CORRESPONDENCE

Neuroendoscopic Observation of a Large Anterior

Communicating Artery Aneurysm
To the Editor:
We report on an 81-year-old woman who, because of a
likely syncope, fell down backward and sustained a scalp
injury. She was known to have dementia and to be under the
care of a neurologist; however, she had not undergone a brain
computed tomographic scan.
At admission, she was lethargic (Glasgow Coma Scale score of
9) and vomited several times in the emergency room. An urgent
computed tomographic scan ruled out traumatic lesions but
revealed markedly dilated ventricles. In the suprasellar area, a FIGURE C2. Neuroendoscopic view showing the aneurysm and related
structures within the third ventricle.
round hypodense lesion with calcifications in the upper slices
was present; the images allowed us to suspect an aneurysm (Fig.
C1). The patient rapidly worsened to a Glasgow Coma Scale After surgery, the patient demonstrated prompt improve-
score of 5. Long-standing hydrocephalus was rapidly decompen- ment; she was able to walk and talk on the third day after
sating, probably after the head trauma and a minor subarachnoid surgery. A magnetic resonance imaging scan with angio-
hemorrhage. We chose an endoscopic ventricular exploration, graphic sequences on the seventh postoperative day con-
because in such huge ventricles, it could be carried out without firmed the presence of the aneurysm, with an axial diameter of
problems even in the presence of the suspected aneurysm; we 1.2 cm and a sagittal diameter of 1.6 cm (Fig. C3). On the ninth
could then place a catheter under endoscopic control, or if it was postoperative day, the patient was discharged home with a
safe enough, we could first attempt an endoscopic third ventric- Glasgow Outcome Scale score of 5. In view of the absence of
ulostomy (ETV). Conversely, we believed that placing the ven- rupture or related neurological deficits and the patient’s age,
tricular catheter as usual, in a blind way, could have the adjunc- no treatment was undertaken for the partially thrombosed
tive risk of hurting the intraventricular mass. AComA aneurysm.
A right precoronary burr hole was drilled, and a rigid The association between hydrocephalus and dementia in cases
endoscope (forward oblique, 30 degrees; Storz-Decq-Hopkins; of giant AComA aneurysms has been reported (2). Ishihara et al.
Karl Storz GmbH & Co., Tuttlingen, Germany) was inserted (1) published a case report on a basilar tip aneurysm diagnosed
into the right frontal horn. As soon as the dilated foramen of
Monro was passed and the third ventricle was entered, a large,
ovoid, yellowish, and pulsatile lesion stemming from the an-
teroinfundibular area was observed. The optic chiasm seemed
to be stretched upward. The ETV was carried out easily,
although the ventricular floor diameters were narrowed by
the pulsatile mass. A large anterior communicating artery
(AComA) aneurysm was observed, together with its relation-
ship with neighboring anatomic intraventricular structures
(Fig. C2).

FIGURE C3. A and B, post-third ventricu-

lostomy magnetic resonance imaging scans
with angiographic sequences showing the
FIGURE C1. Preoperative computed tomographic scans showing hydro- anatomic relationships between the aneu-
cephalus and a suprasellar partially calcified, round lesion. rysm and the brain. Note the patent stoma.

NEUROSURGERY VOLUME 56 | NUMBER 3 | MARCH 2005 | E629

CORRESPONDENCE

during ETV, but, to our knowledge, this is the first reported case
of an AComA aneurysm observed during ETV.
Claudio Schonauer
Aldo Moraci
Naples, Italy
Enrico Tessitore
Nicolas de Tribolet
Geneva, Switzerland
Giuseppe M.V. Barbagallo
Catania, Italy

1. Ishihara S, Kamikawa S, Suzuki C, Katoh H, Ross I, Tsuzuki N, Ohnuki A,

Miyazawa T, Nawashiro H, Shima K: Neuroendoscopic identification of a
basilar artery tip aneurysm in the third ventricle: Case illustration.
J Neurosurg 96:1138, 2002.
2. Lownie SP, Drake CG, Peerless SJ, Ferguson GG, Pelz DM: Clinical presen-
tation and management of giant anterior communicating artery region aneu-
rysms. J Neurosurg 92:267–277, 2000.

DOI: 10.1227/01.NEU.0000155082.62626.OF
Unusual Nerve-Artery Relationship in Microvascular
Exploration for Tic Douloureux
To the Editor:
The patient, a white woman, developed tic douloureux
involving the right first and second divisions at the age of 48
years. She was treated conservatively with carbamazepine
(Tegretol; Novartis Pharmaceutical Corp., East Hanover, NJ),
but after 2 years, her pain had become increasingly difficult to
control with an adequate dosage of Tegretol; thus, surgical
intervention was recommended. After discussing the pros and
cons of microvascular decompression versus percutaneous
thermocoagulation, she elected to undergo decompression.
At surgery, the anteroinferior cerebellar artery initially
seemed to be compressing the superior aspect of the trigemi-
nal nerve. However, careful dissection of arachnoid tissue
around the artery-nerve complex revealed that the artery was,
in fact, penetrating the midportion of the nerve approximately
5 mm distal to the brainstem (Fig. C4). After penetration, the
artery disappeared ventrally and caudally. The portio minor
of the nerve was not involved.
Preoperative magnetic resonance imaging suggested that
the anteroinferior cerebellar artery was adjacent to the nerve.
At surgery, dissection was not extended farther than required
for the procedure; thus, the anteroinferior cerebellar artery
could not be confirmed with certainty. It is possible that the
artery was the superior cerebellar artery, although a persistent
abnormal pontine artery could be considered (1, 2).
Because the pain involved the first division, resection of the upper
portion of the nerve was thought inadvisable and there was concern
that sectioning the lower portion of the nerve would fail to relieve
the pain. Resection of the artery was not considered.
Therefore, with the use of careful blunt dissection, the upper
and lower halves of the trigeminal nerve were carefully sep-
FIGURE C4. Drawing showing the anteroinferior cerebellar artery (AICA)-
nerve complex.
arated distal to the artery, allowing for a large opening for the
artery and precluding compression of the nerve. This enlarge-
ment allowed the artery to be freely movable in its passage
through the nerve. Nothing further was done.
After surgery, the patient was pain-free. Within 6 months,
some pain in the right first division was occasionally felt. This
slowly worsened, again, with inadequate control by Tegretol.
Therefore, 2 years after her decompressive procedure, percu-
taneous thermocoagulation of the first division of the right
trigeminal nerve was carried out with relief of the recurrent
pain. Subsequently, she developed some occasional flicks of
pain along with some return of pinprick pain perception in the
right first division. However, the corneal reflex remains ab-
sent, and she has some continuing problems of dryness of the
cornea and conjunctiva in the right eye requiring ophthalmo-
logical follow-up and the use of artificial tears. The mild pain
is controlled with gabapentin (Neurontin; Pfizer, New York,
NY).
Bernard S. Patrick
Jackson, Mississippi
1. Jannetta PJ: Microvascular decompression of the trigeminal nerve root entry
zone, in Rovit RL, Murali R, Jannetta PJ (eds): Trigeminal Neuralgia. Baltimore,
Williams & Wilkins, 1990, pp 201–222.
2. Rhoton AL Jr: Microsurgical anatomy of decompression operations on the
trigeminal nerve, in Rovit RL, Murali R, Jannetta PJ (eds): Trigeminal Neural-
gia. Baltimore, Williams & Wilkins, 1990, pp 165–200.
DOI: 10.1227/01.NEU.0000155083.39755.53

