Hemispheric Cerebral Ischemia in Traumatic Brain Injury : A Report of Four Cases

135
Case Report
Indian Journal of Neurotrauma (IJNT)
2005, Vol. 2, No. 2, pp. 135-138
Hemispheric cerebral ischemia in traumatic brain injury: A
report of four cases.
Y R Yadav M Ch, Sanjay Pandey M Ch, Alok Agrawal M D*
Departments of Neurosurgery and *Radiodiognosis
NSCB Medical College Jabalpur and Hospital, Jabalpur (MP)
Abstract: Vascular injury to brain as a secondary phenomenon is not uncommon in head injury. Abnormality
in cerebral blood flow after head injury is well documented. There are plenty of reports of focal vascular
insults in head injury; however hemispheric ischemia is not reported so far to the best of our knowledge.
Four patients of hemispheric ischemia were treated in last 13 years time out of the total of 13167 patients
admitted for head injury. Three patients were males of six months, 30 years and 34 years of age while
the fourth patient was a 10-year-old-female. Road traffic accident, assault and fall from height were the
mode of accident in these cases. Both the adults died while both the children survived with gross
neurological deficits. All four patients had subarachnoid and subdural hematomas along with evidence
of hyperextension injury suggested by abrasion on forehead. Severe form of vascular injury like
hemispheric ischemia is rare. Subarachnoid and subdural hematoma and hyperextension injuries could
be risk factors. Prognosis is poor. There is a need to identify a subgroup of patients at risk of such
complications.
Keywords: cerebral infarction, secondary brain injury, traumatic hemispheric cerebral ischemia, vascular
insult
INTRODUCTION
and on the vertex. There was no external evidence of injury
on neck. He was hyperventilating with rate of 44 per minute
Cerebral ischemia is an important contributor to increased
and there were bilateral coarse crepitations in the chest.
morbidity and mortality in patients of head injury. The
He was intubated and ventilated. CT scan showed right
importance of cerebral vascular dysfunction in the patho-
fronto-parietal thin acute subdural haematoma with right
physiology of brain injury, the effect of trauma on cerebral
fronto parieto-temporo-occipital (hemispheric)
circulation has been well studied1,2. The exact incidence is
hypodensity involving the grey white matter sparing basal
not known. Isolated cerebro-vascular injury is thought to
ganglia region suggestive of ischemia with gross midline
be quiet common but we have not come across any
shift (Figure 1). Hypodensity extended on other side
reference of the global hemispheric cerebral ischemia.
adjacent to falx. Subarachnoid bleed in interhemispheric
However diffuse vascular injury was observed in about
fissure was also seen. Tiny hemorrhagic contusions were
11% of patients with fatal diffuse axonal injury2. We are
also seen in the right cerebral convexity. Patient was also
reporting four such patients of diffuse vascular injury
put on osmotic diuretics and ventilation was continued.
producing unilateral hemispheric ischemia.
Inspite of treatment, patient deteriorated and died 17 hours
CASE REPORT
Case 1
A thirty-four-year old male presented with alleged history
of assault by a hard and blunt object.He was unconscious
since injury, and his GCS on admission was 4/15 (E V M ).
1
1
2
There was no history of hypertension, diabetes mellitus
or any cardiac illnesses.His pupils were 4 mm in size, dilated
and not reacting to light bilaterally. He had also developed
left sided hemiplegia following the assault. There were
abrasions and diffuse swelling on forehead on either side
FIGURE 1 : Axial CT shows hypo density involving the grey white matter
Address for correspondence : Y R Yadav M Ch, 105 Nehru Nagar,
of the right fronto parietal and temporo occipital region. There is interhemispheric
Opposite Medical College, Jabalpur MP 482003
subdural bleed, brain swelling ,midline shift and uncal herniation with
E-mail: yadavyr@yahoo.co.in
hypodensity on other side adjacent to falx
Indian Journal of Neurotrauma (IJNT), Vol. 2, No. 2, 2005

