Abstract
IT is common experience that inflamed tissues are hypersensitive to pain. Direct experiments have shown that this hypersensitivity may result from the increased sensitivity of the receptors in the injured tissues1. On the other hand, MacKenzie2, as far back as 1893, suggested that hypersensitivity could be the result of increased sensitivity of structures in the central nervous system. According to this investigator, sensory impulses arising in the injured tissues create an “irritable focus” in the segment of the spinal cord at which they enter. As a result a stimulus which would not evoke a sensation of pain in undamaged tissue begins to do so, if the afferent impulses set up by the stimulus reach the “irritable focus”. Participation of central mechanisms in the development of hyperaesthesia was then confirmed by a number of observations3–7. It has not yet been made clear, however, just where this “irritable focus” is created—that is, at which synaptic relay the facilitation elicited by impulses arising in the injured tissues occurs. A number of suggestions have been made previously5,8,9, but none is satisfactory.
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SMOLIN, L., SAMKO, N. Central Mechanism of Hyperaesthesia. Nature 211, 1412–1413 (1966). https://doi.org/10.1038/2111412a0
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DOI: https://doi.org/10.1038/2111412a0
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