E629 | VOLUME 56 | NUMBER 3 | MARCH 2005 www.neurosurgery-online.com


Results of Multimodality Treatment for 141 Patients
with Brain Arteriovenous Malformations and Seizures:
Factors Associated with Seizure Incidence and Seizure
Outcomes
To the Editor:
After a careful reading of the article published by Hoh et al.
(3) about the results of a multimodality approach to patients
with arteriovenous malformations of the brain associated with
seizures, we thought it appropriate to make some comments.
Obviously, this group has a wide experience in the manage-
ment of these neurovascular lesions; nevertheless, evaluating
the outcome of their patients, our attention was drawn to the
high incidence of postoperative seizures. Only 73 (66%) of the
outcomes could be included in Engel Class I, whereas the
other 34 (30.9%) outcomes were included in the less favorable
Engel Classes II, III, and IV (3).
There is a group of neurological diseases with a proven
relationship with epileptic seizures; some of them can be
cured by epilepsy surgery. Among these diseases are the
neocortical lesions (i.e., tumors), neurovascular lesions (i.e.,
arteriovenous malformations, cavernous angiomas), gliotic ar-
eas, and others related to embryonic maldevelopment (e.g.,
dysplasias, abnormal neuronal migration). In the management
of this last group, the worst results are obtained, with only a
30 to 50% benefit with lesionectomy; however, the outcome in
patients with nondysplastic lesions is variable. Some authors
report a benefit (Engel Class I) between 65 and 90% (1, 2, 4, 6),
and others have reported a discrete benefit in their patients of
56% (5).
What seems to be the cause of these results? Failure to
achieve a seizure-free status after epilepsy surgery for a struc-
tural lesion (e.g., arteriovenous malformation) is often attrib-
uted to inadequate removal of the lesion and/or associated
epileptogenic cortex. The patients with neurovascular lesions
whose main complaint is epilepsy should be approached
through a plan designed for epilepsy surgery. Through this
protocol, it could be established whether the cause of the
seizures is in the underlying tissue or if there are other areas
with epileptogenic activity and even the presence of dual
pathological findings (a condition in which a structural lesion
appears simultaneously with cortical regions without appar-
ent damage but with evident abnormal excitatory activity).
Without this approach, surgeons would not be able to guar-
antee the solution of the main problem in these patients:
seizures.
We agree with the authors that the location of the epilepto-
genic focus could be in the neuronal tissue surrounding the
lesion. If this condition is verified with electrocorticography
and it is not an eloquent area, this tissue could be removed
safely. Conversely, if it is an eloquent area, multiple subpial
transections could be an option.
We are aware that the proposed approach has some draw-
backs (i.e., the role of long-term video-electrocorticographic
recording for localization of seizure foci is limited to lesions
with low or no flow [cryptic arteriovenous malformations]
NEUROSURGERY
CORRESPONDENCE
because of the risk of hemorrhage, mass effect, and edema
secondary to grids or electrodes over the adjacent cortex). In
addition, opioid anesthetic agents can produce false lateraliz-
ing epileptic activity, for example. In such patients, it is ad-
visable that most cortical resections be performed as a second-
stage procedure after the arteriovenous shunt has been
removed.
We consider that the presence of seizures should be evalu-
ated with caution when a patient is to undergo a specific
procedure. When we are applying a minimally invasive
method (endovascular or radiosurgical obliteration), we can-
not properly determine the functional status of the tissue
surrounding the lesion; thus, this could be a problem if the
patient is complaining of epilepsy. For these reasons, we think
that an epileptologist, neurologist, or dedicated neurosurgeon
should be included if a multidisciplinary team is involved in
the management of patients with seizures secondary to any
neurological disease.
Raúl Andrés Pérez Falero
Odalys Hernández León
Pinar del Río, Cuba
1. Engel J Jr, Van Ness PC, Rasmussen TB, Ojemann LM: Outcome with respect
to epileptic seizures, in Engel J Jr (ed): Surgical Treatment of Epilepsies. New
York, Raven Press, 1993, pp 609–621.
2. Frater JL, Prayson RA, Morris HH III, Bingaman WF: Surgical pathologic
findings of extratemporal based intractable epilepsy: A study of 133 consec-
utive resections. Arch Pathol Lab Med 124:545–549, 2000.
3. Hoh BL, Chapman PH, Loeffler JS, Carter BS, Ogilvy CS: Results of
multimodality treatment for 141 patients with brains arteriovenous malfor-
mations and seizures: Factors associated with seizures incidence and seizure
outcomes. Neurosurgery 51:303–309, 2002.
4. Kusty RL: Focal extratemporal epilepsy: Clinical features, EEG, patterns, and
surgical approach. J Neurol Sci 16:1–15, 1999.
5. Schramm J, Kral T, Kurthen M, Blumcke I: Surgery to treat frontal lobe
epilepsy in adults. Neurosurgery 51:644–653, 2002.
6. Smith JR, Lee MR, King DW, Murro AM, Park YD, Lee PG, Meador KJ, Loring
DW: Results of lesional versus non lesional frontal lobe epilepsy surgery.
Stereotact Funct Neurosurg 69:202–209, 1997.
DOI: 10.1227/01.NEU.0000155084.47379.89
Death after Late Failure of Endoscopic Third
Ventriculostomy: A Potential Solution
To the Editor:
The article of Mobbs et al. (1) describes an interesting ap-
proach to prevention of a fearful complication of endoscopic
third ventriculostomy (ETV): rapid deterioration leading to
sudden death. The authors suggest that placement of a ven-
tricular catheter and subcutaneous reservoir at the conclusion
of the procedure may offer the potential to sample cerebro-
spinal fluid, measure intracranial pressure, and, in the case of
deterioration, aspirate cerebrospinal fluid to decrease
pressure.
In our opinion, if a reservoir is to be placed after every ETV,
it might as well be inserted in every shunted patient. After all,
VOLUME 56 | NUMBER 3 | MARCH 2005 | E629
CORRESPONDENCE
shunted patients have a similar or even higher risk of mal-
function and are associated with a significantly higher danger
of “sudden” death throughout their lifetime. We agree with
other commentators that subcutaneous reservoir placement
undoubtedly increases the risk (and cost) of ETV. In addition,
placement of a permanent foreign body compromises the core
rationale for ETV: avoiding reliance on a foreign body.
ETV-associated infections occur in more than 5% of patients
(2). When a foreign body remains in situ, antibiotics are not
enough to clear the infection in most patients and another
operation is required. Furthermore, the reservoir placement
may prolong the operation and compromise wound healing,
especially in infants. Insisting on regular clinical follow-up of
our post-ETV population, and taking seriously any clinical
changes that may occur in this group, seems to be a more
rational and overall safer approach to confront the ETV fail-
ures that are bound to happen, whether early or late.
Shlomi Constantini
Vitaly Siomin
Tel Aviv, Israel
1. Mobbs RJ, Vonau M, Davies MA: Death after late failure of endoscopic third
ventriculostomy: A potential solution. Neurosurgery 53:384–386, 2003.
2. Siomin V, Cinalli G, Grotenhuis A, Golash A, Oi S, Kothbauer K, Weiner H, Roth J,
Beni-Adani L, Pierre-Kahn A, Takahashi Y, Mallucci C, Abbott R, Wisoff J,
Constantini S: Endoscopic third ventriculostomy in patients with cerebrospinal fluid
infection and/or hemorrhage. J Neurosurg 97:519–524, 2002.
DOI: 10.1227/01.NEU.0000155085.47379.CO
Rate of Resolution of Histologically Verified
Intracranial Tuberculomas
To the Editor:
I read the article by Poonnoose and Rajshekhar (1). They
have analyzed a difficult problem on the treatment of tuber-
culoma that does not resolve. Their recommendation on the
duration of antituberculous therapy (ATT) based on the radio-
logical picture is logical. However, Prof. Rabacca from
Moracco has a different opinion and emphasizes in his com-
ment that the problem may be a result of the bad practice by
clinicians in the use of an antitubercular drug regimen.
I understand from the article that 24 patients had their
tissues examined microbiologically. This group of patients
could be further subdivided into Group I (i.e., patients who
received ATT) and Group II (i.e., patients who did not receive
ATT). There were 9 patients in Group I and 15 patients in
Group II (Table C1).
One can conclude from this analysis that the positive yield,
as well as the incidence of multidrug-resistant bacilli, was
higher in Group II. This probably highlights the fact that the
incidence of multidrug resistance is higher in India.
In treating patients with resistant tuberculosis, we have
observed that most of these cases were associated with a
tubercular abscess. The wall of the tubercular abscess proba-
E629 | VOLUME 56 | NUMBER 3 | MARCH 2005
TABLE C1. Rate of resolution of histologically verified
intracranial tuberculomas in 24 patients
Group I (ATTⴙ) Group II (ATTⴚ)
No. of patients 9 15
Positive culture 1 6
Multidrug resistance 1 3
a
ATT, antituberculous therapy.
bly forms a barrier to chemotherapy. The same mechanism
likely holds true for drug-resistant tuberculomas. Surgical
manipulation of these lesions disrupts the barrier; hence, they
respond to ATT after surgery. Therefore, it may not be essen-
tial to excise them totally.
Manas Kumar Panigrahi
Hyderabad, India
1. Poonnoose SI, Rajshekhar V: Rate of resolution of histologically verified
intracranial tuberculomas. Neurosurgery 53:873–879, 2003.
DOI: 10.1227/01.NEU.0000155086.85497.33
Stimulation of the Subthalamic Nucleus in Parkinson’s
Disease Does Not Produce Striatal Dopamine Release
To the Editor:
I would like to make a comment regarding the article of
Abosch et al. (1). The authors conclude that “Our results
suggest that STN [subthalamic nucleus] stimulation does
not mediate its anti-PD [Parkinson’s disease] effects via
the release of dopamine, as assessed with [11C]raclopride
displacement.”
[11C]Raclopride is a D2-dopamine (DA) receptor antagonist
(4). Patients with typical Parkinson’s disease (PD) have re-
duced dopa decarboxylase activity in the putamen (3, 5) and
reduced DA transporter sites (5), with preserved D2 receptors
in positron emission tomographic studies. This is in discor-
dance with cases of progressive supranuclear palsy, which
demonstrate loss of striatal D2 receptors (2, 3).
Diminished DA availability to the striatum of patients with
PD does not lead to a change of [11C]raclopride binding in the
area. I do not consequently expect that any treatment of PD
would change [11C]raclopride binding in the striatum.
Nikolaos Evangelos Sakellaridis
Athens, Greece
1. Abosch A, Kapur S, Lang AE, Hussey D, Sime E, Miyasaki J, Houle S, Lozano
AM: Stimulation of the subthalamic nucleus in Parkinson’s disease does not
produce striatal dopamine release. Neurosurgery 53:1095–1105, 2003
www.neurosurgery-online.com

