Preserved cardiac sympathetic nerve accounts for normal cardiac uptake of MIBG in PARK2
Identifieur interne : 002F04 ( Istex/Corpus ); précédent : 002F03; suivant : 002F05Preserved cardiac sympathetic nerve accounts for normal cardiac uptake of MIBG in PARK2
Auteurs : Satoshi Orimo ; Takeshi Amino ; Masayuki Yokochi ; Tohru Kojo ; Toshiki Uchihara ; Atsushi Takahashi ; Koichi Wakabayashi ; Hitoshi Takahashi ; Nobutaka Hattori ; Yoshikuni MizunoSource :
- Movement Disorders [ 0885-3185 ] ; 2005-10.
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Abstract
We performed [123I] MIBG myocardial scintigraphy in two of three patients with PARK2 from unrelated families and examined the heart tissues from the three patients immunohistochemically using an antibody against tyrosine hydroxylase (TH) to see whether cardiac sympathetic nerve is involved. Cardiac uptake of MIBG was normal except for a slight decrease in the late phase in one of the patients. Postmortem examination revealed that TH‐immunoreactive nerve fibers in the epicardium were well preserved in all three patients. The present study confirmed that cardiac sympathetic nerve is well preserved in PARK2 with a homozygous exon deletion, which accounts for normal cardiac uptake of MIBG. Moreover, normal cardiac uptake of MIBG might be of potential diagnostic value to indicate the absence of Lewy body pathology, even in patients with levodopa‐responsive Parkinsonism, as in PARK2. © 2005 Movement Disorder Society
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DOI: 10.1002/mds.20594
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ISTEX:93A1F555EE9922B77F75A14F22D7C2A6EE6E1916Le document en format XML
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Japan</mods:affiliation></affiliation></author><author><name sortKey="Amino, Takeshi" sort="Amino, Takeshi" uniqKey="Amino T" first="Takeshi" last="Amino">Takeshi Amino</name><affiliation><mods:affiliation>Department of Neurology, Kanto Central Hospital, Tokyo, Japan</mods:affiliation></affiliation></author><author><name sortKey="Yokochi, Masayuki" sort="Yokochi, Masayuki" uniqKey="Yokochi M" first="Masayuki" last="Yokochi">Masayuki Yokochi</name><affiliation><mods:affiliation>Department of Neurology, Ebara Metropolitan Hospital, Tokyo, Japan</mods:affiliation></affiliation></author><author><name sortKey="Kojo, Tohru" sort="Kojo, Tohru" uniqKey="Kojo T" first="Tohru" last="Kojo">Tohru Kojo</name><affiliation><mods:affiliation>Department of Neuropathology, Tokyo Metropolitan Institute for Neuroscience, Tokyo, Japan</mods:affiliation></affiliation></author><author><name sortKey="Uchihara, Toshiki" sort="Uchihara, Toshiki" uniqKey="Uchihara T" first="Toshiki" last="Uchihara">Toshiki 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Cardiac uptake of MIBG was normal except for a slight decrease in the late phase in one of the patients. Postmortem examination revealed that TH‐immunoreactive nerve fibers in the epicardium were well preserved in all three patients. The present study confirmed that cardiac sympathetic nerve is well preserved in PARK2 with a homozygous exon deletion, which accounts for normal cardiac uptake of MIBG. Moreover, normal cardiac uptake of MIBG might be of potential diagnostic value to indicate the absence of Lewy body pathology, even in patients with levodopa‐responsive Parkinsonism, as in PARK2. © 2005 Movement Disorder Society</div></front></TEI><istex><corpusName>wiley</corpusName><author><json:item><name>Satoshi Orimo MD, PhD</name><affiliations><json:string>Department of Neurology, Kanto Central Hospital, Tokyo, Japan</json:string></affiliations></json:item><json:item><name>Takeshi Amino MD</name><affiliations><json:string>Department of Neurology, Kanto Central Hospital, Tokyo, Japan</json:string></affiliations></json:item><json:item><name>Masayuki Yokochi MD, PhD</name><affiliations><json:string>Department of Neurology, Ebara Metropolitan