A potent modifier of behavioral, neuronal, autonomic, and motor responses to visceral stimulation in experimental models inflammation has been commonly used to produce visceral hypersensitivity. The presence of inflammation in visceral structures frequently, but not universally, leads to reports of pain and sensitivity to mechanical and chemical stimuli. Cystitis, esophagitis, gastritis, duodenitis, ileitis, colitis, and proctitis all have evidence of mucosal inflammatory changes, as a hallmark finding. However, profound inflammatory changes of the mucosal lining, such as occurs with ulcerative colitis, may present with nonpainful, bloody stools.
Inflammation produces profound changes in the responsiveness of subsets of previously unresponsive visceral primary afferents and the term "silent" afferents has been coined.56 These afferents are normally non-reactive to most stimuli, but in the presence of products of inflammation become spontaneously active and highly reactive to mechanical stimuli, such as distension. Silent afferents have been frequently noted in visceral structures forming up to 50 percent of the neuronal sample,57 but are only infrequently noted in cutaneous structures. The lack of sensitivity of the viscera at baseline may relate to the sparcity of active visceral afferents which are quantitatively fewer per unit area than similar measures of cutaneous afferents. Because they are few, increased activity may be necessary in order to cross a threshold for perception.
Spinal neurons responsive to visceral stimuli also change their responsiveness to visceral stimuli in the presence of inflammation and when other sensitizing manipulations have been performed (see, for example, Refs 58, 59). Whether this is due to increased afferent activity, altered intrinsic properties of dorsal horn neurons, or altered modulatory influences within the central nervous system is unknown. It is likely that all of these separate mechanisms contribute in some way to the final sensitized state.
Whereas acute inflammation is often obvious with the hallmark features of redness, swelling, pain, and warmth, the more subtle changes related to chronic inflammation are often difficult to identify. Progressive fibrosis, mast cell infiltration, and altered oxidative stress markers all suggest that an ongoing indolent inflammatory process may be present that has sensory consequences equal to that of acute inflammation. Mast cell infiltration has been implicated in the hypersensitivity states of irritable bowel syndrome60 and interstitial cysititis,61 which has, in turn, prompted treatment with antihistamines and cromolyn-related compounds with mixed benefits. Mast cells have been observed to cluster around nerve bun-dles62 and have been noted to express estrogen receptors63
which, in turn, suggests a mechanism for menstrual cycle-associated exacerbations of some visceral pains.
More subtle than the histologically identifiable alterations in cell distribution are the biochemical changes that indicate a low level of chronic inflammation. Alterations in measures of oxidative stress have been observed in several hypersensitivity disorders, such as fibromylagia64 and chronic fatigue syndrome,65 and form a basis for sensory changes in the absence of histological changes. Use of antioxidant/micronutrient therapies (e.g. vitamins C and E, selenium) has had reported utility in the treatment of painful visceral disorders, such as chronic pan-creatitis.66
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If you suffer with asthma, you will no doubt be familiar with the uncomfortable sensations as your bronchial tubes begin to narrow and your muscles around them start to tighten. A sticky mucus known as phlegm begins to produce and increase within your bronchial tubes and you begin to wheeze, cough and struggle to breathe.