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HOME > J Mov Disord > Volume 19(1); 2026 > Article
Letter to the editor
 Deep Brain Stimulation for Hemiballismus: A Case Report and Review of the Literature
Negin Eissazade1,2orcid, Seyedehnarges Tabatabaee3orcid, Mansour Parvaresh-Rizi4orcid, Gholamali Shahidi5, Behnam Safarpour Lima6orcid, Sadra Rohani4, Renato P. Munhoz7,8orcid, Alfonso Fasano7,8,9orcid, Mohammad Rohani10,11corresp_iconorcid
Journal of Movement Disorders 2026;19(1):107-110.
DOI: https://doi.org/10.14802/jmd.25236
Published online: October 1, 2025

1Cellular and Molecular Research Center, Iran University of Medical Sciences, Tehran, Iran

2Brain and Cognition Clinic, Institute for Cognitive Sciences Studies, Tehran, Iran

3Department of Neurology, Iran University of Medical Sciences (IUMS), Tehran, Iran

4Department of Neurosurgery, Iran University of Medical Sciences (IUMS), Tehran, Iran

5Department of Neurology, Hazrat Rasool Hospital, Iran University of Medical Sciences, Tehran, Iran

6Department of Neurology, School of Medicine, Shahid Beheshti University of Medical Sciences, Tehran, Iran

7Edmond J. Safra Program in Parkinson’s Disease, Morton and Gloria Shulman Movement Disorders Clinic, Toronto Western Hospital, University Health Network, Toronto, ON, Canada

8Krembil Brain Institute, Neuroscience, Toronto, ON, Canada

9Center for Advancing Neurotechnological Innovation to Application (CRANIA), Toronto, ON, Canada

10Skull Base Research Center, Five Senses Health Institute, Iran University of Medical Sciences, Tehran, Iran

11Department of Neurology, School of Medicine, Iran University of Medical Sciences, Tehran, Iran

Corresponding author: Mohammad Rohani, MD Department of Neurology, Hazrat Rasool Hospital, Iran University of Medical Sciences, Niyayesh St, Sattarkhan Ave, Tehran 1445613131, Iran / Tel: +98-21-66-52-5331 / E-mail: mohammadroohani@gmail.com
• Received: September 3, 2025   • Revised: September 22, 2025   • Accepted: October 1, 2025

Copyright © 2026 The Korean Movement Disorder Society

This is an Open Access article distributed under the terms of the Creative Commons Attribution Non-Commercial License (http://creativecommons.org/licenses/by-nc/4.0/) which permits unrestricted non-commercial use, distribution, and reproduction in any medium, provided the original work is properly cited.

