IS NEURONAL DEATH NECESSARY FOR ACQUIRED EPILEPTOGENESIS IN THE IMMATURE BRAIN?

被引:19
|
作者
Dudek, F. Edward [1 ]
Ekstrand, Jeffrey J. [2 ]
Staley, Kevin J. [3 ]
机构
[1] Univ Utah, Sch Med, Dept Physiol, Salt Lake City, UT 84108 USA
[2] Univ Utah, Sch Med, Dept Pediat, Salt Lake City, UT 84108 USA
[3] Harvard Univ, Sch Med, Dept Neurol, Massachusetts Gen Hosp, Boston, MA 02115 USA
关键词
PROLONGED FEBRILE SEIZURES; SPONTANEOUS RECURRENT SEIZURES; INDUCED STATUS EPILEPTICUS; TEMPORAL-LOBE EPILEPSY; LONG-TERM; RAT MODEL; HIPPOCAMPAL EXCITABILITY; MESSENGER-RNA; DENTATE GYRUS; INJURY;
D O I
10.1111/j.1535-7511.2010.01369.x
中图分类号
R74 [神经病学与精神病学];
学科分类号
摘要
A central question concerning acquired epileptogenesis in the immature brain is whether neuronal death is required for the development of epilepsy after a brain insult. Results from three different animal models of brain injury during early development have been used to develop the hypothesis that status epilepticus, prolonged febrile seizures, or hypoxia-induced seizures can lead to chronic epilepsy without the occurrence of neuronal death. This brief review will summarize the evidence supporting the hypothesis in each model and then critique the data and published interpretations. A case will be made that the evidence to date neither rules out the occurrence of neuronal death nor demonstrates that epileptogenesis (i.e., spontaneous recurrent seizures) has actually occurred in these animal models of acquired pediatric epilepsy. We also review evidence for the opposing hypothesis: acquired epileptogenesis in the immature brain requires, or at least often involves, neuronal death.
引用
收藏
页码:95 / 99
页数:5
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