2. Brooks DJ: Positron emission tomographic studies of subcortical degenera-
tions and dystonia. Semin Neurol 9:351–359, 1989.
3. Brooks DJ, Ibanez V, Swale G, Quinn N, Lee AJ, Mathias CJ, Bannister R,
Marsden CD, Frackowiak RS: Differing patterns of striatal 18F-dopa uptake in
Parkinson’s disease, multiple system atrophy, and progressive supranuclear
palsy. Ann Neurol 28:547–555, 1990.
4. Farde L, Eriksson L, Blomquist G, Halldin C: Kinetic analysis of central
[11C]raclopride binding to D2-dopamine receptors studied by PET: A comparison to
the equilibrium analysis. J Cereb Blood Flow Metab 9:696–708, 1989.
5. Swale GV, Wroe SJ, Lees AL, Brooks DJ, Frackowiak RS: The identification of
presymptomatic parkinsonism: Clinical and [18F]dopa positron emission to-
mography studies in an Irish kindred. Ann Neurol 32:609–617, 1992.
In Reply:
We thank Dr. Sakellaridis for his comments on our article
(1). In response, we offer the following points.
The administration of l-dopa results in the amelioration of
the motor symptoms of PD. Studies have demonstrated that
this improvement in motor symptoms is associated with bind-
ing of DA to DA receptors as visualized by the competitive
displacement of previously administered labeled [11C]raclo-
pride (2) in the form of occupied striatal receptors.
Stimulation of the subthalamic nucleus (STN) similarly re-
sults in amelioration of the motor symptoms of PD. Given the
similarities in clinical effect between l-dopa administration
and STN stimulation, we tested the hypothesis that effective
STN stimulation would also result in the displacement of
striatal [11C]raclopride. We found, however, that there was no
significant displacement of striatal [11C]raclopride in response
to STN stimulation, and therefore concluded—given the lim-
itations outlined in our Discussion—that this is not the pri-
mary mechanism of action of STN stimulation.
Aviva Abosch
Shitij Kapur
Anthony E. Lang
Doug Hussey
Elspeth Sime
Janis Miyasaki
Sylvain Houle
Andres M. Lozano
Toronto, Ontario, Canada
1. Abosch A, Kapur S, Lang AE, Hussey D, Sime E, Miyasaki J, Houle S, Lozano
AM: Stimulation of the subthalamic nucleus in Parkinson’s disease does not
produce striatal dopamine release. Neurosurgery 53:1095–1105, 2003
2. Tedroff J, Pederson M, Aquilonius SM, Hartvig P, Jacobsson G, Langstrom B:
Levodopa-induced changes in synaptic dopamine in patients with
Parkinson’s disease as measured by [11C]-raclopride displacement and PET.
Neurology 46:1430–1436, 1996.
DOI: 10.1227/01.NEU.0000155087.93120.06
Microsurgical Keyhole Approach for Middle Fossa
Arachnoid Cyst Fenestration
To the Editor:
We read with great interest the recently published article by
Levy et al. (2). Regardless of the original description of this
NEUROSURGERY
CORRESPONDENCE
innovative keyhole approach to arachnoid cyst fenestration as
a safe effective method for treating middle fossa cysts, we had
the impression that during the decision-making process, the
authors focused their attention on the arachnoid cysts, placing
important associated pathological findings in second place,
specifically in the case of children with hydrocephalus.
Arachnoid cysts presumably result from an aberration in
the embryological development of the subarachnoid space (4).
This hypothesis seems to be the reason for the actual disorder
in the cerebrospinal fluid circulation and why subarachnoid
cysts are frequently associated with hydrocephalus. Whether
the cyst is the cause of the ventriculomegalia is a clinical and
therapeutic dilemma. In some patients, the location of the cyst
interferes with the normal cerebrospinal fluid circulation (i.e.,
those compressing the sylvian aqueduct or those obstructing
the outlet foramina in the fourth ventricle); however, in some
cases, there is no evident relationship between the cysts and
the ventricular enlargement. In those situations, some authors
support the idea that the hydrocephalus is communicating
and the actual problem is in the subarachnoid space, similar to
their subarachnoid cyst counterparts (5). This could be the
reason for the low incidence of hydrocephalus (15–18%) in
children with middle fossa arachnoid cysts (1, 3).
In this article, Levy et al. (2) use the microsurgical keyhole
approach as the initial procedure for treatment of middle fossa
arachnoid cysts, including those in three moderately hydro-
cephalic patients. It is about those patients that we have some
concerns. Were their complaints secondary to hydrocephalus
or to the cysts? Why does the ventricular size remain stable
after the surgical procedure? In this situation, it is advisable to
determine whether these stable patients were functioning at
their full potential or whether their neurological function
could be improved after surgical diversion. In these patients,
it is also necessary to define whether they had arrested or
compensated hydrocephalus.
Because this procedure provides communication between the
cyst and the basal cisterns, we agree with the authors that the
proposed technique is useful for arachnoid cysts without hydro-
cephalus. In patients harboring middle fossa arachnoid cysts and
hydrocephalus, the diversion of the cyst could not be effective;
thus, the ventricular enlargement should be approached inde-
pendently, as suggested by Raffel and McComb (3).
Odalys Hernàndez Leòn
Raúl Andrés Pérez Falero
Ivàn F. Arenas Rodrìguez
Carlos Lozano Crespo Palacio
Pinar del Rio, Cuba
1. Ciricillo SF, Cogen PH, Harsh GR, Edwards MS: Intracranial arachnoid cysts
in children: A comparison of the effects of fenestration and shunting.
J Neurosurg 74:230–235, 1991.
2. Levy ML, Wang M, Aryan HE, Yoo K, Meltzer H: Microsurgical keyhole
approach for middle fossa arachnoid cyst fenestration. Neurosurgery 53:
1138–1145, 2003.
VOLUME 56 | NUMBER 3 | MARCH 2005 | E629
CORRESPONDENCE
3. Raffel C, McComb JG: To shunt or to fenestrate: Which is the best surgical
treatment for arachnoid cysts in pediatric patients? Neurosurgery 23:338–342,
1988.
4. Rengachary SS, Watanabe I: Ultrastructure and pathogenesis of intracranial
arachnoid cysts. J Neuropathol Exp Neurol 40:61–83, 1981.
5. Shapiro KN, Swift DM: Intracranial arachnoid cysts, in Tindall GT, Cooper
PR, Barrow DL (eds): The Practice of Neurosurgery. Baltimore, William &
Wilkins, 1996, vol III.
DOI: 10.1227/01.NEU.0000155088.70249.45
Detection of Intracranial Aneurysms with Two-
dimensional and Three-dimensional Multislice Helical
Computed Tomographic Angiography
To the Editor:
The article by Kangasniemi et al. (4) provides useful insight
on the first generation of multislice computed tomographic
angiography (CTA) technology in the detection of intracranial
aneurysms. Their informative and timely study reinforces the
fact that the technique of CTA has evolved progressively since
its inception in tandem with developments in high-resolution
scanning machines and corresponding imaging software.
Since the late 1990s, we have also been advocates of CTA as
the sole diagnostic tool for detecting ruptured aneurysms (2,
3). We also use a protocol of subjecting all patients presenting
with subarachnoid hemorrhage to CTA first. Digital subtrac-
tion angiography (DSA) is performed only if the results of
CTA are negative or inconclusive or if the aneurysmal location
and/or morphology is unusual. The senior author (KAC) has
successfully operated on more than 120 patients with ruptured
aneurysms in the past 5 years on the basis of CTA alone
(unpublished data). During the process, however, we have
observed certain inherent deficiencies in our approach in sur-
gically treating aneurysms on the basis of CTA alone, recent
technical advances in CTA technology notwithstanding.
First, the actual pattern of blood flow is much better demon-
strated by standard DSA as compared with CTA. This, we be-
lieve, is an important requisite for surgery for aneurysms located
in the region of the AComA. Failure to realize the dominance of
any side and to appreciate the precise state of cross-flow across
the AComA with CTA has forced us to preserve the AComA
each time surgery is undertaken in this region. This is not always
mandatory and can be difficult (at times, almost impossible),
hence risky. The relatively simpler option of trapping the
AComA for difficult aneurysms ceases to exist unless adequate
filling of respective distal anterior cerebral arteries (A2) from
their ipsilateral proximal portions (A1) is ensured. In our expe-
rience, CTA, even with the newer generation of scanning ma-
chines, does not always provide sufficient information in this
respect. Conversely, DSA with cross-compression studies can be
invaluable. In addition, if there are any anatomic variations in
this region, as there often are, CTA can, in fact, be misleading (1).
It is possible to miss a vascular malformation on CTA. Only
the flow aneurysms may be detected and erroneously blamed for
the hemorrhage, thereby missing the actual culprit. Even with
the best-quality CTA, the perforators around the aneurysm may
E629 | VOLUME 56 | NUMBER 3 | MARCH 2005
not be picked up as well as on standard DSA and the images
certainly are not comparable to those on three-dimensional DSA.
Learning from our mistakes by operating on the basis of CTA
alone, we are gradually moving back toward DSA, which has
also undergone significant advances during the past few years.
Perhaps the question is not one of “either/or.” Rather, both
techniques have their own sets of advantages and disadvantages
and, in fact, can complement each other in generating valuable
diagnostic information, especially in cases of difficult aneurysms,
irrespective of whether a surgical or endovascular means of
treatment is adopted. Although we agree completely with the
authors’ conclusions about CTA being noninvasive, fast, and
credible in diagnosing ruptured aneurysms, the article stops
short of elaborating on the intrinsic pitfalls of the technique,
which equally deserve to be highlighted. On the basis of experi-
ence at our institute, we can recommend CTA as an excellent
adjuvant but not complete substitute for the “gold standard”
DSA, except in circumstances in which the patient’s rapidly
deteriorating clinical condition is attributable to an expanding
aneurysmal hematoma.
Kishor A. Choudhari
Nidhi Jain
Belfast, United Kingdom
1. Choudhari KA: Fenestrated anterior cerebral artery. Br J Neurosurg 16:525–
529, 2002.
2. Choudhari KA, McKinstry S, Kamel H, Fannin T: Efficacy of computed
tomographic angiography in the setting of aneurysmal subarachnoid haem-
orrhage. Neurosurgery 45:713–714, 1999 (abstr).
3. Choudhari KA, McKinstry S, Kamel HA, Fannin TF: CT Angiography: Pos-
sible non-invasive substitute for conventional angiography in subarachnoid
haemorrhage. Br J Neurosurg 14:76, 2000 (abstr).
4. Kangasniemi M, Mäkelä T, Koskinen S, Porras M, Poussa K, Hernesniemi JA:
Detection of intracranial aneurysms with two-dimensional and three-
dimensional multislice helical computed tomographic angiography. Neuro-
surgery 54:336–341, 2004.
DOI: 10.1227/01.NEU.0000155089.77873.68
Depression in Patients with High-grade Glioma: Results
of the Glioma Project
To the Editor:
Litofsky et al. (5) report an impressive incidence of depression
(93%) in 598 glioma patients enrolled in the Glioma Outcomes
Project. The incidence of mood disorders and the efficacy of
methods of investigation in cancer patients are controversial.
In the literature on cancer and depression, the main issue is
the difficulty in distinguishing major depression from mild
depression. Even standard screening tools often fail to distin-
guish between demoralization and major depression. Situa-
tional or reactive depression should be considered a normal
psychological response to the changes associated with a diag-
nosis of cancer. This type of depression is essentially psycho-
logical in nature rather than physiological and is more respon-
sive to supportive psychotherapy than medication (1).
www.neurosurgery-online.com

