31
views
0
recommends
+1 Recommend
0 collections
    0
    shares
      • Record: found
      • Abstract: found
      • Article: found
      Is Open Access

      Gray Matter Abnormalities in Non-comorbid Medication-naive Patients with Major Depressive Disorder or Social Anxiety Disorder

      research-article

      Read this article at

      Bookmark
          There is no author summary for this article yet. Authors can add summaries to their articles on ScienceOpen to make them more accessible to a non-specialist audience.

          Abstract

          Background

          An overlap of clinical symptoms between major depressive disorder (MDD) and social anxiety disorder (SAD) suggests that the two disorders exhibit similar brain mechanisms. However, few studies have directly compared the brain structures of the two disorders. The aim of this study was to assess the gray matter volume (GMV) and cortical thickness alterations between non-comorbid medication-naive MDD patients and SAD patients.

          Methods

          High-resolution T1-weighted images were acquired from 37 non-comorbid MDD patients, 24 non-comorbid SAD patients and 41 healthy controls (HCs). Voxel-based morphometry analysis of the GMV (corrected with a false discovery rate of p < 0.001) and vertex-based analysis of cortical thickness (corrected with a clusterwise probability of p < 0.001) were performed, and group differences were compared by ANOVA followed by post hoc tests.

          Outcomes

          Relative to the HCs, both the MDD patients and SAD patients showed the following results: GMV reductions in the bilateral orbital frontal cortex (OFC), putamen, and thalamus; cortical thickening in the bilateral medial prefrontal cortex, posterior dorsolateral prefrontal cortex, insular cortex, left temporal pole, and right superior parietal cortex; and cortical thinning in the left lateral OFC and bilateral rostral middle frontal cortex. In addition, MDD patients specifically showed a greater thickness in the left fusiform gyrus and right lateral occipital cortex and a thinner thickness in the bilateral lingual and left cuneus. SAD patients specifically showed a thinner cortical thickness in the right precentral cortex.

          Interpretation

          Our results indicate that MDD and SAD share common patterns of gray matter abnormalities in the orbitofrontal-striatal-thalamic circuit, salience network and dorsal attention network. These consistent structural differences in the two patient groups may contribute to the broad spectrum of emotional, cognitive and behavioral disturbances observed in MDD patients and SAD patients. In addition, we found disorder-specific involvement of the visual processing regions in MDD and the precentral cortex in SAD. These findings provide new evidence regarding the shared and specific neuropathological mechanisms that underlie MDD and SAD.

          Highlights

          • MDD and SAD share common gray matter abnormalities in the orbitofrontal-striatal-thalamic circuit, salience and dorsal attention network.

          • MDD patients show disorder-specific involvement of the visual processing regions.

          • SAD patients show disorder-specific involvement of the precentral cortex.

          An overlap of clinical symptoms between major depressive disorder (MDD) and social anxiety disorder (SAD) suggests similar brain mechanisms for the two disorders. However, few studies have directly compared the brain structures of the two disorders. The aim of this study was to assess gray matter volume and cortical thickness alterations between non-comorbid medication-naive MDD patients and SAD patients. We found that MDD and SAD shared a common pattern of gray matter abnormalities in the orbitofrontal-striatal-thalamic circuit, salience network and dorsal attention network. MDD patients showed disorder-specific involvement of the visual processing regions. SAD patients showed disorder-specific involvement of the precentral cortex.

          Related collections

          Most cited references41

          • Record: found
          • Abstract: found
          • Article: not found

          Distinct genetic influences on cortical surface area and cortical thickness.

          Neuroimaging studies examining the effects of aging and neuropsychiatric disorders on the cerebral cortex have largely been based on measures of cortical volume. Given that cortical volume is a product of thickness and surface area, it is plausible that measures of volume capture at least 2 distinct sets of genetic influences. The present study aims to examine the genetic relationships between measures of cortical surface area and thickness. Participants were men in the Vietnam Era Twin Study of Aging (110 monozygotic pairs and 92 dizygotic pairs). Mean age was 55.8 years (range: 51-59). Bivariate twin analyses were utilized in order to estimate the heritability of cortical surface area and thickness, as well as their degree of genetic overlap. Total cortical surface area and average cortical thickness were both highly heritable (0.89 and 0.81, respectively) but were essentially unrelated genetically (genetic correlation = 0.08). This pattern was similar at the lobar and regional levels of analysis. These results demonstrate that cortical volume measures combine at least 2 distinct sources of genetic influences. We conclude that using volume in a genetically informative study, or as an endophenotype for a disorder, may confound the underlying genetic architecture of brain structure.
            Bookmark
            • Record: found
            • Abstract: found
            • Article: not found

            Targeting abnormal neural circuits in mood and anxiety disorders: from the laboratory to the clinic.

