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Gastrointestinal Complications of Diabetes Mellitus
Published in Jack L. Leahy, Nathaniel G. Clark, William T. Cefalu, Medical Management of Diabetes Mellitus, 2000
Bernard Coulie, Michael Camilleri
The pathogenesis of abnormal gastrointestinal motility in diabetes mellitus is incompletely understood and is likely multifactorial, including extrinsic denervation, enteric neuropathy, and hyperglycemia (1,9,12,14). These result in impaired gastric contractility or abnormal myoelectrical control (1). The syndrome is typically seen in patients with type I or insulin-dependent diabetes mellitus (IDDM). Peripheral neuropathy is present in the majority of patients with enteropathy, and other forms of autonomic neuropathy are common. Previous work has attributed these motility disorders to mainly vagal nerve dysfunction, although dysfunction of the sympathetic innervation has also been implicated and probably causes a reduced internal anal sphincter tone, resulting in nocturnal stool incontinence. Motor abnormalities of the small intestine observed in symptomatic diabetic patients are often indistinguishable from those seen in patients with other syndromes affecting postganglionic sympathetic function. The relative contributions of parasympathetic and sympathetic nerve damage to diabetic visceral neuropathy in the nonsphincteric regions of the digestive tract remains unclear. Vagal dysfunction is probably critical in gastric stasis, but it is unclear whether rapid small bowel transit and diarrhea result from vagal neuropathy or from loss of tonic inhibitory sympathetic input. Electrolyte imbalances caused by diabetic ketoacidosis (e.g., hypokalemia) and uremia may further aggravate impaired motor function in diabetic patients.
Chronic Fatigue Syndrome: Limbic Encephalopathy in a Dysregulated Neuroimmune Network
Published in Jay A. Goldstein, Chronic Fatigue Syndromes, 2020
The cause of irritable bowel syndrome (IBS) is complex, but almost certainly invokes the limbic system. Some studies suggest that panic disorder and numerous other CFS symptoms common to CFS occur in association with IBS. Our work in functional brain imaging in IBS patients reveals abnormalities similar to those seen in CFS patients, although we have a much smaller sample of IBS patients. Descending influences on vagal nuclei from the limbic system could well be involved. There has also been degeneration of the myenteric plexus reported in an IBS patient who had a 95% colectomy for obstipation.57 IBS has been relieved by administration of leuprolide acetate (Lupron), a gonadotropin-releasing hormone (GnRH) agonist used in the treatment of prostatic cancer and endometriosis.58 Cells which stain for GnRH have been found in sympathetic ganglia and the bladder as well as in the limbic system. Neuronal projections from the lateral hypothalamus, insular cortex, solitary tract, and amygdaloid nuclei project directly to sympathetic preganglionic areas and could be affected by GnRH agonists. Lupron also has immunosuppressive actions, primarily on B lymphocytes, and is being used in clinical trials for this purpose. The possibility that a virus which could have a neurotoxic effect on limbic and myenteric structures by expression of a gene product, thus causing an encephalopathy/enteric neuropathy which would be non-inflammatory, could be considered as a possible etiologic factor. Retroviruses may act in this manner, and a human foamy virus has been reported to cause hippocampal as well as intestinal smooth muscle degeneration in transgenic mice.59
Chronic Constipation
Published in Peter Sagar, Andrew G. Hill, Charles H. Knowles, Stefan Post, Willem A. Bemelman, Patricia L. Roberts, Susan Galandiuk, John R.T. Monson, Michael R.B. Keighley, Norman S. Williams, Keighley & Williams’ Surgery of the Anus, Rectum and Colon, 2019
Charles H. Knowles, Adil E. Bharucha
The subject of GI neuromuscular pathology is one that in general is fraught with technical and interpretative uncertainties,80,81 and the study of colonic tissue in chronic constipation is no exception. The interested reader should access more detailed information from specific review.80 Accepting issues of selection bias (patients having colectomy are not representative of the whole); technical processing (many data are based on outdated histologic techniques, e.g. silver staining); reporting (do subtle differences actually deviate from normality?) and interpretation (do findings have a causal relationship with observed clinical phenotype?), the following observations may be briefly summarised in patients with chronic constipation (mainly based on studies of patients with slow transit constipation): Bona fide enteric neuropathy81 is probably not a common finding.Widely reported changes in functional subsets of enteric neurons82,83 or glia may have biological relevance but little current diagnostic utility.Well-established developmental, degenerative and inflammatory myopathic phenotypes81 are at best a very uncommon finding.Quantitative reductions in numbers of interstitial cells of Cajal (pacemaker cells) are the most consistent finding84 (see Figure 17.4) although standardised approaches will be required for diagnosis in individual patients in clinical practice.80
Mechanisms behind diffuse idiopathic peripheral neuropathy in humans – a systematic review
Published in Scandinavian Journal of Gastroenterology, 2023
Hanna Tufvesson, Viktor Hamrefors, Bodil Ohlsson
It is well known that several diseases may lead to diffuse peripheral neuropathy in the autonomic nervous system, including the enteric nervous system, and the sensorimotor system [1]. Since the awareness of enteric neuropathy is limited, it may take time before reaching a correct diagnosis as well as proper treatment of the patient. Signs and symptoms of cardiovascular autonomic neuropathy and sensorimotor neuropathy are more often recognized, whereas enteric neuropathy with gastrointestinal (GI) dysmotility may be classified as psychological and functional disorders instead of organic neuropathy [1]. Undiagnosed, enteric neuropathy may lead to malnutrition and, thereby, further neurological deterioration [2].
Diseases which cause generalized peripheral neuropathy: a systematic review
Published in Scandinavian Journal of Gastroenterology, 2021
Bodil Roth, Danielle Bernadette Schiro, Bodil Ohlsson
Diagnosis and treatment of autonomic neuropathy are important to prevent secondary complications. Cardiovascular neuropathy may impair the possibility for the subjects to exercise or live an active life. Since both impaired microcirculation and sudomotor function lead to dry skin and loss of sweating, these changes can contribute to the development of ulcers and gangrenes. Furthermore, there is a strong association between reduced heart rate variability and silent myocardial ischemia and mortality, with an increased mortality risk of 2.14 (95% confidence interval of 1.83–2.51) in patients with cardiovascular autonomic neuropathy [29]. Enteric neuropathy impairs the possibility to eat regularly and optimally deliver food and drugs to the small intestine. All these factors have a negative impact on the metabolic control of diabetes, which enhances the development of neuropathy [29,30,32]. Thus, neuropathy has a considerable relevance on both quality of life and survival. Gastrointestinal symptoms without objective findings on endoscopy are called irritable bowel syndrome (IBS). These patients are treated with dietary advice, psychological treatment and drugs to reduce gastrointestinal symptoms [65]. A thorough examination of the gastrointestinal tract and its motility may lead to a diagnosis of gastrointestinal dysmotility instead of IBS [17,21], with a different treatment to improve motility with enhanced metabolic control and reduced symptoms [31]. Nevertheless, it is important to recognize that the gastrointestinal symptoms in Sjögren’s syndrome or other disorders may not only depend on enteric neuropathy [17,46]. The finding of a correlation between levels of feces calprotectin, organic gastrointestinal disease and inflammatory rheumatic activity suggests that Sjögren’s syndrome may be situated in the entire gastrointestinal mucosa and not only in the mouth [66].