1. CLINICAL STUDIES
EARLY HYPODENSITY ON COMPUTED
TOMOGRAPHIC SCAN OF THE BRAIN IN
AN ACCIDENTAL PEDIATRIC HEAD INJURY
Paul Steinbok, M.B.B.S. OBJECTIVE: Hypodensities on computed tomographic (CT) brain scans are thought to
Division of Pediatric Neurosurgery, take at least 6 hours to become apparent after blunt head trauma. This finding, in con-
Department of Surgery,
BC Children’s Hospital,
junction with the later evolution of the hypodensities, is used in timing the injury in
and University of British Columbia, children with suspected non-accidental brain injury, in whom the history may be inac-
Vancouver, Canada curate. The purpose of this study is to report the occurrence of diffuse cerebral parenchy-
mal hypodensities on CT scans performed within 5 hours of a well-defined accidental
Ashutosh Singhal, M.Sc., M.D. head injury.
Division of Pediatric Neurosurgery,
Department of Surgery,
METHODS: A retrospective review was performed of five patients admitted to British
BC Children’s Hospital, Columbia Children’s Hospital who had accidental head injury and who were identi-
and University of British Columbia, fied as having diffuse cerebral hemispheric hypodensities on early CT scans.
Vancouver, Canada
RESULTS: We present five patients (age range, 4 mo–14 yr) with well-documented acci-
Ken Poskitt, M.D.C.M. dental head injuries who demonstrated obvious and extensive CT brain scan cerebral
Department of Radiology, hemispheric hypodensity from 60 minutes to 4.5 hours after trauma. All five patients pre-
BC Children’s Hospital sented with severe head injuries and immediate, unremitting coma, and all five pro-
and University of British Columbia, gressed rapidly to brain death within 48 hours.
Vancouver, Canada
CONCLUSION: It is unusual, but possible, to develop CT hypodensities as early as
D. Douglas Cochrane, M.D. 1 hour after accidental head injury. In our small series of cerebral hemispheric hypo-
Division of Pediatric Neurosurgery, density occurring less than 5 hours after trauma, all five patients had a uniformly fatal
Department of Surgery, outcome. These observations may be important medicolegally in the assessment of the
BC Children’s Hospital,
and University of British Columbia,
timing of head injury when the history of the trauma is not clear, as in children with
Vancouver, Canada suspected non-accidentally inflicted injury. It is inappropriate to generalize these find-
ings to patients who are not unconscious immediately after a head injury, who regain
Reprint requests: consciousness after an injury before deteriorating, or who do not progress rapidly to
Paul Steinbok, M.B.B.S.,
Division of Pediatric Neurosurgery,
brain death.
Department of Surgery, KEY WORDS: Cerebral edema, Child abuse, Computed tomographic hypodensity, Head injury, Medicolegal,
BC Children’s Hospital,
Timing of injury
4480 Oak Street, #K3–159,
Vancouver, BC, Canada V6H 3V4.
Neurosurgery 60:689–695, 2007 DOI: 10.1227/01.NEU.0000255398.00410.6B www.neurosurgery-online.com
Email: psteinbok@cw.bc.ca
H
Received, June 7, 2006.
ypodensities on computed tomo- next 3 to 5 days and then regress during the
Accepted, December 8, 2006.
graphic (CT) brain scans after head subsequent few days. Thus, the presence of
trauma have traditionally been attrib- obvious CT scan hypodensities within 6 hours
uted to cerebral ischemia. Previously pub- of a reported head injury may lead physicians
lished reports have suggested that it is diffi- to call into question the timing of the injury or
cult to precisely determine how much time raise the possibility of an etiology other than
must elapse between the injury and the devel- the reported head injury. In young children
opment of hypodensities, particularly diffuse and infants, the apparent inconsistency
hypodensities (6, 20). As commented on by between the CT scan findings and the reported
Dias et al. (9), and in keeping with our experi- history of the trauma may lead to a concern
ence, the standard opinion is that CT scan low regarding non-accidental inflicted injury.
densities do not become readily apparent until There are a number of reports in which the
at least 6 hours after the injury. Typically, they occurrence of parenchymal hypodensities on
become progressively more obvious during the the initial CT scan after non-accidentally
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2. STEINBOK ET AL.
