Prefrontal cortex dysfunction and depression in atypical parkinsonian syndromes
Identifieur interne : 001755 ( PascalFrancis/Corpus ); précédent : 001754; suivant : 001756Prefrontal cortex dysfunction and depression in atypical parkinsonian syndromes
Auteurs : Birgit Herting ; Bettina Beuthien-Baumann ; Katrin Pottrich ; Markus Donix ; Antje Triemer ; Johannes B. Lampe ; Rüdiger Von Kummer ; Karl Herholz ; Heinz Reichmann ; Vjera A. HolthoffSource :
- Movement disorders [ 0885-3185 ] ; 2007.
Descripteurs français
- Pascal (Inist)
English descriptors
- KwdEn :
Abstract
Depressive symptoms are common in patients with neurodegenerative disorders. Imaging studies suggest that a disruption of frontal-subcortical pathways may underlie depression associated with basal ganglia disease. This pilot study tested the hypothesis that frontal dysfunction contributes to depression associated with multiple system atrophy (MSA) and progressive supranuclear palsy (PSP). Depressed patients with MSA (n = 11), PSP (n = 9), and age-matched controls (n = 25) underwent measures of cerebral glucose metabolism applying positron emission tomography with ' 18F-fluorodeoxyglucose. Regional metabolism in the patient groups was compared to the normal subjects using the voxel-based statistical parametric mapping. Depressive symptom severity (Hamilton Depression Rating) and degree of locomotor disability (Hoehn & Yahr) were assessed in the patient groups. The association between prefrontal metabolism and the occurrence of depressive symptoms and the degree of locomotor disability was investigated. When compared to controls, MSA patients revealed significant metabolic decreases in bilateral frontal, parietal, and cerebellar cortex and in the left putamen. In PSP patients, significant hypometabolism was demonstrated in bilateral frontal cortex, right thalamus, and midbrain. Depression severity but not the patients' functional condition was significantly associated with dorsolateral prefrontal glucose metabolism in both patient groups. The findings of this pilot study support the hypothesis that depressive symptoms in MSA and PSP are associated with prefrontal dysfunction.
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Format Inist (serveur)
NO : | PASCAL 07-0210947 INIST |
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ET : | Prefrontal cortex dysfunction and depression in atypical parkinsonian syndromes |
AU : | HERTING (Birgit); BEUTHIEN-BAUMANN (Bettina); POTTRICH (Katrin); DONIX (Markus); TRIEMER (Antje); LAMPE (Johannes B.); VON KUMMER (Rüdiger); HERHOLZ (Karl); REICHMANN (Heinz); HOLTHOFF (Vjera A.) |
AF : | Department of Neurology, Technische Universität Dresden/Allemagne (1 aut., 6 aut., 9 aut.); Department of Nuclear Medicine, Technische Universität Dresden and PET-Center, Research Center Rossendorf/Allemagne (2 aut.); Department of Psychiatry and Psychotherapy, Technische Universität Dresden/Allemagne (3 aut., 4 aut., 5 aut., 10 aut.); Department of Neuroradiology, Technische Universität Dresden/Allemagne (7 aut.); Manchester Molecular Imaging Center/Manchester, England/Royaume-Uni (8 aut.) |
DT : | Publication en série; Niveau analytique |
SO : | Movement disorders; ISSN 0885-3185; Etats-Unis; Da. 2007; Vol. 22; No. 4; Pp. 490-497; Bibl. 43 ref. |
LA : | Anglais |
EA : | Depressive symptoms are common in patients with neurodegenerative disorders. Imaging studies suggest that a disruption of frontal-subcortical pathways may underlie depression associated with basal ganglia disease. This pilot study tested the hypothesis that frontal dysfunction contributes to depression associated with multiple system atrophy (MSA) and progressive supranuclear palsy (PSP). Depressed patients with MSA (n = 11), PSP (n = 9), and age-matched controls (n = 25) underwent measures of cerebral glucose metabolism applying positron emission tomography with ' 18F-fluorodeoxyglucose. Regional metabolism in the patient groups was compared to the normal subjects using the voxel-based statistical parametric mapping. Depressive symptom severity (Hamilton Depression Rating) and degree of locomotor disability (Hoehn & Yahr) were assessed in the patient groups. The association between prefrontal metabolism and the occurrence of depressive symptoms and the degree of locomotor disability was investigated. When compared to controls, MSA patients revealed significant metabolic decreases in bilateral frontal, parietal, and cerebellar cortex and in the left putamen. In PSP patients, significant hypometabolism was demonstrated in bilateral frontal cortex, right thalamus, and midbrain. Depression severity but not the patients' functional condition was significantly associated with dorsolateral prefrontal glucose metabolism in both patient groups. The findings of this pilot study support the hypothesis that depressive symptoms in MSA and PSP are associated with prefrontal dysfunction. |
