PERIPHERAL AND CENTRAL SENSITIZATION

Abstract

Fundamental neurophysiological processes that underlie the onset and persistence of pain, especially in chronic pain disorders, are peripheral and central sensitisation. Tissue damage or inflammation causes peripheral sensitisation, which lowers activation thresholds and increases peripheral nociceptor responsiveness because inflammatory mediators such prostaglandins, bradykinin, cytokines, and nerve growth factor are released. At the location of damage, this increased excitability plays a role in primary hyperalgesia. Central sensitisation, on the other hand, describes activity-dependent amplification of neural signalling in the central nervous system, which raises the excitability of supraspinal pain pathways and spinal dorsal horn neurones. Clinical symptoms include increased receptive fields, allodynia, secondary hyperalgesia, and pain that persists long after tissue repair.