Mechanomyography as a novel marker of nerve dysfunction and recovery in chronic entrapment neuropathy

Introduction There is a need for objective metrics to quantify the degree of nerve dysfunction resulting from chronic entrapment neuropathy. Mechanomyography (MMG) detects mechanical motor activity after nerve stimulation using accelerometry, and it may be a useful tool for quantifying nerve function. Compared to traditional electrodiagnostic testing, MMG offers practical advantages including resistance to electrical interference and non-invasive sensor placement. The aim of this study was to investigate the association between MMG and nerve dysfunction secondary to chronic nerve compression in a rodent model, comparing these results to established electrodiagnostic and histologic metrics. Methods Lewis rats ( n = 60) underwent sciatic nerve compression surgery using silicone conduits on one side and sham surgery on the other side. Nerves were evaluated using a custom-built MMG device and compound muscle action potential (CMAP) prior to compression and after 2, 3, 4, 5, or 6 months of compression. To simulate decompression, the silicone tubes were removed after 3 months in 18 animals, and they recovered for an additional 2, 4, or 6 months. MMG metrics included the stimulus threshold required for a muscle response (MMG-st) and the magnitude of muscle acceleration. At each endpoint, evoked muscle force and muscle mass were measured, and histomorphometry analysis of nerve sections was performed. Results Compared across all timepoints, compressed nerves had increased MMG-st (control: 0.32 ± 0.09 mA, compressed: 0.42 ± 0.11 mA, p < 0.001), with differences becoming statistically significant by 3 months. Compressed nerves demonstrated increased CMAP latency and decreased amplitude, with corresponding histological changes including decreased myelin width and increased G-ratio. Following decompression and recovery, MMG-st decreased, with no detectable difference from controls by 6 months. MMG-st significantly correlated with CMAP latency (r rm = 0.41, p < 0.001), CMAP amplitude (r rm = −0.20, p = 0.021), and myelin width ( r = −0.45, p < 0.001). Using a threshold of ≥0.4 mA, MMG-st demonstrated 76% sensitivity and 80% specificity for identifying compressed nerves in this preclinical model. Discussion MMG-st was elevated after compression and improved following decompression, with statistically significant correlations to other established metrics. These results support a potential role for MMG in chronic entrapment neuropathies as an objective biomarker for quantifying nerve dysfunction and monitoring decompression adequacy.