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Journal Cover British Journal of Pain  
   [11 followers]  Follow    
   Hybrid Journal Hybrid journal (It can contain Open Access articles)
   ISSN (Print) 2049-4637 - ISSN (Online) 2049-4645
   Published by Sage Publications Homepage  [756 journals]
  • Guest Editorial
    • Authors: Farquhar-Smith, P; Bennett, M.
      Pages: 129 - 129
      PubDate: 2014-11-18T03:28:25-08:00
      DOI: 10.1177/2049463714555888|hwp:resource-id:spbjp;8/4/129
      Issue No: Vol. 8, No. 4 (2014)
  • Editorial
    • Authors: Cox; F.
      Pages: 130 - 130
      PubDate: 2014-11-18T03:28:25-08:00
      DOI: 10.1177/2049463714555440|hwp:resource-id:spbjp;8/4/130
      Issue No: Vol. 8, No. 4 (2014)
  • Cancer pain for the 21st century: stepping off the ladder, stepping up to
           new challenges
    • Authors: Ahmedzai; S. H.
      Pages: 131 - 132
      PubDate: 2014-11-18T03:28:25-08:00
      DOI: 10.1177/2049463714557047|hwp:master-id:spbjp;2049463714557047
      Issue No: Vol. 8, No. 4 (2014)
  • Splice variation of the mu-opioid receptor and its effect on the action of
    • Authors: Gretton, S. K; Droney, J.
      Pages: 133 - 138
      Abstract: Summary points
      An individual’s response to opioids is influenced by a complex combination of genetic, molecular and phenotypic factors.
      Intra- and inter-individual variations in response to mu opioids have led to the suggestion that mu-opioid receptor subtypes exist.
      Scientists have now proven that mu-opioid receptor subtypes exist and that they occur through a mechanism promoting protein diversity, called alternative splicing.
      The ability of mu opioids to differentially activate splice variants may explain some of the clinical differences observed between mu opioids.
      This article examines how differential activation of splice variants by mu opioids occurs through alternative mu-opioid receptor binding, through differential receptor activation, and as a result of the distinct distribution of variants located regionally and at the cellular level.
      PubDate: 2014-11-18T03:28:25-08:00
      DOI: 10.1177/2049463714547115|hwp:master-id:spbjp;2049463714547115
      Issue No: Vol. 8, No. 4 (2014)
  • Pain in cancer survivors
    • Authors: Brown, M. R; Ramirez, J. D, Farquhar-Smith, P.
      Pages: 139 - 153
      Abstract: Cancer and its treatment exert a heavy psychological and physical toll. Of the myriad symptoms which result, pain is common, encountered in between 30% and 60% of cancer survivors. Pain in cancer survivors is a major and growing problem, impeding the recovery and rehabilitation of patients who have beaten cancer and negatively impacting on cancer patients’ quality of life, work prospects and mental health. Persistent pain in cancer survivors remains challenging to treat successfully. Pain can arise both due to the underlying disease and the various treatments the patient has been subjected to. Chemotherapy causes painful chemotherapy-induced peripheral neuropathy (CIPN), radiotherapy can produce late effect radiation toxicity and surgery may lead to the development of persistent post-surgical pain syndromes. This review explores a selection of the common causes of persistent pain in cancer survivors, detailing our current understanding of the pathophysiology and outlining both the clinical manifestations of individual pain states and the treatment options available.
      PubDate: 2014-11-18T03:28:25-08:00
      DOI: 10.1177/2049463714542605|hwp:master-id:spbjp;2049463714542605
      Issue No: Vol. 8, No. 4 (2014)
  • Cancer pain physiology
    • Authors: Falk, S; Bannister, K, Dickenson, A. H.
      Pages: 154 - 162
      Abstract: Mechanisms of inflammatory and neuropathic pains have been elucidated and translated to patient care by the use of animal models of these pain states. Cancer pain has lagged behind since early animal models of cancer-induced bone pain were based on the systemic injection of carcinoma cells. This precluded systematic investigation of specific neuronal and pharmacological alterations that occur in cancer-induced bone pain. In 1999, Schwei et al. described a murine model of cancer-induced bone pain that paralleled the clinical condition in terms of pain development and bone destruction, confined to the mouse femur. This model prompted related approaches, and we can now state that cancer pain may include elements of inflammatory and neuropathic pains but also unique changes in sensory processing. Cancer-induced bone pain results in progressive bone destruction, elevated osteoclast activity and distinctive nocifensive behaviours (indicating the triad of ongoing, spontaneous and movement-induced hyperalgesia). In addition, cancer cells induce an inflammatory infiltrate and release growth factors, cytokines, interleukins, chemokines, prostanoids and endothelins, resulting in a reduction of pH to below 5 and direct deformation of primary afferents within bone. These peripheral changes, in turn, drive hypersensitivity of spinal cord sensory neurons, many of which project to the parts of the brain involved in the emotional response to pain. Within the spinal cord, a unique neuronal function reorganization within segments of the dorsal horn of the spinal cord receiving nociceptive input from the bone are discussed. Changes in certain neurotransmitters implicated in brain modulation of spinal function are also altered with implications for the affective components of cancer pain. Treatments are described in terms of mechanistic insights and in the case of opioids, which modulate pain transmission at spinal and supraspinal sites, their use can be compromised by opioid-induced hyperalgesia. We discuss evidence for how this comes about and how it may be treated.
      PubDate: 2014-11-18T03:28:25-08:00
      DOI: 10.1177/2049463714545136|hwp:master-id:spbjp;2049463714545136
      Issue No: Vol. 8, No. 4 (2014)
  • Pain services and palliative medicine - an integrated approach to pain
           management in the cancer patient
    • Authors: O'Brien, T; Kane, C. M.
      Pages: 163 - 171
      Abstract: The vast majority of cancer patients will experience pain during the course of their illness. Thankfully, in most instances, the consistent application of analgesic guidelines, tailored to the unique needs of each individual patient, will deliver a satisfactory outcome. These guidelines recommend the skilled use of analgesic medications, often in conjunction with a range of adjuvant therapies as may be required. Despite the consistent and rational application of such strategies, it is recognised that a small but significant proportion of cancer patients continue to experience more refractory pain. In addition, these patients may experience a plethora of unwanted dose-limiting side effects associated with their analgesic medication, sometimes even at low dose. All such patients with more complex and refractory pain syndromes require a more comprehensive review and many will require interventional therapy and/or adjuvant approaches. Unfortunately, the availability and accessibility of such services are variable. Even in circumstances in which palliative medicine and pain services co-exist in the same region, there may be poor integration between the two services. Each specialty area holds a unique set of skills and competencies, yet there is considerable overlap. Patient care and outcomes will be enhanced by establishing more formal relationships between these two specialty areas.
      PubDate: 2014-11-18T03:28:25-08:00
      DOI: 10.1177/2049463714548768|hwp:master-id:spbjp;2049463714548768
      Issue No: Vol. 8, No. 4 (2014)
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