Neurophysiological Basis of Visceral Pain

Objectives: In spite of visceral pain being a prominent symptom in the clinical setting, its mechanisms have been less explored than those underlying somatic pain. The objectives of this article are to review the current knowledge on pathophysiology of the most prominent phenomena related to visceral nociception, i.e., true visceral pain, referred pain without and with hyperalgesia, visceral hyperalgesia, and viscero-visceral hyperalgesia. Findings: The poor localization and diffuse nature of true visceral pain results from the low density of sensory innervation of the viscera and the extensive functional divergence of the visceral input within the central nervous system [CNS]. Referred pain without hyperalgesia is explained by the phenomenon of "convergence-projection," i.e., convergence of visceral and somatic afferent fibers onto the same sensory neurons at various CNS levels. Referred pain with hyperalgesia is partly due to central sensitization of viscero-somatic convergent neurons [triggered by the massive afferent visceral barrage]. The muscle hyperalgesia also probably results from a reflex arc activation; the visceral input would trigger reflex muscle contraction in turn responsible for sensitization of muscle nociceptors in the area of referral. Recent experimental studies by this group in a rat model of ureteric calculosis support this hypothesis by documenting: a. positivity of a number of morphofunctional indices of skeletal muscle contraction in specimens of the oblique musculature ipsilateral to the stone [site of referred hyperalgesia] and b. c-Fos labeled motoneurons in the spinal cord segments of sensory projection from the ureter. Visceral hyperalgesia, e.g., hypersensitivity of an internal organ due to inflammation, has been attributed to phenomena of both peripheral and central sensitization. Viscero-visceral hyperalgesia, i.e., the enhancement of painful symptoms because of algogenic conditions of two visceral districts sharing part of their sensory innervation [e.g., urinary tract and female reproductive organs] is probably explained, at least in part, by sensitization of viscero-visceral convergent neurons in the CNS. Conclusions: Some aspects of visceral nociception have been fully elucidated, while the pathophysiology of other phenomena-mostly referred hyperalgesia from viscera and viscero-visceral hyperalgesia-still needs clarification. Experimental studies on adequate animal models will hopefully provide a better understanding of these phenomena, leading ultimately to an improvement of diagnostic tools and management of visceral pain in the clinical setting.