clinical neurosurgical vignettes for the oral board and recertification examinations first 2...
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i
Clinical Neurosurgical Vignettes for the
Oral Board and Recertification
Examinations:
A Self Assessment Guide
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iii iii
Clinical Neurosurgical Vignettes for the
Oral Board and Recertification
Examinations:
A Self Assessment Guide
Thomas G. Psarros, MD
Spine and Brain Neurosurgery Center
Reading Hospital and Medical Center
West Reading, Pennsylvania
Jonathan A. White, MD
Assistant Professor and Residency Program Director
Department of Neurological Surgery
Birsner Family Professorship in Neurological SurgeryUniversity of Texas Southwestern School of Medicine
Dallas, Texas
Howard Morgan, MD, MA., MS., FACS
Professor
Department of Neurological Surgery
Trammell Crow Professorship in Neurological Surgery
University of Texas Southwestern School of Medicine
Dallas, Texas
Anotatos Publishing 2008
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Anotatos Publishing, LLC.Allentown, Pennsylvania 18104
2008 by Anotatos Publishing, LLC.
Typeset in Times New Roman
Printed in the United States
All rights including that of translation reserved. No part ofthis publication may be reproduced, stored in a retrieval
system or transmitted in any form or by any means,
including photocopying, electronic, mechanical, recording,
or otherwise, without the prior written permission of thepublisher.
The publisher and/or authors are not responsible (as a matter
of product liability, negligence, or otherwise) for any injury
resulting from any material contained herein. Thispublication contains information relating to general
principles of medical care that should not be construed as
specific instructions for individual patients. Manufacturersproduct information and package inserts should be reviewed
for current information including contraindications, dosages,
and precautions.
Library of Congress Control Number: 2007943015
Psarros, Thomas G., January 2008
Clinical Neurosurgical Vignettes for the Oral
Board and Recertification Examinations: A SelfAssessment Guide.
Thomas G. Psarros, Jonathan A. White, Howard
Morganp. 310
Includes index and bibliographical references.
ISBN-13: 978-0-9802096-0-0 ISBN-10: 0-9802096-0-9
for Library of Congress
The publishers and authors have made every effort to tracecopyright holders for borrowed material and reference all material
in this book in a just manner when appropriate. If they have inadvertently
overlooked any, they will be pleased to make any necessary arrangements
at the first opportunity.
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Dedication
To my young son George for making me the proudest father in the world
To my lovely wife, Sandy, for her unconditional support
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vii vii
Table of Contents
Case 1: Anterior interosseous nerve syndrome............................................ 1-6
Case 2: Posterior communicating artery aneurysm ................................... 7-18
Case 3: Parkinsons disease ..................................................................... 19-28Case 4: Perimesencephalic subarachnoid hemorrhage ............................ 29-36
Case 5: Middle cerebral artery aneurysm ................................................ 37-46
Case 6: Normal pressure hydrocephalus.................................................. 47-52Case 7: Trigeminal neuralgia................................................................... 53-58
Case 8: Carotid-cavernous fistula............................................................ 59-62Case 9: Carotid stenosis........................................................................... 63-72
Case 10: Carpel tunnel syndrome .............................................................. 73-78
Case 11: Basilar apex aneurysm ................................................................ 79-88Case 12: Odontoid fracture........................................................................ 89-98
Case 13: Colloid cyst ............................................................................... 99-104
Case 14: Anterior communicating artery aneurysm .............................. 105-112Case 15: Posterior inferior cerebellar artery aneurysm ......................... 113-118
Case16: Mycotic aneurysm................................................................... 119-122
Case 17: Cerebral venous thrombosis.................................................... 123-128
Case 18: Middle cerebral artery infarct ................................................. 129-138Case 19: Vein of Galen malformation ................................................... 139-142
Case 20: Cerebral arterial venous malformation ................................... 143-150
Case 21: Cerebral amyloid angiopathy.................................................. 151-152Case 22: Far lateral lumbar disc herniation ........................................... 153-156
Case 23: Central nervous system germinoma........................................ 157-166
Case 24: Pituitary adenoma/Cushings disease ..................................... 167-178
Case 25: Vestibular schwannoma.......................................................... 179-186Case 26: Neurocysticercosis .................................................................. 187-192
Case 27: Myelomeningocele.................................................................. 193-198Case 28: Lipomyelomeningocele........................................................... 199-204
Case 29: Upper brachial plexopathy...................................................... 205-210
Case 30: Closed head injury .................................................................. 211-220
Case 31: Cubital tunnel syndrome......................................................... 221-228Case 32: Cervical spine fracture/ligamentous injury............................. 229-236
Case 33: Posterior interosseous nerve entrapment ................................ 237-240
Case 34: Isolated brain metastases......................................................... 241-248Case 35: Thoracic spinal cord tumor ..................................................... 249-254
Case 36: Carotid artery dissection ......................................................... 255-259Case 37: Spinal cord stimulation and failed back surgery syndrome ... 261-270Index: .................................................................................................... 271-282
Bibliography: ......................................................................................... 283-298
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ix
Preface
The thought of preparing a series of books for the written neurosurgery board
examination seemed to be an excellent one, but the task seemed daunting because the
fund of knowledge required to pass the test was felt to be as extensive as the field ofneurosurgery itself. Our first two books entitled The Definitive Neurological Surgery
Board Review andIntensive Neurosurgery Board Review: Neurological Surgery Q & A
primarily focused on the basic science aspects of the field in the form of a textbook and aQ & A book, respectively. This book is primarily intended for neurosurgeons preparing
for the oral board and recertification examinations, although should prove useful toneurosurgical residents studying for the written examination due to the growing number
of clinical-based questions popping up on this exam. It is certainly not meant to be a
comprehensive or authoritative narrative on the plethora of neurosurgical topics tested,but simply a compilation of case studies that I put together while studying for the Oral
Boards that may prove useful during your preparatory efforts. I primarily relied on two
board-certified neurosurgeons from The University of Texas Southwestern MedicalCenter while compiling these case studies, but have benefited tremendously from the
collective experience of many others during my residency in Dallas. This book is a
tribute to all of them because without their mentorship, guidance, and unselfish
dedication to neurosurgical education this book would not be in your hands today.
