Articles: neuralgia.
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Multicenter Study Clinical Trial
Pain catastrophizing predicts poor response to topical analgesics in patients with neuropathic pain.
Previous research suggests that high levels of pain catastrophizing might predict poorer response to pharmacological interventions for neuropathic pain. ⋯ The results of the present study suggest that the development of brief interventions specifically targeting catastrophic thinking might be useful for enhancing the effects of pharmacological interventions for neuropathic pain. Furthermore, failure to account for the level of catastrophizing might contribute to null findings in clinical trials of analgesic medication.
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Diagnostics of neuropathy pain is presented in the article, where most essential are methods of clinical estimation with the use of questionnaires and scales for verification and quantitative estimation of pain. The neurological inspection of patients with suspicion on neuropathy pain must plug in itself of the motive, sensory and vegetative phenomena with the purpose of authentication of all signs of neurological dysfunction. If on a background immunotherapy it is not succeeded fully a pain syndrome preparations of the first row, setting of combined pharmacotherapy allows to promote efficiency of treatment at the less dosages of preparations and reduce the risk of development of by-effects.
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J Pain Symptom Manage · Dec 2011
Multicenter StudyPreliminary assessment of a neuropathic pain treatment and referral algorithm for patients with cancer.
The purpose of this case series study was to pilot test an evidence-based neuropathic pain (NP) treatment and referral algorithm for use by oncology nurses when managing cancer-related NP. ⋯ Evidence from this pilot study suggests that NP evidence-based treatment may result in improved symptoms, function, and patient satisfaction. A randomized controlled trial is needed to further assess algorithm efficacy.
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Randomized Controlled Trial Multicenter Study
Clinical trial of the p38 MAP kinase inhibitor dilmapimod in neuropathic pain following nerve injury.
Current treatments of neuropathic pain arising from conditions such as nerve injury/compression are only partially effective, and limited in their use by side-effects. p38 mitogen-activated protein kinase (MAPK) is involved in the regulation and synthesis of inflammatory mediators, and is the target for a novel class of cytokine-suppressive anti-inflammatory drugs. p38 inhibitors may reduce neuronal sensitisation in preclinical models of neuropathic pain, particularly where there is a substantial inflammatory component. An exploratory, multicentre, double-blind, placebo-controlled, two-period, cross-over trial was undertaken to evaluate the effect of dilmapimod (SB-681323), a selective p38 MAPK inhibitor, on neuropathic pain symptoms and signs. Fifty patients with nerve trauma, radiculopathy or carpal tunnel syndrome were randomised; 43 patients completed the study. ⋯ There was a statistically significant reduction in the primary endpoint of average daily pain score during the second week of treatment among patients treated with dilmapimod (15 mg/day) compared to placebo using NRS [0.80; 95% CI (0.28, 1.33); p=0.0034]. A similar trend for effect was seen in some secondary endpoints. Dilmapimod was well tolerated, with no clinically relevant safety findings. p38 MAPK inhibitors merit further evaluation for neuropathic pain in larger clinical trials, particularly for clinically meaningful analgesic effect size.
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Multicenter Study
The neuropathic components of chronic low back pain: a prospective multicenter study using the DN4 Questionnaire.
The present study investigated the neuropathic components of chronic low back pain (LBP) in patients with and without lower limb pain using the DN4 questionnaire and confirmed its psychometric properties. Patients (n = 132) from 11 French multidisciplinary pain or rheumatology centers were classified by a first investigator into 4 groups derived from the Quebec Task Force Classification of Spinal Disorders (QTFSD): group 1 (pain restricted to the lumbar area); group 2 (pain radiating proximally); group 3 (pain radiating below the knee without neurologic signs); and group 4 (pain radiating towards the foot in a dermatomal distribution, with neurological signs, corresponding to typical radiculopathy). A second investigator applied the DN4 questionnaire to the lower limb (groups 2 to 4) and lower back. A comparison of groups 1 and 4 confirmed the psychometric properties of DN4 (sensitivity 80%; specificity 92%, for a cutoff of 4/10, similar to other neuropathic conditions). In the lower limb, the proportion of patients with neuropathic pain (NP) was related to the distality of pain radiation (15, 39, and 80% in groups 2, 3 and 4, respectively; P < .0001). In the lower back, the proportion of patients with NP was higher for patients with typical radicular pain compared with the other groups (P = .006). Thus, typical radiculopathy has similar characteristics as other neuropathic conditions and is confirmed as the commonest neuropathic syndrome in LBP patients. The observation that neuropathic and nociceptive components of LBP vary in the back and lower limb probably accounts for the discrepancies of reported prevalence rates of NP in LBP. As this study was essentially based on a questionnaire, future studies combining standard clinical sensory testing, specific questionnaires, and more objective assessment of the sensory lesion are now required to further investigate the neuropathic component of chronic LBP. ⋯ This study confirms the psychometric properties of the DN4 questionnaire to assess neuropathic pain in patients with low back pain. Neuropathic mechanisms largely contribute to pain in the lower limb as compared to the back, but neuropathic pain is not restricted to typical radiculopathy. This may have significant implications for the choice of treatment strategy in these patients.