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)

A case of myasthenia gravis accompanied with polymyositis and malignant thymoma, detected immune complexes in the sera and around the muscle fibers, was described. A 37-year-old woman was admitted to Shinshu University Hospital in September, 1987 because of dyspnea, dysphagia and muscle weakness. She first noticed her right blepharoptosis 3 weeks before admission. Weakness of all four limbs and myalgia of lower extremities were noticed one week later. These symptoms got worse and nocturnal dyspnea, dysphagia and easy fatigability at mastication appeared. On admission, she looked ill and neurological examination revealed left blepharoptosis, bilateral facial weakness, weakness of all four limbs, more prominent in proximal muscles and tenderness of lower extremities. Edrophonium test was positive, improving her muscle weakness. Laboratory examination revealed the elevated serum levels of CK, the increased titre of circulating immune complexes and high titres of acetylcholine receptor antibodies and anti-skeletal muscle antibodies. Electromyographic study showed myogenic pattern and Harvey-Masland test revealed waning at low frequency stimulation. Muscle biopsy showed marked perivascular infiltration of lymphocytes, accompanied by phagocytosis and interstitial fibrosis. IgG deposits were shown around the muscle fibers exclusively around the infiltrates of mononuclear cells. Granular deposits of C3 were also shown specifically around the muscle fibers exclusively around the infiltrates of mononuclear cells. Thymectomy was performed on September 21, 1987. Invasion of thymoma, predominantly lymphocytic type, to right lung and pericardium was observed histologically. After thymectomy, she got better. Immunological data and immunohistochemical examination of the present case suggest that in the case of myasthenia gravis accompanied with polymyositis and malignant thymoma, immune complexes may play a primary role on the pathogenesis of myositis.
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PMID:[Detection of immune complexes in the sera and around the muscle fibers in a case of myasthenia gravis and polymyositis]. 253 18

Data from 357 conscious stroke patients taking part in an acute intervention trial and assessed within 48 hours of the onset of symptoms, were used to investigate the prevalence and natural history of swallowing problems. Nearly 30% of patients with single-hemisphere strokes were initially found to have difficulty swallowing a mouthful of water, but in most of those who survived, the deficit had resolved by the end of the first week. Strong correlations were found between dysphagia and speech impairment (comprehension and expression) and with facial weakness, but there was no association with the side of the stroke. After controlling for other markers of overall stroke severity such as conscious level, urinary continence, white blood cell count and strength in the affected limbs, swallowing impairment still showed a significant inverse correlation with functional ability at 1 and 6 months. These results indicate that, even if dysphagia itself is not responsible for much excess mortality in acute stroke, it might still lead to complications which hamper functional recovery.
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PMID:The natural history and functional consequences of dysphagia after hemispheric stroke. 256 84

A sporadic case of spinocerebellar degeneration with prominent involvement of the motor system has recently been encountered. A 54-year-old man without family history noticed speech disturbance at the age of 46 and weakness in his right hand the following year. The muscle weakness and atrophy were slowly progressive and made walk impossible at the age of 50, when his dysphagia increased. At the age of 54, he was admitted to our hospital when neurological findings revealed marked amyotrophy of general skeletal muscle and tongue with fasciculation. Deep tendon reflexes were decreased. Cerebellar ataxia was impossible to evaluate because of profound muscle weakness. And sensory disturbance was suspected in the distal portion of the lower extremities. CT scan revealed progressive atrophy of the brain stem and cerebellum. The patient died at the age of 54 due to CO2 narcosis. The clinical course was 8 years. A summary of the pathological findings was as follows: 1) Marked neuronal loss of the anterior horn of the spinal cord and motor cranial nerve nuclei except for oculomotor nuclei, with mild degeneration of pyramidal tract below lumbosacral level. 2) Degeneration of cerebellipetal system, spinocerebellar tract, Clarke's column and the middle root zone and cerebellifugal system, dentate nucleus, superior cerebellar peduncles, and red nucleus. 3) Mild degeneration of pontine nuclei, inferior olivary nuclei, pontine transverse fibers, the middle and inferior cerebellar peduncles, cerebellar white matter and Purkinje cells as in OPCA.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:[A nosological study of a patient showing ataxia & lower motor neuron involvement]. 259 37

