Severity of REM atonia loss in idiopathic REM sleep behavior disorder predicts Parkinson disease
Identifieur interne : 001C82 ( Main/Exploration ); précédent : 001C81; suivant : 001C83Severity of REM atonia loss in idiopathic REM sleep behavior disorder predicts Parkinson disease
Auteurs : R. B. Postuma [Canada] ; J. F. Gagnon [Canada] ; S. Rompre [Canada] ; J. Y. Montplaisir [Canada]Source :
- Neurology [ 0028-3878 ] ; 2010.
Descripteurs français
- Pascal (Inist)
English descriptors
- KwdEn :
- Aged, Atonia, Behavior, Cohort Studies, Female, Follow-Up Studies, Humans, Idiopathic, Longitudinal Studies, Male, Middle Aged, Nervous system diseases, Parkinson Disease (diagnosis), Parkinson Disease (etiology), Parkinson Disease (physiopathology), Parkinson disease, Polysomnography (methods), Predictive Value of Tests, REM Sleep Behavior Disorder (complications), REM Sleep Behavior Disorder (diagnosis), REM Sleep Behavior Disorder (physiopathology), Rapid eye movement sleep, Severity of Illness Index, Sleep disorder, Sleep, REM (physiology).
- MESH :
- complications : REM Sleep Behavior Disorder.
- diagnosis : Parkinson Disease, REM Sleep Behavior Disorder.
- etiology : Parkinson Disease.
- methods : Polysomnography.
- physiology : Sleep, REM.
- physiopathology : Parkinson Disease, REM Sleep Behavior Disorder.
- Aged, Cohort Studies, Female, Follow-Up Studies, Humans, Longitudinal Studies, Male, Middle Aged, Predictive Value of Tests, Severity of Illness Index.
Abstract
Background: Over 50% of persons with idiopathic REM sleep behavior disorder (RBD) will develop Parkinson disease (PD) or dementia. At present, there is no way to predict who will develop disease. Since polysomnography is performed in all patients with idiopathic RBD at diagnosis, there is an opportunity to analyze if baseline sleep variables predict eventual neurodegenerative disease. Methods: In a longitudinally studied cohort of patients with idiopathic RBD, we identified those who had developed neurodegenerative disease. These patients were matched by age, sex, and follow-up duration to patients with RBD who remained disease-free and to controls. Polysomnographic variables at baseline (i.e., before development of neurodegenerative disease) were compared between groups. Results: Twenty-six patients who developed neurodegenerative disease were included (PD 12, multiple system atrophy 1, dementia 13). The interval between polysomnogram and disease onset was 6.7 years, mean age was 69.5, and 81% were male. There were no differences between groups in sleep latency, sleep time, % stages 2-4, % REM sleep, or sleep efficiency. However, patients with idiopathic RBD who developed neurodegenerative disease had increased tonic chin EMG activity during REM sleep at baseline compared to those who remained disease-free (62.7 ± 6.0% vs 41.0 ± 6.0%, p = 0.020). This effect was seen only in patients who developed PD (72.9 ± 6.0% vs 41.0 ± 6.0%, p = 0.002), and not in those who developed dementia (54.3 ± 10.3, p = 0.28). There was no difference in phasic submental REM EMG activity between groups. Conclusions: In patients with REM sleep behavior disorder initially free of neurodegenerative disease, the severity of REM atonia loss on baseline polysomnogram predicts the development of Parkinson disease.
