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Objective In order to assess the effect of gray matter volumes and cortical thickness on antidepressant treatment response in late-life depression, the authors examined the relationship between brain regions identified a priori and Montgomery-Åsberg Depression Rating Scale (MADRS) scores over the course of an antidepressant treatment trial. Method In a nonrandomized prospective trial, 168 patients who were at least 60 years of age and met DSM-IV criteria for major depression underwent MRI and were enrolled in a 12-week treatment study. Exclusion criteria included cognitive impairment or severe medical disorders. The volumes or cortical thicknesses of regions of interest that differed between the depressed group and a comparison group (N=50) were determined. These regions of interest were used in analyses of the depressed group to predict antide-pressant treatment outcome. Mixed-model analyses adjusting for age, education, age at depression onset, race, baseline MADRS score, scanner, and interaction with time examined predictors of MADRS scores over time. Results Smaller hippocampal volumes predicted a slower response to treatment. With the inclusion of white matter hyperintensity severity and neuropsychological factor scores, the best model included hippocampal volume and cognitive processing speed to predict rate of response over time. A secondary analysis showed that hippocampal volume and frontal pole thickness differed between patients who achieved remission and those who did not. Conclusions These data expand our understanding of the prediction of treatment course in late-life depression. The authors propose that the primary variables of hippocampal volume and cognitive processing speed, subsuming other contributing variables (episodic memory, executive function, language processing) predict antidepressant response.

Different TEMPS versions, few studies comparing BD with ADHD or BPD, no correlation with other questionnaires.

Purpose Violence against healthcare professionals has become an emergency in many countries. Literature in this area has mainly focused on nurses while there are less studies on physicians, whose alterations in mental health and burnout have been linked to higher rates of medical errors and poorer quality of care. We summarized peer-reviewed literature and examined the epidemiology, main causes, consequences, and areas of intervention associated with workplace violence perpetrated against physicians. Recent Findings We performed a review utilizing several databases, by including the most relevant studies in full journal articles investigating the problem. Workplace violence against doctors is a widespread phenomenon, present all over the world and related to a number of variables, including individual, socio-cultural, and contextual variables. During the COVID-19 pandemic, incidence of violence has increased. Data also show the possible consequences in physicians’ deterioration of quality of life, burnout, and traumatic stress which are linked to physical and mental health problems, which, in a domino effect, fall on patients’ quality of care. Summary Violence against doctors is an urgent global problem with consequences on an individual and societal level. This review highlights the need to undertake initiatives aimed at enhancing understanding, prevention, and management of workplace violence in healthcare settings.

Several preclinical studies have demonstrated neuronal effects of glucocorticoids on the hippocampus (HC), a limbic structure with anterior-posterior anatomical and functional segmentation. We propose a volumetric magnetic resonance imaging analysis of hippocampus head (HH), body (HB) and tail (HT) using Cushing's disease (CD) as model, to investigate whether there is a differential sensitivity to glucocorticoid neuronal damage in these segments. We found a significant difference in the HH bilaterally after 12 months from trans-sphenoidal surgical selective resection of the adrenocorticotropic hormone (ACTH)-secreting pituitary micro-adenomas. This pre-post surgery difference could contribute to better understand the pathopysiology of CD as an in vivo model for stress-related hypercortisolemic neuropsychiatric disorders.

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Our data suggest a VNS modulatory effect on hippocampal plasticity as measured by hippocampal gray volume increase in TRD patients. These preliminary findings indicate the fundamental role of hippocampal remodeling as a marker of response to VNS in TRD.

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