ORIGINAL ARTICLE
Contemporary Management of Penetrating Brain Injury
Domenic P. Esposito, MD, FACS and James B. Walker, MD
Abstract: Penetrating brain injury includes all traumatic brain
injury that is not the result of a blunt mechanism. Concerning
these injuries, gunshot wounds are by far the most prevalent.
Despite law enforcement efforts, these injuries unfortunately
continue to be commonplace in large trauma centers as well as
in metropolitan and large community emergency departments.
Great efforts have been undertaken to standardize the medical
and surgical management of these patients. The authors review
the Guidelines of Penetrating Brain Injury published in 2001
and performed an updated literature search concerning this
topic. There is evidence to suggest based upon current data that
aggressive antibiotic prophylaxis and avoidance of aggressive
debridement of deep-seated bone and bullet fragments has
improved morbidity and mortality over the last 35 years.
Key Words: debridement, penetrating brain injury, surgical
management
(Neurosurg Q 2009;19:249–254)
A fter significant multidisciplinary collaboration, the
evidence-based Guidelines for the Management of
Severe Head Injury1 was introduced to the trauma
community in 1995 followed in 20072 by the third edition.
Both of these previous guidelines did not address the
management of patients specifically injured by penetrat-
ing objects including gun shot wounds and stabbing
injuries. In 1998 the International Brain Injury Associa-
tion, the Brain Injury Association of the United States
of America, members of the American Association of
Neurological Surgeons and the Congress of Neurological
Surgeons began to work on this effort.
In August 2001 the Journal of Trauma introduced
the Guidelines for the Management of Penetrating Brain
Injury (PBI),3 which has standardized both the medical
and surgical management of these unique and challenging
injuries. These guidelines are principally founded upon
From the Department of Neurosurgery, University of Mississippi
Medical Center, Jackson, Mississippi.
Financial Disclosure: Neither of the authors has any financial or
commercial interests in association with products or information
mentioned in this manuscript.
Proprietary Statement: Neither of the authors has any proprietary
interests in association with products or information mentioned in
this manuscript. No internal or external grants were received for this
manuscript.
Reprints: James B. Walker, MD, Department of Neurosurgery,
University of Mississippi Medical Center, 2500 North State Street,
Jackson, MS 39216 (e-mail: jbwalker@neurosurgery.umsmed.edu).
Copyright r 2009 by Lippincott Williams & Wilkins
Neurosurg Q  Volume 19, Number 4, December 2009
published literature that mainly includes retrospective
civilian and military analysis. Herein this article, we
review the principles of the Guidelines of Penetrating
Brain Injury3 as well as perform a current literature
search with emphasis on medical and surgical manage-
ment of these challenging patients. In addition, we discuss
some of our adaptations in our fairly extensive cohort of
penetrating injuries.
LITERATURE SEARCH
The Guidelines for the Management of Penetrating
Brain Injury3 was reviewed in its entirety. Additionally,
PubMed and MEDLINE search engines were used to
perform a current literature search using the following key
words in all practical combinations: ‘‘abscess,’’ ‘‘angio-
gram,’’ ‘‘antibiotic,’’ ‘‘arteriogram,’’ ‘‘ballistics,’’ ‘‘brain
injury,’’ ‘‘cerebral injury,’’ ‘‘cerebrospinal fluid (CSF)
leak,’’ ‘‘computed tomography,’’ ‘‘craniocerebral injury,’’
‘‘craniotomy,’’ ‘‘epilepsy,’’ ‘‘gunshot wounds,’’ ‘‘intracranial
pressure,’’ ‘‘magnetic resonance,’’ ‘‘meningitis,’’ ‘‘neuro-
surgery,’’ ‘‘penetrating,’’ ‘‘posttraumatic seizures.’’
BALLISTIC PRINCIPLES INVOLVED IN PBI
The ability to penetrate the skull is determined
primarily by the energy and the shape of the object along
with the angle of the trajectory of the projectile.4,5 In
addition to the shape of the projectile, understanding
the concept of kinetic energy is crucial to the under-
standing of the primary injury involved in PBI. Please
recall that kinetic energy is characterized by the equation:
E = 1/2mv2. In other words, the kinetic energy of a
projectile represents one half of the mass of the projectile
multiplied by the velocity of the projectile to the second
power. Hence the velocity of the projectile has a greater
influence than the mass of the projectile alone.
