Pain
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Central poststroke pain (CPSP) is a specific pain condition arising as a direct consequence of a cerebrovascular lesion. There is limited knowledge about the epidemiology and clinical characteristics of this often neglected but important consequence of stroke. In this population-based study, a questionnaire was sent out to all (n=964) stroke patients identified through the Danish National Indicator Project Stroke Database in Aarhus County, Denmark, between March 2004 and February 2005. ⋯ The minimum prevalence of definite or probable CPSP in this population is 7.3% and the prevalence of CPSP-like dysesthesia or pain is 8.6%. Pinprick hyperalgesia was present in 57%, cold allodynia in 40%, and brush-evoked dysesthesia in 51% of patients with CPSP. Because of its negative impact on quality of life and rehabilitation, pain is an important symptom to assess in stroke survivors.
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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.