Febrile seizures and mesial temporal sclerosis

被引:104
作者
Cendes, F [1 ]
机构
[1] Univ Estadual Campinas, FCM, Dept Neurol, BR-13084970 Campinas, SP, Brazil
关键词
epilepsy; febrile seizures; genetics; hippocampal sclerosis; hippocampus; temporal lobe;
D O I
10.1097/00019052-200404000-00013
中图分类号
R74 [神经病学与精神病学];
学科分类号
摘要
Purpose of review The sequence of febrile seizures followed by intractable temporal lobe epilepsy is rarely seen from a population perspective. However, several studies have shown a significant relationship between a history of prolonged febrile seizures in early childhood and mesial temporal sclerosis. The interpretation of these observations remains quite controversial. One possibility is that the early febrile seizure damages the hippocampus and is therefore a cause of mesial temporal sclerosis. Another possibility is that the child has a prolonged febrile seizure because the hippocampus was previously damaged by a prenatal or perinatal insult or by genetic predisposition. Recent findings Imaging studies have shown that prolonged and focal febrile seizures can produce acute hippocampal injury that evolves to hippocampal atrophy, and that complex febrile seizures can originate in the temporal lobes in some children. Several lines of evidence now indicate that genetic predisposition is an important causal factor of febrile seizures and mesial temporal sclerosis. From recent clinical and molecular genetic studies, it appears that the relationship between febrile seizures and later epilepsy is frequently genetic, and there are several syndrome-specific genes for febrile seizures. Summary Mesial temporal sclerosis probably has different causes. A number of retrospective studies showed that complex febrile seizures are a causative factor for the later development of mesial temporal sclerosis and temporal lobe epilepsy. However, contradictory results have come from several prospective and retrospective studies. The association between febrile seizures and temporal lobe epilepsy probably results from complex interactions between several genetic and environmental factors.
引用
收藏
页码:161 / 164
页数:4
相关论文
共 60 条
[1]   TEMPORAL-LOBE EPILEPSY AFTER PROLONGED FEBRILE CONVULSIONS - EXCELLENT OUTCOME AFTER SURGICAL-TREATMENT [J].
ABOUKHALIL, B ;
ANDERMANN, E ;
ANDERMANN, F ;
OLIVIER, A ;
QUESNEY, LF .
EPILEPSIA, 1993, 34 (05) :878-883
[2]   Two novel SCN1A missense mutations in generalized epilepsy with febrile seizures plus [J].
Annesi, G ;
Gambardella, A ;
Carrideo, S ;
Incorpora, G ;
Labate, A ;
Pasqua, AA ;
Civitelli, D ;
Polizzi, A ;
Annesi, F ;
Spadafora, P ;
Tarantino, P ;
Candiano, ICC ;
Romeo, N ;
De Marco, EV ;
Ventura, P ;
LePiane, E ;
Zappia, M ;
Aguglia, U ;
Pavone, L ;
Quattrone, A .
EPILEPSIA, 2003, 44 (09) :1257-1258
[3]   A deletion in SCN1B is associated with febrile seizures and early-onset absence epilepsy [J].
Audenaert, D ;
Claes, L ;
Ceulemans, B ;
Löfgren, A ;
Van Broeckhoven, C ;
De Jonghe, P .
NEUROLOGY, 2003, 61 (06) :854-856
[5]   Mossy fiber plasticity and enhanced hippocampal excitability, without hippocampal cell loss or altered neurogenesis, in an animal model of prolonged febrile seizures [J].
Bender, RA ;
Dubé, C ;
Gonzalez-Vega, R ;
Mina, EW ;
Baram, TZ .
HIPPOCAMPUS, 2003, 13 (03) :399-412
[6]   Febrile seizures: genetics and relationship to other epilepsy syndromes [J].
Berkovic, SF ;
Scheffer, IE .
CURRENT OPINION IN NEUROLOGY, 1998, 11 (02) :129-134
[7]   Familial temporal lobe epilepsy: A common disorder identified in twins [J].
Berkovic, SF ;
McIntosh, A ;
Howell, RA ;
Mitchell, A ;
Sheffield, LJ ;
Hopper, JL .
ANNALS OF NEUROLOGY, 1996, 40 (02) :227-235
[8]   Hippocampal sclerosis following brief generalized seizures in adulthood [J].
Briellmann, RS ;
Newton, MR ;
Wellard, RM ;
Jackson, GD .
NEUROLOGY, 2001, 57 (02) :315-317
[9]  
CAMFIELD P, 1994, DEV MED CHILD NEUROL, V36, P887
[10]   FREQUENCY AND CHARACTERISTICS OF DUAL PATHOLOGY IN PATIENTS WITH LESIONAL EPILEPSY [J].
CENDES, F ;
COOK, MJ ;
WATSON, C ;
ANDERMANN, F ;
FISH, DR ;
SHORVON, SD ;
BERGIN, P ;
FREE, S ;
DUBEAU, F ;
ARNOLD, DL .
NEUROLOGY, 1995, 45 (11) :2058-2064