Frederik W Bes

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Stephan Anagnostaras

University of California, San Diego

Elizaveta Solomonova

McGill University

Steven J Frenda

California State University, Los Angeles

Nicola Barclay

University of Oxford

Tore Nielsen

Université de Montréal

Ram L. Pandey Vimal

Google

Josie E Malinowski

University of East London

barbara baert

KU Leuven

Ryan Hurd

John F. Kennedy University

Chien-Ming Yang

National Cheng Chi University

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Melatonin Effects in REM Sleep Behavior Disorder Associated with Obstructive Sleep Apnea Syndrome: A Case Series

Current Alzheimer Research, Sep 8, 2017

OBJECTIVES REM sleep behavior disorder (RBD), with its main clinical symptoms of nightmares with ... more OBJECTIVES REM sleep behavior disorder (RBD), with its main clinical symptoms of nightmares with dream-enacting behavior, is considered as a possible precursor of neurodegenerative disease. Obstructive Sleep Apnea Syndrome (OSAS) is known to be capable of provoking RBD-like symptoms by apneic event related arousals. The two sleep related pathologies must coincide in a relevant number of individuals because of overlapping prevalence in similar age groups. Until now RBD symptoms coexisting with OSAS are rarely described in scientific literature and in fact considered as OSAS mimicking RBD. METHODS We report four cases with a severe clinical RBD syndrome which were polysomnographically also diagnosed with concomitant OSAS (AHI range: 10.1 -53.2/h). RESULTS Treatment with 2 mg prolonged release melatonin led to a relevant clinical improvement of RBD symptoms in all patients, so far untreated for the sleep related breathing disorder. Measure of REM sleep without atonia (RSWA) in polysomnography showed values ranging from 5.1 to 20.4% determined with the Montplaisir method. Surprisingly, RSWA values in PSG with melatonin were high, probably because of the still untreated OSAS. CONCLUSION We presume that in patients with RBD and OSAS both pathologies contribute in varying degrees to the emergence of RBD symptoms by a destabilization of REM sleep. We suggest by consequence to consider a therapeutic strategy including the treatment of both disorders for an optimal therapeutic response.

Twenty Years After: Another Case Report of Melatonin Effects on REM Sleep Behavior Disorder, Using Serial Dopamine Transporter Imaging

Neuropsychobiology, 2017

Introduction: REM sleep behavior disorder (RBD) is considered a prodromal phase of α-synucleinopa... more Introduction: REM sleep behavior disorder (RBD) is considered a prodromal phase of α-synucleinopathy like Parkinson disease (PD). PD is characterized by a progressive decline of dopamine (DA) in the striatum. Here we report the surprising increase in DA transporter density over successive years in an RBD patient treated with melatonin. Case Presentation: A then 72-year-old man was clinically suspected to suffer from PD in 2011. DA transporter scintigraphy (DaTSCAN) revealed reduced DA transporter density, and the patient was diagnosed with developing PD. Because of outacting dreams every night (speaking, yelling, kicking, pushing) he was referred to our clinic. Video-assisted polysomnography (PSG) confirmed the diagnosis of RBD in 2012. Management and Outcome: Melatonin treatment (2 mg slow release/day; 30 min prior to habitual bedtime; always at the same clock time) was initiated after PSG and continued. After 6 months of gradual improvement, clinical signs of RBD were absent. Control PSG in 2014 confirmed normalized REM sleep with atonia. Furthermore, no clinical sign of neurodegeneration occurred ever since. Additional DaTSCANs were performed in 2013 and 2015. Whereas the 2011 scan prior to melatonin treatment bore clear signs of PD, the 2013 scan was considered borderline and the 2015 scan without any sign of PD. Discussion: To the best of our knowledge, DA transporter density increase over time has never been reported in a single subject, neither healthy aged individuals nor patients suffering from RBD or PD. We interpret these results as a possible neuroprotective role for melatonin in synucleinopathy.

Progression of clinical markers in prodromal Parkinson’s disease and dementia with Lewy bodies: a multicentre study

Brain, Mar 7, 2023

The neurodegenerative synucleinopathies, including Parkinson’s disease and dementia with Lewy bod... more The neurodegenerative synucleinopathies, including Parkinson’s disease and dementia with Lewy bodies, are characterized by a typically lengthy prodromal period of progressive subclinical motor and non-motor manifestations. Among these, idiopathic REM sleep behaviour disorder is a powerful early predictor of eventual phenoconversion, and therefore represents a critical opportunity to intervene with neuroprotective therapy. To inform the design of randomized trials, it is essential to study the natural progression of clinical markers during the prodromal stages of disease in order to establish optimal clinical end points. In this study, we combined prospective follow-up data from 28 centres of the International REM Sleep Behavior Disorder Study Group representing 12 countries. Polysomnogram-confirmed REM sleep behaviour disorder subjects were assessed for prodromal Parkinson’s disease using the Movement Disorder Society criteria and underwent periodic structured sleep, motor, cognitive, autonomic and olfactory testing. We used linear mixed-effect modelling to estimate annual rates of clinical marker progression stratified by disease subtype, including prodromal Parkinson’s disease and prodromal dementia with Lewy bodies. In addition, we calculated sample size requirements to demonstrate slowing of progression under different anticipated treatment effects. Overall, 1160 subjects were followed over an average of 3.3 ± 2.2 years. Among clinical variables assessed continuously, motor variables tended to progress faster and required the lowest sample sizes, ranging from 151 to 560 per group (at 50% drug efficacy and 2-year follow-up). By contrast, cognitive, olfactory and autonomic variables showed modest progression with higher variability, resulting in high sample sizes. The most efficient design was a time-to-event analysis using combined milestones of motor and cognitive decline, estimating 117 per group at 50% drug efficacy and 2-year trial duration. Finally, while phenoconverters showed overall greater progression than non-converters in motor, olfactory, cognitive and certain autonomic markers, the only robust difference in progression between Parkinson’s disease and dementia with Lewy bodies phenoconverters was in cognitive testing. This large multicentre study demonstrates the evolution of motor and non-motor manifestations in prodromal synucleinopathy. These findings provide optimized clinical end points and sample size estimates to inform future neuroprotective trials.

Polysomnographic diagnosis of REM sleep behavior disorder: a change is needed

Sleep, Dec 15, 2022

Seasonality of human sleep: Polysomnographic data of a neuropsychiatric sleep clinic

Frontiers in Neuroscience, Feb 17, 2023

Frederik W Bes

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