L. Buenaver

Discordance between pain and radiographic severity in knee osteoarthritis: Findings from quantitative sensory testing of central sensitization

OBJECTIVE Radiographic measures of the pathologic changes of knee osteoarthritis (OA) have shown modest associations with clinical pain. We sought to evaluate possible differences in quantitative sensory testing (QST) results and psychosocial distress profiles between knee OA patients with discordant versus congruent clinical pain reports relative to radiographic severity measures. METHODS A total of 113 participants (66.7% women; mean ± SD age 61.05 ± 8.93 years) with knee OA participated in the study. Radiographic evidence of joint pathology was graded according to the Kellgren/Lawrence scale. Central sensitization was indexed through quantitative sensory testing, including heat and pressure-pain thresholds, tonic suprathreshold pain (cold pressor test), and repeated phasic suprathreshold mechanical and thermal pain. Subgroups were constructed by dichotomizing clinical knee pain scores (median split) and knee OA grade scores (grades 1-2 versus 3-4), resulting in 4 groups: low pain/low knee OA grade (n = 24), high pain/high knee OA grade (n = 32), low pain/high knee OA grade (n = 27), and high pain/low knee OA grade (n = 30). RESULTS Multivariate analyses revealed significantly heightened pain sensitivity in the high pain/low knee OA grade group, while the low pain/high knee OA grade group was less pain-sensitive. Group differences remained significant after adjusting for differences on psychosocial measures, as well as age, sex, and race. CONCLUSION The results suggest that central sensitization in knee OA is especially apparent among patients with reports of high levels of clinical pain in the absence of moderate-to-severe radiographic evidence of pathologic changes of knee OA.

Pain-related Catastrophizing and Perceived Social Responses: Inter-relationships in the Context of Chronic Pain

Abstract Pain‐related coping, particularly catastrophizing, plays a significant role in shaping pain responses. One way catastrophizing is hypothesized to amplify pain and disability is via its effect on patients’ social environments (e.g., communal coping model), though empirical support is limited. The present study tested whether the association between catastrophizing and deleterious pain‐related outcomes was mediated by patients’ perceptions of significant others’ responses to their pain in a sample of 1356 pain patients. Regression analyses showed that perceived significant other punishing responses partially mediated catastrophizings relationship with pain‐related disability, and with depressive symptoms. Further, several variables moderated the association between catastrophizing and perceived social responses to pain. Catastrophizing was more strongly associated with greater perceived solicitous responses for patients of relatively short pain duration. Also, higher catastrophizing was more strongly associated with perceived punishing responses among patients perceiving lower social support. In addition, the mediational effects of perceived punishing responses on catastrophizings relationship with depressive symptoms, and with pain‐related disability were only found in individuals reporting low levels of perceived social support. In sum, perceived social responses were found to play a small role in mediating the relationship between catastrophizing and pain‐related outcomes, and these mediational effects may be strongest in particular patient subgroups. The present data suggest that interpersonal mechanisms may not constitute a primary route by which catastrophizing exerts its maladaptive effects on pain responses. The study and further understanding of what principal factors mediate catastrophizings deleterious effects on pain will be important in illuminating the biopsychosocial model of pain.

Symptoms of distress as prospective predictors of pain-related sciatica treatment outcomes

Abstract Prior studies evaluating predictors of pain‐related outcomes following treatment for sciatica have been limited by methodological problems, including retrospective study design, use of unvalidated outcome measures, and short‐term follow‐up periods. Despite these limitations, some reports have suggested that symptoms of psychological distress may predict individual differences in pain treatment‐related outcomes (e.g., higher levels of depressive and anxious symptomatology are associated with greater pain and disability after treatment). In this study, we sought to determine whether acute symptoms of depression and anxiety were prospectively associated with treatment outcomes over a 3‐year follow‐up period in surgically treated and non‐surgically treated patients with sciatica. Patients were recruited from the practices of community‐based physicians throughout the state of Maine, and underwent in‐person baseline assessments, with mailed follow‐up questionnaires at 3, 6, 12, 24, and 36 months. Study outcomes included patient‐reported symptoms of pain and disability. For each outcome variable, we examined whether baseline mood (i.e., mood assessed prior to the initiation of treatment), as well as mood at the immediately preceding assessment point, prospectively predicted outcomes over 3 years in multivariate repeated‐measures analyses. In most analyses, symptoms of depression and anxiety, both at baseline and at the preceding time point, were significant independent predictors of worse pain and function after controlling for relevant covariates. Collectively, elevated distress appears to be a significant risk factor for reduced treatment benefit (i.e., less improvement in pain and disability) over short and medium‐term follow‐up periods in patients with sciatica. Future research should determine whether the prospective identification and treatment of patients with high levels of distress (a “yellow flag”) is associated with improved treatment outcomes.

