Citation

Vargo JM, Grachek RA, Rockswold GL. J. Trauma 1999; 47(2): 265-72; discussion 273-4.

Affiliation

Department of Surgery, Hennepin County Medical Center, University of Minnesota, Minneapolis 55404, USA.

Copyright

(Copyright © 1999, Lippincott Williams and Wilkins)

DOI

unavailable

PMID

10452460

Abstract

BACKGROUND: Light deprivation significantly accelerates recovery from attention deficits (neglect) after cortical ablation in rats. We hypothesized that light deprivation would improve recovery after traumatic contusive brain injury (TBI) and do so by enhancing dopaminergic function in the ipsilateral basal ganglia. METHODS: Adult rats received left frontal contusion injury and were placed into darkness or standard light/dark cycling for 48 hours. Neurologic evaluation included attentional and sensorimotor tasks. Amphetamine-induced production of the immediate early gene protein product Fos was quantified to determine neuronal dopaminergic response in caudate-putamen (striatum). RESULTS: Unilateral frontal TBI produced severe contralateral deficits in all tasks. Postoperative light deprivation resulted in improved recovery from attentional but not sensorimotor deficits. Five days after injury, ipsilateral striatal Fos expression was reduced by 51% in TBI rats experiencing normal light cycling (p < 0.006). In contrast, postoperative light deprivation normalized striatal Fos expression. By 6 weeks, all TBI rats demonstrated nearly full recovery and striatal Fos expression was symmetrical between the two striata. CONCLUSION: Postoperative light deprivation may improve recovery from TBI-induced attention deficits by normalizing basal ganglia function.

Language: en