i

Clinical Neurosurgical Vignettes for the

Oral Board and Recertification
Examinations:



A Self Assessment Guide








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 Surgery
University 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

iv
Anotatos Publishing, LLC.
Allentown, Pennsylvania 18104


2008 by Anotatos Publishing, LLC.


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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. This
publication contains information relating to general
principles of medical care that should not be construed as
specific instructions for individual patients. Manufacturers
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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 Self
Assessment Guide.
Thomas G. Psarros, Jonathan A. White, Howard
Morgan
p. 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 trace
copyright 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.

v v







Dedication


To my young son George for making me the proudest father in the world

To my lovely wife, Sandy, for her unconditional support
























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 ..................................................................... 19-28
Case 4: Perimesencephalic subarachnoid hemorrhage ............................ 29-36
Case 5: Middle cerebral artery aneurysm................................................ 37-46
Case 6: Normal pressure hydrocephalus.................................................. 47-52
Case 7: Trigeminal neuralgia................................................................... 53-58
Case 8: Carotid-cavernous fistula............................................................ 59-62
Case 9: Carotid stenosis........................................................................... 63-72
Case 10: Carpel tunnel syndrome .............................................................. 73-78
Case 11: Basilar apex aneurysm................................................................ 79-88
Case 12: Odontoid fracture........................................................................ 89-98
Case 13: Colloid cyst ............................................................................... 99-104
Case 14: Anterior communicating artery aneurysm.............................. 105-112
Case 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 ................................................. 129-138
Case 19: Vein of Galen malformation................................................... 139-142
Case 20: Cerebral arterial venous malformation ................................... 143-150
Case 21: Cerebral amyloid angiopathy.................................................. 151-152
Case 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.......................................................... 179-186
Case 26: Neurocysticercosis .................................................................. 187-192
Case 27: Myelomeningocele.................................................................. 193-198
Case 28: Lipomyelomeningocele........................................................... 199-204
Case 29: Upper brachial plexopathy...................................................... 205-210
Case 30: Closed head injury .................................................................. 211-220
Case 31: Cubital tunnel syndrome......................................................... 221-228
Case 32: Cervical spine fracture/ligamentous injury............................. 229-236
Case 33: Posterior interosseous nerve entrapment ................................ 237-240
Case 34: Isolated brain metastases......................................................... 241-248
Case 35: Thoracic spinal cord tumor ..................................................... 249-254
Case 36: Carotid artery dissection ......................................................... 255-259
Case 37: Spinal cord stimulation and failed back surgery syndrome ... 261-270
Index: .................................................................................................... 271-282
Bibliography: ......................................................................................... 283-298

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 of
neurosurgery itself. Our first two books entitled The Definitive Neurological Surgery
Board Review and Intensive Neurosurgery Board Review: Neurological Surgery Q & A
primarily focused on the basic science aspects of the field in the form of a textbook and a
Q & A book, respectively. This book is primarily intended for neurosurgeons preparing
for the oral board and recertification examinations, although should prove useful to
neurosurgical 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 Medical
Center 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 journal
articles 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 and
recertification 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
Anterior interosseous nerve syndrome 1

Case 1


A 17-year-old female fractured her
right forearm during a high school
volleyball 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 likely
diagnosis?
Anterior interosseous nerve (AIN)
injury or compression (also known as
Kiloh-Nevin syndrome) causes
weakness of the long flexors of the
thumb (flexor pollicis longus), index
and middle fingers (flexor digitorum
profundus I and II), and the pronator
quadratus muscle. When one tries to
pinch the index finger and thumb, the
end 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, p
14-15 )
[19]
; (Greenberg, 2001, p
540)
[51]
.

2. Describe the course of the AIN?
The AIN originates from the
posterolateral surface of the median
nerve (between the two heads of the
pronator 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 teres
muscle, 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 anterior
interosseous artery (branch of the ulnar
artery) 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 AIN
terminates in the PQ muscle (Wilkins
and Rengachary, 1996, p 3081)
[161]
.

