National Addiction Workshop: A Virtual Adaptation to Support Competency Development in Opioid Use Disorder Management.

BACKGROUND: Accessible, manualized, skill-based training ready for wide dissemination is needed to prepare healthcare staff to meet the needs of people impacted by the opioid epidemic. METHODS: A 2-day workshop and simulation training was designed by an interprofessional substance use disorder (SUD) specialty care team, adapted to a virtual platform, manualized, and offered to healthcare staff and trainees from a large healthcare system. The workshop was offered 6 times over the course of 10 months with a total of 177 participants from across the United States enrolled in the training. Interactive experiential learning strategies including games designed to test knowledge, small-group case discussions, video demonstrations of skills, patient panels, and 3 simulations of a patient with chronic pain who developed opioid use disorder in the context of long-term opioid therapy were utilized in efforts to build skills and confidence managing SUDs in primary care and general mental health settings. RESULTS: Of those who completed the post-workshop survey, most found both content and training structure useful, particularly content related to medication management, stigma, and collaborative care. In addition, overall confidence scores in assessing, diagnosing, and treating SUD increased. Skill building exercises, such as interprofessional team simulations, were highlighted as most beneficial. The workshop received national attention leading to a partnership with the healthcare system's simulation center for wider dissemination. CONCLUSION: Expanding access to SUD treatment requires training healthcare staff to effectively change attitudes, increase knowledge, and improve key skills. This 2-day interprofessional workshop was well-received by participants who reported high acceptability and satisfaction scores and demonstrated improved confidence in the management of SUDs. This type of manualized, collaborative, skill-based learning experience can foster staff preparedness and willingness to conceptualize SUD as a chronic condition amenable to treatment in different healthcare settings.

Poor sleep quality and exaggerated salivary cortisol reactivity to the cold pressor task predict greater acute pain severity in a non-clinical sample.

Poor sleep is often independently associated with greater pain sensitivity and dysregulation of the hypothalamic-pituitary-adrenal (HPA) axis (e.g., greater basal cortisol and exaggerated stress-induced cortisol reactivity). However, the interactions among sleep, pain, and the HPA axis have not been adequately evaluated. In this study, 40 healthy adults provided self-report regarding perceived sleep quality over the past month prior to completion of an acute noxious physical stressor (i.e., cold pressor task; CPT). Following the CPT, they reported on the severity of pain experienced. Salivary cortisol was sampled before, immediately following, and during recovery from CPT. Using bootstrapped confidence intervals with a bias correction, results showed that poor sleep quality was significantly associated with greater reports of CPT-induced pain severity and greater cortisol reactivity (i.e., increase from baseline). Furthermore, greater cortisol reactivity to the CPT was found to significantly mediate the relationship between poor sleep and pain severity.

Experimental pain ratings and reactivity of cortisol and soluble tumor necrosis factor-α receptor II following a trial of hypnosis: results of a randomized controlled pilot study.

OBJECTIVE: Current evidence supports the efficacy of hypnosis for reducing the pain associated with experimental stimulation and various acute and chronic conditions; however, the mechanisms explaining how hypnosis exerts its effects remain less clear. The hypothalamic-pituitary-adrenal (HPA) axis and pro-inflammatory cytokines represent potential targets for investigation given their purported roles in the perpetuation of painful conditions; yet, no clinical trials have thus far examined the influence of hypnosis on these mechanisms. DESIGN: Healthy participants, highly susceptible to the effects of hypnosis, were randomized to either a hypnosis intervention or a no-intervention control. Using a cold pressor task, assessments of pain intensity and pain unpleasantness were collected prior to the intervention (Pre) and following the intervention (Post) along with pain-provoked changes in salivary cortisol and the soluble tumor necrosis factor-α receptor II (sTNFαRII). RESULTS: Compared with the no-intervention control, data analyses revealed that hypnosis significantly reduced pain intensity and pain unpleasantness. Hypnosis was not significantly associated with suppression of cortisol or sTNFαRII reactivity to acute pain from Pre to Post; however, the effect sizes for these associations were medium-sized. CONCLUSIONS: Overall, the findings from this randomized controlled pilot study support the importance of a future large-scale study on the effects of hypnosis for modulating pain-related changes of the HPA axis and pro-inflammatory cytokines.

