Abstract
Text of Abstract Liability to develop posttraumatic epilepsy (PTE) correlates in a general way with trauma dose. While contusion of the brain produces an admixture of extravasated blood, edema fluid and necrotic tissue at the site of skull trauma and in regions remote from the direct force, an unpredictable cascade of shearing injury, torsion and rotation and a myriad of physiological changes occur in structures subject to the mechanical pressure wave. Animal models mimic components of injury, some more thoroughly than others. Designing a treatment that is a prophylaxis for the development of PTE awaits understanding the mechanisms of epileptogenesis initiated by trauma.
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