Litofsky et al. (5) used selected items of a quality of life scale
(Short Form 36) that are not validated for the detection of
mood disorders in cancer patients. The accuracy of a diagnos-
tic tool that reveals depression in almost all patients investi-
gated should be considered with caution. Moreover, the pres-
ence of depressive symptoms was investigated in a selected
series of patients, and, as stated by the authors, “the total
number of patients eligible for enrollment was unknown.”
In the study, the authors reported a relationship between
depression and poor postoperative neurological status and/or
multifocal tumor sites. These are well-known negative prog-
nostic factors (3). Yet, although the influence on shorter sur-
vival of clinical factors such as neurological signs, incomplete
surgical removal, biopsy, and multifocal presentation has been
demonstrated, this is not the case with depression. It is not
clear whether patients presenting with bad prognostic factors
are more likely to present with symptoms of depression or
whether depression itself should be considered a predictor of
poor outcome. Therefore, the need for antidepressant treat-
ment is debatable at the present time.
In a pilot project of continuing home care for brain tumor
patients, we have followed 215 patients affected by malignant
glioma from diagnosis to home-assisted death during the past 3
years. In 73 patients, depressive symptoms were evaluated using
a self-reported quality of life scale (European Organization for
Research and Treatment of Cancer Quality of Life Core Ques-
tionnaire 30), which explores several domains, including emo-
tional functions (6). Patients were evaluated after surgery and
then at 3-month intervals. The score of emotional function was
significantly correlated to the disability scale (Barthel Index; P ⬍
0.05) and general quality of life (P ⬍ 0.01). Comprehensive treat-
ment with psychological support and home neurorehabilitation
led to an improvement in quality of life and a reduction in
depressive symptomatology in patients as well as in caregivers.
Patients treated with neurorehabilitation at home for 3 months
after surgery had lower neurological disability and improved
emotional function and general quality of life scores (Fig. C5). In
FIGURE C5. Graph showing correlation between level of disability (Bar-
thel Index), emotional function (emotional func.) score (P ⬍ 0.05), and
general quality of life (qol) score (P ⬍ 0.05) of the European Organiza-
tion for Research and Treatment of Cancer Quality of Life Core Question-
naire 30 questionnaire, which was evaluated in 73 brain tumor patients.
NEUROSURGERY
CORRESPONDENCE
our experience, depressive symptoms can be related to many
factors, including knowledge of prognosis, different stage of
disease, neurological disability, cognitive function, quality of life,
and socioeconomic condition. Thus, symptoms of depression
should be considered a part of coping strategies in a physiolog-
ical process of adaptation to the disease, at least in those patients
whose depressive symptoms do not meet criteria for major
depression.
In our opinion, the incidence of pathological mood disor-
ders reported by Litofsky et al. (5) is overestimated, probably
because of inadequate diagnostic tools and even selection bias.
Specific diagnostic instruments for the detection of depression
in cancer patients need to be validated to eliminate the influ-
ence of somatic symptoms of medical illness. Psychiatric treat-
ment and medication should be reserved for the few cases in
which major depression is clearly documented (2, 4, 7).
Andrea Pace
Alfredo Pompili
Rome, Italy
1. Angelino AF, Treisman GJ: Major depression and demoralization in cancer
patients: Diagnostic and treatment consideration. Support Care Cancer
9:344–349, 2001.
2. Coyne JC, Palmer SC, Shapiro PL: Prescribing antidepressant to advanced
cancer patients with mild depressive symptoms is not justified. J Clin Oncol
21:295–296, 2004.
3. Curran WJ, Scott CB, Horton J, Nelson JS, Weinstein AS, Fischbach AJ, Chang
CH, Rotman M, Asbell SO, Krisch RE, Nelson DF: Recursive partitioning
analysis of prognostic factors in three Radiation Therapy Oncology Group
malignant glioma trials. J Natl Cancer Inst 85:704–710, 1993.
4. Hahn CA, Dunn RH, Logue PE, King JH, Edwards CL, Halperin EC: Pro-
spective study of neuropsychologic testing and quality-of-life assessment of
adults with primary malignant brain tumors. Int J Radiat Oncol Biol Phys
55:992–999, 2003.
5. Litofsky NS, Farace E, Anderson F Jr, Meyers C, Huang W, Laws ER Jr:
Depression in patients with high-grade glioma: Results of the Glioma Out-
comes Project. Neurosurgery 54:358–367, 2004.
6. Osoba D, Aaronson NK, Muller M, Sneeuw K, Hsu MA, Yung WK, Brada M,
Newlands E: The development and psychometric validation of a brain
quality-of-life questionnaire for use in combination with general cancer-
specific questionnaires. Qual Life Res 5:139–150, 1996.
7. Pringle AM, Taylor R, Whittle IR: Anxiety and depression in patients with an
intracranial neoplasm before and after tumour surgery. Br J Neurosurg 13:46–51,
1999.
DOI: 10.1227/01.NEU.0000155090.77873.BE
Grading of Subarachnoid Hemorrhage: Modification of
the World Federation of Neurosurgical Societies Scale
on the Basis of Data for a Large Series of Patients
To the Editor:
We read with great interest the article written by Rosen and
Macdonald (8). In this article, the authors propose a modifi-
cation of the World Federation of Neurosurgical Societies
(WFNS) scale, adding factors that affect prognosis in a large
series of patients included in different trials for assessing the
effect of tirilazad mesylate (U74006F) (Freedox; Pharmacia &
VOLUME 56 | NUMBER 3 | MARCH 2005 | E629
CORRESPONDENCE
Upjohn, Kalamazoo, MI) on the outcome after spontaneous
subarachnoid hemorrhage (SAH). All of these patients had
experienced aneurysmal SAH diagnosed by angiography
within the first 48 hours after the bleeding, and all were
surgically treated. However, several important concerns arise
from the methodology used in this study that could affect the
validity of its conclusions.
The first concern is whether the sample used to design this
new modified scale represents the whole clinical spectrum of
spontaneous SAH. As different articles have pointed out, the
identification of factors influencing the prognosis after SAH is
essential to a better understanding of the course of the illness
and improvement in the final results (2). The first step to
achieve this goal is to define clearly the population of study. It
has been calculated that 12 to 25% of patients experiencing
aneurysmal SAH die before reaching a hospital. In addition,
17 to 31% of the patients in different global series did not
undergo surgery because of poor clinical condition at admis-
sion or early rebleeding (2, 6, 7, 9, 10). Conversely, it is not
uncommon for patients not to be diagnosed the first time they
go to the emergency department, because SAH can be mis-
taken for other illnesses. In our own series, nearly 17% of
patients with SAH were admitted more than 48 hours after
bleeding (2). There are also patients in whom the first angio-
graphic examination does not detect the source of bleeding
(12). Thus, although the sample used in this study is large and
quite homogeneous, conclusions on the factors related to
prognosis in the patients included may not be representative
of the whole perspective of the illness and therefore not ap-
plicable in every case.
Another important problem with the design of this new
scale is the complexity of its grading scheme. When a new
scale is going to be used, it should be simple, easy to admin-
ister by different personnel involved in the care of the patients
so as to have low interobserver variability, facilitate informa-
tion about the state of the patient, and be a good means for
assessing prognosis. This new scale adds so many factors—up
to eight—that it is difficult to establish the grade of a single
patient if one has to memorize the different scores that each
factor adds to the final grading score. It also makes it difficult
even in large clinical series, such as the huge one used by the
authors for validating the new scale, to assign patients to
every score of the scale. This large number of different grades
also makes it difficult to have different probabilities of good or
bad evolution between grades, something that the authors
have attempted to resolve by “collapsing” the grades of the
new scale into a five-tiered scale, adding more confusion.
As stated previously, using a scale that has to be imple-
mented after angiography could affect its applicability to the
total number of patients experiencing spontaneous SAH, be-
cause many of them do not have initial angiography or be-
cause angiographic results are normal (2, 6, 12). The authors
also introduce another scale for this subpopulation of patients,
including preangiography factors. It is not clearly stated why
they do not add the thickness of the clot in computed tomo-
graphic scans to the factors they propose, when this last factor
E629 | VOLUME 56 | NUMBER 3 | MARCH 2005
seems to be an important variable in the whole sample used
for the multivariate analysis, because a diagnosis of SAH is
made by computed tomography. Therefore, it does not seem
logical to exclude this factor from the “preangiography” scale.
As pointed out by the reviewers, other concerns include the
time at which outcome is measured and the lack of embolized
patients. Three months seems to be too short a period to assess
the final evolution in these patients, because recovery could
progress after this time and embolization could alter the
weight of the different factors influencing the prognosis.
Other scales and modifications of the WFNS scale have been
proposed previously. The WFNS scale (1) was based on the
Glasgow Coma Scale (11) so as to improve the viability of
previous scales that used more ambiguous definitions of the
patient’s level of consciousness. However, this scale is still not
widely accepted, and different authors have questioned its
validity, especially regarding its grouping composition (2, 4,
5). Thus, several corrections were proposed for this classifica-
tion scheme, and new scales appeared, such as the Glasgow
Coma Scale for SAH (5), which uses different cutoff points
between clinical grades. In addition, other factors related to
the outcome of patients experiencing aneurysmal SAH, such
as age or quantity of blood in the initial computed tomo-
graphic scan (2, 4, 8-10), have been included in other scales
that might predict prognosis better than scales based only on
the patient’s level of consciousness. On the basis of informa-
tion acquired from a logistic regression model, Ogilvy and
Carter (4) developed a new grading scheme (Massachusetts
General Hospital [MGH] scale), which applied a simple scor-
ing method to each prognostic factor considered relevant,
such as the level of consciousness, age, quantity of blood in the
first computed tomographic scan, and size of the aneurysm.
Although data regarding the validity of this new grading
scheme, assessed retrospectively and prospectively and in
different subsets of their own series of patients, have been
already presented (4), the results of its applicability in total
management series of patients with SAH or its application in
other centers are still lacking. It would have been interesting to
assess the performance of the MGH scale in Ogilvy and Cart-
er’s patients, because it seems much simpler and easier to use
than the one proposed by the authors of this article. In fact, the
MGH scale is intended for the same population as this new
modified scale, that is, patients with confirmed aneurysmal
SAH treated with surgery.
In a recently published report (2), we attempted to compare
the performance of the MGH scale (4) with that of other level
of consciousness-based scales for SAH, such as the WFNS
scale (1) and the Glasgow Coma Scale for SAH described by
Oshiro et al. (5), in our own series of patients experiencing
spontaneous SAH using the same statistical methodology as
Rosen and Macdonald. The MGH scale was superior to the
other scales in terms of area under the receiver operating
characteristic curve for the subgroup of patients with con-
firmed aneurysmal SAH. However, although increasing the
prognostic capability of previous scales, the MGH scale shares
with the new scale proposed by the authors the lack of uni-
www.neurosurgery-online.com

