Wilfried Diagnostic MRI in Dogs and Cats (VetBooks - Ir)

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ir
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Diagnostic MRI in
Dogs and Cats
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Diagnostic MRI in
Dogs and Cats
WILFRIED MAI, Dr. Méd. Vét., MSc, PhD, Diplomate ACVR,
Diplomate ECVDI
Professor of Radiology
Section Chief of Radiology
University of Pennsylvania
School of Veterinary Medicine
Philadelphia, Pennsylvania
USA
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CRC Press
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Library of Congress Cataloging‑in‑Publication Data
Names: Mai, Wilfried, editor.

Title: Diagnostic MRI in dogs and cats / [edited by] Wilfried Mai.
Description: Boca Raton : CRC Press, [2018] | Includes bibliographical references and index.
Identifiers: LCCN 2017061268 (print) | LCCN 2017061795 (ebook) | ISBN 9781315121055 (General eBook) |
ISBN 9781498737708 (hardback : alk. paper)
Subjects: LCSH: Veterinary radiography. | Magnetic resonance imaging. | MESH: Magnetic Resonance Imaging--veterinary |
Dog Diseases--diagnostic imaging | Cat Diseases--diagnostic imaging
Classification: LCC SF757.8 (ebook) | LCC SF757.8 .D46 2018 (print) | NLM SF 757.8 | DDC 636.089/607572--dc23
LC record available at https://lccn.loc.gov/2017061268
Visit the Taylor & Francis Web site at

http://www.taylorandfrancis.com
and the CRC Press Web site at

http://www.crcpress.com
CONTENTS
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Preface ix
Contributors xi
Abbreviations xii
SeCtion 1 PHYSiCS AnD teCHniCAL ConSiDeRAtionS – iMAGe oPtiMiZAtion
CHAPTER 1 GeneRAL PRinCiPLeS oF MAGnetiC ReSonAnCe iMAGinG 3

Wilfried Mai
CHAPTER 2 iMAGe CHARACteRiStiCS in MRi AnD PRinCiPAL PULSe SeQUenCeS 36

Wilfried Mai
CHAPTER 3 MRi ARtiFACtS 70

J. Fraser McConnell
CHAPTER 4.1 oPtiMiZeD teCHniQUe: BRAin 88

Silke Hecht
CHAPTER 4.2 oPtiMiZeD teCHniQUe: SPine 106

Ruth Dennis
CHAPTER 4.3 GeneRAL FeAtUReS AnD oPtiMiZeD teCHniQUe FoR tHe

MUSCULoSKeLetAL SYSteM 130
Amy R. Zalcman, Cristi Cook, and Wilfried Mai
CHAPTER 4.4 teCHniCAL PARtiCULARitieS WitH LoW-FieLD iMAGinG 153

Wilfried Mai
SeCtion 2 MRi oF tHe BRAin
CHAPTER 5.1 ConGenitAL AnD DeVeLoPMentAL DiSoRDeRS 161

Silke Hecht
vi C on t e n t s
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CHAPTER 5.2 MetABoLiC AnD DeGeneRAtiVe enCePHALoPAtHieS 172

Silke Hecht
CHAPTER 5.3 enCePHALitiS/MeninGoenCePHALitiS 187

Benjamin Young
CHAPTER 5.4 BRAin neoPLASiA 211

Silke Hecht
CHAPTER 5.5 CYStiC ConDitionS 241

Silke Hecht
CHAPTER 5.6 iSCHeMiC BRAin DiSeASe AnD VASCULAR AnoMALieS 251

J. Fraser McConnell
CHAPTER 5.7 BRAin HeMoRRHAGe 282

J. Fraser McConnell
CHAPTER 5.8 BRAin tRAUMA 309

Silke Hecht
CHAPTER 5.9 AGinG CHAnGeS oF tHe BRAin 318

Silke Hecht and Amy Hodshon
CHAPTER 5.10 CRAniAL neRVe DiSeASeS 326

Wilfried Mai
SeCtion 3 MRi oF non-neURoLoGiCAL StRUCtUReS oF tHe HeAD AnD neCK
CHAPTER 6.1 nASAL CAVitY AnD FRontAL SinUSeS 347

Jimmy H. Saunders and Susanne A. E. B. Boroffka
CHAPTER 6.2 eYe AnD oRBit 362

Susanne A. E. B. Boroffka and Jimmy H. Saunders
CHAPTER 6.3 eXteRnAL, MiDDLe, AnD inneR eAR 380

C on t e n t s vii
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CHAPTER 6.4 non-neURoLoGiC ConDitionS oF tHe HeAD AnD neCK 393

SeCtion 4 MRi oF tHe SPine
CHAPTER 7.1 noRMAL MRi SPinAL AnAtoMY, DeGeneRAtiVe DiSC DiSeASe,

AnD DiSC HeRniAtion 413
Wilfried Mai
CHAPTER 7.2 CeRViCAL SPonDYLoMYeLoPAtHY 447

Ronaldo C. da Costa
CHAPTER 7.3 DeGeneRAtiVe LUMBoSACRAL StenoSiS 472

Silke Hecht
CHAPTER 7.4 ConGenitAL AnD DeVeLoPMentAL AnoMALieS AnD MALFoRMAtionS 481

Wilfried Mai
CHAPTER 7.5 inFLAMMAtoRY AnD inFeCtioUS ConDitionS 508

Wilfried Mai
CHAPTER 7.6 SPinAL neoPLASiA 527

Wilfried Mai
CHAPTER 7.7 iSCHeMiC MYeLoPAtHY, SPinAL CoRD HeMoRRHAGe, MYeLoMALACiA 565

Daniela Schweizer-Gorgas
CHAPTER 7.8 eXtRAMeDULLARY CYSt-LiKe ConDitionS oF tHe SPine 584

Wilfried Mai
CHAPTER 7.9 SYRinGoMYeLiA 595

Wilfried Mai
CHAPTER 7.10 MRi oF tHe BRACHiAL AnD LUMBoSACRAL PLeXUSeS 603

Wilfried Mai
CHAPTER 7.11 DeGeneRAtiVe SPinAL DiSeASeS 618

Wilfried Mai
viii C on t e n t s
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CHAPTER 7.12 MRi oF SPinAL tRAUMA 622

Wilfried Mai
CHAPTER 7.13 MRi oF PARASPinAL SoFt tiSSUeS 630

Wilfried Mai
SeCtion 5 MRi oF tHe MUSCULoSKeLetAL SYSteM
CHAPTER 8 MRi oF MUSCULoSKeLetAL DiSeASeS 643

SeCtion 6 MRi oF tHe tHoRAX AnD ABDoMen
CHAPTER 9.1 CARDiAC MRi 687

Wilfried Mai
CHAPTER 9.2 MRi oF non-CARDiAC tHoRACiC ConDitionS 710

Ruth Dennis
CHAPTER 10 ABDoMinAL MRi 723

Wilfried Mai, Ruth Dennis, and Matthew Paek
index 753
PREFACE
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ix
It is my great pleasure and honor to introduce this new this mesmerizing imaging technology. My goal was to select
textbook tackling the vast and increasingly complex topic a few collaborators that are recognized and trusted experts
of clinical magnetic resonance imaging (MRI) in the dog on the topics they would be writing about, either through
and cat. The use of clinical MRI in veterinary medicine is their clinical research experience, publication track record,
no longer the privilege of a few, and the vast majority of or general recognition in the veterinary radiology commu-
university veterinary hospitals worldwide have on-site MRI nity. I was lucky that the people I had elected to collaborate
scanners. In addition, there has been a dramatic increase in all agreed to do so. I was even luckier that they all pro-
the number of veterinary specialty practices that now have vided high-quality contributions, which I had the immense
regular access to MRI capabilities. This has been made even privilege and pleasure to edit and review. Even the chapters
easier with the development of veterinary-specific machines. I wrote were submitted to the scrutiny of a careful editing
With the increasing availability of the technology, there is process by Dr. Silke Hecht from the University of Tennessee
also an increasing need for expertise in interpreting these (former president of the ACVR and former president of
images. Although there have been a large number of sci- the CT & MRI Society). Dr. Hecht is a trusted name in the
entific publications on various aspects of clinical MRI in field of veterinary imaging in general and MRI in particu-
canine and feline practice, there is a paucity of reference lar, with numerous publications and extensive experience on
textbooks that provide a well-illustrated and comprehensive the topic. I cannot thank her enough for taking over this
overview of the current knowledge. task, in addition to contributing many excellent chapters
Having been in the field of veterinary radiology educa- herself. Almost all the contributors are from the radiology
tion for quite a few years now, I saw a need for an updated specialty with a vast expertise in MRI, with the exception of
and thorough text and pictorial review of the current state- Dr. Ronaldo da Costa, chief neurologist at the Ohio State
of-the-art in small animal veterinary MRI. Although MRI University, whom I asked to contribute a chapter on cervical
now constitutes one of six individual examination sections spondylomyelopathy, as he is regarded as a world expert on
at the American College of Veterinary Radiology (ACVR) the topic. Examples of other experts I asked to participate
Specialty board examination, trainees often comment that in this endeavor include Dr. Ruth Dennis, an early pioneer
they are in dire need of a well-documented, evidence-based in the development of clinical veterinary MRI, Drs. Fraser
learning resource. It was to fill this void that I decided to McConnell and Daniela Schweizer-Gorgas, for their expe-
embark on this adventure. rience and knowledge of MRI of ischemic and hemorrhagic
I have been immersed in the field of MRI since my neurologic disorders, Dr. Benjamin Young for his outstand-
younger years when I completed a Masters and then PhD ing publication track record on MRI of inflammatory brain
in Biomedical Engineering, during which I focused more disease, Dr. Susanne Boroffka for her expertise in MRI of
on the physics and basic science aspects of the modality. the orbit, and Dr. Jimmy Saunders for his well-published
I started practicing clinical MRI on a regular basis at the investigative work on cross-sectional imaging of nasal dis-
beginning of my career at the University of Pennsylvania as eases. Dr. Cristi Cook from the University of Missouri con-
an Assistant Professor of Veterinary Radiology, and I sure tributed her vast knowledge on the multimodality imaging
would have loved, back then, to have had access to a good of canine orthopedic conditions, for which MRI is particu-
reference textbook in my learning process. The same strug- larly suitable. Finally, I am indebted to one of my former
gle has been true for many of my earlier radiology trainees. radiology residents, Dr. Matt Paek, for contributing so many
With our gain in experience and comfort, the increasing quality MR images that are the result of his exemplary and
number of quality scientific publications elucidating MRI extensive use of the modality in clinical practice. Through
patterns of various diseases, and the improvement in imag- the careful choice of these collaborators, and a thorough
ing technology, MRI has become much more integrated as a editing process and literature review, I believe that this
routine imaging modality. textbook provides an accurate representation of the current
Still, I had been thinking about putting a group of evidence-based knowledge in veterinary MRI to this date.
experts together to share our experience and summarize Regarding the contents, although countless general refer-
current knowledge to hopefully facilitate the learning of ences exist on the topic, I did not want to pass on dedicating
x P r e fac e
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a few chapters to MRI physics and technology (Section 1), Like Dominique, Corinne always trusted me, even when
because I wanted this book to be a stand-alone reference anyone else would have doubted; her constant and uncon-
for someone to use, whether it be a radiology/neurology ditional support have meant the world to me.
resident in training or a practitioner with a need to learn • Dr. Paul Barthez, my residency mentor/director: he
about veterinary clinical MRI. I tried to keep these chapters trusted I knew something about MRI physics, but he
simple enough, which is challenging because when it comes taught me all the rest.
to MRI, once you pull at the thread there is no end to the • Dr. Allan Johnson, who welcomed me at the Duke
unraveling. My goal was to keep it concise by using many University Center for In Vivo Microscopy. This unbe-
visual aids and diagrams, and trying to avoid abstract con- lievable and amazing human being has got to be the
cepts and equations whenever possible. Within that section, most humble and talented junior researchers’ mentor that
several chapters are dedicated to optimization of imaging I have ever met. His jovial and upbeat attitude, his ‘can-do’
technique and will hopefully be helpful for anyone who is approach, and his insatiable passion to teach, help, mentor,
getting started with MRI scanning, whether it be a veteri- and push his trainees were a true inspiration to me.
nary technologist or a veterinarian. The following book sec-
tions are organized by anatomic regions (brain, head/neck, Of course, no such monumental task could ever be possi-
spine, musculoskeletal, thorax, and abdomen), and within ble to achieve without the help and support of my colleagues
each section, each chapter focuses on a disease category of at PennVet: Drs. Ana Cáceres, Jennifer Reetz, Yael Mosenco,
that body region. I wanted the book to be easily searchable and Jantra Suran; former colleagues Drs. Tobias Schwarz,
and this organization seemed to make the most sense to me. Victoria Johnson, Gabriela Seiler, Jeff Wortman, and
I adopted a ‘bullet-points format’ throughout the book, to Darryl Biery; and the talented imaging technologists that
keep the concepts concise and organized. For the most part, have acquired many of the wonderful images presented in
all the information presented in this book reflects knowl- this book (chronologically, Amy Basatemur, Denise Priore,
edge that is supported by peer-reviewed scientific publi- Russel White, Barb Kaminsky, and Lisa Chant).
cations, which are referenced at the end of each chapter. I also could not have done it without all the residents that
I did not want to deliver a book of ‘opinions’. Such material I was lucky to train over the past 13 years, undoubtedly one
already exists. I wanted to write a book of ‘facts’. Although of the most challenging but also most rewarding parts of
this book is a thorough review of the current knowledge, it my job. They have all in one way or the other shaped me
is also richly illustrated with annotated images showcasing as the instructor and mentor I am today, and have taught
the main features of the disease processes covered in each me so many invaluable lessons. Observing them struggling
chapter. I decided to include images obtained at all magnet with a variety of concepts when it comes to clinical MRI
field strengths, so as to reflect the current reality of veteri- has been an unparalleled resource for me to understand
nary MRI, which uses low-, mid-, and high-field magnets. what works and what doesn’t in terms of teaching this topic,
The magnetic field strength information, where known, is which I hope will translate in this book and help many other
included at the end of each figure caption. residents and practitioners down the road.
I cannot conclude this preface without having a thought Finally, I need to thank my mom and friends who have
for all the mentors that have helped shape my passion for endured my ups and downs over the many years that took
and knowledge of clinical MRI: me to this point and particularly over the past 2 years while
in the process of writing this seemingly never-ending book.
• First and foremost, Dr. Dominique Begon, my radiology A special thank you to my husband Minhtri Thach, who
professor when I was a student and then intern at the has been very patient when the priority of this writing and
École Nationale Vétérinaire d’Alfort in France, who rec- editing process took away from our time together and has
ognized my genuine interest in diagnostic imaging and pushed me so much to make sure it would be the best it
helped me ‘make it happen’. could be.
• Dr. Corinne Fournel, for giving me the unique opportunity I am forever grateful for all these people.
to enroll into an alternative radiology residency training
program under the mentorship of Dr. Paul Barthez. Wilfried Mai
CONTRIBUTORS
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xi
Susanne A. E. B. Boroffka, Dr. med. vet., PhD, J. Fraser McConnell, BVM&S, DVR, Diplomate
Diplomate ECVDI ECVDI, CertSAM, MRCVS
Boroffka Diagnostic Imaging Senior Lecturer in Veterinary Diagnostic Imaging
Utrecht, The Netherlands Small Animal Teaching Hospital
University of Liverpool (Leahurst Campus)
Cristi Cook, DVM, MS, Diplomate ACVR Neston, Cheshire, United Kingdom
Thompson Laboratory for Regenerative Orthopaedics
Missouri Orthopedic Institute Matthew Paek, VMD, MS, Diplomate ACVR
Columbia, Missouri, USA Synergy Veterinary Imaging Partners
Frederick, Maryland, USA
Ronaldo C. da Costa, DMV, MSc, PhD, Diplomate
ACVIM (Neurology) Jimmy H. Saunders, Dr. med. vet., PhD, CertVR,
Professor and Service Head – Neurology and Diplomate ECVDI
Neurosurgery Professor in Medical Imaging
Department of Veterinary Clinical Studies Department of Medical Imaging of Domestic Animals and
The Ohio State University College of Veterinary Medicine Orthopedics of Small Animals
Columbus, Ohio, USA Ghent University Faculty of Veterinary Medicine
Merelbeke, Belgium
Ruth Dennis, MA, VetMB, DVR, Diplomate ECVDI,
FRCVS Daniela Schweizer-Gorgas, Prof. Dr. med. vet.,
Head of the Diagnostic Imaging Unit Diplomate ECVDI
Centre for Small Animal Studies Head of Division of Clinical Radiology
Animal Health Trust Department of Clinical Veterinary Medicine
Newmarket, Suffolk, United Kingdom Vetsuisse-faculty, University of Bern
Bern, Switzerland
Silke Hecht, Dr. med. vet., Diplomate ACVR,
Diplomate ECVDI Benjamin D. Young, DVM, MS, Diplomate ACVR
Professor in Radiology VCA Alameda East Veterinary Hospital
Department of Small Animal Clinical Sciences Denver, Colorado, USA
University of Tennessee College of Veterinary Medicine
Knoxville, Tennessee, USA Amy R. Zalcman, DVM
Resident in Radiology
Amy Hodshon, DVM, Diplomate ACVIM (Neurology) Veterinary Health Center
Assistant Professor in Neurology and Neurosurgery University of Missouri
University of Tennessee College of Veterinary Medicine Columbia, Missouri, USA
Knoxville, Tennessee, USA
Wilfried Mai, Dr. Méd. Vét., MSc, PhD, Diplomate

ACVR, Diplomate ECVDI
Professor and Chief of Radiology
University of Pennsylvania School of Veterinary Medicine
Philadelphia, Pennsylvania, USA
ABBREVIATIONS
xii
ADC apparent diffusion coefficient MHz megahertz

ADM ascending/descending myelomalacia MPS mucopolysaccharidosis
AHNPE acute hydrated nucleus pulposus extrusion MRA magnetic resonance angiography
ATP adenosine triphosphate MRCP magnetic resonance cholangiopancreatography
AVM arteriovenous malformation MRI magnetic resonance imaging
bFFE balanced fast field echo MRS magnetic resonance spectroscopy
CAA ceroid amyloid angiopathy MRV magnetic resonance venography
CBF cerebral blood flow MTT mean transit time
CKCS Cavalier King Charles Spaniel NCL neuronal ceroid lipofuscinosis
CME canine monocytotropic (or monocytic) ehrlichiosis NE necrotizing encephalitis
cMRI cardiac MRI NEX number of excitations
CNS central nervous system NLE necrotizing leukoencephalitis
CPP cerebral perfusion pressure NME necrotizing meningoencephalitis
CSF cerebrospinal fluid NMR nuclear magnetic resonance
CSM cervical spondylomyelopathy N FE number of pixels in the FE direction
CVR cerebrovascular resistance N PE number of pixels in the PE direction
CVT cerebral vein thrombosis NSA number of signal averages
dGEMRIC delayed gadolinium enhanced MRI of cartilage OA-CSM osseous-associated cervical spondylomyelopathy
DISH diffuse idiopathic skeletal hyperostosis PC VIPR phase-contrast vastly undersampled isotropic
DSH domestic short-haired (cat) projection reconstruction
DTI diffusion tensor imaging PD proton density
DWI diffusion-weighted imaging PDW proton density-weighted
ECG electrocardiogram/electrocardiography PE phase-encoding
EPI echoplanar imaging PNET primitive neuroectodermal tumor
FCD focal cortical dysplasia PNST peripheral nerve sheath tumor
FCE fibrocartilaginous embolism PRF pulse repetition frequency
FCEM fibrocartilaginous embolic myelopathy PWI perfusion-weighted imaging
FE frequency-encoding rBW receive bandwidth
FFE fast field echo rCBF relative cerebral blood flow
FID free induction decay RF radiofrequency
FISP fast imaging with steady-state precession ROI region of interest
FISS feline injection site sarcoma SCC squamous cell carcinoma
FLAIR fluid attenuated inversion recovery SE spin echo
FLASH fast low angle shot SE-EPI spin echo EPI
FMPGR fast multiplanar gradient recalled acquisition in the SNR signal-to-noise ratio
steady state SPAIR spectral attenuated inversion recovery
fMRI functional MR imaging SPIR spectral presaturation with inversion recovery
FOV field of view SSFP steady state free precession
FROMS feline restrictive orbital myofibroblastic sarcoma SS-FSE single shot fast spin echo
FSE fast spin echo STIR short tau inversion recovery
GE FISP gradient echo fast imaging with steady-state SWI susceptibility-weighted imaging
precession T1W T1-weighted
GFE frequency-encoding gradient strength T2W T2-weighted
GME granulomatous meningoencephalomyelitis TBI traumatic brain injury
GPE phase-encoding gradient strength TE time of echo (or echo time)
GRE gradient echo TI time from inversion/inversion time (tau)
GRE-EPI gradient echo EPI TIA transient ischemic attack
HASTE half Fourier acquisition single shot turbo TOF time of flight
spin echo TR repetition time
HPE holoprosencephaly TSE turbo spin echo
IR inversion recovery TTP time to peak signal loss
IVDD intervertebral disc disease VOX volume of the voxels
SECTION 1
PHYSICS AND TECHNICAL

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CONSIDERATIONS – IMAGE
OPTIMIZATION
CHAPTER 1 General principles of magnetic resonance imaging
CHAPTER 2 Image characteristics in MRI and principal pulse sequences
CHAPTER 3 MRI artifacts
CHAPTER 4.1 Optimized technique: brain
CHAPTER 4.2 Optimized technique: spine
CHAPTER 4.3 General features and optimized technique for the

musculoskeletal system
CHAPTER 4.4 Technical particularities with low-field imaging

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CHAPTER 1
GENERAL PRINCIPLES OF MAGNETIC

RESONANCE IMAGING 3
Wilfried Mai
CONTENTS
Atomic and nuclear structure.....................................................................................................................................................................................3
What is magnetism? ..................................................................................................................................................................................................4
Spins – magnetic moment ........................................................................................................................................................................................4
Spin angular momentum ...........................................................................................................................................................................................5
The net magnetization (M0): spin-up and spin-down.................................................................................................................................................6
Transverse (Mxy) and longitudinal (Mz) components of the net magnetization ...........................................................................................................8
Measuring the net magnetization: magnetic resonance .............................................................................................................................................9
The return to equilibrium: spin-lattice and spin-spin relaxation .............................................................................................................................. 11
The longitudinal relaxation time: T1 ........................................................................................................................................................................ 12
The transverse relaxation time: T2 ........................................................................................................................................................................... 13
The free induction decay ......................................................................................................................................................................................... 13
T2* versus T2.......................................................................................................................................................................................................... 15
A basic pulse sequence: the spin echo, or how to measure the true T2 ................................................................................................................... 15
What about the repetition time? ............................................................................................................................................................................... 17
The MR image: field of view, matrix, pixel, and voxel ............................................................................................................................................. 18
From image to spatial frequencies: notion of Fourier transform .............................................................................................................................. 19
Spatial encoding: slice selection .............................................................................................................................................................................21
Spatial encoding: notions of frequency-encoding and phase-encoding .................................................................................................................. 24
A bit more about phase-encoding ...........................................................................................................................................................................26
The frequency domain, or k-space, and its relationship to the MR image ...............................................................................................................28
Further reading........................................................................................................................................................................................................35
It is beyond the scope of this textbook to provide in-depth ATOMIC AND NUCLEAR STRUCTURE
details regarding the physics of magnetic resonance imag-
ing (MRI). There are a large number of textbooks, scien- • Atoms are made of a nucleus and orbiting electrons.
tific articles, and free online resources available for readers • The nucleus itself consists of protons and neutrons.
who are interested in a more detailed description. However, • The electrons have a negative charge and weigh about
we will explain the basics and go over the material that is 2,000 times less than protons and neutrons; protons
important for radiologists to understand: have a positive charge while the neutrons have no charge
(Table 1.1).
• The basic principles of nuclear magnetic resonance and the • The number of protons in a nucleus defines the identity
phenomenon of relaxation (longitudinal and transverse). of the element: for example, all hydrogen atoms contain
• The concepts of image formation, and how they influ- 1 proton, all carbon atoms contain 6 protons. This num-
ence image quality such as signal-to-noise ratio, image ber is called the atomic number, Z.
contrast, and spatial resolution. • The total number of protons and neutrons in an atom is
• The mechanisms and pros/cons of the essential pulse called mass number, A.
sequences often used in diagnostic imaging. • Two atoms with the same number of protons but a differ-
• Common image artifacts and prevention/correction. ent number of neutrons are called isotopes.
4 CHAPTER 1
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veterinary patients such as identification microchips,

Table 1.1 Mass and charges of atomic particles. surgical implants, and ballistic projectiles.
• Paramagnetism: refers to materials with some ions
PARtiCLe MASS (g) CHARGe with unpaired electrons such as ions of various metals
Proton 1.6727 × 10 −24 +1 like Fe (iron), Mg (magnesium), and Gd (gadolinium).
Neutron 1.6750 × 10−24 0 The electronic magnetic moment due to the unpaired
Electron 9.110 × 10−28 −1
electrons confers on these ions a positive magnetic
susceptibility capable of effecting magnetization of
other structures around them. This magnetic suscep-
tibility is much less than that of ferromagnetic mate-
• It is customary to represent an element X as A X: X defines rials, but sufficient to cause effects on MR images.
the element (i.e., its number of protons) and A defines This is exploited with some of these ions being used
which isotope of the element is considered. For example, as MRI contrast agents (gadolinium).
13C (six protons) is the isotope of carbon that contains • Super-paramagnetism: these are materials made of
seven neutrons; the most abundant isotope of carbon in discrete individual domains of elements that, when in
nature is 12C (six protons and six neutrons). bulk, have ferromagnetic properties. This results in a
positive magnetic susceptibility that falls somewhere
WHAT IS MAGNETISM? between that of ferromagnetic and paramagnetic
materials; some of these can be used as contrast agents
• Magnetism and displacement of an electric charge can in MRI, such as super-paramagnetic iron particles.
be related to each other: an electrical current running • Diamagnetism: refers to materials that do not possess
through a cable generates a magnetic field that one can intrinsic atomic magnetic moment but, when placed
detect by placing a compass in the vicinity. Conversely, in a strong external magnetic field, slightly repel the
an electrical current can be induced by placing a bar field, resulting in a negative magnetic susceptibility.
magnet in the center of a solenoid cable. Water and most biologic tissues are diamagnetic.
• Magnetism is a fundamental property of matter, caused
by the orbiting electrons at the atomic level. These orbit- SPINS – MAGNETIC MOMENT
ing electrons can cause atoms to possess a small magnetic
field called ‘magnetic moment’. • All fundamental particles (electrons, protons, neutrons)
• In a nucleus, the nucleons (protons and neutrons) rotate spin around their own axis and, therefore, as a result of
around their axis and, given the existence of electric electromagnetism, they have an associated magnetic field
charges, you can already see how the nucleus of an atom called ‘magnetic moment’ or ‘magnetic dipole moment’
also has the potential of intrinsic magnetic properties. (Fig. 1.1). This property is called ‘spin’.
• The units to measure magnetic fields are the Gauss (G) • Spin is a fundamental property of nature, like mass or
and Tesla (T), the official SI unit being the Tesla. The charge. It comes in multiples of ½ and can be positive or
Tesla is defined as such: a particle carrying a charge of 1 negative. Individual unpaired electrons, neutrons, and
Coulomb and passing through a magnetic field of 1 Tesla protons have a spin of +½ or −½.
at a speed of 1 meter per second perpendicular to said • Note that neutrons, although devoid of a net charge,
field experiences a force with magnitude 1 Newton. do possess a magnetic moment (non-zero spin). This
is because at the sub-particle level, they are made (like
1 Tesla ≈ 10,000 Gauss protons) of quarks, which are electrically charged; the
• The Earth’s magnetic field is about 0.5 Gauss or 5 × 10 −5 total charge of a neutron’s quarks is zero, but their spa-
Tesla; compare this with the magnetic field strengths tial distribution within the neutron generates a magnetic
used in high-field MRI, typically 1.5 to 3 Tesla. This is moment when the neutron spins. The magnetic moment
about the strength of electromagnets used to pick up cars of a neutron is equal to about two-thirds that of a proton.
in junk yards. • Particles with similar spin can pair up, with their mag-
• Magnetic properties of materials vary depending on netic moments facing opposite directions, in the same
their composition, and in MRI four different types of way that two identical little magnets would. This in turn
magnetic properties are typically encountered: eliminates the observable manifestations of their indi-
• Ferromagnetism: materials that have a large positive vidual spins. In a nucleus, protons (as well as neutrons)
magnetic susceptibility. When they are placed in a form pairs and their individual magnetic moments cancel
magnetic field, the field strength is much stronger each other out (Fig. 1.2).
inside the material than outside; such materials typ- • As a result, all isotopes that contain an odd number of pro-
ically contain iron, nickel, or cobalt, and include tons and/or neutrons possess an intrinsic ‘nuclear magnetic
magnets and various objects that can be found in moment’ and ‘nuclear spin angular momentum’ (see below),
G e n e r a l P r i nc i pl e s of M ag n e t ic R e son a nc e I m agi ng 5
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North • There are two reasons why hydrogen protons (1H) are
very good for MRI:
m • They are abundant in biologic tissues due to their
richness in water molecules;
• They have the ability to generate a relatively strong
NMR signal compared with other elements that have
H+ a non-zero spin.
• ‘Nuclear magnetism’ refers to the fact that a nucleus with
a non-zero spin will behave as a little bar magnet, with
magnetic field lines around it (Fig. 1.1). This magnetic
field can be described by a vector, where the length of
South the vector describes the magnitude of the magnetic field
generated, and the direction of the vector describes the
Fig. 1.1 The hydrogen atom contains one single proton; as
orientation of the magnetic field generated. Much like
this proton spins around its axis, it generates a small magnetic
the needle of a compass, when that nucleus is placed in a
field, and behaves as a little bar magnet with a magnetic
strong external magnetic field B0, its magnetization vec-
moment vector pointing south to north.
tor will try to align itself parallel to the direction of the

external magnetic field vector B0 .
and can be used for nuclear magnetic resonance (NMR)
experiments. They are said to have a ‘non-zero spin’; spin is
a quantum mechanical feature of the nucleus. In contrast, all SPIN ANGULAR MOMENTUM
isotopes with an even number of protons and neutrons have
an intrinsic nuclear magnetic moment of zero (Fig. 1.2). • If you place a spinning top on a table and spin it, it will
• For example, carbon 13C (seven neutrons [i.e., three pairs quickly deviate from the vertical axis due to interactions
of neutrons + one unpaired neutron] and six protons [three between the rotational force and the gravitational force, and
pairs]) has magnetic properties that make it usable in will start to wobble around the vertical axis. In the absence
NMR, while 12C (three pairs of neutrons and three pairs of friction (which will eventually make it stop spinning and
of protons) does not. fall), it would continue to spin and wobble around the ver-
• In MRI, the signal is derived from hydrogen protons tical axis at a specific angle to that axis due to its specific
(1H, one unpaired proton). In NMR spectroscopy, other ‘angular momentum’, which depends on its mass (Fig. 1.3).
elements can be used to generate an NMR signal, such • There is an analogous property of small nuclear particles
as certain isotopes of phosphorus (31P), carbon (13C), with a non-zero spin that is proportional to their mass,
sodium (23Na), or fluorine (19F). and this is called ‘spin angular momentum’. Because
N S + + =0
N N =0
S N
PAIRED MAGNETS HELIUM NUCLEUS HYDROGEN NUCLEUS

Their opposite poles 2 paired protons (+) 1 unpaired proton
attract each other 2 paired neutrons (N) → Non-zero magnetic moment
→ No magnetic moment
Fig. 1.2 Left: identical bar magnets pair up with their opposite poles, matching up so that their magnetic fields cancel each
other. Middle: the same phenomenon happens in a nucleus with an even number of neutrons and protons; in this example, the
helium nucleus contains two paired protons and two paired neutrons, and therefore has no net magnetic moment. Right: the
hydrogen nucleus contains a single (thus unpaired) proton and therefore possesses a magnetic moment.
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Fig. 1.3 The top is spinning around

its own axis (red arrow). Due to the
interaction of the mass of the spinning
top with the gravitational force, the
rotating axis of the spinning top
has a gyration pattern (blue arrow)
around the axis of the force of gravity
(green arrow). That gyration motion
is called ‘precession’.
Precession motion
B0
Spinning motion of the proton

Fig. 1.4 The spin angular momentum
of a particle with a non-zero spin
causes it to precess around the axis of
the strong external magnetic field B0.
of the spin angular momentum, when a nucleus with a

non-zero spin is placed in an externally applied magnetic
( )
f0 ( MHz ) = γ MHz.Tesla −1 × B0 ( Tesla )
field, it is not perfectly aligned parallel to the external
ω 0 = 2 × π × f0
magnetic field; instead, the angular momentum forces it
to wobble around the magnetic field. The envelope of the • γ is the ‘gyromagnetic ratio’, and is unique for an ele-
trajectory of the spin magnetic vector is therefore cone- ment; for hydrogen protons:
shaped; this particular motion due to the spin angular • γ = 2.67 × 108 rad.s−1.T−1
momentum is called ‘precession’ (Fig. 1.4). • γ = 42.57 MHz.T−1
• Note that the spinning motion of the particle exists even • For example, in a magnetic field of 1 Tesla, the preces-
in the absence of an external magnetic field, but there sion motion of hydrogen protons will be at a frequency of
is no precession in that case. Spin angular momentum 42.57 MHz, or 42.57 million rotations per second.
exists even in the absence of an external magnetic field • The equation ω0 = γ × B0 is called the ‘Larmor equation’.
as an intrinsic property of spins; it is the interaction • ω0 is called the ‘Larmor frequency’.
between the spin angular momentum and the external
magnetic field that causes the motion of precession. THE NET MAGNETIZATION (M0):
• The frequency (ω0, in radians per second [= angular SPIN-UP AND SPIN-DOWN
frequency], or f 0 in megahertz [number or rotations per
second]) of that precession motion is a function of the • Regardless of the body part being imaged, some prin-
particle and the strength B0 (Tesla) of the externally ciples always apply in MRI. The basic principle relies on
applied magnetic field: placing a patient in the bore of a magnet and generating
a signal: the NMR signal.
( ) ( )
ω 0 rad.s−1 = γ rad.s−1.Tesla−1 × B0 ( Tesla ) • Consider a sample of protons (hydrogen nuclei). Outside
of an externally applied magnetic field, at the equilibrium

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the direction of the external magnetic field vector B0 .

However, due to quantum mechanics constraints, they
will not all have the same orientation; some spin vectors

will be pointing in the direction of B0 (‘spin-up’ or paral-
lel), and some in the opposite direction (‘spin-down’ or
anti-parallel).
M0 = 0 • This is different from what physical bar magnets would
do in a magnetic field where they would all be aligned
in the direction of the external magnetic field; this is
because protons obey the rules dictated by ‘quantum
physics’, as opposed to bar magnets, which obey the rules
of ‘classic mechanics’.
• Note that, in reality, the individual spin vectors are pre-

cessing around the direction of B0 , with the tip of the
Fig. 1.5 A theoretical sample of a few protons (hydrogen vectors describing a circular trajectory, the plane of
nuclei). In the absence of a strong external magnetic field,
the circle being perpendicular to the direction of B0
they are oriented in a random fashion so that the sum of their
(Fig. 1.6).
individual magnetization vectors, called the net magnetization
• The reason why the protons, when placed in an external
vector (M0), is equal to 0.
field, can exist in one of these two states is a result of
quantum mechanics physics, which dictate that a particle
state, the magnetic field vectors of protons are oriented with a spin value of s can exist in [2s + 1] orientations,

randomly, so that the vector sum M 0 (macroscopic mag- or ‘states’, when placed in an external magnetic field.
netization, or ‘net magnetization vector’) of the mag- Since protons have a spin of ½, they can adopt two states,

netic fields of all individual protons would equal zero or orientations, when placed in B0 .
(Fig. 1.5). This is the reason why a biologic tissue sample • The population of protons is distributed about equally
at rest has no measurable magnetization. between the spin-up and spin-down groups, but because
• When placed in a strong external magnetic field (B0), a the energy required to remain at the spin-down level
non-zero magnetization is created in the sample of pro- (anti-parallel) is slightly higher, there is a slight excess of

tons, the direction of which is parallel to that of B0 . We protons in the spin-up orientation than in the spin-down.
say that the sample of protons is now ‘magnetized’. This results in the overall sample of protons gaining a

• That net magnetization is due to the fact that, like the net magnetization vector M 0 that is oriented parallel to,

needle of a compass, protons will become parallel to and pointing in the same direction as, B0 (Fig. 1.6).
y
Mz DOWN
x UP UP
Mxy = 0
UP DOWN
B0
DOWN
DOWN
M0
UP
NUP = 5 UP
NDOWN = 4

Fig. 1.6 When placed in a strong external magnetic field B0 , the individual spin vectors are precessing around the direction

of B0 , with the tip of the vectors describing a circular trajectory, the plane of the circle being perpendicular to the

direction of B0 . There is a slight excess of spin-ups versus spin-downs (in this case 5 versus 4), resulting in a non-zero net
magnetization vector M0.
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• According to Boltzmann’s statistics, the ratio between

the number of spins up (Nup) and spins down (Ndown) z
depends on the energy difference (ΔE) between the two
states and the temperature (T) as follows, where kb is the ω0 y
Boltzmann constant:
B0
 ∆E 
N up   z component
= exp k b .T 
N down y component
• The energy difference ΔE between the two states depends
x
on the strength of the magnetic field B0. At the tempera- x component
ture of the human body, and in a 1.5 T magnetic field,
the ratio would be equal to 1.000004, which means that
for every 1 million protons in the anti-parallel direction,
there are one-million-and-four protons in the parallel
direction.
• As you may imagine, the ‘net magnetization’ created by
such a minor difference is pretty small. One could cal-
culate that, assuming the human head has a volume of
Fig. 1.7 Schematic representing a proton oriented parallel
1,500 mL and is made of 80% water, the net magneti-
to B0 and precessing around it, in a Cartesian coordinates
zation at B0 = 1.5 T would be about M0 = 20 μT. This
system (x,y,z). One can consider two vectorial components to
is 75,000 times weaker than the main magnetic field B0.
the magnetic moment vector of that spin. The z component
Thus, specific strategies will be needed to extract such a
is the projection onto the z-axis and the xy component is
weak signal from the strong background created by B0.
the projection onto the (x,y) plane. Note that as the proton
• The magnitude of M 0 depends on the amplitude of the precesses around B0, the z component remains constant and
magnetic field B0, the density of protons in the sample static, while the (x,y) component (red vector) will rotate in the
(proton density [PD]), the temperature T, and the gyro- plane (x,y) at the precession frequency.
 γ 
magnetic ratio γ  =  of the element at hand (h is the
 2π 
Planck constant and kb the Boltzmann constant):
• In that system, once placed in the magnetic field B0 , the
M0 = B0 × PD ×
( γ .h ) 2
protons will all individually precess around the direction
4.k b .T of the z-axis. Although they all have the same preces-
• This relationship shows that: sion frequency ω0, they are doing so incoherently: they are
• Higher magnetic field B0 yields higher net mag- said to not be ‘in phase’, so that the projection of their
netization M0 in a given sample of tissue, hence the magnetic vectors onto the (x,y) plane makes up a group
MRI signal will be better in a 1.5 T MRI (high-field of vectors with random directions and equal magnitude.
magnet) machine than in a 0.2 T MRI (low-field • As a result, the sum of the projections of these vectors
magnet) machine. in the (x,y) plane equals zero; in other words, the total
• Higher PD yields higher net magnetization: tissues component of the net magnetization in the (x,y) plane
rich in protons, such as highly hydrated tissues, will at equilibrium, called the ‘transverse magnetization’, is
be more magnetized and produce more signal than zero: M xy = 0.
tissues with poor PD. You can already start to under- • On the other hand, the projection of the individual pre-
stand why MRI has high sensitivity to pathology; for cessing spin vectors onto the z-axis is either a vector

example, brain edema, richer in water than normal pointing in the direction of B0 (spin-up) or 180° opposite
brain parenchyma, will be readily detectable with (spin-down), and all of these projections have the same
MRI. amplitude, so that the sum of an up-projection and a
down-projection equals zero; since there is a slight excess
of spin-ups in the sample, the resulting vector sum along
TRANSVERSE (Mxy) AND LONGITUDINAL
the z-axis, also called ‘longitudinal magnetization’, Mz,
(Mz) COMPONENTS OF THE NET
is a positive vector pointing in the same direction as B0 .
MAGNETIZATION (Fig. 1.7) • From this it becomes clear that, at equilibrium, there

• Let us consider an (x,y,z) Cartesian coordinate system, exists a net magnetization vector M 0 , which is aligned

with the z-axis parallel to the main magnetic field B0 , exactly with the main magnetic field B0 . The compo-

and the (x,y) plane perpendicular to the direction of B0 . nents of that net magnetization vector in the (x,y) plane
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(transverse magnetization) and along the z-axis (longitu- ω0 = γ × B0. This frequency is called the ‘resonance fre-
dinal magnetization) are such that (Fig. 1.6): quency’. For the experiment to work, the RF pulse and
the protons have to be ‘in resonance’.
M xy = 0 • To understand the concept of ‘resonance’, think about
pushing a child on a playground swing; the swing has an
Mz = M0 intrinsic oscillating frequency that depends on its length
and load. If you swing the child at the same frequency as
MEASURING THE NET MAGNETIZATION: the natural frequency of the swing, you are very efficient
MAGNETIC RESONANCE in transferring energy to the swing; however, if you try
• As you have probably guessed, the aim of MRI will be to to do it ‘out-of-tune’ with regard to the frequency of the
measure the net magnetization in individual voxels, made swinging pattern, it will be less efficient, more difficult
of packets of tissue with different densities of protons, or even counterproductive. The energy transfer will be
and protons with different magnetic behaviors depend- maximum when you swing the child at the exact same
ing on their physicochemical environment. frequency as the natural frequency of the swing (i.e.,
when you are in ‘resonance’ with the swing).
• The net magnetization vector M 0 that we defined in the
previous paragraphs is of much smaller magnitude than • When the RF pulse is applied, two things happen (quan-
tum mechanics interpretation):
the main magnetic field B0 it is parallel to, and therefore
1. The system is provided with energy, allowing
it is virtually impossible to measure that magnetization
more and more protons to transition from the
as this tiny signal is so much smaller than B0.
spin-up (lower energy) to the spin-down (higher
• The strategy to measure that magnetization is to flip the
energy) orientation; the net result of this is that the
net magnetization vector M 0 into a plane perpendicular longitudinal component Mz of the net magnetization

to B0 . Indeed, the projection of B0 in a plane perpendicu- M0 is progressively decreasing, as there are fewer and
lar to it will be null, and therefore if one can selectively fewer protons in the spin-up orientation. When there
shift the net magnetization from its original longitudinal is an equal number of protons in the spin-up as in the
orientation to a plane perpendicular to it, it will become spin-down orientation, the longitudinal component
measurable without being ‘hidden’ by the intense mag- of the net magnetization becomes null.

netic field B0 . For measurement, we will need to use a 2. The precession motions of individual protons are more
detector that only measures magnetic fields in the trans- and more ‘in-phase’ with each other; as a result, the
verse plane. transverse components of the spin vectors are not
• The property used to achieve this goal relies on ‘magnetic oriented randomly in the (x,y) plane anymore, and
resonance’. As you remember, when placed in a strong therefore their sum, the transverse magnetization M xy,
magnetic field, the protons align themselves along the is not equal to 0 and progressively increases. When all

direction of B0 , with about half parallel to (spin-up) and protons in the sample are ‘in-phase’, M xy reaches its

half anti-parallel (spin-down) to the direction of B0 . There maximum value equal to the original magnitude of the
is a slight excess of protons in the ‘spin-up’ orientation, net magnetization, M0.
because this energy level is slightly less than the ‘spin- • The net result of these phenomena is that the net mag-
down’ orientation. The energy difference, ΔE, between netization vector will progressively tilt away from the
the two states is directly proportional to the strength of initial orientation, with its tip describing a spiral motion
the magnetic field B0. that fits in a sphere, from the north pole of that sphere
• One can force protons to transition between the energy to its equator (Fig. 1.8). After a 90° pulse it will end up
levels by providing energy to the sample of protons, equal being completely in the (x,y) plane, perpendicular to both

to the energy difference ΔE between the two states. This B0 and B1 and, like B1, rotating at the Larmor frequency

energy is provided in the form of an electromagnetic in that plane (Figs. 1.8, 1.9). The vector M 0 is said to be

radiation, which is a rotating magnetic field B1. This ‘flipped’ away from B0 .
rotating (or oscillating) magnetic field is: • As this happens, the longitudinal component of the net

• Generated by a radiofrequency (RF) pulse within the magnetization vector M 0 (Mz) progressively decreases,
transmit coil of the MR system. while its transverse component (M xy) progressively

• Perpendicular to B0 (i.e., in the (x,y) plane). increases. M xy reaches a maximum value when M 0 is

• Rotating around the axis of B0 (= the z-axis), at the completely in the transverse (x,y) plane, and its ampli-
Larmor frequency of protons. tude is then equal to the amplitude of the longitudinal
• The principle of resonance is that the protons will only magnetization at equilibrium: M0. At that point in time,
transition between the energy levels if the RF pulse is the longitudinal component Mz of the net magnetization

applied at the proton’s Larmor, or precessional, frequency vector M 0 is equal to 0 (Fig. 1.9).
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B0
M0
M0
M0
During the application of the RF pulse, After a certain time, the magnetization If the RF pulse is kept on, the
the extremity of the magnetization vector vector M0 is completely shifted in the magnetization vector M0 continues
M0 is describing a spiral along the surface transverse plane, the equatorial plane its path along the southern hemisphere
of a sphere, and progressively shifting of the sphere: this is a 90° pulse until it reaches a direction completely
away from B0 opposite to the equilibrium and
to B0: this is a 180° pulse
Fig. 1.8 Trajectory described by the net magnetization vector M0 during the application of the RF pulse.
z z z
M0 M0
y y
90°
y alpha
Mz
MXY Mxymax = M0
x B1 x B1 x
Mxy = M0
Mz = 0
T=0

Fig. 1.9 During the application

of the RF pulse (using a rotating magnetic field B1 ), the longitudinal component of the
net magnetization vector M 0 (Mz) progressively decreases, while its transverse component (M xy) progressively increases.

M xy reaches a maximum value when M 0 is completely in the transverse (x,y) plane, and its amplitude is then equal to the
amplitude of the longitudinal magnetization at equilibrium: M0. At that point in time, the longitudinal component of the net

magnetization vector M 0 is equal to 0, and both M 0 and B1 (perpendicular to each other) are rotating in the transverse (x,y)
plane, at the Larmor frequency.
α is called the ‘flip angle’ and depends on the gyromag-
• If one measures the angle α between M 0 and B0 (z-axis)
during this process, one can observe a steady increase netic ratio, the magnitude of the rotating magnetic field
B1, and the time t that B1 is applied for:
in the value of α from 0 to 90° as M 0 transitions from

being parallel to B0 into the (x,y) plane; the net value of α = γ × B1 × t
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increase in the transverse magnetization M xy until a

Table 1.2 Changes in amplitude of the longitudinal maximal amplitude, equal to M0.
and transverse components
of the net
magnetization vector M0 , depending on the flip • This state is unstable, so that as soon as the RF pulse
angle. stops, these two separate processes are reversed, and the
system returns to equilibrium (stable state):
eQUiLiBRiUM 90˚ PULSe 180˚ PULSe • There are transitions between the two energy levels,
Mz M0 0 −M0 which restore a slight excess of spin-ups in the sample
(maximum) (minimum) (maximum, negative) (the spin-up state is more stable [lower energy] than
Mxy 0 M0 0
the spin-down) and therefore allow the longitudinal
(minimum) (maximum) (minimum) magnetization to progressively grow back to its initial
and maximum value, M0; this phenomenon is called
‘longitudinal, or spin-lattice, relaxation’ because it
relies on energy exchange between the protons and
• If the RF pulse continues to be applied after M 0 has the molecules in their environment (lattice).
been flipped into the transverse plane (a ‘90° pulse’), • The protons undergo progressive dephasing due to
the magnetization vector will continue its course, with local magnetic field inhomogeneities induced by the
its tip describing a spiral along the surface of the south- movement of adjacent spins due to molecular vibra-
ern hemisphere (Fig. 1.8), down to a point where it will tions, rotations, or collisions (Brownian motion). This

be oriented completely parallel to B0 but in a direction results in a rapid decrease in amplitude of the trans-
completely opposite. This corresponds to a flip angle of verse magnetization M xy; this phenomenon is called
α = 180° (a ‘180° pulse’, also called an ‘inversion pulse’). ‘transverse, or spin-spin, relaxation’. The term ‘spin-
• The duration of the RF pulse is very short, in the order spin’ conveys the fact that this relaxation is because
of a few milliseconds. The longer the RF pulse is applied, of interactions between protons, due to the different
the larger the flip angle α. molecular environments they are in, causing local var-
• Table 1.2 describes the changes in amplitude of the longi- iations in the magnetic field the protons experience
tudinal and transverse components of the net magnetiza- (B0 +/− delta); these microvariations in the local mag-
netic field change the precession frequency of individ-
tion vector M 0 , depending on the flip angle.
ual protons due to the Larmor equation (ω = γ × B0),
• Note that, given the relationship between the ‘flip angle’, which in turn causes rapid dephasing of the protons
the amplitude of the RF pulse (B1), and the duration of in any given voxel. These local inhomogeneities are
the pulse (t) [α = γ × B1 × t], the same flip angle can be the same reason why, at equilibrium, the protons are
obtained with various combinations of amplitude of B1 precessing out-of-phase, resulting in a null value of
and application time t. In practice, stronger pulses are the transverse magnetization.
used to increase flip angles, in order to maintain minimal • Due to the relaxation phenomena, after a 90° RF pulse
image acquisition times. there is an exponential regrowth of the longitudinal mag-
• The principal benefit of the magnetic resonance experi- netization Mz and an exponential decrease of the transverse
ment is that it shifts the net magnetization into a plane
magnetization M xy (Figs. 1.10, 1.11). These phenomena
that is now perpendicular to B0 and, since B0 has no are due to two separate processes, respectively: (1) energy
vector component in that plane, the net magnetization exchange between protons and microenvironment (lat-
becomes measurable; therefore, now, the magnetic prop- tice), and (2) rapid dephasing of the precession motion of
erties of every single voxel of the patient become, in the- the protons. Because these processes are independent, the
ory, measurable. rate of regrowth of the longitudinal magnetization Mz is
not the same as the rate at which the transverse magneti-
THE RETURN TO EQUILIBRIUM: SPIN- zation M xy decreases after the end of the RF pulse.
LATTICE AND SPIN-SPIN RELAXATION • The rate of Mz regrowth is characterized by a specific
time, called T1 (‘longitudinal relaxation time’), which
• In the previous paragraph we saw that, during a 90° RF is the time it takes for the longitudinal magnetization
pulse, the net magnetization is shifted into the transverse to reach 63% of its original amplitude before the RF
(x,y) plane, and that this is the result of two phenomena: pulse was applied (which, as you remember, equals the
1. Energy absorption (from the RF pulse) allowing spin- amplitude of the equilibrium net magnetization M0)
ups to transition to the spin-down state until there is (Fig. 1.10). After a 90° pulse, Mz regrows as a function of
an equal number of spins ‘up’ and ‘down’, leading to time (t) according to the following equation:
nulling of the longitudinal magnetization Mz.
2. Synchronization of the precession motion of the  −
t

Mz ( t ) = M0 ×  1 − e T1 
protons, which now precess ‘in-phase’, leading to an  
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Longitudinal magnetization
Mz = 100% = M0
95%
87%
Fig. 1.10 T1 relaxation curve
showing the exponential
63%
regrowth of the longitudinal
magnetization after a 90°
RF pulse. The T1 relaxation
time is a characteristic of
specific biologic tissues and
T1 2xT1 3xT1 4xT1 Time corresponds to the time after
500–1,000 ms which 63% of the maximum
in biologic tissues value at equilibrium, M0, is
reached.
Transverse magnetization
Mxy= 100% = M0
Fig. 1.11 T2 relaxation curve

showing the exponential
decrease of the longitudinal
magnetization after a 90°
37%
RF pulse. The T2 relaxation
13% time is a characteristic of
5% specific biologic tissues and
corresponds to the time after
T2 2xT2 3xT2 4xT2 Time
which 37% of the maximum
50–100 ms in
biologic tissues value at equilibrium, M0, is
reached.
• The rate of M xy decay is characterized by another of 500–1,000 ms. T1 depends on molecular structure
specific time, called T2 (‘transverse relaxation time’), as well a solid or liquid state of tissues; for example, T1
which is the time it takes for the transverse magnetiza- tends to be longer in fluids than in solids and is shorter
tion to decrease by 63% of the amplitude it had at the for fatty versus non-fatty tissues.
end of the RF pulse (which equals the amplitude of the • Tissues have specific T1 because, due to their molecular
net magnetization M0) (Fig. 1.11). In other words, at a structures or state (liquid or solid), the Brownian motion
time of T2 after the end of the RF pulse, M xy will be of the molecules (translations, rotations, collisions) varies
equal to 37% of the maximum value it had at the end significantly between different tissues. The frequency of
of the 90° pulse (M0). At the end of the 90° pulse, the these molecular collisions has an influence on the ability
transverse magnetization M xy decreases as a function of of the protons to exchange energy with the lattice during
time according to the following equation: the relaxation period:
• When the natural frequency of molecular collisions
t t
− − in the tissue is close to the Larmor frequency of
M xy ( t ) = M xy _ max × e T2 = M0 × e T2
protons (condition of ‘resonance’, which maximizes
energy transfer), the energy exchange during relaxa-
THE LONGITUDINAL RELAXATION TIME: T1 tion is maximal and T1 is short. This is, for example,
the case in fatty tissue, which is why fat has a short T1.
• T1 is an intrinsic characteristic of the biologic tissue • Conversely, when the collisional frequency is very
containing protons. In biologic tissues, T1 is in the order low (e.g., in water molecules in ice, which have
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poor mobility), the energy exchange during relaxation averages out the local inhomogeneities of the magnetic
is slow and T1 is long. field induced by said molecules, so that individual
• Another example of long T1 is water, in which the col- protons see, on average, a more homogeneous magnetic
lisional frequency of the highly mobile, small-sized, field. This, in turns, decreases spin-spin interactions
water molecules is much higher than the protons’ and lengthens the transverse relaxation process: T2 is
Larmor frequency. This is a reason why when a therefore longer. This is the reason why fluids, such as
tissue undergoes pathologic change with increased cerebrospinal fluid (CSF) in neuro-MRI, have a long
water content, the T1 of that tissue will increase; an T2. For the same reason, accumulation of free water in
example of that situation is brain edema, and as we tissues, such as seen with brain edema, will also induce an
will see later, this will translate to a darker (hypoin- increase in T2 of these tissues. As we will see later, this is
tense) brain parenchyma on T1-weighted images. why fluids like the CSF, or edematous brain tissue, will
• There is a relationship between the T1 of a given appear bright (‘hyperintense’) on T2-weighted images.
tissue and the magnetic field B0, due to the Larmor • Conversely, in tissues where there is slow motion of
equation (ω = γ × B0). When B0 increases, so does molecules, such as solid tissues, or tissues containing
the Larmor frequency of protons in that field. This large molecules, the T2 will be shorter.
in turn increases the difference between Larmor fre-
quency and Brownian collisional frequencies (which THE FREE INDUCTION DECAY
are constant and independent of B0). This is the reason • As we just saw, during relaxation, Mz regrows and M xy
why, for example, T1 of fat will be longer at 3 Tesla decreases. Due to the differences in T2 (tens of millisec-
than at 1.5 Tesla. onds) versus T1 (hundreds of milliseconds) the decrease
in M xy is much faster than the regrowth of Mz. As a
THE TRANSVERSE RELAXATION TIME: T2
result, if we now combine M xy + M z = M 0 , we can see

that the tip of the vector M 0 during relaxation will have
• Like T1, T2 is a characteristic of each biologic tissue.
an envelope that resembles the bell of a trumpet, some-
• T2 in biologic tissues is a lot shorter than T1 (typically
what conical (Fig. 1.12).
10 times shorter, about 50–100 ms). The shorter the T2,
the faster the transverse magnetization will disappear • This is different from the spherical envelope that was
after the end of the RF pulse. observed during the application of the RF pulse, and
• Like T1, T2 depends on the molecular structure and that difference is inherently due to the specific relaxation
state (solid/liquid) of tissues. This again can be explained times T1 and T2, with T2 << T1.
by the Brownian motion differences in tissues: • These characteristics will influence the signal that we
• In tissues where there is high mobility of small molecules measure in MR imaging, which is precisely acquired
such as free water, the fast motion of the small molecules during that relaxation period.
M0
M0 Fig. 1.12 During

relaxation (right), the
tip of the regrowing net
magnetization vector
follows an envelope
shaped like the bell of
During the RF pulse, the net During relaxation, the net a trumpet, different from
magnetization vector shifts towards magnetization vector returns to its the spherical envelope
the transverse plane while equilibrium position, following the
precessing, following the envelope envelope of a cone or a trumpet- that is followed during the
of a sphere bell application of the RF
pulse (left).
14 CHAPTER 1
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M0, returning to equilibrium position
(x,y) plane
Projection of M0 in the (x,y) plane = Mxy vector
MRI signal
M xy
Receiving
In the (x,y) plane, the tip of the transverse coil
magnetization vector Mxy describes a spiral
Fig. 1.13 During relaxation, the tip of the transverse component of the magnetization vector (M xy) describes a spiral in the (x,y)
plane. This rotating magnetic field in the (x,y) plane can generate an electrical signal in a receiving coil placed in the (x,y) plane:
the MRI signal.
Signal
The envelope of the free induction decay
signal is an exponential characterized by a
time constant T2* (T2* << T2)
Time
Fig. 1.14 The

free induction
decay.
• It has a rotating (spiral) motion; that rotating mag-

• If one decomposes the vector M 0 during relaxation into
netic field induces an electric signal within the receiv-
its transverse component M xy and its longitudinal com-
ing coil (antenna) placed in the (x,y) plane. This signal,
ponent M z , one would see that the tip of the vector M xy , the MR signal, is called the ‘free induction decay’
in the (x,y) plane describes a spiral (Fig. 1.13). (FID) (Fig. 1.13).
• That rotating magnetic field can generate a signal that is • The FID curve has the shape of a damped sine wave
measurable because: (Fig. 1.14). This is a direct result of the way that M xy
• It is in the transverse plane, therefore not influenced decreases in the (x,y) plane, describing a rotating
by B0. motion along a spiral.
2. The fact that the signal measured (FID) does not
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• When the vector M xy points towards the receiving coil

the signal is positive, while when it points away from the only reflect the magnetic properties of the tissue
coil the signal is negative. This explains the ‘sine wave’ itself (T2 relaxation time), but is in fact compounded

appearance. by the constant extrinsic inhomogeneities of B0 .
Think of this as if you were taking pictures with your
• The amplitude of M xy decreases with time (getting
closer and closer to the center of the spiral), explaining camera, and the lens was scratched (permanent, fixed
the ‘damped’ appearance of the sine wave curve. defects); the resulting images would be only a partial
representation of reality, with a constant imperfection
superimposed on all images corresponding to the
T2* VERSUS T2 scratches on the lens. To obtain a picture that is a
• In a perfect situation, the envelope of the FID curve true depiction of reality, you would have to find a
(Fig. 1.14) should decrease according to the transverse way to remove the imperfections from the lens after
relaxation time constant T2, associated with the decrease the images are acquired: this is what the ‘spin echo’
in transverse magnetization M xy. As mentioned earlier, strategy will do (see below).
the decrease of M xy is due to dephasing of the protons
because of the local magnetic field inhomogeneities that
the molecules in the microenvironment of the protons A BASIC PULSE SEQUENCE: THE SPIN ECHO,
create, due to their own small magnetic field and the OR HOW TO MEASURE THE TRUE T2
Brownian molecular motions.
• In practice, however, there are other sources of inhomo- • In MRI, a ‘pulse sequence’ is a programed series of events
geneities, which are constant and inherent to permanent that aim at:
local distortions of the main magnetic field itself. These • Generating a signal from the patient (usually through
can result from several sources: the application of one or several RF pulses using
• B0 imperfections due to magnet manufacturing, phys- transmit coils).
ical environment of the machine, etc. • Measuring this signal with a receiving coil.
• Sample-induced constant inhomogeneities, also called • Spatially localizing the signal (using magnetic field
‘magnetic susceptibility’, are observed at the interface gradients) in order to create a graphic representation
between tissues that have very different magnetic in the form of an MR image, which contains anatomic
polarization causing distortion of the local magnetic information as well as contrast.
field (examples include interfaces with air, interfaces • The very basic scheme is called the spin echo sequence,
with bone, etc.). in which an ‘echo’ of the initial signal from the FID is
• Magnetic field inhomogeneities make dephasing of pro- created some time after the end of the 90° RF pulse.
tons during relaxation much faster, so that M xy actu- • The aim of the spin echo strategy is to (1) lengthen the
ally decreases at a much faster rate than expected. The time during which a signal can be recorded from the sam-
resulting observed decrease in transverse magnetization ple and (2) eliminate the influence of the constant inho-
is characterized by a time constant T2*, with T2* << T2. mogeneities of magnetic field that are associated with
In fact, the main contributor to the dephasing of protons imperfections of B0 and susceptibility effects, which, as
at the end of the 90° pulse is this constant inhomogene- we studied earlier, are causing ultra-fast dephasing of the
ity of B0. As a result, the envelope of the observed FID spins that is not a reflection of the actual proton density
signal decays according to the T2* constant. and biomechanical environment of these protons in the
• T2* is heavily dependent on the strength of B0 because sample.
it is harder to obtain a homogeneous field in a high-field • To understand the principle of the spin echo sequence,
system, and also because magnetic susceptibility differ- one can think of analogous examples. Imagine, for
ences are amplified in a stronger magnetic field. T2, on example, a rabbit and a turtle on a race track (Fig. 1.15).
the other hand, is quite independent from B0. At t = 0 (end of the 90° RF pulse), the turtle and rab-
• In the end, although we were able to create a tissue net bit are at the same level on the start line (all protons in
magnetization reflecting the properties of tissue (density the sample are ‘in-phase’). They start racing, but because
of protons and physicochemical properties of the tis- the rabbit is inherently faster than the turtle (= ‘precesses
sue), and then shift the net magnetization signal into the faster’), it rapidly gets ahead of the turtle (= ‘dephasing’).
transverse plane (x,y) to make it measurable by a receiv- If, at some point, the rabbit and turtle are moved 180°
ing coil, we are now facing two challenges: to the opposite side of the track relative to the horizon-
1. The very rapid dissipation of the signal due to the tal axis, but continue racing in the same direction, the
inherent inhomogeneities of the tissues (intrinsic turtle is now ahead of the rabbit, closer to the finish line.
inhomogeneities) and the constant imperfections of After some time, they will reach the finish line together

the magnetic field B0 (extrinsic inhomogeneities). (= ‘rephasing’).
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START!!!
1 3
Fig. 1.15 The analogy of the rabbit and turtle running allows an understanding of how a 180° pulse applied some time after the
90° pulse allows the formation of an echo.
1 z e 2 z
lus
°p
90
t=0 M0
y y
Mxy1
x x
m
m21
m4 m3
m1 < m2 < m3 < m4
3 z 4 z
e
plus
0°
18 y y
t = t180 t = 2 x t180
m3 m2 m1
m4 x Mxy2 x
The 180° pulse flips the vectors

m1, m2, m3, and m4 symmetrically Mxy2 < Mxy1
relative to the y axis, in the
(x,y) plane
Fig. 1.16 Illustration of the effect of the application of a 180° pulse. (1) At t = 0, all protons are in phase causing the transverse
magnetization M xy1 to be maximum; (2) rapidly, the protons start to lose phase coherence, some precessing slower and others
faster than the central precession frequency; (3) at some time (t180) after the end of the 90° pulse, a 180° pulse is applied causing
the spins to move symmetrically across the y-axis while keeping their speed and direction of precession; (4) after a time equal
to 2 × t180, the spins are again in phase and M xy is maximal: this is the echo. Note that the newly created M xy (M xy2) has less
amplitude than the initial one at t = 0, because the 180° pulse only canceled out the fixed magnetic field inhomogeneities (T2*)
but not the intrinsic spin-spin interactions.
• Similarly, the application of a 180° pulse at some time • If time t180 elapses again (= 2 × t180), then the protons
(t180) after the 90° RF pulse causes the protons to reverse regain their ‘phase coherence’, inducing regrowth of a
their relative phase to the resonant frequency. The rates transverse magnetization and therefore a signal in the
and directions of precession of the protons do not change, receiving coil (Fig. 1.16). This new signal is known as
only their relative phase (Fig. 1.16). the ‘spin echo’.
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• The dephasing due to constant B0 inhomogeneities the 180° pulse at precisely TE/2 seconds after the 90°
(imperfections of B0, local differences in magnetic suscep- RF pulse. You now see that one can manipulate the MR
tibilities within the patient) is eliminated, because the pro- signal temporally and, in this particular case, the time at
tons experience exactly the same interactions prior to and which the echo signal is collected. This will have some
following the 180° pulse. This means that the contributions implications in that this allows one to minimize or maxi-
to T2* relaxation from these static sources will be nulled. mize the differences in T2 times of various tissues in the
Only the irreversible spin-spin relaxation is unaffected by sample. When maximizing the differences in T2 times,
the 180° pulse, so that the loss of phase coherence and signal we say that we are weighting the signal according to T2
amplitude for a spin echo is due only to true T2 relaxation. (= T2-weighted signal, more on this later).
• This process can be repeated by applying additional 180° • Note that the 180° pulse will also influence the longitu-
pulses, with the new signal (echo) generated each time dinal magnetization Mz, which will be regrowing dur-
having a progressively decreasing intensity. If you plot ing the time interval TE/2 and therefore will be flipped
the maximal signal intensity of each echo as a function 180° along the z-axis. This, however, is usually negligible
of time, you obtain a decreasing exponential whose time because TE/2 is usually very short in comparison with
constant is T2 (Fig. 1.17). T1 so that the regrowth of Mz by the time the 180° pulse
• This strategy allows generation of a signal that depends is applied is minimal (Fig. 1.18).
on T2 of tissues over a much longer period of time than
would be observed otherwise. WHAT ABOUT THE REPETITION TIME?
• Note that, as shown on Fig. 1.17, the amplitude of the
echo is less than the initial amplitude of M xy (M xy1), • In the previous paragraph, we introduced the notion
because the 180° pulse only eliminates the dephasing due of TE (echo time). This is a central parameter of MRI
to the constant field inhomogeneities, but not the vari- pulse sequences, but until now we have not mentioned
able inherent dephasing due to spin-spin interactions. another important pulse sequence parameter, the ‘repeti-
This is why the spin echo scheme reveals an MR signal tion time’ (TR).
that is purely dependent on the true T2 relaxation times • As we will study later, the collection of signal through
of tissues within the patient. the generation of a spin echo needs in fact to be repeated
• The longer one waits to apply the 180° pulse, the weaker a number of times to be able to reconstruct an image of
the echo signal will be, as more irreversible spin-spin the patient. For example, for a typical MR image that
relaxation will have occurred in the sample. would contain 256 × 256 pixels (i.e., 256 lines), the sig-
• The time at which the echo signal peaks is called the nal needs to be collected 256 times to be able to spatially
‘echo time’ or ‘time of echo’ and is symbolized by TE. encode the data collected and localize the origin of the
To obtain an echo at a specific TE one needs to apply magnetization measured.
Signal (= transverse magnetization)

This envelope is characterized by
the T2 time: the influence of the
inhomogeneities of B0 has been
Mxy1 = max = M0 removed, and the signal is now a Fig. 1.17 The application of a 180° pulse at
function of the tissue’s some time TE/2 after the 90° pulse causes
Rapid inhomogeneities only
dephasing, Rephasing
regrowth of the transverse magnetization due
according Mxy2 < Mxy1 to rephasing of protons causing formation of
to T2* an echo, which reaches a maximum amplitude
Time at an additional time TE/2 (or TE after the
90° pulse). The amplitude of that echo is
less than that of M0, because the 180° pulse
only cancels the fixed inhomogeneities of B0
(e.g., due to magnet imperfections or local
TE patient magnetic susceptibilities) but does
Time of echo not eliminate the intrinsic dephasing due to
180
90 pure spin-spin interactions within the sample.

If a curve is drawn that joins the maximum
amplitudes of the echoes after successive 180°
TE/2 TE/2 pulses, that curve decays according to the
true T2 time of the tissue sample.
18 CHAPTER 1
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Magnetization
Mz
Very partial regrowth of Mz
Mxy at time of 180° pulse
Time
Mz is flipped 180° at TE/2
ECHO
180
90 90
Echo time (TE)

Repetition time (TR)
Fig. 1.18 A basic spin echo pulse sequence. At t = 0, a 90° pulse is applied causing M z to be nulled and M xy to become
maximum; at TE/2, a 180° pulse is applied, which causes progressive rephasing of the protons and, in turn, regrowth of
M xy, and also flips the longitudinal magnetization M z by 180°. This latter effect is minimal though, because since TE is
usually very short compared with T1, there has been minimal regrowth of M z by the time the 180° pulse is applied. At time
TE (echo time), the echo reaches maximal amplitude. M z continues to regrow, and when it has reached its maximum value
(or a reasonably high value), the process is repeated, with a new 90° pulse applied at some time TR after the previous 90°
pulse: TR is the repetition time.
• For one given line of an image, the sequence of events is it allows primary images to be obtained in any plane
as follows: (transverse, dorsal, sagittal, or any oblique plane).
• 90° pulse, shifts M 0 in the transverse plane, nulls Mz, • An image can be thought of as a matrix (i.e., a series of
and makes M xy maximal. lines and columns containing an array of pixels).
• After TE/2, a 180° pulse is applied, which rephases the • A ‘pixel’ (= picture element) is the compressed informa-
protons and allows an echo to be obtained, at a time tion in one plane of a three-dimensional volume element,
TE, which is when the signal is recorded (= ‘signal called a ‘voxel’ (Fig. 1.19).
read-out’). • The ‘field of view’ (FOV) represents the actual dimen-
• At TE, M xy is maximal again (although <M0, due to sions (height and width, in mm or cm) of the image frame
the irreversible spin-spin dephasing), but Mz has only obtained, while the ‘matrix size’ defines the number of
partially regrown. lines N L and columns NC in the image.
• Therefore, before another 90° pulse is applied to • N L × NC defines the number of pixels in the image,
repeat the experiment in order to obtain a second which is equal to the number of voxels in the anatomic
line of the image, one must wait a sufficient amount slice being imaged. A typical image matrix, for example,
of time for Mz to have regrown enough so that a 90° is one that contains 256 lines and 256 columns (i.e., 256 ×
pulse will be able to shift that new net magnetization 256 = 65,536 pixels).
in the (x,y) plane again. • There is a relationship between FOV, matrix size, and
• The time one waits to apply another 90° pulse is called spatial resolution of the image; for example, for a given
the TR (repetition time) (Fig. 1.18). FOV, if one increases matrix size, the size of each indi-
vidual pixel decreases. In other words, ‘spatial resolution’
increases.
THE MR IMAGE: FIELD OF VIEW, • The surface area of a pixel multiplied by the slice thickness
MATRIX, PIXEL, AND VOXEL determines the volume of an individual voxel (Fig. 1.19).
• Both FOV and matrix can be square or rectangular,
• MRI, like computed tomography or ultrasonogra- which will have an influence on the size and shape of the
phy, produces cross-sectional images (i.e., slices of the pixels and will have some practical implications regard-
patient). One particularity of MRI is that, unlike CT, ing image quality.
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FOVx
wh Fig. 1.19 The physical slice of the

patient (left) has a defined slice
thickness and contains a series
of voxels (volume elements). The
8 VOXELS
8 PIXELS
FOVy
dimension of an individual voxel
is w (width) × h (height) × slice
thickness. The corresponding image
displayed on the screen is made of a
series of pixels (picture elements) of
ce ss
Sli kne dimension w × h. The dimension of
8 VOXELS ic 8 PIXELS the image is called the field of view
th
FOVx / 8 = w (pixel width) (FOV). The FOV divided by the
FOVy / 8 = h (pixel height) number of pixels in a given direction
w x h = surface area of a pixel (mm2) (x or y) gives the dimensions of an
w x h x slice thickness = volume of a voxel (mm3)
individual pixel.
FROM IMAGE TO SPATIAL FREQUENCIES: this is what we call the ‘spatial domain’. We can decom-
NOTION OF FOURIER TRANSFORM pose this spatial signal into a combination of sine and
cosine signals that have various frequencies and ampli-
• Before we go into more detail about spatial encoding and tudes, just as we can decompose a given musical chord
MR signal collection, it is worth going over the concept into the individual frequencies that make it up. This is
of relationships between a physical image and spatial the ‘frequency domain’.
frequencies. • For example, look at the complex signal S(t) in Fig. 1.20.
• An example of a familiar signal that is made of differ- It shows a variation of intensity as a function of time: this
ent frequencies is music. If you have some knowledge is the ‘time domain’. One could show that it is the sum
of music theory, you may be able, just by listening to of three well-defined sine wave signals, S1(t) + S2(t) + S3(t),
a chord (i.e., any harmonic set of three or more notes that which have different frequencies and amplitudes.
is heard as if sounding simultaneously), to decompose the • As shown in Fig. 1.20, we can represent these three sig-
notes that the chord is made of. In other words, your ears nals differently, on a diagram that would have frequencies
and brain are able to perform a complex mathematical on the x-axis and amplitude on the y-axis. This diagram
process that separates the individual frequencies (notes) is a simplified version of a one-dimensional ‘frequency
that make a complex signal (musical chord) heard as the domain’.
combined sum of the individual frequencies. • The mathematical operation that allows one to convert
• An image such as an MR image is a spatial distribution in the signal in the ‘time domain’ or ‘spatial domain’ into
a plane of a series of pixels that have various intensities; the ‘frequency domain’ (i.e., to decompose the signal
1
Time domain Frequency Amplitude
Fig. 1.20 Top left: a complex signal
shown as amplitude variation as a
Time
function of time. Top right: this
Time signal can be decomposed into the
Fourier
transform individual sine wave signals it is
S(t) = S1(t) + S2(t) + S3(t) S1(t) = sin t made of: in this case, three simple
S2(t) = 1.5 × sin(1.5 × t) signals S1(t), S2(t), and S3(t). Bottom
Amplitude S3(t) = 2 × sin(2 × t) left: these three signals can be
Frequency
A3 = 2A1 represented in a different manner
A2 = 1.5A1 S3 domain
S2 with amplitude on the y-axis and
A1
S1 frequency on the x-axis: this is a
ƒ 1.5ƒ 2ƒ Frequency frequency domain representation of
the time domain signal on the top
left.
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Intensity Distance
The intensity profile of the image on the left along

the red line is a rectangular pulse signal
Low frequencies only
create a rough shape of
the original signal, with
blurred edges
Adding together
sinusoidal signals of
increasing frequency
and decreasing
intensities recreates a
profile that resembles
more and more the
original rectangular
pulse signal
As higher frequencies
are added, the edges
and details of the actual
signal are becoming
clearer and clearer
Fig. 1.21 Top left: the image of a simple object (top left) such as a line-pair phantom. Top right: representation of variations
of signal intensity along the red line across the image; this generates a rectangular pulse signal with abrupt variations of signal
from maximum to minimum. Bottom: the original rectangular pulse signal can be represented more and more accurately
by adding up sine wave functions of progressively increasing frequency and decreasing amplitude; the low frequency signal
only gives a rough idea of the general shape and contrast of the original signal (series of mounts and valleys). Adding higher
frequencies of lower amplitudes allows better definition of the detailed edges of the original object (adds ‘spatial resolution’ and
‘detail’). So, in the Fourier transform of a signal, the low frequency/high amplitude signals generally contain information on
general shape and contrast of the object, while the higher frequency/lower amplitude signals contain information about small
detail and edges (i.e., the spatial resolution).
into the many frequencies it is made of) is called the (‘harmonics’), the original shape of the rectangular
‘Fourier transform’. It is beyond the scope of this book pulse signal could be reconstructed. As can be seen in
to go into the complex details of how the mathemat- the Fig. 1.21, if you have only one low frequency, high
ics work, but the very important concept to remember amplitude signal, it only provides a gross representation
here is that the way we usually think of a pixel at some of the variations in signal intensity and its general shape
location in the image (spatial domain, coordinates in (mounts and valleys), but the edges are very blurry. As
mm; pixel intensity) can be thought of, in the frequency you add more and more signals of higher and higher fre-
domain, as a ‘spatial frequency’ (mm−1, or the inverse of quency, the sum of the signals gets sharper and sharper
a distance) and ‘amplitude’. edges, getting closer to the true shape of the original
• Look at the simple image in Fig. 1.21: this could, for signal.
example, be the line pairs of a phantom used to mea- • The important take-home message here is that when
sure resolution of an x-ray or CT machine. At each lead decomposing a spatial domain signal into its frequency
strip, there is an abrupt increase in signal intensity with components:
a very sharp edge. One could get a graph of the horizon- • The high amplitude/low frequency components
tal change in pixel intensity along the image; this is an contain information about the general shape of the
‘image profile’ in the spatial domain (unit on the x-axis signal and gross variations in signal intensities: that is,
is now a distance, not time). It is a ‘rectangular pulse sig- ‘general shape’ and ‘contrast’.
nal’, with very sharp vertical changes in intensity corre- • The higher frequencies contain information about the
sponding to the edges of the lead strips of the phantom. edges/sharp details of the signal: that is, ‘detail’ and
• One could show that by adding a number of sine wave sig- ‘spatial resolution’.
nals of increasing frequencies and decreasing amplitudes
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SPATIAL ENCODING: SLICE SELECTION Z coils
• Without manipulation, the MR signal we have been

studying so far and that is recorded by the receiving
coil in the (x,y) plane originates from the entire sample
(patient) under study.
• However, in order to create an image that is a repre- x y y x Y coils
sentation of the internal anatomy of the patient, one
needs to localize the spatial origin of the signal within
a specific slice in order to attribute to each voxel a sig-
nal intensity that is representative of the true proton
density and biochemical environment of these protons X coils
within each individual voxel. This process is called
Fig. 1.22 Additional coils (x, y, and z coils) are placed
‘spatial encoding’.
within the bore of the magnet and allow, depending on their
• Spatial encoding relies on two essential tools:
orientation, the creation of magnetic field gradients. These
• A physical tool: the magnetic field ‘gradients’.
gradients are additional magnetic fields, which will be added
• A mathematical tool: the ‘Fourier transform’.
to or subtracted from B0 (depending on their polarity) to
• A magnetic field gradient is a predetermined spatial vari-
create linear variations of net magnetic field experienced by
ation of the strength of the magnetic field along a given
protons in the three directions of space. The z coils create
direction. Gradients are essential in spatially localizing
magnetic field gradients along the z-direction (B0), while the
the origin of resonance signal within the patient.
x coils and y coils will generate magnetic field gradients in the
• To understand the relationship between gradient and
perpendicular planes, along the x- and y-axis, respectively.
spatial localization, let us take the example of the tem-
perature in a closed room:
• Physics dictates that there is a continual vertical varia- point of the axis of all magnetic gradients) and a negative
tion of temperature from the bottom to the top of the gradient in the opposite direction (Fig. 1.23).
room, as warm air tends to move upwards. • Gradients are all centered on this isocenter and of oppo-
• As a result, there may be a linear variation of the air site polarity on either side of it; for that reason, they
temperature as a function of altitude; for example, are said to be ‘bipolar’. The strength G of the gradient
the temperature may increase by 0.05° Celsius every defines the ‘slope’ of the linear gradient, and is expressed
10 cm. This is called a ‘positive vertical temperature in milliTesla per meter (mT/m). On one side of the iso-
gradient’. center the slope is positive and on the other side the slope
• If you imagine a staircase in the room with stairs that is negative, so that the strength of the net magnetic field
are each 10 cm in height, the temperature would rise will be (B0 + G × d1) at some distance d1 from the iso-
linearly by 0.05° Celsius every step. If the temperature center in the positive gradient area, and (B0 – G × d2)
at the bottom (floor) is 20° Celsius, you know that if at some distance d2 from the isocenter in the negative
you are on the stairs, and the measured temperature gradient area. At the isocenter, the net magnetic field is
is 20.25° Celsius, you would be on step number 5: 20 unchanged and equal to B0 (Fig. 1.23).
+ 0.05 (1st step) + 0.05 (2nd step) + 0.05 (3rd step) + 0.05 • The first step of spatial localization is to select a slice
(4th step) + 0.05 (5th step) = 20.25° Celsius. within the patient (i.e., the plane of the patient we want
• There is therefore a relationship between the meas- to obtain an image of):
ured signal (temperature) and your spatial localization • In the absence of a gradient, all protons in the body
up the staircase. experience the same magnetic field B0, and therefore
• Regarding MRI, we can create linear gradients of the precess at the same frequency ω0 = γ × B0.
magnetic field within the bore of the magnet by super- • Using a ‘slice selection gradient’, one can force all
imposing additional magnetic fields created by gradient protons in the slice of interest to precess at a given
coils (Fig. 1.22), which generate a secondary magnetic frequency, specific to that slice.
field whose value will be added or subtracted (depend- • For example, as presented in Fig. 1.24, imagine a slice
ing on the direction of the added field) to the value of selection gradient of strength GS applied in the direc-
B0. The result is that the ‘net magnetic field’ can now be tion of the main magnetic field B0 (i.e., along the z-axis).
varied linearly as a function of space (Fig. 1.23). All protons within a plane perpendicular to B0 located
• For example, a linear gradient can be applied in the direc- at some distance d from the isocenter will experi-
tion of B0 (central axis of the bore in a high-field magnet), ence a magnetic field equal to [B0 ± GS × d]. They will
with a positive gradient on one side of the magnetic iso- therefore precess at a frequency ωd = γ × [B0 ± GS × d],
center (center of the bore of the magnet, and also center which depends on the exact location of the slice.
22 CHAPTER 1
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B0
ISOCENTER
- +
t
Negative slope (–G) gradien
In mT/m Posi
tive
+
- rad ient
Positive slope (+G)
In mT/m d2
Distance
from
ve g isocenter
Negati
0 d1 Magnetic
field
strength
B0 – G × d2 B0 B0 + G × d1
Fig. 1.23 Schematic representation of a magnetic field gradient. In this case, a gradient is applied along the axis of the main
magnetic field B0 (called the z-axis). The gradient is centered at the isocenter of the bore, and is positive to its right (slope +G)
and negative to its left (slope –G). As a result, protons located at a distance d1 to the right of the isocenter will experience an
actual magnetic field equal to B0 + G × d1 and will precess faster; on the other hand, protons located at some distance d2 from
the isocenter to the left will experience an actual magnetic field equal to B0 – G × d2 and will precess slower.
Within that slice (perpendicular to

B0, and at a distance d from the
isocenter), protons experience
a magnetic field equal to (B0 – Gs × d).
therefore they precess at a
frequency:
ωd = γ × (B0 – GS × d) B0
ISOCENTER
90°
pul
)
×d
se
– GS
× (B 0
=γ
ω RF
d
+
Transverse image - Slice selection gradient
at the desired amplitude Gs [mT/cm]
location d
Fig. 1.24 Slice selection gradient. The gradient (GS) is applied in the direction of z-axis (B0) and centered at the isocenter,
being positive to the right of the isocenter and negative to the left. In a transverse plane perpendicular to B0 and located at
some distance d from the isocenter, all protons will precess at a unique frequency that is dependent on the strength (slope)
of the gradient and the distance d (i.e., slice selective): ωd = γ × (B0 – GS × d). If we now apply a RF pulse that is tuned to that
specific frequency, only the protons located in the specific slice will experience resonance and be excited; the other protons in
the volume of the bore are precessing at different frequencies and thus will be insensitive to that RF pulse. We have therefore
selectively excited a single slice of the patient.
• If a 90° RF pulse is sent at a frequency ωRF that (i.e., remainder of the patient) will be insensitive to
matches the resonance frequency of the protons that RF pulse.
within the selected slice (ωRF = γ × [B0 ± GS × d]), then • As a result, the MR signal recorded will be exclusively
ONLY the protons within that slice will be sensitive generated by protons within the selected slice.
to the RF pulse, while all protons outside of that slice
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• Assuming patients are placed in the bore of the magnet • The slice selection gradient is also used to determine
with their long axis parallel to B0 (i.e., in sternal or the slice thickness. Remember the 90˚ pulse is sent at a
dorsal recumbency in the bore of a superconductor frequency corresponding to that of the protons in the
magnet): selected slice; in reality the RF pulse contains a small
– Transverse images will be obtained by using a range of frequencies, called the ‘transmit bandwidth’,
slice selection gradient oriented along the caudo- so that it is a slab of a certain thickness, proportional to
cranial axis (i.e., parallel to B0). the frequency range, that gets excited by the RF pulse
– Sagittal images will be obtained by using a slice (e.g., 1 mm, 2 mm, 3 mm…):
selection gradient that is oriented left to right (or • The wider the transmit bandwidth of the RF pulse,
right to left). the thicker the slice (Fig. 1.26). This corresponds to a
– Dorsal images will be obtained by using a slice shorter RF pulse since frequency = 1/time.
selection gradient that is oriented ventral to dorsal • For a fixed transmit bandwidth, slice thickness can
or vice versa (Fig. 1.25). also be modified by changing the strength of the slice
– Images in any desired oblique orientation can be selection gradient, so that the range of frequencies
obtained by simply applying a linear combination included in the RF pulse is ‘spread’ over a thicker
of several gradients simultaneously. Depending on (‘shallow’ gradient slope) or thinner (‘steep’ gradient
which gradient coils are turned on, and the rela- slope) portion of the patient (Fig. 1.27).
tive strength of each gradient, the obliquity of the • Within an MRI pulse sequence, the slice selection gradi-
imaging plane can be controlled. ent is applied at the same time as the 90° RF pulse, so
Dorsal
GS from ventral plane
to dorsal
Fig. 1.25 The orientation of

GS from the slice selection gradient
rostral to
o Transverse
plane will determine the orientation
caudal t
B0 lef of the imaging plane. In any
m
fro ht
G S rig given direction, the polarity of
to
the gradients can be modified;
Sagittal for example, the slice selection
plane gradient for the transverse
plane can be oriented rostral
to caudal (as shown) or caudal
to rostral.
tion tio
n
lec lec
e se t se t
c e
Sli adien c
Sli adien
gr gr
∆ω1 ∆ω2 Fig. 1.26 Slice thickness can

be modified by changing the
transmit bandwidth of the RF
pulse: wide bandwidth (left)
will excite a broader range
Thick slice Thin slice of frequencies, resulting in a
thicker slice.
24 CHAPTER 1
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er
ng t
t ro ien
S ad
gr t
ien
grad
a ker
We
∆ω
Fig. 1.27 For a fixed transmit

bandwidth, slice thickness can
also be changed by modifying
the strength (slope) of the
slice-encoding gradient, with
a stronger (steeper slope)
gradient resulting in a thinner
Thin slice Thick slice slice than a weaker (shallower
slope) gradient.
that only the protons precessing at the frequency of that line-pairs per centimeter’ (i.e., five ‘dark–light’ patterns
RF pulse will resonate and generate a signal from within are contained within a centimeter).
the slice of interest. In a spin echo scheme, the 180° pulse • Regarding MRI, spatial encoding will aim at measur-
should be at the same frequency as the 90° RF pulse and ing the periodic variation in signal spatial distribution or
in the presence of the same slice selection gradient, so image brightness, measured not as line-pairs per centi-
that only the protons in the slice of interest will experi- meter but as ‘cycles per centimeter’.
ence the rephasing pulse. • As was demonstrated by the French physicist Joseph
Fourier, any image can be decomposed into a spectrum
SPATIAL ENCODING: NOTIONS of periodic (sinusoidal) brightness variations or spatial
OF FREQUENCY-ENCODING frequencies. In a digital image with a matrix of 256 × 256
AND PHASE-ENCODING pixels there are 256 × 256 possible spatial frequencies,
allowing for positive and negative values. If we know
• Now that we have selected which slice of the patient we the spatial frequencies, we can calculate an image of the
want to image, we need to be able to decode the signal object that formed them.
coming from within that slice during relaxation, so that • The purpose of MR spatial encoding is to use gradi-
we can assign parts of the signal to where in the patient ents to manipulate the MR signal, so that it gives all the
they originated. spatial frequencies necessary to form an image. These
• The signal measured during relaxation is contributed spatial frequencies will be placed in a matrix called the
to by all the protons within the slice, and is due to the ‘frequency domain’ or ‘k-space’, in which each point of
precession of the protons while they return to the equi- data is a spatial frequency component of the actual MR
librium position. As discussed before, precession is a image. In other words, and this is an important concept,
rotational cyclic motion and therefore can be character- each point of that frequency domain determines a spatial
ized by a frequency ω rad/s (or f, in Hz = cycles/s). frequency that exists across the entire MR image. For a
• ‘Spatial encoding’ takes advantage of that property by digital image with a matrix of 256 × 256 pixels, the cor-
using frequency and phase to detect which part of the slice responding k-space will contain 256 × 256 data points,
the signal is coming from. In principle, spatial encoding representing the 256 × 256 spatial frequencies necessary
reveals the ‘spatial frequencies’ contained in the image to reconstruct the image.
of interest, and then, using a mathematical function (the • To understand the concept of spatial encoding with
‘inverse Fourier transform’) we can reconstruct the image gradients, imagine three discs with a red mark rotating
with all the information of brightness, contrast, and detail. along a horizontal line (similar to a precessing proton)
• One of the easiest ways to understand spatial frequen- (Fig. 1.28a):
cies is to think of a line-pair test object, such as those • At the beginning of this experiment, let us place the
used for testing x-ray or CT imaging systems, as illus- red mark at the same position, 12 o’clock.
trated in Fig. 1.21. The pattern of image brightness pro- • If the discs rotate at the same frequency ω0, every time
duced by this line-pair pattern is like a spatial frequency. we look at the discs, the red mark is at the same level
For example, a specific spatial frequency could be ‘five on all three discs; for example, 2 o’clock (Fig. 1.28b).
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(a) (d) ф1
ф2 ф3
ω0 ω0 ω0
No gradient: all discs precess at ω0 ω3
ω1 ω2
(b) ф ф ф The discs not only precess at different frequencies as
a function of their location along the gradient, but
also acquire a different phase ф
(e)
ω0 ω0 ω0 ф1
ф2 ф3
In the absence of a gradient, at some time t, all discs
are in phase, and still precess at ω0
(c)
ω3
ω2 ω0 ω0 ω0
ω1
A gradient is turned on: the discs now start precessing The gradient is turned off: the discs resume
faster from left to right; their position along the gradient precessing all at the same frequency ω0, but their
determines their precession frequency relative phase is retained
Fig. 1.28 Principle of frequency- and phase-encoding. (a) At the beginning of this experiment, let us place the red mark at the
same position, 12 o’clock. (b) If the discs rotate at the same frequency ω 0, every time we look at the discs, the red mark is at the
same level on all three discs, for example, 2 o’clock. (c) If we now apply a positive gradient so that the discs rotate faster from
left to right at respective frequencies ω1 < ω2 < ω3, and if we now measure the frequency of each disc while the gradient is on,
we can determine which signal frequency corresponds to which disc; this principle is called ‘frequency-encoding’. (d, e) If we
now stop the gradient, all discs start rotating at the initial frequency ω 0 again, so we cannot discriminate which disc is which
by measuring frequency alone. However, when they were under the influence of the gradient, causing differences in rotational
speeds, they acquired different ‘phases’; think of the phase as the angle between the red marker’s radius at its original position
at 12 o’clock, and the position it has at any observation time after the gradient has been applied. The discs have now acquired
different phases Φ1, Φ2, and Φ3, with Φ1 < Φ2 < Φ3. Even though the initial gradient is now turned off, we still have a way to
discriminate spatially the three discs by measuring their phase. This principle is called ‘phase-encoding’ (PE). In other words,
the gradient (called ‘PE gradient’) has ‘tagged’ the spatial localization of each of the discs by conferring on them a specific
phase, which depends on the strength, orientation, and duration of the gradient.
• If we now apply a positive gradient so that the discs discs have now acquired different phases Φ1, Φ2, and
rotate faster from left to right at respective frequen- Φ3 with Φ1 < Φ2 < Φ3. Even though the initial gradient
cies ω1 < ω2 < ω3, and if we now measure the frequency is now turned off, we still have a way to discriminate
of each disc while the gradient is on, we can deter- spatially the three discs by measuring their phase.
mine which signal frequency corresponds to which This principle is called ‘phase-encoding’. In other
disc; this principle is called ‘frequency- encoding’ words, the gradient (called ‘phase-encoding [PE]
(Fig. 1.28c). gradient’) has ‘tagged’ the spatial localization of each
• If we now stop the gradient, all discs start rotating disc by conferring on them a specific phase, which
at the initial frequency ω0 again, so we cannot dis- depends on the strength, orientation, and duration of
criminate which disc is which by measuring frequency the gradient.
alone. However, when the discs were under the influ- • Let us now imagine a theoretical image plane with a
ence of the gradient, causing differences in rotational matrix of 3 × 3 pixels, each containing only one proton:
speeds, they acquired different ‘phases’. Think of the • If no gradient is applied during signal readout at the
phase as the angle between the red marker’s radius time of echo, all protons are precessing at ω0 and
at its original position at 12 o’clock and the position therefore the signal generated by the slice contains
it has at any observation time after the gradient has only one frequency, ω0. It is not possible to detect
been applied. As seen in Figs. 1.28d and 1.28e, the which pixel the signal is coming from (Fig. 1.29).
26 CHAPTER 1
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Fig. 1.29 Effect of the frequency-

encoding (FE) gradient applied
during signal readout. If no gradient
is applied, all protons precess at the
same frequency and the readout
signal only contains one single
frequency. Under the influence of the
FE gradient during signal readout,
protons in the different columns
precess at different frequencies
and, as a result, the signal obtained
ω0 ω0 ω0 ω0 – Δω ω0 ω0 + Δω
contains three different frequencies,
which can be decoded by Fourier
transform.
Single frequency Three frequencies
• If we now apply a gradient along the x-axis, centered • The concept of FE is quite easy to grasp: precession
on the middle column during signal readout: frequencies are varied in the FE direction (for example,
– The protons in the left column will precess slower x-axis) during readout of the MR signal. The MR signal
than those in the central column because they that is collected contains the sum of all these frequen-
experience a weaker magnetic field (remember, cies, but this can then be sorted out using a mathematical
ω = γ × B). function, the Fourier transform, to decode all frequen-
– The protons in the central column will still pre- cies contained in the signal.
cess at ω0, since the gradient is 0 at that level. • The concept of PE is a bit more difficult to grasp. In
– The protons in the right column will precess faster particular, one cannot sort out spatial frequencies
than those in the central column as they experi- using only one PE gradient. In fact, in order to sort
ence a stronger magnetic field. out all spatial frequencies along each line of a 256 × 256
• As a result, the signal collected during readout will matrix, one needs to acquire the MR signal 256 times,
contain three frequencies, one each corresponding to each time using the same FE gradient in the x-direc-
the three columns. The gradient used for this is called tion, but a PE gradient of different strength (mT/m) in
‘frequency-encoding (FE) gradient’, or ‘readout gra- the y-direction. (See Table 1.3 and Fig. 1.30 for further
dient’, since it is applied during signal collection. explanation about this concept, using a simple example
• The principles of FE and PE will be used to encode the with six pixels.)
signal within the imaged slice during MR acquisition: • In reality, an MR image contains many more pixels
• A location dependent phase will be obtained using a (thousands) and therefore the mathematics involved are
PE gradient prior to signal readout in one direction substantially more complex than the simplified exam-
of the image (the PE direction); that phase will be ple presented in Table 1.3, but the point is that you need
retained after the gradient is turned off. two different acquisitions (= two readouts), with the
• An FE gradient will be applied in the other direc- same FE gradient but different PE gradient strengths
tion (FE direction) during signal readout, determin- (= PE steps), to decode phase shifts and spatially local-
ing specific precession frequencies that are location ize two lines of the image. For an image that contains n
dependent as well. lines, you will need n PE steps. So, for example, for an
image matrix that contains 256 × 256 pixels, the pulse
A BIT MORE ABOUT PHASE-ENCODING sequence will need to be repeated 256 times, each with
a different PE gradient, to be able to get enough data
• As described above, specific gradients can be used to tag to localize spatially the signal in all 256 × 256 pixels.
specific locations within the image plane using spatial This is one of the main reasons for the long acquisition
variations in frequency or phase. times in MRI.
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Table 1.3 Simplified mathematical explanation of phase-encoding considering only six pixels of a brain image.
• Let us consider six specific pixels in a brain image (Fig. 1.30). Based on our previous explanations, each pixel in the image plane, during signal
readout, is generating a sinusoidal signal that is a function of time and depends on the specific precession frequency ω in that voxel (a function of
its location along the FE gradient) and phase ϕ (acquired at that location during the application of the PE gradient, before readout). That signal is
in the form ‘A.sin(ωt + ϕ)’, with A being the amplitude of the signal in that pixel, which depends in particular on the proton density in the
corresponding voxel.
• Therefore, based on the spatial location (column and line) of pixels A, B, C, D, E, and F during a given readout, the signal within each voxel A
through F is as follows:
SA(t ) = A × sin(ω1t + ϕA,B,C)
SB(t ) = B × sin(ω2t + ϕA,B,C)
SC(t ) = C × sin(ω3t + ϕA,B,C)
SD(t ) = D × sin(ω1t + ϕD,E,F)
SE(t ) = E × sin(ω2t + ϕD,E,F)
SF(t ) = F × sin(ω3t + ϕD,E,F)
• Note that the pairs {A,D}, {B,E}, and {C,F} resonate at the same frequency, since they are in the same column; also note that during a given
readout, {A,B,C} have the same phase ϕA,B,C relative to {D,E,F} because they are on the same line along the PE gradient.
• Note that pixels A, B, and C are all at the ‘zero’ level of the PE gradient, therefore at each PE step, regardless of the strength of the PE gradient,
they will have a phase of 0 as they will always be experiencing the magnetic field B0 (ϕA,B,C = 0)
• Consider a first acquisition (step 0), before any PE gradient has been applied; the signal in the line containing pixels A, B, and C is in phase with
signal in the line containing pixels D, E, and F (= no phase: ϕA,B,C = ϕD,E,F = 0):
• The signal from column {A,D} would be:
• S 0A,D (t ) = A × sin(ω1t + 0) + D × sin(ω1t + 0) = (A + D) × sin ω1t
• The signal from column {B,E} would be:
• S 0B,E (t ) = B × sin(ω2t + 0) + E × sin(ω2t + 0) = (B + E) × sin ω2t
• The signal from column {C,F} would be:
• S 0C,F (t ) = C × sin(ω3t + 0) + F × sin(ω3t + 0) = (C + F) × sin ω3t
• Consider now a second step, after a PE gradient has been applied (step 1). Imagine the strength of that gradient was such that the pixels along
the bottom line (D, E, F) are now 180° out of phase (= completely opposite) with pixels along the top line (A, B, C):
• The signal from pixel A is unchanged (phase is 0 as this pixel is at the 0 line of the gradient) and is still equal to A × sin(ω1t ).
• The signal from pixel D is now D × sin(ω1t + 180) = – D × sin(ω1t ) (basic trigonometry rule). In other words, that signal is now inverted.
• As a result, signal from column {A,D} would be, for that step 1 signal readout:
• S1A,D (t ) = A × sin(ω1t) + [–D × sin(ω1t )] = (A – D) × sin ω1t
• By the same logic, signal from columns {B,E} and {C,F} would now be:
• S1B,E (t ) = (B – E) × sin(ω2t )
• S1C,F (t ) = (C – F) × sin(ω3t )
• The knowledge of S0A,D(t ) alone, or S1A,D(t ) alone is not sufficient to determine A and D uniquely, but what happens if we calculate their sum and
their difference?
• S0A,D (t ) + S1A,D(t ) = (A + D) × sin ω1t + (A – D) × sin ω1t = (A + D + A – D) × sin ω1t = 2A × sin ω1t (i.e., a signal whose amplitude is ONLY
contributed to by pixel A).
• S0A,D (t ) – S1A,D(t ) = (A + D) × sin ω1t – (A – D) × sin ω1t = (A + D – A + D) × sin ω1t = 2D × sin ω1t (i.e., a signal whose amplitude is ONLY
contributed to by pixel D).
• Using the same algebraic manipulation of signal obtained during the two different readouts (phase of 0° and phase of 180°), one can also
determine uniquely the pairs {B,E} and {C,F}.
• With this overly simplified example, you can understand how signal from these six pixels can now be encoded:
• The first signal is acquired during application of an FE gradient but without preliminary application of a PE gradient (step 0), therefore there is
no phase shift between lines (A,B,C) and (D,E,F). When we apply a Fourier transform on that signal, we reveal three signals of respective
frequencies ω1, ω2, and ω3; their respective amplitudes are (A + D), (B + E), and (C + F).
• The second signal is acquired after a PE gradient has been applied, causing a phase shift of 180° between the two lines (A,B,C) and (D,E,F).
The signal is read out using the same FE gradient, and if a Fourier transform is applied to that signal, it reveals again three signals of respective
frequencies ω1, ω2, and ω3; now, their respective amplitudes are (A – D), (B – E), and (C – F).
• By simple algebraic manipulation of the sum and difference of these signals, one can sort out uniquely A, B, C, D, E, and F.
• Another way to look at this is to realize that measuring mathematical function that can extract the frequency
successive phase shifts of a signal is the same as taking components of a signal.
successive measurements of the same signal over time, as • As these pseudo-frequencies (rate of change of phase)
we are doing with FE: obtained by Fourier transform of the signal in the PE
• The rate at which the phase shifts are occurring can be direction are dependent on location in the PE direc-
thought of as a ‘pseudo-frequency’ and can be decoded tion, this indeed represents another form of spatial
by Fourier transform, which, as you remember, is a localization of signal using frequencies.
28 CHAPTER 1
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Amplitude
C+F
A+D
B+E
Phase-encoding gradient
Frequency
Zero A B C ω1 ω2 ω3
Amplitude
No 180° phase
Phase shift
D E F Shift
A–D C–F
B–E
ω1 ω2 ω3 Phase-encoding Phase-encoding Frequency

Step 0 Step 1
No gradient Gradient ω1 ω2 ω3
turned on
Frequency-encoding gradient
Fig. 1.30 Simplified explanation of the principle of phase-encoding. (Refer to Table 1.3 for a detailed explanation.)
TE/2 180
90
RF pulses
Slice selection GS GS
gradient Gф3
Gф2
Phase-encoding Gф1
gradient
Frequency-encoding GFE
gradient
MR signal
TE
Readout
Fig. 1.31 Simplified diagram representing a standard spin echo pulse sequence. The slice selection gradient (GS) is applied
simultaneously with the RF pulses, so that these pulses are selective of the slice of interest. The phase-encoding gradient is
applied between the 90° and 180° pulses. In this simplified example, three positive gradient steps are represented, each creating
different phases. The frequency-encoding gradient is applied at the same time as the echo is formed, during readout of the MR
signal.
• In practice, the PE gradient in a standard spin echo These will slightly modify the precession frequency or
sequence is applied between the 90° and 180° RF pulses the phase of spins in each direction x and y of the imag-
(Fig. 1.31). It is classically represented on the pulse ing plane. The frequency or phase shifts of the signal
sequence diagram as a stack of rectangles represent- contain information regarding the spatial distribution of
ing the varying strengths (slopes) of all the PE gradient protons along the x and y axes.
steps, each of them encoding a different line of k-space. • The signal obtained during a readout is a complex varia-
tion of amplitude as a function of time, which can be
THE FREQUENCY DOMAIN, OR K-SPACE, decomposed into its individual components with infor-
AND ITS RELATIONSHIP TO THE MR IMAGE mation about frequency/phase/amplitude. This operation
is done using the Fourier transform. Therefore, the MR
• As shown previously, to obtain an MR image gradients of signal, as recorded, does not contain direct information
magnetic field are added to the main magnetic field B0. about spatial coordinates. The MR signal in the ‘time
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domain’ needs to be processed using a Fourier transform

to extract the information about frequencies within it,
which are related to spatial localization. The MR signal
is not recorded directly in the ‘spatial domain’; it is in the
time domain and then Fourier transformed and collected
in the ‘frequency domain’, also called ‘k-space’. For a Nx ×
OBJECT
Ny image matrix, with Nx being the number of pixels in Dimensions d x d (mm)
the FE direction and Ny the number of pixels in the PE
direction, Ny successive 90° pulses are used to generate Gradient
strength
Ny readout signals, each readout being obtained after = slope = Gx
application of a different PE gradient strength (PE step).
• So one can think of that data space (k-space) as a matrix
that contains as many lines and columns as there are lines
and columns in the image. For an Nx × Ny image matrix,
we would have to fill data in a k-space that contains Nx ×
Ny data points.
• Each ‘point’ in k-space contains some information about
frequency/phase shift that was acquired during read- B0
out of the signal at the time that specific data point was
recorded (k x), as well as some information on the phase Frequency-encoding gradient
that was imparted to protons by the previously applied
PE gradient (k y).
Fig. 1.32 Spatial localization along the frequency-encoding
• What is important to understand is that, even though
gradient. Magnetic field at a position x depends on gradient’s
visually the k-space matrix resembles an image matrix,
slope Gx: Bx = B0 ± Gx × x. According to the Larmor equation,
the signal within a specific data point of coordinates
the frequency of signal at position x will be: ω x = γ × Bx = γB0 ±
(k x,k y) does NOT correspond to the pixel of coordinates
γGx × x. There is therefore a relationship between frequencies
(x,y) in the image. Rather, each point in k-space con-
and spatial location along the x-axis; that relationship depends
tains some information that was contributed to by all the
on the slope (strength) of the gradient.
pixels of the image, and represents a ‘spatial frequency’
that exists across the entire image. From a mathematical
standpoint, each point of coordinates (k x,k y) in k-space TFE TFE
has a signal that corresponds to the sum (or integral) of 3× seconds, and the last sample (k xN ) after N ×
N N
all the little signals in all the little pixels across the entire seconds.
image (spatial domain), under that particular PE gradi-
ent strength (step) and that point in time during readout • Therefore, in k-space, there is a relationship between
(FE gradient). k xi (‘i’ is the order of the data point k xi) and the product
T
• It is the decoding of that space, using an ‘inverse Fourier γ × G x × i × FE .
N
transform’, that will allow assigning each pixel in the • It would be easy to think that one could also apply a
spatial domain (physical image plane) a signal intensity FE gradient along the y-axis to encode frequencies in
that corresponds to the actual spins that belong to that that direction and, therefore, encode the signal into the
particular voxel. two directions (x and y), which could then be recorded
• The FE gradient imparts information to the signal during one readout. However, it does not quite work
that is related to the spatial location along the x-axis this way. As shown earlier (see “Spatial encoding: slice
(Figs. 1.32, 1.33): selection”), the simultaneous application of gradients in
• Indeed, when a linear gradient of strength (or slope) different directions results, in effect, in one single gradi-
Gx is applied along the x-direction, the magnetic field ent direction, which is the vectorial sum of the orien-
varies linearly from left to right and, at any position x, tation of the two primary gradients, weighted by their
can be expressed as Bx = B0 ± Gx × x. respective strengths. This is how oblique image planes
• Due to the Larmor equation, this means that signal are obtained. Therefore, that strategy would not work
frequency along the x-axis also depends on location to encode separately the x and the y direction during the
and can be expressed as ωx = γB0 ± γGx × x. same signal readout. This is why another strategy is used,
by imparting a temporally separate PE gradient in the y
• If the FE gradient is applied for TFE seconds, the first
direction, prior to readout.
sample (k x1) is obtained after TFE seconds, the second
N • At each PE step, a gradient of strength Gyj (‘j’ is the order
TFE
sample (k x2) after 2× seconds, the third (k x3) after of the line) is used, and gradient strength is increasing
N
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One readout signal, obtained after N samples (signal amplitude

a specific phase-encoding step as a function of time), every
Ts sec
SAMPLING WINDOW Time Ts = TFE/N
Total duration = TFE
Ts Analog to
digital
converter
OBJECT Discrete Fourier

Dimensions d x d kx1kx2……………………kxN transform
(mm)
k-SPACE N frequencies and

ky Spatial frequencies amplitudes,
xmin = –d/2 xmax = +d/2 (mm–1) placed in k-space
on corresponding line
GFE = Gx
Duration = TFE
kx
Fig. 1.33 The duration of the frequency-encoding gradient determines the sampling window TFE. Within that sampling window,
signal is sampled at a rate that depends on the number of samples needed (N = number of pixels in the image in the frequency-
encoding direction); a sample is obtained every Ts = TFE/N seconds. N discrete samples of the readout signal (amplitude as a
function of time, time-domain) are collected and digitized by an analog to digital converter. A discrete Fourier transform of that
signal is performed and yields N data points (k x1 to k xN, frequencies and amplitudes, frequency domain), which are placed in the
appropriate line of k-space.
ymax = +d/2
kyNy……………………
GyNy
Dimension d
OBJECT k-SPACE
……
Spatial frequencies ky
Dimensions d x d
(mm) Gy2 (mm–1)
Gy1
ky2 ……………………
ky1 ……………………
ymin = –d/2 kx
Fig. 1.34 Phase-encoding (PE) is used to fill lines of k-space. Each line is filled using a different PE gradient strength. If there
are Ny lines in the PE direction, Ny different PE gradients are applied successively (from Gy1 to GyNy). Gradients from Gy1
to GyNy have incremental strengths (slopes Gyj), thereby inducing a different phase shift along the y-axis. That phase shift is
‘memorized’, and recorded during signal readout for that specific PE step. Each readout fills up one line of k-space. The process
is repeated until all the lines from k y1 to k yNy have been encoded.
incrementally (which is why we represent that gradient as • For each line k yj, the phase acquired is a function
a stack of little rectangles) (Fig. 1.34): of the gyromagnetic ratio γ, the strength of the PE
• For each corresponding readout, a specific phase shift gradient Gyj, and the time this gradient is applied for
has been acquired by all protons in all voxels of the (TPE).
imaging plane (during preliminary application of the • Therefore, in k-space, there is a relationship between
PE gradient), and signal is frequency-encoded during k yj and γ × Gyj × TPE .
readout of the echo; that data is used to fill-up one line • Note that the symbol representing the PE gradients
of k-space (Fig. 1.34). That line corresponds to a spe- is a stack of rectangles spread above and below the ‘0’
cific PE step (a specific strength of the PE gradient) value; this is because the successive gradient strengths
and contains all frequencies of the signal from pixels will be creating a phase that varies between –180° and
along the FE direction. +180° (a complete cycle of 360°).
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y 2 cycles per unit length in the ky

x-direction
No variation of spatial
ky1 = 0 (no variation of
frequency in the y-direction
frequency in the y-direction)
x kx
IMAGE K-SPACE kx1 is a low spatial frequency

y = SPATIAL DOMAIN = FREQUENCY DOMAIN ky (only 2 cycles/unit length)
ky2 = 0 (no variation of

frequency in the y-direction)
x kx
8 cycles per unit length in the
x-direction
No variation of spatial
frequency in the y-direction
kx2 is 4 times higher spatial
frequency than kx1
(8 cycles/unit length vs
2 cycles/unit length)
Fig. 1.35 Line-pair phantoms with different spatial frequencies (2 line-pairs per unit length at the top, 8 line-pairs per unit
length at the bottom) and their corresponding Fourier transform represented in a k-space.
• In the end, a specific point of coordinates (k xi, k yj) in

TFE contrast, signal intensity, and detail (spatial resolution).
k-space contains data that is a function of [ γ × G x × i × ]
N The central regions of k-space contain the low frequen-
and [ γ × G yj × TPE]. cies information (i.e., the general shape and contrast of
• To further understand the relationship between spatial the object), while the peripheral portions of k-space con-
frequencies in the object and k-space, look at Fig. 1.35. tain the information on edges and small objects (i.e., the
This shows two simple line-pair phantoms, similar to spatial resolution and detail in the image [Fig. 1.36]).
the one in Fig. 1.21. The first phantom contains only a There are online resources that allow you to play with
single spatial frequency in the x-direction, of 2 line-pairs this concept and obtain the Fourier transform and cor-
per unit length. The second object contains a higher responding k-space of any image, and then reconstruct
spatial frequency of 8 line-pairs per unit length. In both the image by selecting sub-portions of k-space, using an
objects, there is no variation of spatial frequencies in the inverse Fourier transform (http://www.ejectamenta.com/
y-direction (only vertical line pairs). The Fourier trans- ImagingExperiments/fourierimagefiltering.html). If you
form of the low frequency object in k-space would reveal do this on a dorsal MR image of a dog, for example, you
only one frequency with k y = 0 (no variation of spatial fre- can see, as shown in Fig. 1.37, that:
quency in the y-direction) and a low k x value (low spatial • When keeping only the low frequencies (central
frequency, 2 cycles/unit length). The Fourier transform k-space) and removing the higher frequencies (periph-
of the higher frequency object would reveal still a single eral k-space), equivalent of a ‘low-pass filter’, you
point with k y = 0 (no variation of spatial frequency in the obtain an image that has the general shape and con-
y-direction) and a higher k x value with a 4 times higher trast of the original, but with blurry edges and poor
frequency. spatial resolution.
• The k-space, in the end, is the result of a Fourier trans- • When removing the low frequencies and keeping
form of the MR signal in two directions, extracting only the higher frequencies, equivalent to a ‘high-
the variations in spatial frequencies in the x-direction pass filter’, you obtain an image that has only the fine
(FE) and y-direction (PE). We talk about a 2D-FT details of the original but low signal and low contrast.
(two-dimensional Fourier transform). Once that data • Therefore, one can emphasize contrast over detail,
is acquired, the inverse operation is repeated (inverse depending on which part of k-space is acquired and
Fourier transform), to reconstruct an anatomic image, reconstructed. In a typical data acquisition, the central
which contains intensities in the spatial domain. lines of k-space are acquired first, providing the general
• As discussed above, and introduced in the section contrast and shape, and the upper and lower lines are
‘From image to spatial frequencies: notion of Fourier then progressively acquired, adding, every time, more
transform’, k-space contains all the information about details to the image.
32 CHAPTER 1
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+180°
Periphery of k-space
contains lower amplitude,
higher frequency information
Phase-encoding gradient = DETAILS AND EDGES
+90° = SPATIAL RESOLUTION
GyN
Center of k-space contains
…………
0 higher amplitude, lower

Gy2 frequency information
Gy1
= CONTRAST AND GENERAL
SHAPE
–90°
–180°
Fig. 1.36 The central regions of k-space contain the low frequencies information (i.e., the general shape and contrast of the
object), while the peripheral portions of k-space contain the information on edges and small objects (i.e., the spatial resolution
and detail in the image).
K-space Entire image Image

Inverse fourier
transform
Fourier
transform
Low-pass filter High-pass filter
Fig. 1.37 Dorsal MRI image of the head of a dog and corresponding k-space. At the bottom are images obtained when selecting
sub-portions of the k-space to reconstruct an image. The central portion of k-space (bottom left) contains the general shape
and contrast of the object, but without detailed edges and with a blurry appearance/poor spatial resolution. The peripheral
portions of k-space (bottom right) contain the detail and spatial resolution information. These images were created on the web
site http://www.ejectamenta.com/ImagingExperiments/fourierimagefiltering.html, using a dorsal MR image of a dog’s head.
• Various strategies to fill-up data in k-space can be used • Navigation through k-space for spatial encoding is made
to gain time while maintaining adequate information by applying gradients of various directions and strengths,
regarding contrast and spatial resolution, depending on and/or RF pulses (for example, a 180° pulse when in a
the primary goal of the images. For example, in MR angi- certain location [k xi,k yj] will switch the data collection to
ography with gadolinium, rapid spiral encoding of the the point [−k xi,−k yj] of k-space). This opens many possi-
central portions of k-space is used to quickly obtain the bilities for strategies of k-space encoding, which depend
maximum information about contrast during first-pass on the goals and priorities for imaging, as well as con-
of gadolinium across the vascular territory of interest. straints of specific pulse sequences.
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• To take the example of a simple spin echo sequence is repeated, this time with the next PE gradient
(Fig. 1.38): strength, thereby moving the acquisition to the next
• The 90° pulse places us in the center of k-space (no line of k-space.
phase in any direction, all protons in slice at same • Intuitively, you can guess that there is a straightforward
frequency). relationship between k-space (spatial frequencies, unit
• Between the 90° and 180° pulses, the first PE gradient cm−1) and image space (distances, cm). It is beyond the
is applied, in this case the –180° gradient (bottom line scope of this book to get into the complicated mathematical
of the stack). This moves us in k-space down to the explanation for the relationship; however, it is important
bottom line in the vertical direction. Simultaneously, to remember the following points (Fig. 1.39):
a positive gradient in the FE direction is applied, • There is an inverse relationship between spacing
which moves us to the right-hand side of the bottom of successive sampling points in k-space (Δk x and
line (i.e., in the right bottom corner of k-space). Δk y in cm−1 [i.e., column and line spacing]) and the
• After this, a 180° pulse is applied, which reverses the dimensions of the FOV (in cm) in the x-direction and
position of spins and causes us to move in k-space in y-direction:
the opposite corner (top left corner). 1
• We are now ready to read out the signal for the 1st – FOVx = (see demonstration in Table 1.4).
∆k x
(top) line of k-space by applying a positive FE gradient 1
as the echo is forming, which in effect is moving us to – FOVy = .
∆k y
the right along that line. Signal is sampled discretely
– In other words, the more space there is between
as the gradient is applied, obtaining data for all points
lines and columns of k-space, the smaller the FOV
at regular time intervals from the left to the right.
• Some time after the end of signal readout (end of the and vice versa.
TR [repetition time]), a new 90° pulse is applied, and • The maximum frequencies sampled (k xmax and k ymax)
we are now back in the center of k-space. The process are related to the size of the pixels in the x-direction
180
180
90
RF RF 90
GS GS
GPE GPE
GFE GFE
180
180
90 90
RF RF
GS GS
GPE GPE
GFE GFE
Fig. 1.38 Navigation through k-space during a spin echo pulse sequence. Top left: the 90° pulse places us in the center of
k-space (no phase in any direction, all protons in slice at same frequency). Bottom left: between the 90° and 180° pulses, the
first phase-encoding gradient is applied, in this case the –180° gradient (bottom line of the stack). This moves us in k-space
down to the bottom line in the vertical direction; simultaneously, a positive gradient in the frequency-encoding direction
is applied, which moves us to the right-hand side of the bottom line (i.e., in the right bottom corner of k-space). Top right:
After this, a 180° pulse is applied, which reverses the position of spins and causes us to move in k-space in the opposite corner
(top left corner). Bottom right: we are now ready to readout the signal for the 1st (top) line of k-space by applying a positive
frequency-encoding gradient as the echo is forming, which in effect is moving us to the right along that line. Signal is sampled
as the gradient is applied, obtaining data for all points from the left to the right. After this (end of the time of repetition), a
new 90° pulse is applied, and we are now back in the center of k-space. The process is repeated, this time with the next phase-
encoding gradient strength, thereby moving the acquisition to the next line of k-space.
34 CHAPTER 1
VetBooks.ir
K-space Image matrix
1
FOVx =
Δkx
Δx = 1
2kxmax
–kxmax +kxmax
Δkx Δx
2kxmax FOVx = Nx × Δx
Fig. 1.39 Relationships between dimensions in k-space (cm–1) and image matrix (cm). Spacing between lines and columns in
k-space (Δk) relates to the physical dimensions of the image field of view. Pixel size in the image (Δx) is related to the maximum
range of frequencies in k-space (2k max).
Table 1.4 Simplified mathematics behind the relationship between field of view (FOV) and k-space.
FOVx FOVx
• The FOV in the FE direction (FOVx) corresponds to pixels of coordinates − xmax = − to xmax = + in the spatial domain.
2 2
 BW   BW 
• The range of frequencies sampled during signal readout is called the ‘receive bandwidth’ (rBW), and varies from  −  to  +  (for
2  2 
example, a BW of 32 kHz encompasses frequencies from –16 to +16 kHz around the central frequency).
1
• rBW can be thought of as the inverse of FE sampling time .
TFE
 BW 
•  +  can be thought of as the maximum resonant frequency at the far right of the FE gradient.
2 
FOVx
• If the strength of the FE gradient is Gx (T/cm), then the resonant frequency (Hz) at a distance xmax = + along the x-axis in the image plane
FOVx 2
would be (Larmor equation): γ × Gx × .
2
 BW 
• As seen above, that frequency is also equal to  + .
 2 
• Therefore, we have the following relationship:
 BW  FOVx
 +  = γ × Gx ×
2  2
or
BW 1
FOVx = =
γ × Gx TFE × γ × Gx
• As you can see, the stronger the gradient, the smaller the field of view.
• The strength (slope) of the gradient determines how much frequency shift there is between two consecutive points in k-space along the FE
direction: the stronger the gradient, the more spacing there is.
• Therefore, the spacing Δkx between successive kx points in k-space is inversely proportional to the size of the field of view in the frequency-
encoding direction
1
FOVx =
∆k x
and y-direction (i.e., the spatial resolution of the sampled along the echo, which is centered on the null
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image). Intuitively that makes sense, as we noted pre- value of k x, and the echo is itself symmetrical.
viously that the peripheral portions of k-space contain • Therefore, the data at (k xi, k yj) is identical to that at
the high frequency information corresponding to the (–k xi, –k yj).
detail/resolution in the image. Therefore, the higher • This property can be used to our advantage to encode
values of k x and k y correspond to a higher and higher k-space faster without having to actually acquire all
frequency signal and smaller and smaller details in the data points: half-Fourier acquisitions, for example,
image (i.e., smaller pixels). There is, therefore, a rela- utilize this property.
tionship between the size of the pixels (Δx and Δy) and
the maximum range of k x (k xmax – (–k xmax) = 2k xmax) and FURTHER READING
k y (k ymax – (–k ymax) = 2k ymax) in k-space:
1 Below are only a few of the many resources that are avail-
– ∆x = (high values of k xmax correspond to
2k x max able to learn more about the very complex physics of
smaller pixels in the x-direction). MRI. The list only includes the main texts that were used
1 to compile the summary presented herein. Much more
– ∆y = (high values of k ymax correspond to
2k y max detailed information, beyond the scope of this particular
smaller pixels in the y-direction). textbook, can be found in these and many other books/
– Since there is, as noted earlier, a relation- articles/web sites.
ship between (k xi,k yj) and {[ γ × G x × i × TFE ],
N Berry E, Bulpitt A (2009). Fundamentals of MRI: An Interactive
[ γ × G yj × TFE]}, k xmax and k ymax in turn also depend Learning Approach (Series in Medical Physics and Biomedical
on the strength of the FE and PE gradients Gx and Engineering). CRC Press, Boca Raton.
Dale BM, Brown MA, Semelka RC (2015). MRI: Basic Principles and
Gy used.
Applications, 5th edn. Wiley-Blackwell, Hoboken, New Jersey.
• There are symmetrical properties to k-space (‘conjugate Kastler B, Vetter D, Pattay Z, Germain P (2011). Comprendre
symmetry’): l’IRM: Manuel d’auto-apprentissage, 7ème edn. Elsevier Masson,
• The data on the top half of k-space (positive k y) is iden- Issy-les-Moulineaux.
McRobbie DW, Moore EA, Graves MJ, Prince MR (2006). MRI
tical to the data on the bottom half (negative k y). This
from Picture to Proton, 2nd edn. Cambridge University Press,
is because the PE gradients’ strengths (slopes) used Cambridge.
to acquire data in the top half of k-space are identi- Plewes DB, Kucharczyk W (2012). Physics of MRI: a primer.
cal (albeit with a reversed polarity) to those used to JMRI 35:1038–54.
acquire data in the bottom half of k-space. Runge VM, Nitz WR, Schmeets SH (2008). The Physics of
Clinical MR Taught Through Images, 2nd edn. Thieme Medical
• The data in the left half of k-space (negative k x) is the Publishers, New York.
same as that in the right half of k-space (positive k x). Westbrook C, Roth CK, Talbot J (2011). MRI in Practice, 4th edn.
This is because on each line the frequencies are Wiley-Blackwell, Chichester.
CHAPTER 2
IMAGE CHARACTERISTICS IN MRI AND

36 PRINCIPAL PULSE SEQUENCES
Wilfried Mai
CONTENTS
Field of view and spatial resolution .........................................................................................................................................................................36
Relationship between k-space, field of view, and spatial resolution ...................................................................................................................37
Field of view in the phase-encoding direction and phase-wraparound...............................................................................................................39
Field of view in the frequency-encoding direction, notion of receiver bandwidth, and frequency-wraparound ...................................................40
Signal and contrast in MRI and image weighting ....................................................................................................................................................42
Signal-to-noise ratio ...............................................................................................................................................................................................46
Acquisition time ......................................................................................................................................................................................................48
Principal pulse sequences.......................................................................................................................................................................................48
Spin echo ..........................................................................................................................................................................................................48
Fast spin echo/turbo spin echo.......................................................................................................................................................................... 51
Single shot fast spin echo..................................................................................................................................................................................53
Inversion recovery .............................................................................................................................................................................................53
Short tau inversion recovery.........................................................................................................................................................................54
Fluid attenuated inversion recovery ..............................................................................................................................................................55
Gradient echo pulse sequences .........................................................................................................................................................................55
General principles of gradient echo imaging ................................................................................................................................................55
Steady-state gradient echo/rewound gradient echo/coherent gradient echo .................................................................................................61
Spoiled gradient echo (‘incoherent’ gradient echo) .......................................................................................................................................62
Time-reversed gradient echo ........................................................................................................................................................................63
Echo planar imaging ..........................................................................................................................................................................................65
Diffusion-weighted imaging...............................................................................................................................................................................65
Chemical fat saturation technique ......................................................................................................................................................................66
Further reading........................................................................................................................................................................................................68
In this chapter, we will review the characteristics of MR • The FOV is determined by the technologist at the MRI
images, as well as some of the parameters that control them. control work-station and depends on the patient’s size,
We will then describe commonly used MRI pulse sequences area under investigation, and clinical indication for imag-
and their clinical applications in veterinary imaging. ing. The physical parameters that actually control the
size of the FOV are the frequency- and phase-encoding
FIELD OF VIEW AND SPATIAL RESOLUTION gradient strength (GFE and GPE) and, in the frequency-
encoding direction, the receiver bandwidth (rBW, see
• The field of view (FOV) represents the actual dimension below).
of the image obtained and is measured in cm or mm. • Spatial resolution is the ability of the imaging system to
• It is made of a matrix of pixels arranged in lines and col- differentiate and display separately two small objects that
umns. The most common image matrices are squared, so are close to each other. The better the resolution,
that there are equal numbers of lines and columns. A typ- the smaller these objects and the closer to each other
ical matrix has 256 lines and 256 columns (256 × 256 = they can be. Intuitively, it is the volume of the voxel that
65,536 pixels). will determine spatial resolution in MRI.
I m age C h a r ac t e r is t ic s i n M R I a n d P r i nc i pa l P u l s e Se qu e nc e s 37
• There are therefore three parameters that define the spa- Relationship between k-space, field
tial resolution of an MR image (see Fig. 1.19): of view, and spatial resolution
• Dimensions of the FOV. • As you will remember from Chapter 1, data for MR image
• Slice thickness. formation is stored during readout in the frequency
• Size of the image matrix. domain, called k-space. Each line of k-space corresponds
• For a given FOV, increasing the matrix size decreases the to a readout of an MR echo signal, obtained after the
pixel dimension and, therefore, increases resolution. For application of a specific phase-encoding (PE) gradient
example, for a 12.8 cm square FOV and a 128 × 128 pixels (which generates phase differences in the PE direction),
image matrix, the in-plane resolution will be 1 mm. If and during a frequency-encoding (FE) gradient (which
the image matrix is changed to 256 × 256, the pixel size generates frequency differences in the FE direction).
decreases to 0.5 mm, improving in-plane resolution by a • The spacing Δk between the lines of k-space is inversely
factor of 2. related to the FOV (see Chapter 1), so that the wider Δk,
• Increasing slice thickness decreases resolution in the the smaller the FOV (Fig. 2.1). Since what determines
direction perpendicular to the image plane. the spacing between two successive points in k-space
• Larger voxels lead to increased volume averaging, as dif- (frequency or phase differences) is the steepness (slope)
ferent objects of different signal intensity are averaged of the gradient, increasing the gradient strength will
out in the resulting voxel containing them. decrease the FOV.
kxmax kxmax
kxmax/2 kxmax
kymax
k-space
kymax /2
kymax /2
kymax
8 x 8 samples 4 x 4 samples 4 x 4 samples 8 x 4 samples

kxmax = kymax Unchanged kxmax = kymax kxmax and kymax halved Same kxmax , halved kymax
Equal spacing (∆kx = ∆ky) Increased ∆kx = ∆ky Unchanged ∆kx = ∆ky Unchanged ∆kx = ∆ky
Image
8 x 8 pixels 4 x 4 pixels 4 x 4 pixels 8 x 4 pixels

Squared pixels Squared pixels Squared pixels Rectangular pixels
Square FOV Same size pixels Pixels twice as large Pixels twice as large in the
Smaller, square FOV Same square FOV y direction
Same square FOV
(a) (b) (c) (d)
Fig. 2.1 Relationship between k-space, image field of view (FOV), and resolution. (a) Squared k-space with eight samples in
both directions and equal spacing (Δk x = Δk y). This corresponds to an 8 × 8 pixels image; the FOV is square because spacing
in k-space is identical in both directions, and pixels have the same size in both directions (square pixels) because the maximum
extent in k-space (k xmax and k ymax) is identical in both directions. (b) Compared with (a), the extent of k-space (maximum values
of k x and k y) is unchanged, but there are 4 × 4 samples with double space between them; this yields a smaller FOV in the image
(increased Δk in k-space) with 4 × 4 pixels of same resolution (since k xmax and k ymax are unchanged). (c) Compared with (a),
extent of k-space is halved, keeping only 4 × 4 samples while not changing their spacing Δk; this yields an image of same FOV
(unchanged Δk) but 4 × 4 pixels that are twice the size (half the resolution) because k xmax and k ymax were divided by 2. The image
is blurrier due to the decreased resolution. (d) Compared with (a), extent of k-space was halved in the y-direction but maintained
in the x-direction, while spacing of samples is preserved (Δk x = Δk y) resulting in 8 × 4 samples; this yields an image that has 8 × 4
pixels but now they are rectangular because k ymax is decreased, so the pixels are longer in the y-direction than in the x-direction
(= loss of spatial resolution in the y-direction). The FOV, however, is unchanged, since the spacing Δk x and Δk y is unchanged.
38 CHAPTER 2
• The maximum frequencies encoded in k-space in both • Rectangular image matrices are possible, where the num-
the FE and PE direction (k xmax and k ymax) determine the ber of lines is not equal to the number of columns, but the
size of the pixels, with higher frequencies corresponding pixels retain the same size and square shape (Fig. 2.2).
to smaller pixels (Fig. 2.1). This can be useful when the shape of the anatomy of
• Fig. 2.1 illustrates the effects of changing either spacing interest is not square and would fit better in a rectangle;
of data points or extent of k-space on the size and resolu- an example would be a sagittal image of the lumbar spine
tion of the actual image obtained. in which the craniocaudal coverage necessary is larger
• Note that if k xmax = k ymax and ∆k x = ∆k y, then a square than the dorsoventral coverage. Another example is a
image FOV with square pixels is obtained (Fig. 2.1). sagittal or dorsal image of the stifle joint, in which the
However, if the numbers of lines and columns are dif- proximodistal coverage needs to be longer than the cra-
ferent and the FOV is square, the pixels are rectangular, niocaudal or left-to-right coverage, respectively. In such
which alters spatial resolution; this resolution is worse in cases, one could decide to use a rectangular FOV with the
the direction where the pixels are longer (see Fig. 2.1d). longer dimension matching the longer direction of the
kxmax
FREQUENCY-ENCODING kxmax
PHASE-ENCODING
k-space
kymax
kymax
8 x 8 samples 8 x 4 samples
kxmax = kymax kxmax = kymax
Equal spacing (∆kx = ∆ky) Different spacing (∆ky = 2∆kx)
Image
Aliasing or
wraparound
8 x 4 pixels
8 x 8 pixels Squared pixels
Squared pixels Rectangular FOV, which is halved
Square FOV in the y direction
Same resolution
(a) (b) (c)
Fig. 2.2 k-space, rectangular image field of view (FOV), and phase-aliasing. In some cases, rectangular FOVs can be beneficial
when the anatomy of interest is asymmetrical and larger in one of the two directions. In such cases, it can be useful to phase-
encode along the shorter dimension of the object and decrease the number of phase-encoding steps to gain time. (a) We use
again the 8 × 8 k-space with identical extents of k-space (k xmax = k ymax), and same spacing (Δk), yielding a square image with 8 × 8
squared pixels. (b) If we want to obtain a rectangular FOV shorter in the dorsoventral direction (phase-encoding direction), we
can decrease the number of lines encoded by decreasing the number of phase-encoding steps from 8 to 4. The maximum extent
of frequencies encoded stays as in (a) (same k ymax); however, the gradient increment between each step is doubled so that line
spacing (Δk y) is doubled. The result is that FOVy is halved (since we doubled Δk y) but the size of the pixels in the y-direction is
the same (since we did not change k ymax). Therefore, the rectangular FOV has the same resolution (same pixel size as the initial
one). (c) In reality, in that particular example, a phase-wrap or aliasing artifact will happen, because some anatomy exists outside
of the specified smaller FOV in the y-direction. The top part of the head is folded over to the bottom of the rectangular FOV,
and the bottom part of the head is folded over to the top part of the FOV, resulting in an image where erroneously mapped
anatomy is superimposed over the actual desired scanned area. There are strategies to eliminate this problem (see Chapter 3).
anatomic FOV. The square shape and size of the pixels • The larger the difference of GPE between each PE step,
could be preserved by simply reducing the number the larger ∆k y and the smaller the FOV PE .
of pixels in the shorter direction by the same factor as • Along a column of the FOV in the direction of the PE
the decreased coverage in that direction (Fig. 2.2). For gradient, protons acquire a phase during the application
example, a square matrix of 256 × 256 with a FOV of of each PE gradient that depends on their spatial position
256 × 256 mm yields 1 mm square pixels. If one uses a along the gradient (Fig. 2.3).
rectangular FOV of 256 × 128 mm while reducing the • Typically, the gradient strength is chosen so that the
image matrix to 256 × 128 pixels, we still have 1 mm FOV includes the entire anatomy along the direction
square pixels. Typically, the smaller dimension will be the of the PE gradient, imparting phases in that direction
PE direction, as having fewer PE steps to perform (e.g., that vary between –180° and +180° (360° total; i.e., a
128 instead of 256) will allow decreasing acquisition time. full circle of phases) from one extremity of the FOV PE
to the other. However (see Fig. 2.3), the PE gradient
Field of view in the phase-encoding exists all across the bore of the magnet (i.e., it also exists
direction and phase-wraparound outside of the prescribed FOV PE). If there is anything
• The FOV in the PE direction (FOV PE) can be adjusted outside of the prescribed FOV PE that contains protons
by changing the differences in amplitude of the PE gra- and therefore can generate an MR signal, these protons
dient between each PE step, which in effect in k-space will be subjected to the same RF pulse and PE gradi-
changes spacing between the encoded lines (∆k y). ent and generate a signal whose phase is dependent on
Area in purple is within the

bore and subjected to the
encoding gradients, but
outside of the prescribed FOV
+180° Phase = +180°

Outside object is wrapped
+160° around to the opposite Phase = +160°
side of the FOV
Phase-encoding gradient
Phase = +90°
0° Phase = 0°
Phase = –90°
–180° Phase = –180°

Object outside of FOV
–200° but in magnet bore Phase = –200°
Fig. 2.3 Simplified explanation of the ‘phase-wrap artifact’. Phases vary in the direction of the prescribed FOV PE from –180°
to +180° (360° total; i.e., a full circle of phases) from one extremity of the FOV PE to the other. However, the phase-encoding
gradient (as well as the frequency-encoding gradient) exists all across the bore of the magnet (in purple) (i.e., outside of the
prescribed FOV). If there is anything outside of the prescribed FOV PE that contains protons and therefore can generate an MR
signal, these protons will be subjected to the same phase-encoding gradient and generate a signal whose phase is dependent
on their location along the gradient. As shown here, a hypothetical proton-rich object located below the bottom of the FOV
may generate a signal and acquire a phase during phase-encoding; in that case, the phase would be –200°. As you can see on the
right with the clock-face analogy, showing the phase-angle displayed on a circle, a phase of –200° is ‘equivalent’ to a phase of
+160° (basic trigonometry), which will fall within the encoded range (–180° to +180°). Consequently, the Fourier transform will
calculate this signal as originating from within the prescribed FOV, ‘wrapped-around’ to the opposite side of the image. This is
called ‘wraparound’ or ‘aliasing’ artifact and can be a significant issue when the prescribed FOV PE is smaller than the anatomy
existing in that direction within the image plane.
40 CHAPTER 2
their location along the gradient. As shown in Fig. 2.3, center frequency of the echo. For example (Fig. 2.4),
due to the equivalence of angles outside of the –180° to a rBW of 80 kHz represents 40 kHz below to 40 kHz
+180° range, the calculation may erroneously localize above the center frequency (–rBW/2 to +rBW/2). This
these protons within the FOV. In the example shown, a value is an operator-selectable parameter, chosen at the
proton localized outside the FOV at the bottom would control workstation, with total rBWs ranging from 5 to
acquire a phase of –200° at that particular location. As 100 kHz. Due to the Larmor equation (Fig. 2.4), the
shown with the clock-face analogy on the right, a phase rBW of 80 kHz mentioned above would correspond to a
of –200° is equivalent to a phase of +160°, which falls variation of 1.88 mT (= 80 × 10 −3/42.57) from one end of
within the [–180° to +180°] range and therefore will be the FOV FE to the other in the FE direction.
erroneously localized in the FOV PE at the +160° location • In the end, FOV FE will be related to two parameters:
(i.e., ‘wrapped around’ to the opposite side of the image). the strength of the FE gradient (GFE), and the rBW
(Fig. 2.5):
Field of view in the frequency-
encoding direction, notion of receiver rBW
FOVFE =
bandwidth, and frequency-wraparound γ × G FE
• Remember that, during readout of the echo, a FE gra-
dient is applied in the FE direction, which will change • Assuming a fixed FE gradient, narrowing the rBW will
the strength of the magnetic field experienced by pro- yield a smaller FOV (Fig. 2.5). For a given rBW, increas-
tons along that direction as a function of their position ing the FE gradient’s strength will decrease the size of
along this linear gradient. Due to the Larmor equation FOV FE .
(ω0 = γ.B0 or, in MHz, f 0 = γ .B0, see Chapter 1), this will • The total rBW is apportioned equally to each of the N FE
change the precessional frequencies linearly in the direc- pixels in the FE direction, so that each pixel receives a
tion of the gradient. Therefore, there is a ‘range of fre- sub-set Δf of the total bandwidth rBW:
quencies’ from minimal to maximal in the direction of
the gradient, which exists across the bore of the magnet rBW
∆f =
in the FE direction. The ‘receiver bandwidth’ (rBW) N FE
refers to the subset of frequencies that will be sampled
during readout along that direction, and therefore will • Based on the formula above, Δf is in hertz/pixel. Some
be related to the FOV FE . It defines the upper and lower manufacturers use that quantity Δf to express bandwidth
limits of frequencies to be digitized on either side of the at the control workstation.
FOVFE
Fig. 2.4 Illustration of the relationship between
receiver bandwidth (rBW) and the variations
in precessional frequencies and magnetic field
seen by protons across the chosen field of view
(FOV) in the frequency-encoding direction.
In this example, the frequency-encoding
gradient is applied left to right, and the rBW is
set at 80 kHz, which determines the range of
frequencies and magnetic field seen by protons
from the extreme left to the extreme right of
the FOV. The frequency-encoding gradient
does exist outside of these boundaries, but
ISOCENTER
only these frequencies are collected during
signal readout. Using the Larmor equation
Frequencies (MHz) (Υ B0 – 40.10–3) Υ B0 (Υ B0 + 40.10–3) [f(MHz) = γ (MHz.Tesla–1) × B0 (Tesla) and γ
Magnetic field (Tesla) (B0 – 0.94.10 )
–3
B0 (B0 + 0.94.10–3) = 42.57 MHz.T–1], one can calculate that such
a bandwidth corresponds to a net variation of
rBW = 80 kHz (= 80.10–3 MHz) magnetic field amplitude of 1.88 mT from left
Corresponds to a variation of magnetic field of 1.88.10–3 T
to right of the FOV.
f
GFE
Receiver bandwidth
x rBW
FOVFE =
Υ × GFE
FOVFE
Fig. 2.5 Schematic showing the relationship between receiver bandwidth (rBW), field of view (FOV) in the frequency-encoding
direction (FOV FE), and strength of the frequency-encoding gradient (GFE). The GFE in this case is applied left to right (green
arrow), which is the frequency-encoding direction. The slope of the green line represents the gradient’s strength (the steeper,
the stronger). For a given gradient strength, the smaller the bandwidth, the smaller the FOV. For a fixed bandwidth, FOV
can be decreased by increasing gradient strength. In practice, the technologist specifies the FOV desired in the frequency-
encoding direction and has no access to gradient strength. The bandwidth, however, can be modified at the MRI control station
in order, for example, to improve signal-to-noise ratio (by decreasing the bandwidth); the machine automatically adjusts the
frequency-encoding gradient strength to maintain the specified FOV. (Note: the notation γ specifies that the unit used for the
gyromagnetic ratio is MHz.T −1.)
• During acquisition, the readout signal is sampled dis- • As illustrated in Fig. 2.6, the highest frequencies pres-
cretely at a frequency that depends on the duration of ent in a given signal may not be represented accurately
the observation TFE (= duration of the FE gradient) mak- if sampling frequency is not high enough. As a result, a
ing up a ‘sampling window’. The sampling is discrete so high-frequency signal may be represented by a lower fre-
T quency, which will lead to erroneous spatial localization
that it occurs every TS = FE seconds (see Fig. 1.33).
N FE and frequency wraparound or frequency aliasing artifact,
TS is sometimes called the ‘dwell time’. The sampling where part of the anatomy will be displayed on the oppo-
frequency (number of samples per second) is equal to the site side of the FOV FE .
inverse of the dwell time: • During signal readout, the maximum frequency we wish
to record accurately in our signal (f FEmax) is determined
1 N by the total rBW. In effect, that maximum frequency is
Sampling frequency ( Hz ) = = FE
TS TFE equal to rBW/2, since we record a range of frequencies
from (–rBW/2) to (+rBW/2). Therefore, we can write
• When sampling a periodic signal, there is a maximum that:
frequency of signal that can be sampled, depending on
the sampling frequency. This is a well-known phenome- rBW Sampling frequency
fFEmax = =
non in Doppler ultrasound, where the maximum Doppler 2 2
shift that can be recorded without aliasing is equal to half • In the end, for a given rBW, sampling frequency must be
the sampling rate (pulse repetition frequency [PRF]). at least equal to the rBW to record the highest frequency
When it comes to sampling the MR signal during read- in that bandwidth without aliasing.
out of the echo, the sampling frequency also determines • This, however, poses a problem, because if the rBW is
the maximum frequency f FEmax contained in the echo that decreased to decrease FOV FE , there may still be higher
can be sampled accurately: frequencies in the signal (coming from outside of the
rBW/FOV FE range), which will be sampled at an insuf-
Sampling frequency ficient frequency, and will wrap around into our sampled
fFEmax =
2 signal, creating artifact. If there is no anatomy outside of
42 CHAPTER 2
Time domain One cycle

TS TS
Time
Time
Fourier
transform
S(t) = S1(t) + S2(t) + S3(t)

One cycle
S1(t) = sin t Actual signal Time

S2(t) = 1.5 × sin(1.5 × t) due to discrete
S3(t) = 2 × sin(2 × t) sampling
Fig. 2.6 Relationship between sampling frequency and accuracy of representation of the sampled signal depending on signal
frequency. The theoretical MR signal on the top left can be decomposed by Fourier transform into three individual sine
waves of specific frequencies and amplitudes, of which the red signal (S3) has the highest frequency (shortest cycle or period).
During readout, a discrete sampling of the MR signal is performed every TS seconds (the ‘sampling frequency’ is 1/TS). When
looking at what this sampling looks like for each of the three individual signals S1, S2, and S3 (top right), we can see that the red
signal (highest frequency, S3) is sampled less than twice per cycle, which leads to the sampled signal (bottom right) having an
erroneous frequency, lower than that of the original signal. On the other hand, the blue and green signals are sampled at least
twice per cycle (i.e., sampling frequency is at least twice that of the signals) and therefore the sampled signals (bottom right)
are represented at the correct frequency. So, for a given sampling frequency, there is a risk that high frequencies may not be
sampled and represented accurately in the MR signal after sampling, leading to aliasing or wraparound artifact.
the prescribed FOV FE , this will not be a problem, but if defined by the difference in signal intensity divided by
there is anatomy outside of the prescribed FOV FE , these the average signal between the two tissues.
undersampled high frequencies will be mapped inside • The signal generated by a given tissue after a 90° RF
the FOV FE , on the opposite side of the image (frequency pulse depends on three intrinsic properties of that tissue:
wraparound or aliasing). • The proton density (ρ): number of mobile hydrogen
• To avoid this, the MR signal can be oversampled, up protons per unit volume of that tissue; the higher ρ,
to 512 to 1,024 times per echo (when typical display the more signal available from that tissue.
resolution in the FE direction is 256). This causes no • The T1 and T2 relaxation times, which depend on
time penalty, as increasing that sampling frequency is three main inherent characteristics of that tissue:
simply performed by increasing the digitizing rate of – Its inherent ability to absorb energy: some tissues
the sampling circuitry; one inconvenient side effect of easily absorb energy from protons, while others do
this method is that it increases the noise and therefore not. This is important for spin-lattice relaxation,
decreases the signal-to-noise (SNR) ratio. A method and influences the T1 relaxation time.
more commonly used is band-pass filtering, which elimi- – The spatial arrangement of the molecules within
nates the spurious high-frequency components and only the tissue. When molecules are closely packed
keeps the frequency components in the desired band. together, this facilitates the interaction between
These remedies are systematically applied during acqui- magnetic fields of hydrogen nuclei that are close
sition, regardless of the FOV, so that aliasing artifact to each other, and this has an influence on spin-
is usually not an issue in the FE direction, unlike the spin relaxation and T2 relaxation time.
phase-aliasing artifact that we covered earlier. – The closeness between natural Brownian motion
frequency of molecules and Larmor frequency of
SIGNAL AND CONTRAST IN MRI protons. The closer they are to each other, the
AND IMAGE WEIGHTING easier the energy transfer between the protons
and the molecular lattice (this is the resonance
• Image contrast is defined by the differences in signal condition), which facilitates spin-lattice relaxation
intensities between various tissues. More precisely, it is and influences T1 relaxation time.
TR
TE/2
180
90 90
RF pulses
GS GS GS
Slice selection
gradients
Gф3
Gф2
Phase-encoding Gф1
gradients G’ф1
G’ф2
G’ф3
GFE
Frequency-encoding GFE
gradients
MR signal
TE Readout
Fig. 2.7 A standard spin echo pulse sequence. The slice selection gradient (GS) is applied simultaneously with the RF pulses so
that these pulses are selective of the slice of interest. The phase-encoding gradient is applied between the 90° and 180° pulses.
In this simplified example, only six gradient steps are represented, each creating different phases; this would correspond to a
theoretical k-space with six lines. The frequency-encoding gradient is applied at the same time as the echo is formed, during
readout of the MR signal. Note that a frequency-encoding gradient is also applied during the application of phase-encoding
gradients, which allows placing ourselves in the correct location of k-space prior to data collection during readout (see Fig. 1.38).
• In Chapter 1, we studied how, during relaxation, the the rate of regrowth of longitudinal magnetization is
longitudinal magnetization grows back according to a more visibly different between CSF and fat, and con-
T1 time constant due to spin-lattice relaxation, and the trast due to differences in T1 relaxation times will
transverse magnetization fades away according to a T2 be emphasized, a phenomenon called ‘T1-weighting’
time constant due to spin-spin relaxation. (Fig. 2.8).
• During a classic spin echo pulse sequence (Fig. 2.7), the • TE determines the amount of decay of transverse
signal is acquired successively for each line of k-space magnetization that has occurred in tissues before
after a new 90° RF pulse. A new RF pulse is repeated signal is measured. For a given tissue, the longer
every time of repetition (TR), and the echo is read at the the TE, the less signal there will be to measure.
time of echo (TE) after the 90° RF pulse: Since tissues have different spin-spin relaxation
• TR determines the amount of longitudinal relaxation times, T2 and TE have an influence on signal
that has occurred before a new 90° RF pulse is applied. measured for each tissue and on signal differences
If the TR is short, then longitudinal relaxation may between tissues (contrast) (Fig. 2.9). As shown in
not be complete by the time of the next 90° RF, and Fig. 2.9, taking the example of fat and CSF again,
therefore there is less magnetization to be shifted into immediately after the RF pulse all tissues have a
the transverse plane for the next readout, leading to maximum transverse magnetization, and therefore
a decrease in signal. Tissues with a longer T1 will measuring signal early (short TE) will minimize the
be more affected by this, and therefore T1 and TR differences between T2 times of different tissues.
have an influence on signal measured and on signal Conversely, measuring signal later (long TE) will
differences between tissues (contrast) (Fig. 2.8). As yield larger differences in residual transverse mag-
shown in Fig. 2.8, taking the simple example of the netization of tissues, and therefore contrast due to
longitudinal relaxation of fat and cerebrospinal fluid differences in T2 times will be emphasized, a phe-
(CSF) after a 90° RF pulse, if one waits a long time nomenon called ‘T2-weighting’.
(long TR) before the next 90° RF, then all tissues • In the end, for a simple spin echo pulse sequence, the
have recovered close to 100% of their longitudinal amplitude of MRI signal given by a specific tissue depends
magnetization, and therefore longitudinal magneti- on TR, TE (pulse sequence parameters), and intrinsic
zation of all tissue is similar, yielding poor contrast tissue properties T1, T2, and proton density (ρ); it also
between tissues. Conversely, when using a short TR, depends on whether flow (such as CSF flow) is present
44 CHAPTER 2
Longitudinal magnetization
Fat
CSF
Long TR
Small differences in
longitudinal magnetization
of tissues
Poor T1 contrast
Short TR
Large differences in
longitudinal magnetization
of tissues
Good T1 contrast
Short TR Time
Long TR
Fig. 2.8 The rate of longitudinal magnetization regrowth after a 90° RF pulse varies across different types of tissues. The TR
determines how much longitudinal magnetization difference there is between tissues and emphasizes these differences when
TR is short; this is called T1-weighting.
Short TE
Small differences in transverse
magnetization of tissues
Poor T2 contrast
Long TE
Large differences in transverse
magnetizaton of tissues
CSF Good T2 contrast
Fat
Short TE Time
Long TE
Fig. 2.9 The rate of transverse magnetization decay after a 90° RF pulse varies across different types of tissues. The TE
determines how much transverse magnetization was allowed to decay prior to the signal readout. The shorter the TE, the less
difference in residual transverse magnetization there is between tissues; a long TE maximizes differences in tissues based on
their T2 relaxation times: this is called T2-weighting.
• For example, images can emphasize (= maximize)

Table 2.1 Relaxation times (approximate values) of various the differences in T1 relaxation time of tissues: this
tissues at 1.5 Tesla.
is called ‘T1-weighting’. This can be achieved by
using:
1.5 teSLA
– A short TR, which maximizes the differences in
Tissue T1 relaxation T2 relaxation T1 of various tissues.
time (ms) time (ms)
– A short TE, which minimizes the differences in
Gray matter 950 100 T2 of various tissues.
White matter 600 80 • Similarly, images can be ‘T2-weighted’ when they
Cerebrospinal fluid* 4,500 2,200 maximize the differences in T2 relaxation time
between tissues. This can be achieved by using:
Fat 250 60
– A long TR, which minimizes the differences in
Muscle 900 50 T1 of various tissues.
*CSF relaxation times are quite variable due to the influence of flow on – A long TE, which maximizes the differences in
signal measurements. T2 of various tissues.
• ‘Proton density-weighting’ can also be obtained,
within the tissue, and there is therefore a ‘FLOW’ factor where contrast relies mostly on the differences in
in the signal equation as follows: concentration of protons (mobile hydrogen atoms)
between tissues. This can be achieved by using:
 −
TR
 −
TE
– A long TR, which minimizes the differences in
Signal SE = ρ ×  1 − e T1  × e T2 × FLOW
  T1 of various tissues.
– A short TE, which minimizes the differences in
• One can manipulate image contrast in MRI using the T2 of various tissues.
control parameters in order to obtain images that • Other forms of weighting exist, relying on more spe-
emphasize certain characteristics of tissues: this is called cific imaging strategies and tissue characteristics
‘image-weighting’. This is due to their inherent differ- (e.g., diffusion-weighting, susceptibility-weighting),
ences in T1 and T2 relaxation times (Table 2.1), as well as which we will address later when covering various spe-
their differences in density of protons (Fig. 2.10): cific pulse sequences.
TE
T2-W
T1-W PD-W
TR
Fig. 2.10 The combination of TR and TE determines the emphasis on T1 differences, T2 differences, or proton density
differences between tissues, allowing images to be obtained that are respectively T1W (short TE and TR), T2W (long TE
and TR), or proton density-weighted (PDW) (short TE and long TR). A combination of a long TE and short TR is not used
as this will lead to very poor signal: maximum loss of transverse magnetization due to the long TE, and very little recovery of
longitudinal magnetization between two successive 90° RF pulses because of the short TR.
46 CHAPTER 2
SIGNAL-TO-NOISE RATIO • Relaxation times of tissues (T1 and T2), which deter-
mine the rate of regrowth of the longitudinal mag-
• Together with spatial resolution, the SNR is the most netization and decay of the transverse magnetization
important factor of image quality in MRI (as in other imag- during relaxation, and therefore the amount of availa-
ing modalities). It measures how much true signal (reflect- ble magnetization during readout and signal amplitude.
ing actual anatomy) versus random noise an image has. • Controllable factors that influence the SNR are:
• In MRI, the main source of noise is the patient’s body, • The volume of the voxels (VOX). Larger voxels contain
which can emit RF energy due to thermal motion. more protons and therefore generate more signal.
Additional noise is created in the receiver chain (pream- There is an inverse relationship between spatial reso-
plifier, RF receive coil). lution and SNR: when resolution is increased (smaller
• A classic measurement of SNR in MRI is to measure the voxels), SNR is decreased.
difference between signal in the object and the back- • The rBW: remember the relationship between the
ground noise (i.e., air around the object) and then divide dimensions of the FOV FE in the FE direction, the
it by the standard deviation of the background signal. amplitude of the FE gradient (GFE), and the rBW
• Non-controllable factors influencing SNR are: rBW
(FOVFE = ). We can increase the rBW with
• The magnetic field strength (B0). As discussed in γ × G FE
Chapter 1, when B0 increases, there is an increase in a simultaneous increase in the gradient’s amplitude
magnitude of the net magnetization vector in every (steeper gradient), which would preserve the same
voxel, thus creating more magnetization to be shifted FOV FE . As shown in Fig. 2.11, changing the rBW
in the transverse plane and more signal to be read out. can influence SNR. When increasing rBW, the signal
The same column of the FOV, with a doubled rBW

(64 kHz). The summed signal from all voxels of this
This is a column of the FOV at that rBW (32 kHz). column has lower maximum amplitude, but is
In this column, the summed signal from spread over a wider range of frequencies so that
all voxels is about 5 times the noise (SNR = 5) the TOTAL signal is the same (the area of the
rectangle is the same). However, the noise
amplitude is unchanged, resulting in noise covering
more of the surface area of the signal (SNR = 3.5;
i.e., 5 divided by the square root of 2).
–32 kHz –16 kHz 0 +16 kHz +32 kHz –32 kHz –16 kHz 0 +16 kHz +32 kHz
rBW = 32 kHz rBW = 64 kHz

rBW
FOVFE =
γ × GFE
Fig. 2.11 Effect of increasing the bandwidth during readout on the signal-to-noise ratio (SNR). During each readout,
corresponding to a specific phase-encoding step (previously applied), data is sampled at regular intervals during the application
of a frequency-encoding gradient, and then Fourier transformed to extract the frequency components. These diagrams can be
thought of as one-dimensional Fourier transform of the signal from one line of k-space; this is a one-dimensional ‘projection’
of the object, digitized into sections according to the number of pixels (columns) in the frequency-encoding direction (in this
theoretical example: N FE = 7). The total receiver bandwidth (rBW) is apportioned equally to each of the N FE columns in the
frequency-encoding direction. In this example, two rBWs are shown, 32 kHz on the left and 64 kHz (doubled) on the right.
The change in bandwidth spreads the range of frequencies allocated to each column; although the peak amplitude of signal
per column is decreased, the total amount of signal is the same. The noise is constant regardless of the rBW, so when the rBW
is increased, you can see on the diagrams that the noise now makes up a larger percentage of the surface area of signal in each
column; therefore, the SNR has decreased when the rBW was doubled. Another consequence of increasing rBW is that signal is
sampled faster (time is inverse of frequency). Note that to maintain the size of FOV FE, when rBW is doubled, the amplitude of
the frequency-encoding gradient (GFE) should be doubled too (cf. equation relating FOV FE, rBW, and GFE).
recorded per column in the FE direction gets spread in order to get sufficient signal and improve SNR.
out over a larger frequency range; the maximum ampli- When NEX is doubled, SNR is increased by a factor
tude of the signal decreases, but the total signal per of 2. Increasing NEX results in significant increase
column that is collected remains the same. However, in acquisition time, as each line of k-space is acquired
since noise amplitude is constant, the increase in rBW multiple times; if NEX is doubled, then acquisition
results in a lower summed SNR per column. There is time is doubled.
an inverse relationship between SNR and the square • The number of PE steps (= number of pixels in the
root of rBW. So, for example, if rBW is doubled, SNR PE direction [N PE]). Indeed, as we reviewed earlier,
is divided by a factor of 1.4 (square root of 2). The the signal from the entire FOV is recorded as many
benefits of using a larger rBW, however, are: times as a readout is happening, which is determined
– A shorter readout time, so that shorter TEs can be by the number of PE steps. Thus, for a matrix with
used (Table 2.2). 128 PE steps, less signal is accumulated from the FOV
– A reduced chemical shift artifact between fat and than with 256 PE steps; it can be shown that SNR is
water protons (see Chapter 3). a function of the square root of N PE . The increase in
• The number of excitations (NEX). NEX represents N PE causes some increase in SNR. Now, obviously,
the number of times that signal from a given line of it is not that simple, since when going from 128 to
k-space (i.e., a given PE gradient step) is recorded and 256 PE steps, there is also a drop in SNR due to the
averaged with other signal readouts of the same line. pixels now being two times smaller in the PE direc-
The reason for doing this is to improve signal. Noise tion. When increasing N PE from 128 to 256 (with
is random and its amplitude varies in each position same FOV PE), SNR is divided by 2 since pixels are
each time data is stored; signal is not random and two times smaller in that direction, but SNR is also
always occurs at the same place when data is collected. multiplied by the square root of 2 due to the doubling
By collecting the data several times and averaging it, in PE steps. The net change in SNR is 2 , which is a
we then tend to increase the proportion of signal rel- 2
factor of 0.7. This represents a net reduction in SNR.
ative to noise, as the noise partially cancels itself out
• In the end, we can write the following relationship
across different data collections. Typically, each line
between SNR and imaging parameters; FPulseSequence
of k-space is acquired 2–4 times, sometimes more,
represents sequence parameters that can also influ-
ence SNR and vary across pulse sequences:
Table 2.2 Relationship between receiver bandwidth and
readout time (acquisition window). VOX × NEX × N PE × FPulseSequence
SNR ∝
rBW
• The rBW determines the time for readout (i.e., the time during which
the FE gradient will need to be turned on for data acquisition for each
• Other operator-controlled parameters that influence
line of k-space). SNR are the TR, TE, and flip angle, which will vary
• For example, if the image matrix contains 256 pixels in the FE across various MRI pulse sequences. Another important
direction, then 256 data points must be collected and stored during factor is the type of receiver coil used:
the acquisition window per line of k-space filling. Remember that the • TR controls the amount of longitudinal magnetiza-
sampling frequency of data during readout must be equal to the rBW tion that can regrow prior to the next RF pulse, so the
to avoid aliasing of the highest spatial frequencies within the FOV. longer the TR the more magnetization has recovered
Therefore, if we pick a rBW of 32 KHz, the sampling frequency is also
32 KHz, equivalent to 32,000 data points collected per second. As
and the more magnetization is available to be flipped
the sampling interval (dwell time) is 1/sampling frequency, a data during the next pulse sequence, thereby providing
point is acquired every 0.00003125 s. Thus, to acquire 256 data more signal. Obviously this costs time, as when TR
points, the total readout time must be 256 × 0.00003125 s or 8 ms, increases, acquisition time will increase too.
and that will be the duration of the FE gradient (in fact, it lasts a bit • TE controls the amount of transverse magnetiza-
longer as there are ramp-up and ramp-down times as well). tion that can decay before readout of the echo. The
• If we now divide rBW by 2 (16 kHz), the sampling frequency also longer the TE, the less residual transverse magnetiza-
becomes 16 KHz. Therefore, only 16,000 data points are acquired
per second, or one point every 0.0000625 s. To acquire 256 data
tion there is, and the lower the signal.
points, we now need a readout for 16 ms. In other words, reducing • The flip angle for a standard spin echo sequence is
rBW while keeping the number of data points constant results in an 90°, which flips the longitudinal magnetization com-
increase in readout time. pletely in the transverse plane allowing a maximum
• As a side note, decreasing rBW also results in an increase in the transverse magnetization to be obtained. We will see
minimum TE that can be used, because the peak of the echo must be later when studying specific pulse sequences (e.g.,
centered in the middle of the acquisition window. This could have gradient echo), that the flip angle can be <90°, which
some implications depending on the type of image-weighting one is
looking for.
leads to lower amplitude of the transverse magnetiza-
tion and lower SNR.
48 CHAPTER 2
• The type of receiver coil used is also an important • MRI pulse sequences can be grouped in several main
factor that influences SNR. Since the most important ‘families’, and within each family various variations of
source of noise is the patient itself, coils with a smaller the same general scheme exist and are referred to using
sensitive volume will result in lower noise coming acronyms that are quite variable across the different MRI
from structures adjacent to the selected plane, and manufacturers. Table 2.3 summarizes the main pulse
therefore improve SNR. Surface coils have higher sequences and acronyms for a subset of MRI brands.
SNR than body coils due to their limited sensitivity
profile. Quadrature-coils have better SNR because Spin echo
signal is acquired from two different coils. Finally, • The spin echo sequence was introduced in Chapter 1
phased-array coils have increased SNR because signal and is illustrated in Fig. 2.7. This is a very commonly
from several coils are added together. used type of pulse sequence and is included in almost any
MRI protocol.
ACQUISITION TIME • A 90° RF pulse shifts the net magnetization into the
transverse plane and, after a time TE/2, a 180° RF pulse
• One of the differences between MRI and other imaging tuned to the slice of interest causes progressive rephas-
techniques, such as computed tomography, radiography, ing of protons that occurs at time TE (the time of echo).
and ultrasound, is that acquisition times are significantly Signal readout is centered on the peak of the echo, while
longer. The inherent factors that contribute to image the FE gradient is turned on for a time that depends on
formation in MRI are responsible for this difference, the chosen rBW. After readout, a new 90° RF pulse is
and strategies that help decreasing acquisition times in applied, at time TR after the previous 90° pulse, and a
MRI are important and implemented as often as pos- new sequence is repeated, to encode a new line of k-space.
sible, although they are always a compromise with some • Choices of TR and TE determine image weighting, as
aspects of image quality such as spatial resolution, SNR, studied earlier:
etc. • Short TR [300–700 ms]/short TE [10–30 ms]:
• The long acquisition times in MRI make general anes- T1-weighted (T1W) images. Because of the short TR,
thesia necessary when imaging small animal patients to scan time is relatively short (4–6 min depending on
avoid motion artifacts. coverage, matrix size, and NEX).
• In the basic spin echo pulse sequence covered in • Long TR [>2,000 ms]/long TE [>80 ms]: T2-weighted
Chapter 1 (Fig. 2.7), we saw that one signal readout is (T2W) images. Due to the longer TE (low residual
necessary for each of the N PE lines of k-space. In the pre- transverse magnetization during signal readout) they
vious paragraph, we mentioned that in fact a readout for have poor SNR; because of the long TR they also take
a given line is often acquired several times in a row, and longer to acquire (7–15 min depending on coverage,
then averaged to increase SNR. The number of times matrix size, and NEX).
a readout is repeated is called the NEX, or number of • Long TR [>2,000 ms]/short TE [10–30 ms]: proton
signal averages. Therefore, each pulse sequence must be density-weighted (PDW) images.
repeated N PE × NEX times to encode the entire k-space • Because TR is typically much longer than TE in a
with sufficient SNR. Each of these acquisitions takes a spin echo sequence, there is an opportunity to use the
time equal to TR. long TR to excite and record echoes from several slices
• In the end, the overall acquisition time for one image in successively within one TR (Fig. 2.12). This is called
a basic spin echo pulse sequence with normal Cartesian ‘multislice acquisition’ and is a strategy that allows
encoding of k-space (line-by-line, all lines acquired) is: a decrease in the total acquisition time. The maxi-
mum number of slices one can excite during one TR
Tacq = N PE × NEX × TR (this defines a ‘group’) depends on the TR and TE, or
• From this relationship, it is clear that decreasing the more precisely the ratio TR/TE. Reducing TR and/or
acquisition time causes a decrease in spatial resolution increasing TE decreases the number of slices that can be
and/or SNR. acquired with one pulse sequence.
• Clinical applications:
PRINCIPAL PULSE SEQUENCES • T1W images provide good anatomic detail due to
their high SNR (short TE → more residual transverse
• An MRI ‘pulse sequence’ is a programed set of RF pulses magnetization to record). Image contrast (in particu-
and changing magnetic gradients, characterized by sev- lar lesion contrast) is not very good; however, in com-
eral parameters adjustable at the control workstation. bination with the use of contrast agents (gadolinium),
Specific pulse sequences are designed for specific imag- lesion conspicuity can be enhanced. Gadolinium is a
ing goals and, for a given patient/clinical application, paramagnetic metal used as an MRI contrast agent
they are grouped in the form of an ‘MRI protocol’. intravenously in the form of a chelate. When in close
Table 2.3 Summary of the various families of MR pulse sequences and acronyms used by a few MRI manufacturers.
GeneRAL eLeCtRiC PHiLiPS SieMenS HitACHi toSHiBA

Spin echo family Spin echo SE SE SE SE SE
(Spin Echo) (Spin Echo) (Spin Echo) (Spin Echo) (Spin Echo)
Fast spin echo FSE TSE TSE FSE FSE
(Fast Spin Echo) (Turbo Spin Echo) (Turbo Spin Echo) (Fast Spin Echo) (Fast Spin Echo)
Ultra fast spin echo SS-FSE SSH-TSE SS-TSE Single Shot FSE FASE
(single shot techniques) (Single Shot Fast Spin Echo) (Single SHot Turbo Spin (Single Shot Turbo Spin (Single Shot Fast Spin (Fast Advanced Spin
Echo) Echo) Echo) Echo)
UFSE HASTE
(Ultra Fast Spin Echo) (Half fourier Acquisition
Single shot Turbo spin
Echo)
Inversion Inversion recovery IR IR IR IR IR
recovery family (Inversion Recovery) (Inversion Recovery) (Inversion Recovery) (Inversion Recovery) (Inversion Recovery)
Short tau (T1) inversion STIR STIR STIR STIR STIR
recovery (Short Tau Inversion (Short Tau Inversion (Short Tau Inversion (Short Tau Inversion (Short Tau Inversion
Recovery) Recovery) Recovery) Recovery) Recovery)
Fluid attenuated inversion FLAIR FLAIR FLAIR Fast FLAIR FLAIR
recovery (FLuid Attenuated Inversion (FLuid Attenuated (FLuid Attenuated (Fast FLuid Attenuated (FLuid Attenuated
(long tau inversion recovery) Recovery) Inversion Recovery) Inversion Recovery) Inversion Recovery) Inversion Recovery)
or Turbo Dark Fluid
True inversion T1 FLAIR Real IR True IR T1 FLAIR
Gradient echo Gradient echo GRE FFE GRE GE FE
family (Gradient Recalled Echo) (Fast Field Echo) (Gradient Recalled Echo) (Gradient Echo) (Field Echo)
Incoherent RF spoiled SPGR (SPoiled Gradient T1-FFE GFE RF Spoiled FE
(spoiled) Recalled) (T1-weighted Fast Field (Gradient Field Echo) (Field Echo)
gradient echo Echo)
Gradient MPGR FLASH GRE FE
spoiled (MultiPlanar Gradient (Fast Low Angle SHot) (Gradient Recalled Echo) (Field Echo)
Recalled acquisition in the
steady state)
I m age C h a r ac t e r is t ic s i n M R I a n d P r i nc i pa l P u l s e Se qu e nc e s
Coherent (steady-state) GRASS (Gradient Recalled FFE FISP SG FE

gradient echo Acquisition in Steady State) (Fast Field Echo) (Fast Imaging with = SARGE (Field Echo)
Steady-state Precession) Steady-state Acquisition
Fast MPGR Rewound Gradient Echo
(Fast MultiPlanar Gradient
Recalled acquisition in the
steady state)
(Continued)
49
Table 2.3 (Continued) Summary of the various families of MR pulse sequences and acronyms used by a few MRI manufacturers.
50
GeneRAL eLeCtRiC PHiLiPS SieMenS HitACHi toSHiBA

Gradient echo Balanced gradient echo (true FIESTA Balanced FFE (Balanced True FISP BASG True SSFP
family FISP) (Fast Imaging Employing Fast Field Echo) (Fast Imaging with (BAlanced SARGE) (True Steady-State
(Continued ) Steady-sTate Acquisition) Steady-state Precession) Free Precession)
(Contrast enhanced) SSFP T2-FFE PSIF TRSG SSFP
Steady-state free precession (Steady-State Free (T2-weighted contrast- (reverse Fast Imaging (Time-Reversed SARGE) (Steady-State Free
(GE) Precession) enhanced Fast Field Echo) with Steady-state Precession)
Precession = FISP
DE FGR backward)
(Driven Equilibrium Fast
Gradient Recalled acquisition
in the steady state)
Fast gradient echo Fast GRASS T1 TFE Turbo FLASH RGE Fast FE
(Gradient Recalled (T1-weighted Turbo Field (Turbo Fast Low Angle (Rapid Gradient Echo) (Fast Field Echo)
Acquisition in Steady State) Echo) SHot)
Fast GRE (Gradient Recalled

Echo)
Fast SPGR (SPoiled Gradient

Recalled)
Volume interpolated gradient FAME THRIVE VIBE
recalled echo (Fast Acquisition with (T1-weighted High (Volume Interpolated
CHAPTER 2
Multiphase EfGRE3D) Resolution Isotropic Breath-hold Examination)

Volume Examination)
Echo planar Spin echo – echo planar SE EPI SE EPI EPI SE SE EPI SE PEI
family Gradient echo – echo planar GRE EPI FFE-EPI EPI Perf SG-EPI FE-EPI
Diffusion-weighted imaging DWI DWI DWI DWI DWI
TR
ω1 ω2
ω1 ω2 ω1
180
180
90 90 90
RF pulses
Slice selection GS GS GS GS GS
gradients
Gф3 Gф3
Gф2 Gф2
Phase-encoding Gф1 Gф1
gradients G’ф1 G’ф1
G’ф2 G’ф2
G’ф3 G’ф3
GFE GFE
Frequency- GFE GFE
encoding
gradients
MR signal
TE TE
SLICE 1 SLICE 2
Fig. 2.12 Multislice acquisition in spin echo pulse sequences. The TR is typically much longer than the TE, therefore within
one TR, one can utilize the down time to excite additional slices. In this example, two slices are selectively excited using RF
pulses at frequencies ω1 and ω2. The second slice is excited right after the echo from slice 1 has been recorded. The echo from
slice 2 is then recorded and when time hits TR for slice 1, a new 90° pulse at frequency ω1 is applied. In this scheme, during one
TR, data from two slices is encoded. The number of slices that can be excited within one TR depends on the length of TR and
TE (i.e., the type of image-weighting that is being used).
proximity to protons, the strong paramagnetic effect RF pulses are applied (at times TE/2, 1.5 × TE, 2.5 × TE,
of gadolinium shortens the T1 relaxation time of these 3.5 × TE, etc.), each one of them generating an echo fill-
protons, thereby causing a dramatic increase in signal ing one line of k-space. Each of the 180° pulses is preceded
on T1W images (indeed, if T1 is shortened, the lon- by a PE gradient of different amplitude. Because several
gitudinal magnetization recovers much faster between lines are filled during the same TR, k-space is filled much
two 90° RF pulses, thereby generating more measura- faster than with conventional spin echo; for example, if
ble transverse magnetization). four echoes are recorded during the TR, k-space can be
• Lesion contrast is typically good with T2W images filled four times faster and therefore acquisition time is
due to an increase in water content in most lesions divided by four. The number of echoes that are recorded
that will result in a high signal. in one TR is called the ‘turbo factor’ (Siemens, Philips),
‘echo-train length’ (General Electric, Toshiba), or ‘shot
Fast spin echo/turbo spin echo factor’ (Hitachi).
• In conventional spin echo, one echo is obtained per TR, • In conventional spin echo, one TR and one TE are
filling one line of k-space at a time. The ‘90–180-echo’ picked and influence image weighting; all echoes are
sequence needs to be repeated as many times as there are recorded with the same TE. With turbo spin echo
lines of k-space to fill; for instance, if there are 256 lines, (TSE)/fast spin echo (FSE) pulse sequences, data is
this sequence must be repeated 256 times to fill all cor- collected at various TEs within one TR, and therefore
responding 256 lines of k-space. This can be a time- strategies have to be used to apply appropriate weight-
consuming process, especially with T2W images, due to ing to the images obtained. Each echo is collected with
their long TR. a different PE gradient strength. The PE gradients of
• Since TE is typically much shorter than TR, the TR time lower strength/slope (near the ‘zero’ line of k-space)
(time separating two successive 90° RF pulses) can be contain the maximum signal amplitude and contrast
used in a more efficient way by encoding several lines of information, as discussed in Chapter 1. Therefore, if we
k-space during one single TR interval (Fig. 2.13). In that use these shallow gradients for the echoes within the
scheme, after the 90° RF pulse, several successive 180° echo-train that occur at the desired TE, we maximize
52 CHAPTER 2
TR
180
180
180
180
90 90
RF pulses
Slice GS GS GS GS GS GS
selection
gradients
Gф2
Phase- Gф1
encoding G’ф1
G’ф2
gradients
Frequency- GFE GFE GFE GFE

encoding
gradients
MR
signal
TE 1st ECHO 2nd ECHO 3nd ECHO 4th ECHO
Echo-train length or turbo factor = 4
Fig. 2.13 A classic turbo spin echo or fast spin echo scheme. In this scheme, after the 90° RF pulse, several successive 180° RF
pulses are applied (at times TE/2, 1.5 × TE, 2.5 × TE, 3.5 × TE, etc.), each one of them generating an echo that allows filling of
one line of k-space. Each one of the 180° pulses is preceded by a phase-encoding gradient of different amplitude (slope). In this
example, four echoes are obtained, so four lines of k-space are encoded within one TR; this is called the echo-train length or
turbo factor. This allows total acquisition time to be decreased by a factor of 4.
signal and contrast for these echoes and thus obtain an • Susceptibility artifacts are decreased with TSE/FSE
appropriately weighted image. The stronger (steeper) PE sequences due to the multiple 180° RF pulses, which
gradients are used to measure echoes that are at earlier all cause rephasing. This can be beneficial in some
or later TEs than the ‘desired TE’, and generate echoes cases; for example, by minimizing artifacts caused
of lower amplitudes that have less influence on image by metal implants. However, TSE/FSE sequences
weighting but provide detail/resolution. At the control may be less sensitive to small hemorrhages due to the
workstation, this desired TE is called the ‘effective TE’ decreased sensitivity to magnetic susceptibility.
and is chosen by the operator: that effective TE is the • When long echo-trains are used, time saving is
time at which the shallowest PE gradients (central lines optimized; however, overall more echoes with erro-
of k-space) will be applied in the echo-train. This strat- neous weighting are introduced in the pool of data,
egy is called ‘phase-reordering’. so net image weighting may be skewed (this is par-
• Since FSE/TSE pulse sequences rely on similar mecha- ticularly true for T1W images, which can be skewed
nisms to the conventional spin echo pulse sequences, towards T2-weighting when using long echo-trains).
their benefits and uses are similar, with the advantage In addition, the later echoes in the echo-train tend
that acquisition times are reduced. There are a few dif- to have very low signal amplitude due to inevitable
ferences with TSE/FSE pulse sequences that are worth progressive T2 decay. The echoes at the tail-end of
noting: the echo-train are typically obtained with steeper PE
• Fat tends to be brighter on T2W images with TSE/ gradients used to obtain detail/resolution data (edges
FSE sequences, despite its short T2 time. This is of k-space). If the amplitude of these echoes is too low,
because the multiple 180° RF pulses used reduce this may result in loss of detail/resolution in the image
the spin-spin interactions in fat (called ‘J-coupling’), and some blurring of sharp edges/interfaces.
thereby lengthening its T2. High signal from fat • Note that just as with conventional spin echo, the dead
on T2W TSE/FSE images can hinder detection of time within a TR is also used for multislice acquisi-
pathology, but this can be circumvented by the use of tion. In other words, during one TR multiple slices are
fat suppression techniques, when deemed appropriate. excited using successive 90° RF pulses, and for each
slice multiple lines of k-space are encoded using the equilibrium position, and their magnetization progres-
FSE/TSE strategy (multiple successive 180° RF pulses). sively regrows from that point due to the longitudinal
Longer echo-train lengths use up more of the TR time, relaxation process passing through null value at a time
and therefore fewer slices can be excited within one that depends on their specific T1 time.
TR. There is, therefore, a trade-off between these two • The time for null value (TI null) varies for each tissue
quantities, with longer echo-train lengths decreasing according to their intrinsic relaxation times as well as
the number of slices (group size) that can be acquired sequence parameters. When IR is used combined with an
within one pulse sequence. FSE/TSE acquisition sequence, TI null varies as follows,
where TElastecho is time of the last echo in the echo-train
Single shot fast spin echo of the FSE/TSE scheme:
• One can further decrease acquisition time by pushing
the FSE/TSE strategy to the extreme and combining it    TR − TE lastecho   
− 
with a partial Fourier technique: TI null = T1 ×  ln 2 − ln  1 + e  T1

• Using a FSE/TSE scheme, a little over half of the lines    

of k-space needed are acquired within one TR after a
single 90° RF pulse (hence the term ‘single shot’). • One can show that when TR >> T1 (i.e., for tissues with
• The other half is synthesized using the conjugate short T1, such as fat), nulling occurs at a time equal to
symmetry of k-space (cf. Chapter 1). This leads to a about T1*(ln 2) = 0.69*T1, as the second term in between
decrease in SNR. The half acquisition of k-space is the brackets becomes closer to 0. This does not, however,
the reason why this sequence is also called HASTE hold true for tissues with long T1, such as fluids.
(half Fourier acquisition single shot turbo spin echo). • The TI determines the amount of longitudinal magneti-
• The short acquisition time results in low SNR. The long zation that is available from each tissue to be flipped into
echo-train after the single excitation causes severe T2 the transverse plane by the 90° RF pulse.
blurring artifacts in the PE direction, which can signifi- • Obviously, depending on the TI value, some tissues will
cantly degrade the image quality. still have a negative longitudinal magnetization by the
• Clinical applications. Because of these drawbacks, time the 90° RF pulse is applied. In most image recon-
HASTE/single shot fast spin echo (SS-FSE) is typically struction schemes, the sign of the net magnetization of
used to image tissues or structures with long T2 relax- a given tissue does not matter, as signal is displayed as
ation times (e.g., fluids), which are relatively unaffected ‘magnitude’ (i.e., the absolute value of the net magne-
by T2 blurring, with thick slices and low in-plane res- tization vector). This is the ‘magnitude reconstruction’
olution to maintain adequate SNR. One application in where signal will vary from 0 (black) to maximum (white)
dogs and cats is the use of HASTE/SS-FSE to obtain a (Figs. 2.14, 2.16).
‘myelogram effect’ (‘T2-myelogram’) on sagittal images • Some vendors have an option to use ‘phase-corrected’
of the spine. Because of its long relaxation time, CSF reconstruction as opposed to ‘magnitude reconstruction’.
typically appears very bright on a heavily T2W HASTE/ This is called ‘true IR’ or ‘real IR’, and in this scheme, the
SS-FSE pulse sequence, while the surrounding tissues information about the polarity of the net magnetization
are of low signal due to T2 decay. This provides a sagittal during recovery is preserved, with negative values darker
image that highlights the CSF in the subarachnoid space, while positive values are made brighter (hyperintense).
very similar in appearance to a traditional myelogram. It On such images, air (zero signal) is a mid-shade of gray,
provides a quick snapshot of the subarachnoid space in midway between completely black and completely white.
a short time (a few seconds), allowing rapid detection of • IR sequences tend to be T1W as the 180° RF preparatory
spinal cord compressive lesions and areas of dilation of pulse exaggerates the differences in T1 of tissues (i.e., the
the subarachnoid space such as diverticula. inversion pulse increases the ‘T1-dynamic range’ in the
image).
Inversion recovery • The main use of IR sequences today is through their abil-
• Inversion recovery (IR) pulse sequences use the same ity to suppress the signal from specific tissues. Knowing
basic principles as the spin echo pulse sequences studied the T1 relaxation time of specific tissues at specific field
above to generate signal in the form of an echo. strength, one can use IR sequences to suppress selec-
• It includes an additional 180° RF preparation pulse, tively the signal from these tissues, such as fat (short tau
called the ‘inversion pulse’, which occurs at a time TI inversion recovery [STIR]) or fluids (fluid attenuated
(‘time from inversion’ or ‘inversion time’, also called inversion recovery [FLAIR]). This is achieved by using a
‘Tau’) prior to the traditional 90°/180° pulse series. TI equal to the nulling time of the longitudinal magne-
• After the inversion pulse, all tissues have their net tization of the tissue that is targeted (e.g., for tissues with
magnetization flipped opposite (180° away) from the short T1:0.69*T1tissue).
54 CHAPTER 2
Longitudinal
magnetization
Fat
logy
Patho
Signal available
TISTIR
Fluid
Time
180
180
180
180
[…]
180
90
RF pulses
Inversion pulse TSE/FSE scheme STIR
Fig. 2.14 Principle of a STIR pulse sequence. A preparatory 180° inversion RF pulse is used first and flips all protons in the
opposite direction. Protons then start to recover their longitudinal magnetization in the direction of B0 at variable rates,
depending on the T1 relaxation time of the tissue they are in. At variable time points the longitudinal magnetization of all
tissues would cross the 0 line, which defines their nulling point. At an inversion time (TISTIR) equal to the nulling time of
the longitudinal magnetization of fat, the classic fast spin echo sequence is started with the 90° excitation pulse followed by
multiple 180° pulses. The gray scale on the right illustrates the expected signal intensity obtained from tissues as a result of
this imaging scheme when images are displayed using the ‘magnitude reconstruction’. Fat will be black as it does not have any
longitudinal magnetization, therefore will not generate any transverse magnetization or MR signal. Pathology will tend to be
quite intense, as it usually contains a large amount of free water, which lengthens its T1 time, thereby causing a significant
amount of residual negative longitudinal magnetization by the time the 90° RF pulse is applied. Fluids will tend to be very
bright (hyperintense) due to the long relaxation time.
Short tau inversion recovery • The benefits and uses of the STIR pulse sequence are
• In a STIR pulse sequence (Fig. 2.14), the TI is short, multiple:
matching the nulling time of fat; for example, at 1.5T, • It is widely used in musculoskeletal imaging, because
T1 for fat is equal to about 220 ms, so using a TI of about the suppression of the bright signal from the fatty
150 ms (0.69*220) will null the signal from fat when the bone marrow enhances the conspicuity of pathologic
90° pulse is applied. changes to the bone, such as edema, bruising, or neo-
• Nulling of fat signal with STIR is more efficient than plasia (Fig. 2.15).
with the fat saturation techniques, as STIR is not sensi- • Pathologic lesions (e.g., tumors, infection) are often
tive to magnetic field inhomogeneities, which make satu- rich in free water, which lengthens the T1 of the
ration techniques less suitable, especially when imaging lesion. When short to medium TIs are used, this T1
large FOVs, and in newer 1.5T systems, where the lengthening creates a substantial negative longitu-
extremely short bore limits the homogeneity of spectral dinal magnetization of these tissues at the TI time,
fat suppression at the ends of the magnet. causing these lesions to look brighter (hyperintense)
• STIR pulse sequences cannot be used with gadolinium on magnitude reconstructed images. Note that for the
contrast agents, because the T1 of enhancing tissue is same reason, fluids (e.g., CSF, synovial fluid, cysts)
shortened and closer to that of fat, leading to suppres- tend to look quite hyperintense on STIR images, like
sion of signal from enhancing tissues on STIR images. ‘T2-pathology’ scans.
Therefore, if fat suppression is needed on post-contrast • Because hyperintense signal from pathology is
scans, fat saturation techniques are used. enhanced on STIR images while bright signal from
Fig. 2.15 Comparison between a T2W-TSE sagittal image of the shoulder (left) and a STIR image (right) in a dog with
shoulder osteochondrosis. The subchondral bone marrow lesions are more obvious in the STIR image (arrows) and the joint
effusion in the caudal pouch (dotted arrow) is also more conspicuous as its signal is enhanced compared with the suppressed fat
around it (which was hyperintense on the T2W image, arrowhead).
background or surrounding fat is reduced, the lesion- intra- or periventricular lesions in the brain (Fig. 2.17),
to-background contrast tends to be enhanced, which meningeal lesions, or peripheral spinal cord lesions; for
makes STIR images suitable for fast ‘screening’ of example, this can be useful for a diagnosis of meningitis.
large FOVs looking for bright lesions. This pulse sequence is now a standard part of most clini-
cal protocols in neuroimaging.
Fluid attenuated inversion recovery • A T1-FLAIR pulse sequence is not typically part of stan-
• In FLAIR pulse sequences, the TI is calculated so that dard imaging protocols, but it can occasionally be useful
signal from fluid is nulled (Fig. 2.16). to image lesions surrounded by CSF such as meningio-
• Relatively pure fluids, such as CSF, have long intrinsic mas in the subarachnoid space (Fig. 2.18) or intraventric-
T1 relaxation times, therefore their TI null is not simply ular tumors, especially after the application of contrast
a function of 0.69*T1, as for fat, but it more strongly material (gadolinium). The contrast enhancement of the
depends on TR as shown in the TI null equation above, lesion and suppression of the signal from the CSF can
and also depends on TElastecho. lead to an increase in lesion-to-background contrast that
• FLAIR images can be made with different types of can be beneficial.
weighting:
• T1-FLAIR images are obtained with relatively short Gradient echo pulse sequences
TR and TE values in order to minimize T2-weighting.
With these sequences, TI null for fluids is usually General principles of gradient echo imaging
around 800–1,000 ms. • Up until now, we have studied pulse sequences of the
• T2-FLAIR images are obtained with very long TR spin echo family. In this type of pulse sequence, the
and TE values to maximize T2-weighting and hence inhomogeneities of the magnetic field that cause ultrafast
sensitivity to pathology. With these sequences, TI null decay of the transverse magnetization after the 90° RF
for fluids is usually around 2,000–2,500 ms. pulse (according to the T2* time) are corrected for by the
• The benefits and uses of a T2-FLAIR pulse sequence are application of a 180° RF pulse, which rephases protons
due to its high sensitivity to pathology owing to the heavy and generates an echo at the TE time.
T2-weighting. Water-rich lesions are usually very bright • Note that the generation of an echo is essential to
and conspicuous on T2-FLAIR images. T2-FLAIR the way that signal is recorded and spatially encoded
also increases the conspicuity of lesions that are located before being stored in k-space, since the center of the
close to the bright signal of CSF on T2W images such as echo, containing the higher amplitude signals with
56 CHAPTER 2
VetBooks.ir
Longitudinal
magnetization
Fat
e
Tissu
Fluid
Signal available
TIFLAIR Time
180
[…]
180
180
90
Inversion pulse RF pulses

TSE/FSE scheme FLAIR
Fig. 2.16 Principle of a FLAIR pulse sequence. A preparatory 180° inversion RF pulse is used first and flips all protons in
the opposite direction. Protons then start to recover their longitudinal magnetization in the direction of B0 at variable rates,
depending on the T1 relaxation time of the tissue they are in. At variable time points the longitudinal magnetization of all
tissues would cross the 0 line, which defines their nulling point. At an inversion time (TI FLAIR) equal to the nulling time of the
longitudinal magnetization of (pure) fluid, the classic fast spin echo sequence is started with the 90° excitation pulse followed
by multiple 180° pulses. The gray scale on the right illustrates the expected signal intensity obtained from tissues as a result
of this imaging scheme when images are displayed using the ‘magnitude reconstruction’. Fluid (such as CSF) will be black as it
does not have any longitudinal magnetization, therefore will not generate any transverse magnetization or MR signal.
Fig. 2.17 Transverse images of the brain

* * at the same level in a dog with a choroid
plexus tumor. Left is a T2W image and right
is a T2-FLAIR image. There is dilation of
T T
the ventricular system (*). The outline of
the tumor (T) is more conspicuous on the
* * * * T2-FLAIR image where the signal from
the hyperintense CSF around it has been
suppressed.
information on contrast, must correspond to the 0 val- of which will be aligned with the center of the acquisi-
ues of k x (as you remember, the center of k-space con- tion window while the FE gradient is on.
tains the higher amplitude frequencies with information • A relatively long TR is necessary in spin echo pulse
on contrast). That is why in spin echo we let the mag- sequences to allow for enough recovery of the longitudi-
netization dephase naturally, before rephasing it with a nal magnetization prior to the application of the next 90°
180° RF pulse, which will generate an echo, the center RF pulse. However, long TRs equate to long acquisition
VetBooks.ir
Fig. 2.18 Transverse T1-FLAIR pre-contrast (top) and post-

contrast (bottom) images at the level of C1 in a dog with a
meningioma. Even on the pre-contrast image, the outline of
the meningeal tumor (arrows) along the left side is well seen
due to the suppression of the CSF signal (*), which appears
very dark on these images. C, spinal cord.
C
* times, and it would be beneficial to use significantly
shorter TRs to decrease acquisition times. As shown in
Fig. 2.19, when short TRs are used (TR < T1), there is
insufficient recovery of the longitudinal magnetization
between successive 90° RF pulses, a phenomenon known
as ‘saturation’; this results in low amplitude transverse
magnetization induced by each 90° RF pulse, and there-
fore low signal.
• There is another strategy to generate an echo that does
not rely on a 180° RF pulse, but on the use of a ‘rever-
sal gradient’, and for that reason is called ‘gradient echo’
C pulse sequence.
* • As you can see in Figs. 2.20 and 2.21, we can use two
successive gradients of opposite polarities to dephase and
then rephase the protons, thereby generating a regrowth
in transverse magnetization signal in the form of an echo.
This causes the free induction decay (FID) signal to rap-
idly decrease as protons are dephased, to then regrow in
Mzmax = M0
Large MZ_EFF
Mz_eff
90° RF pulse
TR TR TR Large transverse magnetization
Mzmax = M0
Small MZ_EFF
Mz_eff
90° RF pulse
TR TR TR TR TR TR TR Small transverse magnetization
Fig. 2.19 Effect of the TR on the available longitudinal magnetization to generate signal in spin echo. If complete recovery were
allowed during TR, the longitudinal magnetization would fully regrow to reach the maximum value Mzmax = M0 (see Chapter
1), and therefore each 90° RF pulse would generate a maximum transverse magnetization for signal generation. In practice, the
longitudinal magnetization is not allowed to recover completely as this would generate very long acquisition times. Top: When TR
is long and on the order of or superior to T1, there is a large amount of longitudinal magnetization recovered between each TR
(Mz_eff = effective longitudinal magnetization), which will generate a substantial transverse magnetization when the 90° RF pulse
is applied. Bottom: When TR is short (<T1), the amount of longitudinal magnetization recovery is much less, thereby providing
little longitudinal magnetization to be flipped in the transverse plane by the next 90° RF pulse. This is called ‘saturation’. The
result is that the transverse magnetization obtained, and therefore the MR signal, will be of low amplitude.
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φ φ φ φ1 φ2
φ3
ω0 ω0 ω0
ω3
ω2 ω1
(a) (c)
φ φ φ
φ1 φ2 φ3
ω0 ω0 ω0
ω3
ω1 ω2
(b) (d)
Fig. 2.20 Principle of formation of an echo using gradient reversal. This uses the same analogy used in Chapter 1, between
precessing protons and a rotating disc. In (a), right after the 90° RF pulse, the protons are all precessing in the transverse plane
at the same frequency ω 0. In (b), a dephasing gradient is applied, which causes a linear change in precessing frequency in the
direction of the gradient. This is progressively causing a phase shift between the three discs, dependent on their position along
the gradient, the strength of the gradient, and the duration of the gradient. In (c), (time TE/2) the polarity of the gradient is
reversed but its amplitude (slope) is retained, causing the precessing frequencies to be changed in the opposite direction. The
discs that were precessing slower now precess faster and vice-versa; this is causing progressive reversal of the phase differences.
In (d), at time TE (echo time) all discs have returned to the same frequency ω 0 and are now in phase. This is the echo, and
because it was generated by a gradient, it is called a ‘gradient echo’.
Transverse
magnetization The dephasing gradient (negative polarity)
Free induction decay causes faster decay of the transverse
Signal T2* magnetization
The rephasing gradient (positive polarity)
causes progressive regrowth of the transverse
magnetization
The peak of the regrowth is the peak of the echo
and that is the center of the acquisition window;
the gradient is still applied after this (for frequency-
encoding during signal collection), causing more
dephasing and magnetization decay
TE
α
RF pulse
Rephasing
Dephasing/rephasing Dephasing + +
+
frequency-encoding gradients -
Frequency- This is the gradient echo
encoding
MR signal
Acquisition window
Fig. 2.21 Diagram showing the effect of the RF pulse, dephasing, and rephasing gradients on the transverse magnetization
and MR signal. The RF pulse generates a transverse magnetization, which is recorded in the transverse plane but decays fast
due to T2* effects. At a time after the RF pulse, a dephasing gradient (here of negative polarity) is applied causing progressive
dephasing of protons in the frequency-encoding direction. This forced dephasing is causing a faster drop in transverse
magnetization (in red). A rephasing (positive here) gradient is then applied in the frequency-encoding direction, of opposite
polarity but equal strength to the dephasing gradient. This is causing progressive rephasing of protons, hence a regrowth in the
transverse magnetization. This corresponds to the growth of an MR signal, the gradient echo. The acquisition window during
which signal is frequency-encoded and recorded to fill a line of k-space is centered on the peak of the echo (this peak is the
‘time of echo’ [TE]).
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the form of an echo. In that case, the echo is not gener- • Also, since no 180° RF pulse is used, it takes less time
ated by spin reversal as in spin echo sequences, but by for the longitudinal magnetization to regrow, so that
the application of two opposite and successive gradients, TR can now be shortened. In fact, TR can be made even
hence the term ‘gradient echo’. shorter by using excitation RF pulses that are <90°. The
• In a gradient echo pulse sequence, there is therefore only strategy makes sense: if the longitudinal magnetization
one RF pulse, as opposed to the 90°/180° pair in spin is not flipped entirely in the transverse plane to gener-
echo. Fig. 2.22 shows a simplified time line of the basic ate transverse magnetization and signal, it will recover
gradient echo pulse sequence. Because gradients are used its original orientation along B0 faster. This would
rather than a rephasing 180° RF pulse, the formation of allow sooner application of the next excitation RF pulse
the echo is much faster than in spin echo pulse sequences. to acquire the next line of k-space. However, as shown
This allows for much shorter time of echo (TE). in Fig. 2.23, the downside of this strategy is that when
TR
α α α
RF pulses
Slice selection GS GS GS
gradients
Phase-encoding
gradients
+ + + + + +
Frequency-encoding
- - -
gradients
MR signal
Readout Readout Readout
TE
Fig. 2.22 Simplified diagram of a standard gradient echo pulse sequence. A single RF pulse is used to excite protons in the
slice; the flip angle (α) is typically <90° in gradient echo imaging. Dephasing/rephasing gradients are applied in the frequency-
encoding direction to cause the formation of an echo at time TE after the RF pulse. Signal is read out (recorded) with the
acquisition centered on the peak of the echo. At a time TR, a new RF excitation pulse is applied and the sequence is repeated
with a different phase-encoding gradient strength, to fill a different line of k-space.
MZMAX = M0 MZMAX = M0
30° RF pulse
MZRES
90° RF pulse
Full transverse magnetization: MXY = M0 Partial transverse magnetization: MXY < M0
Fig. 2.23 The effect of a flip angle <90° on the amount of transverse magnetization obtained for signal. Left: When a 90° RF
pulse is used as in traditional spin echo, the net magnetization vector in yellow is completely flipped into the transverse plane,
generating a transverse magnetization (orange) that is equal in amplitude to M0. Right: When a flip angle of <90° is used, the
net magnetization vector is tilted partially away from the direction of B0 (in this case, 30° [green]), and its transverse component
(projection onto the (x,y) plane, in orange) is therefore of lower amplitude than M0, generating a weaker signal. However, the
smaller flip angle preserves a residual longitudinal magnetization M ZRES, which is available for the next RF pulse (see Fig. 2.24).
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the net magnetization vector M zmax = M0 is not flipped successive and rapid RF pulses to generate a small but
completely into the transverse plane, the amount of measurable transverse magnetization signal.
transverse magnetization generated and available for • In the end, the general characteristics of a gradient echo
signal generation is less. It corresponds to the geomet- pulse sequence are as follows:
ric projection of the partially tilted net magnetization • Smaller flip angles (<90°).
vector onto the transverse plane. One obtains a ‘partial • Shorter TR and TE → faster acquisition times.
transverse magnetization’ M xy, whose amplitude is <M0. • Echo is created by a bi-phasic gradient (dephasing/
• It is, however, possible to use smaller flip angles when rephasing).
short TRs are used. This is because of the ‘optimal angle • Transverse magnetization decays according to T2*
theory’, which dictates that for any combination of TR and not T2, because the echo is generated through
(sequence specific) and T1 (tissue specific), there is an the use of gradients as opposed to a 180° pulse. Unlike
optimal flip angle that will generate a maximum signal. the 180° pulse, the dephasing/rephasing gradient does
This angle, called the ‘Ernst angle’, therefore represents not compensate for the dephasing of spins caused by
a compromise between the maximum regrowth of Mz inherent magnetic field inhomogeneities or fixed
between two RF pulses (for a given tissue) and the maxi- tissue magnetic susceptibilities in the patient (e.g., at
mum signal available in the transverse plane. For a long interfaces of tissues with different magnetic suscep-
TR (like in spin echo), the optimum flip angle is typically tibilities). Therefore, the transverse magnetization
close to 90°. For short TRs, however, the optimum angle decreases much faster than in spin echo, and signal is
is reduced. One can show that the Ernst angle value is also more susceptible to artifacts.
 −
TR
 • Image contrast in gradient echo depends on proton
equal to cos−1  e T1
 . For example, the T1 of white matter density, T1, T2*, TR, and TE, but also flip angle.
 
• SNR tends to be reduced compared with spin echo
at 1.5T is about 600 ms. The optimum flip angle for that
sequences, due to a smaller flip angle and decreased TR.
tissue with a TR of 2,500 ms would be about 89°. For a • Image weighting with gradient echo pulse sequences
TR of 100 ms (close to the typical values used in gradient depends on TR and TE, but also the flip angle α. In
echo imaging), it would be about 32°. practice, TR is always short with gradient echo pulse
• As shown in Fig. 2.24, the use of a small flip angle and sequences, so the main determinants of image weight-
short TR maintains a significant longitudinal component ing are going to be TE and α. T2*, T1, or proton den-
of the net magnetization that can be flipped partially by sity-weighting are possible, but a significant degree of
MZMAX = M0
MZMAX = M0
*
MZRES
3O°
2nd RF pulse
1st RF pulse
r
cto
ve
MZRES
on
ati
tiz
ne
ag
tm
Ne
TR TR TR TR TR TR TR
Fig. 2.24 This schematic illustrates the benefit of using a smaller flip angle when a very short TR is used. Before the first RF
excitation pulse, the longitudinal magnetization is equal to M ZMAX = M0 (*). Using a smaller flip angle, in this case 30°, the net
magnetization vector (yellow) is only tilted away partially from the z-axis (green), leaving a significant residual longitudinal
magnetization M ZRES (purple). The small flip angle is still able to generate a small but substantial transverse component
in the (x,y) plane (orange), which can produce an MR signal. In this case a tissue with a relatively short T1 relaxation time
is represented, so that its longitudinal magnetization reaches back to the maximum value, even when using a short TR as
illustrated. Therefore, at the second RF excitation pulse, a large amount of longitudinal magnetization is already recovered to
be tilted partially and generate some transverse magnetization that will generate signal.
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Fig. 2.25 Transverse images of

the brain in a dog with metastatic
hemangiosarcoma. On the left, a
gradient echo image is presented
showing a focal markedly
hypointense rounded lesion
(arrow) consistent with magnetic
susceptibility artifact, to which
T2*W gradient echo pulse
sequences are sensitive. On the
right, a post-contrast T1W image
is presented, demonstrating that
(a) (b) the lesion enhances (arrow).
T2*-weighting is always present, due to the absence of a

180° rephasing pulse as is the case in spin echo imaging:
• T1-weighting: large flip angle (70° or more to max-
imize differences in T1) and short TE (to minimize
T2* effects).
• T2*-weighting: small flip angle (<20° to minimize
differences in T1) and long TE (to maximize T2*
effects).
• Proton density-weighting: small flip angle (<20° to
minimize differences in T1) and short TE (to mini-
mize T2* effects).
• The clinical applications of gradient echo pulse sequences
are multiple:
• Due to their high sensitivity to magnetic susceptibil-
ity, they are often used with T2*-weighting to identify
hemorrhage, exploiting the paramagnetic properties
of hemoglobin by-products (Fig. 2.25). To maximize
T2*-weighting (and therefore susceptibility), low flip
angle, long TR and long TE are used.
• Due to the dramatic reduction in scan time, they
can be used for single-slice breath-hold imaging
for abdominal scanning or for dynamic contrast-
enhancement studies.
• Gradient echo pulse sequences are also very sensitive
to flow because the rephasing of spins with gradi-
ents is not slice selective (as is the 180° RF pulse in
spin echo imaging), so flowing nuclei in blood vessels
always give off signal as long as they have been pre-
viously excited (by the excitation RF pulse). This, Fig. 2.26 MR angiography: abdomen, dorsal image post
coupled with fast imaging time, makes the gradient contrast with fast spoiled gradient echo imaging. Renal
echo pulse sequences very suitable for MR angiogra- angiography in a dog. A duplication of the caudal vena cava is
phy (Fig. 2.26). noted caudal to the reno-caval confluence (arrows).
Steady-state gradient echo/rewound gradient echo/ very short TRs, there is the possibility to build-up a
coherent gradient echo ‘steady state’ of the transverse magnetization. When the
• With the imaging strategy used in gradient echo, not TR is shorter than T2, the transverse magnetization
only is a longitudinal component of the magnetization induced by an RF pulse does not have time to completely
maintained throughout the acquisition, but also, with dissipate before the next RF pulse is applied. An RF
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pulse, regardless of its flip angle, contains energy that contrast does not depend on differences in T1 and T2
is capable of rephasing those protons that are still in times of tissues, but on the ratio T2/T1. As a result, in
the transverse plane. If applied early enough, a new RF tissues that have longer T2 or relatively similar T1 and
pulse therefore has the ability to create some rephasing T2 (such as fluids), signal intensity will be high.
of that residual transverse magnetization and, just like • These sequences make fluid (long T2) very bright, and
in a spin echo pulse sequence, this can create a form of can be useful to obtain rapid images confirming the fluid
‘spin echo’ called a ‘stimulated echo’ (Fig. 2.27). These nature of structures or to confirm the patency of blood
echoes coincide with the next RF pulse, can induce a vessels. As they are very sensitive to flow, they can be
voltage in the receiver coil, and therefore generate signal used for angiography. Rapid imaging can allow breath-
that affects contrast. hold acquisitions of slices. Heavy T2* weighting makes
• Thus, in gradient echo pulse sequences with very short them very sensitive to artifacts. Also, because signal is
TR, signal in the transverse plane can originate from the made of ‘fresh’ FID and older stimulated echoes (hence
FID caused by the successive excitation RF pulses (angle signal that is in effect from different time points), they
α) and/or the stimulated echoes. are very sensitive to motion artifacts.
• As shown in Fig. 2.27, a stimulated echo is the result • Balanced gradient echo (true FISP [fast imaging with
of the rephasing of the FID from an RF pulse that hap- steady-state precession]) is a variety of steady-state gra-
pened two cycles prior. Since the stimulated echoes were dient echo sequences where rewinding gradients are
generated by previous RF pulses, they may contain erro- applied in all three directions (slice-selection, frequency-
neous spatial encoding for where they appear within the encoding, phase-encoding), which require very fast gra-
pulse sequences. If these echoes (also called ‘transverse dients. This results in a null net-gradient effect across
coherence’) are not dealt with, they can generate artifact all TRs.
in the form of ‘banding’ due to interferences between
differently phase-encoded signals from different exci- Spoiled gradient echo (‘incoherent’ gradient echo)
tations. Therefore, in order to not corrupt the signal, • In spoiled gradient echo imaging, the residual transverse
this transverse coherence needs to either be eliminated magnetization following signal readout within each TR
(‘spoiling’, see below) or its spatial encoding information cycle is altered (= ‘spoiled’), so that only a longitudinal
needs to be ‘rewound’. component contributes to the net magnetization vector
• The latter strategy is what is performed in ‘steady-state’ by the time of the next RF pulse.
gradient echo imaging. • Because the transverse magnetization is spoiled between
• With this technique, a ‘rewinder’ gradient is used after RF pulses, the resulting signal depends less on T2/T2*
data collection within each cycle, which ‘rewinds’ the effects and is more heavily T1W.
phase that was applied by the actual PE gradient, so • Spoiling of the residual transverse magnetization can be
that the ‘spatial information’ in any existing trans- done in two ways:
verse coherence (stimulated echoes) is lost prior to 1. Application of ‘spoiled’ (also called ‘crusher’) gradients
exploiting this signal after the following RF pulse. to cause dephasing of the transverse magnetization.
The rewinding gradient is of similar amplitude but These spoiler gradients can be applied using the FE,
opposite polarity to the previous PE gradient, and PE, or slice-encoding gradient, or any combination
cancels the dephasing that this first PE gradient had thereof (Fig. 2.29).
caused (Fig. 2.28). 2. Use of excitation RF pulses (α) of variable phase
• As a result, the recorded MR signal in steady-state gradi- in a pseudo-random fashion (‘RF spoiling’). This
ent echo is made of two components (Fig. 2.27a): causes every newly formed transverse magnetization
• The classic echo from the FID induced by the RF caused by the RF pulse to have a different phase to
excitation pulse (α), weighted in T1 or proton density the previous or the next, which prevents build up of
depending on α. transverse coherence in the (x,y) plane; only the FID
• The rephased (= stimulated) echo from the residual created by the RF pulse immediately prior is recorded
transverse magnetization (= transverse coherence, by the receiver-coil.
weighted more in T2*). • Most manufacturers use the RF technique in spoiled
• Due to the mechanism of action, other names for these gradient echo, and even those that use gradient spoilers
pulse sequences include ‘rewound gradient echo’ and typically combine it with some RF spoiling as the latter is
‘coherent gradient echo’. more efficient in eliminating that transverse coherence.
• In steady-state gradient echo imaging, the TR is very • Because with these sequences the residual transverse
short (typically <50 ms), resulting in tissues with longer magnetization containing T2* weighting is spoiled,
T2 not losing their transverse magnetization between the resulting recorded signal is rather T1W or PDW
two excitation RF pulses. Therefore, there is a perma- (Fig. 2.27b). With short TRs, one can obtain fast T1W
nent longitudinal and transverse magnetization so that breath-hold images, which have good T1 contrast and
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TR TR TR
α α α α
RF pulses
Ca
RF3 RF4
Ca
RF1 RF2 2
u
ID1 ID
use
se
F F
ses es
sF
sF
ha as
ID
Rep ph
ID3
Re
2
FID
and
echoes
FID1 from RF1 FID2 from RF2 FID3 from RF3 FID4 from RF4
In blue: spin echo from RF1 In red: spin echo from RF2
= stimulated echo = stimulated echo
MR signal recorded Gradient echo
Coherent/rewound from FID3
(a) gradient echo +
Rephased (stimulated)
echo from RF1
Gradient echo Gradient echo Gradient echo from FID3
Spoiled from FID1 from FID2
(b) gradient echo
Stimulated echo from RF1 Stimulated echo from RF2

Time-reversed
(c) gradient echo
Fig. 2.27 Steady state in gradient echo. When TR is extremely short, typically shorter than T2 and T1 times of tissues, there
is some residual transverse magnetization by the time the next RF pulse is applied. In this example, four successive RF pulses
(flip angle alpha) are shown. The first pulse RF1 generates an FID signal in the transverse plane (FID1), which decays according
to T2*. Very shortly thereafter, the second pulse RF2 is applied which also generates an FID signal (FID2). However, because
there is residual transverse magnetization from FID1, this second RF pulse is going to cause some rephasing of that transverse
magnetization. This will generate an echo, which will peak at the same time as RF pulse 3 is applied; this echo is called a
‘stimulated echo’ and is a form of spin echo, since it was in fact generated by the rephasing effect of an RF pulse. At the time of
RF3, there are therefore two signals superimposed onto each other: the echo from FID1 and the FID3 from RF3. For a similar
reason, at the time of RF4, two signals are superimposed: the echo from FID2, which was caused by the rephasing effect of RF3
on FID2, and the FID4 caused by RF4. In reality (not represented here), TR is so short that the tail ends of these signals are
superimposed on each other, generating in fact a continuous signal in the transverse plane that has varying amplitude; in other
words, a ‘steady-state’ of MR signal, containing FIDs and ‘stimulated echos’. At the bottom of the figure are three time lines that
show the portion of that signal that is used in rewound (coherent) gradient echo (a), in spoiled (incoherent) gradient echo (b), and
time-reversed gradient echo (c). (a) In coherent/rewound gradient echo, after a steady state is reached, both the fresh gradient
echo from the new FID and the echoes from transverse coherence are recorded after rephasing; signal is T2* and T1W because
it is contributed to by transverse coherence and longitudinal magnetization tilted by the RF pulse. (b) In spoiled gradient echo,
only the actual gradient echo from the new FID is used within each TR, by destroying the residual transverse coherence (using
gradient and/or RF spoilers). Because the contribution of the transverse coherence is cancelled, signal is more T1W as it depends
more on the amount of longitudinal magnetization tilted by the RF pulse within each TR. (c) In time-reversed gradient echo,
only the stimulated echoes from the residual transverse coherence are recorded. Using appropriate gradients, they are made to
occur prior to the RF excitation pulses (as opposed to simultaneous to them as happens typically); no gradient echo from the
pure FIDs is recorded in this case, and signal is more T2W because it is generated in the form of a spin echo.
demonstrate pathology well after contrast material injec- RF pulse and also a component of echoes coming from
tion (gadolinium). The excellent T1 contrast and fast the refocusing of residual transverse magnetization from
imaging as well as sensitivity to flow make them also previous RF pulses (= transverse coherence, Fig. 2.27).
suitable for MR angiography (Fig. 2.26). In the previous strategies, we explained how to either
destroy that transverse coherence so that only the true
Time-reversed gradient echo FID is recorded (‘spoiled gradient echo’, mostly T1W)
• Recall that, without intervention, the signal in gradient or to preserve that transverse coherence and record it
echo contains both the signal from FID caused by each as well as the true FID after removing the erroneous
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TR
α α α
RF pulses
gradients
* * *
Phase-encoding
gradients
Frequency-encoding + + + + + +
gradients - - -
MR signal
Readout:
TE
contains signal
from FID + stimulated echoes
Fig. 2.28 Simplified diagram of a coherent gradient echo pulse sequence (steady-state gradient echo/rewound gradient echo).
Rewinding gradients are applied (*) by reversing the phase-encoding gradient prior to the next RF pulse. The rewinding
gradient cancels the phases that were acquired during the actual phase-encoding gradient prior to signal collection, so that the
echoes can be exploited during the next cycle without containing erroneous spatial localization information.
TR
α α α
RF pulses
* * *
gradients
Phase-encoding
gradients
Frequency-encoding + + * + + * + + *
gradients - - -
MR signal
Readout:
TE contains signal only
from rephased FID
Fig. 2.29 Simplified diagram of a spoiled gradient echo pulse sequence using spoiler gradients. Strong spoiler gradients (*) are
applied after echo readout to destroy any residual transverse magnetization coherence prior to the next excitation RF pulse.
spatial encoding information it may contain by the use • In these pulse sequences, the recorded signal is actually
of rewinding gradients (‘steady-state gradient echo/ an echo of the spin echo type created by the FID from an
rewound gradient echo/coherent gradient echo’, mostly RF pulse in the preceding cycle, and therefore this inher-
T2*W). ently contains information that is more T2W as opposed
• None of these strategies allow information to be to T2*W (Fig. 2.27c). The recorded echo occurs at an
obtained that is truly T2W. There is an additional effective TE time equal to TR + TE.
variant of gradient echo pulse sequence that allows • Recording of the echoes from the residual transverse
acquisition of more heavily T2W images by record- magnetization only is performed by the judicious use of
ing only the signal from the echoes from the residual gradients, which will make these echoes appear before
transverse magnetization. This is called ‘time-reversed the next RF pulse so that they can be recorded. It is
gradient echo’ and represents a ‘T2-contrast enhanced beyond the scope of this text to go into the details of how
approach’. this is achieved, especially since, currently, this type of
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gradient echo sequence is not used commonly in veteri- is neoplasia with high cellular density, which com-
nary medicine. presses the extracellular space and restricts free dif-
fusion of water in that extracellular space. Cytotoxic
Echo planar imaging edema is another example, in which water molecules
• Echo planar imaging (EPI) pulse sequences are not rou- move in the intracellular compartment, where their
tinely used in clinical veterinary MRI. In this scheme, movement is impaired by cell membranes and intra-
echoes for each PE step are obtained by successive cellular organelles, in addition to the extracellular
rephasing gradients, instead of the multiple 180° RF space being compressed as the edematous cells swell
pulses as described with FSE/TSE schemes. up. DWI can be used in these circumstances to try
• The initial RF pulse can be a single pulse, as in pure and characterize pathology such as acute brain infarc-
gradient echo imaging (GRE-EPI), or could use a pair tion with cytotoxic edema (DWI with apparent diffu-
of 90/180° RF pulses (spin echo preparation [SE-EPI]) sion coefficient [ADC] maps, see below).
followed by a train of gradient echoes. The SE-EPI • Anisotropic restriction is when motion is prefer-
sequences have longer acquisition times due to the pres- entially restricted in a particular direction. This
ence of the 180° pulse; however, this removes some of happens in some tissues that have a particular
the artifacts associated with the inhomogeneities of the geometric orientation at the microscopic level, such
magnetic field. Other preparation pulses may be used in as neuron fibers in the spinal cord or in the brain
combination with EPI (EPI-FLAIR to null signal from (white matter tracts, for example). Because of the
CSF). geometric orientation of the fibers, water mole-
• This imaging scheme allows acquisition of many lines cules tend to move preferentially along the longi-
of k-space in a very short time. In single-shot EPI, all tudinal orientation of the fibers and their motion is
PE steps (up to 128) can be obtained following only one restricted in the other directions; this principle is
RF excitation pulse, while in multi-shot EPI, a group of used for ‘diffusion tensor imaging’.
k-space lines are encoded for each RF pulse within a TR • DWI aims at revealing the microscopic characteristics of
period. water motion restriction at the level of the voxel:
• EPI sequences are very fast and therefore not very sen- • In classic DWI (Fig. 2.30), two diffusion gradients
sitive to motion. This allows their use to image physi- are used on either side of the 180° pulse in a spin-echo
ologic processes, such as cardiac function or perfusion, echo planar sequence.
and in other forms of functional imaging. • The duration and amplitude of the two gradients are
• One relatively common application of EPI pulse identical.
sequences in veterinary imaging is the use of T2W • The first diffusion gradient causes protons in the
SE-EPI sequences combined with diffusion gradients for direction of that gradient to acquire a phase, which
diffusion-weighted imaging (DWI) (see below). depends on their location along the gradient.
• The 180° RF pulse completely inverts the spins in the
Diffusion-weighted imaging (x,y) plane so the phase they have acquired due to the
• DWI highlights the microscopic motions of water mol- first gradient is reversed.
ecules within voxels of the imaged tissues. • The second diffusion gradient, of similar duration,
• In biologic tissues, water molecules are constantly mov- amplitude, and polarity to the first, will therefore, at
ing due to ‘Brownian motion’. These micro-movements the time of echo, exactly invert the effect of the first
are random and vary depending on the molecular envi- gradient so that no phase remains, provided the water
ronment. Within a voxel of biologic tissue, natural water molecules have not moved between the two gradients
molecule movement occurs at the intracellular level, (i.e., are in the same location with respect to the direc-
within the extracellular space, and between the intra- tion of the gradients).
and extracellular compartments. • In normal brain tissue, typically diffusion of water
• When there is no restriction to water movement, is unrestricted so that the water molecules move
Brownian motion is high, allowing water molecules to between the two gradients and therefore most water
move about the environment easily. This is called ‘unre- molecules do not experience the rephasing effect of
stricted’ (or ‘free’) diffusion. the second diffusion gradient. This leads to a loss of
• Conversely, when water molecules encounter physi- signal in the voxel when the echo is measured, leading
cal barriers that restrict their displacement, Brownian to a hypointense voxel.
motion is low and diffusion is said to be restricted. • In voxels where there is motion restriction (e.g., cyto-
In addition, restriction can have variable spatial toxic edema, cell-dense tumor), most water molecules
distribution: stay trapped in that voxel and therefore experience
• Isotropic restriction is when motion is restricted in a both diffusion gradients so that the phase acquired
similar fashion in all directions of space. An example during the first is reversed by the second. There is,
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180°
DG1 DG2
90°
Time
Fig. 2.30 Diffusion-weighted imaging using a spin echo EPI pulse sequence. Two diffusion gradients (either in slice-selection,
phase-encoding, or frequency-encoding direction) are placed symmetrically on either side of the 180° RF pulse of the spin echo
sequence. The first diffusion gradient (DG1) causes a phase to be acquired by protons in water molecules in the voxel. Top row:
If protons move out of the voxel prior to the application of the second diffusion gradient DG2, that phase is not reversed by the
second diffusion gradient. This causes a drop in signal in the voxel. Bottom row: if the water molecules have restricted motion
and remain in the voxel between the two diffusion gradients, the phase acquired during DG1 and inverted by the 180° pulse is
completely reversed by the second diffusion gradient, which is identical to DG1. This causes a high signal in the voxel.
therefore, phase coherence at time of echo in that diffusion tensor imaging (‘MR tractography’). This
voxel, leading to a high signal. type of imaging exploits the particular restriction of
• Typically, the experiment is repeated three times by motion that exists in tissues with a longitudinal fibrillar
applying the diffusion gradients in the slice-selection, orientation, such as white matter tracts in the brain or
FE, and PE gradients, so that assessment of movement spine. In these tissues, water motion is restricted to the
restriction of water is performed in all three directions longitudinal orientation of these neuronal tracts (path of
of space. least resistance). Diffusion tensor imaging is an exten-
• The amplitude of the diffusion effect can be mod- sion of DWI, which highlights in an image these paths
ulated by what is called the ‘b-value’ at the control of preferential diffusion of water molecules.
workstation. This b-value depends on the amplitude
and duration of the gradient as well as the time sepa- Chemical fat saturation technique
rating the two diffusion gradients. • Fat suppression techniques are commonly used in MRI,
• An image is obtained with a b-value of 0 (no diffusion because suppressing the naturally bright signal of fat
gradient = T2W) and then with a b-value >0 (typi- tends to highlight pathologic lesions. We described ear-
cally around 1,000 = DW). From that information, lier in this chapter a popular technique for fat suppres-
an ADC can be determined within each voxel that sion that uses a 180° preparatory inversion pulse and a
measures the absolute diffusion of water between the time of inversion coinciding with the null magnetization
two images. This is displayed as an ‘ADC’ map, where of fat (STIR pulse sequence, see above). The STIR pulse
restricted motion appears black while unrestricted sequence, however, cannot be used as a post-gadolinium
motion has a brighter signal (Fig. 2.31). sequence because the STIR imaging scheme will sup-
• Other types of diffusion imaging exist and are beginning press signal from all structures that have a short T1,
to be investigated in veterinary medicine; for example, which is the case with gadolinium-enhanced tissues.
VetBooks.ir
(a) (b)
(c) (d)
Fig. 2.31 Dorsal plane T2W (a), T2-FLAIR (b), DWI (c), and corresponding ADC map (d) images of the brain in a female dog
with a history of mammary gland tumors that was presented for dyspnea. The patient was hospitalized for treatment and, during
hospitalization, developed acute vomiting, ataxia, and stiffness on all four limbs. A brain MRI was performed within 2 hours of
the onset of these neurologic signs. No abnormality was noted on T2W and T2-FLAIR images. However, on the DWI image,
a territorial, wedge-shaped hyperintense lesion is seen in the right cerebellum, which corresponds to a hypointense signal on
the ADC map indicative of restricted diffusion (arrows). These changes are suggestive of an acute ischemic event, and were
only detectable on these pulse sequences in this patient that was imaged very early (<2 hours) after the onset of signs of stroke.
This illustrates the sensitivity of DWI in the very early stage of ischemia. (1T MRI system; images courtesy of Drs. Anne-Carole
Duconseille and Arnaud Louvet, Centre d’Imagerie par Résonance Magnétique de l’Animal, France)
Therefore, other strategies exist that can be used on • The simplest example of such sequences, called ‘fat
post-contrast series. saturation’ or ‘chemical shift selective’, uses a narrow
• Chemical fat saturation is also known as spectral fat sup- bandwidth RF pulse tuned to the center of the lipid
pression, and exploits the difference in the precessional resonance. This specifically excites the fat protons,
frequencies of fat and water protons, which is also known which flip in the transverse plane; spoiling gradients
as ‘chemical shift’. For example, at 1.5T, that difference are then applied in both the FE and PE directions,
in precessional frequency between fat and water protons which dephase the fat signal thereby nulling any
is about 220 Hz. transverse magnetization due to fat protons. The fat
• Because of that difference, RF pulses can be specifically protons become ‘saturated’, and therefore will not gen-
tuned to the precessional frequency of fat protons, in erate signal when the actual imaging pulse sequence
order to selectively excite these without affecting protons (e.g., spin echo, gradient echo) is applied immediately
in water molecules or other tissues. after (Fig. 2.32).
68 CHAPTER 2
VetBooks.ir
180
180
[…]
180
90
90
RF pulses
ωfat
TSE/FSE scheme
*
Spoiler
gradients
Fig. 2.32 Schematic representation of the simplest example of ‘fat saturation’. A narrow bandwidth RF pulse tuned to the center
of the lipid resonance is used (ωfat). This specifically excites the fat protons, which flip in the transverse plane. Spoiling gradients
(*) are then applied in both the frequency- and phase-encoding directions, which dephase the fat signal thereby nulling any
transverse magnetization due to fat protons. The fat protons become ‘saturated’, and therefore will not generate signal when the
actual imaging pulse sequence is applied immediately after. In this example, a classic turbo spin echo pulse sequence is activated
after the spoiler gradient, but other pulse sequences such as gradient echo can be used as well in this scheme.
180
180
180
180
[…]
90
RF pulses ωfat
TSE/FSE scheme
*
Spoiler
Longitudinal gradients
magnetization
TI
0
Time
Fig. 2.33 Schematic illustrating the principles of fat saturation using a preparatory fat selective inversion pulse (SPIR,
SPAIR). The fat selective inversion pulse (100° to 180°) inverts the magnetization of lipid protons, which then starts to regrow.
The actual imaging pulse sequence is started at the time of inversion that coincides with the null value of that longitudinal
magnetization of fat. Between the inversion RF pulse and the start of the imaging pulse sequence, spoiler gradients are also
applied to dephase any transverse magnetization components of fat that would have been created by the inversion pulse.
• There are variations of the simple fat saturation scheme FURTHER READING
that use a preparatory fat selective inversion pulse (100°
to 180°). The longitudinal magnetization of fat starts to Below are only a few of the many resources that are available
regrow after that inversion pulse, and the actual imag- to learn more about the very complex physics of MRI. The
ing pulse sequence is started at the TI that coincides list only includes the main texts that were used to compile
with the null value of that longitudinal magnetization the summary presented herein. Much more detailed infor-
of fat (Fig. 2.33). Between the inversion RF pulse and mation, beyond the scope of this particular textbook, can
the start of the imaging pulse sequence, spoiler gradi- be found in these and many other books/articles/web sites.
ents are also applied to dephase any transverse magne- Berry E, Bulpitt A (2009). Fundamentals of MRI: An Interactive
tization components of fat that would have been created Learning Approach (Series in Medical Physics and Biomedical
by the inversion pulse. Examples of these techniques Engineering). CRC Press, Boca Raton.
include SPIR (spectral presaturation with inversion Chavhan GB, Babyn PS, Jankharia BG et al. (2008). Steady-state
recovery) and SPAIR (spectral attenuated inversion MR imaging sequences: physics, classification, and clinical
recovery). applications. Radiographics 28:1147–60.
VetBooks.ir
Dale BM, Brown MA, Semelka RC (2015). MRI: Basic Principles and Pease A, Miller R (2011). The use of diffusion tensor imaging
Applications, 5th edn. Wiley-Blackwell, Hoboken, New Jersey. to evaluate the spinal cord in normal and abnormal dogs.
D’Anjou MA, Carmel EN, Tidwell AS (2011). Value of fat Vet Radiol Ultrasound 52:492–7.
suppression in gadolinium-enhanced magnetic resonance Plewes DB, Kucharczyk W (2012). Physics of MRI: a primer.
neuroimaging. Vet Radiol Ultrasound 52(Supp. 1):S85–S90. JMRI 35:1038–54.
Garosi LS, Mc Connell JF (2005). Ischaemic stroke in dogs and Runge VM, Nitz WR, Schmeets SH (2008). The Physics of
humans: a comparative review. J Small Anim Pract 46:521–9. Clinical MR Taught Through Images, 2nd edn. Thieme Medical
Kastler B, Vetter D, Pattay Z, Germain P (2011). Comprendre Publishers, New York.
l’IRM: Manuel d’auto-apprentissage, 7ème edn. Elsevier Masson, Westbrook C, Roth CK, Talbot J (2011). MRI in Practice, 4th edn.
Issy-les-Moulineaux. Wiley-Blackwell, Chichester.
McRobbie DW, Moore EA, Graves MJ, Prince MR (2006). MRI
from Picture to Proton, 2nd edn. Cambridge University Press,
Cambridge.
CHAPTER 3
MRI ARTIFACTS
70 J. Fraser McConnell
CONTENTS
Motion related artifacts and phase mismapping ......................................................................................................................................................70
Flow-related artifacts ...............................................................................................................................................................................................73
Vascular flow .....................................................................................................................................................................................................73
CSF flow artifacts...............................................................................................................................................................................................75
Phase-encoded motion artifact (pulsatility artifact) ............................................................................................................................................75
Artifacts related to hardware and room shielding ....................................................................................................................................................76
Hardware-related artifacts ..................................................................................................................................................................................76
Shielding-related artifacts ..................................................................................................................................................................................77
Coil artifacts ............................................................................................................................................................................................................77
Artifacts associated with MRI pulse sequences .......................................................................................................................................................78
Poor signal-to-noise ratio..................................................................................................................................................................................78
Cross-excitation ................................................................................................................................................................................................79
Slice overlap/cross talk......................................................................................................................................................................................79
Phase wrap/wraparound artifact .........................................................................................................................................................................79
Gibbs artifact (truncation/ringing artifact) ..........................................................................................................................................................81
B0-sensitive (‘off-resonance’) banding artifact....................................................................................................................................................81
Chemical shift artifacts ......................................................................................................................................................................................81
Misregistration of signal ..............................................................................................................................................................................81
Phase-cancellation artifacts (‘black boundary artifact’) ................................................................................................................................82
Susceptibility artifacts........................................................................................................................................................................................83
Magic angle effect..............................................................................................................................................................................................85
Partial volume averaging ...................................................................................................................................................................................85
References...............................................................................................................................................................................................................86
Artifacts can be defined as any feature on an image that However, some artifacts may be overlooked and misinter-
misrepresents the object in the field of view (FOV).1 All preted as normal anatomy or pathology. To avoid misin-
MR images contain some artifacts and their recognition terpretation, it is important to identify suspect lesions on
is important to avoid misdiagnoses and to allow diagnostic multiple planes and pulse sequences. In most cases, genu-
images to be obtained. While artifacts are visible on every ine pathology will be visible on different imaging planes or
MR image, they can be useful in allowing characterization sequences.
of tissues or identification of lesions such as hemorrhage
or thrombi. MOTION RELATED ARTIFACTS
Artifacts can be divided into those due to patient fac- AND PHASE MISMAPPING
tors (chemical shift, flow effects, motion, susceptibility) and
those due to equipment and software. • Motion artifacts are very common in MRI and occur
In most cases, recognition of artifacts is straight forward, due to ‘phase mismapping’, which occurs because mov-
manifesting as image distortion, poor image quality, or ing protons develop different phase shifts from static tis-
presence of clearly non-anatomically shaped signal changes. sue and therefore are incorrectly spatially located during
M R I A r t i fac t s 71
phase-encoding (PE) (see Chapter 1). Since image data • Gross patient motion generally results in non-diagnostic
acquisition takes a long time, even minor patient move- images with blurring or multiple ghost images:
ment can result in severely degraded images. For this • Correction of gross motion artifacts requires changes
reason, veterinary patients generally need to be anesthe- in anesthesia (e.g., ensuring patient is at appropriate
tized for MRI. plane of anesthesia, use of ventilators, ensuring ade-
• Motion related artifacts can be divided into three types: quate analgesia or, in severe cases, performing neuro-
1. Gross patient movement (Fig. 3.1). muscular blockade [although this is rarely required]).
2. Macroscopic movement due to normal physiology • Patient motion can be damped by use of padding and
(cardiac, respiratory, gastrointestinal motion) (Fig. 3.2). positioning straps and ensuring that the animal is in a
3. Microscopic motion (flow and diffusion effects). comfortable position.
• Motion can be random or periodic, 2 and the more • Painful orthopedic conditions (e.g., hip and stifle oste-
regular and predictable the motion (e.g., respiration) oarthritis) can be exacerbated by positioning for MRI
the easier it is to employ specific techniques to reduce (e.g., lumbosacral spinal studies), which can result in
motion effects. the patient panting or waking up during anesthesia.
• Due to the way that the MR signal is spatially located, • Gross physiologic (respiratory, cardiac motion and peri-
motion artifacts are most severe in the PE direction as stalsis) or pathologic motion (e.g., seizures, myoclonus)
even minor changes in position of tissue result in phase cannot be stopped:
errors (increased or decreased phase dispersion), which • Where physiologic motion is regular, acquisition of
cause errors in spatial localization on the image (‘phase MRI data that is gated to that physiologic process
mismapping’). (electrocardiogram [ECG] or respiratory gating)
• Some ghosting due to phase mismapping is inevitable can be used to generate motion free images (see
(e.g., from larger arteries) and, if it overlies the area of Chapters 9.1, 9.2, and 10).
interest, swapping PE and frequency-encoding (FE) • Gating is required for cardiac and thoracic imaging
directions will move the location of the artifact so it does and is also usually required for cranial abdominal
not obscure the area of interest. Applying saturation imaging (e.g., liver studies).
bands over large blood vessels, the gastrointestinal tract, • During gating, image data is only acquired periodi-
or the source of the artifact will null the signal from the cally (e.g., at the same point during the ECG cycle or
tissue and may also reduce the artifact. phase of respiration).
Fig. 3.1 Gross motion artifact on a transverse T1W post- Fig. 3.2 Transverse T2W images of the cranial abdomen of
contrast image of the brain. The image is non-diagnostic a Greyhound showing motion artifact (phase mismapping)
with multiple ghosting artifacts, which are most severe in the (arrows) in the phase-encoding direction (right to left). The
phase-encoding direction (right to left). (1.5T MRI system) artifact was primarily due to respiratory motion resulting in
regular ghosting but sparing the lumbar spine, which was
static during image acquisition. (1.5T MRI system)
72 CHAPTER 3
• Image acquisition for gated studies takes longer than manually inflating the lungs by compressing the
for non-gated images. rebreathing bag).
• Cardiac imaging requires ECG gating using MRI • As motion tends to generate random signals,1 increas-
compatible electrodes and specific software. ing the number of averages (to at least four) during
• Reduction of respiratory motion can be achieved image acquisition will reduce physiologic motion
by techniques that use external bellows, which artifact, as the signal from static tissue increases with
move with chest wall excursions (respiratory increased averages but the random signal or moving
gating), and respiratory compensation (also uses tissue signals tend to cancel each other out.2 However,
bellows). Techniques for respiratory gating that increasing acquisition time, by increasing the number
do not require external bellows are also available of averages, also increases the chance of gross patient
and are often simpler to use. Navigator echoes, motion during acquisition.
which track movement of the diaphragm, allow • Parallel imaging techniques allow faster acquisition
image acquisition to be timed relative to diaphrag- times, but if there is patient motion this can be worse
matic movement, thus reducing respiratory motion than non-parallel techniques as all of the ghost images
(Fig. 3.3). Breath-hold techniques are commonly may be within tissue boundaries.3
used in people to minimize respiratory motion, and • Some MR pulse sequences are less sensitive to motion
can be performed in veterinary patients (e.g., by (e.g., single-shot and echo planar imaging techniques,
(a) (b)
(c) (d)
Fig. 3.3 Dorsal (a) and transverse (c, d) T2W images of the cranial abdomen and navigator echo trace (b) in a normal dog. This
is an example of respiratory gating using navigator echoes acquisition to minimize movement artifact. A region of interest
(white box in a) is usually placed across the diaphragm (a) and produces a real-time trace of diaphragmatic motion (b), which is
used to time the RF pulses so that each slice is acquired at the same phase of respiration. Respiratory gating usually prolongs
scan time. The transverse T2W image acquired without respiratory gating (c) shows blurring and ghosting due to respiratory
motion, most obviously affecting the liver (solid arrow) and main portal vein (dashed arrow). The transverse T2W image acquired
with respiratory gating using navigator echoes (d) shows almost complete absence of motion artifact. (1.5T MRI system)
which allow very fast image acquisition at the expense at higher velocities.7 The appearance of flow differs
of image resolution and signal). on gradient echo sequences as there is no 180° slice
• Most MRI vendors have produced a variety of pulse selective refocusing pulse, and there is never any flow
sequences, which can be used to reduce the effects of related signal loss. In contrast to spin echo sequences,
patient motion based on radial or rotating overlapping gradient echo sequences show flow-related enhance-
sampling of k-space (e.g., BLADE, PROPELLOR, ment because the whole body receives the refocusing
MULTIVANE).4,5 gradient and the flowing fluid is rephased irrespective
of its slice position.7
FLOW-RELATED ARTIFACTS • Entry slice phenomenon results in differing signal
intensity of blood in different slices within a stack of
Vascular flow slices. The nuclear spins of blood flowing perpendic-
• The appearance of flowing fluids on MRI is complex and ularly through multiple slices become progressively
depends on pulse sequence, imaging parameters (e.g., more saturated as the protons move through the stack
time of repetition [TR], time of echo [TE], slice thick- of slices (Fig. 3.5). The nuclear spins of blood within
ness), direction (within or through plane), profile (lami- the center of the stack of slices will have experienced
nar versus turbulent), and velocity of the flow. Ghosting more excitation pulses than blood that enters the first
artifacts can also occur (pulsatility artifact). slice from adjacent tissue, which will have not expe-
• There are three main effects seen with blood flow: time rienced any RF pulses.7 The effect of this is that the
of flight (TOF) (‘inflow’) effects, entry slice phenome- blood within the entry slice may show greater signal
non, and intravoxel dephasing effects:6,7 than blood in the image slices further away from the
• TOF effects occur when flow is through the plane of entry slice. The degree of entry slice phenomenon
the image and when some or all of the flow is replaced varies with TR, slice thickness, and direction and
between the radiofrequency (RF) pulses. With spin velocity of flow.
echo sequences, the tissue has to receive both an • Flow-related intravoxel dephasing occurs when nuclei
excitation and a refocusing RF pulse to return a signal having different velocities are present in the same
(see Chapters 1 and 2). Stationary fluid or tissue expe- voxel. Due to their different velocities, these nuclei
rience both the 90° and 180° pulses and therefore will have traveled different distances to reach that
can generate a signal. Within faster flowing fluids voxel between the 90° RF pulse and signal readout,
either all, or only part of, the blood experiences both and therefore will have accumulated variable amounts
RF pulses and either no, or only a partial, signal is of phase, depending on the extent of magnetic field
returned (Fig. 3.4). The appearance of flow on spin gradients they have been exposed to during travel.
echo sequences is therefore signal loss, which is greater When they arrive in the voxel, these differences in
(a) (b)
Fig. 3.4 Transverse T2W (a) and T2*W gradient echo (b) images of the normal cervical spine in a dog. There is absence of
signal within the carotid arteries (solid arrows) and jugular veins (dashed arrows) on the T2W image (a) but high signal on the
T2*W image (b) due to ‘time of flight’ effects. Blood within the ventral vertebral venous sinuses (arrowheads) is hyperintense
on the T2W image as there is little time of flight effect due to the slow flow and direction of flow. (1.5T MRI system)
74 CHAPTER 3
(a) (b)
Fig. 3.5 Transverse T1W images of the cranial abdomen showing entry slice phenomenon. Blood flowing into the aorta (solid
arrows) is highest in signal in the entry (cranial) slice (a) and is low signal at the exit (caudal) slice (b). The reverse is seen in the
caudal vena cava (dashed arrows), where the entry slice is caudal and the exit slice is cranial. (1.5T MRI system)
(a) (b)
Fig. 3.6 Transverse T2*W gradient echo images with (a) and without (b) flow compensation of the cervical spine in a French
Bulldog with syringomyelia. Without flow compensation (b) there is low signal within the carotid arteries (solid arrows, b)
due to intravoxel dephasing. With flow compensation (a), the altered phase shifts of the flowing blood are corrected and the
vessels appear higher in signal (solid arrows, a). In addition to correcting for signal changes due to intravoxel dephasing, flow
compensation can reduce other flow related artifacts (e.g., phase-mismapping [dashed arrow, b]). (1.5T MRI system)
phase accrued will cause some destructive interfer- applying additional gradients so there is no phase shift
ences in the amplitude of the signal that is recorded with the moving protons. Gradient moment rephasing
from that voxel, which can cause signal drop from the assumes there is a constant velocity and direction of
affected voxels. This phenomenon can be reduced by flow so works best on slow laminar flow (i.e., venous
using gradient moment rephasing (nulling) (Fig. 3.6), flow).7 An effect of flow compensation is to increase
also known as ‘flow compensation’, which tries to the minimum TE that can be used, which may reduce
correct the altered phases of the flowing nuclei by the number of slices possible.1
CSF flow artifacts