In addition, for understanding the total energy of
the projectile, it is paramount to understand the
pathophysiology6,7 involved in PBI. As the projectile
travels through the brain parenchyma, it is preceded by a
transient sonic wave that has a minimal influence of
surrounding tissue. Soon after the projectile travels in the
brain, it is followed by a temporary cavitation of the brain
parenchyma, which can be several times the diameter of
the projectile. This temporary cavity then collapses upon
itself only to reexpand in progressively smaller undulating
wave-like patterns. Every cycle of temporary expansion
and collapse creates significant surrounding tissue injury
to the brain. This can result in shear-like injury of the
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Esposito and Walker
neurons or can result in epidural hematomas, subdural
hematomas, or parenchymal contusions.5
Another important principle to recognize is the
principle of air resistance’s influence upon the ballistics of
a projectile. A projectile loses its kinetic energy rapidly as
it travels through air because of its resistance.4,5 There-
fore, a PBI is likely to be much more severe if the
projectile source is close to the patient head. Once again
this is due the notion that a large percentage of the initial
kinetic energy is being transferred to the surrounding
brain parenchyma.
NEUROIMAGING IN THE MANAGEMENT OF PBI
Computer tomography (CT) scanning of the head is
strongly recommended in all PBI3 when it is available.
This is largely due to the fact that CT scanning provides a
improved identification of embedded bone fragments and
the missile trajectory.8–10 It is also superior to the plain
films in determining the extent of the brain injury and
the detection of hematomas causing mass effect.11,12
Although plain films may give some indication for the
projectile path,13,14 it can sometimes be misleading in the
case of ricochet injuries. A ricochet injury occurs when
the bullet ricochets against the contralateral skull surface
and then travels in another direction through the brain
parenchyma.
Magnetic residence imaging (MRI) is seldom
indicated in the setting of PBI.15,16 Moreover, MRI
should also be highly discouraged when the substance of
the projectile is unknown. Even in instances when the
projectile is of an MRI compatible substance, CT
scanning provides much more useful and prognostic
information when compared with MRI.
At our institution, CT angiography is often
obtained once the CT scan of the head is reviewed and
suggests a wound tract that travels near major vascular
structures. Projectile trajectories that create concern for
vascular injuries include areas that cross the sylvian
fissure (location of middle cerebral artery), the subfalcine
areas (location of anterior cerebral artery), and around
the carotid canal (location of the internal carotid artery).
If CT angiography is suggestive of a vascular injury or
the patient’s findings on neurologic examination suggest
a vascular injury, a formal cerebral angiogram is then
obtained.
Vascular complications most commonly involved in
PBI patients are the development of traumatic aneurysms
or arteriovenous fistulas.17–19 Once identified, surgical or
endovascular repair may be warranted. Occasionally a
vascular injury will develop in a delayed fashion.18,19 This
often presents as a delayed hematoma formation seen on
a repeat CT scan.
The incidence of subarachnoid hemorrhage after
PBI ranges from 31% to 78% which has been calculated
from various retrospective CT scanning data.3,20,21 The
presence of subarachnoid hemorrhage after PBI has been
shown to correlate significantly with mortality.20 More-
over, subarachnoid hemorrhage is of greatest concern
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Neurosurg Q  Volume 19, Number 4, December 2009
when identified around large vascular territories and in
association with intraventricular hemorrhage.12
A common yet potentially life threatening compli-
cation of subarachnoid hemorrhage is the development of
vasospasm.22 Vasospasm results from a reactive phenom-
enon of smooth muscle contraction within the walls of the
vasculature. This leads to a decrease diameter of the
vasculature with resulting decrease cerebral blood flow
to the brain tissue. When severe, vasospasm can lead to
ischemia and ultimately cerebral infarction. Interestingly,
there was no difference in outcome based on a 3 month
Glasgow Outcome Scale (GOS) when PBI patients with
or without vasospasm were compared.23 When vasos-
pasm is detected (often diagnosed by increased transcra-
nial Doppler ultrasound velocities), therapeutic measures
should be immediately used.
Treatments of vasospasm include intravascular
expansion and endovascular angioplasty. Medical man-
agement of vasospasm includes conventional ‘‘HHH
Therapy’’ where the HHH stands for hypertension,
hypervolemia, and hemodilution. Here, measures are
taken to increase the patient’s blood pressure, to hydrate
the patient with intravenous fluids, as well as dilute the
patient’s blood volume to decrease the hematocrit. All of
these measures have been shown to increase the cerebral
blood flow.24 When HHH therapy fails, the patient
should be considered for selective transluminal balloon
angioplasty of the spasmodic vessels when available.
