The journal of pain : official journal of the American Pain Society
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Neuropathic pain (NP) remains difficult to control for a significant number of patients with cancer. Chemotherapy-induced peripheral neuropathy (CIPN) has been postulated as an initial stage in the development of NP. To assess whether CIPN (defined as National Cancer Institute Common Toxicity Criteria grade 2 or higher) was associated with NP, we conducted a survey of breast cancer patients who had participated in clinical trials of paclitaxel. Of the 430 potential respondents, 240 responded to the survey. Results showed that 64% experienced CIPN during paclitaxel treatment. Follow-up survey data revealed that 27% of those with CIPN were subsequently diagnosed with NP. Logistic regression analyses showed that those who had experienced CIPN were 3 times more likely to develop NP (95% confidence interval = 1.2-7.2; P < .001), which persisted in the multivariate logistic model. In addition, NP patients reported twice as many visits to their health care provider (P = .02) and had taken more prescription (50% vs 19%; P = .001) and over-the-counter medications (62.5% versus 45%; P = .08) for pain than those without NP. The results of this study confirm that CIPN is a predictor of NP, suggesting that survivors treated with paclitaxel should be regularly monitored for NP beyond treatment. ⋯ The survival rates of breast cancer patients have steadily improved over recent years; thus, research into symptoms that persist after treatment is important. We found CIPN as a predictor of NP. Understanding the epidemiology of NP in breast cancer patients has high clinical and public health significance.
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There is evidence suggesting an important role of nociceptive sensitization in lateral epicondylalgia (LE). Our aim was to explore somato-sensory changes in patients with unilateral LE to better understand this musculoskeletal condition. Twelve patients (6 female) with LE with a mean (SD) age 47 (10) years, and 16 controls (7 female), aged 41 (9) years were tested. The following somato-sensory parameters were assessed: pressure-pain threshold (PPT), heat- and cold-pain thresholds, thermal, cold- and vibration-detection thresholds. All these tests were bilaterally assessed over the lateral epicondyle (affected/unaffected in patients; dominant/nondominant in controls) and at the dorsal-lateral surface of the wrist in all patients and controls. The results showed that patients with unilateral LE not only exhibited substantial reductions in PPT on the affected side compared to the unaffected side (mean difference and 95% confidence intervals: 219 kPa [136.8 to 301.1 kPa] but also when compared to controls (581.1 kPa [340.5 to 821.7 kPa]), showing bilateral pressure-pain hyperalgesia. These differences represented an effect size (ie, standardized mean difference) of 1.23 and .94, respectively. In the same cohort, there were no such deficits in cold and heat pain, cold- and warm-detection thresholds, and vibration-detection thresholds, either between affected and unaffected sides in patients with LE or between patients and controls. Effect sizes for the sensory-detection tests were small, which were generally less than the pain tests. Our data imply that LE is largely characterized by peripheral and central mechanical pain hyperalgesia. ⋯ This article reveals the presence of bilateral pressure-pain hypersensitivity in patients with unilateral LE. On the contrary, thermal and vibration tests were not significantly different from controls.
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Our aim was to investigate bilateral, widespread pressure-pain hypersensitivity in nerve, muscle, and joint tissues in women with myofascial temporomandibular disorders (TMD) without concomitant comorbid conditions. Twenty women with myofascial TMD (aged 20 to 28 years old), and 20 healthy matched women (aged 20 to 29 years), were recruited. Pressure-pain thresholds (PPT) were bilaterally assessed over supra-orbital (V1), infra-orbital (V2), mental (V3) nerves, median (C5), radial (C6) and ulnar (C7) nerve trunks, the C5-C6 zygapophyseal joint, the lateral pole of the temporo mandibular joint (TMJ), and the tibialis anterior muscle in a blinded design. The results showed that PPTs were significantly decreased bilaterally over the supra-orbital, infra-orbital, and mental nerves, median, ulnar, and radial nerve trunks, the lateral pole of the TMJ, the C5-C6 zygapophyseal joint, and the tibialis anterior muscle in patients with myofascial TMD as compared to healthy controls (all sites: P < .001). There were no significant differences in the magnitude of PPT decreases between the trigeminal and extratrigeminal test sites. PPT over the mental nerve, the TMJ, C5-C6 zygapophyseal joint and tibialis anterior muscle were negatively correlated to both duration of pain symptoms and TMD pain intensity (P < .05). Our findings revealed bilateral, widespread pressure hypersensitivity in women presenting with myofascial TMD, suggesting that widespread central sensitization is involved in myofascial TMD women. ⋯ This article reveals the presence of bilateral and widespread pressure-pain hypersensitivity in women with myofascial TMD, suggesting that widespread central sensitization is involved in myofascial TMD. This finding has implications for development of management strategies.
