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)

Patients with bulbar amyotrophic lateral sclerosis (ALS) are often referred to the otolaryngologist/head and neck surgeon and speech pathologist for evaluation and management of dysphagia and dysarthria. These patients comprise an unusual group because of the progressive and multi-system nature of their illness. The neuromuscular disabilities associated with bulbar ALS cause a myriad of related symptoms associated with swallowing, speech, and respiration. Although the rate of progression cannot be predicted, a general pattern of progression is noted. Bulbar disease accounts for the majority of the worst symptoms of ALS. The loss of the ability to swallow changes eating from a pleasurable task to a burden of survival. Loss of communication effectively imprisons the patient in a state of isolation. The progressive weakness of respiration, predominantly a spinal rather than bulbar manifestation, is the cause of death for nearly all ALS patients and is also discussed. The general patterns of progression of bulbar ALS are outlined in this paper. The development of symptoms are correlated with specific treatment recommendations to aid the clinician in devising an orderly plan of management for this progressive disease.
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PMID:Bulbar amyotrophic lateral sclerosis: patterns of progression and clinical management. 258 13

Scleromyxedema is an infiltrative skin disease produced by hyaluronic acid deposition in the dermis. A benign monoclonal gammopathy is usually present. We report 2 patients with scleromyxedema and systemic illnesses. Both patients had muscle weakness, dysphagia, and weight loss in addition to the skin changes. One also had sclerodactyly, telangiectasias, and Raynaud's phenomenon. Scleromyxedema with systemic involvement may mimic rheumatic diseases.
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PMID:Scleromyxedema with systemic involvement mimics rheumatic diseases. 294 92

Generalized weakness, intermittent dysphagia, and a 40-pound weight loss developed in an elderly man over a six-month period. Examination revealed weakness, atrophy and fasciculations of extremity musculature, pseudobulbar speech, hyperactive upper extremity reflexes, and extensor toe signs without sensory loss. Results of electrodiagnostic studies were consistent with an axonal polyneuropathy. Endocrinologic results were compatible with hyperthyroidism. Radioiodine therapy resulted in resolution of clinical neurologic symptoms and signs within seven months. This case illustrates a previously undescribed concurrence of hyperthyroid associated polyneuropathy and pyramidal tract dysfunction that led to an initial clinical diagnosis of amyotrophic lateral sclerosis.
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PMID:Pyramidal tract deficits and polyneuropathy in hyperthyroidism, Combination clinically mimicking amyotrophic lateral sclerosis. 299 Feb 4

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

The authors report a case of Isaacs syndrome observed in a 40 years old woman. The clinical picture included progressive muscular weakness, dysphagia, dysphonia, dyspnea and increased perspiration. Fasciculations, facial myokymia and pseudomyotonia were observed on physical examination. Electromyographic study at rest revealed continuous electrical muscle activity. Muscle histochemistry showed type II fibers atrophy and an ultrastructural study of the gastrocnemius muscle disclosed marked cysternal dilatation of the sarcoplasmatic reticulum. An excellent clinical response was observed with the use of carbamazepine. Some recent aspects of this rare syndrome are reviewed and discussed.
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PMID:[Isaacs syndrome: report of a case]. 320 16

Ten patients with spasmodic torticollis were treated by injection of a total dose of 30 ng of botulinum toxin type A into the affected sternomastoid and posterior cervical muscles. Nine patients reported improvement in head position and control, which was confirmed in seven cases by clinical assessment and "blind" videotape ratings before and 6 weeks after injection. Five patients who had pain reported relief. Seven patients had mild transient dysphagia after injection; two who were given a more concentrated solution of the toxin developed more severe dysphagia, but this also recovered. Other minor transient side effects included weakness of the voice and local pain. The beneficial effects of botulinum toxin injections lasted some 2 to 3 months. A slight reduction in the total dose of toxin injected avoided the main side effects, and this method of treatment appears to offer successful control of head position and pain in the majority of patients with torticollis.
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PMID:Botulinum toxin in spasmodic torticollis. 320

A rare case of esophageal cancer with brain metastasis is reported. A 54-year-old man complaining of dysphagia was admitted to our hospital. Endoscopic and radiographic examinations revealed an advanced esophageal cancer with supraclavicular lymph node metastasis. Five months later, muscle weakness of right upper extremities developed. A brain CT scan revealed a low density area with a ring enhancement in the left front parietal region. The patient developed right hemiplegia and delirium, and died seven months later. Autopsy findings showed a hematogenous metastasis of the left precentral gyrus, measuring 3.0 x 2.5 x 2.5 cm.
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PMID:[An autopsy case of esophageal cancer with brain metastasis]. 328 77

