摘要
Interictal brain energy metabolism and glutamate-glutamine cyclingare impaire d in epilepsy and may contribute to seizure generation. We used the zero-flow m icrodialysis method to measure the extracellular levels of glutamate,glutamine, and the major energy substrates glucose and lactate in the epileptogenic and the nonepileptogenic cortex and hippocampus of 38 awake epileptic patients during t he interictal period. Depth electrodes attached to microdialysis probes were use d to identify the epileptogenic and the nonepileptogenic sites. The epileptogeni c hippocampus had surprisingly high basal glutamate levels, low glutamine/glutam ate ratio, high lactate levels, and indication for poor glucose utilization. The epileptogenic cortex had only marginally increased glutamate levels. We propose that interictal energetic deficiency in the epileptogenic hippocampus could con tribute to impaired glutamate reuptake and glutamate-glutamine cycling, resulti ng in persistently increased extracellular glutamate, glial and neuronal toxicit y, increased lactate production together with poor lactate and glucose utilizati on, and ultimately worsening energy metabolism. Our data suggest that a differen t neurometabolic process underlies the neocortical epilepsies.
Interictal brain energy metabolism and glutamate-glutamine cyclingare impaire d in epilepsy and may contribute to seizure generation. We used the zero-flow m icrodialysis method to measure the extracellular levels of glutamate,glutamine, and the major energy substrates glucose and lactate in the epileptogenic and the nonepileptogenic cortex and hippocampus of 38 awake epileptic patients during t he interictal period. Depth electrodes attached to microdialysis probes were use d to identify the epileptogenic and the nonepileptogenic sites. The epileptogeni c hippocampus had surprisingly high basal glutamate levels, low glutamine/glutam ate ratio, high lactate levels, and indication for poor glucose utilization. The epileptogenic cortex had only marginally increased glutamate levels. We propose that interictal energetic deficiency in the epileptogenic hippocampus could con tribute to impaired glutamate reuptake and glutamate-glutamine cycling, resulti ng in persistently increased extracellular glutamate, glial and neuronal toxicit y, increased lactate production together with poor lactate and glucose utilizati on, and ultimately worsening energy metabolism. Our data suggest that a differen t neurometabolic process underlies the neocortical epilepsies.
出处
《世界核心医学期刊文摘（神经病学分册）》
2005年第7期12-12,共1页
Digest of the World Core Medical Journals:Clinical Neurology
