From the Journal of Body Work and Movement Therapies Volume 14, Issue 1, Pages 3-12 (January 2010) Fascia: A missing link in our understanding of the pathology of fibromyalgia Ginevra L. Liptanab Received 26 January 2009; received in revised form 7 August 2009; accepted 11 August 2009. Summary Significant evidence exists for central sensitization in fibromyalgia, however the cause of this process in fibromyalgia—and how it relates to other known abnormalities in fibromyalgia—remains unclear. Central sensitization occurs when persistent nociceptive input leads to increased excitability in the dorsal horn neurons of the spinal cord. In this hyperexcited state, spinal cord neurons produce an enhanced responsiveness to noxious stimulation, and even to formerly innocuous stimulation. No definite evidence of muscle pathology in fibromyalgia has been found. However, there is some evidence for dysfunction of the intramuscular connective tissue, or fascia, in fibromyalgia. This paper proposes that inflammation of the fascia is the source of peripheral nociceptive input that leads to central sensitization in fibromyalgia. The fascial dysfunction is proposed to be due to inadequate growth hormone production and HPA axis dysfunction in fibromyalgia. Fascia is richly innervated, and the major cell of the fascia, the fibroblast, has been shown to secrete pro-inflammatory cytokines, particularly IL-6, in response to strain. Recent biopsy studies using immuno-histochemical staining techniques have found increased levels of collagen and inflammatory mediators in the connective tissue surrounding the muscle cells in fibromyalgia patients. The inflammation of the fascia is similar to that described in conditions such as plantar fasciitis and lateral epicondylitis, and may be better described as a dysfunctional healing response. This may explain why NSAIDs and oral steroids have not been found effective in fibromyalgia. Inflammation and dysfunction of the fascia may lead to central sensitization in fibromyalgia. If this hypothesis is confirmed, it could significantly expand treatment options to include manual therapies directed at the fascia such as Rolfing and myofascial release, and direct further research on the peripheral pathology in fibromyalgia to the fascia. Keywords: Central sensitization, Myofascial release, Manual therapy, Inflammation, Connective tissue, Growth hormone a Dept. of Medicine, Oregon Health & Science University, 3181 SW Sam Jackson Park Road, Portland, OR 97239, United States b Legacy Good Samaritan Pain Management Center, 1130 NW 22nd Ave, Suite 345, Portland, OR 97210, United States Legacy Good Samaritan Pain Management Center, 1130, NW 22nd Ave, Suite 345, Portland, OR 97210, United States. Tel.: +1 503 413 7513; fax: +1 503 413 7503. PII: S1360-8592(09)00094-1 doi:10.1016/j.jbmt.2009.08.003 Does anyone know if there is any studies on Facia inflammation and CFS? Could the inflammation in the facia provide evidence that fibromyalgia may be an autoimmune disease? Where there any biopsies of the facia in those Monkey studies? Could XMRV be hiding out in the facia?