• CSF flow artifacts occur due to altered magnetization of
CSF as it moves. They are most commonly seen on T2W
and T2-FLAIR images where areas of abnormal signal
are seen within accumulations of cerebrospinal fluid
(CSF) (e.g., cisterna magna, hydrocephalus, syrinxes)
with turbulent flow (Fig. 3.7).8
• These should not be mistaken for solid masses and can be
differentiated from true pathology as they are not consistent
on different imaging planes. On images from T2*W gradi-
ent echo or balanced pulse sequences (e.g., bFFE, FISP),
these ‘pseudolesions’ are not usually visible (Fig. 3.8).
• On T2W images CSF flow commonly results in a drop in
the normally high signal of the CSF, while on T2-FLAIR
images it appears bright as it causes a failure of suppres-
sion of CSF adjacent to the brainstem and within the
mesencephalic aqueduct due to entry slice phenomenon
Fig. 3.7 Sagittal T2W image of the cervical spine of a normal (Fig. 3.8). This should not be mistaken for pathologic
Hungarian Vizla. The heterogeneous areas of intermediate causes of increased CSF signal.9
signal (arrow) within the subarachnoid space at the level of C2
are due to CSF flow artifact and should not be mistaken for Phase-encoded motion artifact
intradural pathology. (1.5T MRI system) (pulsatility artifact)
• Pulsatility artifacts are usually associated with the puls-
• Artifacts due to TOF or entry slice phenomenon can ing of larger blood vessels and appear on the image as
be reduced by using saturation bands (pre-saturation multiple ghost images of the vessel in the PE direction.
pulses) adjacent to the FOV or in the slice direction. They occur adjacent to the pulsating blood vessel, heart
The saturation bands give an excitation pulse to the etc. at the same level (Fig. 3.9).
flowing nuclei to fully saturate the net magnetization • The number and brightness of the ghost images depend
vector so there is no transverse magnetization and no on the rate and amplitude of pulsation.2 Image acquisi-
signal. Saturation bands should be placed between the tion parameters (e.g., TR, number of averages, FOV)
flow and the imaging stack.7 Saturation bands increase also affect the position of the ghost images.2
the specific absorption rate and also use time between • Pulsatility artifacts only occur in the PE direction and
the RF pulses, therefore reducing the number of slices will change orientation if the scan is repeated with the
possible. PE and FE directions swapped (Fig. 3.10).8
(a) (b) (c)

Fig. 3.8 Transverse T2W (a), T2-FLAIR (b), and bFFE (c) images of the brain in a 3-month-old crossbred dog with severe
congenital hydrocephalus. There is CSF flow artifact (arrows) within the dilated 4th ventricle visible on the T2W (a) and
T2-FLAIR (b) images but not on the bFFE image (c). CSF flow artifacts can be distinguished from genuine pathology as the
pseudolesions are inconsistent and not visible on different planes or sequences. (1.5T MRI system)
76 CHAPTER 3
(a) (b) (c)

Fig. 3.9 Transverse T1W post-contrast (a), T2W (b), and dorsal T1W post-contrast images in a normal 10-year-old Boxer.
In (a) a pulsatility artifact originating from the venous sinuses (arrowhead) overlies the cerebellum and appears a curvilinear
hyperintensity (solid arrow) on the transverse T1W post-contrast image. Smaller pulsatility artifacts (dashed arrows) are
present overlying the digastricus muscles. Pulsatility artifacts occur in the phase-encoding direction, which in this case is
right to left. The pseudolesion can be recognized as artifactual as it is not visible on other pulse sequences or imaging planes
(b, c). (1T MRI system; reproduced, with permission, from the BSAVA Manual of Canine and Feline Musculoskeletal Imaging,
2nd edn, British Small Animal Veterinary Association, Gloucester.)
Fig. 3.10 Matched post-contrast

transverse T1W images of the
canine brain at the level of the
thalamus. (a) With the phase-
encoding gradient applied in
a ventral to dorsal direction,
vascular pulsations (dashed arrows)
create ghosts superimposed on
brain parenchyma (solid arrows).
(b) When the phase-encoding
direction is changed to a horizontal
orientation (left to right), the
artifact is no longer superimposed
on the brain. (Reproduced, with
permission, from Cooper JJ,
Young BD, Hoffman A et al. (2010).
Intracranial magnetic resonance
imaging artifacts and pseudolesions
in dogs and cats. Vet Radiol
(a) (b)
Ultrasound 51(6):587–595.)
• They are also usually only visible on one imaging plane ARTIFACTS RELATED TO HARDWARE
and are inconsistent, which helps distinguish them from AND ROOM SHIELDING
genuine pathology.
• The brightness of the ghost images is affected by the sig- Hardware-related artifacts
nal intensity of the moving structure, and the brighter • Artifacts due to hardware problems are usually evident to
the structure the brighter the ghost image. For exam- the radiographer as they commonly affect studies from
ple, pulsation artifacts on T1W images are usually more multiple patients in a similar way or may prevent the
marked on post-contrast images and should not be mis- scanner from running normally.
taken for abnormal contrast enhancement (where the • In many cases, hardware problems can only be solved by
ghost image overlies anatomy). engineers. Less severe problems should be detected on
• Flow compensation and radial encoding of k-space may regular quality assurance scans (preventive maintenance)
reduce pulsatility artifacts.4 as recommended by most vendors. As hardware problems
are unrelated to the patient being scanned, they are also often affect all sequences and may be consistent between
often visible on images of phantoms. patients. Correction requires determining the source of
the RF interference and removing it if possible.
Shielding-related artifacts10 • ‘Spike’ or ‘herringbone’ artifacts10,11 appear as multiple
• ‘Zipper artifact’ appears as a narrow linear band of image parallel dark stripes across the image (Fig. 3.12). The
noise (alternating decreased and increased signal appear- spacing width and angulation may vary and the artifact
ing similar to a zip, hence the name) (Fig. 3.11), which may be inconsistent, often only occurring during certain
runs across the entire field of view in the FE direction. sequences when there is a loose electrical connection,
The artifact extends beyond the boundaries of the patient which is most likely to occur when the gradients are applied
and does not distort the image. With parallel imaging at a very high duty cycle. Build up of static electricity may
the appearance of zipper artifacts may appear differ- also result in spike artifacts (e.g., if the room is too dry
ent, with ghosting seen on the image.3 Zipper artifacts due to failure of the humidification system). The artifact
are caused by leakage of external RF signals (e.g., from occurs due to production of a spike of noise, which results
electrical equipment or radio stations) into the MRI in a bad data point in the raw data (k-space). Correction
scanning room. RF interference can occur either due requires the intervention of an MRI engineer. A similar
to a break in the room shielding or arise from electri- appearing artifact can occur due to missing data points
cal equipment in the room (e.g., monitoring equipment, within k-space (‘zero-fill artifact’).
lights). The width and position of artifacts depend on
the frequency of the source and they occur when the RF COIL ARTIFACTS
noise is of a narrow range of frequencies. If the RF noise
covers a large range of frequencies, degradation of the • Most modern MRI coils contain multiple coil elements
whole image may occur rather than a specific zipper arti- to receive and/or transmit the RF signal. Complete fail-
fact. In many MRI scanners, if the scanning room door ure of individual coil elements may result in focal loss
is not closed, the scanner will not operate, but if the door of signal within one area of the image and will affect all
is left partially open or there are dirty/broken contacts images produced using the defective coil. With parallel
on the door, RF interference can occur. Zipper artifacts imaging, in addition to some signal loss, there may be
Fig. 3.11 Zipper artifact (arrow) due to external RF Fig. 3.12 Dorsal T2W image of a cat with simulated spike
interference. Artifacts due to hardware or problems with artifact (arrow). The thickness and angulation of the banding
room shielding will usually affect all sequences. Zipper seen with spike artifacts are variable. If several bad data
artifact occurs in the frequency-encoding direction, which points are present in k-space, several bands of different
helps differentiate it from pulsatility artifact, which happens angulation, criss-crossing each other, may be present creating
in the phase-encoding direction. (1.5T MRI system; image a ‘herringbone pattern’. (1.5T MRI system; image courtesy of
courtesy of Dr. Wilfried Mai, University of Pennsylvania) Dr. Wilfried Mai, University of Pennsylvania)
78 CHAPTER 3
image ghosting due to mismatches between the calibra- gradients become distorted at the edges of the FOV [‘gra-
tion and diagnostic images.3 Correction requires replace- dient non-linearity’]). To avoid this, images should be
ment or repair of the coil. obtained using a smaller FOV.1
• With surface coils or phased-array coils (e.g., spine or
torso coils), which are positioned on one side of a patient, ARTIFACTS ASSOCIATED WITH
the received signal is non-linear and reduces with MRI PULSE SEQUENCES
increasing distance. This results in tissue closer to the
coil having more signal than deeper tissues and leads to Other than motion and intrinsic patient artifacts, the most
variation in signal-to-noise ratio (SNR) across the image common artifacts seen are related to software and pulse
(‘intensity non-uniformity’). Various image filtration sequence options. The MR operator can potentially alter
and data transformations are often used to normalize many variables, which can affect the image quality.
the apparent signal across the image so that superficial
structures appear similar in signal to deeper structures Poor signal-to-noise ratio
(Fig. 3.13). However, even with filtration, it is common • Poor SNR reduces image contrast and can render the
for objects closest to the coil to appear brighter. If not images non-diagnostic.
recognized, this can lead to potential misdiagnoses (e.g., • There is a trade-off in MRI between SNR, image resolu-
in images of heads scanned on a spine coil the part of the tion, and acquisition time, which are interdependent (see
brain closest to the coil appears brighter [Fig. 3.13]). Chapter 2).
• ‘Receive coils’ are designed to image a specific maximum • Some image noise is always present, but if excessive it
FOV but they receive signal from adjacent objects out- will result in a grainy appearing image, which can mask
side the coil. If the images acquired are larger than the potential pathologies. There are numerous factors
coil FOV, there is distortion and loss of signal from any (imaging parameters, coil, hardware faults) that affect
tissue beyond the limits of the coil. the SNR, but in most cases poor SNR is due to operator
• A similar phenomenon occurs if very large FOVs are error, and careful review of the pulse sequence acquisi-
imaged (e.g., body imaging where the magnetic field tion parameters is warranted.
(b)
(a) (c)
Fig. 3.13 Transverse T2W image of the brain (a) and sagittal T2W image of the lumbar spine in a dog (b) obtained with a spine
surface coil. There is variation in signal intensity across the images with greatest signal intensity in the tissues closest to the
coil (circle in a; arrow in b). Filtering of the image (c) to correct for the non-uniformity of signal results in more uniform signal
intensity across the image. (1.5T MRI system)
Cross-excitation FOV wrapping around (aliasing) and overlying the area

• Loss of signal can occur during slice selection if there is of interest (Fig. 3.15).
excitation of a slice from adjacent slices resulting in par- • Phase wrap also occurs with 3D acquisitions in the slice
tial saturation of spins. direction (Fig. 3.16), which is also phase-encoded.1 With
• This can occur during multislice acquisitions because 3D acquisitions, phase wrap can therefore occur in two
of the shape of the frequency profiles of the RF pulse, different directions.
which are imperfect. • The area of overlap is peripheral in the PE direction on
• The artifact occurs if there is no gap between slices, is conventional MRI images.
worst on inversion recovery sequences, and spares the • Phase wrap can also occur with non-anatomic objects
edge slices of a multislice acquisition. The artifact can be that are outside the patient (e.g., drip lines or capnogra-
avoided by having an interslice gap of at least one-third phy tubing containing moisture).
of the slice thickness, using an interleaved acquisition • With parallel imaging the appearance of phase wrap
technique or 3D acquisition. is different, with aliased tissue appearing centrally
within the images associated with increased image noise
Slice overlap/cross talk (Fig. 3.17).3
• If image slices overlap during a multislice, multi-angle • To prevent this artifact, the FOV in the PE direction
acquisition, there is focal band of loss of signal at the needs to be larger than the area of anatomy being imaged,
overlap point (Fig. 3.14). or phase oversampling needs to be used. In phase overs-
• When the second set of slices is acquired some of the ampling, the FOV is enlarged in the PE direction in
tissue will already have experienced the first RF pulses order to cover a wider area of anatomy and to preserve
so the spins will already be saturated and will return no spatial resolution; the number of phase-encoding steps is
signal. This will create dark bands across the images. increased accordingly. This eliminates the wraparound
• The artifact is generally not a problem provided it occurs artifact, but at the cost of an increase in acquisition time
within anatomy outside the area of interest. given the increase in PE steps. This can be compensated
for by reducing the number of excitations (averages) to
Phase wrap/wraparound artifact maintain acquisition time; however, this causes some
• Phase wrap occurs when the FOV in the PE direction reduction in SNR. Some machines automatically reduce
is too small, resulting in areas of anatomy outside the the number of excitations when the imaging option ‘no
(a) (b)
Fig. 3.14 Example of cross-talk artifact. The image on the left (a) is a sagittal plane localizer that shows slice localization of
two sets of dorsal plane images that have been aligned with the vertebral canal for optimal imaging of the cervical (blue) and
thoracic (yellow) spine. There is overlap of the groups in the caudal cervical spine. The resulting dorsal plane image of the
cervical spine (b) shows horizontal black bands where there was overlap from the dorsal plane images of the thoracic spine.
(1.5T MRI system; images courtesy of Dr. Wilfried Mai, University of Pennsylvania)
80 CHAPTER 3
Fig. 3.15 Transverse T2W image of the lumbar spine in

a dog with phase wrap artifact (arrows). The image was
acquired with the field of view in the phase-encoding
direction (right to left) smaller than the area of anatomy,
which results in the lateral parts of the abdomen wrapping
Fig. 3.16 Transverse T1W 3D image of the brain in a normal
over the image. (1T MRI system; reproduced, with
Bulldog with phase wrap artifact in the slice direction (rostral
permission, from the BSAVA Manual of Canine and Feline
to caudal in this case). The rostral extremity of the head has
Musculoskeletal Imaging, 2nd edn, British Small Animal
wrapped into the image with the frontal sinus and orbits
Veterinary Association, Gloucester.)
(arrows) visible superimposed over the brain. (1.5T MRI
system)
(a) (b)
Fig. 3.17 Dorsal magnetic resonance angiography image of the thorax (a) and transverse T1W image of the lumbar spine
(b) in two normal dogs showing phase wrap with parallel imaging. The aliased tissue (solid arrows, a) appears centrally within
the image, in comparison with non-parallel imaging techniques where the aliased signal is peripherally on the image. There is
additional loss of signal (dotted arrow, b) centrally within the image. (1.5T MRI system)
phase wrap’ is used, and then discard the extended por- cord, and could be mistaken for parenchymal pathol-
tions of the FOV to only display the region of initial ogy such as edema or gliosis.13
interest. • In the stifle joints, truncation artifacts may cause
• As the PE process is time consuming, the PE direction is linear structures across the menisci, which can be
often aligned with the shortest anatomic axis of the area mistaken for meniscal tears.2
being imaged (e.g., PE right to left on a dorsal plane image
of the head or spine). B0 -sensitive (‘off-resonance’)
banding artifact
Gibbs artifact (truncation/ringing artifact) • This artifact occurs in balanced steady-state free pre-
• Gibbs artifacts appear as a series of alternating dark cession sequences (e.g., FISP, FIESTA, bFFE) due to
and bright lines, which occur typically at high contrast B 0 non-uniformity, which results in failure of com-
boundaries and follow the contour of the boundary. plete reversal of the signal phase accumulated dur-
• They occur due to data undersampling and cannot be ing the acquisition. This causes phase errors from
totally eliminated.2 The undersampling causes the high- the development of phase shifts, resulting in phase
frequency signal from a high contrast sharp interface to accumulation.14
not be represented accurately. • This artifact appears as black bands (Fig. 3.19) in areas
• As the imaging matrix is usually smaller in the PE direc- of increased B0 non-uniformity (e.g., at the edges of the
tion than the FE direction, the artifact occurs more FOV, adjacent to lung and gastrointestinal tract or close
often in the PE direction.1 to microchips).
• Correction requires sampling at more data points by • The bands occur at frequency intervals of 1/TR,
increasing the size of the image matrix and voxel size. increasing in number and size with longer TR.
Image filtering may reduce the visual appearance of the • This artifact cannot be totally avoided, but shorter TR
artifact. and careful shimming may reduce the severity of the
• Gibbs artifacts can be mistaken for normal anatomy or artifact.14
pathology:
• For example, on sagittal T2W images they can cause a Chemical shift artifacts
linear hyperintensity in the middle of the spinal cord Chemical shift artifacts can occur due to two processes based
that can be mistaken for the central canal (Fig. 3.18).12 on either misregistration of signal or phase cancellations.
• In patients with focal spinal cord compression, a focal
spinal cord hyperintensity may be seen as a result Misregistration of signal
of convergence of hyperintense truncation artifacts • The spatial location of MR signals in the FE direction is
arising from the ventral and dorsal surfaces of the based on the fact that the resonant frequency of the spins
(a) (b)
Fig. 3.18 Sagittal T2W images in a dog with C4-C5 disc extrusion with images acquired with 302 (a) and 476 (b) phase-
encoding steps. The linear T2 hyperintensities (arrows) within the spinal cord, which mimic the central canal, are artifactual
and occur due to truncation (Gibbs) artifact. The severity of the artifact can be reduced by increasing resolution in the phase-
encoding direction. Note that the artifact is reduced with increased number of phase-encoding steps (b). (1.5T MRI system)
82 CHAPTER 3
hydrogen atoms, effectively deshielding them so that

they resonate at a slightly higher frequency. This effect
increases with increasing magnetic field strength and
allows the use of spectral fat saturation techniques
(see Chapter 2).
• The effect of the slightly differing resonant frequencies
of fat and water (fat is lower than water) results in slight
spatial misregistration of the fat signal.
• Chemical shift artifact occurs only in the FE direction
and can result in an artifactual line at fat/soft tissue inter-
faces that is black on one side and white on the opposite
side (Fig. 3.20). This can be mistaken for pathology
(e.g., meningeal thickening).
• Chemical shift artifact cannot be totally avoided, but can
be minimized by increasing the receiver bandwidth or by
using fat suppression techniques (e.g., spectral FATSAT,
mDIXON, see Chapter 2).
• As recognition of pathology on the MRI images is often
based on the asymmetrical appearance of lesions, it is
advisable that for transverse and dorsal plane images the
frequency-encoding direction is dorsoventral or cra-
niocaudal, respectively, so the chemical shift artifact is
Fig. 3.19 Transverse bFFE image of the cervical spine of symmetrical.
a normal dog. The curved black bands (arrows) are due to
B0-sensitive banding artifact. (1.5T MRI system) Phase-cancellation artifacts (‘black boundary artifact’)
• Differences in the resonant frequencies of fat and water
varies across the image due to the varying magnetic gra- can lead to an artifact known as phase cancellation or 2nd
dients used in image acquisition (see Chapter 1). order chemical shift artifact.1
• The resonant frequencies of fat and water are slightly • This occurs on gradient echo sequences but not spin
different based on the configuration of the elec- echo sequences and results in black lines on the bound-
tron clouds. In water, the electronegative oxygen aries of tissues when voxels along the periphery of the
removes some of the electron cloud from the adjacent object contain both water and fatty tissues.
Fig. 3.20 Dorsal T2W images of the

normal lumbar spine in a dog showing the
effect of frequency-encoding direction on
chemical shift artifact. With frequency-
encoding right to left (a) the artifact
is asymmetrical lateral to the spinal
cord and lumbar nerves, and results in
apparent thickening of the meninges and
lumbar nerves (arrows). When frequency-
encoding is craniocaudal, the fat/cord
interface is parallel to the direction of
frequency-encoding, and the dark bands
from the chemical shift artifact are no
longer visible, making interpretation
easier. (1T MRI system; reproduced, with
permission, from the BSAVA Manual of
Canine and Feline Musculoskeletal Imaging,
2nd edn, British Small Animal Veterinary
(a) (b)
Association, Gloucester.)
VetBooks.ir
(a) (b)
Fig. 3.21 Transverse T2*W gradient echo images of the lumbar spine of a normal dog acquired in-phase with TE of 13.8 ms (a)
and out-of-phase (b) with TE of 20.7 ms showing phase cancellation artifact. The black boundary (arrows, b) along the margins
of the bladder and intestines is due to voxels containing fat and water and is most severe in the phase-encoding direction (right
to left). (1.5T MRI system)
• Due to differences in resonant frequencies, the spins of

water and fat lose phase coherence after the initial RF
pulse at slightly different rates. At specific TEs, when
the spins of fat and water are exactly 180° out of phase,
the signals from the water and fat cancel each other out,
resulting in signal loss.
• This can happen at the boundary of organs surrounded
by fat (e.g., kidneys in the retroperitoneal space), when
voxels containing mixed fat and water at the boundaries
of objects appear black (Fig. 3.21). As this artifact only
occurs at specific TEs (2.2 ms, 6.6 ms, 11.0 ms, 15.4 ms,
etc.), it can be avoided by choosing a TE when fat and
water are in-phase.
• Phase cancellation artifact can result in artifactual
changes in thickness of bone.15
Susceptibility artifacts
• Susceptibility artifacts occur at the boundaries between
substances of different magnetic susceptibility (e.g., bone
and air). At these boundaries, there is microscopic varia-
tion in the local magnetic field, which causes alterations
in frequency and phase shifts of the spins. Fig. 3.22 Transverse T2* W gradient echo image of a
• The artifact results in focal distortion of the image normal dog showing susceptibility artifact (arrows) from the
(greatest on gradient echo sequences) and is commonly frontal sinuses. The focal image distortion and blooming are
seen adjacent to the frontal sinuses (Fig. 3.22), tympanic characteristic of susceptibility artifact. (1.5T MRI system)
bullae, and microchips. The susceptibility artifact can be
so large as to prevent normal anatomy from being visual- • Susceptibility artifacts are largest adjacent to ferromag-
ized (Fig. 3.23) (e.g., near to surgical implants). netic objects (e.g., metallic implants),16–19 although they
• The shape, size, and signal intensity of susceptibility also occur with hemorrhage, suture material, some for-
artifacts vary with anatomy, field strength, echo time, eign bodies, and gas.8 Susceptibility artifacts become
bandwidth, and differences in susceptibility. larger with increasing field strength.
84 CHAPTER 3
In this case, it is helpful to change the imaging param-

eters (e.g., increase TE and flip angle on T2*W gradient
echo pulse sequences20) to maximize susceptibility.
• In most cases, however, susceptibility artifacts are
unwanted and should be reduced.
• Optimized metal artifact reduction sequences have
been developed by most MRI vendors (e.g., MAVRIC,
Advanced WARP, O-MAR) (Fig. 3.24) but are often
only available as additional options on specific machines.
• Imaging parameters that can reduce susceptibility arti-
facts include:17,21,22
• Avoid gradient echo pulse sequences.
• Avoid parallel imaging if metal artifacts are present.
• Parallel imaging reduces artifacts due to air in the
sinuses and tympanic bullae.
• Use short echo-spacing,23 which allows collection of
Fig. 3.23 Sagittal T2W image of the cervical spine of a more echoes during the echo-train before the signal
normal cat. There is a large susceptibility artifact (arrows) decays and less time for dephasing of spins.
from the identity chip, which prevents evaluation of the mid- • Use longer echo-train.23
cervical spine. Susceptibility artifacts from metallic implants • Use shorter TE as there is less time for dephasing of
cannot be avoided but choice of pulse sequence and imaging spins.
parameters can reduce the size/orientation of the artifact, • Use high receiver bandwidth.
and in most cases a diagnostic study can be obtained. • Use thin slices.
(1.5T MRI system) • Increase image resolution by increasing the matrix
size in the FE direction.22
• Avoid spectral fat saturation. If suppression of
• The presence of objects with magnetic susceptibility in fat signal is desired, use sequences that do not
the FOV causes spectral fat saturation to not be homo- rely on frequency-specific fat saturation, such as
geneous in large areas around the object, due to the STIR; however, such sequences should not be used
regional changes in precessional frequencies. In these post-contrast (see Chapter 2).
cases, large areas around the object are not appropriately • Maintain adequate SNR.
saturated (i.e., the fat remains bright). • Swap PE and FE directions. This will not eliminate
• Because susceptibility effects are commonly seen with the artifact but will change its shape and the direction
hemorrhage, they can be useful to identify such lesions. of maximum severity, which may lead the artifact to
(a) (b)
Fig. 3.24 Transverse T1W images of the pelvis in a dog with left-sided total hip replacement obtained without (a) and with (b)
metal artifact reduction software. There is reduced size of the susceptibility artifact (arrows, b) due to the implant with the
metal artifact reduction software compared with the conventional image. (1.5T MRI system)
not overlap too much of the region of diagnostic inter- proton density-weighted, T2*W, and STIR sequences).
est. This can be particularly useful when imaging the Because high signal within a tendon can be seen with
cervicothoracic spine in patients with microchips. tendon injuries, this artifact can be mistaken for genuine
• Changing alignment of metallic implants relative to tendon pathology.24,25 The magic angle artifact is not vis-
B0 (e.g., by changing limb or body position). This can ible on sequences with long TE such as T2W images,
reduce artifacts but may not be practical. Susceptibility and therefore comparing the areas of high signal on
artifacts from metal implants are smallest when the T1W images with similar regions of the T2W images
implant is aligned with the main magnetic field.22 will allow differentiation of the artifact from genuine
pathology (Fig. 3.25).
Magic angle effect
• Tendons and ligaments normally have low signal on all Partial volume averaging
MRI pulse sequences, due to their highly ordered colla- • Partial volume averaging artifacts are not unique to MRI
gen with protons bound to water. Normal ligament fibers and occur in all cross-sectional imaging modalities.
will behave similarly, but the more complex organiza- • MR images are generated from data obtained from voxels
tional pattern of ligaments produces less uniform signal (which are cuboidal) but are displayed on the computer
intensity compared with tendons. monitor as pixels (which are two-dimensional).
• In tendons, the dipolar interactions between tissue pro- • The signal intensity of the pixel is the average of all
tons with highly ordered collagen usually result in rapid the different tissues within the individual voxel. If
dephasing of these protons following excitation (‘dipole the voxel contains different tissues that have different
interaction’), leading to little or no signal emanating signal intensities (e.g., CSF and white matter), then
from the tendon. When the tendon’s fibers are oriented the brightness of the pixel on the image will be
at some particular angles to the axis of the main mag- intermediate between the two. This occurs most
netic field (55 ± 10°, or any interval of this, such as 125°, commonly with large voxels and voxels at the boundary
235°, 305°), the dipole interactions are minimized, which of different structures, especially if the interface is
creates a signal of enough intensity to make the structure curved. This effect is called partial volume averaging
look hyperintense, potentially mimicking pathology. and may result in ‘pseudolesions’, which can mimic
• This is called the ‘magic angle artifact’. pathology.
• This causes an increase in signal intensity of the tendon • Partial volume averaging becomes more severe with
on short TE sequences (especially T1W images, but also increasing slice thickness.
(a) (b)
Fig. 3.25 Sagittal PDW (a) and transverse T2W (b) images of the shoulder in a normal dog showing magic angle artifact (arrow, a).
The increased signal within the biceps brachii tendon on the PDW image is artifactual and is not visible on other imaging planes
or T2W images (which have a long TE). (1.5T MRI system; reproduced, with permission, from the BSAVA Manual of Canine and
Feline Musculoskeletal Imaging, 2nd edn, British Small Animal Veterinary Association, Gloucester.)
86 CHAPTER 3
(a) (b)
Fig. 3.26 Transverse (a) and sagittal (b) T2W images of the normal brain in a 5-year-old Akita showing partial volume
averaging artifact causing a pseudolesion on the transverse image (arrow, a). The focal T2 hyperintensity apparently within
the pons on the transverse plane image (a) is artifactual due to partial volume averaging as a result of the voxels containing
both CSF and brain tissue (arrowheads, b). The slice location and width of the transverse image are shown by the lines on the
sagittal image, which allows confirmation that the pseudolesion is artifactual. (1T MRI system; reproduced, with permission,
from the BSAVA Manual of Canine and Feline Musculoskeletal Imaging, 2nd edn, British Small Animal Veterinary Association,
Gloucester.)
• Pseudolesions created due to partial volume averag- 5. Lavdas E, Mavroidis P, Kostopoulos S et al. (2015). Reduction of
ing are easily recognized as artifactual by assessing the motion, truncation and flow artifacts using BLADE sequences in
cervical spine MR imaging. Magn Reson Imaging 33(2):194–200.
‘lesion’ on different imaging planes (Fig. 3.26). Genuine
6. McRobbie DW, Moore EA, Graves MJ et al. (2006). Go with
pathology is usually visible on multiple imaging planes. the flow: MR angiography. In: MRI From Picture to Proton.
• Partial volume averaging cannot be eliminated as the (eds. DW McRobbie, EA Moore, MJ Graves, MR Prince)
image slice always has a finite width, but it can be reduced Cambridge University Press, Cambridge, pp. 258–81.
by obtaining thinner slices. Reducing slice thickness, 7. Westbrook C, Roth CK, Talbot J (2011). Flow phenomena.
however, results in reduction in signal leading to poorer In: MRI in Practice, 4th edn. (eds. C Westbrook, CK Roth,
SNR, which is generally a worse problem than partial J Talbot) Wiley-Blackwell, Chichester, pp. 198–224.
volume averaging artifacts. When evaluating small 8. Cooper JJ, Young BD, Hoffman A et al. (2010). Intracranial
structures that require high resolution, three-dimen- magnetic resonance imaging artifacts and pseudolesions in
dogs and cats. Vet Radiol Ultrasound 51(6):587–95.
sional volumetric acquisitions are usually required.
9. Lisanti C, Carlin C, Banks KP et al. (2007). Normal MRI
appearance and motion-related phenomena of CSF. Am J
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1. McRobbie DW, Moore EA, Graves MJ et al. (2006). Improving 10. Zhuo J, Gullapalli RP (2006). MR artifacts, safety, and quality
your image: how to avoid artefacts. In: MRI from Picture to control. Radiographics 26(1):275–97.
Proton. (eds. DW McRobbie, EA Moore, MJ Graves, MR 11. Heiland S (2008). From A as in Aliasing to Z as in Zipper:
Prince) Cambridge University Press, Cambridge, pp. 79–107. artifacts in MRI. Clin Neuroradiol 18(1):25–36.
2. Arena L, Morehouse HT, Safir J (1995). MR imaging artifacts 12. Bronskill MJ, McVeigh ER, Kucharczyk W et al. (1988).
that simulate disease: how to recognize and eliminate them. Syrinx-like artifacts on MR images of the spinal cord.
Radiographics 15(6):1373–94. Radiology 166(2):485–8.
3. Yanasak NE, Kelly MJ (2014). MR imaging artifacts and 13. Gregori T, Lam R, Priestnall SL et al. (2016). Truncation
parallel imaging techniques with calibration scanning: a new artifact in magnetic resonance images of the canine spinal
twist on old problems. Radiographics 34(2):532–48. cord. Vet Radiol Ultrasound 57(6):582–6.
4. Mavroidis P, Giankou E, Tsikrika A et al. (2016). 14. Huang SY, Seethamraju RT, Patel P et al. (2015). Body
Brain imaging: comparison of T1W FLAIR BLADE with MR imaging: artifacts, k-space, and solutions. Radiographics
conventional T1W SE. Magn Reson Imaging 37:234–42. 35(5):1439–60.
15. Dimock AN, Spriet M (2010). Influence of the chemical shift 21. Hargreaves BA, Worters PW, Pauly KB et al. (2011).
artifact on measurements of compact bone thickness in equine Metal-induced artifacts in MRI. Am J Roentgenol 197(3):
distal limb MR images. Vet Radiol Ultrasound 51(4):415–20. 547–55.
16. David FH, Grierson J, Lamb CR (2012). Effects of surgical 22. Port JD, Pomper MG (2000). Quantification and
implants on high-field magnetic resonance images of the minimization of magnetic susceptibility artifacts on GRE
normal canine stifle. Vet Radiol Ultrasound 53(3):280–88. images. J Comput Assist Tomogr 24(6):958–64.
17. David FH, Grierson J, Lamb CR (2012). Reducing 23. Lee MJ, Kim S, Lee SA et al. (2007). Overcoming artifacts
susceptibility artefacts in magnetic resonance images of the from metallic orthopedic implants at high-field-strength
canine stifle following surgery for cranial cruciate ligament MR imaging and multi-detector CT. Radiographics 27(3):
deficiency. Vet Comp Orthop Traumatol 25(6):488–97. 791–803.
18. Sutherland-Smith J, Tilley B (2012). Magnetic resonance imaging 24. Spriet M, Mai W, McKnight A (2007). Asymmetric signal
metallic artifact of commonly encountered surgical implants and intensity in normal collateral ligaments of the distal
foreign material. Vet Radiol Ultrasound 53(3):312–17. interphalangeal joint in horses with a low-field MRI system
19. Hecht S, Adams WH, Narak J et al. (2011). Magnetic due to the magic angle effect. Vet Radiol Ultrasound 48(2):
resonance imaging susceptibility artifacts due to metallic 95–100.
foreign bodies. Vet Radiol Ultrasound 52(4):409–14. 25. Werpy NM, Ho CP, Kawcak CE (2010). Magic angle effect
20. Liang L, Korogi Y, Sugahara T et al. (1999). Detection of in normal collateral ligaments of the distal interphalangeal
intracranial hemorrhage with susceptibility-weighted MR joint in horses imaged with a high-field magnetic resonance
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CHAPTER 4.1
OPTIMIZED TECHNIQUE: BRAIN

88 Silke Hecht
CONTENTS
Magnetic field strength and coil selection ...............................................................................................................................................................89
Patient preparation and positioning.........................................................................................................................................................................89
MRI pulse sequences, functional imaging techniques, and technical modifications used in brain imaging ............................................................89
Spin echo sequences .........................................................................................................................................................................................89
T1-weighted spin echo pulse sequences ......................................................................................................................................................89
T2-weighted spin echo pulse sequences ......................................................................................................................................................89
Proton density-weighted spin echo pulse sequences ...................................................................................................................................91
Modified spin echo sequences including fast and turbo spin echo techniques ..................................................................................................91
Inversion recovery sequences ......................................................................................................................................................................91
Fast or turbo spin echo techniques ..............................................................................................................................................................92
Single shot techniques ................................................................................................................................................................................92
Gradient echo sequences ...................................................................................................................................................................................92
T2*W GRE sequence ....................................................................................................................................................................................93
2D/3D volumetric acquisitions .....................................................................................................................................................................93
Functional imaging techniques ..........................................................................................................................................................................94
Diffusion-weighted imaging .........................................................................................................................................................................94
Perfusion-weighted imaging ........................................................................................................................................................................95
Functional MR imaging ................................................................................................................................................................................95
Magnetic resonance spectroscopy ...............................................................................................................................................................96
Technical modifications .....................................................................................................................................................................................96
Spatial presaturation ....................................................................................................................................................................................96
Fat saturation ...............................................................................................................................................................................................96
Magnetization transfer imaging ....................................................................................................................................................................96
Optimized brain MRI protocol .................................................................................................................................................................................97
General considerations ......................................................................................................................................................................................97
Contrast media in brain MRI ..............................................................................................................................................................................97
Brain MRI protocol for veterinary patients..........................................................................................................................................................98
Important MRI artifacts in brain imaging .................................................................................................................................................................98
Motion ...............................................................................................................................................................................................................98
Cerebrospinal fluid flow artifacts .....................................................................................................................................................................100
Susceptibility ...................................................................................................................................................................................................101
Partial volume averaging .................................................................................................................................................................................102
References.............................................................................................................................................................................................................102
O p t i m i z e d Te c h n iqu e : Br a i n 89
While the MRI technique will at least in part be dependent • MRI procedures are noisy, with the main source of noise
on the equipment available to the radiologist/clinician, being associated with the rapid switching of gradient
several factors should be taken into consideration to coils. This has potential to cause a significant reduc-
assure optimum image acquisition. Specific imaging pro- tion in frequency specific cochlear function in dogs.
tocols also depend on the clinical indication for brain Therefore, ear-protecting devices such as earplugs may
MRI. This chapter will present general technical consid- be recommended as a routine precautionary measure.5,6
erations for brain MRI in dogs and cats. The particulari- • Identification microchips are typically implanted near
ties of low-field MRI will be covered in a separate chapter the cervical spine and brain. Although they may be
(see Chapter 4.4). associated with significant susceptibility artifacts and
interfere with image interpretation, adverse effects or
MAGNETIC FIELD STRENGTH microchip malfunction have not been observed using
AND COIL SELECTION MRI systems from 0.5 to 3T.7–9
• For brain MRI examinations, positioning of the patient
• MRI systems used in clinical veterinary medicine include in either sternal or dorsal recumbency is possible.
low-field systems (e.g., 0.25T or 0.4T) and high-field sys- Straight positioning is important to obtain true sagittal,
tems (1T, 1.5T, or 3T). There are inherent advantages transverse, and dorsal planes.
to higher field systems regarding signal-to-noise ratio
(SNR), image quality, availability of advanced imaging MRI PULSE SEQUENCES, FUNCTIONAL
sequences, and speed of image acquisition especially in IMAGING TECHNIQUES, AND TECHNICAL
small patients.1,2 Nevertheless, low-field systems can pro- MODIFICATIONS USED IN BRAIN IMAGING
duce diagnostic quality scans of the small animal brain
(see Chapter 4.4). While a detailed description of pulse sequences, signal, and
• In human medicine, quadrature head coils and, more contrast in MRI can be found in Chapter 2, a brief overview
recently, phased array head coils are most commonly of sequences and techniques used for MR examination of
used when imaging the brain.3 However, small diameter the brain is provided here.
orthopedic coils or surface coils wrapped around the area
of interest are in the author’s experience quite useful for Spin echo sequences
imaging the brain in dogs and cats: • These include T1W, T2W, and PDW sequences, which
• Some traditional head coils are closed on one end, are the most basic but also the most commonly used MRI
which makes access to the patient under general sequences.1,10–17
anesthesia difficult and interferes with positioning
of endotracheal tubes and anesthesia monitoring T1-weighted spin echo pulse sequences
equipment. • A short TR is chosen to maximize the differences in T1
• When using a large diameter head coil with a sig- relaxation between tissues. This is combined with a short
nificant gap between the coil and patient, the image TE to minimize T2 effects. Fat has a short T1 relaxation
quality may be limited. time and is hyperintense, while fluid has a long T1 relax-
ation time and appears hypointense.
PATIENT PREPARATION AND POSITIONING • Soft tissues have somewhat variable intermediate T1
relaxation times and signal intensity (Fig. 4.1.1a).
• With few exceptions (e.g., unconscious patients), small • After uptake of paramagnetic contrast agents, physiolog-
animal patients undergoing brain MRI will be examined ically contrast-enhancing tissues (e.g., pituitary gland)
under general anesthesia, and the usual precautions and and contrast-enhancing pathologic lesions (e.g., certain
risk factors associated with general anesthesia apply. brain tumors) are hyperintense (Fig. 4.1.1d).
• Before the animal is brought into the MRI suite, all
superficial metallic structures (e.g., collar, tags, or deco- T2-weighted spin echo pulse sequences
rative hairclips) must be removed. • A long TE is chosen to maximize differences in T2
• Adverse effects have not been reported in animals with relaxation between tissues, combined with a long TR to
skin tattoos (e.g., identification tattoos associated with minimize T1 relaxation effects.
ear or inner thigh). However, the examiner should be • Because of the long TE, tissues with a short T2 relaxation
aware that cutaneous reactions (‘burns’) attributed to time will have completely lost their transverse magneti-
ferromagnetic metallic compounds found in tattoo ink zation and have a low signal at the time of signal read-
are sporadically seen in humans.4 A cold compress placed out, while tissues with longer T2 relaxation times still
on the tattoo may be used prophylactically or symptom- maintain their transverse magnetization, generating more
atically to avoid this problem. signal and therefore appearing hyperintense (brighter).
90 CHAPTER 4.1
(a) (b)
(c) (d)
Fig. 4.1.1 Transverse images of the brain in an 8-year-old Border Collie with a large cystic extra-axial mass (meningioma,
presumptive) associated with the right ventral aspect of the cranium. (a) T1W image showing a fusiform lesion approximately
isointense to the ventricular system (arrowhead) at the dorsal aspect of the mass, which is otherwise isointense to brain
parenchyma and not clearly visible (solid arrows). Note the hyperintensity of the bone marrow fat associated with the skull and
subcutaneous fat (dotted arrows). (b) On the T2W image the mass is mildly hyperintense, and the dorsal cystic component is
strongly hyperintense (isointense to CSF). Note that fat is also hyperintense on this TSE sequence. (c) On the PDW image the
mass is mildly hyperintense. Note the increased conspicuity of gray/white matter distinction on this sequence compared with
the T1W and T2W images. (d) T1W post-contrast image showing strong and homogeneous contrast enhancement of the mass
while the cystic component is non-enhancing.
• Fluid has a long T2 relaxation time and, therefore, is which additional pulses are applied (see below), fat typi-
hyperintense on T2W images. Soft tissues have interme- cally appears hyperintense on today’s T2W MRI studies.
diate T2 relaxation times. Fat has a short T2 relaxation • A T2W sequence can be considered a ‘pathology’
time and appears hypointense on conventional spin echo scan, because abnormal fluid collections and tissues
(SE) T2W images. However, as conventional T2W SE with abnormal increased fluid content (‘juicy tissue’;
sequences have largely been replaced with shorter fast e.g., edema, inflammation, neoplasia) will appear hyper-
spin echo (FSE) or turbo spin echo (TSE) sequences in intense compared with normal tissues (Fig. 4.1.1b).
Proton density-weighted spin echo pulse sequences can be used with T1- or T2-weighting. T2-FLAIR
• These sequences are achieved by choosing a long TR in images are useful in conjunction with regular
combination with a short TE to minimize T1 and T2 T2W SE images in characterizing T2 hyperintense
effects on image contrast. lesions.19,20 Using T2-FLAIR, pure fluid (CSF and
• PDW images are characterized by excellent anatomic fluid in cystic lesions) is suppressed and becomes
detail and are very useful in orthopedic imaging. hypointense while solid lesions remain hyperintense.
• For brain imaging, they also provide a good contrast Additionally, this sequence increases conspicuity
between gray and white matter (Fig. 4.1.1c). Although of T2-hyperintense lesions bordering fluid-filled
their value in neuroimaging of small animals is limited, structures such as the ventricles or the subarach-
anecdotal evidence suggests that they may be helpful in noid space (Fig. 4.1.2). Finally, T2-FLAIR pulse
the evaluation of patients with degenerative brain disease sequences are helpful in differentiating true T2
and skull trauma (see also Chapter 5.8).18 hyperintense parenchymal lesions from pseudole-
sions created by inclusion of fluid-filled structures
Modified spin echo sequences including and brain parenchyma within the same slice thick-
fast and turbo spin echo techniques ness (volume averaging): a pseudolesion typically
• These sequences are based on conventional SE prin- will be suppressed on the T2-FLAIR image com-
ciples, but additional pulses are applied to selectively pared with traditional T2W series. Without modi-
suppress signal from certain tissues (inversion recovery fication of acquisition parameters, FLAIR is unable
sequences) or to accelerate data acquisition (fast spin echo to suppress signal from fluids with high protein
[FSE] or turbo spin echo [TSE] techniques and single content, cell components, or blood by-products, a
shot techniques).1,10–16 potential pitfall when interpreting images. Because
of the long inversion time used in FLAIR imaging,
Inversion recovery sequences there is also some degree of T1-weighting, and this
• These are characterized by an initial 180° pulse (inver- has the potential to demonstrate contrast enhance-
sion pulse). Dependent on the time elapsed between this ment in brain lesions. For this reason, post-contrast
180° pulse and initiation of the regular SE sequence (time T2-FLAIR images have been compared with con-
of inversion; TI) they result in selective suppression of ventional post- contrast T1W SE images, although
fluid (= fluid attenuated inversion recovery; FLAIR) or they do not appear to improve diagnostic perfor-
fat (= short tau inversion recovery; STIR). mance when compared with the combined evalu-
• FLAIR. A long TI prior to initiation of a SE sequence ation of the standard T2-FLAIR pre-contrast and
allows selective suppression of fluid. These sequences T1W post-contrast series.21,22
(a) (b)
Fig. 4.1.2 Transverse T2W (a) and T2-FLAIR (b) images of the brain in an 11-year-old West Highland White Terrier with
meningoencephalitis of undetermined etiology. Note the bilateral periventricular hyperintensity, which is more conspicuous on
T2-FLAIR images due to suppression of signal from CSF in the ventricular system and subarachnoid space.
92 CHAPTER 4.1
(a) (b)
Fig. 4.1.3 Sagittal T2W (a) and STIR (b) images of the head in a 12-year-old Irish Wolfhound. An aggressive infiltrative mass
lesion associated with the presphenoid and sphenoid bones (arrows) is more conspicuous on the STIR image than on the T2W
image due to suppression of adjacent bone marrow fat.
• STIR. A short TI prior to initiation of a SE sequence fluid-filled spaces such as the subarachnoid space and
allows selective suppression of fat. This sequence is ventricular system.
very valuable in orthopedic and spinal imaging and • ‘Quick-brain’ MR imaging was initially introduced as an
provides enhanced anatomic contrast depiction in alternative technique to CT scanning for assessing chil-
brain imaging.23 It is also useful in patients in which dren with hydrocephalus. Other indications in humans
evaluation of the skull, overlying soft tissues, and include macrocephaly, Chiari malformation, intracranial
adjacent regions of the head (e.g., the orbit) is desired cysts, screening prior to lumbar puncture, screening for
(Fig. 4.1.3). congenital anomalies, and trauma.
• These sequences have gained popularity in veterinary
Fast or turbo spin echo techniques24 medicine mostly for spinal imaging, but can add use-
• In conventional SE imaging, one 180° pulse is applied ful information when imaging fluid-filled intracranial
during each TR and one echo (signal) is generated. In FSE structures and evaluating a patient for meningeal disease
and TSE, multiple 180° pulses are applied during each TR where the normal hyperintense signal from CSF may be
and multiple echoes are received, resulting in a decrease obliterated due to the presence of proteins, cells and tis-
in scan time without compromising image quality. sues, or due to adhesions (Fig. 4.1.4).25–27
• FSE/TSE techniques have essentially replaced conven-
tional SE sequences in T2W imaging. One potential Gradient echo sequences
disadvantage is the strong hyperintensity of fat on T2W • Gradient echo (GRE) sequences use smaller flip angles
FSE/TSE images, as hyperintense fat in the bone mar- and shorter TRs than SE sequences, resulting in shorter
row may obscure or mimic skull lesions (see Fig. 4.1.1b). scan times. They also lack a 180° pulse, which has impor-
This disadvantage can easily be compensated for by add- tant implications for image-weighting and quality:
ing a fat saturation technique or comparing T2W images • Conventional GRE sequences can be used to acquire
with other sequences. T1W, PDW, and T2*W images.
• Acquisition of truly T2W images is not possible.
Single shot techniques • GRE sequences are prone to susceptibility artifacts,
• These ultrafast techniques employ a single RF pulse as there is no compensation for external field inhomo-
associated with a very long echo-train and half-Fourier geneities.12,28–31
space encoding, thereby acquiring all the necessary data • A plethora of GRE applications have been developed in
within one TR and further decreasing scan time. recent years, including conventional, coherent (steady
• Examples include HASTE (Siemens), SSH-TSE (Philips), state), incoherent (spoiled), steady-state free precession,
SS-FSE (General Electric), FSE-ADA (Hitachi), or balanced, fast, single shot, and echo-planar imaging
Super-FASE (Toshiba). sequences. Some sequences used routinely for imaging
• The resultant images are characterized by heavy of the CNS in small animals include T2*W GRE and
T2-weighting, and are most beneficial in imaging of 2D/3D volumetric acquisitions.
(a) (b)
Fig. 4.1.4 Sagittal images of the brain in a 6-year-old mixed breed dog with meningoencephalitis of undetermined etiology.
(a) The T2W image demonstrates an indistinct intra-axial lesion associated with the brainstem (arrow), mild crowding of the
caudal fossa with flattening of the caudal cerebellar margin (arrowhead), and an incidental quadrigeminal cistern cyst (asterisk).
(b) The heavily T2W half-Fourier acquisition single-shot TSE sequence shows extensive attenuation of the subarachnoid space
of the cerebrum consistent with inflammatory meningeal infiltration (arrowheads).
(a) (b)
Fig. 4.1.5 Transverse images of the brain in a 17-year-old mixed breed dog. (a) The T2W image does not show any
abnormalities. (b) There are multiple intra-axial punctate susceptibility artifacts on the T2*W image (arrowheads), consistent
with cerebral microbleeds.
T2*W GRE sequence • Additional indications may include identification of intra-

• Gas interfaces, soft tissue mineralization, fibrous tissue, cranial mineralization (e.g., in some forms of meningio-
and certain blood degradation by-products (e.g., methe- mas [‘psammomatous’]) or abnormal gas pockets (e.g., in
moglobin) cause magnetic field inhomogeneities, which brain abscesses).32–34
appear as a signal void (susceptibility artifact) on T2*W
images. 2D/3D volumetric acquisitions
• T2*W is most commonly utilized to identify intracra- • Specific 2D and 3D GRE sequences (e.g., Siemens VIBE,
nial hemorrhage and differentiate it from other lesions Philips THRIVE, General Electric FAME, Hitachi
(Fig. 4.1.5). SARGE, and Toshiba RADIANCE) may be beneficial in
94 CHAPTER 4.1
(a) (b)
Fig. 4.1.6 (a) Transverse image of the brain in a 6-year-old Newfoundland dog with neuritis of the oculomotor nerve
(presumptive). The image was acquired with a 3D T1W GRE sequence. There is focal enlargement of the left oculomotor
nerve (arrow). (b) Dorsal reconstructed image of the 3D dataset showing the enlarged nerve over a greater length (arrows).
Thickening of the nerve had improved at a recheck examination 5 months later.
the evaluation of small structures (inner ear, pituitary • Diffusion-weighted imaging (DWI) utilizes two gradi-
gland, osseous structures, or cranial nerves), as they ents applied on either side of the 180° pulse to produce
allow acquisition of thin slices (<1 mm) without inter- signal differences based on mobility and direction of
slice gap and permit multiplanar reconstruction of the water diffusion. Normal tissues have more water mobil-
3D dataset in additional planes (Fig. 4.1.6).18,29,35–40 ity than abnormal tissues. Mobile water protons do not
• Magnetic resonance angiography (MRA) techniques experience the second diffusion gradient and therefore
maximize vascular contrast by enhancing the signal are not rephased, causing a greater signal loss. In contrast,
from spins in flowing blood and/or suppressing the sig- tissues with less water mobility experience restricted dif-
nal from surrounding stationary tissues. Although this fusion and display higher signal, as the immobile water
can be accomplished without contrast medium admin- protons experience both gradients, and the dephasing
istration (digital subtraction MRA, phase contrast caused by the first diffusion gradient is cancelled out by
MRA, time of flight MRA), contrast-enhanced MRA is the second (= no drop in signal).
considered a superior technique due to improved image • In people, as well as in veterinary patients, DWI is most
quality. In people, evaluation of the intracranial circula- commonly used in the diagnosis of ischemic stroke.48–52
tion provides valuable information in the diagnosis and In acute cerebral ischemia, restricted diffusion occurs
prognosis of various abnormalities such as aneurysms, secondary to failure of the cell membrane ion pump and
arterial and venous steno-occlusive diseases, inflamma- subsequent cytotoxic edema. An acute stroke is charac-
tory arterial diseases, and congenital vascular abnor- terized by marked hyperintensity on a DW image and
malities. Although intracranial vascular abnormalities hypointensity on a synthesized apparent diffusion coeffi-
are infrequently reported in the veterinary literature, cient (ADC) map derived from two or more DW images
MRA might be considered as a quick and low-risk pro- (Fig. 4.1.7). In people, DWI is also used to differentiate
cedure to evaluate intracranial vessels in select cases.41–45 benign from malignant lesions and distinguish neopla-
sia from edema or infarction. While some initial studies
Functional imaging techniques in animals have yielded promising results, the value of
DWI in the diagnosis of neurologic disorders other than
Diffusion-weighted imaging acute stroke remains to be determined.53–56
• Diffusion describes the motion of molecules in • Diffusion tensor imaging is a specialized DWI technique
tissues.46,47 This process is not truly random due to that utilizes strong multidirectional gradients to map white
the presence of physiologic boundaries (e.g., cell mem- matter tracts. Initial studies proved the feasibility of this
branes, intracellular organelles) and is referred to as technique in dogs, which may ultimately aid in the diagnosis
‘apparent diffusion’. of white matter disease and facilitate surgical planning.57,58
(a) (b)
Fig. 4.1.7 Territorial cerebellar infarct (left rostral cerebellar

artery) in a 16-year-old mixed breed dog. (a) The transverse
T2W image demonstrates a sharply marginated wedge-
shaped hyperintense lesion associated with the left cerebellar
hemisphere (arrow). (b, c) The lesion remains hyperintense on
the DW image (arrow, b) and is hypointense on the ADC map
(arrow, c), consistent with restricted diffusion and ischemic
(c)
stroke.
Perfusion-weighted imaging • Other potential applications include assessment of tumor

• Perfusion-weighted imaging (PWI) allows estimation of malignancy based on metabolic activity and evaluation of
blood volume passing through the capillary bed per unit tissue viability of vascular organs.
time. This is most commonly accomplished by dynami-
cally measuring the passage of a bolus of contrast agent Functional MR imaging
through the cerebral vasculature. • Functional MR imaging (fMRI) is a rapidly evolv-
• Perfusion imaging is often used in combination with ing area in human medicine, which allows evaluation
DWI in patients with acute ischemic stroke, where of brain activity during certain activities or following
the difference between diffusion and perfusion abnor- stimulation.
malities provides a measure of the ischemic penumbra • Any activity/stimulus (e.g., viewing a picture or smell-
(area of reversible ischemia that can be salvaged if blood ing food) results in activation of a specific area in the
flow is re-established promptly).52,59 brain, which necessitates an increase in blood flow.
96 CHAPTER 4.1
The resultant focal increase in oxyhemoglobin and patients with ischemic stroke, hepatic encephalopathy,
decrease in deoxyhemoglobin can be detected by means and inflammatory and neoplastic brain lesions have
of MRI due to their inherent difference in magnetic sus- shown promising results.64–73
ceptibility (‘blood oxygen level dependent’ or ‘BOLD’
imaging). Technical modifications
• The result is a map of functional brain areas during a spe-
cific activity or after a specific stimulus. Unfortunately, Spatial presaturation
application of this technique in veterinary patients is thus • Spatial presaturation pulses are used to suppress unde-
far limited due to the need for immobilization or gen- sired signals from anatomic areas within the imaging
eral anesthesia. However, initial attempts in conditioned field of view.74
awake dogs has yielded promising results, and fMRI in • Although these pulses are not commonly applied in brain
animals is likely to gain importance with the develop- imaging, they can be used to suppress signal from neigh-
ment of faster sequences and experience.60–62 boring vessels, thus minimizing ghosting artifacts.
Magnetic resonance spectroscopy Fat saturation

• Magnetic resonance spectroscopy (MRS) is a method • Unlike STIR, which is an entirely separate MR pulse
to measure tissue chemistry by recording signals from sequence, selective (‘spectral’) fat saturation pulses can
specific metabolites. In-vivo MRS is most commonly be applied to any sequence to suppress signal from fat
performed using hydrogen protons (1H [proton] spectros- without affecting the signal intensity of other tissues.23,74
copy). Although other metabolites can be recorded using • Fat saturation has proven especially beneficial when
this technique, proton spectroscopy has the advantages of applied to post-contrast T1W images, as it facilitates dif-
a high SNR and a relatively short examination time so it ferentiation of contrast-enhancing lesions from adjacent
can be added to conventional MR imaging protocols. fat and aids in identification of meningeal enhancement
• Applications in neuroimaging include monitoring of (Fig. 4.1.8).75–77
biochemical changes occurring in tumors, metabolic
disorders, and inflammatory and neurodegenerative Magnetization transfer imaging
diseases.47,63 • Magnetization transfer pulses can be applied in SE or
• With increasing availability of higher strength magnets, GRE sequences to produce additional signal suppression
MRS is gaining popularity in clinical veterinary medi- of tissue water. The technique may be used qualitatively
cine, and initial studies in canine models and clinical to increase the visibility of lesions seen during MRA and
(a) (b)
Fig. 4.1.8 Transverse post-contrast T1W images of the brain in a 4-year-old Yorkshire Terrier with meningoencephalitis.
Although meningeal enhancement is seen along the lateral surfaces of the brain on the image obtained without fat suppression
(arrowheads, a), this finding is more conspicuous on the fat-suppressed image, especially along the dorsal surface where
hyperintense fat in the medullary cavity of the adjacent frontal bone is nulled (arrowheads, b).
following contrast administration, or quantitatively to • Gadolinium-based contrast media decrease the T1

aid in the diagnosis of white matter disease. and T2 relaxation times of protons in their vicinity,
• However, currently this technique has not been well although at clinical concentrations, T1-effects predomi-
documented in canine and feline medicine in clinical nate. Therefore, lesions accumulating gadolinium have
applications.74,78 decreased T1 relaxation time, causing a hyperintense
signal on T1W images.
OPTIMIZED BRAIN MRI PROTOCOL • Certain normal intracranial structures outside of the
blood–brain barrier, such as pituitary gland, choroid
General considerations plexus, trigeminal nerve, and blood vessels, show physi-
• There are several criteria that should be met when estab- ologic contrast uptake.
lishing an MRI protocol:3 • Some disagreement exists as to the optimal timing
• Clinical questions must be answered. of MR image acquisition following contrast medium
• Examination time must be kept as short as possible. administration (immediate versus delayed).76,84,89
• Study results must be reproducible. However, since brain post-contrast images are usu-
• As indicated before, imaging protocols must be adapted ally acquired in more than one plane, some images are
to the equipment available and to radiologist/clinician acquired at a more delayed phase given the acquisition
preferences. There is no consensus regarding the stan- times for each pulse sequence.
dard brain imaging protocol in veterinary medicine. In • Dynamic studies monitoring contrast enhancement
human medicine, there is also great variability in the (wash-in and wash-out) over time are not commonly used
recommendations made. in veterinary medicine at this point, but may be useful
• The following are a few examples of recommendations for the evaluation of the pituitary gland, cerebral perfu-
for brain MRI protocol development found in the human sion, and brain tumors.59,86,88
literature: • In most human hospitals, administration of contrast
• MRI studies of the brain should include at least two medium is not part of a routine MRI brain proto-
imaging planes and two weightings, preferably more.3 col. However, the situation in veterinary medicine is
• The minimum screening brain protocol should different:
include sagittal T1W, axial T2W, axial T2-FLAIR, • Although rare, serious adverse side effects of gado-
T2*W, and DWI pulse sequences. If there is a clin- linium administration have been reported in people,
ical suspicion that the integrity of the blood–brain including nephrogenic systemic fibrosis in patients
barrier may be affected, post-contrast T1W images with reduced renal function.90 MR contrast agents
should be acquired. Specific suggestions for addition are considered safe for use in veterinary patients.81,82
of other sequences depend on the clinical suspicion Reports of significant adverse effects are limited to
(e.g., ‘multiple sclerosis protocol’, ‘tumor protocol’, one publication describing suspected anaphylactoid
‘epilepsy protocol’, ‘cerebrovascular imaging proto- reactions in three dogs.83 The author has observed
col’, ‘ischemic stroke imaging protocol’).17 an anaphylactoid reaction after MR contrast medium
• A large human study found that use of a 3-sequence administration in one white Tiger, which was con-
protocol (consisting of sagittal T1W, axial T2W trolled with antihistamine administration.
FLAIR, and axial DWI) resulted in failure to detect • In one study in human patients, use of a 4-sequence
25% of major abnormalities. This was reduced to 16% protocol not including a post-contrast sequence
of major lesions missed using a 4-sequence protocol resulted in failure to detect 16% of major lesions,
(sequences as above with the addition of a suscepti- 90% of which were contrast enhancing.79 The
bility-weighted sequence), with most of them being authors concluded that this number of missed
contrast-enhancing lesions.79 lesions during the initial MR examination resulted
in an acceptable rate of patients having to return for
Contrast media in brain MRI a second MRI examination. In a similar study in vet-
• The MRI contrast agents most commonly used in veteri- erinary medicine a previously undetected lesion was
nary medicine are gadolinium-based.48,76,80–88 identified on post-contrast images in 2% of cases,
• Contrast medium for brain imaging is administered at a and the authors questioned the routine adminis-
dose of 0.1 mmol/kg, which may be increased to improve tration of contrast media in veterinary patients.91
detection of poorly enhancing lesions or for angiographic However, this study was performed at low-field
studies. (0.2T) and results may be different at high-field.
• Enhancement is seen if a lesion is vascularized, is located In addition, veterinary patients are scanned under
outside of or has disrupted the blood–brain barrier, and general anesthesia, making it difficult to resched-
allows accumulation of contrast medium in the tissue ule a second MRI examination to acquire additional
after extravasation from the vascular system. sequences.
98 CHAPTER 4.1
• Probably more so than in people, there is often a – Evaluate the craniocervical junction.94
delay between the initial diagnosis of clinical signs – Evaluate morphology of the caudal fossa and
and referral for an MRI examination in veterinary cerebellum.95
patients. According to one preliminary study in – Identify concurrent lesions affecting the cranial
small animals, contrast medium administration was cervical spinal cord.96
especially useful in patients with chronic neurologic • Transverse T1W and T2W sequences.
signs.92 • Transverse T2-FLAIR:
– Although one study in dogs did not find a sig-
Brain MRI protocol for veterinary patients nificant advantage when adding a T2-FLAIR to a
• Scout views/localizer planes. Fast sequences are used regular T2W sequence,19 most radiologists agree
to obtain slices in three orthogonal imaging planes, that T2-FLAIR should be part of a standard MRI
which are then used to plan the diagnostic sequence brain protocol.1,15,20,29,92
image acquisition. The localizer should be repeated if • Transverse T2*W sequence:
the quality of initial images is considered insufficient for – According to one study, hemorrhagic intracranial
planning. lesions missed on other sequences are found in 6%
• Sagittal plane images. These are planned using the dor- of veterinary patients using this sequence.32
sal and transverse localizer images. The longitudinal – Additionally, the identification of susceptibil-
fissure separating the two cerebral hemispheres is used ity artifacts consistent with hemorrhage allows
as the guiding anatomic reference, and sagittal slices are a more specific diagnosis for intracranial lesions
acquired parallel to this landmark. Using an odd number compared with evaluation with SE sequences
of slices with the median slice exactly on midline ensures only.
acquisition of one perfect mid-sagittal image. • Transverse (+/- sagittal and dorsal) T1W images after
• Transverse plane images. These are planned using the contrast medium administration:
dorsal and sagittal images (localizer and/or initial sagit- – Post-contrast T2-FLAIR images may be used as
tal images) and are oriented perpendicular to the hard an alternative to conventional post-contrast T1W
palate. Slices should be acquired from rostral to the crib- SE images, although they do not appear to improve
riform plate to caudal to the foramen magnum. diagnostic performance when compared with the
• Dorsal plane images. These are planned using the sag- combined evaluation of the standard T2-FLAIR
ittal and transverse images (localizer and/or diagnostic pre-contrast and T1W post-contrast series.21,22
images) and are oriented parallel to the brainstem. Since T2-FLAIR pulse sequences are more prone
• The slice thickness and number of slices will depend to artifacts19 and take longer to acquire, regular
on the patient’s size. For most small animal patients a T1W SE post-contrast series may be preferred.
slice thickness of 3–4 mm is adequate. – Addition of fat saturation to the T1W post-
• To avoid asymmetry related to chemical shift artifacts, contrast series may improve characterization of
the frequency-encoding (FE) gradient should be applied meningeal enhancement76 and differentiation
in a dorsoventral/ventrodorsal direction on transverse between contrast-enhancing tissues and fat.77
images and in a rostrocaudal/caudorostral direction on • Additional sequences described above (PDW, STIR,
dorsal plane images. Similarly, to avoid motion artifact single shot techniques, 2D/3D volumetric GRE
from large pulsating vessels interfering with evaluation acquisitions, DWI, PWI, fMRI, MRS) may be added
of the brain, the phase-encoding (PE) gradient should be to the protocol depending on clinical suspicion and
applied in a laterolateral direction on transverse images initial findings on routine MRI sequences.
(see below).
• Images of a given patient should be acquired in at least in IMPORTANT MRI ARTIFACTS
two planes (sagittal and transverse). Dorsal plane images IN BRAIN IMAGING
should be added if further evaluation of extent of intra-
cranial lesions (e.g., for surgical or radiation therapy A detailed discussion of MRI artifacts can be found in
planning) or evaluation of adjacent regions (e.g., nasal Chapter 3. Some important artifacts frequently encoun-
cavity or orbit) is desired. tered when imaging the brain in small animals and possible
• Based on information provided in the human and veteri- remedies will briefly be discussed.
nary medical literature, the following sequences should
be included in a standard brain MRI protocol in veteri- Motion
nary patients (Fig. 4.1.9):1 • Motion artifacts are probably less common in veterinary
• Sagittal T2W sequence: than in human medicine as most patients are scanned
– Assess for intracranial mass effect and subtento- under general anesthesia.63,97,98 However, even if the
rial or foramen magnum herniation.1,93 animal does not move during the scan, physiologically
(a)
(b)
(c)
(d)
(e) (f)
Fig. 4.1.9 MRI study of the brain in a 7-year-old Boston Terrier with a large intra-axial forebrain mass (glioma, presumptive).
(a) The sagittal T2W image shows evidence of an ill-defined hyperintensity associated with the forebrain (asterisk) and
associated mass effect. There is displacement of the occipital lobes ventral to the osseous tentorium, foramen magnum
herniation of the cerebellum (arrow), and syringohydromyelia of the cranial cervical spinal cord (arrowhead). The nasopharynx
is fluid-filled, which is incidental. (b–f) The transverse images show a large intra-axial mass lesion associated with the left
frontal lobe, which is heterogeneously hyperintense on the T2W image (b), hypointense on the T1W image (c), remains
moderately hyperintense on the T2-FLAIR image (d), does not show evidence of significant susceptibility artifact on the T2*W
image (e), and shows heterogeneous, mostly peripheral, contrast enhancement on the T1W post-contrast image (f).
100 CHAPTER 4.1
(a) (b)
Fig. 4.1.10 Motion artifact encountered during brain MRI scan. (a) The initial sagittal T2W sequence was acquired with the
patient only lightly sedated due to poor condition. Marked motion artifact is evident as parallel alternating bands extending
dorsally and ventrally in the phase-encoding direction. (b) After induction of anesthesia a diagnostic quality scan was possible.
(a) (b)
Fig. 4.1.11 (a) Motion artifact from a pulsating vessel resulting in the impression of a focal contrast-enhancing lesion associated
with the right thalamus (arrow) on this T1W post-contrast image. (b) After switching of the phase- and frequency-encoding
gradients this ‘lesion’ is no longer identified.
moving structures (e.g., pulsating vessels) will still result techniques, and flipping PE and FE gradients (if motion
in artifacts. Motion artifacts always occur in the direc- artifact interferes with evaluation of area of interest;
tion in which the PE gradient was applied, regardless of Fig. 4.1.11).
the direction of motion. They manifest as ‘ghosts’ of the
moving structure at various locations along the PE axis, Cerebrospinal fluid flow artifacts
blurring, and/or parallel bands (Fig. 4.1.10). • A CSF flow void artifact appears as artificial loss of sig-
• Remedies include adequate restraint of the patient, nal from CSF, which is most commonly encountered on
breath-hold techniques (limited in most systems due T2W images (Fig. 4.1.12).97,99,100
to duration of scan and usually not needed for head/ • It is attributed to rapid or turbulent flow of CSF, where
brain studies), cardiac/respiratory gating, pre-saturation flowing protons move so quickly that they are not exposed
pulses, flow compensation techniques, motion correction to the initial 90° and the 180° refocusing RF pulses,
(a) (b)
Fig. 4.1.12 CSF flow void artifact in a dog with obstructive hydrocephalus secondary to meningoencephalitis. (a) On the
transverse T2W image there is a focal hypointensity associated with the mesencephalic aqueduct (arrow). (b) No corresponding
lesion is identified on the sagittal T2W image.
(a) (b)
Fig. 4.1.13 Susceptibility artifact due to presence of a metallic foreign body in the field of view. (a) On the transverse T1W
image, there is a focal distortion of the magnetic field with alternating areas of signal void and hyperintensity associated with
the right ventral aspect of the head. (b) A radiograph of the head reveals a metallic spring (arrow), which was found to be
embedded in the gums adjacent to the right mandibular ramus.
which are slice-selective. It may occasionally be seen in CSF flow when non-saturated spins enter the imag-
normal dogs, but it seems more common in small breed ing plane and generate a strong signal after applica-
dogs with increased ventricular size and syringomyelia. tion of the 90° pulse. CSF flow-associated artifacts
• As this artifact is more likely to occur with a thinner can easily be identified by comparison with other
slice and a longer TE, modification of imaging param- sequences and image planes, as they will not be con-
eters will decrease severity. However, a decrease in TE sistent findings.
will also result in an undesirable change in weighting and
may not be feasible. Susceptibility
• A similar artifact known as ‘entry slice phenome- • Magnetic susceptibility is a term used to describe the
non’ appears as an artificially high signal at a site of magnetic properties of a material.63,97,98,101
102 CHAPTER 4.1
(a) (b)
Fig. 4.1.14 Volume averaging observed during a brain MRI examination in an 11-year-old mixed breed dog. (a) On the
T2W transverse image there are several T2 hyperintense areas associated with the periphery of the cerebrum (arrowheads).
(b) These are not evident on the corresponding T2-FLAIR image, indicating that these were pseudolesions related to volume
averaging of widened cerebral sulci and adjacent brain parenchyma.
• Diamagnetic materials (e.g., soft tissues) have very low • This artifact can cause hyperintensities adjacent to fluid-
susceptibility and weaken a magnetic field. Paramagnetic filled structures (subarachnoid space, ventricles) on T2W
materials (e.g., gadolinium and certain hemoglobin deg- images, resulting from averaging of brain and CSF sig-
radation by-products) have a slightly stronger susceptibil- nal, and may be misinterpreted as parenchymal lesions
ity and focally enhance a magnetic field. Ferromagnetic (Fig. 4.1.14).
materials (e.g., iron) become strongly magnetized and • Remedies include decreasing slice thickness, verification
experience a large force when placed in an external mag- of lesions on additional planes, and verification of any T2
netic field. abnormality on T2-FLAIR images.
• Presence of materials with differing susceptibility in
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CHAPTER 4.2
OPTIMIZED TECHNIQUE: SPINE

106 Ruth Dennis
CONTENTS
Indications and contraindications.......................................................................................................................................................................... 107
High- versus low-field spinal MRI......................................................................................................................................................................... 107
Handling, restraint, and positioning ......................................................................................................................................................................108
Radiofrequency coil selection................................................................................................................................................................................ 110
Image planes ......................................................................................................................................................................................................... 111
Sagittal plane ................................................................................................................................................................................................... 111
Transverse plane .............................................................................................................................................................................................. 111
Dorsal plane .................................................................................................................................................................................................... 112
Oblique planes................................................................................................................................................................................................. 114
Field of view and slice thickness ........................................................................................................................................................................... 114
Pulse sequences ................................................................................................................................................................................................... 114
MRI protocols .................................................................................................................................................................................................. 114
Image weighting and sequence modifiers ........................................................................................................................................................ 115
Three-plane localizer (= scout images) ....................................................................................................................................................... 115
T2 weighting .............................................................................................................................................................................................. 115
T1 weighting .............................................................................................................................................................................................. 116
Combined T1/T2 weighting ........................................................................................................................................................................ 116
Contrast enhancement and subtraction ...................................................................................................................................................... 117
Fat suppression ......................................................................................................................................................................................... 118
Short tau inversion recovery ...................................................................................................................................................................... 119
Gradient echo sequences ...........................................................................................................................................................................120
Fluid-attenuated inversion recovery ...........................................................................................................................................................122
MR angiography .........................................................................................................................................................................................122
Diffusion-weighted and diffusion tensor imaging .......................................................................................................................................122
Sequences for CSF flow .............................................................................................................................................................................123
Intrathecal gadolinium administration ........................................................................................................................................................123
Artifacts .................................................................................................................................................................................................................123
Motion artifact .................................................................................................................................................................................................123
Partial volume averaging artifact ...................................................................................................................................................................... 124
Chemical shift artifact ...................................................................................................................................................................................... 124
Susceptibility artifact ....................................................................................................................................................................................... 124
Truncation (Gibbs artifact) ............................................................................................................................................................................... 124
Signal changes at injection sites......................................................................................................................................................................125
General principles of spinal MRI interpretation .....................................................................................................................................................126
References............................................................................................................................................................................................................. 127
O p t i m i z e d Te c h n iqu e : Spi n e 107
Magnetic resonance imaging (MRI) is now considered to risk of false-positive diagnoses, such as subclinical disc
be the ‘gold standard’ for most aspects of spinal imaging in lesions, especially at the lumbosacral junction. False-
people and in veterinary patients, both because of the tis- negative diagnoses may also arise due either to lack of
sue information that it yields and its safety compared with MRI changes with certain diseases (e.g., degenerative
radiographic or computed tomography (CT) myelography. myelopathy or mild inflammation) or inadequate tech-
Because of its inherently high tissue contrast, it gives nique or interpretation. MR scans should, therefore,
excellent depiction of the spinal cord parenchyma and always be considered in the light of the clinical findings
so shows lesions even when there are no size changes due and other ancillary tests.
to swelling or compression, which would result in false- • Conditions that may mimic spinal signs must be excluded;
negative findings on myelography. these include metabolic, neuromuscular, peripheral ner-
Cerebrospinal fluid (CSF) and epidural fat surround- vous system, intracranial, and orthopedic diseases.
ing the spinal cord are visible and internal vertebral venous • Indications for spinal MRI include the following:
structures and ligaments can be seen. Although fine bone • Spinal or paraspinal pain.
detail is less well demonstrated than with CT, both the out- • Spinal deformity.
line and internal architecture of the vertebrae are clearly • Mono-/para-/hemi- or tetraparesis or -plegia.
seen by using a combination of different pulse sequences. • Spinal ataxia.
The intervertebral discs are clearly visible, and pathology of • Spinal masses, swellings, and sinus tracts.
discs can be seen directly rather than being inferred from • Surgical planning (e.g., vertebral body and canal
changes in disc space width or myelographic abnormalities. measurements).1
Conditions that cannot be diagnosed using myelography • Weakness or collapsing episodes, which may be
but which may give rise to spinal clinical signs (e.g., nerve attributable to spinal disease.
root pathology, foraminal disc extrusions, and paraspinal • Screening for disease (e.g., syringomyelia secondary
soft tissue inflammation) are well demonstrated and the full to Chiari-like malformation).
extent of lesions that involve both the spine and surround- • Contraindications for spinal MRI are few, but include
ing tissues is shown. the presence of metal in close proximity to the area to be
MRI is therefore invaluable not only for diagnosis of scanned; this will lead to distortion of the image or signal
spinal disorders but also for treatment planning, prognosis, drop-out as a result of susceptibility artifact:
and monitoring response to treatment. • Microchips occasionally cause a problem when scan-
It should also be noted that although certain conditions, ning the cervicothoracic area of cats or small dogs and
such as degenerative myelopathy, do not give rise to changes may need to be removed before diagnostic scans can
on MRI, normal images are valuable to rule out other pos- be obtained, although microchips themselves are not
sible diagnoses. affected by the magnetic field and the chip number is
Good MRI technique is vital in order to avoid the pro- not erased.
duction of non-diagnostic or even misleading images. The • Previous surgery within the field of view (FOV) may
possibility of imaging in multiple planes and using many compromise MRI due to the presence of metallic
different pulse sequences means that judicious selection of implants or fragments of metallic material from
the most appropriate combinations is required in order to drill bits. However, the area of distortion is usually
gain maximum diagnostic information within a reasonable localized and even total hip replacements in larger
scanning time. dogs do not usually interfere with lumbosacral
This chapter aims to show how spinal MRI technique scanning.
in small animals can be optimized by addressing technical • The presence of surgical implants outside the FOV is
issues including patient positioning, selection of the most not usually problematic since these are normally made
appropriate radiofrequency (RF) coil, image planes, and of non-ferrous materials and will not be affected by
pulse sequences, and recognition and reduction of artifacts. the magnetic field.
The importance of technique is demonstrated using images
of a wide range of spinal conditions and the approach to HIGH- VERSUS LOW-FIELD SPINAL MRI
interpretation of spinal images is considered.
• The information presented herein is based on the author’s
INDICATIONS AND CONTRAINDICATIONS experience with a 1.5 Tesla MR system (Signa Echospeed,
General Electric Medical Systems, Milwaukee, WI) and
• It is vital that a complete and precise clinical examina- some aspects related to equipment and choice of pulse
tion is performed prior to MRI, with accurate neuro- sequence vary between high- and low-field systems and
localization of the probable cause of the clinical signs. even between different manufacturers.
MRI should not be abused as a global spinal screen- • Specific aspects of low-field spinal MRI are covered in
ing tool; this is dangerous because of the significant Chapter 4.4.
108 CHAPTER 4.2
• Scanning of the spine is often challenging with low- tissues)3 and CT valuable for showing subtle, non-dis-
field systems, especially in large dogs where long areas placed fractures.
of the spine must be examined. Low-field magnets have • Reference has been made above to the risk of hypother-
a relatively small FOV capability, which often necessi- mia with long scans; MRI suites out of necessity must be
tates repeated repositioning of patients in order to cover kept at a fairly cool temperature, therefore keeping small
the area of interest. This makes it difficult to identify patients warm with bubble wrap, fleeces, and custom-
individual vertebrae in certain parts of the spine, and made jackets and leg warmers is important (Fig. 4.2.1).
also results in extremely long scanning times, potentially • Many dogs and cats are scanned in dorsal recumbency,
exacerbating hypothermia in susceptible patients. especially when surface spinal coils are used, and this has
• Increasing the FOV, slice thickness, and number of acqui- the advantage of reducing the effect of spinal motion due
sitions will increase the inherently poor signal-to-noise to breathing. Very large or narrow dogs may sometimes be
ratio (SNR) but the first two reduce image resolution and more easily scanned in lateral recumbency if they are dif-
the last contributes to long scan time.2 Therefore, if only ficult to restrain in dorsal recumbency or if their large size
low-field MRI is available, consideration could be given prevents them from entering the bore of the scanner when
to performing prior myelography in order to localize the supine. Regardless of positioning, it is essential that the
lesion before performing targeted MRI. patient is stable and will not tilt or move during the scan,
and this is achieved using positioning aids such as sandbags,
HANDLING, RESTRAINT, AND POSITIONING foam wedges, tape, and Velcro bands (Fig. 4.2.2).
• The spine must be as straight as possible in the sagittal
• Most dogs and cats are scanned under general anesthesia, plane and if initial localizer images show that this is not
although heavy sedation is used in some centers for brief the case, repositioning should be attempted. Some ani-
procedures such as syringomyelia screening. mals, such as dogs with syringomyelia, muscle spasm, or
• Great care should be taken in handling patients suspected congenital spinal anomalies such as hemivertebrae, may
of having spinal instability, especially after induction of have genuine scoliosis and inability to obtain sagittal
anesthesia when protective muscle spasm is reduced. In images of reasonable lengths of the spine hampers inter-
these animals, plastic or wooden splints should be used pretation. Gentle traction of the neck and restraint of the
and consideration given to the safest position of the head using medical tape may help in such cases.
animal on the table. Prior radiographic screening for • If the animal may be in some discomfort in the position
fractures or (sub) luxations is recommended. In the first adopted for MRI, for example in cases of lumbosacral
instance, suboptimal positioning for initial MRI may disease or hip arthritis, use of analgesics as part of the
have to be accepted, with further adjustments made if anesthetic protocol is recommended to prevent move-
initial scans suggest that the spine is not unstable. ment or tachypnea during the scan or worsening of pain-
• For trauma cases, MRI and CT are complementary, ful signs on recovery. In such cases, it is also beneficial to
with MRI giving much more information about any support the pelvic limbs with sandbags or foam wedges
soft tissue pathology (spinal cord and paraspinal soft to reduce the strain on the hips.
Fig. 4.2.1 A small dog, prepared for spinal scanning, wearing Fig. 4.2.2 A dog positioned in dorsal recumbency on a
a custom-made woolen body warmer and leggings. Bubble- dedicated spinal coil. Long sandbags are placed along either
wrap and fleeces are also useful. Keeping small patients warm side of the dog’s thorax to help keep it upright and stable.
is especially important if the general anesthesia is likely to be
prolonged by spinal surgery.
• Positional maneuvers may be used during MRI to dem- • Lumbosacral flexion:

onstrate dynamic lesions or to reproduce a more natural – The supine position has the effect of placing the
spinal posture. Some examples are as follows: lumbosacral junction in extension, in effect creating
• Occipitoatlantal flexion: the position that often results in increased discom-
– Positioning in dorsal recumbency usually results fort during clinical examination due to increased
in extension of the occipitoatlantoaxial area, which compression of the cauda equina. This means that
can both reduce and exacerbate various conditions. any compression seen on MRI represents a ‘worst-
– It can reduce or even mask cerebellar herniation case scenario’ and it is therefore unlikely that cauda
in Chiari-like malformation,4,5 and sagittal images equina compression will be missed. It may, how-
with the occipitoatlantal area flexed into a more nat- ever, exaggerate the appearance of a compressive
ural position are recommended for the investiga- lesion compared with a normal physiologic posture.
tion of this condition. This is especially important – A flexed sagittal scan may be obtained by pull-
if cisternal CSF sampling is planned, as it will allow ing the pelvic limbs cranially and restraining
assessment of the risk of the procedure. Gentle flex- them with a band placed over the animal’s body.
ion of the occipitoatlantal area may be achieved by This technique is valuable when planning certain
using small foam wedges to achieve a more natural types of lumbosacral surgery (Fig. 4.2.4). The
angle of approximately 135° between the head and fact that most dogs undergo lumbosacral MRI in
neck (Fig. 4.2.3). Care should be taken with this moderate extension (which worsens a compressive
maneuver if atlantoaxial subluxation is a possibility,
although diagnosis of this condition is usually pos-
sible even in extension by recognizing areas of cord
pathology above the dens.
– Conversely, the hyperextended position will exac-
erbate or even create occipitoatlantal overlap and
it is important not to overdiagnose this condition
based on extended images that are not equivalent
to normal posture. Cord compression at C1-C2
due to dorsal atlantoaxial bands, seen especially
in Cavalier King Charles Spaniels, is also more
prominent in extension.6
(a)
Fig. 4.2.3 A Cavalier King Charles Spaniel positioned for a

(b)
gently-flexed sagittal scan of the occipitoatlantal area, which
is a useful technique for assessing the degree of cerebellar Fig. 4.2.4 Sagittal T2W lumbosacral area images in a
herniation in cases of Chiari-like malformation. The patient Rhodesian Ridgeback with degenerative lumbosacral disease.
is in dorsal recumbency and pads are placed on top of the (a) Slightly extended, with the dog in a normal supine
calvarium to maintain an upright position to the nose, thereby position, showing mild impingement of the cauda equina
creating mild ventroflexion of the head in relation to the long (arrow). (b) Flexed position, which has resulted in reduced
axis of the neck. cauda equina compression. (1.5T MRI system)
110 CHAPTER 4.2
lesion) whereas surgery from the dorsal approach in the degree of compression. Nevertheless, caution
is performed with the lumbosacral spine in flexion is recommended if stressed views, which potentially
(which alleviates it) probably contributes to disap- increase neural compression, are used, with scan
pointing correlation between MRI and surgical times being kept to a minimum.
findings.7
• Cervical traction. Traction using weights may be RADIOFREQUENCY COIL SELECTION
applied to the neck in cases of disc protrusions asso-
ciated with cervical spondylomyelopathy, with the • Types and nomenclature of RF coils vary between manu-
dog in either dorsal or lateral recumbency.8,9 It is facturers and between human and dedicated veterinary
recommended that not more than 20%–25% of the systems.
patient’s body weight is used (e.g., approximately 9 kg • For spinal MRI, phased-array spinal coils are used most
for Doberman Pinschers) as, experimentally, exces- often and are ideal for medium- and large-sized dogs
sive distraction can cause spinal cord damage due (Fig. 4.2.6). These coils consist of multiple adjacent
to ischemia and disruption of interstitial spinal cord transmit/receive coils each of which processes signal
pressure.8 The weight may be applied using either a from its own small FOV before the information is com-
soft tie around the premaxilla behind the canine teeth bined to form a single, longer FOV with reduced overall
or a special collar and plastic straps (Fig. 4.2.5). noise. The best images are acquired when the longitudi-
• Kinematic cervical positioning for evaluation of nal FOV is matched to the length of RF coil segments
disc-associated cervical spondylomyelopathy: that are activated. With surface coils the signal intensity
– One study concerning cervical spondylomyelopa- falls off with increasing distance from the coil, therefore
thy in nine Doberman Pinschers used an MRI- the spine should be as close as possible to the coil and the
compatible positioning device (see Fig. 7.2.15), animal is usually scanned supine, in the same position as
and sagittal and transverse T2W images were a human patient. The animal should lie directly on the
acquired with the spine in neutral, extended, coil rather than being supported in a trough since even
flexed, and traction positions.10 a small gap between coil surface and patient will reduce
– Flexion was associated with improvement or the image quality. Signal drop-off can be a problem with
resolution of spinal cord compression in 4/9 the cervicothoracic junction in larger dogs as the area of
patients, whereas extension caused worsening of interest is some distance from the coil, and in such dogs,
compression in 6/9 patients as well as identifying consideration should be given to scanning them in lateral
compressive lesions not seen in other positions. recumbency if they are narrower from side-to-side than
– Although it was previously assumed that positioning dorsoventrally. Signal drop-off can be compensated for
affected dogs such that compressive lesions might using imaging options such as surface coil intensity cor-
worsen for the length of time required for MRI, in rection (e.g., SCIC in General Electric machines), which
fact none of these dogs suffered subsequent neuro- acts in a similar way to depth-gain compensation in ultra-
logic deterioration. The authors postulated that sonography to even out the signal intensity with distance
worsening of neurologic signs following stress radio- from the coil. Phased-array torso coils are an alternative
graphic myelography is due to the presence of the option for dogs that must be scanned in lateral recum-
subarachnoid contrast medium rather than changes bency, such as giant breeds that may not otherwise fit
9kg
Fig. 4.2.5 Diagram of one technique for traction

of the cervical spine in the investigation of cervical
spondylomyelopathy. A soft tie has been placed around the
maxillary canine teeth and muzzle, to which is attached an Fig. 4.2.6 Dedicated phased-array spinal coil, designed for
appropriate weight. Special collars with straps can also be people but ideal for scanning medium- and large-sized dogs in
used. dorsal recumbency.
in the magnet. Some manufacturers of dedicated veteri-

nary MRI scanners offer spinal phased-array coils that
are V-shaped and fit in a V-shaped patient cradle, which
are more adapted to the conformation of that anatomic
region in dogs and cats. They may provide better signal
compared with the flat human spine coils.
• Extremity coils consisting of two curved surface coils,
which clip together to form a cylindrical structure, are
eminently suitable for scanning the spines of cats and
small dogs. Quadrature coils, such as those designed for
human heads, give rise to more respiratory and cardiac
motion artifact when the thoracic and lumbar spine is
scanned, although such coils may be acceptable for cervi-
cal and lumbosacral spine scanning where moving areas Fig. 4.2.7 Foraminal disc extrusion at L5-6 in a Miniature
are not included in the FOV. If a quadrature coil is used, Short-haired Dachshund with right pelvic limb lameness.
the patient should fill the coil reasonably well; very small This right-sided parasagittal T2W image shows normal
patients in large diameter coils give rise to poor images. intervertebral foramina at other sites, containing
• A further consideration is the length of spine that can hyperintense fat. At the affected disc space, there is loss of
be scanned without moving the patient relative to the the foraminal fat signal due to the presence of hypointense
coil. RF coils with some low-field scanners may only material (arrow). Residual disc space material is mineralized.
allow short areas of the spine to be scanned at any one This lesion was not visible in the midline sagittal image.
time, which creates problems with duration of scan- (1.5T MRI system)
ning and identification of individual vertebrae relative to
landmarks. In such cases a more pragmatic approach for • Positional scans (traction, flexion etc.) are usually
larger dogs may be to perform a screening myelogram obtained in the sagittal plane.
in order to locate the lesion, and then to characterize it • The number of slices should be sufficient to include both
using MRI, although this negates some of the benefits of sides of the spine and parasagittal images must be exam-
using MRI. Fortunately, spine surface coils designed for ined carefully for lateralized lesions affecting the inter-
high-field scanners and human MRI are relatively long vertebral foramina, such as lateralized disc extrusions
and allow larger areas of the spine to be imaged without (Fig. 4.2.7). Careful slice placement such that parasagit-
moving the patient. Even with these scanners, however, tal images on the right and left sides are identical aids
very large dogs may need to be moved part way through this. Reliance on examination of only midline sagittal
the study (e.g., rotating from head first to tail first) if the images means that many lateralized lesions will be over-
whole spine needs to be imaged when multiple lesions are looked. However, good sagittal scans may be impossible
suspected. to acquire in dogs with mechanical scoliosis due to the
presence of malformations such as hemivertebrae.
IMAGE PLANES
Transverse plane
It is essential to obtain images in at least two planes oth- • Transverse images are usually acquired after sagit-
erwise small lesions may be overlooked. When a lesion is tal images, in order to obtain more information about
identified the use of all three planes, sagittal, transverse, and a lesion in the orthogonal plane. It is more accurate to
dorsal, is often helpful in order to provide the maximum set up the transverse scan on a definitive sagittal image
amount of information about the pathology. rather than on a localizer image.
• In some cases, transverse images may show changes that
Sagittal plane are not evident on the sagittal scan, for example lateral
• The sagittal plane will always be part of a spinal scan as cervical stenosis. Therefore, absence of findings on sag-
it provides a good overview of the area of interest. It is ittal images should not prevent the use of the transverse
also the plane that is easiest to relate to radiography when plane.
both imaging techniques are used. • Opinions differ as to placement of transverse images rel-
• Comparison between adjacent disc spaces and vertebrae ative to the vertebral canal in the cervical area, where the
is easy and landmarks such as vertebrae C1, C2, and disc spaces lie obliquely relative to the axis of the spine.
T1 and the lumbosacral junction are readily identified, Some workers recommend aligning transverse images
although determination of the conformation of ribs at parallel to the cervical disc spaces and thus oblique to the
the thoracolumbar junction prior to spinal surgery is vertebral canal. However, since the information required
difficult. usually relates to the presence and degree of spinal cord
112 CHAPTER 4.2
compression (or swelling) relative to the vertebral canal’s incorrectly localized, and recommended that transverse
cross section at a given point, it seems more logical to images through the whole segment of interest were also
place the slices perpendicular to the vertebral canal. acquired.12
Nevertheless, in practice little difference is seen between • Obtaining transverse scans along a large section of the
the two techniques. At the lumbosacral junction, angling spine is time-consuming and may not be practical with
of the transverse plane means that images will simulta- low-field systems when imaging acquisition times are
neously be both parallel to the disc space and perpen- inherently longer. However, if other pathology is pres-
dicular to the vertebral canal (Fig. 4.2.8). ent (e.g., dispersed epidural disc material or hemorrhage,
• When no obvious lesion is detected on sagittal images, diffuse cord parenchymal changes), the area covered
it is often customary to obtain transverse images only at must be extended to include normal spine both cranial
the disc spaces rather than throughout the whole area of and caudal to the abnormal area in order to depict its
interest, using small groups of slices or even single slices full extent. In dogs with cervical spondylomyelopathy all
at each disc space (Fig. 4.2.9). This is essential in the disc spaces should be examined in the transverse plane,
cervical area, when foraminal disc extrusions may easily as vertebral canal stenosis is often present at multiple
be overlooked on the other planes.11 One study showed sites but may be overlooked on sagittal and dorsal planes.
that using only sagittal T2W images for determining Breeds predisposed to cervical spondylomyelopathy may
the location of compressive disc herniations in the tho- also suffer from cranial thoracic stenosis, so acquisition
racolumbar spine resulted in 5%–10% of lesions being of transverse images as far caudally as T5 should also be
included13 as the two conditions can co-exist.
Dorsal plane
• The dorsal plane is greatly underused in veterinary MRI
and indeed is often omitted.
• However, in this author’s experience, it has many advan-
tages and is usually the first plane to be acquired:
• It gives a more detailed image than a localizer on
which to place accurate sagittal images.
• It allows the two sides of the spine to be compared for
symmetry.
• It allows identification of ribs at the thoracolumbar
junction prior to spinal surgery in this area. (Note:
careful examination may be required to identify T13
ribs, especially if they are vestigial [Fig. 4.2.10]).
• It gives the clearest image of transitional vertebrae or
lateral subluxation (Fig. 4.2.11).
• It demonstrates lateralized lesions and often gives the
most accurate depiction of their craniocaudal extent
Fig. 4.2.8 Orientation of transverse MR images at the (Fig. 4.2.12).
lumbosacral junction, so that they are perpendicular to the • The widening of the subarachnoid space cranial and
dural sac. caudal to intradural lesions that are lateralized (‘golf
tee sign’) is easier to see in that plane, facilitating their
classification as ‘intradural’.
• In the cauda equina region it gives the best image of
spinal nerves and intervertebral foramina (Fig. 4.2.13).
• It is valuable for determining the boundaries of tumors
in paraspinal tissue and for evaluation of paravertebral
muscle atrophy.14
• It is ideal for an overview of the soft tissues, especially
using STIR sequences (Fig. 4.2.14).
• The dorsal plane is of most value where the section of spine
imaged is level within the plane (i.e., the lumbar, thoracic,
Fig. 4.2.9 The use of single transverse slices or small groups and mid-cervical areas). Where the spine curves, at the
of slices as a screening technique for all disc spaces within a occipitoatlantal, cervicothoracic, and thoracolumbar junc-
clinical area of interest. This is a helpful technique when no tions, it is less helpful, although if obtained with thicker than
lesions have been identified on the dorsal or sagittal plane. normal slices, it can still be used as an accurate localizer.
Fig. 4.2.10 Dorsal T2W image of the lumbar area in a Fig. 4.2.11 Dorsal T2W image of a DSH cat with paraplegia
Staffordshire Bull Terrier, showing identification of an following trauma. The degree of L2-L3 subluxation in the
asymmetrical transitional vertebra at the thoracolumbar dorsal plane is clearly shown (arrow) and there is an excellent
junction (arrow), which has only a right rib but no left rib. overview of the associated soft tissue trauma forming patchy
Identification of such anomalies is important if spinal surgery hyperintense areas in the paraspinal muscles. (1.5T MRI
is to be performed in this area. (1.5T MRI system) system)
Fig. 4.2.12 Dorsal T2W image of the lumbar area in a Fig. 4.2.13 Dorsal plane image of the lumbar spine providing
paraparetic Great Dane with a lateralized L3-L4 disc clear visualization of lumbar spinal nerves L6 and L7 (arrows)
extrusion. The severity, extent, and extradural location of the as they exit the vertebral canal through the intervertebral
compressive tissue are clearly depicted. (1.5T MRI system) foramina. (1.5T MRI system)
114 CHAPTER 4.2
• Large breed dogs in general are more likely to suffer disc

herniation in the T1-T9 segment compared with small
breeds,16 and German Shepherd Dogs have been shown to
have an increased incidence of cord compression due to
cranial thoracic disc herniation (especially at T2-T3) than
other large breeds. It is therefore recommended that this
area is included in studies of German Shepherd Dogs with
T3-L3 myelopathy,17,18 even when lesions have already
been found around the thoracolumbar area.
• Likewise, pain in the lumbosacral area may be due to spi-
nal disease at the base of the tail such as disc extrusion or
discospondylitis in the sacrocaudal area,19,20 and so this
area must be examined also in such cases.
• The FOV selected depends on several factors includ-
ing the size of the patient, the type of coil used, and the
nature of the study. Larger FOVs give better SNR but
poorer resolution than do smaller FOVs, and very large
FOVs should therefore not be used as a time-saving solu-
tion. When an excessively large FOV is used for sagittal
images it may be difficult to position the spine sufficiently
straight for the whole area of interest to be visible in a sin-
gle image. Generally, sagittal images covering a cranio-
caudal spinal length of no more than 20–30 cm in medium
and large sized dogs are recommended. In the transverse
Fig. 4.2.14 Dorsal STIR image in an English Springer Spaniel plane, only the spine and immediately surrounding soft
with spinal pain, pelvic limb ataxia, and pyrexia. Extensive tissues should be included on the FOV unless a larger
paralumbar soft tissue pathology is seen, centered around area, such as the brachial plexus, is under investigation.21
the L3-L4 disc space on the right side. The L3-L4 disc space Where paraspinal soft tissues may be abnormal a larger
is slightly narrowed (dashed arrow) and the vertebral bodies FOV dorsal plane STIR image series is helpful.
of the adjacent vertebrae show subtle hyperintensity (solid • Slice thickness is also a compromise between SNR and
arrow). The final diagnosis was spondylitis due to a migrating resolution. For most spinal imaging, a 2–4 mm slice
grass awn, with associated focal myositis. Dorsal plane images thickness is used, depending on the size of the patient,
often give the best overview of the extent and location of such the area to be covered, and the nature of the lesion.
lesions. (1.5T MRI system) Often, initial scans may be of larger FOV and slice thick-
ness, with smaller values being used to give more precise
Oblique planes information once a lesion has been identified.
• Oblique planes are rarely required in spinal MRI, • It is recommended that a consistent approach to slice
although they might be used to follow the course of a placement be adopted, for ease of interpretation and to
peripheral nerve lesion or to demonstrate a comminuted avoid confusion if no localizer image is available. It is rec-
fracture. However, in such cases reconstruction of 3D ommended that a stack of transverse images is placed to
images is likely to be more rewarding. run from cranial (first slice) to caudal (last slice), sagittal
• At the lumbosacral junction, the use of a dorsal oblique images are placed from right to left, and dorsal images
plane to follow spinal nerves exiting the spine has been from dorsal to ventral.
advocated, and oblique parasagittal images obtained per-
pendicular to the course of the intervertebral foramina PULSE SEQUENCES
rather than vertically have been shown to demonstrate a
smaller and presumably more accurate depiction of the MRI protocols
foraminal size.15 • Many pulse sequences are available, which differ between
high- and low-field MR scanners and which are often,
FIELD OF VIEW AND SLICE THICKNESS confusingly, given different names by the various manu-
facturers (see Chapter 2).
• It is essential that the entire area of possible neuro- • Low-field systems place more emphasis on gradient
localization based on the clinical examination is included echo rather than spin echo pulse sequences. Three-
in the scan; for example, with T3-L3 myelopathies the dimensional datasets are often acquired for subsequent
study should extend to the cranial thoracic spine. reconstruction in other planes, which reduces the
otherwise longer scanning times. However, gradient the first definitive scan is running, especially if multiple
echo sequences are often of lower contrast and are more images in each plane are produced.
prone to susceptibility artifacts than spin echo sequences. • Since localizers are gradient echo pulse sequences, they
• General principles with reference to spinal MRI only show bone with very low signal and osteolytic neoplasia
are described here, and the reader is again referred to is often clear (Fig. 4.2.15). Occasionally, paraspinal soft
Chapter 4.4 on low-field MRI for further information tissue masses involving the thorax or abdomen as well as
about pulse sequences relating to these systems. the spine, or occult abdominal masses such as splenic or
• Some MR facilities work with set protocols (a group of adrenal tumors, may be seen (Fig. 4.2.15).
MRI pulse sequences selected for specific body parts and
medical indications), which has the advantage that the T2 weighting
scans can be run by technicians. Set protocols must be • With high-field systems, the T2W turbo/fast spin echo
devised to give as much information as possible in order pulse sequence is the ‘workhorse’ sequence, and is often
that potential lesions may be identified on subsequent all that is required for diagnosis of intervertebral disc
interpretation. An alternative approach is for the scan to disease and ischemic myelopathy.
be run under the supervision of a radiologist (or other • Fast (turbo) spin echo sequences are said to give better
interpreter) using a flexible and interactive approach image quality in shorter acquisition times than conven-
in which the protocol is tailored to the findings as the tional spin echo T2W sequences.22 Images are of high
scan progresses. This approach is especially helpful for contrast, with hydrated disc nuclei, CSF, epidural fat,
the spine, in which MRI can be very challenging since and most pathologic processes appearing hyperintense
often large areas must be examined and many combina- due to high hydration (Fig. 4.2.16).
tions of pulse sequence, scan plane, and slice thickness/
orientation are possible. It must be appreciated that the
scan time should not be unnecessarily long, especially if
spinal surgery is to follow under the same anesthesia or
if the patient is small and may suffer hypothermia. For
example, acute disc extrusions in small dogs often only
require T2W images in two or three planes to make a
correct diagnosis and plan surgery, and with a high-field
scanner these can be acquired in under 15 minutes.
• In the author’s clinic, the usual approach to the spine is
as follows: (a)
• Dorsal T2W series, both for its significant diagnostic
value and to use as a localizer for accurate placement
of sagittal slices.
• Sagittal T2W series.
• Transverse T2W series over any areas of abnormality.
• Transverse T2W may also be performed at every
other disc space throughout the area of clinical suspi-
cion as a screen for otherwise occult changes (e.g., in
cases of cervical spondylomyelopathy).
• +/− pre- and post-contrast T1W series (the latter *
usually with fat suppression) and/or T1W or T2*W
gradient echo series depending on the nature of any
lesion identified, in planes as required for diagnosis
and based on the value of the various planes already (b)
performed using T2W series. Fig. 4.2.15 (a) Sagittal gradient echo image from the
• If the patient shows non-specific back pain and no 3-plane localizer in a paraplegic Rottweiler. There is marked
spinal lesion is seen, dorsal STIR images are obtained increased signal of the body of T12 indicative of loss of bone
as the best means of demonstrating paraspinal soft mineral substance and replacement with soft tissue (arrow);
tissue pathology. this was due to an aggressive bone tumor. (1.5T MRI system)
(b) Sagittal gradient echo image from the 3-plane localizer in
Image weighting and sequence modifiers a paraplegic standard Wire-haired Dachshund. An incidental
Three-plane localizer (= scout images) splenic mass is seen (asterisk). The spleen was removed and
• The localizer should not only be used for slice place- was found to be benign. The cause of the clinical signs was a
ment but should also be examined for large lesions while disc extrusion. (1.5T MRI system)
116 CHAPTER 4.2
Fig. 4.2.16 Diffuse cervical spinal cord swelling and Fig. 4.2.17 ‘T2W-myelogram’ with a large field of view
parenchymal T2W hyperintensity in a DSH cat with showing a degenerate disc and protrusion at C6-C7 (arrow) in
tetraparesis. Although non-specific, the extent of pathology an ataxic Dogue de Bordeaux. These sequences can be used as
is clearly seen due to the high contrast of T2W images. On a fast overview of the spine for detection of lesions, although
T1W images, no signal changes were seen and the lesion did image resolution is usually poor. (1.5T MRI system)
not contrast enhance. The histopathologic diagnosis was
astrocytoma. (1.5T MRI system)
‘T2-myelogram’ (Fig. 4.2.17). However, SNR and
image definition are poor, and once a lesion is identi-
• Changes in the location and width of the subarachnoid fied, it must be imaged further using other sequences to
space are readily detected against the adjacent lower sig- delineate changes more clearly and to provide anatomic
nal of the spinal cord and vertebrae, demonstrating cord landmarks. Unfortunately, T2W images are poorer
swelling and extramedullary spinal cord compression, with low-field systems, being of poor resolution and
and T2W scans have been found to give more precise taking longer to acquire, and more reliance is placed on
information about the severity and extent of extruded alternative sequences with these scanners.
disc material compared with T1W and STIR images.23
• Differentiation between extradural and extramedullary– T1 weighting
intradural lesions may be challenging, although acqui- • T1W images give excellent depiction of anatomy,
sition of images in both dorsal and sagittal planes may although with lower contrast than T2W.
show widening or splitting of the subarachnoid space in • T1W contrast is, however, inherently higher with low-
an analogous way to myelography. field than with high-field systems, which explains the
• Within the cord parenchyma, T2W hyperintensity greater reliance on T1W images with the former.
denotes pathologic areas of increased water content • In T1W images, CSF is hypointense and of similar
including edema, myelitis, gliosis, myelomalacia, demye- signal intensity to the cord, but epidural fat remains
lination, necrosis, and syringomyelia as well as neoplasia hyperintense and thus comparison of T1W and T2W
and hemorrhage at certain stages of evolution;24 often, images allows CSF and fat to be distinguished. Bony
T1W images of the same area will be unremarkable. The detail is good and disc space width and vertebral body
presence and extent of spinal cord T2 hyperintensity has sclerosis are more accurately assessed than with T2W
been shown to be a prognostic factor in dogs with com- (Fig. 4.2.18). However, spinal cord changes are only
pressive disc extrusions,25 acute non-compressive disc detected when severe; for example, with the overt fluid
extrusions,26 and ischemic myelopathy.27 pockets of syringomyelia.
• Ultrafast, heavily T2W pulse sequences (e.g., HASTE • T1W images are routinely used for syringomyelia
on Siemens, SSFSE on General Electric) are favored by screening with low-field systems due to their increased
some users. These sequences are excellent for evaluation definition compared with T2W with these systems.
of the subarachnoid space. Conventional T2W images
do not clearly differentiate fat and CSF well, whereas Combined T1/T2 weighting
these show CSF with very hyperintense signal while • Balanced, steady-state free precession, gradient echo
suppressing the background signal, including that of pulse sequences (see Chapter 2), in which contrast
the fat. The combination of rapidity of these sequences depends on the ratio between T2 and T1, are especially
and conspicuity of CSF renders them ideal for provid- popular with low-field scanners, for which they give
ing an overview of large sections of the spine in order higher SNR than spin echo sequences.
to demonstrate changes in the subarachnoid space, • Image contrast depends on the relation of T1 to T2
such as sites of cord compression, intradural pathology, and fluids are seen with hyperintense signal.29 These
and arachnoid diverticula, 2,14,28 giving rise to the term sequences provide high SNR and high resolution and
Fig. 4.2.18 Sagittal T1W image of the cervical spine in a

Bearded Collie with cervical pain. Mild vertebral endplate
signal reduction on either side of a subtly narrowed C5-C6
disc space is seen (arrow). (1.5T MRI system)
are good at demonstrating anatomy and free fluid such

as that around spinal nerves. They are therefore useful
for spinal MRI.
• Acronyms include BASG (Hitachi), FIESTA (General Fig. 4.2.19 Transverse, contrast-enhanced T1W image with
Electric), true FISP (Siemens), and HYCE (Esaote). fat suppression demonstrating clearly the extent of a spinal
nerve root mass (arrow). The margins of the mass were less
Contrast enhancement and subtraction clear on T2W images due to adjacent spinal cord edema.
• Generally, structural lesions (i.e., those producing a (1.5T MRI system)
change in volume or anatomy of tissues) will be identified
on T2W images, and therefore pre- and post-contrast barrier due to severe pathology, as well as neovasculariza-
T1W images are unlikely to demonstrate lesions that tion. Its main value lies in delineation of the extent of neo-
have been overlooked on T2W. plasia, being superior to other sequences for definition of
• However, contrast-enhanced T1W images have several tumor volume (Fig. 4.2.19).14 Other types of spinal cord
benefits: pathology such as myelitis show contrast enhancement
• Outlining mass lesions more precisely by distinguish- much less commonly, and when present this indicates
ing vascularized tissue from surrounding edema. a relatively severe lesion. Subtle contrast enhancement
• Demonstrating meningeal inflammation. may only be evident on subtraction images.
• Delineating extruded disc material when this is hard • Outside the spinal cord, contrast enhancement reflects
to differentiate from the spinal cord. increased vascularity of lesions affecting the menin-
• These features are especially well appreciated when fat ges and subarachnoid space, disc spaces, vertebrae, and
suppression is also applied, as epidural and vertebral paraspinal soft tissues. Examples include meningitis,
body fat signal is reduced.30 In the absence of the ability extramedullary intradural and extradural masses, inflam-
to apply fat suppression (low-field systems or the pres- matory components of discospondylitis and paraspinal
ence of a microchip, which interferes with fat suppres- inflammation, abscesses, and sinus tracts.31,32 Areas of
sion), subtraction (post-contrast images – pre-contrast non-enhancement indicate avascular areas such as calci-
images) can be used as an alternative. fied or recently extruded disc material, spinal empyema,
• In addition, as mentioned above, comparison of corre- paraspinal fluid accumulations and foreign bodies.33
sponding T1W and T2W images is often helpful in dif- Again, fat suppression or subtraction may be helpful,
ferentiating fat and CSF. Loss of hyperintense fat signal especially for areas of contrast enhancement within or
on transverse T1W images is clear evidence of verte- close to fat, such as radiculitis or panniculitis. However,
bral canal stenosis and, similarly, reduction in fat signal it must be remembered that contrast enhancement is a
within intervertebral foramina on transverse and para- non-specific finding, and it may also occur around disc
sagittal T1W images indicates inflammation or stenosis extrusions due to reactive meningitis or granulation tis-
surrounding spinal nerves as they pass through interver- sue, mimicking other pathology.34–36 Careful scrutiny of
tebral foramina. the images for other signs of disc disease may be required
• Within the spinal cord, as with brain lesions, contrast in order to avoid a misdiagnosis of neoplasia when the
enhancement reflects breakdown of the blood–CNS MR appearance is atypical.
118 CHAPTER 4.2
• Opinions differ as to the correct dose of contrast medium • Bone lesions: suppression of high signal from normal
to use with low-field scanners. Conspicuity of contrast bone marrow demonstrates high-signal (‘water rich’)
medium decreases with field strength and it has been pathology on T2W images or areas of enhancement
proposed to use 1.5 to 2 times the recommended dose.37 on T1W post-contrast images, such as in cases of
spondylitis and neoplasia. In the author’s experience,
Fat suppression some dogs, such as sight hounds, have very uneven dis-
• The abundance of fat in and around the spine means tribution of fat in their vertebral bone marrow, which
that hyperintense and contrast-enhancing lesions may can mimic pathology such as multiple myeloma. In
be masked by bright signal from fat, and therefore tech- these dogs, application of fat suppression to a T1W or
niques to suppress it are valuable in improving detection T2W scan will indicate whether the appearance is due
of such lesions. These techniques include chemical or to normal fat or to disease (Fig. 4.2.21).
spectral fat saturation (high-field only), opposed phase
imaging (‘Dixon technique’, all field strengths), and
STIR (all field strengths). They allow differentiation of
normal fat in the vertebral bone marrow, epidural space,
paraspinal musculature, and fascial planes from other
hyperintense tissues, which may be pathologic.30,38,39
They also allow abnormal accumulations of fat such as
lipomata to be identified by suppressing their signal.
STIR is considered separately later in this section.
• Fat suppression using the spectral or Dixon technique is
useful for various types of spinal pathology:
(a)
• Spinal cord lesions: by abolishing fat signal the risk
of partial volume averaging artifact from epidural
fat mimicking or masking spinal cord pathology on
dorsal or sagittal scans is removed.
• Epidural and meningeal lesions: as epidural fat signal
is absent, meningeal contrast enhancement, spinal
nerve alterations, and extradural lesions such as
empyema are more readily detected.
• Disc lesions: fat suppression combined with contrast
medium administration results in a ‘myelographic
effect’ in which contrast medium fills the venous
(b)
sinuses ventral to the cord. Small disc extrusions
cause compression of these areas and are more easily
recognized (Fig. 4.2.20).
(c)
Fig. 4.2.21 (a) Uneven signal intensity of the vertebrae
in a T2W image in a Cocker Spaniel with spinal pain.
Hyperintensity on T2W might be normal fat conversion of
Fig. 4.2.20 Sagittal, post-contrast, fat-suppressed T1W image bone marrow, but could also represent pathology. (b) A similar
in a Whippet with a disc extrusion at C5-C6 (arrow). Contrast appearance on the T1W image suggests that the effect is
medium in the vertebral venous sinuses clearly delineates the due to fat. (c) A fat-suppressed, post-contrast T1W image
extrusion, giving a ‘myelographic-like’ effect. This technique shows that these areas have suppressed and have not contrast-
is especially helpful for small extrusions of non-degenerate enhanced, therefore are unlikely to be due to pathology.
disc material. (1.5T MRI system) (1.5T MRI system)
• Paraspinal soft tissue lesions: demonstration of

inflammation in the soft tissues surrounding the
spine is improved, especially in obese animals in
which there is considerable fat infiltration in muscles.
Fat-suppressed T2W and post-contrast T1W series
are both useful as overviews of paraspinal soft tissues,
especially when used in the dorsal plane, which com-
bines the ability to scan with a large FOV with the
potential to compare right and left sides (the same
is true of the STIR sequence, described later in this
section).
• If the post-contrast T1W sequence is to be fat sup-
pressed, a pre-contrast T1W sequence may in some
cases be omitted in order to reduce overall scan time.
However, this carries several disadvantages:
• Firstly, it means that the chance to perform subtrac-
tion, if it is subsequently deemed desirable, is lost. Fig. 4.2.22 Fat-suppressed images that rely on spectral
• Secondly, inherently low signal intensity areas such suppression of fat signal are severely degraded by metallic
as fibrosis or mineralization cannot be differentiated objects in the FOV, in this case a microchip in a Chihuahua.
from suppressed fat. In these cases, STIR pulse sequences may be preferred to
• Thirdly, the modification of the gray scale, which suppress fat signal. (1.5T MRI system)
occurs with fat suppression,30 means that the degree
of contrast enhancement cannot be judged accurately. the area of interest, and changing the scan plane or
• High-field scanners will permit spectral fat saturation repositioning the patient to obtain more uniform distri-
to be applied to various sequences, including T2W butions of anatomic structures.30
and pre/post-contrast T1W sequences (see Chapter 2). • With low-field scanners, fat suppression can still be
However, it cannot be used with low-field magnets, as obtained using the Dixon fat–water separation tech-
the difference in precessional frequency between fat and nique or ‘opposed-phase imaging’.37 This technique is
water is too small to permit them to be differentiated described in Chapter 4.4.
(precessional frequency increases with field strength,
with water resonating at a higher frequency than fat, see Short tau inversion recovery
Chapter 1). Image quality is usually very good, although • The STIR sequence is a fat-suppressed T2W scan, which
the scan times are likely to be slightly increased. With is useful with both high- and low-field systems, but espe-
spectral fat suppression, anything within the FOV cially the latter in which regular spectral fat suppression
causing inhomogeneities of the external magnetic field is not possible.
will cause the fat saturation to be uneven or to create • The following points should be noted:
areas of signal drop-out, which may render the images • STIR is different to a fat-suppressed, post-contrast
non-diagnostic. Examples of such interfering material T1W scan since with STIR all abnormal hydrated
include microchips, surgical implants, small metal frag- tissue is hyperintense, whereas with the post-contrast
ments remaining after high-speed drills have been used, T1W sequence only vascularized (enhancing) areas
and tiny magnetic foci in ingesta and feces. Sagittal are bright. Thus, the STIR sequence may show a
images are most likely to be affected by these serious lesion to be more extensive by including surrounding
artifacts (Fig. 4.2.22). In some cases, the artifact cre- edema in the hyperintense signal.
ated by a microchip may be reduced by displacing the • STIR is sensitive for bone lesions that do not contrast
tissue around it using tape or a stay suture; alternatives enhance, such as endplate edema on either side of a
include removing the microchip, using a smaller FOV disc lesion. STIR changes in cervical paraspinal soft
or different scan plane to exclude the interfering object, tissues have been shown to be a sensitive indicator of
swapping the frequency-encoding (FE) and phase- spinal cord and meningeal inflammation of unknown
encoding (PE) directions, and obtaining a conventional origin (e.g., steroid-responsive meningitis/arteritis).
post-contrast T1W scan and then performing subtrac- The changes in muscle and perineural fascial planes
tion. Other causes of uneven fat suppression include use are often bilateral but asymmetrical, and may also be
of a large FOV, anatomically irregular areas, and scan- seen to a lesser degree in post-contrast T1W and sub-
ning away from the magnet’s isocenter.30 More uniform traction images.40
fat suppression in these cases may be achieved by using • On STIR images, all tissues with short T1 relaxation
magnetic field shimming, a smaller FOV, centering on times have decreased signal intensity, which includes
120 CHAPTER 4.2
(a) (b)
Fig. 4.2.23 Value of STIR imaging in a dog with left thoracic

limb lameness and muscle atrophy in which a brachial
plexus tumor was suspected. (a) and (b) are dorsal plane
large field of view STIR images and (c) is a transverse STIR
image; these images allow comparison of the left and right
side and detect pathology as bright signal. In (a), the left
triceps muscle (solid arrow) is atrophied and hyperintense,
consistent with denervation atrophy. In (b) and (c), focal
segmental thickening and hyperintensity of the left radial
nerve is noted (dotted arrows) consistent with a nerve sheath
tumor. The arrowheads in (b) indicate the left and right
brachiocephalic veins. (1.5T MRI system) (Images courtesy of
(c)
Dr. Wilfried Mai, University of Pennsylvania)
contrast-enhancing structures as gadolinium causes a Gradient echo sequences

decrease in T1 relaxation time. It is therefore wise, • Gradient echo pulse sequences may be both T1W and
whenever possible, to perform STIR prior to contrast T2W (see Chapter 2). With high-field scanners, they can
medium administration, unless pathology has already be used in both 2D and 3D formats, whereas with low-
been identified on T2W images. field systems, the 3D format is popular, allowing refor-
• STIR images are of higher contrast but poorer reso- matting of isotropic voxels in different planes in order to
lution than spin echo images, and they are also prone reduce scan times.
to movement artifact due to respiration and arterial • T1W gradient echo sequences can be used both pre- and
pulsatility. As well as confirming the presence of fat post-contrast.
within a lesion,39 a STIR sequence is particularly • A 3D post-contrast gradient echo sequence (such as the
helpful as an overview of a relatively large area of the ‘spoiled gradient echo’, or SPGR) is extremely useful for
spine, in order to detect paraspinal and axillary soft delineating subtle disc extrusions when the extruded
tissue pathology. The dorsal plane is often the most material and spinal cord are of similar signal intensity on
helpful as it allows comparison of right and left sides pre-contrast images (Fig. 4.2.24).
over a large area. The inclusion of a STIR sequence • Because of their small slice thickness, both T1W and
is especially important in cases of non-specific spinal T2W 3D gradient echo transverse images provide excel-
pain without neurologic deficits and for suspected lent visualization of the spinal articular processes, and
brachial plexus tumors (Fig. 4.2.23). they are therefore to be recommended for trauma cases.
Fig. 4.2.25 Sagittal T2*W gradient echo image of the

lumbosacral junction in a German Shepherd Dog with sacral
osteochondrosis. The osteochondral fragment (arrow) and
adjacent bony remodeling of the cranial body/endplate of S1
are clearly depicted due to the low signal intensity of bone
Fig. 4.2.24 Transverse post-contrast, fat-suppressed T1W with this technique. (1.5T MRI system)
image in a Greyhound with neck pain and left thoracic limb
lameness. The image was acquired using a T1W 3D gradient
echo sequence (3D-SPGR on General Electric systems).
The slice thickness is 1.5 mm and this image shows a small
foraminal disc extrusion impinging on the spinal nerve,
outlined by contrast enhancement (arrow). (1.5T MRI system)
• The T2W gradient echo sequence is known as a T2*

(‘T2 star’) sequence. It produces images in which bone,
other calcified material, and ligaments appear very
hypointense or void in signal intensity, and soft tissues
are of fairly uniform, medium signal intensity. It is espe-
cially useful for spinal MRI because of this high con-
trast.41 The clear outline of the vertebral bodies means
that subtle changes in disc space width, osteolysis, spon- Fig. 4.2.26 Dorsal extradural hemorrhage secondary to a
dylotic spurs, fractures, and bone fragments are best disc extrusion, which has ruptured the venous sinuses in
appreciated on this sequence (Fig. 4.2.25). Calcified a paraplegic Rottweiler. The hemorrhage has contributed
disc material, the annulus fibrosus of discs, dura mater, significantly to the degree of spinal cord compression
and ligaments such as the dorsal longitudinal ligament (arrows). Hemorrhage is seen as heterogeneous signal void on
and transverse atlantal ligament are also seen as areas of gradient echo sequences. (1.5T MRI system)
very low signal. This pulse sequence has also been rec-
ommended for measuring spinal cord cross-sectional products such as deoxyhemoglobin and methemoglobin,
dimension in cases of osseous-associated cervical spon- which have paramagnetic effects.43 T2*W gradient echo
dylomyelopathy, as the margins of the cord are seen images are therefore highly sensitive for the detection of
more clearly than with other sequences.42 T2*W gradi- both extramedullary and intramedullary spinal hemor-
ent echo sequences are inherently prone to susceptibility rhage (Fig. 4.2.26) (see Chapter 7.7).44,45 In people, it is
artifacts, which are areas of low or absent signal resulting recommended that at least one gradient echo sequence is
from local inhomogeneities in the magnetic field. These performed on patients with spinal trauma for maximum
artifacts are especially prominent with high-field scan- detection of acute intramedullary hemorrhage.34 In small
ners. This can be diagnostically useful, since these arti- animals, the T2*W gradient echo sequence has been
facts can be created by the presence of blood degradation found to be of value in a variety of hemorrhagic spinal
122 CHAPTER 4.2
lesions including disc extrusions accompanied by rup- • In the spine, T2-FLAIR may also be used to investi-
ture of the venous sinuses, intramedullary disc extrusion, gate whether a fluid collection, such as in a subarach-
hematomyelia secondary to lumbar puncture, iatrogenic noid diverticulum or a syrinx, consists of CSF or not.
brainstem injury during cisternal puncture, hemorrhagic However, FLAIR images are of poorer resolution than
myelomalacia, trauma, coagulopathy, neoplasia, vascu- images obtained using other sequences, and flow artifacts
lar malformation, and parasitic infection.44–50 However, in CSF may result in uneven or higher signal intensity.
in the case of calcified disc extrusions accompanied by • T1-FLAIR series can be useful to image intradural lesions
hemorrhage, differentiation of disc material from blood in the cranial cervical spine (C1-C2) where the marked
may not be possible since both produce areas of signal suppression of CSF signal in the large cisterns will high-
void. Unfortunately, sensitivity of T2*W gradient echo light the boundaries of intradural masses (Fig. 4.2.27).
for small foci of hemorrhage is much less with low-
field scanners as the susceptibility artifact is smaller. MR angiography
Therefore, the appearance of hematomata is different • MR angiography (MRA) may be used for both arteries
and the sensitivity of detection of small foci of hemor- and veins, including the internal vertebral venous plexus,
rhage less than with high-field systems. and is occasionally of value for spinal MRI.
• Other lesions that are readily detected as areas of sig- • 2D time-of-flight MRA has been described for identi-
nal void on T2*W gradient echo images, and which have fication of an arterial anomaly in the cervical spine of
relevance for spinal MRI, include foreign bodies, gas a dog.51 If contrast medium is used, subtraction of pre-
in sinus tracts, and vacuum phenomenon in degenerate contrast or ‘mask’ images may be performed.
discs under traction.
Diffusion-weighted and diffusion tensor imaging
Fluid-attenuated inversion recovery • Diffusion-weighted imaging (DWI) is widely used in
• FLAIR is a pulse sequence that uses an inversion recovery people for the detection of areas of restricted diffu-
scheme to suppress the signal of CSF. It can be acquired sion associated with brain infarcts, by conversion to an
with T1 or T2 weighting. ‘apparent diffusion coefficient’ (ADC) map. This tech-
• The T2-FLAIR sequence is widely used for brain MRI, nique is also well established in veterinary patients for
since it nulls the hyperintense signal from CSF, allowing intracranial infarction, but the small size of the small
periventricular lesions and those close to the subarach- animal spinal cord makes it an impractical technique for
noid space to be identified with confidence. the investigation of suspected spinal infarcts.
* C
C
*
(a) (b)
Fig. 4.2.27 T1-FLAIR post-contrast dorsal plane (a) and transverse (b) images at the level of C1 in a dog with a meningioma.
The enhanced tumor (asterisks) is visible and fluid suppression shows the CSF as a dark area (arrows) surrounding the
lesion and outlining its intradural location. Contrast between the CSF and spinal cord (C) is enhanced by using FLAIR.
• Diffusion tensor imaging (DTI) is an advanced DWI ARTIFACTS

technique that uses strong, multidirectional gradients
to map white matter tracts and to examine isotropic Numerous artifacts arise with MRI and a detailed discus-
and anisotropic characteristics of water molecule diffusion is outside the scope of this chapter; useful reviews have
sion.52,53 Isotropic diffusion occurs when the magnitude been published elsewhere,58,59 and most of the important
of diffusion is the same in all directions, as occurs in MRI artifacts are discussed in Chapter 3. It may not be pos-
the normal spinal cord. Pathology results in fractional sible to abolish an artifact but its effect can sometimes be
anisotropy, in which the magnitude of diffusion in differ- reduced by certain maneuvers; for example, altering the PE
ent directions varies markedly, as shown on color-coded and FE directions. Artifacts of relevance to spinal MRI are
diffusion maps created in at least six different directions. motion, chemical shift, susceptibility, and truncation.
DTI is more sensitive than conventional MRI for exam-
ining the effects of both acute and chronic spinal cord Motion artifact
injury, including Wallerian degeneration. In humans, • Motion artifact due to patient movement, respiration,
it is used for early diagnosis, to determine the severity and pulsatile blood flow occurs in the PE direction and is
of injury, and to aid surgical planning for a variety of seen as noise, blurring, or ‘ghosting’ (Fig. 4.2.28).
lesions.53 Although in its infancy in the veterinary field, • For sagittal and transverse spinal MR studies, it is rec-
initial studies in dogs have shown that DTI is feasible in ommended that the PE direction is cranial to caudal and
this species and the technique may ultimately aid diag- right to left, respectively, so that unavoidable motion
nosis of white matter disease and surgical planning as in artifact is not superimposed over the spine itself. Motion
people. artifact is less of a problem with dorsal plane spinal
images.
Sequences for CSF flow • Voluntary movement of the patient can be avoided by
• Cine phase contrast MRI has been used to characterize ensuring patient comfort using a suitable ambient tem-
CSF flow dynamics at the foramen magnum and cervi- perature, and using analgesics in animals for whom posi-
cal spine in Cavalier King Charles Spaniels (CKCSs) tioning may be painful (for example, dogs with severe
with Chiari-like malformation (caudal occipital mal- lumbosacral disease or coxofemoral osteoarthrosis).
formation syndrome) and to compare this with control • The patient must be positioned in a stable manner if
dogs.15,54 supine, to avoid tilting during the scan. Adjustments to
• It has been found that obstruction to flow at the foramen the anesthetic protocol may be made to minimize respi-
magnum may be significantly impaired in most CKCSs, ratory motion if it causes a problem, and saturation bands
and CSF velocity and flow pattern is related to the pres-
ence of syringomyelia.
• More recently, cardiac-gated cine balanced fast field echo
has been used to assess pulsation of the brain in dogs
and to measure the degree of cerebellar pulsation with
the neck in a flexed position.55 CKCSs with Chiari-like
malformation and syringomyelia were found to have a
significantly greater pulsation of the cerebellum than
control dogs.
Intrathecal gadolinium administration

• The use of a small amount of gadolinium-based MR
contrast medium mixed with CSF and administered by
cisternal puncture in a dog has been reported.56 In that
case two small dural tears were demonstrated by leak-
age of the contrast medium out of the subarachnoid
space, supporting the diagnosis of a brachial plexus
avulsion.
• In theory, this technique could also be used to demon- Fig. 4.2.28 Motion artifact due to cardiac movement and
strate communication or lack thereof between cyst-like respiration. Motion artifact occurs in the phase-encoding
lesions (arachnoid diverticula) and the subarachnoid direction, which should be cranial to caudal (horizontal)
space. for sagittal spine scans in order to lie mainly ventral to the
• However, intrathecal use of gadolinium in people is cur- spine, thus avoiding image degradation in the area of clinical
rently not licensed in the USA or Europe.57 interest. (1.5T MRI system)
124 CHAPTER 4.2
(‘SAT bands’) may also be placed over moving areas, such greatest with gradient echo sequences and at high-field
as the heart, within the FOV. Respiratory triggering may strengths.59
be possible with some scanners, although they prolong • This artifact may either obscure or mimic lesions, ren-
acquisition times. Flow artifacts in blood vessels often dering some studies completely non-diagnostic, and is
vary between different pulse sequences and are especially therefore of importance in spinal MRI. The most com-
noticeable on contrast-enhanced T1W scans. mon example of this in spinal MRI is due to the effect of
• High signal in blood vessels may create interpretation a microchip on images of the cervicothoracic area, to the
problems; for example, in a dog with a dermoid sinus, an extent that images in small patients may be non-diagnostic
apparent tract extending to the spine was seen on STIR and require removal of the microchip (Fig. 4.2.29).
images but not found at surgery, and was subsequently Images in the dorsal plane, ventral to the chip, may be
thought to be an interspinous vein.60 satisfactory. Other causes of susceptibility artifact include
metallic spinal implants, microscopic metal fragments
Partial volume averaging artifact remaining from previous spinal surgery,61 and ingested
• Partial volume averaging artifact arises with all tomo- metallic foreign bodies, although problems are not usually
graphic modalities when tissue interfaces are oblique encountered in lumbosacral MRI of dogs with total hip
or curved within a slice. It is well recognized in all MR replacements.
studies and its impact can be reduced by using thinner • The effect of susceptibility artifact may be minimized
slices (reduces through-plane partial volume averaging by changing the slice direction, decreasing voxel size,
artifact) and larger imaging matrices (reduces in-plane decreasing TE, increasing receiver bandwidth, or chang-
partial volume averaging artifact). ing the FE direction.59,62
• It may be more problematic in low-field MRI in which • Since microchips lie in loose subcutaneous tissue it may
thicker slices are often used to improve SNR. In the be possible to displace them slightly using a stay suture.
spine, partial volume averaging artifact is most likely to • Susceptibility artifact may be exploited in order to detect
be an issue in sagittal and dorsal images obtained with hemorrhage or calcified foci,59 especially in cases of disc
thicker slices, than with transverse images in which most disease.
tissue interfaces are perpendicular to the slice plane. • Susceptibility artifacts are less pronounced with low-field
than with high-field systems. This is beneficial when the
Chemical shift artifact artifact is problematic but also means that sensitivity of
• Chemical shift is spatial misregistration of fat and water detection of hemorrhage is less.
protons since those in fat resonate at a slightly lower fre-
quency and are shifted a few pixels on the image with Truncation (Gibbs artifact)
respect to protons in hydrated tissue. This produces bands • Truncation, or Gibbs artifact, is a line of abnormal sig-
of bright and dark signal on either side of fat–water internal that occurs parallel to an interface between tissues of
faces in the FE direction, especially on T2W and contrast- markedly different signal intensity. Although it can arise
enhanced T1W scans.59 It may be seen on either side of the in various locations and with other pulse sequences, it is
spinal cord on dorsal and transverse images when the FE
direction is right to left or left to right, and creates distor-
tion in the appearance of intervertebral discs in sagittal
scans when FE is cranial to caudal or caudal to cranial.
• However, more convenient placement of the FE direc-
tion fortunately complements that of the PE directions
as follows:
• Dorsal plane: PE right to left and FE cranial to caudal.
• Sagittal plane: PE cranial to caudal and FE dorsal to
ventral.
• Transverse plane: PE right to left and FE dorsal to
ventral.
• Chemical shift artifact can also be reduced by decreasing
voxel size and increasing receiver bandwidth.59 Chemical
shift artifact is less noticeable with low-field systems.
Susceptibility artifact Fig. 4.2.29 Severe image distortion due to the presence of
• Susceptibility artifact due to the presence of metal a microchip (susceptibility artifact), rendering this sagittal
in the FOV creates areas of signal loss with bright, image of the cervical spine of a 4-month-old kitten non-
curved margins surrounded by image distortion, and is diagnostic. (1.5T MRI system)
of most significance in small animals in spine imaging, in which orientation of the PE direction parallel to the
especially in sagittal and dorsal T2W studies, in which spine (i.e., cranial to caudal) also reduces superimposition
there is high contrast between the spinal cord and CSF/ of motion artifact over the area of interest (see above).
epidural fat. It is seen as one or more hyperintense lines However, for dorsal plane images the FE direction is bet-
along the spinal cord, wider than the central canal and ter placed parallel to the spinal cord (cranial to caudal)
therefore potentially being misinterpreted as central in order to minimize chemical shift artifact, and thus
canal dilation or syringomyelia. truncation is more obvious. This explains the disparity
• One study showed that with lower resolution images a in appearance between the two planes, in which often
single, wider band was created and that with increasing central canal dilation or syringomyelia may be suspected
spatial resolution it appeared as multiple hyperintense on dorsal images but not replicated in the sagittal plane
zones, since truncation artifact is a function of resolution (Fig. 4.2.30). Truncation may also be reduced by apply-
relative to the dimensions of the object being imaged. ing pre-reconstruction filters or using a post-processing
Importantly, the same study showed that when the spi- optimization technique.63
nal cord was compressed, multiple hyperintense zones
coalesced to a single broad zone, mimicking cord hyper- Signal changes at injection sites
intensity due to pathology such as edema.63 • The epaxial lumbar muscles are a site commonly used
• Truncation is due to insufficient data sampling in both for administration of intramuscular injections, including
FE and PE directions. Reduction of the number of PE anti-inflammatory drugs and anesthetic premedicants.
steps is a common maneuver in low-field systems in order • These often create ill-defined bands of abnormal signal
to shorten scan time, hence it is more often a problem intensity that are hyperintense on T2W and STIR and
with these systems. It cannot be eliminated, but can may show contrast enhancement (Fig. 4.2.31). These
be minimized by increasing spatial resolution either by have the potential to cause confusion when patients
increasing the matrix or reducing the FOV. If the matrix undergo MRI for spinal pain as they may be misdiag-
is asymmetrical, placing the larger matrix dimension nosed as areas of myositis. In these animals, the lumbar
(usually FE) perpendicular to the critical tissue inter- route for injections should be avoided, or at the least the
face is advantageous. This works well for sagittal images, side and location of injection should be recorded.
(b)
Fig. 4.2.30 (a) Truncation artifact creating the impression of central canal
dilation (arrow) in this dorsal T2W image of the thoracic spine. (b) The sagittal
T2W image is unremarkable. Truncation occurs in the phase-encoding direction,
which is normally right to left in dorsal images in order to minimize the effect
of chemical shift artifact (which occurs in the frequency-encoding direction).
(a)
(1.5T MRI system)
126 CHAPTER 4.2
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L2
Fig. 4.2.32 Sagittal lumbar MR image showing the origins

of the celiac and cranial mesenteric arteries (arrows), which
are always visible and can be used as landmarks for vertebrae
in the thoracolumbar area once their exact location has
been established. Although they are usually in the region
of L1, in this Lurcher they are actually ventral to L2.
(1.5T MRI system)
confusion: for example, when the base of an apparent

transverse process is identified but the transverse process
is actually elongated, mimicking a palpable rib, or when
vestigial ribs are present. Therefore, if radiographs are
not available, is it essential that a dorsal plane scan is per-
formed in order to identify rib and transverse process
conformation when surgery is contemplated.
• Around the thoracolumbar junction, the celiac and cra-
Fig. 4.2.31 Dorsal STIR image of the lumbar spine of a nial mesenteric arteries are clear landmarks on sagittal
Cocker Spaniel with lumbar pain. A band of ill-defined
scans. Although their position varies slightly between
hyperintense signal is seen lying obliquely in the epaxial
individuals, once their location has been established in
muscles (arrow), but is likely to be an incidental finding
one pulse sequence, they can be used as identifiers for
caused by prior intramuscular injection. For this reason, the
the closest vertebra (usually L1) on subsequent sequences
lumbar site should not be used for premedication or analgesic
performed on that patient (Fig. 4.2.32).65
injection prior to MRI of this area. (1.5T MRI system)
• Similarly, characteristic spinal features, such as the anti-
clinal disc space, spondylosis, or disc degeneration, may
GENERAL PRINCIPLES OF SPINAL be used as cross-referencing features.
MRI INTERPRETATION • Interpretation of spinal images requires accurate cross-
referencing, especially between transverse and sagit-
• The tomographic nature of spinal MR images means tal images. This is usually possible on dedicated image
that it is often more difficult than with radiography to viewer software. Where computer screens are not present
identify the precise location of a lesion with respect to in an operating theatre and hard copies must be referred
the vertebral segment, and this could have severe conse- to during surgery, it is essential that cross-referencing
quences if spinal surgery is performed. images are also printed, and annotation of images is
• However, with careful acquisition and assessment of the also recommended. Hard copies should be printed with
images, it is usually not necessary for supplementary images of adequate size and using the correct veterinary
radiographs to be obtained. On the sagittal scan, certain orientation.
vertebrae are characteristic in shape and on parasagittal • Assessment of spinal cord compression or swelling usu-
images of the thoracolumbar spine, ribs and transverse ally necessitates differentiation between CSF and epi-
processes can generally be distinguished as the rib heads dural fat. These are often difficult to distinguish from
are rounded whereas the transverse processes are flat- each other on T2W scans, in which both are hyperin-
tened dorsoventrally and lie slightly more ventrally.64 tense. However, comparison of T2W images with iden-
• However, it is unwise to rely on sagittal scans only for tical slices obtained with T1 weighting reveals which
providing surgical landmarks, as the presence of transi- areas are epidural fat (hyperintense on both) and which
tional vertebrae at the thoracolumbar junction can create are CSF (iso- to hypointense on T1W images). This is
VetBooks.ir
especially helpful in the transverse plane. Such com- degenerative lumbosacral stenosis. J Am Vet Med Assoc
parison of identical image slices obtained with different 216(11):1769–74.
image weighting is fundamental to MR interpretation. 8. da Costa RC, Parent J, Dobson H et al. (2006). Comparison
• A systematic approach to assessment of spinal MR of magnetic resonance imaging and myelography in 18
Doberman pinscher dogs with cervical spondylomyelopathy.
images is recommended, examining separately the spinal
Vet Radiol Ultrasound 47(6):523–31.
cord, subarachnoid space, meninges, epidural space, 9. Penderis J, Dennis R (2004). Use of traction during magnetic
vertebrae, intervertebral discs, and paraspinal soft tis- resonance imaging of caudal cervical spondylomyelopathy
sues. Comparison of right and left sides for symmetry (“wobbler syndrome”) in the dog. Vet Radiol Ultrasound
on transverse and dorsal images is helpful, especially for 45(3):216–9.
the detection of muscle wastage, for example with lum- 10. Provencher M, Habing A, Moore SA et al. (2016). Kinematic
bosacral disease.66 Diagnosis of spinal nerve pathology magnetic resonance imaging for evaluation of disc-associated
is often challenging due to their small size and proxim- cervical spondylomyelopathy in Doberman Pinschers. J Vet
ity to blood vessels. In cases of suspected brachial plexus Intern Med 30(4):1121–8.
11. Bersan E, McConnell F, Trevail R et al. (2015). Cervical
disease, the presence of numerous blood vessels in the
intervertebral foraminal disc extrusion in dogs: clinical
axilla is challenging as both vessels and nerve tumors presentation, MRI characteristics and outcome after medical
will show contrast enhancement, but blood vessels can management. Vet Rec 176(23):597.
be followed to the parent vessel through several adjacent 12. Guillem Gallach R, Suran J, Caceres AV et al. (2011).
slices. At the lumbosacral junction, detection of spinal Reliability of T2-weighted sagittal magnetic resonance images
nerve compression by foraminal stenosis or lateral spon- for determining the location of compressive disk herniation in
dylosis is also challenging. Loss of perineural fat signal dogs. Vet Radiol Ultrasound 52(5):479–86.
on T1W images and surrounding contrast enhancement 13. Johnson P, De Risio L, Sparkes A et al. (2012). Clinical,
are helpful signs of pathology, but generally there is poor morphologic, and morphometric features of cranial thoracic
spinal stenosis in large and giant breed dogs. Vet Radiol
correlation between clinical signs and MR features, and
Ultrasound 53(5):524–34.
images must be interpreted in the appropriate clinical 14. Kippenes H, Gavin PR, Bagley RS et al. (1999). Magnetic
context since lumbosacral disease is a common incidental resonance imaging features of tumors of the spine and spinal
finding. cord in dogs. Vet Radiol Ultrasound 40(6):627–33.
15. Zindl C, Tucker RL, Jovanovik J et al. (2017). Effects of image
plane, patient positioning, and foraminal zone on magnetic
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52:S81–S4. German Shepherd dogs and other large breed dogs. Vet Radiol
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resonance imaging characteristics of suspected vertebral 19. Freeman P (2010). Sacrococcygeal intervertebral disc
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dogs. Vet Radiol Ultrasound 53(5):552–9. 20. Lawson CM, Reichle JK, McKlveen T et al. (2011). Imaging
4. Dennis R (2011). Flexed sagittal MRI for evaluation of findings in dogs with caudal intervertebral disc herniation.
the occipital bone and foramen magnum. Annual European Vet Radiol Ultrasound 52(5):487–91.
Veterinary Diagnostic Imaging Conference, London. 21. Kraft S, Ehrhart EJ, Gall D et al. (2007). Magnetic resonance
5. Upchurch JJ, McGonnell IM, Driver CJ et al. (2011). imaging characteristics of peripheral nerve sheath tumors of
Influence of head positioning on the assessment of Chiari- the canine brachial plexus in 18 dogs. Vet Radiol Ultrasound
like malformation in Cavalier King Charles spaniels. Vet Rec 48(1):1–7.
169(11):277. 22. Miyabayashi T, Smith M, Tsuruno Y (2000). Comparison
6. Cerda-Gonzalez S, Olby NJ, Griffith EH (2015). Dorsal of fast spin-echo and conventional spin-echo magnetic
compressive atlantoaxial bands and the craniocervical junction resonance spinal imaging techniques in four normal dogs.
syndrome: association with clinical signs and syringomyelia Vet Radiol Ultrasound 41(4):308–12.
in mature cavalier King Charles spaniels. J Vet Intern Med 23. Naude SH, Lambrechts NE, Wagner WM et al. (2008).
29(3):887–92. Association of preoperative magnetic resonance imaging
7. Jones JC, Banfield CM, Ward DL (2000). Association between findings with surgical features in Dachshunds with
postoperative outcome and results of magnetic resonance thoracolumbar intervertebral disk extrusion. J Am Vet Med
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24. Ohshio I, Hatayama A, Kaneda K et al. (1993). Correlation 41. Dennis R (2005). Use of gradient echo pulse sequences in
between histopathologic features and magnetic resonance MRI of the spine in small animals. Annual European Veterinary
images of spinal cord lesions. Spine 18(9):1140–9. Diagnostic Imaging Conference, Naples.
25. Ito D, Matsunaga S, Jeffery ND et al. (2005). Prognostic value 42. Gasper JA, Rylander H, Stenglein JL et al. (2014). Osseous-
of magnetic resonance imaging in dogs with paraplegia caused associated cervical spondylomyelopathy in dogs: 27 cases
by thoracolumbar intervertebral disk extrusion: 77 cases (2000–2012). J Am Vet Med Assoc 244(11):1309–18.
(2000–2003). J Am Vet Med Assoc 227(9):1454–60. 43. Atlas SW, Thulborn KR (2002). Intracranial haemorrhage.
26. De Risio L, Adams V, Dennis R et al. (2009). Association In: Magnetic Resonance Imaging of the Brain and Spine, 3rd edn.
of clinical and magnetic resonance imaging findings with (ed. SW Atlas) Lippincott Williams and Wilkins, Philadelphia,
outcome in dogs with presumptive acute noncompressive pp. 773–832.
nucleus pulposus extrusion: 42 cases (2000–2007). J Am Vet 44. Hammond LJ, Hecht S (2015). Susceptibility artifacts on T2*-
Med Assoc 234(4):495–504. weighted magnetic resonance imaging of the canine and feline
27. De Risio L, Adams V, Dennis R et al. (2008). Association spine. Vet Radiol Ultrasound 56(4):398–406.
of clinical and magnetic resonance imaging findings with 45. Kent M, Eagleson JS, Neravanda D et al. (2010). Intraaxial
outcome in dogs suspected to have ischemic myelopathy: spinal cord hemorrhage secondary to atlantoaxial subluxation
50 cases (2000–2006). J Am Vet Med Assoc 233(1):129–35. in a dog. J Am Anim Hosp Assoc 46(2):132–7.
28. Seiler GS, Robertson ID, Mai W et al. (2012). Usefulness 46. Lujan Feliu-Pascual A, Garosi L, Dennis R et al. (2008).
of a half-fourier acquisition single-shot turbo spin-echo Iatrogenic brainstem injury during cerebellomedullary cistern
pulse sequence in identifying arachnoid diverticula in dogs. puncture. Vet Radiol Ultrasound 49(5):467–71.
Vet Radiol Ultrasound 53(2):157–61. 47. McConnell JF, Garosi LS (2004). Intramedullary intervertebral
29. Scheffler K, Lehnhardt S (2003). Principles and applications disk extrusion in a cat. Vet Radiol Ultrasound 45(4):327–30.
of balanced SSFP techniques. Eur Radiol 13(11):2409–18. 48. Platt SR, Dennis R, Murphy K et al. (2005). Hematomyelia
30. D’Anjou MA, Carmel EN, Tidwell AS (2011). Value of fat secondary to lumbar cerebrospinal fluid acquisition in a dog.
suppression in gadolinium-enhanced magnetic resonance Vet Radiol Ultrasound 46(6):467–71.
neuroimaging. Vet Radiol Ultrasound 52(1 Suppl 1):S85–90. 49. Platt SR, McConnell JF, Bestbier M (2006). Magnetic
31. Holloway A, Dennis R, McConnell F et al. (2009). Magnetic resonance imaging characteristics of ascending hemorrhagic
resonance imaging features of paraspinal infection in the dog myelomalacia in a dog. Vet Radiol Ultrasound 47(1):78–82.
and cat. Vet Radiol Ultrasound 50(3):285–91. 50. Tidwell AS, Specht A, Blaeser L et al. (2002). Magnetic
32. Naughton JF, Tucker RL, Bagley RS (2005). Radiographic resonance imaging features of extradural hematomas
diagnosis - paraspinal abscess in a dog. Vet Radiol Ultrasound associated with intervertebral disc herniation in a dog.
46(1):23–6. Vet Radiol Ultrasound 43(4):319–24.
33. Schneider AR, Chen AV, Tucker RL (2010). Imaging diagnosis: 51. Westworth DR, Vernau KM, Cullen SP et al. (2006). Vascular
vertebral canal porcupine quill with presumptive secondary anomaly causing subclavian steal and cervical myelopathy in
arachnoid diverticulum. Vet Radiol Ultrasound 51(2):152–4. a dog: diagnosis and endovascular management. Vet Radiol
34. Czervionke LF, Haughton VM (2002). Degenerative diseases Ultrasound 47(3):265–9.
of the spine. In: Magnetic Resonance Imaging of the Brain 52. Pease A, Miller R (2011). The use of diffusion tensor imaging
and Spine, 3rd edn. (ed. SW Atlas) Lippincott Williams and to evaluate the spinal cord in normal and abnormal dogs.
Wilkins, Philadelphia, pp. 1633–713. Vet Radiol Ultrasound 52(5):492–7.
35. Kippenes H, Silver GM, Gavin PR et al. (2000). Magnetic 53. Yoon H, Park NW, Ha YM et al. (2016). Diffusion tensor
resonance imaging of extradural spinal cord masses – imaging of white and grey matter within the spinal cord of
distinguishing contrast-enhancing disc disease from neoplasia. normal Beagle dogs: sub-regional differences of the various
Annual Meeting of the American College of Veterinary Radiology, diffusion parameters. Vet J 215:110–7.
Chicago. 54. March PA, Abramson CJ, Smith M et al. (2005). CSF flow
36. Suran JN, Durham A, Mai W et al. (2011). Contrast abnormalities in caudal occipital malformation syndrome. Annual
enhancement of extradural compressive material on magnetic Meeting of the American College of Veterinary Internal Medicine,
resonance imaging. Vet Radiol Ultrasound 52(1):10–6. Baltimore.
37. Konar M, Lang J (2011). Pros and cons of low-field magnetic 55. Driver CJ, Watts V, Bunck AC et al. (2013). Assessment of
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52:S5–S14. malformation and syringomyelia using cardiac-gated cine
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the diagnosis of spinal diseases in dogs: a preliminary report. diagnosis: traumatic dural tear diagnosed using intrathecal
Annual Meeting of the American College of Veterinary Radiology, gadopentate dimeglumine. Vet Radiol Ultrasound 50(5):502–5.
San Antonio. 57. Munoz A, Mateo I, Lorenzo V et al. (2013). MR
39. Morgan LW, Toal R, Siemering G et al. (2007). Imaging cisternography/myelography of post-traumatic spinal CSF
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40. Eminaga S, Cherubini GB, Villiers E et al. (2013). STIR 58. Kaur P, Kumaran SS, Tripathi RP et al. (2007). Protocol error
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59. Mirowitz SA (1999). MR imaging artifacts. Challenges and 64. Yeamans CL, Haley A, Gutierrez-Quintana R et al. (2015).
solutions. Magn Reson Imaging Clin N Am 7(4):717–32. Surgical anatomical landmarks of the thoracolumbar vertebral
60. Davies ESS, Fransson BA, Gavin PR (2004). A confusing column on magnetic resonance imaging in dogs. Anat Histol
magnetic resonance imaging observation complicating Embryol 45(2):140–4.
surgery for a dermoid cyst in a Rhodesian ridgeback. 65. Dennis R (2005). Assessment of location of the celiac and
Vet Radiol Ultrasound 45(4):307–9. cranial mesenteric arteries relative to the thoracolumbar
61. Freer SR, Scrivani PV (2008). Postoperative susceptibility spine using magnetic resonance imaging. Vet Radiol Ultrasound
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62. Freer SR, Scrivani PV, Gross B (2008). Letter to the Editor. muscle transverse area and symmetry in dogs with and
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63. Gregori T, Lam R, Priestnall SL et al. (2016). Truncation 56(10):618–22.
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cord. Vet Radiol Ultrasound 57(6):582–6.
CHAPTER 4.3
GENERAL FEATURES AND OPTIMIZED TECHNIQUE

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130 FOR THE MUSCULOSKELETAL SYSTEM

CONTENTS
MRI characteristics of musculoskeletal tissues ....................................................................................................................................................130
Normal signal intensity of musculoskeletal structures .....................................................................................................................................130
Cortical bone ............................................................................................................................................................................................. 131
Bone marrow .............................................................................................................................................................................................. 131
Articular cartilage .......................................................................................................................................................................................132
Fibrocartilage .............................................................................................................................................................................................132
Tendons/ligaments ....................................................................................................................................................................................132
Muscle tissue ............................................................................................................................................................................................132
Synovium/synovial fluid .............................................................................................................................................................................133
Changes in signal induced by musculoskeletal pathology ...............................................................................................................................133
Choice of coil ........................................................................................................................................................................................................134
Joint specific MR anatomy, imaging planes, and pulse sequences .......................................................................................................................134
Muscles ...........................................................................................................................................................................................................134
Bone ................................................................................................................................................................................................................134
Shoulder joint ..................................................................................................................................................................................................134
Elbow joint.......................................................................................................................................................................................................139
Stifle joint ........................................................................................................................................................................................................142
Coxofemoral joint ............................................................................................................................................................................................146
Carpus–manus ...............................................................................................................................................................................................146
Tarsus–pes ...................................................................................................................................................................................................... 147
Orthopedic hardware and MRI artifacts .................................................................................................................................................................150
References.............................................................................................................................................................................................................150
MRI provides exquisite soft tissue contrast and is very sensi- system, and will also summarize important MRI anatomic
tive to pathologic processes, which typically cause changes features of the various joints.
in proton density and mobility. As a result, this technique
is particularly suitable to assess musculoskeletal soft tissue MRI CHARACTERISTICS OF
abnormalities, and to some extent bone pathology as well. MUSCULOSKELETAL TISSUES
MRI is indicated in small animals when there is persistent
lameness that cannot be clearly explained by clinical exami- Normal signal intensity of
nation and radiographs. musculoskeletal structures
To gain maximal information, optimal technique should • Signal intensity on MRI is dependent on the density of
be used, including choice of appropriate coils for the region mobile protons in the voxel and how they interact with
under investigation, perfect positioning, and optimization their physicochemical environment, which will influ-
of pulse sequence combination depending on the clinical ence their longitudinal (T1) and transverse (T2) relax-
suspicion and region being imaged. This chapter will focus ation times (see Chapter 1). Table 4.3.1 summarizes
on reviewing important technical considerations to improve the differences in relaxation times of various musculo-
the quality of MRI examination of the musculoskeletal skeletal tissues and Table 4.3.2 summarizes the general
G e n e r a l Fe at u r e s a n d O p t i m i z e d Te c h n iqu e for t h e Musc u l os k e l e ta l Sys t e m 131
Table 4.3.1 Relative relaxation times of musculoskeletal tissues.1
tiSSUe t1 ReLAXAtion tiMe t2 ReLAXAtion tiMe

Muscle Medium Short
Adipose tissue Short Medium
Nerve Medium Medium
Other soft tissue Medium to long Medium to long
Tendon, bone – Very short (depends on fiber orientations relative to B0)
Table 4.3.2 Signal intensity of musculoskeletal tissues and associated structures on common pulse
sequences.1,2
tiSSUe t1-WeiGHteD PRoton DenSitY-WeiGHteD t2-WeiGHteD

Cortical bone Very low Very low Very low
Fat High Intermediate Low/intermediate (high if turbo/
Yellow (fatty) bone marrow fast spin echo [TSE/FSE] is used)
Red (hematopoietic) bone Low Intermediate Low/intermediate
marrow
Hyaline cartilage Intermediate Intermediate Intermediate/high
Muscle Intermediate Intermediate Intermediate/low
Nerves Intermediate (slightly <muscle) Intermediate (slightly <muscle) Intermediate (slightly <muscle)
Fibrocartilage Low Low Low
Ligaments, tendons Low Low Low
Blood vessels Low Low Low or high
Fluid Low/intermediate High High
Proteinaceous fluid High High High
Air Low Low Low
signal intensity of various musculoskeletal structures • In young animals, a large portion of the bone marrow is
on common pulse sequences. The differences in relax- active red marrow, which is hypercellular and contains
ation times between tissues contribute to the excel- <25% fat; in contrast, in older animals, there is a shift to
lent contrast achieved with MRI. That contrast can be inactive yellow bone marrow, which is hypocellular and
modified by using various MRI pulse sequences (see contains >75% fat.5
Chapter 2). • The conversion of red to yellow bone marrow usually
begins at the phalanges before birth, and progresses
Cortical bone proximally along the appendicular skeleton, although red
• The few water protons in cortical bone have an extremely marrow usually persists to some extent in the axial skel-
short transverse relaxation time, resulting from surface eton, ribs, sternum, proximal metaphyses of the humeri,
interactions and diamagnetism of the mineral relative to and femurs.5
water. • Fat is the predominant contributor to the signal of both
• This contributes to the black signal of cortical bone on red and yellow bone marrow; it has very short T1 and
all conventional MRI pulse sequences.3,4 moderately long T2 relaxation times.5
• On conventional T1W imaging, yellow bone marrow has
Bone marrow high signal, similar to that of subcutaneous fat, while the
• The cancellous bone and medullary cavity of bones are red marrow has a lower signal, similar to that of muscles.
richer in protons due to their bone marrow content. The • On T2W FSE/TSE sequences, yellow bone marrow has
bone marrow can be fatty (yellow) or hematopoietic high signal intensity due to the fat content, while the red
(red), the relative amount of each varying with age and bone marrow has intermediate signal (lower than fat but
location. higher than muscle).
132 CHAPTER 4.3
• A drop in signal is observed for the yellow bone marrow

on fat-suppressed pulse sequences (STIR or sequences
with fat saturation). This can be helpful to identify
pathologic high signal on T2W images, which remains
high on fat-suppressed images, whereas normal yellow
bone marrow will have decreased signal.
Articular cartilage
• The articular cartilage has a variable signal intensity that
is dependent on the pulse sequence:3
• Healthy articular cartilage has an intermediate signal
intensity on T1W and T2W images.6
• On STIR and T2W FSE/TSE with fat saturation
images, cartilage appears dark gray and provided it is
thick enough, may be distinguished from the hyperin-
tense synovial fluid, allowing for identifiable pathol-
ogy (thinning, disruption). Spatial resolution may,
however, be insufficient to separate and identify the
very thin articular cartilage in small tight joints such
as the elbow.
• 3D T1W gradient echo pulse sequences with fat satu-
ration are often preferred to image the articular carti-
lage, especially in joints with tight articular space such
as the elbow.7 On these sequences, the articular cartilage
appears bright in contrast with the low signal of synovial
fluid within the joint and suppressed signal from fat in
the adjacent subchondral bone.7 Fig. 4.3.1 Sagittal PDW fat saturated image of the shoulder
showing the biceps brachii tendon at its origin on the
• The distinction between endochondral cartilage and
supraglenoid tubercle. A focal artifactual hyperintensity is
synovial fluid in young dogs is poor.8
present in the tendon (circle) due to a magic angle artifact
where the tendon fibers were oriented at about 55° relative to
Fibrocartilage the direction of the main magnetic field. This hyperintensity
• In fibrocartilage such as menisci, there is decreased was not present on a T2W image where a long TE was used.
mobility and density of protons resulting in a dark Some hyperintense joint effusion is present distending the
appearance on all sequences.3 joint capsule (arrow). (3T MRI system)
• Identification of meniscal tears requires the use of pulse
sequences with short TE (proton density-weighted • Normal ligament fibers will behave similarly, but the
[PDW] or T1W spin echo, T2*W gradient echo). more complex organizational pattern of ligaments pro-
duces less uniform signal intensity compared with
Tendons/ligaments tendons.9,10
• Tendons and ligaments normally have low signal on all • The magic angle artifact is more prominent in pulse
MRI pulse sequences, due to their highly ordered col- sequences with a low to moderate time of echo (TE),
lagen with protons bound to water. such as PDW, T1W, T2*W, and STIR sequences. It can
• In tendons, the dipolar interactions between tissue pro- be recognized by comparing the tendon or ligament sig-
tons with highly ordered collagen usually result in rapid nal in the short TE image with the signal from the same
dephasing of these protons following excitation (‘dipole structure in a long TE image, such as a T2W FSE/TSE
interaction’), leading to little or no signal emanating image.9,10
from the tendon.9,10
• When the tendon’s fibers are oriented at some particular Muscle tissue
angles to the axis of the main magnetic field (55 ± 10°, • Normal muscle has an intermediate to long T1 relax-
or any interval of this such as 125°, 235°, or 305°), the ation time and a short T2 relaxation time.11
dipole interactions are minimized, which creates a signal • On T1W images, it is hyperintense to water and very
of enough intensity to make the structure look hyper- hypointense compared with fat.
intense, potentially mimicking pathology. This is called • On T2W images, it is of much lower signal intensity
the ‘magic angle artifact’ (Fig. 4.3.1). than water and fat.
• On STIR and fat-suppressed T2W images, normal mus- • Many neoplasms have longer relaxation times than
cle signal intensity is much lower than water and higher the host tissue. This is generally thought to be from
than fat. increased water content; this too will induce increased
• Normal muscle fascicles (bundles of muscle fibers) are signal on T2W images for example.
separated from one another by fat-containing septa, • In cases of fibrosis there is a decrease in proton density,
which gives muscle bellies a ‘feathery’ or ‘marbled’ which will be associated with a decreased MR signal.
appearance on non-fat suppressed images. • Fatty infiltration shortens T1 relaxation times, causing
increased signal on T1W images.1 This signal is typically
Synovium/synovial fluid decreased when fat suppression is employed.
• The synovium is not often identified unless there is • Hemorrhage will cause variable changes depending on
pathology causing joint effusion or intra-articular con- the age of hemorrhage and changing concentrations of
trast techniques are employed that allow distension of the different by-products of degradation of hemoglobin
the joint capsule and higher contrast.12–15 over time, which all have different magnetic properties.
• Synovial fluid has very high signal on T2W images and In addition, the associated inflammation and edema may
low signal on T1W images. Its high signal on T2W images prolong T1 and T2 relaxation times and compound the
provides excellent natural contrast to the intra-articular net changes in signal.1 T2*W gradient echo images are
structures (e.g., cruciate ligaments, menisci), which are useful to identify the susceptibility artifacts associated
typically hypointense. Joint effusion therefore creates a with some by-products of hemoglobin, which will form
spontaneous ‘arthrogram’ effect on T2W images. areas of signal void within the lesion.
• Advanced MRI techniques can be used to detect and
Changes in signal induced by quantify early degenerative changes of articular carti-
musculoskeletal pathology lage, although these have been so far only described in
• Pathology will influence the mobility and density of pro- experimental studies:17,18
tons, and these changes will cause modifications in sig- • ‘Delayed gadolinium enhanced MRI of cartilage’
nal that can be emphasized by an appropriate choice of (dGEMRIC) is a technique that quantifies the accu-
the combination of pulse sequences used. The process of mulation of gadolinium in articular cartilage after
‘extracting information about tissue type and pathology intravenous injection, by way of calculation of the
by MR techniques’ has been called ‘tissue characterization’.1 T1 relaxation time of cartilage. In early cartilaginous
• Tissues can be described by signal intensity, texture, and, degeneration, there is depletion of negatively charged
to some degree, size. Table 4.3.3 summarizes the changes glycosaminoglycans, causing relatively more pos-
in relaxation times that are induced by common muscu- itively charged areas. As a result, these degenerated
loskeletal pathologies. areas will accumulate more negatively charged gado-
• Although this has not be thoroughly evaluated in small linium. This causes glycosaminoglycan-poor regions
animals, MRI has demonstrated superiority to radiogra- of cartilage to have a decrease in their T1 relaxation
phy and computed tomography in people for the detec- time. The mean dGEMRIC index value in the normal
tion of subtle osteolysis, both in terms of volume and canine elbow cartilage at 3T was reported to be about
extent.16 Due to its superior soft tissue contrast, MRI is 400 ms.18
also better for assessment of the surrounding tissues.16 • ‘T2-mapping’ employs T2W MRI to map the T2
• Inflammation generally causes a prolongation of T1 and T2 relaxation time of cartilage. Damaged cartilage has
relaxation times, which is attributed to edema resulting in an increase in water content due to changes in the
increased water content.1 This will cause decreased signal interaction of the water molecules with the collagen
on T1W images and increased signal on T2W images. matrix and proteoglycans; this in turn increases the
T2 relaxation time of damaged cartilage, which can
be quantified with MRI. The mean T2 value in the
Table 4.3.3 Changes in relaxation times for common
musculoskeletal diseases.1
normal canine elbow cartilage at 3T was reported to
be about 56 ms.18
t1 ReLAXAtion t2 ReLAXAtion
• Calcification may be difficult to appreciate and diagnose
DiSeASe PRoCeSS tiMe tiMe with MRI, having a variety of appearances that depends
on the acute or chronic deposition and amount of asso-
Inflammation Increased Increased
ciated inflammatory response. Calcification within ten-
Neoplasia Increased Increased dons can be demonstrated as hypointensity (susceptibility
Fibrosis – Decreased artifact) on T2*W gradient echo images but this could
Fatty infiltration Decreased – also represent acute hemorrhage or gas.2 Correlation
Interstitial hemorrhage Increased Increased
with radiographs may therefore be indicated when calci-
fication is suspected on MR images.
134 CHAPTER 4.3
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CHOICE OF COIL Shoulder joint

• The patient is placed in lateral recumbency, with the
• The coil selection depends on the anatomic region under shoulder under investigation resting on top of a sur-
investigation.1 The imaging coil should approximate face or flex coil.12 Dedicated human shoulder receiving
the size and configuration of the anatomy to be investi- coils have also been used both in experimental studies
gated, thereby producing maximum signal-to-noise ratio of isolated limbs harvested from canine cadavers15,27 and
(SNR) and maximal spatial resolution.19 in studies on live dogs.33,34 However, in some cases their
• Quadrature surface coils are often preferred for muscu- shape may not be perfectly adapted to imaging of canine
loskeletal MRI because of their ease in patient position- shoulders due to the general difference in shape of the
ing and increased SNR over linear coils.20 They may be area between humans and dogs.
associated with a drop of signal for the deeper regions, • Although mild flexion of the shoulder joint (around 80°)
which could be a concern when imaging the coxofemoral has been reported to provide adequate visualization of the
joint and medial aspect of the shoulder. biceps tendon proximal to the humerus,27 an angle closer
• Volume coils provide more uniform SNR, but may not to the standing angle of 105°–115° is more appropriate
be suitable to image proximal regions of the limbs due for viewing the entire joint.33 In fact, it was shown that
to their geometry. Again, this is mostly a concern for the a more extended position (120°–150°) improved visual-
shoulder and hip. ization of some joint elements, in particular the medial
capsuloligamentous structures (medial joint capsule
JOINT SPECIFIC MR ANATOMY, IMAGING and medial glenohumeral ligament).12 These angles are
PLANES, AND PULSE SEQUENCES defined by estimating the degree of angulation between
the spine of the scapula and the long axis of the humerus.
There are excellent published resources describing the MRI • Positioning of the limb in the right posture can be
anatomy of the canine joints, and the reader is referred to secured using tape.
them for more in-depth information and illustrations, as an • The standard imaging planes are illustrated in
extensive description of the complex MRI anatomy of all Fig. 4.3.2.12 Sagittal images are parallel to the long axis
joints is beyond the scope of this textbook.12,14,21–29 of the scapula and humerus, dorsal images are parallel
to the long axis of the spine of the scapula and glenohu-
Muscles meral ligament, and transverse images are perpendicular
• Dorsal and transverse planes are ideal for separation of to the long axis of the spine of the scapula and glenohu-
muscle bellies. meral ligaments.12
• Subcutaneous fat, intermuscular fat, and bone marrow • Key anatomic features:
provide inherent contrast;30 however, fat suppression can • The biceps brachii tendon and sheath are best appre-
be useful to suppress the bright signal from fat and high- ciated on sagittal and transverse T2W series
light pathology. (Fig. 4.3.3) or arthrogram T1W series (Fig. 4.3.4).
• Spin echo pulse sequences are generally appropriate for The tendon is uniformly hypointense on T1W and
evaluation of muscles; both T1W and T2W spin echo
can be used. However, sequences with relatively short
TR and short TE (more T1W) are preferred as they have
higher SNR and shorter acquisition times.30
Bone
• Transverse images perpendicular to the long axis of the
120–150°
bones are most useful.

• Pulse sequences that are found valuable for imaging of
bone include T1W, T2W, and proton density spin echo
images as well as STIR. STIR images in particular are
quite useful for identification of abnormalities in the (a) (b) (c)
periarticular bone.31
• The greatest contrast between dense cortical bone and Fig. 4.3.2 Diagram showing the orientation of the imaging
marrow is observed on T1W and proton density spin planes for sagittal (a), dorsal (b), and transverse (c) imaging
echo pulse sequences.32 of the shoulder joint. (Adapted from, with permission,
• As mentioned previously, sequences with fat suppression Agnello KA, Puchalski SM, Wisner ER et al. (2008). Effect
(e.g., STIR) are useful to differentiate high T2 signal in of positioning, scan plane, and arthrography on visibility
the cancellous bone or medullary cavity that is due to of periarticular canine shoulder soft tissue structures on
normal conversion of red to yellow bone marrow from magnetic resonance images. Vet Radiol Ultrasound
pathologic changes (see above). 49(6):529–539.)
GT
(a) (b) (c)
GT
(d) (e) (f)

Fig. 4.3.3 Representative images of the shoulder in a normal dog, showing anatomic features of the shoulder joint. Transverse
T2W image (a) and transverse T1W image (d) at the level of the greater tubercle of the humerus (GT), sagittal T1W images
passing through the infraspinatus muscle tendon (b, c), and sagittal images passing through the supraspinatus muscle and
tendon (e, f). On all the images, the supraspinatus tendon is indicated by an open arrow as it inserts onto the cranial aspect of
the greater tubercle (GT), the infraspinatus muscle is indicated by a dashed arrow as it inserts onto the lateral surface of the
greater tubercle, and the biceps brachii tendon in the intertubercular groove is indicated by a solid arrow. Images (b) and (c)
were obtained along the lateral surface of the greater tubercle of the humerus, optimizing evaluation of the insertion of the
infraspinatus tendon. Images (e) and (f) were obtained through the plane of the greater tubercle, optimizing evaluation of
the insertion of the supraspinatus tendon. On the T2W image (a), a small amount of synovial fluid is seen within the sheath
of the biceps brachii tendon forming a thin hyperintense stripe surrounding the tendon. The arrowheads in (b) and (c) indicate
the spine of the scapula. (1.5T MRI system)
T2W images, originating from the supraglenoid to isointense to the muscles; however, at its broad
tubercle of the scapula and extending distally on the insertion onto the cranial aspect of the greater tuber-
craniomedial aspect of the shoulder joint in the inter- cle of the humerus, a consistent hyperintense signal is
tubercular groove. It transitions into muscle fibers seen on T2W and PDW images,35 as well as on T2*W
medial and slightly cranial to the humerus. This gradient echo images (Fig. 4.3.6).27 Histologically,
tendon is poorly visible on STIR images. The trans- the increased signal correlates to a fibrocartilaginous
verse humeral ligament, holding the biceps tendon in enthesis. This hyperintensity is a normal anatomic
place within the groove, may be seen on transverse feature of the supraspinatus enthesis, and should not be
images connecting the greater to the lesser tubercle mistaken for pathology.35
(Fig. 4.3.5). • The infraspinatus tendon is well visualized in all
• The supraspinatus tendon is well appreciated on sag- imaging planes on T1W and T2W series as well as
ittal and transverse T1W and T2W images and its T1W arthrogram (Fig. 4.3.3). It is poorly visualized
visibility is improved on sagittal T1W arthrogram in STIR images. It appears as a well-defined struc-
images (Fig. 4.3.3). The proximal portion of the ture, flattened in the mediolateral direction that
tendon within the muscle belly is slightly hypointense progressively thickens as it extends distally to insert
136 CHAPTER 4.3
VetBooks.ir
*
*
(a) (b)
Fig. 4.3.4 Sagittal T1W (a) and T1W-arthrogram (b) images of the shoulder in a normal dog. The biceps tendon is indicated by
the arrows. On the arthrogram, the joint capsule is distended by hyperintense fluid (asterisks), which extends down around the
biceps brachii tendon within the sheath.
Fig. 4.3.5 Transverse post-contrast T1W image of the

shoulder showing the biceps brachii tendon within the
intertubercular groove, as well as the transverse humeral Fig. 4.3.6 Sagittal T2W image of the shoulder in a normal dog
ligament (arrowhead). (1.5T MRI system) at the level of the insertion of the supraspinatus tendon onto
the cranioproximal edge of the greater tubercle. This image
shows the normal variations in signal of the insertion of the
tendon (arrow), which often appears hyperintense on T2W and
PDW images, while it is homogeneously hypointense on T1W
images. The rounded structures seen caudal to the humeral
head (arrowhead) correspond to a cross-section of the caudal
circumflex humeral artery and axillobrachial vein outlined by
fat. Note the small amount of markedly hyperintense synovial
fluid in the joint. (1.5T MRI system)
on transverse and dorsal images after intra-articular

injection of gadolinium,12,13 with the dorsal plane
arthrogram being optimal for identification of the
medial glenohumeral ligament (Fig. 4.3.8). On these
T1W arthrograms, the distension of the medial recess
of the joint capsule, located medial to the medial gle-
nohumeral ligament, allows one to identify this lig-
ament as a thin hypointense structure, best seen on
* S
dorsal T1W arthrograms. There is no similar joint
capsular recess along the lateral joint capsule, and
therefore the lateral glenohumeral ligament and
lateral joint capsule form a single ‘capsuloligamentous
complex’. When no arthrogram is performed, T2W
H
images are better than T1W images for evaluating the
capsuloligamentous structures, although at low field
they may not be distinguished, even on T2W images
in the absence of significant joint effusion.13 The joint
capsule may be slightly more visible on T1W images
after intravenous gadolinium injection due to mild
normal enhancement of this structure.
• Recommended pulse sequences, in chronologic order:
• Sagittal and transverse T1W spin echo.
• Sagittal, transverse, and dorsal T2W FSE.
• A sagittal STIR series is useful to evaluate for hyper-
intense lesions of the subchondral bone and entheses
to highlight pathology.
• Transverse T1W spin echo post intravenous injection
Fig. 4.3.7 Dorsal plane T1W image of the humeral joint of gadolinium (preferably with fat saturation).
in a normal dog demonstrating the subscapularis muscle • Sagittal, transverse, and dorsal T1W arthrogram
(asterisk) and tendon (arrow), medial to the joint. S, scapula; (post intra-articular injection of gadolinium):
H, humerus. (1.5T MRI system) – The contrast medium should be diluted in saline
prior to injection into the joint. Clinical studies
onto the lateral margin of the greater tubercle of the have used dilutions of 1:100 of gadolinium concen-
humerus. trated at 0.5 mmol/mL for MR arthrograms,12,13
• The subscapularis muscle and tendon are best appreci- but another study showed that a 1:1,200 dilution
ated in the transverse and dorsal planes on both T1W provided the best contrast without obscuring the
and T2W series (Fig. 4.3.7). The lateral margin of edges of the anatomic structures of interest.15
the tendon is better delineated on a T1W arthro- – 4–6 mL of the diluted solution should be injected
gram where it passes over the medial border of the into the joint after clipping and aseptic prepara-
distended joint capsule. The muscle courses along the tion of the injection site and aspiration of 2–3 mL
medial aspect of the scapula and the tendon inserts on of synovial fluid prior to injection of contrast
the lesser tubercle of the humerus immediately distal medium; 0.2 mL of epinephrine may be injected as
to the joint. well to retard the absorption of contrast medium.13
• The teres minor muscle and tendon are poorly visu- – Fat saturation is a useful modifier of the T1W
alized in any plane; the muscle originates from the arthrogram sequence, as it highlights the joint
caudal border of the scapula and transitions into a structures by suppressing the signal from fat;
hypointense small tendon that inserts on the teres on images without fat suppression, distinction
tubercle of the humerus, immediately caudodistal to between the hyperintense periarticular fat and
the infraspinatus tendon. This humeral insertion, hyperintense contrast medium may be difficult.15
immediately caudal to that of the infraspinatus – Possible pitfalls include the inadvertent injection
tendon, may be best appreciated on transverse plane of gas into the joint, which may lead to the false-
images. positive diagnosis of intra-articular loose bodies.
• The medial and lateral joint capsule and glenohumeral Gas bubbles tend to elevate to non-dependent
ligaments are closely associated and difficult to dis- regions of the joint, whereas loose bodies will
tinguish from each other. They are best appreciated gravitate to dependent locations.2 Extra-articular
138 CHAPTER 4.3
VetBooks.ir
(a) (b) (c)
*
G
(d) (e) (f)

Fig. 4.3.8 Dorsal plane T1W (a), T2W (b), and T1W-arthrogram (c) (after intra-articular injection of diluted gadolinium)
images at the level of the humeral joint, and transverse plane T1W (d), T2W (e), and T1W-arthrogram (f) images at the level of
the glenoid in a normal dog. On all the images, medial is to the left and lateral is to the right. In (a), (b), and (c), the thin arrow
points at the lateral capsuloligamentous complex and the arrowhead points at the tendon of the infraspinatus muscle. In (a), the
thick arrow points at the medial joint capsule together with the medial glenohumeral ligament, which are not resolved as they
are in contact with each other. In (c), after intra-articular contrast material injection, these two structures are now separated and
the medial glenohumeral ligament is visible separately, indicated by the thick arrow. S, scapula; H, humerus. In (d), the thin
arrow points at the medial joint capsule together with the glenohumeral ligament, which are not resolved as they are in contact
with each other. In (f), after intra-articular contrast material injection, these two structures are now separated and the medial
glenohumeral ligament is visible separately and indicated by the thin arrow. The arrowheads in (d) and (f) point at the lateral
capsuloligamentous complex, and the hypointense structure immediately lateral to it is the tendon of the infraspinatus muscle
(circle). *, supraglenoid tubercle; G, glenoid cavity. (1.5T MRI system; adapted with permission from Agnello KA, Puchalski SM,
Wisner ER et al. (2008). Effect of positioning, scan plane, and arthrography on visibility of periarticular canine shoulder soft
tissue structures on magnetic resonance images. Vet Radiol Ultrasound 49(6):529–539.)
leakage may also complicate interpretation and while PDW fat-saturated sequences have been
could mimic tears. To decrease the likelihood of reported for examination of fluid accumulation
extra-articular leakage, it is recommended not to in the joint and surrounding tendons.15,27 The
inject too large a volume of contrast solution and mid intensity of fat in the T2*W gradient echo
use a small gauge needle. sequence allows good separation and distinction
• T2*W gradient echo sequences have also been between closely associated hypointense ligaments
reported for examination of tendons and ligaments, and tendons. 27
Elbow joint distally to the proximolateral aspect of the radius.

• Compared with the shoulder and stifle joints, MRI It is normally thicker proximal to the humeroradial
of the elbow joint is in its infancy and not routinely joint than distal to it. On transverse images, it appears
performed.20,36 oval-shaped, and craniomedial to it on T2W images,
• The patient could be placed in lateral recumbency, with a small hyperintense spot can be seen representing
the elbow under investigation in the dependent portion, synovial fluid.
or in sternal recumbency. The elbow should be placed • The medial collateral ligament is inconsistently seen
roughly in an anatomic physiological position. on dorsal and transverse images, and is best appreci-
• Depending on the size of the patient, a circumferential ated on dorsal T1W images, forming a thin hypoin-
coil such as a human wrist coil can be used and placed tense linear structure running in a proximomedial
around the elbow joint.21 Circular surface coils have also to distolateral direction next to the medial coronoid
been used by applying the coil around the olecranon;37–39 process of the ulna. Like the lateral collateral liga-
with such coils, some degree of flexion of the elbow is ment, it is hypointense, similar to cortical bone.
necessary to fit the coil around the olecranon area. Small • The tendon of the triceps muscle attaching to the caudal
flex coils may also be used. aspect of the olecranon tuberosity is best evaluated
• Imaging planes are illustrated in Fig. 4.3.9.21 The trans- on sagittal images and is mildly hypointense on T1W
verse plane is defined as parallel to the articular surface images and markedly hypointense on T2W images.
of the radial head. The sagittal plane is perpendicular • The pronator teres muscle is best seen on sagittal
to the transverse plane and parallel to the limb’s sagit- images. It originates at the craniomedial aspect of the
tal plane. The dorsal plane is perpendicular to both the distal humerus and passes cranial to the medial epi-
transverse and sagittal planes and roughly parallel to the condyle to extend along the cranioproximal third of
plane of the radioulnar interosseous ligament.21 the radius; its signal intensity is between fat and cor-
• Key anatomic features of the elbow joint have been tical bone, with the tendon having the same intensity
described at low field (Figs. 4.3.10, 4.3.11):21 as the muscle.
• The lateral collateral ligament is best identified in the • The flexor carpi radialis muscle is best seen on sagittal
transverse and dorsal planes, and forms a hypointense and dorsal images. It originates from the medial epi-
band on both T1W and T2W images originating condyle as a hypointense tendon caudal to the prona-
from the lateral humeral epicondyle and attaching tor teres muscle. Its proximal origin is readily seen on
Fig. 4.3.9 Sagittal (a) and

dorsal (b) T1W images of
the elbow in a normal dog,
illustrating the orientation
of the dorsal (solid line),
transverse (dashed line),
and sagittal (dotted line)
planes for elbow imaging in
the dog. (0.2T MRI system;
images courtesy of Dr. Yseult
(a) (b)
Baeumlin, University of Ghent)
140 CHAPTER 4.3
Tric
Bice
eps
ps b
bra
chii
rach
ii
Flexor carpi
radialis tendon Triceps muscle tendon
Flexor digitorum Flexor carpi
(a) profundus tendon (b) ulnaris tendon (c)
Triceps muscle
tendon
Flexor carpi
radialis tendon
*
Flexor
digitorum R
profundus The 2 heads of the flexor U
tendon carpi ulnaris muscle
Flexor digitorum
superficialis muscle
(d) (e) (f)
Fig. 4.3.10 Adjacent sagittal T2W images (a, b, c) and T1W images (d, e, f) of the elbow in a normal dog, outlining the
anatomic features of the elbow joint and periarticular structures that can be identified on MRI. Pairs (a, d), (b, e), and (c, f) are
approximately at the same level of the elbow. Star (a, d), medial humeral epicondyle; asterisk (f), anconeal process; H, humerus;
U, ulna; R, radius. (0.2T MRI system; images courtesy of Dr. Yseult Baeumlin, University of Ghent)
dorsal images extending distally from the most prom- to the caudal margin of the medial epicondyle,
inent part of the medial epicondyle. with a small pocket of synovial fluid seen cranial
• The flexor digitorum superficialis muscle is best seen in to it on the T2W images.
the sagittal plane, caudal to the flexor carpi radialis. Its – The ulnar head originates as a broad-based ten-
origin is at the most caudal aspect of the medial epi- don from the proximomedial aspect of the olecra-
condyle and is well seen on sagittal and dorsal images; non, and extends then caudally and laterally to the
it appears as a moderately hypointense broad-based humeral head. It is best appreciated on sagittal and
band on the dorsal images. transverse images.
• The flexor carpi ulnaris muscle has a humeral and an • The extensor carpi radialis muscle originates from a
ulnar head (Fig. 4.3.11): crest on the lateral aspect of the humeral condyle, and
– The humeral head originates from the caudal can be appreciated on transverse and sagittal images.
margin of the medial epicondyle, and both ori- • The extensor digitorum communis muscle originates
gin and belly can be seen on sagittal images. Its as a markedly hypointense tendon on the lateral
tendon of origin, hypointense on both T1W and humeral epicondyle and extends distally along the
T2W images, is best seen on transverse images, lateral surface of the radius. It is best appreciated on
forming a crescent-shaped structure conforming dorsal plane images.
(a) • The extensor digitorum lateralis muscle also originates

Brachialis muscle on the lateral humeral epicondyle as a hypointense
Biceps brachii muscle tendon immediately lateral and adjacent to the lateral
Extensor carpi collateral ligament, and extends distally traveling
radialis muscle caudal to the extensor digitorum communis, along the
lateral aspect of the radius. It is best appreciated on
dorsal plane images.
• The tendon of origin of the extensor carpi ulnaris muscle
is best appreciated on transverse images as a hypoin-
Lateral collateral tense structure that is rounded to ovoid, located at the
Med Epic Lat Epic ligament caudolateral aspect of the lateral humeral epicondyle,
immediately caudal to the lateral collateral ligament
of the elbow joint (Fig. 4.3.11).
Flexor carpi U Extensor carpi • The biceps brachii muscle and tendon of insertion are
ulnaris tendon ulnaris tendon best appreciated on sagittal and transverse images
(humeral head) Anconeus muscle in the craniomedial aspect of the elbow. The hypoin-
Ulnar head of the flexor carpi ulnaris muscle tense tendon fibers form hypointense structures in
the middle of the muscle at the level of the humeral
(b) condyle (Fig. 4.3.11), which transition into a hypoin-
tense band that distally attaches onto the medial
tuberosity of the proximal radius and tuberosity of the
proximal ulna.
• The subchondral bone has low signal intensity on
T1W/T2W spin echo sequences as well as coherent
(steady-state) gradient echo pulse sequences (e.g., 3D
gradient echo fast imaging with steady-state precession
[3D GE FISP] on Siemens, fast multi-planar gradient
Lat recalled acquisition in the steady state [FMPGR] on
Med General Electric, or fast field echo [FFE] on Phillips),
Epic
Epic
while the bone marrow in the adjacent cancellous
bones and medullary cavities of the distal humerus,
proximal radius, and ulna is hyperintense.39
• The articular cartilage has variable signal intensity
depending on the pulse sequence used:39
U R – On T1W and T2W spin echo images, it is isoin-
tense to muscles.
– On coherent (steady-state) gradient echo images it
is isointense to slightly hyperintense to muscles.
– On incoherent (spoiled) gradient echo sequence
with fat saturation (e.g., 3D fast low angle shot
[FLASH] on Siemens), the articular cartilage is
isointense40 to hyperintense39 to muscle.
– On all pulse sequences, in normal joints, the
opposing articular cartilage surfaces cannot be
Flexor digitorum Extensor digitorum
superficialis muscle lateralis muscle
distinguished from each other and summate with
each other.39 This is true even at higher magnetic
fields such as 3T,40 although in larger dogs and
Flexor digitorum with longer scan times, it may be possible to sepa-
profundus muscle
rate the opposing articular surfaces.7
Fig. 4.3.11 Transverse (a) and dorsal plane (b) T1W images • Clinically relevant osseous structures:
of the elbow in a normal dog. Med Epic, medial humeral – Coherent (steady-state) gradient echo pulse
epicondyle; Lat Epic, lateral humeral epicondyle; U, ulna; sequences (e.g., 3D GE FISP, FMPGR, FFE) are
R, radius; star, anconeal process; open arrow, medial coronoid more adequate for assessment of the subchondral
process of the ulna. (0.2T MRI system; images courtesy of bone, medial coronoid and anconeal processes of
Dr. Yseult Baeumlin, University of Ghent) the ulna.39 3D acquisitions are preferred, as they
142 CHAPTER 4.3
• MR arthrography of the elbow joint can be per-

formed by injecting 5–6 mL of a diluted solution
(1:250; i.e., 0.002 mmol/mL) of gadolinium into the
joint. This typically still does not allow separation
of opposing adjacent articular surfaces, and can in
fact obscure the articular cartilage due to the bloom-
U ing effect of the hyperintense signal from the con-
trast infused synovial fluid. Infusion of gadolinium
into the joint can help to differentiate completely
detached from partially attached fragments of the
R medial coronoid process, although this has low diag-
nostic importance.38
• Recommended pulse sequences, in chronologic order:
• Dorsal, sagittal, transverse T1W spin echo with thin
slices (2–3 mm): assessment of tendons/muscles, col-
lateral ligaments.
• Sagittal T2W TSE/FSE: assessment of tendons/
muscles, presence/degree of joint effusion.
• Dorsal STIR (or fat-saturated T2W spin echo): detec-
tion of inflammation/edema in the articular/periar-
ticular soft tissues, detection of bone marrow lesions
Fig. 4.3.12 Transverse T1W image of a normal canine elbow (e.g., subchondral bone edema, cellular infiltrates),
at the level of the medial coronoid process of the ulna (arrow). detection of incomplete ossification of the humeral
U, ulna; R, radius. (3T MRI system) condyle.
• 3D coherent (steady-state) gradient echo pulse
allow thinner slices to be obtained at a better sequences (e.g., 3D GE FISP, FMPGR, FFE) refor-
SNR, which can be critical for small structures matted in the adequate planes for evaluation of the
such as the medial coronoid process. subchondral bone, medial coronoid and anconeal
– The medial coronoid process of the ulna has a low processes of the ulna, medial ridge of the humeral
signal intensity on T1W/T2W spin echo images trochlea.
(Fig. 4.3.11) as well as gradient echo.39 Its artic- • 3D spoiled gradient echo sequences with fat suppres-
ulation with the medial aspect of the humeral sion may be added for a clear evaluation of the interos-
condyle is best seen on sagittal images, while its seous space for congruity (sagittal images).
articulation with the radial head is best appreci- • Post-contrast (intravenous) dorsal, sagittal, transverse
ated on transverse images (Fig. 4.3.12). T1W spin echo with thin slices (2–3 mm): detection
– The anconeal process is best appreciated on sagit- of enhancement in inflamed tissues (e.g. flexor enthe-
tal images (Fig. 4.3.10). sopathy41).
– The medial ridge of the humeral trochlea, a com-
mon location of osteochondrosis, is best evaluated Stifle joint
on dorsal plane images. • Although commonly performed in people, stifle MRI is
– The congruence of the elbow joint can be assessed not as widely used in veterinary medicine, which in part
on sagittal images such as spoiled gradient echo is due to added cost, lack of comfort, and experience with
sequences with fat suppression (e.g., 3D MPGR, the modality and the ability to perform arthroscopy at
3D FLASH) on which the subchondral bone and the time of surgery. However, arthroscopy provides lim-
marrow signals are very dark in contrast with the ited visibility and is not able to assess the extra-articular
iso- to hyperintense articular cartilage. On sagit- structures, lesions located underneath the articular
tal images, the proximal humeroulnar interosse- surfaces, or lesions affecting the tibial surface of the
ous space at the cranial extremity of the anconeal menisci.6,20,42 In contrast, the menisci, cruciate liga-
process is normally narrower in large breed dogs. ments, collateral ligaments, long digital extensor tendon,
The mid to cranial humeroradial interosseous infrapatellar fat pad, synovium, and synovial fluid can all
space is also normally narrower, in comparison be evaluated with MRI.20
with the interosseous space at the center of the • Several options can be used for positioning:
trochlear notch, giving a visual impression of mild • Lateral recumbency with the investigated limb in
incongruity; this degree of ‘incongruity’ is a nor- the dependent position on a surface coil.20 An addi-
mal variation in these breeds.40 tional flexible surface coil can be also placed along the
medial aspect of the stifle to improve signal from the plane parallel to the tibial plateau or perpendicular to the
non-dependent surface of the joint.43 patellar ligament (Fig. 4.3.13).
• Lateral recumbency with the investigated limb in • Slice thickness should be 3 mm on spin echo sequences
the non-dependent position if an extremity coil is with thin gap or no gap, and can be reduced when using
used.14 Dorsal recumbency can also be used with such 3D gradient echo sequences. The field of view (FOV)
coils.22,28 The smallest extremity coil that can fit the should be small (10–12 cm) and matrix size should be at
stifle joint should be used to improve SNR. least 256 × 192.19
• Although extension of the limb has been recom- • Key anatomic features (Fig. 4.3.14):
mended in some studies, with a femorotibial angle of • The cranial and caudal cruciate ligaments are best
145°,14,28 recent studies showed that a flexed position at appreciated on sagittal images and to a lesser degree
90° improves the visualization of the cranial cruciate in the dorsal plane, forming homogeneous hypoin-
ligament in all imaging planes,44 although the effect tense bands. They may not be entirely visible on a
of flexion on visibility of other structures of interest single image due to their oblique/spiral orientation.
has not been reported so far. The downside of this • The patellar tendon is best evaluated on sagittal
flexed position is that it requires the use of a larger images, forming a hypointense band connecting the
extremity coil to fit the flexed joint in. This may cause apex of the patella to the tibial tuberosity of the prox-
some decrease in SNR, and the smallest extremity coil imal tibia.19
that can accommodate the flexed stifle joint should be • The lateral and medial menisci are best identified on
used to minimize this effect. dorsal and sagittal plane images:14,19,22,28
• Restraining tools, such as tape and foam wedges, – On sagittal images, each meniscus forms a low
should be used to maintain the limb in a stable posi- intensity structure with a characteristic ‘bow-tie’
tion during scanning. shape corresponding to the cranial and caudal
• Several options have been used to define the imaging horns; each horn assumes a triangular shape with
planes for MRI of the stifle; however, in general, the the base located cranially (cranial horn) or cau-
sagittal plane is defined to be parallel to the surface of dally (caudal horn) and the apex pointing towards
the medial femoral epicondyle, which in effect makes the center of the joint.
this plane roughly parallel to the orientation of the cra- – On dorsal plane images, the menisci have a tri-
nial cruciate ligament.14,20,28,44 The dorsal plane should angular shape with their base towards the lateral
be parallel to the patellar ligament and the transverse (lateral meniscus) or medial (medial meniscus)
MED LAT
Fig. 4.3.13 Dorsal (a) and sagittal (b)

PDW fast spin echo images of the stifle
in a dog showing the orientation of
standard imaging planes. The solid line
depicts orientation of the sagittal imaging
plane, parallel to the medial surface
of the medial femoral epicondyle, the
dashed line shows the orientation of the
transverse imaging plane, perpendicular
to the patellar ligament, and the dotted
line shows the dorsal plane orientation,
parallel to the patellar ligament. MED,
(a) (b)
medial; LAT, lateral. (1.5T MRI system)
144 CHAPTER 4.3
MED LAT *
(a) (b) (c)
(d) (e) (f)

Fig. 4.3.14 Dorsal T2W fast spin echo (a) and serial sagittal (b through f, lateral to medial) PDW fast spin echo images of the
stifle in a normal dog, highlighting some anatomic features identifiable with MRI. White arrowheads, caudal horns of the
medial and lateral menisci; solid red arrow, meniscofemoral ligament; open arrow, popliteal sesamoid bone; dotted arrows,
cranial and caudal horns of the lateral meniscus; asterisk, infrapatellar fat pad; red arrowhead, patellar ligament; solid white
arrows, cranial cruciate ligament; dashed arrow, caudal cruciate ligament; open arrowheads, cranial and caudal horns of the
medial meniscus. (1.5T MRI system)
joint surfaces, and their apex pointing towards the • The caudal aspect of the joint capsule is best appreci-
center of the joint. ated on sagittal images, forming a hypointense linear
– On sagittal images, the caudal margin of the lat- structure.22
eral meniscus can appear indistinct in the area • The articular cartilage is of intermediate signal inten-
where it abuts the tendon of the popliteal muscle, sity on T1W and T2W spin echo images and diffi-
especially in smaller dogs and at low field. This cult to distinguish from the synovial fluid.14 It is of
should not be mistaken for a lesion.14,22 high signal intensity on gradient echo images, which
– On T2*W gradient echo imaging, an inhomoge- are preferred for cartilage evaluation.19,22 In large
neous increased signal in the central part of normal breed dogs such as working dogs, the articular carti-
menisci not extending to the periphery has been lage measures about 2 mm thickness with the thick-
reported with low-field magnets.14 Mottled signal est being the patellar cartilage, when imaged using a
of normal menisci has also been reported with gra- fat-saturated 3D spoiled gradient echo pulse sequence.19
dient echo pulse sequences, and should not be mis- • The meniscofemoral ligament is best seen on dorsal
taken for pathology (Fig. 4.3.15).42,43 plane images of the caudal joint region within
• The lateral and medial collateral ligaments are best the intercondylar fossa, forming a thick hypointense
seen on dorsal plane images, where they form hypoin- structure extending from the medial margin of the
tense bands vertically oriented; they can also be caudal horn of the lateral meniscus to the proximolat-
appreciated on transverse images.14,19,22,28 eral border of the medial femoral condyle.14,22,28
(a) (b)
Fig. 4.3.15 Sagittal 3D T2*W spoiled gradient recalled echo image (a) and dorsal PDW fast spin echo image (b) of the stifle
joint in a normal dog. Note the mottled appearance of the meniscus on the gradient echo image (white arrow, a) versus the
homogeneous hypointense appearance on the PDW image (black arrows, b). (1.5T MRI system)
• The transverse ligament of the stifle, which connects be used.14 Reported benefits of stifle MR arthrography
the cranial horns of the medial and lateral menisci, include:
is best appreciated on dorsal images passing by the • Improved visualization of the cranial and caudal cru-
cranial aspect of the menisci. It forms a horizontal ciate ligaments.
hypointense band-like structure.22 • Better differentiation between meniscal tears and
• The tendon of the extensor digitorum longus muscle degenerative changes.
can be seen in the sagittal and transverse planes • At high-field (1.5T), better visualization of some ana-
originating from the extensor fossa at the craniolat- tomic components such as the popliteomeniscal fasci-
eral aspect of the lateral femoral condyle. It forms a cles connecting the caudolateral margin of the lateral
thin elongated band traveling distally in the sagittal meniscus to the musculotendinous portion of the
images and an oval-shaped hypointense structure in popliteal muscle.19
the transverse plane adjacent to the craniodistolateral • Better visualization of the joint capsule when the joint
surface of the lateral femoral condyle.28 is distended by the contrast material.
• The tendon of the popliteus muscle is best seen on • Recommended protocol for stifle imaging, in chrono-
transverse images, forming a hypointense band arising logical order:
from the craniolateral surface of the lateral femoral • Sagittal and dorsal T1W spin echo.
condyle (popliteal fossa, caudal to the extensor fossa) • Sagittal and transverse T2W TSE/FSE, with fat sat-
and running caudodistally from that point along the uration.
lateral surface of the lateral femoral condyle.28 • Dorsal STIR to look for areas of subchondral bone
• MR arthrography of the stifle joint has been reported.14,19 lesions, in particular in the intercondylar fossa of the
Gadolinium diluted in saline at 1:100 (resulting in a con- distal femur and in the intercondylar eminence of the
centration of 0.005 mmol/mL) has been used. In large tibia.31
breed dogs, 10–15 mL of diluted gadolinium are injected • Sagittal and dorsal proton density TSE/FSE for
into the joint after retrieving an equivalent amount of meniscal assessment.
synovial fluid. The limb is then flexed and extended sev- • Fat saturated 3D spoiled gradient echo pulse sequence
eral times to allow good diffusion of the contrast mate- could be considered if specific assessment of the artic-
rial within the joint. A T1W spin echo sequence with ular cartilage is desired.19
fat saturation is then obtained in the sagittal and dorsal • Sagittal and dorsal post-contrast T1W spin echo
planes; a T1W gradient echo pulse sequence can also images could be added if needed.
146 CHAPTER 4.3
• Sagittal and dorsal T1W arthrography after intra-ar- • The short radial collateral ligament is best seen on
ticular injection of diluted gadolinium may be consid- dorsal plane images, and has two portions:
ered, in selected cases. – The straight portion originates on a tubercle prox-
• If specific assessment of the cranial cruciate ligament imal to the styloid process of the radius and inserts
is deemed insufficient on images with a femorotibial on the medial part of the radial carpal bone.
angle of 145°, repeat sagittal images with the limb – The oblique portion originates from the styloid
flexed at 90° may be considered.44 process of the radius and inserts on the palmar
aspect of the radial carpal bone.
Coxofemoral joint • The multiple short intercarpal ligaments that link
• For imaging of the coxofemoral joints, the patient should adjacent carpal bones can be appreciated on dorsal
be placed in dorsal recumbency on a surface coil or flex- plane images.
ible body coil, with the pelvic limbs extended. • The palmar ulnocarpal ligament runs from the
• Sagittal plane for coxofemoral imaging is parallel to the medial aspect of the distal ulna to the palmar surface
patient’s sagittal plane. The dorsal and transverse planes of the radial carpal bone and can be seen on dorsal
may be tilted off a bit from the standard dorsal and trans- plane images.
verse planes to account for the slightly tilted orientation • The palmar radiocarpal ligament runs from the
of the pelvis. palmar aspect of the distal radius and attaches to
• Imaging series may include: the lateral aspect of the radial carpal bone. It is best
• Transverse, sagittal, dorsal planes T1W spin echo. appreciated on sagittal plane images.
• Dorsal plane STIR. • The palmar radiocarpal-metacarpal ligament runs
• Dorsal plane T2W TSE/FSE with fat saturation. from the palmar aspect of the radial carpal bone and
• If indicated, post-contrast T1W spin echo in dorsal attaches to the palmar aspect of the proximal meta-
+/- transverse plane. carpal bones II and III. It is best appreciated on sagit-
tal plane images.
Carpus–manus • The accessorio-ulnocarpal ligament runs from the
• The patient can be scanned in lateral recumbency with dorsodistal border of the accessory carpal bone to the
the affected limb dependent on a surface coil, in a neutral ulnar carpal bone and is best seen on sagittal images.
position similar to that used for a lateral radiograph of • Adjacent to it is the accessorio-quartile ligament,
the carpus.20 Dedicated wrist coils or small flex coils can which runs from the accessory carpal bone to the 4th
also be used to improve circumferential SNR. carpal bone and is also best seen on sagittal images.
• Dorsal plane images are defined as the plane contain- • The accessorio-metacarpal ligaments connect the
ing the metacarpal bones. The sagittal plane is perpen- accessory carpal bone to the bases of the 4th and 5th
dicular to that dorsal plane, and the transverse plane is metacarpal bones and are best seen on sagittal plane
perpendicular to the long axis of metacarpal bones III images.
and IV. • The deep and superficial digital flexor tendons of
• Key anatomic features:25,26 the manus, as well as the common and lateral digital
• Most ligaments of the carpal region can be adequately extensor tendons, are best evaluated on transverse
evaluated with MRI; on T1W spin echo images they images, forming small oval- or crescent-shaped struc-
appear as homogeneous hypointense bands and on tures dorsal (extensors) or palmar (flexors) to the
gradient echo images they appear as uniform or stri- metacarpophalangeal bones (Fig. 4.3.16). They can
ated low signal intensity bands. also be evaluated on sagittal images, although that
• The radioulnar ligament and articular disc between plane may not be perfectly aligned with all individual
the distal radius and ulna cannot be distinguished tendons, especially for digits 2 and 4.
from each other and are best appreciated on dorsal • The digital pads and carpal pad can be seen on the
plane images. transverse images forming rounded to oval-shaped
• The palmar carpal fibrocartilage forms a hypoin- hyperintense structures on T1W images.
tense sheet along the palmar surface of the proxi- • The interosseous muscles are seen proximal to the
mal metacarpal bones and carpal bones (except the carpal pad along the palmar aspect of the metacarpal
accessory carpal bone); it is best appreciated on a region, forming hyperintense structures extending
dorsal plane image passing by the palmar surface of proximally from the metacarpophalangeal sesamoid
the carpus. bones (Fig. 4.3.16).
• The short ulnar collateral ligament runs from the • The abductor pollicis longus tendon can be appreciated
styloid process of the ulna to the ulnar carpal bone on transverse images obtained at the level of the distal
and is seen on dorsal plane images along the more carpal row. Other abductor structures such as the
palmar surface of the carpus. abductor digiti V muscle can also be seen at that level.
* *
(a) (b)
Fig. 4.3.16 Transverse PDW image of the pes (a) and transverse 3D gradient echo T1W image of the manus (b) at the level
of the metatarsal and metacarpal bones, respectively, showing the branches of the flexor digitorum superficialis tendon (open
arrows) and flexor digitorum profundus tendon (solid arrows) along the plantar/palmar surfaces of the pes/manus. Along the
dorsal surface, the branches of the extensor tendons are visible (dotted arrows). Plantar/palmar to the metatarsals/metacarpals,
the interosseous muscles form a lobulated mass of intermediate signal intensity (asterisk). (1.5T MRI system)
• FOV should be kept small (10 × 10 cm) with thin slices dorsal plane is perpendicular to the sagittal and trans-
(2 mm), no interslice gap, and a reasonably large matrix verse planes, aligned with the plane of the metatarsal
size (256 × 192 or 256 × 256). Pulse sequences should bones (Fig. 4.3.17).23
include: • Most soft tissue structures of the tarsus can be identi-
• T1W spin echo in the dorsal and sagittal planes with fied with MRI. Detailed anatomic atlases are available
thin slices. (Figs. 4.3.18, 4.3.19):23
• T2W TSE/FSE with fat saturation in the sagittal • The transverse plane allows good assessment of the
planes. dorsal, plantar, medial, and lateral tendons of the
• PDW fast spin echo with fat saturation in the trans- tarsus. Some intertarsal and tarsometatarsal liga-
verse, dorsal, and sagittal planes. ments can also be seen on transverse images but are
• 3D T2*W gradient recalled echo pulse sequence in generally better visualized in the dorsal plane:
the steady-state can also be used to obtain thinner – The medial and lateral collateral ligaments of the
slices (1 mm or less) that can be useful to identify tarsus are also best identified on transverse images
smaller ligamentous structures. where they form thin hypointense bands along the
• Post-contrast T1W series may be considered in medial and lateral borders of the tibiotarsal joint.
selected cases. – The hypointense tendons of the tibialis cranialis
and extensor digitorum longus muscles can be identi-
Tarsus–pes fied dorsal to the talocrural joint.
• The patient can be scanned in lateral recumbency with – More distally, at the level of the central and distal
the affected limb dependent on a surface coil, with the tarsal rows and proximal metatarsals, the small
limb in a neutral position, similar to that used for a lat- rounded to oval-shaped hypointense tendon of
eral radiograph of the tarsus. Dedicated wrist coils or the extensor digitorum longus muscle can be appre-
small flex coils can also be used to improve circumfer- ciated superficially on midline, while the flat
ential SNR. hypointense tendon of the tibialis cranialis mus-
• The transverse plane is defined as perpendicular to the cle deviates medially to attach onto the vestigial
long axis of the calcaneus. The sagittal plane is defined rudiment of metatarsal I and proximal extrem-
as parallel to the sagittal plane of the calcaneus, and the ity of metatarsal II. At that level, immediately
148 CHAPTER 4.3
(a) (b) (c)

Fig. 4.3.17 Dorsal (a, b) and sagittal (c) T1W images of the tarsus in a normal dog illustrating the general orientation
of standard imaging planes for MRI of the tarsus; transverse plane orientation is shown in (a), sagittal plane orientation
in (b), and dorsal plane orientation in (c). (1.5T MRI system; reproduced, with permission, from Deruddere KJ, Milne ME,
Wilson KM et al. (2014). Magnetic resonance imaging, computed tomography, and gross anatomy of the canine tarsus.
Vet Surg 43(8):912–9.)
C
*
T
CT
T4
T2 T3 CT
T3
(a) (b) (c) (d)

Fig. 4.3.18 Serial dorsal plane T2W fast spin echo images of the tarsus in a normal dog highlighting some anatomic features.
C, calcaneus; CT, central tarsal bone; T4, 4th tarsal bone; T2, 2nd tarsal bone; T3, 3rd tarsal bone; T, talus; asterisk, medial
malleolus; star, lateral malleolus; arrows, medial and lateral ridges of the trochlea of the talus. (1.5T MRI system)
plantar to the tendon of the extensor digitorum hypointense linear structure extending along the
longus muscle, the bellies of the extensor digitorum lateral aspect of the distal calcaneus and over the
brevis muscle can be seen. lateral border of the 4th tarsal bone.
– Plantar to the metatarsal bones, the interosse- – PDW images with fat saturation allow identification
ous muscles are visible and silhouette with each of the intertarsal and tarsometatarsal ligaments,
other, forming a lobulated mass of medium signal plantar ligaments, and other support structures.
intensity. • The sagittal plane images are good for assessment
– Plantar to these muscles, the oval- or of selective bony structures such as the ridges of the
crescent-shaped hypointense branches of the flexor talus, especially on PDW images. PDW images are
digitorum profundus and then flexor digitorum super- also good for evaluation of tendons surrounded by
ficialis tendons are visible (Fig. 4.3.16). fluid, such as the gastrocnemius tendon, flexor digitorum
• The dorsal plane allows excellent assessment of superficialis tendon on images centered on the calcaneal
numerous structures: tuberosity, and the flexor digitorum profundus tendon
– The bones and joints of the tarsus are easily visible on images immediately medial to the calcaneus. On
(Fig. 4.3.18). images centered on the calcaneal tuberosity, the distal
– Tendons attaching onto the calcaneal tuberosity, continuation of the flexor digitorum superficialis tendon
such as the gastrocnemius tendon, flexor digitorum can be appreciated on T1W sagittal images, forming a
superficialis tendon, and common calcaneal ten- thin hypointense structure traveling distally, plantar to
don of the gracilis, semitendinosus, and biceps femoris the tarsal and metatarsal bones (Fig. 4.3.19); on these
muscles, can also be evaluated on images adjacent images, the bellies of the extensor digitorum brevis
to the extremity of the calcaneal tuberosity. muscle can be seen dorsal to the tarsometatarsal joints,
– Medial and lateral tendons, such as the flexor digi- forming a fusiform area of medium signal intensity
torum profundus passing along the medial surface originating from the distodorsal surface of the calca-
of the calcaneus, medial and lateral collateral neus and extending distally. Dorsal to these, the long,
ligaments, thick plantar ligaments, such as the thin, markedly hypointense tendon of the extensor dig-
calcaneo-quartile ligament, and plantar support itorum longus muscle is clearly visible.
structures of the tarsus can be identified on T1W • FOV should be kept small (10 × 10 cm) with thin slices (2
images. The calcaneo-quartile ligament runs mm), no interslice gap, and a reasonably large matrix size
from the lateral surface of the calcaneal body and (256 × 192 or 256 × 256). Pulse sequences should include:20,23
extends distally to attach to the 4th tarsal bone and • T1W spin echo in the dorsal and sagittal planes.
then the base of metatarsals IV and V. On dor- • T2W TSE/FSE with fat saturation in the sagittal
sal T1W images it can be seen forming a thin plane.
Ext Dig Longus

Gastroc
Fig. 4.3.19 PDW fast
spin echo images in the
Tibialis transverse plane (a) and
cranialis sagittal plane (b) in a
C normal dog, highlighting
some anatomic features.
T Ext Dig Longus DDF, flexor digitorum
profundus tendon;
SDF SDF, flexor digitorum
MED LAT superficialis tendon; Ext
Dig Longus, extensor
digitorum longus tendon;
C Gastroc, gastrocnemius
muscle tendon; arrowhead,
mm.
trochlear ridge of the talus;

DDF C, calcaneus; T, talus;
Interosseous
open arrow, talocalcaneal

interosseous ligament.
SDF MED, medial; LAT, lateral.
(a) (b)
(1.5T MRI system)
150 CHAPTER 4.3
VetBooks.ir
• PDW fast spin echo with fat saturation in the trans- This is because in spin echo sequences, the 180°
verse, dorsal, and sagittal planes. refocusing pulse applied between the initial 90° radi-
• 3D T2*W gradient recalled echo pulse sequence in ofrequency pulse and readout of the signal corrects
the steady-state can also be used to obtain thinner for the static field inhomogeneities and limits signal
slices (1 mm or less) that can be useful to identify loss related to intravoxel dephasing (T2* effect); such
smaller ligamentous structures. a rephasing pulse does not exist with gradient echo
• Post-contrast T1W series may be considered in pulse sequences, making them particularly sensitive
selected cases. to field inhomogeneities.45
• TSE/FSE pulse sequences generally decrease the
ORTHOPEDIC HARDWARE intensity of the artifact in comparison with simple
AND MRI ARTIFACTS spin echo sequences, due to the multiple refocusing
180° pulses applied during the TR. The artifact can
• In patients that do not respond favorably, or as well as be even further reduced by using a shorter TE time,
expected, after orthopedic surgery, MRI examination making T1W and PDW images generally less sensi-
can be indicated to evaluate for causes when radiographs tive to the artifact than T2W images.
do not provide a clear explanation. For example, a com- • Pulse sequences using spectral fat saturation are more
mon cause of continued or recurring lameness after cra- sensitive to the artifact as the resonant frequency of fat
nial cruciate surgery is the development of late meniscal is affected by the presence of the metallic implants.45
injuries.45 Although not completely immune to the artifact,
• Metallic objects, such as near ferromagnetic implants pulse sequences using inversion recovery to null the
used in orthopedic surgery, can pose problems when per- signal of fat (STIR) are preferred when fat suppression
forming postoperative MRI, due to the severe suscepti- is desired.45
bility artifacts that they may cause.45,46 • In general, TSE/FSE without fat saturation should be
• Magnetic susceptibility is the degree to which a material preferred when imaging joints with surgical implants.45
becomes magnetized when placed in an external mag- • Dedicated pulse sequences have recently been reported
netic field. to mitigate the effects of implant-associated suscepti-
• Para- and ferromagnetic materials cause local distortion bility artifacts, such as WARP-TSE, which combines
of the magnetic field, which can affect MR images by several strategies (view angle tilting, slice-encoding
causing signal void and misregistration in the vicinity of metal artifact correction, and increased bandwidth)
the susceptible material:45 to decrease the artifact.46 Although they significantly
• Signal void occurs because the heterogeneity of the increase acquisition time, they reduce the severity of
magnetic field caused by the material induces more susceptibility artifacts; for example, in canine stifle
rapid dephasing of protons after a radiofrequency joints after tibial plateau leveling osteotomy.
pulse, resulting in a drop in signal and signal void in • Other than these specific sequences, additional strat-
the images. egies that can be used include:46
• Misregistration occurs because the altered magnetic – Increasing receiver bandwidth.
field changes the precession frequency of protons, – Using TSE sequences with short echo train
which is critical for spatial localization of signal within length.
the imaged sample (see Chapter 1). Specifically, mis- – Orienting the frequency-encoding direction so
registration occurs in the direction of the frequency- that the artifact does not overlap the region of
and slice-encoding gradients. This causes an in-slice main clinical interest.
and through-slice spatial distortion of the image. • In joints/bones with prior orthopedic surgery, micro-
This appears as a hyperintense rim immediately adja- metallic fragments (not visible radiographically) from
cent to the area of signal void, and local distortion of instrumentation can create multiple signal voids on
the imaged anatomy. MR imaging.19 Suture material, even non-metallic,
• The effect of orthopedic surgical implants depends on can also result in signal void.
the nature of the material, size/location of the implants,
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intensity in normal collateral ligaments of the distal 26. Ober CP, Freeman LE (2009). Computed tomographic,
interphalangeal joint in horses with a low-field MRI system magnetic resonance imaging, and cross-sectional anatomic
due to the magic angle effect. Vet Radiol Ultrasound 48(2): features of the manus in cadavers of dogs without forelimb
95–100. disease. Am J Vet Res 70(12):1450–8.
10. Werpy NM, Ho CP, Kawcak CE (2010). Magic angle effect 27. Schaefer SL, Forrest LJ (2006). Magnetic resonance imaging
in normal collateral ligaments of the distal interphalangeal of the canine shoulder: an anatomic study. Vet Surg 35(8):
joint in horses imaged with a high-field magnetic resonance 721–8.
imaging system. Vet Radiol Ultrasound 51(1):2–10. 28. Soler M, Murciano J, Latorre R et al. (2007). Ultrasonographic,
11. May DA, Disler DG, Jones EA et al. (2000). Abnormal signal computed tomographic and magnetic resonance imaging
intensity in skeletal muscle at MR imaging: patterns, pearls, anatomy of the normal canine stifle joint. Vet J 174(2):351–61.
and pitfalls. Radiographics 20 Spec No:S295–315. 29. Widmer WR, Buckwalter KA, Braunstein EM et al. (1994).
12. Agnello KA, Puchalski SM, Wisner ER et al. (2008). Effect Radiographic and magnetic resonance imaging of the
of positioning, scan plane, and arthrography on visibility stifle joint in experimental osteoarthritis of dogs. Vet Radiol
of periarticular canine shoulder soft tissue structures on Ultrasound 35(5):371–84.
magnetic resonance images. Vet Radiol Ultrasound 49(6): 30. Murphy WA, Totty WG, Carroll JE (1986). MRI of normal
529–39. and pathologic skeletal muscle. Am J Roentgenol 146(3):
13. De Rycke LM, Gielen IM, Dingemanse W et al. (2015). 565–74.
Computed tomographic and low-field magnetic resonance 31. Winegardner KR, Scrivani PV, Krotscheck U et al. (2007).
arthrography: a comparison of techniques for observing intra- Magnetic resonance imaging of subarticular bone marrow
articular structures of the normal canine shoulder. Vet Surg lesions in dogs with stifle lameness. Vet Radiol Ultrasound
44(6):704–12. 48(4):312–7.
14. Pujol E, Van Bree H, Cauzinille L et al. (2011). Anatomic 32. Nolte-Ernsting CC, Adam G, Buhne M et al. (1996). MRI
study of the canine stifle using low-field magnetic resonance of degenerative bone marrow lesions in experimental
imaging (MRI) and MRI arthrography. Vet Surg 40(4): osteoarthritis of canine knee joints. Skeletal Radiol 25(5):
395–401. 413–20.
15. Schaefer SL, Baumel CA, Gerbig JR et al. (2010). Direct 33. Murphy SE, Ballegeer EA, Forrest LJ et al. (2008). Magnetic
magnetic resonance arthrography of the canine shoulder. resonance imaging findings in dogs with confirmed shoulder
Vet Radiol Ultrasound 51(4):391–6. pathology. Vet Surg 37(7):631–8.
16. Sofka CM, Potter HG, Adler RS et al. (2006). Musculoskeletal 34. Wall CR, Cook CR, Cook JL (2015). Diagnostic sensitivity
imaging update: current applications of advanced imaging of radiography, ultrasonography, and magnetic resonance
techniques to evaluate the early and long-term complications imaging for detecting shoulder osteochondrosis/
of patients with orthopedic implants. HSS J 2(1):73–7. osteochondritis dissecans in dogs. Vet Radiol Ultrasound
17. Naughton JF, Stewart MC, Ciobanu L et al. (2013). Contrast 56(1):3–11.
magnetic resonance imaging for measurement of cartilage 35. Pownder SL, Hayashi K, Shah P et al. (2015). Magnetic
glycosaminoglycan content in dogs: a pilot study. Vet Comp resonance imaging of the insertion of the canine
Orthop Traumatol 26(2):100–4. supraspinatus: the origin of the signal. American College of
18. Wucherer KL, Ober CP, Conzemius MG (2012). The Veterinary Radiology Conference, Minneapolis.
use of delayed gadolinium enhanced magnetic resonance 36. Cook CR, Cook JL (2009). Diagnostic imaging of canine
imaging of cartilage and T2 mapping to evaluate articular elbow dysplasia: a review. Vet Surg 38(2):144–53.
cartilage in the normal canine elbow. Vet Radiol Ultrasound 37. Snaps FR, Balligand MH, Saunders JH et al.
53(1):57–63. (1997) Comparison of radiography, magnetic resonance
19. Banfield CM, Morrison WB (2000). Magnetic resonance imaging, and surgical findings in dogs with elbow dysplasia.
arthrography of the canine stifle joint: technique and Am J Vet Res 58(12):1367–70.
152 CHAPTER 4.3
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38. Snaps FR, Park RD, Saunders JH et al. (1999). Magnetic 43. Blond L, Thrall DE, Roe SC et al. (2008). Diagnostic accuracy
resonance arthrography of the cubital joint in dogs affected of magnetic resonance imaging for meniscal tears in dogs
with fragmented medial coronoid processes. Am J Vet Res affected with naturally occuring cranial cruciate ligament
60(2):190–3. rupture. Vet Radiol Ultrasound 49(5):425–31.
39. Snaps FR, Saunders JH, Park RD et al. (1998). Comparison 44. Podadera J, Gavin P, Saveraid T et al. (2014). Effects of stifle
of spin echo, gradient echo and fat saturation magnetic flexion angle and scan plane on visibility of the normal canine
resonance imaging sequences for imaging the canine elbow. cranial cruciate ligament using low-field magnetic resonance
Vet Radiol Ultrasound 39(6):518–23. imaging. Vet Radiol Ultrasound 55(4):407–13.
40. Janach KJ, Breit SM, Kunzel WW (2006). Assessment of 45. David FH, Grierson J, Lamb CR (2012). Effects of surgical
the geometry of the cubital (elbow) joint of dogs by use of implants on high-field magnetic resonance images of the
magnetic resonance imaging. Am J Vet Res 67(2):211–8. normal canine stifle. Vet Radiol Ultrasound 53(3):280–8.
41. de Bakker E, Gielen I, Kromhout K et al. (2014). Magnetic 46. Simpler RE, Kerwin SC, Eichelberger BM et al. (2014).
resonance imaging of primary and concomitant flexor enthe- Evaluation of the WARP-turbo spin echo sequence for
sopathy in the canine elbow. Vet Radiol Ultrasound 55(1):56–62. 3 Tesla magnetic resonance imaging of stifle joints in dogs
42. Martig S, Konar M, Schmokel HG et al. (2006). Low-field with stainless steel tibial plateau leveling osteotomy implants.
MRI and arthroscopy of meniscal lesions in ten dogs with Vet Radiol Ultrasound 55(4):414–9.
experimentally induced cranial cruciate ligament insufficiency.
CHAPTER 4.4
TECHNICAL PARTICULARITIES
WITH LOW-FIELD IMAGING 153
Wilfried Mai
CONTENTS
Types of low-field systems ....................................................................................................................................................................................153
Advantages of low-field imaging ...........................................................................................................................................................................154
Disadvantages of low-field imaging ......................................................................................................................................................................154
Strategies to increase diagnostic value of low-field MRI .......................................................................................................................................154
References.............................................................................................................................................................................................................156
As described in Chapters 1 and 2, the strength of the mag- – Air-cored resistive magnets typically comprise
netic field greatly influences image quality (in particular four large coils wound with either copper wire
signal-to-noise ratio [SNR]) as well as acquisition time.1 MR or aluminum bands. An electric current passed
scanners are generally classified into one of the three cate- through the windings generates a magnetic field of
gories of low-, medium-, and high-field strength.1 Low-field up to about 0.2–0.3T.17 Any increase in magnetic
MRI has been defined as magnetic field strength ranging field would require an increase in current, which
from 0.2–0.4T,1,2 medium-field being 0.5–1.0T, and high- would create more resistance in the windings and,
field being >1.0T.1 However, there is some variability in the in turn, would raise the temperature to a level that
literature as to what is regarded as low-, medium-, and high- would ultimately destroy the electromagnet.16
field strength.2 – Iron-cored electromagnets, which use coils wound
Low-field MRI scanners are quite popular in veteri- around soft iron pole pieces, are a variation of
nary medicine due to their relatively low cost and ease of resistive electromagnets. When an electric cur-
installation/housing and maintenance. This popularity is rent flows through the coils, the iron becomes
reflected by the number of publications investigating low- a magnet. The use of iron means that higher
field MRI.2–15 magnetic fields can be achieved compared with
High-field magnets tend to predominate in academic air-cored magnets (0.5–0.6T); however, these sys-
veterinary centers, as they represent expanded research tems are quite heavy due to the large mass of iron
opportunities in advanced imaging studies that would required.17
not be possible using systems with lower field strength. • Permanent magnets use materials in which large
However, in veterinary medicine in general, the bulk of magnetic fields are induced during manufacture;
MRI machines are installed in private practice, where low- they are made of a material that remains magnetic for
field units predominate.2 extremely long periods of time. They have maximum
field strengths around 0.2–0.3T and, like the elec-
TYPES OF LOW-FIELD SYSTEMS tromagnet designs described above, the field is often
oriented vertically. Installation and running costs
• Two types of technologies are found in low-field MRI: are low. It should be remembered that permanent
• Electromagnets produce a magnetic field through magnets cannot be ‘switched off’. Such units are very
circulation of an electrical current through a coil. heavy (typically around 9,500 kg), due to their metal
Although the capital costs of such magnets are rela- composition.17
tively low, the operational costs of resistive magnets • Both human low-field MRI systems and veterinary dedi-
are quite high due to the large amount of power cated systems are found in veterinary practice.
required to maintain the magnetic field. To keep • Human systems are generally more expensive, but pro-
the magnetic field on, power must be supplied to the vide technical advantages including a more homogeneous
system:16 magnetic field, larger fields of view, stronger gradients
154 CHAPTER 4.4
(slew rate = peak gradient strength divided by rise time), diagnostic efficacy is unclear as there are no clear com-
multichannel receiver coils, and more modern/complex parative studies between low- and high-field imaging.
pulse sequences with expanded clinical applications.2 • In general, high-field imaging may be more sensi-
Disadvantages of human systems include limited use of tive to certain features of specific diseases, but over-
coils designed for human applications on animals (due to all, the sensitivity of low- versus high-field scanners in
anatomic differences), and software not adapted to vet- the diagnosis of the disease itself often appears to be
erinary use.2 equivalent.1
• Veterinary systems tend to be cheaper, and offer veteri- • This being said, for some conditions, such as meniscal
nary-specific software (e.g., anatomic part designations, tears in dogs, high-field imaging seems to perform bet-
veterinary-specific orientation and labeling), coils opti- ter than low-field imaging in regard to sensitivity and
mized for veterinary anatomy, and specific applications interobserver agreement.18–21
for veterinary needs.2 Compared with their human coun- • For spinal imaging, a very common indication for MRI
terpart, they tend to have lower technological standards, in small animal patients, several challenges exist:2,22
such as lower gradient slew rate; this has a negative effect • Due to the compact design of low-field magnets,
on imaging speed and spatial resolution. They also tend imaging of the caudal cervical or cranial thoracic
to have a smaller volume of homogeneous magnetic field, spine may not be possible in larger dogs.2
resulting in smaller field of view.2 • Due to the low SNR, it may be difficult to obtain
• As a result, there is considerable variation in MRI quality diagnostic studies of the spine, particularly in small
in veterinary practice. patients.
• The small field of view of low-field units may neces-
ADVANTAGES OF LOW-FIELD IMAGING sitate repositioning the patient repeatedly to obtain
images of the entire region of interest, in particular
• The purchase cost of low-field MRI machines is signifi- the thoracolumbar spine.
cantly less than for medium- or high-field units. • Although some artifacts are reduced at low-field, this
• In addition, costs of installation of low-field units are can also have negative diagnostic consequences, such
much lower, due to the simpler technology and lack of as less sensitivity to diagnosis of hematomas, since
specific requirement such as a shielded room etc. MRI exploits susceptibility artifacts to recognize
• Maintenance is also cheaper, due to lower these lesions.2
electricity costs, lack of need for helium gas, which is • The difference in precessional frequency between fat
necessary with superconductive magnets, and cheaper and water is too small in low-field MRI to allow selective
periodic check-ups of the system. chemical saturation (spectral fat suppression), hence this
• Risk management costs are lower, due to the fact that method cannot be used. This can make differentiation
low-field units are generally safer than high-field units. between contrast-enhanced lesions and fat difficult on
• Fringe fields are smaller, which allows less stringent post-contrast images.
installation requirements, permits installation in a • Image contrast and contrast enhancement both depend
smaller space, and decreases the risk of projectile inci- on field strength, and enhancement of lesions is typically
dents. Conventional anesthesia and monitoring equip- less visible at low-field compared with high-field.23
ment as opposed to specific MR-compatible technology
can be used, provided it is kept at a reasonable distance STRATEGIES TO INCREASE DIAGNOSTIC
from the machine. VALUE OF LOW-FIELD MRI
• Some artifacts are reduced or less conspicuous with
low-field imaging, such as chemical shift artifacts, sus- • The low SNR in low-field systems can to some extent be
ceptibility artifacts, and flow/motion artifacts. Artifacts compensated for by:24
associated with metal hardware are reduced compared • Increasing slice thickness.
with high-field imaging. • Reducing in-plane resolution.
• Increasing number of acquisitions.
DISADVANTAGES OF LOW-FIELD IMAGING • Decreasing the bandwidth.
• These adjustments reduce image resolution and prolong
• The major drawback of low-field MRI is the lower SNR anesthesia and image acquisition time, potentially exac-
compared with high-field imaging (Figs. 4.4.1, 4.4.2). erbating patient hypothermia.22
This results in lower spatial resolution and lower tempo- • If thin slices of high resolution are needed, increasing
ral resolution (i.e., longer acquisition times). the number of acquisitions (averages) will be necessary
• Generally, high-field scanners will produce better qual- to compensate for the decreased SNR, but that will cost
ity images in a shorter time; however, the impact on time.25
Te c h n ic a l Pa r t ic u l a r i t i e s Wi t h L ow-Fi e l d I m agi ng 155
(a) (b)
(c) (d)
Fig. 4.4.1 Sagittal T1W images at high-field (1.5T, a) and low-field (0.25T, b) of the caudal lumbar spine and transverse high-
field (c) and low-field (d) images at the level of the L5-L6 intervertebral disc in the same Belgian Malinois dog. The signal-to-
noise ratio and resolution in (b) and (d) (low-field) are inferior to those in (a) and (c) (high-field); however, major structures of
interest, such as the spinal cord, subarachnoid space, and intervertebral disc, can still be adequately evaluated on the low-field
images.
• Although fat saturation cannot be used with low-field contrast-to-noise ratio and high sensitivity to fluid
scanners, suppression of signal from fat can still be and pathology, but low SNR. Because all structures
obtained using various strategies including: with short T1 relaxation time are suppressed, gado-
• Short tau inversion recovery pulse sequence (STIR), linium-enhanced lesions may also be suppressed on
which is also used in high-field.2 This pulse sequence STIR and therefore this sequence cannot be utilized
(see Chapter 2) utilizes an inversion radiofrequency for fat suppression of post-contrast images.
pulse of 180º followed by a ‘time of inversion’ after • Strategies have been developed to obtain fat suppres-
which the 90º radiofrequency pulse is applied. The sion at low-field, exploiting the small but existing dif-
time of inversion is chosen to match the time at which ferences in precessional frequencies of fat and water
the signal from fat is nulled, so that it is suppressed protons. A popular method is the ‘Dixon method’,
in the final image. These sequences have a high in which two echoes are recorded at times that are
156 CHAPTER 4.4
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(a) (b) (c)
(d) (e) (f)

Fig. 4.4.2 Sagittal T2W (a, d), transverse T2W (b, e), and transverse T2-FLAIR (c, f) images at the level of the interthalamic
adhesion in two Boxer dogs. The dog in the top row was imaged at high-field (1.5T) while the dog in the bottom row was
imaged at low-field (0.25T). Slice thickness was 3 mm in all images. There is in general more detail and better resolution in the
high-field images. For example, the outline of the interthalamic adhesion (asterisks, a and d) is much clearer in (a) than in (d).
calculated to coincide with water and fat protons being • When using a low-field magnet to image the spine in
either in-phase or out-of-phase.2,24,26 In-phase and patients with neurologic signs, there may be an advan-
opposed-phase images are acquired. The sum of these tage in performing myelography as the initial screen-
images produces a pure water image; the difference ing procedure, assuming that CT is not available, at
between these images produces a pure lipid image.26 least in large dogs, 22 so that the MR examination can
The Dixon method requires a minimum of two be focused on areas of concern based on myelographic
data acquisitions (‘two-point Dixon method’). This assessment.
method is very sensitive to magnetic field inhomo-
geneities, due to phase shift errors, which may make REFERENCES
suppression of fat imperfect. To remedy this problem, 1. Hayashi N, Watanabe Y, Masumoto T et al. (2004). Utilization
a third acquisition is sometimes made to compensate of low-field MR scanners. Magn Reson Med Sci 3(1):27–38.
for the magnetic field inhomogeneities (‘three-point 2. Konar M, Lang J (2011). Pros and cons of low-field magnetic
Dixon method’). With T1-weighting, this technique resonance imaging in veterinary practice. Vet Radiol Ultrasound
can be used successfully to detect areas of gadolinium
52:S5–S14.
enhancement while suppressing the signal from fat.2 3. Armbrust LJ, Hoskinson JJ, Biller DS et al. (2004). Low-field
• Conspicuity of gadolinium-enhanced lesions is lower on magnetic resonance imaging of bone marrow in the lumbar
low-field imaging, and some authors have proposed that spine, pelvis, and femur in the adult dog. Vet Radiol Ultrasound
the gadolinium dose should be increased when using low- 45(5):393–401.
field scanners to offset this relatively decreased conspi- 4. Bergknut N, Auriemma E, Wijsman S et al. (2011). Evaluation
cuity. Some authors have proposed 0.15 mmol/kg body of intervertebral disk degeneration in chondrodystrophic and
weight instead of the usual 0.1 mmol/kg,2 although no nonchondrodystrophic dogs by use of Pfirrmann grading of
formal study exists to support the effect of this increased images obtained with low-field magnetic resonance imaging.
Am J Vet Res 72(7):893–8.
dose.
Te c h n ic a l Pa r t ic u l a r i t i e s Wi t h L ow-Fi e l d I m agi ng 157
5. Bergknut N, Grinwis G, Pickee E et al. (2011). Reliability of magnetic resonance imaging of canine focal liver lesions.
macroscopic grading of intervertebral disk degeneration in Vet Radiol Ultrasound 53(4):371–80.
dogs by use of the Thompson system and comparison with 16. Westbrook C, Kaut Roth C, Talbot J (2011). (eds.) MRI
low-field magnetic resonance imaging findings. Am J Vet Res in Practice. 4th edn. Wiley-Blackwell, Ames.
72(7):899–904. 17. McRobbie DW, Moore EA, Graves MJ et al. (2007). MRI
6. De Decker S, Gielen IM, Duchateau L et al. (2011). Intraobserver, From Picture to Proton, 2nd edn. Cambridge University Press,
interobserver, and intermethod agreement for results of Cambridge.
myelography, computed tomography-myelography, and low-field 18. Blond L, Thrall DE, Roe SC et al. (2008). Diagnostic accuracy
magnetic resonance imaging in dogs with disk-associated wobbler of magnetic resonance imaging for meniscal tears in dogs
syndrome. J Am Vet Med Assoc 238(12):1601–8. affected with naturally occuring cranial cruciate ligament
7. De Decker S, Gielen IM, Duchateau L et al. (2010). Low-field rupture. Vet Radiol Ultrasound 49(5):425–31.
magnetic resonance imaging findings of the caudal portion of 19. Bottcher P, Armbrust L, Blond L et al. (2012). Effects
the cervical region in clinically normal Doberman Pinschers of observer on the diagnostic accuracy of low-field MRI
and Foxhounds. Am J Vet Res 71(4):428–34. for detecting canine meniscal tears. Vet Radiol Ultrasound
8. De Decker S, Gielen IMVL, Duchateau L et al. (2011). 53(6):628–35.
Intraobserver and interobserver agreement for results of low- 20. Bottcher P, Bruhschwein A, Winkels P et al. (2010). Value of
field magnetic resonance imaging in dogs with and without low-field magnetic resonance imaging in diagnosing meniscal
clinical signs of disk-associated wobbler syndrome. J Am Vet tears in the canine stifle: a prospective study evaluating
Med Assoc 238(1):74–80. sensitivity and specificity in naturally occurring cranial
9. Kneissl S, Probst A, Konar M (2004). Low-field magnetic cruciate ligament deficiency with arthroscopy as the gold
resonance imaging of the canine middle and inner ear. standard. Vet Surg 39(3):296–305.
Vet Radiol Ultrasound 45(6):520–2. 21. Olive J, d’Anjou MA, Cabassu J et al. (2014). Fast presurgical
10. Kromhout K, van Bree H, Broeckx BJ et al. (2015). Low- magnetic resonance imaging of meniscal tears and concurrent
field magnetic resonance imaging and multislice computed subchondral bone marrow lesions. Study of dogs with
tomography for the detection of cervical syringomyelia in naturally occurring cranial cruciate ligament rupture.
dogs. J Vet Intern Med 29(5):1354–9. Vet Comp Orthop Traumatol 27(1):1–7.
11. Muleya JS, Taura Y, Nakaichi M et al. (1997). Appearance of 22. Robertson I, Thrall DE (2011). Imaging dogs with suspected
canine abdominal tumors with magnetic resonance imaging disc herniation: pros and cons of myelography, computed
using a low field permanent magnet. Vet Radiol Ultrasound tomography, and magnetic resonance. Vet Radiol Ultrasound
38(6):444–7. 52:S81–4.
12. Rousset N, Holmes MA, Caine A et al. (2013). Clinical and 23. Brekenfeld C, Foert E, Hundt W et al. (2001). Enhancement
low-field MRI characteristics of injection site sarcoma in of cerebral diseases: how much contrast agent is enough?
19 cats. Vet Radiol Ultrasound 54(6):623–9. Comparison of 0.1, 0.2, and 0.3 mmol/kg gadoteridol at
13. Seiler G, Hani H, Scheidegger J et al. (2003). 0.2 T with 0.1 mmol/kg gadoteridol at 1.5 T. Invest Radiol
Staging of lumbar intervertebral disc degeneration in 36(5):266–75.
nonchondrodystrophic dogs using low-field magnetic 24. Tavernier T, Cotten A (2005). High- versus low-field MR
resonance imaging. Vet Radiol Ultrasound 44(2):179–84. imaging. Radiol Clin North Am 43(4):673–81, viii.
14. Tamura S, Doi S, Tamura Y et al. (2015). Thoracolumbar 25. Robertson I (2011). Optimal magnetic resonance
intradural disc herniation in eight dogs: clinical, low-field imaging of the brain. Vet Radiol Ultrasound
magnetic resonance imaging, and computed tomographic 52(1 Suppl 1):S15–22.
myelography findings. Vet Radiol Ultrasound 56(2):160–7. 26. Delfaut EM, Beltran J, Johnson G et al. (1999). Fat
15. Yonetomi D, Kadosawa T, Miyoshi K et al. (2012). Contrast suppression in MR imaging: techniques and pitfalls.
agent Gd-EOB-DTPA (EOB.Primovist(R)) for low-field Radiographics 19(2):373–82.
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SECTION 2
MRI OF THE BRAIN

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159
CHAPTER 5.1 Congenital and developmental disorders
CHAPTER 5.2 Metabolic and degenerative encephalopathies
CHAPTER 5.3 Encephalitis/meningoencephalitis
CHAPTER 5.4 Brain neoplasia
CHAPTER 5.5 Cystic conditions
CHAPTER 5.6 Ischemic brain disease and vascular anomalies
CHAPTER 5.7 Brain hemorrhage
CHAPTER 5.8 Brain trauma
CHAPTER 5.9 Aging changes of the brain
CHAPTER 5.10 Cranial nerve diseases

