Pain
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Heart rate variability (HRV) and baroreflex sensitivity (BRS) are indexes reflecting the ability to maintain cardiovascular homeostasis amidst changing conditions. Evidence primarily from small studies suggests that both HRV and BRS may be reduced in individuals with chronic pain (CP), with potential implications for cardiovascular risk. We compared HRV and BRS between individuals with CP (broadly defined) and pain-free controls in a large unselected population sample. ⋯ Results were somewhat weaker for the post-CPT period. Mediation analyses indicated that for 6 of 7 HRV and BRS measures tested, there were significant indirect (mediated) effects of CP status on the presence of comorbid hypertension via reduced HRV or BRS. Results confirm in the largest and broadest sample tested to date that the presence of CP is linked to impaired cardiovascular regulation and for the first time provide support for the hypothesis that links between CP and comorbid hypertension reported in previous population studies may be due in part to CP-related decrements in cardiovascular regulation.
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Pyrethroid insecticides are widely used for pest control in agriculture or in human public health commonly as a topical treatment for scabies and head lice. Exposure to pyrethroids such as permethrin or tetramethrin (TM) causes sensory alterations such as transient pain, burning, stinging sensations, and paraesthesias. Despite the well-known effects of pyrethroids on sodium channels, actions on other channels that control sensory neuron excitability are less studied. ⋯ In TRESK knockout mice, pain-associated behaviors elicited by TM were enhanced, providing further evidence for a role of this channel in preventing excessive neuronal activation. Our results indicate that inhibition of K2P channels facilitates sensory neuron activation and increases their excitability. These effects contribute to the generation of paraesthesias and pain after pyrethroid exposure.
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Chronic pain conditions are highly comorbid with insufficient sleep. While the mechanistic relationships between the 2 are not understood, chronic insufficient sleep may be 1 pathway through which central pain-modulatory circuits deteriorate, thereby contributing to chronic pain vulnerability over time. To test this hypothesis, an in-laboratory model of 3 weeks of restricted sleep with limited recovery (5 nights of 4-hour sleep per night followed by 2 nights of 8-hour sleep per night) was compared with 3 weeks of 8-hour sleep per night (control protocol). ⋯ These changes may reflect abnormalities in central pain-modulatory processes. Limited recovery sleep did not completely resolve these alterations in pain-modulatory processes, indicating that more extensive recovery sleep is required. Results suggest that exposure to chronic insufficient sleep may increase vulnerability to chronic pain by altering processes of pain habituation and sensitization.
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Chronic pain is common and creates a significant burden to the individual and society. Emerging research has shown the influence of the family environment on pain outcomes. However, it is not clear what shared factors between family members associate with chronic pain. ⋯ There was an increase in odds of chronic pain if exposure family member had chronic pain (odds ratio [OR]: 1.30, 95% confidence interval [CI]: 1.02-1.65), if both were women (OR: 1.39, 95% CI: 0.99-1.94), if both were older in age (OR: 1.80, 95% CI: 1.31-2.48), and if both had low household income (OR: 3.27, 95% CI: 1.72-6.21). These findings show that most explanation for chronic pain is still at the individual level. However, some significant shared effects between family members associate with chronic pain, and this highlights the influence of the family context.