Spinal cord injuries (SCI) in dogs are not frequent, but they are serious pathological conditions accompanied with high morbidity and mortality. The pathophysiology of SCI involves a primary insult, disrupting axons, blood vessels, and cell membranes by mechanical force, or causes tissue necrosis by ischemia and reperfusion. The primary injury is followed by a cascade of secondary events, involving vascular dysfunction, edema formation, continuing ischemia, excitotoxicity, electrolyte shifts, free radical production, inflammation, and delayed apoptotic cell death. The most frequent cause of SCI in dogs is an acute intervertebral disc extrusion, exogenous trauma or ischemia. Neurological symptomatology depends on the location, size and the type of spinal cord lesions. It is characterized by transient or permanent, incomplete or complete loss of motor, sensory, autonomic, and reflex functions caudal to the site of the lesion. In a case of partial spinal cord (SC) damage, one of the typical syndromes develops (e. g. Brown-Séquard syndrome, central SC syndrome, ventral SC syndrome, dorsal SC syndrome, conus medullaris syndrome, or traumatic cauda equina syndrome). The severe transversal spinal cord lesion in the cervical region causes paresis or plegia of all four extremities (tetraparesis, tetraplegia); in thoracic or lumbosacral region, paresis or plegia of the pelvic extremities (paraparesis, paraplegia), i. e. sensory-motor deficit, urinary and foecal incontinence and sexual incompetence. The central nervous system in mammals does not regenerate, so the neurological deficit in dogs following severe SCI persists for the rest of their lives and animals display an image of permanent suffering. The research strategy presented here involved a PubMed, Medline (Ovid) and ISI Web of Science literature search from Januray 2001 to December 2017 using the term “canine spinal cord injury” in the English language; also references from selected papers were scanned and relevant articles included.