Postprandial hypotension and parkinsonian state in Parkinson's disease.
Identifieur interne : 004571 ( PubMed/Corpus ); précédent : 004570; suivant : 004572Postprandial hypotension and parkinsonian state in Parkinson's disease.
Auteurs : K R Chaudhuri ; C. Ellis ; S. Love-Jones ; T. Thomaides ; S. Clift ; C J Mathias ; J D ParkesSource :
- Movement disorders : official journal of the Movement Disorder Society [ 0885-3185 ] ; 1997.
English descriptors
- KwdEn :
- Adult, Aged, Autonomic Nervous System Diseases (complications), Autonomic Nervous System Diseases (physiopathology), Blood Glucose, Energy Intake, Humans, Hypotension (complications), Hypotension (diagnosis), Insulin (blood), Male, Middle Aged, Motor Activity, Parkinson Disease (complications), Parkinson Disease (physiopathology), Parkinson Disease, Secondary (complications), Parkinson Disease, Secondary (physiopathology), Severity of Illness Index, Time Factors.
- MESH :
- chemical , blood : Insulin.
- chemical : Blood Glucose.
- complications : Autonomic Nervous System Diseases, Hypotension, Parkinson Disease, Parkinson Disease, Secondary.
- diagnosis : Hypotension.
- physiopathology : Autonomic Nervous System Diseases, Parkinson Disease, Parkinson Disease, Secondary.
- Adult, Aged, Energy Intake, Humans, Male, Middle Aged, Motor Activity, Severity of Illness Index, Time Factors.
Abstract
Abnormal postprandial cardiovascular responses such as postprandial hypotension (PPH) occur in primary autonomic failure and contribute significantly to morbidity. The extent and frequency of PPH and its relationship to the parkinsonian state in idiopathic Parkinson's disease (IPD) is unknown. By studying 20 patients with IPD (without autonomic failure) and 16 age-matched controls after both groups ingested a standard isocaloric balanced liquid meal, we have shown that supine PPH complicates IPD and is related to marked worsening of the parkinsonian state as measured by a cumulative score of tremor, rigidity, bradykinesia, posture, and gait. Furthermore, significant postural hypotension is unmasked that results in postural intolerance due to presyncopal symptoms. Our study indicates that, in patients with IPD, ingestion of a meal may lead to abnormal postprandial cardiovascular responses and aggravation of the parkinsonian stage. The underlying mechanisms are unclear, although vasodilatory gut peptides released in response to food ingestion may be contributory.
DOI: 10.1002/mds.870120608
PubMed: 9399210
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Clift</name></author><author><name sortKey="Mathias, C J" sort="Mathias, C J" uniqKey="Mathias C" first="C J" last="Mathias">C J Mathias</name></author><author><name sortKey="Parkes, J D" sort="Parkes, J D" uniqKey="Parkes J" first="J D" last="Parkes">J D Parkes</name></author></titleStmt><publicationStmt><idno type="wicri:source">PubMed</idno><date when="1997">1997</date><idno type="RBID">pubmed:9399210</idno><idno type="pmid">9399210</idno><idno type="doi">10.1002/mds.870120608</idno><idno type="wicri:Area/PubMed/Corpus">004571</idno></publicationStmt><sourceDesc><biblStruct><analytic><title xml:lang="en">Postprandial hypotension and parkinsonian state in Parkinson's disease.</title><author><name sortKey="Chaudhuri, K R" sort="Chaudhuri, K R" uniqKey="Chaudhuri K" first="K R" last="Chaudhuri">K R Chaudhuri</name><affiliation><nlm:affiliation>University Department of Neurology, Institute of Psychiatry, London, England.</nlm:affiliation></affiliation></author><author><name sortKey="Ellis, C" sort="Ellis, C" uniqKey="Ellis C" first="C" last="Ellis">C. Ellis</name></author><author><name sortKey="Love Jones, S" sort="Love Jones, S" uniqKey="Love Jones S" first="S" last="Love-Jones">S. Love-Jones</name></author><author><name sortKey="Thomaides, T" sort="Thomaides, T" uniqKey="Thomaides T" first="T" last="Thomaides">T. Thomaides</name></author><author><name sortKey="Clift, S" sort="Clift, S" uniqKey="Clift S" first="S" last="Clift">S. Clift</name></author><author><name sortKey="Mathias, C J" sort="Mathias, C J" uniqKey="Mathias C" first="C J" last="Mathias">C J Mathias</name></author><author><name sortKey="Parkes, J D" sort="Parkes, J D" uniqKey="Parkes J" first="J D" last="Parkes">J D Parkes</name></author></analytic><series><title level="j">Movement disorders : official journal of the Movement Disorder Society</title><idno type="ISSN">0885-3185</idno><imprint><date when="1997" type="published">1997</date></imprint></series></biblStruct></sourceDesc></fileDesc><profileDesc><textClass><keywords scheme="KwdEn" xml:lang="en"><term>Adult</term><term>Aged</term><term>Autonomic