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Oxford Specialist
Handbooks in Cardiology

Cardiovascular
Computed
Tomography
2nd edition

Edited by

James Stirrup
Consultant Cardiologist,
Royal Berkshire NHS Foundation Trust,
Reading, UK

Russell Bull
Consultant Radiologist
Royal Bournemouth Hospital,
Bournemouth, UK

Michelle Williams
Clinical Lecturer in Cardiothoracic Radiology,
University of Edinburgh,
Edinburgh, UK

Ed Nicol
Consultant Cardiologist and Head of Cardiovascular CT,
Royal Brompton and Harefield NHS Foundation Trust,
London, UK

1
1
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Second Edition published in 2020
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 v

Foreword

Welcome to the 2nd edition of Cardiovascular Computed Tomography! Over

the last decade, the cardiological community has witnessed an exponential
increase in the use of CT coronary angiography in the evaluation of patients
with suspected or known coronary artery disease. The technology has de-
veloped extremely fast, with the introduction of next generation ultrafast
scanners, significant reduction in radiation exposure, and strong research
providing the scientific fundament for the clinical use of CT coronary angi-
ography. But the use of cardiovascular CT has expanded significantly be-
yond detection of coronary artery disease. Particularly in structural heart
disease and electrophysiology, CT is extremely important in patient selec-
tion, procedural planning and clinical follow-up.
Following the success of the first edition, Drs Stirrup, Williams, Bull, and
Nicol have provided a comprehensive handbook on the use of cardiac CT
in practice. The new handbook is divided into 8 parts, and starts with a
technical section. It addresses important fundamental topics in cardiac CT,
including technological developments, but also radiation, contrast agents,
and scanning protocols for the coronary arteries, the left atrium and pul-
monary veins (in patients considered for atrial fibrillation ablation), and
heart valves (prior to transcatheter heart valve therapies).
The second section addresses in detail the anatomy of the thorax and its
structures, which forms the basis for cardiovascular CT.
The third section is the core of the book, the section on coronary ar-
tery disease. It encompasses all the anatomical details of CT coronary angi-
ography, including calcium score, stenosis severity assessment and plaque
imaging, but also the functional parameters reflecting the stenosis severity
(FFRCT and myocardial perfusion).
The fourth section includes left and right ventricular size and function,
as well as atrial size and function quantification (important in atrial fibrilla-
tion ablation) and left atrial appendage assessment (to evaluate potential
occlusion).
The fifth section provides the information derived from CT to select pa-
tients with structural heart disease who may be candidates for transcatheter
valve therapies. In sections 6 and 7, the use of CT to evaluate congenital
heart disease and assess the various arteries (thoracic aorta, peripheral ar-
teries, and pulmonary arteries).
The last section addresses comparison of CT with other non-invasive
imaging modalities and provides information on guidelines, but also on CT
accreditation and certification.
All in all, this 2nd edition of Cardiovascular Computed Tomography provides
everything the clinician needs to know about cardiac CT imaging. It provides
detailed technical information, but is also very focused on clinical applica-
tions. A “must read” for the general, clinical cardiologist with an interest in
cardiac CT, as well as for the specialist working with cardiac CT.

Jeroen J. Bax, MD, PhD

Dept of Cardiology
Leiden University Medical Center, The Netherlands
 vii

Preface

Cardiovascular computed tomography (CCT) has become increasingly piv-

otal in cardiovascular medicine in the last decade. It is now the primary
technique for the non-​invasive evaluation of the coronary arteries and ar-
guably the cardiovascular system in general in several clinical situations. In
the UK, CT coronary angiography (CTCA) is now the first line test for
those with suspected angina (who do not have established coronary artery
disease) and imminent US and European guidelines are also likely to see an
increasing role for CTCA in this area. CCT is now central to the pre-​and
post-​intervention assessment of structural heart disease (TAVI, mitral valve
intervention and left atrial occlusion); has an increasing role in valve assess-
ment, and also in the assessment of congenital heart disease (both in adults
and children). There has been a relentless and rapid rate of change in CT
technology (which still often outstrips the evidence for its utility) and there
remains a lack of high quality training opportunities in CCT globally. Whilst
many courses exist for CCT training, it is only through hands-​on experience
that true clinical competence results.
This handbook is meant to be a broadly applicable résumé of CCT rather
than a fully comprehensive manual for the use of every CT scanner. Indeed,
the latter would be impossible given the pace of change of CT technology,
coupled with the different engineering approaches used by each CT vendor.
Nonetheless, details that relate to specific CT scanners are provided in the
text. Four broad themes are dealt with in the handbook: the components
of a (generic) CT scanner and the physics associated with them; practical
aspects of cardiovascular CT, including patient set-​up, contrast media and
scan protocols; cardiac CT, particularly CT coronary angiography and
evaluation of cardiac structure and function; and finally broader vascular
imaging using CT. A recurring message in this book is that CCT is one of
many imaging techniques available to assess the heart and broader cardio-
vascular system. We hope to reinforce this context in the final chapter with
some background of the other available cardiac imaging techniques.
This book is written in the familiar, easily accessible Oxford Handbook
style and draws together the experience and opinions of many international
experts in CCT. Our hope is that the reader will carry this updated hand-
book with them whilst they accrue their hands-​on experience. It is aimed at
all students, clinicians, physicists, and radiographers/​technologists involved
in CCT.
JS
RB
MW
EN
May 2019
 ix

Contents
Contributors xi
Symbols and abbreviations xv

1 Historical development of cardiovascular CT 1

2 MSCT scanner components 7
3 Technical principles of cardiovascular CT 19
4 Beyond 64-​detector CT 35
5 Radiation physics, biology, and protection 45
6 Practical aspects of cardiovascular CT 69
7 Intravenous contrast media 83
8 Scan protocols 99
9 Difficult scenarios 111
10 Image reconstruction and processing 125
11 Sources of artefact 149
12 Cross-​sectional anatomy of the thorax 165
13 The coronary arteries and cardiac veins 175
14 Assessment of coronary artery disease 187
15 Coronary stent imaging 223
16 Coronary artery bypass graft imaging 235
17 Ventricular pathology 243
18 Evaluation of myocardial scarring and perfusion 271
19 Evaluation of the left atrium and pulmonary veins 285
20 CT work-​up prior to transcatheter
aortic valve implantation 295
21 Valve imaging 313
22 Pericardial disease 351
23 Adult congenital heart disease 363
24 Non-​cardiac findings on cardiac CT 413
x Contents

25 Thoracic aortic imaging 439

26 Pulmonary artery imaging 455
27 Peripheral arterial imaging 467
28 Systemic veins 477
29 Accreditation and certification
in cardiovascular CT 487
30 Comparison of multimodality imaging 491
31 Future directions of cardiac CT 529

