Epilepsy after head injury.
OBJECTIVE
The purpose of this short review is to provide an update on the epidemiology of posttraumatic epilepsy, associated risk factors, data from prevention studies, and recent breakthroughs in experimental research.


RESULTS
There is increasing evidence that neuroimaging findings, stratification by neurosurgical procedures performed, and genomic information (e.g. apolipoprotein E and haptoglobin genotypes) may provide useful predictors of the individual risk of developing posttraumatic epilepsy. While antiepileptic drug prophylaxis can be effective in protecting against acute (provoked) seizures occurring within 7 days after injury, no antiepileptic drug treatment has been found to protect against the development of posttraumatic epilepsy and therefore long-term anticonvulsant prophylaxis is not recommended. Glucocorticoid administration early after head injury also has not been found to reduce the risk of posttraumatic epilepsy. At the basic research level, there have been advances in the understanding of pathophysiological changes in posttraumatic excitatory and inhibitory synapses, and the critical period for epileptogenesis after head injury has been better defined. Finally, the development of a novel animal model, which mimicks more closely human posttraumatic epilepsy, may facilitate efforts to characterize relevant epileptogenic mechanisms and to identify clinically effective antiepileptogenic treatments.


CONCLUSIONS
Despite the continuing lack of clinically effective agents for posttraumatic epilepsy prophylaxis, recent advances in basic and clinical research offer new hope for success in the development of new strategies for prevention and treatment.
D'Ambrosio
Raimondo
R
Department of Neurological Surgery and Regional Epilepsy Center, University of Washington, Seattle, Washington, USA. raid@u.washington.edu
Perucca
Emilio
E
D000818:Animals; D000927:Anticonvulsants / Q000494:pharmacology / Q000627:therapeutic use; D001921:Brain / Q000473:pathology / Q000503:physiopathology; D001930:Brain Injuries / Q000453:epidemiology / Q000503:physiopathology*; D015984:Causality; D015897:Comorbidity; D006259:Craniocerebral Trauma / Q000453:epidemiology / Q000503:physiopathology*; D004195:Disease Models, Animal; D004827:Epilepsy / Q000188:drug therapy / Q000453:epidemiology / Q000503:physiopathology*; D005938:Glucocorticoids / Q000494:pharmacology / Q000627:therapeutic use; D006801:Humans; D009435:Synaptic Transmission / Q000502:physiology; D017211:Treatment Failure
D000927:Anticonvulsants; D005938:Glucocorticoids