Neurophysiologic and neuroradiologic features of intractable epilepsy after traumatic brain injury in adults

ORIGINAL CONTRIBUTION

Neurophysiologic and Neuroradiologic Features of Intractable Epilepsy After Traumatic Brain Injury in Adults
Ramon Diaz-Arrastia, MD, PhD; Mark A. Agostini, MD; Alan B. Frol, PhD; Bruce Mickey, MD; James Fleckenstein, MD; Eileen Bigio, MD; Paul C. Van Ness, MD

Background: There is controversy regarding the precise mechanism by which epilepsy results after traumaticbrain injury (TBI). Previous reports have suggested that mesial temporal lobe epilepsy may result from TBI only in young children, while neocortical epilepsy arises from TBI in later life. These conclusions were based on surgical series and may be biased because of patient selection. Objective: To determine the frequency of mesial tem-

poral lobe as opposed to neocortical epilepsy in patientswith intractable epilepsy resulting from TBI after the age of 10 years.
Patients and Methods: We identified 23 patients with

Results: Of the 23 patients, 8 (35%) had mesial temporal lobe epilepsy, based on the finding of hippocampal sclerosis on a magnetic resonance imaging scan, consistent interictal and ictal electroencephalographic recordings, evidence of temporal lobe dysfunction onneuropsychologic testing, and characteristic seizure semiology. Two of these patients underwent anterior temporal lobectomies with clinical benefit, and hippocampal sclerosis was confirmed pathologically. In 2 cases, patients were not treated surgically because of bilateral temporal lobe dysfunction noted on intracarotid amobarbital testing. Eleven patients had neocortical epilepsy; 1 had primarygeneralized epilepsy; and, in 3, the site of seizure onset was not localized. Conclusions: Mesial temporal lobe epilepsy can result from TBI in adolescents and adults as well as in children, and can often be bilateral and associated with multifocal injury. This information may be useful in developing prophylactic therapy for posttraumatic epilepsy.

intractable epilepsy who had TBI after the age of 10years, preceding the onset of epilepsy. Patients were studied by simultaneous videotape and scalp electroencephalographic recording of typical seizures; magnetic resonance imaging; neuropsychologic studies; and, when appropriate, intracarotid amobarbital testing. Two patients underwent anterior temporal lobectomies.

Arch Neurol. 2000;57:1611-1616 ated with a risk of PTE of up to 30%.4 In thissetting, the mechanism of epileptogenesis may be partly related to the toxic effects of hemoglobin breakdown products on neuronal function.5 Finally, closed head injury often produces diffuse concussive injury, with shearing of axons, diffuse edema and ischemia, and secondary cellular damage through the release of excitatory amino acids, cytokines, bioactive lipids, or other toxic mediators.6 Theincidence of PTE after diffuse head injury is less established, but is likely to be in the order of 10% in patients who had loss of consciousness for longer than 24 hours.4 Epileptogenesis may arise from diffuse injury as a result of selective damage to vulnerable brain regions, such as the hippocampus.7 Several workers8-10 have studied brain trauma as the cause of intractable temporal lobe epilepsyretrospectively in surgi-

From the Departments of Neurology (Drs Diaz-Arrastia, Agostini, and Van Ness), Psychiatry (Dr Frol), Neurosurgery (Dr Mickey), Neuroradiology (Dr Fleckenstein), and Neuropathology (Dr Bigio), The University of Texas Southwestern Medical Center at Dallas.

brain injury (TBI) is a common cause of epilepsy, accounting for approximately 4% of focal epilepsy in thegeneral population, and is the leading cause of epilepsy with onset in young adults (those aged 15-24 years).1 Epilepsy resulting from brain trauma is often difficult to control with medical therapy, and is the cause of epilepsy in approximately 5% of patients referred to specialized epilepsy centers.2 Traumatic brain injury results in potentially epileptogenic brain damage through several mechanisms,...