CC : | 002B17; 002B17D; 002B17F |
FD : | Système nerveux pathologie; Etat dépressif; Parkinson maladie; Atrophie multisystématisée; Cortex préfrontal; Trouble fonctionnel; Tomographie; Lobe frontal |
FG : | Encéphale pathologie; Système nerveux central; Trouble humeur; Extrapyramidal syndrome; Maladie dégénérative; Système nerveux central pathologie |
ED : | Nervous system diseases; Depression; Parkinson disease; Multiple system atrophy; Prefrontal cortex; Dysfunction; Tomography; Frontal lobe |
EG : | Cerebral disorder; Central nervous system; Mood disorder; Extrapyramidal syndrome; Degenerative disease; Central nervous system disease |
SD : | Sistema nervioso patología; Estado depresivo; Parkinson enfermedad; Atrofia multisistematizada; Corteza prefrontal; Trastorno funcional; Tomografía; Lóbulo frontal |
LO : | INIST-20953.354000145702210060 |
ID : | 07-0210947 |
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<front><div type="abstract" xml:lang="en">Depressive symptoms are common in patients with neurodegenerative disorders. Imaging studies suggest that a disruption of frontal-subcortical pathways may underlie depression associated with basal ganglia disease. This pilot study tested the hypothesis that frontal dysfunction contributes to depression associated with multiple system atrophy (MSA) and progressive supranuclear palsy (PSP). Depressed patients with MSA (n = 11), PSP (n = 9), and age-matched controls (n = 25) underwent measures of cerebral glucose metabolism applying positron emission tomography with ' <sup>18</sup>
F-fluorodeoxyglucose. Regional metabolism in the patient groups was compared to the normal subjects using the voxel-based statistical parametric mapping. Depressive symptom severity (Hamilton Depression Rating) and degree of locomotor disability (Hoehn & Yahr) were assessed in the patient groups. The association between prefrontal metabolism and the occurrence of depressive symptoms and the degree of locomotor disability was investigated. When compared to controls, MSA patients revealed significant metabolic decreases in bilateral frontal, parietal, and cerebellar cortex and in the left putamen. In PSP patients, significant hypometabolism was demonstrated in bilateral frontal cortex, right thalamus, and midbrain. Depression severity but not the patients' functional condition was significantly associated with dorsolateral prefrontal glucose metabolism in both patient groups. The findings of this pilot study support the hypothesis that depressive symptoms in MSA and PSP are associated with prefrontal dysfunction.</div>
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<fC03 i1="06" i2="X" l="FRE"><s0>Trouble fonctionnel</s0>
<s5>10</s5>
</fC03>
<fC03 i1="06" i2="X" l="ENG"><s0>Dysfunction</s0>
<s5>10</s5>
</fC03>
<fC03 i1="06" i2="X" l="SPA"><s0>Trastorno funcional</s0>
<s5>10</s5>
</fC03>
<fC03 i1="07" i2="X" l="FRE"><s0>Tomographie</s0>
<s5>11</s5>
</fC03>
<fC03 i1="07" i2="X" l="ENG"><s0>Tomography</s0>
<s5>11</s5>
</fC03>
<fC03 i1="07" i2="X" l="SPA"><s0>Tomografía</s0>
<s5>11</s5>
</fC03>
<fC03 i1="08" i2="X" l="FRE"><s0>Lobe frontal</s0>
<s5>12</s5>
</fC03>
<fC03 i1="08" i2="X" l="ENG"><s0>Frontal lobe</s0>
<s5>12</s5>
</fC03>
<fC03 i1="08" i2="X" l="SPA"><s0>Lóbulo frontal</s0>
<s5>12</s5>
</fC03>
<fC07 i1="01" i2="X" l="FRE"><s0>Encéphale pathologie</s0>
<s5>37</s5>
</fC07>
<fC07 i1="01" i2="X" l="ENG"><s0>Cerebral disorder</s0>
<s5>37</s5>
</fC07>
<fC07 i1="01" i2="X" l="SPA"><s0>Encéfalo patología</s0>
<s5>37</s5>
</fC07>
<fC07 i1="02" i2="X" l="FRE"><s0>Système nerveux central</s0>
<s5>38</s5>
</fC07>
<fC07 i1="02" i2="X" l="ENG"><s0>Central nervous system</s0>
