Professional Documents
Culture Documents
eBook PDF
Visit to download the full and correct content document:
https://ebooksecure.com/download/100-case-reviews-in-neurosurgery-ebook-pdf/
Any screen.
Any time.
Anywhere.
Activate the eBook version
of this title at no additional charge.
Expert Consult eBooks give you the power to browse and find content,
view enhanced images, share notes and highlights—both online and offline.
4 Click “Redeem”
5 Log in or Sign up
6 Go to “My Library”
It’s that easy!
Place Peel Off
Sticker Here
MICHELE R. AIZENBERG, MD
Associate Professor of Neurological Surgery and Oncology,
Director, Brain and Spine Cancer Center
University of Nebraska Medical Center
Omaha, NE, USA
Edinburgh London New York Oxford Philadelphia St Louis Sydney Toronto 2017
© 2017, Elsevier Inc. All rights reserved.
No part of this publication may be reproduced or transmitted in any form or by any means, electronic or
mechanical, including photocopying, recording, or any information storage and retrieval system, without
permission in writing from the publisher. Details on how to seek permission, further information about the
Publisher’s permissions policies and our arrangements with organizations such as the Copyright Clearance
Center and the Copyright Licensing Agency, can be found at our website: www.elsevier.com/permissions
This book and the individual contributions contained in it are protected under copyright by the Publisher
(other than as may be noted herein).
Notices
Knowledge and best practice in this field are constantly changing. As new research and experience
broaden our understanding, changes in research methods, professional practices, or medical treatment
may become necessary.
Practitioners and researchers must always rely on their own experience and knowledge in evaluating
and using any information, methods, compounds, or experiments described herein. In using such
information or methods they should be mindful of their own safety and the safety of others, including
parties for whom they have a professional responsibility.
With respect to any drug or pharmaceutical products identified, readers are advised to check the most
current information provided (i) on procedures featured or (ii) by the manufacturer of each product to be
administered, to verify the recommended dose or formula, the method and duration of administration,
and contraindications. It is the responsibility of practitioners, relying on their own experience and
knowledge of their patients, to make diagnoses, to determine dosages and the best treatment for each
individual patient, and to take all appropriate safety precautions.
To the fullest extent of the law, neither the Publisher nor the authors, contributors, or editors, assume
any liability for any injury and/or damage to persons or property as a matter of products liability,
negligence or otherwise, or from any use or operation of any methods, products, instructions, or ideas
contained in the material herein.
ISBN: 978-0-323-35637-4
Printed in China
Preface xii
List of Contributors xiii
Acknowledgments xxii
Dedication xxiii
SECTION I
Vascular Neurosurgery
Section Editor: Alexander A. Khalessi, MD
2 Cavernous Malformation 9
Jeffrey A. Steinberg, MD • J. Scott Pannell, MD •
Alexander A. Khalessi, MD
v
vi Contents
14 Cerebellar Hemorrhage 81
Reid Hoside, MD • J. Scott Pannell, MD •
Alexander A. Khalessi, MD
15 Moyamoya Disease 85
Brandon C. Gabel, MD • J. Scott Pannell, MD •
Alexander A. Khalessi, MD
17 Carotid Stenosis 93
Jeffrey A. Steinberg, MD • J. Scott Pannell, MD •
Alexander A. Khalessi, MD
SECTION II
Nontraumatic Cranial Lesions
Section Editor: Griffith R. Harsh IV, MD • J. Dawn Waters, MD
25 Craniopharyngioma 141
Matthew G. MacDougall, MD • David D. Gonda, MD •
Michael L. Levy, MD, PhD
26 Glioblastoma 147
Kevin K.H. Chow, MD, PhD
35 Ependymoma 183
Zachary Medress • Melanie G. Hayden Gephart, MD
SECTION III
Neurosurgical Trauma
Section Editor: Joseph D. Ciacci, MD
SECTION IV
Spinal Neurosurgery
Section Editor: Adam S. Kanter, MD
60 Chordoma 313
Michael M. McDowell, MD • Zachary J. Tempel, MD •
Adam S. Kanter, MD
SECTION V
Pediatric Neurosurgery
Section Editor: Michael L. Levy, MD, PhD
62 Myelomeningocele 327
Alexa Smith, MD • Bond Nguyen •
Michael L. Levy, MD, PhD
SECTION VI
Stereotactic and Functional Neurosurgery
Section Editor: Paul S. Larson, MD
SECTION VII
Peripheral Nerve Neurosurgery
Section Editor: Justin Brown, MD
SECTION VIII
Neurology
Section Editors: Neal Prakash, MD, PhD • Ramsis Benjamin, MD
98 Neurosarcoidosis 521
Ramsis Benjamin, MD
Glossary 533
APPENDICES
Section Editors: Henry E. Aryan, MD • Aasim S. Kazmi, MD
Index 579
Preface
As the most challenging discipline, Neurosurgery rebuffs any single text’s attempt at reveal-
ing its intricacies and complexities. Accordingly, this text and its individual chapters aim
for a more humble goal. Together, they aspire to serve as a primer of essential material
often reviewed during certification examinations and a framework into which deeper
knowledge can be contextualized.
