The results indicate scores on catastrophizing before and after treatment that are clinically meaningful. These results may serve as preliminary guidelines to assess the clinical significance of interventions targeting pain catastrophizing in patients with subacute pain after musculoskeletal injury.

These results further support the validity of the IEQ and provide a guideline for its clinical interpretation in patients with persistent pain and disability following musculoskeletal injury. IEQ scores above the identified cut off may represent a barrier to work return and may warrant targeted intervention.

Emerging evidence suggests that perceived injustice is a risk factor for adverse outcomes associated with chronic pain. To date, however, the processes by which perceived injustice impacts on pain outcomes remain speculative. Evidence from several lines of research suggests that anger may mediate the relationship between injustice and pain outcomes. However, this relationship has not been empirically tested in patients with chronic pain. Thus, the purpose of this study was to examine whether anger mediates the relationships between perceived injustice and pain intensity, depressive symptoms, and self-reported disability. One hundred and seventy-three individuals with chronic musculoskeletal pain completed self-report measures of perceived injustice, anger, pain intensity, depressive symptoms, and disability. Consistent with previous research, high scores on a measure of perceived injustice were associated with greater pain, more severe depressive symptoms, and more pronounced disability. Hierarchical regression analyses indicated that anger variables completely mediated the relationship between perceived injustice and pain intensity, and partially mediated the relationship between perceived injustice and depressive symptoms. Anger did not mediate the relationship between perceived injustice and self-reported disability. The Discussion addresses the theoretical and clinical implications of the findings.

The present study examined the relationship between perceived injustice associated with whiplash injury and displays of pain behavior. Individuals (N=85) with whiplash injuries were filmed while performing a simulated occupational lifting task. They were also asked to complete measures of pain, perceived injustice, catastrophic thinking, depression, and functional disability. Consistent with previous research, high levels of perceived injustice were associated with more intense pain, higher levels of catastrophic thinking, depression, and disability. Analyses revealed that individuals with high levels of perceived injustice displayed more protective pain behaviors than individuals with low levels of perceived injustice, regardless of the level of physical demand of the task. The relation between perceived injustice and protective pain behavior remained significant even when controlling for pain severity, catastrophic thinking, and depression. There was no significant association between perceived injustice and displays of communicative pain behavior. The results of this study suggest that the relation between perceived injustice and pain behavior might underlie the high prevalence of occupational disability in individuals who have sustained whiplash injuries. Implications for intervention are addressed.

This is the first study to examine perceived injustice in a trauma sample. Results support the presence of injustice perception in this group and its associations with pain and quality of life outcomes. Additional research is suggested to explore the impact of perceived injustice on recovery outcomes among individuals who have sustained traumatic injury.

It is well known that chronic pain is prevalent, complex to manage, and associated with high costs, in health care and society in general. Thanks to advances in new forms of cognitive behavioral therapy (known as third-wave CBT), currently clinicians and researchers have an empirically validated psychological treatment with increasing research support for the treatment of chronic pain. This treatment is called acceptance and commitment therapy (ACT). The main aim of this paper is to provide a narrative review that summarizes and integrates the current state of knowledge of ACT in the management of chronic pain as well as discuss current challenges and opportunities for progress. Based on the psychological flexibility model, ACT extends previous forms of CBT and integrates many CBT-related variables into six core therapeutic processes. ACT is a process-based therapy that fosters openness, awareness, and engagement through a wide range of methods, including exposure-based and experiential methods, metaphors, and values clarification. To our knowledge, there are three published systematic reviews and meta-analyses that support the effectiveness of ACT for chronic pain and many studies focused on specific processes derived from the psychological flexibility model. There is also promising support for the cost-effectiveness of ACT; however, the current evidence is still insufficient to establish firm conclusions about cost-effectiveness and the most efficient means of delivery. Additional well-designed economic evaluations are needed. Other research aims include delineating the neurobiological underpinnings of ACT, refining available outcome and process measures or develop new ones for ACT trials, and meeting the challenge of wide dissemination and implementation in real-world clinical practice.

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Summary Background Recessive forms of congenital ichthyosis encompass a group of rare inherited disorders of keratinization leading to dry, scaly skin. So far, 13 genes have been implicated, but there is a paucity of data on genotype–phenotype correlation in some populations. Objectives We compiled an English cohort of 146 individuals with recessive ichthyosis and assessed genotype–phenotype correlation. Methods Deep phenotyping was undertaken by history‐taking and clinical examination. DNA was screened for mutations using a next‐generation sequencing ichthyosis gene panel and Sanger sequencing. Results Cases were recruited from 13 National Health Service sites in England, with 65% of patients aged < 16 years at enrolment. Pathogenic biallelic mutations were found in 83% of cases, with the candidate gene spread as follows: TGM1 29%, NIPAL4 12%, ABCA12 12%, ALOX12B 9%, ALOXE3 7%, SLC27A4 5%, CERS3 3%, CYP4F22 3%, PNPLA1 2%, SDR9C7 1%. Clinically, a new sign, an anteriorly overfolded ear at birth, was noted in 43% of patients with ALOX12B mutations. The need for intensive care stay (P = 0·004), and hand deformities (P < 0·001), were associated with ABCA12 mutations. Self‐improving collodion ichthyosis occurred in 8% of the cases (mostly TGM1 and ALOX12B mutations) but could not be predicted precisely from neonatal phenotype or genotype. Conclusions These data refine genotype–phenotype correlation for recessive forms of ichthyosis in England, demonstrating the spectrum of disease features and comorbidities, as well as the gene pathologies therein. Collectively, the data from these patients provide a valuable resource for further clinical assessment, improving clinical care and the possibility of future stratified management. What's already known about this topic? Recessive forms of ichthyosis are rare but often difficult to diagnose. Mutations in 13 genes are known to cause recessive forms of ichthyosis: ABCA12, ALOX12B, ALOXE3, CERS3, CYP4F22, LIPN, NIPAL4, PNPLA1, SDR9C7, SLC27A4, SULT2B1, ST14 and TGM1. Some phenotypic features may associate with certain gene mutations, but paradigms for genotype–phenotype correlation need refining. What does this study add? The genotypic spectrum of recessive ichthyosis in England (based on 146 cases) comprises TGM1 (29%), NIPAL4 (12%), ABCA12 (12%), ALOX12B (9%), ALOXE3 (7%), SLC27A4 (5%), CERS3 (3%), CYP4F22 (3%), PNPLA1 (2%) and SDR9C7 (1%). New or particular phenotypic clues were defined for mutations in ALOX12B, ABCA12, CYP4F22, NIPAL4, SDR9C7 and TGM1, either in neonates or in later life, which allow for greater diagnostic precision. In around 17% of cases, the molecular basis of recessive ichthyosis remains unknown.