Scleromyxedema is a rare fibromucinous connective tissue disorder characterized by papular skin lesions associated with sclerosis and a serum monoclonal gammopathy. Little is known about either the natural history or the systemic manifestations of this disease. We reviewed the medical records of 19 patients with biopsy-proven scleromyxedema seen from 1950 to 1985 for evidence of systemic disease. There were 10 males and 9 females with a median age at diagnosis of 53 years. Monoclonal gammopathy was present in 13 patients. Eight patients complained of dysphagia; 3 had proximal esophageal dysfunction and 1 had total esophageal aperistalsis on barium swallow. Proximal muscle weakness was noted in 5, with an inflammatory myopathy in 3. Six patients complained of dyspnea on exertion. Of these, 5 had reduced diffusing capacity, 3 had reduced volumes, and 2 developed cor pulmonale. Pathologic changes characteristic of "scleroderma kidney" were demonstrated in 1 patient at postmortem. One patient had Raynaud's phenomenon and 2 had arthralgias/arthritis with noninflammatory synovial fluids. Although 8 of 12 patients treated with melphalan noted regression of their skin changes, no consistent improvement in the extracutaneous manifestations was demonstrated. Furthermore, 2 patients died of sepsis related to melphalan-induced myelosuppression, and 4 developed hematological malignancies following melphalan therapy. In conclusion, systemic manifestations in scleromyxedema are more prevalent than previously recognized, and can resemble those of scleroderma. Significant toxicity occurred with the use of alkylating agents in these patients, with treatment-related complications developing in 45% of patients treated with melphalan. The lack of definitive data regarding the natural history of this disease complicates the question of optimal therapy, but the use of alkylating agents should be reserved for those patients with severe debilitating skin disease.
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PMID:Scleromyxedema: a scleroderma-like disorder with systemic manifestations. 333 81

Four pups in a litter of eight Labrador Retrievers suddenly developed hind limb weakness. In three, paralysis ascended rapidly resulting in quadriplegia, cervical weakness, dysphagia and death. Postmortem examination revealed a severe polyradiculoneuritis in which roots, ganglia, and spinal and cranial nerves were heavily infiltrated by lymphocytes, plasma cells and macrophages and contained abundant protozoan pseudocysts. On sections of the brain and spinal cord protozoa were less frequent and appeared independent of the glial nodules which marked focal areas of necrosis. The organisms initially were thought to be Toxoplasma gondii, but this supposition was not supported by serological, immunocytochemical, or electron microscopic findings. Ultrastructurally the organisms resembled an unidentified sporozoan parasite, which has been reported in the CNS of dogs in Scandinavia. The inflamed spinal roots contained many degenerated and demyelinated axons. Electron microscopic studies indicated that the tachyzoite-like organisms, through their invasive and proliferative activities, brought about many of the degenerative changes in the Schwann cells and axons of the spinal roots and nerves.
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PMID:Canine protozoan polyradiculoneuritis. 339 93

The rapid diagnosis and immediate intervention required in patients with serious drug overdose or poisoning makes toxicological screening of limited value to the emergency department physician. Instead, a careful clinical evaluation using the history, physical examination, and the more readily available laboratory tests may allow a tentative diagnosis and the initiation of life-saving treatment. Laboratory tests should include serum osmolality, electrolytes, glucose, BUN and an estimation of the anion and osmolar gaps. The ECG can also provide useful information. Clinical findings of important include altered blood pressure, pulse, respiration and body temperature, the presence of coma, agitation, delirium or psychosis, and muscular weakness. An ophthalmological examination is also of importance in the acutely poisoned patient. Oral burns or dysphagia may occur following ingestion of any strongly reactive substance, but the absence of oral burns does not preclude the possibility of oesophageal or stomach injury. Odours and skin colour may also contribute to the diagnosis. Comprehensive toxicology screening may not be immediately available, or may be inaccurate, thus adding little to the information obtained during the initial evaluation of the poisoned patient.
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PMID:Physical assessment and differential diagnosis of the poisoned patient. 354 6


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