Dissociation of muscle and cortical response scaling to balance perturbation acceleration.

The role of cortical activity in standing balance is unclear. Here we tested whether perturbation-evoked cortical responses share sensory input with simultaneous balance-correcting muscle responses. We hypothesized that the acceleration-dependent somatosensory signals that drive the initial burst of the muscle automatic postural response also drive the simultaneous perturbation-evoked cortical N1 response. We measured in healthy young adults (N=16) the initial burst of the muscle automatic postural response (100-200ms), startle-related muscle responses (100-200ms), and the perturbation-evoked cortical N1 potential, i.e. a negative peak in cortical EEG activity (100-200ms) over the supplementary motor area. Forward and backward translational support-surface balance perturbations were applied at four levels of acceleration, and were unpredictable in timing, direction, and acceleration. Our results from averaged and single-trial analyses suggest that although cortical and muscle responses are evoked by the same perturbation stimulus, their amplitudes are independently modulated. While both muscle and cortical responses increase with acceleration, correlations between single-trial muscle and cortical responses were very weak. Further, across subjects, the scaling of muscle responses to acceleration did not correspond to scaling of cortical responses to acceleration. Moreover, we observed a reduction in cortical response amplitude across trials that was related to a reduction in startle-related, but not balance-correcting, muscle activity. Therefore, cortical response attenuation may be related to a reduction in perceived threat rather than motor adaptation or changes in sensory inflow. We conclude that the cortical N1 reflects integrated sensory inputs simultaneously related to brainstem-mediated balance-correcting muscle responses and startle-reflexes.