“…Severity of neurologic injury spans a spectrum up to and including sensorimotor complete injury, with predictable patterns of recovery across different severities (Olby et al, 2003, 2004; Bergknut et al, 2012). Primary and secondary mechanisms of SCI in dogs are consistent with those observed in humans, and include central gray matter hemorrhage, necrosis, cavitation, sparing of subpial axons, axonal degeneration, and variable degrees of demyelination (Smith and Jeffery, 2006; Moore and Oglesbee, 2014; Henke et al, 2014, 2015). Accordingly, clinical dog models can serve as a “bridge” between rodent models of SCI and human patients because they address many translational issues.…”