Vol.:(0123456789) 1 3 Acta Neurol Belg DOI 10.1007/s13760-017-0839-y ORIGINAL ARTICLE An investigation on the efects of carbamazepine and sodium valproate on neuromuscular transmission Halil Ay 1  · Özlem Ethemoğlu 1   Received: 8 August 2017 / Accepted: 18 September 2017 © Belgian Neurological Society 2017 telithromycin, fuoroquinolones, aminoglycosides, mac- rolides, and anaesthetics cause worsening of the disease [1]. In mammalians, calcium (Ca 2+ ) has been shown to enter the nerve terminals through at least three diferent channels at neuromuscular junction. While the L- and N-type Ca 2+ channels have been demonstrated to be mostly associated with spontaneous release of acetylcholine, P/Q-type Ca 2+ channels have been shown to be associated with neurotrans- mitter release induced by depolarisation [2]. In a reported study, investigation of neuromuscular junction by electron microscopy in rats indicated that the voltage-gated sodium (Na + ) channels were concentrated in depths of postsynaptic membrane and perijunctional region [3]. Sodium valproate (SV) is an antiepileptic drug that is used commonly in treatment of both partial and general- ised epileptic seizures [4]. Currently, antiepileptic mecha- nism of action of SV has been described by the multiple mechanisms of action including potentiation of GABAergic (gamma-aminobutyric acid) system, inhibition of glutamate receptors, and potential blockade of voltage-gated Na + chan- nels [5]. In a study, SV has been found to block the T-type calcium channels in acutely isolated thalamocortical neurons from rats [6]. SV also has efects on L-type calcium chan- nels, sodium channels, and voltage-gated potassium chan- nels [7]. Carbamazepine (CBZ) is used in treatment of simple and complex partial seizures of epilepsy and generalised convul- sions. It inhibits release of glutamate and the like neuro- transmitters by blocking the presynaptic voltage-sensitive sodium channels in central nervous system. It also blocks N-methyl-D-aspartate and adenosine receptors [8]. Another mechanism of action of CBZ is blockade of L-type calcium channels [9]. Currently, there are limited studies that investigated the relationship of antiepileptic drugs with neuromuscular Abstract The aim of this study was to investigate the efects of sodium valproate (SV) and carbamazepine (CBZ) on neuromuscular transmission using single-fbre electro- myography (SFEMG) in patients with epilepsy. We per- formed SFEMG during the voluntary contraction of extensor digitorum communis muscle. 30 epileptic patients taking SV, 25 epileptic patients taking CBZ, and 25 age-matched healthy volunteers were included in the study. Mean jitter values (MCD) of subjects taking SV and CBZ were com- pared with normal controls. MCD values of subjects tak- ing SV and CBZ were statistically signifcantly higher than those of control group. Review of the correlation between disease duration and MCD values of patients showed that MCD values were increased with the prolonged use of drugs, and thus, indicated a positive relationship between these two parameters. These results suggest that both SV and CBZ reduce neuromuscular transmission in patients without a neuromuscular junction disease. Keywords Sodium valproate · Carbamazepine · Neuromuscular disease · Single-fbre electromyography · Epilepsy Introduction Many drugs have been reported to adversely interact with neuromuscular transmission in Myasthenia Gravis (MG) disease. Several agents including D-penicillamine, * Halil Ay ayhalil27@hotmail.com 1 Department of Neurology, Harran University, Medical Faculty, Şanlıurfa, Turkey