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Brain Sciences
Special Issues
Advances in Neuroinflammation and Pain Medicine
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Advances in Neuroinflammation and Pain Medicine

A special issue of Brain Sciences (ISSN 2076-3425). This special issue belongs to the section "Sensory and Motor Neuroscience".

Deadline for manuscript submissions: closed (31 January 2025) | Viewed by 6407

Special Issue Editors

Dr. Giovane S. Galdino

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Guest Editor
Pain Neuroimmunobiology Laboratory, Institute of Motricity Sciences, Federal University of Alfenas, Alfenas 37130-001, MG, Brazil
Interests: pain; analgesia; neuroinflammation; neuroimmune response; glial cells; pharmacology; physiology
Special Issues, Collections and Topics in MDPI journals
Dr. Tayllon dos Anjos-Garcia

E-Mail Website
Guest Editor
Multicenter Graduate Program in Physiological Sciences, Institute of Biomedical Sciences - PPGMCF-ICB), Federal University of Alfenas, Alfenas 37130-001, MG, Brazil
Interests: pain; endocannabinoid signaling; fear-related disorders; neural circuits

Special Issue Information

Dear Colleagues,

Recently, science has demonstrated that a specific relationship exists between the immune system and the development of pain. In this context, studies involving the investigation of neuroinflammation have been of great interest to pain medicine, both for unveiling new mechanisms of action and the development of treatment strategies.

Present in the scientific literature are articles elucidating mechanisms involved in the neuroinflammatory responses to different types of pain, as well as treatment strategies for controlling these mechanisms and, consequently, the associated pain.

We are focusing on devising strategies that allow scientific innovation, mainly through new tools, technologies, and studies that help us to uncover mechanisms involved in neuroinflammation and pain medicine.

Authors are invited to submit relevant original research articles, as well as reviews and systematic review articles.

Dr. Giovane S. Galdino
Dr. Tayllon dos Anjos-Garcia
Guest Editors

Manuscript Submission Information

Manuscripts should be submitted online at www.mdpi.com by registering and logging in to this website. Once you are registered, click here to go to the submission form. Manuscripts can be submitted until the deadline. All submissions that pass pre-check are peer-reviewed. Accepted papers will be published continuously in the journal (as soon as accepted) and will be listed together on the special issue website. Research articles, review articles as well as short communications are invited. For planned papers, a title and short abstract (about 100 words) can be sent to the Editorial Office for announcement on this website.

Submitted manuscripts should not have been published previously, nor be under consideration for publication elsewhere (except conference proceedings papers). All manuscripts are thoroughly refereed through a single-blind peer-review process. A guide for authors and other relevant information for submission of manuscripts is available on the Instructions for Authors page. Brain Sciences is an international peer-reviewed open access monthly journal published by MDPI.

Please visit the Instructions for Authors page before submitting a manuscript. The Article Processing Charge (APC) for publication in this open access journal is 2200 CHF (Swiss Francs). Submitted papers should be well formatted and use good English. Authors may use MDPI's English editing service prior to publication or during author revisions.

Keywords

  • pain medicine
  • neuroinflammation
  • immune system
  • nociception
  • pain treatment
  • analgesia

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Further information on MDPI's Special Issue policies can be found here.

Published Papers (3 papers)

