Objectives: The anterior cingulate is thought to be essentially involved in impulsivity and affect regulation and in the pathogenesis of depression as well as of attention deficit/hyperactivity disorder. At the same t...Objectives: The anterior cingulate is thought to be essentially involved in impulsivity and affect regulation and in the pathogenesis of depression as well as of attention deficit/hyperactivity disorder. At the same time alterations in glutamatergic neurotransmission in the frontal forebrain have been found in imaging studies in Attention Deficit Hyperactivity Disorder (ADHD) and in depressive patients. Therefore we hypothesized that glutamate/glutamine (Glx) signals in the anterior cingulate cortex (ACC) of depressed ADHD patients might differ from that in non-depressed patients. Methods: Fourteen male adult patients with ADHD were included into the study. Chemical Shift Imaging of ACC was performed. Subgroups were defined based on scores on the Beck Depression Inventory (BDI) and ratios of metabolites were compared between groups. Additionally correlation analyses of BDI scores with metabolite ratios were calculated. Results: Significantly lower Glx signals and N-acetyl-aspartate (NAA) signals were found in the left anterior cingulate cortex of depressed ADHD patients. The Glx/Cr and NAAX/Cr ratios in the left ACC correlated significantly with BDI-scores. Conclusions: To our knowledge this is the first report about a relationship between depressive symptoms and metabolite disturbances in ACC of adult patients with ADHD. Our preliminary data produce first evidence for a putative link between neurochemical alterations in the ACC and depressive symptoms. They should be controlled for in further studies.展开更多
文摘Objectives: The anterior cingulate is thought to be essentially involved in impulsivity and affect regulation and in the pathogenesis of depression as well as of attention deficit/hyperactivity disorder. At the same time alterations in glutamatergic neurotransmission in the frontal forebrain have been found in imaging studies in Attention Deficit Hyperactivity Disorder (ADHD) and in depressive patients. Therefore we hypothesized that glutamate/glutamine (Glx) signals in the anterior cingulate cortex (ACC) of depressed ADHD patients might differ from that in non-depressed patients. Methods: Fourteen male adult patients with ADHD were included into the study. Chemical Shift Imaging of ACC was performed. Subgroups were defined based on scores on the Beck Depression Inventory (BDI) and ratios of metabolites were compared between groups. Additionally correlation analyses of BDI scores with metabolite ratios were calculated. Results: Significantly lower Glx signals and N-acetyl-aspartate (NAA) signals were found in the left anterior cingulate cortex of depressed ADHD patients. The Glx/Cr and NAAX/Cr ratios in the left ACC correlated significantly with BDI-scores. Conclusions: To our knowledge this is the first report about a relationship between depressive symptoms and metabolite disturbances in ACC of adult patients with ADHD. Our preliminary data produce first evidence for a putative link between neurochemical alterations in the ACC and depressive symptoms. They should be controlled for in further studies.
