Extrapyramidal symptoms in Wilson's disease are associated with olfactory dysfunction.
Identifieur interne : 001731 ( Ncbi/Merge ); précédent : 001730; suivant : 001732Extrapyramidal symptoms in Wilson's disease are associated with olfactory dysfunction.
Auteurs : Antje Mueller [Allemagne] ; Ulrike Reuner ; Basile Landis ; Hagen Kitzler ; Heinz Reichmann ; Thomas HummelSource :
- Movement disorders : official journal of the Movement Disorder Society [ 0885-3185 ] ; 2006.
English descriptors
- KwdEn :
- Adult, Aged, Basal Ganglia (physiopathology), Basal Ganglia Diseases (diagnosis), Basal Ganglia Diseases (genetics), Basal Ganglia Diseases (physiopathology), Blood Glucose (metabolism), Chromosome Aberrations, Copper (metabolism), Extrapyramidal Tracts (physiopathology), Female, Fluorodeoxyglucose F18 (diagnostic use), Genes, Recessive, Hepatolenticular Degeneration (diagnosis), Hepatolenticular Degeneration (genetics), Hepatolenticular Degeneration (physiopathology), Humans, Magnetic Resonance Imaging, Male, Middle Aged, Neurodegenerative Diseases (diagnosis), Neurodegenerative Diseases (genetics), Neurodegenerative Diseases (physiopathology), Olfaction Disorders (diagnosis), Olfaction Disorders (genetics), Olfaction Disorders (physiopathology), Olfactory Pathways (physiopathology), Parkinsonian Disorders (diagnosis), Parkinsonian Disorders (genetics), Parkinsonian Disorders (physiopathology), Positron-Emission Tomography, Sensory Thresholds (physiology), Statistics as Topic.
- MESH :
- chemical , diagnostic use : Fluorodeoxyglucose F18.
- chemical , metabolism : Blood Glucose, Copper.
- diagnosis : Basal Ganglia Diseases, Hepatolenticular Degeneration, Neurodegenerative Diseases, Olfaction Disorders, Parkinsonian Disorders.
- genetics : Basal Ganglia Diseases, Hepatolenticular Degeneration, Neurodegenerative Diseases, Olfaction Disorders, Parkinsonian Disorders.
- physiology : Sensory Thresholds.
- physiopathology : Basal Ganglia, Basal Ganglia Diseases, Extrapyramidal Tracts, Hepatolenticular Degeneration, Neurodegenerative Diseases, Olfaction Disorders, Olfactory Pathways, Parkinsonian Disorders.
- Adult, Aged, Chromosome Aberrations, Female, Genes, Recessive, Humans, Magnetic Resonance Imaging, Male, Middle Aged, Positron-Emission Tomography, Statistics as Topic.
Abstract
Wilson's disease is a rare autosomal recessive disorder characterized by the accumulation of copper, mainly in the liver and the brain. As copper accumulation in the brain leads to disturbances in basal ganglia function, neurological-type patients typically present with hypo- and hyperkinetic extrapyramidal symptoms, with Parkinsonism being very common. Although there are numerous reports on olfactory deficits in primary neurodegenerative disorders, olfactory function has not been investigated in metabolic disorders presenting with extrapyramidal features. Twenty-four patients with Wilson's disease participated in the investigation. All patients were treated pharmacologically. They comprised patients with liver disease alone (including mild enzyme elevation in asymptomatic individuals; n = 11) and/or neurological symptoms (n = 13) at the time of testing. Twenty-one patients underwent both [18F]fluoro-2-deoxy-D-glucose positron emission tomography ([18F]FDG-PET) and magnetic resonance imaging (MRI). The severity of extrapyramidal symptoms was judged using a clinical score system ranging from 0 (no symptoms) to 3 (severe symptoms). In all patients, psychophysical testing was performed using the Sniffin' Sticks, which involved tests for odor threshold, discrimination, and identification. Results from the present study revealed that Wilson's disease patients with neurological symptoms show a significant olfactory dysfunction compared to hepatic-type patients. Individuals who are more severely neurologically affected also present with a more pronounced olfactory deficit. Of interest, there was no significant effect of long-term treatment with penicillamine on olfactory function. Olfactory function did not correlate significantly with the presence of MRI visible lesions in the basal ganglia or with any regional glucose metabolism as measured by [18]F-FDG-PET. In conclusion, these findings indicate that the underlying pathological alterations with degeneration in the basal ganglia and neuronal loss in association with a marked increase of the copper content in this brain region play a role in the olfactory deficit.