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136
Y R Yadav, Sanjay Pandey, Alok Agrawal
after the injury.
Case 2.
A six-month-old male child had a fall from bed of about 2
feet in height, and became unconscious. He had an episode
of generalized tonic-clonic seizures after the fall, and at the
time of admission, GCS was 5/15 (E V M ). Pupils were 2
1
1
3
mm in size and reacting to light. He was not moving his
right side. There was abrasion on left side of his forehead,
and his vitals were stable. There was no external evidence
of neck injury. CT scan showed left sided fronto-parieto-
FIGURE 3 : Follow up axial CT shows interval development of left
hemispheric atrophy and chronic left sided subdural collection.
Case3.
A 30-year-old-male was brought in 20 hours after a road
traffic accident. He had developed hemiplegia on the right
since the time of the accident, and had become unconscious
3-4 hours after the accident. He had one episode of
generalized seizures, and vomited 5-6 times. There was no
history of hypertension, diabetes mellitus or any cardiac
illnesses. On admission his GCS was 4/15 (E V M ), pupils
1
1
2
were fully dilated and sluggishly reacting to light. There
were abrasions on right side of his forehead. There was no
FIGURE 2 : Axial CT shows extensive hypodensity involving the
external evidence of injury in neck. CT showed thin subdural
grey white matter of the left fronto parietal and temporo occipital
region.
hematoma in left fronto- parietal region with left hemispheric
hypodensity and midline shift of 12 mm (Figure 4). There
temporal thin acute subdural haematoma and hemispheric
hypodensity suggesting of ischemia (Figure 2). There was
blood in posterior part of interhemispheric fissure. He was
put on conservative management with frusemide and
antiepileptic drugs. Doppler for neck vessels revealed
normal blood flow through both the internal and external
carotids. Patient showed gradual improvement for 20 days
after which his neurological status plateaued. Repeat CT
showed chronic subdural hematoma in left fronto-parietal
region, which was managed by repeated tapping. He
showed gradual improvement in sensorium and partial
resolution of weakness in right half. He was discharged
three weeks after the injury with spontaneous eye opening,
no verbal response and right-sided hemiparesis. Child
showed gradual improvement in his hemiperesis and
speech at follow up. CT done after two years showed
cerebral atrophy of left hemisphere with ipsilateral
ventriculomegaly (Figure 3). Child is having hemiperesis
(power grade 3-4 in proximal group and 1-2 in distal group).
He is able to speak few words only with spastic speech,
however his comprehension is fairly good. He is able to
perform his daily activity without any help. His school
FIGURE 4: Axial CT showing extensive hypo density involving
performance is below average
the grey white matter of the left fronto parietal and temporo
occipital region including the ipsilateral basal
ganglia.interhemispheric subdural bleed, brain swelling, midline shift
and uncal herniation is also seen.
Indian Journal of Neurotrauma (IJNT), Vol. 2, No. 2, 2005

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Hemispheric cerebral ischemia in traumatic brain injury: A report of four cases.
137
was blood in the interhemispheric fissure. He was intubated
Based on the observations of forehead bruise in all cases
and hyperventilated and mannitol and frusemide were
and associated unilateral injury to the lateral aspect of the
administered. There was no response to treatment, and the
skull in two of our cases we propose that hyperextension
patient deteriorated and died 30 hours after the accident.
and rotation mechanism leading to dissection/thrombosis
of intracranial portion of carotid artery could be the cause
Case 4:
of vascular injury in our cases. Association of subarachnoid
A ten-year-old girl sustained head injury in a road traffic
bleed and subdural hematoma in all our cases suggest that
accident. She became unconscious immediately after the
vasospasm could also be responsible for ischemia. The
accident. There was no history of seizures or ear, nose and
posterior cerebral artery (PCA) involvement could be
throat bleeding. There was no history of hypertension,
explained on the basis of either compression of the vessel
diabetes mellitus or any cardiac illnesses. Her Glasgow coma
in the ambient cistern secondary to midline shift or to the
scale was 4/15 (E M V ), and pupils were normal sized,
fetal origin of the PCA. The anterior cerebral artery (ACA)
1
2
1
reacting to light. There was no external evidence of injury
involvement could be due to absence of anterior
in neck. She had abrasions on right forehead. CT done on
communicating artery. In one of our patient evidence of
the day of injury showed normal-sized ventricles including
ischemia was not there in first CT scan suggesting that it
basal cisterns. There was subarachnoid hemorrhage in
was secondary insult which can be prevented. Doppler
posterior interhemispheric fissure. Her condition remained
study of the neck vessel was possible in only two cases,
status quo for the next 5 days. MRI of brain was done
which did not show any lesion in the neck, other two cases
looking to her very minimal findings in CT and poor
were in very poor condition and both of them died before
neurological status. MRI revealed gyral swelling and signal
these investigations could be done.
alteration in left hemisphere. Gyral signal alterations were
Although exact incidence and pathophysiology of
hyper intense in T2 and FLAIR and iso to hypo intense in
cerebral ischemia is not known, however various
T1-weighted images. Left lateral ventricle was effaced. There
pathological finding were reported in the literature. Varying
was minimal subdural bleed in bilateral temporal lobe and
degree of cerebral ischemia in head injury has been
adjacent right cerebellum(Figure 5). She was shifted to our
reported1,2,3. Intravascular thrombosis has been associated
hospital for further treatment, and was put on frusemide,
with ischemia4. Multiple cerebrovascular abnormalities
mannitol and anticonvulsants. Doppler for neck vessels
including subarachnoid hemorrhage, focal platelet
revealed normal blood flow through both carotids in its
accumulation, and severe ischemia are seen in traumatic
course in the neck. She showed gradual neurological
brain injuries5. Three stages of hemodynamic changes are
recovery, and repeat CT done after 28 days of injury showed
observed in severe head injury: hypoperfusion, hyperemia
and vasospasm. Isolated vascular injury like infarct in
distribution of artery of Heubner is well reported6. Diffuse
vascular injury has been reported in 11.7% of patients in
fatal diffuse axonal injury2. Vascular endothelial growth
factor was increased in CSF after brain injury suggesting
that vascular injury occurs in head injury patients7.
Microvascular basal lamina damage was also seen in brain
injury. Ischemic damage in intracranial hematomas was
thought to be more commonly due to artery compression
secondary to brain shift and herniation8.
Pathophysiological studies in traumatic brain injuries
revealed primary membrane damage to neuronal cell bodies,
FIGURE 5 : T2W axial images reveal gyral swelling and hyper
white matter structure and vascular beds due to shear
intensity of the left cerebral hemisphere.
forces. These injuries were similar to strokes.
infarct in left occipital lobe. GCS at the time of discharge 45
The definite evidences of proof of benefit of any drug
days later was E M V . There was right-sided hemiparesis
4
6
2
altering coagulation in human being are lacking.
with power grade 1-2 in proximal joints and no power in
Enoxaparin reduced brain edema, cerebral lesions, and
distal joints. She was advised physiotherapy and to come
improves motor and cognitive impairments induced by
for follow up after one month.
traumatic brain injuries in rats9. However in the other study
DISCUSSION
antithrombin treatment in patients with traumatic brain
injury resulted only in marginal reduction of hyper
Indian Journal of Neurotrauma (IJNT), Vol. 2, No. 2, 2005

