PubMed · 11320993
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D J Hewitt. 2001. Web alert.. https://doi.org/10.1007/s11916-001-0002-5
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Complex regional pain syndrome consists of pain and other symptoms that are unexpectedly severe or protracted after an injury. In type II complex regional pain syndrome, major nerve injury, often with motor involvement, is the cause; in complex regional pain syndrome I, the culprit is a more occult lesion, often a lesser injury that predominantly affects unmyelinated axons. In florid form, disturbances of vasoregulation (eg, edema) and abnormalities of other innervated tissues (skin, muscle, bone) can appear. Because of these various symptoms and the difficulty in identifying causative lesions, complex regional pain syndrome is difficult to treat or cure. Complex regional pain syndrome has not been systematically investigated; there are few controlled treatment trials for established complex regional pain syndrome. This article reviews the existing studies (even if preliminary) to direct clinicians toward the best options. Treatments for other neuropathic pain syndromes that may be efficacious for complex regional pain syndrome also are discussed. Some common treatments (eg, local anesthetic blockade of sympathetic ganglia) are not supported by the aggregate of published studies and should be used less frequently. Other treatments with encouraging published results (eg, neural stimulators) are not used often enough. We hope to encourage clinicians to rely more on evidence-supported treatments for complex regional pain syndrome.
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This study examines immediate nitric oxide (NO) release from monocytes following interleukin-1beta (IL-1beta), interferon-gamma (IFN-gamma), and tumor necrosis factor-alpha (TNF-alpha) challenge in patients with complex regional pain syndrome (CRPS). Study patients exhibited the following: (1), mechanical allodynia; (2), evidence of either vasomotor or sudomotor disturbance; and (3), concordant painful allodynia documented with quantitative sensory testing that was temporarily abolished with sympathetic block. Ten subjects (CRPS, N=5; control, N=5) were enrolled. Peripheral blood monocytes were challenged with 100 microl of IL-1beta (1 ng), IFN-gamma (1 ng), TNF-alpha (0.01 ng), and normal saline (NS) and the resultant immediate NO release measured. Subjects with CRPS exhibited a statistically significant increase in NO release in response to IFN-gamma (P<0.012) compared with controls. The NO responses to IFN-gamma in excess of NS (P<0.025) and as the ratio IFN-gamma/NS (P<0.022) were also significantly increased.