From the perspective of didactic utility, the standard, time-tested neurosurgical text-
books offer a distillation of the most useful art and schemata. Therefore, figures from these
familiar texts have been incorporated into this book, along with new art and imaging, in
the hope that the aggregate will constitute a robust visual fabric within 100 Case Reviews
in Neurosurgery.
The book is divided into intuitive sections. The information provided and the questions
posed follow the experience of a neurosurgeon being consulted in the hospital or seeing
a new patient in clinic that has come to them for care. The vascular section covers surgical
and nonsurgical elements that are key elements of essential vascular cases. The peripheral
nerve section is particularly detailed since this is a specialized field most general neuro-
surgeons have limited exposure to in daily practice. The appendices provide information
that is vital yet cumbersome to include in the flow of the chapters. The layout and pre-
sentation of information follows the formats of common grand rounds and examinations
most readers have experienced from the beginning of their neurosurgical training through
their current continuing education.
The most challenging part of constructing the book you now read has been to find that
elusive balance invaluable to the modern pedagogical text between comprehensiveness
and concision, between textual explanation and visual illustration, between esoteric speci-
ficity and simple intelligibility. My hope is that the content presented here has been
insightfully and incisively curated for your purposes.
Rahul Jandial
xii
List of Contributors
xiii
xiv List of Contributors
For those that have not had the opportunity to assemble a text, the immense collaborative
effort can be lost behind the bold, large font names on the cover. Yes, the editors are key
to the process. Equally important is the publishing team. Alexandra Mortimer, Louisa
Talbott and Andrew Riley have been thoughtful and attentive companions in making this
book. The book would be porous and flawed without them. Most importantly Charlotta
Kryhl has helped shepherd us through the original idea, its need in the neurosurgical
community and ultimately the spirit of this textbook. Thank you for your support and
leadership.
xxii
For boundless love
For unwavering support
For my mother, Sushma Jandial
Rahul Jandial
This page intentionally left blank
Chen, Ph.D, for gifting me his disdain of the conventional-and
to my mother, Professor S.J. Chen,
for my brutal endurance and voice of reason.
Mike Y. Chen
Presentation
An 18-year-old female presents to the ED with severe headaches, nausea, vomiting, and
complex partial seizure beginning on the right side of the body. She has no history of prior
seizures. She has had headaches in the past, but this headache is worse than usual.
• PMH: otherwise unremarkable; no recent trauma
• Exam: mild left-sided weakness
Differential Diagnosis
• Vascular
• Ischemic/embolic stroke
• Arteriovenous malformation (AVM)
• Cavernous hemangioma
• Aneurysm rupture
• Moyamoya disease
• Infectious
• CNS infection (herpes simplex encephalitis)
• Neoplastic
• Primary cerebral tumor
• Metastasis (most commonly lung, renal cell carcinoma, melanoma, breast)
• Metabolic/toxic/nutritional
• Alcohol withdrawal
• Drug intoxication
• Electrolyte abnormalities
• Hypoglycemia
• Congenital/developmental
• Osler-Weber-Rendu disease
• Sturge-Weber syndrome
• Wyburn-Mason syndrome (“Bonnet–Dechaume–Blanc syndrome”)
1
2 SECTION I Vascular Neurosurgery
Initial Imaging
FIGURE 1-1
FIGURE 1-2
1 Cerebral Arteriovenous Malformation 3
Further Imaging
Anterior parietal
artery
Posterior parietal
artery
Angular artery
Temporo-occipital
artery
Superior division
of left MCA
M1 segment of
the left MCA
Fetal PCA
FIGURE 1-3 PA and lateral left anterior circulation digital subtraction angiogram.
