Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0011168 (dysphagia)
 15,644 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Three cases of esophageal intramural pseudodiverticulosis (EIP) are described and the literature reviewed. We conclude that EIP is an inflammatory disease of unknown etiology characterized by dilatation of the esophageal submucosal glandular elements. The classic radiographic picture which is that of collar-button-shaped outpouchings projecting in a perpendicular fashion from the luminal surface is mainly related to dilatation in the glandular ductal system. It is usually diagnosed in the sixth and seventh decades, but all ages may be affected. Dysphagia is a very common but not universal symptom of the disease process. Approximately one third of these patients have diabetes mellitus. Strictures of the esophagus are frequently seen, and varying degrees of esophagitis may be manifest endoscopically. Esophageal motility disturbances are common and may be severe. Candida infestation with and without tissue invasion has been seen in a number of patients and should be searched for in all cases of EIP.
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PMID:Esophageal intramural pseudodiverticulosis. 40 82

Detailed roengenological examinations of the esophagus were carried out in 110 diabetics and 130 controls. In 50 (45%) diabetic patients functional abnormalities were detected. Wavy esophageal contours, irregular spontaneous contractions and functional diverticula were observable. In diabetes, these changes occurred at an earlier age and more frequently than in controls. Esophageal transit time was markedly prolonged. The clinical symptoms of dysphagia were usually mild or absent. Diabetic dysphagia is one of the manifestations of diabetic visceral neuropathy. It is attributed mainly to the diabetic damage of the vagus nerve.
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PMID:Esophageal dysfunction in diabetes mellitus. 52 9

In two cases of chronic schizophrenia complicated by diabetes mellitus, the concomitant use of the neuroleptica and oral antidiabetics was attended by the appearance of symptoms simulative of syndrome malin, i.e. hyperpyrexia, tachycardia, blood pressure instability, disturbances of consciousness, muscle rigidity, tremor, dysphagia, salivation and urinary incontinence. In one of these cases, the patient, a 47-year-old man, died 10 days later. In the other case, a 62-year-old woman, almost all the symptoms subsided after 14 days, and oral dyskinesia persisted for only one additional month. In both cases, hypoglycemia due to oral antidiabetics was not seen. In Case 2, a combined regimen of oral antidiabetics and neuroleptica was later resumed. Again, a similar set of symptoms as seen initially were noted, along with an elevation of the serum CPK level. Parenterally administered biperiden proved to be highly effective in the control of the symptoms. The pathogenetic mechanism of these symptoms might possibly be explained as potentiation of the action of the neuroleptica by oral antidiabetics.
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PMID:"Syndrome malin"-like symptoms probably due to interaction between neuroleptica and oral antidiabetic agents. 65 48

The gastrointestinal complications of diabetes mellitus are the outward forms of the diabetic visceral neuropathy. The diabetic damage of the vagus nerve leads to disturbances of the tonus and the motility resembling to postvagotomy like conditions in the following clinical forms: diabetic dysphagia, diabetic gastroparesis, diabetic diarrhoea, diabetic megacolon, diabetic cholecystomegaly. These are in general late complications of labile diabetes. The mild abdominal symptoms are not in proportion to the severe radiological changes, proper diagnosis may be obtained only by means of roentgenological examinations in most cases.
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PMID:[Gastrointestinal complications of diabetes mellitus]. 117 96

The existence of specific, age-related changes in gastrointestinal motility with clinical significance is controversial. Beside the more infrequent primary motility disorders, secondary motility disturbances associated with collagen vascular diseases, endocrinopathies, and neuromuscular diseases are prominent in the older and often multimorbid patients. Especially in geriatric patients, motility associated symptoms are undesired side-effects of drug therapy. The pathophysiology, clinical syndromes, and therapeutic principles of motility disorders in the elderly are discussed. The major symptoms of esophageal dysfunction are dysphagia, chest pain, heartburn, and regurgitation. Oropharyngeal dysphagia, mostly caused by cerebrovascular accidents and other neurologic disorders, leads to disturbances in food intake, and is often complicated by broncho-pulmonary infections arising from recurrent aspiration of food or saliva. Gastrointestinal reflux disease and spastic motility disorders of the esophagus are regarded as possible causes of angina-like chest pain after exclusion of cardiac diseases. Motility disturbances of the stomach and small bowel are often related to systemic disease (i.e., diabetes mellitus, chronic intestinal pseudo-obstruction) of drug side-effects. Mental and physical decline, reduced fluid intake, and constipating drugs are the most relevant factors for idiopathic constipation in the elderly. Fecal incontinence means a great psychological strain for older patients and leads to social isolation.
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PMID:[Gastrointestinal motility in the elderly]. 144 9

