Tardive dyskinesia in dopa-responsive dystonia: a reappraisal of the dopamine hypothesis of tardive dyskinesia.
Dopa-responsive dystonia, an autosomal-dominant disorder caused by mutations in the guanosine triphosphate (GTP)-cyclohydrolase I gene, is characterized by severe striatal dopamine depletion. Tardive dyskinesia, on the other hand, has often been associated with striatal dopamine overactivity. This article reports on a 44-year-old man with dopa-responsive dystonia who developed tardive dyskinesia on long-term haloperidol therapy. Nigrostriatal dopamine deficiency may be necessary for the development of tardive dyskinesia.
de la Fuente-Fernández
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Department of Neurology, EuroEspes Biomedical Research Center, La Coruña, Spain.
D000328:Adult; D018726:Anti-Dyskinesia Agents / Q000009:adverse effects*; D004298:Dopamine / Q000096:biosynthesis / Q000502:physiology; D015259:Dopamine Agents / Q000009:adverse effects; D004409:Dyskinesia, Drug-Induced / Q000188:drug therapy*; D004421:Dystonia / Q000188:drug therapy* / Q000235:genetics; D005192:Family Health; D005260:Female; D006136:GTP Cyclohydrolase / Q000235:genetics; D006220:Haloperidol / Q000009:adverse effects*; D006801:Humans; D007980:Levodopa / Q000009:adverse effects; D008297:Male; D017354:Point Mutation
D018726:Anti-Dyskinesia Agents; D015259:Dopamine Agents; D007980:Levodopa; D006136:GTP Cyclohydrolase; D006220:Haloperidol; D004298:Dopamine