Balloon angioplasty involves the insertion of an inflatable
compliant balloon that stretches the vascular wall to
increase the cerebral blood flow.
ICP MONITORING
One of the greatest advancements in modern
management of traumatic brain injuries and PBI injuries
is the development of monitoring of intracranial pressure
(ICP). ICP monitoring involves drilling a burr hole in the
skull and the insertion of a monitoring device or a bolt
that couples to a water column (or monitoring device)
that can produce continuous pressure measurements.
It is crucial to understand that the principle of
intracranial pressure results from the fact that the
intracranial space is a fixed volume (once the fontanelles
have fused). Moreover, the rigidity of the skull accounts
for its noncompliance where small increases in volume
result in larger increases in pressure. Consequently, there
exists a limited area for the brain to swell as a result of
cytotoxic edema or expanding hematomas. In addition,
cerebral blood flow is also a common influence upon
ICP. As cerebral blood flow increases then there is more
blood volume within the intracranial space which raises
intracranial pressure in concordance with the Monro-
Kellie doctrine (ICP is determined by the relative cranial
contents of brain tissue, CSF, and blood].25 Paradoxi-
cally, cerebral blood flow can decrease to a point where
the brain parenchyma is not adequately perfused leading
to ischemia and subsequent cytotoxic edema which raises
intracranial pressure.
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Neurosurg Q  Volume 19, Number 4, December 2009 Penetrating Brain Injury

The indications for ICP monitoring and its applica-

tions in PBI have been incompletely studied. This is more
prominent in regards to civilian data when compared with
military data. However from the available data, elevated
ICP seems to be frequent after PBI11,26–28 and when
present is predictive of worse outcomes.12,29 In one
particular earlier series, 92% of patients who underwent
ICP monitoring demonstrated intracranial hypertension
(ICP>20 mm Hg).27 Unfortunately when compared with
the Guidelines for the Management of Traumatic Brain
Injury, there is little data to reveal how successful
management of intracranial pressure improves outcomes
in PBI patients.3 Although because of these short comings,
general aspects of ICP management discussed in the
literature of nonpenetrating traumatic brain injury has
been generalized to the PBI population. At our institu-
tion, threshold to begin treatment for elevated ICP is set
at 20 mm Hg. This value is slightly above normal ICP
measurements in normal individuals. Medical manage-
ment of intracranial hypertension includes sedation with
benzodiazepines and narcotics, nondepolarizing paralytics,
mannitol, and gentle hypothermic induction (35.51C).
Long-term hyperventilation and steroid administration
should be strictly avoided and has been conclusively shown
to increase morbidity and mortality in all traumatic brain
injury.1,2 FIGURE 1. This axial noncontrasted computed tomography
scan demonstrates a gunshot wound with a trajectory
confined to the bifrontal convexity where the majority of the
SURGICAL MANAGEMENT OF PBI bullet fragments are confined to the left frontal white matter.
Note there are minimal skull and tissue disruption and no
Immediately upon arrival of a PBI patient to an significant hematoma formation. Such cases can be treated
emergency facility, a thorough inspection of the super- with local wound debridement and closure.