A 66-year-old female suffering from HTLV-1 associated myelopathy (HAM) for more than 30 years was hospitalized because of memorial impairment, deafness, dysarthria, dysphagia, and complete paraplegia. She first noticed stiffness and weakness of the right leg at 35 years of age. Gait disturbance was slowly progressed and complete paraplegia developed 18 years later. Neurological examinations on admission revealed that she was bedridden with decubitus, mental deterioration (pre-dementia of subcortical type), bilateral optic nerve atrophy, severe sensory-neural deafness, dysarthria, complete paraplegia, and marked neurogenic bladder. Laboratory data showed mild normocytic anemia and moderate diabetes mellitus. Anti-HTLV-1 antibody titers in serum and CSF were 78,192X and 1,024X, respectively (PA method). Serum levels of soluble IL-2 receptor was markedly elevated (2,200 U/ml). Peripheral blood lymphocytes showed spontaneous proliferation when cultured for 5 days (3H-thymidine uptake; 45,285 cpm/5 X 10(4) cells). MRI examinations of the spinal cord disclosed a predominant atrophy of lower thoracic cord without any compressive lesions. Brain MRI showed diffuse high intensity lesions of the periventricular area on T2 weighted images. Such abnormalities were predominantly found in fronto-parietal region and were quite similar to those of leuko-ariosis. Single photon emission CT using 123I-iodoamphetamine showed hypoperfusion of cerebral white matter on delayed image. It has been reported that intellectual impairment and brain atrophy are not usually seen in HAM patients. The present case, however, shows that such abnormalities of the central nervous system could occur in HAM patients with a long duration of illness.
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PMID:[A case of HTLV-1 associated myelopathy progressed in course over 30 years]. 189 70

We describe four men from two kinships affected with X-linked recessive bulbospinal neuronopathy, and one sporadic case. All developed postural tremor, weakness, and fasciculations, with onset from age 25 to 39 years. Weakness began in the pelvic girdle or hands, with dysphagia or dysarthria occurring years later in two. Sensory symptoms were present in only one, who also had diabetes mellitus. In contrast, sural nerve action potentials were small or absent in all. Needle EMG showed widespread chronic partial denervation with reinnervation. The characteristic twitching of the chin produced by pursing of the lips consisted of repetitive or grouped motor unit discharges, rather than fasciculations. Broader awareness of the distinctive features of bulbospinal neuronopathy will probably increase the frequency of its recognition. Diagnosis is important for purposes of providing a prognosis for affected men and genetic counseling for affected families.
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PMID:Clinical and electrodiagnostic features of X-linked recessive bulbospinal neuronopathy. 153 Jul 14

61 of 1,590 (3.8%) patients with cerebrovascular disease showed suprabulbar palsy of the pure form (42 patients; 2 had autopsy) and striate form (19 patients; 3 had autopsy). 25 patients with the pallidopyramidal syndrome were included since the clinical picture bordered on the striate form. The pure variety was characterized by dysarthria, dysphagia and automatic voluntary dissociation of facial movements. Half of the patients also had hemiparesis, primitive reflexes and short-step gait. In the striate form, the main signs were dysarthria, dysphagia, automatic voluntary dissociation, rigidity and hypokinesia. Brisk tendon reflexes, primitive reflexes, short-step gait and mental deterioration were also present in half of the patients. The pure variety was caused by multiple infarcts and/or lacunae (85.7%), while the striate form had vascular lesions by computed tomography in only 36.8% of the cases. Histological findings, showing lipohyalinosis of the arterial wall leading to stenosis and occlusion of the lumen and tissue rarefaction and disintegration, support the assumption that microinfarctions, sometimes found only by histopathological examination, are the leading pathogenetic factor in this form. Hypertension, cardiopathy, smoking habit, dyslipemia and diabetes are the most frequent risk factors in both forms.
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PMID:Pseudobulbar palsy: a clinical computed tomography study. 229 26

Although diverticulopexy for the treatment of Zenker's diverticulum was described more than 75 years ago, its use has been infrequently reported in the surgical literature. Between 1974 and 1987, thirty-two patients manifested dysphagia caused by a pharyngoesophageal diverticulum. Twelve patients underwent diverticulopexy with cricopharyngeal myotomy, whereas the others had a one-stage resection of the diverticulum with myotomy. Complications of diverticulectomy were rare, but included an instance of esophageal leak, which responded to conservative therapy. Despite this low complication rate, diverticulopexy with myotomy was used in patients who possessed risk factors that made them unsuitable candidates for diverticulectomy. These factors included a debilitated state from effects of the diverticulum, a history of postsurgical complications, multiple medical illnesses, advanced age with inability to ambulate, and insulin-dependent diabetes mellitus. A nasogastric tube was not necessary after diverticulopexy. This allowed oral intake on the first postoperative day, immediate ambulation, and a shorter hospital stay. Objective recurrence occurred in one patient who underwent diverticulopexy and myotomy caused by manipulation of the sac during a subsequent surgical procedure, but significant dysphagia did not occur. Thus, although diverticulectomy has proved to be a relatively safe procedure, diverticulopexy with cricopharyngeal myotomy is recommended for high-risk patients in whom potential complications from diverticulum excision and prolonged hospitalization could be devastating.
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PMID:Diverticulopexy and cricopharyngeal myotomy: treatment for the high-risk patient with a pharyngoesophageal (Zenker's) diverticulum. 249 11

Although diffuse idiopathic skeletal hyperostosis generally affects the lumbar spine, any segment of the spine may be involved. When the cervical spine is affected, dysphagia may occur. Diabetes mellitus is commonly present. A history of previous cervical trauma is an indication to obtain cervical spine radiographs. Barium swallow and endoscopy provide confirmation of etiology. Surgery is curative.
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PMID:Dysphagia due to diffuse idiopathic skeletal hyperostosis. 265 Apr 99


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