Evidence map›Paper›PMID 42158854›Full record

ArticleFrontiers in immunology2026

Precuneus hyperexcitability mediates inflammatory-driven pain hypersensitivity following sleep disruption: a multimodal neuroimaging study.

Chao Li, Yang Wang, Kechong Zhou, Peng Zhang, Gang Chen, Xufeng Jiang, Yuhong Guo

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Article in Frontiers in immunology, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.

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1 · What the graph read from it

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3 · Its place in the literature

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4 · The record

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5 · Who and what money

Authors and funding

7 authors.

Chao Li *Department of Orthopedics, Xiangyang Central Hospital, Affiliated Hospital of Hubei University of Arts and Science, Xiangyang, Hubei, China.
Yang Wang *Department of Orthopedics, Xiangyang Central Hospital, Affiliated Hospital of Hubei University of Arts and Science, Xiangyang, Hubei, China.
Kechong Zhou *Department of Urology, Xiangyang Central Hospital, Affiliated Hospital of Hubei University of Arts and Science, Xiangyang, Hubei, China.
Peng ZhangDepartment of Orthopedics, Xiangyang Central Hospital, Affiliated Hospital of Hubei University of Arts and Science, Xiangyang, Hubei, China.
Gang ChenDepartment of Orthopedics, Xiangyang Central Hospital, Affiliated Hospital of Hubei University of Arts and Science, Xiangyang, Hubei, China.
Xufeng JiangDepartment of Orthopedics, Xiangyang Central Hospital, Affiliated Hospital of Hubei University of Arts and Science, Xiangyang, Hubei, China.
Yuhong GuoDepartment of Orthopedics, Xiangyang Central Hospital, Affiliated Hospital of Hubei University of Arts and Science, Xiangyang, Hubei, China.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Background: Sleep disruption(SD) has been shown to amplify inflammatory signaling and promote pain hypersensitivity, but how inflammation interacts with brain functional alterations to drive pain sensitization remains unclear. This study therefore aims to investigate inflammatory associated pain hypersensitivity induced by SD and characterize neural correlates for mediating neuroimmune-pain interactions. Materials and methods: This study employed two complementary designs: 1) A experimental design comparing forced awakening (FA) and uninterrupted sleep (US) groups, with polysomnography (PSG), task-fMRI, structural MRI, inflammatory cytokines, and quantitative sensory testing post-intervention; 2) A longitudinal cohort of chronic pain patients assessed pre- and 3-months postoperatively using neuroimaging, clinical pain metrics, and sleep quality indices (PSQI). Mass univariate analyses were performed to reveal differences in pain-elicited brain response between FA and US group. Structural and functional metrics were analyses within resultant brain regions using patient cohort. Multivariate correlations and mediation models were performed to test neuroimmune interactions. Results: FA subjects exhibited reduced total/slow-wave sleep, elevated IL-6, and lowered pain-thresholds versus US. Task-fMRI revealed hyperactivation in the precuneus and middle temporal gyrus during pain processing after FA. Serum IL-6 inversely correlated with pain thresholds and positively with precuneus activation. Mediation analysis demonstrated a mediating effect of precuneus hyperexcitability on the IL-6-pain hypersensitivity relationship. Longitudinal data from patient cohort complemented these findings, showing aberrant precuneus normalization correlated with improvement in pain and sleep quality. Conclusion: Across experimental and clinical cohorts, we identified the precuneus as a cortical hub linking sleep disruption, inflammation, and pain hypersensitivity, thereby revealing a novel neuroimmune pathway for sleep-related pain amplification.

Indexed as

HyperalgesiaInflammationSleep Wake DisordersAdultFemaleHumansMagnetic Resonance ImagingMaleMiddle AgedMultimodal ImagingNeuroimagingNociplastic PainPain ThresholdPolysomnographySleepfunctional MRIgeneral liner modelinflammationpain hypersensitivitysleep disruption

Identifiers

PMID42158854
PMCPMC13180543

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