Decision-making under stress: A psychological and neurobiological integrative model.

Understanding the impact of stress on cognitive processes, particularly decision-making, is crucial as it underpins behaviors essential for survival. However, research in this domain has yielded disparate results, with inconsistencies evident across stress-induction paradigms and drug administration protocols designed to investigate specific stress pathways or neuromodulators. Building upon empirical studies, this research identifies a multifaceted matrix of variables contributing to the divergent findings. This matrix encompasses factors such as the temporal proximity between stressors and decision tasks, the nature of stressors and decision contexts, individual characteristics including psychobiological profiles and affective states at the time of decision-making and even cultural influences. In response to these complexities, we propose a comprehensive model that integrates these relevant factors and their intricate interplay to elucidate the mechanisms governing decision-making during stressful events. By synthesizing these insights, our model not only refines existing paradigms but also provides a framework for future study designs, offering avenues for theoretical advancements and translational developments in the field of stress's impact on cognitive functions. This research contributes to a deeper understanding of the nuanced relationship between stress and decision-making, ultimately advancing our knowledge of cognitive processes under challenging conditions.

Cortical activity involved in perception and imagery of visual stimuli in a subject with aphantasia. An EEG case report.

Aphantasia has been described as the inability to voluntarily evoke mental images using the "mind's eye." We studied a congenital aphantasic subject using neuropsychological testsand 64 channel EEG recordings, in order to studycortical activity involved in perception and imagery evaluating event-related potentials(N170, P200, N250). The subject is in the normal range of the neuropsychological tests performed, except for specific imagery tests. The EEG results show that when he evokes the same mental image, he starts the evoking process from left temporal instead of frontal areas, he does not activate occipital visual nor left anterior parietal areas.

Pharmacological Treatment of Anxiety Disorders: The Role of the HPA Axis.

Stress in general, and early life stress in particular, has been associated with the development of anxiety and mood disorders. The molecular, biological and psychological links between stress exposure and the pathogenesis of anxiety and mood disorders have been extensively studied, resulting in the search of novel psychopharmacological strategies aimed at targets of the hypothalamic-pituitary-adrenal (HPA) axis. Hyperactivity of the HPA axis has been observed in certain subgroups of patients with anxiety and mood disorders. In addition, the effects of different anti-anxiety agents on various components of the HPA axis has been investigated, including benzodiazepines, tricyclic antidepressants (TCAs), and selective serotonin reuptake inhibitors (SSRIs). For example, benzodiazepines, including clonazepam and alprazolam, have been demonstrated to reduce the activity of corticotrophin releasing factor (CRF) neurons in the hypothalamus. TCAs and SSRIs are also effective anti-anxiety agents and these may act, in part, by modulating the HPA axis. In this regard, the SSRI escitalopram inhibits CRF release in the central nucleus of the amygdala, while increasing glucocorticoid receptor (GRs) density in the hippocampus and hypothalamus. The molecular effects of these anti-anxiety agents in the regulation of the HPA axis, taken together with their clinical efficacy, may provide further understanding about the role of the HPA axis in the pathophysiology of mood and anxiety disorders, paving the way for the development of novel therapeutic strategies.

The Links Between Stress and Depression: Psychoneuroendocrinological, Genetic, and Environmental Interactions.

The role of stress in the origin and development of depression may be conceived as the result of multiple converging factors, including the chronic effect of environmental stressors and the long-lasting effects of stressful experiences during childhood, all of which may induce persistent hyperactivity of the hypothalamic-pituitary-adrenal axis. These changes, including increased availability of corticotropin-releasing factor and cortisol, are also associated with hyperactivity of the amygdala, hypoactivity of the hippocampus, and decreased serotonergic neurotransmission, which together result in increased vulnerability to stress. The role of other monoaminergic neurotransmitters, genetic polymorphisms, epigenetic mechanisms, inflammatory processes, and altered cognitive processing has also been considered in the development of a comprehensive model of the interactions between different factors of vulnerability. Further understanding of the underlying mechanisms that link these factors may contribute significantly to the development of more effective treatments and preventive strategies in the interface between stress and mood disorders.

Regulation of hypothalamic-pituitary-adrenal activity in response to cognitive therapy in patients with generalized anxiety disorder.

The aim of this study was to evaluate the efficacy of cognitive therapy (CT) in the treatment of generalized anxiety disorder (GAD), as it would be reflected through both psychological and psychoneuroendocrinological parameters. For this purpose, a group of outpatients with GAD were treated with CT for up to a maximum of 24 sessions. In order to assess psychological and biological changes, anxiety-related symptoms were evaluated according to the Hamilton Anxiety Rating Scale (HAM-A), and the hypothalamic-pituitary-adrenal (HPA) function was determined through assessment of circulating cortisol levels. A significant decrease in the HAM-A scores, along with significant changes in plasma cortisol levels, were observed after completion of treatment with CT. These observations contribute to demonstrate that the effect of certain psychotherapeutic approaches, such as CT, may be observed at both psychological and biological levels.

Psychoneuroendocrinological studies on chronic stress and depression.

The adaptive response to stress is characterized by activation of neural and neuroendocrine cascades mediated mainly by the noradrenergic/sympathetic and limbic-hypothalamic-pituitary-adrenal (HPA) systems, respectively. Chronic psychosocial stress has long been associated with the origin and development of depression, where increased levels of cortisol have been observed in both conditions. In this regard, increased levels of cortisol could be directly involved in the mood changes observed in depression, and direct connections between these and alterations of the serotonergic neurotransmission have been also proposed. Therefore, we investigated the potential link between alterations of the limbic-HPA system with the serotonergic hypothesis of depression at both the molecular and clinical levels. Our findings support the notion that chronic psychosocial stress may lead to depression in certain individuals depending on the psychobiological background and their particular psychological resources. Therefore, certain interventions aimed at normalization of the HPA system could potentially prevent the development of depression in chronically stressed subjects. This would be possible through either pharmacological interventions or psychotherapeutic strategies, such as cognitive therapy, aimed at improving resilience and controllability in stressful situations.

Psychoneuroendocrinological links between chronic stress and depression.

OBJECTIVE: The goal of this report is to develop a comprehensive model, which integrates psychosocial and neurobiological aspects, for better understanding the link between chronic stress and mood disorders. METHOD: A selective review of the relevant bibliography was conducted. The significant data were integrated with clinical and preclinical findings, particularly focusing on the effect of the hypothalamo-pituitary-adrenal (HPA) activity on the serotonergic neurotransmission in the CNS. RESULTS: The reviewed data shows that chronic application of stress responses may lead to alterations in the regulation of the HPA system, and the resulting hypercortisolism may be reflected in various psychoneuroendocrinological processes, such as the observed in the serotonergic system, which was implicated in the origin and development of depression. CONCLUSIONS: The analysis of the interactions between the different components of this process, suggests that normalization of the HPA system, either directly through psychopharmacologic strategies, or indirectly through psychotherapeutic approaches oriented to improve the cognitive appraisal of stressful situations, may provide us with more effective diagnostic, preventive, and therapeutic methods in the treatment of widespread anxiety and mood disorders.