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B." last="Postuma">R. B. Postuma</name><affiliation wicri:level="4"><inist:fA14 i1="01"><s1>Department of Neurology, McGill University, Montreal General Hospital</s1><s2>Montreal</s2><s3>CAN</s3><sZ>1 aut.</sZ></inist:fA14><country>Canada</country><placeName><settlement type="city">Montréal</settlement><region type="state">Québec</region><settlement type="city">Montréal</settlement></placeName><orgName type="university">Université McGill</orgName></affiliation><affiliation wicri:level="3"><inist:fA14 i1="02"><s1>Centre d'Etude du Sommeil et des Rythmes Biologiques, Hôpital du Sacre-Coeur</s1><s2>Montreal</s2><s3>CAN</s3><sZ>1 aut.</sZ><sZ>2 aut.</sZ><sZ>3 aut.</sZ><sZ>4 aut.</sZ></inist:fA14><country>Canada</country><placeName><settlement type="city">Montréal</settlement><region type="state">Québec</region></placeName></affiliation></author><author><name sortKey="Gagnon, J F" sort="Gagnon, J F" uniqKey="Gagnon J" first="J. F." last="Gagnon">J. F. Gagnon</name><affiliation wicri:level="3"><inist:fA14 i1="02"><s1>Centre d'Etude du Sommeil et des Rythmes Biologiques, Hôpital du Sacre-Coeur</s1><s2>Montreal</s2><s3>CAN</s3><sZ>1 aut.</sZ><sZ>2 aut.</sZ><sZ>3 aut.</sZ><sZ>4 aut.</sZ></inist:fA14><country>Canada</country><placeName><settlement type="city">Montréal</settlement><region type="state">Québec</region></placeName></affiliation><affiliation wicri:level="1"><inist:fA14 i1="03"><s1>Department of Psychiatry, Université de Montréal</s1><s2>Quebec</s2><s3>CAN</s3><sZ>2 aut.</sZ><sZ>4 aut.</sZ></inist:fA14><country>Canada</country><wicri:noRegion>Quebec</wicri:noRegion></affiliation></author><author><name sortKey="Rompre, S" sort="Rompre, S" uniqKey="Rompre S" first="S." last="Rompre">S. Rompre</name><affiliation wicri:level="3"><inist:fA14 i1="02"><s1>Centre d'Etude du Sommeil et des Rythmes Biologiques, Hôpital du Sacre-Coeur</s1><s2>Montreal</s2><s3>CAN</s3><sZ>1 aut.</sZ><sZ>2 aut.</sZ><sZ>3 aut.</sZ><sZ>4 aut.</sZ></inist:fA14><country>Canada</country><placeName><settlement type="city">Montréal</settlement><region type="state">Québec</region></placeName></affiliation></author><author><name sortKey="Montplaisir, J Y" sort="Montplaisir, J Y" uniqKey="Montplaisir J" first="J. Y." last="Montplaisir">J. Y. Montplaisir</name><affiliation wicri:level="3"><inist:fA14 i1="02"><s1>Centre d'Etude du Sommeil et des Rythmes Biologiques, Hôpital du Sacre-Coeur</s1><s2>Montreal</s2><s3>CAN</s3><sZ>1 aut.</sZ><sZ>2 aut.</sZ><sZ>3 aut.</sZ><sZ>4 aut.</sZ></inist:fA14><country>Canada</country><placeName><settlement type="city">Montréal</settlement><region type="state">Québec</region></placeName></affiliation><affiliation wicri:level="1"><inist:fA14 i1="03"><s1>Department of Psychiatry, Université de Montréal</s1><s2>Quebec</s2><s3>CAN</s3><sZ>2 aut.</sZ><sZ>4 aut.</sZ></inist:fA14><country>Canada</country><wicri:noRegion>Quebec</wicri:noRegion></affiliation></author></analytic><series><title level="j" type="main">Neurology</title><title level="j" type="abbreviated">Neurology</title><idno type="ISSN">0028-3878</idno><imprint><date when="2010">2010</date></imprint></series></biblStruct></sourceDesc><seriesStmt><title level="j" type="main">Neurology</title><title level="j" type="abbreviated">Neurology</title><idno type="ISSN">0028-3878</idno></seriesStmt></fileDesc><profileDesc><textClass><keywords scheme="KwdEn" xml:lang="en"><term>Aged</term><term>Atonia</term><term>Behavior</term><term>Cohort Studies</term><term>Female</term><term>Follow-Up Studies</term><term>Humans</term><term>Idiopathic</term><term>Longitudinal Studies</term><term>Male</term><term>Middle Aged</term><term>Nervous system diseases</term><term>Parkinson Disease (diagnosis)</term><term>Parkinson Disease (etiology)</term><term>Parkinson Disease (physiopathology)</term><term>Parkinson disease</term><term>Polysomnography (methods)</term><term>Predictive Value of Tests</term><term>REM Sleep Behavior Disorder (complications)</term><term>REM Sleep Behavior Disorder (diagnosis)</term><term>REM Sleep Behavior Disorder (physiopathology)</term><term>Rapid eye movement sleep</term><term>Severity of Illness Index</term><term>Sleep disorder</term><term>Sleep, REM (physiology)</term></keywords><keywords scheme="MESH" qualifier="complications" xml:lang="en"><term>REM