inflicted injury has been mentioned (8–10, 15). Because the diag- vehicle collision in one case, and a bicycle accident (without a
nosis of inflicted shaking injury is associated with inaccuracies helmet) in one case.
in the history, it may be argued that the timing of the trauma in None of the patients was documented to have a cardiorespi-
such reports may be unreliable. There are well-documented ratory arrest or any period of hypoxia or hypotension during
reports of brain “swelling” within 6 hours of accidental head initial transfer or during the trauma resuscitation before the
trauma, but no reports of early parenchymal CT scan hypoden- initial CT scan. None of the patients was identified to have
sities in documented accidental injuries in children or adults. radiographic or clinical evidence of spine or spinal cord injury.
We present this case series to demonstrate that diffuse and In one of three patients in whom funduscopy was documented,
obvious CT scan parenchymal hypodensities occur within 5 retinal hemorrhages, consistent with non-accidental trauma,
hours of well-documented accidental pediatric head injury and were identified (Table 1). This patient was one of three in this
to discuss the prognostic and medicolegal implications of these series investigated by our child protection team. On the basis of
findings. corroborating eyewitness accounts, it was concluded that the
injury was genuinely the result of a fall as described by the
PATIENTS AND METHODS family. In another patient, there were bilateral retinal infarcts,
which are not typical of non-accidental injury. In the third
British Columbia’s Children’s Hospital is a tertiary referral patient, funduscopy was normal.
center for pediatric head trauma, with a catchment area includ- All five initial CT scans demonstrated diffuse, obvious, cere-
ing approximately 4.2 million residents of British Columbia, bral hemisphere hypodensity, and, in some scans, there were
Canada. This is a retrospective review of a series of children hypodensities in more-central structures, such as the basal gan-
treated at British Columbia’s Children’s Hospital and identified glia and/or the brainstem (Table 2). All five patients had tento-
as having early CT scan hypodensities after accidental head rial and/or interhemispheric acute subdural blood. In two
injury. The medical records of these patients were reviewed to patients, there were acute convexity subdural hematomas, both
reconfirm the timing and accidental nature of the injury. All of which were of mixed density; a right frontoparietal convex-
information in the medical record, including ambulance ity hematoma, 7 mm in maximal thickness, and a right frontal
reports, emergency department reports, medical and nurses hematoma, 7 mm in maximal thickness. All five initial CT scans
notes, as well as any social worker notes and discharge sum- showed evidence of brain swelling with basal cistern efface-
maries were reviewed. The time of injury was estimated from ment, and four of the five scans showed complete obliteration
these records and only patients with well-corroborated trauma of the basal cisterns. Only one of five patients had a cranial frac-
histories were included in this review. The timing and find- ture. The distributions of the hypodensities on the initial CT
ings on the CT scans performed after the trauma were ascer- scan are presented in Table 2. Representative early CT scan
tained with the assistance of a pediatric neuroradiologist (KP). images of each patient are shown in Figure 1.
The clinical course of the patients and the results of any addi- In Patients 2 and 4 (Table 1), carotid Doppler ultrasound per-
tional radiological investigations were also determined. The formed 18 and 8 hours, respectively, after injury demonstrated
study was approved by the Ethics Committee of the University reversed diastolic flow. In Patient 3, an intracranial pressure
of British Columbia and the Research Review Committee of monitor was inserted, which demonstrated pressures of greater
British Columbia’s Children’s Hospital. than 65 mmHg. In Patient 4, xenon-CT and magnetic resonance
angiography at approximately 6.5 hours after injury confirmed
RESULTS the absence of cerebral blood flow (CBF). A diffusion-weighted
magnetic resonance imaging scan performed at the same time
Five patients were identified with well-documented acciden- as the magnetic resonance angiography showed marked
tal head trauma and early posttraumatic hypodensities; all restriction of diffusion in the cerebral hemispheres. In Patient 5,
were noted on CT scans performed less than 5 hours after the a craniotomy was performed to evacuate a 1-cm-thick cerebral
injury. In three of the five patients, the possibility of non- convexity acute subdural hematoma, and postoperative
accidental inflicted injury had been raised because of the CT intracranial pressure monitoring demonstrated an intracranial
scan findings and the child protection team had investigated pressure of greater than 40 mmHg.
