ParkinsonFranceV1, Pmc, Curation, bibRecord, 000122

Does Postural Rigidity Decrease during REM Sleep without Atonia in Parkinson Disease?

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Does Postural Rigidity Decrease during REM Sleep without Atonia in Parkinson Disease?

Auteurs : Dario Arnaldi [France, Italie] ; Alice Latimier [France] ; Smaranda Leu-Semenescu [France] ; Fabrizio De Carli [Italie] ; Marie Vidailhet [France] ; Isabelle Arnulf [France]

Source :

Journal of Clinical Sleep Medicine : JCSM : Official Publication of the American Academy of Sleep Medicine [ 1550-9389 ] ; 2016.

RBID : PMC:4877316

Abstract

Study Objectives:

Rigidity is a muscle hypertonia typical of Parkinson disease (PD), whereas rapid eye movement (REM) sleep behavior disorder (RBD) is characterized by abnormally increased muscle tone during REM sleep (REM sleep without atonia) and enacting dream behaviors. Because movements are not bradykinetic during RBD in patients with PD, we investigated whether the background, wake postural rigidity is attenuated during REM sleep without atonia, in absence of movement.

Methods:

The amplitude of levator menti (postural muscle) electromyographic activity during relaxed evening wakefulness (considered as reference) and sleep (N2, N3, atonic REM sleep, and quiet REM sleep without atonia) was measured in 20 patients with PD (with and without RBD), 10 patients with idiopathic RBD patients and 10 healthy subjects.

Results:

The chin tone amplitude progressively decreased from wake to N2, N3, and atonic REM sleep in the four groups, but the highest amplitude was observed in PD patients with RBD during atonic REM sleep. Furthermore, chin muscle tone amplitude did not attenuate from wake to REM sleep without atonia in patients with both PD and RBD but dramatically attenuated (by 40% on average) in patients with idiopathic RBD.

Conclusions:

The high amplitude of chin muscle tone in PD with RBD (but not in idiopathic RBD) during REM sleep with and without atonia suggests that both PD-related hypertonia and RBD-related enhanced muscle tone coexist during REM sleep, together affecting chin muscle tone. Consequently, some rapid RBD movements likely start against a rigid postural tone.

Citation:

Arnaldi D, Latimier A, Leu-Semenescu S, De Carli F, Vidailhet M, Arnulf I. Does postural rigidity decrease during REM sleep without atonia in Parkinson disease? J Clin Sleep Med 2016;12(6):839–847.

Url:

