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Background: Glutamatergic dysfunction and altered membrane lipid and energy metabolism have been repeatedly demonstrated in the frontal/prefrontal and anterior cingulate cortex (ACC) in schizophrenia. Though having been already studied in animals, the presumed link between glutamatergic function and structural plasticity has not been investigated directly in the human brain yet. We measured glutamate (Glu), focal energy metabolism, and membrane phospholipid turnover to investigate main pathologies in those key brain regions of schizophrenia., Methods: (1)H- and (31)P-Chemical Shift Imaging (CSI) was combined in a single session to assess Glu and markers of energy (PCr, ATP) and membrane lipid (PME, PDE) metabolism in 31 neuroleptic-naïve first acute onset psychosis patients and 31 matched healthy controls. Multivariate analyses of covariance were used to assess disease effects on Glu and to investigate the impact of Glu alterations on phospholipid and energy metabolites., Results: Glu levels of patients were increased in the frontal and prefrontal cortex bilaterally and in the ACC. Higher Glu was associated with increased left frontal/prefrontal PME and right frontal/prefrontal PDE in patients, which was not observed in healthy controls. In contrast, higher Glu levels were associated with lower PCr or ATP values in the frontal/prefrontal cortex bilaterally and in the right ACC of controls. This was not observed in the right ACC and left frontal/prefrontal cortex of patients., Conclusion: Frontal glutamatergic hyperactivity is disconnected from physiologically regulated energy metabolism and is associated with increased membrane breakdown in right and increased membrane restoration in left frontal and prefrontal cortical regions. As indicated by previous findings, this pathology is likely dynamic during the course of first acute illness and possibly associated with negative symptoms and cognitive impairment. Our findings underline the importance of further research on neuroprotective treatment options during the early acute or even better for the ultra-high risk state of psychotic illness., (Copyright © 2015. Published by Elsevier B.V.)

Background: The dysfunction of specific brain areas might account for the distortion of body image in patients with anorexia nervosa. The present study was designed to reveal brain regions that are abnormal in structure and function in patients with this disorder. We hypothesized, based on brain areas of altered activity in patients with anorexia nervosa and regions involved in pain processing, an interrelation of structural aberrations in the frontoparietal-cingulate network and aberrant functional activation during thermal pain processing in patients with the disorder., Methods: We determined pain thresholds outside the MRI scanner in patients with anorexia nervosa and matched healthy controls. Thereafter, thermal pain stimuli were applied during fMRI imaging. Structural analyses with high-resolution structural T1-weighted volumes were performed using voxel-based morphometry and a surface-based approach., Results: Twenty-six patients and 26 controls participated in our study, and owing to technical difficulties, 15 participants in each group were included in our fMRI analysis. Structural analyses revealed significantly decreased grey matter volume and cortical thickness in the frontoparietal-cingulate network in patients with anorexia nervosa. We detected an increased blood oxygen level-dependent signal in patients during the painful 45 °C condition in the midcingulate and posterior cingulate cortex, which positively correlated with increased pain thresholds. Decreased grey matter and cortical thickness correlated negatively with pain thresholds, symptom severity and illness duration, but not with body mass index., Limitations: The lack of a specific quantification of body image distortion is a limitation of our study., Conclusion: This study provides further evidence for confined structural and functional brain abnormalities in patients with anorexia nervosa in brain regions that are involved in perception and integration of bodily stimuli. The association of structural and functional deviations with thermal thresholds as well as with clinical characteristics might indicate a common neuronal origin.

Introduction: Both impaired white matter connectivity and alterations in gray matter morphometry have repeatedly been reported in schizophrenia. Neurodevelopmental models propose a close linkage between gray matter alterations and white matter deficits. However, there are no studies investigating alterations in cortical thickness in relation to white matter connectivity changes., Methods: This combined diffusion tensor imaging (DTI) - surface based morphometry study examined a potential linkage between disruption in white matter connectivity and alterations in cortical thickness. Cortical thickness was analyzed using the FreeSurfer software package (version 4.0.5, http://surfer.nmr.harvard.edu) in a sample of 19 patients with schizophrenia and 20 healthy controls., Results: Whole brain node-by-node correlational analysis revealed a highly significant association ( r= -.8, p < .0001) between disturbed white matter connectivity in the superior temporal cortex and diminished cortical thickness in the posterior part of the cingulate cortex (Brodmann area 23/31)., Conclusions: This result indicates a significant linkage between disturbed white matter connectivity and reduced cortical thickness in a relevant node of the default mode network that is held to be of high pathophysiological relevance in schizophrenia. The result moreover provides support for the assumption of a neurodevelopmental pathogenesis of the disorder., (Copyright © 2012 Elsevier Ltd. All rights reserved.)

Objectives: Evidence for working memory (WM) deficits in obsessive-compulsive disorder (OCD) is increasing. However, findings regarding the underlying neural substrates are heterogeneous. Moreover, the influence of cognitive demand on the severity of these deficits and associated activation alterations is a matter of debate., Methods: To further address this question the present fMRI study examined a sample of 21 predominantly medication-free inpatients with OCD and 21 matched healthy volunteers using a parametric verbal n-back task., Results: In agreement with earlier studies patients exhibited focused activation alterations that could be found to be critically dependent on WM demands: There were no differences in activation between patients and healthy volunteers under low cognitive demands. However, patients exhibited a significantly decreased activation in the dorsal anterior cingulate cortex (dACC) in association with increasing task demands. While dACC activation in controls showed a linear increase with increasing task demands, this linearity was not detectable in patients with OCD., Conclusions: Present findings provide further support for the relevance of the anterior cingulate in OCD and illustrate that both task demands and task processes are of major influence in this context., (Copyright © 2012 Elsevier Ltd. All rights reserved.)

Background: The anterior cingulate cortex plays a central role in altered processes of cognitive control in schizophrenia. However, the cortical foundations of disturbed anterior cingulate cognitive activation are poorly understood. Therefore, this study investigated the association of anterior cingulate cognitive activation and cortical thickness in schizophrenia combining functional magnetic resonance imaging (fMRI) and surface-based morphometry., Methods: Fifty-three patients with schizophrenia according to DSM-IV and 53 age- and sex-matched healthy subjects were included and underwent fMRI and high-resolution T1-weighted MRI. fMRI data was analyzed using SPM5. Cortical thickness was calculated using an automated computerized algorithm (Freesurfer Software). Statistical cortical maps were created correlating anterior cingulate activation and cortical thickness on a node-by-node basis covering the entire cortex in schizophrenia and healthy control subjects., Results: Patients demonstrated a significantly reduced anterior cingulate cognitive activation. Significantly differing associations of anterior cingulate activation and cortical thickness were found in a pattern of dorsolateral prefrontal, superior frontal-anterior cingulate, and superior temporal cortical regions, where patients but not healthy control subjects demonstrated a significant association of reduced anterior cingulate activation and cortical thinning. A direct comparison of cortical thickness between the diagnostic groups revealed a significantly reduced cortical thickness of these prefrontotemporal regions in schizophrenia., Conclusions: To our best knowledge, this is the first study indicating that prefrontotemporal cortical thinning constitutes a relevant cortical pathomechanism for altered cognitive activation in schizophrenia. Our data additionally reveal a profound disruption of structural and functional integration in the prefrontotemporal system in schizophrenia., (Copyright © 2012 Society of Biological Psychiatry. Published by Elsevier Inc. All rights reserved.)