FIBROMYALGIA--CENTRAL FACTORS IN ITS ETIOPATHOGENESIS

这项研究的目的是完成为期5年的NIH研究的第二年， 在1996年7月的资金周期，是为了更好地了解中心因素 参与疼痛感知改变的发病机制 纤维肌痛（FM）。 我们测试了从一个模型中得出的3个假设， 神经内分泌和免疫异常， 脑脊液（CSF）5-羟色胺减少，CSF P物质（SP）可引起中枢神经系统致敏 参与疼痛感知的结构，即，丘脑和尾状核 原子核 局部脑血流量（rCVF）减少， 结构作为这种敏化过程的标记， 与全身性低痛阈和其他改变有关 在疼痛感知中，独立于心理的影响 status. 该模型还假设，SCF SP升高可能部分是由于 CSF白细胞产生SP信使（m）RNA。 我们测量（1） 皮质、丘脑和尾状核的rCBF，（2）CSF水平 5-羟色胺代谢产物5-羟吲哚乙酸（5-HIAA），SP，CSF 白细胞数和白细胞SP mRNA水平;（3）痛阈和 (4)心理状态

The aim of this study, which completed the second year of a 5-year NIH funding cycle in July, 1996, is to better understand the central factors involved in the etiopathogenesis of altered pain perception in fibromyalgia (FM). We test 3 hypotheses drawn from a model which posits that neuroendocrine and immunologic abnormalities, characterized by decreases in cerebrospinal fluid (CSF) serotonin and increases in CSF substance P (SP), lead to sensitization of central nervous system structures involved in pain perception, i.e., thalamus and caudate nucleus. Decreases in regional cerebral blood flow (rCVF) to these structures serve as markers for this sensitization process and are associated with generalized low pain thresholds and other alterations in pain perception, independently of the effects of psychological status. The model also posits that elevated SCF SP may in part be due to SP messenger (m) RNA production by CSF leukocytes. We measure (1) rCBF to cortex, thalamus, and caudate nucleus, (2) CSF levels of serotonin metabolite 5-hydroxyindole acetic acid (5-HIAA), SP, CSF leukocyte number, and leukocyte SP mRNA level, (3) pain thresholds and (4) psychological status.