            Recent decades have witnessed tremendous advances in the neuroscience of emotion, learning and memory, and in animal models for understanding depression and anxiety. This review focuses on new rationally designed psychiatric treatments derived from preclinical human and animal studies. Nonpharmacological treatments that affect disrupted emotion circuits include vagal nerve stimulation, rapid transcranial magnetic stimulation and deep brain stimulation, all borrowed from neurological interventions that attempt to target known pathological foci. Other approaches include drugs that are given in relation to specific learning events to enhance or disrupt endogenous emotional learning processes. Imaging data suggest that common regions of brain activation are targeted with pharmacological and somatic treatments as well as with the emotional learning in psychotherapy. Although many of these approaches are experimental, the rapidly developing understanding of emotional circuit regulation is likely to provide exciting and powerful future treatments for debilitating mood and anxiety disorders.
              Bookmark
              • Record: found
              • Abstract: found
              • Article: not found

              Regional and progressive thinning of the cortical ribbon in Huntington's disease.

              Huntington's disease (HD) is a fatal and progressive neurodegenerative disease that is accompanied by involuntary movements, cognitive dysfunction, and psychiatric symptoms. Although progressive striatal degeneration is known to occur, little is known about how the disease affects the cortex, including which cortical regions are affected, how degeneration proceeds, and the relationship of the cortical degeneration to clinical symptoms. The cortex has been difficult to study in neurodegenerative diseases primarily because of its complex folding patterns and regional variability; however, an understanding of how the cortex is affected by the disease may provide important new insights into it. Novel automated surface reconstruction and high-resolution MR images of 11 patients with HD and 13 age-matched subjects were used to obtain cortical thickness measurements. The same analyses were performed on two postmortem brains to validate these methods. Regionally specific heterogeneous thinning of the cortical ribbon was found in subjects with HD. Thinning occurred early, differed among patients in different clinical stages of disease, and appeared to proceed from posterior to anterior cortical regions with disease progression. The sensorimotor region was statistically most affected. Measurements performed on MR images of autopsy brains analyzed similarly were within 0.25 mm of those obtained using traditional neuropathologic methods and were statistically indistinguishable. The authors propose that the cortex degenerates early in disease and that regionally selective cortical degeneration may explain the heterogeneity of clinical expression in HD. These measures might provide a sensitive prospective surrogate marker for clinical trials of neuroprotective medications.
                Bookmark

                Author and article information

                Contributors
                Journal
                EBioMedicine
                EBioMedicine
                EBioMedicine
                Elsevier
                2352-3964
                15 June 2017
                July 2017
                15 June 2017
                : 21
                : 228-235
                Affiliations
                [a ]Huaxi MR Research Center (HMRRC), Department of Radiology, West China Hospital of Sichuan University, Chengdu, PR China
                [b ]Mental Health Center, West China Hospital of Sichuan University, Chengdu, PR China
                Author notes
                [* ]Corresponding authors at: Huaxi MR Research Center (HMRRC), Department of Radiology, West China Hospital of Sichuan University, No. 37 Guo Xue Xiang, Chengdu 610041, PR China.Huaxi MR Research Center (HMRRC)Department of RadiologyWest China Hospital of Sichuan UniversityNo. 37 Guo Xue XiangChengdu610041PR China qiyonggong@ 123456hmrrc.org.cn lusuwcums@ 123456tom.com
                Article
                S2352-3964(17)30248-7
                10.1016/j.ebiom.2017.06.013
                5514428
                28633986
                fe2439ee-1958-4362-a70e-08da2be29c8a
                © 2017 The Authors

                This is an open access article under the CC BY-NC-ND license (http://creativecommons.org/licenses/by-nc-nd/4.0/).

                History
                : 15 May 2017
                : 14 June 2017
                : 14 June 2017
                Categories
                Research Paper

                major depressive disorder (mdd),social anxiety disorder (sad),voxel-based morphometry (vbm),diffeomorphic anatomical registration through exponentiated lie algebra (dartel),gray matter volume (gmv),cortical thickness

                Comments

                Comment on this article