Abstract
Almost without exception man is familiar with the experience we call “pain”. It is a matter of concern because of its frequent, though not infallible, warning of personal damage or danger, arousing protective reflexes and courses of action. From Plato and Aristotle until about the time of Avicenna, in the 11th century (see Dallenbach, 1939; K. D. Keele, 1962; Procacci, 1969) it was regarded as a “passion of the soul” believed to result from “overstimulation” of any of the senses. Avicenna’s suggestion of its being a separate sense was borne out experimentally by the work of Schiff (1858), who by appropriate cord section was able to distinguish touch and pain as separate events following separate tracts and not mutually extinguishable. Even later, Goldscheider (1916) still adhered to the physical overstimulation theory but limited his ideas to those of “pressure overstimulation”. He was opposed, chiefly by von Frey (1922), who not only believed pain to be a separate sense but also that it was mediated by receptor organs of its own—free nerve endings This does not imply that pain is the only sensation initiated by stimulation of free nerve endings (Nafe and Wagoner, 1937; Sjöquist, 1938). Weddell (1947) showed that some presumed pain-nerve endings are connected to myelinated nerve fibers (rapidly conducting) and some to unmyelinated (slowly conducting) nerve fibers. Head (1920), Woollard et al. (1940), Iggo (1962), and others suggest that the complete pain picture will be modified by the relative distribution of stimulation between the peripheral nerve elements affected, and that the general distribution of stimulation in space, peripherally, will also affect the mental picture as a whole.
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Armstrong, D. (1970). Pain. In: Erdös, E.G., Wilde, A.F. (eds) Bradykinin, Kallidin and Kallikrein. Handbook of Experimental Pharmacology / Handbuch der experimentellen Pharmakologie, vol 25 / 25. Springer, Berlin, Heidelberg. https://doi.org/10.1007/978-3-642-46222-1_22
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