Tourniquet‐induced ischemia and somatosensory evoked potentials

Abstract

We studied the effect of tourniquet-induced ischemia on the somatosensory evoked potential (SEPI. During 24 minutes of ischemia, short-latency components (P9, P14, and N18) and Erb9s potential were abolished earlier than the iong-latency components iP22, N30, P40, and N60). The latency increase was the same for Erbs potential and for P9, P14, and N18, but it was greater for P22, N30, and P40 and greatest for N60. These dissociated effects suggest that SEP components are not transmitted through a single pathway but are mediated through independent routes, possibly involving different first-order afferent fibers. Selective abnormalities of the early SEP peaks in association with relative preservation of late peaks may occur in peripheral nerve disorders.