Index 537

Contributors
Amir Ahmadi
Assistant Clinical Professor
of Cardiovascular Disease,
The Mount Sinai Hospital,
New York, USA
Mona Bhatia
Director and Head of the
Department of Radiology and
Imaging, Fortis Escorts Heart
Institute, New Delhi, India
Matthew Budoff
Professor of Medicine, David
Geffen School of Medicine,
University of California Los
Angeles, California, USA
Russell Bull
Consultant Radiologist, Royal
Bournemouth Hospital,
Bournemouth, UK
Patricia Carrascosa
Medical Specialist in
Cardiovascular Imaging, Spectral
Tomography, and Virtual Studies,
Diagnóstico Maipú, Buenos
Aires, Argentina
Mark Cassar
Oxford University Hospitals NHS
Foundation Trust, Oxford, UK
Elly Castellano
Consultant Physicist, The Royal
Marsden NHS Foundation Trust,
London, UK
Sally Copperwaite
Superintendent Radiographer,
Royal Brompton & Harefield
NHS Foundation Trust,
London, UK
xi
Maros Ferencik
Assistant Professor of Medicine,
Oregon Health and Science
University, Oregon, USA
Borek Foldyna
Department of Diagnostic
and Interventional Radiology,
University of Leipzig, Leipzig,
Germany
Natalie Gartland
Radiographer, Department of
Radiology, Royal Brompton &
Harefield NHS Foundation Trust,
London, UK
Kelly Han
Paediatric Cardiologist,
The Children's Heart Clinic,
Minnesota, USA
Gareth Morgan Hughes
Consultant Cardiologist,
University Hospitals Plymouth
NHS Trust, Plymouth, UK
U. Joseph Schoepf
Director of Cardiovascular
Imaging, Medical University
of South Carolina,
Charleston, USA
Laurence King
Principal Physicist (Diagnostic
Radiology), The Royal Marsden
NHS Foundation Trust,
London, UK
Olga Lazoura
Consultant Radiologist, Royal
Free London NHS Foundation
Trust, London, UK
xii Contributors
Jonathon Leipsic
Professor, Department of
Radiology, UBC and St Paul’s
Hospital, Vancouver, Canada
Pierre LePage
Cardiology Registrar, University
Hospitals Plymouth NHS Trust,
Plymouth, UK
Lakshman Manjunath
Department of Medicine,
Stanford University, Stanford, USA
Pal Maurovich-​Horvat
Director of the Cardiovascular
Imaging Research Group,
Semmelweis University,
Budapest, Hungary
Rine Nakanishi
Program Director of Cardiac
CT, University of California
Los Angeles Medical Centre,
California, USA
David Newby
BHF John Wheatley Chair
of Cardiology, University of
Edinburgh, Edinburgh, UK
Ed Nicol
Consultant Cardiologist and
Head of Cardiovascular CT,
Royal Brompton and Harefield
NHS Foundation Trust,
London, UK
Koen Nieman
Associate Professor of
Cardiovascular Medicine and
Radiology, Stanford University,
Stanford, USA
Simon Padley
Consultant Radiologist, Royal
Brompton & Harefield NHS
Foundation Trust, London, UK
Francesca Pugliese
Consultant in Advanced
Cardiovascular Imaging, Queen
Mary University of London,
London, UK
Ronak Rajani
Consultant Cardiologist, Guy’s
and St Thomas’ NHS Foundation
Trust, London, UK
Gaston A.
Rodriguez-​Granillo
Staff Cardiologist, Diagnóstico
Maipú, Buenos Aires, Argentina
Carl Roobottom
Professor and Honorary
Consultant, University
Hospitals Plymouth NHS Trust,
Plymouth, UK
Nik Sabharwal
Consultant Cardiologist, Oxford
University Hospitals NHS
Foundation Trust, Oxford, UK
Rebecca Schofield
Consultant Cardiologist, North
West Anglia NHS Foundation
Trust, Peterborough, UK
James Shambrook
Consultant Cardiothoracic
Radiologist, University Hospital
Southampton NHS Foundation
Trust, Southampton, UK
Elizabeth Shaw
Radiographer, Royal Brompton
and Harefield NHS Foundation
Trust, London, UK
Leslee Shaw
Professor of Medicine and
Radiology, Weill University,
New York, USA

James Stirrup
Consultant Cardiologist, Royal
Berkshire NHS Foundation
Trust, Reading, UK
Bálint Szilveszter
Cardiovascular Imaging Research
Group, Semmelweis University,
Budapest, Hungary
Katharine Thomas
Clinical Research Fellow in the
Department of Cardiovascular
Medicine, University of
Oxford, UK
Contributors
xiii
Todd Villines
Executive Editor, Journal of
Cardiovascular Computed
Tomography, and Walter Reed
National Military Medical Center,
Maryland, USA
Michelle Williams
Clinical Lecturer in
Cardiothoracic Radiology,
University of Edinburgh,
Edinburgh, UK
 xv

Symbols and abbreviations

E cross reference AVSD atrioventricular septal defect

M online resource/​web address AZ azygous vein
∴ therefore BAC broncheoalveolar cell
carcinoma
pP primary
BAV bicuspid aortic valve
2° secondary
BCA brachiocephalic artery
i increase
BHA beam hardening artefacts
d decrease
BMI body mass index
l produces
BMS bare-​metal stents
3DE 3D echocardiography
BPM beats per minute
AA aortic arch
BSCI British Society of
AAOCA anomalous aortic origin of a
Cardiovascular Imaging
coronary artery
BTS British Thoracic Society
ACA anomalous coronary arteries
C carina
ACCF American College of
Cardiology Foundation CABG coronary artery bypass
grafting
ACHD adult congenital heart disease
CAC coronary artery calcium
AF atrial fibrillation
CAC-​DRS Coronary Artery Calcium
AIVG anterior
Data and Reporting System,
interventricular groove
CAC-​DRS
ALARA as low as reasonably
CAD coronary artery disease
achievable
CCS coronary artery calcium score
ALCAPA anomalous coronary artery,
arising anomalously from the CCT cardiac computed
pulmonary artery tomography
AMVL anterior mitral valve leaflet CCT cardiovascular CT
AOA aortic arch CCTGA congenitally corrected
transposition of the great
AOR aortic root
arteries
AP aortopulmonary
CFD computational fluid dynamics
AR aortic regurgitation
CHD congenital heart disease
ARCAPA anomalous coronary artery,
CHSS Congenital Heart Surgeon
arising anomalously from the
Society
pulmonary artery
CMPR curved MPR
ARVC arrhythmogenic right
ventricular cardiomyopathy CMR cardiovascular magnetic
resonance
AS aortic valve stenosis
CNR contrast-​to-​noise ratio
ASD atrial septal defects
CO coronary ostia
AV atrioventricular
CONFIRM COronary CT Angiography
AVA aortic valve area
EvaluatioN For Clinical
AVNRT atrioventricular nodal re-​ Outcomes: An InteRnational
entrant tachycardia Multicentre Registry
xvi Symbols and abbreviations

CT computerized tomography ICA interpretation of coronary

angiography
CTA CT angiography
ICA invasive coronary angiography
CTCA CT coronary angiography
ICD implantable cardiac
CTDI CT dose index
defibrillator
CTEPH chronic thromboembolic
ICRP International Commission on
pulmonary hypertension
Radiological Protection
CTP CT perfusion
IMA internal mammary artery
CTPA CT pulmonary angiography
IMH intramural haematoma
CTPV CT pulmonary venography
IR iterative reconstruction
CZT cadmium-​zinc-​telluride
IRMER Ionising Radiation (Medical
DA descending aorta Exposure) Regulations
DCM dilated cardiomyopathy IVC inferior vena cava
DE delayed enhancement IVS interventricular septum
DECT dual-​energy CT IVUS intravascular ultrasound
DENSE displacement encoding with IWOS ischaemic lesions without
stimulated echoes stenosis
DES drug-​eluting stents KD Kawasaki’s disease
DLP dose–​length product KEV kiloelectronvolts
DRL diagnostic reference level LA left atrium
DSCT dual-​source CT LAA left atrial appendage
EAT epicardial adipose tissue LAD left anterior descending
EBCT electron beam CT LAVG left atrioventricular groove
ECG electrocardiogram LBCV left brachiocephalic vein
EDE effective dose equivalent LBV left brachiocephalic vein
EF ejection fraction LCCA left common carotid artery
EGFR estimated glomerular LCS left coronary sinus
filtration rate
LCX left circumflex artery
EP electrophysiology
LGE late gadolinium enhancement
ESC European Society of
LIMA left internal mammary arteries
Cardiology
LMS left main stem
ESR erythrocyte
sedimentation rate LN lymph nodes
FBP filtered back-​projection LPA left pulmonary artery
18F-​FDG 18F-​fluorodeoxyglucose LPH lipomatous hypertrophy
FFR fractional flow reserve LSA left subclavian artery
FOV field of view LSPV left superior pulmonary vein
GTN glyceryl trinitrate LSVC left superior vena cava
GY gray LV left ventricular/​ventricle
HALT hypoattenuating leaflet LVAP left ventricular apex
thickening LVEDV left ventricular
HCM hypertrophic cardiomyopathy end-​diastolic volume
HR heart rate LVEF left ventricular ejection fraction
HU Hounsfield units LVNC left ventricular
non-​compaction
 Symbols and abbreviations
xvii

