These data suggest that ICAD causing high-grade stenosis and occlusion are more likely to lead to intracranial obstructions and cerebral or retinal ischemic events. Conversely, ICAD without luminal narrowing cause more local signs and symptoms.

Background and Purpose-Autopsy studies found that lacunar strokes differ in the size of the underlying brain infarct and that small lacunes are usually caused by hypertensive small-artery disease (SAD) and larger ones by atheromatous or embolic perforator occlusion. These findings suggest that larger lacunar infarcts might cause more severe neurological deficits and a higher detection rate on brain imaging compared with lacunar strokes caused by SAD. This prospective observational study was performed to investigate whether (1) neurological outcome, (2) prevalence of stroke risk factors, (3) prevalence of clinically asymptomatic occlusive cerebral artery disease, and (4) detection rate of underlying lacunar infarcts at brain imaging differ in ischemic lacunar strokes with (non-SAD) and without potential etiologies other than SAD. Methods-Consecutive patients with lacunar stroke (nϭ244), defined by both clinical findings and brain imaging, were studied. Neurological deficit was quantified at presentation with the use of the National Institutes of Health Stroke Scale (NIHSS) and after 3 months with the NIHSS and the modified Rankin Scale (mRS). Cerebral arteries were investigated by ultrasound. Results-Compared with patients with SAD lacunar strokes (nϭ155; 64%), patients with non-SAD lacunar strokes (nϭ89; 36%) had (1) higher NIHSS scores at presentation and higher NIHSS and mRS scores after 3 months (PϽ0.05); a higher prevalence of (2)

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This study suggests that ICAD has a benign long-term prognosis with low rates of ipsilateral carotid territory and any stroke and that the stroke rate in ICAD is not related to the persistence of severe carotid stenosis or occlusion. These results question the rationale of surgical or catheter-based revascularization in patients with ICAD.