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Review

40 pages, 5811 KiB  
Review
Metabolic Dysfunction and Dietary Interventions in Migraine Management: The Role of Insulin Resistance and Neuroinflammation—A Narrative and Scoping Review
by Cinzia Cavestro
Brain Sci. 2025, 15(5), 474; https://doi.org/10.3390/brainsci15050474 - 29 Apr 2025
Abstract
Introduction: Migraine is a prevalent neurological disorder characterized by recurrent headaches with autonomic and neurological symptoms, significantly impacting quality of life globally. Its pathogenesis involves genetic, neurological, inflammatory, and metabolic factors, with insulin resistance and metabolic dysfunction increasingly recognized as important contributors. Historically, [...] Read more.
Introduction: Migraine is a prevalent neurological disorder characterized by recurrent headaches with autonomic and neurological symptoms, significantly impacting quality of life globally. Its pathogenesis involves genetic, neurological, inflammatory, and metabolic factors, with insulin resistance and metabolic dysfunction increasingly recognized as important contributors. Historically, it has been known that certain foods can trigger migraine attacks, which led for many years to the recommendation of elimination diets—now understood to primarily target histamine-rich foods. Over the past two decades, attention has shifted toward underlying metabolic disturbances, leading to the development of dietary approaches specifically aimed at addressing these dysfunctions. Methods: A scoping literature review was conducted using PubMed and Embase to evaluate the relationships among migraine, insulin-related mechanisms, neurogenic inflammation, and dietary interventions. Initial searches focused on “MIGRAINE AND (neurogenic inflammation)” (2019–15 April 2025), followed by expanded searches from 1950 onward using terms such as “MIGRAINE AND (insulin, insulin resistance, hyperinsulinism)”, and “MIGRAINE AND (diet, dietary, nutrition, nutritional)”. A specific search also targeted “(INSULIN OR insulin resistance OR hyperinsulinism) AND (neurogenic inflammation)”. Abstracts were screened, full texts were retrieved, and duplicates or irrelevant publications were excluded. No filters were applied by article type or language. Systematic reviews and meta-analyses were prioritized when available. Results: Migraine pathogenesis involves trigeminovascular system activation, neurogenic inflammation mediated by CGRP and PACAP, immune dysregulation, mast cell activation, and cortical spreading depression (CSD). Emerging evidence highlights significant associations between migraine, insulin resistance, and hyperinsulinism. Hyperinsulinism contributes to migraine through TRPV1 sensitization, increased CGRP release, oxidative stress, mitochondrial dysfunction, and systemic inflammation. Metabolic dysfunction, including obesity and insulin resistance, exacerbates migraine severity and frequency. Dietary interventions, particularly anti-inflammatory, Mediterranean, and ketogenic diets, show promise in reducing migraine frequency and severity through mechanisms involving reduced inflammation, oxidative stress, improved mitochondrial function, and glucose metabolism stabilization. Conclusions: The interplay between insulin resistance, metabolic dysfunction, and neuroinflammation is crucial in migraine pathophysiology. Targeted dietary interventions, including ketogenic and Mediterranean diets, demonstrate significant potential in managing migraines, emphasizing the need for personalized nutritional strategies to optimize therapeutic outcomes. Full article
(This article belongs to the Special Issue Advances in Neuroinflammation and Pain Medicine)
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Graphical abstract

18 pages, 1124 KiB  
Review
Neuroinflammatory and Immunological Aspects of Fibromyalgia
by Kate Findeisen, Emma Guymer and Geoffrey Littlejohn
Brain Sci. 2025, 15(2), 206; https://doi.org/10.3390/brainsci15020206 - 17 Feb 2025
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Abstract
Fibromyalgia is a common, high-impact condition of chronic widespread pain and sensory dysfunction associated with altered central and peripheral sensory processing. A growing body of evidence supports the role of neuroinflammation and immune changes in fibromyalgia, and a narrative review of this literature [...] Read more.
Fibromyalgia is a common, high-impact condition of chronic widespread pain and sensory dysfunction associated with altered central and peripheral sensory processing. A growing body of evidence supports the role of neuroinflammation and immune changes in fibromyalgia, and a narrative review of this literature was undertaken. Published data suggest that the interactions between the neural pain networks and the immune system in fibromyalgia appear to be bidirectional and operate both centrally and peripherally. There is a growing focus on processes occurring in the dorsal root ganglia and the role of maladaptive microglial cell activation. Ongoing insight into neuroinflammatory mechanisms in fibromyalgia opens potential avenues for the development of mechanism-based therapies in what is, at present, a challenging-to-manage condition. Full article
(This article belongs to the Special Issue Advances in Neuroinflammation and Pain Medicine)
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14 pages, 3834 KiB  
Review
The Role of the Thalamus in Nociception: Important but Forgotten
by Giovane Galdino, Flavio Protasio Veras and Tayllon dos Anjos-Garcia
Brain Sci. 2024, 14(8), 741; https://doi.org/10.3390/brainsci14080741 - 25 Jul 2024
Cited by 1 | Viewed by 3295
Abstract
Pain is a complex response to noxious stimuli. Upon detection of the nociceptive stimulus by first-order neurons or nociceptors, an action potential ascends to the spinal dorsal horn, a crucial site for synapsing with second-order neurons. These second-order neurons carry the nociceptive stimulus [...] Read more.
Pain is a complex response to noxious stimuli. Upon detection of the nociceptive stimulus by first-order neurons or nociceptors, an action potential ascends to the spinal dorsal horn, a crucial site for synapsing with second-order neurons. These second-order neurons carry the nociceptive stimulus to supraspinal regions, notably the thalamus. Although extensive research has focused on spinal-level nociceptive mechanisms (e.g., neurotransmitters, receptors, and glial cells), the thalamus is still poorly elucidated. The role of the thalamus in relaying sensory and motor responses to the cortex is well known. However, a comprehensive understanding of the mechanisms in the synapse between the second-order and third-order neurons that transmit this impulse to the somatosensory cortex, where the response is processed and interpreted as pain, is still lacking. Thus, this review investigated the thalamus’s role in transmitting nociceptive impulses. Current evidence indicates the involvement of the neurotransmitters glutamate and serotonin, along with NMDA, P2X4, TLR4, FGR, and NLRP3 receptors, as well as signaling pathways including ERK, P38, NF-κB, cytokines, and glial cells at nociceptive synapses within the thalamus. Full article
(This article belongs to the Special Issue Advances in Neuroinflammation and Pain Medicine)
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