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Cerebral glucose metabolism abnormalities in patients with major depressive symptoms in pre‐dialytic chronic kidney disease: Statistical parametric mapping analysis of F‐18‐FDG PET, a preliminary study
Author(s) -
Song Sang Heon,
Kim In Joo,
Kim SeongJang,
Kwak Ihm Soo,
Kim YongKi
Publication year - 2008
Publication title -
psychiatry and clinical neurosciences
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.609
H-Index - 74
eISSN - 1440-1819
pISSN - 1323-1316
DOI - 10.1111/j.1440-1819.2008.01849.x
Subject(s) - statistical parametric mapping , orbitofrontal cortex , prefrontal cortex , medicine , gyrus , anterior cingulate cortex , temporal cortex , superior frontal gyrus , superior parietal lobule , psychology , endocrinology , neuroscience , psychiatry , functional magnetic resonance imaging , magnetic resonance imaging , radiology , cognition
Aims: The aim of the present study was to investigate the relationship between depressive symptoms and cerebral glucose metabolism in pre‐dialytic chronic kidney disease (PDCKD) patients. Methods: Twenty‐one patients with stage 5 CKD and 21 healthy volunteers underwent depressive mood assessment and statistical parametric mapping (SPM) using F‐18‐fluorodeoxyglucose (FDG) positron emission tomography (PET). Results: Several voxel clusters of significantly decreased cerebral glucose metabolism were found in PDCKD patients. The largest cluster was left prefrontal cortex (Brodmann area [BA] 9). The second largest cluster was also left prefrontal cortex (BA 9). The third largest clusters were right prefrontal cortex (BA 10) and right basolateral prefrontal cortex (BA 46). Other brain areas also showed decreased cerebral glucose metabolism including left anterior cingulate gyrus (BA 32), left premotor cortex (BA 6), left transverse temporal gyrus (BA 41), left superior temporal gyrus (BA 42), right basolateral prefrontal cortex (BA 44), right inferior parietal lobule (BA 39), left middle temporal gyrus (BA 19), and left angular gyrus (BA 39). Hypermetabolized brain areas, however, were not found in PDCKD patients compared to normal controls. For the right orbitofrontal cortex there was a negative correlation of cerebral glucose metabolism with Hamilton Depression Rating Scale (HDRS) in PDCKD patients (BA 11). Conclusion: PDCKD patients with depressive symptoms had decreased cerebral glucose metabolism in several brain areas. For the right orbitofrontal cortex there was a negative correlation with HDRS in PDCKD patients. The present findings provide functional neuroimaging support for abnormal cerebral glucose metabolism in PDCKD patients with depressive symptoms.