versal applicability to every patient experiencing spontaneous
SAH, including untreated and idiopathic or “angiography-
negative” SAH cases. This means that this scale could not be
applied in our center in nearly 40% of the patients experienc-
ing spontaneous SAH (3).
Alfonso Lagares
José F. Alen
Pedro A. Gómez
Ramiro D. Lobato
Madrid, Spain
1. Drake CG, Hunt WE, Sano K, Kassell N, Teasdale G, Pertuiset B, Devilliers
JC: Report of the World Federation of Neurological Surgeons Committee on
a Universal Subarachnoid Hemorrhage Grading Scale. J Neurosurg 68:985–
986, 1988.
2. Lagares A, Gómez PA, Alén JF, Lobato RD, Rivas JJ, Alday R, Campollo J,
de la Camara AG: A comparison of different grading scales for predicting
outcome after subarachnoid haemorrhage. Acta Neurochir (Wien) 147:5–16,
2005.
3. Lagares A, Gómez PA, Lobato RD, Alén JF, Alday R, Campollo J: Prognostic
factor on hospital admission after spontaneous subarachnoid hemorrhage.
Acta Neurochir (Wien) 143:665–672, 2001.
4. Ogilvy CS, Carter BS: A proposed comprehensive grading system to predict
outcome for surgical management of intracranial aneurysms. Neurosurgery
42:959–970, 1998.
5. Oshiro EM, Walter KA, Piantadosi S, Witham TF, Tamargo RJ: A new sub-
arachnoid hemorrhage grading system based on the Glasgow Coma Scale: A
comparison with the Hunt and Hess and World Federation of Neurological
Surgeons Scale in a clinical series. Neurosurgery 41:140–148, 1997.
6. Qu F, Aiyagari V, Cross DT, Dacey RG Jr, Diringer MN: Untreated sub-
arachnoid hemorrhage: Who, why and when? J Neurosurg 100:244–249,
2004.
7. Roos YB, de Haan RJ, Beenen LFM, Groen RJM, Albrecht KW, Vermeulen M:
Complications and outcome in patients with aneurysmal subarachnoid
hemorrhage: A prospective hospital based cohort study in The Netherlands.
J Neurol Neurosurg Psychiatry 68:337–341, 2000.
8. Rosen DS, Macdonald RL: Grading of subarachnoid hemorrhage: Modifica-
tion of the World Federation of Neurosurgical Societies Scale on the basis of
data for a large series of patients. Neurosurgery 54:566–576, 2004.
9. Säveland H, Brand L: Which are the major determinants for outcome in
aneurysmal subarachnoid hemorrhage? A prospective total management
study from a strictly unselected series. Acta Neurol Scand 90:245–250, 1994.
10. Säveland H, Hillman J, Brandt L, Edner G, Jakobson K, Algers G: Overall
outcome in aneurysmal subarachnoid hemorrhage: A prospective study
from neurosurgical units in Sweden during a 1-year period. J Neurosurg
76:729–734, 1992.
11. Teasdale G, Jennett B: Assessment of coma and impaired consciousness: A
practical scale. Lancet 2:81–84, 1977.
12. Topcuoglu MA, Ogilvy CS, Carter BS, Buonanno FS, Koroshetz WJ, Singhal
AB: Subarachnoid hemorrhage without evident cause on initial
angiographic studies: Diagnostic yield of subsequent angiography and other
neuroimaging tests. J Neurosurg 98:1235–1240, 2003.
In Reply:
I have read the comments of Dr. Lagares and his colleagues
and thank them for taking such an interest in our article (3). They
raise several concerns. First, the population included in the da-
tabase that we used may not include the whole clinical spectrum
of spontaneous SAH. This is a fact. Patients had to get to the
hospital alive to be considered for the tirilazad mesylate studies.
I do not consider this a particularly grave flaw, because we are
only interested in grading, for the purposes of estimating prog-
NEUROSURGERY
CORRESPONDENCE
nosis among other reasons, among those patients we treat at the
hospital. It is irrelevant in those already fatally affected. The more
serious concern is that clinical trials may enroll selected groups of
patients. It is widely discussed that clinical trials of patients with
SAH selectively enroll good-grade patients, although I was un-
able to find a systematic review of this on a search of the litera-
ture. Conversely, as long as there are some patients from all
grades, as there were in the tirilazad mesylate database, the full
spectrum of SAH could be represented but the relative weighting
of prognostic factors could be altered. There is, however, no
assurance of this.
The second concern regarding the grading scale we devel-
oped was its complexity. I agree and do not believe this is a
practical scale to use. This disadvantage is cited in the conclu-
sion of the article. The comments of the reviewers are relevant
and precisely summarize the issues. Outcome prediction is
inexact at present, and clinical decisions are made on the basis
of factors other than a computer-generated statistical analysis
of a database. I draw attention to a recent article by Claassen
et al. (1), which exemplifies our thinking in the area as well as
that of some of the reviewers, which is to explore biochemical
and other types of markers as predictors of outcome.
I was not certain about the point of some of the other issues
raised by Dr. Lagares and his colleagues. We do include clot
thickness in the scale. Also, the time at which recovery is assessed
is only important if certain groups of patients cross categories.
Whether or not this occurs is unknown. The lack of endovascular
treatment is a limitation of the database. Patients treated with
coils were excluded from these trials. It would have been inter-
esting to compare the MGH scale (2) with our scale, but the
database we have does not include the necessary information.
There is no information on the Hunt and Hess grade. The Fisher
grade is not included but probably could be estimated.
In summary, I thank Dr. Lagares and his colleagues for their
interest. My recommendations stand as written at the end of
the article. To advance knowledge in the area, data should be
collected on as many prognostic factors as possible and re-
ported. On-line data supplementation could be allowed for
journals with word limitations so that as much information as
possible is available.
R. Loch Macdonald
Chicago, Illinois
1. Claassen J, Vu A, Kreiter KT, Kowalski RG, Du EY, Ostapkovich N, Fitzsim-
mons BF, Connolly ES, Mayer SA: Effect of acute physiologic derangements
on outcome after subarachnoid hemorrhage. Crit Care Med 32:832–838,
2004.
2. Ogilvy CS, Carter BS: A proposed comprehensive grading system to predict
outcome for surgical management of intracranial aneurysms. Neurosurgery
42:959–968, 1998.
3. Rosen DS, Macdonald RL: Grading of subarachnoid hemorrhage: Modifica-
tion of the World Federation of Neurosurgical Societies Scale on the basis of
data for a large series of patients. Neurosurgery 54:566–576, 2004.
DOI: 10.1227/01.NEU.0000155091.15992.3B
VOLUME 56 | NUMBER 3 | MARCH 2005 | E629
