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PAIN

CLASSIC TEACHING RELATING TO PAIN

As anaesthesia is invoked to prevent appreciation of pain, any study of the discipline of anaesthesia must be related to an understanding of what constitutes pain. The old classic teaching on pain involved a hard-wired, modality specific, line specific, single pathway which coupled stimulus with pain sensation. Anatomists labelled the axons and nerve cells according to this single relay transmission system. It commenced in the periphery with fine myelinated (Aδ) and unmyelinated (C-fibre) afferents which possessed such high thresholds for stimulation that they only responded to noxious stimuli. Sherrington (1900) termed these structures ‘nociceptors’ but he realized that impulses in them would not necessarily lead to pain sensation unless the central nervous system accepted them and conveyed them to a pain-perceiving region of the brain. The nociceptor fibres were found to end preferentially on cells in laminae 1, 2 and 5 of the dorsal horn and from there impulses were believed to reach the thalamus by way of spinothalamic fibres which ran in the ventrolateral white matter of the spinal cord. From the thalamus impulses were said to reach a site of pure pain sensation (pain centre) in the association areas of the cerebral cortex. Afferent mechanisms In recent years pain studies have resulted in an almost explosive expansion of knowledge relating to pain mechanisms in the body and have shown that these earlier ideas must be abandoned in favour of an interlocking, dynamic series of biological processes which need still further investigation. It is apparent that in the periphery the old picture of fixed property nociceptor cells in damaged tissue passively detecting the products of cell breakdown does not accurately represent what is actually happening. The tissue breakdown products have been shown to have both direct and indirect effects on sensory afferent nerves. The role of unmyelinated sensory fibres themselves in inflammation as proposed by Lewis (1942) is, however, now well established. Leucocytes attracted into damaged tissues secrete cytokines which have both powerful systemic and local effects. Substances such as nerve growth factor synthetized locally in damaged tissue are also involved in pain production (McMahon et al., 1995). The sympathetic nerves play a role in the inflammatory process, new α adrenergic, bradykinin and opiate receptors appear and there are a group of C-fibres which seem to be completely silent in normal tissue but which are activated by ongoing inflammation. It is now also clear that certain types of pain are produced by afferents with large diameters outside the range of nociceptors.

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