Performance of a concurrent cognitive task modifies pre- and post-perturbation-evoked cortical activity.

Preparation for postural instability engages cortical resources that serve to optimize compensatory balance responses. Engagement of these cortical resources in cognitive dual-task activities may impact the ability to appropriately prepare and optimize responses to instability. The purpose of this study was to determine whether cognitive dual-task activities influenced cortical activity preceding and following postural instability. Postural instability was induced using a lean-and-release paradigm in 10 healthy participants. Perturbations were either temporally predictable (PRED) or unpredictable (UNPRED) and presented with (COG) or without a cognitive dual-task, presented in blocks of trials. The electroencephalogram was recorded from multiple frontal electrode sites. EEG data were averaged over 25-35 trials across conditions. Area under the curve of pre-perturbation cortical activity and peak latency and amplitude of post-perturbation cortical activity were quantified at the Cz site and compared across conditions. Performance of the concurrent cognitive task reduced the mean (SE) magnitude of pre-perturbation cortical activity in advance of predictable bouts of postural instability (PRED: 18.7(3.0)mVms; PRED-COG; 14.0(2.3)mVms). While the level of cognitive load influenced the amplitude of the post-perturbation N1 potential in the predictable conditions, there were no changes in N1 with a cognitive dual task during unpredictable conditions (PRED: -32.1(3.2)µV; PRED-COG: -50.8(8.4)µV; UNPRED: -65.0(12.2)µV; UNPRED-COG: -64.2(12.7)µV). Performance of the cognitive task delayed and reduced the magnitude of the initial gastrocnemius response. The findings indicate that pre- and post-perturbation cortical activity is affected by a cognitive distractor when postural instability is temporally predictable. Distraction also influences associated muscle responses.

Frequency characteristics of cortical activity associated with perturbations to upright stability.

Cortical evoked potentials are evident in the control of whole-body balance reactions in response to transient instability. The focus of this work is to continue to advance understanding of the potential cortical contributions to bipedal balance control. Temporally unpredictable postural perturbations evoke a negative potential (N1), which has drawn parallels to error-related negativity (ERN) as well as visual and auditory evoked N1 responses. The mechanism underlying the generation of event-related potentials (ERPs) has been a matter of debate for the past few decades. While the evoked model proposes that ERPs are generated by the addition of fixed latency and fixed polarity responses, the phase reorganization model suggests that ERPs are the result of stimulus-induced phase reorganization of the ongoing oscillations. Previous studies have suggested phase reorganization as a possible mechanism in auditory N1, visual N1 and error-related negativity (ERN). The purpose of the current study was to explore the frequency characteristics of the cortical responses to whole-body balance perturbations. Perturbations were evoked using a lean and release protocol. The results revealed a significant power increase and phase-locking of delta, theta, alpha, and beta band activity during perturbation-evoked N1. This may suggest that the stimulus-induced phase reorganization of the ongoing electroencephalographic (EEG) activity could account for the features of cortical ERPs in response to perturbation of upright stability.

Localizing evoked cortical activity associated with balance reactions: does the anterior cingulate play a role?

The ability to correct balance disturbances is essential for the maintenance of upright stability. Although information about how the central nervous system controls balance reactions in humans remains limited, recent literature highlights a potentially important role for the cerebral cortex. The objective of this study was to determine the neural source of the well-reported balance-evoked N1 response. It was hypothesized that the N1 is associated with an "error-detection" event in response to the induced perturbation and therefore may be associated with activity within the anterior cingulate cortex (ACC). The localized source of the N1 evoked by perturbations to standing balance was compared, within each participant, to the location of an error-related negativity (ERN) known to occur within the ACC while performing a flanker task. In contrast to the main hypotheses, the results revealed that the location of the N1 was not within the ACC. The mean Talairach coordinates for the ERN were (6.47, -4.41, 41.17) mm, corresponding to the cingulate gyrus [Brodmann area (BA) 24], as expected. However, coordinates for the N1 dipole were (5.74, -11.81, 53.73) mm, corresponding to the medial frontal gyrus (BA 6), specifically the supplementary motor area. This may suggest the N1 is linked to the planning and execution of elements of the evoked balance reactions rather than being associated with error or event detection. Alternatively, it is possible that the N1 is associated with variation in the cortical representation due to task-specific differences in the activation of a distributed network of error-related processing. Subsequent work should focus on disentangling these two possible explanations as they relate to the cortical processing linked to reactive balance control.