Although every attempt has been made to ensure the clarity and accuracy of the questions
and answers, the reader is referred to the multiple referenced textbooks and journalarticles for further clarification should the need arise. Each vignette is generally
formulated with a differential diagnosis, most likely diagnosis, treatment
recommendations, and surgical approaches and techniques. This volume will serve as an
eye-opening refresher for busy neurosurgeons studying for the oral board andrecertification examinations, and should prove to be a valuable vehicle for rapid and
systematic pre-test review for neurosurgery residents preparing for the written boards.We wish you luck during your preparatory efforts.
Thomas G. Psarros, MD
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Anterior interosseous nerve syndrome 1
Case 1
A 17-year-old female fractured her
right forearm during a high schoolvolleyball game and required casting.
Two-months after removal of the cast
she complained of a painful right hand.
Her neurologic examination was
normal except that she was unable to
perform the maneuver depicted below
with the right hand.
_______________________________
_______________________________
1. What is the most likelydiagnosis?
Anterior interosseous nerve (AIN)
injury or compression (also known as
Kiloh-Nevin syndrome) causesweakness of the long flexors of the
thumb (flexor pollicis longus), index
and middle fingers (flexor digitorumprofundus I and II), and the pronator
quadratus muscle. When one tries to
pinch the index finger and thumb, theend of the fingers extend and instead of
the tips of the fingers, the pulps touch
producing the classic pinch sign, as
depicted above. (Brazis, et al., 1996, p14-15 )
[19]; (Greenberg, 2001, p
540)[51]
.
2. Describe the course of the AIN?
The AIN originates from theposterolateral surface of the median
nerve (between the two heads of thepronator teres muscle) approximately 5
to 8 cm distal to the medial epicondyle.Typically, the AIN branches just distal
to the proximal border of the
superficial head of the pronator teresmuscle, and accompanies the median
nerve through the fibrous arch of the
flexor digitorum superficialis (FDS)muscle. The AIN then comes to lie in
front of the interosseous membrane,
coursing distally with the anteriorinterosseous artery (branch of the ulnarartery) to the level of the wrist. The
AIN supplies motor branches to the
flexor pollicis longus (FPL) muscle,flexor digitorum profundus (FDP)
muscles of the index and long fingers,
and pronator quadratus (PQ) muscle.The branches to the FPL and FDP
muscles arise near the tendinous origin
of the FDS muscle approximately 4 cm
distal to AIN origin. The AINterminates in the PQ muscle (Wilkinsand Rengachary, 1996, p 3081)
[161].
3. What is the etiology of a painfulhand with this syndrome?
The AIN has no cutaneous innervationand is most often considered a purely
motor nerve. The AIN, however, does
have terminal sensory branches fromthe wrist radiocarpal, radioulnar,
intercarpal, and carpometacarpal joints.
Damage to the terminal sensory
branches can cause chronic, naggingvolar wrist and forearm pain (Brazis, et
al., 1996, p 14-15)[19]
; (Wilkins and
Rengachary, 1996, p 3081)[161]
.
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4. What are some causes of AINsyndrome?
Trauma including supracondylar
humeral fracture, forearm fracture(as in this case), dislocation of the
elbow, penetrating missile injury,stab wounds, and crush injuries
Compression of the AIN bymusculotendinous bands or other
anomalous structures within the
forearm (from pronator teresmuscle, flexor digitorum
superficialis arch)
Iatrogenic injury
Arterial or venous access(cutdowns, catheterization,venipuncture)
Anomalous AIN course deep topronator teres muscle
Accessory muscles: Gantzersmuscle, aberrant head of flexor
carpi radialis muscle
Forearm mass
Enlarged bicipital bursa
Aberrant radial artery
Thrombosed ulnar collateral artery
Inflammation
The AIN may be involved as partof neuralgic amyotrophy
Infection (cytomegalovirus)
Arteritis (polyarteritis nodosa)(Brazis, et al., 1996, p 14)
[19]
5. What are typical features of acomplete AIN syndrome?
There is a history of spontaneous pain
in the proximal volar wrist and
forearm. Symptoms tend to increasewith activity, especially repetitive
forearm motion. Weakness is usually
preceded by pain, with the pain oftensubsiding partially or completely over
weeks to months. There is classically
weakness of the FPL, FDP of the index
and long fingers, and PQ muscles. Thisoften leaves patients complaining of
difficulty with writing or picking up
small objects. On clinical examination,
the most prominent feature is weaknessof the thumb FPL and index and long
finger FDP muscles causing the
"classic attitude" of the weak pinch(Wilkins and Rengachary, 1996, p
3081)[161]
.
6. What are the typical features ofan incomplete AIN syndrome
and how is it usually caused?
There are reports of various"incomplete AIN syndromes, alsoreferred to as pseudo-anterior
interosseous nerve syndromes. These
atypical presentations may be causedby anatomic variations including:
A. The ulnar nerve may innervate thelong finger (partial or complete in half
the population), which will preserve
the long finger FDP muscle strength.
B. The Martin-Gruber anastomosis,present in approximately 17% of the
population has a connection between
the median and ulnar nerves. One
common variant has a connectionbetween the anterior interosseous to
ulnar nerve. In this situation, many of
the ulnar-mediated hand intrinsicmuscles will be affected as well.
C. The AIN may innervate the entireFDP muscle, which would result inweakness of all fingers.
D. The AIN may also supply part ofthe FDS muscle (30% of people)
(Brazis, et al., 1996, p 15)[19]
.
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Anterior interosseous nerve syndrome 3
7. What is the differential diagnosisof AIN syndrome?
The most commonly misdiagnosed
problem is a tendon rupture, usually ofthe FPL muscle, but also of the FDP
muscle. Hill reported that 10 of 33patients with AIN syndrome were
initially diagnosed as having a tendon
rupture (three had FPL explorationunnecessarily) (Hill, et al., 1985, p 4-
16)[59]
. Electrical stimulation of the
FPL or FDP muscle can help identifythe presence of an intact tendon
(Howard, 1986, p 737-785)[62]
. Other
common conditions in the differentialinclude acute brachial plexusneuropathy, partial proximal median
nerve injury, thoracic outlet syndrome,
and cervical radiculopathy (especiallyC8, although relatively uncommon).
History, clinical examination, and
electrophysiologic studies can helpexclude these other entities (Brazis, et
al., 1996, p 15)[19]
.
