Effects of hypothermia on short latency somatosensory evoked potentials in humans

Short latency somatosensory evoked potentials (SSEPs) elicited by median nerve stimulation were monitored in 14 adult patients undergoing cardiac surgery under cardiopulmonary bypass and induced hypothermia. SSEPs were recorded at 1–2°C steps as the body temperature was lowered from 37°C to 20°C to determine temperature-dependent changes. Hypothermia produced increased latencies of the peaks of N 10, P 14 and N 19 components, the prolongation was more severe for the later components so that N 10−P 14 and P 14−N 19 interpeak latencies were also prolonged. The temperature-latency relationship had a linear correlation. The magnitude of latency prolongation (msec) with 1°C decline in temperature was 0.61, 1.15, 1.56 for N 10,P 4 and N 19 components, respectively, and 0.39 and 0.68 for interpeak latencies N 10−P 14 and P 14−N 19, respectively. The rise time and duration of the 3 SSEP components increased progressively with cooling. Cortically generated component, N 19 was consistently recordable at a temperature above 26°C, usually disappearing between 20°C and 25°C. On the other hand, more peripherally generated components, N 10 and P 14, were more resistant to the effect of hypothermia; P 14 was always elicitable at 21°C or above, whereas N 10 persisted even below 20°C. The amplitude of SSEP components had a poor correlation with temperature; there was a slight tendency for N 10 and P 14 to increase and for N 19 to decrease with declining temperature. Because incidental hypothermia is common in comatose and anesthetized patients, temperature-related changes must be taken into consideration during SSEP monitoring under these circumstances.