ReviewPain2013
Glia and pain: is chronic pain a gliopathy?
Review in Pain, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. It is linked to trial NCT04631471 (Regeneration in Cervical Degenerative Myelopathy - a Multi-centre, Double-blind, Randomised, Placebo Controlled Trial Assessing the Efficacy of Ibudilast as an Adjuvant Treatment to Decompressive Surgery for Degenerative Cervical Myelopathy), which is not on this map. Cited by 649 papers, 4 of them syntheses that pooled it.
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.
Regeneration in Cervical Degenerative Myelopathy - a Multi-centre, Double-blind, Randomised, Placebo Controlled Trial Assessing the Efficacy of Ibudilast as an Adjuvant Treatment to Decompressive Surgery for Degenerative Cervical Myelopathy
Who cites it
649 citing papers in PubMed, 4 syntheses or guidelines pooled it, 1,164 citations in OpenAlex.
- Role of Supraspinal Neuroinflammation in Chronic Pain After Experimental Spinal Cord Injury-A Systematic Review.International journal of molecular sciences · 2026Pooled it
- Sexually Dimorphic Neuroimmune Pathways in Chronic Pain: A Comprehensive Systematic Review of Cellular and Molecular Mechanisms.Biomolecules · 2026Pooled it
- Molecular targets in bone cancer pain: a systematic review of inflammatory cytokines.Journal of molecular medicine (Berlin, Germany) · 2024Pooled it
- The core of maintaining neuropathic pain: Crosstalk between glial cells and neurons (neural cell crosstalk at spinal cord).Brain and behavior · 2023Pooled it
- Trial
- Impact of repeated exposure to CPM on CPM efficiency and pain sensitivity in healthy adults: a randomized controlled trial.Frontiers in pain research (Lausanne, Switzerland) · 2025Trial
- Neuroimmune alterations and nociceptive behavior in oral carcinogenesis in rats.European journal of oral sciences · 2026Article
- Glial cells in neuropathic pain.Physiological reviews · 2026Review
- Targeting Spinal Dorsal Horn Sensitisation in Chronic Pain: Mechanisms and Translational Strategies.Neuroscience bulletin · 2026Review
- Teriparatide reduces spinal neuroinflammatory phenotypes in ovariectomized rats revealed by an artificial intelligence-driven glial cell morphometry of bright-field tissue sections.Microscopy (Oxford, England) · 2026Article
- Neurobiological and Neuroimmune Mechanisms Linking Chronic Pain, Sleep Disturbances and Mental Health Disorders.International journal of molecular sciences · 2026Review
- Reactive aldehyde species-mediated neuropathic pain in spinal cord injury: Mechanisms and therapeutic opportunities.Neural regeneration research · 2026Article
- Preventive Treatment With Ceftriaxone Attenuates Neuropathic Pain and Anxiety-Like Behaviour in a Mouse Model of Partial Sciatic Nerve Ligation.European journal of pain (London, England) · 2026Article
- The Pathophysiological Mechanisms of Glia in Animal Models of Chronic Orofacial Pain: A Systematic Review.Pathophysiology : the official journal of the International Society for Pathophysiology · 2026Review
- Targeting Supramolecular Active Complexes of NaAdvanced science (Weinheim, Baden-Wurttemberg, Germany) · 2026Article
- Glial fibrillary acidic protein in fibromyalgia: its serum levels and antibodies.Advances in rheumatology (London, England) · 2026Article
- TGF-β1 modulates PFC glial cell activation to facilitate exercise-induced analgesia in mice with spared nerve injury.IBRO neuroscience reports · 2026Article
- Losmapimod, an Oral Anti-p38 MAP Kinase, Demonstrates Anti-Neuropathic and Anti-Inflammatory Effects in Rat Acute Pain.Journal of clinical medicine · 2026Article
- Differential Modulation of Spinal Angiotensin-Converting Enzymes Plays a Critical Role in the Development of Trigeminal Neuropathic Pain.Pharmaceuticals (Basel, Switzerland) · 2026Article
- Spinal Cord Stimulation Alleviates Neuropathic Pain Involves Regulation of the CaCellular and molecular neurobiology · 2026Article
589 more citing papers are in PubMed but not listed here.
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
3 authors at 1 institution in 1 country.
Funding
Abstract
Activation of glial cells and neuro-glial interactions are emerging as key mechanisms underlying chronic pain. Accumulating evidence has implicated 3 types of glial cells in the development and maintenance of chronic pain: microglia and astrocytes of the central nervous system (CNS), and satellite glial cells of the dorsal root and trigeminal ganglia. Painful syndromes are associated with different glial activation states: (1) glial reaction (ie, upregulation of glial markers such as IBA1 and glial fibrillary acidic protein (GFAP) and/or morphological changes, including hypertrophy, proliferation, and modifications of glial networks); (2) phosphorylation of mitogen-activated protein kinase signaling pathways; (3) upregulation of adenosine triphosphate and chemokine receptors and hemichannels and downregulation of glutamate transporters; and (4) synthesis and release of glial mediators (eg, cytokines, chemokines, growth factors, and proteases) to the extracellular space. Although widely detected in chronic pain resulting from nerve trauma, inflammation, cancer, and chemotherapy in rodents, and more recently, human immunodeficiency virus-associated neuropathy in human beings, glial reaction (activation state 1) is not thought to mediate pain sensitivity directly. Instead, activation states 2 to 4 have been demonstrated to enhance pain sensitivity via a number of synergistic neuro-glial interactions. Glial mediators have been shown to powerfully modulate excitatory and inhibitory synaptic transmission at presynaptic, postsynaptic, and extrasynaptic sites. Glial activation also occurs in acute pain conditions, and acute opioid treatment activates peripheral glia to mask opioid analgesia. Thus, chronic pain could be a result of "gliopathy," that is, dysregulation of glial functions in the central and peripheral nervous system. In this review, we provide an update on recent advances and discuss remaining questions.
Indexed as
Identifiers
What OpenQuestion holds
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.