# Clinical and electrophysiological characteristics of myasthenia gravis patients with concomitant type 2 diabetes mellitus

## TL;DR

This study finds that myasthenia gravis patients with type 2 diabetes show unique nerve function patterns, suggesting a link between metabolic issues and neuromuscular symptoms.

## Contribution

The study identifies a novel electrophysiological phenotype in MG patients with T2DM, including an 'L-shaped' decrement pattern in nerve stimulation.

## Key findings

- MG patients with T2DM show peripheral neuropathy signs like prolonged motor latencies and reduced nerve conduction.
- T2DM MG patients exhibit an 'L-shaped' decrement pattern in facial nerve stimulation, differing from non-T2DM patients.
- LFRNS decrement correlates with blood glucose levels and diabetes duration, indicating metabolic influence on nerve function.

## Abstract

Type 2 Diabetes Mellitus (T2DM) is a common comorbidity in late-onset myasthenia gravis (MG), with pre-existing T2DM in some MG patients hinting at a possible pathogenic connection between the two disorders. This study aims to explore the clinical and neurophysiological features of MG, with a particular focus on the electrophysiological disparities between MG patients with and without T2DM.

In this retrospective study, 170 MG inpatients were recruited and divided into T2DM (n = 51) and non-T2DM groups. Clinical profiles and electrophysiological characteristics were compared.

There were no significant differences between the two groups in terms of MG clinical classification, Quantitative MG (QMG) scores, or antibody profiles. Electrophysiologically, the T2DM group exhibited peripheral neuropathy, characterized by prolonged distal motor latencies, decreased compound muscle action potential (CMAP) amplitudes, slowed motor nerve conduction velocities, extended F-wave latencies, and sensory nerve dysfunction. In low-frequency repetitive nerve stimulation (LFRNS) of the facial nerve, the decrement pattern was predominantly “L-shaped” (minimal recovery) in T2DM patients, in contrast to the “U-shaped” pattern in non-T2DM patients. Accessory nerve LFRNS decrement showed a positive correlation with QMG score, fasting blood glucose levels, and diabetes duration.

Patients with MG and concomitant T2DM demonstrate electrophysiological evidence of peripheral nerve impairment and a unique “L-shaped” decrement pattern on LFRNS of the facial nerve. This distinct electrophysiological phenotype likely reflects a complex interplay of metabolic derangements at the neuromuscular junction (NMJ). These results highlight the critical role of glycemic control in the management of MG.