ReviewJournal of pain research2026
Cognitive Behavioral Therapy and Pain Chronification: Neuroimmune Rationale, Evidence Boundaries, and Trial Design Priorities: A Structured Narrative Review.
Review in Journal of pain research, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
0 citing papers in PubMed.
No citing paper in PubMed yet.
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
5 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Background: Pain chronification is a dynamic transition in which persistent pain may be shaped by interacting nociceptive, peripheral, spinal, supraspinal, neuroimmune, endocrine and cognitive-affective processes. Cognitive Behavioral Therapy (CBT) has clinical value in chronic pain, but claims about glial modulation and disease modification require careful qualification. Objective: To evaluate CBT as an early, mechanism-informed and hypothesis-generating intervention while distinguishing clinical efficacy, neuroimmune plausibility, prevention hypotheses and disease-modifying claims. Methods: We conducted a structured narrative review using prespecified evidence domains. PubMed/MEDLINE searches covering January 2014 to September 10, 2026 were complemented by citation chasing and selected landmark mechanistic articles. Sources were organized by evidence domain, study type and interpretive role, including pain chronification, neuroimmune and glial mechanisms, brain-network mechanisms, CBT outcomes, psychoneuroimmune pathways, perioperative prevention hypotheses, risk phenotyping and scalable delivery. No quantitative pooling or formal systematic/scoping-review workflow was performed. Results: Experimental and translational studies support neuroimmune contributions to central sensitization and pain maintenance, whereas human evidence for direct CBT effects on microglial or astrocytic activation remains insufficient. CBT produces reproducible, generally small effects on pain intensity and more consistent benefits for interference, disability, distress, coping, sleep and function. Conclusion: CBT should be presented as a clinically valuable component of multimodal care and as a testable psychoneuroimmune hypothesis, not as a proven preventive, glial-targeting or disease-modifying treatment. Risk-stratified, early, component-specific and mechanism-embedded trials are needed before prevention claims are made.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.