Catastrophizing and pain-coping in young adults: associations with depressive symptoms and headache pain.

UNLABELLED Cognitive and behavioral pain-coping strategies, particularly catastrophizing, are important determinants of the pain experience. Most studies of pain-coping are performed in samples of treatment-seeking patients with longstanding pain complaints. Individual differences in pain-coping styles may also significantly affect day-to-day pain and quality of life in nonclinical samples, though this has rarely been investigated. In particular, headache pain is common in the general population, and little is known about how pain-related coping affects pain and quality of life among headache sufferers from a nonclinical setting. In this study, 202 generally healthy subjects were divided into 2 groups, those who reported problem headaches and pain-free control subjects. Reports of pain-related catastrophizing and the use of active pain-coping strategies did not differ between the groups, but differential associations between pain-coping strategies and emotional functioning were observed. Specifically, within the headache group only, those reporting higher levels of pain catastrophizing and lower levels of active pain-coping showed the highest level of depressive symptoms. Further, higher catastrophizing was associated with greater headache pain and pain-related interference. These findings suggest that catastrophizing has little influence on emotional functioning in those without ongoing pain complaints and highlight the importance of coping in modulating the consequences of pain on day-to-day functioning, even in samples from nonclinical settings. Moreover, these findings indirectly suggest that interventions that increase adaptive coping and decrease catastrophizing may help to buffer some of the deleterious functional consequences of headache pain. PERSPECTIVE This study adds to a growing literature that conceptualizes catastrophizing as a diathesis, or risk factor, for deleterious pain-related consequences. These data suggest that catastrophizing may require the presence of a pain condition before its detrimental effects are exerted.

The SBSM Guide to Actigraphy Monitoring: Clinical and Research Applications

The SBSM Guide to Actigraphy Monitoring: Clinical and Research Applications Sonia Ancoli-Israel, Jennifer L. Martin, Terri Blackwell, Luis Buenaver, Lianqi Liu, Lisa J. Meltzer, Avi Sadeh, Adam P. Spira & Daniel J. Taylor a Departments of Psychiatry and Medicine, University of California, San Diego b David Geffen School of Medicine at the University of California, Los Angeles c VA Greater Los Angeles Healthcare System, Geriatric Research, Education and Clinical Center d Research Institute, California Pacific Medical Center, San Francisco e Department of Psychiatry and Behavioral Sciences, Johns Hopkins University School of Medicine f Department of Psychiatry, University of California, San Diego g Department of Pediatrics, National Jewish Health, Denver h School of Psychological Sciences, Tel Aviv University, Israel i Department of Mental Health, Johns Hopkins Bloomberg School of Public Health j Department of Psychiatry and Behavioral Sciences, Johns Hopkins School of Medicine k Department of Psychology, University of North Texas Published online: 14 Aug 2015.

Evidence for indirect effects of pain catastrophizing on clinical pain among myofascial temporomandibular disorder participants: the mediating role of sleep disturbance.

Summary Pain catastrophizing was associated with greater sleep disturbance, and both pain catastrophizing and pain‐related rumination indirectly affected clinical pain and pain‐related interference through alterations in sleep. ABSTRACT Sleep disturbance and pain catastrophizing are important mediators of the chronic pain experience. To date, these factors have not been considered concurrently despite compelling theoretical rationale to do so. In the present study, we examined whether pain catastrophizing not only has direct effects on clinical pain and pain‐related interference, but also indirect effects through its association with sleep disturbance. We evaluated this hypothesis using a cohort (n = 214) of myofascial temporomandibular disorder participants using a statistical bootstrapping technique recommended for tests of indirect effects. Results suggested that pain catastrophizing was associated with greater sleep disturbance, and that a significant portion of variance in clinical pain severity and pain‐related interference attributable to pain catastrophizing was mediated by sleep disturbance. Supplementary analyses revealed that the rumination component of catastrophizing seemed to be indirectly related to clinical outcomes through sleep disturbance. No evidence for indirect effects was observed for helplessness and magnification components. These results suggest that rumination about pain may contribute to clinical pain indirectly through alterations in sleep. Prospective studies are needed to examine lagged associations between these constructs. These findings have important theoretical and clinical implications. Critically, interventions that reduce pain catastrophizing may concurrently improve sleep and clinical pain.

