The widespread myofascial pain of fibromyalgia is sympathetically maintained and immune mediated.

The recent demonstration of antibody-induced passive transfer of pain hypersensitivity from fibromyalgia (FM) subjects to mice brings renewed focus to the role of the immune system in generating FM pain. However, this data must be interpreted in the context of known myofascial pathology in FM, which includes impaired muscle relaxation and elevated intramuscular pressure. In addition, FM fascial biopsies demonstrate elevated inflammatory and oxidative stress markers and increased endomysial collagen deposition. This article proposes a unifying hypothesis for FM pain generation that connects known muscle and fascia abnormalities with the newly discovered role of antibodies. FM is characterized by persistent sympathetic nervous system hyperactivity which results in both pathologic muscle tension and an impaired tissue healing response. Although autoantibodies play a key role in normal tissue healing, sympathetic nervous system hyperactivity impairs the resolution of inflammation, and promotes autoimmunity and excessive autoantibody production. These autoantibodies can then bind with myofascial-derived antigen to create immune complexes, which are known to trigger neuronal hyperexcitability in the dorsal root ganglion. These hyperexcited sensory neurons activate the surrounding satellite glial cells and spinal microglia leading to pain hypersensitivity and central sensitization. Although immune system modulation may become an important treatment tool in FM, direct manual treatments that lessen myofascial inflammation and tension must not be neglected. Myofascial release therapy significantly reduces FM pain, with residual benefits even after the conclusion of treatment. Self-myofascial release techniques and gentle stretching programs also ease fibromyalgia pain, as do trigger point injections and dry-needling.
Competing Interests: Declarations of competing interest None.
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