Neurogastroenterology and motility : the official journal of the European Gastrointestinal Motility Society
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Neurogastroenterol. Motil. · Oct 2011
ReviewDevelopment of pharyngo-esophageal physiology during swallowing in the preterm infant.
Poor feeding is a common cause of prolonged hospitalization of preterm infants. Pharyngeal and upper esophageal sphincter (UES) function of preterm infants has been technically difficult to assess and is therefore poorly characterized. The aim of this study was to assess the development of pharyngeal motility, UES function, and their coordination during nutritive swallowing in preterm infants. ⋯ Results show developmental changes in infant swallow physiology that can be clearly linked to the effectiveness of nutritive swallowing. Most preterm infants demonstrated poor pharyngeal pressures at the laryngeal inlet coupled with poor coordination of pharyngeal propulsion with UES relaxation. These pressure patterns were less efficient than those demonstrated by older infants who were more adept at feeding. These observations may explain why infants under 34 weeks are physiologically unable to feed effectively and experience frequent choking and fatigue during feeding.
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Neurogastroenterol. Motil. · Aug 2011
ReviewDiagnosis and treatment of chronic constipation--a European perspective.
Although constipation can be a chronic and severe problem, it is largely treated empirically. Evidence for the efficacy of some of the older laxatives from well-designed trials is limited. Patients often report high levels of dissatisfaction with their treatment, which is attributed to a lack of efficacy or unpleasant side-effects. Management guidelines and recommendations are limited and are not sufficiently current to include treatments that became available more recently, such as prokinetic agents in Europe. ⋯ We present an overview of the pathophysiology, diagnosis, current management and available guidelines for the treatment of chronic constipation, and include recent data on the efficacy and potential clinical use of the more newly available therapeutic agents. Based on published algorithms and guidelines on the management of chronic constipation, secondary pathologies and causes are first excluded and then diet, lifestyle, and, if available, behavioral measures adopted. If these fail, bulk-forming, osmotic, and stimulant laxatives can be used. If symptoms are not satisfactorily resolved, a prokinetic agent such as prucalopride can be prescribed. Biofeedback is recommended as a treatment for chronic constipation in patients with disordered defecation. Surgery should only be considered once all other treatment options have been exhausted.
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Neurogastroenterol. Motil. · Apr 2011
ReviewUnderstanding gut-brain interactions in gastrointestinal pain by neuroimaging: lessons from somatic pain studies.
Neuroimaging research on gut-brain interactions has greatly improved our understanding of the brain mechanisms involved in processing and perceiving visceral pain in health and functional gastrointestinal disorders (FGID). However, discrepancies in the results of these studies continue to exist, which is at least partially due to the fact that important factors contributing to the intrinsic heterogeneity of symptom-based FGID, including psychological processes and psychiatric comorbidity, are insufficiently integrated in visceral pain neuroimaging research. ⋯ This review will defend the thesis that, to increase our understanding of the heterogeneous etiopathogenesis of FGID, visceral pain neuroimaging studies need to be integrated with: (i) epidemiological and behavioral evidence on the influence of psychological processes on visceral pain in health and FGID, and (ii) methodology and evidence from affective, cognitive, and psychiatric neuroimaging studies. To illustrate this point, the somatic pain neuroimaging field will be taken as an example before giving an overview of novel and integrative visceral pain studies in health and FGID. Some limitations of current pain neuroimaging studies will be outlined, before providing a summary of suggestions for moving the visceral pain neuroimaging field forward.
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Neurogastroenterol. Motil. · Dec 2010
ReviewGastrointestinal hormonal dysfunction in gastroparesis and functional dyspepsia.
Numerous hormones secreted by the gut, during both the fasted state and in response to a meal, influence gastrointestinal motor and/or sensory function, and appear to contribute to the pathogenesis of delayed gastric emptying associated with gastroparesis, functional dyspepsia (FD) and feed intolerance in critical illness. Gut hormones are, accordingly, potential targets for the management of these patients. ⋯ This article will discuss the hypersensitivity to enteral fat and endogenous (nutrient-stimulated) and exogenous cholecystokinin (CCK) in patients with FD, and the elevation in both fasting and postprandial CCK levels evident in this group. It will review the use of pharmacological agonists of motilin and ghrelin, which accelerate gastric emptying, in the management of gastroparesis and FD. The frequent finding of markedly delayed gastric emptying in the critically ill will be examined; this is associated with elevated plasma CCK and peptide YY in both the fasted and postprandial states, which may account for the increase in small intestinal nutrient inhibitory feedback on gastric motility in this group. The concepts that the rate of gastric emptying is a major determinant of postprandial glycemic excursions in diabetes, and that modulation of gastric emptying may improve glycemic control, will be addressed; in type 1 and insulin-treated type 2 diabetic patients, co-ordination of insulin administration with nutrient delivery and absorption should be optimized, while type 2 patients who are not on insulin are likely to respond to dietary and/or pharmacological interventions which slow gastric emptying.
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Neurogastroenterol. Motil. · May 2010
ReviewRole of spinal cord glia in the central processing of peripheral pain perception.
The discovery that glial activation plays a critical role in the modulation of neuronal functions and affects the spinal processing of nociceptive signalling has brought new understanding on the mechanisms underlying central sensitization involved in chronic pain facilitation. Spinal glial activation is now considered an important component in the development and maintenance of allodynia and hyperalgesia in various models of chronic pain, including neuropathic pain and pain associated with peripheral inflammation. In addition, spinal glial activation is also involved in some forms of visceral hyperalgesia. ⋯ We discuss the signalling pathways engaged in central glial activation, including stress pathways, and the neuron-glia bidirectional relationships involved in the modulation of synaptic activity and pain facilitation. In this expanding field of research, the characterization of the mechanisms by which glia affect spinal neuro-transmission will increase our understanding of central pain facilitation, and has the potential for the development of new therapeutic agents for common chronic pain conditions.