Salivary cortisol and soluble tumor necrosis factor-α receptor II responses to multiple experimental modalities of acute pain.

The present study compared cortisol and soluble tumor necrosis factor-α receptor II (sTNFαRII) responses provoked by cold pressor, hot water, ischemic, and neutral water (i.e., room temperature) modalities. Oral fluid samples were collected before, immediately after, and during recovery to assess physiological responses. From baseline, the cold pressor, but not hot water or ischemic modalities, produced a significant time-dependent elevation in cortisol, whereas cortisol significantly decreased for the neutral water task. When compared to baseline, the cold pressor, hot water, and ischemic modalities were associated with decreased sTNFαRII responses over time. The sTNFαRII response to neutral water initially decreased but returned to approximate baseline levels. Pain ratings were positively associated with cortisol increase from baseline and the overall cortisol response was negatively associated with the overall sTNFαRII response.

Enhanced cortisol increase upon awakening is associated with greater pain ratings but not salivary cortisol or soluble tumor necrosis factor-α receptor II responses to acute pain.

OBJECTIVES: The cortisol awakening response (CAR) is related to psychosocial factors and health in potentially significant ways, suggesting that it may be a distinctive marker of hypothalamic-pituitary-adrenal axis function and dysfunction. This study sought to expand upon previous work that examined the association between CAR and ratings of laboratory-evoked acute pain stimulation. In addition to evoked pain ratings, this study also tested whether CAR was prospectively related with salivary cortisol and soluble tumor necrosis factor-α receptor II responses to acute pain stimulation. METHODS: This study included 36 healthy, pain-free volunteers of both sexes recruited through posted study flyers. Prior to completion of laboratory pain testing, salivary cortisol samples were obtained at home over the course of a single morning according to the following time frame: upon awakening, and 15, 30, and 60 minute after awakening. After collection of saliva, study participants brought their home saliva samples to the laboratory for assay and subsequently completed acute experimental pain testing procedures. RESULTS: Cluster analysis of CAR revealed two distinct groups with similar patterns of cortisol response to awakening; increased and flattened. Relative to flattened CAR, increased CAR was associated with greater ratings of pain intensity and unpleasantness. Salivary cortisol was significantly increased and soluble tumor necrosis factor-α receptor II significantly decreased after pain testing, but neither of these responses differed as a function of increased versus flattened CAR. DISCUSSION: CAR may be a marker for stress sensitivity and/or the anticipation of impending stress, which could explain why the increased CAR cohort reported greater acute pain ratings.

Pain catastrophizing mediates the relationship between self-reported strenuous exercise involvement and pain ratings: moderating role of anxiety sensitivity.

OBJECTIVE: To investigate the cross-sectional associations among self-reported weekly strenuous exercise bouts, anxiety sensitivity, and their interaction with pain catastrophizing and pain responses to the cold pressor task (CPT) in healthy, ethnically diverse young adults (n = 79). Exercise involvement has been shown to have hypoalgesic effects and cognitive factors may partially explain this effect. Particularly, alterations in pain catastrophizing have been found to mediate the positive pain outcomes of multidisciplinary treatments incorporating exercise. Further, recent evidence suggests that exercise involvement and anxiety sensitivity may act together, as interacting factors, to exert an effect on catastrophizing and pain outcomes; however, further research is needed to clarify the nature of this interaction. METHODS: Before the CPT, participants were asked to complete the Godin Leisure-Time Exercise Questionnaire, the Beck Depression Inventory, and the Anxiety Sensitivity Index. After the CPT, participants completed a modified version of the Pain Catastrophizing Scale and the Short Form-McGill Pain Questionnaire. RESULTS: At a high level of anxiety sensitivity, controlling for depressive symptoms, CPT immersion time, and sex differences, a bias-corrected (BC), bootstrapped confidence interval revealed that pain catastrophizing significantly mediated the relationship between self-reported weekly strenuous exercise bouts and pain response (95% BC Confidence Interval = -9.558, -0.800 with 1000 resamples). At intermediate and low levels of anxiety sensitivity, no significant mediation effects were found. CONCLUSIONS: These findings support that, for pain catastrophizing to mediate the strenuous exercise-pain response relation, individuals must possess a high level of anxiety sensitivity.