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)

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

The authors present a review of 21 cases with the diagnosis of type I amyloid neuropathy based on epidemiological data, clinical evolution and histopathological findings. They call attention to the possibility of cranial nerves involvement (hyposmia, diplopia, masseterian hypotrophy, peripheral facial paralysis, hypoacusis, dysphonia, laryngeal paralysis, dysphagia, and trapezium muscle hypotrophy), to the severeness of the digestive symptoms, to the precocity of the autonomic disorders, and to the rather high incidence (6 cases) of heart involvement. The electromyography showed anterior horn involvement in 3 cases. The electrocardiography showed repolarization disorders in 11 cases, left ventricular overload in 6 cases and atrioventricular block in 5 cases. The serum proteins electrophoresis showed frequent abnormalities, but no typical curve could be obtained. The barium-contrasted X-rays of the gastrointestinal tract showed no anatomical lesions, but functional abnormalities (hypo or hypermotility) were found in 14 examination. The Schilling test showed impairment of vitamin B12 absorption in 50% of the cases. However, with the concomitant administration of intrinsic factor (3 cases) there was improvement of it absorption. This proves that the gastric mucosa plays an important role in the disease malabsorption. The test with labeled-triolein showed slow absorption in 2 cases and steatorrhea in 3 (6 tests). For the confirmation of the amyloid deposits, the best histopathological procedure was nerve biopsy. In men, when the nerve biopsy was negative, testicular biopsy has shown to be a good option.
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PMID:Type I primary neuropathic amyloidosis (Andrade, portuguese). 114 94

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

During aging, secretion and motility of the upper GI tract slow down. The reduction of these functions, however, does not create complaints. In the higher age groups, a number of symptoms from age-dependent diseases occur more frequently, e.g., dysphagia in response to cerebral ischemia, or disturbed gastric emptying caused by diabetic visceral neuropathy. Moreover, certain GI diseases occur more often in the elderly, e.g., chronic atrophic gastritis, NSAR-induced gastric ulcers, malignancies, and others. In contrast, almost nothing is known about diseases or symptoms of the GI tract that might be specific for the elderly. With only a few exceptions, there are no age-dependent clinical differences. Nevertheless, intestinal diseases often develop more rapidly and the mortality is higher in the elderly than in younger people.
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PMID:[Geriatric diseases of the upper digestive tract]. 144 7

We report the cases of two patients who developed cranial nerve palsies after drinking ethylene glycol. A 33-year-old man developed multiple cranial nerve deficits nine days after the ingestion of ethylene glycol in a suicide attempt. Clinical findings included profound bilateral cranial nerve VII palsies and severe dysfunction of cranial nerves IX and X. The neuropathy occurred despite treatment with hemodialysis. The dysphagia completely cleared within two weeks, but at six months a severe bilateral cranial nerve VII dysfunction persisted. A 22-year-old man undergoing hemodialysis for ethylene glycol-induced renal failure developed bilateral cranial nerve VII dysfunction 14 days after ingestion. At a three-month follow-up, the patient demonstrated only moderate functional recovery. The etiology of the cranial nerve deficits is unknown but may be related to oxalate crystal deposition of ethylene glycol-induced pyridoxine dysfunction.
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PMID:Multiple cranial nerve deficits after ethylene glycol poisoning. 199 9

Nineteen cases are described, including 12 cases from three different families and 7 nonfamilial cases, in which multisystem neurological disease was associated with acanthocytosis in peripheral blood and normal plasma lipoproteins. Mild acanthocytosis can easily be overlooked, and scanning electron microscopy may be helpful. Some neurologically asymptomatic relatives with significant acanthocytosis were identified during family screening, including some who were clinically affected. The mean age of onset was 32 (range 8-62) yrs and the clinical course was usually progressive but there was marked phenotypic variation. Cognitive impairment, psychiatric features and organic personality change occurred in over half the cases, and more than one-third had seizures. Orofaciolingual involuntary movements and pseudobulbar disturbance commonly caused dysphagia and dysarthria that was sometimes severe, but biting of the lips or tongue was rarely seen. Chorea was seen in almost all symptomatic cases but dystonia, tics, involuntary vocalizations and akinetic-rigid features also occurred. Two cases had no movement disorder at all. Computerized tomography often demonstrated cerebral atrophy. Caudate atrophy was seen less commonly, and nonspecific focal and symmetric signal abnormalities from the caudate or lentiform nuclei were seen by magnetic resonance imaging in 3 out of 4 cases. Depression or absence of tendon reflexes was noted in 13 cases and neurophysiological abnormalities often indicated an axonal neuropathy. Sural nerve biopsies from 3 cases showed evidence of a chronic axonal neuropathy with prominent regenerative activity, predominantly affecting the large diameter myelinated fibres. Serum creatine kinase activity was increased in 11 cases but without clinical evidence of a myopathy. Postmortem neuropathological examination in 1 case revealed extensive neuronal loss and gliosis affecting the corpus striatum, pallidum, and the substantia nigra, especially the pars reticulata. The cerebral cortex appeared spared and the spinal cord showed no evidence of anterior horn cell loss. Two examples of the McLeod phenotype, an X-linked abnormality of expression of Kell blood group antigens, were identified in a single family and included 1 female. The genetics of neuroacanthocytosis are unclear and probably heterogeneous, but the available pedigree data and the association with the McLeod phenotype suggest that there may be a locus for this disorder on the short arm of the X chromosome.
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PMID:Neuroacanthocytosis. A clinical, haematological and pathological study of 19 cases. 199 79

