140 Muscle Accelerometry as a Novel Marker of Axonal Injury in Chronic Entrapment Neuropathy

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. Muscle accelerometry quantify mechanical-motor-activity after stimulation of neuromuscular tissue and may enable evaluation of underlying nerve function. METHODS: Experimental Lewis-rats underwent compressions at proximal- and distal-sites of sciatic nerves using silicone-conduits. To simulate chronic-entrapment, sciatic nerves were compressed for 2-, 3-, and 4-months (n = 6 in each month) and were serially evaluated by accelerometry, compound-muscle-action-potential (CMAP), and compound-neural-action-potential (CNAP). To simulate recovery, sciatic nerves were decompressed at 3-months and tracked for additional 2-months with accelerometry, CMAP, and CNAP. In each group, the left-side served as control nerve and right-side served as experimental nerve. Accelerometry was acquired by custom-built-device after direct electrical-nerve-stimulation from 0.1-mA to 1.5-mA current. The accelerometry was quantified by composite magnitude of muscle movement in x-, y-, and z-axis. At each endpoint, histomorphometry analysis was performed to evaluate nerve injury and recovery. RESULTS: After each month of nerve compression, there was a trend in worsening of nerve function indicated by decline in accelerometry at higher stimulation current of 1.5-mA .This finding was correlated with CMAP and CNAP.At each endpoint of 2-, 3-, and 4-month, there was significant worsening in g-ratio of compressed nerve as compared to the control nerves. After decompression at 3-months, muscle accelerometry at 0.5 mA current indicated a clear trend in recovery of nerve function. This finding was correlated with CNAP, however, CMAP results were variable. CONCLUSIONS: The muscle accelerometry may serve as a quantitative marker of axonal function and neuromuscular reinnervation in chronic entrapment neuropathy.