Definition and research guide
This page combines a MeSH definition, publication statistics and selected research abstracts. It is a starting point for reading the literature, not a medical textbook or a systematic evidence review.
Content available: 3 complete abstracts (551 words), 9 references. Full article text is not stored or reproduced here; follow the PMID, DOI or PMC links to read the original sources and their access terms.
Definition
Intense or aching pain that occurs along the course or distribution of a peripheral or cranial nerve.
Definition: NLM Medical Subject Headings (MeSH) scope note (Public domain (U.S. National Library of Medicine); attribution requested). View the MeSH record.
Also known as: Neuralgias; Neurodynia; Neurodynias; Neuropathic Pain; Neuropathic Pains; Pain, Neuropathic; Pains, Neuropathic; Nerve Pain.
Where it fits in the MeSH classification
- Broader topics
- Peripheral Nervous System Diseases; Pain
- Narrower topics
- Causalgia; Morton Neuroma; Neuralgia, Postherpetic; Piriformis Muscle Syndrome; Pudendal Neuralgia; Sciatica
Research landscape
PubMed indexes 28,414 records tagged with the MeSH heading “Neuralgia” (counts retrieved 2026-10-29). 7,915 of them (27.9%) were published from 2020 onward, and the busiest period so far is 2010-2019 with 9,989 records.
Reviews account for 4,547 records (16.0%) and meta-analyses for 414. Randomized controlled trials number 1,202 (4.2%) as a share of all records on the topic.
Show the data
| Period | Records |
|---|---|
| through 1999 | 6,764 |
| 2000-2009 | 3,746 |
| 2010-2019 | 9,989 |
| 2020 onward | 7,915 |
Publication-type chart data
| Type | Records | Share |
|---|---|---|
| Reviews | 4,547 | 16.0% |
| Meta-analyses | 414 | 1.5% |
| Randomized controlled trials | 1,202 | 4.2% |
Method: PubMed query "Neuralgia"[MeSH Terms] with publication-type and date filters, retrieved 2026-10-29.
Reading the evidence in neuroscience
Neuroscience draws on tools with different strengths: cellular and animal work can manipulate circuits directly, while human imaging and electrophysiology observe the living brain at lower resolution. Small imaging studies are prone to false positives, and findings in animals do not always carry over to people. Clinical neurology and psychiatry rely on trials and cohort studies whose outcomes are often symptom scales. Check the species, the sample size, how the outcome was measured and whether results were replicated.
Evidence from open-access studies
These open-access studies come from PubMed’s best-match results for this heading (papers whose main topic it is), ranked here by citation count, with one recent addition. Each abstract is reproduced in full under its recorded open licence so that you can read the authors’ own words. They illustrate the literature; they are not a systematic summary of it. Citation counts measure attention, not reliability or clinical benefit.
| Study / authors | Year | Source label / design | Europe PMC citations | Licence / source |
|---|---|---|---|---|
| Translational control in the spinal cord regulates gene expression and pain hypersensitivity in the chronic phase of neuropathic pain | 2026 | Research article Design not recorded in structured metadata | 9 | cc by PMID 41960785 · DOI · PMC13068433 |
| Integrative Proteomics Reveal Neuroimmune and Dopaminergic Alterations Across the Nociceptive Neuraxis in Neuropathic Pain | 2026 | Research article Design not recorded in structured metadata | 8 | cc by PMID 41677653 · DOI · PMC12896955 |
| MDFIC2 is a PIEZO channel modulator that can alleviate mechanical allodynia associated with neuropathic pain | 2025 | Research article Design not recorded in structured metadata | 7 | cc by PMID 41201821 · DOI · PMC12626003 |
Translational control in the spinal cord regulates gene expression and pain hypersensitivity in the chronic phase of neuropathic pain [1]
Abstract reading summary — source excerpts
- Opening excerpt
- Sensitization of spinal nociceptive circuits plays a crucial role in neuropathic pain.
- Closing excerpt
- Together, these findings advance our understanding of translational control mechanisms in the spinal cord during neuropathic pain and highlight their cell type- and phase-specific contributions to gene expression and pain hypersensitivity.
- Interpretation limits
- Verbatim excerpts from the authors’ abstract; the closing excerpt may describe a finding, limitation or recommendation. Design, population, effect size and uncertainty have not been independently extracted or appraised. Read the complete abstract and linked paper before interpreting the findings.
