Contribution of anti-ryanodine receptor antibody to impairment of excitation–contraction coupling in myasthenia gravis

Abstract

ObjectiveThe aim of this study was to elucidate the relationship between the impairment of excitation–contraction (E–C) coupling and anti-ryanodine receptor (RyR) antibody in patients with myasthenia gravis (MG). MethodsMasseteric compound muscle action potential (CMAP) and mandibular movement-related potentials (MRPs) were recorded simultaneously after stimulating the trigeminal motor nerve with a needle electrode. The E–C coupling time (ECCT) was calculated as the latency difference between CMAP and MRP. For each patient, we selected a representative data set when there was no abnormal decrement in response to repetitive nerve stimulation. The 26 data sets were divided into an anti-RyR-positive group (n=12) and an anti-RyR-negative group (n=14). ResultsMasseteric ECCT was significantly longer (p=0.017) in anti-RyR-positive group (median, mean, range; 3.6, 3.8, 3.0–5.9ms) than in anti-RyR-negative group (3.1, 3.1, 2.7–4.0) although there were no significant differences in masseteric CMAP amplitude and % decrement between the two groups. The bite force was significantly lower in anti-RyR-positive group than in normal controls. ConclusionsPresence of anti-RyR antibodies is associated with significantly prolonged masseteric ECCT compared to absence of the antibodies in MG. SignificanceAnti-RyR antibody contributes to E–C coupling impairment in the masseter muscle in patients with MG.