The journal of pain : official journal of the American Pain Society
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Randomized Controlled Trial
An explanatory study evaluating the muscle relaxant effects of intramuscular magnesium sulphate for dystonia in complex regional pain syndrome.
The treatment of dystonia related to complex regional pain syndrome (CRPS) remains unsatisfactory, raising the need of alternative targets for intervention. In dystonia, pathologic muscle changes may occur, which contributes to stiffness. Because magnesium sulphate may act as a muscle relaxant through its actions on the neuromuscular junction and muscle, we performed an explanatory study of the muscle relaxant effect and safety of intramuscular magnesium sulphate (IMMG) in CRPS patients with dystonia. In a double-blind randomized placebo-controlled crossover study, 30 patients were assigned to 3-week treatments of IMMG and placebo. Treatments were separated by a 1-week washout period. The daily dose of IMMG was 1,000 mg in week 1, 1,500 mg in week 2, and 2,000 mg in week 3. The primary outcome measure was the difference in change in Burke-Fahn-Marsden scores after 3 weeks of treatment between both interventions. Secondary outcomes involved severity of dystonia, myoclonus, tremor, and pain, and functional activity. Data of 22 patients available for the explanatory analysis revealed no significant differences between IMMG and placebo treatment in any of the outcomes. In conclusion, we found no indication of efficacy of IMMG in a daily dose of 2,000 mg as a muscle relaxant in CRPS-related dystonia. ⋯ In this double-blind placebo-controlled crossover study there was no evidence found of a muscle relaxant effect of intramuscular magnesium sulphate in dystonia related to CRPS. Consequently, there is insufficient support for new studies evaluating the efficacy of other routes of MG administration in CRPS-related dystonia.
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Despite the high prevalence of neck pain among women, menstrual effects on regional pain outcomes have not been investigated in this clinical population. This study evaluated menstrual effects on mechanical pain sensitivity (pressure pain threshold [PPT]), neck pain intensity (numeric pain rating scale [NPRS]), and neck-related disability (Neck Disability Index [NDI]) in 22 normally menstruating (NM) and 17 hormonal contraceptive users with chronic neck pain. Sex hormones, PPT, and NDI were measured during the early follicular (F1), late follicular (F2), and luteal (L) menstrual phases. Daily NPRS scores were recorded in an online symptom diary and averaged within each phase. Estradiol and progesterone increased only for NM women in F2 and L, respectively. Phase effects on PPT (η(2) = .003), NDI (η(2) = .003), and NPRS (η(2) = .016) for NM women were small and did not differ from those for the hormonal contraceptive users (P ≥ .386). Averaged across the menstrual cycle, PPT scores explained 29% of the variance in NPRS scores for NM women but were not associated with NDI scores in either group. Results indicate that the magnitude of menstrual effects on mechanical pain sensitivity and the severity of neck pain and disability do not exceed thresholds of clinically detectable change in women with chronic neck pain. ⋯ Fluctuations in evoked and clinical pain outcomes across the menstrual cycle do not appear to be of sufficient magnitude to impact clinical decision making for women with chronic neck pain.
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Randomized Controlled Trial
Determinants of pain treatment response and nonresponse: identification of TMD patient subgroups.
The purpose of the present study was to determine if we could identify a specific subtype of temporomandibular disorder (TMD) pain patients that does not respond to treatment. Patients were 101 men and women with chronic TMD pain recruited from the community and randomly assigned to 1 of 2 treatment conditions: a standard conservative care (STD) condition or a standard care plus cognitive-behavioral therapy condition (STD + CBT) in which patients received all elements of STD but also received cognitive-behavioral coping skills training. Growth mixture modeling, incorporating a series of treatment-related predictors, was used to distinguish several distinct classes of responders or nonresponders to treatment based on reported pain over a 1-year follow-up period. Results indicated that treatment nonresponders accounted for 16% of the sample and did not differ from treatment responders on demographics or temporomandibular joint pathology, but that they reported more psychiatric symptoms, poorer coping, and higher levels of catastrophizing. Treatment-related predictors of membership in treatment responder groups versus the nonresponder group included the addition of CBT to STD, treatment attendance, and decreasing catastrophization. It was concluded that CBT may be made more efficacious for TMD patients by placing further emphasis on decreasing catastrophization and on individualizing care. ⋯ This article provides evidence that the TMD chronic pain population is heterogeneous and that a subsample of patients will be unresponsive to standard or psychosocial approaches. The addition of CBT to treatment may be helpful for this group, but new individualized approaches will be needed to treat all patients effectively.
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Factorial validity of the English-language version of the Pain Catastrophizing Scale--child version.
The Pain Catastrophizing Scale (PCS) was developed in English to assess 3 components of catastrophizing (rumination, magnification, helplessness). It has been adapted for use and validated with Flemish-speaking children (Pain Catastrophizing Scale for Children [PCS-C]) and French-speaking adolescents. The PCS-C has been back-translated to English and used extensively in research with English-speaking children; however, the factorial validity of the English PCS-C has not been empirically examined. This study assessed the factor structure of the English PCS-C among a community sample of 1,006 English-speaking children (aged 8-18 years). Exploratory factor analysis was conducted using a random subsample (n = 504) to assess the underlying factor structure. Items with poor factor loadings were removed. Confirmatory factor analysis, using the second subsample (n = 502), was used to cross-validate the factor structure revealed by exploratory factor analysis and compare it to the original 3-factor model and other model variants. Exploratory factor analysis revealed that the original PCS-C and a revised 3-factor model comprising 11 of the original 13 PCS-C items, all loading on their original factors, provided adequate fit to the data. The revised model provided statistically better fit to the data compared to all other model variants, suggesting that the English PCS-C may be better understood using a revised 11-item oblique 3-factor model. ⋯ This is the first examination of the factorial validity of the widely used English version of the PCS-C in a large community sample of English-speaking children. A revised 11-item, 3-factor model provided statistically better fit to the data compared to the original model and other model variants.
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Mechanical sensitivity of muscle nociceptors was previously shown to increase 2 days after lengthening contractions (LC), but heat sensitivity was not different despite nerve growth factor (NGF) being upregulated in the muscle during delayed-onset muscle soreness (DOMS). The discrepancy of these results and lack of other reports drove us to assess heat sensitivity during DOMS in humans and to evaluate the effect of NGF on the heat response of muscle C-fibers. Pressure pain thresholds and pain intensity scores to intramuscular injection of isotonic saline at 48°C and capsaicin were recorded in humans after inducing DOMS. The response of single unmyelinated afferents to mechanical and heat stimulations applied to their receptive field was recorded from muscle-nerve preparations in vitro. In humans, pressure pain thresholds were reduced but heat and capsaicin pain responses were not increased during DOMS. In rats, the mechanical but not the heat sensitivity of muscle C-fibers was increased in the LC group. NGF applied to the receptive field facilitated the heat sensitivity relative to the control. The absence of facilitated heat sensitivity after LC, despite the NGF sensitization, may be explained if the NGF concentration produced after LC is not sufficient to sensitize nociceptor response to heat. ⋯ This article presents new findings on the basic mechanisms underlying hyperalgesia during DOMS, which is a useful model to study myofascial pain syndrome, and the role of NGF on muscular nociception. This might be useful in the search for new pharmacologic targets and therapeutic approaches.