Current Treatment Options in Neurology

, Volume 7, Issue 3, pp 231–236 | Cite as

Tardive dystonia

  • Frank Skidmore
  • Stephen G. Reich

Opinion statement

Tardive dyskinesia is a movement disorder that develops after exposure to dopamine receptor blocking agents. Less well-appreciated are other, more recently described tardive syndromes that are phenomenologically distinct from tardive dyskinesia and respond to different treatments. Patients may simultaneously have more than one tardive syndrome. Major subtypes of tardive syndromes include tardive dyskinesia, characterized by orobuccolingual, truncal, or appendicular, choreiform movements; tardive dystonia, characterized by sustained, stereotyped muscle spasms of a twisting or turning character; and tardive akathisia, characterized by an inner sense of restlessness or unease. The sensation often is unpleasant and may be accompanied by repetitive, purposeless move-ments (stereotypies), such as pacing. Less common tardive syndromes include tardive myoclonus, tardive tourettism, and tardive tremor. Tardive syndromes often are a source of great distress and disability to patients and may be permanent, despite discontinuing the responsible medication. Prevention, early detection, and prompt management are the major clinical focus. When a patient develops a tardive syndrome appropriate actions include 1) review of the primary diagnosis that prompted starting a dopamine receptor blocking agent; 2) characterization of the movement disorder(s); 3) where possible, discontinuation of dopamine blocking agent or replacement with a less potent alternative agent; 4) gradual withdrawl of the offending drug because some patients have an exacerbation of a tardive syndrome after abrupt withdrawal; and 5) assessment of the severity of symptoms and development of a treatment plan based on the phenomenology, with the goal of maximizing patient comfort and function. Although tardive dyskinesia typically develops after chronic exposure to dopamine receptor blocking agents, it, and other variants (such as tardive dystonia) can develop very rapidly after treatment. There seems to be no minimal safe duration of exposure for the development of a tardive syndrome. It is important to recognize that anti-emetics, which are dopamine receptor blockers, such as prochlorperazine, promethazine and metoclopramide, can cause tardive syndromes. Clinicians should become familiar with antipsychotic agents that have a lower risk of causing tardive syndromes, such as clozapine, quetiapine, and olanzapine. We review treatment options for tardive dystonia.


Clozapine Olanzapine Dystonia Deep Brain Stimulation Botulinum Toxin 
These keywords were added by machine and not by the authors. This process is experimental and the keywords may be updated as the learning algorithm improves.


Unable to display preview. Download preview PDF.

Unable to display preview. Download preview PDF.

