Pain
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Little is known about risk factors for emergency department (ED) attendance for chronic pain (CP) management and the relative service burden. We examined ED utilisation in patients with CP, identified risk factors associated with attendance for chronic musculoskeletal pain (CMP), and estimated the comparative cost of treatment. The study cohort comprised a random sample of 3700 adults from the general population in Tayside, Scotland. ⋯ Characteristics protective of ED attendance for CMP were: being in receipt of strong opioids (OR = 0.21); transitioning from nonopioid to opioid analgesics (OR = 0.25); recent analgesic dose increases (OR = 0.24); and being prescribed tricyclic antidepressants (OR = 0.10), benzodiazepines (OR = 0.46), or hypnotics (OR = 0.45). Chronic musculoskeletal pain was one of the most expensive conditions to treat (£17,680 [∼$22,668] per annum), conferring a substantial burden on ED services. Improved understanding of the risk/protective factors could inform healthcare redesign to reduce avoidable ED attendances for CMP management.
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Although clinical studies support the suggestion that stress is a risk factor for painful chemotherapy-induced peripheral neuropathy (CIPN), there is little scientific validation to support this link. Here, we evaluated the impact of stress on CIPN induced by oxaliplatin, and its underlying mechanisms, in male and female rats. A single dose of oxaliplatin produced mechanical hyperalgesia of similar magnitude in both sexes, still present at similar magnitude in both sexes, on day 28. ⋯ Also, a risk factor for CIPN, early-life stress, was evaluated by producing both stress-sensitive (produced by neonatal limited bedding) and stress-resilient (produced by neonatal handling) phenotypes in adults. Although neonatal limited bedding significantly enhanced CIPN only in female adults, neonatal handling significantly attenuated CIPN, in both sexes. Our study demonstrates a sexually dimorphic role of the 2 major neuroendocrine stress axes in oxaliplatin-induced neuropathic pain.
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Under some conditions, people persist in their attempts to control their pain even when no such control is possible. Theory suggests that such pain-control attempts arise from actual pain experiences. Across 3 experiments we examined how (1) losing control over pain and (2) instructions concerning pain, moderated pain-control attempts. ⋯ Instead, participants lost control over pain because of an unannounced change in the learning task. Results indicated that when participants lost control over pain, they generally stuck to the previously effective pain-control strategy, and that this tendency was larger if they received instructions from others than when they developed a strategy by themselves. These findings suggest that when pain is no longer controllable, very persistent pain-control attempts might be the result of adherence to previously effective pain-control instructions.
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Quadriparesis after intramuscular trigger point injections for myofascial pain syndrome has been rarely reported in the literature. A 37-year-old male patient presented with myofascial pain syndrome and was given trigger point injections in trapezius muscles under ultrasound guidance. The patient noticed weakness in all the 4 limbs at approximately 12 hours after the procedure, which gradually progressed to functional quadriplegia at the time of presentation to the emergency department. ⋯ Immediate potassium correction with intravenous and oral potassium chloride was initiated, and the patient showed improvement within 6 hours of initiating correction. Stress of the procedure, use of steroids with mineralocorticoid effects such as methylprednisolone, or deranged thyroid function tests may have acted as triggers to precipitate hypokalemic paralysis in the patient. Knowledge of this complication is essential as prompt diagnosis and timely management of hypokalemia can result in complete resolution of the symptoms.
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A common experimental neurophysiological method to study synaptic plasticity is pairing activity of somatosensory afferents and motor cortical circuits, so-called paired associative stimulation (PAS). Dysfunctional inhibitory and excitatory PAS mechanisms within the sensorimotor system were described in patients with migraine without aura (MO) between attacks. We have recently observed that the same bidirectional PAS rules also apply to the visual system. ⋯ Although vPAS-25 significantly enhanced and vPAS + 25 reduced VEP amplitude habituation in healthy volunteers, the same protocols did not significantly change VEP amplitude habituation in MO between attacks. We provide evidence for lack of habituation enhancing and habituation suppressing visual PAS mechanisms within the visual system in interictal migraine. This finding, in combination with those previously obtained studying the sensorimotor system, leads us to argue that migraine disease-related dysrhythmic thalamocortical activity prevents the occurrence of physiological bidirectional synaptic plasticity induced by vPAS.