Read complete abstract (193 words)
Sensitization of spinal nociceptive circuits plays a crucial role in neuropathic pain. This sensitization depends on new gene expression that is primarily regulated via transcriptional and translational control mechanisms. The relative roles of these mechanisms in regulating gene expression in the clinically relevant chronic phase of neuropathic pain are not well understood. Here, we show that, in mice, changes in gene expression in the spinal cord during the chronic phase of neuropathic pain are substantially regulated at the translational level. Downregulating spinal translation at the chronic phase alleviated pain hypersensitivity. Cell type-specific profiling revealed that spinal inhibitory and excitatory neurons exhibited substantial changes in translation after peripheral nerve injury. Notably, increasing translation selectively in all inhibitory neurons or parvalbumin-positive (PV+) interneurons, but not excitatory neurons, promoted mechanical pain hypersensitivity. Furthermore, increasing translation in PV+ neurons decreased their intrinsic excitability and spiking activity. Conversely, reducing translation in spinal PV+ neurons prevented the nerve injury-induced decrease in excitability but did not alleviate mechanical hypersensitivity. Together, these findings advance our understanding of translational control mechanisms in the spinal cord during neuropathic pain and highlight their cell type- and phase-specific contributions to gene expression and pain hypersensitivity.
Abstract reproduced from the open-access article under the recorded cc by licence; © the authors. PMID 41960785 · DOI · PMC13068433
Integrative Proteomics Reveal Neuroimmune and Dopaminergic Alterations Across the Nociceptive Neuraxis in Neuropathic Pain [2]
Abstract reading summary — source excerpts
- Opening excerpt
- Neuropathic pain (NP) arises from maladaptive changes in peripheral and central nociceptive circuits, yet molecular alterations spanning the entire pain neuraxis remain poorly understood.
- Closing excerpt
- This integrative molecular map highlights potential therapeutic targets, including glial-derived S100 proteins and dopamine modulators for the comprehensive management of NP.
- Interpretation limits
- Verbatim excerpts from the authors’ abstract; the closing excerpt may describe a finding, limitation or recommendation. Design, population, effect size and uncertainty have not been independently extracted or appraised. Read the complete abstract and linked paper before interpreting the findings.
Read complete abstract (221 words)
Neuropathic pain (NP) arises from maladaptive changes in peripheral and central nociceptive circuits, yet molecular alterations spanning the entire pain neuraxis remain poorly understood. Neuroinflammation is increasingly recognized as a central mechanism in NP chronification, yet the region-specific molecular events linking immune activation to affective pain processing remain inadequately defined. In this study, we employed high-resolution LC-HRMS-based quantitative proteomics to investigate chronic constriction injury (CCI)-induced molecular alterations in the sciatic nerve (SN), spinal cord (SC), and orbitofrontal cortex (OFC) of male Wistar rats, a region critical for affective and cognitive pain modulation. Behavioral assessments confirmed the development of NP phenotypes and motor deficits. Proteomic profiling revealed exclusive and differentially expressed proteins enriched in neuroinflammatory pathways across all regions. S100 proteins (S100A8 and S100B) were significantly elevated in SN, SC, and OFC, as confirmed by immunofluorescence. Their up-regulation coincided with increased astrocyte (GFAP) and microglial (Iba-1) activation, highlighting a pervasive inflammatory milieu. Intriguingly, the OFC proteome demonstrated marked up-regulation of dopamine-regulating proteins and positive regulation of dopaminergic neurotransmission, suggesting involvement of reward-related analgesic circuits. Together, our findings delineate a "nociceptive neuraxis" driven by neuroimmune activation and neuromodulatory adaptations that interfaces with dopaminergic signaling to influence sensory and affective components of pain. This integrative molecular map highlights potential therapeutic targets, including glial-derived S100 proteins and dopamine modulators for the comprehensive management of NP.
Abstract reproduced from the open-access article under the recorded cc by licence; © the authors. PMID 41677653 · DOI · PMC12896955
MDFIC2 is a PIEZO channel modulator that can alleviate mechanical allodynia associated with neuropathic pain [3]
Abstract reading summary — source excerpts
- Opening excerpt
- PIEZO channels are mechanical force sensors involved in various biological processes, including somatosensation.
- Closing excerpt
- These findings demonstrate a mechanism for regulating mechanosensation and highlight a potential therapeutic route for treating mechanical allodynia.
- Interpretation limits
- Verbatim excerpts from the authors’ abstract; the closing excerpt may describe a finding, limitation or recommendation. Design, population, effect size and uncertainty have not been independently extracted or appraised. Read the complete abstract and linked paper before interpreting the findings.