CORRESPONDENCE
Evolution of the Brain: From Behavior to Consciousness
in 3.4 Billion Years
To the Editor:
Dr. Oro’s article (6) is a fine review of the development of
the brain from the perspective of Darwin’s theory of evolution.
That is its weakness. Darwin’s theory that life can be explained
by the purely materialistic mechanism of natural selection
acting on variation is increasingly under assault for substan-
tive reasons by scientists (1, 4, 5) and philosophers (4, 8). The
Darwinian explanation for consciousness is particularly
problematic.
Dr. Oro asserts that we are conscious because we have
evolved brains that are computers made of meat and that
parallel processing of complex sensations led to conscious-
ness. However, if our consciousness evolved because of nat-
ural selection, natural selection would only hone conscious
activities that favor procreation. Other conscious activities,
such as pondering theories of evolution, would be selectively
neutral or even selected against (skimming the Journal of Hu-
man Evolution is not notably procreative). Our scientific opin-
ions would bear no necessary relation to the truth, because the
discernment of truth is not selected; procreation is selected. In
the evolutionary paradigm, all conscious activity that evolved
by natural selection is directed to procreation, including the
thinking that produced the theory itself. If our consciousness
evolved, we have no claim on the ability to discern scientific
truth. Evolved consciousness is a tool for mating rather than a
tool for science.
The materialistic aspects of Darwinism are dubious as well.
The assertion that consciousness is the result of “adaptive
representational networks” that are “individualized circuitries
that generate behavioral solutions that precisely fit the specific
environmental conditions, bioenergetic needs, personal expe-
riences, and unique life history of the individual” (6, p 1294) is
so vague that it is even difficult to ascertain how it could be
proven right or wrong. What experiments could be done to
test its predictions? What are its predictions? What is the
scientific basis for asserting that complexity of “circuitries” is
sufficient for consciousness? Can consciousness even be de-
fined in material terms? A professor is smarter than a school-
boy, but is he more conscious? A person with normal vision
and normal hearing certainly processes more complex sensory
information than a person who is born blind and deaf, but is
he or she more conscious than the disabled person? Does
consciousness correlate with intelligence quotient? Are adults
more conscious than children? Is a computer running Win-
dows 2000 closer to consciousness than a computer running
Windows 98? Where is there even a shred of evidence that
brain complexity causes consciousness rather than mediates
it?
The fundamental weakness of Darwinism is that it restricts
itself to materialistic explanations for life, including material-
istic causes for consciousness and for what most of us would
call the “soul.” An alternative explanation for life and con-
sciousness, of course, is that it was designed by a higher
E629 | VOLUME 56 | NUMBER 3 | MARCH 2005
intelligence. During the past decade, several biochemists and
mathematicians have suggested that it is possible to identify
intelligent design (ID) in biological processes. Perhaps the
most cogent recent evidence for ID has been the recognition of
irreducible complexity (1). Irreducible complexity is the char-
acteristic of many molecular systems, such as metabolic path-
ways and bacterial flagella, in which it seems necessary that all
of the individual components be in place before the system as
a whole can function. These molecular systems are too com-
plex to have arisen fully formed by a single mutation; thou-
sands or even millions of individual mutations would be
necessary to create them from nonfunctional precursors. Evo-
lutionary theory requires that each minute intermediate mu-
tation must have conferred procreative advantage by itself;
yet, the irreducibly complex system does not work until all the
mutations have occurred and all the components are in place.
It is difficult to ascertain how undirected evolutionary mech-
anisms could have assembled intricate molecular systems of
such complexity and specificity without functional intermedi-
ates. How did such systems evolve by natural selection?
Among modern theories in physical science, Darwinism is
unique for the paucity of quantitative evidence to support its
fundamental hypothesis—the hypothesis that the extraordi-
nary specified complexity of living organisms is the result of
the undirected process of natural selection acting on random
variation without intervention by an intelligent agent. Re-
cently, investigators have applied the mathematics of infor-
mation theory to biological complexity. Mathematician Wil-
liam Dembski (4, p 166), using Emile Borel’s probability
method to detect design (3), has proposed that any contingent
system that contains more than 500 bits of information has
sufficient complexity and specificity that it is almost certainly
intelligently designed. The chance that a system with more
than 500 bits of information arose without an intelligent
150
agency would be less than 10⫺ , which is no chance. A single
strand of human deoxyribonucleic acid encodes information
that is many orders of magnitude greater than that threshold
for detection of design; in any other branch of science except
evolutionary biology, the genetic code would be recognized as
an artifact of ID. The hypothesis that some of the complexity
of living systems is the result of ID has been excluded from
biology for philosophical rather than scientific reasons. Scien-
tific materialism is the secular religion of modern biology.
The detection of ID is common in other fields of science. It
forms the basis for forensic science, cryptography, and archae-
ology. The a priori exclusion of the possibility of ID as an
explanation for biological complexity leads to absurdities. If
an archaeological site were unearthed and found to contain a
man’s corpse with a primitive ax wedged in the man’s skull,
an archaeologist would affirm that the ax was designed, a
forensic scientist would conclude that the man’s death was
intentional, and an evolutionary biologist would conclude that
the man was an accident.
The ethical implications of Darwinism are gaining credibil-
ity at the same time that the scientific implications are losing
credibility. If consciousness is what makes us human, and
www.neurosurgery-online.com

