ReviewFrontiers in molecular neuroscience2025
Environmental enrichment for neuropathic pain via modulation of neuroinflammation.
Review in Frontiers in molecular neuroscience, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 2 papers.
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Who cites it
2 citing papers in PubMed.
- Melatonin Mitigates Central Sensitization and Nociplastic Pain in Spinal Cord and Dorsal Root Ganglia of FM Rat Model: Modulation of SIRT1/PGC-1α/MAPK/NF-κB Signaling.Journal of neuroimmune pharmacology : the official journal of the Society on NeuroImmune Pharmacology · 2026Article
- Targeted muscle reinnervation attenuates neuropathic pain and neuroma development in a rat model of tibial nerve transection.Frontiers in bioengineering and biotechnology · 2026Article
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Authors and funding
3 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Neuropathic pain causes tremendous biological and psychological suffering to patients worldwide. Environmental enrichment (EE) is a promising non-pharmacological strategy with high cost-effectiveness to reduce neuropathic pain and support rehabilitation therapy. Three researchers reviewed previous studies to determine the efficacy of EE for neuropathic pain to research how EE improves neuropathic pain through neuroinflammation. For this review, Embase, PubMed, and Cochran were searched. Three authors did study selection and data extraction. Out of 74 papers, 7 studies met the inclusion criteria. In the chronic constriction injury rats with acute or chronic detrimental stimulation, the change of pain behavior was influenced by environmental settings like start time, and cage size. Besides, physical EE has a larger effect than socially EE in inflammatory pain. These articles suggest employing various EE to regulate the release of pain-causing substances and changes in ion channels in the peripheral and central nerves to improve neuropathic pain behavior and depression and anxiety conditions. The existing proof provides important knowledge for upcoming preclinical investigations and the practical use of EE in clinical pain treatment. This analysis aids in the advancement of improved approaches for managing chronic pain, with a focus on internal mechanisms for controlling pain.
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Registered trials
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