Michaud Martin, Soucy Jean-Paul, Chabli Allal, Lavigne Gilles, Montplaisir Jacques
Département de Psychiatrie Faculté de Médecine Université de Montréal, Canada.
J Neurol. 2002 Feb;249(2):164-70. doi: 10.1007/pl00007859.
Restless legs syndrome (RLS) is a common sleep-related disorder principally characterised by leg paresthesia associated with an irresistible urge to move. A majority of RLS patients experience periodic leg movements during sleep (PLMS) and wakefulness. Pharmacological evidence suggests that RLS-PLMS may be caused by a central nervous system dopaminergic (DA) dysfunction. The aim of the present study was to evaluate the striatal pre- and postsynaptic DA status in patients suffering from both RLS and PLMS, by means of [123I] beta-CIT and [123I]IBZM SPECT respectively. Ten drug-naïve patients and ten age-matched controls participated in this study. All participants were recorded for at least one night of polysomnography before the SPECT studies. No difference was seen in DA transporter ([123I] beta-CIT) binding between RLS-PLMS patients (MD=4.89) and controls (MD=4.81; p=0.81). The study of the striatal D2-receptor binding ([123I]IBZM) revealed a significantly lower binding in patients (MD= 1.72) compared with controls (MD=1.85; p=0.006). These results support the hypothesis that a central DA dysfunction is involved in the physiopathology of RLS-PLMS. Several mechanisms may be responsible for the decrease of the D2-receptor binding. However, since [123I] beta-CIT binding is normal, a decreased number of D2-receptors or a decreased affinity of D2-receptors for [123I]IBZM is more likely than an increased level of synaptic DA with attendant downregulation of D2-receptors.
不宁腿综合征（RLS）是一种常见的与睡眠相关的疾病，主要特征是腿部感觉异常，并伴有无法抑制的活动冲动。大多数RLS患者在睡眠（PLMS）和清醒时会出现周期性腿部运动。药理学证据表明，RLS-PLMS可能由中枢神经系统多巴胺能（DA）功能障碍引起。本研究的目的是分别通过[123I]β-CIT和[123I]IBZM SPECT评估同时患有RLS和PLMS的患者纹状体突触前和突触后DA状态。10名未服用过药物的患者和10名年龄匹配的对照者参与了本研究。在进行SPECT研究之前，所有参与者均记录了至少一晚的多导睡眠图。RLS-PLMS患者（平均差异=4.89）和对照者（平均差异=4.81；p=0.81）之间的DA转运体（[123I]β-CIT）结合未见差异。对纹状体D2受体结合（[123I]IBZM）的研究显示，与对照者（平均差异=1.85；p=0.006）相比，患者的结合显著降低（平均差异=1.72）。这些结果支持了中枢DA功能障碍参与RLS-PLMS病理生理过程的假说。几种机制可能导致D2受体结合减少。然而，由于[123I]β-CIT结合正常，D2受体数量减少或D2受体对[123I]IBZM的亲和力降低比突触DA水平升高伴D2受体下调更有可能。
