PROLACTIN LEVELS IN RESTLESS LEGS SYNDROME

该子项目是利用NIH/NCRR资助的中心赠款提供的资源的许多研究子项目之一。子项目和研究者（PI）可能从另一个NIH来源获得了主要资金，因此可以在其他CRISP条目中表示。所列机构为中心机构，不一定为研究者机构。不宁腿综合征（RLS）是一种病因不明的疾病。现有的证据主要来自临床工作，表明存在多巴胺功能异常：Sinemet和多巴胺激动剂治疗症状的有效性为95-99%。 PET和SPECT扫描结果显示，纹状体中的D2受体和DAT有小但显著的减少。本研究的目的是寻找一种替代多巴胺敏感系统，催乳素分泌，作为一个可能的生物标记多巴胺功能及其特点的RLS人口。催乳素的分泌受抑制性多巴胺的控制。Greenspan等人（1991）证明了催乳素脉动的昼夜节律模式与已知的多巴胺分泌一致。多巴胺在早上最高，催乳素在早上最低。多巴胺处于最低水平，催乳素在深夜和凌晨达到最高水平。在不宁腿综合征的症状有一个昼夜节律模式：在晚上更糟，最小或没有在早上。据推测，大脑内多巴胺能系统的昼夜变化是造成症状的昼夜变化的原因。夜间多巴胺减少会导致症状发作。因此，研究遵循昼夜节律模式的多巴胺机制是合适的，特别是那些遵循RLS症状预期模式的机制。也就是说，随着夜间多巴胺的减少，催乳素和RLS症状一样升高。两者都是由于多巴胺能活性的降低。因此，我们可以假设，与年龄匹配的对照组相比，不宁腿综合征患者的平均催乳素水平升高，脉冲高度增加，夜间脉冲幅度增加。Greenspan等人1991年的论文（1）评价了这些指标，发现其对多巴胺能活性变化最敏感。

This subproject is one of many research subprojects utilizing the resources provided by a Center grant funded by NIH/NCRR. The subproject and investigator (PI) may have received primary funding from another NIH source, and thus could be represented in other CRISP entries. The institution listed is for the Center, which is not necessarily the institution for the investigator. Restless legs syndrome (RLS) is a disorder of unclear etiology. There is existing evidence primarily from clinical work that suggests there is an abnormality of dopamine function: Sinemet and the dopamine agonists are 95-99% effective in treating symptoms. PET and SPECT scanning results showed small but significant decreases in the D2 receptors and the DAT in the striatum. The purpose of this study is to look at an alternative dopamine sensitive system, prolactin secretion, as a possible biological marker for dopamine function and its characteristics in the RLS population. Prolactin secretion is under inhibitory dopamine control. Greenspan et al (1991) demonstrated a circadian pattern to the prolactin pulsatility in line with what is known about dopamine secretion. Dopamine is at its highest and prolactin at its lowest in the morning. Dopamine is at its lowest and prolactin is at its highest late night and early hours of the morning. In Restless legs syndrome the symptoms have a circadian pattern: worse at night minimal or absent in the morning. It has been postulated that circadian variations in the dopaminergic system within the brain are responsible for this circadian variation in symptoms. Decreasing dopamine at night leads to the onset of symptoms. Therefore, it would be appropriate to look at dopamine mechanisms which follow a circadian pattern, particularly those that follow the expected pattern of RLS symptoms. That is, with a decrease in dopamine at night, prolactin rises as do RLS symptoms. Both supposedly are due to a decrease in dopaminergic activity. One would therefore hypothesize that patients with restless legs syndrome would have increased mean prolactin levels, increased pulse height and increased pulse amplitude at night compared to age-matched controls. These are the measures, which were evaluated and found most sensitive to changes in dopaminergic activity in the Greenspan et al 1991 paper (1).