DOI: 10.1002/mds.20989
PubMed: 16763975
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Reuner</name></author><author><name sortKey="Landis, Basile" sort="Landis, Basile" uniqKey="Landis B" first="Basile" last="Landis">Basile Landis</name></author><author><name sortKey="Kitzler, Hagen" sort="Kitzler, Hagen" uniqKey="Kitzler H" first="Hagen" last="Kitzler">Hagen Kitzler</name></author><author><name sortKey="Reichmann, Heinz" sort="Reichmann, Heinz" uniqKey="Reichmann H" first="Heinz" last="Reichmann">Heinz Reichmann</name></author><author><name sortKey="Hummel, Thomas" sort="Hummel, Thomas" uniqKey="Hummel T" first="Thomas" last="Hummel">Thomas Hummel</name></author></titleStmt><publicationStmt><idno type="wicri:source">PubMed</idno><date when="2006">2006</date><idno type="doi">10.1002/mds.20989</idno><idno type="RBID">pubmed:16763975</idno><idno type="pmid">16763975</idno><idno type="wicri:Area/PubMed/Corpus">002C05</idno><idno type="wicri:Area/PubMed/Curation">002C05</idno><idno type="wicri:Area/PubMed/Checkpoint">002D28</idno><idno 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(genetics)</term><term>Olfaction Disorders (physiopathology)</term><term>Olfactory Pathways (physiopathology)</term><term>Parkinsonian Disorders (diagnosis)</term><term>Parkinsonian Disorders (genetics)</term><term>Parkinsonian Disorders (physiopathology)</term><term>Positron-Emission Tomography</term><term>Sensory Thresholds (physiology)</term><term>Statistics as Topic</term></keywords><keywords scheme="MESH" type="chemical" qualifier="diagnostic use" xml:lang="en"><term>Fluorodeoxyglucose F18</term></keywords><keywords scheme="MESH" type="chemical" qualifier="metabolism" xml:lang="en"><term>Blood Glucose</term><term>Copper</term></keywords><keywords scheme="MESH" qualifier="diagnosis" xml:lang="en"><term>Basal Ganglia Diseases</term><term>Hepatolenticular Degeneration</term><term>Neurodegenerative Diseases</term><term>Olfaction Disorders</term><term>Parkinsonian Disorders</term></keywords><keywords scheme="MESH" qualifier="genetics" xml:lang="en"><term>Basal Ganglia 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Topic</term></keywords></textClass></profileDesc></teiHeader><front><div type="abstract" xml:lang="en">Wilson's disease is a rare autosomal recessive disorder characterized by the accumulation of copper, mainly in the liver and the brain. As copper accumulation in the brain leads to disturbances in basal ganglia function, neurological-type patients typically present with hypo- and hyperkinetic extrapyramidal symptoms, with Parkinsonism being very common. Although there are numerous reports on olfactory deficits in primary neurodegenerative disorders, olfactory function has not been investigated in metabolic disorders presenting with extrapyramidal features. Twenty-four patients with Wilson's disease participated in the investigation. All patients were treated pharmacologically. They comprised patients with liver disease alone (including mild enzyme elevation in asymptomatic individuals; n = 11) and/or neurological symptoms (n = 13) at the time of testing. Twenty-one patients underwent both [18F]fluoro-2-deoxy-D-glucose positron emission tomography ([18F]FDG-PET) and magnetic resonance imaging (MRI). The severity of extrapyramidal symptoms was judged using a clinical score system ranging from 0 (no symptoms) to 3 (severe symptoms). In all patients, psychophysical testing was performed using the Sniffin' Sticks, which involved tests for odor threshold, discrimination, and identification. Results from the present study revealed that Wilson's disease patients with neurological symptoms show a significant olfactory dysfunction compared to hepatic-type patients. Individuals who are more severely neurologically affected also present with a more pronounced olfactory deficit. Of interest, there was no significant effect of long-term treatment with penicillamine on olfactory function. Olfactory function did not correlate significantly with the presence of MRI visible lesions in the basal ganglia or with any regional glucose metabolism as measured by [18]F-FDG-PET. In conclusion, these findings indicate that the underlying pathological alterations with degeneration in the basal ganglia and neuronal loss in association with a marked increase of the copper content in this brain region play a role in the olfactory deficit.