CORRESPONDENCE
Should Cervical Fusions Ever Be Done for
Cervicalgia Alone?
To the Editor:
Now that I am semiretired and no longer performing operative
neurosurgery, I have been disappointed to find that some of my
younger colleagues decline to perform cervical fusions for patients
whom I refer to them if those patients have only neck pain and do
not have severe radicular symptoms and/or neurological deficit. I
am told that this is because of an impression of a universally poor
outcome, although perhaps it is also in part a reaction to some of
the excessive surgical zeal for doing cervical fusions that we all
encounter in the community. My own recollection, based on
more than 40 years of performing cervical spine surgery, has not
been so pessimistic, and I believe that it is a disservice to my
patients for them not to be able to undergo potentially quite
beneficial fusion surgery. Surgery for painful joints elsewhere in
the body is certainly widely practiced and accepted, with large
numbers of artificial hips, knees, and so on being used to treat
painful joints as our population ages. Because the cervical disc is
another joint that can be locally damaged, producing arthralgic
pain, I fail to see the logic of not operating on a painful cervical
disc when indicated.
To reinforce my memory, I did a quick chart review of my own
last 10 patients operated on for arthralgic cervicalgia during the
years 1995 to 2002. Like most spinal neurosurgeons, the majority
of the cervical operations that I performed were for disc ruptures
with radiculitis, cervical fractures, spondylotic myelopathy, tu-
mors, and other conditions. However, I did retrieve the records
for 10 patients on whom I had operated for neck pain as their
principal symptom. All these patients had severe 1- or 2-level
cervical disc degeneration, and none had associated neurological
deficits. All were incapacitated by intolerable pain despite
aggressive and often prolonged therapy, including anti-in-
flammatory drugs, bracing, exercises, and often intradiscal steroid
injections. There were 5 men and 5 women, 8 with single-level
disease and 2 with adjacent 2-level disease. Their ages were
younger than those of typical patients with degenerative spon-
dylopathy (mean age 45.5 years, range 36-64 years), most having
a history of remote neck injury of limited severity. All underwent
anterior cervical fusion, 4 with a Cloward technique and 6 with
instrumentation. Follow-up varied from 2 to 64 months (mean 8
months). Four patients reported excellent results (fully functional
without medication), 3 good results (functional but requiring
medication), and 2 fair results (decreased pain intensity but
functionally limited), and only 1 reported a poor result (no pain
relief).
Undoubtedly the results that can be achieved with cervical
fusion for cervicalgia will be determined chiefly by patient se-
lection because most neurosurgeons and orthopedists are likely to
be technically adept at such surgery. My patients were selected
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after I got to know them, all had severe and focal degenerative disc
disease on imaging, and all had intolerable neck pain despite
vigorous and varied alternative therapy. It should not be overly
difficult for neurosurgeons to select patients likely to benefit from
fusion surgery for cervicalgia, just as they select appropriate pa-
tients for surgery for other disorders. It seems to me that ‘‘the
myth of poor outcome from fusion surgery for cervicalgia’’ is
likely to become self-fulfilling if proper patient selection is not
carried out, but these patients do exist, many suffer greatly, and
many of them can benefit greatly from surgery to become grateful
patients.
Harold A. Wilkinson
Boston, Massachusetts
10.1227/NEU.0b013e31820208bf
Anaplastic Foci Within Gliomas
To the Editor:
The comment provided by Dr Engh1 about intraoperative vi-
sualization of anaplastic foci in gliomas points out the elegant usage
of 5-aminolevulinic acid for this purpose but misses the already
available, published techniques to achieve this goal in nonenhancing
gliomas. Publications back to the 1990s demonstrate radiological
and nuclear medicine techniques (xenon-enhanced computer to-
mography, positron emission tomography, especially amino acid
positron emission tomography with methionine or fluoro-ethyl-
thyrosine)2-4 to investigate nonenhancing gliomas for anaplastic foci.
This preoperative radiological information is used intraoperatively by
implementation into the neuronavigation to target these pre-
operatively identified anaplastic areas4 (Figure). This technique is
used in many centers routinely with good success and should not be
withheld from the readers of Neurosurgery as a much cheaper
technique, especially in the United States, where 5-aminolevulinic
acid apparently is not available yet. This is of great interest to the
neurosurgical community because all suspected low-grade gliomas
without contrast enhancement should be considered to have ana-
plastic areas as long as positron emission tomography or histology
can exclude it.
Karl Roessler
Iris Zachenhofer
Feldkirch, Austria
1. Engh JA. Improving intraoperative visualization of anaplastic foci within gliomas.
Neurosurgery. 2010;67(2):N21–N22.
2. Roessler K, Gatterbauer B, Becherer A, et al. Surgical target selection in cerebral
glioma surgery: linking methionine (MET) PET image fusion and neuronavigation.
Minim Invasive Neurosurg. 2007;50(5):273-280.
3. Roessler K, Czech T, Dietrich W, et al. Frameless stereotactic-directed tissue
sampling during surgery of suspected low-grade gliomas to avoid histological un-
dergrading. Minim Invasive Neurosurg. 1998;41(4):183-186.
www.neurosurgery-online.com
 CORRESPONDENCE

FIGURE. Suspected low grade glioma, right hemisphere. A and B, Computed tomography and magnetic resonance imaging
showing diffuse infiltrative tumor frontal and temporo-parietal, without any contrast enhancement. C and D, Image fusion with
methionine positron emission tomography demonstrating an anaplastic focus in the deep frontal periventricular area. E,
A stereotactic needle biopsie of this focus revealed highly anaplastic tumor histology with MIB-1 proliferation index of 33%,
corresponding to a glioblastoma (modified from Roessler et al3).

4. Roessler K, Nasel C, Czech T, Matula C, Lassmann H, Koos WT. Histological
heterogeneity of neuroradiologically suspected adult low grade gliomas detected by
xenon enhanced computerized tomography (CT). Acta Neurochir (Wien).
1996;138(11):1341-1347.
10.1227/NEU.0b013e3182041797
Anaplastic Foci Within Gliomas
I greatly appreciate the thoughtful comments from Drs
Roessler and Zachenhofer. Their group has been a leader in the
evaluation of methionine positron emission tomography and
xenon-enhanced computed tomography in the delineation of
anaplastic foci within gliomas. Their technique is much more
widely available than 5-aminolevulinic acid and has been used at
multiple centers with success.
The novelty of the technique proposed by Widhalm et al1 is
not the integration of metabolic imaging into neurosurgical image
guidance, which has been well demonstrated by Dr Roessler.
Rather, the real-time feedback that is provided by intraoperative
fluorescence of high-grade areas is further confirmation to the
operating surgeon that anaplastic foci are being sent for histo-
pathological evaluation. Whether this information translates into
meaningful clinical outcomes for patients with these tumors re-
mains to be seen.
Johnathan A. Engh
Pittsburgh, Pennsylvania
1. Widhalm G, Wolfsberger S, Minchev G, et al. 5-Aminolevulinic acid is a promising
marker of detection of anaplastic foci in diffusely infiltrating gliomas with non-
significant contrast enhancement. Cancer. 2010;116(6):1545-1552.
