Glucose hypermetabolism in the thalamus of patients with hemifacial spasm.
Identifieur interne : 000E58 ( PubMed/Curation ); précédent : 000E57; suivant : 000E59Glucose hypermetabolism in the thalamus of patients with hemifacial spasm.
Auteurs : Megumi Shimizu [Japon] ; Yukihisa Suzuki ; Motohiro Kiyosawa ; Masato Wakakura ; Kenji Ishii ; Kiichi Ishiwata ; Manabu MochizukiSource :
- Movement disorders : official journal of the Movement Disorder Society [ 1531-8257 ] ; 2012.
English descriptors
- KwdEn :
- Adult, Aged, Botulinum Toxins, Type A (pharmacology), Botulinum Toxins, Type A (therapeutic use), Disability Evaluation, Electromyography, Female, Fluorodeoxyglucose F18 (diagnostic use), Functional Laterality (drug effects), Functional Laterality (physiology), Glucose (metabolism), Hemifacial Spasm (drug therapy), Hemifacial Spasm (pathology), Humans, Male, Middle Aged, Neuromuscular Agents (pharmacology), Neuromuscular Agents (therapeutic use), Positron-Emission Tomography, Thalamus (drug effects), Thalamus (metabolism), Thalamus (radionuclide imaging).
- MESH :
- chemical , diagnostic use : Fluorodeoxyglucose F18.
- chemical , metabolism : Glucose.
- chemical , pharmacology : Botulinum Toxins, Type A, Neuromuscular Agents.
- chemical , therapeutic use : Botulinum Toxins, Type A, Neuromuscular Agents.
- drug effects : Functional Laterality, Thalamus.
- drug therapy : Hemifacial Spasm.
- metabolism : Thalamus.
- pathology : Hemifacial Spasm.
- physiology : Functional Laterality.
- radionuclide imaging : Thalamus.
- Adult, Aged, Disability Evaluation, Electromyography, Female, Humans, Male, Middle Aged, Positron-Emission Tomography.
Abstract
The purpose of this study was investigate functional alteration in the brains of patients with hemifacial spasm using positron emission tomography (PET). We studied cerebral glucose metabolism using PET with (18) F-fluorodeoxyglucose in 13 patients with right lateral hemifacial spasm and 13 with left lateral hemifacial spasm. All patients underwent 2 PET scans before treatment (active state) and after treatment (suppressive state) with the botulinum neurotoxin type A. At the time of the PET scans, the severity of the spasm was rated according to the Jankovic Disability Rating Scale. We also used magnetic resonance imaging to evaluate the grade of neurovascular compression in each patient using scores of 1 to 3 (1 = mild, 3 = severe). Fifty-two normal volunteers were examined as controls. Compared with controls, patients with right and left hemifacial spasm showed bilateral cerebral glucose hypermetabolism in the thalamus in both the active and suppressive states. However, thalamic glucose metabolism after the suppressive state was significantly reduced compared with that in the active state using region of interest analysis. There was a positive correlation between the severity of the spasm in the active state and the score of neurovascular compression (rs = 0.65) that was estimated using Spearman order correlation coefficient. We observed bilateral cerebral glucose hypermetabolism in the thalamus of patients with hemifacial spasm. The thalamic glucose hypermetabolism may be attributed to multiple sources, including afferent input from the skin and muscle spindle, antidromic conduction of the facial nerve, and secondary alteration in the central nervous system.
