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      Transmission of risk from parents with chronic pain to offspring : an integrative conceptual model

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      PAIN

      Ovid Technologies (Wolters Kluwer Health)

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          Abstract

          Offspring of parents with chronic pain are at increased risk for pain and adverse mental and physical health outcomes (Higgins et al, 2015). Although the association between chronic pain in parents and offspring has been established, few studies have addressed why or how this relation occurs. Identifying mechanisms for the transmission of risk that leads to the development of chronic pain in offspring is important for developing preventive interventions targeted to decrease risk for chronic pain and related outcomes (eg, disability and internalizing symptoms). This review presents a conceptual model for the intergenerational transmission of chronic pain from parents to offspring with the goal of setting an agenda for future research and the development of preventive interventions. Our proposed model highlights 5 potential mechanisms for the relation between parental chronic pain and pediatric chronic pain and related adverse outcomes: (1) genetics, (2) alterations in early neurobiological development, (3) pain-specific social learning, (4), general parenting and family health, and (5) exposure to stressful environment. In addition, the model presents 3 potential moderators for the relation between parent and child chronic pain: (1) the presence of chronic pain in a second parent, (2) timing, course, and location of parental chronic pain, and (3) offspring's characteristics (ie, sex, developmental stage, race or ethnicity, and temperament). Such a framework highlights chronic pain as inherently familial and intergenerational, opening up avenues for new models of intervention and prevention that can be family centered and include at-risk children.

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          Most cited references 126

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          Pain catastrophizing: a critical review.

          Pain catastrophizing is conceptualized as a negative cognitive-affective response to anticipated or actual pain and has been associated with a number of important pain-related outcomes. In the present review, we first focus our efforts on the conceptualization of pain catastrophizing, highlighting its conceptual history and potential problem areas. We then focus our discussion on a number of theoretical mechanisms of action: appraisal theory, attention bias/information processing, communal coping, CNS pain processing mechanisms, psychophysiological pathways and neural pathways. We then offer evidence to suggest that pain catastrophizing represents an important process factor in pain treatment. We conclude by offering what we believe represents an integrated heuristic model for use by researchers over the next 5 years; a model we believe will advance the field most expediently.
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            Why rejection hurts: a common neural alarm system for physical and social pain.

            Numerous languages characterize 'social pain', the feelings resulting from social estrangement, with words typically reserved for describing physical pain ('broken heart', 'broken bones') and perhaps for good reason. It has been suggested that, in mammalian species, the social-attachment system borrowed the computations of the pain system to prevent the potentially harmful consequences of social separation. Mounting evidence from the animal lesion and human neuroimaging literatures suggests that physical and social pain overlap in their underlying neural circuitry and computational processes. We review evidence suggesting that the anterior cingulate cortex plays a key role in the physical-social pain overlap. We also suggest that the physical-social pain circuitry might share components of a broader neural alarm system.
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              Genetic basis for individual variations in pain perception and the development of a chronic pain condition.

              Pain sensitivity varies substantially among humans. A significant part of the human population develops chronic pain conditions that are characterized by heightened pain sensitivity. We identified three genetic variants (haplotypes) of the gene encoding catecholamine-O-methyltransferase (COMT) that we designated as low pain sensitivity (LPS), average pain sensitivity (APS) and high pain sensitivity (HPS). We show that these haplotypes encompass 96% of the human population, and five combinations of these haplotypes are strongly associated (P=0.0004) with variation in the sensitivity to experimental pain. The presence of even a single LPS haplotype diminishes, by as much as 2.3 times, the risk of developing myogenous temporomandibular joint disorder (TMD), a common musculoskeletal pain condition. The LPS haplotype produces much higher levels of COMT enzymatic activity when compared with the APS or HPS haplotypes. Inhibition of COMT in the rat results in a profound increase in pain sensitivity. Thus, COMT activity substantially influences pain sensitivity, and the three major haplotypes determine COMT activity in humans that inversely correlates with pain sensitivity and the risk of developing TMD.
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                Author and article information

                Journal
                PAIN
                PAIN
                Ovid Technologies (Wolters Kluwer Health)
                0304-3959
                2016
                December 2016
                : 157
                : 12
                : 2628-2639
                Article
                10.1097/j.pain.0000000000000637
                5592972
                27380502
                © 2016

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