ArticlePain reports2025
Evidence for spinal disinhibition as a pain-generating mechanism in fibromyalgia syndrome.
Article in Pain reports, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 4 papers.
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Who cites it
4 citing papers in PubMed.
- Pain Mechanisms in Fibromyalgia: An Integrative Narrative Review of Central, Peripheral, Neuroimmune, and Psychobiological Factors.Biomedicines · 2026Review
- Human pain transcriptomics: lessons learned so far.Pain reports · 2026Review
- CRISPR-guided nanotherapy for rare central sensitization syndromes.Annals of medicine and surgery (2012) · 2025Article
- Integrating nociplastic pain into neuropathic pain framework: a proposal for a revised classification.Frontiers in pain research (Lausanne, Switzerland) · 2025Review
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Authors and funding
6 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Introduction: Pain phenomenology in patients with fibromyalgia syndrome (FMS) shows considerable overlap with neuropathic pain. Altered neural processing leading to symptoms of neuropathic pain can occur at the level of the spinal cord, and 1 potential mechanism is spinal disinhibition. A biomarker of spinal disinhibition is impaired H-reflex rate-dependent depression (HRDD). Objectives: This study investigated whether patients with FMS exhibit evidence of spinal disinhibition. Methods: Thirty-one individuals with FMS and 20 healthy volunteers underwent testing of Hoffman reflex including HRDD, along with assessment of clinical signs and symptoms, pressure pain thresholds, temporal summation of pain (wind-up), and conditioned pain modulation (CPM). Small nerve fibre structure was quantified using intraepidermal nerve fibre density and corneal confocal microscopy. Results: Patients with FMS had significantly impaired HRDD at 1 Hz ( Conclusion: We demonstrate for the first time that people with FMS show evidence of spinal disinhibition, which is most dominant in shorter duration of disease and may represent a putative mechanism of pain generation in FMS. Identifying people with impairment of central pain processing at an early stage may provide opportunities for targeted mechanistically directed interventions. Longitudinal studies are warranted to tease out the precise contribution of these mechanisms.
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