Pain Catastrophizing and Salivary Cortisol Responses to Laboratory Pain Testing in Temporomandibular Disorder and Healthy Participants

UNLABELLED Pain catastrophizing is an important variable in the context of acute and chronic pain. The neurophysiological correlates of pain catastrophizing, however, have not been rigorously evaluated. We examined the relationship between trait-pain catastrophizing and morning salivary cortisol levels before and following a 45-minute laboratory pain-testing session in healthy, pain-free (n = 22), and temporomandibular disorder (TMD) participants (n = 39). We also examined whether TMD patients evidenced generalized hyperalgesia and hypercortisolism. Pain catastrophizing was associated with a flattened morning salivary cortisol profile in the context of pain testing, irrespective of pain status. Cortisol profiles did not differ between healthy and TMD participants. TMD was associated with mechanical hyperalgesia only at the masseter. These data are the first to show an association between pain catastrophizing and elevated salivary cortisol profiles in the context of standardized experimental pain testing. These findings in both healthy individuals and those with chronic orofacial pain suggest that aberrant adrenocortical responses to pain may serve as a neurophysiologic pathway by which pain catastrophizing enhances vulnerability for development of chronic pain and maintains and/or exaggerates existing pain and associated morbidity. PERSPECTIVE Neurophysiological mechanisms by which pain catastrophizing is related to acute and chronic pain recently have come under empirical study. Understanding of these mechanisms has the unique potential to shed light on key central-nervous-system factors that mediate catastrophizing-pain relations and therapeutic benefits associated with changes in catastrophizing and related cognitive processes.

Cognitive-behavioral therapy for insomnia in knee osteoarthritis: a randomized, double-blind, active placebo-controlled clinical trial.

Insomnia is prevalent among patients with knee osteoarthritis (OA). Research indicates that sleep disruption may amplify clinical pain by altering central pain modulation, suggesting that treatment of insomnia may improve pain. The aims of this study were to evaluate the efficacy of cognitive–behavioral therapy for insomnia (CBT‐I) in patients with knee OA, to determine whether improvements in sleep predict reduced pain, and to determine whether alterations in pain modulation mediate improvements in clinical pain.

Sleep, Pain Catastrophizing, and Central Sensitization in Knee Osteoarthritis Patients with and Without Insomnia

Osteoarthritis (OA), a chronic degenerative joint disorder, is characterized by joint pain. Emerging research demonstrates that a significant number of patients evidence central sensitization (CS), a hyperexcitability in nociceptive pathways, which is known to amplify and maintain clinical pain. The clinical correlates of CS in OA, however, are poorly understood. Insomnia is prevalent in older adults with OA, and recent experiments suggest associations between poor sleep and measures of CS. Catastrophizing, a potent predictor of pain outcomes, has also been associated with CS, but few studies have investigated possible interactions between catastrophizing, sleep, and CS.

Increased sensitivity to physical activity among individuals with knee osteoarthritis: Relation to pain outcomes, psychological factors, and responses to quantitative sensory testing

Summary Sensitivity to physical activity was related to measures of central sensitization and pain catastrophizing and cross‐sectionally predicted worse pain, function, and physical performance. ABSTRACT Recent findings suggest that certain individuals with musculoskeletal pain conditions have increased sensitivity to physical activity (SPA) and respond to activities of stable intensity with increasingly severe pain. This study aimed to determine the degree to which individuals with knee osteoarthritis (OA) show heightened SPA in response to a standardized walking task and whether SPA cross‐sectionally predicts psychological factors, responses to quantitative sensory testing (QST), and different OA‐related outcomes. One hundred seven adults with chronic knee OA completed self‐report measures of pain, function, and psychological factors, underwent QST, and performed a 6‐min walk test. Participants rated their discomfort levels throughout the walking task; an index of SPA was created by subtracting first ratings from peak ratings. Repeated‐measure analysis of variance revealed that levels of discomfort significantly increased throughout the walking task. A series of hierarchical regression analyses determined that after controlling for significant covariates, psychological factors, and measures of mechanical pain sensitivity, individual variance in SPA predicted self‐report pain and function and performance on the walking task. Analyses also revealed that both pain catastrophizing and the temporal summation of mechanical pain were significant predictors of SPA and that SPA mediated the relationship between catastrophizing and self‐reported pain and physical function. The discussion addresses the potential processes contributing to SPA and the role it may play in predicting responses to different interventions for musculoskeletal pain conditions.