Distinct Patterns of Regional Cerebral Glucose Metabolism in Parkinson's Disease with and without Mild Cognitive Impairment
Identifieur interne : 000E98 ( PascalFrancis/Corpus ); précédent : 000E97; suivant : 000E99Distinct Patterns of Regional Cerebral Glucose Metabolism in Parkinson's Disease with and without Mild Cognitive Impairment
Auteurs : Yoshiyuki Hosokai ; Yoshiyuki Nishio ; Kazumi Hirayama ; Atsushi Takeda ; Toshiyuki Ishioka ; Yoichi Sawada ; Kyoko Suzuki ; Yasuto Itoyama ; Shoki Takahashi ; Hiroshi Fukuda ; Etsuro MoriSource :
- Movement disorders [ 0885-3185 ] ; 2009.
Descripteurs français
- Pascal (Inist)
English descriptors
- KwdEn :
Abstract
There is no consensus with regard to the clinical and neuroimaging characteristics of prodromal dementia in Parkinson's disease (PD). To delineate functional neuroimaging features of PD with mild cognitive impairment (PDMCI) and with no cognitive impairment (PDNC), we compared regional cerebral glucose metabolism (CMRglc) amongst 13 patients with PDMCI, 27 with PDNC, and 13 healthy controls. The PDNC patients had limited areas of hypometabolism in the frontal and occipital cortices. In the PDMCI patients, there were extensive areas of hypometabolism in the posterior cortical regions, including the temporo-parieto-occipital junction, medial parietal, and inferior temporal cortices. The present results suggest that posterior cortical dysfunction is the primary neuroimaging feature of PD patients at risk for dementia.
Notice en format standard (ISO 2709)
Pour connaître la documentation sur le format Inist Standard.
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Format Inist (serveur)
NO : | PASCAL 09-0223194 INIST |
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ET : | Distinct Patterns of Regional Cerebral Glucose Metabolism in Parkinson's Disease with and without Mild Cognitive Impairment |
AU : | HOSOKAI (Yoshiyuki); NISHIO (Yoshiyuki); HIRAYAMA (Kazumi); TAKEDA (Atsushi); ISHIOKA (Toshiyuki); SAWADA (Yoichi); SUZUKI (Kyoko); ITOYAMA (Yasuto); TAKAHASHI (Shoki); FUKUDA (Hiroshi); MORI (Etsuro) |
AF : | Department of Radiological Technology and Science, School of Health Science, Tohoku University/Sendai/Japon (1 aut.); Department of Behavioral Neurology and Cognitive Neuroscience, Graduate School of Medicine, Tohoku University/Sendai/Japon (1 aut., 2 aut., 3 aut., 5 aut., 6 aut., 7 aut., 11 aut.); Department of Neurology, Graduate School of Medicine, Tohoku University/Sendai/Japon (4 aut., 8 aut.); Department of Clinical Neuroscience, Graduate School of Medicine, Yamagata University/Yamagata/Japon (7 aut.); Department of Diagnostic Radiology, Graduate School of Medicine, Tohoku University/Sendai/Japon (9 aut.); Department of Radiology and Nuclear Medicine, Institute of Development, Aging, and Cancer, Tohoku University/Sendai/Japon (10 aut.) |
DT : | Publication en série; Niveau analytique |
SO : | Movement disorders; ISSN 0885-3185; Etats-Unis; Da. 2009; Vol. 24; No. 6; Pp. 854-862; Bibl. 32 ref. |
LA : | Anglais |
EA : | There is no consensus with regard to the clinical and neuroimaging characteristics of prodromal dementia in Parkinson's disease (PD). To delineate functional neuroimaging features of PD with mild cognitive impairment (PDMCI) and with no cognitive impairment (PDNC), we compared regional cerebral glucose metabolism (CMRglc) amongst 13 patients with PDMCI, 27 with PDNC, and 13 healthy controls. The PDNC patients had limited areas of hypometabolism in the frontal and occipital cortices. In the PDMCI patients, there were extensive areas of hypometabolism in the posterior cortical regions, including the temporo-parieto-occipital junction, medial parietal, and inferior temporal cortices. The present results suggest that posterior cortical dysfunction is the primary neuroimaging feature of PD patients at risk for dementia. |
