Phys Med Rehab Kuror 2015; 25 - IS06
DOI: 10.1055/s-0035-1554819

Hot Topics in Life Sciences: Genetic Variability, Pain and Disability

J Gjerstad 1
  • 1University of Oslo and Research Scientist at National Institute of Occupational Health (NIOH), Oslo, NO

Most pain states are temporary, i.e. the pain intensity is reduced along with the healing process. For some patients, however, pain persists and may become chronic. Such persistent pain conditions are often associated with a prolonged inflammatory process, which in turn may be related to functional cellular changes in the pain pathways.

Earlier studies show that tissue damage associated with long-lasting inflammation enhances the neuronal activity in the sensory system. For example previous findings show that intervertebral disc herniation, and subsequent leakage of nucleus pulposus (NP) out of the disc, increases the excitability of the primary afferent nerve roots and dorsal horn neurons. NP induces inflammatory and immunological responses that involve interleukin-1 (IL-1) and human leukocyte antigen II (HLA II). In addition, the mu-opioid receptor 1 (OPRM1) and the enzyme Catechol-O-metyltransferase (COMT) in the brain may be important for the supraspinal nociceptive modulation.

We all carry the same genes, but the exact DNA code may vary between individuals that affects a number of physiological processes. Hence, genetic variability may also be important for pain. The present lecture emphasizes that genetic variability may affect both the local inflammatory and immunological responses following disc herniation mentioned above, as well as the supraspinal nociceptive modulation. Better understanding of the mechanisms underlying these neurobiological features may be important for future management of persistent pain conditions.


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