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Extracellular metabolites in the cortex and hippocampus of epileptic patients
Author(s) -
Cavus Idil,
Kasoff Willard S.,
Cassaday Michael P.,
Jacob Ralph,
Gueorguieva Ralitza,
Sherwin Robert S.,
Krystal John H.,
Spencer Dennis D.,
AbiSaab Walid M.
Publication year - 2005
Publication title -
annals of neurology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 4.764
H-Index - 296
eISSN - 1531-8249
pISSN - 0364-5134
DOI - 10.1002/ana.20380
Subject(s) - microdialysis , glutamate receptor , glutamine , ictal , hippocampus , epilepsy , neuroscience , cortex (anatomy) , medicine , biology , endocrinology , chemistry , biochemistry , central nervous system , amino acid , receptor
Interictal brain energy metabolism and glutamate–glutamine cycling are impaired in epilepsy and may contribute to seizure generation. We used the zero‐flow microdialysis 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 the interictal period. Depth electrodes attached to microdialysis probes were used to identify the epileptogenic and the nonepileptogenic sites. The epileptogenic hippocampus had surprisingly high basal glutamate levels, low glutamine/glutamate 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 contribute to impaired glutamate reuptake and glutamate–glutamine cycling, resulting in persistently increased extracellular glutamate, glial and neuronal toxicity, increased lactate production together with poor lactate and glucose utilization, and ultimately worsening energy metabolism. Our data suggest that a different neurometabolic process underlies the neocortical epilepsies. Ann Neurol 2005;57:226–235