Effect of hypothermia on kainic acid-induced limbic seizures: an electroencephalographic and [formula omitted]-deoxyglucose autoradiographic study

Abstract

The effect of body temperature on kainic acid (KA)-induced limbic seizures was examined in Wistar rats. In rats undergoing limbic seizure induced by 1 μg intra-amygdaloid injection of KA, the post-injection latency of initial ictal discharges in the left amygdala was significantly longer in rats whose body temperature was lowered to 30°C (2.55±0.94 min at 37°C, 13.19±5.70 min at 30°C; p=0.0017). The post-injection latency of initial ictal discharges in the left hippocampus was also significantly longer under the same conditions (23.68±9.96 min at 37°C, 43.85±17.98 min at 30°C; p=0.0253). The number of limbic seizures occurring in the first 2 h post-injection was significantly lower in hypothermic rats (30.0±10.7 at 37°C, 8.71±2.69 at 30°C; p=0.0017), as was the total duration of limbic seizures over the same period (23.61±8.45 min at 37°C, 10.30±4.48 min at 30°C; p=0.0060). Local cerebral glucose utilization (LCGU), measured 2 h post-injection, was significantly lower in hypothermic rats, mainly in the limbic structures. 14 C -deoxyglucose autoradiograms showed decreased radiation density not only in the left amygdala and bilateral hippocampus, but also in the cerebral cortex of hypothermic rats. The results of the present experiment demonstrate that the use of hypothermia, which has been shown to be effective in the treatment of acute cerebral ischemia and brain injury, may also be effective in the treatment of status epileptics.