Pain pathways in orthopaedic practice.

Abstract

DESPITE Steindler's (1959) admirable lectures on the subject, pain in orthopiedic practice remains a difficult problem. To some extent the difficulty is exaggerated by the adoption of diagnoses based on pathological processes which are insusceptible of proof-diagnoses for which it is impossible to establish an association between symptoms and their alleged origin, let alone a direct causal link. For instance a nipped zygapophyseal synovial fringe may well cause acute symptoms, but as there is no means of examining the synovia of zygapophyseal joints, to make this the diagnosis is purely speculative. Nevertheless pathological guesswork of this sort is regrettably common, and when some of the latest advances in neurophysiology, for example the experimental evidence that higher brain activity may modify incoming sensory impulses, are added to the mixture, one even hears talk of such things as the psychosomatic causes of slipped disc. This is a pity because with adequate precision in both history taking and examination, particularly with regard to the mechanistic and neurological aspects, there is usually enough objective evidence at hand to obviate the need for guessing. Furthermore such evidence will probably fit in quite logically with what is known of the physiology of pain. Unfortunately there is little reference made by the authorities to what in orthopoedic medicine is a common clinical phenomenon. This is that pain pathways in general, and referred pain in particular, are pathological rather than physiological processes; or in other words local pathological changes have to be present before peripherally referred pain can be manifest. Healthy tissue may eventually become the seat of referred pain either because the primary lesion imposes a mechanical strain upon it, or because the primary lesion subjects it to unrelieved nervous irritation, or a combination of both. But until local changes of one sort or another have deprived it of health and caused an increased nervous discharge of impulses to originate from it, it cannot be the site for referred pain. A number of pathological factors,