• Ramon Diaz-Arrastia, Mark A Agostini, Christopher J Madden, and Paul C Van Ness.
• Department of Neurology, University of Texas Southwestern Medical Center, Comprehensive Epilepsy Center, Parkland Memorial Hospital, Dallas, Texas 75390-9036, USA. Ramon.Diaz-Arrastia@UTSouthwestern.edu
• Epilepsia. 2009 Feb 1;50 Suppl 2:14-20.

AbstractPosttraumatic epilepsy is a common complication of traumatic brain injury (TBI), occurring in up to 15-20% of patients with severe brain trauma. Trauma accounts for approximately 5% of chronic epilepsy in the community. Because it is a common condition, and because of the relatively short latency period between injury and onset of chronic seizures, posttraumatic epilepsy represents a good model to test antiepileptogenic therapies. However, several well-conducted clinical trials have failed to demonstrate antiepileptogenic efficacy for several common anticonvulsants. Posttraumatic epilepsy can arise through a number of mechanisms, which often coexist within a single patient. Penetrating brain injury produces a cicatrix in the cortex and is associated with a risk of posttraumatic epilepsy of approximately 50%, whereas nonpenetrating head injury may produce focal contusions and intracranial hemorrhages, and is associated with a risk of posttraumatic epilepsy of up to 30%. Furthermore, closed head injury often produces diffuse concussive injury, with shearing of axons and selective damage to vulnerable brain regions, such as the hippocampus. The clinical, neurophysiologic, imaging, and neuropathologic features or epileptogenicity differ between these alternate mechanisms. It is likely that better understanding of the subtypes of epilepsy resulting from brain trauma will be required to successfully identify antiepileptogenic therapies.

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