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The extent of participation of supraspinal structures in the generation of the long latency (M2) electromyographic (EMG) response to imposed joint displacement may be reflected in the effect of lesions of the central nervous system. M2 activity has been reported in a variety of studies to be either present or absent following supraspinal lesions. Since other studies have shown different characteristics of long latency activity in proximal as compared to distal upper limb muscles in primates, the present experiments were conducted to determine the effect of motor cortical (area 4) lesions on reflex activity generated in a proximal versus a distal upper limb muscle. Chronic experiments were performed on squirrel monkeys with unilateral lesions of the forelimb motor cortex (area 4) which was mapped with the aid of electrical stimulation. Input-output relationships were determined between torque motor-imposed joint rotation and the EMG response in the stretched muscles (flexor digitorum profundus (FDP) and short head of biceps (SHB)). The EMG responses were reported as a percentage of maximum EMG output and controlled for base line EMG level. The “gain” (slope of EMG response versus torque load) for FDP M2 activity was markedly decreased in the limb contralateral to the area 4 lesion as compared to the opposite limb. This decrease was independent of base line EMG levels. In SHB, early latency (M1) EMG activity was significantly increased, but M2 activity appeared unaffected on the side contralateral to the lesion. The results demonstrate that the central and peripheral mechanisms generating M2 activity in FDP differ from those in SHB in terms of motor cortical dependency.

The effect of cortical lesions on the electromyographic response to joint displacement in the squirrel monkey forelimb