the circumstances of the injury. In all cases, there was incontro- Autopsies were performed in two patients (Patients 2 and
vertible evidence that the injury was a bona fide accident. The 4). In both patients, there was marked cerebral edema with
demographic data, mechanism of injury, initial Glasgow Coma uncal and tonsillar herniation. In Patient 2, there was a thin
Scale (GCS) score, pupillary reaction at initial assessment, CT subdural hematoma, with an associated contusion and lacera-
scan findings, and outcome are summarized in Table 1. All five tion of the right cerebral hemisphere, diffuse subarachnoid
patients had severe blunt head injuries and were immediately blood, and diffuse hypoxic-ischemic changes, with no definite
unconscious, with a GCS score of less than 8. The age range histopathological evidence of acceleration/deceleration brain
was 4 months to 14 years; four of the five patients were injury. No abnormalities were noted in the brainstem. In
younger than 2 years of age at the time of injury. There were Patient 4, there were thin diffuse subdural hemorrhages over
two girls and three boys. The mechanism of injury was a fall in the cerebral hemispheres and neuroaxonal spheroids at the cer-
three cases, one of which was from a moving vehicle, a motor vicomedullary junction, but not in the remainder of the brain,
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3. COMPUTED TOMOGRAPHIC SCAN HYPODENSITIES AFTER HEAD INJURY
TABLE 1. Patient summarya
Patient no. Age/sex Mechanism GCS Pupils Funduscopy CT scan Outcome
1 4 mo/F MVC 3 2 fixed Not performed 3.5 hr: SAH, IVH, tentorial 24 hr: brain death
ASDH, PH
2 7 mo/M Fall down stairs 3 1 fixed Bilateral retinal and 2 hr: falx, tentorial and con- 24 hr: brain death
preretinal hemorrhages vexity ASDH, mild IVH, PH
3 14 yr/M Bike accident 4 2 fixed Not performed 4.5 hr: DAI, mild falx ASDH, 36 hr: brain death
mild SAH, mild IVH, PH
4 12 mo/F Fall from fast 5 2 fixed Bilateral retinal infarcts 3.5 hr: mild SAH, mild falx 24 hr: brain death
moving hay wagon and tentorial ASDH, PH
5 2 yr/M Fall from stool 4 2 fixed Normal 1 hr: tentorial and convexity 48 hr: death
ASDH, PH
a
GCS, Glasgow coma scale; CT, computed tomographic; MVC, motor vehicle collision; SAH, subarachnoid hemorrhage; IVH, intraventricular hemorrhage; ASDH, subdural
hematoma; PH, parenchymal hypodensities; DAI, diffuse axonal injury.
and extensive bilateral retinal hemorrhages. The vertebral and
carotid arteries were normal. TABLE 2. Distribution of low densities on initial computed tomographic
scana
DISCUSSION Patient
Bilateral
Lentiform Brain- Cere-
cerebral Thalamus Caudate
no. nucleus stem bellum
The patients reported in this study all experienced acciden- hemispheres
tal severe traumatic brain injuries, characterized on CT scans 1
within 5 hours by severe diffuse brain swelling and parenchy- 2
mal hypodensities and resulting in rapid brain death. The 3
mechanisms of injury varied from a relatively mild type of 4
trauma, a fall from a stool, to a high-energy impact, a motor 5
vehicle collision. There was nothing special regarding the a
, hypodensity was present in that anatomical location.
mechanism of injury in any of the patients that would have
suggested the rapid progression to death that occurred there-
after. The patients in this study did not necessarily experience hypodensity of the gray matter, but the authors did not com-
severe diffuse axonal injury because neither of the two autop- ment specifically regarding hypodensities.
sied brains showed evidence of acceleration and deceleration Early CT scan hypodensities after head injury have been
injury in the cerebral hemispheres. demonstrated previously in non-accidental injuries (8–10, 15).
