The ability to perceive pain from cutaneous to deeper tissues and organs is part of the normal sensory repertoire of many animal species. Nonetheless, ongoing chronic pain substantially reduces the quality of life of suffering patients, often accompanied with co-morbidities that further add to the socioeconomic burden of chronic pain. Pain harnesses many neuronal systems from the periphery along the central neuraxis to higher centres of the brain. Following tissue or nerve injury, sustained activity in peripheral afferents can significantly increase the excitability of spinal cord neurones and higher centres in the brain, producing central sensitisation with ensuing pain and altered sensory function.
This talk will outline our current understanding of pain pathways in the peripheral and central nervous system. The significant role of supraspinal influences and changes in spinal excitability in the development and maintenance of abnormal sensitivity in chronic pain states will be discussed. Indeed, descending projections from the brain to the spinal cord can protect again persistent pain, e.g. in placebo analgesia, and central sensitization can occur in the absence of peripheral pathology, e.g. after opioid-induced hyperalgesia. This talk will cover the pro-nociceptive changes that occur in peripheral, spinal and supraspinal centres in chronic pain states and relate this to potential improvement of targeted analgesic therapies.
Disclosure of Interest None declared