Hemichorea–hemiballism syndrome following a thrombo-embolic striatal infarction

Abstract

A 70-year-old man was admitted to our emergency department for sudden onset of abnormal involuntary movements involving his upper and lower left limbs. Hemichoreal movements were restricted to his left limbs, associated with rare episodes of hemiballism (video). There were no cranial nerve alterations, no sensory loss or limb weakness. The patient reported mild hypertension under treatment. There was no history of diabetes mellitus or epilepsy, no prior exposure to neuroleptics or recent change in therapy. He denied any similar previous episode or family history of movement disorders.Chest radiography, electrocardiography, and laboratory tests including glucose, glycated hemoglobin, coagulation parameters, and immunoglobulin electrophoresis were normal. Brain non-contrast CT scan on admission showed no signs of acute ischemia (Fig. 1a). A supra-aortic-trunk Doppler sonography revealed an irregular surface plaque, partly ulcerated, on the origin of the right internal carotid artery with stenosis of about 90 %, confirmed at CT angiography (Fig. 1b).

Movement Disorders Associated With Cerebral Artery Stenosis: A Nationwide Study

“…Traditionally, the subthalamic nucleus was considered to be a typical anatomical correlate for hemichorea and hemiballism (9). However, it has been found that various stroke lesions involved in the striato-pallido-thalamo-cortical feedback loop, including the caudate nucleus, putamen, thalamus, and subcortical white matter, also cause chorea or ballism (10)(11)(12)(13). Moreover, there is accumulated evidence of CAS-associated chorea without overt stroke lesions (14)(15)(16)(17).…”

Case Report: Ischaemic Stroke Presented with Hemichorea-Hemiballism

“…A their distribution zone lacks a collateral blood supply and is functionally characterized as "terminal" (Guida et al, 2013). The regular basal ganglia circuitry transmission pattern would be interrupted by increased dopamine release brought on by ischemia.…”

“…The regular basal ganglia circuitry transmission pattern would be interrupted by increased dopamine release brought on by ischemia. Acute circuitry dysfunction would cause excessive motor facilitation and a lack of thalamic movement control (Guida et al, 2013;Laganiere et al, 2016).…”

“…Hemichorea typically appears within a few hours of the start of the stroke (as in our patient's case), although delays of up to five days have also been documented. The idea of pathogenesis mediated by restorative neuroplasticity has been brought forward as a result of this delay (Guida et al, 2013;Ueta et al, 2021). Hemichorea appears to happen a few days after stroke, whereas hemiballism is typically seen to happen promptly with the onset of stroke.…”

“…Minimal functional impairment may linger in post-ischemic hemichorea-hemiballismus. The prognosis for syndromes connected to cortical ischemia localizations is believed to be better (Guida et al, 2013).…”