Abstracts

Post-traumatic seizures (PTS) are a complication of head trauma. Hemorrhagic injury to the cortex has an increased risk of PTS, possibly due to reaction of free hemoglobin (Hb) with lipid rich environment. Hb and iron can enhance oxidative stress. The brain is susceptible to oxidative damage due to is high oxygen consumption, high lipid content and low antioxidant activity. Haptoglobin (Hp) is a plasma glycoprotein that removes free Hb and prevents Hb-induced damage. Hp has three different phenotypes, HP-1-, Hp 2-1 and Hp 2-2. Hp 1-1 is biologically the most and Hp 2-2 is the least active in Hb binding, antioxidant activity. Polymorphisms of apoliprotein E (APOE) plays an important role in neuropathological finding in patients with head injuries. Of the three common alleles, e2, e3 and e4, the presence of e4 has been shown to have a less favorable outcome. We hypothesized that patients who develop PTS have a 1)lower concentration of haptoglobin and/or a higher frequency of low capacity haptoglobin phenotype; 2)higher oxidant stress as reflected in increased 8-isoprostane (8-isoP), a lower total antioxidant capacity (TAOC); 3)higher frequency of APOE e4 allele., Patients were recruited from our valproate prophylaxis study ([italic]Temkin et al. J Neurosurg 1999;91:593-600)[/italic]. Of the 51 who had developed PTS, 25 cases and 26 controls, matched for age, sex, PTS risk factor and treatment group. Baseline information on seizure history, current alcohol use and medications, and 50 ml of blood were obtained. Plasma/serum were used for the biochemical analysis and blood cells for genetic analysis. Statistical analysis was performed using unpaired t-test for the biochemical markers and Chi-square analysis for the genotyping., [table1][underline]PTS Cases vs.Controls
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[underline]8-IsoP[/underline]: 246[plusmn]170 pg/ml vs 172[plusmn]152 pg/ml (p=0.1)
[underline]TAOC[/underline]: 1.2[plusmn]0.1mM vs 1.1[plusmn]0.1mM (p=0.38)
[underline]Hp:[/underline] 122[plusmn]39 mg/dl vs 142[plusmn]69 mg/dl (p=0.22)
[underline]Ferritin[/underline] 96[plusmn]87 [mu]g/ml vs 154[plusmn]131 [mu]g/ml (p=0.069)., We found no difference in Hp concentration or phenotype, oxidative activity or capacity, or APOE genotype in the head trauma patients who developed PTS. There was a trend towards an increased oxidative stress and decreased ferritin concentrations. In contrast to microhemorrhagic gradual brain injury that may be mediated by free Hb/iron, direct physical damage in this case may be the most contributing factor in developing PTS., (Supported by Research Initiative Award from the American Epilepsy Society.)