Abstracts

RATIONALE: Traumatic brain injury (TBI) is a serious health problem associated with significant long-term mortality and morbidity. Over 2 million people in the US sustain brain injury yearly. For individuals 35 or younger, TBI represents a major cause of death and disability. Chronic sequelae of TBI, including post-traumatic epilepsy (PTE), may produce greater disability than the original injury. The development of PTE is related to the degree of brain injury and the presence of intracranial blood. Studies have shown that the presence of blood, specifically of iron, plays an important role in epileptogenesis. In the parenchyma of the brain, iron-induced free radical (FR) reactions represent a fundamental mechanism affecting brain injury responses and epileptogenesis. TBI has been shown to be associated with overload of free radicals. Biologic mechanisms consisting of complex enzymatic reactions normally maintain adequate FR balance. The availability and efficiency of FR scavenging enzymes is genetically determined. Patients who have a deficiency in total free radical scavenging capacity may be at increased risk of developing PTE. METHODS: We conducted a pilot study in which blood concentrations of FR enzymes and trace elements were measured in 17 TBI patients. Nine TBI patients with PTE (TBI+E) and 8 TBI patients with no history of seizure disorder post-trauma (TBI-E, controls)were recruited. Control subjects were matched by severity of injury and were more than 2 years post trauma. RESULTS: There was no difference in age, gender, duration of LOC, or penetrating TBI. A substantial difference was found between the 2 groups for mean glutathione peroxidase levels (72.8 IU/gm Hgb and 54.9 IU/gm Hgb in the TBI-E & TBI+E, respectively)and mean peroxidation indexes (10.9 and 13.6 for the TBI-E & TBI+E groups, respectively). Glutathione peroxidase of ? 60 and glutathione peroxidation index > 10 have been used as predictors of patients genetically deficient in FR enzyme system. This criteria correctly identified 75% of patients with and without PTE. CONCLUSIONS: Deficiency in FR scavenging capacity is associated with increased risk of PTE. A genetic ability to detoxify FR is important in the occurrence of PTE.