Effects of hypothermia on median nerve somatosensory evoked potentials during spontaneous circulation.

Perioperative-induced hypothermia is a common means of reducing ischemic injury in neurosurgical procedures and cardiac surgery, and it may occur accidentally. Somatosensory evoked potentials (SSEPs) are used frequently for neurophysiologic monitoring of these procedures. The effects of hypothermia on SSEPs have been studied widely in humans with cardiopulmonary bypass (CPB) during nonpulsatile flow. However, changes of latency and amplitude of early SSEP components during spontaneous circulation have not yet been studied. Median nerve SSEPs were recorded in 21 patients during rewarming from 32 to 36 degrees C core temperature. Latencies and amplitudes of N9, N13, N20, and central conduction time were registered at 32, 34, and 36 degrees C. Latencies of N9, N13, and N20 were prolonged at 32 degrees C compared with 36 degrees C (N9: 13.4 +/- 1.4 msec versus 11.8 +/- 1.4 msec, P <.05; N13: 17.6 +/- 1.9 msec versus 15.4 +/- 1.4 msec, P <.01; N20: 26.5 +/- 1.8 msec versus 22.4 +/- 1.6 msec, P <.001). Amplitude of N20 was higher at 32 degrees C compared with 36 degrees C (2.86 +/- 1.94 microV versus 2.07 +/- 1.47 microV, P < .05). Central conduction time decreased by 27%, and peripheral latency of N13 decreased by 14%. The increase in SSEP latency (N9, N13, and N20) and central conduction time during moderate hypothermia of 32 degrees C and spontaneous circulation are comparable with those during nonpulsatile flow on CPB. In contrast to nonpulsatile flow, the amplitude of N20 was increased significantly (P < .05) during moderate hypothermia and pulsatile circulation. These results suggest to be cautious about generalizing the effects of hypothermia on SSEP during CPB to spontaneous circulation.