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Quick Look
Does central sensitization adequately explain most symptoms of fibromyalgia?
Science: Many symptoms cannot be explained as a consequence of central sensitization.
Conclusion: Central sensitization occurs in fibromyalgia, but although it exacerbates certain symptoms, it is not a primary cause of fibromyalgia.
Fibromyalgia results from a dysfunction of the immune system.
Immune Cells
The authors of the study briefly summarized below (full text version here) begin by mentioning the theory of central sensitization, noting both its significance, as well as its inability to account for many of the common symptoms of fibromyalgia. Specifically, “mood disorders, fatigue, specific sleep disturbances, stiffness and post-exertional pain cannot be fully explained by the abnormalities of central pain processing.”
It is noted that fibromyalgia shares many symptoms with ‘sickness syndrome’, including lethargy, fatigue, somnolence, and mood disorders (primarily depression,) and that in sickness syndrome these symptoms are generally believed to result from activation of the immune system. Specifically, many symptoms of sickness syndrome are believed to result from excess production of pro-inflammatory cytokines, and perhaps the activation of glial cells by those cytokines.
While it is true that fibromyalgia is not generally considered to be an inflammatory disorder, the authors suggest several reasons why fibromyalgia might be considered to result from an inflammatory process. Persistent elevation of several pro-inflammatory cytokines has been reported in fibromyalgia, and may account for much pain production.
While the publication referenced primarily concerns the role of growth hormone (or the lack thereof) as an exacerbating factor, it also presents significant evidence supporting a role for inflammation in the symptoms of fibromyalgia, and that the condition may result from a fundamental (if unknown) dysfunction of the immune system.
2010
Preliminary Evidence of Increased Pain and Elevated Cytokines in Fibromyalgia Patients with Defective Growth Hormone Response to Exercise.
Summary of the Abstract
There is mounting evidence that fibromyalgia symptoms are influenced by dysfunction of the hypothalamic-pituitary-hormonal axes – the “HPHA” – and the immune response system (also known as the inflammatory response system.)
The predominant fibromyalgia symptoms of pain, fatigue, sleep disturbance, depression, stiffness and exercise intolerance may be related to ‘sickness behavior’ – a syndrome that results from an excess of pro-inflammatory cytokines that are produced in response to stress.
It is hypothesized that serum levels of pro-inflammatory cytokines and fibromyalgia symptom severity will be higher in those patients who, upon exercising, exhibit a diminished growth hormone response. Growth hormone dysfunction was found to be associated with increased pain, more tender points, and higher levels of pro-inflammatory cytokines prior to exercise, including IL-1, IL-6, and IL-8.
These results suggest that a defective growth hormone response to exercise may be associated with increased levels of blood cytokines and greater pain in certain fibromyalgia patients.
With all due respect, most of the ‘objective’ measures of fibromyalgia are found in post traumatic stress disorder, bipolar, major depressive, and other psych patients. This is not to belittle the condition as a psych diagnosis, but to emphasize that the rationale of depending on such artificial measures as ‘proof’ of fibromyalgia as a disease is fallacious. Fibro is a condition, like hypertension, that has genetic risk factors to produce a condition that can be managed, but not cured. This is not a disease to be eradicated, since it would be disrupting the genetic code of the sufferers. Please, stop using ‘immune changes’ and such nonsense as proof in this condition.