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

Abstract

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.

Neural mechanisms and functional correlates of altered postural responses to perturbed standing balance with chronic low back pain

“…Instead, the N1 potential appears to be an event detector for unexpected postural error such that the amplitude of the N1 potential (a) increases when the timing of the perturbation is unpredictable, (b) decreases with attention distraction that is elicited by dual tasking, and (c) increases with enhanced fear of postural perturbation that is elicited, for example, by manipulating the height of the ledge on which a subject stands (Bolton, 2015). The N1 potential has also been found unchanged by direction of perturbation, delayed but unchanged in amplitude by peroneal nerve damage that slows peripheral conduction velocity, unchanged in timing or amplitude by ischemic nerve block or vestibular loss, and estimated to arise from the supplementary motor area, thus further supporting the interpretation of a higher-order function such as detection of postural error rather than pure sensory processing (Dietz et al, 1985; Marlin et al, 2014; Mierau et al, 2015). Although the neural generators of the P2 potential are not yet known, the P2 potential appears to reflect ongoing monitoring of postural challenge.…”

“…Thus, N1 and P2 amplitudes did not significantly differ and were highly correlated when generated from a waveform representing an average of 15, 20, or 25 trials. When reviewing 19 past studies of perturbation evoked potentials (Dietz et al, 1984; Dietz et al, 1985; Quintern et al, 1985; Ackermann et al, 1986; Berger et al, 1990; Duckrow et al, 1999; Quant et al, 2004a; Quant et al, 2004b; Quant et al, 2005; Adkin et al, 2006; Adkin et al, 2008; Mochizuki et al, 2008; Mochizuki et al, 2009a; Mochizuki et al, 2009b; Mochizuki et al, 2010; Sibley et al, 2010; Marlin et al, 2014; Little and Woollacott, 2015; Mierau et al, 2015), the number of subjects included per group was: mean = 11, median = 10, mode = 10, range = 4–37; the number of trials performed per condition was: mean = 33, median = 30, mode = 30, range = 10–64. Some studies, however, only reported the number of trials performed and not the number retained for analysis following artifact rejection.…”

“…The number of trials retained for analysis is reported in the results. The FCz (midline frontal-central), Cz, (midline central) and CPz (midline central-parietal) electrodes were chosen for analysis based on previous studies that described the topography of maximal potential amplitudes and estimated sources of the perturbation evoked potential (Quant et al, 2004b; Mochizuki et al, 2009a; Marlin et al, 2014; Mierau et al, 2015). …”

Neuroimaging of Human Balance Control: A Systematic Review

“…Marlin et al (2014) investigated if the perturbation evoked N100 and the ERN both originated in the ACC using a lean-and-release protocol to invoke a feet-in-place balance response [similar to those in: Adkin et al (2006) and Mochizuki et al (2008)] and used dipole analysis to locate the N100 response. The ERN was localized to the ACC, as expected.…”

“…Gwin et al (2011) used a similar approach but excluded components if the current dipole model to scalp accounted for less than 80% of the scalp variance - criteria used by six other studies (Sipp et al, 2013; Kline et al, 2014; Lau et al, 2014; Bradford et al, 2015; Bulea et al, 2015; Snyder et al, 2015). Lastly, 6 studies used PCA to identify and remove movement artifact (Bulea et al, 2014, 2015; Huang et al, 2014; Marlin et al, 2014; Luu et al, 2016; Nathan and Contreras-Vidal, 2016). …”