Hospital, Tokyo, Japan</json:string></affiliations></json:item><json:item><name>Tohru Kojo MD, PhD</name><affiliations><json:string>Department of Neuropathology, Tokyo Metropolitan Institute for Neuroscience, Tokyo, Japan</json:string></affiliations></json:item><json:item><name>Toshiki Uchihara MD, PhD</name><affiliations><json:string>Department of Neuropathology, Tokyo Metropolitan Institute for Neuroscience, Tokyo, Japan</json:string></affiliations></json:item><json:item><name>Atsushi Takahashi MD, PhD</name><affiliations><json:string>Organ and Function Pathology Division, Yokufukai Geriatric Hospital, Tokyo, Japan</json:string></affiliations></json:item><json:item><name>Koichi Wakabayashi MD, PhD</name><affiliations><json:string>Department of Neuropathology, Hirosaki University School of Medicine, Hirosaki, Japan</json:string></affiliations></json:item><json:item><name>Hitoshi Takahashi MD, PhD</name><affiliations><json:string>Department of Pathology, Brain Research Institute, University of Niigata, Niigata, Japan</json:string></affiliations></json:item><json:item><name>Nobutaka Hattori MD, PhD</name><affiliations><json:string>Department of Neurology, Juntendo University School of Medicine, Tokyo, Japan</json:string></affiliations></json:item><json:item><name>Yoshikuni Mizuno MD, PhD</name><affiliations><json:string>Department of Neurology, Juntendo University School of Medicine, Tokyo, Japan</json:string></affiliations></json:item></author><subject><json:item><lang><json:string>eng</json:string></lang><value>PARK2</value></json:item><json:item><lang><json:string>eng</json:string></lang><value>Parkinson's disease</value></json:item><json:item><lang><json:string>eng</json:string></lang><value>MIBG myocardial scintigraphy</value></json:item><json:item><lang><json:string>eng</json:string></lang><value>cardiac sympathetic nerve</value></json:item><json:item><lang><json:string>eng</json:string></lang><value>denervation</value></json:item></subject><language><json:string>eng</json:string></language><abstract>We performed [123I] MIBG myocardial scintigraphy in two of three patients with PARK2 from unrelated families and examined the heart tissues from the three patients immunohistochemically using an antibody against tyrosine hydroxylase (TH) to see whether cardiac sympathetic nerve is involved. Cardiac uptake of MIBG was normal except for a slight decrease in the late phase in one of the patients. Postmortem examination revealed that TH‐immunoreactive nerve fibers in the epicardium were well preserved in all three patients. The present study confirmed that cardiac sympathetic nerve is well preserved in PARK2 with a homozygous exon deletion, which accounts for normal cardiac uptake of MIBG. 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Japan</p></note><affiliation>Department of Neurology, Kanto Central Hospital, Tokyo, Japan</affiliation></author><author><persName><forename type="first">Takeshi</forename><surname>Amino</surname><roleName type="degree">MD</roleName></persName><affiliation>Department of Neurology, Kanto Central Hospital, Tokyo, Japan</affiliation></author><author><persName><forename type="first">Masayuki</forename><surname>Yokochi</surname><roleName type="degree">MD, PhD</roleName></persName><affiliation>Department of Neurology, Ebara Metropolitan Hospital, Tokyo, Japan</affiliation></author><author><persName><forename type="first">Tohru</forename><surname>Kojo</surname><roleName type="degree">MD, PhD</roleName></persName><affiliation>Department of Neuropathology, Tokyo Metropolitan Institute for Neuroscience, Tokyo, Japan</affiliation></author><author><persName><forename type="first">Toshiki</forename><surname>Uchihara</surname><roleName type="degree">MD, 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Cardiac uptake of MIBG was normal except for a slight decrease in the late phase in one of the patients. Postmortem examination revealed that TH‐immunoreactive nerve fibers in the epicardium were well preserved in all three patients. The present study confirmed that cardiac sympathetic nerve is well preserved in PARK2 with a homozygous exon deletion, which accounts for normal cardiac uptake of MIBG. 