VetBooks.ir
CHAPTER 5.1
CONGENITAL AND DEVELOPMENTAL DISORDERS

Silke Hecht 161
CONTENTS
Hydrocephalus ......................................................................................................................................................................................................161
Meningocele and meningoencephalocele..............................................................................................................................................................163
Holoprosencephaly/corpus callosum abnormalities ..............................................................................................................................................163
Lissencephaly .......................................................................................................................................................................................................165
Polymicrogyria ......................................................................................................................................................................................................165
Focal cortical dysplasia .........................................................................................................................................................................................165
Dyke–Davidoff–Masson-like syndrome ................................................................................................................................................................166
Cerebellar malformations ......................................................................................................................................................................................166
Congenital cerebellar aplasia and hypoplasia .................................................................................................................................................166
Dandy–Walker malformation complex ............................................................................................................................................................166
Chiari-like malformation (= caudal occipital malformation syndrome) .................................................................................................................. 167
References.............................................................................................................................................................................................................168
This chapter describes congenital and developmental disor- include failure to thrive, malformation of the skull,
ders of the brain, including Chiari-like malformation. Other ventrolateral strabismus, abnormal behavior, cog-
abnormalities of the craniocervical junction are covered nitive dysfunction, ataxia, blindness, and vestibular
in Chapter 7.4. Cystic intracranial anomalies (hydranen- dysfunction, may not be evident until several months
cephaly, porencephaly, intracranial intra-arachnoid diver- of age.4–6
ticula [‘cysts’], intracranial epidermoid and dermoid cysts, • Acquired hydrocephalus can occur at any age and devel-
Rathke cleft cysts, ependymal and choroid plexus cysts) are ops secondary to CSF flow obstruction caused by
described in Chapter 5.5. Congenital anomalies of brain a variety of diseases of the central nervous system
metabolism (neuronal lipofuscinosis etc.) are covered in including neoplasia and other mass lesions, intra-
Chapter 5.2. ventricular hemorrhage, or meningoencephalitis.7–12
With the exception of skull malformations, clinical
HYDROCEPHALUS signs are similar to those in young animals but may
also reflect the underlying cause of the hydrocepha-
• Hydrocephalus is defined as an abnormal distension of lus.4 Even though technically this form of hydroceph-
the ventricular system of the brain related to inadequate alus is not congenital/developmental, it is illustrated
passage of cerebrospinal fluid (CSF) from its point of and covered in this chapter.
production within the ventricular system to its point of • Differentiating between moderate but pathologic hydro-
absorption:1,2 cephalus and normal variations of the ventricular system
• Congenital hydrocephalus is predominantly seen in toy can be challenging:
and brachycephalic breed dogs.3 The most commonly • In one ultrasonographic study in dogs with persis-
identified cause is stenosis of the mesencephalic aque- tent fontanelles, normal height of the lateral ventri-
duct associated with fusion of the rostral colliculi; cles measured at the level of the pituitary gland was
however, in many cases an obvious site of obstruction reported to be 0%–14% of the dorsoventral height
is not found.4 Genetic factors and in-utero exposure of the brain measured on midline; moderate ven-
to toxins or infectious agents have also been associ- tricular enlargement was defined as 15%–25% and
ated with congenital hydrocephalus. Although the >25% was considered indicative of severe ventricular
condition is present at birth, clinical signs, which enlargement.13
162 CHAPTER 5.1
• In another ultrasonographic study, the size of the • Atrophy of the interthalamic adhesion.29,31
lateral ventricles at the level of the interthalamic adhe- • Periventricular edema resulting from transependymal
sion in normal dogs ranged from slit-like to 0.35 cm.14 migration of CSF (best seen on T2-FLAIR images as
• Ventriculomegaly and ventricular asymmetry are periventricular hyperintensity, and most common in
common findings in asymptomatic dogs, and this acute cases) (Fig. 5.1.3).4,27,33,34
finding may or may not be clinically significant.15–19 • Periventricular diverticula, tears, and clefts, which
An increased size and volume of the cerebral ven- may be associated with parenchymal hemorrhage as
tricles has been reported in Yorkshire Terriers16 and high pressure CSF dissects along the white matter
English Bulldogs.18,20 tracts; this is usually best seen on gradient echo
• Progressive dilation of the ventricles and sub- T2*W images, appearing as signal voids associated
arachnoid space is also anticipated with increasing age with susceptibility artifacts caused by hemoglobin
and, therefore, dilated ventricles in older dogs may by-products.4,29,31,33
not be pathologic.21,22 • Empty sella (herniation of the subarachnoid space
• Normal cats have small ventricles,23 and noticeable into the sella turcica);35 this is particularly visible as a
ventricular enlargement is considered abnormal unless hyperintense area within the sella on the T2W series
mild and related to age-associated brain atrophy, in due to accumulation of fluid within it.
which case additional signs such as widened cerebral • CSF signal void in mesencephalic aqueduct on T2W
sulci are present.24 images attributed to high velocity or turbulent CSF
• Common MRI findings in cases of hydrocephalus flow (see Fig. 4.1.12a).36
include: • Subtentorial herniation of a dilated ventricle.31
• Ventricular enlargement (Fig. 5.1.1).25–30 • Additional MRI findings in congenital hydrocephalus
• Thinning of the cerebral cortices.29,31 may include:
• Less common MRI findings may include: • Enlargement of the calvarium +/− open fonta-
• Absence of the septum pellucidum leading to continu- nelles.4,6,25–27
ity between the lateral ventricles.31 • Other congenital anomalies including meningomye-
• Dilation of the olfactory recesses of the lateral ventri- locele, Chiari-like malformation, occipital dysplasia/
cles (located in the olfactory bulb and normally not hypoplasia, syringohydromyelia, Dandy–Walker syn-
visible), and the infundibular recess (Fig. 5.1.2).29,31,32 drome, and cerebellar hypoplasia.4,29,37–39
Fig. 5.1.1 Congenital hydrocephalus in a 10-month-old Fig. 5.1.2 Obstructive hydrocephalus in a 2-year-old cat
Chihuahua. This transverse T2W image shows severe subsequently diagnosed with feline infectious peritonitis.
symmetric dilation of the lateral and third ventricles, This dorsal T2W image shows bilaterally symmetric dilation
cortical thinning, and absence of a septum pellucidum. of the recesses of the olfactory bulbs (arrows) along with
(1.5T MRI system) generalized ventriculomegaly. (1.5T MRI system)
C onge n i ta l a n d D e v e l opm e n ta l D isor de r s 163
Fig. 5.1.4 Ethmoidal meningoencephalocele in a 10-month-

old mixed breed dog. This sagittal T2W image demonstrates
Fig. 5.1.3 Obstructive hydrocephalus in a 3-year-old Bouvier absence of part of the cribriform plate and herniation of the
des Flandres with cryptococcal meningitis. On this transverse olfactory bulb into the caudal nasal cavity (arrowhead), with
T2-FLAIR image, CSF in the ventricles is black due to concurrent formation of a cyst-like lesion in the most rostral
suppression of fluid signal (asterisk). There is bilateral aspect (arrow). (1.5T MRI system)
periventricular hyperintensity consistent with transependymal
migration of CSF, which was most severe in the rostral part of
• Superficial (parietal) meningoencephaloceles may be
the brain in this patient (arrow). (1T MRI system)
diagnosed clinically due to a fluctuant palpable swell-
ing over the calvarium. Diagnosis of basal or ethmoidal
• MRI findings that may be useful in discriminating clini- (nasal) meningoencephaloceles requires advanced imag-
cally relevant hydrocephalus from incidental ventriculo- ing, even though they may be associated with concurrent
megaly include:40 external deformity of the head.31,44
• A ventricle/brain index >0.6 on dorsal plane images. • Age at presentation is variable and ranges from weeks
The ventricle/brain index is evaluated on dorsal T2 to several years. Clinical signs are also variable and
images and defined as the maximum continuous dis- include behavioral abnormalities, seizures, and abnormal
tance between the internal borders of the ventricles mentation.
divided by the maximum width of the brain paren- • MRI findings include:
chyma in the same image. • Calvarial defect with herniation of meninges +/−
• Elevation of the corpus callosum and dorsoventral brain tissue in cases of superficial/parietal (meningo)
flattening of the interthalamic adhesion, best seen on encephalocele.42,47
sagittal plane images. • Cribriform plate defect with herniation of meninges
• Periventricular edema (Fig. 5.1.3). +/− brain tissue in cases of nasal/ethmoidal (meningo)
• Dilation of the olfactory recesses (Fig. 5.1.2). encephalocele (Fig. 5.1.4).42,44–46
• Thinning of the cortical sulci and/or subarachnoid • Concurrent facial/calvarial deformity.42,44
space. • Meningeal enhancement of protruded tissue.47
• Disruption of the internal capsule adjacent to the • Porencephaly (in cases of parietal meningoencepha-
caudate nucleus. locele).47
MENINGOCELE AND HOLOPROSENCEPHALY/CORPUS

MENINGOENCEPHALOCELE CALLOSUM ABNORMALITIES
• Protrusion of meninges alone or meninges along with • Holoprosencephaly (HPE) is a failure of the forebrain to
brain tissue through a calvarial defect (cranioschisis, sufficiently divide into two hemispheres, and is char-
cranium bifidum) are termed meningocele and meningoen- acterized by absent or smaller midline prosencephalic
cephalocele, respectively.41 structures (corpus callosum, septum pellucidum, septal
• These conditions have been described in dogs and nuclei, fornix, and optic nerves), incomplete separation of
cats.31,42–47 Most lesions are congenital, although devel- normally paired forebrain structures (lateral ventricles,
opment of a meningomyelocele secondary to trauma cingulate gyri, and caudate nuclei), and hydrocephalus.
or surgery is possible.46 A genetic basis is reported in • Dependent on severity, HPE can be subdivided into
Burmese cats.48,49 alobar, semilobar, and lobar HPE:29,31
164 CHAPTER 5.1
• In alobar HPE (syn. arrhinencephaly), prosencephalic • Agenesis or dysgenesis of the corpus callosum is a feature of
cleavage fails, resulting in a single midline forebrain HPE, but may also occur as an isolated abnormality:
with a primitive monoventricle. This condition is • Staffordshire Bull Terriers and Miniature Schnauzers
usually associated with severe facial malformation appear predisposed to both conditions but other
including a single cycloptic globe. Reports in small breeds may be affected. The age at presentation is
animals are rare,41,50 and descriptions of diagnostic very variable and has been reported to range from 3
imaging findings are lacking. MRI findings in people to 81 months.52
with alobar HPE include:51 • Adipsia/hypodipsia (associated with hypernatremia)
– A large monoventricle often associated with a dor- is the most common presenting complaint.53–56
sal cyst. Animals may be neurologically normal or show var-
– Ball-, cup-, or pancake-like appearance of brain iable signs including tremors, proprioceptive deficits,
on sagittal images. ataxia, reduced menace, obtundation, and vestib-
– Absence of olfactory bulbs and fusion of basal ular signs. Dermatologic abnormalities, including
ganglia and hypothalamic and thalamic nuclei. hyperkeratosis, ichthyosis, seborrhea, and alopecia,
• With semilobar HPE the occipital lobes are dis- have also been reported.52,53
tinct while the rostral cerebral hemispheres fail to • MRI findings in dogs with lobar HPE and agenesis or
separate.31 No reports were found describing this dysgenesis of the corpus callosum include:52–56
condition in small animal patients. • Agenesis or dysgenesis of the corpus callosum, which
• In lobar HPE only the most rostral and ventral is best visualized on mid-sagittal or transverse T2W
portions of the cerebral hemispheres are fused. images (Fig. 5.1.5a).
(a) (b)
(c) (d)
Fig. 5.1.5 Dysgenesis of the corpus callosum in a 4-month-old female Miniature Schnauzer presented with hypodipsic
hypernatremia (a, c) compared with MR images of the brain of a normal 8-year-old dog of the same breed (b, d). The sagittal
T2W image (a) shows that the hypointense corpus callosum (arrows) is small compared with the normal dog (b). The transverse
T2*W image (c) shows that the lateral ventricles have unusually upturned and pointed corners (arrowheads) compared with the
normal dog (d). (1T MRI system)
• Fusion of the ventral frontal lobes, cingulate gyri, POLYMICROGYRIA

lateral ventricles, and part of the diencephalon
with associated loss of some normal midline struc- • This is a disorder of cerebrocortical development result-
tures. ing in an increased number of small, disorganized gyri in
• Unusually upturned, pointed corners of the lateral the dorsal and lateral cerebral cortex.
ventricles seen on transverse images (Fig. 5.1.5c). • It has been reported in Standard Poodles, in which a
• Less commonly, a focal circular T2 hyperintensity hereditary basis is suspected.63,64
dorsal to the midbrain thought to represent either • Affected dogs present with cortical blindness and other
dilatation of the pineal recess or an arachnoid diver- neurologic abnormalities including gait and behavioral
ticulum.52 changes. Age at presentation ranges from 7 weeks to 5 years.
• MRI findings include:
LISSENCEPHALY • Increased numbers of disorganized shallow gyri in
the occipital lobes, most easily visualized on dorsal
• This disorder of cortical neuronal migration is charac- plane T2W images (Fig. 5.1.7).63,64
terized by paucity, absence, and/or hypoplasia of cere- • Less common MRI findings include ventriculomegaly/
bral gyri (pachygyria) and thickening of the cerebral hydrocephalus63 and thinning of the subcortical white
cortex.29 matter in the occipital lobes.
• The disease has been reported in dogs and cats and it
appears to be hereditary in Lhasa Apsos.57–59 FOCAL CORTICAL DYSPLASIA
• Clinical signs can range from mild to severe and include
abnormal mentation, behavioral abnormalities, visual • These lesions are sporadically reported in the veterinary lit-
problems, and seizures. Affected animals present from erature in dogs and cats ranging from 1 to 13 years of age.65–69
less than 1 to several years of age.57–61 • As in people, these conditions are speculated to have epi-
• MRI findings include: leptogenic potential.70 However, the significance of focal
• A smooth cerebral surface and a thick neocortex with cortical dysplasia (FCD) in animals remains uncertain,
absence of the corona radiata (Fig. 5.1.6).58,60–62 as all reported cases were diagnosed post mortem and
• Less commonly, concurrent anomalies such as cer- most had concurrent abnormalities that were considered
ebellar hypoplasia, corpus callosum abnormalities, more significant (porencephaly, meningoencephalitis, or
ventriculomegaly, or arachnoid cysts.58,60 intracranial neoplasia).65–68
(a) (b)
Fig. 5.1.6 Lissencephaly in a 1-year-old Chinese Crested dog (a) compared with a normal mixed breed dog of the same age (b).
The transverse T2W image shows that the cerebral surface lacks gyri and sulci and appears smooth compared with the dog
with normal cerebral gyrification. The neocortex is thick and the corona radiata (fan-like white matter tracts extending into
the cerebral cortex; indicated by arrows in b) is absent. (1.5T MRI system; images courtesy of Dr. Robert L. Bergmann and
Dr. Lindsay Williams, Carolina Veterinary Specialists Medical Center)
166 CHAPTER 5.1
Fig. 5.1.8 Dyke–Davidoff–Masson-like syndrome in an

Fig. 5.1.7 Polymicrogyria in a 12-year-old Standard Poodle. 11-year-old female spayed DSH cat that was presented
This transverse T2W image shows an increased number for seizures. This transverse T1W image shows partial
of disorganized shallow gyri, especially in the left absence/hypoplasia of the right cerebral hemisphere with
cerebral hemisphere. (1.5T MRI system; image courtesy compensatory thickening (hyperostosis) of the overlying
of Drs. Charles Vite and Wilfried Mai, University of skull. (1.5T MRI system; image courtesy of Daniel Cuff, Bush
Pennsylvania) Veterinary Neurological Services)
• MRI was performed in one dog and failed to demonstrate • In kittens, this is most commonly observed following in-
structural abnormalities.69 MRI findings in people vary utero infection with the panleukopenia virus.76,77 Although
with the type of FCD and range from no abnormalities an association with parvovirus infection has been proposed,
to changes in cortical thickness, T2 hyperintensities, the condition is most likely inherited in dogs.75,76,78–80
hemispheric atrophy, and linear tracks of gray matter • Clinical signs (cerebellar ataxia) are present at birth or
extending to the cortical mantle.70 shortly thereafter, and do not progress.31,73,81 This is dif-
ferent from ‘cerebellar abiotrophy’, in which animals
DYKE–DAVIDOFF–MASSON-LIKE SYNDROME are normal at birth and clinical signs develop at several
weeks to years of age (see also Chapter 5.2).73
• Dyke–Davidoff–Masson-like syndrome is a syndrome • MRI findings include:31,62,77,82
described in people with intrauterine or early child- • An absent or abnormally small cerebellum with CSF
hood loss of unilateral brain parenchyma and subsequent filling the space normally occupied by cerebellar
asymmetric changes to the cranium.71 parenchyma (Fig. 5.1.9). This is particularly visible
• A single case of this condition has been reported in a on T2W images due to the hyperintensity of the sur-
3.5-year-old DSH cat presented with new-onset seizures.72 rounding CSF.
• MRI findings include: • Less commonly, concurrent anomalies such as lissen-
• Hypoplasia/partial absence of a cerebral hemisphere. cephaly and hydranencephaly are seen.58,77
• Changes in the overlying cranium including hyper-
ostosis and expansion of the diploic space (Fig. 5.1.8). Dandy–Walker malformation complex
• In human patients, this refers to a group of congenital
CEREBELLAR MALFORMATIONS central nervous system anomalies that primarily involve
the cerebellum and adjacent tissues.
Congenital cerebellar aplasia • In people, the primary abnormalities are partial or com-
and hypoplasia plete absence of the cerebellar vermis, cystic dilation of
• These conditions are rare in dogs and cats:73 the fourth ventricle, and enlargement of the posterior
• Cerebellar aplasia/agenesis is defined as complete fossa.83 Comparable cases of cerebellar vermian aplasia
absence of cerebellar tissue.74,75 or hypoplasia with or without associated cystic dilation
• Cerebellar hypoplasia is characterized by uniform of the fourth ventricle have been reported in dogs.84–89
paucity of cerebellar tissue. Eurasier dogs are genetically predisposed.90,91
Fig. 5.1.10 Dandy–Walker-like malformation in a 5-year-old

male Eurasier dog. This sagittal T2W image demonstrates
absence of the caudal portion of the cerebellar vermis and
the caudal aspect of the cerebellar hemispheres. A large
accumulation of fluid is noted in the caudal fossa (asterisk) and
the fourth ventricle has a cyst-like dilation (arrow). (1.5T MRI
Fig. 5.1.9 Congenital cerebellar defect of undetermined system; reproduced, with permsission, from Bernardino F,
etiology in a 4-month-old Golden Retriever. This dorsal Rentmeister K, Schmidt MJ et al. (2015). Inferior cerebellar
T2W image demonstrates that the majority of the cerebellar hypoplasia resembling a Dandy-Walker-like malformation in
parenchyma of the left cerebellar hemisphere is missing and purebred Eurasier dogs with familial non-progressive ataxia:
has been replaced by CSF. Note also the shrunken, atrophied a retrospective and prospective clinical cohort study. PloS One
right eye (phthisis bulbi). (1.5T MRI system) 10(2):e0117670. doi:10.1371/ journal.pone.0117670.)
• Common MRI findings include (Fig. 5.1.10): spinal cord, and surrounding bony structures. Chiari
• Hypoplasia/agenesis of the cerebellar vermis.84,86,89,90 malformations 1–3 represent different degrees of her-
• Cyst-like dilation of the fourth ventricle.84,86,90 niation of posterior fossa content into the upper cervical
• Enlargement of the caudal fossa.84,86,90 canal (Chiari types 1 and 2) or through an upper cervical
• Less common MRI findings may include: meningocele (Chiari type 3). In Chiari type 4 there is
• Concurrent focal or generalized hypoplasia of the hypoplasia of the cerebellum.92
cerebellar hemispheres.84,86,90 • A disorder similar to Chiari type 1 malformation in
• Ventricular dilation. 84,86,90 people has been reported in dogs and is characterized by
• Extension of the cystic fourth ventricle into the supraten- a relatively small size of the caudal fossa and resultant
torial space with displacement of the occipital lobes.84 overcrowding of the neural structures.93–97 An earlier
• Absence/poor visibility of the corpus callosum and closure of the spheno-occipital synchondrosis has been
septum pellucidum.85,90 identified in predisposed breeds, and may be respon-
• Dorsal displacement of the osseous tentorium.84,86,90 sible for underdevelopment of the caudal fossa.98 The
• Widening and irregular gyrification of cerebral sulci.86 bony malformation leads to cerebellar compression and,
• Note that congenital cerebellar abnormalities may not in severe cases, herniation into or through the foramen
always be apparent on MRI examination. For example, magnum and kinking of the medulla.93,94
no abnormalities were detected in Coton de Tulear dogs • Several pathophysiologic mechanisms have been pro-
with neonatal cerebellar ataxia.81 posed to explain concurrent syringomyelia, which is a
common sequela in this condition (see Chapter 7.9).99–102
CHIARI-LIKE MALFORMATION (= CAUDAL • Cavalier King Charles Spaniels (in which an autosomal
OCCIPITAL MALFORMATION SYNDROME) recessive mode of inheritance is suspected) and Brussels
Griffons are predisposed, but Chiari-like malformations
• In humans, Chiari malformations are a group of struc- and syringomyelia are commonly seen in other small and
tural defects involving brainstem, cerebellum, upper toy breeds as well.38,95,96,103–105
168 CHAPTER 5.1
• Less commonly, concurrent ventriculomegaly and/

or occipital dysplasia manifesting as widening and
abnormal shape of the foramen magnum (likely unre-
lated to clinical signs).62,93,94,107
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170 CHAPTER 5.1
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10(4):365–7.
CHAPTER 5.2
METABOLIC AND DEGENERATIVE

172 ENCEPHALOPATHIES
Silke Hecht
CONTENTS
Lysosomal storage diseases.................................................................................................................................................................................. 172
Glycoproteinoses ............................................................................................................................................................................................. 173
Fucosidosis ............................................................................................................................................................................................... 173
Alpha-mannosidosis ................................................................................................................................................................................. 173
Sphingolipidoses............................................................................................................................................................................................. 173
Globoid cell leukodystrophy ...................................................................................................................................................................... 173
Gangliosidoses ......................................................................................................................................................................................... 173
Mucopolysaccharidoses .................................................................................................................................................................................. 174
MPS I (Hurler syndrome) .......................................................................................................................................................................... 174
MPS III (Sanfilippo syndrome type IIIB) .................................................................................................................................................... 175
Proteinoses...................................................................................................................................................................................................... 175
Neuronal ceroid lipofuscinosis (Batten disease) ........................................................................................................................................ 175
Cerebellar cortical abiotrophy in American Staffordshire Terriers ............................................................................................................... 176
L-2-hydroxyglutaric aciduria ................................................................................................................................................................................. 176
Hereditary polioencephalomyelopathies................................................................................................................................................................ 176
Hepatic encephalopathy ........................................................................................................................................................................................177
Kernicterus ............................................................................................................................................................................................................ 178
Hypoglycemic encephalopathy .............................................................................................................................................................................. 179
Thiamine deficiency .............................................................................................................................................................................................. 179
Hypocobalaminemic encephalopathy ....................................................................................................................................................................180
Myelinolysis/osmotic demyelination syndrome ....................................................................................................................................................180
Neuroaxonal dystrophies....................................................................................................................................................................................... 181
Spongy degeneration ............................................................................................................................................................................................ 181
Leukoencephalomyelopathy .................................................................................................................................................................................. 181
Cerebellar cortical abiotrophy (cerebellar cortical degeneration) ........................................................................................................................... 181
Idiopathic superficial neocortical degeneration and atrophy in young adult dogs .................................................................................................182
References.............................................................................................................................................................................................................182
A wide and heterogeneous range of diseases falls under this should alert the clinician to the possibility of a metabolic,
category. Description of specific conditions in this chapter nutritional or degenerative encephalopathy.
will be limited to disorders for which MRI findings in dogs
and/or cats have been reported. While imaging findings in LYSOSOMAL STORAGE DISEASES
different disorders vary, bilaterally symmetric signal inten-
sity changes to deep gray matter nuclei, with or without • Lysosomal storage diseases (LSDs) comprise a wide
abnormal contrast enhancement, symmetric and diffuse variety of abnormalities, which are characterized by the
signal intensity changes to gray and/or (subcortical) white intracellular accumulation of one or more products of an
matter, and/or brain atrophy are common and, if identified, interrupted metabolic pathway.1
M e ta bol ic a n d D e ge n e r at i v e E nc e ph a l opat h i e s 173
• More than 50 individual disorders have been reported to • In addition to progressive neurologic signs (tremors,
date.2 Most are inherited in an autosomal recessive fash- ataxia, dysmetria, and weakness), emaciation, skeletal
ion and involve single enzyme deficiencies. abnormalities, hepatomegaly, thymic aplasia, gingival
• Depending on the nature of the intracellular accumula- hyperplasia, ocular abnormalities, and polycystic kidney
tion, the main subgroups are the glycoproteinoses, the disease may also be encountered.2,25–28
oligosaccharidosis, the sphingolipidoses, the mucopoly- • Although morphologic or signal intensity changes on the
saccharidoses (MPS), and the proteinoses.3 common MRI pulse sequences have not been reported,
• Although many disorders affect the central nervous sys- quantitative MRI has been used in such animals, and
tem, ocular and musculoskeletal manifestations may also findings include:
be observed. • On DWI, a decrease in apparent diffusion coefficient
• LSDs do not usually have a gender predilection and the values of white and gray matter and, on quantita-
age at presentation is variable. tive T2-mapping, an increase in T2 values of white
• Clinical signs are often insidious in onset but always matter, corresponding to neuronal swelling, abnormal
progressive. A wide variety of neurologic signs may be myelin, and astrogliosis.29
observed including behavioral changes, loss of learned • A decrease in the magnetization transfer ratio in white
behavior, ataxia, proprioceptive deficits, apparent blind- matter of affected cats compared with normal cats.30
ness, deafness, and seizures. Cerebellar and cerebello- • A significant difference in MR spectroscopy spec-
vestibular signs such as tremors, ataxia, dysmetria, and tral patterns in the occipital cortex and the cerebellar
nystagmus with progression to paresis and paralysis are vermis between affected and unaffected cats.8
common.3
• In recent years, the increased awareness of these condi- Sphingolipidoses
tions has led to publication of an increasing number of Globoid cell leukodystrophy
individual case reports and case series of various natu- • Globoid cell leukodystrophy (Krabbe’s disease) is caused
rally occurring LSDs in small animal patients.4–9 In by mutations in the gene for galactocerebrosidase and
addition, research dogs have been used as a model not has been reported in a variety of dog breeds (West
only for human LSDs but also for canine and human Highland White Terrier, Cairn Terrier, Bluetick Hound,
aging as clinical, neuropathologic, and biochemical Australian Kelpie, Beagle, Irish Setter, Miniature Poodle)
changes in some diseases (e.g., ceroid lipofuscinosis and and cats.31–44
MPS type I) are similar between old dogs and people, • Clinical signs in affected animals occur by approximately
which allows both cross-sectional and longitudinal stud- 3–4 months of age and include tremors, ataxia, dysmet-
ies of disease progression in related animals with short ria, paresis/paralysis, urinary disorders, and visual and
life spans (see also Chapter 5.9).2,10–24 cognitive impairment. Neurologic status progressively
deteriorates until euthanasia/death.31–33,38,40,43
Glycoproteinoses • MRI findings include:
Fucosidosis • Changes consistent with diffuse, symmetric white
• Fucosidosis has been reported in a 2-year-old spayed matter disease (Fig. 5.2.1):43,45,46
female DSH cat presented with a 10-day history of pro- – Increased signal intensity in the corpus callosum
gressive incoordination.5 on T1W images.
• MRI findings include: – Symmetric T2 hyperintensity of corpus callosum,
• Extensive and diffuse hyperintensity of the white centrum semiovale, internal capsule, corona radi-
matter on T2W images, resulting in poor white and ata, and cerebellar white matter.
gray matter distinction in both the forebrain and cer- – Decreased T2 signal intensity of thalamus and
ebellum. caudate nucleus.
• Poor definition of the sulci. – Mild hydrocephalus.
• Bilaterally symmetric T2 hyperintensity of the – Symmetric contrast enhancement of the corpus
caudate nucleus, rostral thalamus, and ventral region callosum, internal capsule, and corona radiata.
of the internal capsule, and T1 hyperintensity in the • Hypointensity of white matter tracts on magnetiza-
internal capsule, rostral thalamus, and basal nuclei. tion transfer-weighted images consistent with demy-
• No contrast enhancement. elination.46
Alpha-mannosidosis Gangliosidoses
• Alpha-mannosidosis has been reported in Persian, long- • Gangliosidoses are characterized by excessive neuronal
hair and shorthair cats. Affected animals present as early accumulation of ganglioside and are subdivided depend-
as 8 weeks of age. ing on the type of enzyme deficiency.
174 CHAPTER 5.2
(a) (b)
Fig. 5.2.1 Globoid cell leukodystrophy in a 3-month-old Cairn Terrier. (a) This transverse T2W image shows generalized
diffuse increase in signal intensity of cerebral white matter (arrows) and hypointensity of the thalamus (asterisk). (b) This
transverse T1W image shows mild increased signal intensity of the corpus callosum (arrow). (1.5T MRI system; images
courtesy of Drs. Wilfried Mai and Charles Vite, University of Pennsylvania)
• GM1-gangliosidosis has been reported in cats and a variety disorders, tremors, depression, dementia, ataxia, and
of dog breeds including Shiba Inu dogs, Alaskan Huskies, blindness.7,9,56,61,62 MRI findings include:
Portuguese Water Dogs, English Springer Spaniels, and • Diffuse T2 hyperintensity and T1 hypointensity of
mixed breed dogs.47–54 Neurologic signs start at approxi- the subcortical cerebral white matter.9,61
mately 4 (cats) or 5 (dogs) months of age and consist of • Bilaterally symmetric T2 hyperintensity and T1
progressive tremors, muscle weakness, and ataxia result- hypointensity to the caudate nucleus without contrast
ing eventually in the inability to stand.2,20 MRI findings enhancement (later stages).7,9
include: • Cerebral and cerebellar atrophy of variable severity
• A relative increase in gray matter with thinning of the (later stages).7,9
white matter. • Absent, partially missing, or small corpus callosum
• An abnormal signal intensity of cerebral and cerebel- and rostral commissure.56
lar white matter on T2W images (Fig. 5.2.2).55
• Diffuse T2 hyperintensity of the cerebral white Mucopolysaccharidoses
matter and brain atrophy.20 Mucopolysaccharidoses (MPS) are a complex group of
• Absent, partially missing, or small corpus callosum diseases caused by various anomalies of metabolism of
and rostral commissure (Fig. 5.2.3). It has been glycosaminoglycan. Dogs and cats may be affected by
suggested that hypoplasia of the corpus callosum on various subtypes.3 Depending on the type, clinical abnor-
midline sagittal images may be a useful indicator of malities may involve the musculoskeletal, cardiovascu-
lysosomal storage disease, in particular juvenile-onset lar, respiratory, ocular, auditory, and central nervous
gangliosidoses.56 systems.2,3,63,64
• GM2-gangliosidosis has been reported in dogs (e.g.,
Golden Retriever and Toy Poodle) and cats (e.g., Korat MPS I (Hurler syndrome)
cats and DSH cats).7,9,57–60 In cats, neurologic signs occur • MPS I in dogs causes enlargement of the internal organs,
as early as 2–3 weeks of age and include head tremors and cardiac valvular disease, arteriosclerotic-like lesions in
cerebellar, mental, postural reaction, and spinal reflex large blood vessels, umbilical hernias, corneal clouding,
abnormalities. In dogs, clinical signs typically occur at bony deformities, poor growth, and a shortened life span
approximately 9–12 months of age and include motor (<3 years).
(a) (b)
Fig. 5.2.2 GM1 gangliosidosis in a 3-month-old dog. Transverse T2W (a) and T2-FLAIR (b) images demonstrating diffuse
T2 hyperintensity in the subcortical white matter of the cerebrum (arrows). (1.5T MRI system; reproduced, with permission,
from Hasegawa D, Yamato O, Nakamoto Y et al. (2012). Serial MRI features of canine GM1 gangliosidosis: a possible
imaging biomarker for diagnosis and progression of the disease. Scientific World Journal, Article ID 250197, http://dx.doi.
org/10.1100/2012/250197.)
(a) (b)
Fig. 5.2.3 Sagittal T2W images of the brain in a normal 4-month-old Beagle control (a) and a 6-month-old Shiba Inu dog with
GM1 gangliosidosis (b). In the normal dog (a), the corpus callosum (arrows), fornix (black arrowhead), and rostral commissure
(white arrowhead) are well identified. In contrast, in the affected dog (b) a normal corpus callosum is not identified. (1.5T MRI
system; images courtesy of Dr. Hasegawa, Nippon Veterinary and Life Science University)
• MRI findings have been reported in a Plott Hound including dysmetria, hindlimb ataxia, and a wide-based
research colony18 and include: stance on clinical examination.
• Cerebral ventricular enlargement and cortical atrophy • MRI examination of the brain was unremarkable in
at 12 months of age. these patients.65
• Abnormally small corpus callosum.
Proteinoses
MPS III (Sanfilippo syndrome type IIIB) Neuronal ceroid lipofuscinosis (Batten disease)
• MPS III has been reported in two Schipperke dogs who • Neuronal ceroid lipofuscinosis (NCL) is characterized
presented at 3 years of age with tremors and episodes by the abnormal accumulation of lipoprotein pigment
of stumbling and showed evidence of cerebellar disease within cellular lysosomes.
176 CHAPTER 5.2
• The disease has been reported in cats and a variety of • It has been described in Staffordshire Bull Terriers, West
dog breeds including English Setters, Chinese Crested Highland White Terriers, and Yorkshire Terriers.78–84
dogs, Dachshunds, Australian Cattle Dogs, Chihuahuas, Affected animals typically present between 6 months
Tibetan Terriers, and Border Collies.4,14,16,66–75 It has and 1 year of age, although initial presentation at as late
also been studied in canine models of human NCL and as 7 years of age is possible.
aging.10–13,24 Different variants exist, with both juvenile- • Neurologic signs are progressive and include seizures,
and adult-onset forms of the disease. altered behavior, dementia, head tremors, muscle stiff-
• Clinical signs include seizures, motor dysfunction, ness, and cerebellar ataxia.
impaired vision, progressive cognitive decline, impaired • MRI findings include:
memory, and behavioral problems. Most animals show • Bilaterally symmetric gray matter abnormalities
clinical signs between 1 and 3 years of age. (polioencephalopathy) affecting the cerebrum, cer-
• MRI findings include: ebellum, diencephalon, mesencephalon, and meten-
• Widening of the cerebral sulci and cerebellar fissures cephalon (Fig. 5.2.5):78–84
and ventriculomegaly indicative of brain atrophy – Abnormal swelling, T2 hyperintensity, and T1
(Fig. 5.2.4).4,6,69,74 isointensity or mild hypointensity of gray matter
• Abnormally small corpus callosum.56 with no contrast enhancement.
• Less common MRI findings include: – Cerebral cortex, thalamus, caudal colliculi, and
• Enhancement and thickening of meninges.4 dorsomedian tegmentum commonly affected.
• Subdural hematoma formation.76 – Symmetric changes to gray matter nuclei.
• Lack of gray and white matter distinction on T2W • T2 hyperintensity of peripheral subcortical white
images,6 although others have reported a normal matter.82
gray–white matter junction.74
HEREDITARY
Cerebellar cortical abiotrophy in American POLIOENCEPHALOMYELOPATHIES
Staffordshire Terriers
(See specific section below on this condition.) • Mitochondrial encephalopathies resembling subacute
• Cerebellar cortical abiotrophy in American Staffordshire necrotizing encephalomyelopathy (Leigh syndrome)
Terriers linked to an arylsulfatase G mutation is a special in people have been reported in a variety of dog breeds
type of NCL equivalent to rare adult-onset NCL (Kufs’ including Yorkshire Terriers, American Staffordshire
disease) in people.24,77 Bull Terriers, Alaskan Huskies, Australian Cattle Dogs,
Shi Tzus, English Springer Spaniels, and mixed breed
L-2-HYDROXYGLUTARIC ACIDURIA dogs.85–93
• A recent publication found that the ‘Alaskan Husky
• This is an autosomal recessive inborn error of metabo- encephalopathy’ previously attributed to a mitochondrial
lism caused by failure to break down L-2-hydroxyglutaric defect was in fact associated with a mutation in a thia-
acid, causing levels to rise in urine, plasma, and CSF. mine transporter protein.94
(a) (b) (c)

Fig. 5.2.4 Neuronal ceroid lipofuscinosis in a 1.5-year-old Chihuahua. The T2W sagittal image (a) shows generalized
cerebral atrophy with widened sulci, ventriculomegaly, and a small and irregularly shaped interthalamic adhesion (arrow).
There is also atrophy of the cerebellum, with increased CSF fluid signal separating the folia. The dorsal T1W pre- (b) and
post-contrast (c) images show thickening and enhancement of the meninges, especially along the right cerebrum (arrows, c).
(1.5T MRI system; images courtesy of Drs. Wilfried Mai and Charles Vite, University of Pennsylvania)
(a) (b)
Fig. 5.2.5 L-2-Hydroxyglutaric aciduria in a 9-month-old Staffordshire Bull Terrier. Transverse T2W (a) and T1W (b) images
showing bilaterally symmetric gray matter abnormalities characterized by abnormal swelling, T2 hyperintensity, and T1
hypointensity. (1.5T MRI system; images courtesy of Dr. Chris Lamb, Royal Veterinary College)
Fig. 5.2.6 Alaskan Husky encephalopathy (polioencephalopathy) in a 1-year-old dog. T2W images showing multifocal regions
of abnormal hyperintensity affecting the lateral aspect of the caudate nucleus, claustrum, putamen, thalamus, gray–white
matter junction, medulla, and cerebellum (arrows). (1.5T MRI system; reproduced, with permission, from Vernau KM,
Runstadler JA, Brown EA et al. (2013). Genome-wide association analysis identifies a mutation in the thiamine transporter 2
(slc19a3) gene associated with Alaskan Husky encephalopathy. PLoS One 8(3):e57195. doi:10.1371/journal.pone.0057195.)
• Affected animals present between 6 weeks and 5 years of contrast enhancement) of various brain and brainstem
age with a wide range of possible clinical signs including nuclei.90–92,94
ataxia, head tilt, nystagmus, strabismus, seizures, behav- • Symmetric spinal cord lesion(s) affecting the
ioral changes, disorientation, gait abnormalities, central gray matter (same signal characteristics as brain
visual deficits, reduced mentation, thoracic limb weak- lesions).90,91
ness, and progressive spastic tetraparesis.
• Histopathologically, there are bilaterally symmetric HEPATIC ENCEPHALOPATHY
areas of cavitation/necrosis/malacia of various brain and
brainstem nuclei, possibly associated with poliomalacia • Failure of the liver to remove toxic substances absorbed
of the spinal cord. from the gastrointestinal tract may result in hepatic
• MRI findings include (Fig. 5.2.6): encephalopathy. Portosystemic shunts are the most
• Bilaterally symmetric abnormalities (T2 hyperinten- common cause in veterinary patients, and most affected
sity and T1 iso- or hypointensity without evidence of animals present at a young age.
178 CHAPTER 5.2
• Onset of neurologic signs in older animals is possible and

often related to other liver diseases (e.g., cirrhosis).
• Neurologic manifestations include behavioral changes,
ataxia, pacing, head pressing, circling, blindness, sei-
zures, and coma.95–97
• Brain atrophy (Fig. 5.2.7).98,99
• Significantly higher concentration of the glutamine–
glutamate complex and significantly lower concentration
of myoinositol on magnetic resonance spectroscopy.100
• Less common MRI findings include:
• Bilaterally symmetric T1 hyperintensity to the len-
tiform nuclei attributed to increased concentration
of manganese, which decreases with treatment of the
underlying cause (Fig. 5.2.8).99,101
• Bilateral extensive T2 hyperintense lesions along the
cerebral cortex.98
Fig. 5.2.7 Generalized brain atrophy in a 7-year-old KERNICTERUS

Yorkshire Terrier presented with hepatic encephalopathy due
to a congenital portosystemic shunt. This T2W transverse • Kernicterus (bilirubin encephalopathy) is most com-
image shows generalized cerebral atrophy with widened sulci monly recognized in human infants and describes vary-
and ventriculomegaly. (1.0T MRI system) ing degrees of brain damage secondary to deposition of
bilirubin in the gray matter of the brain (especially the
basal ganglia) and spinal cord, accompanied by nerve cell
degeneration.102
(a) (b)
Fig. 5.2.8 Bilateral spontaneous (pre-contrast) T1 hyperintensities of the lentiform nuclei in a 2-year-old dog with acquired
portosystemic shunts secondary to liver fibrosis. Dorsal (a) and transverse (b) T1W images showing hyperintensity of the
lentiform nuclei (arrows). (1.0T MRI system; images courtesy of Dr. Wilfried Mai, University of Pennsylvania)
(a) (b)
Fig. 5.2.9 Kernicterus in a 9-year-old mixed-breed dog, treated for immune-mediated hemolytic anemia and increased serum
bilirubin concentration, that became comatose with cluster seizures. Transverse T2W (a) and T2-FLAIR (b) images showing
bilaterally symmetric hyperintensity of the caudate nuclei (asterisk, b) and cingulate gyri (arrow, b). (Images courtesy of
Dr. Andrew Specht, University of Florida)
• The condition has been reported in a 7-year-old Wheaten • MRI findings include:
Terrier103 with fulminant liver failure and a 9-year-old • Bilaterally symmetric lesions in the caudate nuclei:
mixed breed dog with immune-mediated hemolytic ane- – Strongly hyperintense on T2W and T2-FLAIR
mia, who underwent an MRI examination of the brain.104 images.
• MRI findings include: – Hyperintense rim with a hypointense center on
• Bilaterally symmetric T2 and T2-FLAIR hyperinten- T1W images.
sity of thalamus, lateral and medial geniculate nuclei, – No evidence of contrast enhancement.
caudate nuclei, regions of other basal nuclei, deep – Improvement of lesions after treatment.
cerebellar nuclei, and throughout the cerebral cortical
gray matter (Fig. 5.2.9). THIAMINE DEFICIENCY
• Slight increases in T2 signal intensity in regions of sub-
thalamic nuclei, substantia nigra, and hippocampus. • This is one of the few nutritional deficiencies still
• Mild T1 hyperintensity of caudate nuclei, region of relatively commonly reported in dogs and cats. In addi-
the globus pallidus, and deep cerebellar nuclei, with tion to the possibility of a deficiency in commercial pet
no evidence of contrast enhancement. foods, a deficiency may arise in dogs and cats with medi-
cal conditions. Thiamine deficiency results in insuf-
HYPOGLYCEMIC ENCEPHALOPATHY ficient ATP production in the brain, with subsequent
neuronal dysfunction.
• Due to the central role of glucose in the metabolism of the • Neurologic signs are highly variable and include altered
brain, severe hypoglycemia can induce neurologic lesions. mentation, acute blindness, proprioceptive deficits, ataxia,
• MRI findings in a 6-year-old West Highland White polyneuropathy, spastic ventroflexion of the head and neck,
Terrier presented with seizures and a staggering gait and extensor rigidity, vestibular signs, paresis, hyperesthesia,
subsequently diagnosed with an insulinoma have been tremors, seizures, and coma. Ocular, gastrointestinal, or
reported.105 cardiac abnormalities may also be present.106
180 CHAPTER 5.2
(a) (b)
Fig. 5.2.10 Thiamine deficiency in a 5-year-old cat. Transverse T2W images showing bilaterally symmetric hyperintense
lesions of the lateral geniculate nuclei (arrow, a) and the medial vestibular nuclei (arrow, b).
• MRI findings include: • MRI findings include:

• Bilaterally symmetric multifocal abnormalities affect- • Bilaterally symmetric abnormalities mostly affecting
ing nuclei of brain and brainstem: the gray matter.
– In dogs:107,108 • T2 hyperintense lesions in thalamus, mesencephalon,
– T2, T2-FLAIR, and post-contrast T1 hyper- pons, caudal cerebellar peduncles, and interposital
intensities in the red nuclei, caudal colliculi, nuclei (deep cerebellar nuclei).
vestibular nuclei of the brainstem, and the cer- • Resolution of changes after cobalamin supplemen-
ebellar nodulus. tation.
– Bilaterally symmetric T2 hyperintensities in
the caudate nuclei and rostral colliculi. MYELINOLYSIS/OSMOTIC
– In cats (Fig. 5.2.10):109–111 DEMYELINATION SYNDROME
– T2, T2-FLAIR, and T2* hyperintense non-
enhancing lesions associated with the lateral • This neurologic condition is typically caused by rapid
geniculate nuclei, caudal colliculi, periaque- correction of chronic hyponatremia and is most com-
ductal gray matter, medial vestibular nuclei, monly seen in human patients with electrolyte derange-
cerebellar nodulus, and facial nuclei. ments (alcoholics, liver transplant recipients, and patients
– T1 hyperintensity of the caudal colliculi, taking diuretics).
medial vestibular nuclei, and facial nuclei. • Lesions were originally thought to be limited to the
• Improvement or resolution with implementation of pons, but extrapontine locations including the thalamus,
thiamin supplementation.107,109,110 midbrain, cerebellum, basal nuclei, and cerebrocortical
gray and white matter junctions have been reported in
HYPOCOBALAMINEMIC ENCEPHALOPATHY human patients.116
• Myelinolysis has been experimentally induced in dogs and
• Cobalamin deficiency may be related to a congenital results in rigid quadriparesis.117 Naturally affected dogs
defect resulting in malabsorption, may result from a show neurologic deterioration following rapid correction of
variety of intestinal, hepatic and pancreatic diseases, or hyponatremia.118,119 A similar condition has been reported
may be related to malnutrition.112,113 in a cat and was attributed to severe malnutrition.120
• Clinical signs often include lethargy and inappetence; • MRI findings include:
neurologic abnormalities are less common.113–115 • Bilaterally symmetric T2/T2-FLAIR hyperin-
• MRI findings have been reported in an 8-year-old tense non-enhancing lesions within the thalamus,
British Shorthair cat presented with waxing and waning caudate nuclei, and along the cerebrocortical gray–
forebrain signs.115 white matter junction (Fig. 5.2.11).119
(a) (b)
Fig. 5.2.11 Myelinolysis following correction of hyponatremia in an 8-year-old mixed breed dog. Transverse T2W (a) and
T2-FLAIR (b) images showing bilaterally symmetric T2 hyperintensities associated with the thalamus (arrows).
(1.0T MRI system; images courtesy of Dr. Anthony Fischetti, Animal Medical Center)
NEUROAXONAL DYSTROPHIES • Smaller lesions within the thalamus ventromedial to

the lateral ventricles.
• These are a group of neurodegenerative disorders that
have been reported in several dog breeds (including LEUKOENCEPHALOMYELOPATHY
Rottweilers, Jack Russell Terriers, Collies, and Papillons)
and cats.121–129 • This is a rare degenerative disorder of undetermined
• Age at presentation and clinical signs vary between dif- etiology and reported in Rottweilers.132 Affected ani-
ferent types of the disease. mals develop signs consistent with general proprio-
• Imaging findings have been reported in Papillons: ceptive ataxia and upper motor neuron tetraparesis at
affected dogs present at approximately 3–4 months of 1.5–3.5 years of age. MRI changes with this condition
age with a variety of progressive clinical signs includ- have more commonly been reported in the spinal cord
ing tetraparesis, depressed postural reflexes, ataxia, head (see Chapter 7.11).
tremors, absent menace, and hypermetria.124,125,129 • MRI abnormalities of the brain have been reported in
• MRI findings include: one 22-month-old male Rottweiler, and included:133
• A normal MRI examination.124,129 • Bilaterally symmetric T2/T2*/T2-FLAIR hyperin-
• Progressive generalized brain atrophy.129 tense, T1 isointense, and non-enhancing intra-axial
lesions in the pyramids and ventral aspect of the crus
SPONGY DEGENERATION cerebri.
• A series of progressive neurologic diseases have been CEREBELLAR CORTICAL ABIOTROPHY

summarized under the nondescript term ‘spongy degenera- (CEREBELLAR CORTICAL DEGENERATION)
tion’. These conditions are primarily, but not exclusively,
diseases of white matter, may be hereditary, and may • This condition is characterized by degeneration of
result in a variety of clinical manifestations.130 initially normal neuronal cell populations within the
• Imaging findings have been reported in a 7-month-old cerebellar cortex after birth and can be considered a
Labrador Retriever evaluated for progressive tetraparesis subcategory in the complex group of ‘canine hereditary
and cerebellar dysfunction and subsequently diagnosed with ataxias’. In addition to familial reports in at least nine
a leukodystrophy similar to Canavan disease in children.131 breeds of dog, sporadic reports of this condition can be
• MRI findings include: found for at least 13 breeds to date.134–143 Reports in cats
• Large, ovoid, bilaterally symmetric T2 hyperintense are rare.144–146
and T1 hypointense non-enhancing lesions in the • Clinical signs consistent with cerebellar dysfunction
region of the deep cerebellar nuclei. are insidious in onset and progressive. Age at onset of
182 CHAPTER 5.2
IDIOPATHIC SUPERFICIAL NEOCORTICAL

DEGENERATION AND ATROPHY
IN YOUNG ADULT DOGS
• This is a recently recognized degenerative cerebral dis-

ease reported in 1–2-year-old dogs of a variety of breeds
(Irish Wolfhound, Poodle, Great Dane, Scottish Deer
Hound). Presenting neurologic signs include ataxia, dys-
phagia, blindness, and mentation changes.156
• MRI findings include severe bilateral cerebrocortical
atrophy and enlarged lateral and third ventricles.156
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186 CHAPTER 5.2
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CHAPTER 5.3
ENCEPHALITIS/MENINGOENCEPHALITIS
Benjamin Young 187
CONTENTS
General features of meningoencephalitis and meningitis ......................................................................................................................................188
Idiopathic or immune-mediated meningoencephalitis/meningitis .........................................................................................................................189
Meningoencephalitis of unknown etiology.......................................................................................................................................................189
Granulomatous meningoencephalomyelitis ................................................................................................................................................189
Necrotizing encephalitis .............................................................................................................................................................................190
Canine idiopathic eosinophilic (granulomatous) meningoencephalitis ............................................................................................................ 191
Idiopathic hypertrophic pachymeningitis .........................................................................................................................................................192
Viral encephalitis ..................................................................................................................................................................................................192
Distemper virus encephalitis............................................................................................................................................................................192
Feline coronavirus – feline infectious peritonitis .............................................................................................................................................193
Fungal meningoencephalitis .................................................................................................................................................................................194
Cryptococcosis ................................................................................................................................................................................................194
Blastomycosis .................................................................................................................................................................................................196
Coccidioidomycosis ........................................................................................................................................................................................ 197
Aspergillosis....................................................................................................................................................................................................199
Phaeohyphomycosis........................................................................................................................................................................................199
Rickettsial meningoencephalitis ............................................................................................................................................................................202
Canine monocytotropic ehrlichiosis ................................................................................................................................................................202
Bacterial meningoencephalitis, brain abscess, empyema ......................................................................................................................................202
Protozoal meningoencephalitis ............................................................................................................................................................................205
Neosporosis ....................................................................................................................................................................................................205
Toxoplasmosis .................................................................................................................................................................................................206
Parasitic meningoencephalitis...............................................................................................................................................................................206
References.............................................................................................................................................................................................................208
Meningoencephalitis may result from infection (bacterial, signs are rare, but pyrexia and systemic leukocytosis occa-
viral, protozoal, rickettsial, fungal, or parasitic) or from sionally accompany these conditions.1
non-infectious causes (idiopathic or immune-mediated). MRI is an essential diagnostic tool in the investigation
The clinical presentation of meningoencephalitis is vari- of brain disease; however, the MRI appearance of menin-
able and typically reflects the arrangement and location of goencephalitis can vary greatly depending on the cause and
the central nervous system (CNS) lesions.1 The spinal cord nature of the lesions. There is substantial variability even
may be affected simultaneously, adding to the complexity of within specific pathological entities. In addition, it is impor-
the clinical presentation. Meningoencephalitis commonly is tant to note that there is a great degree of overlap in MRI
acute in onset, progressive in nature, and associated with findings between different disease categories (inflamma-
a multifocal to diffuse neuroanatomic localization.1 More tory, neoplastic, vascular), and MRI signal characteristics
localized signs are possible in some forms of meningoen- are often not predictive of lesion etiology.2,3 The diagnosti-
cephalitis that manifest as mass lesions, and can mimic the cian must consider the combination of various MRI lesion
clinical presentation of neoplastic diseases. Extraneural characteristics and lesion distribution along with patient
188 CHAPTER 5.3
signalment and clinical history to develop a reasonable dif- sequences.9,10 T2-FLAIR images have been found to
ferential diagnosis list.3–5 have little benefit over T2W for identifying menin-
geal lesions in several studies.6,11,12
GENERAL FEATURES OF • Two patterns of meningeal contrast enhancement
MENINGOENCEPHALITIS AND MENINGITIS have been described:
– Enhancement of the leptomeninges (the arach-
• In general, when compared with neoplasia, the MRI noid and pia mater, ‘pial’ enhancement), which
appearance of meningoencephalitis is more likely to: extends into the cerebral sulci.
• Be multifocal (i.e., have multiple lesions).2,3,6,7 – Enhancement of the pachymeninges (the dura
• Involve both supratentorial and infratentorial por- mater and adjacent periosteum, ‘dural’ enhance-
tions of the brain (Fig. 5.3.1).3 ment), which does not extend into the sulci.13,14
• Have irregular lesion shape with ill-defined margins.2,3,6,7 • Several techniques have been shown to increase the
• Have uniform T2W and T2-FLAIR signal hyperin- visibility of meningeal contrast enhancement, includ-
tensity.3 ing the application of chemical fat suppression to
• Have meningeal contrast enhancement.3,6,7 T1W sequences and subtraction MRI (post-process
• In general, when compared with neoplasia, the MRI subtraction of the pre-contrast T1W image from
appearance of meningoencephalitis is less likely to: the post-contrast image).10,11,15 Normal dogs have
• Have strong contrast enhancement (although contrast been shown to have consistently identifiable contrast
enhancement is common).3,6 enhancement of the meninges when dynamic subtrac-
• Have heterogeneous T2W or T2-FLAIR signal tion is applied to the images, attributable mainly to
intensity.3 the pachymeningeal vessels.10 However, in dogs with
• Have mass effect (although still frequently seen).2,3,6 confirmed inflammatory conditions of the brain,
• General features of meningitis: dynamic subtraction does not appear to increase sen-
• Infectious or non-infectious inflammation of the sitivity of detection of meningeal enhancement, com-
meninges may occur independently or in conjunction pared with the standard comparison of pre- versus
with encephalitis.8 post-contrast images.16 This said, dynamic subtrac-
• Normal meninges are typically not visible on stand- tion appears to increase the sensitivity of MRI to
ard pre-contrast MRI sequences and may be incon- detect intra-axial inflammatory lesions in dogs16 and
spicuous or faintly enhanced on post-contrast T1W may therefore still be recommended when meningo-
encephalitis is suspected.
• Delayed acquisition time following gadolinium
administration has been reported to provide marginal
improvement of contrast enhancement of meninges.9,15
• Overall, MRI has been shown to have low sensitiv-
ity for identifying meningeal pathology, particularly
disease affecting the leptomeninges.11 Meningeal con-
trast enhancement is also not highly sensitive for iden-
tifying dogs with inflammatory cerebrospinal fluid
(CSF) and is non-specific, occurring variably with
infectious, non-infectious inflammatory, and neoplas-
tic conditions.2,3,6,11,13,15,17–19 Therefore, the absence of
abnormal meningeal contrast enhancement does not
rule out meningitis.
• When present, the MRI findings that can indicate
meningitis include:
– T2W and T2-FLAIR hyperintensity of the
meninges (Fig. 5.3.2).11,13
– Increased meningeal contrast enhancement,
which may or may not extend into the cerebral
sulci depending on the meningeal layers involved
Fig. 5.3.1 Granulomatous meningoencephalitis in a (Fig. 5.3.2).6,11,13,15,17,20,21
4-year-old Basset Hound. Transverse T2W image showing – Increased thickness (smooth or nodular) of the
bilateral hyperintensity of both cerebral hemispheres and meninges.11,15,18
the left aspect of the brainstem (arrows). (3T MRI system; – These meningeal abnormalities may be focal,
image courtesy of Dr. Jay Griffin, Texas A&M University) regional, or diffuse.11,15,18
E nc e ph a l i t is / M e n i ng oe nc e ph a l i t is 189
(a) (b)
Fig. 5.3.2 Idiopathic eosinophilic meningoencephalitis in a 3-year-old mixed breed dog. (a) Transverse T2-FLAIR image
showing hyperintensity of the right cerebral leptomeninges extending into the sulci (arrows) as well as an ill-defined
hyperintensity in the right brain parenchyma (dotted arrow). (b) Dorsal post-contrast T1W image showing increased
enhancement of the right cerebral leptomeninges extending into the sulci (arrows). (1.5T MRI system; images courtesy of
IDIOPATHIC OR IMMUNE-MEDIATED • Multifocal lesions of the white and gray matter, which
MENINGOENCEPHALITIS/MENINGITIS can involve the forebrain, brainstem, and cerebel-
lum.1,20,24,25
Meningoencephalitis of unknown etiology • Irregular lesion margins, T2W and T2-FLAIR
Meningoencephalitis of unknown etiology (MUE) is an hyperintensity, and T1W hypo- or isointensity.1,6,25
umbrella term used when an antemortem diagnosis of idio- • Contrast enhancement is variable and can have a ring-
pathic meningoencephalitis is suspected but histopathologic like pattern.1,24–26
diagnosis has not been established.1,22 The various catego- • T2W perilesional hyperintensity (indicating edema).1,25
ries of MUE share similar clinical and neuropathologic • Meningeal enhancement is not typical but may be
features and include granulomatous meningoencephalomy- present.13
elitis (GME), necrotizing meningoencephalitis (NME), and • MRI findings of focal GME may be indistinguishable
necrotizing leukoencephalitis (NLE).1 from neoplasia, and include (Fig. 5.3.4):
• A single mass.27,28
Granulomatous meningoencephalomyelitis • Mass effect with compression or displacement of the
• GME most commonly affects young and middle-aged adjacent structures.13,28,29
dogs, and lesions can have diffuse, focal, or ocular distri- • Variable, occasionally strong, contrast enhancement.27,28
bution.1,22,23 Therefore, the MRI appearance is variable • T2W hypointense foci associated with hemorrhage.29
and reflects that distribution. • MRI findings of ocular GME have been described in a
• The onset of disease is often acute and progressive. single case including:
A combination of signalment, clinical signs, CSF analy- • T1W and T2W isointense mass-like enlargement of
sis, and MRI findings is often used to make a presump- the optic chiasm.30
tive antemortem diagnosis.22 • Strong contrast enhancement of the optic nerves.30
• Common MRI findings of the diffuse form of GME • T2W hyperintensity (edema) of the optic pathway,
include (Fig. 5.3.3): ventral thalamus, and forebrain.30
190 CHAPTER 5.3
(a) (b)
Fig. 5.3.3 Diffuse granulomatous meningoencephalitis in a

4-year-old Dachshund. Transverse T2W (a) and MP-RAGE
(a T1W sequence) (b) images showing bilaterally asymmetric
lesions of the cerebral white and gray matter that are T2W
hyperintense (dotted arrows, a) and T1W hypointense (b).
Transverse post-contrast MP-RAGE with fat saturation
image (c) showing strong multifocal contrast enhancement
(black arrows). There is also contrast enhancement of the
leptomeninges on the right (white arrow). (3T MRI system;
(c)
images courtesy of Dr. Jay Griffin, Texas A&M University)
Necrotizing encephalitis Pekingese) and more recently also in the Papillon, Shih
• It has been proposed that both NME (formerly known Tzu, Coton de Tulear, Brussels Griffon, and a large
as ‘Pug dog encephalitis’) and NLE (formerly known mixed-breed dog. This led some authors to suggest that
as ‘necrotizing encephalitis of Yorkshire Terriers’) may this condition is not breed restricted.31,33
represent a spectrum of necrotizing inflammatory brain • Common MRI findings of NME are listed below
disease of unknown etiology with similar pathogenesis, (Fig. 5.3.5):
thought to be invariably fatal.1 There is overlap in neuro- • Multifocal, asymmetric lesions with ill-defined
pathologic findings between both conditions, and breeds margins affecting the cortical gray and subcortical
predisposed to one form have been diagnosed with the white matter, causing loss of gray–white matter dis-
other based on histopathology.1 However, the anatomic tinction. Lesions can be found in the cerebral hem-
distributions of lesions in these two variants of necrotiz- ispheres, hippocampus, thalamus, caudal brainstem,
ing encephalitis (NE) have been described in numerous and cerebellum.19,31,33,34
reports and are worth listing separately. • Lesions are iso- or mildly hypointense on T1W
images and hyperintense on T2W and T2-FLAIR
Necrotizing meningoencephalitis images.19,20,31,33,34
• NME typically affects young animals (mean • Variable and mild contrast enhancement of parenchy-
27.5 months).1,31,32 It was first described in several small mal lesions.19,31,33,34
dog breeds (Pug, Yorkshire Terrier, Maltese, Chihuahua, • Mild contrast enhancement of the leptomeninges.19,31,34
VetBooks.ir
(b)
Fig. 5.3.4 Focal granulomatous meningoencephalitis in a

6-year-old Dachshund. (a) Dorsal T2W image showing a large,
ill-defined heterogeneously hyperintense mass of the right
cerebral hemisphere causing leftward displacement of the falx
cerebri (arrowhead). (b) Transverse post-contrast MP-RAGE
image (a T1W sequence) showing well-defined strong contrast
enhancement of the mass (arrow). (3T MRI system; images
(a)
courtesy of Dr. Jay Griffin, Texas A&M University)
• Asymmetric lateral ventriculomegaly.19,31,34 but also the cortical gray matter, thalamus, and brain-
• Mass effect causing falx cerebri shift.19,31,33,34 stem.1,36,39,40
• Perilesional T2W and T2-FLAIR hyperintensity • Lesions are hypointense on T1W images and hyper-
(edema).19,33,34 intense on T2W and T2-FLAIR images.37,39,40
• Occasional MRI findings of NME include: • Contrast enhancement is variable and can have a ring-
• Cerebellar herniation through the foramen like pattern.36,37,39,40
magnum.19,31,33,34 • Lateral ventriculomegaly.35,36,40
• Sharply margined cyst-like lesions (T1W hypoin- • Perilesional T2W hyperintensity (edema).36
tense/T2W hyperintense) characteristic of necrotic • Sharply delineated cyst-like lesions (T1 hypointense/
fluid.19,33 T2 hyperintense) have been reported, but are
• In some cases, lesions are confined to the caudal uncommon.37
brainstem.19
Canine idiopathic eosinophilic
(granulomatous) meningoencephalitis
Necrotizing leukoencephalitis • Idiopathic eosinophilic meningoencephalitis has been
• This type of necrotizing encephalitis has been reported described in a number of dog breeds, most commonly in
with similar lesion distribution in the Yorkshire Terrier young to middle-aged, large breed dogs.41
and French Bulldog.35–39 • CSF eosinophilia is commonly seen with this condi-
• It affects primarily young animals, with a mean age of tion, and the clinical outcome is more favorable than in
4.5 years.1,35 dogs with parasitic, protozoal, or mycotic causes of CSF
• Both cerebral and brainstem lesions are seen.35–39 eosinophilia.41,42
• MRI findings of NLE include: • The MRI appearance is quite variable, which may indi-
• Multifocal, asymmetric irregularly shaped lesions cate a variety of underlying etiologies, including breed-
with ill-defined margins, predominantly affecting the associated encephalitides.41–43
subcortical white matter of the cerebral hemispheres, • MRI findings in dogs include (Fig. 5.3.2):
192 CHAPTER 5.3
(a) (b)
Fig. 5.3.5 Necrotizing meningoencephalitis in a 1-year-

old Pug dog. Transverse T2W (a) and MP-RAGE (a T1W
sequence) (b) images showing bilaterally asymmetric
lesions of the gray and white matter, including hippocampal
involvement. Most lesions are ill-defined T2W hyperintense
and T1W iso- or mildly hypointense (black arrows, a
and b). There is a well-defined T2W hyperintense and
T1W hypointense cystic lesion (white arrow, a and b).
(c) Transverse post-contrast MP-RAGE with fat saturation
image showing no contrast enhancement of the lesions.
(3T MRI system; images courtesy of Dr. Jay Griffin, Texas
(c)
A&M University)
• Widening of the cerebral sulci indicating cortical (i.e., limited to the dura with no extension into the
atrophy.41,43 sulci), which can be severe.
• Patchy cerebral T2W hyperintensity.41,42 • In some cases, the enhanced dura has a layered
• Diffuse T1W hypointensity of the cerebral gray matter.43 pattern, with two enhancing layers surrounding an
• Patchy or diffuse contrast enhancement of the cere- iso- to hypointense central layer.
bral cortex or meninges.41,42
• Intra-axial mass lesions.41 VIRAL ENCEPHALITIS
Idiopathic hypertrophic pachymeningitis Distemper virus encephalitis

• Idiopathic hypertrophic pachymeningitis is a reported • Distemper virus can affect both young and mature
condition affecting the dura mater in which no infec- animals, causing brain gray matter demyelination and
tious or other underlying cause can be determined on necrosis in acute infection and lymphoplasmacytic
CSF analysis. The prognosis is fair to poor with immu- inflammation, humoral response, and oxidative destruc-
nomodulating drug therapy.18 tion of white matter in animals that survive to suffer
• MRI findings with this condition include (Fig. 5.3.6): chronic or latent infections.22,44–46
• Thickening, increased T2W hyperintensity, and • The appearance of MRI lesions differs markedly depend-
increased contrast enhancement of the pachymeninges ing on the chronicity of infection.45
(a) (b)
Fig. 5.3.6 Idiopathic hypertrophic pachymeningitis in a 6-year-old Greyhound. (a, b) Transverse post-contrast T1W images
showing severe thickening and strong enhancement of the pachymeninges, which does not extend into the cerebral sulci.
There is a subtle non-enhancing layer within the thickened meninges (arrows, a). (1.5T MRI system; images courtesy of
• In the acute form, MRI findings include (Fig. 5.3.7): Feline coronavirus – feline
• Large, ill-defined lesions affecting the cerebral infectious peritonitis
gray matter that are T2W and T2-FLAIR hyperin- • Feline infectious peritonitis (FIP) is a pyogranulomatous
tense and T1W iso- or hypointense. These cerebral vasculitis occurring in a small number of cats infected with
lesions are seen most commonly in the temporal lobes the ubiquitous enteric feline coronavirus.47 Neurologic
and may be attributed to the acute, post-ictal brain manifestation of FIP is reportedly common, and may be
edema.44 concurrent with ocular or intra-abdominal lesions.48
• T2W hyperintense, T1W hypointense lesions in the • As with FIP in general, cats with neurologic manifesta-
cerebellum and brainstem with loss of gray–white tions of FIP are most commonly young (less than 2 years
matter distinction, corresponding histopathologically of age).7,47,48
to areas of demyelination.44 • In the brain, histopathologic lesions include meningitis,
• Variable contrast enhancement of these lesions.44 ventriculitis, choroiditis, and periventricular vasculi-
• The MRI findings of chronic distemper meningoen- tis; this explains the common MRI findings of contrast
cephalitis have been reported in a single dog,45 and enhancement of the meninges and ventricular lining.48
include (Fig. 5.3.8): Brain parenchymal granulomas can also be present.48
• Bilaterally symmetric hyperintense T2W lesions of • MRI findings of neurologic FIP include:
the white matter just deep to the gray–white matter • Meningeal, ependymal, or periventricular contrast
junction of the parietal and frontal lobes. enhancement (mild to strong); this sign appears to
• T2W hyperintensity of the arbor vitae of the cere- be more common with FIP than with other causes of
bellum causing loss of cerebellar gray–white matter feline meningoencephalitis (Fig. 5.3.9).20,48–50
junction. • Dilation of lateral, third, or fourth ventricles
• Ill-defined hyperintense T2W lesion of the caudal (Fig. 5.3.9).7,48,49
brainstem. • When present, parenchymal lesions have distinct
• These lesions are not visible on T1W pre- and margins in most cases, a trend noted more frequently
post-contrast images. with FIP than with other causes of feline meningoen-
• Pachymeningeal contrast enhancement. cephalitis.7
194 CHAPTER 5.3
VetBooks.ir
(a) (b) (c)

Fig. 5.3.7 Distemper encephalitis in a 7-year-old Boxer dog with refractory seizures. (a) Transverse T2W image showing
ill-defined hyperintensity throughout the right temporal and piriform gray and white matter with a smaller lesion in the
hippocampus and left piriform lobe. (b) Lesions are iso- to hypointense on this T1-FLAIR image. (c) Transverse post-contrast
T1-FLAIR with fat saturation image showing subtle enhancement of the right piriform lesion and enhancement of the
leptomeninges (arrows). (3T MRI system; images courtesy of Dr. Jay Griffin, Texas A&M University)
(a) (b)
Fig. 5.3.8 Sagittal (a) and transverse (b) T2W images at the level of the interthalamic adhesion in a 3-year-old Chihuahua with
chronic distemper meningoencephalitis. There is hyperintensity of the arbor vitae (arrow, a) with partial loss of cerebellar
cortical gray–white matter demarcation and nearly symmetric hyperintensity of the cortical gray–white matter junction of
the parietal lobes (b). (1T MRI system; reproduced, with permission, from Griffin JF, Young BD, Levine JM (2009). Imaging
diagnosis: chronic distemper meningoencephalitis. Vet Radiol Ultrasound 50(2):182–4.)
• Lesions can be focal or multifocal and can involve the FUNGAL MENINGOENCEPHALITIS
cerebellum.7,48
• They are T2W iso- or hyperintense and T1W iso- or Cryptococcosis
hypointense,7 and most have moderate to strong con- • CNS infection caused by the saprophytic fungus
trast enhancement.7 Cryptococcus neoformans is seen in dogs (most less than 4
• Often, additional lesions are visible following contrast years old) and cats (over 5 years of age in one report),
administration that were not visible on pre-contrast likely acquired through inhalation.51–56
images. In some cats, lesions are only visible on • Dogs typically have a histologically greater inflamma-
post-contrast T1W images.7 tory response within lesions than cats, which may affect
• Cerebellar herniation can be present.7 the appearance on MRI.46,54,57
• In some cases no abnormality is seen.7
(a) (b)
Fig. 5.3.9 Sagittal T1W post-contrast (a) and T2W (b) images in a cat with FIP, in which there is marked dilation of the
fourth ventricle and moderate dilation of the third ventricle. The ependymal lining of the ventricle has enhanced signal
after gadolinium contrast medium intravenous administration (arrowheads, a). (1.5T MRI system; reproduced, with
permission, from Negrin A, Lamb CR, Cappello R et al. (2007). Results of magnetic resonance imaging in 14 cats with
meningoencephalitis. J Feline Med Surg 92(2):109–116.)
• The development of intracranial pseudocysts is com-

mon; they correspond histopathologically to cavitations
filled with gelatinous material, resulting from a prolif-
eration of fungi and gelatinous capsular material in the
Virchow–Robin space.57 The disease can also cause dif-
fuse meningoencephalitis, focal granulomas, or ventric-
ulitis, which will also determine the MRI appearance of
lesions.57
• MRI findings of cryptococcosis in dogs include:
• Multifocal or, less commonly, isolated, parenchymal
(forebrain, cerebellum, midbrain) and meningeal
lesions.54,56–59
• Parenchymal lesions have an equal predilection for
gray and white matter involvement,54,57–59 and are typ-
ically T2W and T2-FLAIR hyperintense and T1W
hypointense with indistinct margins; well-defined
lesions can be seen in cases with granulomas or pseu-
docyts.54,56–59
• Perilesional T2W hyperintensity (edema).54,56,57,59
• Occasional mass lesions with mass effect and brain
herniation, most commonly in the frontal and olfac-
tory lobes (Fig. 5.3.10).54,56,57
• Very common contrast enhancement. In some cases,
lesions are only seen on post-contrast images. Patterns
of enhancement include:58
– Focal or diffuse meningeal enhancement (present
in most cases), and occasionally meningeal thick-
ening (Fig. 5.3.11); in some dogs, this is the only
abnormality seen on MRI.57 Fig. 5.3.10 Cryptococcal encephalitis in a 2-year-old Golden
– Ill-defined mild-to-moderate (sometimes strong) Retriever. T2W dorsal image showing focal enlargement of
enhancement of parenchymal lesions. the right olfactory lobe with hyperintensity of the gray and
– Occasional faint ring-like enhancement,58 though white matter (arrow). (3T MRI system; image courtesy of
less frequent than in cats.57 Dr. Jay Griffin, Texas A&M University)
196 CHAPTER 5.3
– Enhancement of the choroid plexus.13,56–59

– Possible contrast enhancement of periocular soft
tissues.57
• Nasal cavity or paranasal sinuses lesions extending
through the cribriform plate.57
• Medial retropharyngeal and mandibular lymphade-
nomegaly.57
• Reversal of some MRI changes has been reported fol-
lowing long-term treatment with antifungal drugs,
with persistence of well-defined contrast-enhancing
lesions in the frontal cortex, presumably due to gran-
uloma formation.59
• MRI findings of cryptococcosis in cats include:
• Multifocal or, less commonly, isolated parenchymal
(forebrain, cerebellum, midbrain) and meningeal
lesions.54,56,57,60
• Parenchymal lesions have an equal predilection for
gray and white matter involvement, and are typi-
cally T2W and T2-FLAIR hyperintense and T1W
hypointense with indistinct margins;56,57,60 well-
defined lesions can be seen in cases with granulomas
or pseudocysts (Fig. 5.3.12).
• Contrast enhancement of lesions is almost always
(a) present and can be focal or multifocal; strong
enhancement is most common. Meningeal enhance-
ment is present in most cases.54,57,60 Poor enhancement
or lack of enhancement is, however, possible (personal
observation) and may be due to the minimal inflam-
matory response seen on histopathology in cats with
cryptococcosis.54
• Pseudocysts (well-marginated focal T2W hyperin-
tense, T1W hypointense lesions) can have periph-
eral contrast enhancement (some also have central
enhancement) (Fig. 5.3.12).57
• Mass effect with herniation can be present.54,60
• Occasionally the MRI examination can be normal.57
Blastomycosis
• Intracranial disease caused by Blastomyces dermatitidis
infection is typically seen in young dogs (and rarely in
cats) in the Midwest river valleys and the South of the
USA.61–63 Reported MRI lesions caused by blastomycosis
fall into two categories: mass lesions or ependymal and
ventricular changes.
• MRI findings of focal lesions caused by blastomycosis
include:
• Intra- or extra-axial, single or multifocal masses, some
of which extend from the nasal cavity or retrobulbar
(b) space into the cranial cavity.64,65
Fig. 5.3.11 Transverse T1W pre- (a) and post-contrast (b) • Most lesions are T2W hyperintense and T1W iso-
images in a 1-year-old dog with cryptococcosis (identified in or hypointense; however, some lesions have been
the CSF). There is marked meningeal enhancement extending reported to be T2W iso- or hypointense.64,65
deep into the sulci, characteristic of leptomeningitis. • Strong uniform contrast enhancement of lesions
(1.5T MRI system; images courtesy of Dr. Wilfried Mai, is reported in almost all cases, with occasional ring
University of Pennsylvania) enhancement; meningeal thickening and enhance-
ment with a dural tail sign is also described.64,65
E nc e ph a l i t i s / M e n i ng oe nc e ph a l i t i s 197
(a)
(b) (c)
Fig. 5.3.12 Transverse T2W (a), sagittal T2W (b), and dorsal T1W (c) images in a 2-year-old cat with progressive neurologic
signs, diagnosed with cryptococcosis based on CSF analysis. On the transverse image (a), there are punctate T2W
hyperintensities in both caudate nuclei (solid arrows) and a larger focal irregular hyperintense lesion in the left cerebral
hemisphere (dashed arrow). On the sagittal image (b), a well-defined markedly hyperintense lesion is seen in the left temporal
lobe (arrow) corresponding to a hypointense oval-shaped lesion on the dorsal T1W image (arrowhead), consistent with a
Cryptococcus pseudocyst. (1.5T MRI system; images courtesy of Dr. Wilfried Mai, University of Pennsylvania)
• Perilesional T2 hyperintensity (edema) is common.64,65 dogs and cats in the Southwest of the USA, clinical dis-
• Mass effect with midline shift is common.64,65 ease occurs at a much lower rate, most commonly seen
• MRI findings of ventricular lesions caused by blastomy- in dogs less than 3 years of age and cats around 5 years
cosis include:62 of age.66–68
• Bilaterally enlarged lateral ventricles with occasional • Systemic disease is spread hematogenously after inhala-
dilation of the olfactory recesses. tion of the soil-based organism.68
• Enlarged or compressed third ventricle. • Intracranial lesions can include granulomatous mass-
• Compressed mesencephalic aqueduct. like lesions or granulomatous meningitis.54,69 The MRI
• T2W and T2-FLAIR hyperintensity surrounding the appearance of solitary CNS Coccidioides lesions reportedly
rostral horn and occipital portions of the lateral ven- shares many similarities with neoplasia including glioma,
tricles, third ventricle, mesencephalic aqueduct, and meningiomas, and round cell neoplasia.69 Indistinct
fourth ventricle. lesion borders and indeterminate lesion compartmental-
• Ependymal or periventricular contrast enhancement ization (i.e., intra-axial versus extra-axial) were suggested
of the lateral ventricles, third ventricle, mesencephalic as possible characteristics of coccidioidomycosis to help
aqueduct, and fourth ventricle. distinguish it from neoplasia.69
• MRI findings of coccidioidomycosis include:
Coccidioidomycosis • Solitary parenchymal or meningeal lesions.69
• Although the infection rate of the dimorphic fungi Although it has been observed, the MRI appear-
Coccidioides immitis and Coccidioides posadasii is high among ance of non-solitary disease (multifocal) has not been
198 CHAPTER 5.3
reported at the time of writing; parenchymal lesions • Perilesional T2 hyperintensity (edema) is common
often cause a mass effect.69 (Fig. 5.3.13).69
• Most lesions have entirely indistinct margins or a • Homogeneous mild to marked contrast enhancement
mixture of distinct and indistinct regions.69 is most common (Fig. 5.3.13), although heterogene-
• Most lesions are T2W hyperintense and T1W isoin- ous or absent contrast enhancement is possible;54,69 a
tense to normal gray matter. However, lesions with dural tail sign can be present.69
T2W iso- or hypointensity and T1W hypo- or hyper- • T2W hyperintensity and contrast enhancement of the
intensity were also reported (Fig. 5.3.13).54,69 cranial musculature has been reported.54
(a)
(c)
Fig. 5.3.13 Transverse T2W (a), transverse T1W post-

contrast (b), and dorsal T1W post-contrast (c) images
in a 3-year-old Boxer with coccidioidomycosis. On
the T2W image (a) there is a focal heterogeneous
lesion with areas of T2W hypointensity (solid
arrow), surrounded by marked poorly marginated
perilesional edema (dashed arrows). Marked
heterogeneous enhancement of the focal lesion is
seen on post-contrast images (b, c). (1.5T MRI system;
images courtesy of Dr. Wilfried Mai, University of
(b) Pennsylvania)
Aspergillosis • Occasional signal voids on T2*W gradient echo

• Nasal or systemic aspergillosis (caused by Aspergillus images, indicating intralesional hemorrhage.72
fumigatus, A. terreus, A. deflectus, and other species) can • Absence of MRI abnormality does not rule out CNS
lead to CNS infection.70–73 involvement with aspergillosis.72
• Young to middle-aged dogs are most commonly affected • Changes outside of the CNS include abnormal signal
by this opportunistic organism.70 German Shepherd intensity or contrast enhancement of the cochlear
Dogs are notably susceptible to systemic infection, which fluid or intraocular structures.72
may indicate a genetic predisposition.70,71
• The MRI appearance of dogs with intracranial aspergil- Phaeohyphomycosis
losis is quite variable in the few cases reported.71,72 MRI • Infections caused by a variety of opportunistic, pig-
findings include: mented fungi are referred to as phaeohyphomycoses.
• Asymmetric multifocal intra-axial lesions of the cere- Affected dogs and cats can be immunocompetent, immu-
brum, thalamus, or brainstem.71,72 nocompromised, or have concurrent disease.74,75 The
• Occasionally, a plaque-like extra-axial mass.72 most common of these organisms to cause intracranial
• Lesions are typically T2W and T2-FLAIR hyperin- disease is Cladophialophora (previously called Cladosporium
tense or mixed intensity, T1W iso- or mildly hypoin- and Xylohypha).75 The prognosis for intracranial infection
tense.71,72 is considered grave, although there are case reports of
• Inconsistent perilesional T2W hyperintensity indi- long-term survival following a combination of surgical
cating edema.71,72 debulking and antifungal therapy.54,74
• Possible mass effect with larger intra-axial mass • Fungal granulomas in the brain associated with this
causing falx shift.71,72 fungal species are often isolated but are occasionally
• Contrast enhancement (often strong) in most lesions multiple. Description of the MRI appearance of phaeo-
(both intra- and extra-axial);71,72 meningeal enhance- hyphomycosis is limited to a few individuals (two dogs
ment is occasionally seen (Fig. 5.3.14).72 and one cat).
(a) (b) (c)

Fig. 5.3.14 Aspergillosis in a 3-year-old German Shepherd Dog. (a) T2W dorsal image showing multiple focal hyperintensities
in the left cerebral white matter (black arrows), which could not be identified on pre-contrast T1W images. (b, c) Dorsal post-
contrast MP-RAGE with fat saturation (a T1W sequence) images showing multiple focal enhancing lesions (white arrows).
(3T MRI system; images courtesy of Dr. Jay Griffin, Texas A&M University)
200 CHAPTER 5.3
• The reported MRI appearance of phaeohyphomycosis • Ill-defined T2W hyperintense/T1W hypointense

includes two patterns: mass-like enlargement of a cerebral hemisphere, with
• Large well-defined solitary mass, with a T2W strong non-uniform contrast enhancement, causing
hyperintense/T1W hypointense non-enhancing mass effect (falx shift, lateral ventricular compression,
center, and a thick peripheral rim, which is T2W caudal transtentorial, and foramen magnum hernia-
iso- or hypointense, T1W-isointense, and strongly tion).76 More focal and distinct mass lesions are also
enhancing (Fig. 5.3.15); perilesional T2W hyper- possible (Fig. 5.3.16).
intensity is present consistent with edema.54,74 This
cavitated appearance is due to abscessation.74
Fig. 5.3.15 Transverse T2W (a), T1W pre-contrast (b), and

T1W post-contrast (c) images of the brain in a 12-month-
old castrated male Boxer with acute progressive neurologic
signs, with a subsequent diagnosis of an intracranial
phaeohyphomycotic abscessed granuloma. On the transverse
T2W image (a), at the level of the center of the mass, the
lesion has a hyperintense center (star) and a hypointense
rim; there is midline shift and severe perilesional edema of
surrounding white matter tracts (arrows). On the transverse
post-contrast T1W image (c), there is strong contrast
enhancement of the rim of the lesion. (1.5T MRI system;
reproduced, with permission, from Bentley RT, Faissler D,
Sutherland-Smith J (2011). Successful management of an
intracranial phaeohyphomycotic fungal granuloma in a dog.
J Am Vet Med Assoc 239(4):480–5.)
(a)
(b) (c)
(a) (b)
(c) (d)
Fig. 5.3.16 Sagittal T2W (a), transverse T2-FLAIR (b), T1W pre-contrast (c), and T1W post-contrast (d) images of the brain in
a 4-year-old Jack Russell Terrier presented with acute onset of progressive central vestibular signs. There is a mass associated
with the left rostral colliculus, which is T2W heterogeneously hyperintense, T2-FLAIR heterogeneously iso- to hyperintense,
and T1W hypointense (solid arrows, a, b, and c). There is marked contrast enhancement (solid arrow, d). There is perilesional
edema (dashed arrows, a and b). The mass is causing mass effect on the cerebellum, with caudal displacement and foramen
magnum herniation (arrowhead, a). Poorly defined T2W hyperintense signal is seen in the cranial cervical spinal cord and
likely represents early syringomyelia secondary to the cerebellar herniation through the foramen magnum. At necropsy,
a dense inflammatory infiltrate of neutrophils and epithelioid macrophages was present centered on pigmented fungal
hyphae with non-parallel walls, variably distinct septae, and non-dichotomous branching; rare pigmented fungal yeasts were
present. The morphology and pigmentation were consistent with phaeohyphomycosis. (1.5T MRI system; images courtesy of
202 CHAPTER 5.3
RICKETTSIAL MENINGOENCEPHALITIS BACTERIAL MENINGOENCEPHALITIS,

BRAIN ABSCESS, EMPYEMA
Canine monocytotropic ehrlichiosis
• Infection caused by the rickettsial organism Ehrlichia • Bacterial meningoencephalitis can be the result of sep-
canis is known as canine monocytotropic (or monocytic) ticemia, external trauma (including bite wounds), direct
ehrlichiosis (CME).77 The brown dog tick Rhipicephalus extension from middle ear infections/nasal disease/dental
sanguineus is the vector of transmission. disease, contamination of the CSF, foreign body migra-
• Neurologic signs of CME are caused by perivascu- tion, and cribriform plate fracture or malformation.80–86
lar plasma cell infiltration, meningitis, and meningeal • Depending on the underlying cause, MRI lesions may
bleeding.77 Intraparenchymal lesions may result from be focal or multifocal and mass-like or diffuse.7,81–83,86,87
arterial infarction.78 Descriptions of localized bacterial infection, including
• The MRI appearance of a single case of CME has been brain abscesses, from direct inoculation or extension
reported fully and is similar to that seen in people from adjacent structures predominate the literature.
with rickettsial meningoencephalitis.78 MRI findings • The key MRI findings distinguishing confirmed and
included: presumed brain abscesses in dogs and cats have included
• Multifocal punctate lesions of the caudate nuclei and (Fig. 5.3.17):
thalamus, which were T2W hyperintense and centrally • Focal mass lesions, typically T2W hyperintense and
T1W hypointense, occasionally contrast-enhancing. T1W hypointense. Many of these lesions have a
• Mild contrast enhancement of the leptomeninges. central necrotic or cystic center (T1W hypointense
• Partial description of an MRI examination in one with absence of central contrast enhancement).81–83,86,88
additional case of CME has been reported. The find- • A T2W hypointense peripheral rim can be present
ings were of high signal intensity and hypertrophy of and has been reported in humans as a distinguishing
the meninges.79 feature of brain abscessation, caused by paramagnetic
(a) (b)
Fig. 5.3.17 Transverse T2W (a), T2-FLAIR (b), T2*W gradient echo (c), T1W pre-contrast (d), and T1W post-contrast
(e) images of the brain in an 18-month-old intact female German Shepherd Dog presented with an acute onset of depression,
hyperthermia, and anorexia/adypsia. The patient was moving slowly with unsteady gait, and a brain MRI was performed.
The dog had been treated for several weeks with steroids because of an unspecified dermatologic condition. There is a large
ovoid mass in the rostroventral aspect of the left frontal lobe, with a central core that is heterogeneously T2 hyperintense,
with several peripheral concentric ‘onion skin-like’ hypointense rims (a). The center of the lesion (asterisks, a, b, d, and e)
is partially suppressing on T2-FLAIR (= not pure fluid, b), T1W pre-contrast hypointense (d), and non-enhancing (e). On
the T2*W gradient echo image (c), there are areas of hypointensity in the peripheral ring around that core, suggestive
of susceptibility artifacts (arrow). The peripheral ring of the lesion is strongly contrast-enhancing (e). There is marked
perilesional hyperintensity in the left and right white matter appearing hyperintense on the T2W and T2-FLAIR images (a, b).
A smaller lesion with similar characteristics was present in the rostral aspect of the right frontal lobe (not shown). At necropsy,
the two lesions were diagnosed as encapsulated brain abscesses of unknown origin. (Images courtesy of the Clinical Radiology
Department of the Vetsuisse-Faculty, Bern (Switzerland), and the Online Atlas of Domestic Animal Neurological Pathology
and MRI [http://www.vetsuisse-bern.ch/~vet-iml/lernmodule/htmls/npintro.html?neuropatho|npintro].) (Continued)
(c) (d)
(e)
Fig. 5.3.17 (Continued)
free radicals within phagocytic macrophages. This abscesses or rupture into an adjacent ventricle. In
can also cause susceptibility artifacts in the rim on cases of communication with the ventricle, abnor-
T2*W gradient echo images (Fig. 5.3.17).81,86,88–90 mal T1W intensity and incomplete T2-FLAIR
• The majority of lesions have an often thick, strong suppression of the ventricular CSF may be expected
peripheral rim contrast enhancement (Fig. 5.3.17), (Fig. 5.3.18).86,88
with a smaller proportion having variable peripheral • Mass effect, perilesional T2W hyperintensity (edema),
contrast enhancement.81–83,86,88 and brain herniation can be present and occasionally
• It has been suggested that, because of the rela- are severe.81,88
tively lower blood supply of cerebral white matter, • Concurrent signs of skull trauma (bone defect, intrac-
abscess lesions that span the gray and white matter ranial bone fragment displacement, and adjacent
can have relatively thinner medial rims, a feature subcutaneous fluid [T2W hyperintense] or gas accu-
that is important both as a diagnostic feature and as mulation [signal void]) may be present in post-trau-
predisposing to abscess rupture, causing additional matic brain abscesses.81
204 CHAPTER 5.3
(a) (b)
Fig. 5.3.18 Sagittal T2W (a) and T1W post-contrast (b) and
transverse T2-FLAIR (c) images in an 8-year-old spayed female
Kerry Blue Terrier presented for evaluation of progressive
neurologic signs including dullness, lethargy, circling, and
disorientation that had occurred during the previous 3 days. On
the sagittal T2W image (a), there is a mass in the left frontal lobe
(arrow) having a hypointense rim and hyperintense center. It is
surrounded by hyperintense tissue consistent with perilesional
edema. On the post-contrast T1W image (b), there is strong
enhancement of the rim of that mass (arrow), as well as the lining
of the left lateral ventricle (ventriculitis). On the transverse
T2-FLAIR image, note the lack of suppression of CSF signal
in the left lateral ventricle (arrow) compared with the right
one. These characteristics are consistent with an abscess with
extension/rupture into the left lateral ventricle (changing the
chemical composition of fluid in that ventricle and explaining the
lack of T2-FLAIR suppression). Staphylococcus sp. was cultured
from blood and CSF and a vegetative lesion of the mitral valve
(endocarditis) was identified on echocardiography. (1.5T MRI
system; reproduced, with permission, from Bach JF, Mahony OM,
Tidwell AS et al. (2007). Brain abscess and bacterial endocarditis
in a Kerry Blue Terrier with a history of immune-mediated
(c) thrombocytopenia. J Vet Emerg Crit Care 17:409.)
• MRI findings in dogs and cats with intracranial exten- • Occasionally, intracranial bacterial infection may
sion of middle ear infection include (Fig. 5.3.19): cause accumulation of purulent material in the sub-
• Plaque-like extra-axial masses with mass effect adjacent dural (between dura mater and arachnoid membrane)
to the brainstem and the tympanic bullae, with heteroge- or epidural spaces, a condition known as ‘empyema’.
neous T2W signal and strong contrast enhancement.7,87 Recognition of this condition should spur consideration
• Variable degrees (absent to extensive) of T2W hyper- of surgical drainage.80 MRI features of empyema include:
intensity of the cortical gray matter.7,87 • Focal or regional thickening of the extra-axial space,
• T2W meningeal hyperintensity and thickening, with which is T2W and T2-FLAIR hyperintense, often
T1W contrast enhancement ipsilateral to the affected described as crescent-shaped in cases of subdural
middle ear.7,87 This enhancement can affect the pachy- empyema or fusiform/biconvex/lentiform in cases of
meninges (dural enhancement) or leptomeninges (pial epidural empyema.80,82,91,92
enhancement).13 • Strong contrast enhancement of the meninges sur-
• Heterogeneously T1W and T2W hyperintense tissue rounding non-enhancing material.80,82,91
in the affected middle ear cavity. Contrast enhance- • Extra-axial material may cause mass effect and brain
ment of this tissue and lining of the middle ear cavity herniation.80,82,91
is common.87
* *
(a) (b)

post-contrast (c) images at the level of the tympanic bullae
in a 7-year-old cat with circling and head tilt. On the T2W
image (a), there is hyperintense material filling the lumen of
both tympanic bullae (asterisks) and ill-defined hyperintensity
along the left ventral aspect of the cranial cavity (arrow). On
the T1W pre-contrast image (b), the material in the tympanic
bullae is isointense to the muscles, and on the post-contrast
image (c), there is marked enhancement of the lining of the
bullae indicating otitis media. There is a fusiform area of
strong contrast enhancement along the left ventral aspect
of the cranial cavity adjacent to the left tympanic bulla
(arrow, c), consistent with focal meningitis and possibly early
epidural empyema formation, secondary to extension of the
infection in the middle ear into the brain cavity. (1.5T MRI
system; images courtesy of Dr. Wilfried Mai, University of
(c)
Pennsylvania)
PROTOZOAL MENINGOENCEPHALITIS (affecting dogs) and Toxoplasma gondii (dogs and cats) have
been reported separately.
Protozoa are obligate intracellular parasites passed transpla-
centally or through ingestion of oocyst-containing soil, feces Neosporosis
or infected intermediate hosts. Dogs and cats developing • The MRI changes with neosporosis have been reported
protozoal meningoencephalitis tend to be younger animals, to include:
but can be of any age and may have concurrent myopathy.93 • Atrophy of the cerebellum, with decreased distinc-
The MRI appearance of lesions caused by Neospora caninum tion between gray and white matter, and widening of
206 CHAPTER 5.3
the sulci between the folia. These may be the only • Lesions are T2W hyperintense, iso- to hypointense on
changes seen in some patients.94,95 T1W images,98 and strongly contrast-enhancing,98–100
• Multifocal T2W hyperintense, T1W isointense or with occasionally a dural tail.98,99
hypointense, and variably contrast-enhancing lesions • Perilesional T2W hyperintensity (edema).98
of the brainstem, thalamus, internal capsule, or cere-
bral cortex (Fig. 5.3.20).95 PARASITIC MENINGOENCEPHALITIS
• Perilesional and white matter edema seen in the cere-
bellum as well as the cerebral and brainstem lesions.94,95 • Migrating parasites may invade the CNS causing single
• Occasional contrast enhancement or thickening of or multifocal lesions, often with acute clinical signs.22
the meninges around the cerebellum, brainstem, or The resultant granulomatous lesions of the brain or
diencephalon.94–96 meninges often have variable degrees of inflammation,
• Concurrent spinal cord lesions in some animals.95 necrosis, or hemorrhage (MR characteristics of hem-
• Concurrent masticatory muscles atrophy, T2W orrhage are specifically discussed in Chapter 5.7). The
hyperintensity, and contrast enhancement suggestive infection can also cause diffuse meningoencephalitis of
of myositis in some cases.94 the cerebrum or brainstem.101,102
• Reports of the MRI appearance of intracranial para-
Toxoplasmosis sitic lesions in dogs and cats are limited and are often
• Both diffuse meningoencephalitis and focal mass- single case reports, including those caused by Cuterebra,
like granulomas secondary to toxoplasmosis have been Eucoleus (Capillaria), Taenia (coenurosis), Angiostrongylus,
reported in dogs and cats. and Baylisascaris species.41,50,103–108
• MRI features with toxoplasmosis-associated diffuse • MRI findings of various parasitic lesions include:
meningoencephalitis include multifocal T2W hyperin- • Extra-axial or intra-axial cyst-like lesions contain-
tense, T1W isointense, variably contrast-enhancing, and ing T2W hyperintense, T1W hypointense fluid that
poorly marginated lesions of the cerebral hemispheres suppress on T2-FLAIR images and do not contrast
and brainstem.6,7,97 enhance; this seems to be a distinguishing feature of
• MRI features with toxoplasmosis-associated granulomas most reported parasitic lesions. In some cases, focal
include: mass lesions are present adjacent to the cyst-like
• Intra-axial or extra-axial mass lesion of the cerebrum; lesion(s) and have strong uniform contrast enhance-
the appearance of extra-axial masses can be similar to ment.103,104,109
meningioma.98–100
(a) (b)
Fig. 5.3.20 Protozoal meningoencephalitis in a 3-year-old Boston Terrier. (a) Transverse T2W image showing a partially
defined hyperintense lesion ventrally in the left frontal lobe (arrow). There is also extensive asymmetric diffuse hyperintensity
(edema) of the white matter extending into the gray matter. (b) Transverse post-contrast T1-FLAIR with fat saturation
image showing multifocal strong contrast enhancement within the white matter lesions. At histopathology, protozoal cysts
consistent with either Toxoplasma gondii or Neospora caninum infection were identified. (3T MRI system; images courtesy of
Dr. Jay Griffin, Texas A&M University)
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• Cyst-like lesions can be very large with associated mass • In cases of presumed Cuterebra spp. larva migrans,
effect and potentially cause brain herniation.103,109 a curvilinear T2W hyperintense and T1W hypoin-
• A case of Baylisascaris procyonis migration had diffuse tense tract through the cerebral gray and white matter
T2W hyperintensity of the cerebral gray matter causing with strong enhancement following contrast medium
marked loss of distinction between the gray and white administration was reported (Fig. 5.3.21).106,107
matter. The dog also had cerebellar herniation.41
(a) (b)
Fig. 5.3.21 Dorsal T2W (a), dorsal T1W post-contrast (b), and
transverse T1W post-contrast (c) images of the brain in a 1-year-old
castrated male mixed-breed dog with a 3-day history of progressively
deteriorating mentation. Three days prior to referral, the owners
witnessed the dog sneezing several times in succession with
subsequent development of generalized urticaria. On the dorsal
images, there is a well-defined tortuous and tubular lesion that is
T2W hyperintense with hypointense periphery (white arrows, a). On
the dorsal and transverse post-contrast images, the tubular tract is
hypointense with strong peripheral enhancement (black arrow, c).
This lesion extends from the left hippocampus caudomedially
across the falx cerebri to the right occipital lobe, ending at the
calvarium. There was also a T2W hyperintensity of the right frontal
lobe extending to the cribriform plate (not shown). Given the
circuitous path of the lesion, the concurrent hyperintense lesion
near the cribriform plate and the history of sneezing several days
prior to presentation, a parasitic migratory tract with a nasal route
(c) of entry was suspected, such as from migrating Cuterebra. There
was CSF eosinophilia and histopathology showed severe subacute
encephalomalacia and subacute neutrophilic and eosinophilic meningoencephalitis with areas of hemorrhage and necrosis,
consistent with a migrating parasite. (1.5T MRI system; Fig. 5.3.21b is reproduced, with permission, from Thawley VJ, Suran JN,
Boller EM (2013). Presumptive central nervous system cuterebriasis and concurrent protein-losing nephropathy in a dog. J Vet
Emerg Crit Care 23(3):335–9; Figs. 5.3.21a and 5.3.21c are courtesy of Dr Wilfried Mai, University of Pennsylvania)
208 CHAPTER 5.3
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CHAPTER 5.4
BRAIN NEOPLASIA
Silke Hecht 211
CONTENTS
Brain masses: Intra- versus extra-axial origin ....................................................................................................................................................... 212
Associated findings with intracranial masses ........................................................................................................................................................ 212
Hydrocephalus................................................................................................................................................................................................. 212
Syringomyelia.................................................................................................................................................................................................. 212
Perilesional edema ......................................................................................................................................................................................... 212
Mass effect ......................................................................................................................................................................................................213
Brain herniation ...............................................................................................................................................................................................213
Accuracy of MRI in the diagnosis of intracranial neoplasia ................................................................................................................................... 213
MRI findings in specific tumor types .....................................................................................................................................................................214
Meningeal tumors............................................................................................................................................................................................214
Meningioma ...............................................................................................................................................................................................214
Other tumors with meningeal involvement .................................................................................................................................................216
Glial tumors .....................................................................................................................................................................................................216
Oligodendrogliomas and astrocytomas ...................................................................................................................................................... 217
Glioblastoma multiforme ............................................................................................................................................................................ 217
Gliomatosis cerebri/cerebelli ...................................................................................................................................................................... 218
Ventricular tumors ........................................................................................................................................................................................... 219
Choroid plexus tumors ............................................................................................................................................................................... 219
Ependymomas ............................................................................................................................................................................................220
Ventricular meningiomas............................................................................................................................................................................220
Other ventricular tumors .............................................................................................................................................................................220
Central primitive neuroectodermal tumors including medulloblastomas .........................................................................................................220
Hamartomas, borderline tumors, and tumor-like lesions .................................................................................................................................222
Hamartomas ...............................................................................................................................................................................................222
Meningioangiomatosis ..............................................................................................................................................................................223
Cerebral hemangiomas and hemangioblastomas .......................................................................................................................................224
Cholesterol granulomas .............................................................................................................................................................................224
Intracranial extension of extracranial mass-like lesions..............................................................................................................................225
Central nervous system-associated tumors .....................................................................................................................................................225
Pituitary tumors..........................................................................................................................................................................................225
Other sellar or suprasellar masses .............................................................................................................................................................227
Trigeminal nerve sheath tumors .................................................................................................................................................................228
Olfactory neuroblastoma ...........................................................................................................................................................................228
Intracranial extension of extracranial tumors .............................................................................................................................................228
Metastatic central nervous system tumors .......................................................................................................................................................229
Other intracranial neoplasms ...........................................................................................................................................................................229
Round cell tumors ......................................................................................................................................................................................229
Intravascular lymphoma .............................................................................................................................................................................229
Granular cell tumors ...................................................................................................................................................................................229
References.............................................................................................................................................................................................................235
212 CHAPTER 5.4
Intracranial masses, whether neoplastic or not, can be sub- in classifying a lesion as intra-axial in those cases
divided based on location into intra-axial (arising from (Figs. 5.4.5, 5.4.6).
within the brain axis) and extra-axial.1–3 They can be fur- • Finally, while presence and degree of contrast
ther characterized by number, location, size, margination, enhancement of intra-axial masses is highly variable,
signal intensity, homogeneity, contrast enhancement, and and while moderate to strong enhancement can be
concurrent imaging findings (ventriculomegaly, changes seen with both intra- and extra-axial masses, absent or
associated with cranium and/or meninges, hemorrhage, poor enhancement is most consistent with intra-axial
mineralization, mass effect, edema, cystic or necrotic com- origin as a result of the protection of the mass by the
ponent etc.).4–7 Co-existing intracranial masses of differ- blood–brain barrier (Figs. 5.4.11, 5.4.12).
ent histogenesis in the same patient are rare but have been
reported.8–12 This chapter will cover possible associated ASSOCIATED FINDINGS WITH
findings with intracranial masses, the accuracy of MRI in INTRACRANIAL MASSES
the diagnosis of intracranial neoplasia, and MRI findings
reported with specific tumor types. A variety of pathologic sequelae can be associated with
intracranial masses, including hydrocephalus, cervicotho-
BRAIN MASSES: INTRA- VERSUS racic syringomyelia, peritumoral edema, mass effect, and
EXTRA-AXIAL ORIGIN brain herniation.1,3,13–16
• Classification of a mass as intra- or extra-axial in origin Hydrocephalus

can be helpful in establishing a presumptive diagnosis.1,2,7 • Hydrocephalus is defined as dilation of the ventricular
• Extra-axial masses arise from tissues other than actual system.17 A detailed description of types and pathophysi-
brain parenchyma: ology is provided in Chapter 5.1. Obstructive hydro-
• Many are located in the periphery of the brain and cephalus is a fairly common finding in animals with
compress rather than invade brain parenchyma intracranial neoplasia, especially with tumors associated
(e.g., meningiomas) (Figs. 5.4.1–5.4.4). with the ventricular system or caudal fossa.5,17
• Some are in a typical location (e.g., intraventricular • MRI findings include (Figs. 5.4.7, 5.4.10):6,17–19
choroid plexus tumors or pituitary tumors originating • Ventricular enlargement and thinning of the cerebral
from the pituitary fossa; Figs. 5.4.7–5.4.10, 5.4.14, cortices.
5.4.15), and most are strongly contrast-enhancing • Periventricular edema resulting from transependy-
as they are not protected by the blood–brain barrier mal flow of CSF (best seen on T2-FLAIR images as
(Figs. 5.4.1–5.4.4, 5.4.7–5.4.10, 5.4.14, 5.4.15, periventricular hyperintensity).
5.4.17). • Periventricular diverticula, tears, and clefts, which
• Other signs that suggest an extra-axial origin include: may be associated with parenchymal hemorrhage
– Concurrent changes to the skull (e.g., cribriform (best seen on T2*W images).
plate lysis seen with nasal tumors or hyperos-
tosis occasionally present with meningiomas; Syringomyelia
Figs. 5.4.1, 5.4.3, 5.4.17). • Syringomyelia is characterized by the development of
– A broad-based contact of the lesion with menin- fluid-filled cavities within the spinal cord, which is most
ges forming an obtuse angle (comparable to the commonly seen in dogs with caudal occipital malforma-
‘extrapleural sign’ seen with masses originating tion syndrome (Chiari-like malformation).20,21 However,
from the thoracic wall on thoracic radiographs; other diseases resulting in abnormal cerebrospinal fluid
Fig. 5.4.2). dynamics at the craniocervical junction, including
– Meningeal thickening and enhancement adjacent intracranial masses, have been reported as underlying
to a mass (‘dural tail’, Fig. 5.4.4). cause.14,22–24 A detailed description of types and patho-
• Intra-axial masses originate from the brain parenchyma: physiology of syringomyelia is provided in Chapter 7.9.
• They may be completely surrounded by normal brain • MRI findings include tubular (sometimes with irregular,
tissue, in which case determination of the origin scalloped margins) parenchymal T2 hyperintense, T1
of the mass is straightforward (Fig. 5.4.18). hypointense, and non-enhancing cord cavitation extend-
• In contrast, peripherally located or very large masses ing over several vertebral segments (Figs. 5.4.1, 5.4.2,
may be in contact with overlying meninges, which 5.4.5).14,16,21,22,24
may make diagnosis challenging. An acute rather than
obtuse angle of the mass with the meninges (similar Perilesional edema
to a pulmonary mass bordering the thoracic wall, • Perilesional edema may be seen concurrently with many
using the thoracic radiograph analogy) and absence intracranial diseases including neoplasms.1,3,25,26 Under
of adjacent meningeal enhancement may be helpful normal circumstances, exchange of substances between
Br a i n Ne opl a si a 213
the blood and the brain is limited by the blood–brain ACCURACY OF MRI IN THE DIAGNOSIS
barrier. Damage to brain capillaries results in leakage OF INTRACRANIAL NEOPLASIA
of fluid into the extracellular space (vasogenic edema).
This extracellular fluid may migrate along the white • There is general agreement that MRI is the modality
matter fiber tracts and accumulate to create a mass of choice for imaging of most intracranial disorders in
effect.27 small animals.1,4–6,27,31–33
• MRI findings include perilesional T2/T2-FLAIR hyper- • Several studies have been performed to evaluate the abil-
intensity, T1 hypointensity, and swelling of white mat- ity of MRI to distinguish neoplastic from non-neoplastic
ter without contrast enhancement (Figs. 5.4.14, 5.4.17, brain diseases, sometimes with conflicting results:
5.4.18, 5.4.22).6,19,27 • One study found seven MRI signs that had a signif-
icant association with neoplasia: single lesion, shape,
Mass effect mass effect, dural contact, dural tail, lesions affecting
• Space occupying lesions within the cranial vault (e.g., the adjacent bone, and contrast enhancement.34
tumors) and secondary changes (e.g., edema) are com- • Another study found only strong contrast enhance-
monly associated with a mass effect.3,6,25,27 ment, extra-axial origin, T2-FLAIR mixed intensity,
• MRI findings include (Figs. 5.4.1–5.4.6, 5.4.14, 5.4.17, and defined lesion margins to be predictive of neo-
5.4.18, 5.4.22):3,6,25,27 plasia.35
• Displacement of the falx cerebri/midline shift. • A study evaluating interobserver agreement and
• Displacement of brain parenchyma, which may ulti- diagnostic accuracy of brain MRI in dogs found
mately lead to brain herniation (see below). not only substantial to almost perfect agreement
• Compression of the ventricular system. (0.64 < κ < 0.86) between observers in lesion identi-
fication but also moderate to substantial agreement
Brain herniation (0.56 < κ < 0.69) for categorization by diagnosis
• Increase in intracranial pressure (due to an intracranial (normal, neoplastic, inflammatory, vascular, meta-
mass and/or associated changes) can lead to compres- bolic/toxic, or other).36
sion and displacement of brain parenchyma and brain • Another study evaluating the reliability and validity
herniation. of MRI for detecting neoplastic, inflammatory, and
• MRI findings include (Figs. 5.4.1, 5.4.2, 5.4.5, cerebrovascular brain lesions in dogs found a high
5.4.14):6,13,15,28–30 sensitivity (94.4%) and specificity (95.5%) of MRI
• Herniation of the caudal portion of the cerebellum for detecting a brain lesion, with a similarly high
into and through the foramen magnum (‘foramen performance for classifying neoplastic disease (sensi-
magnum herniation’), which is best appreciated on tivity 87.4%, specificity 91.7%). Additionally, inter-
T2W sagittal images where the ventral part of the cer- rater agreement was very good for overall detection
ebellar vermis extends caudally through the foramen of structural brain lesions (κ = 0.895) and neoplastic
magnum. This is usually secondary to the develop- lesions (κ = 0.771).37
ment of masses in the caudal fossa, but can also result • In one study comparing MRI findings between
from masses in the cranial fossa. gliomas and presumed cerebrovascular accidents in
• Herniation of part of the cerebral cortex across dogs, 10%–47% of the presumed cerebrovascular
midline into the opposite half of the cranial vault accidents were misdiagnosed as gliomas and 0%–12%
(‘subfalcine herniation’), which is best appreciated on of the gliomas were misdiagnosed as cerebrovascular
transverse images. With this type of herniation, the accidents. Agreement between observers was moder-
ipsilateral cingulate gyrus is pushed ventrally and, ate (κ = 0.48).38
under the rigid midline falx, the contralateral cingu- • Initial studies have been performed evaluating advanced
late gyrus is compressed by the herniated tissue and MRI techniques to allow specific diagnosis of intracra-
there is depression of the ipsilateral corpus callosum. nial lesions:
Depending on the size of the mass, there will be com- • DWI, with measurement of apparent diffusion coef-
pression or displacement of the ipsilateral lateral ven- ficients, has a wide range and significant overlap in
tricle. various intracranial diseases in dogs and is likely
• Displacement of portions of the cerebral cortex ventral not useful in determination of the histologic type of
to the tentorium cerebelli (‘caudal transtentorial her- lesion.39
niation’) resulting in displacement of the brainstem • This being said, advanced techniques such as DWI
and rostral aspect of the cerebellum away from the may be useful in differentiating specific tumor types
mass lesion. Obstructive hydrocephalus can be seen that otherwise share similar MRI characteristics; for
with this type of herniation due to compression of the example, preliminary results indicate that there may
mesencephalic aqueduct. be differences in apparent diffusion coefficients and
214 CHAPTER 5.4
fractional anisotropy between extra-axial histiocytic sporadic reports of meningioma in young animals can be
sarcomas and meningiomas.40 found in the literature.47,48
• Multivoxel proton MRS is a technique that inter- • Clinical signs are variable and depend on tumor size and
rogates the presence and concentration of various location. Altered consciousness, seizures, and vestibu-
metabolites in brain tissue and has proven effective for lar dysfunction are most commonly reported.44,46 The
differentiating inflammatory from neoplastic lesions most common tumor location is rostrotentorial (espe-
in the canine brain (for example, the accuracy of the cially fronto-olfactory),2,4,44,45,49 but association with
N-acetylaspartate-to-choline ratio was 82.7%).41 the caudal fossa or the ventricular system (see below) is
possible.14,24,50–54
MRI FINDINGS IN SPECIFIC TUMOR TYPES • MRI findings include (see also Fig. 4.1.1):
• Round/ovoid (Figs. 5.4.1, 5.4.2) or plaque-like
Meningeal tumors (Fig. 5.4.3), usually smoothly marginated mass asso-
Meningioma ciated with the brain, typically in broad-based contact
• Meningiomas are the most common brain tumors in with underlying bone (except tumors in ventricular
dogs and cats, accounting for 45%–51.5% and 73% of location).2,3,19,30,44,45,49,55,56
reported cases, respectively.25,30,42,43 They originate from • Usually single lesion, but presence of multiple tumors
the meningeal lining of the brain. possible.19,55,57,58
• Golden Retrievers, Boxers, and Domestic Short-haired • Typically hypointense to isointense on T1W images,
cats are predisposed.25,30,44–46 Affected animals typically hyperintense on T2W/T2-FLAIR images, and strongly
present at middle to higher age (mean age at presenta- contrast-enhancing (homogeneous, heterogeneous, or
tion 10 years in dogs and 12 years in cats),26,45 although ring enhancement possible).1–3,5,25,30,44,45,49,55,59,60
(a)
(b)
Fig. 5.4.1 Meningioma (meningothelial subtype) in a 9-year-
old DSH cat. (a) Sagittal T2W image demonstrating a large
mildly hyperintense lesion associated with the forebrain
(asterisk), with associated mass effect. There is subtentorial
and foramen magnum herniation (arrowheads) and cervical
syringomyelia is noted (arrow). (b) Transverse T2W image
demonstrating a large well-circumscribed mildly hyperintense
mass with a strongly hyperintense rim in the periphery of the
left frontal, parietal, and temporal lobes, which is in broad-
based contact with the overlying skull. There is a significant
mass effect with associated midline shift and compression of
the ventricular system. (c) On the transverse T1W image, the
mass is isointense to mildly hypointense. Thickening of the
(c)
overlying cortical bone (hyperostosis) is evident (arrows).
(Continued)
(d) (e)
(f) (g)
Fig. 5.4.1 (Continued) Meningioma (meningothelial subtype) in a 9-year-old DSH cat. (d) The mass does not suppress on
T2-FLAIR. (e) PDW image again demonstrating hyperostosis of the overlying skull. (f) T2*W image showing a small focal
susceptibility artifact associated with the mass, most consistent with focal mineralization considering the tumor type (arrow).
(g) Post-contrast T1W image showing strong and fairly homogeneous enhancement of the mass. There is a focal cortical
erosion (arrow), with extension of the mass into the thickened portion of the skull. (1.5T MRI system)
• Concurrent brain edema (hyperintense on T2W/ • Bone changes adjacent to the tumor including hyper-
T2-FLAIR images) and mass effect.3,4,19,45 ostosis, pressure atrophy, or tumor invasion of bone
• ‘Dural tail sign’: thickening and enhance- (cats) (Figs. 5.4.1, 5.4.3, 5.4.4).19,26,30,64
ment of the dura adjacent to an extra-axial mass • Single or multiple tumor-associated cyst-like changes
(Fig. 5.4.4).19,61 (more common in dogs than cats). Cystic menin-
• Less common MRI findings include: giomas occur predominantly in the rostral fossa
• Mineralization or hemorrhage associated with the (Fig. 5.4.2).19,30,65–68
mass causing T2 hypointense foci and/or susceptibil- • Cervical syringomyelia, especially secondary to
ity artifact (signal void) on T2*W images.19,30,62,63 tumors in the caudal fossa.14,24,53
216 CHAPTER 5.4
VetBooks.ir
(a) (b)
Fig. 5.4.2 Cystic meningioma in a 7-year-old Chihuahua. (a) Sagittal T2W image showing a large and well-circumscribed
cystic lesion associated with the ventral aspect of the rostral cranial vault, which has a ventral soft tissue component in broad-
based contact with the underlying skull (arrow). Subtentorial herniation and cervical syringomyelia (arrowhead) are also
evident. (b) Sagittal post-contrast T1W image showing homogeneous contrast enhancement of the ventral (solid) aspect of the
mass (arrow) while the cystic component (asterisk) is non-enhancing. (1.5T MRI system)
(a) (b)
Fig. 5.4.3 Transverse T1W pre- (a) and post-contrast (b) images in a 12-year-old Golden Retriever with an ‘en-plaque’
meningioma along the right temporal lobe. There is sclerosis/hyperostosis of the calvarial bone (solid arrows, a) with the
hyperintense bone marrow being replaced by hypointense bone sclerosis; compare with the normal bone marrow on the
contralateral side (dashed arrow, a). On the post-contrast image (b), there is marked plaque-like meningeal thickening and
enhancement (arrows, b). (1.5T MRI system; images courtesy of Dr. Wilfried Mai, University of Pennsylvania)
Other tumors with meningeal involvement Glial tumors

• Other tumor types that may affect the meninges include Glial tumors are fairly common in dogs, accounting for
disseminated histiocytic sarcoma, lymphoma, granular approximately 35%–37% of primary brain tumors in this
cell tumor, and metastatic disease (meningeal carcino- species.25,43 Boxer dogs and Boston Terriers are predis-
matosis).69–74 These tumor types are covered in more posed.25 In contrast, glial tumors account for only approxi-
detail below. mately 8% of feline primary brain tumors.26
Fig. 5.4.4 Transverse T1W post-contrast image of the brain

in a 12-year-old DSH cat with a large meningioma. Strong
contrast enhancement of the mass is noted and there is
tapering meningeal enhancement/thickening on the margins
of the mass (arrows) consistent with a ‘dural tail’. This sign is
commonly seen with meningiomas, although it is not specific
for that type of tumor. (1.5T MRI system; image courtesy of
Oligodendrogliomas and astrocytomas • Oligodendrogliomas have been reported to be more

• Oligodendrogliomas and astrocytomas are the most likely to cause ventricular distortion than astrocyto-
common glial tumors reported in veterinary patients.25,26 mas;79 however, others found no difference between
• Mean age at presentation in dogs is 8–9 years; how- astrocytomas and oligodendrogliomas regarding rela-
ever, several cases have been reported in young patients tionship to the lateral ventricles.82
including puppies.25,75–78 Clinical signs are variable, but • Oligodendrogliomas can occasionally have an intra-
seizures, mentation change, vision loss, and vestibular ventricular location86,87 mimicking other types of
signs seem fairly common.25 Mean age in cats is 10–13 intraventricular tumors. Although rare, CSF drop
years, but younger cats may be affected.26 Circling, sei- metastases have been reported in cases of primary
zures, and altered consciousness are the most common intraventricular oligodendrogliomas, similar to what
presenting complaints in feline patients.26,46 is observed with other more common intraventricular
• MRI findings in astrocytomas and oligodendrogliomas neoplasms such as choroid plexus tumors.87
include (Fig. 5.4.5; see also Fig. 4.1.9): • Tumor histologic grade cannot be definitively deter-
• Intra-axial, often heterogeneous, ovoid to amorphous, mined using MRI. The following features are more
well defined to infiltrative T1 isointense to hypoin- common in high-grade gliomas compared with low-
tense and T2 isointense to hyperintense mass lesions grade gliomas:
with variable contrast enhancement.2,3,5,19,25,38,59,60,78–83 • Contrast enhancement.79,82
• Commonly located in cerebrum or thalamus, less • Cystic regions within the tumor.79
commonly found in cerebellum and caudal brain- • Involvement of deeper structures (e.g., thalamus).79
stem.2,25,30,59,78,82 • Gradient echo signal void indicative of hemorrhage.79
• Typically single lesions, although cases of multiple
concurrent tumors have been reported.1,4,5,84,85 Glioblastoma multiforme
• Cyst-like and/or necrotic regions in the mass • Glioblastoma multiforme is a high-grade astrocytoma
(T2 hyperintense, T1 hypointense, non-enhancing that is sporadically reported in dogs.25,42,88
areas), intralesional hemorrhage (susceptibility arti- • MRI features of glioblastoma multiforme include
facts on T2*W images), vasogenic edema, and mass (Fig. 5.4.6):19,88
effect.2–5,19,25,30,38,59,79,82 • Typically sharply marginated but occasionally diffuse
• MRI is not reliable for differentiating astrocytomas from intra-axial heterogeneous T2 hyperintense, and T1
oligodendrogliomas, although select MRI features tend isointense to hypointense mass with variable contrast
to be more common in specific tumor types: enhancement.
• Caudal fossa location is more common in astrocyto- • Concurrent necrosis, peritumoral edema, mass effect,
mas.2,25,82 and cyst-like changes.
• Oligodendrogliomas are more likely to contact the • Less commonly, a broad-based or pedunculated mass
brain surface than astrocytomas.82 with both intra- and extra-axial features can be seen.25
218 CHAPTER 5.4
*
(a) (b)
(c) (d)
Fig. 5.4.5 Glioma (oligodendroglioma) in a 7-year-old Boxer. (a) Sagittal T2W image showing a large intra-axial mass
associated with the right frontal lobe with severe associated mass effect (ventricular compression [arrow], subtentorial
herniation [arrowhead], and foramen magnum herniation [dashed arrow]). Cervical syringomyelia is also evident (asterisk).
(b–d) The mass is heterogeneously hyperintense on the transverse T2W image (b), hypointense on the T1W image (c), and
shows moderate ring enhancement (d). (1.5T MRI system)
Gliomatosis cerebri/cerebelli Affected animals present with a wide age range (1–13 years)
• Gliomatosis cerebri/cerebelli is a rare tumor-like disease and with variable clinical signs dependent on tumor
of glial cells characterized by diffuse widespread infiltra- location.
tion, usually with preservation of brain structures.42 • MRI findings include:
• This tumor type has been reported in Boxers, other • Focal or multifocal ill-defined T2W/T2-FLAIR
brachycephalic breeds, and large breed dogs.16,89–93 hyperintense areas associated with brain and/or
(a) (b)
Fig. 5.4.6 Glioblastoma multiforme in a 5-year-old mixed breed dog. (a) The T2W transverse image shows a large intra-
axial mass associated with the right thalamus and temporal lobe, with marked associated mass effect indicated by ventricular
compression (arrow) and midline shift (arrowhead). (b) Following administration of contrast medium, there is moderate ring
enhancement of a central portion of the mass. (1.5T MRI system)
spinal cord.1,60,90–92 The lesions are typically not • Clinical signs are variable dependent on location, size,
contrast-enhancing; however, mild parenchymal and degree of concurrent hydrocephalus and include
enhancement and meningeal enhancement is possible. mentation change, vestibular syndrome, and neck pain.25
• Several adjacent cerebral lobes are typically simulta- • MRI findings in choroid plexus tumors include
neously affected. (Figs. 5.4.7, 5.4.8):1–5,19,59,94,95
• Focal mass-like changes are possible in the midst of • Papilliform (more commonly seen with papilloma than
diffuse lesions, and concurrent astrocytoma or oligo- carcinoma) or globular ventricular mass in expected
dendroglioma may be identified.16 anatomic location of the choroid plexus.
• Normal MRI study.16,92 • Usually hyperintense on T2W images and of variable
intensity on T1W images.
Ventricular tumors • Strong contrast enhancement.
Several tumor types can affect the ventricular system • Signal heterogeneity secondary to cyst formation,
including choroid plexus tumors (papillomas and carcino- mineralization, hemorrhage, or necrosis possible.
mas), ependymomas and meningiomas in dogs and cats, and • Concurrent ventriculomegaly/hydrocephalus, perile-
neurocytomas in dogs. Extension of other tumor types (e.g., sional/periventricular edema, mass effect, and brain
gliomas or round cell neoplasms such as lymphoma) into the herniation.
ventricular system is also possible.4,26 • Additional findings reported in choroid plexus carci-
noma include:
Choroid plexus tumors • Evidence of intraventricular or subarachnoid metas-
• Choroid plexus tumors are the most common ventricular tases (detected in 35% of carcinomas but not in pap-
tumors in dogs, with choroid plexus carcinomas being illomas).94
more common than choroid plexus papillomas. • Multiple intra-axial cyst-like lesions (T2 hyperintense,
• Golden Retrievers are overrepresented. Median age at T1 hypointense, with or without peripheral enhance-
presentation is 5 years (range, 3–14 years) for choroid ment of the wall) associated with cerebrum, cerebellum,
plexus papillomas and 7 years (range, 3–12 years) for and brainstem, without evidence of a distinct primary
choroid plexus carcinomas. Choroid plexus tumors most ventricular mass.69,96 These lesions are due to leptome-
commonly occur in the 4th ventricle followed by the 3rd ningeal spread (carcinomatosis) of the primary choroid
and lateral ventricles.94 plexus carcinoma, which may remain unidentified.
220 CHAPTER 5.4
Fig. 5.4.7 Large mass associated with the ventricular Fig. 5.4.8 Choroid plexus carcinoma in a 6-year-old mixed
system (choroid plexus tumor, presumptive) in a 3-year-old breed dog. This post-contrast T1W image shows a large
Bull Terrier. This dorsal post-contrast T1W image with fat strongly contrast-enhancing mass in the right caudal cranial
suppression shows a large irregularly marginated strongly fossa, which is contiguous with the choroid plexus of the
contrast-enhancing mass associated with the right lateral fourth ventricle (arrows). (1.0T MRI system)
ventricle, extending across the midline and resulting in severe
obstructive hydrocephalus. (1.5T MRI system) • Ventricular meningiomas are rare in dogs. MRI findings
have been reported in one dog with a microcystic ven-
Ependymomas tricular meningioma53 and included:
• Ependymomas are less common ventricular tumors in • T1 isointense to hypointense and heterogeneously T2
dogs, but in cats they are more common than choroid hyperintense mass within the 4th ventricle with inho-
plexus tumors. They arise from the ependymal cells that mogeneous ring enhancement.
line the ventricles of the brain. These tumors may extend • Hydrocephalus, mass effect, perilesional edema, and
from the ventricular wall into the ventricular lumen or cervical syringomyelia.
into the adjacent brain parenchyma.
• MRI findings in ependymomas include (Fig. 5.4.9):19,97–99 Other ventricular tumors
• Fairly well-circumscribed smooth or lobulated mass • Intraventricular neurocytoma is a rare tumor of neu-
in ventricular and/or periventricular location. ronal or mixed neuroglial origin associated with the
• Typically T1W isointense, T2W hyperintense, and ventricular lining. MRI findings with this tumor were
variably contrast-enhancing. reported in one dog and included T1 isointense, T2 and
• Associated cyst-like structure(s). T2-FLAIR heterogeneously hyperintense, and markedly
• Secondary hydrocephalus, mass effect, and brain her- heterogeneously contrast-enhancing mass lesions within
niation. both lateral ventricles.100
• Lymphoma affecting the choroid plexus and ventricular
Ventricular meningiomas system has been reported in cats.26
• Meningiomas account for the majority of ventricular • Oligodendrogliomas (see above).
tumors in cats.26 Clinical signs are similar to other brain
tumors and include altered mentation, circling, seizures, Central primitive neuroectodermal
and non-specific signs such as lethargy and inappetence. tumors including medulloblastomas
MRI findings in ventricular meningiomas in cats include • Primitive neuroectodermal tumors (PNETs) are a het-
(Fig. 5.4.10):19,26,30 erogeneous group of poorly differentiated neoplasms
• Smoothly marginated T1 isointense and T2 hyperin- derived from germinal neuroepithelial cells.42,101 They
tense mass, most commonly within the 3rd ventricle, have been classified based on location as peripheral
with strong and homogeneous contrast enhancement. (arising from nervous tissue within bone or soft tissues)
• Hydrocephalus. or central (originating from brain or spinal cord).
* *
(a) (b)
(c) (d)
Fig. 5.4.9 Ependymoma in the right ventricle in a 5-year-old Domestic Long-haired cat. Sagittal T2W (a), transverse T1W
pre-contrast (b), dorsal T1W post-contrast (c), and transverse T1W post-contrast (d) images. A well-defined rounded mass
is present within the right lateral ventricle (solid arrow in a), which is hyperintense on the T2W image (a), isointense on the
T1W pre-contrast image (b), and strongly contrast-enhancing (c, d). There is a central cavitation in the mass, which is T2
hyperintense, T1 pre-contrast hypointense, and non-enhancing, consistent with cyst-like changes or necrosis. Midline shift
to the left is noted. There is fluid dilation of the right lateral ventricle rostral and caudal to the mass (asterisks, a). Note the
foramen magnum herniation of the cerebellum (dashed arrow, a). (1.5T MRI system; images courtesy of Dr. Wilfried Mai,
University of Pennsylvania)
222 CHAPTER 5.4
(a) (b)
Fig. 5.4.10 Ventricular mass (intraventricular meningioma) in a 10-year-old DSH cat. Transverse T1W pre- (a) and post-
contrast (b) images showing a soft tissue intensity moderately contrast-enhancing nodule associated with the third ventricle
(arrows). Concurrent obstructive hydrocephalus is noted. (1.5T MRI system; images courtesy of Dr. Stephanie Nykamp,
Ontario Veterinary College)
• Medulloblastomas are cerebellar tumors arising from Hamartomas, borderline tumors,

the external granular layer of the cerebellum and sharing and tumor-like lesions
histopathologic features with PNETs.42,102 A variety of conditions are included in this group and
• Similar to humans, most cases in dogs and cats have overlap exists with disorders described in other chapters.
been reported in young patients (18 months to 4 years of Fluid-filled mass lesions of the brain (e.g., arachnoid cysts,
age),25,103–110 although older animals (up to 8 years) may be ependymal cysts, dermoid and epidermoid cysts) are cov-
affected.25,109,110 Clinical signs vary with tumor location. ered in Chapter 5.5.
• MRI findings with these tumors include (Fig. 5.4.11):
• Typically intra-axial mass.106,107,108,111,112 Hamartomas
• PNETs: • Hamartomas are masses formed by disorderly
– Anywhere in the central nervous system overgrowth of tissue elements normally present at that
(CNS).103–104,112 site. Most intracranial hamartomas are either neural or
– Isointense to hypointense on T1W images, hypervascular and produce clinical signs according to their
intense on T2W images, and variably but typically neuroanatomic location.113
moderately to strongly contrast-enhancing.25,103,105,112 • Age at presentation in dogs and cats is extremely vari-
– Associated hemorrhage possible and expected able, ranging from 3 months to 15 years.25,114–118
to result in susceptibility artifacts on T2*W • There are rare descriptions of the MRI appearance of
images.104 these lesions:
– Involvement of soft tissues of the head, nasal cav- • MRI findings in a 16-month-old cat with a vascular
ity, or tympanic bullae has been reported in a case hamartoma included:118
of intracranial extension of a peripheral PNET101 – Symmetric, circular, intra-axial cerebellar mass.
and in a case of suspected extracranial extension – Heterogeneously T2 hyperintense and mildly
of a central PNET; however, extracranial origin T1 hyperintense with heterogeneous contrast
with intracranial extension could not be excluded enhancement.
in the latter case.106 – Mass effect, cerebellar herniation, compression of
• Medulloblastomas (Fig. 5.4.12): brainstem, and obstructive hydrocephalus.
– Associated with the cerebellum.106,107,109–111 • MRI findings in a 3-month-old dog with a thalamic
– Predominantly isointense to hypointense on T1W astrocytic hamartoma (and concurrent meningoangi-
images, variably hyperintense on T2W images, omatosis, see below) included:116
with variable contrast enhancement.7,60,106,107,109,111 – Intra-axial mass caudal to the 3rd ventricle.
(a) (b)
(c) (d)
Fig. 5.4.11 Primitive neuroectodermal tumor in a 9-year-old mixed breed dog. An extensive infiltrative lesion is associated
with predominantly the white matter tracts of the right cerebral hemisphere and extends via the interthalamic adhesion
towards the left. The tumor is T2 (a) and T2-FLAIR (b) hyperintense, T1 hypointense (c), and shows only minimal contrast
enhancement (d). There is associated mass effect with compression of the ventricular system and midline shift towards the
left. (1.5T MRI system)
– Homogeneously T2 hypointense and T1 hyper- adjacent parenchyma.42 Histopathologically, it is caused

intense with homogeneous contrast enhancement. by leptomeningeal and meningovascular proliferation.
– Obstructive hydrocephalus and periventricular • The brainstem is a predilection site for this disease in
edema. dogs, but other intracranial or spinal locations are pos-
sible, and clinical signs depend on the size and location
Meningioangiomatosis of the lesion.
• Meningioangiomatosis is a rare benign lesion character- • Most animals present at a young age (3–14 months),
ized by a leptomeningeal plaque that extends from the but a diagnosis in dogs as old as 9 years has been
subarachnoid space along the perivascular spaces into the reported.116,119–123
224 CHAPTER 5.4
Fig. 5.4.12 Medulloblastoma in a 7-year-old Boxer. There is

a well-marginated mass in the right part of the cerebellum
adjacent to the tentorium (solid arrows, a). The lesion
is hyperintense on the T2W image (a), with perilesional
edema (dashed arrow) and leftward displacement of the
4th ventricle (arrowhead). The mass is hypointense on the
T1W image (b) and mildly/heterogeneously enhancing after
gadolinium injection (c). (1.5T MRI system; images courtesy
(a)
of Dr. Wilfried Mai, University of Pennsylvania)
(b) (c)
• MRI findings include (Fig. 5.4.13):119,121,122 • Variable intensity on spin echo sequences, with hetero-
• T1 hyperintense or isointense and T2, T2*, and geneous or peripheral (hemangiomas) or homogeneous
T2-FLAIR hyperintense lesion. (hemangioblastomas) contrast enhancement.60,124–127
• Variable contrast enhancement. • Signal void (susceptibility artifact) indicative of hem-
• Lesion is usually superficial but extends into brain orrhage on T2*W images.124,126
parenchyma. • T1 and/or T2 hypointense rim surrounding mass
attributed to hemosiderin deposition.124,125
Cerebral hemangiomas and hemangioblastomas • Associated vasogenic edema and mass effect.124–127
• Cerebral hemangiomas and hemangioblastomas are rare
vascular tumors reported in dogs between 13 months Cholesterol granulomas
and 9 years of age presented with forebrain signs of vari- • Cholesterol granulomas are non-neoplastic lesions
able duration and severity.122–125 resulting from a chronic inflammatory reaction to pro-
• MRI findings include: gressive cholesterol accumulation; they have most com-
• Intra-axial mass of variable size.124–127 monly been reported in horses.42 A few cases have been
Intracranial extension of extracranial mass-like lesions

• Similar to intracranial extension of nasal and skull neo-
plasms (see “Central nervous system-associated tumors”
below), extension of extracranial non-neoplastic masses
into the cranial vault is possible.133,134 For example, MRI
findings in a 3-year-old Yorkshire Terrier with intracra-
nial extension of a nasal mucocele have been reported134
and included a multilobulated and relatively sharply mar-
ginated T2 and T2-FLAIR hyperintense, T1 isointense,
ring enhancing mass with concurrent mass effect and
brain edema.
Central nervous system-associated tumors

This group includes tumors originating from structures
adjacent to the brain and extending locally to affect the
CNS either through compression or invasion.
Pituitary tumors
• Pituitary tumors are fairly common in dogs and cats,
accounting for approximately 14% and 9% of intracra-
nial neoplasms, respectively.2,26 They can be classified
according to histologic type and size:
• Histologic type: Adenomas are slow-growing and
non-invasive. Invasive adenomas and carcinomas
are similar in that they are locally invasive and grow
rapidly, but only carcinomas will result in regional or
Fig. 5.4.13 Cerebellar meningioangiomatosis in a 4-year-old
distant metastatic disease.135 However, intracranial
Jack Russell Terrier. This dorsal post-contrast T1W image
metastatic lesions from carcinoma, even when present,
shows a superficial extra-axial plaque-like lesion along the
are not usually visible on MRI, making differentiation
caudal margin of the left cerebellar hemisphere and additional
of the different tumor types based on imaging find-
intra-axial lesions, all of which are moderately to strongly
ings impossible.
contrast-enhancing. (1.0T MRI system)
• Size: Pituitary macrotumors extend beyond the pitui-
tary fossa and measure >10 mm in dorsoventral height,
reported in cats presented between 4 and 13 years of while pituitary microtumors are small and may not be
age with variable clinical signs,128–130 and in a 2-year-old visible on MRI.2,5,135–138
American Bulldog presented with staggering, altered • In cats, median age at presentation is 10.1 years (4.2–17.0
consciousness, and hyperesthesia.131 Two additional years). Blindness and altered consciousness are the most
cases have been reported in cats: one where a cholesterol common neurologic signs in this species.26 Signs related
granuloma was present along with an intraventricular to a functional tumor (hyperadrenocorticism or acro-
meningioma, and one where an abundance of choles- megaly) are rare.139,140
terol crystals was present within a meningioma, posing • Mean age at presentation in dogs with pituitary adeno-
a potential pitfall in diagnosis.12,132 mas and invasive adenomas is 10.6 years and 8.3 years,
• MRI findings include: respectively. Age at presentation in dogs with pituitary
• Large extra-axial well-circumscribed mass origi- carcinomas ranges from 5 to 11 years.135 Large breed
nating from the ventricular system, brain surface/ dogs are most commonly affected.136 Clinical signs may
subarachnoid space, or fissures between cerebral occur secondary to compression of surrounding brain
hemispheres.12,128–131 parenchyma by an enlarging pituitary mass (e.g., dis-
• In cats, a solid lesion of variable T1 and T2 signal orientation, ataxia, conscious proprioceptive or cranial
intensity (often with T2 hypointense foci); heteroge- nerve deficits), may be secondary to a functional pitu-
neous on pre- and post-contrast sequences.12,128–131 itary tumor (most commonly hyperadrenocorticism),
• In dogs, a cyst-like lesion (homogeneously T2 hyper- or may be non-specific (e.g., dullness, poor appetite,
intense and T1 hypointense; fluid-fluid line on lethargy).135,136,138,141
T2-FLAIR; ring enhancement).131 • Pituitary apoplexy characterized by acute neurologic
• Associated mass effect, compression of adjacent brain signs related to hemorrhage of a pituitary mass has been
tissue, hydrocephalus, and/or syringomyelia.12,128–131 reported in dogs and cats.142,143
226 CHAPTER 5.4
• MRI findings in pituitary macrotumors (adenomas and – Larger tumors have a worse prognosis for radia-
adenocarcinomas) include (Fig. 5.4.14): tion therapy than smaller tumors.147
• Oval or irregular mass measuring more than 10 mm, • Variable signal intensity, but most commonly isoin-
originating from the pituitary fossa.2,5,19,30,135,136,138,141, tense on T1W images, mildly hyperintense on T2W
144–146 and T2-FLAIR images, and strongly homogeneously
– Invasive adenomas are significantly larger than or heterogeneously contrast-enhancing.2,5,19,30,135,136,
adenomas (1.8 +/− 0.7 cm versus 1.2 +/− 0.7 cm).135 138,141,144–146
(a) (b)
(c) (d)
Fig. 5.4.14 Pituitary macrotumor in a 6-year-old mixed breed dog. (a) On the T2W sagittal image, a large mass is centered
on the pituitary fossa. There is marked associated mass effect with subtentorial herniation (solid arrow, a). (b–f) The lesion is
mostly hyperintense but heterogeneous with isointense and hypointense areas on the T2W image (dashed arrow, b), and shows
attenuation of some T2 hyperintense areas, while others remain hyperintense on the T2-FLAIR image (c). This is consistent
with tumor-associated cyst-like changes, some of which contain proteinaceous or cellular fluid (c). The mass displays multiple
large susceptibility artifacts on the T2*W image consistent with hemorrhage (d), is iso- to hypointense on the T1W image (e), and
shows strong fairly homogeneous contrast enhancement (f). When comparing the T2W and T2-FLAIR images with the post-
contrast image, diffuse peritumoral hyperintensity is noted, consistent with peritumoral edema. (1.5T MRI system) (Continued)
(e) (f)

– Cystic and/or hemorrhagic component.2,5,19,145
– Peritumoral edema.2,5,19
– Secondary hydrocephalus.2
– Invasion into surrounding structures including
sphenoid bone (Fig. 5.4.15).5,135,146
– Thickened frontal bone and abnormal soft tis-
sue accumulation in the nasal cavity, sinuses, and
pharynx in acromegalic cats.140
• MRI findings in pituitary microtumors include:
• No abnormality.135,138,141
• Increased convexity to the dorsal pituitary margin.5,19,138
• On T1W pre-contrast images, displacement of the
vasopressin-containing and, therefore, spontaneously
T1 hyperintense neurohypophysis.19,148,149
• Possibly alteration of normal pituitary enhance-
ment pattern during dynamic image acquisition.19,150
Dynamic enhancement of the pituitary gland after
gadolinium injection typically shows first enhance-
ment of the stalk of the gland (pars tuberalis and
neurohypophysis) about 50–60 seconds after injec-
tion, followed by uniform enhancement at 100–140
seconds.
Fig. 5.4.15 Pituitary adenocarcinoma in a 14-year-old
Other sellar or suprasellar masses Yorkshire Terrier. The transverse T1W post-contrast
• Other masses that may occur in the sellar or suprasellar image shows a well-circumscribed and homogeneously
region, and which may be difficult to distinguish from enhancing pituitary mass invading the basisphenoid bone and
primary pituitary tumors, include tumors covered else- extending into the dorsal aspect of the nasopharynx (arrow).
where in this chapter (meningioma, lymphoma, granular (1.5T MRI system)
228 CHAPTER 5.4
cell tumor, gliomatosis cerebri), very rare tumor types • MRI findings reported in three dogs with metastases to
such as craniopharyngiomas or germ cell tumors the pituitary gland from a pancreatic carcinoma and two
(Fig. 5.4.16), and metastases to the pituitary gland.4,5,19 thyroid carcinomas included:
• MRI findings in two cats with malignant craniopharyn- • Well-circumscribed pituitary mass with variable con-
giomas included:151 trast enhancement.152,153
• Large contrast-enhancing mass at the skull base. • Additional intra-axial brain lesions consistent with
• Extensive bone lysis and cerebral displacement. additional metastases.153
Trigeminal nerve sheath tumors

• Trigeminal nerve sheath tumors manifest as extra-axial
masses in the middle or caudal fossa, which may result
in atrophy of the masticatory muscles, compression or
distortion of the adjacent brainstem, and enlargement of
the skull foramina.154
• These are discussed in detail in Chapter 5.10.
Olfactory neuroblastoma
• Olfactory neuroblastoma (also referred to as esthe-
sioneuroblastoma or neuroesthesioblastoma) is a rare
malignant neuroectodermal tumor derived from the
olfactory neuroepithelium. It arises at the cribriform
plate and can extend into both the cranial vault and the
nasal cavity.155–158
• Age reported at presentation ranges from 6 to 15 years in
dogs and 3 to 13 years in cats.155,158
• Affected animals may show nasal and/or variable neuro-
logic signs.155
• MRI findings reported in one dog included a T1 and T2
isointense moderately contrast-enhancing mass with an
associated large cyst centered on the cribriform plate
and extending into the nasal cavity and cranial vault
Fig. 5.4.16 Suprasellar germ cell tumor in an 8-year-old (Fig. 5.4.17).156
mixed breed dog. The transverse T1W post-contrast image
demonstrates a large contrast-enhancing mass located in the Intracranial extension of extracranial tumors
ventral cranium, extending from the level of the pituitary • Primary nasal tumors (e.g., adenocarcinoma, squamous
fossa dorsally into the hypothalamic and thalamic regions. cell carcinoma) may invade the brain through the cribri-
(1.5T MRI system) form plate.1,146
(a) (b)
Fig. 5.4.17 Olfactory neuroblastoma in a 2-year-old mixed breed dog. The parasagittal T2W (a) and post-contrast T1W
(b) images show a large heterogeneous mass extending through the cribriform plate into the caudal aspect of the nasal cavity
and the rostral cranial vault. On the T2W image, there is marked diffuse hyperintensity extending along the white matter
tracts caudally to the mass, consistent with vasogenic edema. (1.0T MRI system)
• Tumors of the skull, such as multilobular tumor of bone, • MRI findings include (Figs. 5.4.20–
or masses originating from adjacent structures (ear, 5.4.23):19,25,26,60,70,71,146,167–172
orbit) may also extend into the cranial vault and result in • Poorly or well-defined, single or multifocal, intra-ax-
compression or invasion of the brain.159–161 ial or extra-axial masses, with extra-axial location
• These disorders are covered in Chapters 6.1, 6.2, and 6.3. more common in histiocytic sarcoma.166
• Variable intensity but typically isointense to hypoin-
Metastatic central nervous system tumors tense on T1W images and isointense to hyperintense
• Many primary tumors, including hemangiosarcoma, on T2W images, with moderate to strong contrast
melanomas, and carcinomas, have the potential for wide enhancement.
dissemination including spread to the CNS. Affected • Meningeal involvement (masses, thickening, contrast
animals are typically older, although isolated cases of enhancement, ‘dural tail sign’). In dogs with histio-
younger patients are found in the literature.146,162,163 cytic sarcoma, meningeal enhancement tends to be
• Neurologic signs may or may not be present and depend quite extensive and is often not only seen adjacent to
on the extent and location of intracranial metastases. the mass lesion, but also in non-contiguous regions of
Seizures, vestibular signs, and mentation change were the CNS (Fig. 5.4.23).166
common in a cohort of dogs with intracranial heman- • Concurrent edema and mass effect.
giosarcoma and carcinoma metastases.146 Acute blind- • Intracranial extra-axial histiocytic sarcomas share
ness was reported in a dog with metastatic disease to the common imaging features with meningiomas, and
pituitary gland.152 A dog with meningeal carcinomatosis the distinction is challenging. For example, the dural
presented with seizures and central blindness.73 tail sign is commonly observed in both tumor types.
• MRI findings include: Transtentorial herniation of forebrain masses and
• Multifocal (less commonly single) lesions associated syringomyelia in the cranial cervical spinal cord, sug-
with brain parenchyma, often near the gray–white gesting crowding of the foramen magnum, seem to be
matter interface.1,4,5,19,164 more prevalent with histiocytic sarcoma than menin-
• Lesions are rounded to ovoid, distinctly or indis- gioma, and may be indicative of the rapidly growing
tinctly marginated, typically isotense to hypointense aggressive nature of these tumors.166 Another feature
on T1W images, hyperintense on T2W images, and that may be more specific of histiocytic sarcoma com-
strongly homogeneously or ring enhancing.1,4,19,60,153,162 pared with meningioma is the leptomeningeal involve-
• Hemorrhage, indicated by susceptibility artifact on ment, with contrast enhancement extending into the
T2*W images, common in hemangiosarcoma metas- sulci that often appears to spread apart the adjacent
tases (Fig. 5.4.18).4,5,62 gyri by growth of the neoplastic mass lesion.40
• Melanoma metastases may be T1 hyperintense,
T2 hypointense, and associated with signal void on Intravascular lymphoma
T2*W images because of the combined paramagnetic • Intravascular lymphoma (malignant angioendothe-
effects of melanin and hemorrhagic changes com- liomatosis, angiotrophic lymphoma) is a rare tumor in
monly present with these lesions (Fig. 5.4.19).19,165 dogs and cats, and is characterized by neoplastic prolif-
• Associated vasogenic edema.1,153,164 eration of malignant lymphoid cells within the lumen
• Less common MRI findings include: of blood vessels, with little to no extension into adjacent
– Lack of contrast enhancement of parenchymal parenchyma.173–175
lesions.60,164 • MRI findings include:
– Involvement of extraparenchymal structures (e.g., • Multifocal small parenchymal T2 and T2-FLAIR
pituitary gland and meninges).73,152,153 hyperintense, T1 isointense to hypointense lesions
with variable contrast enhancement consistent with
Other intracranial neoplasms brain infarcts.4,173,175
Round cell tumors • Less common MRI findings include:
• Lymphoma is the second most common intracranial – Small susceptibility artifacts on T2*W images.4
neoplasm in cats, accounting for 14% of cases.26 In dogs, – Meningeal enhancement.173
lymphoma accounts for approximately 4% of primary – Asymmetry of cerebral cortices with cortical
and 12% of secondary intracranial neoplasms.25,146 thickening, T2 hyperintensity, and poorly defined
• Histiocytic sarcoma affecting the CNS in dogs is uncom- gyri.175
mon.25,43 Although the neurologic form may be part of a
disseminated, multi-organ process, it is confined to the Granular cell tumors
CNS in most canine patients.166 • Granular cell tumors are rare CNS neoplasms, the his-
• Age at presentation and clinical signs are highly variable togenesis of which remains uncertain to date. They have
for both tumor types.25,26,146,166 been reported in 10–12-year-old dogs of various breeds,
230 CHAPTER 5.4
(a) (b)
(c) (d)
Fig. 5.4.18 Probable hemangiosarcoma metastases to the brain in a 14-year-old mixed breed dog presented with hemoabdomen
and a splenic mass. (a, c) Transverse T2-FLAIR images showing multiple intra-axial lesions of variable size and intensity,
which are surrounded by extensive hyperintensity to the white matter tracts consistent with vasogenic edema. The largest
lesion within the right temporal lobe (a) is associated with mass effect and midline shift towards the left. (b, d) Corresponding
T2*W images demonstrating susceptibility artifacts of variable size and distribution associated with the parenchymal lesions,
consistent with hemorrhage. The lesion within the right temporal lobe (b) shows layering of variable intensity hemorrhagic
strata. (1.5T MRI system)
(a) (b)
(c) (d)
Fig. 5.4.19 Metastatic melanoma in a 12-year-old Labrador Retriever with a history of melanoma removal from a toe 1 year
prior. There is a T2-heterogeneous lesion in the right frontal lobe (a), with marked susceptibility artifacts on T2*W gradient
echo (b), spontaneous T1 hyperintensity (arrow, c), and contrast enhancement (d). Several additional lesions with similar signal
characteristics were present throughout the brain. Spontaneous T1 hyperintensity and susceptibility artifacts are common with
melanoma lesions, due to the combined paramagnetic effects of melanin and hemorrhagic changes present in these lesions.
232 CHAPTER 5.4
VetBooks.ir
Fig. 5.4.20 Intracranial lymphoma in a 14-year-old DSH cat.

The transverse post-contrast T1W image shows a poorly
marginated contrast-enhancing mass lesion associated with
the dorsal rostral aspect of the parietal lobes with concurrent
meningeal enhancement along the falx cerebri. (1.5T MRI
system; image courtesy of Dr. Matthew Baron, MedVet
Cincinnati)
(a) (b)
Fig. 5.4.21 Disseminated lymphoma in a 5-year-old Mastiff. The transverse T2W image (a) and post-contrast T1W gradient
recalled echo image with fat suppression (b) show a large heterogeneous T2 hyperintense and mildly contrast-enhancing intra-
axial mass associated with the right occipital lobe, with associated mass effect. Multifocal contrast enhancement of the masticatory
musculature and the bones of the skull (most severely the temporal bones and mandible) is also noted. (1.5T MRI system)
and in a 6-year-old cat. Neurologic signs are variable cerebrum.19,72,74,176,177 The plaque-like lesions may be
and include seizures, proprioceptive deficits, behavior confused with the ‘en-plaque’ form of meningioma
changes, abnormal mentation, and ataxia.72,74,176–180 (compare Figs. 5.4.3, 5.4.24).175
• In most reported cases, the tumors were meningeal/ • Isointense to hyperintense to gray matter on T2W and
extra-axial;72,74,176,177,179,180 however, intra-axial location T2-FLAIR images, hyperintense on T2*W images,
has also been reported.178 and of variable intensity on T1W images (although
• MRI findings include (Fig. 5.4.24): spontaneous hyperintensity on T1W pre-contrast
• Typically, meningeal/extra-axial mass, often images is common, and may be a distinctive feature),
plaque-like and extensive along the convexity of the with strong contrast enhancement.72,74,176
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(a) (b)
Fig. 5.4.22 Intracranial disseminated histiocytic sarcoma in a 12-year-old mixed breed dog. (a) The T2W transverse image
shows extensive T2 hyperintensity to the white matter tracts of the right cerebral hemisphere with associated mass effect
(midline shift towards the left and compression of the right lateral ventricle), consistent with vasogenic edema. The post-
contrast T1W image shows extensive meningeal enhancement (both pachymeningeal and leptomeningeal) along the surface of
the right cerebral hemisphere. (1.5T MRI system)
(a) (b)
Fig. 5.4.23 Intracranial histiocytic sarcoma in a 7-year-old Basset Hound. Transverse T2-FLAIR (a), transverse T1W post-
contrast (b), and dorsal T1W post-contrast (c) images at the level of the tentorium cerebelli, and transverse T1W post-contrast
image at the level of C1 (d). The tumor is centered around the tentorium and falx cerebri, with a mostly extra-axial meningeal
component but possible intra-axial involvement (dashed arrows, b and c). The mass is strongly enhancing (b, c), and extensive
meningeal thickening/enhancement is seen extending far from the margins of the mass (open arrow, b). At the level of C1, there
is evidence of meningeal enhancement and a small meningal nodular lesion that was not directly connected to the tentorial
lesion (arrowhead, d). On the T2-FLAIR image, extensive white matter edema is noted (solid arrow, a). (1.5T MRI system;
images courtesy of Dr. Wilfried Mai, University of Pennsylvania) (Continued)
234 CHAPTER 5.4
VetBooks.ir
(c) (d)
(a) (b)
Fig. 5.4.24 Transverse MR images of the brain in an 11-year-old Boston Terrier dog with a granular cell tumor. A plaque-like
tumor extends across the right lateral meninges conforming to the convexity of the cerebrum (solid arrows, a and c). The lesion
is iso- to hypointense to gray matter with a heterogeneous appearance on the T2W (a) and T2-FLAIR (b) images, hyperintense
on the T1W pre-contrast image (c), and uniformly contrast-enhancing on the post-contrast T1W image (d). Extensive
perilesional edema (dashed arrows, b), mass effect with midline shift (arrowhead, a), and compression of the right lateral
ventricle are seen. (1.5T MRI system; images courtesy of Dr. Wilfried Mai, University of Pennsylvania) (Continued)
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c
(c) (d)
• Meningeal enhancement/dural tail extending from 9. Kishimoto M, Yamada K, Seok JS et al. (2008). Analysis
periphery of mass. 72,74,176,177 of blood flow in a third ventricular ependymoma and an
• Associated peritumoral edema, mass effect, and brain olfactory bulb meningioma by using perfusion computed
herniation.72,74,176 tomography. J Vet Med Sci 70(9):981–3.
10. MacKillop E, Thrall DE, Ranck RS et al. (2007). Imaging
diagnosis – synchronous primary brain tumors in a dog.
– Intra-axial mass.178 Vet Radiol Ultrasound 48(6):550–3.
– Transcalvarial extension.177 11. Alves A, Prada J, Almeida JM et al. (2006). Primary and
– Obstructive hydrocephalus.72 secondary tumours occurring simultaneously in the brain of a
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Vet Radiol Ultrasound 42(6):504–10. cell tumor in a cat. Vet Pathol 43(5):797–800.
175. Lapointe JM, Higgins RJ, Kortz GD et al. (1997). 180. Spoor MS, Kim DY, Kanazono S et al. (2013). What is your
Intravascular malignant T-cell lymphoma (malignant diagnosis? Impression smears of a cerebral mass from a dog.
angioendotheliomatosis) in a cat. Vet Pathol 34(3):247–50. Vet Clin Pathol 42(2):240–1.
CHAPTER 5.5
CYSTIC CONDITIONS
Silke Hecht 241
CONTENTS
Congenital and developmental cystic lesions ........................................................................................................................................................ 241
Hydranencephaly and porencephaly ................................................................................................................................................................ 241
Hydranencephaly ........................................................................................................................................................................................ 241
Porencephaly ............................................................................................................................................................................................. 241
Intracranial intra-arachnoid diverticula (‘cysts’) ...............................................................................................................................................242
Intracranial epidermoid cysts (syn. cholesteatomata) and dermoid cysts .........................................................................................................244
Rathke’s cleft cysts ..........................................................................................................................................................................................245
Ependymal cysts .............................................................................................................................................................................................. 247
Choroid plexus cysts ....................................................................................................................................................................................... 247
Other congenital/developmental conditions associated with increased fluid accumulation within the cranium ................................................ 247
Acquired cystic lesions ......................................................................................................................................................................................... 247
‘Hydrocephalus ex vacuo’ (‘compensatory hydrocephalus’) and ‘lacunae’ ........................................................................................................ 247
Neurocysticercosis ..........................................................................................................................................................................................248
Malignant and benign cystic intracranial masses.............................................................................................................................................248
References............................................................................................................................................................................................................. 249
Fluid-filled lesions within the cranium are a common find- other etiologies including hypoperfusion/hypoxia have
ing in human and veterinary patients. Most cystic brain been proposed.4–8
conditions described in small animals are congenital/ • Unless other brain lesions are present, clinical signs reflect
developmental in nature. Traumatic or vascular events may the loss of cerebral cortex (circling, behavioral abnormali-
also result in fluid-filled cavities of variable size within the ties, seizures, lethargy, blindness) while gait is maintained.
cranium, or cystic lesions may develop secondary to, or in • Age at presentation in naturally affected dogs and cats
association with, inflammatory or neoplastic intracranial ranges from 8 weeks to 13 months.5–8
conditions. As in people, cystic intracranial lesions may result • MRI findings include:
in clinical signs or may be silent and found incidentally.1–3 • Uni- or bilateral reduction of size of the cerebral cortex
to a thin mantle surrounding a large fluid-filled cavity
CONGENITAL AND DEVELOPMENTAL contiguous with the lateral ventricle (Fig. 5.5.1).7
CYSTIC LESIONS • Total loss of parietal and temporal lobes and partial
loss of frontal and occipital lobes on the affected side
Hydranencephaly and porencephaly are reported in dogs.5
These disorders are infrequently reported in companion
animals and describe the presence of fluid-filled cavities in Porencephaly
the cerebral cortex. • In porencephaly, cystic cavities are present in the cere-
brum due to cell destruction or failure of development.4
Hydranencephaly • Affected animals may be asymptomatic, present with
• In hydranencephaly, there is near complete destruction clinical signs related to the affected area of the brain
and/or lack of development of the neocortex due to a including seizures, or, surprisingly, may show neuro-
destructive process occurring in utero, typically associ- logic signs not normally localized to the forebrain such
ated with viral infection (e.g., panleukopenia), although as nystagmus. Clinical signs may not become apparent
242 CHAPTER 5.5
(a) (b)
Fig. 5.5.1 Hydranencephaly in a 6-month-old West Highland White Terrier. Parasagittal (a) and transverse (b) T2W images
show a large cystic lesion, which is contiguous with the left lateral ventricle and has reduced the adjacent cerebral cortex to a
thin rim. Doming of the overlying skull is noted. (1.5T MRI system) (Images courtesy of Dr. Lizza Baines, Willows Veterinary
Professionals)
(a) (b)
Fig. 5.5.2 Porencephaly in a 9-year-old Old English Sheepdog. Transverse T2W (a) and T2-FLAIR (b) images show a focal
lesion associated with the left forebrain, which is isointense to CSF and contiguous with the left lateral ventricle. The right
tympanic bulla contains hyperintense material, consistent with otitis media. (1.5T MRI system)
until later in life, and age at presentation reported in the Intracranial intra-arachnoid
literature ranges from 12 weeks to 7 years.5,9–11 diverticula (‘cysts’)
• MRI findings include: • These fluid-filled intracranial lesions have traditionally
• Cerebral cavities of variable size with MRI signal been termed ‘cysts’, but as they lack an epithelial lin-
identical to CSF (Fig. 5.5.2).5,9–11 ing, they are more appropriately termed ‘diverticula’ or
• Lesions may be unilateral or bilateral, single or multi- ‘pseudocysts’.2
ple, and are commonly wedge shaped.9 • They arise from splitting/duplication of the arachnoi-
• Cavities may communicate with the ventricles or sub- dae and occur in close association with the intracranial
arachnoid space.2,5,9–11 arachnoid cisterns, which are focal expansions of the
Cys t ic C on di t ions 243
subarachnoid space with increased anatomic separation • MRI findings include:13–20,22–24

between the pia mater and arachnoid, pooling of CSF, • Sharply demarcated lesions dorsal to the quadri-
and decreased number of trabeculae. geminal plate (= supracollicular fluid collections),
• They can occasionally have an intraventricular location at the cerebellomedullary/cerebellopontine angle
(e.g., 4th ventricle), in which case the pathophysiology is (= cerebellomedullary/cerebellopontine angle arach-
somewhat unclear. In people, one hypothesis is hernia- noid cyst/diverticulum) or associated with the 4th
tion of external arachnoid of the cisterna magna into the ventricle (= 4th ventricle arachnoid diverticulum)
4th ventricle (‘internal meningocele’). The close associa- (Figs. 5.5.3–5.5.5).
tion with the choroid plexus led to another hypothesis, • Lesions contain fluid isointense to CSF, with sup-
whereby these diverticula may arise from arachnoid tis- pression on T2-FLAIR and no evidence of contrast
sue that has been displaced into the ventricles by ingrow- enhancement.
ing vascular mesenchyma at the time of formation of the • Dependent on size and location of the lesion, flatten-
choroid plexus.12 ing, compression or displacement of adjacent structures
• They are usually considered a primary malformation, (cerebellum, brainstem, occipital lobes). With supra-
although they may develop secondary to inflammation collicular fluid collections, there is compression of the
or trauma.13–15 rostral margin of the cerebellum and caudal margin
• In dogs, diverticula in the region of the quadrigeminal of the occipital lobes, which are displaced caudally
cistern (located between the splenium of the corpus cal- and rostrally, respectively. With a 4th ventricle diver-
losum and the rostral portion of the cerebellum, and ticulum, the focal expansion of the ventricle causes
anatomically separated from the 3rd ventricle by a thin dorsal displacement of the cerebellum, which assumes
membrane) are most common, and have often been called a typical ‘crescent shape’ on sagittal images, and there
‘quadrigeminal cysts’.13–20 However, a recent anatomic is ventral displacement of the brainstem (Fig. 5.5.5).
and imaging study suggested that such fluid collections • In cases of supracollicular fluid collections, identi-
should instead be termed ‘supracollicular fluid accumu- fication of the thin membrane normally separating
lations’,21 and a recent review suggested use of the term
‘rostrocerebellar diverticula’.2 These alternative terms
refer to the general anatomic location and three possible
different origins of these lesions:21
• Pattern 1. Most common; caudodorsal expansion of
the 3rd ventricle, with normal or minimally enlarged
quadrigeminal cistern.
lv qc
• Pattern 2. Expansion of both the caudodorsal aspect
of the 3rd ventricle and the quadrigeminal cistern.
• Pattern 3. Less common; isolated expansion of the ita
tv
* C
quadrigeminal cistern, with normal 3rd ventricle (true

‘quadrigeminal cistern diverticulum’).
• It has been hypothesized that expansion of the 3rd ven-
tricle may in fact be part of a generalized congenital
hydrocephalus rather than an isolated anomaly, as it
is often seen in dogs with concurrent variable degrees
of lateral ventricular enlargement and in breeds
predisposed to congenital hydrocephalus.21 Fig. 5.5.3 Intracranial arachnoid diverticulum associated
• Cerebellomedullary/cerebellopontine cistern cysts and with the quadrigeminal cistern in a 10-year-old Shi Tzu
diverticula associated with the 4th ventricle have also presented with recent onset seizures. The sagittal T2W
been reported.15,22–24 image shows a large, sharply marginated, triangular cystic
• Small breed dogs (especially the Shi Tzu and other lesion in the caudodorsal cranial vault due to marked
brachycephalic breeds) are most commonly affected.13,16 expansion of the quadrigeminal cistern (qc), which results in
The disorder is rare in cats, and Persians seem to be cranial displacement and compression of the occipital lobes
predisposed.19,24 and in caudoventral displacement and compression of the
• Intra-arachnoid diverticula are commonly an incidental cerebellum (C). The thin membrane that normally separates
finding.13,17 If clinical signs are present, they depend on the third ventricle (tv) from the quadrigeminal cistern
location and size of the lesion, and may include hyperes- (qc) is visible (arrow). There is also dilation of the lateral
thesia, vestibular or facial nerve signs, cerebellar signs, ventricles (lv). The association between this lesion and the
obtundation, and seizures.13,15,18,22–24 Age at diagnosis is recent clinical signs is uncertain. (ita, interthalamic adhesion,
variable and ranges from a few months to several years. asterisk, quadrigeminal plate). (1.5T MRI system)
244 CHAPTER 5.5
Fig. 5.5.4 Intracranial arachnoid diverticulum associated

with the 4th ventricle in a 2-year-old Pekingese. The sagittal
STIR image shows a focal ovoid lesion, which is isointense
to CSF, associated with the caudal aspect of the 4th ventricle
and extending into the foramen magnum (arrow). The lesion Fig. 5.5.5 Intracranial arachnoid diverticulum associated
is separate from the cisterna magna (arrowhead) and results with the 4th ventricle. Sagittal T1W image in a 5-month-
in obstructive hydrocephalus and marked compression of the old dog presented with obtunded mental status, decreased
brainstem from dorsally. postural reactions, and marked cervical hyperesthesia.
Note the focal expansion of the 4th ventricle, causing dorsal
the 3rd ventricle from the quadrigeminal cistern
displacement of the cerebellum, which now has a ‘crescent
can be seen on sagittal T2W images, and should be
shape’ (asterisk). The brainstem is displaced ventrally
used to determine the origin of the fluid collection
and compressed. There is a thin membrane at the caudal
(Fig. 5.5.3).21 Sagittal reformatting of 3D balanced
aspect of the 4th ventricle extending from its roof (arrow).
steady-state free precession series has been reportedly
(0.4T MRI system) (Image reproduced, with permission, from
useful in identifying this thin membrane.21
Bazelle J, Caine A, Palus V et al. (2015). Characteristics of
• In cases of 4th ventricle arachnoid diverticula, a thin
fourth ventricle arachnoid diverticula in five dogs. Vet Radiol
membrane can be noted at the caudal aspect of the
Ultrasound 56(2):196–203)
distended ventricle, extending ventrally from its roof,
and thought to represent disruption of the dorsal or
ventral veli of the 4th ventricle (Fig. 5.5.5).22 epithelial ectoderm becomes entrapped within nervous
• Less common findings may include: tissue and forms a slowly expanding cystic mass (see
– Obstructive hydrocephalus.13,19,22 Fig. 7.4.8); they can also result from invagination of sec-
– Altered signal intensity of intralesional fluid due ondary neural vesicles, such as the otic vesicle.2,4
to hemorrhage.20 • Epidermoid cysts contain keratin squames and few
– Concurrent syringomyelia in the cervical spinal inflammatory cells, and the cyst wall consists of a strati-
cord, especially with 4th ventricle diverticula.22 fied squamous epithelium supported by connective tissue
• For quadrigeminal cistern region cysts, there is a rela- stroma.
tionship between size of the lesion and presence of • In dermoid cysts, the cyst wall is complex and con-
clinical signs. Cysts causing >14% compression of the tains adnexa (sweat glands, hair follicles, and sebaceous
occipital lobe on mid-sagittal images are always asso- glands).4 These lesions are also described dorsal to the
ciated with clinical signs, while there is no association spine due to a similar pathogenesis (see Chapter 7.4).
between degree of cerebellar compression and clinical • Intracranial epidermoid and dermoid cysts are usually
signs.13 located in the cerebellopontine angle or the 4th ventri-
cle.2,25–27 Few case reports of this condition exist in dogs;
Intracranial epidermoid cysts (syn. reports in cats are lacking to date.
cholesteatomata) and dermoid cysts • Clinical signs typically do not occur until adult-
• These are benign slow-growing space-occupying lesions hood;25,28–33 the lesions may also remain clinically silent
that are caused by a failure of neural tube closure when and be incidentally discovered at necropsy or when
imaging a patient for other reasons.4,26,27,34 Due to the T2W images, suppression on fat suppressed images,
common location of these lesions, vestibular dysfunc- and presence of a dark edge on one side of the droplet
tion is the most common presenting complaint; focal sei- in the frequency-encoding direction on T2W images
zures, aggressiveness, ataxia, and hemiparesis have also due to the chemical shift artifact (Fig. 5.5.7).2,26,32
been reported.
• MRI findings include: Rathke’s cleft cysts
• Mass of variable size in the caudal fossa, most com- • These are cystic malformations of the Rathke’s cleft that
monly within the 4th ventricle; the mass typically sits are thought to arise from failure of obliteration of the
on the midline between the brainstem and the cere- lumen of the Rathke’s pouch, the precursor of the ante-
bellum and causes variable degrees of compression of rior lobe, intermediate lobe, and pars tuberalis of the
these structures. pituitary gland, which forms as a rostral outpouching of
• Due to the location of these structures, there can be the primitive oral cavity during embryologic develop-
evidence of secondary obstructive hydrocephalus and/ ment. During development, the lumen of this pouch is
or cervical syringohydromyelia.28,29,32 narrowed down to a cleft, which is supposed to regress;
• With epidermoid cysts, the mass is typically heter- it is the persistence of this cleft and subsequent cystic
ogeneously hyperintense on T2W images, hypoin- enlargement that causes a Rathke’s cleft cyst.
tense on T1W images, and remains hyperintense on • The lumen of these cysts contains mucoid or, less com-
T2-FLAIR (which differentiates them from intrac- monly, serous fluid and cellular debris. They develop in
ranial intra-arachnoid diverticula). It may contain the pituitary fossa and are often an incidental finding in
internal septations and may show ring enhancement human patients.35,36
(Fig. 5.5.6).28,30,31 • Only few reports exist in the veterinary literature. An asso-
• With dermoid cysts, the mass is typically heteroge- ciation of Rathke’s cleft cysts with congenital dwarfism has
neously hyperintense on T1W and T2W images due been reported in German Shepherd Dogs; however, they
to fat content, remains hyperintense on T2-FLAIR, may not cause any clinical signs, especially if small.37,38
may have low signal on fat suppressed sequences, may • MRI findings include:3,37,39
contain suspended low intensity foci due to presence • Single or loculated cystic lesion(s) within the pitu-
of calcification or hair, may show ring enhancement, itary fossa with or without suprasellar extension
and may be associated with fat droplets within the (Fig. 5.5.8).
ventricular system or subarachnoid space resulting • Cysts are hypointense on T1W images, hyperintense
from rupture of the cyst and communication with on T2W images, may not suppress on T2-FLAIR
the CSF-filled spaces. These fat droplets are recog- due to composition of fluid, and may show mild ring
nized by their non-dependent position (fat floats on enhancement.
top of CSF), high signal intensity on both T1W and
(a) (b)
Fig. 5.5.6 Epidermoid cyst in a 4-year-old English Setter

presented with a 5-day history of paraparesis. An MRI
examination of the cervical spine was performed in dorsal
recumbency. Sagittal T2W (a) and pre-contrast T1W (b) images
reveal a well-circumscribed round cystic mass associated
with the 4th ventricle, with gravity-dependent sedimentation
of cellular/proteinaceous contents dorsally, obstructive
hydrocephalus, and extensive cervical syringomyelia. (c) The
post-contrast T1W image with fat suppression shows ring
(c)
enhancement of the mass.
246 CHAPTER 5.5
(a) (b)
(c) (d)
Fig. 5.5.7 Intracranial dermoid cyst in a dog. On the T2W sagittal image (a), a heterogeneous, mostly hyperintense mass is
seen between the cerebellum and brainstem, causing mild ventral displacement of the brainstem. On the transverse T1W
image (b), the mass (arrows) is on the midline between the brainstem and the cerebellum, and its content is heterogeneous,
with some hyperintense areas compared with CSF. Transverse T1W (c) and T2W (d) images at the level of the lateral
ventricles show a small, well-defined oval structure within the non-dependent part of the right lateral ventricle (the patient
was positioned in dorsal recumbency for scanning). This structure is markedly T1 hyperintense and T2 isointense compared
with CSF. On the T2W image (d), the hypointense crescent-shaped dorsal border (solid arrow) and hyperintense ventral border
of the lesion (dashed arrow) are the result of a chemical shift artifact. This is consistent with lipid content of the structure,
which also explains its non-dependent location in the ventricular lumen. (Reproduced, with permission, from MacKillop E
(2011). Magnetic resonance imaging of intracranial malformations in dogs and cats. Vet Radiol Ultrasound 52(Suppl 1):S42–51)
(Images in the original article were courtesy of Dr. C.R. Lamb, Royal Veterinary College)
(a) (b)
Fig. 5.5.8 Incidental Rathke cleft cyst (presumptive) in a 13-year-old Chihuahua presented with a hemorrhagic stroke of the
right frontal lobe (not shown). The transverse T2W (a) and T2-FLAIR (b) images show a sharply marginated and thin-walled
cystic lesion within the pituitary fossa (arrows). The hyperintensity of the white matter tracts of the right cerebral hemispheres
with associated mass effect is consistent with vasogenic edema secondary to the hemorrhagic stroke in this patient.
Ependymal cysts • Lesions are non-enhancing, ring enhancing, or

• These cysts are lined by ependymal cells rather than a strongly enhancing.41–43 The strong enhancement is
basement membrane or connective tissue. In humans, quite atypical for a cyst-like structure, and has been
they are often located deep within brain parenchyma, attributed to neo-vascularization within the cyst or
may be incidental or be associated with a variety of clini- disruption of the blood–brain barrier.42
cal signs.36
• A case of a large cerebellar ependymal cyst has been Other congenital/developmental
reported in an 11-week-old Staffordshire Bull Terrier conditions associated with increased
who presented with generalized ataxia and falling since fluid accumulation within the cranium
birth.40 • Congenital hydrocephalus manifests as ventricular dila-
• MRI findings included a well-circumscribed cystic lesion tion, which ranges from mild to severe.44
filled with fluid of signal similar to CSF. In people, they • Holoprosencephaly is a failure of the forebrain to bifur-
can be found in variable locations, but separate from the cate normally and is characterized by an absence or
ventricular system.36,40 reduction in size of midline prosencephalic structures,
incomplete separation of normally paired forebrain
Choroid plexus cysts structures, and hydrocephalus.2
• Choroid plexus cysts develop when neuroepithelium lin- • Dandy–Walker malformation is characterized by partial
ing the interlobar clefts invaginates into the stroma with or complete absence of the cerebellar vermis and cystic
subsequent accumulation of CSF and debris. In people, dilation of the fourth ventricle.2,45,46
they are most commonly located in the lateral ventri- • These conditions are described in more detail in
cles and are often asymptomatic. Two cases have been Chapter 5.1.
reported in dogs: one in the cerebellopontine angle loca-
tion in a 6-year-old Doberman Pinscher with a head tilt ACQUIRED CYSTIC LESIONS
and ataxia,41 and one within the 4th ventricle in a 3-year-
old Toy Fox Terrier presented for ‘fly-biting’ episodes.42 ‘Hydrocephalus ex vacuo’ (‘compensatory
• MRI findings include: hydrocephalus’) and ‘lacunae’
• Well-circumscribed lesions, which are typically isoin- • A number of insults to the brain parenchyma including
tense to CSF, although signal intensity can be altered necrosis, trauma, and vascular compromise can result in
due to variations in protein content.42,43 focal loss of brain tissue, leaving a space that passively fills
248 CHAPTER 5.5
with CSF. Although these conditions should technically • MRI findings include:52,56,57
not be classified as ‘hydrocephalus’, which is defined as • Single or multifocal rounded, parenchymal, menin-
an active distension of the ventricular system,47,48 ‘hydro- geal/subarachnoid, and/or ventricular cysts isointense
cephalus ex vacuo’ or ‘compensatory hydrocephalus’ are to CSF on T1W and T2W images, ranging from
still used due to lack of a better term.49,50 4–20 mm.
• The term ‘lacunae’ has also been applied to small cystic • Tapeworm scolex may be visible as an internal asym-
brain lesions observed in a population of older dogs and metric nodule (‘hole-with-dot’).
attributed to chronic lacunar infarcts.51 • Nodular or ring enhancement and perilesional edema
• Age at diagnosis and clinical findings are variable, and in degenerate cysts.
the lesions may be discovered incidentally when imaging
a patient for other reasons. Malignant and benign cystic
• MRI findings include: intracranial masses
• Dependent on the underlying cause, variably sized • A variety of benign or malignant intracranial masses may
and shaped lesion(s) isointense to CSF and replacing be associated with cavitation and/or cyst-like changes.
normal brain parenchyma without a noticeable mass However, they usually have a solid component allowing
effect (Fig. 5.5.9; see also Chapter 5.8, Fig. 5.8.8 and differentiation from most cystic lesions and diverticula
Chapter 5.9, Fig. 5.9.4).49–51 described above.
• In cases of previous trauma, concurrent osseous • Brain tumors that may have a cystic component
lesions or evidence of chronic hematoma in the vicin- include meningiomas, gliomas, choroid plexus
ity of the fluid-filled lesion. tumors, nasal tumors, and others.58–66 These condi-
tions are described in more detail in Chapter 5.4.
Neurocysticercosis • Intracranial extension of nasal mucoceles has been
• Infection of the central nervous system with cystic larvae reported in one dog and one cat.67,68
of Taenia solium is a frequent cause of seizures in people, • A cholesterol granuloma within the 4th ventricle
especially in resource-poor countries.52 and secondary obstructive hydrocephalus have been
• A diagnosis of neurocysticercosis in dogs is typically described in a 2-year-old American Bulldog. The mass
made at necropsy.53–55 had a cystic appearance on MR images but appeared
• Clinical signs vary dependent on the number and loca- solid on gross pathology.69
tion of the cysts.
• One case of MRI diagnosis of this condition has been
reported in the veterinary literature: a 2-year-old
Whippet with a 3-month history of circling and falling.56
(a) (b)
Fig. 5.5.9 Residual cystic brain lesion (‘lacuna’) following a previous ischemic infarct in a French Bulldog with polycythemia
vera. (a, b) Transverse T2W (a) and T2-FLAIR (b) images at time of initial presentation show a wedge-shaped hyperintense
lesion associated with the right mesencephalon (arrows). (c, d) Transverse T2W (c) and T2-FLAIR (d) images at recheck MR
examination 2 years later show a focal punctate lesion isointense to CSF at the site of the previous infarct (arrows). (Continued)
(c) (d)
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CHAPTER 5.6
ISCHEMIC BRAIN DISEASE AND

VASCULAR ANOMALIES 251
J. Fraser McConnell
CONTENTS
Pathophysiology of stroke .....................................................................................................................................................................................251
Normal brain perfusion ....................................................................................................................................................................................252
Pathophysiology of brain ischemia ..................................................................................................................................................................252
Ischemic penumbra .........................................................................................................................................................................................252
Classification of stroke ..........................................................................................................................................................................................253
Technical considerations for MRI investigation of stroke.......................................................................................................................................254
General considerations ....................................................................................................................................................................................254
Diffusion-weighted imaging in stroke ..............................................................................................................................................................254
Perfusion-weighted imaging in stroke .............................................................................................................................................................257
MRI features of arterial infarction .........................................................................................................................................................................259
General features ..............................................................................................................................................................................................261
Acute large artery/territorial infarcts .................................................................................................................................................................266
Chronic large artery/territorial infarcts .............................................................................................................................................................266
Small vessel disease (‘lacunar infarcts’)...........................................................................................................................................................266
Differential diagnoses for arterial infarcts.........................................................................................................................................................272
Transient ischemic attacks.....................................................................................................................................................................................272
Global brain ischemia ........................................................................................................................................................................................... 274
Venous infarction and thrombosis.........................................................................................................................................................................275
Hypertensive encephalopathy ................................................................................................................................................................................277
Vascular anomalies ...............................................................................................................................................................................................277
References.............................................................................................................................................................................................................279
In this chapter, the pathophysiologic and imaging features the brain).1 The term stroke is often used to describe
of non-hemorrhagic cerebrovascular disorders of the brain the clinical syndrome of acute onset of persistent
are described. Hemorrhagic complications are often seen neurologic deficits.2
concomitant with the conditions described in this chapter, • Strokes are generally divided into ischemic stroke (due
and are covered separately in Chapter 5.7. to obstruction of blood vessels) and hemorrhagic stroke
(as a result of vessel rupture).1 In small animals, ischemic
PATHOPHYSIOLOGY OF STROKE disease is more common than hemorrhagic stroke.
• On MRI the appearance usually differs considerably, and
• The appearance of ischemic brain disease on MRI is there are often different underlying causes and patho-
related to the pathophysiology of the disease. An under- physiology. Hemorrhagic stroke is covered in Chapter 5.7.
standing of the disease mechanisms is helpful to ade- • The most common cause of stroke is obstruction or
quately interpret the imaging findings. rupture of a cerebral blood vessel, but ischemia can also
• Stroke, or cerebrovascular accident, is the clinical occur as a result of impaired brain perfusion due to a
manifestation of cerebrovascular disease (defined as reduction in cardiac output (e.g., global brain ischemia
pathology or rupture of the blood vessels supplying due to cardiac arrest).
252 CHAPTER 5.6
Normal brain perfusion • Within the brain, some areas such as the occipital and
• Cerebral perfusion (circulation through the vascular bed parietal lobes, certain regions of the hippocampus
of tissue) is determined by the cerebral perfusion pres- such as the cornu ammonis 1 (CA1), cerebellum, and
sure (CPP), which is the gradient between mean arterial caudate nucleus are particularly vulnerable.7
pressure and intracranial pressure.
• The flow of blood within brain tissue (cerebral blood Ischemic penumbra
flow [CBF]) is determined by the CPP and cerebrovascu- • Reduction in CBF following arterial thrombosis is not
lar resistance (CVR), where CBF = CPP/CVR. uniform within lesions, with severity increasing from the
• Due to autoregulatory mechanisms, CBF remains rela- periphery to the center.
tively constant despite variations in mean arterial blood • The volume of ischemic tissue is often larger than the
pressure. volume that is infarcted. Peripheral areas of ischemia
• CBF is greater in gray matter than white matter and may potentially recover normal function if blood sup-
there is some coupling of CBF with metabolism, so that ply is restored, while in areas of severe or prolonged
metabolically active areas of the brain (e.g., the thalamus) ischemia, known as the core, irreversible infarction
have greater perfusion.3,4 occurs.
• Perfusion within the brain is non-uniform, with greater • The area of ischemic tissue within the lesion that is
perfusion in the occipital/parietal lobes versus olfactory potentially salvageable with treatment is known as the
lobe.5 ‘ischemic penumbra’.
• Values of relative CBF (rCBF) vary depending on the • Surrounding the penumbra there is an area of tissue with
measurement technique. Normal rCBF in gray matter mild reduction in blood flow, which is more likely to sur-
is approximately 55–75 +/− 25 mL/100 g/min on CT vive, called the ‘oligemic region’.2,8
and 145–280 mL/100 g/min when measured on MRI.4,6 • In people, the volume of the infarcted core has prog-
Loss of cellular function occurs when CBF falls below nostic and therapeutic importance.2,9 The correlation
15–20 mL/100 g/min.2 between infarct core size and prognosis is unknown in
small animals.
Pathophysiology of brain ischemia • The size of the ischemic penumbra can be estimated
• Brain tissue requires a constant supply of oxygen and using a combination of diffusion-weighted imag-
glucose to maintain normal function. ing (DWI) and perfusion-weighted imaging (PWI)
• Ischemic damage to the brain occurs secondary to a (Fig. 5.6.1):
reduction in oxygen supply to the tissue, typically caused • DWI shows the infarct core and PWI the area of
by reduced perfusion. This rapidly leads to loss of neu- ischemia.
ronal activity. • The difference between lesion size measured on
• As a result of brain ischemia, a cascade of events happens: PWI and DWI represents the volume of tissue that
• Due to energy depletion within the affected cells, is underperfused but which is potentially salvageable
there is loss of ATP and depolarization of the cell with treatment.
membrane. • The initial ischemic penumbra comprises two parts:
• This causes an influx of sodium and calcium across the an area that progresses to infarction, and an area that
cell membrane followed by water, leading to increased typically normalizes on follow-up imaging. In people,
intracellular water (‘cytotoxic edema’). PWI has been used to try and differentiate these two
• If the hypoxia or reduced perfusion is severe or pro- areas of the penumbra and establish quantitative via-
longed, the ischemic tissue may undergo infarction. bility thresholds. Using reference points in symmet-
• Over time there is activation of a cascade of neuro- rically located, normally perfused areas of the brain,
chemical events leading to lipolysis, cell necrosis, rCBF ratios and mean transit time (MTT) ratios can
inflammation, and apoptosis.2 be computed. An rCBF ratio <0.59 and a MTT ratio
• Breakdown of the cell membranes and the blood– >1.63 in the acute stages of stroke have been suggested
brain barrier results in development of vasogenic to predict progression of the penumbra to infarction.10
edema after 24 hours, and this increases with time, However, different studies have shown a wide range of
peaking at 3–4 days. cut-off values, and there are marked differences with
• There is variable susceptibility to ischemia within dif- the technique and equipment used, which limits their
ferent tissues and locations in the brain, leading to the value.11 There is conflicting evidence as to whether
concept of ‘selective vulnerability’. Those areas with the the tissue identified by a PWI/DWI mismatch reper-
highest metabolic activity are the most susceptible to fuses following treatment and the evidence support-
ischemia: ing the use of PWI in clinical cases is weak.8,11 The
• Gray matter is more sensitive than white matter to value of PWI in clinical small animal cases has not
ischemia. been demonstrated.
I sc h e m ic Br a i n D is e a s e a n d Va sc u l a r A nom a l i e s 253
(a) (b)
Fig. 5.6.1 Acute cerebellar infarct in a 6-year-old Maltese

presenting with acute-onset non-ambulatory tetraparesis,
cerebellar rigidity, and nystagmus. Transverse T2W (a)
and DW (b) images and relative CBF map (c) showing that
the T2W image underestimates the area of ischemia (solid
arrows), which is larger on the DW image (b) and extends
more laterally along the left side of the cerebellum (open
arrow). The PW image (c) shows severe hypoperfusion
(dashed arrows) typical of an acute ischemic infarct. The size
of the lesion on DWI (b) and PWI (c) is similar, suggesting
(c)
that the ischemic penumbra is small. (1.5T MRI system)
CLASSIFICATION OF STROKE – Cardioembolic stroke.

– Other causes.
• Strokes can be classified in a variety of ways, and there is – Unknown etiology (cryptogenic).
no agreed single classification scheme in people or small • Historically on MRI, strokes were divided into territo-
animals. rial (large vessel disease) or lacunar (small vessel disease),
• Strokes are commonly classified according to clinical based on the size and location of the infarcts. Classifying
presentation, results of imaging, underlying risk factors, strokes as either large vessel or small vessel infarcts can
and results of diagnostic tests. help predict the underlying cause:
• Strokes are usually broadly classified according to:12,13 • In people, the most common cause of large artery
• Hemorrhagic versus ischemic stroke. stroke is thrombosis due to atherosclerosis, which
• Arterial versus venous stroke. occurs either at the site of plaques or results from
• The vessel(s) affected. embolism from blood vessels located upstream such
• Type of stroke: as the carotid arteries.2
– Large vessel (atherosclerotic stroke/territorial • Lacunar strokes by contrast were originally thought
infarcts). to occur due to intrinsic small vessel disease (rather
– Small vessel (e.g., lacunar infarcts). than embolic disease). The classification of small
254 CHAPTER 5.6
infarcts is complex, and the assumption that lacunar • MRA may be performed to document site of throm-
infarcts only represent intrinsic small vessel disease bosis or vascular abnormality.
has been shown to be unreliable.14 Small deep infarcts • PWI to confirm reduced perfusion and to evaluate
may also occur secondary to embolic disease, and the penumbra.
intrinsic small vessel disease may cause multiple other • In people with ischemic stroke due to thrombosis, medi-
changes on MRI in addition to small deep infarcts.15 cal treatment with thrombolytics needs to be performed
• The exact underlying mechanism of most brain infarcts within ~4.5 hours after onset of stroke, thus early imag-
in small animals is unknown, although predisposing ing is essential.9 As veterinary patients are very rarely
medical conditions are commonly identified.16 In contrast imaged within this timeframe, MRI for treatment plan-
to people, naturally occurring atherosclerosis appears to ning is generally not required.
be relatively rare in small animals and, in dogs, is most
commonly associated with hypothyroidism17,18 or lipid Diffusion-weighted imaging in stroke
metabolism disorders.19 Cardioembolic causes of stroke • DWI (see Chapter 2) is an important technique for the
also appear to be rare in small animals.1 investigation of ischemic brain disease and is used to
highlight the changes in MRI signal associated with the
TECHNICAL CONSIDERATIONS FOR cytotoxic edema that develops quickly after the onset of
MRI INVESTIGATION OF STROKE ischemia.
• DWI is significantly more sensitive than conventional
General considerations pulse sequences (e.g., T2W or T2-FLAIR) in the per-
• In people, specific MRI protocols are used in cases where acute stages when standard MRI images may be normal
a stroke is suspected, with the aims of confirming stroke, (see Fig. 2.31).20 After occlusion of cerebral arteries,
classifying the type of stroke, treatment planning, iden- there is a rapid reduction in CBF and within minutes
tifying underlying causes, and prognosis.2 increased signal on DWI may be seen.
• A typical human stroke protocol often includes, in addi- • DWI is almost 100% sensitive for detection of acute
tion to the standard pulse sequences: infarction in people,11 although negative results can occur
• T2*W gradient echo or susceptibility-weighted with mild ischemia (e.g., transient ischemic attacks).21
imaging (SWI) to detect the presence of hemorrhage, • In acute arterial stroke, there is reduced diffusion on
which is a contraindication for thrombolytic therapy. DWI (Fig. 5.6.2), which can be quantified by calculating
• DWI to confirm restricted diffusion. the apparent diffusion coefficient (ADC). A reduction in
(a) (b)
Fig. 5.6.2 Acute cerebellar infarct in a 6-year-old Maltese presenting with acute-onset non-ambulatory tetraparesis, cerebellar
rigidity, and nystagmus (same dog as in Fig. 5.6.1). Transverse T2W (a) and DW (b) images, ADC map (c), and exponential
ADC map (d) showing severe restricted diffusion within the lesion typical of an acute ischemic infarct (arrows). The ADC map
(c) shows low signal confirming restricted diffusion and excluding T2 shine-through effects. The exponential ADC map (d)
is calculated from the ADC values, and leads to an inverted scale more similar to the DW images, where restricted diffusion
appears bright, but again eliminating T2 shine-through effects like the regular ADC map; these exponential ADC maps may be
more sensitive than ADC images for recognizing restricted diffusion in periventricular areas as a bright signal adjacent to the
dark CSF. (1.5T MRI system)
(c) (d)
the ADC occurs when CBF drops below 15–20 mL/100 have a maximal decrease at approximately 24 hours after
g/min.2 onset of ischemia.2
• The exact cause of restricted diffusion due to cytotoxic • An important use of DWI in people is in estimating the
edema is unknown. A possible cause is movement of age of ischemic infarcts using ADC values, and this may
water into the intracellular compartment where the pres- be applicable in animals as well (Fig. 5.6.3). In clinical
ence of organelles and cell membranes impedes motion studies in people, ADC values continue to drop for sev-
of water.22 Swelling of affected cells also occurs and this eral days after the onset of stroke, and remain reduced
may cause reduced diffusion of water and increased cyto- for 4–5 days before pseudo-normalizing between 4 and
plasmic viscosity.23 In experimental models, ADC values 10 days.2 After 10 days, ADC values become elevated.
(a) (b)
Fig. 5.6.3 Acute cerebellar infarct and chronic lacunar infarct in the left caudate nucleus in a 9-year-old Cocker Spaniel
presenting with acute-onset ataxia, falling to the right, and tetraparesis. The dog had protein-losing nephropathy, hypertension,
and hypercoagulopathy, which are all predisposing factors for stroke. Transverse T2W (a, e) and DW (b, f) images, ADC maps
(c, g), and exponential ADC maps (d, h) showing an acute cerebellar infarct (solid arrows, a–d) and chronic lacunar infarct within
the left caudate nucleus (dotted arrows, e, g, and h). Both lesions appear hyperintense on the T2W images but DWI shows that
the cerebellar infarct is acute with restricted diffusion, which is hyperintense on the DW image (b) and exponential ADC map
(d) and with low signal on the ADC map (c). The DW image of the lacunar infarct (f) shows increased diffusion, which appears of
low signal on the exponential ADC map (h) and of high signal on the ADC map (g), indicating chronicity. In this case the DWI
shows that the cerebellar lesion is the reason for the clinical signs and also that there have been at least two episodes of ischemia
occurring at different time points. (Continued)
256 CHAPTER 5.6
(c) (d)
(e) (f)
(g) (h)
• In people, DWI is also of value to estimate the core • Relative brain perfusion can be measured in two main
infarct volume by measuring the volume of DWI ways on MRI, including contrast based techniques and
abnormality. The amplitude of ADC decrease is highly non-contrast based techniques:
correlated with areas of infarction.2 A volume of the core • Contrast based T2*W echo planar imaging tech-
infarct of >70 mL is an indicator of poor prognosis, and niques (e.g., dynamic susceptibility contrast imaging)
this threshold is often used for guiding the use of endo- are used most commonly, and rely on measuring the
vascular techniques of clot removal in humans. reduction in signal caused by the susceptibility effects
of gadolinium-based contrast medium (Fig. 5.6.4).
Perfusion-weighted imaging in stroke The contrast is given using a pressure injector fol-
• Ischemic brain disease also usually results in perfusion lowed by a saline flush and a dynamic acquisition is
abnormalities; these can be assessed using MRI, which, used to obtain the images representing the first arte-
in some cases, can show changes that may not be visible rial pass of contrast material through the vascular bed
on other techniques. of interest.
(a) (b)
–5
–10
Relative percentage
–15
–20
–25
–30
–35
–40
Dynamic reference line (0)
–45 Region of interest
0 5 10 15 20 25 30 35 40 45 50 55 60 65 70
(c) Dynamics (seconds)
Fig. 5.6.4 Dynamic susceptibility contrast imaging in a 6-year-old Maltese. Transverse T2*W echo planar images pre- (a) and
during (b) contrast injection showing signal loss (hypointensity) within the parenchyma and blood vessels (arrows, b) due to
the T2-shortening effects of gadolinium. The signal-versus-time graph (c) shows a marked signal drop as the bolus of contrast
passes through the brain. Deconvolution and mathematical transformations using the signal-versus-time graph are used to
generate relative perfusion and bolus timing graphs. (1.5T MRI system)
258 CHAPTER 5.6
• Non-contrast based techniques, such as arterial spin • Depending on the technique used, a variety of perfusion
labelling, use magnetically labelled arterial blood to parameters can be measured to quantify brain perfusion
act as an endogenous tracer to allow perfusion to be (Figs. 5.6.5, 5.6.6).11 The main measurements used are
measured.24 During image acquisition, alternating relative rCBF, relative cerebral blood volume (rCBV),
control and arterially labelled images are acquired MTT, time to peak signal loss (TTP), and the time
and are then subtracted from each other, to allow at which the deconvoluted residue function reaches its
perfusion to be calculated. The difference in signal maximum value (Tmax):
is approximately proportional to the CBF. Although • CBV is the total blood volume within a voxel of
this technique allows non-invasive measurement of interest (mL/100 g), which in dogs is approximately
brain perfusion without contrast material administra- 2.5–3.0 mL/100 g.4
tion, it yields a weak MR signal, and can be affected • CBF measured using MRI in normal dogs is greater
by a large number of technical factors.25 in gray matter compared with white matter and
(a) (b)
(c) (d)
Fig. 5.6.5 Perfusion parametric maps of a 6-year-old Maltese. Relative cerebral blood flow (a) and relative cerebral blood
volume (b) maps show greater perfusion within gray matter and arteries compared with white matter. In normal animals,
perfusion in the left and right sides should be symmetric and analysis generally involves comparing contralateral regions of
interest to quantify differences in relative perfusion. Multiple assumptions are made when generating perfusion maps on MRI
and numerical values can vary depending on technique. Maps showing bolus characteristics including MTT (c) and TTP (d) are
less technique-dependent and can give some information on timing delays and other abnormalities, but do not show perfusion
of the brain.
(a) (b)
(c) (d)
Fig. 5.6.6 Perfusion parametric maps of a 6-year-old Maltese with acute left cerebellar infarct (same dog as in Figs. 5.6.1 and
5.6.2). Images are obtained at the level of the cerebellum. Relative cerebral blood flow (a) and relative cerebral blood volume
(b) maps show severe reduced relative blood flow and volume within the infarct (arrows). The MTT (c) and TTP (d) maps show
delay in arrival of contrast within the infarct.
varies from approximately 145 to 280 mL/100 g/min • In cases of suspect stroke in small animals, a standard
depending on the region of the brain.26 brain protocol including T2-FLAIR and T1W post-
• MTT (= CBV/CBF) represents the mean time for contrast plus T2*W gradient echo or SWI and DWI if
blood to pass though the voxel of interest. available is recommended.
• Anatomic and physiologic variations can result in asym- • DWI is useful for diagnosis of stroke in small animals
metry on perfusion studies in people, which complicates as some infarcts may be more obvious on DWI (see
interpretation of PWI studies.8,27 Fig. 2.31), and if classical DWI abnormalities are pres-
ent this may help differentiation of stroke from other
MRI FEATURES OF ARTERIAL INFARCTION pathologies.28 However, low ADC values can also be seen
in other pathologies (Fig. 5.6.7).29
• Rapid diagnosis (within 4 hours) of onset of stroke is • MRA can show many of the normal cerebral arteries
rarely possible in small animals, therefore imaging tech- larger than 0.4 mm diameter in dogs,30 but is rarely used
niques used in people for treatment planning are usually diagnostically in stroke (Fig. 5.6.8).
only of academic interest in veterinary medicine.
260 CHAPTER 5.6
(a) (b)
Fig. 5.6.7 Intravascular lymphoma in a 3-year-old crossbred dog presented with progressive central vestibular signs. The
transverse T2-FLAIR (a) and DW (b) images show multifocal lesions (arrows) within gray and white matter, more obvious
on the DW image. The ADC maps derived from DWI (not shown) confirmed that the lesions had restricted diffusion and
histopathology confirmed lymphoma. DWI for some pathologies is more sensitive than conventional sequences, as in this case.
(1.5T MRI system)
(a) (b)
Fig. 5.6.8 Cerebellar infarct in a 6-year-old Maltese presenting with acute-onset non-ambulatory tetraparesis, cerebellar
rigidity, and nystagmus (same dog as in Figs. 5.6.1, 5.6.2, and 5.6.6). Sagittal T2W (a) and 3D-time-of-flight MRA (b) of the
cranial arteries (ventral view). The appearance of the lesion on the T2W image is typical of an acute ischemic infarct within
the territory of the rostral cerebellar artery (arrow, a). The MRA shows normal flow in the right internal carotid artery (open
arrow, b) but complete absence of flow within the left internal carotid artery (not visible due to complete absence of flow).
(1.5T MRI system)
General features • Definitive diagnosis of arterial ischemic stroke relies on

• In dogs, most infarcts are presumed to be due to in-situ documenting occlusion of the abnormal artery, supported
thrombosis of cerebral vessels, although embolism may by DWI abnormalities concurrent with altered perfusion
also occur.1 on PWI. Several PWI abnormalities are typically seen in
• Typically, ischemic stroke presents acutely/peracutely, acute ischemia, such as reduced CBF and increased rela-
with minimal progression31 or gradual improvement, tive MTT and Tmax. PWI abnormalities are, however,
over time, depending on the severity. variable and complex depending on the degree of collat-
• There are numerous predisposing medical conditions eral circulation and autoregulatory mechanisms, which
for stroke in small animals including: atherosclerosis can compensate for a reduced CPP.11 For example, CBV
due to hypothyroidism or hyperlipoproteinemia, renal may be maintained or even elevated due to vasodilation
disease, sepsis, neoplasia, coagulopathy, endocrinopathy, and development of a collateral leptomeningeal circula-
fibrocartilaginous embolism, aortic or cardiac embolism, tion. In the acute stages, PWI abnormalities are often
Leishmania, Dirofilaria, Cuterebra, and granulomatous larger than DWI abnormalities, but over time the DWI
meningoencephalitis.16,31–34 An underlying cause for abnormalities may increase in size to match PWI lesions.
stroke was found in approximately 50% of cases in one • Due to the small size of canine and feline cerebral arter-
study, with the most common predisposing factors being ies, direct visualization of the primary vascular abnor-
renal disease and hyperadrenocorticism.35 mality is rarely possible. MRA may show occlusion of
• Breed predispositions are reported for ischemic infarcts larger arteries in some cases (Fig. 5.6.8), but due to limi-
in dogs, with sighthounds and spaniels predisposed.35–37 tations of spatial resolution, the sensitivity is relatively
The increased incidence of infarction in Greyhounds low.32
may be due to hypertension.37 • MRI features of ischemic arterial infarcts include:28,35
• It is not uncommon for animals with ischemic stroke to • Most commonly solitary, uncommonly multi-
suffer multiple further infarctions if an underlying cause ple lesion(s) that is/are hyperintense on T2W and
cannot be corrected. The diagnosis of ischemic disease T2-FLAIR images (Fig. 5.6.9), unless hemorrhagic
on brain MRI is an indication for investigation of poten- transformation is present (Fig. 5.6.10).
tial underlying causes. • The lesion may be homogeneous or heterogeneous.
• The appearance of ischemia on MRI is complex and • The lesion is often sharply marginated.
depends on the time of imaging from onset of ischemia, • Lesion confined to specific vascular territories
the parts of the brain affected, the blood vessels involved, (Fig. 5.6.11).
and the underlying cause of the ischemia. • Cerebellum is the most common site of territorial
• Due to the development of cytotoxic edema, arterial infarcts in dogs.
strokes typically are homogeneously hyperintense on • Gray matter only, or preferentially affecting gray
T2W images. In people, 90% of patients with acute arte- matter (Fig. 5.6.9).
rial infarction show increased T2W signal by 24 hours • Mass effect is generally mild to moderate, depending
post onset.2 on the size of the infarction (Fig. 5.6.12). Vasogenic
• On DWI in the acute stages of infarction, there is edema contributes to the mass effect seen with large
restricted diffusion, which appears hyperintense on the infarctions on MRI and mass effect peaks at days 3–4
DWI and of low signal on ADC maps. As DWI images post onset of infarction.2
usually have some T2-weighting, lesions that are • Enhancement pattern variable, often no enhancement
hyperintense on T2W images may also appear hyper- (especially small infarcts) (Figs. 5.6.9, 5.6.13).
intense on DWI; this high signal on DWI due to T2 • Contrast enhancement usually occurs after resolution
effects is known as ‘T2 shine-through’, and may mimic of any mass effect (i.e., enhancement with an obvious
restricted diffusion. This underscores the importance mass effect is rare). This is a key imaging feature that
of a comparison with the ADC map to prove restricted helps differentiate large infarcts from other mass
diffusion. lesions.
• Because of selective vulnerability, the changes are typi- • Contrast enhancement may occur within 24–48 hours
cally predominately, or exclusively, within the gray mat- post onset, but is more commonly seen at 1–8 weeks.
ter, with relative sparing of the white matter. In people, early parenchymal enhancement may be
• Another key feature of ischemic infarcts is that lesions predictive of hemorrhagic transformation.38
are confined to specific vascular territories supplied by • Reduced CBF, increased MTT and Tmax on PWI
the affected arteries. In most territorial infarcts, a single (Fig. 5.6.6).
artery is involved. Therefore, lesions are confined to a • Restricted diffusion on DWI in acute stages (high
single vascular territory, which helps differentiate arte- DWI signal, low ADC map signal) (Fig. 5.6.2).
rial infarction from other causes of cytotoxic edema. • Occlusion of supplying artery on MRA (Fig. 5.6.8).
262 CHAPTER 5.6
(b)
(a)
(c)
(d)
Fig. 5.6.9 Acute non-hemorrhagic cerebellar infarct in a

12-year-old Pug presented with peracute onset of severe
vestibular signs. Dorsal (a) and transverse T2W (b), DW (c),
T1W (d), and T1W post-contrast (e) images showing a sharply
marginated homogeneous T2 hyperintense lesion, which is
most severe within the gray matter and with minimal to no
mass effect (arrows, a and b). The lesion is confined to the
vascular territory of the left rostral cerebellar artery and
is hypointense on the T1W images (d) with only very faint
peripheral enhancement (e). The DW image (c) shows severe
restricted diffusion typical of acute ischemia. (1.5T MRI
(e)
system)
(a) (b)
(c) (d)
Fig. 5.6.10 Ischemic infarct within the territory of the left middle cerebral artery in a Greyhound imaged on day 1 (a, b) and
7 days (c, d) after onset of signs. Transverse T2-FLAIR (a, c) images showing progressive increase in size of the initial lesion
(solid arrow) due to development of vasogenic edema and a heterogeneous appearance in the subacute stage (c) compared with
the peracute stage (a). The T2*W images (b, d) show no evidence of hemorrhage initially (b) but development of hemorrhage by
day 7 (d) due to reperfusion (dotted arrow). (1.5T MRI system)
• Estimation of the age of the infarction using MRI cri- been used to estimate the time of onset of isch-
teria has been reported: emia.20,40 A significant correlation between degree
– In people, gyral enhancement occurs in sub- of T2-FLAIR–DWI mismatch and onset time of
acute infarcts, beginning at ~7 days post onset of stroke has been reported, and may be used to age
signs, and persists for 6–8 weeks.2 Parenchymal peracute infarcts when onset time is unknown.40
enhancement with subacute infarcts is common • In addition to the MRI features described above, there
but is usually mild.39 are several imaging findings reported in human arterial
– In experimental canine models, at the early stages infarction,2 which have not been reported in naturally
of infarction, quantification of differences in sig- occurring infarcts in small animals but may potentially
nal intensity on T2-FLAIR and DWI images has be seen:
264 CHAPTER 5.6
Fig. 5.6.11 Schematic representation of the vascular

Rostral cerebral a. arterial supply to the brain in dogs on a ventral view
of the brain (a), as well as approximate distribution of
Internal carotid a. territories supplied by the different vessels overlaid
on T2W transverse images of the brain of a dog (b).
Middle cerebral a.
(Images courtesy of Dr. Wilfried Mai, University of
Pennsylvania)
Caudal cerebral a.
Rostral
cerebellar a.
Basilar a.
Caudal cerebellar a.
Vertebral a.
(a)
Rostral cerebral arteries Middle cerebral arteries Striate arteries Caudal cerebral arteries
(b) Perforating arteries Rostral cerebellar arteries Caudal cerebellar arteries Vertebral arteries
(a) (b)
Fig. 5.6.12 Acute ischemic infarcts in a 10-year-old Cavalier King Charles Spaniel (a) and an 11-year-old West Highland White
Terrier. Transverse T2W images showing that mass effect with acute infarcts is variable. In (a), a severe mass effect is seen in
a large left cerebral infarct in the territory of the left middle cerebral artery, resulting in compression of adjacent structures
and midline shift to the right. In (b), a small cortical infarct (arrow) in the right frontal lobe shows mild swelling of the affected
parenchyma but no mass effect. (1T MRI system)
(a) (b)
Fig. 5.6.13 Subacute (5 days old) lacunar infarct in the left caudate nucleus in an 8-year-old Bullmastiff presented with acute
onset disorientation. The transverse T1W (a) and T1W post-contrast (b) images show moderately severe enhancement (arrow)
within the center of the infarct. This degree of enhancement is uncommon and in many ischemic infarcts there is no or
minimal enhancement. (1T MRI system)
266 CHAPTER 5.6
• Hypointensity of the subcortical white matter in the

acute stages on T2W images. Table 5.6.1 Vascular territories of the canine brain.1
• Absence of signal void from arterial flow.
• Susceptibility changes in the affected cortex. MAJoR ARteRieS VASCULAR teRRitoRY
• Early arterial contrast enhancement without signifi- Rostral cerebral artery Rostromedial and dorsal surfaces of the
cant parenchymal enhancement. cerebral cortex along each side of the
• Prominent hypointense veins on SWI.41 medial longitudinal fissure
• While in many cases the imaging and clinical features Middle cerebral artery Lateral cerebral cortex
are highly suggestive of ischemic infarction, diagnosis Caudal cerebral artery Caudomedial and dorsal surfaces of the
can be difficult in large infarcts, especially where there cerebral cortex along each side of the
is hemorrhagic transformation. In some cases, follow-up medial longitudinal fissure
imaging is required to differentiate large infarcts from Rostral cerebellar artery Rostral part of the cerebellar hemisphere,
other mass lesions (e.g., neoplasia). vermis, and dorsolateral brainstem
Caudal cerebellar artery Caudal and ventral cerebellum
Acute large artery/territorial infarcts Lateral medulla
• The part of the brain affected during ischemic stroke is
dependent on which artery or arterial branch is occluded.
A key imaging feature of ischemic stroke is the localiza- • In dogs, the most common territorial infarcts are
tion of lesions within specific vascular territories and within the regions supplied by the rostral cerebel-
therefore knowledge of vascular territories is important lar and middle cerebral arteries.35–37 Rostral cerebral
(Fig. 5.6.11). There are individual anatomic variations, artery infarcts are less common, while caudal cere-
primarily in the origin of the smaller arteries. bral and caudal cerebellar artery infarcts are the least
• The primary arterial supply to the brain in dogs is via the commonly reported.35,44
internal carotid and basilar arteries, which form an arte-
rial ring on the ventral surface of the brain adjacent to the Chronic large artery/territorial infarcts
pituitary gland. Small communicating arteries (the ros- • Infarcts are classified as chronic when there is resolution
tral and caudal communicating arteries) join the internal of edema, resorption of necrotic tissue, and restoration
carotid and basilar arteries forming the ‘circle of Willis’. of the blood–brain barrier.2 This is usually complete
• The cerebrum is supplied by three large arteries – within 6 weeks.
the rostral, middle, and caudal cerebral arteries, which are • Serial imaging of infarcts has shown that chronic infarcts
bilateral and arise from the circle of Willis. The middle are smaller and more sharply marginated than acute
cerebral arteries are the largest arteries supplying the infarcts. There is often parenchymal volume loss and
brain. Small terminal cortical branches supply the corti- there may be areas of cavitation as the lesions become
ces whilst central branches, arising from near the origin chronic (Fig. 5.6.14).36,45 As the integrity of the blood–
of the middle cerebral artery, supply the basal nuclei and brain barrier is restored, there is absence of parenchymal
adjacent tracts. contrast enhancement.2 Secondary changes (atrophy due
• The rostral part of the cerebellum is supplied by the ros- to Wallerian degeneration) may be seen downstream of
tral cerebellar arteries, which usually arise from the cau- the areas of infarction (Fig. 5.6.15).2
dal communicating artery. • Table 5.6.2 summarizes imaging features that may be
• Small arteries arising directly from the basilar artery used to determine the age of infarcted lesions.
provide blood supply to the brainstem, pons, and caudal
cerebellum.42 Small vessel disease (‘lacunar infarcts’)
• All the vessels anastomose with adjacent vessels on the • Small (‘lacunar’) infarcts deep within the brain are more
surface of the brain, providing some collateral circulation. common than large territorial infarcts. They occur due
• The arterial supply to the brain is not uniform, and the to pathology affecting the tissue supplied by the small
gray matter has a larger capillary network than the white perforating arteries of the brain.
matter. • The location of lacunar infarcts is determined by which
• The arterial supply to the brain is different in cats, with of the perforating arteries are involved. Lacunar infarcts
the main supply via the maxillary and pharyngeal arter- are most commonly solitary, but multiple infarcts do
ies. The circle of Willis in cats is incomplete, and the occur and they may also occur in combination with ter-
external carotid artery supplies almost the entire brain, ritorial infarcts.46
except for the caudal brainstem, which is supplied by the • Classically, the term ‘lacunar infarct’ is used for infarcts
vertebral arteries.33,43 arising from small end (terminal) arteries and does not
• Table 5.6.1 summarizes the territories supplied by the include small cortical infarcts, which occasionally occur
individual arteries in dogs. within small cortical end arteries.
(a) (b)
(c) (d)
Fig. 5.6.14 Left cerebral infarct in a Persian cat presenting with sudden-onset right hemiparesis and circling. Dorsal T2W (a, c)
and transverse T2-FLAIR (b, d) images acquired 1 day post onset of signs (a, b) and 15 months later (c, d). The latter images
(c, d) show focal atrophy of the lesion, which is smaller and more sharply defined than initially. The T2-FLAIR image (d) shows
development of low signal areas (arrow, d) consistent with cavitation/cyst formation within the infarcted area. (1T MRI system)
• In dogs, the main perforating arteries are the medial striate arteries on each side. The distribution and num-
striate arteries, which arise from the circle of Willis at ber of lateral striate arteries is more variable.47
the junction of the ethmoidal and middle cerebral artery, • The origin of the perforating arteries is also variable,
and the lateral striate arteries, which arise from the mid- and they may arise from the communicating arteries, the
dle cerebral artery.47 rostral, or the middle cerebral arteries. Some anastomo-
• The number of striate arteries varies, but they are usually ses and small overlap of vascular territories occurs.
symmetric, and there is no association between number • Clinical signs vary depending on which vascular ter-
and the dog’s size. In most dogs, there are two medial ritory is involved.46 Table 5.6.3 describes the territories
268 CHAPTER 5.6
(a) (b)
Fig. 5.6.15 Chronic ischemic right frontal and thalamic infarcts plus right-sided atrophy in a 12-year-old Labrador Retriever.
Transverse T2W images at the level of the thalamus (a) and cerebellum (b) show reduced volume of the right thalamus (solid
arrows, a) and right pyramidal tract (dotted arrow, b) presumed due to Wallerian degeneration secondary to the ischemic
infarcts more rostrally. (1T MRI system)
Table 5.6.2 Imaging features and age of ischemic arterial infarcts.
MASS eFFeCt ContRASt enHAnCeMent ADC VALUeS

Peracute None None, early arterial, parenchymal enhancement uncommon Decreased
Acute Variable None, vascular enhancement or parenchymal (~50%) Decreased
Subacute Variable Gyral or parenchymal enhancement common Normal (pseudo-normalization)
Chronic None or reduced volume None Elevated
Table 5.6.3 Vascular territories of main perforating arteries.
BLooD VeSSeL VASCULAR teRRitoRY

Rostral choroidal artery Choroid plexus of the lateral ventricles, caudal crus of the internal capsule,
caudal caudate nucleus, optic tract, putamen, globus pallidus
Medial striate arteries/lenticulostriate arteries Basal nuclei (globus pallidus, putamen, part of the head of the caudate
nucleus) and medial part of the internal capsule
Lateral striate arteries/lenticulostriate arteries Claustrum, external capsule, insula, lateral part of the internal capsule, and
dorsal part of the caudate nucleus
Proximal perforating artery arising from the caudal communicating Rostromedial aspect of the thalamus
artery
Distal perforating artery arising from the caudal communicating artery Caudolateral aspect of the thalamus and subthalamus
Caudal perforating artery arising from the basilar bifurcation and Median and paramedian aspect of the caudal thalamus, rostral pons, and
paramedian branches arising from the proximal portion of the caudal midbrain
cerebral artery
supplied by the main perforating arteries. Four ‘lacunar • As lacunar infarcts may occur due to intrinsic small
syndromes’ have been described in dogs, based on the vessel disease, there may also be other MRI changes
topographical location of the infarcts:35,46 suggestive of vascular pathology (e.g., cerebral micro-
• Striate arteries: ipsilateral circling, head and neck bleeds, white matter hyperintensities) (Fig. 5.6.16).48
turn, contralateral menace deficit with normal pupil- Microbleeds are small foci of hemosiderin-containing
lary light reflex, contralateral postural reaction macrophages in normal brain parenchyma, which are
deficit, contralateral hemiparesis/ataxia.35,46 remnants of previous hemorrhage; these lesions appear
• Paramedial lesions: signs of vestibular dysfunction. as round, hypointense foci measuring ≤4 mm on T2*W
• Extensive dorsal lesion: vestibular ataxia, circling, and gradient recalled echo images, iso- or hypointense on
contralateral menace response deficit. T2W images, are not visible on T1W images, and do not
• Ventrolateral lesions: circling and contralateral pro- contrast-enhance (see Chapter 5.7).49
prioceptive deficits.
(a) (b)
Fig. 5.6.16 Acute cerebellar infarct (a), presumed age-

related white matter hyperintensities (b), and cerebral
microbleed (c) in a 14-year-old mixed breed dog. Dorsal T2W
(a), transverse T2-FLAIR (b), and T2*W gradient echo (c)
images show a small ischemic infarct in the cerebellar vermis
(solid arrow, a) and bilaterally symmetric white matter T2
hyperintensity, which is most severe caudally and best seen
on the T2-FLAIR image (dotted arrows, b). White matter
hyperintensities are not uncommon in old dogs and are
an apparently incidental finding, but can also occur with
other pathologies (e.g., hypertension) (in this case blood
pressure was normal). The T2*W image (c) shows a cerebral
microbleed (open arrow) indicating intrinsic small vessel
disease. It is not uncommon with ischemic brain disease for
(c)
multiple pathologies to be present. (1T MRI system)
270 CHAPTER 5.6
• In people, most lacunar infarcts are clinically silent but • Located within territory of small vessels (thalamus,
increase the risk of dementia and cognitive dysfunction.14 basal ganglia, internal capsule, brainstem).
It is not uncommon in dogs also to see chronic lacunar • Mass effect usually absent or mild (Fig. 5.6.17).
infarcts with no history of stroke. • Hyperintense on T2W images.
• The MRI features of lacunar infarcts include:35,46,50 • Commonly solitary but may be multiple (Fig. 5.6.18).46
• Small focal lesions that are irregular or angular in Multiple infarcts in differing vascular territories are
shape (Fig. 5.6.17). suggestive of an embolic cause.
(a) (b)
(c) (d)
Fig. 5.6.17 Acute lacunar infarcts in three different dogs. In dog 1 (a), the transverse T2-FLAIR image shows an infarct
within the territory of the right striate arteries (solid arrow). In dog 2 (b, c), transverse and dorsal T2W images show an infarct
within the territories of the perforating arteries (dotted arrows). In dog 3 (d), there is an infarct also in the territories of the
perforating arteries (open arrow). Acute lacunar infarcts have variable shapes. Often on one imaging plane lacunar infarcts
have an angular appearance and are relatively sharply marginated with minimal or no mass effect. Note the difference in shape
of the infarct on the transverse (b) and dorsal (c) images in dog 2. Small lacunar infarcts adjacent to the lateral ventricles are
often best seen on dorsal plane T2W images. Clinical history, CSF analysis, and DWI may be required to differentiate some
lacunar infarcts from inflammatory disease. The distribution of lacunar infarcts depends on which arteries are involved. It is
not uncommon for there to be multiple lacunar infarcts in different vascular territories, in contrast to large territorial infarcts,
which are usually solitary.
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• Usually contrast enhancement is absent or mild. • In chronic stages, cavitation and loss of volume are
• DWI pulse sequences may show restricted diffusion common (Fig. 5.6.19).
in the early stages, but due to small size lesions may • Hemorrhagic transformation is uncommon.
not be visible.
(a) (b)
Fig. 5.6.18 Multiple lacunar infarcts and left territorial cerebellar infarct in a 12-year-old Dalmatian. Transverse (a) and dorsal
(b) T2W images show small lacunar infarcts within the left caudate nucleus (solid arrow) and right thalamus (dotted arrow)
in addition to the large cerebellar infarct (open arrow). Multiple infarcts in differing vascular territories are suggestive of an
embolic cause. (1T MRI system)
(a) (b)
Fig. 5.6.19 Lacunar infarct in a 3-year-old Cavalier King Charles Spaniel. Transverse T2W (a, b) and T1W post-contrast
(c) images obtained 24 hours post onset of signs (a) and 2 years later (b, c). On the latter images (b, c), the lesion is smaller
with sharper margination, and appears as a fluid signal (dotted arrow, b) on the T2W image (b) with no enhancement (dotted
arrow, c) on the T1W post-contrast image (c). (1T MRI system) (Continued)
272 CHAPTER 5.6
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Table 5.6.4 Differential diagnoses for lesions appearing

bright on DWI imaging.52,53
Artifactual
• ‘T2 shine-through’
Lesions containing viscous/proteinaceous fluid
• Early abscessation
Cytotoxic edema
• Infarction/ischemia
• Post-ictal edema
• Some metabolic diseases and toxicoses
• Hypertensive encephalopathy
• Viral encephalitis
• Leukodystrophies
• Encephalitis
Densely cellular masses
• Lymphoma
• Some gliomas
(c) • Granulomas
– Differences on DWI images with gliomas being
Differential diagnoses for more often bright on ADC maps while infarcts are
arterial infarcts more often dark.28
• In general, agreement between radiologists for classify- – Wedge-shaped lesions are more commonly seen
ing pathology on MRI is only moderate to substantial with infarcts.
(0.56 < Kappa < 0.69).51 Substantial discordancy between • Seizure-induced (‘post-ictal’) changes seen on MRI
MRI diagnoses and confirmed diagnoses is reported in are reported in dogs,54 but are often bilateral with
small animal MRI.51 Since brain biopsy is rarely available a predilection for the piriform lobes, hippocam-
in animals, follow-up MRI may be required to differenti- pus, cingulum, and frontal cortex. As seizures
ate some infarcts from other diseases. are uncommon in small animals presenting with
• While many infarcts have a characteristic appearance on infarcts,35 the history may be helpful in differenti-
MRI, significant error rates in diagnosis are reported in ation. In addition, with post-ictal changes there is
dogs.28 hyperperfusion of the affected region,55 in contrast
• As ischemic infarcts primarily result in cytotoxic edema, to acute infarcts, which are underperfused; PWI
other disease processes that also cause cytotoxic edema series may be helpful in highlighting these perfusion
may resemble infarcts. On DWI, restricted diffusion differences (Fig. 5.6.21).
due to cytotoxic edema appears similar irrespective • Some metabolic disorders have a gray matter distribu-
of the cause. There are also other potential causes of tion with no mass effect, and may also mimic infarc-
DWI abnormalities that can mimic acute ischemia, as tion.56,57 Metabolic diseases typically have a bilateral
described in Table 5.6.4. distribution and often involve multiple areas of the
• A number of conditions may share imaging features with brain, which differentiates metabolic disease from
infarction: most infarcts.
• One study comparing infarcts and gliomas showed • Inflammatory diseases can also resemble vascular
that with some observers, infarcts could be mistaken disease with gray matter involvement and minimal
for gliomas in up to 47% of cases and gliomas for mass effect.58
infarcts in up to 12% of cases (Fig. 5.6.20).28 Features
that may help differentiate infarcts from gliomas TRANSIENT ISCHEMIC ATTACKS
include (see Table 5.6.5):28
– Lesion location (gliomas are not confined to vas- • Transient ischemic attacks (TIAs) are brief episodes
cular territories). of neurologic dysfunction resulting from focal cere-
– Size (gliomas tend to be larger). bral ischemia not associated with permanent cerebral
– Mass effect (more pronounced with gliomas). infarction.59
– Perilesional edema (more pronounced with • Suspected TIAs have been reported in dogs, preceding
gliomas). the development of infarction.36 Historically, part of the
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Fig. 5.6.20 Acute ischemic infarct in a 10-year-old Cavalier

King Charles Spaniel (a) and glioma in a 10-year-old Boxer
(b, c, same location 3 weeks apart). These transverse T2W
images show that occasionally large ischemic infarcts (a) can
resemble glial cell tumors (b). There is a greater mass effect
associated with the infarct in this case (a). In the Boxer dog,
repeat MRI (c) 3 weeks later shows increased size of the
mass compared with the initial MRI (b), which supports a
diagnosis of neoplasia. (1T MRI system)
(a)
Table 5.6.5 Common differential diagnoses for ischemic

arterial infarcts.
DiFFeRentiAL DiSCRiMinAtinG FeAtUReS

(b) Glioma May see enhancement with significant mass effect
Mass effect usually more severe than with infarct
Lesions not confined to vascular territories
Lesions are hyperintense on ADC maps while infarcts
tend to be hypointense
Post-ictal Distribution of lesions (hippocampus, piriform lobes,
changes cingulum, frontal lobes)
Lesions not confined to vascular territories
History of seizures (uncommon with stroke)
Affected regions are hyperperfused on PWI while
infarcts are hypoperfused
Trauma Lesions not confined to vascular territories
Often changes in the extracranial tissues
Usually known history of trauma
Metabolic Bilaterally symmetric distribution
disease Lesions not confined to vascular territories
Inflammatory Often white matter preferentially affected
disease Lesions not confined to vascular territories
Lesions often multifocal and poorly marginated
Often progressive onset of signs and multifocal
(c) neurolocalization
274 CHAPTER 5.6
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(a) (b)
Fig. 5.6.21 Post-ictal changes in a 12-year-old Cocker

Spaniel. Transverse T2-FLAIR (a), DW (b), and PW
(c) images show bilateral T2 hyperintensity within the
hippocampi (a), with restricted diffusion on the DW image
(arrows, b). The relative CBF map (c) shows increased
perfusion (dotted arrow) within the hippocampi in contrast to
ischemia, where reduced perfusion is expected. Note the DW
(b) and PW (c) images are at slightly different levels so are not
(c)
directly comparable. (1.5T MRI system)
diagnostic criteria of TIAs was based on the duration of GLOBAL BRAIN ISCHEMIA
episodes (<24 hours). Histologic studies have shown the
presence of permanent ischemic injury even with short- • Global brain ischemia may occur if there is a transient
lived episodes of ischemia.60 period of complete ischemia of the whole brain, followed
• Small ischemic infarcts may be seen in people present- by reperfusion.7
ing with short-lived neurologic episodes. The presence • There is usually a history of anesthetic complication
of acute infarcts, even if clinical signs are short lived, is or airway obstruction, but it may also occur following
a high-risk factor for the future development of stroke. apparently normal general anesthesia.7,61
• As conventional MRI has relatively low sensitivity for • The pathophysiology is similar to other causes of brain
very small infarcts, DWI +/− PWI is recommended for ischemia, but as the period of hypoxia is often short,
the diagnosis of a TIA. The diagnosis of TIA requires much of the tissue damage is thought to be due to reper-
demonstration of absence of infarction. As conventional fusion injury. The distribution of lesions reflects the
MRI is expected to be normal in cases of TIA, the diag- general pattern of selective vulnerability of neurons to
nosis is presumptive, largely based on history. TIAs hypoxia.
without infarction in people are considered a low risk for • Global brain ischemia should be included as a cause of
further stroke.60 any peracute non-progressive neurologic dysfunction
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(a) (b)
Fig. 5.6.22 Transverse T2W (a) and T2-FLAIR (b) images in an 8-year-old Maltese who had general anesthesia the day prior
for a dental procedure. The dog was previously healthy but was slow to recover from anesthesia and then developed generalized
tremor with altered mentation; he became stuporous and non-ambulatory tetraplegic. There is increased signal intensity in the
gray matter of both frontoparietal lobes, symmetric but worse on the left. The changes together with the history are consistent
with global brain ischemia. (1.5T MRI system) (Images courtesy of Dr. Matthew Paek, Bush Advanced Veterinary Imaging)
that occurs after anesthesia or post cardiopulmonary • The major cerebral veins are divided into cortical and
resuscitation.61 A delay in the development of neurologic central veins, with the cortical veins further subdivided
deficits is characteristic for this condition.7 Clinical signs into dorsal and ventral cerebral veins (Fig. 5.6.23):
commonly include blindness, compulsive pacing, ataxia, • There are multiple asymmetrical dorsal cerebral
and seizures.61 veins, which drain nearly the entire cerebral cortex
• Reported MRI findings suggestive of global brain isch- and empty into the dorsal sagittal sinus.
emia include (Fig. 5.6.22):7,61 • The ventral cerebral veins drain the temporal lobe
• T2W and T2-FLAIR hyperintensity within the cor- cortex and join the dorsal petrous sinus.
tical gray matter of the parieto-occipital lobes. • The central veins drain into the great cerebral vein,
• T2W and T2-FLAIR hyperintensity within the which joins with the vein of the corpus callosum to
caudate nuclei. form the straight sinus.
• Bilateral distribution, most commonly symmetric but • As in people, anatomic variations are common in the
may be asymmetric. intracranial dural venous sinus system of dogs, and these
• Mild or no involvement of subcortical white matter. variations have been described.62
• Mild diffuse cortical and caudate nucleus contrast • Cerebral veins thrombosis (CVT) is much less com-
enhancement in some cases. monly recognized than arterial thrombosis,63 and is
• Follow-up MRI may show reduced size and severity rarely reported in small animals,64 although this condi-
of lesions but gray matter hyperintensities may persist tion may be underdiagnosed.
permanently.7 • Cerebral venous infarctions in people rarely present with
a ‘stroke syndrome’, and have a very varied clinical pre-
VENOUS INFARCTION AND THROMBOSIS sentation. Headache is the most common symptom, but
venous thrombosis often also results in seizures and non-
• In dogs, the venous drainage of the brain and meninges specific focal or multifocal encephalopathy. Less com-
is via a collection of sinuses that join the paired max- mon presentations include cavernous sinus syndrome
illary, internal jugular, and vertebral veins and also the and subarachnoid hemorrhage.63
ventral internal vertebral venous plexuses.42 The sinuses • There are many underlying causes of cerebral venous
are divided into a dorsal and a ventral set, which freely thrombosis reported in people, often extracranial
intercommunicate.42 (pro-thrombotic conditions), 63 but intracranial causes
276 CHAPTER 5.6
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(a) (b)
Fig. 5.6.23 (a) Transverse, maximal intensity projection (MIP) MRV

image at the level of the confluence of the dorsal sagittal, transverse,
and straight sinuses. The image illustrates dorsal dural venous sinus
anatomy that is consistent with standard canine anatomic reference
texts. The following vessels are labelled: dorsal sagittal sinus (DSS),
transverse sinus (TR), temporal sinus (TE), sigmoid sinus (SI),
and maxillary vein (MV). (b) Sagittal MIP MRV image of the same
dog showing standard normal anatomy of the dorsal sagittal sinus
(DSS), straight sinus (ST, open arrowheads), sigmoid sinus (SI),
transverse sinus (TR), and temporal sinus (TE). (c) Dorsal MIP
MRV image of the same dog showing standard normal anatomy as
viewed dorsally. Dorsal sagittal sinus (DSS), dorsal cerebral veins
(DCV), transverse sinuses (TR), and sigmoid sinuses (SI) are labelled.
(1.5T MRI system) (Reproduced, with permission, from Fenn J, Lam
R, Kenny PJ (2013). Variations in magnetic resonance venographic
anatomy of the dorsal dural venous sinus system in 51 dogs. Vet Radiol
(c)
Ultrasound 54(4):373–80.)
or extension of pathology from adjacent structures • The diagnosis of CVT is based on demonstrating the
(e.g., sinuses) are possible.65,66 presence of thrombi within the cerebral veins/sinuses,
• In dogs, pathology involving the cerebral venous sinuses and often requires the use of venography (e.g., magnetic
is rarely reported.64 Most cases present as cavernous resonance venography [MRV]).
sinus syndrome,66–69 with the most common underlying • The typical MRI features of CVT thrombosis include
cause being neoplasia involving that sinus. The imaging abnormal signal within a sinus and corresponding
features in these cases are primarily those of a CNS or absence of flow on MRV:63
extracranial mass lesion, rather than a primary vascular • In people, the normal dural sinuses are isointense on
disease.66–69 Vascular malformations are also reported.70 T1W, hypointense on T2W and T2-FLAIR images,
• Thrombosis of the sinuses (e.g., secondary to masses and of high signal on T2*W gradient echo images.
or surgery) may be well tolerated in small animals due • In cases of acute thrombosis, signal may be unchanged
to collateral flow. In dogs, acute occlusion of the sagit- on T1W and T2-FLAIR images, but becomes low on
tal, transverse, and dorsal sagittal sinuses appears to be T2*W images due to the presence of deoxyhemoglo-
generally well tolerated with minimal adverse effects.71 bin.65 SWI is also useful in demonstrating the pres-
However, experimental studies in cats have shown altera- ence of thrombi in the acute stage.73
tions in rCBF and venous infarction with occlusion of • In the subacute stage, with the conversion of deoxy-
the dorsal sagittal sinus.72 hemoglobin to methemoglobin during the 2nd week,
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thrombi become hyperintense on all sequences • DWI images show increased signal on ADC maps
including T2*W gradient echo. indicative of increased diffusion due to vasogenic
• The appearance of chronic clots is variable, depend- edema.
ing on the degree of organization of the clot. It is
typically isointense on T1W images, iso- to hyper- VASCULAR ANOMALIES
intense on T2W images, and hypointense on T2*W
images.65 • Primary vascular anomalies involving the brain are most
• Parenchymal MRI findings of cerebral venous infarc- commonly congenital, although they may not present
tion are not reported in small animals, and are variable clinically until much later in life.
in people, including:65 • Acquired vascular disease commonly occurs with many
• Vasogenic edema, which can be accompanied by cyto- pathologies (e.g., neoplasia, trauma, ischemia), and the
toxic edema. clinical and imaging findings primarily reflect the under-
• Cortical/subcortical location not following arterial lying disease rather than alterations in the appearance or
vascular territories. number of the vessels involved.
• Hemorrhage in 30%–50% of cases, often in subcorti- • Vascular anomalies involving the brain and meninges
cal zones, with a multinodular appearance. include:77,78
• Variable mass effect. • Absence or hypoplasia of normal vessels.
• Variable DWI abnormalities. • Persistent transient embryonic vessels.
• Thalamic edema (uni- or bilateral) in cases of throm- • Vessels with abnormal morphology.
bosis of the deep cerebral veins. • Arteriovenous malformations.
• Dural arteriovenous fistulas.
HYPERTENSIVE ENCEPHALOPATHY • Aneurysms.
• Cavernous malformation.
• Neurologic dysfunction secondary to systemic hyper- • Capillary telangiectasis (unreported in small
tension is known as ‘hypertensive encephalopathy’, and animals).
the diagnosis is based on documenting hypertension and • Variations in vessel number and morphology occur in
resolution of the neurologic signs following control of small animals but are not reported to be clinically signif-
the hypertension.74 icant.79 If vascular abnormalities are hemodynamically
• Hypertensive encephalopathy is thought to result in compensated, they may be clinically silent and may be
vasogenic and interstitial edema due to failure of auto- found incidentally on MRI.77
regulation of the cerebral vasculature,74 although it could • In most cases of congenital arteriovenous vascular mal-
also be due to inflammation and ischemia as a result of formation (except capillary telangiectasis) the MRI
hypoperfusion and vasoconstriction.74 changes are associated with secondary brain hemorrhage
• The caudal brain is predisposed due to regional differ- (see Chapter 5.7).
ences in sympathetic innervation of the cerebral blood • A definitive diagnosis and differentiation of the type
vessels.74 The pathology within the affected regions of vascular malformation requires angiography. In
is primarily vasogenic edema, but additional findings people, the detection of arteriovenous malforma-
reflecting vascular disease such as microbleeds may be tions, dural arteriovenous fistulas, and aneurysm is
seen. important as these conditions carry a risk of recur-
• The MRI findings reported with hypertensive encepha- rent intracranial hemorrhage, but may be amenable to
lopathy include (Fig. 5.6.24):74–76 treatment.80
• T2 hyperintensities within the white matter due to • Arteriovenous malformations (AVMs) of the brain are
vasogenic edema. assumed to be developmental in origin, and comprise
• Isointense on T1W images and usually non-con- feeding arteries, draining veins, and a nidus of abnor-
trast-enhancing or, if present, contrast enhancement mal vessels between the two. The vessels of the nidus
is mild. differ histologically from capillaries and function as an
• Lesions preferentially involve the mid-caudal cere- arteriovenous shunt.81 In people, most AVMs are soli-
brum (parietal and occipital lobes), although lesions tary, and if symptomatic, most commonly present as
can be extensive within the cerebrum and involve the spontaneous intraparenchymal hemorrhage and account
frontal regions. for 15% of people presenting with spontaneous bleeds.81
• Caudate nuclei/thalamus are less commonly affected. Diagnosis is usually made from intra-arterial digital
• Lesions may be bilaterally symmetric or asymmetric. subtraction angiography to demonstrate the tangle of
• Clear differentiation between white and gray matter dilated arteries and veins without a capillary network.
in affected area. The presence of hemorrhage may mask the underlying
278 CHAPTER 5.6
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(a) (b)
(c) (d)
Fig. 5.6.24 Hypertensive encephalopathy in a cat. Transverse T2W (a), T2-FLAIR (b), ADC map (c), and T1W post-contrast
(d) images of the brain in an 18-year-old cat presented recumbent and stuporous after seizure, with a history of chronic renal
disease and hyperthyroidism with systemic hypertension. Note the clear T2 and T2-FLAIR hyperintensity in the white matter
(a, b), which is also hyperintense on the ADC map (c), indicating increased diffusion due to vasogenic edema. The lesions are
hypointense on the T1W image (d) with no contrast enhancement. (1.5T MRI system) (Images courtesy of Dr. Matthew Paek,
Bush Advanced Veterinary Imaging)
vascular malformation. Indirect MRI features suggestive • Cavernous malformations are closely packed, thin-
of AVMs in people include:81 walled vessels without normal interposed brain paren-
• Flow voids on T1W and T2W images. chyma. They may occur anywhere in the brain but are
• Hemorrhagic foci. most commonly found within the subcortical white mat-
• Perilesional T2 hyperintensity. ter and may be multiple.81 In people, the MRI features
• Lack of a mass effect but localized cerebral distortion. are similar to AVMs, and appear as focal hemorrhages
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without associated edema. Cavernous malformations 16. Garosi L, McConnell JE, Platt SR et al. (2005). Results
classically have a complete rim of hemosiderin.78 of diagnostic investigations and long-term outcome of
• The MRI appearance of confirmed AVMs and other 33 dogs with brain infarction (2000–2004). J Vet Intern Med
19(5):725–31.
vascular anomalies in small animals has not yet been
17. Patterson JS, Rusley MS, Zachary JF (1985). Neurologic
reported. manifestations of cerebrovascular atherosclerosis associated
with primary hypothyroidism in a dog. J Am Vet Med Assoc
186(5):499–503.
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35. Garosi L, McConnell JF, Platt SR et al. (2006). Clinical and 53. Karaarslan E, Arslan A (2008). Diffusion weighted MR
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36. McConnell JF, Garosi L, Platt SR (2005). Magnetic resonance 54. Mellema LM, Koblik PD, Kortz GD et al. (1999). Reversible
imaging findings of presumed cerebellar cerebrovascular magnetic resonance imaging abnormalities in dogs following
accident in twelve dogs. Vet Radiol Ultrasound 46(1):1–10. seizures. Vet Radiol Ultrasound 40(6):588–95.
37. Kent M, Glass EN, Haley AC et al. (2014). Ischemic stroke 55. Cole AJ (2004). Status epilepticus and periictal imaging.
in Greyhounds: 21 cases (2007–2013). J Am Vet Med Assoc Epilepsia 45(Suppl 4):72–7.
245(1):113–7. 56. Penderis J, McConnell JF, Calvin J (2007). Magnetic
38. Kim EY, Na DG, Kim SS et al. (2005). Prediction of resonance imaging features of thiamine deficiency in a cat.
hemorrhagic transformation in acute ischemic stroke: Vet Rec 160(8):270–2.
role of diffusion-weighted imaging and early parenchymal 57. Garosi LS, Dennis R, Platt SR et al. (2003). Thiamine
enhancement. Am J Neuroradiol 26(5):1050–5. deficiency in a dog: clinical, clinicopathologic, and magnetic
39. Karonen JO, Partanen PL, Vanninen RL et al. (2001). resonance imaging findings. J Vet Intern Med 17(5):719–23.
Evolution of MR contrast enhancement patterns during 58. Terzo E, McConnell JF, Shiel RE et al. (2012). Unique
the first week after acute ischemic stroke. Am J Neuroradiol topographic distribution of greyhound nonsuppurative
22(1):103–11. meningoencephalitis. Vet Radiol Ultrasound 53(6):636–42.
40. Xu XQ, Zu QQ, Lu SS et al. (2014). Use of FLAIR imaging 59. Easton JD, Saver JL, Albers GW et al. (2009). Definition and
to identify onset time of cerebral ischemia in a canine model. evaluation of transient ischemic attack: a scientific statement
Am J Neuroradiol 35(2):311–6. for healthcare professionals from the American Heart
41. Kim YW, Kim HJ, Choi SH et al. (2014). Prominent Association/American Stroke Association Stroke Council;
hypointense veins on susceptibility weighted image in the cat Council on Cardiovascular Surgery and Anesthesia; Council
brain with acute infarction: DWI, SWI, and PWI. Acta Radiol on Cardiovascular Radiology and Intervention; Council on
55(8):1008–14. Cardiovascular Nursing; and the Interdisciplinary Council
42. Bezuidenhout A (2013). The heart and arteries. In: Miller’s on Peripheral Vascular Disease. The American Academy
Anatomy of the Dog, 4th edn. (eds. HE Evans, A de Lahunta) of Neurology affirms the value of this statement as an
Elsevier Saunders, St. Louis, pp. 441–76. educational tool for neurologists. Stroke 40(6):2276–93.
43. Gillilan LA (1976). Extra- and intra-cranial blood supply to 60. Sorensen AG, Ay H (2011). Transient ischemic attack:
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44. Negrin A, Gaitero L, Anor S (2009). Presumptive caudal North Am 21(2):303–13, x.
cerebellar artery infarct in a dog: clinical and MRI findings. 61. Panarello GL, Dewey CW, Barone G et al. (2004). Magnetic
J Small Anim Pract 50(11):615–8. resonance imaging of two suspected cases of global brain
45. Major AC, Caine A, Rodriguez SB et al. (2012). Imaging ischemia. J Vet Emerg Crit Care 14(4):269–77.
diagnosis – magnetic resonance imaging findings in a 62. Fenn J, Lam R, Kenny PJ (2013). Variations in magnetic
dog with sequential brain infarction. Vet Radiol Ultrasound resonance venographic anatomy of the dorsal dural venous
53(5):576–80. sinus system in 51 dogs. Vet Radiol Ultrasound 54(4):373–80.
46. Goncalves R, Carrera I, Garosi L et al. (2011). Clinical and 63. Ferro JM, Canhao P (2014). Cerebral venous sinus
topographic magnetic resonance imaging characteristics of thrombosis: update on diagnosis and management. Curr
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47. St-Jacques R, Gorczyca W, Mohr G (1996). Microvascular 64. Swayne DE, Tyler DE, Batker J (1988). Cerebral infarction
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18(2):157–62. 65. Bonneville F (2014). Imaging of cerebral venous thrombosis.
48. Wardlaw JM, Lewis SC, Keir SL et al. (2006). Cerebral Diagn Interv Imaging 95(12):1145–50.
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clinically and radiologically, independently of white matter Bilateral cavernous sinus syndrome in dogs: 6 cases
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49. Fulkerson CV, Young BD, Jackson ND et al. (2012). MRI 67. Theisen SK, Podell M, Schneider T et al. (1996). A
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50. Rossmeisl JH, Jr., Rohleder JJ, Pickett JP et al. (2007). 68. Hernandez-Guerra AM, Del Mar Lopez-Murcia M et al.
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weighted gradient-echo MRI for the diagnosis of cerebral 80. Josephson CB, White PM, Krishan A et al. (2014). Computed
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CHAPTER 5.7
BRAIN HEMORRHAGE
282 J. Fraser McConnell
CONTENTS
Mechanisms of MRI contrast in hemorrhage .........................................................................................................................................................282
Etiology of intracranial hemorrhage.......................................................................................................................................................................285
Various types of intracranial hemorrhage .............................................................................................................................................................288
Focal intraparenchymal hemorrhage ................................................................................................................................................................288
Non-traumatic, non-neoplastic intraparenchymal hemorrhage ...................................................................................................................288
Neoplastic hemorrhage ..............................................................................................................................................................................289
Multifocal intraparenchymal hemorrhage.........................................................................................................................................................289
Multifocal non-traumatic large hemorrhages ..............................................................................................................................................289
Cerebral microbleeds .................................................................................................................................................................................299
Extra-axial hemorrhage ....................................................................................................................................................................................302
Subarachnoid hemorrhage .........................................................................................................................................................................302
Subdural hemorrhage .................................................................................................................................................................................302
Epidural hemorrhage ..................................................................................................................................................................................306
Intraventricular hemorrhage .......................................................................................................................................................................306
Miscellaneous causes of hemorrhage ..............................................................................................................................................................307
References.............................................................................................................................................................................................................307
Historically, computed tomography (CT) was the preferred • With hemorrhage, two main physical mechanisms deter-
modality for the identification of intracranial hemorrhage; mine the MR signal intensity:
however, with the development of gradient echo pulse • Relaxivity effects.
sequences, MRI now has greater sensitivity and accuracy • Susceptibility effects.
for this diagnosis.1 • Both relaxivity and susceptibility effects are the result of
iron within the heme molecule.
MECHANISMS OF MRI CONTRAST • In general, materials can be grouped into four categories
IN HEMORRHAGE (diamagnetic, paramagnetic, superparamagnetic, and
ferromagnetic) based on their behavior when exposed
• An understanding of the underlying mechanisms of to a magnetic field, which is determined by the arrange-
MRI contrast that occur with intracranial hemorrhage ment of electrons in the material (see Chapter 1).
helps with image interpretation. The appearance of brain • Within hemorrhage, the magnetic properties of iron will
hemorrhage on MRI is complex, and varies depending on depend on the state of hemoglobin degradation and oxy-
many factors including:2,3 genation, but also on the integrity of the cell membranes
• Intrinsic factors, such as age of the hemorrhage (which of erythrocytes. Following bleeding, there is a progres-
dictates the relative amounts of various by-products of sive change in the biochemical state of the heme mol-
the degradation of hemoglobin), size and location of ecule and structure of the red blood cell:
bleeding, erythrocyte integrity, recurrent bleeding. • In hyperacute hemorrhage, hemoglobin is oxygenated
• Technical factors such as magnetic field strength, (oxyhemoglobin) and intracellular because the red cell
MRI pulse sequence. membrane is still intact.
• Biological factors such as local pH, arterial versus • Subsequently there is loss of oxygen from the hemo-
venous origin, blood–brain barrier integrity, and globin (deoxyhemoglobin) within intact red cells.
oxygen tension.3
Br a i n H e mor r h age 283
• Over time the iron within the heme becomes oxidized or minimal effects on relaxivity (T1 signal) are seen on
(ferrous Fe2+ to ferric Fe3+), resulting in formation of the image (Table 5.7.1).
methemoglobin, initially intracellular. • Magnetic susceptibility is the temporary induction of a
• With erythrolysis, methemoglobin progressively magnetic field (magnetization), which occurs within a
becomes extracellular. material/tissue when it is placed within a strong mag-
• Extracellular methemoglobin is ultimately converted netic field. Susceptibility effects result in generation of
into ferritin and hemosiderin, and stored within mac- local effective magnetic fields, which can differ between
rophages and glial cells. tissues and can generate image contrast by increasing
• As the magnetic properties of iron vary across these dif- magnetic field inhomogeneity, thereby shortening T2*
ferent stages, contrast and signal intensity will also vary relaxation time. A common example of susceptibility
and allow estimation of the age of hemorrhage based on effect is seen at the boundaries between tissue and air
the MRI appearance. However, many other factors com- or bone: at these interfaces, susceptibility differences can
plicate the interpretation. result in quite marked disturbance of the local magnetic
• Relaxivity of a substance relates to the changes it induces field, resulting in susceptibility artifacts (blooming and
in the relaxation rates of neighboring protons (i.e., its focal image distortion), particularly visible on T2*W
effects on the relaxation times T1 and T2 of protons images. In the case of hemorrhage, local magnetic field
that are in its immediate vicinity). In hemorrhagic distortions induced by the iron result in shortening of
lesions, relaxivity effects are caused by the iron content T2 relaxation and rapid loss of the neighboring protons’
of the heme, and they depend on the degradation form phase coherence. Compartmentalization of iron within
of hemoglobin and biochemical form of the iron within cells is an important factor in causing local heteroge-
the heme, which can either reduce the local magnetic neity in the magnetic field resulting in acceleration of
field (negative magnetic susceptibility, diamagnetism) or spin dephasing. Weak paramagnetic substances, such as
augment it (positive magnetic susceptibility, paramag- methemoglobin, may not cause significant magnetic field
netism and superparamagnetism). This is a function of heterogeneity when non-compartmentalized (e.g., within
the number of unpaired electrons in the outer orbital. In extra-axial or extracellular spaces), and in these cases
most of the degradation states of hemoglobin, the iron has will have minimal susceptibility effects.4 Susceptibility
unpaired electrons in the outer orbital resulting in para- effects increase with increasing magnetic field strength
magnetic or superparamagnetic effects (Table 5.7.1).2,3 and are greater in T2*W gradient echo and susceptibility-
Paramagnetic and superparamagnetic effects accelerate weighted imaging (SWI) than on fast spin echo sequences
both longitudinal and transverse proton relaxation (i.e., (Fig. 5.7.1). While at certain stages of hemorrhage sus-
decrease the T1 and T2 relaxation times), but the effects ceptibility effects on T2*W gradient echo images may be
are most obvious on T1W images where shortening of minimal, lesions are typically non-uniform, containing
the T1 relaxation time results in increased signal (= T1 degradation by-products of different ages. The net result
hyperintensity). In addition, the interaction between is the presence of susceptibility effects within some areas
the outer electrons of the iron within the heme and of the hemorrhage (e.g., subacute hematomas are hyper-
adjacent protons is inversely proportional to the sixth intense centrally and hypointense peripherally). On
power of distance, and therefore decreases very rapidly T2W images, hemorrhage is hypointense in all stages,
with increasing distance. For paramagnetic effects to except the hyperacute and subacute stages. In hyperacute
be seen, water molecules must be in close proximity to hemorrhage where there is oxyhemoglobin and intact
the iron atoms. Although the iron in deoxyhemoglobin cells, hemorrhage appears as fluid (T2 hyperintense). In
and hemosiderin/ferritin is paramagnetic or superpara- subacute stages when there is erythrolysis, there is loss
magnetic,2,3 the molecular configuration of these mol- of compartmentalization of the heme molecule resulting
ecules shields the iron from water molecules so that no in loss of magnetic non-uniformity, and also increased
Table 5.7.1 Magnetic properties of the different forms and by-products of hemoglobin.
FoRM oF HeMoGLoBin MAGnetiC PRoPeRtY t1 SiGnAL