ficial wound should be noted after routine resuscitation
maneuvers have been applied. An entrance wound should
be identified and its location recorded as well as any exit because this has been shown to correlate with worse
wounds when they exist. The superficial scalp should be outcomes.9,31 This has marked a significant trend since
observed for powder burns, which would imply a close Vietnam era to proceed with a more conservative,
range firearm injury. Any CSF, bleeding, or brain paren- minimally invasive approach toward cerebral debride-
chyma emerging from the wound should be documented. ment as this has been shown to improve outcomes and
In addition, the size of the deficit should be documented lower morbidity.27,30,32
and when extensive complex skin flap closure may be Once a patient has been classified as a surgical
needed. After the wound has been inspected, a thorough candidate, attempts should be made to operate within 12
neurologic examination should be noted and a postre- hours of the injury to prevent infection and resulting
suscitative GCS should be obtained. It is important to abscesses.10,30,33 As with bone fragments, only acces-
document any cranial nerve or motor deficits. The eyes sible missile fragments in noneloquent brain should be
should be carefully inspected and pupillary responses and retrieved although there has been some suggestion that
size recorded. When the patient has been adequately removal of all missile fragments may decrease the risk of
resuscitated and stabilized for transfer, a CT scan should seizures.34
be immediately obtained. When not available, plain skull When the trajectory of the bullet has been noted on
films should obtained. CT scan to violate an open air sinus (Fig. 2), an operation
Treatment of small entrance wounds with local is recommended for water-tight closure of the damaged
wound care and closure in patients whose scalp has dura.3 It has been suggested that this may decrease the
not been devitalized and have no significant intracranial risk of abscess formation and CSF fistulas.33,35,36
pathologic findings on CT scan (Fig. 1) is not only ade- In summary, the surgical management of PBI is
quate but recommended according to the guidelines.3 based largely on Class III data. There are no randomized-
However, in the presence of significant mass effect, control studies that have examined the relative effect of
debridement of necrotic brain tissue along with safely various treatment of debridement to prevent infection
accessible bone fragments is recommended.30 It should be and minimize the development of seizure disorders. The
noted that any deeply seated bone fragments especially current trend is to minimize the degree of debridement
those in eloquent brain areas should not be retrieved whereas by obtaining a water-tight dura closure. In addition

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Esposito and Walker
FIGURE 2. This axial noncontrasted computed tomography
scan demonstrates a penetrating brain injury with significant
disruption of the left frontal bone and violation of the frontal
sinus marked by the associated pneumocephalus. Such
patients should undergo surgical debridement and dural
repair to prevent subsequent cerebrospinal fluid leaks and
infectious complications. In addition, this patient demon-
strates inappropriate midline shift and should also be
considered for a decompressive craniectomy.
at our institution, any patient with a salvageable examina-
tion and midline shift that exceeds 5 mm where the midline
shift is greater than the width of the associated subdural
or epidural hematoma is considered for a decompressive
hemicraniectomy (Fig. 2).
MANAGEMENT OF CSF LEAK
A common finding among PBI patients is the
development of a CSF leak, which has an incidence of
28% in one large series.33 This complication develops as a
result of the projectile’s violation of the dura along with
failure to adequately seal the defect through normal tissue
healing responses. CSF leaks can present through the
entry or exit sites of the projectile as well as through the
ear or nose when the mastoid air cells and the open-air
sinuses have been violated, respectively.
As stated in the guidelines, surgical correction is
currently recommended for CSF leaks that do not stop
spontaneously or are refractory to temporary CSF diver-
sion through a ventricular catheter or lumbar drain.3
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Neurosurg Q  Volume 19, Number 4, December 2009
During surgery every effort should be made to close the
dura.3 When the dura cannot be closed primarily with
suture approximation, a tissue graft can be used from the
patient’s pericranium, temporalis fascia, or fascia lata.
Synthetic grafts can be used as well, however, they can act
as a foreign body and thus increase the risk of infection,
especially in grossly contaminated wounds.37 When
closing the wound, a water tight closure of all layers is
ideal.
When a CSF leak occurs remote from the projec-
tile’s entrance, CSF diversion should be considered.37
The patient’s CT scan of the head should be carefully
inspected before the placement of the lumbar drain
because mass effect from hematomas and midline shift
are relative contraindications for lumbar drainage com-
pared to a ventriculostomy because of the risk of her-
niation syndromes. It has been demonstrated in several
retrospective studies that CSF leaks that persist after
surgery have a high likelihood of developing meningitis
or abscess.36,38–40
ANTIBIOTIC PROPHYLAXIS FOR PBI
One of the most dreaded complications of PBI is
the development of infectious complications. These may
present as local wound infections, meningitis, ventriculi-
tis, or cerebral abscess. Unfortunately, infectious compli-
cations are not uncommon and occur in as many as 15%
of all PBI cases based on one series.41 It is highly
suggested from multiple retrospective studies that the
presence of air sinus wounds and CSF fistulas may further
increase the risk of infection33,36,38 with an incidence as
high as 49.5%.38
The early administration of broad spectrum anti-
biotics likely decreases these infectious complications
based upon preantibiotic military data where infectious
complications reached as high as 58.8% in all penetrating
head injuries.42 Although performed in 1946 under poorly
controlled conditions, Munslow43 additionally noted a
decrease in infectious complications from 21% to 5.6%
after the advent of parenteral penicillin. In one of the
largest retrospective reviews which included civilian
PBI data, Benzel et al18 demonstrated a rate of infection
of 1% to 5% overall and less than a 1% rate of
development of brain abscess with use of broad spectrum
antibiotics.
