Psychology

Objectives Contemporary fear-avoidance models of chronic pain posit that fear of pain, and overgeneralization of fear to non-threatening stimuli is a potential pathway to chronic pain. While increasing experimental evidence supports this hypothesis, a comprehensive investigation requires testing in multiple modalities due to the diversity of symptomatology among individuals with chronic pain. In the present study we used an established tactile fear conditioning paradigm as an experimental model of allodynia and spontaneous pain fluctuations, to investigate whether stimulus generalization occurs resulting in fear of touch spreading to new locations. Methods In our paradigm, innocuous touch is presented either paired (predictable context) or unpaired (unpredictable context) with a painful electrocutaneous stimulus (pain-US). In the predictable context, vibrotactile stimulation to the index or little finger was paired with the pain-US (CS+), whilst stimulation of the other finger was never paired with pain (CS-). In the unpredictable context, vibrotactile stimulation to the index and little fingers of the opposite hand (CS1 and CS2) was unpaired with pain, but pain-USs occurred unpredictable during the intertrial interval. During the subsequent generalization phase, we tested the spreading of conditioned responses (self-reported fear of touch and pain expectancy) to the (middle and ring) fingers between the CS+ and CS-, and between the CS1 and CS2. Results Differential fear acquisition was evident in the predictable context from increased self-reported pain expectancy and self-reported fear for the CS + compared to the CS-. However, expectancy and fear ratings to the novel generalization stimuli (GS+ and GS-) were comparable to the responses elicited by the CS-. Participants reported equal levels of pain expectancy and fear to the CS1 and CS2 in the unpredictable context. However, the acquired fear did not spread in this context either: participants reported less pain expectancy and fear to the GS1 and GS2 than to the CS1 and CS2. As in our previous study, we did not observe differential acquisition in the startle responses. Conclusions Whilst our findings for the acquisition of fear of touch replicate the results from our previous study (Biggs et al., 2017), there was no evidence of fear generalization. We discuss the limitations of the present study, with a primary focus on procedural issues that were further investigated with post-hoc analyses, concluding that the present results do not show support for the hypothesis that stimulus generalization underlies spreading of fear of touch to new locations, and discuss how this may be the consequence of a context change that prevented transfer of acquisition.

Chronic pain and sleep disturbance are highly comorbid disorders, which leads to barriers to treatment and significant healthcare costs. Understanding the underlying genetic and neural mechanisms of the interplay between sleep disturbance and chronic pain is likely to lead to better treatment. In this study, we combined 1206 participants with phenotype data, resting-state functional magnetic resonance imaging (rfMRI) data and genotype data from the Human Connectome Project and two large sample size genome-wide association studies (GWASs) summary data from published studies to identify the genetic and neural bases for the association between pain and sleep disturbance. Pittsburgh sleep quality index (PSQI) score was used for sleep disturbance, pain intensity was measured by Pain Intensity Survey. The result showed chronic pain was significantly correlated with sleep disturbance (r = 0.171, p-value < 0.001). Their genetic correlation was r = 0.598 using linkage disequilibrium (LD) score regression analysis. Polygenic score (PGS) association analysis showed PGS of chronic pain was significantly associated with sleep and vice versa. Nine shared functional connectivity (FCs) were identified involving prefrontal cortex, temporal cortex, precentral/postcentral cortex, anterior cingulate cortex, fusiform gyrus and hippocampus. All these FCs mediated the effect of sleep disturbance on pain and seven FCs mediated the effect of pain on sleep disturbance. The chronic pain PGS was positively associated with the FC between middle temporal gyrus and hippocampus, which further mediated the effect of chronic pain PGS on PSQI score. Mendelian randomization analysis implied a possible causal relationship from chronic pain to sleep disturbance was stronger than that of sleep disturbance to chronic pain. The results provided genetic and neural evidence for the association between pain and sleep disturbance, which may inform future treatment approaches for comorbid chronic pain states and sleep disturbance.

