Prince David A, Parada Isabel, Li Huifang, McDonald Whitney, Graber Kevin
Department of Neurology and Neurological Sciences, Stanford University School of Medicine, Stanford, California, U.S.A.
Epilepsia. 2010 Dec;51 Suppl s5:30. doi: 10.1111/j.1528-1167.2010.02816.x.
Development of new excitatory connectivity and decreases in γ-aminobutyric acid (GABA)ergic inhibition are mechanisms underlying posttraumatic epileptogenesis in animal models. Experimental strategies that interfere with these processes, applied between the trauma and seizure onset, are antiepileptogenic in the laboratory, and have promise for prophylaxis of epileptogenesis after cortical injury in humans. For an expanded treatment of this topic see Jasper's Basic Mechanisms of the Epilepsies, Fourth Edition (Noebels JL, Avoli M, Rogawski MA, Olsen RW, Delgado-Escueta AV, eds) National Library of Medicine Bookshelf [NCBI] at http://www.ncbi.nlm.nih.gov/books).
新的兴奋性连接的形成以及γ-氨基丁酸（GABA）能抑制作用的减弱是动物模型创伤后癫痫发生的潜在机制。在创伤和癫痫发作开始之间应用的干扰这些过程的实验策略，在实验室中具有抗癫痫发生作用，并且有望预防人类皮质损伤后的癫痫发生。有关该主题的扩展论述，请参阅《贾斯珀癫痫基本机制》第四版（Noebels JL、Avoli M、Rogawski MA、Olsen RW、Delgado-Escueta AV主编），可在国家医学图书馆书架[NCBI]上查阅，网址为http://www.ncbi.nlm.nih.gov/books 。