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Dear Editor,
Hemiballismus (HB) is a hyperkinetic movement disorder affecting one side of the body that is characterized by involuntary, flinging movements and is most often caused by subthalamic nucleus (STN) lesions. While stroke is the most common etiology, HB has also been linked to metabolic disturbances such as nonketotic hyperglycinemia, as well as infectious, neoplastic, neurodegenerative, and traumatic causes [1].
Most cases improve spontaneously or respond to pharmacological therapy, including treatment with dopamine receptor antagonists and botulinum toxin injections [2]. However, a subset of patients remains severely disabled despite optimal medical management. For such refractory cases, deep brain stimulation (DBS) has emerged as a promising intervention, offering adjustability, reversibility, and sustained symptom relief.
Here, we present a case of poststroke HB successfully treated with unilateral globus pallidus internus (GPi) DBS, followed by a literature review summarizing DBS targets, stimulation parameters, and outcomes across various etiologies of HB.
A 53-year-old man with a history of ischemic heart disease, coronary artery bypass grafting, and type 2 diabetes mellitus (T2DM) presented with right-sided HB following an ischemic stroke involving the left STN in 2019 (Supplementary Video 1 in the online-only Data Supplement). His symptoms were refractory to pharmacological treatment, including consumption of up to 25 mg tetrabenazine three times daily, and led to significant functional impairment, requiring assistance with daily activities (modified Rankin Scale [mRS] score=4). Neurological examination was remarkable only for generalized hyporeflexia. Brain magnetic resonance imaging confirmed an ischemic stroke in the left STN (Supplementary Figure 1 in the online-only Data Supplement).
One year after symptom onset, the patient underwent DBS targeting the left posteroventral GPi (Supplementary Figure 2 in the online-only Data Supplement). The procedure was uneventful, and the two middle contacts were activated in double-monopolar mode shortly thereafter. Six weeks post-operatively, his mRS score improved to 2, indicating greater independence in daily activities.
After one year, the stimulation settings were optimized to an amplitude of 2.3 V, a frequency of 130 Hz, and a pulse width of 60 μs. The patient reported a marked improvement in quality of life and was able to perform daily activities with minimal assistance (Supplementary Video 1 in the online-only Data Supplement).
To further explore DBS targets, stimulation parameters, and clinical outcomes in hemichorea-hemiballismus (HC-HB), we conducted a literature review. In May 2025, we systematically searched PubMed/MEDLINE, Embase, and Scopus using relevant keywords, including “hemichorea,” “hemiballismus,” and “deep brain stimulation.” We included peer-reviewed English-language studies without time restrictions that reported adult patients (≥18 years) with HC-HB of any etiology treated with DBS. The reference lists of eligible articles were also screened to identify additional reports.
To date, 17 cases of HC-HB treated with DBS have been reported, including 10 male patients aged 22–82 years (Table 1). When classified by etiology, vascular causes were the most frequent (ischemic stroke, n=5; subarachnoid hemorrhage, n=3; traumatic brain injury, n=2; developmental venous anomaly, n=1), followed by metabolic disturbances (nonketotic hyperglycinemia in the setting of T2DM, n=4). Less common etiologies included neoplasia (n=1) and infection (Propionibacterium acnes contamination of a DBS electrode, n=1). Overall, 11 patients underwent GPi DBS, although the use of alternative targets such as the ventral intermediate nucleus (Vim) also yielded clinical benefit, with stimulation parameters ranging from 0.8 to 4.5 V in amplitude and 60 to 185 Hz in frequency. The outcomes were generally favorable across groups: vascular and metabolic cases both showed marked or complete improvement, whereas a single patient with an infection experienced symptom recurrence following device removal [1].
Consistent with prior reports, our patient achieved significant functional recovery and reduced disability following left GPi-DBS, with an enhanced overall quality of life. Beyond HB, GPi-DBS has demonstrated efficacy in other choreiform movement disorders, including Huntington’s disease and choreaacanthocytosis, leading to improvements in both movement and functional independence. Compared with alternative targets such as the STN or thalamus, which have yielded more variable results and stimulation-related side effects, the GPi generally offers a more consistent balance of efficacy and safety [3].
The therapeutic rationale for GPi-DBS is supported by the basal ganglia circuitry: lesions, particularly those involving the STN, reduce excitatory input to the GPi, leading to excessive thalamic disinhibition and cortical hyperexcitation that underlie hyperkinetic movements [4,5]. In some cases, multifocal or combined stimulation strategies have been employed to permit lower stimulation amplitudes, thereby reducing the incidence of side effects and prolonging device longevity. While other procedures (e.g., pallidotomy and thalamotomy) have also been used for patients with HB [6], their irreversible nature and risks of complications limit their appeal. DBS, by contrast, is both reversible and adjustable, allowing parameters to be fine-tuned over time, with side effects managed through programming rather than reoperation.
Despite encouraging results, challenges remain in identifying appropriate candidates, as outcomes vary across etiologies and individual patients, and predictors of efficacy have not been fully defined. Standardized, multicenter studies are needed to establish patient selection criteria, optimize stimulation parameters, and assess long-term outcomes across HB subtypes. Future research should also focus on the development of validated clinical scales, neuroimaging biomarkers of treatment responsiveness, and adaptive stimulation technologies to further personalize therapy.
Taken together, our case and the available literature suggest that GPi-DBS represents a promising therapeutic option for select patients with refractory HC-HB, with potential benefits in terms of functional recovery and quality of life. Nevertheless, given the rarity of this condition and the limited evidence to date, larger collaborative studies are essential to establish its efficacy and optimize treatment strategies for this disabling disorder.
The online-only Data Supplement is available with this article at https://doi.org/10.14802/jmd.25236.
Video 1.
This video shows ballistic movements of the right upper and lower extremities when the patient is sitting on a bed and walking and significant improvement in these movements after deep brain stimulation.
Supplementary Material.
jmd-25236-Supplementary-Material.pdf
Supplementary Figure 1.
Axial T1-weighted (A) and T2-weighted (B) brain MRI scans showing a lacunar infarction (arrow) in the left subthalamic nucleus. MRI, magnetic resonance imaging.
jmd-25236-Supplementary-Figure-1.pdf
Supplementary Figure 2.
Postoperative axial brain CT scan showing the left GPi DBS electrode placement (arrow). CT, computed tomography; GPi, globus pallidus internus; DBS, deep brain stimulation.
jmd-25236-Supplementary-Figure-2.pdf

Ethics Statement

Ethical approval was waived by the local Ethics Committee of Iran University of Medical Sciences due to the nature of the study, as all procedures were part of routine care. Written informed consent was obtained from the patient for participation.