3. What is the etiology of a painful
hand with this syndrome?
The AIN has no cutaneous innervation
and is most often considered a purely
motor nerve. The AIN, however, does
have terminal sensory branches from
the wrist radiocarpal, radioulnar,
intercarpal, and carpometacarpal joints.
Damage to the terminal sensory
branches can cause chronic, nagging
volar wrist and forearm pain (Brazis, et
al., 1996, p 14-15)
[19]
; (Wilkins and
Rengachary, 1996, p 3081)
[161]
.
2 Clinical Neurosurgical Vignettes


4. What are some causes of AIN
syndrome?
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 by
musculotendinous bands or other
anomalous structures within the
forearm (from pronator teres
muscle, flexor digitorum
superficialis arch)
Iatrogenic injury
Arterial or venous access
(cutdowns, catheterization,
venipuncture)
Anomalous AIN course deep to
pronator teres muscle
Accessory muscles: Gantzers
muscle, 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 part
of neuralgic amyotrophy
Infection (cytomegalovirus)
Arteritis (polyarteritis nodosa)
(Brazis, et al., 1996, p 14)
[19]


5. What are typical features of a
complete AIN syndrome?
There is a history of spontaneous pain
in the proximal volar wrist and
forearm. Symptoms tend to increase
with activity, especially repetitive
forearm motion. Weakness is usually
preceded by pain, with the pain often
subsiding partially or completely over
weeks to months. There is classically
weakness of the FPL, FDP of the index
and long fingers, and PQ muscles. This
often leaves patients complaining of
difficulty with writing or picking up
small objects. On clinical examination,
the most prominent feature is weakness
of 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 of
an incomplete AIN syndrome
and how is it usually caused?
There are reports of various
"incomplete AIN syndromes, also
referred to as pseudo-anterior
interosseous nerve syndromes. These
atypical presentations may be caused
by anatomic variations including:

A. The ulnar nerve may innervate the
long 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 connection
between the anterior interosseous to
ulnar nerve. In this situation, many of
the ulnar-mediated hand intrinsic
muscles will be affected as well.

C. The AIN may innervate the entire
FDP muscle, which would result in
weakness of all fingers.
D. The AIN may also supply part of
the FDS muscle (30% of people)
(Brazis, et al., 1996, p 15)
[19]
.
Anterior interosseous nerve syndrome 3

7. What is the differential diagnosis
of AIN syndrome?
The most commonly misdiagnosed
problem is a tendon rupture, usually of
the FPL muscle, but also of the FDP
muscle. Hill reported that 10 of 33
patients with AIN syndrome were
initially diagnosed as having a tendon
rupture (three had FPL exploration
unnecessarily) (Hill, et al., 1985, p 4-
16)
[59]
. Electrical stimulation of the
FPL or FDP muscle can help identify
the presence of an intact tendon
(Howard, 1986, p 737-785)
[62]
. Other
common conditions in the differential
include acute brachial plexus
neuropathy, partial proximal median
nerve injury, thoracic outlet syndrome,
and cervical radiculopathy (especially
C8, although relatively uncommon).
History, clinical examination, and
electrophysiologic studies can help
exclude these other entities (Brazis, et
al., 1996, p 15)
[19]
.

8. What diagnostic studies may help
confirm the diagnosis?
Electromyography can help confirm
the diagnoses of AIN syndrome by
helping to localize the muscles
affected. It may show evidence of
abnormal membrane irritability with
loss of motor units in any or all of the
muscles supplied by the AIN. Needle
examination of these muscles may
prove difficult, however, due to their
fairly deep location (Hill, et al., 1985, p
4-16)
[59]
.