8. What diagnostic studies may helpconfirm the diagnosis?
Electromyography can help confirm
the diagnoses of AIN syndrome byhelping to localize the muscles
affected. It may show evidence of
abnormal membrane irritability withloss of motor units in any or all of the
muscles supplied by the AIN. Needle
examination of these muscles mayprove difficult, however, due to their
fairly deep location (Hill, et al., 1985, p
4-16)[59]
.
9. What are some characteristics ofnormal and abnormal single-
motor-unit potentials on
electromyography (EMG)?
In order to understand abnormalities on
EMG, it is imperative that one have asound understanding of how a needle
EMG study is conducted and what the
expected norms should be. EMGinvolves placing a recording needle
into specific muscles and recording
action potentials from muscle fibers,which can be used to determine if any
pathology exists in motoneurons and/or
muscles. There are generally 2 aspectsof an EMG examination that meritdiscussion. They include: 1) assessing
whether there is spontaneous muscle
fiber action potentials, and 2)measuring motor unit action potential
(MUAP) duration, amplitude, and
phases.
Spontaneous muscle activity
When a patient is not moving andunder resting conditions, muscles areessentially silent with no significant
activity. If a motor neuron or muscle is
damaged, however, it is common to see
spontaneous muscle fiber activity onEMG due to hypersensitivity of
denervated muscles. The most common
spontaneous activities that have clinicalsignificance are fibrillation potentials,
positive sharp waves, and complex
repetitive discharges. Fibrillationpotentials are abnormal, spontaneous
contractions of single muscle fibers
that are not visible through the skin,but have a characteristic EMG
waveform. They usually occur
rhythmically and are thought to result
from oscillations of the restingmembrane potential in denervated
muscles. They have a characteristic
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4 Clinical Neurosurgical Vignettes
biphasic or triphasic waveform that canoften be distinguished from normal end
plate potentials. Positive sharp waves
are similar to fibrillation potentials and
appear on EMG as a downward waveafter needle insertion, which is
indicative of needle irritation of
denervated muscle fibers. Denervationof muscle fibers results in fibrillation
potentials and positive sharp waves
within approximately two weeks, buttheir onset may take up to five weeks
in certain cases. These findings usually
persist until the muscle is reinnervated,typically within 3 to 4 months in mild
injuries, or until the injured muscleundergoes complete atrophy (may takeyears). Complex repetitive discharges
are generated from muscle fibers that
have been denervated for longer
periods of time (> 2 months) resultingin chronic muscle fiber necrosis. The
disorders causing complex repetitive
discharges are similar to the onescausing fibrillation potentials and
positive sharp waves, except that
complex repetitive discharges occurwith chronic disease states. Insertional
activity is the discharge of a singlemuscle fiber during insertion of the
EMG needle, and does not necessarily
indicate abnormality unlesssignificantly increased activity is seen
(Winn and Youmans, 2004, p 3856-
3857)[162]
.
MUAP amplitude, duration, and
phases
Muscle potentials appear normally as
waveforms with duration of 5-15 ms,
2-4 phases, and amplitude of 0.5-3 mV.The size of the MUAP is related to the
number of muscle fibers within the
recording range of the EMG needle. If
the MUAP is larger than normal
(increased amplitude and duration),there must be an increased number of
summated action potentials per motor
unit. An increased number of muscle
fibers per motor unit are usually theresult of reinnervation of a previously
injured nerve, suggesting that there was
some insult to the motor nerveapproximately 2 months earlier. If the
MUAP is smaller than normal
(decreased amplitude and duration),there is decreased number of muscle
fibers per motor unit, which generally
occurs with neuromuscular junctiondisorders or myopathies. Polyphasic
units (greater than 4 phases) areabnormal, and can be seen in bothneurogenic and myogenic disorders.
With neurogenic disorders, however,
motor units have a longer duration and
higher amplitude than normalpotentials, while with myopathic
potentials, they are just the opposite
(shorter durations and smalleramplitudes) (Rowland and Merritt,
2000, p 75-76)[136]
; (Winn and
Youmans, 2004, p 3856-3857)[162]
.
10.What are the treatment optionsfor AIN syndrome?
The treatment of patients with AINsyndrome depends primarily on the
cause of the injury. Closed crush
injuries or those related tomusculoskeletal trauma are usually
treated expectantly. Patients are
oftentimes followed closely with serialclinical examinations and diagnostic
studies (electromyograms), and, if,
after 3 to 4 months there is norecovery, surgery is considered. Most
insidious or spontaneous cases are
initially treated nonoperatively, as well.
Immediate exploration is usuallyindicated for penetrating trauma.
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Anterior interosseous nerve syndrome 5
Nonoperative treatment
The initial treatment is generally rest,
avoidance of aggravating factors,
splinting, and nonsteroidal anti-inflammatory medication. If
signs/symptoms persist, some have
advocated corticosteroid injections intothe region of the pronator teres muscle.
Controversy arises as to the duration of
conservative or nonsurgical treatment.The surgical literature generally still
supports nonoperative treatment for 2
to 3 months. If there is noimprovement, surgical exploration is
advocated. When the deficit is partialor slowly improving, the observationperiod can be extended.
In spontaneous or unexplained cases,
treatment depends upon whethercompression or inflammation is the
suspected cause. Features suggestive of
entrapment include slow development,mild pain (primarily volar
wrist/forearm pain), or neurological
deficits isolated to the AIN.Inflammation may be suspected if the
pain is severe, extends above the elbowinto the shoulder region, precedes the
neurological deficit by a matter of
days, and/or there is an associatedipsilateral or contralateral brachial
plexopathy.
If inflammation is suspected, somesuggest that nonsurgical treatment be
carried out for 6 months, while othersargue it may not be needed at all sincereports document improvement even
beyond 2.5 years (Hill, et al., 1985, p
4-16)[59]
. All patients in one reportexperienced full recovery when treated
without surgery (England and Sumner,
1987, p 60)[41]
. The surgical literature
suggests exploration at 3 months if
entrapment is the suspected cause aftera trial of nonsurgical therapy (Kaye
and Black, 2000, p 2092)[77]
.