10.1227/NEU.0b013e31820417bd

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CORRESPONDENCE
Keyhole and Key-Bur-Hole
To the Editor:
We read with great interest the anatomical study done on
MacCarty’s keyhole.1 This bur-hole is typically performed
when an orbito-zygomatic component is added to a pure fronto-
temporal or supra-orbital craniotomy as clearly illustrated in the
article. However any burr hole in this area is often referred to as a
‘‘key hole,’’ also quoted as ‘‘key-bur-hole’’.2 Hence we highlight
the technical difference in performing a bur-hole for a pure
supraorbital or fronto-temporal/Pterional craniotomy.
History of Keyhole
Historically, the word ‘‘keyhole’’ was coined during the era of
the Gigli saw when it is used to open the cranium for a fronto-
temporal craniotomy. It is a keyhole because the guide for the
Gigli saw has to be introduced both superiorly and inferiorly from
this hole (the latter can alternatively be rongeured).
Pure Fronto-Temporal/Supraorbital Craniotomy
However, for a pure fronto-temporal or supra-orbital crani-
otomy the orbital contents should not be exposed. Perneczky
et al3 use the term ‘‘frontobasal burr hole’’ for a supraorbital
craniotomy. For a supra-orbital craniotomy performed using
a high-speed drill, a single frontobasal burr hole is sufficient and,
for cosmetic reasons, should be placed posterior to the temporal
FIGURE. Key-burr-hole showing a more posteriorly angled drilling (B) and a more anteriorly angled drilling (A) for MacCarty’s
keyhole.
E594 | VOLUME 68 | NUMBER 2 | FEBRUARY 2011
Copyright © Congress of Neurological Surgeons. Unauthorized reproduction of this article is prohibited.
line. Special attention must be given to the placement of this bur
hole, particularly with regard to its relationship to the frontal
cranial base and the orbit. Even after correct placement, incorrect
direction of the drilling procedure can result in penetration of
the orbit and not the anterior fossa. While performing a pure
fronto-temporal craniotomy, Michael Salcman et al4 states
that the ‘‘crucial’’ bur hole lies on the ‘‘external orbital process’’
antero-superior to the pterion. The angle of drilling is such that
the tip of the drill points a bit more postero-superiorly so as not to
enter the orbital contents (Figure).
MacCarty’s Keyhole
On the other hand, the Maccarty’s keyhole is a specific entity
which is drilled in such an angle that the tip of the drill points
more antero-inferiorly. And the orbital roof divides the burr-hole
into a superior (anterior cranial fossa) and an inferior (orbital
content) compartment. This enables removal of the orbital rim
and the zygomatic component, as rightly pointed out in the
article.1
In the era of motorized craniotomes, the term keyhole is rarely
used for the purpose it was originally coined.
Chandramouli Balasubramanian
London, United Kingdom
www.neurosurgery-online.com

Balamurugan Mangaleswarar
Hariprakash Chakravarthy
Reginauld John
Chennai, India
1. Tubbs RS, Loukas M, Shoja MM, Cohen-Gadol AA. Refined and simplified
surgical landmarks for the MacCarty keyhole and orbitozygomatic craniotomy.
Neurosurgery. 2010;66(6):ons230–ons233.
2. Menovsky T, De Vries J, Wurzer JA, Grotenhuis JA. Intraoperative ventricular
puncture during supraorbital craniotomy via an eyebrow incision: technical note.
J Neurosurg. 2006;105(3):485-486.
3. Resich R, Perneczky A. Ten-year experience with the supraorbital subfrontal ap-
proach through an eyebrow skin incision. Neurosurgery. 2005;57(4 Suppl):242-255.
4. Salcman M, Kempe LG, Heros, RC. Kempe’s Operative Neurosurgery. Vol. 1 2nd ed.
New York: Springer-Verlag; 2004.
10.1227/NEU.0b013e31820417aa
Keyhole and Key-Burr-Hole
We thank Dr Balasubramanian and colleagues for their
interest in our article and for drawing the readers’ attention to
the historical derivation of the term keyhole. As is the case with
many terms, time dulls and often changes their original
meanings. Another good example of a structure that has been
modified with time and an example that is even more remote in
history is the term ‘‘torcular Herophili.’’ Originally, the term
‘‘torcular’’ referred to the depression in the occipital bone that
houses the confluens of sinuses.1,2 However, over time, this
word began to be applied to the confluens of sinuses and
currently is used without fail to describe the venous sinus
and not the underlying bone. Therefore, although perhaps not
the original use of the term keyhole, current terminology now
embraces its association with the maneuver described by
MacCarty.3
R. Shane Tubbs
Birmingham, Alabama
Aaron Afshin Cohen-Gadol
Indianapolis, Indiana
1. Tubbs RS, Salter G, Oakes WJ. Superficial surgical landmarks for the transverse
sinus and torcular herophili. J Neurosurg. 2000;93(2):279-281.
2. Tubbs RS, Oakes WJ. Letter to the Editor. Neuroanatomy. 2002;1:14.
3. Tubbs RS, Loukas MM, Shoja MM, Cohen-Gadol AA. Refined and simplified
surgical landmarks for the MacCarty keyhole and orbitozygomatic craniotomy.
Neurosurgery. 2010;66(6):ons230-ons233.
10.1227/NEU.0b013e31820417e3
Real-Time Facial Nerve Monitoring
To the Editor:
With great interest I read the article about the strategy of
intraoperative facial nerve monitoring developed by Prell et al.1
NEUROSURGERY
Copyright © Congress of Neurological Surgeons. Unauthorized reproduction of this article is prohibited.
CORRESPONDENCE
In the abstract, the authors state that when periods of A-trains
(a specific electromyographic activity of the facial muscles)
are automatically detected and their length summed up
(ie, ‘‘traintime’’), there was a ‘‘high correlation between traintime
as measured by real-time analysis and functional outcome im-
mediately after the operation (Spearman correlation coefficient
[r] = 0.664, P , .001) and in long-term outcome (r = 0.631,
P , .001).’’ In the text of the article, this statement is similarly
expressed with the exception that a 2-sided P value of ,.0001 is
reported for the correlation between traintime and short-term
(10 days postoperatively) clinical outcome of facial nerve function
in the given 30 patients.
Although it is common to assume that the amount of elec-
tromyographic activity related to mechanical irritation of the
facial nerve during surgery electromyography is somehow related
to facial palsy after the operation, caution should be exercised
with the data presented here for 2 reasons. First, a nerve that had
been severely attached to the tumor and therefore has been se-
verely irritated by the surgical preparation will take at least 6
months to even show the first clinical signs of regeneration in the
facial muscles. More than a year after surgery, however, it can still
recover to grades 2 or even 1 on the House and Brackman scale.
The second consideration is a statistical issue that relates to the
clinically important issue of false-positive electromyographic re-
sponses in prognosticating facial nerve palsy.
The Spearman rank correlation coefficient was used to analyze
the statistical dependence between ‘‘overall traintime’’ and clin-
ical outcome in this study. This coefficient is a measure to assess
how well the relationship between 2 variables can be described
with a monotone function. A perfect Spearman correlation of +1
or 21 occurs when each of the variables is a perfect monotone
function of the other. However, it does not say anything about
the linearity of this function.
