Tardive Dystonia Workup
- Author: Daniel Schneider, MD, MA; Chief Editor: Iqbal Ahmed, MBBS, FRCPsych(UK) more...
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:
CBC count with peripheral smear
Thyroid hormone indices
Liver enzyme values
Erythrocyte sedimentation rate
Antinuclear antibody level
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.
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. 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.
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.
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