Anterior parietal
artery
Posterior parietal
branch of left MCA
Angular artery
Parieto-occipital Temporo-occipital
branch of left PCA artery
Inferior division
Calcarine branch of left MCA
of left PCA
Superior division
of left MCA
Anterior choroidal
artery
Fetal posterior
cerebral artery
Internal carotid
artery
FIGURE 1-4 PA and lateral left anterior circulation digital subtraction angiogram.
4 SECTION I Vascular Neurosurgery
Superior
anastomotic
vein of Trolard
Superior
sagittal sinus
Parietal cortical
bridging veins
Superficial middle
temporal vein
Straight sinus
Torcula Inferior
anastamotic
vein of Labbe
Transverse sinus
Sigmoid sinus
• Figures 1-3 and 1-4 are digital subtraction angiograms of PA and lateral left anterior
circulation performed by left ICA injection. They depict a large 6 cm AVM nidus sup-
plied by multiple MCA and foetal variant PCA pedicles.
• Figure 1-5 is a lateral venous phase digital subtraction angiogram performed by left ICA
injection and demonstrates superficial and deep venous drainage from the AVM.
• Findings are consistent with Spetzler-Martin (SM) scale grade 5 AVM.
Further Workup
• Imaging
• ECG
• Grading
• SM or supplemented SM grading (SM-supp)
• Laboratory
• CMP, CBC, ESR, and CRP
• Consultants
• Cardiology (ECHO)
Pathophysiology
Cerebral AVM is a rare disorder with an estimated prevalence of 0.01% to 0.5% that com-
monly presents with intracranial hemorrhage or seizures. It is the most common cause of
spontaneous intraparenchymal hemorrhage in adults <40 years old. The majority of lesions
(~88%) are superficially located, with approximately 20% having associated aneurysms.
The natural history is heterogeneous, with an approximate 2.2% annual risk of rupture
for previously unruptured AVMs and 4.5% for ruptured. This risk is significantly altered
by several factors including prior hemorrhage, venous drainage, and associated aneurysms;
increasing the annual risk of hemorrhage to as high as 34% in patients having all three
risk factors. Furthermore, the cumulative risk of rupture increases with age. Ruptured
AVMs result in major mortality and morbidity; the associated death rate is as high as 29%
and only 55% of survivors are capable of independent living (mRS ≤2). A majority of
patients will be diagnosed with an AVM before the age of 40, and there is substantial risk
of at least one hemorrhage during their lifetime; therefore these lesions should be treated.
1 Cerebral Arteriovenous Malformation 5
Of note, the recently published ARUBA trial argued for the superiority of medical manage-
ment versus interventional therapy for unruptured AVMs; however, methodological flaws
within the trial and other more recent studies cast significant doubt on those findings.
Treatment Options
Treatment of AVMs is often multimodal, tailored to the specifics of the lesion, and com-
monly assessed by the SM grading scale.
• Surgery
• Resection is the most definitive treatment, resulting in complete obliteration of the
AVM in nearly all patients
• Appropriate for lesions with SM grade ≤5 or SM-supp grade ≤6
• May be combined with embolization for larger AVMs
• Stereotactic radiosurgery
• Appropriate for lesions ≤3cm in diameter with a compact nidus or location in an
eloquent area where resection would result in significant neurologic deficits
• Long latency to lesion obliteration period (1–3 years) and does not completely elimi-
nate the risk of hemorrhage
• May be combined with embolization
• Embolization
• Facilitates both surgery and stereotactic radiosurgery
• May be appropriate for complete AVM obliteration in select cases
Surgical Technique
The approach must be tailored to the AVM location and key associated vascular structures,
including arterial feeders, draining veins, and boundaries of the nidus. Extranidal aneu-
rysms should also be accounted for when planning an approach. Intraoperative monitoring
is important when the AVM is located in or near an eloquent cortex; electrophysiological
monitoring with continuous bilateral upper and lower somatosensory and motor evoked
potentials may aid in the resection. Preoperative staging for embolizations may be per-
formed if deemed appropriate. The significant majority of AVMs are located in the cerebral
convexity, and this surgical approach is outlined next.
