The journal of pain : official journal of the American Pain Society
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Patients with chronic pain often present with hyperalgesia, possibly due to hyperexcitability of nociceptive pathways. The aim of the present study was to investigate alterations in flexor withdrawal reflex (FWR) excitability in individuals with knee osteoarthritis (OA) and the potential effect of specific physical inputs or therapeutic interventions (ie, joint compression and mobilization) on these behaviors. Ten subjects with and 10 without knee OA (age 45-75) were recruited. The FWR was examined utilizing suprathreshold, noxious electrocutaneous stimuli applied at the medial foot. Surface electromyographic (EMG) was recorded from the tibialis anterior (TA) and biceps femoris (BF), and peak joint torques recorded at the hip, knee, and ankle. FWR threshold was ascertained and responses at 2x threshold recorded after the following conditions: a maximal, volitional, joint-compression task, a sham hands-on intervention, and a Grade III oscillatory joint-mobilization intervention. A decreased threshold-to-flexor withdrawal response was found in the OA vs control group (P < .01). EMG and joint-torque FWR responses were further augmented in the OA group following the maximal joint-compression task (P < .05), yet remained unchanged or diminished in controls. Joint mobilization, but not sham intervention, reduced reflex responses significantly, although primarily by decreasing BF activity and knee torques (P < .05). ⋯ Application of specific physical inputs to individuals with knee OA similar to those encountered during activity of daily living or during therapeutic interventions appear to modulate involuntary, nociceptive reflex responses. Routine weight-bearing activities such as walking may potentially enhance heightened FWR responses, while joint mobilization, a commonly used clinical intervention, may diminish reflex excitability.
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Data on 1,700 patients pooled from 5 randomized, placebo-controlled duloxetine studies (3 in diabetic peripheral neuropathic pain and 2 in fibromyalgia) were analyzed to determine clinically important differences (CIDs) in the 0 to 10 Numeric Rating Scale-Pain Intensity (NRS-PI) for patient-reported "worst" and "least" pain intensity while validating the previously published level for "average" pain. The correspondence between the baseline-to-endpoint raw and percentage change in the NRS-PI for the worst, least, and average pain were compared to patients' perceived improvements at endpoint as measured by the 7-point Patient Global Impression of Improvement (PGI-I) scales. Stratification by baseline pain separated the raw but not the percent change scores. The PGI-I category of "much better" or above was our a priori definition of a CID. Cutoff points for the NRS-PI change scores were determined using a receiver operator curve analysis. A consistent relationship between the worst and average NRS-PI percent change and the PGI-I was demonstrated regardless of the study, pain type, age, sex, or treatment group with a reduction of approximately 34%. The least pain item CID was slightly higher at 41%. Raw change CID cutoff points were approximately -2, -2.5 and -3 for least, average, and worst pain respectively. ⋯ We determined an anchor-based value for the change in the worst, least, and average pain intensity items of the Brief Pain Inventory that best represents a clinically important difference. Our findings support a standard definition of a clinically important difference in clinical trials of chronic-pain therapies.
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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. ⋯ 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.
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Do past pain events systematically impact pain ratings of healthy subjects or fibromyalgia patients?
We previously reported that 3 different electronic visual analogue and numerical pain scales are useful in providing refined capacity to discriminate discrete levels of pain intensity. Using the same subjects and scales, we now investigated whether pain scaling is influenced by past pain events and by recalled memories of these events in the rating of pain. Normal control subjects (NC: 19 male, 30 female) and female fibromyalgia (FM) (n = 17) patients received 5-second suprathreshold heat stimuli (45-49 degrees C) to both forearms. The participants rated these experimental heat stimuli using the previously described electronic pain scales. Subsequently, they were asked to report whether they used any prior pain experiences during the process of rating their pain. Out of 49 NC, only 6 females (12.2%) and 7 males (14.3%), and out of 17 FM patients, only 3 females (17.6%) stated that they had used past pain experiences during scaling. Notably, pain ratings of experimental heat stimuli did not statistically differ between subjects who used past pain experiences during scaling as compared to those who did not. Furthermore, ratings of their most severe past pains were not significantly correlated with ratings of experimental pain stimuli. These results do not provide support for the strong assertion that pain rating scales are elastic, ie, being used differently depending on the severity of past pain events such as childbirth. ⋯ Less than 25% of subjects used memories of past pain events during pain scaling. In addition, if they were used, these pain memories did not influence pain scaling with electronic eVAS and eNUM scales. Thus, use of these scales allows reliable comparisons of experimental and clinical pain ratings within and between subjects.
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Attachment and pain outcomes in adolescents: the mediating role of pain catastrophizing and anxiety.
This study examined the relations between attachment styles and pain severity/depression in adolescents. Analyses examined whether anxiety and the 3 dimensions of pain catastrophizing mediated the associations between attachment styles, pain severity and depression. A total of 382 high-school students completed questionnaires assessing attachment styles, catastrophizing, depression, anxiety and, for those who reported pain during the last month, pain severity. Results revealed that secure attachment was associated with lower levels of pain severity, depression, pain catastrophizing and anxiety. Preoccupied and fearful attachment styles were associated with heightened pain severity, depression, pain catastrophizing and anxiety. Dismissing attachment style was only associated with high levels of depression and anxiety. Regression analyses revealed that anxiety and the helplessness dimension of pain catastrophizing mediated the relations between secure, preoccupied and fearful attachment styles and pain severity. Moreover, anxiety and the rumination dimension of pain catastrophizing mediated the relation between secure, preoccupied and fearful attachment styles and depression. These findings suggest that anxiety, pain catastrophizing and attachment styles are related processes but nevertheless make independent contributions to the prediction of pain severity and depression. In addition, these findings suggest that attachment styles and cognitive-affective factors might increase the risk of problematic outcomes in adolescents with pain conditions. Theoretical and clinical implications of these results are discussed. ⋯ The results of this study revealed that anxiety and the helplessness dimension of pain catastrophizing mediated the relation between attachment and pain severity whereas anxiety and rumination mediated the relation between attachment and depression. Attachment style and cognitive-affective factors might increase vulnerability for problematic pain outcomes in adolescents.