Read complete abstract (137 words)
PIEZO channels are mechanical force sensors involved in various biological processes, including somatosensation. To date, only a few PIEZO-binding partners have been identified, including MyoD-family inhibitor proteins (MDFI and MDFIC). Here, we show that MDFIC2, a third member of the MDFI protein family with an as-yet-unknown function, is expressed in a subset of nociceptive sensory neurons. MDFIC2 modulates both PIEZO1 and PIEZO2 gating properties by slowing their kinetics and shifting mechanical sensitivity to higher forces. Interestingly, Mdfic2 is downregulated in mouse neuropathic pain models in which mechanical allodynia is a hallmark symptom. We found that intrathecal administration of adeno-associated virus vector encoding MDFIC2 cDNA reduces mechanical sensitivity and attenuates mechanical allodynia in the spared nerve injury neuropathic pain model. These findings demonstrate a mechanism for regulating mechanosensation and highlight a potential therapeutic route for treating mechanical allodynia.
Abstract reproduced from the open-access article under the recorded cc by licence; © the authors. PMID 41201821 · DOI · PMC12626003
Key reviews and meta-analyses
The most cited review-type papers among PubMed’s best-match results for this heading, listed with bibliographic details only. Follow the links for the full text and access terms.
- Research article Pharmacotherapy for neuropathic pain in adults: a systematic review and meta-analysis [4]
- Research article Prevalence of chronic pain in the UK: a systematic review and meta-analysis of population studies [5]
- Research article A systematic review of antidepressants in neuropathic pain [6]
- Research article Neuropathic pain prevalence following spinal cord injury: A systematic review and meta-analysis [7]
- Research article Cannabis-based medicines for chronic neuropathic pain in adults [8]
- Research article Duloxetine for treating painful neuropathy, chronic pain or fibromyalgia [9]
References
- Lister KC, Wong C, Uttam S, Parisien M, Stecum P, Brown N, et al.. Translational control in the spinal cord regulates gene expression and pain hypersensitivity in the chronic phase of neuropathic pain. . 2026. PMID 41960785 · DOI · PMC13068433
- Majumdar S, Prajapati SK, Dande A, Yata VK, Choudhary K, Peraman R, et al.. Integrative Proteomics Reveal Neuroimmune and Dopaminergic Alterations Across the Nociceptive Neuraxis in Neuropathic Pain. . 2026. PMID 41677653 · DOI · PMC12896955
- Habib AM, Li S, Zhang C, Ji M, Osorio N, Penalba V, et al.. MDFIC2 is a PIEZO channel modulator that can alleviate mechanical allodynia associated with neuropathic pain. . 2025. PMID 41201821 · DOI · PMC12626003
- Finnerup NB, Attal N, Haroutounian S, McNicol E, Baron R, Dworkin RH, et al.. Pharmacotherapy for neuropathic pain in adults: a systematic review and meta-analysis. Lancet Neurol. 2015. PMID 25575710 · DOI · PMC4493167
- Fayaz A, Croft P, Langford RM, Donaldson LJ, Jones GT. Prevalence of chronic pain in the UK: a systematic review and meta-analysis of population studies. BMJ Open. 2016. PMID 27324708 · DOI · PMC4932255
- McQuay HJ, Tramèr M, Nye BA, Carroll D, Wiffen PJ, Moore RA. A systematic review of antidepressants in neuropathic pain. Pain. 1996. PMID 9121808 · DOI
- Burke D, Fullen BM, Stokes D, Lennon O. Neuropathic pain prevalence following spinal cord injury: A systematic review and meta-analysis. Eur J Pain. 2017. PMID 27341614 · DOI
- Mücke M, Phillips T, Radbruch L, Petzke F, Häuser W. Cannabis-based medicines for chronic neuropathic pain in adults. Cochrane Database Syst Rev. 2018. PMID 29513392 · DOI · PMC6494210
- Lunn MP, Hughes RA, Wiffen PJ. Duloxetine for treating painful neuropathy, chronic pain or fibromyalgia. Cochrane Database Syst Rev. 2014. PMID 24385423 · DOI · PMC10711341
About this article
- Sources
- NLM Medical Subject Headings (definition, synonyms); NCBI PubMed (counts, identifiers); Europe PMC (open-access abstracts and citation counts).
- Verification
- Every reference was resolved against PubMed on 2026-10-31; title, year and DOI matched.
- Review state
- automated source verified; no human expert review has been recorded yet.
- Version
- 1, last updated 2026-10-29.
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Evidence strength
EvidenceHelix's computed view of the study designs behind this topic: how common meta-analyses, randomized trials and reviews are, how recent the literature is, and a plain-language reading. It describes the design mix of the literature. It is not a quality appraisal of any study, and it is not medical advice.