Resiliencia ante el dolor: algunas cuestiones sobre favorecer la adaptación dinámica al dolor crónico

In recent years, there has been increasing interest in processes and characteristics that may underlie resilient adaptation to chronic pain. With this recent increase in empirical inquiry, there has emerged a degree of ambiguity in terms between pain resilience and other constructs previously connected to effective pain adaptation, such as pain acceptance, psychological flexibility, and pain self-efficacy. Objectives of the current paper included reviewing recent clinical and empirical evidence in the area of chronic pain resilience and offering a synthesis of these findings, with a specific focus on issues of defining and operationalizing this construct, compared to other constructs relevant to pain adaptation. We conclude that resilience is best defined as a dynamic process related to both stable individual characteristics and contextual and state factors, such as goal contexts and affective states. Finally, the implications of this model are discussed in the context of the extant literature on psychological interventions for chronic pain.En los últimos años ha habido un creciente interés por los procesos y las características que subyacen a la adaptación resiliente al dolor crónico. El amplio número de investigaciones empíricas al respecto, ha puesto de manifiesto la ambigüedad en la definición de conceptos relacionados con la adaptación al dolor como la aceptación del dolor, la flexibilidad psicológica y la auto-eficacia relacionada con el dolor. El objetivo del presente trabajo es revisar la reciente evidencia empírica y clínica, en el área de la resiliencia frente al dolor crónico, ofreciendo una síntesis de los hallazgos, centrando el interés en definir y operacionalizar este constructo, comparado con otros constructos relevantes en la adaptación al dolor. Se concluye que la resiliencia es un proceso dinámico relacionado con características estables individuales y factores situacionales, como las metas o los estados afectivos. Por último, se discuten las implicaciones de este modelo en el contexto de la extensa literatura sobre la intervención psicológica en pacientes con dolor crónico

Pain resilience: issues of modeling dynamic adaptation in chronic pain

In recent years, there has been increasing interest in processes and characteristics that may underlie resilient adaptation to chronic pain. With this recent increase in empirical inquiry, there has emerged a degree of ambiguity in terms between pain resilience and other constructs previously connected to effective pain adaptation, such as pain acceptance, psychological flexibility, and pain self-efficacy. Objectives of the current paper included reviewing recent clinical and empirical evidence in the area of chronic pain resilience and offering a synthesis of these findings, with a specific focus on issues of defining and operationalizing this construct, compared to other constructs relevant to pain adaptation. We conclude that resilience is best defined as a dynamic process related to both stable individual characteristics and contextual and state factors, such as goal contexts and affective states. Finally, the implications of this model are discussed in the context of the extant literature on psychological interventions for chronic pain.En los últimos años ha habido un creciente interés por los procesos y las características que subyacen a la adaptación resiliente al dolor crónico. El amplio número de investigaciones empíricas al respecto, ha puesto de manifiesto la ambigüedad en la definición de conceptos relacionados con la adaptación al dolor como la aceptación del dolor, la flexibilidad psicológica y la auto-eficacia relacionada con el dolor. El objetivo del presente trabajo es revisar la reciente evidencia empírica y clínica, en el área de la resiliencia frente al dolor crónico, ofreciendo una síntesis de los hallazgos, centrando el interés en definir y operacionalizar este constructo, comparado con otros constructos relevantes en la adaptación al dolor. Se concluye que la resiliencia es un proceso dinámico relacionado con características estables individuales y factores situacionales, como las metas o los estados afectivos. Por último, se discuten las implicaciones de este modelo en el contexto de la extensa literatura sobre la intervención psicológica en pacientes con dolor crónico

Sertoli Cell-Specific Deletion of the Androgen Receptor Compromises Testicular Immune Privilege in Mice1

In the mammalian testis, meiotic and postmeiotic germ cell antigens are granted immune privilege. Both local immune suppression and specialized intercellular junctions between somatic Sertoli cells have been proposed to contribute to a highly restricted and effective blood-testis barrier (BTB) that helps maintain tolerance to germ cell antigens. Several studies have suggested that androgens play a role in immune suppression, although direct evidence for this is lacking. We previously reported that Sertoli cell-specific ablation of the androgen receptor (Ar) decreases expression of Cldn3, an androgen-regulated gene and component of Sertoli cell tight junctions, and increases the permeability of the BTB to biotin, a small-molecular-weight tracer. The physiological consequences of Sertoli cell-specific Ar (S-Ar) ablation on immune privilege are unknown. Here we show that in the testes of S-Ar mutant mice, the ultrastructure of Sertoli cell tight junctions is defective and testicular IgG levels are elevated. The interstitium of S-Ar mutant testes becomes populated with macrophages, neutrophils, plasma cells, and eosinophils, and serum samples of mutant mice contain antibodies against germ cell antigens. Together, these results suggest that Sertoli cell-specific deletion of the androgen receptor results in loss of testicular immune privilege. Suppressed levels of androgen signaling may be a contributing factor in idiopathic male infertility

Sertoli cell-specific deletion of the androgen receptor compromises testicular immune privilege in mice.

