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      Review of childhood pain highlights the role of negative stress

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          Abstract

          Aim

          Recurrent pain of unknown origin is a major problem in children. The aim of the present review was to examine the hypothesis of negative stress as an aetiology of recurrent pain from different aspects.

          Methods and Results

          Epidemiological studies, clinical experience and hormonal data give support for such a hypothesis. Negative stress as a tentative aetiology for recurrent pain is reviewed. Stress, muscular tension, the startle reaction and its tentative relation to pain is illuminated. Deviations of hormonal secretion supporting a stress aetiology are mentioned. The role of central sensitisation for recurrent pain is discussed. Possible aetiological implications of recurrent pain as a local symptom or a general disorder are presented. Brain changes due to stress are shortly reviewed. Stress and pain in the clinic are highlighted. The importance of biological, psychological and social factors, as well as genetic elements, is discussed.

          Conclusion

          Stress elicits neurobiological mechanisms. They may lead to many neurophysiological deviances. Increase of muscle tension and neuromuscular excitability and enhanced startle reaction may be of importance for recurring pain. The identification of stress as a primary cause of recurrent pain can have huge implications for understanding signs and treatment in clinical practice.

          Abstract

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          Most cited references61

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          Central role of the brain in stress and adaptation: links to socioeconomic status, health, and disease.

          The brain is the key organ of stress reactivity, coping, and recovery processes. Within the brain, a distributed neural circuitry determines what is threatening and thus stressful to the individual. Instrumental brain systems of this circuitry include the hippocampus, amygdala, and areas of the prefrontal cortex. Together, these systems regulate physiological and behavioral stress processes, which can be adaptive in the short-term and maladaptive in the long-term. Importantly, such stress processes arise from bidirectional patterns of communication between the brain and the autonomic, cardiovascular, and immune systems via neural and endocrine mechanisms underpinning cognition, experience, and behavior. In one respect, these bidirectional stress mechanisms are protective in that they promote short-term adaptation (allostasis). In another respect, however, these stress mechanisms can lead to a long-term dysregulation of allostasis in that they promote maladaptive wear-and-tear on the body and brain under chronically stressful conditions (allostatic load), compromising stress resiliency and health. This review focuses specifically on the links between stress-related processes embedded within the social environment and embodied within the brain, which is viewed as the central mediator and target of allostasis and allostatic load.
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            Stress- and allostasis-induced brain plasticity.

            The brain is the key organ of stress processes. It determines what individuals will experience as stressful, it orchestrates how individuals will cope with stressful experiences, and it changes both functionally and structurally as a result of stressful experiences. Within the brain, a distributed, dynamic, and plastic neural circuitry coordinates, monitors, and calibrates behavioral and physiological stress response systems to meet the demands imposed by particular stressors. These allodynamic processes can be adaptive in the short term (allostasis) and maladaptive in the long term (allostatic load). Critically, these processes involve bidirectional signaling between the brain and body. Consequently, allostasis and allostatic load can jointly affect vulnerability to brain-dependent and stress-related mental and physical health conditions. This review focuses on the role of brain plasticity in adaptation to, and pathophysiology resulting from, stressful experiences. It also considers interventions to prevent and treat chronic and prevalent health conditions via allodynamic brain mechanisms.
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              Stress effects on the hippocampus: a critical review

              Uncontrollable stress has been recognized to influence the hippocampus at various levels of analysis. Behaviorally, human and animal studies have found that stress generally impairs various hippocampal-dependent memory tasks. Neurally, animal studies have revealed that stress alters ensuing synaptic plasticity and firing properties of hippocampal neurons. Structurally, human and animal studies have shown that stress changes neuronal morphology, suppresses neuronal proliferation, and reduces hippocampal volume. Since the inception of stress research nearly 80 years ago, much focus has been on the varying levels of hypothalamic-pituitary-adrenal (HPA) axis neuroendocrine hormones, namely glucocorticoids, as mediators of the myriad stress effects on the hippocampus and as contributing factors to stress-associated psychopathologies such as post-traumatic stress disorder (PTSD). However, reports of glucocorticoid-produced alterations in hippocampal functioning vary widely across studies. This review provides a brief history of stress research, examines how the glucocorticoid hypothesis emerged and guides contemporary stress research, and considers alternative approaches to understanding the mechanisms underlying stress effects on hippocampal functioning.
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                Author and article information

                Contributors
                gosta.alfven@slmk.org
                Journal
                Acta Paediatr
                Acta Paediatr
                10.1111/(ISSN)1651-2227
                APA
                Acta Paediatrica (Oslo, Norway : 1992)
                John Wiley and Sons Inc. (Hoboken )
                0803-5253
                1651-2227
                26 June 2019
                December 2019
                : 108
                : 12 ( doiID: 10.1111/apa.v108.12 )
                : 2148-2156
                Affiliations
                [ 1 ] Clintec Karolinska Institute Stockholm Sweden
                [ 2 ] Department of Neuroscience Karolinska institute Stockholm Sweden
                [ 3 ] Swedish School of Sport and Health Sciences Stockholm Sweden
                Author notes
                [*] [* ] Correspondence

                G Alfven, Clintec, Karolinska Institute, SE 11620 Stockholm, Sweden.

                Tel: +46 739660835 |

                Email: gosta.alfven@ 123456slmk.org

                Article
                APA14884
                10.1111/apa.14884
                6899754
                31162723
                e2d2923e-f2e7-4ea0-ae48-7647b48d26e4
                ©2019 The Authors. Acta Pædiatrica published by John Wiley & Sons Ltd on behalf of Foundation Acta Pædiatrica

                This is an open access article under the terms of the http://creativecommons.org/licenses/by-nc/4.0/ License, which permits use, distribution and reproduction in any medium, provided the original work is properly cited and is not used for commercial purposes.

                History
                : 14 March 2019
                : 14 May 2019
                : 03 June 2019
                Page count
                Figures: 4, Tables: 0, Pages: 9, Words: 6502
                Funding
                Funded by: University of Gothenburg Centre for Person‐Centered Care, GPCC
                Funded by: Swedish School of Sport and Health Sciences
                Categories
                Review Article
                Review Articles
                Custom metadata
                2.0
                December 2019
                Converter:WILEY_ML3GV2_TO_JATSPMC version:5.7.2 mode:remove_FC converted:05.12.2019

                Pediatrics
                electromyography,muscle,pain,startle,stress
                Pediatrics
                electromyography, muscle, pain, startle, stress

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