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Key Features

  • Small lesions (usually < 1.5 cm in diameter) occur in the distribution of

    • Short, penetrating arteries in the basal ganglia

    • Pons

    • Cerebellum

    • Internal capsule

    • Thalamus

    • Deep cerebral white matter (less common) (Table 24–3)

  • Risk factors include poorly controlled hypertension and diabetes mellitus

  • Generally has a good prognosis, with partial or complete resolution often occurring over 4–6 weeks

Clinical Findings

  • There are several clinical syndromes

    • Contralateral pure motor hemiparesis or pure hemisensory deficit

    • Ipsilateral ataxia with crural paresis

    • Dysarthria with clumsiness of the hand

  • Deficits may progress over 24–36 hours before stabilizing

Diagnosis

  • Sometimes visible on CT scans as small, punched-out, hypodense areas, but in other patients no abnormality is seen

  • In some instances, patients with a clinical syndrome suggestive of lacunar infarction are found to have a severe hemispheric infarct on CT scanning

  • Diffusion-weighted MRI is sensitive to acute lesions, which later evolve into areas of T2 hyperintensity and eventually into small, punched-out, cerebrospinal fluid–filled spaces

Treatment

  • Treatment is similar to transient ischemic attack and cerebral infarction

  • Control hypertension or diabetes mellitus

  • Avoid tobacco use

  • Anticoagulation is not indicated

  • Aspirin, 325 mg once daily orally, is of uncertain benefit

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