Corpus callosum in neurodegenerative diseases : Findings in Parkinson's disease
Identifieur interne : 000808 ( PascalFrancis/Checkpoint ); précédent : 000807; suivant : 000809Corpus callosum in neurodegenerative diseases : Findings in Parkinson's disease
Auteurs : Katie Wiltshire [Canada] ; Sheri Foster [Canada] ; Jeffrey A. Kaye [États-Unis] ; Brent J. Small [États-Unis] ; Richard Camicioli [Canada]Source :
- Dementia and geriatric cognitive disorders [ 1420-8008 ] ; 2005.
Descripteurs français
- Pascal (Inist)
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Abstract
Corpus callosum area has been examined in neurodegenerative diseases as a marker for cortical pathology and for differential diagnosis; however, it has not been examined in Parkinson's disease (PD). We compared callosal area in patients with PD and PD with dementia (PDD) to healthy controls and patients with Alzheimer's disease (AD). We subsequently compared our results to a meta-analysis of studies examining callosal area in AD, frontotemporal dementia (FTD), progressive supranuclear palsy (PSP), and corticobasal degeneration (CBD). For the imaging study, midsagittal T1-weighted MRIs were analyzed and the callosal area was determined in patients with PD (n = 24), PDD (n = 25), AD (n = 16) and controls (n = 27). The meta-analysis combined results from all publications (Medline or PubMed) representing unique samples and measuring callosal area in AD, FTD, PSP, and CBD. We found that PD and PDD patients did not show statistically significant callosal atrophy compared to controls (effect size d, 95% Cl, d = 0.13, -0.26 to 0.52, and d = 0.05, -0.44 to 0.33, respectively) or AD. The AD patients had a significant loss of callosal area compared to controls (d = -0.58, -1.01 to -0.15). Dementia severity was correlated with total callosal atrophy in AD (R = 0.66, p < 0.01) but not in PDD patients (R = 0.18, p> 0.1). The meta-analysis revealed significant combined effect sizes for callosal atrophy of: AD (d = -1.03, -1.13 to -0.93), FTD (d = -1.21, -1.56 to - 0.86), PSP (d = -1.09, -1.38 to -0.81), and CBD (d = -1.80, -2.18 to -1.43). We conclude that PD and PDD patients do not have callosal atrophy in contrast to other neurodegenerative diseases, including AD. Callosal atrophy was correlated with dementia severity in patients with AD but not PDD.
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Kaye</name><affiliation wicri:level="1"><inist:fA14 i1="02"><s1>Oregon Health and Science University</s1><s2>Portland, Oreg</s2><s3>USA</s3><sZ>3 aut.</sZ></inist:fA14><country>États-Unis</country><wicri:noRegion>Oregon Health and Science University</wicri:noRegion></affiliation></author><author><name sortKey="Small, Brent J" sort="Small, Brent J" uniqKey="Small B" first="Brent J." last="Small">Brent J. Small</name><affiliation wicri:level="4"><inist:fA14 i1="03"><s1>University of South Florida</s1><s2>Tampa, Fla</s2><s3>USA</s3><sZ>4 aut.</sZ></inist:fA14><country>États-Unis</country><placeName><settlement type="city">Tampa</settlement><region type="state">Floride</region></placeName><orgName type="university">Université de Floride du Sud</orgName></affiliation></author><author><name sortKey="Camicioli, Richard" sort="Camicioli, Richard" uniqKey="Camicioli R" first="Richard" last="Camicioli">Richard Camicioli</name><affiliation wicri:level="1"><inist:fA14 i1="01"><s1>University of Alberta</s1><s2>Edmonton</s2><s3>CAN</s3><sZ>1 aut.</sZ><sZ>2 aut.</sZ><sZ>5 aut.