Oxyhemoglobin Diamagnetic Isointense
Deoxyhemoglobin Paramagnetic Isointense
Methemoglobin Paramagnetic Hyperintense
Ferritin Superparamagnetic Isointense to slightly hyperintense
Hemosiderin Superparamagnetic Isointense to slightly hyperintense
284 CHAPTER 5.7
(a) (b)
Fig. 5.7.1 Intra-axial hemorrhagic mass in a 14-year-old Jack Russell Terrier. Transverse T2W (a) and T2*W gradient echo
(b) images showing susceptibility artifact associated with the periphery of the lesion, especially visible on the T2*W image.
Note the greater size and blooming of the hypointense rim (dashed arrow, b) on the T2*W image (b) compared with the T2W
image (a). There is also intraventricular hemorrhage within the dependent aspect of the temporal horns of the lateral ventricles
bilaterally (solid arrows, b) visible on the T2*W image but not the T2W image, illustrating the greater sensitivity of the T2*W
gradient echo sequence for the detection of hemorrhage. (1.5T MRI system)
water content from the lysed cells, both of which cause usually contains areas of signal void (black) plus sus-
increased signal on the T2W images.2 ceptibility artifact. Without the use of T2*W gradient
• Both relaxivity and susceptibility effects occur simulta- echo images, the agreement between veterinary radi-
neously, but relaxivity effects are greatest on T1 relax- ologists for detection of hemorrhage was poor in one
ation, whereas susceptibility effects affect T2 relaxation study,7 highlighting the difficulties of diagnosis when
only. The effects on relaxivity are predominately seen on only routine T1W, T2W, and T2-FLAIR sequences are
T1W images, and susceptibility effects are seen on T2W used. The sensitivity for detection of cerebral hemor-
images, especially T2*W gradient echo or SWI images. rhage increases with magnetic field strength, and as low-
In general, the presence of high signal on pre-contrast field MRI is still widely used in veterinary medicine, it
T1W images within the brain (due to methemoglobin) is likely that hemorrhagic diseases are underdiagnosed.
and/or very low signal on T2W and T2*W gradient echo SWI has been shown in people to be significantly more
images are suggestive of hemorrhage (Fig. 5.7.2). The sensitive in detection of cerebral microbleeds compared
appearance of hemorrhage on T1W images is useful in with T2*W gradient echo images (Fig. 5.7.3),8 and as
differentiating acute (iso-hypointense) from subacute this technology becomes more widely available in veteri-
bleeds (hyperintense). The T2W images allow differen- nary medicine, an increase in diagnosis rates of hemor-
tiation of early subacute (hypointense) from late subacute rhage is expected.
(hyperintense) stages in people,2 but this may not apply • When evaluating images, it is important to consider the
in dogs.5 Overall, it is important to remember that the signal changes seen on T1W, T2W, and T2*W globally
MRI signal depends on the age of the hemorrhage and as opposed to individually, as the specific signal changes
relative amounts and spatial distribution of the various seen on the various pulse sequences can be caused by
by-products of hemoglobin; therefore, different regions other processes. For example, hyperintensity on a T1W
of the hematoma may have different signal characteris- brain images is not 100% specific for hemorrhage and
tics (Table 5.7.2). may be seen with melanin, high protein, flow artifacts, or
• Of the commonly available pulse sequences in vet- paramagnetic effects (e.g., due to manganese) (Table 5.7.3
erinary practice, T2*W gradient echo sequences are and Fig. 5.7.4).3 Similarly, other conditions (e.g., calci-
the most sensitive for visualizing hemorrhage,6 which fication, flow artifacts) can cause signal voids on T2*W
(a) (b)
Fig. 5.7.2 Intra-axial hematoma in a 4-month-old Cocker

Spaniel due to a suspected coagulation disorder. T2W (a),
T1W (b), and T2*W gradient echo (c) images showing
hypointensity (arrows, a and c) on the T2W (a) and T2*W
(c) images and hyperintensity (arrow, b) on the T1W image,
which are typical of brain hemorrhage. The T2*W gradient
echo image shows susceptibility artifact associated with
the lesion, which helps differentiate bleeding from other
causes of T2 hypointensity. The T1 and T2 hyperintensity
centrally within the lesion suggests the hematoma is late-
subacute/chronic (the MRI was performed 6 days after onset
of signs). The complete hypointense hemosiderin rim on the
T2W and T2* gradient echo images is more commonly seen
with benign hematomas than with neoplastic hemorrhage.
(c)
(1.5T MRI system)
images (Fig. 5.7.4), and the presence of susceptibil- ETIOLOGY OF INTRACRANIAL HEMORRHAGE
ity artifact (signal void with geometric distortion and
blooming) is important in differentiating hemorrhage • Intracranial hemorrhage can be classified as primary or
from these other causes (Table 5.7.3).9 secondary based on the underlying etiology.
• The MRI appearance of brain hemorrhage is complex and • Primary causes of hemorrhage are hypertension and
due to a combination of many factors. Several mnemon- ceroid amyloid angiopathy (CAA), resulting in spontane-
ics have been developed to help memorize the main signal ous rupture of small vessels, and these are rare in small
changes on T1W and T2W images as hemorrhage ages. animals.17,18
An example is: ‘I Bleed, I Die, Bleed Die, Bleed Bleed, Die Die’: • Secondary causes include neoplasia, thromboses,
• Hyperacute hemorrhage: T1 Isointense and T2 infectious/parasitic disease, trauma, arteriovenous
Bright. malformations, cerebral cavernous malformations,
• Acute hemorrhage: T1 Isointense and T2 Dark. aneurysms, and coagulopathy.19,20
• Early subacute hemorrhage: T1 Bright and T2 Dark. • Where possible, the underlying cause of the bleed-
• Late subacute hemorrhage: T1 Bright and T2 Bright. ing should be identified, but in some cases, this is not
• Chronic hemorrhage: T1 Dark and T2 Dark. possible.
286
Table 5.7.2 The theoretical signal characteristics of intraparenchymal hemorrhage.3–5,10
intenSitY on APPARent
BioCHeMiCAL FoRM/ tiMe oF intenSitY on t2*W intenSitY on DiFFUSion CoeFFiCient
DiStRiBUtion CLiniCAL StAGe APPeARAnCe intenSitY on t1W intenSitY on t2W GRADient eCHo DWi (ADC) MAPS
Oxyhemoglobin/ Hyperacute Immediate to Hypo- to isointense Hyperintense Markedly hypointense rim Hyperintense Hypointense to intermediate
intracellular few hours but rapidly develops due to rapid conversion of
rim of hypointensity oxyhemoglobin into
due to rapid conversion deoxyhemoglobin
of oxyhemoglobin into (intracellular oxyhemoglobin
deoxyhemoglobin is hyperintense)
Deoxyhemoglobin/ Acute Hours to days Hypo- to isointense Hypointense +/− Markedly hypointense Hypointense Hypointense
intracellular +/− thin hyperintense hyperintense peripheral
periphery (due to early rim (due to edema)
oxidation of
deoxyhemoglobin into
methemoglobin)
Methemoglobin/ Early subacute First few days Hyperintense Hypointense Hypointense Hypointense Hypointense
intracellular
CHAPTER 5.7
Methemoglobin/ Late subacute to Days to Hyperintense Hyperintense Hyperintense center due to Hyperintense Hypointense to intermediate
extracellular early chronic months extracellular methemoglobin
dissolved in water-containing
hematoma cavity.
Hypointense periphery due to
early peripheral accumulation
of ferritin and hemosiderin
Ferritin and Chronic Days to Iso- to hypointense Hyperintense center Hyper- to isointense centrally. Hypointense center Variable – hypo- or
hemosiderin/ indefinitely center. (mostly water). Intensely hypointense rim hyperintense center.
extracellular Iso- to slightly Hypointense periphery (ferritin and hemosiderin) Possible hypointense
hyperintense periphery periphery due to
‘T2-blackout’ susceptibility
artifact
Br a i n H e mor r h ag e 287
(a) (b)
(c) (d)
Fig. 5.7.3 Cerebral microbleeds in a 13-year-old Border Collie dog presented with seizure-like episodes. Transverse T2*W
gradient echo (a, b) and SWI (c, d) images showing small signal voids at the gray–white matter junction and right caudate
nucleus, which represent hemosiderin deposits (dotted arrows, a and b; solid arrows, c and d). Note the increased number and
conspicuity of the lesions (solid arrows) on the SWI images. (1.5T MRI system)
Table 5.7.3 Potential mimics of intracranial hemorrhage.
t1 HYPeRintenSitY11,12 t2 HYPointenSitY13
Melanin (e.g., melanoma metastases, melanosis) Gas
Flow artifacts Calcification
Lipid (e.g., dermoid cyst, lipoma) Flow effects – turbulent or rapid flow
Protein effects – macromolecules, protein denaturation Protein effects – high protein levels
(e.g., colloid cysts, Rathke’s cleft cyst, epidermoid, laminar cortical necrosis) High cellularity (e.g., lymphoma)
Manganese/iron/gadolinium/copper deposition Iron or copper deposition
Calcification Secretory granules in pituitary adenomas15,16
Vasopressin within the pituitary gland14
288 CHAPTER 5.7
(a) (b)
Fig. 5.7.4 Pneumocephalus secondary to craniotomy in a

dog (a, b) and lacunar infarct in the left caudate nucleus in
an 8-year-old Mastiff (c). In the dog with pneumocephalus,
transverse T2W (a) and T1W (b) images show signal void
within the ventricular system (solid arrows) due to air.
(1T MRI system) In the dog with a lacunar infarct (c), the
faint hyperintensity on the periphery of the infarct (dotted
arrow) seen on this T1W transverse image was not visible
on T2*W gradient echo images, excluding hemorrhage;
it is likely due to the paramagnetic effects of protein
(c)
macromolecules as a result of necrosis. (1T MRI system)
VARIOUS TYPES OF INTRACRANIAL • In dogs, in most cases of spontaneous non-traumatic,

HEMORRHAGE non-neoplastic intraparenchymal hematomas, no under-
lying cause is found.18
Focal intraparenchymal hemorrhage • Where an underlying medical condition is found, coagu-
Non-traumatic, non-neoplastic intraparenchymal lopathy is common, such as secondary to Angiostrongylus
hemorrhage vasorum infection.17,18,21 Presently, this parasitic infection
• A wide range of pathologies resulting in spontaneous non- is mostly endemic in Europe, although it has reportedly
traumatic, non-neoplastic intracranial hemorrhage have spread to Canada (Newfoundland and Labrador prov-
been reported in dogs including vasculitis, hypertension, inces). Where bleeding is due to coagulopathy, it is not
degenerative disease, vascular malformations, hemorrhagic uncommon for other sites of hemorrhage to be present
transformation of ischemic stroke, and coagulopathies. (e.g., cutaneous, sclera, intramuscular).17
• Clinical signs are variable, but acute onset of central and bleeding of different ages within the lesion are sug-
neurologic abnormalities, which may be progressive, is gestive of neoplasia;25 however, presence of a complete
common.17 T2/T2* hypointense hemosiderin rim can also occur
• For solitary, non-traumatic, non-neoplastic larger hem- with neoplastic hemorrhage.26
orrhages, the prognosis has been reported to be good to • Vasogenic edema is common with both non-neoplastic
excellent in approximately 60% of cases.18 hematomas and hemorrhagic neoplasms, but in people
• Intraparenchymal hematomas should be considered there is a trend for tumors to have more severe perile-
as a differential diagnosis for a focal intraparenchymal sional edema.27 Perilesional edema tends to regress as
lesion when the signal characteristics indicate the pres- non-neoplastic hematomas age, while it does not resolve
ence of hemorrhage (especially susceptibility artifacts, with tumors.
high signal on T1W images, low signal on T2W images). • When a hemorrhagic lesion presents with features sug-
Classically, there are five stages of evolution of cerebral gestive of underlying neoplasia, such as marked contrast
hematoma formation described in people, which are enhancement, repeat MRI may be required to monitor
used to age cerebral bleeds on MRI (Table 5.7.2).3 Similar progression of the lesion (Fig. 5.7.10). This can also be
appearances are reported in dogs, with the exception of useful in cases of masses with a large hemorrhagic com-
the early subacute stage where, in one study, hematomas ponent but no clear evidence of underlying tumor, when
were hyperintense on T2W and T2*W gradient echo the clinical progression suggests underlying ongoing
images.5 The accuracy of MRI for aging intracranial pathology. The persistence of perilesional edema and
hemorrhage in small animals is unknown, but in people failure to follow the expected evolution of a pure hema-
is known to be unreliable.22,23 toma are suggestive of neoplasia.
• The MRI features of non-traumatic, non-neoplastic • MRI features which, in people, have been reported to be
intraparenchymal hemorrhage include:3,20 suggestive of hemorrhagic neoplasia include:3,25,27
• Mass lesion, often rounded/globular in shape. • Irregular or incomplete hemosiderin rim
• Larger hematomas may appear cystic with a sediment– (T2/T2* hypointense).
fluid line. • Non-hemorrhagic neoplastic tissue (Fig. 5.7.11).
• Signal intensity varies with stage (Table 5.7.2), but • Marked signal heterogeneity and generally more
presence of T1 hyperintensity and T2 hypointensity complex compared with benign hematomas
is suggestive of hemorrhage (Fig. 5.7.2). (Fig. 5.7.9).
• Susceptibility artifact seen on T2*W gradient echo • Delayed evolution of the hematoma (may require
and SWI images. serial imaging or evidence of discordancy between
• Variable perilesional edema (Fig. 5.7.5), which apparent age of the bleed on MRI and the clinical
decreases with time and is absent in chronic stages picture).
(Fig. 5.7.6). • Persistent perilesional edema.
• Regular markedly hypointense periphery in subacute • Central or eccentric, rather than peripheral, distribu-
and chronic stages on T2*W images (Fig. 5.7.2). tion of the methemoglobin-induced T1 hyperinten-
• Usually absence of contrast enhancement in the acute sity.26
stage, but thin rim of enhancement may be seen in the • Irregular or nodular contrast enhancement outside
subacute stage; enhancement at the acute stage is not the areas of hemorrhage or focal enhancement within
typical, but occasionally seen (Figs. 5.7.7, 5.7.8). the hematoma.
• In people with primary intraparenchymal hemor- • Clear contrast enhancement within a clinically acute
rhages, additional lesions (small infarcts, white matter hematoma (Fig. 5.7.11).
hyperintensity, microbleeds) indicating small vessel
disease or hypertension are commonly visible.24 Multifocal intraparenchymal hemorrhage
• Multifocal hemorrhages are divided into two main types:
Neoplastic hemorrhage cerebral microbleeds (see below) and larger multifocal
• Although there are no published data to support this hemorrhagic masses.
observation, neoplasia is probably the most common • The distinction is based primarily on size, but other fac-
cause of intraparenchymal brain hemorrhage in dogs and tors such as location, mass effect, presence of edema, and
cats. contrast enhancement should also be considered.
• Hemorrhage is commonly seen in tumors, but the MRI
appearance is predominately of a solid mass rather than Multifocal non-traumatic large hemorrhages
a hematoma. Hemorrhagic tumors are often complex • Multifocal non-traumatic large (≥5 mm) hemorrhages
masses with solid, contrast enhancing parts (Fig. 5.7.9). are mainly reported with secondary (metastatic) neopla-
Lack of a distinct, complete T2/T2* hypointense rim sia or coagulopathy, with other causes being rare.
290 CHAPTER 5.7
(a) (b)
(c) (d)
Fig. 5.7.5 Acute/subacute hematoma secondary to

hypertension due to an adrenal pheochromocytoma in
a 10-year-old Coton de Tulear. Transverse T2W (a),
T2-FLAIR (b), T2*W gradient echo (c), T1W
pre-contrast (d), and T1W post-contrast (e) images
showing a large solitary intra-axial mass with signal
characteristics of hemorrhage. There is extensive
perilesional edema (arrows, a and b) and the mass appears
complex, which makes differentiation between benign
and neoplastic hemorrhage difficult, particularly when
there is an already known primary neoplasm (in this
case an adrenal tumor). The T2*W image (c) shows the
mass is predominately hemorrhage and the absent to
minimal contrast enhancement (e) is consistent with a
large benign hemorrhage (confirmed at post-mortem).
(e)
(1.5T MRI system)
(a) (b)
(c) (d)
Fig. 5.7.6 Spontaneous intra-axial hemorrhage in a 13-year-old Yorkshire Terrier presented for peracute onset of seizures,
presumably due to small vessel pathology. Transverse T2W (a), T2-FLAIR (b), T1W pre-contrast (c), and T2*W gradient
echo (d) images acquired 6 days after onset of signs. Transverse T2W (e) and T1W (f) images were obtained 3 months after
the initial study. The initial images (a–d) show a hemorrhagic mass in the right piriform lobe, which has peripheral edema
(arrows, a and b) and signal characteristics consistent with an early subacute hematoma. Follow-up MRI shows the expected
evolution of a benign hemorrhage with resolution of edema, reduced size, and development of signal intensity consistent with a
chronic bleed, with low signal on the T2W (e) and T1W images (f). (1.5T MRI system) (Continued)
292 CHAPTER 5.7
(e) (f)
(a) (b)
Fig. 5.7.7 Multifocal acute intra-axial brain hematomas and left frontal sinus hemorrhage in a 2-year-old English Springer
Spaniel with a coagulation disorder. Transverse T2W (a, b), T1W (c), T1W post-contrast (d), and T2*W gradient echo
(e) images showing hematomas in the left temporal lobe (a, c–e) and right frontal lobe regions (b). Hemorrhage in the left
frontal sinus is also seen in (b) (dotted arrow). It is not uncommon for animals with clotting disorders to show multiple sites
of hemorrhage as in this case. The large amount of perilesional edema (a) and absence of contrast enhancement (d) are only
seen in the early stages of benign hematoma formation. A narrow complete hypointense rim on the T2*W image (solid arrow)
is consistent with a benign etiology. The signal characteristics of the lesion are compatible with a hyperacute–acute lesion.
The MR images were obtained 48 hours after onset of neurologic signs. (1T MRI system)
(c) (d)
(e)
294 CHAPTER 5.7
(a) (b)
(c) (d)
Fig. 5.7.8 Acute intraparenchymal and intraventricular

hemorrhage in a 2-year-old Border Collie with confirmed
hemophilia A. Transverse T2W (a), T1W pre-contrast (b),
T1W post-contrast (c), and T2*W gradient echo (d, e) images
showing a large intra-axial mass with extensive perilesional
edema (dotted arrow, a) within the right frontotemporal lobe.
There is a severe midline shift to the left due to the mass effect
(arrowhead, c). The appearance of the mass is non-specific
on the T2W and T1W images but the T2*W image (d) shows
signal void and susceptibility artifact typical of hemorrhage.
The intraventricular hemorrhage (dotted arrows, e) seen on the
T2*W image was not visible on other sequences. The appearance
of the hematoma is consistent with a peracute hemorrhage.
There is mild peripheral enhancement and central contrast
enhancement within the lesion (solid arrows, c), which is
unusual, as with benign hematomas there is generally absence of
(e) enhancement in the acute stages. (1T MRI system)
(a) (b)
(c) (d)
Fig. 5.7.9 Hemorrhagic pituitary tumor in a 14-year-

old Yorkshire Terrier with pituitary-dependent
hyperadrenocorticism and recent onset of altered
mentation. Sagittal T2W (a), transverse T2W (b), T1W
pre-contrast (c), T1W post-contrast (d), and T2*W
gradient echo (e) images showing a large irregular mass
in the region of the pituitary gland causing compression
of the adjacent parenchyma. The presence of low signal
on the T2W (a, b) and high signal on the pre-contrast
T1W (c) images is suggestive of hemorrhage, which is
confirmed on the T2*W image (e). Note the presence of
contrast-enhancing non-hemorrhagic tissue associated
with the mass (d) and the heterogeneous appearance and
absence of a complete hemosiderin rim (e), which are all
suggestive of an underlying neoplastic cause of bleeding.
Acute bleeding within pituitary masses can occur and is
(e) known as ‘pituitary apoplexy’. (1T MRI system)
296 CHAPTER 5.7
(a) (b)
(c) (d)
Fig. 5.7.10 Small hemorrhagic mass within the subcortical

region of the left cerebrum in a 13-year-old Griffon Bleu de
Gascogne presenting with acute onset of cluster seizures.
There were no neurologic abnormalities within the inter-ictal
period. Transverse T2W (a), T2-FLAIR (b), T2*W gradient
echo (c), T1W pre-contrast (d), and T1W post-contrast (e)
images showing a small mass with extensive perilesional T2
hyperintensity assumed to represent edema. The signal intensity
of the lesion and the T2/T2* peripheral hypointense rim are
consistent with a benign hematoma; however, the presence of
marked enhancement with concurrent edema are features that
are atypical of a benign lesion and are suggestive of underlying
neoplasia. In this case there were no abnormal neurologic signs
in the following 7 months and extensive investigation for an
underlying cause of hemorrhage was normal, with no evidence
of neoplasia, making a primary spontaneous bleed the most
likely etiology. Overlap in imaging features between benign and
malignant hemorrhage is common and in many cases, follow-up
(e) MRI is required to differentiate them. (1T MRI system)
VetBooks.ir
(a) (b)
(c) (d)
Fig. 5.7.11 Intra-axial mass, presumed neoplastic, in a 13-year-old crossbreed dog with acute-onset neurologic signs of 6 days’
duration. Transverse T2W (a), T2*W gradient echo (b), and T1W post-contrast (c, d) images showing a large intra-axial mass
with areas of low signal intensity in the T2*W image (arrow, b) suggestive of hemorrhage. Image (d) was obtained at a level
rostral to (a), (b), and (c) and shows a large enhancing soft tissue component to the mass (d), which together with the subacute
history is incompatible with a benign hematoma. (1T MRI system)
• The prognosis for multifocal hemorrhages secondary to extracranial metastases (e.g., lung, muscle) are usually
coagulopathy (e.g., due to A. vasorum infection) is gener- present in addition to the primary tumor. Hemorrhagic
ally good.18 metastases (from hemangiosarcoma or other neoplasia)
• Where multifocal hemorrhagic lesions are due to neopla- typically show large amounts of perilesional edema for
sia, the most common underlying cause is hemangiosar- the size of the lesion and nodules usually show contrast
coma; these metastases are often very hemorrhagic, and enhancement (Fig. 5.7.12).
298 CHAPTER 5.7
(a) (b)
(c) (d)
Fig. 5.7.12 Metastatic neoplasia within the brain

and muscles in an older American Cocker Spaniel
presenting with acute-onset multifocal neurologic
abnormalities. The coagulation profile was normal
and thoracic radiographs showed a severe nodular
lung pattern. Transverse T2W (a), T2-FLAIR (b),
T2*W gradient echo (c), T1W pre-contrast (d), and
T1W post-contrast (e) images showing multifocal
variably sized nodules within the brain (arrows, a
and b). A large hemorrhagic lesion is seen on the left
side on the T2*W image and a smaller one on the right
side (arrows, c). Enhancing nodules are also present
in the cranial muscles such as the right temporalis
(arrows, e). The presence of extensive edema (a, b) and
enhancement of the nodules (e) is typical of metastatic
(e) neoplasia. (1T MRI system)
Cerebral microbleeds • The MRI and histologic appearance of microbleeds is

• Cerebral microbleeds are common in people, and have similar in dogs and people, most commonly arising from
also been proven to occur in dogs.28 They result from the gray–white matter junction of the cerebral cortices.28
chronic hemorrhage presumed to be due to leakage from • Strict criteria for diagnosis of cerebral microbleeds exist
small blood vessels and are markers of underlying vascu- in people,29,30 and include:
lar pathology. The MRI changes associated with these • Small round/ovoid signal void with associated bloom-
are caused by small foci of hemosiderin within macro- ing on T2*W gradient echo images (Fig. 5.7.13).
phages, within an otherwise normal brain. • Well-defined lesions.
(a) (b)
(c) (d)
Fig. 5.7.13 Cerebral microbleeds and white matter T2 hyperintensity in a 14-year-old Lurcher dog with chronic systemic
hypertension due to renal disease and pheochromocytoma. Transverse T2W (a), T1W post-contrast (b), T2*W gradient echo (c),
and T2-FLAIR (d) images show small focal bleeds on the T2*W image (c) within the left caudate nucleus, cingulum, and right
temporal lobe (arrows, c). Microbleeds are often only visible on T2*W gradient echo or SW images. Note the signal void and
blooming of the bleed in the left caudate nucleus on the T2*W image compared with the T2W image on which it is barely
visible (dotted arrow, a). The absence of enhancement (b) and perilesional edema, the shape, size, and signal intensity are all
characteristic of microbleeds. The bilaterally symmetric white matter hyperintensity in the caudal periventricular regions on the
T2-FLAIR image (arrows, d) is not uncommon in elderly dogs; it can also occur in association with hypertension and should not
be mistaken for perilesional edema. (1T MRI system)
300 CHAPTER 5.7
• Homogeneously hypointense on T2*W gradient echo intraparenchymal hemorrhage. As mentioned above,

images or SWI. metastatic tumors are easily differentiated from micro-
• Absence of T1 and T2 hyperintensity. bleeds by the presence of peripheral vasogenic edema and
• At least half of the lesion is surrounded by brain contrast enhancement of the lesions.
parenchyma. • The sensitivity of MRI for the detection of small spon-
• Absence of concurrent macrobleeds (>5–10 mm), spe- taneous intraparenchymal hemorrhages is highly depen-
cific causes of bleeding (e.g., coagulopathy, trauma) dent on the magnetic field strength and pulse sequences
(Fig. 5.7.14), and non-hemorrhagic causes of signal used. In people, at higher field strengths and using pulse
void (e.g., vessels) (Fig. 5.7.15). sequences sensitive to susceptibility artifacts (SWI), the
• In dogs, most microbleeds are multiple, and the main dif- commonest cause of intraparenchymal hemorrhage is
ferential diagnosis is metastasis from hemangiosarcoma, cerebral microbleeds, with a prevalence of up to 35% in
which is one of the most common causes of multifocal the general elderly population.9,31
(a) (b)
(c) (d)
Fig. 5.7.14 Traumatic brain injury in a 2-year-old Weimaraner following being hit by a car. Transverse T2W (a), T2-FLAIR (b),
and T2*W gradient echo (c at same level as a and b; d at a different location) images showing multifocal small sized bleeds.
The lesions (solid arrows, c) resemble cerebral microbleeds, but the presence of perilesional edema (dotted arrows on the
T2-FLAIR image, b) is atypical for microbleeds. In addition, diagnosis of cerebral microbleeds requires exclusion of other
causes of multifocal brain hemorrhage, which in this case are likely due to trauma. (1T MRI system)
• In people, the two main causes of cerebral microbleeds with other pathologies caused by hypertension (e.g.,
are hypertensive vasculopathy and CAA: lacunar infarcts, white matter lesions) (Fig. 5.7.13).31
• The distribution of microbleeds within the brain In people, higher numbers of microbleeds are a pre-
differs between the two, with lesions in the basal dictor of future hemorrhagic stroke in patients sur-
ganglia, thalamus, brainstem, and cerebellum asso- viving intracranial hemorrhage. The presence of
ciated with hypertensive vasculopathy and a lobar microbleeds has also been shown to increase the risk
(especially caudal) distribution consistent with CAA. of future ischemic stroke, and may be considered a
• In people, while cerebral microbleeds are common precursor of symptomatic intracranial hemorrhage.
and increase in prevalence with age, hypertension is • In dogs, both hypertension and CAA can be found:
the most consistent predictor of their development, • Although microbleeds have been rarely reported,
with positive odds ratios of ~2–4. The prevalence a high prevalence (5/12 dogs) of hypertension was
of microbleeds is also, not surprisingly, associated reported in one study and was associated with a poor
(a) (b)
(c) (d)
Fig. 5.7.15 Cerebral microbleed in the cingulum of a 13-year-old Border Collie presented for acute-onset seizures due to
spontaneous benign hematoma in another part of the brain (not shown), secondary to systemic hypertension. Transverse T2*W
gradient echo (a, c) and T2W (b, d) images showing a cerebral microbleed at the gray–white matter junction (a, b). The lesion (solid
arrows, a and b) is round, homogeneous, and completely surrounded by brain tissue. The cross-sections of the rostral cerebral
arteries also appear as clearly defined round hypointensities (dotted arrows, c and d) on the transverse T2W image (c) and T2*W
gradient echo image (d), and could be mistaken for cerebral microbleeds, but are not surrounded by brain tissue and do not show
focal image distortion and blooming due to susceptibility artifact, as would be the case with a microbleed (a). (1.5T MRI system)
302 CHAPTER 5.7
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outcome compared with dogs with microbleeds where barrier.2 It can be difficult in some cases to differenti-
no underlying cause was found.18 ate extra-axial hemorrhages from other fluid collections,
• Pathologic studies in dogs have shown changes within as many conditions result in T2-FLAIR hyperintensity,
cerebral blood vessels to be common in aged animals, and susceptibility effects on T2*W gradient echo may be
usually involving small diameter veins with adventi- difficult to visualize (e.g., small lesions adjacent to bone
tial thickening. or sinuses) or may be absent (Fig. 5.7.16).
• In one necropsy-based study of apparently normal old
dogs, microhemorrhages were present in 25% of dogs. Subarachnoid hemorrhage
In the same study, cerebrovascular amyloidosis was • Subarachnoid hemorrhage occurs as the result of bleed-
detected in 65% of dogs but this was not associated ing into the CSF spaces from surface vessels on the pia or
with hemorrhage or vascular degeneration or reac- arachnoidal meninges.2 Rupture of aneurysms and head
tion. Amyloid deposits were found most commonly trauma are the most common underlying etiologies of
in the frontotemporal parts of the cerebral cortex, subarachnoid hemorrhages in people.3,35
with sparing of the basal nuclei and brainstem.32 In • In people, the distribution of the subarachnoid hemor-
a larger canine pathology based study, CAA was also rhage can be suggestive of the underlying etiology,36 but
commonly present (81%) with amyloid deposits seen no such association has been shown in small animals.
around capillaries and the tunica media of arterioles, • Subarachnoid hemorrhage is toxic to the brain, resulting
with a similar frontotemporal cortical distribution.33 in release of inflammatory mediators, which cause vaso-
• There are no studies in dogs comparing distribution spasm, edema, and additional neurologic injuries.37
of microbleeds and association with CAA, but given • The MRI changes associated with subarachnoid hemor-
similarities in amyloid distribution between people rhage include:
and dogs, a similar association seems likely. • Focal or diffuse hemorrhage confined to the suba-
rachnoid space within the basal cisternae and/or adja-
Extra-axial hemorrhage cent to the cerebral hemispheres (Fig. 5.7.16).
• Extra-axial hemorrhages include subarachnoid, subdu- • Serpentine or linear in shape.
ral, epidural, and intraventricular hemorrhages. • Follows adjacent sulci, resulting in displacement
• They are uncommon in small animals and occur much of cortical gray matter away from adjacent bone
less frequently than intraparenchymal bleeding.18 Most (Fig. 5.7.16).38
cases result from hemostatic disorders or severe trauma • Variable mass effect depending on the size of the
(e.g., road traffic accidents). Small hemorrhages are easily hemorrhage.
overlooked on MRI, and T2-FLAIR and T2*W gradient • Variable signal intensity dependent on age of bleed,
echo images should be obtained. but T1 hyperintensity, T2 hypointensity, or T2* gra-
• In people, classification of the anatomic location of extra- dient echo hypointensity +/- susceptibility artifact is
axial hemorrhages is helpful in predicting the underlying suggestive.
cause. However, in small animals, no association between • In chronic cases, superficial siderosis (subpial accu-
anatomic location of hemorrhage and etiology has been mulation of hemosiderin) is reported in people and
reported. appears as linear T2/T2* gradient echo hypointensity
• The appearance of extra-axial hemorrhage is variable, following the cortex and, in later stages, cyst forma-
being dependent on the time of imaging from onset of tion and brain atrophy.3,39
bleeding amongst other factors. Accurate determination
of age of bleed is even less reliable than with intrapa- Subdural hemorrhage
renchymal hemorrhage.34 In the first four stages (hyper- • Subdural hemorrhages occur within the space between
acute to chronic) of hemorrhage the signal progression the dura and arachnoid, usually due to venous bleeding.40
is the same as for intraparenchymal bleeding. However, • Few cases have been reported in dogs41–46 and the condi-
due to higher oxygen tension in the vascularized dura or tion is unreported in cats. Reported causes in dogs include
CSF the progression between stages is slower, especially external trauma,43,47 overshunting by ventriculoperito-
for subarachnoid and intraventricular hemorrhage, than neal shunts,48 and suspected tearing of blood vessels sec-
for intraparenchymal hemorrhage.2 The appearance of ondary to brain atrophy due to ceroid lipofuscinosis.42
very chronic hemorrhage in the extra-axial spaces dif- • In dogs, reported neurologic signs include tremor, ataxia,
fers from intraparenchymal bleeds, as there is formation seizures, and mentation changes but as concurrent
of non-paramagnetic hemichromes when methemoglo- pathologies are usually present, it is difficult to attribute
bin undergoes oxidative denaturation, due to the greater clinical signs directly to subdural hemorrhage.
oxygen levels.2 With chronic extra-axial hemorrhages • The MRI appearance of subdural hemorrhage includes:
there is absence of a hemosiderin rim unless there is • Single or multiple crescent-shaped hemorrhages
repeated bleeding, as they are outside the blood–brain superficial to the brain (Fig. 5.7.17).45
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(a) (b)
(c) (d)
Fig. 5.7.16 Acute traumatic brain injury and extra-axial (probable subarachnoid) hemorrhage and small skull fracture in
a 3-year-old Cavalier King Charles Spaniel hit by a car 3 days previously and showing signs of mild ataxia. Dorsal (a) and
transverse T2W (b), T2-FLAIR (c), and T2*W gradient echo (d) images showing a small fracture in the left temporal bone on
the dorsal plane image (solid arrow, a) and linear T2 hyperintensity conforming to the surface of the left cerebrum consistent
with an acute small subarachnoid hemorrhage (dotted arrows, a and c). The fluid accumulation is best seen on the T2-FLAIR
image (c). The presence of corresponding reduced signal within the fluid on the T2*W image (d) is difficult to visualize due to
the small size of the lesion and adjacent bone. (1T MRI system)
304 CHAPTER 5.7
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(b)
(a)
(d)
(c)
Fig. 5.7.17 Subdural hemorrhage in a 14-month-

old mixed breed dog secondary to overshunting by a
ventriculoperitoneal shunt placed to treat hydrocephalus.
Dorsal (a) and transverse T2-W (b), T2-FLAIR (c), T2*W
gradient echo (d), and T1W post-contrast (e) images
showing large bilateral extra-axial fluid accumulations,
which result in abaxial displacement and compression of
the brain. The fluid crosses suture lines (solid arrows, a)
but not the midline, which distinguishes subdural from
epidural hemorrhage. The T2*W gradient echo image (d)
shows low signal in the dependent areas of the subdural
fluid collections, consistent with hemorrhage (dotted
(e)
arrows, d). (1T MRI system)
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• Signal intensity varies with chronicity but the main hemispheres and cerebrum/cerebellum, respectively,
component is usually hyperintense or of mixed signal and block subdural hemorrhage from crossing.2
intensity on T2W images and low signal intensity on • Usually significant mass effect.
T1W images in the chronic stages.3,34 Signal intensity • Repeated bleeding may result in irregular hypointense
in acute and subacute stages is similar to intraparen- membranes separating areas of different chronicity or
chymal hemorrhages. fluid-fluid levels.3
• Subdural hemorrhage may cross the suture lines of the • In chronic cases, meninges may be markedly thickened
cranium (Fig. 5.7.17),40 but does not cross the midline and show diffuse increased contrast enhancement.44,49
or between supra- and infratentorial compartments, • Repeated bleeding may result in low signal periph-
because it is limited by the falx and tentorium, which ery due to hemosiderin deposits, which overwhelm
are dural extensions located between the cerebral normal clearance mechanisms (Fig. 5.7.18).2
(a) (b)
(c) (d)
Fig. 5.7.18 Chronic subdural hemorrhage in a 14-month-old mixed breed dog (same dog as in Fig. 5.7.17) secondary to
overshunting by a ventriculoperitoneal shunt placed to treat hydrocephalus. Transverse T2W (a), T2-FLAIR (b), T2*W
gradient echo (c), and T1W post-contrast (d) images showing multiple irregular membranes within the subdural space.
Note the characteristic crescent shape of the subdural hematomas. (1T MRI system)
306 CHAPTER 5.7
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Epidural hemorrhage • Signal intensity varies with chronicity and is similar

• Epidural hemorrhage occurs within the space between to subdural hematomas.
the inner cortex of the cranium and the dura mater, and • Low signal from the fibrous dura may be visible
is most commonly arterial in origin.40 between the hematoma and surface of the cerebral
• Intracranial epidural hematomas are rare and may occur cortex.2
secondary to trauma or coagulopathy.50 In people, epi-
dural hemorrhage is commonly traumatic in origin and Intraventricular hemorrhage
there are often concurrent skull fractures or other signs • Intraventricular hemorrhage can occur due to bleed-
of trauma. ing from subependymal veins, extension from adjacent
• MRI features of epidural hemorrhage include: parenchyma, or reflux of blood due to subarachnoid
• Most commonly convex or biconvex (‘lenticular’) in hemorrhage through the normal apertures.2
shape (Fig. 5.7.19). • Predisposing causes in people include hypertension,
• Epidural hemorrhage may cross dural folds (e.g., falx) aneurysm, arteriovenous malformation, trauma, and
but does not cross suture lines (Fig. 5.7.19) where the idiopathic causes.51 In most cases, intraventricular
dura is tightly adhered to the overlying calvarium.2 hemorrhage is seen in conjunction with other sites of
(a) (b)
(c) (d)
Fig. 5.7.19 Acute epidural hematoma in a 1-year-old Labrador Retriever secondary to Angiostrongylus vasorum infection.
Sagittal (to the left of midline, a) and transverse T2W (b), T2*W gradient echo (c), and T1W (d) images showing a biconvex
(‘lenticular’) extra-axial fluid accumulation, which does not cross the frontoparietal suture line (arrow, a). Within the
hematoma, there is dependent fluid-fluid level (arrow, b). The presence of peripheral T1 hyperintensity (dotted arrow, d) and
low signal on the T2*W (c) image is consistent with an acute hemorrhage. (1T MRI system)
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hemorrhage, which are often larger or more obvious, and 8. Cheng AL, Batool S, McCreary CR et al. (2013).
small intraventricular hemorrhages are easily overlooked Susceptibility-weighted imaging is more reliable than
and possibly underrecognized. Isolated intraventricu- T2*-weighted gradient-recalled echo MRI for detecting
microbleeds. Stroke 44(10):2782–6.
lar hemorrhage is rare in people,52 where three forms
9. Greenberg SM, Vernooij MW, Cordonnier C et al. (2009).
of intraventricular hemorrhage are described: clot-
Cerebral microbleeds: a guide to detection and interpretation.
ted hematoma, layered hemorrhage, and red blood cell Lancet Neurol 8(2):165–74.
deposits.53 10. Macellari F, Paciaroni M, Agnelli G et al. (2014). Neuroimaging
• The MRI features of intraventricular hemorrhage in intracerebral hemorrhage. Stroke 45(3):903–8.
include: 11. Ginat DT, Meyers SP (2012). Intracranial lesions with high
• Changes often only visible on T2*W gradient echo signal intensity on T1-weighted MR images: differential
images appearing as signal void with susceptibility diagnosis. RadioGraphics 32(2):499–516.
artifact within the gravity-dependent parts of the ven- 12. Cakirer S, Karaarslan E, Arslan A (2003). Spontaneously
T1-hyperintense lesions of the brain on MRI: a pictorial
tricular system (Fig. 5.7.1).
review. Curr Probl Diagn Radiol 32(5):194–217.
• Changes are most common in the lateral ventricles,
13. Zimny A, Neska-Matuszewska M, Bladowska J et al. (2015).
especially in temporal horns and rostrally (Fig. 5.7.1). Intracranial lesions with low signal intensity on T2-weighted
• Changes are often bilateral. MR images – review of pathologies. Pol J Radiol 80:40–50.
• In cases of a large volume of hemorrhage, fluid–fluid 14. Bonneville F, Cattin F, Marsot-Dupuch K et al. (2006). T1
levels may be seen within the CSF. signal hyperintensity in the sellar region: spectrum of findings.
• Large blood clots may appear as solid intraventricular RadioGraphics 26(1):93–113.
masses with similar appearance to intraparenchymal 15. Heck A, Ringstad G, Fougner SL et al. (2012). Intensity
hematomas. of pituitary adenoma on T2-weighted magnetic resonance
imaging predicts the response to octreotide treatment in
• Lack of CSF signal suppression on T2-FLAIR
newly diagnosed acromegaly. Clin Endocrinol 77(1):72–8.
images.2
16. Potorac I, Petrossians P, Daly AF et al. (2015). Pituitary
MRI characteristics in 297 acromegaly patients based on
Miscellaneous causes of hemorrhage T2-weighted sequences. Endocr Relat Cancer 22(2):169–77.
In addition to primary hemorrhagic diseases, microscopic 17. Garosi LS, Platt SR, McConnell JF et al. (2005). Intracranial
hemorrhage is seen with many pathologies (e.g., thiamine haemorrhage associated with Angiostrongylus vasorum infection
deficiency, hypoxia),54 which potentially may be visible on in three dogs. J Small Anim Pract 46(2):93–9.
MRI sequences that are sensitive to hemorrhage (T2*W 18. Lowrie M, De Risio L, Dennis R et al. (2012). Concurrent
gradient echo, SWI), especially at higher field strengths. medical conditions and long-term outcome in dogs with
nontraumatic intracranial hemorrhage. Vet Radiol Ultrasound
Where hemorrhage is a minor component of the pathology,
53(4):381–8.
the appearance of the lesion on MRI will primarily be due
19. Schlunk F, Greenberg SM (2015). The pathophysiology of
to the non-hemorrhagic parts. intracerebral hemorrhage formation and expansion. Transl
Stroke Res 6(4):257–63.
REFERENCES 20. Ciura VA, Romero JM (2014). Nontraumatic acute
1. Kidwell CS, Chalela JA, Saver JL et al. (2004). Comparison of intraparenchymal hemorrhage: algorithm for workup and
MRI and CT for detection of acute intracerebral hemorrhage. differential diagnosis. Semin Roentgenol 49(1):112–26.
JAMA 292(15):1823–30. 21. Wessmann A, Lu D, Lamb CR et al. (2006). Brain and spinal
2. Parizel P, Makkat S, Van Miert E et al. (2001). Intracranial cord haemorrhages associated with Angiostrongylus vasorum
hemorrhage: principles of CT and MRI interpretation. infection in four dogs. Vet Rec 158(25):858–63.
Eur Radiol 11(9):1770–83. 22. Alemany Ripoll M, Stenborg A et al. (2004). Detection and
3. Atlas SW, Thulborn KR (2017). Intracranial hemorrhage. appearance of intraparenchymal haematomas of the brain
In: Magnetic Resonance Imaging of the Brain and Spine, 5th edn. at 1.5 T with spin-echo, FLAIR and GE sequences: poor
(ed. SW Atlas) Wolters Kluwer, Philadelphia, pp. 484–530. relationship to the age of the haematoma. Neuroradiology
4. Whang JS, Kolber M, Powell DK et al. (2015). Diffusion- 46(6):435–43.
weighted signal patterns of intracranial haemorrhage. 23. Zyed A, Hayman LA, Bryan RN (1991). MR imaging of
Clin Radiol 70(8):909–16. intracerebral blood: diversity in the temporal pattern at
5. An D, Park J, Shin JI et al. (2015). Temporal evolution of MRI 0.5 and 1.0 T. Am J Neuroradiol 12(3):469–74.
characteristics in dogs with collagenase-induced intracerebral 24. Offenbacher H, Fazekas F, Schmidt R et al. (1996). MR of
hemorrhage. Comp Med 65(6):517–25. cerebral abnormalities concomitant with primary intracerebral
6. Kuker W, Thiex R, Rohde I et al. (2000). Experimental acute hematomas. Am J Neuroradiol 17(3):573–8.
intracerebral hemorrhage. Value of MR sequences for a safe 25. Atlas SW, Grossman RI, Gomori JM et al. (1987).
diagnosis at 1.5 and 0.5 T. Acta Radiol 41(6):544–52. Hemorrhagic intracranial malignant neoplasms: spin-echo
7. Leclerc MK, d’Anjou MA, Blond L et al. (2013). Interobserver MR imaging. Radiology 164(1):71–7.
agreement and diagnostic accuracy of brain magnetic 26. Destian S, Sze G, Krol G et al. (1989). MR imaging of
resonance imaging in dogs. J Am Vet Med Assoc 242(12): hemorrhagic intracranial neoplasms. Am J Roentgenol
1688–95. 152(1):137–44.
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27. Tung GA, Julius BD, Rogg JM (2003). MRI of intracerebral 42. Asakawa MG, MacKillop E, Olby NJ et al. (2010). Imaging
hematoma: value of vasogenic edema ratio for predicting the diagnosis – Neuronal ceroid lipofuscinosis with a chronic
cause. Neuroradiology 45(6):357–62. subdural hematoma. Vet Radiol Ultrasound 51(2):155–8.
28. Fulkerson CV, Young BD, Jackson ND et al. (2012). MRI 43. Hopkins AL, Wheeler SJ (1991). Subdural hematoma in a dog.
characteristics of cerebral microbleeds in four dogs. Vet Radiol Vet Surg 20(6):413–7.
Ultrasound 53(4):389–93. 44. Kitagawa M, Okada M, Koie H et al. (2008). Magnetic
29. Charidimou A, Krishnan A, Werring DJ et al. (2013). Cerebral resonance imaging and computed tomography appearance
microbleeds: a guide to detection and clinical relevance in of chronic subdural haematoma in a dog. Aust Vet J 86(3):
different disease settings. Neuroradiology 55(6):655–74. 100–1.
30. Greenberg SM, Vernooij MW, Cordonnier C et al. (2009). 45. Nykamp S, Scrivani P, DeLahunta A et al. (2001). Chronic
Cerebral microbleeds: a guide to detection and interpretation. subdural hematomas and hydrocephalus in a dog. Vet Radiol
Lancet Neurol 8(2):165–74. Ultrasound 42(6):511–4.
31. Poels MM, Vernooij MW, Ikram MA et al. (2010). Prevalence 46. Yashon D, Small E, Jane JA (1965). Congenital hydrocephalus
and risk factors of cerebral microbleeds: an update of the and chronic subdural hematoma in a dog. J Am Vet Med Assoc
Rotterdam scan study. Stroke 41(10 Suppl):S103–6. 147(8):832–6.
32. Borras D, Ferrer I, Pumarola M (1999). Age-related changes 47. Yanai H, Tapia-Nieto R, Cherubini GB et al. (2015). Results
in the brain of the dog. Vet Pathol 36(3):202–11. of magnetic resonance imaging performed within 48 hours
33. Sasaki M, Pool R, Summers BA (2003). Vasculitis in a dog after head trauma in dogs and association with outcome: 18
resembling isolated angiitis of the central nervous system in cases (2007–2012). J Am Vet Med Assoc 246(11):1222–9.
humans. Vet Pathol 40(1):95–7. 48. Kitagawa M, Kanayama K, Sakai T (2005). Subdural
34. Sieswerda-Hoogendoorn T, Postema FA, Verbaan D et al. accumulation of fluid in a dog after the insertion of a
(2014). Age determination of subdural hematomas with CT ventriculoperitoneal shunt. Vet Rec 156(7):206–8.
and MRI: a systematic review. Eur J Radiol 83(7):1257–68. 49. Blitshteyn S, Mechtler LL, Bakshi R (2004). Diffuse dural
35. Macdonald RL, Schweizer TA (2017). Spontaneous gadolinium MRI enhancement associated with bilateral
subarachnoid haemorrhage. Lancet 389(10069):655–66. chronic subdural hematomas. Clin Imaging 28(2):90–2.
36. Marder CP, Narla V, Fink JR et al. (2014). Subarachnoid 50. Cabassu J, Cabassu J-P, Brochier L et al. (2008). Surgical
hemorrhage: beyond aneurysms. Am J Roentgenol 202(1):25–37. treatment of a traumatic intracranial epidural haematoma in a
37. Miller BA, Turan N, Chau M et al. (2014). Inflammation, dog. Vet Comp Orthopaed 21(5):457–61.
vasospasm, and brain injury after subarachnoid hemorrhage. 51. Bakshi R, Kamran S, Kinkel PR et al. (1999). MRI in cerebral
BioMed Res Internat 2014:384342. intraventricular hemorrhage: analysis of 50 consecutive cases.
38. Heit JJ, Iv M, Wintermark M (2017). Imaging of intracranial Neuroradiology 41(6):401–9.
hemorrhage. J Stroke 19(1):11–27. 52. Barnaure I, Liberato AC, Gonzalez RG et al. (2017).
39. Kumar N (2010). Neuroimaging in superficial siderosis: an Isolated intraventricular haemorrhage in adults. Br J Radiol
in-depth look. Am J Neuroradiol 31(1):5–14. 90(1069):20160779.
40. Krees B (2008). Trauma. In: Brain Imaging: Direct Diagnosis 53. Hernalsteen D, Dignac A, Oppenheim C et al. (2007).
in Radiology. (eds. K Sartor, S Haehnel, B Kress) Thieme, Hyperacute intraventricular hemorrhage: detection and
Stuttgart, pp. 1–24. characterization, a comparison between 5 MRI sequences.
41. Adamo PF, Crawford JT, Stepien RL (2005). Subdural J Neuroradiol 34(1):42–8.
hematoma of the brainstem in a dog: magnetic resonance 54. Summers BA, Cummings JF, de Lahunta A (1995). Veterinary
findings and treatment. J Am Anim Hosp Assoc 41(6):400–5. Neuropathology. Mosby Year Book, St.Louis.
CHAPTER 5.8
BRAIN TRAUMA
Silke Hecht 309
CONTENTS
Classification of traumatic brain injuries ...............................................................................................................................................................309
CT versus MRI for traumatic brain injuries ............................................................................................................................................................ 310
MRI pulse sequences for the head trauma patient ................................................................................................................................................. 310
Primary traumatic brain injury............................................................................................................................................................................... 310
Extra-axial lesions ........................................................................................................................................................................................... 311
Epidural hematomas .................................................................................................................................................................................. 311
Subdural hematomas ................................................................................................................................................................................ 311
Subarachnoid and ventricular hemorrhage ................................................................................................................................................ 311
Intra-axial lesions ............................................................................................................................................................................................ 312
Intra-axial hematomas ............................................................................................................................................................................... 312
Brain contusions ....................................................................................................................................................................................... 312
Diffuse axonal injury ................................................................................................................................................................................. 313
Vascular lesions .............................................................................................................................................................................................. 313
Secondary traumatic brain injury .......................................................................................................................................................................... 313
Acute secondary injury .................................................................................................................................................................................... 313
Diffuse cerebral swelling ........................................................................................................................................................................... 313
Brain herniation .......................................................................................................................................................................................... 313
Post-traumatic brain ischemia and infarction ............................................................................................................................................ 313
Infection ..................................................................................................................................................................................................... 314
Pneumocephalus ....................................................................................................................................................................................... 314
Chronic secondary injury ................................................................................................................................................................................ 315
MRI prognostic indicators in head trauma............................................................................................................................................................. 315
References............................................................................................................................................................................................................. 315
Traumatic brain injury (TBI) is defined as an injury to the imaging should be considered in patients who fail to respond
intracranial structures following physical trauma to the to aggressive medical management, patients who deteriorate
head. The term head injury is preferred if injuries to other after an initial response to medical therapy, and/or patients
structures such as the scalp and skull are present.1 Head with focal or asymmetric neurologic signs.12
injuries and TBI are common in veterinary patients and
are associated with increased mortality in trauma patients.2 CLASSIFICATION OF TRAUMATIC
Possible etiologies include road traffic accidents, injuries BRAIN INJURIES
caused by other animals (e.g., kicks or bites), falls, and
human inflicted trauma including ballistic and iatrogenic • TBI can be subdivided into primary and secondary
injuries.3–11 Animals at all ages may be affected, and clinical injuries. Primary injury is the direct result of traumatic
and neurologic signs are highly variable dependent on sever- impact. Secondary injury usually begins within minutes
ity of the brain trauma and presence of concurrent injuries. of injury and can last days, weeks, or even longer.1,12,13
Not all patients presented with head trauma will undergo • The possible pathophysiologic sequelae of primary and
advanced imaging of the head/brain. However, cranial secondary brain injury can be categorized as follows:1,10,14
310 CHAPTER 5.8
• Primary injury: • Additional considerations in human head trauma patients

– Extra-axial: epidural hematoma, subdural hema- include:
toma, subarachnoid hemorrhage, intraventricular • Magnetic resonance angiography: recommended to
hemorrhage. evaluate patients for suspected dissection or other
– Intra-axial: parenchymal hematoma/hemorrhage, vascular injury.26
contusion, diffuse axonal injury. • Diffusion-weighted imaging: recommended to eval-
– Vascular (e.g., arteriovenous fistula). uate for trauma-induced infarcts and diffuse axonal
• Secondary injury: injury.26
– Acute: diffuse cerebral swelling, brain hernia- • Susceptibility-weighted imaging: recommended to
tion, ischemia and infarction, infection, (tension) evaluate for diffuse axonal injury.26
pneumocephalus. • Several advanced MR technologies including diffu-
– Chronic: hydrocephalus, ‘hydrocephalus ex vacuo’, sion tensor imaging, functional MRI, magnetization
encephalomalacia, diffuse cortical atrophy. transfer imaging, and magnetic resonance spec-
troscopy have not yet demonstrated clinical utility,
CT VERSUS MRI FOR TRAUMATIC although they may have long-term prognostic value
BRAIN INJURIES in subacute, chronic, and repetitive TBI.19,30–32
• There is general agreement that CT is the modality of PRIMARY TRAUMATIC BRAIN INJURY
choice to evaluate patients with acute head trauma, espe-
cially in moderate and severe cases, as it is quick and highly • The by-products of the progressive degradation of hemo-
accurate in the diagnosis of conditions that may impact globin in hemorrhagic lesions cause changes in signal on
clinical management such as fractures, intracranial hem- T1W and T2W images, the intensity of which depends
orrhage, brain swelling, and brain herniation.1,12,15-20 on the degradation stage (see Chapter 5.7).15,20,33,34
• MRI is indicated in patients with acute TBI when CT • Depending on the location, intracranial hemorrhage
fails to explain the neurologic findings, and is the pre- can be categorized as epidural, subdural, subarachnoid,
ferred imaging modality for subacute and chronic ventricular, or intra-axial (Fig. 5.8.1). With any of these
TBI.1,19–21 types of intracranial hemorrhage, general changes may
• In people, MRI and CT have similar sensitivity in be seen including associated mass effect, concurrent skull
the detection of acute epidural and subdural hemato- fractures, and lesions of overlying soft tissues. Specific
mas.22,23 MRI is superior in the detection of non-hem- MRI morphologic features that can be used to classify
orrhagic lesions, brainstem injuries, and subarachnoid hemorrhage into these different categories are described
hemorrhage.23–25 below.
MRI PULSE SEQUENCES FOR THE

HEAD TRAUMA PATIENT
• In addition to conventional T1W and T2W images,

the following sequences may add valuable information
in the evaluation of patients with head trauma (see also SA
Chapter 4.1):
SD
• T2-FLAIR: improved detection of brain contusions,
white matter shearing/diffuse axonal injuries, and IV
subarachnoid hemorrhage.1,9,24–27
• Gradient recalled echo T2*W: highly sensitive in the ED IP
detection of blood degradation products and espe-
cially useful in the evaluation of patients with sub-
acute and chronic head trauma.1,11,27,28 May also be
helpful in evaluation of bony structures.9
• T1W, PDW, and/or 3D T1W gradient recalled echo
sequences: may be superior to other MR sequences in
the evaluation of bony structures.9,29
• STIR: most helpful in identifying extracranial soft
tissue trauma.9 Fig. 5.8.1 Schematic image illustrating the appearance of
• In general, the combination of T2W and T2-FLAIR intracranial hemorrhage. ED, epidural; IP, intraparenchymal;
series provides the most diagnostic information.9 IV, intraventricular; SA, subarachnoid; SD, subdural.
Br a i n Tr au m a 311
Extra-axial lesions • Lesion may cross suture lines but is limited by the falx
Epidural hematomas and tentorium, which are dural extensions that extend
• Epidural hematomas accumulate in the potential space between cerebral hemispheres and cerebrum/cere-
between the inner surface of the skull and the dura bellum, respectively, and block subdural hemorrhage
mater. from crossing.
• They are typically caused by laceration or tearing of a
meningeal artery by a skull fracture, and are often rap- Subarachnoid and ventricular hemorrhage
idly expanding due to the high pressure in arteries.1,20 • With subarachnoid and ventricular hemorrhage, there
• MRI findings include:1,9,15,16,19,20,27 is bleeding into the CSF-filled subarachnoid space and
• Well-defined biconvex (lenticular) extra-axial mass of ventricular system, respectively.
variable signal intensity dependent on age of hemat- • In addition to rupture of small vessels of the pia mater,
oma. traumatic subarachnoid hemorrhage may result from
• Lesion may cross dural folds such as the falx cerebri extension of a contusion or hematoma, or from transep-
and osseous tentorium cerebelli, but usually does not endymal diffusion of intraventricular hemorrhage.1,20
cross suture lines where the dura is tightly adhered to • MRI findings include:9,25,40
the overlying calvarium. • In acute cases, there may be no abnormal findings
on conventional T1W and T2W images, as acute
Subdural hematomas hemorrhage is isointense to CSF. However, hyperin-
• Subdural hematomas accumulate within the potential tense signal will be noted in the subarachnoid space
space between the pia-arachnoid and the dura mater. on T2-FLAIR images. Ventricular hemorrhage can
• They are usually caused by tearing of veins that traverse cause a gravity-dependent fluid–precipitate level in
the subdural space and are less common in small animals the ventricular lumen.
than in people.1,20 Subdural hematomas may also occur • In subacute or chronic cases, hemoglobin degradation
secondary to reasons other than trauma.35–37 by-products may be visible on conventional spin echo
• MRI findings include (Fig. 5.8.2):1,15,16,19,20,27,38,39 sequences, dependent on the stage of degradation,
• Peripheral crescent-shaped collection of hemor- and appear iso-, mixed, or hypointense to CSF on
rhage of variable signal intensity, which is often very T2-FLAIR. Susceptibility artifacts (signal voids) will
extensive. be noted on T2*W images.
(a) (b)
Fig. 5.8.2 Subdural hematoma in a 3-year-old French Bulldog presented with pain and acute onset of seizures after a fall.
(a) The T2-FLAIR image shows crescent shaped symmetric hyperintensity adjacent to the piriform lobes and extending
dorsally bilaterally (arrowheads). (b) On the T2*W image, a thin peripheral susceptibility artifact demarcates the subdural
lesion from adjacent tissue (arrowheads). (1T MRI system)
312 CHAPTER 5.8
(a) (b)
Fig. 5.8.3 Intraparenchymal hemorrhage and skull fractures in a 5-year-old Fox Terrier after being hit by a car. (a) On the
T2*W image multiple susceptibility artifacts indicative of hemorrhage are associated with the olfactory bulbs bilaterally,
markedly more severe on the left (arrow). Skull fractures and subcutaneous soft tissue swelling are also evident. (b) A post-
contrast 3D T1W gradient recalled echo image obtained at the same level allows improved visualization of skull fractures with
the fractured and displaced fragments forming linear hypointense structures. (1T MRI system)
Intra-axial lesions
Intra-axial hematomas
• Intra-axial hematomas result from shear injury causing
rupture of intraparenchymal blood vessels resulting in
hemorrhage.1
• MRI findings include (Fig. 5.8.3):1,20,41,42
• Intraparenchymal mass of variable size and intensity.
• Perilesional T2W and T2-FLAIR hyperintensity
consistent with edema.
Brain contusions
• Brain contusions are common sequelae to head trauma
and consist of heterogeneous regions of hemorrhage,
edema, and necrosis, often located in the superficial gray
matter.1,20
• MRI findings include (Fig. 5.8.4):1,9,15,20,21,26,39,43
• Ill-defined intra-axial lesions close to the brain
surface.
• Lesion may be on side of primary injury or occur on
the opposite side, in a ‘contrecoup’ pattern.
• Lesions are T2 hyperintense if edema predominates. Fig. 5.8.4 Brainstem contusion in an 8-year-old Jack Russell
In the presence of hemorrhagic lesions the lesions Terrier after a dog attack. The transverse T2W image shows
have variable signal intensity and exhibit susceptibil- a focal intra-axial T2 hyperintense lesion within the left
ity artifacts on T2*W images. aspect of the brainstem (arrow). Focal hyperintensity of the
• Hemosiderin from chronic contusion may persist adjacent musculature is also evident, consistent with trauma
indefinitely and cause signal voids from susceptibility (arrowhead). (1T MRI system)
artifacts on T2*W gradient echo images.
Diffuse axonal injury Brain herniation

• Diffuse axonal injury (DAI) results from rapid accel- • The increase in intracranial pressure related to both pri-
eration head trauma causing shearing injuries related mary and secondary injuries can lead to compression and
to differences in elastic and inertial properties between displacement of brain parenchyma.1,9,44–46
different but adjacent brain tissues.1,20 This results in • MRI findings include (Fig. 5.8.5):3,9,44,45
disruption of axons, especially at the gray–white matter • Herniation of the caudal portion of the cerebellum
junction of the cerebrum, at the corpus callosum, basal into and through the foramen magnum (‘foramen
nuclei, and rostral aspect of the brainstem. DAI is poorly magnum herniation’).
documented in animals.9 • Herniation of part of the cerebral cortex across
• MRI findings in people include:1,26 midline into the opposite half of the cranial vault
• Hemorrhagic acute lesions: small, petechial hemor- (‘subfalcine herniation’).
rhages at the gray–white matter junction of the cer- • Displacement of portions of the cerebral cortex
ebral hemispheres, best seen on T2*W images (focal ventral to the tentorium cerebelli (‘caudal transtento-
signal voids due to susceptibility artifacts). rial herniation’).
• Non-hemorrhagic acute lesions: multiple small T2 • Displacement of portions of the cerebellum dorsal to
hyperintense foci consistent with edema and best seen the tentorium cerebelli (‘rostral transtentorial herni-
on T2-FLAIR images. ation’).
• Chronic lesions: • Herniation through a fracture site or through a
– Brain atrophy (widening of the sulci). pre-existing calvarial defect (e.g., open fontanelle).
– Gliosis manifesting as T2 and T2-FLAIR hyper-
intense parenchymal lesions. Post-traumatic brain ischemia and infarction
– Hemosiderin deposits seen as signal voids on • Post-traumatic brain ischemia and infarction may occur
T2*W images, which may persist for the rest of secondary to diffuse increased intracranial pressure or a
the patient’s lifetime. focal compressive lesion such as a hematoma, bone frag-
ment, or part of the skull in the case of brain herniation.1
Vascular lesions • MRI findings overlap with other post-traumatic brain
• Post-traumatic intracranial arterial dissection, aneu- changes (edema and contusion). Specific MR imaging
rysms, pseudoaneurysms, and arteriovenous fistulas are findings in cerebral vascular compromise are covered in
reported in human patients and warrant evaluation by Chapter 5.6.
means of CT angiography or MRA.1,26
• MRI findings reported in a dog with an arterialized
aneurysm secondary to traumatic arteriovenous fistuli-
zation included:5
• An expansile mass along the right intracranial cavern-
ous sinus and extending through the orbital fissure
into the retrobulbar space.
• Signal void due to presence of rapidly flowing blood
on conventional MR sequences.
• Vascular connection confirmed with MRA.
SECONDARY TRAUMATIC BRAIN INJURY
Acute secondary injury

Diffuse cerebral swelling
• Diffuse cerebral swelling may develop secondary to an
increase in cerebral blood volume or vasogenic and cyto-
toxic edema. Fig. 5.8.5 Transverse T2W image of the caudal head
• MRI findings include:1,26,41,44 in an 8-year-old Pomeranian following a dog attack.
• Effacement of the cerebral sulci and ventricular com- Findings include soft tissue injuries to the head indicated
pression. by swelling and multifocal patchy muscle hyperintensities,
• Loss of gray–white matter differentiation in cytotoxic hyperintensity and swelling to the left cerebellum consistent
edema. with contusion, and herniation of part of the cerebellum
• Diffuse T2 hyperintensity along the cerebral white through a defect in the skull secondary to fractures (arrow).
matter tracts in vasogenic edema. (1T MRI system)
314 CHAPTER 5.8
Infection – Susceptibility artifacts may be seen on T2*W

• A penetrating injury to the calvarium, such as a bite images, appearing as signal voids in the wall of the
wound, migrating foreign body, ballistic injury, or medi- abscess.
cal procedure, may result in infection of intracranial tis- – Strong peripheral (ring) enhancement on post-
sues (meningitis or abscessation).1,6,16,47–49 contrast images.
• On occasion, patients with minor head trauma may not • Associated vasogenic edema, mass effect, and brain
present to the veterinarian right away as the initial lesion herniation.
may be considered clinically insignificant or may go • Adjacent skull fracture(s) and soft tissue lesion(s).
entirely unnoticed. This is especially true in the case of
small lesions in very young animals (e.g., scratch or bite Pneumocephalus
wound in a puppy or kitten). If the initial head trauma • Pneumocephalus is defined as intracranial accumulation
resulted in introduction of bacteria into the calvarium, of air, which most commonly occurs following crani-
affected animals may present days to weeks later with otomy or craniectomy, although traumatic causes have
new onset of neurologic signs related to intracranial been reported in people and dogs.8,14,49–54
infection. • Clinical signs in affected patients are variable. If the
• MRI findings in inflammatory brain diseases are accumulation of intracranial gas occurs under pressure
covered in detail in Chapter 5.3. MRI findings of (‘tension pneumocephalus’), affected patients show rap-
intracranial infection secondary to trauma include idly progressive neurologic signs, and this condition is a
(Fig. 5.8.6): 6,47–49 potentially life-threatening emergency.
• Meningitis: meningeal thickening and strong con- • MRI findings include (Fig. 5.8.7):50–53
trast enhancement. • Air within the ventricular system or, less commonly,
• Abscessation: the subarachnoid or epidural space appearing as a
– Epidural, intraparenchymal, or, less commonly, signal void on all sequences.
subdural mass lesion. • Variable distension and asymmetry of the ventricular
– T1 hypointense and T2 hyperintense, often with system.
T2 hypointense rim. • A meniscus between adjacent normal CSF and air.
* *
Fig. 5.8.7 Pneumocephalus in a canine model of

post-mortem-induced head injury. There is deformation of
Fig. 5.8.6 Meningitis and brain abscessation in a 2-year-old the right frontal sinus, consistent with skull fractures. Focal
dog several weeks after sustaining a bite wound to the head. areas of signal void (asterisks) dorsal to the right and, to a
The transverse post-contrast T1W image demonstrates an lesser degree, the left olfactory bulbs on this PDW image
irregularly shaped strongly contrast enhancing mass with are consistent with traumatic fistulas between the frontal
small non-enhancing central foci in the right cerebrum. sinuses and cranial vault and subsequent intracranial air
Additional findings include adjacent meningeal enhancement, accumulation. (1.5T MRI system)
soft tissue irregularities, a defect in the overlying skull
(arrow), and hypointensity and mass effect to the entire right
cerebral hemisphere consistent with edema. (1T MRI system)
• Mass effect such as midline shift in cases of tension • Evidence of chronic subdural hemorrhage with asso-
pneumocephalus, often with progressive neuropathy ciated susceptibility artifacts on T2*W images.
clinically. • Chronic skull fractures.
• Post-surgical or post-traumatic skull and soft tissue • Other late effects of head trauma, especially in cases of
changes, typically with a fistula between the ventricu- chronic repetitive injury, are still poorly understood. In
lar system and an air-filled space (e.g., frontal sinus). people, repetitive brain trauma such as sustained by box-
ers or football players has been linked to chronic traumatic
Chronic secondary injury encephalopathy and various neurodegenerative diseases
• Late-term effects of head trauma may include:1,16,20 including Alzheimer’s disease.30,55 Although the histopath-
• Hydrocephalus secondary to intraventricular or ologic findings reported in a dog with chronic traumatic
subarachnoid hemorrhage and resultant impaired brain injury were different from those reported in people,
reabsorption of CSF. cortical atrophy was also observed, which is a common
• ‘Hydrocephalus ex vacuo’, corresponding to CSF- finding in many human and animal neurodegenerative
filled enlargements of the ventricles and/or subarach- diseases.10 There is agreement that conventional MR
noid space due to loss of adjacent parenchymal brain sequences are not sufficient for evaluating changes associ-
substance resulting from brain tissue destruction or ated with repetitive brain injury, and extensive research
atrophy. is being conducted evaluating the utility of advanced MR
• Encephalomalacia. technologies in diagnosis and prognostication.1,19,30,32,56,57
• Residual chronic changes from hemorrhage, espe-
cially subdural, may cause lifelong abnormalities on MRI PROGNOSTIC INDICATORS
MR examination. IN HEAD TRAUMA
• MRI findings include (Fig. 5.8.8):1,16,20
• Ventricular dilation of variable severity. • Negative prognostic MRI findings reported in dogs with
• Focal or multifocal brain parenchymal defects filled head trauma include:
with CSF. • Degree of midline shift.3,9
• The extent of intraparenchymal lesions.3
• Brain herniation.3
• Skull fractures.3
• Injuries affecting the caudal fossa or both the rostral
and caudal fossae.9
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CHAPTER 5.9
AGING CHANGES OF THE BRAIN

318 Silke Hecht and Amy Hodshon
CONTENTS
MRI changes during brain maturation in juvenile animals .................................................................................................................................... 318
Aging changes of the brain.................................................................................................................................................................................... 318
General considerations .................................................................................................................................................................................... 318
Neurobiologic/neuropathologic changes in the aging brain............................................................................................................................. 319
MRI changes in the aging brain .......................................................................................................................................................................320
References.............................................................................................................................................................................................................323
The canine and feline brain undergoes changes with age, • MRI maturation of the corpus callosum is reached at
such as changes in iron content, volume, and relative amount 6 weeks on T1W images, 8 weeks on T2W and STIR
of white matter. These structural and morphologic changes images, and at 12 weeks on T2-FLAIR images.
cause variations in the MRI appearance of the brain, which • Significant changes in diffusion parameters are
the radiologist needs to be aware of when interpreting noted.5
imaging studies. This chapter will cover both changes with • Maturation of cerebral gyri and sulci continues after
maturation in juvenile animals as well as changes occurring birth and is complete by 14 days post partum.6 The
with advanced age. sequence and time course of gyrification are identi-
cal for all breeds studied, and the symmetry of gyri is
MRI CHANGES DURING BRAIN maintained during this development.
MATURATION IN JUVENILE ANIMALS
AGING CHANGES OF THE BRAIN
• While the central nervous system is relatively mature
at birth in some species, extensive postnatal neurologic General considerations
development occurs in others. Changes occurring with • Physiologic and pathologic changes occurring in the
maturation include general growth, blood–brain barrier brains of aging dogs and in dogs with certain storage dis-
development, and postnatal neurogenesis, synaptogen- eases are similar to changes observed in humans. As a
esis, and myelination.1 result, the dog has been used as a model for normal and
• The following information pertains to dogs unless oth- pathologic human brain aging to improve understanding
erwise indicated. of conditions ranging from mild cognitive impairment to
• MRI findings with maturation include: Alzheimer’s disease/dementia (see also Chapter 5.2).7–15
• Expansion of lateral ventricles (first detected at • Canine cognitive dysfunction syndrome is believed to
3–4 weeks of age).2 affect as many as 14%–30% of older (>7–10 years) dogs,
• Changes in gray and white matter signal intensity due with the prevalence increasing to over 45% in dogs
to progressive myelination of the brain (Fig. 5.9.1).3,4 >15 years.16–20 The condition is still underrecognized, as
These changes occur from caudal to rostral in the the clinical signs (including staring into space, disorien-
brainstem and from central to peripheral in the cer- tation, changes in social interactions, changes in sleep–
ebrum. The changes in signal intensity of the cere- wake cycles, house soiling, anxiety, vocalizing, pacing,
bral hemispheres occurring with brain maturation are and deficits in learning and memory) are insidious in
summarized in Table 5.9.1. onset and are commonly mistaken for normal age-related
• MRI maturation of the cerebellum and brainstem is behavioral changes.11,15,18,21–23
reached at 4 weeks on T1W images, 6 weeks on T2W • Cognitive dysfunction syndrome has only been recently
and STIR images, and at 12 weeks on T2-FLAIR recognized in feline patients. Pathologic and clini-
images. cal findings are similar to dogs.22,24–26 Clinical signs in
A gi ng C h a nge s of t h e Br a i n 319
(a) (b)
Fig. 5.9.1 Transverse T2W images of canine brain

maturation. The subcortical white matter is hyperintense
to gray matter during the juvenile phase (weeks 1–4; a),
isointense during the transition phase (6 weeks; b), and
exhibits hypointensity during the maturing phase and into
adulthood (8–36 weeks; c). The relative decrease in white
matter intensity is predominantly due to a decrease in water
content during myelination. (1.5T MRI system; reproduced,
with permission, from Gross B, Garcia-Tapia D, Riedesel E
et al. (2010). Normal canine brain maturation at magnetic
(c)
resonance imaging. Vet Radiol Ultrasound 51(4):361–73.)
Table 5.9.1 Changes in signal intensity of the cerebral hemispheres occurring with brain maturation in dogs.
T1W images T2W and STIR images T2-FLAIR images

• Juvenile (white matter isointense • Juvenile (white matter isointense • ‘Pseudomature’ (white matter hypointense to gray matter):
or hyperintense to gray matter): or hyperintense to gray matter): 1–2 weeks
1–3 weeks 1–4 weeks • 1st isointense transition: 3 weeks
• Isointense transition: 3–4 weeks • Isointense transition: 4–8 weeks • Juvenile (white matter hyperintense to gray matter): 4–6 weeks
• Mature (white matter hypointense • Mature (white matter hypointense • 2nd isointense transition: 6–12 weeks
to gray matter): 16 weeks to gray matter): 16 weeks • Mature (white matter hypointense to gray matter): 36 weeks
affected cats include house soiling, excessive vocaliza- Neurobiologic/neuropathologic

tion, disorientation, restlessness, aggression, and clingy changes in the aging brain
attachment. • Although neurobiologic changes and imaging findings
• As other diseases (e.g., renal, hepatic, or central ner- tend to be more severe in animals with cognitive dys-
vous system disorders) may result in similar behavioral function, there is considerable overlap with ‘normal’
changes, the diagnosis of cognitive dysfunction syn- older pets.
drome is challenging, and is made by exclusion.22,27
320 CHAPTER 5.9
• Neurobiologic changes with age in normal dogs and cats • MRI findings in normal aging dogs, and dogs with cog-
and in patients with cognitive dysfunction include: nitive dysfunction include:
• Cerebral cortical atrophy (with resultant narrowing of • Morphologic changes:
gyri, widening of sulci, and ventriculomegaly), which – Widening of the cerebral sulci and ventriculo-
begins in the frontal lobes and is more severe in dogs megaly (Fig. 5.9.2).8,56,61,62
than cats.7,9,11,12,15,24,28–31 – Cerebral atrophy, most pronounced in mesatice-
• Neuron loss and decreased neurogenesis in various phalic and brachycephalic dogs.62
areas of the brain.7,9,11–13,24,28–30,32–35 – Change in size of frontal lobes:
• Accumulation of beta-amyloid (Aβ) in the form of diffuse – Gray matter atrophy that can be bilateral or
senile plaques in dogs and cats (can be large and less well unilateral; the prefrontal cortex shows larger
defined in cats compared with people) and as toxic Aβ losses in males than females while the tempo-
oligomers in dogs.7,9,12,15,33,36–41 Amyloid load correlates ral cortex shows larger losses in females than
with clinical signs of cognitive dysfunction in dogs.36,42 males.58
• Hyperphosphorylation of Tau protein in the brain, – The age-related decrease in frontal lobe
changing it from soluble and monomeric to insoluble volume precedes decreases in total brain
and filamentous (Tau pathology). Unlike in humans, volume.9
neurofibrillary tangles are not observed; however, – Smaller frontal lobe volumes are associated
hyperphosphorylated tau is reported in animals and with poor performance on certain cognitive
may be associated with neuronal degeneration and tests and with larger Aβ loads.9
cognitive impairment.12,39,40,43,44 – Small size of the interthalamic adhesion has
• Accumulation of multiple end-products of oxidative been described as an indicator of cognitive dys-
damage to proteins, lipids, and nucleotides (e.g., car- function in dogs, but may also be seen in normal
bonyl groups due to oxidative damage to proteins and older dogs (Fig. 5.9.2). The height of the inter-
lipofuscin/ lipofuscin-like products due to lipid perox- thalamic adhesion measured on transverse plane
idation). Such changes have been shown in dogs and images was reported to be 6.79 +/− 0.70 mm in
are suspected in cats.9,10,13,24,26,28,45–47 normal dogs and 3.82 +/− 0.79 mm in demented
• Vascular and circulatory abnormalities: dogs.63
– Deposition of Aβ in association with blood vessels – Change in size of hippocampus with age in dogs
(cerebrovascular amyloid angiopathy), which may is debated:
compromise the blood–brain barrier and impair – Hippocampal volume in dogs >11 years was
vascular function.8,12,13,22,42,48–53 significantly smaller than younger animals
– In dogs: in a study of 66 Beagles aged 3 months to
– Thickening, fibrosis, and hyalinosis of small 15 years.9
arteries; calcification of the tunica externa of – No correlation between hippocampus size and
blood vessels.10,28 age was observed in a study of 19 Beagles aged
– Microhemorrhages and infarcts.12,13,28,42,48–56 8 months to 16 years.61
– In cats: • White matter abnormalities:
– Compromised blood flow and hypoxia within – Regional bilateral decline in volume with age.
the brain due to decreased cardiac output, hyper- Both males and females show equivalent atrophy
tension, anemia, and altered blood viscosity.24,27 of the internal capsule. Females show greater atro-
• Additional neuropathologic changes reported in dogs phy of the hippocampal white matter, males show
include: a reduction in the white matter tract volume of the
– Diffuse white matter abnormalities (demyelin- optic nerve bundle.58
ation, degeneration).10,13,28,57–59 – Spontaneous development of white matter T2
– Gliosis characterized by astrocytosis.13,28,33,60 hyperintensities, particularly adjacent to the lat-
– Other changes (meningeal calcification, mito- eral ventricles, attributed to perivascular demy-
chondrial dysfunction, caspase activation, DNA elination and axonal loss caused by chronic
fragmentation, inflammation, spheroids in the ischemia, blood–brain barrier compromise, and
cerebral white matter, accumulation of polygluco- amyloid angiopathy (Fig. 5.9.3).10,57,61,64 These
san bodies).10,12,13,28 seem to correspond to age-related white matter
changes and leukoaraiosis originally reported in
MRI changes in the aging brain elderly people and more recently in dogs.65–68 In
• The neurobiologic/neuropathologic changes described people they are known to contribute to dementia,
above can induce changes in the MRI appearance of the while their significance in dogs is undetermined
brains of aging dogs and cats. to date.
(a) (b)
(c) (d)
Fig. 5.9.2 MR images of a 13-year-old mixed breed dog with generalized brain atrophy (a, c) compared with a 4-year-old
normal dog (b, d). The transverse T2W image in the older dog (a) shows prominence (deepening and widening) of the cerebral
sulci, a small interthalamic adhesion, and moderate generalized ventriculomegaly compared with the younger animal (b). An
incidental subcutaneous cyst is associated with the right dorsal aspect of the head (a). On the sagittal T2W image, small size
and abnormal shape (triangular [arrow, c] rather than circular [arrow, d]) of the interthalamic adhesion are observed in the
older dog (c) compared with the younger dog (d). (1.5T MRI system)
• Focal or multifocal lesions related to vascular • Additional MRI findings in old dogs include:
damage: – At very high field (4.7T MRI system), progressive
– Lacunar infarcts commonly affect the caudate T2 hypointense areas in the globus pallidus and
nucleus and thalamus and appear as sharply mar- substantia nigra attributed to iron deposition.61
ginated, well defined, and homogeneous T2 hyper- – Changes in metabolite ratios with age on mag-
intense lesions (Fig. 5.9.4; see also Fig. 5.5.9).54,55 netic resonance spectroscopy:
In a longitudinal study, chronic infarcts appeared – Age-related decline in markers of neuronal health
isointense to CSF and increased in number with (N-acetyl containing compounds) in dogs.72
advancing age.56 – Decrease in choline-to-creatine ratio com-
– Microbleeds (silent cerebral hemorrhages) best pared with young dogs.73
seen as (multi)focal small susceptibility artifacts – N-acetyl aspartate-to-choline ratio signifi-
on T2*W images (Fig. 5.9.5).69–71 cantly lower in young and geriatric dogs than
in adult dogs.73
322 CHAPTER 5.9
(a) (b)
Fig. 5.9.3 Bilaterally symmetric periventricular T2 (a) and T2-FLAIR (b) hyperintensities associated with cerebral white
matter in a 15-year-old Basset Hound with canine cognitive dysfunction syndrome. T2 hyperintense material within the
tympanic bullae was incidental. (1.5T MRI system)
(a) (b)
Fig. 5.9.4 Chronic lacunar infarct in a 9-year-old Greyhound. A triangular, sharply marginated lesion, which is isointense to
CSF on the T2W (a) and T2-FLAIR (b) images, is associated with the right thalamus (arrows). (1.5T MRI system)
• Although there is also clear evidence of age-associated • Small multifocal areas of decreased signal intensity
brain pathology in cats, reports on related imaging on T1W images, predominantly in the piriform
changes are scarce.26 MRI findings reported include: lobes.29
• Cerebral atrophy (decrease in both gray and white • MRS alterations with decreased levels of creatine,
matter volume) with increased ventricular size and inositol, and N-acetyl-aspartate observed in senior
widening of sulci, although this may not be as marked cats.74
as that seen in the dog (Fig. 5.9.6).29
(a) (b)
Fig. 5.9.5 Cerebral microbleeds in a 14-year-old West Highland White Terrier. (a) The transverse T2W image reveals mild
generalized brain atrophy. (b) The T2*W image shows multifocal punctate signal voids (susceptibility artifacts) associated with
the right caudate nucleus and the parietal lobes. (1.5T MRI system)
(a) (b)
Fig. 5.9.6 Aging changes of the brain in a cat. Transverse T2W MR image at the level of the thalamus in a 16-year-old cat
(a) showing mild prominence to the cerebral sulci and lateral ventricles consistent with brain atrophy, compared with an MR
image of the brain at the same level in a 3-year-old cat (b). The degree of brain atrophy is less severe than that typically seen in
dogs. (1.5T MRI system)
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CHAPTER 5.10
CRANIAL NERVE DISEASES

326 Wilfried Mai
CONTENTS
Technical considerations .......................................................................................................................................................................................327
Normal MRI anatomy of the cranial nerves............................................................................................................................................................327
General features ...............................................................................................................................................................................................327
Hypoglossal nerve (XII) ...................................................................................................................................................................................327
Glossopharyngeal (IX), vagus (X), and accessory (XI) nerves..........................................................................................................................332
Vestibulocochlear nerve (VIII) ..........................................................................................................................................................................332
Facial nerve (VII)..............................................................................................................................................................................................332
Abducens nerve (VI) ........................................................................................................................................................................................332
Trigeminal nerve (V) and its branches..............................................................................................................................................................332
Orbital fissure group (abducens nerve [VI], ophthalmic branch of trigeminal nerve [V], trochlear nerve [IV], oculomotor nerve [III]) ............332
Optic nerve (II) .................................................................................................................................................................................................333
Olfactory nerves (I) ..........................................................................................................................................................................................333
Contrast enhancement .....................................................................................................................................................................................333
Olfactory nerve diseases .......................................................................................................................................................................................333
Optic nerve diseases .............................................................................................................................................................................................333
Anatomic and pathologic considerations .........................................................................................................................................................333
Optic neuritis ...................................................................................................................................................................................................333
Optic nerve neoplasia ......................................................................................................................................................................................334
Idiopathic oculomotor neuropathy.........................................................................................................................................................................334
Trigeminal nerve diseases .....................................................................................................................................................................................335
Idiopathic trigeminal neuropathy .....................................................................................................................................................................335
Trigeminal nerve sheath tumors .......................................................................................................................................................................336
Cavernous sinus syndrome ...................................................................................................................................................................................338
Facial nerve diseases ............................................................................................................................................................................................340
Facial nerve paralysis secondary to otitis media/interna ..................................................................................................................................340
Idiopathic facial paralysis ...............................................................................................................................................................................340
Facial and vestibular neuropathy of unknown origin ........................................................................................................................................341
Vestibulocochlear nerve diseases..........................................................................................................................................................................341
References.............................................................................................................................................................................................................342
Due to the complex anatomy of the cranial nerves, the difficult to see with MRI. Conversely, CT provides excel-
evaluation of patients with cranial neuropathies requires lent bony detail to identify these osseous landmarks, but
an in-depth understanding of the normal course of these the soft tissue contrast is very poor in comparison with
important structures. The cranial nerves are small and MRI, and identification of the individual nerves is not pos-
have a tortuous path at the base of the skull, making MRI sible. With the improved technology available in veterinary
challenging, especially since bony landmarks such as the medicine, in particular higher magnetic field strengths and
skull foramina and canals through which they travel are optimized coils and pulse sequences, MRI has become the
C r a n i a l Ne rv e D is e a s e s 327
technique of choice to image dogs and cats with cranial NORMAL MRI ANATOMY OF
nerve disease. THE CRANIAL NERVES
TECHNICAL CONSIDERATIONS General features

• In dogs, cranial nerves II, III, V and its divisions, and
• Studies reporting on the normal MRI anatomy of the VIII are usually consistently visualized. Cranial nerves
cranial nerves in dogs and cats have found transverse IV, VII, and the group of IX, X, and XI are inconsis-
plane T2W images to be the most useful in their identifi- tently seen, and cranial nerves VI and XII are very dif-
cation.1,2 T1W images can also be useful, as they provide ficult to identify or not seen at all. The emergence of
improved visualization of some bony landmarks. cranial nerves II, III, IV, V, VII, VIII, and the IX/X/XI
• Dorsal and sagittal planes are less useful because of the group can also typically be identified.1
curvilinear course of the cranial nerves. • In cats, cranial nerves II, V and its divisions, VII and
• 2 mm slice thickness was reported to provide the best VIII are typically visualized while cranial nerves IV
results in both dogs and cats.1,2 and VI are typically not individually visible; cranial
• In people, steady state free precession (SSFP) MRI nerve III is occasionally poorly visualized. The emer-
pulse sequences are preferred for imaging of the cra- gence of cranial nerves IX, X, XI, XII, and the common
nial nerves. These pulse sequences have various acro- path of nerves IX, X, and XI through the tympano-
nyms depending on the manufacturer, such as FIESTA, occipital fissure can only be visualized as a single ill-
TrueFISP, balanced-FFE (see Chapter 2). Steady state defined structure.2
pulse sequences generate a constant longitudinal and • Cranial nerves typically are isointense to the gray matter
transverse magnetization by keeping the TR shorter of the brain on both T1W and T2W images, although in
than the T2 relaxation times of the tissue. Because the cats the structure corresponding to the group of cranial
TR is shorter than T2, there is not enough time for nerves IX, X, XI, and XII is reportedly hyperintense on
the transverse magnetization to decay completely T2W images.1,2
before the next radiofrequency pulse, so that there will • A schematic showing the area of origin of the cranial
be some residual transverse magnetization left over. nerves from a ventral view is provided in Fig. 5.10.1,
That residual transverse magnetization will be fed back together with a table summarizing anatomic features and
into longitudinal magnetization with the next radio- function of each nerve.
frequency pulse; that pulse also flips some of the lon- • Figs. 5.10.2a–l show transverse MRI images in a cat,
gitudinal magnetization into the transverse plane. If reformatted from a 3D-balanced SSFP volumetric data-
this process is repeated, after several TR periods this set. Transverse images are serially presented from cau-
constant exchange between longitudinal and transverse dal to rostral, with the position of each transverse plane
magnetization results in a ‘steady state’, with a steady image referenced on a median sagittal T1W image
magnitude of both magnetizations.3 These sequences (Fig. 5.10.2a). As most nerves have a transverse or
provide a strong signal in tissues that have a high T2/ caudal-to-rostral trajectory after their emergence, they
T1 ratio, such as cerebrospinal fluid (CSF) and fat, tend to be more easily identified and traced when scroll-
thereby allowing excellent contrast between the darker ing through transverse images from caudal to rostral.
nerves and the CSF when they leave the brain and travel For this reason, the MR anatomy of the cranial nerves,
through the base of the skull, all this at excellent spa- with references to internal landmarks, is described below
tial resolution with submillimetric slice thickness, and for each nerve on transverse images starting from caudal
shorter acquisition time compared with traditional spin to rostral.
echo sequences. When used in 3D mode, multiplanar
reformatting is possible, allowing optimization of imag- Hypoglossal nerve (XII)
ing planes for various structures. The main disadvan- • The hypoglossal nucleus is located in the medulla, adja-
tages of these pulse sequences include reduced contrast cent to midline in the floor of the 4th ventricle.
resolution between different soft tissues, poor depiction • The nerve emerges from the brainstem, lateral to the
of global landmarks due to the submillimetric section pyramids, as a longitudinal series of small rootlets on
thicknesses,4 and common banding artifacts across the the ventral surface of the medulla; these rootlets are very
images due to phase shift errors, particularly promi- small, which is why they are usually not individually vis-
nent in the skull base where there are distortions of ible on MRI.1
the magnetic field due to susceptibility differences (see • The emergence of the hypoglossal nerve in cats may be
Chapter 3). Therefore, these pulse sequences should be seen on the ventrolateral part of the myelencephalon
considered as complementary to the traditional T2W as a hyperintense focus on T2W images, but is poorly
and T1W sequences. defined.2
328
NERVE EXITS THE BRAIN CASE THROUGH FUNCTION
Many small bundles of fibers

CN I
from olfactory bulb through Sensory from olfactory epithelium
(Olfactory n.)
cribriform plate to nasal mucosa
Olfactory bulbs CN II
Optic canal Sensory from retina (vision)
(Optic n.)
Motor to dorsal, medial, and ventral rectus mm., ventral oblique and
CN III
Orbital fissure levator palpebrae mm.
(Oculomotor n.)
Parasympathetic to iris sphincter m.
Optic chiasm
CN IV
Orbital fissure Motor to dorsal oblique m.
(Trochlear n.)
Infundibulum Ophthalmic branch → Trigeminal Sensory from globe (including cornea), periorbital tissue, nasal mucosa,
Mammillary bodies canal → Orbital fissure medial canthus of the eye. Parasympathetic to lacrimal gland
Maxillary branch → Trigeminal
Sensory from maxillary area, lateral canthus of the eye
CN V canal → Foramen rotundum → Alar
Parasympathetic to lacrimal gland
(Trigeminal n.) canal* → Rostral alar foramen
Sensory from mandibular area and auriculotemporal area.
Mandibular branch → Trigeminal
Cerebral peduncles Motor to masticatory mm. (temporalis, masseter, medial/lateral pterygoid,
canal → Foramen ovale
(midbrain) rostral part of digastricus mm.) and tensor veli palatini m.
CN VI
Orbital fissure Motor to retractor bulbi m. and lateral rectus m.
Pons (Abducens n.)
Motor to muscles of facial expression and caudal part of digastricus m.

CN VII Internal acoustic meatus → Facial
Sensory (taste) from the rostral two-thirds of the tongue and palate
(Facial n.) canal → Stylomastoid foramen
CHAPTER 5.10
Parasympathetic to salivary and lacrimal glands
Cerebellum CN VIII Internal acoustic meatus → Inner

Sensory from inner ear (hearing and balance)
(Vestibulocochlear n.) ear
Sensory from the caudal third of the tongue and pharyngeal mucosa
CN IX Jugular foramen → Tympano-
Medulla Motor to the pharynx
(Glossopharyngeal n.) occipital fissure
oblongata Parasympathetic to parotid and zygomatic salivary glands
Motor to pharynx and esophagus; larynx via recurrent laryngeal n.
CN X Jugular foramen → Tympano-
Sensory to ear canal and laryngeal mucosa
(Vagus n.) occipital fissure
Parasympathetic to heart, lungs, and abdominal viscera
CN XI Jugular foramen → Tympano-

occipital fissure Motor to trapezius, sternocephalicus, brachiocephalicus mm.
(Accessory n.)
CN XII
Hypoglossal canal Motor to extrinsic and intrinsic mm. of the tongue
(Hypoglossal n.)
Fig. 5.10.1 Schematic ventral view of the brain showing emergence of the cranial nerves (left) and associated anatomic features and function of the corresponding
nerves (right). *: in cats, there is no alar canal; CN, cranial nerve; n, nerve; m, muscle; mm, muscles.
Cerebellum
EEC
st
l
Ve
TB CN VIII
NP
k j i hg f e d cb
(a) (b)
Rostral aspect
of cerebellum
CN VII
Colliculi
EE
CN V
C
Pons CN V
CN VII Pons
TB TB
Cochlea NP NP
(c) (d)
Fig. 5.10.2 Images of the brain of a cat showing the origin and paths of selective cranial nerves. Images (b–k) are reformatted
transverse images obtained from a 3D dataset of a FIESTA pulse sequence; (l) is a dorsal oblique image showing the course of
the optic nerves from the optic chiasm to the retina; (a) is a median sagittal T1W image showing the orientation of reformatted
planes in images (b–l). CN, cranial nerve; TB, tympanic bulla; Vest, vestibule of the inner ear; EEC, external ear canal;
NP, nasopharynx. (1.5T MRI system) (Continued)
330 CHAPTER 5.10
Mesencephalic
aqueduct
CN V
TB CN V ganglion CN V ganglion
CN V NP
NP
(e) (f)
Caudal aspect of the 3rd ventricle

Dorsal and ventral parts Interthalamic adhesion
of the 3rd ventricle
Pituitary gland
Mandibular branch of CN V Maxillary branch of CN V

exiting through foramen ovale exiting through foramen rotundum
(g) (h)
Optic chiasm
Orbital fissure nerve group Maxillary artery Orbital fissure nerve group
Maxillary artery
Maxillary branch of CN V Maxillary branch of CN V
(i) (j)
CN II
CN II
Orbital fissure nerve group

Maxillary artery
Maxillary branch of V
(k) (l)
332 CHAPTER 5.10
• The hypoglossal canal, through which the nerve exits can be identified together with the other nerves travel-
the skull, cannot be identified on MR images.1,2 ing through that fissure, and described below under the
‘orbital fissure group’.
Glossopharyngeal (IX), vagus (X),
and accessory (XI) nerves Trigeminal nerve (V) and its branches
• These nerves emerge very close to each other, lateral • The emergence of the trigeminal nerve can be identi-
to the myelencephalon, at the level of the lateral recess fied roughly level with the caudal colliculi of the mesen-
of the 4th ventricle and caudal cerebellar peduncles. cephalon and the pons (Fig. 5.10.2d). The nerve then
• When seen, they form a small and ill-defined structure continues rostrally along the floor of the cranial cav-
that is T2 hypointense in dogs and T2 hyperintense in ity, enclosed within the trigeminal canal, although this
cats, traveling towards the ipsilateral tympano-occipital osseous landmark cannot be identified on MRI. A focal
fissure located caudomedial to the tympanic bulla; they rounded enlargement of the nerve, corresponding to the
cannot be differentiated from each other.1,2 trigeminal ganglion, can be identified (Fig. 5.10.2f).1,2
• The first branch off the trigeminal nerve is the man-
Vestibulocochlear nerve (VIII) dibular branch, which exits ventrolaterally through the
• The vestibulocochlear nerve can typically be identi- large foramen ovale (oval foramen), roughly at the level of
fied immediately dorsal to the vestibule of the inner the caudal margin of the interthalamic adhesion/caudal
ear, traveling lateroventrally from the myelencephalon aspect of the 3rd ventricle, a useful landmark easily iden-
(Fig. 5.10.2b).1,2,5 tified when correlating transverse with sagittal images
• The vestibules (each containing a utricle and a sac- (Figs. 5.10.2a, 5.10.2g).1,2
cule) represent an easily identified landmark dorsal • Immediately rostral to this, the maxillary branch of the
to the tympanic bullae, as they form recognizable trigeminal nerve exits the cranial cavity ventrally through
structures on transverse images, looking like ‘ducks’ the foramen rotundum (round foramen) (Fig. 5.10.2h). In
heading laterally.6,7 They are hyperintense on T2W dogs, it immediately joins the alar canal (within the basi-
images, due to the intralabyrinthine fluid,7 contrast- sphenoid bone), through which the nerve travels together
ing with the surrounding bony labyrinth that appears with the maxillary artery to exit rostrally through the
as a signal void.6,8 The ‘duck pattern’ has previously rostral alar foramen; in cats, there is no alar canal. The
been attributed to the semicircular canals,6,7 but at the alar canal cannot be identified on MR images due to
resolution obtained on standard fast spin echo T2W its bony nature. After entering the round foramen, the
images, these canals are too small to be seen, and the maxillary branch of the trigeminal nerve can be traced
duck pattern corresponds, in fact, to the vestibule (see rostrally as a small rounded to oval-shaped hypointense
also Chapter 6.3).9,10 structure, ventrolateral to the orbital fissure. It is accom-
panied by a rounded, markedly hypointense structure
Facial nerve (VII) immediately lateral to it, corresponding to the maxillary
• Immediately rostral to the vestibule, the cochlea of the artery (Figs. 5.10.2i–k).1,2
inner ear is easily recognized due to its typical spiral- • The third branch of the trigeminal nerve is the
shape, with a high internal T2 signal due to the fluid ophthalmic branch, and is described below together with
within it. the remainder of the ‘orbital fissure group’. It may be
• The cochlea is a useful landmark to identify cranial observed on a few slices rostral to the round foramen,
nerve VII, which can be seen emerging from the pons before it joins the rest of the ‘orbital fissure group’ (see
and traveling laterally, forming a thin structure dorsal below).1,2
to the cochlea, corresponding to the path of the nerve
through the facial canal, after it exits the brain cavity Orbital fissure group (abducens
through the internal acoustic meatus (Fig. 5.10.2c).1,2 nerve [VI], ophthalmic branch of
Typically, the rostral aspect of the cerebellum is visible trigeminal nerve [V], trochlear
in the same image plane.1,2 nerve [IV], oculomotor nerve [III])
• Immediately rostral to the pituitary fossa, at the level of
Abducens nerve (VI) the rostral clinoid process, is the opening of the orbital
• In dogs, the proximal course of the abducens nerve can- fissure through the floor of the cranial cavity, through
not be identified due to its size; its emergence may be which the ‘orbital fissure group’ of cranial nerves travels
seen at the rostral part of the myelencephalon, caudal to reach the orbital space.
to the pons on the lateral side of the rostral part of the • This group includes the abducens nerve (VI), the oph-
pyramids. thalmic branch of the trigeminal nerve (V), the trochlear
• Although the nerve itself cannot be identified due to its nerve (IV), and the oculomotor nerve (III). The indi-
small size, its rostral path through the orbital fissure vidual paths of these nerves are difficult to recognize,
although nerve III may be seen lateral to the pituitary • Mild enhancement of the trigeminal ganglion is typi-
gland in most patients.1,2,11 cally seen in normal cats.2
• The orbital fissures containing these nerves are easily
recognized as paired symmetrical oval-shaped or lentic- OLFACTORY NERVE DISEASES
ular structures on transverse images, located ventrolat-
erally to the optic chiasm (Figs. 5.10.2i–k). • As described in the imaging anatomy paragraph above,
• Besides the cranial nerves III, IV, V ophthalmic, and VI, the olfactory nerve does not form a distinct trunk as do
the orbital fissure also contains vascular structures and other nerves and therefore is not identified as a separate
muscles (e.g., the retractor bulbi muscle); the individual structure. Instead, it consists of a large number of sepa-
nerves are difficult or impossible to distinguish from rate non-myelinated sensory fibers; the neurosensory
each other, especially in small dogs and cats. cells reside in the nasal epithelium, and axons from these
cells pass through the cribriform plate as the fila olfacto-
Optic nerve (II) ria, to synapse in the olfactory bulbs.16
• The optic chiasm can easily be identified as an oval- • These fibers can be involved in pathologic processes that
shaped structure along the floor of the cranial cavity, affect the cribriform plate:
dorsomedial to the orbital fissures, roughly at the level • Nasal cavity disease extending caudally into the
of the rostral margin of the 3rd ventricle (Fig. 5.10.2j).1,2 cranial vault, such as nasal neoplasia, or destructive
• From there, the optic nerves can be traced rostrally, rhinitis such as fungal.
forming two distinct oval-shaped structures coursing in • Neoplasia involving the olfactory bulb of the brain
the direction of the eyes through the optic canal. Their (e.g., olfactory neuroblastoma, also referred to as
entire course can be depicted using dorsal oblique imag- esthesioneuroblastoma or neuroesthesioblastoma,
ing planes (Figs. 5.10.2k, l).1,2 see Chapter 5.4) or meningioma located in the rostral
• A thin hyperintense rim surrounds the nerves on T2W meninges.
images due to the CSF within the extension of the
meninges.1,2,12 OPTIC NERVE DISEASES
• In dogs, the normal diameter of the intracanalicular and
intracranial portion of the optic nerve measured at 0.2T Anatomic and pathologic considerations
is 2.2 +/− 0.15 mm, while the intraorbital portion mea- • The optic nerves are white matter tracts of the dienceph-
sures 1.7 +/− 0.06 mm (3.7 +/− 0.27 mm when the optic alon composed of retinal ganglion cell axons.13
nerve sheath complex is included).13 Another study at • The optic nerve is surrounded by a sheath composed of
higher magnetic field strength (1.5T) found the diam- external (vagina externa nervi optici) and internal (vagina
eter of the intraorbital portion including the sheath to interna nervi optici) layers; the outer layer is a continua-
be closer to 3 mm;12 however, it also found a positive cor- tion of the dura mater while the internal layer is a contin-
relation with body weight, and introduced a nerve sheath uation of the pia mater. These two layers are separated by
diameter/body weight ratio, with a normal value around CSF, and this space communicates with the intracranial
0.21 mm/kg. The mean height and width of the optic subarachnoid space.
chiasm (0.2T) is 2.1 +/− 0.08 mm and 4.8 +/− 0.16 mm, • Dogs with intracranial hypertension may have an
respectively.13 increased value of the ratio between the intraorbital optic
nerve sheath diameter (measured on transverse T2W
Olfactory nerves (I) images) and body weight.12
• The olfactory nerves consist of small separate bundles of • MRI of the optic nerves may be indicated in cases of vision
nerve fibers that pass from the olfactory mucosa to the loss with lack of significant ocular lesions and a normal
olfactory bulbs at the rostral aspect of the telencepha- electroretinogram, which indicate a process located any-
lon and, as such, are not identified individually on MR where along the afferent visual pathway (postretinal blind-
images.1,2 ness).17 Any lesion causing a mass effect on, or invasion
into, the visual pathways can cause postretinal blindness;
Contrast enhancement examples include orbital or rostral intracranial meningio-
• In normal dogs, mild contrast enhancement of the tri- mas, pituitary tumors (especially in cats), or nasal tumors
geminal nerve ganglion is typically seen. In most dogs, invading the cranial cavity through the cribriform plate.
contrast enhancement of the trigeminal nerve itself is Optic neuritis is another potential cause.17
also seen. The degree of enhancement is typically less
than that of the pituitary gland, or equal to it in some Optic neuritis
dogs.1,14 The enhancement may be due to an incomplete • Optic neuritis is an inflammation of the optic nerve lead-
blood–nerve barrier for this particular nerve, as has been ing to primary demyelination, and typically manifests as
shown in other species like the rabbit.15 a visual deficit.18
334 CHAPTER 5.10
• Optic neuritis may occur secondary to granulomatous progress to develop, disseminated central nervous system
meningoencephalitis (GME), necrotizing leukoencepha- lesions.21 Involvement of the optic nerves and chiasm in
litis/meningoencephalitis, infectious encephalomyelitis GME can be part of the disseminated or the ocular form
(viral, bacterial, fungal, rickettsial, protozoal, and para- of the disease.20,22
sitic), toxic, or neoplastic processes.18,19 Spread of infec- • MRI features of optic neuritis include uni- or bilateral
tion or inflammation from the eye and orbit can also enhancement of the optic nerves and chiasm after gado-
sometimes involve the optic nerves, including extraocu- linium injection, with or without enlargement of the
lar or masticatory myositis, Toxoplasma gondii infection, optic chiasm (Fig. 5.10.3).18,22
Hepatozoon canis infection, and fungal infection (crypto-
coccosis, blastomycosis, histoplasmosis). In cats, spread Optic nerve neoplasia
from orbital and nasal cavity infection, feline infectious • Retrobulbar meningioma is a common nervous system
peritonitis (FIP), toxoplasmosis, and mycoses can also tumor that arises from the meninges covering the optic
cause optic neuritis.20 nerve within the orbit.23 The mass is typically T2 hyper-
• GME is an inflammatory condition of unknown etiol- intense, T1 isointense, and strongly enhancing after gad-
ogy, although an autoimmune disorder or delayed type olinium administration (see Fig. 6.2.15). Occasionally
hypersensitivity reaction is suspected.20 The condi- the optic nerve may be seen within the mass surrounded
tion has three presentations: disseminated, focal mass, by neoplastic tissue (Fig. 5.10.4). The mass often
or ocular.21 In the ocular form, there is acute onset of deforms the caudal aspect of the globe and causes rostral
visual impairment, variable pupillary changes, variable displacement of the eye. It may extend through the optic
degrees of optic disc edema, and occasionally chorioreti- canal into the cranial cavity.23
nitis. Dogs with ocular GME may concurrently have, or • Other tumors affecting the optic nerves, chiasm, or
sheath include peripheral nerve sheath tumors,24 lym-
phoma,25 and glial cell tumors.26,27
IDIOPATHIC OCULOMOTOR NEUROPATHY
• Although the oculomotor nerve is usually affected

concurrently with the trochlear (IV), ophthalmic
branch of trigeminal (V), and abducens (VI) nerves
by space-occupying lesions in the area around the
pituitary fossa (‘cavernous sinus syndrome’, described
below), isolated idiopathic oculomotor neuropathy has
been reported.11
• Clinical signs include unilateral areflexive mydriasis
(internal ophthalmoplegia), a smaller palpebral fissure
due to ptosis, neuromuscular dorsolateral strabismus,
and external ophthalmoparesis (decreased adduction of
the affected eye when testing physiologic nystagmus
[‘vestibulo-ocular reflex’]).
• The condition has been reported in adult dogs, with no
sex predilection and in a variety of breeds, such as Boxers
and Border Collies.
• MRI features of the condition include (Fig. 5.10.5; see
also Fig. 4.1.6):11
• Mild to marked enlargement of the affected oculo-
motor nerve at the level of the middle cranial fossa,
lateral to the pituitary gland, occasionally extending
Fig. 5.10.3 Transverse T1W post-contrast image in a 7-year- rostrally into the orbital fissure.
old Pomeranian with left optic neuritis. Hyperintensity of the • Signal intensity is variable, but typically iso- to
left optic nerve and optic chiasm and thickening are present, hyperintense to gray matter on T2W images (less
consistent with unilateral optic neuritis (arrow). (1.5T MRI commonly T2 hypointense), isointense on T1W
system; reproduced, with permission, from Armour MD, pre-contrast images, and iso-, hypo-, or hyperintense
Broome M, Dell’Anna G et al. (2011). A review of orbital and on T2-FLAIR images, with mild to marked enhance-
intracranial magnetic resonance imaging in 79 canine and 13 ment on T1W post-contrast images; occasionally,
feline patients (2004–2010). Vet Ophthalmol 14(4):215–26.) contrast enhancement may be absent, especially
(a) (b)
Fig. 5.10.4 Dorsal T1W post-contrast with fat saturation (a) and transverse T1W post-contrast (b) images at the level of
the orbit in a 9-year-old Cocker Spaniel with a left optic nerve meningioma. An elongated, enhancing, somewhat lobulated
mass extending from the opening of the optic canal to the caudal aspect of the globe is seen (arrows, a), causing flattening/
indentation of the caudal aspect of the globe and mild focal thickening/protrusion at the level of the optic disc of the left
retina (arrowhead, a). On the transverse image, the cross section of the optic nerve is seen (arrow, b) surrounded by enhancing
meningeal neoplastic tissue. (1.5T MRI system)
in cases where enlargement of the affected nerve is • The main clinical manifestation of idiopathic trigemi-
not clear. Contrast enhancement is more commonly nal neuropathy is an acute onset of ‘dropped jaw’ due
focal but can be diffuse. to an inability to close the mouth, with no other signs
• Clinical and MRI signs may improve over time, of systemic disease or other cranial nerve deficits.28
although they remain stable and non-progressive in Concurrent sensory deficits in the territory innervated
most patients. In cases with marked nerve enlarge- by the trigeminal nerve may be seen, such as decreased
ment confusion with a neoplasm is possible.11 facial and corneal sensation.28 In some cases it may be
associated with Horner’s syndrome, due to involve-
TRIGEMINAL NERVE DISEASES ment of the postganglionic sympathetic fibers running
together with the ophthalmic branch of the trigeminal
Idiopathic trigeminal neuropathy nerve.14 Enophthalmia and decreased lacrimation with
• Idiopathic trigeminal neuropathy is the most com- corneal ulceration may also be seen.32 Concurrent deficits
mon cause of ‘dropped jaw syndrome’ in dogs, result- associated with the facial nerve (VII) can be present.28
ing from flaccid paralysis of the muscles innervated by Clinically appreciable muscle atrophy of the temporalis
the mandibular branch of the trigeminal nerve.28 Other and masseter muscles may be present, although less com-
terms used to refer to this condition include ‘trigemi- mon than with neoplastic conditions,28 and may be bilat-
nal neuropathy’, ‘trigeminal neuritis’, or ‘trigeminal eral or unilateral.28,32,33
neurapraxia’.28 • The etiology of the condition is not clear, and histopath-
• Differential diagnoses for a ‘dropped jaw’ include neo- ologic data are scarce due to the self-limiting nature of
plastic infiltration involving both trigeminal nerves, the condition; a few studies report inflammatory changes
such as lymphoma29 or myelomonocytic leukemia,30,31 such as lymphohistiocytic ganglioneuritis or suppurative
and infectious conditions such as rabies.28 neuritis.32,33
336 CHAPTER 5.10
(a) (b)
(c) (d)
Fig. 5.10.5 Transverse MR images obtained at the level of the pituitary gland (asterisk, c) in a 6-year-old male neutered Beagle
presented with internal ophthalmoplegia and external ophthalmoparesis of the right eye. There is marked enlargement of
the right oculomotor nerve with isointensity on T2W (arrow, a), hypointensity on T2-FLAIR (arrow, b), and isointensity on
T1W pre-contrast (arrow, c) with marked focal homogeneous enhancement following contrast administration (arrow, d).
(Reproduced, with permission, from Tetas Pont R, Freeman C, Dennis R et al. (2017). Clinical and magnetic resonance imaging
features of idiopathic oculomotor neuropathy in 14 dogs. Vet Radiol Ultrasound 58(3):334–43.)
• MRI features of trigeminal neuritis include (Fig. 5.10.6): Trigeminal nerve sheath tumors
• Diffuse enlargement of the trigeminal nerve within • While other types of neoplastic involvement of the
the calvarium and trigeminal canal. trigeminal nerves, such as lymphoma and myelo-
• Affected nerves are isointense on T1W images, iso- monocytic leukemia, have been reported, 28–31 nerve
to hyperintense on T2W images, and have homoge- sheath tumors (schwannoma, neurofibroma) are most
neous or heterogeneous contrast enhancement after common.34
gadolinium injection.32 • Clinical presentation is typically chronic, with clinical
• Concurrent atrophy of the masticatory muscles may signs reflecting unilateral dysfunction of the trigemi-
be present. nal nerve, including unilateral atrophy of the temporalis
*
#
+
(a) (b)
Fig. 5.10.6 Transverse T2W image at the level of the frontal

* lobes (a) and transverse T2W (b) and T1W post-contrast
(c) images at the level of the midbrain in a 9-year-old
Labrador Retriever with unilateral (right-sided) trigeminal
neuropathy. In (a), there is atrophy of the right temporalis
(*), masseter (#), and pterygoid muscles (+) with ill-defined
internal T2 hyperintensities, consistent with denervation.
In (b), mild T2 hyperintensity of the right trigeminal nerve
(dashed arrow) compared with the left (solid arrow) is noted.
The corresponding T1W post-contrast image (c) shows
marked contrast enhancement of the right trigeminal nerve
(dashed arrow) compared with the left (solid arrow). Mild
enhancement of the left trigeminal nerve is physiologic.
(c) (1.5T MRI system)
and masseter muscles, reduced facial sensation, absent • In most cases, multiple branches of the trigeminal
palpebral reflex with normal menace response, reduced nerve are involved simultaneously, with the mandib-
corneal sensation, and corneal ulceration. Signs of dys- ular and maxillary branches being most commonly
function of other areas of the nervous system, such as affected.37
hemiparesis, forebrain signs etc., are typically the result • Distortion of the associated brainstem may be seen.32,34,36
of expansion of the mass causing subsequent damage to • The neoplastic mass is commonly isointense on T1W
adjacent brain structures.34,35 images and iso- to hyperintense on T2W images, and
• MRI features of trigeminal nerve sheath tumors include most commonly homogeneously enhances, although
(Fig. 5.10.7): heterogeneous enhancement is possible.32,34,36
• Extra-axial mass on the ventral aspect of the cranial • Unilateral atrophy of the masticatory muscles inner-
vault in the anatomic location of the trigeminal nerve vated by the mandibular branch of the trigeminal
in either the middle or caudal fossa.32,34,36 nerve (temporalis, masseter, and pterygoid muscles) on
338 CHAPTER 5.10
(a) (b)
Fig. 5.10.7 Transverse T2W (a) and T1W post-contrast (b) images in an 11-year-old dog with a left-sided trigeminal nerve
sheath tumor. There is a large, ventrolateral, broad-based, T2 hyperintense and strongly enhancing mass associated with the
origin of the left trigeminal nerve (solid arrows, a), with marked muscle atrophy of the left temporalis muscle (arrowhead, a)
and areas of muscle hyperintensity (denervation atrophy). There is also some T2 hyperintense and mildly T1 hyperintense
material in the left tympanic bulla (dashed arrow, a) consistent with fluid accumulation secondary to denervation of the tensor
veli palatini muscle. (1.5T MRI system)
the same side as the mass lesion, with areas of hyper- of fluid and development of effusion in the bulla.38,39
intensity on T1W and T2W images consistent with Tympanic cavity effusion can be seen in 33% to 63%
denervation muscle atrophy.32 Denervation causes a of affected dogs.38,41
reduction in muscle mass and replacement by fatty
tissue, explaining the hyperintensity on T1W and CAVERNOUS SINUS SYNDROME
T2W and decreased volume of the affected muscles.
These atrophied muscles can have some degree of • Isolated conditions of the oculomotor (III), trochlear
contrast enhancement after gadolinium injection.38 (IV), and abducens (VI) nerves are very rare. More typi-
• Presence of fluid in the ipsilateral tympanic bulla (T2 cally, concurrent involvement of these nerves is observed
hyperintense and of variable T1 signal intensity), with when a space-occupying lesion affecting the area around
or without enhancement of the lining of the tympanic the pituitary fossa (cavernous sinus) is present.19
bulla after gadolinium injection.38–41 This is due to • The cavernous sinuses are paired channels lying on the
dysfunction of the auditory (Eustachian) tube that floor of the cranial cavity, providing venous drainage for
connects the tympanic cavity to the nasopharynx. In the orbit and brain.42 They extend from the tympano-
the context of trigeminal nerve neoplasia, this dys- occipital fissure to the orbital fissure, and flank the pitu-
function is due to paralysis of the tensor veli palatini itary fossa and dorsum sellae. They communicate rostrally
muscle, which is innervated by a nerve of the mandib- with the ophthalmic plexus through the orbital fissures
ular branch of the trigeminal nerve. This muscle con- and caudally with the ventral petrosal sinuses through
trols opening of the nasopharyngeal orifice during the petro-occipital foramina.42 In the dog, the internal
swallowing, which normally allows pressure equaliza- carotid artery as well as cranial nerves III, IV, ophthal-
tion between the tympanic bulla and the atmosphere, mic branch of V, and VI travel through the sinus and
as well as drainage of secretions created by the epithe- exit together rostrally through the orbital fissure. A por-
lial lining of the tympanic cavity and auditory tube. tion of the maxillary branch of V also travels with these
The lack of opening of the nasopharyngeal orifice of structures before it exits through the foramen rotundum.42
the auditory tube causes negative pressure to build Lesions involving this anatomic area may therefore pro-
up in the tympanic cavity, resulting in transudation duce a variety of clinical signs corresponding to deficits
of these nerves and are collectively known as ‘cavernous for the maxillary branch of V travel, can cause similar
sinus syndrome’.42–47 clinical signs,43 and therefore MRI is an important tool
• Because cranial nerves III, IV, and VI provide innervation to establish the cause.
to the extraocular muscles and the parasympathetic effer- • The most common cause of cavernous sinus syndrome is
ent fibers of cranial nerve III are responsible for pupillary neoplastic infiltration of the cavernous sinus; examples
constriction (Fig. 5.10.1), the most common clinical man- include meningioma, lymphoma, metastatic carcinoma,
ifestations of cavernous sinus syndrome include external pituitary tumors, germ cell tumors, glial cell tumors,
and internal ophthalmoparesis/ophthalmoplegia, mydria- primitive neuroectodermal tumor, and retropharyngeal
sis (with no direct or consensual pupillary light reflex), neuroendocrine tumors invading the base of the skull
and ptosis. Vision is usually unaffected. Involvement of through the internal carotid sheath.45–47 Trauma, vas-
the ophthalmic and maxillary branches of the trigeminal cular anomalies,42 and inflammatory (infectious or non-
nerve (V) can cause sensory deficits including reduced or infectious) diseases (e.g., cryptococcosis, FIP) can also be
absent corneal sensation and periorbital/nasofacial hypal- considered.47
gesia. Because postganglionic sympathetic fibers also lie • MRI features of lesions associated with cavernous sinus
in close proximity to the cavernous sinus, there can also syndrome are variable depending on the etiology of the
be signs of oculosympathetic denervation (Horner’s syn- condition, but commonly include a mass invading into at
drome).46 The signs can be unilateral or bilateral, depend- least one of the cavernous sinuses on the floor of the cra-
ing on the extent and localization of the primary disorder nial cavity around the pituitary fossa, of variable signal
causing infiltration of the cavernous sinuses.46 intensity and contrast enhancement, and with variable
• Disease processes that involve the retro-orbital space or types and degrees of involvement of extrasinusal struc-
orbital fissure, through which all of these nerves except tures (Fig. 5.10.8).46
(a) (b)
Fig. 5.10.8 Transverse T1W post-contrast images at the level of the pituitary gland (a) and more rostrally at the level of the
orbital fissure (b) in a 7-year-old Boxer with absent direct and consensual pupillary light reflex in the left eye, left eye ptosis,
ophthalmoparesis, and left-sided mydriasis consistent with a left-sided cavernous sinus syndrome. There is a large suprasellar
neoplasm (solid white arrows, a) that extends along the floor of the cranial cavity on the left thereby impinging onto the area
of the left cavernous sinus and causing dorsal displacement of the left internal carotid artery (solid black arrow, a) compared
with the right (dashed arrow, a). More rostrally (b), enhancing neoplastic tissue is seen extending into the left orbital fissure
(solid arrow) compared with the right (dashed arrow); the rostral margin of the suprasellar mass remains visible at this level
(arrowhead). (1.5T MRI system)
340 CHAPTER 5.10
FACIAL NERVE DISEASES Other conditions affecting the facial nerve include otitis
media/interna and idiopathic facial paralysis.
• The facial nerve emerges from the cranial cavity through
the internal acoustic meatus together with the vestibulo- Facial nerve paralysis secondary
cochlear nerve. After a short distance, it enters the facial to otitis media/interna
canal of the petrous temporal bone; it then bends at the • Due to the close association of the facial nerve with the
level of the geniculate ganglion. At this point, the major middle/inner ear, it is not uncommon for the facial nerve
petrosal nerve branches off and runs rostroventrally in to be involved in patients with otitis media/interna, with
the petrosal canal. The nerve opens into the cavity of the inflammatory changes extending to the nerve (see also
middle ear, and continues in the S-shaped facial canal Chapter 6.3).35
to finally emerge from the stylomastoid foramen located • Signs associated with the primary condition of the middle/
caudal to the external acoustic meatus, at the dorsocau- inner ear will be present (see below, “Vestibulocochlear
dolateral aspect of the tympanic bulla.48 nerve diseases”), and abnormal post-contrast enhance-
• Clinical signs due to dysfunction of the facial nerve ment of the facial nerve may be seen, immediately dorsal
include impairment of the facial muscles, causing to the cochlea on transverse images (Fig. 5.10.9).
drooping of the ear and corner of the mouth, drool-
ing of saliva, and impaired closure of the eyelids; Idiopathic facial paralysis
decreased eyelid closure and tear production (parasym- • In the absence of otitis media, idiopathic facial neu-
pathetic dysfunction) can lead to corneal dryness and ropathy is the most common cause of peripheral facial
ulceration.48 nerve paralysis in dogs.48 It is usually acute in onset and
• The facial nerve, due to its area of origin (Fig. 5.10.1), unilateral.35
can be secondarily affected by space-occupying lesions • The pathophysiology of the condition is not clear, but
of the cerebellopontine angle, such as meningiomas or studies found Wallerian degeneration characterized by
other mass lesions. The vestibulocochlear nerve is often active demyelination of the larger diameter fibers and
concurrently affected due to its anatomic proximity. Schwann cell proliferation.48
(a) (b)
Fig. 5.10.9 Transverse T1W pre- (a) and post-contrast (b) images at the level of the facial canals in a 6-year-old Bulldog with
right-sided facial paralysis (facial neuropathy) and head tilt (peripheral vestibular syndrome). The patient had otitis media and
interna. On these images, hyperintense material is seen in the right tympanic bulla (arrowhead, a), with enhancement of the
lining of the bulla on post-contrast image (arrowhead, b), consistent with otitis media. There is also significant enhancement
of the right facial nerve (solid arrows) compared with the left (dashed arrows), consistent with right facial neuritis secondary to
otitis media. (See Fig. 5.10.10 for images at the level of the vestibules in the same dog.) (1.5T MRI system)
• MRI features of idiopathic facial paralysis include: disorder’, which includes head tilt (in the direction of the
• Abnormal enhancement of the intratemporal facial lesion), horizontal or rotary nystagmus, falling, rolling,
nerve, involving all segments or only portions of it;48 and ataxia.16,51 With central vestibular disorders, which
volumetric interpolated breath-hold examination affect the brainstem vestibular nuclei, additional signs
pulse sequences have been shown to be more sensitive such as abnormal mental status, ipsilateral paresis, and
and specific than regular T1W spin echo sequences conscious proprioceptive deficits are present.51
to detect abnormal enhancement of the facial nerve in • Diseases causing central vestibular disorders are dis-
dogs with idiopathic facial neuropathy.49 cussed in other chapters of this book. MRI is warranted
• Absence of concurrent abnormality affecting the ipsi- in patients with clinical signs of peripheral vestibular
lateral cerebellopontine angle or middle/inner ear. disease, to determine the etiology of the condition, plan
• Absence of MRI abnormality of the facial nerve is also treatment, and establish prognosis.
possible.48 • The most common diseases causing peripheral vestibular
• Some authors suggested that absence of contrast disorder include otitis media/interna, middle ear neopla-
enhancement of the facial nerve on MRI in dogs with sia, idiopathic peripheral vestibular disease, and, less com-
a clinical diagnosis of idiopathic facial neuropathy monly, cerebellopontine angle space-occupying lesions.51
could predict a better chance of clinical recovery; • MRI features of otitis media include (see also Chapter 6.3):
however, the number of patients was very small and • T2 hyperintense/T1 isointense material filling the
this conclusion should be interpreted with caution.48 lumen of the tympanic bulla.51
• Others suggested that enhancement of the affected • Post-contrast enhancement of the lining of the
nerve may be due to some degree of inflammatory affected tympanic bulla.51
changes in the earlier stages of the disease (although • Absence of bony abnormality, or sclerosis/thicken-
this was not demonstrated histopathologically), and that ing of the wall of the bulla appearing hypointense on
lack of enhancement may represent later stages of the T1W and T2W images.
condition, where inflammation has subsided and only • Possible T2 hyperintensity in the area of the ipsilat-
residual changes (e.g., loss of nerve fibers) are present.49 eral vestibular nerve.
• MRI features of otitis interna include (see also
Facial and vestibular neuropathy Chapter 6.3):51,52
of unknown origin • Concurrent signs of otitis media described above.
• Concomitant facial and vestibular neuropathy of • Loss of the normally markedly T2 hyperintense
unknown origin has been reported.50 signal of fluid in the vestibule of the inner ear, which
• Affected dogs are middle-aged and present with acute typically form a ‘duck-shaped’ pattern on transverse
onset of facial paralysis and peripheral vestibular syn- images.7 This can be caused by fibrous obliteration
drome. CSF analysis often shows increased total protein of the fluid-containing spaces of the inner ear in the
with normal cell count. No infectious etiology is identi- chronic phase of inflammation. In the less chronic
fied, and clinical signs of facial paralysis and peripheral phase, there can be normal or decreased signal on
vestibular syndrome may resolve or persist, indepen- T2W images due to changes in composition of the
dently from each other. fluid and/or early fibrous proliferation; lack of sup-
• MRI features are similar to those seen with idiopathic pression of the bright T2-signal on T2-FLAIR images
facial paralysis described above, including possible can indicate changes in composition of the fluid in
enhancement of the affected facial nerve especially at the inner ear secondary to inflammatory changes
high-field (1.5T) and no abnormality of the ipsilateral (Fig. 5.10.10).
vestibulocochlear nerve.50 • Possible ill-defined enhancement of the petrous
portion of the temporal bone on post-contrast images.
VESTIBULOCOCHLEAR NERVE DISEASES • Possible T2 hyperintensity in the area of the ipsilat-
eral vestibular nerve.
• The vestibulocochlear nerve has a vestibular part, respon- • MRI features of middle ear neoplasia include material
sible for sensory information for maintenance of balance of variable signal intensity and variable patterns/degrees
and orientation of the head with respect to gravity, and a of contrast enhancement in the lumen of the bulla, with
cochlear part, responsible for hearing. It originates from destruction of the wall of the bulla and local invasion
the pons, together with the facial nerve, and passes with into adjacent structures.51
it through the internal acoustic meatus to reach the inner • In cases of idiopathic peripheral vestibular disease, no
ear. Due to the anatomic proximity between these two abnormality is seen.
nerves, disease processes affecting the vestibulocochlear • In cases of cerebellopontine masses, an extra-axial
nerve commonly also affect the facial nerve.16 mass in the cerebellopontine angle is noted, of variable
• Conditions affecting specifically the inner ear, ves- signal intensity and contrast enhancement depending on
tibular ganglion, or nerve cause a ‘peripheral vestibular histopathologic nature (see Chapter 5.4).
342 CHAPTER 5.10
(a) (b)
Fig. 5.10.10 Transverse T2W (a) and T2-FLAIR (b) images at the level of the vestibules of the inner ear in the same dog as in
Fig. 5.10.9. On these images, hyperintense material is seen in the right tympanic bulla (white arrowheads), with hyperintensity
of the lining of the bulla, consistent with otitis media; the origin of each vestibulocochlear nerve is visible (black arrowheads, a)
and does not show significant abnormality. In (a), the ‘duck-shaped’ T2 hyperintense signal of fluid in the right (solid arrows)
and left (dashed arrows) vestibules of the inner ears is visible; however, in (b), the fluid signal is not suppressed in the right
vestibule (solid arrows) as it is in the normal left vestibule (dashed arrows). This indicates changes in the composition of the
fluid in the canals, consistent with otitis interna. (1.5T MRI system)
REFERENCES after surgical and medical treatment of otogenic intracranial

1. Couturier L, Degueurce C, Ruel Y et al. (2005). Anatomical infection in 11 cats and 4 dogs. J Vet Intern Med 20(3):648–56.
study of cranial nerve emergence and skull foramina in 9. Probst A, Kneissl S (2006). Computed tomographic anatomy
the dog using magnetic resonance imaging and computed of the canine temporal bone. Anat Histol Embryol 35(1):19–22.
tomography. Vet Radiol Ultrasound 46(5):375–83. 10. Wolf D, Lupke M, Wefstaedt P et al. (2011). Optimising
magnetic resonance image quality of the ear in healthy dogs.
2. Gomes E, Degueurce C, Ruel Y et al. (2009). Anatomic
Acta Vet Hung 59(1):53–68.
study of cranial nerve emergence and associated skull
11. Tetas Pont R, Freeman C, Dennis R et al. (2017). Clinical and
foramina in cats using CT and MRI. Vet Radiol Ultrasound
magnetic resonance imaging features of idiopathic oculomotor
50(4):398–403.
neuropathy in 14 dogs. Vet Radiol Ultrasound 58(3):334–43.
3. Chavhan GB, Babyn PS, Jankharia BG et al. (2008). Steady-
12. Scrivani PV, Fletcher DJ, Cooley SD et al. (2013). T2-weighted
state MR imaging sequences: physics, classification, and
magnetic resonance imaging measurements of optic nerve
clinical applications. Radiographics 28(4):1147–60.
sheath diameter in dogs with and without presumed intracranial
4. Sheth S, Branstetter BFt, Escott EJ (2009). Appearance of hypertension. Vet Radiol Ultrasound 54(3):263–70.
normal cranial nerves on steady-state free precession MR 13. Boroffka SA, Gorig C, Auriemma E et al. (2008). Magnetic
images. Radiographics 29(4):1045–55. resonance imaging of the canine optic nerve. Vet Radiol
5. Kneissl S, Probst A (2006). Magnetic resonance imaging Ultrasound 49(6):540–4.
features of presumed normal head and neck lymph nodes in 14. Pettigrew R, Rylander H, Schwarz T (2009). Magnetic
dogs. Vet Radiol Ultrasound 47(6):538–41. resonance imaging contrast enhancement of the trigeminal
6. Garosi LS, Dennis R, Schwarz T (2003). Review of diagnostic nerve in dogs without evidence of trigeminal neuropathy.
imaging of ear diseases in the dog and cat. Vet Radiol Vet Radiol Ultrasound 50(3):276–8.
Ultrasound 44(2):137–46. 15. Cooper JJ, Young BD, Hoffman A et al. (2010). Intracranial
7. Lamb CR, Garosi L (2000). Two little ducks went swimming magnetic resonance imaging artifacts and pseudolesions in
one day. Vet Radiol Ultrasound 41(3):292. dogs and cats. Vet Radiol Ultrasound 51(6):587–95.
8. Sturges BK, Dickinson PJ, Kortz GD et al. (2006). Clinical 16. Parry AT, Volk HA (2011). Imaging the cranial nerves.
signs, magnetic resonance imaging features, and outcome Vet Radiol Ultrasound 52(1 Suppl 1):S32–41.
17. Seruca C, Rodenas S, Leiva M et al. (2010). Acute postretinal 35. Penderis J (2003). Common cranial nerve disorders in dogs
blindness: ophthalmologic, neurologic, and magnetic and cats – 2. CN V and CN VII. In Practice 25:256–63.
resonance imaging findings in dogs and cats (seven cases). 36. Saunders JH, Poncelet L, Clercx C et al. (1998). Probable
Vet Ophthalmol 13(5):307–14. trigeminal nerve schwannoma in a dog. Vet Radiol Ultrasound
18. Armour MD, Broome M, Dell’Anna G et al. (2011). A review 39(6):539–42.
of orbital and intracranial magnetic resonance imaging in 79 37. Swift KE, McGrath S, Nolan MW et al. (2017). Clinical and
canine and 13 feline patients (2004–2010). Vet Ophthalmol imaging findings, treatments, and outcomes in 27 dogs with
14(4):215–26. imaging diagnosed trigeminal nerve sheath tumors: a multi-
19. Penderis J (2003). Common cranial nerve disorders in dogs center study. Vet Radiol Ultrasound 58(6):679–89.
and cats – 1. CN I to IV and CN VI. In Practice 25:178–89. 38. Kent M, Glass EN, de Lahunta A et al. (2013). Prevalence of
20. Nell B (2008). Optic neuritis in dogs and cats. Vet Clin North effusion in the tympanic cavity in dogs with dysfunction of
Am Small Anim Pract 38(2):403–15, viii. the trigeminal nerve: 18 cases (2004–2013). J Vet Intern Med
21. Talarico LR, Schatzberg SJ (2010). Idiopathic granulomatous 27(5):1153–8.
and necrotising inflammatory disorders of the canine central 39. Kent M, Talarico LR, Glass EN et al. (2015). Denervation of
nervous system: a review and future perspectives. J Small Anim the tensor veli palatini muscle and effusion in the tympanic
Pract 51(3):138–49. cavity. J Am Anim Hosp Assoc 51(6):424–8.
22. Kitagawa M, Okada M, Watari T et al. (2009). Ocular 40. Owen MC, Lamb CR, Lu D et al. (2004). Material in the
granulomatous meningoencephalomyelitis in a dog: magnetic middle ear of dogs having magnetic resonance imaging
resonance images and clinical findings. J Vet Med Sci for investigation of neurologic signs. Vet Radiol Ultrasound
71(2):233–7. 45(2):149–55.
23. Regan DP, Kent M, Mathes R et al. (2011). Clinicopathologic 41. Wessmann A, Hennessey A, Goncalves R et al. (2013). The
findings in a dog with a retrobulbar meningioma. J Vet Diagn association of middle ear effusion with trigeminal nerve mass
Invest 23(4):857–62. lesions in dogs. Vet Rec 173(18):449.
24. Haak CE, Breshears MA, Lackner PA (2007). What is 42. Tidwell AS, Ross LA, Kleine LJ (1997). Computed
your diagnosis? Retrobulbar neoplasia. J Am Vet Med Assoc tomography and magnetic resonance imaging of cavernous
231(6):863–4. sinus enlargement in a dog with unilateral exophthalmos.
25. Nagel C, Silver T, Grahn B (2013). Optic chiasm B-cell Vet Radiol Ultrasound 38(5):363–70.
lymphoma in a 20-month-old Mastiff dog. Vet Ophthalmol 43. Durden AC, Kent M, Platt SR (2011). What is your
16(Suppl 1):164–7. neurologic diagnosis? Orbital lymphoma of the T-cell origin.
26. Naranjo C, Schobert C, Dubielzig R (2008). Canine ocular J Am Vet Med Assoc 239(3):303–5.
gliomas: a retrospective study. Vet Ophthalmol 11(6):356–62. 44. Fransson B, Kippenes H, Silver GE et al. (2000). Magnetic
27. Siso S, Lorenzo V, Ferrer I et al. (2003). An anaplastic resonance diagnosis: cavernous sinus syndrome in a dog.
astrocytoma (optic chiasmatic-hypothalamic glioma) in a dog. Vet Radiol Ultrasound 41(6):536–8.
Vet Pathol 40(5):567–9. 45. Guevar J, Gutierrez-Quintana R, Peplinski G et al. (2014).
28. Mayhew PD, Bush WW, Glass EN (2002). Trigeminal Cavernous sinus syndrome secondary to intracranial
neuropathy in dogs: a retrospective study of 29 cases lymphoma in a cat. J Feline Med Surg 16(6):513–6.
(1991–2000). J Am Anim Hosp Assoc 38(3):262–70. 46. Rossmeisl JH Jr., Higgins MA, Inzana KD et al. (2005).
29. Pfaff AM, March PA, Fishman C (2000). Acute bilateral Bilateral cavernous sinus syndrome in dogs: 6 cases
trigeminal neuropathy associated with nervous system (1999–2004). J Am Vet Med Assoc 226(7):1105–11.
lymphosarcoma in a dog. J Am Anim Hosp Assoc 36(1):57–61. 47. Theisen SK, Podell M, Schneider T et al. (1996).
30. Carpenter JL, King NW Jr., Abrams KL (1987). Bilateral A retrospective study of cavernous sinus syndrome in 4 dogs
trigeminal nerve paralysis and Horner’s syndrome associated and 8 cats. J Vet Intern Med 10(2):65–71.
with myelomonocytic neoplasia in a dog. J Am Vet Med Assoc 48. Varejao AS, Munoz A, Lorenzo V (2006). Magnetic resonance
191(12):1594–6. imaging of the intratemporal facial nerve in idiopathic facial
31. Christopher MM, Metz AL, Klausner J et al. (1986). Acute paralysis in the dog. Vet Radiol Ultrasound 47(4):328–33.
myelomonocytic leukemia with neurologic manifestations in 49. Smith PM, Goncalves R, McConnell JF (2012). Sensitivity
the dog. Vet Pathol 23(2):140–7. and specificity of MRI for detecting facial nerve abnormalities
32. Schultz RM, Tucker RL, Gavin PR et al. (2007). Magnetic in dogs with facial neuropathy. Vet Rec 171(14):349.
resonance imaging of acquired trigeminal nerve disorders in 50. Jeandel A, Thibaud JL, Blot S (2016). Facial and vestibular
six dogs. Vet Radiol Ultrasound 48(2):101–4. neuropathy of unknown origin in 16 dogs. J Small Anim Pract
33. Panciera RJ, Ritchey JW, Baker JE et al. (2002). Trigeminal 57(2):74–8.
and polyradiculoneuritis in a dog presenting with masticatory 51. Garosi LS, Dennis R, Penderis J et al. (2001). Results of
muscle atrophy and Horner’s syndrome. Vet Pathol 39(1): magnetic resonance imaging in dogs with vestibular disorders:
146–9. 85 cases (1996–1999). J Am Vet Med Assoc 218(3):385–91.
34. Bagley RS, Wheeler SJ, Klopp L et al. (1998). Clinical features 52. Garosi LS, Lamb CR, Targett MP (2000). MRI findings in
of trigeminal nerve-sheath tumor in 10 dogs. J Am Anim Hosp a dog with otitis media and suspected otitis interna. Vet Rec
Assoc 34(1):19–25. 146(17):501–2.
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SECTION 3
MRI OF NON-NEUROLOGICAL
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345
STRUCTURES OF THE HEAD

AND NECK
CHAPTER 6.1 Nasal cavity and frontal sinuses
CHAPTER 6.2 Eye and orbit
CHAPTER 6.3 External, middle, and inner ear
CHAPTER 6.4 Non-neurologic conditions of the head and neck

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CHAPTER 6.1
NASAL CAVITY AND FRONTAL SINUSES

Jimmy H. Saunders and 347
Susanne A. E. B. Boroffka
CONTENTS
Technical considerations ......................................................................................................................................................................................347
Anatomy, MRI anatomy, and normal variants ........................................................................................................................................................348
Nasal cavity and paranasal sinuses in carnivores ............................................................................................................................................348
Feline anatomic specificities ...........................................................................................................................................................................350
Nasal cycle ......................................................................................................................................................................................................350
Clinical features in nasal disorders .......................................................................................................................................................................350
Malformation/developmental disorders .................................................................................................................................................................350
Nasal dermoid cyst/sinus ................................................................................................................................................................................350
Nasal epidermoid cyst .....................................................................................................................................................................................350
Meningoencephalocele ....................................................................................................................................................................................351
Inflammatory non-infectious disorders .................................................................................................................................................................351
Nasal polyps ....................................................................................................................................................................................................351
Lymphoplasmacytic rhinitis ............................................................................................................................................................................352
Infectious rhinitis ..................................................................................................................................................................................................353
Fungal rhinitis: aspergillosis ...........................................................................................................................................................................353
Fungal rhinitis: cryptococcosis ........................................................................................................................................................................355
Parasitic rhinitis...............................................................................................................................................................................................355
Bacterial rhinitis...............................................................................................................................................................................................355
Foreign body rhinitis ............................................................................................................................................................................................355
Traumatic rhinitis ..................................................................................................................................................................................................356
Feline idiopathic chronic rhinitis ...........................................................................................................................................................................357
Sinonasal neoplasia ..............................................................................................................................................................................................357
References.............................................................................................................................................................................................................360
MRI is a reliable, non-invasive technique for diagnosing to those used for brain imaging. Symmetric position-
nasal pathologies.1–3 In contrast to CT, MRI allows dif- ing should be achieved, with the plane of the hard palate
ferentiation between the nasal mucosa and other soft tis- parallel to the table. Images in the transverse plane are
sues or fluid.3 This can be an advantage in distinguishing defined as perpendicular to the plane of the hard palate
pathologic conditions where the nasal cavity contains many and long axis of the patient; dorsal plane images are par-
structures of differing physical densities, even though it allel to the hard palate and sagittal plane images parallel
does not always result in a superior diagnostic capability of to the nasal septum.
MRI over CT.4 • On at least the dorsal and sagittal plane images, scan-
ning is advised from the tip of the nose back through
TECHNICAL CONSIDERATIONS the mid portion of the brain.5 These two planes are
most appropriate to determine the integrity of the crib-
• MRI of the nasal passages should be performed with riform plate in dogs with a nasal tumor or fungal infec-
the patient in sternal recumbency, using similar coils tion, such as aspergillosis. Images through the dorsal
348 CHAPTER 6.1
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plane also provide a more general view of the entire cribriform plate and nasopharynx caudally and appear
nasal passages, allowing easier characterization of the on MRI as a signal void.6
disease process.5 • The cribriform plate is a sieve-like partition between
• Images in the transverse plane allow symmetric evalu- the nasal and cranial cavities that is perforated by ~300
ation of the nasal turbinates, which is essential for the foramina (<1.5 mm in diameter) serving for the passage
diagnosis of diseases that affect the nasal region.6 of olfactory nerve bundles. The cribriform plate is not a
• MRI pulse sequences generally used for diagnosing linear flat structure as the name would imply, but a com-
pathologic abnormalities of the nasal cavity and fron- plex dome-shaped structure with its base towards the
tal sinuses are T1W spin echo before and after contrast brain and apex towards the nostrils.6 Thus, continuity
administration and T2W fast/turbo spin echo.5 and integrity of the cribriform plate are best evaluated in
the sagittal and dorsal planes.5,6
ANATOMY, MRI ANATOMY, AND • The right and left nasal passages are separated by a nasal
NORMAL VARIANTS septum (cartilaginous and membranous rostrally, osse-
ous caudally). Some curvature of the rostral aspect of the
Nasal cavity and paranasal sinuses nasal septum is commonly seen in normal animals and
in carnivores (Fig. 6.1.1) represents an incidental variation.6 The potential clinical
• The bony structure of the nasal cavity and frontal sinuses impact on nasal airflow of a curved septum and its role
consists of the incisive, nasal, maxillary, lacrimal, zygo- in the pathophysiology of some respiratory disorders,
matic, palatine, vomer, presphenoid, and ethmoid bones. such as brachycephalic airway syndrome, is still under
These bones extend from the nostrils rostrally to the investigation.7
• The rostral half of the nasal passages contains the dor-
sal and ventral nasal conchae, which are usually referred
to as ‘nasal turbinates’. The dorsal nasal turbinate is a
smooth, curved plate that arises from the nasal bone
as an extension of the first endoturbinate. The ventral
nasal turbinate is thick but short and occupies the rostral
two-thirds of the nasal cavity. It arises from the maxilla
as an extension of the second endoturbinate that breaks
1 2
3
1
4
(a) (b)
Fig. 6.1.1 Normal nasal MRI anatomy in a 2-year-old Bernese Mountain Dog. (a) Dorsal T1W post-contrast image: 1, nasal
turbinates; 2, maxillary recess. (b) Transverse T1W post-contrast image at the level of the rostral nasal cavity: 1, common nasal
meatus; 2, dorsal nasal meatus; 3, middle nasal meatus; 4, ventral nasal meatus. (Continued)
Na s a l C av i t y a n d Fron ta l Si n us e s 349
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3
1 3 1
4
2
2
5
(c) (d)
Fig. 6.1.1 (Continued) Normal nasal MRI anatomy in a 2-year-old Bernese Mountain Dog. (c) Transverse T1W post-
contrast image at the level of the middle nasal cavity: 1, nasal septum; 2, hard palate; 3, endoturbinates; 4, vomer bone; 5,
oral cavity. (d) Transverse T1W image at the level of the caudal nasal cavity: 1. endoturbinates; 2, nasopharynx; 3, cribriform
plate; 4, frontal sinus. (1T MRI system)
up to form many longitudinal scrolls, greatly enlarging • The middle nasal meatus lies between the dorsal and
the richly vascularized covering mucosa. The nasal tur- ventral nasal turbinates.
binates restrict the airflow. The caudal half of the nasal • The ventral nasal meatus is located between the
cavity is largely filled by the ethmoidal turbinates, which ventral nasal turbinate and the floor of the nasal
attach caudally to the cribriform plate and are covered by cavity.
the orbital lamina of the ethmoid bone. The ethmoidal • The common nasal meatus is a longitudinal narrow
turbinates are so extensive that they invade the lower space bounded medially by the nasal septum and lat-
part of the frontal sinuses. They are composed of four erally by the ipsilateral turbinates; it communicates
long endoturbinates (I to IV) and six small ectoturbi- with the three other meatuses.6
nates (1 to 6). The difference between the two groups • The nasopharyngeal meatus extends from the
is based on their location. Each ethmoidal element pos- dilated caudal portion of the ventral nasal meatus to
sesses a basal bony leaf, which attaches to the orbital the choana and opens into the nasal portion of the
lamina of the ethmoid bone. pharynx.6
• MRI provides good detail of the nasal turbinates because • The paranasal sinuses consist of the frontal sinuses,
of their distinct mucosal covering. They appear moder- the maxillary sinuses (or recesses), and the sphenoidal
ately intense on T1W images and hyperintense on T2W sinuses.6 All of them communicate with the nasal cavity.6
images.6 Normal turbinates are scrolled and symmetric The frontal sinuses are composed of three compartments
when observed on transverse images.6 (rostralis, medialis, lateralis), with the rostral one being
• Variations in the structure of the ethmoidal turbinates further subdivided into three parts (medialis, intermedius,
are commonly observed on MRI mainly in brachyce- lateralis), which drain separately into the nasal cavity via
phalic animals.7 the ethmoidal meatuses.6 The lateral compartment of the
• Four narrow nasal passages, the nasal meati, are present rostral frontal sinus is the largest and occupies much of
between and along the turbinates:6 the frontal bone, including the zygomatic process. The
• The dorsal nasal meatus is a passage between the frontal crest separates the right and left frontal sinuses
dorsal nasal turbinate and the dorsal wall of the nasal from each other. The air-containing frontal sinuses
cavity. appear as a signal void on MR.
350 CHAPTER 6.1
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Feline anatomic specificities • The clinical differentiation of nasal disorders is often

• The structure of the nasal conchae in cats is similar to challenging and frustrating, even using multiple diag-
the dog. The rostral half of the nasal cavity contains nostic procedures at substantial cost to the owner.11
the dorsal conchae and the short, but very thick, ventral • Chronic nasal discharge and sneezing are the most com-
conchae.8 mon clinical signs, but they lack specificity even when
• The ethmoturbinates are (more) strongly developed in considering the type and uni- or bilateral nature of the
cats compared with dogs and also invade the ventral part discharge.12 Other signs such as epistaxis (dogs > cats),
of the frontal sinuses.8 These sinuses are large cavities coughing, stertor, reverse sneezing, or concurrent neu-
that are not divided into compartments. rologic deficits help orientate the diagnosis. A thorough
• Compared with dogs, the maxillary recesses are very physical examination and, in some cases, laboratory tests
small and the sphenoidal sinuses are larger.8 may also help to refine the diagnosis.12
• Distortion of the nasal conchae associated with a mal- • However, ultimately, in most patients with chronic nasal
formation of the nasal septum and ethmoid bone occurs disease, diagnostic imaging and rhinoscopy, eventually
occasionally in cats and may be a consequence of viral combined with nasal biopsy, will be required to deter-
rhinitis at young age (see below under “Feline idiopathic mine the underlying cause of the disorder.11
chronic rhinitis”).
MALFORMATION/DEVELOPMENTAL
Nasal cycle DISORDERS
• The nasal cycle is a physiologic phenomenon that causes
variation in size of the nasal passage and change in air- Nasal dermoid cyst/sinus
flow in the nasal cavity due to cyclical congestion and • Nasal dermoid cyst/sinus is a failure of separation of
decongestion of the venous sinusoids lining the nasal the surface ectoderm (forming the epidermis) and
mucosa.9 neuroectoderm (forming the nervous system) during
• It has been described in many species, including the embryogenesis.13
dog and the cat. Possible causes for this phenomenon • Due to the topographic pattern of that separation, der-
include: moid sinuses/cysts typically occur on midline, connect-
• The need to synchronize the process of mucosal reju- ing the skin to deeper structures, and can be seen in the
venation. nasal region, cranium, and vertebral column. A tract
• Facilitation of the replacement of mucosal moisture. extending from the skin into the subcutaneous tissues is
• Opportunity for the mucosa to clean itself of con- mostly, but not always, present.14
taminants and debris on one side, while the other side • A classification of dermoid cysts into five categories and
maintains essential functions.9 three subtypes has been proposed.15
• In fact, it is still unclear if the phenomenon appears in • MRI findings include (Figs. 6.1.2, 6.1.3):16,17
all dogs and cats, as it is not observed in 20% of people.9 • Presence of a tract starting on the midline of the nasal
• In dogs and cats, the precise duration of the cycle is still plane and running along the nasal septum.
unknown but has been suggested to be between 15 min- • Signal intensity depends on the cellular content of the
utes and 6 hours. cyst and is generally hypointense on T1W images and
• On MRI, the nasal cycle results in an asymmetric nasal hyperintense on T2W images.
mucosa in the rostral part of the nasal cavity best visible • On post-contrast T1W images, there may be periph-
on T2W images.9 The asymmetry is due to unilateral eral enhancement of the cyst, allowing better delin-
vasoconstriction causing increased mucosal perfusion eation. Additionally, it may help to differentiate
in the contralateral side, resulting in signal intensity dermoid cysts (non-enhancing) from other masses
and mucosal thickening. The frontal sinuses are not such as neoplasia, typically enhancing.
involved. • A contrast-enhanced sinogram may help to better
• The normal nasal cycle may mimic the MR features define the direction of the tract.
reported with inflammatory rhinitis.9 • Intracranial extension has been reported in about
25%–30% of human patients, but has not been described
CLINICAL FEATURES IN NASAL DISORDERS in dogs. This may be due to anatomic differences of the
nasal cavity between people and dogs and to the shorter
• In dogs, sinonasal neoplasia, fungal rhinitis, and lym- anteroposterior length of the nasal cavity in humans.13
phoplasmacytic rhinitis are the most common causes of
chronic nasal disease,10,11 while neoplasia and chronic Nasal epidermoid cyst
rhinosinusitis represent two-thirds of chronic nasal dis- • Nasal epidermoid cyst has been described in brachyce-
eases in cats.12 phalic breeds.18 This cyst is a type of epithelial cyst that
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Fig. 6.1.2 Nasal dermoid cyst in an adult Shi-Tzu. Fig. 6.1.3 Nasal dermoid cyst in a 3-year-old Border Collie.
Sagittal T1W image showing a round, well-defined, mildly Transverse T2W image showing a small hyperintense ovoid
heterogeneous and hyperintense lesion (arrow) visible on lesion located in the midline of the nasal plane (arrow).
the rostrodorsal aspect of the nasal bone. (Reproduced, with It runs along the nasal septum and widens it. (0.3T MRI
permission, from Sturgeon C (2008). Nasal dermoid sinus cyst system; image courtesy of Dr. Kaatje Kromhout, Ghent
in a shih tzu. Vet Rec 163(7):219–20.) University)
has a stratified, keratinized squamous epithelium and evaluate the content of the meningoencephalocele, and
contains intraluminal breakdown products of desqua- detect additional intracranial anomalies, CT and MRI
mated epithelial cells. should be used in combination.21
• This condition can be congenital (similar to the dermoid • MRI findings include (Fig. 6.1.4):21,22
cyst described above), traumatic, or associated with a for- • Brain tissue, mainly olfactory bulb, bulging into the
eign body.18 A predominant inflammatory component, nasal cavity.
which is absent in simple epithelial cyst, is present.18 • Defect in the cribriform plate, best appreciated on
• MRI findings include:18 dorsal or sagittal plane images.
• Thin-walled cystic structure filling one of the nasal • Deformation or deviation of adjacent structures,
passages. mainly the ethmoid conchae and the nasal septum.
• The content of the cyst is hypointense on T1W • Signs of meningoencephalitis may be present (see
images and hyperintense on T2W images. Chapter 5.3).
• Moderate enhancement of the wall on post-contrast
T1W images. INFLAMMATORY NON-
INFECTIOUS DISORDERS
Meningoencephalocele
• Herniation of brain cavity content into the nasal cavity Nasal polyps
occurs through defects in the cribriform plate; they are • Nasal inflammatory polyps (also referred to as ‘inflam-
called intranasal meningoceles when only meninges are matory polyps of the nasal turbinates’ or ‘feline mesen-
herniated, or meningoencephaloceles when both cere- chymal nasal hamartoma’)23 are an uncommon cause of
bral tissue and meninges are herniated.19 nasal obstruction in young cats (6–24 months).23 Their
• The disorder is usually caused by a disturbance in sepa- precise etiopathogenesis is still unknown, even if devel-
ration of surface ectoderm (epithelial layer) and neuro- opment secondary to chronic inflammation has been
ectoderm (nervous tissue) on midline during the final suggested. Polyps within the nasal cavity are rare in dogs
phase of neural tube formation, causing displacement of and are usually unilateral.24
the normal bone tissue, allowing a herniation to occur.20 • These polyps should not be confused with nasopharyn-
The type of encephalocele depends on the location of the geal polyps. Nasal inflammatory polyps arise in the nasal
disturbance within the neural tube. passages and occasionally extend into the nasophar-
• In order to better delineate the location and extent of the ynx, while nasopharyngeal polyps originate from the
bony defect on the one hand and, on the other hand, out- Eustachian tube and can grow into the nasopharynx, the
line the connection with the intracranial compartment, middle ear, or both.23
352 CHAPTER 6.1
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(a) (b)
Fig. 6.1.4 Intranasal meningoencephalocele in a 5-month-old Border Collie. (a) Dorsal T2W spin echo image through the
ventral part of the nose. Clearly visible is the asymmetry caused by the presence of brain tissue (arrow) and the absence of the
normal bony structures in the caudal part of the right nasal passage. There is a slight deviation of the nasal septum to the left
side. The protruding brain tissue has a normal appearance. (b) Sagittal T1W image through the skull (slightly parasagittal
towards the right side). The right cerebral olfactory bulb is seen extending into the caudoventral aspect of the right nasal
passage (arrow). (Reproduced, with permission, from Martle VA, Caemaert J, Tshamala M et al. (2009). Surgical treatment of a
canine intranasal meningoencephalocele. Vet Surg 38(4):515–9.)
• MRI findings include: • Periapical infections of the maxillary teeth may result
• Intranasal soft tissue mass that replaces the normal in a purulent nasal discharge if the infection extends
turbinates (without active lysis). to the nasal mucosa.27 Recently, an association between
• The mass is hypo- to isointense on T1W and hyper- lymphoplasmacytic rhinitis and odontogenic infection
intense on T2W images (compared with the normal was reported, with 55% of the patients with rhinitis also
turbinates). having odontogenic infection. Rhinitis secondary to
• Absent or minimal contrast enhancement compared dental disease may also be due to abnormal tooth growth
with the normal nasal structures. (e.g., an impacted tooth).27
• Mineralization may be present, appearing as areas of • MRI findings in cases of lymphoplasmacytic rhinitis
signal void within the lesion. include (Fig. 6.1.5):2
• Contrary to tumors and fungal rhinitis, osteoly- • Diffuse, localized or randomly distributed lesions,
sis is rarely identified in patients with nasal polyps. more often bilateral than unilateral.
• Turbinate destruction is typically absent or mild,
Lymphoplasmacytic rhinitis while moderate turbinate destruction occurs less fre-
• Lymphoplasmacytic rhinitis, also referred to as ‘idiopathic quently.
lymphoplasmacytic rhinitis’, ‘inflammatory rhinitis’, or • Hypointense or isointense turbinates on T1W images
‘non-specific rhinitis’, is characterized microscopically compared with muscle.
by a bilateral infiltration of lymphocytes and plasma cells • Hypointense or isointense turbinates on T2W images
into the nasal mucosa, although variable numbers of neu- compared with fat.
trophils and eosinophils may also be present.25,26 Affected • Accumulation of hyperintense (compared with muscle
animals show a disruption of the mucociliary clearance on T1W and brain tissue on T2W) fluid in the nasal
system causing accumulation of secretions, mucosal concavity and/or frontal sinus.
gestion, edema, and hyperplasia, creating an ideal micro- • Mild to moderate bone lysis of the nasal boundaries
environment for bacterial proliferation.26 The underlying such as facial bones or hard palate.
etiopathogenesis of lymphoplasmacytic rhinitis has still to
be fully elucidated.25,26
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(a) (b)
Fig. 6.1.5 Lymphoplasmacytic rhinitis in a 14-year-old Jack Russell Terrier. (a) Dorsal T1W spin echo post-contrast image
showing increased bilateral nasal turbinate contrast enhancement consistent with proliferation of the mucosa (arrows).
(b) Dorsal T2W spin echo image showing hyperintense signal within the nasal turbinates (arrow) consistent with accumulation
of exudates. (0.2T MRI system; images courtesy of Prof. Michael Herrtage, University of Cambridge)
• Differential diagnosis: nasal aspergillosis may be consid- This colonization and invasion of the nasal mucosa by
ered. However, in nasal aspergillosis turbinate destruc- the fungus causes a destructive rhinitis often accom-
tion is more severe, the turbinates are hyperintense on panied by bone reaction (frontal sinus osteomyelitis),
T1W images, and lytic lesions of the bony nasal bound- presumably due to an endotoxin responsible for the
aries are more frequently present.2 turbinate necrosis. 28,29
• Cats, mostly brachycephalic, are affected by two forms of
INFECTIOUS RHINITIS upper respiratory tract aspergillosis:30
• Sinonasal aspergillosis, most often due to A. fumigatus
Fungal rhinitis: aspergillosis (quite similar to the disease in dogs).
• Sinonasal aspergillosis in dogs typically affects young • Sino-orbital aspergillosis, in which A. felis is often iso-
to middle-aged dogs with a mesati- or dolichocephalic lated.
head conformation. 28,29 This disease process is nearly • The pathogenesis of fungal infections is still poorly
always due to Aspergillus fumigatus and is character- understood.28–30 Defects of innate and adaptive immune
ized by the formation of superficial mucosal fungal mechanisms are not typically observed in sinonasal
plaques within the nasal cavity and/or frontal sinus aspergillosis.28–30 Concurrent disease or systemic immu-
in otherwise healthy animals. 28,29 The fungus does nodeficiency is not typically recognized. However, facial
not invade beneath the level of mucosal epithelium trauma, nasal foreign bodies, and dental disease are occa-
but incites a severe chronic inflammatory response. 28 sionally implicated.11,28
354 CHAPTER 6.1
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• Clinically, fungal rhinitis is characterized by a chronic • MRI findings include (Fig. 6.1.6):3,31–33
mucopurulent nasal discharge, often in dogs with nasal • Turbinate destruction, mostly severe, resulting in
pain and nasal plane ulceration and/or depigmentation, cavitation in the affected nasal cavity (variably sized
which has sometimes been present for months or even areas that are gas filled [signal void] with absence of
years.28–30 Additionally, sneezing, epistaxis (sometimes turbinate structures).
severe), decreased appetite, signs of depression, and, in • Hyperintense signal of the remaining turbinates on
severe cases, facial deformity, epiphora, and seizures may T1W images.
be observed, as well as mild mandibular lymphadenopa- • Hyperintense rim of tissue or thickened mucosal
thy.28–30 In cats with sino-orbital aspergillosis, additional lining of the inner wall of the nasal cavity and/or
ocular (keratitis, prolapse of the nictitating membrane, frontal sinuses on T2W and T1W post-contrast
conjunctival hyperemia, exophthalmos, deviation of the images.
globe) and generalized signs (fever, neurologic signs) may • Bone changes:
be observed.30 Differentiation from other chronic nasal – Thickened reactive bone, especially in the fron-
disorders, mainly nasal neoplasia, based on clinical pre- tal sinus, appears as hypointense thickening of the
sentation is challenging, highlighting the importance of bone margins (‘frontal bone sclerosis’).
diagnostic imaging.29
(a)
(b) (c)
Fig. 6.1.6 Sinonasal aspergillosis in a 2-year-old Dachshund. (a) Transverse T1W spin echo post-contrast image showing
bilateral turbinate destruction and nasal septum destruction (solid arrow) resulting in obvious nasal passage cavitation.
Contrast enhancement (dotted arrows) of the hypertrophic mucosa is present. (b) Transverse T2W spin echo image showing a
signal void (solid arrow) within the nasal cavity due to turbinate destruction and cavitation. Hyperintensity (dotted arrows) of
the hypertrophic mucosa is present. (c) Dorsal T2W spin echo image showing bilateral turbinate destruction (arrow) and nasal
septum destruction (asterisk). (1T MRI system; images courtesy of AJ van Belt, Utrecht University)
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– Destruction of thin bone structures (frontal crest, or body cavity/organ involvement (nasal + disseminated
cribriform plate, medial border of the maxillary form).
recesses), causing discontinuity and interruption • The MRI features of feline nasal cryptococcosis have
of the normal hypointense MRI signal from these not been described. Based on reported descriptions of its
structures. appearance on CT,35 expected lesions include:
• Although the MRI appearance of feline sino-orbital • Localized rhinitis with a variable amount of soft tissue
aspergillosis has not been reported, some distinctive in the nasal cavity and variable degrees of turbinate
features from the classic sinonasal form have been lysis (nasal form).
described at CT, and may also be encountered if such • Fungal masses/granulomas with severe bone erosion,
patients were to be imaged with MRI:34 possibly involving the cribriform plate.
– Orbital mass causing mass effect with exophthalmos. • Regional lymphadenopathy is usually present.
– Abnormal paranasal soft tissue thickening.
– Solid mass effect in the nasal cavity, frontal Parasitic rhinitis
sinuses, sphenoid sinuses, and nasopharynx. • Nasal parasites are rare in dogs and cats.
– Evidence of naso-orbital communication due to • Cuterebra spp. (arthropod) and Linguatula serrata (arthro-
lysis of the orbital lamina. pod) have been reported in both species. Eucoleus boehmi
– The MRI features may be similar to naso-orbital (nematode) and Pneumonyssoides caninum (arthropod) have
neoplasia. been specifically reported in dogs and Mammomonogamus
• Despite the superiority of MRI over CT for evalu- (nematode) in cats.
ation of soft tissue structures in general, it is often • In most cases, the MR examination will be unremarkable
not possible to differentiate fungal mycetomas and with a non-specific mucosal thickening.
inspissated secretions in the sinuses.3,31,32 Indeed, the
protein content of sinonasal secretions can signifi- Bacterial rhinitis
cantly affect signal intensity on both T1W and T2W • No single bacterium has been identified as a potential
images, causing various combinations of hypointense cause of primary bacterial rhinitis.
or hyperintense signals. While protein concentra- • Secondary bacterial infection is common in dogs with
tion increases, the signal intensity on T1W images chronic nasal disease and explains the transient response
will change from hypo- to hyperintense and T2 to antibiotics seen in some dogs.
signal will change from hyper- to hypointense. Once • Proliferation of bacterial organisms in dogs with chronic
the protein concentration exceeds 28%, the secre- nasal disease could result from mucus trapping and
tions become inspissated and appear hypointense on decreased nasal mucosal defense mechanisms.
both T1W and T2W images.31,33 Additionally, the • The MRI appearance has not been specifically reported,
differentiation between soft tissue and secretions but one would expect non-specific changes including
may be affected by image quality and technique. In increased fluid/soft tissue material accumulation in the
people, acquisition of T2-FLAIR images may help nasal passages, mucosal thickening and enhancement,
differentiate solid soft tissue structures from fluid and mild turbinate lysis in chronic cases.
in the sinuses and improve recognition of cribriform
plate erosion.31 Fat suppression techniques are often FOREIGN BODY RHINITIS
used in human sinonasal imaging to help delineate
soft tissue structures in the sinuses and periorbital • Foreign body rhinitis is frequent in dogs, particularly
regions.33 Whether these techniques would be useful hunting dogs, and infrequent in cats. The sneeze reflex
in dogs is unknown because of the lack of fatty tissue is in most cases an effective way of expelling foreign
in the sinuses of dogs. material from the nose. However, sometimes a foreign
body can become lodged in the nasal turbinates and
Fungal rhinitis: cryptococcosis cause local chronic inflammation, possibly accompa-
• Cryptococcosis (C. neoformans, C. gattii) is frequently iso- nied by secondary aspergillosis.28 Less frequently, for-
lated in fungal rhinitis in Australia but it has also been eign material may wind up within the nasal cavity by
reported in New Zealand and North America. Unlike entry through the nasopharyngeal meatus after being
other systemic mycoses, cryptococcosis is more common gagged or vomited, inadvertently transferring the for-
in cats than in dogs. Patients with cryptococcosis may eign material into the nasopharynx and then into the
be presented with only involvement of the nasal cavity caudal nasal cavity.
and/or nasal plane (nasal form), with a more extensive • The most commonly reported foreign bodies are wooden
nasal cavity disease and local spread (nasal + local form), sticks and grass awns in dogs, while blades of grass are
or with cutaneous tissue, ocular/central nervous system, more common than seeds or grass awns in cats.36,37
356 CHAPTER 6.1
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• The search for a nasal foreign body should start with pieces of wood may become more intense on MRI as
radiography or CT, as CT is superior for imaging for- they become soaked with fluid.
eign bodies surrounded by air, as is commonly the case • Collection of fluid or abscessation, forming focal
with nasal or paranasal sinus foreign bodies and as accumulation of material of variable intensity on T1W
MRI is contraindicated for imaging some types of for- images and hyperintense on T2W images around the
eign bodies such as metallic ones (see also Chapter 6.4). foreign body.
If radiography or CT is inconclusive, MRI may be help- • In more chronic cases, unilateral, localized turbinate
ful. If a foreign body cannot be visualized on imaging, destruction secondary to the inflammatory response.
the radiologist should look for signs associated with its
presence such as unilateral (bilateral is exceptional) focal
turbinate destruction, thickening of the remaining tur- TRAUMATIC RHINITIS
binates, regional accumulation of fluid, and mucoid exu-
date while the frontal sinuses remain unaffected. • Traumatic rhinitis is caused by depression fractures, bony
• MRI findings include (Fig. 6.1.7): sequestra, and subsequent osteomyelitis. Most fractures
• Focal signal void corresponding to the foreign body are caused by dog bites or blunt trauma (car accidents).
itself, which may be elongated or geometrically • The MRI features are related to the trauma (fracture,
shaped depending on the nature of the foreign body; sequestra, osteomyelitis) with possibly an increased
however, in chronic cases, foreign bodies such as intensity of the nasal turbinates.
(a) (b)
* Fig. 6.1.7 Stick foreign body rhinitis in a 10-year-old English

Setter. (a, b) Transverse T1W fast spin echo post-contrast
images of the same dog on different levels. A small rounded
structure (solid arrows) is observed in the left dorsal nasal
meatus. There is contrast enhancement (dotted arrows) of the
thickened mucosa of the left turbinates. A very mild amount
of turbinate destruction (open arrow) is present. (c) Sagittal
T2W fast spin echo image showing the tubular foreign object
(arrow) ending in the endoturbinates at a safe distance from
the cribriform plate (asterisk). (3T MRI system; images
(c)
courtesy of Dr. Kari L. Anderson, University of Minnesota)
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FELINE IDIOPATHIC CHRONIC RHINITIS carcinoma) or mesenchymal (e.g., chondrosarcoma) in

origin.40 In cats, lymphoma and epithelial neoplasms are
• Feline idiopathic chronic rhinitis is a common cause of the most common tumor types.40 In addition to these,
chronic rhinitis, and is seen in cats of any age, although more than 20 other malignant tumor types have been
younger cats are most often affected.38 reported in the nasal cavity, with only a few case reports
• This disorder is likely the consequence of a complex pro- of benign processes.
gression of microbial, physiologic, anatomic, genetic, • The nasal cavity and paranasal sinuses can also be sec-
and immunologic interactions combined with environ- ondarily affected by some neoplasms arising from the
mental factors (e.g., stress).38,39 face (e.g., squamous cell carcinoma of the nasal plane,
• Feline herpes virus type 1 has been suggested as an osteosarcoma, multilobular tumor of bone), which are
important pathogen factor for initiating the condition, often locally invasive and may extend into the nasal cav-
following acute viral cytolysis during a bout of acute ity. These neoplasms should be differentiated from the
severe rhinitis.39 It is then perpetuated by recurrent bac- typical ‘nasal cavity’ neoplasms because they require a
terial infection, an exuberant inflammatory response, or different treatment. Other structures included in the
permanent or cumulative destruction of nasal epithelium nasal cavity may undergo neoplastic transformation (e.g.,
and bony turbinates following chronic reactivation of the infraorbital nerve).
virus from the trigeminal ganglia into nasal tissue.39 • In dogs, sinonasal tumors seem to correlate with nasal
• Affected cats with this condition typically have a recur- length and, thus, with the amount of surface area that
rent history of chronic intermittent or progressive sneez- is exposed to environmental carcinogens. Therefore,
ing, stertor, and nasal discharge.39 Older cats may develop dolicho- and mesaticephalic dogs have a higher risk of
anorexia due to loss of smell, which may exacerbate other developing sinonasal neoplasia than open-mouth breath-
underlying disease conditions (e.g., chronic kidney, liver, ing brachycephalic dogs, which are more prone to lower
or gastrointestinal disease).39 respiratory tract disorders.
• The MRI features of feline idiopathic chronic rhinitis • Clinical manifestations of sinonasal neoplasia are similar
have not been described. Expected lesions are mucosal to fungal rhinitis, including nasal discharge, epistaxis,
edema and mucopurulent debris causing accumulation of facial deformity, and neurologic signs such as seizures in
variable amounts of soft tissue intense material, variable cases of brain invasion.
degree of turbinate and nasal, maxillary, or frontal bone • MRI features of sinonasal neoplasia have been
destruction, and presence of osseous malformations such reported,1,4,32,41 and although individual features are often
as nasal turbinate distortion and asymmetry of the crib- best seen in one plane, the use of all three imaging planes
riform plate. (Fig. 6.1.8). (transverse, dorsal, and sagittal) is recommended to give
the most complete picture of the extent of the tumor
SINONASAL NEOPLASIA • MRI findings may include (Figs. 6.1.9, 6.1.10):
• Space-occupying mass with heterogeneous signal
• Sinonasal tumors are nearly always malignant in dogs intensity replacing the nasal turbinates in nearly all
and cats and mostly arise in the caudal two-thirds of the cases.
nasal cavity. In dogs, tumors may be epithelial (adeno- • The signal characteristics of the mass lesions are var-
carcinoma, undifferentiated carcinoma, squamous cell iable:
(a) (b)
Fig. 6.1.8 Feline chronic rhinitis in a 6-year-old Burmese cat. Transverse T1W spin echo (a) and T2W turbo spin echo (b)
images showing mucosal edema and mild bilateral turbinate destruction (arrows). (1T MRI system; images courtesy of AJ van
Belt, Utrecht University)
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* *
(a) (b)
Fig. 6.1.9 Sinonasal neoplasia in an 8-year-old American

Staffordshire Terrier. (a, b) Transverse T2W images at
different levels showing a horizontal fluid level (solid arrow)
and moderate amount of fluid (dotted arrows) in the right
* frontal sinus. Replacement of the endoturbinates by a solid
mass of intermediate signal intensity (asterisks) is present.
The delineation of the brain is still visible. (c) Dorsal T1W
3D turbo spin echo post-contrast image showing a space-
occupying soft tissue mass (arrow) with heterogeneous
signal intensity replacing the nasal turbinates on the right
side and extending into the caudal aspect of the left nasal
passage. The mass has a hyperintense signal compared with
the masticatory muscle (asterisk). (1T MRI system; images
(c)
courtesy of AJ van Belt, Utrecht University)
– Mildly hyperintense (~80% of cases) or isointense • Trapped fluid in the (caudal) nasal passages and in
(~15% of cases) compared with the masticatory one or both frontal sinuses on T2W images (~60% of
muscles on T1W images. cases). Fluid can be readily differentiated from tumor
– Hyperintense (~90% of cases), isointense (~10% of tissue on MRI by its distribution (gravity dependent)
cases), rarely hypointense compared with the mas- and high signal on T2W images and by preservation
ticatory muscles on T2W images. of the turbinate bones in the affected part of the nasal
– Isointensity on T1W images combined with cavity. In the case of trapped frontal sinus fluid, thick-
hyperintensity on T2W images is more compat- ening and inflammation of the frontal sinus lining
ible with a carcinoma, while mild hyperinten- can be seen on post-contrast T1W scans, which may
sity on T1W and iso- or hypointensity on T2W represent secondary sinusitis.
images is more indicative of a sarcoma. • Destruction of the nasal septum (~70% of cases),
• On T1W post-contrast images, enhancement of the nasal, maxillary, and/or frontal bones (~50% of cases)
mass and mucosa of the remaining turbinates is mild resulting in disruption of the normal signal void of
to moderate, allowing easier identification of turbinate these bony boundaries, and replacement by neoplastic
destruction (best evaluated on transverse images). tissue with higher signal.
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(a)
(b) (c)
Fig. 6.1.10 Sinonasal neoplasia in an 8-year-old Argentinian dog. Transverse T1W 3D turbo spin echo post-contrast
(a), transverse T2W turbo spin echo (b), and dorsal T1W 3D turbo spin echo post-contrast (c) images showing a space-
occupying soft tissue mass with heterogeneous signal intensity replacing the nasal turbinates on the left side and invading the
nasopharynx and the maxillary recess (solid arrows). The mass has a hyperintense signal compared with the masticatory muscle
(asterisk, c). Secondary fluid accumulation in the left frontal sinus is present (dotted arrows). The cribriform plate is intact
(open arrow, c). (1T MRI system; images courtesy of AJ van Belt, Utrecht University)
• Extension of the tumor into the cranial cavity (~20% • Therapeutic and prognostic considerations:
of cases): – Radiation therapy planning: fluid accumulation
– Loss of the normal signal void of the cribriform without bony destruction in the frontal sinus sup-
plate, best appreciated on sagittal or dorsal plane ports the diagnosis of obstructive frontal sinusitis
images. as opposed to sinus invasion, which is important
– Meningeal (dural) hyperintensity on T2W for radiotherapy treatment planning as the gross
sequences, with corresponding meningeal tumor volume will exclude the frontal sinuses and
enhancement on T1W post-contrast images. thus decrease the overall radiotherapy treatment
– Local cerebral edema causing increase in signal volume.4
intensity of brain parenchyma in the olfactory or – Tumor extension into the caudal recesses, menin-
frontal lobes of the brain on T2W or T2-FLAIR geal hyperintensity on T2W images, and tumor
images. extension into the cranium in dogs without neuro-
– Intracranial extra-axial mass effect. logic signs at the time of diagnosis have not been
360 CHAPTER 6.1
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associated with shorter survival time in dogs with 16. Hayward N, Baines S, Mahoney P et al. (2005). Abstract
nasal tumor treated by radiation therapy.42 from the Annual Conference of the European Association
– Compared with CT, MRI provides similar infor- of Veterinary Diagnostic Imaging: MRI appearance of a
mation regarding the assessment of bony involve- nasal dermoid sinus cyst in two dogs. Vet Radiol Ultrasound
47(4):419.
ment in dogs with nasal neoplasia, but appears
17. Sturgeon C (2008). Nasal dermoid sinus cyst in a shih tzu.
to yield higher tumor measurements, leading to Vet Rec 163(7):219–20.
possible higher tumor staging.43 MRI may also 18. Murgia D, Pivetta M, Bowlt K et al. (2014). Intranasal
be more sensitive than CT to identify menin- epidermoid cyst causing upper airway obstruction in three
geal enhancement,43 and may overall provide vital brachycephalic dogs. J Small Anim Pract 55(8):431–5.
information on tumor stage, prognosis, and treat- 19. Martle VA, Caemaert J, Tshamala M et al. (2009). Surgical
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magnetic resonance imaging, computed tomographic, and Inflammatory polyps of the nasal turbinates of cats:
rhinoscopic features of nasal aspergillosis in dogs. J Am Vet an argument for designation as feline mesenchymal nasal
Med Assoc 225(11):1703–12. hamartoma. J Feline Med Surg 13(4):213–9.
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the evaluation of canine intranasal neoplasia. J Small Anim 25. Lobetti R (2014). Idiopathic lymphoplasmacytic rhinitis in
Pract 50(7):334–40. 33 dogs. J S Afr Vet Assoc 85(1):1151.
5. Gavin PR, Holmes SP (2009). Head – non CNS. In: Practical 26. Windsor RC, Johnson LR (2006). Canine chronic
Small Animal MRI, 1st edn. (eds. PR Gavin, RS Bagley) Wiley- inflammatory rhinitis. Clin Tech Small Anim Pract 21(2):76–81.
Blackwell, Ames, pp. 309–32. 27. Stepaniuk KS, Gingerich W (2015). Suspect odontogenic
6. De Rycke LM, Saunders JH, Gielen IM et al. (2003). Magnetic infection etiology for canine lymphoplasmacytic rhinitis.
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sinuses in mesaticephalic dogs. Am J Vet Res 64(9):1093–8. aspergillosis. Vet Clin North Am Small Anim Pract 37(5):
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Clin Tech Small Anim Pract 21(2):89–94. comparison of tumor staging using computed tomography
41. Petite AF, Dennis R (2006). Comparison of radiography and versus magnetic resonance imaging findings in dogs
magnetic resonance imaging for evaluating the extent of nasal with nasal neoplasia: a pilot study. Vet Radiol Ultrasound
neoplasia in dogs. J Small Anim Pract 47(9):529–36. 58(3):315–25.
CHAPTER 6.2
EYE AND ORBIT

362 Susanne A. E. B. Boroffka
and Jimmy H. Saunders
CONTENTS
Technical considerations ......................................................................................................................................................................................362
General considerations..........................................................................................................................................................................................363
Ocular malformations and developmental conditions ............................................................................................................................................365
Anophthalmia and microphthalmia ..................................................................................................................................................................365
Persistent hyperplastic tunica vasculosa lentis/persistent hyperplastic primary vitreous and persistent hyaloid artery....................................365
Orbital malformations and developmental conditions ...........................................................................................................................................366
Nasolacrimal cysts...........................................................................................................................................................................................366
Orbital varix .....................................................................................................................................................................................................366
Ocular degenerative disorders ...............................................................................................................................................................................366
Cataract ...........................................................................................................................................................................................................366
Retinal detachment ..........................................................................................................................................................................................367
Inflammatory and infectious disorders ..................................................................................................................................................................367
Endophthalmitis and panophthalmitis..............................................................................................................................................................367
Extraocular polymyositis..................................................................................................................................................................................368
Optic neuritis ...................................................................................................................................................................................................369
Orbital cellulitis and abscessation ...................................................................................................................................................................369
Ocular form of granulomatous meningoencephalitis........................................................................................................................................369
Other inflammatory disorders and pseudotumors ............................................................................................................................................371
Traumatic disorders...............................................................................................................................................................................................371
Traumatic rupture of the globe .........................................................................................................................................................................371
Traumatic proptosis of the globe ......................................................................................................................................................................373
Orbital fractures ...............................................................................................................................................................................................373
Ocular and orbital neoplasms................................................................................................................................................................................373
Ocular neoplasia ..............................................................................................................................................................................................373
Orbital neoplasia.............................................................................................................................................................................................. 374
Feline restrictive orbital myofibroblastic sarcoma ............................................................................................................................................377
References.............................................................................................................................................................................................................378
TECHNICAL CONSIDERATIONS • The slice thickness should be chosen as thin as possible,

while taking other factors into consideration, such as
• MRI is less sensitive than CT for the evaluation of the the magnetic field strength, to preserve signal-to-noise
orbital bone and mineralized tissue, but is superior in ratio.
the assessment of the globe, optic nerve, and/or optic • Intravenous injection of contrast medium (gadolinium)
chiasm.1–8 provides additional information on tissue perfusion and
• An MRI examination should include T1W, T2W, +/– vascular permeability, and enhances the differentiation
PDW pulse sequences with a slice thickness of 2–4 mm. between normal and pathologic structures.
Ey e a n d O r bi t 363
• Due to the high fat content in the orbital space, fat sup- • The optic disc may be seen as a small, round hypointense
pression techniques may be useful to prevent misreg- structure at the caudal margin of the globe.
istration at the border of fat and water (chemical shift) • The sclera, choroid, and retina cannot be differentiated
that may challenge assessment of the optic nerve sheath, from one another.
extraocular muscles, and/or ocular globe. They are also • The anterior and posterior chamber and the vitreous are
useful on post-contrast images as they facilitate the iden- hypointense on T1W and hyperintense on T2W images.
tification of enhancing material, which may otherwise be • The orbit is mainly osseous and formed by six bones:
obscured by the abundant hyperintense fat. the frontal, lacrimal, maxillary, zygomatic, palatine,
• Fluid-attenuated sequences (e.g., T2-FLAIR) allow visu- and sphenoid bones. The posterolateral one-fifth of the
alization of underlying pathology possibly obscured by orbital margin is completed by the thick fibrous orbital
the bright signal of normal cerebrospinal fluid.3,8 ligament, connecting the zygomatic process of the fron-
• In addition to the transverse scan planes, dorsal oblique tal bone with the frontal process of the zygomatic bone.
(from rostrodorsal to caudoventral at an angle of 43–45° • Shape and size of the orbit depend on the breed; brachyce-
to the hard palate) and sagittal oblique (from rostrolat- phalic breeds have a considerately shallower bony orbit than
eral to caudomedial at an angle of 33° to the mid-sagittal dolicho- or mesaticephalic breeds. The cortical bone of the
plane) planes parallel to the optic nerve and extraocular orbit is seen as a signal void on all MRI pulse sequences.
muscles planes are useful for a thorough evaluation of all • The ocular adnexa are composed of the seven extraocu-
orbital structures.9 lar muscles, the eyelids, and the nasolacrimal apparatus.
Six extraocular muscles originate in the vicinity of the
ANATOMY, MRI ANATOMY, AND optic foramen at the apex of the orbital cone, the sev-
NORMAL VARIANTS (Fig. 6.2.1) enth arises from a small depression in the palatine bone.
In normal animals, these muscles enhance to a greater
• The eye is embedded in the orbital fat within the orbit, degree than the surrounding musculature.10
and consists of the globe including its intraocular struc- • The optic nerve forms the connection between the eye
tures and ocular adnexa. and brain. It is covered by a sheath composed of two lay-
• In general, T1W images of the orbit are characterized ers, an external layer (vagina externa nervi optici) and an
by the high signal intensity of the orbital fat, whereas the internal layer (vagina interna nervi optici), which are a con-
lens has low signal intensity and the extraocular muscles, tinuation of the dura mater and pia mater of the brain,
optic nerve, ciliary body, and iris have intermediate sig- respectively. As a result, these two layers are separated
nal intensity. Signal intensity of the vitreous lies between by CSF continuous with the CSF in the intracranial
that of the lens and extraocular muscles and signal inten- subarachnoid space. It originates from the optic chi-
sity of the lens capsule lies between that of the orbital fat asm (intracranial part), passes through the optic canal/
and extraocular muscles. foramen with the internal ophthalmic artery and vein
• T2W images show high signal intensity of the vitreous and (intracanalicular part) to enter the orbit (intraorbital
cerebrospinal fluid. Fluid-filled lesions will be easily dif- part) and join the retina (intraocular part).9
ferentiated from a soft tissue lesion due to their very high • The lacrimal gland is a small, flat, oval-shaped lobulated
signal on these pulse sequences. The relative order of signal gland lying dorsolaterally between the globe, the orbital
intensity of ocular and orbital structures from high to low ligament, and the zygomatic process of the frontal bone.
is: vitreous body and aqueous humor in the anterior and Its specific MRI appearance has not been reported in
posterior chambers, orbital fat, brain, extraocular muscles, dogs and cats, but in people it has a lobulated shape and
optic nerve and iris, eyelids and skin, lens, and air. intermediate signal intensity on T1W images.3
• Due to its very low water and high protein content, the
lens has relatively long T1 and short T2 relaxation times. GENERAL CONSIDERATIONS
This explains its hypointense appearance, in comparison
with the surrounding fluid-laden tissues, on most pulse • Many ocular diseases can be diagnosed by direct oph-
sequences. The nucleus of the lens has both a lower water thalmologic examination; however, in some cases, ocular
content (i.e., lower proton density) and a shorter T2 structures may be obscured by opaque material such as
relaxation time than the cortex, allowing in some cases edema, pigmentation induced by congenital abnormali-
differentiation between the two on MR images. ties, inflammation, degeneration, trauma, and/or neo-
• The ciliary body may be visible as a small hypointense plasia. Also, hemorrhage, due to high blood pressure or
structure at the periphery of the lens, at the corneo- coagulation disorders, or idiopathic, may occur. Imaging
scleral junction. can be useful in these cases, allowing structures not
• The iris forms a very thin line anterior to the lens, and directly visible with ophthalmologic examination to be
due to its transverse orientation is easier to see on sagittal imaged. Other conditions that may benefit from imaging
or dorsal plane images. include alterations of the structure of the aqueous humor
364 CHAPTER 6.2
(a) (b)
(c) (d)
(e) (f)
Fig. 6.2.1 Normal orbital and ocular MRI anatomy in a 2-year-old Bernese Mountain Dog. (a) Sagittal T1W image showing
the normal intraocular structures and extraocular muscles embedded in the orbital fat (open arrow). (b) Dorsal T1W image
showing the normal intraocular structures including the anterior chamber (dotted arrow), the lens (arrowhead), the vitreous
(solid arrow), and the extraocular muscles embedded in the orbital fat (open arrow). Note that in the lens the nucleus and cortex
can be differentiated due to their slight difference in signal intensity. (c) Transverse T1W post-contrast image at the level of the
lens showing the attachment of the extraocular muscles to the globe. (d) Transverse T2W, (e) T1W, and (f) 3D turbo field echo
post-contrast images caudal to the ocular globe showing the hypointense extraocular muscles outlined by the hyperintense
orbital fat. (1.5T MRI system; images courtesy of AJ van Belt, Utrecht University)
of the anterior and posterior chambers and the vitreous,

alterations of the position, structure, shape, and size of
the lens and globe, and folding and/or detachment of the
retina.
• Orbital diseases originate from tissues located within the
orbit, from the periorbital structures (muscles, blood ves-
sels, nerves, fat, bone), or can result from orbital exten-
sion of nasal, oral, or paranasal sinuses conditions. The
latter group is not uncommon, due to the relatively thin
medial orbital bone wall with several anatomic interrup-
tions for vessels and nerves. Examples of orbital diseases
include:11–13
• Congenital alterations (such as craniofacial deformi-
ties, arteriovenous fistula).
• Inflammatory diseases (such as orbital cellulitis with
or without abscess formation, myositis, extraocular
polymyositis, or sialoadenitis of the zygomatic sali-
vary gland).
• Traumatic lesions.
• Cystic or proliferative diseases (such as cranioman-
dibular osteopathy).
• Primary or metastatic neoplastic disease.
• Optic nerve lesions, such as optic nerve sheath men- Fig. 6.2.2 Dorsal T2W image in a 6-month-old Cairn Terrier
ingiomas, inflammatory fluid collection in the nerve showing congenital microphthalmia of the right eye, visibly
sheath, optic nerve hypoplasia, or optic neuritis. smaller than the left. (Image courtesy of Dr. Ruth Dennis,
• Changes within the orbit are typically clinically char- Animal Health Trust)
acterized by exophthalmos with increase of retrobulbar
pressure with or without protrusion of the nictitating unknown; it is often associated with other ocular anoma-
membrane, whereas enophthalmos rarely occurs:13 lies involving the cornea, lens, uvea (iris, choroid layer,
• Exophthalmos is usually caused by space-occupying ciliary body), vitreous, and retina. In the miniature
lesions caudal to the eye due to traumatic, inflam- Schnauzer and Australian Shepherd Dog this anomaly is
matory, degenerative, or neoplastic orbital disease.13 suspected to be recessively inherited.22,23
Less common causes are enlargement of the tempo- • MRI findings include either no eyeball or small eyeball
ral muscles, extension of processes from the nasal or with a poorly developed orbit (Fig. 6.2.2).
oral cavity, sinuses, and teeth,14 zygomatic or lacrimal
gland mucoceles,15–18 or vascular anomalies behind Persistent hyperplastic tunica vasculosa
the globe.19,20 lentis/persistent hyperplastic primary
• Enophthalmos may occur in patients in whom the vitreous and persistent hyaloid artery
retrobulbar support is reduced due to dehydration, • Persistent hyperplastic tunica vasculosa lentis/persis-
resorption of the retrobulbar fat (cachexia), muscle tent hyperplastic primary vitreous (PHTVL/PHPV)
atrophy (due to chronic myositis), and occasionally and persistent hyaloid artery are congenital, develop-
with nasal processes or diseases located on the nasal mental ocular abnormalities in which the hyaloid artery
side of the orbit with marked bone destruction or with or large portions of the fetal ocular hyaloid system
Horner’s syndrome (uni- or bilateral). fail to regress. The anomalies may be associated with
lenticonus, cataract, and elongated ciliary processes, and
OCULAR MALFORMATIONS AND sometimes with abnormalities of the retina, optic nerve,
DEVELOPMENTAL CONDITIONS and globe. This anomaly has been described incidentally
in different breeds, but in the Doberman Pinscher and
Anophthalmia and microphthalmia Staffordshire Bull Terrier the occurrence of PHTVL/
• Congenital abnormalities of the orbit occur very rarely PHPV is hereditary.24,25
in dogs and only a few reports of anophthalmia, orbital • MRI findings include:
dysplasia, and cysts have been published.21 • Normal or small eyeballs.
• Congenital anophthalmia (absent ocular globe) and • Retrolental soft tissue in the anatomic location of the
microphthalmia (hypoplastic ocular globe) have been Cloquet’s canal (perivascular sheath surrounding the
described in several breeds and the cause remains hyaloid artery in the embryonic eye), forming a fine
366 CHAPTER 6.2
linear structure extending from the disc of the optic • Although MRI is typically not used as a primary diag-
nerve to the posterior surface of the lens. nostic tool for this condition, the increased lenticular
• Retinal detachment (see below for MRI appearance). opacification may be appreciated on MR images inciden-
In some cases, the retinal detachment may be fun- tally when imaging the head for other reasons.
nel-shaped (as seen on sagittal or dorsal plane images), • MRI findings include (Fig. 6.2.3):28
with the tip of the funnel towards the lens and the • Decreased signal intensity of the lens.
base towards the posterior wall of the globe. The sub- • Lenticular deformation, which may result in increased
retinal fluid is hyperintense to the vitreous on both or decreased anterior–posterior diameter.
T1W and T2W images; a fluid–sediment level may • The lens may be luxated into the anterior chamber or
be seen, with the gravity-dependent portion being the vitreous.
hypointense on both T1W and T2W images, likely
due to the presence of hemorrhage in the subretinal
space with subsequent sedimentation of blood cells.
ORBITAL MALFORMATIONS AND

DEVELOPMENTAL CONDITIONS
Nasolacrimal cysts
• Alteration of the nasolacrimal duct due to head confor-
mation or developmental cysts of the lacrimal system can
result in obstruction of the lacrimal canal and deforma-
tion of surrounding bones.
• MRI findings include:26,27
• Mass lesion arising from the lacrimal bone region
with T2W hyperintense and T1W hypointense signal
intensity.
• Deformation of surrounding bones (lacrimal, max-
illary, and frontal) resulting from pressure atrophy
caused by the space-occupying lesion.
• On T2W images, there may be a fluid– sediment level
with a hypointense gravity-dependent layer.
• On post-contrast T1W images, there is enhancement
of the wall of the cyst.
(a)
Orbital varix
• An orbital varix is a venous malformation characterized
by abnormal dilation of the orbital veins and usually
results from congenital vessel weakness or other orbital
vascular malformations.
• Orbital varices occur extremely rarely in dogs and only
single case reports have been published.19,20
• Exophthalmos caused by abnormal, distended orbital
vessels.
• Tortuous anomalous orbital vessels (varices) with
strong enhancement.
• Thrombi within the varix may form laminated struc-
tures with mixed signal intensity due to blood break-
down products and fibrin.
(b)
OCULAR DEGENERATIVE DISORDERS Fig. 6.2.3 Transverse (a) and sagittal (b) T1W post-contrast
images of the right eye and orbit in an 11-year-old Siberian
Cataract Husky showing the hypointense nucleus of the right lens
• Cataract is a degenerative disease of the lens that occurs (arrows), consistent with a nuclear cataract. (1.5T MRI
commonly in dogs and less frequently in cats. system; images courtesy of AJ van Belt, Utrecht University)
Retinal detachment • Orbital inflammation is most often caused by penetrat-

• Retinal detachment is an uncommon finding on MR ing foreign bodies entering the orbital space via the con-
images. It may occur in patients with trauma to the junctiva or oral cavity. Bite and scratch wounds near the
eye and orbit, cataract, inflammatory or neoplastic dis- orbit may also induce orbital inflammation.
ease, congenital anomalies, or secondary to systemic • These inflammatory changes may occur diffusely (cel-
hypertension. lulitis) or form abscesses.
• MRI findings include (Fig. 6.2.4):29
• V-shaped or ‘seagull’-shaped linear intraocular leaf- Endophthalmitis and panophthalmitis
lets converging posteriorly towards the optic disc, and • Endophthalmitis is an inflammation of the anterior and
limited anteriorly by their attachment point at the posterior ocular structures, whereas in panophthalmitis
ora serrata, at 10 and 2 o’clock on dorsal plane images the scleroretinal rim is also inflamed.
(this differentiates retinal detachment from choroidal • Causes are often infectious and may include bacteria,
detachment, which is not limited by the ora serrata fungi, or viruses. Triggering factors are varied, and
anteriorly). include migrating foreign bodies (grass awns), cor-
• Subretinal fluid collection, which is usually hyperin- neal ulceration/perforation, lens luxation, surgery (e.g.,
tense to the vitreous on T1W and T2W images. retained lens material after cataract surgery), toxic
agents, or primary neoplasia.
INFLAMMATORY AND INFECTIOUS DISORDERS • Portals for ocular infection include local extension, ocu-
lar blood supply, cerebrospinal fluid via the optic nerve
• Ocular inflammatory disorders are typically dealt with sheath, or the optic nerve itself.2,11,14,30,31
using direct clinical and ophthalmoscopic examination • MRI findings include (Fig. 6.2.5):
as well as ultrasound. • Deformation of the globe.
• MRI may, however, be useful for inflammatory condi- • T2W hyperintensity of the scleroretinal rim and sur-
tions confined to or extending into the orbital region. rounding orbital structures.
• On post-contrast T1W images, heterogeneous
enhancement and thickening of the intraocular struc-
tures and scleroretinal rim.
• Linear structure parallel to the sclera or seagull
appearance due to retinal detachment; the subretinal
Fig. 6.2.4 Dorsal T2W image in a 5-month-old DSH cat Fig. 6.2.5 Dorsal plane T1W post-contrast image in a
showing bilateral retinal detachment. The detached retina 4-year-old Labrador Retriever showing strong enhancement
forms a characteristic ‘seagull pattern’ (arrows) that attaches of the extraocular muscles and scleroretinal rim, consistent
posteriorly at the papilla and anteriorly at the ora serrata. with endophthalmitis and orbital cellulitis. The left globe
(1.5T MRI system; image courtesy of Dr. Ruth Dennis, also is misshaped due to cellulitis. (1.5T MRI system; image
Animal Health Trust) courtesy of AJ van Belt, Utrecht University)
368 CHAPTER 6.2
fluid is hyperintense to the vitreous on T1W and • This condition is a rare idiopathic inflammatory disorder
T2W images. of single or multiple extraocular eye muscles. Unilateral
• A foreign body may be depicted as a T1W and T2W or sequential bilateral subacute painful exophthalmos is
hypointense structure without contrast enhancement. the main symptom of extraocular polymyositis.10
• Loss of definition of the extraocular muscles and fat if • MRI findings include (Fig. 6.2.6):
orbital cellulitis is also present. • In acute extraocular polymyositis:
– Uni- or bilateral rostral displacement of the
Extraocular polymyositis globe(s) (exophthalmos).
• Extraocular polymyositis affects large breed dogs, among – T2W hyperintensity of the orbital structures.
which the Golden Retriever is overrepresented. Affected – Increase in volume and loss of definition of the
dogs are usually 6 to 24 months old, and females are most extraocular muscles.
frequently affected.10
(a) (b)
(c) (d)
Fig. 6.2.6 Fat-saturated dorsal T1W pre- (a) and post-contrast (b) images, sagittal STIR image at the level of the right orbit (c),
and fat-saturated transverse T1W post-contrast image (d) in a 1-year-old Golden Retriever dog with extraocular polymyositis,
showing the markedly thickened extraocular muscles in both orbits, which are hyperintense on the STIR image (c) and T1W
pre-contrast image (a), and strongly diffusely enhancing (b, d). (1.5T MRI system; images courtesy of Dr. Wilfried Mai,
University of Pennsylvania)
– On T2W images, hyperintensity of the extraocu- Orbital cellulitis and abscessation

lar muscles. • Cellulitis and inflammation/infection of the orbital soft
– Diffuse enhancement of the extraocular muscles tissues often cause exophthalmos and/or periorbital
on post-contrast T1W images. swelling.
• In chronic extraocular polymyositis: • Hematogenous, translocation of infectious organisms
– Caudal displacement of the globes (enophthalmos). through the sclera or mucosa (conjunctiva, oral, nasal),
– Atrophy of the optic nerve. penetrating trauma, foreign bodies, extension of sinusitis,
– T1W and T2W hyperintensity and decreased vol- bone sequestration and tooth root abscesses, periodontal
ume of the extraocular muscles. or endodontic disease can result in orbital cellulitis with
or without abscessation. Contrast enhancement is best
Optic neuritis appreciated on fat-suppressed T1W images.2,11,14,30,31
• Optic neuritis is an inflammation of the optic nerve • MRI findings include (Figs. 6.2.8, 6.2.9):2,11,14,27,30,31
resulting in primary demyelination. • Increased T2W hyperintensity of the non-fatty
• Possible causes in dogs include granulomatous meningo- orbital soft tissues.
encephalitis (see below), infections with distemper virus, • Increase of volume of the orbital soft tissues with loss
tick-borne encephalitis virus, or Ehrlichia canis.32 In some of definition of the normal fat and extraocular muscles.
cases, no specific causal agent is identified (‘idiopathic • Eyelids and periorbital structures may be involved
immune-mediated optic neuritis’). (see above, “Endophthalmitis and panophthalmitis”).
• In the cat, causes include spread of orbital and nasal cav- • On T1W post-contrast images, diffuse or heteroge-
ity infections,1 feline infectious peritonitis, toxoplasmo- neous enhancement of the affected orbital soft tissues.
sis, mycotic infections (cryptococcosis), histoplasmosis,33 • Abscess formation is recognized as a mass lesion with
systemic hypertension, and lymphoma.32 T2W hyperintense and T1W hypointense center and
• If optic nerve disease is suspected, fat suppression tech- peripheral (ring) contrast enhancement.
niques such as STIR are recommended to eliminate the • When intracranial involvement is present, T2W,
hyperintense signal from orbital fat that surrounds the STIR, and T2-FLAIR hyperintensity of the tissues
optic nerve.9 Post-contrast images should be obtained in the optic nerve canal and orbital fissure and menin-
with fat saturation for the same reason. geal enhancement on T1W post-contrast images may
• MRI findings include (Fig. 6.2.7):34 be visible.
• Normal orbital structures. • Close inspection of the caudal maxillary teeth and
• Thickening of the optic nerve and optic nerve sheath. alveolar bone is recommended to rule out dental
• Diffuse contrast enhancement of the optic nerve on disease as a cause for orbital infection or abscessation
T1W post-contrast images (easier to appreciate on (Fig. 6.2.9). These teeth have a very close proximity
images with fat suppression). to the orbit and the floor of the orbit is composed of
soft tissue structures, facilitating extension of peri-
apical infection into the orbital space. In dogs, the
maxillary fourth premolar and the first and second
molars are the teeth that are most commonly the
cause of orbital disease. Periapical abscess formation
of those teeth may result in orbital inflammation.
T1W or PDW images are useful for evaluation of the
integrity of the alveolar bone and teeth structures and
will show alterations of the normal low signal of these
structures, with hyperintense tissue connecting the
periapical region to the orbital inflammation.31
• Foreign bodies may be recognized as a signal void
that does not correspond to an anatomic structure;
however, many foreign bodies may not be visible
on MRI due to their small size and hydration status
(Fig. 6.2.10).35
Fig. 6.2.7 Dorsal T1W post-contrast image in a 4-year-old
Labrador Retriever (same dog as in Fig. 6.2.5) with optic Ocular form of granulomatous
neuritis showing the thickened and enhanced extraocular meningoencephalitis
muscles and thickened hypointense optic nerve of the left eye • Granulomatous meningoencephalitis (GME) most
(arrow). (1.5T MRI system; image courtesy of AJ van Belt, commonly affects young and middle-aged dogs, and
Utrecht University) lesions can have diffuse, focal, or ocular distribution.
370 CHAPTER 6.2
(a) (b)
Fig. 6.2.8 Transverse T1W post-contrast (a), T2W (b),

and sagittal T1W post-contrast (c) images in a 4-year-
old Domestic Long-haired cat showing a left orbital mass
consisting of central cavities filled with T2W hyperintense
(b) and T1W hypointense (a, c) material that is non-
enhancing. There is strong peripheral enhancement of the
wall of this lesion (c). These changes are consistent with an
orbital abscess, in this case secondary to a scratch injury.
There is also ventrolateral indentation of the left globe and
moderate exophthalmos. (1.5T MRI system; images courtesy
(c)
of Dr. Ruth Dennis, Animal Health Trust)
Fig. 6.2.9 Transverse T1W post-contrast image in a

4-year-old English Bulldog showing enhancement of the
left temporal muscle (asterisk) and orbital structures with
a large orbital hypointense non-enhancing fluid pocket
(open arrow), consistent with abscess formation. There is
lysis of the alveolar bone of the left maxillary 2nd molar tooth
(solid arrow), consistent with alveolitis, which was the source
of the orbital infection and abscessation. (1.5T MRI system;
image courtesy of AJ van Belt, Utrecht University)
(a)
Fig. 6.2.10 T2W sagittal oblique image of the right orbit (a) in a 9-year-
old English Springer Spaniel showing a geometric stratified hypointense
structure with hyperintense halo (arrow) compatible with a foreign body
with surrounding inflammation. (b) Surgically removed foreign body
(piece of wood). (1.5T MRI system; images courtesy of Dr. Ruth Dennis,
(b)
Animal Health Trust)
Therefore, the MRI appearance is variable and reflects • Although not documented in dogs in the current veteri-
that distribution. The intracranial manifestations are nary literature, the authors have seen cases reminiscent
covered in Chapter 5.3. of this feline condition that shared similar clinical and
• MRI findings of ocular GME have been described in a imaging features (Fig. 6.2.11).
single case including:36 • Other rare inflammatory immune-mediated disorders
• T1W and T2W isointense mass-like enlargement of can affect the orbit and occasionally form mass lesions,
the optic chiasm. especially in young dogs. An example is nodular granulo-
• Strong contrast enhancement of the optic nerves. matous episcleritis,39 which can form well-defined orbital
• T2W hyperintensity (edema) of the optic pathway, masses and may be confused with neoplasia.
ventral thalamus, and forebrain. • MRI findings include:27,40,41
• T1W hypointense and T2W hyperintense space-
Other inflammatory disorders occupying mass lesion with well-defined borders
and pseudotumors within the orbit.
• Orbital pseudotumor, or ‘idiopathic sclerosing orbital • Rostral, dorsal, and/or lateral displacement of the
pseudotumor’, is a condition that has been reported in globe (with or without indentation) together with the
cats.31 It is a rare sclerosing orbital disease with a grad- extraocular muscles and optic nerve.
ual onset of clinical signs including exophthalmos with • Definition of the orbital fat and soft tissues is often
progressive lack of motility of the globe and surround- preserved.
ing tissues, resistance to retropulsion, protrusion of the
third eyelid, and progressive lack of eyelid function. It TRAUMATIC DISORDERS
may lead to exposure keratitis and entropion, and cor-
neal perforation. Recent reports, however, have proposed Traumatic rupture of the globe
a reclassification of this condition as a neoplastic disease, • Globe rupture occurs when the integrity of the
namely ‘feline restrictive orbital myofibroblastic sar- scleroretinal rim is disrupted by blunt or penetrating
coma’ (FROMS) (see below).37,38 Cross-sectional imag- trauma. These concussive forces can result in forward
ing reveals thickening of the sclera and adjacent tissues displacement of the eye from the bony eye socket (pro-
in most cases,37,38 while a distinct orbital mass can be seen ptosis), lens displacement (luxation), bleeding within
in other cases (see below).31 the anterior chamber of the eye (hyphema), retinal
372 CHAPTER 6.2
(a) (b)
(c) (d)
Fig. 6.2.11 Parasagittal T2W (a) and transverse T2W (b), T1W pre-contrast (c), and T1W post-contrast (d) images in a
7-month-old Golden Retriever presented with ocular discomfort, chemosis, and reduced, painful retropulsion. There is a
well-defined oblong mass in the right orbit (arrows) that is mildly hyperintense on the T2W images and moderately enhancing
on the T1W post-contrast image. Fine-needle aspiration revealed hemorrhage and after NSAID and antibiotic treatment,
the dog presented normal after 15 days. Although neoplasia was suspected initially, based on cytology and response to
treatment, the final presumptive diagnosis was ‘pseudotumor’ in the right orbital space. (1.5T MRI system; images courtesy
of Dr. Ruth Dennis, Animal Health Trust)
(a) (b)
Fig. 6.2.12 Sagittal oblique T1W post-contrast (a) and T2W (b) images in a 9-year-old Jack Russell Terrier with a ruptured
globe. There is leakage of T1W hypointense (a) and T2W hyperintense (b) vitreous into the orbit (solid arrows) through a
tear in the scleroretinal rim (dashed arrow). There is also a posterior lens subluxation. (1.5T MRI system; images courtesy of
Dr. Ruth Dennis, Animal Health Trust)
detachment, fractures of the bones around the eye, and asymmetry may occur. Fractures involving the parana-
rupture and collapse of the ocular globe (Fig. 6.2.12).42 sal sinus may cause orbital emphysema with crepitus. In
• MRI findings include:27,40,41 chronic fractures, deformation of the orbit may be pres-
• Irregular contour of the globe with possible interrup- ent due to malunion and bony callus formation.
tions of the scleroretinal rim. • For evaluation of the bony structures, CT examination is
• Decreased volume of the ocular globe. preferred, but MRI may provide more detailed informa-
• Leakage of T2W hyperintense and T1W hypointense tion regarding the nature and extent of concurrent soft
vitreous within the orbit, sometimes through a visible tissue injuries.
scleroretinal rent. • MRI findings include:43
• Rostral displacement of the globe, with the eyelids
Traumatic proptosis of the globe trapped caudal to the globe (proptosis).
• Proptosis is an acute rostral displacement of the globe • Mass effect caudal to the globe (hemorrhage or edema)
from the orbit caused by trauma. It can occur in any with loss of the normal orbital anatomy.
breed and both in cats and dogs, but brachycephalic • Fractures of the frontal, temporal, and zygomatic bones
breeds are predisposed.27,40,41 are visible as interruption of the normally hypointense
• MRI findings include: (black) cortical bone and irregularly shaped signal voids
• Rostral displacement of the globe (eyelids are trapped within the orbital or periorbital region corresponding
caudal to the globe). to bone fragments; such changes may be easier to
• Mass effect caudal to the globe (hemorrhage and/or identify on T1W or PDW images.
edema) with loss of the normal orbital anatomy. • Orbital emphysema may also cause signal voids within
• Rupture of the rectus extraocular muscles may be the orbital space.
seen.
OCULAR AND ORBITAL NEOPLASMS
Orbital fractures
• After head trauma, fractures of the frontal, temporal, Ocular neoplasia
and zygomatic bones may occur and either exophthal- • Intraocular neoplasia may mimic or induce ocular
mos (with proptosis of the globe) or enophthalmos, stra- inflammatory disease; it can also cause hyphema and/or
bismus, orbital and periocular hemorrhage, and facial secondary glaucoma.
374 CHAPTER 6.2
• Intraocular tumors arise mostly from the iris and cili- • In melanoma, the mass may be hyperintense on T1W
ary body, with the most common ones being melanoma and hypointense on T2W images due to the paramag-
or carcinoma.21,44–48 Tumors affecting the posterior seg- netic properties of melanin in the mass (Fig. 6.2.14).
ments and possibly infiltrating the optic nerve are less These paramagnetic properties result from the high
common (e.g., the rare choroidal melanoma).49 affinity of melanin for metal ions.
• MRI findings include (Fig. 6.2.13): • In posterior segment neoplasia, a mass in the area of
• Focal thickening or mass lesion associated with the the vitreous and choroidal/retinal region may be seen,
iris and/or ciliary body; these changes are best appre- often with evidence of retinal detachment.
ciated on sagittal or dorsal plane imaging.
• Focal mass lesion, which is T2W hyperintense and Orbital neoplasia
T1W hypointense with contrast enhancement. • In dogs and cats, more than 90% of orbital neoplasms
• Diffuse enhancement of the scleroretinal rim after are malignant with regional invasion (including into the
contrast injection due to inflammation secondary to brain) and/or distant metastasis.2,21,37,38,48,50
the neoplasia.
(a) (b)
Fig. 6.2.13 Transverse T2W (a), T1W (b), and T1W

post-contrast (c) images in an 11-year-old mixed
breed dog showing a T2W hypointense (compared
with the vitreous), T1W hyperintense, and strongly
contrast-enhancing mass lesion of the ventrolateral
ciliary body of the right eye (arrows). Histopathology
revealed a ciliary body adenocarcinoma. (1.5T MRI
system; images courtesy of Dr. Ruth Dennis, Animal
(c)
Health Trust)
(a) (b)
Fig. 6.2.14 Transverse T2W (a) and T1W post-contrast (b) images in an 11-year-old Collie-mix dog showing a T2W
hypointense (a) and enhancing (b) mass lesion of the iris in the right eye (arrows). The T2W hypointense signal is characteristic
for ocular melanoma. (1.5T MRI system; images courtesy of Dr. Ruth Dennis, Animal Health Trust)
• Orbital neoplasia may include primary neoplasia, local • Possible enlargement and heterogeneous enhance-
extension of neoplasia arising from adjacent structures ment of the mandibular lymph nodes.
(adjacent skull, nasal cavity and paranasal sinuses or oral • In cases of optic nerve meningioma: expansile, par-
cavity), or metastatic disease from distant sites. tially mineralized (signal voids) soft tissue mass caudal
• Reported orbital tumors include orbital chondroma
rodens, osteosarcoma, chondrosarcoma, hemangiosar-
coma, adenocarcinoma (lacrimal gland, third eyelid
gland, zygomatic salivary gland), granular cell myo-
blastoma, orbital hemangiopericytoma, fibrosarcoma,
neurofibrosarcoma, lobular gland adenoma, orbital
meningioma, lymphoma, squamous cell carcinoma, optic
nerve glioma, peripheral nerve sheath tumors, lipomas,
myxosarcoma, and undifferentiated neoplasms.2,39
• General MRI features of orbital neoplasia include
(Figs. 6.2.15, 6.2.16):
• T1W hypointense and T2W hyperintense space-
occupying mass lesion with well-defined borders
within the orbit; signal intensity may, however, be
heterogeneous and variable depending on the type of
neoplasm and presence of secondary changes such as
hemorrhage, necrosis, or mineralization.
• Rostral, dorsal, and/or lateral displacement of the
globe (with or without indentation) together with the
extraocular muscles and optic nerve. Fig. 6.2.15 Sagittal oblique T1W post-contrast image of the
• Definition of the orbital fat and soft tissues is often right eye in an 8-year-old English Springer Spaniel showing
preserved. a large, strongly contrast-enhancing mass lesion originating
• Tumor extension into the surrounding soft tissues from the optic nerve. Histopathology revealed a meningioma.
and/or paranasal sinuses (lysis of the medial bony (1.5T MRI system; image courtesy of Dr. Ruth Dennis,
orbital wall and/or zygomatic bone). Animal Health Trust)
376 CHAPTER 6.2
(a) (b)
Fig. 6.2.16 Transverse T2W (a), T1W (b), and T1W post-
contrast (c) images in a 9-year-old Staffordshire Bull Terrier
showing a lobulated contrast-enhancing mass lesion at the
ventrolateral aspect of the left orbit causing exophthalmos.
Histopathology revealed an orbital round cell tumor.
(1.5T MRI system; images courtesy of Dr. Ruth Dennis,
(c) Animal Health Trust)
to the eye that can be tracked to the optic nerve. • The lesions often form communicating, sometimes
There is often significant bone atrophy of the orbital multiloculated, fluid-filled cavities (T2W hyperin-
wall and optic canal. tense, T1W hypointense, and non-enhancing) with
• The specific MRI appearance of orbital myxosarcoma small areas of solid tissue. On post-contrast T1W
has been reported (Fig. 6.2.17):50 images there is strong peripheral enhancement of the
• Extensive disease is usually present within and beyond wall of these fluid-filled/mucinous lesions.
the confines of the orbit, resulting in various degrees • A more solid presentation is also possible, with small
of exophthalmos and pterygopalatine fossa swelling. fluid pockets within the bulk of the mass; in these
• The lesions are typically well-defined, appearing to cases, the mass is heterogeneously T2W and T1W
lie mainly within the fascial planes rather than invad- hyperintense to muscles and has slight patchy contrast
ing the soft tissues; there is often caudal extension enhancement after gadolinium administration.
between the zygomatic salivary gland and ptery- • Osteolysis of the neighboring bone structures such as
goid muscles medially, and the mandibular coronoid the mandibular coronoid process and temporoman-
process and temporal muscle laterally. dibular joint may be seen.
(a) (b) (c)

Fig. 6.2.17 Transverse (a), dorsal (b), and sagittal (c) T2W images in a 9-year-old female neutered Labrador Retriever with
a left orbital myxosarcoma. Note the extensive, multiloculated accumulation of markedly T2W hyperintense material in the
orbit, extending ventrally in the intermandibular space and caudally to the temporomandibular joint. (1.5T MRI system;
reproduced, with permission, from Dennis R (2008). Imaging features of orbital myxosarcoma in dogs. Vet Radiol Ultrasound
49(3):256–63.)
Feline restrictive orbital • MRI findings include (Fig. 6.2.18):38

myofibroblastic sarcoma • Mild thickening of the episclera, sclera, and adjacent
• FROMS is a rare, progressive, and fibrosing condition of orbital structures.
the orbit and adjacent connective tissues. • Signal reduction and partial effacement of the orbital
• Recent reports indicate that this condition was previ- fat.
ously described as being inflammatory and referred to as • On T1W post-contrast images, marked contrast
‘idiopathic sclerosing orbital pseudotumor’.37,38 enhancement of the sclera and episcleral tissues.
• Clinically, most cats present with unilateral ocular • Decrease in volume and definition of the extraocular
involvement and subsequently the tumor may spread muscles with no specific contrast enhancement.
along fascial planes to the contralateral orbit and eyelids
and/or the lips and oral cavity.37,38
(a) (b)
Fig. 6.2.18 Dorsal plane MR images of the orbits in an 11-year-old Siamese cat. Pre-contrast (a) T1W and (b) T2W images.
Note the mild thickening of the episclera and adjacent retrobulbar soft tissues (arrowheads). (Continued)
378 CHAPTER 6.2
(c) (d)
Fig. 6.2.18 (Continued) Dorsal plane MR images of the orbits in an 11-year-old Siamese cat. (c) Post-contrast T1W image
with chemical fat saturation demonstrating marked contrast enhancement of the retrobulbar tissues, especially on the left
(arrow). (d) STIR image depicting heterogeneous, increased signal intensity of the left retrobulbar soft tissues (open arrow).
Reproduced, with permission, from Thomasy SM, Cissell DD, Arzi B et al. (2013). Restrictive orbital myofibroblastic sarcoma
in a cat – cross-sectional imaging (MRI & CT) appearance, treatment, and outcome. Vet Ophthalmol 16(Suppl 1):123–9.)
• Additional features that have been reported at CT and 7. Penninck D, Daniel GB, Brawer R et al. (2001). Cross-
may also be seen on MRI include:37 sectional imaging techniques in veterinary ophthalmology.
– Thickening of the adjacent gingiva and hard palate Clin Tech Small Anim Pract 16(1):22–39.
8. Tamraz JC, Outin-Tamraz C, Saban R (1999). MR imaging
as well as interorbital nasofrontal cutis.
anatomy of the optic pathways. Radiol Clin North Am 37(1):
– Lysis of the orbital wall with extension of a soft
1–36, ix.
tissue mass into the nasal cavity. 9. Boroffka SA, Gorig C, Auriemma E et al. (2008). Magnetic
• Recent case series mention that typically no mass resonance imaging of the canine optic nerve. Vet Radiol
lesions are present;37,38 however, other authors Ultrasound 49(6):540–4.
described the presence of distinct orbital mass 10. Joslyn S, Richards S, Boroffka S et al. (2014). Magnetic
lesions.31 resonance imaging contrast enhancement of extra-ocular
muscles in dogs with no clinical evidence of orbital disease.
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159(4):110–5.
CHAPTER 6.3
EXTERNAL, MIDDLE, AND INNER EAR

380 Jimmy H. Saunders and
CONTENTS
External ear ......................................................................................................................................................................................................380
Middle ear .......................................................................................................................................................................................................381
Inner ear ..........................................................................................................................................................................................................381
Bulla effusion ........................................................................................................................................................................................................383
Otitis externa .........................................................................................................................................................................................................383
Otitis media ...........................................................................................................................................................................................................384
Otitis interna..........................................................................................................................................................................................................385
Otogenic intracranial infection secondary to otitis media or interna ......................................................................................................................386
Aural cholesteatoma ..............................................................................................................................................................................................386
Inflammatory polyps ............................................................................................................................................................................................388
Neoplasia ..............................................................................................................................................................................................................390
References.............................................................................................................................................................................................................391
sequences particularly suited for imaging of the inner

TECHNICAL CONSIDERATIONS ear and associated nerves, and they are routinely used in
people.2,5
• Both high- and low-field MRI can be used for exami- • With regard to image plane orientation, dorsal and
nation of the external, middle, and inner ear.1,2 In par- transverse planes are favored because they allow left-to-
ticular, MRI has opened a new field of investigation in right comparison.1
the pathology of the inner ear and neighboring neural
structures using volume acquisition and very thin slices ANATOMY, MRI ANATOMY, AND
of 1 mm or less.1,3 NORMAL VARIANTS (Fig. 6.3.1)
• In aural disorders, T2W sequences are useful for iden-
tifying fluid (high signal intensity),4 whereas pre- and External ear
post-contrast T1W sequences are mandatory to demon- • The external ear greatly varies in shape and size among
strate blood–brain barrier or hemato-perilymphatic bar- dog and cat breeds.6 The auricular and annular cartilages
rier breakdown, as well as hypervascular lesions such as form the support for the majority of the ear canal while
otitis interna.4 the small, separate scutiform cartilage serves as attach-
• Three-dimensional balanced gradient echo sequences, ment for several medial auricular muscles.6
such as FIESTA (General Electric), True FISP (Siemens), • The lateral segment of the external ear canal is vertically
or balanced FFE (Phillips), have short acquisition times, oriented, and only supported by cartilage; the medial
and provide images with high spatial resolution with segment is oriented 45° to the vertical (90° in cats) and
outstanding image contrast between the cranial nerves has cartilaginous and osseous support.6
and cerebrospinal fluid, and hyperintense signal from • Spaniel breeds tend to have narrow external ear canals
fluid-filled structures such as the endolymph and peri- while chondrodystrophic breeds commonly show miner-
lymph in the inner ear. These characteristics make these alized auricular and annular cartilage.7
E x t e r n a l , M i ddl e , a n d I n n e r E a r 381
5
2
1
3 1
(a) (b)
Fig. 6.3.1 Six-year-old normal German Shepherd Dog. Transverse T1W (a) and T2W (b) images at the level of the ear. 1,
tympanic cavity; 2, wall of the external ear canal; 3, horizontal portion of the ear canal; 4, internal acoustic meatus; 5, external
acoustic meatus. (1T MRI system)
Middle ear • The inner ear comprises the bony and membranous lab-
• The tympanic membrane spans the entrance to the tym- yrinth, with the latter being embedded inside the for-
panic cavity, separating the external from the middle mer. The bony labyrinth consists of a central chamber
ear.6 called the vestibule, the three semicircular canals, and
• The middle ear is contained within the petrous temporal the spirally coiled cochlea. The membranous labyrinth
bone and is comprised of the air-filled tympanic bulla fills each of these compartments, including a semicircu-
containing the three auditory ossicles (the lateral mal- lar duct in each semicircular canal, a utricle and saccule
leolus, the intermediate incus, and the medial stapes).6 in the vestibule, and a cochlear duct in the cochlea, as
• The tympanic bulla is round to ovoid in shape. There well as a vestibular aqueduct.6
are, however, breed variations of its shape; for example, it • The endolymph is contained within the membranous
tends to be more flattened in the Cavalier King Charles labyrinth, while the perilymph fills the space between
Spaniel. the outer wall of the membranous labyrinth and the
• The feline tympanic bulla has one or more septae, inner wall of the bony labyrinth.
incompletely dividing the tympanic cavity into a dorso- • Intralabyrinthine fluid is visible as high signal intensity
lateral and ventromedial portion.6 on T2W sequences contrasting with the surrounding
• On MRI, the normal bulla is visible as a signal void on bony labyrinth that appears as a signal void.3,4 On most
all imaging sequences because it contains air bounded by images, only the vestibule (containing the utricle and
cortical bone, both of which produce no MRI signal.8 saccule) as well as the cochlea are visible. In the trans-
• Low-field MRI does not allow identification of the tym- verse plane, each vestibule forms the pattern of a ‘duck
panic membrane or the auditory ossicles.2 silhouette’ swimming to the lateral aspect, while the
• Dorsomedially, the auditory (Eustachian) tube connects fluid in the cochlea has a characteristic spiral shape.2,4,9
the middle ear to the nasopharynx.6 Normal function of The ‘duck pattern’ has previously been attributed to the
this organ is essential to prevent middle ear disorders.5 semicircular canals,4,10 but at the resolution obtained on
• The facial nerve (cranial nerve VII), sympathetic inner- standard fast spin echo T2W images, these structures
vation of the eye, and the parasympathetic innervation are too small to be seen, and the duck pattern corre-
of the lacrimal gland are anatomically closely associated sponds in fact to the vestibule.2,9 On 3D gradient echo
with the middle ear.6 pulse sequences in the steady state, such as FIESTA,
True-FISP, Balanced FFE, or the more modern CISS or
Inner ear (Fig. 6.3.2) FIESTA-C, higher spatial resolution, higher signal-to-
• The inner ear is enclosed within the petrous temporal noise ratio and excellent contrast to noise, especially for
bone, dorsomedial to the middle ear.6 fluid-filled structures, allow visualization of part or all
382 CHAPTER 6.3
(a) (b)
(c) (d)
Fig. 6.3.2 Transverse 3D-FIESTA images at the level

of the inner ear in a normal dog. (a) Transverse image
through the vestibule of the inner ear showing bright
signal within the utricle and saccule (arrowhead).
(b) Transverse image at the level of the cochlea
(arrowhead). (c–e) 3D volume rendering of the endo- and
perilymph content of the inner ear segmented from the
3D-FIESTA series. Images from different perspectives
show the vestibule (solid arrowheads) and cochlea
(open arrowheads), as well as the thin semicircular canals
(dotted arrows). (1.5T MRI system; images courtesy of
(e)
of the semicircular canals; when visible, they form three thickening and erythema of the ear canal, and aural dis-
distinct hyperintense, very thin semicircular structures charge in cases of bacterial infection.7
adjacent to the vestibule (Fig. 6.3.2).2 • MRI is rarely used to primarily diagnose otitis externa,
but may be used in dogs with chronic otitis externa to
BULLA EFFUSION evaluate for signs of otitis media/interna. Otitis externa
could also be identified while scanning a patient for other
• Fluid in the middle ear is regularly seen on MRI stud- reasons (e.g., brain MRI).
ies performed for reasons unrelated to ear disease, and is • MRI findings include (Fig. 6.3.3):
easily recognized on T2W images.11 Some of these cases • In acute cases, often strong contrast enhancement
may represent a subclinical form of otitis media. In oth- of the thin lining of the external ear canal on T1W
ers, no reason can be demonstrated and it must be con- post-contrast images, with less pronounced hyperin-
sidered an incidental finding.11 tensity on T2W images.
• Although fluid may accumulate in the middle ear of dogs • In chronic cases:8,17
without otitis media, its presence may predispose to – Non-enhancing soft tissue material, mainly exu-
infection and inflammation.11 date, in the external ear canal, typically hyperin-
• Auditory (Eustachian) tube dysfunction is suspected to tense on T2W images and of variable intensity on
be a predisposing factor promoting fluid accumulation T1W images (depending on cellular and macro-
in the middle ear, particularly in brachycephalic breeds molecular content of the exudative fluid).
such as the Cavalier King Charles Spaniel.12–14 – Thickening of the ear canal lining with strong
• The auditory tube is a musculotubal conduit extending contrast enhancement on T1W post-contrast
from the rostral aspect of the tympanic cavity to the naso- images due to increased vascularization of the
pharynx. It allows for pressure equalization between the inflamed tissue; mild hyperintensity of this thick-
tympanic cavity and the atmosphere, and also allows for ened wall on T2W images.
drainage of fluid from the tympanic cavity.15,16 Normally – Beneath the epithelium, fibrous tissue is often
closed, the pharyngeal orifice is opened by the action of present that is hypointense on T1W and even
the tensor veli palatini muscle,15,16 which is innervated by more so on T2W images.
the nerve of the tensor veli palatini muscle, a small branch – Subjective narrowing of the external ear canal.
of the mandibular nerve. The mandibular nerve is one of – Mineralization of the auricular and annular carti-
the three main branches of the trigeminal nerve. Thus, lages in chronic cases produces a signal void that
conditions affecting normal function of the trigeminal
nerve, such as trigeminal nerve sheath tumors or neuri-
tis, can cause dysfunction of the tensor veli palatini muscle
leading to accumulation of fluid in the ipsilateral tym-
panic bulla. Effusion is observed in the tympanic cavity
ipsilateral to a disorder of the trigeminal nerve in 30% of
dogs.15,16 When identifying fluid in the bulla in dogs with
no clinical signs of otitis externa/media, careful inspec-
tion of the area of the trigeminal nerve is recommended.
• Fluid accumulating in the tympanic bulla contains vari-
able amounts of proteinaceous material mixed with pure
fluid and usually appears hyperintense on T2W images
and isointense on T1W images (although the T1 inten-
sity may vary) compared with brain tissue.4,11
OTITIS EXTERNA
• Inflammation of the external ear canal may be caused

by infection, allergic and hypersensitivity reactions,
mechanical irritation (parasites or foreign bodies such as
grass seeds/awns), or be idiopathic.7 Fig. 6.3.3 Otitis externa in a 7-year-old German Shepherd
• Small ear canals (Shar Pei) or long floppy ear flaps (Basset Dog. Transverse T1W spin echo post-contrast image
Hound, Cocker Spaniel) prevent airflow and are there- showing thickening of the wall of the left horizontal ear
fore predisposing factors.7,12 canal (solid arrow) and contrast enhancement of the mucosa
• Clinically, affected patients present with ear scratch- (dotted arrow). (0.3T MRI system; image courtesy of
ing (pruritus), head shaking, malodor from the ear, Dr. Kaatje Kromhout, Ghent University)
384 CHAPTER 6.3
should be differentiated from normal auricular • Some predisposing factors have been identified in cats
cartilage. such as nasopharyngeal disorders/polyps and soft pal-
– Foreign body material, such as a grass awn, often ate abnormalities such as a cleft palate, or palatine
has a similar appearance to the surrounding soft hypoplasia.19,20 Breed predisposition has been dem-
tissues and is therefore difficult to detect. onstrated in dogs such as the Cavalier King Charles
Spaniel.13,21
OTITIS MEDIA • Typically, dogs with otitis media have a history of recur-
rent chronic bacterial external ear infections.18 Clinically,
• In dogs, otitis media (= inflammation of the tympanic the condition presents with copious aural exudate,
bulla) is usually secondary to an external ear inflamma- head shaking, and pain on palpation of the ear canal.
tion and/or damage to the tympanic membrane.18 Additionally, patients may show pain when opening the
• In cats, otitis media is more commonly secondary to viral mouth; facial nerve and sympathetic nerve disturbances
or bacterial upper respiratory infections, with extension may be seen, due to association with the wall and lumen
through the auditory tube.18 of the tympanic bulla.18
• Less common routes of infection in both cats and dogs • MRI findings include (Figs. 6.3.4, 6.3.5):4,8,17
include extension via the temporohyoid joint, direct • In acute to subacute cases:4,8
extension via erosion of the wall of the tympanic bullae, – Exudative effusion in the lumen of the tympanic
or migration along vascular or neural pathways.6 bulla, which is hypo- to isointense on T1W and
(a) (b)
Fig. 6.3.4 Otitis media in a 4-year-old Pug. Transverse

T2W (a), PDW (b), and T1W post-contrast (c) images
showing the left tympanic bulla filled with hyperintense
material. The right tympanic bulla is partially filled as well.
(1T MRI system; images courtesy of AJ van Belt, Utrecht
(c)
University)
(a) (b)
Fig. 6.3.5 Chronic otitis media in a 14-year-old European

Short-haired cat. Transverse T1W post-contrast (a), T2W
(b), and PDW (c) images showing the right tympanic bulla
filled with material that is hypointense on the T1W and
PDW images and hyperintense on the T2W image. There is
irregular thickening of the mucosal lining of the tympanic
cavity, which is moderately hyperintense on the T2W and
PDW images and strongly contrast enhancing (solid arrow).
Very mild enhancement (dotted arrow) of the ventral wall of
the left tympanic bulla is visible, consistent with early/mild
otitis media on that side as well. (1T MRI system; images
(c)
courtesy of AJ van Belt, Utrecht University)
hyperintense on T2W images; in cats, this effu- – Non-uniform, irregular thickening (reactive oste-
sion is usually initially located in the dorsolateral itis) or sometimes osteolysis of the bony wall of the
compartment and in most severe cases fills up the bulla. The thickened wall forms a curved hypoin-
tympanic cavity.4 tense signal (signal void) on all pulse sequences
– Thickened, inflamed mucosal lining of the inner along the margins of the bulla, with or without
wall of the bulla, resulting in a hyperintense signal irregular margins; interruptions of this signal void
(bright rim) on T1W post-contrast images.8 may be seen when lysis is present.
• In chronic cases:8,17 – Intracranial extent with involvement of the brain-
– Inspissation (progressive dehydration) of the stem (see below: “Otogenic intracranial infection
fluid in the lumen, resulting in increased protein secondary to otitis media or interna”).
concentration and increased tissue proliferation,
which leads to increased signal intensity (com- OTITIS INTERNA
pared with cerebral cortex) on T1W images and
decreased signal intensity on T2W images. • Otitis interna is usually caused by extension of inflam-
– Mixed signal intensity of the mucosa of the tym- mation of the middle ear (otitis media).
panic bulla on T2W images, with hypointense • Clinically, the condition is characterized by signs of a
areas representing fibrous tissue. peripheral vestibular syndrome, suggesting injury to
– Enlarged tympanic bulla because of the pressure the vestibular nerve or receptor organs.22 Head tilting,
of the fluid/material within it. falling, rolling, circling, nystagmus, strabismus, and
386 CHAPTER 6.3
OTOGENIC INTRACRANIAL INFECTION

