BackgroundVascular depression is regarded as a subtype of late-life depression characterized by a distinct clinical presentation and an association with cerebrovascular damage. Although the term is commonly used in research settings, widely accepted diagnostic criteria are lacking and vascular depression is absent from formal psychiatric manuals such as the Diagnostic and Statistical Manual of Mental Disorders, 5th edition – a fact that limits its use in clinical settings. Magnetic resonance imaging (MRI) techniques, showing a variety of cerebrovascular lesions, including extensive white matter hyperintensities, subcortical microvascular lesions, lacunes, and microinfarcts, in patients with late life depression, led to the introduction of the term “MRI-defined vascular depression”.DiscussionThis diagnosis, based on clinical and MRI findings, suggests that vascular lesions lead to depression by disruption of frontal–subcortical–limbic networks involved in mood regulation. However, despite multiple MRI approaches to shed light on the spatiotemporal structural changes associated with late life depression, the causal relationship between brain changes, related lesions, and late life depression remains controversial. While postmortem studies of elderly persons who died from suicide revealed lacunes, small vessel, and Alzheimer-related pathologies, recent autopsy data challenged the role of these lesions in the pathogenesis of vascular depression. Current data propose that the vascular depression connotation should be reserved for depressed older patients with vascular pathology and evident cerebral involvement. Based on current knowledge, the correlations between intra vitam neuroimaging findings and their postmortem validity as well as the role of peripheral markers of vascular disease in late life depression are discussed.ConclusionThe multifold pathogenesis of vascular depression as a possible subtype of late life depression needs further elucidation. There is a need for correlative clinical, intra vitam structural and functional MRI as well as postmortem MRI and neuropathological studies in order to confirm the relationship between clinical symptomatology and changes in specific brain regions related to depression. To elucidate the causal relationship between regional vascular brain changes and vascular depression, animal models could be helpful. Current treatment options include a combination of vasoactive drugs and antidepressants, but the outcomes are still unsatisfying.

This list serves as a starting point to enhance coping with stressors as a healthcare student or professional in order to help mitigate burnout, depression, and suicidality. The next steps include adapting digital health strategies to specifically fit the needs of healthcare providers, with the ultimate goal of facilitating in-person care when warranted.

During the past decade, research on the biological basis of sensory processing sensitivity (SPS)—a genetically based trait associated with greater sensitivity and responsivity to environmental and social stimuli—has burgeoned. As researchers try to characterize this trait, it is still unclear how SPS is distinct from seemingly related clinical disorders that have overlapping symptoms, such as sensitivity to the environment and hyper-responsiveness to incoming stimuli. Thus, in this review, we compare the neural regions implicated in SPS with those found in fMRI studies of—Autism Spectrum Disorder (ASD), Schizophrenia (SZ) and Post-Traumatic Stress Disorder (PTSD) to elucidate the neural markers and cardinal features of SPS versus these seemingly related clinical disorders. We propose that SPS is a stable trait that is characterized by greater empathy, awareness, responsivity and depth of processing to salient stimuli. We conclude that SPS is distinct from ASD, SZ and PTSD in that in response to social and emotional stimuli, SPS differentially engages brain regions involved in reward processing, memory, physiological homeostasis, self-other processing, empathy and awareness. We suggest that this serves species survival via deep integration and memory for environmental and social information that may subserve well-being and cooperation.This article is part of the theme issue ‘Diverse perspectives on diversity: multi-disciplinary approaches to taxonomies of individual differences’.

ObjectivesMeditation has been shown to have physical, cognitive, and psychological health benefits that can be used to promote healthy aging. However, the common and specific mechanisms of response remain elusive due to the diverse nature of mind–body practices.MethodsIn this review, we aim to compare the neural circuits implicated in focused-attention meditative practices that focus on present-moment awareness to those involved in active-type meditative practices (e.g., yoga) that combine movement, including chanting, with breath practices and meditation.Recent FindingsRecent meta-analyses and individual studies demonstrated common brain effects for attention-based meditative practices and active-based meditations in areas involved in reward processing and learning, attention and memory, awareness and sensory integration, and self-referential processing and emotional control, while deactivation was seen in the amygdala, an area implicated in emotion processing. Unique effects for mindfulness practices were found in brain regions involved in body awareness, attention, and the integration of emotion and sensory processing. Effects specific to active-based meditations appeared in brain areas involved in self-control, social cognition, language, speech, tactile stimulation, sensorimotor integration, and motor function.SummaryThis review suggests that mind–body practices can target different brain systems that are involved in the regulation of attention, emotional control, mood, and executive cognition that can be used to treat or prevent mood and cognitive disorders of aging, such as depression and caregiver stress, or serve as “brain fitness” exercise. Benefits may include improving brain functional connectivity in brain systems that generally degenerate with Alzheimer’s disease, Parkinson’s disease, and other aging-related diseases.

Background In comparison with the general population, physicians, and physicians‐in‐training are at greater risk for suicide. Although key gender differences in suicide risk factors and behaviors have been identified in the general population, the extent to which these differences apply to physicians and physicians‐in‐training is unclear. Here, we aimed to identify gender differences in risk factors, clinical presentation, and help‐seeking behaviors of medical students, house staff, and physician faculty at high risk for suicide. Methods We explored gender differences among 450 physicians and trainees meeting criteria for high suicide risk on anonymous online questionnaires completed between 2009 and 2017. Results High‐risk female trainees and physicians had higher mean Patient Health Questionnaire‐9 (PHQ‐9) scores compared with the males (11.1, standard deviation [SD] 5.1 vs. 9.8, SD 4.7) and were more likely to endorse feeling worried (73.8% vs. 61.2%), irritable (60.4% vs. 49.4%), and stressed (79.6% vs. 70%). High‐risk male trainees and physicians were more likely than females to endorse suicidal thoughts (31.2% vs. 22.1%), intense anger (24.3% vs. 16.1%), drinking too much (31.2% vs. 22.3%), and recreational drug or prescription medication use without clinically appropriate follow‐up (9.4% vs. 4.3%). There were no gender differences in help‐seeking behaviors. Conclusions This is the first study to report gender differences among risk factors, presentation, and help‐seeking behaviors of physicians, and trainees at high risk for suicide. Our findings are mostly consistent with those of the general population and show that only a minority of at‐risk men and women in healthcare sought treatment, highlighting the importance of intervention and suicide prevention in this population.