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Abstract
Visceral pain has a temporal evolution. Its first phase is a poorly defined, midline sensation (true visceral pain) that soon becomes referred to a somatic region; there it may manifest with or without hyperalgesia. The pathophysiology of symptoms in the various phases differs. The diffuse localization of true visceral pain is probably due to the low density of visceral sensory innervation and extensive divergence of the visceral input within the central nervous system. Although referred pain without hyperalgesia is attributable to the well-documented convergence of both visceral and somatic afferent inputs onto the same central neurons, referred pain with hyperalgesia is more difficult to explain. Central mechanisms may be involved in the hyperalgesia, in terms of a spinal irritable focus triggered by the visceral barrage, which facilitates messages from somatic structures. The intervention of a reflex mechanism has also been suggested.