ArticleBrain, behavior, & immunity - health2025
How does chronic psychosocial distress induce pain? Focus on neuroinflammation and neuroplasticity changes.
Article in Brain, behavior, & immunity - health, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 7 papers.
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Who cites it
7 citing papers in PubMed.
- Meditations on Methodological Issues in Clinical Investigations of "Central Sensitization" (Jonah XII).Journal of clinical medicine · 2026Article
- Article
- A systematic scoping review and conceptual analysis of new-onset fibromyalgia manifestations after non-hospitalized COVID-19: empirics, definitions, methodologies, pathophysiology, mapping of literature, and knowledge gaps.Journal of translational medicine · 2026Article
- Effects of Physical Exercise on Anxiety and Depression of People with Fibromyalgia: Umbrella Review of Systematic Reviews and Meta-Analyses.Journal of functional morphology and kinesiology · 2026Review
- Editorial on the special issue "Emerging PNI research: future leaders in focus - second edition".Brain, behavior, & immunity - health · 2026Article
- Microglial CX3CR1 signaling mediates stress-induced pain behavior in mice.Frontiers in immunology · 2026Article
- Dry Eye Disease and Psychiatric Disorders: Neuroimmune Mechanisms and Therapeutic Perspectives.International journal of molecular sciences · 2025Review
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Authors and funding
3 authors.
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Abstract
Chronic primary pain including fibromyalgia for the musculoskeletal system persists for more than 3 months. Its etiological factors and the pathophysiological mechanisms are not known, and therefore, there is no satisfactory therapy, it is an unmet medical need condition. The only etiological and aggravating factor is chronic psychosocial distress, which is known to cause neuroimmune and endocrine changes both in the periphery and the central nervous system. In this short review, we introduce our research perspective by summarizing the recent literature on the interactions between chronic pain, stress, and commonly co-morbid mood disorders. Immune activation, autoimmunity, neuro-immune-vascular crosstalks and neuroinflammation play roles in the pathophysiology of these conditions. Data on stress-induced neuroplasticity changes at cellular and molecular levels were also collected in relation to chronic primary pain both from clinical studies and animal experiments of translational relevance. Understanding these mechanisms could help to identify novel therapeutic targets for chronic primary pain including fibromyalgia.
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