Peripheral Nerve Compression: Etiology, Critical Pressure Threshold, and Clinical Assessment

Abstract

A number of experimental studies in our laboratory have been designed to evaluate the functional response of the median nerve at the wrist to various degrees of acute local compression in healthy volunteers and hypertensive patients. The relative significance of ischemia and mechanical deformation in early nerve compression, the critical threshold pressure for nerve conduction impairment, and the clinical sensibility testing system most accurate for evaluating and following patients with acute and chronic compressive neuropathies have been determined using a human model for median nerve compression in the carpal tunnel. Between 40 mmHg and 50 mmHg there exists a critical threshold pressure in normotensive people at which peripheral nerve is acutely jeopardized. The critical pressure threshold is higher in hypertensive patients. The threshold exists at 30 mmHg below diastolic blood pressure and 45 mmHg below mean arterial blood pressure in both normotensive and hypertensive individuals. The correlation between systemic blood pressure and the function of the nerve in response to local compression favors the concept that reduced microvascular perfusion plays the major role in the early stages of low pressure nerve compression. In acute and chronic compression neuropathy, threshold tests (Semmes-Weinstein pressure, vibratory sensibility) detect the earliest abnormalities of nerve function.