Nervous System Diseases (complications)</term><term>Autonomic Nervous System Diseases (physiopathology)</term><term>Blood Glucose</term><term>Energy Intake</term><term>Humans</term><term>Hypotension (complications)</term><term>Hypotension (diagnosis)</term><term>Insulin (blood)</term><term>Male</term><term>Middle Aged</term><term>Motor Activity</term><term>Parkinson Disease (complications)</term><term>Parkinson Disease (physiopathology)</term><term>Parkinson Disease, Secondary (complications)</term><term>Parkinson Disease, Secondary (physiopathology)</term><term>Severity of Illness Index</term><term>Time Factors</term></keywords><keywords scheme="MESH" type="chemical" qualifier="blood" xml:lang="en"><term>Insulin</term></keywords><keywords scheme="MESH" type="chemical" xml:lang="en"><term>Blood Glucose</term></keywords><keywords scheme="MESH" qualifier="complications" xml:lang="en"><term>Autonomic Nervous System Diseases</term><term>Hypotension</term><term>Parkinson Disease</term><term>Parkinson Disease, Secondary</term></keywords><keywords scheme="MESH" qualifier="diagnosis" xml:lang="en"><term>Hypotension</term></keywords><keywords scheme="MESH" qualifier="physiopathology" xml:lang="en"><term>Autonomic Nervous System Diseases</term><term>Parkinson Disease</term><term>Parkinson Disease, Secondary</term></keywords><keywords scheme="MESH" xml:lang="en"><term>Adult</term><term>Aged</term><term>Energy Intake</term><term>Humans</term><term>Male</term><term>Middle Aged</term><term>Motor Activity</term><term>Severity of Illness Index</term><term>Time Factors</term></keywords></textClass></profileDesc></teiHeader><front><div type="abstract" xml:lang="en">Abnormal postprandial cardiovascular responses such as postprandial hypotension (PPH) occur in primary autonomic failure and contribute significantly to morbidity. The extent and frequency of PPH and its relationship to the parkinsonian state in idiopathic Parkinson's disease (IPD) is unknown. By studying 20 patients with IPD (without autonomic failure) and 16 age-matched controls after both groups ingested a standard isocaloric balanced liquid meal, we have shown that supine PPH complicates IPD and is related to marked worsening of the parkinsonian state as measured by a cumulative score of tremor, rigidity, bradykinesia, posture, and gait. Furthermore, significant postural hypotension is unmasked that results in postural intolerance due to presyncopal symptoms. Our study indicates that, in patients with IPD, ingestion of a meal may lead to abnormal postprandial cardiovascular responses and aggravation of the parkinsonian stage. The underlying mechanisms are unclear, although vasodilatory gut peptides released in response to food ingestion may be contributory.</div></front></TEI><pubmed><MedlineCitation Owner="NLM" Status="MEDLINE"><PMID Version="1">9399210</PMID><DateCreated><Year>1998</Year><Month>02</Month><Day>10</Day></DateCreated><DateCompleted><Year>1998</Year><Month>02</Month><Day>10</Day></DateCompleted><DateRevised><Year>2011</Year><Month>11</Month><Day>17</Day></DateRevised><Article PubModel="Print"><Journal><ISSN IssnType="Print">0885-3185</ISSN><JournalIssue CitedMedium="Print"><Volume>12</Volume><Issue>6</Issue><PubDate><Year>1997</Year><Month>Nov</Month></PubDate></JournalIssue><Title>Movement disorders : official journal of the Movement Disorder Society</Title><ISOAbbreviation>Mov. Disord.</ISOAbbreviation></Journal><ArticleTitle>Postprandial hypotension and parkinsonian state in Parkinson's disease.</ArticleTitle><Pagination><MedlinePgn>877-84</MedlinePgn></Pagination><Abstract><AbstractText>Abnormal postprandial cardiovascular responses such as postprandial hypotension (PPH) occur in primary autonomic failure and contribute significantly to morbidity. The extent and frequency of PPH and its relationship to the parkinsonian state in idiopathic Parkinson's disease (IPD) is unknown. By studying 20 patients with IPD (without autonomic failure) and 16 age-matched controls after both groups ingested a standard isocaloric balanced liquid meal, we have shown that supine PPH complicates IPD and is related to marked worsening of the parkinsonian state as measured by a cumulative score of tremor, rigidity, bradykinesia, posture, and gait. Furthermore, significant postural hypotension is unmasked that results in postural intolerance due to presyncopal symptoms. Our study indicates that, in patients with IPD, ingestion of a meal may lead to abnormal postprandial cardiovascular responses and aggravation of the parkinsonian stage. The underlying mechanisms are unclear, although vasodilatory gut peptides released in response to food ingestion may be contributory.