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Bilateral anterior cerebral artery infarction resulting from explosion-type injury to the head
and neck.
J H Lipschutz, R M Pascuzzi, J Bognanno and T Putty
Stroke. 1991;22:813-815
doi: 10.1161/01.STR.22.6.813
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813
Case Report
Bilateral Anterior Cerebral Artery
Infarction Resulting From Explosion-Type
Injury to the Head and Neck
Joshua H. Lipschutz, MD; Robert M. Pascuzzi, MD;
James Bognanno, MD; and Tim Putty, MD
A 43-year-old woman suffered a blast-type injury to the head and neck. She subsequently
developed bilateral internal carotid artery occlusion and bilateral anterior cerebral artery
infarction not demonstrated by magnetic resonance imaging scan 24 hours after the explosion,
but confirmed by a second scan 8 days after the explosion. In patients with blast-type injury to
the head and neck who develop coma with a nonfocal neurological exam, the possibility of
bilateral carotid artery occlusion and bilateral ischemic infarction should be considered.
C
arotid artery occlusion is a well-recognized,
although infrequent, complication of nonpenetrating trauma to the head and neck.1-3
We report a patient who suffered a blast-type injury
to the head and neck and subsequently developed
bilateral internal carotid artery occlusion and bilateral anterior cerebral artery infarction.
Case Report
A 38-year-old woman with a history of mild hypertension and Graves' disease was preparing Christmas
dinner for her family when, in attempting to light her
gas stove, the stove exploded, producing minor burns
to her neck, face, and scalp. There was no loss of
consciousness. She was noted initially to be fully alert
and neurologically intact, with first- and seconddegree burns on the face, ears, scalp, posterior neck,
and upper back estimated to cover approximately 4%
of the total body surface area. Eleven hours after the
explosion, she became acutely unresponsive and developed episodic decerebrate posturing with episodic
hypertension. She had slow roving conjugate eye
movements, normal pupillary reaction, normal funduscopic examination, and symmetric lower cranial
nerve function. Bilateral limb hypertonia, hyperactive reflexes, and extensor toe signs were present.
Emergency computed tomogram of the head with
and without contrast was normal. An electroencephalogram showed mild diffuse slowing. Intracranial pressure, cerebrospinal fluid profile, screens
From the Departments of Internal Medicine (J.H.L.), Neurology (R.M.P.), Radiology (J.B.), and Neurosurgery (T.P.), Indiana
University School of Medicine, Indianapolis, Ind.
Address for correspondence: Robert M. Pascuzzi, MD, 1001 W.
10th St., 6th Floor, Indianapolis, IN 46202.
Received November 5, 1990; accepted March 1, 1991.
for metabolic disturbance, standard toxicological
screens, Westergren sedimentation rate, antinuclear antibodies, thryoid function tests, blood cultures, and echocardiogram were all within normal
limits. Magnetic resonance imaging was performed
24 hours after the explosion and was read initially
as normal, although, in retrospect, there was a
faintly increased signal in the cortical gray matter of
the anterior cerebral artery distribution. A single
photon emission computed tomogram 4 days after
the explosion showed bifrontal perfusion defects. A
second magnetic resonance imaging scan 8 days
after the explosion showed large bilateral frontal
and parasaggital abnormalities indicative of acute
ischemic infarction in the anterior cerebral artery
distribution (Figure 1). Mild abnormalities were
seen in patchy fashion in territories supplied by the
lenticulostriate arteries. A cerebral angiogram
demonstrated narrow internal carotid arteries distal
to the carotid bifurcation, with abrupt occlusion of
the internal carotid arteries bilaterally just distal to
the ophthalmic arteries (Figure 2). Over the next 4
weeks, the patient's neurological status remained
unchanged. She became septic from a urinary tract
infection and died 7 weeks after the explosion.
Discussion
Carotid artery occlusion due to nonpenetrating
trauma is uncommon and was first described by
Verniel in 1872.4 Although carotid arterial trauma
accounts for approximately 10% of all arterial injuries in both civilian2 and military practice,1 only
3-5% of carotid arterial injuries are due to nonpenetrating trauma. Rubio and associates5 reviewed 72
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814
Stroke
Vol 22, No 6 June 1991
FIGURE 1. Long repetition time, long echo time axial
magnetic resonance image obtained on day 8. Extensive
symmetric edema in the anterior cerebral artery distribution and the lenticulostriate distributions, right greater
than left (arrows).
cases of carotid arterial trauma in which only two
were caused by nonpenetrating injuries.
Accurate diagnosis of carotid arterial injury due to
nonpenetrating trauma at the time of hospital presentation is difficult. In a compilation of 96 cases by
Krajewski and Hertzer,6 only 6% of the patients with
carotid arterial injury due to nonpenetrating trauma
had symptoms within 1 hour after injury. Most developed symptoms within 24 hours, but 17% had no
symptoms for days or weeks after the injury. Symptoms included aphasia, altered consciousness, seizures, and motor and sensory disturbances.