Although the use of broad spectrum antibiotics is
primarily speculative owing to a paucity of evidence
and lack of randomized controlled trials, they are still
recommended because there is data to suggest a wide
variety of organisms are pathogenic in PBI settings where
Gram negative organisms were most common based on
a large military series.36 Considerable variation exists
in antibiotic preference; however, cephalosporins have
become the preferred agent nationally.44 At our institu-
tion, we routinely use prophylactic parenteral broad
spectrum antibiotics for all of our PBI patients. We
commonly use intravenous cephtriaxone, metronidazole,
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Neurosurg Q  Volume 19, Number 4, December 2009
and vancomycin and continue them for a minimum of
6 weeks. As we have initiated this protocol, we have
yet to encounter our first infectious complication over
40 consecutive patients although we did have 1 case of
ventriculitis after a patient inadvertently stopped his
antibiotics after 1 week.
ANTISEIZURE PROPHYLAXIS FOR PBI
Not only is the development of posttraumatic
seizures a potential cause of morbidity for PBI patient,
it is often a cause fear and concern for family members
involved in their care. Furthermore, seizures during the
first week after an initial injury can be a cause of
morbidity and mortality because of the development of
raised intracranial pressures and increased metabolic
demands. Thus antiseizure medications are recommended
in the first week after PBI. This has been suggested to
prevent early posttraumatic seizures in these patients
based upon military data analysis.45–48 Prophylactic
treatment with anticonvulsants beyond the first week
after PBI has not been shown to prevent the development
of new seizures and is currently not recommended. In our
series that includes 187 patients since 2002, an incidence
of approximately 50% of posttraumatic epilepsy has
been observed. This has prompted us to continue anti-
seizure prophylaxis in all but the most minimally injured
patients.
PROGNOSIS IN PBI
Before determining the appropriate medical or
surgical management of PBI patients, it is paramount to
determine the prognosis of the patient based on the head
CT and neurologic examination findings. Great care
should be executed when obtaining an appropriate GCS
score because surgery should only be considered for
neurologically salvageable patients. It is imperative to
ensure that the patient’s GCS score is not obscured owing
to simultaneous seizure activity or medications that can
influence cognition and motor activity. These can include
sedative or hypnotic agents used for intubation or
paralytics that have been recently administered to the
patient.
Several factors have been suggestive to contribute to
a worse outcome3 and include:
 increase in age
 suicide attempts
 associated coagulopathy
 GCS score of 3 with bilaterally fixed and dilated pupils
 high-initial ICP
Moreover several CT scan findings (Fig. 3) have
been suggested to be correlative to a worse outcome3 and
include:
 bihemispheric lesions
 multilobar injuries
 intraventricular hemorrhage
 uncal herniation
 subarachnoid hemorrhage.
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Penetrating Brain Injury
FIGURE 3. This axial noncontrasted CT scan demonstrates a
bihemispheric gunshot wound with marked intraventricular
hemorrhage, subarachnoid hemorrhage, and early ischemic
changes. In concordance with a low GCS score, a conservative
approach is an appropriate means of management and
surgical intervention should be discouraged.
CONCLUSIONS
Care of patients with PBI has changed dramatically
as the advent of Guidelines for the Management of
Penetrating Brain Injury. There has been a move over the
last 35 years to avoid aggressive debridement of deep-
seated bone and bullet fragments as this appears to
improve functional outcome. In its place, aggressive
administration of prophylactic parenteral antibiotics has
been used to prevent infectious complications. Although
there is a paucity of Class I and II data on this topic, there
is adequate data on its cousin counterpartynonpenetrat-
ing traumatic brain injury. There has been a call to
perform large multicentered randomized controlled trials,
which could alter our care of these challenging patients in
the future.
REFERENCES
1. Bullock R, Chestnut RM, Clifton G, et al. Guidelines for the
management of severe head injury. J Neurotrauma. 1995;13:
641–734.
2. Bullock R, Chestnut RM, Clifton G, et al. Guidelines for the
management of severe head injury-3rd edition. J Neurotrauma. 2007;
24(suppl):S1–106.
