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      Absence of change in the gray matter volume of patients with ulcerative colitis in remission: a voxel based morphometry study

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          Abstract

          Background

          Recent neuroimaging studies have investigated the brain involvement in patients with Crohn's disease (CD) and Ulcerative Colitis (UC). Functional studies found abnormalities in cognitive and emotional functions in CD and UC, while a voxel based morphometry (VBM) study found morphological changes in CD. We conducted a VBM study to compare the gray matter (GM) volume of UC patients and controls.

          Methods

          Eighteen UC patients in remission and eighteen healthy controls underwent structural MRI. VBM is a fully automated technique allowing identification of regional differences in the amount of GM, which enables an objective analysis of the whole brain. VBM was used for comparisons between patients and controls.

          Results

          UC patients were all in remission and had a mild clinical course. There were no differences between patients and controls in GM volume.

          Conclusion

          The brain morphology of patients with UC in remission is similar to controls. The lack of GM abnormalities in UC patients might reflect the mild clinical course of the inflammatory bowel disorder. Further research involving patients with different degrees of disease severity or during flares could shed more light on potential brain structural changes in UC.

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          Most cited references 20

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          Voxel-based morphometry--the methods.

          At its simplest, voxel-based morphometry (VBM) involves a voxel-wise comparison of the local concentration of gray matter between two groups of subjects. The procedure is relatively straightforward and involves spatially normalizing high-resolution images from all the subjects in the study into the same stereotactic space. This is followed by segmenting the gray matter from the spatially normalized images and smoothing the gray-matter segments. Voxel-wise parametric statistical tests which compare the smoothed gray-matter images from the two groups are performed. Corrections for multiple comparisons are made using the theory of Gaussian random fields. This paper describes the steps involved in VBM, with particular emphasis on segmenting gray matter from MR images with nonuniformity artifact. We provide evaluations of the assumptions that underpin the method, including the accuracy of the segmentation and the assumptions made about the statistical distribution of the data. Copyright 2000 Academic Press.
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            From inflammation to sickness and depression: when the immune system subjugates the brain.

            In response to a peripheral infection, innate immune cells produce pro-inflammatory cytokines that act on the brain to cause sickness behaviour. When activation of the peripheral immune system continues unabated, such as during systemic infections, cancer or autoimmune diseases, the ensuing immune signalling to the brain can lead to an exacerbation of sickness and the development of symptoms of depression in vulnerable individuals. These phenomena might account for the increased prevalence of clinical depression in physically ill people. Inflammation is therefore an important biological event that might increase the risk of major depressive episodes, much like the more traditional psychosocial factors.
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              Inflammation and its discontents: the role of cytokines in the pathophysiology of major depression.

              Recognition that inflammation may represent a common mechanism of disease has been extended to include neuropsychiatric disorders including major depression. Patients with major depression have been found to exhibit increased peripheral blood inflammatory biomarkers, including inflammatory cytokines, which have been shown to access the brain and interact with virtually every pathophysiologic domain known to be involved in depression, including neurotransmitter metabolism, neuroendocrine function, and neural plasticity. Indeed, activation of inflammatory pathways within the brain is believed to contribute to a confluence of decreased neurotrophic support and altered glutamate release/reuptake, as well as oxidative stress, leading to excitotoxicity and loss of glial elements, consistent with neuropathologic findings that characterize depressive disorders. Further instantiating the link between inflammation and depression are data demonstrating that psychosocial stress, a well-known precipitant of mood disorders, is capable of stimulating inflammatory signaling molecules, including nuclear factor kappa B, in part, through activation of sympathetic nervous system outflow pathways. Interestingly, depressed patients with increased inflammatory biomarkers have been found to be more likely to exhibit treatment resistance, and in several studies, antidepressant therapy has been associated with decreased inflammatory responses. Finally, preliminary data from patients with inflammatory disorders, as well as medically healthy depressed patients, suggest that inhibiting proinflammatory cytokines or their signaling pathways may improve depressed mood and increase treatment response to conventional antidepressant medication. Translational implications of these findings include the unique opportunity to identify relevant patient populations, apply immune-targeted therapies, and monitor therapeutic efficacy at the level of the immune system in addition to behavior.
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                Author and article information

                Contributors
                alessandro.furey@tiscali.it
                massimo.campieri@unibo.it
                angelabertani@hotmail.com
                antonallascarcel@hotmail.com
                daniela.ballotta@unimore.it
                carlo.calabrese2@unibo.it
                fernando.rizzello@unibo.it
                paolo.gionchetti@unibo.it
                nichelli@unimore.it
                benuzzi@unimore.it
                Journal
                Biopsychosoc Med
                Biopsychosoc Med
                Biopsychosocial Medicine
                BioMed Central (London )
                1751-0759
                7 January 2015
                7 January 2015
                2015
                : 9
                : 1
                Affiliations
                [ ]Department of Psychology, University of Bologna, Bologna, Italy
                [ ]Department of Clinical Medicine, IBD Unit, S. Orsola-Malpighi Hospital, University of Bologna, Bologna, Italy
                [ ]Department of Biomedical, Metabolic Sciences, and Neurosciences, Nuovo Ospedale Civile S. Agostino-Estense, University of Modena and Reggio Emilia, Modena, Italy
                [ ]Department of Gastroenterology, IBD Unit, Policlinico Hospital, Modena, Italy
                Article
                28
                10.1186/s13030-014-0028-7
                4302580
                © Agostini et al.; licensee BioMed Central. 2015

                This is an Open Access article distributed under the terms of the Creative Commons Attribution License ( http://creativecommons.org/licenses/by/4.0), which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly credited. The Creative Commons Public Domain Dedication waiver ( http://creativecommons.org/publicdomain/zero/1.0/) applies to the data made available in this article, unless otherwise stated.

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                © The Author(s) 2015

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