Citation

Li H, McDonald W, Parada I, Faria L, Graber K, Takahashi K, Ma Y, Prince D. Neurosci. Lett. 2011; 497(3): 172-176.

Affiliation

Epilepsy Research Laboratory, Department of Neurology and Neurological Sciences, Stanford Univ. Sch. of Medicine, 300 Pasteur Dr., Stanford CA 94305.

Copyright

(Copyright © 2011, Elsevier Publishing)

DOI

10.1016/j.neulet.2011.02.042

PMID

21354270

Abstract

Prophylaxis of posttraumatic epilepsy will require a detailed knowledge of the epileptogenic pathophysiological processes that follow brain injury. Results from studies of experimental models and human epilepsy highlight alterations in GABAergic interneurons and formation of excessive new excitatory synaptic connectivity as prominent targets for prophylactic therapies. Promising laboratory results suggest that it will be possible to experimentally modify these aberrant processes and interfere with epileptogenesis. However, a number of key issues must be addressed before these results can be used to frame clinical antiepileptogenic therapy.

Language: en