Abstract
Seizure following traumatic brain injury (TBI) leads to morbidity and mortality in acute, sub-acute, and chronic phases. Post-traumatic seizure in the acute phase involves several mechanisms: blood–brain barrier disruption with iron deposition, albumin leakage, inflammatory cascades, microglial activation, glutamate excitotoxicity, and oxidative stress. Subsequently, Tau aggregation, neurogenesis, synaptic plasticity, gene expression, and epigenetic alterations cause post-traumatic epilepsy in the sub-acute and chronic phases. When we know the pathogenesis of seizure after traumatic brain injury and epileptogenesis, we will understand the post-traumatic complications. This chapter summarizes the essential pathophysiology of seizures following TBI.
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