What is the pathophysiology of nonarticular rheumatism/regional pain syndromes?

Updated: Apr 04, 2018
  • Author: T P Sudha Rao, MD; Chief Editor: Herbert S Diamond, MD  more...
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Answer

Tendonitis presents as local pain, inflammation, dysfunction, and degeneration. It can be associated with overuse, infection, systemic rheumatic disease, or metabolic disturbance such as calcium apatite or pyrophosphate deposition. Fluoroquinolone antibiotic use can be associated with tendonitis and rupture. Inflammation can cause "triggering," in which the digit locks and a snapping sensation is felt upon release. [3]

Bursitis presents as local pain and inflammation of the synovial fluid filled saclike structures that protect soft tissues from underlying bone. Overuse, infection, systemic rheumatic disease, and metabolic disturbance such as calcium apatite and pyrophosphate deposition can also cause bursitis. Gout often causes olecranon bursitis and prepatellar bursitis.

Structural disorders such as scoliosis, lateral patellar subluxation, and flatfoot can cause local pain but are not always a source of pain or dysfunction. [4] The hypermobility syndrome presents with arthralgias due to increased joint laxity in the face of muscle disuse.

Neurovascular entrapment can occur centrally (eg, in spinal stenosis), in deep tissues (eg, thoracic outlet syndrome), or peripherally (eg, carpal or tarsal tunnel syndromes). [5, 6, 7, 8]  Bone enlargement due to osteophytes, muscular tension, and inflammation can contribute to narrowing of a neurovascular passage. Pain and paresthesia usually occur distal to the site of entrapment.

Regional myofascial pain syndromes, such as temporomandibular joint syndrome, may represent a pain-spasm pain cycle triggered by mechanical injury, such as strain or overuse. [9]

Multiple bursitis and tendonitis syndrome presents with anatomically localized areas of pain and dysfunction. Pain can be widespread, but the muscle tender points observed in fibromyalgia are absent. Usually, much less fatigue occurs, and responses to local therapies are better than in fibromyalgia.

Fibromyalgia, in many cases, presents as a form of allodynia, in which usually painless stimuli are perceived as painful, and hyperalgesia, in which normally painful stimuli is amplified. Cerebrospinal fluid levels of substance P are elevated, and additional abnormalities in the serotonin system and in the regulation of cortisol exist. Fibromyalgia can also coexist with various autoimmune diseases and onset often follows a severe flulike syndrome, a defined infection (eg, Lyme disease), or trauma. Sleep is often disturbed, and nonrestorative sleep is associated with increased pain. The increased prevalence in females may point to a hormonal influence. Few abnormalities occur in the peripheral musculature. Studies that show abnormalities of cerebral blood flow in the thalamus and caudate nucleus help support the likelihood that pain processing in the central nervous system behaves abnormally. [10, 11, 12]

A study by Light and colleagues found that patients with chronic fatigue syndrome have an increased expression of sensory, adrenergic, and immune genes during moderate exercise. [13] Abnormalities of the neuroendocrine immune system are well documented, but none has yet been proven to be sensitive and specific enough to be used as a criterion for diagnosis.

Psychological, personality, and social factors may play important roles in many chronic cases of local and generalized pain syndromes. The image below depicts possible factors that contribute to the generation of these syndromes.

Possible factors that lead to myofascial pain synd Possible factors that lead to myofascial pain syndromes.

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