Operative Treatment
The operative treatment is generally
similar to the techniques used for thepronator syndrome. A curvilinear
incision can be made on the
anteromedial side of the armapproximately 8 cm above the elbow,
and carried across the flexor crease into
the midforearm. The median nervecan then be identified proximal to the
take-off of the AIN and followeddistally being sure it is decompressedat all potential sites of entrapment.
Approximately 4-5 cm above the
elbow, one needs to look for a fibrousband connecting the medial epicondyle
to a rare bony prominence of the
humerus called the ligament ofStruthers. It only occurs in about 2% of
the population, but if identified, needs
to be divided. The next commonentrapment site of the median nerve is
at the lacertus fibrosis, which arisesfrom the biceps tendon. The median
nerve generally runs under the lacertus
fibrosis, which may cause entrapmentif hypertrophic or fibrotic. The median
nerve then courses between the two
heads of the pronator teres muscle. At
the level of the pronator teres muscle,the AIN arises from the median nerve.
Together they may be entrapped by afibrotic pronator teres muscle,especially adjacent to the deep or ulnar
head of this muscle. The deep head of
the pronator teres muscle can bedivided to relieve the compression on
the nerve if the ulnar head is fibrotic or
hypertrophic. The dissection is then
carried distally to the level of the
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6 Clinical Neurosurgical Vignettes
sublimis bridge, which is the fibrousarch of the flexor digitorum
superficialis muscle. The AIN travels
under the sublimis bridge, and needs to
be transected to relieve anycompression on the AIN. The AIN is
then followed further distally to ensure
there is no entrapment from anomalousmuscle origins (i.e. Gantzer's muscle,
flexor carpi radialis brevis muscle).
Dissection adjacent to the origin of theAIN may be difficult due to a
constellation of multiple small arteries
and veins that tend to congregate nearorigin of the FDS muscle, which need
to be preserved (Kaye and Black, 2000,p 2092-2093)
[77]; (Wilkins and
Rengachary, 1996, p 3081)[161]
; (Winn
and Youmans, 2004, p 3925)[162]
(Batjer and Loftus, 2003, p 1757)[13]
.
End of case
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Posterior communicating artery aneurysm 7
Case 2
A 62-year-old female with a history ofmalignant hypertension and aortic
valve insufficiency was brought to the
emergency room by paramedics
complaining of severe headache, neck
stiffness, and photophobia. There was
no history of trauma. On examination,
she was fully alert with no ocular gaze
restriction or neurological deficit. Her
noncontrast computed tomography
(CT) scan is depicted below.
1. As the consulting neurosurgeon,you inform the emergency room
physician that the next course of
action should include?
After making a diagnosis of
subarachnoid hemorrhage (SAH) by
CT scan (will demonstrate blood in85% of patients scanned within 48
hours), cerebral angiography should be
performed as soon as possible.Traditional catheter-based angiography
remains the gold standard for
diagnosing cerebral aneurysms,although other imaging modalities are
gaining widespread popularity
including computed tomographic
angiography (CTA) and magneticresonance angiography (MRA).
During cerebral angiography, it isimperative to identify the entire course
of blood vessels in two planes,
including the posterior inferiorcerebellar arteries and anterior
communicating artery complex. The
angiogram should demonstrate, ifpossible, the etiology of the SAH, the
aneurysmal neck and projection, thevessels arising next to the aneurysm,determine whether multiple aneurysms
exist (up to 20% of cases), and assess
the degree of concomitant vasospasm
that may be present (althoughvasospasm is extremely unlikely in the
hours immediately following a SAH)
(Hughes, 2003, p 253)[63]
.
The experience with MRA is rapidly
evolving as acquisition protocols andMRI technology improve. Earlier
studies suggest 86% sensitivity indetecting aneurysms greater than 3 mm
compared to digital subtraction
angiography (Ross, et al., 1990, p 449-456)
[135]; (Ronkainen, et al., 1997, p
380-384)[133]
, while other studies show
that MRA sensitivity approaches 95%
when compared to angiography (Atlas,1994, p 1-16)
[9]. The false positive rate
for MRA is approximately 16%(Ronkainen, et al., 1997, p 380-384)
[133]. There are a number of
variables that affect MRAs ability to
detect aneurysms including: aneurysmsize, rate and direction of blood flow in
the aneurysm in relation to the
magnetic field, thrombosis, and
calcification. Moreover, it has limited
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8 Clinical Neurosurgical Vignettes
resolution in the setting of vasospasmand in detecting blood products in the
acute period following SAH. MRI,
however, has proven invaluable and
highly effective in the evaluation ofgiant intracranial aneurysms. Because
giant aneurysms are often partially
thrombosed, they often opacifyincompletely during angiography,
which can result in an underestimation
of their true size (Hackney, et al., 1986,p 878-880)
[53]; (Barboriak and
Provenzale, 1998, p 1469)[10]
;
(Greenberg, 2001, p 757)[51]
.
CTA is a more recent development,and its role is becoming better defined.Evidence suggests that it has similar
sensitivity to conventional angiography
in detecting aneurysms, and its use
among cerebrovascular surgeons forsurgical planning has steadily grown.
It has a reported sensitivity and
specificity of 95% and 83%,respectively, in detecting aneurysms as
small as 2.2 mm. Unlike conventional
angiography, however, CTA has theadvantage of showing a 3-dimensional
image and demonstrating theaneurysms relationship to adjacent
structures. Bone artifact may hinder
adequate visualization of certainaneurysms adjacent to the skull base
(Anderson, et al., 1997, p 522-528)[6]
;
(Zouaoui, et al., 1997, p 125-130)[170]
;
(Greenberg, 2001, p 758)[51]
; (Korogi,et al., 1999, p 497)
[85]; (Liang, et al.,
1995, p 1497)[90]
.
Lumbar puncture (LP) after SAH is
risky, and should not be performed in
the patient presented here. In onestudy, 13% of patients undergoing
lumbar puncture after SAH
deteriorated neurologically. Whether or
not clinical deterioration was related to
the LP is unclear, but since it carries arisk of brain herniation or aneurysmal
rebleeding, this procedure should
generally be reserved for patients
where the diagnosis remains uncertainfollowing CT scanning.
Xanthochromia develops only after redblood cells lyse, and is usually
detectable after 4 hours, is maximal at
1 week, and is typically undetectableby 3 weeks. If cerebrospinal fluid is
bloody due to SAH, the blood will
usually not clot if left to stand (Duffy,1982, p 1163-1164)
[35].
