Mice deficient in the recognition molecules, close homolog of L1 (CHL1) and tenascin-C, show improved and reduced functional recovery, respectively, after spinal cord injury compared with wild-type littermates. In this study, we addressed the question whether the differential functional outcome was paralleled by differences in blood-spinal cord barrier (BSCB) repair in the two mouse strains. We conducted spinal cord compression injuries in knock-out and wild-type mice. BSCB permeability was assessed by measuring the Evans blue spread within the spinal cord tissue at 14-21 days after injury. Results show that CHL1 reduces and tenascin-C enhances BSCB permeability, suggesting a correlation between functional outcome and BSCB repair.