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Cited by 13Pain Management and TreatmentFibromyalgia and Chronic Fatigue Syndrome ResearchPain Mechanisms and Treatments

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Complex Regional Pain Syndrome Evolving to Full-Blown Fibromyalgia: A Proposal of Common Mechanisms

Martínez-Lavín, Manuel, Vargas, Angelica, Silveira, Luis H., Amezcua-Guerra, Luis M., Martínez-Martínez, Laura-Aline, Pineda, Carlos·2021·JCR: Journal of Clinical Rheumatology
DOI 10.1097/rhu.0000000000001304
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Abstract

Background: Spread of complex regional pain syndrome (CRPS) outside the affected limb is a well-recognized phenomenon; nevertheless, the actual evolution from CRPS to fibromyalgia is poorly documented. Similar mechanisms have been recently put forward to explain the development of CRPS and fibromyalgia including dorsal root ganglia (DRG) hyperexcitability and small fiber neuropathy. Objectives: The aims of this study were to describe 3 cases with typical CRPS evolving to full-blown fibromyalgia and to discuss the potential pathogenetic mechanisms linking these debilitating illnesses. Methods: This was a review of medical records and PubMed search on the relationship between CRPS-fibromyalgia with DRG and small nerve fiber neuropathy. Results: Our 3 cases displayed over time orderly evolution from CRPS to fibromyalgia. Dorsal root ganglion hyperexcitability and small fiber neuropathy have been recently demonstrated in CRPS and in fibromyalgia. Dorsal root ganglia contain the small nerve fiber cell bodies surrounded by glial cells. After trauma, DRG perineuronal glial cells produce diverse proinflammatory mediators. Macrophages, lymphocytes, and satellite glial cells may drive the immune response to more rostrally and caudally located DRG and other spinal cord sites. Dorsal root ganglion metabolic changes may lead to small nerve fiber degeneration. This mechanism may explain the development of widespread pain and autonomic dysfunction. Conclusions: Clinicians should be aware that CRPS can evolve to full-blown fibromyalgia. Spreading of neuroinflammation through DRG glial cell activation could theoretically explain the transformation from regional to generalized complex pain syndrome.

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Metadata

Authors
Martínez-Lavín, M., Vargas, A., Silveira, L. H., Amezcua-Guerra, L. M., Martínez-Martínez, L.-A., & Pineda, C.
Affiliations
  • Rheumatology Department, National Institute of Cardiology
  • Instituto Nacional de Cardiología (MX)
  • Instituto Nacional de Rehabilitación (MX)
Corresponding author
  • Silveira, Luis H.
  • Amezcua-Guerra, Luis M.
  • Martínez-Martínez, Laura-Aline
ORCID
Venue
JCR: Journal of Clinical Rheumatology
Publisher
Ovid Technologies (Wolters Kluwer Health)
Published
2020-02-06
Volume
27
Issue
6S
Pages
S274-S277
ISSN
  • 1076-1608 (ISSN-L)
  • 1536-7355
DOI
10.1097/rhu.0000000000001304
OpenAlex
W3005064316
Cited by
13
References
1
Citations by year
2026: 1 · 2025: 1 · 2024: 2 · 2023: 3 · 2022: 2 · 2021: 2 · 2020: 2
FWCI
2.64
Type
journal article
Language
en
Open access
closed
Locations
  • JCR Journal of Clinical Rheumatology (publishedVersion)
  • PubMed (publishedVersion)
Topics
  • Health Sciences › Medicine › Anesthesiology and Pain Medicine › Pain Management and Treatment
  • Health Sciences › Medicine › Psychiatry and Mental health › Fibromyalgia and Chronic Fatigue Syndrome Research
  • Health Sciences › Medicine › Physiology (medical) › Pain Mechanisms and Treatments
Keywords
complex regional pain syndrome, fibromyalgia, small fiber neuropathy, satellite glial cells, neuroinflammation, widespread pain, autonomic dysfunction, pro-inflammatory mediators
MeSH terms
Fibromyalgia, Ganglia, Spinal, Humans, Pain, Complex Regional Pain Syndromes, Pain Management

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