Background and Purpose-Internal carotid artery dissection (ICAD) is a
frequent cause of ischemic stroke in young patients. Whether cerebral
ischemia is of embolic or hemodynamic origin remains to be determined.
Heparin is often administered in ICAD; however, a drug trial can hard
ly be conducted because of the low recurrence rate after the acute sta
ge. Therefore, the best therapeutic approach should be determined on t
he basis of the presumed mechanism of cerebral ischemia. One way to ap
proach the mechanism of stroke in ICAD is to determine stroke patterns
. We postulated that most cortical and large subcortical infarcts (gre
ater than or equal to 15 mm) are of embolic origin and that small subc
ortical infarcts (<15 mm) and junctional infarcts are not. The aim of
our study was to determine the stroke patterns in 40 consecutive patie
nts with ICAD. Methods-The patients (26 women and 14 men; mean age, 42
.8 years) had a total of 65 ICADs. Seventeen patients were free of any
vascular risk factor. CT scans, MRI scans, and angiographic features
were analyzed by observers who were blinded to the clinical findings.
Results-We found 34 cortical infarcts, 25 large subcortical infarcts,
1 small subcortical infarct, and 5 junctional infarcts. Conclusions-Mo
st infarcts related to ICAD are cortical infarcts or large subcortical
infarcts; small subcortical infarcts and junctional infarcts are infr
equent. Therefore, these findings suggest that most infarcts occurring
in carotid artery dissection (CAD) are probably embolic rather than h
emodynamic in origin. According to this presumed mechanism, anticoagul
ation seems a logical treatment at the early stage of CAD.