Sleep Behavior Disorder</term></keywords><keywords scheme="MESH" qualifier="diagnosis" xml:lang="en"><term>Parkinson Disease</term><term>REM Sleep Behavior Disorder</term></keywords><keywords scheme="MESH" qualifier="etiology" xml:lang="en"><term>Parkinson Disease</term></keywords><keywords scheme="MESH" qualifier="methods" xml:lang="en"><term>Polysomnography</term></keywords><keywords scheme="MESH" qualifier="physiology" xml:lang="en"><term>Sleep, REM</term></keywords><keywords scheme="MESH" qualifier="physiopathology" xml:lang="en"><term>Parkinson Disease</term><term>REM Sleep Behavior Disorder</term></keywords><keywords scheme="MESH" xml:lang="en"><term>Aged</term><term>Cohort Studies</term><term>Female</term><term>Follow-Up Studies</term><term>Humans</term><term>Longitudinal Studies</term><term>Male</term><term>Middle Aged</term><term>Predictive Value of Tests</term><term>Severity of Illness Index</term></keywords><keywords scheme="Pascal" xml:lang="fr"><term>Trouble du sommeil</term><term>Maladie de Parkinson</term><term>Pathologie du système nerveux</term><term>Atonie</term><term>Idiopathique</term><term>Sommeil paradoxal</term><term>Comportement</term></keywords></textClass></profileDesc></teiHeader><front><div type="abstract" xml:lang="en">Background: Over 50% of persons with idiopathic REM sleep behavior disorder (RBD) will develop Parkinson disease (PD) or dementia. At present, there is no way to predict who will develop disease. Since polysomnography is performed in all patients with idiopathic RBD at diagnosis, there is an opportunity to analyze if baseline sleep variables predict eventual neurodegenerative disease. Methods: In a longitudinally studied cohort of patients with idiopathic RBD, we identified those who had developed neurodegenerative disease. These patients were matched by age, sex, and follow-up duration to patients with RBD who remained disease-free and to controls. Polysomnographic variables at baseline (i.e., before development of neurodegenerative disease) were compared between groups. Results: Twenty-six patients who developed neurodegenerative disease were included (PD 12, multiple system atrophy 1, dementia 13). The interval between polysomnogram and disease onset was 6.7 years, mean age was 69.5, and 81% were male. There were no differences between groups in sleep latency, sleep time, % stages 2-4, % REM sleep, or sleep efficiency. However, patients with idiopathic RBD who developed neurodegenerative disease had increased tonic chin EMG activity during REM sleep at baseline compared to those who remained disease-free (62.7 ± 6.0% vs 41.0 ± 6.0%, p = 0.020). This effect was seen only in patients who developed PD (72.9 ± 6.0% vs 41.0 ± 6.0%, p = 0.002), and not in those who developed dementia (54.3 ± 10.3, p = 0.28). There was no difference in phasic submental REM EMG activity between groups. Conclusions: In patients with REM sleep behavior disorder initially free of neurodegenerative disease, the severity of REM atonia loss on baseline polysomnogram predicts the development of Parkinson disease.</div></front></TEI><affiliations><list><country><li>Canada</li></country><region><li>Québec</li></region><settlement><li>Montréal</li></settlement><orgName><li>Université McGill</li></orgName></list><tree><country name="Canada"><region name="Québec"><name sortKey="Postuma, R B" sort="Postuma, R B" uniqKey="Postuma R" first="R. B." last="Postuma">R. B. Postuma</name></region><name sortKey="Gagnon, J F" sort="Gagnon, J F" uniqKey="Gagnon J" first="J. F." last="Gagnon">J. F. Gagnon</name><name sortKey="Gagnon, J F" sort="Gagnon, J F" uniqKey="Gagnon J" first="J. F." last="Gagnon">J. F. Gagnon</name><name sortKey="Montplaisir, J Y" sort="Montplaisir, J Y" uniqKey="Montplaisir J" first="J. Y." last="Montplaisir">J. Y. Montplaisir</name><name sortKey="Montplaisir, J Y" sort="Montplaisir, J Y" uniqKey="Montplaisir J" first="J. Y." last="Montplaisir">J. Y. Montplaisir</name><name sortKey="Postuma, R B" sort="Postuma, R B" uniqKey="Postuma R" first="R. B." last="Postuma">R. B. Postuma</name><name sortKey="Rompre, S" sort="Rompre, S" uniqKey="Rompre S" first="S." last="Rompre">S. Rompre</name></country></tree></affiliations></record>Pour manipuler ce document sous Unix (Dilib)
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