The contribution of force-sensitive muscular afferents to prolonged flexion withdrawal reflexes, or flexor spasms, following human spinal cord injury (SCI) was investigated. In three separate experimental conditions, flexion reflexes were triggered in subjects with SCI using trains of electrocutaneous stimuli delivered at the foot and lower leg and compared to reflexes elicited via intramuscular (IM) electrical stimuli. In the first experiment, flexion reflexes were elicited using IM stimuli to the tibialis anterior (TA) in the majority of subjects tested. The ratio of peak isometric ankle to hip torques during IM-triggered reflexes were proportionally similar to those evoked by electrocutaneous foot or shank stimulation, although the latency to onset and peak flexion torques were significantly longer with IM stimulation. In the second experiments, the amplitude and frequency of IM TA stimulation were varied to alter the stimulus-induced muscle torque. Peak ankle and hip torques generated during the flexion reflex responses were correlated to a greater extent with stimulus-induced muscle torques as compared to the modulated stimulus parameters. In the third experimental series, IM stimuli delivered to the gastrocnemius (GS) elicited flexion reflexes in approximately half of the subjects tested. The combined data indicate a potentially prominent role of the stimulus-induced muscle contraction to the magnitude and latency of flexor reflex behaviors following IM TA stimulation. Results following IM GS stimulation indicate multi-joint flexion reflexes can also be elicited, although to a lesser extent than IM TA stimulation.