DOI: 10.36347/sasjm.2015.v01i03.009

Pages: Page: 102-107

Anatomy of human pain pathway is complex. It starts with the primary sensory neurons in the periphery, conduction to the spinal cord through afferent neurons, and processing at multiple higher levels that include the dorsal horn, spinal projections, thalamus, and cortex. Transmission of painful stimulus and its processing involves different ion channels, receptors, and various chemical mediators. Different sodium channels, especially Nav1.7 are expressed preferentially in most slowly conducting nociceptive neurons and in sympathetic neurons. Dysregulated expression of voltage-gated sodium channels can produce neuronal hyperexcitability associated with severe pain, whereas loss of the Nav1.7 channel in patients leads to indifference to pain. Interestingly, certain factors of human pain perception can be inherited like acute pain thresholds, efficacy of analgesics, inclination of developing chronic pain, etc. Mutation of the genes encoding for ion channels can cause heritable pain disorders by abnormal channel function or expression. Discovery of genetic mutations and of additional variants that likely to be identified in the future will open up the possibility of understanding chronic pain accurately, at the molecular level. The understanding of the pain pathway at the molecular level may lead to new therapeutic strategies that will bring us closer to more effective treatments for pain.