CC : | 002B17; 002B17G |
FD : | Maladie de Parkinson; Déficit cognitif léger; Trouble cognitif; Pathologie du système nerveux; Encéphale; Glucose; Métabolisme; Tomoscintigraphie; Tomographie par émission de positons |
FG : | Système nerveux central; Pathologie de l'encéphale; Syndrome extrapyramidal; Maladie dégénérative; Pathologie du système nerveux central |
ED : | Parkinson disease; mild cognitive impairment; Cognitive disorder; Nervous system diseases; Encephalon; Glucose; Metabolism; Emission tomography; Positron emission tomography |
EG : | Central nervous system; Cerebral disorder; Extrapyramidal syndrome; Degenerative disease; Central nervous system disease |
SD : | Parkinson enfermedad; Disturbio cognitivo ligero; Trastorno cognitivo; Sistema nervioso patología; Encéfalo; Glucosa; Metabolismo; Tomocentelleografía; Tomografía emisión positrones |
LO : | INIST-20953.354000186181820090 |
ID : | 09-0223194 |
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Pascal:09-0223194Le document en format XML
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<series><title level="j" type="main">Movement disorders</title>
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<profileDesc><textClass><keywords scheme="KwdEn" xml:lang="en"><term>Cognitive disorder</term>
<term>Emission tomography</term>
<term>Encephalon</term>
<term>Glucose</term>
<term>Metabolism</term>
<term>Nervous system diseases</term>
<term>Parkinson disease</term>
<term>Positron emission tomography</term>
<term>mild cognitive impairment</term>
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<keywords scheme="Pascal" xml:lang="fr"><term>Maladie de Parkinson</term>
<term>Déficit cognitif léger</term>
<term>Trouble cognitif</term>
<term>Pathologie du système nerveux</term>
<term>Encéphale</term>
<term>Glucose</term>
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<term>Tomoscintigraphie</term>
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<front><div type="abstract" xml:lang="en">There is no consensus with regard to the clinical and neuroimaging characteristics of prodromal dementia in Parkinson's disease (PD). To delineate functional neuroimaging features of PD with mild cognitive impairment (PDMCI) and with no cognitive impairment (PDNC), we compared regional cerebral glucose metabolism (CMRglc) amongst 13 patients with PDMCI, 27 with PDNC, and 13 healthy controls. The PDNC patients had limited areas of hypometabolism in the frontal and occipital cortices. In the PDMCI patients, there were extensive areas of hypometabolism in the posterior cortical regions, including the temporo-parieto-occipital junction, medial parietal, and inferior temporal cortices. The present results suggest that posterior cortical dysfunction is the primary neuroimaging feature of PD patients at risk for dementia.</div>
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<sZ>9 aut.</sZ>
</fA14>
<fA14 i1="06"><s1>Department of Radiology and Nuclear Medicine, Institute of Development, Aging, and Cancer, Tohoku University</s1>
<s2>Sendai</s2>
<s3>JPN</s3>
<sZ>10 aut.</sZ>
</fA14>
<fA20><s1>854-862</s1>
</fA20>
<fA21><s1>2009</s1>
</fA21>
<fA23 i1="01"><s0>ENG</s0>
</fA23>
<fA43 i1="01"><s1>INIST</s1>
<s2>20953</s2>
<s5>354000186181820090</s5>
</fA43>
<fA44><s0>0000</s0>
<s1>© 2009 INIST-CNRS. All rights reserved.</s1>
</fA44>
<fA45><s0>32 ref.</s0>
</fA45>
<fA47 i1="01" i2="1"><s0>09-0223194</s0>
</fA47>
<fA60><s1>P</s1>
</fA60>
<fA61><s0>A</s0>
</fA61>
<fA64 i1="01" i2="1"><s0>Movement disorders</s0>
</fA64>
<fA66 i1="01"><s0>USA</s0>
</fA66>
