Amyloid and glucose imaging in dementia with Lewy bodies and multiple systems atrophy

Abstract Background Multiple Systems Atrophy (MSA) and Dementia with Lewy bodies (DLB) can present with both REM behavior disorder and severe autonomic dysfunction. In rare occasions, patients with MSA progress to cognitive impairment and even dementia. Positron emission topography (PET) imaging usi...

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Veröffentlicht in:Parkinsonism & related disorders 2011-03, Vol.17 (3), p.160-165
Hauptverfasser: Claassen, Daniel O, Lowe, Val J, Peller, Patrick J, Petersen, Ronald C, Josephs, Keith A
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creator Claassen, Daniel O
Lowe, Val J
Peller, Patrick J
Petersen, Ronald C
Josephs, Keith A
description Abstract Background Multiple Systems Atrophy (MSA) and Dementia with Lewy bodies (DLB) can present with both REM behavior disorder and severe autonomic dysfunction. In rare occasions, patients with MSA progress to cognitive impairment and even dementia. Positron emission topography (PET) imaging using both the amyloid ligand Pittsburgh Compound B (11C-PiB) and 18 flurodeoxyglucose (18F-FDG) was used to ascertain the presence of amyloid and pattern of glucose metabolic derangement in both disorders. Methods Patients diagnosed with probable DLB or MSA, with clinical symptoms of either REM Behavior Disorder (RBD), Parkinsonism, or dysautonomia were prospectively identified. All underwent both 11C-PiB and 18F-FDG PET imaging. Statistical comparison between DLB, MSA, and normal controls was performed. Results Six patients, 3 with DLB, 2 with Parkinson predominant MSA (MSA-P), and 1 with cerebellar predominant MSA (MSA-C) were identified. Increased level of PiB retention was noted in all patients diagnosed with DLB, but was absent in MSA. In those with DLB, glucose hypometabolism corresponded with regions of amyloid presence, and included prefrontal, parietotemporal, occipital and primary visual cortex regions. MSA patients were distinguished by cerebellar glucose hypometabolism. Conclusions These findings emphasize the distinguishing characteristics between the alpha-synuclein related disorders of DLB and MSA. The absence of amyloid in the cases of MSA is a possible distinguishing characteristic of the disorder.
doi_str_mv 10.1016/j.parkreldis.2010.12.006
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In rare occasions, patients with MSA progress to cognitive impairment and even dementia. Positron emission topography (PET) imaging using both the amyloid ligand Pittsburgh Compound B (11C-PiB) and 18 flurodeoxyglucose (18F-FDG) was used to ascertain the presence of amyloid and pattern of glucose metabolic derangement in both disorders. Methods Patients diagnosed with probable DLB or MSA, with clinical symptoms of either REM Behavior Disorder (RBD), Parkinsonism, or dysautonomia were prospectively identified. All underwent both 11C-PiB and 18F-FDG PET imaging. Statistical comparison between DLB, MSA, and normal controls was performed. Results Six patients, 3 with DLB, 2 with Parkinson predominant MSA (MSA-P), and 1 with cerebellar predominant MSA (MSA-C) were identified. Increased level of PiB retention was noted in all patients diagnosed with DLB, but was absent in MSA. In those with DLB, glucose hypometabolism corresponded with regions of amyloid presence, and included prefrontal, parietotemporal, occipital and primary visual cortex regions. MSA patients were distinguished by cerebellar glucose hypometabolism. Conclusions These findings emphasize the distinguishing characteristics between the alpha-synuclein related disorders of DLB and MSA. The absence of amyloid in the cases of MSA is a possible distinguishing characteristic of the disorder.</description><identifier>ISSN: 1353-8020</identifier><identifier>EISSN: 1873-5126</identifier><identifier>DOI: 10.1016/j.parkreldis.2010.12.006</identifier><identifier>PMID: 21195652</identifier><language>eng</language><publisher>England: Elsevier Ltd</publisher><subject>Aged ; Amyloid - metabolism ; Aniline Compounds ; Autonomic diseases ; Brain Mapping ; Dementia with Lewy bodies ; Female ; Fluorodeoxyglucose F18 ; Glucose - metabolism ; Humans ; Lewy Body Disease - diagnostic imaging ; Lewy Body Disease - pathology ; Male ; Middle Aged ; Multiple system atrophy ; Multiple System Atrophy - diagnostic imaging ; Multiple System Atrophy - pathology ; Neurology ; Parasomnias ; PIB PET ; Positron-Emission Tomography - methods ; Thiazoles ; Tomography, X-Ray Computed - methods</subject><ispartof>Parkinsonism &amp; related disorders, 2011-03, Vol.17 (3), p.160-165</ispartof><rights>Elsevier Ltd</rights><rights>2010 Elsevier Ltd</rights><rights>Copyright © 2010 Elsevier Ltd. 