The present study examined the effect of chronic corticosterone exposure on motor and cognitive deficits following traumatic brain injury (TBI). Adults rats were treated with either corticosterone acetate (15 ug/ml) added to their drinking water or vehicle (0.5% alcohol) for 3 months. Following this 3-month treatment, corticosterone-treated rats (n = 8) and vehicle-treated rats (n = 10) were injured at a mild level of fluid percussion injury (1.7-1.8 atm). Additional corticosterone-treated (n = 8) and vehicle-treated rats (n = 8) were surgically prepared for injury but were not injured. Both motor (beam balance and beam walking) and cognitive (Morris water maze) performances were assessed following injury. Motor deficits were transiently enhanced following injury in rats treated with corticosterone. Rats treated with corticosterone were also slower in learning the Morris water maze than vehicle-treated rats. These findings demonstrate that elevated corticosterone levels potentiate the behavioral deficits observed after traumatic brain injury. Applied to aging research, these results suggest that the elevated basal levels of corticosterone present in aged animals may mediate the enhanced vulnerability of aged animals to traumatic brain injury.