9. What are some characteristics of
normal and abnormal single-
motor-unit potentials on
electromyography (EMG)?
In order to understand abnormalities on
EMG, it is imperative that one have a
sound understanding of how a needle
EMG study is conducted and what the
expected norms should be. EMG
involves 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 aspects
of an EMG examination that merit
discussion. 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 and
under resting conditions, muscles are
essentially silent with no significant
activity. If a motor neuron or muscle is
damaged, however, it is common to see
spontaneous muscle fiber activity on
EMG due to hypersensitivity of
denervated muscles. The most common
spontaneous activities that have clinical
significance are fibrillation potentials,
positive sharp waves, and complex
repetitive discharges. Fibrillation
potentials 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 resting
membrane potential in denervated
muscles. They have a characteristic
4 Clinical Neurosurgical Vignettes


biphasic or triphasic waveform that can
often be distinguished from normal end
plate potentials. Positive sharp waves
are similar to fibrillation potentials and
appear on EMG as a downward wave
after needle insertion, which is
indicative of needle irritation of
denervated muscle fibers. Denervation
of muscle fibers results in fibrillation
potentials and positive sharp waves
within approximately two weeks, but
their 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 muscle
undergoes complete atrophy (may take
years). Complex repetitive discharges
are generated from muscle fibers that
have been denervated for longer
periods of time (> 2 months) resulting
in chronic muscle fiber necrosis. The
disorders causing complex repetitive
discharges are similar to the ones
causing fibrillation potentials and
positive sharp waves, except that
complex repetitive discharges occur
with chronic disease states. Insertional
activity is the discharge of a single
muscle fiber during insertion of the
EMG needle, and does not necessarily
indicate abnormality unless
significantly 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 the
result of reinnervation of a previously
injured nerve, suggesting that there was
some insult to the motor nerve
approximately 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 junction
disorders or myopathies. Polyphasic
units (greater than 4 phases) are
abnormal, and can be seen in both
neurogenic and myogenic disorders.
With neurogenic disorders, however,
motor units have a longer duration and
higher amplitude than normal
potentials, while with myopathic
potentials, they are just the opposite
(shorter durations and smaller
amplitudes) (Rowland and Merritt,
2000, p 75-76)
[136]
; (Winn and
Youmans, 2004, p 3856-3857)
[162]
.

10. What are the treatment options
for AIN syndrome?
The treatment of patients with AIN
syndrome depends primarily on the
cause of the injury. Closed crush
injuries or those related to
musculoskeletal trauma are usually
treated expectantly. Patients are
oftentimes followed closely with serial
clinical examinations and diagnostic
studies (electromyograms), and, if,
after 3 to 4 months there is no
recovery, surgery is considered. Most
insidious or spontaneous cases are
initially treated nonoperatively, as well.
Immediate exploration is usually
indicated for penetrating trauma.

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 into
the 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 no
improvement, surgical exploration is
advocated. When the deficit is partial
or slowly improving, the observation
period can be extended.

In spontaneous or unexplained cases,
treatment depends upon whether
compression 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 elbow
into the shoulder region, precedes the
neurological deficit by a matter of
days, and/or there is an associated
ipsilateral or contralateral brachial
plexopathy.

If inflammation is suspected, some
suggest that nonsurgical treatment be
carried out for 6 months, while others
argue it may not be needed at all since
reports document improvement even
beyond 2.5 years (Hill, et al., 1985, p
4-16)
[59]
. All patients in one report
experienced 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 after
a trial of nonsurgical therapy (Kaye
and Black, 2000, p 2092)
[77]
.

Operative Treatment

The operative treatment is generally
similar to the techniques used for the
pronator syndrome. A curvilinear
incision can be made on the
anteromedial side of the arm
approximately 8 cm above the elbow,
and carried across the flexor crease into
the midforearm. The median nerve
can then be identified proximal to the
take-off of the AIN and followed
distally being sure it is decompressed
at all potential sites of entrapment.

