Pain has been defined as ‘an unpleasant sensory and emotional experience associated with actual or potential tissue damage’ by the International Association for the Study of Pain (IASP), which has become the parent organisation for many national pain societies. This definition has arisen from a consideration of some of the features of pain as a multimodal experience. These include:

• Pain has a protective function, and may or may not be associated with tissue damage.

• Pain should not be equated to nociception. Nociception is usually a component of pain symptoms but not necessarily so.

• Intrinsic modulatory mechanisms exist in the body which attenuate the intensity of the pain experience.

• Sensitisation mechanisms exist which intensify pain symptoms, resulting in the phenomenon of hyperalgesia.

• Pain possesses a subjective and affective element as a result of connections between the pain system, the cortical centres and the limbic system.

• Pain levels are also influenced by past experience and anticipation, due to interaction between the pain system and the prefrontal cortex.

• Pain can affect visceral and neuroendocrine function as a result of interconnections with medullary centres and the hypothalamus.

Nociception

Nociception is the sensory modality by which noxious stimuli are detected peripherally, and transmitted centrally to the central nervous system (Figure PP1). Noxious stimuli may or may not be associated with tissue damage. The pathway by which nociception is mediated consists of:

• Nociceptors

• Dorsal root ganglia containing the body of the nociceptor

• The dorsal horn of the spinal cord

• The primary synapse

• Ascending tracts

• The thalamus and higher centres

Nociceptors

The primary afferent neurones for pain are referred to as nociceptors, which possess specialised nerve endings existing in almost all tissues of the body.