Brainstem respiratory control: substrates of respiratory failure of multiple system atrophy.
Identifieur interne : 002936 ( PubMed/Checkpoint ); précédent : 002935; suivant : 002937Brainstem respiratory control: substrates of respiratory failure of multiple system atrophy.
Auteurs : Eduardo E. Benarroch [États-Unis]Source :
- Movement disorders : official journal of the Movement Disorder Society [ 0885-3185 ] ; 2007.
English descriptors
- KwdEn :
- Apnea (complications), Apnea (physiopathology), Brain Stem (metabolism), Brain Stem (physiology), Catecholamines (deficiency), Glutamic Acid (metabolism), Humans, Multiple System Atrophy (complications), Multiple System Atrophy (physiopathology), Muscle Weakness (physiopathology), Muscle, Skeletal (physiopathology), Neurons (metabolism), Periodicity, Pons (metabolism), Receptors, Neurokinin-1 (metabolism), Respiratory Insufficiency (complications), Respiratory Insufficiency (metabolism), Respiratory Insufficiency (physiopathology), Respiratory Physiological Phenomena, Respiratory Sounds (physiopathology), Serotonin (metabolism), Solitary Nucleus (metabolism).
- MESH :
- chemical , deficiency : Catecholamines.
- complications : Apnea, Multiple System Atrophy, Respiratory Insufficiency.
- metabolism : Brain Stem, Glutamic Acid, Neurons, Pons, Receptors, Neurokinin-1, Respiratory Insufficiency, Serotonin, Solitary Nucleus.
- physiology : Brain Stem.
- physiopathology : Apnea, Multiple System Atrophy, Muscle Weakness, Muscle, Skeletal, Respiratory Insufficiency, Respiratory Sounds.
- Humans, Periodicity, Respiratory Physiological Phenomena.
Abstract
Multiple system atrophy may manifest with severe respiratory disorders, including sleep apnea and laryngeal stridor, which reflect a failure of automatic control of respiration. This function depends on a pontomedullary network of interconnected neurons located in the parabrachial/Kölliker Fuse nucleus in the pons, nucleus of the solitary tract, and ventrolateral medulla. Neurons in the preBötzinger complex expressing neurokinin-1 receptors are critically involved in respiratory rhythmogenesis, whereas serotonergic neurons in the medullary raphe and glutamatergic neurons located close to the ventral medullary surface are involved in central chemosensitivity to hypercapnia, hypoxia, or both. Pathological studies using selective neurochemical markers indicate that these neuronal groups are affected in multiple system atrophy. This finding may provide potential anatomical substrates for the respiratory manifestations of the disease.
DOI: 10.1002/mds.21236
PubMed: 17133520
Affiliations:
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This function depends on a pontomedullary network of interconnected neurons located in the parabrachial/Kölliker Fuse nucleus in the pons, nucleus of the solitary tract, and ventrolateral medulla. Neurons in the preBötzinger complex expressing neurokinin-1 receptors are critically involved in respiratory rhythmogenesis, whereas serotonergic neurons in the medullary raphe and glutamatergic neurons located close to the ventral medullary surface are involved in central chemosensitivity to hypercapnia, hypoxia, or both. Pathological studies using selective neurochemical markers indicate that these neuronal groups are affected in multiple system atrophy. This finding may provide potential anatomical substrates for the respiratory manifestations of the disease.</div></front></TEI><pubmed><MedlineCitation Owner="NLM" Status="MEDLINE"><PMID Version="1">17133520</PMID><DateCreated><Year>2007</Year><Month>02</Month><Day>05</Day></DateCreated><DateCompleted><Year>2007</Year><Month>03</Month><Day>23</Day></DateCompleted><DateRevised><Year>2013</Year><Month>11</Month><Day>21</Day></DateRevised><Article PubModel="Print"><Journal><ISSN IssnType="Print">0885-3185</ISSN><JournalIssue CitedMedium="Print"><Volume>22</Volume><Issue>2</Issue><PubDate><Year>2007</Year><Month>Jan</Month><Day>15</Day></PubDate></JournalIssue><Title>Movement disorders : official journal of the Movement Disorder Society</Title><ISOAbbreviation>Mov. Disord.</ISOAbbreviation></Journal><ArticleTitle>Brainstem respiratory control: substrates of respiratory failure of multiple system atrophy.