Motor Control During Rapid Eye Movement (REM) Sleep Behaviour Disorder

Patient with severe Parkinson's disease (PD) with motor fluctuations are akinetic and bradykinetic during the "off" phases. Their motor status dramatically improves during "on" phases, due to the effect of dopaminergic agents. In the off phases, the plasmatic levels of dopaminergic drugs are the lowest. The plasmatic levels of dopaminergic drugs are also very low during nocturnal sleep. Nevertheless, PD patients may show vigorous and rapid movements during REM Behaviour Disorder (RBD). Thirty-three to 46% of the patients with PD have RBD. Akinesia and bradykinesia are the consequence of a hyperactivity of the SubThalamic Nuclei (STN). The electrophysiological correlate of this hyperactivity causing akinesia and bradykinesia is represented by STN beta activity, recorded by local field potentials. STN beta activity is not present during the execution of a voluntary movement at an "on" phase. Levodopa therapy, which can revert akinesia and bradykinesia, also suppress STN beta activity in PD patients The STN is the surgical target for Deep Brain Stimulation (DBS) of the basal ganglia to improve the motor symptoms of PD. The STN has bilateral connections with the laterodorsal nucleus/pedunculopontine tegmentum (LDT/PPN), a key structure for REM sleep regulation. The investigators hypothesize that during the execution of the phasic motor behaviours of RBD the pattern of discharge of STN differs from the one observed during voluntary movements in the "off" phase, in PD patients. In other terms, we expect the STN beta activity to disappear during the execution of phasic motor behaviors of RBD.