Light deprivation soon after frontal brain trauma accelerates recovery from attentional deficits and promotes functional normalization of basal ganglia

Background: Light deprivation significantly accelerates recovery from atten tion deficits (neglect) after cortical ablation in rats. We hypothesized th at light deprivation mould improve recovery after traumatic contusive brain injury (TBI) and do so by enhancing dopaminergic function in the ipsilater al basal ganglia, Methods: Adult rats received left frontal contusion injury and were placed into darkness or standard light/dark cycling for 48 hours. Neurologic evalu ation included attentional and sensorimotor tasks. Amphetamine-induced prod uction of the immediate early gene protein product Fos was quantified to de termine neuronal dopaminergic response in caudate-putamen (striatum). Results: Unilateral frontal TBI produced severe contralateral deficits in a ll tasks. Postoperative light deprivation resulted in improved recovery fro m attentional but not sensorimotor deficits. Five days after injury, ipsila teral striatal Fos expression was reduced by 51% in TBI rats experiencing n ormal light cycling (p < 0.006), In contrast, postoperative light deprivati on normalized striatal Fos expression, ES 6 weeks, all TBI rats demonstrate d nearly full recovery and striatal Fos expression was symmetrical between the two striata, Conclusion: Postoperative light deprivation may improve recovery from TBI-i nduced attention deficits by normalizing basal ganglia function.