It is well documented that diffuse brain swelling can be iden- However, only Dias et al. (9) tried to time the first CT scan
tified on CT scans performed within hours of a severe trau- after the injury; in their report, parenchymal CT scan hypo-
matic brain injury in both children and adults (1, 5, 12, 18). densities were noted on scans performed an average of 3.2
However, the establishment of early and extensive hypo- hours after the “suspected” time of the injury. The authors tried
densities in association with the brain swelling after well- to pinpoint the time of the injury but, in some cases, had to date
documented accidental pediatric head injury, as noted in the the injury to the time of “an apneic spell, seizure, abrupt coma,
cases presented in this series, is, to our knowledge, a novel or other significant and immediate event,” which might not
observation in the literature. represent the precise timing of the actual injury itself. In the
The radiological diagnosis of diffuse brain swelling after cases reported herein, the injuries were accidental and the time
trauma has typically been based on the findings of obliterated of injury was precisely documented.
or compressed basal cisterns, with or without small lateral and The CT scan hypodensities in our cases were diffuse, severe,
third ventricles, in the absence of significant midline shift ( 3–6 and very obvious. The hypodensities affected primarily the
mm, depending on the study) or significant intracranial focal cerebral hemispheres (Table 2), which were uniformly hypo-
mass lesion (1, 12). In one study by Willman et al. (18), “poor dense, and the findings were similar to the cases described by
gray-white differentiation” was also included as one of the CT Han et al. (11) as having the so-called “reversal sign.” Han et al.
scan criteria of brain swelling. None of the studies included used the term reversal sign to indicate diffuse cerebral edema
comments regarding the presence of hypodensities on the CT on CT scan, with decreased density of the cortical gray and
scans in the patients with a diagnosis of early diffuse brain white matter, and relatively increased density of the thalami,
swelling. It can be argued that the presence of poor gray-white brainstem, and cerebellum. In their study, there were eight chil-
differentiation, as in the study by Willman et al. (18), implies dren with the reversal sign present at the time of the first CT
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4. STEINBOK ET AL.
to the occurrence of the reversal sign in the list of parenchymal
A B abnormalities among the 15 patients with well-defined times of
the initial CT scan relative to the injury. However, they note in
their discussion that “among infants with the reversal sign,
50% were evident on the initial scans performed an average of
3.5 hours after the injury was reported.” The findings in our
patients with accidental head injury support the contention of
Dias et al. (9) with respect to the abused child, namely that
hypodensities may not take 6 to 48 hours to develop. In our
series, there was no doubt regarding the accidental nature or
the timing of the trauma and all patients had extensive cerebral
hemisphere hypodensity, similar to the reversal sign, between
1 and 5 hours after the head injury.
C D The pathophysiology of the parenchymal hypodensities
noted in the children in this series is not clear. These CT scan
findings indicate the presence of cerebral edema, as was iden-
tified in the two patients who had autopsies. However, the
pathophysiology of such extensive edema within hours of the
trauma is not clear. In the series by Han et al. (11) of children
with reversal sign, when trauma was the etiology, child abuse
was the most common cause. The authors opined that in this
group of children with abuse, the posttraumatic reversal sign
may have been the result of repeated trauma to the brain,
resulting in repeated “edema induced hypoperfusion of the
brain, in turn resulting in stress induced hyperglycemic cere-
bral patterns of anoxic injury.” However, in our series, repeated
E traumatic brain injury cannot be implicated.
FIGURE 1. A, Patient 1, CT scan Acute posttraumatic diffuse brain swelling without cerebral
obtained 3.5 hours after injury in a hypodensities has been attributed to cerebral vascular engorge-
motor vehicle collision. B, Patient 2, ment secondary to hyperemia, on the basis of the initial report
CT scan obtained 2 hours after a fall of Bruce et al. (7) on so-called “malignant brain swelling” in
down stairs. C, Patient 3, CT scan children. Studies that are more recent, with CT scan dynamic
obtained 4.5 hours after a fall off a scanning (19) and CT scan xenon assessment of CBF within a
fast-moving bicycle. D, Patient 4, CT
few hours of head injury, have indicated that, in the most severe
scan obtained 3.5 hours after a fall off
of a fast-moving wagon during a hay
brain injuries, decreased CBF, sometimes to ischemic levels,
ride. E, Patient 5, CT scan obtained 1 rather than cerebral hyperemia may be present (4, 5, 14). On
hour after a fall from a stool. serial CBF measurements, the decreased CBF may be replaced
by cerebral hyperemia after 24 hours (4, 5, 14); thus, if CBF is not
measured within hours of the injury, the period of decreased
CBF may be missed. It may, therefore, be that the reduced CBF,
scan after admission; of these, two had an accidental head which can occur early after trauma, is enough to cause ischemia
injury and three were thought to have experienced child abuse. and infarction in some patients. This could, in turn, lead to rap-
In these patients with an acute reversal sign, the time of the idly apparent low densities and swelling on CT scans.
