A primary central source determines perturbation-evoked N1 amplitudes in younger adults

The balance perturbation-evoked N1 potential is a reliable cortical response during reactive balance control that is correlated to a variety of cognitive and motor functions. Although the supplementary motor area (SMA) has been identified as the primary source of the N1, it is less understood whether other brain regions contribute to the N1 recorded at the scalp. We used source localization on electroencephalography (EEG) data from 25 younger adults recorded during backward whole body perturbations during stance. We identified the sources that contribute to channel-based N1 recordings and quantified their impact on N1 amplitude and latency. In younger adults, N1 amplitudes can be explained by one single source in a central midline cortical region covering the SMA. When reconstructing N1 signals using backprojections with one versus all independent components (ICs) identified as brain sources there was no difference in peak amplitudes and a small but significant difference in N1 peak latencies. Parallel brain sources thus deflect the time course of the N1, but not its magnitude. Brain areas associated with ICs contributing to the shift in N1 latency varied between participants. Our results emphasize the dominant influence of central cortical areas on the N1 response, informing hypotheses regarding the nature of the signal and its functional role. Importantly, the extent and location of other cortical structures that influence N1 timing, such as parietal cortex areas and the anterior cingulate cortex, may further elucidate cortical contributions to balance. These markers could be crucial for the early detection of balance problems in clinical populations.NEW & NOTEWORTHY We demonstrate that channel-level amplitudes of the balance perturbation-evoked N1 in younger adults primarily reflect neural activity originating from cortical central midline regions, particularly the supplementary motor area (SMA). In contrast, contributions from parallel active brain regions evoked by balance perturbations are indicated by an effect on N1 peak latencies. Our findings imply that the perturbation-evoked N1, unlike other evoked potentials, is not a mixture of multiple neural sources in younger adults.