Pain
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Regional decreases in grey matter volume as detected by magnetic resonance imaging-based volumetry have been reported in several clinical chronic pain cohorts. Here, we used voxel-based morphometry in a nonclinical cohort to investigate whether grey matter alterations also occur in older individuals (aged 40-85 years) from the general population. Based on self-report of pain, we identified 31 pain-free controls, 45 subjects with ongoing pain (low back pain, headache, or lower extremity joint pain) who had at least moderate pain on more than 3 days/month, and 29 individuals with past pain (stopped for >12 months). ⋯ No grey matter volume decreases were found in the group with pain that had stopped for >12 months. These results show that pain-related grey matter volume decreases are present in individuals from the general population. The lack of morphometric anomalies in subjects with past pain supports recent evidence suggesting that pain-related grey matter changes are reversible after cessation of pain.
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Editorial Comment Review
Acupuncture's claims punctured: not proven effective for pain, not harmless.
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Neuropathic pain is associated with reorganization of spinal synaptic circuits, implying that adhesion proteins that normally build and modify synapses must be involved. The adhesion proteins E- and N-cadherin delineate different synapses furnished by nociceptive primary afferents, but dynamic aspects of cadherin localization in relationship to onset, maintenance or reversibility of neuropathic pain are uncharacterized. Here, we find very different responses of these cadherins to L5 spinal nerve transection (SNT)-induced mechanical allodynia and to intrathecal glial derived neurotrophic factor (GDNF), which has potent analgesic effects in this pain model. ⋯ Patterns of immunolabeling for GDNF receptor components GFRα1, NCAM, and RET after L5 SNT suggest that GFRα1 and NCAM are the principal receptors operative in this model. In addition, GFRα1 codistributes with E-cadherin, but not N-cadherin, profiles. Together, these data indicate strikingly divergent patterns of temporal and molecular regulation of different cadherins at distinct nociceptive circuits in response to spinal nerve injury, suggesting that the two cadherins and the circuits with which they are affiliated participate in different aspects of synaptic and circuit reorganization associated with neuropathic pain.
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Many different psychosocial treatments for pain have been described in the literature. All of these treatments have at least some evidence supporting their efficacy. ⋯ An overarching model or framework that includes all of the factors hypothesized to play a role in the effects of these treatments would be useful for (1) understanding the similarities and differences between existing and future psychosocial pain treatments, (2) guiding the psychosocial evaluation of patients with chronic pain, and (3) giving clinicians greater flexibility for including psychosocial interventions that have proven efficacy, but that may not be explained by their preferred (but perhaps limited) model. This article proposes an initial version of such a framework, with the hope that it will increase our understanding of the role that psychosocial factors play in the experience of pain and its negative effects on functioning, and informs future research seeking to identify the common and specific factors associated with psychosocial pain treatments.
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Pain catastrophizing is associated with enhanced temporal summation of pain (TS-Pain). However, because prior studies have found that pain catastrophizing is not associated with a measure of spinal nociception (nociceptive flexion reflex [NFR] threshold), this association may not result from changes in spinal nociceptive processes. The goal of the present study in healthy participants was to examine the relationship between trait (traditional) and state (situation-specific) pain catastrophizing and temporal summation of NFR (TS-NFR) and TS-Pain. ⋯ Trait catastrophizing was not related to TS-Pain or TS-NFR. Together, these results confirm prior studies that indicate that catastrophizing enhances pain via supraspinal processes rather than spinal processes. Moreover, because catastrophizing was associated with TS-Pain but not TS-NFR, caution is warranted when using pain ratings to infer temporal summation of spinal nociceptive processes.