The journal of pain : official journal of the American Pain Society
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Bestrophin-1, a calcium-activated chloride channel (CaCC), is involved in neuropathic pain; however, it is unclear whether it has a dimorphic role in female and male neuropathic rats. This study investigated if 17β-estradiol and estrogen receptor alpha (ERα) activation regulate bestrophin-1 activity and expression in neuropathic rats. Neuropathic pain was induced by L5-spinal nerve transection (SNT). ⋯ PERSPECTIVE: The mechanisms involved in neuropathic pain differ between male and female animals. Our data suggest that ERα is necessary for expression and function of bestrophin-1 in neuropathic female but not male rats. Data support the idea that a therapeutic approach to relieving neuropathic pain must be based on patient's gender.
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Exacerbation of pain by chronic stress and comorbidity of pain with stress-related disorders such as depression and post-traumatic stress disorder, represent significant clinical challenges. Previously we have documented that chronic forced swim (FS) stress exacerbates neuropathic pain in spared nerve injury (SNI) rats, associated with an up-regulation of GluN2B-containing N-methyl-D-aspartate receptors (GluN2B-NMDARs) in the central nucleus of the amygdala (CeA). However, the molecular mechanisms underlying chronic FS stress (CFSS)-mediated exacerbation of pain sensitivity in SNI rats still remain unclear. ⋯ These findings suggest that activation of CRF/CRFR1 signaling in the CeA contributes to chronic stress-induced exacerbation of neuropathic pain by enhancing GluN2B-NMDAR-mediated synaptic plasticity in rats subjected to nerve injury. PERSPECTIVE: Our present study provides a novel mechanism for elucidating stress-induced hyperalgesia and highlights that the CRF/CRFR1 signaling and the GluN2B-NMDAR-mediated synaptic plasticity in the CeA may be important as potential therapeutic targets for chronic stress-induced pain exacerbation in human neuropathic pain. DATA AVAILABILITY: The data that support the findings of this study are available from the corresponding author upon reasonable request.
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Review Meta Analysis
SOMATOSENSORY PROFILING OF PATIENTS WITH CLUSTER HEADACHE: A SYSTEMATIC REVIEW AND META-ANALYSIS.
The objectives were 1) to synthesize quantitative sensory testing results in cluster headache (CH) patients and to identify somatosensory differences from healthy subjects (HS), and 2) between symptomatic and asymptomatic sides in CH patients. Two independent reviewers conducted a literature search in MEDLINE, EMBASE, Web of Science, and CINAHL databases. Studies with observational designs were included. ⋯ These results are of clinical relevance because their presence could be associated with a poorer prognosis, chronification, and treatment response. PERSPECTIVE: This study provides consistent findings on the somatosensory profile characterizing patients with CH. Clinicians should assess PPTs and other quantitative sensory testing variables in the trigeminal and extratrigeminal (cervical) regions.
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Though pain sensitivity impairments contribute to chronic pain in younger adults, it is unclear if pain hypersensitivity manifests with aging and is heightened in the geriatric chronic low back pain population. The cross-sectional study preliminarily addressed this gap by measuring pain sensitivity in older adults with chronic low back pain (n = 25) as well as pain-free sex-matched older (n = 25) and younger adults (n = 25). Pain sensitivity was quantified by 8 distinct measures that were subdivided as static (ie, pressure pain thresholds, heat pain thresholds, fixed mechanical pain, and fixed cold pain) and dynamic pain sensitivity (ie, mechanical temporal summation, thermal ramp and hold, heat pain aftersensations, and conditioned pain modulation). ⋯ Further study is needed to more definitively parse out whether pain hypersensitivity is comparatively heightened in older adults with chronic LBP beyond the influence of chronological aging. PERSPECTIVE: This article establishes that surrogate measures of centrally mediated pain sensitization are heightened with aging. Impaired endogenous pain modulation may influence chronic pain development, maintenance, treatment efficacy, and/or ensuing disability, necessitating research to comprehensively characterize how pain hypersensitivity contributes to geriatric chronic pain conditions.