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affiliationRef="#af1"><personName><givenNames>Takeshi</givenNames><familyName>Amino</familyName><degrees>MD</degrees></personName></creator><creator xml:id="au3" creatorRole="author" affiliationRef="#af2"><personName><givenNames>Masayuki</givenNames><familyName>Yokochi</familyName><degrees>MD, PhD</degrees></personName></creator><creator xml:id="au4" creatorRole="author" affiliationRef="#af3"><personName><givenNames>Tohru</givenNames><familyName>Kojo</familyName><degrees>MD, PhD</degrees></personName></creator><creator xml:id="au5" creatorRole="author" affiliationRef="#af3"><personName><givenNames>Toshiki</givenNames><familyName>Uchihara</familyName><degrees>MD, PhD</degrees></personName></creator><creator xml:id="au6" creatorRole="author" affiliationRef="#af4"><personName><givenNames>Atsushi</givenNames><familyName>Takahashi</familyName><degrees>MD, PhD</degrees></personName></creator><creator xml:id="au7" creatorRole="author" affiliationRef="#af5"><personName><givenNames>Koichi</givenNames><familyName>Wakabayashi</familyName><degrees>MD, PhD</degrees></personName></creator><creator xml:id="au8" creatorRole="author" affiliationRef="#af6"><personName><givenNames>Hitoshi</givenNames><familyName>Takahashi</familyName><degrees>MD, PhD</degrees></personName></creator><creator xml:id="au9" creatorRole="author" affiliationRef="#af7"><personName><givenNames>Nobutaka</givenNames><familyName>Hattori</familyName><degrees>MD, PhD</degrees></personName></creator><creator xml:id="au10" creatorRole="author" affiliationRef="#af7"><personName><givenNames>Yoshikuni</givenNames><familyName>Mizuno</familyName><degrees>MD, PhD</degrees></personName></creator></creators><affiliationGroup><affiliation xml:id="af1" countryCode="JP" type="organization"><unparsedAffiliation>Department of Neurology, Kanto Central Hospital, Tokyo, Japan</unparsedAffiliation></affiliation><affiliation xml:id="af2" countryCode="JP" type="organization"><unparsedAffiliation>Department of Neurology, Ebara Metropolitan Hospital, Tokyo, Japan</unparsedAffiliation></affiliation><affiliation xml:id="af3" countryCode="JP" type="organization"><unparsedAffiliation>Department of Neuropathology, Tokyo Metropolitan Institute for Neuroscience, Tokyo, Japan</unparsedAffiliation></affiliation><affiliation xml:id="af4" countryCode="JP" type="organization"><unparsedAffiliation>Organ and Function Pathology Division, Yokufukai Geriatric Hospital, Tokyo, Japan</unparsedAffiliation></affiliation><affiliation xml:id="af5" countryCode="JP" type="organization"><unparsedAffiliation>Department of Neuropathology, Hirosaki University School of Medicine, Hirosaki, Japan</unparsedAffiliation></affiliation><affiliation xml:id="af6" countryCode="JP" type="organization"><unparsedAffiliation>Department of Pathology, Brain Research Institute, University of Niigata, Niigata, Japan</unparsedAffiliation></affiliation><affiliation xml:id="af7" countryCode="JP" type="organization"><unparsedAffiliation>Department of Neurology, Juntendo University School of Medicine, Tokyo, Japan</unparsedAffiliation></affiliation></affiliationGroup><keywordGroup xml:lang="en" type="author"><keyword xml:id="kwd1">PARK2</keyword><keyword xml:id="kwd2">Parkinson's disease</keyword><keyword xml:id="kwd3">MIBG myocardial scintigraphy</keyword><keyword xml:id="kwd4">cardiac sympathetic nerve</keyword><keyword xml:id="kwd5">denervation</keyword></keywordGroup><fundingInfo><fundingAgency>Japan Foundation for Neuroscience and Mental Health (Tama Nakagawa Foundation)</fundingAgency></fundingInfo><abstractGroup><abstract type="main" xml:lang="en"><title type="main">Abstract</title><p>We