According to American College of Reumatology definition in 1990 (and the latest revision of 2010), fibromyalgia is a clinical, “chronic pain syndrome” mainly characterized by the presence of widespread and diffuse pain (as the core symptom), that is usually associated with fatigue (more than 90% of patients), morning stiffness, nonrestorative sleep (more than 75% of patients), cognitive dysfunction (fibrofog or brainfog, Glass, 2010), mood disorder (up to 75% of patients) and other somatic complains (IBS, muscular soreness, muscle cramps, Reynaud’s phenomenon, headaches etc). Currently, this syndrome is affecting between 2-4% of population (women 3,7%, Men 0,5%, Denmark 0,7%, Norwegian 10,5%) (McBeth J et al, 2007). There is strong comorbidity between FM and Chronic Fatigue Syndrome (CFS). These syndromes are considered separate but related disorders, sharing the fatigue (but also unrefreshing sleep, widespread muscle pain and weakness, sore throat, headaches etc) as a common symptom. Fatigue is also the most common symptom of fibromyalgia, second only to the muscle pain and diffuse body aches.
The cause of fibromyalgia is unknown, but some evidence exists about genetic predisposition, HPA and SAM axis dysfunction, DNIC dysfunction, hormonal imbalance etc. Psychoneurobiological dysfunctions are also discussed.
At the 1990’s, the original concept of fibromyalgia was entirely focused on the presence of pain and tender points at specific locations (18 points symmetrically located at both sites of the body). Tender points “were synonymous with fibromyalgia” (Mary-Ann Fitzcharles et al, 2013). Not anymore. American College of Rheumatology (2010) and Canadian Fibromyalgia Guidelines (2012) agreed that the presence of tender points is not of great value and fibromyalgia can be positively diagnosed as a “polysymptomatic distress syndrome” characterized of chronic widespread pain and associated symptoms. Today, due to lack of signs of peripheral inflammation (localize lesions, joint or tissue damage, muscle pathology), we are focus on pain-related and cognitive symptomatology.
Indeed, many researchers tried to investigate the central component of the disease using fMRI technology in order to localize and describe specific brain areas that are involved in processing of pain signals (Mercado et al, 2013). There are evidence that pain processing abnormalities could be a) due to specific defect in pain matrix (excitatory neurotransmitters, increase of NMDA, AMPA population), and b) close related to the dysfunction of descending opioid and non-opioid pain-inhibitory system (serotonine – norepinephrine – opioidergic pathway). Neuroimaging investigations have found a) abnormal activity within prefrontal and parietal regions (working memory, demanding tasks, control and execution), b) both morphological and functional brain anomalies related to widespread and diffuse pain (fronto-cingulated regions) and c) cognitive symptoms. Many of them support the idea that FM is a real “pain amplification syndrome” characterized of multiple changes into the brain.
Research on peripheral nervous system involvement was less advanced. But recently, a reduction in dermal unmyelinated nerve fibers bundles was found in skin samples of FM patients compared with patients with depression or health controls. This finding supports the hypothesis of impaired small fiber function, towards a neuropathic nature of pain in FM patients (a peripheral, small fiber polyneuropathy) (Nurcan U et al, Brain 2013). A parallel study from US (Oaklander Anne Louise, Pain 2013) also announced that some patients labeled as fibromyalgia had unrecognized small fiber polyneuropathy that was confirmed with distal-leg neurodiagnostic skin biopsies. These results demonstrate that 50% of FM patients may have a “small fiber polyneuropathy” as the main reason for their pains.
So, the debate between clinicians and researchers regarding the etiological importance of peripheral and central sensitization signs (hyperalgesia, allodynia, hyperpathia, brainfog) is still open.
In the present round table we will describe all the above mentioned basic data, in addition with the local, segmental and systemic acupoints that are related with fibromyalgia and chronic fatigue syndrome treatment. Furthermore we’ll talk about different acupuncture techniques (electroacupuncture, minimal acupuncture, auricular acupuncture etc) and how we’ll choose the appropriate technique according to patient’s history and symptoms. In addition, symptomatic points and points according to TCM etiology of FM/CFS will be analyzed.
Miltiades Y. Karavis, MD, FICAE, physiatrist
President of Hellenic Medical Acupuncture Society
•Francisco Mercado, Paloma Barjola, Marisa Fernandez Sanchez, Virginia Guerra, Francisco Gomez-Esquer. Brain Function in fibromyalgia: Altered Pain Processing and Cognitive Dysfunction, Madrid, Spain, 2013.
•Glass JM, Cognitive dysfunction in fibromyalgia syndrome. Journal of Musculoskeletal Pain, 2010, 18 (4), 367-372.
•Mary-Ann Fitzcharles MB, Peter A, Ste-Marie BA, Pereira MD, Fibromyalgia:evolving concepts over the past 2 decades, CMAJ, 2013.
•Nurcan Uceyler, Daniel Zeller, Ann-Kathrin Kahn, Susanne Kewenig, Sarah Kittel-sxhneider, annina Schmid, Jordi Casanova-molla, Karlheinz Reiners, Claudia Sommer. Small fiber pathology in patiens with fibromyalgia syndrome, Brain 2013:136; 1857-1867.
•Wolfe F, Clauw DJ, Fitzcharles M-A et al. The American College of Reumatology Preliminary Diagnostic Criteria for Fibromyalgia and Measurement of Symptom Severity. Arthritis Care Res (Hoboken) 2010;62:600-10.
•Wolfe F, Smythe HA, Yunus MB et al. The American College of Reumatology 1990 Criteria for Classification of Fibromyalgia. Report of the Multicenter Criteria committee. Arthritis Rheum 1990;33:160-72.