Der Schmerz
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Pain is the leading symptom of inflammatory joint diseases. It is immediately caused by the release of prostaglandins (and potentially leukotrienes) from cells of the inflamed tissues, which sensitizes the pain receptors. The synthesis of these mediators depends on the activation of infiltrated inflammatory cells, as well as recruitment of tissue born cells, predominantly by the inflammatory cytokines Interleukin-1 (IL-1) or tumor necrosis factor (TNF). ⋯ Anti-inflammatory drugs as the glucocorticoids predominantly decrease the synthesis of cytokines, and thereby the stimuli leading to prostaglandin synthesis. Together with a decrease of the synthesis of arachidonate metabolizing enzymes this leads to correction of pain. Although not directly analgetic, immunosuppressive drugs, too, by decreasing the immune reaction dependent inflammation, contribute to pain relief.
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Myofascial pain syndromes, fibromyalgia, and articular dysfunctions may all be contributing to our patients' ubiquitous musculoskeletal pain problems that generally are poorly understood and poorly managed. Thepectoralis minor myofascial pain syndrome, for example, results from trigger points (TrPs) activated by stress overload of the muscle. ⋯ Snapping palpation at the TrP elicits a local twitch response (LTR). The increased muscle tension of a pectoralis minor syndrome commonly entraps the lower trunk of the brachial plexus, producing symptoms of a cervical radiculopathy.