LVOT left ventricular outflow tract PDA posterior descending

coronary artery
MA milliamperes
PD A patent ductus arteriosus
MAS milliampere-​seconds
PE pulmonary embolism
MAC mitral annular calcification
PET positron emission tomography
MACE major adverse cardiac events
PFO patent foramen ovale
MAPCA major aorto-​pulmonary
collateral artery PICC peripherally inserted central
catheter
MBIR model-​based iterative
reconstruction PIVG posterior (inferior)
inter-​ventricular groove
MDCT multidetector CT
PMT photomultiplier tubes
MESA Multi-​Ethnic Study of
Atherosclerosis POBA plain old balloon angioplasty
MFH malignant fibrous histiocytoma PPV positive predictive value
MIBG metaiodobenzylguanidine PR positive remodelling
MIP maximum intensity projection PR pulmonary regurgitation
MLA minimal luminal area PS pulmonary stenosis
MLD minimal luminal diameter PT pulmonary trunk
MPA main pulmonary artery PTL pre-​test likelihood
MPR multiplanar reformatting PV pulmonary vein
MPS myocardial perfusion PVC premature ventricular
scintigraphy complexes
MR mitral regurgitation PVR pulmonary vascular resistance
MRI magnetic resonance imaging RA right atrium
MSCT multi-​slice CT RAA right atrial appendage
MVA mitral valve area RAVG right atrioventricular groove
NCS non-​coronary sinus RCA right coronary artery
NICE National Institute for Health RCCA right common carotid artery
and Clinical Excellence RCS right coronary sinus
NPV negative predictive value RF radiofrequency
NSF nephrogenic systemic fibrosis RIMA right internal mammary
OCT optical coherence tomography arteries
OES oesophagus RLL right lobe of liver
PA pulmonary artery RML right middle lobe
PACS picture archiving and RNV radionuclide ventriculography
communication system ROA regurgitant orifice area
PAH pulmonary artery ROI region of interest
hypertension
RPA right pulmonary artery
PAPVC partial anomalous pulmonary
venous connection RSA right subclavian artery

PAR para-​aortic regurgitation RUL right upper lobe

PAT pericardial adipose tissue RV right ventricular/​ventricle

PCI percutaneous coronary RVEF RV ejection fraction

intervention RVEDV right ventricular
end-​diastolic volume
xviii Symbols and abbreviations

RVESV right ventricular TA transapical

end-​systolic volume TAO transaortic
RVOT right ventricular outflow tract TAPVC total anomalous pulmonary
RWT relative wall thickness venous connection
SCCT Society of Cardiovascular CT TAVI transcatheter aortic valve
implantation
SIHD stable ischaemic heart disease
TAVR transcatheter aortic valve
SLE systemic lupus erythematosis
replacement
SNR signal-​to-​noise ratio
TCFA thin cap fibrous atheroma
SOV sinuses of Valsalva
TGA transposition of the great
SPECT single photon emission arteries
computed tomography
TMVR
SPL secondary pulmonary lobule
TOE transoesophageal
SQUEEZ stretch quantifier of echocardiography
endocardial engraved zones
TOF Tetralogy of Fallot
SSCT single-​slice CT
TR tricuspid regurgitation
SSD shaded-​surface display
TRO triple rule-​out
ST sinotubular
TTE transthoracic
STE speckle-​tracking echocardiography
echocardiography
TVL tricuspid valve leaflets
STJ sinotubular junction
VA ventriculoarterial
STS-​MIP sliding thin slab MIP
VHD valvular heart disease
SV sievert
VMI virtual monochromatic
SVC superior vena cava imaging
SVG saphenous vein graft VR volume rendering
SWOI stenotic lesions without VSD ventricular septal defects
ischaemia
Chapter 1 1

Historical development
of cardiovascular CT
Introduction 2
Origins of X-​ray computed tomography 3
Scanner development 4
Electron beam CT 6
2 Chapter 1 Historical development of CCT

Introduction
The use of X-​ray computed tomography (CT) to image the heart has in-
creased exponentially over the last decade. This i is largely the result of
technological improvements that have rendered cardiac images less suscep-
tible to artefacts arising from cardiac motion and significantly reduced radi-
ation doses. However, these artefacts have not been abolished entirely. The
ability to reliably acquire low-​dose, high-​quality cardiovascular CT (CCT)
datasets is predicated in part on an understanding of the hardware and
software used to generate them, which in turn may be better understood
by reviewing briefly the development of the CT scanner from initial models
to the current state-​of-​the-​art equipment.
 Origins of X-ray computed tomography
3

Origins of X-​ray computed tomography

The invention of X-​ray CT is credited to Sir Godfrey Hounsfield, an en-
gineer working for EMI Laboratories, and Allan Cormack, a South African
physicist at Tufts University, Massachusetts.
The major hurdle to the initial development of CT was mathematical.
Acquiring image data through multiple projections was straightforward but
converting this into a resultant image was not. The theoretical basis for
determining the nature of heterogenous tissues that attenuate a transmitted
X-​ray beam was laid out by Allan Cormack in the early 1960s but remained
unexploited as it had uncertain practical application. Unaware of this work,
Godfrey Hounsfield pursued an engineering solution to the problem, which
led to the development of a CT scanner prototype in the late 1960s and, ul-
timately, the first clinical CT scanner, which was installed in Atkinson Morley
Hospital, London in 1971. This scanner was dedicated to imaging the brain
and took around 4 min. to acquire each axial image. A whole-​body CT
scanner was to follow. For their combined work, Cormack and Hounsfield
shared the Nobel Prize for Physiology and Medicine in 1979.
4 Chapter 1 Historical development of CCT

Scanner development
To date, four broad generations of conventional CT scanners have been de-
veloped (Fig. 1.1). Each modifies the geometric arrangement of X-​ray tube
and detector array. Although intuition would suggest that current scanners
are of the fourth generation, this is not the case. In fact, all modern CT
scanners are based on third-​generation technology. The technical aspects
of modern CT are easier to understand with a little background knowledge
of successive iterations of CT scanner geometry.

A C A C
D D

(i) B (ii) B

A A

C C

(iii) B (iv) B

Fig. 1.1 The four generations of CT scanning technology. (i) First generation. X-​rays
are emitted from the source (A) to reach the detector (B). The assembly is then
translated in stages across the patient (C) until complete coverage is obtained. The
assembly is rotated (D) and the process is repeated. (ii) Second generation. Similar
to first-​generation technology, although fan-​beam X-​rays used and detector numbers
i (iii) Third generation. X-​rays are emitted from the source (A), pass through the
patient and reach the detectors (B). The whole assembly then rotates around the
patient to a new view (C). Translation is no longer necessary. (iv) Fourth generation.
Similar to third-​generation CT, except that the detector array (B) is arranged
circumferentially around the patient and does not move during the acquisition.
 Scanner development
5