consciousness is the result of material complexity of the brain,
it is inevitable that the conclusion will be drawn that smart
people are more human than simple people. Newborn babies
and some neurologically handicapped people demonstrate
less behavioral complexity than many animals do. Are they
less conscious than animals? Are they less than human?
Princeton University’s Peter Singer, the world’s preeminent
ethicist, has suggested that newborns and some people with
severe cognitive handicaps ought to have fewer legal rights
than some animals and that it is ethical for their parents or
caretakers to kill them if they wish (7).
The emergence of such ethics is not surprising. Philosopher
Benjamin Wilker (8, p 27) has pointed out that every philoso-
phy of science necessarily includes a worldview; there are no
separate magesteria in which scientific theories do not have
philosophical and ethical implications. In the 20th century, the
worldview of Darwinism had a profound impact on human-
ity. Social Darwinism, the application of Darwinism to the
social sciences, served as the basis for a vast program of
eugenics and involuntary sterilization in the United States (2).
It fell into disrepute in the 1930s when “survival of the fittest”
emerged as a philosophy of government in Europe. The
worldview engendered by Darwinism has since taken more
subtle but perhaps more pervasive forms. During the past
half-century, abortion, infanticide, genetic screening, the pros-
pect of therapeutic and reproductive human cloning, the use
of fetal tissue for experimentation, and voluntary and even
involuntary euthanasia, all of which benefit the fit at the
expense of the less fit, have been gaining acceptance.
Neurosurgeons practice an applied science; we care for
many people who are not particularly “fit,” and we have a
special responsibility to understand the ethical implications of
scientific theories published in our journals. Dr. Oro’s review
of the evolutionary development of the human brain is a
retelling of a dubious scientific theory with a disturbing eth-
ical pedigree. Evolutionary theories are collections of stories,
some quite fanciful, such as the assertion that “we started to
eat meat, got smarter, and thought of cleverer ways to obtain
more meat . . .” (6, p 1293) or “tools and increasing cognition
allowed procurement of a richer diet that led to a smaller gut,
thus freeing more energy for brain expansion” (6, p 1287).
Although there is no other area of modern physical science in
which such tales would be accepted as meaningful theories,
the ethical implications of Darwinism have been taken quite
seriously and seem to be gaining currency again. Philosopher
Daniel Dennett has called Darwinism a “universal acid” that
gradually transforms any culture in which it gains ascendance
(8). The corrosive ethics of Darwinism are proving far more
durable than the science (6).
Michael Robert Egnor
Stony Brook, New York
1. Behe MJ: Darwin’s Black Box: The Biochemical Challenge to Evolution. New
York, Touchstone, 1996.
NEUROSURGERY
CORRESPONDENCE
2. Black E: War Against the Weak: Eugenics and America’s Campaign to Create a
Master Race. New York, Four Walls Eight Windows, 2003.
3. Borel E: Probabilities and Life. Baudin M (trans). New York, Dover, 1962, p 28.
4. Dembski WA: Intelligent Design: The Bridge Between Science & Theology.
Downers Grove, InterVarsity Press, 1999.
5. Margulis L, Sagan D: Acquiring Genomes: A Theory of the Origins of Species.
New York, Basic Books, 2002.
6. Oro J: Evolution of the brain: From behavior to consciousness in 3.4 billion
years. Neurosurgery 54:1287–1297, 2004.
7. Singer P: Writings on an Ethical Life. New York, Harper Collins, 2000, pp
225–235.
8. Wilker B: Moral Darwinism: How We Became Hedonists. Downers Grove,
InterVarsity Press, 2002.
In Reply:
I appreciate Dr. Egnor’s comments on my article (20). It is
unclear whether he opposes the theory of the evolution of life
or just of the evolution of human life and consciousness.
However, it is clear that he advocates ID. A brief review of the
ID movement may benefit readers new to the subject.
In 1987, the Supreme Court in Edwards v. Aguillard ruled
that creation science was not science but religion. In his 1993
book, Darwin on Trial, University of California law professor
Philip Johnson (10) suggested the use of “intelligent design” as
an alternative. In 1996, he established the Center for Science
and Culture at the Discovery Institute in Seattle (28, p 3) and
subsequently published The Wedge of Truth: Splitting the Foun-
dations of Naturalism (11). In her book, Creationism’s Trojan
Horse: The Wedge of Intelligent Design, Barbara Forrest notes
that Johnson’s book is part of a “wedge strategy” designed to
get intelligent design “theory” into the public schools (7). (We
should credit Johnson for revealing his bias that “. . . scientific
evidence is not really needed to prove the theory true any
more than scientific evidence is needed to prove that two plus
two equals four” [10, p 45].)
Among the leading advocates of ID is biochemist Michael J.
Behe. His central argument, which Dr. Egnor views as “perhaps
the most cogent recent evidence for intelligent design,” is pre-
sented in the book Darwin’s Black Box: The Biochemical Challenge to
Evolution (3). Behe argues that the presence of biological “irre-
ducibly complex” structures (by definition, a structure that
would not work after the loss of one of its component parts)
indicates that they were designed and could not have evolved.
He uses the analogy of the common mousetrap: take away the
hammer, spring, or pin, and the trap will not work. Behe believes
that several biological structures or systems are irreducibly com-
plex, among which are the flagellum, blood clotting, and the
immune system. The argument, a modern version of the 19th
century notion that the eye could not have evolved, is flawed. As
biologist Kenneth Miller states: “Multiple parts of complex, in-
terlocking biological systems do not evolve as individual parts,
despite Behe’s claim that they must. They evolve together, as
systems that are gradually expanded, enlarged, and adapted to
new purposes” (18).
The mechanisms of evolution are more robust and dynamic
than Dr. Egnor suggests. Exaptation, the use an adaptive
structure for a different function than that for which it was
initially developed, plays an important role in the develop-
VOLUME 56 | NUMBER 3 | MARCH 2005 | E629
CORRESPONDENCE
ment of complex structures. Instead of being irreducibly com-
plex, homeostasis is being demonstrated to have rapidly
evolved in vertebrates (1). These studies further reveal the
“power and versatility of gene duplications and exon shuf-
fling.” Computer modeling indicates that the number of mu-
tations needed to generate some complex functions can be
startlingly small and that initially deleterious mutations can
serve “as stepping-stones to the evolution of complex fea-
tures” (14). Furthermore, recent studies of the genome’s silent
areas have uncovered a hidden function: regulating the devel-
opment of complex structures (15). As the mechanisms of
biological complexity are revealed and the evolution of ho-
meostasis, the flagellum (6, 19), and the immune system (9) are
defined, the complexity argument fades. Even Behe’s analogy
of an irreducibly complex mousetrap has lost its vigor (16).
Mathematician William Dembski (5) proposes the concept of
specified complexity. A suitable pattern, which he calls specifi-
cation, combined with complexity (measured by probability and
pattern) indicates ID. He developed an explanatory filter to de-
termine whether an event is caused by necessity (natural law),
chance, or design. An event of high probability is a result of law,
and one of low probability is a result of chance or design de-
pending on the presence of a suitable pattern meeting the con-
dition detachability. Detachability, crucial in Dembski’s scheme
for differentiating chance from design, seems to be subjective (21,
p 25). Furthermore, the outcome of the filter depends on how
tightly its probability limits are set. The management of change is
also problematic. Does an event such as a cometary impact,
highly probable during Earth’s period of heavy bombardment
and now highly improbable, change from law to a chance?
Finally, the definition of design itself is unclear, because Dembski
suggests design without a designer in some cases (21, pp 21–22).
Although one ID advocate described Dembski as “the Isaac
Newton of information theory” (21, p 20), other reviewers are not
convinced (21, 28).
A new “carefully nuanced” (8, p 314) argument is moving to
center stage. In their book, Rare Earth: Why Complex Life Is
Uncommon in the Universe, paleontologist Peter Ward and as-
tronomer Donald Brownlee discuss various observations sug-
gesting that Earth-like planets are rare (27). ID advocates
Guillermo Gonzalez, an astronomer/physicist, and Jay W.
Richards, a philosopher/theologist and vice president of the
Discovery Institute, have expanded on this theme in their
book, The Privileged Planet: How Our Place in the Cosmos Is
Designed for Discovery. Gonzalez and Richards argue that be-
cause the “Earth’s conditions allow for a stunning diversity of
measurements” (8, p xiii), which render it “optimal for making
scientific discoveries” (8, p xv), and because our planet is
habitable, we must have been designed. This “correlation
between habitability and measurability” is their “compelling
discovery” (8, p 332). Given that we would not be here if Earth
were not habitable, the debate centers on our possible unique-
ness. The thrust of my article, that conscious life appeared on
this habitable terrestrial planet after billions of years of evo-
lution altered by a series of catastrophic events, suggests that
human life and consciousness may indeed be unique.
E629 | VOLUME 56 | NUMBER 3 | MARCH 2005
Gonzalez and Richards suggest what they mean by design: it
does not have to be perfect, moral, or efficient (8, p 330). Because
the authors do not debate evolution, support the history of
catastrophic impacts, and are likely to agree that asteroidal col-
lisions are caused by law or chance and not by design, let’s
briefly review our planet’s history. The Earth is created by accre-
tion and then by heavy bombardment of comets and asteroids. A
proto-moon of just the right size hits the Earth in just the right
direction so that it avoids destruction yet is able to capture much
of the material to create the Moon, which stabilizes Earth’s orbit
and limits extreme fluctuations in climate. Once life begins and is
well established, a huge asteroid slams into the Earth, destroying
90% of marine life and 70% of terrestrial life. Vertebrates make it
through this “bottleneck” and evolve into mammals and dino-
saurs. The huge reptiles dominate the Earth for 100 million years,
whereas mammals remain “small creatures confined to the
nooks and crannies of a dinosaur’s world” (13). Another cata-
strophic impact destroys the dinosaurs and finally allows mam-
mals to flourish and evolve into conscious beings. Is this history,
dependent on what Dembski’s filter would detect as law or
chance events (the impacts) (5), the result of design? When con-
sidered from this wider perspective, defining the options as law,
chance, and design is not revealing. I suggest that the mystery
lies deeper.
Consciousness is likely latent in all creation and becomes
apparent in organisms with highly complex brains. The lim-
ited self-awareness in chimpanzees (12, 24) and the partial
consciousness of extinct Homo neanderthalensis (able to shape
stone tools and bone awls, occasionally bury the dead, and
possibly stitch crude clothing [2]) suggest an evolved emer-
gence. In humans, the neural correlates of consciousness are
being defined by functional brain imaging (12, 22, 25, 26).
Whether adaptive representational networks or other theory
enriches our understanding of consciousness, it is a wonder
we live in this age of discovery.
The remainder of Dr. Egnor’s critique seems to be based on
the view that science requires the philosophy of materialism.
It does not. Forty percent of scientists reject materialism and
accept an active and personal God (13), which is a figure
similar to that in the general population. In Finding Darwin’s
God, biologist Kenneth Miller (17) writes: “Darwin lifted the
curtain that allowed us to see the world as it really is” and
“ultimately brought us closer to an understanding of God.”
The wedge strategy is unnecessary. A millennia-old Ara-
maic translation of Genesis reads: “And God saw all that had
been done and behold it was a unified order” (23). Darwin (4)
revealed the unified order of life and concluded in the last line
of On the Origin of Species: “There is grandeur in this view of
life, with its several powers, having been originally breathed
by the Creator into a few forms or into one; and that, whilst
this planet has gone cycling on according to the fixed law of
gravity, from so simple a beginning endless forms most beau-
tiful and most wonderful have been, and are being evolved.”
John Oro
Columbia, Missouri
www.neurosurgery-online.com

