Fibromyalgia (FM) is a chronic, widespread pain condition that has important prevalence in general population. Despite the musculoskeletal pain, the majority of people with fibromyalgia also experience fatigue, sleep disorders, visceral pain, exercise intolerance and neurological symptoms. This syndrome is considered a functional syndrome because it is better characterized by its symptoms, suffering and disability rather than well seen organic structure impairment. A substantial literature has been produced in order to explain the pathophysiology of fibromyalgia: researches on genetics, biogenic amines, neurotransmitters, hypothalamic-pituitary-adrenal axis hormones, oxidative stress, mechanisms of pain modulation, central sensitization and autonomic function in FM revealed various abnormalities indicating that multiple factors and mechanisms may be involved in the pathogenesis of FM. Dysautonomia may have a main role at FM pathophysiology, even though it is not clear if cause, consequence or a component of this mosaic syndrome. Future research must be encouraged in order to evaluate the real role of autonomic nervous system or its impaired function in the complex pathophysiology of the syndrome and in order to assess efficacy of therapeutics interventions through well designed assays. The development of effective therapeutics measures has been delayed due to lack of knowledge of the main mechanisms in the pathogenesis of FM. A thorough understanding of mechanisms will be required to develop and document convenient therapies. This review aims to describe the most recent articles that document autonomic system impairment in SFM and to discuss dysautonomia as a potential mechanism that plays a role in the symptoms genesis, symptoms maintenance and comorbidity in SFM.
fibromyalgia; autonomic nervous system; pathophysiology; rheumatic disease; adrenergic receptor; dystautonomia