Istvan Papp, Zoran Cvetkovic, Nazanin Biabani, Jan Rosenzweig, Camilla Speicher, Alessio Delogu, Alexander D Nesbitt, Panagis Drakatos, Ines R Violante, Dijana Vilic, Clive Ballard, David O'Regan, Peter J Goadsby, Ivana Rosenzweig
{"title":"Nightmare disorder shows reduced slow oscillation-dominant spindle coupling in NREM sleep.","authors":"Istvan Papp, Zoran Cvetkovic, Nazanin Biabani, Jan Rosenzweig, Camilla Speicher, Alessio Delogu, Alexander D Nesbitt, Panagis Drakatos, Ines R Violante, Dijana Vilic, Clive Ballard, David O'Regan, Peter J Goadsby, Ivana Rosenzweig","doi":"10.1038/s44323-026-00094-0","DOIUrl":null,"url":null,"abstract":"<p><p>Nightmare disorder is historically conceptualised as a rapid eye movement (REM) sleep parasomnia, but evidence also points to altered non-rapid eye movement (NREM) sleep physiology. Here, in a retrospective case-control study, we analysed overnight polysomnography from 26 adults with nightmare disorder and 32 controls using a harmonised event-based EEG pipeline. Nightmare disorder showed reduced frontal slow-oscillation-spindle coupling, whereas delta-spindle coupling was preserved, yielding lower coupling dominance than in controls (0.137 ± 0.083 versus 0.238 ± 0.096; p = 6.8 × 10<sup>-5</sup>). Stage-adjusted K-complex density across the first 6 h from sleep onset was also lower in nightmare disorder (0.463 ± 0.345 versus 0.723 ± 0.475 events per minute of available N2/N3 sleep; p = 0.019), whereas peak-timing differences were not robust. These findings suggest altered NREM sleep microarchitecture in nightmare disorder rather than a phenotype confined to REM sleep, and warrant prospective confirmation in harmonised, clinically phenotyped cohorts.</p>","PeriodicalId":501704,"journal":{"name":"npj Biological Timing and Sleep","volume":"3 1","pages":""},"PeriodicalIF":0.0000,"publicationDate":"2026-06-22","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13287732/pdf/","citationCount":"0","resultStr":null,"platform":"Semanticscholar","paperid":null,"PeriodicalName":"npj Biological Timing and Sleep","FirstCategoryId":"1085","ListUrlMain":"https://doi.org/10.1038/s44323-026-00094-0","RegionNum":0,"RegionCategory":null,"ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":null,"EPubDate":"","PubModel":"","JCR":"","JCRName":"","Score":null,"Total":0}
引用次数: 0
Abstract
Nightmare disorder is historically conceptualised as a rapid eye movement (REM) sleep parasomnia, but evidence also points to altered non-rapid eye movement (NREM) sleep physiology. Here, in a retrospective case-control study, we analysed overnight polysomnography from 26 adults with nightmare disorder and 32 controls using a harmonised event-based EEG pipeline. Nightmare disorder showed reduced frontal slow-oscillation-spindle coupling, whereas delta-spindle coupling was preserved, yielding lower coupling dominance than in controls (0.137 ± 0.083 versus 0.238 ± 0.096; p = 6.8 × 10-5). Stage-adjusted K-complex density across the first 6 h from sleep onset was also lower in nightmare disorder (0.463 ± 0.345 versus 0.723 ± 0.475 events per minute of available N2/N3 sleep; p = 0.019), whereas peak-timing differences were not robust. These findings suggest altered NREM sleep microarchitecture in nightmare disorder rather than a phenotype confined to REM sleep, and warrant prospective confirmation in harmonised, clinically phenotyped cohorts.