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Problems within schemes included health provider engagement, recruiting those with low agency and communication between professionals and patients about social prescribing. Based on our findings, we propose a number of recommendations for enhancing social prescribing schemes. Professionals, including neurologists, we argue, can benefit from engaging in the concept and practice of social prescribing and referring patients and clients to social prescribing link workers where appropriate. Neurologists are also part of a larger team, as they work alongside allied health professionals such as occupational therapists and physiotherapists, some of whom are already performing aspects of the link worker role.Compelling evidence have highlighted the role of inflammation as a possible mechanism linking environmental stress to the development of depression. In particular, the communication between the peripheral and the brain immune system might lead to brain inflammatory processes, in turn causing impaired neurogenesis and neural plasticity. JNJ-64619178 concentration As a consequence, measuring brain inflammation and its possible correlation with peripheral inflammatory processes has become the focus (and a challenge) for a number of recent studies. In this chapter we review the evidence on the link between stress, peripheral and brain inflammation and the way to measure it, through preclinical, post-mortem and clinical models of depression and in healthy humans. We describe the concept of microglial activation as a marker of neuroinflammation and the potential use of anti-inflammatory treatments in depression. The paper concludes by highlighting the unresolved questions and challenges for future studies.In this chapter we review the existing literature regarding the interactions between stress and the mechanisms that maintain balance. Evidence suggests that the interplay between neuro-endocrine and psychological factors may have a significant role in balance function. For example, in healthy individuals vestibular stimulation has been shown to trigger the stress response as indicated by increased blood cortisol levels, whereas in patients with vestibular pathology factors such as resilience and anxiety may be the key focus of interactions with stress. Critically, factors such as anxiety are known to influence clinical outcomes, despite our mechanistic understanding of these processes remaining in their infancy.Stress is ubiquitous in chronic medical conditions; however, the connections to psychiatric and neurologic conditions are not always clearly established. Epilepsy is a unique illness that is intimately intertwined with stress and anxiety not only as a result of the disease process but also as a cause of disease exacerbation. Anxiety and depression also involve stress management and often overlap with epilepsy. Anxiety symptoms themselves may be present as intrinsic aspects of seizure phenomena, either during the events or closely related to them. The pathways of stress and anxiety involve the hypothalamic pituitary adrenal (HPA) axis and explain at least in part how stress may lead to worsening seizure control. Ultimately, the study of stress, anxiety, and epilepsy offers insight into mind and body connections, and furthers understanding of neuropsychiatric illness.AD is a complicated multi-systemic neurological disorder that involves different biological pathways. Several risk factors have been identified, including chronic stress. Chronic stress produces an alteration in the activity of the hypothalamic pituitary adrenal (HPA) system, and the autonomic nervous system (ANS), which over time increase the risk of AD and also the incidence of cardiovascular disease (CVD) and risk factors, such as hypertension, obesity and type 2 diabetes, associated with cognitive impairment and AD. Considering the multi-factorial etiology of AD, understanding the complex interrelationships between different risk factors is of potential interest for designing adequate strategies for preventing, delaying the onset or slowing down the progression of this devastating disease. Thus, in this review we will explore the general mechanisms and evidence linking stress, cardiovascular disease and AD, and discuss the potential benefits of physical activity for AD by counteracting the negative effects of chronic stress, CVD and risk factors.Stress is ubiquitous with many factors contributing to its effects, including psychological responses and associated biological factors, including cortisol related physiological responses, and inflammation. Also in Parkinson's disease there is growing evidence for the role of stress in some key symptoms, even stretching to the prodromal stage. Here we discuss the possible contributions of the range and nature of stress in PD and we aim to summarize the current knowledge about the role of stress-related responses on motor and non-motor symptoms, the underlying pathophysiology, and the potential implications for treatment.Suicide is a global health issue accounting for at least 800,000 deaths per annum. Numerous models have been proposed that differ in their emphasis on the role of psychological, social, psychiatric and neurobiological factors in explaining suicide risk. Central to many models is a stress-diathesis component which states that suicidal behavior is the result of an interaction between acutely stressful events and a susceptibility to suicidal behavior (a diathesis). This article presents an overview of studies that demonstrate that stress and dysregulated hypothalamic-pituitary-adrenal (HPA) axis activity, as measured by cortisol levels, are important additional risk factors for suicide. Evidence for other putative stress-related suicide risk factors including childhood trauma, impaired executive function, impulsivity and disrupted sleep are considered together with the impact of family history of suicide, perinatal and epigenetic influences on suicide risk.This chapter reviews the relationship between stress and brain function in patients with neuropsychiatric disorders, with an emphasis on disorders that have most clearly been linked to traumatic stress exposure. These disorders, which have been described as trauma spectrum disorders, include posttraumatic stress disorder (PTSD), a subgroup of major depression, borderline personality disorder (BPD) and dissociative disorders; they share in common a neurobiological footprint, including smaller hippocampal volume, and are distinguished from other disorders that may share symptom similarities, like some of the anxiety disorders, but are not as clearly linked to stress. The relationship between environmental events such as stressors, especially in early childhood, and their effects on brain and neurobiology is important to understand in approaching these disorders as well as the development of therapeutic interventions. Addressing patients with stress-related disorders from multiple developmental (age at onset of trauma) as well as levels of analysis (cognitive, cultural, neurobiological) approaches will provide the most complete picture and result in the most successful treatment outcomes.