DOI: 10.1002/mds.24925
PubMed: 22344604
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sort="Wakakura, Masato" uniqKey="Wakakura M" first="Masato" last="Wakakura">Masato Wakakura</name></author><author><name sortKey="Ishii, Kenji" sort="Ishii, Kenji" uniqKey="Ishii K" first="Kenji" last="Ishii">Kenji Ishii</name></author><author><name sortKey="Ishiwata, Kiichi" sort="Ishiwata, Kiichi" uniqKey="Ishiwata K" first="Kiichi" last="Ishiwata">Kiichi Ishiwata</name></author><author><name sortKey="Mochizuki, Manabu" sort="Mochizuki, Manabu" uniqKey="Mochizuki M" first="Manabu" last="Mochizuki">Manabu Mochizuki</name></author></titleStmt><publicationStmt><idno type="wicri:source">PubMed</idno><date when="2012">2012</date><idno type="doi">10.1002/mds.24925</idno><idno type="RBID">pubmed:22344604</idno><idno type="pmid">22344604</idno><idno type="wicri:Area/PubMed/Corpus">000E58</idno><idno type="wicri:Area/PubMed/Curation">000E58</idno></publicationStmt><sourceDesc><biblStruct><analytic><title xml:lang="en">Glucose hypermetabolism in the thalamus of patients with hemifacial spasm.</title><author><name sortKey="Shimizu, Megumi" sort="Shimizu, Megumi" uniqKey="Shimizu M" first="Megumi" last="Shimizu">Megumi Shimizu</name><affiliation wicri:level="1"><nlm:affiliation>Department of Ophthalmology and Visual Science, Tokyo Medical and Dental University, Itabashi, Tokyo, Japan.</nlm:affiliation><country xml:lang="fr">Japon</country><wicri:regionArea>Department of Ophthalmology and Visual Science, Tokyo Medical and Dental University, Itabashi, Tokyo</wicri:regionArea></affiliation></author><author><name sortKey="Suzuki, Yukihisa" sort="Suzuki, Yukihisa" uniqKey="Suzuki Y" first="Yukihisa" last="Suzuki">Yukihisa Suzuki</name></author><author><name sortKey="Kiyosawa, Motohiro" sort="Kiyosawa, Motohiro" uniqKey="Kiyosawa M" first="Motohiro" last="Kiyosawa">Motohiro Kiyosawa</name></author><author><name sortKey="Wakakura, Masato" sort="Wakakura, Masato" uniqKey="Wakakura M" first="Masato" last="Wakakura">Masato Wakakura</name></author><author><name sortKey="Ishii, Kenji" sort="Ishii, Kenji" uniqKey="Ishii K" first="Kenji" last="Ishii">Kenji Ishii</name></author><author><name sortKey="Ishiwata, Kiichi" sort="Ishiwata, Kiichi" uniqKey="Ishiwata K" first="Kiichi" last="Ishiwata">Kiichi Ishiwata</name></author><author><name sortKey="Mochizuki, Manabu" sort="Mochizuki, Manabu" uniqKey="Mochizuki M" first="Manabu" last="Mochizuki">Manabu Mochizuki</name></author></analytic><series><title level="j">Movement disorders : official journal of the Movement Disorder Society</title><idno type="eISSN">1531-8257</idno><imprint><date when="2012" type="published">2012</date></imprint></series></biblStruct></sourceDesc></fileDesc><profileDesc><textClass><keywords scheme="KwdEn" xml:lang="en"><term>Adult</term><term>Aged</term><term>Botulinum Toxins, Type A (pharmacology)</term><term>Botulinum Toxins, Type A (therapeutic use)</term><term>Disability Evaluation</term><term>Electromyography</term><term>Female</term><term>Fluorodeoxyglucose F18 (diagnostic use)</term><term>Functional Laterality (drug effects)</term><term>Functional Laterality (physiology)</term><term>Glucose (metabolism)</term><term>Hemifacial Spasm (drug therapy)</term><term>Hemifacial Spasm (pathology)</term><term>Humans</term><term>Male</term><term>Middle Aged</term><term>Neuromuscular Agents (pharmacology)</term><term>Neuromuscular Agents (therapeutic use)</term><term>Positron-Emission Tomography</term><term>Thalamus (drug effects)</term><term>Thalamus (metabolism)</term><term>Thalamus (radionuclide imaging)</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>Glucose</term></keywords><keywords scheme="MESH" type="chemical" qualifier="pharmacology" xml:lang="en"><term>Botulinum Toxins, Type A</term><term>Neuromuscular Agents</term></keywords><keywords scheme="MESH" type="chemical" qualifier="therapeutic use" xml:lang="en"><term>Botulinum Toxins, Type A</term><term>Neuromuscular Agents</term></keywords><keywords scheme="MESH" qualifier="drug effects" xml:lang="en"><term>Functional Laterality</term><term>Thalamus</term></keywords><keywords scheme="MESH" qualifier="drug therapy" xml:lang="en"><term>Hemifacial Spasm</term></keywords><keywords scheme="MESH" qualifier="metabolism" xml:lang="en"><term>Thalamus</term></keywords><keywords scheme="MESH" qualifier="pathology" xml:lang="en"><term>Hemifacial Spasm</term></keywords><keywords scheme="MESH" qualifier="physiology" xml:lang="en"><term>Functional Laterality</term></keywords><keywords scheme="MESH" qualifier="radionuclide imaging" xml:lang="en"><term>Thalamus</term></keywords><keywords scheme="MESH" xml:lang="en"><term>Adult</term><term>Aged</term><term>Disability