Lesions of which basal ganglia structure commonly cause hemiballismus?

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Hemiballismus mainly reflects disruption of the indirect pathway in the basal ganglia, most classically from a lesion of the subthalamic nucleus. The subthalamic nucleus normally excites the internal segment of the globus pallidus (GPi), which tonically inhibits the thalamus to limit movement. When the subthalamic nucleus is damaged, this excitatory drive to GPi weakens, reducing inhibitory control over the thalamus. The thalamus then drives motor cortex more strongly, producing the large, abrupt, flinging movements of one side of the body (contralateral to the lesion). This typical pattern is most often due to a vascular event affecting the subthalamic nucleus.

Lesions to the putamen or caudate can cause chorea or other hyperkinetic or cognitive features, but they do not classically produce the abrupt, ballistic movements of hemiballismus. Lesions of the globus pallidus tend to lead to dystonia or bradykinesia more than hemiballismus.