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Prefrontal cortex dysfunction and depression in atypical parkinsonian syndromes
Author(s) -
Herting Birgit,
BeuthienBaumann Bettina,
Pöttrich Katrin,
Donix Markus,
Triemer Antje,
Lampe Johannes B.,
von Kummer Rüdiger,
Herholz Karl,
Reichmann Heinz,
Holthoff Vjera A.
Publication year - 2007
Publication title -
movement disorders
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 3.352
H-Index - 198
eISSN - 1531-8257
pISSN - 0885-3185
DOI - 10.1002/mds.21237
Subject(s) - putamen , statistical parametric mapping , prefrontal cortex , psychology , progressive supranuclear palsy , depression (economics) , basal ganglia , medicine , thalamus , late life depression , frontal lobe , dorsolateral prefrontal cortex , atrophy , neuroscience , cardiology , central nervous system , magnetic resonance imaging , cognition , macroeconomics , economics , radiology
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 18 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. © 2007 Movement Disorder Society