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(Stroke. 2003;34:653.)
© 2003 American Heart Association, Inc.

Original Contributions

Ischemic Lacunar Stroke in Patients With and Without Potential Mechanism Other Than Small-Artery Disease

Ralf W. Baumgartner, MD; Claude Sidler, MD; Maria Mosso, MD Dimitrios Georgiadis, MD

From the Department of Neurology, University Hospital of Zürich, Zürich, Switzerland.

Correspondence to Ralf W. Baumgartner, MD, Department of Neurology, University Hospital, Frauenklinikstrasse 26, CH-8091 Zürich, Switzerland. E-mail Ralf.Baumgartner{at}nos.usz.ch

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 (n=244), 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 (n=155; 64%), patients with non-SAD lacunar strokes (n=89; 36%) had (1) higher NIHSS scores at presentation and higher NIHSS and mRS scores after 3 months (P<0.05); a higher prevalence of (2) hypertension (P<0.05), (3) coronary artery disease (P<0.0001), (4) previous transient ischemic attacks (P<0.01), and (5) asymptomatic stenoses of intracranial cerebral (P<0.01 to P<0.0001) and extracranial carotid (30% to 50% narrowing; P<0.01) arteries; and (6) a higher detection rate of the underlying lesion at brain imaging (P<0.01).

Conclusions— Our data suggest that patients with non-SAD lacunar strokes have a worse clinical outcome and a higher prevalence of large cerebral and coronary artery disease than patients with SAD lacunar strokes.

Editorial Comment

Louis R. Caplan, MD, Guest Editor

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