SECONDARY TO OTITIS MEDIA OR INTERNA
• Brainstem dysfunction resulting from central spread of

inflammation from otitis media/interna is an infrequent
complication.
• MRI is effective in characterizing the location and extent
of the intracranial pathologic changes as well as patholo-
gies within the middle/inner ear structures.
• The MRI signs of brainstem involvement are related to
the stage of the disorder and may be classified as acute,
subacute, or chronic.3 Besides the otitis media lesions in
the tympanic bulla described above, the MRI features of
intracranial extension include (Fig. 6.3.7):3
• In cases of acute neurologic dysfunction:
– T2W hyperintense thickening of the meninges
and subjacent neuropil of the brainstem, cerebel-
lum, and cerebrum ipsilateral to the middle/inner
ear changes with, on T1W post-contrast images,
Fig. 6.3.6 Otitis interna in a 1-year-old European Short-
moderate to strong contrast enhancement (some-
haired cat. Transverse T2W image showing a decrease in
times ring enhancement). Ring-like enhancement
MRI signal intensity of the endo- and perilymph of the
with lack of enhancement of the space-occupy-
vestibule of the right inner ear (solid arrow) in comparison
ing parameningeal tissue can suggest empyema
with the left (dotted arrow). (0.3T MRI system; image
formation.
courtesy of Dr. Kaatje Kromhout, Ghent University)
– T2W and T2-FLAIR hyperintense signal in the
adjacent brain tissue corresponding to a variable
asymmetric ataxia in the presence of a normal mental amount of cerebral edema; this may be mild and
status and normal postural reaction can be observed.22 limited to the cortical gray matter or extensive
If associated neural structures in the petrous temporal throughout the white matter on the affected side.
bone are involved (cranial nerves VII/VIII, sympathetic – A mild mass effect may be present.
nerve), facial paralysis (VII) and Horner’s syndrome • In cases of subacute neurologic dysfunction:
may be present.22 In dogs with vestibular disorders, the – Mass(-es) extending into the cerebellomedullary
presumed localization of the lesion identified with MRI angle, with a variable intensity on T2W images
matches the surgical findings in 90% of the cases.23 and variable enhancement on T1W post-contrast
• MRI findings include (Fig. 6.3.6):20,23,24 images.
• In cases of acute inflammation of the internal ear: – Lack of, or only mild, brain edema on T2W
normal signal intensity on T2W images (fluid inten- images
sity, similar to CSF) and strong enhancement inside – Possible localized mass effect.
the membranous labyrinth on post-contrast T1W • In cases of chronic neurologic dysfunction:
images due to leakage of contrast into the intralabyrin- – Mass(-es) extending into the brainstem and cer-
thine fluid following breakdown of the hemoperilym- ebellomedullary angle, with a variable signal
phatic barrier or uptake of contrast by inflammatory intensity on pre- and post-contrast T1W images
tissue. (sometimes ring enhancement) and homogeneous
• Chronic inflammation of the internal ear with fibrous or heterogeneous hyperintensity on T2W images.
obliteration of the intralabyrinthine fluid-containing – Brain edema, which may be mild (especially in
spaces will cause a decrease in the normal hyperin- cats) or more extensive (especially in dogs).
tense MRI signal associated with the vestibule and – Limited mass effect on parenchymal tissues adja-
cochlea on T2W images.22 Post-contrast T1W images cent to the mass.
show absence of, or minimal, enhancement.
• Osteomyelitis may be present, characterized by oste- AURAL CHOLESTEATOMA
osclerosis (irregular signal voids) and osteolysis with
irregular contrast enhancement of the petrous tem- • An aural cholesteatoma is an epidermoid cyst located in
poral bone. the middle ear.26 It contains keratin and/or sebaceous
• Meningeal and/or cranial nerve (VII and VIII) material causing a mild to severe inflammatory response
enhancement on contrast-enhanced T1W images.25 of the surrounding tissues.27,28
(a) (b)
Fig. 6.3.7 Otogenic intracranial infection in an 8-year-old European Short-haired cat. Transverse T1W spin echo (a) and T1W
3D fast field echo post-contrast (b) images (at two different levels) showing the right tympanic bulla filled with material that is
slightly hyperintense to the brain parenchyma (solid arrow, a). The lesion extends to the inner ear and the brain parenchyma.
In the brain, there is a large round hypointense cavitary lesion (asterisk, b) in direct connection with the ear with marked
peripheral rim enhancement (dotted arrows, b). (1T MRI system; images courtesy of AJ van Belt, Utrecht University)
• The disorder is mostly secondary to a chronic otitis isointense on T1W images compared with brain
externa causing a retraction of the tympanic membrane tissue; limited case reports or series describe a lack
into the middle ear or the migration of stratified squa- of enhancement on T1W images after gadolinium
mous epithelium from the external auditory meatus into administration,3,26,30 although contrast enhancement
the infected middle ear cavity through a perforated tym- (heterogeneous or diffuse) has been reported with
panic membrane.26–28 CT,26 and may conceivably also be seen with MRI in
• Congenital inclusion of a squamous epithelial cyst behind some cases.
an intact tympanic membrane can occur as a develop- • There may be partial enhancement of the lining of the
mental defect with similar consequences.26–28 bulla on post-contrast T1W images due to inflamma-
• Auditory tube dysfunction has been suggested to predis- tion.
pose brachycephalic dogs to the development of primary • A distinctive common feature of aural cholesteatoma
cholesteatoma.13 is the progressive expansion of the lumen of the bulla
• In both primary and secondary cholesteatomas, the con- by the slowly growing mass causing widening of the
tinuous keratin production results in shedding of keratin- bulla with distension of its wall.
ized squamous cells into the cyst, which leads to gradual • Thickening of the wall of the tympanic bulla and
enlargement, compression, and subsequent destruction petrous temporal bone, appearing hypointense on
of nearby structures, including bone and neural tissue, T1W images and hypointense or of mixed signal on
leading to the clinical signs.26,27 T2W images, suggesting sclerosis and obliteration of
• Clinically, a history and signs of chronic otitis externa the medullary fat.
(otorrhea, pawing at the ear) associated with pain on pal- • Depending on the direction in which the process
pation of the bulla, pain or even inability to open the extends, additional changes may be seen, including:
mouth, and/or head shaking or tilting suggest aural cho- – Remodeling of the temporomandibular joint.
lesteatoma.29 Neurologic signs such as unilateral facial – Compression of the nasopharynx.
paralysis, ataxia, or circling (vestibular syndrome) may – Meningeal enhancement or even cerebral tissue
be observed.29 enhancement with or without a space-occupying
• MRI findings include (Figs. 6.3.8, 6.3.9):30,31 lesion at the level of the cerebellomedullary junction.
• Tympanic bulla filled by a mass that is mostly hyper- – Regional muscular involvement.
intense, sometimes of mixed intensity on T2W and • Increased size of the loco-regional lymph nodes is
T2-FLAIR sequences compared with brain tissue, observed in ~50% of cases.
388 CHAPTER 6.3
* *
(a) (b)
Fig. 6.3.8 Aural cholesteatoma in a 10-year-old English

Bulldog. Transverse T1W (a), T1W post-contrast (b),
and T2W (c) images showing the right tympanic bulla
filled by a soft tissue mass (dotted arrows, a and b) with
moderate expansion of the tympanic cavity. There is
thickening of the tympanic bulla wall (solid arrows) with
mild enhancement on the post-contrast image (b). There is
no contrast enhancement of the tympanic cavity content.
Severe dilatation of the lateral ventricles (asterisks, b) is
visible. (0.25T MRI system; images courtesy of Dr. Johan
(c)
van Ommen, Orion Dierenkliniek)
• In human medicine, diffusion-weighted MRI sequences tympanic bulla, or within the auditory tube and extend
have been used to detect cholesteatoma, with a into the nasopharynx (‘nasopharyngeal polyps’).
hypersignal on DW images attributed to a T2 shine- • Concurrent otitis externa or media can be present
through effect;32 however, this has not been evaluated depending on the location of the polyp.
in dogs. • Suggested etiologies are an ascending infection or con-
• The only treatment for aural cholesteatoma is surgery genital origin.19
(total ear canal ablation – lateral or ventral bulla oste- • Clinical signs typically result from the obstruction of the
otomy). Early surgical treatment is essential as inability nasopharynx (upper airway obstruction), with Horner’s
to open the mouth, neurologic signs on admission, and syndrome and head tilt being consistent with otitis media
lysis of any portion of the temporal bone are risk factors and otitis interna, respectively.19
for recurrence, which happens in approximately 50% of • MRI findings include (Fig. 6.3.10):33
cases.30 • Soft tissue mass, arising within the tympanic bulla or
auditory tube, possibly extending into the external ear
INFLAMMATORY POLYPS canal or nasopharynx.
• The polyps have heterogeneous signal intensity on
• Inflammatory polyps are commonly seen in young adult T2W images, and on T1W post-contrast images
cats and are rare in dogs. They can originate in the there is strong homogeneous contrast enhancement
external ear canal epithelium, the epithelial lining of the or peripheral enhancement only.
(a) (b)
(c) (d)
Fig. 6.3.9 Aural cholesteatoma in a 7-year-old male French Bulldog presented with a 1-year history of otitis externa, partially
responsive to antibiotics. Four months prior to MRI, the dog developed a head tilt (to the left) and left facial nerve paralysis.
Transverse T2W (a), T2-FLAIR (b), T1W (c), and T1W 3D post-contrast with fat saturation (d) images showing the left
tympanic bulla filled and severely expanded by a mass (arrow, a). The mass has heterogeneous signal intensity and is partially
contrast enhancing, mainly at the periphery, and there is a focal meningeal enhancement (dashed arrow, d) adjacent to the mass.
The wall of the affected tympanic bulla is severely thickened and irregular (arrowhead, d). (Images courtesy of Dr. Nagata,
Synergy Animal General Hospital)
390 CHAPTER 6.3
(a) (b)
Fig. 6.3.10 Inflammatory nasopharyngeal polyp in a 2-year-old Maine Coon cat. Serial transverse T1W 3D fast field echo
post-contrast images at the level of the auditory tube (a) and at its nasopharyngeal opening (b). In (a), the left auditory tube is
expanded by soft tissue material (solid arrow); at its rostral nasopharyngeal opening, there is a hyperintense, rounded, well-
defined polyp-like structure protruding into the nasopharyngeal lumen from the left dorsal wall (dotted arrow, b), with rim
enhancement. (1T MRI system; images courtesy of AJ van Belt, Utrecht University)
NEOPLASIA • Advanced imaging is an essential tool for final diagnosis

next to histopathologic examination,34 to localize the ori-
• Tumors of the auricular structures are quite uncommon, gin of the lesion and evaluate extension into the neigh-
and cats are more frequently affected than dogs.34 boring tissues, either for surgical debulking or radiation
• Squamous cell carcinoma (SCC) is a common neoplasm therapy planning.
and can affect the pinna and periauricular area in cats • MRI findings include (Fig. 6.3.11):8,22,35
where it is secondary to ultraviolet radiation exposure, • Ceruminous gland adenoma: local mass respecting
with white cats being predisposed to this condition.34 the integrity of the external ear canal wall.
SCC can also affect the external ear canal, more com- • Ceruminous gland adenocarcinoma:
monly in dogs. SCC is the most common neoplasm – Usually large, aggressive, highly invasive (from
affecting the middle ear and may arise directly from that external to middle and inner ear) and destruc-
region, or extend into the middle ear from a primary tive mass (osseous bulla and petrous temporal
tumor located in the external ear canal.34 bone).
• Adnexal neoplasms are also common tumors that may – The mass is usually of heterogeneous signal inten-
affect the external ear canal, including ceruminous or sity on T2W images and strongly enhancing on
sebaceous gland adenoma and adenocarcinoma. Chronic post-contrast T1W images.
local inflammation with increased exposure to cerumen – Invasion of adjacent structures (muscles, pharynx)
is considered a predisposing factor for development of or intracranial extension is common.
adnexal ear tumors.34 – Mandibular and retropharyngeal lymph node
• Clinical signs of ear neoplasia are quite like those of enlargement can be noted.
chronic otitis, and in general, neoplasia should be con- • Feline SCC may have a similar MRI aspect to ceru-
sidered in patients with signs of chronic otitis that are minous gland adenocarcinomas, from which they
non-responsive to medical management or recurring. are difficult to differentiate, which underscores the
Neoplasia involving the temporal bone (e.g., osteosar- importance of histopathologic confirmation.
coma, osteochondrosarcoma) may produce clinical signs
mimicking primary middle or internal ear disease.34
(a) (b)
Fig. 6.3.11 Infiltrative ceruminous gland adenocarcinoma in

a 7-year-old DSH cat presented with right-sided vestibular
signs. Transverse T2W (a), T1W (b), and T1W post-contrast
(c) images showing a diffuse soft tissue swelling on the right
side, involving the temporal muscles (solid arrow, a), the
horizontal ear canal, middle and inner ear, the mandibular
salivary gland (dotted arrow, a), and the other surrounding
tissues. There is a mild mass effect on the nasopharynx
(arrowhead, a). The lesion is heterogeneous on the T2W image,
isointense on the T1W image, and shows strong enhancement
in the T1W post-contrast image. There is enhancement of
the meninges on the side of the lesion (open arrow, c) and the
normal signal void of the petrous portion of the temporal bone
is partially lost, indicative of lysis and intracranial extension.
The left vertical ear canal is missing due to previous surgery
to remove a polyp. (1.5T MRI system; images courtesy of
(c)
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14. McGuinness SJ, Friend EJ, Knowler SP et al. (2013). 28. Persaud R, Hajioff D, Trinidade A et al. (2007). Evidence-
Progression of otitis media with effusion in the Cavalier King based review of aetiopathogenic theories of congenital and
Charles spaniel. Vet Rec 172(12):315. acquired cholesteatoma. J Laryngol Otol 121(11):1013–9.
15. Kent M, Glass EN, de Lahunta A et al. (2013). Prevalence of 29. Greci V, Travetti O, Di Giancamillo M et al. (2011). Middle
effusion in the tympanic cavity in dogs with dysfunction of ear cholesteatoma in 11 dogs. Can Vet J 52(6):631–6.
the trigeminal nerve: 18 cases (2004–2013). J Vet Intern Med 30. Harran NX, Bradley KJ, Hetzel N et al. (2012). MRI findings
27(5):1153–8. of a middle ear cholesteatoma in a dog. J Am Anim Hosp Assoc
16. Kent M, Talarico LR, Glass EN et al. (2015). Denervation of 48(5):339–43.
the tensor veli palatini muscle and effusion in the tympanic 31. Newman AW, Estey CM, McDonough S et al. (2015).
cavity. J Am Anim Hosp Assoc 51(6):424–8. Cholesteatoma and meningoencephalitis in a dog with chronic
17. Dvir E, Kirberger RM, Terblanche AG (2000). Magnetic otitis externa. Vet Clin Pathol 44(1):157–63.
resonance imaging of otitis media in a dog. Vet Radiol 32. Vercruysse JP, De Foer B, Pouillon M et al. (2006). The
Ultrasound 41(1):46–9. value of diffusion-weighted MR imaging in the diagnosis
18. Gotthelf LN (2004). Diagnosis and treatment of otitis of primary acquired and residual cholesteatoma: a surgical
media in dogs and cats. Vet Clin North Am Small Anim Pract verified study of 100 patients. Eur Radiol 16(7):1461–7.
34(2):469–87. 33. Allgoewer I, Lucas S, Schmitz SA (2000). Magnetic resonance
19. Kudnig ST (2002). Nasopharyngeal polyps in cats. Clin Tech imaging of the normal and diseased feline middle ear.
Small Anim Pract 17(4):174–7. Vet Radiol Ultrasound 41(5):413–8.
20. Woodbridge NT, Baines EA, Baines SJ (2012). Otitis media 34. Sula MJ (2012). Tumors and tumorlike lesions of dog and cat
in five cats associated with soft palate abnormalities. Vet Rec ears. Vet Clin North Am Small Anim Pract 42(6):1161–78.
171(5):124. 35. Negrin A, Cherubini GB, Lamb C et al. (2010). Clinical signs,
21. Stern-Bertholtz W, Sjostrom L, Hakanson NW (2003). magnetic resonance imaging findings and outcome in 77 cats
Primary secretory otitis media in the Cavalier King Charles with vestibular disease: a retrospective study. J Feline Med Surg
spaniel: a review of 61 cases. J Small Anim Pract 44(6):253–6. 12(4):291–9.
CHAPTER 6.4
NON-NEUROLOGIC CONDITIONS
OF THE HEAD AND NECK 393
Jimmy H. Saunders and

CONTENTS
Oral cavity/maxilla and mandibles ........................................................................................................................................................................394
Masticatory muscles .............................................................................................................................................................................................394
Anatomy, MRI anatomy, and normal variants ...................................................................................................................................................394
Masticatory muscle infection and abscessation ...............................................................................................................................................395
Canine masticatory myositis ............................................................................................................................................................................396
Temporomandibular joint ......................................................................................................................................................................................397
Pathology of the temporomandibular joints .....................................................................................................................................................397
Salivary glands .....................................................................................................................................................................................................398
Clinical signs of salivary gland disorders ........................................................................................................................................................398
Zygomatic sialadenitis .....................................................................................................................................................................................398
Sialocele .........................................................................................................................................................................................................399
Neoplasia ........................................................................................................................................................................................................400
Lymph nodes ........................................................................................................................................................................................................400
Neoplasia/inflammation/infection ....................................................................................................................................................................401
Pharynx, auditory (eustachian) tube ......................................................................................................................................................................401
Pharyngeal foreign body ..................................................................................................................................................................................401
Pharyngeal/laryngeal neoplasia .......................................................................................................................................................................404
Nasopharyngeal polyps ..................................................................................................................................................................................404
Larynx ...................................................................................................................................................................................................................404
Thyroid/parathyroid glands ...................................................................................................................................................................................404
Thyroid carcinoma (dogs)................................................................................................................................................................................406
Thyroid adenoma .............................................................................................................................................................................................407
Parathyroid gland disease................................................................................................................................................................................407
Carotid bodies.......................................................................................................................................................................................................407
Anatomy and physiology ................................................................................................................................................................................407
Carotid body paragangliomas ..........................................................................................................................................................................408
Other conditions....................................................................................................................................................................................................409
References.............................................................................................................................................................................................................409
394 CHAPTER 6.4
In this chapter, non-neurologic structures of the head and

neck, including the oral cavity, masticatory muscles, tem-
poromandibular joints, salivary glands, lymph nodes, phar-
ynx and larynx, thyroid/parathyroid glands, and carotid
bodies, are discussed. Conditions of the nasal cavity/
paranasal sinuses, ear, eye, and orbit are covered in other
chapters (Chapters 6.1–6.3).
ORAL CAVITY/MAXILLA AND MANDIBLES
• Despite promising preliminary results, the value of MRI

for diagnosis of oral cavity disorders has still to be dem-
onstrated and only a few studies have described some
MRI features of this region.1,2
• One study suggested a superiority of MRI compared
with CT to differentiate neoplastic from non-neoplastic
disorders, determine the size of oral masses, and assess
the degree of extension and invasion into adjacent
structures.1
• Dental structures are hypointense on all MRI pulse
sequences. The difference of intensity with the sur-
rounding alveolar bone enables detection of odontogenic
tumors, and the gross extent of the lesion can be clearly
defined with MRI.3
• Mandibular and retropharyngeal lymph nodes should
always be included in studies of the oral cavity and can
be easily evaluated with MRI (see below).
• There are only rare reports of the MRI appearance of
oral neoplasia in dogs.1 Masses of variable signal inten-
sity and contrast enhancement are easily depicted with Fig. 6.4.1 Left mandibular fibrosarcoma in a 10-year-old
MRI (Fig. 6.4.1). The soft tissue margins are typically Golden Retriever. An enhancing mass centered on the left
clearly visible, and the extension of the tumor within mandible is clearly visible and causing destruction of the
the adjacent bone is usually easily seen on MRI images, cortex, with loss of the normal hypointense cortical signal
reportedly better than with CT,1 likely because of the in the left mandibular body (compare with the other side).
superior soft tissue contrast of MRI. At the caudal limit of the lesion, extension of the neoplastic
• Maxillary or mandibular osteosarcomas were reported to tissue within the medullary cavity of the left mandible is
form very mottled, multiloculated masses, with markedly clearly appreciated (solid arrow). The hypointense roots
hyperintense, ‘popcorn-like’ pockets of fluid accumula- of the mandibular teeth are clearly visible (dotted arrows).
tion on T2W images.1 These pockets of fluid are thought (1.5T MRI system; image courtesy of Dr. Wilfried Mai,
to be due to hemorrhagic cystic cavities that form as a University of Pennsylvania)
result of the severe and aggressive bone destruction that
takes place in this tumor type.1
• MRI pulse sequences should include T2W images and
MASTICATORY MUSCLES T1W pre- and post-contrast images in the three planes;
STIR images and the use of fat saturation on post-
• MRI is an interesting tool for the early diagnosis of contrast images may enhance the conspicuity of lesions
inflammatory myopathies in dogs.4–9 by suppressing the bright inter- and intramuscular signal
• However, non-specific patterns often do not permit dis- of fat.
tinction between necrotic and inflammatory myopathies.
In addition, infectious and immune-mediated etiologies Anatomy, MRI anatomy, and
cannot be differentiated either.4,6,10 normal variants (Fig. 6.4.2)
• However, MRI may be used for evaluation of location • The muscles of mastication are the temporal, masseter,
and distribution of lesions, allowing one to determine the and medial pterygoid muscles (all jaw closers), the lat-
best site for tissue sampling. MRI is also useful for moni- eral pterygoid muscles (medial temporomandibular joint
toring the progression of lesions and treatment efficacy.9 translation), and the digastric muscles (jaw opener).11
Non-Ne u rol o gic C on di t ions of t h e H e a d a n d Ne c k 395
5
*
5 2 3
3
2
4 4
(a) (b)
Fig. 6.4.2 Normal masticatory musculature in a 1-year-old French Bulldog. Transverse T1W images of the head at the level
of the temporomandibular joints (a) and slightly caudal to these joints (b). 1, right temporal muscle; 2, right masseter muscle;
3, left medial pterygoid muscle; 4, left digastric muscle; 5, nasopharynx. The asterisk indicates the condylar process of the
right mandible, the solid arrow points at the left temporomandibular joint, and the dashed arrow points at the soft palate.
(1T MRI system)
• The temporal muscle is the largest of the masticatory canal, round foramen, and orbital fissure. It travels
muscles; it occupies the temporal fossa and is tightly ventrolaterally and attaches on the medial surface
attached to the lateral surface of the parietal, temporal, of the neck of the mandibular condyle. It is also best
frontal, and occipital bones. It arises from the sagittal evaluated on transverse images.11
crest, and becomes thicker in the more ventral region • The digastric muscle extends from the ventral part of the
(which is best appreciated on transverse images). From occipital bone to the ventromedial surface of the man-
its large origin, the muscle fibers curve rostrally and ven- dible (best appreciated on sagittal images). The origin of
trally underneath the zygomatic arch to insert onto the the muscle largely surrounds the tympanic bulla.
mandibular coronoid process; this insertion is also best • All muscles of mastication are innervated by branches
appreciated on transverse images.11 of the mandibular nerve, a branch of the trigeminal
• The masseter muscle is rectangular and rests on the lat- nerve.11
eral surface of the ramus of the mandible; it has some
well-developed bundles from the zygomatic arch to the Masticatory muscle infection
mandibular bone. It is a large muscle consisting of bellies and abscessation
that are clearly separated into two or three layers in MRI • Infection and abscessation of the masticatory muscles
transverse images.11,12 can result from:
• The medial and lateral pterygoid muscles lie between the • Oral and pharyngeal traumatic lacerations, with or
medial surface of the mandible and the pterygoid, pala- without a migrating foreign body.
tine, and basisphenoid bones: • External injuries and bite wounds.
• The medial pterygoid muscle has a well-developed • Cellulitis, sialadenitis, alveolitis, and otitis externa/
belly originating from the lateral surface of the ptery- media spreading into the surrounding musculature.
goid, palatine, and sphenoid bones (medial to the • MRI findings include (Fig. 6.4.3):13
zygomatic salivary gland), and travels caudolaterally • Intramuscular patchy areas of hyperintensity on T2W
to attach onto the medial and caudal aspects of the or STIR images.
angular process of the mandible. It is best evaluated • On post-contrast T1W images:
on transverse MRI images.11,12 – Marked patchy muscular contrast enhancement.
• The lateral pterygoid muscle is much smaller, orig- – In cases of abscess, central non-enhancing cavity
inating from the sphenoid bone, ventral to the alar surrounded by a rim of contrast enhancement.
396 CHAPTER 6.4
• MRI features reflect the stage of the disease and the

underlying pathologic changes (Fig. 6.4.4):4–10
• In the early stages, there is increased volume of the
affected muscles, with multifocal to coalescing ill-
defined, poorly demarcated areas of hyperintensity
on T2W images that are iso- to slightly hypo- or
hyperintense on T1W images compared with normal
muscle. These areas are also typically hyperintense on
STIR images. These changes are due to accumulation
of edema-like fluid and inflammatory cells in the dis-
eased muscles.
Fig. 6.4.3 Abscess in the right temporal muscle in a 5-year-

old French Bulldog. Transverse T1W post-contrast image
showing central irregularly shaped non-enhancing cavities,
containing fluid that is isointense to muscles (arrows).
There is marked peripheral enhancement of muscle tissues
surrounding these fluid pockets. The right temporal muscle
is enlarged compared with the contralateral one. (0.25T MRI
system; image courtesy of Dr. Johan van Ommen, Orion
Dierenkliniek)
• Mandibular and/or medial retropharyngeal lymph (a)

node enlargement.
• Additional MRI changes associated with the primary/
causal disorder (e.g., foreign body [signal void], otitis).
Canine masticatory myositis

• Canine masticatory myositis is an immune-mediated
disorder in which dogs develop auto-antibodies against
type 2M muscle fibers, which are exclusively found in the
masticatory muscles.4,5,14 The digastricus muscle is, how-
ever, typically less affected or not affected by the condi-
tion, because it contains predominantly type 2A fibers.15
• This condition is usually seen in large breed, young to
middle-aged dogs. In the acute phase, patients are pre-
sented with pain on yawning or masticating, whereas in
the more chronic phase, restricted jaw opening and mas-
ticatory muscle atrophy is visible.
• There is a juvenile form of masticatory myositis seen
in Cavalier King Charles Spaniel puppies with bilateral
masticatory muscle atrophy.16 This poorly understood (b)
condition results in difficulty opening the mouth. Fig. 6.4.4 Masticatory myositis in a 1-year-old Beagle dog.
• MRI is sensitive to the changes seen with myopathies Transverse T1W post-contrast (a) and T2W (b) images
and may be used to diagnose the condition, identify the showing ill-defined patchy hyperintense areas within
best sites for initial diagnostic tissue sampling, and then both temporal muscles on the T2W image (arrows, b)
follow up disease progression to assess response to ther- corresponding to areas of contrast enhancement (a). (1T MRI
apy, thereby obviating the need for repeated biopsies. system; images courtesy of AJ van Belt, Utrecht University)
• At the chronic stage, there is muscle atrophy, with

sometimes accumulation of fibrous connective tissue
causing areas of iso- to hypointensity on T1W and
T2W images. In people with chronic inflammatory
myopathies, affected muscles are typically hyperin-
tense on T1W and T2W images due to fatty infil-
tration; however, fatty infiltration is rarely seen in
animals.
• There is heterogeneous patchy contrast enhancement 3
of the diseased muscles. Areas of non-enhancement
are often seen, consistent with necrotic regions. 1
• Areas of low signal on T1W, T2W, and T2*W gradi-
ent echo images may be seen, suggesting mineraliza-
tion and/or hemorrhage.
• Mild mandibular and/or medial retropharyngeal lym-
phadenopathy may be present. 2
TEMPOROMANDIBULAR JOINT
Anatomy, MRI anatomy, and

normal variants (Fig. 6.4.5)
• The temporomandibular joint is a condylar joint formed
by the condylar process of the mandible and the man-
Fig. 6.4.5 Normal temporomandibular joint in an adult
dibular fossa of the temporal bone, with a thin articu-
Beagle dog. Transverse T1W post-contrast image.
lar disc that facilitates hinge and gliding movements.17
1, temporomandibular joint; 2, condylar process of the right
The disc is poorly developed in dogs because of the
mandible; 3, mandibular fossa of the right temporal bone.
simplistic jaw movements.18
(1T MRI system)
• The ossification of the mandibular condyle is completed
relatively late, so that its margins can appear irregular in
dogs up to 12 months old. In cats, the condyle is more Pathology of the
uniformly cylindric. There is an unnamed fossa in the temporomandibular joints
rostrolateral aspect of the condyle in the dog that can be • No specific study of the MRI appearance of temporoman-
pronounced in some breeds.14 dibular joint pathology exists in the veterinary literature
• The MRI anatomy of the temporomandibular joint in currently; however, like CT, this cross-sectional imaging
the normal dog has been described using high-field 1T technique may be useful for evaluation of patients with
MRI.19 disorders of these joints.13
• The cancellous bone of the condylar process of the man- • Some conditions, such as temporomandibular dysplasia,
dible and the mandibular fossa of the temporal bone are osteoarthrosis, or subtle traumatic injuries, may be dif-
hyperintense to muscle and isointense to hypointense to ficult to diagnose and evaluate with MRI, and are usually
fat on T1W images, mildly hyperintense to muscle on better assessed with CT.
T2W images, and are frequently heterogeneous.19 Their • Subchondral cysts appear as rounded well-defined
cortex forms a shell of signal void as typically seen on structures in the subchondral bone of the mandibular
MRI. condylar process and are hyperintense on T2W images,
• The articular disc is visible in ~70% of normal dogs on hypointense on T1W images, and non-enhancing.13
T1W and T2W images.19 It appears iso- to hyperintense • Tumors near the temporomandibular joint may affect
to muscle on T1W images and varies from hypo- to the joint either by extension of lysis (e.g., osteosarcoma,
hyperintense to muscle on T2W images.19 The lateral squamous cell carcinoma) or by mechanical encroach-
collateral ligament cannot be identified.19 ment with proliferative bony tumors such as benign oste-
• Another study focused on the use of a low-field 0.5T omas or multilobular tumors of bone arising from the
MRI system for imaging the temporomandibular joint.20 mandible or temporal bone. This latter type of tumor
It concluded that low-field MRI systems are able to dis- may appear as a mass with prominent irregular signal
play subtle anatomic structures using a dedicated coil voids on MRI, due to the new bone formation associated
and a small field of view. with these lesions.
398 CHAPTER 6.4
SALIVARY GLANDS • The mandibular gland is hyperintense compared with

the parotid gland.
Anatomy, MRI anatomy, and • The mandibular and major sublingual glands are overall
normal variants (Fig. 6.4.6) homogeneous on MR images, while the zygomatic and
• The salivary system is composed of the zygomatic, man- parotid glands are more heterogeneous.21
dibular, parotid, sublingual (monostomatic and polysto-
matic), and ventral buccal salivary glands. In cats, there Clinical signs of salivary gland disorders
is an additional molar salivary gland.20 • The symptoms of salivary gland disorders are related to
• The polystomatic sublingual, ventral buccal, and molar their anatomic location and type of disorder.
salivary glands cannot be identified as well as the normal • Although the zygomatic gland is less frequently involved
papillae and ducts of the different glands using low-field in disease processes, pathology of this gland is the most
MRI.21 documented in veterinary MRI literature, probably
• The ‘crescent-shaped’ parotid glands surround the exter- because of clinical signs similar to retrobulbar disease,
nal ear canals ventrally, which serve as a consistent ana- which are usually investigated using cross-sectional
tomic landmark; they are located dorsal and adjacent to imaging.22
the mandibular salivary glands. • Zygomatic gland disorders commonly result in pro-
• The zygomatic gland is in the pterygopalatine fossa, a trusion of the third eyelid, exophthalmos, decreased
consistent landmark, lateral to the origin of the ptery- or absent retropulsion of the globe, signs of pain on
goid muscle; it has an irregular trapezoid shape in the opening the mouth, papilla swelling, and periorbital
transverse plane. swelling.22
• The mandibular salivary gland is the biggest salivary
gland, located caudal to the mandibular ramus. It is oval- Zygomatic sialadenitis
shaped in the transverse plane. • Inflammation of the zygomatic gland is uncommon in
• The small (monostomatic) sublingual gland is located at small animals. Etiologies include:
the caudal level of the mandible between the base of the • Primary (immune-mediated).
tongue and the mylohyoid muscle. The digastric muscle • Secondary to trauma (blunt trauma, penetrating inju-
can serve as a landmark for visualization of the mandibu- ries such as bite wounds, foreign bodies).
lar and sublingual glands.20 • Extension of a systemic (viral) or local (tooth root)
• Compared with muscles, the normal salivary glands are infectious or neoplastic process.
iso- (7%–40%) to hyperintense (60%–90%) on T1W • Severe inflammation often results in secondary sialocele
images and hyperintense on T2W images. Moderate to and/or abscessation or even rupture of the gland.
marked contrast enhancement is observed on T1W post- • Zygomatic sialadenitis is often associated with inflam-
contrast images. mation of the adjacent masticatory muscles.
*
1
2
2
(a) (b)
Fig. 6.4.6 Normal salivary glands in an adult Beagle dog. Transverse T1W (a) and T2W (b) images. 1, right parotid salivary
gland; 2, right mandibular salivary gland. The asterisk (b) indicates the right external ear canal. (1T MRI system)
(a) (b)
Fig. 6.4.7 Zygomatic sialadenitis in a 10-year-old Labrador Retriever. Transverse T1W (a) and T2W (b) images at the level of
the orbits showing severe enlargement of the right zygomatic salivary gland (solid arrows) that extends ventrally; compare with
the normal left zygomatic gland (dotted arrow, b). The right medial pterygoid muscle (asterisk, b) is compressed by the enlarged
salivary gland and not well delineated compared with the left one (arrowhead, b). There is mild soft tissue swelling of the right
upper maxillary tissues (dashed arrow, a). The right salivary duct is distended (circle, b). (1T MRI system; images courtesy of
AJ van Belt, Utrecht University)
• MRI findings include (Fig. 6.4.7):22,23 more refractory to medical treatment. The presence of
• In the early stage, minimal alteration of signal inten- an abscess necessitates surgical drainage and/or removal
sities. of the gland.22
• Signal changes suggestive of inflammation of the
gland include hypointensity on T1W images and Sialocele
hyperintensity on T2W images compared with adja- • A sialocele is a fluid cavitation within the connective tis-
cent muscle. sue consisting of collected mucin. It may be due to local
• Marked homogeneous enhancement on post-contrast trauma to a salivary gland or obstruction of a salivary
T1W images. duct (by mucus retention or sialolithiasis).
• Enlarged volume of the gland and adjacent cellulitis • Clinically, this condition is characterized by a gradually
causing ocular globe displacement (dorsal, rostral, enlarging, fluctuant, painless swelling in the upper cer-
and/or lateral) in severe cases. vical or intermandibular region. The sublingual glands
• Mild to moderate T2W hyperintensity and varia- are most commonly affected; with further enlargement,
ble post-contrast T1W enhancement of the adjacent the sialocele may extend along the ventral neck, giv-
tissues (optic nerve, extraocular muscles, orbital fat, ing the animal a ‘frog-like’ neck shape (hence the name
masticatory muscles). ‘ranula’).
• Abscessation of the gland may form a cavitated lesion • MRI findings include (Fig. 6.4.8):23,24
with non-enhancing central areas of fluid (pus) • Fluid cavitation within or adjacent to the affected
that is T2 hyperintense, T1 hypointense, and non- salivary gland forming a well-defined fluid-
enhancing, and a strongly enhancing wall. distended sac; the content is hypointense on T1W
• Zygomatic sialadenitis usually resolves rapidly with images, hyperintense on T2W images, and non-
medical treatment. Patients with a large sialocele seem enhancing
400 CHAPTER 6.4
(a) (b)
Fig. 6.4.8 Zygomatic gland sialocele in a 7-year-old Shi Tzu with progressive exophthalmos. Transverse T1W post-contrast
(a) and T2W (b) images showing a large space-occupying fluid-filled loculated lesion in the right orbit (hypointense signal on
T1W and hyperintense signal on T2W) indicated by the solid arrows. The walls of the cavitated lesions are mildly enhancing
on the T1W post-contrast image (a). The ventral aspect of the lesion is in close contact with the right zygomatic salivary gland
(asterisk). (1T MRI system; images courtesy of AJ van Belt, Utrecht University)
• The wall of the sialocele usually enhances on T1W aspect of the angular process of both mandibles, along
post-contrast images. both sides of the facial vein and rostral to the mandibu-
• Cross-sectional imaging such as MRI is useful for lar salivary gland. They measure about 1–2 cm in length
surgical planning, which is the treatment of choice in dogs. Afferent lymphatic vessels to the mandibular
since drainage alone results in recurrence in 40% of lymph nodes drain the entire head, except the tongue,
affected animals.24 pharynx, larynx, and ear. The efferent vessels lead to the
medial retropharyngeal lymph node.25
Neoplasia • A single parotid lymph node, measuring about 1 cm in
• Primary salivary gland neoplasia, such as adenocarci- dogs and 5 mm in cats, is located caudoventral to the
noma, is very rare in dogs and cats. Surrounding soft temporomandibular joint. Its caudal half is covered
tissue tumors such as fibrosarcoma can infiltrate the sali- by the rostral aspect of the parotid salivary gland, and
vary glands. is therefore almost never discernible when normal. It
• Clinically, this condition usually manifests as a painless drains similar territories to the mandibular lymph nodes
swelling. with the addition of the ipsilateral parotid gland and the
• MRI findings include:23 ear. The efferent vessels lead to the medial retropharyn-
• An irregular mass originating from a salivary gland, geal lymph node.25
obliterating the corresponding gland. • The medial retropharyngeal lymph node measures
• The mass is usually of mixed signal intensity on T1W 3–4 cm in length in dogs. It is located on the dorsolateral
and T2W images with mostly strong, heterogeneous aspect of the pharynx, caudal to the digastric muscle and
contrast enhancement. The signal intensity depends ventrolateral to the longus capitis muscle. Its rostrolateral
on the tissue content and presence of fluid or necrosis. border is in contact with the mandibular salivary gland.
It drains the parotid and mandibular lymph nodes, the
LYMPH NODES cranial aspect of the esophagus and trachea (including the
thyroid gland), and almost the entire neck musculature.
Anatomy, MRI anatomy, The efferent vessels drain into the tracheal trunk.25
and normal variants • The lateral retropharyngeal lymph node is inconsis-
• Generally, two to three mandibular lymph nodes (up to tent and only present in about 30% of dogs, where it
five) are very superficially located near the caudoventral is very small. It is almost always present in cats.26 It is
superficially located, between the ear base and the wing PHARYNX, AUDITORY (EUSTACHIAN) TUBE
of C1. It drains the parotid salivary gland and the exter-
nal ear. Its efferent lymphatics lead to the medial retro- Anatomy, MRI anatomy,
pharyngeal node.25 and normal variants
• The superficial cervical lymph nodes (formerly named • The pharynx includes the oropharynx cranioventrally,
‘prescapular lymph nodes’) are usually paired, located the nasopharynx craniodorsally, and the larger laryngo-
cranial to the supraspinatus muscle, in between the cer- pharynx caudally.
vical muscles. They measure up to 4 cm in length in dogs. • The nasopharynx is cranially delimited by the choanae
They are composed of two dorsal nodes and a smaller and bilaterally bounded by the hamulus processes of
ventral one in cats, in which they also are more deeply the pterygoid bone. Its ventral limit is the soft palate.
located. They drain the cutaneous tissues of the head, Both the choanae and nasopharynx should be patent and
neck, and ears, the entire thoracic limb, and the cranial gas-filled.
thorax. Efferent vessels lead to the tracheal trunk, tho- • The rostroventral margin of the oropharynx is the base
racic duct, or external jugular vein.25 of the tongue while its dorsal margin is the soft palate.
• The cranial deep cervical lymph node is present in 30% Its lumen is generally collapsed, except when the patient
of dogs, is small (1 to 6 mm), and located cranial to the is intubated.
thyroid gland. This lymph node is absent in cats. • Caudally, the laryngopharynx is separated from the
• The middle deep cervical node is rarely present in dogs nasopharynx by the palatopharyngeal arches and from
and cats, is located along the mid-portion of the trachea, the oropharynx by the epiglottis. The laryngopharynx
and has a similar size to the cranial deep node. is bounded caudally by the larynx at approximately the
• The caudal deep cervical node is present in 30% of dogs, level of the axis.20
larger than the cranial and middle ones, and is located • The auditory tube is normally collapsed and not visible
ventral to the trachea, underneath the sternothyroid and on MRI. The tube exits the tympanic bulla rostrome-
sternohyoid muscles at the thoracic inlet. This lympho- dially via a short bony canal and continues rostrally as
center is composed of multiple smaller nodes in cats. a musculotubular canal, entering the dorsolateral naso-
• The facial vein is a consistent landmark to identify man- pharynx via a small ostium at a level just caudal to the
dibular lymph nodes, and the mandibular salivary gland hamulus process of the pterygoid bone.30
is a useful landmark to localize the medial retropha-
ryngeal lymph nodes. The parotid salivary gland or the Pharyngeal foreign body
external acoustic meatus are useful markers to identify • Most commonly reported oropharyngeal foreign bod-
the parotid lymph nodes, which are not consistently ies are wooden sticks (>70%), often found in medium to
seen. In some dogs, nodules within the lymphoreticular large breed dogs.31 This predisposition may reflect stick
tissue of the soft palate are seen.25 chasing activity in these breeds and posture of the head
• Compared with surrounding fat, lymph nodes are while retrieving.31
hypointense on T1W and T2W images and isointense • Other common foreign bodies include pieces of metal
on post-contrast T1W images. Compared with muscles, (fishhooks, needles), bones, and migrating foreign bodies
lymph nodes are isointense on T1W and hyperintense on like grass awns.31
T2W images. In T1W and T2W images, a hypointense • Clinically, the condition is characterized by:
band, created by the chemical shift artifact, can be seen • In acute cases, cervical swelling, hypersalivation, dys-
at the lymph node–fat boundary along the direction of phagia, and oral pain.
the frequency encoding gradient.27 • In chronic cases, swelling, abscessation, and a recur-
rent draining tract.31
Neoplasia/inflammation/ • In general, CT is considered a better modality for the
infection (Fig. 6.4.9) detection of foreign bodies while radiography has the
• Somewhat subjective MRI features that may be used lowest sensitivity.32,33 However, the sensitivity of an
to differentiate inflammatory and neoplastic condi- imaging method for diagnosis of foreign bodies depends
tions have been reported for the medial retropharyngeal on the type of foreign body. For example, radiography is
lymph nodes.28 adequate for glass and metal; ultrasonography for glass,
• Inflammatory lymph nodes are mildly to moderately metal, and plastic; CT for glass, porcelain, and fresh
enlarged, show moderate to marked perinodal enhance- wood; and MRI for dry wood, plastic, or porcelain.32,33
ment, homogeneous to heterogeneous contrast enhance- Conversely, radiography and CT are not indicated
ment, and local muscle contrast enhancement.28 for plastic foreign bodies. Ultrasonography is not the
• Metastatic lymph nodes are moderately to severely modality of choice for the detection of foreign bodies
enlarged and become more heterogeneous on T2W and located deep in the body or foreign objects surrounded
post-contrast T1W images than normal lymph nodes.28,29 by gas.
402 CHAPTER 6.4
(a) (b)
Fig. 6.4.9 Neoplastic right medial retropharyngeal lymph

node in a 6-year-old Newfoundlander with a tonsillar
squamous cell carcinoma. Transverse T1W post-contrast
(a), subtraction (T1W post- minus pre-contrast) (b), and
T2W (c) images showing moderate enlargement of the
right medial retropharyngeal lymph node (arrows) with
heterogeneous signal and areas of enhancement. 1, right
parotid salivary gland; 2, right mandibular salivary
gland. (1T MRI system; images courtesy of AJ van Belt,
(c)
Utrecht University)
• MRI may not be appropriate to identify metallic foreign • Various MRI findings have been reported
bodies because of the magnetic susceptibility artifacts (Fig. 6.4.10):32–37
that are associated with them. MRI is also less favor- • Typically, foreign bodies appear hypointense relative
able for locating foreign objects with low signal intensity to muscle and fat on both T1W and T2W images.
when they are surrounded by other low intensity struc- • The surrounding inflammatory response is usually
tures such as scar tissue, tendons, or calcifications.33 hypointense on T1W images and hyperintense on
• Several types of foreign bodies are associated with sus- T2W images. Avid contrast enhancement of the
ceptibility artifacts on MRI, including porcelain, metal, inflamed tissues is usually present on T1W post-
gas-containing wood (typically dry wood), certain types contrast images.
of nylon found in clothing, and stone.33 Detection of • Fluid pockets and sinus tracts are hypointense on
these foreign bodies can be improved by selecting pulse T1W and hyperintense on T2W images.
sequences that enhance this artifact, such as gradient • The appearance of wooden foreign bodies depends
echo pulse sequences, frequency-specific fat suppression, on their size, hydration, composition of surrounding
and pulse sequences with long time of echo. tissue, and presence of an inflammatory response.
(a) (b)
(c) (d)
Fig. 6.4.10 Pharyngeal foreign body (stick) in a 6-year-old German Shepherd Dog. Transverse (a) and sagittal (b) T2W and
transverse (c) and sagittal (d) T1W post-contrast images showing a large, cylindrical retropharyngeal foreign body (arrows).
On the T2W transverse images, alternating hyper- and hypointense concentric layers are noted (arrow, a); the outermost,
very hypointense layer represents fibrous tissue. Strong peripheral enhancement is noted in (c) and (d). (1.5T MRI system;
reproduced, with permission, from Dobromylskyj MJ, Dennis R, Ladlow JF et al. (2008). The use of magnetic resonance
imaging in the management of pharyngeal penetration injuries in dogs. J Small Anim Pract 49(2):74–9.)
The hyperintense signal around wooden foreign rich in water, may not be reliably identified at MRI
bodies on T2W images may serve as natural contrast, because of its higher signal intensity. Small wooden
improving their visualization, unless the foreign foreign bodies or wooden foreign bodies without
body has adsorbed enough fluid to increase its T2 associated collection of fluid are not easily identified.
signal. They typically appear as a geometric markedly A wooden object may fracture and fragments migrate
hypointense structure on T1W and T2W images to various locations including the retro-orbital space,
compared with the surrounding muscles, although retropharyngeal region, and submandibular and cer-
variations in signal intensity on T1W images have vical soft tissues, causing multiple simultaneous foci
been described. Fresh (green) wood, which is often of inflammation and infection.
404 CHAPTER 6.4
• Focal susceptibility artifacts may be seen with some LARYNX

foreign bodies, although if the artifact is too strong,
as with metal, image distortion may prevent accurate • Although the MRI appearance of pathologic conditions
localization of the foreign body.33 of the larynx has not been reported, the MRI anatomy of
• Regional lymphadenopathy is often present. the normal canine larynx has been described using T1W
• Oropharyngeal foreign bodies are challenging to treat sequences.39
effectively.38 In most cases, the owner has no knowledge • The laryngeal cartilages have variable signal intensity
of an initial injury and the original site of penetration, (Fig. 6.4.11):39
mostly the sublingual area, is only visible in 30% of the • The epiglottic and cuneiform cartilages, the cunei-
cases.31 More than 80% of animals present with signs of form and corniculate processes, and other parts of
chronic disease, which complicates surgical exploration the arytenoid cartilages have higher signal intensity
and decreases the chance of successful treatment.31,38 because of their collagen type II content, as well as the
The use of cross-sectional imaging with high sensitiv- presence of the laryngeal ligaments.39
ity to foreign material, such as CT or MRI, is therefore • Conversely, the cricoid and thyroid cartilages have
important in the management of these cases. lower signal intensity due to their hyaline nature.
• The laryngeal cavity and its ventricles are air-filled and
Pharyngeal/laryngeal neoplasia well seen as a signal void.39
• Pharyngeal neoplasia shares common features with oral • Laryngeal pathology is rarely investigated with MRI.
neoplasia. Laryngeal tumors are uncommon and their MRI appear-
• The most common oropharyngeal neoplasia includes ance has not been reported. One would expect a mass
malignant melanoma, squamous cell carcinoma, and fibro- lesion of variable signal intensity associated with the lar-
sarcoma in dogs, and squamous cell carcinoma in the cat.39 ynx. Destructive masses centered on the basihyoid bone
• These tumors are more commonly investigated with CT. may be seen with ectopic thyroid carcinoma.40
No consistent imaging features have been reported with
MRI; a mass of irregular shape and variable signal inten- THYROID/PARATHYROID GLANDS
sity is usually identified, with variable degrees and pat-
terns of contrast enhancement. Anatomy, MRI anatomy, and
normal variants (Fig. 6.4.12)
Nasopharyngeal polyps • The thyroid gland comprises two separate oblong lobes
• This condition has been covered in Chapter 6.3. that span the dorsolateral aspect of the trachea with the
1 2
(a) (b)
Fig. 6.4.11 Normal larynx in an adult Beagle dog. Transverse T1W (a) and T2W (b) images. 1, larynx; 2, transverse arytenoid
muscle; 3, lateral cricoarytenoid muscle. (1T MRI system)
T T
(a) (c)
T T
(b) (d)
Fig. 6.4.12 Normal thyroid glands in two adult dogs. Transverse (a) and parasagittal (b) T1W images and transverse (c) and
parasagittal (d) T2W images showing the thyroid glands (solid arrows). The glands are located between the carotid arteries
(dashed arrows, a) and the trachea (T). The open arrows point at the external jugular veins. A syrinx is present in the spinal
cord (dotted arrows, a and b). (1T MRI system; images courtesy of Stefanie Veraa, Utrecht University)
maximal cross-sectional area of the lobes located ventral • On post-contrast T1W images, there is a diffuse increase
to C2–C3 or C3 in more than 85% of dogs.41 in signal intensity, reaching an intermediate level between
• Most lobes are ovoid on transverse images and the right muscle and fat or becoming equal to fat; the parenchyma
lobe is slightly more cranially located than the left lobe also becomes more homogeneous.41
in dogs.41 • On T2W images, the parenchyma is heterogeneous
• In only a few large breed dogs does an isthmus connect with a relatively high intensity compared with pre-
the caudal aspect of both lobes.41 contrast T1W images, intermediate between muscle
• The cranial and caudal thyroid arteries and veins can be and fat.41
recognized after intravenous contrast injection.41 • On 2D T2*W gradient echo images, the intensity is gen-
• The mean maximal thyroid lobe diameter on transverse erally high, often being equal to or higher than CSF.41
images is 8.1 mm in dogs, being twice the mean diam- On this pulse sequence, the parenchyma appears homo-
eter of the common carotid artery.41 This ratio is an easy geneous in 65% and heterogeneous in 35% of cases, due
method for estimating normal thyroid gland size, avoid- to the presence of focal hypointense areas.41
ing the necessity of using reference values for different • On 3D T2*W gradient echo images (different repetition
dog sizes.41 time, time of echo, and flip angle, and a higher spatial
• On pre-contrast T1W images, the thyroid gland is isoin- resolution compared with the 2D acquisition mode), the
tense or slightly hyperintense compared with muscle, parenchyma is more frequently heterogeneous with pres-
with hypointense areas conferring an inhomogeneous ence of hypointense areas.41 The signal intensity of the
structure.41 gland is always equal to CSF in this sequence.41
406 CHAPTER 6.4
• On PDW images, the intensity of thyroid tissue is at least • Since canine thyroid tumors are almost always non-
higher than surrounding muscles, sometimes isointense secreting and therefore do not result in hyperthyroid-
to fat.41 Compared with T2W images, the thyroid paren- ism, thyroid masses will usually only be detected after
chyma is most often homogeneous.41 becoming large enough to become palpable/visible or
• In all pulse sequences, a difference in homogeneity cause clinical signs from mechanical compression of the
between the left and right lobes is rarely seen, while a surrounding structures.42 The lungs are the primary
difference in signal intensity is never observed. site of metastatic spread after local invasion of the thy-
• Normal parathyroid glands are not routinely recognized roid veins. Other sites of metastatic spread include the
on MR images, although large‐diameter glands may regional lymph nodes, kidneys, spleen, liver, bone, and
appear as focal hyperintensities on T2W images.41 spine.42
• MRI findings include (Fig. 6.4.13):43
Thyroid carcinoma (dogs) • Large mass along the dorsolateral aspect of the
• More than 70% of thyroid masses in dogs are thyroid trachea, just caudal to the larynx, that usually dis-
carcinomas.42 These are mostly unilateral, large, and fast places the ipsilateral common carotid artery laterally.
growing masses that are poorly encapsulated and locally • The mass is hyperintense on T1W (95%) and T2W
aggressively invasive.42 Ectopic thyroid tissue located images. A marked and heterogeneous enhancement is
anywhere from the base of the tongue to the base of the observed on T1W post-contrast images.
heart can undergo neoplastic transformation.42 • Cystic areas (T2 hyperintense and T1 hypointense)
• Carcinomas are non-functional in 90% of cases and or areas of dystrophic mineralization (T1 and T2
therefore do not result in hyperthyroidism.42 hypointense) are common.
T T
(a) (b)
Fig. 6.4.13 Thyroid carcinoma in a 9-year-old Staffordshire

Terrier. Transverse T2W (a), transverse T1W post-
contrast (b), and parasagittal T1W post-contrast (c) images
showing a large rounded mass at the level of the left
thyroid gland (solid arrows). This mass is hyperintense
to the surrounding muscles on the T2W image (a) and
heterogeneously contrast enhancing (b, c). The left carotid
artery (dashed arrows, a and b) is displaced dorsally and
medially by the mass. Dotted white arrows, esophagus.
(c)
(1T MRI system)
• Capsule disruption occurs in two-thirds of cases, fre- • The mass is hypointense on T1W and hyperintense
quently followed by local tissue invasion (blood vessels, on T2W images. A moderate to marked and heter-
musculature, nerves, larynx, trachea, esophagus). ogeneous enhancement is observed on T1W post-
• MRA images may highlight the deviated common contrast images.
carotid artery, engorged cranial and caudal thyroid • Cystic areas may be present, appearing as rounded
arteries, and vascularization and perfusion of the structures that are markedly hyperintense on T2W
thyroid masses. images, hypointense on T1W images, and non-
• Ectopic thyroid masses show similar features to in-situ enhancing. Nodular lesions of intermediate signal
thyroid masses. intensity may be seen lining the walls of these cystic
• Thyroid carcinomas and carotid body tumors show simi- cavities. On T2W images, less hyperintense material
lar MRI and histologic features. However, carotid body may be present in the dependent portion of these flu-
tumors are located dorsolaterally to the larynx at the id-filled cavities and may correspond to proteinaceous
level of the bifurcation of the common carotid artery.43 material sedimenting with gravity.44
Thyroid adenoma Parathyroid gland disease

• Hyperthyroidism is a common disorder in older cats, • The MRI appearance of parathyroid gland pathology has
nearly always due to thyroid adenoma or adenomatous not been well described in dogs and cats.
hyperplasia. In 70% of these, bilateral involvement of the • Benign or malignant parathyroid nodules may appear
lobes is present.42 the same as reported in people, forming well-defined
• Although less common than in cats, thyroid adenomas lesions within or adjacent to the thyroid glands, which
also occur in dogs and are mostly incidental findings are hypointense on T1W images and hyperintense on
discovered at necropsy, as these tumors do not produce T2W image, as was anecdotally illustrated in veterinary
clinical signs.42 texts.13
• Adenoma-associated hyperthyroidism affects mainly
cats older than 10 years.42 Clinically, the affected ani- CAROTID BODIES
mals show weight loss, increased appetite, hyperactivity/
nervosity, polydipsia and polyuria, vomiting, and Anatomy and physiology
regurgitation.42 • The carotid bodies are chemoreceptors located at the
• MRI findings include (Figs. 6.4.14, 6.4.15):44 carotid bifurcation into the internal and external carotid
• Well-marginated ovoid or rounded mass along the arteries. They detect changes in the composition of
dorsolateral aspect of the trachea, just caudal to the blood in the common carotid artery.45
larynx, that may displace the ipsilateral common • The chemoreceptors/paraganglionic cells composing
carotid artery laterally if large enough. the carotid bodies originate embryologically from the
(a) (b)
Fig. 6.4.14 Bilateral thyroid cystadenomas in a 9-year-old Boxer. Transverse T1W post-contrast (a) and T2W (b) images at the
level of the thyroid glands showing a moderately enlarged, very rounded right thyroid gland (solid arrows). Both glands are
homogeneously hyperintense on the T2W image and markedly homogeneously contrast enhancing (dashed arrows, left thyroid
gland). (1T MRI system; images courtesy of Dr. Silke Hecht, University of Tennessee)
408 CHAPTER 6.4
(a) (b)
Fig. 6.4.15 Thyroid adenoma found incidentally during brain imaging (cerebellar meningioma) in an 11-year-old mixed breed
dog. Parasagittal T1W post-contrast (a) and T2W (b) images. The thyroid gland (arrows) is enlarged, with multiple, small,
rounded hyperintense structures in the parenchyma on the T2W image and poor, heterogeneous contrast enhancement on the
T1W image. (1T MRI system; images courtesy of Dr. Silke Hecht, University of Tennessee)
neural crest and migrate along the branchial arches, in

close association with autonomic ganglion cells. In the
adult, extra-adrenal paraganglia form clusters of neuro-
endocrine cells that are closely associated with the auto-
nomic nervous system and are located at several sites
within the body.46
• Carotid bodies in normal dogs and cats are not visible on
MRI,45 but become visible when they undergo neoplastic
transformation.
Carotid body paragangliomas

• Carotid body paragangliomas are an uncommon cause of
neck masses in dogs.
• Clinically, the condition is marked by the presence of a
palpable cranial cervical mass. Clinical signs result from T
the space-occupying effects of the mass,47 with respira-
tory signs such as dyspnea, stertor, or increased respi-
ratory noise being the most common.46 Furthermore,
swallowing difficulties, sometimes ‘swallowing syn-
cope’, and circulatory disturbances due to compression
of the carotid artery are noted.48 Local tissue invasion Fig. 6.4.16 Carotid body tumor in a 5-year-old Labrador
may cause neurologic signs such as Horner’s syndrome, Retriever. Transverse T2W image at the caudal aspect of the
head tilt, or facial nerve paralysis.43,46 Distant metastases skull showing a large well-defined, very heterogeneous mass
to the lungs, mediastinal lymph nodes, liver, brain, and on the left side (arrow) displacing the trachea (T) to the right.
heart have been reported.45 (0.3T MRI system; image courtesy of Dr. Kaatje Kromhout,
• MRI findings include (Fig. 6.4.16):46–48 Ghent University)
• Large mass centered at the carotid bifurcation, with
poor or discrete margination. The carotid artery is of paragangliomas in people. The ‘salt’ components
often ‘entrapped’ by the mass. are the high-signal regions that correspond with slow
• Masses are heterogeneously hyperintense to muscles flow or hemorrhage and the ‘pepper’ components are
on T1W and T2W images. the multiple signal voids of vessels on both T1W and
• ‘Salt-and-pepper’ heterogeneity on T2W images, T2W images.
referring to hyper- and hypointense foci within the • Strong and heterogeneous contrast enhancement on
tumor, has been reported to be a characteristic feature post-contrast T1W images.
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foreign body in a Weimaraner. Vet Ophthalmol 10(6):390–3. dogs. Vet Radiol Ultrasound 48(6):544–9.
SECTION 4
MRI OF THE SPINE

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411
CHAPTER 7.1 Normal MRI spinal anatomy, degenerative disc disease, and
disc herniation
CHAPTER 7.2 Cervical spondylomyelopathy
CHAPTER 7.3 Degenerative lumbosacral stenosis
CHAPTER 7.4 Congenital and developmental anomalies and malformations
CHAPTER 7.5 Inflammatory and infectious conditions
CHAPTER 7.6 Spinal neoplasia
CHAPTER 7.7 Ischemic myelopathy, spinal cord hemorrhage, myelomalacia
CHAPTER 7.8 Extramedullary cyst-like conditions of the spine
CHAPTER 7.9 Syringomyelia
CHAPTER 7.10 MRI of the brachial and lumbosacral plexuses
CHAPTER 7.11 Degenerative spinal diseases
CHAPTER 7.12 MRI of spinal trauma
CHAPTER 7.13 MRI of paraspinal soft tissues

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CHAPTER 7.1
NORMAL MRI SPINAL ANATOMY, DEGENERATIVE

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DISC DISEASE, AND DISC HERNIATION 413
Wilfried Mai
CONTENTS
Basic anatomy of non-discal spinal structures ...................................................................................................................................................... 413
Normal MRI appearance of non-discal spinal structures ....................................................................................................................................... 415
The intervertebral disc: histology and normal MR appearance ..............................................................................................................................421
Spinal MRI technique and surgical landmarks ......................................................................................................................................................422
Classification of intervertebral disc disease ..........................................................................................................................................................423
Comparative imaging ............................................................................................................................................................................................427
MRI features of disc degeneration .........................................................................................................................................................................427
General MRI features of compressive degenerative IVDD ......................................................................................................................................427
MRI features of uncommon/atypical degenerative disc extrusion ..........................................................................................................................434
Intervertebral foraminal disc extrusion .............................................................................................................................................................434
Intradural or intramedullary extrusion ..............................................................................................................................................................434
Intravertebral disc herniation (Schmorl’s node)................................................................................................................................................438
Correlation between MRI, clinical signs, and prognosis in dogs with compressive degenerative disc disease .....................................................438
Cervical spine ..................................................................................................................................................................................................438
Thoracolumbar spine .......................................................................................................................................................................................438
Sacrococcygeal or intercoccygeal disc herniation............................................................................................................................................441
Lumbosacral stenosis ......................................................................................................................................................................................441
MRI features of acute hydrated nucleus pulposus extrusion ..................................................................................................................................441
References.............................................................................................................................................................................................................443
For many years, MRI has been considered the best method • Dorsal and ventral support for the intervertebral discs is
for identification of disc degeneration in dogs.1 Currently, provided by the longitudinal ligaments of the vertebral
MRI is recognized as a very accurate method for localiza- column (Fig. 7.1.1):8
tion of disc herniation and determination of laterality and • The dorsal longitudinal ligament (lig. longitudinale
degree of spinal cord compression,2–5 which are important dorsale) extends along the floor of the vertebral canal.
considerations for surgical planning. The procedure is non- – It is wider and thicker in the cervical region,
invasive and produces high-resolution multiplanar images which explains why lateral disc extrusion and
of the intervertebral discs, spinal cord parenchyma, and radiculopathy (root signature) are more common
subarachnoid and epidural spaces. The unique information in this region.9
provided by MRI (e.g., presence and extent of spinal cord – It is thinner and centered on midline in the
edema, signs of myelomalacia, presence of hemorrhage) also thoracolumbar area, allowing easier dorsal pro-
carries a prognostic value.6,7 trusion of disc material, and subsequent cord
compression.
BASIC ANATOMY OF NON-DISCAL – Unlike the intervertebral disc, the dorsal longi-
SPINAL STRUCTURES tudinal ligament is extensively innervated and
as a result, stretching and tearing of the outer
• There are reference texts available describing the detailed annulus fibrosus and dorsal longitudinal liga-
anatomy of the spine and intervertebral discs.8 We will ment, which are seen with disc protrusion and
only review the key anatomic features that are important extrusion, are proposed as a cause for ‘discogenic
to keep in mind when interpreting spinal MRI images. pain’ in dogs.10
414 CHAPTER 7.1
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• The ventral longitudinal ligament (lig. longitudinale not be mistaken for pathologic cord swelling on MR
ventrale) spans the ventral surface of the vertebral images.8,12
column.8 • By convention, spinal cord segments and vertebrae
• Additional ligaments of the spine include the intercapital have the same numeric order, with the exception of
and yellow ligaments: cord segment C8. However, the location of each cord
• The intercapital ligaments (lig. intercapitale) are short, segment is usually cranial to the corresponding verte-
transverse fibrous bands that join the heads of paired bral segment.8
ribs. They are located ventral to the dorsal longitu- • The ratio between the diameter of the spinal cord
dinal ligament (Fig. 7.1.1). They are only present and the diameter of the vertebral canal varies
between T2 and T11.8 They buttress the dorsal part between dog breeds, being higher in Dachshunds
of the annulus fibrosus, preventing dorsal disc herni- and generally in chondrodystrophic breeds versus
ation between these vertebrae. non-chondrodystrophic breeds.13 Regardless of the
• The yellow ligaments (ligg. flava) are also called inter- chondrodystrophic status, there is an increase in
arcuate ligaments. They are loose, thin, elastic sheets thoracolumbar vertebral canal diameter as a func-
and bridge the space between the arches of adjacent tion of weight in dogs, but the spinal cord diameter
vertebrae.8 does not vary significantly; this results in an inverse
• The spinal cord and spinal nerve roots are contained relationship between spinal cord-to-canal diameter
within the vertebral canal (juxtaposition of all the indi- and dog weight.12 This was also reported in the cer-
vidual vertebral foramina of the spine): vical spine based on myelographic findings.14 These
• The cranial and caudal extremities of the spinal cord features should be kept in mind when evaluating
are located respectively at the foramen magnum and the spinal cord for signs of swelling (e.g., edema) or
the ‘conus medullaris’, which is located caudal to L6 atrophy (e.g., degenerative myelopathy).
in smaller breeds of dogs and in cats and cranial to L6 • There are three meningeal layers surrounding the spinal
in larger breeds of dogs.11 cord (Fig. 7.1.1):
• Anatomically, normal regional widening of the spinal • The innermost is the ‘pia mater’ (pia mater spinalis),
cord is observed at the level of the cervical and lumbar firmly attached to the spinal cord and highly vascular.15
‘intumescences’, located at the 6th–7th cervical and • The ‘arachnoid membrane’ (arachnoidea spinalis) forms
4th–5th lumbar vertebrae, respectively; these should the middle layer.
Dorsal
longitudinal
ligament
Rib head Dura mater
Subdural
Intercapital space
ligament Arachnoid
membrane
Ventral Subarachnoid
longitudinal space
ligament Pia mater
(a) (b)
Fig. 7.1.1 Schematics representing (a) the location of the ventral/dorsal longitudinal ligaments and intercapital ligaments in the
thoracic spine and (b) a cross section of the spinal cord illustrating the arrangement of the meningeal layers.
Nor m a l M R I Spi n a l A n at om y, D e ge n e r at i v e D isc D is e a s e , a n d D isc H e r n i at ion 415
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• The outermost layer is the ‘dura mater’ (dura mater • On T1W images (Figs. 7.1.2–7.1.4):
spinalis). • Epidural and paraspinal fat appear hyperintense.16
• A layer of ‘dural border cells’ closely attaches the • The epidural fat provides contrast with the other
arachnoid membrane and dura mater to each other.15 spinal structures.
The virtual space between the arachnoid and dura • The spinal cord, nerve roots, and bone marrow are
mater is called the ‘subdural space’.15 isointense or slightly hypointense compared with the
• Between the arachnoid and pia mater is the ‘subarach- intervertebral discs.
noid space’, which contains CSF as well as arachnoid • With images of good contrast and spatial resolution,
trabeculae, forming a web that loosely attaches the the difference between gray and white matter can be
arachnoid to the pia mater. appreciated on transverse images, with the central
• Outside of the dura mater is the ‘epidural space’, which butterfly-shaped gray matter being hyperintense to
contains fat, fluid, and the internal vertebral venous the peripheral white matter (Fig. 7.1.4). This is an
plexus.15 inverse relationship to that observed in the brain, and
• The nerve roots exit the vertebral canal through the in people this is reportedly due to longer T1 relaxa-
paired intervertebral foramina. The collection of spinal tion times of the spinal cord white matter.17
nerve roots in the lumbosacral area is called the ‘cauda • On sagittal images, the gray matter of the spinal
equina’. cord can occasionally form a hyperintense line in the
• The spinal portion of the subarachnoid space is filled center of the cord (Fig. 7.1.2).
with CSF. It begins cranially at the foramen magnum • On transverse images, a low signal circumferential
(where it communicates with the intracranial subarach- ring is seen around the cord, representing a combi-
noid space) and ends caudally at the filum terminale near nation of the CSF in the subarachnoid space, chem-
the lumbosacral junction. ical shift artifact, and the meningeal structures
• CSF is also found in the central canal of the spinal cord, (Figs. 7.1.3, 7.1.4).16
which communicates with the 4th ventricle cranially and • The dorsal and ventral longitudinal ligaments as
terminates caudally blindly at the conus medullaris or, well as the ligamentum flavum may be visible in the
in some cases, is continuous with the lumbar subarach- intervertebral areas, where they appear as low inten-
noid space.8 The central canal is lined by ependymal sity structures separate from the bone.16
cells. • The joint capsule and synovial fluid of the articular
process joints are not clearly visible, although the
NORMAL MRI APPEARANCE OF NON- summation of the articular cartilage and synovial
DISCAL SPINAL STRUCTURES fluid can form a line separating the dark bone of the
articular facets (Fig. 7.1.5).
• On all pulse sequences, the vertebral cortical bone • The internal vertebral venous plexus consists of two
appears as a black shell (Fig. 7.1.2).16 sharply marginated symmetric hypointense ovoid
structures. They are located ventral to the cord in the
mid-region of the vertebral bodies, and then diverge
slightly abaxially at the level of the intervertebral disc
spaces (Fig. 7.1.5).
* • On fast spin echo (turbo spin echo) T2W series:
• The epidural and paraspinal fat are hyperintense
and the cord and the nerve roots are hypointense
(Figs. 7.1.3, 7.1.6).
• With images of good contrast and spatial resolution,
the difference between gray and white matter can be
Fig. 7.1.2 Sagittal T1W image of the cranial cervical vertebral appreciated on transverse images, with the central
column in an 8-year-old male castrated Beagle. The spinal butterfly-shaped gray matter being hyperintense to
cord is indicated by the double-headed arrow. The vertebral the peripheral white matter; in people this is report-
cortex forms a dark shell around the bones (arrowhead edly due to longer T2 relaxation times of the gray
pointing at the dens of the axis). A white thin stripe (arrow) matter (Fig. 7.1.4).17
is seen in the middle of the cord and likely represents the • The bone marrow is hypointense compared with the
gray matter of the spinal cord parenchyma. The CSF in the fat, iso- or hypointense to the spinal cord, and iso-
subarachnoid space forms a hypointense space conforming to intense to the muscles.18,19 Occasional patchy T1 and
the outer boundaries of the spinal cord (asterisk). (1.5T MRI T2 hyperintensities of the vertebral bone marrow can
system; image courtesy of Dr. Tobias Schwarz, University of be seen, which represent normal red hematopoietic
Edinburgh) bone marrow conversion into yellow fatty marrow.19,20
416 CHAPTER 7.1
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* *
NP
AF
(a) (b)
Fig. 7.1.3 Transverse T1W (a) and T2W (b) images at the
level of a lumbar intervertebral disc in a normal dog, and
transverse T1W post-contrast with fat saturation image (c)
of the cervical spine at C5-C6 in another normal dog. The
subarachnoid space, filled with CSF, forms a hypointense
ring around the cord on T1W images (asterisk, a), which is
markedly hyperintense on the T2W image (asterisk, b). The
epidural fat is hyperintense on the T1W and T2W images
(arrowheads, a and b), while it is suppressed and hypointense
after fat saturation (arrowhead, c). The hyperintense tissue
around the spinal cord on the post-contrast image (c)
corresponds to enhanced vascular structures associated with
the internal venous plexus. The nucleus pulposus (NP) of
the intervertebral disc is hyperintense on the T2W image (b)
while the annulus fibrosus (AF) is hypointense. On the T1W
image (a), the disc is iso- to hypointense to the spinal cord.
The central canal is visible on the T2W image, forming a
hyperintense dot in the middle of the cord (arrow) due to its
(c)
CSF content. (1.5T MRI system)
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(a) (b)
Fig. 7.1.4 Transverse T1W (a) and T2W (b) images of the cervical spine in two dogs at the level of C6 and C3, respectively,
showing the normally butterfly-shaped hyperintense gray matter (arrows) compared with the hypointense white matter. On
the T2W image (b), the nucleus pulposus shows mottled areas of low signal consistent with degenerative changes (arrowhead).
The CSF in the subarachnoid space (dashed arrows) is hypointense on the T1W image and hyperintense on the T2W image.
(1.5T MRI system)
They should not be mistaken for pathologic changes; on direction and velocity of blood flow within these
the use of fat suppression techniques can help dif- sinuses.
ferentiate these incidental signal changes from true • The basivertebral venous canal can occasionally be
pathology (Fig. 7.1.7).21 seen on T2W images forming a Y-shaped slightly
• Depending on patient size and image resolution, the hyperintense structure on transverse images and a
T2 hyperintense synovial fluid can be seen forming vertical hazy hyperintense area in the middle of the
a bright line separating corresponding articular pro- vertebral body on sagittal images (Fig. 7.1.9).
cesses of adjacent vertebrae (Fig. 7.1.8). • Sequences with heavy T2 weighting, such as T2W
• The CSF in the subarachnoid space forms a thin single-shot fast spin echo (SS-FSE), enhance the
hyperintense ring around the cord,16 but may be signal from CSF while suppressing the signal from
difficult to differentiate from the hyperintense epi- background tissue, giving a natural ‘myelographic’
dural fat depending on the amount of T2 weighting effect; they are often referred to as ‘T2-myelograms’
(Figs. 7.1.3, 7.1.4, 7.1.6). for that reason.22–24
• The internal vertebral venous plexus can also be seen • As described above, the spinal cord-to-vertebral
on T2W images, forming two sharply marginated canal diameter ratios vary inversely with dog size.
symmetric ovoid structures ventral to the cord in the Pathologic changes in spinal cord size can be appreci-
mid-region of the vertebral bodies, and then diverg- ated on MRI, and Table 7.1.1 can be used as a general
ing slightly abaxially at the level of the intervertebral guideline for the normal thoracolumbar spinal cord-
disc spaces; their signal intensity varies depending to-canal ratios in dogs.12
418 CHAPTER 7.1
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(a) (b)
(c) (d)
Fig. 7.1.5 Transverse T1W pre-contrast images at the level of the C5-C6 space (a) and mid C6 (c) and corresponding post-
contrast images with fat saturation at C5-C6 (b) and mid C6 (d). The internal venous plexus is visible forming two rounded
structures over the vertebral body in the mid-body region (arrowheads, c and d). Over the disc space, the internal venous plexus
is abaxially displaced (dashed arrow, b), and gets closer to the intervertebral veins (dotted arrows, b). The open arrows in (b) and
(d) point at the vertebral veins. Note the contrast enhancement of these vascular structures in (b) and (d). The articular process
joints are visible, with the articular cartilage and synovial fluid forming a hypointense line between the dark vertebral cortical
bone margins (solid arrow, a). (1.5T MRI system)
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* *
NP
AF
(a) (b)
Fig. 7.1.6 Transverse T1W (a) and T2W (b) images at the level of L5 in a dog. The thecal sac (juxtaposed dura mater and
arachnoid membrane) forms a hypointense ring (arrowhead, b) around the conus medullaris (dotted arrows) and cauda equina,
and is filled with T2 hyperintense (b) and T1 hypointense (a) CSF. The nerve roots appear as hypointense small rounded
structures, some located in the epidural space and others in the thecal sac (solid arrows). The epidural fat (asterisks) outside of
the thecal sac is hyperintense in both images. AF, annulus fibrosus; NP, nucleus pulposus. (1.5T MRI system)
(a) (b)
Fig. 7.1.7 Sagittal T2W (a) and STIR (b) images of the caudal lumbar spine in a dog. On the T2W image, there is a focal area of
hyperintense signal in the cranial endplate of L5 (arrowhead), which is suppressed on the STIR image (arrowhead), indicative of
normal red hematopoietic bone marrow conversion into yellow fatty marrow. Nuclear clefts are visible in the nucleus pulposus of
all discs on the T2W image, indicative of early degenerative changes (arrows). (1.5T MRI system)
420 CHAPTER 7.1
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* *
* *
(a) (b)
Fig. 7.1.8 Parasagittal T2W image (a) and reformatted parasagittal CT image (b) of the cervical spine in a dog showing the
corresponding articular processes of two adjacent cervical vertebrae (asterisks). On the T2W image, the hyperintense synovial
fluid within the articular process joint is visible (arrow).
(a) (b)
Fig. 7.1.9 Sagittal (a) and transverse (b) T2W images of the lumbar spine in a dog showing the linear (a) and Y-shaped (b)
hyperintense structure formed in the middle of the vertebral body by the basivertebral venous canal (arrowheads), which serves
as a communicating venous branch between the internal and external vertebral venous plexus. Nuclear clefts are present in the
middle of the nuclei of the discs, consistent with early degenerative changes (arrow, a). (1.5T MRI system)
Table 7.1.1 Spinal cord-to-vertebral canal diameter ratio

measured on T2W sagittal images in dogs of
various weights, at the level of T4, T9, and L3;
presented as median and range (T4) or mean
+/– standard deviation (T9 and L3).12
BODY WEIGHT T4 T9 L3
1–10 kg 0.78 (0.69–0.80) 0.74±0.09 0.76±0.09
11–20 kg 0.67 (0.67–0.76) 0.74±0.06 0.68±0.08
21–30 kg 0.56 (0.53–0.57) 0.60±0.11 0.58±0.08
>30 kg 0.55 (0.53–0.59) 0.49±0.05 0.51±0.08
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THE INTERVERTEBRAL DISC: HISTOLOGY • There is more collagen (primarily collagen type I)
AND NORMAL MR APPEARANCE and less ground substance in the annulus than in the
nucleus.
• The intervertebral disc is made of a peripheral ‘annulus • Water, bound to large proteoglycan molecules, is the
fibrosus’ and a central ‘nucleus pulposus’.25 Histologically, principal component of the nucleus pulposus (80%–
they are separated by a transition zone.10,26 The ventral 88%), and confers its gelatinous consistency.28 This
part of the annulus is thicker than the dorsal part.25 In allows the disc to function as a hydroelastic cushion
the adult animal the nucleus pulposus is the surviving that maintains its width during loading.10
structure of the embryologic notochord.27 • On MR images, the difference between nucleus
• The disc lies in close contact with the cartilaginous end- pulposus and annulus fibrosus of the normal (non-
plates of adjacent vertebrae, with fibers from the nucleus degenerated) disc is best appreciated on T2W images,
pulposus and annulus fibrosus being interwoven with the where the nucleus has a very bright signal caused by
collagen fibers of the cartilaginous endplates and bony the long relaxation time of water (Figs. 7.1.3, 7.1.10).25
trabeculae.16 The endplates play an essential role in sup- The inner portion of the annulus fibrosus is also water
plying the disc with nutrients and oxygen by diffusion rich and hyperintense.18,25
and osmosis from the capillary buds through the semi- • On T1W transverse images, the intervertebral disc
permeable endplates.26 has medium signal intensity (Fig. 7.1.3).18 On trans-
• Both the annulus and the nucleus are made of fibro- verse images, the annulus fibrosus should form a low
cartilage but contain different amounts of collagen and signal intensity continuous ring of fibers around the
ground substance (composed of hyaluronic acid and nucleus.25
glycosaminoglycans that hold water due to their strong
negative charge):18
SC
SC *
NP
NP
*
(a) (b)
Fig. 7.1.10 Sagittal (a) and transverse (b) T2W images of the cervical spine in a canine specimen (a) and a normal dog (b)
showing the hyperintense signal of a normal nucleus pulposus (NP) surrounded by the hypointense annulus fibrosus (asterisks).
The spinal cord is indicated (SC). The bright signal around the spinal cord results from the summation of the CSF in the
subarachnoid space and epidural fat. (1.5T MRI system)
422 CHAPTER 7.1
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SPINAL MRI TECHNIQUE AND

SURGICAL LANDMARKS
• The optimized MRI technique for spinal imaging

is described in Chapter 4.2 and also detailed in the
literature.29
• Although spontaneous resorption of compressive disc
material has been rarely described,30 orthopedic and
neurosurgical veterinarians typically agree that surgi-
cal decompression is the treatment of choice,10 and MR Fig. 7.1.11 Parasagittal T2W image of the thoracolumbar
spine in a dog. The rounded rib heads (arrowheads) and
images are used not only to diagnose the condition at
ellipsoid lumbar transverse processes (arrows) are visible and
hand but also to localize compressive lesions in order
have distinctly different shapes that can be used as imaging
to plan the surgical approach. An accurate localization
landmarks. (1.5T MRI system)
of the compressive site is important to avoid errors and
minimize surgical and anesthetic times.
• The tomographic nature of MRI can cause problems in
localization because anatomic features that are helpful
landmarks may be excluded from the images, especially
when a small FOV is used. T13
• For cervical or lumbosacral compressive lesions, local- AO
ization is usually quite straightforward due to distinctive
anatomic features such as the atlas, axis, or sacrum.
• For thoracolumbar compressive lesions, bony landmarks
such as the ribs and sacrum can be used for localization. Fig. 7.1.12 Sagittal T2W image of the thoracolumbar spine in
If diagnostic series have relatively small FOVs (to opti- a dog. The celiac artery (arrowhead) and cranial mesenteric
mize resolution), it is important to obtain large FOV artery (arrow) are visible coming off the aorta (AO) and
localizer (scout) images in order to be able to count the are both located ventral to T13 in this particular dog as
vertebrae accurately and reduce the risk of missing a determined by evaluation of additional parasagittal images or
vertebral malformation that could affect accurate local- images of the lumbosacral spine (not shown). There is variable
ization of individual disc spaces at surgery. This is impor- degree of loss of the normal T2 hyperintense signal of the
tant, as dogs can have unusual numbers of vertebrae; for nucleus pulposus and decreased width of all discs between
example, about 10% of Dachshunds are reported to have T4-T5 and T11-T12, consistent with disc degeneration.
variations in the number of vertebrae in some segments (1.5T MRI system)
of the spine.31 However, large FOV scout images may
not be feasible depending on equipment, such as type of • The celiac and cranial mesenteric arteries, typically well
MRI machine, or selected coil. If the scout images are visible on sagittal images ventral to the spine, are poor
not of sufficient quality to identify skeletal abnormali- anatomic landmarks, and should be used with caution.
ties, or confidently count the vertebrae, it may be useful Although they are located ventral to L1 in most cases,
to obtain a routine survey radiograph in all animals prior there is considerable variation (Fig. 7.1.12), and there-
to, or immediately after, the MRI scan. fore it is not advisable to use these landmarks for accurate
• Dorsal images can be used to identify the last ribs and identification of vertebral order at the thoracolumbar
costovertebral articulations, but are not necessarily level.29,33 However, once the vertebral segment immedi-
part of the standard imaging protocol for disc disease.32 ately dorsal to them has been confidently identified in a
When dorsal images are not available, sagittal images specific patient, these two vessels are useful landmarks to
can be used to identify the last pair of ribs. On parasagit- identify vertebral segments across FOVs.32
tal images along the lateral edges of the vertebral bod- • Recommendations for spinal MRI protocols are presented
ies, the rib heads and transverse processes have distinctly in Chapter 4.2; however, it is worth mentioning here that
different shapes:33 limited MRI examinations for disc herniation (e.g., con-
• Costovertebral articulations appear as small, round, sisting of a T2W sagittal series to determine suspicious
well-demarcated hypointense areas at the level of the sites followed by a focal transverse series limited to these
base of the vertebral canal (Fig. 7.1.11). levels) should be exercised with caution. It was reported
• In contrast, transverse processes appear as ellipsoid that the evaluation of sagittal T2W series to localize
or oval-shaped, well-demarcated hypointense areas compressive disc herniation was not 100% accurate and
located at the level of the middle or ventral third of could lead to erroneous localization of significantly com-
the vertebral body height (Fig. 7.1.11). pressive lesions.34 If sagittal images are used to guide a
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limited transverse series in dogs with disc herniation, it intervertebral disc degeneration is in many ways similar
is recommended that transverse images are obtained not to that observed in humans.26
only of the suspicious site, but also the disc spaces imme- • Canine degenerative IVDD was historically first classi-
diately cranial and caudal to this. If multiple sites of com- fied by Hansen:48
pression are suspected, then transverse images across the • In ‘chondroid degeneration’ (Hansen type 1 IVDD),
entire spinal segment are recommended to determine there is early notochordal and chondrocyte-like cell
the most significant compressions.34 senescence within the nucleus pulposus. This results
• A recent study with low-field imaging, comparing sagit- in shifting concentrations of glycosaminoglycan, loss
tal T2W and STIR series (either isolated or in combina- of water and proteoglycan content, and increased
tion) to identify sites of disc extrusion in dogs, showed collagen content. The disc becomes more cartilag-
that sagittal STIR series should be considered a useful inous, and its nucleus becomes more granular, loses
adjunctive sequence to improve the radiologist’s con- its hydroelastic shock-absorbing qualities, and often
fidence and help minimize false-negative diagnoses, mineralizes.27 Ultimately, this degenerative process
whenever a lesion has not been identified on preliminary can lead to herniation of the nucleus pulposus through
T2W sagittal screening. The study suggested that sag- the annular fibers, with subsequent ‘extrusion’ of
ittal STIR series should be given consideration before degenerated nuclear material into the vertebral canal.
concluding that intervertebral disc extrusion does not This type of disc degeneration starts early in life, and
exist within the scanned field.35 is found most commonly in young chondrodystrophic
• Along the same line, the use of only ultrafast, heavily dogs.49
T2-weighted pulse sequences (e.g., SS-FSE, HASTE) to • In ‘fibroid degeneration’ (Hansen type 2 IVDD),
localize compressive lesions is also not recommended. there is progressive increase in fibrous content of the
These pulse sequences, often called ‘T2-myelograms’, nucleus, with shifts in proteoglycan ratios, dehydra-
highlight the bright signal from CSF in the subarach- tion, and possible mineralization as well (although
noid space, yielding images that resemble the traditional less common than with chondroid degeneration).
radiographic myelogram, and can help quickly local- Ultimately, this can cause rupture of the inner layers
ize areas of extradural compressions due to the focal of the annulus fibrosus and partial displacement of
attenuation/deviation of the subarachnoid space signal. the nucleus pulposus into the disrupted portion of the
However, a study showed poor agreement with the regu- annulus (‘protrusion’); this results in outward protru-
lar T2W pulse sequences when compressive lesions are sion of the peripheral portion of the annulus, due to the
present, and therefore regular T2W series should always mass effect from the displaced nucleus, together with
be acquired in conjunction.22 T2-myelogram series may subsequent hypertrophy of the peripheral annulus.27
have diagnostic value in that they slightly improve the This type of herniation is more commonly observed
accuracy of the T2W sagittal series to identify signifi- in non-chondrodystrophic dogs, and the degenerative
cant compressive sites, especially when multiple areas of process starts later in life.49 However, some studies
disc herniation are present.22,34 showed that 62%–92% of non-chondrodystrophic
dogs weighing more than 20 kg with thoracolum-
CLASSIFICATION OF INTERVERTEBRAL bar compressive disc disease had disc extrusions as
DISC DISEASE opposed to protrusions.50,51
• This simplified histopathologic classification of degen-
• ‘Intervertebral disc disease’ (IVDD) is an imprecise erative processes of the disc has practical limitations, and
umbrella term, used to indicate any form of interverte- is in fact not used in human medicine by the American
bral disc change, whether it is associated with displace- Society of Spine Radiology.27 With the more detailed
ment (‘herniation’) of portions of the disc or not, and imaging of the patterns of disc herniation that it is pos-
whether it is clinically significant or not.27 sible to achieve with MRI, more recent studies have
• In most cases, IVDD follows degeneration of the inter- divided IVDDs into several categories based on MRI
vertebral disc.25,36,37 The exception is the acute extrusion appearance:52
of non-degenerated (i.e., hydrated) disc material,27 often • ‘Disc bulging’ corresponds to circumferential exten-
associated with some form of traumatic event (see spe- sion of the disc beyond the margins of the vertebral
cific paragraph below, MRI features of acute hydrated endplates; on transverse images, there is extension of
nucleus pulposus extrusion).28,38–47 the outer rim of the annulus beyond the margin of the
• Degeneration of the intervertebral disc is a complex and intervertebral disc space over >50% of the disc cir-
multifactorial process that is characterized by changes in cumference (Fig. 7.1.13a).27,52
the composition of the cells and extracellular matrix of • ‘Disc protrusion’ (Figs. 7.1.13b, 7.1.14) is defined
the nucleus pulposus, annulus fibrosus, transition zone, as partial extension of the nucleus and portion of
and vertebral endplates. The pathophysiology of canine the annulus through disrupted fibers of the annulus
424 CHAPTER 7.1
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(b)
(a)
Fig. 7.1.13 Disc bulging (a), protrusion (b), and extrusion (c).

(a) Transverse T2W image at the C5-C6 disc space in a dog.
There is moderate disc bulging causing mild deformity of the
ventral margin of the cord but no significant compression.
(b) Transverse T2W image at the C5-C6 disc space in a dog
with focal disc protrusion causing mild left ventral spinal cord
compression. (c) Transverse T2W image at the C2-C3 disc
space in a 6-year-old female dog with disc extrusion causing
marked left ventral cord compression. A large hypointense left
ventral irregular extradural mass is present, corresponding to
(c)
extruded disc material. (1.5T MRI system)
but without complete rupture of the annulus (corre- to type 1 in Hansen’s classification system). This
sponding to type 2 in Hansen’s classification system); extruded material can completely detach from the
the compressive material has an attachment with the disc it originates from and form a free extradural
annulus fibrosus that is greater in length than the dis- mass lesion, with various degrees of dispersion of this
tance of displacement into the vertebral canal, in any material in the epidural space (‘disc herniation with
imaging plane.2 fragmentation’).52
• ‘Disc extrusion’ (Figs. 7.1.13c, 7.1.14) is seen when • ‘Acute hydrated nucleus pulposus extrusion’
portions of the nucleus +/− inner annulus traverse (AHNPE):27 if a disc with a well hydrated nucleus
through all layers of the outer annulus and form a pulposus (i.e., completely normal or with only early
focal mass in the extradural space, deviating epidural degenerative changes) is placed under a stress exceed-
fat and, depending on the size of the herniation, the ing its normal strength, the dorsal annulus fibro-
subarachnoid space and spinal cord (corresponding sus may rupture and some of the normal jelly-like
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(a) (b)
Fig. 7.1.14 Schematic representation of disc extrusion and protrusion. Disc extrusion (a) is present when portions of the nucleus
+/− the inner annulus traverse through all layers of the outer annulus and form a focal mass in the extradural space. Disc
protrusion (b) is defined as partial extension of the nucleus and a portion of the annulus through disrupted fibers of the annulus
but without complete rupture of the annulus.
nucleus pulposus may be extruded into the vertebral these cases showed material consistent with nucleus
canal. Because the non-degenerated nucleus mate- pulposus, with various degrees of mild degeneration.60
rial is normally hydrated, it has the ability to diffuse It is therefore preferable to use the terminology ‘com-
in the epidural space, leaving only the secondary pressive acute hydrated nucleus pulposus extrusion’ to
changes attributable to acute spinal cord contusion, describe this condition in dogs.27,60,61
with no or only subtle extradural spinal cord com- • Although in the majority of cases compressive disc dis-
pression.28,39,41,43,53 However, the condition can also ease occurs in the absence of a significant traumatic
cause spinal cord compression,38,54,55 mostly in the event and as a result of chronic degenerative changes in
cervical region. Therefore, there are both ‘com- the disc, traumatic disc extrusion does occur, and may
pressive’ and ‘non-compressive’ forms of AHNPE. be more frequent than initially thought. Traumatic disc
Several terms have been used to describe the non- extrusion can involve non-degenerated hydrated discs
compressive form of this syndrome, including ‘trau- (AHNPE described above), but also degenerated discs.
matic disc prolapse’, ‘traumatic disc herniation’, ‘disc A recent study found that disc extrusion appears to be
explosion’, ‘non-compressive nucleus pulposus extru- more common than previously reported in dogs with
sion’, ‘Hansen type 3 disc disease’, ‘high-velocity- spinal trauma,41 affecting 62% of 50 dogs with spinal
low-volume disc disease’, ‘traumatic intervertebral injury. Spinal cord compression as a result of these trau-
disc extrusion’, ‘hydrated nucleus pulposus extrusion’, matic extrusions was not common (29% of cases), and was
and ‘acute non-compressive nucleus pulposus extru- more often seen in older and chondrodystrophic dogs,
sion’.27,28,38,39,43,45,46,53–55 The compressive form of the suggesting that some degree of disc degeneration prior
disease was previously improperly referred to as ‘discal to trauma would make it more likely for the extruded
cyst’ or ‘ventral intraspinal cyst’,56–58 in reference to a material to cause spinal cord compression.41
human condition, where cysts that communicate with • Atypical degenerative disc extrusion: extrusion of degen-
the intervertebral disc form in the ventral aspect of erated disc material of clinical significance can have a
the vertebral canal and cause spinal cord compression. different presentation than the classic extrusion into the
In spite of sharing similar MRI characteristics, the epidural space causing spinal cord compression. Types of
canine condition actually has a different clinical pres- extrusion in that category would include:
entation and pathophysiology.38,54,55 Microsurgical • Foraminal extrusion causing nerve root compression
studies showed that the lesion is caused by hydrated instead of spinal cord compression/contusion. This
disc material extruded within the fibers of the dorsal is an uncommon condition, which has probably been
longitudinal ligament forming a contained ventral underdiagnosed prior to the advent of MRI in veteri-
extradural compressive mass lesion.59 Cytology and nary medicine. The condition may be more common
histopathology of compressive material removed in in the cervical segment due to anatomic particularities
426 CHAPTER 7.1
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in that area: the dorsal longitudinal ligament is wider longitudinal ligament, and annulus fibrosus, which
in the cervical area than the thoracolumbar region, may easily rupture during a recurring extrusion and
forcing the herniation to occur in a dorsolateral direc- facilitate the translocation of disc material into the
tion. There are also anecdotal reports of this condi- subarachnoid space or spinal cord.68 Most reported
tion occurring at L6-L7 and L7-S1.62–64 Dorsolateral intradural or intramedullary extrusions were located
(foraminal) extrusion may happen in these locations near the thoracolumbar junction,42,65–70 with only a
due to the dorsal and ventral portions of the annulus few reports in the cervical and lumbar areas.44,47,71 In
being thicker than at the thoracolumbar junction this type of disc extrusion, the extruded disc material
(where dorsal, compressive extrusions are typi- may be normal,72 but typically shows some degree
cally seen).63 Dogs of various ages and breeds can be of degenerative changes histopathologically.42,47,65–68
affected. In the cervical location, neurologic exam- The affected spinal cord segment shows areas of
ination is often normal, with cervical hyperesthesia malacia and hemorrhage of the white and gray matter
and lameness being the most common presenting with loss of architecture.72
complaints.9 The condition seems to respond well to • Intravertebral disc herniation, also known as ‘Schmorl’s
medical management as a first-line approach.9 In the node’, corresponds to herniation of intervertebral disc
lumbosacral segment, clinical signs include lumbar material into the vertebral body, which can be facilitated
pain, pain on extension of the pelvic limbs, various by underlying weakness of the cartilaginous endplate or
neurologic deficits, and muscle atrophy, depending on subchondral trabeculae of the vertebral body.73 In dogs,
which nerves are compressed by the displaced mate- they may occur in the cervical, lumbar, or sacral ver-
rial.62,63 tebrae,74 although they have been reported more com-
• Intradural or intramedullary disc extrusion: in some monly at the lumbosacral space.73 They usually affect
cases, acute forceful extrusion of disc material can the central portion of the endplate and, less commonly,
cause tearing of the dura mater.40,45 This dural tear the marginal regions.73 They may or may not be associ-
can allow extruded disc material to end up in an ated with clinical signs. When present, clinical mani-
intradural65–68 or intramedullary location.42,44,47,68–70 festations may include pain, which is thought to arise
Intradural or intramedullary extrusions are often from concurrent disc herniation dorsally and nerve
associated with strenuous activity or a traumatic root compression and/or inflammation in the cancel-
event, but can also happen without such signifi- lous bone marrow of the vertebral body with exposure
cant events; in the latter case, it is speculated that to disc material.74
previous disc disease may have predisposed to sub- • A summary of the general classification of IVDD in dogs
sequent intradural/intramedullary extrusion by and cats proposed based on the discussion above is pre-
causing adhesions between the dura mater, dorsal sented in Fig. 7.1.15.
Intervertebral disc disease
Degenerated disc Non-degenerated disc

= acute hydrated nucleus pulposus extrusion
(usually trauma or exercise-associated)
Disc Disc
In situ Disc extrusion
bulging protrusion
Uncommon and
Non-traumatic Traumatic Non-compressive Compressive
atypical disc extrusion
Foraminal Cord contusion
Intradural/
Dural tear
intramedullary
Intravertebral Intramedullary
(Schmorl's node) disc material
Fig. 7.1.15 Proposed classification of intervertebral disc disease in dogs and cats.
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COMPARATIVE IMAGING breeds,77,78 MRI is still overall more accurate for lesion
localization in dogs with thoracolumbar myelopathy,
• Current imaging techniques available to confirm even in chondrodystrophic breeds. 2 MRI is also more
a clinical suspicion of disc herniation in veterinary accurate than conventional CT for differentiating
medicine include myelography, CT with or without disc extrusion from protrusion, and has overall higher
intrathecal injection of iodinated contrast material sensitivity. 2
(CT-myelography), and MRI.
• Although a recent study suggested that patient outcome is MRI FEATURES OF DISC DEGENERATION
not significantly improved when using MRI for diagnosis
of IVDD,75 it is still considered the method of choice for • Whether or not disc degeneration is associated with sig-
pre-surgical diagnosis as it is non-invasive and provides nificant compressive myelopathy or radiculopathy, MRI
superior anatomic detail as well as potential prognostic is recognized as a very sensitive tool to identify disc
indicators (e.g., myelomalacia). degeneration.25,36,37
• Myelography is more readily available and less expensive • Various classification systems have been evaluated,25,36,37
than MRI, but is also more invasive and requires specific and have validated MRI as an accurate method to iden-
technical skills for adequate injection of iodinated con- tify and grade IVDD non-invasively, with good to excel-
trast material into the subarachnoid space. In dogs with lent correlation with histopathology25,79,80 and gross
acute first-time thoracolumbar disc extrusion, MRI was pathology,37 as well as good inter- and intraobserver
found to be more accurate than myelography for deter- agreement.36
mination of site and side of compression, with the big- • The Pfirrmann grading system is widely used in human
gest advantage in identification of side of compression.76 medicine and has proved to be reliable in dogs as well,
Inter-reviewer agreement for determination of side of allowing comparative studies regarding diagnosis and
compression was also substantially better for MRI.76 treatment of disc disease.36,37
However, the myelographic protocol in that study did not • Regardless of the grading system used, early MRI signs
include oblique projections, which may have improved of disc degeneration include decreased T2 signal of the
the performance of myelography in determining side nucleus pulposus, with or without a linear hypointense
of compression. Although the accuracy of T2W series signal parallel to the endplates called ‘nuclear cleft’
alone was higher than that of myelography, MRI accu- (Figs. 7.1.7, 7.1.9).25 This cleft is caused by biochemical
racy was further improved with the combined evaluation changes with areas of lower water and higher collagen
of T2W, T1W, and T1W post-contrast series, reaching content than adjacent portions of the nucleus, and can
100% for site and side of compression.76 This, however, be seen before histopathologically detectable changes
may be attributed to a relative lack of MRI experience occur.25 As degenerative changes progress, the T2 signal
of some reviewers in this study, who may not have per- intensity of the disc decreases more and more, and the
formed as well with T2W series alone as an experienced width of the disc decreases (Fig. 7.1.12). Loss of continu-
radiologist. MRI is also superior to myelography in dif- ity and integrity of the annulus become apparent,25,36,37
ferentiating extradural hemorrhage from extradural and ultimately disc protrusion or extrusion can develop.
intervertebral disc material or spinal cord swelling, a dif- These may or may not cause significant spinal cord or
ferentiation that can prove challenging with myelogra- nerve root compression, depending on location and
phy. Extensive cord swelling or extradural hemorrhage extent of disc herniation.
can impede localization of the exact origin of compres-
sion on myelography, due to the extensive interruption GENERAL MRI FEATURES OF
of the myelographic contrast columns often seen in these COMPRESSIVE DEGENERATIVE IVDD
cases.76
• CT is less widely available than myelography, but still • MRI is reportedly very accurate in determining the site
more available than MRI, even in referral practices. of origin, side of the compressive lesion, and craniocau-
Some authors have advocated the use of conventional dal extension of extruded intervertebral disc material
CT (without intrathecal injection of iodinated con- (especially using the T2W series).4,76,81
trast material) to diagnose disc herniation in chon- • General MRI findings in dogs with compressive disc dis-
drodystrophic breeds, on the premise that herniated ease include (Figs. 7.1.13, 7.1.16):
discs in these breeds are often mineralized and there- • Extradural compression of the spinal cord centered at
fore readily identified on conventional CT. CT also the level of an intervertebral disc, recognized by:
has the benefit of being faster and cheaper.77 Even – Loss of the epidural fat hyperintense signal.
though conventional CT has been found to be rela- – Change in the shape of the spinal cord, as well as a
tively adequate for the diagnosis and localization of change in the normal ovoid shape of the disc, best
mineralized disc extrusions in chondrodystrophic appreciated on transverse images.
428 CHAPTER 7.1
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(a)
(b)
Fig. 7.1.16 C3-C4 disc extrusion in a 6-year-old female

Beagle. Sagittal T2W (a) image of the cervical spine and
transverse T2W (b) and T1W (c) images at the level of the
cranial endplate of C4. The dorsally extruded disc material
is causing marked dorsal displacement and compression of
the spinal cord (mostly left ventral). The ventral epidural
fat and subarachnoid space are attenuated and compressed/
displaced by the compressive material, which is markedly
hypointense on both the T2W and T1W images (arrows). The
corresponding disc space is narrowed (a). Nuclear clefts are
seen in the C2-C3, C4-C5, and C5-C6 discs consistent with
(c)
degenerative changes. (1.5T MRI system)
– Presence of extradural material causing a mass

effect, with compression/displacement of the
hyperintense subarachnoid space (T2W images):
– That material mostly represents displaced
degenerated disc material that is typically T1
and T2 hypointense and is in close association
with the corresponding intervertebral disc.
– In dispersed or sequestered disc extrusions,
continuity with the affected disc may not be
readily observed on MR images (Fig. 7.1.17).
• Degenerative changes of the corresponding interver- Fig. 7.1.17 Sagittal T2W image of the lumbar spine in a
tebral disc (loss of T2 hyperintense signal from the 2-year-old dog with an acute traumatic L4-L5 disc extrusion
disc). following a car accident. The L4-L5 disc space is narrowed
• Narrowing of the intervertebral disc space, which is and hypointense disc material is seen over the mid-body of
best evaluated on sagittal series, particularly T1W L4 in the ventral vertebral canal causing severe ventral spinal
series.82 compression. The continuity between the disc of origin
• The differentiation between disc extrusion and protru- (L4-L5) and the disc material that migrated cranially (arrow)
sion can sometimes be challenging with MRI. Some and is now sequestered over L4 is difficult to establish.
criteria have been reported to be useful in large breed (1.5T MRI system)
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dogs to increase accuracy and interobserver agreement of dogs with intervertebral disc extrusion, and is more
MRI in differentiating these two types of herniation:83,84 severe when extruded disc material is calcified and when
• Midline disc herniation and partial instead of com- epidural hemorrhage is present.86 Both epidural hemor-
plete intervertebral disc degeneration are more likely rhage and inflammation can contribute to visible MRI
to be associated with protrusion. changes:
• Single instead of multiple disc herniations and disper- • Their MRI appearance is variable: hyperintense to
sion of the disc material beyond the borders of the the spinal cord or heterogeneous on T2W images, and
intervertebral disc space are more likely to be associ- hyper-, hypo-, or isointense to the spinal cord on T1W
ated with extrusion. images.87 This appearance likely reflects changes in
• Heavily T2W pulse sequences (SS-FSE, HASTE) pro- magnetic properties depending on the age of the hem-
vide a ‘myelographic’ effect by enhancing the signal of orrhage and amount of disc-associated inflammation
the CSF and suppressing the signal from other struc- (Fig. 7.1.20). Such MRI changes can be seen in about
tures, and can be used to quickly spot areas of cord 10% of dogs with thoracolumbar or lumbosacral disc
compression identified by interruption and/or deviation herniation.87 They are more common in the caudal
of the columns of CSF (Fig. 7.1.18).23 It is not recom- lumbar spine and more often observed when there has
mended to rely only on this pulse sequence as it is often been migration of disc material. These secondary epi-
in disagreement with the traditional T2W series; it can, dural changes are difficult to differentiate from the
however, be useful in determining the most significant extruded disc material.
lesions(s), which are associated with more pronounced • T2*W sequences (gradient recalled echo) are sensitive
attenuation/deviation of the subarachnoid space, in cases to the paramagnetic properties of deoxyhemoglobin
where multiple protrusions are present.22 and methemoglobin and can demonstrate signal voids
• T2*W pulse sequences (gradient recalled echo) have been due to susceptibility artifacts associated with recent
reported to highlight susceptibility artifacts in extradu- hemorrhage or hematomas in the epidural space
ral compressive material, whether macroscopic hemor- (Fig. 7.1.21).85
rhage is present or not.71 These susceptibility artifacts • Contrast enhancement is seen in more than 50% of
take the form of multiple hypointense foci admixed with dogs with epidural hemorrhage/inflammation.87
the extradural material, or a partial or complete hypoin- • Altogether, these features can cause erroneous diag-
tense ring surrounding that material. This hypointense nosis of neoplastic conditions, and this variability
ring can allow clearer demarcation between spinal cord needs to be considered when interpreting MR images
and extradural material when the distinction is blurred in dogs with an acute neurologic presentation.
on T2W images (Fig. 7.1.19).71 • Although contrast enhancement was initially reported to
• Epidural hemorrhage and epidural inflammation can be not be a common feature in compressive disc disease in
present in addition to the epidural disc material, and dogs and cats, recent studies have shown that it actually
may complicate the MRI appearance. Epidural hemor- occurs relatively commonly with this condition:
rhage is due to tearing of the internal vertebral venous • In dogs with compressive disc disease, contrast
plexuses during forceful disc extrusion.85 Epidural enhancement of the extradural material has been
inflammation is histopathologically present in most reported in about 50% of cases, and appears more
L5
(a) (b)
Fig. 7.1.18 Sagittal T2W (a) and SS-FSE (‘T2-myelogram’, b) images of the lumbar spine in an 8-year-old dog with acute
disc extrusion at L4-L5. The L4-L5 disc space is narrowed and markedly hypointense. The extruded disc material has
migrated cranially and is now present in the ventral aspect of the vertebral canal at the level of caudal L4 (arrows). On the
T2-myelogram, focal attenuation of the normal hyperintense signal from the subarachnoid space is visible (arrowhead). Note
that the site of subarachnoid space attenuation (over the length of L4) on this sequence can only be established by comparison
with the corresponding T2W image. (1.5T MRI system)
430 Chapter 7.1
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(a) (b)
Fig. 7.1.19 Transverse T2W (a) and T2*W gradient echo (b) images over the body of L4 in a 2-year-old dog with acute
traumatic disc extrusion at L4-L5 following a car accident. The compressive extradural material (arrows) is seen in the
left ventral aspect of the vertebral canal displacing the cord dorsally and to the right. The compressive material is better
differentiated from the cord (C) on the gradient echo image. (1.5T MRI system)
L4
(a)
L4
(b) (c)
Fig. 7.1.20 T2W images in a dog with acute disc extrusion at L3-L4. Sagittal (a), right parasagittal (b), and transverse (c)
images over the body of L4. There is a large amount of heterogeneous, mostly hypointense, material in the dorsolateral aspect
of the vertebral canal (arrows, a and b; arrowheads, c), causing left dorsolateral spinal cord compression (asterisk, c). This dog
underwent an extensive left-sided hemilaminectomy over L4 and L5 and a large amount of hemorrhage and disc material was
retrieved. (1.5T MRI system)
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L5
(b)
C
* Fig. 7.1.21 Transverse fast spin echo T2W image over the body of L4 (a) and
parasagittal (along the right side of the vertebral canal) T2*W gradient echo
image (b) in a dog with acute disc herniation at L4-L5. On the transverse image,
a large amount of T2 heterogeneous extradural material (asterisk) is seen causing
compression and displacement of the spinal cord (C). The parasagittal T2*W
gradient echo image is obtained through the plane of that extradural material
and shows multiple irregular markedly hypointense structures (arrows), called
‘signal voids’, consistent with hemorrhage extending over several vertebral
(a) bodies. Extensive epidural hemorrhage was seen surgically. (1.5T MRI system)
common with extrusion than protrusion and in dogs • Lack of post-surgical improvement or acute worsening
with subacute to chronic presentation (Fig. 7.1.22).87,88 of clinical signs after surgery is an indication to repeat
• Contrast enhancement of the meninges adjacent to spinal imaging:
the extruded extradural compressive material has • Although myelomalacia (see Chapter 7.3) is a potential
been also reported to occur in up to 40% of cases cause for lack of post-surgical improvement in dogs
(Fig. 7.1.23).88 with acute compressive disc extrusion, a recent study
• MRI contrast enhancement is not a significant indica- showed that persistence of compressive disc material
tor of the presence of epidural hemorrhage or inflam- due to incomplete initial removal or erroneous initial
mation.87,88 surgical site was the cause of the lack of improvement
• Patterns of enhancement of extradural compres- in 80% of Dachshunds with acute thoracolumbar disc
sive material are variable, and can be diffuse/homo- disease.93
geneous, heterogeneous, central, or peripheral • In dogs that show initial post-surgical improvement,
(rim-like).87,89 or static clinical status, acute deterioration of neu-
• There is no association between the pattern of rologic function is often due to early reherniation
enhancement and the duration of clinical signs, neu- at the site of previous hemilaminectomy. In a recent
rologic grade, type of herniation, or presence of hem- study on more than 500 dogs that received decom-
orrhage.89 pressive surgery for thoracolumbar disc disease, acute
• There are no well-defined guidelines to grade the sever- post-surgical deterioration was seen in 2% of cases. In
ity of spinal cord compression on MR images; however, all cases, it was caused by reherniation (Fig. 7.1.24).94
several studies have used some form of ‘spinal cord com- Reherniation can happen on the contralateral side,
pression ratios’.90–92 Examples include measuring the which underscores the importance of repeat imaging
percentage of the cross-sectional area of the vertebral in these cases to confirm lateralization of compressive
canal that is occupied by compressive extradural mate- material and plan the surgical approach accordingly.94
rial, or the ratio of the cross-sectional area of the spinal • Susceptibility artifacts due to microscopic metal frag-
cord at the point of maximal compression to the cross- ments from normal wear of surgical instruments has
sectional area of the spinal cord on the closest transverse been reported when performing spinal MRI on patients
image without compression. Commonly used cut-off that received prior spinal surgery.95 This could make
points to describe compression severity are: MRI interpretation challenging in dogs with lack of
• Mild compression: up to 25% of the vertebral canal improvement or early post-operative worsening, since
cross-sectional area occupied by compressive mate- in these cases the compressive material is located at
rial. the initial surgical site. However, in a recent study,
• Moderate compression: 25%–50%. investigators did not observe susceptibility artifacts in
• Severe compression: >50%. any of 10 dogs re-imaged 1–10 days after the initial
432 CHAPTER 7.1
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(a) (b)

T1W post-contrast (c) images of the lumbar spine at L5-L6
in an 8-year-old male Beagle with spinal cord compression
due to disc extrusion. The hypointense and heterogeneous
extruded disc material (arrow, a) is causing marked left
ventral cord compression on the T2W image; the material is
also hypointense on the T1W pre-contrast image (arrow, b)
and on the T1W post-contrast image there is moderate
patchy enhancement of the compressive material (arrow, c).
(c)
(1.5T MRI system)
surgery.93 In another study of 10 dogs presenting with • When susceptibility artifacts due to metallic debris
delayed recurrent disc extrusion at another site, MRI are present adjacent to the site of interest, they can
did not identify such artifacts either, and performed be reduced by implementing a number of technical
better than myelography at determining the side of adjustments:97
the new compressive lesions. Therefore, MRI seems – Fast spin echo sequences are preferable, as the
to be an appropriate tool to re-image dogs with lack multiple 180° pulses compensate in part for the
of post-surgical improvement, acute worsening in the fixed inhomogeneities of magnetic field associated
early post-surgical period, or delayed recurrence of with the metallic debris; if spin echo sequences
clinical signs suspected to be due to recurring hernia- are used, a short time of echo (TE) should be
tion at another site.96
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(a) (b)
Fig. 7.1.23 Transverse T1W pre-contrast (a) and post-contrast (b) images at C5-C6 in a dog with disc extrusion causing right
ventral spinal cord compression. On the post-contrast image, there is linear meningeal enhancement along the ventral aspect of
the spinal cord (arrow). (1.5T MRI system)
*
*
(a) (b)
Fig. 7.1.24 Transverse T2W images at the level of the cranial aspect of L4 in a 5-year-old Dachshund with disc extrusion at L3-L4.
(a) Image at initial presentation showing marked ventral left-sided compression of the spinal cord (asterisk) due to disc extrusion.
The arrowhead indicates the left articular process joint. (b) Repeat MRI 11 days after left-sided hemilaminectomy at L3-L4 due to
acute decompensation; there is recurrent compression of the spinal cord (asterisk) due to reherniation of additional disc material.
The left articular processes (arrowhead) are missing secondary to the surgery, and there are patchy hyperintense areas in the
epaxial musculature (arrow) representing normal post-surgical changes. Reherniation of additional disc material was confirmed
during repeat surgical exploration. (1.5T MRI system)
434 CHAPTER 7.1
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preferred to decrease the influence of dephasing contralateral nerve, with strong contrast enhancement
induced by the metallic debris. (Fig. 7.1.25).64 Such lesions can easily be mistaken for a
– Decreasing the voxel size by increasing the matrix peripheral nerve sheath tumor.
at constant FOV or decreasing the FOV while
keeping the same image matrix, or, alternatively, Intradural or intramedullary extrusion
decreasing slice thickness: this decreases signal- • The vast majority of intradural or intramedullary disc
to-noise ratio, but can be compensated for by extrusions in dogs and cats so far have been imaged with
increasing the number of excitations (NEX). myelography or CT-myelography.42,65–69 There are rare
– Increasing the receiver bandwidth: this too reports of the MRI appearance of these conditions.44,47,68,71
decreases signal-to-noise ratio and may require • MRI findings suggestive of intradural extrusion include:
increasing NEX to maintain a good signal. • A T2 hypointense mass extending from the disc into
– Swapping phase- and frequency-encoding direc- the vertebral canal causing displacement and com-
tion, to change the main orientation of the arti- pression of the cord.
fact. This could potentially propagate flow-artifact • T2 hyperintense signal cranial and caudal to that
over the area of interest, but these are less intense mass, due to focal dilation of the subarachnoid space
than the susceptibility artifacts. along the margins of the compressive lesion. This
may be an indicator of the intradural location of the
MRI FEATURES OF UNCOMMON/ATYPICAL compressive lesion, similar to the ‘golf tee’ sign on
DEGENERATIVE DISC EXTRUSION myelograms.68
• MRI findings suggestive of intramedullary extrusion
Intervertebral foraminal disc extrusion include:
• The MRI appearance of several cases of cervical inter- • Focal cord swelling and changes in T2-signal inten-
vertebral foraminal disc extrusion has been reported.9 sity of the spinal cord parenchyma immediately dorsal
The most common affected sites are C6-C7 and C5-C6. to the affected disc, and extending cranial and caudal
Careful examination of transverse images across the disc to it, in the absence of significant extradural compres-
space and intervertebral foramina is important for cor- sive material. Most commonly, a combination of both
rect identification of this condition; extruded disc mate- T2 hyperintensities and hypointensities can be seen,
rial can be present within the intervertebral foramen or and are most likely due to a mixture of extruded disc
more distolaterally (Fig. 7.1.25). Gradient echo images material, edema, malacia, and hemorrhage.72
can be useful, as they allow better contrast between the • Occasionally, a tract can be seen extending from the
venous sinus and intervertebral disc. On sagittal images, disc space dorsally into the spinal parenchyma;44,47,70
the affected disc has often decreased signal intensity on this presumably represents the path of the extruded
T2W images. Differentiation between foraminal steno- disc into the spinal cord parenchyma (Fig. 7.1.27).
sis due to foraminal disc extrusion and overgrowth of the Although this tract has been reported to be T2 hyper-
articular process can prove challenging.9 intense44,47 and T1 hypointense with mild peripheral
• The MRI appearance of foraminal or extraforaminal hyperintensity,44 its actual signal intensity on various
(‘far lateral’) disc herniation is rarely reported in the MRI pulse sequences will vary depending on the
lumbar or lumbosacral segments, with anecdotal reports respective amounts of edema/malacia/hemorrhage
at L6-L7 and L7-S1.62,63 Transverse images show T2 and on whether the acutely extruded disc material in
hypointense material associated with the affected disc the cord is degenerated or not (Fig. 7.1.27).
extruded in a dorsolateral direction and causing impinge- • Decreased T2-signal intensity of the affected disc.44,47
ment of the nerve roots in the foramen or lateral to it. Occasionally, a T2 hyperintense focal rent can be seen
Contrast enhancement around the compressive lesion is across the annulus fibrosus and presumably represents
reported (Fig. 7.1.26).63 the area of acute annulus fracture through which the
• Occasionally, foraminal disc extrusion can cause gan- extrusion occurred (Fig. 7.1.27).47
glioneuritis.64 Disc fragments extruded into the inter- • Occasionally, a T2W hypointense focus can be seen
vertebral foramen can cause mechanical and chemical within the spinal cord, representing degenerated disc
damage to the perineurium of the nerve sheath, and material extruded into the parenchyma.44,68
may penetrate the nerve root, leading to inflammatory • Gradient echo images can demonstrate areas of
changes. These changes can cause thickening of the hypointense cord parenchymal susceptibility artifacts
nerve root and ganglion; in addition, the disc material consistent with hemorrhage following the extrusion
can contribute to the impression of a soft tissue mass (Fig. 7.1.27).44,71
in the area. These changes appear as a tubular space- • Mild enhancement can be seen around the tract or
occupying lesion in the intervertebral foramen, which is extruded material after gadolinium administra-
T1 isointense and T2 hyperintense compared with the tion.44,68,70
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(a)
(b) (c)
(d) (e)
Fig. 7.1.25 Sagittal T2W (a), parasagittal (to the left of midline) T2-myelogram (SS-FSE, b), transverse T2W (c), T1W pre-
contrast (d), and T1W post-contrast (e) images at the level of the C2-C3 intervertebral disc space in a male Beagle presented
with cervical pain. On the sagittal T2W image (a), the C2-C3 space is narrowed and hypointense and there is mild ventral
cord compression due to disc material extrusion (arrowhead). On the parasagittal SS-FSE (b), hypointense material is seen
obliterating the CSF signal at the entrance of the left C2-C3 intervertebral foramen (dashed arrow). On the transverse images,
there is irregular hypointense material in the ventral aspect of the left intervertebral foramen (arrows) with thickening of
the C3 nerve root, as well as mild ventral spinal cord compression; the left nerve root is T2 hyperintense and T1 isointense
(c, d). There is marked focal contrast enhancement of the left C3 ganglion and nerve root (e). This was presumed to be due
to foraminal herniation of disc material causing secondary ganglioneuritis. The dog improved on steroids so no surgery was
performed. (1.5T MRI system; images courtesy of Dr. Matthew Paek, Bush Advanced Veterinary Imaging)
436 CHAPTER 7.1
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L5
(a) (b)
(d)
(c)
Fig. 7.1.26 Sagittal T2W (a), parasagittal T2W (to the right

of midline) (b), dorsal STIR (c), transverse T2W (d), and
transverse T1W post-contrast with fat saturation (e) images
of the lumbar spine in a 5-year-old Dachshund presented
for lameness in the right pelvic limb. (a) The L5-L6 disc
space is narrowed and hypointense (arrowhead), but no cord
compression is noted. (b) On the parasagittal image across
the right intervertebral foramen, a rounded hypointense
structure is seen in the right L5-L6 intervertebral foramen
corresponding to extruded disc material (dashed arrow).
(c) On the dorsal STIR image, this material is seen again, (e)
and is surrounded by hyperintense signal suggestive of
edema/inflammation (dashed arrow). (d) The dorsolaterally
extruded disc material is clearly visible on the transverse T2W image (arrow) causing obliteration of the exit of the right L5-L6
intervertebral foramen. (e) There is strong enhancement around the extruded material due to focal inflammation (arrow).
(1.5T MRI system)
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(a) (b)
Fig. 7.1.27 Transverse T1W (a), T2W (b), and T2*W

gradient echo (c) images at the level of mid T13 and
sagittal T2W (d) image of the thoracolumbar spine
in a 7-year-old dog that became acutely paraplegic
after going into the yard and yelping. On the sagittal
image (d), there is mild reduction in size of the
nucleus pulposus of the T13-L1 disc and a thin
hyperintense linear tract (arrow) is seen through the
dorsal annulus. This is consistent with acute extrusion
of hydrated nucleus pulposus through the annulus.
The extruded material has penetrated the spinal cord
(intramedullary herniation), causing a hypointense
tract extending dorsally and cranially into the spinal
(c) cord parenchyma (arrowhead). The transverse images
(a, b, c) are obtained at the mid-level of T13 across
c the aforementioned intramedullary tract, which is
isointense with a hyperintense rim on the T1W image
(a), hypointense with a hyperintense rim on the T2W
image (b), and hyperintense with a hypointense rim
on the T2*W gradient echo image (c). The tract is due
T13 to intramedullary disc material and accompanying
hemorrhage. On the sagittal image, there is extensive
spinal cord parenchyma T2 hyperintensity concerning
(d) for myelomalacia. (1.5T MRI system)
438 CHAPTER 7.1
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Intravertebral disc herniation CORRELATION BETWEEN MRI, CLINICAL

(Schmorl’s node) SIGNS, AND PROGNOSIS IN DOGS WITH
• Although typically diagnosed radiographically, intra- COMPRESSIVE DEGENERATIVE DISC DISEASE
vertebral disc herniation may occasionally be seen at
MRI when imaging a patient for non-specific spinal Cervical spine
pain. • Cervical IVDD accounts for 14%–16% of IVDD in
• The herniation causes a defect in the endplate adja- dogs.98 Disc extrusion secondary to Hansen type 1
cent to the disc, which is filled with material that is degeneration is common in small breed dogs (especially
isointense to the disc and typically involves the cen- Dachshund and Beagle) but is also seen in large breed
tral portion rather than the periphery of the endplate dogs (especially Labrador Retriever, German Shepherd
(Fig. 7.1.28).20 This is best identified on sagittal or dor- Dog, Rottweiler, Dalmatian).99,100
sal plane images. • In small breed dogs the most common sites of herniation
• Reactive endplate changes, characterized by T2 and are C2-C3, C3-C4, and C4-C5 whereas in large breed
STIR hyperintensity and T1 hypointensity with or dogs the most common sites are C4-C5 and C6-C7.99,100
without endplate enhancement, are typically seen, while • Paresis or paralysis is less common with cervical her-
in some cases endplate sclerosis is present (T1 and T2 niation than thoracolumbar herniation; a possible
hypointense with no enhancement).20 explanation is that the dorsal longitudinal ligament
is wider in the cervical area than the thoracolumbar
region, forcing the herniation to occur in a dorsolateral
direction (between the dorsal longitudinal ligament
and vertebral venous sinus). The other reason is that
in the cervical area, the spinal cord occupies a smaller
proportion of the vertebral canal so that the degree of
spinal cord compression caused by an equal volume of
herniated disc material is less than in the thoracolum-
bar area.14,98
• Due to these features, the clinical manifestations of cer-
vical disc herniation tend to be cervical pain and root
signature due to nerve root compression.
• In the cervical area, there is a positive correlation
between the degree of spinal cord compression caused
by disc herniation, measured on transverse images, and
neurologic grade at time of imaging. However, there is
no correlation with the post-surgical neurologic status or
the clinical outcome after surgical intervention.98
Thoracolumbar spine
• Overall, the most commonly affected discs in the thora-
columbar region are T13-L1 and T12-T13;101 however,
in large breed dogs, L1-L2, T13-L1, and L2-L3 are more
commonly affected.50,51
• Compressive disc disease cranial to T10 is uncommon
because of the intercapital ligaments, which run between
the heads of corresponding ribs (between T2 and T11),
ventral to the dorsal longitudinal ligament. These liga-
Fig. 7.1.28 Dorsal reformatted image of a 3D-T1W gradient ments create a band, shielding the spinal cord from the
echo series of the lumbosacral area in a 7-year-old Labrador intervertebral disc in those locations.
Retriever with lumbar back pain. On survey radiographs, • Cranial thoracic disc herniation causing spinal cord
moderate lumbosacral spondylosis and partial joint collapse compression has been reported to be more common
were observed. The focal defect in the cranial endplate of S1 in German Shepherd Dogs compared with other large
(arrow) represents an intravertebral disc herniation (Schmorl’s breed dogs, especially at T2-T3, T3-T4, and T4-T5
node). (0.3T MRI system; reproduced, with permission, from (Fig. 7.1.29).102–104 Therefore, it is important to include
Gendron K, Doherr MG, Gavin P et al. (2012). Magnetic the cranial thoracic spine (including T2-T3) when
resonance imaging characterization of vertebral endplate imaging dogs of this breed with T3-L3 myelopathy.
changes in the dog. Vet Radiol Ultrasound 53(1):50–6.) • Correlation with clinical signs and prognosis:
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T2 T2-T3
(a) (b)
Fig. 7.1.29 Transverse T2W images at the level of T2 (a),

T2-T3 disc space (b), and T3 (c) in a 9-year-old German
T3 Shepherd Dog presented for progressive ataxia of the pelvic
limbs. There is compressive disc herniation at T2-T3.
Note the different size and shape of the spinal cord at the
compressive site (b) compared with cranial and caudal to it
(c)
(a, c). (1.5T MRI system)
440 CHAPTER 7.1
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• In dogs with neurologic deficit due to thoracolumbar dogs, T2 hyperintensity exceeding the length of
disc extrusion, it appears that there is no definitive L2 is associated with a poor outcome in about 55%
association between the degree of spinal cord com- of cases (Fig. 7.1.30).6
pression as defined on T2W transverse images, – Regardless of the severity of neurologic deficits
and the neurologic grade at presentation or clinical at presentation, an increase in the length of the
outcome after surgery.101,105 T2 hyperintensity increases the likelihood of an
• However, the length over which the spinal cord is unsuccessful outcome (remaining non-ambulatory
compressed may be associated with the neurologic after surgery),105 especially when the length of the
grade at presentation,105 but not with outcome.81,105 hyperintensity exceeds three times the length
• In dogs with acute thoracolumbar disc extrusion, of L2.6
areas of spinal cord hyperintensity on T2W series can – Even in dogs with intact deep pain perception,
be identified. Their exact cause is not clear but possi- areas of spinal cord T2 hyperintensity may be a
ble origins include necrosis, myelomalacia, intramed- predictor of poor outcome.6
ullary hemorrhage, inflammation, and edema.6 This • In dogs with thoracolumbar disc extrusion, hetero-
feature carries clinical and prognostic significance: geneous epidural material associated with epidural
– They have been associated with more severe neu- hemorrhage or inflammation does not appear to be
rologic deficits at presentation.87,88,105 associated with clinical outcome compared with dogs
– Areas of T2 hyperintensity have been associated without these changes.87
with a poor outcome.6,81,105 In acutely paraplegic
(a) (b)
Fig. 7.1.30 Transverse T2W images at the level of T13-L1 (a)

and mid T13 (b) and sagittal T2W image (c) in a 9-year-old
Dachshund with acute compressive disc extrusion at T13-L1.
The ventral cord compression is visible in (a) and (c, arrow),
and there is an area of T2 hyperintensity in the spinal cord
parenchyma (dotted arrow, b) extending longitudinally
over the bodies of T13 and L1 (over two vertebral bodies in
length). This dog did not recover complete motor function
(c)
after decompressive surgery. (1.5T MRI system)
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Sacrococcygeal or intercoccygeal short period (<24 hours) of deterioration followed by

disc herniation a static or improving clinical course; the clinical pres-
• There have been anecdotal reports of sacrococcy- entation is usually quite similar to ischemic myelop-
geal or intercoccygeal (Cd1-Cd2) disc protrusions or athy.39,53
extrusions causing tail pain, pain during defecation, or • In the compressive form, there does not appear to
abnormal tail position.106,107 be an association with exercise or trauma although
• Resolution of these clinical signs occurred after surgical the presentation is acute as well.38 In this case, the
correction, while some dogs were managed medically. extruded hydrated disc material does not diffuse
• MRI and CT can be useful in confirming the presence of but accumulates ventral to the spinal cord, centered
extruded disc material in the sacrococcygeal canal.106,107 on midline, immediately dorsal to the affected disc.
On MRI, heterogeneous or hypointense disc material is This form is almost exclusively reported in the cer-
seen extending dorsal to the affected disc space, obliter- vical spine, with C4-C5 being the most commonly
ating the vertebral canal and obscuring the spinal nerves affected space, followed by C3-C4 and C5-C6.38,54–58
and perineural fat. Typically, the condition is characterized by an acute
onset of non-painful cervical myelopathy with tetra-
Lumbosacral stenosis plegia or non-ambulatory tetraparesis and progressive
• Degenerative lumbosacral stenosis is an umbrella term deterioration within 24–48 hours from the onset;
defined by an abnormal narrowing of the L5-S3 ver- occasionally respiratory dysfunction is observed.38,54
tebral canal or intervertebral foramina, with compres- • MRI features of the non-compressive form of the disease
sion of the cauda equina nerve roots and/or their blood include (Fig. 7.1.31):28,39,72
supply.108 • Focal hyperintensity on T2W images in the spinal
• It is a multifactorial condition including: intervertebral cord overlying an intervertebral disc; the area of
disc degeneration, intervertebral disc protrusion (less maximal hyperintensity is usually just dorsal to the
commonly extrusion), bone proliferation on the vertebral affected intervertebral disc space, but can sometimes
endplates and articular processes, vertebral subluxation, be seen just cranial or caudal to the space.28,39 It is gen-
and hypertrophy of the joint capsules and interarcuate erally less than one vertebral body in length, and on
ligament (ligamentum flavum).27,108 transverse T2W images is often lateralized.72 It typi-
• Due to its particular nature and the fact that disc disease cally affects both the gray and white matter.
only contributes partially to this syndrome, this condi- • This region is usually isointense on T1W pre-contrast
tion will be covered separately in a specific chapter (see images but can occasionally be mildly hyperintense,
Chapter 7.3). hypointense, or heterogeneous.
• Mild post-contrast enhancement is uncommon, but is
MRI FEATURES OF ACUTE HYDRATED possible especially if the dog is imaged several days
NUCLEUS PULPOSUS EXTRUSION after clinical onset.28,72
• T2*W gradient recalled echo images occasionally
• As mentioned earlier (Classification of intervertebral disc show hypointensity in the spinal cord consistent with
disease), acute nucleus pulposus extrusion without sig- parenchymal hemorrhage.28,39
nificant pre-existing degenerative disc disease is now a • Reduction in volume and signal intensity of the
well-recognized entity.28,38,39,43,46,53–55,61 nucleus pulposus of the corresponding disc on T2W
• The condition has non-compressive and compressive images; this can cause narrowing of the correspond-
forms, with the non-compressive form being more coming intervertebral disc space, which is best appreciated
monly reported: on sagittal images.
• In the non-compressive form, extrusions typically • Extraneous material or signal changes within the
occur during performance of strenuous exercise or epidural space dorsal to the affected disc space with
following trauma. The acutely extruded hydrated absence of, or minimal, spinal cord compression.
nucleus pulposus material causes spinal cord contu- • A communicating T2 hyperintense tract can
sion immediately dorsal to the affected disc; there is occasionally be seen on transverse or sagittal
no significant spinal cord compression due to diffu- images traversing the dorsal annulus between the
sion of the gel-like hydrated disc material in the epi- residual nucleus pulposus and the vertebral canal;28
dural space. This form is seen in the T3-L3 segment this likely represents the site of acute rupture of the
more commonly (67%–72% of cases), followed by the annulus through which the hydrated nucleus was
C1-C5 segment (14%–27%) and less often the C6-T2 extruded.
and L4-S3 segments.28,39,46,53 Typically, the condi- • MRI features related to prognosis:
tion is characterized by an acute or hyperacute, often – Overall, affected patients are reported to have an
markedly lateralizing paresis or plegia, with an initial unsuccessful outcome in up to 33% of cases.39
442 CHAPTER 7.1
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(a) (b)
Fig. 7.1.31 Parasagittal (along left side of the cord) (a) and transverse (b) T2W images at the level of cranial C4 in a dog that
sustained cervical trauma and a chip fracture of the caudoventral aspect of the body of C3 (not shown). There is a focal area of
patchy T2 hyperintensity in the spinal cord over the affected disc space C3-C4 and extending caudal to it. The hyperintensity
is clearly asymmetrical and more left-sided on the transverse image (arrows). Both the gray and white matter are affected. The
C3-C4 disc (arrowhead, a) has decreased volume and signal intensity of its nucleus pulposus when compared with the adjacent
normal discs. No significant extradural compressive material is noted, but a small amount of non-compressive epidural material,
which is hypointense to the epidural fat, is seen along the left side of the cord (dashed arrow, b). These signs are consistent with
a non-compressive acute hydrated nucleus pulposus extrusion secondary to the trauma. Note the patchy hyperintensities in
the hypaxial muscles ventral to C3 close to the fracture site on the sagittal image (a), consistent with hemorrhage/edema. (1.5T
MRI system)
– There is an association between the cross- dorsal to a slightly narrowed intervertebral disc space
sectional area of the T2W hyperintense lesion on (most commonly C4-C5, C3-C4, C5-C6).
transverse images and a poor outcome; a cross- • On sagittal T2W images the extruded material has an
sectional area exceeding 90% of the cord area is elongated shape and is difficult to distinguish from
associated with a 92% chance of an unsuccessful the hyperintense epidural fat and CSF because it has
outcome.39 similar signal intensity.
– The presence of hypointense signal in the cord • On transverse T2W images centered on the affected
on T2*W images, suggesting hemorrhage, is also disc space, the extruded material lies symmetrically
associated with a poor outcome.39 on the midline, ventral to the spinal cord, and often
• There is some overlap in the MRI appearance of has a characteristic ‘seagull’ shape (Fig. 7.1.32).
non-compressive AHNPE and ischemic myelopa- • On T2-FLAIR images, the extruded material typi-
thy (fibrocartilaginous embolism, see Chapter 7.7), cally retains a hyperintense signal,57,58 but sometimes
with studies showing moderate inter-observer agree- is suppressed.56,58
ment in diagnosing non-compressive AHNPE and • There is ventral compression of the spinal cord
ischemic myelopathy with MRI, and moderate to causing dorsal displacement centered at the interver-
good intra-observer agreement.53 Although more tebral disc space.
investigation is needed, there is some suggestion • Focal intramedullary T2W hyperintensity dorsal to
that AHNPE lesions on MRI tend to be more often the affected disc may be noted, which is T1W isoin-
lateralized and have shorter length compared with tense and non-enhancing after gadolinium injection.
ischemic lesions.53 • This focal intramedullary T2W hyperintensity is
• MRI features of the compressive form of the disease usually iso- to hyperintense on T2*W images, con-
include (Fig. 7.1.32):38,54–58 sistent with spinal cord contusion.
• Presence of T2 hyperintense material ventral to the • There is inconstant mild diffuse38 or peripheral57,58
spinal cord, on midline and centered immediately contrast enhancement of the extruded material.
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(a) (b)
Fig. 7.1.32 Sagittal T2W image of the cervical spine (a) and transverse T2W image at the level of the C3-C4 disc space in
an 11-year-old dog presented for acute tetraplegia. There is narrowing of the C3-C4 disc space, with loss of normal signal
intensity and volume of its nucleus pulposus (arrowhead, a). There is T2 hyperintense material ventral to the spinal cord
on midline and centered immediately dorsal to the C3-C4 disc space. On the sagittal T2W image (a), this material has an
elongated shape and is difficult to distinguish from the hyperintense epidural fat and CSF (arrow). On the transverse T2W
image centered on the affected disc space (b), this material lies symmetrically on the midline, ventral to the spinal cord, and has
a characteristic ‘seagull’ shape (dashed arrow). There is moderate ventral spinal cord compression. The appearance of the lesion
is characteristic of a compressive form of acute hydrated nucleus pulposus extrusion. (1.5T MRI system)
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Intervertebral disc degeneration in the dog. Part 1: Anatomy 42. Liptak JM, Allan GS, Krockenberger MB et al. (2002).
and physiology of the intervertebral disc and characteristics of Radiographic diagnosis: intramedullary extrusion of an
intervertebral disc degeneration. Vet J 195(3):282–91. intervertebral disc. Vet Radiol Ultrasound 43(3):272–4.
27. Fingeroth JM, Thomas WB (2015). Advances in Intervertebral 43. Lu D, Lamb CR, Wesselingh K et al. (2002). Acute
Disc Disease in Dogs and Cats. Wiley Blackwell, Ames. intervertebral disc extrusion in a cat: clinical and MRI
28. Chang Y, Dennis R, Platt SR et al. (2007). Magnetic resonance findings. J Feline Med Surg 4(1):65–8.
imaging of traumatic intervertebral disc extension in dogs. 44. McConnell JF, Garosi LS (2004). Intramedullary intervertebral
Vet Rec 160(23):795–9. disk extrusion in a cat. Vet Radiol Ultrasound 45(4):327–30.
29 Dennis R (2011). Optimal magnetic resonance imaging of the 45. McKee WM, Downes CJ (2008). Rupture of the dura mater
spine. Vet Radiol Ultrasound 52:S72–S80. in two dogs caused by the peracute extrusion of a cervical disc.
30. Steffen F, Kircher PR, Dennler M (2014). Spontaneous Vet Rec 162(15):479–81.
regression of lumbar Hansen type 1 disk extrusion detected 46. McKee WM, Downes CJ, Pink JJ et al. (2010). Presumptive
with magnetic resonance imaging in a dog. J Am Vet Med Assoc exercise-associated peracute thoracolumbar disc extrusion in
244(6):715–8. 48 dogs. Vet Rec 166(17):523–8.
31. Olby NJ, Dyce J, Houlton JEF (1994). Correlation of plain 47. Sanders SG, Bagley RS, Gavin PR (2002). Intramedullary
radiographic and lumbar myelographic findings with surgical spinal cord damage associated with intervertebral disk
findings in thoracolumbar disc disease. J Small Anim Pract material in a dog. J Am Vet Med Assoc 221(11):1594–6, 74–5.
35(7):345–50. 48. Hansen H (1952). A pathologic-anatomical study on disc
32. Dennis R (2005). Assessment of location of the celiac and degeneration in the dog. Acta Orthop Scand Suppl 11:1–117.
cranial mesenteric arteries relative to the thoracolumbar 49. Smolders LA, Bergknut N, Grinwis GC et al. (2013).
spine using magnetic resonance imaging. Vet Radiol Ultrasound Intervertebral disc degeneration in the dog. Part 2:
46(5):388–90. chondrodystrophic and non-chondrodystrophic breeds. Vet J
33. Yeamans CL, Haley A, Gutierrez-Quintana R et al. (2016). 195(3):292–9.
Surgical anatomical landmarks of the thoracolumbar vertebral 50. Cudia SP, Duval JM (1997). Thoracolumbar intervertebral
column on magnetic resonance imaging in dogs. Anat Histol disk disease in large, nonchondrodystrophic dogs: a
Embryol 45(2):140–4. retrospective study. J Am Anim Hosp Assoc 33(5):456–60.
34. Guillem Gallach R, Suran J et al. (2011). Reliability of 51. Macias C, McKee WM, May C et al. (2002). Thoracolumbar
T2-weighted sagittal magnetic resonance images for disc disease in large dogs: a study of 99 cases. J Small Anim
determining the location of compressive disk herniation in Pract 43(10):439–46.
dogs. Vet Radiol Ultrasound 52(5):479–86. 52. Besalti O, Pekcan Z, Sirin YS et al. (2006). Magnetic
35. Housley D, Caine A, Cherubini G et al. (2017). Evaluation resonance imaging findings in dogs with thoracolumbar
of T2-weighted versus short-tau inversion recovery sagittal intervertebral disk disease: 69 cases (1997–2005). J Am Vet
sequences in the identification and localization of canine Med Assoc 228(6):902–8.
intervertebral disc extrusion with low-field magnetic 53. Fenn J, Drees R, Volk HA et al. (2015). Inter- and
resonance imaging. Vet Radiol Ultrasound 58(4):433–43. intraobserver agreement for diagnosing presumptive ischemic
36. Bergknut N, Auriemma E, Wijsman S et al. (2011). Evaluation myelopathy and acute noncompressive nucleus pulposus
of intervertebral disk degeneration in chondrodystrophic and extrusion in dogs using magnetic resonance imaging. Vet
nonchondrodystrophic dogs by use of Pfirrmann grading of Radiol Ultrasound 57(1):33–40.
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54. Hamilton T, Glass E, Drobatz K et al. (2014). Severity of 74. Baltzer WI, Hillebrand L, Smith TJ et al. (2012). Surgical
spinal cord dysfunction and pain associated with hydrated management of a Schmorl’s node in an Airedale Terrier and
nucleus pulposus extrusion in dogs. Vet Comp Orthop Traumatol review of the literature. Vet Comp Orthop Traumatol 25(2):
27(4):313–8. 167–71.
55. Manunta ML, Evangelisti MA, Bergknut N et al. (2015). 75. Parry AT, Harris A, Upjohn MM et al. (2010). Does choice of
Hydrated nucleus pulposus herniation in seven dogs. Vet J imaging modality affect outcome in dogs with thoracolumbar
203(3):342–4. spinal conditions? J Small Anim Pract 51(6):312–7.
56. Kamishina H, Ogawa H, Katayama M et al. (2010). 76. Bos AS, Brisson BA, Nykamp SG et al. (2012). Accuracy,
Spontaneous regression of a cervical intraspinal cyst in a dog. intermethod agreement, and inter-reviewer agreement for use
J Vet Med Sci 72(3):349–52. of magnetic resonance imaging and myelography in small-
57. Kang BJ, Jung Y, Park S et al. (2015). Discal cysts of the breed dogs with naturally occurring first-time intervertebral
cervical spine in two dogs. J Vet Sci 16(4):543–5. disk extrusion. J Am Vet Med Assoc 240(8):969–77.
58. Konar M, Lang J, Fluhmann G et al. (2008). Ventral intraspinal 77. Olby NJ, Munana KR, Sharp NJ et al. (2000). The
cysts associated with the intervertebral disc: magnetic resonance computed tomographic appearance of acute thoracolumbar
imaging observations in seven dogs. Vet Surg 37(1):94–101. intervertebral disc herniations in dogs. Vet Radiol Ultrasound
59. Dolera M, Malfassi L, Marcarini S et al. (2015). Hydrated 41(5):396–402.
nucleus pulposus extrusion in dogs: correlation of magnetic 78. Dennison SE, Drees R, Rylander H et al. (2010). Evaluation of
resonance imaging and microsurgical findings. Acta Vet Scand different computed tomography techniques and myelography
57:58. for the diagnosis of acute canine myelopathy. Vet Radiol
60. Falzone C (2017). Canine acute cervical myelopathy: Ultrasound 51(3):254–8.
Hydrated nucleus pulposus extrusion or intraspinal discal 79. Bergknut N, Meij BP, Hagman R et al. (2013). Intervertebral
cysts? Vet Surg 46(3):376–80. disc disease in dogs – part 1: a new histological grading
61. Lowrie ML, Platt SR, Garosi LS (2014). Extramedullary scheme for classification of intervertebral disc degeneration in
spinal cysts in dogs. Vet Surg 43(6):650–62. dogs. Vet J 195(2):156–63.
62. Chambers JN, Selcer BA, Sullivan SA et al. (1997). Diagnosis 80. Kranenburg HJ, Grinwis GC, Bergknut N et al. (2013).
of lateralized lumbosacral disk herniation with magnetic Intervertebral disc disease in dogs – part 2: comparison of
resonance imaging. J Am Anim Hosp Assoc 33(4):296–9. clinical, magnetic resonance imaging, and histological findings
63. Fadda A, Lang J, Forterre F (2013). Far lateral lumbar disc in 74 surgically treated dogs. Vet J 195(2):164–71.
extrusion: MRI findings and surgical treatment. Vet Comp 81. Besalti O, Ozak A, Pekcan Z et al. (2005). The role of extruded
Orthop Traumatol 26(4):318–22. disk material in thoracolumbar intervertebral disk disease:
64. Mouradian-Darby AE, Young BD, Griffin JF et al. (2014). a retrospective study in 40 dogs. Can Vet J 46(9):814–20.
Lymphocytic ganglioneuritis secondary to intervertebral disc 82. Levitski RE, Lipsitz D, Chauvet AE (1999). Magnetic
extrusion in a dog. J Small Anim Pract 55(9):471–4. resonance imaging of the cervical spine in 27 dogs. Vet Radiol
65. Barnoon I, Chai O, Srugo I et al. (2012). Spontaneous Ultrasound 40(4):332–41.
intradural disc herniation with focal distension of the 83. De Decker S, Gomes SA, Packer RM et al. (2016). Evaluation
subarachnoid space in a dog. Can Vet J 53(11):1191–4. of magnetic resonance imaging guidelines for differentiation
66. Packer RA, Frank PM, Chambers JN (2004). Traumatic between thoracolumbar intervertebral disk extrusions and
subarachnoid–pleural fistula in a dog. Vet Radiol Ultrasound intervertebral disk protrusions in dogs. Vet Radiol Ultrasound
45(6):523–7. 57(5):526–33.
67. Poncelet L, Heimann M (2011). Intradural vertebral disc 84. Gomes SA, Volk HA, Packer RM et al. (2016). Clinical and
herniation in a dog. Vet Rec 168(18):486a. magnetic resonance imaging characteristics of thoracolumbar
68. Tamura S, Doi S, Tamura Y et al. (2015). Thoracolumbar intervertebral disk extrusions and protrusions in large breed
intradural disc herniation in eight dogs: clinical, low-field dogs. Vet Radiol Ultrasound 57(4):417–26.
magnetic resonance imaging, and computed tomographic 85. Tidwell AS, Specht A, Blaeser L et al. (2002). Magnetic
myelography findings. Vet Radiol Ultrasound 56(2):160–7. resonance imaging features of extradural hematomas
69. Kent M, Holmes S, Cohen ELI et al. (2011). Imaging associated with intervertebral disc herniation in a dog.
diagnosis – CT myelography in a dog with intramedullary Vet Radiol Ultrasound 43(4):319–24.
intervertebral disc herniation. Vet Radiol Ultrasound 52(2):185–7. 86. Fadda A, Oevermann A, Vandevelde M et al. (2013). Clinical and
70. Kitagawa M, Okada M, Kanayama K et al. (2012). pathological analysis of epidural inflammation in intervertebral
Identification of ventrolateral intramedullary intervertebral disk extrusion in dogs. J Vet Intern Med 27(4):924–34.
disc herniation in a dog. J S Afr Vet Assoc 83(1):103. 87. Mateo I, Lorenzo V, Foradada L et al. (2011). Clinical,
71. Hammond LJ, Hecht S (2015). Susceptibility artifacts on T2*- pathologic, and magnetic resonance imaging characteristics of
weighted magnetic resonance imaging of the canine and feline canine disc extrusion accompanied by epidural hemorrhage or
spine. Vet Radiol Ultrasound 56(4):398–406. inflammation. Vet Radiol Ultrasound 52(1):17–24.
72. De Risio L (2015). A review of fibrocartilaginous embolic 88. Suran JN, Durham A, Mai W et al. (2011). Contrast
myelopathy and different types of peracute non-compressive enhancement of extradural compressive material on magnetic
intervertebral disk extrusions in dogs and cats. Front Vet Sci resonance imaging. Vet Radiol Ultrasound 52(1):10–6.
2:24. 89. Freeman AC, Platt SR, Kent M et al. (2012). Magnetic
73. Gaschen L, Lang J, Haeni H (1995). Intravertebral disc resonance imaging enhancement of intervertebral disc disease
herniation (Schmorl’s node) in five dogs. Vet Radiol Ultrasound in 30 dogs following chemical fat saturation. J Small Anim
36(6):509–16. Pract 53(2):120–5.
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90. da Costa RC, Parent JM, Partlow G et al. (2006). Morphologic 99. Cherrone KL, Dewey CW, Coates JR et al. (2004).
and morphometric magnetic resonance imaging features A retrospective comparison of cervical intervertebral disk
of Doberman Pinschers with and without clinical signs of disease in nonchondrodystrophic large dogs versus small
cervical spondylomyelopathy. Am J Vet Res 67(9):1601–12. dogs. J Am Anim Hosp Assoc 40(4):316–20.
91. De Decker S, Gielen IM, Duchateau L et al. (2012). 100. Hillman RB, Kengeri SS, Waters DJ (2009). Reevaluation
Evolution of clinical signs and predictors of outcome after of predictive factors for complete recovery in dogs with
conservative medical treatment for disk-associated cervical nonambulatory tetraparesis secondary to cervical disk
spondylomyelopathy in dogs. J Am Vet Med Assoc 240(7): herniation. J Am Anim Hosp Assoc 45(4):155–63.
848–57. 101. Penning V, Platt SR, Dennis R et al. (2006). Association
92. Provencher M, Habing A, Moore SA et al. (2016). Kinematic of spinal cord compression seen on magnetic resonance
magnetic resonance imaging for evaluation of disc-associated imaging with clinical outcome in 67 dogs with thoracolumbar
cervical spondylomyelopathy in Doberman Pinschers. J Vet intervertebral disc extrusion. J Small Anim Pract 47(11):
Intern Med 30(4):1121–8. 644–50.
93. Forterre F, Gorgas D, Dickomeit M et al. (2010). Incidence 102. Gaitero L, Anor S (2009). Cranial thoracic disc protrusions in
of spinal compressive lesions in chondrodystrophic dogs with three German Shepherd dogs. Vet J 182(2):349–51.
abnormal recovery after hemilaminectomy for treatment of 103. Gaitero L, Nykamp S, Daniel R et al. (2013). Comparison
thoracolumbar disc disease: a prospective magnetic resonance between cranial thoracic intervertebral disc herniations in
imaging study. Vet Surg 39(2):165–72. German Shepherd dogs and other large breed dogs. Vet Radiol
94. Hettlich BF, Kerwin SC, Levine JM (2012). Early reherniation Ultrasound 54(2):133–8.
of disk material in eleven dogs with surgically treated 104. Jaderlund KJ, Hansson K, Lindberg R et al. (2002).
thoracolumbar intervertebral disk extrusion. Vet Surg T3-T4 disc herniation in a German shepherd dog. Vet Rec
41(2):215–20. 151(25):769–70.
95. Freer SR, Scrivani PV (2008). Postoperative susceptibility 105. Levine JM, Fosgate GT, Chen AV et al. (2009). Magnetic
artifact during magnetic resonance imaging of the vertebral resonance imaging in dogs with neurologic impairment due
column in two dogs and a cat. Vet Radiol Ultrasound 49(1): to acute thoracic and lumbar intervertebral disk herniation.
30–4. J Vet Intern Med 23(6):1220–6.
96. Reynolds D, Brisson BA, Nykamp SG (2013). Agreement 106. Freeman P (2010). Sacrococcygeal intervertebral disc
between magnetic resonance imaging, myelography, and extrusion in a dachshund. Vet Rec 167(16):618–9.
surgery for detecting recurrent, thoracolumbar intervertebral 107. Lawson CM, Reichle JK, McKlveen T et al. (2011). Imaging
disc extrusion in dogs. Vet Comp Orthop Traumatol 26(1):12–8. findings in dogs with caudal intervertebral disc herniation.
97. Freer SR, Scrivani PV, Gross B (2008). Letter to the editor. Vet Radiol Ultrasound 52(5):487–91.
Vet Radiol Ultrasound 49(3):317–8. 108. Jones JC, Banfield CM, Ward DL (2000). Association
98. Ryan TM, Platt SR, Llabres-Diaz FJ et al. (2008). between postoperative outcome and results of magnetic
Detection of spinal cord compression in dogs with cervical resonance imaging and computed tomography in working
intervertebral disc disease by magnetic resonance imaging. dogs with degenerative lumbosacral stenosis. J Am Vet Med
Vet Rec 163(1):11–5. Assoc 216(11):1769–74.
CHAPTER 7.2
CERVICAL SPONDYLOMYELOPATHY
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Ronaldo C. da Costa 447
CONTENTS
Anatomic considerations .......................................................................................................................................................................................447
Pathophysiology of cervical spondylomyelopathy.................................................................................................................................................449
General MRI features of cervical spondylomyelopathy ..........................................................................................................................................453
Disc-associated cervical spondylomyelopathy.................................................................................................................................................453
Osseous-associated cervical spondylomyelopathy ..........................................................................................................................................453
Spinal cord signal changes..............................................................................................................................................................................454
Associated pathology.......................................................................................................................................................................................457
Dynamic and kinematic MRI of cervical spondylomyelopathy ...............................................................................................................................457
Traction MRI ....................................................................................................................................................................................................457
Kinematic MRI .................................................................................................................................................................................................461
Comparative imaging ............................................................................................................................................................................................462
MRI features related to prognosis..........................................................................................................................................................................465
References.............................................................................................................................................................................................................468
• Cervical spondylomyelopathy (CSM) or ‘wobbler syn- ANATOMIC CONSIDERATIONS

drome’ is a common disease of the cervical vertebral col-
umn of large- and giant-breed dogs. It is characterized • The reader is referred to Chapter 7.1 for a detailed
by dynamic and static compressions of the cervical spinal description of the anatomic structures of the cervical
cord, nerve roots, or both, leading to variable degrees of spine as well as the normal MRI appearance of structures
neurologic deficits and neck pain.1 of the vertebral column.
• A variety of names (at least 15) have been used to describe • The cervical region is unique in the sense that a larger
the disease; cervical vertebral instability, cervical malfor- degree of anatomic variation is seen in the cervical verte-
mation/malarticulation syndrome, and disc-associated brae compared with other vertebral regions. Not only are
wobbler syndrome are some of the terms most com- the cervical vertebrae different, but also the shape of and
monly used. relationship between the spinal cord and the vertebral
• Even though the disease can affect essentially all canine canal vary according to the location within the cervical
breeds, the Doberman Pinscher and the Great Dane rep- column (Fig. 7.2.1).2,6
resent approximately 60%–70% of all affected dogs. • It is also important to be aware that imaging changes are
• Cervical spondylomyelopathy is a complex disease, and commonly seen in large-breed dogs predisposed to CSM
many aspects of its pathogenesis remain unclear. An without associated clinical signs:
example of its complexity is the fact that Doberman • Two MRI studies showed that 25%–30% of clinically
Pinschers and Great Danes can have spinal cord com- normal Doberman Pinschers have clinically silent
pression secondary to intervertebral disc protrusion and spinal cord compression (Fig. 7.2.2).2,4
osseous compression while demonstrating no clinical • Other vertebral column changes previously thought
signs of cervical spondylomyelopathy.2–5 to be associated with CSM have also been found in
448 CHAPTER 7.2
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(a) (b)
Fig. 7.2.1 Transverse T2W images at the level of the C2-C3

(a), C5-C6 (b), and C7-T1 (c) intervertebral discs of a clinically
normal Doberman Pinscher. Note the different shapes of
the spinal cord at each cervical level. The normal spinal cord
at C7-T1 (c) has a somewhat trapezoid shape. (1.5T MRI
system; images courtesy of Dr. Wilfried Mai, University of
(c)
Pennsylvania)
a high percentage of clinically normal Doberman compression and foraminal stenosis as the causes of clini-
Pinschers, including intervertebral disc degeneration cal signs in canine CSM, and prompted consideration of
(75% of dogs), intervertebral disc protrusion (100%), other mechanisms potentially involved in the pathogen-
and intervertebral foraminal stenosis (69%).2 esis of the disease.3,5
• A similar study in clinically normal Great Danes • The shape of the vertebral canal may be one of the
also revealed a significant number of abnormal ana- mechanisms involved in the predisposition of Doberman
tomic findings, with foraminal stenosis seen in 73% Pinschers and Great Danes to CSM. An ex-vivo morpho-
of normal dogs, whereas spinal cord compression was metric study demonstrated that the height of the cranial
only present in 6.6% (Fig. 7.2.3).6 aspect of the vertebral canal of large-breed dogs is sig-
• These findings in clinically normal dogs called into nificantly smaller than that in small breeds, resulting in
question the traditional assumptions of spinal cord a funnel-shaped vertebral canal, particularly affecting
C e rv ic a l Sp on dy l om y e l opat h y 449
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the caudal cervical vertebrae.7 Among the large canine

breeds studied, this funnel-shaped pattern was most sig-
nificant in Doberman Pinschers.7
• Anatomic differences were thought to explain why CSM
rarely occurs in small-breed dogs in contrast to its high
incidence in large-breed dogs. It was initially thought
that the vertebral canal of small-breed dogs is propor-
tionately larger than that of large- and giant-breed dogs.8
However, a recent morphometric MRI study could not
confirm this hypothesis.9 In this study, a comparison of
the proportion of the vertebral canal occupied by the
Fig. 7.2.2 Sagittal T2W image of the cervical vertebral
spinal cord in Doberman Pinschers, Great Danes, and
column of a clinically normal 7-year-old, male neutered
small-breed dogs actually revealed that the canal occu-
Doberman Pinscher. Note the complete loss of T2 signal
pancy was highest for small-breed dogs and lowest in
of all the intervertebral discs except for the C3-C4 disc,
Great Danes.9 This finding highlights the importance
consistent with degeneration; C3-C4 retains partial bright
of vertebral canal dynamic biomechanical factors in the
T2 signal, consistent with partial degeneration. Mild ventral
pathophysiology of CSM.10
spinal cord compression is seen at C5-C6. C2 and C6 = second
and sixth cervical vertebrae, respectively. (1.5T MRI system;
reproduced, with permission, from da Costa RC, Parent JM,
PATHOPHYSIOLOGY OF CERVICAL
Partlow G et al. (2006). Morphologic and morphometric
SPONDYLOMYELOPATHY
magnetic resonance imaging features of Doberman
• It is important to have a solid understanding of the basis
pinscher dogs with and without clinical signs of cervical
of the pathogenesis of CSM because, as previously stated,
spondylomyelopathy. Am J Vet Res 67(10):1601–12.)
morphologic changes suggestive of CSM can be seen
without clinical signs of the disease.
• The pathophysiology involves both static and dynamic
factors. The key static factor is vertebral canal stenosis.
(a) (b)
Fig. 7.2.3 Transverse T2W images centered at the C4-C5 (a) and C5-C6 (b) intervertebral spaces in a clinically normal
Great Dane showing lateral spinal cord compression secondary to articular process joint proliferation. The compression is
mild and unilateral on the left at C4-C5 (a) and moderate and bilateral at C5-C6 (b). The arrows indicate bilateral foraminal
stenosis. R = right side. (3T MRI system; reproduced, with permission, from Martin-Vaquero P, da Costa RC (2014). Magnetic
resonance imaging features of Great Danes with and without clinical signs of cervical spondylomyelopathy. J Am Vet Med Assoc
245(4):393–400.)
450 CHAPTER 7.2
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Studies show that Doberman Pinschers and Great Danes a respective incidence of 87% and 100% in CSM affected
with cervical spondylomyelopathy have a stenotic cervi- dogs.2,6 Even though most normal dogs had mild to mod-
cal vertebral canal when compared with clinically nor- erate stenosis compared with a more severe stenosis in
mal dogs. This stenosis affects the entire cervical spine, CSM dogs, there still remained a high incidence of sub-
not just at the caudal cervical region, where compressive clinical foraminal stenosis.
lesions are commonly located.2,6 A narrow canal lowers • Despite some degree of overlap, the pathophysiology of
the threshold at which the cumulative effects of various the spinal cord compressions can be divided into osseous
structures encroaching on the spinal cord cause signs or disc-associated compressions.17 Disc-associated CSM
of myelopathy.11 It is well established in humans that is typically seen in middle-aged large-breed dogs (pri-
a smaller vertebral canal is an important factor for the marily Doberman Pinschers), whereas the osseous form
development of cervical spondylotic myelopathy.12–14 of CSM is mostly seen in young adult giant-breed dogs
• This vertebral canal stenosis might be an absolute steno- such as Great Danes.
sis (which then causes direct spinal cord compression and • Disc-associated CSM is caused by a combination of inter-
neurologic signs) or a relative vertebral stenosis, which vertebral protrusion with or without ligament hypertro-
by itself does not lead to myelopathic signs, but predis- phy (either the dorsal longitudinal ligament or the yellow
poses the patient to develop myelopathy.2,3,6 ligament [ligamentum flavum]) (Fig. 7.2.4):
• Foraminal stenosis has been demonstrated as one of the • Three factors act in combination to explain the patho-
key factors contributing to the ischemic insult in the physiology of disc-associated CSM:2,18–20
pathogenesis of human cervical spondylotic myelopa- – Relative vertebral canal stenosis.
thy.15,16 In contrast, it is difficult to establish a direct – More pronounced torsion in the caudal cervi-
association between foraminal stenosis and spinal cord cal vertebral region leading to intervertebral disc
injury in most canine CSM cases. Foraminal stenosis was degeneration.
found in 69% and 73% of clinically normal Doberman – Protrusion of larger volume discs in the caudal
Pinschers and Great Danes, respectively, compared with cervical spine.
Fig. 7.2.4 Schematic illustrating the changes associated with disc-associated cervical spondylomyelopathy. The top image
shows ventral spinal cord compression and nerve root compression at C5-C6 caused by intervertebral disc protrusion. Dorsally,
hypertrophy of the ligamentum flavum (in yellow) causes mild spinal cord compression. Bottom row: left: transverse section
at the level of the C4-C5 disc region showing normal spinal cord and vertebral canal; middle: ventral compression at C5-C6
caused by intervertebral disc protrusion and hypertrophy of the dorsal longitudinal ligament (in yellow) and ligamentum flavum
(causing mild dorsal compression); right: asymmetric intervertebral disc protrusion at C6-C7, causing spinal cord and nerve
root compressions. (Reproduced, with permission, from da Costa RC (2010). Cervical spondylomyelopathy (wobbler syndrome)
in dogs. Vet Clin North Am Small Anim Pract 40(5):881–913.)
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Fig. 7.2.5 Schematic illustrating the changes associated with osseous-associated cervical spondylomyelopathy. Top row: left:
severe dorsolateral spinal cord compression at C2-C3 caused by osseous malformation and osteoarthritic changes; middle:
normal C3-C4 disc region; right: bilateral compression at C4-C5 caused by osteoarthritic changes and medial proliferation
of the articular processes, resulting in absolute vertebral canal stenosis and foraminal stenosis leading to spinal cord and
nerve root compressions, respectively. The bottom image shows dorsal spinal cord compression at C3-C4 caused by lamina
malformation and hypertrophy of the ligamentum flavum. Osteoarthritic changes are also shown at C2-C3. (Reproduced, with
permission, from da Costa RC (2010). Cervical spondylomyelopathy (wobbler syndrome) in dogs. Vet Clin North Am Small Anim
Pract 40(5):881–913.)
• Affected dogs are apparently born with a congenital • Critical to the development of clinical signs in CSM
vertebral canal stenosis that worsens over time.21 The affected large-breed dogs is the concept of dynamic
vertebral canal stenosis per se does not lead to clini- lesions (i.e., lesions that worsen or improve with differ-
cal signs, but predisposes them to the development of ent positions of the cervical spine). Dynamic spinal cord
clinical signs. compressions are present in both disc- and osseous-
• The vast majority of disc-associated spinal cord com- associated CSM.1,10 Repetitive flexion and extension of
pressions are located in the caudal cervical spine, the cervical spine can lead to spinal cord elongation caus-
affecting the discs C5-C6 and C6-C7. ing axial parenchymal strain and stress, which has been
• Osseous-associated CSM (OA-CSM) is different because proposed as a key mechanism of spinal cord injury in cer-
it is typically related to absolute vertebral canal stenosis vical spondylotic myelopathy in humans.25,26
secondary to proliferation of the vertebral arch (dorsally), • These dynamic changes in the vertebral canal were
articular processes (dorsolaterally), or articular facets recently documented in the caudal cervical vertebral
and pedicles (laterally) (Fig. 7.2.5).22–24 The cause of the region (C4-C5, C5-C6, C6-C7) of dogs.27 Extension of
compression appears to be a combination of vertebral the cervical spine resulted in a 28.9% reduction in the
malformation and osteoarthritic/osteoarthrotic changes diameter of the vertebral canal compared with flexion.27
at the level of the articular processes. Occasionally, these Moving from a neutral position to extension decreased
compressions are complicated by disc protrusion, espe- the canal diameter by 16.5%.27 Significant narrowing of
cially in older dogs. the caudal cervical intervertebral foramina was also dem-
• Ligamentous compression (ligamentum flavum) may be onstrated during cervical extension.28
contributing to the pathophysiology of the disease in • The concept of dynamic compression is very differ-
giant- and large-breed dogs, but pure ligamentous com- ent from instability, which has been defined as the loss
pression as the single source of compression appears of ability of the cervical spine under physiologic loads
uncommon. to maintain its normal pattern of displacement so that
452 CHAPTER 7.2
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there is no damage to the spinal cord or nerve roots.29,30

Instead, it appears that a restricted, rather than an exces-
sive, intervertebral motion is more likely to exist at the
sites of disc degeneration and severe arthritic changes
affecting the articular processes, as has been shown in
people.6,31,32 Instability has not yet been proven in dogs
with CSM. By the time of diagnosis, when severe degen-
erative changes are already present either affecting the
articular processes or intervertebral disc, it is likely
that those joints are not unstable. Instability might be
a pre-clinical condition that leads to the degenerative
changes, and if so, documenting its existence might be
very difficult.
• Due to the importance of dynamic compressions in the
pathogenesis of CSM, it is clear that advanced imaging
modalities need to evaluate the dynamic component of
CSM.
TECHNICAL CONSIDERATIONS
• The optimal MRI technique for spinal imaging is

described in Chapter 4.2. Listed below are some of the
Fig. 7.2.6 CT myelogram showing left dorsolateral
key points used by the author when investigating cases
spinal cord compression at the level of T2-T3 in a
suspected of having CSM.
1-year-old Mastiff with osseous-associated cervical
• Dorsal recumbency is attempted in all dogs with CSM.
spondylomyelopathy. (Reproduced, with permission, from
Some very deep chested dogs cannot fit into the MRI
da Costa RC, Echandi RL, Beauchamp D (2012). Computed
bore of high-field MR units, and therefore need to be
tomography myelographic findings in dogs with cervical
imaged in lateral recumbency. It is important to note
spondylomyelopathy. Vet Radiol Ultrasound 53(1):64–70.)
the change in orientation of the chemical shift artifact
when switching from dorsal to lateral recumbency (see
Chapters 3 and 4.2). Due to machine configuration, Chapter 2) and sagittal and transverse T2W and T1W
large-breed dogs scanned in low-field MR units are pulse sequences.34 Occasionally, T2-FLAIR, STIR, and
imaged in lateral recumbency. contrast-enhanced T1W pulse sequences may be used.
• Field of view (FOV): even though CSM is a cervical • If foraminal stenosis needs to be objectively assessed, a
myelopathic disease that causes compressive lesions pri- gradient echo pulse sequence with magnetization trans-
marily in the caudal cervical region (C5-C6 and C6-C7), fer and contrast enhancement has been reported in peo-
almost 10% of dogs with CSM have lesions in the cra- ple to be the best sequence to evaluate the foramen in the
nial thoracic vertebral region (Fig. 7.2.6).33 In addition, transverse plane.35–37
compressive lesions are also occasionally identified at the • Transverse images should be acquired through all inter-
dorsal aspect of the C1-C2 region. Therefore, the FOV vertebral disc spaces because lateralized compressions
should extend from C1 to T3. or foraminal stenosis are difficult to identify on sagittal
• Imaging planes: the sagittal and transverse planes are images.38 Dorsal images cannot be used as a screening
the most important. Dorsal plane images are occasion- method for that purpose, as their reliability in identify-
ally useful, although due to the natural curvature of the ing lateralized compressions has not been evaluated.
cervical vertebral region compared with the thoraco- • The orientation of the transverse slices needs to be
lumbar region, comparison of multiple vertebral levels defined and oriented consistently throughout all inter-
is difficult. vertebral disc spaces. One study found significant differ-
• Considering that more than half of dogs with CSM have ences in the size of the vertebral canal in the cervical
multiple compressive lesions, proper straight alignment vertebral column when comparing slices oriented paral-
of the vertebral column is of paramount importance, as lel to the endplates versus perpendicular to the vertebral
comparison of severity of compression at different sites canal.39
will be made on the sagittal and transverse images. • Due to the importance of dynamic compressions in the
• The basic pulse sequences routinely used when sus- pathogenesis of CSM, it is clear that advanced imaging
pecting CSM are: sagittal heavily T2W sequence modalities need to evaluate the dynamic component of
(‘T2-myelogram’ such as HASTE or SS-FSE, see CSM. In contrast with reports of clinical worsening
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after flexion and extension myelographic studies in dogs, • The severity of the intervertebral disc protrusion is
this complication has not been observed with kinematic determined based on the amount of disc displacement
MRI. It appears that extension and traction views are in relation to the cranial and caudal endplates on the
particularly useful.40,41 sagittal images.
• Diffusion tensor imaging (DTI) with tractography is • Degenerative changes of the corresponding interver-
becoming a common technique in people and prelimi- tebral disc (loss of T2 hyperintense signal from the
nary evidence suggests it might be useful in the diagnos- disc).
tic evaluation of canine CSM.42–45 • Frequently combined with dorsal spinal cord compres-
sion caused by malformation of the dorsal lamina and/
GENERAL MRI FEATURES OF CERVICAL or hypertrophy of the ligamentum flavum (Fig. 7.2.7).
SPONDYLOMYELOPATHY • Dogs with disc-associated CSM have relative verte-
bral canal stenosis, although this might be difficult to
Disc-associated cervical identify without objective assessment.
spondylomyelopathy • Spinal cord signal changes: typically, hyperintensity
• MRI can accurately reveal sites of disc-associated com- on T2W images centered over the compressive lesion
pressive lesions. Most disc-associated compressive lesions is seen in over half of disc-associated CSM cases.49
are located at C5-C6 and C6-C7. Note that mild ventral • Foraminal stenosis is frequently seen in the caudal
compression of the subarachnoid space and spinal cord cervical vertebral column.
is commonly seen at C2-C3 on sagittal images; however,
this is usually not associated with significant spinal cord Osseous-associated cervical
compression on transverse images. spondylomyelopathy
• General MRI findings in dogs with disc-associated • Dogs with OA-CSM (typically giant-breed dogs) often
canine CSM include:2,46–48 have multiple sites of spinal cord compression, mostly
• Extradural ventral compression of the spinal cord cen- from C4-C5 through C6-C7.
tered at the level of an intervertebral disc, recognized by: • Occasionally, vertebral canal stenosis and spinal cord
– Deformation and dorsal displacement of the spi- compression are also found at C2-C3, C3-C4, and the
nal cord and ventral subarachnoid space (on T2W cranial thoracic vertebral column.33
images) (Fig. 7.2.7). • In dogs with OA-CSM, MRI frequently reveals:
– Variable degrees of ventral spinal cord compres- • Hypointense T1W and T2W proliferative changes
sion, centered over the intervertebral disc space associated with the articular processes, lamina, and/
and caused by intervertebral disc protrusion. or pedicles, consistent with hypertrophic degener-
• The compressive material is hypointense on T1W and ative changes of these osseous structures.6,22,23,50–52
T2W images. This often causes variable degrees of foraminal steno-
sis, usually best appreciated on transverse and dorsal
plane images (Figs. 7.2.8, 7.2.9).
• Reduction or loss of the normally hyperintense syno-
vial joint fluid signal is often found on T2W images,
in association with the articular process joint degen-
erative changes.
• The presence of osseous proliferative changes causes
absolute vertebral canal stenosis and secondary extra-
dural spinal cord compression, which most often has
a lateral, dorsal, and/or dorsolateral distribution, and
can be uni- or bilateral (Fig. 7.2.8).
• Due to the lateral and dorsolateral localization of the
compressions, the compressed spinal cord can change
Fig. 7.2.7 Sagittal T2W image in a 10-year-old Doberman shape and become triangular, trapezoid, or square-
Pinscher with disc-associated cervical spondylomyelopathy. shaped on transverse images, with loss of the normally
This image shows multiple sites of ventral spinal cord hyperintense signal from epidural fat/cerebrospinal
compression, more severe at C5-C6 and C6-C7. Spinal cord fluid (CSF) on T2W images.
hyperintensity is also seen at C6-C7. Mild dorsal spinal • If post-contrast T1W images are obtained, no spinal
cord compressions are seen at C3-C4, C4-C5, and C6-C7. cord contrast enhancement is typically seen in
Intervertebral disc degeneration is also seen at multiple OA-CSM.22
levels with severe sclerotic changes of the endplates at C6-C7 • Given the lateral or dorsolateral localization of com-
causing decreased signal. (3T MRI system) pression in the majority of cases with OA-CSM, the
454 CHAPTER 7.2
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(a) (b)
Fig. 7.2.8 Transverse T2W images at the level of C4-C5

(a), C5-C6 (b), and C6-C7 (c) in a Great Dane with osseous-
associated cervical spondylomyelopathy. Bilateral, lateral
spinal cord compression secondary to articular joint processes
proliferation is present at all levels. (3T MRI system;
reproduced, with permission, from Martin-Vaquero P,
da Costa RC, Drost WT (2014). Comparison of non-
contrast computed tomography and magnetic resonance
imaging in the evaluation of Great Danes with cervical
(c)
combined use of parasagittal, dorsal, and transverse MR • Areas of hyperintensity on T2W images, along with
images may be necessary to fully characterize the extent isointensity on T1W images, corresponded to regions
of these compressions (Fig. 7.2.9). of slight loss of nerve cells, gliosis and edema in the
gray matter, as well as demyelination, edema, and
Spinal cord signal changes Wallerian degeneration in the white matter.
• The spinal cord parenchyma should be scrutinized for • The combination of T2 hyperintensity and T1
changes in signal intensity. hypointensity corresponded to severe changes such
• Signal intensity in the abnormal area is characterized as as necrosis, myelomalacia, and spongiform changes
increased (= hyperintense) or decreased (= hypointense) in the gray matter, as well as white matter necrosis
compared with the normal parenchyma cranial and cau- (Fig. 7.2.11).53
dal to the lesion. The most common signal change is • Interestingly, experimentally induced chronic cervical
hyperintensity on T2W images (Figs. 7.2.7–7.2.10). spinal cord compression in dogs produced spinal cord
• In people, the correlation of spinal cord signal changes signal changes that histopathologically corresponded to
on MRI and histopathology has been well described.53 lesions affecting mostly the gray matter (motor neuron
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(a)
(c) (b)
Fig. 7.2.9 MR images of a 5-year-old Great

Dane with osseous-associated CSM. In (a), a
sagittal T2W image shows dorsal and ventral
spinal cord compression at C2-C3 and areas of
hypointensity suggestive of dorsal and lateralized
spinal cord compression at C5-C6 and C6-C7. In
(b), a dorsal T2W image shows bilateral spinal
cord compressions at C4-C5, C5-C6, and C6-C7
(arrows). In (c), a transverse image at C2-C3 shows
dorsolateral compression. In (d), a transverse
image shows bilateral compression at C6-C7.
(d)
(3T MRI system)
456 CHAPTER 7.2
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(a) (b)
Fig. 7.2.10 Doberman Pinscher with disc-associated cervical spondylomyelopathy. In (a), a sagittal T2W image shows mild
ventral spinal cord compression at the level of C6-C7 and mild dorsal compressions at C3-4 and C4-5, with well-defined spinal
cord hyperintensity at C5-C6 and C6-C7. The corresponding sagittal T1W image (b) shows spinal cord hypointensity at C5-C6
and C6-C7. (3T MRI system)
(a)
(b)
Fig. 7.2.11 Mid-sagittal T2W image (a) of the cervical spine,

transverse T2W image (b), and corresponding T1W image (c)
at C6-C7 in a Great Dane with cervical spondylomyelopathy.
The mid-sagittal image reveals two areas of spinal cord
hyperintensity: at C5-C6 (ill-defined) and C6-C7 (well-
defined). Transverse images through C6-C7 reveal marked
spinal cord T2 hyperintensity and T1 hypointensity,
secondary to severe compression due to bilateral lateral
articular process joint proliferation with irregular articular
surfaces and sclerosis causing severe vertebral canal stenosis
with a vertically elongated appearance of the spinal cord.
(3T MRI system; reproduced, with permission, from
Martin-Vaquero P, da Costa RC (2014). Magnetic resonance
imaging features of Great Danes with and without clinical
signs of cervical spondylomyelopathy. J Am Vet Med Assoc
(c)
245(4):393–400.)
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loss and necrosis), but there was no evidence of demy- DYNAMIC AND KINEMATIC MRI OF
elination or axonal degeneration.54 CERVICAL SPONDYLOMYELOPATHY
• These experimental findings contrast with the patho-
logic changes described in the spinal cord of CSM Traction MRI
affected dogs, where there is a predominance of white • The concept of static and dynamic lesions in dogs
matter lesions with myelin degeneration and secondary with CSM was first established in 1982.17 Lesions that
axonal injury.55–57 improved or disappeared on traction or flexion/extension
• One study looked specifically at factors associated with views were considered dynamic. Due to the risk of neuro-
spinal cord signal changes in 102 dogs with CSM. The logic deterioration after myelography with these cervical
overall incidence of spinal cord signal changes was manipulations, only traction positions continued to be
55.9%. They were significantly more common in dogs routinely used.61 Lesions that improved or disappeared
with a chronic history, more severe neurologic deficits, with traction were determined to be dynamic, whereas
and with moderate or severe spinal cord compressions.49 those that did not improve were called static.
The location and direction of the compressive lesions • The technique for traction was rather subjective, since it
had no influence on the development of spinal cord sig- was described as grasping the dog behind the base of the
nal changes in dogs with CSM. skull while applying firm linear traction.17 Based on this
concept, a multitude of surgical techniques were devel-
Associated pathology oped for the treatment of dynamic lesions.62–64 It is sur-
• In addition to the changes described above, extradural prising that so many surgical techniques were based on
synovial cysts originating from the articular process such a subjective diagnostic criterion, especially since it
joints have also been reported in dogs with OA-CSM. was never established how much traction should be used
They are often associated with abnormally enlarged and how it should be consistently performed.
articular process joints.22,58–60 Parasagittal, dorsal, and • More recently, guidelines for traction MRI studies were
transverse images aid in the visualization and localiza- reported.46,65 The original method of grasping and hold-
tion of these extradural synovial cysts (Fig. 7.2.12). ing the dog’s head for dynamic myelographic studies
Occasionally, the extradural synovial cysts may partially violates MR safety guidelines and cannot be directly
enhance on post-contrast images.22 transposed to MR imaging. Instead, traction can be
• Importantly, a recent study showed that kinematic MRI applied with a rope attached to the dog’s maxilla or,
may aid in the visualization of these extradural synovial preferably, with a cervical harness anchored on the dog’s
cysts (see below and Fig. 7.2.19).41 mandible (see Fig. 4.2.5 in Chapter 4.2).46,65
(a)
Fig. 7.2.12 Synovial cyst in a Rottweiler dog with cervical

spondylomyelopathy. Sagittal (a) and transverse (b) T2W
images showing the synovial cyst at C5-C6 (arrows). Note
the enlarged articular processes associated with the cyst
on the transverse image (b). (3T MRI system; reproduced,
with permission, from da Costa RC, Cook LB (2016). Cystic
abnormalities of the spinal cord and vertebral column.
Vet Clin North Am Small Anim Pract 46(2):277–93.) (b)
458 CHAPTER 7.2
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• It is recommended to avoid using more than 20% or 25% • It is also important to understand how subjective and
of the patient’s body weight. Even though weights of discrepant the MRI and myelographic findings can be
50% of the patient’s body weight have been used,65 the in determining lesions as static or dynamic, as shown
author has used 20% of body weight consistently and in the case illustrated in Fig. 7.2.13. The issue of sub-
been able to appreciate matching amounts of interver- jectivity associated with interpretation of these studies
tebral distraction in morphometric evaluations of the was already identified with myelography many years
intervertebral discs.2 ago.69
• In people, there are very few reports about traction MRI • The dura mater and the spinal cord have elastic prop-
studies. The traction force used ranged between 20% and erties to adjust themselves to changes in neck position
33% of the weight of an average person.30,66 These rec- according to movement. A traction study in normal
ommendations were based on non-anesthetized human cats demonstrated that the caudal cervical region has
patients. In an anesthetized dog, muscle tone would not significantly higher vertebral and spinal cord motion
counteract the traction force; therefore, it is reasonable compared with the cranial cervical spine.70 Because of
to assume that less traction would be needed to produce the inherent elastic properties of the cervical spinal
the same degree of spinal distraction as in people. cord and vertebral structures, it is possible that many
• It has been demonstrated in experimental studies that lesions that would be considered dynamic on myelog-
excessive traction can cause ischemia and disruption of raphy would in fact be static on MR evaluation, as seen
the spinal cord interstitial pressure, causing permanent in Fig. 7.2.14.
cord damage.67,68
(a)
(b)
Fig. 7.2.13 Cervical myelogram and T2W MR images of a 7-year-old Doberman

Pinscher with disc-associated cervical spondylomyelopathy. (a) Pre-traction
cervical myelogram showing ventral extradural compression at C6-C7.
(b) The post-traction cervical myelogram reveals improvement in the degree of
ventral compression. This lesion could be considered dynamic. (c) Ventrodorsal
myelogram showing bilateral extradural compression at C6-C7, worse on the
(c)
right. (Continued)
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(d)
(e)
(f) (g)
Fig. 7.2.13 (Continued) Cervical myelogram and T2W MR images of a 7-year-old Doberman Pinscher with disc-associated
cervical spondylomyelopathy. (d) Pre-traction sagittal T2W showing ventral and dorsal spinal cord compression with
marked spinal cord hyperintensity at C6-C7. Complete intervertebral disc degeneration is also seen at C6-C7. (e) The post-
traction sagittal T2W image reveals minimal improvement in ventral spinal cord compression. On MR imaging, the lesion
appears static. (f) Transverse T2W image at the cranial region of the spinal cord compression showing bilateral spinal cord
compression with cord hyperintensity. (g) Transverse T2W image at the central aspect of the cord compression. Marked
circumferential compression reveals a small, atrophic spinal cord that is seen as an irregular area of hyperintensity (arrow).
C7 = seventh cervical vertebra. (1.5T MRI system; reproduced, with permission, from da Costa RC, Parent JP, Dobson H
et al. (2006). Comparison of magnetic resonance imaging and myelography in 18 Doberman pinscher dogs with cervical
460 CHAPTER 7.2
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(a)
(b)
(c)
(d)
(e)
Fig. 7.2.14 Cervical myelogram and T2W MR images of a 9-year-old
Doberman Pinscher with cervical spondylomyelopathy. (a) Pre-
traction cervical myelogram showing ventral extradural compression
at C6-C7 and splitting of the ventral contrast column at C5-C6.
(b) The post-traction cervical myelogram shows improvement in (f)
ventral compression and in splitting of the contrast column. This
lesion can be considered dynamic. (c) Ventrodorsal myelogram
showing focal divergence of the contrast columns at C5-C6. No asymmetric compression is seen. (d) Pre-traction sagittal
T2W image showing marked spinal cord compression at C5-C6, with minimal cord compression at C6-C7. Intervertebral
disc degeneration is observed at C4-C5, C5-C6, and C6-C7. (e) The post-traction sagittal T2W image still shows marked
spinal cord compression at C5-C6. On MR imaging, the lesion appears static. (f) Transverse T2W image at C5-C6 showing
markedly asymmetric spinal cord compression, worse on the right side (arrow). C7 = seventh cervical vertebra; R = right.
(1.5T MRI system; reproduced, with permission, from da Costa RC, Parent JP, Dobson H et al. (2006). Comparison of
magnetic resonance imaging and myelography in 18 Doberman pinscher dogs with cervical spondylomyelopathy. Vet Radiol
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Kinematic MRI
• As previously discussed in the pathophysiology sec-
tion, the presumed instability widely discussed in dogs
with CSM might in fact be dynamic-related spinal cord
lesions. The dynamic nature of CSM-associated lesions
needs to be quantified and assessed with MRI.
• Even though much less is known about vertebral column
biomechanics in dogs compared with humans, recent
canine studies provide support to the concept of both
dynamic vertebral canal and foraminal stenosis.27,28
• A biomechanical study showed that the vertebral
canal diameter of the caudal cervical vertebral column
increased by 7.7% from a neutral position to flexion,
whereas in extension the canal diameter decreased by Fig. 7.2.15 Great Dane positioned in extension on a board
16.5%. When comparing the variation in the vertebral used for kinematic MRI.
canal between flexion and extension, the difference in
vertebral canal diameter was 28.9%.27
• In another biomechanical study, it was found that flexion neutral position, mainly at C4-C5. It also showed wors-
of the caudal cervical vertebral column caused an increase ening of compressive lesions, primarily at C5-C6 and
in width and height of the intervertebral foramina by 3.5% C6-C7. In some patients, there was worsening of both
and 11.1%, respectively. Extension caused a decrease in dorsal and ventral compressive lesions, a phenomenon
both width (11.3%) and height (17.2%) of the interverte- called the ‘pincer effect’ (Figs. 7.2.16, 7.2.17).76 Flexion
bral foramina. These changes occurred both in normal frequently caused improvement or resolution of ventral,
dogs and in dogs with intervertebral disc degeneration.28 disc-related spinal cord compressions.40 Resolution
• In human medicine, the dynamic component of cervi- of ventral spinal cord compression during flexion had
cal spondylotic myelopathy has been evaluated using been noted on myelography previously,17 and it might
kinematic MRI for many years. Patients are placed in be related to an increase in the vertebral canal height,
a positioning device that allows controlled flexion and which has been documented by biomechanical studies
extension +/– lateral bending and axial rotation of the in dogs.27
cervical vertebral column.71–75 It has been shown that • Kinematic MRI in dogs with OA-CSM also revealed
kinematic MRI will reveal lesions that are not noted on new compressive lesions, and extension resulted in
standard imaging.74,75 the identification of a new primary site of spinal cord
• Findings on kinematic MRI in people have been used compression in one-third of patients in one study
to direct patient management. One study showed that (Fig. 7.2.18).41 In one patient, kinematic MRI allowed
kinematic MRI changed therapeutic management in easy identification of a synovial cyst, which became
28% of patients with cervical disc disease.72 The results compressive with extension of the cervical vertebral
of kinematic MRI changed surgical management in column (Fig. 7.2.19). The effect of flexion on spinal
87% of patients with cervical spondylotic myelopathy. cord compression was variable. In some patients, flex-
Intraoperative patient positioning was modified in 27% ion resulted in improvement or resolution of compres-
of patients based on kinematic MRI findings.72 Based on sive lesions, while in others it identified new areas of
these results, it appears that kinematic MRI studies may compression.
also be important in canine CSM, to assess and docu- • Contrary to the reports of dynamic myelography,
ment the dynamic nature of lesions. where clinical worsening was reported in approximately
• An MRI compatible positioning device was recently 20% of dogs,17 worsening after kinematic MRI was not
designed for evaluation of kinematic MRI in dogs.40,41 observed in any dog to date.40,41 However, it is impor-
The kinematic board allowed controlled flexion and tant to closely monitor patients during the procedure.
extension in 10° increments. The patient was posi- During flexion, there is a risk for the positioning device
tioned in lateral recumbency to allow maximum flexion to cause compression of both the trachea and the vago-
and extension within the constraints of the MRI bore sympathetic trunk. As a result, special attention needs
(Fig. 7.2.15). to be paid to heart rate, blood pressure, capnometry,
• In dogs with disc-associated CSM, extension revealed and pulse oximetry in all patients undergoing these
new areas of compression that were not present in a procedures.
462 CHAPTER 7.2
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(a) (b)
(c) (d)
Fig. 7.2.16 Kinematic sagittal T2W images of a dog with disc-associated cervical spondylomyelopathy. Neutral position
(a), traction (b), flexion (c), and extension (d) are represented. Flexion of the cervical vertebral column (c) results in cranial
migration of the T2W hyperintensities within the spinal cord that were level with C5-C6 and C6-C7 on the neutral position
image (a). Extension is associated with both ventral and dorsal compression (‘pincer effect’) at C5-C6 and C6-C7. (3T MRI
system; reproduced, with permission, from Provencher M, Habing A, Moore SA et al. (2016). Kinematic magnetic resonance
imaging for evaluation of disc-associated cervical spondylomyelopathy in Doberman Pinschers. J Vet Intern Med 30(4):1121–8.)
COMPARATIVE IMAGING incidence of post-myelographic seizures appears higher

in dogs with CSM compared with other spinal diseases.79
• MRI has been considered the best imaging technique for • Conventional CT can be done under sedation and offers
people with cervical spondylotic myelopathy for almost exquisite bone detail.80 This higher bone definition
three decades,77,78 and is also the imaging modality of would be potentially important in dogs with OA-CSM,
choice for dogs with suspected CSM.22,46 allowing more precise evaluation of the degenera-
• Other imaging methods that have been used to evaluate tive changes of the cervical vertebral articular process
CSM in dogs include conventional myelography, con- joints.23 For example, in a comparative CT and MRI
ventional CT, and CT myelography. study in dogs with OA-CSM, there was overall a better
• In a study comparing MRI and myelography in dogs with interobserver agreement for both the regularity of the
disc-associated CSM,46 MRI allowed identification of articular surfaces and the degree of articular process joint
more sites of abnormalities than myelography. Although proliferation for CT when compared with MR images
myelography could identify the location of the lesion (Fig. 7.2.20).80 Similar findings, specifically concern-
in most patients, MRI was more accurate in predicting ing the articular facets, have also been found in people.81
the site, severity, and nature of the spinal cord compres- However, although conventional CT had a substantial
sion. Spinal cord MRI signal changes were seen in the agreement with MRI regarding the site of main spinal
majority of patients and provided assistance in precise cord compression (Fig. 7.2.21),80 this technique cannot
lesion identification. It is also important to note that the be recommended as a sufficient diagnostic modality due
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(a) (b)
(c) (d)
Fig. 7.2.17 Kinematic sagittal T2W images of a dog with disc-associated cervical spondylomyelopathy. Neutral position
(a), traction (b), flexion (c), and extension (d) are represented. With extension of the cervical vertebral column (d), there is
significant worsening of the C6-C7 compression primarily dorsally, as well as a new compressive lesion identified at C5-C6.
(3T MRI system; reproduced, with permission, from Provencher M, Habing A, Moore SA et al. (2016). Kinematic magnetic
resonance imaging for evaluation of disc-associated cervical spondylomyelopathy in Doberman Pinschers. J Vet Intern Med
30(4):1121–8.)
to the possibility of not identifying the main site of com- cord compressions are seen in approximately 63% of dogs
pression or missing additional lesions. with CSM.33,85
• CT myelography has been shown to be complementary • In a study comparing myelography, CT myelography,
to standard myelography in the evaluation of Doberman and MRI in 22 dogs with disc-associated CSM, there
Pinschers with cervical spondylomyelopathy.82 An were significant discrepancies in interpretation amongst
advantage of CT myelography is visualization of spinal imaging modalities and amongst observers. The study
cord atrophy, which is associated with poor prognosis.82 found moderate agreement between all modalities
A disadvantage of both conventional myelography and regarding identification of the most severe compressive
CT myelography is their invasiveness as compared with lesions. The authors concluded that CT myelography
MRI. Post-myelographic seizures and temporary dete- and MRI could be seen as complementary modalities.48
rioration of the patient’s neurologic status are important • Although it is unquestionable that there is diagnostic
disadvantages.46,79,83 value to a multimodality approach combining CT and
• CT myelography is still used in people for equivocal MRI studies, in clinical practice, most cases will only
cases where cervical radiculopathy secondary to forami- have one imaging modality, and in these cases high-field
nal stenosis is the main clinical problem.84 However, MRI would be the modality of choice, as it is in people.
unlike MRI, CT myelography is unable to detect spinal • High-field MRI also offers the possibility of perform-
cord parenchymal changes that are helpful to determine ing advanced techniques such as DTI with tractography
the most significant spinal cord lesion(s) in cases with (Fig. 7.2.22), as well as kinematic MRI (traction, flexion,
multiple compressions. This is an important advantage extension) with a large FOV, which is useful to assess the
of MRI over CT myelography, because multiple spinal dynamic components of CSM.40–43
464 CHAPTER 7.2
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(a) (b)
(c) (d)
(e) (f)
Fig. 7.2.18 Kinematic sagittal T2W images (a, c, e) and transverse T2W images at the level of C5-C6 (b, d, f) of a dog with
osseous-associated cervical spondylomyelopathy. Neutral position (a, b), flexion (c, d), and extension (e, f) are represented.
There are mild ventral compressions at C4-C5 and C5-C6 and a moderate dorsal compression at C5-C6 in a neutral
position (a, b). Flexion of the cervical vertebral column results in mild improvement in the dorsal compression at C5-C6,
but the ventral compressions remain unchanged (c, d). Extension is associated with worsening of both the ventral and dorsal
compression at C5-C6, improvement in the ventral compression at C4-C5, and a new, mild dorsal compression at C6-C7
(e, f). (3T MRI system; reproduced, with permission, from Provencher M, Habing A, Moore SA et al. (2017). Evaluation of
osseous-associated cervical spondylomyelopathy in dogs using kinematic magnetic resonance imaging. Vet Radiol Ultrasound
58(4):411–21.)
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C5
(a) (b)
(c) C5 (d)
Fig. 7.2.19 Kinematic sagittal T2W images (a, c) and transverse T2W images at the level of C3-C4 (b, d) in a dog with osseous-
associated cervical spondylomyelopathy. Neutral position (a, b) and extension (c, d) are represented. No spinal cord compression
or cyst is seen on the transverse image in neutral position (b), although the right dorsolateral aspect of the vertebral foramen
appears enlarged. With extension (d), there is enlargement of a synovial cyst associated with the right articular process causing
moderate right dorsolateral compression of the spinal cord. There are new dorsal compressions at C4-C5, C5-C6, and C6-C7
with a new ventral compression at C6-C7. (3T MRI system; reproduced, with permission, from Provencher M, Habing A,
Moore SA et al. (2017). Evaluation of osseous-associated cervical spondylomyelopathy in dogs using kinematic magnetic
resonance imaging. Vet Radiol Ultrasound 58(4):411–21.)
MRI FEATURES RELATED TO PROGNOSIS • In spite of some controversy, spinal cord signal changes
have also been used to predict outcome in humans. A
• In people, several MRI studies have shown a correlation study from 1990 reported that the hyperintensity of the
between the decrease in cross-sectional area of the spinal spinal cord on T2W images was associated with a poor
cord and the clinical severity of myelopathy.13,86 There outcome.89 In contrast, two subsequent studies suggested
is a consistent correlation between the degree of spinal that T2 hyperintense areas in the spinal cord were not
cord compromise at the level of greatest compression and correlated with outcome.90,91 It appears, however, that
prognosis for recovery. In general, those patients with the the presence of larger, well-defined areas of spinal cord
greatest degree of cord compression have a lesser chance hyperintensity on T2W images, as well as multifocal
of recovery after surgical decompression.87 Recent stud- areas of hyperintensity, are associated with a worse prog-
ies also substantiate that the transverse cross-sectional nosis.92,93 Human patients with postoperative regres-
area of the spinal cord can be used to predict outcome.88 sion of intramedullary hyperintensity had a significantly
466 CHAPTER 7.2
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(a)
(b) (c)
(d) (e)
Fig. 7.2.20 Great Dane with osseous-associated CSM. (a) Mid-sagittal T2W MR image of the cervical spine, (b) transverse
T2W MR image at C5-C6 and (c) corresponding transverse non-contrast CT image using a bone window, (d) transverse
T2W MR image at C6-C7 and (e) corresponding transverse non-contrast CT image using a bone window. The T2W mid-
sagittal image reveals two areas of spinal cord hyperintensity at C5-C6 (ill-defined, mild) and C6-C7 (well-defined, severe),
without showing any clear indication of spinal cord compression in this image. Severe proliferation of the pedicles and bilateral
lateral articular process joint proliferation with irregular articular surfaces and sclerosis are present at the C5-C6 and C6-C7
intervertebral spaces, visible on both transverse T2W and CT images. While MR imaging provides information about the
severity of the spinal cord signal changes and is suggestive of spinal cord atrophy at C6-C7, the CT images more clearly depict
the irregular surface and sclerotic changes of the articular processes. (3T MRI system; reproduced, with permission, from
Martin-Vaquero P, da Costa RC, Drost WT (2014). Comparison of non-contrast computed tomography and magnetic resonance
imaging in the evaluation of Great Danes with cervical spondylomyelopathy. Vet Radiol Ultrasound 55(5):496–505.)
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(a)
(b) (c)
Fig. 7.2.21 Great Dane with osseous-associated CSM. (a) Mid-sagittal T2W MR image, (b) transverse T2W MR image at
the C4-C5 intervertebral space, and (c) corresponding transverse non-contrast CT image using a bone window. Severe dorsal
compression of the spinal cord is present at C4-C5 on both the mid-sagittal and transverse MR and CT images. The transverse
T2W MR images show hypointense dorsal tissue hypertrophy as the cause of the compression, consistent with either abnormal
proliferative dorsal lamina or ligamentous hypertrophy. The corresponding CT image is supportive of an osseous-associated
compression secondary to dorsal lamina proliferation. (3T MRI system; reproduced, with permission, from Martin-Vaquero P,
da Costa RC, Drost WT (2014). Comparison of non-contrast computed tomography and magnetic resonance imaging in the
evaluation of Great Danes with cervical spondylomyelopathy. Vet Radiol Ultrasound 55(5):496–505.)
better outcome than those where the signal intensity did progression of spinal cord signal changes, mostly T2
not change.94 hyperintensity, has been documented in spite of success-
• Due to the controversy on the actual significance of sig- ful decompressive spinal surgery in dogs.97 The true sig-
nal changes on T2W images, the focus shifted to T1W nificance of spinal cord hyperintensity on T2W images in
images.95 Although it is more difficult to reliably iden- dogs is therefore still unclear. Nonetheless, preliminary
tify, most of the current human literature agrees that evidence suggests that the combination of hyperintensity
the presence of intramedullary hypointensity on T1W on T2W images combined with hypointensity on T1W
images generally implies irreversible spinal cord injury images might be associated with a poorer prognosis.
and a poor prognosis.92,93,96 • Recent studies in people have focused on advanced MRI
• There is limited information in the veterinary literature techniques to assist in prognostication for human patients
to draw conclusions about the true significance of MRI with cervical spondylotic myelopathy. Studies have
spinal cord signal changes in dogs. It appears that in spite looked at magnetic resonance spectroscopy and DTI,
of clear spinal cord hyperintensity on T2W images, some primarily the latter, with very interesting results.98–101
dogs remain clinically stable for long periods of time; DTI with tractography (Fig. 7.2.22) is being inves-
therefore, by itself, spinal cord hyperintensity does not tigated in dogs with CSM and may become a valuable
appear to be indicative of a poor prognosis. Additionally, prognostic tool in the future.
468 CHAPTER 7.2
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Fig. 7.2.22 Tractographic image of the spinal cord of a dog with cervical spondylomyelopathy. Diffusion tensor imaging (DTI)
was first acquired using single-shot spin-echo planar imaging. Data was processed to generate DTI maps. The fractional
anisotropy maps from C2 to C7 were used to generate this tractographic image. (3T MRI system; reproduced, with permission,
from Hecht S, da Costa RC (2015). Principles and applications of magnetic resonance imaging. In: Practical Guide to Canine and
Feline Neurology, 3rd edn (eds. CW Dewey, RC da Costa) Wiley-Blackwell, Ames.)
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in patients with cervical spondylotic myelopathy. Spine (Phila neural recovery in cervical spondylotic myelopathy. Spine
Pa 1976) 40(3):171–8. (Phila Pa 1976) 42(1):8–13
CHAPTER 7.3
DEGENERATIVE LUMBOSACRAL STENOSIS

472 Silke Hecht
CONTENTS
Etiopathology of DLSS ..........................................................................................................................................................................................472
Clinical signs ........................................................................................................................................................................................................472
MRI features ..........................................................................................................................................................................................................473
References.............................................................................................................................................................................................................478
Degenerative lumbosacral stenosis (DLSS) is a common • German Shepherd Dogs and structurally related breeds,
disorder, seen mainly in large-breed dogs, with a multi- such as the Belgian Malinois, are particularly suscep-
factorial etiology, in which degeneration of the lumbosa- tible to DLSS; German Shepherd Dogs represent an
cral intervertebral disc plays a central role. Several names estimated 25%–57% of all dogs presented for this condi-
have been used over the past decades to describe this tion.22,26,44 The reason for this breed predisposition is not
condition, including ‘cauda equina compression’, ‘cauda well understood, but a reduced spinal mobility at L7-S1
equina syndrome’, ‘lumbosacral malarticulation and mal- attributed to reduced angulation of the articular facets,32
formation’, ‘lumbosacral disease’, ‘lumbosacral stenosis’, an increased prevalence of predisposing factors such as
‘lumbosacral instability’, and ‘degenerative lumbosacral sacral osteochondrosis45 or transitional lumbosacral ver-
stenosis’.1–13 tebrae,46 and a predisposition for degenerative changes of
Many conditions described in other chapters in this text- the lumbosacral intervertebral disc21 are believed to be
book, such as acute intervertebral disc extrusion,14 spinal contributing factors.
neoplasia,15 trauma,16 epidural abscess,17 and discospon- • Clinical signs usually develop in middle-aged or older
dylitis,18–20 have been reported to affect the lumbosacral dogs, with an average presenting age of 7 years. Males
junction, and some may potentially mimic DLSS. MRI are overrepresented, with odds ratios from 1.3:1 to 5:1
findings associated with these conditions are described in reported.2,12,22,26,44
Chapters 7.1, 7.5, 7.6, 7.10, and 7.12. • Although less common, degenerative lumbosacral disease,
lumbosacral intervertebral disc herniation, and predispos-
ETIOPATHOLOGY OF DLSS ing factors such as transitional vertebra and sacral osteo-
chondrosis have been reported in small dogs and cats.47–52
• There are multiple etiopathologic factors that may con-
tribute to this condition: CLINICAL SIGNS
• Intervertebral disc degeneration and herniation (most
commonly protrusion).1,2,5,7,10–12,21–29 • Clinical signs typically result from compression or
• Lumbosacral instability/subluxation with ventral dis- inflammation of the cauda equina within the vertebral
placement of the sacral lamina.4,5,9,12,24 canal or the L7 nerves passing through the intervertebral
• Malalignment of the articular facet joints.30–32 foramina.
• Stenosis of the lumbosacral intervertebral foram- • They are usually insidious in onset and include:1,2,10,24
ina.2,7,10,29,33,34 • Lumbosacral pain elicited by palpation.
• Vertebral anomalies including transitional verte- • Uni- or bilateral pelvic limb lameness.
brae3,8,35,36 and sacral osteochondrosis.37–41 • Difficulty jumping, standing, lying down, or climbing
• Proliferation of spinal and paraspinal soft tissues stairs.
including spinal ligaments (especially interarcuate • Altered tail carriage.
and dorsal longitudinal ligament) and synovial joint • Paresthesia/dysesthesia manifested as licking or
capsules.5,29,42,43 chewing the tail, the perineum, or the extremities.
• Vascular compromise.12 • Urinary and/or fecal incontinence.
D e ge n e r at i v e Lu m bos ac r a l St e nosis 473
MRI FEATURES • Swelling of spinal nerve roots (Fig. 7.3.4).26,53

• Transitional lumbosacral vertebra, most commonly
• Many imaging modalities have been used to evaluate the lumbarization of S1, which is not completely fused to
canine lumbosacral region including conventional radi- S2 (best seen on sagittal or dorsal images) and may
ography, stress radiography, myelography, epidurogra- have an asymmetric conformation with a partially or
phy, osseous and intraosseous venography, discography, completely formed transverse process on one side and
linear tomography, and cross-sectional imaging (CT and asymmetric articulation with the corresponding iliac
MRI).2,13 wing (best seen on dorsal images) (Fig. 7.3.6).36
• MRI findings in DLSS include: • Hypertrophy of the interarcuate and/or dorsal lon-
• Degeneration (decrease in normal T2 signal inten- gitudinal ligaments, forming hypointense material
sity of the nucleus pulposus) and herniation of the associated with the dorsal and/or ventral vertebral
lumbosacral intervertebral disc (typically protrusion canal (Figs. 7.3.6, 7.3.7).26,53
of annulus fibrosus) into the vertebral canal and/or • Sacral osteochondrosis,28,37 forming a defect in the
intervertebral foramina (Figs. 7.3.1, 7.3.2, 7.3.4, outline of the cranial endplate of S1, which will
7.3.5).12,23,26,28–31,53 usually be best visible on sagittal images. The oste-
• Effacement of the signal from epidural fat within the ochondral fragment, if present, can be identified and
vertebral canal (Figs. 7.3.1, 7.3.2, 7.3.4–7.3.7).12,23,33 localized within the vertebral canal. Reactive endplate
• Displacement +/− compression of the dural sac or changes can be present, characterized by T2W and
nerve roots of the cauda equina (Figs. 7.3.1, 7.3.2, STIR hyperintensity and T1W endplate hypointen-
7.3.4–7.3.6).12,23,26,53 sity, with or without endplate enhancement. Areas of
• Evidence of a step in the vertebral alignment between bone sclerosis (T1W and T2W hypointense) can sur-
L7 and S1 and/or ventral displacement of the dorsal round these reactive changes (Fig. 7.3.8).
lamina of the sacrum (‘telescoping’).26 This is typi- • Spondylosis deformans, appearing as smoothly mar-
cally best appreciated on sagittal images (Figs. 7.3.2, ginated T1 and T2 hypointense new bone forma-
7.3.4, 7.3.7). tion arising from the margins of the endplates and
• Narrowing/stenosis of the lumbosacral intervertebral bridging the intervertebral space (Figs. 7.3.1, 7.3.4,
foramen (uni- or bilateral), best seen on transverse or 7.3.7).26,29,53
parasagittal images (Figs. 7.3.2, 7.3.3).29,33,53 • Although CT and MRI are superior to other imaging
• Symmetric or asymmetric decrease in paraspinal techniques, definitive criteria for a reliable diagnosis of
muscle mass (Figs. 7.3.2, 7.3.4, 7.3.5).54 DLSS remain elusive.5,28,56 Limitations of both CT and
• Synovial or ganglion cysts, appearing as T1 hypoin- MRI include:
tense and T2 hyperintense rounded or oval-shaped • Effect of positioning and degree of limb extension/
lesions associated with the articular process joints at flexion on appearance of the lumbosacral junc-
L7-S1 (Fig. 7.3.5).29–31,55 tion.6,24,57
(a) (b)
Fig. 7.3.1 DLSS with degenerative intervertebral disc disease in an 8-year-old mixed breed dog. The sagittal T2W image (a)
shows diffuse hypointensity of the lumbosacral intervertebral disc with protrusion into the vertebral canal and attenuation
of the epidural fat. The transverse T2W image (b) shows that the herniation is fairly central and results in almost complete
obliteration of epidural fat and compression of the nerve roots of the cauda equina (arrow). Mild ventral spondylosis deformans
(arrowheads) is also noted. (1T MRI system)
474 CHAPTER 7.3
(a) (b)
Fig. 7.3.2 DLSS in an 11-year-old Belgian Malinois. The
sagittal T2W image (a) shows diffuse hypointensity of
the lumbosacral intervertebral disc with protrusion into
the vertebral canal. There is mild ventral deviation of the
sacral lamina (‘telescoping’, arrow). Ventral spondylosis
deformans is present (arrowhead). The sagittal heavily T2W
half-Fourier-acquisition single-shot turbo spin-echo image
(‘T2-myelogram’, b) demonstrates focal displacement and
compression of the hyperintense CSF signal within the dural
sac at the lumbosacral junction (arrow). On the transverse
T2W image (c), lateral spondylosis deformans encroaches on
the left intervertebral foramen, which is completely obliterated
by hypointense material (arrowhead), compared with the
contralateral foramen. The vertebral canal does not appear
significantly compromised at this level. Severe muscle atrophy
and diffuse T2 hyperintensity of the left gluteal musculature
is noted. (1T MRI system) (c)
(a) (b)
Fig. 7.3.3 DLSS with foraminal stenosis in a 5-year-old German Shepherd Dog. Mid-sagittal T2W MR image (a) and
corresponding reformatted sagittal CT image (b) showing only minor protrusion of the lumbosacral intervertebral disc with no
obvious additional lumbosacral abnormalities detected (solid arrows). (Continued)
D e g e n e r at i v e Lu m bos ac r a l St e nosi s 475
(c) (d)
(e) (f)
Fig. 7.3.3 (Continued) DLSS with foraminal stenosis in a 5-year-old German Shepherd Dog. Parasagittal (c) and transverse (e)
T2W MR images and corresponding CT images (d, f) demonstrating stenosis of the L7-S1 intervertebral foramina bilaterally
(dashed arrows). Lateralized spondylosis deformans is also noted (arrowheads, e and f ). (1.5T MRI system)
(a) (b)
Fig. 7.3.4 DLSS in an 11-year-old German Shepherd Dog. The sagittal T2W image (a) shows hypointensity of the lumbosacral
intervertebral disc (along with other lumbar discs) and protrusion into the ventral vertebral canal. There is ventral displacement of
the dorsal lamina of the sacrum (arrow). Both processes result in reduction of the dorsoventral diameter of the vertebral canal. Mild
spondylosis deformans is also noted. The transverse T2W image (b) shows marked thickening of the left L7 nerve root (arrowhead)
and severe asymmetric atrophy and diffuse hyperintensity of the paraspinal and gluteal musculature (more severe on right side).
(Continued)
476 CHAPTER 7.3
Fig. 7.3.4 (Continued) DLSS in an 11-year-old German

Shepherd Dog. The transverse T1W fat suppressed post-
contrast image (c) demonstrates moderate diffuse contrast
(c) enhancement of the thickened nerve root (arrowhead). (1T
MRI system)
(b)
(a)
Fig. 7.3.5 DLSS with intervertebral disc protrusion and

articular process joint synovial/ganglion cysts in a 9-year-
old German Shepherd Dog. The sagittal T2W image (a)
shows hypointensity of the lumbosacral intervertebral disc
and protrusion into the vertebral canal. Additionally, there
is a well-circumscribed round T2 hyperintense lesion with a
hypointense rim (arrow) associated with the dorsal aspect of
the vertebral canal, presumably associated with the articular
process joint. Both lesions result in complete attenuation
of epidural fat. The transverse T2W (b) and STIR (c)
images show well-circumscribed and strongly T2 and STIR
(c)
hyperintense lesions associated with the articular process
joints bilaterally (arrowheads). These lesions are consistent
with synovial or ganglion cysts. They extend into the vertebral canal from dorsolaterally and in combination with the centrally
protruding disc result in moderate cauda equina compression. Note also the severe muscle atrophy of the right paraspinal and
gluteal musculature (b). (1T MRI system)
T13
L1
(b)
Fig. 7.3.6 DLSS with a symmetric transitional lumbosacral
vertebra and ligamentous hypertrophy in a 4-year-old
German Shepherd Dog. The dorsal STIR image (a) shows
only six normal lumbar vertebrae and sacralization of
L7. The sagittal T2W image (b) shows a large amount
of hypointense material within the ventral aspect of the
vertebral canal consistent with hypertrophy of the dorsal
longitudinal ligament and protrusion of the annulus fibrosus
(dashed arrow). A large amount of hypointense material is
also associated with the dorsal aspect of the vertebral canal,
L6
consistent with hypertrophy of the interarcuate ligament
(solid arrow). There is complete obliteration of the vertebral
L7 canal with loss of visualization of epidural fat and with severe
compression of the cauda equina. The arrowhead shows
incomplete fusion of the sacralized L7 segment with the
(a)
remainder of the sacrum. (1T MRI system)
(a) (b)
Fig. 7.3.7 Sagittal T2W (a) and T1W post-contrast (b) images of the lumbar spine in a 7-year-old dog with clinical signs of
lumbosacral disease. There is malalignment of L7 and S1 with ventral tipping of the cranial endplate of S1, creating a step
between the floor of the vertebral canal of L7 and the floor of the vertebral canal of S1, consistent with lumbosacral instability.
There is ventral displacement of the dorsal lamina of the sacrum (arrow). There is hypertrophy of the dorsal longitudinal
ligament and ventral spondylosis deformans. The combination of vertebral malalignment and dorsal longitudinal ligament
hypertrophy is causing reduction of the dorsoventral diameter of the vertebral canal with dorsal displacement and compression
of the cauda equina. (1.5T MRI system; images courtesy of Dr. Wilfried Mai, University of Pennsylvania)
478 CHAPTER 7.3
(a) (b)
Fig. 7.3.8 DLSS with sacral osteochondrosis in a 1-year-old German Shepherd Dog. The sagittal T1W image (a) shows
flattening of the craniodorsal margin of the sacrum, with a large amount of hypointense material being located in the ventral
aspect of the vertebral canal, obliterating the epidural fat and resulting in displacement and compression of the nerve roots
of the cauda equina. Diffuse hypointensity of the L7-S1 vertebral endplates consistent with sclerosis is also noted. The
corresponding radiograph (b) confirms these findings and in addition shows a well-circumscribed osseous fragment in the plane
of the vertebral canal, consistent with osteochondrosis dissecans.
• Effect of acquisition parameters and interobserver 5. Jeffery ND, Barker A, Harcourt-Brown T (2014). What
variability on measurements of intervertebral foram- progress has been made in the understanding and treatment
inal area.6,58,59 of degenerative lumbosacral stenosis in dogs during the past
• Evaluation of the actual significance of degeneration 30 years? Vet J 201(1):9–14.
6. Jones JC, Davies SE, Werre SR et al. (2008). Effects of body
and bulging/herniation of the lumbosacral interverte-
position and clinical signs on L7-S1 intervertebral foraminal
bral disc and other lumbosacral degenerative changes, area and lumbosacral angle in dogs with lumbosacral
since such changes are commonly seen in dogs with disease as measured via computed tomography. Am J Vet Res
no clinical signs of DLSS.5,21,60,61 69(11):1446–54.
• Poor correlation between imaging and clinical find- 7. Mayhew PD, Kapatkin AS, Wortman JA et al. (2002).
ings, imaging and surgical findings, and between Association of cauda equina compression on magnetic
imaging findings and clinical outcome.7,25,27 resonance images and clinical signs in dogs with degenerative
• CT studies with the pelvic limbs flexed and extended lumbosacral stenosis. J Am Anim Hosp Assoc 38(6):555–62.
have been used to assess dynamic changes in verte- 8. Morgan JP, Bahr A, Franti CE et al. (1993). Lumbosacral
transitional vertebrae as a predisposing cause of cauda equina
bral canal diameter and intervertebral foraminal area
syndrome in German shepherd dogs: 161 cases (1987–1990).
in dogs with lumbosacral disease, and these studies J Am Vet Med Assoc 202(11):1877–82.
may be useful for diagnosis of dynamic lesions.6,58,62 9. Oliver JE, Jr., Selcer RR, Simpson S (1978). Cauda equina
However, standardized protocols for these techniques compression from lumbosacral malarticulation and
using MRI are lacking. malformation in the dog. J Am Vet Med Assoc 173(2):207–14.
10. Tarvin G, Prata RG (1980). Lumbosacral stenosis in dogs.
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20. Kraft SL, Mussman JM, Smith T et al. (1998). Magnetic Vet Radiol Ultrasound 47(1):32–8.
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of lumbosacral intervertebral disc degeneration in clinically 40(4):338–44.
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Vet Radiol Ultrasound 53(3):289–95. resonance imaging in the diagnosis and surgical management
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216(11):1769–74. 42. Palmer RH, Chambers JN (1991). Canine lumbosacral
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retrospective analysis of degenerative lumbosacral stenosis Comp Cont Educ Pract 13(2):213–22.
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Traumatol 21(3):285–93. diseases. 1. Anatomy, pathophysiology, and clinical
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Agreement between computed tomography, magnetic 44. De Risio L, Sharp NJ, Olby NJ et al. (2001). Predictors
resonance imaging, and surgical findings in dogs with of outcome after dorsal decompressive laminectomy
degenerative lumbosacral stenosis. J Am Vet Med Assoc for degenerative lumbosacral stenosis in dogs: 69 cases
229(12):1924–9. (1987–1997). J Am Vet Med Assoc 219(5):624–8.
28. Worth AJ, Thompson DJ, Hartman AC (2009). Degenerative 45. Ondreka N, Amort KH, Stock KF et al. (2013). Skeletal
lumbosacral stenosis in working dogs: current concepts and morphology and morphometry of the lumbosacral junction
review. N Z Vet J 57(6):319–30. in German shepherd dogs and an evaluation of the possible
29. Adams WH, Daniel GB, Pardo AD et al. (1995). Magnetic genetic basis for radiographic findings. Vet J 196(1):64–70.
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3–13. 40(4):167–72.
30. Rossi F, Seiler G, Busato A et al. (2004). Magnetic resonance 47. Cariou MP, Stork CK, Petite AF et al. (2008). Cauda equina
imaging of articular process joint geometry and intervertebral syndrome treated by lumbosacral stabilisation in a cat.
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480 CHAPTER 7.3
50. Harris JE, Dhupa S (2008). Lumbosacral intervertebral disk 57. Di Concetto S, Mandsager RE, Riebold TW et al. (2012).
disease in six cats. J Am Anim Hosp Assoc 44(3):109–15. Effect of hind limb position on the craniocaudal length of
51. Newitt AL, German AJ, Barr FJ (2009). Lumbosacral the lumbosacral space in anesthetized dogs. Vet Anaesth Analg
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52. Archer R, Sissener T, Connery N et al. (2010). Asymmetric body position, imaging plane, and observer on computed
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53. Wisner ER, Zwingenberger AL (2015). Intervertebral disk 59. Reynolds D, Tucker RL, Fitzpatrick N (2014). Lumbosacral
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in dogs: will we see progress in the next 30 years? Vet J
202(2):201–2.
CHAPTER 7.4
CONGENITAL AND DEVELOPMENTAL

VetBooks.ir
ANOMALIES AND MALFORMATIONS 481
Wilfried Mai
CONTENTS
Vertebral congenital or developmental abnormalities ............................................................................................................................................481
Hemivertebrae, butterfly vertebrae, block vertebrae ..........................................................................................................................................481
Transitional vertebrae .......................................................................................................................................................................................485
Vertebral articular processes dysplasia ............................................................................................................................................................486
Vertebral canal stenosis ...................................................................................................................................................................................486
Cranial thoracic stenosis in large-breed dogs ............................................................................................................................................486
Cervical vertebral arch anomaly in the Basset Hound .................................................................................................................................487
Neural tube defects (dysraphism) ..........................................................................................................................................................................489
Embryology of the neural tube ........................................................................................................................................................................489
Spina bifida, meningocele, myelomeningocele ................................................................................................................................................489
Split cord malformation ...................................................................................................................................................................................493
Dermoid sinus .................................................................................................................................................................................................493
Lumbosacral osteochondrosis ..............................................................................................................................................................................496
Craniocervical junction anomalies ........................................................................................................................................................................498
Atlantoaxial instability......................................................................................................................................................................................498
Dorsal angulation of the dens ..........................................................................................................................................................................500
Atlantoaxial dural bands ..................................................................................................................................................................................501
Atlanto-occipital overlapping ...........................................................................................................................................................................501
Occipitoatlantoaxial malformation....................................................................................................................................................................502
Incomplete ossification of the atlas ..................................................................................................................................................................503
Vascular anomalies ...............................................................................................................................................................................................503
References.............................................................................................................................................................................................................505
Most congenital or developmental anomalies of the ver- VERTEBRAL CONGENITAL OR

tebral column can be diagnosed radiographically; how- DEVELOPMENTAL ABNORMALITIES
ever, MRI can provide more information regarding
the consequences of these anomalies, such as presence/ Hemivertebrae, butterfly
location/degree of spinal cord compression, and associated vertebrae, block vertebrae
soft tissue abnormalities such as syringomyelia or arach- • Malformations of the vertebral bodies are caused by
noid diverticula.1,2 Primary soft tissue anomalies such as abnormal development, fusion, or both, of the ver-
myelomeningocele or dermoid sinus will also be better tebral ossification centers during embryonic or fetal
evaluated with MRI. In many cases, MRI and CT imaging development.1,3–5
will complement each other and provide different types of • Such anomalies are common in brachycephalic breeds,
important information. especially those that have screw tails (English Bulldogs,
482 CHAPTER 7.4
VetBooks.ir
French Bulldogs, Boston Terriers, Pugs), likely because – Ventral aplasia or hypoplasia of the vertebral
the screw tail conformation is due to a hemivertebrae body causes the ventral aspect of the vertebra
conformation of the coccygeal vertebrae,4 a trait that to be absent or underdeveloped, resulting in a
has been selected as a desirable phenotype for many true ‘dorsal hemivertebra’ or a ‘ventral wedge-
generations.3 They are also occasionally seen in other shaped vertebra’.
small and large breeds; in German Shorthaired Pointers – Combined ventral and median aplasia of the
the anomaly is hereditary with an autosomal recessive vertebral body causes a more central under-
transmission.1 development resulting in a ‘butterfly vertebra’,
• These anomalies can be single or multiple, and three in reference to the shape of the vertebral body
main types are encountered (Fig. 7.4.1):3 when viewed in a dorsal plane.
• ‘Block vertebrae’, resulting from a failure of vertebral – Kyphoscoliotic abnormalities cause a focal exces-
segmentation, in which portions of adjacent vertebral sive convex dorsal curvature, together with a focal
elements fail to divide; these typically do not cause exaggerated lateral curvature of the spine, the
spinal deformity. latter being best appreciated on dorsal images.
• ‘Hemivertebrae’ (also called ‘wedge-shaped vertebrae’ These are caused by ventrolateral aplasia of the
or ‘cuneiform vertebrae’) and ‘butterfly vertebrae’, vertebral body, resulting in a ‘dorsolateral hemi-
resulting from an abnormal development of a portion vertebra’ conformation and secondary deformi-
of a vertebral element. Depending on the type of ver- ties both in the sagittal and in the dorsal plane
tebral anomaly, several types of spinal deformities are (kyphoscoliosis).
seen: • ‘Short vertebrae’ result from symmetric hypoplasia
– Kyphotic abnormalities cause a focal excessive and are characterized by a vertebral body that is
convex dorsal curvature of the spine, best appreci- shorter but retains overall normal shape; this does not
ated on sagittal images: result in spinal deformity.
NO SPINAL DEFORMITY KYPHOSIS KYPHOSCOLIOSIS
DORSAL HEMIVERTEBRA DORSOLATERAL HEMIVERTEBRA

NORMAL VERTEBRAE
Ventral aplasia Ventrolateral aplasia
BLOCK VERTEBRAE
VENTRAL WEDGE-SHAPED
Ventral hypoplasia
SHORT VERTEBRA BUTTERFLY VERTEBRA

Symmetric hypoplasia Ventral and median aplasia
Fig. 7.4.1 Schematic classification of congenital vertebral anomalies resulting from abnormal development and/or fusion of
the vertebral ossification centers during embryonic or fetal development. For each category, the appearance is shown from
a cranial perspective, lateral perspective, and dorsal perspective. (Adapted, with permission, from Gutierrez-Quintana R,
Guevar J, Stalin C et al. (2014). A proposed radiographic classification scheme for congenital thoracic vertebral malformations
in brachycephalic “screw-tailed” dog breeds. Vet Radiol Ultrasound 55(6):585–91.)
C onge n i ta l a n d D e v e l opm e n ta l A nom a l i e s a n d M a l for m at ions 483
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• In screw-tail dogs, the most common anomalies are the

butterfly vertebra, the ventral wedge-shaped vertebra,
and the short vertebra.3
• The most common location of these anomalies is the
mid- to caudal thoracic spine, especially between T6 and
T9,1 although in a recent study in screw-tail dogs T12
was commonly affected as well.3
• They are most commonly asymptomatic and there-
fore often represent incidental findings (Fig. 7.4.2).6
However, they can result in clinical signs due to progres-
sive vertebral canal stenosis and vertebral column insta-
bility, especially in Pugs (Figs. 7.4.3, 7.4.4).3,5,6 There is
Fig. 7.4.2 Sagittal T2W image in a 7-year-old male English a suggestion that dorsal and dorsolateral hemivertebrae
Bulldog. A ventral wedge-shaped hemivertebra is seen are more commonly associated with neurologic deficits,
(arrow) causing mild kyphosis but no significant spinal which may be the result of more pronounced scoliosis
cord compression. There is decreased signal of multiple and secondary spinal canal stenosis.3 In these cases, clini-
intervertebral discs consistent with degeneration. There is cal signs are suggestive of a chronic progressive trans-
ventral spondylosis deformans at the level of the abnormal verse myelopathy affecting the T3-L3 segment of the
vertebra, causing a hypointense stripe bridging the spinal cord.4 These include pelvic limb ataxia to paresis
intervertebral spaces ventrally. (1.5T MRI system) with intact segmental reflexes. Acute presentation with
non-ambulatory paraparesis or paraplegia is possible.1
(a) (b)
Fig. 7.4.3 Parasagittal (a) and midline sagittal (b) T2W

images of the thoracolumbar spine and transverse T2W
image at the level of T12 (c) in an 8-year-old French
Bulldog with a 1-month history of paresis. There is a
butterfly conformation of T12, with two paramedian
wedge-shaped fragments (asterisks, c) on the transverse
* * image; one of these portions can be seen on the
parasagittal image (arrow, a) but not on the midline sagittal
image (dotted arrow, b), which shows the narrowest point
of the abnormally formed vertebral body. The anomaly
is causing focal kyphosis, seen on the sagittal images,
and right ventral compression of the spinal cord, seen on
the transverse image, due to the stenosis of the vertebral
canal from the vertebral anomaly. T2 hyperintense signal
is present in the spinal cord parenchyma consistent with
edema or gliosis. (See corresponding radiographs in
(c)
Fig. 7.4.4.) (1.5T MRI system)
484 CHAPTER 7.4
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(a)
Fig. 7.4.4 Lateral (a) and ventrodorsal (b) close-up views of

the thoracolumbar spine in the same dog as in Fig. 7.4.3. The
butterfly conformation of the body of T12 is appreciated
(arrows). (b)
• Although these vertebral anomalies are typically readily consequences of the condition on the spinal canal and
identified radiographically (Fig. 7.4.4), advanced imag- spinal cord:
ing is necessary in patients with neurologic deficits to • T1W and/or PDW images are preferred to provide
determine the cause and location of spinal cord changes. bony detail, while T2W and/or myelographic
Conventional myelography and CT myelography can be (e.g., SS-FSE, HASTE) images should be obtained
used, but in some cases the filling of the subarachnoid to evaluate for secondary changes such as arach-
space in the affected area is poor, which can make inter- noid diverticula (see Chapter 7.8), syringomyelia (see
pretation difficult, especially when secondary changes Chapter 7.9), and spinal cord parenchyma T2 hyper-
such as an arachnoid diverticulum are present. In addi- intensity, which may be associated with edema or
tion, these techniques do not allow a good assessment of gliosis secondary to compression.1
spinal cord parenchymal changes, such as syringomyelia, • In dogs with severe kyphoscoliosis, there is often
which may be present in association with the vertebral a 3D spiral conformation to the spine in the area
anomaly. of deformity that makes it difficult to assess spinal
• In cases where surgical correction is contemplated, MRI cord compression with cross-sectional imaging
should be followed by CT, which allows a better evalu- such as MRI.7,8 Oblique imaging aimed at obtaining
ation of bony detail and of the 3D trajectory of the ver- ‘true’ transverse images of the abnormal spinal seg-
tebral column in all planes, especially when using 3D ments, depending on their orientation, is often nec-
reconstructed CT images.1 essary for a thorough assessment of the spinal cord,
• In dogs with neurologic deficits, MRI can determine and can be quite time-consuming. These transverse
the cause and location of the disease as well as identify images allow assessment for presence or absence of
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vertebral canal stenosis causing spinal cord com- with thoracic kyphosis/kyphoscoliosis associated with
pression:4 vertebral anomalies is observed more commonly in
– Dorsoventral compression caused by gross reduc- the L1-L5 segment.7
tion in the dorsoventral height of the pedicles.
– Ventrolateral compression (uni- or bilateral) asso- Transitional vertebrae
ciated with the imperfectly formed dorsal aspect • The normal spinal division of the vertebral column in
of the affected vertebral bodies (Fig. 7.4.3). dogs and cats includes seven cervical, 13 thoracic, seven
• Spinal deformities such as kyphosis and scoliosis are lumbar, three sacral, and a variable number of caudal
best appreciated on sagittal and dorsal images, respec- (coccygeal) vertebrae.
tively (Figs. 7.4.2, 7.4.3). • Transitional vertebrae are congenital defects of seg-
• Examination of the entire segment at hand should mentation during embryologic development in which,
be conducted, as the clinical signs may be associated at the cervicothoracic, thoracolumbar, or lumbosacral
with concurrent conditions such as intervertebral disc junctions, characteristics of adjacent divisions are
herniation. Although there is a greater likelihood exhibited in a single vertebra.5 The anomaly can be
for early disc degeneration in the spaces immedi- uni- or bilateral, and when bilateral can have an asym-
ately adjacent to the vertebral anomaly,9 compressive metric appearance. An example would be development
disc herniation at these adjacent spaces is in fact of transverse processes at S1 and absent fusion with S2,
uncommon.7 This may be due to their common local- a condition called ‘lumbarization’ of S1 (Fig. 7.4.5).
ization in the thoracic segment, where the intercapi- Another common example is the absence of ribs at T13
tal ligament prevents compressive disc herniation. In with or without developed transverse processes (lum-
fact, compressive disc herniation in French Bulldogs barization of T13).
S1
L7
(a)
Fig. 7.4.5 Sagittal T2W image (a) and transverse T2W (b)
images at the level of the lumbosacral disc (b) and cranial
body of S1 (c) in a 7-year-old male German Shepherd Dog
with cauda equina syndrome signs. The first sacral vertebra
(S1) is not united to S2 (dotted arrow, a). On the transverse
image, S1 has developed rudimentary transverse processes
(arrows, b), and there is malarticulation with the right
iliac wing (asterisk, c). These signs are consistent with S1
being a transitional vertebra (‘lumbarization’). In German
Shepherd Dogs, this is often associated with some degree of
lumbosacral instability, leading to progressive lumbosacral
stenosis due to a combination of disc protrusion, hypertrophy *
of the dorsal longitudinal ligament and ligamentum flavum,
fibrous tissue, and bony proliferations. In this case, there is
subtotal obliteration of the vertebral canal at the lumbosacral
level because of these progressive changes (arrowheads, a
and b), which cause compression of the nerve roots of the
cauda equina. (1.5T MRI system)
(c)
486 CHAPTER 7.4
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• These anomalies are quite commonly seen in both dogs one or several vertebrae in the thoracic and/or lumbar
and cats,5,10 and are typically of no clinical significance. region.13,14
However, in the lumbosacral segment, their presence has • There is fibrocartilage and new bone proliferation of
been associated with the development of clinical lumbo- the remaining cranial articular processes, filling the
sacral stenosis in German Shepherd Dogs and related gap left by the hypoplastic/aplastic caudal articular pro-
breeds (Fig. 7.4.5).11 cesses. Eventually, this can cause impingement of the
• Another important consideration when interpreting dorsal aspect of the vertebral canal, worsened by variable
MRI studies is that unusual vertebral counts in a spe- degrees of hypertrophy of the ligamentum flavum, result-
cific segment due to the presence of transitional verte- ing in dorsal or dorsolateral spinal cord compression. In
brae can challenge accurate localization of compressive Pugs, granulation tissue originating from the dura mater
lesions, which is important for surgical planning. For and contributing to spinal cord compression was also
example, about 10% of Dachshunds are reported to have reported.13 Histopathologically, evidence of loss of sub-
variations in the number of vertebrae in some segments stance (atrophy) is noted in the spinal cord with axonal
of the spine (for example, eight lumbar vertebrae due degeneration and gliosis.13
to lumbarization of S1 or T13).12 This can particularly • There is one case report of concurrent aplasia of both the
be a problem when small fields of view (FOVs) are used cranial and caudal articular processes in the thoracolum-
to optimize resolution. In such cases it is important to bar area of a Pomeranian dog;15 in that case, the articu-
obtain large FOV localizer (scout) images in order to be lar process joints were replaced by fibrous tissue, but the
able to count the vertebrae accurately and to reduce the anomaly was not causing spinal cord compression.
risk of missing a vertebral malformation that could affect • The MRI features of the condition include (Fig. 7.4.6):13,14
accurate localization of individual disc spaces at surgery. • Dorsolateral or dorsal compression of the spinal cord
However, large FOV scout images may not be feasible centered at the level of the affected articular process
depending on MRI equipment and coil selection. If the joints.
scout images are not of sufficient quality to identify skel- • Absent or poorly visible caudal articular processes,
etal abnormalities or confidently count the vertebrae, it particularly appreciated on dorsal or transverse
may be useful to obtain a routine survey radiograph in all images. These changes may be easier to identify on
animals prior to or following the MRI scan. T1W or PDW pulse sequences.
• In non-Pug dogs, compensatory hypertrophy of the
Vertebral articular processes dysplasia cranial articular processes, forming amorphous masses
• Abnormal development of the vertebral primary ossifi- of low T1 and T2 signal intensity tissue extending
cation centers results in the well-recognized conditions between the dorsal laminae of the vertebrae. These
described above, such as block vertebrae, hemivertebrae, or masses have higher signal than the cortical bone and
butterfly vertebrae. Abnormal development of secondary similar signal to the vertebral cancellous bone. There
ossification centers such as dysplasia/hypoplasia/aplasia may or may not be concurrent disc bulging/protrusion
of the vertebral articular processes is less common. There or hypertrophy of the dorsal longitudinal ligament,
are only a few reports, both in asymptomatic dogs and in which case the spinal cord assumes an ‘hour-glass’
in dogs with neurologic signs.13–15 In addition, a few ear- appearance on sagittal images.14
lier reports of dorsal or dorsolateral spinal cord compres- • T2 hyperintense signal can be seen in the dorsal
sion in the t horacolumbar area in dogs presenting with aspect of the spinal cord parenchyma, interpreted as
chronic progressive pelvic limb ataxia and paresis16,17 early syrinx formation, edema, gliosis, or malacia.14
shared striking morphologic similarities with the more • In Pugs, there is typically no hypertrophy of the
recent well-documented cases,13–15 and may have, in fact, cranial articular facets as seen in other dogs; however,
represented variations of the same condition. there is constrictive compression of the spinal cord at
• Typical clinical presentation in affected dogs is progres- the level of the articular process joints, caused by a
sive pelvic limb ataxia at a variable age (17 weeks to 11 fibrous band surrounding and sometimes infiltrating
years).13,14 There is usually no pain on spinal palpation. the dura mater, which in some cases penetrates the
Urinary and fecal incontinence is also reported.13 subarachnoid space (Fig. 7.4.6).13
• The most common location of the anomaly is in the cau-
dal thoracic and cranial lumbar spine.13,14 Vertebral canal stenosis
• Breeds affected so far have included a series of Pugs, and Cranial thoracic stenosis in large-breed dogs
single or few cases in the German Shepherd Dog, Shiloh • Cranial thoracic stenosis is a primarily developmental
Shepherd, Cavalier King Charles Spaniel, mixed breed osseous stenosis of the cranial thoracic vertebral canal,
dog, Pomeranian, and Basset Hound.13–17 sharing similar features to the osseous-associated cer-
• Most commonly, the condition is characterized by vical spondylomyelopathy seen in giant-breed dogs (see
hypoplasia or aplasia of the caudal articular processes of Chapter 7.2).18
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T12
T11
(a) (b)
Fig. 7.4.6 Sagittal T2W image (a) and transverse T2W

images at the level of T11-T12 (b) and T12-T13 (c) in a
10-year-old Pug with progressive ataxia and paresis. A
constrictive myelopathy is seen at the level of T11-T12
(arrowhead, a). On the transverse image at T11-T12 (b), the
laterally positioned cranial articular processes of T12 are well
visible (arrows), but no distinct caudal articular processes
of T11 are visible, consistent with hypoplasia/aplasia;
attenuation of the subarachnoid space and dorsoventral
narrowing of the cord consistent with constrictive myelopathy
are present. At T12-T13 (c), both the laterally positioned
cranial articular processes of T13 (solid arrows) and the
medially located caudal articular processes of T12 (dotted
(c)
arrows) are visible. (1.5T MRI system)
• It affects primarily young (median 9.5 months), male dogs • Variable degrees of irregular hypointense bulbous
of the Molosser breeds (Dogue de Bordeaux, Bullmastiff, enlargement of these joints.
Rottweiler, St Bernard) but other breeds can also be • Vertebral canal stenosis best appreciated in the trans-
affected (Chow-Chow, German Shepherd Dog).19,20 verse plane, with patterns of stenosis including dorso-
• The clinical manifestation is ambulatory or non- lateral, lateral, or dorsoventral stenosis in decreasing
ambulatory paresis with a T3-L3 neurolocalization, order of frequency. The stenosis can be symmetric or
typically without spinal hyperesthesia. In some dogs, asymmetric.
no neurologic deficits are present, even when the cord • In compressive cases, mild focal syringohydromyelia
appears compressed visually. cranial to the stenotic site can be present, and paren-
• Most commonly affected sites with compressive stenosis chymal T2 hyperintensity can be seen at the sites of
are T2-T3 and T3-T4, and multiple locations are com- stenosis.
mon. Non-compressive stenosis is also common at T4-T5.
• The MRI features of the condition include:18 Cervical vertebral arch anomaly in the Basset Hound
• On parasagittal images, abnormal positioning and ori- • This is a developmental abnormality reported in the
entation of the articular process joints, with a steeper Basset Hound, affecting the dorsal laminae and spinous
angle of the joints to the dorsal plane. processes of two or more adjacent cervical vertebrae;19
488 CHAPTER 7.4
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a somewhat similar stenosis in the thoracic region caused the cranially located vertebra is dorsally enlarged,
by smooth bony malformation of the caudal lamina of forming a convex protuberance that fits into a concave
T12 and cranial lamina of T13 has been reported in a area of the enlarged spinous process of the caudally
Basset Hound and could represent a variation of this cer- located vertebra.
vical stenosis.21 The author has seen similar anomalies in • These deformities are made of dense compact bone
other breeds, too (Fig. 7.4.7). and are hypointense on all pulse sequences; they are
• Clinical signs vary from cervical hyperesthesia to non- separated by a cleft of intermediate signal intensity
ambulatory tetraparesis, but the most common pre- formed by fibrous soft tissue.
sentation is ataxia affecting all four limbs and paresis • The bony protuberances can cause some degree of
affecting predominantly the thoracic limbs (‘central cord dorsal spinal cord compression but, most commonly,
syndrome’, seen in cases of midline dorsal cervical spi- dorsal, midline cord compression is caused by tissue
nal cord compression and attributable to the somatotopic of intermediate signal intensity corresponding
organization of the cervical spinal cord). to hyperplasia and remodeling of the ligamentum
• Most dogs are male, young, often less than 2 years of age flavum.
at time of presentation, although presentation at an older • T2 hyperintensity can be seen in the spinal cord at
age is possible. the level of these abnormalities, likely due to gliosis
• The C4-C5 intervertebral articulation is most com- or edema.
monly affected, followed by C5-C6 and C3-C4. • The condition is dynamic in nature, and ligamentum
• MRI features include (Fig. 7.4.7): flavum hypertrophy can progress over time to become
• A well-defined smooth abnormality involving the more and more compressive. This suggests that lig-
dorsal laminae and spinous processes of two or more amentous hypertrophy occurs secondarily to the
adjacent vertebrae: the caudal part of the lamina of primary osseous abnormalities.
(a) (b)
Fig. 7.4.7 Sagittal T2W (a) and T1W (b) images and
transverse T2W image at the level of C4-C5 (c) in a
10-year-old male Boxer with ataxia of all four limbs
and neck pain. The caudal part of the dorsal lamina of SC
C4 forms a well-defined and smooth enlarged convex
protuberance, which extends dorsally and ventrally
(dotted arrows, a and b). The spinous process of C5 is
enlarged and extends cranioventrally (solid arrows, a
and b). There is dorsal spinal cord (SC) compression at
this level (arrowhead, c). Similar abnormalities, but to a
lesser extent, are present between C3 and C4. (1.5T MRI
(c)
system)
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NEURAL TUBE DEFECTS (DYSRAPHISM) Neural plate Neural crest
Non-neural ectoderm
Embryology of the neural tube
• Neural tube defects are congenital malformations result- Notochord
ing from abnormal development and/or closure of the
neural tube during embryogenesis.22,23 Neural folds
• Because this process is highly interconnected with
the development of vertebrae, paravertebral muscula-
Neural
ture, and overlying skin, the term ‘neural tube defects’ groove
includes by extension developmental anomalies of these Paraxial mesoderm
structures (for example, spina bifida), and they all can be
seen in isolation or in combination.
• During embryologic development, the neuroectoderm,
which will form the central nervous system, is derived
Neural crest
from the ectoderm germ layer (Fig. 7.4.8). It first forms cells
a ‘neural plate’ that is located dorsal to the notochord
and connected on each side to the non-neural ectoderm;
the connection between these two parts of the ectoderm
is the ‘neural crest’. The notochord will eventually form
Somites
the nuclei pulposi of the intervertebral discs. The neural
plate progressively bends dorsally, forming a longitudi- Neural tube Neural canal
nal neural groove and two folds at the neural crest (the
‘neural folds’). The two neural folds eventually meet each Fig. 7.4.8 Schematic illustration of the embryologic
other dorsally and fuse, at which time there is separation development of the neural tube. The neuroectoderm, which
between the non-neural ectoderm, the neural crest, and will form the central nervous system, is derived from the
the neuroectoderm, resulting in a full neural tube with ectoderm germ layer. It first forms a ‘neural plate’ that is
a central neural canal and two neural crests dorsolateral located dorsal to the notochord and connected on each side
to the neural tube. The non-neural ectoderm forms a to the non-neural ectoderm; the connection between these
superficial layer dorsal to the neural tube and will form two parts of the ectoderm is the ‘neural crest’. The notochord
the epidermis. The neural crests will form the primor- will eventually form the nuclei pulposi of the intervertebral
dial ganglions distributed regularly along the dorsolat- discs. The neural plate progressively bends dorsally forming a
eral aspect of the neural tube. longitudinal ‘neural groove’ and two folds at the neural crest
• On each side of the neural tube, the ‘paraxial mesoderm’ (the ‘neural folds’). The two neural folds eventually meet
develops into ‘somites’, which subdivide into the ‘der- each other dorsally and fuse, at which time there is separation
matome’ (future dermis), ‘myotome’ (future axial and between the non-neural ectoderm, the neural crest, and the
appendicular muscles), and ‘sclerotome’ (future vertebrae neuroectoderm, resulting in a full neural tube with a central
and ribs).23 neural canal and two neural crests dorsolateral to the neural
tube. The non-neural ectoderm forms a superficial layer
Spina bifida, meningocele, dorsal to the neural tube and will form the epidermis. The
myelomeningocele neural crests will form the primordial ganglions distributed
• Spina bifida is a condition in which one or a few of the regularly along the dorsolateral aspect of the neural tube. On
vertebral arches fail to close over the spinal cord.22,23 each side of the neural tube, the ‘paraxial mesoderm’ develops
• It is asymptomatic when the underlying neural tissues into ‘somites’, which subdivide into the ‘dermatome’ (future
are not involved (‘spina bifida occulta’) (Fig. 7.4.9). dermis), ‘myotome’ (future axial and appendicular muscles),
• It can become symptomatic (‘spina bifida manifesta’) when and ‘sclerotome’ (future vertebrae and ribs).
the underlying neural structures are displaced dorsally
into the neural arch defect on midline between the epax-
ial muscles: paraxial mesoderm, and neural plate during neu-
• If only meningeal tissue is displaced into the defect, a rulation). One example is myeloschisis, a failure of
‘meningocele’ is formed. neural tube closure resulting in a cleft in the dorsal
• If both meningeal tissue and neural tissue (e.g., nerves) aspect of the cord and associated with spina bifida
are displaced, a ‘myelomeningocele’ is formed; the (Figs. 7.4.10, 7.4.11).2
neural components of the myelomeningocele often • The meningocele/myelomeningocele can connect
undergo myelodysplasia (= spinal cord malformation to the skin where it can remain closed (‘spina bifida
because of abnormal interaction of the notochord, cystica’) or can open to the exterior (‘spina bifida aperta’),
490 CHAPTER 7.4
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(a) (b)
Fig. 7.4.9 Transverse T2W images at the level of T2 (a) and T3 (b) in a 4-year-old Pit Bull Terrier with spina bifida occulta
at T3. Note the split appearance of the spinous process of T3 (arrows, b) compared with the normal appearance of the spinous
process of T2. There is a normal shape and position of the subarachnoid space and spinal cord in the vertebral canal at that
level, indicating that no meningocele or myelomeningocele is present. (1.5T MRI system)
in which case CSF can leak to the outside through most commonly reported in the lumbosacrococcygeal
the opening.23 The point of attachment of the mye- region.22,23,25–28 Myelomeningocele was occasionally
lomeningocele to the skin can cause ‘tethering’ of reported in the thoracic segment.24
the spinal cord (i.e., progressive traction on the cord • The clinical signs in cases of spinal bifida and concurrent
and nerves during postnatal axial skeleton elongation myelomeningocele are related to the amount of primary
cranial to that point of attachment, causing secondary neuronal damage involved (myelodysplasia) and the sec-
damage to the cord such as ischemic lesions).24,25 ondary effects of spinal cord tethering. They are con-
• Association with other neural tube defects such as der- sistent with the lumbosacrococcygeal localization of the
moid sinus is possible (Fig. 7.4.11).26 condition and include:
• Some breeds are predisposed to these conditions, such • Urinary and fecal incontinence, pelvic limb ataxia,
as the English Bulldog or the Manx cat. In the latter, and proprioceptive deficits.
an autosomal dominant inheritance is suspected and • Upper motor neuron signs can be seen when the lesion
likely associated with the sacrococcygeal dysgenesis that is located more cranially,24 but also secondary to lum-
is a characteristic of the breed.2 Other breeds, however, bosacrococcygeal lesions, in which case they are asso-
can be affected, such as the German Shepherd Dog, ciated with progressive tethering of the spinal cord.25
French Bulldog, and Yorkshire Terrier.2,22–28 • A depression can be felt on palpation of the affected
• Although spina bifida occulta can affect any vertebral region,25–27 or occasionally a focal dermal cyst-like
segment, the clinical form of the condition (spina bifida mass.24,28 Clear fluid (CSF) can ooze from the lesion
manifesta) with meningocele or myelomeningocele is when there is an open communication.23,24,28
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• MRI findings include (Figs. 7.4.10, 7.4.11):22–24 • In cases of meningocele or myelomeningocele, the
• Incomplete dorsal lamina of the affected vertebra, subarachnoid space is seen to extend dorsally through
best appreciated in transverse images, especially on the absent vertebral arch or split spinous process with
T1W images, which provide better bony detail. variable degrees of dorsal extension. The menin-
• Split appearance of the dorsal spinous process of the geal sac can extend up to the skin with or without
affected vertebrae, or absent dorsal spinous process, direct communication to the exterior. This is par-
also best appreciated on transverse images. ticularly well appreciated on T2W images, due to
(a) (b)
T4
(c)
Fig. 7.4.10 Transverse T2W (a) and T1W (b) images at the level of T4 and sagittal T2W image (c) of the thoracic spine in an
8-year-old Bichon Frise with progressive paresis of the pelvic limbs. There is spina bifida at T4 evidenced by the split appearance
of the spinous process (solid arrows, a and b). There is dorsal displacement of the meninges and spinal cord into the defect
created dorsally, consistent with a myelomeningocele; this dorsal displacement results in widening of the ventral epidural space
(arrowheads, a and c). There is a large area of T2 hyperintensity in the dorsal aspect of the spinal cord over T2-T5 (asterisk, c)
corresponding to a large syrinx. A thinner syrinx extends caudally to that level (dashed arrow, c). (1.5T MRI system)
492 CHAPTER 7.4
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L7 L7
(a) (b)
SC *
SC * L7
L7
(c) (d)
Fig. 7.4.11 Myelomeningocele with associated dermoid

sinus in a 4-year-old male castrated English Bulldog
presented with intermittent urinary straining and
incontinence, intermittent colitis, and decreased
perineal reflexes. Transverse T1W (a) and T2W
(b), sagittal T1W (c) and T2W (d), and HASTE
(‘T2-myelogram’) (e) images. The dorsal lamina and
spinous process of L7 are absent, best appreciated SC
on the transverse images. The meningeal sac *
extends dorsally through the defect of L7, forming
a characteristic ‘candle flame’ appearance on the
transverse images; the triangular dorsal extension (e)
of the CSF-filled thecal sac is also well appreciated
on the sagittal HASTE image (white arrow, e). The
spinal cord (SC) dorsally extends into the defect when approaching L7, causing relative widening of the ventral
subarachnoid space (asterisks, c–e). Neural structures extend dorsally into the displaced meningeal sac. These
findings are consistent with spina bifida at L7 and secondary myelomeningocele. In addition, a hypointense tract
(black arrows, a–d) is seen extending from the dorsal extremity of the myelomeningocele to an area of focal
invagination of the cutaneous tissues (arrowheads, a–d), consistent with a type IV or VI dermoid sinus. (1T MRI
system; images courtesy of Dr. Silke Hecht, University of Tennessee College of Veterinary Medicine)
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the hyperintensity of the CSF within the displaced separating the spinal cord into two approximately equal
meningeal sac. On transverse images, the dorsally hemicords; the extent and location of the split abnormal-
displaced meningeal sac can look like a ‘candle flame’. ity are variable (Fig. 7.4.12).
Fat suppression can highlight the meningocele by
suppressing the hyperintense signal of adjacent fat. Dermoid sinus
Heavily T2W sequences such as single-shot fast spin • Dermoid sinus (also called dermoid sinus tract, dermoid
echo (‘T2-myelogram’) can also demonstrate the cyst) results from failure of separation of the surface ecto-
hyperintense, CSF-filled meningeal sac extending derm (forming the epidermis) and neuroectoderm (form-
dorsally into the vertebral defect (Fig. 7.4.11). ing the nervous system) during embryogenesis.26,30–48
• In cases of myelomeningocele, neural tissue is seen This results in cutaneous ectoderm sequestration and
traveling dorsally within the expanded subarachnoid internal migration along with the folding of the neural
space. Nerves entering the myelomeningocele form tube, forming a ‘dermoid sinus’ (i.e., a dorsal midline
linear structures that are hypointense to the CSF and skin opening extending deeper ventrally in the form of
iso- to hypointense to the spinal cord. a blind-ending tube of varying depth and thickness).
• On sagittal and transverse images, dorsal elevation of Histopathologically, the sinus is lined by stratified squa-
the thecal sac and internal neural structures as they mous epithelium and contains adnexal structures (hair
approach the abnormal vertebral lamina defect can be follicles, sebaceous and sweat glands).31 The term ‘piloni-
seen. The epidural space is widened ventrally due to dal sinus/cyst’ is also occasionally encountered to describe
this displacement, and typically filled with fat (bright this condition but is probably inappropriate as it refers to
on T1W and T2W images and suppressed on fat sup- a human condition, which, although similar in presenta-
pressed images) (Figs. 7.4.10, 7.4.11). tion, differs from the canine/feline dermoid sinus from a
• In cases of association with a dermoid sinus, a stalk of pathophysiologic and histopathologic standpoint.5,31
variable signal intensity can be seen connecting the • Due to the topographic pattern of ectodermal separa-
dorsal tip of the myelomeningocele to the skin, and tion, dermoid sinuses typically occur on midline, con-
there is typically a focal ventral invagination of the necting the skin to deeper structures, and can be seen in
cutaneous tissues at the point of connection with the the nasal region, cranium, and vertebral column. They
skin (Fig. 7.4.11). can be single or multiple.
• Depending on how deep the connecting tract penetrates,
Split cord malformation spinal dermoid sinus falls into one of six categories
• Split cord malformation refers to a longitudinal separa- (Fig. 7.4.13):
tion of a portion of the spinal cord, and ranges from a • Type I: tubular sac extending from the skin to the
partially cleft cord in a single dural sac to a completely supraspinous or nuchal ligament.
duplicated cord within dual dural sacs with an interven- • Type II: more superficial tract, with a deep fibrous
ing bony spur.29 strand connecting to the supraspinous or nuchal lig-
• Partial split cord malformation (myeloschisis, with a dor- ament.
sal cleft separating the dorsal horns) is often associated • Type III: superficial tract with no connection to the
with spina bifida as a result of the incomplete dorsal clo- supraspinous or nuchal ligament.
sure of the neural tube.2,5 • Type IV: deep tract that communicates with the ver-
• Complete split cord malformation, also called ‘diaste- tebral canal and is attached to the dura mater.
matomyelia’, is a rare condition that has been reported • Type V: true dermoid ‘cyst’, with a closed capsule and
in veterinary medicine mostly in calves, although a no deeper connection or opening to the skin.
recent report describes its MRI appearance in a German • Type VI: deep tract that extends to the supraspinous
Shepherd Dog that was presented with lifelong diffi- or nuchal ligament and continues deeper as a fibrous
culty urinating, associated with a chronic neurogenic strand, which connects to the dura mater.39
bladder.29 • Only types IV and VI may be associated with neurologic
• Symptoms in people may include increased urinary fre- signs due to their relationship with the dura mater. In
quency, increased urgency, feeling of incomplete voiding, these cases, neurologic signs can be the result of:
post-void dribbling, poor voluntary control, and urge or • Infection (abscessation, meningitis, meningomyelitis,
stress incontinence. Neurogenic bladder conditions are etc.).
static from birth in some patients and only recent in • Compression of the spinal cord due to progressive
onset in others. Recurrent urinary tract infection, likely enlargement of the deeper portion of the tract with
due to incomplete voiding of the urinary bladder, is a fre- accumulated debris (hair follicles, sebum, keratin,
quent consequence.29 desquamated epithelial cells).
• MRI appearance is that of a dorsoventrally oriented, • Tethering of the spinal cord.39
mid-sagittal T2 hyperintense, T1 hypointense band • Syringomyelia.39
494 CHAPTER 7.4
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(a) (b)
Fig. 7.4.12 Transverse T2W (a) and T1W (b) images at the level of the cranial aspect of T7 in a 9-year-old female German
Shepherd Dog presented with a chronic, lifelong problem with difficulty urinating. On the T2W image (a), there is a vertical
hyperintense line separating the cord into two halves, consistent with a split cord malformation; this longitudinal split extends
over several vertebrae (T6 to T10). On the T1W image (b) this corresponds to a faint hypointense area in the sagittal plane of
the spinal cord. (1.5T MRI system; images courtesy of Dr. Brian Allett, Advanced Veterinary Medical Imaging)
Type I Type II Type III Type IV Type V Type VI
Skin
Subcutis
Muscles
Supraspinous or
nuchal ligament
Bone
Dura mater Spinal cord
Bone
Fig. 7.4.13 Schematic classification of dermoid sinus reported in the literature. See text for details of the various types of
dermoid sinus.
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• Dermoid sinus can be associated with other congenital tortuous; both T2W and T1W series are useful to assess
abnormalities such as spina bifida, spinous process mal- soft tissues and bone structures optimally. Fat suppres-
formations, hemivertebrae, or block vertebrae.30,33,36,39,40,47 sion techniques can help highlight the sinus and tract
Concomitant anomalies of the dorsal laminae or spi- better. Thin slices with no gaps techniques may be pre-
nous processes of the vertebrae deep to the sinus should scribed to increase the ability to track the sinus from ori-
raise concern for a communication with the vertebral gin to end. An external marker, such as a lipid capsule
canal.32,33,36,39,42,47 Although rare, the association between taped on the skin at the level of the opening of the sinus,
dermoid sinus and spina bifida can lead to a communicat- is useful.
ing dermoid sinus and myelomeningocele.26 • The MRI abnormalities reported with spinal dermoid
• Although the Rhodesian Ridgeback is predisposed to sinus are as follows (Fig. 7.4.14):
the condition due to a hereditary transmission,38 spinal • A focal invagination of the cutaneous tissues towards
dermoid sinuses have been reported in numerous breeds, the spinous processes corresponding to the clinically
including:41 palpable lesion. Deep to that area, there may be a focal
• Cervical region: Borboel, Chow Chow, Golden rounded or lenticular subcutaneous lesion, corre-
Retriever, Pyrenean Mountain Dog, Rhodesian sponding to the main cavity of the sinus, followed by
Ridgeback and Domestic Short-haireded cat.37 a tubular tract extending ventrally to a variable depth,
• Thoracic region (most commonly cranial portion): depending on the type of dermoid sinus.
Boxer, Chinese Crested Dog, Chow-Chow, Rhodesian • The lumen of the sinus and its tract is often filled with
Ridgeback, Shih-Tzu, Siberian Husky, Swedish sebum, keratin debris, and hair, resulting in a vari-
Vallhunds, Victorian Bulldog, Yorkshire Terrier, able and unpredictable MR signal. Compared with
Burmese cat,39,46,47 and Balinese cat.49 muscles, the lesions tend to be T2 hyperintense while
• Lumbosacral region: English Springer Spaniel, T1W signal is more variable (hypo-, iso-, hyperin-
French Bulldog.26 tense).37,43,47 Areas that are hyperintense on both T1W
• Sacrococcygeal region: Rhodesian Ridgeback. and T2W images may correspond to lipid lining.37 In
• Spinal MR imaging in patients with dermoid sinuses is a case report where gadolinium contrast was admin-
typically performed because of concurrent neurologic istered intravenously, only minimal enhancement was
signs, but may also be performed in the absence of neu- seen.37 In a case where the sinus was abscessed, the
rologic deficits to assess for possible subclinical vertebral lesion was markedly T2 hyperintense and T1 hypoin-
canal/dura mater involvement. Other imaging modali- tense with a hypointense wall on both T1W and T2W
ties such as contrast fistulography or CT fistulography images, suggestive of a thick capsule.35
have been used to determine the extent of the sinus, but • In types IV and VI, which have a dural connection,
false-negative results with these imaging studies may additional signs include (Fig. 7.4.14):
occur due to presence of luminal debris. In these cases, – Presence of a linear, somewhat tortuous tract of
myelography can also be used to identify involvement of variable signal intensity, extending deep to the
the dura mater/subarachnoid space deep to the dermoid skin towards the spine and entering the vertebral
sinus.50 canal, connecting with the dura mater, usually
• The accuracy of MRI in determining the true extent of through an interarcuate space and in some cases
a dermoid sinus is not known, since only isolated case through a defect of the dorsal arch (schisis).32,37,40,47
reports or small case series are available. A number of – Concurrent vertebral malformations such as
these studies were performed at low-field, which may spina bifida, block vertebrae, partial fusion of
challenge the identification of the tract. In reported cases adjacent spinous processes, or incomplete dorsal
where MRI was used and in which there was a confirmed lamina.32,37,39,40,47 Such anomalies seem to be more
connection with the dura mater (types IV and VI), MRI commonly associated with dermoid sinuses that
was generally successful in determining the presence of have connection with the dura mater, and there-
that connection, either through direct visualization of fore their identification should trigger a careful
the tract,32,37,40,47 or highly suspected through the con- examination of the meninges, subarachnoid space,
comitant presence of focal spinal cord abnormalities and spinal cord.
deep to the dermoid sinus.39 In other cases where no – Focal dorsal tenting of the meninges of the spi-
dural connection or concurrent dural/spinal cord abnor- nal cord, due to the dural connection pulling the
malities were seen, there was indeed no connection at dura dorsally. In cases of tenting, the dorsal sub-
surgery (type I).43 In one case, vascular structures seem- arachnoid space is focally widened and assumes
ingly extending from the sinus area have been mistaken a characteristic triangular shape on transverse
for extension of the tract.35 images.32,37 In cases of tethering there is dorsal
• MRI of dermoid sinus should include multiple imag- displacement of the cord at the level of the sinus.39
ing planes, as the geometry of the tract can be complex/
496 CHAPTER 7.4
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L7
L7
(a) (b)
Fig. 7.4.14 Type IV dermoid sinus in a 22-month-old female

