Cerebral evoked potentials associated with the compensatory reactions following stance and gait perturbation.

We have studied the gastrocnemius electromyographic (EMG) responses and the cerebral potentials evoked in normal subjects by perturbations of stance and gait in the form of short treadmill acceleration impulses. In the stance condition a small EMG response (LM1; latency around 40 ms) was followed by a strong muscle activation (LM2; latency 75-90 ms). Following perturbation during gait, LM1 was lacking and LM2 appeared a little earlier (65-75 ms). In the stance condition, the cerebral potentials appeared with shorter latency (42 ms as compared to 83 ms) and a larger amplitude (41 microV as compared to 21 microV) than those seen in the gait condition. These changes can be explained by a presynaptic inhibition of group I afferent signals during gait, which are assumed to be responsible for the early EMG and EEG responses. It is suggested that the LM2 and the cerebral responses evoked by gait perturbation are mediated by signals from group II and III afferents.