In the mammalian testis, meiotic and postmeiotic germ cell antigens are granted immune privilege. Both local immune suppression and specialized intercellular junctions between somatic Sertoli cells have been proposed to contribute to a highly restricted and effective blood-testis barrier (BTB) that helps maintain tolerance to germ cell antigens. Several studies have suggested that androgens play a role in immune suppression, although direct evidence for this is lacking. We previously reported that Sertoli cell-specific ablation of the androgen receptor (Ar) decreases expression of Cldn3, an androgen-regulated gene and component of Sertoli cell tight junctions, and increases the permeability of the BTB to biotin, a small-molecular-weight tracer. The physiological consequences of Sertoli cell-specific Ar (S-Ar) ablation on immune privilege are unknown. Here we show that in the testes of S-Ar mutant mice, the ultrastructure of Sertoli cell tight junctions is defective and testicular IgG levels are elevated. The interstitium of S-Ar mutant testes becomes populated with macrophages, neutrophils, plasma cells, and eosinophils, and serum samples of mutant mice contain antibodies against germ cell antigens. Together, these results suggest that Sertoli cell-specific deletion of the androgen receptor results in loss of testicular immune privilege. Suppressed levels of androgen signaling may be a contributing factor in idiopathic male infertility

Greater Post-Surgical Pain Predicts Long-Term Depressed Affect in Breast Cancer Patients The Role of Coping

Background: Depressed affect is observed during primary treatment for early-stage breast cancer and often persists into survivorship. Pain can influence the long-term emotions of women with breast cancer. Behavioral mechanisms explaining this relationship are less clear. Coping during primary treatment may play a role in the association between pain and depressed affect. Aims: Our observational study examined a longitudinal mediation model testing whether post-surgical pain intensity predicted depressed affect 5 years later via disengagement and/or engagement coping at the end of treatment. Method: Women ( N = 240) with stage 0–III breast cancer completed measures of pain, coping, and depressed affect 4–10 weeks post-surgery, and 12 months and 5 years later. Results: Structural modeling yielded measurement models of 12-month disengagement and engagement coping. Direct effects emerged between post-surgical pain intensity and 12-month disengagement (β = .37, p < .001) and engagement coping (β = .16, p < .05). Post-surgical pain intensity was also related to 5-year depressed affect (β = .25, p < .05). Disengagement and engagement coping were not associated with depressed affect at 5-year follow-up, and there was no evidence of mediation. Limitations: This is a secondary analysis of data from a trial conducted several years ago, and may not generalize due to a homogenous sample with attrition at long-term follow-up. Conclusions: Greater post-surgical pain intensity predicts more disengagement and engagement coping at the end of primary treatment, as well as depressed affect during survivorship. Managing post-surgical pain may influence the emotions of survivors of breast cancer up to 5 years later, possibly through coping or non-coping processes

Effects of brief stress management interventions on distress and leukocyte nuclear factor kappa B expression during primary treatment for breast cancer: A randomized trial

