2018 Volume 46 Issue 2 Pages 85-94
Several studies have shown the failure of excitation-contraction (E-C) coupling in myasthenia gravis (MG). However, there had been few useful methods to measure E-C coupling in vivo. In 2000s, we developed new E-C coupling testing procedures using accelerometer to record movement-related potentials (MRPs). The compound muscle action potentials (CMAPs) and MRPs were recorded simultaneously after stimulating the dominant nerve, and the E-C coupling time (ECCT) was calculated by the latency difference between CMAP and MRP. Moreover, the amplitude of MRP (=maximum acceleration) was analyzed to examine the twitch force of innervated muscles. The new method has been applied to masseter and jaw movement after trigeminal nerve stimulation (Imai’s method), or abductor pollicis brevis (APB) muscle and thumb movement after median nerve stimulation. As a result, we reported several interesting findings in MG: (1) impaired E-C coupling contributes to muscle weakness apart from neuromuscular transmission in the masseter; (2) anti-ryanodine receptor (RyR) antibody contributes to E-C coupling impairment in the masseter; (3) the early effect of tacrolimus may imply a pharmacological enhancement of RyR function to improve E-C coupling; (4) post-tetanic potentiation of APB muscle twitch is diminished, suggesting impaired E-C coupling; (5) the ice-pack test induces a prolonged effect of ameliorating impaired E-C coupling.
