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Disease

Neuralgia

Late-stage therapeutic developmentEmerging researchRising momentum
17
Publications
20
Clinical trials
6
Related conditions
1
Related treatments
3
Related proteins
2025
Latest publication
Latest activity
beta

Recent clinical, regulatory, research and industry developments relating to this disease.

Disease applications of spinal cord stimulation: Chronic nonmalignant pain.

Research2024-01-05Neurotherapeutics : the journal of the American Society for Experimental NeuroTherapeutics

Central neuropathic pain.

Research2023-12-21Nature reviews. Disease primers

mGluR5 from Primary Sensory Neurons Promotes Opioid-Induced Hyperalgesia and Tolerance by Interacting with and Potentiating Synaptic NMDA Receptors.

Research2023-07-14The Journal of neuroscience : the official journal of the Society for Neuroscience

Partial peripheral nerve injury promotes a selective loss of GABAergic inhibition in the superficial dorsal horn of the spinal cord.

Research2002-08-01The Journal of neuroscience : the official journal of the Society for Neuroscience

What's happening now

An analyst briefing on current research, clinical, regulatory and industry activity surrounding this disease.

Clinical Milestones7View
Activity timeline7

Research-associated treatments

Drugs and agents co-studied with this disease across the research literature — associative, not necessarily established treatments. Number shows shared papers.

Clinical trials

18 sponsors · 1 new · 1 completed in the last 12 months (net +1)

The current development programme across all trial phases.

Clinical programme
20
All trials
6
Active
17
Late-stage
6
Completed
Late-stage studies
Recruiting
Recently completed

Research activity

17 papers

Key research shaping understanding of this disease, combining the latest publications with the most influential evidence.

Publications over time
20022025
Most influential

Prevention and management of chemotherapy-induced peripheral neuropathy in survivors of adult cancers: American Society of Clinical Oncology clinical practice guideline.

Journal of clinical oncology : official journal of the American Society of Clinical Oncology · 2014 · 831 cites

Partial peripheral nerve injury promotes a selective loss of GABAergic inhibition in the superficial dorsal horn of the spinal cord.

The Journal of neuroscience : the official journal of the Society for Neuroscience · 2002 · 592 cites

Neuropathic Pain: Mechanism-Based Therapeutics.

Annual review of pharmacology and toxicology · 2020 · 208 cites
Recent publications
Major themes8
  • Neuralgia8
  • Chronic Pain4
  • Amygdala1
  • Anxiety1
  • Astrocytes1
  • Dipeptidyl-Peptidase IV Inhibitors1
  • gamma-Aminobutyric Acid1
  • Glucagon-Like Peptide-1 Receptor Agonists1
Leading journals6
  • Mediators of inflammation2
  • The Journal of neuroscience : the official journal of the Society for Neuroscience2
  • ACS nano1
  • Anesthesiology1
  • Annual review of pharmacology and toxicology1
  • Autophagy1
Leading researchers8
  • Liu S2
  • Ali U1
  • Attal N1
  • Baba H1
  • Bak K1
  • Bannister K1
  • Baron R1
  • Berman BM1
Affiliations (unnormalised)6
  • Aarhus University Hospital1
  • Baylor College of Medicine1
  • Brain Science Institute1
  • Cathay General Hospital1
  • Center for Cognition and Sociality1
  • Center for Neuroplasticity and Pain (CNAP)1

Disease biology

3 matches

Key proteins & gene products studied in this disease. Number shows shared papers.

Related conditions

6 matches

Diseases frequently studied alongside this one. Number shows shared papers.

Disease profile

A grounded synthesis of the condition — overview, causes, mechanism, risk factors and current standard of care.

Overview

Neuralgia is intense or aching pain that occurs along the course or distribution of a peripheral or cranial nerve. In the supplied literature, it is discussed within the broader category of neuropathic pain and peripheral neuropathic pain.

Causes

Neuralgia is associated in the literature with lesions or disease of the central or peripheral somatosensory nervous system. Reported sources of neuropathic pain include nerve compression, channelopathies, autoimmune disease, incision, and diabetic neuropathy as a frequent cause of peripheral neuropathic pain.

Pathophysiology

The literature describes neuralgia in terms of neuropathic pain mechanisms involving neuroinflammation, altered synaptic transmission, signal transduction, and neuronal plasticity. Cytokine dysregulation and microglial activation are linked to neuronal and glial injury, while TNF-alpha can increase excitatory signaling through NMDA receptors and reduce inhibitory GABA-A receptor activity, shifting the balance toward excitation.

Risk factors

Conditions that damage or disease the central or peripheral somatosensory nervous system increase risk. The grounding specifically identifies nerve compression, channelopathies, autoimmune disease, incision, and diabetic neuropathy as associated settings.

Current standard of care

Management is described at the level of mechanism-based and drug-therapy approaches for neuropathic pain, with emphasis on improving analgesia through better diagnostic classification. The supplied abstracts also support use of pharmacologic strategies targeting neuropathic pain mechanisms and nonpharmacologic approaches such as acupuncture-electroacupuncture in persistent pain, but they do not provide a single unified standard regimen for neuralgia.

AI-generated summary grounded in MeSH and 6 peer-reviewed sources. Informational only — not medical advice. Generated 2026-07-07.

Reference

Authoritative identity, definition & identifiers.

Defined in MeSH

Intense or aching pain that occurs along the course or distribution of a peripheral or cranial nerve.

Identifiers
References & data sources
  • Disease identity & definition — NLM Medical Subject Headings (MeSH), public domain
  • Clinical trials — ClinicalTrials.gov (U.S. National Library of Medicine)
  • Research activity — Europe PMC (EMBL-EBI) + OpenAlex-derived paper links
  • Related entities are derived from literature co-mention (studied together) — associative, not causal.