Hypothermia amplifies somatosensory-evoked potentials in uninjured rats.

Temperature fluctuations significantly impact neurological injuries in intensive care units. As the benefits of therapeutic hypothermia continue to unfold, many of these discoveries are generated by studies in animal models undergoing experimental procedures under the influence of anesthetics. We studied the effect of induced hypothermia on neural electrophysiological signals of an uninjured brain in a rodent model while under isoflurane. Fourteen rats were divided into 2 groups (n=7 each), on the basis of electrode placement at either frontal-occipital or primary somatosensory cortical locations. Neural signals were recorded during normothermia (T=36.5 to 37.5°C), mild hypothermia (T=32 to 34°C), and hyperthermia (T=38.5 to 39.5°C). The burst-suppression ratio was used to evaluate electroencephalography (EEG), and amplitude-latency analysis was used to assess somatosensory-evoked potentials (SSEPs). Hypothermia was characterized by an increased burst-suppression ratio (mean±SD) of 0.58±0.06 in hypothermia versus 0.16±0.13 in normothermia, P<0.001 in frontal-occipital; and 0.30±0.13 in hypothermia versus 0.04±0.04 in normothermia, P=0.006 in somatosensory. There was potentiation of SSEP (2.89±1.24 times the normothermic baseline in hypothermia, P=0.02) and prolonged peak latency (N10: 10.8±0.4 ms in hypothermia vs. 9.1±0.3 ms in normothermia; P15: 16.2±0.8 ms in hypothermia vs. 13.7±0.6 ms in normothermia; P<0.001), whereas hyperthermia was primarily marked by shorter peak latencies (N10: 8.6±0.2 ms, P15: 12.6±0.4 m; P<0.001). In the absence of brain injury in a rodent model, hypothermia induces significant increase to the SSEP amplitude while increasing SSEP latency. Hypothermia also suppressed EEGs at different regions of the brain by different degrees. The changes to SSEP and EEG are both reversible with subsequent rewarming.