</ArticleTitle><Pagination><MedlinePgn>155-61</MedlinePgn></Pagination><Abstract><AbstractText>Multiple system atrophy may manifest with severe respiratory disorders, including sleep apnea and laryngeal stridor, which reflect a failure of automatic control of respiration. This function depends on a pontomedullary network of interconnected neurons located in the parabrachial/Kölliker Fuse nucleus in the pons, nucleus of the solitary tract, and ventrolateral medulla. Neurons in the preBötzinger complex expressing neurokinin-1 receptors are critically involved in respiratory rhythmogenesis, whereas serotonergic neurons in the medullary raphe and glutamatergic neurons located close to the ventral medullary surface are involved in central chemosensitivity to hypercapnia, hypoxia, or both. Pathological studies using selective neurochemical markers indicate that these neuronal groups are affected in multiple system atrophy. This finding may provide potential anatomical substrates for the respiratory manifestations of the disease.</AbstractText><CopyrightInformation>(c) 2006 Movement Disorder Society.</CopyrightInformation></Abstract><AuthorList CompleteYN="Y"><Author ValidYN="Y"><LastName>Benarroch</LastName><ForeName>Eduardo E</ForeName><Initials>EE</Initials><AffiliationInfo><Affiliation>Mayo Clinic, Department of Neurology, Rochester, Minnesota 55905, USA. benarroch.eduardo@mayo.edu</Affiliation></AffiliationInfo></Author></AuthorList><Language>eng</Language><GrantList CompleteYN="Y"><Grant><GrantID>P01 NS32352-P2</GrantID><Acronym>NS</Acronym><Agency>NINDS NIH HHS</Agency><Country>United States</Country></Grant></GrantList><PublicationTypeList><PublicationType UI="D016428">Journal Article</PublicationType><PublicationType UI="D052061">Research Support, N.I.H., Extramural</PublicationType><PublicationType 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UI="Q000503">physiopathology</QualifierName></MeshHeading><MeshHeading><DescriptorName MajorTopicYN="N" UI="D018908">Muscle Weakness</DescriptorName><QualifierName MajorTopicYN="N" UI="Q000503">physiopathology</QualifierName></MeshHeading><MeshHeading><DescriptorName MajorTopicYN="N" UI="D018482">Muscle, Skeletal</DescriptorName><QualifierName MajorTopicYN="N" UI="Q000503">physiopathology</QualifierName></MeshHeading><MeshHeading><DescriptorName MajorTopicYN="N" UI="D009474">Neurons</DescriptorName><QualifierName MajorTopicYN="N" UI="Q000378">metabolism</QualifierName></MeshHeading><MeshHeading><DescriptorName MajorTopicYN="N" UI="D010507">Periodicity</DescriptorName></MeshHeading><MeshHeading><DescriptorName MajorTopicYN="N" UI="D011149">Pons</DescriptorName><QualifierName MajorTopicYN="N" UI="Q000378">metabolism</QualifierName></MeshHeading><MeshHeading><DescriptorName MajorTopicYN="N" UI="D018040">Receptors, Neurokinin-1</DescriptorName><QualifierName MajorTopicYN="N" UI="Q000378">metabolism</QualifierName></MeshHeading><MeshHeading><DescriptorName MajorTopicYN="N" UI="D012131">Respiratory Insufficiency</DescriptorName><QualifierName MajorTopicYN="Y" UI="Q000150">complications</QualifierName><QualifierName MajorTopicYN="N" UI="Q000378">metabolism</QualifierName><QualifierName MajorTopicYN="Y" UI="Q000503">physiopathology</QualifierName></MeshHeading><MeshHeading><DescriptorName MajorTopicYN="Y" UI="D012143">Respiratory Physiological Phenomena</DescriptorName></MeshHeading><MeshHeading><DescriptorName MajorTopicYN="N" UI="D012135">Respiratory Sounds</DescriptorName><QualifierName MajorTopicYN="N" UI="Q000503">physiopathology</QualifierName></MeshHeading><MeshHeading><DescriptorName MajorTopicYN="N" UI="D012701">Serotonin</DescriptorName><QualifierName MajorTopicYN="N" UI="Q000378">metabolism</QualifierName></MeshHeading><MeshHeading><DescriptorName MajorTopicYN="N" UI="D017552">Solitary Nucleus</DescriptorName><QualifierName MajorTopicYN="N" UI="Q000378">metabolism</QualifierName></MeshHeading></MeshHeadingList><NumberOfReferences>68</NumberOfReferences></MedlineCitation><PubmedData><History><PubMedPubDate PubStatus="pubmed"><Year>2006</Year><Month>11</Month><Day>30</Day><Hour>9</Hour><Minute>0</Minute></PubMedPubDate><PubMedPubDate PubStatus="medline"><Year>2007</Year><Month>3</Month><Day>24</Day><Hour>9</Hour><Minute>0</Minute></PubMedPubDate><PubMedPubDate PubStatus="entrez"><Year>2006</Year><Month>11</Month><Day>30</Day><Hour>9</Hour><Minute>0</Minute></PubMedPubDate></History><PublicationStatus>ppublish</PublicationStatus><ArticleIdList><ArticleId IdType="doi">10.1002/mds.21236</ArticleId><ArticleId IdType="pubmed">17133520</ArticleId></ArticleIdList></PubmedData></pubmed><affiliations><list><country><li>États-Unis</li></country></list><tree><country name="États-Unis"><noRegion><name sortKey="Benarroch, Eduardo E" sort="Benarroch, Eduardo E" uniqKey="Benarroch E" first="Eduardo E" last="Benarroch">Eduardo E. 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