Abstracts

Pediatric traumatic brain injury (TBI) is a common cause of childhood death and disability. Post-traumatic epilepsy (PTE) and cognitive disabilities are common sequelae that may manifest years after TBI. PTE afflicts 10% of children after severe TBI but remains poorly understood. To test the hypothesis that TBI during brain development increases seizure susceptibility later in life, we used standard electrical stimulation techniques to assess seizure thresholds in a rat TBI model., Immature, male Sprague-Dawley rats (n=20/grp) underwent TBI by controlled cortical impact (6-mm rounded tip, 4 m/sec velocity, 2-mm deformation, 100 msec duration) to left parietal cortex using isoflurane anesthesia (1%) on post-natal day (PND) 16-18. Results were compared to those obtained from age-matched sham (craniotomy only using isoflurane) and naive rats (n=20/grp). Seizure thresholds were assessed during adolescence and adulthood for tonic (PND 34 and 60), clonic (PND 37 and 63) and limbic (PND 40) seizures. Full convulsive current (CC) curves were generated by staircase procedure and the median CC (CC50) was calculated using Probit analysis. A p-value [lt] 0.05 was considered significant., Tonic and clonic seizure thresholds increased with age in naive rats (p[lt]0.05). As shown in Table 1, seizure responses during adolescence (PND 34-40) were similar among groups for tonic and clonic seizures; however, limbic seizure responses showed a trend toward lower thresholds after TBI. In adults (PND 60-63), tonic seizure thresholds were decreased in both sham and TBI (vs. naive) groups. Conversely, clonic seizure thresholds were similar among sham and naive rats but decreased after TBI (vs. either naive or sham)., TBI to left parietal cortex during brain development attenuates normal maturational increases in clonic seizure thresholds and may increase susceptibility to limbic seizures. Given the involvement of frontal cortex and limbic system in learning and decision-making functions, this finding may have implications not only for PTE, but also for post-injury learning and behavioral deficits. Delineation of the incidence of PTE and cognitive deficits, as well as further characterization of longitudinal maturational changes in seizure thresholds post-TBI are ongoing.[table1], (Supported by NIH K12-HD 01410; PCMC Foundation; University of Utah Child Health Research Center.)