Resting regional cerebral glucose metabolism in advanced Parkinson's disease studied in the Off and On conditions with [18F]FDG-PET
Identifieur interne : 002886 ( PascalFrancis/Corpus ); précédent : 002885; suivant : 002887Resting regional cerebral glucose metabolism in advanced Parkinson's disease studied in the Off and On conditions with [18F]FDG-PET
Auteurs : Georg Berding ; Per Odin ; David J. Brooks ; Guido Nikkhah ; Cordula Matthies ; Thomas Peschel ; Mona Shing ; Hans Kolbe ; Jörg Van Den Hoff ; Harald Fricke ; Reinhard Dengler ; Madjid Samii ; Wolfram H. KnappSource :
- Movement disorders [ 0885-3185 ] ; 2001.
Descripteurs français
- Pascal (Inist)
English descriptors
- KwdEn :
Abstract
Studies of resting regional cerebral glucose consumption (rCMRGlc) in nondemented patients with Parkinson disease (PD) have produced conflicting results, reporting both reduced and normal metabolism in advanced disease and reduced or normal metabolism after dopaminergic therapy. To investigate these issues, [18F]fluorodeoxyglucose (FDG) positron emission tomography (PET) was performed in 1 nondemented PD patients with advanced disease and 10 age-matched controls. PD patients were studied after withdrawal of all dopaminergic medication to produce a practically defined off condition, and a second time I hour after levodopa, resulting in a clinical on state. Dynamic PET scans and simultaneous arterialised venous blood samples of [18F] acticvity were obtained. A graphical approach was used to generate parametric images of rCMRGlc and statistical parametric mapping to localise significant metabolic changes in PD. Compared with controls, global rCMRGlc was reduced in the on but not in the off condition in PD. In both states, significant regional reductions of glucose uptake were found in the parietal, frontal, temporal cortex, and caudate nucleus, Reductions correlated with the severity of disability in frontal and temporal cortex. Direct comparison between on and off conditions revealed relatively greater reductions of uptake in the ventral/orbital frontal cortex and the thalamus during on. Results suggest that cortical and caudate hypometabolism are common in advanced PD and that caution is mandatory if [18F]FDG PET is being used to differentiate advanced PD from dementia and progressive supranuclear palsy where similar reductions are seen. Furthermore, in PD, administration of levodopa is associated with further hypometabolism in orbitofrontal cortex; an area known to be relevant for reversal learning where performance is typically impaired after dopaminergic treatment.
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Pour connaître la documentation sur le format Inist Standard.
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Format Inist (serveur)
NO : | PASCAL 02-0177036 INIST |
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ET : | Resting regional cerebral glucose metabolism in advanced Parkinson's disease studied in the Off and On conditions with [18F]FDG-PET |
AU : | BERDING (Georg); ODIN (Per); BROOKS (David J.); NIKKHAH (Guido); MATTHIES (Cordula); PESCHEL (Thomas); SHING (Mona); KOLBE (Hans); VAN DEN HOFF (Jörg); FRICKE (Harald); DENGLER (Reinhard); SAMII (Madjid); KNAPP (Wolfram H.) |
AF : | Department of Nuclear Medicine, University Medical School/Hannover/Allemagne (1 aut., 9 aut., 10 aut., 13 aut.); Department of Neurology, University of Marburg/Marburg/Allemagne (2 aut., 7 aut.); Medical Research Council Clinical Sciences Centre, Imperial College School of Medicine, Hammersmith Hospital/London/Royaume-Uni (3 aut.); Department of Neurosurgery, Nordstadt Hospital and University Medical School/Hannover/Allemagne (4 aut., 5 aut., 12 aut.); Department of Neurology, University Medical School/Hannover/Allemagne (6 aut., 7 aut., 8 aut., 11 aut.) |
DT : | Publication en série; Niveau analytique |
SO : | Movement disorders; ISSN 0885-3185; Etats-Unis; Da. 2001; Vol. 16; No. 6; Pp. 1014-1022; Bibl. 53 ref. |
LA : | Anglais |
