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Published on: February 14, 2012
Does peripheral neuropathy allow for the clinical expression of tardive dyskinesia by unmasking central nervous
R S El-Mallakh1, B Pant, R Caudill
1Mood Disorders Research Program, University of Louisville School of Medicine, Kentucky 40292, USA.
Abstract:
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.
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