Medscape is available in 5 Language Editions – Choose your Edition here.


Tardive Dystonia Clinical Presentation

  • Author: Daniel Schneider, MD, MA; Chief Editor: Iqbal Ahmed, MBBS, FRCPsych(UK)  more...
Updated: Aug 12, 2015


Tardive dystonia starts insidiously and progresses over months or years, until it becomes static.

Young male psychiatric patients commonly develop tardive dystonia after variable periods (weeks or years) of exposure to dopamine antagonists.

In most patients, tardive dystonia begins in the face or neck; less commonly, the dystonia may begin in one of the arms and, rarely, as a focal foot dystonia.

In 1992, Burke et al conducted a study of patients at the time of maximum severity of their illness.[17] Most patients had involvement of cranial nerves. The neck was involved in almost 80% of the cases; retrocollis was characteristic, occurring in 50% of those with neck involvement. The trunk was affected in 35% of the patients, and most of them had back-arching movements. The arms were affected in 42% of the patients, often in the form of sustained extension to the elbow, especially when walking. The legs were affected in a minority of patients. According to Burke et al, the diagnosis of tardive dystonia requires the following 4 criteria

  1. The patient must have dystonic movements defined as sustained muscle contractions, frequently causing twisting and repetitive movements or abnormal postures.
  2. The dystonia must develop either during or within 3 months of a course of neuroleptic treatment. The 3-month cutoff recognizes the fact that neuroleptics may suppress tardive dyskinesia, which often does not become apparent until sometime after drugs are stopped.
  3. No other neurologic signs should be present to suggest one of the many known causes of secondary dystonia, such as Wilson disease.
  4. The patient must have a negative family history for dystonia. In the presence of a positive family history, knowing whether the affected individual has neuroleptic-induced dystonia or simply expresses an inherited form that is coincident with neuroleptic use is not possible.

A history of recent trauma in the same body region as the focal dystonia or head trauma suggests a posttraumatic dystonia. Hemidystonia is almost always related to a brain lesion on the contralateral side of the abnormal movements.


Physical Examination

The movements evident in patients with tardive dystonia are not dissimilar to those observed in patients with primary torsion dystonia. Dystonic movements can be focal, segmental, generalized, multifocal, or hemidystonic (as described in the Introduction).

A detailed movement disorders examination should be performed. This should include an evaluation for dystonia and abnormal movement disorders such as dyskinesias, parkinsonism, and akathisia.

Dystonia typically presents in a twisting pattern with deviations on multiple anatomical planes. For instance, torticollis usually presents with both a deviation to one side as well as a head tilt. A hand dystonia often presents with an ulnar deviation as well as fingers in flexion or extension. This twisting pattern can be stable or more dynamic in an athetoid pattern.

Dystonia can present with a tremor. One helpful hint in identifying a tremor as dystonic is if it resolves when the patient is asked to allow their affected body part to go into the position that the dystonia is trying to make it go (ie, not fight the movement). Although it does not rule out a dystonic tremor if it does not go away with this maneuver, it is pathognomonic if it does resolve.

Dystonia frequently presents with a sensory trick or geste antagonist. This involves a point on the body where sensory stimulation can frequently overcome or reduce the dystonic symptoms. For instance, patients with torticollis (dystonic neck rotation) frequently find that pressure on their chin or sides of their face can cause the dystonic movements to subside. Patients with jaw or lingual dystonia may find that holding a straw or toothpick inside their mouth helps to reduce their symptoms. These tricks can be helpful diagnostically, but also can be used in developing treatment plans.

Dystonia can be surprisingly task specific. For instance, symptoms can occur with speech but resolve with silence or occur while walking but resolve with running or walking backwards. Again, this can be used to assist with diagnosis and occasionally in developing nonpharmacologic treatment strategies.

A routine physical and neurologic examination should also be included, with an ophthalmologic examination with a slit-lamp if indicated, to look for other symptoms. If general physical examination signs or neurologic signs other than dystonia are present, then tardive dystonia may be associated with other pathologic conditions, because neuroleptics do not induce progressive changes in intellect, such as sensory function, pyramidal motor systems, and cerebellar function.

A mental status examination should be performed, but the results can be completely normal since tardive dystonia does not indicate a psychiatric disease. It is merely a secondary dystonia and any patient who takes a dopamine receptor blocker chronically for any reason (including patients taking antinausea medications) can develop this condition. Given that this is a neurologic and not a psychiatric condition, the mental status examination is not helpful for diagnostic purposes and is most useful in determining whether a patient needs to remain on dopamine blocking agents or can be weaned off.