EA : | Studies of resting regional cerebral glucose consumption (rCMRGlc) in nondemented patients with Parkinson disease (PD) have produced conflicting results, reporting both reduced and normal metabolism in advanced disease and reduced or normal metabolism after dopaminergic therapy. To investigate these issues, [18F]fluorodeoxyglucose (FDG) positron emission tomography (PET) was performed in 1 nondemented PD patients with advanced disease and 10 age-matched controls. PD patients were studied after withdrawal of all dopaminergic medication to produce a practically defined off condition, and a second time I hour after levodopa, resulting in a clinical on state. Dynamic PET scans and simultaneous arterialised venous blood samples of [18F] acticvity were obtained. A graphical approach was used to generate parametric images of rCMRGlc and statistical parametric mapping to localise significant metabolic changes in PD. Compared with controls, global rCMRGlc was reduced in the on but not in the off condition in PD. In both states, significant regional reductions of glucose uptake were found in the parietal, frontal, temporal cortex, and caudate nucleus, Reductions correlated with the severity of disability in frontal and temporal cortex. Direct comparison between on and off conditions revealed relatively greater reductions of uptake in the ventral/orbital frontal cortex and the thalamus during on. Results suggest that cortical and caudate hypometabolism are common in advanced PD and that caution is mandatory if [18F]FDG PET is being used to differentiate advanced PD from dementia and progressive supranuclear palsy where similar reductions are seen. Furthermore, in PD, administration of levodopa is associated with further hypometabolism in orbitofrontal cortex; an area known to be relevant for reversal learning where performance is typically impaired after dopaminergic treatment. |
CC : | 002B17G |
FD : | Parkinson maladie; Tomoscintigraphie; Positon; Métabolisme; Glucose; Encéphale; Repos; Exploration; Homme |
FG : | Système nerveux pathologie; Système nerveux central pathologie; Encéphale pathologie; Extrapyramidal syndrome; Maladie dégénérative; Exploration radioisotopique; Système nerveux central |
ED : | Parkinson disease; Emission tomography; Positron; Metabolism; Glucose; Brain (vertebrata); Rest; Exploration; Human |
EG : | Nervous system diseases; Central nervous system disease; Cerebral disorder; Extrapyramidal syndrome; Degenerative disease; Radionuclide study; Central nervous system |
SD : | Parkinson enfermedad; Tomocentelleografía; Positrón; Metabolismo; Glucosa; Encéfalo; Descanso; Exploración; Hombre |
LO : | INIST-20953.354000094252170030 |
ID : | 02-0177036 |
Links to Exploration step
Pascal:02-0177036Le document en format XML
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<series><title level="j" type="main">Movement disorders</title>
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<term>Parkinson disease</term>
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<term>Tomoscintigraphie</term>
<term>Positon</term>
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<front><div type="abstract" xml:lang="en">Studies of resting regional cerebral glucose consumption (rCMRGlc) in nondemented patients with Parkinson disease (PD) have produced conflicting results, reporting both reduced and normal metabolism in advanced disease and reduced or normal metabolism after dopaminergic therapy. To investigate these issues, [<sup>18</sup>
F]fluorodeoxyglucose (FDG) positron emission tomography (PET) was performed in 1 nondemented PD patients with advanced disease and 10 age-matched controls. PD patients were studied after withdrawal of all dopaminergic medication to produce a practically defined off condition, and a second time I hour after levodopa, resulting in a clinical on state. Dynamic PET scans and simultaneous arterialised venous blood samples of [<sup>18</sup>