http://www.ncbi.nlm.nih.gov/pmc/articles/PMC4877316

DOI: 10.5664/jcsm.5882
PubMed: 26857056
PubMed Central: 4877316

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<series><title level="j">Journal of Clinical Sleep Medicine : JCSM : Official Publication of the American Academy of Sleep Medicine</title>
<idno type="ISSN">1550-9389</idno>
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<front><div type="abstract" xml:lang="en"><sec><title>Study Objectives:</title>
<p>Rigidity is a muscle hypertonia typical of Parkinson disease (PD), whereas rapid eye movement (REM) sleep behavior disorder (RBD) is characterized by abnormally increased muscle tone during REM sleep (REM sleep without atonia) and enacting dream behaviors. Because movements are not bradykinetic during RBD in patients with PD, we investigated whether the background, wake postural rigidity is attenuated during REM sleep without atonia, in absence of movement.</p>
</sec>
<sec><title>Methods:</title>
<p>The amplitude of levator menti (postural muscle) electromyographic activity during relaxed evening wakefulness (considered as reference) and sleep (N2, N3, atonic REM sleep, and quiet REM sleep without atonia) was measured in 20 patients with PD (with and without RBD), 10 patients with idiopathic RBD patients and 10 healthy subjects.</p>
</sec>
<sec><title>Results:</title>
<p>The chin tone amplitude progressively decreased from wake to N2, N3, and atonic REM sleep in the four groups, but the highest amplitude was observed in PD patients with RBD during atonic REM sleep. Furthermore, chin muscle tone amplitude did not attenuate from wake to REM sleep without atonia in patients with both PD and RBD but dramatically attenuated (by 40% on average) in patients with idiopathic RBD.</p>
</sec>
<sec><title>Conclusions:</title>
<p>The high amplitude of chin muscle tone in PD with RBD (but not in idiopathic RBD) during REM sleep with and without atonia suggests that both PD-related hypertonia and RBD-related enhanced muscle tone coexist during REM sleep, together affecting chin muscle tone. Consequently, some rapid RBD movements likely start against a rigid postural tone.</p>
</sec>
<sec><title>Citation:</title>
<p>Arnaldi D, Latimier A, Leu-Semenescu S, De Carli F, Vidailhet M, Arnulf I. Does postural rigidity decrease during REM sleep without atonia in Parkinson disease? <italic>J Clin Sleep Med</italic>
 2016;12(6):839–847.</p>
</sec>
</div>
</front>
</TEI>
<pmc article-type="research-article"><pmc-comment>The publisher of this article does not allow downloading of the full text in XML form.</pmc-comment>
  <front><journal-meta><journal-id journal-id-type="nlm-ta">J Clin Sleep Med</journal-id>
<journal-id journal-id-type="iso-abbrev">J Clin Sleep Med</journal-id>
<journal-id journal-id-type="publisher-id">JCSM</journal-id>
<journal-title-group><journal-title>Journal of Clinical Sleep Medicine : JCSM : Official Publication of the American Academy of Sleep Medicine</journal-title>
</journal-title-group>
<issn pub-type="ppub">1550-9389</issn>
<issn pub-type="epub">1550-9397</issn>
<publisher><publisher-name>American Academy of Sleep Medicine</publisher-name>
</publisher>
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<article-meta><article-id pub-id-type="pmid">26857056</article-id>
<article-id pub-id-type="pmc">4877316</article-id>
<article-id pub-id-type="publisher-id">jc-00334-15</article-id>
<article-id pub-id-type="doi">10.5664/jcsm.5882</article-id>
<article-categories><subj-group subj-group-type="heading"><subject>Scientific Investigations</subject>
</subj-group>
</article-categories>
<title-group><article-title>Does Postural Rigidity Decrease during REM Sleep without Atonia in Parkinson Disease?</article-title>
</title-group>
<contrib-group><contrib contrib-type="author"><name><surname>Arnaldi</surname>
<given-names>Dario</given-names>
</name>
<degrees>MD</degrees>
<xref ref-type="aff" rid="aff1"><sup>1</sup>
</xref>
<xref ref-type="aff" rid="aff2"><sup>2</sup>
</xref>
</contrib>
<contrib contrib-type="author"><name><surname>Latimier</surname>
<given-names>Alice</given-names>
</name>
<degrees>MS</degrees>
<xref ref-type="aff" rid="aff3"><sup>3</sup>
</xref>
</contrib>
<contrib contrib-type="author"><name><surname>Leu-Semenescu</surname>
<given-names>Smaranda</given-names>
</name>
<degrees>MD</degrees>
<xref ref-type="aff" rid="aff1"><sup>1</sup>
</xref>
<xref ref-type="aff" rid="aff3"><sup>3</sup>
</xref>
</contrib>
<contrib contrib-type="author"><name><surname>De Carli</surname>
<given-names>Fabrizio</given-names>
</name>
<degrees>MPhys</degrees>
<xref ref-type="aff" rid="aff4"><sup>4</sup>
</xref>
</contrib>