Background and Aims Higher chronic pain acceptance is associated with lower pain and disability. Clinician beliefs are associated with patients' beliefs. This study therefore aimed to develop the Chronic Pain Acceptance Questionnaire for Clinicians (CPAQ-C) to measure clinicians' beliefs regarding the importance of levels of acceptance in patients with chronic pain, and to examine the questionnaire's psychometric properties. Methods Phase one: the CPAQ-C was adapted from the Chronic Pain Acceptance Questionnaire. Data on 162 completed questionnaires were analysed using Rasch analysis. Phase Two: the cohort completed the Healthcare Providers Pain and Impairment Relationship Scale, and the association (Pearson's correlation co-efficient) between these questionnaires examined to assist CPAQ-C validation. Twenty-four participants completed the CPAQ-C one-week later. Test re-test reliability was examined using intraclass correlation co-efficient (2,1) and standard error of measurement. Phase Three: to examine responsiveness 17 clinicians attending a workshop on Acceptance and Commitment Therapy completed the CPAQ-C before and immediately after the workshop, and six-months later. The Skillings Mack test was used to determine whether CPAQ-C scores differed across different timepoints. Results Rasch analysis supported two subscales: activity engagement and pain willingness. Five poorly functioning items were excluded. There was good correlation between the CPAQ-C and Healthcare Providers Pain and Impairment Relationship Scale (-.54). The CPAQ-C demonstrated good reliability (ICC (2,1): .81; standard error of measurement: 4.76). There was significant improvement in CPAQ-C scores following the workshop (p=<.001). Conclusions The CPAQ-C appears a valid, reliable and responsive measure of clinicians' beliefs regarding the importance of levels of acceptance in patients with chronic pain. Implications Where the CPAQ-C reveals that clinicians have low perceived levels of importance regarding acceptance in patients with chronic pain those clinicians may benefit from specific education, however, this requires further examination.

The IMPACT study focuses on chronic low back pain (CLBP) and depression symptoms, a prevalent and complex problem that represents a challenge for health professionals. Acceptance and Commitment Therapy (ACT) and Brief Behavioural Activation Treatment for Depression (BATD) are effective treatments for patients with persistent pain and depression, respectively. The objectives of this 12 month, multicentre, randomised, controlled trial (RCT) are (i) to examine the efficacy and cost-utility of adding a group-based form of ACT or BATD to treatment-as-usual (TAU) for patients with CLBP and moderate to severe levels of depressive symptoms; (ii) identify pre-post differences in levels of some physiological variables and (iii) analyse the role of polymorphisms in the gene, psychological process measures and physiological variables as mediators or moderators of long-term clinical changes.

Pain self-management is an effective, evidence-based treatment for chronic pain. Peer support, in which patients serve as coaches for other patients, has been effective in other chronic conditions and is a potentially promising approach to implementing pain self-management programs using fewer clinical resources.

Youth with chronic pain and their parents face uncertainty regarding their diagnosis, treatment, and prognosis. Given the uncertain nature of chronic pain, and high comorbidity of anxiety among youth, intolerance of uncertainty (IU) may be critical to the experience of pediatric chronic pain. This study longitudinally examined major tenets of the Interpersonal Fear Avoidance Model of Pain, and included parent and youth IU as key factors in the model. Participants included 152 youth with chronic pain (Mage=14.23 years; 72% female) and their parents (93% female). At baseline, parents and youth reported on their IU and catastrophic thinking about youth pain; youth reported on their fear of pain, pain intensity, and pain interference; and parents reported on their protective responses to child pain. Youth reported on their pain interference three months later. Cross-lagged panel models, controlling for baseline pain interference, showed that greater parent IU predicted greater parent pain catastrophizing which, in turn, predicted greater parent protectiveness, greater youth fear of pain, and subsequently greater youth 3-month pain interference. Youth IU had a significant indirect effect on 3-month pain interference via youth pain catastrophizing and fear of pain. The results suggest that parent and youth IU contribute to increases in youth pain interference over time via increased pain catastrophizing, parent protectiveness, and youth fear of pain. Thus, parent and youth IU play important roles as risk factors in the maintenance of pediatric chronic pain over time and may be important targets for intervention.

A growing body of research has demonstrated a robust link between parental chronic pain and child pain and psychological function. Although the association between parent and child pain is strong, there are limited data to understand environmental and behavioral processes that account for the association and how this develops over time. This longitudinal cohort study was designed to understand potential mechanisms that confer risk or resilience for chronic pain among child offspring of mothers with chronic pain.