References and Recommended Reading

  1. 1.
    Urhbrand O, Faurbye A: Reversible and irreversible dyskinesia after treatment with perphenazine, chlorpromazine, reserpine, ECT therapy. Psycho-pharmacologia 1960, 1:408–418.Google Scholar
  2. 2.
    Faurbye A, Rasch PJ, Peterson PB, et al.: Neurological syndromes in pharmacotherapy of psychosis. Acta Psychiatr Scand 1964, 40:10–27.PubMedGoogle Scholar
  3. 3.
    Burke RE, Fahn S, Jankovic J, et al.: Tardive dystonia: late onset and persistent dystonia caused by anti-psychotic drugs. Neurology 1982, 32:1335–1346. This seminal case series presents 42 cases of tardive dystonia and is the first extensive description of the phenomena. Age of onset of tardive dystonia ranged from 13 to 60 years, and persistent dystonia developed as early as 3 days after exposure to neuroleptics (and as late as 11 years after onset of therapy).PubMedGoogle Scholar
  4. 4.
    Kang UJ, Burke RE, Fahn S: Natural history and treat-ment of tardive dystonia. Mov Disord 1986, 1:193–208. This report of 67 cases of tardive dystonia extends the observations of the previous reference. The authors again note that a significant portion (21%) of their patients developed the syn-drome within a year of starting neuroleptics. Withdrawal of dopamine-blocking therapy resulted in a low rate of remission (five of the 42 patients in whom dopamine blocking agents were withdrawn). The authors describe medical management with anticholinergics, reserpine, and tetrabenazine.PubMedCrossRefGoogle Scholar
  5. 5.
    Braude WM, Barnes TRE: Late-onset akathisia—an indicant of covert dyskinesia: two case reports. Am J Psychiatry 1983, 140:611–612.PubMedGoogle Scholar
  6. 6.
    Little JT, Jankovic J: Tardive myoclonus. Mov Disord 1987, 2:307–312.PubMedCrossRefGoogle Scholar
  7. 7.
    Bharucha KJ, Sethi KD: Tardive tourettism after exposure to neuroleptic therapy. Mov Disord 1995, 10:791–793.PubMedCrossRefGoogle Scholar
  8. 8.
    Stacy M, Jankovic J: Tardive tremor. Mov Disord 1992, 7:53–57.PubMedCrossRefGoogle Scholar
  9. 9.
    Kiriakakis V, Bhatia KP, Quinn NP, Marsden CD: The natural history of tardive dystonia. A long-term follow-up study of 107 cases. Brain 1998, 121:2053–2066. This article is the most extensive description of the clinical variability of tardive dystonia. One-hundred and seven individual cases were followed up for a mean 8.3 years. Onset of symptoms ranged from 4 days to 23 years after initiation of dopamine-blocking therapy. Only 14% of patients observed had a remission of symptoms during follow-up, but discontinuing dopamine-blocking therapy resulted in a four-fold increase in the rate of remission. Although onset was focal in 83%, symptoms progressed in most patients and remained focal in only 17% of patients.PubMedCrossRefGoogle Scholar
  10. 10.
    Correll CU, Leucht S, Kane JM: Lower risk for tardive dyskinesia associated with second-generation anti-psychotics: a systematic review of 1-year studies. Am J Psychiatry 2004, 161:414–425. This meta-analysis evaluates double-blind, randomized trials comparing the atypical antipsychotics and traditional anti-psychotic agents with regard to their propensity to cause tardive dyskinesia. Risperidone, olanzapine, quetiapine, amisulpride, and ziprasidone are compared. As a group, these atypical antipsychotic agents were less likely to cause tardive dyskinesia.PubMedCrossRefGoogle Scholar
  11. 11.
    Tarsy D, Baldessarini RJ, Tarazi FI: Effects of newer antipsychotics on extrapyramidal function. CNS Drugs 2002, 16:23–45.PubMedCrossRefGoogle Scholar
  12. 12.
    Jankovic J: Tardive syndromes and other drug-induced movement disorders. Clin Neuropharmacol 1995, 18:197–214. This is a good general review of tardive dyskinesia and other tardive syndromes.PubMedCrossRefGoogle Scholar
  13. 13.
    Fernandez HH, Friedman JH: Classification and treat-ment of tardive syndromes. Neurologist 2003, 9:16–27. This is another good general review of tardive dyskinesia and other tardive syndromes.PubMedCrossRefGoogle Scholar
  14. 14.
    Skidmore F, Weiner WJ, Burke R: Tardive dyskinesia variants. Drug Induced Movement Disorders. Edited by Weiner WJ, Lang A. Malden, MA: Blackwell Publishing; 2005:257–284. This is a good review of the available literature on tardive dystonia, tardive akathisia, tardive myoclonus, tardive tics, and tardive tremor.Google Scholar
  15. 15.
    Fahn S: Concept and classification of dystonia. In Dystonia 2, Advances in Neurology. Edited by Fahn S, Marsden CD, Calne DB. New York: Raven Press; 1988:2–8.Google Scholar
