Challenges in cancer pain management-bone pain

L. Colvin, M. Fallon

Research output: Contribution to journalArticlepeer-review

Abstract

Whilst not strictly a neuropathic injury, cancer-induced bone pain (CIBP) is a unique state with features of neuropathy and inflammation. Recent work has demonstrated that osteoclasts damage peripheral nerves (peptidergic C fibres and SNS) within trabeculated bone leading to deafferentation, In addition, glia cell activation and neuronal hyperexcitability within the dorsal horn, are all similar to a neuropathy. Gabapentin and carbamazepine (both anti-convulsants that modulate neuropathy) are effective at attenuating dorsal horn neuronal excitability and normalizing pain-like behaviours in a rat model of CIBP. However alterations in neuroreceptors in the dorsal horn do not mimic neuropathy, rather only dynorphin is upregulated, glia cells are active and hypertrophic and c-fos expression is increased post-noxious behavioural stimulus. CIBP perhaps illustrates best the complexity of cancer pains. Rarely are they purely neuropathic, inflammatory, ischaemic or visceral but rather a combination. Management is multimodal with radiotherapy, analgesics (opioids, NSAIDs), bisphosphonates, radioisotopes and tumouricidal therapies. The difficulty with opioids relates to efficacy on spontaneous pain at rest and movement- related pain. Potential adjuvants to standard analgesic therapies for CIBP are being explored in clinical trials and include inhibitors of glutamate release. (c) 2008 Elsevier Ltd. All rights reserved.

Original languageEnglish
Pages (from-to)1083-1090
Number of pages8
JournalEuropean Journal of Cancer
Volume44
Issue number8
DOIs
Publication statusPublished - May 2008

Keywords

  • palliative care
  • cancer-induced bone pain
  • cancer pain
  • DORSAL-HORN NEURONS
  • NERVE GROWTH-FACTOR
  • MURINE MODEL
  • SPINAL-CORD
  • SENSORY NEURONS
  • DESCENDING FACILITATION
  • NEUROCHEMICAL CHANGES
  • SELECTIVE-INHIBITION
  • INFLAMMATORY PAIN
  • PROSTATE-CANCER

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