2. What is the clinical Hunt andHess grade of this patient?
Once a diagnosis of SAH has beenestablished, patients are given a clinical
grade based on one of the accepted
grading schemes. Although numerousgrading scales have been devised since
the 1930s, one of the most universally
accepted grading scales is that of Hunt
and Hess, described originally in 1968(see Table 2.2a).
Table 2.2a Hunt and Hess clinical grading scale afterSAH
Grade Clinical symptomatology
Grade I Awake, mild headache, + nuchal rigidity
Grade II Awake, moderate- to- severeheadaches, nuchal rigidity
Grade III Drowsy or confused + focal deficits
Grade IV Stuporous, mild- to- moderatehemiparesis, and signs of increasedintracranial pressure
Grade V Comatose, severe disability, severeincreased intracranial pressure
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Posterior communicating artery aneurysm 9
Of note, the Hunt and Hess gradingscale places the patient into the next
worse grade if serious systemic disease
or vasospasm is present (Hunt and
Hess, 1968, p 14-20)[64]
. This gradingscale was later revised by Hunt in 1974
to include two additional grades. Grade
0 was added to include patients withunruptured aneurysms without
symptoms, and grade 1a to include
patients with no acute meningealreaction, but a fixed neurological
deficit (Hunt and Kosnik, 1974, p 79-
84)[65]
. The patient in this casepresented with a severe headache,
photophobia, nuchal rigidity, and nodecline in her level of consciousness;all characteristic of a Hunt and Hess
grade II category. Her comorbid
conditions (malignant hypertension and
aortic valve insufficiency), however,drop her one grade into a grade III
category (Hughes, 2003, p 255-256)[63]
.
Although the Hunt and Hess grading
system remains the most widely used
grading scale for patient assessmentfollowing SAH, some have proposed
using other scales to improvepredictive value. For example, Oshiro,
et al., developed a grading scale
(World Federation of NeurologicalSurgeons, WFNS) based on the
Glasgow Coma Scale (GCS). In the
WFNS grading scheme, GCS scores of
15, 12-14, 9-11, 6-8, and 3-5 replacedthe Hunt and Hess scores of 1-5,
respectively (see Table 2.2b). Theauthors of this scale (WFNS) felt thattheir grading scheme was better than
the Hunt and Hess system at predicting
overall patient outcomes while at thesame time being more reproducible
across observers (Hughes, 2003, p 255-
256)[63]
; (Oshiro, et al., 1997, p 140-
148)[115]
.
Table 2.2b World Federation of NeurologicalSurgeons Scale
3. What is the Fisher grade of thispatient?
Fisher (1980) developed a four-tieredgrading scale for the appearance of
SAH on CT scanning dependent upon
the severity and location of the bloodpattern. Grade I patients had noevidence of blood detectable on CT
scanning, while grade II patients had a
thin layer of blood (< 1 mm thick)diffusely spread throughout the
subarachnoid space. Grade III patients
had a thicker amount of cisternalsubarachnoid blood (>1mm thickness
as depicted in this case), while grade
IV patients had intraventricular or
intraparenchymal blood with orwithout a significant subarachnoid
component. The Fisher grading system
can help predict the probability ofdeveloping vasospasm by the amount
of blood detected on CT scan . Patients
with Grade I, II, and IV bleeds had noor minimal incidence of clinically
significant vasospasm, while grade III
patients had a 95.8% incidence in
Grade Clinical findings
Grade I Glasgow coma score 15, no motordeficit
Grade II Glasgow coma score 13 14, nomotor deficit
Grade III Glasgow coma score 13 14, motordeficit
Grade IV Glasgow coma score 7 12, with orwithout motor deficit
Grade V Glasgow coma score 3 6, with orwithout motor deficit
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10 Clinical Neurosurgical Vignettes
Fishers original paper (Fisher, et al.,1977, p 1-9)
[44]. These findings suggest
that blood breakdown products are an
important factor in the genesis of
cerebral vasospasm, with largerquantities of blood increasing the
likelihood that vasospasm will occur
(Hughes, 2003, p 252)[63]
.
4. The cerebral angiogram for thispatient is depicted below. What is
the diagnosis?
This angiogram of the left internal
carotid artery (ICA) depicts a bilobedposterior communicating artery
(PcomA) aneurysm originating at the
level of a fetal PcomA (Wilkins andRengachary, 1996, p 2306)
[161].
5. Describe two angiographic
findings in this patient that areimportant for surgical planning?
Care needs to be taken when evaluating
angiograms of patients with a PComA
aneurysm, SAH, and no third nervedeficit because the aneurysms often
project laterally onto the medial edge
of the temporal lobe rather than inmore common posterolateral or
downward directions. This is important
during surgical planning sincepremature retraction of the temporallobe may result in aneurysm rupture.
Additionally, the integrity of a fetal
PComA needs to be preserved duringsurgery and aneurysm clip placement.
If the area supplied by the PComA is
small, inadvertently placing this vesselinto the clip construct may not cause
any adverse sequelae, however, if the
PComA is fetal or there is a
hypoplastic P1, it may result in aclinically significant PCA infarct(Wilkins and Rengachary, 1996, p
2306)[161]
; (Psarros, 2006, p 199)[124]
.
6. The emergency room physicianreviews the CT scan with you and
wants to begin an infusion of
epsilon-aminocaproic acid
(AMICAR). What are some
important factors to consider
about this medication?
