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Short communication
Middle Cerebral Artery Dissection
By Coleen dams' and Cynthia ~ r e v e n e d

A 12-year-oldgirl had minor head trauma,
with resultant mild headache, one day prior to onset of an
apparently generalized tonic clonic seizure, right herniparesis and dysphasia.A cranial CT scan showed evidence of a
left middle cerebral artery infarct. Despite ventilation, fluid
restriction, mannitol, thiopental infusion and intracranial
pressure monitoring she deteriorated and died. Autopsy
demonstrated dissection of the Ieft middle cerebral artery
with an intact internal carotid artery and no evidence of
vasculitis. Middle cerebral artery dissection in children is
very rare. Most reported cases are diagnosed at autopsy. The
pathogenesis of cerebral artery dissection may include preceeding minor head trauma or exertjon and this should be
sought for in the history.

Key words
Childhood stroke - Cerebral artery dissec-

Mddle cerebral artery (MCA) dissection in
children is rare. We present this case to demonstrate the
diffculty in diagnosis and to increase awareness of this as a
cause of ischemic stroke.
Case report

A 12-year-old girl presented with a seizure,
right hemiparesis and reduced level of wnsciousness. The day
prior to the seizure she had minor trauma, hitting her head on a
coffee table, without loss of consciousness.
resulted in a
small abrasion and headache but she continued to have an
active day. The following day she had an apparently generalized
10-minute tonic-clonic seizure. Subsequently she was drowsy
and confused with dysphasia and a right hemiparesis.
She had previously been well with no history of
seizures, congenital heart defect or evidence of a coagulopathy.
She was taking no medication. There was no family history of
seizures or thrombotic disorder.
An initial cranial computerized tomography
(CT) scan a few hours after seizure onset showed early evidence
of a left MCA infarct with hypodensity in this region. On

admission she had blood pressure 160/100 mmHg and heart
rate 88/rnin. No cardiac or carotid or cranial bruits were heard.
She was intubated but was able to respond appropriately to her
parents' faces and requests. She had a gaze preference to the left
and a right hemiparesis involving the face, arin and leg.
Examination of the cerebrospinal fluid showed protein
0.25 gA,no WBC, 14 x106/l RBC and negative bacterial and
viral culture. Blood culture was sterile. Serum electrolytes,
glucose, calcium, urea and creatinine were normal. Blood count
was normal apart born slightly reduced platelets at 1 3 3 x 1 0 ~ ~ .
Pmthrornbin time and activated partial thromboplastin time
were normal. Sedimentation rate was 4 rnm/hr and anti-nuclear-antibody (ANA) and anti-cardiolipin antibody were neIl (chromogenicand antigen) and protein
gative. Antithrombin J
S antigen (total and free) were normal. Protein C activity and
antigen were both borderline low. hothrombin antigen, thornbin time and plasrninogen were normal. Plasma amino acids,
cholesterol and triglycerides were normal and no abnormalities
were detected on electrocardiogram and transthoracic echocardiogram. Electroencephalogram (EEG) showed marked slowing over the left hemisphere and normal right hemispheric
activity.
She initially improved sl~ghtlybut 29 hours
after her seizure she deteriorated with a drop in heart rate,
dilatation of the left pupil and reduced level of consciousness.
On examination she did not have papilledema but venous
pulsations of the left optic drsc were absent. Extraocular movements and corneal rdexes were present. She had response to
pain on the left side only. A repeat CT scan at that time showed
a much larger area of Infarction with midline shift (Fig. 1). She
was treated with mannitol, fluid restriction, hyperventilation
and intracranial pressure monitoring with thiopental &on
to produce a burst suppression pattern on EEG. She was not
Dven anticoagulants. A repeat cranial CT scan 2 days later
showed further increase in the area of darction and midline
duft and effacement of the basal cisterns. She continued to
deteriorate, developing diabetes insipidus. Five days after her
admission she was brain dead with absent cerebral perfusion on
nuclear brain scan.
At autopsy sections from all the cerebral arteries were examined. These demonstrated dissection of the left
MCA and no involvement of the internal carotid artery (ICA)
(Fig. 2). The smooth muscle of the media was elsewhere histologically unremarkable with no evidence of vasculitis. There
was infarction of most of the left cerebral hemisphere with
cerebral edema, cerebellar tonsillar herniation and ischemic
necrosis of the anterior lobe of the pituitary.

