The epidemiology of this disease has not been reported in China, and there are few accurate statistical data abroad. However, from the literature, the disease is not uncommon, reportedly accounting for 2% of the U.S. population. With such a high incidence, patients may not always be seen by rheumatologists, so the importance of awareness of the disease among other physicians should be emphasized. Etiology and pathogenesis 1, muscle pathology: because muscle pain is the main symptom of the syndrome, so scholars have long been committed to muscle research, but the conclusions are not the same. In the early period (1950), some scholars reported the presence of muscle morphological abnormalities in FS patients, but subsequent studies showed that there were no characteristic changes in muscle morphology or only slight changes in muscle metabolism at the point of tenderness. More recently (1980-1990), analysis using magnetic resonance spectroscopy showed no significant abnormalities in muscle metabolism. It has been widely believed that the mechanism of myalgia in FS is due to muscle hypertonicity that overexcites muscle pain receptors and produces myospasm and chronic myalgia, but recently some scholars have not obtained the above evidence using electromyography, and it is difficult to base this inference. 2, central neurotransmitter secretion: The literature reports that the hypothalamic-pituitary-adrenaline (HPA) axis, sympathetic nervous system (SNS), and abnormal function of the emergency defense system may play an important role in the pathogenesis of the disease. 3, immune mechanisms: Some scholars have proposed that immune regulation disorders and abnormal levels of cytokines in vivo may be related to the pathogenesis of FS. Preliminary studies have found elevated levels of interleukin-2, increased CD+4 lymphocytes and higher CD+4/CD8+ ratios in FS.