Skip to main content

Advertisement

Log in

Opinion statement

Hemiballismus is the most dramatic movement disorder seen in clinical practice. Its emergence points to a structural lesion or metabolic dysfunction in the region of the subthalamic nucleus, its afferent or efferent pathways, or interconnected deep brain nuclei, usually on the side contralateral to the movements. Any focal process may be to blame, but elderly sufferers generally have had vascular events, whereas the etiology is infectious or inflammatory in younger patients. Severe nonketotic hyperglycemia is another important cause of hemiballismus in the elderly. Hemiballismus patients require treatment both for the underlying etiology of the movement and for the movements themselves. There are no large controlled clinical trials to guide anti-ballismus therapy. However, dopamine receptor blocking agents have an established track record in suppressing choreic and ballistic movements, and are first-line agents for acute treatment. Standard neuroleptics such as haloperidol and perphenazine are started at low doses and titrated as tolerated until the movements are controlled. Atypical antipsychotics such as risperidone and clozapine have been used in small series and may have a reduced risk of extrapyramidal side effects. Catecholamine-depleting agents such as reserpine and tetrabenazine may be considered when longterm therapy is required. Other pharmacologic agents have met with varying success. The course of hemiballismus may be complicated by exhaustion, injury, or metabolic disorders, but with good supportive care, acute survival is good, and long-term survival reflects the prognosis of the underlying etiology. In time, the ballistic movements themselves tend to subside allowing withdrawal of drugs in many cases. When movements persist, stereotactic functional neurosurgical procedures may be considered in good surgical candidates.

This is a preview of subscription content, log in via an institution to check access.

Access this article

Price excludes VAT (USA)
Tax calculation will be finalised during checkout.

Instant access to the full article PDF.

Similar content being viewed by others

References and Recommended Reading

  1. Dewey Jr RB, Jankovic J: Hemiballism-hemichorea. Clinical and pharmacologic findings in 21 patients. Arch Neurol 1989, 46:862–867.

    PubMed  Google Scholar 

  2. Pekmezovic T, Svetel M, Ristic A, et al.: Incidence of vascular hemiballism in the population of Belgrade. Mov Disord 2004, 19:1469–1472. This population-based study of vascular hemiballismus persons over 40 in Belgrade over the period between 1/1/1991 and 12/31/1992 found an annual incidence from 0.14/100,000 to 0.87/100,000 (average 0.45/100,000).

    Article  PubMed  Google Scholar 

  3. Postuma RB, Lang AE: Hemiballism: revisiting a classic disorder. Lancet Neurol 2003, 2:661–668. Postuma and Lang reviewed cases from their own subspecialty movement disorders practice and literature cases to challenge the notion that most cases resulted from structural lesions in the subthalamic nucleus. In only 26% of 120 cases, a lesion was definitely or possibly located in that structure. This article also is an excellent review of etiology, pathophysiology, and treatment.

    Article  PubMed  Google Scholar 

  4. Lee BC, Hwang SH, Chang GY: Hemiballismus-hemi-chorea in older diabetic women: a clinical syndrome with MRI correlation. Neurology 1999, 52:646–648. Nonketotic hyperglycemia has emerged as one of the most important causes of hemiballismus. This paper shows the typ-ical MRI changes associated with this form of hemiballismus.

    PubMed  CAS  Google Scholar 

  5. Kostic V, Djuricic B, Paschen W: Hemiballismus: changes in cerebrospinal fluid. Acta Neurol Scand 1988, 78:115–17.

    PubMed  CAS  Google Scholar 

  6. Crossman AR, Sambrook MA, Jackson A: Experimental hemichorea/hemiballismus in the monkey. Studies on the intracerebral site of action in a drug-induced dyskinesia. Brain 1984, 107:579–596.

    Article  PubMed  Google Scholar 

  7. Ristic A, Marinkovic J, Dragasevic N, et al.: Long-term prognosis of vascular hemiballismus. Stroke 2002, 33:2109–2111. Ristic et al. report that the long term prognosis of vascular hemiballismus reflects that of stroke.

    Article  PubMed  Google Scholar 

  8. Ghika-Schmid F, Ghika J, Regli F, Bogousslavsky J: Hyperkinetic movement disorders during and after acute stroke: the Lausanne Stroke Registry. J Neurol Sci 1997, 146:109–116.

    Article  PubMed  CAS  Google Scholar 

  9. Klawans HL, Moses H, Nausieda PA, et al.: Treatment and prognosis of hemiballismus. N Engl J Med 1976, 295:1348–1350.

    Article  PubMed  CAS  Google Scholar 

  10. Johnson WG, Fahn S: Treatment of vascular hemichorea and hemiballismus with perphenazine. Trans Am Neurol Assoc 1974, 99:222–224.

    PubMed  CAS  Google Scholar 

  11. Evidente VG, Gwinn-Hardy K, Caviness JN, Adler CH: Risperidone is effective in severe hemichorea/ hemiballismus. Mov Disord 1999, 14:377–379.

    Article  PubMed  CAS  Google Scholar 

  12. Stojanovic M, Sternic N, Kostic VS: Clozapine in hemiballismus: report of two cases. Clin Neuropharmacol 1997, 20:171–174.

    Article  PubMed  CAS  Google Scholar 

  13. Pearce J: Reversal of hemiballismus by tetrabenazine. JAMA 1972, 219:1345.

    Article  PubMed  CAS  Google Scholar 

  14. Obeso JA, Marti-Masso JF, Astudillo W, et al.: Treatment with hemiballism with reserpine. Ann Neurol 1978, 4:581.

    Article  PubMed  CAS  Google Scholar 

  15. Kothare SV, Pollack P, Kulberg AG, Ravin PD: Gabapentin treatment in a child with delayed-onset hemichorea/ hemiballismus. Pediatr Neurol 2000, 22:68–71.

