The referral of visceral sensations to superficial somatic tissues, a constant feature in visceral nociception, has been known for a long time clinically, but the pathophysiological bases of the phenomenon have been the subject of research investigation only in relatively recent times. The execution of studies in patients in standardized conditions involving quantitative measurement of referred phenomena and the setting up of a number of animal models of visceral nociception (with clear behavioral indicators of referred changes) reproducing the clinical conditions are important advances of the last decades. Basic research studies on these models, often using sophisticated technical approaches, have represented a fundamental step toward identification of neurophysiological and molecular mechanisms underlying referred phenomena, especially the hyperalgesia. Though some interpretative questions still remain open—like the nature of referred dystrophic changes accompanying secondary hyperalge-sia—the results so far obtained cast a new light on the generation and the mediators of the referred component of nociception from internal organs. This opens new avenues for treatment strategies, not merely symptomatic, of one of the most prominent forms of pain that a human being can experience in the medical context.

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