Pain
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Posttraumatic stress disorder (PTSD) symptoms and other negative psychosocial factors have been implicated in the transition from acute to persistent pain. Women (N = 375) who presented to an inner-city emergency department (ED) with complaints of acute pain were followed up for 3 months. They completed a comprehensive battery of questionnaires at an initial visit and provided ratings of pain intensity at the site of pain presented in the ED during 3 monthly phone calls. ⋯ The no recovery group reported significantly greater PTSD symptoms, anger, sleep disturbance, and lower social support at the initial visit than both the early recovery and delayed recovery groups. Results suggest that women with high levels of PTSD symptoms, anger, sleep disturbance, and low social support who experience an acute pain episode serious enough to prompt an ED visit may maintain elevated pain at this pain site for at least 3 months. Such an array of factors may place women at an increased risk of developing persistent pain following acute pain.
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The sodium channel Nav1.7 is a master regulator of nociceptive input into the central nervous system. Mutations in this channel can result in painful conditions and produce insensitivity to pain. Despite being recognized as a "poster child" for nociceptive signaling and human pain, targeting Nav1.7 has not yet produced a clinical drug. ⋯ No changes were observed in CRMP2 mice to inflammatory, acute, or visceral pain. By contrast, in a neuropathic model, CRMP2 mice failed to develop persistent mechanical allodynia. Our study suggests that CRMP2 SUMOylation-dependent control of peripheral Nav1.7 is a hallmark of chronic, but not physiological, neuropathic pain.
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Musculoskeletal pain is the greatest cause of disability worldwide. Owing to its increasing prevalence and burden, the importance of affordable treatments has been highlighted. Text message interventions are accessible, low cost, and effective in promoting healthy behaviour and managing chronic diseases. ⋯ Moreover, text message and telephone counselling interventions had similar effects on function. Overall included studies were of limited methodological quality and heterogeneous. However, our results indicate potential benefits of text messages in the treatment of musculoskeletal pain, which need to be confirmed in future trials.
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Migraine is one of the most disabling disorders worldwide but the underlying mechanisms are poorly understood. Stress is consistently reported as a common trigger of migraine attacks. Here, we show that repeated stress in mice causes migraine-like behaviors that are responsive to a migraine therapeutic. ⋯ Finally, mice received either the calcitonin gene-related peptide monoclonal antibody ALD405 (10 mg/kg) 24 hours before SNP or a coinjection of sumatriptan (0.6 mg/kg). ALD405, but not sumatriptan, blocked the facial hypersensitivity due to SNP. This stress paradigm in mice and the subsequent primed state caused by stress allow further preclinical investigation of mechanisms contributing to migraine, particularly those caused by common triggers of attacks.
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Cancer invading into nerves, termed perineural invasion (PNI), is associated with pain. Here, we show that oral cancer patients with PNI report greater spontaneous pain and mechanical allodynia compared with patients without PNI, suggesting that unique mechanisms drive PNI-induced pain. We studied the impact of PNI on peripheral nerve physiology and anatomy using a murine sciatic nerve PNI model. ⋯ Perineural invasion resulted in nerve damage, including axon loss, myelin damage, and axon degeneration. Electrophysiological evidence of nerve injury included decreased conduction velocity, and increased percentage of both mechanically insensitive and electrically unexcitable neurons. We conclude that PNI-induced pain is driven by nerve injury and peripheral sensitization in HTMRs.