# Hemiballismus as the Sole Manifestation of Acute Thalamic Hemorrhagic Stroke: A Case Report

**Authors:** Yoseph M Habte, Binyam M Habte, Esimael M Abdu, Abdulkerim A Temam, Amira A Mohammed

PMC · DOI: 10.7759/cureus.93719 · Cureus · 2025-10-02

## TL;DR

A 68-year-old man developed hemiballismus after a thalamic hemorrhagic stroke, showing how rare movement disorders can arise from brain injuries.

## Contribution

This case report presents hemiballismus as a rare manifestation of thalamic hemorrhage, expanding understanding of its neuroanatomical origins.

## Key findings

- Hemiballismus occurred following a left thalamic hemorrhagic stroke in a patient with vascular comorbidities.
- Symptomatic treatment provided partial improvement but not full resolution of movement disorder.
- The case emphasizes the need for individualized therapy and close follow-up in post-stroke hyperkinetic disorders.

## Abstract

Post-stroke movement disorders are uncommon, with hyperkinetic types occurring in less than 1% of cases. Hemiballism-hemichorea is the most frequent post-stroke hyperkinetic movement disorder and is typically associated with lesions in subcortical structures. We report a case of a 68-year-old man with hypertension, diabetes, and prior ischemic stroke who developed right-sided hemiballismus within days of a left thalamic hemorrhagic stroke. Brain MRI revealed a hemorrhagic lesion in the left thalamus alongside chronic small vessel ischemic changes and lacunar infarcts. The patient exhibited continuous, high-amplitude involuntary movements that significantly impaired function. Symptomatic treatment with haloperidol, sodium valproate, and clonazepam led to partial improvement, though complete resolution was not achieved during the hospitalization. This case highlights the clinical complexity of post-stroke hemiballismus, the broad neuroanatomical substrates beyond the subthalamic nucleus, and challenges in management, particularly in patients with multiple vascular comorbidities. Given the variability in onset and recovery, close neurological follow-up and individualized therapy are essential. Further research is warranted to better understand the pathophysiology and optimize treatment strategies for post-stroke hyperkinetic movement disorders.

## Linked entities

- **Chemicals:** haloperidol (PubChem CID 3559), sodium valproate (PubChem CID 16760703), clonazepam (PubChem CID 2802)
- **Diseases:** diabetes (MONDO:0005015), ischemic stroke (MONDO:1060198)

## Full-text entities

- **Diseases:** Post-stroke (MESH:D020521), hypertension (MESH:D006973), ischemic (MESH:D002545), movement disorders (MESH:D009069), hyperkinetic (MESH:D006948), diabetes (MESH:D003920), lacunar infarcts (MESH:D059409), Thalamic Hemorrhagic Stroke (MESH:D000083302), ischemic stroke (MESH:D002544), hemorrhagic lesion (MESH:D006470), Hemiballism-hemichorea (MESH:D020820)
- **Chemicals:** clonazepam (MESH:D002998), haloperidol (MESH:D006220), sodium valproate (MESH:D014635)
- **Species:** Homo sapiens (human, species) [taxon 9606]

## Full text

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## Figures

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## References

11 references — full list in the complete paper: https://tomesphere.com/paper/PMC12580584/full.md

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Source: https://tomesphere.com/paper/PMC12580584