Citation

Zaidat OO, Kaminski HJ, Berenson F, Katirji B. Muscle Nerve 1999; 22(9): 1293-1296.

Affiliation

Department of Neurology, University Hospitals of Cleveland, Case Western Reserve University, 11100 Euclid Avenue, Cleveland, Ohio 44106-5098, USA.

Copyright

(Copyright © 1999, John Wiley and Sons)

DOI

unavailable

PMID

10454730

Abstract

The clinical effect of carbamazepine (CBZ) on neuromuscular transmission is described in two children who presented in coma with diffuse hypotonia and areflexia following CBZ overdose. Repetitive nerve stimulation (RNS) showed a decremental response only at high-frequency stimulation. With supportive care, the patients made an uneventful recovery. Follow-up RNS was normal. This is the first report of a clinically evident neuromuscular transmission defect produced by CBZ. We postulate that CBZ's known effect on decreasing sodium channel depolarization produced a defect in neuromuscular transmission. The report emphasizes the contribution of RNS in the evaluation of coma of uncertain etiology, particularly in cases of possible intoxication, and the potential for CBZ to compromise neuromuscular transmission in normal individuals or in patients with a decreased neuromuscular transmission safety factor.

Language: en