F] acticvity were obtained. A graphical approach was used to generate parametric images of rCMRGlc and statistical parametric mapping to localise significant metabolic changes in PD. Compared with controls, global rCMRGlc was reduced in the on but not in the off condition in PD. In both states, significant regional reductions of glucose uptake were found in the parietal, frontal, temporal cortex, and caudate nucleus, Reductions correlated with the severity of disability in frontal and temporal cortex. Direct comparison between on and off conditions revealed relatively greater reductions of uptake in the ventral/orbital frontal cortex and the thalamus during on. Results suggest that cortical and caudate hypometabolism are common in advanced PD and that caution is mandatory if [<sup>18</sup>
F]FDG PET is being used to differentiate advanced PD from dementia and progressive supranuclear palsy where similar reductions are seen. Furthermore, in PD, administration of levodopa is associated with further hypometabolism in orbitofrontal cortex; an area known to be relevant for reversal learning where performance is typically impaired after dopaminergic treatment.</div>
</front>
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<sZ>13 aut.</sZ>
</fA14>
<fA14 i1="02"><s1>Department of Neurology, University of Marburg</s1>
<s2>Marburg</s2>
<s3>DEU</s3>
<sZ>2 aut.</sZ>
<sZ>7 aut.</sZ>
</fA14>
<fA14 i1="03"><s1>Medical Research Council Clinical Sciences Centre, Imperial College School of Medicine, Hammersmith Hospital</s1>
<s2>London</s2>
<s3>GBR</s3>
<sZ>3 aut.</sZ>
</fA14>
<fA14 i1="04"><s1>Department of Neurosurgery, Nordstadt Hospital and University Medical School</s1>
<s2>Hannover</s2>
<s3>DEU</s3>
<sZ>4 aut.</sZ>
<sZ>5 aut.</sZ>
<sZ>12 aut.</sZ>
</fA14>
<fA14 i1="05"><s1>Department of Neurology, University Medical School</s1>
<s2>Hannover</s2>
<s3>DEU</s3>
<sZ>6 aut.</sZ>
<sZ>7 aut.</sZ>
<sZ>8 aut.</sZ>
<sZ>11 aut.</sZ>
</fA14>
<fA20><s1>1014-1022</s1>
</fA20>
<fA21><s1>2001</s1>
</fA21>
<fA23 i1="01"><s0>ENG</s0>
</fA23>
<fA43 i1="01"><s1>INIST</s1>
<s2>20953</s2>
<s5>354000094252170030</s5>
</fA43>
<fA44><s0>0000</s0>
<s1>© 2002 INIST-CNRS. All rights reserved.</s1>
</fA44>
<fA45><s0>53 ref.</s0>
</fA45>
<fA47 i1="01" i2="1"><s0>02-0177036</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>Studies of resting regional cerebral glucose consumption (rCMRGlc) in nondemented patients with Parkinson disease (PD) have produced conflicting results, reporting both reduced and normal metabolism in advanced disease and reduced or normal metabolism after dopaminergic therapy. To investigate these issues, [<sup>18</sup>
F]fluorodeoxyglucose (FDG) positron emission tomography (PET) was performed in 1 nondemented PD patients with advanced disease and 10 age-matched controls. PD patients were studied after withdrawal of all dopaminergic medication to produce a practically defined off condition, and a second time I hour after levodopa, resulting in a clinical on state. Dynamic PET scans and simultaneous arterialised venous blood samples of [<sup>18</sup>
F] acticvity were obtained. A graphical approach was used to generate parametric images of rCMRGlc and statistical parametric mapping to localise significant metabolic changes in PD. Compared with controls, global rCMRGlc was reduced in the on but not in the off condition in PD. In both states, significant regional reductions of glucose uptake were found in the parietal, frontal, temporal cortex, and caudate nucleus, Reductions correlated with the severity of disability in frontal and temporal cortex. Direct comparison between on and off conditions revealed relatively greater reductions of uptake in the ventral/orbital frontal cortex and the thalamus during on. Results suggest that cortical and caudate hypometabolism are common in advanced PD and that caution is mandatory if [<sup>18</sup>
