Nociception & Peripheral Sensitisation

Nociception and peripheral sensitization are introduced as key peripheral contributors to pain within a broader clinical model. The teaching reviews how different stimuli—mechanical, thermal, and chemical—activate receptors in tissues, generate action potentials, and send signals through primary afferent fibers to the spinal cord and brain. It also clarifies the roles of A-alpha, A-beta, A-delta, and C fibers, with emphasis on nociceptors as warning systems rather than “pain receptors.” Inflammation is then linked to increased sensitivity in peripheral nerves. Learners are shown how tissue injury can alter local chemistry, open ion channels, and lower the threshold for nociceptor activation, producing peripheral sensitization. Common clinical features such as primary and secondary hyperalgesia are explained, along with situations where sensitization may become persistent, including recurrent inflammation and systemic low-grade inflammation. The session also develops clinical reasoning for acute and persistent pain: whether symptoms fit expected healing, whether healing is delayed, and when central mechanisms should be considered. A case of longstanding low back pain is used to identify possible peripheral nociceptive sources and to consider movement-based strategies that may reduce ongoing nociceptive input.