Does peripheral neuropathy allow for the clinical expression of tardive dyskinesia by unmasking central nervous system changes?
Tardive dyskinesia (TD) is a severe and troubling complication of long-term typical neuroleptic use whose etiology remains obscure. While it is widely believed that central nervous system (CNS) dopamine receptor super-sensitivity is involved in the pathogenesis of the condition, it is unclear why some patients develop TD while others do not. It is proposed that a subclinical peripheral motoneuropathy with consequent enlarging of the motor units may act to unmask neuroleptic-induced CNS changes allowing for the expression of TD. To investigate this hypothesis we examined motor unit size with electrographic examinations in 14 patients (six with mild TD; eight without and all with psychotic illness). There were no differences between the two groups of patients. While the data do not appear to support the hypothesis, a larger study with more severely affected patients is required to more adequately test the hypothesis.
El-Mallakh
R S
RS
Mood Disorders Research Program, University of Louisville School of Medicine, Kentucky 40292, USA.
Pant
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Caudill
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Bacani-Oropilla
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D000328:Adult; D002490:Central Nervous System / Q000503:physiopathology*; D004409:Dyskinesia, Drug-Induced / Q000209:etiology*; D004576:Electromyography; D005260:Female; D006801:Humans; D008297:Male; D008875:Middle Aged; D017933:Peripheral Nervous System / Q000503:physiopathology; D010523:Peripheral Nervous System Diseases / Q000150:complications*