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Alison Escherich, Terry Patterson, Mark M Stecker, Joseph E Bavaria, Albert T Cheung
Med Sci Monit 2002; 8(4): CR223-228
BACKGROUND: Hypothermia is used clinically to prevent neurologic injurybut the degree of protection which it affords at various levels of the nervous system in humans is difficultto establish. MATERIAL/METHODS: The temporal changes in EEG amplitude and somatosensory evoked potential(SEP) amplitudes in a patient experiencing acute normothermic hypoxemia, a patient experiencing acutecirculatory arrest at moderate hypothermia and a collection of patients undergoing deep hypothermic circulatoryarrest were analyzed to determine the rate at which changes occur during acute lack of oxygen deliveryat various temperatures. RESULTS: In each case, it was found that more rostrally generated potentialsdisappeared more quickly than more peripheral potentials. All potentials decayed more slowly during acutenormothermic hypoxemia than during circulatory arrest. During circulatory arrest at 14.4 degrees C, theamplitude of the Erb's point, N13 and N18 potentials in the SEP took 5 times longer to drop to 50% oftheir value at the onset of ischemia than with circulatory arrest at 30.9 degrees C. CONCLUSIONS: Thelonger times to disappearance of the SEP potentials during deep hypothermia compared to moderate hypothermiawas consistent with the predicted 3.5-6.5 fold reduction in metabolic activity at deep hypothermia comparedto moderate hypothermia. The prolonged time to disappearance of the SEP during normothermic hypoxemiademonstrates that even with reduced oxygen delivery the continued delivery of metabolic substrate canbe critical to neural function.