Current rheumatology reports
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The lumbar spine is a common location for osteoarthritis. The axial skeleton demonstrates the same classic alterations of cartilage loss, joint instability, and osteophytosis characteristic of symptomatic disease in the appendages. Despite these similarities, questions remain regarding the lumbar spine facet joints as a source of chronic back pain. ⋯ Single photon emission computed tomography scans of the axial skeleton are able to identify painful facet joints with increased activity that may be helped by local anesthetic injections. Low back pain is responsive to therapies that are effective for osteoarthritis in other locations. Osteoarthritis of the lumbar spine does cause low back pain.
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Catastrophic antiphospholipid syndrome, defined and documented in 1992, is a potentially fatal complication seen in patients with antiphospholipid antibody. It may arise de novo in patients not previously suspected as having an antiphospholipid syndrome, or it may complicate the course of patients currently treated for this syndrome. Precipitating or "trigger" factors have been identified in 55% of patients; the most common of these factors is infection. ⋯ The clinical manifestations are those of multiorgan failure, and unusual vessels or organs can be involved. Treatment of the condition, with emphasis on effective anticoagulation, intravenous steroids, intravenous immunoglobulin, or plasma exchange, should be aggressive to achieve a satisfactory outcome. Regrettably, despite all available therapeutic options at this time, the mortality is still high (greater than 50%).
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The application of functional imaging techniques has revolutionized the field of human pain physiology and has elaborated the understanding of mechanisms involved in pain processing at the cortical and subcortical levels. With these insights, new therapeutic interventions are being developed in the treatment of acute and chronic pain conditions.
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Fibromyalgia syndrome (FMS) is characterized by widespread pain, fatigue, sleep abnormalities, and distress. Because FMS lacks consistent evidence of tissue abnormalities, recent investigations have focused on central nervous system mechanisms of pain. Abnormal temporal summation of second pain (wind-up) and central sensitization have been described recently in patients with FMS. ⋯ However, central pain mechanisms of fibromyalgia may not depend exclusively on neuronal activation. Neuroglial activation has been found to play an important role in the induction and maintenance of chronic pain. These findings may have important implications for future research and the treatment of fibromyalgia pain.