Spasticity is common feature of human spinal cord injury. It contributes to motor impairment and it also promotes joint deformity in patients who have sustained such injury. The classical definition of spasticity highlights the increased resistance of a joint to externally imposed motion. This resistance is attributable largely to changes in stretch reflex excitability, and it is manifested primarily in those muscles being stretched by the motion. Under this definition, there would be little activity in muscles crossing other joints. In spinal cord injury, however, muscles innervated from distal spinal segments often exhibit little hypertonia, yet patients report the occurrence of disabling spasms. These spasms appear as coordinated patterns of muscle activation throughout the limb, involving either limb flexors or extensors. These patterns are therefore quite different from those of classical spasticity. The receptor origins and neural pathways responsible for the spasms in spinal cord injury will be addressed.