1. Aird WC: Hemostasis and irreducible complexity. J Thromb Haemost
1:227–230, 2003.
2. Balter M: Dressed for success: Neandertal culture wins respect. Science
306:40–41, 2004.
3. Behe MJ: Darwin’s Black Box: The Biochemical Challenge to Evolution. New
York, Touchstone, 1996.
4. Darwin C: On the Origin of Species by Means of Natural Selection. (A facsimile
of the sixth edition of 1872). Norwalk, The Eaton Press, 1991.
5. Dembski WA: Intelligent Design: The Bridge Between Science & Theology.
Downers Grove, InterVarsity Press, 1999.
6. Faugy DM, Farrel K: A twisted tale: The origin and evolution of motility and
chemotaxis in prokaryotes. Microbiology 145:279–280, 1999.
7. Forrest BC, Gross PR: Creationism’s Trojan Horse: The Wedge of Intelligent
Design. Oxford, Oxford University Press, 2003.
8. Gonzalez G, Richards JW: The Privileged Planet: How Our Place in the Cosmos
Is Designed for Discovery. Washington, DC, Regnery Publishing, Inc., 2004.
9. Inlay M: Evolving immunity: A response to Chapter 6 of Darwin’s Black Box.
Available at: http://www.talkdesign.org/faqs/Evolving_Immunity.html.
Accessed January 4, 2005.
10. Johnson PE: Darwin on Trial. Downers Grove, InterVarsity Press, 1993.
11. Johnson PE: The Wedge of Truth: Splitting the Foundations of Naturalism.
Downers Grove, InterVarsity Press, 2002.
12. Keenan J, Gallup GG, Falk D: The Face in the Mirror: The Search for the Origins
of Consciousness. New York, Ecco, 2003.
13. Larson E, Witham L: Scientists and religion in America. Sci Am 281:88–93,
1999.
14. Lenski RE, Ofria C, Pennock RT, Adami C: The evolutionary origin of
complex features. Nature 423:139–144, 2003.
15. Mattick JS: The hidden genetic program of complex organisms. Sci Am
291:60–67, 2004.
16. McDonald JH: A reducibly complex mousetrap—last revised October 1,
2002. Available at: http://udel.edu/~mcdonald/mousetrap.html. Accessed
January 4, 2005.
NEUROSURGERY
CORRESPONDENCE
17. Miller KR: Finding Darwin’s God: A Scientist’s Search for Common Ground
Between God and Evolution. New York, Perennial, 2000.
18. Miller KR: Review of Darwin’s Black Box: The Biochemical Challenge to Evolu-
tion by Michael J. Behe. Available at: http://biomed.brown.edu/Faculty/
M/Miller/Behe.html. Accessed January 4, 2005.
19. Musgrave I: Evolution of the bacterial flagella. Available at: http://
rnaworld.bio.ku.edu/ribozone/resource/transport/
Ian%20Musgrave_flagella.htm. Accessed January 4, 2005.
20. Oro J: Evolution of the brain: From behavior to consciousness in 3.4 billion
years. Neurosurgery 54:1287–1297, 2004.
21. Perakh M: Why Intelligent Design Fails: A Scientific Critique of the New
Creationism. Amherst, Prometheus Books, 2003.
22. Ruby P, Decety J: What you believe versus what you think they believe: A
neuroimaging study of conceptual perspective-taking. Eur J Neurosci 17:
2475–2480, 2003.
23. Schroeder GL: The Hidden Face of God: Science Reveals the Ultimate Truth. New
York, Touchstone, 2001.
24. Smith JD, Shields WE, Washburn DA: The comparative psychology of
uncertainty monitoring and metacognition. Behav Brain Sci 26:317–339,
2003.
25. Vogeley K, Bussfeld P, Newen A, Herrmann S, Happe F, Falkai P, Maier W,
Shah NJ, Fink GR, Zilles K: Mind reading: Neural mechanisms of theory of
mind and self-perspective. Neuroimage 14:170–181, 2001.
26. Vogeley K, May M, Ritzl A, Falkai P, Zilles K, Fink GR: Neural correlates of
first-person perspective as one constituent of human self-consciousness.
J Cognit Neurosci 16:817–827, 2004.
27. Ward PD, Brownle D: Rare Earth: Why Complex Life Is Uncommon in the
Universe. New York, Copernicus, 2000.
28. Young M, Edis T: Why Intelligent Design Fails: A Scientific Critique of the New
Creationism. New Jersey, Rutgers University Press, 2004.
DOI: 10.1227/01.NEU.0000155095.08368.CF
VOLUME 56 | NUMBER 3 | MARCH 2005 | E629