</AbstractText></Abstract><AuthorList CompleteYN="Y"><Author ValidYN="Y"><LastName>Chaudhuri</LastName><ForeName>K R</ForeName><Initials>KR</Initials><AffiliationInfo><Affiliation>University Department of Neurology, Institute of Psychiatry, London, England.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Ellis</LastName><ForeName>C</ForeName><Initials>C</Initials></Author><Author ValidYN="Y"><LastName>Love-Jones</LastName><ForeName>S</ForeName><Initials>S</Initials></Author><Author ValidYN="Y"><LastName>Thomaides</LastName><ForeName>T</ForeName><Initials>T</Initials></Author><Author ValidYN="Y"><LastName>Clift</LastName><ForeName>S</ForeName><Initials>S</Initials></Author><Author ValidYN="Y"><LastName>Mathias</LastName><ForeName>C J</ForeName><Initials>CJ</Initials></Author><Author ValidYN="Y"><LastName>Parkes</LastName><ForeName>J D</ForeName><Initials>JD</Initials></Author></AuthorList><Language>eng</Language><PublicationTypeList><PublicationType UI="D003160">Comparative Study</PublicationType><PublicationType UI="D016428">Journal Article</PublicationType></PublicationTypeList></Article><MedlineJournalInfo><Country>UNITED STATES</Country><MedlineTA>Mov Disord</MedlineTA><NlmUniqueID>8610688</NlmUniqueID><ISSNLinking>0885-3185</ISSNLinking></MedlineJournalInfo><ChemicalList><Chemical><RegistryNumber>0</RegistryNumber><NameOfSubstance UI="D001786">Blood Glucose</NameOfSubstance></Chemical><Chemical><RegistryNumber>0</RegistryNumber><NameOfSubstance UI="D007328">Insulin</NameOfSubstance></Chemical></ChemicalList><CitationSubset>IM</CitationSubset><MeshHeadingList><MeshHeading><DescriptorName MajorTopicYN="N" UI="D000328">Adult</DescriptorName></MeshHeading><MeshHeading><DescriptorName MajorTopicYN="N" UI="D000368">Aged</DescriptorName></MeshHeading><MeshHeading><DescriptorName MajorTopicYN="N" UI="D001342">Autonomic Nervous System Diseases</DescriptorName><QualifierName MajorTopicYN="N" UI="Q000150">complications</QualifierName><QualifierName MajorTopicYN="N" UI="Q000503">physiopathology</QualifierName></MeshHeading><MeshHeading><DescriptorName MajorTopicYN="N" UI="D001786">Blood Glucose</DescriptorName></MeshHeading><MeshHeading><DescriptorName MajorTopicYN="Y" UI="D002149">Energy Intake</DescriptorName></MeshHeading><MeshHeading><DescriptorName MajorTopicYN="N" UI="D006801">Humans</DescriptorName></MeshHeading><MeshHeading><DescriptorName MajorTopicYN="N" UI="D007022">Hypotension</DescriptorName><QualifierName MajorTopicYN="N" UI="Q000150">complications</QualifierName><QualifierName MajorTopicYN="Y" UI="Q000175">diagnosis</QualifierName></MeshHeading><MeshHeading><DescriptorName MajorTopicYN="N" UI="D007328">Insulin</DescriptorName><QualifierName MajorTopicYN="N" UI="Q000097">blood</QualifierName></MeshHeading><MeshHeading><DescriptorName MajorTopicYN="N" UI="D008297">Male</DescriptorName></MeshHeading><MeshHeading><DescriptorName MajorTopicYN="N" UI="D008875">Middle Aged</DescriptorName></MeshHeading><MeshHeading><DescriptorName MajorTopicYN="N" UI="D009043">Motor Activity</DescriptorName></MeshHeading><MeshHeading><DescriptorName MajorTopicYN="N" UI="D010300">Parkinson Disease</DescriptorName><QualifierName MajorTopicYN="Y" UI="Q000150">complications</QualifierName><QualifierName MajorTopicYN="N" UI="Q000503">physiopathology</QualifierName></MeshHeading><MeshHeading><DescriptorName MajorTopicYN="N" UI="D010302">Parkinson Disease, Secondary</DescriptorName><QualifierName MajorTopicYN="Y" UI="Q000150">complications</QualifierName><QualifierName MajorTopicYN="N" UI="Q000503">physiopathology</QualifierName></MeshHeading><MeshHeading><DescriptorName MajorTopicYN="N" UI="D012720">Severity of Illness Index</DescriptorName></MeshHeading><MeshHeading><DescriptorName MajorTopicYN="N" UI="D013997">Time Factors</DescriptorName></MeshHeading></MeshHeadingList></MedlineCitation><PubmedData><History><PubMedPubDate PubStatus="pubmed"><Year>1997</Year><Month>12</Month><Day>17</Day></PubMedPubDate><PubMedPubDate PubStatus="medline"><Year>1997</Year><Month>12</Month><Day>17</Day><Hour>0</Hour><Minute>1</Minute></PubMedPubDate><PubMedPubDate PubStatus="entrez"><Year>1997</Year><Month>12</Month><Day>17</Day><Hour>0</Hour><Minute>0</Minute></PubMedPubDate></History><PublicationStatus>ppublish</PublicationStatus><ArticleIdList><ArticleId IdType="pubmed">9399210</ArticleId><ArticleId IdType="doi">10.1002/mds.870120608</ArticleId></ArticleIdList></PubmedData></pubmed></record>Pour manipuler ce document sous Unix (Dilib)
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