scan relative to the time of the injury was not reported. In the One of the concerns with the proposition that the hypoden-
study by Dias et al. (9), in which a concerted attempt was made sities in our cases were caused by ischemia is that the time
to time the CT scan abnormalities in infants after non-acciden- course of such extensive low densities, as noted in our patients,
tal head injury, there were 15 patients out of a total of 33 in is not in keeping with the CT scan findings observed after
whom the authors thought that the time of the alleged abuse known ischemic events. For example, CT scan hypodensities
could be pinpointed. Six of these 15 patients had parenchymal are usually not observed for the first 12 hours after neonatal
hypodensities on a CT scan performed an average of 3.2 hours asphyxial injures (3) and become more obvious and extensive
after injury. The extent of the hypodensities in these six patients during a 72-hour time course (13). Similarly, in typical cere-
was not reported but they were not extensive enough to be brovascular accidents in adults, CT scan hypodensities are dif-
categorized as showing the reversal sign because those authors ficult to identify until at least 6 hours (16). Indeed, for entry into
indicated the presence of the reversal sign as a separate cate- one multicenter trial for stroke, CT scan evidence of the
gory. In their results, Dias et al. (9) noted that six patients exhib- ischemic event within 6 hours of a clinical middle cerebral
ited the reversal sign on CT scans but they make no reference artery territory stroke included loss of density contrast of the
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5. COMPUTED TOMOGRAPHIC SCAN HYPODENSITIES AFTER HEAD INJURY
lentiform nucleus and/or the insular ribbon and hemispheric accidentally inflicted injury was queried and the child protec-
sulcus effacement (2) but not hypodensity. tion team was asked to investigate because the CT scan find-
In support of the hypothesis that ischemia may be the cause ings of severe low density changes were thought to be incom-
of the early hypodensities observed in our patients, there is patible with the time of the injury as indicated in the history
evidence that, in the most severe ischemic situations, CT scan taken at the time of arrival to the hospital. The case series of
hypodensities may be present earlier than in typical cases. Our children with non-accidentally inflicted head injury reported by
patients, all of whom died, certainly qualify for being in that Dias et al. (9) and this case series of children with accidental
most severely affected group. In the study of hypoxic ischemic head injury indicate that the traditional expectation regarding
term neonates by Lupton et al. (13), the most severely involved the timing of onset of CT scan brain hypodensities after head
children had patchy CT scan hypodensities on the first day of trauma may not always be correct. We think the usual expected
life, although the specific time in hours was not reported. In evolution of low densities on CT scan is still what one would
addition, they had evidence of intracranial hypertension and observe in the vast majority of patients and that the five cases
went on to die or have poor outcomes. Furthermore, CT scan reported with early diffuse hypodensities are unusual. Hence,
hypodensities have been described within 5 hours of proven a question regarding possible child abuse in some of our cases
middle cerebral artery occlusions, and extensive hypodensities was, and still would be, appropriate. However, the knowledge
associated with local brain swelling in the middle cerebral that obvious and diffuse intracerebral low densities on CT scan
artery distribution predicted a fatal outcome (17). In two of can occur, albeit rarely, as early as 1 hour after a documented
our five patients, absent CBF was demonstrated, and it may be accidental head injury may have allayed some of the concerns
that extensive low densities on CT scan can occur rapidly, even regarding the possibility of non-accidental injury in these chil-
as early as 1 hour after trauma, in special and unusual situa- dren. Furthermore, in cases of suspected non-accidental fatal
tions in which there is total ischemia with no blood flow into head injury in which the time of the head injury is not clear, the
the brain. If so, these findings may predict inevitable brain possibility of very early appearance of diffuse low densities on
death, as occurred in all of the patients reported in this article. the CT scan has to be considered in the estimation of the tim-
The outcomes of our patients are consistent with those reported ing of the severe head injury.
by Han et al. (11), who noted that four out of eight children
(five had head trauma) with acute reversal sign on CT scans CONCLUSIONS
died; the other four children had poor outcomes.
