Psychophysiology of arterial baroreceptors and the etiology of hypertension

Rau, Harald; Elbert, Thomas

doi:10.1016/s0301-0511(01)00094-1

Cited by 161 publications

(155 citation statements)

References 41 publications

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“…First, multiple heartbeat-evoked potentials affect neural processing (Schandry and Montoya, 1996;Pollatos et al, 2007;Kern et al, 2013), with marked consequences for sensory processing contingent on the presentation of a stimulus during systole versus diastole (Rau and Elbert, 2001). Such heartbeat-related signals in the visual system could modulate the perception of fine detail via stochastic resonance (Simonotto et al, 1997) and subsequently triggered microsaccades.…”

Section: Discussionmentioning

confidence: 99%

Microsaccades Are Coupled to Heartbeat

et al. 2016

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During visual fixation, the eye generates microsaccades and slower components of fixational eye movements that are part of the visual processing strategy in humans. Here, we show that ongoing heartbeat is coupled to temporal rate variations in the generation of microsaccades. Using coregistration of eye recording and ECG in humans, we tested the hypothesis that microsaccade onsets are coupled to the relative phase of the R-R intervals in heartbeats. We observed significantly more microsaccades during the early phase after the R peak in the ECG. This form of coupling between heartbeat and eye movements was substantiated by the additional finding of a coupling between heart phase and motion activity in slow fixational eye movements; i.e., retinal image slip caused by physiological drift. Our findings therefore demonstrate a coupling of the oculomotor system and ongoing heartbeat, which provides further evidence for bodily influences on visuomotor functioning.

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Section: Discussionmentioning

confidence: 99%

Microsaccades Are Coupled to Heartbeat

et al. 2016

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“…When supine, gravity stimulates cardiopulmonary and arterial baroreceptors, reducing sympathetic system activation (Mohrman & Heller, 2003). This process decreases noradrenergic output from the locus coeruleus (Berridge & Waterhouse, 2003) and in turn dampens down cortical excitability (Rau & Elbert, 2001). Postural influences on EEG recordings, therefore, putatively involve alterations in both CSF thickness and noradrenergic output.…”

Section: Discussionmentioning

confidence: 99%

Posture alters human resting-state

Thibault

Lifshitz

Jones

et al. 2014

Cortex

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Neuroimaging is ubiquitous; however, neuroimagers seldom investigate the putative impact of posture on brain activity. Whereas participants in most psychological experiments sit upright, many prominent neuroimaging techniques (e.g., functional magnetic resonance imaging (fMRI)) require participants to lie supine. Such postural discrepancies may hold important implications for brain function in general and for fMRI in particular. We directly investigated the effect of posture on spontaneous brain dynamics by recording scalp electrical activity in four orthostatic conditions (lying supine, inclined at 45°, sitting upright, and standing erect). Here we show that upright versus supine posture increases widespread high-frequency oscillatory activity.Our electroencephalographic findings highlight the importance of posture as a determinant in neuroimaging. When generalizing supine imaging results to ecological human cognition, therefore, cognitive neuroscientists would benefit from considering the influence of posture on brain dynamics.

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“…For example, pain catastrophizing is associated with elevated negative affect (Hirsh et al 2007), which in turn is often associated with heightened cardiovascular stress reactivity (Burns 1995;Feldman et al 1999;Kamarck et al 1998;Prkachin et al 1999). Prior work indicates that elevations in systolic blood pressure trigger endogenous analgesic mechanisms through functional links between the cardiovascular and pain regulatory systems (e.g., Bruehl and Chung 2004;Edwards et al 2001Edwards et al , 2003Ghione 1996;Rau and Elbert 2001). In this context, a mediation model would predict that catastrophizing would be associated with lower pain intensity through activation of blood pressure-related analgesia.…”

Section: Introductionmentioning

confidence: 99%

Pain catastrophizing, physiological indexes, and chronic pain severity: tests of mediation and moderation models

et al. 2007

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Catastrophizing about pain is related to elevated pain severity and poor adjustment among chronic pain patients, but few physiological mechanisms by which pain catastrophizing maintains and exacerbates pain have been explored. We hypothesized that resting levels of lower paraspinal muscle tension and/or lower paraspinal and cardiovascular reactivity to emotional arousal may: (a) mediate links between pain catastrophizing and chronic pain intensity; (b) moderate these links such that only patients described by certain combinations of pain catastrophizing and physiological indexes would report pronounced chronic pain. Chronic low back pain patients (N = 97) participated in anger recall and sadness recall interviews while lower paraspinal and trapezius EMG and systolic blood pressure (SBP), diastolic blood pressure (DBP) and heart rate (HR) were recorded. Mediation models were not supported. However, pain catastrophizing significantly interacted with resting lower paraspinal muscle tension to predict pain severity such that high catastrophizers with high resting lower paraspinal tension reported the greatest pain. Pain catastrophizing also interacted with SBP, DBP and HR reactivity to affect pain such that high catastrophizers who showed low cardiovascular reactivity to the interviews reported the greatest pain. Results support a multi-variable profile approach to identifying pain catastrophizers at © Springer Science+Business Media, LLC 2007 john.burns@rosalindfranklin.edu. NIH Public Access NIH-PA Author ManuscriptNIH-PA Author Manuscript NIH-PA Author Manuscript greatest risk for pain severity by virtue of resting muscle tension and cardiovascular stress function. KeywordsPain catastrophizing; Chronic pain severity; Lower paraspinal muscle tension; Cardiovascular reactivity; Profile approachCatastrophizing about pain is linked to elevated pain severity and poor adjustment among chronic pain patients (Sullivan et al. 1995). It is defined as a tendency to rumi-nate, magnify and feel helpless about pain (Sullivan et al. 1995), and as a negative automatic appraisal of painful stimuli rooted in activation of maladaptive beliefs or pain schemas (Michael and Burns 2004;Spanos et al. 1979;Sullivan et al. 2001). Irrespective of theoretical conceptualization, only a few physiological mechanisms by which pain catastrophizing maintains and exacerbates chronic pain intensity have been explored (e.g., Edwards and Fillingim 2005).Physical and psychological stress may lead to frequent and intense, or low level but sustained muscular contractions (Sjegaard et al. 2000). This muscle activity can increase pain through ischemia and hypoxia (Fields 1987), and through changes in mechanoreceptor sensitivity (Mense 1993). Flor and colleagues (Flor et al. 1985(Flor et al. , 1991(Flor et al. , 1992 proposed a "symptom-specificity" model of chronic pain, which proposes that patients with certain kinds of musculoskeletal disorders can be distinguished from patients with other kinds of musculoskeletal disorders by substantial stres...

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Psychophysiology of arterial baroreceptors and the etiology of hypertension

Cited by 161 publications

References 41 publications

Microsaccades Are Coupled to Heartbeat

Microsaccades Are Coupled to Heartbeat

Posture alters human resting-state

Pain catastrophizing, physiological indexes, and chronic pain severity: tests of mediation and moderation models

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