We studied 65 consecutive patients with a first stroke who had an appropriate CT-proven small infarct in the territory of the lateral (61 patients), medial (3 patients) or both lateral and medial lenticulostriate arteries (1 patient) from the middle cerebral artery. While more than 75% of these patients were either hypertensive or diabetic (having at least one cause for small-artery disease), embolic sources were encountered in 35%, either from large vessels (28%), and/or from the heart (15%). Other causes (angiitis, migraine) were found in only 9%. The neurologic deficit was purely motor in more than 50% of the patients (in half of them with neuropsychological dysfunctions), a sensori-motor deficit was present in 30% (in half of them with neuropsychological dysfunctions), and only 20% had ataxic hemiparesis. No one had pure sensory stroke. None of the classical lacunar syndrome or the modality of sensory, motor or ataxic deficits were specific for any topographic subdivision of LS territory, but there was a tendency for clinical features to be linked with the involved basal ganglia and the topography of pathways in the internal capsule as delineated by anatomical studies. Pure motor deficits were associated with infarcts in the medial and posterior part of LS territory, visual field deficits and hemineglect always corresponded to posteriorly situated infarcts. Neuropsychological deficits were common in infarcts in the anterior and posterior subdivisions of LS territory, with a major effect of the size of infarct. Sensory deficits were not correlated with any location in LS territory, probably because thalamo-efferent fibres have a more diffuse course through the internal capsule.