Neuropathic pain mechanisms and imaging

Semin Musculoskelet Radiol. 2015 Apr;19(2):103-11. doi: 10.1055/s-0035-1547371. Epub 2015 Mar 12.

Abstract

Molecular and cellular imaging of neuropathic pain, utilizing the myriad of receptors and inflammatory mediators involved in nociceptive activity, is a promising approach toward objectively identifying peripheral pain generators. Neuropathic conditions arise from injured and inflamed nerves, which have been shown to elaborate several molecular and cellular elements that give rise to the neuropathic phenotype and can be exploited for imaging purposes. As such, in vivo approaches to image neuropathic pain mechanisms include imaging voltage-gated sodium channels with radiolabeled saxitoxin, calcium signaling with manganese-enhanced magnetic resonance imaging, and inflammatory changes and nerve metabolism with (18)F-fluorodeoxyglucose. Imaging approaches exploiting other mediators of nociceptive activity, such as substance P (neurokinin-1) receptor, sigma-1 receptor, and macrophages, have shown promising early advances in animal models. By combining the sensitivity and specificity of molecular imaging with the high anatomical, spatial and contrast resolution afforded by computed tomography and MRI, radiologists can potentially identify sites of nerve injury or neuroinflammation that are implicated as peripheral pain drivers with greater accuracy and confidence. In addition to guiding therapy, these approaches will aid in new drug designs for analgesia and more individualized treatment options.

Publication types

  • Review

MeSH terms

  • Contrast Media
  • Humans
  • Image Enhancement / methods
  • Image Interpretation, Computer-Assisted / methods
  • Inflammation Mediators / analysis
  • Ion Channels / metabolism
  • Magnetic Resonance Imaging / methods*
  • Neuralgia / diagnosis*
  • Neuralgia / physiopathology*
  • Peripheral Nerves / pathology*
  • Peripheral Nervous System Diseases / diagnosis*
  • Positron-Emission Tomography / methods*

Substances

  • Contrast Media
  • Inflammation Mediators
  • Ion Channels