Pain
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Activity pacing has been suggested as a behavioural strategy that may protect patients with fibromyalgia (FM) against activity dysregulation and disability. The aim of the present study was to empirically test whether the construct of activity pacing is distinct from other behavioural strategies assessed with the Chronic Pain Coping Inventory (CPCI), such as guarding, resting, asking for assistance, relaxation, task persistence, exercise/stretch, seeking social support, and coping self-statements. The second objective was to test whether pacing was associated with physical disability when controlling for pain catastrophizing, pain severity and the other behavioural strategies as measured with CPCI. ⋯ Moreover, guarding and asking for assistance, but not pacing, were associated with disability. These findings are in line with fear-avoidance models and suggest that specifically active avoidance behaviours are detrimental in FM. The authors recommend developing cognitive-behavioural and exposure-based interventions and challenge the idea that pacing as an intervention is essential in pain self-management programs.
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A wide variety of risk factors for the occurrence and prognostic factors for persistence of non-specific musculoskeletal pain (MSP) are mentioned in the literature. A systematic review of all these factors is not available. Thus a systematic review was conducted to evaluate MSP risk factors and prognostic factors, classified according to the dimensions of the International Classification of Functioning, Disability and Health. ⋯ For whiplash-associated disorders these factors were older age, being female, having angular deformity of the neck, and having an acute psychological response. Similarly, for persistence of low back pain, high evidence was found for having fear-avoidance beliefs and meagre social support at work. For low back pain, high evidence was found for meagre social support and poor job content at work as not being risk factors.
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Individual differences in sensitivity to fentanyl, a widely used opioid analgesic, can hamper effective pain treatment. Still controversial is whether the single nucleotide polymorphisms (SNPs) of the human OPRM1 gene encoding the mu-opioid receptor influence the analgesic effects of opioids. We examined associations between fentanyl sensitivity and the two SNPs, A118G and IVS3+A8449G, in the human OPRM1 gene in 280 Japanese patients undergoing painful orofacial cosmetic surgery, including bone dissection. ⋯ Furthermore, the IVS3+A8449G SNP in intron 3, which represents a complete linkage disequilibrium block with more than 30 SNPs from intron 3 to the 3' untranslated region, was associated with 24-h postoperative fentanyl requirements. Subjects carrying the minor G allele of the IVS3+A8449G SNP required significantly less fentanyl for 24-h postoperative pain control (median: 1.5microg/kg) compared with subjects not carrying this allele (median: 2.5microg/kg, p=0.010). Although further validation is needed, the present findings shed light on the involvement of OPRM1 3' untranslated region polymorphisms in fentanyl sensitivity in addition to the A118G SNP and open new avenues for personalized pain treatment with fentanyl.
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Facial pain has a considerable impact on quality of life. Accurate incidence estimates in the general population are scant. The aim was therefore to estimate the incidence rate (IR) of trigeminal neuralgia (TGN), postherpetic neuralgia (PHN), cluster headache (CH), occipital neuralgia (ON), local neuralgia (LoN), atypical facial pain (AFP), glossopharyngeal neuralgia (GPN) and paroxysmal hemicrania (PH) in the Netherlands. ⋯ The IR increased with age for all diseases except CH and ON, peaking in the 4th and 7th decade, respectively. Postherpetic neuralgia, CH and LoN were more common in men than women. From this we can conclude that facial pain is relatively rare, although more common than estimated previously based on hospital data.
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Cold allodynia is a common sign of neuropathic pain patients but its underlying mechanisms are still largely unknown, partly because the populations of neurons responding to cold stimuli and their transduction mechanisms have not been fully determined. We report a patient with a small-fiber neuropathy of unknown origin, whose main complaint is cold allodynia. ⋯ These findings provide the first direct evidence in human of abnormal peripheral nociceptor behavior potentially responsible for cold allodynia. The responsiveness of C-nociceptors to menthol suggests an abnormal expression or function of TRPM8 channels in this patient with a small-fiber polyneuropathy.