    Article  PubMed  CAS  Google Scholar 

  16. Gonce M, Schoenen J, Charlier M, Delwaide PJ: Successful treatment of hemiballismus with progabide, a new GABA-mimetic agent. J Neurol 1983, 229:121–124.

    Article  PubMed  CAS  Google Scholar 

  17. Hordnes J, Moen G, Tysnes OB: [Hemiballismus in cerebral infarction]. Tidsskr Nor Laegeforen 2001, 121(22):2593–2595.

    PubMed  CAS  Google Scholar 

  18. Dressler D, Wittstock M, Benecke R: Treatment of persistent hemiballism with botulinum toxin type A. Mov Disord 2000, 15:1281–1282.

    Article  PubMed  CAS  Google Scholar 

  19. Levesque MF, Markham C, Nakasato N: MR-guided ventral intermediate thalamotomy for posttraumatic hemiballismus. Stereotact Funct Neurosurg 1992, 58:88.

    Article  PubMed  CAS  Google Scholar 

  20. Jallo GI, Dogali M: Ventral intermediate thalamotomy for hemiballismus. Stereotact Funct Neurosurg 1995, 65:23–25.

    Article  PubMed  CAS  Google Scholar 

  21. Tsubokawa T, Katayama Y, Yamamoto T: Control of persistent hemiballismus by chronic thalamic stimulation. Report of two cases. J Neurosurg 1995, 82:501–505.

    PubMed  CAS  Google Scholar 

  22. Slavin KV, Baumann TK, Burchiel KJ: Treatment of hemiballismus with stereotactic pallidotomy. Case report and review of the literature. Neurosurg Focus 2004, 17:E7.

    PubMed  Google Scholar 

  23. Kurita H, Kawamoto S, Sasaki T, et al.: Relief of hemiballism from a basal ganglia arteriovenous malformation after radiosurgery. Neurology 1999, 52:188–190.

    PubMed  CAS  Google Scholar 

  24. Johnson WG, Fahn S: Treatment of vascular hemiballism and hemichorea. Neurology 1977, 27:634–636.

    PubMed  CAS  Google Scholar 

  25. Emre M, Landis T: Haloperidol in hemichorea-hemiballismus. J Neurol 1984, 231:280.

    Article  PubMed  CAS  Google Scholar 

  26. Gilbert GJ: Response of hemiballismus to haloperidol. JAMA 1975, 233:535–536.

    Article  PubMed  CAS  Google Scholar 

  27. Carella A: [A case of hemiballismus cured with chlorpromazine and butyrophenone]. Acta Neurol (Napoli) 1966, 21:46–54.

    CAS  Google Scholar 

  28. Friedman JH: Atypical antipsychotics in the EPS-vulnerable patient. Psychoneuroendocrinology 2003, 28(Suppl 1):39–51.

    Article  PubMed  CAS  Google Scholar 

  29. Chandra V, Wharton S, Spunt AL: Amelioration of hemiballismus with sodium valproate. Ann Neurol 1982, 12:407.

    Article  PubMed  CAS  Google Scholar 

  30. Okun MS, Riestra AR, Nadeau SE: Treatment of ballism and pseudobulbar affect with sertraline. Arch Neurol 2001, 58:1682–1684.

    Article  PubMed  CAS  Google Scholar 

  31. Krauss JK, Mundinger F: Functional stereotactic surgery for hemiballism. J Neurosurg 1996, 85:278–286.

    Article  PubMed  CAS  Google Scholar 

  32. Vitek JL, Chockkan V, Zhang JY, Kaneoke Y, et al.: Neuronal activity in the basal ganglia in patients with generalized dystonia and hemiballismus. Ann Neurol 1999, 46:22–35.

    Article  PubMed  CAS  Google Scholar 

  33. Carod-Artal FJ, Vargas AP, Marinho PB, et al.: [Tourettism, hemiballism and juvenile Parkinsonism: expanding the clinical spectrum of the neurodegeneration associated to pantothenate kinase deficiency (Hallervorden Spatz syndrome)]. Rev Neurol 2004, 38:327–331.

    PubMed  CAS  Google Scholar 

  34. Bujanover S, Levy Y, Katz M, et al.: Lack of association between anti-phospholipid antibodies (APLA) and Attention Deficit/Hyperactivity Disorder (ADHD) in children. Clin Dev Immunol 2003, 10:105–109.

    Article  PubMed  CAS  Google Scholar 

  35. Burstein L, Breningstall GN: Movement disorders in bacterial meningitis. J Pediatr 1986, 109:260–264.

    Article  PubMed  CAS  Google Scholar 

  36. Im SH, Oh CW, Kwon OK, et al.: Involuntary movement induced by cerebral ischemia: pathogenesis and surgical outcome. J Neurosurg 2004, 100:877–882.

    Article  PubMed  Google Scholar 

Download references

Author information

Authors and Affiliations

Authors

Rights and permissions

Reprints and permissions

About this article

Cite this article

Shannon, K.M. Hemiballismus. Curr Treat Options Neurol 7, 203–210 (2005). https://doi.org/10.1007/s11940-005-0013-3

Download citation

  • Issue Date:

  • DOI: https://doi.org/10.1007/s11940-005-0013-3

Keywords

Navigation