Objective: To report a transient hemichorea–hemiballismus episode associated with a punctate centrum semiovale/corona radiata infarct and emphasize that strategic white-matter ischemia can produce prominent hyperkinesia despite minimal lesion burden.

Background: Hemichorea–hemiballismus is most often linked to basal ganglia or subthalamic nucleus lesions, but vascular lesions outside these structures can cause hyperkinesia through disruption of basal ganglia–thalamo–cortical connectivity. Because acute hemichorea may also occur with metabolic, toxic, or epileptic etiologies, a focused diagnostic approach is required.

Method: Single-patient case report with clinical observation and video documentation of abnormal movements, targeted laboratory evaluation to assess common secondary causes of acute hemichorea–hemiballismus, brain MRI (DWI/ADC and T2/FLAIR), and routine scalp EEG obtained after symptom resolution.

Results: A 53-year-old man developed abrupt left-sided numbness with involuntary movements characterized by intermittent left perioral twitching and head jerks, large-amplitude flinging of the left arm/hand, and writhing movements of the left leg with dystonic-appearing foot posturing. He remained fully alert, speaking, and cooperative but unable to suppress the movements. Symptoms lasted ~2–2.5 hours from ictus and did not recur. Laboratory evaluation did not demonstrate a metabolic or systemic trigger for hyperkinesia (including no marked hyperglycemia; HbA1c 5.7%). MRI showed a tiny focus of restricted diffusion with corresponding ADC signal drop and T2/FLAIR hyperintensity in the right parietal centrum semiovale/corona radiata; a tiny GRE-only susceptibility focus was noted in the right thalamus without diffusion restriction. Routine EEG obtained after resolution was within normal limits without epileptiform discharges.

Conclusion: Punctate centrum semiovale/corona radiata infarction can present as brief, dramatic hemichorea–hemiballismus with preserved awareness and minimal persistent deficits. Recognition of this phenotype and exclusion of common secondary causes through targeted testing can prevent diagnostic delay and supports a disconnection/network mechanism for hyperkinesia from extra-basal ganglia lesions.

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MDS Abstracts - https://www.mdsabstracts.org/abstract/transient-hemichorea-hemiballismus-from-a-punctate-centrum-semiovale-corona-radiata-infarct/