Movement Disorders (revue)

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Prefrontal cortex dysfunction and depression in atypical parkinsonian syndromes

Identifieur interne : 001767 ( Istex/Checkpoint ); précédent : 001766; suivant : 001768

Prefrontal cortex dysfunction and depression in atypical parkinsonian syndromes

Auteurs : Birgit Herting [Allemagne] ; Bettina Beuthien-Baumann [Allemagne] ; Katrin Pöttrich [Allemagne] ; Markus Donix [Allemagne] ; Antje Triemer [Allemagne] ; Johannes B. Lampe [Allemagne] ; Rüdiger Von Kummer [Allemagne] ; Karl Herholz [Royaume-Uni] ; Heinz Reichmann [Allemagne] ; Vjera A. Holthoff [Allemagne]

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RBID : ISTEX:A43B0A917467E2851A077B30164C622F8DD0A8D8

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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. © 2007 Movement Disorder Society

Url:
DOI: 10.1002/mds.21237


Affiliations:


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ISTEX:A43B0A917467E2851A077B30164C622F8DD0A8D8

Le document en format XML

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<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 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. © 2007 Movement Disorder Society</div>
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