</sZ></inist:fA14><country>Canada</country><wicri:noRegion>University of Alberta</wicri:noRegion></affiliation></author></titleStmt><publicationStmt><idno type="wicri:source">INIST</idno><idno type="inist">06-0002537</idno><date when="2005">2005</date><idno type="stanalyst">PASCAL 06-0002537 INIST</idno><idno type="RBID">Pascal:06-0002537</idno><idno type="wicri:Area/PascalFrancis/Corpus">000875</idno><idno type="wicri:Area/PascalFrancis/Curation">000448</idno><idno type="wicri:Area/PascalFrancis/Checkpoint">000808</idno><idno type="wicri:explorRef" wicri:stream="PascalFrancis" wicri:step="Checkpoint">000808</idno></publicationStmt><sourceDesc><biblStruct><analytic><title xml:lang="en" level="a">Corpus callosum in neurodegenerative diseases : Findings in Parkinson's disease</title><author><name sortKey="Wiltshire, Katie" sort="Wiltshire, Katie" uniqKey="Wiltshire K" first="Katie" last="Wiltshire">Katie Wiltshire</name><affiliation wicri:level="1"><inist:fA14 i1="01"><s1>University of Alberta</s1><s2>Edmonton</s2><s3>CAN</s3><sZ>1 aut.</sZ><sZ>2 aut.</sZ><sZ>5 aut.</sZ></inist:fA14><country>Canada</country><wicri:noRegion>University of Alberta</wicri:noRegion></affiliation></author><author><name sortKey="Foster, Sheri" sort="Foster, Sheri" uniqKey="Foster S" first="Sheri" last="Foster">Sheri Foster</name><affiliation wicri:level="1"><inist:fA14 i1="01"><s1>University of Alberta</s1><s2>Edmonton</s2><s3>CAN</s3><sZ>1 aut.</sZ><sZ>2 aut.</sZ><sZ>5 aut.</sZ></inist:fA14><country>Canada</country><wicri:noRegion>University of Alberta</wicri:noRegion></affiliation></author><author><name sortKey="Kaye, Jeffrey A" sort="Kaye, Jeffrey A" uniqKey="Kaye J" first="Jeffrey A." last="Kaye">Jeffrey A. Kaye</name><affiliation wicri:level="1"><inist:fA14 i1="02"><s1>Oregon Health and Science University</s1><s2>Portland, Oreg</s2><s3>USA</s3><sZ>3 aut.</sZ></inist:fA14><country>États-Unis</country><wicri:noRegion>Oregon Health and Science University</wicri:noRegion></affiliation></author><author><name sortKey="Small, Brent J" sort="Small, Brent J" uniqKey="Small B" first="Brent J." last="Small">Brent J. Small</name><affiliation wicri:level="4"><inist:fA14 i1="03"><s1>University of South Florida</s1><s2>Tampa, Fla</s2><s3>USA</s3><sZ>4 aut.</sZ></inist:fA14><country>États-Unis</country><placeName><settlement type="city">Tampa</settlement><region type="state">Floride</region></placeName><orgName type="university">Université de Floride du Sud</orgName></affiliation></author><author><name sortKey="Camicioli, Richard" sort="Camicioli, Richard" uniqKey="Camicioli R" first="Richard" last="Camicioli">Richard Camicioli</name><affiliation wicri:level="1"><inist:fA14 i1="01"><s1>University of Alberta</s1><s2>Edmonton</s2><s3>CAN</s3><sZ>1 aut.</sZ><sZ>2 aut.</sZ><sZ>5 aut.</sZ></inist:fA14><country>Canada</country><wicri:noRegion>University of Alberta</wicri:noRegion></affiliation></author></analytic><series><title level="j" type="main">Dementia and geriatric cognitive disorders</title><title level="j" type="abbreviated">Dement. geriatr. cogn. disord.</title><idno type="ISSN">1420-8008</idno><imprint><date when="2005">2005</date></imprint></series></biblStruct></sourceDesc><seriesStmt><title level="j" type="main">Dementia and geriatric cognitive disorders</title><title level="j" type="abbreviated">Dement. geriatr. cogn. disord.</title><idno type="ISSN">1420-8008</idno></seriesStmt></fileDesc><profileDesc><textClass><keywords scheme="KwdEn" xml:lang="en"><term>Cognitive disorder</term><term>Corpus callosum</term><term>Degenerative disease</term><term>Dementia</term><term>Nervous system diseases</term><term>Nuclear magnetic resonance imaging</term><term>Parkinson disease</term></keywords><keywords scheme="Pascal" xml:lang="fr"><term>Système nerveux pathologie</term><term>Démence</term><term>Trouble cognition</term><term>Parkinson maladie</term><term>Maladie dégénérative</term><term>Corps calleux</term><term>Imagerie RMN</term></keywords></textClass></profileDesc></teiHeader><front><div type="abstract" xml:lang="en">Corpus callosum area has been examined in neurodegenerative diseases as a marker for cortical pathology and for differential diagnosis; however, it has not been examined in Parkinson's disease (PD). We compared callosal area in patients with PD and PD with dementia (PDD) to