Pain
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Diabetic polyneuropathy (DPN) is a common complication of diabetes and is often associated with neuropathic pain. The mechanisms underlying development and maintenance of painful DPN are largely unknown, and quantification of intraepidermal nerve fiber density from skin biopsy, one of the neuropathological gold standard when diagnosing DPN, does not differentiate between patients with and without pain. Identification of possible pain pathophysiological biomarkers in patients with painful DPN may increase our knowledge of mechanisms behind neuropathic pain. ⋯ Peptidergic nerve fiber density correlated with pain ratings in patients with pain (R = 0.33; P = 0.019), but not with quantitative sensory testing results. In this article, we show, for the first time in humans, an increased density of dermal peptidergic fibers in painful DPN. These findings provide new insight in the pathophysiological mechanisms of pain in diabetes and open the research towards new therapeutic targets.
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This article consists of 2 separate studies in which the overarching aim was to examine the relationships between caregiver-child behaviours in the vaccination context (infant and preschool) and preschool attachment outcomes. It provides for the first time an examination of acute pain behaviours during early childhood and how it relates to a critical aspect of child development (ie, attachment status) at the end of early childhood. Study 1 examined the longitudinal relationships between caregiver-infant behaviours during infants' first routine vaccination (2 months) and preschool attachment (n = 84). ⋯ Specifically, higher caregiver sensitivity at preschoolers' 4- to 5-year vaccinations was related to higher preschooler attachment security. The study findings provide evidence that child-caregiver behavioural patterns during the infant and preschool routine vaccination relate to preschoolers' patterns of attachment. Moreover, it underscores the potential importance of health professionals teaching and supporting attuned caregiving to the child in pain.
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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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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.