Patients with muscle aches, pain, and fatigue have long been known to medicine. The roots of fibromyalgia can be traced to the early part of the 20th century with references to “fibrositis”, “muscular rheumatism”, and “lumbago”, terms used interchangeably to describe pain in lumbar muscles with contraction or extension. During the Second World War physicians diagnosed fibrositis in more than three-quarters of soldiers attending military hospitals, often with similar non-specific complaints and symptomatology.  It became the most frequent cause of disability in 450 consecutive recruits.  The concept of so called painful trigger points and nodular indurations at common sites, such as along the neck, shoulder, elbow, wrist, palms, low back, and at times in a more generalized distribution were later noted by English physicians.  Therapy included administration of analgesics, immobilization of the affected areas, infiltration of trigger points with procaine and corticosteroids, local heat, massage, and postural exercises.  Investigators proposed that the demonstration of 12 or more tendon points from 14 typical sites of deep tenderness in clinically affected patients with fibrositis differentiated them from other soft tissue pain syndromes, malingering, and rheumatic disorders.  The terms fibrositis and fibromyalgia became interchangeable in the 1980s by rheumatologists. Yet even before the American College of Rheumatology established “fibromyalgia syndrome” as a distinctive diagnosis, extending the criteria for tender points to 11 of 18 or the presence of widespread pain for at least 3 months duration, there was continuing parallel interest in the emotional aspects of the disorder. It soon became evident that pathophysiological insight was lacking in the fibromyalgia syndrome and that circular reasoning argued the evidence on which the diagnosis was based since its very nature was only valid in the sense that it included virtually all possibilities despite poor reproducibility of trigger and tender points even among experts. The disorder is clinically characterized by generalized pain with widespread tender points in specific areas and is frequently accompanied by fatigue, stiffness, and a non-restorative sleep pattern. 

The contribution of autoimmunity or dysimmunity in the pathogenesis of fibromyalgia was suggested In one retrospective study in which a subgroup of patients had clinically important markers of inflammation, notably an elevated erythrocyte sedimentation rate, C-reactive protein, antinuclear antibody, and rheumatoid factor; a group that was considered representative of inflammatory fibromyalgia. None of their patients developed a documented coexisting autoimmune illness during the retrospective review period.
 
It is generally believed that there is no primary peripheral abnormality in fibromyalgia. One model of the disorder proposes functional dysregulation of central pain pathways in the form of abnormal central sensitization. The neuronal connections implicated in this hypothesis vary widely, but appear to involve ascending pain tracts commencing in the dorsal root ganglia to the periaqueductal gray matter, thalamus, and primary and secondary somatosensory, prefrontal, premotor, and anterior cingulate cortices.  One recent study employing nuclear medicine imaging documented reduced thalamic and pontine tegmentum cerebral blood flow.

Evidenced based guidelines of the American Pain Society, Association of the Scientific Medical Societies in Germany, Canadian Pain Society and the European League Against Rheumatism were reviewed. Treatment with aerobic exercise, cognitive-behavioral therapy, the antidepressant amitriptyline, and multicomponent therapies were advocated most highly.  It is still not certain whether a routine neuromuscular evaluation really contributes anything to patients with classic fibromyalgia, nonetheless, the current data on its prevalence suggests that up to 2% of the adult U.S. population may be affected, and the cost of health care and disability for this segment of the population continues to rise. It appears reasonable to avoid denying its existence, and attempt to understand the plight of such patients.