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)

Clinical signs in dogs with pseudorabies (Aujeszky's disease) were tabulated from 25 confirmed cases. The duration of disease was short, ranging from 6 to 96 hours. Eight dogs were euthanatized. Of those not euthanatized, 12 (71%) died within 24 hours of onset, 16 (94%) died within 48 hours, and only 1 (6%) lived longer than 48 hours (96 hours) after the onset of clinical signs. All of the dogs had ptyalism, 84% were restless, 84% were anorectic, 76% were atactic, and 64% wandered aimlessly. Sixty-four percent of the dogs had tachypnea, 60% had dyspnea, 56% vocalized, 52% were pruritic, 48% held their necks rigidly, 36% vomited, 36% had muscle spasms, 36% were aggressive, 28% had trismus, and 24% had dysphagia. Five of 25 dogs (20%) had abnormal pupillary light responses. Two of the 25 dogs circled and 2 walked backwards. Each of the following were detected once: blindness, ptosis, facial paresis, excessive lacrimation, head-tilt, head-pressing, signs of abdominal pain, and photophobia. All dogs had been exposed to swine, although in some instances the farmer was unaware pseudorabies existed in the herd or believed it was not in the herd on the basis of negative results on serologic testing.
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PMID:Clinical signs associated with pseudorabies in dogs. 277 5

A 37-year-old man suffered from photosensitivity and urinary casts with serological findings of positive anti-DNA antibody, LE cells and false positive VD reaction in September of 1979. He developed general fatigue, dyspnea and diplopia with ptosis of bilateral eyelids in November of 1979, which were improved by the anti-cholinesterase drugs. In January of 1980, he had an attack of unconsciousness and his chest X-ray film showed several tumorous shadows in the anterior mediastinum and middle and lower lung fields. Treating him with chemotherapy of VEMP, the pulmonary shadows disappeared. However, he developed severe muscle weakness with an elevated CPK (430 mU/ml) and a myogenic EMG pattern along with an increased anti-acetylcholine receptor antibody (243 n Mol/l), dysphagia and eyelid-ptosis. He died in September of 1985 and his autopsy disclosed a malignant thymoma of mixed type in the anterior mediastinum and an atrophy and fibrosis with infiltration of inflammatory cells in the striated muscles.
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PMID:[An autopsy case of a patient with myasthenia gravis who showed various symptoms of collagen diseases and complicated with malignant thymoma]. 281 7

Oculopharyngeal muscular dystrophy is a rare, autosomal dominant disorder which has been traced through 11 generations of a French Canadian family. The classic presenting complaints are palpebral ptosis and oropharyngeal dysphagia. The dysphagia is usually progressive and leads to repetitive regurgitation, increased alimentation time, and weight loss. Immunologic studies generally reveal elevated levels of IgA and IgG, while manometry demonstrates poor pharyngeal contraction. The dysphagia is frequently relieved by cricopharyngeal myotomy. We present two case reports and also a new ultrastructural finding of abnormal metallic mitochondrial inclusions. This finding has not been previously described in this disorder.
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PMID:Oculopharyngeal muscular dystrophy: recent ultrastructural evidence for mitochondrial abnormalities. 300

Oculopharyngeal muscular dystrophy is an autosomal dominant myopathy that exhibits the symptoms of progressive dysphagia, with ptosis usually occurring after the age of 40. Literature review of this rare disease reveals a high incidence in the French-Canadian population, as well as in five other ethnic groups. Our article details the clinical history and genealogy of the disease through four generations in a family of English descent. Radiographic studies show a cricopharyngeal bar and aspiration. Results of electron microscopic examination of muscle biopsy specimens from the vastus lateralis and cricopharyngeus muscles confirm a chronic, active, severe, myopathic process that is more pronounced in the cricopharyngeus muscle. The recommended treatment for blepharoptosis and the cricopharyngeus muscle pathosis is discussed.
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PMID:Oculopharyngeal muscular dystrophy: clinical and histopathologic correlations. 310 51

