eMedicine Specialties > Psychiatry > Psychosomatic

Dystonia, Tardive: Differential Diagnoses & Workup

Author: Daniel Schneider, MD, MA, Chief Resident, Departments of Psychiatry and Neurology, University of Massachusetts
Coauthor(s): Paula D Ravin, MD, Associate Professor of Clinical Neurology, University of Massachusetts Memorial Health Care
Contributor Information and Disclosures

Updated: Aug 31, 2009

Differential Diagnoses

Huntington Disease Dementia

Other Problems to Be Considered

Hallervorden-Spatz syndrome
Friedreich ataxia
Olivopontocerebellar atrophy
Lesch-Nyhan syndrome
Metachromatic leukodystrophy
Perinatal injury

Workup

Laboratory Studies

  • To differentiate tardive dystonia from all causes of dystonia, base the workup on the history findings and clinical presentation of the dystonic movements. Diagnostic studies used to differentiate among these numerous causes may need to be extensive in some cases.
  • Any CNS disorder affecting the basal ganglia can produce dyskinetic movements, which can be misleading to the diagnosis of tardive dystonia. A routine evaluation may include the following:
    • Electrolyte levels
    • CBC count with peripheral smear
    • Thyroid hormone indices
    • Calcium level
    • Magnesium level
    • Liver enzyme values
    • Erythrocyte sedimentation rate
    • Antinuclear antibody level
    • VDRL test
    • HIV antibody titer
    • Serum, copper, and ceruloplasmin values
    • Electroencephalogram, CT scan, or MRI of the brain
    • Additional tests - May be warranted in specific cases
  • These tests are expensive; therefore, consider the cost-to-benefit ratio to avoid unnecessary tests.

Imaging Studies

  • Most neuroimaging studies used for dystonia have been performed on patients with idiopathic torsion dystonia. A problem with several of the PET studies on dystonia is the heterogeneity of the patient group recruited. Familial, sporadic, and acquired dystonia have been considered together, and patients with focal or hemidystonia have been favored to provide a side-to-side comparison of basal ganglia function.
  • Increased resting lentiform nucleus metabolism has been described in patients with dystonia.
  • In 1988, Chase et al published a study of 6 patients with sporadic idiopathic dystonia with fluorodeoxyglucose, all of whom had normal findings from CT scan or MRI studies.16 Three patients had increased lenticular glucose use contralateral to the more affected limbs.
  • PET activation findings in patients with idiopathic and acquired dystonia are compatible with inappropriate overactivity of the basal ganglia and their frontal projections on limb movements underlying this condition. Whether the frontal association area overactivity is simply secondary to primary basal ganglia overactivity or represents an adaptive phenomenon in a conscious attempt to suppress the syndrome is unclear.

Other Tests

  • Tardive dystonia is not associated with a characteristic pathological finding. In some reports, the brain is normal, whereas other reports show inferior olive damage, substantia nigra, or nigrostriatal degeneration or swelling of the large neurons of the caudate.
  • Postmortem neurochemical studies found alterations in dopamine concentrations and receptor binding in the brains of persons with schizophrenia, but no specific change correlated with tardive dystonia. In 1987, Arai et al examined the brains of patients with drug-treated schizophrenia who had orofacial dyskinesia and found markedly inflated neurons in the cerebellar dentate nucleus without accompanying neuronal loss or gliosis.17

More on Dystonia, Tardive

Overview: Dystonia, Tardive
Differential Diagnoses & Workup: Dystonia, Tardive
Treatment & Medication: Dystonia, Tardive
Follow-up: Dystonia, Tardive
References

References

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

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

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

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

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

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

  16. 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].

  17. 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].

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  25. Franzini A, Marras C, Ferroli P, Zorzi G, Bugiani O, Romito L. Long-term high-frequency bilateral pallidal stimulation for neuroleptic-induced tardive dystonia. Report of two cases. J Neurosurg. Apr 2005;102(4):721-5. [Medline].

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Further Reading

Keywords

tardive dystonia, muscle contractions, dyskinesia, repetitive movement, abnormal posture, muscle twitch, twitching, involuntary movement, writer's cramp, blepharospasm, geste antagonistique, abnormal muscle spasm, anti-psychotic drug treatment, antipsychotic drug treatment, anti-psychotics, antipsychotics, neuroleptic-induced tardive dyskinesia, dystonic movement, focal striatal lesion, dystonic posture, Westphal phenomenon, neuroleptics, neuroleptic agents, neuroleptic drugs, torticollis, oromandibular dystonia, dystonic adductor dysphonia, focal dystonia, segmental cranial dystonia, segmental axial dystonia, segmental brachial dystonia, segmental crural dystonia, multifocal dystonia, generalized dystonia, hemidystonia, hemi-dystonia, stereotactic thalamotomy, thalamotomy, selective denervation

Contributor Information and Disclosures

Author

Daniel Schneider, MD, MA, Chief Resident, Departments of Psychiatry and Neurology, University of Massachusetts
Disclosure: Nothing to disclose.

Coauthor(s)

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 Headache Society, American Medical Association, Massachusetts Medical Society, and National Headache Foundation
Disclosure: Santhera Phameuticals Grant/research funds Other; Kyowa Pharmaceuticals Grant/research funds Other; Acadia Pharmaceuticals Grant/research funds Other; Bayer Pharmaceuticals None None

Medical Editor

Alan D Schmetzer, MD, Professor, Vice-Chair for Education, and Director of Residency Training in General and Addiction Psychiatry, 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 College of Physician Executives, American Medical Association, American Neuropsychiatric Association, American Psychiatric Association, and Association for Convulsive Therapy
Disclosure: Nothing to disclose.

Pharmacy Editor

Francisco Talavera, PharmD, PhD, Senior Pharmacy Editor, eMedicine
Disclosure: eMedicine Salary Employment

Managing Editor

Iqbal Ahmed, MBBS, Professor, Department of Psychiatry, John A Burns School of Medicine, University of Hawaii
Iqbal Ahmed, MBBS is a member of the following medical societies: Academy of Psychosomatic Medicine, American Association for Geriatric Psychiatry, American Neuropsychiatric Association, and American Psychiatric Association
Disclosure: Nothing to disclose.

CME Editor

Harold H Harsch, MD, Program Director of Geropsychiatry, Department of Geriatrics/Gerontology, Associate Professor, Department of Psychiatry and Department of Medicine, Froedtert Hospital, Medical College of Wisconsin
Harold H Harsch, MD is a member of the following medical societies: American Psychiatric Association
Disclosure: lilly Honoraria Speaking and teaching; Forest Labs Honoraria Speaking and teaching; AstraZeneca Honoraria Speaking and teaching; Pfizer Grant/research funds Speaking and teaching; Northstar Grant/research funds Research; Novartis Grant/research funds research; Pfizer  Speaking and teaching; Sanofi-avetis Grant/research funds research; Otsuke Grant/research funds reseach; GlaxoSmithKline Grant/research funds research

Chief Editor

Stephen Soreff, MD, President of Education Initiatives, Nottingham, NH; Faculty, Metropolitan College of Boston University, Boston, MA
Stephen Soreff, MD is a member of the following medical societies: American College of Mental Health Administration and American Psychosomatic Society
Disclosure: Nothing to disclose.

 
 
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