Bilateral anterior cerebral artery occlusion with
resultant frontal lobe lesions, as occurred with our
patient, can produce akinetic mutism7 and coma.8
Although the lesions are primarily in the frontal
lobes, they may result in more widespread disruption
of hemispheric function. Plum and Posner8 note that
large, deep, midline frontal lesions in humans interrupt the major reciprocal pathways that interconnect
the frontal lobe with the thalamus, the amygdala, and
the midbrain. Such interruptions not only affect
frontal lobe function directly but secondarily influence large parts of the remaining neocortex that
normally receive cortical-cortical connections and
limbic modulation transmitted via the frontal lobe.8
These effects could account for the coma seen in our
patient.
The source of trauma is probably the principal
factor that determines the site of carotid injury.6 A
blow to the head initiating sudden hyperextension
and rotation or lateral flexion can stretch the distal
internal carotid artery across the transverse processes of the first three cervical vertebrae, leading to
distal internal carotid arterial injury. This occurs
more commonly in young people, probably because
of the fact that in elderly patients, the carotid arteries
are more tortuous and tend to straighten rather than
stretch when sudden hyperextension and rotation
occurs.1 Focal disruption of the intima providing a
nidus for thrombus formation may be the mechanism
for carotid arterial occlusion after nonpenetrating
trauma, especially when the injury involves sudden
hyperextension of the neck.9 Our patient may have
suffered sudden hyperextension of the neck caused
either by the force of the blast or as a reaction to the
blast. The symmetry of the force could account for
the bilaterality of the internal carotid arterial occlusion. Internal carotid arterial dissection could have
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Lipschutz et al
Bilateral Anterior Cerebral Artery Infarction
815
FIGURE 2. Late phase of the
left internal carotid angiogram
(day 10). Occlusion of the internal carotid artery just distal to
the ophthalmic artery is present
(arrow). Collateral filling of the
anterior falx artery via ethmoidal
branches of the ophthalmic artery is present (arrowheads).
Some reflux into the external carotid circulation was encountered (open arrows).
occurred in our patient even though it was not
demonstrated on the angiogram.
Several features of this case are noteworthy. Bilateral internal carotid arterial occlusion is rare and, to
our knowledge, has never been described in the
setting of a blast-type injury. In a review by Scherman
and Tucker,3 only 11 cases of bilateral internal carotid arterial occlusion have been reported, and in
only two of these was there complete occlusion of
both internal carotid arteries, as occurred with our
patient. Additionally, our patient had extensive bilateral anterior cerebral artery infarction in association
with the carotid arterial occlusion. Acute internal
carotid arterial occlusion more commonly produces a
middle cerebral artery infarction rather than an
anterior cerebral artery infarction.1'2
The reason for the anterior cerebral artery involvement in our case is unclear. Acute thrombus in the
internal carotid artery may have embolized into the
anterior cerebral artery. Alternatively, acute internal
carotid arterial occlusion may have produced anterior
and middle cerebral artery involvement, with the
latter having sufficient collateral blood flow to limit
the infarction to the anterior cerebral artery territory.
Regarding treatment, when the diagnosis is delayed and the ischemic infarction completed, as
occurred with our patient, there is little to be gained
from carotid reconstruction, and hemorrhagic cerebral infarction could occur after revascularization.6
Although acute heparinization shortly after the detection of carotid arterial injury might logically limit
the propagation of thrombus, several anecdotal reports of subarachnoid hemorrhage as well as progres-
sion of ischemic deficit during treatment
suggest
caution with early anticoagulation.10
In summary, in patients who suffer a blast-type
injury to the head and neck and who subsequently
develop coma with a nonfocal neurological exam, the
possibility of bilateral carotid artery occlusion and
bilateral ischemic infarction should be considered in
the differential diagnosis.
References
1. Davis JM, Zimmerman RA: Injury of the carotid and vertebral
arteries. Neuroradiology 1983;25:55-69
2. Mooney RP, Bessen HA; Delayed hemiparesis following nonpenetrating carotid artery trauma. Am J Emerg Med 1988;6:
341-345
3. Scherman BM, Tucker WS: Bilateral traumatic thrombosis of
the internal carotid arteries in the neck: A case report with
review of the literature. Neurosurgery 1982;10:751-753
4. Verniel M: Contusion multiples; delire violent; hemiplegie a
droite, signes de compression cerebrale. De LAcademie De
Medicine (Paris) 1872;l:46-56
5. Rubio PA, Ruel GJ, Beall AC Jr, Jordan GL Jr, DeBakey ME:
Acute carotid artery injury: 25 years experience. / Trauma
1974; 14:967-973
6. Krajewski LP, Hertzer NR: Blunt carotid artery trauma:
Report of two cases and review of the literature. Ann Surg
198O;191:341-346
7. Freemon FR: Akinetic mutism and bilateral anterior cerebral
artery occlusion. / Neurol Neurosurg Psychiatry 1971;34:
693-697
8. Plum F, Posner J: The pathologic physiology of signs and
symptoms of coma, in The Diagnosis of Stupor and Coma, ed 3.
Philadelphia, FA Davis Co, 1982, pp 24-26
9. Crissey MM, Bernstein EF: Delayed presentation of carotid
intimal tear following blunt craniocervical trauma. Surgery
1974;75:543-549
10. Hart RG, Easton JD: Dissections and trauma of cervicocerebral arteries, in Barnett HJM, Mohr JP, Stein BM, Yatsu FM
(eds): Stroke: Pathophysiology, Diagnosis, and Management
New York, Churchill Livingstone, Inc, 1986, pp 775-788
KEY WORDS • carotid artery diseases • cerebral infarction
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