Contributor Information and Disclosures

Daniel Schneider, MD, MA Assistant Professor of Neurology, Division of Movement Disorders and Behavioral Neurology, Medical Director for Neurologic and Psychiatric Deep Brain Stimulation, Rutgers Robert Wood Johnson Medical School

Disclosure: Nothing to disclose.


Paula D Ravin, MD Associate Professor of Clinical Neurology, University of Massachusetts Memorial Health Care

Paula D Ravin, MD is a member of the following medical societies: American Academy of Neurology, American Medical Association, Massachusetts Medical Society, American Headache Society, National Headache Foundation

Disclosure: Received grant/research funds from Chelsea Pharmaceuticals for independent contractor; Received grant/research funds from Kyowa Pharma for independent contractor; Received consulting fee from Best Doctors Inc for consulting; Received grant/research funds from Beth Israel IRB for independent contractor.

Specialty Editor Board

Francisco Talavera, PharmD, PhD Adjunct Assistant Professor, University of Nebraska Medical Center College of Pharmacy; Editor-in-Chief, Medscape Drug Reference

Disclosure: Received salary from Medscape for employment. for: Medscape.

Chief Editor

Iqbal Ahmed, MBBS, FRCPsych(UK) Faculty, Department of Psychiatry, Tripler Army Medical Center; Clinical Professor of Psychiatry, Uniformed Services University of the Health Sciences; Clinical Professor of Psychiatry, Clinical Professor of Geriatric Medicine, University of Hawaii, John A Burns School of Medicine

Iqbal Ahmed, MBBS, FRCPsych(UK) is a member of the following medical societies: Academy of Psychosomatic Medicine, American Neuropsychiatric Association, American Society of Clinical Psychopharmacology, Royal College of Psychiatrists, American Association for Geriatric Psychiatry, American Psychiatric Association

Disclosure: Nothing to disclose.

Additional Contributors

Alan D Schmetzer, MD Professor Emeritus, Department of Psychiatry, Indiana University School of Medicine

Alan D Schmetzer, MD is a member of the following medical societies: American Academy of Addiction Psychiatry, American Academy of Clinical Psychiatrists, American Academy of Psychiatry and the Law, American Association for Physician Leadership, American Medical Association, American Psychiatric Association, International Society for ECT and Neurostimulation, American Neuropsychiatric Association

Disclosure: Nothing to disclose.


The authors and editors of Medscape Reference gratefully acknowledge the contributions of previous authors, Nestor Galvez-Jimenez, MD, and Perla Periut, MD, to the development and writing of this article.

  1. Bhidayasiri R, Fahn S, Weiner WJ, Gronseth GS, Sullivan KL, Zesiewicz TA. Evidence-based guideline: treatment of tardive syndromes: report of the Guideline Development Subcommittee of the American Academy of Neurology. Neurology. 2013 Jul 30. 81(5):463-9. [Medline].

  2. Burke RE, Fahn S, Jankovic J, et al. Tardive dystonia: late-onset and persistent dystonia caused by antipsychotic drugs. Neurology. 1982 Dec. 32(12):1335-46. [Medline].

  3. Adityanjee, Aderibigbe YA, Jampala VC, Mathews T. The current status of tardive dystonia. Biol Psychiatry. 1999 Mar 15. 45(6):715-30. [Medline].

  4. 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 Nov. 121 (Pt 11):2053-66. [Medline].

  5. Fahn S, Marsden, CD, Calne DB. Classification and Investigation of Dystonia. Marsden CD, Fahn S. Movement Disorders, Vol. 2. London: Butterworths; 1987. 332-358.

  6. Fahn, Stanley and Jankovic, Joseph. Principles and Practice of Movement Disorders. Philadelphia, PA: Churchill Livingston Elveiser; 2007.

  7. Stacy, Mark A. Handbook of Dystonia. New York, NY: Informa Healthcare; 2007.

  8. Keegan DL, Rajput AH. Drug induced dystonia tarda: treatment with L-dopa. Dis Nerv Syst. 1973 Mar. 34(3):167-9. [Medline].

  9. Kang UJ, Burke RE, Fahn S. Tardive dystonia. Adv Neurol. 1988. 50:415-29. [Medline].

  10. Sachdev P. Risk factors for tardive dystonia: a case-control comparison with tardive dyskinesia. Acta Psychiatr Scand. 1993 Aug. 88(2):98-103. [Medline].

  11. Mihara K, Kondo T, Higuchi H, Takahashi H, Yoshida K, Shimizu T. Tardive dystonia and genetic polymorphisms of cytochrome P4502D6 and dopamine D2 and D3 receptors: a preliminary finding. Am J Med Genet. 2002 Aug 8. 114(6):693-5. [Medline].