In this study with all but 3 patients falling into 3 House and
Brackman classes at 6 months (half of them were House and
Brackman grade 1), the data are neither normally distributed nor
linearly related to the second parameter, the intraoperatively
assessed ‘‘overall traintime.’’ In 15 of the patients, these periods of
electromyography trains—the sum of the duration of A-trains
measured at the nose, at the mouth, and at the eye—amounted to
just 2 seconds.
When we reanalyzed the data from this group of patients, we
found that the Spearman correlation coefficient remains signifi-
cant at the 5% level (even though it drops to 0.585). However,
when ‘‘overall traintime’’ exceeds 2 seconds, the coefficient is just
0.449 and no longer reaches statistical significance.
In addition, the authors themselves report 5 false-positive
results with respect to their method of intraoperative facial nerve
monitoring and facial nerve outcome.
Both these facts support the clinical observation that a number
of patients, despite having sustained intraoperative electromyo-
graphic activity, including longer periods of A-trains, exhibit no
facial palsy at all after surgery. This in turn raises questions about
the clinical applicability of the, albeit desirable, idea of
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CORRESPONDENCE
establishing a ‘‘traffic light’’ warning algorithm presented to the
surgeon based on traintime. Should we trust an automatically
calculated variable when deciding to break up? What if we stop
surgery because the light went yellow or red and the tumor is not
even halfway out? On the other hand, what happens to surgical
confidence if we decide to go on despite a red signal?
With the interpretational difficulties of ‘‘overall traintime’’
resulting from the statistical issue described above, one would
hesitate to implement the method in rigid decision-making
algorithms for surgery involving the facial nerve as it stands. Still,
we are confident that methods of online automated data analysis
will complement existing routine strategies for intraoperative
monitoring in the future. Therefore, we are grateful to Dr Prell
and colleagues, who have repeatedly raised this issue and continue
to work toward clinically applicable solutions.
Steffen Klaus Rosahl
Wuppertahl, Germany
1. Prell J, Rachinger J, Scheller C, Alfieri A, Strauss C, Rampp S. A real-time
monitoring system for the facial nerve. Neurosurgery. 2010:66(6):1064-1073.
10.1227/NEU.0b013e318204197b
Real-Time Facial Nerve Monitoring
We appreciate the interest in our article1 and would like to
thank Dr Rosahl for his insightful remarks and the effort he took
in calculating additional statistics. However, we do not fully agree
with his conclusions.
Dr Rosahl states that a compromised facial nerve will take at
least 6 months to show first signs of clinical recovery. However, in
our experience, first signs will be seen after 3 to 4 months in high-
grade paresis (In low-grade paresis, it may even be within weeks);
further improvement will be quick over the next months. The
lion’s share of functional recovery will usually be reached after
6 months, so we are sure that this is an adequate point of time
to state a definite clinical result for our patients.
Dr Rosahl is skeptical regarding the Spearman correlation
coefficients that we calculated because he has observed that our
data were not normally distributed and did not show a linear
function. This observation is correct; in our article, we have
described the correlation as resembling a logarithmic function.
However, neither a linear function nor normally distributed data
are needed to calculate the Spearman coefficient because of its
nature as a rank correlation.
Dr Rosahl has recalculated the Spearman rank correlation for
subgroups of our patients. He calculated traintime correlation to
functional outcome for a subgroup of 15 patients and the re-
maining patients; he states that he used a dividing line of 2
seconds of traintime for this subdivision. However, there were 14
patients with , 2 seconds of traintime, not 15 patients. Although
it would be interesting to know which patients were actually
taken into consideration for this calculation, it is quite clear either
E596 | VOLUME 68 | NUMBER 2 | FEBRUARY 2011
Copyright © Congress of Neurological Surgeons. Unauthorized reproduction of this article is prohibited.
way that these were patients with small amounts of traintime and
good clinical results. Naturally, selective exclusion of these pa-
tients from the statistical calculation will not improve correla-
tions. Apart from this, direct comparison of 2 correlation
coefficients needs a certain number of values to hold statistical
significance. The smaller the difference between the 2 coefficients
is, the higher the needed number of values will be. In this light,
comparing a coefficient of 0.664 against 0.585 or 0.449 with
subdivided groups of 15 patients is questionable.
Dr Rosahl asks if we should ‘‘trust an automatically calculable
variable when deciding to break up.’’ We should not. Release
from responsibility for reasonable decisions was not our in-
tention. As we have discussed in a very detailed way, the operating
surgeon still needs to integrate several crucial information sources
to decide about breaking up. Traintime is an additional source of
information that might be very valuable in cerebellopontine
surgery, but it is not supposed to make us ignore other sources of
information.
Julian Prell
Halle, Germany
1. Prell J, Rachinger J, Scheller C, Alfieri A, Strauss C, Rampp S. A real-time
monitoring system for the facial nerve. Neurosurgery. 2010:66(6):1064-1073.
10.1227/NEU.0b013e31820417d1
History and Evidence Regarding
Hydrostatic Shock
Without citing data in support for the claim, the otherwise
excellent review paper, Ballistics for the Neurosurgeon,1 asserts that
‘‘hydrostatic shock’’ is a ‘‘relatively recent myth.’’ However, the
remote effects of ballistic pressure waves known as ‘‘hydrostatic
shock’’ or ‘‘hydraulic shock’’ have considerable support and a long
history. Reference to ‘‘hydraulic shock’’ can be found as early
as 1898 in an article describing experiments in which fish were
killed by a remote pressure mechanism similar to underwater
dynamite explosions by firing a rifle into the water within 24
inches or so of the fish.2 Upon inspection, no easily discernable
wound was discoverable on the body, and death was attributed
to the remote effects of the pressure wave caused by the bullet
impacting the water.
In the 1940s, Harvey and coworkers3,4 investigated inter-
actions between ballistic waves and tissue in a series of experi-
ments conducted at Princeton University. The fast pressure
transients caused by projectiles hitting fluids and fluid-filled
tissues were detected with piezoelectric pressure transducers and
spark shadowgraph photography. Without conducting sensitive
histological tests or functional tests on living test subjects, this
work concluded that the only easily observable injury caused by
the observed pressure transients are associated with gas pockets in
the body. (The same thinking has long been associated with blast
injury.) However, hunters have long attributed instant
www.neurosurgery-online.com

incapacitation of game animals with the remote effects of a rapid
pressure transient caused by bullet impact.5,6
In 1954, Ochsner reported results of experiments in goats
comparing high-speed projectile impacts to the thigh with a small
high-explosive charge taped to the same location.7 Ochsner found
it notable that blood transfusions alone could not save these
animals and reported an average survival time of 12 hours. He
attributed these observations to the pressure changes that had
been documented by Harvey.