The role of antifibrinolytics for the
purpose of preventing or decreasingclot breakdown following SAH is
controversial (Kassell, et al., 1984, p
225-230)[74]
; (Adams, 1982, p 256-259)
[2]; (Mizoi, et al., 1991, p 807-
813)[99]
; (Findlay, et al., 1988, p 723-
735)[43]
. During normal fibrinolysis,
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Posterior communicating artery aneurysm 11
plasminogen is converted to plasmin,which facilitates the digestion of fibrin
and aids in clot lysis. AMICAR
inhibits the conversion of plasminogen
to plasmin, and reduces the extent offibrinolysis and clot breakdown after
SAH. Intravenous injection of
AMICAR generally peaks in thebloodstream in about 20 minutes. It
crosses the blood-brain barrier and
achieves maximal antifibrinolyticactivity within the cerebrospinal fluid
approximately 48 hours later (Findlay,
et al., 1988, p 723-735)[43]
. A typicalregimen includes infusing 2 g/ hour
intravenously for 48 hours, and then1.5 g/ hour until surgery is performed.Review of the results of one study
found a reduction in rehemorrhage and
death at 14 days from 21% to 10% with
its use (Burchiel, et al., 1984, p 57-63)
[21]. Although it halved the
rebleeding rate the first 14 days
following SAH, there was an increasedrisk in associated medical morbidity,
the most frequent being diarrhea in
approximately 24% of patients.Additionally, communicating
hydrocephalus was 25% more likelywith antifibrinolytic therapy (Burchiel,
et al., 1984, p 57-63)[21]
. The greatest
concern over its use, however, was theincreased risk of vasospasm that
negated its benefits in some studies
(Kassell, et al., 1984, p 225-230)[74]
.
The general consensus about the role ofantifibrinolytics is that they have little
role in acute SAH, especially if surgeryis anticipated within a few hours ordays of admission (Hughes, 2003, p
267)[63]
.
7. What is the rate of rebleedingfollowing a SAH?
The frequency of rebleeding is in the
range of 4% within the first 24 to 48
hours, and approximately 1.5% eachday for the next 13 or 14 days. It
approaches 20% within the first 2
weeks, and approximately 50% at 6
months. Thereafter, the risk is believedto level off to approximately 3% per
year. The mortality rate from
aneurysmal rebleeding is between 44%and 78%. Early surgery or aneurysm
coiling offers the best protection
against rebleeding and its attendantcomplications (Hughes, 2003, p
267)[63]
; (Kassell, et al., 1982, p 337-
343)[73]
.
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12 Clinical Neurosurgical Vignettes
8. What are some advantages anddisadvantages of early versus
delayed surgery after SAH?
Table 2.8 Advantages and disadvantages of earlyversus delayed surgery after SAH
Despite the potential microsurgicalchallenges associated with operating on
a swollen brain, the majority of grade
I-III patients at various institutions stillundergo surgery early after SAH to
minimize the incidence of rebleeding.
Although early surgery can certainly betechnically more challenging,
experience has shown that patient
outcomes are not necessarily adversely
affected, as demonstrated by theInternational Cooperative Study on the
Timing of Aneurysm Surgery
(ICSTAS) (Kassell, et al., 1990, p 37-47)
[75]. Intraoperative ventriculostomy
placement and aggressive gravity
drainage of cerebrospinal fluid haveproven to be very useful in overcoming
an initially swollen brain soon after
SAH (Paine, et al., 1988, p 1107-1109)
[117].
9. The patient is taken to theoperating room for aneurysm
clipping. After elevating a
pterionally-centered bone flap
and modestly craniectomizing the
squamosal portion of the
temporal bone, attention is
directed toward the sphenoid
ridge. This bony wing is
typically removed from lateral
to medial to the level of origin ofwhat structure?
One of the most useful adjuncts to
avoid brain retraction for anterior
circulation aneurysms during initialexposure is to aggressively remove the
bony wing (or sphenoid ridge) of the
sphenoid bone. It is removed usingrongeurs and a power drill from
lateral to medial for a distance of
approximately 4 cm, to the level of theorbital meningeal artery. This
maneuver must include removing the
thin spine of the sphenoid ridge,which, oftentimes, is very adherent to
the underlying dura adjacent to the
horizontal portion of the Sylvian
fissure. If the spine is left intact, thedegree of initial frontal lobe elevation
necessary to expose the carotid cistern
Early approach Delayed approach
ADVANTAGES ADVANTAGES
Decreases rebleeding risk
Allows for aggressivemanagement ofvasospasm
Early removal ofsubarachnoid blood andpossible prevention of
hydrocephalus
Earlier patient ambulationand rehabilitation;perhaps reduced hospitalstay
Reduced medicalcomplications associatedwith bedrest
Evacuation of hematoma,if applicable
Brain less swollen
Easier microdissection
Stable patient
DISADVANTAGES DISADVANTAGES
Swollen brain may makesurgery more difficult
Unstable patient in someinstances
Scheduling problems,possibility ofinexperienced operativeteam
Higher rebleeding risk
Does not facilitate or allowfor aggressivemanagement ofvasospasm
Delayed ambulation,longer hospital stay
Increased risk of medicalcomplications whileawaiting surgery
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Posterior communicating artery aneurysm 13
is increased, and surgical access alongthe flattened ridge and frontal fossa
floor can be markedly hindered. After
the sphenoid ridge is removed and
bony and dural hemostasis is obtained,the dura can be opened in a routine
curvilinear fashion and held with
retention sutures flat against theinferior aspect of the craniectomy and
adjacent muscle (Samson and Batjer,
1990, p 57)[138]
.
10.Describe the pertinent stepsduring surgery for a PcomA
aneurysm?
Initial exposure after dura opened
InIntracranial Aneurysm Surgery:Techniques, Samson and Batjereloquently describe the steps for
clipping PcomA aneurysms (Samson
and Batjer, 1990, p 57-58)[138]
.Withthe aid of a microscope, a small self-
retaining brain retractor is used to
gently elevate the frontal lobe adjacent
to the horizontal portion of the Sylvianfissure. The retractor is then advancedin a step-by-step fashion as the
arachnoid opening is extended from the
horizontal portion of the Sylvian
fissure to its junction with the carotidcistern. As frontal lobe elevation brings
the optic nerve and internal carotid
artery (ICA) covered by arachnoid intoview, the arachnoid covering the
Sylvian fissure usually thickens.
Oftentimes, a small vein will be foundbridging the temporal to frontal lobe
immediately under this thicker
arachnoidal layer adjacent to theSylvian fissure. This vein usually lies
above the origin of the middle cerebral
artery (MCA), and can be coagulated
and cut to complete the opening of thehorizontal portion of the Sylvian
fissure. The retractor blade can then be
advanced to expose the arachnoid layerthat surrounds the optic nerve and ICA.
