Posttraumatic epilepsy is also known as or subsumes Immediate posttraumatic seizure, Early posttraumatic seizures, and Late posttraumatic epilepsy. -ed.
Traumatic brain injury is one of the most common causes of morbidity and mortality, with posttraumatic epilepsy and functional disability being its major sequelae. Once posttraumatic epilepsy has developed, it remits less often than previously reported. Patients with posttraumatic epilepsy appear to have a higher mortality rate than patients with traumatic brain injury without epilepsy. The mechanisms of posttraumatic seizures on cellular level are poorly understood. Several animal models have been used to explore the structural, chemical, and physiologic changes that are responsible for seizures in traumatic brain injury. Animal studies suggested 2 potential mechanisms of epileptogenesis in patients with head injury, occurrence of disinhibition and development of new functional excitatory connectivity. Possibly, reorganization of astrocytes may, along with dendritic sprouting and new synapse formation, form the structural basis for recurrent excitation in the epileptic brain. Acute posttraumatic nonconvulsive seizures may also occur after traumatic brain injury and, in a selected subgroup, appear to be associated with disproportionate long-term hippocampal atrophy. Although potentially preventable, no effective prophylaxis for posttraumatic epilepsy currently exists. Experimental studies suggest alterations in GABAergic interneurons and formation of excessive new excitatory synaptic connectivity as prominent targets for prophylactic therapies. In this review, RK Garg summarizes the current data on epileptogenesis of posttraumatic epilepsy. Dr. Garg also provides the updated information on epidemiology, clinical features, differential diagnosis, and management of posttraumatic epilepsy.