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<p>Sleep’s microstructure emerges from the continual coupling of intrinsic arousal with the homeostatic descent of the night. To ask how this coupling unfolds across disorders, we mapped the nocturnal trajectory of phasic events in idiopathic REM sleep behaviour disorder (iRBD; <i>n</i> = 19), narcolepsy type 1 (NT1; <i>n</i> = 19), NREM parasomnia (<i>n</i> = 18), fibromyalgia (<i>n</i> = 13) and healthy controls (<i>n</i> = 40). Using an automated, cyclic alternating pattern (CAP)- inspired, A‑phase index (API), a B‑phase–agnostic, 60‑s read‑out of phasic burden, we profiled subtype‑specific activity across normalised nights in retrospective polysomnography. In controls, early‑night slow‑wave–dominant phasic responses rose steeply and decayed with dissipating pressure, consistent with thalamocortical homeostasis. In iRBD and NT1, early-night A1 prominence was attenuated, and in fibromyalgia it was broadly reduced across the night. NREM parasomnias showed a distinctive pattern: transient amplification of phasic drive in early, with later attenuation in deep NREM sleep. Stage‑wise comparisons showed the largest group separations in N2 for A1/A2; between group differences were described from normalised time curves without inferential testing. These trajectories suggest that disorders may differ in how intrinsic arousal couples to homeostatic drift across the night. However, findings are hypothesis‑generating given unmatched controls, small groups and lack of adjustment for additional confounds. Descriptive prospective work combining A- and B-phase estimation is warranted.</p>

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Mapping nocturnal arousal across sleep and pain disorders

  • 期刊论文

  • 出版模式：

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  • 发表日期：

    2026年3月5日

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  • Nazanin Biabani,
  • Fábio Mendonça,
  • Carlotta Mutti,
  • Panagis Drakatos,
  • Fernando Morgado-Dias,
  • Antonio G. Ravelo-García,
  • Gulcin Benbir Senel,
  • Heidur Gretarsdottir,
  • Peter J. Goadsby,
  • Robert J. Thomas,
  • Oliviero Bruni,
  • Raffaele Ferri,
  • Liborio Parrino,
  • Ivana Rosenzweig

摘要

Sleep’s microstructure emerges from the continual coupling of intrinsic arousal with the homeostatic descent of the night. To ask how this coupling unfolds across disorders, we mapped the nocturnal trajectory of phasic events in idiopathic REM sleep behaviour disorder (iRBD; n = 19), narcolepsy type 1 (NT1; n = 19), NREM parasomnia (n = 18), fibromyalgia (n = 13) and healthy controls (n = 40). Using an automated, cyclic alternating pattern (CAP)- inspired, A‑phase index (API), a B‑phase–agnostic, 60‑s read‑out of phasic burden, we profiled subtype‑specific activity across normalised nights in retrospective polysomnography. In controls, early‑night slow‑wave–dominant phasic responses rose steeply and decayed with dissipating pressure, consistent with thalamocortical homeostasis. In iRBD and NT1, early-night A1 prominence was attenuated, and in fibromyalgia it was broadly reduced across the night. NREM parasomnias showed a distinctive pattern: transient amplification of phasic drive in early, with later attenuation in deep NREM sleep. Stage‑wise comparisons showed the largest group separations in N2 for A1/A2; between group differences were described from normalised time curves without inferential testing. These trajectories suggest that disorders may differ in how intrinsic arousal couples to homeostatic drift across the night. However, findings are hypothesis‑generating given unmatched controls, small groups and lack of adjustment for additional confounds. Descriptive prospective work combining A- and B-phase estimation is warranted.