Labrador Retriever. Parasagittal (a) and mid-line sagittal (b)
T2W images and transverse T1W image at the level of caudal
L7 (c). A dermoid sinus and tract is seen extending from a skin
opening (arrowhead, a) ventrally to the vertebral canal (black
arrows, a and c), entering the canal in the interarcuate space
at L7-S1 (solid white arrows, b). The tract has a heterogeneous
signal with hypointense wall and hyperintense lumen on
T2W images, and is more homogeneously isointense to
slightly hyperintense to muscles on T1W images. Within
*
the vertebral canal at L7 there is enlargement of the ventral
extremity of the dermoid tract due to accumulation of
debris and cells (asterisk, c), causing dorsal compression and
ventral displacement of the cauda equina (dotted arrows, c).
(1.5T MRI system; images courtesy of Dr. Cristi Cook,
(c)
University of Missouri College of Veterinary Medicine)
– Syringomyelia adjacent to the dural connection, LUMBOSACRAL OSTEOCHONDROSIS

likely associated with focal alterations of the CSF
flow dynamics caused by the dural connection or • Osteochondrosis is a disturbance of endochondral ossi-
concurrent adhesions or vertebral anomalies.39 fication, and in dogs affects predominantly the cau-
– Rarely, presence of an intradural– extramedullary dal aspect of the humeral head, the medial ridge of the
T2 hyperintense mass lesion compressing/dis- humeral trochlea, the femoral condyles, and the ridges of
placing the spinal cord.47 This is due to extension the trochlea of the talus.
of the distal end of the sinus through the dura • The lumbosacral joint is a rare location of canine osteo-
mater forming a progressively enlarging, debris- chondrosis (see also Chapter 7.3), and this location is
filled blind-ended cystic component. A meningeal even less common in cats.51–55
lesion with no dorsal extension to the subcutane- • In dogs, middle-aged male German Shepherd Dogs are
ous or cutaneous area was anecdotally reported in most commonly affected. Boxers and Rottweilers have
a Balinese cat at the level of T3, although no imag- also been reported to be overrepresented.53 The lesion
ing study was performed (postmortem examina- is typically found on the craniodorsal border of the
tion).49 Although rare, if identified on MRI, these sacrum52,55 and, much less commonly, the caudal end-
lesions could potentially be confused with spinal plate of L7.51,53
neoplasia.
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• The condition is uncommon in cats, with animals pre- the cranial endplate of the sacrum, resulting in lipping
senting as young adults, and as in dogs, the cranial sacral of the craniodorsal sacral border with impingement
endplate is more commonly affected than the caudal end- onto the lumbosacral vertebral canal.55 Ultimately, frag-
plate of L7.54 mentation occurs, leaving a corresponding defect in the
• Clinical signs are those typically associated with cauda dorsal aspect of the sacral endplate. The osteochondral
equina syndrome, including lumbosacral pain, reluc- fragment can move dorsally to various extents, causing
tance to rise or sit, and pelvic limb lameness. The onset compression of the cauda equina. Secondary degenera-
of clinical signs tends to be later than with other forms of tive changes including lumbosacral intervertebral disc
osteochondrosis, probably because they are the result protrusion, spondylosis, and ligamentous hypertrophy
of progressive compression of the cauda equina by the are common in older dogs.
enlarging osteochondral fragment and associated degen- • Osteochondrosis can occasionally affect the caudodorsal
erative changes, as opposed to direct sacral pain due to endplate of L7, with imaging changes similar to those
the osteochondral lesion itself. This may be related to seen in the sacral form.53
the fact that in this condition, the osteochondral frag- • On MRI, the defect in the outline of the affected end-
ment occurs in a non-synovial joint. plate will usually be best visible on sagittal images
• Although diagnosis of lumbosacral osteochondro- (Fig. 7.4.15).51 The osteochondral fragment, if pres-
sis can be made radiographically, small fragments may ent, can be identified and localized within the vertebral
remain undetected radiographically, necessitating cross- canal. Presence and degree of cauda equina compression
sectional imaging for diagnosis. MRI is also useful to can be readily appreciated as well as secondary changes
evaluate the effects of the lesion on the cauda equina and such as degenerative lumbosacral disc disease and liga-
to assess the lumbosacral area for location and degree of mentous hypertrophy. Reactive endplate changes can be
secondary degenerative changes that may not be visible present, characterized by T2W and STIR hyperinten-
radiographically, but which are important for surgical sity and T1W endplate hypointensity, with or without
planning. endplate enhancement.51 Areas of bone sclerosis (T1W
• Early signs of sacral osteochondrosis include elongation and T2W hypointense) can surround these reactive
and abnormal caudal angulation of the dorsal aspect of changes.52
(a)
Fig. 7.4.15 Osteochondrosis of the dorsal aspect of the caudal
endplate of L7 in a 4-year-old male German Shepherd Dog
with a 6-month history of progressive and cortisone-responsive
difficulty rising. Sagittal T2W fast spin echo (a, with dotted
line referencing the plane of image b) and dorsal T1W gradient
echo (b) images of the lumbosacral junction. An osteochondral
bone fragment originating from the caudal endplate of L7 is
visible (arrow, a) with adjacent T2W hyperintense subchondral
(b)
marrow changes, interpreted as reactive endplate changes.
The defect in the margin of the caudal endplate of L7 is well
appreciated on the dorsal image (0.3 T MRI system; reproduced, with permission, from Gendron K, Doherr MG, Gavin P
et al. (2012). Magnetic resonance imaging characterization of vertebral endplate changes in the dog. Vet Radiol Ultrasound
53(1):50–6.)
498 CHAPTER 7.4
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CRANIOCERVICAL JUNCTION ANOMALIES • The apical ligament of the dens extends from the
cranial apex of the dens to the basioccipital bone,
The term ‘craniocervical junction anomalies’ encompasses attaching at the caudoventral aspect of the foramen
a number of malformations that occur in the craniocervical magnum; it is best seen on sagittal images, where is
region including the occipital region of the skull, the atlas appears as a homogeneous thin hypointense band
(C1), and the axis (C2).56–58 The most common disorder, (4–10 mm length and 1–2 mm width and height in
Chiari-like malformation, is covered in Chapters 5.1 and 7.9. small-breed dogs). Hyperintense fat ventral to the lig-
Often, various abnormalities are present concomitantly, and ament separates it from the ventral atlanto-occipital
a full assessment typically requires both MR and CT imag- membrane (the cranial continuation of the dorsal lon-
ing for a complete understanding of the soft tissue and bony gitudinal ligament of the vertebral column).
components of these complex conditions, and to facilitate • The paired alar ligaments originate lateral to the
adequate surgical planning. apical ligament and extend craniolaterally to attach
medially to the occipital condyles. They are best iden-
Atlantoaxial instability tified on dorsal oblique plane images that are angled
• Congenital atlantoaxial instability/subluxation is a com- about 20° in a craniodorsal–caudoventral direction
mon condition in small-breed dogs, especially of the toy relative to the ventral floor of the vertebral canal.71
type, documented in numerous case reports and series. Their visualization in a dog with altered alignment
• Yorkshire Terriers, Toy Poodles, and Chihuahuas are the between C1 and C2 due to instability may, however,
breeds most commonly affected.59 Large canine breeds need further adjustment to coincide with the plane of
and cats can also occasionally be affected.60–62 the alar ligaments. In small dogs their length is 4–8
• Mean age at onset of clinical signs is 21.3 months. mm and width/height range from 1 to 2 mm. They
• Clinical signs occur due to increased flexion of the joint, are the strongest stabilizers of the atlantoaxial joint
resulting in dorsal subluxation of the axis relative to the in dogs.72
atlas, thereby causing ventral compression and trauma • Looser stabilizing elements include the atlantoaxial
to the spinal cord. These signs range from neck pain joint capsule and the dorsal atlantoaxial ligament,
with or without ataxia to tetraplegia,59 and in the most which spans the dorsal arch of the atlas and the ver-
severe forms can lead to respiratory paralysis and death. tebral arch of the axis. The ligament may be seen as a
Clinical onset can be acute or insidious.58 thin structure that is hypointense to muscles.
• The most common causes for the instability include • MRI features of atlantoaxial instability include
aplasia and hypoplasia of the dens (odontoid process) (Fig. 7.4.17):71,73
of the axis, observed in 24% and 32% of affected dogs, • Abnormal shape of the dens, which can be absent,
respectively.59 Other causes include dorsal angulation/ blunted, or fragmented.
degeneration/separation of the dens, failure or absence • On sagittal images, increased space between the base
of ligamentous support structures,63 cervical block ver- of C1 and the ventral surface of the dens, usually best
tebrae caudal to C2, and incomplete ossification of the appreciated on T2W images. This widened space may
atlas.63–69 Traumatic (i.e., non-congenital) subluxation/ be due to hypoplasia/aplasia of the dens and/or dorsal
instability can also be the result of trauma without pre- displacement of the dens.
existing predisposing factors, and can be observed in • On sagittal images, increased distance between the
dogs and cats of any age or breed.58 dorsal arch of C1 and spinous process of C2; this,
• The anatomy of the atlantoaxial joint differs from the however, may be difficult to observe, as the thin
remainder of the spine due to its specialized function, dorsal spinous process of C2 may not be fully included
allowing axial rotational movements of the head. The in sagittal images.
dens of the axis lies in a depression in the ventral arch of • Attenuation of the dorsal and ventral subarachnoid
the atlas called the ‘fovea of the dens’ (‘fovea dentis’). The space at the level of the dens.
normal alignment between the atlas and axis is ensured • Dorsal deviation of the cord, which is ventrally com-
by a number of structures, which can be evaluated with pressed by the cranial aspect of the axis/dens; this is
MRI (Fig. 7.4.16):58,70,71 best appreciated on sagittal images.
• The transverse (atlantal) ligament, dorsal to the dens • Focal T2W hyperintensity in the spinal cord
and oriented perpendicular to its long axis, is visible parenchyma dorsal to the dens. This may represent
as a thin T1 and T2 hypointense structure crossing edema, hemorrhage, or chronic gliosis and Wallerian
from left to right within the vertebral canal of the degeneration.
atlas, immediately dorsal to the dens. It is best visu- • Focal T2 or T2* hypointensity/signal void in the cord
alized on transverse images as well as sagittal images. parenchyma may be present in cases of spinal cord
Its length in small dogs ranges between 10 and 17 mm hemorrhage associated with traumatic injuries to the
and its width/height is about 1 mm. cord.73
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(a) (b)
(c) (d) (e)

Fig. 7.4.16 (a) Sagittal prosection of the atlanto-occipital region in a dog. The marker at the bottom of the image is 1 cm in
length. 1, apical ligament of the dens; 2, alar ligament; 3, transverse atlantal ligament; 4, fat surrounding the dorsal atlantoaxial
ligament; 5, connective tissue; 6, basioccipital bone; 7, supraoccipital bone; 8, dorsal lamina of the atlas; 9, axis; 10, dens of
the axis; 11, m. longus capitis; 12, m. longus colli; 14, occipitoatlantoaxial joint capsule; 16, ventral atlanto-occipital membrane;
17, articular cartilage of the atlas; 18, communication between the composite atlanto-occipital and atlantoaxial joint spaces.
(b) Sagittal T1W image of the atlanto-occipital region. 1, apical ligament of the dens (hypointense line); 3, transverse atlantal
ligament; 4, dorsal atlantoaxial ligament; 5, connective tissue (hyperintense); 6, basioccipital bone; 7, supraoccipital bone; 8,
dorsal lamina of the atlas; 9, axis; 10, dens of the axis; 11, m. longus capitis; 12, m. longus colli; 14, occipitoatlantoaxial joint
capsule; 16, ventral atlanto-occipital membrane (hypointense line); 17, articular cartilage of the atlas; 18, communication
between the composite atlanto-occipital and atlantoaxial joint spaces. (c) Dorsal prosection of the atlas at the level of
the odontoid process of the axis. 1, apical ligament of the dens; 2, paired alar ligaments; 3, transverse atlantal ligament;
6, basioccipital bone; 8, junction between the dorsal arch and lateral mass of the atlas; 9, cranial articular extremity of the axis;
10, dens of the axis; 13, basioccipital bone; 14, occipitoatlantoaxial joint capsule. (d) Sagittal T1W image showing the non-
angled dorsal (dotted line) and 20°-angled craniodorsal–caudoventral scan planes used to visualize the alar ligaments. (e) Dorsal
20°-angled PDW image at the level of the dens of the axis. The arrows point to the alar ligaments, which appear as hypointense
bands that are nearly isointense to the surrounding tissue. (Reproduced, with permission, from Middleton G, Hillmann DJ,
Trichel J et al. (2012). Magnetic resonance imaging of the ligamentous structures of the occipitoatlantoaxial region in the dog.
Vet Radiol Ultrasound 53(5):545–51.)
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(a) (b)
transverse T2W image at the level of the apex of the dens
of the axis (c) in a 2-year-old mixed breed dog with a 3-day
history of ataxia. Atlantoaxial subluxation is noted, evidenced
by widening of the space between the body of the atlas and
the dens (solid arrows, a and b), and of the space between
the arch of the atlas and the cranial extremity of the spinous
process of the axis (double-headed arrow, b). The apical
ligament of the dens is mildly thickened and irregular
(dotted arrow, a). The displaced dens is causing ventral
compression of the spinal cord, as seen on the transverse
image (arrowhead, c), and there is mild T2 hyperintensity
in the spinal cord parenchyma at that level consistent with
edema/gliosis. (1.5T MRI system)
(c)
• Syringomyelia extending caudally along the cervical Dorsal angulation of the dens
spinal cord may be present as a result of obliteration • Dorsal angulation of the dens without associated dynamic
of the subarachnoid space in the atlantoaxial region. instability of the atlantoaxial junction has been reported,
• If ligaments are specifically evaluated, one could especially in dogs with Chiari-like malformations.75–77
observe:71 • This can cause abnormal tension on the transverse liga-
– A lack of visualization of the transverse ligament. ment due to the abnormally angled dens, and this pro-
– An irregularly thickened/elongated apical ligament. gressive damage/weakening of the ligament can result in
– Thickening of the alar ligaments. rupture with clinical exacerbation.75
• Although MRI is useful to determine the extent of soft • On MRI, this is best recognized on sagittal images,
tissue lesions associated with atlantoaxial instability, CT where the dens is abnormally pointing in a craniodorsal
is still warranted to provide a complete assessment of the direction, causing medullary kinking and ventral cord
bony structures and information on bone corridor mea- compression (Fig. 7.4.18). T2 hyperintensities in the
surements, as well as to obtain 3D reconstructions and spinal cord parenchyma can be seen at that level from
possibly 3D printing that can be very useful for surgical the chronic compression exerted by the dorsally point-
planning.74 ing dens.75
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Fig. 7.4.19 Sagittal T2W image in a 10-year-old Pug with an

atlantoaxial fibrous band (arrow) causing dorsal compression
of the subarachnoid space and mild dorsal cord compression.
Fig. 7.4.18 Sagittal T2W image in a 6-month-old dog with
There is a long irregular T2 hyperintense syrinx in the
tetraparesis. There is an abnormally formed dens, which is
cervical spinal cord (dotted arrows). (1.5T MRI system)
short and angulated dorsally causing ventral compression of
the spinal cord. There is focal T2 hyperintense signal at that
level in the spinal cord parenchyma, which may represent
• On MRI, atlantoaxial dural bands are best visible
edema or gliosis. There is mild widening of the space between
on T2W sagittal images, forming hypointense well-
the dens and body of the atlas, which may suggest some
marginated tissue that is bulging ventrally at the level
degree of atlantoaxial instability (arrow). (1.5T MRI system)
of the dorsal atlantoaxial junction, causing variable
degrees of subarachnoid space attenuation, and spinal
cord compression (Fig. 7.4.19). There may be dilation of
Atlantoaxial dural bands the subarachnoid space cranial and caudal to the band.80
• Atlantoaxial dural bands are fibrous bands located at Secondary changes such as syringomyelia are common.
the atlantoaxial junction and causing variable degrees • The degree of compression is more pronounced in an
of attenuation of the dorsal subarachnoid space and cord extended position of the head/neck (standard MR posi-
compression.57,78 Other terminology found in the litera- tioning for head imaging) as opposed to flexion (closer
ture includes ‘atlantoaxial dorsal compressive lesions’ or to physiologic neutral position).80 Other abnormalities
‘constrictive lesions’ as well as ‘dural fibrous bands’.76–79 associated with craniocervical anomalies, such as cer-
Latest studies and review articles have referred to them ebellar herniation, can be more pronounced in flexion.82
as ‘atlantoaxial bands’.57,80 Therefore, imaging patients in both the flexed and
• Although they are commonly associated with Chiari-like extended position may be important to obtain full diag-
malformations, they can also be associated with other nostic information across the range of motion of the cra-
craniocervical malformations such as dorsal angulation niocervical region.
of the dens.75 Such bands are present in 38% of small • Atlantoaxial bands and degree of resultant spinal cord
and toy breeds that have Chiari-like malformation77 and compression have been associated with presence/severity
were reported in up to 42% of symptomatic and non- of syringomyelia and also presence (but not severity) of
symptomatic Cavalier King Charles Spaniels.76 In older clinical signs. Clinical signs may be the result of direct
dogs of this breed, the prevalence of these bands can neural compression/damage or the effect of associated
reach >80%,80 suggesting a progressive nature of the syringomyelia.
condition.
• Surgical removal can be associated with improvement of Atlanto-occipital overlapping
the clinical signs.78 • As with other craniocervical abnormalities, atlantoaxial
• At surgery, these bands are mostly composed of soft overlapping is observed in small and toy-breed dogs.
tissue, although in some patients a bony component is • This condition is characterized by abnormal cranial dis-
appreciated. Some hypothesize that they may be associ- placement of the atlas into the foramen magnum, thereby
ated with instability of C1-C2.78 causing variable degrees of overlap between the supraoc-
• Histopathologically, there is fibrosis and proliferation of cipital bone and the dorsal arch of the atlas. A similar
the ligamentum flavum and dura mater, with an irregular condition in people is called ‘basilar invagination’ or
pattern of collagen fascicles including hyalinous nodules ‘impression’.
and occasional areas of calcification and/or ossification.76 • This condition is often found as one of multiple abnor-
Similar thickened tissue has been reported at the atlanto- malities of the craniocervical junction but is typically
occipital level in dogs with Chiari-like malformation.81 associated with occipital dysplasia, which may allow the
502 CHAPTER 7.4
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atlas to move cranially into the abnormally wide fora- cerebellum. The overlapping can be accentuated by
men magnum.79 Other abnormalities such as Chiari-like head/neck extension.79
malformation or atlantoaxial subluxation are common. • Elevation and compression of the medulla oblongata
• Age at presentation varies from juvenile to young adult, at the atlanto-occipital junction (‘medullary kinking’).
but typically patients present by 4 years of age.57 The clin- • Obliteration of the cerebellomedullary cistern and of
ical signs include neck pain and ataxia of all four limbs. the subarachnoid space throughout the length of the
Additional signs associated with secondary syringomyelia atlas.
are common, including spinal hyperpathia, scratching • Secondary changes such as syringomyelia can be
activity, and scoliosis. identified.
• MRI features of this condition are best recognized on
mid-sagittal images (Fig. 7.4.20): Occipitoatlantoaxial malformation
• Cranial displacement of the atlas, with the cranial • Occipitoatlantoaxial malformation is uncommon in dogs
margin of the dorsal arch of the atlas crossing the and even less common in cats.61 It results from errors
foramen magnum to extend cranially into the caudal in development/fusion of the ossification centers of the
fossa, causing indentation of the caudal aspect of the atlas and axis.
(a) (b)
corresponding sagittal reformatted CT image (bone window)
(c) in a 6-year-old Chihuahua with acute onset of tetraparesis.
There is increased space between the dens of the axis and the
body of the atlas (solid arrows), consistent with atlantoaxial
subluxation. The dens is causing ventral compression of the
spinal cord and there is focal T2 hyperintense signal at that
level in the spinal cord parenchyma (a), which may represent
edema or gliosis. There is atlanto-occipital overlap, with the
cranial margin of the arch of the atlas displaced cranial to the
foramen magnum (dotted arrows), likely associated with an
incompletely ossified supraoccipital bone (occipital dysplasia).
(c)
(1.5T MRI system)
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• Affected patients typically present as juveniles or young compression, atlantoaxial instability, and abnormal sig-
adults, and various breeds can be affected. nal within the spinal cord.
• Clinical signs include neck pain, ataxia, and propriocep- • The MRI features of the condition include (Fig. 7.4.21):69
tive deficits in all four limbs. • Incomplete fusion between the left and right neural
• CT is the preferred imaging modality to visualize these arches dorsally, and incomplete fusion between the
complex malformations, especially as it provides high- intercentrum and typically one of the two neural
quality 3D reconstructions of the bony structures. MRI arches, with a wide appearance of these sutures; this is
characteristics have rarely been described,83 and are vari- best appreciated on transverse images.
able as the morphologic features of the anomaly are not • The extremities of the unfused centers typically have
consistent across patients: thickened and flared or blunted ends; malalignment
• Uni- or bilaterally absent or hypoplastic occipital con- can be present resulting from instability or fracture.
dyles. • Atlantoaxial subluxation can be appreciated on sagit-
• Enlargement or lateral narrowing of the foramen tal images, accompanied by variable degrees of ventral
magnum. compression of the spinal cord by the dorsally dis-
• Asymmetric atlas, with foreshortened body and/or placed dens of the axis.
thickened lateral processes or dorsal lamina. • Focal T2 hyperintensity of the spinal cord paren-
• Asymmetric atlanto-occipital or atlantoaxial fusion. chyma dorsal to the dens.
• Fusion between C2 and C3.
• Abnormal position of the axis (axial rotation or sub- VASCULAR ANOMALIES
luxation).
• Cranial displacement of the axis into the foramen • Spinal vascular anomalies are rare in dogs and cats and
magnum, causing dorsal displacement of the medulla not very well documented, with only few case reports
oblongata (medullary kinking). available.86–93 Reports on their MRI appearance are even
• Incompletely developed, blunted odontoid process. scarcer.86,87,90–93
• Variable degrees of spinal cord compression/deviation • Reported vascular anomalies in dogs include cavernous
associated with the above abnormalities, which cause malformations (unclassified hamartoma and cavernous
stenosis of the vertebral canal. angioma),89,90 arteriovenous malformations,88 and aneu-
rysmal lesions (venous aneurysms or arterial ectasia of
Incomplete ossification of the atlas various origins),87,92,93 as well as undetermined intramed-
• The atlas is formed from three centers of ossification: ullary vascular hemorrhagic anomalies.86
the body (intercentrum) located ventrally, and the left and • Animals are typically adult or elderly at presentation, and
right neural arches, located dorsolaterally.69,84 The left clinical signs include various progressive neurologic defi-
and right dorsolateral neural arches form respectively cits depending on the location of the lesions, although
the left and right pedicles and transverse processes; these acute presentation is possible; for example, due to acute
arches fuse dorsally on midline to complete the dorsal thrombotic episodes in the vascular anomaly.
lamina. In Beagles that fusion happens by 106 days, while • Cavernous malformations and arteriovenous malforma-
the intercentrum fuses with the pedicles by 115 days.85 tions can form intramedullary masses of variable signal
• Incomplete ossification of the atlas is a sporadic con- intensity on MRI. Contrast enhancement may be pres-
dition that can affect various breeds but is more com- ent in the form of rim-enhancement or strong diffuse/
monly encountered in gun dogs.68 The clinical form of patchy enhancement, making these lesions difficult to
the condition, associated with atlantoaxial subluxation, differentiate from neoplasia.90
has been reported in various breeds, including Rough • Extramedullary vascular anomalies have been rarely
Collie, Cavalier King Charles Spaniel, Bearded Collie, reported:
English Springer Spaniel, Bull Mastiff, and Wirehaired • In two dogs, focal arterial ectasia in the cervical spine
Fox Terrier.68,69,84 with tortuous/saccular enlargement of some spinal
• Small or partial defects of the neural arch are typically branches of the vertebral arteries and ventral spinal
clinically silent, but larger defects of the neural arch artery was causing spinal cord deviation and compres-
and, more commonly, defects involving the intercentrum sion.87,92,93 In one case, the arterial ectasia appeared
are frequently associated with atlantoaxial instability in to be a primary abnormality,87 while in the other it
breeds that are not typically affected by this condition.68 was associated with an absent right subclavian artery.
• Although the bony abnormalities associated with the This caused increased blood flow (‘steal’) from the
condition are best appreciated with CT, MRI can allow left subclavian and vertebral arteries to the right side
identification of the abnormality, while also allow- through the radicular arteries in order to supply blood
ing assessment of its consequences such as spinal cord to the right vertebral artery and right thoracic limb
(Fig. 7.4.22).93
504 CHAPTER 7.4
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(a) (b)
Fig. 7.4.21 Transverse T2W (a) and T1W (b) images at the
level of C1 and sagittal T2W image of the cervical spine (c) in
a 5-year-old Newfoundland dog with cervical pain and ataxia
that was suspected to have spondylomyelopathy (wobbler
syndrome). There is incomplete ossification of C1 with lack
of fusion between the left and right neural arches dorsally
(dotted arrows, a and b) and between the right neural arch
and the intercentrum lateroventrally (solid arrows, a and b).
There is proliferative tissue at the levels of non-union,
likely from chronic instability, and dorsal attenuation of the
subarachnoid space and mild cord compression are noted at
the level of the caudal border of the arch of C1 (arrowhead, c).
(c)
(1.5T MRI system)
Fig. 7.4.22 T2W sagittal image of the cervical region in a

3-year-old neutered female German Shorthaired Pointer
with progressive ataxia and tetraparesis of 6 weeks’ duration.
Large flow voids consistent with abnormally dilated
vascular structures are evident at C5–C6 (arrow) causing
marked spinal cord compression. Additional smaller flow
voids are present at the level of the bodies of C3 and C4
(arrowheads). These corresponded to multilevel ectatic
anastomotic radicular arterial branches connecting the
left and right vertebral arteries, secondary to a non-patent
proximal segment of the right subclavian artery. (1.5T MRI
system; reproduced, with permission, from Westworth DR,
Vernau KM, Cullen SP et al. (2006). Vascular anomaly causing
subclavian steal and cervical myelopathy in a dog: diagnosis
and endovascular management. Vet Radiol Ultrasound
47(3):265–9.)
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• Abnormalities of the vertebral venous system were thoracolumbar caudal articular processes in Pugs: 11 cases
reported in a population of sighthounds.91 Such (1993–2009). J Am Vet Med Assoc 242(2):223–9.
abnormalities were found in 12% of dogs of this 14. Penderis J, Schwarz T, McConnell JF et al. (2005). Dysplasia
of the caudal vertebral articular facets in four dogs: results of
type undergoing spinal MRI, and were character-
radiographic, myelographic and magnetic resonance imaging
ized by abnormal enlargement of the internal verte- investigations. Vet Rec 156(19):601–5.
bral venous plexus, external vertebral venous plexus, 15. Werner T, McNicholas WT, Kim J et al. (2004). Aplastic
and/or intervertebral veins. Most abnormalities were articular facets in a dog with intervertebral disk rupture of the
unilateral and right sided, and the most common 12th to 13th thoracic vertebral space. J Am Anim Hosp Assoc
location was C6-C7. Although most affected dogs 40(6):490–4.
did not have a definitive diagnosis, the location of 16. McDonnell JJ, Knowles KE, deLahunta A et al. (2003).
the vascular venous abnormality was in most cases Thoracolumbar spinal cord compression due to vertebral
in a neuroanatomic localization that could wholly or process degenerative joint disease in a family of Shiloh
Shepherd dogs. J Vet Intern Med 17(4):530–7.
partly explain the clinical signs (spinal pain, ataxia,
17. Nykamp SG, Scrivani PV, Kennedy S et al. (2001). What is
paresis, lameness). your diagnosis? Attenuation of the dorsal and lateral columns
of contrast material and slight ventral deviation of the
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CHAPTER 7.5
INFLAMMATORY AND INFECTIOUS CONDITIONS

508 Wilfried Mai
CONTENTS
Discospondylitis ...................................................................................................................................................................................................508
Spinal epidural empyema ...................................................................................................................................................................................... 511
Vertebral osteomyelitis .......................................................................................................................................................................................... 512
Meningomyelitis ................................................................................................................................................................................................... 512
Viral meningomyelitis ...................................................................................................................................................................................... 513
Bacterial meningomyelitis................................................................................................................................................................................ 513
Protozoal meningomyelitis .............................................................................................................................................................................. 515
Toxoplasmosis ........................................................................................................................................................................................... 515
Neosporosis ............................................................................................................................................................................................... 515
Leishmaniasis ............................................................................................................................................................................................ 516
Fungal meningomyelitis .................................................................................................................................................................................. 516
Cryptococcosis .......................................................................................................................................................................................... 516
Coccidioidomycosis ................................................................................................................................................................................... 516
Blastomycosis ............................................................................................................................................................................................ 517
Aspergillosis .............................................................................................................................................................................................. 519
Histoplasmosis .......................................................................................................................................................................................... 519
Parasitic meningomyelitis................................................................................................................................................................................520
Non-infectious meningomyelitis ......................................................................................................................................................................520
Granulomatous meningoencephalomyelitis ................................................................................................................................................520
Steroid-responsive meningitis-arteritis ......................................................................................................................................................520
Necrotizing meningomyelitis ......................................................................................................................................................................520
Idiopathic sterile pyogranulomatous inflammation of epidural fat .........................................................................................................................522
Hypertrophic ganglioneuritis .................................................................................................................................................................................522
Meningeal inflammatory pseudotumor..................................................................................................................................................................525
References.............................................................................................................................................................................................................525
Infectious and non-infectious inflammatory conditions of The thoracic, lumbar, and lumbosacral areas are more
the spine are not very common in dogs and cats, but should commonly affected than the cervical area, and simulta-
be considered in patients with spinal pain with or without neous involvement of multiple sites is common.2
neurologic signs attributable to spinal cord abnormalities. • Large-breed dogs are more commonly affected,2 with
Inflammatory lesions are commonly widespread and often mean age at time of diagnosis ranging from 4.1 to
affect the entire central nervous system (CNS). As a result, 9 years. Some studies have reported a predisposition in
clinical signs may reflect multifocal lesions.1 male dogs,3,4 although this was not observed other case
series.2
DISCOSPONDYLITIS • Clinical signs are non-specific and highly vari-
able, including lethargy, anorexia, weight loss, fever,
• Discospondylitis is an infection of two adjacent verte- and spinal pain. Various degrees of neurologic signs
bral endplates and the associated intervertebral disc. may be present, ranging from none to spinal pain,
I n f l a m m at ory a n d I n f e c t ious C on di t ions 509
paresis, or paralysis with or without loss of nociception. • Changes in signal intensity of the adjacent endplates
Ambulatory paraparesis is the most common neuro- compared with normal bone marrow:
logic sign observed. 2 – Mixed intensity on T2W images with multiple
• Neurologic deficits can result from a number of comor- areas of hyperintensity.
bidities, including disc material herniation, osseous or – Mixed to hypointense signal on T1W images.
soft tissue proliferation in the vertebral canal, vertebral – Hyperintense signal on STIR images.
subluxation, pathologic fracture, epidural empyema, and • Changes in signal intensity of the adjacent vertebral
meningitis/myelitis due to extension of inflammation bodies compared with normal bone marrow:
into the neural tissues. – Hypo- or isointense, less commonly hyperintense
• Bacterial causes are more common than fungal infec- on T2W images; the hypointense signal may be
tion, with the most common bacterial agents being due to sclerotic changes within the affected ver-
coagulase-positive staphylococcal species (S. intermedius tebral bodies.
and S. aureus), Streptococcus spp., Brucella canis, Escherichia – Hypo- or isointense on T1W images.
coli, and, less commonly, coagulase-negative staphylo- – Hyperintense to isointense on STIR images.
coccal species, Corynebacterium spp., Actinomyces spp., • Narrowing/collapse of the intervertebral disc space,
Bacteroides spp., Bordetella spp., Erysipelothrix rhusiopathiae, with changes in signal intensity of the space:
Mycobacterium avium, Nocardia spp., Pasteurella multocida, – Hyperintense on T2W images.
Proteus spp., and Salmonella spp.2,5,6 Of the fungal agents, – Isointense, mixed signal intensity, or hyperintense
Aspergillus and Paecilomyces spp. are the most common.2 on T1W images.
• The urinary tract is a common source of hematogenous – Hyperintense on STIR images.
bacterial infection, even when there is no clinicopatho- • Changes in signal intensity of the paravertebral soft
logic evidence of lower urinary tract infection.2 Other tissues around the affected site:
possible sites of origin include abscesses, open wounds, – Iso- to hyperintense to adjacent soft tissues on
respiratory tract, and oral cavity infections.2 The pre- T2W images.
cise physiopathology of hematogenous discospondyli- – Isointense on T1W images.
tis is not clear, but may be related to the presence of – Hyperintense on STIR images. Hyperintense
subchondral vascular loops in the vertebral epiphysis signal in the paravertebral soft tissues may be
causing a slow sluggish blood flow, which may allow detected in STIR images in areas of normal signal
colonization by blood-borne bacteria. These bacteria intensity on T2W, which underscores the useful-
then diffuse through the cartilaginous endplate of the ness of this pulse sequence for this condition.2
vertebral body to reach the disc and eventually the adja- • Diffuse or heterogeneous contrast enhancement
cent endplate. Extension to other vertebral endplates of the intervertebral disc, vertebral endplates, and
can then occur through freely communicating venous paravertebral soft tissues. Paravertebral soft tissue
sinuses.5 enhancement typically affects the tissues ventral to
• Traditionally, the diagnosis of discospondylitis is made the affected disc space(s) but can extend laterally and
based on characteristic radiographic changes together dorsally as well.8
with laboratory findings. Radiographic evaluation, how- • Endplate erosion is usually appreciated and is best
ever, is not optimal, as, on the one hand, there can be a seen on sagittal T1W images as well as PDW images,
delay of up to a few weeks between the onset of clinical appearing as loss of definition of cortical continu-
signs and detection of radiographic changes, and on the ity and destruction of the cortical margins.8 In the
other hand, there is a discrepancy between clinical and early stages of the disease where endplate erosion is
radiographic signs during recovery.7 not present yet, the only change may be STIR and
• MRI can be used to confirm a tentative diagnosis of dis- T2 hyperintensity (+/− T1 hypointensity) of the bone
cospondylitis.2,8–11 Compared with plain radiography, marrow adjacent to the endplates.8
MRI can assess the soft tissue components of the ver- • Extension of the process in the epidural space can be
tebral canal including the epidural structures and spinal seen (‘spinal epidural empyema’, see below), forming
cord, and thereby provide additional information on the an elongated irregular soft tissue structure that is iso-
degree of involvement of these structures and presence to hypointense on T1W images, hyperintense/heter-
and severity of spinal cord compression. MRI is more ogeneous on T2W images, with rim-like or diffuse
sensitive to early changes, and can reveal abnormalities contrast enhancement.
suggestive of discospondylitis in dogs that have normal • Vertebral subluxation, and occasionally pathologic
radiographs, thereby allowing an earlier diagnosis in dogs fracture, best appreciated on sagittal and/or dorsal
with suggestive clinical signs but normal radiographs.8 images.
• Typical MRI changes seen with discospondylitis include • Mild to severe spinal cord compression at the affected
(Fig. 7.5.1):2,5,6,8,9,12 site(s) is common, and can result from secondary disc
510 CHAPTER 7.5
(a) (b)
(c) (d)
(e) (f)
Fig. 7.5.1 Sagittal T2W (a) and STIR (b) images and transverse T2W (c), T1W pre-contrast (d), and T1W post-contrast with fat
saturation (e, f) images of the lumbosacral spine in a 6-year-old female Bullmastiff dog with discospondylitis at L7-S1, presumably
secondary to a severe urinary tract infection with cocci (Staphyloccocus pseudointermedius). The transverse images (c, d, e) are
centered at the L7-S1 disc space, while the transverse image (f) is at the level of the cranial body of L7. On the sagittal images (a,
b), note the irregular lytic changes of the adjacent endplates at L7-S1 with disruption of the cortex and loss of the normal structure
of the intervertebral disc, which is replaced by heterogeneous material that is mostly hyperintense on the T2W and STIR images
(arrow, a). On the STIR image (b) there is patchy hyperintense signal of the bone marrow of the caudal body of L7 and cranial
aspect of the sacrum. The irregular material in the L7-S1 intervertebral disc space is strongly enhancing after gadolinium
injection (e), and there is also marked patchy multifocal enhancement of the paraspinal muscles around the lumbosacral space.
In addition, on the sagittal T2W image, a fusiform extradural lesion is noted in the ventral aspect of the vertebral canal, extending
from the L7-S1 space cranially to the level of cranial L6 and consistent with epidural empyema. This material is mostly slightly
hyperintense to the spinal cord on the T2W and STIR images, with a focal oval-shaped markedly T2 hyperintense region in
its center (arrowhead, a), which on the transverse post-contrast image corresponds to a rounded non-enhancing portion of that
extradural lesion (dotted arrow, f); this is consistent with a fluid pocket, presumably pus. Note that the ventral extradural material
is causing dorsal displacement and compression of the cauda equina (open arrow, f). (1.5T MRI system)
protrusion/extrusion, vertebral subluxation or frac- Bacterial agents that have been reported in cases of
ture, or extension of infection into the epidural space canine spinal epidural empyema include Enterobacter
(spinal epidural empyema). cloacae, coagulase-positive staphylococci, Pasteurella mul-
• Spinal cord parenchyma hyperintensity on T2W tocida, Escherichia coli,13,14 and Salmonella spp.6
images, either focal or diffuse;2 these sites are often • Although CT myelography has been used for the diagno-
(but not always) associated with areas of spinal cord sis of spinal epidural empyema in dogs,15 this technique
compression. can allow spread of the infection in the subarachnoid
• The patterns of MRI changes observed in dogs with space due to iatrogenic contamination during contrast
discospondylitis are not correlated with chronicity of material injection.
the condition.2 • MRI is the imaging modality of choice as it does not
• The number of compressive lesions and degree of require subarachnoid injection of contrast material.13
spinal cord compression seen on MRI are correlated • MRI findings in cases of spinal epidural empyema
with the neurologic score at the time of MRI exami- include (Figs. 7.5.1, 7.5.2):6,13,14,16
nation.2 • Somewhat well-defined epidural mass in the vertebral
canal, causing variable degrees of spinal cord com-
SPINAL EPIDURAL EMPYEMA pression:
– The lesion is hyperintense or of mixed signal on
• Spinal epidural empyema is a relatively rare condition T2W images, heterogeneously hyperintense on
in dogs, and is defined as an accumulation of purulent T2-FLAIR images, and hypointense on T1W
material in the epidural space of the vertebral canal.13 It images, obliterating the normal hyperintense sig-
is a neurologic emergency for which a prompt diagnosis nal from the epidural fat.
is important for treatment decision and to avoid perma- – After gadolinium injection, a peripheral (rim-like)
nent neurologic disability or mortality. pattern of enhancement is commonly seen, while
• The clinical signs include pyrexia, spinal pain, and typi- the pus-filled central cavity is non-enhancing;
cally rapidly progressive myelopathy. less often, a diffuse pattern of enhancement is
• Dogs affected are more commonly of large or giant observed.
breeds.13 – On T2*W gradient echo images, focal areas of
• Possible causes include extension of adjacent osteo- signal void, consistent with susceptibility artifacts
myelitis or discospondylitis, or hematogenous spread. from hemorrhage, may be identified.
(a) (b)
Fig. 7.5.2 Transverse T1W pre- (a) and post-contrast (b) images of the lumbosacral area in a dog with lumbosacral
discospondylitis. The vertebral canal contains heterogeneous material that is irregularly enhancing after contrast material
injection and causes moderate ventral spinal cord (asterisk, a) compression. There is a hypointense non-enhancing lacunar area
on the right consistent with fluid collection (arrows), corresponding to surgically confirmed epidural empyema secondary to
extension of the infectious process from the disc space into the caudal lumbar vertebral canal. (1.5T MRI system; reproduced,
with permission, from Mai W (2013). Magnetic resonance imaging and computed tomography features of canine and feline
spinal cord disease. In: Textbook of Veterinary Diagnostic Radiology, 6th edn. (ed. DE Thrall) Elsevier, St. Louis, pp. 194–221.)
512 Chapter 7.5
VetBooks.ir
• T2 hyperintense lesions in the gray matter of the

spinal cord adjacent to the epidural mass can be seen,
which may represent edema from compression of the
cord by the mass lesion, ischemic changes, myelitis
due to extension of the infection into the spinal cord
parenchyma, or focal areas of malacia.13
• Hyperintense signal of the paraspinal soft tissues
on T2W images and enhancement on post- contrast
images, which may indicate previous soft tissue
injury to the spine or concurrent infection of the
soft tissues (e.g., foreign body migration). In cases
of a migrating foreign body, a hyperintense and
enhancing tract in the paraspinal soft tissue may be
seen, extending to the vertebral canal in the area of
*
empyema.14,17
• Possible signs of discospondylitis adjacent to the area
of epidural empyema (see above for MRI features of (a)
discospondylitis).
• Enhancement of the vertebrae adjacent to the area of
empyema has also been reported, which may be due to
concurrent osteomyelitis.13
VERTEBRAL OSTEOMYELITIS
• Bacterial osteomyelitis is usually caused by direct inocu-

lation after penetrating trauma or surgical contamina-
tion, or by extension from soft tissue infection. Vertebral
infection secondary to grass awn migration is an example
of the latter, and in this case the infection is typically
located between L2 and L4 and affects primarily the
ventral aspect of the vertebrae and hypaxial muscles.18
Hematogenous bacterial osteomyelitis is rare in compar-
ison, but has been reported in various bones including
the vertebrae.19
• Fungal osteomyelitis is also possible, especially with
coccidioidomycosis, blastomycosis, or systemic asper-
gillosis,20 and vertebrae can be affected,21 with the most (b)
common route for infection being hematogenous in Fig. 7.5.3 Sagittal STIR image of the cervicothoracic region
these cases. (a) and T1W post-contrast (b) image at the level of mid-T1 in
• The MRI appearance of vertebral osteomyelitis in a 1-year-old German Shepherd Dog with a large paravertebral
dogs and cats is poorly documented in the literature.19 abscess in the craniodorsal mediastinum. The abscess is
Changes include disruption of the normally hypointense seen as a large fusiform hyperintense structure (asterisk, a)
vertebral cortex on T1W and T2W images, and abnor- ventral to the cranial thoracic spine (a). There are areas of
mal signal intensity in the vertebral body with various patchy hyperintensity within the vertebral bodies of T1 and
degrees of patchy contrast enhancement (Fig. 7.5.3).19 T2 (solid arrows, a), which are moderately enhancing on the
Abnormal signal intensity and variable enhancement of post-contrast image (dotted arrows, b); these changes are
the paravertebral soft tissues in the affected areas are consistent with osteomyelitis. There is also loss of signal
also possible.19 intensity of the nucleus pulposus of the intervertebral disc
at T1-T2, which may suggest early discospondylitis. On the
MENINGOMYELITIS post-contrast image (b), there is enhancement of the thick
wall of the abscess (arrowheads) with large central non-
• Meningomyelitis is defined as inflammation of the spinal enhancing cavities consistent with purulent fluid collections.
cord parenchyma and surrounding meninges. It is rare in A large paravertebral abscess was debrided surgically, and
dogs and cats and can have infectious or non-infectious culture of surgical samples grew colonies of Staphylococcus
origins.1,22 pseudointermedius. (1.5T MRI system)
• Although the cervical spinal cord is considered anecdot- hyperintensity may enhance mildly to moderately
ally to be the most commonly affected site, lesions can after gadolinium injection.
be present in any spinal cord segment and can result in • The MRI pattern is not specific for meningomyelitis,
multifocal myelopathy.22 and other conditions such as myelomalacia, ischemic
• Infectious agents that may cause meningomyelitis in myelopathy and neoplastic conditions such as lym-
dogs include viruses (e.g., canine distemper), bacteria phoma, histiocytic sarcoma, or glial cell neoplasia can
(e.g., Staphylococcus, Pasteurella, Actinomyces, and Nocardia produce similar changes.25,30,32,33 Therefore, correla-
spp.), fungi (e.g., Cryptococcus, Blastomyces, Coccidioides, tion with the clinical signs and laboratory test results
and rarely Histoplasma spp.), rickettsiae (e.g., Ehrlichia is necessary.
spp., Rickettsia ricketsii), protozoa (e.g., Toxoplasma gon-
dii, Neospora caninum), parasites (e.g., Spirocerca lupi, Viral meningomyelitis
Dirofilaria immitis, Angiostrongylus spp.), and rarely algae • In cats, spinal lesions associated with FIP include lep-
(e.g., Prototheca wickerhamii, Prototheca zopfii).22–24 tomeningeal granulomatous changes and vasculitis, with
• In cats, feline infectious peritonitis (FIP) and toxoplas- secondary myelitis.34,35 Concurrent brain lesions involv-
mosis have been reported.25 ing the ventricular system, ependymal lining, and cho-
• Non-infectious causes of meningomyelitis include roid plexus are more common, and their MRI features
granulomatous meningoencephalomyelitis,26 steroid- have been reported (see Chapter 5.3). There is, so far, no
responsive meningitis-arteritis,27 and various poorly report on the spinal cord MRI changes associated with
characterized entities such as pyogranulomatous menin- this condition.
gomyelitis, necrotizing meningoencephalomyelitis, or • Although canine distemper virus can cause meningomy-
necrotizing leukoencephalomyelitis.1,22–24 elitis,24,36 spinal cord MRI changes associated with this
• Meningomyelitis of unknown origin represents a condition have not been reported in the literature so
substantial group of meningomyelitides for which far.22 The author has observed cases of multifocal myeli-
a definitive etiology cannot be determined using the tis caused by distemper virus infection characterized by
standard battery of tests, including CSF analysis and multifocal ill-defined intramedullary lesions scattered
specific testing on CSF/serum (viral, protozoal, fungal, over the cervical, thoracic, and lumbar spine, which were
etc.).28 hyperintense on T2W and STIR images, mildly hypoin-
• Clinical signs associated with meningomyelitis reflect tense on T1W images, and moderately enhancing after
the region of the CNS that is affected, and include para- gadolinium injection (Fig. 7.5.5).
spinal hyperesthesia, general proprioceptive ataxia, and
pelvic/thoracic limb paresis or paralysis.22 Bacterial meningomyelitis
• Some studies suggested a predisposition in toy and hound • The most common routes of bacterial infection of the
breeds, especially older than 2 years, as well as younger CNS are:
dogs of other breeds.22 • Hematogenous resulting from mucous membrane
• There is some overlap between MRI features of menin- colonization or a distant pyogenic focus.
gomyelitis and other intramedullary conditions such • Direct invasion (e.g., after a dog bite or a traumatic
as neoplasia or ischemic myelopathy. Taking into injury).
account the clinical history and results of CSF analy- • Contiguous extension (e.g., vertebral osteomyelitis or
sis may improve the sensitivity of MRI in diagnosing discospondylitis).
meningomyelitis.29 • Communication between the subarachnoid space and
• General MRI features of meningomyelitis include: body surfaces (e.g., dermoid sinus, iatrogenic infec-
• Irregular areas of spinal cord parenchymal hyperin- tion after CSF tap).37
tensity on T2W images. • Common bacterial agents are Escherichia coli, Streptococcus
• These areas are either isointense or hypointense to spp. and Klebsiella spp.37 Other species include
the cord on pre-contrast T1W images. Staphylococcus spp., Pasteurella multocida, Actinomyces spp.,
• Variable contrast enhancement of the meninges and/ and Nocardia spp.1
or spinal cord parenchyma after gadolinium injec- • Bacterial infection of the CNS can rapidly disseminate
tion.23,26,30 and lead to serious illness and death.
• Hyperintense areas in the paraspinal muscles on • Meningeal inflammation is largely responsible for the
STIR and T2W images have been reported in dogs clinical signs. Bacterial cell wall components released
with inflammatory spinal cord disease of unknown into the CSF stimulate local production and release
origin (Fig. 7.5.4).31 In the cervical region, commonly of cytokines and prostaglandins, which attract white
affected muscles include the longus colli, intertransver- blood cells and promote meningitis and ependymitis.
sarii cervicis, and longus capitis muscles. The changes are Meningitis causes increased blood–brain barrier perme-
often bilateral but asymmetric. These areas of STIR ability, vasculitis of penetrating vessels with subsequent
514 CHAPTER 7.5
(a)
(b)
Fig. 7.5.4 Parasagittal STIR (a), transverse T2W (b), and

T1W post-contrast with fat saturation (c) images at the level
of C5 in a 2-year-old Labrador Retriever dog presenting with
neck pain and fever and a presumed diagnosis of steroid-
responsive meningitis-arteritis. There are multifocal areas of
patchy hyperintense signal visible on the STIR (a) and T2W
(b) images, with mild contrast enhancement (c), affecting the
longus colli muscles (solid arrows, a–c) and intertransversarius
muscles (dashed arrows, b and c). Such paravertebral
hyperintense areas, particularly well visible on STIR images,
have been associated with inflammatory conditions of the
(c)
spinal cord and meninges. (1.5T MRI system)
(a) (b)
Fig. 7.5.5 Sagittal T2W (a) and T1W post-contrast (b) images in a 1-year-old Dachshund presented with a 3-week history of
progressive pelvic limb neurologic deficits, which started with knuckling on the left pelvic limb and progressed to bilateral
non-ambulatory pelvic limb paresis. There are multifocal ill-defined intramedullary lesions that are hyperintense on the T2W
image (a) and moderately enhancing after gadolinium injection (b). Histopathologically, there were eosinophilic intranuclear
inclusion bodies in glial cells, with malacia, demyelination, and lymphocytic perivascular cuffing in the medulla and spinal cord,
consistent with canine distemper virus infection. (1.5T MRI system)
infarction/thrombosis, parenchymal edema, and second- and inflammatory infiltrates of the parenchyma, and
ary inflammation of the neural tissues adjacent to the focal severe mononuclear meningitis; protozoal cysts can
meninges (brain and spinal cord).37 be seen within the parenchymal lesions.
• Clinical signs are typically multifocal, reflecting involve- • MRI features are non-specific and rarely reported in
ment of various regions of the CNS including the brain the literature. Changes in a cat were described in one
and spinal cord.37 case report, and included a focal parenchymal lesion
• The MRI features of bacterial meningomyelitis have with spinal cord swelling over T6-T9. The lesion was
not been reported so far, but one would expect the non- hyperintense on T2W and T2-FLAIR images, hypoin-
specific changes described above (bullet point General tense on T1W images, with strong diffuse contrast
MRI features of meningomyelitis, p. 513). enhancement.30
• The author has observed cases of spinal cord lesions
Protozoal meningomyelitis caused by T. gondii in dogs and cats, where there were
Toxoplasmosis diffuse or multifocal intramedullary lesions with cord
• Toxoplasmosis is caused by the protozoal agent Toxoplasma swelling that were T2/T2-FLAIR/STIR hyperintense,
gondii. T1 isointense, and mildly to markedly contrast enhanc-
• Involvement of the spinal cord is very rare, and includes ing (Fig. 7.5.6).
segmental myelopathy extending over several vertebral
bodies, characterized by lateralized malacia of areas of Neosporosis
white and gray matter with prominent perivascular cuffs • Neosporosis is an infection caused by Neosporum caninum.
(a) (b)
Fig. 7.5.6 Sagittal T2W (a) and STIR (b) images of the
cervical spine and transverse T1W post-contrast image at the
level of C6 (c) in a 9-year-old Siamese cat with toxoplasmosis.
The cat presented with a several months’ history of
progressive thoracic limb ataxia with muscle atrophy and mild
pelvic limb ataxia. There are multifocal areas of ill-defined
hyperintense signal in the spinal cord in the cervicothoracic
region on the T2W and STIR images (a, b). After gadolinium
injection, there is marked contrast enhancement primarily
affecting the gray matter of the ventral horns (c). On
histopathology, there was severe lymphoplasmacytic and
histiocytic meningoencephalomyelitis with malacia, astroglial
scarring, and numerous intralesional apicomplexan protozoal
(c)
cysts, consistent with Toxoplasma gondii. (1.5T MRI system)
516 CHAPTER 7.5
• Dogs of any age can be affected by this polysystemic dis- • Pseudocyst formation due to expansion of cryptococ-
ease, which can cause inflammation of the brain, spinal cal organisms along the Virchow–Robin spaces; these
cord, meninges, nerve roots, skeletal muscles, myocar- appear as rounded lesions that are T2 hyperintense,
dium, liver, lungs, skin, and pancreas.38 T1 hypointense with rim enhancement after gadolin-
• In the CNS, the infection causes multifocal areas of non- ium injection.
suppurative inflammation and malacia of the gray and • Meningeal thickening with enhancement (Fig. 7.5.7).
white matter or cerebellar atrophy, and therefore various • Parenchymal lesions that are T2 hyperintense, T1
neurologic signs may be present, including ataxia, pare- iso- to hypointense with variable degrees of homoge-
sis, paralysis, head tilt, head tremors, and seizures. neous or heterogeneous contrast enhancement.
• Spinal cord lesions have been reported, but are usually • Isolated spinal involvement is very rare, and has only
present in conjunction with brain lesions (especially been described in a couple of case reports:
cerebellar atrophy, but also multifocal lesions of the • In a dog, a focal spinal cord compression caused by
cerebrum). a ventral epidural cryptococcoma at C6-C7 was
• MRI features of spinal cord lesions associated with reported and initially thought to represent disc her-
neosporosis that have been reported include a poorly niation on myelography; this dog did not undergo
delineated, intramedullary focal lesion that is hyperin- MRI.41
tense on T2W and T2-FLAIR images, iso- to hypoin- • In a cat, a spinal cryptococcoma in the cranial thoracic
tense on T1W images, with no or minimal contrast spinal cord was reported.42 On MRI, heterogeneous
enhancement.38 areas of T2 hyperintensity and T1 hypointensity of
the spinal cord parenchyma were seen in the cervical
Leishmaniasis and thoracic spine; after contrast injection, an oval-
• Leishmaniasis in dogs is a severe systemic disease caused shaped, well-demarcated hypointense non-enhancing
by the protozoan parasite Leishmania infantum. parenchymal mass was seen at the level of T3, with
• Involvement of the nervous system is rare, but has been enhancement of the spinal cord parenchyma around
detected in both people and dogs.39 Various parts of the that lesion (Fig. 7.5.8). Histopathologically, the
CNS can be affected. In the spine, lesions that have been non-enhancing mass was diagnosed as a cryptococ-
reported include myelitis, radiculoneuritis, meningitis, coma (granulomatous lesion with intra- and extracel-
and extradural granulomas.39 lular yeasts and necrosis).
• MRI findings have been rarely reported.39 In a case of
myelitis associated with leishmaniasis, a poorly defined Coccidioidomycosis
markedly hyperintense intramedullary lesion was seen on • Coccidioidomycosis is caused by Coccidioides immitis,
T2W images in the cervical spine, extending over several a soil-borne dimorphic fungus that rarely affects the
vertebral segments, with spinal cord swelling causing CNS.21 It is endemic to the lower Sonoran desert areas of
obliteration of the signal from the epidural fat and CSF in North America, including parts of Arizona, California,
the subarachnoid space. On T1W pre-contrast images, a New Mexico, Texas, and northern Mexico.43
focal slightly hyperintense mass was seen, which on post- • Coccidioides granulomas can affect the spinal cord both
contrast T1W images had a target-like appearance, with in dogs and in cats, although brain involvement is more
an enhancing core surrounded by isointense tissue and common (see Chapter 5.3).
then a peripheral ring of enhancement.39 • Mass-like lesions due to fungal granuloma formation are
more common than meningitis.44
Fungal meningomyelitis • MRI features of spinal Coccidioides granulomas include:43,44
Cryptococcosis • Intramedullary or intradural–extramedullary and,
• Cryptococcosis is caused by Cryptococcus neoformans, and rarely, extradural lesions.
has a predilection for the CNS. It is the most common • Signal intensity is variable including:
systemic fungal disease in cats.21 CNS infection rarely – Most commonly T2 hyperintense, less commonly
affects the spinal cord in isolation. More commonly, T2 isointense, possibly T2 hypointense.
brain lesions are present concomitantly, and these are – Most commonly T1 hypo- to isointense, less com-
described in Chapter 5.3. monly T1 hyperintense.
• Concurrent spinal cord lesions in cases of intracranial • Perilesional T2 hyperintensity consistent with spinal
cryptococcosis are more commonly seen in dogs than in cord edema.
cats.40 • Contrast enhancement is usually present, stronger
• The MRI appearance of concurrent spinal cord lesions with extramedullary lesions and more variable
in dogs and cats with intracranial cryptococcosis has not with intramedullary lesions. Extension of contrast
been reported specifically, but it may be similar to the enhancement along the meningeal margins around
brain lesions, which include:40 the granuloma, giving the appearance of a ‘dural tail’,
(a)
(c)
Fig. 7.5.7 Sagittal T2W (a) and transverse T1W pre-contrast

(b) and post-contrast (c) images at the level of C2 in a dog
with meningomyelitis due to Cryptococcus infection. On the
T2W image (a), ill-defined extensive areas of hyperintense
signal are seen in the spinal cord (dashed arrows, a). On
the T1W post-contrast image (c) there is strong contrast
enhancement (solid arrow, c) of the meninges compared
with the pre-contrast image at the same level (b). (1.5T MRI
system; reproduced, with permission, from Mai W (2013).
Magnetic resonance imaging and computed tomography
features of canine and feline spinal cord disease. In: Textbook
of Veterinary Diagnostic Radiology, 6th edn. (ed. DE Thrall)
(b)
Elsevier, St. Louis, pp. 194–221.)
may be seen with both intramedullary and intradural– The intramedullary lesions are typically peripheral
extramedullary lesions. in the parenchyma, giving the impression of a broad
• Imaging characteristics are non-specific, and con- base towards the dura mater, sometimes with a ‘dural
fusion with gliomas for the intramedullary lesions tail’ on post-contrast images, leading to the confusing
and meningiomas for the intradural– extramedullary appearance (Fig. 7.5.9). Although subjective, fuzzy
lesions is possible. Single lesions are common, which margins on post-contrast images may be a distin-
increases possible confusion with neoplasia. guishing feature from meningiomas, which typically
• One feature that seems to be recurrent regarding have clear borders.44
the MRI features of fungal granulomas is the fre-
quently reported difficulty in definitively classify- Blastomycosis
ing the lesions based on imaging characteristics as • Blastomycosis is caused by Blastomyces dermatitidis, which
intramedullary or intradural–extramedullary.43,44 grows in moist, acidic soil with decaying vegetation and
518 CHAPTER 7.5
(a)
Fig. 7.5.8 Sagittal T1W post-contrast image of the cranial

thoracic spine in an 11-year-old cat presented with progressive
paraparesis. There is a large non-enhancing intramedullary
lesion dorsal to T3, with marked, poorly marginated
contrast enhancement of the parenchyma around that lesion
(arrowhead). On necropsy, the large non-enhancing lesion was
diagnosed as an intramedullary cryptococcoma. (Reproduced,
with permission, from Belluco S, Thibaud JL, Guillot J et al.
(2008). Spinal cryptococcoma in an immunocompetent cat.
J Comp Pathol 139(4):246–51.)
fecal matter. It is endemic in large waterway systems in

Northern America such as the Mississippi, Missouri,
and Ohio river valleys,21 as well as southeast and west-
ern Canada.45 It is more commonly diagnosed in young
sporting dogs living near water bodies.45
• Blastomycosis affects the CNS in about 4%–6% of dogs. (b)
It is rare in cats, although pyogranulomatous inflamma- Fig. 7.5.9 Parasagittal T2W (a) and dorsal T1W post-
tion of the brain and spinal cord has been reported.21 contrast (b) images of the cervical spine in a dog with
• Brain lesions are more common but spinal cord involve- coccidioidomycosis. On the T2W image (a) there is a focal
ment is possible. hypointense lesion (arrow) that appears intramedullary; there
• In the brain, intra-axial or extra-axial masses are more is mild perilesional edema indicated by hyperintense spinal
commonly seen, but non-mass lesions involving the epen- cord signal. On the dorsal T1W post-contrast image (b), the
dymal and periventricular regions have been reported lesion is strongly enhancing and seems to be broad-based
(see Chapter 5.3). laterally towards the dura mater, with the impression of a
• The MRI appearance of spinal cord blastomycosis has ‘dural tail’ along the caudal margin of the mass. Although the
been rarely reported, and findings are somewhat similar appearance on the dorsal image would suggest an intradural–
to the brain lesions including: extramedullary location, an intramedullary lesion was found
• Focal intramedullary mass lesion that is:46 at surgery. (Reproduced, with permission, from Bentley RT,
– Hypointense with hyperintense rim on T2W Heng HG, Thompson C et al. (2015). Magnetic resonance
images, with perilesional hyperintensity con- imaging features and outcome for solitary central nervous
sistent with edema; the T2 hypointensity may system coccidioides granulomas in 11 dogs and cats. Vet Radiol
occur because of hemosiderin content in the Ultrasound 56(5):520–30.)
macrophages and dense population of fungal by local extension of discospondylitis and resultant
organisms (this appearance was also reported with empyema or disc herniation, as described above in the
coccidioidomycosis, see above). section on discospondylitis.
– Isointense on T1W pre-contrast images.
– Strongly, homogeneously contrast enhancing. Histoplasmosis
• Absence of a mass lesion but changes around the • Histoplasmosis is a mycotic infection of people and
central canal of the spinal cord that are:47 animals caused by the dimorphic soil-borne fungus
– Hyperintense on T2W and T2-FLAIR images Histoplasma capsulatum.49 It has a worldwide distribu-
extending into the gray matter and dorsal funiculi. tion in temperate and subtropical climates, and it is
– Marked contrast enhancement of the ependymal endemic in the Ohio river and Mississippi river valleys
lining of the central canal +/- adjacent paren- in North America, Mexico, Argentina, Brazil, Colombia,
chyma (Fig. 7.5.10). Venezuela, and in other tropical countries in Southeast
Asia and sub-Saharan Africa. It also occurs sporadically
Aspergillosis outside recognized endemic areas; for example, Canada,
• Aspergillosis (Aspergillus spp.) most commonly causes Australia, and Central California. In Europe, a few cases
sinonasal disease, but can also be associated with pulmo- have been reported in Italy.49
nary lesions or cause disseminated disease.48 • It produces a wide spectrum of symptoms ranging from
• Systemic aspergillosis in dogs can cause discospondyli- a mild influenza-like illness to disseminated forms virtu-
tis, osteomyelitis, lymphadenitis, nephritis, splenitis, and ally involving any tissue.49 The CNS is rarely affected
CNS inflammation, and young adult German Shepherd with only few reports available.
Dogs are predisposed to this form of the disease.20,48 • The MRI appearance of an epidural granuloma associ-
• CNS lesions associated with disseminated disease most ated with histoplasmosis was reported. An elongated
commonly affect the brain. When the spine is affected, epidural compressive mass lesion was present that was
discospondylitis in multiple locations is typically seen, relatively isointense to epidural fat and moderately con-
with primary involvement of the spinal cord parenchyma trast enhancing.49 Mild patchy hyperintensity of the
and meninges not observed or reported so far.48 The spi- paraspinal muscles on T2W images was noted in the
nal cord and epidural space can be secondarily affected region of the mass.
(a) (b)
Fig. 7.5.10 Transverse T2-FLAIR (a) and T1W post-contrast (b) images at the level of C1 in a dog with blastomycosis. Note the
ill-defined hyperintense signal around the central canal on the T2-FLAIR image (a) and the ependymal enhancement (arrow)
on the T1W post-contrast image (b). (1.5T MRI system; reproduced, with permission, from Bentley RT, Reese MJ, Heng HG
et al. (2013). Ependymal and periventricular magnetic resonance imaging changes in four dogs with central nervous system
blastomycosis. Vet Radiol Ultrasound 54(5):489–96.)
520 CHAPTER 7.5
Parasitic meningomyelitis • The spinal cord may be affected in isolation or, more
• Aberrant parasitic migration to the spine in dogs is rare, commonly, in combination with intracranial changes.
with only few case reports or small case series found in • MRI features are non-specific and include (Fig. 7.5.12):26
the veterinary literature. Examples include Spirocerca • Ill-defined areas of hyperintense parenchymal
lupi,50–52 Dirofilaria immitis,53 Angiostrongylus cantonensis,54 signal in the white and/or gray matter on T2W and
and Strongyloides spp.55 T2-FLAIR images.
• Depending on the parasite, the aberrant migration can • These areas are isointense, hypointense, or of mixed
occur in the epidural space or in the spinal cord paren- signal intensity on T1W images, and have variable
chyma. The clinical signs depend on the extent and loca- degrees of contrast enhancement varying from none
tion of the aberrant parasitic tract: to marked.
• In epidural locations, focal spinal cord compression • Perilesional edema is commonly seen.
may be present, either due to the parasite itself or due • Meningeal enhancement is uncommon but possible.
to secondary hematomas.51,53
• Direct damage to the spinal cord parenchyma with Steroid-responsive meningitis-arteritis
granulomatous inflammation, hemorrhage, and necro- • Steroid-responsive meningitis-arteritis is a systemic
sis is seen when aberrant migration occurs inside the immune disorder characterized by inflammatory lesions
spinal cord.52,55 of the leptomeninges and associated arteries that is typi-
• The MRI appearance of spinal epidural larva migrans cally responsive to corticosteroids.27
has not been reported so far. On myelography, confu- • Other historical terminology referring to this condition
sion with intervertebral disc herniation or extradural includes ‘necrotizing vasculitis’, ‘polyarteritis’, ‘panarteri-
neoplasia is possible, and it is likely that such confu- tis’, ‘juvenile polyarteritis syndrome’, ‘Beagle pain syn-
sion could also occur on MRI, especially with S. lupi, drome’, ‘corticosteroid-responsive meningitis’, ‘aseptic
which occurs typically in the thoracolumbar region, a suppurative meningitis’, and ‘sterile purulent meningitis’.27
common location for disc herniation.51,53 • Any breed of dog can be affected, with an overrepre-
• MRI changes associated with intramedullary spi- sentation of Beagles, Boxers, Bernese Mountain Dogs,
rocercosis were reported, and included regional Weimaraners, and Nova Scotia Duck Tolling Retrievers.
intramedullary T2 hyperintensity in the thora- • Affected dogs are typically immature or young adults
columbar/cranial lumbar area. Lateralized focal mild (6–18 months), although older adults and elderly dogs
parenchymal enhancement was observed in the thora- can occasionally be affected.27
columbar or cranial lumbar area on T1W post-con- • Clinical signs include profound cervical hyperesthesia,
trast images, corresponding to the site of parasitic depression, and fever, and result directly from the men-
tract (Fig. 7.5.11).50 ingitis/leptomeningeal arteritis lesions. Arteritis may
also involve other organs such as the heart, mediastinum,
Non-infectious meningomyelitis or thyroid gland; concurrent immune-mediated polyar-
Non-infectious causes of meningomyelitis include granu- thritis is possible.27
lomatous meningoencephalomyelitis,26 steroid-responsive • Presentation is more commonly acute and less commonly
meningitis-arteritis,27 and various poorly characterized chronic/protracted.27 The latter may be seen following
groups such as pyogranulomatous meningomyelitis, nec- relapses of acute disease and/or inadequate treatment; in
rotizing meningoencephalomyelitis, and necrotizing this form, additional CNS lesions and clinical signs (e.g.,
leukoencephalomyelitis.1,22–24 motor and proprioceptive deficits, cranial nerve deficits)
can develop resulting from meningeal fibrosis/adhesions,
Granulomatous meningoencephalomyelitis with subsequent obstruction to CSF flow or vascular
• Granulomatous meningoencephalomyelitis is an inflam- obstruction.
matory, non-suppurative condition of the CNS charac- • On MRI, meningeal enhancement may be observed on
terized by an accumulation of mononuclear cells in the T1W images after gadolinium administration.27
parenchyma and/or meninges of the brain and/or spinal
cord.26 Necrotizing meningomyelitis
• It is fairly common in dogs and has been occasionally • Necrotizing meningomyelitis is a poorly characterized
reported in cats. form of meningomyelitis.
• Although its etiology is unclear, an autoimmune disorder • MRI changes associated with this condition have been
with organ-specific T-cell-mediated delayed-type hyper- reported in a young Weimaraner that had concurrent
sensitivity is suspected.26 non-erosive polyarthritis.23 Findings included diffuse,
• Three clinical presentations of the condition are asymmetric increase in signal of the thoracolumbar spi-
reported: focal, multifocal/disseminated, and a rare ocu- nal cord on T2W images, with patchy contrast enhance-
lar form. The cerebral/ocular forms of the condition are ment on T1W images after gadolinium injection,
described in Chapter 5.3. affecting predominantly the gray matter.
(a) (b)
Fig. 7.5.11 Transverse T1W post-contrast image at the level of L2 (a) and corresponding histologic cross-section of the
spinal cord with hematoxylin and eosin staining (b) in a 7-year-old male German Shepherd Dog presented with back pain
and acute pelvic limb paresis. Note the enhancing focus in the left dorsolateral aspect of the spinal cord (white arrow, a) and
corresponding adult Spirocerca lupi nematode within the spinal cord (black arrow, b). (1.5T MRI system; reproduced, with
permission, from Chai O, Shelef I, Brenner O et al. (2008). Magnetic resonance imaging findings of spinal intramedullary
spirocercosis. Vet Radiol Ultrasound 49(5):456–9.)
(a)
Fig. 7.5.12 Sagittal T2W image of the thoracolumbar area
(a) and transverse T2W (b) and T1W pre- (c) and post-contrast
(d) images at the level of mid-T10 in a 9-month-old French
Bulldog with a 1-month history of progressive ataxia. There
are patchy areas of hyperintense signal within the spinal cord
on the sagittal T2W image (a). A hyperintense focus is seen
in the spinal cord on the T2W transverse image (arrow, b),
corresponding to mild hypointensity on the T1W pre-contrast
image (arrow, c), with subtle enhancement after gadolinium
injection (arrow, d). Granulomatous meningomyelitis was
(b)
confirmed on histopathology. (1.5T MRI system) (Continued)
522 CHAPTER 7.5
(c) (d)
IDIOPATHIC STERILE PYOGRANULOMATOUS • Epidural lesions may be focal or multifocal, and com-
INFLAMMATION OF EPIDURAL FAT monly affect the caudal thoracic, thoracolumbar, or
cranial lumbar area.56,58,59
• Idiopathic sterile pyogranuloma, or sterile panniculitis, • MRI features of epidural idiopathic sterile pyogranu-
is a dermatologic disease of unknown etiopathogenesis, lomatous inflammation have been rarely reported, and
forming single or multifocal subcutaneous nodules mea- include (Fig. 7.5.13):58
suring a few millimeters to several centimeters, progress- • A focal, well-circumscribed, elongated epidural mass
ing to a generalized skin disease that is cystic, ulcerated, causing spinal cord compression.
and may develop draining tracts.56 The condition may • Signal intensity is similar to fat (i.e., hyperintense on
also be purely granulomatous, suppurative, eosinophilic, T1W and T2W images with suppressed signal when
necrotizing, or fibrosing.57 In the generalized form, fat suppression techniques are used).
systemic signs such as pyrexia, anorexia, lethargy, and • These MRI features may be similar to those seen with
depression may be seen.57 Association with pancreatitis or epidural myelolipoma (see Chapter 7.6).
intra-abdominal steatitis has been reported.56 The condi- • The MRI appearance of the suppurative form of idio-
tion is typically responsive to glucocorticoid treatment. pathic sterile inflammation of epidural fat has only been
• A pyogranulomatous or suppurative inflammation of the reported once,57 and formed a dorsolateral epidural
epidural fat with histopathologic characteristics similar compressive lesion that was hyperintense on T1W and
to the cutaneous condition has been reported in dogs.56–59 T2W images and mildly contrast enhancing; no fat sup-
• Most reported dogs were Dachshunds, as well as one pressed series were obtained. There was focal myositis
Shih Tzu and one mixed-breed dog.56–59 All the dogs of the epaxial muscles adjacent to the affected region of
were adult or elderly. the spine.
• Clinical signs are similar to compressive intervertebral
disc disease, also common in these breeds, and include
chronic progressive or acute pelvic limb ataxia, parapa- HYPERTROPHIC GANGLIONEURITIS
resis, or paraplegia. In the suppurative form, generalized
signs such as depression, anorexia, and pyrexia may also • Hypertrophic neuritis is a rare inflammatory disorder
be seen.57 of unknown etiology. In people, the condition causes
• Systemic manifestations of the condition involving the a chronic demyelinating polyneuropathy with ‘onion
cutaneous tissues or intra-abdominal area are not uncom- bulb’ formation secondary to proliferating Schwann cells
mon in Dachshunds, either prior to or after the neuro- after repeated episodes of demyelination/remyelination;
logic presentation due to the epidural lesion(s).56,58,59 in dogs the condition is more focal, and characterized
VetBooks.ir
(a) (b)
(c)
(d)
Fig. 7.5.13 Sagittal T1W (a), T2W (b), and T1W with fat
suppression (c) images and transverse T1W (d) and T2W (e)
images at the level of T11 in a 12-year-old male Shih Tzu
with progressive pelvic limb paresis and a confirmed epidural
idiopathic sterile pyogranulomatous inflammatory lesion
located ventrally in the vertebral canal at the level of T11.
The ventral epidural compressive lesion (arrowheads) has
(e) high signal on the T1W (a, d) and T2W (b, e) images and
there is partial suppression of signal with fat suppression (c),
indicative of fat content. (0.4T MRI system; reproduced, with permission, from Murata D, Miura N, Iwanaga T et al. (2012).
CT and MRI imaging diagnosis of epidural idiopathic sterile pyogranulomatous inflammation in a dog spinal canal. J Vet Med
Sci 74(7):913–5.)
by marked chronic lymphocytic inflammation without • In the veterinary literature, inflammation of the C2
‘onion bulb’ formation.60 nerve roots has been most commonly reported. Nerve
• Inflammatory neuropathies affecting the brachial plexus roots are typically affected bilaterally and symmetri-
nerves have been reported in dogs and cats and are cally62 and, less commonly, unilaterally.60
described in Chapter 7.10. • The enlarged nerve roots may cause spinal cord com-
• Focal, unilateral ganglioneuritis secondary to lateralized pression and clinical signs, or may be found inciden-
intervertebral disc extrusion has been reported,61 and tally when imaging the cervical spinal cord for other
this condition is described in Chapter 7.1. reasons.62
• Idiopathic focal hypertrophic neuritis of the nerve roots • Clinical signs may include uni- or bilateral thoracic
and associated ganglion has been rarely reported in the limb lameness, thoracic and pelvic limb progres-
veterinary literature.60,62 Although rare, this condition sive ataxia and paresis, and neck pain. These symp-
should be kept in mind when identifying focal thicken- toms may respond to immunosuppressive doses of
ing of nerve roots on MRI, especially since, when unilat- corticosteroids.62
eral, their appearance can be confused with nerve root • Staffordshire Bull Terriers may be predisposed.62
neoplasia, which carries a different prognosis.60
524 CHAPTER 7.5
(a) (b)
Fig. 7.5.14 Transverse T2W (a) and T1W pre-contrast (b)

and T1W post-contrast with fat saturation (c) images at the
level of the C1-C2 intervertebral foramina in a Pug with
idiopathic hypertrophic ganglioneuritis. Note the bilateral
and symmetric thickening of the C2 nerve roots, which are
mildly hyperintense on the T2W image (arrows, a), isointense
on the T1W pre-contrast image (b), and strongly enhancing
after gadolinium injection (c). The thickened nerve roots are
causing mild dorsolateral compression of the spinal cord,
which assumes a somewhat triangular shape on the T2W
(c)
image (a). (1.5T MRI system)
• MRI features of idiopathic hypertrophic ganglioneuritis • In some cases, extension into the intradural–
include (Fig. 7.5.14):60,62 extramedullary compartment via the dorsal and
• Severe focal enlargement of the affected nerve roots, ventral rootlets can be seen, especially on post-con-
extending into the intervertebral canal, forming an trast images.60
extradural space-occupying lesion and resulting in • Enlarged nerves are hyperintense on T2W images, iso-
variable degrees of compression of the spinal cord. intense on T1W images, and strongly homogeneously
• In the bilateral form, the right and left dorsolateral contrast enhancing.60,62
aspects of the cord may be compressed by the enlarged • Focal area of intramedullary hyperintense signal on
nerve roots, resulting in triangular deformation of the T2W images at the level of compression, likely repre-
cord on transverse images.62 senting edema or gliosis.62
• Focal dilation of the central canal.62 findings in a dog with discospondylitis. Vet Radiol Ultrasound
• Ipsilateral paraspinal muscle atrophy with possible 41(2):142–4.
changes in signal consistent with denervation atrophy 10. Kraft SL, Mussman JM, Smith T et al. (1998). Magnetic
resonance imaging of presumptive lumbosacral
(hyperintensity on T1W and T2W images).60
discospondylitis in a dog. Vet Radiol Ultrasound 39(1):9–13.
11. Lipscomb VJ, Muir P (2000). Magnetic resonance imaging of
MENINGEAL INFLAMMATORY PSEUDOTUMOR a dog with sciatic nerve root signature. Vet Rec 147(14):393–4.
12. Gendron K, Doherr MG, Gavin P et al. (2012). Magnetic
• Inflammatory pseudotumors are distinctive lesions com- resonance imaging characterization of vertebral endplate
posed of myofibroblastic spindle cells accompanied by an changes in the dog. Vet Radiol Ultrasound 53(1):50–6.
infiltrate of inflammatory cells such as plasma cells, lym- 13. De Stefani A, Garosi LS, McConnell FJ et al. (2008).
phocytes, and eosinophils. In dogs and cats, most cases Magnetic resonance imaging features of spinal epidural
have been reported in the orbital cavity, with less com- empyema in five dogs. Vet Radiol Ultrasound 49(2):135–40.
14. Whitty CC, Milner HR, Oram B (2013). Use of magnetic
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nervous system neosporosis. Vet Radiol Ultrasound 55(5):539–46. sterile pyogranulomatous inflammation causing spinal cord
39. Jose-Lopez R, de la Fuente C, Pumarola M et al. (2014). compressive injury in five Miniature Dachshunds. Vet Surg
Intramedullary spinal cord mass presumptively associated with 37(6):594–601.
leishmaniasis in a dog. J Am Vet Med Assoc 244(2):200–4. 57. Cornelis I, De Decker S, Gielen I et al. (2013). Idiopathic
40. Sykes JE, Sturges BK, Cannon MS et al. (2010). Clinical sterile inflammation of the epidural fat and epaxial muscles
signs, imaging features, neuropathology, and outcome in cats causing paraplegia in a mixed-breed dog. J Am Vet Med Assoc
and dogs with central nervous system cryptococcosis from 242(10):1405–9.
California. J Vet Intern Med 24(6):1427–38. 58. Murata D, Miura N, Iwanaga T et al. (2012). CT and
41. Kerwin SC, McCarthy RJ, VanSteenhouse JL et al. (1998). MRI imaging diagnosis of epidural idiopathic sterile
Cervical spinal cord compression caused by cryptococcosis in pyogranulomatous inflammation in a dog spinal canal. J Vet
a dog: successful treatment with surgery and fluconazole. J Am Med Sci 74(7):913–5.
Anim Hosp Assoc 34(6):523–6. 59. Nishida H, Tanaka H, Kitamura M et al. (2012). Three cases of
42. Belluco S, Thibaud JL, Guillot J et al. (2008). Spinal idiopathic sterile pyogranulomatous inflammation of epidural
cryptococcoma in an immunocompetent cat. J Comp Pathol fat in Miniature Dachshunds. J Vet Med Sci 74(8):1071–4.
139(4):246–51. 60. Rodenas S, Summers BA, Saveraid T et al. (2013). Chronic
43. Foureman P, Longshore R, Plummer SB (2005). Spinal cord hypertrophic ganglioneuritis mimicking spinal nerve
granuloma due to Coccidioides immitis in a cat. J Vet Intern Med neoplasia: clinical, imaging, pathologic findings, and outcome
19(3):373–6. after surgical treatment. Vet Surg 42(1):91–8.
44. Bentley RT, Heng HG, Thompson C et al. (2015). Magnetic 61. Mouradian-Darby AE, Young BD, Griffin JF et al. (2014).
resonance imaging features and outcome for solitary central Lymphocytic ganglioneuritis secondary to intervertebral disc
nervous system coccidioides granulomas in 11 dogs and cats. extrusion in a dog. J Small Anim Pract 55(9):471–4.
Vet Radiol Ultrasound 56(5):520–30. 62. Joslyn S, Driver C, McConnell F (2015). Magnetic resonance
45. de Lorimier LP, Fan TM (2010). Delayed diagnosis of fungal imaging of suspected idiopathic bilateral C2 hypertrophic
osteomyelitis with early scintigraphic lesions in a dog. Can Vet ganglioneuritis in dogs. J Small Anim Pract 56(3):184–9.
J 51(12):1394–6. 63. Loderstedt S, Walmsley GL, Summers BA et al. (2010).
46. Lipitz L, Rylander H, Forrest LJ et al. (2010). Clinical and Neurological, imaging and pathological features of a
magnetic resonance imaging features of central nervous system meningeal inflammatory pseudotumour in a Maltese terrier.
blastomycosis in 4 dogs. J Vet Intern Med 24(6):1509–14. J Small Anim Pract 51(7):387–92.
CHAPTER 7.6
SPINAL NEOPLASIA
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Wilfried Mai 527
CONTENTS
Classification of spinal neoplasia ..........................................................................................................................................................................528
Extradural tumors ..................................................................................................................................................................................................529
Malignant vertebral tumors ..............................................................................................................................................................................529
Benign vertebral tumors...................................................................................................................................................................................532
Osteochondroma ........................................................................................................................................................................................532
Chondroma ................................................................................................................................................................................................532
Synovial myxoma/myxosarcoma .....................................................................................................................................................................532
Peripheral nerve sheath tumors .......................................................................................................................................................................535
Fat containing tumors ......................................................................................................................................................................................535
Infiltrative lipoma .......................................................................................................................................................................................535
Epidural myelolipoma ................................................................................................................................................................................536
Other extradural neoplasms .............................................................................................................................................................................536
Peripheral primitive neuroectodermal tumors.............................................................................................................................................536
Paraspinal invasive paragangliomas ..........................................................................................................................................................537
Other paravertebral soft tissue tumors ........................................................................................................................................................537
Intradural–extramedullary tumors .........................................................................................................................................................................537
Meningioma ....................................................................................................................................................................................................538
Nephroblastoma .............................................................................................................................................................................................542
Other tumors....................................................................................................................................................................................................547
Intramedullary tumors ...........................................................................................................................................................................................547
Spinal tumors with variable localization ................................................................................................................................................................554
Histiocytic sarcoma .........................................................................................................................................................................................554
Lymphoma .......................................................................................................................................................................................................556
Meningioangiomatosis ....................................................................................................................................................................................559
Hemangiosarcoma ...........................................................................................................................................................................................559
Chordoma........................................................................................................................................................................................................560
Plasma cell tumor ............................................................................................................................................................................................560
References.............................................................................................................................................................................................................562
Although plain radiographs can allow diagnosis of some subarachnoid space. However, this technique is invasive, as
types of spinal neoplasia, such as aggressive bone tumors, it requires injection of contrast material into the subarach-
a number of neoplastic conditions remain unidentifiable on noid space; it also lacks sensitivity for some types of spinal
radiographs. Myelography increases sensitivity because it neoplasia, and lacks specificity. Both CT and MRI are sen-
outlines the spinal cord and identifies areas of spinal cord sitive techniques to diagnose spinal tumors. CT is excel-
compression/deviation and can, to some extent, determine lent for osseous lesions, which are commonly observed with
localization of compressive lesions with respect to the spinal tumors; however, identification of soft tissue lesions
528 CHAPTER 7.6
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may be challenging, even after intravenous administration • Intradural–extramedullary tumors are located
of iodinated contrast material. Injection of contrast material between the dura mater and the spinal cord. Examples
in the subarachnoid space (CT myelography) may be useful include nerve sheath tumors and meningiomas. The
and increases the ability to differentiate between extradural neoplastic mass causes focal expansion of the suba-
and intradural tumors. Due to its superior soft-tissue reso- rachnoid space and various degrees of compression
lution, MRI is currently the preferred imaging method for and displacement of the adjacent spinal cord. T2W
spinal neoplasia in dogs and cats.1 images are particularly good at demonstrating the
focal expansion of the subarachnoid space due to the
CLASSIFICATION OF SPINAL NEOPLASIA hypersignal of the CSF. The focal dilation of the sub-
arachnoid space along the cranial and caudal margins
• Spinal neoplasia can be classified on the basis of loca- of the intradural mass lesion can form a ‘golf tee’ sign
tion relative to the dura mater, and can be described as similar to that observed on myelographic images.
intramedullary, intradural– extramedullary, or extradu- This will be easier to see on sagittal images for lesions
ral (Fig. 7.6.1):2 located dorsal or ventral to the spinal cord, and on
• Extradural tumors arise from spinal structures dorsal images for lesions located to the left or right
outside of the dura mater including the epidural space of the spinal cord. Pulse sequences with a ‘myelo-
(epidural fat, extradural portion of the spinal nerves), graphic effect’ (so-called ‘T2-myelogram’, such as
the vertebrae, the articular process joints, and the SS-FSE or HASTE pulse sequences) can be helpful
paraspinal soft tissues (e.g., soft tissue tumors sec- in recognizing these features as they isolate the signal
ondarily invading into the spinal structures). MRI from the CSF and lower the signal from the back-
assessment of the extent of neoplastic infiltration into ground tissues.4 Large intradural lesions may be dif-
the vertebral bone marrow, epidural space, or para- ficult to differentiate from intramedullary tumors.4
vertebral tissues can be improved with fat suppression Although variable depending on the histopathologic
on post-contrast images. Without fat suppression, nature, intradural–extramedullary tumors tend to
normal adipose tissue can be difficult to differenti- enhance significantly on post-contrast T1W images.
ate from contrast-enhancing lesions in or adjacent to Fat saturation may be useful to determine the extent
the vertebrae. Pre-contrast T1W images without fat of intradural neoplasia on post-contrast images, by
suppression should still be obtained though, as most suppression of the hypersignal from the epidural fat
lesions affecting the vertebral bone marrow tend to immediately adjacent to the dura mater; for example,
have low signal on T1W images, and may therefore the dural tail (focal thickening/infiltration of the
be identified on these pre-contrast images due to meninges adjacent to a meningeal mass lesion) com-
the natural contrast provided by the fat surrounding monly associated with meningiomas is often more
them.3 conspicuous on post-contrast fat suppressed images.3
Dura mater
and arachnoid
Pia mater
Rootlets
Spinal cord
Extradural Intradural Intramedullary
Fig. 7.6.1 Schematic representation of the relationship between spinal neoplasia and spinal structures depending on the
extradural, intradural–extramedullary, or intramedullary location of the neoplasm. The neoplasm is represented in light
purple color, the spinal cord in yellow, and the subarachnoid space in brown.
Spi n a l Ne opl a si a 529
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• Intramedullary neoplasms affect the spinal cord EXTRADURAL TUMORS

parenchyma and are usually of glial cell origin, such
as astrocytomas or ependymomas. Multicentric neo- MRI is very good at determining the primary vertebral or
plasia of non-neural origin or metastatic lesions can extravertebral nature of spinal neoplasia and invasiveness
also occur (e.g., lymphoma, hemangiosarcoma). On into the vertebral canal. Presence and degree of spinal cord
MRI, focal swelling of the spinal cord will be iden- compression is also easily determined.4
tified, causing circumferential attenuation of the
bright signal from CSF +/− epidural fat on T2W Malignant vertebral tumors
images. Intramedullary masses typically have an iso- • The most common primary vertebral neoplasia in dogs
to hypointense signal on T1W images and may be and cats is osteosarcoma. Chondrosarcoma is also fairly
hyperintense on T2W images, although there is great common in dogs.7,11,14 Metastatic vertebral tumors are
variability and often a heterogeneous signal pattern; common in dogs while they are uncommon in cats.7,11
they often have ill-defined margins, making them dif- • Primary vertebral bone neoplasia tends to affect only
ficult to differentiate from the adjacent normal spinal one vertebral segment whereas metastatic neoplasia com-
cord parenchyma. Contrast enhancement is variable, monly affects multiple vertebrae. However, involvement
but typically less than with intradural or extradural of multiple adjacent vertebrae has been reported with
neoplasia. both chondrosarcoma and osteosarcoma in dogs.7
• Another classification scheme used for spinal tumors • MRI features of malignant vertebral neoplasia include
is whether they are primary (arising from cells native (Figs. 7.6.2–7.6.5):
to the spinal, meningeal, or paraspinal tissues) or sec- • Variable degrees of bone lysis and osteoproliferation
ondary tumors (metastatic from another location in the causing alteration of the shape of the affected vertebra.
body).2
• In dogs, spinal neoplasia is most commonly extradural,
followed by intradural–extramedullary neoplasms and,
less commonly, intramedullary neoplasia:5,6
• Common extradural tumors include peripheral nerve
sheath tumors, osteosarcoma, synovial myxoma/
myxosarcoma, plasma cell tumor, lymphoma, and
metastatic neoplasia (in particular from prostatic car-
cinoma or transitional cell carcinomas of the bladder
and urethra).7 Solitary or disseminated histiocytic
sarcoma can also affect the vertebrae and cause spinal
*
cord compression.8
• Common intradural–extramedullary neoplasms
include nerve sheath tumors, meningioma, and
nephroblastoma.5
• Intramedullary tumors include ependymoma, met-
astatic neoplasia (in particular from transitional cell
carcinoma and hemangiosarcoma), and, less com-
monly, astrocytoma, nephroblastoma, chordoma, and
oligodendroglioma.6
• In cats, the most common spinal neoplasia is lym- Fig. 7.6.2 Transverse T1W post-contrast image with
phoma.9–12 Extradural and mixed extradural/intradural fat saturation at the level of C5 in a 12-year-old German
are the most common locations of spinal lymphoma in Pointer dog with a primary osteosarcoma. A lobulated
cats,9,11,13 while purely intradural (meningeal) and intra- heterogeneously contrast-enhancing mass extends dorsally
medullary locations are less common.9,11 and ventrally to the left side of the affected vertebra (solid
• In cats, aside from lymphoma, common extradural white arrows) and infiltrates the body, left pedicle, and
tumors include osteosarcoma (the second most common left transverse process (dashed white arrow), causing focal
spinal neoplasia in cats overall), fibrosarcoma, undif- disruption of the hypointense signal of the cortex along
ferentiated sarcoma, plasma cell tumors, and, less com- the left ventral aspect of the vertebral canal (black arrow).
monly, other soft tissue sarcomas, nerve sheath tumors, At this level, enhancing neoplastic tissue is seen invading
and metastatic disease. Common intradural tumors the vertebral canal and causing left ventral compression of
include meningioma and histiocytic neoplasia, while the spinal cord (asterisk). The pattern of enhancement is
intramedullary tumors include tumors of glial cell origin heterogeneous, which may reflect areas of mineralization
and primitive neuroectodermal tumors.11,12 commonly seen with osteosarcoma. (1.5T MRI system)
530 CHAPTER 7.6
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(a) (b)
(c) (d)
Fig. 7.6.3 Transverse T2W (a), T2*W gradient echo (b), and T1W pre- (c) and post-contrast (d) images at the level of C5 in a
6-year-old Dogue de Bordeaux with a primary vertebral hemangiosarcoma. On the T2W image (a), a primarily hyperintense
infiltrative mass is seen affecting the right pedicle and lamina, causing expansion of the vertebral canal with invasion by
hyperintense neoplastic tissue, which compresses the spinal cord (asterisk). Extension of T2 hyperintense neoplastic tissue
is seen around the vertebra and dorsally into the epaxial musculature, which enhances after contrast administration (dashed
arrows, a and d). Focal areas of T2 hypointensity are noted in the epidural component of the tumor, which on the T2*W
gradient echo image (b) correspond to hypointense susceptibility artifacts consistent with hemorrhage (solid arrow, b). The
mass is isointense to the spinal cord on the T1W pre-contrast image (c) and strongly contrast enhances after gadolinium
injection (d). (1.5T MRI system)
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• The MRI appearance of specific vertebral tumors

has been rarely reported. For example, chondrosar-
coma tends to form lobulated masses often in the
dorsal vertebral compartment, which are markedly
T2 hyperintense with few foci of hypointensity, iso-
to hypointense on T1W images with mild to marked
peripheral or heterogeneous contrast enhancement.14
• Vertebral lesions appearing hyperintense on T1W
and T2W images should also be evaluated with fat
suppression to differentiate bone marrow fat accu-
mulation from pathology: fat accumulation will be
suppressed on fat-suppressed pulse sequences (STIR,
fat saturation), whereas neoplastic infiltration will
remain hyperintense.3,15
Fig. 7.6.4 Sagittal T1W post-contrast with fat saturation • The MRI features of metastatic versus primary ver-
image in an 8-year-old male Border Collie dog with a
tebral neoplasia are very similar, although they are
metastatic lesion from a prostatic carcinoma at the level
poorly documented in the literature.16–18 There are
of T1. A heterogeneously hyperintense enhancing mass is
few case reports on the MRI appearance of meta-
seen infiltrating the body of T1 and extending both dorsally
static neuroendocrine tumors in dogs (a metastasized
into the vertebral canal, where it causes ventral spinal
chemodectoma and a metastasized adrenal pheo-
cord compression, as well as ventrally into the hypaxial
chromocytoma).17,18 In both cases, multiple vertebrae
musculature and soft tissues. (1.5T MRI system)
were involved with the metastatic lesions forming
intra- and perivertebral amorphous invasive tissue
• Disruption of the normally hypointense vertebral that extended into the vertebral canal, intervertebral
cortex, abnormal signal intensity of the cancellous foramina, and paravertebral musculature, causing
bone portion. variable degrees of spinal cord compression. The met-
• Periosteal reaction, forming irregular hypointense astatic tissue was iso- to hyperintense to the spinal
material surrounding the lesion. cord on T1W pre-contrast images, hyperintense to
• The signal intensity of the neoplastic lesion itself is the spinal cord on T2W images, and moderately to
very variable, ranging from iso- to hyper- or hypoin- strongly enhancing. A similar pattern of extensive and
tense on both T1W and T2W images.1 multifocal intra- and perivertebral amorphous neo-
• Contrast enhancement is also variable, although often plastic infiltrate with contrast enhancement was also
heterogeneous due to the mixture of mineralized reported with metastasized adenocarcinoma in a dog
material and soft tissue in the neoplastic mass. (Fig. 7.6.5).16
Fig. 7.6.5 Sagittal STIR image in a 6-year-old Lhasa Apso dog with a metastatic cholangiocellular carcinoma. Multiple
hyperintense lesions are visible in vertebral bodies and spinous processes at T4, L1, L2, and L3 (arrows). The lesions were also
hyperintense on T2W images (not shown) but unlike incidental fatty infiltrate, they are not suppressed on this STIR image,
indicative of pathology. The lesion at T4 causes attenuation of the bright signal from the CSF around the cord, due to vertebral
canal invasion and cord compression. The patient presented for neurologic deficits and the primary hepatic tumor was found at
necropsy. (1.5T MRI system)
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Benign vertebral tumors processes, or could evolve from hyperplastic immature

Osteochondroma spinal cartilage or from metaplastic connective tissue in
• Osteochondroma is a cartilage-capped exostosis with contact with the spine.22
a cortex and medulla that blend smoothly with those • A case of vertebral chondroma causing spinal cord com-
of the parent bone. The lesion generally arises prior to pression was reported and described as a small, well-
skeletal maturity from the metaphyseal or juxta-epiph- marginated rounded mass arising from the right caudal
yseal regions of the axial and appendicular skeleton. It articular process of C4. Compared with the spinal cord,
can be single or multiple (‘multiple cartilaginous exosto- the lesion was mildly T2 hyperintense, T1 isointense,
ses’).19,20 Common locations of these lesions include the and moderately heterogeneously enhancing on post-
long bones, ribs, and vertebrae. Malignant transforma- contrast T1W images.22 Moderate cord compression was
tion into osteosarcoma and chondrosarcoma is described associated with the mass. This pattern is somewhat sim-
with both isolated osteochondroma and multiple carti- ilar to the MRI appearance of a chondrosarcoma aris-
laginous exostoses.19 ing from the articular process of a cervical vertebra that
• Although they can be clinically silent, signs associated was reported in another dog,23 and therefore the smooth
with spinal osteochondromas may include pain and neu- margins and absence of extensive lysis may not predict
rologic deficits as a result of spinal cord compression and the benign or malignant nature of these cartilaginous
impingement of adjacent nerves.20 tumors.
• Although these lesions are usually easily recognized • In people, endplate chondromas may mimic interverte-
radiographically, they may be difficult to delineate in bral disc disease, as both could cause a ventral extradu-
regions of complex anatomy and where there is super- ral compressive lesion associated with the intervertebral
imposition of numerous structures such as in the spine. disc space. This has not been reported in dogs so far, but
MRI is then useful to evaluate the exact location/extent one would expect this confusion to be possible as well.
of the lesion, location and severity of spinal cord com- Although herniated disc material is typically T2 hypoin-
pression, and other soft tissue impingement for surgical tense, it can be hyperintense in cases of concurrent hem-
planning. orrhage and depending on the degree of pre-existing disc
• MRI features of vertebral osteochondromas include degeneration, and could conceivably appear similar to a
(Fig. 7.6.6):20 chondroma. In addition, contrast enhancement can be
• A well-defined mass arising from the surface of the seen also within herniated disc material.24
affected vertebra and of similar signal intensity to the
adjacent normal bone. Synovial myxoma/myxosarcoma
• Presence of a thin cartilaginous cap recognized as a • Tumors associated with the synovium of the spinal artic-
curvilinear T2 hyperintense, T1 iso- to hypointense ular process joints are rare.
structure conforming to the surface of the mass. • Myxoma or myxosarcoma is most common in this group
• Variable degrees of spinal cord compression or foram- of spinal tumors.25–28 These are neoplasms of fibroblast
inal impingement, depending on the location of the origin, which contain a mucinous matrix.26 Histologically,
mass. synovial myxomas appear as pale, poorly vascularized
• In people, it was shown that increased thickness of the myxoid nodules formed by stellate mesenchymal cells set
cartilaginous cap might be associated with malignant in a loose matrix of delicate collagen fibrils and a large
transformation, although this has not been demon- amount of proteoglycan, which replace the normal syno-
strated with dogs and cats. vial architecture. Once the tumor penetrates beyond the
• In a case of osteochondroma imaged with MRI,21 fibrous layer of the joint capsule, the border of the tumor
the signal pattern of the lesion was more heteroge- is indistinct, and tumor tissue extends along the fascial
neous and the cartilaginous cap was T2 hypointense; planes.25 Their growth is slow but progressive.
however, this lesion was also mixed with areas of cal- • The distinction between myxoma and myxosarcoma can
cinosis circumscripta, which may have contributed only be made with histopathology, as grossly both tumor
to the different appearance; in addition, there can be types have a similar appearance and are locally invasive.
variable degrees of mineralization of the cap as the • Dogs affected are typically adult or elderly, and present
lesion matures, which can also alter the MRI signal with progressive proprioceptive ataxia affecting the pel-
intensity. vic limbs or all four limbs depending on the location of
the tumor.
Chondroma • The MRI features of synovial myxoma/myxosarcoma
• Chondromas are rare benign tumors characterized by are similar, and include (Figs. 7.6.7, 7.6.8):25–28
the formation of mature cartilage, more common in flat • A lobulated mass associated with an articular process
bones and ribs. In the spine, they may originate from the joint, causing distortion/lysis of the adjacent articular
vertebral body, lamina, pedicles, or transverse or spinous processes and possibly widening of the joint space.
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(a) (c)
(b) (d)
Fig. 7.6.6 Transverse (a) and sagittal (b) T2W images and transverse (c) and sagittal (d) T1W images of the lumbar spine in a
2-year-old Golden Retriever with progressive chronic bilateral pelvic limb ataxia and no pain on palpation. There is a smooth
bony proliferation arising from the caudal lamina of a lumbar vertebra and impinging on the vertebral canal, causing dorsal
spinal cord compression. The mass is homogeneous and seamlessly blends with the normal bone tissue of the affected vertebra.
It has a distinct, smooth, curvilinear T2 hyperintense and T1 hypointense cap, characteristic of a cartilaginous cap seen with
osteochondromas (arrows, a and c). An osteochondroma was confirmed at histopathology. (1.5T MRI system; images courtesy
of Dr. Orima, Synergy Animal General Hospital)
• The mass typically invades into the adjacent muscles On T1W images the mass is hypointense and there
and into the vertebral canal, causing variable degrees is moderate to strong enhancement on post-contrast
of spinal cord compression. images, which can be diffuse, patchy, or rim-like.
• The mass is markedly hyperintense on T2W images, Central non-enhancing areas are common, corre-
with signal intensity similar to that of the CSF. sponding to pockets of mucinous substance.
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(a)
(b) (c)
Fig. 7.6.7 Sagittal STIR (a), transverse T2W (b), and transverse T1W post-contrast (c) images in a 2-year-old Shi Tzu with
progressive paraparesis. There is a lobulated STIR and T2W markedly hyperintense mass (arrow, a) associated with the
right articular process joint at L2-L3 (a and b), which is peripherally contrast enhancing on the T1W image after gadolinium
injection (c) with large non-enhancing central areas. The mass is causing right-sided spinal cord (asterisk, c) compression. The
appearance is typical of a synovial myxoma/myxosarcoma, which was confirmed histopathologically. (1.5T MRI system)
Fig. 7.6.8 Sagittal T2W image in a 10-year-old mixed

breed female dog with a synovial myxosarcoma at T9-T10.
A dorsally located, multilobulated, markedly T2 hyperintense
mass is seen associated with the articular processes
region, causing dorsal compression of the spinal cord.
(1.5T MRI system)
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Peripheral nerve sheath tumors

• Peripheral nerve sheath tumors (see “Intradural–
extramedullary tumors”) associated with the spine and
nerve roots can occasionally have a strict extradural
location.29
• There is a single case report of the MRI appearance of
an intraspinal, extradural benign nerve sheath tumor
(schwannoma), in which the extradural mass was located
at the level of C1 in the dorsal epidural space and caused
spinal cord compression. The mass had smooth margins,
was isointense to the cord on T1W images, hyperintense *
on T2W images, and strongly homogeneously contrast
enhancing.29
Fat containing tumors

(a)
One of the benefits of MRI is its ability to gain informa-
tion on the composition of tissues based on their MRI
signal on various pulse sequences. Adipose tissue is easily
recognized based on its homogeneous hyperintensity on
T1W and T2W images and decreased signal when fat sup-
pression techniques are used (STIR, SPAIR, fat saturation).
Therefore, MRI is useful in recognizing fat-rich neoplasms
such as infiltrative lipomas or myelolipomas.
Infiltrative lipoma
• Although histologically benign with no metastatic
potential, infiltrative lipomas are locally aggressive and
can infiltrate the surrounding normal tissues.30–34
• They are diagnosed on the basis of a histologically nor-
mal adipose tissue with microscopic and/or imaging-
based evidence of infiltration of adjacent tissue.
• When originating in a paravertebral location, these
lesions can invade the vertebral canal and cause neuro-
logic signs.
• The MRI features of infiltrative lipomas involving the
spine include (Fig. 7.6.9):31,32,34
• A paraspinal mass with rounded, lobulated or irregu-
(b)
lar margins.
• The mass is hyperintense on T1W and T2W (turbo Fig. 7.6.9 Transverse (a) and sagittal (b) T2W images in a
or fast spin echo) images with a signal intensity similar dog with progressive paraparesis. There is a large markedly
to that of normal subcutaneous fat. hyperintense lobulated mass along the left paravertebral
• Fat-suppression techniques are useful to confirm the region, causing vertebral destruction and invading into
fatty nature of these masses, as their signal is sup- the vertebral canal with resultant spinal cord compression
pressed similarly to that of normal fat.3 (asterisk, a). The mass has signal intensity similar to that
• A key feature is the local invasiveness into adja- of subcutaneous fat. This was histologically diagnosed as
cent muscles and, depending on the case, into the a lipoma, which, based on the imaging findings, is of the
vertebral canal, either through the intervertebral infiltrative type. Although not performed in this case, fat
foramina and/or through direct invasion of the ver- suppression techniques could be useful to confirm the fatty
tebrae; areas of bony lysis/invasion are typically well composition of this neoplasm. (1.5T MRI system; fig. 7.6.9a is
marginated. reproduced, with permission, from Mai W (2013). Magnetic
• There is typically no contrast enhancement, although resonance imaging and computed tomography features
mild enhancement of the muscles infiltrated by the of canine and feline spinal cord disease. In: Textbook of
mass may be present, presumably due to associated Veterinary Diagnostic Radiology, 6th edn. (ed. DE Thrall)
myositis.31 Elsevier, St. Louis, pp. 194–221.)
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Epidural myelolipoma with the spinal cord, interspersed with more hypoin-
• Myelolipoma is a benign tumor consisting of mature tense areas, conferring overall a heterogeneous
fat interspersed with myeloid and erythroid elements, appearance.
resembling bone marrow tissue.35,36 • On fat suppression pulse sequences, suppression of
• They are reported in dogs and cats in the spleen, adrenal the hyperintense signal is consistent with fatty com-
glands, and liver. Their etiology and classification into ponents within the mass.
the neoplasia group are controversial, and some consider • No contrast enhancement is noted.
them as being ectopic proliferations, hamartomas, or
choristomas.35,36 Other extradural neoplasms
• These lesions are typically asymptomatic; however, large Peripheral primitive neuroectodermal tumors
tumors may cause clinical signs as a result of the mass • Primitive neuroectodermal tumors are rare embryonal
effect. When developing adjacent to the spinal cord, they undifferentiated tumors of neural crest origin, which in
can cause neurologic deficits and pain. dogs and cats most commonly develop in the central ner-
• There are a few reports of myelolipomas in the dog in vous system (CNS), in particular the cerebellum where
an epidural location, causing spinal cord compression they are referred to as ‘medulloblastomas’ (see Chapter 5.4).
resulting in proprioceptive ataxia and spinal hyperesthe- • The ‘peripheral’ form of the disease develops outside
sia. All the dogs were older male and sled dogs (a Siberian of the CNS; other terminology found in the literature
Husky, an Alaskan Malamute, and a Husky-cross) and all includes ‘neuroblastoma’. It is derived from germinal
the lesions were in the thoracolumbar junction area.35–37 neuroepithelial cells of the neural crest that are known
• MRI features of epidural myelolipoma include to differentiate into autonomic ganglia, dorsal root gan-
(Fig. 7.6.10):35,36 glia, adrenal medulla, skin melanoblasts, and parts of
• An elongated, irregularly shaped but relatively the peripheral nervous system. As a result, these tumors
well-marginated lesion in the epidural space, causing can develop in various locations and in dogs have been
spinal cord compression. reported in the bone marrow, subcutaneous tissue
• The mass has mixed signal intensity with a bulk of T1 with visceral metastases, cranial nerves, and paraspinal
hyperintense and T2 hyperintense tissue compared location.38,39
*
*
NP
(a) (b)
Fig. 7.6.10 Transverse T1W (a) and transverse SPAIR (a fat suppressed sequence, b) images of the spine at the level of L1-L2 in
an 11.5-year-old castrated male Husky-cross dog evaluated for a 3-week history of thoracolumbar spinal hyperesthesia. There
is a well-marginated mass in the left epidural space (arrows), which has heterogeneous signal on the T1W image and suppresses
on the SPAIR image, consistent with a significant fat content. The mass is causing left-sided spinal cord compression (asterisks).
The epidural mass was diagnosed histopathologically as an epidural myelolipoma. R, right; NP, nucleus pulposus. (3.0T MRI
system; reproduced, with permission under the Creative Commons Attribution License 4.0, from Hoffmann MV, Ludwig DC,
Lempp C et al. (2013). Epidural myelolipoma in a Husky-cross: a case report. Acta Vet Scand 55:28.)
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• When developing in a paraspinal location (e.g., adrenal INTRADURAL–EXTRAMEDULLARY TUMORS

medulla, autonomic ganglia, or peripheral nerves), the
tumor can cause spinal cord compression through inva- The most common intradural–extramedullary tumors
sion into the vertebral canal.38,39 in dogs are meningiomas and peripheral nerve sheath
• Rare reports of the MRI appearance of peripheral primi- tumors.43 Nephroblastoma is a less common intradural–
tive neuroectodermal tumors are available and describe extramedullary tumor.44–50 In cats, the most common
a locally invasive mass with heterogeneous signal on intradural– extramedullary tumor is lymphoma, although
T2W and T1W images, heterogeneous or homogeneous most of these also have an extradural component.11
contrast enhancement, and extension into the vertebral
canal causing extradural spinal cord compression.38,39 Peripheral nerve sheath tumors
Abnormal signal of the vertebrae was also noted in one • Peripheral nerve sheath tumors are spindle cell tumors
case.39 that arise from Schwann cells, perineural cells, or
fibroblasts. They are divided into benign or malignant
Paraspinal invasive paragangliomas depending on morphologic features and biologic behav-
• Extra-adrenal paragangliomas include a diverse group ior. In dogs and cats, benign nerve sheath tumors are
of neuroendocrine tumors that arise from paraganglia, most commonly schwannomas. However, most canine
which are located in multiple sites in the body. nerve sheath tumors are malignant.29,51
• Paraganglia are typically (but not always)40 derived from • They can arise anywhere from the nerve roots to the
the neural crest cells, and arise in association with the most distal portions of the nerves, and for this reason
autonomic nervous system. The paraganglionic system can be found in intraspinal locations, paravertebral loca-
is made up of the adrenal medulla, chemoreceptors, vagal tions (especially at the level of the brachial plexus, see
body, and small groups of cells associated with the tho- Chapter 7.10), or in various regions of the body such as
racic, intra-abdominal, and retroperitoneal ganglia.41 the limbs or the head.
Adrenal and extra-adrenal pheochromocytomas, as well • Intraspinal peripheral nerve sheath tumors most com-
as chemodectomas, arising from aortic or pulmonary monly affect the nerve roots of the caudal cervical and
artery chemoreceptors are examples of paragangliomas; cranial thoracic spine.51 Clinical signs in that location
paragangliomas can also develop from any of the para- include lameness, muscle atrophy, pain on palpation of
ganglia in the autonomic chain.41 the axillary region, and occasionally a palpable mass in
• Paragangliomas that develop from the sympathetic para- the axillary area when the lesion is located or extends
ganglia in the mediastinum or the retroperitoneal space distally enough. When the lesion extends proximally and
may be locally invasive and extend into the vertebral causes spinal cord compression, neurologic deficits may
canal, causing extradural spinal cord compression.41 develop in the pelvic limbs as well.51
• Although a case report describes CT changes in a dog • Intraspinal peripheral nerve sheath tumors are most
with an invasive mediastinal paraganglioma causing ver- commonly found in the intradural–extramedullary
tebral lysis and vertebral canal invasion with cord com- compartment, although extension to the extradural com-
pression,41 to date their MRI appearance has not been partment is common.52 Extension into the spinal cord
reported; one would expect a similar pattern to that parenchyma is possible.
described above with paraspinal peripheral primitive • MRI features of intradural–extramedullary peripheral
neuroectodermal tumors. nerve sheath tumors include (Figs. 7.6.12, 7.6.13):
• A well-marginated mass, typically iso- to hypointense
Other paravertebral soft tissue tumors to the spinal cord on T1W images and hyperintense
• Various soft tissue tumors arising from the paraspinal to the cord on T2W images, with moderate to marked
soft tissues can secondarily invade the vertebral column contrast enhancement on T1W post-contrast images.
and ultimately the vertebral canal and cause spinal cord Contrast enhancement may be homogeneous or het-
compression or even invasion and neurologic deficits. erogeneous.1,29
• Examples include fibrosarcoma, rhabdomyosarcoma, • The combined intradural–extradural location, follow-
other soft tissue sarcomas.42 ing the proximal path of the nerve and closely associ-
• On MRI, a locally invasive mass in the paravertebral ated with the corresponding intervertebral foramen,
tissues with extension into the vertebral canal and vari- is the more common presentation.52
able degrees of vertebral destruction (disruption of the • The shape of the lesion varies but owing to its origin
hypointense cortex, abnormal intravertebral signal) and within the nerve sheath, an elongated, tubular, or
spinal cord compression will be noted. Signal intensity fusiform shape is common. The classic appearance is
will be variable, but commonly the lesions are iso- to that of a tubular mass extending from the intradural
hypointense on T1W images, hyperintense on T2W compartment across the intervertebral foramen and
images, and contrast enhancing (Fig. 7.6.11). into the paravertebral soft tissues. The lesion may be
538 CHAPTER 7.6
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(a) (b)
(c) (d)
Fig. 7.6.11 Serial transverse T1W post-contrast images of the lumbar spine in a cat with a paralumbar fibrosarcoma invading
into the vertebral canal and causing spinal cord compression (asterisk, a). An irregular mass is seen along the right side of
the lumbar spine with areas of strong enhancement and non-enhancing regions. The mass is disrupting the ventral vertebral
cortex, infiltrating the vertebra and entering the vertebral canal, causing severe right ventral spinal cord compression.
(1.5T MRI system; reproduced, with permission, from Mai W (2013). Magnetic resonance imaging and computed tomography
features of canine and feline spinal cord disease. In: Textbook of Veterinary Diagnostic Radiology, 6th edn. (ed. DE Thrall)
Elsevier, St. Louis, pp. 194–221.)
mildly constricted at the level where the nerve trav- a ‘golf-tee’ sign, similar to that observed on myelo-
erses the dura mater or where it crosses the interver- graphic images, particularly on sagittal or dorsal
tebral foramen, which may confer on the lesion a plane images depending on the location of the lesion
dumbbell appearance.2 relative to the spinal cord.
• The intradural component of the lesion causes focal
expansion of the subarachnoid space; as described Meningioma
earlier, this is more easily seen on T2W images owing • Meningioma is the most common primary CNS neo-
to the hyperintense signal of the CSF outlining the plasm affecting the spine in dogs.53 In cats it is the second
intradural mass. The focal expansion of the subarach- most common spinal tumor after lymphoma.9
noid space along the cranial and/or caudal margins • Meningiomas are slow-growing tumors of the meninges
of the intradural component of the lesion can form that cause neurologic deficits primarily by compression
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(a) (b)
(c) (d)
Fig. 7.6.12 Serial T2W (a–d) and T1W post-contrast (e–h) images at the level of C6-C7 in an 11-year-old Brussels Griffon with
a peripheral nerve sheath tumor on the left at C6-C7. The mass (asterisk, b) is isointense to the cord on T2W images and has
an intradural–extramedullary component, which causes focal expansion of the left side of the subarachnoid space immediately
cranial to the lesion; this is forming a focal T2 hyperintense and T1 hypointense crescent-shaped expansion of the CSF space
(arrows, a and e), indicative of a space occupying lesion within the left subarachnoid space. The mass then extends across the
left intervertebral foramen (extradural component). There is strong contrast enhancement (f–h) of both the intradural and
extradural components of the neoplasia. (1.5T MRI system) (Continued)
540 CHAPTER 7.6
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(e) (f)
(g) (h)
of the adjacent neural parenchyma. In the spinal loca- underlying spinal cord parenchyma thereby giving the
tion, they typically cause a chronic, progressive myelopa- impression of an intramedullary mass.53
thy with mild to moderate spinal pain.53 • The cranial cervical spine is most commonly affected
• Affected dogs are typically older (8–9 years of age) and (especially cranial to, or at the level of, C3) and, less com-
although some have reported an overrepresentation of monly, the lumbar spine; the thoracic spine is not com-
Boxers, this was never definitely demonstrated.53 monly affected.53
• Although they occasionally can grow in the epidural • Typically, a single mass is present; however, multifocal
space, most meningiomas in dogs and cats are intradural– lesions or extensive lesions encompassing numerous ver-
extramedullary lesions.54 Rarely, meningiomas arising tebral bodies have been reported.55,56
from the leptomeninges can infiltrate and efface the
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(a) (b)
Fig. 7.6.13 Transverse T2W (a), dorsal T2W (b), and

transverse T1W post-contrast (c) images in an 11-year-old
Cocker Spaniel dog with a peripheral nerve sheath tumor
of the left C4 nerve. There is an isointense to slightly
hyperintense tubular space-occupying lesion in the left
intervertebral foramen at C4-C5 (white arrowhead, a) and
atrophy with T2 hyperintense signal of the left sided epaxial
musculature (black arrowhead, a). On the dorsal image (b),
there is focal expansion of the left subarachnoid space (solid
arrow) along the cranial margin of the intradural component
of the lesion (dotted arrow) causing a golf-tee sign. On the
post-contrast image (c), there is strong enhancement of the
infiltrated nerve and the intradural component (arrow) and
patchy enhancement of the spinal cord parenchyma, which
may indicate intramedullary extension of the neoplasm. (1.5T
(c)
MRI system)
• The MRI features of spinal meningiomas include plane, creating a ‘golf tee’ sign similar to that
(Figs. 7.6.14, 7.6.15):4,52–54,57,58 observed with conventional myelography or CT
• A well-defined focal mass in the extradural–intradural myelography; heavily T2W MR pulse sequences
compartment causing variable degrees of spinal cord (‘T2-myelograms’) can be useful in recognizing
compression: this sign.4,59
– Broad-based dural margin seen on at least one of • Extension of the lesion into the adjacent intervertebral
the imaging planes. foramen along with the nerve roots can occasionally
– Gradual expansion of the subarachnoid space cra- be seen, and may mimic the appearance of a periph-
nial and caudal to the mass, which can be detected eral nerve sheath tumor.54,58
on T2W images, especially in the dorsal or sagittal
542 CHAPTER 7.6
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(a) (b)
Fig. 7.6.14 Sagittal T2-myelogram (SS-FSE, a) and T2W

(b) and T1-FLAIR post-contrast (c) images of the cranial
cervical spine in a 6-year-old dog with cervical pain due
to a meningioma. There is an intradural oval-shaped mass
in the dorsal subarachnoid space over C2 (solid arrows).
On the T2-myelogram and T2W images, widening of the
dorsal subarachnoid space cranial and caudal to the mass
is seen, forming a golf-tee sign (dashed arrows, a and b).
On the T2-myelogram the mass is creating an oval-shaped
defect in the dorsal subarachnoid space column (arrow, a).
The mass is hyperintense on the T2W image and strongly
contrast enhancing with a dural tail extending cranial and
(c)
caudal to it (dotted arrows, c).
• Location in both the intradural and extradural com- spine, with signal intensity similar to that of CSF
partments has been reported.53 (T2 hyperintense, T1 hypointense, suppressed
• The mass is usually hyperintense to the spinal cord on T2-FLAIR, and non-enhancing) has been
on T2W images or, less commonly, isointense; ill-de- reported in one case of a spinal cystic meningioma.
fined areas of spinal cord parenchyma T2 hyperinten- The myelographic and MRI appearance was simi-
sity around the margins of the mass are occasionally lar to that of a spinal arachnoid diverticulum.58
seen, and may represent edema. – Very rarely, leptomeningeal meningiomas can
• Spontaneous hyperintensity on pre-contrast T1W infiltrate and efface the underlying spinal cord
images, ranging from mild to marked, has been parenchyma and give the impression of an intra-
reported quite frequently with meningiomas53,58 medullary mass lesion (Fig. 7.6.16).53 If adjacent
and may be a distinctive feature of this tumor in meningeal enhancement is present, the appear-
dogs; however, its cause has not been elucidated ance may be confused with other neoplasms such
(Fig. 7.6.16). The lesion can also be iso- to hypoin- as histiocytic sarcoma.
tense on T1W pre-contrast images.4,52–54
• Strong, homogeneous contrast enhancement, com- Nephroblastoma
monly with a ‘dural tail’ sign, seen as strong linear • Nephroblastoma is a rare embryonic tumor arising from
enhancement of the border of the tumor confluent the primitive metanephric blastema. During embryonic
with the adjacent meninges.54 development, this tissue normally differentiates into
• Atypical presentations are possible: epithelial and stromal components to form the neph-
– A cyst-like mass lesion associated with the dor- rons and connective tissue of the kidneys. Cells that
sal subarachnoid space in the cranial cervical do not differentiate comprise the ‘nephrogenic rest’
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(a) (b)
(c) (d)
Fig. 7.6.15 Transverse (a) and dorsal (b) T2W images, transverse T1W post-contrast image (c), and dorsal T1W post-
contrast image with fat saturation (d) of the cranial thoracic spine in an 8-year-old Pug dog with progressive ataxia. There is
a well-marginated intradural–extramedullary mass, which is slightly T2 hyperintense (a, b) compared with the spinal cord,
and strongly and homogeneously contrast enhancing (c, d). On the dorsal T2W image (b), there is focal widening of the
subarachnoid space along the cranial and caudal margins of the left-sided intradural mass lesion, forming a characteristic
golf-tee sign (solid arrows). On the dorsal post-contrast image (d), there is a focal thickening/enhancement of the meninges
extending caudally from the mass lesion (dural tail sign, dotted arrow). On that image, the lesion is broad-based laterally, a
common feature of intradural lesions (in this case, a meningioma). (1.5T MRI system)
544 CHAPTER 7.6
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(a) (b)
(c) (d)
Fig. 7.6.16 Transverse T2W (a), T1W pre-contrast (b), T1W post-contrast (c), and dorsal T1W post-contrast (d) images at
the level of C1 in an 11-year-old Labrador Retriever with progressive cervical myelopathy. There is an oval-shaped mass that
appears to be intramedullary at the level of C1. The mass is eccentric and more left sided but appears to invade the spinal cord
parenchyma rather than expand the subarachnoid space. The mass is slightly hyperintense and heterogeneous on the T2W
image (a), hyperintense on the T1W pre-contrast image (b), and markedly diffusely contrast enhancing (c, d). At necropsy an
intramedullary mass was present, and histopathology diagnosed an extensive leptomeningeal intramedullary meningothelial
meningioma (grade 2). Leptomeningeal meningiomas may appear as intramedullary lesions as opposed to intradural–
extramedullary ones. The spontaneous pre-contrast T1 hyperintensity could be a clue that the lesion is of meningeal origin.
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and eventually undergo apoptosis. A nephroblastoma is • MRI features of spinal nephroblastoma include
thought to arise from neoplastic transformation of per- (Figs. 7.6.17, 7.6.18):45,47–49
sistent nephrogenic rest that did not undergo apoptosis. • A focal rounded, oval-shaped or lobulated mass in the
This can develop in the kidney itself, but also in the intradural–extramedullary compartment or, less com-
spine, when embryonic tissue becomes trapped in the monly, intramedullary location (rarely extradural).
dura during development.45,60 Spinal nephroblastomas • The mass is typically isointense to the cord on T2W
typically have histomorphometric features of malignant images or, occasionally, has a T2 heterogeneous signal
lesions, although metastatic disease is rare.45 or a T2 hyperintense peripheral rim. Areas of T2
• Spinal nephroblastoma occurs typically in young (less hyperintensity in the spinal cord parenchyma adjacent
than 3 years old) dogs. Some studies have suggested a to the mass lesion may be present, and could represent
predisposition in German Shepherd Dogs, although edema or gliosis.
other series did not observe this predisposition.44–49 • The mass is isointense to the cord on T1W images
• Dogs typically present with subacute to chronic progres- and shows moderate to strong, often homogeneous,
sive pelvic limb ataxia or paraparesis consistent with a contrast enhancement after gadolinium injection.
T3-L3 myelopathy.45 • Transverse and dorsal images typically show the
• The tumor is most commonly intradural– extramedullary peripheral location of the mass in the dural sac, often
and located consistently between T9 and L3.44,46–48,61 with a broad base towards the meninges. Widening of
However, intramedullary location is also possible,46,48,49 the subarachnoid space cranial or caudal to the mass
while extradural location is very uncommon.60 can be present and help in determining the intra-
• A single mass is usually present, although there is one dural location of the mass; however, this sign is not
case report of possible intraspinal metastases, with a clas- consistently seen and it can be difficult to determine
sic lesion in the typical T9-L3 location and an additional the intradural–extramedullary versus intramedullary
spinal lesion with less differentiated cells suggestive of origin of the mass, especially when the tumor focally
metastatic disease at T11-T12.50 invades the cord or arises from the pia mater.
(a) (b)
Fig. 7.6.17 Serial transverse T2W images (a–f) at the level of T13-L1 and dorsal post-contrast T1W image with fat saturation
(g) in a 4-year-old American Pit Bull Terrier with a nephroblastoma. On the T2W images (a–f), there is a right-sided
hyperintense mass (m in b) causing leftward displacement and compression of the spinal cord (asterisk, b). At the cranial (solid
arrow, a) and caudal (dashed arrows, e) extremities of the mass, there is focal widening of the hyperintense subarachnoid space
consistent with an intradural–extramedullary location of the mass, which was confirmed surgically. On the dorsal post-contrast
image (g) the mass is strongly enhancing and also broad-based laterally, a common feature of intradural lesions. (1.5T MRI
system) (Continued)
546 CHAPTER 7.6
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(c) (d)
(e) (f)
(g)
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(a) (b)
Fig. 7.6.18 Sagittal T2W (a), T1-FLAIR pre-contrast (b),

and T1-FLAIR post-contrast (c) images of the cranial lumbar
spine in a dog with a nephroblastoma. There is an intradural–
extramedullary, well-marginated oval-shaped mass in the
subarachnoid space (arrow, a) surrounded by hyperintense
CSF on the T2W image and hypointense (suppressed)
CSF on the T1-FLAIR images. A golf-tee sign is seen on
the margins of the lesion, characteristic of an intradural
lesion. The mass is slightly hyperintense to the spinal cord
on the T2W image (a), hypointense on the T1-FLAIR
(c) pre-contrast image (b), and markedly homogeneously
contrast enhancing (c). (1.5T MRI system; reproduced,
with permission, from Mai W (2013). Magnetic resonance imaging and computed tomography features of canine and feline
spinal cord disease. In: Textbook of Veterinary Diagnostic Radiology, 6th edn. (ed. DE Thrall) Elsevier, St. Louis, pp. 194–221.)
(Images courtesy of Dr. Shannon Holmes, University of Georgia)
• The only MRI criterion that may be associated with the lesion was strictly intradural–extramedullary or
prognosis is the location of the lesion, with intradural– intramedullary.63
extramedullary lesions having a better prognosis than • Diffuse spinal meningeal oligodendrogliomato-
intramedullary lesions.45 sis has been reported in two older Boxer dogs and a
Staffordshire Bull Terrier.64,65 This rare condition con-
Other tumors sists of extensive leptomeningeal neoplastic infiltration
• Intradural spinal metastases from intracranial cho- by oligodendroglial neoplasia with (‘secondary men-
roid plexus carcinomas have been reported in up to ingeal oligodendrogliomatosis’) or without (‘primary
19% of dogs, although their MRI appearance was not meningeal oligodendrogliomatosis’) evidence of a con-
described.62 Findings of one or several spinal intradural– current intraparenchymal oligodendroglioma. On MRI,
extramedullary mass(es) in a dog with a choroid plexus there is a regional or extensive (over the entire length of
mass lesion may raise concern for the mass to be a carci- the spinal cord), sometimes circumferential, enhancing
noma and for the spinal intradural lesion(s) to represent intradural lesion causing mild compression of the spinal
metastatic disease. cord. The leptomeningeal thickening is T2 hyperintense
• An intradural lumbosacral choroid plexus papilloma and T1 isointense, with strong and diffuse enhancement
was reported in a Shar-Pei dog, extending over the cau- on T1W post-contrast images. The appearance may be
dal lumbar and sacral area and presumed to have arisen similar to some forms of leptomeningeal histiocytic sar-
from neoplastic transformation of choroid plexus coma (see below).
metaplasia occurring from residual traces of ependy-
mal tissue or from ectopic choroid plexus remnants.63 INTRAMEDULLARY TUMORS
The tumor formed an extensive mass in the dural sac,
with areas of fluid-like signal (T2 hyperintense, T1 • Intramedullary tumors are relatively rare in dogs and
hypointense, and suppressed on T2-FLAIR) inter- cats.2 Most of them are primary neural tumors of glial
spaced with more solid regions of contrast-enhancing origin.66 Intramedullary spinal cord tumors are less
tissue, effacing the normal pattern of the nerves of the common than extradural or intradural–extramedullary
cauda equina in the area; it was not possible to tell if tumors.
548 CHAPTER 7.6
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• In dogs, intramedullary tumors account for about 15% of space +/− epidural fat at the level of the lesion, best appre-
all spinal tumors:6 ciated on T2W images, and swelling of the cord in all
• In a recent study, the most common canine primary planes, with variable amounts of intraparenchymal con-
intramedullary tumor was ependymoma, followed by trast enhancement.
astrocytoma and, less commonly, nephroblastoma, • The MRI appearance of canine intramedullary tumors
chordoma, oligodendroglioma, and teratoma.6 has been rarely reported.4,6,73–75 Some of the reported fea-
• Gliomatosis cerebri is a diffuse glial CNS neoplasia tures are described below (Figs. 7.6.19–7.6.22):
where neoplastic cells reminiscent of astrocytes, oli- • Ependymomas can form fusiform or oval-shaped,
godendrocytes, or cells with a transitional appearance focal, or multifocal lesions on sagittal images; on
insinuate among normal structures with minimal transverse images the lesions are centrally located
damage to neurons and axons. It is a widespread (due to their association with the ependymal lining
disease that frequently involves multiple divisions of the central canal) (Fig. 7.6.19).6,75 They are iso-
the CNS, including the spinal cord.67 or hypointense on T1W images, heterogeneously
• Other rare spinal cord neoplasms include:68–70 hyperintense on T2W images, with marked contrast
– Hemangioblastoma, a rare benign highly vascular enhancement, and can contain cyst-like components
CNS tumor of uncertain origin. (T2 hyperintense, T1 hypointense, non-enhancing,
– Hemangioma, a rare benign vasoproliferative or ring-enhancing).
lesion derived from endothelial cells or their pro- • Astrocytomas and oligodendrogliomas form ovoid
genitors, with various subtypes reported such or elliptical mass lesions that are well margin-
as capillary or cavernous; they can occur in any ated and located eccentrically in the spinal cord
tissue but in dogs are usually subcutaneous with on transverse images, causing variable degrees of
CNS involvement being rare. spinal cord expansion (Fig. 7.6.20). The lesions
• The most common metastatic lesions are transi- are iso- or hypointense on T1W images, hyperin-
tional cell carcinoma and hemangiosarcoma, with less tense on T2W and STIR images, with moderate
common metastatic lesions including pheochromocy- enhancement on T1W images post contrast injec-
toma, mammary/pancreatic/prostatic carcinoma, and tion. Mucinous oligodendroglioma may form exten-
sarcoma of unknown origin.6 sive lesions replacing the normal cord parenchyma;
• Although, on average, dogs with intramedullary this variant is formed of neoplastic cells separated by
neoplasia are adult or elderly, patients with primary mucin causing a discontinuous patchy enhancement
intramedullary tumors are typically younger than pattern (Fig. 7.6.21).
dogs with metastatic intramedullary tumors.6 • Metastatic transitional cell carcinoma forms
• In dogs, intramedullary tumors overall tend to be intramedullary masses that are T1 isointense, T2
more common in the T3-L3 segment, although hyperintense, with mild uniform enhancement
primary tumors tend to be more common in the cer- on T1W post-contrast images. Additional abnor-
vical spine.6 malities that may be captured in the field of view
• Dogs with intramedullary tumors typically have a (FOV) include enlargement of the caudal sublumbar
protracted clinical course, shorter in dogs with met- lymph nodes (such as the medial iliac lymph nodes),
astatic disease than in dogs with primary tumors. which appear T2 and STIR hyperintense second-
Dogs with primary intramedullary tumors typically ary to metastatic infiltration. Concurrent lytic ver-
present with myelopathic signs, which depend on tebral lesions may also be present. The appearance
the location of the lesion; myelopathic signs may or of intramedullary metastatic disease is likely varia-
may not be present in dogs with metastatic lesions, ble depending on the nature of the primary tumor
and these may also present with non-specific, non- (Fig. 7.6.22).
neurologic signs. Hyperpathia on spinal palpation is • Metastatic hemangiosarcoma is also described
commonly observed with both primary and meta- below (Spinal tumors with variable localization).
static lesions.6 It has variable signal intensity on T1W images, is
• Intramedullary neoplasia is even less common in cats, hyperintense on T2W images, with marked diffuse
and most are glial cell tumors (most commonly astro- contrast enhancement or ring-like enhancement.
cytomas, but also ependymomas and oligodendroglio- Areas of low signal secondary to hemorrhagic foci
mas).11,71,72 They seem to be more common in the cervical may be present on T2W images and T2*W images
spinal cord.11,71,72 In one study, the median age of affected (see Fig. 7.6.29).4,6,73
cats was 8 years, with most cats being 6 years or older.71 • Glioblastoma multiforme is a rare astrocytic tumor
• General MRI features of intramedullary neoplasia that most commonly affects the brain, but has been
include thinning or attenuation of the subarachnoid reported in the spinal cord of a dog.74 In that case, it
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(a) (b)
Fig. 7.6.19 Sagittal T2W (a), sagittal T1W post-contrast (b),

and transverse T2W (c) images at the level of T7 in a dog
with multisegmental ependymoma. An elongated fusiform,
intramedullary mass extends from T2 to T7 (arrows, b). On
the T2W image there are multifocal fusiform hyperintense
areas associated with the area of the central canal. A
focal markedly T2 hyperintense structure is noted at T7,
which is hypointense on the T1W image, consistent with
a cyst-like change. There is patchy contrast enhancement
around the central canal on the sagittal post-contrast
image. (Reproduced, with permission, from Pancotto TE,
Rossmeisl JH, Jr., Zimmerman K et al. (2013). Intramedullary
spinal cord neoplasia in 53 dogs (1990–2010): distribution,
clinicopathologic characteristics, and clinical behavior. J Vet
(c)
Intern Med 27(6):1500–8.)
formed multifocal lesions in the thoracolumbar spinal there is either diffuse strong contrast enhancement
cord, which were rounded, and hypo- to isointense on or rim enhancement.
T2W images with T2 hypersignal of the parenchyma • The MRI appearance of spinal cord hemangioma has
around these lesions. The lesions were isointense on been rarely reported as well:69
T1W pre-contrast images and contrast enhancing – A capillary hemangioma formed an intramed-
after gadolinium injection. ullary mass that was heterogeneous but mostly
• Gliomatosis cerebri in the spinal cord has been rarely hyperintense on T2W images, mildly hyperin-
reported, but may form an ill-defined intramedullary tense on T1W images, and with strong homoge-
expansile lesion causing attenuation of the subarach- neous contrast enhancement except for a central
noid space and epidural fat; the lesion is hyperintense area.
on T2W images and T2-FLAIR, and isointense on – A cavernous hemangioma formed a focal intra-
T1W images, with no contrast enhancement.76 Spinal medullary mass with a target-like appearance: on
cord lesions may be present even in the absence of T2W images there was a small isointense cen-
MRI abnormality.67 ter surrounded by a large hyperintense area and
• The appearance of spinal cord hemangioblas- a peripheral hypointense region, and on T1W
toma has been rarely reported.68,70 A well-defined images there was a large hypointense center sur-
intramedullary mass is seen, which is T2 hypo- or rounded by a small hyperintense periphery and a
hyperintense, and mildly hyperintense on T1W peripheral hypointense region; there was no con-
pre-contrast images. On T1W post-contrast images, trast enhancement.
550 CHAPTER 7.6
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(a) (b)
Fig. 7.6.20 Transverse T2W (a), T1W pre-contrast with fat

saturation (b), and T1W post-contrast with fat saturation
(c) images at the level of L3-L4 in a 3-year-old mixed
breed dog with a 4-month history of paraparesis. There
is an intramedullary mass invading the gray matter and
expanding peripherally into the white matter. The mass is
hyperintense on the T2W image, isointense on the T1W
image, and markedly heterogeneously contrast enhancing.
Histopathologically, the lesion was diagnosed as a pilocytic
(c)
astrocytoma. (1.5T MRI system)
• Reports of the MRI appearance of intramedullary hyperintense on T2-FLAIR images, and mild
tumors in cats are even more scarce; some features of to strong enhancement, sometimes ring-like, on
glial cell tumors include (Fig. 7.6.23):11,71,72 post-contrast T1W images.
• An intraparenchymal ovoid or elliptical mass. • Ill-defined T2 hyperintensity in the spinal cord
• Variable signal intensity: iso- to hypointense on parenchyma around the mass lesion, which may rep-
T1W images, iso- to hyperintense on T2W images, resent edema.
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(a)
(b)
(c) (d)
Fig. 7.6.21 Sagittal T2W (a) and T1W post-contrast with fat saturation (b) images of the cervicothoracic spine and transverse
T2W (c) and T2-FLAIR (d) images at the level of T1 in a 3-year-old male castrated German Shepherd Dog presented for
progressive gait abnormalities non-responsive to prednisone. A cervicothoracolumbar MRI showed an elongated severe
discontinuous contrast-enhancing space-occupying intramedullary lesion extending from C2 to T9. From C2 to the level of
the C4-C5 disc (not shown) there was an elongated T2 and T2-FLAIR hyperintensity around the central canal of the spinal
cord, which was T1 hypointense with T2-FLAIR attenuation of the central canal and no contrast enhancement. Caudal to
C4-C5, there is progressive dilation of the central canal (a, b), which at the level of C7-T1 occupies >90% of the spinal cord area
and causes swelling of the cord. The material expanding the central canal is T2 hyperintense (a, c) and does not suppress on
T2-FLAIR (d), which indicates it is not made of pure CSF. On the T1W post-contrast image (b) this material is hypointense
with patchy areas of marked contrast enhancement. At necropsy, a mucoid space-occupying infiltrative destructive process
was seen extending longitudinally in the spinal cord. Histopathology showed a mucinous oligodendroglioma. (Images courtesy
of the Clinical Radiology Department of the Vetsuisse-Faculty, Bern (Switzerland), and the Online Atlas of Domestic Animal
Neurological Pathology and MRI [http://www.vetsuisse-bern.ch/~vet-iml/lernmodule/htmls/npintro.html?neuropatho|npintro])
552 CHAPTER 7.6
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(a)
(b)
(c) (d)
Fig. 7.6.22 Sagittal T2W (a) and T1W post-contrast (b) images of the cervical spine, transverse T1W post-contrast fat
saturated image at the level of C3 (c), and dorsal T1W post-contrast image with fat saturation of the axillary region (d)
in an 11-year-old female Labrador Retriever with a mammary gland tumor, pulmonary metastases, and presented with
neurologic deficits with a C1-C5 neurolocalization. There is a metastasis in the spinal cord at the level of C3 that is rounded,
T2 heterogeneous (solid arrow, a), contrast enhancing (solid arrow, b), and with a rim-enhancement pattern on the T1W
post-contrast image with fat saturation (c). On the T2W sagittal image (a), there is a diffuse hyperintensity of the spinal
cord parenchyma extending cranial and caudal to the lesion consistent with perilesional edema. On the dorsal image across
the axillary region (d), there is marked enlargement of the right axillary lymph node (arrowhead) secondary to neoplastic
infiltration. (1.5T MRI system)
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(a) (b)
(c) (d)
Fig. 7.6.23 Transverse T2W (a) and T1W (b) images at the level of C6 and sagittal (c) and transverse (d) T1W post-contrast
images with fat saturation in a 14-year-old cat with an oligodendroglioma. There is a well-marginated intramedullary
T2 hyperintense mass (a) that is iso- to slightly hyperintense to the cord on the T1W pre-contrast image (b) and moderately
diffusely enhancing (arrows, c) (c, d). Small cyst-like changes are seen within the mass forming tiny T2 hyperintense,
T1 hypointense, non-enhancing rounded structures. (1.5T MRI system)
554 CHAPTER 7.6
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SPINAL TUMORS WITH VARIABLE LOCALIZATION They may arise from the soft tissues around the bone and
invade bone secondarily, or may grow initially within the
Histiocytic sarcoma bone marrow and extend to the cortex and adjacent soft
• Histiocytes are a category of leukocytes that have an inte- tissues. The appearance is similar to that of other aggres-
gral role in immune system function and occur in many sive vertebral neoplasia, with bone lysis and soft tissue
tissues throughout the body. They are derived from stem proliferation.
cell precursors and differentiate into cells of the mono- • Direct involvement of the CNS can occur both in the
cyte/macrophage lineage or dendritic cell lineage.77 disseminated form of histiocytic sarcoma and as an
• Histiocytic sarcoma is due to neoplastic transforma- entity isolated to the CNS (‘primary CNS histiocytic
tion of interstitial dendritic cells, with the exception of sarcoma’). In both cases, all parts of the neuraxis can be
a hematophagocytic variant, which occurs within the affected.77–79
splenic red pulp and arises from macrophages.78 • Retrievers and Pembroke Welsh Corgis may be predis-
• Canine breeds predisposed to histiocytic sarco- posed to CNS involvement with histiocytic sarcoma, with
mas include the Bernese Mountain Dog, Rottweiler, Corgis possibly predisposed to the primary CNS form.78
Golden Retriever, Flat-coated Retriever, and Labrador • Histopathologically, neoplastic infiltration in the sub-
Retriever.77 The condition is less common in cats and arachnoid space and leptomeninges with infiltration
poorly documented, although histiocytic tumors can into the white matter of the spinal cord and nerve roots
affect the spinal cord in this species as well.9,11,12 is commonly found. Meningeal infiltration is consis-
• Histiocytic sarcoma can be localized (most commonly a tently seen; even lesions that appear intramedullary on
soft tissue mass along the limbs) or disseminated, affect- MRI typically have some form of meningeal association
ing multiple organ systems including the spleen, liver, histopathologically.78,80
lungs, lymph nodes, bone marrow, and CNS.78 • MRI features of CNS histiocytic sarcoma include
• The spinal cord can be secondarily affected in histiocytic (Figs. 7.6.24, 7.6.25):77–79
sarcoma arising from a vertebra. This has been reported • Focal or multifocal intramedullary and/or intradural–
more commonly in the disseminated form than the local- extramedullary mass lesion(s), most commonly isoin-
ized form.8 Such lesions can cause extradural spinal cord tense (less commonly hypo- or hyperintense) on T1W
compression when they invade into the vertebral canal. images, hyperintense or of mixed signal intensity on
(a) (b)
Fig. 7.6.24 Sagittal T2W (a), T1W pre-contrast (b), and

T1W post-contrast (c) images of the caudal lumbar spine
in a 6-year-old male castrated Greyhound with a 4-week
history of spinal pain and paraparesis. On the T2W image,
intramedullary patchy hyperintensity is noted with partial
loss of the CSF and epidural fat signal consistent with diffuse
cord swelling. After contrast injection, diffuse meningeal
enhancement and patchy intramedullary enhancement are
noted. CSF analysis showed marked, mixed, predominantly
histiocytic inflammation with underlying neoplasia, most
likely histiocytic sarcoma. At necropsy, infiltration of
the meninges, subarachnoid space, and spinal cord with
(c)
histiocytic sarcoma was confirmed. (1.5T MRI system;
reproduced, with permission, from Tzipory L, Vernau KM, Sturges BK et al. (2009). Antemortem diagnosis of localized
central nervous system histiocytic sarcoma in 2 dogs. J Vet Intern Med 23(2):369–74.)
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(a) (b)
(c) (d)
Fig. 7.6.25 Transverse T2W (a), T2-FLAIR (b), and T1W post-contrast (c) images at the level of caudal T11 and transverse
T2W (d), T1W pre- (e), and post-contrast (f) images at the level of T12-T13 in a 6-year-old Rhodesian Ridgeback with spinal
histiocytic sarcoma. There are multifocal areas of the spinal cord that are T2W hyperintense (a, d) and T1W isointense (e) with
mild to moderate contrast enhancement (f). The subarachnoid space has normal T1 hypointensity (e) and T2 hyperintensity (a,
d); however, it fails to suppress on the T2-FLAIR (b), and on the T1W post-contrast images (c, f) the meninges/subarachnoid
space are diffusely homogeneously contrast enhancing; these changes suggest meningeal thickening and subarachnoid space
invasion by abnormal tissue. (Continued)
556 CHAPTER 7.6
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(e) (f)
T2W images, hyperintense on STIR, with moderate whether neoplastic lymphocytes are or are not identi-
to marked contrast enhancement after gadolinium fied in other organ systems, respectively. Clinical signs
injection. depend on the distribution of the lesions in the CNS
• Ill-defined diffuse intramedullary T2 hyperintensity and on the presence and extent of other organ system
with loss of the epidural fat and gray/white matter involvement.
definition, moderate parenchymal contrast enhance- • In cats, lymphoma is the most common tumor affect-
ment after gadolinium injection, and mild diffuse ing the spine.11,12 Affected cats are typically young, with
meningeal enhancement. short duration of clinical signs.9,11,13 The most common
• Meningeal enhancement in the vicinity of focal mass location of spinal lymphoma in cats is extradural or
lesions, sometimes with a dural tail sign. mixed extra- and intradural (affecting the leptomeninges
• Meningeal enhancement often extends over long and/or the spinal cord).11,13 Exclusive intradural location
distances from the mass lesion, and isolated areas of is rare.11 Extramedullary hematopoietic tissue has been
meningeal enhancement distant and separate from cited as the possible tissue of origin for the development
the mass lesion are also possible, suggestive of met- of primary lymphoma of the spine.13 Involvement of other
astatic spread of the condition through the subarach- organ systems is common in cats with spinal lymphoma,
noid space. with bone marrow and kidneys being more commonly
• In some cases, the only abnormality may be menin- affected.9,11,13 In some reported case series, affected cats
geal enhancement without a mass lesion (‘leptomenin- had lesions in multiple regions of the CNS including the
geal histiocytic sarcoma’). brain,11 while in other series, single epidural lesions were
• MRI features of spinal histiocytic sarcoma, such more common.13
as focal mass lesions, meningeal thickening, and • Lymphoma is one of the most common neoplasms in
enhancement, can also be seen with other neoplasms the dog, and the multicentric form accounts for about
such as lymphoma or rare tumors such as meningeal 80% of cases. In this species, lymphoma can affect the
oligodendrogliomatosis, and are therefore non-spe- epidural tissues of the vertebral canal, vertebrae, nerve
cific. Intradural–extramedullary masses with dural roots, paraspinal soft tissues, and, less commonly,
tail can also be seen with meningioma. the spinal cord (although the spinal cord is commonly
affected secondary to compression by extradural neo-
Lymphoma plastic infiltrates).4,81–88
• In both dogs and cats, lymphoma can involve many tis- • MRI features of lymphoma affecting the spine in dogs
sues outside of the lymphatic system, including the CNS. include (Figs. 7.6.26–7.6.28):
Spinal lymphoma can be secondary or primary, based on • Multifocal disease more common than focal disease.81
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(a) (b)
Fig. 7.6.26 Sagittal T2W (a) and STIR (b) images of the cervical spine in a 7-year-old spayed female mixed breed dog with a
1-week history of progressive cervical pain and tetraparesis. There is a focal, fairly distinctly marginated and homogeneous T2
and STIR hyperintense lesion of the 5th cervical vertebra affecting the medullary cavity, vertebral canal, and paraspinal soft
tissues (arrows). The lesion is causing ventral spinal cord compression. (1.5T MRI system) Ultrasound-guided aspirates of the
liver, kidney, and spleen showed lymphoma. (Reproduced, with permission, from Allett B, Hecht S (2016). Magnetic resonance
imaging findings in the spine of six dogs diagnosed with lymphoma. Vet Radiol Ultrasound 57(2):154–61.)
(a) (b)
Fig. 7.6.27 Transverse T2W (a) and T1W post-

contrast (b) images at the level of cranial C4 and
sagittal T2W image (c) in a 10-year-old Bulldog
with lymphoma diagnosed in the spleen through
fine-needle aspirates. CSF analysis showed severe
lymphocytic pleocytosis consistent with lymphoma.
There are patchy multifocal T2 hyperintensities
within the spinal cord parenchyma (c), and irregular
isointense slightly heterogeneous areas of infiltration
of the cord are noted on the T2W image (a, especially
in the dorsal aspect of the cord), which show moderate
(c)
contrast enhancement (b). (1.5T MRI system)
558 CHAPTER 7.6
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(a) (b)
Fig. 7.6.28 Transverse T2W (a), STIR (b), and T1W

post-contrast with fat saturation (c) images at the level of
L5-L6 in a dog with large cell lymphoma in the sacral and
paralumbar area. Multifocal patchy T2 (a) and STIR (b)
hyperintense areas are seen in the paravertebral muscles,
infiltrating the vertebral canal through the intervertebral
foramina and causing dorsal compression of the spinal
cord (asterisk, a). This abnormal tissue is moderately
heterogeneously enhancing on the post-contrast image (c).
(c)
(1.5T MRI system)
• Common simultaneous regional involvement of mul- lesions can be hyperintense on T1W pre-contrast
tiple compartments (vertebrae, paraspinal soft tissues, images.4,88 Heterogeneous signal on T2W images,
epidural space).81,83,86,88 The paraspinal lesions are with hypo- and hyperintense areas, is also reported,86
often ill defined. The vertebral canal and paraspinal as well as isointensity to surrounding muscles.4
components may be seen to communicate through the • Visible vertebral lesions can involve none, one,
intervertebral foramina. several, or all vertebrae, and consist of patchy hyper-
• Variable degrees of spinal cord compression by the intense areas on T2W images, which, unlike fat,
epidural component of the neoplasm.81,86,88 remain hyperintense on STIR images. In one series,
• Signal characteristics are similar for the lesions in the vertebral cortical involvement was not observed,
paraspinal and vertebral canal areas, being T1 iso- to even when paravertebral and epidural infiltration
hypointense, T2 and STIR hyperintense, moderately around the affected vertebrae was present;81 however,
to strongly contrast enhancing.81 In some cases, the other reports have described changes in the shape of
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the affected vertebra with cortical involvement, seen Meningioangiomatosis

as T2W and STIR hyperintense signal with enhance- • Meningioangiomatosis is not a true neoplasm but a rare,
ment on T1W post-contrast images, disrupting the tumor-like, benign focal lesion of the leptomeninges and
normal hypointense signal of the cortex.83 Cortical underlying neural parenchyma, characterized by lepto-
involvement has also been reported in pathologic meningeal and meningovascular proliferation. Grossly,
studies.84 there is a visible plaque composed of proliferative menin-
• Visible vertebral bone marrow involvement on MRI is gothelial or fibroblastic spindle-shaped cells that extends
not necessarily present, even in cases of simultaneous from the subarachnoid space along the perivascular
paravertebral and epidural infiltration.86,88 Depending spaces into the adjacent parenchyma.91
on the cellularity of the infiltrate, vertebral bone • Its origin is unknown and it has been classified as a ham-
marrow involvement with lymphoma may be present artomatous proliferation of meningothelial cells, blood
even in the absence of changes in MRI signal, includ- vessels, and fibroblasts in variable proportion. Others
ing on fat suppressed images.89 have considered it to represent a vascular malformation
• Leptomeningeal involvement with enhancement on that induces perivascular meningothelial proliferation of
post-contrast images is also reported,87 as well as cells from vessel walls or from pluripotent arachnoid cap
involvement of the nerve roots and spinal cord paren- cells in Virchow–Robin spaces.91
chyma.85 • Affected animals are typically juvenile or young adults,
• Additional lesions that can be seen in the FOV include although presentation at an older age is also possible.91,92
lymphadenopathy, hepatomegaly, splenomegaly, and • Although lesions of meningioangiomatosis are more
splenic nodules. commonly reported in the brain, particularly the brain-
• The MRI appearance of feline spinal lymphoma is not stem,91–93 there are reports of lesions in the cervical and
very well documented.87 Both intradural and extradural thoracic spine.91,92
lesions have been reported, which were hypointense on • MRI features of the lesions are variable, but typically a
T1W images, hyperintense on T2W images, with homo- focal parenchymal lesion with an intramedullary pattern
geneous enhancement on post-contrast T1W images.87 close to or extending to the meningeal surface is noted.
Another study where MRI was used reported intramed- The reported spinal cord lesion on MRI was hypointense
ullary location of lymphoma in just under half the cases with peripheral hyperintensity on T2W images, mildly
of spinal lymphoma, although it did not describe details hyperintense on T1W pre-contrast images, and contrast
of the MRI appearance.10 A pathologic study reports that enhancing after gadolinium injection. As in people, the
feline spinal lymphoma often affects multiple areas of the T2W hypointense area corresponded to areas of dense
spine and often involves extra- and intradural structures collagen,91 while the peripheral T2 hyperintense regions
of the vertebral canal simultaneously, including the spi- may have represented edema or gliosis.
nal cord parenchyma and nerve roots.12 There are also
reports on specific infiltration of the nerves of the bra- Hemangiosarcoma
chial plexus, forming mass-like lesions of the affected • Hemangiosarcoma is a malignant neoplasm of vascular
plexus, resembling a peripheral nerve sheath tumor and endothelial origin and can arise from any vascular tissue.
extending into the subarachnoid space and spinal cord • Spinal hemangiosarcoma has been reported in dogs,
parenchyma proximally.13,90 The MRI appearance of in both intramedullary4,6,73 and extradural locations.
these lesions has not been reported, but this should be The extradural form can arise from the vertebrae,94,95
kept in mind when identifying mass-like lesions infiltrat- accounting for approximately 2%–3% of primary bone
ing the brachial plexus and extending into the vertebral tumors of the vertebral column in dogs (Fig. 7.6.3).
canal in cats. Rarely, hemangiosarcoma can affect the epidural
• Atypical forms of lymphoma affecting the CNS, includ- space.96,97 Intramedullary hemangiosarcoma is usually
ing the spinal cord, have been reported. Intravascular metastatic,6,73 while the vertebral and the rare epidural
lymphoma is a proliferation of neoplastic lymphocytes form are typically primary tumors.
within the lumen and wall of blood vessels and has been • MRI features of primary vertebral hemangiosarcoma
reported in both dogs and cats. The progressive occlu- have not been reported but one would expect them to
sion of blood vessels with neoplastic cells leads to throm- have a similar appearance to other primary bone tumors,
bosis, hemorrhage, and infarction. It is most common in with a predominantly lytic pattern as described radio-
middle aged, large-breed dogs, and rare in cats. In dogs, graphically.94,95 T2*W gradient echo images may show
there is a propensity for this form of lymphoma to affect prominent signal voids due to susceptibility artifacts
the CNS and lungs. Progression is rapid and often fatal. associated with hemorrhagic changes, which are com-
On MRI, T2 hyperintense foci in the brain and spinal mon with this highly vascular tumor (Fig. 7.6.3).
cord are seen, with parenchymal lesions and meningeal • MRI features of epidural or intramedullary hemangio-
enhancement.82 sarcoma include (Figs. 7.6.29. 7.6.30):4,6,73,96,97
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(b)
Fig. 7.6.29 Transverse T2*W gradient echo image (a) and
sagittal T1W post-contrast image (b) of the thoracic spine
in a German Shepherd Dog presented with a several-month
history of lameness and a 2-day history of pelvic limb
paralysis. There is a focal susceptibility artifact in the spinal
cord (arrow, a), with patchy intramedullary enhancement
(a) on the post-contrast image (arrow, b). Necropsy revealed
right atrial hemangiosarcoma with numerous splenic and
pulmonary metastases. The spinal cord lesion was identified histopathologically as hemorrhagic myelomalacia and metastatic
hemangiosarcoma. (Reproduced, with permission, from Hammond LJ, Hecht S (2015). Susceptibility artifacts on T2*-weighted
magnetic resonance imaging of the canine and feline spine. Vet Radiol Ultrasound 56(4):398–406.)
• A focal mass lesion, usually well defined, that is either vertebrae rather than the CNS itself, they can also affect
in the epidural location, causing spinal cord compres- the epidural or intramedullary areas. They most com-
sion, or intramedullary. monly involve the cranial and caudal extremities of the
• Epidural lesions are isolated (primary tumor) while axial skeleton.98–101
intramedullary lesions, being metastatic, can be mul- • They have been reported to metastasize in a cat but not
tifocal.6 in dogs.98
• The signal of the mass is typically hyperintense to • There are few case reports of chordoma affecting the
normal spinal cord parenchyma on T2W images spine, although a succinct MRI description is only
(homogeneous or heterogeneous), hyperintense on available for one of them, in which an ill-defined focal
STIR images, isointense to hyperintense on T1W area of parenchymal hyperintensity was seen on T2W
pre-contrast images, and moderately to strongly con- images dorsal to an intervertebral disc space, and ini-
trast enhancing (sometimes rim-like). tially interpreted as an acute non-compressive hydrated
• Signal voids associated with hemorrhage can be seen nucleus pulposus extrusion.98 No information regard-
within the lesion on T2*W gradient echo images.73 ing signal characteristics on T1W images and on post-
The spontaneous hyperintensity on T1W images may contrast series was provided. Other reports using CT
also reflect the presence of blood degradation prod- describe extradural masses, often with amorphous min-
ucts. eralization causing compression of the spinal cord, or
intramedullary masses with areas of mineralization.
Chordoma Focal destruction of the adjacent vertebral tissue is
• Chordomas are slow growing, locally destructive tumors reported.99–101
arising in the cerebrospinal axis from remnants or
derivatives of the notochord. In higher vertebrates, the Plasma cell tumor
nucleus pulposus is believed to be the only derivative • Plasma cell tumors represent monoclonal proliferations
of notochordal tissue; however, remnants of notochord of cells of the B-lymphocyte lineage. They include soli-
may persist outside of the intervertebral discs anywhere tary osseous plasmacytoma, extramedullary plasmacy-
along the vertebral column. As a result, although they toma (i.e., outside of the bone marrow), and multiple
are more commonly extradural tumors affecting the myeloma.
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(a) (b)
(c) (d)
Fig. 7.6.30 Sagittal STIR (a), transverse T2W (b), and T1W pre-contrast (c) and post-contrast (d) images at the level of
T11 in an 8-year-old male Boxer presented for acutely progressive pelvic limb weakness of 2 days’ duration. There is a left
dorsal extradural mass lesion (asterisks) that is hyperintense on the T2W and STIR images (a, b), mildly hyperintense on
the T1W pre-contrast image (c), and strongly contrast enhancing (d). At necropsy, a well-defined, reddish, friable epidural
mass was present on the left side of the vertebral canal from T10 to T13, and histopathology showed a primary epidural
hemangiosarcoma. (0.2T MRI system; reproduced, with permission, from de la Fuente C, Pumarola M, Anor S (2014). Imaging
diagnosis – spinal epidural hemangiosarcoma in a dog. Vet Radiol Ultrasound 55(4):424–7.)
• Multiple myeloma can cause multifocal lytic lesions with These tumors are typically recognized radiographically
a characteristic punched-out appearance involving multi- and not imaged with MRI.
ple bones including the vertebrae. These can secondarily • The MRI appearance of plasma cell tumors is not well
affect the spinal cord when there is a pathologic fracture documented and has only been reported in a few cats.
of an affected vertebra causing spinal cord compression. In one case, which was part of a larger series of tumors
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5. Levy MS, Kapatkin AS, Patnaik AK et al. (1997). Spinal

tumors in 37 dogs: clinical outcome and long-term survival
(1987–1994). J Am Anim Hosp Assoc 33(4):307–12.
6. Pancotto TE, Rossmeisl JH, Jr., Zimmerman K et al. (2013).
Intramedullary spinal cord neoplasia in 53 dogs (1990–2010):
distribution, clinicopathologic characteristics, and clinical
behavior. J Vet Intern Med 27(6):1500–8.
7. Morgan JP, Med V, Ackerman N et al. (1980). Vertebral
tumors in the dog: a clinical, radiologic, and pathologic study
of 61 primary and secondary lesions. Vet Radiol 21(5):197–212.
* 8. Schultz RM, Puchalski SM, Kent M et al. (2007). Skeletal
lesions of histiocytic sarcoma in nineteen dogs. Vet Radiol
9. Bradshaw JM, Pearson GR, Gruffydd-Jones TJ (2004).
A retrospective study of 286 cases of neurological disorders of
the cat. J Comp Pathol 131(2-3):112–20.
10. Goncalves R, Platt SR, Llabres-Diaz FJ et al. (2009).
Clinical and magnetic resonance imaging findings in 92 cats
with clinical signs of spinal cord disease. J Feline Med Surg
11(2):53–9.
11. Marioni-Henry K, Van Winkle TJ, Smith SH et al. (2008).
Tumors affecting the spinal cord of cats: 85 cases (1980–2005).
J Am Vet Med Assoc 232(2):237–43.
Fig. 7.6.31 Transverse T1W post-contrast image at the level 12. Marioni-Henry K, Vite CH, Newton AL et al. (2004).
Prevalence of diseases of the spinal cord of cats. J Vet Intern
of C4 in a 10-year-old male mixed breed dog with a plasma
Med 18(6):851–8.
cell tumor. There is a contrast-enhancing, irregular mass 13. Lane SB, Kornegay JN, Duncan JR et al. (1994). Feline spinal
infiltrating the paravertebral soft tissues along the right lymphosarcoma: a retrospective evaluation of 23 cats. J Vet
pedicle, causing lysis/infiltration of the right pedicle and Intern Med 8(2):99–104.
part of the lamina, and entering the vertebral canal where it 14. Roynard PF, Bilderback A, Falzone C et al. (2016). Magnetic
causes right-sided spinal cord compression. The spinal cord is resonance imaging, treatment and outcome of canine vertebral
labeled with an asterisk. (1.5T MRI system) chondrosarcomas. Six cases. J Small Anim Pract 57(11):610–6.
15. Dennis R (2011). Optimal magnetic resonance imaging of the
affecting the spine in cats, the MRI appearance was spine. Vet Radiol Ultrasound 52:S72–S80.
reportedly normal.11 In another cat, which had a radio- 16. Besalti O, Caliskan M, Can P et al. (2015). Imaging and
surgical outcomes of spinal tumors in 18 dogs and one cat.
graphically visible subtle lytic lesion of the body of L5,
J Vet Sci 17(2):225–34.
an ill-defined focally invasive lesion was seen on MRI 17. Naude SH, Miller DB (2006). Magnetic resonance imaging
around the L5 region affecting the paraspinal muscles, findings of a metastatic chemodectoma in a dog. J S Afr Vet
nerve roots, and epidural space +/− the meninges.102 The Assoc 77(3):155–9.
lesion was hyperintense on T2W and STIR images, 18. Spall B, Chen AV, Tucker RL et al. (2011). Imaging diagnosis –
isointense on T1W pre-contrast images, and enhanced metastatic adrenal pheochromocytoma in a dog. Vet Radiol
after gadolinium injection. The radiographically visible Ultrasound 52(5):534–7.
lytic lesion at L5 was seen as a hyperintense focus in the 19. Green EM, Adams WM, Steinberg H (1999). Malignant
vertebra on STIR images. This pattern is similar to what transformation of solitary spinal osteochondroma in two
mature dogs. Vet Radiol Ultrasound 40(6):634–7.
has been reported in dogs with spinal lymphoma (see
20. Silver GM, Bagley RS, Gavin PR et al. (2001). Radiographic
above) (Fig. 7.6.31). diagnosis: cartilaginous exostoses in a dog. Vet Radiol
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25. Blair WH, Levine JM, Kerwin SC et al. (2011). Imaging 46. Macri NP, Van Alstine W, Coolman RA (1997). Canine spinal
diagnosis – synovial myxoma of lumbar vertebrae articular nephroblastoma. J Am Anim Hosp Assoc 33(4):302–6.
process joint. Vet Radiol Ultrasound 52(3):309–12. 47. McConnell JF, Garosi LS, Dennis R et al. (2003). Imaging
26. Khachatryan AR, Wills TB, Potter KA (2009). What is your of a spinal nephroblastoma in a dog. Vet Radiol Ultrasound
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257–60. 48. Nakade T, Inoue A, Shimazaki H et al. (2006). Spinal
27. Kunkel KA, Palmisano MP, Stefanacci JD (2007). Imaging nephroblastoma in a miniature Dachshund. J Vet Med Sci
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48(6):557–9. 49. Sale CS, Skerritt GC, Smith KC (2004). Spinal
28. Neary CP, Bush WW, Tiches DM et al. (2014). Synovial nephroblastoma in a crossbreed dog. J Small Anim Pract
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and surgical removal. J Am Anim Hosp Assoc 50(3):198–202. 50. Terrell SP, Platt SR, Chrisman CL et al. (2000). Possible
29. Oliveira M, De La Fuente C, Pumarola M et al. (2014). intraspinal metastasis of a canine spinal cord nephroblastoma.
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30. Agut A, Anson A, Navarro A et al. (2013). Imaging resonance imaging and ultrasonography in the diagnosis of a
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lumbar nerve root compression in a dog. Vet Radiol Ultrasound 40(4):367–71.
Ultrasound 54(4):381–3. 52. Levitski RE, Lipsitz D, Chauvet AE (1999). Magnetic
31. Hobert MK, Brauer C, Dziallas P et al. (2013). Infiltrative resonance imaging of the cervical spine in 27 dogs. Vet Radiol
lipoma compressing the spinal cord in 2 large-breed dogs. Ultrasound 40(4):332–41.
Can Vet J 54(1):74–8. 53. Petersen SA, Sturges BK, Dickinson PJ et al. (2008). Canine
32. Kim HJ, Chang HS, Choi CB et al. (2005). Infiltrative lipoma intraspinal meningiomas: imaging features, histopathologic
in cervical bones in a dog. J Vet Med Sci 67(10):1043–6. classification, and long-term outcome in 34 dogs. J Vet Intern
33. McEntee MC, Thrall DE (2001). Computed tomographic Med 22(4):946–53.
imaging of infiltrative lipoma in 22 dogs. Vet Radiol Ultrasound 54. McDonnell JJ, Tidwell AS, Faissler D et al. (2005).
42(3):221–5. Magnetic resonance imaging features of cervical spinal cord
34. Morgan LW, Toal R, Siemering G et al. (2007). Imaging meningiomas. Vet Radiol Ultrasound 46(5):368–74.
diagnosis – infiltrative lipoma causing spinal cord compression 55. Wall M, Platt S, Selcer B et al. (2005). Multifocal spinal papillary
in a dog. Vet Radiol Ultrasound 48(1):35–7. meningioma in a dog. Vet Radiol Ultrasound 46(4):309–12.
35. Hoffmann MV, Ludwig DC, Lempp C et al. (2013). Epidural 56. Yeomans SM (2000). Short paper – extensive spinal
myelolipoma in a Husky-cross: a case report. Acta Vet Scand meningioma in a young dog. J Comp Pathol 122(4):303–6.
55:28. 57. Asperio RM, Marzola P, Zibellini E et al. (1999). Use of
36. Ueno H, Miyake T, Kobayashi Y et al. (2007). Epidural spinal magnetic resonance imaging for diagnosis of a spinal tumor in
myelolipoma in a dog. J Am Anim Hosp Assoc 43(2):132–5. a cat. Vet Radiol Ultrasound 40(3):267–70.
37. Newman SJ, Inzana K, Chickering W (2000). Extradural 58. Jose-Lopez R, de la Fuente C, Pumarola M et al. (2013).
myelolipoma in a dog. J Vet Diagn Invest 12(1):71–4. Spinal meningiomas in dogs: description of 8 cases including a
38. Gains MJ, Leclerc MK, Bedard C (2011). novel radiological and histopathological presentation. Can Vet
A primitive neuroectodermal tumor with extension into the J 54(10):948–54.
cranial vault in a dog. Can Vet J 52(11):1232–6. 59. Pease A, Sullivan S, Olby N et al. (2006). Value of a single-shot
39. Junginger J, Rothlisberger A, Lehmbecker A et al. (2013). turbo spin-echo pulse sequence for assessing the architecture
Peripheral primitive neuroectodermal tumour in a dog. of the subarachnoid space and the constitutive nature of
J Comp Pathol 149(4):424–8. cerebrospinal fluid. Vet Radiol Ultrasound 47(3):254–9.
40. DeLellis RA (2001). The neuroendocrine system and its 60. Gasser AM, Bush WW, Smith S et al. (2003). Extradural
tumors: an overview. Am J Clin Pathol 115 Suppl:S5–16. spinal, bone marrow, and renal nephroblastoma. J Am Anim
41. Rizzo SA, Newman SJ, Hecht S et al. (2008). Malignant Hosp Assoc 39(1):80–5.
mediastinal extra-adrenal paraganglioma with spinal cord 61. Sale CS, Smith KC (2007). Extradural spinal juxtafacet
invasion in a dog. J Vet Diagn Invest 20(3):372–5. (synovial) cysts in three dogs. J Small Anim Pract 48(2):116–9.
42. Chang HW, Ho SY, Lo HF et al. (2006). Vaccine-associated 62. Westworth DR, Dickinson PJ, Vernau W et al. (2008).
rhabdomyosarcoma with spinal epidural invasion and Choroid plexus tumors in 56 dogs (1985–2007). J Vet Intern
pulmonary metastasis in a cat. Vet Pathol 43(1):55–8. Med 22(5):1157–65.
43. Wheeler SJ, Sharp NJH (1995). Neurological deficits in 63. Giannuzzi AP, Gernone F, Ricciardi M et al. (2013). A sacro-
multiple limbs: spinal disorders. In: Manual of Small Animal caudal spinal cord choroid plexus papilloma in a shar-pei dog.
Neurology, 2nd edn. (ed. SJ Wheeler) British Small Animal J Small Anim Pract 54(10):551–4.
Veterinary Association, Cheltenham pp. 143–58. 64. Kovi RC, Wunschmann A, Armien AG et al. (2013). Spinal
44. Brewer DM, Cerda-Gonzalez S, Dewey CW et al. (2011). meningeal oligodendrogliomatosis in two boxer dogs.
Spinal cord nephroblastoma in dogs: 11 cases (1985–2007). Vet Pathol 50(5):761–4.
J Am Vet Med Assoc 238(5):618–24. 65. Lobacz MA, Serra F, Hammond G et al. (2016). Imaging
45. Liebel FX, Rossmeisl JH Jr., Lanz OI et al. (2011). Canine diagnosis – magnetic resonance imaging of diffuse
spinal nephroblastoma: long-term outcomes associated with leptomeningeal oligodendrogliomatosis in a dog with “dural
treatment of 10 cases (1996–2009). Vet Surg 40(2):244–52. tail sign”. Vet Radiol Ultrasound 59(1):E1–6.
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66. Jeffery ND, Phillips SM (1995). Surgical treatment of 85. Long SN, Johnston PE, Anderson TJ (2001). Primary T-cell
intramedullary spinal cord neoplasia in two dogs. J Small lymphoma of the central nervous system in a dog. J Am Vet
Anim Pract 36(12):553–7. Med Assoc 218(5):719–22.
67. Bentley RT, Burcham GN, Heng HG et al. (2016). 86. Ortega M, Castillo-Alcala F (2010). Hind-limb paresis in a
A comparison of clinical, magnetic resonance imaging and dog with paralumbar solitary T-cell lymphoma. Can Vet J
pathological findings in dogs with gliomatosis cerebri, 51(5):480–4.
focusing on cases with minimal magnetic resonance imaging 87. Palus V, Volk HA, Lamb CR et al. (2012). MRI features
changes. Vet Comp Oncol 14(3):318–30. of CNS lymphoma in dogs and cats. Vet Radiol Ultrasound
68. Cantile C, Baroni M, Tartarelli CL et al. (2003). Intramedullary 53(1):44–9.
hemangioblastoma in a dog. Vet Pathol 40(1):91–4. 88. Veraa S, Dijkman R, Meij BP et al. (2010). Comparative
69. Jull P, Walmsley GL, Benigni L et al. (2011). Imaging imaging of spinal extradural lymphoma in a Bordeaux dog.
diagnosis – spinal cord hemangioma in two dogs. Vet Radiol Can Vet J 51(5):519–21.
Ultrasound 52(6):653–7. 89. Feeney DA, Sharkey LC, Steward SM et al. (2013).
70. Michaels J, Thomas W, Ferguson S et al. (2015). Clinical Applicability of 3T body MRI in assessment of nonfocal bone
features of spinal cord hemangioblastoma in a dog. Front Vet marrow involvement of hematopoietic neoplasia in dogs.
Sci 2:39. J Vet Intern Med 27(5):1165–71.
71. Hammond JJ, deLahunta A, Glass EN et al. (2014). Feline 90. Linzmann H, Brunnberg L, Gruber AD et al. (2009).
spinal cord gliomas: clinicopathologic and diagnostic features A neurotropic lymphoma in the brachial plexus of a cat.
of seven cases. J Vet Diagn Invest 26(4):513–20. J Feline Med Surg 11(6):522–4.
72. Tamura S, Hori Y, Tamura Y et al. (2013). Long-term 91. Goncalves R, Johnston P, Wessmann A et al. (2010). Imaging
follow-up of surgical treatment of spinal anaplastic diagnosis – canine meningioangiomatosis. Vet Radiol
astrocytoma in a cat. J Feline Med Surg 15(10):921–6. Ultrasound 51(2):148–51.
73. Hammond LJ, Hecht S (2015). Susceptibility artifacts on 92. Bishop TM, Morrison J, Summers BA et al. (2004).
T2*-weighted magnetic resonance imaging of the canine and Meningioangiomatosis in young dogs: a case series and
feline spine. Vet Radiol Ultrasound 56(4):398–406. literature review. J Vet Intern Med 18(4):522–8.
74. Rothlisberger A, Lehmbecker A, Beineke A et al. (2012). 93. Lorenzo V, Pumarola M, Munoz A (1998).
Suspected primary glioblastoma multiforme in the canine Meningioangiomatosis in a dog: magnetic resonance
spinal cord. J Small Anim Pract 53(10):604–7. imaging and neuropathological studies. J Small Anim Pract
75. Ueno H, Morimoto M, Kobayashi Y et al. (2006). Surgical 39(10):486–9.
and radiotherapy treatment of a spinal cord ependymoma in a 94. Mackenzie GB, Bellah JR, Threatte RM (2003). What is your
dog. Aust Vet J 84(1-2):36–9. diagnosis? Hemangiosarcoma of the cervical vertebrae. J Am
76. Plattner BL, Kent M, Summers B et al. (2012). Gliomatosis Vet Med Assoc 222(8):1075–6.
cerebri in two dogs. J Am Anim Hosp Assoc 48(5):359–65. 95. Reed AL, Payne JT, Aronson E (1994). What is your
77. Taylor A, Eichelberger B, Hodo C et al. (2015). Imaging diagnosis? Primary hemangiosarcoma of the sixth lumbar
diagnosis – spinal cord histiocytic sarcoma in a dog. Vet Radiol vertebra in a dog. J Am Vet Med Assoc 204(11):1749–50.
Ultrasound 56(2):E17–20. 96. de la Fuente C, Pumarola M, Anor S (2014). Imaging
78. Mariani CL, Jennings MK, Olby NJ et al. (2015). Histiocytic diagnosis – spinal epidural hemangiosarcoma in a dog.
sarcoma with central nervous system involvement in dogs: 19 Vet Radiol Ultrasound 55(4):424–7.
cases (2006–2012). J Vet Intern Med 29(2):607–13. 97. Paek M, Glass E, Kent M et al. (2015). Primary lumbar
79. Tzipory L, Vernau KM, Sturges BK et al. (2009). extradural hemangiosarcoma in a dog. J Am Anim Hosp Assoc
Antemortem diagnosis of localized central nervous system 51(3):191–6.
histiocytic sarcoma in 2 dogs. J Vet Intern Med 23(2):369–74. 98. Gruber A, Kneissl S, Vidoni B et al. (2008). Cervical spinal
80. Uchida K, Morozumi M, Yamaguchi R et al. (2001). Diffuse chordoma with chondromatous component in a dog.
leptomeningeal malignant histiocytosis in the brain and Vet Pathol 45(5):650–3.
spinal cord of a Tibetan Terrier. Vet Pathol 38(2):219–22. 99. Pease AP, Berry CR, Mott JP et al. (2002). Radiographic,
81. Allett B, Hecht S (2016). Magnetic resonance imaging computed tomographic and histopathologic appearance of
findings in the spine of six dogs diagnosed with lymphoma. a presumed spinal chordoma in a dog. Vet Radiol Ultrasound
Vet Radiol Ultrasound 57(2):154–61. 43(4):338–42.
82. Bush WW, Throop JL, McManus PM et al. (2003). 100. Stigen O, Ottesen N, Gamlem H et al. (2011). Cervical
Intravascular lymphoma involving the central and peripheral chondroid chordoma in a standard dachshund: a case report.
nervous systems in a dog. J Am Anim Hosp Assoc 39(1):90–6. Acta Vet Scand 53:55.
83. Kornder J, Platt SR, Eagleson J et al. (2016). Imaging 101. Woo GH, Bak EJ, Lee YW et al. (2008). Cervical chondroid
diagnosis – vertebral polyostotic lymphoma in a geriatric dog. chordoma in a Shetland sheep dog. J Comp Pathol
Vet Radiol Ultrasound 57(4):E42–5. 138(4):218–23.
84. Lamagna B, Lamagna F, Meomartino L et al. (2006). 102. Appel SL, Moens NM, Abrams-Ogg AC et al. (2008).
Polyostotic lymphoma with vertebral involvement and Multiple myeloma with central nervous system involvement
spinal extradural compression in a dog. J Am Anim Hosp Assoc in a cat. J Am Vet Med Assoc 233(5):743–7.
42(1):71–6.
CHAPTER 7.7
ISCHEMIC MYELOPATHY, SPINAL CORD

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HEMORRHAGE, MYELOMALACIA 565
Daniela Schweizer-Gorgas
CONTENTS
Anatomic features..................................................................................................................................................................................................565
Ischemic myelopathy/spinal cord infarction ..........................................................................................................................................................566
Spinal hemorrhage ................................................................................................................................................................................................569
Etiology and classification ...............................................................................................................................................................................569
General MRI features of hemorrhage and technical considerations ..................................................................................................................570
Intramedullary hemorrhage ..............................................................................................................................................................................573
Extramedullary hemorrhage .............................................................................................................................................................................573
Myelomalacia ........................................................................................................................................................................................................578
References.............................................................................................................................................................................................................582
A benefit of MRI as opposed to CT is its high soft tissue diameter vessels found in the thoracic part of the
contrast providing detailed information on the structural spinal cord.1
changes to the spinal cord. This makes MRI a powerful • At the ventral median fissure of the spinal cord, the
imaging tool to diagnose conditions that otherwise would radicular arteries connect to the ventral spinal artery
be difficult to identify with CT. Some changes, such as with an ascending and descending branch. Due to
hemorrhage, induce modifications of the magnetic proper- opposing blood flow directions, watershed regions
ties of tissue in which they occur, which can be highlighted may manifest with very little or even no flow in either
using specific MRI pulse sequences. This chapter illustrates direction.2
the use of MRI to diagnose ischemic myelopathy, spinal • The unpaired ventral spinal artery and vein extend the
hemorrhage, and myelomalacia. complete length of the spinal cord along the ventral
median fissure.
ANATOMIC FEATURES • Along the dorsal surface of the cord there are paired dor-
sal spinal arteries and one median vein.3
• A good knowledge of the vascular anatomy of the spi- • The intrinsic arteries of the spinal cord can be separated
nal cord is important for an understanding of the patho- into a central and a peripheral system:
physiology and imaging characteristics of ischemic and • The central system is derived from the ventral spinal
hemorrhagic conditions affecting this structure. artery forming central segmental arteries, which
• The arterial supply (Fig. 7.7.1a) of the spinal cord arises extend dorsally into the spinal cord via the ventral
segmentally from vertebral (cervical spine), intercostal median fissure. The number of central arteries varies
(thoracic spine), lumbar, and sacral arteries: between different parts of the spinal cord and there
• Their spinal branches enter the intervertebral foram- are fewest arteries in the thoracic region. They
ina, cross the dura, and split into ventral and slightly may be distributed either unilaterally or bilaterally
smaller dorsal radicular arteries, which supply the (the percentage of bilateral central arteries increases
adjacent nerve roots. from cranial to caudal along the spinal cord). The
• The radicular arteries run within the subarachnoid central arteries have centrifugal blood flow and supply
space and follow the nerve roots toward the midline two-thirds of the spinal cord including most parts of
surface of the spinal cord. the gray matter.1,2
• The contribution of radicular arterial supply to • In the peripheral system, the blood flows centripetally
the spinal cord is variable, with the smallest per- from the dorsal and ventral spinal arteries into the
centage of radicular contributions and the smallest cord, supplying the outer portion of the ventral and
566 CHAPTER 7.7
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(a) (b)
Fig. 7.7.1 Vascular anatomy of the lumbar spine showing the arterial supply (a) and venous drainage (b). C, central artery; DRA,
dorsal radicular artery; DSA, dorsal spinal artery (paired); L, lumbar artery; LaDbch, lumbar artery dorsal branch; LASbch,
lumbar artery spinal branch; VSA, ventral spinal artery; VRA, ventral radicular artery; BV, basivertebral vein; DEVP, dorsal
external vertebral venous plexus; DL, dorsolateral vein (paired); DRV, dorsal radicular vein; DS, dorsal spinal vein; IVbch,
intervertebral vein branch; VEVP, ventral external vertebral venous plexus; VIVP, ventral internal vertebral venous plexus; VL,
ventrolateral vein (paired); VRV, ventral radicular vein; VS, ventral spinal vein. (Reproduced, with permission, from De Risio L,
Platt SR (2010). Fibrocartilaginous embolic myelopathy in small animals. Vet Clin North Am Small Anim Pract 40(5):859–69.)
lateral white matter columns and the most dorsal part • The most common reported cause of ischemic myelopa-
of the gray matter. thy is embolization of fibrocartilaginous material, a con-
• The central and peripheral arterial systems have no dition known as ‘fibrocartilaginous embolism (FCE)’ or
precapillary interconnections and are functionally ‘fibrocartilaginous embolic myelopathy (FCEM)’.
end arteries.1,2 • The embolus is made of material that is histologically and
• The venous drainage of the spinal cord (Fig. 7.7.1b) is histochemically identical to the nucleus pulposus; how-
ensured by intraparenchymal small veins distributed in a ever, the source and pathway into the vasculature are still
radial pattern to form a dense network on the surface of unclear, and different hypotheses have been proposed:
the cord. These veins drain into the ventral internal ver- • Direct penetration of degenerated disc material into
tebral venous plexus, mainly consisting of two valve-less spinal vessels.
large veins on the floor of the vertebral canal. These veins • Penetration into newly formed inflammatory blood
converge at the mid-vertebral body level and diverge vessels within a degenerated intervertebral disc.
over the intervertebral disc. They drain at the level of • Penetration into embryonic remnant vessels within
the intervertebral foramina via intervertebral veins into the nucleus pulposus.
the major veins of each region. • Penetration into sinusoidal vessels of the bone
marrow.4,5
ISCHEMIC MYELOPATHY/ • Other potential causes of ischemic infarction are
SPINAL CORD INFARCTION thrombi; bacterial, parasitic, neoplastic, or fat emboli;
and neoplastic emboli.4–6
• Occlusion of intraparenchymal spinal cord arteries • Underlying medical conditions may be predisposing fac-
results in ischemic damage of the spinal cord. tors leading to embolization or thrombosis, including
I sc h e m ic My e l opat h y, Spi n a l C or d H e mor r h age , My e l om a l ac i a 567
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cardiomyopathy, hypothyroidism, hyperadrenocorti- • An intramedullary lesion, which often extends over

cism, chronic kidney disease, and systemic hypertension. several vertebral bodies and is often present in spinal
• The imaging appearance of spinal cord infarction/isch- cord segments near a degenerated intervertebral disc.
emia is non-specific for the underlying cause. • The spinal cord changes are often not centered
• The incidence of ischemic myelopathy seems to be higher directly over a disc space (Fig. 7.7.3a).
in dogs than in cats, and middle-aged (median 4–6 years), • The lesion is usually focal, relatively sharply demar-
large- and giant-breed non-chondrodystrophic dogs are cated, and predominantly affects the gray matter
most commonly affected.7 (Fig. 7.7.3b).
• The typical clinical presentation is a hyperacute onset • Lesions are most commonly lateralized or asymmet-
(<6 hours) of non-progressive, non-painful, symmetric (Fig. 7.7.4), but can be symmetric (Fig. 7.7.2b).
ric or asymmetric motor dysfunction depending on the The location of the lesion typically corresponds well
affected spinal cord segment. Owners often report clini- with the clinical findings.
cal signs following immediate exercise or minor trauma. • Depending on the size of the affected area and time
• Ischemic myelopathy might occur in all spinal cord seg- of imaging relative to onset of signs, focal swelling
ments, but predisposed sites reported in dogs are L4-S3 of the spinal cord due to edema is often present in
and C6-T2 (in histologically confirmed cases) or T3-L3 the acute stages (Fig. 7.7.5). This swelling causes an
(antemortem diagnosis). In cats, the cervical spinal cord attenuation of the hyperintense signal of the CSF in
is most commonly affected.7 the subarachnoid space on regular T2W images and
• In cats cervical ischemic myelopathy has been reported even more visible on T2-myelograms (heavily T2W
to be associated with hyaline degeneration of the ven- images with a ‘myelogram’ effect, such as HASTE or
tral spinal artery, basilar artery, or associated branches, SS-FSE pulse sequences, which highlight the signal
resulting in aneurysmal dilation and thrombosis of these from CSF while suppressing the signal from the other
vessels (Fig. 7.7.2).8 tissues). This is usually easier to assess on sagittal
• The imaging modality of choice for the diagnosis of plane images.
FCE is MRI; however, it is important to understand that • Affected areas have hyperintense signal in T2W
MRI can be normal in ischemic myelopathy in contrast and T2-FLAIR images compared with normal gray
to acute hydrated nucleus pulposus extrusion (AHNPE; matter. Signal intensity on T1W images is usually
see Chapter 7.1) and other causes of myelopathy where iso- to hypointense, but signal varies depending on
MRI abnormalities are usually seen.9 Therefore, a nor- the amount of edema (hypointense signal on T1W) or
mal MRI in a patient with a typical clinical history and concurrent hemorrhagic changes (hyperintense signal
findings is suggestive of ischemic myelopathy. on T1W).
• MRI findings suggestive of ischemic myelopathy • Mild, heterogeneous contrast enhancement of the
include:5,9–12 affected area is possible, probably due to disruption of
(a) (b)
Fig. 7.7.2 Presumed ischemic myelopathy in a 6-year-old female DSH cat with known hyperthyroidism and systemic
hypertension (systolic blood pressure 300 mmHg) presented because of an acute onset of non-ambulatory tetraparesis. Sagittal
(a) and transverse (b) T2W images showing a symmetric intramedullary hyperintensity in the cervical spinal cord at the level of
C2 (arrow, a). (1T MRI system)
568 CHAPTER 7.7
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L3
(a)
Fig. 7.7.3 Presumed ischemic myelopathy in a 4-year-old male Spitz dog
presented because of a sudden onset of non-painful paraplegia that developed
when the patient was defecating. Sagittal T2W image (a) showing an
intramedullary hyperintensity extending over several segments of the lumbar
spine (L3, 3rd lumbar vertebra). On the transverse T2W image (b) at the level
of L3, a butterfly-shaped lesion associated with the gray matter of the spinal
(b)
cord is visible. (1T MRI system)
(a) (b)
Fig. 7.7.4 Presumed ischemic myelopathy in a 4-year-old female mixed breed dog with a 2-day history of a non-painful
tetraparesis. Sagittal T2W (a) and transverse T2W (b) images showing a well-delineated asymmetric left-sided intramedullary
hyperintensity mainly within the gray matter of the cervical spinal cord. Note on the sagittal image the high signal of the well-
hydrated nuclei pulposi of the cervical spine. (1T MRI system)
the blood–spinal cord barrier; this is generally seen on artifacts of bone, and motion artifacts of CSF. Using
the 5th to 7th day of disease (Fig. 7.7.5). a multishot technique improves signal-to-noise ratio
• Less commonly, a signal void on T2*W gradient echo and decreases sensitivity to off-resonance effects.15
images or hyperintense signal on T1W images sug- • Presence of MRI changes depends on time of clini-
gestive of hemorrhage may be seen. cal onset to examination, and it is not uncommon for
• In diffusion weighted (DW) images, hyperintense MRI performed less than 72 hours after the clinical
signal with decreased apparent diffusion coefficient has onset to show no abnormality, while the likelihood of
been described in people, and was reported to have the changes increases after 72 hours.
highest sensitivity for spinal stroke.13,14 Similar DWI • Prognostic factors for an unsuccessful outcome are:
findings have been reported in veterinary medicine • Severe neurologic score at the time of initial exami-
in experimental canine models of infarction,15 and nation.
the author has observed it in clinical patients as well • Extent of the T2W hyperintensity seen on MR images:
(Fig. 7.7.6). Clinical application of DWI is, however, the sensitivity of using a lesion length-to-vertebral
technically challenging in small animals, due to its length ratio >2.0 or a percentage cross-sectional area
poor spatial resolution, sensitivity to susceptibility of the lesion ≥67% to predict an unsuccessful outcome
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(a) (b)
(c) (d)
Fig. 7.7.5 Presumed ischemic myelopathy in a 4-year-old male Pug dog with a 3-day history of an ambulatory, non-painful
monoparesis of the left pelvic limb. On the sagittal T2W image (a) there is an ill-defined intramedullary hyperintensity in the
lumbar spinal cord (solid arrow). Mild attenuation of the ventral and dorsal CSF space (dashed arrow) is seen on the sagittal
heavily T2W single-shot turbo-spin echo sequence (T2-myelogram sequence) (b), indicating swelling of the spinal cord. On the
sagittal pre-contrast T1W image (c), the lesion is isointense and on the post-contrast fat-suppressed T1W image (d), there is
mild contrast enhancement of the affected area. (1T MRI system)
has been reported to be 100%. The specificity of these SPINAL HEMORRHAGE

signs is 62% and 52%, respectively.9
• The presence of intramedullary or extramedullary Etiology and classification
hemorrhage is associated with more severe spinal • Spinal hemorrhage can be due to rupture of veins or
cord damage and development of secondary myelo- arteries, or vascular malformations.
malacia.16,17 • In dogs and cats, any traumatic insult, such as interverte-
• Differentiation from the non-compressive form of bral disc herniation, direct trauma, atlantoaxial instability,
AHNPE is challenging, and in some cases it is not pos- or iatrogenic trauma, can cause spinal cord hemorrhage.19
sible to differentiate these two conditions:18 • Several non-traumatic conditions can also cause spi-
• A recent study showed a moderate inter-, and moderate nal cord hemorrhage: coagulopathies (e.g., rodenticide
to good intraobserver agreement for a presumptive diag- toxicity, hemophilia, Angiostrongylus vasorum infection,
nosis of FCE versus non-compressive AHNPE when snake envenomation), rupture of vascular malformations/
using published criteria to identify each condition.18 aneurysms,20–22 and breakdown of blood vessel walls due
• MRI characteristics differentiating ischemic myelop- to myelomalacia. Spinal cord hemorrhage may also be seen
athy from non-compressive intervertebral disc extru- with neoplasia such as granular cell neoplasia23 or hem-
sions are listed in Table 7.7.1. The location of the lesion angiosarcoma;24 however, with neoplastic hemorrhage the
relative to the intervertebral disc appears to be a more primary imaging finding is that of a mass lesion.
useful criterion to differentiate these conditions.18 • If no cause of hemorrhage can be identified, lesions are
Length of the intramedullary T2W hyperintensity often referred to as spontaneous and if clot formation
(longer with FCE than non-compressive extrusion) can be identified, the term ‘hematoma’ is used instead of
may also be a useful criterion. hemorrhage.
• Although earlier studies showed that FCE tends to • Depending on the location of the ruptured vessel,
cause asymmetric T2W hyperintensity while AHNPE the hemorrhage is classified as either extramedullary
causes more central/symmetric hyperintensity, a recent (epidural or intradural) or intramedullary. In people,
study suggested a tendency for FCE lesions to show epidural spinal hematomas are by far the most com-
no lateralization while acute hydrated disc extrusions mon type of spinal hematoma, followed by subarachnoid
tended to show more lateralization.18 hematomas and subdural hematomas.25
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(a) (b)
Fig. 7.7.6 Nine-year-old DSH cat presented with acute-

onset non-ambulatory tetraparesis. MRI revealed a focal
myelopathy within the cervical spinal cord at the level of C2
manifesting as a rather well-delineated hyperintensity on the
T2W image (arrow, a). An ischemic myelopathy was suspected
based on the high signal intensity on the diffusion-weighted
sagittal image (arrow, b) and low signal on the apparent
diffusion coefficient map (arrow, c), indicating restricted
diffusion. (1.5T MRI system; images courtesy of Dr. Fraser
(c)
McConnell, University of Liverpool)
• The clinical signs of spinal hemorrhage vary with ana- • Late subacute (extracellular methemoglobin, short T1
tomic location and severity. Both intramedullary as well and long T2).
as extramedullary hemorrhage may lead to severe spinal • Chronic (ferritin and hemosiderin, short T2).26,27
cord dysfunction. • The signal intensity of hemorrhage depends on these
relaxation times but also on the magnetic field strength,
General MRI features of hemorrhage which also affects the resulting signal intensity of the
and technical considerations different stages.
• In general, MRI is a sensitive imaging modality for • Additional variability in signal depends on whether there
detecting hemorrhage associated with the central ner- is clot formation (hematoma) versus non-clotted intrapa-
vous system. The signal intensity of hemorrhage varies renchymal hemorrhage. This is because of differences in
with time, because the various by-products of hemoglo- the pattern of hemoglobin degradation.28
bin have different magnetic properties depending on • Signal intensity characteristics of hematomas are depen-
whether they contain unpaired electrons. dent on many factors, which can include patient age/
• Five distinct stages of hemorrhage have been defined: size/location of the lesion, hemoglobin oxidation state
• Hyperacute (intracellular oxyhemoglobin, long T1 within the hematoma, clot matrix formation, degree of
and T2 relaxation times). clot retraction, edema surrounding the hematoma, tissue
• Acute (intracellular deoxyhemoglobin, long T1 and pH, and hematocrit of the patient.
short T2). • The presence of iron in hemorrhage and blood clots
• Early subacute (intracellular methemoglobin, short causes susceptibility artifacts to which gradient echo
T1 and short T2). pulse sequences are very sensitive. Compared with spin
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Table 7.7.1 Typical MRI features of ischemic myelopathy, non-compressive acute hydrated nucleus pulposus extrusion,
myelomalacia, and myelitis.
ACUTE NON-COMPRESSIVE
ISCHEMIC HYDRATED NUCLEUS
MYELOPATHY PULPOSUS EXTRUSION MYELOMALACIA MYELITIS
Intraparenchymal Asymmetric, Midline, lateralization possible Diffuse T2 hyperintensity, fuzzy T2 hyperintense/T1
spinal cord changes symmetric possible central canal hypointense lesion with
possible contrast enhancement
Spinal cord swelling Possible, mild Possible, mild Marked Moderate to marked
Extent of the lesion Longer than one Focal Focal or diffuse, 6–20 times the Variable
vertebral length length of L2.
Ascending/descending myelomalacia
if more than four segments affected
Location in relation to Near a disc Overlying a disc Possibly related to disc, either Not related to a disc
the intervertebral disc overlying or distant to disc
(cranially, caudally, or both)
Nucleus pulposus of Signs of degeneration Hyperintense in T2W images, Not applicable Not applicable
the associated disc or reduced volume of reduction in volume
non-degenerate disc
Annulus pulposus No signs of rupture Rupture on gradient recalled Not applicable Not applicable
echo or high resolution images
Epidural fat No abnormality Presence of epidural fat Attenuated due to cord swelling Attenuated due to cord
disruption with heterogeneous swelling
signal
Vertebral canal No material within Possible disc material within Extradural material may be present No extraneous material in the
the vertebral canal the vertebral canal when the cause of myelomalacia is vertebral canal
disc extrusion
echo pulse sequences, gradient echo sequences do not at fat–water interfaces; this is sometimes referred to as
use a refocusing 180° radiofrequency pulse and therefore the ‘black boundary’ or ‘India ink’ artifact,31 or ‘out-of-
do not correct for the dephasing caused by inhomogene- phase’ imaging. The dark signal results from voxels with
ities of the magnetic field (cf. Chapter 2). This results in roughly equal amounts of fat and water, when, at cer-
images that are more T2*W and therefore highlight the tain echo times (2.2 msec, 6.6 msec, 11 msec, etc.), the
local inhomogeneities of a magnetic field such as caused fat and water spins are 180° out-of-phase because of the
by paramagnetic by-products of hemoglobin degrada- phase induced by their different precessing frequencies.
tion. For example, hemosiderin is strongly paramagnetic This causes the signals of fat protons and water protons
and augments the local magnetic field, leading to a more to cancel each other out and the overall signal within the
rapid dephasing of protons and therefore a low signal voxel to drop. This artifact, unlike the classic chemi-
(‘signal void’) in gradient echo images. The T2*W pulse cal shift artifact seen on spin echo sequences, happens
sequences are therefore valuable to identify hemorrhage in both the frequency- and phase-encoding directions.
and distinguish it from other material within the spinal Since CSF and epidural fat are surrounding the spinal
canal.29,30 cord, this artifact is visible on gradient echo sequences of
• However, their use in spinal imaging is more challeng- the spine forming a circumferential black boundary on
ing, since susceptibility artifact can also be induced by transverse images.
surrounding bones of vertebral bodies, mineralized disc • SWI is a magnetic resonance technique that uses phase
material, and aerated lung (this is important concerning images that contain information about local susceptibil-
imaging of the thoracic spine). Therefore, differentiation ity changes between tissues.32 It is exquisitely sensitive
of hemorrhage from other compressive material within to paramagnetic substances, such as deoxygenated blood,
the vertebral canal is based on comparison with signal hemoglobin by-products, iron, and calcium, and, in
intensity in T1W and T2W images (Fig. 7.7.7). people, it was shown to be more sensitive to spinal cord
• In gradient echo sequences, a chemical shift/misreg- hemorrhage in spinal cord injury compared with conven-
istration artifact may be present, forming a black line tional MRI methods.33
572 CHAPTER 7.7
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(a)
* S
* S
(b) (c)
Fig. 7.7.7 Spinal cord compression due to acute disc

extrusion and epidural hemorrhage in a 6-year-old male
Small Swiss Hound. On the transverse T2W (b), T1W (c),
and T2*W gradient echo (d) images, there is low signal
intensity compressive material in the right ventral aspect
of the vertebral canal (asterisks). Note the susceptibility
*
S
artifact on the T2*W image (d) caused by the high calcium
content of mineralized disc material. The spinal cord (S) is
displaced to the left by this compressive material. Dorsal to
the spinal cord, there is material that is hyperintense on the
sagittal T2W (a) and transverse T2W (b) images (arrows)
and separated from the spinal cord by a black outline in all
sequences, which is suggestive of epidural hemorrhage. This
hemorrhage is contributing to some dorsal compression of the
(d)
cord. (1T MRI system)
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Intramedullary hemorrhage intensity of the affected area is often heterogeneous with

• Intramedullary or parenchymal hemorrhage is also hyperintense and/or hypointense areas on T2W images.
named ‘hematomyelia’. On T1W images, the signal may be isointense or hyper-
• The most common cause of parenchymal hemorrhage in intense (Fig. 7.7.8), but a hypointense center has also
people is trauma due to compression, contusion, lacera- been described. Contrast enhancement is a rare finding,
tion, transection, or traction of the cord. Most acute spi- depending on the breakdown of the blood– spinal cord
nal cord injuries result in rupture of the central artery as a barrier and chronicity. On T2*W images, there are usu-
result of stretching and shear. Therefore, intraparenchy- ally one to several foci or areas of signal void/hypointen-
mal hemorrhage affects mainly the gray matter. In the sity consistent with susceptibility artifact (Fig. 7.7.9).21,37
transverse plane, there is radial spread of hemorrhage, • Because of vasogenic edema within the surrounding
while in the long axis of the cord, the spread usually fol- neuropil, perilesional T2W hyperintensity is often pres-
lows the dorsal column due to the organization of the ent, which is difficult to differentiate from hemorrhage.
spinal longitudinal tracts.34 • In people with chronic spinal cord injury, there can be
• In dogs and cats, traumatic spinal hemorrhage most shrinking of the cranial and caudal boundaries of the
commonly occurs following intervertebral disc extru- damaged area with possible formation of a post-trau-
sion or, less commonly, after other traumatic insults matic intramedullary cyst and focal spinal cord atrophy
such as atlantoaxial instability or fractures.19 Non- after several months, which on MRI looks like myeloma-
traumatic conditions are described: primary (sponta- lacia or spongiform changes.38
neous or idiopathic) hemorrhage has been suspected in • In people, intramedullary hemorrhage is associated with
dogs,35 and secondary hematomyelia has been identified poor neurologic recovery. In dogs, it has been observed
in animals with coagulopathies (inherited or acquired),36 that intramedullary hemorrhage occurring secondary to
rupture of vascular malformations, 20 infarcts, neopla- intervertebral disc disease is associated with more severe
sia, aneurysm, syrinx, or infection with Angiostrongylus damage of the white and gray matter.16
vasorum.21
• MRI findings depend on the extent, age, and severity of Extramedullary hemorrhage
hemorrhage. Lesions can be focal or extending over sev- • Hemorrhage within the spinal canal but outside the spi-
eral spinal segments.37 Loss of epidural fat and attenu- nal cord parenchyma is considered ‘extramedullary’, and
ation of the CSF space due to an increased spinal cord can affect the subarachnoid space, the subdural space
diameter, suggesting spinal cord swelling, are often vis- (between the dura and arachnoid), or the epidural space;
ible (Fig. 7.7.8).35 simultaneous involvement of these different compart-
• Signal alterations are predominantly within the gray ments is also possible. An additional rare location of
matter but may affect the whole spinal cord. The signal extramedullary spinal hemorrhage is subperiosteal.
(a)
Fig. 7.7.8 Hematomyelia in a 9-year-old female Dachshund

with hemorrhagic infarction of the spinal cord. Sagittal
T2W (a), transverse T2W (b), T1W (c), and T2*W (d)
images showing increased diameter of the spinal cord and
parenchymal hemorrhage with heterogeneous signal. (1T
(b)
MRI system) (Continued)
574 CHAPTER 7.7
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(c) (d)
• In people, different MRI features of subdural hemor- which is an important feature to distinguish it from
rhage versus subarachnoid hemorrhage are described: subdural hematoma. Spinal subarachnoid hemorrhage
• Subarachnoid hemorrhage occurs when there is hem- rarely presents as a hematoma owing to the dilut-
orrhage within the subarachnoid space (i.e., between ing and redistributing effect of the CSF, unless the
the arachnoid and pia mater). On MRI, CSF is seen hematoma is sufficiently large to block the CSF flow.
surrounding the hemorrhage or hematoma and sepa- • The subdural space is the potential space between the
rating it from the internal surface of the dura mater, dura mater and arachnoid mater, a mere ‘capillary slit’
(a)
Fig. 7.7.9 Intraparenchymal hemorrhage within the cervical

spinal cord due to acute non-compressive hydrated nucleus
pulposus extrusion in a 3-year-old mixed breed dog. The
parenchymal lesion is hyperintense on the T2W sagittal
(arrow, a) and transverse (b) images, and is isointense on the
T1W transverse image (c). There is a signal void consistent
with a susceptibility artifact on the T2*W image (dashed
arrow, d). In (d), the dark area along the left side of the spinal (b)
musculature is due to a large susceptibility artifact (asterisk)
caused by the microchip placed on the left side of the neck. (1T MRI system) (Continued)
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(c) (d)
under physiologic conditions, which may extend into • A direct continuity with the adjacent osseous struc-
a genuine space only under pathologic conditions tures, with extension along the nerve routes into the
such as hemorrhage. A subdural hematoma may have intervertebral foramen.
a semicircular appearance, and tends to be more cres- • The hyperintense fat forms a curved margin along the
centic on transverse images. A ‘Mercedes star’ pattern border of the epidural hemorrhage (capping), creating
has been reported on transverse images in the lumbar a pattern resembling the ‘golf tee’ sign, but in the epi-
region, due to the encasement of blood around the dural location (Fig. 7.7.12).40
arachnoid-lined cauda equina nerves. • If the dura mater is visible, dural displacement towards
• In dogs and cats, an intact subarachnoid membrane is the spinal cord is seen.
usually not present and it is typically not possible to dif- • The epidural hemorrhagic lesion in people is often
ferentiate subdural from subarachnoid hemorrhage. For located posterolaterally in the spinal canal, which the
this reason, such hemorrhages are usually grouped under author also has observed in dogs (i.e., dorsolateral
the name ‘intradural hemorrhage’. Intradural hemor- location).
rhage should be considered when the following changes • Epidural hemorrhage may be widespread in the
are present: vertebral canal and often extends over many
• The epidural fat is visible without displacement of the segments.41
dura mater and there is tissue with signal character- • In one study, epidural hemorrhage or inflammation
istic of hemorrhage conforming to the surface of the following intervertebral disc herniation appeared
spinal cord (Fig. 7.7.10). more commonly associated with extrusions in the L2
• T2 hyperintense subarachnoid CSF signal with some to L5 segment, with the most prevalent location being
widening of the subarachnoid space. L4-L5.28
• Hypointense dura mater visible between the lesion • Depending on the amount of hemorrhage within the
and the epidural fat.39 vertebral canal, there may be severe compression of
• Intradural hemorrhage is easier to identify on mye- the spinal cord or a complete or semicircular cuff
lography compared with MRI due to the classic ‘golf surrounding the spinal cord, as seen on transverse
tee sign’ described with this imaging modality. images.
• Epidural hemorrhage and hematoma are most often asso- • A hypointense curved line between the spinal cord
ciated with intervertebral disc herniation and concurrent and the compressive material on T2W and T2*W
laceration of the vertebral internal venous plexus;40–42 images delineating fresh blood silhouetting against
however, spontaneous extraparenchymal hematomas the dural sac/spinal cord.29,42
have been reported.43 MRI findings suggesting epidural • Contrast enhancement of epidural hemorrhagic mate-
hemorrhage include (Figs. 7.7.11, 7.7.12): rial varies from absent to strong.43
576 CHAPTER 7.7
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T13
(a)
Fig. 7.7.10 Confirmed subdural hemorrhage in a 6-year-old male mixed

breed dog presented with acute paraparesis that progressed to tetraplegia
secondary to ascending myelomalacia. The sagittal T2W image (a) shows a
hyperintensity within the spinal cord extending from T9 to L2 (the arrow
indicates the caudal aspect of the lesion). On the transverse T2W image
(b) at the level of T13 the subdural hemorrhage is visible as a crescent-
shaped hypointensity on the left side of the spinal cord (arrow). There is no
(b)
alteration/displacement of the surrounding epidural fat. (1T MRI system)
(a)
(b)
Fig. 7.7.11 Epidural hemorrhage caused by acute disc extrusion in a 5-year-old male Dachshund. Note the extent of attenuation
of the dorsal and ventral CSF columns on the single-shot turbo spin echo sequence (‘T2-myelogram’, a), and the typical dorsal
location of the hemorrhage on the T2W sagittal image (arrow, b). On the transverse T2W (c) and T1W (d) images, the epidural
hemorrhage forms an epidural mass in the left dorsal aspect of the vertebral canal (arrows) that is causing compression of the
spinal cord and displacement of the epidural fat; there is a clear demarcation between the epidural hemorrhage and the spinal
cord by a dark line. The transverse T2*W image (e) shows the susceptibility artifact (arrow) associated with the hemorrhage.
(1T MRI system) (Continued)
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(c) (d)
(e)
Fig. 7.7.12 Sagittal T2W image in a 6-year-old male mixed

breed dog with acute thoracolumbar disc extrusion. There
is heterogeneous epidural material in the dorsal aspect of
the vertebral canal (dashed arrow) consistent with epidural
hemorrhage. At the cranial margin of this material, the
epidural fat molds itself around this material (capping)
(solid arrow). (1T MRI system)
578 CHAPTER 7.7
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(a) (b)
Fig. 7.7.13 Subperiosteal hematoma in a 4-year-old,

spayed female Greyhound presented with an acute onset
of paraplegia. The extradural hematoma is visible along
both sides of the spinal cord (arrows, a) causing moderate
compression, and it is hyperintense to gray matter on the
T2W (a) and isointense on the T1W pre-contrast (b) and
post-contrast (c) images with no evidence of enhancement.
(1.5T MRI system; images courtesy of Dr. Anita Shea
(c)
[formerly Theobald], The Animal Health Trust)
• Spinal subperiosteal hematoma is a rare condition and MYELOMALACIA

only described in a small number of dogs with extradural
spinal cord compression. Development of subperiosteal • In general, the term malacia describes ‘softening’ of
hemorrhage has been reported to result from trauma, tissue. Concerning the spinal cord, the term is used
infection/inflammation, or an underlying coagulopathy. if histologically there is necrosis of neural tissue with
In the reported canine cases, a cause was not identified and a complete loss of structural integrity of spinal cord
the condition was considered to be spontaneous. There parenchyma.45
exists only one report describing the MRI appearance in • The cause of myelomalacia is any sudden mechani-
a Greyhound. The hematoma showed hyperintense sig- cal impact on the spinal cord, such as external trauma
nal compared with gray matter on T2W images with, in or intervertebral disc herniation. The initial trauma
some areas, a T2W hypointense rim. On T1W images, is considered as a primary injury, which is followed by
the material was isointense to gray matter with no evi- secondary injury due to vascular compromise, shift of
dence of contrast enhancement (Fig. 7.7.13). On gradient electrolytes, and release of free radicals, cellular enzymes,
echo images, the material was isointense to gray matter.44 and vasoactive substances.46–48
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• If four or fewer spinal cord segments are affected, the suggesting that hemorrhage is a biochemical contribu-
disease is considered as focal and clinical signs are tor that promotes the progression of myelomalacia.16
non-progressive. However, the exact pathophysiologic mechanisms of
• In a small percentage of patients, a cranial and/or cau- ADM are still poorly understood. In particular, it is still
dal progression from the initial site is seen and often unknown why ADM develops in some dogs, but not in
ends up affecting more than four consecutive spinal seg- others with seemingly similar initial spinal cord injury.
ments. In these cases, the disease is called ascending/ • ADM spinal cord damage is irreversible and, currently,
descending myelomalacia (ADM), diffuse or progressive ADM appears to be unaffected by any medical or surgi-
hemorrhagic myelomalacia, ascending syndrome, or cal intervention. Therefore, return to normal function
progressive hemorrhagic necrosis of the spinal cord. with adequate quality of life is not possible, and the con-
ADM usually develops within the first 24 hours after dition is considered fatal.
initial spinal cord injury, but can occur up to several days • MRI findings of focal myelomalacia are focal hyper-
after spinal cord injury.46 intense areas on T2W images that are either iso- or
• In dogs, the incidence of ADM is low and ranges hypointense on T1W images.
between 1% and 9% of dogs with acute thoracolumbar • The MRI features of ADM have been described in 18
spinal cord injury.46 In cats, there are rare case reports of dogs and one cat:49,51,52
ADM and reported causes include trauma and systemic • Affected areas encompass most often the initial site
hypertension.49 of spinal cord damage/compression and extend over
• The typical history of a patient with ADM is an initial several segments cranially and/or caudally.
focal spinal cord injury, with subsequent progression of • The length of signal alterations within the cord in
neurologic deficits that cannot be attributed to a spe- dogs with ADM ranges from 6 to 20 times the length
cific segmental area. The neurologic findings depend on of L2. The extension of the lesions is not associated
whether there is cranial (ascending), caudal (descending), with the interval between onset of clinical signs and
or bidirectional (ascending and descending) progression. MRI. As seen on pathology, areas of the spinal cord
The clinical findings of ascending myelomalacia are a distant from and not directly related to the initial site
migration of the line of analgesia cranially, including of damage may be affected.
Horner’s syndrome and fatal progression to respiratory • There is spinal cord swelling in affected areas causing
paralysis. Descending myelomalacia results in destruc- attenuation of the subarachnoid space and CSF
tion of gray matter of the lower motor neurons with signal often over more than four segments.52 This
(ongoing) paraplegia, lack of nociception, and loss of is best appreciated on T2W or heavily T2W images
urinary bladder and anal tone. In addition to neurologic (‘T2-myelogram’ such as SS-FSE or HASTE pulse
deficits, excruciating pain and/or fever over a period of sequences).
hours up to several days can be present. • In a retrospective study of dogs presented for acute
• Pathologically, very large sections of the entire spinal paraplegia and loss of deep pain perception, the mean
cord can show malacic changes. The changes are often length of attenuation of the CSF signal as a ratio to
not continuous and malacic segments may be inter- the length of L2 (as seen on ‘T2-myelogram’ images)
rupted by unaffected ones. The site of initial spinal cord was significantly longer in five dogs developing ADM
damage may even be unaffected, with malacia present compared with 16 control dogs. In this study, a cut-off
distant from the initial site. The most severe changes value of this ratio of 7.4 was determined: dogs with a
are often found in the dorsal white matter, whereas only ratio ≤7.4 were unlikely to develop ADM, while dogs
the periphery of the gray matter might be involved.50 with a ratio >7.4 were indeterminate for progressive
Often, the changes have a triangular shape in the trans- myelomalacia.53
verse plane, with the base of the triangle towards the • The signal intensity of the spinal cord in affected areas
periphery and the tip in close proximity to the central is increased on T2W fast spin echo images and usually
canal. hypointense on T1W images. On T2*W gradient echo
• Histopathologically, necrotico-hemorrhagic material is sequences, affected areas may show a diffuse reduced
found inside the central canal, leading to massive disten- signal intensity indicating subdural/arachnoid or
tion or even rupture with extrusion of the hemorrhagic intramedullary hemorrhage (Figs. 7.7.14, 7.7.15).17
debris in the area of the dorsal cord. The histopathologic • Usually, there is no contrast enhancement in the
findings located even several segments away from the affected areas.
initial damage suggest that both vascular factors50 and • Other possible findings are a mildly dilated central
biomechanical effects might play a role in progression canal, with a general loss of definition and irregular
of ADM.16 Furthermore, an association between the margination (Figs. 7.7.15 e–g).
degree of intramedullary and subdural hemorrhage and • In people, myelomalacia appears as areas of increased
craniocaudal extension of myelomalacia has been found, apparent diffusion coefficient in DWI.54
580 CHAPTER 7.7
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(a)
(b) (c)
(d) (e)
Fig. 7.7.14 Ascending/descending hemorrhagic myelomalacia in a 10-year-old female Whippet. After jumping out of the car,
the dog showed first monoparesis of the left pelvic limb, which then developed into paraplegia without deep pain sensation. The
sagittal (a) and transverse T2W (b) images show a diffuse hyperintensity in the center of the lumbar spinal cord associated with
the gray matter. Susceptibility artifact is seen on the transverse T2*W image (c), indicating hemorrhage. On the T1W pre- (d)
and post-contrast (e) images, the lesion is isointense and shows no contrast enhancement. Note the marked and diffuse swelling
of the lumbar spinal cord, attenuating the CSF space and epidural fat in all images. (1T MRI system)
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(a)
(b)
(c)
(d)
(e) (f)
Fig. 7.7.15 Myelomalacia in a 7-year-old French Bulldog with acute disc herniation at L5-L6 and subdural and epidural
hemorrhage. At presentation, the sagittal and transverse T2W images (a, b) show a focal hyperintensity over L3 to L5 affecting
the whole cross-section of the spinal cord. The transverse T2*W image (c) shows pinpoint signal void in the dorsal aspect of
the cord, consistent with focal hemorrhage. Six days later, the sagittal T2W images show ascending myelomalacia within the
cervical (d), thoracic (e), and whole lumbar spinal cord (f). Note the fuzzy delineation of the central canal with hyperintensity
dorsal to the central canal and the swelling of the spinal cord. (1T MRI system)
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REFERENCES 18. Fenn J, Drees R, Volk HA et al. (2016). Inter- and

1. Caulkins SE, Purinton PT, Oliver JE Jr. (1989). Arterial supply intraobserver agreement for diagnosing presumptive ischemic
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Vet Clin North Am Small Anim Pract 30(1):155–67, vii. 23. Rao D, Rylander H, Drees R et al. (2010). Granular cell
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Foundation, Oxford, pp. 115–20.
CHAPTER 7.8
EXTRAMEDULLARY CYST-LIKE
584 CONDITIONS OF THE SPINE
Wilfried Mai
CONTENTS
Meningeal cyst-like conditions .............................................................................................................................................................................584
Organization of the meninges ..........................................................................................................................................................................584
Intradural arachnoid diverticulum ....................................................................................................................................................................584
Extradural spinal perineurial (Tarlov) cysts ......................................................................................................................................................588
Non-meningeal cyst-like conditions......................................................................................................................................................................588
Articular process joint cysts (synovial/ganglion cysts) ....................................................................................................................................588
Ligamentous/discal cysts ................................................................................................................................................................................590
References.............................................................................................................................................................................................................593
Extramedullary cyst-like spinal conditions are fluid-filled • The space between the pia mater and the arachnoid is
collections associated with the spinal structures outside of called the ‘subarachnoid space’ and contains the cerebro-
the spinal cord, and they can be clinically silent or produce spinal fluid (CSF).
clinical signs through compression of the spinal cord or • Dorsal and ventral nerve roots travel through the sub-
nerve roots.1 They have been referred to as ‘spinal cysts’ in arachnoid space covered by pia mater and pierce the dura
the literature, although for the most part they do not cor- mater, taking a sleeve of arachnoid with them, before
respond sensu stricto to a true cyst, which by definition is a joining a prolongation of the dura distal to the spinal
‘closed, epithelium-lined sac or capsule containing liquid, ganglion. The dural sheath of the spinal nerves fuses
air or semisolid substance’. A number of the conditions with the epineurium at about the level of the interverte-
referred to as ‘cysts’ in the literature do not correspond to bral foramen.
true cysts, as they either are not completely enclosed or lack • Within each spinal nerve, individual nerve fibers are
an epithelial lining. covered by the endoneurium; fascicles of nerve fibers
Extramedullary cyst-like lesions can be divided into are covered by the perineurium and fascicles of nerves
meningeal and non-meningeal lesions. Non-meningeal are enclosed in the epineurium, a continuation of the
cysts most commonly originate from the articular process dura mater.
joints (synovial and ganglion cysts), while the existence of
cysts of ligamentous or discal origin is controversial in dogs Intradural arachnoid diverticulum
and cats. Meningoceles and dermoid sinuses, which also • Spinal arachnoid ‘cysts’ are a rare cause of spinal
form extramedullary fluid-filled structures adjacent to the cord compression in dogs and are very uncommon in
spinal cord, are covered in Chapter 7.4. cats.1–25
• They correspond to a focal dilation of the subarachnoid
MENINGEAL CYST-LIKE CONDITIONS space filled with CSF, covered by dura mater (i.e., they
are intradural) (Fig. 7.8.1). They are equivalent to the
Organization of the meninges type III meningeal cysts reported in people.26
• There are three concentric meningeal layers around the • The terminology found in the literature regarding this
spinal cord (Fig. 7.8.1). condition is inconsistent, and includes: ‘meningeal cysts’,
• The pia mater is the most internal layer and covers the ‘intra-arachnoid cysts’, ‘subarachnoid cysts’, ‘arachnoid
surface of the spinal cord. cysts’, ‘leptomeningeal cysts’, and ‘spinal arachnoid
• The next layer is the arachnoid membrane and the pseudocysts’.1,2,4–14,16–20,22,24,25
outermost layer is the dura mater; these two layers are • The term ‘cyst’ is inappropriate since these structures
intimately attached to each other and the virtual space lack an epithelial lining, are typically not enclosed, and
between them is called the ‘subdural space’. communicate freely with the anatomic subarachnoid
E x t r a m e du l l a ry Cys t -L i k e C on di t ions of t h e Spi n e 585
Arachnoid
diverticulum
Synovium
Dura mater Epineurium

