Introduction to temporal lobe epilepsy

被引:327
作者
Engel, J
机构
[1] UNIV CALIF LOS ANGELES, SCH MED, DEPT NEUROL, LOS ANGELES, CA 90024 USA
[2] UNIV CALIF LOS ANGELES, SCH MED, DEPT NEUROBIOL, LOS ANGELES, CA 90024 USA
[3] UNIV CALIF LOS ANGELES, SCH MED, BRAIN RES INST, LOS ANGELES, CA 90024 USA
关键词
temporal lobe epilepsy; hippocampal sclerosis; discrete lesions; cryptogenic; animal models;
D O I
10.1016/S0920-1211(96)00043-5
中图分类号
R74 [神经病学与精神病学];
学科分类号
摘要
Epileptic disorders are classified as idiopathic when they are genetically transmitted conditions that consist of epilepsy only, with no structural lesions in the brain and no associated neurological deficits, and symptomatic when they result from some other primary brain lesion or insult. Symptomatic temporal lobe epilepsy can be further divided into mesial temporal lobe epilepsy (MTLE), the condition associated with hippocampal sclerosis; lesional temporal lobe epilepsy due to specific identifiable lesions localized to areas that preferentially project to mesial temporal structures; and cryptogenic temporal lobe epilepsy, for which no etiology can be determined. Intensive clinical and basic research on MTLE, perhaps the most common form of human epilepsy, is currently being carried out in epilepsy research centers, and a number of experimental animal models have now been developed to help elucidate the pathophysiology of this condition. Animal models are also important for determining how specific lesions induce epileptogenicity, and whether the neuronal mechanisms in mesial temporal lobe limbic structures are the same as those in neocortex. Cryptogenic temporal lobe epilepsy remains a major clinical challenge, and much more information needs to be derived from research on patients before relevant experimental animal models can be created.
引用
收藏
页码:141 / 150
页数:10
相关论文
共 42 条
[21]   INTERICTAL METABOLIC ANATOMY OF MESIAL TEMPORAL-LOBE EPILEPSY [J].
HENRY, TR ;
MAZZIOTTA, JC ;
ENGEL, J .
ARCHIVES OF NEUROLOGY, 1993, 50 (06) :582-589
[22]   INTERICTAL CEREBRAL METABOLISM IN PARTIAL EPILEPSIES OF NEOCORTICAL ORIGIN [J].
HENRY, TR ;
SUTHERLING, WW ;
ENGEL, J ;
RISINGER, MW ;
LEVESQUE, MF ;
MAZZIOTTA, JC ;
PHELPS, ME .
EPILEPSY RESEARCH, 1991, 10 (2-3) :174-182
[23]  
HOUSER CR, 1992, MOL NEUROBIOLOGY EPI, P41
[24]   INHIBITION IN SYNCHRONOUSLY FIRING HUMAN HIPPOCAMPAL-NEURONS [J].
ISOKAWAAKESSON, M ;
WILSON, CL ;
BABB, TL .
EPILEPSY RESEARCH, 1989, 3 (03) :236-247
[25]   THE BENIGN PARTIAL NONROLANDIC EPILEPSIES [J].
LERMAN, P ;
KIVITY, S .
JOURNAL OF CLINICAL NEUROPHYSIOLOGY, 1991, 8 (03) :275-287
[26]   SURGICAL-TREATMENT OF LIMBIC EPILEPSY ASSOCIATED WITH EXTRAHIPPOCAMPAL LESIONS - THE PROBLEM OF DUAL PATHOLOGY [J].
LEVESQUE, MF ;
NAKASATO, N ;
VINTERS, HV ;
BABB, TL .
JOURNAL OF NEUROSURGERY, 1991, 75 (03) :364-370
[27]  
Luders H, 1987, EPILEPSY ELECTROCLIN, P303, DOI [10.1007/978-1-4471-1401-7_13, DOI 10.1007/978-1-4471-1401-7_13]
[28]  
MATSUMOTO H, 1964, EXP NEUROL, V9, P305, DOI 10.1016/0014-4886(64)90026-3
[29]  
MEENCKE HJ, 1992, MOL NEUROBIOLOGY EPI, P31
[30]   EPILEPTIC BRAIN-DAMAGE IN ADOLESCENT BABOONS FOLLOWING SEIZURES INDUCED BY ALLYLGLYCINE [J].
MELDRUM, BS ;
HORTON, RW ;
BRIERLEY, JB .
BRAIN, 1974, 97 (JUN) :407-&