J Sleep Res. 2026 May 26:e70368. doi: 10.1111/jsr.70368. Online ahead of print.
ABSTRACT
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.
PMID:42186730 | DOI:10.1111/jsr.70368
