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<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; <i>p</i> = 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; <i>p</i> = 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>

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Nightmare disorder shows reduced slow oscillation-dominant spindle coupling in NREM sleep

  • 期刊论文

  • 出版模式：

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  • 发表日期：

    2026年6月22日

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  • 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

摘要

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.