Posttraumatic epilepsy

Ravindra Kumar Garg MD (Dr. Garg of King George's Medical University in Lucknow, India, has no relevant financial relationships to disclose.)
C P Panayiotopoulos MD PhD, editor. (Dr. Panayiotopoulos of St. Thomas' Hospital has no relevant financial relationships to disclose.)
Originally released March 4, 1997; last updated March 26, 2020; expires March 26, 2023

This article includes discussion of posttraumatic epilepsy, post-traumatic epilepsy, early posttraumatic seizures, immediate posttraumatic seizure, and late posttraumatic epilepsy. The foregoing terms may include synonyms, similar disorders, variations in usage, and abbreviations.


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 penetrating head trauma have a very high incidence of posttraumatic epilepsy because of dural tear with intracerebral blood and metallic fragments. 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. Several genetic studies have suggested there is a significant genetic contribution to the development of posttraumatic epilepsy. Abnormalities in neuronal glutamate transporter genes were found to be associated with increased risk of epileptogenesis following severe traumatic brain injury. Epileptiform abnormalities in EEG performed in the acute period following traumatic brain injury predict first-year posttraumatic epilepsy. No effective prophylaxis for posttraumatic epilepsy currently exists. Levetiracetam is now considered a preferred drug over phenytoin because use of phenytoin was associated with longer length of hospital stay and more dizziness. Vagus nerve stimulation should be considered in patients with medically refractory posttraumatic epilepsy who are not good candidates for resection. Long-term mortality is higher in patients with posttraumatic epilepsy than in other patients with traumatic brain injury. In this article, the author summarizes the current data on epileptogenesis of posttraumatic epilepsy. The author also provides updated information on the 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.

Historical note and terminology

Hippocrates (460 BC to 357 BC), in "Injuries of the Head," observed that a wound of 1 side of the head could cause convulsions on the other side of the body. By the time of the Renaissance, physicians were aware of the potential for head injuries to cause both acute convulsions and chronic epilepsy (Temkin 1979). In the 19th century, John Hughlings Jackson provided a detailed description of the association between the character of epileptic attacks and the location of causative head injury wounds (Taylor et al 1931). Penfield and colleagues extended Jackson's observations relating injury location to symptomatology and recognized meningocerebral scar formation in the pathophysiology of posttraumatic epilepsy (Penfield and Erickson 1941; Penfield and Rasmussen 1950; Penfield and Kristiansen 1951; Penfield and Jasper 1954).

Military conflicts have been a major cause of head injuries throughout recorded history, and studies of posttraumatic epilepsy have been conducted following World War I (Ascroft 1941), World War II (Whitty 1947; Walker 1957; Walker 1969; Walker and Jablon 1961), the Korean War (Weiss and Caveness 1972), and the Vietnam War (Caveness et al 1979; Salazar et al 1985; Salazar et al 1995). Studies of posttraumatic epilepsy in nonmilitary personnel have been fewer and reported most extensively by Jennett and colleagues (Jennett and Lewin 1960; Jennett 1972; Jennett 1973; Jennett 1974; Jennett 1975a; 1975b) and later by several other groups (da Silva et al 1992; De Santis et al 1992; Manaka 1992; Lee et al 1995; Temkin et al 1995).

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