A randomized controlled trial (RCT) of 5-week stress management interventions teaching cognitive behavioral therapy (CBT) or relaxation training (RT) techniques showed decreases in stress and serum inflammatory markers over 12 months in women undergoing treatment for breast cancer (BCa). To understand the molecular mechanisms involved, we examined the effects of these interventions on the transcription factor NF-κB DNA binding activity in leukocytes in parallel with circulating inflammatory markers, stress management skill efficacy and multiple distress indicators. This is a secondary analysis using blood samples of 51 BCa patients (Stage 0–III) with high cancer-specific distress selected from a completed RCT (NCT02103387). Women were randomized to one of three conditions, CBT, RT or health education control (HE). Blood samples and self-reported distress measures (Affects Balance Scale-Negative Affect [ABS-NA], Impact of Events Scale-hyperarousal [IES-H] and intrusive thoughts [IES-I]) were collected at baseline (T0) and 12-month follow-up (T2). Self-reported distress measures and perceived stress management skills (PSMS) were also measured immediately post-intervention (baseline + 2 months: T1). Repeated measures analyses compared changes in distress and NF-κB expression among conditions, controlling for age, stage of cancer, days from surgery to baseline, and receipt of chemotherapy and radiation. Regression analyses related T0 to T2 change in NF-κB expression with T0 to T1 changes in self-reported PSMS and distress measures. Exploratory regression analyses also associated change in NF-κB expression with change in serum cytokines (IL-1β, IL-6 and TNF-α); and s100A8/A9, a circulating inflammatory marker important in breast cancer progression. There was a significant condition (CBT/RT, HE)xtime (T0, T2) effect on NF-κB, F(1, 39)= 5.267, p = 0.036, wherein NF-κB expression significantly increased over time for HE but did not change for RT or CBT. Greater increases in PSMS from T0 to T1 were associated with less increase in NF-κB expression over 12 months (β = −0.426, t(36) = −2.637, p = 0.048). We found that women assigned to active intervention (CBT/RT) had significant decreases in ABS-NA (F(1, 40)= 6.537, p = 0.028) and IES-I (F(1, 40)= 4.391, p = 0.043) from T0 to T1 compared to women assigned to HE, who showed no change over time (p’s > 0.10). For women assigned to CBT or RT, lower NF-κB expression at T2 was related to less ABS-NA, IES-H, and IES-I, all p’s < 0.05, although T0–T1 change in distress was not related to T0–T2 change in NF-κB expression for those in an active intervention. Brief CBT or RT stress management interventions can mitigate increases in pro-inflammatory leukocyte NF-κB binding over 12 months of primary treatment in highly distressed BCa patients. These effects are likely brought about by improved stress management skills. •Stress management mitigates leukocyte NF-kB signaling increases during BCa treatment.•Patients maintaining lower distress at 12 month follow-up show less NF-kB DNA binding.•Greater increase in perceived stress management skills predicts less NF-κB signaling.•CBT and relaxation affect molecular mediators of inflammation by reducing distress.•Reducing inflammation during BCa treatment may have long-term health effects

Effects of a Pain Catastrophizing Induction on Sensory Testing in Women with Chronic Low Back Pain: A Pilot Study

Pain catastrophizing, a pattern of negative cognitive-emotional responses to actual or anticipated pain, maintains chronic pain and undermines response to treatments. Currently, precisely how pain catastrophizing influences pain processing is not well understood. In experimental settings, pain catastrophizing has been associated with amplified pain processing. This study sought to clarify pain processing mechanisms via experimental induction of pain catastrophizing. Forty women with chronic low back pain were assigned in blocks to an experimental condition, either a psychologist-led 10-minute pain catastrophizing induction or a control (10-minute rest period). All participants underwent a baseline round of several quantitative sensory testing (QST) tasks, followed by the pain catastrophizing induction or the rest period, and then a second round of the same QST tasks. The catastrophizing induction appeared to increase state pain catastrophizing levels. Changes in QST pain were detected for two of the QST tasks administered, weighted pin pain and mechanical allodynia. Although there is a need to replicate our preliminary results with a larger sample, study findings suggest a potential relationship between induced pain catastrophizing and central sensitization of pain. Clarification of the mechanisms through which catastrophizing affects pain modulatory systems may yield useful clinical insights into the treatment of chronic pain

Does the Broaden-and-Build Theory Explain Reduction in Social Disruption After a Brief Relaxation Intervention for Women With Breast Cancer Undergoing Treatment?

•A 5-week relaxation protocol resulted in greater reductions to social disruption.•Positive affect increased over time but this was not driven by group condition.•Increased positive affect correlated with decreased social disruption.•Change in positive affect did not drive change in social disruption. Women with breast cancer experience social disruption during and after treatment. Brief cognitive-behavioral (CBT) and relaxation (RT) interventions may improve social disruption by increasing positive affect. Using the Broaden-and-Build Theory as a framework, this study examined whether short-term CBT- and RT-related increases in positive affect mediate long-term reductions in social disruption in women with breast cancer undergoing treatment (N = 183). This secondary analysis used latent change score and growth models to test 6- and 12-month intervention effects on positive affect and social disruption, respectively; a parallel-process model assessed mediation. RT demonstrated larger reductions in social disruption across 12 months compared to CBT and a health education control. Six-month latent change in positive affect was significant but not driven by condition. There was a significant direct effect linking the latent slopes of positive affect and social disruption but meditation was not observed. These preliminary findings hint at the value of promoting positive affect and inform the development of brief behavioral interventions that aim to augment social functioning among women surviving breast cancer