Pain
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Conditioned pain modulation (CPM) (ie, diffuse noxious inhibitory controls) is characterized by reduced perception of pain caused by intense pain in a remote body area. The conditioning stimuli used to trigger CPM causes pain, but also important cardiovascular responses. Higher blood pressure has been associated with reduced pain sensitivity. ⋯ A significant positive association was observed between CPM magnitude and the increase in blood pressure during the CPT. These results show that resting blood pressure values are related to acute pain tolerance, while descending pain inhibition is associated with increases in blood pressure. The rise in blood pressure caused by the conditioning stimulus is an important factor predicting the extent of endogenous pain inhibition in healthy subjects.
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The frequency of not being able to self-report pain after a stroke has not been previously assessed in a population-based sample. We studied the epidemiology of this problem using a cohort of patients hospitalized after a stroke in Olmsted County, Minnesota, from June 1, 2008, to June 1, 2012. Overall, 52 of 388 (13.4%) individuals were unable to provide a meaningful response to either a Faces Pain Scale or Numerical Rating Scale on admission. ⋯ Inability to self-report pain on admission was further associated with either subsequent death during the hospitalization (P<.0001) or an inability to provide self-report on dismissal (P<.0001). Our study further defines the epidemiology of the inability to self-report pain after a stroke as being less common than previously thought. Attempts to validate observational pain scales for poststroke patients should focus on those individuals with aphasia and/or depressed levels of consciousness.
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Temporomandibular joint disorder (TMJD) is known for its mastication-associated pain. TMJD is medically relevant because of its prevalence, severity, chronicity, the therapy-refractoriness of its pain, and its largely elusive pathogenesis. Against this background, we sought to investigate the pathogenetic contributions of the calcium-permeable TRPV4 ion channel, robustly expressed in the trigeminal ganglion sensory neurons, to TMJ inflammation and pain behavior. ⋯ Mice with genetically-impaired MEK/ERK phosphorylation in neurons showed resistance to reduction of bite force similar to that of Trpv4(-/-) mice. Thus, TRPV4 is necessary for masticatory sensitization in TMJ inflammation and probably functions upstream of MEK/ERK phosphorylation in trigeminal ganglion sensory neurons in vivo. TRPV4 therefore represents a novel pronociceptive target in TMJ inflammation and should be considered a target of interest in human TMJD.