F]FDG PET is being used to differentiate advanced PD from dementia and progressive supranuclear palsy where similar reductions are seen. Furthermore, in PD, administration of levodopa is associated with further hypometabolism in orbitofrontal cortex; an area known to be relevant for reversal learning where performance is typically impaired after dopaminergic treatment.</s0>
</fC01>
<fC02 i1="01" i2="X"><s0>002B17G</s0>
</fC02>
<fC03 i1="01" i2="X" l="FRE"><s0>Parkinson maladie</s0>
<s5>01</s5>
</fC03>
<fC03 i1="01" i2="X" l="ENG"><s0>Parkinson disease</s0>
<s5>01</s5>
</fC03>
<fC03 i1="01" i2="X" l="SPA"><s0>Parkinson enfermedad</s0>
<s5>01</s5>
</fC03>
<fC03 i1="02" i2="X" l="FRE"><s0>Tomoscintigraphie</s0>
<s5>04</s5>
</fC03>
<fC03 i1="02" i2="X" l="ENG"><s0>Emission tomography</s0>
<s5>04</s5>
</fC03>
<fC03 i1="02" i2="X" l="SPA"><s0>Tomocentelleografía</s0>
<s5>04</s5>
</fC03>
<fC03 i1="03" i2="X" l="FRE"><s0>Positon</s0>
<s5>05</s5>
</fC03>
<fC03 i1="03" i2="X" l="ENG"><s0>Positron</s0>
<s5>05</s5>
</fC03>
<fC03 i1="03" i2="X" l="SPA"><s0>Positrón</s0>
<s5>05</s5>
</fC03>
<fC03 i1="04" i2="X" l="FRE"><s0>Métabolisme</s0>
<s5>07</s5>
</fC03>
<fC03 i1="04" i2="X" l="ENG"><s0>Metabolism</s0>
<s5>07</s5>
</fC03>
<fC03 i1="04" i2="X" l="SPA"><s0>Metabolismo</s0>
<s5>07</s5>
</fC03>
<fC03 i1="05" i2="X" l="FRE"><s0>Glucose</s0>
<s2>NK</s2>
<s5>08</s5>
</fC03>
<fC03 i1="05" i2="X" l="ENG"><s0>Glucose</s0>
<s2>NK</s2>
<s5>08</s5>
</fC03>
<fC03 i1="05" i2="X" l="SPA"><s0>Glucosa</s0>
<s2>NK</s2>
<s5>08</s5>
</fC03>
<fC03 i1="06" i2="X" l="FRE"><s0>Encéphale</s0>
<s5>10</s5>
</fC03>
<fC03 i1="06" i2="X" l="ENG"><s0>Brain (vertebrata)</s0>
<s5>10</s5>
</fC03>
<fC03 i1="06" i2="X" l="SPA"><s0>Encéfalo</s0>
<s5>10</s5>
</fC03>
<fC03 i1="07" i2="X" l="FRE"><s0>Repos</s0>
<s5>13</s5>
</fC03>
<fC03 i1="07" i2="X" l="ENG"><s0>Rest</s0>
<s5>13</s5>
</fC03>
<fC03 i1="07" i2="X" l="SPA"><s0>Descanso</s0>
<s5>13</s5>
</fC03>
<fC03 i1="08" i2="X" l="FRE"><s0>Exploration</s0>
<s5>17</s5>
</fC03>
<fC03 i1="08" i2="X" l="ENG"><s0>Exploration</s0>
<s5>17</s5>
</fC03>
<fC03 i1="08" i2="X" l="SPA"><s0>Exploración</s0>
<s5>17</s5>
</fC03>
<fC03 i1="09" i2="X" l="FRE"><s0>Homme</s0>
<s5>20</s5>
</fC03>
<fC03 i1="09" i2="X" l="ENG"><s0>Human</s0>
<s5>20</s5>
</fC03>
<fC03 i1="09" i2="X" l="SPA"><s0>Hombre</s0>
<s5>20</s5>
</fC03>
<fC07 i1="01" i2="X" l="FRE"><s0>Système nerveux pathologie</s0>
<s5>37</s5>
</fC07>
<fC07 i1="01" i2="X" l="ENG"><s0>Nervous system diseases</s0>
<s5>37</s5>
</fC07>
<fC07 i1="01" i2="X" l="SPA"><s0>Sistema nervioso patología</s0>
<s5>37</s5>
</fC07>
<fC07 i1="02" i2="X" l="FRE"><s0>Système nerveux central pathologie</s0>
<s5>38</s5>
</fC07>
<fC07 i1="02" i2="X" l="ENG"><s0>Central nervous system disease</s0>
<s5>38</s5>
</fC07>
<fC07 i1="02" i2="X" l="SPA"><s0>Sistema nervosio central patología</s0>
<s5>38</s5>
</fC07>
<fC07 i1="03" i2="X" l="FRE"><s0>Encéphale pathologie</s0>
<s5>39</s5>
</fC07>
<fC07 i1="03" i2="X" l="ENG"><s0>Cerebral disorder</s0>
<s5>39</s5>
</fC07>
<fC07 i1="03" i2="X" l="SPA"><s0>Encéfalo patología</s0>
<s5>39</s5>
</fC07>
<fC07 i1="04" i2="X" l="FRE"><s0>Extrapyramidal syndrome</s0>
<s5>40</s5>
</fC07>
<fC07 i1="04" i2="X" l="ENG"><s0>Extrapyramidal syndrome</s0>
<s5>40</s5>
</fC07>
<fC07 i1="04" i2="X" l="SPA"><s0>Extrapiramidal síndrome</s0>
<s5>40</s5>
</fC07>
<fC07 i1="05" i2="X" l="FRE"><s0>Maladie dégénérative</s0>
<s5>41</s5>
</fC07>
<fC07 i1="05" i2="X" l="ENG"><s0>Degenerative disease</s0>
<s5>41</s5>
</fC07>
<fC07 i1="05" i2="X" l="SPA"><s0>Enfermedad degenerativa</s0>
<s5>41</s5>
</fC07>
<fC07 i1="06" i2="X" l="FRE"><s0>Exploration radioisotopique</s0>
<s5>45</s5>
</fC07>
<fC07 i1="06" i2="X" l="ENG"><s0>Radionuclide study</s0>
<s5>45</s5>
</fC07>
<fC07 i1="06" i2="X" l="SPA"><s0>Exploración radioisotópica</s0>
<s5>45</s5>
</fC07>
<fC07 i1="07" i2="X" l="FRE"><s0>Système nerveux central</s0>
<s5>61</s5>
</fC07>
<fC07 i1="07" i2="X" l="ENG"><s0>Central nervous system</s0>
<s5>61</s5>
</fC07>
<fC07 i1="07" i2="X" l="SPA"><s0>Sistema nervioso central</s0>
<s5>61</s5>
</fC07>
<fN21><s1>098</s1>
</fN21>
<fN82><s1>PSI</s1>
</fN82>
</pA>
