Respiratory Variables in Response to a Pain-Fear Stimulus and in Experimental Asthma
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Abstract:
Ventilatory variables and the mechanical properties of the lungs as response to a pain-fear stimulus, electric shock, and in experimental asthma were measured in the guinea pig. The respiratory pattern after exposure to electric shock was characterized by shortened inspiration and a prolonged expiratory phase. This pattern was similar to that observed in experimental allergic asthma. The mechanical properties of the lungs, however, were different in the two situations. In experimental allergic asthma in the guinea pig there was evidence of bronchiolar obstruction as measured by an increase in airway resistance and decrease in compliance. No evidence of increased airway resistance was found in the animals exposed to electric shock. The respiratory pattern after the pain-fear stimulus appeared to be related to screeching of the animals. The findings of this report suggest that it is important to differentiate the respiratory response to a pain-fear stimulus from that of asthma. Such a distinction is possible if indices of bronchiolar function are considered in the definition of bronchial asthma.Keywords:
Stimulus (psychology)
Chronic pain patients are often confronted with repeated failure to achieve pain relief. The aim of this study was to experimentally investigate the effects of repeated failing attempts to control pain on pain impact (pain intensity, emotional and physiological responses). Perceived control over an electrocutaneous pain stimulus was manipulated between subjects by success or failure feedback on a task by which control over pain could be acquired. In addition, success or failure at the task was manipulated without suggesting a possibility to control pain. It was hypothesized that successful control would lead to lowest pain impact, whereas failure to control pain would lead to even higher pain impact than absent control. Furthermore, it was hypothesized that failure feedback would increase pain impact when compared to success feedback. Results indicated that repeated failure to control pain increased anger and heart rate responses compared to the other conditions, but not pain intensity. It is concluded that persistent efforts to control pain in the face of failure may lead to the maintenance or exacerbation of physiological and emotional responses.
Stimulus (psychology)
Pain catastrophizing
Pain tolerance
Pain control
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The purpose of this study was to examine psychosocial influences on exercise-induced hypoalgesia (EIH).Randomized controlled trial.Clinical research unit in a hospital.Fifty-eight healthy men and women (mean age = 21 ± 3 years) participated in this study.Participants were first asked to complete a series of baseline demographic and psychological questionnaires including the Pain Catastrophizing Scale, the Fear of Pain Questionnaire, and the Family Environment Scale. Following this, they were familiarized with both temporal summation of heat pain and pressure pain testing protocols. During their next session, participants completed the Profile of Mood States, rated the intensity of heat pulses, and indicated their pressure pain thresholds and ratings before and after three minutes of submaximal, isometric exercise. Situational catastrophizing was assessed at the end of the experimental session.Results indicated that experimental pain sensitivity was significantly reduced after exercise ( P < 0.05). Men and women did not differ on any of the measured psychosocial variables ( P > 0.05). Positive family environments predicted attenuated pain sensitivity and greater EIH, whereas negative and chronic pain-present family environments predicted worse pain and EIH outcomes. Situational catastrophizing and negative mood state also predicted worse pain and EIH outcomes and were additionally associated with increased ratings of perceived exertion and muscle pain during exercise.This study provides preliminary evidence that psychosocial variables, such as the family environment and mood states, can affect both pain sensitivity and the ability to modulate pain through exercise-induced hypoalgesia.
Hypoalgesia
Pain catastrophizing
Affect
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Several studies have recently suggested that an abnormal processing of respiratory interoceptive and nociceptive (painful) stimuli may contribute to eating disorder (ED) pathophysiology. Mood and anxiety disorders (MA) are also characterized by abnormal respiratory symptoms, and show substantial comorbidity with ED. However, no studies have examined both respiratory and pain processing simultaneously within ED and MA. The present study systematically evaluated responses to perturbations of respiratory and nociceptive signals across the levels of physiology, behavior, and symptom report in a transdiagnostic ED sample (n = 51) that was individually matched to MA individuals (n = 51) and healthy comparisons (HC; n = 51). Participants underwent an inspiratory breath-holding challenge as a probe of respiratory interoception and a cold pressor challenge as a probe of pain processing. We expected both clinical groups to report greater stress and fear in response to respiratory and nociceptive perturbation than HCs, in the absence of differential physiological and behavioral responses. During breath-holding, both the ED and MA groups reported significantly more stress, feelings of suffocation, and suffocation fear than HC, with the ED group reporting the most severe symptoms. Moreover, anxiety sensitivity was related to suffocation fear only in the ED group. The heightened affective responses in the current study occurred in the absence of group differences in behavioral (breath hold duration, cold pressor duration) and physiological (end-tidal carbon dioxide, end-tidal oxygen, heart rate, skin conductance) responses. Against our expectations, there were no group differences in the response to cold pain stimulation. A matched-subgroup analysis focusing on individuals with anorexia nervosa (n = 30) produced similar results. These findings underscore the presence of abnormal respiratory interoception in MA and suggest that hyperreactivity to respiratory signals may be a potentially overlooked clinical feature of ED.
