Hippocampal sclerosis: Development in adult life

被引:41
作者
Jackson, GD
Chambers, BR
Berkovic, SF
机构
[1] ARMC, Boronia Ctr, Brain Imaging Res Inst, W Heidelberg, Vic 3081, Australia
[2] Univ Melbourne, Howard Florey Inst, Dept Med, Dept Neurol,Austin & Repatriat Med Ctr, Melbourne, Vic, Australia
关键词
hippocampal sclerosis; magnetic resonance imaging; neuropathology; epilepsy; temporal lobe epilepsy; T-2; relaxometry;
D O I
10.1159/000017400
中图分类号
Q [生物科学];
学科分类号
07 ; 0710 ; 09 ;
摘要
Hippocampal sclerosis (HS) is the most common pathological lesion underyling intractable temporal robe epilepsy. It is not known whether HS exists before the onset of epilepsy or whether it is caused by seizures. Its has been proposed that childhood seizures cause HS, Optimized magnetic resonance imaging (MRI), hippocampal volumes and T-2 signal quantitation were performed 2 weeks and 8 months following at tonic-clonic seizure in a 23-year-old man, MRI 14 days after the seizure showed symmetrical hippocampal volumes (ratio R/L = 1.03) with intact internal architecture bilaterally but marked signal change in the right hippocampus (T-2 right = 121, T-2 left = 103, normal less than or equal to 108 ms). Eight months later this hippocampus showed severe atrophy with a volume ratio of 0.65 and T-2 values of 117 (right) and 109 ms (left). High-resolution imaging showed that volume loss occurred mainly in the CA1 region which showed high signal in the initial study. Characteristic MRI features of HS can develop in adults and HS cannot always be assumed to have its origins in childhood. Hypoxia in the context of seizures may be an important component in hippocampal damage. HS may be a preventable lesion and MRI signal change seen in the neuronal layers of the hippocampus may be an indication for neuroprotection. Copyright (C) 1999 S. Karger AG, Basel.
引用
收藏
页码:207 / 214
页数:8
相关论文
共 36 条
[1]   DISTRIBUTION OF PYRAMIDAL CELL-DENSITY AND HYPEREXCITABILITY IN THE EPILEPTIC HUMAN HIPPOCAMPAL-FORMATION [J].
BABB, TL ;
LIEB, JP ;
BROWN, WJ ;
PRETORIUS, J ;
CRANDALL, PH .
EPILEPSIA, 1984, 25 (06) :721-728
[2]  
Babb TL., 1987, Surgical Treatment of the Epilepsies, P511
[3]   THE HIPPOCAMPUS IN EXPERIMENTAL CHRONIC EPILEPSY - A MORPHOMETRIC ANALYSIS [J].
BERTRAM, EH ;
LOTHMAN, EW ;
LENN, NJ .
ANNALS OF NEUROLOGY, 1990, 27 (01) :43-48
[4]   Hemicranial volume deficits in patients with temporal lobe epilepsy with and without hippocampal sclerosis [J].
Briellmann, RS ;
Jackson, GD ;
Kalnins, R ;
Berkovic, SF .
EPILEPSIA, 1998, 39 (11) :1174-1181
[5]   STRUCTURAL-CHANGES IN ASTROCYTES INDUCED BY SEIZURES IN A MODEL OF TEMPORAL-LOBE EPILEPSY [J].
CASTIGLIONI, AJ ;
PETERSON, SL ;
SANABRIA, EL ;
TIFFANYCASTIGLIONI, E .
JOURNAL OF NEUROSCIENCE RESEARCH, 1990, 26 (03) :334-341
[6]   PROGRESSIVE NEURONAL LOSS INDUCED BY KINDLING - A POSSIBLE MECHANISM FOR MOSSY FIBER SYNAPTIC REORGANIZATION AND HIPPOCAMPAL SCLEROSIS [J].
CAVAZOS, JE ;
SUTULA, TP .
BRAIN RESEARCH, 1990, 527 (01) :1-6
[7]   TEMPORAL-LOBE EPILEPSY CAUSED BY DOMOIC ACID INTOXICATION - EVIDENCE FOR GLUTAMATE RECEPTOR-MEDIATED EXCITOTOXICITY IN HUMANS [J].
CENDES, F ;
ANDERMANN, F ;
CARPENTER, S ;
ZATORRE, RJ ;
CASHMAN, NR .
ANNALS OF NEUROLOGY, 1995, 37 (01) :123-126
[8]   HIPPOCAMPAL VOLUMETRIC AND MORPHOMETRIC STUDIES IN FRONTAL AND TEMPORAL-LOBE EPILEPSY [J].
COOK, MJ ;
FISH, DR ;
SHORVON, SD ;
STRAUGHAN, K ;
STEVENS, JM .
BRAIN, 1992, 115 :1001-1015
[9]   ETIOLOGY + PATHOGENESIS OF TEMPORAL LOBE EPILEPSY [J].
FALCONER, MA ;
SERAFETINIDES, EA ;
CORSELLIS, JAN .
ARCHIVES OF NEUROLOGY, 1964, 10 (03) :233-&
[10]   GENETIC AND RELATED AETIOLOGICAL FACTORS IN TEMPORAL LOBE EPILEPSY - REVIEW [J].
FALCONER, MA .
EPILEPSIA, 1971, 12 (01) :13-&