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138
Y R Yadav, Sanjay Pandey, Alok Agrawal
coagulation, and could not produce any obvious influence
in traumatic brain injury.
on the progression of brain injury, on CT scan, on outcome
Neurosurgery 2004; 53 : 687-91
or time needed for intensive care10. Early and late
5.
Dietrich WD, Alonso O, Busto R, Prado R, Zao W, Dewanjee
intravenous infusion of nor epinephrine has is seen to
MK, Ginsberg MD. Posttraumatic cerebral ischemia after fluid
percussion brain injury: an auto radiographic and
increase cerebral perfusion in rats11, and this can also be
histopathological study in rats.
used as a treatment option to decrease ischemic insult to
Neurosurgery 1998; 43:585-93.
the brain. L- Arginine was found to improve
6.
Fujimura M , Kameyama M, Motohashi O, Kon H, Ishi K,
microcirculation in missile injury which was decreased in
Onuma T. Cerebral infarction in the caudate nucleus associated
early stage of injury in an experimental study on cats12.
with acute epidural haematoma and diffuse brain injury in a
child after severe head injury.
Routine use of methods detecting cerebral blood flow
Childs Nerv Syst 2004; 20:430-3.
in head injury can identify subgroup of patients in all head
7.
Shore PM, Jackson EK, Wisniewski SR, Clark RS, Adelson PD,
injury likely to get secondary insult due to vascular insults.
Kochanek PM. Vascular endothelial growth factor is increased
It has been seen that the post concussion syndrome in
in cerebrospinal fluid after traumatic brain injury in infants
mild head injuries could be due to vascular insults.
and children.
Hyperventilation or lowering of blood pressure can in fact
Neurosurgery 2004: 54:605-11.
be detrimental in such cases13.
8.
Abe M, Udono H, Tabuchi K, Uchino A, Yshikai T, Taki K.
Analysis of ischemic brain damage in cases of acute subdural
CONCLUSION
Hematomas.
Surg Neurol 2003; 59:464-72.
There is a need to identify subgroup of patients at risk of
9.
Wahl F, Grosjean-Piot O, Bareyre F, Ujan A, Stutzmann JM.
vascular complications by use of methods detecting
Enoxaparin reduces brain edema, cerebral lesions, and improves
cerebral blood flow. Association of hyperextension and
motor and cognitive impairments induced by traumatic brain
rotation injuries, patients with subarachnoid hemorrhage
injuries in rats.
and subdural hematoma in such patients may point towards
J Neurotrauma 2000; 17:1055-65.
certain path physiological mechanism. Management
10. Grenander A, Bredbacka S, Rydvall A, Aroch R, Edner G,
strategies useful in prevention of such insults and early
Koskinen LO, Olivecrona M. Antithrombin treatment in
patients with traumatic brain injury: a pilot study.
management of such complications when they occur can
J Neurosurg Anesthesiol 2001; 13:49-56.
improve prognosis.
11. Kroppenstedt SN, Thomale UW, Griebenow M, Sakowitz OW,
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Indian Journal of Neurotrauma (IJNT), Vol. 2, No. 2, 2005

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