Conflicts of Interest

The authors have no financial conflicts of interest.

Funding Statement

None

Acknowledgments

Authors would like to thank the patient and their family for their kind cooperation.

Author Contributions

Conceptualization: Seyedehnarges Tabatabaee, Mansour Parvaresh-Rizi, Gholamali Shahidi, Behnam Safarpour Lima, Sadra Rohani, Renato P. Munhoz, Alfonso Fasano, Mohammad Rohani. Data curation: Negin Eissazade, Seyedehnarges Tabatabaee, Mohammad Rohani. Formal analysis: Negin Eissazade, Seyedehnarges Tabatabaee, Mohammad Rohani. Investigation: Negin Eissazade, Seyedehnarges Tabatabaee, Sadra Rohani, Mohammad Rohani. Methodology: Negin Eissazade, Seyedehnarges Tabatabaee, Mohammad Rohani. Project administration: Negin Eissazade, Seyedehnarges Tabatabaee, Gholamali Shahidi, Behnam Safarpour Lima, Renato P. Munhoz, Alfonso Fasano, Mohammad Rohani. Resources: Mohammad Rohani. Supervision: Renato P. Munhoz, Alfonso Fasano, Mohammad Rohani. Validation: Mohammad Rohani. Writing—original draft: Negin Eissazade, Seyedehnarges Tabatabaee, Mohammad Rohani. Writing—review & editing: Seyedehnarges Tabatabaee, Mansour Parvaresh-Rizi, Behnam Safarpour Lima, Sadra Rohani, Renato P. Munhoz, Alfonso Fasano, Mohammad Rohani.

Table 1.
Detailed overview of refractory HC-HB cases treated with DBS
Study* Year Patient Presentation Symptom duration/Etiology Target (stimulation parameters) Outcome Follow-up
Metabolic disturbances
 Ozturk et al. S1 2024 75/F Lt HC-HB 6 mo/T2DM Rt GPi (2.4 mA, 60 μs, 130 Hz) + Rt Vim (1.7 mA, 60 μs, 130 Hz) Improved 14 mo/Improved
 Masood et al. S2 2023 68/F Lt HC 5 yr/T2DM Rt GPi (C+1–, 3.5 V, 90 μs, 130 Hz) Mild improvement 5 yr/Improved
71/M Lt HC 5 mo/T2DM Rt GPi (C+1–, 2.4 V, 60 μs, 130 Hz) Improved 4 mo/Improved
 Son et al. S3 2017 46/F Lt HC-HB T2DM Rt GPi (2+1–, 3.5 mA, 110–130 μs, 130 Hz) Improved in 16 mo 16 wk/Improved, with minimal HC
 Nakano et al. S4 2005 65/M Rt HC-HB 5 mo/T2DM Lt Voa + Vop (C0-, C1 and 2 off, and C3+, 2 V, 90 μs, 130 Hz) Improved 9 mo/Improved
Vascular causes
 Parker et al. S5 2020 60/F Lt HC-HB Rt thalamic intraparenchymal hemorrhage traumatic brain injury Rt GPi + Vop Improved 4 yr/Improved
 Ganapa et al. S6 2019 46/M Lt HB 5 yr/Rt PCA ischemic stroke Rt GPi (N/A) Improved -
 Ramirez-Zamora et al. S7 2018 53/F Lt HB Peripartum Rt thalamic cerebral infarction Rt GPi (C+0–, 3.0 V, 90 μs, 130 Hz) Improved in 6 mo 28 mo/Improved
 Pabaney et al. S8 2015 54/M Rt HB Post-fall hemorrhage in Lt STN Lt GPi (C+1−, 2.0 V, 90 µs, 160 Hz) Improved Several weeks/Improved
 Franzini et al. S9 2014 77/M Rt HB Lt capsule-thalamic junction hemorrhage + Lt parietal SAH Lt Voa + Vop (C+, 0–, 1–, 2–, 3–, 3.5 V, 210 ms, 185 Hz) Improved 18 mo/Improved
82/F Lt HB Thalamic ischemic stroke Rt Voa + Vop (C+, 0−, 1−, 2−, 3−, 3.4 V, 90 µs, 180 Hz) Improved 12 mo/Improved
 Xie et al. S10 2014 22/M Lt HC Hemorrhage (developmental venous anomaly) Rt GPi (C+1–, 3.6 V, 120 μs, 60 Hz) Improved 10 mo/Improved
 Oyama et al. S11 2014 44/M Lt HB Rt STN (bilat STN-DBS for PD) stroke Rt GPi (1(2)C+), 3.3 V, 90 ms, 135 Hz) Improved 1 wk/Improved
 Franzini et al. S12 2012 NA/M HB Mesencephalic stroke Vim Improved -
 Hasegawa et al. S13 2009 56/M Lt HB 3 yr/Hemorrhage in Rt pons, midbrain, and subthalamic region Rt GPi (C+1–, 1.5 V (to 4.5 V over 6 mo), 60 μs, 130 Hz) Improved 15 mo/Improved
Neoplasm
 Capelle et al. S14 2011 52/F Rt HC-HB Approximately 4 yr/post-craniopharyngioma resection Lt GPi + Vim (3+0–, 0.8 V, 210 μs, 130 Hz) Improved 25 mo/Improved
Infection
 Masood et al. S2 2023 67/M Lt HC-HB 12 mo/DBS electrode infection Rt GPi (8+9–, 4.1 V, 60 μs, 120 Hz) + Lt GPi (C+1–, 4.5 V, 60 μs, 120 Hz) Improved 2 mo/Improved