performed [<sup>123</sup>I] MIBG myocardial scintigraphy in two of three patients with PARK2 from unrelated families and examined the heart tissues from the three patients immunohistochemically using an antibody against tyrosine hydroxylase (TH) to see whether cardiac sympathetic nerve is involved. Cardiac uptake of MIBG was normal except for a slight decrease in the late phase in one of the patients. Postmortem examination revealed that TH‐immunoreactive nerve fibers in the epicardium were well preserved in all three patients. The present study confirmed that cardiac sympathetic nerve is well preserved in PARK2 with a homozygous exon deletion, which accounts for normal cardiac uptake of MIBG. Moreover, normal cardiac uptake of MIBG might be of potential diagnostic value to indicate the absence of Lewy body pathology, even in patients with levodopa‐responsive Parkinsonism, as in PARK2. © 2005 Movement Disorder Society</p></abstract></abstractGroup></contentMeta></header></component></istex:document></istex:metadataXml><!--Version 0.6 générée le 3-12-2015--><mods version="3.6"><titleInfo lang="en"><title>Preserved cardiac sympathetic nerve accounts for normal cardiac uptake of MIBG in PARK2</title></titleInfo><titleInfo type="abbreviated" lang="en"><title>Preserved Cardiac Sympathetic Nerve in PARK2</title></titleInfo><titleInfo type="alternative" contentType="CDATA" lang="en"><title>Preserved cardiac sympathetic nerve accounts for normal cardiac uptake of MIBG in PARK2</title></titleInfo><name type="personal"><namePart type="given">Satoshi</namePart><namePart type="family">Orimo</namePart><namePart type="termsOfAddress">MD, PhD</namePart><affiliation>Department of Neurology, Kanto Central Hospital, Tokyo, Japan</affiliation><description>Correspondence: Department of Neurology, Kanto Central Hospital, 6‐25‐1 Kami‐Yoga, Setagaya‐ku, 158‐8531 Tokyo, Japan</description><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">Takeshi</namePart><namePart type="family">Amino</namePart><namePart type="termsOfAddress">MD</namePart><affiliation>Department of Neurology, Kanto Central Hospital, Tokyo, Japan</affiliation><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">Masayuki</namePart><namePart type="family">Yokochi</namePart><namePart type="termsOfAddress">MD, PhD</namePart><affiliation>Department of Neurology, Ebara Metropolitan Hospital, Tokyo, Japan</affiliation><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">Tohru</namePart><namePart type="family">Kojo</namePart><namePart type="termsOfAddress">MD, PhD</namePart><affiliation>Department of Neuropathology, Tokyo Metropolitan Institute for Neuroscience, Tokyo, Japan</affiliation><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">Toshiki</namePart><namePart type="family">Uchihara</namePart><namePart type="termsOfAddress">MD, PhD</namePart><affiliation>Department of Neuropathology, Tokyo Metropolitan Institute for Neuroscience, Tokyo, Japan</affiliation><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">Atsushi</namePart><namePart type="family">Takahashi</namePart><namePart type="termsOfAddress">MD, PhD</namePart><affiliation>Organ and Function Pathology Division, Yokufukai Geriatric Hospital, Tokyo, Japan</affiliation><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">Koichi</namePart><namePart type="family">Wakabayashi</namePart><namePart type="termsOfAddress">MD, PhD</namePart><affiliation>Department of Neuropathology, Hirosaki University School of Medicine, Hirosaki, Japan</affiliation><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">Hitoshi</namePart><namePart type="family">Takahashi</namePart><namePart type="termsOfAddress">MD, PhD</namePart><affiliation>Department of Pathology, Brain Research Institute, University of Niigata, Niigata, Japan</affiliation><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">Nobutaka</namePart><namePart type="family">Hattori</namePart><namePart