SCI has traditionally been classified as traumatic and nontraumatic. Traumatic SCI is usually due to motor vehicle collisions (MVCs) (MVAs) (20% to 25%), motorcycle collisions (MCCs) (25% to 30%), or falls (20% to 25%). The most common locations for traumatic SCI are the cervical spine (50% to 55%), followed by the thoracolumbar region (15% to 20%), thoracic spine (10% to 15%), and the lumbosacral region (10%).

Nontraumatic causes of SCI are numerous. Such conditions include: various bacterial (including spinal epidural abscesses), viral, fungal, or parasitic infections; neoplastic lesions (usually extramedullary primary or metastatic tumors); vascular events (infarctions or hemorrhages from vascular malformations); demyelinating lesions such as multiple sclerosis; toxins; autoimmune disorders; and nutritional abnormalities such as vitamin B₁₂ deficiency.

Neurologic damage and the ensuing clinical manifestations will depend on the extent and level of the SCI. Physical examination usually reveals muscle weakness and a sensory level below the level of the lesion in complete lesions. In those patients with incomplete SCI there is some preservation of motor and sensory functions below the level of compromise. Initially patients with SCI will present with atonia and arreflexia below the level of the lesion (spinal shock) and within a few days or weeks will experience spasticity and hyperreflexia.