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      Differential effects of experimentally induced anxiety and fear on pain: the role of anxiety sensitivity

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          Abstract

          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.

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          Most cited references 34

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          A systematic review of psychological factors as predictors of chronicity/disability in prospective cohorts of low back pain.

          A systematic review of prospective cohort studies in low back pain. To evaluate the evidence implicating psychological factors in the development of chronicity in low back pain. The biopsychosocial model is gaining acceptance in low back pain, and has provided a basis for screening measurements, guidelines and interventions; however, to date, the unique contribution of psychological factors in the transition from an acute presentation to chronicity has not been rigorously assessed. A systematic literature search was followed by the application of three sets of criteria to each study: methodologic quality, quality of measurement of psychological factors, and quality of statistical analysis. Two reviewers blindly coded each study, followed by independent assessment by a statistician. Studies were divided into three environments: primary care settings, pain clinics, and workplace. Twenty-five publications (18 cohorts) included psychological factors at baseline. Six of these met acceptability criteria for methodology, psychological measurement, and statistical analysis. Increased risk of chronicity (persisting symptoms and/or disability) from psychological distress/depressive mood and, to a lesser extent, somatization emerged as the main findings. Acceptable evidence generally was not found for other psychological factors, although weak support emerged for the role of catastrophizing as a coping strategy. Psychological factors (notably distress, depressive mood, and somatization) are implicated in the transition to chronic low back pain. The development and testing of clinical interventions specifically targeting these factors is indicated. In view of the importance attributed to other psychological factors (particularly coping strategies and fear avoidance) there is a need to clarify their role in back-related disability through rigorous prospective studies.
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            Robust dimensions of anxiety sensitivity: development and initial validation of the Anxiety Sensitivity Index-3.

            Accumulating evidence suggests that anxiety sensitivity (fear of arousal-related sensations) plays an important role in many clinical conditions, particularly anxiety disorders. Research has increasingly focused on how the basic dimensions of anxiety sensitivity are related to various forms of psychopathology. Such work has been hampered because the original measure--the Anxiety Sensitivity Index (ASI)--was not designed to be multidimensional. Subsequently developed multidimensional measures have unstable factor structures or measure only a subset of the most widely replicated factors. Therefore, the authors developed, via factor analysis of responses from U.S. and Canadian nonclinical participants (n=2,361), an 18-item measure, the ASI-3, which assesses the 3 factors best replicated in previous research: Physical, Cognitive, and Social Concerns. Factorial validity of the ASI-3 was supported by confirmatory factor analyses of 6 replication samples, including nonclinical samples from the United States and Canada, France, Mexico, the Netherlands, and Spain (n=4,494) and a clinical sample from the United States and Canada (n=390). The ASI-3 displayed generally good performance on other indices of reliability and validity, along with evidence of improved psychometric properties over the original ASI. (c) 2007 APA, all rights reserved
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              The influence of negative emotions on pain: behavioral effects and neural mechanisms.

              The idea that pain can lead to feelings of frustration, worry, anxiety and depression seems obvious, particularly if it is of a chronic nature. However, there is also evidence for the reverse causal relationship in which negative mood and emotion can lead to pain or exacerbate it. Here, we review findings from studies on the modulation of pain by experimentally induced mood changes and clinical mood disorders. We discuss possible neural mechanisms underlying this modulatory influence focusing on the periaqueductal grey (PAG), amygdala, anterior cingulate cortex (ACC) and anterior insula as key players in both, pain and affective processing.
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                Author and article information

                Journal
                J Pain Res
                J Pain Res
                JPR
                jpainres
                Journal of Pain Research
                Dove
                1178-7090
                06 June 2019
                2019
                : 12
                : 1791-1801
                Affiliations
                [1 ]Department of Physiological Psychology, University of Bamberg , Bamberg, Germany
                Author notes
                Correspondence: Silvia MetzgerPhysiological Psychology, Otto-Friedrich-University of Bamberg , Markusplatz 3, BambergD-96045, GermanyTel +49 951 863 2249Email silvia.metzger@ 123456uni-bamberg.de
                Article
                189011
                10.2147/JPR.S189011
                6559761
                © 2019 Metzger et al.

                This work is published and licensed by Dove Medical Press Limited. The full terms of this license are available at https://www.dovepress.com/terms.php and incorporate the Creative Commons Attribution – Non Commercial (unported, v3.0) License ( http://creativecommons.org/licenses/by-nc/3.0/). By accessing the work you hereby accept the Terms. Non-commercial uses of the work are permitted without any further permission from Dove Medical Press Limited, provided the work is properly attributed. For permission for commercial use of this work, please see paragraphs 4.2 and 5 of our Terms ( https://www.dovepress.com/terms.php).

                Page count
                Figures: 4, References: 49, Pages: 11
                Categories
                Original Research

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