Pain
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Multicenter Study
Normative data for common pain measures in chronic pain clinic populations: closing a gap for clinicians and researchers.
Normative data for chronic pain questionnaires are essential to the interpretation of aggregate scores on these questionnaires, for both clinical trials and clinical practice. In this study, we summarised data from 13,343 heterogeneous patients on several commonly used pain questionnaires that were routinely collected from 36 pain clinics in Australia and New Zealand as part of the electronic Persistent Pain Outcomes Collaboration (ePPOC) including the Brief Pain Inventory (BPI); the Depression Anxiety and Stress Scales (DASS); the Pain Self-Efficacy Questionnaire (PSEQ); and the Pain Catastrophizing Scale (PCS). The data are presented as summarised normative data, broken down by demographic (age, sex, work status, etc) and pain site/medical variables. ⋯ Scores tended to worsen with age until 31 to 50 years, after which they improved. Scores were worse for those who had a greater number of pain sites, were unemployed, were injury compensation cases, or whose triggering event was a motor vehicle accident or injury at work or home. These results and comparisons with data on the same measures from other countries, as well as their uses in both clinical practice and clinical trials, are discussed.
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Small families carrying rare mutations, which I call "pointer-kindreds," can teach us important lessons. Here, I provide some examples from the field of pain.
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Neuropathic itch is clinically important but has received much less attention as compared to neuropathic pain. In the past decade, itch-specific pathways have been characterized on a cellular and molecular level, but their exact role in the pathophysiology of neuropathic itch is still unclear. Traditionally, mutually exclusive theories for itch such as labeled line, temporal/spatial pattern, or intensity theory have been proposed, and experimental studies in mice mainly favor the specificity theory of itch. ⋯ Rarefication of skin innervation in neuropathy could provide a "spatial contrast" discharge pattern, and axotomy could induce de novo expression of the itch-specific spinal neuropeptide, gastrin-releasing peptide, in primary afferent nociceptors, thereby modulating itch processing in the dorsal horn. Thus, clinical neuropathy may generate itch by changes in the spatial and temporal discharge patterns of nociceptors, hijacking the labeled line processing of itch and abandoning the canonical scheme of mutual exclusive itch theories. Moreover, the overlap between itch and pain symptoms in neuropathy patients complicates direct translation from animal experiments and, on a clinical level, necessitates collaboration between medical specialities, such as dermatologists, anesthesiologists, and neurologists.
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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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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.