The journal of pain : official journal of the American Pain Society
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Multiple abnormalities in pain processing have been reported in patients with chronic musculoskeletal pain syndromes. These changes include mechanical and thermal hyperalgesia, decreased thresholds to mechanical and thermal stimuli (allodynia), and central sensitization, all of which are fundamental to the generation of clinical pain. Therefore, we hypothesized that quantitative sensory tests may provide useful predictors of clinical pain intensity of such patients. Our previous studies of fibromyalgia (FM) patients have shown statistically significant correlations of quantitative sensory test results with clinical pain intensity, including mechanical spatial summation, number of pain areas, wind-up, and wind-up aftersensations. Although these tests predicted up to 59% of the variance in FM clinical pain intensity, their expense and technical complexities limited widespread use in clinical practice and trials. Thus, we developed practical tests of primary (mechanical) and secondary (heat) hyperalgesia that also strongly predict clinical pain intensity in patients with chronic musculoskeletal pain disorders. Thirty-six individuals with FM, 24 with local musculoskeletal pain, and 23 normal controls underwent testing of mechanical and heat hyperalgesia at the shoulders and hands. All subjects rated experimental pains using an electronic visual analog scale. Using either heat or pressure pain ratings as well as tender point counts and negative affect as predictors, up to 49.4% of the patients' variance of clinical pain intensity could be estimated. Results of this study emphasize the important contributions of peripheral and central factors to both local and widespread chronic pain. Overall, measures of mechanical and heat hyperalgesia in combination with tender point and negative affect provided powerful predictors of clinical pain intensity in chronic musculoskeletal pain patients that can be readily used in clinical practice and trials. ⋯ Simple tests of mechanical and heat hyperalgesia can predict large proportions of the variance in clinical pain intensity of chronic musculoskeletal pain patients and thus are feasible to be included in clinical practice and clinical trials.
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Sexual assault (SA) is common, but the epidemiology of acute pain after SA has not previously been reported. We evaluated the severity and distribution of pain symptoms in the early aftermath of SA among women receiving Sexual Assault Nurse Examiner (SANE) care, and the treatment of pain by SANE nurses. Severe pain (≥7 on a 0-10 numeric rating scale) was reported by 53/83 women sexual assault survivors (64% [95% CI, 53-74%]) at the time of SANE evaluation and 43/83 women (52% [95% CI, 41-63%]) 1 week later. Pain in 4 or more body regions was reported by 44/83 women (53% [95% CI, 42-64%]) at the time of initial evaluation and 49/83 women (59% [95% CI, 48-70%]) at 1 week follow-up. Among survivors with severe pain at the time of initial postassault evaluation, only 7/53 (13% [95% CI, 6-26%]) received any pain medication at the time of initial SANE treatment. These findings suggest that pain is common in SA survivors in the early postassault period, but rarely treated. ⋯ Acute pain is common after sexual assault. Practice guidelines for SANE nurses and others who provide care to sexual assault survivors in the early aftermath of assault should include specific recommendations for pain evaluation and treatment. Prospective longitudinal studies of pain outcomes among sexual assault survivors are needed.
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Randomized Controlled Trial
Respiration-induced hypoalgesia: exploration of potential mechanisms.
Slow breathing is used as a means to reduce pain, yet the mechanisms responsible for respiration-induced hypoalgesia are poorly understood. The present study asked 30 healthy participants (M(age) = 21 years, M(education) = 15 years, 80% white non-Hispanic) to breathe at normal, slow (50% normal), and fast (125% normal) rates while constant-intensity, suprathreshold electric stimulations were delivered to the sural nerve to elicit pain and the nociceptive flexion reflex (NFR, a measure of spinal nociception). Stimulations were equally balanced across inhalations and exhalations to determine whether parasympathetic activation during exhalations contributes to hypoalgesia. Respiration rate, heart rate variability (HRV, a measure of parasympathetic activity), heart rate, and subjective arousal were assessed as manipulation checks. Slow breathing reduced pain relative to normal breathing and fast breathing, but NFR was not influenced by breathing. Further, pain and NFR did not differ between exhalations and inhalations, and changes in HRV did not correlate with changes in pain or NFR. Together, these findings suggest that respiration-induced hypoalgesia does not require gating of spinal nociception or changes in parasympathetic activity. ⋯ Slow breathing reduced pain relative to normal and fast breathing. This respiration-induced hypoalgesia does not appear to be due to gating of spinal nociception or changes in parasympathetic activity.
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In the present study, patients with musculoskeletal pain conditions (n = 55) were filmed while performing a lifting task designed to elicit pain behaviors. Patients were asked to perform the lifting task twice, under 2 distinct conditions. In the first condition, patients were asked to rate their pain while lifting a series of weights. In the second condition, patients were asked to estimate the weight of the objects they lifted. The weight estimation condition was conceived as a way to increase the cognitive load associated with the lifting task. The primary purpose of the present study was to examine whether manipulation of cognitive load differentially influenced the expression of pain behaviors in high and low catastrophizers. During the pain rating condition, results indicated that high catastrophizers displayed significantly higher levels of communicative and protective pain behaviors than low catastrophizers. During the weight estimation condition, however, high and low catastrophizers no longer differed in the expression of communicative pain behaviors. These results suggest that increasing cognitive load during a pain-eliciting task may interfere with the expression of communicative pain behaviors in high catastrophizers. The discussion addresses the potential role of automatic and cognitive control processes in the expression of pain behaviors. ⋯ The present study provides new insights into the processes that might underlie the expression of pain behaviors in patients with high levels of catastrophizing. Our findings could have implications for the management of patients presenting with pain conditions, particularly those with high levels of catastrophizing.
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We previously showed evidence for a genetic association of the human leukocyte antigen (HLA) system and complex regional pain syndrome (CRPS) with dystonia. Involvement of the HLA system suggests that CRPS has a genetic component with perturbed regulation of inflammation and neuroplasticity as possible disease mechanisms. However, it is at present unclear whether the observed association with HLA-B62 and HLA-DQ8 in CRPS patients with dystonia also holds true for patients without dystonia. Therefore, we tested the possible association with HLA-B62 and HLA-DQ8 in a clinically homogeneous group of 131 CRPS patients without dystonia. In addition, we investigated the possible association with other alleles of the HLA-A, HLA-B, HLA-C, HLA-DR, and HLA-DQ loci. We showed an increased prevalence of HLA-DQ8 (molecularly typed as HLA-DQB1*03:02; OR = 1.65 [95% CI 1.12-2.42], P = .014) in CRPS without dystonia, whereas no association was observed for HLA-B62 (molecularly typed as HLA-B*15:01; OR = 1.22 [95% CI .78-1.92], P = .458). Our data suggest that CRPS with and CRPS without dystonia may be genetically different, but overlapping, disease entities because only HLA-DQ8 is associated with both. The findings also indicate that distinct biological pathways may play a role in both CRPS subtypes. ⋯ This study is the first to replicate a specific HLA region conferring genetic risk for the development of CRPS. Moreover, associations of HLA-DQ8 with both CRPS with and CRPS without dystonia, and HLA-B62 only with CRPS with dystonia, suggest that these disease entities may be genetically different, but overlapping.