It was well-documented that tissue, including neural tissue,
could be torn or damaged by temporary cavitation.8 Docu-
mentation of remote damage beyond the reach of the temporary
cavity came later, in research reported by groups in Sweden and
China. In a series of articles, a Swedish research team reported
remote injury to the peripheral nerves, the spinal cord, and the
brain with use of electron microscopy of pigs shot in the thigh.9-12
These studies used high-speed pressure sensors implanted in the
thigh, abdomen, neck, and brain of test animals. The pressure
transient was shown to propagate from the impact site to the
brain at close to the speed of sound. A Chinese study published in
1990 also reported in vivo measurements of fast pressure tran-
sients and related remote pressure wave injuries in experiments
including pigs and dogs.13 A later Chinese experiment used
sensitive biochemical techniques to detect remote brain injury in
dogs shot in the thigh.14
Analysis of data relating to rifle wounds from the Vietnam
War described a number of cases of distant wounding, including
broken bones, abdominal wounding in cases where the bullet
did not penetrate the abdominal cavity, a lung contusion re-
sulting from a bullet hit to the shoulder, and distant effects on
the central nervous system.15 A case study of a World War II
soldier sustaining a handgun wound attributed the much later
onset of epilepsy to a hydrodynamic effect.16 Another case study
of a gunshot victim attributed a spinal cord injury to the fo-
cusing of shock waves remote from the bullet path.17 A 2007
article reviewed this and other evidence and predicted that re-
mote brain injury would be common for handgun wounds
centered in the chest.18 Research published in 2009 reported
human autopsy results that showed ‘‘cufflike pattern haemor-
rhages around small brain vessels were found in all speci-
mens.’’19 This remote brain injury was attributed to the pressure
transient caused by the bullet hitting the chest. Easily visible
brain hemorrhaging has also been correlated with instant in-
capacitation in wild animals shot in the chest with much more
powerful firearms.20 Noting similarities between blast and
ballistic waves, a recent paper estimated mild traumatic brain
injury (TBI) thresholds for the thoracic mechanism of blast-
induced TBI by analyzing data from ballistic pressure wave and
behind armor blunt trauma studies.21
A myth is an assertion that has either been disproved by
careful experiment or for which there is no historical or scientific
evidence in cases where it is reasonably expected. Belief in the
remote effects of penetrating projectiles may have originated
with hunters and soldiers, but their reality is now well
NEUROSURGERY
Copyright © Congress of Neurological Surgeons. Unauthorized reproduction of this article is prohibited.
CORRESPONDENCE
established in a broad body of scientific literature, even though
the clinical significance for the practicing neurosurgeon might
be debatable. Perhaps the clinical significance will become
greater with anticipated advancements in detection and treat-
ment of mild TBI.
Michael Courtney
Amy Courtney
Colorado Springs, Colorado
1. Jandial R, Reichwage B, Levy M, Duenas V, Sturdivan L. Ballistics for the
neurosurgeon. Neurosurgery. 2008;62(2):472-480.
2. Science and Industry. The New York Times. November 27, 1898:14. http://
query.nytimes.com/mem/archive-free/pdf?_r=1&res=9F01EED61139E433A257
54C2A9679D94699ED7CF. Accessed June 8, 2010.
3. Harvey EN. The mechanism of wounding by high velocity missiles. Proc Am Philos
Soc. 1948:92(4):294-304. http://www.jstor.org/stable/3143359. Accessed June
26, 2008.
4. Harvey EN, McMillen JH. An experimental study of shock waves resulting from the
impact of high velocity missiles on animal tissues. J Exp Med. 1947:85(3):321-328.
http://jem.rupress.org/content/85/3/321.full.pdf+html. Accessed June 8, 2010.
5. Powell EB. Killing Power, a pamphlet published by National Rifle Association,
Washington, DC, 1944. As cited by Harvey EN, McMillen JH. An experimental
study of shock waves resulting from the impact of high velocity missiles on animal
tissues. J Exp Med. 1947:85(3):321-328. http://jem.rupress.org/content/85/3/
321.full.pdf+html. Accessed June 8, 2010.
6. Super speed bullets knock ’em dead. Popular Mechanics. 1942;77(4):8-10.
7. Ochsner EWA Jr. Experimental wound ballistics. In: Recent Advances in Medicine
and Surgery (19-30 April 1954) Based on Professional Medical Experiences in Japan
and Korea 1950-1953), vol I. US Army Medical Service Graduate School Walter
Reed Army Medical Center, Washington, DC. Medical Science Publication 4.
http://history.amedd.army.mil/booksdocs/korea/recad1/ch4-2.html. Accessed
June 8, 2010.
8. Robinson MD, Bryant PR. Peripheral nerve injuries. In: Zajtchuk R, ed. Textbook
of Military Medicine, Part IV: Surgical Combat Casualty Care: Rehabilitation of the
Injured Combatant, vol 2. Washington, DC: Office of the Surgeon General, US
Department of the Army; 1999:419-574.
9. Suneson A, Hansson HA, Seeman T. Peripheral high-energy missile hits cause
pressure changes and damage to the nervous system: experimental studies on pigs.
J Trauma. 1987;27(7):782-789.
10. Suneson A, Hansson HA, Seeman T. Central and peripheral nervous damage following
high-energy missile wounds in the thigh. J Trauma. 1988;28(1 suppl):S197–S203.
11. Suneson A, Hansson HA, Seeman T. Pressure wave injuries to the nervous system
caused by high-energy missile extremity impact: part I. local and distant effects on
the peripheral nervous system. A light and electron microscopic study on pigs.
J Trauma. 1990:30(3):281-294.
12. Suneson A, Hansson HA, Seeman T. Pressure wave injuries to the nervous system
caused by high energy missile extremity impact, part II: distant effects on the
central nervous system. A light and electron microscopic study on pigs. J Trauma.
1990;30(3):295-306.
13. Liu Y, Chen Y, Li S. Mechanism and characteristics of the remote effects of
projectiles. J Trauma (China). 1990;6(1 suppl):16-20.
14. Wang Q, Wang Z, Zhu P, Jiang J. Alterations of the myelin basic protein and
ultrastructure in the limbic system and the early stage of trauma-related stress
disorder in dogs. J Trauma. 2004:56(3):604-610.
15. Bellamy RF, Zajtchuk R. The physics and biophysics of wound ballistics. In: Con-
ventional Warfare: Ballistic, Blast, and Burn Injuries. Washington, DC: Office of the
Surgeon General, US Department of the Army. Zajtchuk R, ed. Textbook of Military
Medicine, Part I: Warfare, Weaponry, and the Casualty, vol 5; 1990:107-162.
16. Treib J, Haass A, Grauer MT. High-velocity bullet causing indirect trauma to the
brain and symptomatic epilepsy. Mil Med. 1996;161(1):61-64.
17. Sturtevant B. Shock wave effects in biomechanics. Sadhana. 1998:23(5):579-596.
18. Courtney A, Courtney M. Links between traumatic brain injury and ballistic
pressure waves originating in the thoracic cavity and extremities. Brain Inj.
2007:21(7):657-662.
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19. Krajsa J. Přı́činy vzniku perikapilárnı́ch hemoragiı́ v mozku při střelných poraněnı́ch
(Causes of pericapillar brain haemorrhages accompanying gunshot wounds). Brno,
Czech Republic: Institute of Forensic Medicine, Faculty of Medicine, Masaryk
University; 2009. http://is.muni.cz/th/132384/lf_d/. Accessed June 8, 2010.
