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.