Fibromyalgia, chronic fatigue syndrome, and myofascial pain.
Bennett, R · Current opinion in rheumatology · 1998 · DOI
Quick Summary
This review examines how fibromyalgia, chronic fatigue syndrome, and widespread pain are related conditions that share similar features. Researchers found that these conditions run in families, involve abnormal pain processing in the nervous system, and may share some underlying biological problems like growth hormone imbalances and low blood pressure. Several medications and treatments showed promise in reducing symptoms.
Why It Matters
This work demonstrates that fibromyalgia and ME/CFS share multiple biological abnormalities, suggesting they may lie on a disease spectrum rather than being entirely distinct conditions. Understanding these shared mechanisms is crucial for developing treatments that may benefit both populations and for recognizing that patients with overlapping symptoms need integrated diagnostic and therapeutic approaches.
Observed Findings
Chronic widespread pain is several times more prevalent than fibromyalgia diagnosed by 1990 ACR criteria.
Familial clustering of fibromyalgia has been documented, particularly in female relatives.
Neurally mediated hypotension and growth hormone-IGF-1 axis abnormalities occur in both fibromyalgia and chronic fatigue syndrome.
High prevalence of autoantibodies to cytoskeletal and nuclear envelope proteins found in chronic fatigue syndrome.
Ketamine and combined fluoxetine-amitriptyline showed benefit in fibromyalgia pain in experimental settings.
Inferred Conclusions
Fibromyalgia exists on a spectrum of chronic widespread pain disorders rather than as a discrete disease entity.
Abnormal sensory processing and central sensitization are integral mechanisms in fibromyalgia pathophysiology.
Fibromyalgia and ME/CFS share common pathophysiologic features including neuroendocrine and immune abnormalities.
Targeting NMDA receptors and combining specific medications may provide symptomatic benefit in fibromyalgia.
Remaining Questions
Is the familial clustering of fibromyalgia primarily genetic or environmental in origin?
What This Study Does Not Prove
This review does not prove causation for any of the described associations, nor does it establish whether familial clustering results from genetic or environmental factors. The article cannot determine whether shared biomarkers (like autoantibodies or hormone abnormalities) are causative, reactive, or incidental findings. Anecdotal associations mentioned (such as silicone implants) require prospective validation.
About the PEM badge: “PEM required” means post-exertional malaise was an explicit required diagnostic criterion for participant inclusion in this study — not that PEM was studied, observed, or discussed. Studies using criteria that do not require PEM (e.g. Fukuda, Oxford) are tagged “PEM not required”. How the atlas works →
What is the mechanistic relationship between autoantibodies found in ME/CFS and symptom severity?
What proportion of fibromyalgia cases result from identifiable triggers such as trauma, and why do outcomes differ geographically (100% return to work in Israel vs. lower rates in North America)?
Are the shared biomarkers between fibromyalgia and ME/CFS causative or secondary manifestations?