The authors reported a 47-year-old man with hypopharyngeal stenosis caused by late radiation injuries. At the age of ten he underwent irradiation (3000rads) to the neck because of the cervical lymphadenopathy. He had keroid skin change at the age of 19, hypothyroidism since 26, right cervical and brachial plexus neuropathy since 33, and paralysis and papilloma of right vocal cord at 34. And at the age of 41 he underwent tracheostomy owing to laryngeal stenosis. In November 1984 (at age 43) he felt abnormal sensation on the throat but had no dysphagia nor misdiglutition. On November 1987 he had difficulties of swallowing, and could not take anything but fluid. At that time he was diagnosed as hypopharyngeal stenosis. With steroids and antibiotics his difficulties of swallowing were reduced. He experienced the same difficulties on April 1988. Since December 1988 his dysphagia got worse and was not recovered with medication. On May 17 1989, laryngopharyngectomy was performed. At the level of cricoid cartilage hypopharynx was resected. As for the posterior wall, pharynx and cervical esophagus were fixed to prevertebral fascia and anastomosed with end-to-end. And antero-lateral defects were reconstructed with myomucosal tongue flap. Postoperatively he could eat orally. On the basis of the experience of this case and the review of the literature the authors conclude that myomucosal tongue flap is one of alternatives for hypopharyngeal reconstruction.
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PMID:[A case of hypopharyngeal stenosis caused by late radiation injuries--reconstruction of the hypopharynx with myomucosal tongue flap]. 221 61

Esophageal function was prospectively studied in 50 consecutive insulin-requiring diabetes mellitus patients. The patients were stratified in three groups: A) 18 without peripheral neuropathy (PN); B) 20 with PN but no autonomic neuropathy; C) 12 with PN and autonomic neuropathy. Twelve patients (four B, eight C) had gastrointestinal symptoms including six with dysphagia. Radionuclide esophageal emptying was abnormal in 55, 70, and 83% of patients in groups A, B, and C, respectively. Eleven of the 12 (92%) symptomatic and 23 of the 38 (60%) asymptomatic diabetes mellitus patients had abnormal emptying. Five of six patients with dysphagia had abnormal emptying. Esophageal manometry was also performed in 15 patients. Twelve patients had abnormal manometry. These included nutcracker esophagus in two, achalasia in one, and increased percentage of multipeaked and simultaneous contractions in nine. There were no significant correlations between radionuclide esophageal emptying, manometric changes and symptoms. Gastrointestinal symptoms were more common in the presence of autonomic neuropathy. Delayed esophageal emptying was more profound in the presence of PN, but abnormal esophageal emptying was present in patients with neuropathy as commonly as patients without. Furthermore, the presence of diabetic retinopathy, duration or control of diabetics, and fasting blood sugar did not influence the frequency of abnormal esophageal emptying. Our data indicate that esophageal dysfunction is common in male diabetics even in the absence of clinical PN and retinopathy, suggesting that diabetic gastroenteropathy can occur in the absence of significant diabetic complications. Commonly observed abnormal esophageal manometry in diabetics is not necessarily accompanied by significant functional disturbances or symptoms.
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PMID:Radionuclide esophageal emptying and manometric studies in diabetes mellitus. 360 23

Three patients exhibited an unusual variant of chronic relapsing polyneuritis in which extraocular muscle palsies developed 19 days, 20 days, and 3 1/2 months, respectively, before the neuropathy affected the limbs. The peripheral neuropathy evolved over 7 to 12 weeks, lasted 15 months to 13 years, and relapsed in every case. Each patient had dysphagia, areflexia, sensory loss, and weakness of all four limbs, which in two was asymmetrical. Slowed motor nerve conduction and prolonged F wave latencies were present, and the cerebrospinal fluid protein level was elevated without increased cell count. No patient recovered fully despite treatment with immunosuppressant drugs.
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PMID:Ocular palsy preceding chronic relapsing polyneuropathy by several weeks. 398 86

Hemifacial spasm is usually an isolated symptom resulting from facial nerve root compression. Three patients had, in addition, tinnitus, hearing loss, facial sensory loss, diminished gag reflex, dysphagia, and dysarthria. Acoustic reflexes were abnormal, and facial nerve conduction studies showed evidence of ephaptic transmission and ectopic excitation. Brain CT and metrizamide cisternography were normal. Surgical exploration showed compression of cranial nerve roots by posterior inferior cerebellar artery branches. After decompression, symptoms abated, and electrical signs of hemifacial spasm disappeared. Vascular compression of nerve roots in the cerebellopontine recess may cause multiple cranial neuropathy.
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PMID:Vascular compression, hemifacial spasm, and multiple cranial neuropathy. 399 Sep 69


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