title: [Pathophysiology of abdominal pain].
abstract: Abdominal pain can be induced by stimulation of visceral nociceptors. Activation of nociceptors usually requires previous sensitization by pathological events, such as inflammation, ischemia or acidosis. Although abdominal pain can obviously be caused by pathology of a visceral structure, clinicians frequently observe that such a pathology explains only part of the pain complaints. Occasionally, there is lack of objective signs of visceral lesions. There is clear evidence that pain states are associated with profound changes of the central processing of the sensory input. The main consequences of such alterations for patients are twofold: 1) a central sensitization, i.e. an increased excitability of the central nervous system; 2) an alteration of the endogenous pain modulation, which under normal conditions inhibits the processing of nociceptive signals in the central nervous system. Both phenomena lead to a spread of pain to other body regions and an amplification of the pain perception. The interactions between visceral pathology and alterations of the central pain processes represent an at least partial explanation for the discrepancy between objective signs of peripheral lesions and severity of the symptoms. Today, both central hypersensitivity and alteration in endogenous pain modulation can be measured in clinical practice. This information can be used to provide the patients with an explanatory model for their pain. Furthermore, first data suggest that alterations in central pain processing may represent negative prognostic factors. A better understanding of the individual pathophysiology may allow in the future the development of individual therapeutic strategies.
authors.affiliation: Universitätsklinik für Anästhesiologie und Schmerztherapie, Inselspital, Bern. michele.curatolo@insel.ch
authors.forename: Michele
authors.initials: M
authors.lastname: Curatolo
mesh_terms: D015746:Abdominal Pain / Q000209:etiology / Q000503:physiopathology*; D002490:Central Nervous System / Q000503:physiopathology; D006801:Humans; D017774:Long-Term Potentiation / Q000502:physiology; D009433:Neural Inhibition / Q000502:physiology; D009473:Neuronal Plasticity / Q000502:physiology; D009619:Nociceptors / Q000502:physiology; D017288:Pain Threshold / Q000502:physiology; D010525:Peripheral Nerves / Q000503:physiopathology; D011379:Prognosis; D014781:Viscera / Q000294:innervation