OBJECTIVE: To examine the cortical activity associated with 'central set' preparations for induced whole-body instability. METHODS: Self-initiated and temporally unpredictable perturbations to standing balance were caused by the release of a load coupled to a cable affixed to a harness while participants stood on a force plate. Electroencephalographic and electromyographic signals were recorded. RESULTS: Peak activity was located at the Cz electrode. The predictable condition elicited a DC shift 950 ms prior to perturbation onset and was 18.0+/-10.5 micro V in magnitude. Pre-perturbation activity was not associated with the motor act of perturbation initiation and was dissociable from cortical activity related to anticipatory postural muscle activation. Following perturbation onset, N1 potentials were observed with a peak amplitude of 17.6+/-7.2 micro V and peak latency of 140.1+/-25.9 ms. In unpredictable trials, pre-perturbation activity was absent. The peak amplitude (32.0+/-14.8 micro V) and latency (156.5+/-11.8 ms) of the post-perturbation N1 potential were significantly larger (p=0.002) and later (p<0.001) than for predictable trials. CONCLUSIONS: Self-initiated postural instability evokes cortical activity prior to and following perturbation onset. Pre-perturbation cortical activity is associated with changing central set to modulate appropriate perturbation-evoked balance responses. SIGNIFICANCE: These findings establish a link between reactive balance control and cortical activity that precedes and follows perturbations to stability.
OBJECTIVE: To examine the cortical activity associated with 'central set' preparations for induced whole-body instability. METHODS: Self-initiated and temporally unpredictable perturbations to standing balance were caused by the release of a load coupled to a cable affixed to a harness while participants stood on a force plate. Electroencephalographic and electromyographic signals were recorded. RESULTS: Peak activity was located at the Cz electrode. The predictable condition elicited a DC shift 950 ms prior to perturbation onset and was 18.0+/-10.5 micro V in magnitude. Pre-perturbation activity was not associated with the motor act of perturbation initiation and was dissociable from cortical activity related to anticipatory postural muscle activation. Following perturbation onset, N1 potentials were observed with a peak amplitude of 17.6+/-7.2 micro V and peak latency of 140.1+/-25.9 ms. In unpredictable trials, pre-perturbation activity was absent. The peak amplitude (32.0+/-14.8 micro V) and latency (156.5+/-11.8 ms) of the post-perturbation N1 potential were significantly larger (p=0.002) and later (p<0.001) than for predictable trials. CONCLUSIONS: Self-initiated postural instability evokes cortical activity prior to and following perturbation onset. Pre-perturbation cortical activity is associated with changing central set to modulate appropriate perturbation-evoked balance responses. SIGNIFICANCE: These findings establish a link between reactive balance control and cortical activity that precedes and follows perturbations to stability.
Authors: Rahul Goel; Recep A Ozdemir; Sho Nakagome; Jose L Contreras-Vidal; William H Paloski; Pranav J Parikh Journal: Exp Brain Res Date: 2018-05-11 Impact factor: 1.972