Posttraumatic epilepsy

Introduction
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By Ravindra Kumar Garg MD

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. A recent report suggests that interleukin-1β gene variability is a risk factor for posttraumatic epilepsy in patients with traumatic brain injury. Although potentially preventable, no effective prophylaxis for posttraumatic epilepsy currently exists. Among newer drugs, levetiracetam looks promising in children with posttraumatic seizures. Vagus nerve stimulation should be considered in patients with medically refractory posttraumatic epilepsy who are not good candidates for resection. 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.

Key Points

  • Posttraumatic seizures may occur almost simultaneously with head injury or be delayed for several years.
  • 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.
  • Posttraumatic epilepsy appears in many cases as temporal lobe epilepsy that possibly originates from the hippocampus.
  • Neither phenytoin nor any other antiepileptic drugs have proven valuable for preventing the development of late posttraumatic epilepsy.
  • The most effective way to prevent posttraumatic epilepsy is to prevent head trauma.

In This Article

Introduction
Historical note and nomenclature
Clinical manifestations
Etiology
Pathogenesis and pathophysiology
Epidemiology
Prevention
Differential diagnosis
Diagnostic workup
Prognosis and complications
Management
Pregnancy
Anesthesia
References cited
Contributors