  12. Trugman JM, Leadbetter R, Zalis ME, Burgdorf RO, Wooten GF. Treatment of severe axial tardive dystonia with clozapine: case report and hypothesis. Mov Disord. 1994 Jul. 9(4):441-6. [Medline].

  13. Yassa R, Nair V, Iskandar H. A comparison of severe tardive dystonia and severe tardive dyskinesia. Acta Psychiatr Scand. 1989 Aug. 80(2):155-9. [Medline].

  14. Friedman JH, Kucharski LT, Wagner RL. Tardive dystonia in a psychiatric hospital. J Neurol Neurosurg Psychiatry. 1987 Jun. 50(6):801-3. [Medline].

  15. Sethi KD, Hess DC, Harp RJ. Prevalence of dystonia in veterans on chronic antipsychotic therapy. Mov Disord. 1990. 5(4):319-21. [Medline].

  16. Gimenez-Roldan S, Mateo D, Bartolome P. Tardive dystonia and severe tardive dyskinesia. A comparison of risk factors and prognosis. Acta Psychiatr Scand. 1985 May. 71(5):488-94. [Medline].

  17. Burke RE. Neuroleptic-induced tardive dyskinesia variants. Lang AE, Weiner WJ, eds. Drug-Induced Movement Disorders. New York, NY: Futu; 1992. 168-98.

  18. Vandel P, Bonin B, Leveque E, et al. Tricyclic antidepressant-induced extrapyramidal side effects. Eur Neuropsychopharmacol. 1997 Aug. 7(3):207-12. [Medline].

  19. Gabellini AS, Pezzoli A, De Massis P, Sacquegna T. Veralipride-induced tardive dystonia in a patient with bipolar psychosis. Ital J Neurol Sci. 1992 Oct. 13(7):621-3. [Medline].

  20. Chakrabarti S, Chand PK. Lithium - induced tardive dystonia. Neurol India. 2002 Dec. 50(4):473-5. [Medline].

  21. Chase TN, Tamminga CA, Burrows H. Positron emission tomographic studies of regional cerebral glucose metabolism in idiopathic dystonia. Adv Neurol. 1988. 50:237-41. [Medline].

  22. Arai N, Amano N, Iseki E, et al. Tardive dyskinesia with inflated neurons of the cerebellar dentate nucleus. Case reports and morphometric study. Acta Neuropathol (Berl). 1987. 73(1):38-42. [Medline].

  23. Kaufman DM. Use of botulinum toxin injections for spasmodic torticollis of tardive dystonia. J Neuropsychiatry Clin Neurosci. 1994 Winter. 6(1):50-3. [Medline].

  24. Hennings JM, Krause E, Bötzel K, Wetter TC. Successful treatment of tardive lingual dystonia with botulinum toxin: case report and review of the literature. Prog Neuropsychopharmacol Biol Psychiatry. 2008 Jul 1. 32(5):1167-71. [Medline].

  25. Shapleske J, Mickay AP, Mckenna PJ. Successful treatment of tardive dystonia with clozapine and clonazepam. Br J Psychiatry. 1996 Apr. 168(4):516-8. [Medline].

  26. Blake LM, Marks RC, Nierman P, Luchins DJ. Clozapine and clonazepam in tardive dystonia. J Clin Psychopharmacol. 1991 Aug. 11(4):268-9. [Medline].

  27. Trottenberg T, Volkmann J, Deuschl G, Kühn AA, Schneider GH, Müller J. Treatment of severe tardive dystonia with pallidal deep brain stimulation. Neurology. 2005 Jan 25. 64(2):344-6. [Medline].

  28. Zhang JG, Zhang K, Wang ZC. Deep brain stimulation in the treatment of tardive dystonia. Chin Med J (Engl). 2006 May 5. 119(9):789-92. [Medline].

  29. Thobois S, Ballanger B, Xie-Brustolin J, Damier P, Durif F, Azulay JP, et al. Globus pallidus stimulation reduces frontal hyperactivity in tardive dystonia. J Cereb Blood Flow Metab. 2008 Jun. 28(6):1127-38. [Medline].

  30. Gruber D, Trottenberg T, Kivi A, Schoenecker T, Kopp UA, Hoffmann KT, et al. Long-term effects of pallidal deep brain stimulation in tardive dystonia. Neurology. 2009 Jul 7. 73(1):53-8. [Medline].

All material on this website is protected by copyright, Copyright © 1994-2016 by WebMD LLC. This website also contains material copyrighted by 3rd parties.