Pain
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Although gender differences in pain and analgesia are well known, it still remains unclear whether men and women vary in response to multimodal pain treatment. This study was conducted to investigate whether men and women exhibited different outcomes after an intensive multimodal pain treatment program. The daily outpatient program consisted of individual treatment as well as group therapy, with a total amount of therapy of 117.5h per patient. ⋯ Consistently, women (ES .694) improved more in pain-related disabilities in daily life than men (ES .436). These distinctions are not due to differences in pain duration, received medication, psychiatric comorbidities, pain chronicity stage, or application for a disability pension. Therefore, gender differences not only refer to chronic pain prevalence, pain perception, or experimental pain measurement, but also seem to have a clinically relevant impact on the response to pain therapy.
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The aim of this study was to examine the joint role of demographic, clinical, and psychological variables as predictors of acute postsurgical pain in women undergoing hysterectomy due to benign disorders. A consecutive sample of 203 women was assessed 24 hours before (T1) and 48 hours after (T2) surgery. Baseline pain and predictors were assessed at T1 and postsurgical pain and analgesic consumption at T2. ⋯ Findings revealed an integrative heuristic model that accounts for the joint influence of demographic, clinical, and psychological factors on postsurgical pain intensity and severity. In further mediation analysis, pain catastrophizing emerged as a full mediator between presurgical anxiety and postsurgical pain intensity. The potential clinical implications for understanding, evaluating, and intervening in postsurgical pain are discussed.
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Medication-overuse headache (MOH) is relatively common, but its incidence has not been calculated and there are no prospective population-based studies that have evaluated risk factors for developing MOH. The aim of this study was to estimate incidences of and identify risk factors for developing chronic daily headache (CDH) and MOH. This longitudinal population-based cohort study used data from the Nord-Trøndelag Health Surveys performed in 1995-1997 and 2006-2008. ⋯ In contrast, these factors did not increase the risk of CDHwoO. In this large population-based 11-year follow-up study, several risk factors for MOH did not increase the risk for CDHwoO, suggesting these are pathogenetically distinct. If the noted associations are causal, more focus on comorbid condition, physical activity, and use of tobacco and tranquilizers may limit the development of MOH.
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Emerging evidence supports an important role of posterior parasylvian areas in both pain and touch processing. Whether there are separate or shared networks for these sensations remains controversial. The present study compared spatial patterns of brain activation in response to unilateral nociceptive heat (47.5°C) or innocuous tactile stimulation (8-Hz vibration) to digits through high-resolution functional magnetic resonance imaging (fMRI) in squirrel monkeys. ⋯ Single voxels within each activation cluster showed robust BOLD signal changes during each block of nociceptive stimulation. Across animals (n=11), nociceptive response magnitudes of contralateral VS and pIns and ipsilateral Ri were significantly greater than corresponding areas in the opposite hemisphere. In sum, both distinct and shared areas in regions surrounding the posterior sylvian fissure were activated in response to nociceptive and tactile inputs in nonhuman primates.
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Peripheral injury or inflammation leads to a release of mediators capable of binding to a variety of ion channels and receptors. Among these are the 7-transmembrane receptors (G protein-coupled receptors) coupling to G(s), G(i/o), G₁₂/₁₃, or G(q/11) G proteins. Each of the G protein-coupled receptor pathways is involved in nociceptive modulation and pain processing, but the relative contribution of individual signaling pathways in vivo has not yet been worked out. ⋯ Surprisingly, our behavioral and electrophysiological experiments also indicated defects in basal mechanical sensitivity in G(q/11) mutant mice, suggesting a novel function for G(q/11) in tonic modulation of acute nociception. Patch-clamp recordings revealed changes in voltage-dependent tetrodotoxin-resistant and tetrodotoxin-sensitive sodium channels in nociceptors upon a loss of G(q/11), whereas potassium currents remained unchanged. Our results indicate that the functional role of the G(q)/G₁₁ branch of G-protein signaling in nociceptors in vivo not only spans sensitization mechanisms in pathological pain states, but is also operational in tonic modulation of basal nociception and acute pain.