Severity of REM atonia loss in idiopathic REM sleep behavior disorder predicts Parkinson disease
Identifieur interne : 000312 ( PascalFrancis/Checkpoint ); précédent : 000311; suivant : 000313Severity 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.
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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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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. 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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>Atonia</term><term>Behavior</term><term>Idiopathic</term><term>Nervous system diseases</term><term>Parkinson disease</term><term>Rapid eye movement sleep</term><term>Sleep disorder</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><inist><standard h6="B"><pA><fA01 i1="01" i2="1"><s0>0028-3878</s0></fA01><fA02 i1="01"><s0>NEURAI</s0></fA02><fA03 i2="1"><s0>Neurology</s0></fA03><fA05><s2>74</s2></fA05><fA06><s2>3</s2></fA06><fA08 i1="01" i2="1" l="ENG"><s1>Severity of REM atonia loss in idiopathic REM sleep behavior disorder predicts Parkinson disease</s1></fA08><fA11 i1="01" i2="1"><s1>POSTUMA (R. B.)</s1></fA11><fA11 i1="02" i2="1"><s1>GAGNON (J. F.)</s1></fA11><fA11 i1="03" i2="1"><s1>ROMPRE (S.)</s1></fA11><fA11 i1="04" i2="1"><s1>MONTPLAISIR (J. Y.)</s1></fA11><fA14 i1="01"><s1>Department of Neurology, McGill University, Montreal General Hospital</s1><s2>Montreal</s2><s3>CAN</s3><sZ>1 aut.</sZ></fA14><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></fA14><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></fA14><fA20><s1>239-244</s1></fA20><fA21><s1>2010</s1></fA21><fA23 i1="01"><s0>ENG</s0></fA23><fA43 i1="01"><s1>INIST</s1><s2>6345</s2><s5>354000180878260100</s5></fA43><fA44><s0>0000</s0><s1>© 2010 INIST-CNRS. All rights reserved.</s1></fA44><fA45><s0>29 ref.</s0></fA45><fA47 i1="01" i2="1"><s0>10-0094009</s0></fA47><fA60><s1>P</s1></fA60><fA61><s0>A</s0></fA61><fA64 i1="01" i2="1"><s0>Neurology</s0></fA64><fA66 i1="01"><s0>USA</s0></fA66><fC01 i1="01" l="ENG"><s0>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.</s0></fC01><fC02 i1="01" i2="X"><s0>002B17</s0></fC02><fC02 i1="02" i2="X"><s0>002B17G</s0></fC02><fC03 i1="01" i2="X" l="FRE"><s0>Trouble du sommeil</s0><s5>01</s5></fC03><fC03 i1="01" i2="X" l="ENG"><s0>Sleep disorder</s0><s5>01</s5></fC03><fC03 i1="01" i2="X" l="SPA"><s0>Trastorno sueño</s0><s5>01</s5></fC03><fC03 i1="02" i2="X" l="FRE"><s0>Maladie de Parkinson</s0><s2>NM</s2><s5>02</s5></fC03><fC03 i1="02" i2="X" l="ENG"><s0>Parkinson disease</s0><s2>NM</s2><s5>02</s5></fC03><fC03 i1="02" i2="X" l="SPA"><s0>Parkinson enfermedad</s0><s2>NM</s2><s5>02</s5></fC03><fC03 i1="03" i2="X" l="FRE"><s0>Pathologie du système nerveux</s0><s5>03</s5></fC03><fC03 i1="03" i2="X" l="ENG"><s0>Nervous system diseases</s0><s5>03</s5></fC03><fC03 i1="03" i2="X" l="SPA"><s0>Sistema nervioso patología</s0><s5>03</s5></fC03><fC03 i1="04" i2="X" l="FRE"><s0>Atonie</s0><s5>09</s5></fC03><fC03 i1="04" i2="X" l="ENG"><s0>Atonia</s0><s5>09</s5></fC03><fC03 i1="04" i2="X" l="SPA"><s0>Atonía</s0><s5>09</s5></fC03><fC03 i1="05" i2="X" l="FRE"><s0>Idiopathique</s0><s5>10</s5></fC03><fC03 i1="05" i2="X" l="ENG"><s0>Idiopathic</s0><s5>10</s5></fC03><fC03 i1="05" i2="X" l="SPA"><s0>Idiopático</s0><s5>10</s5></fC03><fC03 i1="06" i2="X" l="FRE"><s0>Sommeil paradoxal</s0><s5>11</s5></fC03><fC03 i1="06" i2="X" l="ENG"><s0>Rapid eye movement sleep</s0><s5>11</s5></fC03><fC03 i1="06" i2="X" l="SPA"><s0>Sueño paradojal</s0><s5>11</s5></fC03><fC03 i1="07" i2="X" l="FRE"><s0>Comportement</s0><s5>12</s5></fC03><fC03 i1="07" i2="X" l="ENG"><s0>Behavior</s0><s5>12</s5></fC03><fC03 i1="07" i2="X" l="SPA"><s0>Conducta</s0><s5>12</s5></fC03><fC07 i1="01" i2="X" l="FRE"><s0>Cycle veille sommeil</s0><s5>37</s5></fC07><fC07 i1="01" i2="X" l="ENG"><s0>Sleep wake cycle</s0><s5>37</s5></fC07><fC07 i1="01" i2="X" l="SPA"><s0>Ciclo sueño vigilia</s0><s5>37</s5></fC07><fC07 i1="02" i2="X" l="FRE"><s0>Trouble neurologique</s0><s5>39</s5></fC07><fC07 i1="02" i2="X" l="ENG"><s0>Neurological disorder</s0><s5>39</s5></fC07><fC07 i1="02" i2="X" l="SPA"><s0>Trastorno neurológico</s0><s5>39</s5></fC07><fC07 i1="03" i2="X" l="FRE"><s0>Pathologie de l'encéphale</s0><s5>40</s5></fC07><fC07 i1="03" i2="X" l="ENG"><s0>Cerebral disorder</s0><s5>40</s5></fC07><fC07 i1="03" i2="X" l="SPA"><s0>Encéfalo patología</s0><s5>40</s5></fC07><fC07 i1="04" i2="X" l="FRE"><s0>Syndrome extrapyramidal</s0><s5>41</s5></fC07><fC07 i1="04" i2="X" l="ENG"><s0>Extrapyramidal syndrome</s0><s5>41</s5></fC07><fC07 i1="04" i2="X" l="SPA"><s0>Extrapiramidal síndrome</s0><s5>41</s5></fC07><fC07 i1="05" i2="X" l="FRE"><s0>Maladie dégénérative</s0><s5>42</s5></fC07><fC07 i1="05" i2="X" l="ENG"><s0>Degenerative disease</s0><s5>42</s5></fC07><fC07 i1="05" i2="X" l="SPA"><s0>Enfermedad degenerativa</s0><s5>42</s5></fC07><fC07 i1="06" i2="X" l="FRE"><s0>Pathologie du système nerveux central</s0><s5>43</s5></fC07><fC07 i1="06" i2="X" l="ENG"><s0>Central nervous system disease</s0><s5>43</s5></fC07><fC07 i1="06" i2="X" l="SPA"><s0>Sistema nervosio central patología</s0><s5>43</s5></fC07><fN21><s1>060</s1></fN21><fN44 i1="01"><s1>OTO</s1></fN44><fN82><s1>OTO</s1></fN82></pA></standard></inist><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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