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Background: Depersonalization/derealization disorder (DPD) is a chronic and distressing condition characterized by detachment from oneself and/or the external world. Neuroimaging studies have associated DPD with structural and functional alterations in a variety of distinct brain regions. Such local neuronal changes might be mediated by altered interregional white matter connections. However, to our knowledge, no research on network characteristics in this patient population exists to date. Methods: We explored the structural connectome in 23 individuals with DPD and 23 matched, healthy controls by applying graph theory to diffusion tensor imaging data. Mean interregional fractional anisotropy (FA) was used to define the network weights. Group differences were assessed using network-based statistics and a link-based controlling procedure. Results: Our main finding refers to lower FA values within left temporal and right temporoparietal regions in individuals with DPD than in healthy controls when using a link-based controlling procedure. These links were also associated with dissociative symptom severity and could not be explained by anxiety or depression scores. Using network-based statistics, no significant results emerged. However, we found a trend for 1 subnetwork that may support the model of frontolimbic dysbalance suggested to underlie DPD symptomatology. Limitations: To ensure ecological validity, patients with certain comorbidities or psychotropic medication were included in the study. Confirmatory replications are necessary to corroborate the results of this explorative investigation. Conclusion: In patients with DPD, the structural connectivity between brain regions crucial for multimodal integration and emotion regulation may be altered. Aberrations in fibre tract communication seem to be not solely a secondary effect of local grey matter volume loss, but may present a primary pathophysiology in patients with DPD., Introduction Depersonalization/derealization disorder (DPD) is a dissociative disorder (1) estimated to affect 1%-2% of the general population. (2) However, a German study found a 12-month prevalence of 0.007 based on [...]

The human brain is unusually large. It has tripled in size from Australopithecines to modern humans.sup.1 and has become almost six times larger than expected for a placental mammal of human size.sup.2. Brains incur high metabolic costs.sup.3 and accordingly a long-standing question is why the large human brain has evolved.sup.4. The leading hypotheses propose benefits of improved cognition for overcoming ecological.sup.5-7, social.sup.8-10 or cultural.sup.11-14 challenges. However, these hypotheses are typically assessed using correlative analyses, and establishing causes for brain-size evolution remains difficult.sup.15,16. Here we introduce a metabolic approach that enables causal assessment of social hypotheses for brain-size evolution. Our approach yields quantitative predictions for brain and body size from formalized social hypotheses given empirical estimates of the metabolic costs of the brain. Our model predicts the evolution of adult Homo sapiens-sized brains and bodies when individuals face a combination of 60% ecological, 30% cooperative and 10% between-group competitive challenges, and suggests that between-individual competition has been unimportant for driving human brain-size evolution. Moreover, our model indicates that brain expansion in Homo was driven by ecological rather than social challenges, and was perhaps strongly promoted by culture. Our metabolic approach thus enables causal assessments that refine, refute and unify hypotheses of brain-size evolution.Using estimates of metabolic costs of the brain and body, mathematical predictions suggest that the evolution of adult Homo sapiens-sized brains and bodies is driven by ecological rather than social challenges and is perhaps strongly promoted by culture., Author(s): Mauricio González-Forero [sup.1] , Andy Gardner [sup.1] Author Affiliations:(1) School of Biology, University of St Andrews, St Andrews, UKMain The leading hypotheses for the evolution of brain size make [...]

Codependent behaviors have taken root in mainstream American culture with dire consequences for the physiology of the brain. This dysfunctional cycle triangulating relationships, families, communities and corporations has become so normalized as to be invisible. These patterned deflections of powerlessness are disintegrating the very foundation of the Self. Journey through the neurological underpinnings of dementia, shrouded in codependency; originating in infancy, and threatening our basic human purpose, i.e., conscious evolution. Triangulated relationships, splitting, powerlessness and other states developing within codependent relationships progress into persistent, progressive damage to the brain and body. When codependency is explored as the cause of Alzheimer's, the brain plaques and tangles formed in Alzheimer's can be redefined as a result of life-long restraint-stress, dissociation, and codependent defense formation. Codependency as defined by the Victim, Persecutor and Rescuer triangle is choking individuation and decapitating our golden years while masquerading under the cloak of dementias. A focus on codependent behaviors and recognition of the psychological origin of dementia is necessary to stop the plague of the twenty-first century. Codependence is more than a triangulation of relational patterns of Victim, Persecutor, and Rescuer occurring in substance abuse cohorts. Codependence has become a cultural norm. Compensatory behavioral strategies, ubiquitous self-soothing of powerlessness, result in a defense postured brain; ultimately retarding individuation into the tangled web of dementias., Author Note Many studies cited within were derived from work on mice and monkeys. These and many other animals have experienced horrific cruelty for the sake of scientific knowledge and [...]

Given the crucial role of the gastrointestinal tract and associated organs in handling nutrient assimilation and metabolism, it has long been known that its communication with the brain is important for the control of ingestive behavior and body weight regulation. It is also clear that gut-brain communication is bidirectional and utilizes both rapid neural and slower humoral mechanisms and pathways. However, progress in understanding these mechanisms and leveraging them for the treatment of obesity and metabolic disease has been hindered by the enormous dimension of the gut mucosa, the complexity of the signaling systems, and lack of specific tools. With the ascent of modern neurobiological technology, our understanding of the role of vagal afferents in gut-brain communication has begun to change. The first function-specific populations of vagal afferents providing nutritional feedback as well as feed-forward signals have been identified with genetics- guided methodology, and it is hoped that extension of the methodology to other neural communication pathways will follow soon. Currently, efficient clinical leveraging of gut-brain communication to treat obesity and metabolic disease is limited to a few gut hormones, but a more complete understanding of function-specific and projection-specific neuronal populations should make it possible to develop selective and more effective neuromodulation approaches., Introduction Given that the prevalence of obesity is approaching 50% in some countries (1), it is hard to argue that body weight/adiposity is regulated at healthy levels through biological mechanisms [...]