Pain
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Comparative Study
Multidimensional Pain Inventory derived classifications of chronic pain: evidence for maladaptive pain-related coping within the dysfunctional group.
This study examines maladaptive pain-related fear-avoidance and endurance coping in subgroups of patients with chronic back pain. Hypotheses were derived from the avoidance-endurance model of pain [Hasenbring M. Attentional control of pain and the process of chronification. ⋯ Furthermore, the DYS group showed more thought suppression compared to AC; however, subgroups did not differ significantly with regard to avoidance of social and physical activity, and endurance behavior. Further, DYS as well as ID group showed more non-verbal pain behavior compared to AC, which refers to the special role of operant conditioning. Implications are considered for further investigation of endurance coping to provide a more comprehensive assessment and treatment for subgroups of chronic pain patients.
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Comparative Study
Transition from acute to chronic pain and disability: a model including cognitive, affective, and trauma factors.
This study evaluated a theoretically and empirically based model of the progression of acute neck and back pain to chronic pain and disability, developed from the literature in chronic pain, cognition, and stress and trauma. Clinical information and standardized psychosocial measures of cumulative traumatic events exposure (TLEQ), depressed mood (CES-D), pain (DDS), physical disability (PDI), and pain beliefs (PBPI) were collected at baseline from 84 acute back pain patients followed at an Acute Back Clinic over 3 months. Path analysis was used for the longitudinal prediction of perceived pain and disability. ⋯ More cumulative traumatic life events, higher levels of depression in the early stages of a new pain episode, and early beliefs that pain may be permanent significantly contribute to increased severity of subsequent pain and disability. Replication in a larger sample is desirable to confirm these paths. Early detection of elevated depressive symptoms and high trauma exposure may identify individuals at greater risk for developing chronic pain syndromes who may benefit from early multidisciplinary intervention.
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Comparative Study
Visceral and somatic hypersensitivity in a subset of rats following TNBS-induced colitis.
Chronic abdominal pain is one of the most common gastrointestinal symptoms experienced by patients. Visceral hypersensitivity has been shown to be a biological marker in many patients with chronic visceral pain. We have previously shown that IBS patients with visceral hypersensitivity also have evidence of thermal hyperalgesia of the hand/foot. ⋯ Transient colonic inflammation leads to chronic visceral and somatic hypersensitivity in a subset of rats. These findings are similar to the subset of patients who develop chronic gastrointestinal symptoms following enteric infection.
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We assessed whether intrathecal administration of the uncompetitive and competitive NMDA receptor antagonists ketamine and (+/-)CPP, respectively, could produce differential modulation on chemical and mechanical nociception in normal and monoarthritic rats. In addition, the antinociceptive interaction of ketamine and (+/-)CPP on monoarthritic pain was also studied using isobolographic analysis. Monoarthritis was produced by intra-articular injection of complete Freund's adjuvant into the tibio-tarsal joint. ⋯ Irrespective of the nociceptive test employed, both antagonists showed greater antinociceptive activity in monoarthritic than in healthy rats. Combinations produced synergy of a supra-additive nature in the capsaicin test, but only additive antinociception in paw pressure testing. The efficacy of the drugs, alone or combined, is likely to depend on the differential sensitivity of tonic versus phasic pain and/or chemical versus mechanical pain to NMDA antagonists.
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Comparative Study
Activation of the 5-HT1B/D receptor reduces hindlimb neurogenic inflammation caused by sensory nerve stimulation and capsaicin.
Activation of the 5-HT(1B/D) receptor inhibits cerebrovascular neurogenic inflammation (NI). The aim of this study was to determine if the 5-HT(1B/D) receptor agonist sumatriptan can also inhibit NI in other regions of the body. NI was assessed by measuring plasma extravasation (PE) and changes in blood flow in the rat hindpaw. ⋯ The systemic and local inhibitory actions of sumatriptan are mediated by the 5-HT(1B/D) receptor as pre-treatment with the 5-HT(1B/D) antagonist GR127935 (GR; 15 microl, 1 microM, s.c. or 0.2 micromol/kg, i.v.) completely blocked the inhibitory effect of sumatriptan on capsaicin-induced vasodilation and reduced the inhibitory effect of sumatriptan on capsaicin and electrically induced-PE. Neither PE induced by local injection of substance P (SP) (20 pmol, 20 microl, s.c.) nor vasodilation induced by local CGRP injection was affected by pre-treatment with sumatriptan. These findings indicate that both local and systemic activation of the 5-HT(1B/D) receptor by sumatriptan reduce NI induced by nerve stimulation or capsaicin presumably by inhibiting neuropeptide release. 5-HT(1B/D) receptor agonists may be useful for the treatment of non-trigeminal pain conditions involving NI.