Next, surface feeding arteries are identified and occluded. The dissection of the nidus
may then begin in a circumferential pattern. Deep feeding arteries should be coagulated
and cut or clipped as needed. Upon completion of the nidus dissection, the deep arterial
pedicles must be identified and dissected.
Deep venous drainage is approached last. Major draining veins must first be occluded
with a temporary aneurysm clip and the AVM observed to identify indications of intact
arterial pedicles, such as increased distension of the AVM. Following control of these veins,
the AVM is removed en bloc and blood pressure may be transiently elevated to confirm
adequate hemostasis.
FIGURE 1-10 After the AVM nidus has been removed, the resection bed must be examined for residual
nidi and areas of bleeding. Continuous bleeding often means residual nidi and should be examined closely.
Intraoperative imaging may consist of digital subtraction angiography, with or without supplementary indo-
cyanine green dye video angiography. The resection bed must be completely dry because increases in
systolic blood pressure can easily lead to re-bleeds, necessitating evacuation. Systolic blood pressure can
be increased temporarily to high-normal levels to check for areas of potential bleeding. (Reprinted with
permission. Jandial R, McCormick P, Black PM. Core Techniques in Operative Neurosurgery. Philadelphia:
Philadelphia: Elsevier/Saunders; 2011, ©2011.)
Once confirmed, an EVD or ICP monitor is placed if deemed appropriate. The dura is
then closed, bone flap replaced, and skin closed.
KEY PAPERS
Al-Shahi R, Bhattacharya JJ, Currie DG, et al. Prospective, population-based detection of intracranial vascular
malformations in adults the Scottish intracranial vascular malformation study (SIVMS). Stroke.
2003;34(5):1163-1169.
8 SECTION I Vascular Neurosurgery
Brown RD, Wiebers DO, Forbes G, et al. The natural history of unruptured intracranial arteriovenous malforma-
tions. J Neurosurg. 1988;68(3):352-357.
Friedlander RM. Arteriovenous malformations of the brain. N Engl J Med. 2007;356(26):2704-2712.
Gross BA, Du R. Natural history of cerebral arteriovenous malformations: a meta-analysis. J Neurosurg.
2013;118(2):437-443.
Kim H, Abla AA, Nelson J, et al. Validation of the supplemented Spetzler-Martin grading system for brain arte-
riovenous malformations in a multicenter cohort of 1009 surgical patients. Neurosurgery. 2015;25-31.
Korja M, Bervini D, Assaad N, et al. Role of surgery in the management of brain arteriovenous malformations
prospective cohort study. Stroke. 2014;45(12):3549-3555.
Mohr JP, Parides MK, Stapf C, et al. Medical management with or without interventional therapy for unruptured
brain arteriovenous malformations (ARUBA): a multicentre, non-blinded, randomised trial. Lancet.
2014;383(9917):614-621.
Potts MB, Zumofen DW, Raz E, et al. Curing arteriovenous malformations using embolization. Neurosurg Focus.
2014;37(3):E19.
Stapf C, Mast H, Sciacca RR, et al. Predictors of hemorrhage in patients with untreated brain arteriovenous
malformation. Neurology. 2006;66(9):1350-1355.
van Beijnum J, van der Worp H, Buis DR, et al. Treatment of brain arteriovenous malformations: a systematic
review and meta-analysis. JAMA. 2011;306(18):2011-2019.
Case 2
Cavernous Malformation
Jeffrey A. Steinberg, MD •Alexander
J. Scott Pannell, MD •
A. Khalessi, MD
Presentation
A healthy 45-year-old female presents to the emergency room with seizure.