Approximately 4-5 cm above the
elbow, one needs to look for a fibrous
band connecting the medial epicondyle
to a rare bony prominence of the
humerus called the ligament of
Struthers. It only occurs in about 2% of
the population, but if identified, needs
to be divided. The next common
entrapment site of the median nerve is
at the lacertus fibrosis, which arises
from the biceps tendon. The median
nerve generally runs under the lacertus
fibrosis, which may cause entrapment
if 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 a
fibrotic pronator teres muscle,
especially adjacent to the deep or ulnar
head of this muscle. The deep head of
the pronator teres muscle can be
divided 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
6 Clinical Neurosurgical Vignettes


sublimis bridge, which is the fibrous
arch of the flexor digitorum
superficialis muscle. The AIN travels
under the sublimis bridge, and needs to
be transected to relieve any
compression on the AIN. The AIN is
then followed further distally to ensure
there is no entrapment from anomalous
muscle origins (i.e. Gantzer's muscle,
flexor carpi radialis brevis muscle).
Dissection adjacent to the origin of the
AIN may be difficult due to a
constellation of multiple small arteries
and veins that tend to congregate near
origin 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
Posterior communicating artery aneurysm 7

Case 2



A 62-year-old female with a history of
malignant 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 in
85% 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 magnetic
resonance angiography (MRA).

During cerebral angiography, it is
imperative to identify the entire course
of blood vessels in two planes,
including the posterior inferior
cerebellar arteries and anterior
communicating artery complex. The
angiogram should demonstrate, if
possible, the etiology of the SAH, the
aneurysmal neck and projection, the
vessels 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 (although
vasospasm 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 and
MRI technology improve. Earlier
studies suggest 86% sensitivity in
detecting 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: aneurysm
size, rate and direction of blood flow in
the aneurysm in relation to the
magnetic field, thrombosis, and
calcification. Moreover, it has limited
8 Clinical Neurosurgical Vignettes

resolution in the setting of vasospasm
and in detecting blood products in the
acute period following SAH. MRI,
however, has proven invaluable and
highly effective in the evaluation of
giant intracranial aneurysms. Because
giant aneurysms are often partially
thrombosed, they often opacify
incompletely 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 for
surgical 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 the
advantage of showing a 3-dimensional
image and demonstrating the
aneurysms relationship to adjacent
structures. Bone artifact may hinder
adequate visualization of certain
aneurysms 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 one
study, 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 a
risk of brain herniation or aneurysmal
rebleeding, this procedure should
generally be reserved for patients
where the diagnosis remains uncertain
following CT scanning.

Xanthochromia develops only after red
blood cells lyse, and is usually
detectable after 4 hours, is maximal at
1 week, and is typically undetectable
by 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 and
Hess grade of this patient?
Once a diagnosis of SAH has been
established, patients are given a clinical
grade based on one of the accepted
grading schemes. Although numerous
grading 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 after
SAH

Grade Clinical symptomatology
Grade I Awake, mild headache, +nuchal rigidity
Grade II Awake, moderate- to- severe
headaches, nuchal rigidity
Grade III Drowsy or confused +focal deficits
Grade IV Stuporous, mild- to- moderate
hemiparesis, and signs of increased
intracranial pressure
Grade V Comatose, severe disability, severe
increased intracranial pressure
Posterior communicating artery aneurysm 9

Of note, the Hunt and Hess grading
scale 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 grading
scale was later revised by Hunt in 1974
to include two additional grades. Grade
0 was added to include patients with
unruptured aneurysms without
symptoms, and grade 1a to include
patients with no acute meningeal
reaction, but a fixed neurological
deficit (Hunt and Kosnik, 1974, p 79-
84)
[65]
. The patient in this case
presented with a severe headache,
photophobia, nuchal rigidity, and no
decline 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 assessment
following SAH, some have proposed
using other scales to improve
predictive value. For example, Oshiro,
et al., developed a grading scale
(World Federation of Neurological
Surgeons, 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 replaced
the Hunt and Hess scores of 1-5,
respectively (see Table 2.2b). The
authors of this scale (WFNS) felt that
their grading scheme was better than
the Hunt and Hess system at predicting
overall patient outcomes while at the
same 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 Neurological
Surgeons Scale