First-​generation CT
The original CT scanner was developed by Godfrey Hounsfield in the 1970s.
A single X-​ray source was collimated to produce a thin beam of X-​rays,
which were detected on the opposite side of the patient by two detectors
lined up along the axis of rotation. The assembly was then translated across
the patient to begin a new measurement. Once the entire field had been
covered, the assembly was rotated by ° and the translation procedure
started afresh (‘translate–​rotate’ motion). This was repeated over an arc of
180° to generate the data required to reconstruct an axial slice. Although by
modern standards the image acquisition time was lengthy (around 6 min.),
at the time of introduction the technique was truly revolutionary.
Second-​generation CT
This generation improved on the initial CT design by using multiple narrow
fan-​beam X-​ray sources and detectors with multiple elements. Images were
still acquired using a translate–​rotate mechanism, but scan times were re-
duced substantially due to simultaneous data acquisition from multiple
detector channels. The major factor limiting the advancement of second-​
generation CT scanners was difficulty in engineering X-​ray source/​detector
configurations through the translate–​rotate mechanism.
Third-​generation CT
CT technology was improved further still by widening the X-​ray fan-​beam
to encompass the patient. The patient lies in the centre of an imaginary
circle, on the circumference of which lie the X-​ray source on one side and
an arc of detector elements on the other. The entire mechanism is ro-
tated around the patient, but translation is no longer necessary. Acquisition
times are substantially improved (down to 165 ms on conventional 64-​slice
scanners).
Fourth-​generation CT
This generation evolved only slightly later than third-​generation CT and
offers no significant advantages. A 360° array of fixed detectors is positioned
around the patient, with only the X-​ray source rotating. Fourth-​generation
scanners have a few disadvantages (scatter is a particular problem), but
were dealt a mortal blow by the advent of multi-​slice CT. Although an issue
even for third-​generation scanners, the costs of engineering this technology
for fourth-​generation scanners were impossibly prohibitive.
6 Chapter 1 Historical development of CCT

Electron beam CT
Although third-​generation conventional CT scanners were in use by the
1980s, their temporal resolution was rather poor, precluding cardiac scan-
ning. Electron beam CT (EBCT) scanners were developed to circumvent
this limitation and are occasionally referred to as fifth-​generation scanners.
Rather than using a rotating X-​ray gantry, EBCT employs a fixed electron
beam that is selectively targeted by means of electromagnetic deflection
coils onto a 210° arc of tungsten anodes located beneath the patient
(Fig. 1.2). The electron beam has a current in the region of 640 milliam-
peres (mA); when it strikes the tungsten anodes, X-​rays are emitted in a
process similar to current passing through the tungsten anode of a conven-
tional X-​ray tube (see E X-​ray tube, p. 10). The fan-​shaped X-​ray beam is
collimated to travel vertically; X-​rays are attenuated as they pass through
the patient and are detected by an array of detectors on the opposite side.
The absence of moving parts, coupled with the speed at which the elec-
tron beam can be swept over the tungsten anodes, means that the temporal
resolution (see E Temporal resolution, p. 26) of EBCT is significantly faster
(733 ms) than even modern multi-​slice computed tomography (MSCT)
scanners (65–​165 ms). Radiation exposure is comparable to a prospect-
ively gated calcium score acquisition using MSCT.
Three factors limit the usefulness of EBCT. First, the spatial resolution
(see E Chapter 3 p. 24) is relatively poor (1.5 mm, compared with 0.5 mm
for MSCT). Second, EBCT scanners are essentially limited to cardiac appli-
cations and are less suitable for general purpose CT radiology. Third, EBCT
scanners were more expensive than their 64-​slice MSCT equivalents.
The major clinical use of EBCT is coronary calcium scoring (see
E Coronary artery calcium scoring (1), p. 104), although the technology
has been almost entirely supplanted by MSCT.

Detector array
Detector array

X-ray beam X-ray beam

X-ray tube with deflection coils

Electron beam

Source collimator Tungsten target ring

Tungsten target ring

Fig. 1.2 Electron beam CT.

Chapter 2 7

MSCT scanner components

Gantry 8
X-​ray tube 10
Collimators 12
Detectors 13
Detector terminology 14
Detectors, data channels, and slices 16
8 Chapter 2 MSCT scanner components

Gantry
Modern CT scanners use a rotating gantry onto which the X-​ray tube and
detectors are mounted. Limitations in gantry technology led to the intro-
duction of EBCT for cardiac imaging, but third-​generation CT scanners
eventually supplanted this technology because of two main advances:
• Slip-​ring technology.
• Switch-​mode power supply.
Slip-​ring technology
Previously, conventional CT required power to be supplied via electric
cabling, necessitating a reversal of gantry rotation after every few turns to
allow unwinding of the cable. Slip-​ring technology dispenses with the power
cable: both power and data are transferred to and from the gantry using
metal brushes fixed to the housing of the scanner, but in permanent elec-
trical contact with the rotating gantry. This allows continuous rotation of
the gantry and paved the way for helical CT scanning (see E Acquisition
mode, p. 34).
Switch-​mode power supply
A major problem for rotating gantry CT was the construction of a power
supply that was small enough to be mounted on the gantry but powerful
enough to generate the voltages required. The advent of switch-​mode
power supplies solved this problem, allowing higher efficiency power sup-
plies with reduced size and weight. Most switch-​mode power supplies work
by converting AC to DC current via a switching circuit. The DC current is
then converted back to AC but at a much higher frequency than that sup-
plied by the mains. The increased efficiency allows higher tube voltages to
be achieved, with only limited generation of heat.
Gantry rotation time
This is the time taken for one full rotation of the X-​ray tube/​detector array
around the axis of rotation. The speed of gantry rotation was the limiting
factor in early CT, particularly before the advent of slip-​ring technology.
For many contemporary scanners, approximately half a revolution (180°)
is needed to acquire a single image (the angle of the X-​ray fan beam must
also be considered, so in practice a 7220° arc is required). This is known as
a half-​scan algorithm (see E Temporal resolution, p. 58). A CT scanner
with a gantry rotation time of 330 ms can hence acquire a single image set
in 7165 ms. Thus, the temporal resolution of this scanner is around 165 ms.
Gantry
9
10 Chapter 2 MSCT scanner components

X-​ray tube
Production of X-​rays
In CT, X-​rays are produced by an X-​ray tube (Fig. 2.1):
• Electrons are emitted by heating the filament with an electric current.
This is called thermionic emission.
• A voltage is applied between the cathode and the anode which
accelerates the electrons towards the positively charged anode. The
flow of electrons is described by the tube current (see E X-​ray tube
current, p. 20), measured in milliamperes (mA). The electrons gain
energy equivalent to the applied voltage: in CT, this is typically 120 kVp
(see E X-​ray tube voltage, p. 21).
• The electron beam strikes the anode at the focal spot. Most of the
electron energy is dissipated as heat; about 4% is released as X-​rays.
The X-​ray spectrum
X-​rays are emitted with a range of energies between a few kiloelectronvolts
(keV) and the applied tube voltage. The distribution of energies is described
by the X-​ray spectrum (Fig. 2.2).
There are two types of X-​ray:
• Characteristic X-​rays, which appear as peaks with discrete energies
corresponding to the energy transitions between electron shells.
• Bremmsstrahlung X-​rays, which form a continuum that falls in intensity
towards the higher energies.

High voltage (kVp)

Cathode Anode Stator

Filament Tube insert

Tube housing
Electron beam (mA)

X-ray beam

Fig. 2.1 X-​ray tube.

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Neuralgic attacks are usually characterized, besides the pain, by a
highly-interesting series of symptoms, which are in part transitory
and functional, and in part due to structural changes in the tissues.4
4 See Notta, Arch. gén. de Méd., 1854; Anstie, Neuralgia and its Counterfeits.

The spasm and subsequent dilatation of blood-vessels in the

affected area have already been alluded to. A disturbance of
secreting organs in the neighborhood of the painful region, the
lachrymal gland, the skin, the mucous membranes, the salivary
glands, is of equally common occurrence, and is probably in great
measure due to direct irritation of the glandular nerves, since the
increased secretion is said to occur sometimes unattended by
congestion.

