Ataxic Hemiparesis Due to Pontine Infarction
OBJECTIVES
To describe the clinical characteristics of ataxic hemiparesis.
To review the pathogenesis of lacunar infarcts.
To highlight the many localizations responsible for ataxic hemiparesis (homolateral ataxia and crural paresis).
To review variants of this syndrome.
VIGNETTE
A 75-year-old woman with hypertension and hyperlipidemia had sudden onset of dizziness followed by slurred speech and right-sided weakness.

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Every year at least 795,000 Americans experience a new or recurrent stroke. Strokes result from either ischemia or hemorrhage. Ischemic strokes resulting from small vessel or penetrating artery disease (lacunes) have unique clinical, radiological, and pathological features. Lacunar infarcts are small ischemic infarctions involving the deep regions of the brain or brainstem ranging in diameter from 0.5 to 15.0 mm resulting from occlusion of a single
perforating artery, chiefly the anterior choroidal, middle cerebral, posterior cerebral, and basilar arteries. Lacunes usually occur in patients with long-standing arterial hypertension or diabetes mellitus. Lacunar infarcts could also be the result of occlusion of penetrating arteries by atherosclerosis of the parent artery or by microembolism from extracranial arterial or cardiac sources. The most frequent sites of lacunes are the putamen, pontis, thalamus, posterior limb of the internal capsule, and caudate nucleus.
perforating artery, chiefly the anterior choroidal, middle cerebral, posterior cerebral, and basilar arteries. Lacunes usually occur in patients with long-standing arterial hypertension or diabetes mellitus. Lacunar infarcts could also be the result of occlusion of penetrating arteries by atherosclerosis of the parent artery or by microembolism from extracranial arterial or cardiac sources. The most frequent sites of lacunes are the putamen, pontis, thalamus, posterior limb of the internal capsule, and caudate nucleus.

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