Treatment of Hemiballismus

  • Oksana SuchowerskyEmail author
  • Aakash Shetty
Part of the Current Clinical Neurology book series (CCNEU)


Hemiballismus/hemichorea is characterized by unilateral, involuntary writhing and flinging movements of acute or subacute onset. It is seen most commonly secondary to stroke or nonketotic hyperosmolar hyperglycemia. The subthalamic nucleus was previously thought to be the responsible anatomical site but recent studies have shown that lesions in other structures in the basal ganglia and cortex can produce a similar clinical picture. The majority of the cases have a good prognosis and most resolve spontaneously. Dopamine depleters (including VMAT2 inhibitors) and dopamine antagonists are the mainstay of the treatment. In severe cases, deep brain stimulation (DBS) or pallidotomy can be considered as a treatment option.


Hemiballismus Hemichorea Chorea Ballismus Hyperglycemia, Stroke 

Supplementary material

Video 1

The video Hemiballismus patient history demonstrates random continuous irregular movements involving the proximal and distal extremities, face, and trunk on the right side. These movements are characteristic of chorea with occasional larger amplitude movements signifying hemiballismus (MP4 45682 kb)

Suggested Reading

  1. Chung SJ, Im J-H, Lee MC, Kim JS. Hemichorea after stroke: clinical-radiological correlation. J Neurol. 2004;251:725–9.CrossRefGoogle Scholar
  2. Dewey RB Jr, Jankovic J. Hemiballism-hemichorea: clinical and pharmacologic findings in 21 patients. Arch Neurol. 1989;46:862–7.CrossRefGoogle Scholar
  3. Hasegawa H, Mundil N, Samuel M, Jarosz J, Ashkan K. The treatment of persistent vascular hemidystonia-hemiballismus with unilateral GPi deep brain stimulation. Mov Disord. 2009;24:1697–8.CrossRefGoogle Scholar
  4. Hawley JS, Weiner WJ. Hemiballismus: current concepts and review. Parkinsonism Relat Disord. 2012;18(2):125–9.CrossRefGoogle Scholar
  5. Hyland HH, Forman DM. Prognosis in hemiballismus. Neurology. 1957;7:381–91.CrossRefGoogle Scholar
  6. Klawans HL, Hamilton M, Nausieda PA, Bergen D, Weiner WJ. Treatment and prognosis of hemiballismus. N Engl J Med. 1976;295:1348–50.CrossRefGoogle Scholar
  7. Martin JP. Hemichorea resulting from a local lesion of the brain: the syndrome of the body of Luys. Brain. 1927;50:637–51.CrossRefGoogle Scholar
  8. Parees I, Hernandez-Vara J, Alvarez-Sabin J. Post-stroke hemichorea: observation-based study of 15 cases. Rev Neurol. 2010;51(8):460–4.PubMedGoogle Scholar
  9. Postuma RB, Lang AE. Hemiballism: revisting a classic disorder. Lancet Neurol. 2003;2:661–8.CrossRefGoogle Scholar
  10. Vidakovic A, Dragasevic N, Kostic VS. Hemiballism: report of 25cases. J Neurol Neurosurg Psychiatry. 1994;57:945–9.CrossRefGoogle Scholar
  11. Xie T, Awad I, Kang UJ, Warnke P. DBS reduced hemichorea associated with a developmental venous anomaly and microbleeding in STN. Neurology. 2014;82:636–7.CrossRefGoogle Scholar
  12. Zaitout Z. CT and MRI findings in the basal ganglia in non-ketotic hyperglycaemia associated hemichorea and hemi-ballismus (HC-HB). Neuroradiology. 2012;54:1119–20.CrossRefGoogle Scholar

Copyright information

© Springer Nature Switzerland AG 2019

Authors and Affiliations

  1. 1.Department of Medicine (Neurology), Pediatrics, and Medical GeneticsUniversity of AlbertaEdmontonCanada
  2. 2.Department of Medicine (Neurology)University of AlbertaEdmontonCanada

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