Somatosensory Evoked Potentials: Objective Measures of Antinociception in the Anesthetized Patient?

Abstract

The most critical problems in pain research and clinical practice are the quantitation of nociception and the subjective experience of pain. From a physiologic point of view, pain is a consequence of the activation of nociceptive afferents and neural activity induced by noxious stimuli. The increased nociceptive signal transmission induces changes in brain electrical activity which may be assessed by physiologic measures. One of these neurophysiologic measures is the somatosensory evoked potential (SEP). SEPs reflect changes in brain electrical activity induced by electrical, mechanical, thermal, chemical, or tactile stimulation of peripheral neves. SEPs represent the activities of a rather large number of subcortical and cortical neural generators and are widely used as objective measures of sensory function [56]. The evoked cerebral potential reflects activation of specific afferent sensory systems. However, the evoked response is not specific for a unique stimulus modality. The early SEP components show peak latencies of less than 80 ms. They are separated into early farfield potentials with origins in subcortical structures (e.g., spinal cord, brain stem, thalamus) and early nearfield potentials generated by stimulus-induced summated postsynaptic activity of cortical neurons [22] (Fig. 1). Late SEP components with peak latencies of 80 ms or more may coincide with cognitive signal recognition or magnitude estimation [3, 4, 11, 12, 14–17]. They can best be recorded over the vertex. Both early and late SEPs reflect activity in large myelinated peripheral nerve fibers which activate the dorsal column [23].