</standard>
<server><NO>PASCAL 02-0177036 INIST</NO>
<ET>Resting regional cerebral glucose metabolism in advanced Parkinson's disease studied in the Off and On conditions with [<sup>18</sup>
F]FDG-PET</ET>
<AU>BERDING (Georg); ODIN (Per); BROOKS (David J.); NIKKHAH (Guido); MATTHIES (Cordula); PESCHEL (Thomas); SHING (Mona); KOLBE (Hans); VAN DEN HOFF (Jörg); FRICKE (Harald); DENGLER (Reinhard); SAMII (Madjid); KNAPP (Wolfram H.)</AU>
<AF>Department of Nuclear Medicine, University Medical School/Hannover/Allemagne (1 aut., 9 aut., 10 aut., 13 aut.); Department of Neurology, University of Marburg/Marburg/Allemagne (2 aut., 7 aut.); Medical Research Council Clinical Sciences Centre, Imperial College School of Medicine, Hammersmith Hospital/London/Royaume-Uni (3 aut.); Department of Neurosurgery, Nordstadt Hospital and University Medical School/Hannover/Allemagne (4 aut., 5 aut., 12 aut.); Department of Neurology, University Medical School/Hannover/Allemagne (6 aut., 7 aut., 8 aut., 11 aut.)</AF>
<DT>Publication en série; Niveau analytique</DT>
<SO>Movement disorders; ISSN 0885-3185; Etats-Unis; Da. 2001; Vol. 16; No. 6; Pp. 1014-1022; Bibl. 53 ref.</SO>
<LA>Anglais</LA>
<EA>Studies of resting regional cerebral glucose consumption (rCMRGlc) in nondemented patients with Parkinson disease (PD) have produced conflicting results, reporting both reduced and normal metabolism in advanced disease and reduced or normal metabolism after dopaminergic therapy. To investigate these issues, [<sup>18</sup>
F]fluorodeoxyglucose (FDG) positron emission tomography (PET) was performed in 1 nondemented PD patients with advanced disease and 10 age-matched controls. PD patients were studied after withdrawal of all dopaminergic medication to produce a practically defined off condition, and a second time I hour after levodopa, resulting in a clinical on state. Dynamic PET scans and simultaneous arterialised venous blood samples of [<sup>18</sup>
F] acticvity were obtained. A graphical approach was used to generate parametric images of rCMRGlc and statistical parametric mapping to localise significant metabolic changes in PD. Compared with controls, global rCMRGlc was reduced in the on but not in the off condition in PD. In both states, significant regional reductions of glucose uptake were found in the parietal, frontal, temporal cortex, and caudate nucleus, Reductions correlated with the severity of disability in frontal and temporal cortex. Direct comparison between on and off conditions revealed relatively greater reductions of uptake in the ventral/orbital frontal cortex and the thalamus during on. Results suggest that cortical and caudate hypometabolism are common in advanced PD and that caution is mandatory if [<sup>18</sup>
F]FDG PET is being used to differentiate advanced PD from dementia and progressive supranuclear palsy where similar reductions are seen. Furthermore, in PD, administration of levodopa is associated with further hypometabolism in orbitofrontal cortex; an area known to be relevant for reversal learning where performance is typically impaired after dopaminergic treatment.</EA>
<CC>002B17G</CC>
<FD>Parkinson maladie; Tomoscintigraphie; Positon; Métabolisme; Glucose; Encéphale; Repos; Exploration; Homme</FD>
<FG>Système nerveux pathologie; Système nerveux central pathologie; Encéphale pathologie; Extrapyramidal syndrome; Maladie dégénérative; Exploration radioisotopique; Système nerveux central</FG>
<ED>Parkinson disease; Emission tomography; Positron; Metabolism; Glucose; Brain (vertebrata); Rest; Exploration; Human</ED>
<EG>Nervous system diseases; Central nervous system disease; Cerebral disorder; Extrapyramidal syndrome; Degenerative disease; Radionuclide study; Central nervous system</EG>
<SD>Parkinson enfermedad; Tomocentelleografía; Positrón; Metabolismo; Glucosa; Encéfalo; Descanso; Exploración; Hombre</SD>
<LO>INIST-20953.354000094252170030</LO>
<ID>02-0177036</ID>
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