Neuromuscular transmission defect caused by carbamazepine1

✍ Scribed by Osama O. Zaidat; Henry J. Kaminski; Frank Berenson; Bashar Katirji

• Book ID: 101254443
• Publisher: John Wiley and Sons
• Year: 1999
• Tongue: English
• Weight: 99 KB
• Volume: 22
• Category: Article
• ISSN: 0148-639X
• DOI: 10.1002/(sici)1097-4598(199909)22:9<1293::aid-mus21>3.0.co;2-j

✦ Synopsis

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.