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Fibromyalgia syndrome (FMS) is a chronic pain disorder associated with widespread musculoskeletal pain, tenderness, and fatigue. Additionally, correlational research suggests negative affect (eg, depression, anxiety) and deficits in positive affect may contribute to FMS symptomatology. However, well-controlled, experimental research is necessary to ascertain whether patients with FMS have problems in affective processing. The present study used a well-validated picture-viewing paradigm to evoke emotional responses in 17 patients with FMS and 17 sex- and age-matched healthy control participants. Each participant viewed pleasant (erotica), neutral, and unpleasant (attack related) pictures, and abrupt white noises were delivered during two-thirds of the pictures to evoke startle eyeblinks. Appetitive and defensive responding was assessed from subjective (valence/pleasure and arousal ratings) and physiological (corrugator EMG, heart rate, skin-conductance response, startle-reflex modulation) reactions to pictures. Results suggested FMS was associated with greater defensive activation (displeasure, subjective arousal, corrugator EMG) to the unpleasant, threat-related pictures, but not deficits in appetitive activation to erotic pictures. Although preliminary, these data suggest individuals with FMS have deficits in affective processing, but this dysregulation may be limited to defensive activation. Implications for treatment and future research are discussed. ⋯ Fibromyalgia is a debilitating disease associated with affective distress. Results from the present study suggest that FMS is associated with enhanced defensive activation to nonpainful threat-related stimuli, but not deficits in appetitive reactions to erotic stimuli. These findings have implications for the treatment and study of FMS.
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NFkappaB is involved in several pathogenic mechanisms that are believed to underlie the complex regional pain syndrome (CRPS), including ischemia, inflammation and sensitization. Chronic postischemia pain (CPIP) has been developed as an animal model that mimics the symptoms of CRPS-I. The possible involvement of NFkappaB in CRPS-I was studied using CPIP rats. Under sodium pentobarbital anesthesia, a tourniquet was placed around the rat left ankle joint, producing 3 hours of ischemia, followed by rapid reperfusion (IR injury). NFkappaB was measured in nuclear extracts of muscle and spinal cord tissue using ELISA. Moreover, the anti-allodynic (mechanical and cold) effect was tested for systemic, intrathecal, or intraplantar treatment with the NFkappaB inhibitor pyrrolidine dithiocarbamate (PDTC). At 2 and 48 hours after IR injury, NFkappaB was elevated in muscle and spinal cord of CPIP rats compared to shams. At 7 days, NFkappaB levels were normalized in muscle, but still elevated in spinal cord tissue. Systemic PDTC treatment relieved mechanical and cold allodynia in a dose-dependent manner, lasting for at least 3 hours. Intrathecal-but not intraplantar-administration also relieved mechanical allodynia. The results suggest that muscle and spinal NFkappaB plays a role in the pathogenesis of CPIP and potentially of human CRPS. ⋯ Using the CPIP model, we demonstrate that NFkappaB is involved in the development of allodynia after a physical injury (ischemia and reperfusion) without direct nerve trauma. Since CPIP animals exhibit many features of human CRPS-I, this observation indicates a potential role for NFkappaB in human CRPS.