Seven patients with myasthenia gravis (MG) unresponsive to thymectomy and steroid treatment (Osserman group III) underwent plasma perfusion (PP). All patients showed palpebral ptosis, diplopia, dysphonia, dysphagia, and muscle weakness; five of them had impaired ventilatory function. Separated plasma was perfused onto a column to adsorb anti-AChR-Ab. Each patient received a treatment cycle of six PP sessions. Clinical conditions were assessed before and after the treatment, with evaluation of muscular strength, ventilatory function, and electromyographic testing (RSS). Immunologic markers were tested before and after each PP. Clinical improvement in bulbar symptoms and respiratory function was noted in all patients after one to three PP. Limb muscle strength began to improve later. Serum concentration decreased (mean % +/- SD) after each PP:anti-AChR-Ab 36.47 +/- 17.43; IgA 20.44 +/- 11.26; IgG 21.24 +/- 32.56; IgM 23.22 +/- 11.40; C3 36.78 +/- 10.15; C4 42.69 +/- 14.82. In five of seven patients the improvement continues (follow-up 1 to 10 months). In one patient it lasted only 1 month, and in another a relapse occurred after 10 months of benefit, but was successfully reversed by retreatment.
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PMID:Plasma perfusion in myasthenia gravis. 319 71

Oculopharyngeal muscular dystrophy (OPMD) is a rare progressive disease characterized by bilateral ptosis and dysphagia. A case report of a patient of French-Canadian descent is presented. The importance of OPMD is emphasized, not only in its differential of ptosis, but also because of the possible sequella from the dysphagia of weight loss, pulmonary infection, choking and tracheal aspiration.
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PMID:Oculopharyngeal muscular dystrophy. 358 10

Experimental autoimmune myasthenia gravis (EAMG) was induced in rhesus monkeys using purified acetylcholine receptor (AChR) from Torpedo california. A single dose of 80 micrograms induced antibody formation two weeks after injection. Two subsequent doses at two-week intervals caused clinical signs (anorexia, fatigability, weight loss, ptosis and dysphagia) which initially responded to treatment with neostigmine. Histologic examination of post-mortem tissues revealed lesions characteristic of myasthenia gravis in man: muscular atrophy, fibrous degeneration and lymphocytic infiltration. Antibodies were quantitated in the sera of three other monkeys which received only 60 micrograms of purified AChR. Abnormally high titers persisted for two years (60-200 micrograms /ml versus 0-10 micrograms/ml for controls). A monkey injected with 60 micrograms AChR as part of reconstituted membrane vesicles had lower titers (30-50 micrograms/ml) than those which received purified receptor. Only those monkeys with antibody titers exceeding 800 micrograms/ml developed overt disease. These titers were 4-100 times higher than those reported for myasthenic humans. The antibody-antigen molar ratios were higher for monkeys with disease than for asymptomatic animals. These data suggest that the diversity of antibody molecules synthesized by the sensitized monkeys determined the appearance of clinical signs, and that the cross reaction of anti-torpedo antibodies with monkey receptor was primarily responsible for the development of EAMG.
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PMID:Induction of experimental myasthenia gravis in rhesus monkeys: a model for the study of the human disease. 379 23

A case of oculopharyngeal muscular dystrophy in an elderly woman of French-Canadian background presenting with dysphagia is discussed. Typical features of the clinical presentation include bilateral ptosis and dysphagia with significant potential for morbid outcomes of aspiration pneumonia and malnutrition. Although relatively uncommon, this diagnosis should be considered in an elderly person with dysphagia, a history of ptosis, and the proper family background. Surgical treatment appears to improve the signs and symptoms of this disease.
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PMID:Oculopharyngeal muscular dystrophy as a cause of dysphagia in the elderly. 394 5

The natural history of a moderate intoxication with botulin (probably type B) in six patients is presented and discussed. All patients complained of a persistent and almost complete failure of accommodation, and marked dryness of the mouth. Reduced lacrimation was also noticeable. A disturbance of efferent pupillary reaction was noted only in four patients, and resolved relatively early. On testing with highly diluted pilocarpine solution, a denervation hypersensitivity reaction of the sphincter pupillae was seen. An optic nerve lesion could not be demonstrated in any of the cases. Manifest involvement of the striated musculature, such as a bilateral lateral rectus palsy and ptosis, was found in only one patient. In four patients the presenting symptom was gastroenteritis. Other systemic symptoms were dysphagia, persistent constipation, problems with micturition, general malaise and postural symptoms. All of the patients made a full recovery at the latest after 10 weeks.
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PMID:[Botulism--observations on its course with emphasis on ophthalmologic symptoms]. 397 56

Oculopharyngeal muscular dystrophy is a localized or restricted variety of muscular dystrophy, characterized by bilateral ptosis, myopathic facies, external ophthalmoplegia and dysphagia. A patient with this unusual myopathy is described and detailed esophageal motility studies are presented that provide conclusive evidence of both striated and smooth muscle involvement.Because these unusual localized forms of muscular dystrophy exist and may be of late onset, previous rigid concepts concerning the dystrophies should be discarded.
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PMID:Late-onset muscle dystrophy: oculopharyngoesophageal variety. 594 Mar 25


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