The arachnoid incision, which was
started over the horizontal portion of
the Sylvian fissure, is then extendedposteriorly and anteriorly for better
visualization of the ICA and optic
nerve. The release of cerebrospinalfluid from the subarachnoid Sylvian
and prechiasmatic cisterns will
generally help relax the brain tofacilitate further microdissection and
eventual aneurysm clipping (Samson
and Batjer, 1990, p 57-58)[138]
.
Microdissection after basal cisternsopen
After the basal cisterns open, the next
step should be to focus attention on
securing proximal arterial control priorto more definitive microdissection
distally. Because of the most common
location of PComA aneurysms(projecting posterior and laterally), it is
advantageous to accomplish this
control by beginning the exposure ofthe ICA on its anterior-medial aspect at
the apex of the opticocarotid triangleand then carrying the microdissection
laterally, across the ICA. This should
complete the establishment of proximalarterial control and simultaneously
establish initial exposure of the
proximal aneurysm complex in most
cases. Initial microdissection ofthickened arachnoid and clot in the
posterior carotid cistern should belimited to meticulous proximal-to-distal exposure of the ICA only, as the
surgeon defines in succession the
following vessels: the origin of theposterior communicating artery,
posterior communicating artery (PCA)-
proximal aneurysm junction, aneurysm
neck, the distal origin of the aneurysm
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14 Clinical Neurosurgical Vignettes
neck from the carotid wall, and finallythe anterior choroidal artery origin.
Extensive removal of subarachnoid clot
or identification of the distal posterior
communicating and anterior choroidalvessels or aneurysm fundus should be
postponed until satisfactory exposure
of the entire posterior carotid wall hasbeen exposed to permit safe and early
distal temporary arterial control, should
it be necessary. In most instances,distal control of the ICA is obtained, if
necessary, by placing a temporary clip
just proximal to the ICA bifurcation.After appropriate preparations have
been made for proximal and distalarterial control and with satisfactorypreliminary inspection of the posterior,
anterior and medial carotid walls, the
surgeon is nearly ready to begin
definitive dissection of the aneurysmneck in preparation for clip application
(Samson and Batjer, 1990, p 57-
65)[138]
.
It is first important to identify the distal
PComA for temporary clip placement,if possible, because obtaining proximal
and distal control of the ICA may notbe enough to stop back bleeding from
the PComA if intraoperative rupture
occurs. Sometimes, this cansignificantly hinder visualization and
make further microdissection and
aneurysm clipping difficult. Moreover,
if the PComA is not identified prior toclip placement, the surgeon runs the
risk of including this vessel into theclip construct, especially if vision isimpaired by intraoperative rupture
(Samson and Batjer, 1990, p 63)[138]
;
(Psarros, 2006, p 199)[124]
.
11.Postoperatively, the patient wasfound to have a homonymous
visual field defect of both upper
and lower quadrants. This was
most likely the result of intra-operative injury to what
structure/s?
Occlusion of the anterior choroidal
artery (AchA) may cause ahomonymous defect in the upper and
lower quadrants with sparing of the
horizontal sector (quadruplesectoranopia), which is diagnostic of a
lateral geniculate body infarct in the
AchA distribution. Injury or ligation ofthis vessel may also produce theclassically reported features of
contralateral hemiplegia,
hemianesthesia, and hemianopsia(Brazis, et al., 1996, p 132-140)
[19];
(Psarros, 2006, p 199)[124]
.
The AchA arises from the ICA in 75%
of patients, but can arise from either
the MCA or PcomA in up to 25% of
patients. The AchA supplies: 1) thetemporal lobe - uncus, pyriform cortex,and a portion of the amygdala; 2) the
visual system - optic tract, lateral
geniculate nucleus, and a portion of the
optic radiations; 3) the internal capsuleand basal ganglia - medial globus
pallidus, tail of caudate, genu and
posterior limb of internal capsule; 4)the diencephalon - lateral thalamus and
subthalamus; 5) the mesencephalon -
middle one-third of cerebral peduncleand substantia nigra.
Generally, the sites for temporary clipplacement chosen during surgery for
PComA aneurysms include the
proximal ICA near the anterior clinoid
process, on the distal ICA immediatelyproximal to the carotid bifurcation, and
on the PComA distal to the aneurysm
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Posterior communicating artery aneurysm 15
fundus. Obviously, the territorysupplied by the AchA will be rendered
ischemic during the period of
temporary occlusion, which can result
in a choroidal infarct shouldprolonged temporary occlusion time be
necessary.
Samson and Batjer describe the
following steps for clipping a PcomA
aneurysm after preparation of thevessels to receive temporary clips
(Samson and Batjer, 1990, p 57-
58)[138]
. The arterial blood pressureshould be normalized, and either
etomidate (0.3 mg/kg) or a barbiturate(often pentobarbital) should be given toachieve burst suppression.
Subsequently, temporary clips are
applied from proximal to distal, and the
aneurysm fundus could be moreaggressively manipulated. If necessary,
a small gauge spinal needle could be
used to puncture the aneurysm dome(for larger aneurysms), well away from
the aneurysm neck for easier
manipulation. The suction can then beintermittently placed over the puncture
site and despite continued bleeding ofthe PcomA (if temporary clip
application not possible), suction will
transiently decompress the aneurysmadequately enough to allow dissection
to progress sufficiently to permit
permanent clip placement. Should
protracted microdissection be required,at intervals of approximately 10 to 15
minutes, a small cottonoid can beplaced over the puncture site and thetemporary clips removed to allow for
reperfusion of the carotid (and anterior
choroidal artery) territory, with thebleeding from the aneurysm being
controlled with suction and tamponade
(Samson and Batjer, 1990, p 63-
64)[138]
.
12.What percent of patients withaneurysmal SAH develop
angiographic and clinical
vasospasm?
Vasospasm is one of the greatest
causes of morbidity in patientssurviving the initial SAH.