* the references (S1-S14) cited in this table are provided in the Supplementary Material.

HC, hemichorea; HB, hemiballismus; DBS, deep brain stimulation; NA, not available; T2DM, type 2 diabetes mellitus; GPi, globus pallidus interna; Voa, ventralis oralis anterior; Vop, ventralis oralis posterior nuclei; Vim, ventral intermediate nucleus; PCA, posterior cerebral artery; PD, Parkinson’s disease; SAH, subarachnoid hemorrhage; STN, subthalamic nucleus.

  • 1. Masood Z, Domino JS, Gragg A, Burchiel K, Kinsman M, Sharma VD. Deep brain stimulation for the treatment of hemichorea: case series and literature review. Tremor Other Hyperkinet Mov (N Y) 2023;13:21.ArticlePubMedPMC
  • 2. Ganapa SV, Ramani MD, Ebunlomo OO, Rahman RK, Herschman Y, Mammis A. Treatment of persistent hemiballism with deep brain stimulation of the globus pallidus internus: case report and literature review. World Neurosurg 2019;132:368–370.ArticlePubMed
  • 3. Edwards TC, Zrinzo L, Limousin P, Foltynie T. Deep brain stimulation in the treatment of chorea. Mov Disord 2012;27:357–363.ArticlePubMed
  • 4. Postuma RB, Lang AE. Hemiballism: revisiting a classic disorder. Lancet Neurol 2003;2:661–668.ArticlePubMed
  • 5. Compston A. Hemichorea resulting from a local lesion of the brain. (The syndrome of the body of Luys.) By James Purdon Martin, MD (London). Brain 1927: 50; 637–651; Hemichorea associated with a lesion of the corpus Luysii. By James Purdon Martin and N.S. Alcock. Brain 1934: 57; 504–516; and Hemichorea (hemiballismus) without lesions in the corpus Luysii. By J. Purdon Martin (From the National Hospital, Queen Square, W.C.1) Brain 1957: 80; 1–10. Brain 2006;129:1633–1636.Article
  • 6. Hawley JS, Weiner WJ. Hemiballismus: Current concepts and review. Parkinsonism & Related Disorders 2012;18:125-129. Hawley JS, Weiner WJ. Hemiballismus: current concepts and review. Parkinsonism Relat Disord 2012;18:125–129.PubMed