• PMH: otherwise unremarkable
• Exam: mildly slowed cognition
• Pupils equal and reactive
• Moves all extremities with full strength
• Face/smile symmetric
• No drift
Differential Diagnosis
• Vascular
• Stroke/TIA
• Hemorrhage of vascular malformation
• Neurologic
• Seizure
• Neoplastic
• Brain tumor
• Infectious
• Meningitis, abscess
• Other
• MS
• Systemic/metabolic
9
10 SECTION I Vascular Neurosurgery
Initial Imaging
FIGURE 2-1
FIGURE 2-2
2 Cavernous Malformation 11
FIGURE 2-3
FIGURE 2-4 Brainstem cavernous malformations are often removed through a parenchymal incision much
smaller than the malformation itself. In contrast to many supratentorial cavernous malformations, the prin-
ciples of piecemeal resection are applied here. After incision the lesion is emptied, internally targeting cavi-
ties with liquefied old blood. (Reprinted with permission. Jandial R, McCormick P, Black PM. Core
Techniques in Operative Neurosurgery. Philadelphia: Elsevier/Saunders, ©2011.)
12 SECTION I Vascular Neurosurgery
A B
FIGURE 2-5 When the malformation has been partially internally decompressed, a cleavage plane between the lesion and
the surrounding gliotic hemosiderin-stained parenchyma is developed beginning in the portion of the capsule and surface of
the malformation closest to the entry point. Specifically designed round dissectors (A) or gentle spread of the bipolar forceps
(B) can be used for this maneuver. During this maneuver, gentle traction is applied to the cavernous malformation with the
suction in the surgeon’s left hand, minimizing the mechanical trauma to the surrounding parenchyma. (Reprinted with permis-
sion. Jandial R, McCormick P, Black PM. Core Techniques in Operative Neurosurgery. Philadelphia: Elsevier/Saunders,
©2011.)
FIGURE 2-6 After further internal emptying of the malformation, the cleavage plane is dissected further with a round dis-
sector. Because of the depth of the field and the limited size of the entry incision, this portion of the operation is done more
by “feel” than by direct vision. Extreme caution and gentle touch must be exercised to avoid any damage to portions of
parenchyma not in direct vision. (Reprinted with permission. Jandial R, McCormick P, Black PM. Core Techniques in Opera-
tive Neurosurgery. Philadelphia: Elsevier/Saunders, ©2011.)
2 Cavernous Malformation 13
FIGURE 2-7 After the bulk of the cavernous malformation has been released from the surrounding paren-
chyma, gentle traction with pituitary forceps is applied to the edges of the most superficial portion of the
lesion. If the cavernous malformation has been properly separated, very gentle but steady traction at this
point often leads to the malformation eventually “giving in.” (Reprinted with permission. Jandial R, McCor-
mick P, Black PM. Core Techniques in Operative Neurosurgery. Philadelphia: Elsevier/Saunders, ©2011.)
Further Workup
• Laboratory
• Routine labs
• Imaging
• MRI brain including gradient echo sequences
• Cerebral angiography generally not necessary for classically appearing lesions, but
may be useful in atypical lesions to rule out other vascular anomalies
Pathophysiology
Cavernoma is defined as a vascular malformation composed of dilated capillary-like vessels
without intervening neuronal parenchyma. Cavernomas may occur in the brain or spinal
cord; they can range in size from a few millimeters to several centimeters, are often associ-
ated with venous lesions, and may be congenital or acquired. Grossly they appear as
purple-blue multilobulated “mulberry” lesions, often with gliotic, yellow-stained sur-
rounding tissue from repeated small hemorrhages. Microscopically cavernomas are thin-
walled vessels that lack smooth muscle and elastin and are composed of a single cell layer
of endothelial cells that can contain areas of thrombosis.
Treatment Options
• Observation
• Serial imaging in patients with asymptomatic lesions, lesions in deep locations, or
eloquent regions
• Monitor for hemorrhage or secondary growth/changes in recurrent hemorrhage.
• Medical management
• Focus on symptom management of headaches and seizures.
14 SECTION I Vascular Neurosurgery
• Surgery
• Surgical resection is the only treatment that is curative for cavernomas. Complete
resection eliminates the risk of hemorrhage and improves seizures and headaches.
• Stereotactic radiosurgery
• Controversial in the treatment of cavernomas, generally only considered for inoper-
able lesions with progressive symptoms. Results and evidence vary.
