An Overview of the Mechanisms Involved in Neuralgia

Abstract

Neuralgia is a frequently occurring condition that causes chronic pain and burdens both patients and their families. Earlier research indicated that anti-inflammatory treatment, which was primarily utilized to address conditions like neuralgia, resulted in positive outcomes. However, recent years have witnessed the emergence of various novel mechanisms associated with pain-related disorders. This review provides a concise overview of the inflammatory mechanisms involved in neuralgia. It also examines recent advancements in research, exploring the influence of ion channels and synaptic proteins on neuralgia and its complications. Additionally, the interactions between these mechanisms are discussed with the aim of suggesting innovative therapeutic approaches and research directions for the management of neuralgia.

Keywords:

• neuralgia
• inflammatory mechanisms
• innovative therapeutic approaches

Abbreviations

IASP, The International Association for the Study of Pain; NP, neuropathic pain; CX3CL1, chemokine C-X3-C motif ligand 1; CSF1R, colony stimulating factor 1 receptor; IL-34, interleukin-34; TGF-β1, transforming growth factor β1; TLR4, Toll- like receptor 4; TREM2, triggering receptor expressed on myeloid cells 2; IRF8, interferon regulator factor 8; BDNF, brain-derived neurotrophic factor; SNI, sciatic nerve injury; CCI, chronic constrictive injury; DRG, dorsal root ganglion; VGSCs, voltage gated sodium channels; NAc, nucleus accumbens; Nmb, neuromedin B; TET1, ten-eleven translocation methylcytosine dioxygenase 1; Kv, voltage-gated potassium channel; MSNs, medium spiny neurons; CRMP2, collapsin response mediator protein 2; LTP, long-term potentiation; LTD, long-term depression; RTX, resiniferatoxin; NALCN, sodium leak channel; PNI, peripheral nerves injuries; LIFU, Low-intensity focused ultrasound; CaMKIV, calmodulin-dependent protein kinase IV.

Disclosure

The authors report no conflicts of interest in this work.