3. What is the Fisher grade of this
patient?
Fisher (1980) developed a four-tiered
grading scale for the appearance of
SAH on CT scanning dependent upon
the severity and location of the blood
pattern. Grade I patients had no
evidence 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 cisternal
subarachnoid blood (>1mm thickness
as depicted in this case), while grade
IV patients had intraventricular or
intraparenchymal blood with or
without a significant subarachnoid
component. The Fisher grading system
can help predict the probability of
developing vasospasm by the amount
of blood detected on CT scan . Patients
with Grade I, II, and IV bleeds had no
or 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 motor
deficit
Grade II Glasgow coma score 13 14, no
motor deficit
Grade III Glasgow coma score 13 14, motor
deficit
Grade IV Glasgow coma score 7 12, with or
without motor deficit
Grade V Glasgow coma score 3 6, with or
without motor deficit
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 larger
quantities of blood increasing the
likelihood that vasospasm will occur
(Hughes, 2003, p 252)
[63]
.

4. The cerebral angiogram for this
patient is depicted below. What is
the diagnosis?




This angiogram of the left internal
carotid artery (ICA) depicts a bilobed
posterior communicating artery
(PcomA) aneurysm originating at the
level of a fetal PcomA (Wilkins and
Rengachary, 1996, p 2306)
[161]
.

5. Describe two angiographic
findings in this patient that are
important for surgical planning?
Care needs to be taken when evaluating
angiograms of patients with a PComA
aneurysm, SAH, and no third nerve
deficit because the aneurysms often
project laterally onto the medial edge
of the temporal lobe rather than in
more common posterolateral or
downward directions. This is important
during surgical planning since
premature retraction of the temporal
lobe may result in aneurysm rupture.
Additionally, the integrity of a fetal
PComA needs to be preserved during
surgery and aneurysm clip placement.
If the area supplied by the PComA is
small, inadvertently placing this vessel
into the clip construct may not cause
any adverse sequelae, however, if the
PComA is fetal or there is a
hypoplastic P
1
, it may result in a
clinically significant PCA infarct
(Wilkins and Rengachary, 1996, p
2306)
[161]
; (Psarros, 2006, p 199)
[124]
.

6. The emergency room physician
reviews 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 decreasing
clot 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,
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 of
fibrinolysis and clot breakdown after
SAH. Intravenous injection of
AMICAR generally peaks in the
bloodstream in about 20 minutes. It
crosses the blood-brain barrier and
achieves maximal antifibrinolytic
activity within the cerebrospinal fluid
approximately 48 hours later (Findlay,
et al., 1988, p 723-735)
[43]
. A typical
regimen includes infusing 2 g/ hour
intravenously for 48 hours, and then
1.5 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 increased
risk in associated medical morbidity,
the most frequent being diarrhea in
approximately 24% of patients.
Additionally, communicating
hydrocephalus was 25% more likely
with antifibrinolytic therapy (Burchiel,
et al., 1984, p 57-63)
[21]
. The greatest
concern over its use, however, was the
increased risk of vasospasm that
negated its benefits in some studies
(Kassell, et al., 1984, p 225-230)
[74]
.
The general consensus about the role of
antifibrinolytics is that they have little
role in acute SAH, especially if surgery
is anticipated within a few hours or
days of admission (Hughes, 2003, p
267)
[63]
.

7. What is the rate of rebleeding
following a SAH?
The frequency of rebleeding is in the
range of 4% within the first 24 to 48
hours, and approximately 1.5% each
day 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 believed
to 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 attendant
complications (Hughes, 2003, p
267)
[63]
; (Kassell, et al., 1982, p 337-
343)
[73]
.
12 Clinical Neurosurgical Vignettes

8. What are some advantages and
disadvantages of early versus
delayed surgery after SAH?
Table 2.8 Advantages and disadvantages of early
versus delayed surgery after SAH