<fC01 i1="01" l="ENG"><s0>There is no consensus with regard to the clinical and neuroimaging characteristics of prodromal dementia in Parkinson's disease (PD). To delineate functional neuroimaging features of PD with mild cognitive impairment (PDMCI) and with no cognitive impairment (PDNC), we compared regional cerebral glucose metabolism (CMRglc) amongst 13 patients with PDMCI, 27 with PDNC, and 13 healthy controls. The PDNC patients had limited areas of hypometabolism in the frontal and occipital cortices. In the PDMCI patients, there were extensive areas of hypometabolism in the posterior cortical regions, including the temporo-parieto-occipital junction, medial parietal, and inferior temporal cortices. The present results suggest that posterior cortical dysfunction is the primary neuroimaging feature of PD patients at risk for dementia.</s0>
</fC01>
<fC02 i1="01" i2="X"><s0>002B17</s0>
</fC02>
<fC02 i1="02" i2="X"><s0>002B17G</s0>
</fC02>
<fC03 i1="01" i2="X" l="FRE"><s0>Maladie de Parkinson</s0>
<s2>NM</s2>
<s5>01</s5>
</fC03>
<fC03 i1="01" i2="X" l="ENG"><s0>Parkinson disease</s0>
<s2>NM</s2>
<s5>01</s5>
</fC03>
<fC03 i1="01" i2="X" l="SPA"><s0>Parkinson enfermedad</s0>
<s2>NM</s2>
<s5>01</s5>
</fC03>
<fC03 i1="02" i2="X" l="FRE"><s0>Déficit cognitif léger</s0>
<s2>NM</s2>
<s5>02</s5>
</fC03>
<fC03 i1="02" i2="X" l="ENG"><s0>mild cognitive impairment</s0>
<s2>NM</s2>
<s5>02</s5>
</fC03>
<fC03 i1="02" i2="X" l="SPA"><s0>Disturbio cognitivo ligero</s0>
<s2>NM</s2>
<s5>02</s5>
</fC03>
<fC03 i1="03" i2="X" l="FRE"><s0>Trouble cognitif</s0>
<s5>03</s5>
</fC03>
<fC03 i1="03" i2="X" l="ENG"><s0>Cognitive disorder</s0>
<s5>03</s5>
</fC03>
<fC03 i1="03" i2="X" l="SPA"><s0>Trastorno cognitivo</s0>
<s5>03</s5>
</fC03>
<fC03 i1="04" i2="X" l="FRE"><s0>Pathologie du système nerveux</s0>
<s5>04</s5>
</fC03>
<fC03 i1="04" i2="X" l="ENG"><s0>Nervous system diseases</s0>
<s5>04</s5>
</fC03>
<fC03 i1="04" i2="X" l="SPA"><s0>Sistema nervioso patología</s0>
<s5>04</s5>
</fC03>
<fC03 i1="05" i2="X" l="FRE"><s0>Encéphale</s0>
<s5>09</s5>
</fC03>
<fC03 i1="05" i2="X" l="ENG"><s0>Encephalon</s0>
<s5>09</s5>
</fC03>
<fC03 i1="05" i2="X" l="SPA"><s0>Encéfalo</s0>
<s5>09</s5>
</fC03>
<fC03 i1="06" i2="X" l="FRE"><s0>Glucose</s0>
<s2>NK</s2>
<s5>10</s5>
</fC03>
<fC03 i1="06" i2="X" l="ENG"><s0>Glucose</s0>
<s2>NK</s2>
<s5>10</s5>
</fC03>
<fC03 i1="06" i2="X" l="SPA"><s0>Glucosa</s0>
<s2>NK</s2>
<s5>10</s5>
</fC03>
<fC03 i1="07" i2="X" l="FRE"><s0>Métabolisme</s0>
<s5>11</s5>
</fC03>
<fC03 i1="07" i2="X" l="ENG"><s0>Metabolism</s0>
<s5>11</s5>
</fC03>
<fC03 i1="07" i2="X" l="SPA"><s0>Metabolismo</s0>
<s5>11</s5>
</fC03>
<fC03 i1="08" i2="X" l="FRE"><s0>Tomoscintigraphie</s0>
<s5>12</s5>
</fC03>
<fC03 i1="08" i2="X" l="ENG"><s0>Emission tomography</s0>
<s5>12</s5>
</fC03>
<fC03 i1="08" i2="X" l="SPA"><s0>Tomocentelleografía</s0>
<s5>12</s5>
</fC03>
<fC03 i1="09" i2="X" l="FRE"><s0>Tomographie par émission de positons</s0>
<s5>13</s5>
</fC03>
<fC03 i1="09" i2="X" l="ENG"><s0>Positron emission tomography</s0>
<s5>13</s5>
</fC03>
<fC03 i1="09" i2="X" l="SPA"><s0>Tomografía emisión positrones</s0>
<s5>13</s5>
</fC03>
<fC07 i1="01" i2="X" l="FRE"><s0>Système nerveux central</s0>
<s5>37</s5>
</fC07>
<fC07 i1="01" i2="X" l="ENG"><s0>Central nervous system</s0>
<s5>37</s5>
</fC07>
<fC07 i1="01" i2="X" l="SPA"><s0>Sistema nervioso central</s0>
<s5>37</s5>
</fC07>
<fC07 i1="02" i2="X" l="FRE"><s0>Pathologie de l'encéphale</s0>
<s5>38</s5>
</fC07>
<fC07 i1="02" i2="X" l="ENG"><s0>Cerebral disorder</s0>
<s5>38</s5>
</fC07>
<fC07 i1="02" i2="X" l="SPA"><s0>Encéfalo patología</s0>
<s5>38</s5>
</fC07>
<fC07 i1="03" i2="X" l="FRE"><s0>Syndrome extrapyramidal</s0>
<s5>39</s5>
</fC07>
<fC07 i1="03" i2="X" l="ENG"><s0>Extrapyramidal syndrome</s0>
<s5>39</s5>
</fC07>
<fC07 i1="03" i2="X" l="SPA"><s0>Extrapiramidal síndrome</s0>
<s5>39</s5>
</fC07>