The hair may become dry and brittle and inclined to fall out, or may
lose its color rapidly, regaining it after the attack has passed.

The increased secretion of urine already alluded to attends not only

renal neuralgias, but those of the fifth pair, intercostal, and other
nerves. There may be unilateral furring of the tongue (Anstie).

The muscles supplied by the branches of the affected nerve or of

related nerves may be the seat of spasm, or, on the other hand, may
become paretic; and this is true even of the large muscles of the
extremities.

Vision may be temporarily obscured or lost in the eye of the affected

side in neuralgia of the fifth pair, and hearing, taste, and smell are
likewise deranged, though more rarely. I am not aware that distinct
hemianopsia is observed except in cases of true migraine, where it
forms an important prodromal symptom.

In connection with these disorders of the special senses the

occasional occurrence of typical anæsthesia of the skin of one-half
of the body should be noted, which several observers have found in
connection with sciatica. The writer has seen a cutaneous
hyperæsthesia of one entire half of the body in a case of cervico-
occipital neuralgia of long standing. These symptoms are probably
analogous to the hemianæsthesia which comes on after epileptic or
other acute nervous seizures, or after concussion accidents, as has
lately been observed both in this country and in Europe, and it is
perhaps distantly related to the hemianæsthesia of hysteria. Local
disorders of the sensibility in the neuralgic area are far more
common than this, and, in fact, are usually present in some degree.
The skin is at first hyperæsthetic, but becomes after a time
anæsthetic; and this anæsthesia offers several interesting
peculiarities. When this loss of sensibility is well marked, areas
within which the anæsthesia is found are apt to be sharply defined,
but they may be either of large size or so small as only to be
discovered by careful searching (Hubert-Valleroux). The sensibility
within these areas may be almost wanting, but in spite of this fact it
can often be restored by cutaneous faradization around their
margins, and the functional or neurosal origin of the anæsthesia is
thus made apparent. Where the anæsthesia is due, as sometimes
happens, to the neuritis with which the neuralgia is so often
complicated, it is more lasting, but usually less profound and less
sharply defined.

These changes may be transient, or, if a neuralgia is long continued

and severe, they may pass into a series of more lasting and deeper
affections of the nutrition.

The skin and subjacent tissues, including the periosteum, from being
simply swelled or œdematous may become thickened and
hypertrophied. The writer has known a case of supraorbital
neuralgia, at first typically intermittent, to lead to a thickening of the
periosteum or bone over the orbit, which even at the end of several
years had not wholly disappeared.

Neuralgias of the fifth pair, which are as remarkable in their outward

results as they are in their severity and their relation to other
neuroses, are said to give rise to clouding and ulceration of the
cornea, to iritis, and even to glaucoma.
Herpetic eruptions on the skin sometimes occur, of which herpes
zoster is the most familiar instance.

Muscular atrophy is very common, especially in sciatica, and in

some cases this occurs early and goes on rapidly, while in others it
may be only slight and proportioned to the disease and relaxation of
the muscles, even where the neuralgia has lasted for weeks or
months.

Neuritis of the affected nerve is a common result or attendant of

neuralgia, and may remain behind for an indefinite period after the
acute pain has gone, manifesting itself by subjective and objective
disorders of sensibility, by occasional eruptions on the skin, or by
muscular atrophy.

It is plain that in this list of symptoms a variety of conditions have

been described which would never all be met with in the same case,
and which, as will be shown in the section on Pathology, are
probably due to different pathological causes.

Neuralgia of the Viscera.

These neuralgias are less definitely localized by the sensations of

the patient than those of the superficial nerves, and it is not definitely
known what set of nerves are at fault.

They are deep-seated and are referred to the general neighborhood

of the larynx, œsophagus, heart, or one of the abdominal or genital
organs, as the case may be.

The pain is usually of an intense, boring character, and does not dart
like the pain of superficial neuralgia, but is either constant or comes
in waves, which swell steadily to a maximum and then die away,
often leaving the patient in a state of profound temporary prostration.
Deep pressure often brings relief. A patient of the writer, who is
subject to attacks of this kind in the right hypochondrium, will bear
with her whole weight on some hard object as each paroxysm comes
on, or insist that some one shall press with his fists into the painful
neighborhood with such force that the skin is often found bruised and
discolored.

The functions and secretions of the visceral organs are apt to be

greatly disordered during a neuralgic attack, and it is often difficult or
impossible to tell with certainty which of these conditions was the
parent of the other. Undoubtedly, either sequence may occur, but the
pain excited by disorder of function, or even organic disease of any
organ, is not necessarily felt in that immediate neighborhood. Thus I
have known the inflammation around an appendix cæci, of which the
patient shortly afterward died, to cause so intense a pain near the
edge of the ribs that the passage of gall-stones or renal calculus was
at first suspected.

There seems to be as much variation as to modes of onset and

duration among the visceralgias as among the superficial neuralgias,
but the tendency to short typical attacks of frequent recurrence
seems to be greater with the former.

The visceral neuralgias are quite closely enough related to certain of

the superficial neuralgias to show that they belong in the same
general category. The two affections are often seen in the same
person, and not infrequently at the same time or in immediate
succession. Thus in the case of the patient just alluded to above, the
attacks of deep-seated neuralgia in the neighborhood of the right
flank are at times immediately preceded by severe neuralgia of the
face or head. Similarly, intercostal neuralgia may occur in immediate
connection with neuralgias of the cardiac or gastric nerves.

The phenomenon of tender points is not entirely wanting in the

visceralgias, though less constant and definite than in the superficial
neuralgias.
The liver and the uterus especially become the seat of more or less
localized tenderness, and possibly the tenderness in the ovarian
region which is so common, and so often unattended by real
inflammation, is, in part, of this order.

The secondary results of the visceralgias are not easy to study.

Besides the disorders of secretion and function above alluded to,
swelling of the liver with jaundice and paresis of the muscular walls
of the hollow viscera may be mentioned as having been ascribed to
neuralgia.

It is not known to what degree neuritis occurs as a cause or

complication of these neuralgias, and this is a question which is
greatly in need of further study.

Migraine, or Sick Headache.

This is often classified as an affection of a different order from the

neuralgias, but there seem to be no real grounds for this distinction.

The superficial neuralgias themselves are probably not one, but a

group of affections, with the common bond of severe and
paroxysmal pain.

Neither is what is called migraine always one and the same disease.

Although in its most typical form it presents very striking

characteristics, such as a marked preliminary stage, with peculiar
visual and sensory auras, sometimes occupying one entire half of
the body, a short and regular course and periodical return, deep-
seated pain without tender points, and prominent unilateral vascular
disorders, yet these symptoms shade off by imperceptible degrees
into those of neuralgia of the fifth pair, or more often into one or
another form of unilateral neuralgic headache which stands midway
between the two.
The vascular phenomena of migraine are believed by various
observers, as is well known, to constitute the primary and essential
pathological feature of the disease, and to be the cause of the pain.
But this is a pure hypothesis, and as a matter of fact the cases are
abundant in which no greater vascular changes are present than in
other neuralgias of equal severity.

Migraine seems to occupy an intermediate position between the

grave neuroses, especially epilepsy, and the neuralgias of neurosal
origin.

The symptomatology will be described at greater length below.

GENERAL ETIOLOGY.—The causes of neuralgia may be divided into

predisposing and exciting causes.

The most important of the first group are—

1. Hereditary tendencies;

2. The influences associated with the different critical periods of

life;

3. The influences attached to sex;

4. The action of constitutional diseases, such as phthisis,

anæmia, gout, syphilis, diabetes, nephritis, malarial poisoning,
metallic poisoning.

The most important of the second group of causes are—

1. Atmospheric influences and the local action of heat and cold;

2. Injuries and irritation of nerves;

3. Irritation of related nerves (so-called reflex and sympathetic

neuralgias);

4. Acute febrile diseases.

In most cases more than one cause is to blame, and each should be
separately sought for.

