Future studies should include control group for the evaluation of REM sleep without atonia as marker for neurodegeneration also in non-clinical population and target RBD as precursor of neurodegeneration to develop protective trials.
We visually quantified phasic, "any," and tonic RSWA in the submentalis (SM) and anterior tibialis (AT) muscles, and the automated Ferri REM Atonia Index during polysomnography in adults without RBD aged 21-88.
The percentages of movements and the median inter-movement distance during REM and non-REM (NREM) sleep were used for distinguishing C, RBD and PLMD by combining three optimized classifiers in a 5-fold cross-validation scheme.
We found that Parkinson's disease patients with RBD showed decreased locus coeruleus neuromelanin signal on MRI (P < 0.001) and widespread reduced binding of 11C-MeNER (P < 0.001), which correlated with amount of REM sleep without atonia.
Clinical profiles and radiological findings by cardiac [<sup>123</sup> I]-metaiodobenzylguanidine ([<sup>123</sup> I]-MIBG) scintigraphy and imaging for the dopamine transporter (DAT) were compared between patients with and without RBD symptoms.
Dream enacting behavior (DEB) during REM sleep is a characteristic feature of REM sleep behavior disorder (RBD), the most specific prodromal symptom for Parkinson's disease (PD) and related synucleinopathies.
Participants belonging to the following cohorts of the Parkinson Progression Markers Initiative (PPMI) study were included: de novo PD with dopamine transporter binding deficit (n = 423), idiopathic REM sleep behavior disorder (RBD, n = 39), hyposmia (n = 26) and non-PD mutation carrier (NMC; Leucine-rich repeat kinase 2 (LRRK2) G2019S (n = 88) and glucocerebrosidase (GBA) gene (n = 38) mutations)).
Study subjects included 19 patients with late-onset psychiatric disorders who exhibited REM sleep without atonia (RWA), which is a hallmark of RBD on polysomnography, at our psychiatric ward.
In the late 50s Michel Jouvet discovered the presence of muscle atonia during REM sleep in cats and created the first model of REM sleep behavior disorder.
Patients with rapid eye movement (REM) behavior disorder (RBD) can develop synucleinopathies, and such risk is higher with dopamine transporter single photon emission tomography (123I-FP-CIT SPECT) evidence of nigro-striatal dysfunction.
RBD patients seem to have a milder OSA phenotype (possible reflecting a protective role conferred by the maintenance of muscle tone during REM sleep) and to be less prone to obesity and snoring than non-RBD patients.
These results demonstrated that the presence of RBD in patients with PD is associated with different patterns of both motor deficit distribution and striatal DAT depletion, suggesting that the presence of RBD represents a distinct PD subtype with a malignant motor parkinsonism.