<fC07 i1="04" i2="X" l="FRE"><s0>Maladie dégénérative</s0>
<s5>40</s5>
</fC07>
<fC07 i1="04" i2="X" l="ENG"><s0>Degenerative disease</s0>
<s5>40</s5>
</fC07>
<fC07 i1="04" i2="X" l="SPA"><s0>Enfermedad degenerativa</s0>
<s5>40</s5>
</fC07>
<fC07 i1="05" i2="X" l="FRE"><s0>Pathologie du système nerveux central</s0>
<s5>41</s5>
</fC07>
<fC07 i1="05" i2="X" l="ENG"><s0>Central nervous system disease</s0>
<s5>41</s5>
</fC07>
<fC07 i1="05" i2="X" l="SPA"><s0>Sistema nervosio central patología</s0>
<s5>41</s5>
</fC07>
<fN21><s1>166</s1>
</fN21>
<fN44 i1="01"><s1>OTO</s1>
</fN44>
<fN82><s1>OTO</s1>
</fN82>
</pA>
</standard>
<server><NO>PASCAL 09-0223194 INIST</NO>
<ET>Distinct Patterns of Regional Cerebral Glucose Metabolism in Parkinson's Disease with and without Mild Cognitive Impairment</ET>
<AU>HOSOKAI (Yoshiyuki); NISHIO (Yoshiyuki); HIRAYAMA (Kazumi); TAKEDA (Atsushi); ISHIOKA (Toshiyuki); SAWADA (Yoichi); SUZUKI (Kyoko); ITOYAMA (Yasuto); TAKAHASHI (Shoki); FUKUDA (Hiroshi); MORI (Etsuro)</AU>
<AF>Department of Radiological Technology and Science, School of Health Science, Tohoku University/Sendai/Japon (1 aut.); Department of Behavioral Neurology and Cognitive Neuroscience, Graduate School of Medicine, Tohoku University/Sendai/Japon (1 aut., 2 aut., 3 aut., 5 aut., 6 aut., 7 aut., 11 aut.); Department of Neurology, Graduate School of Medicine, Tohoku University/Sendai/Japon (4 aut., 8 aut.); Department of Clinical Neuroscience, Graduate School of Medicine, Yamagata University/Yamagata/Japon (7 aut.); Department of Diagnostic Radiology, Graduate School of Medicine, Tohoku University/Sendai/Japon (9 aut.); Department of Radiology and Nuclear Medicine, Institute of Development, Aging, and Cancer, Tohoku University/Sendai/Japon (10 aut.)</AF>
<DT>Publication en série; Niveau analytique</DT>
<SO>Movement disorders; ISSN 0885-3185; Etats-Unis; Da. 2009; Vol. 24; No. 6; Pp. 854-862; Bibl. 32 ref.</SO>
<LA>Anglais</LA>
<EA>There is no consensus with regard to the clinical and neuroimaging characteristics of prodromal dementia in Parkinson's disease (PD). To delineate functional neuroimaging features of PD with mild cognitive impairment (PDMCI) and with no cognitive impairment (PDNC), we compared regional cerebral glucose metabolism (CMRglc) amongst 13 patients with PDMCI, 27 with PDNC, and 13 healthy controls. The PDNC patients had limited areas of hypometabolism in the frontal and occipital cortices. In the PDMCI patients, there were extensive areas of hypometabolism in the posterior cortical regions, including the temporo-parieto-occipital junction, medial parietal, and inferior temporal cortices. The present results suggest that posterior cortical dysfunction is the primary neuroimaging feature of PD patients at risk for dementia.</EA>
<CC>002B17; 002B17G</CC>
<FD>Maladie de Parkinson; Déficit cognitif léger; Trouble cognitif; Pathologie du système nerveux; Encéphale; Glucose; Métabolisme; Tomoscintigraphie; Tomographie par émission de positons</FD>
<FG>Système nerveux central; Pathologie de l'encéphale; Syndrome extrapyramidal; Maladie dégénérative; Pathologie du système nerveux central</FG>
<ED>Parkinson disease; mild cognitive impairment; Cognitive disorder; Nervous system diseases; Encephalon; Glucose; Metabolism; Emission tomography; Positron emission tomography</ED>
<EG>Central nervous system; Cerebral disorder; Extrapyramidal syndrome; Degenerative disease; Central nervous system disease</EG>
<SD>Parkinson enfermedad; Disturbio cognitivo ligero; Trastorno cognitivo; Sistema nervioso patología; Encéfalo; Glucosa; Metabolismo; Tomocentelleografía; Tomografía emisión positrones</SD>
<LO>INIST-20953.354000186181820090</LO>
<ID>09-0223194</ID>
</server>
</inist>
</record>
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