Received October 28, 1996; accepted November 18,1996
Neuropediatrics 27 (1996)331-332
@ Hippokrates Verlag Stuttgart

Seven children wjth intracranial artery dissection were reported recently (8).All patients had an ischemic

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'Pediatric Neurology and 'Pediatric Pathology, AIberta Childrens Hospital, University of Calgary, 1820 Richmond Rd SW,Calgary,
Alberta, T2T 5C7, Canada

332 Neuropediatrics 27 (1996)
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suggested that trauma may predispose a minor congenital
defect to dissection (9). This may add to the increased incidence
of intracranial artery dssections in the younger age group (8).
Also reported are gap defects in the internal elastic lamina near
the site of dissection in adults and this author postulated that
the gap defects underlies the spontaneous dissection in arteries
(12).Primary arterial diseases such as fibromuscular dysplasia
have been suspected or described although some patients have
no pathological change (6).
Anticoagulation therapy is usually recommended in patients with ischemic symptoms in the absence of
intracranial hemorrhage or an already completed major a c t .
Intracranial artery dissections usually have diagnosis made at
postmortem, reflectmg the ~ c u l t of
y making an antemortern
diagnosis and institutmg therapy. Thls may account for the
poorer prognosis than is seen in extracranial dissections.Early
angiography has been suggested in childhood stroke to assess
for dissection and consider anticoagulation (10).In retrospect
in this case the minor head trauma and headache were clues to
the etiology and an anaogram may have given the diagnosis
prior to death. However the mfarct was large and already
completed at the time of the initial CT scan and anticoagulant
therapy would have been contraindicated. Surgical intervention
and repair of the aneurysm is generally reserved for patients
with a subarachnoid hemorrhage due to an intracranial dissecting aneurysm or those with embolus fkom an extracranial
dissecting aneurysm (8).
In conclusion it is important to remember
intracranial artery dissection as a cause of stroke in children
especially in the context of minor head trauma or exertion
accompanied by headache. Early angiography may be helpful
in these circumstances to guide management.
References
Chang, V., N. B. Rewcastle, D. C. E Hanuood-Nash, M. G. Norman:
Bilateral h c t i n g aneurysms of the intracranial internal carotid Wries
in an 8-year-oldboy. Neurology 25 (1975) 573-579
Deck, 1. H. N.: Pathology of spontaneous dissection of intracranial
arteries. Can. J. Neurol. Sci. 14 (1987) 88-91

Hochberg, E H., C. Bean, M. Fisher, G. H. Robmon: Stroke in a 15year-old girl secondary to terminal carotid dissection. Neurology 25
(1975) 726-729
Jacob, 1. C., F. B. Maroun, W. D. Heneghan, A. M. House: Uncommon
cerebmvascular lesions in children. Dev. Med. Child. Neurol. 12 (1970)
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Manz, H. I., J. Vester, B. Lnuensfein: Dissecting aneurysm of cerebral
Fig. 2 Cross sectlon of the left middle cerebral artery showlng acute1
arteries in childhood and adolescene. VU~IOWS
Arch. (Pathol. Anal.)
dissection with elevation and displacement of the Internal elastic lamlna
384 (1979) 325-335
larrowl by erythrocytes, fibrin and entrapped neutrophlls. The lumen Is
Mokri, B.: Dissections of C ~ M C and
~ cephalic arteries. In: Sundt, T. M.
virtually obliterated by this process.This Is a van Glesorls elastic Stain with
Jr. (ed.): Occlusive Cerebrovascular Disease: Diagnosis and Surgical
origlnal magnification X 25.
Management. Philadelphia, WB Saunders (1987) 38-59
Nass, R., A. Hays,A. Chuforian: Intracranial dissecting aneurysms in
childhood. Stroke 13 (1982) 204-207
Schievink, W.I., B. Mokri, D. G. Piepgras: Spontaneous dissections of
preceded by headache. Seizures occurred in 2. physical
cwicocephalic arteries in childhood and adolescence. Neurology 44
exertion
onset in 3 and one had hypertension and co(1994) 1607-1612
arctation of the aorta. AngiOgraphy in showed an
Scott, G. E., K. T. Neuberger, 1. Denst: Dissecting aneurysms of the
area of irregular stenosis. Treatment consisted of antiplatelet
inWacranid arteries. Neumlogy 10 (1960) 22-27
therapy in 2 and supportive measures in 5. One boy died and 'O Wood, E. 19, S. Churmg: The important of early angiography in the
investigationof childhood stroke. Can. J. Neurol. Sci. Suppl. 2 (1993)S14
&-tion
of the right distal TCA and
autopsy

proximal branches of the right MCA. In autopsy reports of
children with dissection of the MCA or dutal ICA in all cases the CoIeen Adams, M. B.
plane of dssection is between the internal elastic lamina and Alberta
Hospital
the media, rather than within the media as is seen with cervical 1820 Richmond Rd SW
carotid and aortic dissection (1, 3, 4, 5, 7). Mmor preceding a g a r y , ~lbertaT ~ 5c7
T
trauma, as in the present case, is offen noted. It has been Canada

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Fig. 1 Cranial CT scan 29 hour; after her seizure. This shows a large
hypodense area representing Infarction of the left middle cerebral artery
distribution [anowl. There is mldline shlft t o the rlght and effacement of
the left lateral ventrlcle.

Coleen Adams and Cyn thin Trevenen