20. Carmichael J. Knockdown power. Outdoor Life, July 31, 2003. http://
www.outdoorlife.com/node/45560. Accessed June 8, 2010.
21. Courtney MW, Courtney AC, Working toward exposure thresholds for blast-
induced traumatic brain injury: thoracic and acceleration mechanisms. Neuro-
Image. doi:10.1016/j.neuroimage.2010.05.025. Accessed June 8, 2010.
10.1227/NEU.0b013e3182041992
Regarding ‘‘Retroclival Epidural Hematomas: A
Clinical Series’’
To the Editor:
We read the study reported by Tubbs and collaborators1 with
great interest. Tubbs et al have performed the first prospective
study of retroclival epidural hematomas (REDHs) and have re-
ported more than 3 cases2 of this extremely rare subset of pos-
terior cranial fossa hematomas representing less than 15% of all
intracranial epidural hematomas.3 In fact, retroclival epidural
hematomas are mostly misdiagnosed by standard computed to-
mography (CT), multiplanar reformatted high-resolution CT
and magnetic resonance imaging (MRI) being the gold standard
examination.2,4,5
However, a systematic review of all literature using PubMed
has retrieved 27 previous cases of REDHs since the first report by
Orrison et al in 1986.4,6-9 All but 5 were subsequent to motor
vehicle accidents. A moderate trauma by a running fall was re-
sponsible for the REDH in a 12-year-old girl.10 Calli et al11
reported a fortuitous REDH at a 1-month postoperative MRI of
a posterior fossa decompressive surgery for the management of
an acute cerebellar infarction. Another case was associated with
a pituitary apoplexy.12 Finally, Cho et al7 reported the only
‘‘spontaneous’’ case.
REDH is not a purely pediatric entity: 5 adult cases have been
reported (range, 26-62 years), among which were 2 traumatic
cases.3,13
Craniovertebral junction injury was found in 10 cases (37%).
Only 3 were instable: 1 patient died soon after injury6 and
2 patients required fusion associated with evacuation of the
hematoma because of tetraplegia and, in one case, respiratory
difficulties.14,15 Two other cases were evacuated16 or decompressed.12
Cranial nerve disorders have occurred in 64% of cases (14 in
the sixth, 6 in the ninth, and 8 in the twelfth cranial nerve) and
were completely resolved by 2 months postinjury as the retroclival
blood collection at control imaging. The mean Glasgow Coma
Scale (GCS) score was 9.5, and there effectively was no corre-
lation between hematoma size and presenting symptoms.17
Exceptionally, acute hydrocephalus could be associated with
REDH (2 cases, both fatal).6,18
At our institution, in 5 years, we found only 2 cases of REDH,
subsequent to high-energy road accidents, in adults. These cases
have never been reported. The first one presented with a GCS
E598 | VOLUME 68 | NUMBER 2 | FEBRUARY 2011
Copyright © Congress of Neurological Surgeons. Unauthorized reproduction of this article is prohibited.
score of 7 and delayed bilateral sixth and twelfth cranial nerve
palsies with spontaneous resolution. The other patient had an
initial GCS score of 3 and remained comatose 3 months after
the accident; this was explained by a diffuse axonal injury. No
craniovertebral instability was found, and conservative manage-
ment was performed in all cases.
Tubb et al have described well the hypothetical mechanisms
of the formation of REDHs, which are still controversial. We also
believe that disruption of the tectorial membrane is an important
factor for the formation of hematoma. Bleeding may arise from
the basilar venous plexus or the neuromeningeal trunk, branch of
the ascending pharyngeal artery, which anastomoses with the me-
ningohypophyseal trunk, the inferolateral trunk, and the odontoid
arterial arch system.19 Tubb et al have also written 2 excellent articles
on the tectorial membrane and the basilar venous plexus.20,21
REDH could be associated with retroclival subdural hema-
tomas (RSDHs), particularly in violent injuries, as in our second
patient.6 Isolated RSDHs are rarer than REDHs: only 7 cases
have been reported,22-28 but the context, clinical presentation,
and mechanisms of formation are different. Only 1 patient was
younger than 16 years of age (range, 4-78 years). Four cases were
spontaneous. The only fatal case was subsequent to a minor
trauma in a patient with hemophilia.24 The 2 other traumatic
cases were subsequent to an aggression25 and a fall from a
building.26 The mean GCS score was 14 (range, 11-15).
Because subdural hematoma is not limited by the boundaries
of the tectorial membrane, it is quickly redistributed from the
intracranial to the subdural space.26 Frequently, there was blood
contamination when lumbar puncture was performed.22,23 Two
cases of sixth cranial nerve palsies were found.27,28 Imaging
showed complete resolution within a month and no evacuation
was necessary.
Damien Petit
Philippe Mercier
Angers, France
1. Tubbs RS, Griessenauer CJ, Hankinson T, et al. Retroclival epidural hematomas:
a clinical series. Neurosurgery. 2010;67(2):404-407.
2. Yama N, Kano H, Nara S, et al. The value of multidetector row computed
tomography in the diagnosis of traumatic clivus epidural hematoma in children:
a three-year experience. J Trauma. 2007;62(4):898-901.
3. Ratilal B, Castanho P, Vara Luiz C, Antunes JO. Traumatic clivus epidural
hematoma: case report and review of the literature. Surg Neurol. 2006;66(2):200-
202; discussion 202.
4. Calisaneller T, Ozdemir O, Altinors N. Posttraumatic acute bilateral abducens
nerve palsy in a child. Childs Nerv Syst. 2006;22(7):726-728.
5. Suliman HM, Merx HL, Wesseling P, van der Sluijs B, Vos PE, Thijssen HO.
Retroclival extradural hematoma is a magnetic resonance imaging diagnosis.
J Neurotrauma. 2001;18(11):1289-1293.
6. Orrison WW, Rogde S, Kinard RE, et al. Clivus epidural hematoma: a case report.
Neurosurgery. 1986;18(2):194-196.
7. Cho CB, Park HK, Chough CK, Lee KJ. Spontaneous bilateral supratentorial
subdural and retroclival extradural hematomas in association with cervical epidural
venous engorgement. J Korean Neurosurg Soc. 2009;46(2):172-175.
8. Schneck MJ, Smith R, Moster M. Isolated bilateral abducens nerve palsy associated
with traumatic prepontine hematoma. Semin Ophthalmol. 2007;22(1):21-24.
www.neurosurgery-online.com

9. Kim MS, Cho MS, Kim SH. Delayed bilateral abducens nerve palsy after head
trauma. J Korean Neurosurg Soc. 2008;44(6):396-398.
10. Itshayek E, Goldman J, Rosenthal G, Chikoya L, Gomori M, Segal R. Extradural
hematoma of the clivus, not limited to the severely injured patient: case report and
review of the literature. J Trauma. 2006;60(2):417-420.
11. Calli C, Katranci N, Guzelbag E, Alper H, Yunten N. Retroclival epidural
hematoma secondary to decompressive craniectomy in cerebellar infarction:
MR demonstration. J Neuroradiol. 1998;25(3):229-232.