type="termsOfAddress">MD, PhD</namePart><affiliation>Department of Neurology, Juntendo University School of Medicine, Tokyo, Japan</affiliation><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">Yoshikuni</namePart><namePart type="family">Mizuno</namePart><namePart type="termsOfAddress">MD, PhD</namePart><affiliation>Department of Neurology, Juntendo University School of Medicine, Tokyo, Japan</affiliation><role><roleTerm type="text">author</roleTerm></role></name><typeOfResource>text</typeOfResource><genre authority="originalCategForm">article</genre><originInfo><publisher>Wiley Subscription Services, Inc., A Wiley Company</publisher><place><placeTerm type="text">Hoboken</placeTerm></place><dateIssued encoding="w3cdtf">2005-10</dateIssued><dateCaptured encoding="w3cdtf">2004-12-24</dateCaptured><dateValid encoding="w3cdtf">2005-01-31</dateValid><copyrightDate encoding="w3cdtf">2005</copyrightDate></originInfo><language><languageTerm type="code" authority="rfc3066">en</languageTerm><languageTerm type="code" authority="iso639-2b">eng</languageTerm></language><physicalDescription><internetMediaType>text/html</internetMediaType><extent unit="figures">2</extent><extent unit="tables">1</extent><extent unit="references">21</extent><extent unit="words">2539</extent></physicalDescription><abstract lang="en">We performed [123I] MIBG myocardial scintigraphy in two of three patients with PARK2 from unrelated families and examined the heart tissues from the three patients immunohistochemically using an antibody against tyrosine hydroxylase (TH) to see whether cardiac sympathetic nerve is involved. Cardiac uptake of MIBG was normal except for a slight decrease in the late phase in one of the patients. Postmortem examination revealed that TH‐immunoreactive nerve fibers in the epicardium were well preserved in all three patients. The present study confirmed that cardiac sympathetic nerve is well preserved in PARK2 with a homozygous exon deletion, which accounts for normal cardiac uptake of MIBG. Moreover, normal cardiac uptake of MIBG might be of potential diagnostic value to indicate the absence of Lewy body pathology, even in patients with levodopa‐responsive Parkinsonism, as in PARK2. © 2005 Movement Disorder Society</abstract><note type="funding">Japan Foundation for Neuroscience and Mental Health (Tama Nakagawa Foundation)</note><subject lang="en"><genre>Keywords</genre><topic>PARK2</topic><topic>Parkinson's disease</topic><topic>MIBG myocardial scintigraphy</topic><topic>cardiac sympathetic nerve</topic><topic>denervation</topic></subject><relatedItem type="host"><titleInfo><title>Movement Disorders</title><subTitle>Official Journal of the Movement Disorder Society</subTitle></titleInfo><titleInfo type="abbreviated"><title>Mov. Disord.</title></titleInfo><subject><genre>article category</genre><topic>Brief Report</topic></subject><identifier type="ISSN">0885-3185</identifier><identifier type="eISSN">1531-8257</identifier><identifier type="DOI">10.1002/(ISSN)1531-8257</identifier><identifier type="PublisherID">MDS</identifier><part><date>2005</date><detail type="volume"><caption>vol.</caption><number>20</number></detail><detail type="issue"><caption>no.</caption><number>10</number></detail><extent unit="pages"><start>1350</start><end>1353</end><total>4</total></extent></part></relatedItem><identifier type="istex">93A1F555EE9922B77F75A14F22D7C2A6EE6E1916</identifier><identifier type="DOI">10.1002/mds.20594</identifier><identifier type="ArticleID">MDS20594</identifier><accessCondition type="use and reproduction" contentType="copyright">Copyright © 2005 Movement Disorder Society</accessCondition><recordInfo><recordOrigin>Wiley Subscription Services, Inc., A Wiley Company</recordOrigin><recordContentSource>WILEY</recordContentSource></recordInfo></mods></metadata><serie></serie></istex></record>Pour manipuler ce document sous Unix (Dilib)
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