Articles: neuralgia.
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Better tools are required for the earlier identification and management of orofacial pain with different aetiologies. The painDETECT questionnaire is a patient-completed screening tool with utility for identification of neuropathic pain in a range of contexts. 254 patients, referred from primary care for management of orofacial pain and attending a secondary care centre, were prospectively recruited, and completed the painDETECT prior to consultation. The aim of this study was to determine the accuracy of the painDETECT to detect neuropathic components of orofacial pain, when compared to a reference standard of clinical diagnosis by experienced physicians, in a cohort of hospital-based patients. ⋯ In secondary care settings, the painDETECT performed modestly at identifying neuropathic components, and underestimates the complexity of orofacial pain in its mixed presentations and with multiple diagnoses. Prior to clinical applications or research use, the painDETECT and other generic screening tools must be adapted and revalidated for orofacial pain patients, and separately in primary care, where orofacial pain is considerably less common.
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Clinical rheumatology · Nov 2018
Multicenter StudyValidity of the central sensitization inventory with measures of sensitization in people with knee osteoarthritis.
Our purpose was to determine the validity of the Central Sensitization Inventory (CSI) with psychophysical tests, psychological and physical factors in patients with Knee Osteoarthritis (KOA). Patients with KOA were recruited from three Montreal hospitals. Psychophysical tests (pressure pain threshold, conditioned pain modulation, temporal summation) were conducted and questionnaires administered to determine the presence of neuropathic pain, somatization, anxiodepressive symptoms, pain catastrophizing (PC), and widespread pain (WSP). ⋯ After adjustment for covariates, a multivariable linear regression determined WSP (unstandardized ß 4.161(0.067, 8.255) p = 0.046), somatization (unstandardized ß 1.828 (1.368, 2.288) p < 0.005), and anxiodepressive symptoms (unstandardized ß 0.419 (0.107, 0.730) p = 0.009) significantly predicted CSI scores. The CSI is more strongly associated with psychological factors than psychophysical test results in a KOA population. Its moderate sensitivity and specificity suggest it should be used as part of a more comprehensive evaluative toolkit.
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It is widely believed that cortical changes are a consequence of longstanding neuropathic pain (NP). In this article, we demonstrate that NP in individuals with subacute spinal cord injury (SCI) has characteristic electroencephalography markers (EEG) that precede the onset of pain. EEG was recorded in a relaxed state and during motor imagination tasks in 10 able-bodied participants and 31 patients with subacute SCI (11 with NP, 10 without NP, and 10 who had pain develop within 6 months of EEG recording). ⋯ Clinical Trial Registration Number: NCT02178917 PERSPECTIVE: We demonstrate that brain activity in patients with subacute SCI reveals both early markers and predictors of NP, which may manifest before sensory discomfort. These markers and predictors may complement known sensory phenotypes of NP. They may exist in other patient groups suffering from NP of central origin.
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Tobacco smoking is particularly evident in individuals experiencing chronic pain. This complex relationship is poorly understood at both molecular and behavioral levels. Here, we describe experiments aimed at understanding whether a chronic pain state induces neuroadaptations into the brain or peripheral nerves that involve nicotinic acetylcholine receptors (nAChRs) and whether these neuroadaptations directly lead to increased vulnerability to nicotine addiction or to the development of coping strategies to relieve pain symptoms. ⋯ Spinal nerve ligation and sham rats were equally sensitive to nicotine-induced anxiety-like behavior and antinociception; however, nicotine produced a potent and long-lasting antiallodynic effect in spinal nerve ligation rats. These results demonstrate that chronic pain leads to plasticity of nAChRs that do not directly facilitate nicotine addictive behaviors. Instead, nicotine potently decreases allodynia, an effect that could lead to increased nicotine consumption in chronic pain subjects.
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MicroRNAs (miRNAs) are recognized as significant regulators of neuropathic pain. Moreover, neuroinflammation can contribute a lot to the progression of neuropathic pain. MiR-28-5p has been reported to be involved in many pathological diseases. ⋯ Theoverexpression of Zeb1 can disturb neuropathic pain development, which was repressed by the increase of miR-28-5p by upregulating Cox-2, IL-6, and IL-1β levels. By taking all of these together, it was indicated in our study that miR-28-5p can reduce neuropathic pain progression by targeting Zeb1 in vivo. Our data implied that miR-28-5p/Zeb1 axis can be a novel therapeutic target for neuropathic pain treatment.