12. Goodman JM, Kuzma B, Britt P. Retroclival hematoma secondary to pituitary
apoplexy. Surg Neurol. 1997;47(1):79-80.
13. Fuentes S, Bouillot P, Dufour H, Grisoli F. Occipital condyle fractures and clivus
epidural hematoma. Case report [in French]. Neurochirurgie. 2000;46(6):563-567.
14. Marks SM, Paramaraswaren RN, Johnston RA. Transoral evacuation of a clivus
extradural haematoma with good recovery: a case report. Br J Neurosurg.
1997;11(3):245-247.
15. Papadopoulos SM, Dickman CA, Sonntag VK, Rekate HL, Spetzler RF. Traumatic
atlantooccipital dislocation with survival. Neurosurgery. 1991;28(4):574-579.
16. Muller JU, Piek J, Kallwellis G, Stenger RD. Prepontine epidural hemorrhage [in
German]. Zentralbl Neurochir. 1998;59(3):185-188.
17. Kwon TH, Joy H, Park YK, Chung HS. Traumatic retroclival epidural hematoma
in a child: case report. Neurol Med Chir (Tokyo). 2008;48(8):347-350.
18. Vera M, Navarro R, Esteban E, Costa JM. Association of atlanto-occipital
dislocation and retroclival haematoma in a child. Childs Nerv Syst. 2007;23(8):
913-916.
19. Lasjaunias P, Moret J, Theron J. The so-called anterior meningeal artery of the
cervical vertebral artery. Normal radioanatomy and anastomoses. Neuroradiology.
1978;17(1):51-55.
20. Tubbs RS, Kelly DR, Humphrey ER, et al. The tectorial membrane: anatomical,
biomechanical, and histological analysis. Clin Anat. 2007;20(4):382-386.
21. Tubbs RS, Hansasuta A, Loukas M, et al. The basilar venous plexus. Clin Anat.
2007;20(7):755-759.
22. Tomaras C, Horowitz BL, Harper RL. Spontaneous clivus hematoma: case report
and literature review. Neurosurgery. 1995;37(1):123-124.
23. Schievink WI, Thompson RC, Loh CT, Maya MM. Spontaneous retroclival
hematoma presenting as a thunderclap headache. Case report. J Neurosurg.
2001;95(3):522-524.
24. Myers DJ, Moossy JJ, Ragni MV. Fatal clival subdural hematoma in a hemo-
philiac. Ann Emerg Med. 1995;25(2):249-252.
25. Casey D, Chaudhary BR, Leach PA, Herwadkar A, Karabatsou K. Traumatic clival
subdural hematoma in an adult. J Neurosurg. 2009;110(6):1238-1241.
26. Ahn ES, Smith ER. Acute clival and spinal subdural hematoma with spontaneous
resolution: clinical and radiographic correlation in support of a proposed patho-
physiological mechanism. Case report. J Neurosurg. 2005;103(2 suppl):175-179.
27. Guilloton L, Godon P, Drouet A, Guerard S, Aczel F, Ribot C. Retroclival
hematoma in a patient taking oral anticoagulants [in French]. Rev Neurol (Paris).
2000;156(4):392-394.
28. van Rijn RR, Flach HZ, Tanghe HL. Spontaneous retroclival subdural hematoma.
JBR-BTR. 2003;86(3):174-175.
10.1227/NEU.0b013e31820419a7
Response to Letter to the Editor
We thank the authors for their interest in our article and for
their additional comments with which we agree. We would also
add that other cases of retroclival hematomas may exist in the
literature and may be reported using different nomenclature
(skull base hematoma, etc), thereby making a complete capture
of these cases problematic. Conservative treatment appears to
be appropriate in the overwhelming number of cases. With
improved imaging modalities, we believe these pathologic entities
will become increasingly diagnosed.
R. Shane Tubbs
Birmingham, Alabama
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CORRESPONDENCE
Aaron Afshin Cohen-Gadol
Indianapolis, Indiana
10.1227/NEU.0b013e31820419bd
Surgical Approach and Safety of Spinal Cord Stem
Cell Transplantation
The October 2009 edition of Neurosurgery featured the timely
report of our team’s preclinical work to develop safe techniques
for ventral horn spinal cord stem cell transplantation.1 The report
coincided with Food and Drug Administration (FDA) approval
of the first trial to examine the safety of spinal cord stem cell
transplantation for motor neuron disease. We anticipate that this
trial will be followed by a series of trials in North America,
Europe, and Asia. These trials will coincide with similar ap-
proaches applied to traumatic and demyelinating spinal cord
disease.
The FDA approved protocol is entitled ‘‘A Phase I, Open–
label, First–in–human, Feasibility and Safety Study of Human
Spinal Cord–Derived Cell Transplantation for the Treatment of
Amyotrophic Lateral Sclerosis.’’ As alluded to in the title, the
therapeutic product is derived from NIH–banked human fetal
spinal cord. Technology developed originally in Ron McKay’s
laboratory was used as the intellectual property platform of
a company called NeuralStem, Inc. (Rockville, Maryland). Un-
like many protocols for the propagation of stem cells, Neural-
Stem’s cells are propagated on laminar surface rather than as free–
floating neurospheres.2-4 Hopes for amyotrophic lateral sclerosis
(ALS) therapy rest on experiments in the SOD1 mutant rodent
model of familial ALS conducted published in 2006. The SOD1
gene has been found to have a variety of point mutations in
a subset of patients with familial ALS. When mutant human
SOD1 is expressed in transgenic animals (rodents and pigs), they
develop a phenotype that closely resembles human ALS. Xu et al
demonstrated that spinal cord grafts of the NeuralStem cells had
the ability to preserve motor neuron numbers in the spinal cords
of SOD1 rodents and also prolonged their survival. Several
mechanisms are postulated to explain the efficacy of the grafts.
First, a fraction of the cells are found to develop a gabaergic
neuronal phenotype. These inhibitory cells form synapses with
surrounding cells providing a means to suppress excitotoxicity
thought to play a role in the etiology of degenerative motor
neuron death. The remaining cells develop an astrocytic phe-
notype. Excitotoxicity in ALS has been ascribed to defects in glial
excitatory amino acid scavenging. Thus, it is possible that the
remaining cells prevent toxic build up of excitatory transmitters.
Finally, the cells are demonstrated to secrete a variety of neural
growth factors that may contribute to neural protection. It is clear
that these cells do not replace lost motor neurons and neuro-
muscular junctions.
As mentioned, a variety of competing approaches exist for both
molecular and cellular spinal cord therapies of motor neuron
diseases, spinal cord injury, and demyelinating diseases. Our team
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CORRESPONDENCE
began work on the techniques for safe and accurate ventral
horn targeting in collaboration with Clive Svendsen, PhD (Ce-
dars–Sinai, Los Angeles, California; and Madison, Wisconsin),
coauthor on our October Neurosurgery manuscript in 2004.
Dr Svendsen’s team had documented the neuroprotective prop-
erties of human fetal cortically derived cells.
