Abstract Changes in EMG activity in the wrist flexor muscles were studied in response to electrical stimulation of digital nerves and to sudden extension perturbations at the wrist produced by a torque motor in human subjects with unilateral cerebral hemisphere lesions. With the subjects maintaining a steady voluntary contraction against a constant load, digital nerve stimulation produced a series of excitatory and inhibitory changes in tonic EMG activity from the wrist flexors in both the normal and paretic arm. The most consistent response was a period of EMG inhibition beginning approximately 38 msec after the stimulus and lasting approximately 35 msec. With relatively weak electrical stimuli, there was less EMG inhibition in the paretic arm than in the normal arm; with stronger stimuli, the inhibitory response was similar in the two arms. The electrical stimuli and mechanical perturbations were then delivered together, with the interval between them adjusted so that the expected period of inhibition following electrical stimulation coincided with either the early (M1) or the long latency (M2) components of the stretch reflex. In the normal arm electrical stimulation produced more inhibition of the M2 component than of the M1 component. In the paretic arm, inhibition during the M2 component was less marked and similar in degree to that which occurred during M1. These results are compatible with the view that M1 and M2 are normally mediated by separate neural pathways. The long latency EMG activity evoked by muscle stretch in the paretic arm of hemiplegic patients may be generated by pathways or mechanisms different from those in the intact arm.