The term "spinal shock" applies to all phenomena surrounding physiologic or anatomic transection of the spinal cord that results in temporary loss or depression of all or most spinal reflex activity below the level of the injury. Hypotension due to loss of sympathetic tone is a possible complication, depending on the level of the lesion. The mechanism of injury that causes spinal shock is usually traumatic in origin and occurs immediately, but spinal shock has been described with mechanisms of injury that progress over several hours. Spinal cord reflex arcs immediately above the level of injury may also be severely depressed on the basis of the Schiff-Sherrington phenomenon. The end of the spinal shock phase of spinal cord injury is signaled by the return of elicitable abnormal cutaneospinal or muscle spindle reflex arcs. Autonomic reflex arcs involving relay to secondary ganglionic neurons outside the spinal cord may be variably affected during spinal shock, and their return after spinal shock abates is variable. The returning spinal cord reflex arcs below the level of injury are irrevocably altered and are the substrate on which rehabilitation efforts are based.