European journal of pain : EJP
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The aim of the present study was to compare the subjectively reported and objectively assessed activity-related characteristics of patients with Chronic Low Back Pain (CLBP) who were classified according to their scores on the Patterns of Activity Measure-Pain (POAM-P) into avoiders, persisters, mixed performers (i.e. high scores on both avoidance and persistence behaviour) or functional performers (i.e. low scores on avoidance and persistence behaviour). Patients carried an electronic diary during 14 days to assess the self-reported activity and pain intensity levels in daily life. An accelerometer was used to objectively assess their activity level during the same time period. ⋯ A further analysis tested the association between pain intensity levels and self-reported and objectively assessed daily life activity levels in avoiders and persisters. In persisters, a higher level of self-reported activities in daily life was related to increased pain. The objectively assessed activity level was not associated with pain intensity.
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This study examined differences between Asians and non-Hispanic Whites (Whites) in pain sensitivity, and its relationship to mean arterial pressure (MAP) and heart rate (HR). In 30 Whites (50% female) and 30 Asians (50% female), experimental pain sensitivity was assessed with a hand cold pressor task, yielding measures of pain threshold, tolerance, intensity, and unpleasantness. Mean arterial pressure and HR measurements taken at rest and in response to speech stress were assessed. ⋯ These results indicate that Asian Americans are more sensitive to experimental pain than Whites and suggest ethnic differences in endogenous pain regulatory mechanisms (e.g. MAP and HR). The results may also have implications for understanding ethnic differences in clinical pain.
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While the etiology of fibromyalgia syndrome (FMS) remains unclear, it is assumed that both peripheral and central components are involved. ⋯ Repetitive proton/PGE(2)-induced excitation of muscle tissue led to a more prolonged perception of pain and more wide-spread activation in pain-related brain areas in FMS, especially in the left (ipsilateral) insula, whereas acute protons/PGE(2)-induced pain processing was similar in the two groups. These data provide further evidence for enhanced central pain processing in FMS patients.
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Phantom phenomena are frequent following amputation, but how this often painful experience is modified or triggered by spontaneous events or sensations often puzzles amputees and clinicians alike. We explored triggers of phantom phenomena in a heterogeneous sample of 264 upper and lower limb adult amputees with phantom sensations. Participants completed a structured questionnaire to determine the prevalence and nature of the triggers of phantom phenomena. ⋯ Finally, habitual "forgetting" behaviors were most common soon after amputation, whereas other more adaptive schemata (e.g., self-defense) were equally likely to be performed at any time following amputation. Various likely inter-related mechanisms are discussed in relation to phantom triggers. Ultimately, optimizing stump and neuroma management, as well as restoring function of central networks for pain, limb movement, and amputation-related memories, should help manage spontaneously triggered phantom phenomena.
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Trigeminal neuropathic pain is due to lesion or dysfunction of the nervous system. Dynamic mechanical allodynia is a widespread symptom of neuropathic pain for which mechanisms are still poorly understood. Recent studies demonstrate that forebrain neurons, including neurons in the medial prefrontal cortex (mPFC) are important for the perception of acute and chronic pain. ⋯ Stimulus-evoked pERK-1/2 immunopositive cell bodies displayed a rostrocaudal gradient and layer-selective distribution in the ventral mPFC, being predominant in the rostral ventral mPFC and in layers II-III and V-VI of the ventral mPFC. In layers II-III, intense pERK-1/2 also extended into distal dendrites, up to layer I. These results demonstrate that trigeminal nerve injury induces a significant alteration in the ventral mPFC processing of tactile stimuli and suggest that ERK phosphorylation contributes to the mechanisms underlying abnormal pain perception under this condition.