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)

Botulinum A toxin was injected into the affected muscles in 20 patients with blepharospasm, 8 with torticollis and 12 with hemifacial spasm. In all cases blepharospasm and hemifacial spasm was abolished or markedly reduced. The only side effect was transient ptosis and diplopia. Patients with torticollis had a mild to moderate improvement of the dystonic posture and pain; dysphagia was the most troublesome side effect. Botulinum A toxin is an effective therapy in patients with focal dystonia and spasms.
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PMID:Botulinum A toxin injection in patients with blepharospasm, torticollis and hemifacial spasm. 208 84

In late September 1986, we found 7 patients from a printing factory in Chang-Hwa city who developed an endemic disease manifested by general malaise, ptosis, double vision, dysarthria, dysphagia, and proximal limb weakness. After clinical, epidemiological, microbiological, and toxicological investigations, an outbreak of botulism was confirmed 2 weeks later, Commercially canned peanuts made by an unlicensed cannery were identified as the vehicle of botulinum toxin transmission. Antitoxin was given to 2 patients who needed ventilator support. One of the 7 victims died from medical complications and the remaining 6 patients recovered. Several administrative problems exposed in this outbreak were the poor governmental supervision of canned food, the inadequate quantities of "orphan drugs" stored in this country, the inefficient system for recalling the problem products, and the delayed broadcasting of warnings to the public. Since commercially processed food is increasingly popular with modernization, the possibility of future botulism outbreaks should not be overlooked.
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PMID:Outbreak of type A botulism caused by a commercial food product in Taiwan: clinical and epidemiological investigations. 217 23

Symptoms compatible with vertebrobasilar ischemia have been reported in patients with unilateral or bilateral carotid occlusive disease. Intracranial steal phenomena have been proposed to explain the symptoms. In a review of 54 patients with angiographically documented severe bilateral carotid stenosis (less than or equal to 2 mm residual lumen) or occlusion, eight had symptoms suggesting vertebrobasilar insufficiency. Five patients were identified retrospectively, and the other three were evaluated prospectively. Symptoms included various combinations of hemodynamically mediated, transient bilateral motor, sensory, or visual impairment. Dysarthria, dysphagia, and diplopia were generally absent. Each patient also described additional symptoms compatible with transient hemispheric or retinal ischemia. The anatomic regions subserving the bilateral vertebrobasilar-like symptoms could be correlated with angiographically estimated arterial border zones in both hemispheres and may thus represent bilateral hemispheric border zone ischemia rather than brain stem ischemia. An intracranial steal need not be invoked.
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PMID:The syndrome of bilateral hemispheric border zone ischemia. 226 72

Hepatolenticular degeneration (Wilson's disease) is a hereditary disease in which metabolic disorder of copper leads to its accumulation in the liver, brain, cornea and kidneys with consequent pathologic changes in those organs. Hereditary mechanism of the disease is autosomal recessive with prevalence of 30-100 per 1,000,000 inhabitants. Etiology of this disease is not yet explained. There are two hypotheses. The first one is that it is the disorder of ceruloplasmine metabolism caused by insufficient synthesis of normal ceruloplasmine, or synthesis of functionally abnormal ceruloplasmine. The second one is: the block of copper biliar excretion which is the consequence of the liver lysosomes functional defect. Pathogenetic mechanism of disease is firstly long-term accumulation of copper in the liver, and later, when the liver depo is full, its releasing in circulation and accumulation in the brain, cornea, kidneys and bones, which causes adequate pathologic changes. Toxic activity of copper is the consequence of its activity on enzymes, particularly on those with -SH group. There are two basic clinical forms of the disease: liver disease or neurologic disease. Before puberty the liver damage is more frequent, while in adolescents and young adults neurologic form of the disease is usual. The liver disease is nonspecific and characterized by symptoms of cirrhosis and chronic aggressive hepatitis. The only specificity is hemolytic anemia which, in combination with previous symptoms, is important for diagnosis of the disease. Neurologic symptoms are the most frequent consequence of pathologic changes in the basal ganglia. In our patients the most frequent symptoms were tremor (63%); dysarthria, choreoathetosis and rigor (38%); ataxia and mental disorders (31%); dysphagia and dystonia (12%), diplopia, hypersalivation, nystagmus and Babinski's sign (6%). Among pathologic changes in other tissues and organs the most important is the finding of Kayser-Fleischer ring in the cornea as a result of copper accumulation. Its importance for precise diagnosis is great. The diagnosis of the disease is based on anamnesis, clinical examination, specific and nonspecific laboratory tests. The therapy of choice is penicillamine. If we use it early, the result will be good remission in the majority of patients. Late diagnosis or delay in treatment cause death which is the result of bleeding from esophageal varices or basal ganglia disease. Immunologic damages caused by penicillamine demand interruption of therapy and substitution by three-ethyl-tetra-amine (TETA). We also use zinc salts and tetratiomolibdate in therapy of this disease. Pathogenesis, clinical picture and therapy of the disease are based on our own results.
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PMID:[Hepatolenticular degeneration]. 226 49

