Functional connectivity of the default mode network predicts subsequent polysomnographically measured sleep in people with symptoms of insomnia.
William D S Killgore, Samantha Jankowski, Kymberly Henderson-Arredondo, Daniel A Lucas, Salma I Patel, Lindsey L Hildebrand, Alisa Huskey, Natalie S Dailey
Neuroreport October 4, 2023 DOI: 10.1097/WNR.0000000000001949 via PubMed
Summary
AI-generated from the abstractAmong 20 young adults with insomnia symptoms, resting-state functional connectivity between the default mode network (DMN) and certain cortical regions before bedtime predicted objectively measured sleep quality. Greater connectivity between the DMN and cortical areas involved in executive function and complex cognition was associated with more total sleep time, more REM sleep, and higher sleep efficiency, while connectivity with the pons was linked to lower sleep efficiency. The findings suggest that pre-sleep DMN activation may contribute to insomnia by supporting ruminative thinking, and that interventions to suppress such activation could improve sleep.
Study at a glance
| Characteristics | Observational cohort Peer reviewed |
|---|---|
| Sample size | 20 |
| Population | Young adults with symptoms of insomnia |
| Duration | One evening scan followed by one night of polysomnographic measurement |
| Citations | 19 |
| Key finding | Resting-state functional connectivity between the default mode network and cortical regions involved in executive function and complex cognition predicted better objectively measured sleep, while connectivity with the pons predicted worse sleep efficiency. |
Abstract
Insomnia is often accompanied by excessive pre-sleep rumination. Such ruminative thinking is also associated with increased connectivity of the default mode network (DMN). It is likely that DMN connectivity and associated rumination contribute to the pathogenesis of insomnia. We hypothesized that resting state functional connectivity (rsFC) between the DMN and other brain regions prior to bedtime would predict objectively measured sleep among individuals with insomnia. Twenty participants (12 female; M age = 26.9, SD = 6.6 years) with symptoms of insomnia underwent an rsFC scan in the early evening followed by a night of polysomographically (PSG) measured sleep. Connectivity of the DMN with other brain regions was regressed against several PSG sleep metrics, including time in wake, N1, N2, N3, REM, total sleep time (TST), and sleep efficiency (SE) at a cluster corrected false discovery rate (FDR) correction P < 0.05. The connectivity between DMN and cortical regions was negatively correlated with PSG indices of poorer sleep including time in wake (right angular gyrus) and N1 (precuneus) but positively correlated with time in REM (orbitofrontal cortex), TST (insula, orbitofrontal cortex, superior frontal gyrus, paracingulate gyrus), SE (orbitofrontal cortex). Connectivity between DMN and the pons was negatively correlated with SE. Among individuals with symptoms of insomnia, better sleep was predicted by rsFC between the DMN and cortical regions involved in executive functioning, consciousness, and complex cognition. Findings raise the possibility that future interventions aimed at suppressing pre-sleep DMN activation may weaken synergy between pre-sleep ruminative worry and complex cognitions, potentially ameliorating problems falling asleep.