Evaluation</term><term>Electromyography</term><term>Female</term><term>Humans</term><term>Male</term><term>Middle Aged</term><term>Positron-Emission Tomography</term></keywords></textClass></profileDesc></teiHeader><front><div type="abstract" xml:lang="en">The purpose of this study was investigate functional alteration in the brains of patients with hemifacial spasm using positron emission tomography (PET). We studied cerebral glucose metabolism using PET with (18) F-fluorodeoxyglucose in 13 patients with right lateral hemifacial spasm and 13 with left lateral hemifacial spasm. All patients underwent 2 PET scans before treatment (active state) and after treatment (suppressive state) with the botulinum neurotoxin type A. At the time of the PET scans, the severity of the spasm was rated according to the Jankovic Disability Rating Scale. We also used magnetic resonance imaging to evaluate the grade of neurovascular compression in each patient using scores of 1 to 3 (1 = mild, 3 = severe). Fifty-two normal volunteers were examined as controls. Compared with controls, patients with right and left hemifacial spasm showed bilateral cerebral glucose hypermetabolism in the thalamus in both the active and suppressive states. However, thalamic glucose metabolism after the suppressive state was significantly reduced compared with that in the active state using region of interest analysis. There was a positive correlation between the severity of the spasm in the active state and the score of neurovascular compression (rs = 0.65) that was estimated using Spearman order correlation coefficient. We observed bilateral cerebral glucose hypermetabolism in the thalamus of patients with hemifacial spasm. The thalamic glucose hypermetabolism may be attributed to multiple sources, including afferent input from the skin and muscle spindle, antidromic conduction of the facial nerve, and secondary alteration in the central nervous system.</div></front></TEI><pubmed><MedlineCitation Owner="NLM" Status="MEDLINE"><PMID Version="1">22344604</PMID><DateCreated><Year>2012</Year><Month>04</Month><Day>10</Day></DateCreated><DateCompleted><Year>2012</Year><Month>08</Month><Day>08</Day></DateCompleted><DateRevised><Year>2013</Year><Month>11</Month><Day>21</Day></DateRevised><Article PubModel="Print-Electronic"><Journal><ISSN IssnType="Electronic">1531-8257</ISSN><JournalIssue CitedMedium="Internet"><Volume>27</Volume><Issue>4</Issue><PubDate><Year>2012</Year><Month>Apr</Month></PubDate></JournalIssue><Title>Movement disorders : official journal of the Movement Disorder Society</Title><ISOAbbreviation>Mov. Disord.</ISOAbbreviation></Journal><ArticleTitle>Glucose hypermetabolism in the thalamus of patients with hemifacial spasm.</ArticleTitle><Pagination><MedlinePgn>519-25</MedlinePgn></Pagination><ELocationID EIdType="doi" ValidYN="Y">10.1002/mds.24925</ELocationID><Abstract><AbstractText>The purpose of this study was investigate functional alteration in the brains of patients with hemifacial spasm using positron emission tomography (PET). We studied cerebral glucose metabolism using PET with (18) F-fluorodeoxyglucose in 13 patients with right lateral hemifacial spasm and 13 with left lateral hemifacial spasm. All patients underwent 2 PET scans before treatment (active state) and after treatment (suppressive state) with the botulinum neurotoxin type A. At the time of the PET scans, the severity of the spasm was rated according to the Jankovic Disability Rating Scale. We also used magnetic resonance imaging to evaluate the grade of neurovascular compression in each patient using scores of 1 to 3 (1 = mild, 3 = severe). Fifty-two normal volunteers were examined as controls. Compared with controls, patients with right and left hemifacial spasm showed bilateral cerebral glucose hypermetabolism in the thalamus in both the active and suppressive states. However, thalamic glucose metabolism after the suppressive state was significantly reduced compared with that in the active state using region of interest analysis. There was a positive correlation between the severity of the spasm in the active state and the score of neurovascular compression (rs = 0.65) that was estimated using Spearman order correlation coefficient. We observed bilateral cerebral glucose hypermetabolism in the thalamus of patients with hemifacial spasm. The thalamic glucose hypermetabolism may be attributed to multiple sources, including afferent input from the skin and muscle spindle, antidromic conduction of the facial nerve, and secondary alteration in the central nervous system.</AbstractText><CopyrightInformation>Copyright © 2012 Movement Disorder Society.