Postdoctoral Scholar Washington University School of Medicine St. Louis, Missouri, United States
Introduction: Chronic entrapment neuropathy results in a clinical syndrome ranging from mild pain to debilitating atrophy. There remains a lack of objective metrics that quantify nerve dysfunction and guide surgical decision-making. Mechanomyography (MMG) reflects mechanical motor activity quantified by muscle accelerometry following stimulation of neuromuscular tissue and may indicate underlying nerve dysfunction. The objective of this preclinical study is to establish MMG activation threshold as a marker of axonal injury and accelerometry (g- metric) as a marker of neuromuscular innervation in chronic entrapment neuropathies.
Methods: Experimental Lewis rats underwent sciatic nerve compressions at proximal and distal sites using silastic tubes. The rats were divided in mild (3-month compression), moderate (6-month compression), and severe (8-month compression) groups n=12 in each. MMG activation and accelerometry was acquired by custom-built device. Prior to nerve compression, electromyography (EMG) of tibialis anterior muscle, MMG activation thresholds, and accelerometry was acquired. Direct electrical nerve stimulation was performed with 0.1 mA to 1.5 mA current. The MMG activation was defined as threshold at which first motor response was seen. The accelerometry sensors detected muscle lift in z-axis fixed at ultrasensitive threshold of 30mV/G.
Results: Only baseline results are currently available from this ongoing study. 18 nerve compression surgeries have been performed thus far. At baseline, the mean EMG amplitude for the normal sciatic nerve was 11.29 (+/-4.53) mV and mean MMG activation threshold was 0.31 (+/-0.08) mA. There was a slight negative correlation between EMG amplitudes and MMG activation thresholds (rs -0.29 to -0.42) showing that lower MMG activation thresholds indicate integrity of the nerve. At each stimulus threshold from 0.1 mA to 1.5 mA, accelerometry signal appropriately quantified the muscle response ranging from 0.99 (+/-0.03) g at 0.1 mA, indicating no activation, to a maximal 2.54 (+/-0.42) g at 1.5 mA.
Conclusion : The MMG activation thresholds and muscle accelerometry may serve as a quantitative marker of axonal function and neuromuscular innervation. The validation of these metrics in varying grades of nerve injury would provide indication of axonal injury and prognostication of outcomes in chronic entrapment neuropathy.
How to Improve Patient Care: MMG may improve surgical care of patients with chronic entrapment neuropathy in future.
