The nonarticular pain syndromes have been demonstrated to have definite associations with a group of conditions including nonrestorative sleep, irritable bowel syndrome, chronic fatigue, various mood disorders, chronic and migrainous cephalgia, morning stiffness, tender points as well as temporomandibular joint, carpal tunnel syndrome, plantar fasciitis, and cervical neuralgia.

Nonarticular rheumatic disorders can be differentiated from arthritis by accurate localization of tenderness and pain by the absence of clinical and radiographic signs of joint pathology and systemic disease. However, we have learned that, especially in the case of fibromyalgia, the mechanistic characterization of pain including peripheral, neuropathic, and central types can, in combination, be present in a given individual. Thus, our ability to differentiate these different types of pain in a given individual will also aid our diagnosis and treatment.

Tendonitis and bursitis virtually always present as local pain and inflammation, although bursitis affects the synovial fluid–filled saclike structures protecting soft tissues from underlying bone. Both disorders can be associated with overuse, infection, and systemic disease as well calcium apatite and pyrophosphate deposition disorders, but, in addition, gout frequently causes olecranon and prepatellar bursitis.

Structural conditions can be associated with local pain, but disorders such as lateral patellar subluxation, scoliosis, and flatfeet may not necessarily be the primary source of pain or dysfunction.

Neurovascular entrapment can occur centrally or peripherally, and whether this is secondary to carpal or tarsal tunnel syndrome or spinal stenosis, bony enlargement from osteophytes, inflammation, or muscular spasm can add to narrowing of a neurovascular canal and cause discomfort and paresthesias distal to the point of entrapment.

Fibromyalgia is a condition seen most commonly in women in their fifth decade of life with a female-to-male ratio of 8 : 1. It presents as a form of allodynia, in which painless stimuli are perceived as painful, and hyperalgesia, in which normally painful stimuli are amplified. There appears to be a familial predisposition, suggesting a greater than 8 odds ratio for first-degree relatives and much less familial aggregation with major mood disorders but stronger associations with bipolar and obsessive-compulsive disorders. Levels of substance P, glutamate, excitatory amino acid (EAA), and nerve growth factor can all be elevated, as well as abnormalities of the serotonin system. The cause of fibromyalgia remains unclear, but a recent study links a little known retrovirus to chronic fatigue syndrome. Whether this retrovirus can be associated as well to fibromyalgia remains in question. A host of associated conditions that can occur in association with fibromyalgia but are not necessarily etiologic factors include physical trauma, chronically disturbed sleep, emotional trauma, autoimmune disease (rheumatoid arthritis and systemic lupus erythematosus), female sex, defined infections such as Lyme disease, hepatitis C or human immunodeficiency virus infection, and a family history of fibromyalgia. Tender point examinations for fibromyalgia are performed using digital thumb pressure at nine bilateral upper and lower extremity sites. Control points including the forehead, midanterior thigh, mid deltoid, thumb, and big toe are useful regarding the patient’s sense of general hyperesthesia.

Treatment of nonarticular rheumatism can be very broad and often involves multiple pharmacologic, procedural, and patient-generated approaches guided it is hoped by a single physician source. The pivotal key for appropriate treatment is to understand the various mechanisms that may be contributing to chronic pain and which of the three types, including nociceptive, neuropathic, and non-nociceptive, may be present in combination in a given individual.