Surgical Technique
The goal of surgery is complete removal of the cavernoma. As with many other neurosur-
gical pathologies, the approach is critical in facilitating resection without injury to normal
parenchyma. Intraoperative navigation and ultrasound may be beneficial for localization.
Because these lesions are not highly vascularized, piecemeal removal is possible (Figure
2-4, cavernoma dissection). Dissection between the lesion and the surrounding gliotic
hemosiderin-stained parenchyma is achieved. Decompression of the cavernoma may facili-
tate dissection by allowing folding in of the lesion from the normal tissue (Figures 2-4,
2-5, 2-6, Cavernoma dissection). Once the lesion is completely removed, hemostasis of
the cavity should be achieved with irrigation and a hemostatic agent, as opposed to bipolar
cautery, to decrease risk of injury to parenchymal tissue.
KEY PAPERS
Brown RD Jr, Flemming KD, Meyer FB, et al. Natural history, evaluation, and management of intracranial vascular
malformations. Mayo Clin Proc. 2005;80:269-281.
Lanzino G, Spetzler RF. Cavernous Malformations of the Brain and Spinal Cord. New York: Thieme; 2008.
Porter RW, Detwiler PW, Spetzler RF, et al. Cavernous malformations of the brainstem: experience with 100
patients. J Neurosurg. 1999;90:50-58.
Case 3
Ruptured Middle Cerebral
Artery Aneurysm
Vincent J. Cheung, MD
J. Scott Pannell, MD •• Jayson A. Sack, MD •
Alexander A. Khalessi, MD
Presentation
A 47-year-old woman with no significant past medical history presents to the emergency
department with acute onset headache, nausea, and vomiting. Upon presentation, she is
lethargic but able to answer orientation questions and briskly follow commands in all
extremities. Cranial nerves and motor strength are all grossly intact.
Differential Diagnosis
• Vascular
• Ruptured aneurysm
• Ruptured dural arteriovenous fistula
• Ruptured arteriovenous malformation
• Hypertensive hemorrhage
• Infectious
• Rupture of mycotic cerebral aneurysm (in setting of IV drug use)
• Meningitis
• Other
• Traumatic hemorrhage
• Cocaine-induced intracerebral hemorrhage
• Migraine
Initial Imaging
15
FIGURE 3-1
16 SECTION I Vascular Neurosurgery
FIGURE 3-2
Imaging Description
• Figure 3-1: Noncontrast CT scan of the head. Dense subarachnoid hemorrhage is
present in the right sylvian fissure.
• Figure 3-2: AP projection digital subtraction angiography, right internal carotid injec-
tion. An elongated M1 segment MCA aneurysm is shown.
Further Workup
Following a subarachnoid hemorrhage, the first priority should be given to “ABCs” (airway,
breathing, circulation). If there is significant intraventricular hemorrhage, or the patient
must be intubated and sedated for airway protection or poor neurologic status, an external
ventricular drain should be placed. Strict blood pressure control is critical.
Following subarachnoid hemorrhage, patients are at risk for vasospasm. Vasospasm is
a pathologic constriction of blood vessels that can result in ischemic stroke and is a major
cause of morbidity and mortality after aneurysmal rupture. After securing a ruptured
aneurysm through endovascular embolization or craniotomy for clip ligation, patients are
typically observed for at least 2 weeks. Vasospasm risk peaks from 3 to 14 days after
rupture. During this time, efforts are made to monitor for and mitigate the effects of
vasospasm.
Pathophysiology
Aneurysms are pathologic dilatations in the wall of a blood vessel. When the aneurysm
weakens to the point of rupture, blood extravasates into the subarachnoid space. The
development of a cerebral aneurysm is multifactorial and includes focal structural defects
in the vessel wall, hemodynamic stress from turbulent blood flow or branch point, and
familial factors. Hereditary syndromes associated with cerebral aneurysms include Ehlers-
Danlos syndrome, fibromuscular dysplasia, Osler-Weber-Rendu syndrome, and polycystic
kidney disease. Aneurysms may also form from trauma or infection. Traumatic aneurysms
differ from true aneurysms in that they typically result from dissection between layers of
a vessel wall. In contrast, saccular aneurysms involve all layers of the vessel wall. Infectious
aneurysms (also known as mycotic aneurysms) typically occur in distal cortical branches
and can form in response to focal weakening of the vessel wall due to septic emboli from
bacterial endocarditis, meningitis, or fungal infection.