3. Aarabi B, Alden TD, Chestnut RM, et al. Guidelines for the
management of penetrating brain injury. J Trauma. 2001;
51(suppl):S1–86.
4. Levy MI, Davis SE, et al. Ballistics and forensics. In: Marion DW,
ed. Traumatic Brain Injury. New York: Thieme; 1999:201–213.
5. Ordog GJ, Wasserberger J, Subramarion B. Wound ballistics:
theory and practice. Am Emerg Med. 1984;13:1113–1122.
www.neurosurgery-quarterly.com | 253
Esposito and Walker
6. Barach E, Tomlanovich M, Nowak R. A pathophysiologic
examination of the wounding mechanisms of firearms-part 1.
J Trauma. 1986;26:225–235.
7. Carey ME. Experimental missile wounding of the brain. Neurosurg
Clin N Am. 1995;6:629–642.
8. Aarabi B. Comparative study of bacteriological contamination
between primary and secondary exploration of missile head wounds.
Neurosurgery. 1987;20:610–616.
9. Chaudhri KA, Choudhury AR, al Moutaery KR, et al. Penetrating
craniocerebral shrapnel injuries during ‘‘Operation Desert Storm’’:
early results of a conservative surgical treatment. Acta Neurochir
(Wien). 1994;126:120–123.
10. Helling TS, McNabney WK, Whittaker CK, et al. The role of early
surgical intervention in civilian gunshot wounds to the head.
J Trauma. 1992;32:398–400.
11. Levi L, Borovich B, Guilburd JN. Wartime neurosurgical experience
in Lebanon, 1982-85, I: Penetrating craniocerebral injuries. Isr
J Med Sci. 1990; 26:548–554.
12. Nagib MG, Rockswold GI, Sherman RS, et al. Civilian gunshot
wounds to the brain: prognosis and management. Neurosurgery.
1986;18:533–537.
13. Ameen AA. The management of acute craniocerebral injuries caused
by missiles: analysis of 110 consecutive penetrating wounds of the
brain form Basrah. Injury. 1984;16:88–90.
14. Rish BL, Dillon JD, Weiss GH. Mortality following penetrating
craniocerebral injuries. J Neurosurg. 1983;59:775–780.
15. Oliver C, Kabala J. Air gun pellet injuries: the safety of MR
imaging. Clin Radiol. 1997;52:299–300.
16. Teitelbaum GP, Yee CA, Van Horn DD, et al. Metallic ballistic
fragments: MR imaging safety and artifacts. Radiology. 1990;
175:855–859.
17. Aarabi B. Management of traumatic aneurysms caused by high
velocity missile head wounds. Neurosurg Clin N Am. 1995;
6:775–797.
18. Benzel EC, Day WT, Kesterson L. Civilian craniocerebral gunshot
wounds. Neurosurgery. 1991;29:67–71; discussion 71–72.
19. Amirjamshidi A, Rahmat H, Abbassioun K. Traumatic aneurysms
and arteriovenous fistulas of intracranial vessels associated
with penetrating head injuries occurring during war: principles and
pitfalls in diagnosis and management. A survey of 31 cases and
review of the literature. J Neurosurg. 1996;84:769–780.
20. Kaufman HH, Makela ME, Lee KF, et al. Gunshot wounds to the
head: a perspective. Neurosurgery. 1986;18:689–695.
21. Aldrich EF, Eisenberg HM, Saydjari C, et al. Predictors of mortality
in severely head-injured patients with civilian gunshot wounds: a
report from the NIH Traumatic Coma Data Bank. Surg Neurol.
1992;38:418–423.
22. Shimura T, Mukai T, Teramoto A, et al. Clinicopathological studies
of craniocerebral gunshot wound injuries. No Shinkei Geka. 1997;
25:607–612.
23. Kordestani RK, Counelis GJ, McBride DQ, et al. Cerebral arterial
spasm after penetrating craniocerebral gunshot wounds: transcra-
nial Doppler and cerebral blood flow findings. Neurosurgery.
1997;41:351–359; discussion 359–360.
24. Muench E, Horn P, Bauhuf C, et al. Effects of hypervolemia and
hypertension on regional cerebral blood flow, intracranial pressure,
and brain tissue oxygenation after subarachnoid hemorrhage. Crit
Care Med. 2007;35:1844–1851.
