Two different attentional networks have been associated with visuospatial attention and conflict resolution. In most situations either one of the two networks is active or both are increased in activity together. By using functional magnetic resonance imaging and a flanker task, we show conditions in which one network (anterior attention system) is increased in activity whereas the other (visuospatial attention system) is reduced, showing that attentional conflict and selection are separate aspects of attention. Further, we distinguish between neural systems involved in different forms of conflict. Specifically, we dissociate patterns of activity in the basal ganglia and insula cortex during simple violations in expectancies (i.e., sudden changes in the frequency of an event) from patterns of activity in the anterior attention system specifically correlated with response conflict as evidenced by longer response latencies and more errors. These data provide a systems-level approach in understanding integrated attentional networks.
These data suggest that sleep duration is a significant correlate of the metabolic syndrome. Additional studies are needed to evaluate temporal relationships among these measures, the behavioral and physiologic mechanisms that link the two, and their impact on subsequent cardiometabolic disease.
In this study we investigated the effects of nonevaluative social interaction on the cardiovascular response to psychological challenge. Thirty-nine college-age females appeared accompanied ("Friend" condition) or unaccompanied ("Alone" condition) to an experimental laboratory. In the Friend condition, partners were present while the subject participated in two laboratory tasks, and the partners' evaluation potential was minimized by design. Subjects in the Friend condition showed reduced heart rate reactivity to both tasks, relative to the Alone group, an attenuated task-related systolic blood pressure response to one of the tasks, and a reduced diastolic blood pressure increase during a solitary interview. In two other instances, partner-related response reductions were apparent only for Type A subjects. None of these effects was accompanied by differences in task performance or self-reported emotional response. Interpersonal support may reduce cardiovascular responsivity to stress, an effect with possible implications for understanding the association between social relationships and cardiovascular risk.
These results support the hypothesis that hemodynamic responses under conditions of mental stress may influence the progression of atherosclerosis.
The aim of the present study was to characterize the functional relationships between behaviorally evoked regional brain activation and cardiac autonomic activity in humans. Concurrent estimates of regional cerebral blood flow (rCBF; obtained by positron emission tomography), heart period, and high-frequency heart period variability (HFHPV; an indicator of cardiac parasympathetic activity) were examined in 93 adults (aged 50-70 years) who performed a series of increasingly difficult working-memory tasks. Increased task difficulty resulted in decreased heart period (indicating cardioacceleration) and decreased HF-HPV (indicating decreased cardiac parasympathetic activity). Task-induced decreases in heart period and HF-HPV were associated with concurrent increases and decreases in rCBF to cortical and subcortical brain regions that are speculated to regulate cardiac autonomic activity during behavioral processes: the medialprefrontal, insular, and anterior cingulate cortices, the amygdala-hippocampal complex, and the cerebellum. These findings replicate and extend a small number of functional neuroimaging studies that suggest an important role for both cortical and subcortical brain systems in human cardiac autonomic regulation. KeywordsCentral cardiac autonomic regulation; Heart period; High-frequency heart period variability; Positron emission tomography The cortical and subcortical brain systems that regulate cardiac autonomic activity during behavior have been detailed by extensive research in nonhuman animals (reviewed by Bennarroch, 1997;Buchanan & Powell, 1993;Loewy & Spyer, 1990 NIH-PA Author ManuscriptNIH-PA Author Manuscript NIH-PA Author ManuscriptHurley, Ruit, & Frysztak, 1993). An open question is whether similar brain systems regulate behaviorally integrated cardiac autonomic activity in humans. Answering this question is important because the brain's regulation of cardiac autonomic activity is purported to influence a range of behavioral processes: attending to novel stimuli (Porges, 1995), processing environmental information (Lacey & Lacey, 1974), making decisions (Damasio, 1994), experiencing fear and anxiety (Berntson, Sarter, & Cacioppo, 1998), perceiving pain (Dworkin et al., 1994;Rosen et al., 1996), and reacting to stressors (Lovallo & Gerin, 2003) are examples of such processes.Drawing on the support of nonhuman animal research, the cortical brain systems that are hypothesized to regulate cardiac autonomic activity during behavior include the medialprefrontal (Brodmann Areas 10 and 11), insular, and anterior cingulate (Brodmann Areas 24, 25, and 32) regions of the cortex. A prevailing view is that these cortical systems act as a network with subcortical systems to initiate and represent cardiac autonomic adjustments that support behavioral responses to environmental, psychological, and social stimuli (Bennarroch, 1997;Cechetto, 1994;Groenewegen & Uylings, 2000;Loewy & Spyer, 1990;Thayer & Lane, 2000). Subcortical regions that are thought to regulate behaviorally integrated cardiac ...
