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Is Pain Intensity Associated With Sleep-Spindle Activity in Persons With Chronic Spinal Pain and Chronic Insomnia Disorder? A Polysomnography Study

  • Nils Runge
  • , Nyissa Walsh
  • , Thien Thanh Dang-Vu
  • , Liesbet De Baets
  • , Céline Labie
  • , Thomas Bilterys
  • , Sabine Verschueren
  • , Dieter Van Assche
  • , Jo Nijs
  • , Anneleen Malfliet
  • , Lieven Danneels
  • , Kelly Ickmans
  • , Maarten Moens
  • , Dorien Goubert
  • , Olivier Mairesse
  • , Arsenio Paez
  • Pain in Motion Research Group (PAIN)
  • VUB University
  • Faculty of Movement and Rehabilitation Sciences
  • Brain
  • Pain in Motion International Research Consortium
  • Concordia University
  • Concordia University
  • University Hospital Gasthuisberg
  • University of Warwick
  • Practice for Pain Management
  • University of Gothenburg
  • University Hospital Brussels
  • Fonds Wetenschappelijk Onderzoek—Vlaanderen
  • University of Ghent
  • Laboratoire de Psychologie Médicale et d'Addictologie (ULB312)
  • Brugmann University Hospital
  • University of Oxford Medical Sciences Division

Onderzoeksoutput: Bijdrage aan een tijdschrift › Artikel › peer review

Samenvatting

Chronic spinal pain is associated with fragmented sleep, yet the neurophysiological mechanisms linking the two remain unclear. Given their role in sensory gating and sleep stability, sleep spindles may represent a key mechanism connecting chronic spinal pain and sleep fragmentation. This study examined whether pain intensity over the past 4 weeks was associated with sleep spindle density and related characteristics in individuals with chronic low back or neck pain and chronic insomnia disorder. Data from 120 participants, classified by self-reported pain severity (mild, moderate, severe), were compared on spindle density derived from C4–A1A2 and F4–A1A2 EEG channels. No significant group differences were found in spindle density (respectively, C4: p = 0.372 and F4: p = 0.744). Regression analyses adjusted for age, sex and medication use showed that pain intensity did not significantly predict spindle density (p > 0.05). However, exploratory regression models revealed small but statistically significant associations between pain intensity and both spindle power (p = 0.047) and amplitude (p = 0.038) on the C4 channel. These findings suggest that while spindle density does not vary meaningfully with pain intensity in this clinical population, alterations in spindle power and amplitude may reflect pain-related modulation of thalamocortical activity. This highlights the complexity of pain–sleep interactions in the presence of chronic spinal pain and insomnia. More nuanced, temporally resolved assessments of pain are needed to clarify the dynamic interactions between chronic pain, insomnia, and sleep microarchitecture.

Originele taal-2Engels
Artikelnummere70368
TijdschriftJournal of Sleep Research
Volume35
Nummer van het tijdschrift5
DOI's
StatusGepubliceerd - okt 2026

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