Despite the potential microsurgical
challenges associated with operating on
a swollen brain, the majority of grade
I-III patients at various institutions still
undergo surgery early after SAH to
minimize the incidence of rebleeding.
Although early surgery can certainly be
technically more challenging,
experience has shown that patient
outcomes are not necessarily adversely
affected, as demonstrated by the
International 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 have
proven 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 the
operating 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 of
what structure?
One of the most useful adjuncts to
avoid brain retraction for anterior
circulation aneurysms during initial
exposure is to aggressively remove the
bony wing (or sphenoid ridge) of the
sphenoid bone. It is removed using
rongeurs and a power drill from
lateral to medial for a distance of
approximately 4 cm, to the level of the
orbital 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, the
degree of initial frontal lobe elevation
necessary to expose the carotid cistern
Early approach Delayed approach
ADVANTAGES ADVANTAGES
Decreases rebleeding risk
Allows for aggressive
management of
vasospasm
Early removal of
subarachnoid blood and
possible prevention of
hydrocephalus
Earlier patient ambulation
and rehabilitation;
perhaps reduced hospital
stay
Reduced medical
complications associated
with bedrest
Evacuation of hematoma,
if applicable
Brain less swollen
Easier microdissection
Stable patient
DISADVANTAGES DISADVANTAGES
Swollen brain may make
surgery more difficult
Unstable patient in some
instances
Scheduling problems,
possibility of
inexperienced operative
team
Higher rebleeding risk
Does not facilitate or allow
for aggressive
management of
vasospasm
Delayed ambulation,
longer hospital stay
Increased risk of medical
complications while
awaiting surgery
Posterior communicating artery aneurysm 13

is increased, and surgical access along
the 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 the
inferior aspect of the craniectomy and
adjacent muscle (Samson and Batjer,
1990, p 57)
[138]
.

10. Describe the pertinent steps
during surgery for a PcomA
aneurysm?
Initial exposure after dura opened

In Intracranial Aneurysm Surgery:
Techniques, Samson and Batjer
eloquently describe the steps for
clipping PcomA aneurysms (Samson
and Batjer, 1990, p 57-58)
[138]
. With
the 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 Sylvian
fissure. The retractor is then advanced
in a step-by-step fashion as the
arachnoid opening is extended from the
horizontal portion of the Sylvian
fissure to its junction with the carotid
cistern. As frontal lobe elevation brings
the optic nerve and internal carotid
artery (ICA) covered by arachnoid into
view, the arachnoid covering the
Sylvian fissure usually thickens.
Oftentimes, a small vein will be found
bridging the temporal to frontal lobe
immediately under this thicker
arachnoidal layer adjacent to the
Sylvian 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 the
horizontal portion of the Sylvian
fissure. The retractor blade can then be
advanced to expose the arachnoid layer
that surrounds the optic nerve and ICA.
The arachnoid incision, which was
started over the horizontal portion of
the Sylvian fissure, is then extended
posteriorly and anteriorly for better
visualization of the ICA and optic
nerve. The release of cerebrospinal
fluid from the subarachnoid Sylvian
and prechiasmatic cisterns will
generally help relax the brain to
facilitate further microdissection and
eventual aneurysm clipping (Samson
and Batjer, 1990, p 57-58)
[138]
.

Microdissection after basal cisterns
open

After the basal cisterns open, the next
step should be to focus attention on
securing proximal arterial control prior
to 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 of
the ICA on its anterior-medial aspect at
the apex of the opticocarotid triangle
and then carrying the microdissection
laterally, across the ICA. This should
complete the establishment of proximal
arterial control and simultaneously
establish initial exposure of the
proximal aneurysm complex in most
cases. Initial microdissection of
thickened arachnoid and clot in the
posterior carotid cistern should be
limited to meticulous proximal-to-
distal exposure of the ICA only, as the
surgeon defines in succession the
following vessels: the origin of the
posterior communicating artery,
posterior communicating artery (PCA)-
proximal aneurysm junction, aneurysm
neck, the distal origin of the aneurysm
14 Clinical Neurosurgical Vignettes

