The understanding of pain pathophysiology is continuously evolving. Identifying underlying cellular and subcellular pathways helps create opportunities for targeted therapies that may prove to be effective interventions.1
Nociceptive pain is caused by the ongoing activation of A-δ and C-nociceptors in response to a noxious stimulus (e.g. injury, disease, inflammation).
Generally, there is a close correspondence between pain perception and stimulus intensity, and the pain is indicative of real or potential tissue damage.
Differences in how stimuli are processed across tissue types contribute to the pain’s varying characteristics.2
Central sensitization is a major phenomenon, together with peripheral sensitization, which helps understanding chronic or amplified pain.
There is central sensitization after intense or repetitive stimulus of the nociceptor present in the periphery, leading to reversible increase of excitability and of synaptic efficacy of central nociceptive pathway neurons.3
Pain that is classified on the basis of its presumed underlying pathophysiology is broadly categorized as nociceptive, neuropathic and nociplastic pain.2,4
