RSD/CRPS: the end of the beginning.
RSD/CRPS: the end of the beginning.
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DOI：
10.1016/j.pain.2008.08.006
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发表时间：
2008-10-15
期刊：
影响因子：
7.4
通讯作者：
Oaklander, Anne Louise
中科院分区：
文献类型：
--
作者：
Oaklander, Anne Louise
The history of medicine provides perspective invisible from PubMed. Past theories and practices seem risible until one considers which moderns medical ‘‘facts” will amuse future generations. Neurological disorders have been particularly difficult to resolve since anatomy and function are so complex. Primitive societies blamed the gods for seizures and strokes. Disease causality was eventually internalized, but localization of neural function and dysfunction remained poor for centuries, wandering through the uterus (hysteria) and heart (emotions) among other organs en route to the nervous system. Then, during the mid-20th century Freudian era, neurological disorders without visible localizing lesions (including movement disorders, autism, and schizophrenia) were often attributed to neurotic reactions to psychological traumas rather than to disease. Imperfect mothers figured prominently. These dead-end theories still circulate in some cultures, but have faded in western medicine as identification of cellular and molecular underpinnings of neurological conditions map the path towards diagnosis and cure. We are witnessing such a transition in the complex regional pain syndrome (CRPS).CRPS certainly seemed suspicious. How could a minor or healed limb injury cause pain, swelling, abnormal color and temperature, disordered sweating and movement, for months or even years? And the sex ratio among patients (consistently P 75% women) furthered suspicions of hysteria or neurosis in physicians (consistently P 75% men). In the 1990s Dutch surgeon/scientist, RJA Goris and his coworkers pioneered modern study of CRPS-I, the subtype then thought not to involve nerve injury. In addition to large-scale phenotyping [17], they identified the first evidence of nerve injuries [16] and conducted controlled treatment trials [11] among other achievements. Further support for biological causality came from discovering high levels of pro-inflammatory cytokines in skin, cerebrospinal fluid, and blood of CRPS-I patients [2, 6, 15], and identification of microcirculatory abnormalities including hypoxia and endothelial dysfunction [8, 13]. Confirmation of chronic focal axonal injuries in CRPS-I [1, 10] united the CRPS-I and II subtypes.
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影响因子：
4.6
作者：
Huygen, FJPM;de Bruijn, AGJ;Zijlstra, FJ
通讯作者：
Zijlstra, FJ
影响因子：
7.4
作者：
Oerlemans, HR;Oostendorp, RAB;Goris, RJA
通讯作者：
Goris, RJA
影响因子：
9.9
作者：
van der Laan, L;ter Laak, HJ;Goris, RJA
通讯作者：
Goris, RJA
影响因子：
7.4
作者：
Sandroni, P;Benrud-Larson, LM;Low, PA
通讯作者：
Low, PA
影响因子：
7.4
作者：
Albrecht, PJ;Hines, S;Rice, FL
通讯作者：
Rice, FL