<contrib contrib-type="author"><name><surname>Vidailhet</surname>
<given-names>Marie</given-names>
</name>
<degrees>MD, PhD</degrees>
<xref ref-type="aff" rid="aff3"><sup>3</sup>
</xref>
<xref ref-type="aff" rid="aff5"><sup>5</sup>
</xref>
</contrib>
<contrib contrib-type="author"><name><surname>Arnulf</surname>
<given-names>Isabelle</given-names>
</name>
<degrees>MD, PhD</degrees>
<xref ref-type="aff" rid="aff1"><sup>1</sup>
</xref>
<xref ref-type="aff" rid="aff3"><sup>3</sup>
</xref>
<xref ref-type="corresp" rid="cor1"></xref>
</contrib>
<aff id="aff1"><label>1</label>
APHP- Pitié-Salpêtrière Hospital, Sleep Disorders Unit, Paris, France</aff>
<aff id="aff2"><label>2</label>
Clinical Neurology, Department of Neuroscience (DINOGMI), University of Genoa, Italy</aff>
<aff id="aff3"><label>3</label>
Brain Research Institute- UPMC Paris 6 Univ, Inserm U 1127; CNRS UMR 7225, IHU neuroscience, Paris, France</aff>
<aff id="aff4"><label>4</label>
Institute of Bioimaging and Molecular Physiology, National Research Council, Genoa, Italy</aff>
<aff id="aff5"><label>5</label>
APHP- Pitié-Salpêtrière Hospital, Neurology Department, Paris, France</aff>
</contrib-group>
<author-notes><corresp id="cor1">Address correspondence to: Isabelle Arnulf, MD, <addr-line>Service des Pathologies du Sommeil, Hôpital Pitié-Salpêtrière, 47-83 Boulevard de l'Hôpital, 75651 Paris Cedex 13, France</addr-line>
<phone>33 1 42 16 77 02</phone>
<fax>33 1 42 16 77 00</fax>
<email>isabelle.arnulf@aphp.fr</email>
</corresp>
</author-notes>
<pub-date pub-type="epub"><day>15</day>
<month>6</month>
<year>2016</year>
</pub-date>
<volume>12</volume>
<issue>6</issue>
<fpage>839</fpage>
<lpage>847</lpage>
<history><date date-type="received"><month>8</month>
<year>2015</year>
</date>
<date date-type="rev-recd"><month>1</month>
<year>2016</year>
</date>
<date date-type="accepted"><month>1</month>
<year>2016</year>
</date>
</history>
<permissions><copyright-statement>© 2016 American Academy of Sleep Medicine</copyright-statement>
<copyright-year>2016</copyright-year>
</permissions>
<abstract><sec><title>Study Objectives:</title>
<p>Rigidity is a muscle hypertonia typical of Parkinson disease (PD), whereas rapid eye movement (REM) sleep behavior disorder (RBD) is characterized by abnormally increased muscle tone during REM sleep (REM sleep without atonia) and enacting dream behaviors. Because movements are not bradykinetic during RBD in patients with PD, we investigated whether the background, wake postural rigidity is attenuated during REM sleep without atonia, in absence of movement.</p>
</sec>
<sec><title>Methods:</title>
<p>The amplitude of levator menti (postural muscle) electromyographic activity during relaxed evening wakefulness (considered as reference) and sleep (N2, N3, atonic REM sleep, and quiet REM sleep without atonia) was measured in 20 patients with PD (with and without RBD), 10 patients with idiopathic RBD patients and 10 healthy subjects.</p>
</sec>
<sec><title>Results:</title>
<p>The chin tone amplitude progressively decreased from wake to N2, N3, and atonic REM sleep in the four groups, but the highest amplitude was observed in PD patients with RBD during atonic REM sleep. Furthermore, chin muscle tone amplitude did not attenuate from wake to REM sleep without atonia in patients with both PD and RBD but dramatically attenuated (by 40% on average) in patients with idiopathic RBD.</p>
</sec>
<sec><title>Conclusions:</title>
<p>The high amplitude of chin muscle tone in PD with RBD (but not in idiopathic RBD) during REM sleep with and without atonia suggests that both PD-related hypertonia and RBD-related enhanced muscle tone coexist during REM sleep, together affecting chin muscle tone. Consequently, some rapid RBD movements likely start against a rigid postural tone.</p>
</sec>
<sec><title>Citation:</title>
<p>Arnaldi D, Latimier A, Leu-Semenescu S, De Carli F, Vidailhet M, Arnulf I. Does postural rigidity decrease during REM sleep without atonia in Parkinson disease? <italic>J Clin Sleep Med</italic>
 2016;12(6):839–847.</p>
</sec>
</abstract>
<kwd-group><kwd>REM sleep behavior disorder</kwd>
<kwd>synucleinopathy</kwd>
</kwd-group>
</article-meta>
</front>
</pmc>
</record>

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	La maladie de Parkinson en France (serveur d'exploration)
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La maladie de Parkinson en France (serveur d'exploration)

Does Postural Rigidity Decrease during REM Sleep without Atonia in Parkinson Disease?

Does Postural Rigidity Decrease during REM Sleep without Atonia in Parkinson Disease?

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