Abstract
The confusion amongst clinicans and basic scientists as to what precisely pain is, is emblematic of the difficulties that confront all who attempt to elucidate its pathogenesis. A major contributor to this state of affairs would appear to have been Charles Sherrington. At the turn of the century, with great insight, he focussed attention away from pain itself onto the stimulus in the periphery. In attempting to link stimulus and response in a quantifiable way, he argued that while pain may be caused by a diversity of circumstances, it was commonly associated with peripheral injury. For those categories of stimuli that were of sufficient intensity to threaten, or to produce tissue injury, he coined the term “noxious”. Noxious stimuli he argued, are detected by specialized high threshold sense organs, “nociceptors” and these uniquely signal to the central nervous system, the occurence of tissue damage (Sherrington 1906). The appeal of Sherrington’s analysis lies in its simplicity, for it implies that once a noxious stimulus activates a set of nociceptors, a chain of circumstances (sensory processing within the central nervous system) is initiated that concludes with the perception of a sensory state that we call pain. Such a view has for long dominated the study of the neurobiology of pain (Perl 1985, Willis 1985).
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Woolf, C.J. (1987). Physiological, Inflammatory and Neuropathic Pain. In: Symon, L., et al. Advances and Technical Standards in Neurosurgery. Advances and Technical Standards in Neurosurgery, vol 15. Springer, Vienna. https://doi.org/10.1007/978-3-7091-6984-1_2
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