The observation that pathology and symptomatology may not correlate is readily apparent in numerous visceral pain disorders. Some disorders, such as chronic pancreatitis, have definable pathology, but alterations in pain appear out of proportion to objective radiographic or laboratory findings. Other disorders, such as irritable bowel syndrome, noncardiac chest pain, and postcholecystectomy syndrome, appear to have no grossly apparent histo-pathological basis for the discomfort and pain. Instead, visceral discomfort and pain in such conditions are termed functional and are associated with altered patterns/pressures associated with motility, production of gas, and ingestion of food or beverage. Hence, natural visceral stimuli in the physiologic range can be associated with discomfort and pain in the absence of obvious visceral pathology.
Hypersensitivity to somatically applied stimuli is typically associated with histological evidence of ongoing tissue damage/inflammation. Exception to this statement are neuropathic pain disorders in which there may be a history of nerve injury, but no apparent local histopathological changes. In this case, routine tissue examination would suggest that neuropathic pain disorders are functional.
With an increased sophistication of testing related to visceral disorders, there may prove to be identifiable markers or imaging studies that allow for a reduced reliance on subjective reports of sensation. An example of this comes from the painful bladder disorder, interstitial cystitis (IC). In general, the urothelium of patients with the nonulcerative form of IC appears normal on routine cystoscopic and microscopic examination. It takes a highly sophisticated analysis to discern any quantitative differences between the tissues of IC patients and normal healthy controls such that most measures have been deemed to be of little use in diagnosis. However, when the urothelium of IC patients is examined using a scanning electron microscope, defects in the urothelial surface and tight junctions are common5 and a laboratory marker for a factor that suppresses urothelial cell proliferation may prove diagnostic for the disorder.6 Until similar subtleties of evaluation become routine, the current state-of-the-art for diagnosis of painful visceral disorders requires full consideration of the entire constellation of signs, symptoms, and tests.
Psychophysical studies have demonstrated evidence for hypersensitivity in virtually all clinically relevant visceral pain disorders. This includes hypersensitivity to gastric distension in patients with functional dyspepsia,7 intestinal and rectal distension in patients with irritable bowel syndrome,8, 9 biliary and/or pancreatic duct distension in patients with postcholecystectomy syndrome or chronic pancreatitis,10 and bladder distension in patients with interstitial cystitis.11 In these studies, pain could be evoked at intensities of stimulation lower than those required to produce the same quality and intensity of sensation in a healthy population. A more sophisticated testing of visceral sensitivity using random order, graded distension of the rectum in irritable bowel patients suggest that the population of subjects is heterogenous,12 with subgroups demonstrating hyper-sensitivity and others hypervigilance.
Dissociating potential psychological modifiers of sensory reports from other more physiological pathologies has proven to be difficult. It represents a sometimes insurmountable methodological problem and, perhaps more importantly, due to observations related to the phenomenon of stress-induced hyperalgesia (where psychological factors alter physiological responses) it may not be appropriate to perform such a dissociation. Psy-chophysical studies related to visceral sensation in normal healthy subjects have suggested a basis for some of the emotional factors that may affect pain reports. Strigo et al.13 compared sensations evoked by balloon distension of the esophagus with thermal stimulation of the skin overlying the sternum and found that greater anxiety was evoked by esophageal distension. Furthermore, they found unpleasantness ratings were higher when the esophageal stimulus was administered and a stronger affective component to the visceral sensation was measured using the McGill Pain Questionnaire.
Other psychophysical studies of experimental visceral pain sensation in humans have identified that a sensiti-zation process occurs with repeated stimulation of the gut14,15 and of the urinary bladder16 consistent with observations in nonhuman animals, where repeated presentation of the same visceral stimuli produces increasing vigor of neuronal, cardiovascular, and visceromotor reflex
Clinically, there are three entities that are accepted as potential sources of painful hypersensitivity: (1) inflammation; (2) stress (anxiety); and (3) altered neural function that may be due to injury during critical periods of development (e.g. the neonatal period) or more direct neuropathic processes. These will be discussed below after a description of the anatomy of visceral pain.
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It seems like you hear it all the time from nearly every one you know I'm SO stressed out!? Pressures abound in this world today. Those pressures cause stress and anxiety, and often we are ill-equipped to deal with those stressors that trigger anxiety and other feelings that can make us sick. Literally, sick.