</div></front></TEI><pubmed><MedlineCitation Owner="NLM" Status="MEDLINE"><PMID Version="1">16763975</PMID><DateCreated><Year>2006</Year><Month>10</Month><Day>18</Day></DateCreated><DateCompleted><Year>2007</Year><Month>02</Month><Day>02</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>21</Volume><Issue>9</Issue><PubDate><Year>2006</Year><Month>Sep</Month></PubDate></JournalIssue><Title>Movement disorders : official journal of the Movement Disorder Society</Title><ISOAbbreviation>Mov. Disord.</ISOAbbreviation></Journal><ArticleTitle>Extrapyramidal symptoms in Wilson's disease are associated with olfactory dysfunction.</ArticleTitle><Pagination><MedlinePgn>1311-6</MedlinePgn></Pagination><Abstract><AbstractText>Wilson's disease is a rare autosomal recessive disorder characterized by the accumulation of copper, mainly in the liver and the brain. As copper accumulation in the brain leads to disturbances in basal ganglia function, neurological-type patients typically present with hypo- and hyperkinetic extrapyramidal symptoms, with Parkinsonism being very common. Although there are numerous reports on olfactory deficits in primary neurodegenerative disorders, olfactory function has not been investigated in metabolic disorders presenting with extrapyramidal features. Twenty-four patients with Wilson's disease participated in the investigation. All patients were treated pharmacologically. They comprised patients with liver disease alone (including mild enzyme elevation in asymptomatic individuals; n = 11) and/or neurological symptoms (n = 13) at the time of testing. Twenty-one patients underwent both [18F]fluoro-2-deoxy-D-glucose positron emission tomography ([18F]FDG-PET) and magnetic resonance imaging (MRI). The severity of extrapyramidal symptoms was judged using a clinical score system ranging from 0 (no symptoms) to 3 (severe symptoms). In all patients, psychophysical testing was performed using the Sniffin' Sticks, which involved tests for odor threshold, discrimination, and identification. Results from the present study revealed that Wilson's disease patients with neurological symptoms show a significant olfactory dysfunction compared to hepatic-type patients. Individuals who are more severely neurologically affected also present with a more pronounced olfactory deficit. Of interest, there was no significant effect of long-term treatment with penicillamine on olfactory function. Olfactory function did not correlate significantly with the presence of MRI visible lesions in the basal ganglia or with any regional glucose metabolism as measured by [18]F-FDG-PET. In conclusion, these findings indicate that the underlying pathological alterations with degeneration in the basal ganglia and neuronal loss in association with a marked increase of the copper content in this brain region play a role in the olfactory deficit.</AbstractText></Abstract><AuthorList CompleteYN="Y"><Author ValidYN="Y"><LastName>Mueller</LastName><ForeName>Antje</ForeName><Initials>A</Initials><AffiliationInfo><Affiliation>Smell & Taste Clinic, Department of Otorhinolaryngology, University of Dresden Medical School, Dresden, Germany. antje.mueller@uniklinikum-dresden.de</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Reuner</LastName><ForeName>Ulrike</ForeName><Initials>U</Initials></Author><Author ValidYN="Y"><LastName>Landis</LastName><ForeName>Basile</ForeName><Initials>B</Initials></Author><Author ValidYN="Y"><LastName>Kitzler</LastName><ForeName>Hagen</ForeName><Initials>H</Initials></Author><Author ValidYN="Y"><LastName>Reichmann</LastName><ForeName>Heinz</ForeName><Initials>H</Initials></Author><Author ValidYN="Y"><LastName>Hummel</LastName><ForeName>Thomas</ForeName><Initials>T</Initials></Author></AuthorList><Language>eng</Language><PublicationTypeList><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>0Z5B2CJX4D</RegistryNumber><NameOfSubstance UI="D019788">Fluorodeoxyglucose F18</NameOfSubstance></Chemical><Chemical><RegistryNumber>789U1901C5</RegistryNumber><NameOfSubstance 