BACKGROUND AND PURPOSE Motor deficits after traumatic brain injury (TBI) remain poorly understood. In animals, a localized unilateral brain injury produces hindlimb postural asymmetry (HL-PA) that correlates with contralesional motor impairment. Here we evaluate if a unilateral injury to the sensorimotor cortex by the controlled cortical impact (CCI), a model of clinical focal TBI induces HL-PA in rats, and if this asymmetry is spinally encoded and mediated by the opioid system. EXPERIMENTAL APPROACH HL-PA was assessed after the right-side CCI as difference in limb position. Effects of general opioid antagonist naloxone and selective µ- (β-Funaltrexamine), δ- (naltrindole) and κ- (nor-Binaltorphimine and [(S)-3-fluoro-4-(4-((2-(3-fluorophenyl)pyrrolidin-1-yl)methyl)phenoxy)benzamide]) antagonists on HL-PA were analyzed before and after complete spinal cord transection. HL-PA induced by κ-agonist U50,488H and spinal expression of opioid receptor genes were studied in intact animals. KEY RESULTS The right-side CCI induced HL-PA with contralesional (left) flexion that retained after spinalization. Naloxone and µ-Funaltrexamine but not naltrindole and κ-antagonists abolished HL-PA. Surprisingly, treatment with κ-antagonists resulted in the left-to-right reversal of the flexion side; not contra- (left) but ipsilesional (right) limb was flexed. Furthermore, κ-agonist induced HL-PA with left flexion, while expression of subtypes of opioid receptors and their proportion was different between the left and right lumbar spinal cord. CONCLUSIONS AND IMPLICATIONS We report that the focal TBI-induced HL-PA is encoded at the spinal level and mediated through opioid receptors. The side-specific effects may be induced through lateralized opioid receptors. These findings suggest that the TBI-induced asymmetric motor deficits may be pharmacologically corrected.