A sixty-year-old man was admitted to our hospital on January, 1989. He had suffered a hemorrhage in the right side of pontine tegmentum on April, 1988. He had been in deep coma for about a week, and then he had showed diplopia, mild right deafness, right facial palsy, left hemiparesis, dysarthria, dysphagia, and urinary disturbance. He showed slight improvement of these symptoms and signs, but had developed thereafter extremity myorhythmia on the left side. On admission, rightward slow eye movement (absence of saccadic eye movement and preservation of pursuit eye movement of both eyes) was present. MRI revealed a hypointensity lesion with a hyperintensity spot on T2-weighted images showing an old hemorrhage in the right pontine tegmentum and a hyperintensity lesion on T2-weighted images showing an olivary pseudohypertrophy on the right. We concluded that the extremity myorhythmia in this patient was caused by the damage of the right central tegmental tract followed by right olivary pseudohypertrophy. The rightward slow eye movement was considered to be due to the damage of the right paramedian pontine reticular formation and/or its afferent fibers in the pontine tegmentum.
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PMID:[Left-sided extremity myorhythmia and rightward slow eye movement caused by a hemorrhage in the right pontine tegmentum]. 233 25

We evaluated and presented here, the features of the eleven cases of food-borne botulism who admitted to the Infectious Diseases Department of Ibni Sina Hospital of Ankara University. Three of the cases admitted in 1984 and eight of them admitted in 1987. All of the cases were caused by home-prepared foods which had been eaten without cooking; the types of the food were green beans and pepper with sauce. In these cases the main symptoms and signs were generalized muscular weakness, dry mouth, dysphagia, diplopia, ptosis of the eyelids; besides these the other clinical symptoms and signs were seen in some patients. Although toxin couldn't be detected in the patients' sera by mouse-toxin neutralization, the EMG findings supported our diagnoses. To the three patients in the first group, botulinal anti-toxin was not given and two of them died. Anti-toxin was administered to the seven patients in the second group, none of them died.
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PMID:[Food-borne botulism and its epidemiological features as seen in our country during the last few years]. 248 35

Chondrosarcoma of the skull base is a rare neoplasm. The most common presenting symptoms are hoarseness, dysphagia, and diplopia, which is associated with palsies of cranial nerves X, IX, and VI. The temporal bone is the most common site of tumor origin, followed by the sphenoid bone. These tumors must be differentiated from chordoma, chondroid chordoma, osteogenic sarcoma, enchondroma, and meningioma. Diagnosis is made by patient history, radiologic imaging, and biopsy. The treatment is surgical excision followed by radiation therapy. Five-year survival rates for grades I, II, and III are 90, 81, and 43%, respectively.
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PMID:Extracranial skull base chondrosarcoma. 268 2

We reported a 71-year-old male with lateral medullary syndrome presented acute respiratory arrest after ataxic respiration. The patient had experienced transient diplopia repeatedly for about 2 weeks and then the developed persistent diplopia and vertigo. On the third day he was admitted to our hospital because of neurological deterioration and aspiration pneumonia. He showed left Horner's sign and double vision. And he had sensory disturbances of pain and temperature in the left face and the right side of the body, left limb ataxia and truncal ataxia. He showed dysarthria, severe dysphagia and left mild central facial paresis, but no hemiparesis. This case was clinically considered to be a typical case of left lateral medullary syndrome. When he was admitted to our hospital, he showed hypoxia with hypercapnea in spite of no history of chronic obstructive pulmonary disease. This condition was considered to be a central alveolar hypoventilation. He had two episodes of sudden-onset respiratory arrest following ataxic respiration on the 4th and 5th days, but no cardiac arrest. He was supported his respiration by mechanical ventilation until he was able to breathe spontaneously on the 29th day. The 22nd day MRI disclosed high intensity area in the left lateral and dorso-medial medulla in T2-weighted image, and this lesion was 1.5 cm in length. Therefore this case was diagnosed medullary infarction. This case developed ipsilateral facial pain in chronic stage. Pain existed around the eye and in the cheek, and pain was like toothache and unbearable like thalamic pain.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:[A case of medullary infarction presented lateral medullary syndrome and respiratory arrest after ataxic respiration]. 268 32

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

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


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