A 64-year-old male patient of amyotrophic lateral sclerosis (ALS) with frozen gait, axial rigidity and supranuclear upper gaze palsy was reported. We have followed this patient more than four years. He was well until November 1982, when he noticed weakness of left arm. In March 1983, he noticed hypogeusia and in July, he developed dysarthria and frozen gait. On admission, he was alert and oriented. Neurological examination revealed dysarthria, dysphagia and muscular weakness and atrophy in bilateral upper extremities, dominantly in left side. He showed remarkable frozen gait, retropulsion and could not walk. Brain CT showed mild dilatation of the third ventricle. In August 1988, he showed tongue atrophy, and weakness and atrophy of the extremities progressed during these four years. He also showed axial rigidity and frozen gait. Brain CT showed severe third ventricular dilatation and atrophy of tegmentum of the midbrain and cerebellum that were compatible with progressive supranuclear palsy (PSP). Six months later, he developed upper gaze palsy. From these findings, we concluded that this patient had a quite unique clinical features of both ALS and PSP.
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PMID:[A case of amyotrophic lateral sclerosis associated with clinical features of progressive supranuclear palsy]. 259 46

A 57-year-old woman suffered from polyarthralgia for 7 years, and was treated by using NSAID with the diagnosis of RA. From Jan. 20th 1987, she complained of back pain and numbness of both hands, and from May 7th 1987, she also complained of dysphagia and dysarthria, and she was not able to button up. Soon afterwards she could eat only one custard pudding a day, so she admitted to our hospital on March 17th 1987. The neurological examination showed hyporeflexia and muscle weakness of the four extremities; and hypesthesia of the 7th to 11th intercostal nerve area and both lateral sides of the dorsum pedis. The laboratory examination showed ESR 17 mm/h, gamma-glob 1.66 g/dl, CRP(+), RAHA 80 x, CH50 24.0 U/dl, HLA-antigen; DR 4(+). Cerebrospinal fluid examination showed cell 5/mm3, protein 63 mg/dl, IgG 13 mg/dl, IgG% 20.6%. X-ray examination indicated destruction of both wrists, left elbow, right 2-5th MTP, and left 5th MTP joints. A light microscopic examination of the left sural nerve showed perivascular infiltration with lymphocyte, occasional macrophages and giant cells at the epineurium, and no demyelination or Wallerian degeneration at the nerve fiber. These histological findings were the same as type-I arteritis in nerves in RA proposed by D.L. Conn. Clinical improvement was obtained after administration of prednisolone 30-60 mg/day.
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PMID:[A case of rheumatoid arthritis associated with polyneuritis]. 266 32

Tubular aggregates (TA) are unusual intramuscular structures stained basophilic on hematoxilin and eosin (HE) staining and red on modified Gomori trichrome (GT) staining. The structures are said to be originated from sarcoplasmic reticulum and are collections of tubules with double membranes on electron microscopic studies. The TA are usually seen in biopsy muscles from patients with muscle pain and cramps but without muscle weakness, periodic paralysis or alcoholic myopathy. In addition, there are five reports on families with progressive myopathy and tubular aggregates in the literature. We presented here a 48-year-old postman without any family history, who had had progressive muscle weakness for 17 years. He had never noticed pain or cramps in his muscles, not taken any particular medicine, and not had regular alcoholic beverages. There was no ptosis, facial weakness, masticatory muscle weakness or dysphagia. Muscle wasting, started from the proximal part of four extremities had progressed to the distal part of them. He could not walk on heels or toes and walked with waddling gait. He stood up with Gowers' maneuver. Serum GOT, GPT and CK were elevated. EMG showed myogenic pattern and MCV was normal. The muscle biopsies were performed; the first one taken from quadriceps femoris muscle at 42 years old showed myopathic changes including marked variation in fiber sizes, with scattered necrotic fiber splitting and TA in type 2B fibers. The second biopsy from biceps brachii muscle at the age of 48 years, showed densely proliferated fibrous tissues, marked variation fiber sizes and scattered split fibers. The TA were rarely seen and type 2B fibers were decreased in number.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:[A case of progressive myopathy with tubular aggregates]. 268 70