Unlike the NeuralStem’s cells, these cells are grown as neu-
rospheres. In addition, these cells do not form neurons on
transplantation, but rather all differentiate into astrocytes. To
augment the protective capacity of these cells, Dr Svendsen’s
team used lentiviral vectors to induce the expression and secretion
of glial cell-derived neurotrophic factor (GDNF). Thus, the
Svendsen cells act as organic minipumps for growth factors in
addition to scavenging excitatory amino acids. His team has
demonstrated the ability of these grafts to preserve spinal cord
motor neurons in the SOD1 rat model.5 In 2005, Dr Svendsen
and I submitted a PreIND application for transplantation of these
cells into humans. The manuscript published in October 2009
reports on some of the critical preclinical work conducted to
support this application. The master cell bank has now been
completed, and vector production has been funded by the Na-
tional Gene Vector Laboratories.
We anticipate a final FDA application with Dr Svendsen’s cells
sometime in the next year. We are also supporting the preclinical
development of stem cells intended for use in spinal cord
transplantation for the treatment of ALS and transverse myelitis
by Q Therapeutics (Salt Lake City, Utah), and the academic team
of Angelo Vescovi in Italy. Other teams are pursuing the idea of
embryonic stem cell transplantation for spinal muscular atrophy
in infants.
Extensive work has been done in the Far East with human
application of spinal cord grafting. Most notably Dr Huang
(Beijing) has reported a large series of olfactory ensheathing cell
grafts into the spinal cords of patients with chronic spinal cord
injuries.6-8 He has also transplanted these cells into the brains of
ALS patients, a limited group of which received free hand cervical
injections as well. The results of this work have not, to our
knowledge, been published as yet. In my personal correspondence
with Dr Huang, it has become clear that he has abandoned this
procedure, though it is not clear why.
Anecdotal evidence supports efficacy of the transplants for
spinal cord injury, and it is clear that this approach bears further
scrutiny. However, based on our work in over a hundred pigs, we
are emphatically opposed to free hand cord injections. This ap-
proach has no reproducible targeting accuracy, and more im-
portantly leaves the patient vulnerable to sheer injuries, pressure
injury, and graft reflux.
The FDA approved NeuralStem trial is aimed at establishing
safety and feasibility. We have developed the concept of ‘‘risk
escalation’’ to replace the common ‘‘dose escalation’’ used in
pharmacological trials. We envision the ultimate therapy in-
volving staged lumbar and cervical transplants using multiple
bilateral lumbar injections to preserve ambulation, and mul-
tiple unilateral cervical injections (C3–C5) to preserve
E600 | VOLUME 68 | NUMBER 2 | FEBRUARY 2011
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diaphragmatic and proximal upper extremity function. To
begin with the least risk possible, we will initially enroll non–
ambulatory patients for lumbar unilateral injections,
proceeding to lumbar bilateral injections in non–ambulatory
patients. The main risk of these first cohorts is pain and bowel
and bladder dysfunction. We will then proceed to ambulatory
patients, starting with unilateral multiple injections and
proceeding to bilateral multiple injections. The increased risk
to these cohorts involves potential loss of ambulation. Next, we
will move to unilateral cervical injection with the risk of
quadriplegia, followed finally by staged bilateral lumbar fol-
lowed by unilateral cervical injection. The device described in
the October 2009 manuscript has been modified in a variety of
ways to optimize safety and accuracy. Subsequent reports de-
scribing this development are in production or review at
present.
While preclinical studies address the safety of a specific bi-
ological product, very little work has been done in large animals
that models spinal cord transplantation into humans. That is,
when we transplant human cells into pigs, they are, by definition,
xenografts. While this is the required safety data requested for an
IND, it is not a good model for human allografts proposed for
trials. As such, our team at Emory has recently submitted an RO1
application for continued study of surgical techniques, graft re-
jection, imaging, and graft control in the pig model. It is not clear
which cell line will prove the most beneficial for ALS patients.
However, we have great hopes that much will be learned from
these initial trials about the best way to conduct human spinal
cord transplantation.
Nicholas Boulis
Thais Federici
Atlanta, Georgia
1. Riley J, Federici T, Park J, et al. Cervical spinal cord therapeutic delivery: preclinical
safety validation of a stabilized microinjection platform. Neurosurgery.
2009;65(4):754–762.
2. Xu L, Yan J, Chen D, et al. Human neural stem cell grafts ameliorate motor neuron
disease in SOD–1 transgenic rats. Transplantation. 2006;82(7):865–875.
3. Xu L, Ryugo DK, Pongstaporn T, Johe K, Koliatsos VE. Human neural stem cell
grafts in the spinal cord of SOD1 transgenic rats: differentiation and structural in-
tegration into the segmental motor circuitry. J Comp Neurol. 2009;514 (4):297–309.
4. Yan J, Xu L, Welsh AM, et al. Combined immunosuppressive agents or CD4 anti-
bodies prolong survival of human neural stem cell grafts and improve disease outcomes
in amyotrophic lateral sclerosis transgenic mice. Stem Cells. 2006;24(8):1976–1985.
5. Suzuki M, McHugh J, Tork C, et al. GDNF secreting human neural progenitor
cells protect dying motor neurons, but not their projection to muscle, in a rat model
of familial ALS. PLoS ONE. 2007;2(1):e689.
6. Chen L, Huang H, Zhang J, et al. Short–term outcome of olfactory ensheathing
cells transplantation for treatment of amyotrophic lateral sclerosis. Zhongguo Xiu Fu
Chong Jian Wai Ke Za Zhi. 2007;21(9):961–966.
7. Huang H, Chen L, Wang H, et al. Safety of fetal olfactory ensheathing cell
transplantation in patients with chronic spinal cord injury. A 38–month followup
with MRI. Zhongguo Xiu Fu Chong Jian Wai Ke Za Zhi. 2006;20(4):439–443.
8. Huang H, Chen L, Wang H, et al. Influence of patients’ age on functional recovery
after transplantation of olfactory ensheathing cells into injured spinal cord injury.
Chin Med J (Engl). 2003;116(10):1488–1491.
10.1227/NEU.0b013e3182095e2e
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Direct Posterior Reduction and Fixation
To the Editor:
Having read the article by Dr Feng-Zeng Jian et al1 entitled
‘‘Direct posterior reduction and fixation for the treatment of basilar
invagination with atlantoaxial dislocation,’’ we are attracted by the
surgical technique and its excellent efficacy which they reported.
However, some issues still confused us and we wish to bring them
to the authors and readers of Neurosurgery.
The authors described a method using C2 pedicle screws and
occipital instruments, which was claimed to provide reductive
force to correct the cervico-medullary angle (CMA) and de-
compress the craniovertebral junction.1 After the reduction they
performed posterior fixation and fusion. The authors stated their
procedure was ‘‘novel.’’ To our knowledge, however, this tech-
nique of posterior reduction and fixation used by Jian et al was
first introduced by Abumi et al2 in 1999. Calling it ‘‘a novel
posterior approach’’ without referring to the original author is
unacceptable and unfair for the originality.
