Pain
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Chronic pain is associated with brain atrophy with limited evidence on its impact in the older adult's brain. We aimed to determine the associations between chronic pain and a brain aging biomarker in persons aged 60 to 83 years old. Participants of the Neuromodulatory Examination of Pain and Mobility Across the Lifespan (NEPAL) study (N = 47) completed demographic, psychological, and pain assessments followed by a quantitative sensory testing battery and a T1-weighted magnetic resonance imaging. ⋯ An "older" brain was significantly associated with decreased vibratory (r = 0.323; P = 0.033) and thermal (r = 0.345; P = 0.023) detection, deficient endogenous pain inhibition (F[1,25] = 4.6; P = 0.044), lower positive affect (r = -0.474; P = 0.005), a less agreeable (r = -0.439; P = 0.020), and less emotionally stable personality (r = -0.387; P = 0.042). Our findings suggest that chronic pain is associated with added "age-like" brain atrophy in relatively healthy, community-dwelling older individuals, and future studies are needed to determine the directionality of our findings. A brain aging biomarker may help identify people with chronic pain at a greater risk of functional decline and poorer health outcomes.
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Multiple sclerosis (MS) is a neurodegenerative autoimmune disease with many known structural and functional changes in the central nervous system. A well-recognized, but poorly understood, complication of MS is chronic pain. Little is known regarding the influence of sex on the development and maintenance of MS-related pain. ⋯ We propose that tactile hypersensitivity in female EAE mice may be more immune-driven, whereas pain in male mice with EAE may rely more heavily on neurodegenerative and plasticity-related mechanisms. Morphological and inflammatory differences in the spinal cord associated with pain early in EAE progression supports the idea of differentially regulated pain pathways between the sexes. Results from this study may indicate future sex-specific targets that are worth investigating for their functional role in pain circuitry.
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The traditional translational approach in neuropathic pain research has mainly consisted to date in translating basic findings from animal models of nerve injury to the clinic. Because of the difficulty to extrapolate mechanisms from animals to humans, an inverse translational approach ("top-down") has been advocated and contributed to the development of therapy. ⋯ The biggest trend in recent translational research is to investigate mechanisms or predict therapeutic response in patients by integrating multimodal approaches. The present narrative review emphasizes these various aspects of translational research in neuropathic pain.
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Post-traumatic headache (PTH) is one of the most common, debilitating, and difficult symptoms to manage after a traumatic head injury. Although the mechanisms underlying PTH remain elusive, recent studies in rodent models suggest the potential involvement of calcitonin gene-related peptide (CGRP), a mediator of neurogenic inflammation, and the ensuing activation of meningeal mast cells (MCs), proalgesic resident immune cells that can lead to the activation of the headache pain pathway. Here, we investigated the relative contribution of MCs to the development of PTH-like pain behaviors in a model of mild closed-head injury (mCHI) in male rats. ⋯ Our data, however, also reveal that the development of latent sensitization, manifested as persistent hypersensitivity upon the recovery from mCHI-evoked acute cranial hyperalgesia to the headache trigger glyceryl trinitrate requires intact MC content during and immediately after mCHI. Collectively, our data implicate the acute activation of meningeal MCs as mediator of chronic pain hypersensitivity after a concussion or mCHI. Targeting MCs may be explored for early prophylactic treatment of PTH.