PREDISPOSING CAUSES.—1. Hereditary Tendencies.—It is generally

admitted as beyond question that neuralgias are most common in
families in which other signs of the neuropathic taint are prominent.
Such affections as hysteria, neurasthenia, epilepsy, asthma, chorea,
dipsomania, and even gout and phthisis as it would seem, are akin
to the neuralgic tendency.

The neuropathic family is thought to contain, in fact, a much larger

number of members than this,5 but there is danger of exaggerating
the importance of an influence of which we know as yet so little.
5 Féré, Arch. de Névrologie, 1884, Nos. 19 and 20, “La famille névropathique.”

It should be remembered, moreover, that even where an inherited

taint is present its influence may be but slight as compared with that
of some special exciting cause.

Some neuralgias are more closely associated with the inherited

neuropathic diathesis than others. The connection is especially close
in the case of migraine;6 then follow other forms of periodical
headache and the visceral neuralgias. Even the superficial
neuralgias7 are more or less subject to this influence. This is thought
to be especially true of the facial neuralgias.
6 There is a witty French saying (quoted by Liveing), “La migraine est le mal des
beaux esprits;” which might be rendered, “The disease of nervous temperaments.”

7 For tables of illustrative cases see Anstie, Neuralgia and its Counterfeits, and J. G.
Kerr, Pacific Med. and Surg. Journ., May, 1885.

Reasons will be offered later for suspecting that many cases usually
classed as neuralgia, and characterized by gradual onset and
protracted course, are essentially cases of neuritis; and there is need
of further inquiry as to how far hereditary influences are concerned in
producing them, and whether such influences act by increasing the
liability of the peripheral nerves to become inflamed, or only by
increasing the excitability of the sensory nervous centres.

2. Age.—Neuralgia is oftenest seen in middle life and at the epochs

marked by the development and the decline of the sexual functions.
The affection, when once established, may run over into advanced
age, but cases beginning at this period are relatively rare and very
intractable (Anstie).

Childhood is commonly said to be almost exempt from neuralgia,

but, in fact, there seems no sufficient reason for withholding this term
from the so-called growing pains of young children8 so long as it is
accorded to the almost equally irregular neuralgias of anæmia in the
adult. The same remark applies to the attacks of abdominal pain in
children, which often seem to be entirely disconnected from digestive
disorders.
8 Probably due to anæmia or imperfect nutrition (see Jacobi, “Anæmia of Infancy and
Childhood,” Archives of Med., 1881, vol. v.).

Adolescents and children also suffer from periodical headaches,

both of the migrainoid and of the neuralgic type. These are obstinate
and important affections.9 Migraine especially, coming on in early life,
points to a neuropathic constitution, and will be likely to recur at
intervals through life, or possibly to give place to graver neuroses.
9 Blache, Revue mensuelle de l'enfance, Mar., 1883, and Keller, Arch. de Névroloqie.
1883.

3. Sex.—Women show a stronger predisposition than men to certain

forms of neuralgia, as to the other neuroses, but it is generally
conceded that whereas neuralgias of the fifth and occipital and of the
intercostal nerves are met with oftenest among them, the brachial,
crural, and sciatic neuralgias are commoner among men. This
probably indicates that the neurosal element is of greater weight in
the former group, the neuritic element in the latter.
4. Constitutional Diseases.—The blood-impoverishment of phthisis
and anæmia, the poison of malaria, syphilis, and gout, and the
obscurer forms of disordered metamorphosis of tissue, undoubtedly
predispose to neuralgia and the other neuroses, as well as to neuritis
and others of the direct causes of neuralgic attacks.

Anstie regards the influence of phthisis as so important as to place it

fairly among the neuroses. Gout is likewise reckoned by some
observers among the neuroses,10 but we tread here upon uncertain
ground. Anstie does not regard gout as a common cause of
neuralgia, but most writers rate it as more important, and gouty
persons are certainly liable to exhibit and to transmit an impaired
nervous constitution, of which neuralgia may be one of the
symptoms. The neuralgias of gout are shifting, irregular in their
course, and sometimes bilateral.
10 Dyce-Duckworth, Brain, vol. iii., 1880.

Syphilitic patients are liable to suffer, not only from osteocopic pains
and pains due to the pressure of new growths, but also from attacks
of truly neuralgic character. These may occur either in the early or
the later stages of the disease. They may take the form of typical
neuralgias, as sciatica or neuralgia of the supraorbital nerve
(Fournier11), or they may be shifting, and liable to recur in frequent
attacks of short duration, like the pains from which many persons
suffer under changes of weather, anæmia, or fatigue.
11 Cited by Erb in Ziemssen's Encyclopædia.

There are other obscure disorders of the nutrition, as yet vaguely

defined, in connection with which neuralgia of irregular types is often
found. Some of these are classed together under the name of
lithæmia, and are believed to be due to imperfect oxidation of
albuminoid products.12
12 See DaCosta, Am. Journ. of Med. Sciences, Oct., 1881, and W. H. Draper, New
York Med. Record, Feb. 24, 1883.
Diabetes seems also to be an occasional cause of neuralgia,
especially sciatica, and Berger,13 who has recently described them,
says that they are characterized by limitation of the pain to single
branches of the sacral nerves, by a tendency to occur at once on
both sides of the body, by the prominence of vaso-motor symptoms,
and, finally, by their long duration and obstinacy. There may not, at
the moment, be any of the characteristic symptoms of diabetes
present.
13 Neurologisches Centralblatt, 1882, cited in the Centralbl. für Nervenheilk., etc.,
1882, p. 455.

Chronic nephritis also causes neuralgia, either directly or indirectly;

and severe neuralgic attacks may accompany the condition, which is
as yet but imperfectly known, characterized pathologically by a
general arterio-fibrosis and by increased tension of the arterial
system.

True rheumatism does not appear to be a predisposing cause of

neuralgia.

Anæmia, both acute and chronic, is a frequent cause of neuralgia,

both through the imperfect nutrition of the nervous tissues, to which it
leads, and, it is thought, because the relatively greater carbonization
of the blood increases the irritability of the ganglionic centres.

Even a degree of anæmia which might otherwise be unimportant

becomes of significance in the case of a patient who is otherwise
predisposed to neuralgia; for such persons need to have their health
kept at its fullest flood by what would ordinarily seem a surplus of
nourishment and care.

Under the same general heading comes the debility from acute and
chronic diseases, and the enfeeblement of the nervous system from
moral causes, such as anxiety, disappointment, fright, overwork and
over-excitement, and especially sexual over-excitement, whether
gratified or suppressed (Anstie), or, on the other hand, too great
monotony of life; also from the abuse of tea, coffee, and tobacco.
Lead, arsenic, antimony, and mercury may seriously impair the
nutrition of all the nervous tissues, and in that way prepare the way
for neuralgia.

IMMEDIATE CAUSES.—1. Atmospheric and Thermic Influences.—

Neuralgia is very common in cold and damp seasons of the year, in
cold and damp localities, and in persons whose work entails frequent
and sudden changes of temperature. Exposures of this sort may at
once excite twinges of pain here and there over the body, and may
eventually provoke severe and prolonged attacks of neuralgia.

The action of damp cold upon the body is complicated, and it exerts
a depressing influence on the nervous centres in general which is
not readily to be explained. One important factor, however, is the
cooling of the superficial layers of the blood, which occurs the more
easily when the stimulus of the chilly air is not sufficiently sharp and
sudden to cause a firm contraction of the cutaneous vessels, while
the moisture rapidly absorbs the heat of the blood. From this result,
indirectly, various disorders of nutrition of the deeper-lying tissues or
distant organs; and, among these, congestion and neuritis of the
sensitive nerves.

