Objective: To report a case of ipsilateral chorea secondary to thalamic hemorrhage and discuss neurophysiological mechanisms of hyperkinetic movement disorders

Background: Cerebrovascular disease accounts for up to 22% of secondary movement disorders; it occurs in 1–4% of strokes. Hemichorea–hemiballism is the most frequent hyperkinetic manifestation. Lesions most commonly involve the basal ganglia (44%), followed by the thalamus (37%) (1). In thalamic stroke, dystonia is most common, with chorea third (2)

Method: A 74-year-old man presented in stroke code with vertigo, headache, and hemibody weakness. On admission, blood pressure was 192/105 mmHg. He had rightward gaze deviation and left-sided deficits, including homonymous hemianopia, facial palsy, hemiparesis (2/5), sensory loss, and spatial neglect. Contralateral choreiform movements involving rotatory movements of the wrist and fingers were observed. Brain CT demonstrated a right thalamic hematoma (5.6 cc) with extension into the ipsilateral lateral ventricle. Persistent chorea was treated with risperidone 1 mg nightly, with marked improvement

Results: Post-stroke chorea is thought to result from disruption of the cortico-striato-pallido-thalamo-cortical loop (3). Acute interruption of inhibitory GABAergic pallido-thalamic fibers projecting from the globus pallidus interna to ventroanterior and ventrolateral thalamic nuclei may produce thalamocortical disinhibition and chorea (2,3). Additional pathways implicated include glutamatergic thalamostriatal projections and cerebello-thalamo-cortical circuits involved in motor coordination (2). Although chorea typically occurs contralateral to the lesion, rare ipsilateral cases have been described, possibly due to masking by hemiparesis, bilateral basal ganglia control of motor output, or disinhibition of ipsilateral motor pathways (4). Lesion-network mapping studies further show that heterogeneous lesions producing hemichorea converge within a shared functional network connected to the posterolateral putamen (5). Among thalamic stroke-related movement disorders, the posterolateral thalamus—particularly the ventrolateral and ventroposterior nuclei—is most frequently involved (2)

Conclusion: Ipsilateral vascular chorea after thalamic hemorrhage likely reflects pallido-thalamic disinhibition and disruption of distributed motor networks, supporting a network-based mechanism of post-stroke hyperkinesia

References: 1. Mehanna R, Jankovic J. Movement disorders in cerebrovascular disease. Lancet Neurol. 2013;12(6):597-608.
2. Gupta N, Pandey S. Post-thalamic stroke movement disorders: a systematic review. Eur Neurol. 2018;79(5-6):303-314.
3. Li ZS, Yang H, Li Z, et al. Hemichorea due to ipsilateral thalamic infarction: a case report. World J Clin Cases.2021;9(19):5287-5293.
4. Kobayashi M, et al. Hemichorea associated with nigrostriatal dysfunction: case report of a patient with an ipsilateral infarct in the lenticular nucleus and internal capsule. Neurol Sci. 2025.
5. Laganiere S, Boes AD, Fox MD. Network localization of hemichorea-hemiballismus. Neurology. 2016;86(23):2187-2195.

« Back to 2026 International Congress

MDS Abstracts - https://www.mdsabstracts.org/abstract/ipsilateral-chorea-due-to-thalamic-hemorrhage-insights-into-network-mechanisms-of-post-stroke-hyperkinetic-disorders/