Angiographic vasospasm has been
reported to occur in approximately70% of patients following SAH, with
approximately 20-30% having
clinically significant narrowing. It hasa peak incidence around the seventh
day following SAH, although it can
occur anytime up to approximately 13-14 days post-bleed, beyond of which itis fairly uncommon (Heros, et al.,
1983, p 599-608)[58]
; (Ropper and
Zervas, 1984, p 909-915)[134]
. Whenvasospasm develops, it may last for
several weeks (Heros, et al., 1983, p
599-608)[58]
; (Weir, 1982, p 39-43)[157]
.The most common indicator
predisposing to vasospasm is the
amount of subarachnoid blood on the
CT scan. Thick blood in the basalcisterns (Fisher grade III) carries ahigher vasospasm risk than focal
loculations (Fisher, et al., 1977, p 245-
248)[44]
. Lobar hematomas and
interhemispheric blood are associatedwith a low risk of vasospasm, while
subarachnoid blood in the Sylvian
fissure appears to carry an intermediatevasospasm risk (Pasqualin, et al., 1984,
p 344-353)[118]
; (Kistler, et al., 1983, p
424-436)
[81]
.
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16 Clinical Neurosurgical Vignettes
13.On postoperative day 9 thepatient developed new right arm
and leg weakness while
recovering in the ICU, but her
level of consciousness remainedunchanged. Her ventriculostomy
continued to function properly.
This neurologic change from
baseline was preceded by slight
fever and leukocytosis. What
should be the next course of
action in this patients care?
Clinical vasospasm usually develops
slowly over hours or days and may be
associated with a slow decline inneurologic status. Headache, fever, andleukocytosis may precede and herald
the onset of vasospasm prior to
neurological deterioration. Permanentneurological deficit or death has been
reported to occur in approximately
12% of patients who develop severeclinical vasospasm (Heros, et al., 1983,
p 599-608)[58]
; (Fisher, et al., 1977, p
245-248)[44]
. Although this clinical
history is highly suggestive ofvasospasm, obtaining an emergent CTscan in the face of a new neurologic
deficit is often the first step in
management. This is done to rule out
any structural abnormality(hemorrhage, hydrocephalus, etc.) that
may require alternative treatment
strategies.
14.What is the mainstay of
treatment of clinically significantcerebral vasospasm?
In the chapter on management of SAHinNeurological Emergencies,
Kopitnik, et al., give a thorough
discussion on the management ofcerebral vasospasm, which is
summarized below (Hughes, 2003, p
278-281)[63]
. Presently, the mainstay of
treatment for clinically significantcerebral vasospasm is the induction of
hypervolemia, systemic hypertension,
and hemodilution, commonly referred
to as triple-H therapy orhyperdynamic therapy. The
neurologic deficits seen with
vasospasm result from arterialnarrowing and increased
cerebrovascular resistance.
Autoregulation is often disruptedfollowing SAH, and any intervention/s
that increase cerebral perfusion
pressure can increase cerebral bloodflow in the hypoperfused regions of the
brain and potentially improveoutcomes (Symon, 1979, p 7-22)
[150];
(Pritz, et al., 1978, p 364-368)[123]
.
Patients undergoing Triple H therapy
are best treated in an intensive care unit
(ICU) environment with arterial andcentral venous lines, an indwelling
foley catheter, and pulse oximetry. An
arterial catheter or A-line assessesblood pressure continuously and lends
itself well to frequent blood draws for
blood gas measurements should theybe necessary. A SwanGanz catheter
monitors pulmonary capillary wedgepressure (or central venous pressure if
central venous line is used), a
transcutaneous pulse oximetermonitors oxygen saturation, and an
indwelling foley catheter can be a
useful adjunct to arterial and central
venous lines to gauge volume statusand certain urine electrolytes.
Desaturations may indicate earlypulmonary decompensation fromhypervolemic therapy. Fluid balance is
assessed hourly.
Specifically, the initial therapy for
symptomatic vasospasm consists of
volume expansion with crystalloid
and/or albumin to create a positive
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Posterior communicating artery aneurysm 17
fluid balance. Pulmonary artery wedgepressure is generally maintained
between 14 and 18 mm Hg and central
venous pressure is kept at
approximately 10 mm Hg. If clinicalimprovement is not seen soon after
volume expansion or blood pressure
can not adequately be raised withvolume expansion alone, arterial blood
pressure can be elevated with
dopamine, dobutamine, and/ornorepinephrine and systolic pressures
typically maintained between 180 and
220 mm Hg. Kassell reported goodresults in 58 patients treated for
cerebral vasospasm with volumeexpansion and induced arterialhypertension in which he demonstrated
reversal of neurological deficits in 75%
of patients. Neurological improvement
was permanent in 74% of patients(Kassell, et al., 1982, p 337-343)
[73]. As
intravascular volume is expanded,
patients, oftentimes, undergo asecondary diuresis, which can make
artificial elevation of the pulmonary
capillary wedge pressure difficult.Under these circumstances, the use of
low dose vasopressin can helpminimize the diuresis and maintain an
elevated intravascular fluid volume, if
necessary. Triple H therapy can becontinued until one of the following
conditions are met: neurologic
symptoms resolve, vasospasm clears as
demonstrated by arteriography orDoppler monitoring, or complications
from hyperdynamic therapy occur.Complications may include congestiveheart failure, brain edema, pulmonary
edema, hypertensive cerebral
hemorrhage, systemic complications ofprolonged vasopressor use, and
myocardial infarction (Shimoda, et al.,
1993, p 423-429)[145]
. Calcium channel
blockers may improve SAH patient
outcome (nimodipine 60 mg orallyevery four hours for 21 days) and are
now part of the overall management
algorithm at most institutions. Their
efficacy in reducing the detrimentaleffects of vasospasm has been shown
in controlled studies, (Allen, et al.,
1983, p 619-624)[5]
although the truemechanism of action remains
somewhat elusive (Kassell, et al., 1992,
p 848-852)[72]
.
When hyperdynamic therapy has
proven ineffective, other interventionsmay prove useful. Selective intra-
arterial infusion of papaverinehydrochloride or calcium channelblockers into the symptomatic vascular
territory may reverse angiographic
vasospasm in some patients. The
results of this therapy can be clinicallydramatic but, in a similar fashion, may
be extremely fleeting or completely
unsuccessful (Minami, et al., 2001, p169-179)
[98]. Additionally, transluminal
balloon angioplasty of the large
intracranial vessels (ICA, M1segmentof MCA, vertebral and basilar arteries)
may also prove beneficial. A numberof investigators have reported
encouraging results with the use of
these techniques (Zubkov, et al., 1984,p 65-79)
[171]; (Newell, et al., 1989, p
654-660)[106]
; (Hughes, 2003, p 278-
281)[63]
.
End of case