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Tardive Dystonia Workup

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

Approach Considerations

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.

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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.[21] 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.

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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.[22]

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Contributor Information and Disclosures
Author

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.

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 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.

Acknowledgements

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.

References
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