Neuralgia often coincides with the presence or advent of storms. A

noteworthy and systematic study of this relationship was carried on
through many years under the direction of S. Weir Mitchell14 by a
patient of his, an officer who suffered intensely from neuralgia of the
stump after amputation of the leg. The attacks of pain were found to
accompany falling of the barometer, yet were not necessarily
proportionate to the rapidity or amount of the fall. Saturation of the
air with moisture seemed to have a certain effect, but the attacks
often occurred when the centre of the storm was so remote that
there was no local rainfall. It was impossible to study the electrical
disturbances of the air with accuracy, but a certain relationship was
observed between the outbreak of the attacks and the appearance of
aurora borealis.
14 Am. Journ. of Med. Sci., April, 1877, and Philada. Med. News, July 14, 1883.
This patient's neuralgic attacks were almost certainly of neuritic
origin, and it is possible that the exacerbations were due to changes
of blood-tension in and around the nerve-sheaths. It is also possible
that they were the result of circulatory changes and disordered
nutrition of the nervous centres, already in a damaged condition from
the irritation to which they had been exposed.

2. Injuries and Irritation of Nerves.—Wounds and injuries of nerves15

and the irritation from the pressure of scars, new growths, and
aneurisms are prolific causes of neuralgic pain, partly by direct
irritation, partly by way of the neuritis which they set up. Neuralgias
are likewise common during the period of the healing of wounds, as
Verneuil long since pointed out. The pain may be near the wound
itself or in some distant part of the body.
15 See S. Weir Mitchell, Injuries of Nerves.

Neuralgia due to the pressure and irritation of tumors, new growths,

or aneurisms requires a special word. The pain is apt to be intensely
severe, but what is of especial importance is that the symptoms may
not present anything which is really characteristic of their origin,
except their long continuance; and this should always excite grave
suspicion of organic disease.

These attacks of pain may be distinctly periodical; and this is true

whether they are felt in the distribution of the affected nerve or of
distant nerves.

Not only are direct injuries of nerves a cause of neuralgia, but

sudden concussion or jar may have a like effect—whether by setting
up neuritis or in some other way is not clear. Ollivier16 reports a case
where a blow beneath the breast caused a neuralgia which
eventually involved a large portion of the cervico-brachial plexus;
and the writer has seen a like result from a blow between the
shoulders.
16 Cited by Axenfeld and Huchard, p. 116.
Peripheral irritations, such as caries of the teeth (see below, under
Facial Neuralgia) and affections involving other important plexuses,
such as those of the uterine nerves, are a frequent cause of
neuralgia, and should always be sought for. They act in part by
setting up neuritis, and in part evidently in some more indirect
manner, since the neuralgia which they excite may be referred to
more or less distant regions, forming the so-called—

3. Reflex and Sympathetic Neuralgias.—The term reflex, as here

used, is ill chosen, and the term sympathetic only covers our
ignorance of the real processes involved, and which we should seek
for in detail. Thus, disease of the uterus or ovaries may cause facial,
mammary, intercostal, or gastric neuralgia.

Hallopeau17 suggests that some of these results may be brought

about by the pressure of enlarged lymphatic glands attached to the
affected organ.
17 Loc. cit., p. 766.

Another important centre of nervous irritation is the eye. Slight errors

of refraction, or weakness of the muscles of fixation, especially the
internal recti, are a source of frontal headaches and other nervous
symptoms, and even of typical migraine,18 to a degree which is not
usually appreciated. It is improbable that in the latter case the
irritation acts as more than an exciting cause, but it may
nevertheless be a conditio sine quâ non of the attack.
18 St. Barthol. Hosp. Repts., vol. xix.

Acute and chronic inflammations of the mucous membrane of the

frontal sinuses, perhaps even of the nasal membrane, are likewise
important; and although it is probable that the opinions sometimes
expressed as to the significance of these causes are exaggerated, it
is equally true that obstinate and, as it were, illogical persistence in
their removal will sometimes be richly rewarded.
It is especially worthy of note that there need be no local sign
whatever to call the attention of the patient to the presence of the
peripheral irritation.

Nothnagel19 has described neuralgias which come on in the first

week of typhoid, and are to be distinguished from the general
hyperæsthesia of later stages. He describes an occipital neuralgia of
this sort which finally disappeared under the use of a blister. Other
acute diseases may have a like effect. The writer has seen a severe
facial neuralgia in the first week of an insidious attack of pneumonia
in a person who was not of neuralgic habit, and before the fever or
inflammation had become at all severe.
19 Virch. Arch., vol. liv., 1872, p. 123.

PATHOLOGY AND DIAGNOSIS.—In surveying the clinical history of the

neuralgias and the circumstances under which they occur, we have
grouped together a large number of symptoms of very different
character from each other, and we have now to inquire to what
extent these symptoms are really united by a pathological bond.

Two opposite opinions have been held concerning the pathology of

neuralgic affections. According to one opinion, every neuralgic
attack, no matter how it is excited, is the manifestation of a neurosis
—that is, of a functional affection of the nervous centres—to which
the term neuralgia may properly be applied. This view is based on
the resemblance between the different forms of neuralgia, or the
apparent absence, in many cases, of any adequate irritation from
without, and the fact that the persons in whom neuralgias occur
usually show other signs of a neuropathic constitution.

According to the other opinion, the various forms of neuralgia are so

many different affections, agreeing only in their principal symptom,
and are due sometimes to congestion or anæmia of the nerves or
the nerve-centres; sometimes to neuritis, the pressure of tumors, or
the irritation of distant nerves; sometimes, finally, to a functional
disorder of the nervous centres. The arguments in favor of this
opinion are that the difference between the symptoms of the different
neuralgias as regards their mode of onset and decline, their duration,
the persistence of the pain, and the degree to which the attacks are
accompanied by organic changes of nutrition in the tissues and in
the nerve itself, are so great as to make it appear improbable that we
are dealing in every case simply with one or another modification of
a single affection.

This is a valid reasoning, and it is certainly proper to exhaust the

possibilities of explaining the symptoms that we find in a particular
case by referring them to morbid processes which we can see or of
which we can fairly infer the presence, before we invoke an influence
of the nature of which we understand so little as we do that of the
functional neuroses. At the same time, it must be distinctly borne in
mind that the symptoms of certain neuralgias, and the relation which
the neuralgias in general bear to other neuroses, can only be
accounted for on the neurosal theory, and that in a given case we
can never be sure that this neurosal tendency is not present and is
not acting as at least a predisposing cause. It is especially important
to bear this possible influence in mind in deciding upon prognosis
and treatment.

We may now review briefly the signs which should lead us to

diagnosticate or suspect the presence of the various special causes
of neuralgic symptoms.

Neuritis is indicated by the presence of organic disorders of nutrition

affecting the skin, hair, or nails, or of well-marked muscular wasting;
by pain, not only occurring in paroxysms, but felt also in the
intermissions between the paroxysms, or continuous sensations of
prickling and numbness, even without pain; by tenderness along the
course of the nerve; by anæsthesia, showing itself within the first few
days of the outbreak of a neuralgia; by persistent paralysis or paresis
of muscles.

Neuritis may be suspected, even if one or all of these signs are

absent, in the prolonged neuralgias which follow wounds or strains of
nerves or exposure to damp cold, or which occur in nerves which are
in the immediate neighborhood of diseased organs; also where the
pain is relieved by compression of the nerve above the painful part,
or, on the other hand, where pressure on the nerve excites a pain
which runs upward along the course of the nerve.

It may also be suspected in the large class of superficial neuralgias

which follow a regular and protracted course with gradual onset and
decline, and where the pain is felt not only in the region of
distribution of a nerve, but also along its course—that is, in the
nerve-fibres (either the recurrent nerves or the nervi nervorum)
which are distributed in the sheath of the main trunk or the adjoining
tissues.20
20 See Cartaz, Des Névralgics envisagés au point de vue de la sensibilité récurrente,
Paris, 1875.