Arachnoid Perineurium
Pia mater Endoneurium
NP
Dorsal root
ganglion AF
Normal anatomy
Cerebrospinal fluid
Spinal cord, meninges

and nerve sheaths Ganglion
cyst
Discal Tarlov
cyst Synovial
cyst
cyst
Non-meningeal cyst-like lesions Meningeal cyst-like lesions
Fig. 7.8.1 Schematics showing the general organization of the meningeal layers and nerve sheaths and illustrating the location
and origin of various extramedullary cyst-like structures seen in dogs and cats. Cyst-like conditions are divided into meningeal
(arachnoid diverticulum and Tarlov [perineurial] cyst) and non-meningeal cysts (ganglion/synovial cysts and discal cysts).
NP, nucleus pulposus; AF, annulus fibrosus.
space. For these reasons, the term ‘intradural arachnoid Thoracolumbar diverticula are more common in small-
diverticulum’ is more appropriate.1,15,27,28 and medium-breed dogs, with a predisposition in Pugs
• The pathophysiology of arachnoid diverticulum forma- and French Bulldogs.15 In these two breeds, concurrent
tion is not clear, although most cases seem to be con- spinal conditions are more common, such as interver-
genital and associated with an abnormal development of tebral disc disease or hemivertebrae.15 However, one
the arachnoid membrane, such as duplicating or splitting recent study reported cervical arachnoid diverticula in
during embryologic development, allowing slow expan- a series of seven related Pugs, with no obvious predis-
sion through life and subsequent progressive compres- posing cause, suggesting that a hereditary component
sion of the spinal cord.1,9,21,22 Occasionally, arachnoid is possible in a subset of dogs of this breed, and result-
diverticula have been reported in dogs related to each ing in a different localization than typically seen in
other,17,21 supporting congenital/developmental factors Pugs. 21
with a possible hereditary component. • Arachnoid diverticula are more common in male dogs
• Arachnoid diverticula have also been reported in asso- overall.15 Median age at presentation in a recent meta-
ciation with other conditions of the spine such as analysis was found to be 27 months,1 while a recent
trauma, intervertebral disc herniation, hemivertebrae, large retrospective series reported a median and mean
scoliosis, stenosis due to articular process hypertrophy, age at presentation of 36 and 46 months, respectively.15
arachnoiditis, atlantoaxial instability, and spinal dysra- Although previous studies suggested that dogs with cer-
phism,4,7–9,15,19,22,24,29,30 although a causal relationship has vical diverticula tended to be younger,24 this study did
not been established so far. not find a significant age difference in dogs with cervical
• Arachnoid diverticula most commonly develop in versus thoracolumbar diverticula.15
the cervical (C2-C3 and, less commonly, C5-C6) and • Histopathologically, the wall of the diverticulum is com-
thoracolumbar regions (T9-T13, more commonly posed of a normal to slightly thickened meningothelial
at T13-L1).1,9,15,22,24 Lumbar diverticula are uncom- cell layer and is separated from the spinal cord by an
mon. Cervical diverticula are more common in larger intact pia mater; leptomeningeal inflammatory infiltrates
dogs with a predisposition in Rottweilers.1,9,15,21,22 are possible.9
586 CHAPTER 7.8
• Most diverticula are located dorsally, while ventral and with the subarachnoid space is seen. This lesion is
lateral locations are less common. Occasionally, diver- most commonly located dorsal to the spinal cord
ticula encircling the spinal cord are observed and this (Figs. 7.8.2, 7.8.3), less commonly ventrally or later-
presentation is more common in large-breed dogs and in ally (Fig. 7.8.4).15
the cervical region.15 • The lesion most often extends over two vertebral
• The most common clinical signs include ataxia and hyper- bodies, although longer diverticula are occasionally
metria, which may reflect the common dorsal position of seen.15 A single lesion is usually present, but multiple
the diverticula: impairment of the dorsally located ascend- diverticula are possible. Multilobulated diverticula
ing proprioceptive pathways may explain the ataxia and are occasionally seen, and are more common in the
compression of the dorsolaterally located spinocerebellar cervical region.15
tracts may explain the hypermetria.15 Another relatively • The signal intensity is similar to CSF, being T1
common clinical sign is urinary and fecal incontinence. hypointense and T2 hyperintense (Figs. 7.8.2–7.8.4).
Fecal incontinence may be related to the dorsal compression • In some cases, visualization of the lesion on a T2W series
of sensory pathways important for conscious defecation.2 may be challenging, due to the similar hyperintense
Although the condition is typically not painful,24 spinal signal of the fluid in the subarachnoid space and the
hyperesthesia can be observed in 18%–24% of dogs.15,22 epidural fat, leading to false-negative diagnoses.27 The
• MRI is considered the modality of choice to image use of heavily T2W pulse sequences (‘T2-myelogram’)
arachnoid diverticula because unlike other techniques such as single-shot fast spin echo (SS-FSE) or half-Fou-
it allows assessment of the spinal cord parenchyma and rier acquisition single-shot turbo spin echo (HASTE)
detection of comorbidities such as syringomyelia. can significantly increase the likelihood of identifying
• MRI features of the condition are listed below: arachnoid diverticula by highlighting the signal from
• On sagittal images, a discrete teardrop-shaped fluid-filled structures and suppressing the signal from
lesion adjacent to the spinal cord and contiguous surrounding structures (Fig. 7.8.4).27
T13
(a) (b) (c)
Fig. 7.8.2 Sagittal T2W (a) and transverse T2W (b–d) images at the level of T13 in an 8-year-
old Pug with a 4-week history of ataxia and intermittent fecal incontinence. The transverse
T2W images (b–d) are serial slices from caudal to cranial and show the progressive expansion
of the dorsal subarachnoid space causing progressive dorsal compression of the spinal cord.
The sagittal T2W image (a) shows the classic tear-drop shape of the cranial end of the
arachnoid diverticulum (arrow). The T11-T12 and T12-T13 discs are degenerated with loss
of signal and there is mild dorsal protrusion causing ventral cord compression. Cranial to the
diverticulum, there is patchy hyperintensity in the central aspect of the spinal cord, likely
(d)
representing early syrinx formation and some gliosis (arrowhead). (1.5T MRI system)
*
(a)
(b)
Fig. 7.8.3 Sagittal T2W (a), transverse T2W (b), and

T1-FLAIR (c) images at the level of mid-C3 in a 9-year-old
* Pug with hypermetria of the thoracic limbs. A dorsal arachnoid

diverticulum is seen over C2-C3 (arrows) causing dorsal spinal
cord (asterisks, b and c) compression. The diverticulum is
markedly hyperintense on the T2W images and hypointense
on T1-FLAIR, characteristic of a fluid-filled lesion. Caudal to
the diverticulum, there is ill-defined patchy hyperintensity in
the spinal cord parenchyma consistent with pre-syrinx stage
(c)
(arrowhead, a). (1.5T MRI system)
(d)
Fig. 7.8.4 Transverse T2W images at the
level of T7 (a, b) and T9 (c) and sagittal
T2-myelogram (SS-FSE slab, d) image in
a 9-year-old Cocker Spaniel presented for
paraparesis. There is a ventral and right-sided
ventrolateral arachnoid diverticulum at T7
(arrows, a and b). This dog had a previous
history of meningitis and this diverticulum
may therefore be acquired and secondary to the
(a) (b) (c)
previous meningitis. The T2-myelogram image
shows the focal expansion of the ventral subarachnoid space (arrowhead, d). At T9 there is a central hyperintensity in the
spinal cord parenchyma consistent with a syrinx (dotted arrow, c). (1.5T MRI system)
588 CHAPTER 7.8
• Although signal is typically suppressed on flu- traumatic etiology with mechanical injury to the nerve
id-attenuated inversion recovery pulse sequences sheath leading to cyst formation.
(T2-FLAIR), a lack of suppression on T2-FLAIR has • MRI showed a well-marginated rounded, extradural,
been reported.15 This may reflect that occasionally lateralized lesion associated with the region of the dor-
the fluid in the diverticulum is of different chemical sal nerve root and the intervertebral foramen. The MR
composition than CSF, as has been reported in intrac- signal was T1 hypointense, T2 hyperintense, and sup-
ranial arachnoid cysts in people.31 pressed on T2-FLAIR, characteristic of a fluid-filled
• The spinal cord is compressed to various degrees at lesion (Fig. 7.8.5).33 In the dog with the lumbosacral
the level of the lesion (Figs. 7.8.2–7.8.4). lesion, there was also thinning of the dorsal lamina of
• Concurrent syringomyelia is occasionally the sacrum at the level of the lesion, a finding that is also
seen,5,8,14,18,22,24 and has been reported to improve reported in people32 (Fig. 7.8.5) and is attributed to pres-
after surgical management of the diverticulum sure atrophy caused by slow progressive enlargement of
(Figs. 7.8.2–7.8.4).18 the cyst, similar to what is seen with peripheral nerve
• In cases of acquired diverticula, additional abnor- sheath tumors.
malities may be noted, such as chronic intervertebral
disc herniation, or congenital abnormalities such as NON-MENINGEAL CYST-LIKE CONDITIONS
hemivertebrae; their MRI signs are described in other
chapters in this book. • Spinal non-meningeal cyst-like conditions are degenera-
tive intraspinal fluid-filled structures arising from the
Extradural spinal perineurial (Tarlov) cysts vertebral articulations, ligamentous or discal structures
• Perineurial or perineural cysts, also called Tarlov cysts, of the vertebral column.1 Almost all such cystic struc-
originate from the dorsal nerve root and ganglion sheath, tures reported thus far in veterinary medicine have been
close to the point where the pia and arachnoid membrane associated with the articular process joints.1,3
differentiate into endoneurium and perineurium, respec-
tively. Unlike arachnoid diverticula, they are therefore Articular process joint cysts
extradural lesions filled with CSF and contain neural (synovial/ganglion cysts)
structures pertaining to the nerve root and ganglion • There are four articular processes on most vertebrae: the
(Fig. 7.8.1).1,32,33 left and right cranial articular processes and the left and
• The etiology of these cysts is largely unknown, and pos- right caudal articular processes. They are located on the
sible causes in people include trauma, genetic predisposi- vertebral arch at the junction between the pedicles and
tion (e.g., collagen disorder), or inflammatory processes, lamina. The cranial articular processes of a given verte-
causing focal weakness of the nerve sheath and allowing bra articulate with the caudal articular processes of the
pulsatile and hydrostatic forces of CSF, along with a ball- vertebra located immediately cranially, thereby forming
valve effect, to cause continued dilation of the cyst.32 In the paired articular process joints. The portion of the
people they are common incidental findings on MRI of articular processes that is covered by articular cartilage
the lumbosacral spine and are rarely symptomatic, often is called the facet; however, this term should not be used
multiple, and more frequent in women.32 to designate the entire articular process or to describe
• Histopathologically, the cyst wall is formed of a fibro- the joint.34 Therefore, the term ‘articular facet joint’ is
collagenous capsule. In theory, neural elements such incorrect. The articular process joints are synovial joints
as nerve fibers or cell bodies should be identified for a and therefore contain synovial fluid and are lined by
definitive diagnosis of Tarlov cyst, although these could synovium (Fig. 7.8.1).
be missed if cyst wall resection was incomplete.1 • Articular process joint cysts are extradural fluid-filled
• To date, these cysts have only been reported in two rounded or oval-shaped well-defined structures that
female dogs (a 10-year-old German Shepherd Dog and develop as a result of degeneration of these joints.25,35,36
a 10-year-old Labrador Retriever).33 One was located at • They are histologically divided into (Fig. 7.8.1):
C5-C6, causing moderate right dorsolateral cord com- • Synovial cysts, resulting from outpouching of syn-
pression, and one was located at L7-S1, causing moderate ovial membrane through weakened capsular tissue,
to marked right S1 nerve compression (Fig. 7.8.5). lined by synovium-like epithelial cells.
• Clinical signs included progressive neck pain and ataxia • Ganglion cysts, which are the result of mucinous
in the dog with a cervical cyst, and intermittent and pro- degeneration of periarticular connective tissue and do
gressive non-weight-bearing lameness of the right pelvic not have a synovial lining.
limb with radicular pain in the dog with a lumbosacral • Clinically and imaging-wise, the two entities are
cyst. indistinguishable and some have grouped them under
• In both dogs, there was adjacent intervertebral disc the terminology ‘juxtafacet cysts’,36 although the ter-
degeneration and protrusion, which may support a minology ‘articular process cysts’ is preferable.
(a) (b)
(c) (d)
Fig. 7.8.5 Sagittal T2W (a), transverse T2W (b), sagittal T1W (c), and transverse T1W (d) images at the level of the cranial
aspect of the sacrum in a 10-year-old female intact Labrador Retriever presented with a 2-month history of intermittent but
progressive non-weight-bearing lameness of the right pelvic limb and pronounced radicular pain. There is degeneration and
dorsal protrusion of the L7-S1 intervertebral disc (asterisks, a and c), thinning of the dorsal lamina of the sacrum on the right
(dashed arrows, b and d), and an oval-shaped T2 hyperintense, T1 hypointense lesion (solid arrows) caudomedial to the right
lumbosacral intervertebral foramen causing moderate to marked compression of the S1 nerve root. This was diagnosed as a
perineurial (Tarlov) cyst. (1.5T MRI system; reproduced, with permission, from Liebel F-X, Platt S, Matiasek K et al. (2013).
Diagnosis and management of perineurial (Tarlov) cysts in two dogs. Vet Rec 172(19):504.)
• In dogs, almost all reports of articular process cysts as spondylosis and osteoarthritis of the articular process
have been synovial cysts,35–40 with only one report of a joints, which may reflect increased stress on these joints
ganglion cyst in a German Shepherd Dog with multi- in these areas, leading to the formation of cysts.
ple lesions at L6-L7 and L7-S1.41 • Cysts in the mid- to caudal cervical area are more com-
• Most documented cases have been reported in the mid- monly seen in young giant-breed dogs and are often mul-
to caudal cervical region,35,39 thoracolumbar junction tiple and bilateral. Commonly affected breeds include
area,35,36,40 and lumbosacral junction area.36,37,41 There Mastiffs and Great Danes.35,39 In these dogs, there is
are isolated reports of cysts in the cranial cervical spine an association with degenerative compressive osseous
(C1-C3) in a Chihuahua, which were associated with proliferation from cervical spondylomyelopathy. The
atlantoaxial instability, or articular process hypertro- degenerative changes at these joints with associated insta-
phy similar to spondylomyelopathy in a Cavalier King bility may predispose to the development of cysts. Cystic
Charles Spaniel.38,42 changes associated with the articular process joints are a
• Cysts in the thoracolumbar and lumbosacral area tend common feature reported on MRI in descriptive series of
to occur mostly in older large-breed dogs. They are dogs with cervical spondylomyelopathy, affecting about
often associated with spinal degenerative changes such 20% of patients.43,44
590 CHAPTER 7.8
• Clinical signs associated with these conditions depend • The signal of the lesions is similar to CSF in most cases
on the location of the cysts, and vary from spinal pain and characteristic of fluid-filled lesions: hypointense
to ataxia and tetra- or paraparesis, although in a number on T1W images, hyperintense on T2W images,36,38,41,42
of cases the clinical signs are not attributable to the cysts and suppressing on T2-FLAIR.38
only, but also to concurrent causes of cord compression • In some cases, signal intensity can vary and become T1
such as disc herniation, articular process hypertrophy, or hyperintense if proteinaceous fluid or paramagnetic
vertebral instability. blood breakdown products accumulate within the cyst.37
• The MRI appearance of the lesions includes • Faint rim-enhancement after gadolinium injection
(Figs. 7.8.6–7.8.8): has been reported.37,38
• Well-defined rounded extradural lesions associated
with the articular process joints, causing variable Ligamentous/discal cysts
degrees of compression of the nerve roots and/or • Extradural intraspinal cysts can also rarely develop from
spinal cord. The cysts can be present inside the verte- the ligaments and discal structures of the spine such as
bral canal if they grow medially (Figs. 7.8.6, 7.8.7) or the dorsal longitudinal ligament, ligamentum flavum, or
outside if they grow laterally (Fig. 7.8.8). annulus fibrosus.1
(a) (b)
Fig. 7.8.6 Transverse T2W (a) and T1W (b) and sagittal T2W
(c) images in a 9-year-old male Dachshund dog presented
with severe neck pain. The patient had a disc extrusion at
C2-C3 causing significant spinal cord compression (not
shown). There is a left-sided articular process joint cyst at
the level of C3-C4 (arrows). Ventrally at this site, there is
mild intervertebral disc protrusion. The cyst is oval-shaped,
well-marginated, T2-hyperintense, and T1-hypointense. It is
causing mild left dorsolateral compression of the spinal cord.
Enlargement and remodeling of the left articular processes is
seen, consistent with osteoarthritis (arrowhead, b). (1.5T MRI
(c)
system)
(a) (b)
Fig. 7.8.7 Transverse T2W (a) and T1W (b) images at the level of C6-C7 in a 6-year-old Rottweiler dog with cervical
spondylomyelopathy. A well-marginated T2-hyperintense, T1-hypointense articular process cyst is seen on the right side
(arrows), causing mild dorsolateral compression of the cord, which is also contributed to by hypertrophy of the articular
processes causing lateral narrowing of the vertebral canal. (1.5T MRI system)
• So far, no intraspinal cyst of ligamentous origin has been

reported in the veterinary literature.
• Although some authors reported a series of ventral intra-
spinal cysts seemingly associated with the intervertebral
disc and similar to ‘discal cysts’ seen in people,45,46 more
recent studies and increasing evidence suggest that these
structures were in fact due to acute extrusion of hydrated
nucleus pulposus material (cf. Chapter 7.1), and do not
correspond to the more chronic, degenerative entity seen
in people.47–49
• In people, discal cysts are ventral intraspinal fluid-filled
structures with a wall made of dense fibrous connective
tissue and communicating with the intervertebral disc
through a ruptured annulus.1 They appear as ventral
extradural lesions in the vertebral canal immediately
adjacent to the intervertebral disc, and clinically mani-
fest as chronic painful lumbar radiculopathy.
• In contrast, the condition initially deemed to repre-
sent ‘discal cysts’ in dogs45,46 has a more acute presenta-
Fig. 7.8.8 Transverse T2W image at L4-L5 in a 15-year-old tion, similar to that seen with acute disc herniation, is
German Shepherd Dog. A small incidental articular process more common in the cervical region, and is typically
joint cyst (arrow) is seen on the left side, bulging to the non-painful.47–49 The term ‘discal cyst’ therefore seems
outside of the joint and not causing any significant spinal cord inappropriate in patients with this type of clinical pre-
compression. (1.5T MRI system) sentation and MRI findings of an extradural fluid-filled
lesion ventral to the cord and associated with the dorsal
aspect of the disc.
592 CHAPTER 7.8
• There is only one report in the veterinary literature of • The lesion was somewhat bilobed in the transverse
a condition that resembles the true degenerative dis- plane, T2 hyperintense with a hypointense rim, and
cal cysts seen in people:50 a 6-year-old Rottweiler with T1 hypointense with mild rim enhancement after
chronic episodic thoracolumbar pain and pelvic limb gadolinium injection.
ataxia: • On gradient echo T2*W images, the lesion was hyperin-
• On MRI, a ventral extradural compressive lesion was tense and there was a vertical linear hyperintensity inter-
seen associated with the dorsal aspect of the T13-L1 rupting the dorsal aspect of the annulus fibrosus and
intervertebral disc (Fig. 7.8.9). communicating with the cystic structure (Fig. 7.8.9).
*
*
(a)
(b)
Fig. 7.8.9 Transverse T2W (a), T1W (b), and gradient-

echo T2*W (c) images at the level of T13-L1 in a 6-year-
old Rottweiler with chronic episodic thoracolumbar pain
and pelvic limb ataxia. There is a ventral extradural lesion
(solid arrows, a and b) that is T2 hyperintense with a thin *
hypointense rim and T1 hypointense, causing compression
of the spinal cord (asterisks). On the gradient-echo image (c),
the lesion has an isointense to cerebrospinal fluid center and a
hypointense rim; the T13-L1 annulus fibrosus is interrupted
dorsally by a vertical hyperintensity located ventral to the
extradural cystic lesion (dashed arrow). This was diagnosed
as a degenerative intraspinal cyst, likely of discal origin.
(1.5T MRI system; reproduced, with permission, from
Penning VA, Benigni L, Steeves E et al. (2007). Imaging
diagnosis – degenerative intraspinal cyst associated with an
(c)
intervertebral disc. Vet Radiol Ultrasound 48(5):424–7.)
• At surgery, the cystic lesion was attached to the 20. Parker AJ, Smith CW (1974). Meningeal cyst in a dog. J Am
annulus fibrosus with adhesions to the dura mater. Anim Hosp Assoc 10:595–7.
The wall of the lesion was made of moderately cellu- 21. Rohdin C, Nyman HT, Wohlsein P et al. (2014). Cervical
spinal intradural arachnoid cysts in related, young pugs.
lar fibrous connective tissue occasionally expanded by
cartilaginous foci, and overlain by one or more layers 22. Rylander H, Lipsitz D, Berry WL et al. (2002). Retrospective
of small spindle-shaped lining cells, consistent with a analysis of spinal arachnoid cysts in 14 dogs. J Vet Intern Med
degenerative intraspinal cyst. 16(6):690–6.
23. Sessums KB, Ducote JM, American College of Veterinary
Radiology (2006). What is your diagnosis? Spinal arachnoid
REFERENCES cysts. J Am Vet Med Assoc 228(7):1019–20.
1. Lowrie ML, Platt SR, Garosi LS (2005). Extramedullary 24. Skeen TM, Olby NJ, Munana KR et al. (2003). Spinal
spinal cysts in dogs. Vet Surg 43(6):650–62. arachnoid cysts in 17 dogs. J Am Anim Hosp Assoc 39(3):
2. Chen AV, Bagley RS, West CL et al. (2005). Fecal 271–82.
incontinence and spinal cord abnormalities in seven dogs. J 25. Webb AA (1999). Intradural spinal arachnoid cyst in a dog.
Am Vet Med Assoc 227(12):1945–51, 1928. Can Vet J 40(8):588–9.
3. da Costa RC, Cook LB (2016). Cystic abnormalities of the 26. Nabors MW, Pait TG, Byrd EB et al. (1988). Updated
spinal cord and vertebral column. Vet Clin North Am Small assessment and current classification of spinal meningeal cysts.
Anim Pract 46(2):277–93. J Neurosurg 68(3):366–77.
4. Dyce J, Herrtage ME, Houlton JEF et al. (1991). Canine 27. Seiler GS, Robertson ID, Mai W et al. (2012). Usefulness
spinal ‘arachnoid cysts’. J Small Anim Pract 32:433–7. of a half-fourier acquisition single-shot turbo spin-echo
5. Foss KD, Berry WL (2009). What is your neurologic pulse sequence in identifying arachnoid diverticula in dogs.
diagnosis? Spinal arachnoid cysts. J Am Vet Med Assoc Vet Radiol Ultrasound 53(2):157–61.
234(8):1009–11. 28. Mai W (2013). Magnetic resonance imaging and computed
6. Frykman OF (1999). Spinal arachnoid cyst in four dogs: tomography features of canine and feline spinal cord
diagnosis, surgical, treatment and follow-up results. J Small disease. In: Textbook of Veterinary Diagnostic Radiology, 6th edn.
Anim Pract 40(11):544–9. (ed. DE Thrall) Elsevier, St. Louis, pp. 194–221.
7. Gage ED, Hoerlein BF, Bartels JE (1968). Spinal cord 29. Bagley RS, Silver GM, Seguin B et al. (1997). Scoliosis and
compression resulting from a leptomeningeal cyst in the dog. associated cystic spinal cord lesion in a dog. J Am Vet Med
J Am Vet Med Assoc 152:1664–70. Assoc 211(5):573–5.
8. Galloway AM, Curtis NC, Sommerlad SF et al. (1999). 30. Vignoli M, Rossi F, Sarli G (1999). Spinal subarachnoid cyst in
Correlative imaging findings in seven dogs and one cat with a cat. Vet Radiol Ultrasound 40(2):116–9.
spinal arachnoid cysts. Vet Radiol Ultrasound 40(5):445–52. 31. Berle M, Wester KG, Ulvik RJ et al. (2010). Arachnoid cysts
9. Gnirs K, Ruel Y, Blot S et al. (2003). Spinal subarachnoid cysts do not contain cerebrospinal fluid: a comparative chemical
in 13 dogs. Vet Radiol Ultrasound 44(4):402–8. analysis of arachnoid cyst fluid and cerebrospinal fluid in
10. Goncalves R, Hammond G, Penderis J (2008). Imaging adults. Cerebrospinal Fluid Res 7:8.
diagnosis: erroneous localization of spinal arachnoid cyst. Vet 32. Burke JF, Thawani JP, Berger I et al. (2016). Microsurgical
Radiol Ultrasound 49(5):460–3. treatment of sacral perineural (Tarlov) cysts: case series and
11. Hardie RJ, Linn KA, Rendano VT (1996). Spinal meningeal review of the literature. J Neurosurg Spine 24(5):700–7.
cyst in a dog: a case report and literature review. J Am Anim 33. Liebel FX, Rossmeisl JH, Jr., Lanz OI et al. (2011). Canine
Hosp Assoc 32(6):477–80. spinal nephroblastoma: long-term outcomes associated with
12. Hashizume CT (2000). Cervical spinal arachnoid cyst in a treatment of 10 cases (1996–2009). Vet Surg 40(2):244–52.
dog. Can Vet J 41(3):225–7. 34. Thrall DE, Robertson ID (2015). Atlas of Normal Radiographic
13. Itamoto K (2010). A case involving a dog with a cervical Anatomy and Anatomic Variants in the Dog and Cat, 2nd edn.
arachnoid cyst treated with marsupialization surgery. J Japan Elsevier, St. Louis.
Vet Med Assoc 63:375–8. 35. Dickinson PJ, Sturges BK, Berry WL et al. (2001). Extradural
14. Jurina K, Grevel V (2004). Spinal arachnoid pseudocysts in spinal synovial cysts in nine dogs. J Small Anim Pract
10 rottweilers. J Small Anim Pract 45(1):9–15. 42(10):502–9.
15. Mauler DA, De Decker S, De Risio L et al. (2014). 36. Sale CS, Smith KC (2007). Extradural spinal juxtafacet
Signalment, clinical presentation, and diagnostic findings in (synovial) cysts in three dogs. J Small Anim Pract 48(2):116–9.
122 dogs with spinal arachnoid diverticula. J Vet Intern Med 37. Forterre F, Kaiser S, Garner M et al. (2006). Synovial cysts
28(1):175–81. associated with cauda equina syndrome in two dogs. Vet Surg
16. McKee WM, Renwick PW (1994). Marsupialisation of an 35(1):30–3.
arachnoid cyst in a dog. J Small Anim Pract 35:108–11. 38. Forterre F, Reves NV, Stahl C et al. (2012). Atlantoaxial
17. Ness MG (1998). Spinal arachnoid cysts in two shih tzu synovial cyst associated with instability in a Chihuahua.
littermates. Vet Rec 142(19):515–6. Case Rep Vet Med Vol. 2012 (Article ID 898241):4 pages.
18. Oxley W, Pink J (2012). Amelioration of caudal thoracic 39. Levitski RE, Chauvet AE, Lipsitz D (1999). Cervical
syringohydromyelia following surgical management of an myelopathy associated with extradural synovial cysts in 4 dogs.
adjacent arachnoid cyst. J Small Anim Pract 53(1):67–72. J Vet Intern Med 13(3):181–6.
19. Parker AJ, Adams WM, Zachary JF (1983). Spinal arachnoid 40. Perez B, Rollan E, Ramiro et al. (2000). Intraspinal synovial
cysts in the dog. J Am Anim Hosp Assoc 19:1001–8. cyst in a dog. J Am Anim Hosp Assoc 36(3):235–8.
594 CHAPTER 7.8
41. Webb AA, Pharr JW, Lew LJ et al. (2001). MR imaging resonance imaging observations in seven dogs. Vet Surg
findings in a dog with lumbar ganglion cysts. Vet Radiol 37(1):94–101.
Ultrasound 42(1):9–13. 47. Beltran E, Dennis R, Doyle V et al. (2012). Clinical and
42. Harris KP, Saveraid TC, Rodenas S (2011). Dorsolateral spinal magnetic resonance imaging features of canine compressive
cord compression at the C2-C3 junction in two Cavalier King cervical myelopathy with suspected hydrated nucleus pulposus
Charles spaniels. Vet Rec 169(16):416. extrusion. J Small Anim Pract 53(2):101–7.
43. Lipsitz D, Levitski RE, Chauvet AE et al. (2001). Magnetic 48. Hamilton T, Glass E, Drobatz K et al. (2014). Severity of
resonance imaging features of cervical stenotic myelopathy in spinal cord dysfunction and pain associated with hydrated
21 dogs. Vet Radiol Ultrasound 42(1):20–7. nucleus pulposus extrusion in dogs. Vet Comp Orthop Traumatol
44. Martin-Vaquero P, da Costa RC (2014). Magnetic resonance 27(4):313–8.
imaging features of Great Danes with and without clinical 49. Manunta ML, Evangelisti MA, Bergknut N et al. (2015).
signs of cervical spondylomyelopathy. J Am Vet Med Assoc Hydrated nucleus pulposus herniation in seven dogs. Vet J
245(4):393–400. 203(3):342–4.
45. Kang BJ, Jung Y, Park S et al. (2015). Discal cysts of the 50. Penning VA, Benigni L, Steeves E et al. (2007). Imaging
cervical spine in two dogs. J Vet Sci 16(4):543–5. diagnosis – degenerative intraspinal cyst associated with an
46. Konar M, Lang J, Fluhmann G et al. (2008). Ventral intraspinal intervertebral disc. Vet Radiol Ultrasound 48(5):424–7.
cysts associated with the intervertebral disc: magnetic
CHAPTER 7.9
SYRINGOMYELIA
VetBooks.ir
Wilfried Mai 595
CONTENTS
Normal cerebrospinal fluid production and flow....................................................................................................................................................595
Pathophysiology of syringomyelia ........................................................................................................................................................................595
MRI appearance of syringomyelia .........................................................................................................................................................................598
References.............................................................................................................................................................................................................601
From a strict standpoint, ‘hydromyelia’ refers to pathologic • CSF accumulating in the subarachnoid space is progres-
dilation of the central canal of the spinal cord, whereas in sively removed through absorption by the arachnoid villi,
‘syringomyelia’ the fluid dissects through the ependymal which are finger-like endothelium-lined protrusions of
lining of the central canal, which creates a focal fluid collec- the arachnoid outer layer through the dura mater and
tion within the spinal cord outside of the central canal.1,2 The into the lumen of calvarial venous sinuses (cranial arach-
clinical manifestations are identical between both entities, noid villi) and epidural venous sinuses (spinal arachnoid
and there is often some overlap between them: a dilated cen- villi). Alternative pathways of CSF absorption include
tral canal can rupture, allowing cerebrospinal fluid (CSF) to the cranial and spinal nerve sheaths, the cribriform plate,
extend into the parenchyma, and, conversely, a parenchymal and the adventitia of cerebral arteries.4
cavitation adjacent to the central canal can rupture into it. • The CSF flow from the sites of production to the sites
In addition, research has shown that the abnormal collec- of absorption is pulsatile, corresponding to the systolic
tion of fluid is not in fact pure CSF, but extracellular fluid. pulse wave in the choroidal arteries.4
As a result, the term ‘syringomyelia’ is now accepted to refer
to all spinal cord cavitations containing fluid that is identical PATHOPHYSIOLOGY OF SYRINGOMYELIA
to or closely resembling CSF.2,3 Synonymous terms com-
monly used include ‘syringohydromyelia’ and ‘syrinx’. • There are a number of theories to explain the develop-
ment of syringomyelia, but they all rely on the premise
NORMAL CEREBROSPINAL FLUID that there is some form of obstruction or impairment to
PRODUCTION AND FLOW the normal pulsatile flow of CSF in the subarachnoid space
that is normally associated with the cardiac cycle.2,3,5–33
• The majority of the CSF is produced by the choroid plex- • Regardless of etiology, the driving force of syringomy-
uses located in the lateral, 3rd, and 4th ventricles. A small elia is the systolic CSF pulse pressure: the pressure wave
amount also comes from the brain interstitial fluid, the of CSF displaced from the head during each arterial
parenchymal capillaries, and the ependymal lining of the pulsation.2
ventricles,4 although their exact contribution to the total • With any compression of the spinal subarachnoid space,
amount of CSF produced is controversial. there is, during the systolic pressure wave, a high-pressure
• In normal mammals, the flow of CSF is directed from compartment cranial to the obstructive site and a lower-
the lateral ventricles through the interventricular fora- pressure compartment caudal to the obstructive site:2,20
men into the 3rd ventricle, and then caudally through the • If there is complete obstruction to flow of CSF
mesencephalic aqueduct into the 4th ventricle. The CSF (e.g., circumferential constriction due to an extra-
then enters the subarachnoid space through the lateral dural lesion or arachnoid adhesions), the systolic
apertures of the 4th ventricle, while only a small amount pressure wave is transmitted through the spinal
enters the central canal of the spinal cord. Once in the cord parenchyma caudal to the obstruction, and
cranial subarachnoid space, the CSF circulates rostrally some is reflected backwards (i.e., cranially) into the
to the cranial villous sites of absorption, or caudally into spinal cord parenchyma cranial to the obstruction.
the spinal subarachnoid space.4 This causes repeated, cyclic mechanical distension
596 CHAPTER 7.9
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of the cord, resulting in accumulation of extracel- encroachment of the craniocervical or spinal subarach-
lular fluid originating from the microcirculation of noid space.
the spinal cord. After a potentially reversible phase • A very common cause for syringomyelia in dogs is
of spinal cord edema, this fluid eventually coalesces the Chiari-like malformation/syringomyelia complex
into cavities (i.e., the syrinx) (Fig. 7.9.1). A syrinx can (see Chapter 5.1), which is a multifactorial disease pro-
form both caudal and cranial to the obstructive site cess governed by the effects of increased hindbrain
due to the bidirectional pressure wave transmission volume and impaired occipital bone development.33
into the spinal cord parenchyma.2,20 This causes a volume mismatch between the caudal
• If there is an incomplete obstruction, an open, albeit fossa and brain parenchyma it contains, resulting in
narrow, subarachnoid space channel is left for the CSF crowding of the hindbrain parenchyma. The main mor-
to flow through during each systolic pressure wave; phologic features of the condition are indentation of the
the narrowed window causes the velocity of CSF cerebellum by the supraoccipital bone and/or hernia-
flow to increase through the opening (CSF flow jet). tion of a part of the cerebellum through the foramen
The Venturi effect then takes place, a fluid dynam- magnum (Fig. 7.9.2).33 However, cerebellar indentation
ics law stipulating that the total mechanical energy can be seen in 37%–51% of non-Cavalier King Charles
of flowing fluids remains constant, so that if there is Spaniels without signs of Chiari-like malformation, and
an area of increased velocity, the hydrostatic pressure therefore may not in isolation constitute an accurate
decreases accordingly. This causes a ‘suction effect’ MRI indicator of this anomaly.34 The herniation of the
on the spinal cord that distends it during each systole, cerebellum through the foramen magnum causes vari-
thereby contributing to the increase in the mechani- able degrees of encroachment of the dorsal subarach-
cal distension of the spinal cord and leading to syrinx noid space at that level. In turn, this causes disturbance
formation.2,20 to CSF flow dynamics in the craniocervical area, lead-
• Such alterations of the CSF hydrodynamics can result ing to progressive syringomyelia in the spinal cord.33
from a variety of conditions causing some degree of Abnormal CSF flow dynamics have been demonstrated
(a)
Fig. 7.9.1 Transverse T2W images at the level of caudal

C1 (a) and mid-T1 (b) in a 7-year-old Jack Russell
Terrier with Chiari-like malformation and secondary
syringomyelia in the cervical spine. At the level of C1,
a small syrinx is present (arrow) and there is pre-syrinx
interstitial edema in the dorsal parenchyma (arrowhead).
At the level of T1, a large well-formed syrinx (dashed
arrow) is visible. The syrinx is markedly T2 hyperintense
(b)
due to its fluid content. (1.5T MRI system)
Sy r i ng om y e l i a 597
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(a)
(b)
(c)
Fig. 7.9.2 Sagittal T2W image of the cervical spine (a) and
transverse T2W (b), T1W (c), and T2-FLAIR (d) images
at the level of C2-C3 in a 5-year-old female Cavalier King
Charles Spaniel with Chiari-like malformation and secondary
syringomyelia. There is herniation of the cerebellar vermis
through the foramen magnum (arrow, a). A large syrinx
extends from cranial C2 to C5, which has a circular shape on
the transverse images and is T2 hyperintense, T1 hypointense,
and suppressed on T2-FLAIR (arrowheads, b–d).
(d)
(1.5T MRI system)
with phase-contrast cine MRI in Cavalier King Charles affected with Chiari-like malformation and syringo-
Spaniels affected by Chiari-like malformation, includ- myelia compared with control dogs and Cavalier King
ing interrupted flow at the foramen magnum and inho- Charles Spaniels with Chiari-like malformation only,
mogeneous flow (turbulence or jets) at the foramen supporting the pulse pressure theory (see above) as an
magnum or the C2-C3 space.9 Inhomogeneous flow important contributing factor to syrinx development.17
is associated with the presence and severity of syrin- Chiari-like malformation is common in the Cavalier
gomyelia.9 Cardiac-gated cine balanced fast field echo King Charles Spaniel, but is reported in other breeds
studies demonstrated significantly greater pulsation such as the Griffon Bruxellois and many other small-
of the cerebellum in Cavalier King Charles Spaniels breed dogs as well.3,19,25,34–36
598 CHAPTER 7.9
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• Other anomalies of the caudal fossa or craniocervical flank (resulting in ‘phantom scratching’), scoliosis, signs
junction such as quadrigeminal cysts (see Chapter 5.5), of cervical myelopathy, or cerebellovestibular signs.19,36
atlanto-occipital overlapping, atlantoaxial instability,
occipitoatlantoaxial malformations, atlantoaxial dural MRI APPEARANCE OF SYRINGOMYELIA
bands, or dens abnormalities (see Chapter 7.4) can lead
to the development of syringomyelia through similar • Although a recent study showed that CT performed as
mechanisms (Figs. 7.9.3, 7.9.4).37 well as MRI in identifying and measuring syringomyelia
• Other conditions such as tethered spinal cord (e.g., sec- lesions in dogs,47 MRI is still considered a better imag-
ondary to dermoid sinus or myelomeningocele),38,39 ing modality than CT to assess the presence and extent
trauma, arachnoiditis, caudal fossa space-occupying of the syrinx and, in particular, allow assessment of pre-
lesions (such as brain stem tumors40,41 or epidermoid syrinx interstitial edema, which is not visible on CT.
cyst42), and spinal arachnoid diverticula43–46 can also be • A syrinx appears as longitudinally elongated T2 hyper-
associated with syringomyelia (Fig. 7.9.5). intense/T1 hypointense cavities within the spinal
• Treatment of the underlying cause can lead to resolution cord, with a similar signal intensity to that of the CSF
of the syrinx on follow-up imaging, underscoring the (Figs. 7.9.2–7.9.4).36 On T2-FLAIR images the signal
dynamic process at play in the formation of syringomy- within these cavities is suppressed. These characteristics
elia (Fig. 7.9.3).40,46 are due to the fluid-filled nature of the lesions.
• In some cases, syringomyelia can be present without obvi- • The shape of the spinal cord cavities may be complex
ous identifiable craniocervical junction abnormality.19,25 with septations. Portions of the central canal may be
As some of these dogs are found to have concomitant dilated and can communicate with syrinx cavities.
dilation of the ventricular system, it is hypothesized that • The longitudinal extent of the syrinx can be well appre-
they may have some form of obstruction of the fora- ciated on sagittal images, especially T2W images, due
men magnum (e.g., arachnoiditis) other than Chiari- to the hyperintense signal of the lesions. However, the
like malformation or classic craniocervical junction dimensions of the syrinx may be overestimated on T2W
anomalies.19,25 images due to summation with areas of pre-syrinx inter-
• Clinical signs of syringomyelia associated with cranio- stitial spinal cord edema that precede the cavitation, and
cervical abnormalities may occur at any age and include some authors advocate the use of T1W series to obtain
hyperesthesia, allodynia and paresthesia of neck and more accurate measurements of the lesions.48
(a) (b)
(c) (d)
Fig. 7.9.3 Sagittal T1W image of the head (a), initial sagittal T2W images over the cervicothoracic (b) and thoracolumbar (c) spine,
and sagittal T2W image (d) of the cervicothoracic spine a few weeks after placement of a ventriculoperitoneal shunt in a 10-year-old
Toy Poodle with a quadrigeminal cyst, hydrocephalus, and secondary syringomyelia. The quadrigeminal cyst is indicated in (a) by
the arrow and is causing compression of the cerebellum (asterisk). There is irregular discontinuous syringomyelia involving
the cervical, thoracic, and lumbar spine (dashed arrows, b and c). After treatment (d), there is mild improvement of the cervical
syringomyelia and marked improvement of the cranial thoracic syringomyelia (arrowhead). (1.5T MRI system)
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(a)
(b)
Fig. 7.9.4 Sagittal T2W (a) and transverse T1W (b) and T2W
(c) images at the level of cranial C3 in a 10-year-old Pug
with an atlantoaxial fibrous band (arrow, a) causing dorsal
compression of the subarachnoid space and mild dorsal cord
compression; there is a long irregular syrinx in the cervical
spine, which appears T1 hypointense and T2 hyperintense
(c)
(dotted arrows, b and c). (1.5T MRI system)
• Although in dogs with craniocervical junction anomalies features of these conditions (e.g., arachnoid diverticula,
(e.g., Chiari-like malformation) and concurrent syrin- quadrigeminal cyst, space-occupying neoplastic lesion,
gomyelia the cervical spinal cord is often affected, other meningitis with adhesions) will be present. These are
parts of the spinal cord are commonly involved as well, described in detail in other chapters (Figs. 7.9.4, 7.9.5).
and therefore the entire spine should be imaged to evalu- • The potential association between morphologic fea-
ate the extent of the condition.48 In Cavalier King Charles tures of the syrinx on MRI and clinical signs has been
Spaniels with Chiari-like malformation, syringomyelia studied:23,30
when present affects the C1-C4 segment in 100% of cases, • Although the presence of a syrinx is not necessarily
the C5-L2 segment in 76%, and the L3-L7 segment in associated with neurologic signs,11,12 larger syringo-
49% of cases (Fig. 7.9.3).48 The maximal dorsoventral myelia lesions increase the likelihood of these signs.11
syrinx size can occur in any region of the spinal cord.48 According to one study, maximum syrinx width is a
• In Cavalier King Charles Spaniels with Chiari-like mal- strong predictor of pain, scratching behavior, and sco-
formation/syringomyelia, there is a correlation between liosis; 95% of Cavalier King Charles Spaniels with a
syrinx size and extent and the patient’s age, indicating maximum syrinx width of 0.64 cm or more will have
that the condition is progressive and not static.14,48 associated clinical signs.23 However, other studies
• In cases of Chiari-like malformation, the cerebellum failed to demonstrate a relationship between syrinx
and medulla are seen on sagittal MR images to extend width and persistent pain.30
into or through the foramen magnum, which is occluded • Association of syrinx size with neurologic deficits was
with little or no CSF around the neural structures also found in American Brussels Griffon dogs.19
(see Chapter 5.1) (Fig. 7.9.2). The size of the cerebellar • Larger lesions with involvement of the dorsal horns
herniation does not correlate with the severity of clinical of the gray matter of the spinal cord and asymmetric
signs.11,12 Ventricular dilation is common, and the degree appearance of the syrinx on transverse images may be
of dilation correlates with the syrinx dimensions.15,36 associated with persistent neuropathic pain, although
• When syringomyelia is developing secondary to condi- the relative contribution of the asymmetry and syrinx
tions other than Chiari-like malformations, specific MRI size is controversial (Fig. 7.9.6).23,30
600 Chapter 7.9
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(a)
(b)
Fig. 7.9.5 Sagittal T2W image of the cervical spine (a)

and transverse T2W images at the level of mid-C3 (b) and
cranial C4 (c) in a 2-year-old dog with a previous history
of cryptococcal meningitis that was successfully treated.
A dorsal arachnoid diverticulum developed over C2 and C3,
presumably secondary to adhesions from previous meningitis
(arrows, a and b). Early syrinx formation is noted in the spinal
cord parenchyma caudal to the lesion (arrowheads, a and c).
(c)
(1.5T MRI system)
Fig. 7.9.6 Transverse T2W image of the cervical spine in a

9-year-old male Cavalier King Charles Spaniel with Chiari-
like malformation and syringomyelia showing a large syrinx
involving the dorsal horns of the gray matter, which is very
asymmetric, more severe on the left side. (1.5T MRI system)
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1. Kirberger RM, Jacobson LS, Davies JV et al. (1997). magnetic resonance imaging. Vet J 198(1):88–91.
Hydromyelia in the dog. Vet Radiol Ultrasound 38(1):30–8. 18. Fenn J, Schmidt MJ, Simpson H et al. (2013). Venous sinus
volume in the caudal cranial fossa in Cavalier King Charles
2. Rusbridge C, Greitz D, Iskandar BJ (2006). Syringomyelia:
spaniels with syringomyelia. Vet J 197(3):896–7.
current concepts in pathogenesis, diagnosis, and treatment.
19. Freeman AC, Platt SR, Kent M et al. (2014). Chiari-like
J Vet Intern Med 20(3):469–79.
malformation and syringomyelia in American Brussels Griffon
3. Driver CJ, Volk HA, Rusbridge C et al. (2013). An update on
dogs. J Vet Intern Med 28(5):1551–9.
the pathogenesis of syringomyelia secondary to Chiari-like
20. Greitz D (2006). Unraveling the riddle of syringomyelia.
malformations in dogs. Vet J 198(3):551–9.
Neurosurg Rev 29(4):251–63; discussion 64.
4. Sakka L, Coll G, Chazal J (2011). Anatomy and physiology of 21. Hu HZ, Rusbridge C, Constantino-Casas F et al. (2012).
cerebrospinal fluid. Eur Ann Otorhinolaryngol Head Neck Dis Histopathological investigation of syringomyelia in the
128(6):309–16. Cavalier King Charles spaniel. J Comp Pathol 146(2-3):
5. Bagley RS, Harrington ML, Tucker RL et al. (1996). Occipital 192–201.
dysplasia and associated cranial spinal cord abnormalities in 22. Marino DJ, Loughin CA, Dewey CW et al. (2012).
two dogs. Vet Radiol Ultrasound 37(5):359–62. Morphometric features of the craniocervical junction region
6. Carrera I, Dennis R, Mellor DJ et al. (2009). Use of magnetic in dogs with suspected Chiari-like malformation determined
resonance imaging for morphometric analysis of the caudal by combined use of magnetic resonance imaging and
cranial fossa in Cavalier King Charles Spaniels. Am J Vet Res computed tomography. Am J Vet Res 73(1):105–11.
70(3):340–5. 23. Rusbridge C, Carruthers H, Dube MP et al. (2007).
7. Carruthers H, Rusbridge C, Dube MP et al. (2009). Syringomyelia in cavalier King Charles spaniels: the
Association between cervical and intracranial dimensions and relationship between syrinx dimensions and pain. J Small
syringomyelia in the cavalier King Charles spaniel. J Small Anim Pract 48(8):432–6.
Anim Pract 50(8):394–8. 24. Rusbridge C, Knowler SP (2006). Coexistence of occipital
8. Cerda-Gonzalez S, Dewey CW, Scrivani PV et al. (2009). dysplasia and occipital hypoplasia/syringomyelia in the
Imaging features of atlanto-occipital overlapping in dogs. cavalier King Charles spaniel. J Small Anim Pract 47(10):
Vet Radiol Ultrasound 50(3):264–8. 603–6.
9. Cerda-Gonzalez S, Olby NJ, Broadstone R et al. (2009). 25. Rusbridge C, Knowler SP, Pieterse L et al. (2009). Chiari-like
Characteristics of cerebrospinal fluid flow in Cavalier King malformation in the Griffon Bruxellois. J Small Anim Pract
Charles Spaniels analyzed using phase velocity cine magnetic 50(8):386–93.
resonance imaging. Vet Radiol Ultrasound 50(5):467–76. 26. Schmidt MJ, Amort KH, Failing K et al. (2014). Comparison
10. Cerda-Gonzalez S, Olby NJ, Griffith EH (2015). Dorsal of the endocranial and brain volumes in brachycephalic dogs,
compressive atlantoaxial bands and the craniocervical junction mesaticephalic dogs and Cavalier King Charles spaniels in
syndrome: association with clinical signs and syringomyelia relation to their body weight. Acta Vet Scand 56:30.
in mature cavalier King Charles spaniels. J Vet Intern Med 27. Schmidt MJ, Kramer M, Ondreka N (2012). Comparison of
29(3):887–92. the relative occipital bone volume between Cavalier King
11. Cerda-Gonzalez S, Olby NJ, McCullough S et al. (2009). Charles spaniels with and without syringohydromyelia and
Morphology of the caudal fossa in Cavalier King Charles French bulldogs. Vet Radiol Ultrasound 53(5):540–4.
Spaniels. Vet Radiol Ultrasound 50(1):37–46. 28. Schmidt MJ, Neumann AC, Amort KH et al. (2011).
12. Couturier J, Rault D, Cauzinille L (2008). Chiari-like Cephalometric measurements and determination of general
malformation and syringomyelia in normal cavalier King skull type of Cavalier King Charles Spaniels. Vet Radiol
Charles spaniels: a multiple diagnostic imaging approach. Ultrasound 52(4):436–40.
J Small Anim Pract 49(9):438–43. 29. Schmidt MJ, Ondreka N, Sauerbrey M et al. (2012). Volume
13. Driver CJ, Chandler K, Walmsley G et al. (2013). The association reduction of the jugular foramina in Cavalier King Charles
between Chiari-like malformation, ventriculomegaly and seizures Spaniels with syringomyelia. BMC Vet Res 8:158.
in cavalier King Charles spaniels. Vet J 195(2):235–7. 30. Schmidt MJ, Roth J, Ondreka N et al. (2013). A potential role
14. Driver CJ, De Risio L, Hamilton S et al. (2012). Changes for substance P and interleukin-6 in the cerebrospinal fluid of
over time in craniocerebral morphology and syringomyelia in Cavalier King Charles Spaniels with neuropathic pain. J Vet
cavalier King Charles spaniels with Chiari-like malformation. Intern Med 27(3):530–5.
BMC Vet Res 8:215. 31. Schmidt MJ, Volk H, Klingler M et al. (2013). Comparison of
15. Driver CJ, Rusbridge C, Cross HR et al. (2010). Relationship closure times for cranial base synchondroses in mesaticephalic,
of brain parenchyma within the caudal cranial fossa and brachycephalic, and Cavalier King Charles Spaniel dogs.
ventricle size to syringomyelia in cavalier King Charles Vet Radiol Ultrasound 54(5):497–503.
spaniels. J Small Anim Pract 51(7):382–6. 32. Shaw TA, McGonnell IM, Driver CJ et al. (2012). Increase
16. Driver CJ, Rusbridge C, McGonnell IM et al. (2010). in cerebellar volume in Cavalier King Charles Spaniels with
Morphometric assessment of cranial volumes in age- Chiari-like malformation and its role in the development of
matched Cavalier King Charles spaniels with and without syringomyelia. PLoS One 7(4):e33660.
syringomyelia. Vet Rec 167(25):978–9. 33. Shaw TA, McGonnell IM, Driver CJ et al. (2013). Caudal
17. Driver CJ, Watts V, Bunck AC et al. (2013). Assessment of cranial fossa partitioning in Cavalier King Charles spaniels.
cerebellar pulsation in dogs with and without Chiari-like Vet Rec 172(13):341.
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34. Harcourt-Brown TR, Campbell J, Warren-Smith C et al. 42. MacKillop E, Schatzberg SJ, De Lahunta A (2006).
(2015). Prevalence of Chiari-like malformations in clinically Intracranial epidermoid cyst and syringohydromyelia in a dog.
unaffected dogs. J Vet Intern Med 29(1):231–7. Vet Radiol Ultrasound 47(4):339–44.
35. Loughin CA (2016). Chiari-like malformation. Vet Clin North 43. Foss KD, Berry WL (2009). What is your neurologic
Am Small Anim Pract 46(2):231–42. diagnosis? Spinal arachnoid cysts. J Am Vet Med Assoc
36. Lu D, Lamb CR, Pfeiffer DU et al. (2003). Neurological signs 234(8):1009–11.
and results of magnetic resonance imaging in 40 cavalier King 44. Galloway AM, Curtis NC, Sommerlad SF et al. (1999).
Charles spaniels with Chiari type 1-like malformations. Vet Rec Correlative imaging findings in seven dogs and one cat with
153(9):260–3. spinal arachnoid cysts. Vet Radiol Ultrasound 40(5):445–52.
37. Loughin CA, Marino DJ (2016). Atlantooccipital overlap and 45. Goncalves R, Hammond G, Penderis J (2008). Imaging
other craniocervical junction abnormalities in dogs. Vet Clin diagnosis: erroneous localization of spinal arachnoid cyst.
North Am Small Anim Pract 46(2):243–51. Vet Radiol Ultrasound 49(5):460–3.
38. Kiviranta AM, Lappalainen AK, Hagner K et al. (2011). 46. Oxley W, Pink J (2012). Amelioration of caudal thoracic
Dermoid sinus and spina bifida in three dogs and a cat. J Small syringohydromyelia following surgical management of an
Anim Pract 52(6):319–24. adjacent arachnoid cyst. J Small Anim Pract 53(1):67–72.
39. Ricci E, Cherubini GB, Jakovljevic S et al. (2011). 47. Kromhout K, van Bree H, Broeckx BJ et al. (2015). Low-
MRI findings, surgical treatment and follow-up of a field magnetic resonance imaging and multislice computed
myelomeningocele with tethered spinal cord syndrome in a tomography for the detection of cervical syringomyelia in
cat. J Feline Med Surg 13(6):467–72. dogs. J Vet Intern Med 29(5):1354–9.
40. da Costa RC, Parent JM, Poma R et al. (2004). Cervical 48. Loderstedt S, Benigni L, Chandler K et al. (2011).
syringohydromyelia secondary to a brainstem tumor in a dog. Distribution of syringomyelia along the entire spinal cord
J Am Vet Med Assoc 225(7):1061–4, 48. in clinically affected Cavalier King Charles Spaniels. Vet J
41. Jung DI, Park C, Kang BT et al. (2006). Acquired cervical 190(3):359–63.
syringomyelia secondary to a brainstem meningioma in a
Maltese dog. J Vet Med Sci 68(11):1235–8.
CHAPTER 7.10
MRI OF THE BRACHIAL AND

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LUMBOSACRAL PLEXUSES 603
Wilfried Mai
CONTENTS
Neoplasia ..............................................................................................................................................................................................................604
Other tumors....................................................................................................................................................................................................607
Inflammatory changes ........................................................................................................................................................................................... 611
Traumatic injuries..................................................................................................................................................................................................613
References............................................................................................................................................................................................................. 617
The peripheral nervous system forms the ultimate link lesions and depict their anatomy and relationship to the
between the central integrating pathways of the nervous surrounding structures, especially the intervertebral
system and the body structures performing a specific func- foramen and spinal cord.2
tion. It is responsible for projecting information to (affer- • Imaging of the nerves is challenging because of the fat
ent/sensory) and from (efferent/motor) the central nervous and blood vessels throughout the muscles that usually
system. Due to its exquisite soft tissue contrast and multi- surround the nerve(s) of interest. The use of fat sup-
planar imaging capabilities, spinal MRI is the technique of pression techniques and contrast-enhanced imaging
choice to investigate conditions of the spinal nerve roots and will, therefore, be extremely important for that specific
proximal portions of the spinal nerves close to the interver- application.3
tebral foramina. In this chapter, we will focus on conditions • Imaging should be performed with perfect positioning
affecting the brachial and lumbosacral plexuses, as diseases of the patient, usually in dorsal recumbency with sym-
of these specific structures often cause characteristic clinical metric positioning of the limbs,2 as comparison between
syndromes that lead to focused imaging with MRI. The bra- the affected and the healthy side is very useful, especially
chial plexus is a complex network of interconnected nerves when lesions are subtle. For the brachial plexus, the
formed from contributions from spinal nerves C6, C7, C8, thoracic limbs should be extended cranially and for the
T1, and T2, giving rise to the sensory and motor nerves of lumbosacral plexus the pelvic limbs should be extended
the thoracic limbs.1 It is anatomically located immediately caudally.
cranial to the first rib, medial to the shoulder joint. The • On pre-contrast series, short tau inversion-recovery
lumbosacral plexus is a network of interconnected nerves pulse sequences (STIR) are useful for outlining nerve
formed from contributions from spinal nerves L4 to S2, giv- lesions, which are usually hyperintense and readily vis-
ing rise to the nerves of the pelvic limbs. Most of the nerves ible when the hyperintense background signal from fat is
of the lumbosacral plexus are formed in the hypaxial mus- suppressed.2,3 At the author’s institution, a large field of
cles, ventral to the caudal lumbar spine and sacrum, or close view (FOV) STIR series in the dorsal plane, extending
to them. The most common conditions of the brachial or from dorsal to the spine ventrally to encompass both the
lumbosacral plexus that are imaged with MRI include neo- left and right brachial plexuses (or lumbosacral plexus, if
plasia, trauma, and, less commonly, inflammatory changes. applicable), is usually the first series obtained, in order to
get a general idea of the most likely area affected and to
TECHNICAL CONSIDERATIONS evaluate symmetry of musculature, which would bring
attention to the area of interest.
• With MRI, multiplanar imaging using multiple pulse • A recommended protocol for imaging suspected brachial
sequences is necessary to identify peripheral nerve sheath plexus lesions is described in Table 7.10.1.2
604 CHAPTER 7.10
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Table 7.10.1 Recommended MRI protocol to evaluate the brachial plexus.
• Dorsal recumbency, paying attention to perfect symmetry and identical positioning of the left and right thoracic limbs to obtain perfect symmetry
on transverse and dorsal images.
• Large field of view series including both axillae and vertebral canal from C5 to T3:
• Body coil or flexible torso-array coil.
• 4–5 mm slice thickness.
• Dorsal STIR series encompassing both the right and left shoulder regions.
• Transverse T2W series centered on midline to compare right and left axillary regions.
• Sagittal T2W series (over the affected side, from the spine to the shoulder joint).
• Transverse pre- and post-contrast T1W series.
• Smaller field of view series, over the C5-T3 area:
• Spinal coil or torso-array coil with good signal-to-noise ratio.
• Thinner slices (2–3 mm).
• Transverse, sagittal, and dorsal plane series, T1W post-contrast (preferably with fat saturation), centered over the spine and encompassing the
nerve roots and proximal nerve paths.
Source: Modified from Kraft S, Ehrhart EJ, Gall D et al. (2007). Magnetic resonance imaging characteristics of peripheral nerve sheath tumors of the canine brachial plexus
in 18 dogs. Vet Radiol Ultrasound 48(1):1–7.
they often form palpable masses that are amenable

NEOPLASIA to direct sampling or ultrasound-guided sampling.
More proximal tumors can occasionally be identified
Peripheral nerve sheath tumors on the edge of the FOV on a spinal or plexus MRI
• Primary neoplasms of the peripheral nervous system are series when imaging patients with clinically suspected
rare. These tumors include those in the brachial and plexus tumors. In these cases, the radiologist can
lumbosacral plexuses and represent 26% of canine ner- re-image the patient with readjustment of position-
vous system tumors.1 ing/size of the FOV.6
• Peripheral nerve sheath tumors (PNSTs) arise from the • There is often overlap between these categories, as a
cells surrounding the axons and have been previously tumor originating in one of these three areas com-
classified as neurinomas, neurilemmomas, schwannomas, monly extends proximally and/or distally to involve
neurofibromas, and neurofibrosarcomas.4,5 The Schwann the adjacent regions.
cells are the presumed cells of origin of these neoplasms. • Most plexus PNSTs are found in the brachial plexus, and
Although well recognized in people, the distinction as such are located medial or ventromedial to the shoul-
between schwannoma, neurofibroma, and malignant der joint in the axilla. In this location, affected patients
PNSTs is not as clear in dogs and cats and they are usu- may present with lameness, monoparesis, muscle atro-
ally referred to as ‘peripheral nerve sheath tumors’; they phy, and pain on palpation of the axillary area; various
can be high-grade malignant, low-grade malignant, or sensory deficits are noted, the territorial distribution
benign.4 of which depends on which nerve(s) of the plexus is/are
• PNSTs can affect the cranial or spinal nerves (cranial affected. With time, there is often proximal extension
nerve tumors are covered in Chapter 5.10). Although any through tracking along the nerves; the tumor can sec-
nerve can be affected, spinal PNSTs commonly affect ondarily invade the intervertebral foramen and spinal
the caudal cervical and cranial thoracic area (i.e., the canal and cause variable degrees of spinal cord com-
region of the brachial plexus) and, less commonly, the pression/invasion, at which time neurologic deficits can
lumbosacral plexus. develop in the pelvic limbs.6
• Based on location, spinal PNSTs can be divided into:5 • MRI features of brachial plexus tumors include:2,5–7
• Root tumors, affecting the dorsal or ventral nerve • Variable shape:
roots, which are intradural/extramedullary with – Circumscribed mass, which can be rounded, oval-
possible extradural and/or intramedullary extension shaped, or lobulated (Fig. 7.10.1).
(these are covered in Chapter 7.6). – Diffuse brachial plexus nerve thickening forming
• Plexus tumors, affecting nerves of the brachial/lum- tubular lesions affecting one or several branches
bosacral plexuses or portions of the nerves distal to of the plexus (Figs. 7.10.2–7.10.5; see also
the intervertebral foramen. Fig. 4.2.23).
• Peripheral tumors, which occur distal to the plexus, • Compared with the surrounding skeletal muscles,
forming mass lesions more distally, commonly along the lesions are usually hyperintense on T2W
the limbs but possibly in any region of the body. images, although mixed signal intensity (hyper- and
These are typically not imaged with spinal MRI, as isointense) is possible.2,8
M R I of t h e Br ac h i a l a n d Lu m bos ac r a l P l e x us e s 605
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(a) (b)
Fig. 7.10.1 Dorsal STIR (a), transverse T2W (b), and T1W
post-contrast (c) images at the level of the brachial plexus in
an 11-year-old Golden Retriever with a several-month history
of left thoracic limb monoparesis, muscle atrophy, and biting
of the nails of that limb. There is a large lobulated mass in
the left brachial plexus (solid arrows), which is hyperintense
on the STIR (a) and T2W images (b) and has heterogeneous
contrast enhancement after gadolinium injection (c). On the
dorsal STIR image (a), there is visible thickening of the left
radial nerve extending distally from the lobulated mass due
to neoplastic infiltration tracking along that nerve (dashed
(c)
arrow). (1.5T MRI system)
• Lesions are most commonly isointense to surrounding hyperintense signal on T2W images, STIR images,
muscles on T1W pre-contrast images and occasionally and pre-contrast T1W images with mild contrast
hyperintense or mixed hyper- and isointense. enhancement; such changes are consistent with neu-
• Most lesions have moderate to strong contrast rogenic atrophy, edema, fatty infiltrate, and fibrosis
enhancement;2,8 minimal/mild enhancement is possi- (Fig. 7.10.6).2
ble, and absence of enhancement is rare. • MRI features of lumbosacral PNSTs have been rarely
• The enhancement pattern is more commonly hetero- reported in the veterinary literature:4,9
geneous than homogeneous. • Sciatic nerve PNSTs form well-marginated tubular
• Using fat saturation techniques to suppress the hyper- masses in the pelvic canal, ventral to the lumbosacral
intense signal from fat on post-contrast images can spine and sacrum, in a location consistent with the
help identify lesions by increasing the contrast of sciatic nerve (Figs. 7.10.7, 7.10.8): ventromedial to
enhancing tissue compared with the background.3 the ipsilateral iliac wing and then crossing over cau-
• Ipsilateral atrophy of the muscles innervated by the dolaterally, dorsal to the greater ischiatic notch and
affected nerve(s); often, the atrophied muscles have ischiatic spine, bending ventrally to pass caudomedial
606 CHAPTER 7.10
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(a) (b)
(c) (d)
Fig. 7.10.2 Serial dorsal plane STIR images of the cervicothoracic spine and brachial plexus region in a 12-year-old Miniature
Pinscher with a brachial plexus peripheral nerve sheath tumor affecting the right spinal nerves C6, C7, and C8. Images
progress from dorsal to ventral from (a) to (f). In (a) and (b), the thickened roots of the right spinal nerves at C5-C6 (solid
arrow), C6-C7 (dashed arrow), and C7-T1 (dotted arrow) are visible. Progressing ventrally, the infiltrated nerves of the brachial
plexus form an irregular lobulated hyperintense mass (arrowheads, e and f ). Fat suppression aids in the identification of the
lesion by eliminating the bright signal from the fat, which is typically abundant in the axillary region. Note the atrophy and
diffuse hyperintense signal of the supraspinatus, infraspinatus, and subscapularis muscles secondary to denervation atrophy
(dashed circle, e). (See also the sagittal and transverse images in Figs. 7.10.3 and 7.10.4.) (1.5T MRI system) (Continued)
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(e) (f)
to the greater trochanter as it travels distally. Proximal

extension into the ipsilateral L7-S1 intervertebral
foramen may be seen.4 Mass effect and compression
of the colon can be seen with larger mass-like lesions
in the pelvic canal. The lesions are slightly hyper-
intense to muscles on T2W images, isointense with
hyperintense areas on T1W pre-contrast images, with
strong heterogeneous contrast enhancement after
gadolinium injection.
• Femoral nerve PNSTs form elongated/tubular lesions
ventral to L5-L6, closely associated with or within
the corresponding iliopsoas muscle, again matching
the anatomic course of that nerve.9 The reported
lesions were iso- to slightly hyperintense to surround-
ing muscles on T1W images, hyperintense on T2W
images, and enhancing after gadolinium injection.
Other tumors
• Other tumors of the brachial plexus have been reported,
including poorly differentiated sarcomas, myxosarcoma,
and lymphoma.1,10–12 Malignant sarcomas infiltrating the
femoral nerves have also been reported in two dogs.13
• In a series of feline spinal lymphoma, three out of 23 cats
Fig. 7.10.3 Parasagittal STIR image to the right of midline
had infiltration of a brachial plexus forming a mass-like
in the area of the brachial plexus in the same dog as in
lesion affecting several nerves of the plexus, with proxi-
Fig. 7.10.2. The thickened and markedly hyperintense C7
mal extension into the subarachnoid space.10 The MRI
(dashed arrow) and C8 (dotted arrow) nerves traveling
appearance of a feline brachial plexus lymphoma has only
caudoventrally are readily visible. (1.5T MRI system)
been reported once.11 An axillary mass was seen in the
area of the affected brachial plexus extending from cra-
nial C5 to cranial T1; the mass was slightly hyperintense
to muscle on T1W images and markedly hyperintense
608 CHAPTER 7.10
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(a) (b)
(c) (d)
Fig. 7.10.4 Transverse T2W (a) and T1W post-contrast with fat saturation (b) images at the level of C6-C7 and transverse
T2W (c) and T1W post-contrast with fat saturation (d) images at the level of C7-T1 in the same dog as in Figs. 7.10.2 and
7.10.3. On the T2W images (a, c), the thickened right C7 (dashed arrow) and C8 (dotted arrow) nerves are visible and appear
hyperintense to the skeletal muscles. The thickened C7 nerve is causing very mild right ventral compression of the spinal
cord (a). On the T1W post-contrast images (b, d) there is marked diffuse heterogeneous enhancement of the thickened
C7 (dashed arrow, b) and C8 (dotted arrow, d) nerves. In (c), atrophy and mild hyperintensity of the muscles around the right
scapula are noted. In (c) and (d), note the focal thickening and enhancement of the dorsal and ventral rootlets of the right
C8 nerve (arrowheads). (1.5T MRI system)
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(a)
(b)
(c) (d)
Fig. 7.10.5 Transverse pre- and post-contrast T1W images with fat saturation at the level of C7-T1 (a, b) and mid-T2 (c, d) in a
9-year-old Labrador Retriever presented with chronic lameness on the right thoracic limb with atrophy of the triceps muscle.
There is a tubular structure with peripheral enhancement in the anatomic area of the radial nerve (solid arrows, a and b;
dashed arrows, c and d) that can be traced to the right triceps muscle. The triceps muscle is atrophied and has mild increased
signal intensity on pre-contrast images with mild contrast enhancement after gadolinium injection (arrowheads, c and d).
Histopathology of the radial nerve after amputation revealed a malignant peripheral nerve sheath tumor and denervation
myofiber atrophy of the triceps muscle. (1.5T MRI system)
610 CHAPTER 7.10
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on T2W images. It invaded the vertebral canal through foramen into the vertebral canal. The mass was heteroge-
the widened C7-T1 intervertebral foramen and caused neously hyperintense to muscles on T2W images, iso- to
displacement of the spinal cord at that level. mildly hypointense on T1W images pre-contrast, and
• The MRI appearance of a femoral nerve sarcoma associ- had mild heterogeneous peripheral contrast enhancement
ated with the lumbosacral plexus was reported in a dog.13 after gadolinium injection. There was also atrophy of the
A paravertebral mass was seen ventral to the transverse ipsilateral paravertebral lumbar muscles. These MRI fea-
processes of L5–L7 within the corresponding psoas mus- tures are similar to other types of neoplasia of the femoral
cle, with dorsal extension through the L5-L6 intervertebral nerve, such as PNST or lymphoma (Fig. 7.10.9).
Fig. 7.10.6 Dorsal STIR image in the same

dog as in Fig. 7.10.5, with a final diagnosis of
a malignant peripheral nerve sheath tumor
of the right radial nerve and denervation
myofiber atrophy of the triceps muscle.
On this image, hyperintense signal of the
right triceps muscle (arrowheads) is evident
compared with the contralateral side.
(1.5T MRI system)
* *
(a) (b)
Fig. 7.10.7 Serial transverse T1W post-contrast images with fat saturation at the lumbosacral and pelvic level from cranial
to caudal (a–f) in a 6-year-old German Shepherd Dog with a peripheral nerve sheath tumor of the right sciatic nerve. The
thickened and strongly enhancing nerve (arrows) is seen exiting the right L7-S1 intervertebral foramen (a), then traveling
ventromedial to the right iliac body (b), crossing dorsally over the greater ischiatic notch (c and d) and then extending
caudolateroventrally, passing caudal and medial to the right greater trochanter (indicated by the hash sign, e). Note the atrophy
of the right gluteal muscles (asterisks, a and b). (1.5T MRI system) (Continued)
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(c) (d)
(e) (f)
INFLAMMATORY CHANGES • Bilateral hypertrophic neuritis of the brachial plexus

was reported in a 9-year-old Burmese cat that pre-
• Inflammatory changes of the brachial or lumbosacral sented with subacute progressive bilateral thoracic
plexus nerves are rare; the clinical presentation mimics limb lameness with muscle atrophy, postural reaction
that of neoplasia except that signs are more commonly deficits, and territorial sensory deficits in the areas of
bilateral with these conditions as both sides are typically the radial, ulnar, and median nerves.14 On MRI, there
affected. was marked bilateral enlargement of the nerve roots at
612 CHAPTER 7.10
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(a) (b)
(c) (d)
Fig. 7.10.8 Serial dorsal T1W post-contrast images with fat saturation at the lumbosacral and pelvic level from ventral to dorsal
(a–d) in the same dog as in Fig. 7.10.7. The thickened and strongly enhancing right sciatic nerve is seen exiting the right L7-S1
intervertebral foramen (a), and then crossing dorsally over the greater ischiatic notch (b–d) (arrows). Note the atrophy of the
right gluteal muscles. (1.5T MRI system)
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(a) (b)
Fig. 7.10.9 Transverse T1W post-contrast images at the level of L5-L6 (a) and L7 (b) in a 4-year-old Russian Blue cat with
a few-months’ history of left pelvic limb lameness with atrophy of the muscles innervated by the femoral nerve. The cat
had recently become paraplegic. There is thickening and enhancement of the left spinal nerve L5 as it exits the left L5-L6
intervertebral foramen (solid arrows, a), extending into the left iliopsoas muscle, where it forms an enhancing lobulated
mass consistent with infiltration of the left femoral nerve (dashed arrow, b). Compare with the normal right iliopsoas muscle
(asterisk, b). At L5-L6 (a), there is patchy enhancement in the spinal cord consistent with intramedullary/intradural extension of
the neoplasm, explaining the development of paraplegia. The final diagnosis was lymphoma. (1.5T MRI system)
C6-C7, C7-T1, and T1-T2 extending into the interver- nerves were hyperintense on T2W images, hypointense
tebral foramina; the thickened nerves were hyperintense on T1W images, and non-enhancing.
to muscles on T2W images, isointense on T1W images,
and moderately enhancing particularly in the periph- TRAUMATIC INJURIES
ery (Fig. 7.10.10). One of the enlarged nerves at C6-C7
formed a mass-like lesion in the vertebral canal, causing • Traumatic injuries to the brachial plexus, often due to
moderate lateral spinal cord compression. Histologically, avulsion at the origin of the nerves near the interverte-
there was hypertrophic neuritis involving both brachial bral foramina, are occasionally seen in dogs and cats and
plexuses with no underlying neoplastic or infectious are typically suspected/diagnosed based on history, clini-
cause visible. The appearance is non-specific, and dif- cal signs, and electrophysiologic findings.
ferential diagnoses in felines should include idiopathic • Imaging can be used to try and confirm the diagnostic
neuritis (suspected immune-mediated), infectious neuri- suspicion and also evaluate comorbitities in the area of
tis (such as mycobacteria, which have been reported in the plexus, such as concurrent fracture/luxation, trau-
the sciatic/femoral/common fibular nerves15), metabolic matic disc disease, or soft tissue injuries.
neuropathies, and neoplastic neuropathies.10,11,14 • In veterinary medicine, CT myelography after intra-
• Idiopathic brachial plexus neuritis has also been reported thecal administration of water soluble iodinated con-
in dogs.16,17 Recently, a case report describing MRI trast material has been used to identify brachial plexus
changes in a 7-month-old Vizsla dog with chronic inflam- avulsions.19
matory demyelinating polyradiculoneuropathy affecting • In people, MRI findings in cases of brachial plexus avul-
both brachial plexuses from C6 to T1 was published.18 sion include:20
The dog presented with neurologic deficits and muscle • Intramedullary T2 hyperintensity in the area of the
atrophy of both thoracic limbs. On MRI, there was bilat- plexus (C6-T2) suggesting focal edema or malacia and/
eral thickening of the nerve roots from C6-T1 extend- or intramedullary T2 hypointense signal suggesting
ing across the intervertebral foramina. The thickened susceptibility artifacts associated with hemorrhage
614 CHAPTER 7.10
VetBooks.ir
(a) (b)
(c) (d)
Fig. 7.10.10 Transverse T2W images at the level of C7-T1 (a) and T1-T2 (b) and transverse T1W images pre- (c) and post-
contrast (d) at the level of T1-T2 in a 9-year-old cat presented with a 6-day history of subacute onset, progressive, bilateral
thoracic limb weakness. Intermittent right thoracic limb lameness over the previous 2 months was reported. The C8 and T1
spinal nerves and proximal part of the brachial plexus are thickened bilaterally (arrows), with hyperintense signal compared
with skeletal muscles on the T2W images (a, b), isointensity to muscle on the T1W pre-contrast image (c), and moderate
contrast enhancement (d). The plexus portion of the thickening almost forms a mass-like lesion. The appearance could easily
be mistaken for neoplasia such as lymphoma. Histopathologic examination showed changes consistent with hypertrophic
neuritis of the brachial plexus. (1.5T MRI system; reproduced, with permission, under the STM permission guidelines (2014).
from Garosi L, de Lahunta A, Summers B et al. (2006). Bilateral, hypertrophic neuritis of the brachial plexus in a cat: magnetic
resonance imaging and pathological findings. J Feline Med Surg 8(1):63–8.)
VetBooks.ir
in the areas of avulsion, in cases with preganglionic hyperintense signal in the area of the plexus and close
injuries. to the foramina is often seen on T2W or STIR images,
• Contrast enhancement of intradural nerve roots and associated with focal inflammation/edema secondary to
root stumps. the soft tissue trauma (Figs. 7.10.11, 7.10.12).
• Contrast enhancement of paraspinal muscles. • In a case report, the authors used an intrathecal injection of
• In the author’s experience, similar changes can be 0.5 mL gadolinium (Gd-DTPA at 500 mmol/mL) diluted
expected in dogs and cats with these injuries. Irregular in 1 mL of CSF in a 2-year-old Jack Russell Terrier with
(a) (b)
C7-T1
(c) (d)
Fig. 7.10.11 Transverse STIR images across the C7-T1 (a–c) and T1-T2 (d–f) area in a 2-year-old German Shepherd Dog with a
2-week history of non-weight-bearing lameness on the right thoracic limb after a traumatic event. The dog had palpable muscle
atrophy of the right thoracic limb and sensory deficits especially on the lateral aspect of the limb below the elbow. There is
evidence of a traumatic avulsion of the right brachial plexus. An irregular area of marked increased signal is seen in the right
axillary region in the general area of the right brachial plexus (arrowheads, a and d). There is thickening and hyperintense
signal of the right C8 (solid arrows, a–c) and T1 (dotted arrows, d–f) spinal nerves. Atrophy of the muscles of the right thoracic
limb is visible with faint areas of patchy hyperintense signal. (1.5T MRI system) (Continued)
616 CHAPTER 7.10
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T1-T2
(e) (f)
C7 T1
(a) (b)
Fig. 7.10.12 Transverse T2W (a) and parasagittal T2W to the right of midline (b) images at the level of C7-T1 in a 2-year-old
Bichon Frise that was hit by a car. There is marked thickening and hyperintensity of the right C8 nerve (solid arrow, a).
Continuous with the proximal aspect of the nerve, there is a rounded mass-like structure extending into the vertebral canal
(arrowhead, a) and causing marked right-sided compression of the spinal cord (dashed arrow, a). This mass has heterogeneous
T2 signal (dotted arrows, b) consistent with hemorrhagic changes. At surgery, there was traumatic injury to the right C8
nerve and the dorsal root of the nerve was avulsed, while the ventral root could not be clearly identified. A large hematoma
was present in the vertebral canal on the right side in the area of the avulsion, causing severe spinal cord compression.
(1.5T MRI system)
VetBooks.ir
a suspected traumatic avulsion of the right brachial plexus 8. Levitski RE, Lipsitz D, Chauvet AE (1999). Magnetic
after being hit by a car.20 Note that, in people, this route resonance imaging of the cervical spine in 27 dogs. Vet Radiol
of administration of gadolinium is not currently approved Ultrasound 40(4):332–41.
9. Harcourt-Brown TR, Granger N, Smith PM et al. (2009).
by the United States Food and Drug Administration and
Use of a lateral surgical approach to the femoral nerve in the
European Medicines Agency. Changes observed were con-
management of two primary femoral nerve sheath tumours.
sistent with a plexus avulsion including: Vet Comp Orthop Traumatol 22(3):229–32.
• On T2W images, a focal hyperintensity in the spinal 10. Lane SB, Kornegay JN, Duncan JR et al. (1994). Feline spinal
cord at the level of T2 and diffuse hyperintensity of lymphosarcoma: a retrospective evaluation of 23 cats. J Vet
the ventral paravertebral soft tissues in the general Intern Med 8(2):99–104.
area of the right brachial plexus. 11. Mellanby RJ, Jeffery ND, Baines EA et al. (2003). Magnetic
• On T1W images with fat saturation after intrathecal resonance imaging in the diagnosis of lymphoma involving
injection of gadolinium mixed with CSF, there was the brachial plexus in a cat. Vet Radiol Ultrasound 44(5):
522–5.
leakage of hyperintense material through the right
12. Ueno H, Miyoshi K, Fukui S et al. (2014). Extranodal
intervertebral foramina at C7-T1 and T1-T2, follow-
lymphoma with peripheral nervous system involvement in a
ing the corresponding right nerve pathways into the dog. J Vet Med Sci 76(5):723–7.
right ventral paraspinal musculature and pooling in 13. Montoliu P, Pumarola M, Zamora A et al. (2008). Femoral
the interfascial paravertebral spaces. mononeuropathy caused by a malignant sarcoma: two case
reports. Vet J 178(2):298–301.
REFERENCES 14. Garosi L, de Lahunta A, Summers B et al. (2006). Bilateral,
1. Rudich SR, Feeney DA, Anderson KL et al. (2004). Computed hypertrophic neuritis of the brachial plexus in a cat: magnetic
tomography of masses of the brachial plexus and contributing resonance imaging and pathological findings. J Feline Med
nerve roots in dogs. Vet Radiol Ultrasound 45(1):46–50. Surg 8(1):63–8.
2. Kraft S, Ehrhart EJ, Gall D et al. (2007). Magnetic resonance 15. Paulsen DB, Kern MR, Weigand CM (2000).
imaging characteristics of peripheral nerve sheath tumors of Mycobacterial neuritis in a cat. J Am Vet Med Assoc
the canine brachial plexus in 18 dogs. Vet Radiol Ultrasound 216(10):1589–91.
48(1):1–7. 16. Cummings JF, Lorenz MD, de Lahunta A et al. (1973). Canine
3. D’Anjou MA, Carmel EN, Tidwell AS (2011). Value of fat brachial plexus neuritis: a syndrome resembling serum neuritis
suppression in gadolinium-enhanced magnetic resonance in man. Cornell Vet 63:589–617.
neuroimaging. Vet Radiol Ultrasound 52(1 Suppl 1):S85–90. 17. Alexander JW, de Lahunta A, Scott DW (1974). A case of
4. Abraham LA, Mitten RW, Beck C et al. (2003). Diagnosis of brachial plexus neuropathy in a dog. J Am Anim Hosp Assoc
sciatic nerve tumour in two dogs by electromyography and 10:515–6.
magnetic resonance imaging. Aust Vet J 81(1-2):42–6. 18. Kathmann I, Bottcher I, von Klopmann T et al. (2006).
5. Platt SR, McConnell F (2002). What is your diagnosis? Chronic inflammatory demyelinating polyradiculoneuropathy
Malignant nerve sheath tumour. J Small Anim Pract 43(3):103, with hypertrophy of cervico-thoracal nerve roots in a dog.
39–40. Schweiz Arch Tierheilkd 148(6):297–302.
6. Platt SR, Graham J, Chrisman CL et al. (1999). Magnetic 19. Forterre F, Gutmannsbauer B, Schmahl W et al. (1998). CT
resonance imaging and ultrasonography in the diagnosis of a myelography for diagnosis of brachial plexus avulsion in small
malignant peripheral nerve sheath tumor in a dog. Vet Radiol animals. Tierarztl Prax Ausg K Kleintiere Heimtiere 26(5):
Ultrasound 40(4):367–71. 322–9.
7. Kippenes H, Gavin PR, Bagley RS et al. (1999). Magnetic 20. Munoz A, Mateo I, Lorenzo V et al. (2009). Imaging
resonance imaging features of tumors of the spine and spinal diagnosis: traumatic dural tear diagnosed using intrathecal
cord in dogs. Vet Radiol Ultrasound 40(6):627–33. gadopentate dimeglumine. Vet Radiol Ultrasound 50(5):502–5.
CHAPTER 7.11
DEGENERATIVE SPINAL DISEASES

618 Wilfried Mai
CONTENTS
Spondylosis deformans ........................................................................................................................................................................................ 618
Diffuse idiopathic skeletal hyperostosis ................................................................................................................................................................ 619
Degenerative myelopathy ...................................................................................................................................................................................... 619
Leukoencephalomyelopathy .................................................................................................................................................................................. 619
References.............................................................................................................................................................................................................621
Degenerative spinal disease can affect various portions of laterally) of the endplates of the vertebral bodies, and
the spine, including the intervertebral discs, the vertebrae, which attempt to bridge the intervertebral disc spaces.
and the spinal cord. Degenerative intervertebral disc disease The ventral and lateral cortex of the body of affected ver-
is covered in Chapter 7.1. Degenerative conditions particu- tebrae is preserved. Sclerosis of the adjacent endplates is
lar to the lumbosacral junction are covered in Chapter 7.3. common.1
Degenerative conditions involving the articular process • It is commonly (but not systematically) associated with
joints, such as osteoproliferative or cystic changes, are cov- degenerative intervertebral disc disease.
ered in Chapters 7.2 and 7.8. There are a number of often • The condition itself is typically considered incidental
breed-specific neurodegenerative diseases that commonly and of no clinical significance, although spinal stiffness,
affect the brain, with occasional involvement of the spinal lameness, gait abnormalities, and back pain can be seen,
cord; these are described in Chapter 5.2. The conditions possibly associated with concurrent intervertebral disc
described in this chapter are degenerative spinal conditions disease.
for which specific MRI descriptions have been reported in • MRI features associated with spondylosis deformans
the veterinary literature. include (Figs. 7.11.1, 7.11.2):1
• Ventral, markedly hypointense, smoothly margin-
SPONDYLOSIS DEFORMANS ated new bone formation arising from the periphery
of adjacent endplates and tending to bridge over the
• Spondylosis deformans is characterized by focal or mul- space.
tifocal osteophytes or larger bone spurs that appear • The signal from the new bone is hypointense on all pulse
along the periphery (most commonly ventrally but also sequences compared with the vertebral bone marrow.
Fig. 7.11.1 Sagittal T2W image of

the thoracolumbar spine in a 7-year-
old Shiba Inu dog with multiple sites
of disc herniation including L1-L2,
L2-L3, and L3-L4 (arrowheads).
There is multifocal ventral
spondylosis deformans forming
smoothly marginated markedly
hypointense new bone arising
from the margins of the endplates
and bridging the spaces ventrally
(arrows). (1.5T MRI system)
D e ge n e r at i v e Spi n a l D is e a s e s 619
• Moderate to marked degenerative changes of the Welsh Corgi, Chesapeake Bay Retriever, Rhodesian
associated intervertebral discs are common. Disc pro- Ridgeback, Bernese Mountain Dog, Standard Poodle,
trusion or extrusion may be present, with or without Kerry Blue Terrier, Cardigan Welsh Corgi, Golden
associated spinal cord compression. Retriever, Wire Fox Terrier, American Eskimo Dog,
Soft-coated Wheaten Terrier, and Pug.2 Cats have also
DIFFUSE IDIOPATHIC SKELETAL rarely been affected by the condition.3
HYPEROSTOSIS • Age at onset is typically 5 years and older.2
• Clinically, the condition is characterized by progressive
• Diffuse idiopathic skeletal hyperostosis (DISH) is a sys- ataxia of the pelvic limbs, beginning with loss of pro-
temic non-inflammatory disorder manifesting by ossifi- prioception and absence of paraspinal hyperesthesia.2
cation of soft tissues such as ligaments and attachments Typically, upper motor neuron signs of the pelvic limbs
of tendons and joint capsules to bone.1 are seen on presentation, although less commonly, lower
• Although the condition can affect other parts of the skel- motor neuron signs may be present; later in the course
eton, the spine is commonly affected. In that location, of the disease (several months), the thoracic limbs may
DISH appears radiographically as flowing ossification become affected.3
with a trabecular pattern along the lateral and ventral • Histopathologically, there is progressive, non-inflamma-
aspects of the vertebral column, extending over consecu- tory, segmental axonal degeneration and associated loss
tive (at least three or four) vertebrae. The intervertebral of myelin.2
disc width is typically preserved. • Antemortem diagnosis of degenerative myelopathy
• The etiology of DISH is unclear, although a hereditary relies on recognition of the clinical pattern followed
basis has been suggested in some breeds such as the by completion of a series of diagnostic steps to rule out
Boxer, as they appear predisposed; hypothyroidism and other disorders that could have a similar presentation
hypercalcitonism have also been proposed as etiopatho- (CSF analysis, electrodiagnostic testing, spinal cord
logic factors.1 imaging such as myelography, CT, or MRI). A presump-
• Clinical significance is variable, and the condition can tive diagnosis of degenerative myelopathy is usually
be clinically silent or cause spinal pain and dysfunction. made based on absence of clinically significant myelopa-
• MRI features of DISH are best appreciated on sagittal thy on the basis of imaging; MRI is preferred, as it allows
images and include (Fig. 7.11.2):1 exclusion of both extradural compressive lesions such
• Smoothly marginated new bone formation over as intervertebral disc herniation, and intramedullary or
several consecutive vertebral segments, spanning intradural lesions that may be overlooked with myelog-
the bodies and intervertebral spaces in a continuous raphy or CT. DNA testing is now also available that can
manner. support an antemortem diagnosis of the condition.
• The new bone has signal intensity similar to the • Although rare studies using CT-myelography have
bone marrow of the vertebrae. This is attributed to reported morphologic changes in dogs with degenerative
the presence of fat, a characteristic of bone marrow, as myelopathy (such as a smaller than normal spinal cord
the new bone in DISH is made of normal trabecular with associated widening of the subarachnoid space or
bone. change in shape of the spinal cord, becoming triangular
• The high signal within DISH lesions typically is sup- instead of rounded/oval-shaped on transverse images4),
pressed on fat-suppressed pulse sequences such as no such morphologic changes have been reported to date
STIR. with MRI.
• The intervertebral discs in the affected segments • MRI is reportedly normal in dogs with confirmed degen-
have normal appearance or only mild degenerative erative myelopathy.2,3,5
changes, with a preserved high T2 signal of their • Sensitive imaging techniques such as MRI may reveal
nuclei pulposi. areas of disc protrusions causing variable degrees of spi-
• Disc herniation at sites immediately adjacent to seg- nal cord compression, which may confound the diagno-
ments affected by DISH may be observed. sis of degenerative myelopathy, and the clinician must in
these cases be guided by clinical experience and take into
DEGENERATIVE MYELOPATHY account rapidity of disease progression, presence of para-
spinal hyperesthesia, and amount of spinal cord com-
• Degenerative myelopathy is a chronic progressive pression to account for the severity of the myelopathy.
degenerative spinal cord disease that frequently occurs
in large-breed dogs. Some breeds, such as German LEUKOENCEPHALOMYELOPATHY
Shepherd Dogs, are predisposed. Mixed breed dogs can
also be affected, as well as many other breeds including • Leukoencephalomyelopathy is a rare degenerative disor-
Siberian Husky, Miniature Poodle, Boxer, Pembroke der of unknown etiology recognized in the Rottweiler.6
620 CHAPTER 7.11
(a)
(b)
(c)
Fig. 7.11.2 Lateral radiograph of the thoracolumbar spine (a) and sagittal T2W (b) and T1W (c) MR images of the same area
in a 10-year-old mixed breed dog with progressive pelvic limb paresis. Extensive undulating homogeneous new bone is seen
spanning the ventral surface of the spine, including the vertebral bodies and disc spaces in the caudal thoracic and cranial
lumbar area (solid arrows). This appearance is consistent with diffuse idiopathic skeletal hyperostosis (DISH). In the mid-
thoracic region, there is ventral new bone arising from the margins of the endplates bridging the disc spaces ventrally (dotted
arrows). This appearance is consistent with spondylosis deformans. On the MR images (b, c), note that the DISH lesions
form smoothly marginated new bone spanning the ventral surface of the vertebral column and that the proliferation has high
T1W and T2W signal, similar to that of the vertebral bone marrow (solid arrows), while the spondylosis deformans lesions
are markedly hypointense and centered on the intervertebral disc spaces (dotted arrows). Also note that several discs in the
regions affected by DISH have a preserved high T2 signal of their nuclei pulposi, indicating absence of significant degenerative
disease (arrowheads, b), while the discs in the regions of spondylosis deformans have low T2 signal consistent with concurrent
degenerative disc disease. (1.5T MRI system)
D e ge n e r at i v e Spi n a l D is e a s e s 621
A similar condition has also been reported in Leonberger dogs are typically euthanized due to progressive disease
dogs.7 In Rottweilers, a genetic basis for the disorder within 1 year of diagnosis.6
has been suggested because of the familial relationship • Histopathologically, the white matter is affected, espe-
among the dogs, but the mode of inheritance could not cially in the dorsal aspect of the lateral funiculi of the
be elucidated. cervical spinal cord and pyramidal tracts of the medulla
• In Rottweilers, it is clinically characterized by a long- oblongata; there is primarily myelin loss with much less
strided gait with the appearance of stiffness and over- pronounced involvement of the axons, and concurrent
reaching as the limbs are advanced when walking, astrogliosis and astrocytosis.6
consistent with general proprioceptive ataxia and upper • MRI features were reported in a Rottweiler and included:6
motor neuron tetraparesis.6 In Leonbergers, ataxia, dys- • Bilateral and symmetric lesions in the white matter of
metria, and stumbling are reported.7 the dorsolateral funiculi in the cervical spinal cord.
• Age at onset is between 1.5 and 3.5 years. The thoracic • Concurrent lesions in the brain, affecting the pyra-
limbs are typically affected first, and the pelvic limbs are mids of the medulla oblongata, and ventral aspect of
affected later, usually less severely. Prognosis is poor, and the crus cerebri.
• Lesions were hyperintense on T2W, T2*W, and
T2-FLAIR images, isointense on T1W images, with
no contrast enhancement after gadolinium adminis-
tration.
• MRI changes were also reported in two Leonberger dogs
(Fig. 7.11.3) and included similar but more focal changes,
with bilateral, symmetric T2W, and T2-FLAIR hyper-
intensity within the dorsolateral funiculi of the cervical
spinal cord from C1 to C4 in one dog and only over C2
in the other. In these dogs, lesions were also found in
the brain histopathologically, but were not visible on
MRI. The lesions were isointense on T1W images and
non-enhancing.7
REFERENCES
1. Togni A, Kranenburg HJ, Morgan JP et al. (2014).
Radiographic and MRI characteristics of lumbar disseminated
idiopathic spinal hyperostosis and spondylosis deformans in
dogs. J Small Anim Pract 55(7):343–9.
2. Coates JR, Wininger FA (2010). Canine degenerative
myelopathy. Vet Clin North Am Small Anim Pract 40(5):
929–50.
Fig. 7.11.3 Transverse T2W image in a 2.5-year-old
3. Okada M, Kitagawa M, Kanayama K et al. (2009). Negative
female Leonberger dog presented with a 1-year history of MRI findings in a case of degenerative myelopathy in a dog.
intermittent knuckling in the thoracic limbs. Both lateral J S Afr Vet Assoc 80(4):254–6.
funiculi of the spinal cord show increased signal intensity 4. Jones JC, Inzana KD, Rossmeisl JH et al. (2005). CT
(arrows). At necropsy, lesions were most prominent in the myelography of the thoraco-lumbar spine in 8 dogs with
lateral corticospinal tract, but encroached on the dorsal degenerative myelopathy. J Vet Sci 6(4):341–8.
spinocerebellar, rubrospinal, and lateral spinothalamic 5. Coates JR, March PA, Oglesbee M et al. (2007). Clinical
tracts. Histopathologically, severe myelin breakdown was the characterization of a familial degenerative myelopathy in
Pembroke Welsh Corgi dogs. J Vet Intern Med 21(6):1323–31.
most prominent change, and axons were largely preserved,
6. Eagleson JS, Kent M, Platt SR et al. (2013). MRI findings in
consistent with a primary degenerative myelinolytic
a rottweiler with leukoencephalomyelopathy. J Am Anim Hosp
leukoencephalomyelopathy. (Reproduced, with permission, Assoc 49(4):255–61.
from Oevermann A, Bley T, Konar M et al. (2008). A novel 7. Oevermann A, Bley T, Konar M et al. (2008). A novel
leukoencephalomyelopathy of Leonberger dogs. J Vet Intern leukoencephalomyelopathy of Leonberger dogs. J Vet Intern
Med 22(2):467–71.) Med 22(2):467–71.
CHAPTER 7.12
MRI OF SPINAL TRAUMA

622 Wilfried Mai
CONTENTS
Vertebral bony and ligamentous traumatic injuries................................................................................................................................................622
Traumatic disc herniation ......................................................................................................................................................................................623
Hemorrhage ..........................................................................................................................................................................................................625
Spinal cord parenchymal lesions ..........................................................................................................................................................................626
Traumatic dural tears .............................................................................................................................................................................................628
References.............................................................................................................................................................................................................629
Acute spinal trauma can cause instability, which can result strapped to a spinal board, thus protecting against fur-
in failure of the vertebral column to protect the spinal cord ther damage.3
and nerve roots from severe damage, resulting in myelora- • In people, MRI is more sensitive for assessing spinal cord
diculopathy with associated temporary or permanent pare- and supporting soft tissue injuries secondary to spinal
sis/paralysis. Adequate treatment planning and informed trauma. However, spinal fractures may be missed with
prognosis are highly dependent on a rapid and accurate MRI,2 and this is likely the case in dogs and cats as well.
evaluation of the vertebral column and status of the spinal Combined MRI and CT imaging of the trauma patient
cord. There is little documentation about the utility of MRI is therefore recommended when possible, as it provides
in the evaluation of spinal trauma in dogs and cats, but it is the most complete assessment of extent, location, and
a valuable tool, especially to evaluate the soft tissue compo- anatomy of both bone and soft tissue damage.5 However,
nents and secondary spinal cord injury.1,2 this approach depends on imaging availability, inter-
pretative expertise, rapidity of imaging in the presence
VERTEBRAL BONY AND LIGAMENTOUS of challenging clinical scenarios, and, of course, cost
TRAUMATIC INJURIES consideration.
• Despite its limitations, MRI is still capable of identify-
• Radiography is insensitive for diagnosis of vertebral frac- ing traumatic spinal injuries such as fractures. In people,
tures and subluxations in the acute canine spinal trauma like CT, MRI is more sensitive than plain radiographs in
patient, and is a poor diagnostic tool to assess the stabil- the identification and classification of vertebral traumatic
ity of spinal fractures. Plain radiographs are also not use- injuries.5 Studies in people have even shown a slight
ful to detect compressive spinal cord lesions. superiority in accuracy of MRI versus CT for identifica-
• CT, where available, is therefore recommended in tion and correct classification of some types of thoraco-
patients with a high clinical suspicion of such injury, and lumbar spinal injuries.5
has been reported to be superior to radiography in the • In people, the sensitivity and specificity of MRI for diag-
canine spinal trauma patient.3 Multidetector CT scan- nosing vertebral traumatic injuries is quite variable:
ners now provide the ability to obtain submillimeter • For vertebral fractures:
CT slices in a bone kernel in a short time, and CT has – Sensitivity of 37%–100%, specificity of 98%–100%
become the standard of care for the spinal trauma patient for the vertebral body.
at many referral and university hospitals. High-quality – Sensitivity of 12%–45%, specificity of 90%–97%
multiplanar reformatted images, as well as surface and for the posterior vertebral elements (pedicles,
volume rendering, are very useful for surgical planning arch, spinous processes).
and can be obtained with CT.4 With multidetector CT – For acute vertebral subluxation and acute verte-
units, short acquisition times make it possible to per- bral articular process joint subluxation, sensitivity
form a study with the anesthetized or sedated patient is about 45% and 59%, respectively.
M R I of Spi n a l Tr au m a 623
• Overall sensitivity of MRI to detect spinal soft tissue • Vertebral subluxation or luxation can be spotted on MR
injuries (e.g., longitudinal ligaments, ligamentum images in various planes, depending on the location of
flavum, or interspinous ligaments) varies between the injury and direction of the subluxation/luxation
46% and 71%.6 (Figs. 7.12.5, 7.12.6). Combined assessment of multipla-
• To date, there is no report on the sensitivity and specific- nar images, especially in the sagittal and dorsal planes, is
ity of MRI in the diagnosis of traumatic spinal injuries recommended to better evaluate for subtle intervertebral
in dogs and cats. subluxation, paying particular attention to the alignment
• Determining the location and severity of soft tissue/ and congruence of the articular process joints and adja-
bony trauma and resulting spinal instability is impor- cent vertebral bodies (see Fig. 4.2.11).
tant for surgical planning. Similar to people, a three- • Injuries to the supporting soft tissue structures of the
compartment model has been developed in canine and spine are best identified on T2W images, preferably with
feline patients that divides the vertebral column into fat saturation.7 These ligamentous structures normally
dorsal, middle, and ventral compartments. When there appear as thin hypointense bands on all pulse sequences.7
is involvement of two or three compartments, a trau- MRI features of injuries to these structures include
matic injury is considered unstable:2 (Figs. 7.12.4, 7.12.6, 7.12.7):2
• The dorsal compartment comprises the vertebral • Increased T2W intensity and changes in appearance
arch, which is made up of the spinous process, artic- (fuzziness, irregular/interrupted margins, or com-
ular processes, lamina, and pedicles and also includes plete lack of identification) of the interspinous, inter-
the soft tissue structures of the ‘dorsal ligamentous arcuate, dorsal, and ventral longitudinal ligaments.
complex’ (articular process joint capsules, interarcu- • Poor definition, increased T2 signal, interruption, or
ate ligaments, interspinous ligaments, supraspinous complete lack of identification of the normally hypoin-
and intertransverse ligaments). tense dorsal and ventral portions of the annulus fibro-
• The middle compartment includes the dorsal longitu- sus.
dinal ligament, dorsal aspect of the annulus fibrosus, • Distortion of the intervertebral disc with increased/
and dorsal margin of the vertebral body. heterogeneous signal extending in the area of the
• The ventral compartment includes the remainder of annulus fibrosus on T2W images, with widening or
the vertebral body, lateral and ventral aspects of the narrowing of the corresponding intervertebral disc
annulus fibrosus, nucleus pulposus, and ventral longi- space. Concurrent disc herniation in various direc-
tudinal ligament. tions may be present (see below).
• General MRI assessment of the spine in the trauma • MRI evidence of rupture of both the ventral and
patient should start with careful assessment of large field dorsal disc annulus and associated ventral and dorsal
of view sagittal and dorsal plane images, scrutinizing the longitudinal ligaments may indicate spinal instability
paravertebral soft tissue, looking for focal areas of hyper- even in the absence of concurrent fracture/sublux-
intense signal on fat-suppressed images such as STIR ation, and may warrant further investigation with
series, which would pinpoint areas of traumatic injury.2 stress radiographs and surgical stabilization.2
• Vertebral fractures may be recognized on MRI due to the
focal interruption of the normal hypointense vertebral TRAUMATIC DISC HERNIATION
cortex, together with changes in contour and changes
in signal intensity of the vertebral body due to hemor- • The MRI appearance of intervertebral disc herniation
rhage and edema.2,7 T1W and proton density images are is covered extensively in Chapter 7.1, and the reader is
particularly useful for this specific assessment. Variable referred to that specific chapter for more information.
degrees of relative displacement of the fractured frag- • Disc extrusion secondary to trauma is relatively common
ments may be identified (Figs. 7.12.1–7.12.4). The frac- in dogs, even in the absence of concurrent vertebral frac-
ture line itself may appear as a hypointense line on T2W ture and/or subluxation/luxation.8
or T2*W images due to the focal hemorrhage along the • In most cases, traumatic disc extrusion is non-compres-
margins of the fracture. Minimally or non-displaced fac- sive,8 and spinal cord trauma is due to contusion or intra-
tures can be spotted on MRI as focal, somewhat linear medullary disc herniation, as typically seen with acute
areas of T2W hyperintense signal due to bone marrow non-compressive hydrated nucleus pulposus extrusion,
edema (Fig. 7.12.1). In people, sensitivity of MRI for covered in Chapter 7.1 (Fig. 7.12.1).
detection of non- or minimally displaced fractures pos- • Pre-existing degenerative intervertebral disc disease
terior to the vertebral body (pedicles, lamina, arch, and may be a predisposing factor for spinal cord compres-
spinous process) is less than for the vertebral body, due sion after traumatic extrusion;8 as a result, older dogs and
to the lesser amount of cancellous bone in these verte- chondrodystrophic breeds are more likely to have spinal
bral segments.6 CT is reportedly far superior to MRI for cord compression following traumatic intervertebral disc
diagnosis of fractures of the neural arch in people.7 herniation.
624 CHAPTER 7.12
(a) (b)
(c) (d)
Fig. 7.12.1 Sagittal T2W image of the cervical spine (a), transverse T2W (b) and T2*W gradient echo (c) images at the level of
caudal C3, and transverse T2*W gradient echo image (d) at the level of cranial C4 in a 5-year-old Labrador Retriever after a
collision with another dog. A wedge fracture of the caudoventral body of C3 is visible (solid arrows, a–c). There are ill-defined
hyperintense areas in the hypaxial muscles ventral to C3 and C4 (dashed arrows, a–c). The C3-C4 intervertebral disc space is
collapsed and the signal from the disc is absent (dotted arrow, a), consistent with concurrent acute traumatic disc herniation
of hydrated disc material. There are intramedullary hyperintense areas (arrowhead, a), consistent with contusion/edema
secondary to the traumatic event. On the T2*W gradient echo transverse image at the level of cranial C4 (d), a curvilinear
hypointense area is seen in the left epidural region conforming to the left lateral border of the spinal cord, consistent with
susceptibility artifact from epidural hemorrhage (open arrow). (1.5T MRI system)
(a) (b) (c)

Fig. 7.12.2 Dorsal T1W (a) and T2W (b) images at the level of C1-C2 and ventrodorsal radiograph of the cervical spine (c) in a
7-year-old Afghan Hound that was hit by a car. There is a chip fracture of the apex of the dens of the axis (arrows). (1.5T MRI
system)
(a) (b)
Fig. 7.12.3 Sagittal T2W image (a) and corresponding sagittal reformatted CT image (b) of the thoracic spine in a 1-year-old
mixed breed dog that was hit by a car. A comminuted compression fracture of the body of T11 (arrows) is visible, causing
shortening, misshaping, and heterogeneous signal in the body of T11, with impingement into the vertebral canal causing
ventral spinal cord compression. (1.5T MRI system)
• Compressive disc herniation secondary to trauma is hemoglobin by-products are typically seen, and improve
more common in the cranial cervical, thoracolumbar, sensitivity of MRI in the identification of these specific
and cranial lumbar segments.8 changes.9,10
• Epidural hemorrhage in dogs with traumatic verte-
HEMORRHAGE bral subluxation was reported to form areas of signal
void partially surrounding and conforming to the out-
• Specific MRI features of spinal hemorrhage are covered line of the spinal cord on T2*W gradient echo images
in Chapter 7.7. (Fig. 7.12.1); these areas are of variable signal on T1W
• Paravertebral, intraspinal extradural, or intramedullary and T2W spin echo images.10 Susceptibility artifacts can
hemorrhage can occur secondary to traumatic spinal be observed in the paraspinal soft tissues adjacent to the
injuries in dogs and cats. region of spinal trauma due to intramuscular hemor-
• Although no systematic study exists on specifically trau- rhage. Epidural space hemorrhage (hematomas) can also
matic cases, T2*W gradient echo pulse sequences have cause focal epidural masses that are of variable signal,
been reported to be useful in identification of extradural depending on the age of the lesion, and rarely contrast
or intramedullary hemorrhagic changes in dogs. Signal enhance. T2*W imaging signal voids due to suscepti-
voids due to susceptibility artifacts associated with bility artifacts were also reported.2,9 Variable degrees of
626 CHAPTER 7.12
(a) (b)
Fig. 7.12.4 Transverse T2W image (a) and corresponding

transverse CT image (b) at the level of C5-C6, and sagittal
T2W image (c) of the cervical spine in a 7-year-old mixed breed
dog that was attacked by a larger dog. On the transverse T2W
image (a), there is subluxation of the left articular process joint
(dashed arrow), with mild lateral displacement of the cranial
articular process of C6 relative to the caudal articular process
of C5. An ill-defined, irregular, hypointense fragment is seen
immediately ventral to the joint (solid arrow, a), which on the
CT image corresponds to a small irregular fracture fragment
(solid arrow, b). There is discontinuity and hyperintense
signal in the dorsal annulus fibrosus of the C5-C6 disc
(dotted arrow, a) and on the sagittal image (dotted arrow, c),
and interruption of the dorsal longitudinal ligament is noted;
these changes are consistent with middle compartment
ligament alteration and rupture. Patchy areas of hyperintensity
within the spinal cord parenchyma are noted on the T2W
(c)
images (a, c), consistent with edema. (1.5T MRI system)
spinal cord compression may be present secondary to (T2W hyperintensity), multilevel edema, and edema
these epidural lesions. with concurrent hemorrhage (T2/T2*W hypointense
• Intramedullary hemorrhagic changes are also associated foci). The severity of the initial neurologic grade and the
with susceptibility artifacts causing low-signal foci on degree of clinical improvement respectively increase and
T2*W and, potentially, T2W images;2,10,11 they are typi- decrease when progressing from normal cord to single
cally associated with a more severe neurologic grade at level edema, multilevel edema, and mixed edema and
presentation and poorer prognosis (see below).6,11 hemorrhage. Sagittal T2W series are recommended in
people for this prognostic evaluation.6
SPINAL CORD PARENCHYMAL LESIONS • No systematic large scale study exists in veterinary medi-
cine on the prevalence and prognostic values of such pat-
• Generally, in people, MR signal changes in the spi- terns, although MRI allows identification of spinal cord
nal cord parenchyma following trauma are catego- changes such as presence/location/degree of spinal cord
rized in four levels: normal spinal cord, focal edema compression and parenchymal signal intensity changes
(a) (b)
(c) (d)
Fig. 7.12.5 Transverse T1W (a) and T2W (b) images at the level of C1, transverse CT image cranial to the apex of the dens (c), and
left parasagittal T2*W gradient echo image (d) of the cervical spine in a 2-year-old Golden Retriever that was hit by a car. On the
transverse images, there is subluxation of the dens of the axis to the right relative to the mid-sagittal plane (solid arrows, a and b).
There is irregular hypointense material in the left ventral aspect of the vertebral canal on the T2W image (dotted arrow, b),
corresponding to irregular hypointense signal voids on the parasagittal T2*W gradient echo image (dotted arrow, d), consistent
with hemorrhage. On the CT image (c), tiny mineral bodies are seen in the area of the alar ligaments, consistent with small
avulsion fractures (dotted arrows). (1.5T MRI system)
628 CHAPTER 7.12
Fig. 7.12.6 Sagittal T2W image in a dog with a traumatic

subluxation at L2-L3. The ventral displacement of the
cranial endplate of L3 relative to the caudal endplate of L2
is visible (arrow). There is an irregular signal within the
corresponding disc, with lack of differentiation between the
nucleus pulposus and annulus fibrosus. There is an elongated
area of hyperintensity in the spinal cord parenchyma dorsal
to L2-L3, consistent with edema and contusion. (1.5T MRI
system; reproduced, with permission, from Johnson P,
Beltran E, Dennis R et al. (2012). Magnetic resonance
imaging characteristics of suspected vertebral instability
associated with fracture or subluxation in eleven dogs.
Fig. 7.12.7 Sagittal T2W image of the lumbar spine in a

dog demonstrating MRI characteristics consistent with
dorsal compartment ligament alteration and rupture.
There is alteration of the interspinous ligament creating
irregular hyperintense areas between the spinous processes
(arrowheads). There is no widening of the interspinous
space. There is rupture of the annulus fibrosus of the L2-L3
disc, both dorsally and ventrally, as well as heterogeneous
hyperintense signal within the disc. (1.5T MRI system;
reproduced, with permission, from Johnson P, Beltran E,
Dennis R et al. (2012). Magnetic resonance imaging
characteristics of suspected vertebral instability associated
with fracture or subluxation in eleven dogs. Vet Radiol
such as edema (bright on T2W and T2-FLAIR images) been described in a case report and a small case series.
and hemorrhage (signal void due to susceptibility arti- It is, however, not currently approved worldwide for this
facts on T2*W images).2 specific indication, and is off-label in the USA and many
European countries.12,13
TRAUMATIC DURAL TEARS • The technique reported includes the following steps,
performed after standard MRI without contrast
• Dural tears secondary to trauma are potentially seri- administration:
ous injuries that, if left unrepaired, may cause hernia- • Atlantoaxial puncture with removal of 1 mL of CSF.
tion of neural elements through the defect. These neural • That CSF is then mixed with 0.2–0.5 mL of
elements may become entrapped in scar tissue, causing Gd-DTPA and reinjected via the same atlantoaxial
chronic pain and/or neurologic deficits. Continuous leak puncture site.12,13
of CSF through the tear can also lead to intracranial • The animal is then positioned upright for 5–6 minutes
hypotension syndrome. Dural tears can also increase the to allow for diffusion of contrast material along the
risk for meningitis or focal infection.12,13 subarachnoid space and, after repositioning of
• Intrathecal administration of gadolinum-based contrast the patient, sagittal and transverse T1W images
agent (Gd-DTPA) to diagnose traumatic dural tears has are obtained with fat saturation.
• Leakage of enhanced CSF is readily visible on T1W 5. Rajasekaran S, Vaccaro AR, Kanna RM et al. (2017). The value
images with fat saturation, with various patterns identi- of CT and MRI in the classification and surgical decision-
fied, including:12,13 making among spine surgeons in thoracolumbar spinal
injuries. Eur Spine J 26(5):1463–9.
• Well-defined tracks of leakage following a linear or
6. Bozzo A, Marcoux J, Radhakrishna M et al. (2011). The role
curvilinear path and pinpointing the area of dural
of magnetic resonance imaging in the management of acute
tear; this is commonly associated with less extensive spinal cord injury. J Neurotrauma 28(8):1401–11.
traumatic lesions with nerve root or sleeve avulsion. 7. Saifuddin A (2001). MRI of acute spinal trauma. Skeletal Radiol
• Diffuse leakage, with dissemination into extensive 30(5):237–46.
areas adjacent to the region of injury around the 8. Henke D, Gorgas D, Flegel T et al. (2013). Magnetic
vertebral column, in cases of more extensive dural resonance imaging findings in dogs with traumatic
lacerations. intervertebral disk extrusion with or without spinal cord
• Focal outpouching of enhanced CSF in cases of trau- compression: 31 cases (2006–2010). J Am Vet Med Assoc
242(2):217–22.
matic meningocele.
9. Hague DW, Joslyn S, Bush WW et al. (2015). Clinical,
magnetic resonance imaging, and histopathologic findings in
REFERENCES 6 dogs with surgically resected extraparenchymal spinal cord
hematomas. J Vet Intern Med 29(1):225–30.
1. da Costa RC, Samii VF (2010). Advanced imaging of the
10. Hammond LJ, Hecht S (2015). Susceptibility artifacts on
spine in small animals. Vet Clin North Am Small Anim Pract
T2*-weighted magnetic resonance imaging of the canine and
40(5):765–90.
feline spine. Vet Radiol Ultrasound 56(4):398–406.
2. Johnson P, Beltran E, Dennis R et al. (2012). Magnetic
11. Wang M, Dai Y, Han Y et al. (2011). Susceptibility weighted
resonance imaging characteristics of suspected vertebral
imaging in detecting hemorrhage in acute cervical spinal cord
instability associated with fracture or subluxation in eleven
injury. Magn Reson Imaging 29(3):365–73.
dogs. Vet Radiol Ultrasound 53(5):552–9.
12. Muñoz A, Mateo I, Lorenzo V et al. (2009). Imaging
3. Kinns J, Mai W, Seiler G et al. (2006). Radiographic sensitivity
diagnosis: traumatic dural tear diagnosed using intrathecal
and negative predictive value for acute canine spinal trauma.
gadopentate dimeglumine. Vet Radiol Ultrasound 50(5):502–5.
13. Muñoz A, Mateo I, Lorenzo V et al. (2013). MR
4. Robertson I, Thrall DE (2011). Imaging dogs with suspected
cisternography/myelography of post-traumatic spinal CSF
disc herniation: pros and cons of myelography, computed
fistulae and meningeal lesions in small animals. Acta Radiol
tomography, and magnetic resonance. Vet Radiol Ultrasound
54(5):569–75.
52:S81–4.
CHAPTER 7.13
MRI OF PARASPINAL SOFT TISSUES

630 Wilfried Mai
CONTENTS
Normal MRI appearance of muscles ......................................................................................................................................................................630
Inflammatory myopathies ......................................................................................................................................................................................630
General features ...............................................................................................................................................................................................630
Acute necrotizing myopathy .............................................................................................................................................................................631
Iliopsoas myopathy..........................................................................................................................................................................................631
Paraspinal infection and abscessation...................................................................................................................................................................634
Panniculitis ...........................................................................................................................................................................................................634
Post-surgical complications..................................................................................................................................................................................635
Paraspinal neoplasia .............................................................................................................................................................................................635
References.............................................................................................................................................................................................................640
Paraspinal conditions that may be imaged with advanced INFLAMMATORY MYOPATHIES

cross-sectional imaging such as MRI include inflamma-
tory non-infectious or infectious myopathies, paraspinal General features
abscesses, congenital conditions (e.g., dermoid sinus), trau- • Inflammatory myopathies are characterized by non-
matic injuries, and various neoplastic conditions affecting suppurative infiltration of inflammatory cells into stri-
the muscles (e.g., rhabdomyosarcoma), fat (e.g., lipoma, ated muscles,2 and can have a generalized or focal
infiltrative lipoma, liposarcoma), or connective tissue (e.g., distribution. This is a heterogeneous group of diseases
fibrosarcoma). Congenital diseases such as dermoid sinuses with various etiologies including immune-mediated and
are covered in Chapter 7.4 and neoplastic conditions are also infectious causes such as protozoal (toxoplasmosis, neo-
covered in Chapter 7.6. sporosis), bacterial, and, rarely, rickettsial and parasitic.2
• Clinical signs include paraspinal pain, stiff gait, abnor-
NORMAL MRI APPEARANCE OF MUSCLES mal stance, and lameness. Systemic signs such as fever
and lethargy may be present as well.
• Normal muscle has an intermediate to long T1 relax- • Diagnosis is established through a combination of clini-
ation time and short T2 relaxation time. cal, serologic, electromyographic, and histopathologic
• On T1W images, it is hyperintense to water and very criteria. Muscle biopsy is the most important test for a
hypointense compared with fat.1 definitive confirmation, and therefore sensitive imaging
• On T2W images, it is of much lower signal intensity techniques that allow determination of the best sites for
than water and fat.1 diagnostic sampling are important.2,3 MRI, due to its
• On inversion recovery and fat-suppressed T2W images, high sensitivity to changes in soft tissue structure and
normal muscle signal intensity is much lower than water biochemical environment, is a very good tool for this
and higher than fat.1 purpose.2
• Normal muscle fascicles (bundles of muscle fibers) are • MRI of paraspinal muscles should include T1W and
separated from one another by fat-containing septa, T2W spin echo sequences and T1W post-contrast
which gives muscle bellies a ‘feathery’ or ‘marbled’ images. The addition of fat-suppressed sequences
appearance on non-fat-suppressed images. such as STIR or T2W images with fat saturation is
M R I of Pa r a spi n a l S of t Tiss u e s 631
strongly recommended, as they are more sensitive Iliopsoas myopathy

to detect changes in T2 relaxation time associated • The iliopsoas muscle is a sublumbar muscle formed by
with increased intra- and extracellular water content fusion of the major psoas and iliac muscles. It originates
(muscle edema).1 from the ventrolateral aspect of the lumbar vertebrae, and
• MRI features of inflammatory myopathies include continues caudally in the retroperitoneal space to the pel-
(Fig. 7.13.1):2,4 vis where it inserts onto the lesser trochanter of the femur.
• Focal or multifocal ill-defined, patchy intramuscular • Traumatic injuries to the iliopsoas muscle can occur
lesions. Multifocal lesions may be bilateral but are in the dog when the pelvic limb is caught in extension.
usually asymmetric. It can be uni- or bilateral.
• Lesions are typically hyperintense on T2W images, of • In more chronic forms, fibrotic myopathy may develop,
variable signal on T1W images (hyperintense, isoin- where there is myofiber atrophy and separation of mus-
tense or hypointense), hyperintense on STIR images, cle fibers by fibrous tissue composed of fibroblasts and
and contrast enhancing. mature collagen.5–7 Chronic fibrotic myopathy has also
• High signal on T2W images is typically caused by been reported secondary to focal abscessation due to
edema, which is hypointense on T1W images. grass awn migration.6
• High signal on both T2W and T1W images may • Clinical signs include lameness with pain on extension
reflect fatty replacement, 2 which occurs later in the or internal rotation of the ipsilateral hip joint. Femoral
course of the disease. These changes may be con- neuropathy may be present due to the close anatomic
fused with signal abnormalities associated with den- relationship between the femoral nerve and the iliopsoas
ervation myopathy, which can also be of high signal muscle.8 In chronic contracture with fibrosis, abnormal
on T2W and T1W images with contrast enhance- gait is seen with ‘bunny hopping’ steps and hips main-
ment; however, in this case the abnormal signal tained in flexed position while standing.7
is generally more diffuse as opposed to patchy in • Although CT and ultrasound can be used to identify
inflammatory myopathies; there also tends to be iliopsoas pathology in the dog, it has been reported that
more pronounced muscle atrophy in cases of den- these modalities may reveal no abnormalities, while
ervation. 2 changes are seen on MRI.8
• There are rare descriptions of the MRI appearance of
Acute necrotizing myopathy iliopsoas myopathy in animals:
• Acute necrotizing myopathy (myonecrosis) is a rare • In a dog, atrophy of the affected iliopsoas muscle was
condition of unclear etiology in dogs, characterized seen. There were small focal areas of mild increased
by an acute onset of myalgia, with or without mobility signal within the belly of the affected muscle on T1W
impairment depending on the extent and distribution of images, corresponding to more pronounced increased
affected muscles. Transient myoglobinuria may be pres- signal on T2W images; these areas did not enhance.8
ent, and there is generally progressive improvement with In this case, histopathology showed myofiber atrophy,
supportive care.3 degeneration, occasional necrosis and regeneration,
• There is only one case report of the MRI appearance and fatty replacement. There was no significant
of this condition in a dog with acute onset of non- inflammation, indicating a more chronic phase of the
ambulatory tetraparesis and severe cervical pain.3 The condition.
thoracic girdle muscles were bilaterally affected with • In another dog with bilateral chronic contracture and
involvement of the serratus ventralis, subscapularis, fibrosis of the iliopsoas muscles, there was decreased
supraspinatus, and rhomboideus muscles. size of the muscles with hyperintense areas within the
• MRI features included: muscle bellies on T2W images; no information was
• Swelling of the muscles, with preserved fiber pattern. provided regarding the appearance on T1W images.7
• Hyperintense signal on T2W images with focal areas • Whether the muscles are enlarged or atrophied likely
of hypointense signal. depends on the stage at which the patient is imaged. In
• The hypointense areas on T2W images were also the acute/subacute phase, the muscles are more likely to
hypointense on T2*W images. be enlarged, becoming atrophied at the more chronic
• Patchy slightly hyperintense areas on T1W images fibrosing phase. Enlargement of the muscles has been
pre-contrast. reported on CT.5,6,9
• On post-contrast images, patchy contrast enhance- • Variable degrees of heterogeneous contrast enhance-
ment was seen and there were focal areas of absent ment have been reported on CT,5,6,9 and this also likely
enhancement; the latter corresponded to the hypoin- depends on chronicity of the condition. In the author’s
tense areas on T2W and T2*W images (hemorrhage experience, contrast enhancement can also be seen on
or hemorrhage mixed with necrosis). MRI (Fig. 7.13.2).
632 CHAPTER 7.13
(a) (d)
(b) (e)
(c) (f)
Fig. 7.13.1 Transverse T2W (a, d), T1W (b, e), and T1W post-contrast (c, f) images at the level of mid-C2 (a–c) and mid-C4
(d–f) in a 4-year-old male Boxer dog with a 5-day history of neck pain and diagnosed with neosporosis based on very high
Neospora caninum serology and CSF eosinophilia and a quick complete response to anti-protozoal therapy. Multifocal myositis
is visible forming patchy areas in various paraspinal muscles that are hyperintense on T2W images, mildly hyperintense on
T1W pre-contrast images, and markedly enhanced after gadolinium injection (arrows, a–d). (1.5T MRI system; images courtesy
of Dr. Emily Davis, Sugar Land Veterinary Specialists)
(a) (b)
(c) (d)
Fig. 7.13.2 Dorsal STIR image (a) and transverse T2W (b), T1W (c), and T1W post-contrast with fat saturation (d) images at
the level of the caudal lumbar spine in a dog with iliopsoas myopathy. The left iliopsoas muscle is hyperintense on the STIR
image (arrow, a). On the T2W image ill-defined patchy hyperintense areas are visible in the belly of the muscle (arrow, b).
Abnormal areas are isointense to normal muscle and inconspicuous on the T1W image (c). Irregular diffuse enhancement
is noted on the post-contrast image (arrow, d) compared with the contralateral unaffected side. (1.5T MRI system; images
courtesy of Dr. Matthew Paek, Bush Veterinary Neurology Services)
634 CHAPTER 7.13
PARASPINAL INFECTION AND ABSCESSATION • Loco-regional cellulitis is often seen surrounding the
abscess, and forms diffuse areas of low signal intensity
• Paraspinal infection and abscessation is uncommon, on T1W images and high intensity on T2W images,
and may result from penetrating trauma such as bite with thickening of the skin and a reticular, lace-like
wounds, endogenous migration of plant material (e.g., pattern in the subcutaneous fat.
wood, thorn, grass awn)10 or other foreign material,11,12 • Foreign bodies are difficult to identify on MRI,
or extension of infectious foci in the spine such as disco- as they are typically small and of low signal inten-
spondylitis or vertebral osteomyelitis.13 sity; often they are not visible or very subtle.13
• The cranial sublumbar muscles are commonly affected Conspicuity of the foreign body may be increased on
in cases of migrating foreign bodies such as grass awns. post-contrast images due to the enhancement of the
The reason for this is that the common route of penetra- surrounding inflamed tissue.10 Post-contrast images
tion is via the respiratory system after inhalation. The may also increase suspicion for a migrating foreign
foreign body then penetrates the lung and pleural cav- body by highlighting a linear or tubular fistulous
ity, and is forced between the pleural layers in a caudal tract corresponding to the path of the foreign body
direction by respiratory movements. The foreign body (Fig. 7.13.5).12,13
eventually becomes trapped in the peripheral attachment • Extension of the infectious process into the vertebral
of the diaphragm, ventral to L3 and L4, or penetrates canal (epidural empyema, see Chapter 7.5) may be
further from this point into the intercostal, abdominal, present and identified on MRI.
or sublumbar musculature.11
• Clinical signs typically include focal, regional, or dif- PANNICULITIS
fuse paraspinal pain, focal swelling of the affected region
with clinical evidence of inflammation (redness, heat), or • Idiopathic sterile panniculitis is a dermatologic disease
presence of a fistula.13 These signs may not be evident of unknown etiopathogenesis, forming single or multi-
in cases of involvement of the hypaxial region. Systemic focal subcutaneous nodules measuring a few millime-
signs such as fever and lethargy are typically present. ters to several centimeters, progressing to a generalized
Neurologic deficits such as paraparesis or paraplegia may skin disease that is cystic, ulcerated, and may develop
be present when there is extension of the infection into draining tracts. The condition may be granulomatous,
the vertebral canal. pyogranulomatous, suppurative, eosinophilic, necro-
• MRI features of paraspinal infection or foreign body tizing, or fibrosing.4 In the generalized form, systemic
reaction without abscessation are similar to non-infec- signs such as pyrexia, anorexia, lethargy, and depression
tious myopathies and include:11,13 may be seen. An association with pancreatitis or intra-
• Focal or multifocal poorly marginated lesions within abdominal steatitis has been reported. The condition is
the affected muscles. typically responsive to glucocorticoid treatment. Focal
• Lesions are hyperintense on T2W images, iso-, involvement of the epidural fat has been reported and can
hypo-, or hyperintense on T1W pre-contrast images, cause spinal cord compression; this particular presenta-
and typically enhancing on post-contrast images. tion is covered in Chapter 7.5.
• Spontaneous T1 hyperintensity on pre-contrast • Although the cutaneous form of the condition typically
images seems to be quite common with paraspinal does not necessitate MRI for diagnosis, some patients
infection or foreign body reaction.11,13 This may be may undergo MRI examination due to clinical mani-
caused by the presence of high-protein fluid, micro- festations that mimic primary spinal disease, including
scopic hemorrhage, or redistribution of intra- and severe generalized paraspinal pain and fever.
extracellular water.13 • On MRI, regional or diffuse changes of the superficial
• MRI features of paraspinal abscessation include:12–14 paraspinal tissues may be seen, with thickening of the
• Focal lesion with smooth or irregular contour, causing skin and a reticular, lace-like pattern in the subcutaneous
focal enlargement of the affected muscle or intermus- fat. STIR images may show heterogeneous hyperinten-
cular space. sity of the thickened subcutaneous fat, and diffuse het-
• Compared with normal muscles, the lesion is typically erogeneous enhancement may be seen on post-contrast
hyperintense on T2W and STIR images and iso- to images; fat-suppressed post-contrast images facili-
hypointense on T1W images. Mildly hyperintense tate identification of the enhancement, which may be
signal on T1W pre-contrast images is possible.13 obscured on non-fat-suppressed images due to the natural
• On post-contrast images, there is typically periph- hyperintense signal from subcutaneous fat. Alternatively,
eral enhancement corresponding to the wall of the subtracted series (post-contrast minus pre-contrast) may
abscess, while the central cavity filled with purulent allow detection of subtle diffuse enhancement consistent
material does not enhance (Figs. 7.13.3, 7.13.4). with diffuse inflammation (Fig. 7.13.6).
(a) (b)
(c)
Fig. 7.13.3 Sagittal T2W (a), T1W (b), and T1W post-contrast
with fat saturation (c) images and transverse T1W post-
contrast (without fat saturation) (d) image at the level of C3 in
a 9-year-old mixed breed dog with fever and neck pain. A large
abscess (arrows, b) is visible dorsal to the cranial cervical
spine. The lumen of the abscess is hyperintense on the T2W
image (a), hypointense on the T1W pre-contrast image (b),
and non-enhancing (c, d). The wall of the abscess is irregular
and strongly enhancing (dotted arrows, d). Internal enhancing (d)
septations are visible (d). There is focal myositis around the
abscess forming ill-defined patchy hyperintense areas on the T2W (a) and T1W post-contrast fat saturated (c) images.
Inflammation of the subcutaneous fat is also visible dorsal to the abscess. (1.5T MRI system)
POST-SURGICAL COMPLICATIONS PARASPINAL NEOPLASIA
• Complications after spinal surgery such as laminec- • Various tumors can affect the paraspinal tissues, includ-
tomy include infection (cellulitis, abscess formation, see ing tumors of muscular origin (rhabdomyosarcoma),
above), hemorrhage/hematoma, or seroma formation. vascular origin (hemangiosarcoma), connective tissue
• Depending on the nature and extent of these compli- (fibrosarcoma), peripheral nerve sheath tumors, periph-
cations, severe pain or spinal cord compression may be eral primitive neuroectodermal tumors, paragangliomas,
present, leading to patients being re-imaged with MRI. tumors of fat origin (lipoma, liposarcoma, infiltrative
• Seroma appears as areas of fluid pocketing (high T2 sig- lipoma), and round cell tumors.16–23
nal and low T1 signal) disrupting the normal organiza- • Most of these tumors can directly affect the spinal cord
tion of the soft tissues and dissecting between the fascial through invasion into the vertebral canal, and their MRI
planes at the surgical site.15 characteristics are covered in Chapter 7.6.
• Hematomas form masses of variable size and variable • Clinical signs will be variable, depending on the location
signal intensity depending on the age of the hematoma; of the tumor and local invasiveness. Neurologic deficits
signal voids due to susceptibility artifacts on T2*W gra- may be present when there is invasion of the vertebral
dient echo images are useful for their recognition. canal or invasion/compression of peripheral nerves in
636 CHAPTER 7.13
(a)
(b)
(c)
Fig. 7.13.4 Sagittal STIR image of the cervicothoracic region

(a) and transverse T2W (b), T1W pre-contrast (c), and T1W
post-contrast with fat saturation (d) images at the level of T1-T2
in a 1-year-old German Shepherd Dog with a large paravertebral
abscess in the craniodorsal mediastinum. The abscess is seen
as a large fusiform hyperintense structure ventral to the
cranial thoracic spine (dotted arrows, a). There are areas of (d)
patchy hyperintensity within the vertebral bodies of T1 and
T2 consistent with osteomyelitis. There is also loss of signal intensity of the nucleus pulposus of the intervertebral disc at
T1-T2, which may suggest early discospondylitis. On the transverse images, the lumen of the abscess is filled with pus that is
hyperintense on the T2W image (b), isointense to muscles on the T1W pre-contrast image (c) and non-enhancing (d), while its
wall is hypointense on the T2W image (solid arrows, b) and strongly contrast enhancing (d). A large paravertebral abscess was
debrided surgically, and culture of surgical samples grew colonies of Staphylococcus pseudointermedius. (1.5T MRI system)
(a) (b)
(c) (d)
Fig. 7.13.5 Transverse T2W (a), T1W (b), and T1W post-contrast (c) images at the level of L2, dorsal T1W post-contrast
image with fat saturation immediately ventral to the spine (d), and sagittal T2W image of the diaphragmatic insertion onto
the ventral aspect of the cranial lumbar spine (e) in a dog with a cranial sublumbar infection/fistula secondary to a chronic
grass awn migration, which was removed surgically (f). The foreign body tract is visible on the transverse images as a rounded
structure (arrows, a–c), which is hyperintense on the T2W image (a), heterogeneously hyperintense on the T1W pre-contrast
image (b), and peripherally enhancing on the post-contrast image (c). Heterogeneous enhancement of the muscular insertion of
the diaphragm ventral to L2 due to inflammation is appreciated on the transverse post-contrast image (c). On the dorsal post-
contrast image (d), the linear, somewhat tortuous tract is visible with enhancement of its wall and hypointense lumen (arrows).
On the sagittal T2W image (e), the hyperintense tract is visible ventral to the spine (arrows). (1.5T MRI system; images courtesy
of Dr. Matthew Paek, Bush Veterinary Neurology Services) (Continued)
638 CHAPTER 7.13
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(e) (f)
(a)
(b)
Fig. 7.13.6 Sagittal STIR image of the thoracolumbar spine
(a) and transverse T2W (b) and subtracted (post-contrast
minus pre-contrast) T1W (c) images at the level of T13-L1
in a 12-year-old dog with back pain and fever. There are
diffuse changes of the superficial paraspinal tissues with
thickening of the skin and multifocal hyperintense areas in
the subcutaneous fat on the STIR image (dotted arrows, a),
corresponding to a reticular, lace-like pattern in the
subcutaneous fat on the T2W image (arrowheads, b), which
are enhancing after gadolinium injection (c). Histopathology
showed multifocal nodular pyogranulomatous panniculitis.
A focal area of inflammation deeper in the epaxial muscle is
visible on the transverse images, which is hyperintense on
the T2W image (b) and contrast enhancing (solid arrow, c).
(c)
(1.5T MRI system)
the vicinity of the neoplasia. For example, neoplasia in • MRI of paraspinal tumors may be performed in patients
the iliopsoas muscle could mimic a peripheral femoral without neurologic signs for assessment of tumor exten-
neuropathy.23 sion and to help define surgical margins. One example
• On MRI, a focal mass in the paraspinal soft tissues will is feline vaccine-associated fibrosarcoma.24 In most cases
be identified, of variable signal intensity depending on these lesions present as single tumors, although multiple
the histopathologic nature of the lesion. tumors are possible, especially in patients with recurrence
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(a) (b)
Fig. 7.13.7 Transverse T1W (a), T1W post-contrast (b),

and T2W (c) images at the level of T5 in a cat with an
injection site sarcoma. The tumor directly contacts the
dorsal margins of both scapulae (arrows, a). Infiltrative
margins of the tumor are evident on the post-contrast
image, forming cords extending into the neighboring
tissues (arrows, b). The tumor is moderately and
heterogeneously contrast enhancing (b). Cavitations
are seen on the T2W image as regions that are
homogeneously hyperintense relative to the rest of the
tumor (arrow, c). (0.2T MRI system; reproduced, with
permission, from Rousset N, Holmes MA, Caine A et al.
(2013). Clinical and low-field MRI characteristics of
injection site sarcoma in 19 cats. Vet Radiol Ultrasound
(c)
54(6):623–9.)
after previous surgery. The lesions are of variable MRI images. Focal infiltration appearing as irregular tumor
appearance, but typically heterogeneously hyperintense margins with infiltrative cords extending into the neigh-
to muscle on both T1W and T2W images, with mod- boring tissues is more common in recurring cases after
erate to marked heterogeneous contrast enhancement.24 previous excisional biopsy (Fig. 7.13.7). A T2W hyper-
Cavitations are common, forming focal homogeneous intense perilesional halo is common as well, especially in
T2 hyperintense, T1 iso- or hypointense areas that do cases with previous excisional biopsy, and its significance
not contrast enhance. Calcification may be present and is not clear (e.g., edema, scarring, inflammation).24 Bone
appears as hypointense foci on both T1W and T2W invasion with osteolysis is uncommon.
640 CHAPTER 7.13
REFERENCES 12. Naughton JF, Tucker RL, Bagley RS (2005). Radiographic

1. May DA, Disler DG, Jones EA et al. (2000). Abnormal signal diagnosis – paraspinal abscess in a dog. Vet Radiol Ultrasound
intensity in skeletal muscle at MR imaging: patterns, pearls, 46(1):23–6.
and pitfalls. Radiographics 20 Spec No:S295–315. 13. Holloway A, Dennis R, McConnell F et al. (2009). Magnetic
resonance imaging features of paraspinal infection in the dog
2. Platt SR, McConnell JF, Garosi LS et al. (2006). Magnetic
and cat. Vet Radiol Ultrasound 50(3):285–91.
resonance imaging in the diagnosis of canine inflammatory
14. Grosslinger K, Lorinson D, Hittmair K et al. (2004). Iliopsoas
myopathies in three dogs. Vet Radiol Ultrasound 47(6):532–7.
abscess with iliac and femoral vein thrombosis in an adult
3. De Risio L, McConnell JF, de Stefani A et al. (2009). Imaging
Siberian husky. J Small Anim Pract 45(2):113–6.
diagnosis – acute necrotizing myopathy in a dog. Vet Radiol
15. Matiasek LA, Platt SR, Dennis R et al. (2006). Subfascial
seroma causing compressive myelopathy after cervical dorsal
4 Cornelis I, De Decker S, Gielen I et al. (2013). Idiopathic
laminectomy. Vet Radiol Ultrasound 47(6):581–4.
sterile inflammation of the epidural fat and epaxial muscles
16. Chang HW, Ho SY, Lo HF et al. (2006). Vaccine-associated
causing paraplegia in a mixed-breed dog. J Am Vet Med Assoc
rhabdomyosarcoma with spinal epidural invasion and
242(10):1405–9.
pulmonary metastasis in a cat. Vet Pathol 43(1):55–8.
5. Adrega Da Silva C, Bernard F, Bardet JF et al. (2009). Fibrotic 17. DeLellis RA (2001). The neuroendocrine system and its
myopathy of the iliopsoas muscle in a dog. Vet Comp Orthop tumors: an overview. Am J Clin Pathol 115 Suppl:S5–16.
Traumatol 22(3):238–42. 18. Hobert MK, Brauer C, Dziallas P et al. (2013). Infiltrative
6. Laksito MA, Chambers BA, Hodge PJ et al. (2011). Fibrotic lipoma compressing the spinal cord in 2 large-breed dogs.
myopathy of the iliopsoas muscle in a dog. Aust Vet J Can Vet J 54(1):74–8.
89(4):117–21. 19. Junginger J, Rothlisberger A, Lehmbecker A et al. (2013).
7. Ragetly GR, Griffon DJ, Johnson AL et al. (2009). Bilateral Peripheral primitive neuroectodermal tumour in a dog.
iliopsoas muscle contracture and spinous process impingement J Comp Pathol 149(4):424–8.
in a German Shepherd dog. Vet Surg 38(8):946–53. 20. Kim HJ, Chang HS, Choi CB et al. (2005). Infiltrative lipoma
8. Stepnik MW, Olby N, Thompson RR et al. (2006). Femoral in cervical bones in a dog. J Vet Med Sci 67(10):1043–6.
neuropathy in a dog with iliopsoas muscle injury. Vet Surg 21. McEntee MC, Thrall DE (2001). Computed tomographic
35(2):186–90. imaging of infiltrative lipoma in 22 dogs. Vet Radiol Ultrasound
9. Rossmeisl JH Jr., Rohleder JJ, Hancock R et al. (2004). 42(3):221–5.
Computed tomographic features of suspected traumatic 22. Rizzo SA, Newman SJ, Hecht S et al. (2008). Malignant
injury to the iliopsoas and pelvic limb musculature of a dog. mediastinal extra-adrenal paraganglioma with spinal cord
Vet Radiol Ultrasound 45(5):388–92. invasion in a dog. J Vet Diagn Invest 20(3):372–5.
10. Young B, Klopp L, Albrecht M et al. (2004). Imaging 23. Tucker DW, Olsen D, Kraft SL et al. (2000). Primary
diagnosis: magnetic resonance imaging of a cervical wooden hemangiosarcoma of the iliopsoas muscle eliciting a peripheral
foreign body in a dog. Vet Radiol Ultrasound 45(6):538–41. neuropathy. J Am Anim Hosp Assoc 36(2):163–7.
11. Frendin J, Funkquist B, Hansson K et al. (1999). Diagnostic 24. Rousset N, Holmes MA, Caine A et al. (2013). Clinical and
imaging of foreign body reactions in dogs with diffuse back low-field MRI characteristics of injection site sarcoma in
pain. J Small Anim Pract 40(6):278–85. 19 cats. Vet Radiol Ultrasound 54(6):623–9.
SECTION 5
MRI OF THE
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641
MUSCULOSKELETAL
SYSTEM
CHAPTER 8 MRI of musculoskeletal diseases

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CHAPTER 8
MRI OF MUSCULOSKELETAL DISEASES

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Amy R. Zalcman, Cristi Cook, 643

and Wilfried Mai
CONTENTS
Shoulder joint .......................................................................................................................................................................................................644
Supraspinatus tendinopathy ............................................................................................................................................................................644
Biceps tendinopathy .......................................................................................................................................................................................649
Infraspinatus muscle contracture and injuries .................................................................................................................................................650
Other tendinous and ligamentous conditions...................................................................................................................................................651
Medial glenohumeral ligament injury ........................................................................................................................................................652
Subscapularis tendon injury.......................................................................................................................................................................652
Lateral glenohumeral ligament injury .........................................................................................................................................................653
Teres minor tendon injury ..........................................................................................................................................................................653
Osteochondrosis/osteochondritis dissecans....................................................................................................................................................653
Adhesive capsulitis ..........................................................................................................................................................................................655
Elbow joint ............................................................................................................................................................................................................655
Fragmented medial coronoid process ..............................................................................................................................................................655
Ununited anconeal process..............................................................................................................................................................................659
Humeral condyle osteochondrosis/osteochondritis dissecans.........................................................................................................................660
Flexor enthesopathy.........................................................................................................................................................................................660
Traumatic triceps tendon avulsion ...................................................................................................................................................................660
Incomplete ossification of the humeral condyle ..............................................................................................................................................660
Joint incongruence ..........................................................................................................................................................................................663
Coxofemoral joint..................................................................................................................................................................................................663
Avascular necrosis of the femoral head............................................................................................................................................................663
Hip dysplasia ...................................................................................................................................................................................................663
Stifle joint..............................................................................................................................................................................................................663
Cranial cruciate ligament disease ....................................................................................................................................................................664
Meniscal tears .................................................................................................................................................................................................664
Collateral ligament injury.................................................................................................................................................................................667
Osteochondrosis/osteochondritis dissecans....................................................................................................................................................667
Long digital extensor tendon avulsion .............................................................................................................................................................668
Gastrocnemius musculotendinopathy ..............................................................................................................................................................669
Extremity of the limbs............................................................................................................................................................................................670
Traumatic injuries ............................................................................................................................................................................................670
Foreign bodies.................................................................................................................................................................................................670
Tarsal osteochondrosis/osteochondritis dissecans ..........................................................................................................................................671
Other conditions....................................................................................................................................................................................................673
Myopathies ......................................................................................................................................................................................................673
Joint neoplasia ................................................................................................................................................................................................677
Bone neoplasia ................................................................................................................................................................................................677
Osteomyelitis/septic arthritis ...........................................................................................................................................................................679
References.............................................................................................................................................................................................................683
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The reader is referred to Chapter 4.3 for information

regarding image optimization for the musculoskeletal sys-
tem, as well as basic anatomic descriptions of the various
appendicular skeleton joints that can be imaged with MRI.
This chapter will focus on the MRI features of common
pathologic conditions of the musculoskeletal system. We
will first cover joint-specific conditions that may be investi-
gated with MRI, and then briefly cover conditions that can
affect any regions of the limbs, such as myopathies, neopla-
sia, and infection.
SHOULDER JOINT
MRI of the shoulder is one of the most common indica-

tions for musculoskeletal MRI in dogs, as shoulder lame-
ness may often be caused by non-osseous lesions affecting
the articular or peri-articular soft tissue structures of the
shoulder joint, which are not amenable to a straightfor-
ward radiographic or CT diagnosis. MRI provides exqui-
site soft tissue contrast with very good resolution, and its
multiplanar imaging capabilities with a large field of view
also allow the ruling out of underlying cervical spinal, bra-
Fig. 8.1 Sagittal T2W image of the shoulder in a dog with
chial plexus, or bone disease in a non-invasive manner.1
supraspinatus tendinopathy. The tendon is swollen with
Ultrasound is another imaging method that can be used to
diffuse and marked hyperintensity (arrow). (1.5T MRI
evaluate the soft tissue components of the shoulder joint,
system)
but it is limited by its small field of view and inability to
evaluate the structures of the medial compartment of the
shoulder joint.1 arthroscopy to identify this impingement because
the joint is distended with fluid during arthroscopic
Supraspinatus tendinopathy examination, which may mask actual impingement.1,5
• Supraspinatus tendinopathy/tendinosis is a chronic • Heterogeneous signal intensity on T1W, T2*W gra-
degenerative condition of the supraspinatus tendon and dient echo, and PDW pulse sequences.5
enthesis, characterized histopathologically by myxoma- • Hyperintense signal of the tendon at the insertion
tous degeneration and chondroid metaplasia with dis- over the greater tubercle on T2W (greater than signal
continuous and disorganized collagen fibers,2–4 with or of muscle), fat suppressed PDW or STIR images.2–4
without areas of mineralization.3 • As mentioned in Chapter 4.3, a physiologic hyper-
• The calcifying form of the disease appears to be more intense signal of the broad insertion of the tendon
common than the non-calcifying type.3 on the greater tubercle can be seen in normal dogs
• Typically, no inflammatory cells are present. on T2W and PDW images, attributed to the fibro-
• The condition generally affects large-breed dogs espe- cartilaginous nature of the enthesis, in which there
cially the Labrador Retriever and Rottweiler. is more variability in water content as well as lack of
• There is no known inciting cause; however, contributing uniform collagen orientation, as seen in the tendon
factors include aging, overuse, trauma, and hypoxia sec- proper.6
ondary to supraspinatus tendon hypovascularity. • Intermixed hypointensities (signal voids) in the
• Affected dogs present with a chronic, intermittent tho- enlarged tendon may be present if mineralization is a
racic limb lameness. component of the pathology (Fig. 8.3).5
• The MRI characteristics of this condition are as follows • With chronicity, there is progressive fatty replace-
(Figs. 8.1–8.5): ment at the musculotendinous junction, which then
• Enlargement of the tendon, which can result in appears hyperintense on T2W and T1W images and
impingement on the biceps brachii tendon.2–5 This suppresses on STIR images or with fat saturation.1
impingement is best seen on the transverse images, • On a contrast MR arthrogram, a lack of filling of the
causing medial displacement of the biceps brachii sheath between the biceps tendon and supraspinatus
tendon, which may also appear somewhat flattened tendon may be seen as a result of the compression by
(Figs. 8.3, 8.4). MRI may be more sensitive than the enlarged supraspinatus tendon.5
M R I of Musc u l os k e l e ta l D is e a s e s 645
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(a) (b)
(c) (d)
Fig. 8.2 Sagittal T2W (a), STIR (b), T1W pre-

contrast (c) and post-contrast (d), and transverse
T2W (e) images in a 2-year-old mixed breed dog with
non-calcifying supraspinatus tendinopathy. Note
GT the enlarged supraspinatus tendon (open arrows,
a–d), with hyperintense signal on the sagittal T2W
(a) and STIR images (b). On the post-contrast T1W
image (d), there is mild enhancement of the distal
insertion of the tendon indicative of active disease.
On the transverse T2W image (e), the enlarged
supraspinatus tendon (large arrow) is compressing
the biceps brachii tendon (solid arrow) within
the intertubercular groove. GT, greater tubercle.
(e) (1.5T MRI system).
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(a) (b)
GT
(c) (d)
Fig. 8.3 Lateral radiograph of the shoulder (a) and sagittal STIR (b), sagittal T2W (c), transverse T2W (d), and sagittal
T1W pre-contrast (e) and post-contrast (f) images in a 2-year-old Labrador Retriever that has been lame for 6 months. The
radiograph (a) shows an irregular margin to the greater tubercle and mineral bodies (solid arrow) in the general region of the
supraspinatus tendon. On the MR images, the supraspinatus tendon (open arrows, b–f) is enlarged and there is hyperintense
signal within it on the STIR (b) and T2W (c) images. On the T1W images, a well-defined hypointense signal void is seen within
the tendon (dotted arrow, e) corresponding to a calcifying body secondary to chronic tendinopathy (same body as indicated by
the arrow on the radiograph in a). After gadolinium administration (f), there is mild patchy enhancement of the supraspinatus
tendon. On the transverse T2W image (d), the enlarged and heterogeneous supraspinatus tendon is compressing the biceps
brachii tendon within the intertubercular groove (dashed arrow), which appears flattened, instead of oval-shaped; this may be a
contributing factor to the pain. GT, greater tubercle. (1.5T MRI system) (Continued)
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(e) (f)
Fig. 8.3 (Continued)
Fig. 8.4 Nine-year-old German Shepherd Dog presented

with chronic shoulder lameness. Lateral radiograph of the
shoulder (a) and sagittal T2W (b), transverse STIR (c), and
transverse T1W post-contrast with fat saturation (d–f) MR
images. Images (c) and (f) were obtained at level 3 on the
radiograph (= insertion of the supraspinatus tendon on the
greater tubercle [GT]) and images (d) and (e) are respectively
at levels 1 and 2 on the radiograph, across the intertubercular
groove. On the radiograph, there is osteophytosis at the
caudal margin of the humeral head; two well-defined rounded
mineral bodies are seen superimposed on the proximal
humerus (solid and dashed white arrows). Note the slightly
3 flattened/irregular margin of the caudal articular surface
of the humeral head (black dashed arrow). On the sagittal
T2W image (b), there is distension of the caudal synovial
2 pouch of the shoulder joint (dotted arrow) consistent with
joint effusion. The articular cartilage of the caudal humeral
head and corresponding subchondral bone are slightly
1
irregular (dashed arrow). On the transverse STIR image (c),
the insertion of the supraspinatus tendon onto the greater
(a) tubercle (GT) is indicated by the arrowhead and is thickened
and hyperintense, causing mild medial displacement and
compression of the biceps tendon (open arrow). On the corresponding T1W post-contrast image (f), the supraspinatus tendon
is enhancing (arrowhead) and there is also enhancement of the biceps tendon sheath (open arrow). On the transverse images
obtained more distally at the level of the osseous bodies seen radiographically (d, e), the osseous bodies are clearly visualized
(dashed arrow in d; solid arrow in e) and associated with the biceps tendon sheath, which is distended with fluid (open arrow).
The final diagnosis was chronic osteochondritis dissecans, with healing of the original caudal humeral head osteochondral
lesion, and chronic joint mice that migrated into the biceps tendon sheath causing chronic supraspinatus tendonitis and biceps
tenosynovitis. (1.5T MRI system) (Continued)
648 CHAPTER 8
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GT
(b) (c)
(d) (e)
GT
(f)
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Biceps tendinopathy
• Biceps tendinopathy may be secondary to supraspina-
tus tendinopathy, which can cause impingement of the
biceps brachii tendon (see above), or could be secondary
to other conditions such as shoulder joint trauma with
instability, primary shoulder instability, compressive
mass lesion in the vicinity of the tendon, or joint mouse
migration in the biceps tendon sheath resulting from
chronic osteochondritis dissecans of the humeral head.5
Primary pathology of the biceps tendon, such as partial/
complete tearing or primary biceps tenosynovitis, is also
possible.5
• Physical examination findings include thoracic limb
lameness with pain on hyperflexion of the joint, often
with pain response on direct pressure of the tendon as it
traverses the bicipital groove.
• The MRI characteristics of this condition include
(Figs. 8.6, 8.7):5
• Thickening of the tendon with heterogeneous signal
intensity on T1W, T2*W gradient echo and PDW
pulse sequences.5
• Increased signal intensity on T2*W gradient echo and
PDW pulse sequences,5 as well as on T2W and STIR
images,1 resulting from core tendon damage.
• Tendon tears may be seen on T2W and PDW images
as a hyperintense linear signal across the tendon in
Fig. 8.5 Partial tear (arrow) of the supraspinatus tendon at the area of attachment onto the supraglenoid tubercle
the musculotendinous junction on a sagittal T2W image. of the scapula.1,5
(3T MRI system)
(a) (b)
Fig. 8.6 (a) Sagittal T1W image of the shoulder in a dog with biceps tendinopathy; a focal hyperintense signal is seen in
the tendon of the biceps brachii muscle (arrow). (1.5T MRI system) (b) Transverse T2W image of the shoulder at the level
of the biceps brachii tendon in another dog with biceps tendinopathy; note the focal hyperintensity in the tendon (arrow).
(3T MRI system)
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• Bright tendon signal observed on pulse sequences

with a short time of echo (TE) (such as PDW) should
be confirmed on long TE sequences such as T2W
images (Fig. 8.6) to make sure the bright signal is
not caused by magic angle artifact (see Chapters 3
and 4.3).
Infraspinatus muscle
contracture and injuries
• Fibrotic contracture is the most common condition
affecting the infraspinatus muscle; acute tendon injury
is also possible.5,7
• Fibrotic contracture is mainly diagnosed in mature
hunting, sporting, and working dogs. The etiology is
unknown. In most cases, it is associated with repetitive
minor trauma, caused during periods of vigorous exer-
cise, such as while hunting or working. However, infra-
spinatus muscle contractures induced by blunt trauma
have also been reported.7
• Clinically, the acute phase is characterized by lame-
ness, swelling, pain when the shoulder is extended, and a
reluctance to bear weight. Dogs suffering from subacute
contractures (1–4 months after injury) show typical gait
abnormalities including external rotation of the distal
thoracic limb with the elbow in adduction when the dog
is sitting and a circumductive movement of the affected
limb when walking.7 In chronic cases, the gait abnormal-
ity and lameness may subside; however, there is atrophy
of the infraspinatus muscle and reduction in the range of
Fig. 8.7 Sagittal T2W image in a dog with bicipital shoulder flexion with an inability to adduct and flex the
tenosynovitis. The arrow points to the actual tendon and the limb at the same time.7
hyperintensity around it represents marked effusion in the • The MRI characteristics of infraspinatus fibrotic con-
tendon sheath. Effusion in the remainder of the shoulder tracture include (Fig. 8.8):5,7
joint is also present, causing distension of the caudal synovial • Heterogeneous signal intensity within the muscle and
pouch. (3T MRI system) musculotendinous junction, with minimal extension
into the tendon.5
• Because the tendon sheath communicates with the • In subacute fibrotic contracture, there is increased
synovial joint, distension of the shoulder joint capsule volume of the muscle, best appreciated on transverse
and accumulation of T2 hyperintense fluid are com- images, with a circular hyperintense signal within the
monly seen (Fig. 8.7).1 muscle on T2W and fat saturated PDW images and
• In chronic cases: a peripheral heterogeneous halo. Histopathologically,
– Progressive fraying of the tendon causes it to this corresponds to variable degrees of muscle fiber
become thinner; this can eventually lead to spon- degeneration/necrosis, hemorrhage, and interstitial
taneous rupture.1 edema.7
– Thickening of the synovium due to synovitis • In chronic fibrotic contracture, there is reduced
is seen as a hypointense thick lining on T2W volume of the muscle with a central hypointense
images, with strong enhancement on T1W images signal on T2W and fat saturated PDW images.
obtained after intravenous gadolinium injection.1 An irregular peripheral halo is observed that is
• Evaluation may be enhanced with MR arthrography; hypointense on fat saturated PDW images and
the distension of the tendon sheath may outline syn- mixed hypo- and hyperintense on T2W images.
ovial proliferations and adhesions better, and small Histopathologically, this corresponds to areas of
tears may be more conspicuous as contrast material myofiber degeneration, fibrosis, calcification, and
dissects through the defect. adipose tissue replacement.7
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(a) (b)
(c) (d)
Fig. 8.8 Dorsal plane T2W (a, c) and fat saturated PDW (b, d) images in a dog with chronic fibrotic contracture of the right
infraspinatus muscle (a, b) and subacute fibrotic contracture of the left infraspinatus muscle (c, d). In the chronic lesion, there
is a heterogeneous hypointense signal (arrowheads, a and b), while a heterogeneous hyperintense signal (arrowheads, c and d) is
seen in the subacute lesion. (3T MRI system; reproduced, with permission, from Orellana-James NG, Ginja MM, Regueiro M
(2013). Sub-acute and chronic MRI findings in bilateral canine fibrotic contracture of the infraspinatus muscle. J Small Anim
Pract 54(8):428–31.)
• Acute injuries to the infraspinatus tendon and muscle Other tendinous and
can also be encountered and MRI findings may include ligamentous conditions
(Figs. 8.9, 8.10):5 Other structures that can be evaluated with MRI include
• An enlarged infraspinatus tendon with heterogene- the medial and lateral glenohumeral ligaments and joint
ous signal intensity and increased intensity within capsule, the subscapularis tendon, and the teres minor ten-
the muscle belly on T2*W gradient echo and PDW don. Differentiation between the glenohumeral ligaments
pulse sequences. and joint capsule can be challenging, as these structures are
• Fluid distension of the small bursa associated with intimately associated with each other, especially when no
the tendon insertion, with contrast enhancement on arthrography is obtained. Precise recognition of the type
T1W post-gadolinium images. of injury (inflammation versus partial tear) of these small
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(a) (b)
Fig. 8.9 Dorsal T2W (a) and T1W post-contrast (b) images of the shoulder in a 2-year-old mixed breed dog. The infraspinatus
tendon insertion on the lateral surface of the greater tubercle is indicated by the solid arrows. There is mild fluid distension
of the bursa associated with the infraspinatus tendon (open arrow, a) with mild enhancement after gadolinium injection
(open arrow, b), consistent with infraspinatus bursitis. S, scapula; H, humerus. (1.5T MRI system)
structures may be difficult. Partial tears may remain unde-

tected at MRI; on the other hand, overdiagnosis of abnor-
malities such as inflammation has been reported.5
Medial glenohumeral ligament injury

• Physical examination findings include thoracic limb
lameness, which is often chronic and toe-touching by the
time of presentation. Orthopedic evaluation may reveal
shoulder instability through translational manipulation
of the humeral joint.
(Figs. 8.11, 8.12):5
• A heterogeneous signal intensity with capsuloliga-
mentous thickening in cases of purely inflammatory
changes. This is best appreciated on T2*W gradient
echo and PDW images in the dorsal plane.
• Minor disruption of the ligament silhouette may be
seen in cases of partial tear.
• Major disruption of the ligament silhouette is seen in
cases of complete tear. In this case, an irregular undu-
lating pattern on contrast MR arthrography is seen.
Subscapularis tendon injury

• Full or partial tears of the subscapularis tendon can be
seen.
Fig. 8.10 Dorsal oblique plane T2W image of the proximal • MRI characteristics include:5
humerus in a dog with tendinopathy of the infraspinatus. • In cases of inflammation, tendon enlargement with
The arrow indicates the infraspinatus tendon with a heterogeneous signal intensity on T2*W gradient
hyperintense fluid around it. echo and PDW images.
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Fig. 8.11 Transverse T2W image of the shoulder in a dog with Fig. 8.13 Dorsal plane T1W post-contrast fat saturated image
a chronic partial tear of the subscapularis tendon and medial of the shoulder in a 6-year-old Labrador Retriever with a
glenohumeral ligament. The arrow identifies thickening of lateral glenohumeral ligament tear. There is enhancement
the subscapularis tendon and medial glenohumeral ligament; in the area of the lateral glenohumeral ligament and lack of
the two structures are difficult to distinguish due to their visualization of that ligament (arrow). (1.5T MRI system)
intimate association. (1.5T MRI system)
• Capsuloligamentous disruption is noted in cases of

tears. These are easier to identify on dorsal plane
images and are usually seen near the scapular attach-
ment of the tendon.
• Discontinuity of the ligament may be easier to iden-
tify on positive contrast MR arthrography.
Teres minor tendon injury

• The normal teres minor tendon is inconsistently seen on
MRI;8 however, when injured it may be visible more eas-
Fig. 8.12 Dorsal plane PDW image in a dog with a partial tear ily due to enlargement and changes in signal.
of the medial glenohumeral ligament on the scapular side of • Teres minor tendon injuries have been reported in dogs
the right shoulder (arrow). The contralateral normal left joint with medial shoulder instability.5
is included. (3T MRI system) • The MRI characteristics of this condition include:5
• Thickening of the tendon insertion, best seen on
transverse images, caudal and caudoproximal to the
• Positive contrast arthrography may enhance assess- insertion of the infraspinatus tendon along the lateral
ment of fiber disruption and may highlight the void surface of the proximal humerus.
between tendon and bone in cases of complete avul- • Increased signal on T2*W gradient echo and PDW
sion. images.
Lateral glenohumeral ligament injury Osteochondrosis/osteochondritis

• Physical findings include thoracic limb lameness. dissecans
Orthopedic evaluation may reveal shoulder instability • Shoulder osteochondrosis/osteochondritis dissecans is a
through translational manipulation of the humeral joint. common cause of thoracic limb lameness in dogs, with
• MRI findings include (Fig. 8.13):5 the caudal aspect of the humeral head being most com-
• Capsuloligamentous thickening in inflammatory cases. monly affected.
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• The lesion may be symptomatic or subclinical, and

subclinical lesions may or may not progress to become
symptomatic.
• Symptomatic dogs present with thoracic limb lameness
and may exhibit pain with internal rotation and direct
pressure along the caudal aspect of the joint.
• Compared with radiography, MRI is more sensitive
and slightly less specific for diagnosing osteochondro-
sis/osteochondritis dissecans lesions, but is much more
accurate than radiography for detecting cartilaginous
flaps and moderately more accurate for detecting free
fragments (joint mice).9
• The sagittal T2W and PDW fast/turbo spin echo with
fat saturation sequences are the most suitable to identify
lesions of osteochondrosis or osteochondritis dissecans
of the humeral head.9
(Figs. 8.14–8.17; see also Fig. 8.4):1,9,10
• Joint effusion, easy to detect on T2W or PDW images
where the synovial fluid is markedly hyperintense and
distends the joint capsule.
(a)
Fig. 8.14 Sagittal PDW fat saturated fast spin echo image (b)
of the shoulder in a dog with osteochondritis dissecans and Fig. 8.15 Lateral radiograph of the shoulder (a) and sagittal
an in-situ flap. The arrowhead is at the level of the flap. PDW image (b) in a dog with osteochondritis dissecans. The
Hyperintense joint fluid is present on the cranial and caudal arrowheads denote the flap. (1.5T MRI system; reproduced,
aspects of the flap. The arrows delineate the associated with permission, from Wall CR, Cook CR, Cook JL (2015).
hyperintense bone marrow lesion of the caudal humeral Diagnostic sensitivity of radiography, ultrasonography,
head. (1.5T MRI system; reproduced, with permission, from and magnetic resonance imaging for detecting shoulder
Wall CR, Cook CR, Cook JL (2015). Diagnostic sensitivity of osteochondrosis/osteochondritis dissecans in dogs. Vet Radiol
radiography, ultrasonography, and magnetic resonance imaging Ultrasound 56(1):3–11.)
for detecting shoulder osteochondrosis/osteochondritis
dissecans in dogs. Vet Radiol Ultrasound 56(1):3–11.)
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most commonly in the caudal joint pouch; occasion-

ally, they can migrate cranially and enter the synovial
recess around the biceps brachii tendon, causing sec-
ondary biceps tenosynovitis (see Fig. 8.4).
Adhesive capsulitis
• Adhesive capsulitis (‘frozen shoulder’) is a syndrome
appreciated in human sports medicine and defined by a
loss of range of motion of the shoulder joint impairing the
patient’s ability to sleep, work, or perform daily activities
or desired recreational activities.11 It may represent the
end-stage manifestation of several primary conditions
including trauma, previous surgery, prolonged immobi-
lization, endocrine disorders, or idiopathic causes.
• This condition has been rarely described in dogs;11
affected patients have a history of chronic unilateral tho-
racic limb lameness and severe restriction of shoulder
extension (<110°) and flexion (>90°), with pain on manip-
ulation of the shoulder.
• Arthroscopically, significant adhesions, fibrous scar tis-
sue of the joint capsule, severe synovitis, and severe soft
tissue contracture are seen, together with concurrent
abnormalities of various components of the joint includ-
Fig. 8.16 Sagittal T2W fat saturated image in a dog with ing biceps/supraspinatus tendinopathy and fraying/
osteochondritis dissecans of the caudal humeral head. disruption of the subscapularis tendon, medial glenohu-
The hyperintense joint fluid is coursing underneath the meral ligament and/or joint capsule.11
flap (solid arrow) and free mineralized bodies (joint mice) • MRI findings that have been reported include:11
are seen in the caudal joint pouch (open arrow). • Severe atrophy of the shoulder musculature.
(1.5T MRI system) • Moderate shoulder joint effusion causing distension
of the joint capsule with hyperintense fluid on T2W
• Flattening or concave defect in the margin of the or PDW images.
subchondral bone of the caudal humeral head, best • On post-contrast T1W images, enhancement of the
appreciated on sagittal images. synovial lining of the shoulder joint including around
• When resolution and contrast are sufficient to ade- the biceps brachii tendon (Fig. 8.18).
quately appreciate the articular cartilage, defects and • Concurrent conditions such as severe biceps, supraspi-
inhomogeneities within it may be seen. natus, infraspinatus, teres minor tendinopathy/inser-
• T2W or PDW hyperintensity of the subchondral tionopathy, medial glenohumeral ligament injury, or
bone underlying the cartilaginous lesion may be seen, joint capsule thickening.
corresponding to subchondral bone marrow lesions;
these are due to cellular infiltration, fluid accumula- ELBOW JOINT
tion, or necrosis.9 They are typically hypointense on
T1W images. Compared with the shoulder and stifle joints, MRI of the
• Conversely, hypointense areas of the subchondral elbow joint is in its infancy and not routinely performed.1,12
bone on T1W, T2W, and PDW images are due to This is largely due to the fact that most elbow conditions
bone sclerosis, which may represent a more chronic can be accurately diagnosed with radiographs or CT.
stage of the disease. However, MRI can also diagnose these osteoarticular
• Cartilage and osseous flaps and fragments are conditions, with the added benefit that concomitant articu-
observed when the flap is partially or completely lar and periarticular soft tissue lesions can also be accurately
separated from the articular surface. Cartilage flaps evaluated with MRI, while they would be difficult to char-
form elongated linear hypointense structures con- acterize, even with CT.
forming to the curvature of the caudal aspect of the
humeral head, and on T2W or PDW images, a linear Fragmented medial coronoid process
hyperintense tract can be seen separating that flap • Medial coronoid process disease is part of the ‘canine
from the underlying subchondral bone.9 Fragments elbow dysplasia’ complex, and is the most common cause
(joint mice) form elongated or irregularly shaped of thoracic limb lameness in juvenile and adult medium-
hypointense structures that are free within the joint, to large-breed dogs.13
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* *
(a) (b)
(c) (d)
Fig. 8.17 Sagittal T2W (a), T1W pre-contrast (b), STIR (c), and T1W post-contrast (d) images of the shoulder in a dog with
chronic shoulder osteochondrosis. There is an irregular margin of the subchondral bone of the caudal aspect of the humeral
head (arrow, a) and distension of the caudal synovial pouch with fluid (asterisks, a and b). On the post-contrast image (d), there
is thickening and enhancement of the synovium (dashed arrow, d) indicative of chronic synovitis. (1.5T MRI system)
• The underlying etiology is not known but may be mul- dysplastic changes such as ununited anconeal process,
tifactorial, including joint incongruity, trauma, genetics, humeral condyle osteochondrosis, or elbow incongruity.
growth rate, nutrition, ischemia, or osteochondrosis.13 A radiographically distinct osteochondral fragment
• The condition can manifest as isolated fragmentation or is rarely identified due to the complex anatomic con-
fissuring of the cartilage and/or subchondral bone of the formation of the elbow and many superimpositions on
medial coronoid process, as well as symptomatic carti- 2D radiographic images. This is the reason why tomo-
lage erosion.13 graphic techniques such as CT or MRI are preferred for
• Medial coronoid disease is often considered a ‘rule out’ the diagnosis and grading of this condition.
diagnosis made when there is radiographic evidence of • MRI is more accurate and sensitive but mildly less spe-
elbow osteoarthritis without definitive evidence of other cific than radiography for the diagnosis of fragmented
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(a) (b)
Fig. 8.18 Sagittal T2W (a), transverse STIR (b), and T1W
post-contrast (c) images of the shoulder in a 10-year-old dog
with chronic lameness and chronic hypertrophic villonodular
synovitis of the shoulder. There is diffuse irregular
thickening of the synovium (arrows) and diffuse marked
(c)
contrast enhancement (c). H, humerus. (1.5T MRI system)
medial coronoid process as well as concomitant lesions stage of fragmentation.13 Several patterns have been
(‘kissing lesions’) along the medial ridge of the humeral described including focal hyperintense signal involv-
trochlea;14 MRI also has a better negative predictive ing only the tip of the medial coronoid process, focal/
value than radiography.14 Some authors suggested that linear hypersignal within the subchondral bone, and
MRI may out-perform CT to identify cartilaginous diffuse hypersignal involving the entire coronoid
fragments of the medial coronoid process, which may process. However, there is no correlation between the
be missed with CT,14 although the two techniques have pattern/extent of these bone marrow lesions seen on
never been formally compared. MRI and the severity of arthroscopic or histopatho-
• The MRI characteristics of medial coronoid disease logic changes.13
include (Figs. 8.19, 8.20): • Abnormal morphology of the medial coronoid process
• Bone marrow lesions, characterized by hyperintense is best appreciated on transverse or sagittal plane
signal in the coronoid process as seen on gradient images; 3D coherent (steady state precession) gradi-
echo images; these changes are typically seen in dis- ent echo pulse sequences (Fast MPGR on General
eased coronoid processes and are present prior to the Electric, FISP on Siemens, FFE on Phillips; see
658 CHAPTER 8
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(a) (b)
Fig. 8.19 Transverse T1W images of the right (a) and left (b) elbows at the level of the medial coronoid process in a dog. In (a),
a normal medial coronoid process is seen (arrow); the process is homogeneously hypointense, smoothly marginated, and has a
normal shape. In (b), the medial coronoid process has an irregular shape and heterogeneous signal intensity, with a fissure seen
across it consistent with non-displaced fragmentation (arrow). (3T MRI system)
(a) (b)
Fig. 8.20 Transverse CT image (a) and T1W (b) and T2W (c) MR images of the elbow obtained at the level of the medial
coronoid process of the ulna in a dog with fragmentation of the medial coronoid process. The fragment is readily seen on
the CT image (arrow, a) but also appreciated on the MR images (arrows, b and c). The heterogeneous signal intensity of the
underlying portion of the medial coronoid process is also visible on the MR images. U, ulna; R, radius. (1.5T MRI system)
(Continued)
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(c)
Fig. 8.20 (Continued) Fig. 8.21 Sagittal T2W image of the elbow in a dog with
an ununited anconeal process. There is a hypointense cleft
(arrow) separating the anconeal process (asterisk) from the
remainder of the ulna. (3T MRI system)
Chapter 2) are suitable as they allow thin slices to be surrounded by a hypointense halo.14,15 They are more
obtained and good detail of the margins of the medial conspicuous on fat suppressed images.
coronoid process and can be reformatted in various • Intra-articular injection of gadolinium (MR arthro-
planes. Contrast is dependent on the ratio T2/T1 on gram) can be useful to differentiate completely
these sequences, so synovial fluid appears hyperin- fractured from partially fractured medial coronoid
tense and gadolinium-rich regions will enhance on processes, although the clinical importance of this
post-contrast images. MRI changes include:14,15 differentiation is limited.15
– Fragmented displaced coronoid process with a
low signal intensity compared with surrounding Ununited anconeal process
muscles. • The anconeal process of the ulna has a separate cen-
– Non-displaced, mineralized in-situ abnormal ter of ossification in breeds affected by this condi-
coronoid process, hypointense with an irregular tion; a separate center of ossification is, however, not
outline. observed in all breeds, in particular small dog breeds
– Non-displaced, non-mineralized in-situ abnormal do not have one.16
coronoid process, hyper- to isointense compared • A radiographically apparent opened physis across the
with the surrounding muscles. anconeal process beyond 20–22 weeks of age represents
• Fragments can also be seen on fat suppressed T2W or an ununited anconeal process.12
PDW spin echo images where the hyperintense syn- • Affected animals typically present with thoracic limb
ovial fluid extends into the fissure and highlights the lameness and pain on flexion and extension of the elbow
margins of the fragments; STIR images can also show joint.
fragments, although their low signal-to-noise ratio • Radiographic diagnosis is typically straightforward
makes assessment of tiny fragments challenging.1 and MRI has therefore not been used for this diagno-
• Concurrent lesions may be seen on the medial ridge sis. The sagittal plane T2W spin echo or 3D coherent
of the humeral trochlea (‘kissing lesions’). They are (steady state precession) gradient echo images similar to
easier to see on dorsal plane images and typically those used for medial coronoid process evaluation are
appear as somewhat circular subchondral lesions the most useful. A cleft is seen separating the anconeal
that are hyperintense on T2W or PDW images, process from the remainder of the ulna (Fig. 8.21).17
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Humeral condyle osteochondrosis/ attachment on the medial humeral epicondyle. These

osteochondritis dissecans typically appear as hypointense discrete structures
• This condition occurs most commonly in juvenile, fast within or between the muscles on T1W images.
growing, large-breed dogs and is more common in male • In dogs with concomitant flexor enthesopathy, con-
dogs compared with females.18 current abnormalities associated with elbow dysplasia
• It is predominantly found in the area of the medial ridge are seen, including abnormal shape and signal or frag-
of the humeral trochlea.12 mentation of the medial coronoid process, and abnor-
• The imaging characteristics are difficult to differentiate mal signal in the subchondral bone of the medial ridge
from the ‘kissing lesions’ seen secondary to fragmenta- of the humeral trochlea (see above).
tion of the medial coronoid process and described above. • Other than the presence/absence of signs of elbow dys-
• Dorsal and sagittal plane images are preferred for diag- plasia, there is no significant difference in the aforemen-
nosis of this condition. tioned MRI features between dogs with primary flexor
• MRI findings have not been reported so far, but expected enthesopathy and dogs with concomitant flexor enthe-
findings may include:12 sopathy. In addition, the same features are observed in
• Thickening of the articular cartilage of the medial dogs with clinical or subclinical flexor enthesopathy.19
ridge of the humeral trochlea.
• Flattening of the subchondral bone of that area of the Traumatic triceps tendon avulsion
condylar surface. • This condition has been rarely reported.20
• Cartilage erosions/irregularities; small articular carti- • Affected patients present with an acute onset of tho-
lage lesions without subchondral changes may be diffi- racic limb lameness with poor response to symptomatic
cult to identify due to insufficient spatial resolution.12 medical management. Pain and swelling close to the
• Subchondral bone lesions similar to the humeral elbow in the area of insertion of the triceps muscle onto
condyle ‘kissing lesions’ secondary to medial coronoid the olecranon tuberosity is observed. With chronicity,
process fragmentation (somewhat circular subchon- there is development of a firm swelling proximal to the
dral lesions that are hyperintense on T2W or PDW olecranon and secondary atrophy of the heads of the
images, surrounded by a hypointense halo).14,15 triceps.
• Reported MRI characteristics of this condition include:20
Flexor enthesopathy • In cases of complete rupture, sagittal T1W images
• Flexor enthesopathy of the elbow is a pathologic condition show proximal retraction of the triceps tendon.
of the flexor muscles and their attachment onto the medial • High signal on T2W and STIR images and, depend-
humeral epicondyle. It can occur as a primary entity, when ing on chronicity, some degree of contrast enhance-
underlying pathology of the elbow is absent, and may also ment around the olecranon may also be expected.
be observed concomitant with elbow dysplasia.19
• Clinical signs include non-specific thoracic limb lame- Incomplete ossification of
ness with pain on extension of the elbow. the humeral condyle
• The MRI characteristics of this condition include • Incomplete ossification of the humeral condyle is charac-
(Fig. 8.22):19 terized by an incomplete fusion between the two centers
• An irregular outline of the medial humeral epicon- of ossification of the humeral condyle, which normally
dyle, best appreciated on dorsal or transverse plane fuse at around 70 +/− 14 days in dogs.21 Before that fusion,
images. a cartilaginous plate is present between the medial and
• Thickening of the cortex of the medial humeral epi- lateral aspects of the condyle.
condyle. • This condition has been reported in several canine breeds
• Bone marrow lesions (secondary to subcortical edema with a higher incidence in middle-aged male Spaniels.21
and cellular infiltration), seen as a patchy hyperintense In these, a polygenic, recessive inherited ossification
signal within the subcortical region of the medial epi- weakness of the humeral condyle is suspected.22
condyle on STIR and T2W images. • This condition can lead to spontaneous complete frac-
• Thickening of the flexor muscles, best appreciated on ture of the humeral condyle with no or minimal trauma.
sagittal T2W images, although also commonly seen on • Concurrent elbow conditions such as medial coronoid
transverse T2W and sagittal/transverse T1W images. process fragmentation or humeral condyle osteochon-
• Hyperintense signal of the flexor muscles on T2W drosis are not uncommon.
and STIR images. • Incomplete ossification of the humeral condyle is often
• Contrast enhancement on T1W post-gadolinium bilateral and therefore when identified in one elbow,
injection in the majority of cases. screening of the contralateral limb should be performed.21
• In approximately one-third of cases, a calcified body • Affected patients present with intermittent mild tho-
is seen within or between the flexor muscles near the racic limb lameness.21,22 There is pain with antebrachial
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(a) (b)
(c) (d) (e) (f)

Fig. 8.22 Magnetic resonance images of the elbow from a male mixed breed dog diagnosed with primary flexor enthesopathy.
Transverse T1W pre- (a) and post-contrast (b) images at the level of the humeral epicondyles, dorsal STIR images (c at the level
of the humeral epicondyles; d more caudally at the level of the ulna), and sagittal pre-contrast T1W (e) and T2W (f) images.
In (a) and (b), the flexor carpi ulnaris muscle is thickened (white arrow, a) with contrast enhancement present within the flexor
muscle (black arrow, b). A large calcified body is also visible (open arrows), forming a signal void. In (c) a hyperintense signal
is evident within the medial humeral epicondyle, indicating bone marrow edema (arrowhead). In (d), the flexor carpi ulnaris
muscle shows a hyperintense signal (arrow). In (e) and (f), new bone formation is present at the caudodistal border of the
medial humeral epicondyle (black arrow, e). A large calcified body is visible within the flexor muscles (open arrows) with T2
hyperintense signal in the surrounding muscles (white arrow, f). (0.2T MRI system; reproduced, with permission, from de
Bakker E, Gielen I, Kromhout K et al. (2014). Magnetic resonance imaging of primary and concomitant flexor enthesopathy in
the canine elbow. Vet Radiol Ultrasound 55(1):56–62.)
supination and direct pressure on the medial coronoid • In dorsal and transverse planes, a regular or irregular
process.22 Acute non-weight-bearing lameness with linear signal change is seen when the orientation of
severe elbow pain is seen in dogs with complete humeral the slices crosses the center of the condyle:
condylar fracture. – On T1W images, it appears isointense to the nor-
• Although craniocaudal or craniocaudal oblique elbow mal condyle.
radiographs may identify a fissure in affected patients, – On T2W, gradient echo or STIR images, it
this imaging test lacks sensitivity, and cross-sectional appears hyperintense to the normal condyle.
imaging techniques such as MRI or CT are preferred.21 When T2W pulse sequences are used, fat satura-
• The most sensitive MRI pulse sequences to identify this tion is useful to suppress the bright signal of the
condition include STIR and T1W gradient echo.21 bone marrow and highlight the linear defect.
• MRI characteristics include (Fig. 8.23):21,22 • This cleft may be complete or incomplete (i.e., only par-
• Periarticular osteophytic remodeling, best seen on tially separating the lateral and medial aspects of the
sagittal T1W images. humeral condyle).
• Moderate amount of elbow joint effusion, best seen on • In most cases the defect is well identified on dorsal or
T2W images. transverse plane images; however, in some cases of
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(a) (b)
(c) (d) (e) (f)

Fig. 8.23 Dorsal spin echo T1W (a) and STIR (b) images of the elbow in a dog with incomplete ossification of the humeral
condyle. There is a clear intracondylar line visible at the level of the distal humerus (arrows). The humeral condyle is
heterogeneous in both images. Dorsal spin echo T1W (c), dorsal STIR (d), transverse spin echo T1W (e), and transverse STIR
(f) images in a dog that has incomplete ossification of the humeral condyle on the contralateral limb. No clear intracondylar line
is seen at the level of the distal humerus, but it has a heterogeneous appearance in both pulse sequences, with an evident central
focus of hyperintensity at the level of the condyle (circles). (0.2T MRI system; reproduced, with permission, from Piola V,
Posch B, Radke H et al. (2012). Magnetic resonance imaging features of canine incomplete humeral condyle ossification.
incomplete defect, combined assessment in both planes is STIR images.21 These changes most likely represent
necessary for a confident identification.21 bone marrow lesions (e.g., edema, cellular infiltrates)
• There is heterogeneous signal within the central por- around the fissure area.
tion of the humeral condyle around the fissure, which • In dogs with unilateral fissure or fracture secondary
is usually hypointense on T1W images, variable on to incomplete ossification, MRI of the contralateral
T2W images, and hyperintense on gradient echo and limb may reveal a heterogeneous signal of the humeral
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condyle on T1W and STIR images, with a small focus of

central condylar hyperintensity noted on STIR images;
this may be an indicator of subclinical disease in the con-
tralateral limb, as progression to a complete fissure has
been observed in some of these dogs.21
Joint incongruence
• So far, no formal assessment of the value of MRI in dogs
with elbow joint incongruence has been performed.
However, MRI measurement of elbow joint congruence
has been reported in non-arthritic elbows of various dog
breeds.23
• Elbow joint congruence can be readily assessed on sag-
ittal and dorsal plane images such as spoiled gradient
echo sequences with fat suppression (e.g., 3D MPGR, 3D
FLASH), in which the subchondral bone and marrow FH
FH
signals are very dark in contrast with the iso- to hyperin-
tense articular cartilage. On sagittal images, the proximal
humero-ulnar interosseous space at the cranial extrem-
ity of the anconeal process, as well as the mid to cranial Fig. 8.24 Dorsal T2W image of the pelvis in a dog with
humeroradial interosseous space, are normally narrower chronic coxofemoral dysplasia and osteoarthritis. There
in large-breed dogs compared with the interosseous is marked subluxation of the femoral heads (FH) and
space at the center of the trochlear notch, giving a visual osteophystosis and femoral head remodeling. The decreased
impression of mild incongruity; this degree of ‘incongru- volume of soft tissue is consistent with chronic muscle
ity’ is therefore a normal variation in these breeds.23 atrophy.
COXOFEMORAL JOINT • As early as 7 days post induction of avascular necrosis,

changes can be seen at MRI including decreased signal
Avascular necrosis of the femoral head intensity of the femoral head on T1W images, mod-
• Avascular necrosis of the femoral head, also known erate increased signal intensity on T2W images, and
as Legg–Perthes–Calvé disease, is a condition seen in marked increased signal intensity on STIR images.
immature dogs, most commonly of toy breeds, second-
ary to impairment of the blood supply to the femoral Hip dysplasia
head resulting in necrosis. • Although MRI does not represent the most commonly
• Affected dogs typically present with pelvic limb lame- employed imaging modality to diagnose and grade hip
ness that may progress to non-weight-bearing; there is dysplasia, primary and secondary changes can be identi-
pain with manipulation of the coxofemoral joint through fied (Fig. 8.24); for example, when imaging the pelvis for
a normal range of motion. suspect iliopsoas, gracilis, or sartorius myopathies.
• MRI is not typically used for this diagnosis, as the clini- • Findings may include:
cal presentation and radiographic changes are usually • Subluxation of the coxofemoral joints is seen in the
straightforward; however, experimental studies in dogs dorsal plane when the limbs are extended.
after induction of acute avascular necrosis showed that • Degenerative changes and chronic disuse muscle
MRI may demonstrate early changes, which would allow atrophy.
diagnosis prior to the appearance of classic radiographic
abnormalities.24 MRI may therefore be useful in cases STIFLE JOINT
of high clinical suspicion but absence of characteristic
radiographic abnormalities. • Even though there are numerous experimental and clini-
• Reported abnormalities in surgically induced acute avas- cal studies demonstrating the benefits of stifle MRI in
cular necrosis include:24 dogs,25–38 it is not yet as widely used in veterinary medi-
• At the acute phase, no changes in signal are seen on cine as it is in human medicine.
T1W, T2W, or STIR images; however, there is sig- • This may be in part due to added cost, lack of comfort
nificant decrease in gadolinium enhancement of the and experience with the modality, and the ability to per-
avascular femoral head. This becomes particularly form arthroscopy at the time of surgery.
apparent when comparing dynamic enhancement • However, arthroscopy provides limited visibility and is
profiles between affected and unaffected femurs. not able to assess the extra-articular structures, lesions
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located underneath the articular surfaces, or meniscal intercondylar eminence) of the ligament.1,38 These are
lesions affecting the tibial surface of the menisci.1,31,39 best seen on dorsal plane fluid-sensitive fat-suppressed
• In contrast, the menisci, cruciate ligaments, collateral sequences such as T2W spin echo with fat suppres-
ligaments, long digital extensor tendon, infrapatellar sion or STIR images. These lesions are hypointense
fat pad, synovium, and synovial fluid can all be evalu- on T1W images.38 Although they are commonly seen
ated with MRI.1 MRI provides a comprehensive and in dogs with naturally occurring partial or complete
non-invasive evaluation of all these structures at once in ligament tear, these high STIR signal lesions have
patients with stifle lameness, allowing better treatment also been observed in dogs with stifle lameness but an
planning and prognostication. intact cruciate ligament, and may therefore also rep-
resent a precursor stage of cruciate ligament disease as
Cranial cruciate ligament disease opposed to a consequence of cruciate injury, although
• Cranial cruciate ligament tear is one of the most com- the pathogenesis is not clearly established yet.38
mon orthopedic injuries in the dog. • Joint effusion is commonly observed, especially in
• It is characterized by an acute lameness that may tempo- acute and subacute cases; this is best identified on
rarily resolve, or by an acute and persistent toe-touching T2W or PDW images where synovial fluid appears
lameness. hyperintense; fat saturation should be used to sup-
• Orthopedic examination findings include quadriceps press the high signal from fat and highlight the fluid
femoris muscle atrophy, soft tissue thickening around signal of joint effusion.29 Joint effusion is particularly
the stifle joint, and joint effusion. Specific tests to evalu- well visible in the caudal synovial pouch on sagittal
ate stifle instability include the cranial drawer test and images. In chronic cases, there may not be a signif-
tibial compression test.27 icant amount of joint effusion anymore. Joint effu-
• PDW images in the sagittal oblique plane, optimized for sion may cause compression and altered shape of the
assessment of the cranial cruciate ligament (see Chapter infrapatellar fat pad on sagittal images. This may also
4.3), are preferred for evaluation of integrity of this be contributed to by synovial hyperplasia or synovi-
structure.27 tis causing thickening of the synovium and overall
• With this pulse sequence, in dogs undergoing MRI enlargement of the synovial space.36 Synovial hyper-
(1.5T) for suspected soft tissue injury to the stifle, sen- plasia is well recognized on T2W images as a tissue of
sitivity for diagnosing cranial cruciate ligament lesion moderate signal intensity protruding into the hyper-
was reported to be 93%, specificity was 100%, positive intense synovial fluid.29
predictive value was 100%, and negative predictive value • In chronic cases, osteophytes and enthesophytes
was 67%. There is generally good agreement between are observed in and around the stifle joint, and well
surgical findings and MRI.27 appreciated on T1W images with thin slices, such
• MRI characteristics of cranial cruciate injury include as T1W fast gradient recalled echo images.29 They
(Fig. 8.25):26,27,31,36,37 form low or intermediate signal irregularly shaped
• In cases of complete tear, a lack of visualization or spurs on the surface of the cortical bone at the peri-
only partial visualization of the cranial cruciate liga- articular margins or areas of ligament insertion such
ment on sagittal images. as the intercondylar fossa or near the intercondylar
• Most patients undergoing MRI for cruciate ligament eminence of the tibial plateau.29 Subchondral bone
investigation have partial tears and stable stifles on sclerosis, which appears as a signal void confluent
physical examination.1 In this case, there is disrup- with the subchondral plate, may also be seen on
tion of the normal linear collagen fibers that normally T1W images.29
extend the entire length of the ligament, from origin
to insertion. At MRI, on PDW or T2W images, the Meniscal tears
ligament appears irregularly marginated, often with • There have been more studies evaluating MRI for menis-
increased signal intensity; this is best appreciated on cal tears, due to the fact that they are a common sequela
sagittal images. False positive for hyperintense signal to cruciate ligament lesions and that clinical diagnosis
in the ligament can result from volume averaging with is challenging.28,39–42 Meniscal tears can also occur inde-
the adjacent synovial fluid, especially at the origin pendently from cruciate ligament injury.
of the ligament where it is fan-shaped.1 Therefore, • Presurgical recognition of meniscal tears is impor-
using thin enough slices and cross-referencing signal tant, as outcome may be poor if they are not surgically
changes in multiple planes are important to increase addressed.1
diagnostic confidence. • Patients with meniscal injuries present with non-specific
• Subchondral bone marrow lesions are often seen in lameness with pain on manipulation of the stifle. On
the areas of origin (caudolateral aspect of the inter- orthopedic examination, a ‘meniscal click’ may be pres-
condylar fossa) and insertion (deep to the tibial ent but this is an inconsistent finding.
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(a) (b)
(c) (d)
Fig. 8.25 Sagittal T2W (a), PDW (b), and T1W (c) and dorsal T2W with fat saturation images of the stifle in a 1.5-year-
old Newfoundland with a 3-month history of lameness. No instability was palpated on orthopedic examination. There is a
heterogeneous hyperintense signal in the cranial cruciate ligament (solid arrows) on the T2W and PDW images (a, b) and the
tendon is not clearly visible on the T1W image (c), probably because it is isointense to the surrounding structures. The caudal
cruciate ligament (dashed arrows) is visible and well defined. On the dorsal T2W fat saturated image (d), patchy hyperintense
signal is seen in the subchondral bone of the intercondylar fossa and tibial plateau, consistent with bone marrow lesions
(e.g., edema, cellular infiltrates) in the areas of origin and insertion of the cranial cruciate ligament (open arrows, d). There is
distension of the joint capsule (asterisks, a and b) consistent with joint effusion. These changes are consistent with a partial tear
of the cranial cruciate ligament. (1.5T MRI system)
• Sagittal and dorsal PDW turbo/fast spin echo images pulse sequences used in the different studies may be a
are preferred for meniscal assessment.27,40 Sagittal T2W contributing factor.27,28,39–42,44
images with fat saturation may also be useful.43 • Generally, high-field MRI appears to perform bet-
• The sensitivity and specificity of MRI in diagnos- ter than low-field MRI, 27,40 and MRI appears better
ing meniscal tears is variable depending on the study for lesions in the medial meniscus than in the lateral
(Table 8.1). Variability in magnetic field strengths and meniscus.
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Table 8.1 Summary table reporting sensitivity, specificity, positive predictive value, negative predictive value, and interobserver agreement for diagnosis of
meniscal tears in dogs across various published studies.
MAGNETIC FIELD NUMBER GOLD POSITIVE NEGATIVE INTEROBSERVER

REFERENCE STRENGTH OF STIFLES STANDARD SENSITIVITY SPECIFICITY PREDICTIVE VALUE PREDICTIVE VALUE AGREEMENT
Blond et al.40 1.5T 11 Surgery Overall: 100%; Overall: 94%; n/a n/a n/a
medial meniscus: 100%; medial meniscus: 83%;
lateral meniscus: n/a lateral meniscus: 90.9%
Barrett et al.27 1.5T 18 Surgery 90% 96% 90% 96% Very good to
perfect
Böttcher 0.5T 42 Arthroscopy Overall: 64%; Overall: 90%; Overall: 88%; medial Overall: 69%; n/a
et al.28 medial meniscus: 64%; medial meniscus: 95%; meniscus: 93%; medial meniscus: 69%;
lateral meniscus: 0% lateral meniscus: 97% lateral meniscus: 0% lateral meniscus: 93%
Harper et al.42 0.2T 15 Histopathology 90%–91% but not correlated n/a n/a n/a n/a
CHAPTER 8
with severity of changes

Böttcher 0.5T 50 Arthroscopy Overall: 69%; Overall: 92%; Overall: 73%; Overall: 88%; Fair
et al.41 medial meniscus: 74%; medial meniscus: 89%; medial meniscus: 83%; medial meniscus: 79%;
lateral meniscus: 0% lateral meniscus: 94% lateral meniscus: 5% lateral meniscus: 94%
Taylor-Brown 1.5T 8 (post-TTA Surgery 100% 100% n/a n/a n/a
et al.44 procedure)
Olive et al.43 1.5T 14 Surgery or 75% 100% n/a n/a Excellent
arthroscopy
Abbreviations: TTA = tibial tuberosity advancement; n/a = not applicable.
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• Interobserver agreement appears to be very good at high- • Subchondral bone marrow lesions appearing hyper-
field imaging but only fair with low-field imaging. intense on PDW or T2W images with fat satura-
• MRI characteristics of normal and abnormal menisci tion may be seen in the caudomedial and caudoaxial
have been reported, and the reader should refer to aspects of the tibial plateau and call the radiologist’s
Chapter 4.3 for information on normal MR appearance attention to the possibility of medial meniscal tear.43
and variations of the canine menisci (Fig. 8.26): If a meniscal tear is not visible in cases where such
• Abnormal high signal within the substance of the bone marrow lesions are seen, acquisition of addi-
meniscus may be seen in menisci with damage or tional pulse sequences or planes may be necessary to
degenerative changes but no tear;40,44 however, careful definitely rule out a meniscal tear.43
inspection of all images should be performed in such • Potential pitfalls include:
cases as a subtle tear may in fact be present and – Irregular appearance of the caudal margin of the
overlooked at first glance.43 In addition, menisci that lateral meniscus where it abuts the tendon of the
are healing or have healed will demonstrate a persis- popliteal muscle, especially in smaller dogs and at
tently high signal intensity, and this may be observed low-field; this could be mistaken for a lesion.25,33,40
for upward of 6 months.40 – On T2*W gradient echo imaging, an inhomoge-
• Menisci in which an area of high signal intersects with neous increased signal in the central part of normal
at least one of the meniscal margins are classified as menisci not extending to the periphery has been
torn.27,40 There is inconclusive evidence about use reported with low-field magnets.33 Mottled signal
of intra-articular contrast to better define meniscal of normal menisci has also been reported with
injury.26 gradient echo pulse sequences, and should not be
• The MRI grading system used in people with menis- mistaken for pathology (see Fig. 4.3.15).39,40
cal lesions appears to not be adapted for canine lesions, • Discoid lateral meniscus is a very rare anatomic vari-
at least at low-field.39 ant, in which the meniscus has an oval or circular shape
instead of its normal crescent shape. It has been reported
only once in dogs.45 Although in people this is usually
asymptomatic, the abnormally shaped meniscus can
make it prone to injuries and clinical signs. In the dog,
physical examination findings have included a mild,
intermittent pelvic limb lameness and joint effusion in
the absence of a cranial drawer sign. The MRI charac-
teristics of this condition included:45
• On T1W dorsal plane images, the normally tapering
mid-zone of the lateral meniscus appeared thickened
and covered the entire lateral tibial plateau.
• Mild joint effusion was noted.
Collateral ligament injury

• Although not clearly documented in the veterinary liter-
ature, such injury has been observed by the authors and
may cause chronic stifle lameness.
• MRI findings are best appreciated on the transverse and
dorsal planes, and include:
• Thickening of the affected collateral ligament.
• Heterogeneous signal intensity to hyperintensity
within the affected collateral ligament.
Osteochondrosis/osteochondritis
dissecans
Fig. 8.26 Sagittal T2W image of the stifle in a dog that • This disruption of the endochondral ossification process
received a fibular head transposition a few months prior to resulting in cartilaginous lesions commonly involves the
address a cranial cruciate ligament tear and presented for medial or lateral femoral condyles in dogs.31
recurring stifle lameness. A vertical hyperintense line is • It is observed mostly in large-breed juvenile fast-growing
seen across the caudal horn of the medial meniscus (arrow) dogs and is associated with pelvic limb lameness and pain
reaching the articular surfaces, consistent with a full- isolated to the stifle joint.
thickness meniscal tear. (1.5T MRI system)
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• Although the MRI appearance of this condition has not allow one to avoid this issue. If fat suppression is not
been documented in the veterinary literature, it causes a used, frequency-encoding should be in a direction where
focal cartilage defect along the articular margin of the chemical shift artifact will not affect evaluation of the
affected condyle, with abnormal shape of the underlying articular cartilage surface.
subchondral bone such as flattening or concavity. Fat sat-
urated 3D spoiled gradient echo pulse sequences should Long digital extensor tendon avulsion
be considered for a specific assessment of the articular • Avulsion of the origin of the long digital extensor ten-
cartilage.26 don is an uncommon condition, and is typically seen in
• The lesions are best appreciated on sagittal or dorsal young large- and giant-breed dogs.46
plane images (Fig. 8.27). • Affected dogs present with a unilateral pelvic limb lame-
• Fluid-sensitive sequences with fat suppression (T2W ness, stifle pain and joint effusion, and soft tissue thick-
fat suppressed or STIR images) are useful to detect ening lateral to the stifle.46 Diagnosis at the acute stage
the focal bone marrow lesions in the subchondral bone may be difficult and most dogs receive advanced imaging
at the level of the defect, which will typically appear at the more chronic stage of the disease.46
hyperintense on these pulse sequences and hypointense • The long digital extensor tendon originates at the level of
on T1W images. the extensor fossa of the lateral femoral epicondyle (cra-
• A subchondral bone cyst-like lesion may be present, niolateral aspect of the distal femur) and passes through
forming a rounded markedly T2 hyperintense focal the extensor groove (sulcus extensorius) of the tibia. The
lesion at the level of the cartilaginous defect. proximal tendon is underlaid on its deep surface by a pouch
• Joint effusion is typically present. of the meniscotibial portion of the stifle joint capsule;
• Chemical shift artifact at the interface between carti- because this bursa extends slightly around the caudal mar-
lage and subchondral bone may challenge identifica- gin of the tendon, it is also referred to as a ‘synovial sheath’.
tion of small lesions; however, fat suppression should • Although radiographic changes suggestive of long digital
extensor tendon avulsion have been described (avulsion
fragments near the extensor fossa, osseous defect at the
extensor fossa, soft tissue swelling in the area of the
extensor fossa and distal to it, dystrophic mineralization
in the area of the tendon), MRI allows better evaluation
of the soft tissue structures including the tendon itself,
muscle, and cartilage in addition to bone.46 MRI may
provide a better assessment and recognition of lesions at
the acute phase of the condition.
• The MRI characteristics of long digital extensor tendon
avulsion include:46
• An osseous defect in the lateral condyle of the left
femur at the level of the extensor fossa.
• On T1W images, there is decreased signal intensity
around that defect, consistent with bone sclerosis or
bone marrow lesions secondary to the avulsion.
• A decrease in signal intensity in the proximal portion
of the long digital extensor muscle when compared
with the other regional muscles can be seen on T1W
images, consistent with effusion in the tendon sheath
and edema/hemorrhage in the proximal muscle.
• Although not reported in the literature so far, addi-
tional changes that would be expected would include:
– On T2W or PDW images, distension of the ten-
don sheath with hyperintense fluid.
– Abnormal hyperintense T2 signal in the tendon
and musculotendinous junction due to edema.
– Disruption and distal displacement of the long
Fig. 8.27 Sagittal 3D spoiled gradient echo image of the stifle digital extensor tendon, which may be best
in a dog with femoral condyle osteochondrosis. The arrow appreciated on sagittal or dorsal plane images.
indicates a cartilage and subchondral bone defect with filling Displacement of the tendon secondary to avul-
by synovial fluid. (1.5T MRI system) sion should be considered when the normal
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hypointense tendon in the extensor fossa cannot • Affected dogs have severe lameness, sometimes with a
be clearly identified. plantigrade stance.47 Pain on palpation of the affected
– In chronic cases, thickening of the synovium of gastrocnemius head may be present. A number of dogs
the tendon sheath and enhancement on T1W present with chronic lameness with no history of trauma
images after gadolinium administration should be from athletic activities.48
expected. • Distal displacement of the sesamoid bone of the affected
gastrocnemius head may be seen radiographically; how-
Gastrocnemius musculotendinopathy ever, direct assessment of the injury necessitates imaging
• The gastrocnemius muscle is divided into a lateral and techniques with good soft tissue contrast such as MRI.47
medial head, which arise out of a large tendon from the Osteophytic changes around the lateral fabella may also
lateral and medial supracondylar tuberosities of the cau- be seen radiographically.48
dodistal femur, respectively. Each tendon contains a large • The lateral head appears to be more commonly affected,
sesamoid bone (medial and lateral fabellae) that articu- although the medial head can be affected as well.
lates with the corresponding condyle. The two heads of Concurrent lateral and medial head involvement with
the gastrocnemius fuse distally, forming a single tendon more pronounced changes in the lateral head is common.
that attaches onto the calcaneal tuberosity.47 • The MRI characteristics of this condition include
• Myotendinous strain of the proximal portion of the gas- (Fig. 8.28):47,48
trocnemius muscle origin, with or without total/partial • Altered signal intensity in the affected head of the
avulsion, can be seen with or without prior known proximal gastrocnemius, which can be discrete/focal
trauma.47 It is common in athletic dogs, such as racing or extensive with increased volume:
Greyhounds and field trial dogs, as well as herding dogs, – Hyperintense on T2W fast spin echo, T2*W gra-
but has also been reported in non-working family dogs.48 dient echo, and STIR images.
In people, these strains are classified as stretch injury – Iso- to mildly hyperintense compared with the
(first-degree strain), partial tear (second-degree strain), surrounding muscles on T1W spin echo images.
or complete tear (third-degree strain).47 Occasionally T1 hypointensity is observed.
(a) (b)
Fig. 8.28 Dorsal STIR (a), transverse T2W (b), dorsal T2W (c), and sagittal T2W (d) images of the left stifle in a 7-year-old,
neutered female Border Collie with gastrocnemius musculotendinopathy. High signal intensity with a feathery appearance is
seen in the lateral head of the gastrocnemius muscle (arrows) near the sesamoid bone. (0.2T MRI system; reproduced, with
permission, from Stahl C, Wacker C, Weber U et al. (2010). MRI features of gastrocnemius musculotendinopathy in herding
dogs. Vet Radiol Ultrasound 51(4):380–5.) (Continued)
670 CHAPTER 8
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(c) (d)
• Enhancement of these areas of abnormal signal is seen • The extent of the soft tissue trauma caused by such
on post-contrast T1W images. Contrast enhance- injuries is typically underestimated with other imaging
ment within the sesamoid bone of the affected head modalities, whereas the improved soft tissue contrast of
may also be seen. MRI allows a more thorough assessment of the lesions
• Occasional T2W, T2*W, and STIR hyperintensity in at hand.1
the fascial plane between the lateral head of the gas- • Partial or complete tears of the ligaments of the acces-
trocnemius muscle and the superficial digital flexor sory carpal bone that occur secondary to hyperextension
muscle, best seen on transverse plane images. injuries can be identified with MRI, best seen on fluid-
• Mineralization around the sesamoid bone of the sensitive sequences with suppression of fat signal such
affected head and local soft tissues may be seen as STIR or T2W/PDW sequences with fat saturation
in more chronic lesions, and appear as hypoin- (Fig. 8.29).1 Joint effusion and peritendinous fluid accu-
tense, irregularly marginated foci on various pulse mulation will be seen; the distinct low signal of these
sequences. ligaments, typically well seen on sagittal images, will not
be seen in cases of rupture.1
EXTREMITY OF THE LIMBS • In the tarsus, high-resolution MRI is also good to evalu-
ate the location and extent of soft tissue injuries such as
• MRI of the extremities (carpus/manus and tarsus/pes) is damage to the calcaneal tendon and digital flexor ten-
not commonly used in dogs and cats, in part because the dons (Fig. 8.30).
small size of the structures of these regions and com- • Traumatic injuries to the metacarpophalangeal/metatar-
plex anatomy make assessment challenging. However, sophalangeal sesamoid bones and secondary lesions of
with higher field machines becoming more available and the flexor tendons may be evaluated accurately with MRI
improvement in coil technology, optimal imaging of (Fig. 8.31).
these areas has become possible.
• MRI can be used efficiently for the diagnosis of traumatic Foreign bodies
injuries, foreign bodies, or neoplasia of the extremities. • Foreign bodies affecting the integumentary and muscu-
loskeletal systems are common in dogs, with the distal
Traumatic injuries extremities being commonly affected sites.49
• Hyperextension carpal injuries are common in athletic • Non-radiopaque foreign bodies are a diagnostic chal-
and working dogs. lenge. Undetected chronic foreign bodies can lead to
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(a) (b) (c)

Fig. 8.29 Dorsal T1W pre- (a) and post-contrast (b) fat saturated images and transverse PDW image (c) of the carpus in a
working dog with an acute injury to the extremity. Images (a) and (b) are obtained along the palmar surface of the carpus; the
accessory carpal bone is visible in cross section (dashed arrows) and there is irregular shape and signal within the accessorio-
metacarpal ligament (solid arrows), with marked diffuse enhancement and swelling around it (open arrows). (1.5T MRI system)
complications such as neurapraxia, abscessation, septic In some breeds, such as Rottweilers, it is more commonly
arthritis, or osteomyelitis. seen in the lateral trochlear ridge of the talus.50
• With MR imaging, acute wooden foreign material is usu- • Although the diagnosis of this condition is typically
ally T1 and T2 hypointense to the surrounding muscu- made with radiographs and/or CT, MRI may also be use-
lature, often appearing as a signal void.49 More hydrated ful and allow a thorough assessment of the bony and also
(versus desiccated) pieces of wood may appear T2 hyper- soft tissue changes associated with the condition, which
intense or isointense due to their higher water content.49 may be overlooked with CT or radiography.1 It can also
Chronic wooden foreign bodies may also have progres- be useful in chronic cases with migrated joint mice in
sively increased T2 signal due to long-term soaking. order to correctly localize these mice and facilitate surgi-
• Acute foreign bodies may be more challenging to iden- cal planning and approach (Fig. 8.32).
tify with MRI, especially if they are small. In experimen- • MRI features would be expected to be similar to those
tal studies, CT and ultrasound performed better.49 seen with osteochondrosis of other joints that have been
• Chronic foreign bodies may be more easily identified described earlier, including:1
with MRI because a T2 hyperintense inflammatory • Flattening or a concave defect in the margin of the
response could accentuate an embedded T2 hypoin- subchondral bone of the trochlear ridge, best appre-
tense foreign body;1 this inflammatory reaction is typi- ciated on sagittal or dorsal plane images (Fig. 8.32).
cally T1 hypointense (occasionally T1 hyperintense) • A fragment associated with that subchondral bone
and contrast enhancing. Fluid-cavitation due to absces- defect is seen in cases of osteochondritis dissecans.
sation (T2 hyperintense, T1 hypointense, and non- • Joint effusion, easy to detect on T2W or PDW images.
enhancing) may be seen, and draining tracts can be • T2W, PDW, or STIR hyperintensity and T1W
highlighted on post-contrast images, due to strong hypointensity of the subchondral bone underlying
enhancement of their wall. the cartilaginous lesion may be seen, corresponding
to subchondral bone marrow lesions.
Tarsal osteochondrosis/ • Conversely, hypointense areas of the subchondral
osteochondritis dissecans bone on T1W, T2W, and PDW images are due to
• Tarsal osteochondrosis most commonly affects the bone sclerosis, which may represent a more chronic
medial trochlear ridge of the talus and is often bilateral. stage of the disease.
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IV
*
(a) (b)
Fig. 8.30 Sagittal T2W image at the level of the 4th metatarsophalangeal joint (a), dorsal T1W fat saturated post-contrast
image immediately plantar to the 3rd /4th metatarsophalangeal joints (b), transverse T1W fat saturated post-contrast image at a
level immediately proximal to the 3rd /4th metatarsophalangeal joints (c), and corresponding transverse STIR image at the same
level (d). Images are of the right foot in a 2-year-old Belgian Malinois dog, 1 month after sustaining an acute foot injury. At the
time of the injury, there was swelling at the level of the metatarsophalangeal joints, with pain elicited during extension/flexion
of these joints. At the time of the MR examination, 1 month after injury, the dog had a more plantigrade stance, centered at the
metatarsophalangeal joints. There was residual swelling associated mostly with the 3rd digit and the extremity of that digit was
dorsally deviated. On the sagittal image passing through the 4th metatarsal joint (a), there is effusion and synovial distension of
the metatarsosesamoidean joint (asterisk); the imaging plane passes through the superficial (solid arrow) and deep digital flexor
tendons (arrowhead) of that 4th digit. When tracing the deep digital flexor tendon distally, progressive swelling and increased
signal intensity within that tendon is visible (solid circle). On the dorsal post-contrast image (b), the transition of normal,
homogeneously hypointense (arrowhead) to abnormally thickened and hyperintense 3rd deep digital flexor tendon (dashed
circle) is visible; the abnormal extremity of the 4th deep digital flexor tendon seen in (a) is also visible in that plane (solid circle).
On the transverse images (c, d), the thickened and heterogeneous 3rd deep digital flexor tendon is readily visible again
(dashed circles), and there is also abnormal hyperintense irregular signal in the deep digital flexor tendons of the 2nd, 4th, and
5th digits (dashed arrows). Lesions are more severe in the 3rd and 4th tendons with significant swelling. There is enhancement
of the soft tissues around the plantar aspect of the 3rd and 4th metatarsal bones (c) and corresponding STIR hyperintense
signal (d). In (d), the metatarsophalangeal sesamoid bones are indicated by the thick arrows. Changes are consistent with
severe tear/strain of the deep digital flexor tendons of the right foot, more pronounced in the 3rd and 4th digits, explaining the
plantigrade stance. II, III, IV, and V = 2nd, 3rd, 4th, and 5th metatarsal bones, respectively. (1.5T MRI system; images courtesy of
Dr. Matthew Paek, Bush Advanced Veterinary Imaging) (Continued)
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IV III
V II
(c) (d)
• Chronic thickening/inflammation of the synovium Shepherd Dogs, with an active lifestyle are reportedly
and joint capsule as well as bone remodeling can cause predisposed to specific myopathies such as gracilis, sar-
impingement of the deep digital flexor tendon along torius, or semitendinosus muscles. Clinical signs vary
the medial aspect of the calcaneus, best appreciated depending on the specific muscle(s) affected, but the
on transverse plane images (Fig. 8.32).1 muscle(s) of origin can be difficult to determine based
on physical examination alone; for example, contrac-
OTHER CONDITIONS ture of the sartorius muscle is clinically similar to graci-
lis muscle contracture.55 Therefore, MRI may prove to
Myopathies be the best imaging method to determine the muscle(s)
• When myopathies affect the appendicular skeleton, they affected and plan for the most appropriate treatment.
can cause lameness. Radiographs will typically be normal • When localized close to a joint, myopathies will cause
or show non-specific findings such as soft tissue swelling clinical signs mimicking joint disease and may be rec-
in acute cases or muscle atrophy in chronic cases, and ognized during specific joint imaging. Examples of
advanced imaging such as MRI is very useful to localize such conditions have been covered previously in this
and characterize the muscular changes due to its excel- chapter, in the joint-specific paragraphs; for exam-
lent soft tissue contrast. ple, infraspinatus contracture and gastrocnemius
• Inflammatory myopathies are characterized by non-sup- musculotendinopathy.
purative infiltration of inflammatory cells into striated • Iliopsoas myopathy may cause clinical signs that mimic
muscles, and can have a generalized or focal distribu- coxofemoral pain.56,57 This condition is covered in
tion.51 This is a heterogeneous group of diseases with Chapter 7.13.
various etiologies including immune-mediated and infec- • Diagnosis is established through a combination of clini-
tious causes such as protozoal (toxoplasmosis, neospo- cal, serologic, electromyographic, and histopathologic
rosis), bacterial, and, rarely, rickettsial and parasitic.51,52 criteria. Muscle biopsy is the most important test for a
As many muscles can be involved simultaneously, clinical definitive confirmation, and therefore sensitive imag-
signs will depend on the distribution of the lesions, and ing techniques that allow determination of the best sites
can include paraspinal pain, stiff gait, abnormal stance, for diagnostic sampling are important. MRI, due to its
or lameness. Systemic signs such as fever and lethargy high sensitivity to changes in soft tissue structure and
may be present as well. biochemical environment, is an excellent tool for this
• Fibrotic myopathies and muscle contractures are purpose.
typically focal diseases that affect specific muscles • MR imaging of appendicular muscles should include
(e.g., infraspinatus, supraspinatus, gracilis, sartorius, T1W and T2W spin echo sequences and T1W post-
semitendinosus)53–55 or muscle groups (e.g., quadriceps contrast images. The addition of fat suppressed
femoris, iliopsoas).56,57 Their etiology is not clearly sequences such as STIR or T2W images with fat satura-
established, but excessive exercise over a long period tion is strongly recommended, as they are more sensitive
resulting in tearing or stretching of muscle fibers has in detecting changes in T2 relaxation time associated
been proposed as a possible cause; acute trauma has with increased intra- and extracellular water content
also been implicated.54 Some breeds, such as German (muscle edema).
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(b)
(a) (c)
(d) (e)
Fig. 8.31 One-year-old working dog with chronic lameness and pain at the 3rd metacarpophalangeal joint of the right manus.
There is a fracture of the medial metacarpophalangeal sesamoid bone with secondary interosseous myositis, deep digital flexor
tendon tenosynovitis, and metacarpophalangeal joint effusion. Sagittal PDW image at the level of the 3rd digit (a) showing
distension of the third metacarpophalangeal joint with synovial fluid (joint effusion, solid arrow). The dorsal plane reformatted
image from a 3D MPGR series passing through a plane palmar to the 3rd digit metacarpophalangeal joint (b) shows the
fractured sesamoid bone (arrowhead) compared with the normal 3rd lateral metacarpophalangeal sesamoid (open arrow).
The fractured sesamoid is also appreciated on the transverse 3D MPGR image (c, arrowhead). Images (d) and (e) are passing
through the deep digital and superficial digital flexor tendons. On the PDW image with fat saturation (d), there is effusion
in the sheath around the 3rd digital branch of the deep digital flexor tendon (dashed arrow) and this sheath is enhancing on
the T1W post-contrast image with fat saturation (e, dashed arrow). There is also mild enhancement and swelling of the
interosseous muscle dorsal to that tendon. (1.5T MRI system)
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(a) (b)
Fig. 8.32 Tarsal MRI in a 4-year-old mixed breed dog with chronic lameness and lack of range of motion of the tarsus. On
the dorsal 3D MPGR image (a), there is flattening of the proximoplantar aspect of the medial trochlear ridge of the talus
(arrowhead). On the dorsal T1W post-contrast with fat saturation image (b), an oval-shaped well-defined osseous body is seen
in the sheath of the deep digital flexor tendon, with marked enhancement of the sheath (solid arrow). There is severe chronic
soft tissue swelling along the medial aspect of the tarsus. On the transverse PDW image with fat saturation (c), the deep digital
flexor tendon (open arrow) is squeezed between the talus (T) and the calcaneus (C) secondary to bony proliferations along these
bones impinging onto the tendon and sheath. When imaged in the sagittal plane (d, e) this part of the tendon is focally widened
in the dorsoplantar direction (open arrows), because of it being squeezed lateromedially. Images (d) and (e) are sagittal T2W
fat saturated and PDW fat saturated images passing through the plane of the deep digital flexor tendon. Lobulated expansion
of the tendon sheath filled with hyperintense fluid is seen (dashed arrows) corresponding to tenosynovitis with adhesions, and
the previously mentioned osseous body is seen, sitting within a fluid-filled expansion of the sheath (solid arrows). Image (f) is a
sagittal T1W image showing osteophytosis and lipping of the plantar aspects of the tibia and talus (dotted arrow) due to chronic
osteoarthritis. The final diagnosis is chronic osteochondritis dissecans of the proximoplantar aspect of the medial ridge of the
trochlea of the talus, with a chronic osteochondral fragment (joint mouse) that has migrated proximally into the sheath of the
deep digital flexor tendon, causing chronic tenosynovitis. There is secondary chronic hypertrophic synovitis and osteoarthritis,
worse along the medial and plantar aspects of the tarsus. Note that the joint mouse on all pulse sequences has a trabecular
pattern, similar to normal subchondral bone as is often observed when chronic osteochondral fragments undergo normal
endochondral ossification. (1.5T MRI system) (Continued)
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T
C
(c) (d)
(e) (f)
• MRI features of inflammatory myopathies include • High signal on T2W images is typically caused by
(Figs. 8.28, 8.33–8.35):7,47,51,52 edema, which is hypointense on T1W images.
• Focal or multifocal ill-defined, patchy intramuscular • High signal on both T2W and T1W images may
lesions. Multifocal lesions may be bilateral but are reflect fatty replacement, which occurs later in the
usually asymmetric. course of the disease. These changes may be con-
• Lesions are typically hyperintense on T2W images, of fused with signal abnormalities associated with den-
variable signal on T1W images (hyperintense, isoin- ervation myopathy, which can also be of high signal
tense or hypointense), hyperintense on STIR images, on T2W and T1W images with contrast enhance-
and contrast enhancing. ment; however, in this case the abnormal signal is
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• Although CT and radiography are sensitive to bone lysis,

many neoplasms, in particular those of joint origin, have
only a soft tissue component initially.
• Synovial cell sarcoma and histiocytic sarcoma are the
most common joint neoplasms in dogs. Other tumors of
synovial origin that can be seen are synovial myxomas/
myxosarcomas, which are more common in the stifle and
digits.58
• The MRI appearance of synovial cell sarcoma has rarely
been described in dogs.59
• Joint neoplasms may appear as an enhancing soft tissue
mass associated with the synovium, with variable degrees
of lysis of the adjacent bones causing cortical disruption
(best seen on T1W images) and abnormal intraosse-
ous signal intensity (best detected on T2W sequences
with fat saturation) (Fig. 8.36). Marked joint disten-
sion is usually present and readily seen on T2W images.
Irregular synovial thickening with decreased T2 signal
(a) may be seen as well, with strong contrast enhancement
on T1W post-gadolinium images.1
• The MRI appearance of synovial myxoma affecting the
appendicular skeleton has been reported only once,60
and the MRI features were similar to those reported for
the spinal myxomas/myxosarcomas (see Chapter 7.6),61
including:
• A lobulated mass associated with the affected joint,
causing distortion/lysis of the adjacent bones.
• The mass typically invades into the adjacent muscles
or dissects between the intermuscular fascial planes.
• The mass is markedly hyperintense on T2W images.
On T1W images the mass is hypointense, and
there is moderate to strong enhancement on post-
contrast images, which can be diffuse, patchy, or
rim-like. Central non-enhancing areas are common,
corresponding to pockets of mucinous substance.
(b)
Bone neoplasia
Fig. 8.33 Dorsal (a) and transverse (b) T1W post-contrast • MRI is rarely used to image bone tumors in dogs;
images of the pelvic region in a 7-year-old German Shepherd however, with the development of surgical alternatives
Dog with gracilis fibrotic myopathy/contracture. The to limb amputations (e.g., ‘limb-salvage’ procedures),
proximal portion of the right gracilis muscle is mildly swollen sensitive imaging techniques to accurately evaluate the
and diffusely contrast enhancing. (1.5T MRI system; image extent of the neoplastic tissue within the affected bone
courtesy of Dr. Matthew Paek, Bush Advanced Veterinary are useful.62,63
Imaging) • MRI is capable of early identification of neoplastic infil-
tration as the focal water content that is caused by tumor
infiltration may be depicted early, prior to the develop-
generally more diffuse as opposed to being patchy ment of changes on radiographs or CT; the soft tissue
in inflammatory myopathies; there also tends to be component of bone tumors is also best demonstrated
more pronounced muscle atrophy in cases of dener- with MRI (Fig. 8.37).1 Early lesions may be identified as
vation. focal hypersignal on fluid-sensitive pulse sequences with
fat suppression, such as STIR or fat-saturated T2W or
Joint neoplasia PDW images.1
• MRI is useful to rule out aggressive disease as an under- • On MRI, osteosarcomas cause a focal alteration of the
lying cause of lameness that would otherwise not be signal intensity of the affected metaphyseal cancellous
detected with other imaging techniques. bone and adjacent medullary cavity (Figs. 8.38, 8.39).
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(a) * (b) *
Fig. 8.34 Transverse images through the pelvic region in

a 6-year-old male intact German Shepherd Dog with acute
left-sided gracilis myopathy. On the STIR (a) and T2W
fat saturated (b) images there is enlargement of the left
gracilis muscle (arrows) compared with the right muscle
(asterisks), with patchy hyperintense signal. Marked patchy
enhancement of the T2/STIR hyperintense regions is noted
(c) * on the T1W post-contrast fat saturated image (c, arrow).