</CopyrightInformation></Abstract><AuthorList CompleteYN="Y"><Author ValidYN="Y"><LastName>Shimizu</LastName><ForeName>Megumi</ForeName><Initials>M</Initials><AffiliationInfo><Affiliation>Department of Ophthalmology and Visual Science, Tokyo Medical and Dental University, Itabashi, Tokyo, Japan.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Suzuki</LastName><ForeName>Yukihisa</ForeName><Initials>Y</Initials></Author><Author ValidYN="Y"><LastName>Kiyosawa</LastName><ForeName>Motohiro</ForeName><Initials>M</Initials></Author><Author ValidYN="Y"><LastName>Wakakura</LastName><ForeName>Masato</ForeName><Initials>M</Initials></Author><Author ValidYN="Y"><LastName>Ishii</LastName><ForeName>Kenji</ForeName><Initials>K</Initials></Author><Author ValidYN="Y"><LastName>Ishiwata</LastName><ForeName>Kiichi</ForeName><Initials>K</Initials></Author><Author ValidYN="Y"><LastName>Mochizuki</LastName><ForeName>Manabu</ForeName><Initials>M</Initials></Author></AuthorList><Language>eng</Language><PublicationTypeList><PublicationType UI="D016428">Journal Article</PublicationType><PublicationType UI="D013485">Research Support, Non-U.S. Gov't</PublicationType></PublicationTypeList><ArticleDate DateType="Electronic"><Year>2012</Year><Month>02</Month><Day>16</Day></ArticleDate></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="D009465">Neuromuscular Agents</NameOfSubstance></Chemical><Chemical><RegistryNumber>0Z5B2CJX4D</RegistryNumber><NameOfSubstance UI="D019788">Fluorodeoxyglucose F18</NameOfSubstance></Chemical><Chemical><RegistryNumber>EC 3.4.24.69</RegistryNumber><NameOfSubstance UI="D019274">Botulinum Toxins, Type A</NameOfSubstance></Chemical><Chemical><RegistryNumber>IY9XDZ35W2</RegistryNumber><NameOfSubstance UI="D005947">Glucose</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="D019274">Botulinum Toxins, Type A</DescriptorName><QualifierName MajorTopicYN="N" UI="Q000494">pharmacology</QualifierName><QualifierName MajorTopicYN="N" UI="Q000627">therapeutic use</QualifierName></MeshHeading><MeshHeading><DescriptorName MajorTopicYN="N" UI="D004185">Disability Evaluation</DescriptorName></MeshHeading><MeshHeading><DescriptorName MajorTopicYN="N" UI="D004576">Electromyography</DescriptorName></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="D007839">Functional Laterality</DescriptorName><QualifierName MajorTopicYN="N" UI="Q000187">drug effects</QualifierName><QualifierName MajorTopicYN="Y" UI="Q000502">physiology</QualifierName></MeshHeading><MeshHeading><DescriptorName MajorTopicYN="N" UI="D005947">Glucose</DescriptorName><QualifierName MajorTopicYN="Y" UI="Q000378">metabolism</QualifierName></MeshHeading><MeshHeading><DescriptorName MajorTopicYN="N" UI="D019569">Hemifacial Spasm</DescriptorName><QualifierName MajorTopicYN="N" UI="Q000188">drug therapy</QualifierName><QualifierName MajorTopicYN="Y" UI="Q000473">pathology</QualifierName></MeshHeading><MeshHeading><DescriptorName MajorTopicYN="N" UI="D006801">Humans</DescriptorName></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="D009465">Neuromuscular Agents</DescriptorName><QualifierName MajorTopicYN="N" UI="Q000494">pharmacology</QualifierName><QualifierName MajorTopicYN="N" UI="Q000627">therapeutic use</QualifierName></MeshHeading><MeshHeading><DescriptorName MajorTopicYN="N" UI="D049268">Positron-Emission Tomography</DescriptorName></MeshHeading><MeshHeading><DescriptorName MajorTopicYN="N" UI="D013788">Thalamus</DescriptorName><QualifierName MajorTopicYN="N" UI="Q000187">drug effects</QualifierName><QualifierName MajorTopicYN="Y" UI="Q000378">metabolism</QualifierName><QualifierName MajorTopicYN="N" UI="Q000531">radionuclide imaging</QualifierName></MeshHeading></MeshHeadingList></MedlineCitation><PubmedData><History><PubMedPubDate PubStatus="received"><Year>2011</Year><Month>1</Month><Day>31</Day></PubMedPubDate><PubMedPubDate PubStatus="revised"><Year>2011</Year><Month>11</Month><Day>28</Day></PubMedPubDate><PubMedPubDate PubStatus="accepted"><Year>2012</Year><Month>1</Month><Day>3</Day></PubMedPubDate><PubMedPubDate PubStatus="aheadofprint"><Year>2012</Year><Month>2</Month><Day>16</Day></PubMedPubDate><PubMedPubDate PubStatus="entrez"><Year>2012</Year><Month>2</Month><Day>21</Day><Hour>6</Hour><Minute>0</Minute></PubMedPubDate><PubMedPubDate PubStatus="pubmed"><Year>2012</Year><Month>2</Month><Day>22</Day><Hour>6</Hour><Minute>0</Minute></PubMedPubDate><PubMedPubDate PubStatus="medline"><Year>2012</Year><Month>8</Month><Day>9</Day><Hour>6</Hour><Minute>0</Minute></PubMedPubDate></History><PublicationStatus>ppublish</PublicationStatus><ArticleIdList><ArticleId IdType="doi">10.1002/mds.24925</ArticleId><ArticleId IdType="pubmed">22344604</ArticleId></ArticleIdList></PubmedData></pubmed></record>Pour manipuler ce document sous Unix (Dilib)
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