Browsing by Subject "Autonomic Nervous System"
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Item Open Access A Window Into Autonomic Nervous System Functioning in Autism: Pupillometry in Adults on the Autism Spectrum(2021) Harris, Adrianne AThe autonomic nervous system (ANS) regulates physiological processes throughout the body and disruption or imbalance of that system has been associated with negative physical and psychological outcomes. Pupil responsivity is controlled by the autonomic nervous system and has been show to index activity of the locus coeruleus-norepinephrine (LC-NE) pathway of innervation. Dysregulation of that pathway has been proposed to relate to differences in attentional control in autism. The current study looked at autonomic nervous system functioning in adults on the autism spectrum through the lens of pupil responsivity to tasks probing reactions to changes in environmental lighting and to complex stimuli. The primary aims of the study evaluated the questions: (1) Do measures of pupil response to different types of stimuli yield different results based on autism diagnostic status? and (2) Are there relationships between measures of pupil response, features of autism and self-reported symptoms of depression and anxiety? Pupillometry and symptom measures were conducted with a sample of adults on the autism spectrum (N=11) and adults without a diagnosis of autism (N=14). Primary variables were baseline pupil diameter, amplitude of dilation/constriction, latency to reach maximal dilation/constriction and recovery velocity. Regarding pupil response to environmental lighting, results indicated timing differences of pupillary response over both light and dark conditions based on autism diagnostic status. In particular, adults on the autism spectrum showed longer latency of pupil response to flashes of dark after being accustomed to a light and slower recovery to the accustomed dark condition after being exposed to flashes of light. Regarding tasks evoking pupil responses to complex stimuli (an auditory reversal learning task and an auditory oddball task), results indicated magnitude of response (amplitude) and variability of response differences related to autism diagnostic status. In particular, adults on the autism spectrum showed larger amplitude of response to all trials in the reversal learning task and greater variability of baseline pupil size across trials in the auditory oddball task than adults without a diagnosis of autism. Across tasks evoking pupil response related to environmental lighting or complex stimuli, associations between autism traits—in particular, intense interests/repetitive behaviors, depression, and anxiety—and different pupillometry measures were found in both the autism and non-autism groups. However, these relationships were different for the different groups. The current study explores differences in pupillary light reflex in adults on the autism spectrum and the results support extant findings of individuals on the autism spectrum potentially having an alternate time course of pupil response. The implications these results may have in terms of understanding of ANS functioning, particularly different sympathetic engagement of the LC-NE pathway and differences in attentional control or reward sensitivity, in autism are discussed. Results also suggest that certain features of autism as well as depression and anxiety seem to co-vary with differences in certain pupillometry measure—especially in the context of increased cognitive demands. Limitations of the study, including sample size and measurement issues, are discussed. Overall, the results suggest future research directions, which may increase understanding of relationships between individual behavior and brain functioning across the autism spectrum. These include possible comparisons of pupil response measures to other direct measures of ANS or brain function as well as the need for controlling for additional measures of psychological well-being and reward sensitivity.
Item Open Access Autonomic cardiovascular dysregulation as a potential mechanism underlying depression and coronary artery bypass grafting surgery outcomes.(J Cardiothorac Surg, 2010-05-13) Dao, Tam K; Youssef, Nagy A; Gopaldas, Raja R; Chu, Danny; Bakaeen, Faisal; Wear, Emily; Menefee, DeleeneBACKGROUND: Coronary artery bypass grafting (CABG) is often used to treat patients with significant coronary heart disease (CHD). To date, multiple longitudinal and cross-sectional studies have examined the association between depression and CABG outcomes. Although this relationship is well established, the mechanism underlying this relationship remains unclear. The purpose of this study was twofold. First, we compared three markers of autonomic nervous system (ANS) function in four groups of patients: 1) Patients with coronary heart disease and depression (CHD/Dep), 2) Patients without CHD but with depression (NonCHD/Dep), 3) Patients with CHD but without depression (CHD/NonDep), and 4) Patients without CHD and depression (NonCHD/NonDep). Second, we investigated the impact of depression and autonomic nervous system activity on CABG outcomes. METHODS: Patients were screened to determine whether they met some of the study's inclusion or exclusion criteria. ANS function (i.e., heart rate, heart rate variability, and plasma norepinephrine levels) were measured. Chi-square and one-way analysis of variance were performed to evaluate group differences across demographic, medical variables, and indicators of ANS function. Logistic regression and multiple regression analyses were used to assess impact of depression and autonomic nervous system activity on CABG outcomes. RESULTS: The results of the study provide some support to suggest that depressed patients with CHD have greater ANS dysregulation compared to those with only CHD or depression. Furthermore, independent predictors of in-hospital length of stay and non-routine discharge included having a diagnosis of depression and CHD, elevated heart rate, and low heart rate variability. CONCLUSIONS: The current study presents evidence to support the hypothesis that ANS dysregulation might be one of the underlying mechanisms that links depression to cardiovascular CABG surgery outcomes. Thus, future studies should focus on developing and testing interventions that targets modifying ANS dysregulation, which may lead to improved patient outcomes.Item Open Access Effects of striatal nitric oxide production on regional cerebral blood flow and seizure development in rats exposed to extreme hyperoxia.(Journal of applied physiology (Bethesda, Md. : 1985), 2015-12) Gasier, Heath G; Demchenko, Ivan T; Allen, Barry W; Piantadosi, Claude AThe endogenous vasodilator and signaling molecule nitric oxide has been implicated in cerebral hyperemia, sympathoexcitation, and seizures induced by hyperbaric oxygen (HBO2) at or above 3 atmospheres absolute (ATA). It is unknown whether these events in the onset of central nervous system oxygen toxicity originate within specific brain structures and whether blood flow is diverted to the brain from peripheral organs with high basal flow, such as the kidney. To explore these questions, total and regional cerebral blood flow (CBF) were measured in brain structures of the central autonomic network in anesthetized rats in HBO2 at 6 ATA. Electroencephalogram (EEG) recordings, cardiovascular hemodynamics, and renal blood flow (RBF) were also monitored. As expected, mean arterial blood pressure and total and regional CBF increased preceding EEG spikes while RBF was unaltered. Of the brain structures examined, the earliest rise in CBF occurred in the striatum, suggesting increased neuronal activation. Continuous unilateral or bilateral striatal infusion of the nitric oxide synthase inhibitor N(ω)-nitro-L-arginine methyl ester attenuated CBF responses in that structure, but global EEG discharges persisted and did not differ from controls. Our novel findings indicate that: 1) cerebral hyperemia in extreme HBO2 in rats does not occur at the expense of renal perfusion, highlighting the remarkable autoregulatory capability of the kidney, and 2) in spite of a sentinel increase in striatal blood flow, additional brain structure(s) likely govern the pathogenesis of HBO2-induced seizures because EEG discharge latency was unchanged by local blockade of striatal nitric oxide production and concomitant hyperemia.