25. Mokri B. The Monro-Kellie hypothesis: applications in CSF volume
depletion. Neurology. 2001;56:1746–1748.
26. Crockard HA. Early intracranial pressure studies in gunshot
wounds of the brain. J Trauma. 1975;15:339–347.
254 | www.neurosurgery-quarterly.com
Neurosurg Q  Volume 19, Number 4, December 2009
27. Lillard PL. Five years experience with penetrating craniocerebral
gunshot wounds. Surg Neurol. 1978;9:79–83.
28. Sarnaik AP, Kopec J, Moylan P, et al. Role of aggressive intracranial
pressure control in management of pediatric craniocerebral gunshot
wounds with unfavorable features. J Trauma. 1989;29:1434–1437.
29. Miner ME, Ewing-Cobbs L, Kopaniky DR, et al. The results of
treatment of gunshot wounds to the brain in children. Neurosurgery.
1990;26:20–25.
30. Hubschmann O, Shapiro K, Baden M, et al. Craniocerebral gunshot
injuries in civilian practice: prognostic criteria and surgical manage-
ment experience with 82 cases. J Trauma. 1979;19:6–12.
31. Hammon WM, Kempe G. Analysis of 2187 consecutive penetrating
wounds of the brain from Vietnam. J Neurosurg. 1971;34(2 Pt 1):
127–131.
32. Brandvold B, Levi L, Feinsod M, et al. Penetrating craniocerebral
injuries in the Israeli involvement in the Lebanese conflict.
J Neurosurg. 1990;72:15–21.
33. Arendall RE, Meinowsky AM. Air sinus wounds: an analysis of 163
consecutive cases incurred in the Korean War, 1950-1952. Neuro-
surgery. 1983;13:377–380.
34. Salazar AM, Jabbari B, Vance SC, et al. Epilepsy after penetrating
head injury, I. Clinical correlates: a report of the Vietnam Head
Injury Study. Neurology. 1985;35:1406–1414.
35. Gonul E, Baysefer A, Kahraman S. Causes of infections and
management results in penetrating craniocerebral injuries. Neuro-
surg Rev. 1997;20:177–181.
36. Aarabi B, Taghipour M, Alibaii E, et al. Central nervous system
infections after military missile head wounds. Neurosurgery. 1998;
42:500–509.
37. Vrankovic D, Hecimovic I, Dmitrovic B. Management of missile
wounds of the cerebral dura mater: experience with 69 cases.
Neurochirurgia. 1992;35:150–155.
38. Meirowsky AM, Caveness WF, Dillon JD, et al. Cerebrospinal fluid
fistulas complicating missile wounds of the brain. J Neurosurg. 1981;
54:44–48.
39. Rish BL, Caveness WF, Dillon JD, et al. Analysis of brain abscess
after penetrating craniocerebral injuries in Vietnam. Neurosurgery.
1981;9:535–541.
40. Taha JM, Haddad FS, Brown JA. Intracranial infection after missile
injuries to the brain: report of 30 cases from the Lebanese conflict.
Neurosurgery. 1991;29:864–868.
41. Carey ME, Young HF, Mathis JL. A bacterial study of cranio-
cerebral missile wounds from Vietnam. J Neurosurg. 1971;34:145–154.
42. Whitaker R. Gunshot wounds of the cranium: with special reference
to those of the brain. Br J Surg. 1916;3:708–735.
43. Munslow RA. Penetrating head wounds: experiences from the
Italian campaign. Ann Surg. 1946;123:180–189.
44. Kaufman HH, Schwab K, Salazar AM. A national survey of
neurosurgical care for penetrating head injury. Surg Neurol. 1991;
36:370–377.
45. Rish B, Caveness W. Relation of prophylactic medication to the
occurrence or early seizures following craniocerebral trauma.
J Neurosurg. 1973;38:155–158.
46. Young B, Rapp RP, Norton JA, et al. Failure of prophylactically
administered phenytoin to prevent late posttraumatic seizures.
J Neurosurg. 1983;58:236–241.
47. Glotzner FL, Haubitz I, Miltner F, et al. Seizure prevention using
carbamazepine following severe brain injuries. Neurochirurgia.
1983;26:66–79.
48. Temkin NR, Dikmen SS, Anderson GD, et al. Valproate therapy
for prevention of posttraumatic seizures: a randomized trial.
J Neurosurg. 1999;91:593–600.
r 2009 Lippincott Williams & Wilkins