  16. 16.
    Sachdev P: Tardive blepharospasm. Mov Disord 1998, 13:947–951.PubMedCrossRefGoogle Scholar
  17. 17.
    Levin H, Reddy R: Clozapine in the treatment of neuroleptic-induced blepharospasm: a report of 4 cases. J Clin Psychiatry 2000, 61:140–143.PubMedCrossRefGoogle Scholar
  18. 18.
    Tan EK, Jankovic J: Tardive and idiopathic oromandib-ular dystonia: a clinical comparison. J Neurol Neurosurg Psychiatry 2000, 68:186–190.PubMedCrossRefGoogle Scholar
  19. 19.
    Molho ES, Feustel PJ, Factor SA: Clinical comparison of tardive and idiopathic cervical dystonia. Mov Disord 1998, 13:486–489.PubMedCrossRefGoogle Scholar
  20. 20.
    Brashear A, Ambrosius WT, Eckert GJ, Siemers ER: Comparison of treatment of tardive dystonia and idiopathic cervical dystonia with botulinum toxin type A. Mov Disord 1998, 13:158–161. This open-label case control study evaluates the efficacy of botulinum toxin A in seven patients with tardive dystonia compared with 149 patients with idiopathic cervical dystonia. A slightly higher dose of botulinum toxin was required in patients with tardive dystonia (P=0.0045), but efficacy of this therapy was similar in both patient groups.PubMedCrossRefGoogle Scholar
  21. 21.
    Krack P, Schneider S, Deuschl G: Geste device in tardive dystonia with retrocollis and opisthotonic posturing. Mov Disord 1998, 13:155–157.PubMedCrossRefGoogle Scholar
  22. 22.
    Soares KVS, McGrath JJ: Vitamin E for neuroleptic-induced tardive dyskinesia. The Cochrane Database of Systematic Reviews 2001; 4. This meta-analysis of 10 controlled trials evaluates the available literature on the effectiveness of vitamin E in improving tardive dyskinesia. The analysis concluded that available data do not support the hypothesis that vitamin E provides a symptomatic benefit in tardive dyskinesia.Google Scholar
  23. 23.
    Friedman JH: Clozapine treatment of psychosis in patients with tardive dystonia: Report of three cases. Mov Disord 1994, 9:321–324.PubMedCrossRefGoogle Scholar
  24. 24.
    Wolf ME, Mosnaim AD: Improvement of axial dystonia with the administration of clozapine. Int J Clin Pharm Ther 1994, 32:282–283.Google Scholar
  25. 25.
    Trugman JM, Leadbetter R, Zalis ME, et al.: Treatment of severe axial tardive dystonia with clozapine: case report and hypothesis. Mov Disord 1994, 9:441–446.PubMedCrossRefGoogle Scholar
  26. 26.
    Shapleske J, McKay AP, McKenna PJ: Successful treatment of tardive dystonia with clozapine and clonazepam. Br J Psych 1996, 168:516–518.CrossRefGoogle Scholar
  27. 27.
    Lucetti C, Bellini G, Nuti A, et al.: Treatment of patients with tardive dystonia with olanzapine. Clin Neuropharmacol 2002, 25:71–74.PubMedCrossRefGoogle Scholar
  28. 28.
    Greene P: Baclofen in the treatment of dystonia. Clin Neuropharmacol 1992, 15:276–288.PubMedCrossRefGoogle Scholar
  29. 29.
    Dressler D, Oeljeschlager RO, Ruther E: Severe tardive dystonia: treatment with continuous intrathecal baclofen administration. Mov Disord 1997, 12:585–587.PubMedCrossRefGoogle Scholar
  30. 30.
    Jankovic J: Botulinum toxin in clinical practice. J Neurol Neurosurg Psychiatry 2004, 75:951–957.PubMedCrossRefGoogle Scholar
  31. 31.
    Tarsy D, Kaufman D, Sethi KD, et al.: An open-label study of botulinum toxin A for treatment of tardive dystonia. Clin Neuropharmacol 1997, 20:90–93.PubMedCrossRefGoogle Scholar
  32. 32.
    Chatterjee A, Forrest Gordon M, Giladi N, Trosch R: Botulinum toxin in the treatment of tardive dystonia. J Clin Psychopharmacol 1997, 17:497–498.PubMedCrossRefGoogle Scholar
  33. 33.
    Comella CL, Shannon KM, Jaglin J: Extensor truncal dystonia: successful treatment with botulinum toxin injections. Mov Disord 1998, 13:552–555.PubMedCrossRefGoogle Scholar
  34. 34.
    Trottenberg T, Volkmann J, Deuschl G, et al.: Treatment of severe tardive dystonia with pallidal deep brain stimulation. Neurology 2005, 64:344–346. The authors describe improvement of symptoms after pallidal deep brain stimulation in five patients with refractory tardive dystonia.PubMedGoogle Scholar
  35. 35.
    Trottenberg T, Paul G, Meissner W, et al.: Pallidal and thalamic neurostimulation in severe tardive dystonia. J Neurol Neurosurg Psychiatry 2001, 70:557–559.PubMedCrossRefGoogle Scholar

Copyright information

© Current Science Inc 2005

Authors and Affiliations

  • Frank Skidmore
  • Stephen G. Reich
    • 1
  1. 1.Department of NeurologyUniversity of Maryland School of MedicineBaltimoreUSA

Personalised recommendations