healthy controls and patients with Alzheimer's disease (AD). We subsequently compared our results to a meta-analysis of studies examining callosal area in AD, frontotemporal dementia (FTD), progressive supranuclear palsy (PSP), and corticobasal degeneration (CBD). For the imaging study, midsagittal T<sub>1</sub>-weighted MRIs were analyzed and the callosal area was determined in patients with PD (n = 24), PDD (n = 25), AD (n = 16) and controls (n = 27). The meta-analysis combined results from all publications (Medline or PubMed) representing unique samples and measuring callosal area in AD, FTD, PSP, and CBD. We found that PD and PDD patients did not show statistically significant callosal atrophy compared to controls (effect size d, 95% Cl, d = 0.13, -0.26 to 0.52, and d = 0.05, -0.44 to 0.33, respectively) or AD. The AD patients had a significant loss of callosal area compared to controls (d = -0.58, -1.01 to -0.15). Dementia severity was correlated with total callosal atrophy in AD (R = 0.66, p < 0.01) but not in PDD patients (R = 0.18, p> 0.1). The meta-analysis revealed significant combined effect sizes for callosal atrophy of: AD (d = -1.03, -1.13 to -0.93), FTD (d = -1.21, -1.56 to - 0.86), PSP (d = -1.09, -1.38 to -0.81), and CBD (d = -1.80, -2.18 to -1.43). We conclude that PD and PDD patients do not have callosal atrophy in contrast to other neurodegenerative diseases, including AD. Callosal atrophy was correlated with dementia severity in patients with AD but not PDD.</div></front></TEI><inist><standard h6="B"><pA><fA01 i1="01" i2="1"><s0>1420-8008</s0></fA01><fA03 i2="1"><s0>Dement. geriatr. cogn. disord.</s0></fA03><fA05><s2>20</s2></fA05><fA06><s2>6</s2></fA06><fA08 i1="01" i2="1" l="ENG"><s1>Corpus callosum in neurodegenerative diseases : Findings in Parkinson's disease</s1></fA08><fA11 i1="01" i2="1"><s1>WILTSHIRE (Katie)</s1></fA11><fA11 i1="02" i2="1"><s1>FOSTER (Sheri)</s1></fA11><fA11 i1="03" i2="1"><s1>KAYE (Jeffrey A.)</s1></fA11><fA11 i1="04" i2="1"><s1>SMALL (Brent J.)</s1></fA11><fA11 i1="05" i2="1"><s1>CAMICIOLI (Richard)</s1></fA11><fA14 i1="01"><s1>University of Alberta</s1><s2>Edmonton</s2><s3>CAN</s3><sZ>1 aut.</sZ><sZ>2 aut.</sZ><sZ>5 aut.</sZ></fA14><fA14 i1="02"><s1>Oregon Health and Science University</s1><s2>Portland, Oreg</s2><s3>USA</s3><sZ>3 aut.</sZ></fA14><fA14 i1="03"><s1>University of South Florida</s1><s2>Tampa, Fla</s2><s3>USA</s3><sZ>4 aut.</sZ></fA14><fA20><s1>345-351</s1></fA20><fA21><s1>2005</s1></fA21><fA23 i1="01"><s0>ENG</s0></fA23><fA43 i1="01"><s1>INIST</s1><s2>22106</s2><s5>354000135170660030</s5></fA43><fA44><s0>0000</s0><s1>© 2006 INIST-CNRS. 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For the imaging study, midsagittal T<sub>1</sub>-weighted MRIs were analyzed and the callosal area was determined in patients with PD (n = 24), PDD (n = 25), AD (n = 16) and controls (n = 27). The meta-analysis combined results from all publications (Medline or PubMed) representing unique samples and measuring callosal area in AD, FTD, PSP, and CBD. We found that PD and PDD patients did not show statistically significant callosal atrophy compared to controls (effect size d, 95% Cl, d = 0.13, -0.26 to 0.52, and d = 0.05, -0.44 to 0.33, respectively) or AD. The AD patients had a significant loss of callosal area compared to controls (d = -0.58, -1.01 to -0.15). Dementia severity was correlated with total callosal atrophy in AD (R = 0.66, p < 0.01) but not in PDD patients (R = 0.18, p> 0.1). The meta-analysis revealed significant combined effect sizes for callosal atrophy of: AD (d = -1.03, -1.13 to -0.93), FTD (d = -1.21, -1.56 to - 0.86), PSP (d = -1.09, -1.38 to -0.81), and CBD (d = -1.80, -2.18 to -1.43). We conclude that PD and PDD patients do not have callosal atrophy in contrast to other neurodegenerative diseases, including AD. 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