Does peripheral neuropathy allow for the clinical expression of tardive dyskinesia by unmasking central nervous system changes

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.