A recent paper published under the auspices of the Royal College of Physicians aims to provide “succinct, relevant information for patients and clinicians about FMS (fibromyalgia syndrome) and its diagnosis” [Berwick et al. 2022]. But although the clinical features of FMS are well described, the paper only contains a single sentence that mentions causation:
“Although the aetiology is still abstruse, advances in research have shown that alterations in pain processing within the nervous system are likely causative.” (p.570)
But because pain is an experience (i.e. an abstraction) and not a “thing” that can be processed, this sentence is not illuminating. But all may not be lost!
A research project led by the Institute of Psychiatry, Psychology & Neuroscience at King’s College London, in collaboration with the University of Liverpool and the Karolinska Institute in Stockholm, provides evidence that autoimmune processes might be responsible for at least some of the clinical features of the condition [Goebel et al. 2021].
Mice were injected with antibodies in serum obtained from people with FMS. As a result, they rapidly developed an increased sensitivity to mechanical pressure and cold and reduced muscle strength and mobility. In addition, nerve fibres supplying their skin were reduced in number.
In contrast, mice injected with antibodies from healthy people were unaffected. The results suggest that patient antibodies cause or at least are a major contributor to the condition. After a few weeks, antibodies had been cleared from their system, and the mice recovered.
Dr Andreas Goebel, the study’s principal investigator, believes “the results offer amazing hope that the invisible, devastating symptoms of fibromyalgia will become treatable.”
Professor Camilla Svensson, the study’s primary investigator from Karolinska Institute said, “Antibodies from people with FMS living in two different countries, the UK and Sweden, gave similar results, which adds enormous strength to our findings.”
Antibodies obtained from patients with FMS accumulate in macrophages (large phagocytic* cells) within the dorsal root ganglia** (DRG) of the mice. Such antibodies can also activate other cells (known as satellite glial cells) that are closely applied to the dorsal nerve roots. These types of cell can release powerful chemicals that excite nearby nervous tissues within the DRG. Such excitation results in the person experiencing pain [Hanani & Spray 2020].
Furthermore, Albrecht et al.  have shown evidence of positron emission tomography (PET) of activation of glial cells occurring within the nervous system of patients with fibromyalgia.
Taken together, the findings provide support for an underlying complex autoimmune aetiology in patients with FMS.
The next step in the research will be identifying the cells to which the symptom-inducing antibodies bind. This may be helpful in developing novel treatment strategies for FMS and devising much-needed blood-based tests for diagnosis.
By John Quintner, Physician in Pain Medicine & Rheumatology (retired)
*Phagocytes are capable of engulfing and absorbing bacteria and other small cells and particles.
**A cluster of neurons in a dorsal root of a spinal nerve.
Albrecht DS, Fosberg A, Sandstrom A, et al. Brain-glial activation in fibromyalgia – a multi-site positron emission tomography investigation. Brain Behav Immun 2019;75:72-83. doi: 10.1016/j.bbi.2018.09.018.
Berwick R, Barker C, Goebel A. The diagnosis of fibromyalgia syndrome. Clin Med 2022;22(6):570-574. doi: 10.7861/clinmed.2022-0402.
Goebel A, Krok E, Gentry C, et al. Passive transfer of fibromyalgia symptoms from patients to mice. J Clin Invest 2021;131(13):e144201. doi: 10.1172/JCI201.
Hanani M, Spray DC. Emerging importance of satellite glia in nervous system function and dysfunction. Nature Reviews Neuroscience 2020;21:485-498. doi: 10.1038/s41583-020-0333-z.
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