{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,6,20]],"date-time":"2026-06-20T13:39:23Z","timestamp":1781962763028,"version":"3.54.5"},"reference-count":64,"publisher":"Wiley","issue":"10","license":[{"start":{"date-parts":[[2026,2,23]],"date-time":"2026-02-23T00:00:00Z","timestamp":1771804800000},"content-version":"vor","delay-in-days":0,"URL":"http:\/\/creativecommons.org\/licenses\/by\/4.0\/"},{"start":{"date-parts":[[2026,2,23]],"date-time":"2026-02-23T00:00:00Z","timestamp":1771804800000},"content-version":"tdm","delay-in-days":0,"URL":"http:\/\/doi.wiley.com\/10.1002\/tdm_license_1.1"}],"content-domain":{"domain":["physoc.onlinelibrary.wiley.com"],"crossmark-restriction":true},"short-container-title":["The Journal of Physiology"],"published-print":{"date-parts":[[2026,5]]},"abstract":"<jats:sec>\n                    <jats:title>Abstract<\/jats:title>\n                    <jats:p>\n                      Standing balance relies on rapid reflexes as well as longer\u2010latency subcortical and cortical processes to generate corrective responses to postural disturbances. EEG studies consistently identify two perturbation\u2010evoked markers of cortical activity, the balance N1 and midfrontal theta power, associated with changes in body orientation and corrective actions. It remains unclear, however, whether these markers depend on the nervous system's active control of posture or reflect a more general evaluation of unexpected sensory input. We tested this by measuring cortical and muscle activity during support\u2010surface perturbations while systematically manipulating whether or not participants actively controlled posture. In Experiment 1 (\n                      <jats:italic>n<\/jats:italic>\n                      \u00a0=\u00a010), participants experienced identical perturbations while either actively balancing or being passively moved through equivalent motion. Despite large reductions in balance\u2010correcting muscle activity during passive trials (\u223c30\u201360%), N1 and theta responses persisted with only modest amplitude reductions (\u223c10%). In Experiment 2 (\n                      <jats:italic>n<\/jats:italic>\n                      \u00a0=\u00a016), we created passive conditions increasingly removed from balance by varying sensory feedback (footplate + whole\u2010body\n                      <jats:italic>vs<\/jats:italic>\n                      . footplate\u2010only motion) and motor engagement (isometric contraction\n                      <jats:italic>vs<\/jats:italic>\n                      . relaxed posture). Relaxed postures markedly suppressed muscle responses, yet cortical responses persisted, showing only modest modulation with sensory feedback (larger during footplate\u2010only rotations) and no dependence on motor engagement. Together, these results indicate that N1 and midfrontal theta are not dependent on active postural control and persist even without matching sensory feedback or motor engagement. Rather than reflecting the generation or scaling of corrective actions, they index the early detection and evaluation of unexpected sensory events, consistent with prediction error or surprise processing.\n                      <jats:boxed-text content-type=\"graphic\" position=\"anchor\">\n                        <jats:graphic xmlns:xlink=\"http:\/\/www.w3.org\/1999\/xlink\" mimetype=\"image\/png\" position=\"anchor\" specific-use=\"enlarged-web-image\" xlink:href=\"graphic\/tjp70407-gra-0001-m.png\">\n                          <jats:alt-text>image<\/jats:alt-text>\n                        <\/jats:graphic>\n                      <\/jats:boxed-text>\n                    <\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>Key points<\/jats:title>\n                    <jats:p>\n                      <jats:list list-type=\"bullet\">\n                        <jats:list-item>\n                          <jats:p>When standing balance is disturbed by a perturbation, the brain shows characteristic electrical responses called the balance N1 and theta activity, which are thought to contribute to balance\u2010correcting actions.<\/jats:p>\n                        <\/jats:list-item>\n                        <jats:list-item>\n                          <jats:p>We tested whether these cortical responses depend on actively controlling posture or instead reflect the detection of unexpected motion irrespective of balance conditions.<\/jats:p>\n                        <\/jats:list-item>\n                        <jats:list-item>\n                          <jats:p>Participants stood in a robotic balance simulator and experienced identical perturbations while actively balancing or being passively moved, and when whole\u2010body sensory feedback and muscle engagement were removed.