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      Deep Brain Stimulation for Hemiballismus: A Case Report and Review of the Literature
      Deep Brain Stimulation for Hemiballismus: A Case Report and Review of the Literature
      Study* Year Patient Presentation Symptom duration/Etiology Target (stimulation parameters) Outcome Follow-up
      Metabolic disturbances
       Ozturk et al. S1 2024 75/F Lt HC-HB 6 mo/T2DM Rt GPi (2.4 mA, 60 μs, 130 Hz) + Rt Vim (1.7 mA, 60 μs, 130 Hz) Improved 14 mo/Improved
       Masood et al. S2 2023 68/F Lt HC 5 yr/T2DM Rt GPi (C+1–, 3.5 V, 90 μs, 130 Hz) Mild improvement 5 yr/Improved
      71/M Lt HC 5 mo/T2DM Rt GPi (C+1–, 2.4 V, 60 μs, 130 Hz) Improved 4 mo/Improved
       Son et al. S3 2017 46/F Lt HC-HB T2DM Rt GPi (2+1–, 3.5 mA, 110–130 μs, 130 Hz) Improved in 16 mo 16 wk/Improved, with minimal HC
       Nakano et al. S4 2005 65/M Rt HC-HB 5 mo/T2DM Lt Voa + Vop (C0-, C1 and 2 off, and C3+, 2 V, 90 μs, 130 Hz) Improved 9 mo/Improved
      Vascular causes
       Parker et al. S5 2020 60/F Lt HC-HB Rt thalamic intraparenchymal hemorrhage traumatic brain injury Rt GPi + Vop Improved 4 yr/Improved
       Ganapa et al. S6 2019 46/M Lt HB 5 yr/Rt PCA ischemic stroke Rt GPi (N/A) Improved -
       Ramirez-Zamora et al. S7 2018 53/F Lt HB Peripartum Rt thalamic cerebral infarction Rt GPi (C+0–, 3.0 V, 90 μs, 130 Hz) Improved in 6 mo 28 mo/Improved
       Pabaney et al. S8 2015 54/M Rt HB Post-fall hemorrhage in Lt STN Lt GPi (C+1−, 2.0 V, 90 µs, 160 Hz) Improved Several weeks/Improved
       Franzini et al. S9 2014 77/M Rt HB Lt capsule-thalamic junction hemorrhage + Lt parietal SAH Lt Voa + Vop (C+, 0–, 1–, 2–, 3–, 3.5 V, 210 ms, 185 Hz) Improved 18 mo/Improved
      82/F Lt HB Thalamic ischemic stroke Rt Voa + Vop (C+, 0−, 1−, 2−, 3−, 3.4 V, 90 µs, 180 Hz) Improved 12 mo/Improved
       Xie et al. S10 2014 22/M Lt HC Hemorrhage (developmental venous anomaly) Rt GPi (C+1–, 3.6 V, 120 μs, 60 Hz) Improved 10 mo/Improved
       Oyama et al. S11 2014 44/M Lt HB Rt STN (bilat STN-DBS for PD) stroke Rt GPi (1(2)C+), 3.3 V, 90 ms, 135 Hz) Improved 1 wk/Improved
       Franzini et al. S12 2012 NA/M HB Mesencephalic stroke Vim Improved -
       Hasegawa et al. S13 2009 56/M Lt HB 3 yr/Hemorrhage in Rt pons, midbrain, and subthalamic region Rt GPi (C+1–, 1.5 V (to 4.5 V over 6 mo), 60 μs, 130 Hz) Improved 15 mo/Improved
      Neoplasm
       Capelle et al. S14 2011 52/F Rt HC-HB Approximately 4 yr/post-craniopharyngioma resection Lt GPi + Vim (3+0–, 0.8 V, 210 μs, 130 Hz) Improved 25 mo/Improved
      Infection
       Masood et al. S2 2023 67/M Lt HC-HB 12 mo/DBS electrode infection Rt GPi (8+9–, 4.1 V, 60 μs, 120 Hz) + Lt GPi (C+1–, 4.5 V, 60 μs, 120 Hz) Improved 2 mo/Improved
      Table 1. Detailed overview of refractory HC-HB cases treated with DBS

      the references (S1-S14) cited in this table are provided in the Supplementary Material.

      HC, hemichorea; HB, hemiballismus; DBS, deep brain stimulation; NA, not available; T2DM, type 2 diabetes mellitus; GPi, globus pallidus interna; Voa, ventralis oralis anterior; Vop, ventralis oralis posterior nuclei; Vim, ventral intermediate nucleus; PCA, posterior cerebral artery; PD, Parkinson’s disease; SAH, subarachnoid hemorrhage; STN, subthalamic nucleus.

      Table 1.

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