The Hyperpathic Syndrome: A Challenge to Specificity Theory
Yngve Zotterman influenced our way of thinking in many ways. One was the tactic he shared with his master, Lord Adrian, which was to start in the periphery and to attribute as many sensory phenomena as possible to particular types of afferent fibres. This eminently sensible initial tactic has been carried to an extreme by a number of authors, into the claim that the sole origin of pain is activity in a particular type of fibre, the nociceptor. Since they have assigned the monopoly of extracting this quality of sensory experience to a specific fibre type in the periphery, the only role they can allow to central synaptic processes is to control the amplitude of sensation without affecting its quality or location. The central nervous system is seen to consist of a series of labelled line pain specific pathways whose gain may change but not their information content. The adherents of the specificity theory are wrong for many reasons, one of which is the subject of this paper, the hyperpathic syndrome. Like any syndrome, this consists of a grouping of signs and symptoms, each present in varying degrees in particular cases. It is necessary to propose a theory to explain the syndrome as an entity and not to explain one fraction such as primary hyperalgesia and then to imply that the whole is explained. We have to explain why the following characteristics are grouped together.
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