<\/jats:p>\n                        <\/jats:list-item>\n                        <jats:list-item>\n                          <jats:p>The balance N1 and theta activity persisted in conditions where participants were not controlling their movement and even when whole\u2010body sensory feedback and motor engagement were removed, whereas balance\u2010correcting muscle responses were strongly diminished.<\/jats:p>\n                        <\/jats:list-item>\n                        <jats:list-item>\n                          <jats:p>This shows that cortical responses to balance perturbations are not specific to active balance control but probably represent the brain's detection and evaluation of unexpected sensory events.<\/jats:p>\n                        <\/jats:list-item>\n                      <\/jats:list>\n                    <\/jats:p>\n                  <\/jats:sec>","DOI":"10.1113\/jp290280","type":"journal-article","created":{"date-parts":[[2026,3,8]],"date-time":"2026-03-08T21:07:17Z","timestamp":1773004037000},"page":"3914-3933","update-policy":"https:\/\/doi.org\/10.1002\/crossmark_policy","source":"Crossref","is-referenced-by-count":1,"title":["Cortical responses to balance perturbations persist without active postural control"],"prefix":"10.1113","volume":"604","author":[{"ORCID":"https:\/\/orcid.org\/0009-0004-9766-4790","authenticated-orcid":false,"given":"Daphne N. R.","family":"Jansen","sequence":"first","affiliation":[{"name":"Department of Neuroscience, Erasmus MC University Medical Center Rotterdam  Rotterdam The Netherlands"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"ORCID":"https:\/\/orcid.org\/0009-0004-3113-7162","authenticated-orcid":false,"given":"Lucas","family":"Mensink","sequence":"additional","affiliation":[{"name":"Department of Neuroscience, Erasmus MC University Medical Center Rotterdam  Rotterdam The Netherlands"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"ORCID":"https:\/\/orcid.org\/0009-0009-8728-0589","authenticated-orcid":false,"given":"Matto","family":"Leeuwis","sequence":"additional","affiliation":[{"name":"Department of Neuroscience, Erasmus MC University Medical Center Rotterdam  Rotterdam The Netherlands"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"ORCID":"https:\/\/orcid.org\/0000-0002-0230-9971","authenticated-orcid":false,"given":"Patrick A.","family":"Forbes","sequence":"additional","affiliation":[{"name":"Department of Neuroscience, Erasmus MC University Medical Center Rotterdam  Rotterdam The Netherlands"}],"role":[{"vocabulary":"crossref","role":"author"}]}],"member":"311","published-online":{"date-parts":[[2026,2,23]]},"reference":[{"key":"e_1_2_5_2_1","doi-asserted-by":"publisher","DOI":"10.1016\/j.neulet.2008.02.018"},{"key":"e_1_2_5_3_1","doi-asserted-by":"publisher","DOI":"10.1007\/s00221-005-0310-9"},{"key":"e_1_2_5_4_1","doi-asserted-by":"publisher","DOI":"10.1038\/s41598-022-12911-0"},{"key":"e_1_2_5_5_1","doi-asserted-by":"publisher","DOI":"10.1371\/journal.pcbi.1011562"},{"key":"e_1_2_5_6_1","doi-asserted-by":"publisher","DOI":"10.1016\/j.neubiorev.2015.08.014"},{"key":"e_1_2_5_7_1","doi-asserted-by":"publisher","DOI":"10.1007\/BF00230477"},{"key":"e_1_2_5_8_1","doi-asserted-by":"publisher","DOI":"10.1016\/S0167-8760(98)00040-3"},{"key":"e_1_2_5_9_1","doi-asserted-by":"publisher","DOI":"10.1016\/j.neuroscience.2009.07.042"},{"key":"e_1_2_5_10_1","doi-asserted-by":"publisher","DOI":"10.1007\/s002210050940"},{"key":"e_1_2_5_11_1","doi-asserted-by":"publisher","DOI":"10.1016\/j.tics.2014.04.012"},{"key":"e_1_2_5_12_1","doi-asserted-by":"publisher","DOI":"10.3390\/brainsci15050531"},{"key":"e_1_2_5_13_1","doi-asserted-by":"publisher","DOI":"10.3109\/00016487009123358"},{"key":"e_1_2_5_14_1","doi-asserted-by":"publisher","DOI":"10.7554\/eLife.21792"},{"key":"e_1_2_5_15_1","doi-asserted-by":"publisher","DOI":"10.1016\/j.neuroimage.2021.118809"},{"key":"e_1_2_5_16_1","doi-asserted-by":"publisher","DOI":"10.1016\/j.tins.2023.08.009"},{"key":"e_1_2_5_17_1","doi-asserted-by":"publisher","DOI":"10.1113\/jphysiol.1993.sp019824"},{"key":"e_1_2_5_18_1","doi-asserted-by":"publisher","DOI":"10.1016\/j.jneumeth.2003.10.009"},{"key":"e_1_2_5_19_1","doi-asserted-by":"publisher","DOI":"10.1113\/jphysiol.2009.168690"},{"key":"e_1_2_5_20_1","doi-asserted-by":"publisher","DOI":"10.1113\/jphysiol.1994.sp020257"},{"key":"e_1_2_5_21_1","doi-asserted-by":"publisher","DOI":"10.1113\/jphysiol.1994.sp020240"},{"key":"e_1_2_5_22_1","first-page":"61","volume-title":"Handbook of clinical neurology","author":"Forbes P. 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