It must be remembered that the study of neuritis, and especially of

chronic neuritis, is still in its infancy, and that we are by no means in
possession of its complete clinical history.21
21 See Pitres and Vaillard, Arch. de Névrologie, 1883.

The presence of congestion of the sensory nerves or nerve-centres

may be inferred with some degree of probability where neuralgic
attacks of relatively sudden onset and short duration occur in parts
which have been exposed to heat or cold, or in connection with
suppression of the menstruation, or, it is said, as a result of
intermittent fever. The exacerbations of pain which take place in
cases of chronic neuritis under changes of weather and after fatigue
are very likely due to this cause; and the same may be true of some
of the fleeting pains which occur in chlorotic and neuropathic
persons who are subject to fluctuations of the circulation of vaso-
motor origin.

The same vaso-motor influences which cause congestion may also

cause the correlative state of anæmia, which becomes thus a cause
of transient and shifting though often severe attacks, which may be
irregular in their distribution. General anæmia is also a predisposing
cause of severe typical seizures, as has been pointed out above.
The pressure of new growths or of aneurisms is to be suspected
when neuralgic attacks are unusually severe and prolonged, recur
always in the same place, and occur in persons who are not
predisposed to neuralgias. The pains from this cause are apt to be
relatively continuous, but they may, on the other hand, be distinctly
paroxysmal, and may occupy a part of the body far removed from
the irritating cause.

Bilateral pains should also excite suspicion of organic disease,

though they may be due to other causes, such as gout, diabetes,
and metallic poisoning.

Neuralgic attacks may be supposed to be of neurosal origin when

they are of sudden onset and short duration, or when they occur in
persons of neuropathic constitution, and, by exclusion, when no
other cause is found. These conditions are best fulfilled in the case
of migraine and the visceral neuralgias. It must, however, be borne in
mind that the neuropathic predisposition is sometimes well marked
even in the case of the superficial neuralgias, especially the
epileptiform neuralgia of the face.

GENERAL TREATMENT.—To treat neuralgia with satisfaction it is

necessary to look beyond the relief of the particular attack and
search out the causes by which it was provoked. As has already
been remarked, these are usually multiple, and among them will be
found, in the great majority of cases, some vice of nutrition or faulty
manner of life.

It is safe to say that any dyscrasia occurring simultaneously with

neuralgia, whether gout, phthisis, malaria, or diabetes, should
receive its appropriate treatment, whatever theory we may hold as to
the real connection between the two conditions.

In protracted neuralgias it is always proper to assume that neuritis

may be present—i.e. to treat the nerve itself by galvanism and local
applications. Local irritations, such as diseases of the eye, ear, teeth,
nose, or uterus, should be sought out and removed; and attention
may here be called again to the fact that a neuralgia may be due to
some local condition which does not of itself attract the patient's
attention.

Patients who are subject to pain at changes of weather or on

exposure should be suitably protected by clothing, and should have
their cutaneous regulatory apparatus strengthened by baths and
friction. The best protection, however, is incapable of entirely
warding off the effect of atmospheric changes upon the nervous
centres. Vaso-motor changes of neurotic origin can be, in a
measure, prevented by removing the patient from the influence of
irregularity of life and emotional excitement and through an improved
nutrition.

If the patient has been subjected to chronic fatigue or nervous strain,

not only must these be avoided, but their action should be
counteracted by the requisite rest and tonic treatment.

Long hours of sleep at night may often be supplemented to

advantage by rest during certain hours of the daytime. If the patient
cannot take active exercise, massage is indicated, and in some
cases of anæmia this may advantageously be combined with the wet
pack, in the manner described by Mary Putnam Jacobi.22
22 Massage and Wet Pack in the Treatment of Anæmia.

Where these measures cannot be carried out, the writer has found it
of much service in these, as in a large class of debilitated conditions,
to let the patient rub himself toward the end of the forenoon in a
warm room with a towel wet in cold or warm water, and then lie down
for an hour or so or until the next meal. If acceptable, the same
operation may be repeated in the afternoon.

Neuralgic patients are apt to be underfed, and even where this is not
distinctly the case, a systematic course of over-feeding,23 with
nourishing and digestible food, such as milk, gruel, and eggs, given
at short intervals, is often of great service if thoroughly carried out.
The full benefit of this treatment cannot always be secured unless
the patient is removed from home, and, if need be, put to bed and
cared for by a competent nurse.
23 See S. Weir Mitchell, Fat and Blood; and Nervous Diseases, especially of Women.

A change of climate, and especially the substitution of a dry and

warm for a moist and cold climate, will sometimes break up the
neuralgic habit, for the time at least. In making choice of climate or
locality, however, the physician should keep distinctly in view the end
that he desires to gain. Thus, the debility or anæmia which is the
essential condition of many neuralgias may often be relieved by
surroundings which would not be thought favorable to the neuralgic
tendency as such. Oftentimes the sedative influence of quiet country
life is all that is required.

Of the tonic drugs, cod-liver oil, iron, arsenic, and quinine are by far
the most important, and it is often well to give them simultaneously.
Iron may be used in large doses if well borne, for a short time at
least. Quinine may be given in small doses as a tonic, or in larger
doses to combat the neuralgic condition of the nervous system. This
remedy has long been found to be of great value in the periodical
neuralgias of the supraorbital branch of the fifth pair, but its
usefulness is not limited to these cases. It may be of service in
periodical neuralgias of every sort, and often even in non-periodical
neuralgia.

When the attacks recur at stated intervals care should be taken to

anticipate them with the quinine by about four hours, even if the
patient has to be waked in the early morning for the purpose. Single
doses of fifteen, twenty, or even thirty grains may check the attacks
where smaller doses have failed. Such doses cannot, however, be
long continued, and are not to be classed as tonic.

Of other remedies which directly influence the neuralgic condition,

the following are the most important: opium, aconite, gelsemium,
phosphorus, belladonna, chloride of ammonium, cannabis Indica,
croton-chloral, electricity, hydropathy, massage, counter-irritation,
subcutaneous injections of water, chloroform, osmic acid, etc.;
surgical operations.

Opium is usually employed only for the momentary relief of pain, but
it has also been claimed that in small and repeated doses it may
exert a really curative action. This should not, however, be too much
counted on. Opium should never be used continuously for the simple
relief of pain unless under exceptional circumstances, the danger of
inducing the opium habit is so much to be dreaded. Moreover, both
patient and physician are less likely to seek more permanent means
of cure if this temporary remedy can always be appealed to. It is best
given by subcutaneous injections of the various salts of morphine.
The dose should always be small at first (gr. 1/12 and upward), unless
the idiosyncrasy of the patient is already known; and there is
probably no advantage in making the injections at the seat of pain or
in the immediate neighborhood of the nerve supplying the affected
part, except such as might attend the injection of any fluid (see
below).

Belladonna (atropia), which is so often given with morphine to

diminish its unpleasant effects, seems at times, even when given
alone, to have an effect on neuralgia out of proportion to its
anæsthetizing action, which is very slight. It is considered to be
especially useful in the visceralgias.

Aconite, given, if necessary, in doses large enough and repeated

often enough to cause numbness and tingling of the lips and the
extremities for some days, will sometimes break up an attack,
especially of trigeminal neuralgia,24 better than any other means; but
its use is liable to depress the heart, and it is a dangerous remedy if
not carefully watched. Some patients complain that it causes a
marked sense of depression or faintness, and a feeling of coldness;
and indeed its full therapeutic effect is sometimes not obtained until
such symptoms as these are induced to some degree. The use of
the crystallized alkaloid, aconitia, has the advantage of ensuring
certainty of dose.
24 See Seguin, Arch. of Med., vol. i., 1879; vol. vi., 1881.