Role of cortical dysplasia in epileptogenesis following prolonged febrile seizure.

作者: Kyung-Il Park , Kon Chu , Keun-Hwa Jung , Jin-Hee Kim , Kyung-Muk Kang

DOI: 10.1111/J.1528-1167.2010.02676.X

关键词:

摘要: SUMMARY Purpose: Hippocampal sclerosis, characterized by prominent neuronal loss and reactive gliosis, is the most common pathology in human temporal lobe epilepsy (TLE). Although prolonged febrile convulsion (FC) a risk factor of TLE, it not clear whether FC provokes hippocampal sclerosis subsequent TLE. Given that underlying brain lesions, such as cortical dysplasia (CD), immature predispose patients to FC, CD may link However, role epileptogenesis after also unclear. Here, we investigated inborn increases later induced using rat model. Methods: Experimental was utero exposure methylazoxymethanol (MAM). Rat pups from MAM-treated or control rats were then subjected FC. We examined morphologic changes hippocampi with respect loss, synaptogenesis, evaluated spontaneous recurrent seizures (SRS) long-term video-EEG (electroencephalography). Results: The MAM+FC group had significantly lower density CA1 dentate hilus than other groups. A robust increase glial cells synaptic reorganization detected Furthermore, SRS occurred all 50% 25% FC-only MAM-only group, respectively. frequency total duration highest group. Discussion: Our results suggest preexisting augments proepileptogenic effects leading

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