Ingvar M, Shapiro H M
Anesthesiology. 1981 Jan;54(1):33-7. doi: 10.1097/00000542-198101000-00007.
Neurophysiologic studies indicate that local anesthetic-induced seizures are generated in subcortical brain structures. The authors utilized a quantitative autoradiographic technique to measure cerebral metabolism during lidocaine-induced seizure activity in rats anesthetized with nitrous oxide. Local cerebral metabolic rate for glucose (l-CMRg) was determined when lidocaine infusion resulted in sustained electroencephalographic patterns consisting of approximately 100--125-mu volt discharges with a frequency of about 9 Hz, lasting 1-2 sec, and superimposed upon almost isoelectric periods lasting 1-3 sec. Significant reductions in 1-CMRg (30-70 per cent decreases) occurred in 19 of 26 regions surveyed. All areas of cerebral cortex had decreased glucose uptake following lidocaine administration. The hippocampus developed a striking increase in 1-CMRg of 237 per cent, while the amygdala and other related nuclei sustained metabolic rates similar to those present before lidocaine was given. This study demonstrates a coupling of metabolic activity with functional activity in subcortical structures recognized to be involved in the generation of local anesthetic seizure activity. Additionally, it reveals a heterogeneous response of cerebral metabolism to lidocaine infusion in the presence of subcortically localized seizures.
神经生理学研究表明，局部麻醉药诱发的癫痫发作是在大脑皮质下结构中产生的。作者利用定量放射自显影技术，在一氧化二氮麻醉的大鼠中测量利多卡因诱发癫痫活动期间的脑代谢。当利多卡因输注导致脑电图模式持续，包括频率约为9Hz、持续1 - 2秒、幅度约为100 - 125微伏的放电，并叠加在持续1 - 3秒的几乎等电位期时，测定局部脑葡萄糖代谢率（l - CMRg）。在26个被检测区域中的19个区域，l - CMRg出现显著降低（降低30 - 70%）。利多卡因给药后，大脑皮质的所有区域葡萄糖摄取均减少。海马体的l - CMRg显著增加237%，而杏仁核和其他相关核团的代谢率维持在利多卡因给药前的水平。这项研究证明了在被认为与局部麻醉药癫痫活动产生有关的皮质下结构中，代谢活动与功能活动之间的耦合。此外，它揭示了在皮质下局限性癫痫发作存在的情况下，脑代谢对利多卡因输注的异质性反应。
