ReviewPain2017
The role of calcitonin gene-related peptide in peripheral and central pain mechanisms including migraine.
Review in Pain, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 309 papers, 1 of them a synthesis 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.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
309 citing papers in PubMed, 1 synthesis or guideline pooled it, 565 citations in OpenAlex.
- Effectiveness of intraoral splints in the treatment of migraine and tension-type headache: A systematic review.Clinical and experimental dental research · 2023Pooled it
- Trial
- Cutaneous allodynia as predictor for treatment response in chronic migraine: a cohort study.The journal of headache and pain · 2023Trial
- CGRP-induced migraine-like headache in persistent post-traumatic headache attributed to mild traumatic brain injury.The journal of headache and pain · 2022Trial
- Tolerability and safety of galcanezumab in patients with chronic cluster headache with up to 15 months of galcanezumab treatment.Headache · 2022Trial
- Review
- Article
- Chronic pain after thoracic surgery: mechanisms, risk factors, and limitations of current preventive strategies-a narrative review.Journal of thoracic disease · 2026Review
- Elucidating the nociceptive role of CGRP in migraine headache.Brain : a journal of neurology · 2026Article
- Senolytic Therapy as a Preventive Strategy for Spine Degeneration and Pain.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2026Article
- Neuropathic pain in traumatic brain injury: consequences, mechanisms, and therapeutic avenues.Inflammopharmacology · 2026Review
- Untangling neuropathic pain: pathophysiological insights and future directions for targeted therapy.Naunyn-Schmiedeberg's archives of pharmacology · 2026Review
- Comparison of the Effectiveness of Greater Occipital Nerve (GON) Block and Sphenopalatine Ganglion (SPG) Block in the Treatment of Chronic Migraine.Healthcare (Basel, Switzerland) · 2026Article
- A delayed endothelial-glial mechanism for CGRP-induced migraine.The journal of headache and pain · 2026Review
- Dorsal horn DCC amplification loop induced by endplate osteoclasts generates chronic nociplastic low back pain in male mice.Nature communications · 2026Article
- Cochlear Functional Changes and CGRP Modulation in a Chronic Nitroglycerin Migraine-Like Rat Model.The European journal of neuroscience · 2026Article
- Novel Role for CGRP in Aqueous Humor Outflow.Investigative ophthalmology & visual science · 2026Article
- CXCL10 knockdown attenuates vestibular migraine in rats by inhibiting PI3K-mediated neuroinflammation and central sensitization.The journal of headache and pain · 2026Article
- Early life stress induces brain-wide electrical network predisposition to migraine.The journal of headache and pain · 2026Article
- Varenicline-mediated cholinergic activation through α4β2 nAChR inhibits microglial neuroinflammation and alleviates neuropathic pain and depression following spinal cord injury.Journal of translational medicine · 2026Article
249 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
No grant is acknowledged in the PubMed record.
Abstract
Calcitonin gene-related peptide (CGRP) is a 37-amino acid peptide found primarily in the C and Aδ sensory fibers arising from the dorsal root and trigeminal ganglia, as well as the central nervous system. Calcitonin gene-related peptide was found to play important roles in cardiovascular, digestive, and sensory functions. Although the vasodilatory properties of CGRP are well documented, its somatosensory function regarding modulation of neuronal sensitization and of enhanced pain has received considerable attention recently. Growing evidence indicates that CGRP plays a key role in the development of peripheral sensitization and the associated enhanced pain. Calcitonin gene-related peptide is implicated in the development of neurogenic inflammation and it is upregulated in conditions of inflammatory and neuropathic pain. It is most likely that CGRP facilitates nociceptive transmission and contributes to the development and maintenance of a sensitized, hyperresponsive state not only of the primary afferent sensory neurons but also of the second-order pain transmission neurons within the central nervous system, thus contributing to central sensitization as well. The maintenance of a sensitized neuronal condition is believed to be an important factor underlying migraine. Recent successful clinical studies have shown that blocking the function of CGRP can alleviate migraine. However, the mechanisms through which CGRP may contribute to migraine are still not fully understood. We reviewed the role of CGRP in primary afferents, the dorsal root ganglion, and in the trigeminal system as well as its role in peripheral and central sensitization and its potential contribution to pain processing and to migraine.
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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.