It is widely accepted that the reducible atlantoaxial dislocation
can be corrected by posterior reduction alone. It is noticed that 5
(17.2%) of Jian’s 29 cases were reducible atlantoaxial dislocation
(AAD), even though the author did not specify the cases. These
cases should not be counted in calculation of reduction rate. To
our experience, however, favorable outcome for the irreducible
AAD (IAAD) cannot be achieved by posterior procedure without
additional anterior AA release.3–5 In the setting of IAAD, the
‘‘single posterior longitudinal distraction’’1 between C2 and the
occiput will be resisted by the contracted tissues at the front
(longus capitis, longus colli, anterior longitudinal ligament, alar,
FIGURE 1. Jian’s Figure 6C and 6A had very different shape of the odontoid. A horizontal line via the center point of C1 arch
was drawn. The subdental synchondrosis (pointed by the broken arrow) was not pulled down enough to be defined as complete
reduction.
NEUROSURGERY
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CORRESPONDENCE
and apical ligaments). As a result, the effect of reduction is
limited. In fact, the 2 cases whom Jian et al claimed to achieve
anatomic reduction in their Figure 4 and 5 are not completely
reduced. In their Figure 6C, where the authors also claimed to
achieve anatomic reduction, it is clear that the shape of the
odontoid, clivus and C2 spinous process is inconsistent with
those in Jian’s Figure 6A (Figure 1), hence they must be taken
from different sections. The reductive effect should be evaluated
in the same mid-sagittal computed tomographic (CT) scan.
Moreover, if we draw a horizontal line via the center point of C1
arch, we can find that the subdental synchondrosis (pointed by
the broken arrow) was not pulled down enough to be defined as
complete reduction (Figure 1).
For IAAD, in order to achieve the reduction procedure, the
odontoid should have two motions: descending and tilting for-
ward (Figure 2). To our experience, cervical traction and transoral
atlantoaxial release lead the migrated odontoid to descend. For-
ward-bending of the locked plates and C2 pedicle screws can
cause the odontoid to tilt forward and achieve the anatomic
reduction (Figure 2 and 3). After the anatomic reduction, the
facet joint should be wedge-shaped and opened anteriorly (Figure
3I and 3J). However, Jian’s posterior distraction only provided
extension force for the odontoid and caused the facet joint to
open posteriorly (Figure 4). Consequently, it leads to an aggra-
vated kyphosis of the craniovertebral junction (shown by Jian’s
Figure 1) and the potential compression by the odontoid ex-
tension. Unfortunately, we believe the technique Jian et al used
for IAAD and basilar invagination is reducing the AAD in
a wrong direction.
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FIGURE 2. During the reduction procedure, the odontoid has 2 motions: descending and tilting forward. Forward-bending of
the locked plates and C2 pedicle screws can cause the odontoid to tilt forward and achieve the anatomic reduction.

FIGURE 3. A, a 20-year-old male had basilar invagination, AAD and C1 occipitalization. B, reconstructive CT showed upward migration of
the odontoid. C, preoperative MRI revealed the ventral compression and Chiari malformation. D, preoperative CT revealed the facet joint slide
anteriorly and inferiorly. E, the contralateral facet joint. F, the patient underwent transoral release and posterior occiput-C2 fixation and fusion.
Postoperative lateral X-ray showed an anatomic reduction. G, postoperative MRI obtained 5 days after surgery showed complete decompression.
H, at the 4 months follow-up, CT showed anatomic reduction and solid fusion. I, after the anatomic reduction, the facet joint should be wedge-
shaped and opened anteriorly. J, the contralateral facet joint was also opened anteriorly. K, MRI obtained 6 months after surgery showed the
reduction of Chiari malformation.

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 CORRESPONDENCE

FIGURE 4. Jian’s posterior distraction only provided extension force for the odontoid and caused the facet joint to open
posteriorly. Consequently, it leads to an aggravated kyphosis of the craniovertebral junction.

FIGURE 5. For case 14 in Jian’s report (the only 38-year-old female), the preoperative and postoperative CMA was all 135 degrees.

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CORRESPONDENCE
FIGURE 6. For Jian’s case 7 (the only 44-year-old female), the preoperative CMA was 127 degree, while the postoperative angle
was 132 degrees.
For the patients with AAD and basilar invagination, the ventral
compression from the upward migrated odontoid is the primary
pathology. The complete reduction of the odontoid is the most
important factor to improve the CMA and restore the herniated
cerebellar tonsils5 (Figure 3K). In doing so, the posterior de-
compression is not reasonable. The authors removed part of the
posterior margin of the foramen magnum for all 29 cases.1
However, only 7 of them had Chiari malformations. The in-
dications for the remaining 22 cases were unreasonable. In ad-
dition, the postoperative evaluation lost its anatomic landmark
because of removal of the osseous margin6 and the evaluation of
Chamberlain’s line and McRae’s line was trustless.
Some information in Jian’s report was unbelievable. Jian’s
Figure 4 was from case 14 (the only 38-year-old female in Jian’s
Table 2), and the postoperative CMA was actually 135 degrees
(Figure 5). However, the authors reported it as 150 degrees (from
Jian’s Table 3). Jian’s Figure 5 was from case 7 (the only 44-year-
old female), and they reported the CMA was 142 degrees. But we
can find the actual angle was only 132 degrees (Figure 6). The
authors confirmed the fusion using a lateral X-ray in their Figure
5. It is not an objective confirmation. The fusion status should be
judged on the reconstructive CT scan like their Figure 4D.
Furthermore, readers can find the images in Jian’s Figure 6 were
not from the same patient because: 1) the odontoid in Jian’s
Figure 6A, 6C, and 6E had different shape. 2) the pedicle screw in
Jian’s Figure 6D have different trajectory with that in 6F. 3) the
images in Jian’s Figure 6E and 6F had uncommon small C2
spinous process and large C3 process, which differed with those in
6A and 6C. 4) subdental synchondrosis of C2 found in Jian’s
E604 | VOLUME 68 | NUMBER 2 | FEBRUARY 2011
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Figure 6C was near the level of C1 anterior arch, while that in 6E
was far underneath the level of C1 anterior arch (both of 6C and
6E were postoperative and should have the same position of the
subdental synchondrosis).
Again we thank the authors’ report and extremely expect to
participate in the discussion on this issue.
Chao Wang
Shenglin Wang
Beijing, China
1. Jian FZ, Chen Z, Wrede KH, Samii M, Ling F. Direct posterior reduction and
fixation for the treatment of basilar invagination with atlantoaxial dislocation.
Neurosurgery. 2010;66(4):678-687; discussion 687.
2. Abumi K, Takada T, Shono Y, Kaneda K, Fujiya M. Posterior occipitocervical
reconstruction using cervical pedicle screws and plate-rod systems. Spine (Phila Pa
1976). 1999;24(14):1425-1434.
3. Wang C, Yan M, Zhou HT, Wang SL, Dang GT. Open reduction of irreducible
atlantoaxial dislocation by transoral anterior atlantoaxial release and posterior in-
ternal fixation. Spine (Phila Pa 1976). 2006;31(11):E306-E313.
4. Wang C, Wang S. Visocchi M, Pietrini D, Tufo T, Fernandez E, Di Rocco C,
(2009). Pre-operative irreducible C1-C2 dislocations: intra-operative reduction and
posterior fixation. The ‘‘always posterior strategy’’. Acta Neurochir (Wien).
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