ArticlebioRxiv : the preprint server for biology2026
A Primary Central Source Determines Perturbation-Evoked N1 Amplitudes but not Latencies in Younger Adults.
Article in bioRxiv : the preprint server for biology, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
0 citing papers in PubMed.
No citing paper in PubMed yet.
Corrections and comments
- Updated by
Authors and funding
4 authors.
Funding
Abstract
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 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 (IC) 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 IC's 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 hypothesizes 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.
Indexed as
Identifiers
What OpenQuestion holds
Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.