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In rare occasions, patients with MSA progress to cognitive impairment and even dementia. Positron emission topography (PET) imaging using both the amyloid ligand Pittsburgh Compound B (11C-PiB) and 18 flurodeoxyglucose (18F-FDG) was used to ascertain the presence of amyloid and pattern of glucose metabolic derangement in both disorders. Methods Patients diagnosed with probable DLB or MSA, with clinical symptoms of either REM Behavior Disorder (RBD), Parkinsonism, or dysautonomia were prospectively identified. All underwent both 11C-PiB and 18F-FDG PET imaging. Statistical comparison between DLB, MSA, and normal controls was performed. Results Six patients, 3 with DLB, 2 with Parkinson predominant MSA (MSA-P), and 1 with cerebellar predominant MSA (MSA-C) were identified. Increased level of PiB retention was noted in all patients diagnosed with DLB, but was absent in MSA. In those with DLB, glucose hypometabolism corresponded with regions of amyloid presence, and included prefrontal, parietotemporal, occipital and primary visual cortex regions. MSA patients were distinguished by cerebellar glucose hypometabolism. Conclusions These findings emphasize the distinguishing characteristics between the alpha-synuclein related disorders of DLB and MSA. The absence of amyloid in the cases of MSA is a possible distinguishing characteristic of the disorder.</description><subject>Aged</subject><subject>Amyloid - metabolism</subject><subject>Aniline Compounds</subject><subject>Autonomic diseases</subject><subject>Brain Mapping</subject><subject>Dementia with Lewy bodies</subject><subject>Female</subject><subject>Fluorodeoxyglucose F18</subject><subject>Glucose - metabolism</subject><subject>Humans</subject><subject>Lewy Body Disease - diagnostic imaging</subject><subject>Lewy Body Disease - pathology</subject><subject>Male</subject><subject>Middle Aged</subject><subject>Multiple system atrophy</subject><subject>Multiple System Atrophy - diagnostic imaging</subject><subject>Multiple System Atrophy - pathology</subject><subject>Neurology</subject><subject>Parasomnias</subject><subject>PIB PET</subject><subject>Positron-Emission Tomography - methods</subject><subject>Thiazoles</subject><subject>Tomography, X-Ray Computed - methods</subject><issn>1353-8020</issn><issn>1873-5126</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2011</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><recordid>eNqNksuO1DAQRS0EYh7wC8g7VunxI3bcG6RhxEtqiQXM2nLb5R73OHGwE0b5exx6AIkNrKpUureudKoQwpRsKKHy6rgZTb7PEF0oG0bWMdsQIp-gc6o63gjK5NPac8EbRRg5QxelHAkhnSD8OTpjlG6FFOwc3V73S0zBYTM4fIizTQVw6M0hDAccBuygh2EKBj-E6Q7v4GHB--QClJ-Gfo5TGCPgspQJ-jqcchrvlhfomTexwMvHeolu37_7evOx2X3-8OnmetdY3ompcabdS9V6SQXIjhrrvDAdU04S0oJ3HZdgiTSEKWF951vBWy-AUu4c33vgl-j1ae-Y07cZyqT7UCzEaAZIc9Fqu6U1ibF_KwXbEq44r0p1UtqcSsng9ZgrkLxoSvRKXx_1H_p6pa8p05V-tb56DJn3Pbjfxl-4q-DtSQAVyvcAWRcbYLDgQgY7aZfC_6S8-WuJjWEI1sR7WKAc05yHCl1TXapBf1m_YH0CWu_PiaL8By-3sL0</recordid><startdate>201103</startdate><enddate>201103</enddate><creator>Claassen, Daniel O</creator><creator>Lowe, Val J</creator><creator>Peller, Patrick J</creator><creator>Petersen, Ronald C</creator><creator>Josephs, Keith A</creator><general>Elsevier Ltd</general><scope>CGR</scope><scope>CUY</scope><scope>CVF</scope><scope>ECM</scope><scope>EIF</scope><scope>NPM</scope><scope>AAYXX</scope><scope>CITATION</scope><scope>7X8</scope><scope>7TK</scope></search><sort><creationdate>201103</creationdate><title>Amyloid and glucose imaging in dementia with Lewy bodies and multiple systems atrophy</title><author>Claassen, Daniel O ; Lowe, Val J ; Peller, Patrick J ; Petersen, Ronald C ; Josephs, Keith A</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c375t-da4b684f615e671acdf5a728d6004efd736ec06a0285cf7f4534f5e113dd3bfe3</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2011</creationdate><topic>Aged</topic><topic>Amyloid - metabolism</topic><topic>Aniline Compounds</topic><topic>Autonomic diseases</topic><topic>Brain Mapping</topic><topic>Dementia with Lewy bodies</topic><topic>Female</topic><topic>Fluorodeoxyglucose F18</topic><topic>Glucose - metabolism</topic><topic>Humans</topic><topic>Lewy Body Disease - diagnostic imaging</topic><topic>Lewy Body Disease - pathology</topic><topic>Male</topic><topic>Middle Aged</topic><topic>Multiple system atrophy</topic><topic>Multiple System Atrophy - diagnostic imaging</topic><topic>Multiple System Atrophy - pathology</topic><topic>Neurology</topic><topic>Parasomnias</topic><topic>PIB PET</topic><topic>Positron-Emission Tomography - methods</topic><topic>Thiazoles</topic><topic>Tomography, X-Ray Computed - methods</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Claassen, Daniel O</creatorcontrib><creatorcontrib>Lowe, Val J</creatorcontrib><creatorcontrib>Peller, Patrick J</creatorcontrib><creatorcontrib>Petersen, Ronald C</creatorcontrib><creatorcontrib>Josephs, Keith A</creatorcontrib><collection>Medline</collection><collection>MEDLINE</collection><collection>MEDLINE (Ovid)</collection><collection>MEDLINE</collection><collection>MEDLINE</collection><collection>PubMed</collection><collection>CrossRef</collection><collection>MEDLINE - Academic</collection><collection>Neurosciences Abstracts</collection><jtitle>Parkinsonism &amp; related disorders</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Claassen, Daniel O</au><au>Lowe, Val J</au><au>Peller, Patrick J</au><au>Petersen, Ronald C</au><au>Josephs, Keith A</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Amyloid and glucose imaging in dementia with Lewy bodies and multiple systems atrophy</atitle><jtitle>Parkinsonism &amp; related disorders</jtitle><addtitle>Parkinsonism Relat Disord</addtitle><date>2011-03</date><risdate>2011</risdate><volume>17</volume><issue>3</issue><spage>160</spage><epage>165</epage><pages>160-165</pages><issn>1353-8020</issn><eissn>1873-5126</eissn><abstract>Abstract Background Multiple Systems Atrophy (MSA) and Dementia with Lewy bodies (DLB) can present with both REM behavior disorder and severe autonomic dysfunction. In rare occasions, patients with MSA progress to cognitive impairment and even dementia. Positron emission topography (PET) imaging using both the amyloid ligand Pittsburgh Compound B (11C-PiB) and 18 flurodeoxyglucose (18F-FDG) was used to ascertain the presence of amyloid and pattern of glucose metabolic derangement in both disorders. Methods Patients diagnosed with probable DLB or MSA, with clinical symptoms of either REM Behavior Disorder (RBD), Parkinsonism, or dysautonomia were prospectively identified. All underwent both 11C-PiB and 18F-FDG PET imaging. Statistical comparison between DLB, MSA, and normal controls was performed. Results Six patients, 3 with DLB, 2 with Parkinson predominant MSA (MSA-P), and 1 with cerebellar predominant MSA (MSA-C) were identified. Increased level of PiB retention was noted in all patients diagnosed with DLB, but was absent in MSA. In those with DLB, glucose hypometabolism corresponded with regions of amyloid presence, and included prefrontal, parietotemporal, occipital and primary visual cortex regions. MSA patients were distinguished by cerebellar glucose hypometabolism. Conclusions These findings emphasize the distinguishing characteristics between the alpha-synuclein related disorders of DLB and MSA. The absence of amyloid in the cases of MSA is a possible distinguishing characteristic of the disorder.</abstract><cop>England</cop><pub>Elsevier Ltd</pub><pmid>21195652</pmid><doi>10.1016/j.parkreldis.2010.12.006</doi><tpages>6</tpages></addata></record>
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subjects Aged
Amyloid - metabolism
Aniline Compounds
Autonomic diseases
Brain Mapping
Dementia with Lewy bodies
Female
Fluorodeoxyglucose F18
Glucose - metabolism
Humans
Lewy Body Disease - diagnostic imaging
Lewy Body Disease - pathology
Male
Middle Aged
Multiple system atrophy
Multiple System Atrophy - diagnostic imaging
Multiple System Atrophy - pathology
Neurology
Parasomnias
PIB PET
Positron-Emission Tomography - methods
Thiazoles
Tomography, X-Ray Computed - methods
title Amyloid and glucose imaging in dementia with Lewy bodies and multiple systems atrophy
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