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Hemiballismus – STN Lesion Mechanism — SCE Neurology MCQ

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HardMovement DisordersHemiballismus – STN Lesion MechanismSCE Neurology

A 60-year-old woman presents with sudden onset of contralateral hemichorea and hemiballismus affecting the left arm and leg. CT brain shows a small haemorrhagic lesion in the right subthalamic nucleus. What is the mechanism?

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Correct answer: D — Loss of subthalamic nucleus excitatory drive to the globus pallidus internus, reducing inhibitory output from GPi to the thalamus, resulting in excessive thalamocortical excitation and involuntary movements

The subthalamic nucleus (STN) provides excitatory (glutamatergic) drive to the globus pallidus internus (GPi). When the STN is damaged, GPi output is reduced, leading to disinhibition of the thalamus and excessive thalamocortical excitation — manifesting as contralateral hemichorea/hemiballismus. This is the classic mechanism of hemiballismus and demonstrates the indirect pathway of the basal ganglia motor circuit. Treatment includes dopamine-depleting agents (tetrabenazine) or dopamine blockers. A: Motor tract damage causes weakness, not involuntary movements. C: Cerebellar dysfunction causes ataxia. D: Dopamine excess is not the primary mechanism. E: The lesion is central.

Reference: Clinical Neuroanatomy; Basal Ganglia Circuitry