Cortical activity prior to predictable postural instability: is there a difference between self-initiated and externally-initiated perturbations?

Previous work has revealed pre-perturbation cortical activity linked to predictably-timed perturbations to upright stability. Because individuals rely on the ability to anticipate perturbations for independent mobility, we sought to determine whether perturbation-evoked cortical potentials elicited by voluntarily-initiated external perturbations were dissociable from those elicited by externally-cued perturbations. Postural instability was evoked under three experimental conditions: cued external perturbations (EXT-CUE), cued self-initiated perturbations (SELF-CUE), and un-cued self-initiated perturbations (SELF-NO CUE). All conditions were characterized by comparable pre-perturbation slow-wave potentials initiated 1536.83+/-44.94 ms prior to perturbation onset, measuring 11.24+/-0.94 microV in amplitude. There were no differences in pre-perturbation cortical activity across tasks. Post-perturbation N1 potentials were also evoked, reaching peak amplitude at 132.63+/-3.40 ms following perturbation onset. The potentials were significantly larger in the EXT-CUE (17.08+/-2.99 microV) condition than both the SELF-CUE (11.98+/-2.53 microV) and SELF-NO CUE conditions (9.24+/-1.79 microV). There were no significant differences across tasks for measures of tibialis anterior muscle activity prior to or following perturbation onset, nor were there significant differences in centre of pressure excursion amplitude across tasks. This study highlights that despite using different mechanisms to initiate temporally predictable perturbations to upright stability, pre-perturbation cortical events with similar spatio-temporal characteristics and magnitude are evoked, signalling consistency in the cortical processes that optimize compensatory postural responses which are independent from the cues that inform the onset of postural instability. These findings enhance the understanding of cortical involvement in postural control.