The journal of pain : official journal of the American Pain Society
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The purpose of this study was to determine the types of nonverbal cues that informal family caregivers use to evaluate pain in loved ones with dementia. Moreover, we sought to determine the extent to which caregiver characteristics such as mood, empathy, and sex are associated with caregiver ratings of patient pain. Long-term care home residents with dementia were filmed while at rest and while they were engaging in discomforting movements (eg, routine transfers). Informal caregivers (ie, family members) observed the videos of their loved ones and rated the amount of pain that the patients were expressing. Contrary to expectations, caregiver ratings of pain were not related to any specific pain behaviours, suggesting that nonverbal pain cues were either disregarded or not noticed by the caregivers. The total number of pain behaviors expressed by patients was related to caregiver ratings of pain intensity only among caregivers who spent relatively more time with the patient each week. Caregiver empathy, mood, sex or other demographic characteristics were not predictive of caregiver ratings. Instead, it appears that caregivers relied on context in making the pain determinations. ⋯ Informal caregivers (ie, family members) of persons with dementia who reside in long-term care facilities do not generally take into account specific pain behaviors when evaluating pain in their loved ones. Interventions designed to help caregivers become more attentive to specific pain cues might be important to pursue.
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Cytokines, essential mediators of inflammatory and immune responses, play an important role in the pathophysiological processes associated with neuropathic pain following peripheral nerve injury. Recently, a novel proinflammatory cytokine, the interleukin (IL)-17, was found to orchestrate inflammatory responses in a wide range of inflammatory and autoimmune diseases of the nervous system. Here, we investigated the role of IL-17 in mediating neuroinflammation and pain hypersensitivity using the neuropathic pain model of partial ligation of the sciatic nerve in mice. Compared to wild-type, IL-17 knockout (KO) mice displayed significantly decreased mechanical pain hypersensitivity as well as decreased infiltration of T cells and macrophages to the injured sciatic nerves and the L3-L5 dorsal root ganglia and decreased activation of microglia and astrocytes in the L3-5 dorsal and ventral horns of the spinal cord. Further, intraplantar and intraneural injection of recombinant IL-17 into the hind paw and the sciatic nerve, respectively, induced both mechanical allodynia and thermal hyperalgesia, whereas intrathecal injection produced thermal hyperalgesia. IL-17 administration was associated with a significant increase in the numbers of infiltrating neutrophils and activated dendritic cells in the injected hind paws and infiltrating neutrophils in the injected sciatic nerves. Taken together, our results demonstrate that IL-17 contributes to the regulation of immune cell infiltration and glial activation after peripheral nerve injury and the ensuing neuropathic pain. ⋯ IL-17 is an important regulator of immune responses and is involved in inducing and mediating proinflammatory reactions. Using IL-17 KO mice, we have demonstrated that IL-17 contributes to neuroinflammatory responses and pain hypersensitivity following neuropathic injury. This work identifies IL-17 as a potential therapeutic target in neuropathic pain.