3 Ruptured Middle Cerebral Artery Aneurysm 17
Ophthalmic artery
A2 segment Posterior
communicating
artery
Anterior
choroidal
artery
Orbitofrontal Middle cerebral
artery artery (M1 segment)
Medial striate artery
of Heubner
Medial lenticulostriate
arteries Lateral
lenticulostriate
arteries M2 segments
FIGURE 3-3 Anatomy of anterior circulation with the major branches and perforators of the internal
carotid artery, of the M1 segment of the middle cerebral artery, of the A1 and A2 segments of the anterior
cerebral artery, and of the anterior communicating artery. (Reprinted with permission. Winn HR. Youmans
Neurological Surgery. 6th ed. Elsevier; 2011.)
Treatment Options
• Craniotomy for clip ligation
• Endovascular embolization
Surgical Technique
The patient is positioned supine in a head holder, and the head is maintained in a 15- to
20 degree rotation away from the side of the aneurysm. Additionally, the head is extended
roughly 20 degree to allow gravity to retract the frontal lobe from the anterior cranial fossa.
A curvilinear skin incision is performed inferiorly from the zygomatic arch (<1 cm from
tragus) and superiorly to the midline, staying just behind the hairline. The skin and tem-
poralis muscle are elevated together and retracted forward with skin hooks. A standard
frontotemporal craniotomy is performed. Additional bone of the pterion and lesser wing
of the sphenoid are drilled down and/or rongeured until the lateral edge of the superior
orbital fissure is reached. The dura is then opened with a semicircular incision.
FIGURE 3-4 Positioning of the patient for the right-sided
lateral supraorbital approach. (Reprinted with permission.
Quiñones-Hinojosa A. Schmidek and Sweet Operative
Neurosurgical Techniques. 6th ed. Elsevier; 2012.)
20° 20°
Another random document with
no related content on Scribd:
The Project Gutenberg eBook of Satu sydämestä
ja auringosta
This ebook is for the use of anyone anywhere in the United States
and most other parts of the world at no cost and with almost no
restrictions whatsoever. You may copy it, give it away or re-use it
under the terms of the Project Gutenberg License included with this
ebook or online at www.gutenberg.org. If you are not located in the
United States, you will have to check the laws of the country where
you are located before using this eBook.
Language: Finnish
Kirj.
Elina Vaara
SISÄLLYS:
SATU SYDÄMESTÄ JA AURINGOSTA
Kaukaiset metsät.
Satu sydämestä ja auringosta.
Mennyt suvi.
Lumikkosydän.
Järvellä.
Hiiden hovi.
Syysromanssi.
Saaren soittaja.
VILLIVIINI
Karnevaalihuume.
Käsky — kielto..
Kuolleet.
Judithin tuska.
Villiviini.
HILJAISIA AKORDEJA
Puutumus.
Hiljainen huone.
Akordi.
Hiljaisimmat.
Hartaus.
Keväthämärä.
Blayn prinssi.
Trubaduurilaulu.
Aavelinna.
Suleika.
Yö keitaalla.
Oi Sulamith, on päivät hämärtyneet.
Netkron sadusta.
PUISTOKUJA
Kevät.
Kultaiset pallot.
Kellastuneesta vihkosta.
Katkenneiden pilarien kaupunki.
Tähtisumua.
Uneksijat.
Puistokuja.
SATU SYDÄMESTÄ JA AURINGOSTA.
KAUKAISET METSÄT.
MENNYT SUVI.
LUMIKKO-SYDÄN.
Sun nuoruutesi kuninkaallinen on kristalliseen arkkuun
suljettuna, ja parvi kääpiöiden itkee, palvoo sua vuorten yössä
vahakynttilöin.
JÄRVELLÄ.
HIIDEN HOVI.
SAAREN SOITTAJA.
———
KARNEVAALIHUUME.
KÄSKY — KIELTO.
KUOLLEET.
JUDITHIN TUSKA.
VILLIVIINI.
PUUTUMUS.
HILJAINEN HUONE.