The Surgical Treatment And NMD ARK GluR2Expression In Cerebral Cortex Of Intractable Temporal Lobe Epilepsy

Epilepsy (EP) is a common central nervous system disease that has longcourse, repeated episodes and high death rate. It is reported that the morbidityrate of EP was7‰and the morbidity rate of active EP was4.6‰in China,and20%-25%among them were intractable EP that cannot be controlled bymedicines. Now, the surgical effect on intractable temporal lobe epilepsy(TLE) is fairly well. There are many preoperative evaluation methods for TLE,but still no best scheme.The pathogenesis of EP is still not clear now. Some animal experimentalstudies showed that N-methy-D-aspartate (NMDA) and alphaamino-3-hydroxyl-5-methyl-4-isoxazole-propionate (AMPA) receptor mayinvolve in the pathogenesis of EP. N-methy-D-aspartate receptor1(NR1/NMDAR1) subunit is the essential functional subunit of NMDAreceptor; Glutamate receptor2(GluR2) determines the Ca2+permeability ofneurons APMA receptors.This study is to investigate the best preoperative evaluation scheme forintractable TLE by summarizing the preoperative evaluation methods of33cases intractable TLE, operative methods and curative effects. This study alsotries to preliminarily investigate the pathogenesis of TLE by detecting theNMDAR1and GluR2expression in cerebral cortex of TLE patients andnon EP patients with immunohistochemical method.PartⅠ Preoperative evaluation scheme and operative effects of temporallobe epilepsyObjective:To investigate the best preoperative evaluation scheme for intractableTLE by summarizing the preoperative evaluation methods, operative methodsand curative effects. Methods：The clinical data of33TLE patients in Chengde5thHospital from2008.8to2010.10that were treated with operation were summarized. The results ofpreoperative evaluation methods such as clinical features,video-electroencephalogram (V-EEG), intracranial buried electrode V-EEG,cranial magnetic resonance imaging (MRI), single photon emission computedtomography (SPECT) were analyzed; the results of cortex and deep partelectroencephalogram (EEG) monitoring results were also analyzed. Theinformation about curative effects was obtained by rechecking V-EEG andtelephone follow-up. The effects of TLE operation were evaluated accordingto professor QiFu Tan’s standard in1994.Results:1The preoperative evaluation scheme for intractable TLEFollowing steps are needed to determine the EP lesion: First, diagnoseTLE according to clinical appearances and V-EEG results. Second, determinethe epileptiform discharge location and lesion site by V-EEG, cranial MRI andSPECT results. Third, to further determine epileptiform discharge location byintracranial buried electrode V-EEG monitoring for a few TLE patients thatwere difficult to determine epileptiform discharge location.2. Operative effectsAfter1-2years following up, in terms of the operative effects,30cases(90.9%) were satisfied,2cases (6.1%) improved obviously,1case (3%) notsatisfied. The total effective rate of operation was97.0%.Conclusions:1On scientificity, feasibility and practicability, we established apreoperative evaluation scheme of refractory epilepsy, which was based on thepreoperative evaluation experiences of33cases, predecessors’ experience, andthe characteristics of the basic-level hospitals: First, diagnose TLE accordingto clinical appearances and V-EEG results. Second, determine theepileptiform discharge location and lesion site by V-EEG, cranial MRI andSPECT results. Third, for a few TLE patients that were difficult to determine epileptiform discharge location, process intracranially buried electrode V-EEGmonitoring to further determine epileptiform discharge location.2It has been testified by surgical results of33cases intractable TLE thatthe preoperative evaluation scheme established in this study was very feasibleand practical, the cerebral cortex lesion site can be located accurately，the totaleffective rate of operation was97%.Part Ⅱ NMDAR1and GluR2expression in cerebral cortex of TLEpatientsObjective:To investigate the expression and significance of NMDAR1and GluR2in cerebral cortex of TLE patients, and provide experimental base forpreventing and drug treating TLE.Methods:33TLE patients were divided into3groups by interictal epileptiformdischarge (IED) frequency collected by V-EEG at awaking period duringinterictal phase: low frequency group, intermediate frequency group and highfrequency group (n=11). The NMDAR1and GluR2expression in cerebralcortex of TLE patients and non EP patients were detected byimmunohistochemical staining.Results:1NMDAR1expression in cerebral cortexThe NMDAR1immunopositive products were buffy exquisite granulasand located at cytoplasm and nuclear membrane of cerebral cortex neurons,mainly in cytoplasm. Compared with non EP patients, NMDAR1expressionin cerebral cortex of TLE patients increased obviously (P<0.05). NMDAR1expression in cerebral cortex of TLE patients in intermediate frequency groupand high frequency group were obviously higher than that of low frequencygroup (P<0.05). Compared with intermediate frequency group, NMDAR1 expression in cerebral cortex of TLE patients in high frequency groupincreased obviously (P<0.05).2GluR2expression in cerebral cortexThe GluR2immunopositive products were buffy exquisite granulas andlocated at the cytoplasm and cell membrane of cerebral cortex neurons, mainlyin cytoplasm. Compared with high frequency group, GluR2expression incerebral cortex of TLE patients in low frequency group, intermediatefrequency group and non EP patients group increased obviously (P<0.05).GluR2expression in cerebral cortex of TLE patients in low frequency groupwere obviously higher than non EP patients group and intermediate frequencygroup (P<0.05). There is no statistically significant between non EP patientsgroup and intermediate frequency group (P＞0.05).Conclusions:This study first discovers that abnormal expression of NMDAR1andGluR2has close relations with IED frequency of TLE. Moreover, NMDAR1expression has positive correlation with IED frequency of TLE, GluR2expression has negative correlation with IED frequency of TLE.