Respiratory Rate
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Abstract Dyspnea is a debilitating and threatening symptom in various diseases. Affected patients often report the unpredictability of dyspnea episodes being particularly anxiety‐provoking and amplifying the perception of dyspnea. Experimental studies testing dyspnea unpredictability together with related neural processes, physiological fear responses, and dyspnea‐related personality traits are sparse. Therefore, we investigated the impact of unpredictability of dyspnea offset on dyspnea perception and fear ratings, respiratory neural gating and physiological fear indices, as well as the influence of interindividual differences in fear of suffocation (FoS). Forty healthy participants underwent a task manipulating the offset predictability of resistive load‐induced dyspnea including one unloaded safety condition. Respiratory variables, self‐reports of dyspnea intensity, dyspnea unpleasantness, and fear were recorded. Moreover, respiratory neural gating was measured in a paired inspiratory occlusion paradigm using electroencephalography, while electrodermal activity, startle eyeblink, and startle probe N100 were assessed as physiological fear indices. Participants reported higher dyspnea unpleasantness and fear when dyspnea offset was unpredictable compared to being predictable. Individuals with high levels of FoS showed the greatest increase in fear and overall higher levels of fear and physiological arousal across all conditions. Respiratory neural gating, startle eyeblink, and startle probe N100 showed general reductions during dyspnea conditions but no difference between unpredictable and predictable dyspnea conditions. Together, the current results suggest that the unpredictable offset of dyspnea amplifies dyspnea perception and fear, especially in individuals with high levels of FoS. These effects were unrelated to respiratory neural gating or physiological fear responses, requiring future studies on underlying mechanisms.
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Cold pressor test
Stimulus (psychology)
Pain tolerance
Pain catastrophizing
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Abstract Empathy is essential for the survival of social species. In many studies, especially those with animal models, empathy for pain was evaluated by the modulation of pain sensitivity. However, the relationship between pain sensitivity and empathy for pain is not well established. Here, by performing two experiments, we aimed to investigate their relationship at both behavioral and electrophysiological levels. In Experiment 1, we characterized individual pain sensitivity using pain threshold and tolerance in a cold pressor test, self‐report empathy using Interpersonal Reactivity Index, and pain‐related psychological factors, including pain‐related anxiety, depression, pain catastrophizing, and pain‐related fear, using well‐validated questionnaires. We observed that pain sensitivity was positively correlated with emotional empathy, and their relationship was mediated by pain‐related anxiety, pain catastrophizing, and pain‐related fear. In Experiment 2, we quantified empathy for pain using pain intensity and unpleasantness as well as event‐related potentials (ERPs) in an empathy for pain task. Positive correlations were observed between pain sensitivity and psychophysiological empathic responses (i.e., the P3 component and the late positive potential in ERPs), and their relationship was mediated by pain‐related fear. These results suggested that being influenced by some pain‐related psychological factors, individuals with higher pain sensitivity tended to have stronger empathy for pain, manifested as stronger emotional reactions to others' pain. Our results indicated that the conventional strategy of using pain sensitivity to quantify empathy should be treated with caution, as their relationship could be disturbed by experimental manipulations or pathological modulations that could influence individual emotional states or cognitive processes.
Pain catastrophizing
Anxiety sensitivity
Interpersonal Reactivity Index
Cold pressor test
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Atopy
Clinical Significance
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CINAHL
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Background: Anxiety has been associated with both increased and decreased pain perception. Rhudy and Meagher (2000) showed that pain sensitivity is enhanced by anxiety (anticipation of shocks), but diminished by fear (confrontation with shocks). A problem of this approach is the confounding of emotional and attentional effects: Administered shocks (fear induction) divert attention away from pain, which might account for lower pain in this condition. Moreover, heterogeneous findings in the past might be due to inter-individual differences in the proneness to react to anxiety and fear such as ones anxiety sensitivity (AS) level. Objectives: Our aim was to clarify the association between anxiety, fear and pain. We used the NPU paradigm for inducing these emotions and recording pain sensitivity at once with one stimulus to prevent interference by distraction. We assumed that anxiety and fear affect pain differently. Moreover, we hypothesized that subjects with clinically relevant (high) AS (H-AS group) show enhanced pain perception in contrast to low AS subjects (L-AS group). Method: Forty healthy subjects (female: N=20; age M=23.53 years) participated and H-AS or L-AS status was determined by clinically discriminating cut-off scores of the Anxiety Sensitivity Index-3 (ASI-III). Emotions were induced by the application of unpredictable (anxiety) and predictable (fear) electric stimuli. Pain ratings of electric stimuli were compared between the conditions. Startle reflex and anxiety ratings were recorded. Results: Results showed no general effects of anxiety and fear on pain perception. However, anxiety enhanced pain sensitivity in H-AS subjects, whereas fear did not affect pain sensitivity. In L-AS subjects no effects on pain perception were found. Conclusion: Results revealed that anxiety, not fear, enhanced pain perception but only in subjects with clinically relevant AS levels. This indicates that subclinical AS levels are sufficient to increase pain sensitivity, in uncertain situations.
Anxiety sensitivity
Fear-potentiated startle
Sensation
Anticipation (artificial intelligence)
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