Anatomy and physiology of pain

It is apparent that the ‘pain pathway’ is not a static, hard-wired component of the nervous system, but is a very dynamic one. Both the nature of the peripheral stimulus and the degree of tissue damage can influence the level of neuronal activity and even the actual phenotype of the primary sensory neurone. This in turn can have major effects on signal processing at spinal level, initiating long-term changes within the spinal cord which alter all subsequent processing of sensory information. Any attempt to produce analgesia with local anaesthetics or other agents which act at the various accessible points in the pathway (Figure 2.7) must therefore take account of the changes which may already have occurred, and also of the possibility of preventing the development of detrimental long-term changes. Clinical implementation of the theory of ‘pre-emptive analgesia’, that is, inducing impulse block prior to injury to prevent the initiation and development of peripheral and central sensitization, remains controversial. Much of the work from animal studies supports the effectiveness of pre-treatment, but the results from clinical studies have been disappointing (Dahl & Moiniche 2004, Kissin 2000), perhaps because of the complexity and plasticity of the system. It is now clear that a multiplicity of neurotransmitters are involved at a variety of sites so that use of a single agent is almost bound to fail. It has become evident, therefore, that optimal analgesia can only be obtained by using a ‘balanced’ or ‘multi-modal’ approach (Kehlet & Dahl 1993), that is, systemic analgesics (e.g. opioids and non-steroidal anti-inflammatory drugs) combined with site-directed local anaesthetics (Wilmore & Kehlet 2001)