ABSTRACT

Higher cortical centres can modify the sensation of pain through descending pathways to the thalamus and dorsal horn. Furthermore, pain itself can cause amplification of its own pathway.

As well as the initial stimulation of nociceptors, painful stimuli also often cause the initiation of an inflammatory response, leading to the release of inflammatory mediators from plasma activated by tissue damage and from the nerve terminals themselves. These inflammatory mediators, which include cytokines, prostaglandins, leukotrienes and bradykinin, cause vasodilatation and oedema, as well as stimulate nociceptive pathways themselves, and thus worsen the algesia (pain).