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UI="Q000378">metabolism</QualifierName></MeshHeading><MeshHeading><DescriptorName MajorTopicYN="N" UI="D002869">Chromosome Aberrations</DescriptorName></MeshHeading><MeshHeading><DescriptorName MajorTopicYN="N" UI="D003300">Copper</DescriptorName><QualifierName MajorTopicYN="N" UI="Q000378">metabolism</QualifierName></MeshHeading><MeshHeading><DescriptorName MajorTopicYN="N" UI="D005116">Extrapyramidal Tracts</DescriptorName><QualifierName MajorTopicYN="N" UI="Q000503">physiopathology</QualifierName></MeshHeading><MeshHeading><DescriptorName MajorTopicYN="N" UI="D005260">Female</DescriptorName></MeshHeading><MeshHeading><DescriptorName MajorTopicYN="N" UI="D019788">Fluorodeoxyglucose F18</DescriptorName><QualifierName MajorTopicYN="N" UI="Q000176">diagnostic use</QualifierName></MeshHeading><MeshHeading><DescriptorName MajorTopicYN="N" UI="D005808">Genes, Recessive</DescriptorName></MeshHeading><MeshHeading><DescriptorName MajorTopicYN="N" UI="D006527">Hepatolenticular 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UI="Q000503">physiopathology</QualifierName></MeshHeading><MeshHeading><DescriptorName MajorTopicYN="N" UI="D000857">Olfaction Disorders</DescriptorName><QualifierName MajorTopicYN="Y" UI="Q000175">diagnosis</QualifierName><QualifierName MajorTopicYN="N" UI="Q000235">genetics</QualifierName><QualifierName MajorTopicYN="N" UI="Q000503">physiopathology</QualifierName></MeshHeading><MeshHeading><DescriptorName MajorTopicYN="N" UI="D009833">Olfactory Pathways</DescriptorName><QualifierName MajorTopicYN="N" UI="Q000503">physiopathology</QualifierName></MeshHeading><MeshHeading><DescriptorName MajorTopicYN="N" UI="D020734">Parkinsonian Disorders</DescriptorName><QualifierName MajorTopicYN="Y" UI="Q000175">diagnosis</QualifierName><QualifierName MajorTopicYN="N" UI="Q000235">genetics</QualifierName><QualifierName MajorTopicYN="N" UI="Q000503">physiopathology</QualifierName></MeshHeading><MeshHeading><DescriptorName MajorTopicYN="Y" UI="D049268">Positron-Emission Tomography</DescriptorName></MeshHeading><MeshHeading><DescriptorName MajorTopicYN="N" UI="D012684">Sensory Thresholds</DescriptorName><QualifierName MajorTopicYN="N" UI="Q000502">physiology</QualifierName></MeshHeading><MeshHeading><DescriptorName MajorTopicYN="N" UI="D013223">Statistics as Topic</DescriptorName></MeshHeading></MeshHeadingList></MedlineCitation><PubmedData><History><PubMedPubDate PubStatus="pubmed"><Year>2006</Year><Month>6</Month><Day>10</Day><Hour>9</Hour><Minute>0</Minute></PubMedPubDate><PubMedPubDate PubStatus="medline"><Year>2007</Year><Month>2</Month><Day>3</Day><Hour>9</Hour><Minute>0</Minute></PubMedPubDate><PubMedPubDate PubStatus="entrez"><Year>2006</Year><Month>6</Month><Day>10</Day><Hour>9</Hour><Minute>0</Minute></PubMedPubDate></History><PublicationStatus>ppublish</PublicationStatus><ArticleIdList><ArticleId IdType="doi">10.1002/mds.20989</ArticleId><ArticleId IdType="pubmed">16763975</ArticleId></ArticleIdList></PubmedData></pubmed><affiliations><list><country><li>Allemagne</li></country><region><li>District de Dresde</li><li>Saxe (Land)</li></region><settlement><li>Dresde</li></settlement></list><tree><noCountry><name sortKey="Hummel, Thomas" sort="Hummel, Thomas" uniqKey="Hummel T" first="Thomas" last="Hummel">Thomas Hummel</name><name sortKey="Kitzler, Hagen" sort="Kitzler, Hagen" uniqKey="Kitzler H" first="Hagen" last="Kitzler">Hagen Kitzler</name><name sortKey="Landis, Basile" sort="Landis, Basile" uniqKey="Landis B" first="Basile" last="Landis">Basile Landis</name><name sortKey="Reichmann, Heinz" sort="Reichmann, Heinz" uniqKey="Reichmann H" first="Heinz" last="Reichmann">Heinz Reichmann</name><name sortKey="Reuner, Ulrike" sort="Reuner, Ulrike" uniqKey="Reuner U" first="Ulrike" last="Reuner">Ulrike Reuner</name></noCountry><country name="Allemagne"><region name="Saxe (Land)"><name sortKey="Mueller, Antje" sort="Mueller, Antje" uniqKey="Mueller A" first="Antje" last="Mueller">Antje Mueller</name></region></country></tree></affiliations></record>Pour manipuler ce document sous Unix (Dilib)
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