<s5>38</s5>
</fC07>
<fC07 i1="02" i2="X" l="SPA"><s0>Sistema nervioso central</s0>
<s5>38</s5>
</fC07>
<fC07 i1="03" i2="X" l="FRE"><s0>Trouble humeur</s0>
<s5>39</s5>
</fC07>
<fC07 i1="03" i2="X" l="ENG"><s0>Mood disorder</s0>
<s5>39</s5>
</fC07>
<fC07 i1="03" i2="X" l="SPA"><s0>Trastorno humor</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>Système nerveux central pathologie</s0>
<s5>42</s5>
</fC07>
<fC07 i1="06" i2="X" l="ENG"><s0>Central nervous system disease</s0>
<s5>42</s5>
</fC07>
<fC07 i1="06" i2="X" l="SPA"><s0>Sistema nervosio central patología</s0>
<s5>42</s5>
</fC07>
<fN21><s1>141</s1>
</fN21>
<fN44 i1="01"><s1>OTO</s1>
</fN44>
<fN82><s1>OTO</s1>
</fN82>
</pA>
</standard>
<server><NO>PASCAL 07-0210947 INIST</NO>
<ET>Prefrontal cortex dysfunction and depression in atypical parkinsonian syndromes</ET>
<AU>HERTING (Birgit); BEUTHIEN-BAUMANN (Bettina); POTTRICH (Katrin); DONIX (Markus); TRIEMER (Antje); LAMPE (Johannes B.); VON KUMMER (Rüdiger); HERHOLZ (Karl); REICHMANN (Heinz); HOLTHOFF (Vjera A.)</AU>
<AF>Department of Neurology, Technische Universität Dresden/Allemagne (1 aut., 6 aut., 9 aut.); Department of Nuclear Medicine, Technische Universität Dresden and PET-Center, Research Center Rossendorf/Allemagne (2 aut.); Department of Psychiatry and Psychotherapy, Technische Universität Dresden/Allemagne (3 aut., 4 aut., 5 aut., 10 aut.); Department of Neuroradiology, Technische Universität Dresden/Allemagne (7 aut.); Manchester Molecular Imaging Center/Manchester, England/Royaume-Uni (8 aut.)</AF>
<DT>Publication en série; Niveau analytique</DT>
<SO>Movement disorders; ISSN 0885-3185; Etats-Unis; Da. 2007; Vol. 22; No. 4; Pp. 490-497; Bibl. 43 ref.</SO>
<LA>Anglais</LA>
<EA>Depressive symptoms are common in patients with neurodegenerative disorders. Imaging studies suggest that a disruption of frontal-subcortical pathways may underlie depression associated with basal ganglia disease. This pilot study tested the hypothesis that frontal dysfunction contributes to depression associated with multiple system atrophy (MSA) and progressive supranuclear palsy (PSP). Depressed patients with MSA (n = 11), PSP (n = 9), and age-matched controls (n = 25) underwent measures of cerebral glucose metabolism applying positron emission tomography with ' <sup>18</sup>
F-fluorodeoxyglucose. Regional metabolism in the patient groups was compared to the normal subjects using the voxel-based statistical parametric mapping. Depressive symptom severity (Hamilton Depression Rating) and degree of locomotor disability (Hoehn & Yahr) were assessed in the patient groups. The association between prefrontal metabolism and the occurrence of depressive symptoms and the degree of locomotor disability was investigated. When compared to controls, MSA patients revealed significant metabolic decreases in bilateral frontal, parietal, and cerebellar cortex and in the left putamen. In PSP patients, significant hypometabolism was demonstrated in bilateral frontal cortex, right thalamus, and midbrain. Depression severity but not the patients' functional condition was significantly associated with dorsolateral prefrontal glucose metabolism in both patient groups. The findings of this pilot study support the hypothesis that depressive symptoms in MSA and PSP are associated with prefrontal dysfunction.</EA>
<CC>002B17; 002B17D; 002B17F</CC>
<FD>Système nerveux pathologie; Etat dépressif; Parkinson maladie; Atrophie multisystématisée; Cortex préfrontal; Trouble fonctionnel; Tomographie; Lobe frontal</FD>
<FG>Encéphale pathologie; Système nerveux central; Trouble humeur; Extrapyramidal syndrome; Maladie dégénérative; Système nerveux central pathologie</FG>
<ED>Nervous system diseases; Depression; Parkinson disease; Multiple system atrophy; Prefrontal cortex; Dysfunction; Tomography; Frontal lobe</ED>
<EG>Cerebral disorder; Central nervous system; Mood disorder; Extrapyramidal syndrome; Degenerative disease; Central nervous system disease</EG>
<SD>Sistema nervioso patología; Estado depresivo; Parkinson enfermedad; Atrofia multisistematizada; Corteza prefrontal; Trastorno funcional; Tomografía; Lóbulo frontal</SD>
<LO>INIST-20953.354000145702210060</LO>
<ID>07-0210947</ID>
</server>
</inist>
</record>
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