(1.5T MRI system)
Fig. 8.35 Transverse image through the coxofemoral joints

region in a 6-year-old male intact German Shepherd Dog with
acute right-sided iliopsoas myotendinopathy (same dog as in
Fig. 8.34). On this transverse T1W post-contrast image with
fat saturation there is marked patchy contrast enhancement
of the musculotendinous insertion of the right iliopsoas
muscle (solid arrow) onto the lesser trochanter of the right
proximal femur (dashed arrow). Also note the severe bilateral
coxofemoral joint incongruity with poor acetabular coverage,
shallow acetabulae, and osteophytic remodeling along the
acetabular margins.
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* * *
* *
(a) (b) (c)

Fig. 8.36 Dorsal oblique T2W (a) and T1W post-contrast fat saturated (b) and sagittal T1W post-contrast fat saturated (c)
images of the shoulder in a 10-year-old Basset Hound with chronic lameness and pain in the shoulder and no radiographic
abnormality. A multilobulated mass (asterisks) is seen around the shoulder joint with extension in the synovial sheath of the
biceps brachii tendon (arrow, c), consistent with a joint-associated neoplasm. Histopathology confirmed a histiocytic sarcoma.
(1.5T MRI system)
The lesion is usually best seen on pre-contrast T1W reference to the post-contrast images is recommended
images, where it is typically isointense to muscle and as, in some cases, some of the isointense tissue at the
hypointense to the adjacent fat in the medullary cavity; tumor/fat margin does not enhance and is interpreted
the lesion usually enhances, decreasing the T1 contrast as non-tumor tissue (e.g., necrosis, hemorrhage, edema).
between tumor tissue and normal bone marrow. On The leading margin of contrast-enhancing isointense
PDW and T2W images, the tumor tissue is more dif- tissue should be used as a landmark for intramedullary
ficult to differentiate from the medullary fat, resulting in tumor extension.
a fair to poor line of demarcation.63
• Disruption of the hypointense signal from the cortex is Osteomyelitis/septic arthritis
usually best appreciated on T1W images and irregular • In people, MRI has been shown to offer superior sensi-
hypointense signal around the bone corresponding to tivity compared with bone scintigraphy for the detection
mineralization and periosteal reaction is typically seen. of osteomyelitis, and more precisely detects extraosse-
• In determining intraosseous tumor extension with imag- ous complications. A characteristic MRI feature of sub-
ing techniques, one study found MRI to be less accurate acute osteomyelitis, called the ‘penumbra sign’, has been
than radiographs and CT in determining tumor exten- described in people but not yet reported in veterinary
sion, with a trend to overestimate it; however, this study medicine. It refers to the thin layer of granulation tissue
did not include post-contrast T1W imaging in the evalu- that lines the abscess cavity and appears slightly hyper-
ation.62 Another study, using combined T1W pre- and intense on pre-contrast T1-weighted images.64–66 The
post-contrast evaluation, found that MRI was more accu- appearance of osteomyelitis on MRI in dogs has only
rate than radiography, CT, and nuclear scintigraphy for been reported in anecdotal individual cases.65 On T1W
tumor extension. In general, T1W pre-contrast images images, an irregular signal within the medullary cavity
highlight the demarcation between isointense (to muscle) of the bone can be seen, with cortical disruption (lack of
tumor tissue and hyperintense medullary fat; however, visualization of the normal signal void of the cortex) and
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(a) (b)
H H
(c) (d)
Fig. 8.37 Lateral shoulder radiograph (a) and sagittal

T2W (b), transverse STIR (c), T1W pre-contrast
(d), and T1W post-contrast with fat saturation
(e) images in a 9-year-old Bulldog with shoulder
lameness. A very subtle periosteal reaction is noted
along the caudal cortex of the humerus on the H
lateral radiograph (solid arrow, a) and an ill-defined
rounded soft tissue mass is seen caudal to this
(dashed arrows, a). This mass is well visible on the
MR images (dashed arrows, b–e), being hyperintense
on the T2W and STIR images, isointense to muscles
on the T1W pre-contrast image, and with patchy
internal and peripheral rim enhancement after
gadolinium injection. The soft tissue component
of this bone lesion is much better appreciated with
MRI. The final diagnosis was chondrosarcoma.
H = humerus. (1.5T MRI system) (e)
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(a) (b)
Fig. 8.38 Sagittal T1W fat saturated pre- (a) and post-contrast (b) images of the shoulder in a 10-year-old Golden Retriever
with a proximal humeral osteosarcoma. No lesion was seen radiographically, but MRI reveals a patchy abnormal signal in the
proximal humeral metaphysis extending proximally into the epiphysis and distally in the diaphysis. The lesion is hyperintense
on the T1W pre-contrast image, with patchy enhancement after gadolinium injection; the distal margin of the tumor is slightly
more well-defined on the post-contrast image (arrows). (1.5T MRI system)
(a) (b)
Fig. 8.39 Dorsal plane STIR (a), sagittal T2W (b), and transverse T1W post-contrast with fat saturation (c) images at the level
of the scapula in a 6-year-old mixed breed dog with a scapular chondrosarcoma. There is a lobulated STIR and T2 hyperintense
mass in the proximal aspect of the scapula (solid arrows, a and b) causing disruption of the normal hypointense cortex (compare
with the contralateral normal scapula in a, indicated by the dashed arrow). On the T1W fat saturated post-contrast image (c),
the mass is mildly enhancing, more so on the periphery (arrows); the disruption of the normally hypointense scapular cortex is
clearly appreciated (arrowhead) indicative of lytic changes. (1.5T MRI system) (Continued)
682 CHAPTER 8
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extension of the heterogeneous signal within the sur-

rounding soft tissues.65
• Septic arthritis may cause signs similar to joint-associated
neoplasia, although typically there will not be a clear
solid mass-like component in septic arthritis. Findings
may be similar to those reported in people, including
(Fig. 8.40):67
• Irregular synovial thickening with enhancement.
• Joint effusion.
• Periarticular edema.
• Subchondral bone irregularities (typically T2 and
STIR hyperintense) with cortical disruption.
• Marked irregular articular and periarticular contrast
enhancement on T1W post-gadolinium images.
(c)
* *
(a) (b) (c)

Fig. 8.40 Dorsal STIR (a), T1W pre-contrast (b), and T1W post-contrast with fat saturation (c) images of the stifle in a
4.5-month-old Boxer with 3-week history of lameness and swollen stifle joint, diagnosed with septic arthritis. There is
joint effusion (asterisks, a and b), synovial thickening (solid arrows, a), synovial, intra- and periarticular enhancement
(arrowheads, c), and subchondral bone erosions along the tibial plateau (dashed arrows, b). (1.5T MRI system; images
courtesy of Dr. Matthew Paek, Bush Advanced Veterinary Imaging)
VetBooks.ir
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35. Soler M, Murciano J, Latorre R et al. (2007). Ultrasonographic, 50. Wisner ER, Berry CR, Morgan JP et al. (1990).
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resonance imaging of subarticular bone marrow lesions in dogs semitendinosus myopathy in 18 dogs. J Am Anim Hosp Assoc
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47. Stahl C, Wacker C, Weber U et al. (2010). MRI features osteomyelitis. Eur Radiol 15(6): 1268–70.
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SECTION 6
MRI OF THE THORAX

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685
AND ABDOMEN
CHAPTER 9.1 Cardiac MRI
CHAPTER 9.2 MRI of non-cardiac thoracic conditions
CHAPTER 10 Abdominal MRI

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CHAPTER 9.1
CARDIAC MRI
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Wilfried Mai 687
CONTENTS
Cardiac gating .................................................................................................................................................................................................688
Control of respiratory motion...........................................................................................................................................................................688
Animal positioning and image plane orientation ..............................................................................................................................................688
Black-blood cMRI techniques ..........................................................................................................................................................................688
Bright-blood cMRI techniques .........................................................................................................................................................................690
cMRI assessment of cardiac morphology, function, and structure .........................................................................................................................691
Cardiac mass and ventricular volumes ............................................................................................................................................................691
Ventricular systolic hemodynamic function .....................................................................................................................................................693
Ventricular diastolic hemodynamic function ....................................................................................................................................................693
Morphologic assessment and planar measurements .......................................................................................................................................693
Quantitative flow assessment – phase-contrast imaging..................................................................................................................................693
Regional myocardial function – strain imaging (MR tagging) ..........................................................................................................................697
Myocardial structure ........................................................................................................................................................................................697
Contrast-enhanced magnetic resonance angiography......................................................................................................................................700
Clinical applications in veterinary medicine ..........................................................................................................................................................701
Cardiomyopathy ..............................................................................................................................................................................................701
Cardiac tumors ................................................................................................................................................................................................701
Congenital anomalies ......................................................................................................................................................................................703
Mitral insufficiency ..........................................................................................................................................................................................704
References.............................................................................................................................................................................................................708
In people, magnetic resonance imaging is routinely used speed up acquisition times to values compatible with in-vivo
to depict cardiac morphology, flow, and function, as well as imaging.13,15–34 Although cMRI is still in its infancy in vet-
myocardial structure.1–8 In companion animals, the evalu- erinary medicine, the increasing availability of advanced
ation of cardiac morphology and function has mainly been MRI equipment allows easier access to these techniques,
based on echocardiographic evaluation and cardiac cathe- and this chapter provides a brief overview of the informa-
terization. Until recently, cardiac MRI (cMRI) in animals tion that can be gained and examples of some clinical appli-
has been focused on naturally occurring or experimentally cations. For more details on the technical aspects, the reader
produced animal models of human diseases such as cardio- is referred to review and research articles mentioned in the
myopathy,9 muscular dystrophy,10 myocardial infarction,11,12 references.
and pulmonary hypertension.13 Early reports of the thoracic
MR anatomy in dogs produced low-quality images with GENERAL CONSIDERATIONS
little detail of the cardiovascular structures, mostly due to
artifacts resulting from cardiac and respiratory motion.14 The reader is referred to Chapter 2 for more details about
These problems have been overcome through cardiac gat- the concepts and basic principles of the pulse sequences that
ing, respiratory navigation, and encoding strategies that are mentioned below.
688 CHAPTER 9.1
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Cardiac gating in place with tape, is very important. Visual inspection of

• Cardiac gating is a strategy aiming at synchronizing data the quality of the ECG signal at the MRI control station
collection with specific phases of the cardiac cycle, so after placing the electrodes should be performed prior to
as to minimize the effects of cardiac motion in order to moving the patient into the bore of the machine.
improve morphologic imaging. • A torso-array receive-only multicoil (or other appro-
• Most of the time, gating is performed using signal from priate coil providing good signal along all sides of the
an ECG that is integrated with the MRI machine and patient and compatible with cardiac imaging options) is
the imaging software. placed over the thoracic area.
• Cardiac gating can be applied prospectively during • The sagittal and transverse localizers can be used to
acquisition, which involves the use of an arrhythmia obtain a long-axis 4-chamber view of the heart similar to
rejection period or window around the R-wave, during the ‘left apical 4-chamber view’ in echocardiography.27
which the sequence is not played out, or retrospectively, For this, a double-oblique image is obtained by placing a
where the sequence runs continuously and the position first acquisition plane on the sagittal localizer that runs
of the data within the cardiac cycle is determined after roughly from the middle of the left atrium to the car-
data collection.2,35,36 diac apex; these structures are typically well recognized
when scrolling through the images of the sagittal local-
Control of respiratory motion izer. Then a second oblique plane is placed on a trans-
• Cardiac pulse sequences in people are typically run dur- verse localizer image at the level of the left atrium; this
ing breath-hold, and depending on the type of pulse line runs across the middle of the heart, at about a 45°
sequence used and extent of anatomic coverage, several angle from horizontal, from left-ventral to right-dorsal
successive breath-holds may be necessary to record the (Fig. 9.1.1). A fast T1W single slice image can be run
necessary data. using this double-oblique orientation to verify that the
• In dogs and cats, voluntary breath-hold is not possible. resulting acquisition plane is indeed a 4-chamber view
However, these patients are imaged under anesthesia, of the heart, showing the left atrium, left ventricle, right
allowing induction of apnea after periods of hyperventi- atrium, and right ventricle (Fig. 9.1.1). Adjustments may
lation. Even more effective apnea can be obtained using need to be made, depending on the patient, if there is tilt-
constant infusion of cisatracurium.29 This can later be ing of the thorax or in case of shifting of the heart due to
reversed using atropine and neostigmine. either pulmonary atelectasis or cardiothoracic pathology.
• Control of respiratory motion can also be achieved using • When an adequate 4-chamber view has been obtained,
‘respiratory gating’, where data are collected during it can be used to orient true short-axis images of the left
a limited portion of the respiratory cycle, usually near ventricle (similar to the ‘right parasternal short-axis view’
end-expiration when respiratory movement is minimal.37 in echocardiography) by placing the imaging planes per-
This is achieved by means of a belt of bellows placed pendicular to the long axis of the left ventricle, spanning
around the patient’s thorax, within which a transducer the apex to the base (Fig. 9.1.1). This allows acquisition
produces an electronic signal the amplitude of which of standard imaging planes for measurements of ventric-
corresponds to the maximum and minimum excursion of ular mass, ventricular volumes, left atrial size, and aortic
the thoracic wall during respiration.38,39 This is described and main pulmonary artery dimensions.20
in more detail in Chapter 9.2. However, for cardiac imag- • Then, depending on the specific application, additional
ing, this is usually of limited utility due to the small tho- long-axis images of the heart can be obtained, guid-
racic wall excursions during breathing, which are even ing the acquisition planes from either the long-axis
more reduced under anesthesia, and the short duration 4-chamber or short-axis images, in a similar fashion to
of most scans. An exception to this is complex 4D flow the methodology used in echocardiography. Adequate
analysis, which has much longer acquisition times and placement of imaging planes can be challenging in
requires the use of respiratory triggering with bellows.13 cMRI, and requires a good understanding and knowl-
edge of the cardiac anatomy and how it relates to the
Animal positioning and image standard transverse/sagittal/dorsal imaging planes used
plane orientation in regular MRI.
• The patient is typically placed in dorsal recumbency in
the magnet bore. Black-blood cMRI techniques
• For cardiac gating, electrodes are placed on the thoracic • Black-blood (or ‘dark-blood’) methods, as their name
wall after shaving the hair to ensure good contact and suggests, result in the cardiac cavities having a dark sig-
coupling during data acquisition. Poor or inconstant nal due to flowing blood within them. These typically
signal is a common cause of failure to complete a cMRI utilize pulse sequences of the spin echo family.2,35,36
examination, so adequate positioning of these electrodes, • Although standard spin echo sequences provide dark-
ensuring good coupling with the skin and securing them blood signal, modifiers such as double or triple inversion
C a r di ac M R I 689
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SAGITTAL LOCALIZER
LA
RV
LV
RA
(a)
LA
TRANSVERSE LOCALIZER
(c)
LA
LONG-AXIS 4-CHAMBER
(b)
Fig. 9.1.1 Step-by-step approach to obtaining short-axis cMRI images of the heart. Because the long axis is oriented obliquely
with respect to the true sagittal, dorsal, and transverse planes of the patient, a double-oblique plane is necessary to obtain
true long-axis or short-axis views of the heart. The sagittal (a) and transverse (b) localizers can be used to obtain a long-axis
4-chamber view of the heart. A first acquisition plane is placed on the sagittal localizer that runs roughly from the middle of the
left atrium (LA) to the cardiac apex (dotted line, a); these structures are typically well recognized when scrolling through the
images of the sagittal localizer. Then, a second oblique plane is placed on the transverse localizer image at the level of the left
atrium, running across the middle of the heart, at about a 45° angle from horizontal, running from left-ventral to right-dorsal
(dotted line, b). A fast T1W single slice image can be run using this double-oblique orientation to verify that the resulting
acquisition plane is indeed a 4-chamber view of the heart (c), showing the left atrium (LA), left ventricle (LV), right atrium
(RA), and right ventricle (RV). When an adequate 4-chamber view has been obtained, it can be used to orient true short-axis
images of the left ventricle (e) by placing the imaging planes perpendicular to the long axis of the left ventricle, spanning the
apex to the base (dotted lines, d). (Continued)
690 CHAPTER 9.1
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(d)
(e)
recovery can be used to further null signal from blood, • Then, as in all fast or turbo spin echo acquisitions,
thereby improving contrast between the cardiac tissues several 180° pulses are applied before the next R-wave
and blood pool.36 to encode several lines of k-space. This process is
• In the double inversion preparation scheme, two succes- repeated across the following cardiac cycles, until
sive preparatory 180° pulses are applied before a classic enough data are accumulated in k-space to recon-
fast or turbo spin echo acquisition, which consists of a 90° struct the slice of interest. Because of the delay after
radiofrequency pulse followed by multiple 180° pulses: the R-wave before data collection, all images will be
• The first 180° pulse is triggered by the R-wave of the acquired in diastole.
ECG, and is spatially non-selective: it inverts all the • The dark signal of blood provides good contrast between
spins in the entire volume. the cardiac walls and cavities, and these techniques are
• It is immediately followed by a slice-selective 180° useful for assessment of cardiac morphology (Fig. 9.1.2).
pulse, causing the stationary spins within the slice to
come back in their original position, while all spins Bright-blood cMRI techniques
outside of the slice being imaged are still inverted and • These techniques use pulse sequences of the gradient
starting to recover their longitudinal magnetization. echo family. Because with these pulse sequences the
• If the 90° pulse of the fast spin echo sequence is rephasing gradient refocuses flowing spins, the signal
applied at a time when the longitudinal magnetization of blood is bright with this method.35 Areas of turbulent
of the blood reaches zero from the initial inversion blood flow are indicated by signal voids (Fig. 9.1.3).2,35,36
(around 600 ms), blood entering the slice will have a • Bright-blood techniques involve the use of very fast gra-
dark signal. dient echo sequences that are triggered by the R-wave
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LA
Ao
LV
RV
Fig. 9.1.3 Long-axis bright-blood image (balanced turbo field

echo) of the heart in a normal Beagle showing the left atrium
(LA), aortic root (Ao), left ventricle (LV), and right ventricle
(RV). The image is obtained during systole and a dark jet of
trivial mitral regurgitation is seen (arrow). (3T MRI system;
image courtesy of Dr. med. vet. Matthias Dennler, Vetsuisse
Fig. 9.1.2 Short-axis transverse view dark-blood image (fast
Faculty, Universität Zürich)
spin echo with double inversion recovery) of the heart at the
level of the left and right ventricles. The dark signal of blood
provides good contrast between the cardiac walls and cavities. executed rapidly, while providing greater contrast-to-
(1.5T MRI system; reproduced, with permission, from Mai W, noise and signal-to-noise ratios. Examples include:36
Weisse C, Sleeper MM (2010). Cardiac magnetic resonance • Fast Imaging Employing STeady-state Acquisition
imaging in normal dogs and two dogs with heart base tumor. (FIESTA).
Vet Radiol Ultrasound 51(4):428–35.) • Balanced Fast Field Echo (bFFE).
• Fast Imaging with Steady-state Precession (FISP).
of the ECG and repeated several times across the R–R • Echo-planar imaging sequences, which are very fast and
interval (as many time-points as the number of cardiac not very sensitive to motion, can also be used for cardiac
phases of interest). The process is repeated across as imaging, often in combination with gradient echo; they
many cardiac cycles as needed to encode enough lines allow functional assessment in cases in which arrhyth-
of k-space for each phase of the cycle being imaged. mias preclude adequate cardiac gating.36
• The images are then reconstructed for each time-point • Bright-blood cMRI techniques are useful to evaluate
and can be played in a loop reproducing cardiac motion flow, including valvular stenosis, regurgitation, and tur-
across the cycle in a fashion similar to echocardiography: bulent blood flow around lesions.35
this display is called ‘cine-mode’ (Figs. 9.1.4, 9.1.5).
• Fast gradient echo (radiofrequency- or gradient-spoiled) cMRI ASSESSMENT OF CARDIAC
pulse sequences that can be used for bright blood cMRI MORPHOLOGY, FUNCTION, AND STRUCTURE
imaging have various names depending on the manufac-
turers, including (see Table 2.3):36 Cardiac mass and ventricular volumes
• Fast SPoiled Gradient Recalled (fSPGR). • With echocardiography, cardiac mass and volume mea-
• Turbo Fast Low Angle SHot (Turbo-FLASH). surements are derived from a limited 2D dataset, with
• Turbo Field Echo (TFE). assumptions of cardiac outline based on geometric mod-
• Fast Field Echo (FFE). els; this can lead to discrepancies in hearts with abnormal
• More complex gradient echo sequences such as balanced anatomy or contraction patterns.
gradient echo, a variation of the steady state free preces- • With cMRI, actual myocardial mass and volume are
sion scheme, are also used. These sequences incorporate obtained with algorithms such as Simpson’s algorithm,
a short repetition time (TR) with gradient refocusing and are based on 3D datasets resulting from the juxtapo-
that is less susceptible to T2* effects compared with stan- sition of series of adjacent and contiguous slices with no
dard spoiled gradient echo pulse sequences. They can be geometric assumption.2
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Fig. 9.1.4 Short-axis images of the ventricles in a normal dog using a cine bright-blood image sequence (gradient echo cine
stack). The same slice is displayed at eight representative phases of the cardiac cycle from early-systole to end-diastole. Images
are chronologically ordered from left to right on each row. The contraction of the myocardium can be dynamically assessed
when this is played as a cine-loop on the viewing station. (1.5T MRI system; reproduced, with permission, from Mai W,
Weisse C, Sleeper MM (2010). Cardiac magnetic resonance imaging in normal dogs and two dogs with heart base tumor.
(a) (b)
Fig. 9.1.5 Long-axis view of the left ventricle and atrium in a normal dog, similar to the echocardiographic ‘right parasternal
long-axis 4-chamber view’, using a cine bright-blood image sequence displaying an end-diastolic (a) and an end-systolic
(b) image. At end-systole, the left atrium is maximally distended while the left ventricular cavity is reduced to a minimum.
(1.5T MRI system; reproduced, with permission, from Mai W, Weisse C, Sleeper MM (2010). Cardiac magnetic resonance
imaging in normal dogs and two dogs with heart base tumor. Vet Radiol Ultrasound 51(4):428–35.)
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• Ventricular volume and mass can be obtained from serial such as contrast-enhanced echocardiography or real-
transverse bright-blood cine-images obtained from the time triplane echocardiography, improves the correla-
apex of the heart to the atrioventricular annulus: tion with cMRI measurements.23
• Epicardial and endocardial borders can be drawn on • There is generally good to very good agreement between
each transverse image at end-systole and end-diastole. contrast-enhanced CT and cMRI for measurements
• End-diastole and end-systole are visually determined of left or right ventricular stroke volume and ejection
by watching the loops and identifying the images fraction.20,33,34
with maximum ventricular dilation (diastole) and
minimum ventricular dilation (systole). Ventricular diastolic
• This allows calculation of myocardial surface area and hemodynamic function
ventricular lumen surface area per slice. • There are very few reports of the cMRI-derived assess-
• These surface areas multiplied by slice thickness yield ment of ventricular diastolic function in veterinary
myocardial volume and ventricular luminal volume medicine.25
per slice. • Left ventricular diastolic function parameters can
• Adding up myocardial volume across all slices yields be obtained from left ventricular volume versus time
total myocardial volume, and multiplying this by curves, which can be calculated from cine-MR images as
myocardial density (~1.05) yields the ‘total ventricular described above, with volumetric measurements repeated
mass’.25–27 at various time-points across the cardiac cycle. The first
• Adding up ventricular volumes yields total left and derivative of that curve (dV/dt) can then be plotted and
right ventricular volumes at end-systole and end-di- used to calculate diastolic function parameters such as
astole.19,20,23,31,33,34 peak diastolic filling rate, mean diastolic filling rate,
• In normal cats, cMRI with measurements in end-systole early diastolic filling rate, and late diastolic filling rate.25
was found to be more accurate in predicting left ventric- • However, tissue Doppler imaging appears to be more
ular mass than standard echocardiography.27 sensitive than cMRI-derived diastolic function param-
• Standard 2D and M-mode echocardiography, whether eters in identifying diastolic dysfunction in cats with
performed on awake or anesthetized dogs, generally yield moderate to severe hypertrophic cardiomyopathy.25
measurements of canine left ventricular volumes that are
significantly different from cMRI.20,23,31 Advanced ultraso- Morphologic assessment and
nographic applications, such as contrast-enhanced echocar- planar measurements
diography23 or 3D echocardiography (‘real-time triplane’), • cMRI with images in similar planes to the standard
have better agreement with cMRI measurements.31 echocardiographic planes can be used to evaluate car-
• For the right ventricular volume, 3D echocardiogra- diac morphology and obtain similar quantitative planar
phy also showed good agreement with cMRI in nor- measurements, such as: interventricular septum thick-
mal Beagles, with a trend for underestimation with 3D ness (systole/diastole), left ventricular internal diameter
echocardiography.34 (systole/diastole), left ventricular posterior wall thick-
• Comparative studies between contrast-enhanced CT ness (systole/diastole), left atrial diameter, mitral annu-
and cMRI generally showed good agreement between lus diameter, aortic annulus diameter, left atrial/aortic
the two techniques for the left and right ventricular vol- diameter ratio, main pulmonary artery diameter, and
umes,20,33,34 with the exception of the end-diastolic left fractional shortening (Figs. 9.1.6, 9.1.7).20
ventricular volume in some studies.33 • Studies comparing these planar measurements between
contrast-enhanced 64-slice multidetector CT, 3T MRI,
Ventricular systolic hemodynamic function and awake standard echocardiography showed good
• Left ventricular stroke volume can be easily calculated agreement between CT and MRI, but significant differ-
from the ventricular volumes described above: (left ences with awake echocardiography.20
ventricular end-diastolic volume – left ventricular end-
systolic volume). Quantitative flow assessment –
• From the stroke volume, the left ventricular ejection phase-contrast imaging
fraction (%) can be calculated as: (left ventricular stroke • Assessment of flow through the mitral, aortic, tricuspid,
volume/left ventricular end-diastolic volume) × 100. and pulmonic valves is routinely performed clinically by
• Right ventricular stroke volume and ejection fraction Doppler echocardiography in dogs and cats.19
can be calculated in a similar fashion. • Some qualitative assessment of flow is obtained with the
• As for volumetric measurements, standard echocardio- cine-cMRI bright-blood techniques described above, as
graphic techniques tend to yield values of left ventricu- turbulent flow typically creates signal void, forming dark
lar stroke volumes or ejection fraction that are different jet-like structures in the cardiac cavities when visualiz-
from cMRI, but use of advanced ultrasound techniques, ing the cine-loops (Fig. 9.1.3).32
694 CHAPTER 9.1
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RV LA
LA
RA
LV LV
LV
RV
(a) (b) (c)
Ao
LA
RA PA Ao
Ao M RA
MP
A
LV
RV
RV RV
(d) (e) (f)

Fig. 9.1.6 Representative bright-blood images of the heart in a normal Beagle showing the cardiac anatomy in various planes
similar to those typically obtained in 2D echocardiography (balanced turbo field echo). (a) Short-axis transventricular plane;
(b) 4-chamber plane; (c) left-sided 2-chamber plane; (d) left ventricular outflow plane; (e) right-sided 2-chamber plane; (f) right
ventricular outflow plane. LV, left ventricle; RV, right ventricle; LA, left atrium; RA, right atrium; Ao, aorta; MPA, main
pulmonary artery. (3T MRI system; images courtesy of Dr. med. vet. Matthias Dennler, Vetsuisse Faculty, Universität Zürich)
• While cine-cMRI with bright-blood allows morpho- • Therefore, ‘phase images’ can be extracted from the
logic and functional imaging of the heart as described measured MR signal. Flow-dependent phase effects
earlier, quantitative flow imaging can also be performed can be used to measure two datasets, each obtained
with cMRI, using ‘flow-sensitive phase-contrast’ pulse during the application of a bipolar velocity-encoding
sequences. gradient, containing two parts of similar amplitude/
• The detailed physics of phase-contrast imaging are duration, but opposite polarity (negative then pos-
beyond the scope of this book, but briefly: itive or vice versa); the velocity-encoding gradients
• MRI signal in general is sensitive to flow and motion, for each of the two datasets have the same direction,
and this can cause artifacts in many applications. but different amplitude.40 They are applied in the
However, this intrinsic sensitivity to motion can be direction where flow is being assessed. Stationary
exploited to image vessels or cardiac chambers and spins submitted to this bipolar gradient will experi-
then quantify blood flow.40 ence no phase shift overall, as the phase shift induced
• As described in Chapter 1, local spin magnetization is by the first half of the gradient will be cancelled
a vector quantity, and therefore the MRI signal con- out by the second part of the gradient; in contrast,
tains information on both magnitude and phase. spins moving along the velocity-encoding gradient
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RV
RV
IVS IVS
LVID
LVID
LVPW LVPW
(a) (b)
LPA
RPA LA
Ao MPA
RV
LV
RV
(c) (d)
Fig. 9.1.7 Representative bright-blood images in a normal Beagle dog (balanced steady state free precession) showing some
examples of planar measurements that can be obtained with cMRI in a similar fashion to those obtained with echocardiography.
(a) Short-axis transventricular plane in diastole; (b) short-axis transventricular plane in systole; (c) short-axis transaortic
plane; (d) 4-chamber plane in diastole. RV, right ventricle; MPA, main pulmonary artery; LPA, left pulmonary artery; RPA,
right pulmonary artery; LA, left atrium; LV, left ventricle; IVS, interventricular septum thickness; LVID, left ventricular
internal diameter; LVPW, left ventricular posterior wall. The double-headed arrows indicate areas of measurement of the
interventricular thickness, left ventricular internal diameter, left ventricular posterior wall thickness (a in diastole; b in systole),
aortic and main pulmonary artery diameters (c), and mitral annulus (d). (3T MRI system; reproduced, with permission, from
Drees R, Johnson RA, Stepien RL et al. (2015). Quantitative planar and volumetric cardiac measurements using 64 MDCT and
3T MRI vs. standard 2D and M-mode echocardiography: does anesthetic protocol matter? Vet Radiol Ultrasound 56(6):638–57.)
will acquire a net phase shift, which depends on velocity-encoding gradients are used, with otherwise
their velocity. Subtraction of the two resulting identical acquisition parameters, the phase shifts
phase images allows the quantitative assessment induced by the actual imaging gradients (slice selec-
of the phase-shifts, and hence the velocities of the tion, phase and frequency encoding) are eliminated
underlying flow. Because two datasets with different in the subtracted image.
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• These bipolar gradients can be applied successively from the phase difference images. To calculate flow,
along the three anatomic axes x, y, and z to provide cross-sectional images of the vessel of interest must be
flow-sensitivity along these directions, and can obtained so the surface area of the cross section of the
also be combined along different axes simultane- vessel can be determined. The product of the area and
ously, which allows flow measurements in oblique the average velocity over the vessel yields the volume
directions. flow rate (Fig. 9.1.8).19,32
• In phase-contrast imaging, the signal is linearly pro- • Phase contrast methods are sensitive to a ‘range of
portional to the velocity of the spin: faster moving velocities’, which is determined by a user-defined
spins give rise to a larger signal. Spin motion can be ‘velocity-encoding value’ (V ENC) prior to acquisition
encoded using gray-scale or color-scale, with colors (this depends on the amplitude, duration, and spacing
depending on the direction of motion and hue depend- of the bipolar gradients). Blood velocities higher than
ing on velocity. This allows the vascular anatomy to that value will be misrepresented in the image (this is
be assessed, and the speed and direction of blood conceptually similar to ‘aliasing’ in Doppler echocar-
flow to be qualitatively determined. Flow data can diography). Consequently, the user must choose this
be obtained in 1D, 2D, or 3D modes; 4D (3D + time) value carefully depending on the anticipated range of
display is also possible (Figs. 9.1.8, 9.1.9). velocities in the specific target vessel. Different veloc-
• In addition, quantitative information regarding the ity encoding values can be used in different scans to
velocity and volume flow rate of blood can be derived highlight different vessels.
(a) FLOW (b) PHASE (c) SUBTRACTION
Fig. 9.1.8 Quantitative flow at the level of the aortic root using phase-contrast angiography with synchronization to the heart
cycle. (a) Flow image for anatomic detail; (b) phase image – the pixels do not represent signal strength but the phase of the
signal and correlate with flow velocity; (c) subtraction image – compensates for phase differences unrelated to flow. The red
circle in (c) represents a region of interest (ROI) where quantification of flow is measured. The graph shows the flow (y-axis,
mL/s) through the ROI over an entire cardiac cycle (x-axis) Since the ROI is placed at the aortic root, this represents the aortic
stroke volume. (3T MRI system; images courtesy of Dr. med. vet. Matthias Dennler, Vetsuisse Faculty, Universität Zürich)
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Compared with conventional imaging techniques that

measure global functional indices such as fractional
shortening, ejection fraction, or stroke volume, MR tag-
ging has the advantage of comprehensive evaluation of
regional myocardial function, as well as the delineation
of complex wall motion mechanics.5
• Examples of measurements obtained with this technique
include circumferential strain, radial strain, peak strain
timing, myocardial twist, and torsion.5
• These functional parameters can be color-coded and
mapped onto the actual cine-loop to obtain a visual
dynamic assessment of spatial and temporal variations of
these parameters across the myocardium in the slice of
interest (Fig. 9.1.11).
• Although the technique has not been reported in clinical
applications in veterinary medicine to date, it has been
employed in canine models of human diseases such as
Duchenne muscular dystrophy.10 As in people, there is
potential for this tool to be also used in clinical applica-
tions in dogs and cats, such as in the functional evalua-
tion of cardiomyopathies.2
Myocardial structure
• MRI has the unique capability to provide information
on tissue structure based essentially on the density of
protons and their physicochemical environment. This
exquisite sensitivity to changes in tissue structure pro-
Fig. 9.1.9 Multidimensional phase contrast angiography
vides the outstanding soft tissue contrast of MRI.
(volume scan over time). The principle is the same as in
• This can be used in cardiac imaging to identify fine
2D quantitative flow (Fig. 9.1.8) but the measurements are
structural changes of the myocardium, which would
repeated for the entire volume in three directions. Flow
remain invisible using more conventional techniques
velocities in the vessels are coded with colors, with colors
such as echocardiography.
indicating the direction of flow and hue (intensity of the color)
• In people, a common cause of such structural changes is
indicating the velocity. (3T MRI system; image courtesy
myocardial infarction, but this condition is not a com-
of Dr. med. vet. Matthias Dennler, Vetsuisse Faculty,
mon disease in dogs and cats. Other structural changes
Universität Zürich)
that can be seen in dogs and cats are those associated
with cardiomyopathy, where there is myocardial fibrosis
Regional myocardial function – with myocyte loss and collagen replacement producing
strain imaging (MR tagging) an expansion of the extracellular space; this expansion
• Cardiac ‘tagging’ involves labeling the myocardium of the extracellular space in fibrotic myocardium causes
using special saturation pulses that are spatially distrib- pooling of MRI contrast agents such as gadolinium after
uted in the plane of imaging, resulting in parallel low- intravenous injection, with a slow washout compared
signal stripes across the cardiac slice (SPAtial Modulation with healthy myocardium.
of Magnetization, SPAMM).5 • Obtaining post-contrast cMRI images 10–15 min-
• A rectangular grid pattern (two sets of perpendicular utes after gadolinium injection, a technique known as
series of stripes) is typically used on transverse (short- ‘delayed contrast-enhanced MRI’, has the potential to
axis) images of the heart, while a simple set of parallel reveal areas of replacement fibrosis by showing accumu-
stripes is often preferred for long-axis images. lation of gadolinium, forming hyperintense myocardial
• These saturation bands deform across the cardiac cycle regions compared with normal myocardium, in which
with myocardial contraction and expansion, and this washout of gadolinium has occurred by the time of
deformation can be visually assessed in cine-mode acquisition (Fig. 9.1.12).28 However, this technique is less
(Fig. 9.1.10) and subsequently quantified using dedicated sensitive to diffuse interstitial fibrosis, where there is no
software yielding detailed regional analysis of myocar- focal expansion of the interstitial space to allow accumu-
dial contractility and functional parameters (Fig. 9.1.11). lation and retention of gadolinium. Typically, delayed
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(a) (b) (c)
(d) (e) (f)
(g) (h) (i)
(j) (k) (l)

Fig. 9.1.10 cMRI images at the level of the ventricles using spatial modulation of magnetization (SPAMM), or ‘MRI tagging’.
Representative images of a single slice at 12 time-points across a cardiac cycle are displayed, showing the deformation of
the grid induced by saturation bands as the myocardium contracts and expands. This can subsequently be quantified using
dedicated software yielding detailed regional analysis of myocardial contractility and functional parameters (see Fig. 9.1.11).
(1.5T MRI system)
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5%
2 Fig. 9.1.11 Example of a quantitative

6
color display and associated regional
measurement of one of the myocardial
5 3 function parameters that can be
derived from quantitative analysis
4
of SPAMM images such as those in
Fig. 9.1.10. The peak circumferential
–25% strain is displayed; it is color coded
and overlaid onto the actual gray-scale
SPAMM image. This can be played as
1 2 3 4 5 6 Average a cine-loop for subjective assessment
0
or can be quantified at the regional
circumferential strain
level, after defining regions of interest

Average peak
(radial segments 1 through 6 in this

case), to obtain measures of function in
–10
specific areas of the myocardium. This
can be reassessed over time to measure
progression of myocardial disease
–20 or the effects of therapeutic
interventions. (1.5T MRI system)
RV
LV
(a) (b)
Fig. 9.1.12 Delayed contrast enhancement (pre-contrast in a, and 13 min after gadolinium injection in b) cMRI to assess
myocardial fibrosis in a dog model of Duchenne muscular dystrophy. This approach uses a cardiac-gated, inversion recovery-
prepared T1W fast gradient echo sequence during apnea. The inversion recovery scheme allows nulling of signal from normal
myocardium. In (b), patchy areas of contrast retention are noted within the myocardium of the left ventricle and interventricular
septum consistent with delayed gadolinium wash-out in areas of replacement fibrosis. LV, cavity of the left ventricle; RV, cavity of
the right ventricle. (1.5T MRI system)
700 CHAPTER 9.1
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contrast-enhancement techniques involve the use of a • Acquisition can be made faster by use of specific
cardiac-gated, inversion recovery-prepared T1W fast k-space encoding strategies that focus on the contrast
gradient echo sequence during apnea. Several succes- information in the center of k-space, such as elliptic
sive episodes of apnea may be required to obtain all centric view ordering of k-space.
the transverse ventricular slices from apex to base in • Parallel acquisition (e.g., on General Electric
2–3 stages, depending on acquisition duration and size machines: Array Spatial Sensitivity Encoding
of the heart. The inversion-recovery scheme is not man- Technique, ASSET), where each separate element of
datory, and some veterinary studies have not used it;28 its the coil acquires a specific portion of the field of view,
goal is to pick an inversion time that nulls the signal of can also help reduce acquisition times.
normal myocardium (typically 175–250 ms) so that there • A pre-contrast mask is acquired with the same param-
is improved contrast between the normal (washed-out) eters as the actual MRA sequence.
myocardium and the fibrotic (gadolinium-enhanced) • Several (three to four) consecutive 3D volumes are
myocardium. This inversion time may need to be opti- acquired starting immediately after the intravenous
mized for each patient prior to actual image acquisition injection of 0.3 mmol/kg gadolinium followed by
by obtaining single slice, low-resolution breath-hold a saline flush (manual or using a power injector).
images at different inversion times, and inspecting them This method requires no timing of arrival of con-
visually to determine the best time to null the myocar- trast material, as one of the consecutive 3D volumes
dial signal.41 will have maximum contrast enhancement of the
• Another possible structural change of the myocardium vascular structures of interest and will be used for
is fatty replacement, which can occur in some forms analysis.
of canine cardiomyopathies such as the arrhythmo- • The 3D volume with overall best vascular enhance-
genic right ventricular cardiomyopathy of Boxers. Fatty ment is identified, and the mask is subtracted from
replacement can be demonstrated on T1W images as this series before reconstruction.
hyperintense myocardial regions, and proven by using • Images are then examined using maximum intensity
fat-suppressed techniques where the fat signal is elimi- projections in various planes (Fig. 9.1.13).
nated.9,15 Dark-blood imaging, using multislice, short-
axis double inversion recovery fast spin echo sequences
with and without fat saturation can be used for that
purpose.15
Contrast-enhanced magnetic PV
resonance angiography
• Specific vascular imaging encompassing the heart and
thoracic vessels can be obtained using contrast-enhanced
MRA.18,29,42,43 This provides fast, large field of view
BCT
assessment of the cardiovascular structures independent Ao
of the direction of blood flow.
• The 3D nature of the data allows post-processing of the
images off-line and reformatting of maximum intensity LA
Ao
projections or angiographic-like images in any arbitrary
plane; this permits evaluation of anomalous vessels and
understanding of their spatial relationships with neigh- LV
boring vascular or non-vascular structures, similar to LSA
CT angiography.
• Such images can be complementary to the standard non-
contrast enhanced bright-blood and dark-blood cMRI
series described above. Images are acquired in apnea, but
do not require cardiac gating as only the vascular first Fig. 9.1.13 3D contrast-enhanced MR angiography (spoiled
pass of contrast material is registered. gradient echo sequence) in a normal Beagle. Left view of a 3D
• The technique used is similar to abdominal MRA volume after gadolinium injection. Cardiovascular structures
techniques: are clearly visible with this technique. BCT, brachiocephalic
• A 3D volume is prescribed in the dorsal plane and trunk; LSA, left subclavian artery; Ao, aorta; LA, left atrium;
positioned to cover the entire thorax. LV, left ventricle; PV, pulmonary veins. (3T MRI system;
• 3D FSPGR or 3D FLASH pulse sequences can be image courtesy of Dr. med. vet. Matthias Dennler, Vetsuisse
used.18,29,42,43 Faculty, Universität Zürich)
VetBooks.ir
CLINICAL APPLICATIONS IN • Ex-vivo MRI studies of affected Boxer dogs using

VETERINARY MEDICINE T1W images showed hyperintense myocardial lesions
in the right ventricle that matched areas of fatty
Cardiomyopathy replacement on histopathology.9
• cMRI has been evaluated in cats with hypertrophic • In-vivo cMRI studies have also been performed in
cardiomyopathy:25–28 affected and non-affected Boxer dogs, measuring
• cMRI using bright-blood cine-imaging was shown right ventricular systolic and diastolic volumes as well
to be more accurate than standard echocardiography as ejection fraction using bright-blood cine-cMRI.
in quantifying left ventricular mass in normal cats, Visual assessment of the cine images was performed
paving the way to using this tool to monitor progres- to detect presence of right ventricular aneurysms
sion of disease in cats with hypertrophic cardiomyo- and gross wall motion abnormalities. Dark-blood
pathy, and also to assess left ventricular variables in imaging using inversion recovery fast spin echo pulse
response to various therapeutic interventions.27 sequences with and without fat saturation was per-
• Delayed contrast-enhancement cMRI was also eval- formed to detect areas of fatty replacement in the
uated in Maine Coon cats with moderate to severe myocardium.15 In this study, right ventricular ejection
hypertrophic cardiomyopathy but no heart failure.28 fraction was reduced in affected Boxer dogs, and right
Although overall there was no statistically detecta- ventricular aneurysms were identified. However, no
ble difference in myocardial contrast enhancement area of fatty replacement was noted, possibly due to
between cats with cardiomyopathy and normal a less advanced stage of the disease or due to a more
cats, one affected cat had a visually appreciable area of diffuse, microscopic form of fatty infiltration that
delayed myocardial enhancement. may not be detected by the cMRI technique.15
• Diastolic ventricular function in Maine Coon cats
with moderate to severe hypertrophic cardiomyo- Cardiac tumors
pathy was also evaluated using cMRI.25 The study • In people, cMRI is considered the gold standard for the
showed that cMRI was less sensitive than tissue comprehensive imaging of pericardial disease and cardiac
Doppler imaging in detecting early left ventricular masses, as it provides superior tissue characterization rel-
diastolic dysfunction in these cats. ative to CT and all modalities of echocardiography. Also,
• The effect of the angiotensin-converting enzyme unlike echocardiography, it allows imaging in any plane
inhibitor ramipril on left ventricular mass (measured without limitations related to body condition.16
with bright-blood cine-cMRI) and myocardial fibrosis • cMRI has been evaluated in a few studies in dogs with
(measured by delayed contrast-enhancement cMRI) cardiac or pericardial neoplasia.16,22,29
was also studied in Maine Coon cats and Maine Coon • In a small case series, retrospective evaluation of cMRI
crossbred cats with moderate to severe hypertrophic studies in dogs with pericardial effusion confirmed the
cardiomyopathy but without heart failure. No effect presence of a neoplastic mass in cases where transtho-
of this treatment was noted compared with placebo, racic echocardiography was equivocal. It also improved
suggesting that early treatment with ramipril may not confidence regarding the nature of the tumor based on
be indicated in asymptomatic cats with hypertrophic cMRI signal characteristics:16
cardiomyopathy.26 • Confirmed or suspected hemangiosarcoma had high
• cMRI has also been evaluated in some forms of canine heterogeneous signal on both dark-blood and bright-
cardiomyopathy, such as the arrhythmogenic right ven- blood cMRI images compared with normal myocar-
tricular cardiomyopathy seen in Boxer dogs:9,15 dium, and most lesions were located close to the right
• In that condition, there is severe right ventricular atrioventricular groove (Figs. 9.1.14, 9.1.15).16
myocyte loss with replacement by fatty or fibrofatty • A suspected paraganglioma was located around the
tissue; similar but less pronounced focal changes aorta and had high signal intensity on dark-blood
may also be present in the atria and left ventricle.9 series, with strong enhancement after gadolinium
These changes lead to right ventricular dysfunction injection and a central non-enhancing area suggestive
and arrhythmias, as well as formation of focal right of necrosis.16
ventricular aneurysms (focal defects of the ventricu- • In another report of right atrial tumors and ascites in
lar wall creating outpouchings of the ventricular two dogs, bright-blood cine-cMRI, black-blood cMRI,
lumen).15 and 3D contrast-enhanced MRA provided a comprehen-
• Structural and functional disorders therefore pri- sive understanding of the extent of the mass lesions use-
marily affect the right ventricle in this condition, the ful for planning of interventional radiology procedures
assessment of which is challenging using conventional (caval stenting); 3D MRA and bright-blood cine-imaging
echocardiography due to its complex anatomic con- also allowed confirmation of presence of residual flow
formation. through the partially obstructed caudal vena cava as well
702 CHAPTER 9.1
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Ao
MP
LEFT
MPA
M
A
Ao
LEFT
M
LV
(a) DORSAL (b) CAUDAL
Fig. 9.1.14 Suspected hemangiosarcoma in the right atrioventricular groove in a dog: black-blood sequence images (short-axis
transaortic in a; long-axis transaortic in b). A hyperintense heterogeneous mass (M) is seen in the right atrioventricular groove.
A small amount of pericardial effusion is present (arrowhead, a). Ao, aorta; MPA, main pulmonary artery; LV, left ventricle.
(1.5T MRI system; reproduced, with permission, from Boddy KN, Sleeper MM, Sammarco CD et al. (2011). Cardiac magnetic
resonance in the differentiation of neoplastic and nonneoplastic pericardial effusion. J Vet Intern Med 25(5):1003–9.)
RA
Ao
M
(a) (b)
Fig. 9.1.15 Right atrial hemangiosarcoma in a

dog. Short-axis transaortic bright-blood pre-
contrast (a), post-contrast (b), and dark-blood M
parasagittal (c) images. A mass (M) is visible
in the right atrium, which has strong patchy
enhancement after gadolinium injection
(arrow, b). Ao, aorta; RA, right atrium.
(c)
(1.5T MRI system)
VetBooks.ir
PA
RA
Ao
MASS
LA
(a) (b)
L&R
Pulm Art
(c) (d)
Fig. 9.1.16 Four representative dorsal plane images across the heart in a dog using a black-blood cMRI technique. A right atrial
mass (MASS) is visible as a structure isointense to the myocardium, obliterating the lumen of the right atrium and pushing the
atrial septum to the left. RA, right atrium; PA, main pulmonary artery; Ao, aorta; LA, left atrium; L & R Pulm Art, left and
right pulmonary arteries. (1.5T MRI system; reproduced, with permission, from Mai W, Weisse C, Sleeper MM (2010). Cardiac
magnetic resonance imaging in normal dogs and two dogs with heart base tumor. Vet Radiol Ultrasound 51(4):428–35.)
as established alternate venous return through the azy- added advantage of cMRI-guided catheterization and
gos vein (Figs. 9.1.16–9.1.19).29 interventions.44
• In a dog with a pericardial mesothelioma, cMRI showed • Conversely, diagnosis of congenital cardiac disease in
diffuse pericardial thickening and enhancement and also dogs and cats is still made, in the vast majority of cases, by
ruled out a small peri-aortic mass that had been sus- use of echocardiography and/or cardiac catheterization.
pected on echocardiography (Fig. 9.1.20).22 • There are only a handful of individual case reports
describing the use of cMRI in the evaluation of congeni-
Congenital anomalies tal cardiac diseases in veterinary patients:21,24,30,43
• cMRI is now an attractive imaging tool in human pedi- • 3D contrast-enhanced MRA was used in a dog to
atric congenital heart disease as it is non-invasive and diagnose a persistent ductus arteriosus and measure
lacks ionizing radiation. The technological advance- the ductus diameter.43
ments, with improved image resolution and ultra- • T1W black-blood fast spin echo and bright-blood cine
short imaging time, allow real-time imaging with the gradient echo series were used to evaluate a dog with
704 CHAPTER 9.1
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Azygos
Vert v.
CrVC
MASS
CrVC
PA
CdVC
(a)
MASS
Fig. 9.1.17 Sub-volume maximum intensity projections of
contrast-enhanced magnetic resonance angiography in the
same dog as in Fig. 9.1.16. Long-axis oblique view of the
heart (a) and dorsal oblique view of the base of the heart (b).
In (a), note the space occupying mass (MASS) in the caudal
chamber of the right atrium, the reduced flow in the caudal
vena cava (CdVC), and the alternate venous return established
through the vertebral veins (Vert v.) and the dilated azygos (b)
vein (Azygos). The cranial vena cava (CrVC) is enlarged as
a result of the alternate venous return. In (b), note the space-occupying mass (MASS) in the main body (sinus venarium) of
the right atrium and the mass effect on the atrial septum (long arrow). The cranial vena cava (CrVC) is seen and to its left the
main pulmonary artery (PA) with branching caudal lobar pulmonary arteries. The pulmonary veins entering the left atrium
are indicated by the short arrows. (1.5T MRI system; reproduced, with permission, from Mai W, Weisse C, Sleeper MM (2010).
Cardiac magnetic resonance imaging in normal dogs and two dogs with heart base tumor. Vet Radiol Ultrasound 51(4):428–35.)
cor triatriatum dexter that had previously undergone Mitral insufficiency

balloon valvuloplasty. cMRI allowed identification of • Mitral regurgitation associated with myxomatous mitral
the abnormal membrane, the membranostomy orifice valve disease is highly prevalent, especially in older
(Fig. 9.1.21), thickening of the pulmonic valves, a small-breed dogs, and is the third most common cause of
dilated coronary sinus, and the dilated azygos vein death in canine patients.32
emptying into the cranial vena cava.24 • Therefore, there has been historical interest in under-
• In a dog with a rare complex congenital anomaly com- standing the pathophysiology of this progressive condi-
bining several defects, bright-blood cMRI was used to tion using non-invasive ways to follow-up changes over
image the interatrial defect and measure the size of the time and evaluate treatment efficacy. Various modalities
communication. Hypointense signal corresponding to of cMRI have been used in numerous studies investigat-
flow from the left to right atrium through the atrial ing experimentally induced mitral insufficiency in dogs,
defect was identified.21 Measurement of the size of the and these have been thoroughly reviewed recently.45 The
defect was closer to actual dimension when measured advanced post-processing techniques and analyses used
with cMRI compared with echocardiography. in these studies are beyond the scope of this textbook.
• Advanced cMRI using 4D velocity mapping • cMRI has also been evaluated in canine patients with
(phase-contrast vastly undersampled isotropic pro- spontaneous mitral regurgitation.32
jection reconstruction [PC VIPR]) was used in a dog • Mitral regurgitant volume with cMRI can be calculated
with a rare anomalous vessel between the ascending in a few steps:32
aorta and main pulmonary artery that was originally • Left ventricular stroke volume is calculated after
thought to represent a patent ductus arteriosus.30 determining the left ventricular end-systolic and
This technique allowed a more precise assessment of end-diastolic volumes from short-axis cine bright-
hemodynamics associated with this anomalous vessel blood images as described above.
and concurrent anomalies in preparation for surgical • Long-axis images of the left ventricular outflow tract
treatment.30 are obtained in a plane perpendicular to the short-axis
VetBooks.ir
Ao
M
CV
C
(a) (b)
(c) (d)
Fig. 9.1.18 Representative images of a short-axis transaortic bright-blood series in a dog with right atrial neoplasia. Four
images of the same slice at different time points of the cardiac cycle are displayed. The large intra-atrial mass is seen (M) as
well as the caudal vena cava (CVC) and the aorta (Ao) in cross section. The mass invades the atrial septum and extends into
the left atrial lumen (arrow, d). (1.5T MRI system; reproduced, with permission, from Mai W, Weisse C, Sleeper MM (2010).
Cardiac magnetic resonance imaging in normal dogs and two dogs with heart base tumor. Vet Radiol Ultrasound 51(4):428–35.)
706 CHAPTER 9.1
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C
CrV
Ao
CV
C
(a) (b)
Ao
(c) (d)
Fig. 9.1.19 Contrast-enhanced magnetic resonance angiography in the same dog as in Fig. 9.1.18. Dorsal oblique views of the
base of the heart using sub-volume maximum intensity projections. Four representative contiguous projections are shown.
Note the caudal vena cava (CVC), the atrial mass (M), the aorta (Ao), and the cranial vena cava (CrVC); a cranial mediastinal
mass (M in b) was also identified. The liver lobes are separated by hypointense fluid (ascites). The mass invades the left atrium
through the atrial septum (arrow, a). (1.5T MRI system; reproduced, with permission, from Mai W, Weisse C, Sleeper MM
(2010). Cardiac magnetic resonance imaging in normal dogs and two dogs with heart base tumor. Vet Radiol Ultrasound
51(4):428–35.)
VetBooks.ir
RV
LV *
*
(a) (b)
CrVC
Ao
RVOT
RA
LA
LV
CdVC
(c) (d)
Fig. 9.1.20 Short-axis transventricular black-blood (a) and bright-blood (b) images and dorsal reformatted images of a 3D
contrast-enhanced MRA at the level of the base of the heart (c and d) in a dog with pericardial effusion due to a mesothelioma.
On transthoracic echocardiography, a heart base mass had been suspected. Thickening of the pericardium is noted (dotted
arrows, a) and a small amount of hypointense pericardial effusion is present (solid arrow, a). There is a crescent-shaped area
of intermediate signal intensity in the pericardial sac (asterisks, a and b), which was non-enhancing after gadolinium injection
(not shown) and corresponded to blood clots and fibrin. The dorsal 3D MRA images (c and d) do not show any evidence of a
heart base mass. RV, right ventricle; LV, left ventricle; RA, right atrium; CrVC, cranial vena cava; CdVC, caudal vena cava;
LA, left atrium; Ao, aorta; RVOT, right ventricular outflow tract. (1.5T MRI system)
images (similar to Fig. 9.1.3); these images are used to contouring on these images allows measurement of
determine the plane for flow measurement in the aortic the aortic surface area, and the aortic stroke volume
root, aligned parallel to the aortic valve plane (i.e., per- is determined from the aortic flow per heart beat and
pendicular to the blood flow in the outflow tract). the surface area (Fig. 9.1.8).
• Phase-contrast flow measurement is performed in the • Mitral regurgitant volume can then be calculated by
aortic root to obtain velocity-encoded maps and quan- subtracting the aortic stroke volume from the left
titative measurements of aortic blood flow. Active ventricular stroke volume.
708 CHAPTER 9.1
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PV
RVOT RVOT PV
MO
CrRA
* Ao
CrRA Ao
CrRA
MV
CdRA LA LA
CdRA CdRA
CS CS
(a) CdVC (b) CdVC (c)
Fig. 9.1.21 Short-axis dark-blood (T1W turbo spin echo) cMRI images of the heart at the level of the heart base in a Golden
Retriever with an imperforate cor triatriatum dexter and concurrent double-chambered right ventricle. The imperforate
membrane dividing the right atrium was previously opened using balloon dilation, which resolved the signs of right-sided
congestive heart failure. This cMRI was performed 1 year later. In (a), the dilated great coronary vein running around the left
atrioventricular groove (asterisk, a; arrows, a–c), continued by the coronary sinus (CS), opens into the caudal chamber of the
right atrium (CdRA) next to the caudal vena cava (CdVC). The membrane (arrowheads) within the right ventricle outflow tract
(RVOT) corresponds with the double-chambered right ventricle lesion; MV, mitral valve. In (b), the thickened pulmonary
valve (PV) with a domed appearance is visible. In (c), the membranostomy orifice (MO) is present across the membrane
dividing the right atrium into cranial (CrRA) and caudal (CdRA) right atrial chambers; Ao, aorta, LA, left atrium. (1T MRI
system; reproduced, with permission, from Lopez-Alvarez J, Dukes-McEwan J, Martin MW et al. (2011). Balloon dilation of
an imperforate cor triatriatum dexter in a Golden Retriever with concurrent double-chambered right ventricle and subsequent
evaluation by cardiac magnetic resonance imaging. J Vet Cardiol 13(3):211–8.)
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16. Boddy KN, Sleeper MM, Sammarco CD et al. (2011). 29. Mai W, Weisse C, Sleeper MM (2010). Cardiac magnetic
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neoplastic and nonneoplastic pericardial effusion. J Vet Intern base tumor. Vet Radiol Ultrasound 51(4):428–35.
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25. MacDonald KA, Kittleson MD, Garcia-Nolen T et al. (2006). measurement with phase-contrast MR imaging: basic facts and
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effect of ramipril on left ventricular mass, myocardial fibrosis, 42. Contreras S, Vazquez JM, Morales M et al. (2011). Three-
diastolic function, and plasma neurohormones in Maine Coon dimensional MRA study of the normal canine thorax: MIP
cats with familial hypertrophic cardiomyopathy without heart sections and volume rendering. Anat Histol Embryol 40(1):40–6.
failure. J Vet Intern Med 20(5):1093–105. 43. Louvet A, Duconseille AC, Lazard P (2010). Contrast-
27. MacDonald KA, Kittleson MD, Reed T et al. (2005). enhanced magnetic resonance angiography of patent ductus
Quantification of left ventricular mass using cardiac magnetic arteriosus in a dog. J Small Anim Pract 51(8):451–3.
resonance imaging compared with echocardiography in 44. Ntsinjana HN, Hughes ML, Taylor AM (2011). The role of
domestic cats. Vet Radiol Ultrasound 46(3):192–9. cardiovascular magnetic resonance in pediatric congenital
28. MacDonald KA, Wisner ER, Larson RF et al. (2005). heart disease. J Cardiovasc Magn Reson 13:51.
Comparison of myocardial contrast enhancement via cardiac 45. Dillon AR, Dell’Italia LJ, Tillson M et al. (2012). Left
magnetic resonance imaging in healthy cats and cats with ventricular remodeling in preclinical experimental mitral
hypertrophic cardiomyopathy. Am J Vet Res 66(11):1891–4. regurgitation of dogs. J Vet Cardiol 14(1):73–92.
CHAPTER 9.2
MRI OF NON-CARDIAC THORACIC CONDITIONS

710 Ruth Dennis
CONTENTS
Technical considerations ....................................................................................................................................................................................... 710
Choice of radiofrequency coil .......................................................................................................................................................................... 710
Pulse sequence parameters ............................................................................................................................................................................. 711
Patient positioning........................................................................................................................................................................................... 711
Reducing the effects of motion artifacts ........................................................................................................................................................... 711
Clinical application of MRI for selective non-cardiac thoracic conditions ............................................................................................................. 714
Thoracic wall ................................................................................................................................................................................................... 714
Mediastinum.................................................................................................................................................................................................... 717
Lungs ..............................................................................................................................................................................................................720
Other areas ......................................................................................................................................................................................................720
References.............................................................................................................................................................................................................722
In people, thoracic MRI has long been an established tech- the pulmonary air is effaced by pathology such as consolida-
nique in the diagnosis of thoracic disease and is considered tion, neoplasia, or other air-space disease, the susceptibility
complementary to other imaging techniques.1,2 Currently in effects are reduced and the abnormal tissue becomes visible.
veterinary medicine, CT is still the imaging technique of
choice for advanced cross-sectional imaging of the thorax. TECHNICAL CONSIDERATIONS
Despite the potential value of MRI for investigating non-
cardiac thoracic diseases in small animals, and the publi- Factors to consider include the choice of radiofrequency
cation of several papers considering normal anatomy,3–7 (RF) coil, pulse sequence parameters, patient positioning,
there is a dearth of literature available relating to MRI of and, importantly, ways to minimize the adverse effects of
thoracic disease processes. As a result, there is currently a movement artifact. For thoracic wall lesions a useful prac-
lack of evidence base to inform any decision whether to use tice, as with other areas of the body, is to tape one or more oil
MRI or CT in specific circumstances. Prospective stud- capsules to any area of visible swelling, scar, or sinus opening
ies comparing the two modalities in individual patients are to demonstrate its location on the images. However, these
therefore warranted. The clinical use of MRI for the inves- become less visible or disappear altogether if fat suppression
tigation of thoracic disease in small animals depends on the techniques are used (Fig. 9.2.1).
area under investigation. Cardiac MRI using ECG gating
is now a well-established tool in people and is discussed in Choice of radiofrequency coil
Chapter 9.1. The main limitation for thoracic MR images is • This largely depends on the size of the patient and the
image degradation due to respiratory and cardiac motion, type of scanner in use. For larger dogs being scanned
but nevertheless useful information can be obtained about in a human medical system, a body or thorax coil may
the thoracic wall, pleural space, and mediastinum. It must be required, whereas smaller patients may be imaged in
be remembered that images do not have to be perfect to head or extremity coils.
be diagnostic, and even when artifacts are present they • Dedicated veterinary systems come with a different
may yield useful information. MRI is of inferior value for range of RF coils but these are unlikely to be optimized
imaging the lungs compared with CT, not only because of for the thorax. If only one area of the thorax, such as a
respiratory motion but also magnetic susceptibility effects specific region of the thoracic wall, is under investiga-
caused by air in the lungs, which create a magnetic field tion, a surface coil may be used adjacent to that area, and
gradient at every alveolar wall interface.1,2 However, where this will result in less motion artifact since the area of
M R I of Non- C a r di ac Thor ac ic C on di t ions 711
Fig. 9.2.2 American Cocker Spaniel lying in lateral

recumbency on a spinal coil (a phased-array surface coil) for
MRI of a superficial mass on the dependent thoracic wall.
Placing the side of interest adjacent to the coil both reduces
motion artifact due to respiration and increases the signal-to-
Fig. 9.2.1 Dorsal plane T2W image showing an oil capsule
noise ratio. A restraint band as shown may also help to reduce
(arrow, EfavetTM ) taped over the scar from an incompletely
motion artifact.
removed rhabdomyosarcoma on the lateral aspect of the
thorax in a Cocker Spaniel. (1.5T MRI system)
• Other sequences, some of which require special soft-
interest will abut the coil and will therefore move less ware, may be used for cardiac MR angiography and are
(Fig. 9.2.2). described in Chapter 9.1.
• Generally, motion artifacts seem to be less of a problem • In whole body protocols reported in the literature,8 the
with surface coils than with birdcage coils since artifact STIR sequence was found to be best for lesion conspicu-
originating in tissue more distant from the coil will be ity and for detection of lymph nodes outside the thorax,
attenuated. as they were hyperintense against a dark, fat-suppressed
background. However, severe artifacts in the thorax
Pulse sequence parameters associated with cardiac motion prevented assessment
• There are no rigid protocols for thoracic studies since of all thoracic lymph nodes.8 STIR images inherently
each case is unique and the sequences used must be tai- have a relatively low signal-to-noise ratio (SNR) and a
lored to the patient and the lesion. dark, grainy appearance. However, in people, STIR
• A sufficiently large field of view (FOV) must be selected is recommended for thoracic and abdominal MRI as it
to include the entire area of interest without phase-wrap reduces the signal intensity from subcutaneous fat in the
artifact. Slice thickness depends on the size of both the anterior body wall.9
patient and any lesion, but will often be in the order of
5–7 mm. Patient positioning
• The use of relatively thick slices permits coverage of • For thoracic wall lesions, positioning the patient with
the large thoracic area with a reasonable number of the area of interest dependent and the patient lying on
image slices and an acceptable scan time. Smaller lung a surface coil provides the double benefit of reducing
lesions may not be visible, but for primary investiga- motion of the area of interest and giving excellent SNR
tion of lung disease, MRI would not be the technique (Fig. 9.2.2).
of choice. • Although SNR falls off rapidly with distance from the
• Reports of thoracic MRI in anatomic studies of normal surface coil, this is not an issue for superficial disease
dogs describe the use of various pulse sequences, processes (Fig. 9.2.3).
including pre- and post-contrast T1W, T2W, PDW,
STIR, single shot fast spin echo (FSE) and gradient Reducing the effects of motion artifacts
echo.4,5,7,8 • Minimizing the deleterious effect of motion (voluntary,
• Subtraction images (between the post- and pre-contrast respiratory, and cardiac) remains the most significant
T1W series) are also recommended, especially where hurdle in the production of diagnostic thoracic MR
lesions are close to or surrounded by hyperintense fat. images in veterinary patients, especially as techniques
712 CHAPTER 9.2
flow, respiration or cardiac motion9). The intensity of the

ghosting increases with increased amplitude of motion
or increased signal intensity of the moving structure.
Conversely, non-periodic, random motion such as peri-
stalsis produces more diffuse image noise propagated
widely in the phase-encoding direction. Motion arti-
fact due to vessel pulsatility and cardiac motion is much
worse on T1W images following the administration of
contrast medium due to increased signal intensity in the
flowing blood.
• The following maneuvers may be helpful to decrease
motion artifacts:
• Selection of the most appropriate RF coil (see above).
• Mechanical reduction of the amplitude of motion (e.g.,
positioning of the patient to reduce respiratory move-
ment in the area of interest), usually by placing that
area dependently so that the weight of the overlying
body holds the area relatively still (caveat: positioning
must not compromise patient welfare if significant
intrathoracic pathology that might affect lung aera-
Left side - RF coil tion is present). Other methods to restrict movement,
such as the use of a firmly placed restraint band, may
Fig. 9.2.3 Transverse T2W image of the thorax in an English
be considered, provided that they do not interfere
Springer Spaniel with a ventral thoracic wall swelling. The
with the patient’s respiration (Fig. 9.2.2).
dog was in left lateral recumbency on a surface spinal coil
• Choice of image planes least affected by motion,
with the side of interest dependent. There is rapid drop-off of
although it is still recommended to use all three planes
signal with increasing distance from the coil but the area of
for at least one pulse sequence.
interest is clearly seen. The lesion was caused by a kebab stick
• Increasing the number of signal averages (NSA), also
(see also Fig. 9.2.10). The image is oriented to show the dog’s
known as number of excitations (NEX), to increase
position during scanning. (1.5T MRI system)
the SNR and reduce the prominence of signal due
to motion. Since movement tends to be random and
signal is reproducible, the more times each phase-
are often optimized for human patients. Some very sim- encoding step is averaged, the more signal arises from
ple actions can be performed, whereas others are more tissue and the less from movement.10 However, not
complex and may require dedicated scanning hardware only does this increase scan time significantly but
or software. also it fails to reduce the blurring caused by general
• Most high-field scanners used in veterinary medicine are respiratory motion.
made for the human medical market, and therefore may • Orienting the phase-encoding and frequency-
have these software/hardware capabilities as standard. encoding directions so that motion artifact is superim-
In contrast, low-field systems are typically primarily posed over regions of lesser importance (Fig. 9.2.4).
designed for human extremities, in which motion arti- This also confirms signal to be artifact and not due
facts are hardly an issue, and therefore offer no options to real structures. For example, for cranial medias-
for motion artifact reduction.10 tinal masses, the phase-encoding direction would
• In anesthetized veterinary patients, cardiac motion be in the dorsal/ventral direction on sagittal images
usually has greater effect on the images than does res- (labelled ‘AP’ in human medical systems), and right/
piration. Motion artifacts extend in the direction of left on dorsal plane images in order to direct cardiac
phase-encoding, regardless of the direction of move- artifact away from the cranial mediastinum. If neces-
ment, as they are due to the displacement of protons sary, sequences can be repeated after reversal of the
between the application of each phase-encoding gradient phase- and frequency-encoding directions in order to
and that of the frequency-encoding gradient, resulting in examine areas previously obscured. As previously dis-
signal misregistration in the phase-encoding direction. cussed, this does not affect general image blurring due
Discrete, regularly spaced artifacts or ‘ghosts’ occur in to respiratory motion.
the phase-encoding direction whenever the position or • Using ultra-fast pulse sequences (e.g., 20 seconds or
signal intensity of structures within the FOV varies in less), with anesthetized patients under apnea after a
a regular, periodic fashion (e.g., pulsatile blood or CSF period of hyperventilation.
PE
PE
(a) (b)
Fig. 9.2.4 (a) Transverse fat-suppressed, post-contrast T1W image of the thorax in a Cocker Spaniel with an incompletely
resected rhabdomyosarcoma (same dog as in Fig. 9.2.1 showing an oil capsule marker). The phase-encoding direction is right-
to-left (horizontal), which means that cardiac motion artifact is superimposed over the area of interest. (b) Phase-encoding (PE)
has been re-oriented to the vertical direction and the cardiac motion artifact is no longer superimposed over the lateral thoracic
wall. Incomplete fat suppression dorsally is due to the presence of a microchip. (1.5T MRI system)
• Active suppression of signal from tissue generating that they produce. However, a disadvantage of
potential motion artifacts, using techniques such saturation techniques is that they often reduce the
as spatial or spectral saturation, respiratory and/ number of slices available in a given scan time, and
or cardiac gating techniques, phase-reordering, and they can increase heating of the patient’s tissues.10
gradient nulling. However, these techniques require – ‘Gating’ or ‘triggering’ are general terms used to
special equipment and can also result in a time penalty: describe techniques of reducing phase mismap-
– Saturation techniques involve the application of an ping from periodic cardiac or respiratory motion.
initial 90° RF excitation pulse to a volume of tissue They are used to take ‘snapshot’ images of tissues
outside the area of interest in order to reduce or whenever they return to a fixed position. ‘Cardiac
eliminate signal that would cause motion artifacts. gating’ is described in the section on cardiac
‘Spatial saturation pulses’, also known as satura- MRI (Chapter 9.1). During ‘respiratory gating’,
tion bands (‘SAT bands’), are areas applied to the data are collected during a limited portion of the
images used as localizers prior to the scan. Their respiratory cycle, usually near end-expiration
location, width, and centering are adjusted appro- when respiratory movement is minimal.11 This
priately; in people, they are typically 5–10 cm is achieved by means of a bellows device placed
wide and they are especially helpful to reduce the around the patient’s thorax within which a trans-
signal intensity of fat in the anterior thoracic and ducer produces an electronic signal, the amplitude
abdominal wall.11 However, they cannot be placed of which corresponds to the maximum and mini-
over the area of interest. Another technique is to mum excursion of the thoracic wall during breath-
apply SAT bands across blood vessels flowing into ing.10,12 At the end of each expiration, the MRI
the area of interest, parallel to the image slices, to system is triggered to collect a phase-encoding
minimize artifact from blood flow. This is espe- step for each slice, so the image data are acquired
cially valuable for arterial blood but can also be when the least movement is occurring. A major
used to nullify the effect of venous flow. disadvantage of this is the marked prolongation of
– ‘Spectral saturation pulses’ can also be used to sup- imaging time required, by 2–4 times, and the limi-
press signal from a chemical species, usually fat, tation to pulse sequences with long repetition time
thus reducing the signal intensity of the artifact (TR). Although said to work well in anesthetized
714 CHAPTER 9.2
dogs, with typically long and stable expiration applied to correct for phase shifts among a popula-
punctuated by short, sharp intakes of breath,10 the tion of flowing protons at the time of echo collec-
technique fails if the patient is panting or breath- tion. It does not result in an increase in imaging
ing erratically. In addition, the respiratory bellows time but increases the minimum time of echo that
used to register thoracic wall motion were origi- can be used, thereby reducing the number of slices
nally developed for people, and may not be very possible.
reliable in dogs and cats, due to the different size
and shape of their thorax compared with people.13 CLINICAL APPLICATION OF MRI
If available, pediatric bellows should be used in FOR SELECTIVE NON-CARDIAC
smaller dogs and cats to limit this issue. A simpler THORACIC CONDITIONS
technique described is ‘respiratory pseudotrigger-
ing’ in which the length of the average respiratory • Thoracic lesions seen on MR images fall into two
cycle is observed and an appropriate TR selected categories:
to match the cycle. This will naturally be easier • Elective studies, to investigate a known lesion, such
if intermittent positive pressure ventilation is as a thoracic wall mass or other deformity, or an
applied, but pulse sequences are again limited to intrathoracic lesion detected radiographically, such as
those with long TR.11 a cranial mediastinal mass.
– Another technique widely used in people via • Lesions found incidentally during MR scans per-
attachment of the thoracic bellows band is formed for other reasons, usually spinal studies. Some
‘phase reordering’ (respiratory ordered phase- of these findings may be related to the primary lesion
encoding). Data are collected continuously but (e.g., lung metastases from a spinal tumor) whereas
then reordered according to the respiratory cycle others represent separate conditions, such as occult
data recorded simultaneously to simulate the diaphragmatic rupture or heart base tumor. These
pattern of a slow, prolonged respiratory cycle.11 incidental lesions are often seen on the large FOV
Unlike respiratory gating, phase reordering localizers, which should always be examined while the
methods are associated with only a modest time first definitive scan is running.
penalty, although they may permit fewer slices • Examples of thoracic lesions that can be investigated
to be acquired.12 Phase reordering techniques with MRI, based on the author’s experience in using this
assign a specific order to the acquisition of the technique in selected patients, are given below.
phase-encoding steps, synchronizing them with
consistent times within the respiratory cycle. For Thoracic wall
example, in one technique the phase-encoding • Technique tips:
gradient amplitude is maximized during end- • Use an oil capsule as a marker for surface features
inspiration and minimized during end-expiration. such as scars or draining tracts.
This means that the low-order phase-encoding • Position the patient with the area of interest depend-
data (center of k-space, see Chapter 1), which are ent to minimize motion.
highly sensitive to motion, are collected towards • Surface coils are ideal, since the lesions are superficial.
the end of expiration and the beginning of inspi- • Place phase-encoding direction orthogonal to the
ration. The high-order phase- encoding data lesion in each plane.
(outer portions of k-space), which are less sensi- • Use several sequences in one plane and, depending
tive to motion, are collected over the remaining on which one provides the most information, use that
part of each respiratory cycle.9 However, in vet- one in the two other planes.
erinary patients this technique may be less useful • Oblique sagittal plane images, aligned with the ribs
as it relies on successful use of the bellows appa- on the dorsal image used as a localizer, can be helpful
ratus in plotting respiratory motion. It is also for rib lesions.
possible to deliberately maximize mismapping so • Visible or palpable thoracic wall lesions represent the
that artifacts are projected as far away as possible commonest indication for elective thoracic MRI:
from the region of interest.10 • Examples include soft tissue and rib tumors, lipoma-
– ‘Gradient nulling’ also known as ‘gradient tous masses, abscesses, and foreign body reactions
moment rephasing’ or ‘flow compensation’, is a (Fig. 9.2.5).
technique used to reduce flow artifacts, which can • Prior radiographs will have been obtained for many
create ghost images of vascular structures that can of these patients and so, especially in the case of rib
superimpose over areas of interest within the tho- tumors, MRI is performed for surgical planning
rax, especially close to the heart and large vessels. rather than for primary diagnosis. To this end, MRI is
In this technique, additional gradient pulses are superior to CT because of its much greater soft tissue
Fig. 9.2.5 Fibrosarcoma (arrow) on the ventral thoracic wall Fig. 9.2.6 Liposarcoma (arrow) on the ventral thoracic wall
in a Rottweiler; transverse, fat-suppressed, post-contrast T1W in a Labrador Retriever; transverse T2W image. (1.5T MRI
image. (1.5T MRI system) system)
contrast, and most significant bony change should radiographs of the area may help confirm the pres-
already have been seen radiographically. ence of gas/mineralization versus other causes of
• MRI features of thoracic wall masses that should be signal void.
assessed include the size, shape, extent, margination, • General signal characteristics of thoracic wall mass
and the presence of any fluid pockets or foreign mate- lesions are shared with abdominal wall lesions (see
rial. Chapter 10).
• Lipomatous tissue is easily recognized by its fat-signal • MRI is especially valuable for pre-surgical assessment
characteristics: hyperintense on T1W and FSE T2W of feline injection site sarcomas (FISS) as it shows the
series and suppressed on STIR and when fat satura- extent of any pathology, facilitating the obtaining
tion is used (Figs. 9.2.6, 9.2.7). of clean surgical margins.14 Microchips in the area
• Tumors of the ribs are a common cause of thoracic wall of interest may render the study non-diagnostic and
masses and can be evaluated with MRI (Fig. 9.2.8). necessitate removal prior to scanning. Although MRI
Common characteristics include the presence of a is less sensitive for small areas of bone involvement with
well-defined mass surrounding a rib, loss of normal FISS (usually the vertebral spinous processes) than
rib architecture, and displacement of adjacent ribs. radiography or CT, this is of secondary importance
Benign rib lesions may also be detected (Fig. 9.2.9). provided the full extent of pathology is shown. When,
• For fluid collections and other areas of necrosis, as is often the case, one or more unsuccessful surgical
post-contrast T1W (with fat suppression if available) procedures have already been performed, interpreta-
and subtraction images are especially helpful. Fluid tion is hindered by the lack of ability to distinguish
material and necrosis is typically hypointense on T1W between tumor and surgical reaction. In these cases,
images with no enhancement and variable degrees of the aim of surgery is to remove the entire area of abnor-
rim-enhancement after gadolinium injection. mal tissue on the assumption that tumor cells may be
• Foreign bodies are often geometric in shape and present anywhere within it. Of equal importance to
hypointense to signal void on T2* gradient echo patient welfare is the use of MRI to show when the
images, but small areas of hypointensity may also mass is so extensive that surgery is not possible or that
be created by fibrosis, chronic hemorrhage, and a successful outcome is unlikely. One study exam-
gas bubbles and therefore must be interpreted with ined the low-field MRI characteristics of confirmed
caution (Fig. 9.2.10). In particular, examination of FISS in 19 cats.14 All tumors were hyperintense to
716 CHAPTER 9.2
VetBooks.ir
(a)
Fig. 9.2.7 (a) Close-up view of a right lateral recumbent

thoracic radiograph in an Italian Spinone performed as a
(b)
metastasis check for a neoplasm elsewhere. This showed an
apparently extrapleural, rounded mass in the craniodorsal thorax (arrow). (b) Transverse T2W image of the thorax showing
that the mass (arrows) was communicating with a larger extrathoracic mass. This was hyperintense on both T1W and T2W
and suppressed with fat saturation (not shown), indicating that it was adipose tissue. The final diagnosis was lipoma. T, trachea.
(1.5T MRI system)
(b)
Fig. 9.2.8 (a) Close-up view of a dorsoventral radiograph of

the thorax in a Rottweiler with a rib tumor, showing localized
soft tissue swelling (arrows), subtle rib displacement, and
a small amount of unstructured new bone production.
(b) Dorsal T2W image, which shows the extent of the lesion
(a)
(arrow) much more clearly. (1.5T MRI system)
Fig. 9.2.9 Sagittal oblique T2W image of the thoracic wall Fig. 9.2.10 Sagittal oblique T2*W gradient echo image
in an Irish Wolfhound with a firm, painless swelling around of the thorax and cranial abdomen in an English Springer
the costochondral junctions in the mid-left thoracic wall. Spaniel with a firm swelling on the thoracic wall (same dog
Radiography suggested aggressive bony changes in this as in Fig. 9.2.3). A linear, hypointense structure is directed
location, but the MRI appearance is non-aggressive (arrow). cranioventrally from the stomach through the diaphragm and
The presumed diagnosis was of fusion or synostosis between pericardial sac (arrows). It subsequently exited the thoracic
the costochondral junctions, of unknown cause. (1.5T MRI cavity at the site of the swelling. It was removed surgically and
system) found to be a kebab stick. The scan plane was set up by viewing
several transverse images simultaneously, each of which
showed a short segment of the foreign body. (1.5T MRI system)
surrounding musculature on T1W and T2W images • Elective MRI may be performed for known or sus-
and larger tumors were more likely to contain mineral- pected mediastinal mass lesions, but occult lesions are
ization, which appeared as regions of signal void. Most occasionally found on localizer images when imaging a
showed moderate to marked heterogeneous contrast patient for spinal disease (Figs. 9.2.12, 9.2.13). Smaller
enhancement. Indistinct margins and the presence of masses may be missed radiographically, and so nor-
a peripheral T2W hyperintense zone were more prev- mal prior radiographs do not rule out mediastinal dis-
alent following previous excisional biopsy, while cavi- ease. Associated mediastinal +/- pleural fluid may also
tation was more prevalent following incisional biopsy. be evident and appear as homogeneous T1W hypoin-
Tumor volume did not predict tumor-free margins at tense/T2W hyperintense, non-enhancing material in
surgery. Similar features are recognized on high-field the mediastinal +/- pleural spaces with corresponding
MRI in the author’s experience, and fat-suppressed, retraction of the lungs. MRI may be performed for sur-
contrast-enhanced T1W images are often the most gical planning prior to an attempt to resect a mediasti-
helpful in delineating the full extent of macroscopic nal mass, in which case the main purpose of the study is
tissue changes (Fig. 9.2.11). to determine whether or not adjacent structures such as
major blood vessels have been invaded; all three imaging
Mediastinum planes must be used and 3D angiographic images may
• Technique tips: be helpful (Figs. 9.2.14–9.2.16). Despite the technical
• For cranial mediastinal masses, ventral recumbency limitations of thoracic MRI, in the author’s experience
results in least movement of the area of interest. it seems to compare favorably with CT for this purpose,
• Surface coils are less suitable as SNR must be uniform although studies comparing the two techniques are lack-
across the thorax. ing. However, both false positives and false negatives
• For detection of vascular invasion, optimization of for vascular invasion may occur, especially as absence of
slice placement parallel and perpendicular to vessels visible tumor within the vessel lumen does not rule out
will minimize partial volume averaging artifact. infiltration of tumor into the vessel wall. To date, there
718 CHAPTER 9.2
(a)
Fig. 9.2.11 (a) Well-defined and superficial feline injection

site sarcoma (FISS, arrow) in a Bengal cat, seen on a
transverse T2W image. (b) Extensive, ill-defined and deep
FISS in a DSH cat seen on a dorsal plane, fat-suppressed,
post-contrast T1W image. The bulk of the mass is clearly
visible (M) and infiltrative tendrils are also seen extending far
away from the main mass, as indicated by the dashed arrows.
(b)
(1.5T MRI system)
*
*
Fig. 9.2.12 Occult cranial mediastinal mass (asterisk) Fig. 9.2.13 Incidental mediastinal cyst (asterisk) found on
identified on a sagittal three-plane localizer image obtained MRI for a large chest wall mass (granulation tissue) in a cat;
for cervical spine scanning in a Shetland Sheepdog. transverse post-contrast T1W image. (1.5T MRI system)
(1.5T MRI system)
Fig. 9.2.15 Transverse T2W image of the cranial thorax in a

Labrador Retriever with a very large thymoma. The cranial
vena cava is displaced to the right and shows luminal invasion
Fig. 9.2.14 Transverse T2W image of the cranial thorax of by the mass (arrow). (1.5T MRI system)
a German Shepherd Dog with a very large thymoma. Major
blood vessels do not appear to be invaded, although the cranial
vena cava is slightly compressed (arrow). (1.5T MRI system)
is no MRI study reporting the use of MRI characteristics

for histopathologic differentiation of various mediastinal
masses.
• MRI can also be used to investigate cranial mediastinal
lymphadenopathy; for example, when looking for met-
astatic extension of head and neck neoplasia. With the
phase-encoding direction oriented in a dorsal-to-ventral M
direction (for dorsal and sagittal images), the motion arti-
facts from the heart are directed away from the cranial T
mediastinum, allowing good evaluation of the cranial
mediastinal lymph nodes. In a study reporting on a whole
body MRI protocol for cancer patients, the cranial medi-
astinal lymph nodes were consistently seen.8 However,
cardiac motion artifacts challenged assessment of the
tracheobronchial lymph nodes, and only the larger mid-
dle tracheobronchial lymph node could be consistently
evaluated. The left and right tracheobronchial lymph
nodes and sternal lymph nodes were not seen consistently.
For a better assessment of the tracheobronchial lymph Fig. 9.2.16 Dorsal plane T2W image of a tracheal
nodes, it may be advisable to obtain additional series with chondrosarcoma in a Border Collie. The extent of the tumor
the phase-encoding directed cranial-to-caudal for sag- (M) is clearly seen, displacing the trachea (T) to the left. No
ittal and dorsal images and left-to-right for transverse vascular invasion was seen on other images. The tumor was
images, or to use cardiac gating. The best pulse sequence removed successfully. (1.5T MRI system)
720 CHAPTER 9.2
to identify lymph nodes is the STIR sequence, on which especially if associated with volume loss, due to the rela-
they appear hyperintense and well demarcated from the tively long scanning times required for MRI.
dark background; T1W sequences also allow identifica- • Literature reports of the use of MRI for diagnosis of lung
tion of the hypointense nodes when they are surrounded pathology are scant but as part of a whole body MRI pro-
by fat; T2W sequences proved less efficient in identify- tocol for canine cancer patients, demonstration of a pul-
ing the nodes due to poor contrast and poorly defined monary infiltrate thought to be lymphoma was described
margins.8 On T1W and T2W images, lymph nodes as a diffuse, hyperintense signal in the normally hypoin-
typically have low to intermediate signal intensity and tense lung fields on STIR sequences.8 A large pulmonary
high central intensity due to the fatty hilum.15 There are small-cell carcinoma causing clinical signs mimick-
anecdotal reports of the MRI appearance of metastatic ing brachial plexus pathology has been reported, and
mediastinal lymph nodes.16 On T2W images, affected appeared as a heterogeneous mass containing multiple
nodes were fusiform rather than ovoid, had more irregu- T2 hyperintense and T1 hypointense areas thought to
lar to mildly lobulated margins than normally seen, with represent areas of necrosis or cyst-like changes.17
absent central hyperintense signal from the hilar fat, and
contained areas of low signal intensity foci in the central Other areas
and peripheral regions. They had heterogeneous contrast • Other lesions that may be visible on thoracic MRI
enhancement after gadolinium injection. include pleural space, diaphragmatic, and esophageal
lesions. While CT would normally be preferred, occult
Lungs pleural space and diaphragmatic lesions may be identi-
• MRI would not be considered the technique of choice for fied on MRI spinal scans and therefore further investi-
investigation of the lungs, but might be considered if CT gated on the spot with MRI.
is not available. However, lung pathology, especially mass • Spontaneous pneumohemothorax in a Greyhound that
lesions, may be seen incidentally on localizer images for suffered an acute intramedullary thoracolumbar disc
spinal scans and other images in which a larger FOV has extrusion while running, is shown in Fig. 9.2.19. As
been used. the dog was in dorsal recumbency for the MRI study,
• As well as solitary and multiple lung nodules and masses, the free pleural fluid pooled dependently adjacent to the
lung lobe torsion, lobar emphysema, bronchial foreign spine and gas–fluid interfaces due to concomitant pneu-
body, severe bronchiectasis, and pneumonia may all be mothorax was subsequently identified on large FOV
evident on MRI (Figs. 9.2.17, 9.2.18). However, lung images.
consolidation in dependent areas of the lung is likely • Pyothorax and pleural space abscessation may also be
to be due to general anesthesia-associated atelectasis, imaged using MRI, providing sufficient information to
H H
Fig. 9.2.17 Solitary lung mass (M) in a Shih Tzu, Fig. 9.2.18 One sagittal image from a three-plane localizer
demonstrated on a post-contrast T1W image. Generalized scan of a Bichon Frise with acute paraplegia, initially
bronchial thickening was evident but no other masses were suspected clinically to be due to a disc extrusion. The
identified. The lesion was removed surgically and found to be localizer shows numerous lung nodules (arrows) suggestive
an eosinophilic granuloma. H, heart. (1.5T MRI system) of lung metastasis and the definitive scans showed cord
compression caused by pathologic fracture of a presumed
vertebral tumor. (1.5T MRI system)
H
Sp
Fig. 9.2.19 Spontaneous pneumohemothorax in a Greyhound

that suffered from acute paraplegia due to a disc extrusion while
running. The dog was supine for spinal MRI, and for clarity, the
image is oriented in the same way as the dog was lying during
the scan (i.e., the dorsal part of patient is at the bottom of the
image). Free fluid (F) was identified in the dorsal thorax adjacent
Fig. 9.2.20 Dorsal T2W thoracic image in a DSH cat with
to the spine. Subsequent large field of view transverse T2W
acute paraparesis thought to be due to spinal trauma as a
scans showed that free air was also present, creating a gas–fluid
result of a road traffic accident. A ruptured diaphragm is seen,
interface in the pleural space (arrow). A collapsed lung lobe is
with the spleen (Sp) located in the left hemithorax, displacing
visible within the fluid (L). (1.5T MRI system)
the heart (H) to the right. (1.5T MRI system)
guide surgery. Pyothorax produces pleural space fluid,

which is particulate and therefore of higher T1W and
lower T2W signal intensity than other types of fluid such
as CSF and urine. In the case of pleural abscessation,
the fluid is confined to abscess cavities with contrast-
enhancing margins. Lungs are displaced accordingly and
may have rounded margins due to pleurisy.
• Diaphragmatic hernias can also successfully be demon- T
strated with MRI. The cat in Fig. 9.2.20 presented with
acute ataxia and paresis but no signs of trauma: on spinal
MRI a left-sided diaphragmatic rupture was identified in
the absence of spinal lesions, and the presumed diagnosis
*
was of cord concussion due to unknown trauma.
• Esophageal conditions can also be evaluated with
MRI. To limit cardiac motion artifacts, which may
obscure the mid-mediastinal portion of the esophagus,
care should be taken to orient the phase-encoding in
a cranial-to-caudal direction on sagittal and dorsal
images and in a left-to-right direction on transverse Fig. 9.2.21 Transverse T2W image of the mid thorax in an
images. The author has used MRI to assess intratho- English Springer Spaniel presenting with ataxia and paresis.
racic esophageal lesions such as neoplasia, and lack of An extensive and ill-defined dorsal mediastinal mass (asterisk)
patency of the ligamentum arteriosum in a puppy with was identified, involving both the spine and esophagus
a vascular ring anomaly was successfully shown using (arrows). An esophageal tumor was diagnosed. The trachea
MR angiography (Figs. 9.2.21, 9.2.22). (T) is displaced dorsally and to the left.
722 CHAPTER 9.2
REFERENCES
1. Cooper SA, Banerjee AK (1999). Magnetic resonance imaging
of the thorax: a review. Clin MRI/Develop in MR 9(2):41–5.
2. Hatabu H, Stock KW, Sher S et al. (2000). Magnetic resonance
imaging of the thorax. Past, present, and future. Radiol Clin
North Am 38(3):593–620.
3. Contreras S, Arencibia A, Gil F et al. (2010). Black and
bright-blood sequences magnetic resonance angiography and
gross sections of the canine thorax: an anatomical study. Vet J
185(2):231–4.
4. Contreras S, Vazquez JM, Miguel AD et al. (2008). Magnetic
resonance angiography of the normal canine heart and
associated blood vessels. Vet J 178(1):130–2.
5. Contreras S, Vazquez JM, Morales M et al. (2011). Three-
dimensional MRA study of the normal canine thorax: MIP
sections and volume rendering. Anat Histol Embryol 40(1):40–6.
6. Johnson VS, Seiler G (2006). Magnetic resonance imaging
appearance of the Cisterna chyli. Vet Radiol Ultrasound
47(5):461–4.
7. Vilar JM, Arencibia A, Ramirez JA et al. (2003). Magnetic
resonance imaging of the thorax of three dogs. Vet Rec
153(18):566–8.
8. Kraft S, Randall E, Wilhelm M et al. (2007). Development
of a whole body magnetic resonance imaging protocol in
normal dogs and canine cancer patients. Vet Radiol Ultrasound
48(3):212–20.
9. Elster AD, Burdette JH (2001). Questions and Answers in
Magnetic Resonance Imaging, 2nd edn. Mosby, St. Louis.
10. Elliott I, Skerritt GC (2010). Handbook of Small Animal MRI,
1st edn. Wiley-Blackwell, Ames.
11. Mirowitz SA (1999). MR imaging artifacts. Challenges and
solutions. Magn Reson Imaging Clin N Am 7(4):717–32.
12. Westbrook C, Kaut Roth C, Talbot J (2011). MRI in Practice,
4th edn. Wiley-Blackwell, Ames.
13. Gilbert SH, McConnell FJ, Holden AV et al. (2010). The
potential role of MRI in veterinary clinical cardiology. Vet J
183(2):124–34.
14. Rousset N, Holmes MA, Caine A et al. (2013). Clinical and
low-field MRI characteristics of injection site sarcoma in 19
Fig. 9.2.22 Dorsal plane subtraction image in a 3-month- cats. Vet Radiol Ultrasound 54(6):623–9.
old Dalmatian puppy with a vascular ring anomaly due to a 15. Kneissl S, Probst A (2006). Magnetic resonance imaging
persistent right aortic arch. The study was performed in an features of presumed normal head and neck lymph nodes in
attempt to identify whether or not the ductus arteriosus/ dogs. Vet Radiol Ultrasound 47(6):538–41.
ligamentum arteriosum was patent. Although a thread-like 16. Kishi EN, Holmes SP, Abbott JR et al. (2014). Functional
area of contrast medium is seen (arrow), it did not appear to metastatic parathyroid adenocarcinoma in a dog. Can Vet J
link the aorta and pulmonary artery, and at thoracotomy no 55(4):383–8.
17. Ferreira AJ, Peleteiro MC, Correia JH et al. (2005). Small-cell
patency was found.
carcinoma of the lung resembling a brachial plexus tumour.
CHAPTER 10
ABDOMINAL MRI
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Wilfried Mai, Ruth Dennis, and Matthew Paek 723
CONTENTS
Liver, biliary tree, pancreas....................................................................................................................................................................................726
Hepatic nodular and mass lesions ...................................................................................................................................................................726
Liver-specific contrast agents ..........................................................................................................................................................................728
Biliary tree and pancreatic duct ........................................................................................................................................................................730
Pancreas ..........................................................................................................................................................................................................732
Spleen ...................................................................................................................................................................................................................733
Abdominal lymph nodes .......................................................................................................................................................................................735
Urogenital tract......................................................................................................................................................................................................736
Kidneys and ureters .........................................................................................................................................................................................736
Bladder ............................................................................................................................................................................................................738
Genital tract .....................................................................................................................................................................................................738
Adrenal glands ...................................................................................................................................................................................................... 741
Gastrointestinal tract ............................................................................................................................................................................................. 742
Magnetic resonance angiography.......................................................................................................................................................................... 744
Non-contrast-enhanced techniques ................................................................................................................................................................. 744
Contrast-enhanced MRA.................................................................................................................................................................................. 746
References.............................................................................................................................................................................................................751
Although ultrasonography is still the technique of choice acquisition times, breath-holding can be used with these
to image the abdomen in dogs and cats, it can be chal- pulse sequences, minimizing respiratory motion artifacts.
lenging and lack sensitivity, especially for assessment of Respiratory gating detecting thoracic wall movements or
the cranial abdomen in variable situations, including large mapping diaphragmatic excursions can also be applied to
or deep-chested conformation,1 panting/motion, or large acquire data that are free of breathing motion artifacts.2
volumes of gastrointestinal gas. Cross-sectional imag- In addition, hardware related solutions such as coils with
ing techniques, such as CT and MRI, can be beneficial in parallel acquisition, where different coil segments image
these cases. MRI provides the benefits of exquisite soft- specific quadrants of the abdomen, can allow further scan-
tissue contrast, multiplanar imaging capabilities, and lack ning time reduction. Abdominal MRI is a common imag-
of ionizing radiation. 2–4 The need for general anesthesia, ing tool in people; for example, acute abdominal and pelvic
long acquisition times, and respiratory motion artifacts are conditions that can be rapidly diagnosed with MRI include
the main disadvantages associated with MRI.5 However, choledocholithiasis, acute cholecystitis, acute pancreatitis,
advances in hardware and software have allowed acquisi- bowel inflammation in the setting of inflammatory bowel
tion of images that are free of motion artifacts with shorter disease (Crohn’s disease and ulcerative colitis), and appen-
imaging times.2 These advances include the use of faster dicitis. There are very few studies reporting the use of
pulse sequences such as half-Fourier acquisition single MRI for abdominal disease in dogs and cats, and therefore
shot turbo spin echo (HASTE) and sequences of the gra- this chapter will be largely pictorial, illustrating examples
dient echo family such as fast low-angle shot (FLASH) of potential applications of MRI in a clinical setting, based
or spoiled gradient echo (SPGR). Due to their short on the authors’ experience.
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GENERAL CONSIDERATIONS sequences with free breathing are often subject to sig-
nificant motion artifacts that prevent adequate assess-
• The choice of coil depends on the size of the patient and ment of some organs, especially smaller structures in the
the type of scanner in use: cranial abdomen, such as the pancreas.3 A recent study
• For larger dogs being scanned in a human medical found that pulse sequences with breath-hold are gener-
system, a body or thorax coil may be required, whereas ally better than those with respiratory navigation or free
smaller patients may be imaged in head or extremity breathing. However, for the caudal abdomen free breath-
coils. ing pulse sequences may be used as well.2
• Phased-array coils can be beneficial to reduce scan • A recommended protocol may include:2
time when used in parallel (‘parallel imaging’): • Dorsal T2W turbo spin echo with fat saturation and
multiple overlapping small coils individually cover breath-hold.
a smaller volume, but with less noise than with a • Dorsal T2 HASTE or SSFSE with respiratory navi-
larger coil encompassing the entire volume; when gation or breath-hold.
these coils are run in parallel and the data combined, • Transverse T1W FLASH or SPGR with breath-hold
the entire volume under study can be covered in a pre-contrast and post-contrast.
shorter time. The most popular parallel imaging • If the focus is on the caudal abdomen, free breathing
methods are SENSitivity Encoding (SENSE) and transverse T1W spin echo pre- and post-contrast can
Array coil Spatial Sensitivity Encoding Technique also be used.
(ASSET).6 • Dorsal or sagittal plane STIR pulse sequence can help
• Dedicated veterinary systems come with a different to screen for lesions and lymph node identification.
range of radiofrequency coils but these are unlikely to There is excellent image contrast, depicting fluid and
be optimized for the abdomen. solid soft tissue lesions as hyperintense regions, with
• Strategies to minimize the effect of respiratory motion the added advantage of background fat signal suppres-
should be used, especially when imaging the cranial sion.9
abdomen close to the diaphragm. Most of the strategies • Functional pulse sequences such as perfusion-weighted
used for thoracic imaging can also be used for abdomi- or diffusion-weighted imaging have been investi-
nal imaging, and are described in Chapter 9.2. These gated in normal dogs, but not applied clinically at this
include: time.10 They may in the future be helpful to character-
• Breath-hold techniques, if permitted by the acquisi- ize diffuse liver changes or early modifications before
tion time. the appearance of visible morphologic or structural
• Free breathing acquisition while controlling motion alterations.
using different strategies such as ‘respiratory gating’, • Organ-specific pulse sequences and protocols can be
‘respiratory pseudotriggering’, or ‘phase reor- used as well, outlined in the corresponding paragraphs.
dering’ (respiratory ordered phase encoding) (see • Signal intensities of organs vary depending on the pulse
Chapter 9.2): sequences used. In general, the decreasing order of signal
– Detection of the respiratory movements can be intensity in dogs is (Figs. 10.1, 10.2):9
facilitated by the use of a bellows device placed • T1W images: fat > [bile and renal pelvis] > bone
around the patient’s thorax, within which trans- marrow > [liver and lymph nodes] > [renal cortex and
ducers produce an electronic signal, the ampli- spleen] > skeletal muscle > renal medulla > urine.
tude of which corresponds to the maximum and • T2W images: urine > [fat and bile] > [renal medulla
minimum excursion of the thoracic wall during and pelvis] > [spleen and lymph nodes] > bone marrow
breathing.7,8 > renal cortex > liver > skeletal muscle.
– Acquisition can also be triggered using ‘respira- • STIR: urine > renal medulla > [spleen and bile] > renal
tory navigator echoes’ to reduce phase mismapping cortex > lymph nodes > [skeletal muscle, liver and fat]
caused by respiratory motion.2 In this technique, > bone marrow.
a region of interest (ROI) is placed across the dia- • This order of signal intensity is fairly similar in cats,
phragm on either dorsal or sagittal localizers. The except that the renal medulla is slightly hyperintense to
system monitors the signal intensity in real time the skeletal muscles on T1W images.3
within this ROI and omits data acquired outside • Variable degrees of contrast enhancement will be
prescribed boundaries (see Fig. 3.3). While this observed on T1W post-gadolinium injection images,
is an effective method, the scan time may increase depending on the organs, type and dose of contrast
and/or the signal-to-noise ratio (SNR) decrease medium used, type of MRI sequence (spin echo versus
due to the data being removed.8 gradient echo), and timing of imaging after injection.
• A large number of pulse sequences can be used for • The signal intensity of urine will also change after
abdominal imaging. Regular T1W and T2W pulse gadolinium injection due to renal excretion of the
A b d om i n a l M R I 725
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L
GB GB
F F
Pyl Pyl
Sp Sp
(a) (b)
F F
D
Tr Colon D Tr Colon
Sp
Sp
Cec Cec
UB UB
DC DC
(c) (d)
Fig. 10.1 Dorsal T1W images with breath-hold (a, c) and corresponding T2W fast recovery fast spin echo images with breath-
hold (b, d) in a dog at the level of the gallbladder (a, b) and cecum (c, d), illustrating the anatomic relationships and various
signal intensities on T1W and T2W images. Note the hyperintense bile in the gallbladder on the T2W images while it is only
mildly hyperintense on the T1W images. The fluid in the fundus (F, c and d) or pyloric antrum (Pyl, a and b) and the urine
in the urinary bladder (UB, c and d) appear hypointense on the T1W and hyperintense on the T2W images, while gas in the
lumen of the fundus (F, a and b) and in the cecum (Cec, c and d) appears black on all pulse sequences. GB, gallbladder; L, liver;
Sp, spleen; Pyl, pyloric antrum; F, gastric fundus; D, descending duodenum; Cec, cecum; DC, descending colon; Tr Colon,
transverse colon; UB, urinary bladder. (1.5T MRI system)
contrast material. A pseudolayering pattern can be intensity, the middle layer is of very high signal inten-
seen in the dependent portion of the bladder lumen; it sity (lower concentration gadolinium as it starts to mix
appears as three sharply defined layers or bands of dif- with urine), and the bottom layer (dependent) is mark-
ferent signal intensity. On T1W images the upper layer edly hypointense. The cause of this artifact is thought to
(non-dependent) represents normal urine of low signal be the accumulation of highly concentrated gadolinium
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F
F
L Sp
L Sp
Sp
Sp
RK cvc LK
Ao
DC
DC
(a) (b)
F
F
DC
DC
(c) (d)
Fig. 10.2 Dorsal T1W with breath-hold (a, c) and T2W fast recovery fast spin echo with breath-hold (b, d) images in a dog at
the level of the left adrenal gland (arrows, a and b) and right adrenal gland (solid arrows, c and d), illustrating the anatomic
relationships and various signal intensities on T1W and T2W images. L, liver; Sp, spleen; F, gastric fundus; DC, descending
colon; LK, left kidney; RK, right kidney; CVC, caudal vena cava; Ao, aorta. The close relationship between the right adrenal
gland, right kidney, and caudal vena cava, as well as between the left adrenal gland, left kidney, and aorta is visible. Vascular
landmarks such as the celiac and cranial mesenteric arteries (dashed arrows, d) are visible. The fluid in the gastric fundus (F)
appears hypointense on the T1W images and hyperintense on the T2W images. (1.5T MRI system)
in the dependent portion of the urinary bladder shortly LIVER, BILIARY TREE, PANCREAS
after the injection of the contrast medium. At these
concentrations, the T1 and T2 relaxation times of the Hepatic nodular and mass lesions
urine–gadolinium mixture become extremely short, and • Nodular hyperplasia typically is not detected on MRI
the effect of the reduction in T2 time becomes visible, because the lesions are formed of normal hepatocytes
causing the signal intensity to decrease sharply.11 with normal hepatic organization and vasculature, and
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therefore have a similar signal intensity to the surround-

ing normal parenchyma.12 They may appear as distinct
nodules when they deform the margins of the organ
(Fig. 10.3), when there are additional changes such as
glycogen accumulation within them, or when they are
numerous and surrounded by parenchymal atrophy and
fibrosis, such as seen with cirrhosis.12
• There is very little information available in the vet-
erinary literature regarding the MRI appearance of
malignant hepatic lesions,5,12,13 and therefore the actual
diagnostic accuracy of MRI in differentiating malig-
nant versus benign lesions and differentiating various
HEART LIVER types of hepatic malignancies is, at this time, not clearly
established:
• Hepatocellular neoplasia may form masses that are
isointense to normal liver parenchyma on T1W
pre-contrast images, sometimes with a hypointense
Fig. 10.3 Enlarged and nodular liver found incidentally rim corresponding to a capsule or pseudocapsule.
during spinal MRI in a Border Terrier with paraplegia due On T2W images the lesions are more heterogene-
to a T12-T13 disc extrusion. The nodules (arrows) have a ous than the surrounding normal liver parenchyma
similar signal intensity to the liver parenchyma, which could (Figs. 10.4, 10.5). Post-contrast enhancement may be
be consistent with benign nodular hyperplasia. However, a similar to that of the liver parenchyma and may show
definitive diagnosis was not obtained at the time due to the a central non-enhancing hypointense area (‘central
necessity of proceeding to surgery. Although signal intensity scar’) and a more heterogeneous appearance than that
of the liver on this sagittal T2W image is homogeneous, the of the normal liver.
liver architecture was heterogeneous on ultrasonography. • Hemangiosarcoma was reported to form lesions
(1.5T MRI system) that are hypointense to the normal parenchyma
on T1W pre-contrast images and hyperintense on
#
Sp
*
GB
St
Sp
(a) (b)
Fig. 10.4 Transverse (a) and dorsal (b) T1W images of the cranial abdomen in 12-year-old male neutered Poodle-mix dog
presented to the neurology service with non-ambulatory paraparesis. There is a mass in the ventral aspect of the liver (solid
black arrows, a; white arrows, b) that has a heterogeneous signal intensity. The dashed black arrows in (a) indicate ghosting
artifact associated with flow motion in the caudal vena cava (asterisk) and aorta (#). Histopathology showed hepatic adenoma.
Sp, spleen; GB, gallbladder; St, stomach. (1.5T MRI system)
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Liver-specific contrast agents

• Several contrast agents other than the standard gadolin-
ium-DTPA (Magnevist®, Omniscan®) or gadolinium-
DOTA (Dotarem®) can be used to specifically image the
liver.
• Superparamagnetic iron oxide particles (e.g., Resovist®)
can be used due to their specific accumulation in the
reticuloendothelial system. After injection, they are
taken up by the Kupffer cells of the liver. This accumula-
tion of iron-based particles causes a shortening of the T2
relaxation time, and subsequent markedly decreased sig-
nal of the liver parenchyma when using pulse sequences
that are sensitive to changes in T2, such as gradient
echo pulse sequences.14 As most hepatic tumors lack
normal Kupffer cells, the contrast between neoplastic
Sp tissue and normal parenchyma increases after injection
of these particles. Imaging should be performed about
20 minutes after injection.
• More recently, gadolinium-based agents have been used
to specifically image the liver in dogs.15–19 These include
gadoxetate disodium (Gd-EOB-DTPA, Primovist ® in
Europe and Eovist® in the USA) as well as gadobenate
Fig. 10.5 Dorsal T2W turbo spin echo image in a 5-year-old dimeglumine (Gd-BOPTA, Multihance®).
mixed breed dog with a large hepatic mass, diagnosed as a • After intravenous injection, the biodistribution of
hepatocellular carcinoma at histopathology. A large mass of these contrast agents follows two phases:18
complex mixed signal intensity is present in the ventral aspect – A first dynamic phase with distribution of the
of the liver (arrows). Hyperintense areas likely represent contrast agent into the vascular and extracellu-
regions of fluid cavitation (degenerative cyst-like changes or lar space, similar to other extracellular contrast
necrosis). Sp, spleen. (1.0T MRI system; see also Figs. 10.6 media.
and 10.7; images courtesy of Dr. Anne-Carole Duconseille – A hepatocellular phase, where the contrast agent
and Dr. Arnaud Louvet, Centre d’Imagerie par Résonance accumulates in normally functioning hepatocytes
Magnétique de l’Animal) by a canalicular organic anion transporter.
• As a result, these contrast agents are excreted by the
kidneys and the biliary system.
T2W images. Delayed contrast enhancement may • The continuous accumulation of contrast material
be observed due to progressive accumulation of con- in the hepatocytes after injection causes a gradual
trast material in the lesion, while non-enhancing increase in signal intensity of the liver parenchyma
regions corresponding to blood clots may also be on T1W images. Because these contrast agents accu-
seen, conferring a heterogeneous appearance on mulate in normally functioning hepatocytes, the
some lesions. healthy hepatic parenchyma progressively enhances
• Hepatic metastases may form multiple nodules that after administration until a plateau of enhancement
are hypointense to liver parenchyma on T1W images, is reached. In contrast, neoplastic lesions that contain
hyperintense on T2W images, and enhance more abnormal hepatocytes or no hepatocytes will not accu-
than the surrounding normal liver parenchyma on mulate contrast material and will appear hypointense.
post-contrast T1W images. Their MRI appearance Benign hepatic lesions such as nodular hyperplasia,
may, however, be variable depending on the nature of which contain normally functioning hepatocytes, will
the primary tumor. enhance similarly to normal liver tissue. As a result,
• Diffuse hematopoietic neoplasia in the liver (lym- neoplastic lesions in the liver parenchyma are likely
phoma or myelodysplastic syndrome) was reported to appear hypointense compared with the normal
to cause decreased signal intensity of the liver paren- (enhanced) surrounding parenchyma during the
chyma on T2W images, causing it to appear hypoin- hepatobiliary phase of the contrast agent distribution
tense to skeletal muscles.5 It is not clear, however, (Figs. 10.6–10.8).
whether this difference is caused directly by malig- • Reported doses for gadoxetate disodium vary
nant cell infiltrates, extramedullary hematopoiesis, or between 0.0125 and 0.025 mmol/kg, although
tumor-induced metabolic perturbations. the lower dose provides similar results in terms of
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Fig. 10.6 Serial transverse spoiled gradient echo images (3D-FLASH) of the liver in a 5-year-old mixed breed dog with a large
hepatic mass, diagnosed as a hepatocellular carcinoma at histopathology (same dog as in Figs. 10.5 and 10.9). These images were
acquired 20 minutes after injection of the liver-specific contrast medium gadobenate dimeglumine (Gd-BOPTA, Multihance®),
corresponding to the hepatobiliary phase of the biodistribution of the contrast material. The images presented here were
subtraction images (post-contrast minus pre-contrast) to remove the high signal from fat. The goal of this series is to rule out
hypointense lesions in the liver parenchyma outside of the large mass, which would raise concern for metastatic disease. The
mass itself (solid arrows) is hypointense at this phase of the study as it is made of abnormal hepatocytes, which do not take
up the contrast material. The normal liver parenchyma around the mass is markedly hyperintense (dotted arrows) as it has
accumulated contrast material. The gallbladder (asterisk) is starting to accumulate hyperintense bile in the dependent aspect of
its lumen due to the progressive biliary excretion of gadobenate dimeglumine. (1.0T MRI system; images courtesy of Dr. Anne-
Carole Duconseille and Dr. Arnaud Louvet, Centre d’Imagerie par Résonance Magnétique de l’Animal)
liver parenchymal enhancement, and may therefore material, in a manner similar to that described later
suffice.18 For gadobenate dimeglumine, the reported (see “Contrast-enhanced MRA”) (Fig. 10.9).
dose is 0.2 mmol/kg.17 • A post-contrast ‘equilibrium’ T1W series may be
• Pre-contrast T1W images are obtained using rapid obtained about 1.5–2 minutes after injection.17
pulse sequences such as volume interpolated 3D gra- • After the dynamic vascular and equilibrium phases
dient echo T1W sequences (e.g., FAME on General acquisition, a delayed ‘hepatobiliary’ phase is obtained
Electric, VIBE on Siemens, THRIVE on Philips). coinciding with maximum concentration of contrast
These pulse sequences are fairly short and can be material in the normal hepatocytes. Optimal timing
acquired in apnea; however, patients may be curarized for the hepatobiliary phase for gadoxetate disodium
using cisatracurium, for example, to limit respiratory was initially reported to be after 20 minutes,19 but more
motion during apnea. recent studies showed that imaging 10–15 minutes
• The early vascular distribution of these gadolinium- after injection provides optimum liver enhancement,
based contrast agents can be used to image the liver which does not increase significantly later on.15,18 For
vasculature to assess relationship of potential liver gadobenate dimeglumine, imaging at 23–25 minutes
nodules/mass lesions relative to important vascu- after injection appears optimal.17 The hepatobil-
lar structures, which is useful for surgical planning. iary phase can be imaged using various rapid T1W
This is accomplished in a dynamic fashion, using fast pulse sequences, such as 3D spoiled gradient echo
spoiled gradient echo pulse sequences such as 3D T1W (Fast SPGR or Turbo FLASH), as well as volume
Fast-SPGR or Turbo-FLASH. Successive volumes interpolated 3D gradient echo T1W pulse sequences
centered at the porta hepatis and liver are obtained (e.g., FAME on General Electric, VIBE on Siemens,
starting immediately after the injection of contrast THRIVE on Philips).
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GB
GB
(a) (b)
Fig. 10.7 Transverse T2W (a) and T1W 3D-FLASH (b) images obtained 20 minutes after injection of the liver-specific
contrast medium gadobenate dimeglumine (Gd-BOPTA, Multihance®) in a dog diagnosed with a hepatic carcinoid tumor.
Only the largest mass (open arrow, a), presumably the primary tumor, was visible on abdominal ultrasound. On the T2W
image, an additional hyperintense lesion is seen (solid arrow, a) adjacent to the larger mass, suspicious for a metastatic lesion.
On the delayed post-contrast image, both lesions are markedly hypointense (open and solid arrows, b) confirming a neoplastic
origin. There are a number of additional hypointense lesions (dashed arrows, b) that were invisible on the T2W image and on
ultrasound, and correspond to numerous hepatic metastases. Note in (b) the accumulation of hyperintense contrast material in
the dependent lumen of the gallbladder (GB) due to the progressive biliary excretion of contrast material. (1.0T MRI system;
images courtesy of Dr. Anne-Carole Duconseille and Dr. Arnaud Louvet, Centre d’Imagerie par Résonance Magnétique
de l’Animal)
• The time between the dynamic vascular acquisition agents; however, it typically enhances less than the
and the delayed hepatobiliary phase can be used to surrounding normal parenchyma, with the maximum
obtain T2W turbo/fast spin echo images with res- contrast visible around 10 minutes after injection
piratory triggering. These series are important to of gadoxetate disodium.16 Benign lesions, such as
identify fluid-filled lesions such as cysts or cyst-like nodular hyperplasia or vacuolar hepatopathy, may be
changes, which would also appear hypointense on the visible on T2W images but show similar enhancement
T1W images during the hepatobiliary phase (similar to the normal liver at the post-contrast hepatobiliary
to neoplastic lesions), but will appear hyperintense on phase of the study.16,19 Additional malignant lesions
T2W images (Fig. 10.8). Although gadolinium-based not visible on ultrasound may be demonstrated with
agents cause shortening of both T1 and T2 relaxa- MRI, which may be important for staging and surgi-
tion times, the effect on T2 times is usually minimal cal planning.16,17,19
at in-vivo concentrations. It was shown that these
liver-specific contrast agents do not significantly Biliary tree and pancreatic duct
alter the hepatic T2 signal intensity during the time • Magnetic resonance cholangiopancreatography (MRCP)
between injection and hepatobiliary phase acquisi- has been described in cats as a method to image the bili-
tion,15 making it possible to use that waiting time to ary tree and pancreatic duct.20
acquire the T2W series. • Pulse sequences useful for imaging of the pancreatic and
• Both gadoxetate disodium and gadobenate dimeglu- biliary ductal system are modified fast spin echo sequences
mine have been evaluated to assess hepatic nodular with long echo times that are heavily T2W, suppressing
and mass lesions in dogs.16,17,19 Due to impaired but background signal while making static or slow-moving
retained hepatocellular function, hepatocellular carci- fluids such as bile in the biliary tree hyperintense. Pulse
noma can enhance variably when using these contrast sequences that can be used include rapid acquisition with
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GB
GB
(a) (b)
St
GB
GB
(c) (d)
Fig. 10.8 Transverse 3D gradient echo T1W sequence (3D FAME, a and c) obtained 20 minutes after injection of the liver-
specific contrast medium gadobenate dimeglumine (Gd-BOPTA, Multihance®) and corresponding transverse T2W images with
respiratory triggering (b and d) in a 14-year-old Dachshund diagnosed with a hepatic mass on ultrasound. This examination
was performed to rule out additional hepatic lesions not visible on ultrasound. In (a), a hypointense lesion is seen in the liver
(solid black arrow) but this lesion is hyperintense on the T2W image (solid white arrow, b) consistent with a cyst. However,
numerous additional hypointense lesions are seen in the liver parenchyma (dotted black arrows, a and c) that are not visible on
the T2W images and are consistent with metastatic disease. The main lesion that was seen on ultrasound is indicated in (c) and
(d) by the arrowheads. GB, gallbladder; St, stomach. (1.5T MRI system)
rapid enhancement (RARE), half-Fourier acquisition use of secretin (2 U/kg, imaging about 3 minutes after
single-shot turbo spin echo (HASTE), and fast-recovery injection) can enhance its visibility by causing ductal
fast spin echo (FRFSE) sequences. distension.20
• Dorsal oblique planes are used to image as much of the • Other pulse sequences can provide visual assessment
biliary tree as possible. of the biliary tree and pancreatic duct, as well as allow
• Although the gallbladder and common bile duct are simultaneous assessment of the pancreatic tissue and
readily assessed with these sequences, the pancreatic liver parenchyma. They are described in the following
duct is not consistently seen in normal cats, and the section on the pancreas.
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M M
RK Ao RK Ao
(a) (b)
Fig. 10.9 Magnetic resonance angiography in a 5-year-old mixed breed dog with a large hepatic mass, diagnosed as a
hepatocellular carcinoma on histopathology (same dog as in Figs. 10.5 and 10.6). Early imaging after intravenous injection of
the liver-specific contrast medium gadobenate dimeglumine (Gd-BOPTA, Multihance®) allows acquisition of angiographic
images. These T1W FLASH maximum intensity projection images in the dorsal plane show the relationship between the large
hepatic mass (M) and the hepatic vasculature. The portal vein is visible (solid arrow), as well as some afferent vessels such as
the gastroduodenal vein (open arrow) and intrahepatic efferent vessels (dotted arrows and white arrowheads). The hepatic
artery (yellow arrowheads) is also clearly seen as well as the aorta (Ao). RK, right kidney. (1.0T MRI system; images courtesy of
Dr. Anne-Carole Duconseille and Dr. Arnaud Louvet, Centre d’Imagerie par Résonance Magnétique de l’Animal)
• In cats with cholangitis/cholecystitis, changes may be

seen on T1W post-contrast images, including thicken-
ing and enhancement of the gallbladder wall.21,22
Pancreas
• MRCP, as described above, does not allow concurrent
assessment of the liver and pancreatic tissue adjacent
to the ductal system, and therefore additional pulse
sequences may be necessary for that purpose such as:20
• Fast spoiled gradient recalled echo pulse sequences C
(e.g., FSPGR on General Electric, Turbo-FLASH on
Siemens, Turbo Field Echo on Philips). L
• Pre- and post-contrast volume interpolated 3D gradi- St
ent echo T1W pulse sequences (e.g., FAME, VIBE,
THRIVE).
• T2W fast spin echo (Fig. 10.10). Fig. 10.10 Normal pancreatic body (arrows) seen on a
• These pulse sequences allow concurrent assessment parasagittal T2W image in a Jack Russell Terrier undergoing
of the biliary tree and pancreatic duct, which appear MRI for spinal pain. The pancreas is seen as a small, well-
hyperintense on T2W fast spin echo pulse sequences defined, hypointense organ surrounded by hyperintense
(Fig. 10.11), while they are hypointense on fast spoiled abdominal fat. Two incoming branches of the hepatic
gradient recalled echo and volume interpolated 3D gra- portal vein are seen in cross-section dorsal to the pancreas.
dient echo T1W pulse sequences (Fig. 10.12).20 The stomach (St) lies immediately cranial, and part of
• In cats, excellent visualization of the pancreatic tissue the transverse colon (C) is seen ventral to the pancreas.
is achieved with T1W volume interpolated 3D gradient L, liver. Note the hyperintense fluid in the dorsal aspect
echo pulse sequences (FAME, VIBE, THRIVE), and of the gastric lumen and hypointense gas in the ventral
these also allow simultaneous assessment of the biliary lumen as the patient was in dorsal recumbency for scanning.
tree and, after secretin injection, of the pancreatic duct. (1.5T MRI system)
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They may be most appropriate for general evaluation of

hepatobiliary and pancreatic disease in cats (Fig. 10.12).20
• The pancreas is typically uniformly hyperintense relative
to the liver on T1W images and isointense to hypoin-
tense on T2W images with fat saturation. It forms a thin,
flat organ, which is best appreciated in the dorsal and
sagittal planes on various pulse sequences due to its close
CVC relationship with the descending duodenum, portal vein,
CVC greater curvature of the stomach, and spleen.21
• In cats with pancreatitis, pronounced signal intensity
abnormalities can be seen.22 The inflamed pancreas
Heart appears hypointense on T1W pre-contrast images and
GB Pyl hyperintense on T2W images as a result of fibrosis and
edema. It may be enlarged, with or without dilation of
the pancreatic duct. Cystic changes are readily identi-
fied, forming rounded hyperintense structures on T2W
images. Irregular hyperintense areas of the peripancre-
Fig. 10.11 Normal gallbladder (GB) and cystic/common bile atic tissues may be seen on T2W images, indicative of
duct (arrows) seen in a parasagittal T2W image in a Pug focal peritonitis/steatitis.
undergoing spinal MRI for the investigation of paraparesis.
The bile content appears hyperintense and the surrounding SPLEEN
liver parenchyma is hypointense. Note the hyperintense
fluid in the dorsal lumen of the pyloric antrum (Pyl) and • Splenic nodular lymphoid hyperplasia and extramedul-
hypointense gas in the ventral lumen of the antrum, as the lary hematopoiesis have been reported to form nodular
patient was in dorsal recumbency for scanning. CVC, caudal lesions in the parenchyma that are hypointense to the
vena cava. (1.5T MRI system) surrounding splenic tissue on T1W gradient echo and
(a) (b)
Fig. 10.12 Transverse oblique (a) and dorsal (b) images of the cranial abdomen using a T1W 3D SPGR (3D FAME) pulse
sequence after gadolinium injection and post secretin injection in a normal cat. The imaging planes are optimized for
evaluation of the pancreatic parenchyma, which is readily visible as a finely lobulated V-shaped structure on the dorsal plane
image (b). On these post-secretin images, the dilated hypointense pancreatic duct is readily visible (arrow and arrowheads).
(1.5T MRI system; reproduced, with permission, from Marolf AJ, Stewart JA, Dunphy TR et al. (2011). Hepatic and
pancreaticobiliary MRI and MR cholangiopancreatography with and without secretin stimulation in normal cats. Vet Radiol
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T2W fast spin echo images, and less enhancing than the • The MRI appearance of malignant splenic disease has
normal surrounding parenchyma on T1W gradient echo not been well characterized thus far:
images after gadolinium injection.12 However, the number • One limited case series reports a malignant plasma
of cases reported in the literature so far is very low, and cell tumor lesion in the spleen as hypointense on T1W
the authors have observed variable appearance of benign gradient echo and hyperintense on T2W fast spin
lesions. For example, extramedullary hematopoiesis may echo images, with stronger (peripheral and nodular)
form mass-like lesions of heterogeneous signal with enhancement than the surrounding parenchyma;12
hyper- and hypointense regions on both T1W and T2W however, there are not enough data to generalize this
images with irregular contrast enhancement (Fig. 10.13). pattern to other types of malignant splenic lesions.
Sp
(a) (c)
F F
Sp
Sp
Sp
(b) (d)
Fig. 10.13 Transverse (a) and dorsal (b) T1W post-contrast images with fat saturation and corresponding transverse (c) and
dorsal (d) T2W images with fat saturation and breath-hold in an 8-year-old female spayed mixed breed dog presented for
surgical removal of a functional primary adrenal gland mass causing hyperadrenocorticism. There is a left adrenal adenoma
(dotted arrows) and a splenic mass (solid arrows) due to extramedullary hematopoiesis. Both lesions have heterogeneous signal
on both pulse sequences. Sp, spleen; F, gastric fundus. (1.5T MRI system)
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CVC
Ao CVC
R
UB
Fig. 10.14 Transverse T2W image in a dog showing a well- (a)

defined mid-splenic mass (arrows) with distortion of the
splenic margins and markedly heterogeneous signal intensity.
The mass was remarkably subtle on ultrasonography.
Splenectomy was performed and the final diagnosis was
hemangiosarcoma. (1.5T MRI system)
• In another study, a primary splenic hemangiosarcoma

formed a markedly T1 hypointense and T2 isointense
mass compared with normal splenic parenchyma; no
post-contrast images were acquired.5 A case report R
describes a T1 hypointense, T2 hyperintense hetero-
geneous mass with irregular contrast enhancement.23
The MRI appearance of splenic hemangiosarcoma
is likely variable due to the mixed amounts of solid/
fluid-filled components with necrotic changes and
various stages of hemorrhage (Fig. 10.14). P
ABDOMINAL LYMPH NODES
• Normal or pathologic lymph nodes are most visible on

STIR or fat saturated T1W post-contrast pulse sequences (b)
due to their hyperintense signal on these sequences and
suppression of the high signal from the perinodal fat Fig. 10.15 Transverse (a) and dorsal (b) T1W post-contrast
(Fig. 10.15).9,13 images with fat saturation in a 6-year-old German Shepherd
• They are also easily seen on T1W spin echo images on Dog with post-surgical inflammatory changes at the
which they appear hypointense surrounded by hyperin- lumbosacral level (after sacral laminectomy). There is reactive
tense fat. They are least visible on T2W fast spin echo lymphadenopathy of the medial iliac (solid arrows, a and b)
images.9 and internal iliac (dotted arrow, a) lymph nodes. The nodes
• Although enlarged abdominal lymph nodes can be read- are enlarged, hyperintense, and homogeneously enhancing
ily identified with abdominal ultrasound, MRI may be but retain smooth margins and normal shape. This dog
useful in cases where metastasis to the lymph nodes also had incidentally a split caudal vena cava (CVC) seen
located deep in the pelvic canal, such as the sacral lymph on each side of the aorta (Ao). The rectum (R) and urinary
nodes, is suspected.24 These nodes may remain unidenti- bladder (UB) are visible, as well as the prostate gland (P).
fied using ultrasound because their location prevents a (1.5T MRI system)
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good acoustic window. Therefore, MRI may be a better heterogeneous contrast enhancement on post-gadolin-
tool than ultrasound for staging of selective cancers such ium T1W images. Cyst-like changes are sometimes seen
as, for example, anal apocrine gland adenocarcinoma.24 within the abnormal lymph node (Fig. 10.16).24 The
• On MRI, metastatic lymph nodes are enlarged, rounded, MRI appearance of a mesenteric lymph node infiltration
with irregular or undulating margins. They have het- with lymphoma was reported,25 and described a large
erogeneous signal intensity on STIR images and lobulated mass that was isointense to the spleen on T1W
images, heterogeneously hyperintense on T2W images,
and with heterogeneous contrast enhancement.
UROGENITAL TRACT
Kidneys and ureters

• The renal shape, size, and structure including the paren-
chyma and collecting system are readily evaluated on
standard T1W and T2W images:
• Renal neoplasia may cause renal enlargement and
Sp mass lesions with alteration of shape and heteroge-
neous signal (Figs. 10.17, 10.18). The MRI appear-
ance of renal neoplasia is not well documented in the
veterinary literature, although there are anecdotal
Fig. 10.16 Basset Hound with cystic metastatic changes reports of identification of renal carcinoma with
in a sacral lymph node (arrows) secondary to anal sac MRI,5 where a heterogeneous left renal mass with
adenocarcinoma. Multiple sublumbar and pelvic canal lymph a cystic component was visible on T1W and T2W
nodes were affected. In this sagittal T2W image the sacral images; an additional T2W hypointense nodule
lymph node parenchyma is hypointense and the central was seen in the contralateral kidney represent-
cystic material hyperintense. The lymph node is severely ing metastatic disease. This metastatic nodule had
enlarged and has a lobulated irregular margin. Sp, spleen. not been identified on ultrasound, presumably due
(1.5T MRI system) to the large size of the dog and gas interposition.
UB
UB
(a) (b)
Fig. 10.17 Dorsal T1W (a) and STIR (b) images in 3-year-old male neutered Domestic Medium-haired cat presented for
dragging the pelvic limbs. A large lobulated mass is present in the caudal aspect of the right kidney (arrows) and was diagnosed
as large-cell lymphoma. The left kidney has an irregular shape and signal pattern likely due to concurrent underlying chronic
renal disease. There was also infiltration of the 6th lumbar vertebra and sublumbar lymph nodes by lymphoma, which was
causing the neurologic signs (not shown). UB, urinary bladder. (1.5T MRI system)
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Fig. 10.18 Renal adenocarcinoma in a Boxer that was

investigated for episodes of hematuria. On abdominal
ultrasonography an ill-defined, distorting mass was evident
in the cranial pole of the right kidney, but the dog’s obesity
K rendered examination difficult. This sagittal T1W post-
contrast image shows the mass as an irregular area of
reduced contrast enhancement (arrow) deforming the
renal margin. Copious, hyperintense abdominal fat is seen
Sp
and chemical shift artifact is visible along the dorsal and
ventral renal margins as thin hypointense and hyperintense
L crescents, respectively. K, kidney; L, liver; Sp, spleen.
(1.5T MRI system)
Sp
Fig. 10.19 Dorsal plane T1W post-contrast image in a

Tibetan Terrier with pyelonephritis showing bilateral,
moderately severe pyelectasia. The dilated renal pelves
(dotted white arrows) are seen as relatively hypointense areas
surrounded by enhancing renal parenchyma, and dilation of
the right ureter is also noted in this image (solid white arrow).
The adrenal glands (dotted black arrows) are visible on each
side of the midline. (1.5T MRI system)
This underscores the benefit of cross-sectional They will appear hypointense on both T1W and T2W
imaging such as MRI in these patients; in the images due to their mineral content (Fig. 10.20).
authors’ experience MRI can outperform ultrasound • Renal hemorrhage may be recognized due to the sus-
in the visualization and delineation of renal neopla- ceptibility artifacts associated with the by-products of
sia in some dogs (Fig. 10.18). hemoglobin, which appear as signal voids on T2*W
• Pyelectasia, as seen with hydronephrosis or pyelone- gradient echo series (Fig. 10.21).
phritis, may be identified as it causes distension of the • Dynamic magnetic resonance nephro-ureterography has
pelvis and diverticula with fluid that is hypointense been reported in dogs, using serial 3D fast gradient echo
on T1W images and hyperintense on T2W images, pulse sequences (such as Fast SPGR or Turbo FLASH)
although signal intensity may be altered depending on acquired in the dorsal plane:
the degree of cellularity and the protein content in the • Series obtained immediately after gadolinium injec-
fluid (Fig. 10.19). tion allow evaluation of the vascular (arterial/renal)
• Nephroliths may cause variably shaped structures phase of the contrast agent distribution (aorta, renal
associated with the pelvic cavities and diverticula. arteries, renal veins, caudal vena cava).26
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Sp
Sp
LK RK LK
Fig. 10.20 Dorsal T2W image in a Miniature Dachshund Fig. 10.21 Abdominal MRI was performed in this
undergoing MRI for lumbar disc extrusion. There is a very Staffordshire Bull Terrier with intermittent hematuria of
large renal calculus (arrow) seen as a well-defined hypointense unknown origin in an attempt to identify a source of bleeding.
mass in the pelvis of the right kidney, found incidentally. In this dorsal plane T2*W gradient echo image, streaks of
Several large uroliths were also present in the bladder signal void are seen in the cranial pole of the right kidney
(see Fig. 10.25). F, gastric fundus; Sp, spleen; LK, left kidney. consistent with prior hemorrhage (arrow), indicating a renal
(1.5T MRI system) source of hematuria. RK, right kidney; LK, left kidney;
Sp, spleen. (1.5T MRI system)
• Excretory phase series obtained minutes after injection These techniques can be particularly useful when renal
allow good anatomic study of the renal morphology/ function is poor, leading to decreased gadolinium renal
structure as well as the ureters. Fat saturation is useful excretion.
to identify the ureters by suppressing the hyperintense
signal from periureteral fat.27 Bladder
• The combined information from the vascular • On T2W images, urine provides a natural contrast out-
and excretory phases can help identify complex lining the hypointense bladder wall mucosa. This can be
vasculo-ureteral anomalies such as retrocaval used to identify bladder wall thickening, irregularities,
ureters or anomalous positions of the large vessels or masses (Fig. 10.24).
(Fig. 10.22).27 • Cystoliths may be identified as intraluminal hypointense
• Using gadolinium-based contrast agents that are structures of variable size and shape in the dependent
eliminated via glomerular filtration with no tubular portion of the urinary bladder and outlined by hyperin-
reabsorption or secretion, researchers have also used tense urine (Fig. 10.25).
dynamic MR nephrography to measure renal func-
tion, as well as provide a morphologic assessment of Genital tract
renal structure.28 • Prostatic, uterine, and ovarian abnormalities such as
• T2W pulse sequences (fast or turbo spin echo) (‘static enlargement, heterogeneous parenchyma, fluid filling,
MR urography’) are a good addition for evaluation of cyst-like changes, and mass lesions can be identified with
conditions that cause renal pelvic and/or ureteral dila- MRI (Figs. 10.26–10.28).
tion or urinomas, as fluid in these structures will appear • MRI can be particularly beneficial in the evaluation of
hyperintense (Fig. 10.23). Fat saturation is useful as the intrapelvic components of prostatic or uterine dis-
it increases the conspicuity of the fluid-filled ureters ease, which may be inaccessible to ultrasound examina-
versus the suppressed signal of the retroperitoneal fat.27 tion (Figs. 10.26, 10.28).
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(a) (b)
Fig. 10.22 Dynamic magnetic resonance nephro-ureterography in an 8-year-old female Bernese Mountain Dog. Dorsal plane
T1W gradient echo image acquired immediately after intravenous contrast medium injection (vascular phase, a) and delayed
dorsal subvolume maximum intensity projection derived from a 3D T1W SPGR (FLASH) acquisition (excretory phase, b). In
(a), the contrast material is still in the aorta (arrowhead) and early venous return from the kidneys is noted in the renal veins
and cranial abdominal portion of the caudal vena cava, while the post-renal caudal vena cava (asterisk, a) is not yet enhanced.
There is evidence of transposition of the caudal vena cava (asterisk, a) on the left side of the aorta. The left renal pelvis and
proximal ureter are dilated with hypointense urine in this early vascular phase image, obtained prior to onset of renal excretion;
the left ureter (arrow) abruptly tapers as it passes dorsal to the transposed caudal vena cava (retrocaval ureter). In (b), the aorta
is visible and does not compress the left ureter; renal excretion of gadolinium is now causing the dilated left renal pelvis and
ureter to appear markedly hyperintense (arrow). Final diagnosis was transposition of the caudal vena cava with retrocaval left
ureter and secondary ureteral obstruction and hydrouretrer/hydronephrosis. (1.0T MRI system; reproduced, with permission,
from Duconseille AC, Louvet A, Lazard P et al. (2010). Imaging diagnosis – left retrocaval ureter and transposition of the
caudal vena cava in a dog. Vet Radiol Ultrasound 51(1):52–6.)
* Fig. 10.23 Parasagittal T2W image in a Chesapeake Bay

Retriever that showed worsening abdominal or lumbar pain
over 2 weeks following an accident in which a log fell onto
RK
his back. There is a large, hyperintense cystic structure
(asterisk) adjacent to, and displacing, the right kidney (RK).
On laparotomy, this was found to be a urinoma (para-ureteral
pseudocyst), which had formed as a result of a tear in the
proximal ureter. (1.5T MRI system)
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UB
Sp
Fig. 10.24 Dorsal plane T2W image of the caudal abdomen Fig. 10.25 Sagittal T2W image in a Miniature Dachshund
and pelvic canal in a Border Collie with pollakiuria and (same dog as in Fig. 10.20) showing several very large
signs of lumbosacral disease. Diffuse, irregular thickening cystoliths as well-defined geometric hypointense structures
of the left bladder wall is evident (arrow), the lesion being contrasting with hyperintense urine. These were found
hypointense and highlighted against hyperintense urine. incidentally during spinal MRI. The uroliths are in contact
Degenerative lumbosacral stenosis was also diagnosed with the dorsal wall of the urinary bladder (UB) as the
(not shown). Final diagnosis was transitional cell carcinoma. dog was in dorsal recumbency for scanning. Sp, spleen.
(1.5T MRI system) (1.5T MRI system)
R
UB
Fig. 10.26 Sagittal fat-suppressed T2W image in a female

English Springer Spaniel with dyschezia, dysuria, and a
large pelvic mass on radiography and ultrasonography.
There is a very large pelvic canal soft tissue mass (arrows) P
displacing and compressing the rectum (R). The mass
appears as an elongated structure comprising multiple,
hypointense nodules: these were also hypointense on T1W Fig. 10.27 Transverse T2W image at the level of the prostate
gland in an intact, male Staffordshire Bull Terrier with
images. UB, urinary bladder, showing flow artifact near the
lumbosacral clinical signs and severe hind end pain. The
ureteric openings. Final diagnosis was vaginal leiomyoma.
prostate remains bilobed but is markedly enlarged and highly
(1.5T MRI system) heterogeneous in architecture. Prostatitis was suspected
but the owners declined further investigation. P, prostate;
R, rectum. (1.5T MRI system)
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size and the large amount of surrounding retroperito-

neal fat; wider receiver bandwidths and smaller pixel size
may therefore be more suitable for MRI of the adrenal
glands, although this is at the cost of some drop in SNR
(see Chapter 1). Fat suppression (with saturation or use
C of inversion recovery) can also be used to eliminate the
signal from fat around the glands and therefore negate
the chemical shift artifact.
P • The classic anatomic landmarks used in ultrasound to
find the glands can also be used in MRI:29
• The adrenal glands are located roughly at the T12 to
L3 level, cranial to the ipsilateral renal vessels.
UB • The right adrenal gland is closely associated with the
caudal vena cava and usually along the dorsal or dor-
solateral surface of that vessel, approximately at the
level of the celiac artery (Fig. 10.2).
• The left adrenal gland is ventrolateral to the aorta,
approximately at the level of the cranial mesenteric
artery (Fig. 10.2).
Fig. 10.28 Sagittal T2W image in an intact, male Bernese • The phrenicoabdominal vessels are inconsistently
Mountain Dog. There is a large paraprostatic cyst (C), seen, especially the ones associated with the right
seen as a well-defined hyperintense structure caudodorsal adrenal gland. The dorsal and sagittal planes are
to an enlarged prostate gland (P). The prostate gland has better to identify these small vessels.
heterogeneous signal intensity, with small hyperintense • The outline of the right adrenal gland may be unclear
structures consistent with cysts and ductal ectasia, suggesting where the gland is in close contact with the caudal
concurrent benign prostatic hyperplasia. UB, urinary bladder. vena cava, especially in dogs with little retroperito-
(1.5T MRI system) neal fat; the craniodorsal aspect of the right adrenal
gland may also be obscured when it comes in contact
ADRENAL GLANDS with the liver parenchyma.
• On standard dorsal/sagittal or oblique planes the
• Although ultrasound is currently the technique of choice entire gland may not be possible to image on a single
to image the adrenal glands, it may be technically chal- slice due to their somewhat oblique orientation to the
lenging in large dogs, especially those with deep-chested long axis of the patient.
conformation. Furthermore, understanding of local ana- • On pulse sequences with no control for breathing
tomic invasion from large adrenal tumors may be dif- motion, the right adrenal gland may be blurred out by
ficult with ultrasound. Cross-sectional imaging such as respiratory motion artifacts due to its close proximity
CT is often used in these circumstances, but abdomi- to the diaphragm.
nal MRI is an alternative; another benefit of MRI is that • In dogs, both adrenal glands are elongated in the cranial
the entire hypothalamic–pituitary–adrenal axis may be to caudal direction (Fig. 10.19), with the right gland hav-
imaged by combining MRI of the brain and abdomen.29 ing a wider cranial pole that has variable shape and the
• Surface coils such as spinal coils may be inadequate, espe- left gland having a typical peanut-shape in the dorsal or
cially in larger patients, due to drop in signal at the level sagittal planes.
of the glands; however, when combined with a body flex • The glands are easy to identify as they are hypointense
coil over the abdomen to improve circumferential signal, to the surrounding retroperitoneal fat, which appears
they provide adequate imaging. Head coils or extremity hyperintense on standard T1W spin echo and T2W fast/
coils generally provide a good result for adrenal gland turbo spin echo pulse sequences. Their signal intensity
MRI, but cannot be used in larger patients.29 relative to other organs varies depending on the pulse
• A combination of transverse and dorsal plane imaging sequence:
is usually adequate to identify the adrenal glands and • T2W images: hyperintense to the liver, iso- or hypoin-
depict their relationship relative to surrounding struc- tense to the spleen, isointense to the renal cortex.
tures including blood vessels, which is important when • T1W images pre-contrast: isointense to hyperintense
assessing invasiveness of adrenal tumors.29 to the liver, spleen, renal cortex.
• Depending on the pixel size and receiver bandwidth, • T1W images post-contrast: hyper- or isointense to
pronounced chemical shift artifact may impair visualiza- the liver, spleen, renal cortex (occasionally hypoin-
tion of the adrenal gland parenchyma due to their small tense to renal cortex).
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CVC *
RK
Sp
LK
Fig. 10.30 Sagittal T2W image in a Labradoodle with a

right adrenal mass. Careful examination of multiple planes
and sequences suggested invasion of the phrenicoabdominal
vein, extending to the lumen of the caudal vena cava.
This small vessel (arrow) is located cranial to part of the
adrenal mass (asterisk). CVC, caudal vena cava; Sp, spleen.
(1.5T MRI system)
Fig. 10.29 Dorsal T1W post-contrast image with fat
saturation in a 12-year-old male castrated mixed breed dog GASTROINTESTINAL TRACT
with underlying pituitary dependent hyperadrenocorticism
that was presented for paraparesis. Physical examination • Ultrasonographic assessment of the gastrointestinal
yielded poor femoral pulses and subjectively cold limbs. tract can be challenging in larger patients and when
MRI revealed an aortic thrombus (see Fig. 10.40). The large amounts of gastrointestinal gas are present. Cross-
adrenal glands (arrows) are enlarged and retain normal sectional imaging such as CT and MRI can provide valu-
shape, suggesting adrenal hyperplasia consistent with able information in these cases.
hyperadrenocorticism, a predisposing factor for thrombosis. • Although CT has been recently evaluated in dogs to
RK, right kidney; LK, left kidney; F, gastric fundus. (1.5T image the abdominal gastrointestinal tract,31,32 no such
MRI system) study has been performed using MRI.
• In people, the main issues with MRI of the gastrointesti-
• A ‘corticomedullary pattern’, with a hyperintense nal tract are motion-related artifacts (peristalsis) and lack
center surrounded by a hypointense rim on both of adequate luminal distension, since poorly distended
T1W and T2W images can also be seen. loops can simulate or hide pathologic processes, espe-
• Adrenal changes including hyperplasia (Fig. 10.29), cially in less experienced hands.33
nodular changes (Fig. 10.13), and adrenal masses • However, MRI combines the advantages of excellent
(Figs. 10.30, 10.31) are readily identified with MRI. soft tissue contrast, non-invasiveness, functional infor-
• Vascular invasion of adrenal tumors can be evaluated mation, and lack of ionizing radiation. Furthermore,
as well (Fig. 10.31). Magnetic resonance angiography recent developments in MRI have led to improved spa-
(MRA, see below) may be useful for that purpose. tial and temporal resolution as well as decreased motion
• The specific appearance of various adrenal tumors has artifacts.33
not yet been reported in the veterinary literature. A case • In people, adequate gastrointestinal distension is typi-
of metastatic pheochromocytoma arising from the left cally achieved by oral ingestion of water-based contrast
adrenal gland was reported. A large lobulated mass material, since it is easy to implement and provides excel-
replaced the left adrenal gland and had heterogeneous lent signal characteristics, resulting in bright lumen on
signal on T2W images.30 However, in the authors’ expe- T2W and dark lumen on T1W images. Tap water is fre-
rience, the MRI signal as well as the level and pattern of quently used, but because it is rapidly reabsorbed in the
enhancement are quite variable. small intestine, leading to a poor distension of the distal
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(a) (b)
Fig. 10.31 Sagittal T2W images in a 12-year-old female

spayed Golden Retriever presented for an inability to walk.
There is a left adrenal gland carcinoma (solid arrows) that
invades into the caudal vena cava (dotted arrows, b and c).
These are consecutive sagittal plane images showing the mass
entering and expanding the lumen of the caudal vena cava.
Wispy striations within the retroperitoneal space represented
(c)
subsequent hemorrhage. (1.5T MRI system)
Lung
Fig. 10.32 Oblique sagittal T2*W gradient echo image in

an English Springer Spaniel with vomiting, lethargy, and
pyrexia and a history of having eaten kebab sticks 2 weeks
previously. A geometric, rectilinear, hypointense structure
Heart of approximately 15 cm length extends from the stomach
through the diaphragm and into the pericardial sac (arrows).
This oblique plane was aligned to demonstrate the entire
foreign body, which was only seen partially in standard planes.
A kebab stick was removed surgically and the dog made a full
recovery. (1.5T MRI system)
jejunum and ileum, it is often mixed with higher osmo- nasogastric tubing. Obviously, the need for anesthesia
lality and viscosity agents. After a 4–6-hour fast, patients would make this procedure potentially riskier due to
are asked to drink between 1,000 mL and 1,500 mL possible regurgitation and aspiration.
of intraluminal contrast agent 45–55 minutes prior to • At this time, the use of MRI for diagnosis of gastroin-
examination. Metoclopramide may be added directly testinal diseases in dogs and cats remains anecdotal, but
to the oral contrast material to promote gastric empty- the authors have identified gastrointestinal disease using
ing.33 This may be challenging to implement in dogs and the technique, including foreign bodies (Fig. 10.32) and
cats, although in selective cases it could be achieved after neoplastic lesions (Figs. 10.33–10.36).
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LK
UB
*
Sp
Fig. 10.33 Sagittal T2W image in a Cocker Spaniel. During

MR imaging for disc extrusion (dotted arrow), a well-defined
mass (solid arrows) was identified, suspected to be intestinal
in origin. Ultrasound confirmed an intestinal origin, and fine
needle aspiration was non-diagnostic. UB, urinary bladder;
Sp, spleen. (1.5T MRI system)
Fig. 10.34 Dorsal plane STIR image of the caudal abdomen in

a Border Collie with lymphoma in the nictitating membrane.
* * During staging with radiography and ultrasonography a cecal

mass was identified, which was examined further with MRI at
the same time as head MRI was performed. This cecal mass
*
was also subsequently confirmed to be due to lymphoma.
Here it is seen as a lobulated hyperintense mass (asterisk)
lying between two loops of small intestine (arrows). LK, left
kidney. (1.5T MRI system)
UB
MAGNETIC RESONANCE ANGIOGRAPHY
Fig. 10.35 Sagittal STIR image of the pelvic canal in a German MRA allows evaluation of the abdominal vasculature using
Shepherd Dog with a submucosal rectal adenocarcinoma both non-contrast-enhanced and contrast-enhanced tech-
(arrows), which is seen as an elongated area of mural infiltration niques, and can therefore be used to diagnose vascular disease
of the dorsal rectal wall with hyperintense signal. The medial such as thrombosis or vascular congenital anomalies such as
iliac lymph nodes are markedly enlarged and of heterogeneous portosystemic shunts or arteriovenous malformations.
signal intensity (black asterisk) and cause ventral displacement
of the colon (white asterisks); this is consistent with metastatic Non-contrast-enhanced techniques
disease. The gas in the colon and rectum appears as a signal • Spontaneous vascular contrast can be obtained without
void. UB, urinary bladder. (1.5T MRI system) injection of gadolinium by exploiting differences in mag-
netization or phase of flowing protons in blood in relation
to stationary tissues. These techniques are respectively
called ‘time-of-flight’ and ‘phase-contrast’ MRA.34–36
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*
*
(a) (b)
(c) (d)
Fig. 10.36 Transverse (a) and sagittal (b) T2W images and transverse T1W post-contrast (c) and sagittal T1W pre-contrast
(d) images of the pelvic canal in 9-year-old female spayed Rottweiler presented for tenesmus and obstipation. Rectal
examination revealed a dorsally located mural or extramural compressive mass. A well-defined, exophytic, smoothly marginated
mass is seen associated with the dorsal wall of the rectum (arrows). The mass has heterogeneous signal on the T2W images
(a and b), homogeneous isointense signal (to the colonic wall) on the T1W pre-contrast image (d) and patchy moderate contrast
enhancement after gadolinium injection (c). The mass is causing attenuation of the colorectal lumen, which appears as a signal
void on the T2W images (asterisks, a and b) due to its air content. Histopathology after surgical removal diagnosed a rectal wall
leiomyoma. (1.5T MRI system)
• A detailed description of the underlying physics of The signal from stationary protons is suppressed by
time-of-flight and phase-contrast MRA is beyond the the use of successive excitation pulses, causing satura-
scope of this textbook, but basic principles are described tion of their magnetization; this is achieved by the use
below: of a repetition time (TR) much shorter than the T1
• Time-of-flight techniques create a differential in the relaxation time of these tissues and a relatively large
amplitude of magnetization between flowing blood flip angle, combined with a rapid radiofrequency pulse
and stationary tissues. The magnetization is manip- repetition rate.37 When subjecting a slice to these sat-
ulated so that protons flowing into the imaged slice uration pulses, the stationary protons are saturated,
have maximum amplitude and generate signal, while but protons in vessels perpendicular to that slice
the stationary protons within the slice have low regularly enter it fully magnetized as they have not
magnetization and their signal is low or suppressed. been subjected to the slice-specific saturation pulses.
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Therefore, they will have a strong magnetization Contrast-enhanced MRA

and generate a high signal when data are collected. • The non-contrast-enhanced MRA techniques described
As these protons in vessels continuously enter the above have limitations, such as problems associated with
slice fully magnetized and then exit the slice and are in-plane saturation, low sensitivity to slow flow, and
replaced by new fresh protons, there is a continuous motion artifacts. For instance, with time-of-flight MRA,
high signal generated within the vessels perpendicu- the multidirectional flow in complex vascular territories
lar to the slice, while the stationary in-plane protons such as the portal venous system or intrathoracic vascu-
are suppressed by the saturation radiofrequency lature requires imaging in both dorsal and transverse
pulses. Pre-saturation pulses placed adjacent to the planes, which lengthens acquisition and makes assess-
slice being imaged can be used to specifically image ment more cumbersome. With phase-contrast MRA,
arteries or veins by suppressing the signal of flow in a inappropriate choice of the maximum expected velocity
given direction. (inadequate strength of the velocity encoding gradient)
• Phase-contrast MRA exploits the differences in ‘phase’ will result in slow flow not being depicted or fast flow
between stationary protons (non-moving tissues) and being aliased.
moving protons (within blood vessels) to highlight • Similar to CT angiography using iodinated contrast
signal from the moving spins and obtain natural vas- agents, it is possible to enhance the signal from blood
cular contrast. Remember from Chapter 1 that the within vessels by injection of gadolinium-based contrast
‘phase’ is a measure of how far the magnetization material and imaging using fast pulse sequences that are
precesses from the time it is flipped into the trans- timed to coincide with the arterial and then the venous
verse plane until the time it is detected. A specific and distribution of the contrast agent.26,38–40
measurable phase can be applied to protons by apply- • Fast imaging sequences of the gradient echo family are
ing a magnetic field gradient of known amplitude used, usually in a 3D acquisition and using short time of
and direction (called ‘velocity encoding gradient’). repetition and time of echo, and a high radiofrequency
If one applies successively two gradients of the same pulse repetition rate to saturate signal from background
strength but opposite directions, the net effect on sta- tissues; a small flip angle is used to maximize detection
tionary protons will be null, because the phase they of flowing blood that has a shortened T1 relaxation time
acquire during the application of the first gradient due to the presence of intravascular gadolinium.37
will be cancelled out by the second. However, moving • Advantages include shorter imaging time compared
protons will retain a net residual phase at the end of with the non-contrast techniques and ability to image
the second gradient. Indeed, because they move, they larger volumes independent of the direction and velocity
experience a different magnitude of the second gra- of blood flow while minimizing artifacts from flow and
dient compared with the first; that phase shift can be dephasing and providing superior vessel lumen depic-
used to calculate the velocity of the moving protons, tion, including of vessels with slow blood flow.37
as described in Chapter 9.1, or the velocity encoded • A few variations of the technique have been described
image can be subtracted from one acquired without in the literature, but the main steps are outlined below:
the velocity encoding gradients to obtain an image • The patient is positioned in dorsal recumbency in the
where signal intensity is proportional to phase and magnet bore.
therefore flow. In 2D phase-contrast MRA, a thick • A torso-array receive-only multi-coil (or any other
slice is encoded with velocity and the resulting flow coil with good signal in all directions of space) is
displayed in white, resembling a projection angio- placed over the vascular area of interest (for example,
gram. In 3D phase-contrast MRA, velocity encoding cranial abdomen for hepatic portal MRA).
is performed in the three directions of space, allowing • A 20G catheter connected to a Y adaptor designed for
one to obtain a 3D map of blood flow that can then be MRA is placed in the cephalic vein.
displayed in the form of maximum intensity projec- • A 3-plane localizer (sagittal, dorsal, transverse) is used
tions (MIPs). to plan the MRA acquisition (2D T2*W gradient echo
• In veterinary medicine, time-of-flight MRA has been sequence).
used to image congenital portosystemic shunts but the • The 3D volume for MRA is prescribed in a plane
technique missed single shunts in about 21% of dogs,36 that will allow it to cover the target vascular territory
and therefore appears less sensitive than contrast- in the fastest time. For example, for hepatic portal
enhanced techniques.38,39 imaging, a dorsal plane is best, positioned to cover as
• Time-of-flight MRA has also been used to diagnose aor- much of the liver as possible in the dorsal to ventral
tic thrombosis in dogs. Complete absence of vascular sig- direction from the confluence of the left hepatic vein
nal or irregular luminal filling defect may be identified with the caudal vena cava cranially to well past the
depending on the size of the thrombus.34,35 splenoportal confluence caudally.39,40
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• For the MRA acquisition, a 3D fast spoiled gradi- the main portal vein and its efferent branches into dif-
ent recalled echo (3D FSPGR) sequence with ellip- ferent liver lobes can be identified.40
tic centric view ordering is used. In this scheme, fast • Identification and accurate description of the anatomy
encoding of the center of k-space is performed in a of extrahepatic and intrahepatic portosytemic shunts,
spiral fashion, which allows acquisition of information as well as arteriovenous malformations, are possible:38,39
on contrast (central region of k-space, see Chapter 1) – Portosystemic shunting vessels are best identi-
in a faster manner. fied at the portal venous phase of the multiphase
• Parallel acquisition can be used to speed up data acqui- acquisition. Careful mapping of the tributaries
sition, thereby allowing coverage of a larger volume to the portal vein using evaluation of MIPs, 3D
within the same imaging time (see “General considera- volume renderings, and source images in the vari-
tions,” earlier). Use of parallel acquisition will require a ous planes allows identification of the anomalous
short calibration of the coils to be done over the target vessel from its origin to its connection with the
volume prior to actual MRA; this only takes seconds. systemic venous system, such as the caudal vena
• ‘Zero filling’ can be used to obtain a larger interpo- cava or the azygos vein. Differentiation between
lated matrix in the frequency encoding direction with intra- and extrahepatic shunts is feasible, as all
additional overlapping interpolated slices along the branches of the portal venous system are identified.
z-axis; the additional slices obtained will smooth out Differentiation can also be achieved by referenc-
review of serial images during diagnostic evaluation. ing the location of the anomalous vessels in rela-
• Immediately before the acquisition, apnea is induced tion to the liver parenchyma (Figs. 10.37–10.39).
using hyperventilation. Apnea can be further improved – Hepatic arteriovenous malformation can be dem-
by curarization (e.g., constant infusion of cisatracurium, onstrated at the arterial phase of the multiphase
later reversed using atropine and neostigmine). study.39 The celiac artery is seen feeding a fine and
• A pre-contrast mask is acquired with the same param- complex network of tortuous vessels in the liver,
eters just prior to the injection of gadolinium. often near the gallbladder, which then commu-
• The 3D contrast-enhanced MRA multiphase sequence nicates with a dilated portal venous branch; early
is initiated immediately at the end of the injection retrograde enhancement of the portal vein during
of gadolinium at a dose of 0.1–0.3 mmol/kg.26,37–40 the arterial phase can be seen, suggesting hepa-
The contrast medium can be injected manually at an tofugal portal flow resulting from portal hyper-
approximate rate of 2.5–3 mL/sec followed by a flush tension caused by the arteriovenous malformation.
of 5 mL of saline, or using an MRI compatible power On sagittal images, an abrupt decrease in size of
injector. the aorta is observed after the origin of the celiac
• Four consecutive 3D volumes are acquired: typically, artery. The celiac artery is also larger than the cra-
one of them will contain information regarding the nial mesenteric artery due to the ‘blood steal’ from
arterial phase of contrast material distribution and the arteriovenous malformation in the liver. At the
another will contain information on the venous phase. portal phase of the multiphase study, complex net-
This alleviates the need to perform a timing-bolus. works of intrahepatic dilated vascular structures
• The best arterial phase and the best venous phase are can be seen, as well as multiple extrahepatic tortu-
identified by reviewing all series of the multiphase ous vessels, especially in the region of the left kid-
acquisition, and then the mask is subtracted from ney, representing acquired portosystemic varices.
these series prior to reconstruction. • Contrast-enhanced MRA can be used to image the renal
• Full volume MIPs are then reconstructed from these vasculature in dogs (see “Kidneys and ureters,” earlier).
subtracted series. From these, sub-volume MIPs This can be useful to identify anomalies such as large
encompassing the vessels of interest can be obtained vessel transposition that can potentially cause ureteral
and optimized to image specific vessels of interest. compression.26
• Individual source images in the dorsal, transverse, • Contrast-enhanced MRA can be used to diagnose aor-
and sagittal planes can and should also be reviewed to tic thrombosis.37 Aortic thrombi are easily demonstrated
assess specific vessels. on dorsal plane images of the abdominal aorta, forming
• There are few reports of the use of contrast-enhanced hypointense filling defects (Fig. 10.40); presence of resid-
MRA to image the abdominal vasculature in dogs. Most ual flow through the thrombosed aorta and the extent and
studies report its use to image the portal vascular system anatomy of collateral vessels can be clearly outlined on
and identify congenital anomalies such as portosystemic contrast-enhanced MRA images. Aortic thrombosis may,
shunts or arteriovenous malformations.38–40 however, also be detected on regular non-angiographic
• Excellent depiction of the portal venous system is images as thrombi may form intraluminal space-occupying
obtained with this technique, and the tributaries to lesions of different signal intensity than normal blood.34
748 CHAPTER 10
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(a)
CVC
Fig. 10.37 Contrast-enhanced MRA in a dog with a left

PV divisional intrahepatic portosystemic shunt. The panel above
V
GD
(a) shows consecutive dorsal plane images acquired at the

portal phase. These are post-contrast images after mask
Sp V subtraction to highlight contrast-enhanced structures. The
left divisional intrahepatic shunt (arrows) is clearly visible
CVC
extending into the left side of the liver and then entering the
left margin of the caudal vena cava close to the diaphragm.
LK The image on the left (b) shows a 3D volume rendering of
the portal vasculature highlighting the shunting vessel in red
Ao
(arrow). CVC, caudal vena cava; GDV, gastroduodenal vein;

PV, portal vein; Sp V, splenic vein; Ao, aorta; LK, left kidney.
(1.5T MRI system)
(b)
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St
(a) (b) (c)
(d) (e) (f)

Ao
CVC
CVC
(g) (h)
Fig. 10.38 Contrast-enhanced MRA in a dog with a right divisional intrahepatic portosystemic shunt. Consecutive dorsal plane
images acquired at the portal phase are presented. These are post-contrast images after mask subtraction to highlight contrast-
enhanced structures. The right divisional intrahepatic shunt (solid arrows, b and d–g) is clearly visible, originating from the
portal vein (dotted arrows, a and b) then extending into the right side of the liver and entering the right margin of the caudal
vena cava close to the diaphragm. Ao, aorta; CVC, caudal vena cava; St, stomach. (1.5T MRI system)
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(a) (b) (c)
(d) (e)
Fig. 10.39 Contrast-enhanced MRA in 7-year-old male neutered Pug in which routine pre-anesthetic bloodwork revealed
elevated liver enzymes, hypoglycemia, and decreased blood urea nitrogen. There is a single congenital extrahepatic porto-
azygos shunt. Consecutive dorsal plane images acquired at the portal phase are presented. The shunting vessel (solid white
arrows) is visible, originating from the portal vein (dotted white arrow, a) then extending dorsally towards the aortic hiatus
ventral to the spine where it enters a vessel immediately adjacent and to the right of the aorta (asterisk, e) corresponding to the
azygos vein. Note on the first image how the portal vein decreases in size (dotted black arrow, a) after the origin of the shunt.
The black solid arrow in (a) indicates the splenic vein. (1.5T MRI system)
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Fig. 10.40 Dorsal T1W post-contrast with fat saturation

image in a 12-year-old male castrated mixed breed dog with
* underlying pituitary dependent hyperadrenocorticism that

was presented for paraparesis (same dog as in Fig. 10.29).
Physical examination yielded poor femoral pulses and
subjectively cold limbs. There are two areas of filling defect
in the lumen of the aorta, one cranial to the left renal
artery and another one at the caudal extremity of the aorta
extending into the external iliac arteries consistent with sites
of thrombosis (dotted arrows). Normal contrast enhancement
of the aortic lumen is noted between these two sites of aortic
thrombosis (asterisk). A large hypointense cyst is seen in the
left kidney (solid arrow). (1.5T MRI system)
REFERENCES 10. Del Chicca F, Schwarz A, Grest P et al. (2016). Perfusion- and
1. Fields EL, Robertson ID, Osborne JA et al. (2012). diffusion-weighted magnetic resonance imaging of the liver of
Comparison of abdominal computed tomography and healthy dogs. Am J Vet Res 77(5):463–70.
abdominal ultrasound in sedated dogs. Vet Radiol Ultrasound 11. Mai W (2008). Pseudolayering artefact on postcontrast
53(5):513–7. magnetic resonance images of the bladder of 18 dogs and
three cats. Vet Rec 163(4):117–9.
2. Manley R, Matthews AR, Morandi F et al. (2013). Magnetic
12. Clifford CA, Pretorius ES, Weisse C et al. (2004). Magnetic
resonance imaging of the canine abdomen: effect of pulse
resonance imaging of focal splenic and hepatic lesions in the
sequence on diagnostic quality. Vet Radiol Ultrasound
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54(3):253–62.
13. Feeney DA, Sharkey LC, Steward SM et al. (2013).
3. Newell SM, Graham JP, Roberts GD et al. (2000).
Parenchymal signal intensity in 3-T body MRI of dogs with
Quantitative magnetic resonance imaging of the normal feline
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14. Chang D, Kim B, Yun Y et al. (2002). Superparamagnetic iron
4. Samii VF, Biller DS, Koblik PD (1999). Magnetic resonance oxide-enhanced magnetic resonance imaging of the liver in
imaging of the normal feline abdomen: an anatomic reference. beagle dogs. Vet Radiol Ultrasound 43(1):37–42.
Vet Radiol Ultrasound 40(5):486–90. 15. Bratton AK, Nykamp SG, Gibson TW et al. (2015). Evaluation
5. Muleya JS, Taura Y, Nakaichi M et al. (1997). Appearance of of hepatic contrast enhancement with a hepatocyte-specific
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using a low field permanent magnet. Vet Radiol Ultrasound healthy dogs. Am J Vet Res 76(3):224–30.
38(6):444–7. 16. Constant C, Hecht S, Craig L et al. (2016). Gadoxetate
6. Glockner JF, Hu HH, Stanley DW et al. (2005). Parallel MR disodium (Gd-EOB-DTPA) contrast enhanced magnetic
imaging: a user’s guide. Radiographics 25(5):1279–97. resonance imaging characteristics of hepatocellular carcinoma
7. Elliott I, Skerritt GC (2010). Handbook of Small Animal MRI, in dogs. Vet Radiol Ultrasound 57(6):594–600.
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8. Westbrook C, Kaut Roth C, Talbot J (2011). MRI in Practice, metastases in dogs using gadobenate dimeglumine-enhanced
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19. Yonetomi D, Kadosawa T, Miyoshi K et al. (2012). Contrast 30. Spall B, Chen AV, Tucker RL et al. (2011). Imaging diagnosis –
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50(1):58–64. of portosystemic shunts in 10 dogs. Vet Radiol Ultrasound
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28. Fonseca-Matheus JM, Perez-Garcia CC, Ginja MM et al. congenital portal vascular anomalies. Vet Radiol Ultrasound
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nephrography in healthy dogs. Vet J 189(3):341–5. 40. Mai W (2009). Multiphase time-resolved contrast-enhanced
29. Llabres-Diaz FJ, Dennis R (2003). Magnetic resonance portal MRA in normal dogs. Vet Radiol Ultrasound 50(1):
imaging of the presumed normal canine adrenal glands. 52–7.
INDEX
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Note: Page numbers in italics refer to figures.
abdominal imaging 723–51 adrenal glands 741–2 arteritis (steroid-responsive meningitis-

adrenal glands 726–7, 741–2 anatomy 726, 737, 741 arteritis) 514, 520
hyperplasia 742 hyperplasia 742 arthritis
neoplasia 734, 742–3 neoplasia 734, 742–3 osteoarthritis
anatomy 725–6, 732 aging changes in the brain 319–23 cervical spine (OA-CSM) 451, 451,
aortic thrombosis 747, 751 atrophy 162, 320, 321, 322, 323 453–4, 454–5, 461, 462–3, 464–5,
biliary tree/pancreatic duct 730–2, 733 cognitive dysfunction syndrome 318–19, 322 466–7
bladder 724–6, 738, 740 maturation in juveniles 318, 319 limbs 663, 675–6
gastrointestinal tract 742–3, 743–4 metabolic changes on MRS 321, 322 septic 682, 682
genital tract 738, 740–1 vascular damage 321, 322–3 articular cartilage
imaging techniques 724–6 white matter abnormalities 269, 320, 322 degeneration 133
contrast-enhanced MRA 61, 746–7 air-cored resistive magnets 153 normal 132, 141, 144
non-contrast-enhanced MRA 744–6 alar ligaments 498, 500 artifacts 70–86
kidney 736–8 Alaskan Husky encephalopathy 176–7, 177 B0 -sensitive banding 81, 82
hemorrhage 737, 738 aliasing (wraparound) artifacts blood flow 73–5, 73, 74
neoplasia 736–7, 736–7 FE direction 41–2, 42 brain imaging 98–102
pyelectasia 737, 737 PE direction 39–40, 39, 79–81, 80 CSF flow 75, 75, 100–1, 101
stones 737, 738 alpha-mannosidosis 173 chemical shift 81–3, 82–3, 124, 571, 741
liver American Staffordshire Terriers (cerebellar coil-related 77–8, 78
liver-specific contrast agents 728–30, cortical abiotrophy) 176, 182 cross-excitation 79
729–32 amyloid 301–2, 320 cross-talk 79, 79
neoplasia 727–8, 727–8 analgesia 108 Gibbs (truncation) 81, 81, 124–5, 125
nodular hyperplasia 726–7, 727 anconeal process 140 injection sites 125, 126
vasculature 729, 732, 747, 748–50 ununited 659, 659 joint imaging 150
lymph nodes 735–6, 735–6 aneurysm 313 low-field systems 154
pancreas 732–3, 732–3 angioendotheliomatosis, malignant magic angle (tendons) 85, 85, 132, 132
spleen 733–5, 734–5 (intravascular lymphoma) 229, 260, 559 magnetic susceptibility see susceptibility
ureters 738, 739 angiography see magnetic resonance artifacts
abducens nerve (CN VI) angiography (MRA) motion-related 70–3, 71–2
anatomy 328, 332 Angiostrongylus vasorum (heartworm) 288 abdomen 724
cavernous sinus syndrome 338–9, 339 annulus fibrosus 416, 421, 421 brain 98–100, 100
abductor pollicis longus tendon 146 anophthalmia 365 heart 688, 713
abscesses aortic thrombosis 747, 751 spine 123–4, 123
brain apparent diffusion coefficient (ADC) thorax 711–14, 711, 713
bacterial 202–3, 202–3, 314, 314 maps 66, 67 partial volume averaging 85–6, 86, 102, 102,
fungal 200, 200 hemorrhagic stroke 286 124
ruptured 204 ischemic stroke 254–7, 254–5, 255–6, 268 phase-cancellation 82–3, 83
masticatory muscle 395–6, 396 arachnoid membrane pulsatility 75–6, 76
orbital 370 intracranial diverticula 242–4, 243, 244 shielding failure 76–7, 77
paraspinal muscle 634, 635, 636–8 spinal 414–15, 584 and signal-to-noise ratio 78
pleural 720–1 diverticula 584–8, 586–7, 600 spinal imaging see spine, artifacts
accessorio-metacarpal ligaments 146 see also subarachnoid space wraparound (aliasing)
accessorio-quartile ligament 146 arrhinencephaly (alobar holoprosencephaly) FE direction 41–2, 42
accessorio-ulnocarpal ligament 146 164 PE direction 39–40, 39, 79–81, 80
accessory nerve (CN XI) 328, 332 arrhythmogenic right ventricular ascending/descending myelomalacia (ADM)
acquisition times 48, 51, 52–3 cardiomyopathy of Boxer dogs 700–1 579, 580–1
and NEX 47 arterial anatomy aspergillosis
parallel imaging 72, 724, 747 brain 264, 266 brain 199, 199
acute hydrated nucleus pulposus extrusion spinal cord 565–6, 566 nasal 353–5, 354
(AHNPE) 424–5, 441–2, 442–3, 624 arterial ectasia (spinal) 503, 504 spine 519
differential diagnosis of spinal cord arterial spin labelling 258 astrocytoma
ischemia 442, 569, 571 arteriovenous malformations (AVMs) brain 217, 219
acute necrotizing myopathy 631 brain 277–8 glioblastoma multiforme 217, 219, 548–9
adhesive shoulder capsulitis 655, 657 liver 747 spinal cord 116, 548, 548–9, 550
754 I n de x
atherosclerosis 254 brain miscellaneous 307

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atlas (C1) abscesses 319–23 multifocal non-traumatic large 289,

atlantoaxial dural bands 501, 501, 599 bacterial 202–3, 202–3, 314, 314 297, 298
atlantoaxial instability 498, 499–500, 500 fungal 200, 200 subarachnoid 302, 303, 311
atlanto-occipital overlapping 501–2, 502 ruptured 204 subdural 302, 304, 305, 305, 311, 311
incomplete ossification 503, 504 aging 318–23 traumatic 300, 303, 310–12, 311–12
occipitoatlantoaxial malformation 502–3 atrophy 162, 320, 321, 322, 323 herniation
atomic structure 3–4 cognitive dysfunction syndrome meningoencephalocele 163, 163,
auditory (Eustachian) tube 401 318–19, 322 351, 352
bulla effusion 338, 383 leukoaraiosis 320 neoplasia mass effect 213, 214, 216,
inflammatory polyps 390 maturation in juveniles 318, 319 218, 226
avascular necrosis of the femoral head 663 metabolic changes on MRS 321, 322 traumatic 313, 313
axis (C2) vascular damage 321, 322–3 hypertensive encephalopathy 277, 278
atlantoaxial dural bands 501, 501, 599 white matter abnormalities 320, 322 imaging techniques 88–102
atlantoaxial instability 498, 499–500, 500 amyloid 301–2, 320 coil selection 89
dorsal angulation of the dens 500, 501 anatomy (vascular) 264, 266, 275, 276 contrast enhancement 97–8, 188, 189,
occipitoatlantoaxial malformation 502–3 artifacts 98–102 212, 257, 257, 261, 265
CSF flow 75, 75, 100–1, 101 DWI see diffusion-weighted
b-value 66 hemorrhage 61, 283–4, 284 imaging (DWI)
B0 -sensitive banding artifacts 81, 82 cerebral blood flow 252, 258–9, 258–9 fast spin echo 92
bacterial infections congenital/developmental disorders 161–8 field strength 89
discospondylitis 114, 508–11, 510 cerebellar aplasia/dysplasia 166, 167 fMRI 95–6
meningoencephalitis 202–4, 202–5, 314, 314 Chiari-like malformation 109, 123, gradient echo/T2*W 92–4, 93
meningomyelitis 513–15 167–8, 168, 596–7 MRA 94, 259, 260
osteomyelitis 409, 512, 512, 679, 682 cystic 241–7, 242–7 MRS 96, 214
rhinitis 355 Dandy–Walker malformation complex optimized protocols 97–8, 254, 310
balanced gradient echo (true FISP/FIESTA) 166–7, 167, 247 patient preparation 89
50, 62, 116–17 Dyke–Davidoff–Masson-like syndrome PWI 95, 252, 253, 257–9, 257, 258–9, 261
ear 380–1, 382 166, 166 SS-FSE 92, 93
heart 691 focal cortical dysplasia 165–6 STIR 91–2, 92
band-pass filtering 42 holoprosencephaly 163–5, 164, 247 T1-FLAIR 55, 57
basivertebral venous canal 417, 420 hydrocephalus 101, 161–3, 162, 163 T1W/T2W/PDW 89–91, 90
Basset Hounds (cervical vertebral arch lissencephaly 165, 165 T2-FLAIR 55, 56, 91, 91, 98, 310, 319
anomaly) 486–8 meningocele/meningoencephalocele 163, ischemia 251–77
Batten disease (neuronal ceroid lipofuscinosis) 163, 351, 352 age of infarction 255, 255–6, 263, 268
175–6, 176 polymicrogyria 165, 166 cerebellar infarcts 95, 253–6, 259–60,
biceps brachii muscle and tendon vascular anomalies 277–9 262, 269
impingement by supraspinatus tendinopathy cranial nerves see cranial nerves classification of stroke 253–4
644, 645–8 cystic lesions 241–9 differential diagnosis 272, 273–4
normal 134–5, 135–6, 141, 141 arachnoid diverticula 242–4, 243–4 extent/severity of damage 252, 253, 257
tendinopathy 649–50, 649–50 choroid plexus cysts 247 global 274–5, 275
biliary tree 730–1, 732, 733 dermoid cysts 244–5, 246 hemorrhagic transformation 263
bilirubin encephalopathy (kernicterus) ependymal cysts 247 imaging techniques 67, 94–5, 252,
178–9, 179 epidermoid cysts 244–5, 245 254–9, 257
black boundary artifacts (chemical shift) 82–3, hydranencephaly 241, 242 lacunar infarcts (acute) 266–71, 269–71
83, 124, 571 lacunae/hydrocephalus ex vacuo 247–8, lacunar infarcts (chronic) 247–8, 248–9,
black-blood cardiac MRI 688–90, 691 248–9, 315 271–2, 321, 322
bladder 725, 738 neoplasms 215, 216, 248 large artery infarcts (acute) 264, 266
post-contrast appearance (pseudolayering) neurocysticercosis 248 large artery infarcts (chronic) 266, 267–8
724–6 porencephaly 241–2, 242 mass effect variability 265
stones 740 Rathke’s cleft cysts 245, 247 pathophysiology 251–2
wall thickening 740 degenerative disorders 176, 181–2, 182 post-traumatic 313
blastomycosis cognitive dysfunction syndrome TIAs 272–4
brain 196–7 318–19, 322 venous thrombosis/infarction 275–7
spine 517–19, 519 hemorrhage 282–307 meningoencephalitis 187–207
block vertebrae 482, 482 age of 282–3, 286, 302 bacterial 202–4, 202–5, 314, 314
blood flow see hemodynamics causes 285 fungal 194–200, 195–201
body warmers (knitted) 108 contusion 312, 312 general appearance 91, 93, 96, 188, 188
Boltzmann constant 8 epidural 306, 306, 311 idiopathic 91, 93, 188, 189–92, 189–93
bone 131–2, 134 extra-axial (general remarks) 302 parasitic 206–7, 207
bone marrow 131–2, 415, 417, 419 imaging techniques 98, 282–7, protozoal 205–6, 206
Boxer dogs (cardiomyopathy) 700–1 284–5, 287 rickettsial 202
brachial plexus 603–15 intraparenchymal neoplastic 289, 295–7 spread from middle ear infections 204,
anatomy 603 intraparenchymal other 288–9, 290–4 205, 386, 387
imaging techniques 127, 603–4 intraparenchymal traumatic 312, 312 viral 192–4, 194–5
lymphoma 559, 607, 610 intraventricular 284, 306–7, 311 metabolic encephalopathies 172–80
neuritis 611–13, 614 location 310 cobalamin deficiency 180
PNSTs 120, 604–5, 605–10 microbleeds 93, 269, 269, 299–302, 299, hepatic 177–8, 178
trauma 613–17, 615–16 301, 323 L-2-hydroxyglutaric aciduria 176, 177
I n de x 755
brain (continued) canine idiopathic eosinophilic flow artifacts 75, 75, 100–1, 101
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hypoglycemic 179 meningoencephalitis 189, 191–2 leakage via a dural tear 628–9
kernicterus 178–9, 179 canine masticatory myositis 396–7, 396 spinal 415, 416, 417, 417, 419
lysosomal storage diseases 172–6, 174–5 canine monocytotropic ehrlichiosis 202 SS-FSE 53, 116
mucopolysaccharidoses 174–5 capsuloligamentous complex 137, 138 syringomyelia 595–8
myelinolysis 180, 181 cardiac imaging 687–708 cerebrovascular disease see brain, hemorrhage;
neuronal ceroid lipofuscinosis 175–6, 176 black-blood technique 688–90, 691 brain, ischemia
polioencephalomyelopathy 176–7, 177 bright-blood technique 690–1, 691, 693 ceroid amyloid angiopathy (CAA) 301–2
thiamine deficiency 179–80, 180 cine mode 691, 692 ceruminous gland neoplasms 390, 391
neoplasia 211–35 cardiomyopathy 697, 699, 700–1 cervical lymph nodes 401
associated pathology 212–13 congenital anomalies 703–4, 708 cervical masses
cholesterol granuloma 224–5, 248 contrast-enhanced techniques carotid body paraganglioma 408–9, 408
choroid plexus 56, 219, 220, 547 MRA 700, 700, 704, 706 thyroid neoplasms 406–7, 406–7
cystic 215, 216, 248 post-contrast images 697, 699, 700–1 cervical spine
diagnostic accuracy of MRI 213–14 hemodynamics anatomy 413–4, 415–16, 447–9, 448
ependymoma 220, 221 4D velocity mapping 697, 704 atlantoaxial joint 498, 499
glial (glioma) 99, 216–19, 218–19, 272, 273 blood flow 693–6, 696–7, 707 congenital malformations
granular cell tumors 229–35, 234–5 ventricular diastole/systole 693, 701 atlantoaxial dural bands 501, 501, 599
hamartoma 222–3 mass/volume measurements 691–3 atlantoaxial instability 498, 499–500, 500
hemangioma/hemangioblastoma 224 mitral insufficiency 691, 704, 707 atlanto-occipital overlapping 501–2, 502
hemorrhagic 289, 295–7, 297, 298 morphology 693, 694–5 atlas incomplete ossification 503, 504
histiocytic sarcoma 229, 233–4 motion artifacts 688, 713 dorsal angulation of the dens 500, 501
intra- vs extra-axial 212 myocardial function (cardiac tagging) occipitoatlantoaxial malformation 502–3
intracranial spread of extracranial lesions 697, 698–9 vertebral arch anomaly 486–8, 488
225, 228–9, 359 neoplasia 701–3, 702–7 disc disease 425–6, 434, 435, 438
lymphoma 229, 232 planes of imaging 688, 689–90, 693, 694–5 compressive AHNPE 441–2, 443
lymphoma, intravascular 229, 260 carotid body 407–8 cervical spondylomyelopathy (CSM) 447–68
meningeal 57, 90, 214–16, 214–17, paraganglioma 408–9, 408 in cranial thoracic region 452
220, 222 carpus–manus disc-associated 450–1, 450, 453, 453, 456
meningioangiomatosis 223–4, 225 foreign bodies 670–1 kinematic MRI 461, 462–3
metastatic disease 229, 230–1, 297, 298 imaging techniques 146–7 dynamic compression 451–2, 452–3
neurocytoma 220 normal 147 kinematic MRI 110, 461, 461–5
olfactory neuroblastoma 228, 228, 333 trauma 670, 671, 674 traction MRI 110, 110, 457–8, 458–60
pituitary 225–7, 226–7 cartilage imaging techniques 110–12, 452–3
PNET/medulloblastoma 220, 222, 223–4 degeneration 133 CT myelography 462–3, 466–7
sellar/suprasellar 227–8, 228 neoplasia DTI with tractography 467, 468
trauma 309–15 limb 680, 681–2 MRI compared with CT 462–3, 466–7
chronic effects 315, 315 spine 529, 531–2 osseous-associated 451, 451, 453–4, 454–5
classification 309–10 normal 132, 141, 421 kinematic MRI 461, 464–5
contusion 312, 312 cataract 366, 366 MRI compared with CT 462–3, 466–7
diffuse axonal injury 313 cauda equina 109, 109, 113, 415 pathophysiology 449–52, 450–1
diffuse cerebral swelling 313 osteochondrosis 497 preclinical 447–9, 449
hemorrhage 300, 303, 310–12, 311–12 see also degenerative lumbosacral stenosis prognosis 465, 467
herniation 313, 313 caudal deep cervical lymph node 401 spinal cord changes 454, 455–6, 457
imaging techniques 310 cavernous malformations (brain) 278–9 synovial cysts 457, 457, 465, 589, 591
infections 203, 314, 314 cavernous sinus syndrome 338–9, 339 chemical fat saturation (spectral fat saturation)
ischemia/infarction 313 cecum 725 66–8, 68, 96, 119, 713
pneumocephalus 288, 314–15, 314 lymphoma 744 contraindication 84, 154
prognostic features 315 celiac artery 126, 422, 422 chemical shift artifacts 81–3, 82–3, 124, 571, 741
vascular lesions 313 central spinal arteries 565 Chiari-like malformation 109, 167–8, 168
vascular anatomy 264, 266, 275, 276 cerebellopontine angle neoplasia 340–1 atlantoaxial dural bands 501
vascular lesions cerebellum demonstration of CSF flow 123
age-related 320, 321 aplasia/dysplasia 166, 167 syringomyelia 168, 596–7, 597, 599, 600
anomalies 277–9 blood supply 266 cholesteatomata (epidermoid cysts)
traumatic 313 cortical abiotrophy 176, 181–2, 182 intracranial 244–5, 245
brainstem 223, 386 Dandy–Walker malformation complex middle ear 386–8, 388–9
bright-blood cardiac MRI 690–1, 691, 693 166–7, 167, 247 nasal 350–1
cine mode 691, 692 herniation through foramen magnum cholesterol granuloma 224–5, 248
butterfly vertebrae 482, 482, 483–4 see Chiari-like malformation chondroid degeneration of intervertebral
infarcts 95, 253–6, 259–60, 262, 269 discs 423
calcaneo-quartile ligament 149 maturation 318 chondroma (spine) 532
calcaneus 148, 149 medulloblastoma 222, 224 chondrosarcoma
calcification (musculoskeletal) 133 cerebral arteries 266 limb 680, 681–2
calculi cerebral blood flow (CBF) 252 spine 529, 531
bladder 740 perfusion imaging 258–9, 258–9 chordoma 560
kidney 737, 738 cerebrospinal fluid (CSF) choroid plexus
canine distemper virus distinguishing from fat 43, 116, 126–7 cysts 247
encephalitis 192–3, 194 FLAIR 55, 122 tumors 56, 219, 220
meningomyelitis 513, 514 flow 123, 595 spinal metastasis 547
756 I n de x
ciliary body 363 spine 481–505 neoplasms 334, 335, 375–6, 375
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tumors 374, 374 craniocervical junction 498–503, neuritis 189, 333–4, 334, 369, 369
circle of Willis 266 499–502 III (oculomotor)
cMRI see cardiac imaging lumbosacral osteochondrosis 121, 473, anatomy 328, 332–3
cobalamin deficiency 180 478, 496–7, 497 neuropathy 94, 334–5, 336
coccidioidomycosis neural tube defects 489–96, 489–92, IV (trochlear) 328, 332
brain 197–8, 198 494, 496 V (trigeminal)
spine 516–17, 518 transitional vertebrae 113, 126, 473, 477, anatomy 328, 329–31, 332
coccyx 485–6, 485 contrast enhancement 333
disc herniation 441 vascular 503, 504, 505 and middle ear effusion 338, 383
hemivertebrae 482 vertebral articular processes dysplasia nerve sheath tumors 228, 336–8, 338
cochlea 332, 381, 382 486, 487 neuropathy 335–6, 337
cognitive dysfunction syndrome 318–19, 322 vertebral body malformations 481–5, VI (abducens) 328, 332
coherent (steady-state) gradient echo 49, 61–2, 482, 483–4 VII (facial)
63–4, 141 vertebral canal stenosis 486–8, 488 anatomy 328, 329, 332, 340, 381
coil artifacts 77–8, 78 contrast enhancement neuropathy 340–1, 340
coil selection abdominal vessels 746–7 VIII (vestibulocochlear)
abdominal imaging 724, 741 adverse reactions 97 anatomy 328, 329, 332
brain imaging 89 angiography 94, 746–7 neuropathy 341, 342
gradient coils 21 abdominal vessels 729, 732 IX (glossopharyngeal) 328, 332
musculoskeletal imaging 134, 139, 143 cardiovascular 700, 700, 704, 706 X (vagus) 328, 332
and SNR 47–8 bladder 724–6 XI (accessory) 328, 332
spinal imaging 110–11, 110 brachial plexus 615–17 XII (hypoglossal) 327, 328, 332
thoracic imaging 710–11 brain 97–8 anatomy 327–33
collateral ligaments ischemia 257, 257, 261, 265 cavernous sinus syndrome 338–9, 339
carpus 146 meningitis 188, 189 imaging techniques 326–7
elbow 139 neoplasia 212 craniocervical junction
stifle 144, 667 cardiovascular system atlantoaxial dural bands 501, 501, 599
tarsus 147 cardiomyopathy 697, 699, 701 atlantoaxial instability 498, 499–500, 500
compensatory hydrocephalus 247–8, 248–9, 315 tumors 701–3, 704, 706 atlanto-occipital overlapping 501–2, 502
computed tomography (CT) vasculature 700, 700 atlas incomplete ossification 503, 504
foreign bodies 356, 401 cartilage degeneration (dGEMRIC) 133 dorsal angulation of the dens 500, 501
head trauma 310 elbow 142 occipitoatlantoaxial malformation 502–3
spine iron oxide particles 728 see also Chiari-like malformation
CSM 462–3, 466–7 liver 728–30, 729–31 craniopharyngioma 228
DLSS 478 low-field systems 156 cribriform plate 348, 349
intervertebral discs 427 pituitary tumors 227 defective, causing meningoencephalocele
neoplasia 527–8 shoulder 138–9 163, 351
trauma 622 spine 117–18 olfactory neuroblastoma 228, 228, 333
vertebral body abnormalities 484 disc disease 429–31, 432–3 cross-excitation artifacts 79
congenital (developmental) conditions dural tears 628 cross-talk artifacts 79, 79
brain 161–8 intrathecal administration of contrast cruciate ligaments 143, 144, 664, 665
cerebellar aplasia/dysplasia 166, 167 agent 123, 615–17, 628 cryptococcosis
Chiari-like malformation 109, 123, neoplasia 117, 117, 528 meningoencephalitis 194–5
167–8, 168, 596–7 stifle joint 145 in cats 196, 197
choroid plexus cysts 247 TIW images 48, 51 in dogs 195–6, 195, 196
Dandy–Walker malformation complex trigeminal nerve 333 meningomyelitis 516, 517, 518
166–7, 167, 247 contrast (signal intensity) 42–5 nasal 355
dermoid cysts 244–5, 246 conus medullaris 414, 419 cystic lesions
Dyke–Davidoff–Masson-like syndrome convulsions, post-ictal changes 272, 274 brain 241–9
166, 166 cor triatriatum dexter 704, 708 arachnoid diverticula 242–4, 243, 244
ependymal cysts 247 coronoid process 142, 142 choroid plexus cysts 247
epidermoid cysts 244–5, 245 fragmented 655–9, 658–9 dermoid cysts 244–5, 246
focal cortical dysplasia 165–6 corpus callosum ependymal cysts 247
holoprosencephaly 163–5, 164, 247 agenesis/dysgenesis 164–5, 164 epidermoid cysts 244–5, 245
hydranencephaly 241, 242 hypoplasia 174, 175 hydranencephaly 241, 242
hydrocephalus 101, 161–3, 162–3 maturation 318 lacunae/hydrocephalus ex vacuo 247–8,
intra-arachnoid diverticula 242–4, 243–4 cortical bone 131 248–9, 315
lissencephaly 165, 165 costs of low-field systems 154 neoplasms 215, 216, 248
meningocele/meningoencephalocele 163, coxofemoral joint 146 neurocysticercosis 248
163, 351, 352 avascular necrosis of the femoral head 663 porencephaly 241–2, 242
polymicrogyria 165, 166 dysplasia 663, 663 Rathke’s cleft cysts 245, 247
porencephaly 241–2, 242 cranial deep cervical lymph node 401 cryptococcal pseudocysts 195–6, 197, 516
Rathke’s cleft cysts 245, 247 cranial mesenteric artery 422, 422 ear (cholesteatoma) 386–8, 388–9
vascular anomalies 277–9 cranial nerves 326–42 lymph node metastases 736
eye 365–6, 365 I (olfactory) 328, 333 nasal
heart/great vessels 703–4, 708, 722 II (optic) dermoid 350, 351
nose 350–1, 351–2 anatomy 328, 331, 333, 363 epidermoid 350–1
orbit 366 indications for MRI 333 nasolacrimal 366
I n de x 757
cystic lesions (continued) cholesteatoma 386–8, 388–9 epidural myelolipoma 536, 536
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spine 584–93 imaging techniques 380 epidural space 415

arachnoid diverticula (intradural) 584–8, inflammatory polyps 388, 390 Ernst angle 60
586–7, 600 neoplasms 390, 391 esophagus 721, 721
articular process joint cysts otitis externa 383–4, 383 esthesioneuroblastoma (olfactory
588–90, 590–1 otitis interna 341, 342, 385–6, 386 neuroblastoma) 228, 228, 333
dermoid sinuses 492, 493–6, 494, 496 otitis media 384–5, 384–5 ethmoidal meningoencephalocele 163, 351, 352
ligamentous/discal 590–3, 592 and the facial nerve 340, 340 ethmoidal turbinates 348, 350
lumbosacral (in DLSS) 476 intracranial spread 204, 205, 386, 387 Eustachian (auditory) tube 401
perineurial (Tarlov) cysts (extradural) and the vestibulocochlear nerve 341 bulla effusion 338, 383
588, 589 and trigeminal nerve disorders 338, 383 inflammatory polyps 390
synovial cysts in CSM 457, 457, 465, 591 tympanic bulla effusion 338, 383 exophthalmos 365
cytotoxic edema 65, 252, 255, 272 ear protection during scans 89 extensor carpi radialis muscle 140
echo planar imaging (EPI) 50, 65 extensor carpi ulnaris muscle and tendon
degenerative lumbosacral stenosis (DLSS) cardiac imaging 691 141, 141
109, 441, 472–3, 473–8, 478, 485 dynamic susceptibility contrast imaging extensor digitorum brevis muscle 149
dementia (cognitive dysfunction syndrome) 257, 257 extensor digitorum communis muscle 140
318–19, 322 see also diffusion-weighted imaging extensor digitorum lateralis muscle 141, 141
dental disease 352, 369, 394 echo time (TE) 17, 43, 45, 48 extensor digitorum longus muscle and tendon
dermoid cysts/sinuses fast spin echo 51–2 145, 147, 149, 149
intracranial 244–5, 246 and SNR 47 extraocular muscles 363
nasal 350, 351 echo-train length 51, 52–3 polymyositis 368–9, 368
spinal 492, 493–6, 494, 496 elbow joint 655–63 extremity coils 111, 143
diamagnetism 4, 102, 283 flexor enthesopathy 660, 661 eye
diaphragm injuries 721, 721 fragmented medial coronoid process anatomy 363, 364
diffuse axonal injury 313 655–9, 658–9 anophthalmia/microphthalmia 365, 365
diffuse idiopathic skeletal hyperostosis (DISH) imaging techniques 139–42, 655 cataract 366, 366
619, 620 planes 139 diagnosis of disease 363–5
diffusion tensor imaging (DTI) 66 incomplete ossification of the humeral endophthalmitis/panophthalmitis
brain 94 condyle 660–3, 662 367–8, 367
spine 123, 467, 468 incongruence 663 granulomatous meningoencephalitis 189,
diffusion-weighted imaging (DWI) 65–6, 66 normal 140–2 334, 369–71
ADC maps 66, 67, 254–7, 254–6, 286 osteochondrosis of the humeral condyle 660 imaging techniques 362–3
hemorrhagic stroke 286 ununited anconeal process 659, 659 neoplasms 373–4, 374, 375
ischemic stroke 67, 94, 95, 252, 253, 254–7, electrocardiography (ECG) 688 persistence of fetal hyaloid system 365–6
254–5, 259 electromagnet types 153 retinal detachment 366–7, 367
age of infarction 255, 255–6, 263 electromagnetism see magnetism trauma 371–3, 373
problems in interpretation 261, 272 empyema see also optic nerve; orbit
spinal 568 intracranial 204
neoplasms 213–14, 260 pleural 720–1 facial nerve (CN VII)
spine 122–3 spinal 509, 510, 511–12, 511 anatomy 328, 329, 332, 340, 381
digastric muscle 395 encephalitis see meningoencephalitis neuropathy 340–1, 340
discospondylitis 114, 508–11, 510 encephalopathy fast gradient echo (TFE/FFE/FLASH) 50, 691
distemper virus degenerative see neurodegenerative fast imaging with steady-state precession (true
encephalitis 192–3, 194 disorders FISP, balanced gradient echo) 50, 62, 116–17
meningomyelitis 513, 514 hypertensive 277, 278 ear 380–1, 382
Dixon method (fat suppression) 155–6 metabolic see metabolic encephalopathies heart 691
dorsal longitudinal ligament 413, 414, 415 endophthalmitis 367–8, 367 fast (turbo) spin echo (FSE/TSE) 51–3, 52
hypertrophy in DLSS 477 enophthalmos 365 brain 92, 93
dorsal recumbency 108, 108 entry slice phenomenon 73, 74–5, 101 heart 690–1, 691
dorsal spinal arteries 565, 566 eosinophilic meningoencephalitis 189, 191–2 single shot (SS-FSE) 53, 92, 116, 417, 423,
dropped jaw syndrome 335–6, 337 ependymal cysts 247 429, 567
dura mater, spinal 415, 584 ependymoma spine 53, 115–16, 116, 417, 423, 429, 429, 567
tears 628–9 brain 220, 221 fat tissue
dural tail sign spinal cord 548, 549 in bone marrow 131–2
coccidioidomycosis (spinal) epidermoid cysts chemical shift artifacts 81–3, 82–3, 124,
516–17, 518 aural 386–8, 388–9 571, 741
meningioma 217, 542, 542–3 intracranial 244–5, 245 epidural 415, 571
dwell time (T S) 41 nasal 350–1 distinguishing from CSF 43, 116, 126–7
Dyke–Davidoff–Masson-like syndrome epidural empyema sterile panniculitis 522, 523
166, 166 intracranial 204 fast spin echo 52
dynamic susceptibility contrast imaging spinal 509, 510, 511–12, 511 fat-containing tumors
257, 257 epidural fat 415, 571 lipoma 535, 535, 715, 716
distinguishing from CSF 43, 116, 126–7 myelolipoma 536, 536
ear 380–92 sterile panniculitis 522, 523 fatty replacement in myocardium 700
anatomy 381 suppression 118–19, 118, 528 muscle infiltration 133
external ear 380 epidural hemorrhage orbital 363
inner ear 332, 381–3, 382 brain 306, 306, 311 suppression
middle ear 381 disc herniation 429, 430–1 brain imaging 90, 96
758 I n de x
fat tissue (continued) foreign bodies glial tumors (glioma) 99, 216
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chemical fat saturation 67–8, 67, 84, carpal/tarsal 670–1 astrocytoma 116, 217, 548
96, 154 imaging methods 356, 401–2 differential diagnosis of stroke 272, 273
Dixon method 155–6 kebab sticks 712, 715, 717, 743 glioblastoma multiforme 217, 219, 548–9
in low-field systems 155–6 metal 101, 402 gliomatosis cerebri/cerebelli 218–19, 548–9
spinal imaging 118–19, 118, 528 nasal 355–6, 356 oligodendroglioma 217, 218, 548, 551, 553
STIR 54, 55, 66, 155 orbital 369, 371 oligodendrogliomatosis 547
fecal incontinence 586 oropharyngeal 101, 401–4, 403 glioblastoma multiforme
feline idiopathic chronic rhinitis 357, 357 paraspinal 634, 637–8 brain 217, 219
feline infectious peritonitis (FIP) 193–4, wood 402–3, 671 spinal cord 548–9
195, 513 forelimb joints see carpus–manus; elbow; gliomatosis cerebri/cerebelli
feline injection site sarcoma (FISS) 639, shoulder brain 218–19
715–17, 718 Fourier transform 19–20, 20, 27, 31 spinal cord 548–9
feline restrictive orbital myofibroblastic sarcoma free induction decay 13–15, 14 global brain ischemia 274–5, 275
(FROMS) 371, 372, 377–8, 377–8 frequency domain (k-space) 24, 28–35, globoid cell leukodystrophy 173, 174
femoral nerve tumors 607, 610, 613 31–4, 37–8 glossopharyngeal nerve (CN IX) 328, 332
femur frequency-encoding (FE) 24–6, 25–6, 29, 29–30 glycoproteinoses 173
avascular necrosis of the femoral head 663 FOV and receiver bandwidth 40–2, 40–41 GM1-gangliosidosis 174, 175
condylar osteochondrosis 667–8, 668 wraparound (aliasing) artifacts 41–2, 42 GM2-gangliosidosis 174
ferromagnetism 4, 102 frozen shoulder (adhesive capsulitis) 655, 657 golf-tee sign 112, 528, 538, 541–3, 547
fibrocartilage 132, 421 fucosidosis 173 gradient echo pulse sequences (GRE) 57–61, 58
fibrocartilaginous embolism (FCE) 442, functional MRI (fMRI) 95–6 balanced (true FISP/FIESTA) 50, 62,
566–9, 568–70 fungal infections 116–17, 691
fibroid degeneration of intervertebral discs 423 meningoencephalitis ear 380–1, 382
fibrosarcoma aspergillosis 199, 199 brain 92–4, 93
mandibular 394 blastomycosis 196–7 bright-blood cardiac MRI 690–1, 691–2
paraspinal 538 coccidioidomycosis 197–8, 198 coherent (steady-state) 49, 61–2, 63–4, 141
thoracic wall 715 cryptococcosis 194–6, 195–7 fast (TFE/FFE/FLASH) 50, 691
fibrosis 133 phaeohyphomycosis 199–200, 200–1 incoherent (spoiled) 49, 62–3, 64
field strength see magnetic field strength meningomyelitis manufacturers’ terminology 49–50
field of view (FOV) 18, 36 aspergillosis 519 spine 120–2
artifacts in large FOVs 78 blastomycosis 517–19, 519 time-reversed 63–5
FE direction 40–2, 40–1 coccidioidomycosis 516–17, 518 gradient nulling (flow compensation) 74,
and k-space 33–5, 37–8, 37 cryptococcosis 516, 517–8 74, 714
PE direction 39–40, 39, 79 histoplasmosis 519 granular cell tumors 229–35, 234–5
rectangular 38–9, 38 nasal granulomatous meningoencephalomyelitis
spinal imaging 114, 119, 452 aspergillosis 353–5, 354 brain 188, 189, 190–1
FLAIR (fluid attenuated inversion recovery) cryptococcosis 355 ocular 189, 334, 369–71
55, 56 osteomyelitis 512 spinal cord 520, 521–2
brain
T1-FLAIR 55, 57 gadobenate dimeglumine contrast agent hamartoma 222–3
T2-FLAIR 55, 56, 91, 91, 310, 319 728–30, 729–31 Hansen classification of intervertebral disc
spine gadolinium contrast agent see contrast disease 423
T1-FLAIR 122, 122 enhancement hardware-related artifacts 76–8, 77–8
T2-FLAIR 122, 587 gadoxetate disodium contrast agent 728–30 HASTE see single shot fast spin echo (SS-FSE);
flexor carpi radialis muscle 139–40, 140 gallbladder 725, 732 T2-myelograms
flexor carpi ulnaris muscle 140, 140, 141 ganglion cysts 589–90 head coils 89
flexor digitorum profundus tendon (carpus) ganglioneuritis head injuries
146, 147 due to disc extrusion 434, 435 nasal 356
flexor digitorum profundus tendon (tarsus) hypertrophic 522–5, 524 orbital fractures 373
149, 149, 672–3 gangliosidoses 173–4, 175 see also trauma, brain
flexor digitorum superficialis muscle (carpus) gastrocnemius muscle and tendon 149, 149 heart see cardiac imaging
140, 140–1 musculotendinopathy 669–70, 669–70 heartworm (Angiostrongylus vasorum) 288
flexor digitorum superficialis tendon (carpus) gastrointestinal tract 742–3 hemangioma/hemangioblastoma
146, 147 kebab stick lodged in 743 brain 224
flexor digitorum superficialis tendon (tarsus) neoplasia 744, 745 spinal cord 548, 549
149, 149 gating techniques 71–2 hemangiosarcoma
flexor enthesopathy of the elbow 660, 661 cardiac 688 brain metastases 230
flip angle (α) 10–11, 47 respiratory 72, 72, 688, 713–14, 724 heart 701, 702
in gradient echo sequences 59–60, 59–60 General Electric scanners 49–50 liver 727–8
flow artifacts genital tract 738 spine 559–60
blood 73–5, 73–4 enlarged prostate 740, 741 metastatic 548, 560
CSF 75, 75, 100–1, 101 vaginal leiomyoma 740 primary 530, 559, 561
phase-encoded (pulsatility) 75–6, 76 germ cell tumors, suprasellar 228 spleen 735, 735
flow compensation (gradient nulling) 74, ghosting artifacts 71, 71 hematoma, spinal 569–70
74, 714 Gibbs artifacts 81, 81, 124–5, 125 subperiosteal 578, 578
FLOW factor 45 glenohumeral ligaments 651–2 hematomyelia (intramedullary hemorrhage)
fMRI (functional MRI) 95–6 lateral 653, 653 573, 573–4, 626
focal cortical dysplasia 165–6 medial 137, 138, 652, 653 hemivertebrae (wedge-shaped) 482, 482, 483, 483
I n de x 759
hemodynamics Hurler syndrome (MPS I) 174–5 compressive disease (non-degenerative,

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4D velocity mapping 697, 704 hydranencephaly 241, 242 AHNPE) 425, 441–2, 443
artifacts of blood flow 73–5, 73–4 hydrocephalus 161–3, 162–3 and CSM 450–1, 450, 453, 453, 456
cardiac blood flow 693–6, 696–7 acquired 161, 212, 220, 222, 315 kinematic MRI 461, 462–3
cerebral blood flow 252, 258–9, 258–9 CSF flow void 101 cysts 591–3, 592
perfusion-weighted imaging 95, 252, 253, hydrocephalus ex vacuo 247–8, 248–9, 315 degeneration (early changes) 417, 419–20,
257–9, 257–9, 261 hydrogen nuclei (protons) 3, 5, 5, 7–8 422, 427
ventricular diastole/systole 693, 701 L-2-hydroxyglutaric aciduria 76, 177 discospondylitis 114, 508–11, 510
hemoglobin 282–3, 286 hypertension in DLSS 473, 473–6
hemorrhage encephalopathy 277, 278 extrusion (typical form) 113, 424, 424–5
age of 282–3, 286, 302, 570 and microbleeds 301–2 foraminal (dorsolateral) extrusion 111, 121,
brain 282–307 hyperthyroidism 407 425–6, 434, 435–6
causes 285 hypertrophic cardiomyopathy (cats) 701 imaging techniques 121, 427
contusion 312, 312 hypertrophic ganglioneuritis 522–5, 524 fat suppression 118, 118
epidural 306, 306, 311 hypertrophic pachymeningitis, idiopathic FOV 114, 119
extra-axial (general) 302 192, 193 plane 111–12, 112
imaging techniques 98, 282–7, hypoglossal nerve (CN XII) 327–8, 332 intradural/intramedullary extrusion 426,
284–5, 287 hypoglycemic encephalopathy 179 434, 437
intraparenchymal neoplastic 289, 295–7 hyponatremia 180 intravertebral herniation (Schmorl’s node)
intraparenchymal other 288–9, 290–4 hypothermia 108 426, 438, 438
intraparenchymal traumatic 312, 312 normal 416, 421, 421
intraventricular 284, 306–7, 311 identity chips 89 protrusion 116, 423–4, 424, 425, 429
location 310 susceptibility artifacts 84, 107, 119, surgical landmarks 111, 422–3, 422, 486
microbleeds 93, 269, 269, 299–302, 299, 119, 124 and vertebral body abnormalities 485
301, 323 idiopathic meningoencephalitis see intracranial hemorrhage see hemorrhage, brain
miscellaneous 307 meningoencephalitis, idiopathic intravoxel dephasing effects 73–4, 74
multifocal non-traumatic large 289, (immune-mediated) inverse Fourier transform 29, 31
297, 298 idiopathic sclerosing orbital pseudotumor 371, inversion recovery (IR) sequences 53, 700
subarachnoid 302, 303, 311 372, 377–8, 377–8 fluid attenuated see FLAIR
subdural 302, 304, 305, 305, 311, 311 idiopathic sterile panniculitis 522, 523, manufacturers’ terminology 49
trauma 300, 303, 310–12, 311–12 634, 638 short tau see STIR
MRI appearance 133, 282–5, 286–7 idiopathic superficial neocortical degeneration iris 363
SWI 284, 287, 571 and atrophy 182 melanoma 375
T2*W 61, 93, 98, 283–4, 284–5, 287 iliopsoas myopathy 631, 633, 678 iron
renal 737, 738 incoherent (spoiled) gradient echo 49, 62–3, 64 in hemoglobin 282–3
spinal 569–78 infarction see also susceptibility artifacts
causes 569 brain see ischemia, brain iron-cored electromagnets 153
epidural 429, 430–1 spinal cord 442, 566–9, 567–570 iron oxide particles (contrast agent) 728
extramedullary 573–5, 576–8, 578, 625–6 inflammation 133 ischemia, brain 251–77
intramedullary 573, 573–4, 626 inflammatory polyps age of infarction 255, 255–6, 263, 268
MRI techniques 121–2, 121, 570–1, 572 ear 388, 390 classification 253–4
trauma 624, 625–6 nose 351–2 differential diagnosis 272, 273–4
susceptibility artifacts 61 inflammatory pseudotumor 525 extent/severity of damage 252, 253, 257
brain 61, 283–4, 284 infraspinatus muscle contracture 650, 651 general features 261–6, 262
spine 121, 429, 430, 570–1, 572, 625–6 infraspinatus tendon 135–7, 135, 651, 652 global 274–5, 275
hepatic encephalopathy 177–8, 178 injection sites hemorrhagic transformation 263
hepatic imaging see liver artifacts 125, 126 imaging methods
hepatocellular carcinoma 729, 730, 732 sarcoma (FISS) 639, 715–17, 718 angiography 259, 260
herringbone artifacts 77, 77 interarcuate (yellow) ligament 414, 415 contrast enhancement 261, 262, 265
high-field systems 89, 119 hypertrophy 450, 488 DWI 67, 94, 95, 252, 253, 254–7, 254–5,
compared with low-field 154, 155–6 intercapital ligaments 414, 414 259, 261
hindlimb joints see coxofemoral joint; stifle internal vertebral venous plexus 415, 417, 418 protocols 254
joint; tarsus–pes interosseous muscles (carpal) 146, 147 PWI 95, 252, 253, 257–9, 257–9, 261
hip see coxofemoral joint interosseous muscles (tarsal) 149 lacunar infarcts (acute) 266–71, 269–71
hippocampus 320 intervertebral discs 421–43 lacunar infarcts (chronic) 247–8, 248–9,
histiocytic sarcoma AHNPE 424–5, 441–2, 442–3, 624 271–2, 321, 322
brain 229, 233–4 bulging 423, 424 large artery infarcts (acute) 264, 266
joints 677, 679 classification of disease 423–6, 426 large artery infarcts (chronic) 266, 267–8
spine 554, 554–6, 556 compressive disease (degenerative) 427–34 mass effect variability 265
histoplasmosis 519 contrast enhancement 429–31, 432–3 pathophysiology 251–2
Hitachi scanners 49–50 correlation of MRI with clinical signs post-traumatic 313
holoprosencephaly 163–5, 164, 247 and prognosis 438–42, 439–40 TIAs 272–4
humerus epidural hemorrhage/inflammation venous thrombosis/infarction 275–7
flexor enthesopathy of the epicondyle 660, 661 429, 430–1 ischemia, spinal cord 442, 566–9, 567–70
incomplete ossification of the condyle post-surgical deterioration 431–2, 433
660–3, 662 SS-FSE imaging 423, 429, 429 jaw 394, 394
osteochondrosis susceptibility artifacts 429, 430, 431–4 dropped jaw syndrome 335–6, 337
of the condyle 660 T2*W imaging 121, 429, 430–1 temporomandibular joint 397, 397
of the head 653–5, 656 typical signs 424, 427–9, 428 see also masticatory muscles
760 I n de x
joints fat suppression 155–6 magnetism 4

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artifacts caused by orthopedic spine 107–8, 154, 156 magnetic moment (spin) 4–5, 5
implants 150 lumbosacral plexus net magnetization (M0) 6–15
effusions 133 anatomy 603 precession 5–6, 6, 9, 24
neoplasia 677, 679 imaging techniques 603 types of magnets 153
septic arthritis 682, 682 PNSTs 604, 605–7, 610–11, 612 magnetization transfer imaging 96–7
see also individual joints sarcoma 610, 613 mandible 394, 394
lumbosacral spine temporomandibular joint 397, 397
k-space (frequency domain) 24, 28–35, 31–4, interpretation of scans 127 mandibular branch of the trigeminal nerve
37–8 myelomeningocele 490 330, 332
kernicterus 178–9, 179 osteochondrosis 121, 473, 478, 496–7, 497 mandibular lymph nodes 400
kidney plane of imaging 112, 114 mandibular salivary gland 398, 398
anatomy 61, 726 positioning for the scan 109–10 masseter muscle 395
hemorrhage 737, 738 stenosis (DLSS) 109, 441, 472–3, 473–8, masticatory muscles
neoplasia 736–7, 736–7 478, 485 anatomy 394–5, 395
pyelectasia 737, 737 transitional vertebrae 473, 477, 485–6, 485 infections/abscesses 395–6, 396
stones 737, 738 lung 710, 720, 720 myositis 396–7, 396
ureters 738, 739 lymph nodes matrix size 18, 37
‘kissing lesions’ 659 abdominal 735–6, 735–6 rectangular images 38–9, 38
Krabbe’s disease (globoid cell leukodystrophy) head and neck 400–1, 402 maxilla 394
173, 174 metastatic disease 402, 720, 736, 736 maxillary branch of the trigeminal nerve
kyphoscoliosis 482, 482, 484–5 thoracic 719–20 330–1, 332
kyphosis 482, 482–3 lymphoma medial collateral ligament
brain 229, 232, 260 elbow 139
lacrimal gland 363 cecum 744 stifle 144, 667
nasolacrimal cysts 366 intravascular 229, 260, 559 tarsus 147
lacunar (small vessel) infarcts kidney 736 medial coronoid process 142, 142
acute 266–71, 269–71 liver 728 fragmented 655–9, 658–9
chronic 247–8, 248–9, 271–2, 321, 322 spine 556–9, 557–8 medial glenohumeral ligament 137, 138,
Larmor equation/frequency 6, 13, 40 brachial plexus infiltration 559, 607, 610 652, 653
laryngopharynx 401 lymphoplasmacytic rhinitis 352–3, 353 medial pterygoid muscle 395
larynx 404, 404 lysosomal storage diseases 172–3 medial retropharyngeal lymph node 400
lateral collateral ligament alpha-mannosidosis 173 mediastinum 717–20
elbow 139 fucosidosis 173 incidentalomas 718
stifle 144, 667 gangliosidoses 173–4, 175 lymph nodes 719–20
tarsus 147 globoid cell leukodystrophy 173, 174 vascular invasion 717, 719
lateral glenohumeral ligament 653, 653 medulloblastoma 222, 224
lateral pterygoid muscle 395 magic angle artifacts 85, 85, 132, 132 melanoma
lateral retropharyngeal lymph node 400–1 magnetic field strength (B0) brain metastases 231
Legg–Perthes–Calvé disease 663 B0 -sensitive banding artifacts 81, 82 ocular 374, 375
leishmaniasis 516 brain imaging 89 meninges 200
lens 363 classification 153 spinal anatomy 414–15, 414, 584, 585
cataract 366, 366 gradients 21–4, 22–3 meningioangiomatosis 223–4, 225, 559
leukoaraiosis 320 low-field imaging 153–6 meningioma
leukoencephalitis, necrotizing 191 and net magnetization 7–9 brain 57, 90, 214–15, 214–15, 216
leukoencephalomyelopathy 181, 619–21, 621 and SNR 46 dural tail sign 217
ligaments 132, 138 spinal imaging 107–8 intraventricular 220, 222
see also individual ligaments and T1/T2 13, 15 optic nerve 334, 335, 375–6, 375
ligamentum flavum (yellow ligament) 414–5 magnetic resonance angiography (MRA) spine 122, 538–42, 542–4
hypertrophy 450, 488 aortic thrombosis 747, 751 meningitis see meningoencephalitis
lipoma brain 94, 259, 260 meningocele 163, 489
spinal 535, 535 cardiac vessels 700, 700, 704, 706 meningoencephalitis 187–207
thoracic wall 715, 716 flow 693–6, 696–7 bacterial 202
liposarcoma 715 contrast-enhanced 94, 700, 700, 704, 706, abscesses 202–3, 202–3, 204, 314, 314
lissencephaly 165, 165 729, 732, 746–7 empyema 204
liver liver/portal vein 729, 732, 747, 748–50 from middle ear infections 204, 205,
neoplasia 727–8, 727–8 phase-contrast technique 693–6, 696, 697, 386, 387
use of liver-specific contrast agents 707, 746 fungal
728–30, 729–32 renal vessels 61 aspergillosis 199, 199
nodular hyperplasia 726–7, 727 spine 122 blastomycosis 196–7
vasculature 729, 732, 747, 748–50 time-of-flight technique 122, 745–6 coccidioidomycosis 197–8, 198
see also hepatic encephalopathy magnetic resonance cholangiopancreatography cryptococcosis 194–6, 195–7
long digital extensor tendon avulsion 668–9 (MRCP) 730–2 phaeohyphomycosis 199–200, 200–1
longitudinal magnetization (M z) 8–9, 11 magnetic resonance nephro-ureterography general appearance 91, 93, 96, 188, 188
longitudinal relaxation time see T1 737–8, 739 idiopathic (immune-mediated)
low-field imaging 153–6 magnetic resonance spectroscopy (MRS) 96, eosinophilic 189, 191–2
advantages and disadvantages 154 214, 321–2 granulomatous 188, 189, 190–1
compared with high-field 155–6 magnetic susceptibility artifacts see granulomatous, ocular form 189, 334,
equipment 153–4 susceptibility artifacts 369–71
I n de x 761
meningoencephalitis (continued) misregistration artifacts nasal cavity

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hypertrophic pachymeningitis 192, 193 chemical shift 81–2, 124, 571, 741 anatomy 348–9, 348–9
necrotizing 190–1, 192 magnetic susceptibility 150 feline 350
unknown etiology 91, 93, 189 mitral valve insufficiency 691, 704, 707 aspergillosis 353–5, 354
parasitic 206–7, 207 motion-related artifacts 70–3, 71–2 bacterial rhinitis 355
protozoal 206 abdomen 724 cryptococcosis 355
neosporosis 205–6 brain 98–100, 100 dermoid cysts/sinuses 350, 351
toxoplasmosis 206 heart 688, 713 diagnosis of disease 350
rickettsial 202 spine 123–4, 123 epidermoid cysts 350–1
viral thorax 711–14, 711, 713 feline idiopathic chronic rhinitis 357, 357
distemper encephalitis 192–3, 194 mucopolysaccharidoses 174 foreign body rhinitis 355–6, 356
feline infectious peritonitis 193–4, 195 MPS I (Hurler syndrome) 174–5 imaging techniques 347–8, 355, 360
meningoencephalocele 163 MPS III (Sanfilippo syndrome inflammatory polyps (feline) 351–2
intranasal 163, 351, 352 type IIIB) 175 lymphoplasmacytic rhinitis 352–3, 353
meningomyelitis 512–22, 571 multilobular tumor of bone 397 meningoencephalocele 163, 351, 352
bacterial 513–15 multiple myeloma 561 nasal cycle 350
fungal multislice acquisition 48, 51, 52–3 neoplasia 357–60, 358–9
aspergillosis 519 artifacts associated with 79, 79 olfactory neuroblastoma 228, 228, 333
blastomycosis 517–19, 519 muscle parasitic rhinitis 355
coccidioidomycosis 516–17, 518 imaging techniques 134, 394, 630–1 sino-orbital rhinitis (feline) 353–5
cryptococcosis 516, 517–18 infections/abscesses traumatic rhinitis 356
histoplasmosis 519 masticatory muscles 395–6, 396 nasal turbinates 348–9, 350
non-infectious paraspinal 634, 635–8 rhinitis 353–4, 357
granulomatous 520, 521–2 myopathy see myopathy/myositis nasolacrimal cysts 366
necrotizing 520 neurogenic atrophy 606–7, 609–10 nasopharynx 401
steroid-responsive meningitis-arteritis normal 132–3, 630 polyps 388, 390
514, 520 see also individual muscles navigator echoes (respiratory gating) 72,
parasitic 520, 521 musculoskeletal imaging 54, 55, 130–50 72, 724
protozoal see also individual tissues and joints neck see entries at cervical
leishmaniasis 516 myelination 318 necrotizing encephalitis 190
neosporosis 515–16 myelinolysis 180, 181 leukoencephalitis 191
toxoplasmosis 515, 515 myelitis see meningomyelitis meningoencephalitis 190–1, 192
viral 513, 514 myelodysplastic syndrome 728 necrotizing meningomyelitis 520
menisci 143–4, 144–5 myelogram effect (T2-myelograms) 53, 116 neoplasia see under specific parts of the body
tears 132, 664–7, 667 arachnoid diverticula 586, 587 neosporosis
meniscofemoral ligament 144, 144 disc injuries 116, 417, 423, 429, 429, brain 205–6, 206
mesenteric artery 126 435, 576 spinal cord 515–16
mesothelioma, pericardial 703, 707 DLSS 474 nephroblastoma, spinal 542–6, 545–7
metabolic encephalopathies 172–80 ischemic myelopathy 567, 569 net magnetization (M0) 6–15
cobalamin deficiency 180 myelomeningocele 492 neural tube defects 489–96
hepatic 177–8, 178 neoplasia 528, 542 dermoid cysts/sinuses
L-2-hydroxyglutaric aciduria 176, 177 myelography 156 intracranial 244–5, 246
hypoglycemic 179 brachial plexus 613 nasal 350, 351
kernicterus 178–9, 179 CSM 462, 463 spinal 492, 493–6, 494, 496
lysosomal storage diseases 172–3 dural tears 628 embryology 489, 489
alpha-mannosidosis 173 intervertebral discs 427 spina bifida 489–93, 490–2
fucosidosis 173 neoplasia 527–8 split cord malformation 493, 494
gangliosidoses 173–4, 175 myelolipoma, epidural 536, 536 neuritis
globoid cell leukodystrophy 173, 174 myelomalacia 571, 578–9, 580–1 brachial plexus 611–13, 614
mucopolysaccharidoses 174–5 myelomeningocele 489–93, 491–2 ganglioneuritis 434, 522–5, 524
myelinolysis 180, 181 myelopathy optic nerve 189, 333–4, 334, 369, 369
neuronal ceroid lipofuscinosis 175–6, 176 degenerative 181, 619–21, 621 neuroaxonal dystrophies 181
polioencephalomyelopathy 176–7, 177 ischemic 442, 566–9, 567–70 neuroblastoma, olfactory 228, 228, 333
thiamine deficiency 179–80, 180 see also cervical spondylomyelopathy neurocysticercosis 248
metal implants causing susceptibility artifacts myopathy/myositis 673, 676–7 neurocytoma 220
84–5 acute necrotizing myopathy 631 neurodegenerative disorders
foreign bodies 101, 402 extraocular polymyositis 368–9, 368 cerebellar cortical abiotrophy 176,
microchips 84, 107, 119, 119, 124 gastrocnemius musculotendinopathy 181–2, 182
orthopedic 84, 107, 150 669–70, 669–70 cognitive dysfunction syndrome
metastatic disease gracilis 677–8 318–19, 322
brain 229, 230–1, 297, 298 iliopsoas 631, 633, 678 idiopathic superficial neocortical
liver 728 infraspinatus contracture 650, 651 degeneration and atrophy 182
lymph nodes 402, 720, 736, 736 masticatory muscle infections 395–6, 396 leukoencephalomyelopathy 181, 619–21, 621
spine 531, 531, 547, 548, 552, 560 paraspinal 630–1, 632 neuroaxonal dystrophies 181
microchips 89 infections 634, 635–8 spongy degeneration 181
susceptibility artifacts 84, 107, 119, myxoma, synovial 532–3, 534, 677 neuronal ceroid lipofuscinosis 175–6, 176
119, 124 myxosarcoma neutrons 4
microphthalmia 365, 365 orbital 376, 377 nodular granulomatous episcleritis 371
middle deep cervical lymph node 401 synovial 532–3, 534 nose see nasal cavity
762 I n de x
nuclear magnetic resonance (NMR) osteochondritis dissecans perforating arteries 267–9

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spectroscopy 5 shoulder 647–8, 653–5, 654–5 perfusion-weighted imaging (PWI) 95

nuclear magnetism 5 tarsus 671–3, 675–6 ischemic stroke 95, 252, 253, 257–9, 257–9, 261
nucleus pulposus 416, 421, 421 osteochondroma 532, 532 pericardial mesothelioma 703, 707
acute extrusion (AHNPE) 424–5, 441–2, osteochondrosarcoma 409 perineurial (Tarlov) cysts (extradural) 588, 589
442–3, 624 osteochondrosis peripheral nerve sheath tumors (PNSTs) 604
differential diagnosis of ischemia 442, elbow (humeral condyle) 660 brachial plexus 120, 604–5, 605–10
569, 571 lumbosacral 121, 473, 478, 496–7, 497 lumbosacral plexus 604, 605–7, 610–612
degeneration 423 shoulder (humeral head) 653–5, 656 spinal cord 535, 537–8, 539–41
number of excitations (NEX) 47, 712 stifle (femoral condyle) 667–8, 668 trigeminal nerve 228, 336–8, 338
nutritional deficiencies tarsus 671–3, 675–6 peripheral primitive neuroectodermal
cobalamin 180 osteomyelitis tumors 536–7
thiamine 179–80, 180 limb 679, 682 peripheral vestibular syndrome 341, 385–6
skull 409 phaeohyphomycosis 199–200, 200–1
occipital dysplasia 501–2 vertebral 512, 512 pharynx 401
occipitoatlantal flexion 109, 109 osteosarcoma foreign bodies 401–4, 403
occipitoatlantoaxial malformation 502–3 jaw 394 nasopharyngeal polyps 388, 390
ocular conditions see eye limb 677–9, 681 neoplasms 404
oculomotor nerve (CN III) spine 529, 529, 531 phase-cancellation artifacts 82–3, 83, 124, 571
anatomy 328, 332–3 otitis externa 383–4, 383 phase-contrast imaging (blood flow) 694–6,
cavernous sinus syndrome 338–9, 339 otitis interna 341, 342, 385–6, 386 696–7, 746
idiopathic neuropathy 94, 334–5, 336 otitis media 384–5, 384–5 phase-encoding (PE) 25, 25, 26–8, 27, 28,
odontoid process (dens), dorsal angulation 500, 501 and the facial nerve 340, 340 29–30, 30
olfactory nerve (CN I) 328, 333 intracranial spread 204, 205, 386, 387 FOV and wraparound artifacts 39–40, 39,
olfactory neuroblastoma 228, 228, 333 and the vestibulocochlear nerve 341 79–81, 80
oligodendroglioma motion artifacts 71, 712, 714
brain 217, 218 palmar carpal fibrocartilage 146 pulsatility artifacts 75–6, 76
spinal cord 548, 551, 553 palmar radiocarpal ligament 146 and SNR 47
oligodendrogliomatosis 547 palmar radiocarpal-metacarpal ligament 146 phase mismapping 70–1
ophthalmic branch of the trigeminal palmar ulnocarpal ligament 146 see also motion-related artifacts
nerve 332–3 pancreas 732–3, 732–3 phase reordering 64, 714
optic nerve (CN II) pancreatitis 733 pheochromocytoma 742
anatomy 328, 331, 333, 363 pancreatic duct 730–1, 732, 733 Philips scanners 49–50
indications for MRI 333 panniculitis, sterile 522, 523, 634, 638 physics of MRI 3–35
neoplasms 334, 335, 375–6, 375 panophthalmitis 367–8, 367 pia mater 414
neuritis 189, 333–4, 334, 369, 369 paraganglioma pituitary tumors 225–7, 226–7
oral cavity 394, 395 cardiac 701 pixels 18, 19, 37
dental disease 352, 369, 394 carotid body 408–9, 408 plane of images 23, 23
foreign bodies 101, 401–4 paraspinal 537 carpus–manus 146
orbit parallel imaging 72, 724, 747 coxofemoral joint 146
anatomy 363, 364 artifacts 77–8, 80 elbow 139
cellulitis 367, 369 paramagnetism 4, 102, 283 heart 688, 689–90, 693, 694–5
abscesses 370 paranasal sinuses 349, 350 nasal cavity 347–8
congenital malformations 366 neoplasms 357–60, 358–9 shoulder 134
diagnosis of disease 365 parasitic infections spine 111–14, 125, 452
extraocular polymyositis 368–9, 368 intraparenchymal hemorrhage stifle joint 143
foreign bodies 369, 371 (A. vasorum) 288 tarsus–pes 147, 148
fractures 373 meningoencephalitis 206–7, 207 plasma cell tumors 560–2, 562
imaging techniques 362–3 meningomyelitis 520, 521 pleural space 720–1, 721
neoplasms 374–6, 375–7 nasal 355 pneumocephalus 288, 314–15, 314
pseudotumor/FROMS 371, 372, 377–8, neurocysticercosis 248 pneumohemothorax 720, 721
377–8 paraspinal soft tissues 119, 630–9 polioencephalomyelopathy 176–7, 177
nodular granulomatous episcleritis 371 DISH 619, 620 polymicrogyria 165, 166
see also eye; optic nerve infections/abscesses 634, 635, 636–8 popliteus muscle tendon 145
orbital fissure 332–3 inflammatory myopathies 630–1, 632 porencephaly 241–2, 242
orbital varix 366 acute necrotizing myopathy 631 porto-azygos shunt 750
orientation of imaging plane see plane of images iliopsoas 631, 633, 678 portosystemic shunt 747, 748–9
oropharynx 401 neoplasia 537, 538, 635, 638–9, 639 positioning the patient for imaging
foreign bodies 401–4, 403 normal 630 brachial plexus 603
neoplasms 404 panniculitis 522, 523, 634, 638 brain 89
orthopedic implants 84, 107, 150 post-surgical complications 635 carpus–manus 146
osmotic demyelination syndrome 180, 181 parathyroid gland 406, 407 coxofemoral joint 146
osteoarthritis parotid gland 398, 398 lumbosacral plexus 603
cervical spine (osseous-associated CSM) parotid lymph node 400 shoulder 134
451, 451, 453–4, 454–5 partial volume averaging artifacts 85–6, 86, spine 108–10
kinematic MRI 461, 464–5 102, 102, 124 cervical traction 110
MRI compared with CT/CT patellar tendon 143, 144 dorsal recumbency 108, 452
myelography 462–3, 466–7 PDW (proton density-weighting) 45, 45, 61, for kinematic MRI 110, 461
limbs 663, 675–6 91, 131 occipitoatlantal flexion 109
I n de x 763
positioning the patient for imaging (continued) bacterial 355 subscapularis tendon injuries 652–3
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stifle joint 142–3 cryptococcosis 355 supraspinatus tendinopathy 644, 644–9

tarsus–pes 147 feline idiopathic chronic rhinitis 357, 357 teres minor tendon injuries 653
thorax 711, 711–12 foreign body 355–6, 356 sialadenitis 398–9, 399
post-ictal changes 272, 274 lymphoplasmacytic 352–3, 353 sialocele 399–400, 400
precession 5–6, 6, 9, 24 parasitic 355 Siemens scanners 49–50
primitive neuroectodermal tumors (PNETs) sino-orbital (feline) 353–5 signal-to-noise ratio (SNR) 46–8
220, 222, 223 traumatic 356 and artifacts 78, 712
medulloblastoma 222, 224 ribs low-field vs high-field 155, 156
peripheral 536–7 identification of 112, 126, 422, 422 single shot fast spin echo (SS-FSE) 53
pronator teres muscle 139 neoplasia 714–5, 716, 717 brain 92, 93
prostate gland, enlarged 740, 741 vestigial 113 spine see T2-myelograms
proton density of tissues (ρ) 42 rickettsial meningoencephalitis 202 sinonasal aspergillosis 353–5, 354
proton density-weighting (PDW) 45, 45, 61, round cell tumors 229 sinonasal neoplasms 357–60, 358, 359
91, 131 sino-orbital aspergillosis 353, 354, 355
protons 3, 5, 5, 7–8 sacral osteochondrosis 121, 473, 478, sinuses 349, 350
protozoal infections 496–7, 497 neoplasms 357–60, 358–9
meningoencephalitis 206 sacrococcygeal disc herniation 441 skull
neosporosis 205–6 salivary glands 398, 398 atlanto-occipital overlapping 501–2, 502
toxoplasmosis 206 neoplasms 400 imaging techniques 92
meningomyelitis sialadenitis 398–9, 399 meningioma 215, 215–16
leishmaniasis 516 sialocele 399–400, 400 osteochondrosarcoma 409
neosporosis 515–16 sampling frequency 41–2, 42 osteomyelitis 409
toxoplasmosis 515, 515 Sanfilippo syndrome type IIIB (MPS III) 175 slice overlap (cross talk) artifacts 79, 79
pseudocysts (cryptococcal) 195, 196, 197, 516 sarcoma slice selection gradients 21–4, 22–3
pseudotumors (FROMS) 371, 372, chondrosarcoma 529, 531, 680, 681–2 slice thickness 23, 24, 37, 114, 711
377–8, 377–8 fibrosarcoma 394, 538, 715 spatial encoding 21–8
Pug dog encephalitis (necrotizing FROMS 371, 372, 377–8, 377–8 see also frequency-encoding (FE); phase-
meningoencephalitis) 190–1, 192 histiocytic 677, 678 encoding (PE)
pulsatility artifacts 75–6, 76 brain 229, 233–4 spatial frequencies 19–21, 24–6, 31
pyelectasia 737, 737 spine 554, 554–6, 556 spatial modulation of magnetization (SPAMM)
pyothorax 720–1 injection site (FISS) 639, 715–17, 718 697, 698–9
liposarcoma 715 spatial presaturation pulses 96
quadrature coils 111, 134 myxosarcoma 376, 377, 532–3, 534 spatial resolution 18, 31, 32, 36–8
quadrigeminal cysts 243–4, 243–4, 598 synovial cell 677 spatial saturation pulses (saturation bands) 75,
see also hemangiosarcoma; osteosarcoma 697, 712
radicular arteries 565 saturation (short TR) 57, 57 spectral attenuated inversion recovery
radiofrequency (RF) coils see coil selection saturation bands (SAT bands) 75, 697, 712 (SPAIR) 68
radiography 401, 622 Schmorl’s node 426, 438, 438 spectral (chemical) fat saturation 66–8, 68, 96,
radiotherapy (for sinonasal neoplasms) 359–60 schwannoma see peripheral nerve sheath tumors 119, 713
radioulnar ligament 146 sciatic nerve PNSTs 605–7, 610–11 contraindication 84, 154
Rathke’s cleft cysts 245, 247 secretin 731 spectral presaturation with inversion recovery
receiver bandwidth (rBW) 40–2, 40–1 seizures, post-ictal changes 272, 274 (SPIR) 68
and SNR 46–8, 46 semicircular canals 381–3, 382 sphingolipidoses 173–4, 174
rectal tumors 744, 745 septic arthritis 682, 682 spike artifacts 77, 77
red bone marrow 131 shielding-related artifacts 76–7, 77 spin 4–5, 5
relaxation times 11–15, 12–14, 17 short intercarpal ligament 146 spin-up and spin-down states 7–8, 7, 9
hemorrhagic lesions 283, 284 short radial collateral ligament 146 spin angular momentum 5–6, 6
and image weighting 42–5 short tau inversion recovery (STIR) 54–5, 54–5 spin echo pulse sequences 15–17, 16, 18, 48–57
musculoskeletal tissues 131, 133 abdomen 724 black-blood cardiac MRI 688–90, 691
see also T1-weighting (T1W); T2-weighting bone 134 brain imaging 89–92
(T2W); T2*-weighting (T2*W) brain 91–2, 92 fast/turbo 51–3, 52, 92, 93, 690–1, 691
renal imaging see kidney in low-field systems 155 inversion recovery 53, 700
repetition time (TR) 17–18, 43, 44, 45, 48, peripheral nerves 603 see also FLAIR; STIR
56–7, 57 spine 119–20, 423 manufacturers’ terminology 49
gradient echo sequences 59–60 thorax 711 single shot (ultrafast) 53, 92, 116, 116, 417,
and SNR 47 short ulnar collateral ligament 146 423, 429, 429, 567
resonance frequency 9 shoulder joint 644–55 standard form 28, 43, 48–51, 51
respiratory motion artifacts 71, 72, 688, adhesive capsulitis 655, 657 spin-lattice (longitudinal) relaxation 11
713–14, 724 biceps tendinopathy 649–50, 649, 650 spin-spin (transverse) relaxation 11
navigator echoes 72, 72, 724 glenohumeral ligament injuries 651–2, spina bifida 489–93, 490–2
positioning 711, 712 653, 653 spinal cord
pseudotriggering 714 imaging techniques 134–8, 644 anatomy 414, 414, 448, 565–6, 566
retinal detachment 366, 367, 367 planes 134 CSM 454, 455–6, 457
retropharyngeal lymph nodes 400–1 infraspinatus muscle contracture 650, 651 degenerative diseases 619–21, 621
rewinding gradient 62, 64 infraspinatus tendon injuries 651, 652 hemorrhage 569–78, 572, 573–4, 576–8, 624,
RF interference 77, 77 normal 135–8 625–6
rhinitis osteochondrosis/osteochondritis dissecans ischemia 442, 566–9, 567–570
aspergillosis 353–5, 354 647–8, 653–5, 654–6 myelomalacia 570, 578–9, 580–1
764 I n de x
spinal cord (continued) epidural empyema 509, 510, 511–12, 511 in dogs 529, 548–9, 556–9
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neoplasia 116, 117, 529, 547–50, 551–3 ganglioneuritis ependymoma 548, 549
spinal cord-to-vertebral canal diameter ratio due to disc extrusion 434 extradural 528, 528, 529–37
414, 420 hypertrophic 522–5, 524 gliomatosis cerebri 548, 549
split cord malformation 493, 494 hemorrhage 569–78 hemangioma/hemangioblastoma 548, 549
trauma 625–8 causes 569 hemangiosarcoma 530, 548,
see also cervical spondylomyelopathy; epidural 429, 430–1 559–60, 560–1
meningomyelitis; syringomyelia extramedullary 573–5, 576–8, 578, 625–6 histiocytic sarcoma 554, 554–6, 556
spinal nerve roots 127 intramedullary 573, 573–4, 626 imaging techniques 117, 528–9
anatomy 113, 415, 419, 584 MRI techniques 121–2, 121, 570–1, 572 intradural–extramedullary 528, 528, 529,
ganglioneuritis trauma 624, 625–6 537–47
due to disc extrusion 434, 435 imaging techniques 107–27 intramedullary 116, 528, 529, 547–50,
hypertrophic 522–5, 524 angiography 122 551–3
nerve sheath tumors 537 coil selection 110–11, 110 lipoma 535, 535
swollen (in DLSS) 475–6 contrast-enhanced MRI 117–18, 123, lymphoma 556–9, 557–8, 607, 610
see also brachial plexus; lumbosacral plexus 429–31, 615–17, 628 meningioangiomatosis 559
spine for CSF flow 123 meningioma 122, 538–42, 542–4
anatomy 413–15, 414–17, 417, 418–20 CSF vs epidural fat 43, 116, 126–7 metastatic 531, 531, 547, 548, 552, 560
atlantoaxial joint 498, 499 for CSM 110, 112, 452–3, 462–3, 467 myelolipoma (epidural) 536, 536
intervertebral discs 416, 421, 421 CT 427, 462–3, 527–8, 622 nephroblastoma 542–6, 545–7
meninges 414–15, 414, 584, 585 for disc pathology 427 oligodendroglioma 548, 551, 553
vascular anatomy 565–6, 566 DWI/DTI 122–3, 467, 468 oligodendrogliomatosis 547
artifacts 123–5 fat suppression 118–19, 118, 528 osteochondroma 532, 533
chemical shift 82, 83, 124, 571 FOV 114, 119, 452 osteosarcoma 529, 529, 531
coil-related 78, 78 gradient echo 120–2 in the paraspinal soft tissues 537, 538,
Gibbs 81, 81, 124–5, 125 for hemorrhage 121–2, 121, 570–1, 572 635, 638–9, 639
injection sites 125, 126 indications/contraindications for MRI peripheral PNETs 536–7
susceptibility, hemorrhage 121, 429, 460, 107, 413 plasma cell tumors 560–2, 562
570–1, 572, 625–6 interpretation 126–7 PNSTs 535, 537–8, 539–41
susceptibility, metallic/microchips 84, intrathecal contrast 123, 615–17, 628 synovial myxoma/myxosarcoma
107, 119, 119, 124, 124, 431–4 low-field systems 107–8, 154, 156 532–3, 534
cervical spondylomyelopathy see cervical myelography 156, 427, 462, 463, 527–8, osteomyelitis 512, 512
spondylomyelopathy 613, 628 panniculitis (sterile) 522, 523, 634, 638
congenital/developmental disorders 481–505 for neoplasia 117, 527–8 paraspinal soft tissues see paraspinal soft
craniocervical junction 498–503, optimized protocols 114–15, 422–3, 452 tissues
499–502 patient preparation and positioning spondylitis 114, 508–11, 510
lumbosacral osteochondrosis 121, 473, 108–10, 108–110, 452, 461 surgical landmarks 111, 126, 422–3, 422, 486
478, 496–7, 497 plane of imaging 111–14, 125, 452 syringomyelia 500, 595–600, 596, 598–600
neural tube defects 489–96, 489–92, scout images 115 Chiari-like malformation 168, 596–7,
494, 496 SS-FSE see T2-myelograms 597, 599–600
transitional vertebrae 113, 126, 473, 477, STIR 119–20, 423 intracranial causes 212, 214, 216, 218
485–6, 485 T1-FLAIR 122, 122 trauma 113, 622–9
vascular 503, 504, 505 T1-weighting 116, 415 bony injuries 622–3, 624–8
vertebral articular processes dysplasia T1/T2 combined weighting 116–17 disc herniation 424–5, 428, 430, 441–2,
486, 487 T2-FLAIR 122, 587 442–3, 623–5, 624
vertebral body malformations T2-weighting 115–16, 415, 417, 422–3 dural tears 628–9
481–5, 482–4 T2*-weighting 121–2, 429, 430, 431, 571 hemorrhage 624, 625–6
vertebral canal stenosis 486–8, 488 for trauma 622–3, 628 ligamentous injuries 623, 626, 628
cyst-like lesions 584–93 see also spine, artifacts spinal cord parenchymal lesions 626–8
arachnoid diverticula (intradural) 584–8, inflammatory pseudotumor 525 spirocercosis 520, 521
586–7, 600 intervertebral discs see intervertebral discs spleen
articular process joint cysts 588–90, ischemic myelopathy 442, 566–9, 567–70 nodular lesions 733–4, 734
590–1 meningomyelitis 512–22, 571 tumors 734–5, 735
cervical synovial cysts in CSM 457, 457, bacterial 513–15 spoiled (incoherent) gradient echo 49, 62–3, 64
465, 589, 591 fungal 516–19, 517–19 spondylitis 114, 508–11, 510
ligamentous/discal 590–3, 592 non-infectious 514, 520, 521–2 spondylomyelopathy, cervical (CSM) 447–68
perineurial (Tarlov) cysts (extradural) parasitic 520, 521 in cranial thoracic region 452
588, 589 protozoal 515–16, 515 disc-associated 450–1, 450, 453, 453, 456
degenerative diseases 618–21 viral 513, 514 kinematic MRI 461, 462–3
DISH 619, 620 myelomalacia 571, 578–9, 580–1 dynamic compression 451–2, 452–3
leukoencephalomyelopathy 619–21, 621 neoplasia 527–62 kinematic MRI 110, 461, 461, 462, 463–5
lumbosacral stenosis 109, 472–3, 473–8, astrocytoma/glioblastoma multiforme traction MRI 110, 110, 457–8, 458–60
478, 485 116, 548–9, 550 imaging techniques 110, 112, 452–3
myelopathy 619 in cats 529, 548, 550, 556, 559 DTI with tractography 467, 468
spondylosis deformans 473, 474–5, 477, chondroma 532 myelography and CT myelography
483, 618–19, 618, 620 chondrosarcoma 529, 531 462–3, 466–7
see also intervertebral discs, compressive chordoma 560 osseous-associated 451, 451, 453–4, 454–5
disease (degenerative) choroid plexus metastases 547 kinematic MRI 461, 464–5
discospondylitis 114, 508–11, 510 classification 528–9 MRI compared with CT 462–3, 466–7
I n de x 765
spondylomyelopathy, cervical (CSM) (continued) synovial cell sarcoma 677 tarsus–pes

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pathophysiology 449–52, 450–1 synovial cysts foreign bodies 670–1

preclinical 447–9, 449 articular process joint 588–90, 590–1 imaging techniques 147–50
prognosis 465, 467 cervical (in CSM) 457, 457, 465, 589, 591 planes 148
spinal cord changes 454, 455–6, 457 lumbosacral (in DLSS) 476 normal 147–9
synovial cysts 457, 457, 465, 589, 591 synovial myxoma/myxosarcoma 532–3, 534, 677 osteochondrosis/osteochondritis dissecans
spondylosis deformans 483, 618–19, 618, 620 synovium/synovial fluid, normal 133, 417, 420 671–3, 675–6
lumbosacral 473, 474–5, 477 syringomyelia 595–600 trauma 670, 672–3
spongy degeneration (white matter appearance 596, 598–9 tattoos 89
diseases) 181 Chiari-like malformation 168, 596–7, 597, tau protein hyperphosphorylation 320
squamous cell carcinoma 390 599–600 TE (echo time) 17, 43, 45, 48
steady-state (coherent) gradient echo 49, 61–2, intracranial causes 212, 214, 216, 218 fast spin echo 51–2
63–4, 141 other causes 500, 598, 598–600 and SNR 47
steady-state free precession (SSFP) 50, 328 pathophysiology 595–8 temporal muscle 395
steroid-responsive meningitis-arteritis 514, 520 significance of lesion size 599 temporomandibular joint 397, 397
stifle joint 663–70 tendons 132, 138
collateral ligament injuries 667 T1 (longitudinal relaxation time) 11, 12–13, magic angle artifacts 85, 85, 132, 132
cruciate ligament injuries 664, 665 12, 42–3 see also individual tendons
gastrocnemius musculotendinopathy hemorrhagic lesions 283, 284 tensor veli palatini muscle 338, 383
669–70, 669 musculoskeletal tissues 131, 133 teres minor muscle and tendon 137, 653
imaging techniques 142–6, 663–4 T1-FLAIR Tesla (T) 4
planes 143 brain 55, 57 thecal sac 419
long digital extensor tendon avulsion 668–9 spine 122, 122 thiamine deficiency 179–80, 180
meniscal tears 664–7, 667 T1-weighting (T1W) 42–3, 44, 45, 48 thoracic imaging 710–22
normal 144, 145 abdomen 724 diaphragm 721, 721
osteochondrosis 667–8, 668 brain 89, 98, 319 esophagus 721, 721
stimulated echo 62, 63 with contrast agent 48, 51 heart see cardiac imaging
striate arteries 267, 269 eye/orbit 363 imaging techniques 710–11
stroke hemorrhage 284–5, 285–6, 287 lung 710, 720, 720
hemorrhagic see hemorrhage, brain; musculoskeletal tissues 131 mediastinum 717–20
hemorrhage, spinal spine 116, 415 incidentalomas 718
ischemic see ischemia, brain; ischemia, T1/T2 combined weighting 116–17 lymph nodes 719–20
spinal cord T2 (transverse relaxation time) 12, 12, vascular invasion 717, 719
subarachnoid hemorrhage 13, 17, 42–3 motion artifacts 711–14, 711, 713
brain 302, 303, 311 hemorrhagic lesions 283, 284 heart 688, 713
spinal cord 573–5, 576 musculoskeletal tissues 131, 133 oil capsule marking position of lesion 711
subarachnoid space (spinal) 415, 416 T2* 15 patient position 711, 711
CSF flow 595 T2-FLAIR pleural space 720–1, 721
golf-tee sign 112, 528, 538, 541–3, 547 brain 55, 56, 91, 91, 98, 310, 319 thoracic wall 714–17
meningioma 541, 542–3 spine 122, 587 FISS 639, 715–17, 718
nephroblastoma 545 T2-myelograms (SS-FSE/HASTE) 53, 116 foreign bodies 712, 715, 717
PNST 538, 539–41 arachnoid diverticula 586, 587 neoplasms 715, 715–16
subdural hemorrhage disc injuries 116, 417, 423, 429, 429, vascular ring anomaly 722
brain 302, 304, 305, 305, 311, 311 435, 576 thoracic vertebral canal stenosis 486–7
spinal cord 573–5, 576 DLSS 474 thoracolumbar spine
subdural space (spinal) 415, 574–5 ischemic myelopathy 567, 569 disc disease 422, 426, 438–40, 439–40
sublingual salivary glands 398, 399 myelomeningocele 492 surgical landmarks 111, 126, 422, 422, 486
subperiosteal hematoma 578, 578 neoplasia 528, 542 transitional vertebrae 113, 126
subscapularis muscle and tendon 137, T2-weighting (T2W) 17, 43, 44, 45, 48 thromboembolism
137, 652–3 abdomen 724 abdominal aorta 747, 751
superficial cervical lymph nodes 401 brain 89–90, 98, 319 cerebral veins 275–7
superparamagnetism 4, 283 hemorrhage 283–4, 284, 285, thyroid gland
supracollicular fluid accumulations 285, 286– 7 adenoma 407, 407, 408
(quadrigeminal cysts) 243–4, 243–4, 598 eye/orbit 363 anatomy 404–6, 405
suprasellar tumors 227–8, 228 musculoskeletal tissues 131, 133 carcinoma (dog) 406–7, 406
supraspinatus tendon spine 115–16, 415, 417, 422–3 hyperthyroidism 407
normal 135, 135, 136 time-reversed gradient echo 63–5 tibialis cranialis muscle and tendon 147
tendinopathy 644, 644, 645–9 T2*-weighting (T2*W) 15, 60–1 time of flight (TOF) effects 73, 73, 75
susceptibility artifacts 83–5, 83, 101–2 brain hemorrhage 61, 93, 98, 283–4, 284–5, MRA 122, 745–6
foreign bodies 101, 402, 404 286, 287 time-reversed gradient echo 63–5
hemorrhage 61 ligaments and tendons 138 tooth disease 352, 369, 394
brain 61, 283–4, 284 spine 121–2, 429, 430–1, 571 Toshiba scanners 49–50
spine 121, 429, 430, 570–1, 572, 625–6 Taenia solium cysts 248 toxoplasmosis
metallic 84–5, 101, 107, 119, 124, 431–4 tail brain 206
microchips 84, 107, 119, 119, 124 disc herniation 441 spinal cord 515, 515
orthopedic implants 84, 107, 150 screw tail 482, 483 TR (repetition time) 17–18, 43, 44, 45,
in TSE/FSE sequences 52 talus 148, 149 48, 56–7, 57
susceptibility-weighted imaging (SWI) tapeworm cysts 248 gradient echo sequences 59–60
284, 287, 571 Tarlov (perineurial) cysts 588, 589 and SNR 47
766 I n de x
transient ischemic attacks (TIAs) 272–4 ulna 141–2, 141–2 histiocytic sarcoma 554
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transverse ligament of the stifle 145 fragmented medial coronoid process 655–9, lymphoma 558–9
transverse magnetization (M xy) 8, 9, 11, 14–15 658–9 metastatic 531, 531
transverse relaxation time see T2 ununited anconeal process 659, 659 osteochondroma 532, 532
trauma ultrasound, ventricular enlargement 161–2 osteosarcoma 529, 529, 531
brachial plexus 613–17, 615–16 ureters 738, 739 osteomyelitis 512, 512
brain 309–15 urinary incontinence 505 trauma 622–3
chronic effects 315, 315 urinary system see bladder; kidney fractures 624–5, 626
classification 309–10 urinoma 739 subluxation 113, 626–8
contusion 312, 312 vertebral canal 414
diffuse axonal injury 313 vaginal leiomyoma 740 spinal cord-to-vertebral canal diameter ratio
diffuse cerebral swelling 313 vagus nerve (CN X) 328, 332 414, 420
hemorrhage 300, 303, 310–12, 311–12 vascular flow artifacts 73–5, 73–4 stenosis
herniation 313, 313 vascular ring anomaly 722 cervical vertebral arch anomaly
imaging techniques 310 vasogenic edema 213, 228, 252, 277, 278, 573 486–8, 488
infections 203, 314, 314 velocity-encoding value (V ENC) 696 cranial thoracic 486–7
ischemia/infarction 313 venous anatomy and CSM 448–52, 450, 451
pneumocephalus 314–15, 314 brain 275, 276 DLSS 109, 441, 472–3, 473–8, 478, 485
prognostic features 315 hepatic 729, 732, 747, 748–50 vestibulocochlear nerve (CN VIII)
vascular lesions 313 spine 415, 417, 418, 420, 566, 566 anatomy 328, 329, 332
carpus 670, 671, 674 venous malformations neuropathy 341, 342
diaphragm 721, 721 brain 277–9 viral meningoencephalitis
eye/orbit 371–3, 373 orbital varix 366 canine distemper 192–3, 194
nasal 356 spine 505 feline infectious peritonitis 193–4, 195
spine 113, 622–9 venous thrombosis, cerebral 275–7 viral meningomyelitis 513, 514
bony injuries 622–3, 624–8 ventral internal vertebral venous plexus vision, loss of 333–4, 334
disc herniation 424–5, 428, 430, 441–2, 566, 566 vitamin deficiencies
442–3, 623–5, 624 ventral longitudinal ligament 414, 414, 415 cobalamin 180
dural tears 628–9 ventral spinal artery 565, 566 thiamine 179–80, 180
hemorrhage 624, 625–6 ventricles, brain volume interpolated gradient recalled echo 50
ligamentous injuries 623, 626, 628 age-related changes 162, 321, 323 voxels 18, 19, 37, 46
spinal cord parenchymal lesions 626–8 blastomycosis 197 intravoxel dephasing effects 73–4, 74
tarsus 670, 672–3 distension (hydrocephalus) 101,
tendon avulsions 161–3, 162–3 water 13
long digital extensor 668–9 acquired 161, 212, 220, 222, 315 wedge-shaped vertebrae (hemivertebrae) 482,
triceps 660 intraventricular arachnoid diverticula 482, 483, 483
triceps tendon 139, 140, 660 243–4, 243–4, 598 white matter
trigeminal nerve (CN V) intraventricular hemorrhage 284, 306–7, 311 age-related changes 269, 320, 322
anatomy 328, 329–31, 332 tumors imaging 90, 91, 94
contrast enhancement 333 choroid plexus 56, 219, 220 leukoencephalomyelopathy 181,
and middle ear effusion 338, 383 ependymoma 220, 221 619–21, 621
nerve sheath tumors 228, 336–8, 338 meningioma 220, 222 necrotizing leukoencephalitis 191
neuropathy (idiopathic) 335–6, 337 neurocytoma 220 spongy degeneration 181
trochlear nerve (CN IV) ventricles, heart see cardiac imaging see also metabolic encephalopathies
anatomy 328, 332 vertebrae whole body protocols 711
cavernous sinus syndrome 338–9, 339 articular process joint cysts 588–90, 590–1 wobbler syndrome see cervical
truncation (Gibbs) artifacts 81, 81, 124–5, 125 bone spurs (spondylitis deformans) 473, spondylomyelopathy
tumors see neoplasia under specific parts of 474–5, 477, 483, 618–19, 618, 620 wraparound (aliasing) artifacts
the body congenital malformations FE direction 41–2, 42
turbo (fast) spin echo (TSE/FSE) 51–3, 52 dysplasia of the articular processes PE direction 39–40, 39, 79–81, 80
brain 92, 93 486, 487
heart 690–1, 691 transitional vertebrae 113, 126, 473, 477, X-rays 401, 622
single shot (SS-FSE) 53, 92, 116, 417, 423, 485–6, 485
429, 567 vertebral body abnormalities 481–5, yellow bone marrow 131–2
spine 53, 115–16, 116, 417, 423, 429, 482–4 yellow (interarcuate) ligament 414 –15
429, 567 vertebral canal stenosis 486–8, 488 hypertrophy 450, 488
tympanic bulla 381 discospondylitis 114, 508–11, 510
cholesteatoma 387, 388–9 neoplasia zipper artifacts 77, 77
effusion 338, 383 chondroma 532 zygomatic gland 398
otitis media 340, 340, 341, 384–5, 384–5 chondrosarcoma 529, 531 sialadenitis 398–9, 399
tympanic membrane 381, 387 hemangiosarcoma 530, 559 sialocele 399–400, 400

Wilfried Diagnostic MRI in Dogs and Cats (VetBooks - Ir)

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International Standard Book Number-13: 978-1-4987-3770-8 (Hardback)

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SeCtion 1 PHYSiCS AnD teCHniCAL ConSiDeRAtionS – iMAGe oPtiMiZAtion

CHAPTER 1 GeneRAL PRinCiPLeS oF MAGnetiC ReSonAnCe iMAGinG 3

CHAPTER 2 iMAGe CHARACteRiStiCS in MRi AnD PRinCiPAL PULSe SeQUenCeS 36

CHAPTER 3 MRi ARtiFACtS 70

CHAPTER 4.1 oPtiMiZeD teCHniQUe: BRAin 88

CHAPTER 4.2 oPtiMiZeD teCHniQUe: SPine 106

CHAPTER 4.3 GeneRAL FeAtUReS AnD oPtiMiZeD teCHniQUe FoR tHe

CHAPTER 4.4 teCHniCAL PARtiCULARitieS WitH LoW-FieLD iMAGinG 153

SeCtion 2 MRi oF tHe BRAin

CHAPTER 5.1 ConGenitAL AnD DeVeLoPMentAL DiSoRDeRS 161

CHAPTER 5.2 MetABoLiC AnD DeGeneRAtiVe enCePHALoPAtHieS 172

CHAPTER 5.3 enCePHALitiS/MeninGoenCePHALitiS 187

CHAPTER 5.4 BRAin neoPLASiA 211

CHAPTER 5.5 CYStiC ConDitionS 241

CHAPTER 5.6 iSCHeMiC BRAin DiSeASe AnD VASCULAR AnoMALieS 251

CHAPTER 5.7 BRAin HeMoRRHAGe 282

CHAPTER 5.8 BRAin tRAUMA 309

CHAPTER 5.9 AGinG CHAnGeS oF tHe BRAin 318

CHAPTER 5.10 CRAniAL neRVe DiSeASeS 326

SeCtion 3 MRi oF non-neURoLoGiCAL StRUCtUReS oF tHe HeAD AnD neCK

CHAPTER 6.1 nASAL CAVitY AnD FRontAL SinUSeS 347

CHAPTER 6.2 eYe AnD oRBit 362

CHAPTER 6.3 eXteRnAL, MiDDLe, AnD inneR eAR 380

CHAPTER 6.4 non-neURoLoGiC ConDitionS oF tHe HeAD AnD neCK 393

SeCtion 4 MRi oF tHe SPine

CHAPTER 7.1 noRMAL MRi SPinAL AnAtoMY, DeGeneRAtiVe DiSC DiSeASe,

CHAPTER 7.2 CeRViCAL SPonDYLoMYeLoPAtHY 447

CHAPTER 7.3 DeGeneRAtiVe LUMBoSACRAL StenoSiS 472

CHAPTER 7.4 ConGenitAL AnD DeVeLoPMentAL AnoMALieS AnD MALFoRMAtionS 481

CHAPTER 7.5 inFLAMMAtoRY AnD inFeCtioUS ConDitionS 508

CHAPTER 7.6 SPinAL neoPLASiA 527

CHAPTER 7.7 iSCHeMiC MYeLoPAtHY, SPinAL CoRD HeMoRRHAGe, MYeLoMALACiA 565

CHAPTER 7.8 eXtRAMeDULLARY CYSt-LiKe ConDitionS oF tHe SPine 584

CHAPTER 7.9 SYRinGoMYeLiA 595

CHAPTER 7.10 MRi oF tHe BRACHiAL AnD LUMBoSACRAL PLeXUSeS 603

CHAPTER 7.11 DeGeneRAtiVe SPinAL DiSeASeS 618

CHAPTER 7.12 MRi oF SPinAL tRAUMA 622

CHAPTER 7.13 MRi oF PARASPinAL SoFt tiSSUeS 630

SeCtion 5 MRi oF tHe MUSCULoSKeLetAL SYSteM

CHAPTER 8 MRi oF MUSCULoSKeLetAL DiSeASeS 643

SeCtion 6 MRi oF tHe tHoRAX AnD ABDoMen

CHAPTER 9.1 CARDiAC MRi 687

CHAPTER 9.2 MRi oF non-CARDiAC tHoRACiC ConDitionS 710

CHAPTER 10 ABDoMinAL MRi 723

Wilfried Mai, Dr. Méd. Vét., MSc, PhD, Diplomate

ADC apparent diffusion coefficient MHz megahertz

PHYSICS AND TECHNICAL

CHAPTER 1 General principles of magnetic resonance imaging

CHAPTER 2 Image characteristics in MRI and principal pulse sequences

CHAPTER 3 MRI artifacts

CHAPTER 4.1 Optimized technique: brain

CHAPTER 4.2 Optimized technique: spine

CHAPTER 4.3 General features and optimized technique for the

CHAPTER 4.4 Technical particularities with low-field imaging

• It has a rotating (spiral) motion; that rotating mag-