neck from the carotid wall, and finally
the anterior choroidal artery origin.
Extensive removal of subarachnoid clot
or identification of the distal posterior
communicating and anterior choroidal
vessels or aneurysm fundus should be
postponed until satisfactory exposure
of the entire posterior carotid wall has
been 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 distal
arterial control and with satisfactory
preliminary inspection of the posterior,
anterior and medial carotid walls, the
surgeon is nearly ready to begin
definitive dissection of the aneurysm
neck 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 not
be enough to stop back bleeding from
the PComA if intraoperative rupture
occurs. Sometimes, this can
significantly hinder visualization and
make further microdissection and
aneurysm clipping difficult. Moreover,
if the PComA is not identified prior to
clip placement, the surgeon runs the
risk of including this vessel into the
clip construct, especially if vision is
impaired by intraoperative rupture
(Samson and Batjer, 1990, p 63)
[138]
;
(Psarros, 2006, p 199)
[124]
.

11. Postoperatively, the patient was
found 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 a
homonymous defect in the upper and
lower quadrants with sparing of the
horizontal sector (quadruple
sectoranopia), which is diagnostic of a
lateral geniculate body infarct in the
AchA distribution. Injury or ligation of
this vessel may also produce the
classically 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) the
temporal 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 capsule
and 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 peduncle
and substantia nigra.

Generally, the sites for temporary clip
placement chosen during surgery for
PComA aneurysms include the
proximal ICA near the anterior clinoid
process, on the distal ICA immediately
proximal to the carotid bifurcation, and
on the PComA distal to the aneurysm
Posterior communicating artery aneurysm 15

fundus. Obviously, the territory
supplied by the AchA will be rendered
ischemic during the period of
temporary occlusion, which can result
in a choroidal infarct should
prolonged temporary occlusion time be
necessary.

Samson and Batjer describe the
following steps for clipping a PcomA
aneurysm after preparation of the
vessels to receive temporary clips
(Samson and Batjer, 1990, p 57-
58)
[138]
. The arterial blood pressure
should be normalized, and either
etomidate (0.3 mg/kg) or a barbiturate
(often pentobarbital) should be given to
achieve burst suppression.
Subsequently, temporary clips are
applied from proximal to distal, and the
aneurysm fundus could be more
aggressively 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 be
intermittently placed over the puncture
site and despite continued bleeding of
the PcomA (if temporary clip
application not possible), suction will
transiently decompress the aneurysm
adequately 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 be
placed over the puncture site and the
temporary clips removed to allow for
reperfusion of the carotid (and anterior
choroidal artery) territory, with the
bleeding from the aneurysm being
controlled with suction and tamponade
(Samson and Batjer, 1990, p 63-
64)
[138]
.
12. What percent of patients with
aneurysmal SAH develop
angiographic and clinical
vasospasm?
Vasospasm is one of the greatest
causes of morbidity in patients
surviving the initial SAH.
Angiographic vasospasm has been
reported to occur in approximately
70% of patients following SAH, with
approximately 20-30% having
clinically significant narrowing. It has
a peak incidence around the seventh
day following SAH, although it can
occur anytime up to approximately 13-
14 days post-bleed, beyond of which it
is fairly uncommon (Heros, et al.,
1983, p 599-608)
[58]
; (Ropper and
Zervas, 1984, p 909-915)
[134]
. When
vasospasm 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 basal
cisterns (Fisher grade III) carries a
higher vasospasm risk than focal
loculations (Fisher, et al., 1977, p 245-
248)
[44]
. Lobar hematomas and
interhemispheric blood are associated
with a low risk of vasospasm, while
subarachnoid blood in the Sylvian
fissure appears to carry an intermediate
vasospasm risk (Pasqualin, et al., 1984,
p 344-353)
[118]
; (Kistler, et al., 1983, p
424-436)
[81]
.

