Neeck G
Department of Rheumatology, Kerckhoff Clinic and Foundation, Bad Nauheim, Germany.
Scand J Rheumatol Suppl. 2000;113:8-12.
The symptomatology of the fibromyalgia syndrome (FMS) often resembles an alteration in central nervous set points at least in three systems. The patients suffer under chronic pain in the region of the locomotor system, presumably reflecting a disturbed central processing of pain. Anxiety and depression often characterizes the clinical picture. Almost all of the hormonal feedback mechanisms controlled by the hypothalamus are altered. Characteristic for FMS patients are the elevated basal values of ACTH, follicle-stimulating hormone (FSH), and cortisol as well as lowered basal values of insulin-like growth factor 1 (IGF-1, somatomedin C), free triiodothyronine (FT3), and oestrogen. In FMS patients, the systemic administration of the relevant releasing hormones of corticotropin-releasing hormone (CRH), growth hormone-releasing hormone (GHRH), thyreotropin-releasing hormone (TRH), and luteinizing hormone-releasing hormone (LHRH) leads to increased secretion of ACTH and prolactin, whereas the degree to which TSH can be stimulated is reduced. The stimulation of the hypophysis with LHRH in female FMS patients during their follicular phase results in a significantly reduced LH response. All in all, the typical alterations in set points of hormonal regulation that are typical for FMS patients can be explained as a primary stress activation of hypothalamic CRH neurons caused by the chronic pain. In addition to the stimulation of pituitary ACTH secretion, CRH activates somatostatin on the hypothalamic level, which in turn inhibits the release of GH and TSH on the hypophyseal level. The lowered oestrogen levels could be accounted for both via an inhibitory effect of the CRH on the hypothalamic release of LHRH or via a direct CRH-mediated inhibition of the FSH-stimulated oestrogen production in the ovary. Serotonin (5HT), precursors like tryptophan (5HTP), drugs which release 5HT or act directly on 5HT receptors stimulate HPA axis, indicating a stimulatory serotonergic influence on HPA axis function. Therefore activation of the HPA axis may reflect an elevated serotonergic tonus in the central nervous system of FMS patients.
纤维肌痛综合征（FMS）的症状学至少在三个系统中常常类似于中枢神经设定点的改变。患者遭受运动系统区域的慢性疼痛，这可能反映了疼痛的中枢处理紊乱。焦虑和抑郁常常是临床表现的特征。几乎所有由下丘脑控制的激素反馈机制都发生了改变。FMS患者的特征是促肾上腺皮质激素（ACTH）、促卵泡激素（FSH）和皮质醇的基础值升高，以及胰岛素样生长因子1（IGF-1，生长介素C）、游离三碘甲状腺原氨酸（FT3）和雌激素的基础值降低。在FMS患者中，全身给予促肾上腺皮质激素释放激素（CRH）、生长激素释放激素（GHRH）、促甲状腺激素释放激素（TRH）和促黄体生成素释放激素（LHRH）等相关释放激素会导致ACTH和催乳素分泌增加，而促甲状腺激素（TSH）的可刺激程度降低。在卵泡期，对女性FMS患者用LHRH刺激垂体，会导致促黄体生成素（LH）反应显著降低。总而言之，FMS患者典型的激素调节设定点改变可以解释为由慢性疼痛引起的下丘脑CRH神经元的原发性应激激活。除了刺激垂体ACTH分泌外，CRH在下丘脑水平激活生长抑素，进而在垂体水平抑制生长激素（GH）和TSH的释放。雌激素水平降低可能是由于CRH对下丘脑LHRH释放的抑制作用，或者是由于CRH直接介导的对卵巢中FSH刺激的雌激素产生的抑制作用。血清素（5HT）、色氨酸（5HTP）等前体、释放5HT或直接作用于5HT受体的药物会刺激下丘脑-垂体-肾上腺（HPA）轴，表明血清素能对HPA轴功能有刺激作用。因此，HPA轴的激活可能反映了FMS患者中枢神经系统中血清素能张力升高。
