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Surgical experiences are reported, together with considerations on target features and related encephalic circuits.Due to the growing number of chronic traumatic encephalopathy (CTE) cases in the military and contact sports, defining the cellular and molecular substrate of this disorder is crucial. Most classic neuropathological investigations describe cortical tau and, to a lesser extent, amyloid lesions, which may underlie the clinical sequela associated with CTE. The application of modern molecular biologic technology to postmortem human brain tissue has made it possible to evaluate the genetic signature of specific neuronal phenotypes at different stages of CTE pathology. Most recently, molecular pathobiology has been used in the field of CTE, with an emphasis on the cholinergic neurons located within the nucleus basalis of Meynert, which develop tau pathology and are associated with cognitive dysfunction similar to that found in Alzheimer’s disease (AD). Quantitative findings derived from single-cell transcript investigations provide clues to our understanding of the selective vulnerability of neurons containing AD-like tau pathology at different stages of CTE. Since human tissue-based studies provide a gold standard for the field of CTE, continued molecular pathological studies are needed to reveal novel drug targets for the treatment of this disorder.Burnout constitutes a serious health concern in the modern working environment. It is a stress-related condition that has developed as a result of a prolonged psychosocial stress exposure causing a persistent mismatch between demands and resources. The main symptom is emotional exhaustion, but physical fatigue, diminished professional efficacy, cynicism, and cognitive impairments are also associated with this condition. Burnout has been used both as a psychologic term in occupational settings and as a clinical diagnosis in patient populations, and there is currently no universally accepted definition and diagnostic criteria of burnout. It has been hypothesized that the two main stress response systems, the autonomic nervous system (ANS) and the hypothalamus-pituitary-adrenal axis (HPA axis), are involved in the pathogenesis of burnout. A common hypothesis is that in the early stages of chronic stress, the HPA axis and sympathetic ANS activity tend to be higher, while it will decrease with a longer duration of chronic stress to ultimately reach a state of hypoactivity in clinical burnout. The current research in this field shows many contradictory results. Thus there is no compelling evidence of either ANS or HPA dysfunction in burnout. However, there is partial support for the hypothesis of HPA and sympathetic hyperactivity in early stages, and HPA hyporeactivity and low vagal activity in more severe burnout cases, but high-quality studies investigating the causal links are still lacking.At least one in seven pregnant or recently postpartum women will experience a mental illness such as an anxiety disorder, depressive disorder, or substance use disorder. These mental illnesses have detrimental effects on the health of the mother, child, and family, but little is known about the hypothalamic and other neural correlates of maternal mental health concerns. EPZ005687 datasheet The transition to parenthood alone is a time of remarkable neural plasticity, so it is perhaps not surprising that current research is showing that maternal mental illness has unique neural profiles. Furthermore, the neural systems affected by peripartum mental illness overlap and interact with the systems involved in maternal caregiving behaviors, and mother-infant interactions are, therefore, highly susceptible to disruption. This review discusses what we know about the unique neural changes occurring during peripartum mental illness and the role of the hypothalamus in these illnesses. With an improved understanding of the neural correlates of maternal mental health and disease, we will be better equipped to predict risk, develop effective treatments, and ultimately prevent suffering for millions of parents during this critical time in life.In this chapter, light therapy for mood disorders is discussed, including mood disorders during and after pregnancy. In the introduction, we discuss the symptomatology, etiology, and treatment of a specific type of mood disorder, seasonal affective disorder, since it kick-started the first clinical trials with light therapy. Second, we elaborate on the pathophysiology of mood disorders, in particular in the peripartum period. Next, we present an overview of the proposed working mechanisms of light therapy, followed by a discussion of the clinical trials that have followed after the initial research in seasonal affective disorder. Finally, we also focus on the limitations of these trials, such as considerable heterogeneity among studies and many methodological shortcomings. This is complemented by a number of suggestions for future research. Further studies are needed, which stems from the fact that the results have not always been consistent. Despite this, light therapy may be a promising treatment option for various types of mood disorders, since it shows a significant reduction in symptoms in many patients with few adverse effects.Some patients who have been diagnosed as “dead by neurologic criteria” continue to exhibit certain brain functions, most commonly, neuroendocrine functions. In this chapter, we review the pathophysiology of brain death that can lead either to neuroendocrine failure or to preserved neuroendocrine functioning. We review the evidence on continued hypothalamic functioning in patients who have been declared “brain dead,” examine potential mechanisms that would explain these findings, and discuss how these findings create additional confounds for brain death testing. We conclude by reviewing the evidence for the management of hypothalamic-pituitary failure in the setting of brain death and organ transplantation.Following the onset of any life-threatening illness that requires intensive medical care, alterations within the neuroendocrine axes occur which are thought to be essential for survival, as they postpone energy-consuming anabolism, activate energy-producing catabolic pathways, and optimize immunological and cardiovascular functions. The hormonal changes present in the acute phase of critical illness at least partially resemble those of the fasting state, and recent evidence suggests that they are part of a beneficial, evolutionary-conserved adaptive stress response. However, a fraction of patients who survive the acute phase of critical illness remain dependent on vital organ support and enter the prolonged phase of critical illness. In these patients, the hypothalamic-pituitary-peripheral axes are functionally suppressed, which may have negative consequences by which recovery may be hampered and the risk of morbidity and mortality in the long-term increased. Most randomized controlled trials of critically ill patients that investigated the impact on the outcome of treatment with peripheral hormones did not reveal a robust morbidity or mortality benefit.