Since its description more than 150 years ago, clinicians and scientists have been puzzled over the cause(s) of IBS. Current basic and clinical research studies have suggested that this syndrome is a disorder associated with physiologic alterations of several organ systems including the gut, spinal cord, and brain;14 altered signaling among these systems fuels and perpetuates the condition. Just as the gastrointestinal tract sends signals to the brain in response to a variety of local stimuli, sensory input to the brain affects the function of the gut. Integrated signaling occurs between the gut and brain; these connected activities are influenced by a variety of factors. Increased intestinal motility and mucosal hyperemia induced by stressful or painful experiences is an example of alteration of gut function induced by the brain and spinal cord.15 Examples of altered central nervous system functioning as a response to gastrointestinal stimuli seen in IBS include changes in the processing of painful and noxious gut stimuli in the brain, as described below.
Psychological disturbances and past experiences of physical or sexual abuse are risk factors for IBS.1-3 Abnormal integration of the intestinal sensory, motor, and autonomic systems, coupled with the appropriate psychological milieu, ultimately may produce functional-type gut disorders. Neural connections from the brain to the gut allow extrinsic information (including visual, olfactory, and auditory stimulation) and cognitive stimuli such as emotional responses, to subsequently interact with the intestinal nervous system. Neurotransmitters are involved in all of the aforementioned neuronal activities.
When aberrant actions are present in these systems, patients develop symptomatic gut dysfunction as shown in Figure 6.1. The most consistently demonstrated abnormality in patients with IBS is the presence of visceral hyperalgesia. Patients with IBS exhibit a markedly decreased threshold for the sensation of painful stimuli in the gut when compared to controls.16
The most commonly utilized method for demonstrating intestinal hypersensitivity involves the analysis of symptoms produced by the inflation of balloons within the rectosigmoid colon. Multiple research trials have demonstrated that patients with IBS experience discomfort after inflation of smaller volumes of fluid or air into the rectosigmoid colon than do controls.16,17 In fact, the threshold for the initial sensation of discomfort seen at low volumes as well as the development of rectosigmoid pain with larger balloon volumes are both much lower in individuals with IBS compared to normal controls. These types of studies appear to establish the presence of a specific defect of the sensory portion of the enteric nervous system in patients with IBS.4,17,18 Further studies have demonstrated that this rectosigmoid hypersensitivity may also reflect abnormalities in specific portions of the brain that are involved in the regulation of painful stimuli. For example, studies comparing normal individuals with IBS patients using rectosigmoid balloon inflation performed with simultaneous positron emission tomography (PET) scanning have shown that the anterior cingulate gyrus, a portion of the brain normally involved in the downregulation of noxious stimuli, has decreased activity in IBS patients.19 Of interest, repeated distention of the rectosigmoid colon results in stimulation of pre-frontal cortex in IBS patients but not in normal volunteers. The prefrontal cortex is responsible for anticipation of unpleasant stimuli.3,19 These data suggest that IBS patients have altered brain function, characterized by enhanced anticipation of unpleasant gastrointestinal stimuli coupled with an inability to downregulate unpleasant sensations produced by these stimuli. These findings validate the concept that complex alterations in the brain-gut axis play an important role in symptoms experienced by patients with IBS.2-4
Several studies have demonstrated that IBS may occur as a late consequence of gastrointestinal infection, including traveler's diarrhea and acute bacterial gastroenteritis.20-24 One study has shown that the likelihood of developing IBS after an intestinal bacterial infection was approximately 10 times higher than that of the general population.20 Histologic changes, such as the heightened presence of chronic inflammatory cells in the lamina propria, have been demonstrated after a colonic bacterial infec-tion.22 Alteration of local immune function of the gastrointestinal tract following bacterial infections have also been demonstrated.23,24
Gut dysfunction, including rectosigmoid hypersensitivity and increased intestinal motil-ity, occur for at least 6 months in all individuals after a bacterial gastroenteritis.22 However, only a small percentage (for example, 5% of individuals having a salmonella gastroenteritis) will develop the chronic symptoms of IBS by actually experiencing the sensation of altered gut func-tion.21 The appropriate psychological milieu, including anxiety or stress, or a history of childhood trauma, appears to be characteristic of developing IBS.
Psychosocial factors are clearly important in the development of IBS. One study has demonstrated that approximately 50% of individuals with IBS meet the criteria for psychiatric diag-noses,25 compared to less than 20% of patients without IBS. Anxiety, depression, and somatiza-tion disorders are the most common psychiatric diagnoses in individuals with IBS. Patients who have symptoms of IBS and psychosocial disturbances are more likely to complain of abdominal pain and to seek medical therapy.4
Unfortunately, increased seemingly unnecessary abdominal surgeries are also seen in these patients. Insightful studies by Drossman et al26 have demonstrated that a significant number of women with functional gut disorders report a history of physical or sexual abuse.
Clinical experience suggests that mild-to-moderate gut dysfunction in IBS occurs primarily from disturbances in both gut and brain biology, while psychosocial abnormalities predominate in patients with the most severe forms of IBS.4
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