The behavioral and neural responses to social exclusion were examined in women randomized to four conditions, varying in levels of attractiveness and friendliness. Informed by evolutionary theory, we predicted that being socially excluded by attractive unfriendly women would be more distressing than being excluded by unattractive women, irrespective of their friendliness level. Our results contradicted most of our predictions but provide important insights into women's responses to interpersonal conflict.
View Article and Find Full Text PDFIn this narrative review, we examine biological processes linking psychological stress and cognition, with a focus on how psychological stress can activate multiple neurobiological mechanisms that drive cognitive decline and behavioral change. First, we describe the general neurobiology of the stress response to define neurocognitive stress reactivity. Second, we review aspects of epigenetic regulation, synaptic transmission, sex hormones, photoperiodic plasticity, and psychoneuroimmunological processes that can contribute to cognitive decline and neuropsychiatric conditions.
View Article and Find Full Text PDFBullying victimization is a form of psychological stress that is associated with poor outcomes in the areas of mental health and learning. Although the emotional maladjustment and memory impairment following interpersonal stress are well documented, the mechanisms of complex cerebral dysfunctions have neither been outlined nor studied in depth in the context of childhood bullying victimization. As a contribution to the cross-disciplinary field of developmental psychology and neuroscience, we review the neuropathophysiology of early life stress, as well as general psychological stress to synthesize the data and clarify the versatile dynamics within neuronal networks linked to bullying victimization.
View Article and Find Full Text PDFAversive events can evoke strong emotions that trigger cerebral neuroactivity to facilitate behavioral and cognitive shifts to secure physiological stability. However, upon intense and/or chronic exposure to such events, the neural coping processes can be maladaptive and disrupt mental well-being. This maladaptation denotes a pivotal point when psychological stress occurs, which can trigger subconscious, "automatic" neuroreactivity as a defence mechanism to protect the individual from potential danger including overwhelming unpleasant feelings and disturbing or threatening thoughts.
View Article and Find Full Text PDFObjective: We assessed mean heart rate (HR) and HR variability (HRV) across wake, rapid eye movement (REM) sleep, and non-REM (NREM) sleep, and across varying levels of NREM sleep depth in individuals with depression and sleep complaints.
Methods: Retrospective polysomnographic data were obtained for 25 individuals diagnosed as having depression (84% female; mean age = 33.8 ± 12.
Background: Abnormalities in heart rate during sleep linked to impaired neuro-cardiac modulation may provide new information about physiological sleep signatures of depression. This study assessed the validity of an algorithm using patterns of heart rate changes during sleep to discriminate between individuals with depression and healthy controls.
Methods: A heart rate profiling algorithm was modeled using machine-learning based on 1203 polysomnograms from individuals with depression referred to a sleep clinic for the assessment of sleep abnormalities, including insomnia, excessive daytime fatigue, and sleep-related breathing disturbances (n = 664) and mentally healthy controls (n = 529).
Objective: To evaluate alpha and beta components of adrenergic baroreflex sensitivity (BRSa) in Valsalva maneuver (VM).
Methods: BRSa was studied in 89 healthy subjects aged 30±13 [16-75] years. Subjects were divided into three groups per blood pressure (BP) patterns associated with relatively balanced or increased alpha-adrenergic modulation: (1) BAR (n=43) - Balanced Autonomic Response with a BP dip below baseline in late phase II (IIL) and recovery in phase IV; (2) SAR (n=16) - Suppressed Autonomic Response with a non-dipping BP; and (3) AAR (n=30) - Augmented Autonomic Response with a BP recovery in phase IIL.
Am J Physiol Regul Integr Comp Physiol
February 2016
The objective of this study was to assess hemodynamic responses and baroreflex sensitivity (BRS) indexes during Valsalva maneuver (VM) and head-up tilt (HUT) testing in orthostatic intolerance (OI). Patients with neurogenic orthostatic hypotension (NOH, n = 26), postural tachycardia syndrome (n = 26) and symptomatic OI (n = 14) were compared with healthy population (control, n = 107) and inappropriate sinus tachycardia (n = 7). Hemodynamic assessment included patterning and quantification with vagal and adrenergic BRS (BRSa/BRSa1).
View Article and Find Full Text PDFObjective: To investigate hemodynamic trans-phasic fluctuations in Valsalva maneuver (VM) and relate them to adrenergic baroreflex sensitivity (BRSa) indices.
Methods: In a healthy population (n=107) with a young age predominance (32 ± 15 years) systolic blood pressure (SBP) and BRSa indices in VM were studied.
Results: Augmented and Suppressed Autonomic Responses (AAR, 28%; SAR, 15%, respectively), in addition to Balanced Autonomic Response (BAR, 40%), were found.
Our objective was to examine the differences in cardiac autonomic function in Postural Tachycardia Syndrome (POTS) versus inappropriate sinus tachycardia (IST). Subjects (IST, n = 8; POTS, n = 12) were studied using standard measurements of the autonomic reflex screen, baroreflex function and spectral analysis. Data was compared to age/gender-matched controls (n = 20).
View Article and Find Full Text PDFThe reliability of the baroreflex sensitivity measurement has not yet been established. Thus, the objective of this study was to define intra-rater reliability of baroreflex sensitivity (BRS) measurements of the Valsalva maneuver (VM) in healthy individuals. Twenty-two healthy volunteers underwent VM testing at two time points.
View Article and Find Full Text PDFBackground: A significant number of patients admitted to hospital after acute ischemic stroke deteriorate clinically. Deterioration is generally noted within the first 48 h after stroke onset. The mechanisms leading to this deterioration are not fully understood.
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