The accurate evaluation of cardiovascular reactions to psychological challenge requires stable baselines against which change can be evaluated. When more than one challenge is employed, the recovery of this baseline becomes important in order to avoid carryover effects. Resting periods, even those of 20 min or more, do not guarantee baseline stability. We compared a 20‐min resting condition and a new form of baseline condition in 48 college men using video tasks as the psychological challenges. The new form was a minimally demanding color detection task, termed the “vanilla”baseline condition. A 10‐min version and a 20‐min version of this condition were tested. Comparisons to 10‐min resting baselines were made using our prior work and values from the literature. Vanilla baseline conditions were shown to be equal to or better than resting baseline conditions using criteria of between‐ and within‐baseline stability, amplitude and significance of responsivity, and generalizability between sessions on separate days. Ten‐minute resting baselines also showed acceptable stability, questioning the value of lengthy baselines. The good performance of the 10‐min vanilla baseline in initial and replication samples supported its utility for estimating baselines for many purposes.
Chronic stress in non-human animals decreases the volume of the hippocampus, a brain region that supports learning and memory and that regulates neuroendocrine activity. In humans with stressrelated psychiatric syndromes characterized by impaired learning and memory and dysregulated neuroendocrine activity, surrogate and retrospective indicators of chronic stress are also associated with decreased hippocampal volume. However, it is unknown whether chronic stress is associated with decreased hippocampal volume in those without a clinical syndrome. We tested whether reports of life stress obtained prospectively over an approximate 20-year period predicted later hippocampal grey matter volume in 48 healthy postmenopausal women. Women completed the Perceived Stress Scale repeatedly from 1985 to 2004; in 2005 and 2006, their hippocampal grey matter volume was quantified by voxel-based morphometry. Higher Perceived Stress Scale scores from 1985 to 2004-an indicator of more chronic life stress-predicted decreased grey matter volume in the right orbitofrontal cortex and right hippocampus. These relationships persisted after accounting for age, total grey matter volume, time since menopause, use of hormone therapy, subclinical depressive symptoms, and other potentially confounding behavioral and age-related cerebrovascular risk factors. The relationship between chronic life stress and regional grey matter volume-particularly in the hippocampus and orbitofrontal cortex-appears to span a continuum that extends to otherwise healthy individuals. Consistent with animal and human clinical evidence, we speculate that chronicstress-related variations in brain morphology are reciprocally and functionally related to adaptive and maladaptive changes in cognition, neuroendocrine activity, and psychiatric vulnerability.Keywords chronic life stress; hippocampus; orbitofrontal cortex; voxel-based morphometry Stressful experiences can be both constructive and destructive to the body and brain. In the short term, acute stressful experiences mobilize adaptive changes in physiology and behavior that help to meet the demands of environmental challenges and protect against threats to internal homeostasis Selye, 1956). Over the long term, however, chronic
Individuals who exhibit exaggerated blood pressure reactions to psychological stressors are at risk for hypertension, ventricular hypertrophy, and premature atherosclerosis; however, the neural systems mediating exaggerated blood pressure reactivity and associated cardiovascular risk in humans remain poorly defined. Animal models indicate that the amygdala orchestrates stressor-evoked blood pressure reactions via reciprocal signaling with corticolimbic and brainstem cardiovascular-regulatory circuits. Based on these models, we used a multimodal neuroimaging approach to determine whether human individual differences in stressor-evoked blood pressure reactivity vary with amygdala activation, gray matter volume, and functional connectivity with corticolimbic and brainstem areas implicated in stressor processing and cardiovascular regulation. We monitored mean arterial pressure (MAP) and concurrent functional magnetic resonance imaging BOLD signal changes in healthy young individuals while they completed a Stroop color-word stressor task, validated previously in epidemiological studies of cardiovascular risk. Individuals exhibiting greater stressor-evoked MAP reactivity showed (1) greater amygdala activation, (2) lower amygdala gray matter volume, and (3) stronger positive functional connectivity between the amygdala and perigenual anterior cingulate cortex and brainstem pons. Individual differences in amygdala activation, gray matter volume, and functional connectivity with corticolimbic and brainstem circuits may partly underpin cardiovascular disease risk by impacting stressor-evoked blood pressure reactivity.
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