16 Clinical Neurosurgical Vignettes

13. On postoperative day 9 the
patient developed new right arm
and leg weakness while
recovering in the ICU, but her
level of consciousness remained
unchanged. 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 in
neurologic status. Headache, fever, and
leukocytosis may precede and herald
the onset of vasospasm prior to
neurological deterioration. Permanent
neurological deficit or death has been
reported to occur in approximately
12% of patients who develop severe
clinical vasospasm (Heros, et al., 1983,
p 599-608)
[58]
; (Fisher, et al., 1977, p
245-248)
[44]
. Although this clinical
history is highly suggestive of
vasospasm, obtaining an emergent CT
scan 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 significant
cerebral vasospasm?
In the chapter on management of SAH
in Neurological Emergencies,
Kopitnik, et al., give a thorough
discussion on the management of
cerebral vasospasm, which is
summarized below (Hughes, 2003, p
278-281)
[63]
. Presently, the mainstay of
treatment for clinically significant
cerebral vasospasm is the induction of
hypervolemia, systemic hypertension,
and hemodilution, commonly referred
to as triple-H therapy or
hyperdynamic therapy. The
neurologic deficits seen with
vasospasm result from arterial
narrowing and increased
cerebrovascular resistance.
Autoregulation is often disrupted
following SAH, and any intervention/s
that increase cerebral perfusion
pressure can increase cerebral blood
flow in the hypoperfused regions of the
brain and potentially improve
outcomes (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 and
central venous lines, an indwelling
foley catheter, and pulse oximetry. An
arterial catheter or A-line assesses
blood pressure continuously and lends
itself well to frequent blood draws for
blood gas measurements should they
be necessary. A SwanGanz catheter
monitors pulmonary capillary wedge
pressure (or central venous pressure if
central venous line is used), a
transcutaneous pulse oximeter
monitors oxygen saturation, and an
indwelling foley catheter can be a
useful adjunct to arterial and central
venous lines to gauge volume status
and certain urine electrolytes.
Desaturations may indicate early
pulmonary decompensation from
hypervolemic 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
Posterior communicating artery aneurysm 17

fluid balance. Pulmonary artery wedge
pressure is generally maintained
between 14 and 18 mm Hg and central
venous pressure is kept at
approximately 10 mm Hg. If clinical
improvement is not seen soon after
volume expansion or blood pressure
can not adequately be raised with
volume expansion alone, arterial blood
pressure can be elevated with
dopamine, dobutamine, and/or
norepinephrine and systolic pressures
typically maintained between 180 and
220 mm Hg. Kassell reported good
results in 58 patients treated for
cerebral vasospasm with volume
expansion and induced arterial
hypertension 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 a
secondary diuresis, which can make
artificial elevation of the pulmonary
capillary wedge pressure difficult.
Under these circumstances, the use of
low dose vasopressin can help
minimize the diuresis and maintain an
elevated intravascular fluid volume, if
necessary. Triple H therapy can be
continued until one of the following
conditions are met: neurologic
symptoms resolve, vasospasm clears as
demonstrated by arteriography or
Doppler monitoring, or complications
from hyperdynamic therapy occur.
Complications may include congestive
heart failure, brain edema, pulmonary
edema, hypertensive cerebral
hemorrhage, systemic complications of
prolonged vasopressor use, and
myocardial infarction (Shimoda, et al.,
1993, p 423-429)
[145]
. Calcium channel
blockers may improve SAH patient
outcome (nimodipine 60 mg orally
every four hours for 21 days) and are
now part of the overall management
algorithm at most institutions. Their
efficacy in reducing the detrimental
effects of vasospasm has been shown
in controlled studies, (Allen, et al.,
1983, p 619-624)
[5]
although the true
mechanism of action remains
somewhat elusive (Kassell, et al., 1992,
p 848-852)
[72]
.

When hyperdynamic therapy has
proven ineffective, other interventions
may prove useful. Selective intra-
arterial infusion of papaverine
hydrochloride or calcium channel
blockers into the symptomatic vascular
territory may reverse angiographic
vasospasm in some patients. The
results of this therapy can be clinically
dramatic but, in a similar fashion, may
be extremely fleeting or completely
unsuccessful (Minami, et al., 2001, p
169-179)
[98]
. Additionally, transluminal
balloon angioplasty of the large
intracranial vessels (ICA, M
1
segment
of MCA, vertebral and basilar arteries)
may also prove beneficial. A number
of 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