A case of polymyositis with repeated dysphagia and muscle weakness associated with peculiar findings of skin was reported. The patient was a 67-year-old man. His birth and development was normal. There was no family history of neuromuscular disease. On 26th March 1987 he was admitted to a hospital because of dysarthria and dysphagia after fever and diagnosed as having viral myositis. His conditions improved spontaneously with bed rest and he left hospital on 14th April. On 23rd April he had chill and sore throat with fever. On 27th he was admitted to the same hospital because of dysarthria and muscle weakness of the proximal portion of the upper limbs. These symptoms also improved with bed rest. He had repeated these symptoms several times and then he was admitted to our hospital on 12th June. On examination he showed the skin pigmentation under the right eye and the eruption in the back of hands and the buttocks. Muscle weakness was observed in the proximal portion of the upper limbs and the neck flexor. Laboratory tests in admission were as follows: sGOT 49 mU/ml, sGPT 104 mU/ml, LDH 1064 mU/ml, CPK 565 mM/ml, aldolase 25.2 IU/1/37 degrees C. Electromyography showed the typical myogenic changes and biopsy of left biceps brachii revealed inflammatory cells in the muscle fiber which are specific to polymyositis. Immuno-histochemical study is performed to analyse the subpopulation of mononuclear cells in biopsied muscle and skin. Mononuclear cells infiltrated into perimysium, endomysium and epidermis were positive for T11 and T8, but less positive for T4, B1 and Leu11. On the basis of these findings he was diagnosed as having "polymyositis syndrome".
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PMID:[A case of polymyositis with repeated dysphagia and muscle weakness associated with peculiar findings of skin]. 280 15

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

Four elderly patients with inclusion body myositis and dysphagia are described. Dysphagia was the presenting symptom in three, preceding generalised weakness by 1.5 to 7 years. Myotomy of the cricopharyngeal muscle improved the symptoms and signs in 3 of the 4 patients. It is suggested that inclusion body myositis is not an infrequent cause of dysphagia in elderly people, and is amenable to treatment.
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PMID:Dysphagia in inclusion body myositis. 285 42

A 17-year-old girl presented with malaise, weakness, palpitations, dysphagia, myalgias, and weight loss of 1 month's duration. Within 24 hours of admission to the hospital, she had hypotension unresponsive to medical management, intractable congestive heart failure, and arrhythmias; she died. Several empty bottles of syrup of ipecac were later found among her belongings. Syrup of ipecac is commonly used to induce emesis in patients who had ingested toxic substances. The chief pharmacologic property of this agent is due to its alkaloid component, emetine. There have been many previous reports of death due to emetine poisoning in patients receiving ipecac fluid extract and in those treated for amoebic dysentery. However, the literature cites only three case reports of fatalities secondary to chronic ipecac use as a means of losing weight. This is the first report of a death due to chronic ipecac use in an adolescent patient with bulimia. Emetine persists in the body for long periods, and in patients who have ingested it chronically, emetine is extremely toxic, specifically to cardiac smooth and skeletal muscles. With an increased awareness of the importance of weight control in the adolescent age group, the physician must carefully evaluate these patients for the use of emetics.
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PMID:Death due to chronic syrup of ipecac use in a patient with bulimia. 287 30


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