The occurrence of acute obvious diffuse cerebral hypodensity We have presented five children with documented and well-
is rare among head-injured patients, and, on the basis of the lack corroborated accidental head injuries in whom CT scans per-
of reports in the literature, this is probably a rare phenomenon. formed between 1 and 5 hours after injury showed diffuse and
It is difficult to understand why these five patients developed obvious cerebral hemispheric hypodensity. These findings call
this problem. The mechanism of injury, which included a fall into question the commonly held opinion that such extensive
down stairs and a fall from a stool, was less severe than in many parenchymal hypodensities take at least 6 hours to appear after
other head-injured patients. Nonetheless, all patients clearly head trauma. This may be of medicolegal importance in discus-
experienced a severe brain injury with immediate coma and a sions regarding the timing of head injuries in children. It is
poor GCS score and went on to die rapidly. It was somewhat important to recognize that, in our series, diffuse early hypo-
unexpected that, in the two autopsied patients, despite the densities on CT scan were associated with a severe traumatic
apparent clinical severity of the brain injury, neither showed brain injury, immediate unconsciousness that never resolved,
histopathological evidence of diffuse axonal injury and one had and rapid brain death in all patients. It is inappropriate to gen-
findings of axonal injury limited to the cervicomedullary junc- eralize the findings of this case series to patients who are not
tion. It would be interesting to elucidate the factors that may unconscious immediately after a head injury, who regain con-
have precipitated the disastrous outcome in these children. sciousness after an injury before deteriorating, or who do not
The findings in this study of extensive CT scan intracerebral progress rapidly to brain death.
hypodensities within 5 hours of a well-documented head injury
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COMMENTS
T his article highlights the early changes on CT scans that may occur
after severe head trauma and appropriately points out that such
T his report describes five children who were found to have diffuse
hemispheric low density within 5 hours of well documented acci-
dental blunt head trauma. In the past, it has been more or less assumed
changes may occur earlier than has been touted by timing pundits.
The authors make an important point that the low attenuation changes
cannot be used to establish that the onset of the damage had to occur
that this finding was diagnostic of child abuse and that it took 6 to 24
6 to 12 hours before the changes but that they may occur within 1 to 2
hours to develop, although loss of the gray-white junction could be
hours. Diffusion imaging and diffusion tensor magnetic resonance
seen earlier.
imaging have established these facts. Now, in severe trauma cases, the
This report is significant in several regards. The fact that all of these
same has been established for CT scans.
children had clear blunt trauma rather than shaking lends further sup-
port to the hypothesis of impact being required to develop this clinico- Marvin Nelson
radiographic picture, as proposed by Duhaime (1). It is important that Pediatric Neuroradiologist
the finding of diffuse hemispheric low density is not diagnostic of Los Angeles, California
nonaccidental trauma, and this finding alone does not demand this
diagnosis. The recognition that retinal hemorrhages are also not neces-
sarily diagnostic of child abuse makes this diagnosis difficult at times.
A thorough investigation of the circumstances of a childhood injury is
T his study documents early hypodensity in accidental head injury in
five children on CT scans obtained within 5 hours of the injury.
The children were very young (< 2 yr of age), had evidence of very
needed before accusations are made. Finally, this finding carries a uni- poor clinical grade (Glascow Coma Scale score, 3–5), and severely
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7. COMPUTED TOMOGRAPHIC SCAN HYPODENSITIES AFTER HEAD INJURY
increased intracranial pressure, and all died. The finding of “black” edema would be unusual. Early low density has also been reported in
cerebral hemispheres on CT scans is always an ominous sign and, as nonaccidental injury in which the timing issues are much harder to
the authors discuss, probably represents irreversible global cerebral document. When this issue was raised in this series, the patients were
ischemia. Distinguishing this radiological finding from that seen after appropriately investigated by the child protection team.
nonaccidental injury can be difficult. Two of the children were reported
to have fallen down stairs (and had retinal hemorrhages) or from a James M. Drake
stool, both instances in which a rapidly fatal outcome with extensive Toronto, Canada
NEUROSURGERY VOLUME 60 | NUMBER 4 | APRIL 2007 | 695