Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C1762617 (weakness)
 37,932 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

An opportunity to investigate the role of anti-acetylcholine receptor antibody (anti-AcH R-antibody) in neonatal myasthenia gravis was presented when an infant was born to a symptomatic myasthenic mother who elected to breast feed the child. Pyridostigmine bromide determinations in plasma and breast milk were made by quantitative gas liquid chromatography. Anti-AcH R-antibody was assayed by an immunoprecipitation method. Simultaneous maternal blood and milk samples did not suggest concentration of pyridostigmine bromide in milk or significant transfer of medication through demand breast feeding. Weakness was not noted in the neonate in spite of high levels of anti-AcH R-antibody demonstrated in her blood. Presence of a markedly elevated anti-AcH R-antibody in a pregnant patient symptomatic with myasthenia gravis does not necessarily predict a clinically affected offspring, nor does the elevated antibody in the infant, presumably acquired transplacentally, necessarily result in clinical symptomatology in the newborn period.
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PMID:The role of anti-acetylcholine receptor antibody in neonatal myasthenia gravis. 75 66

A 12-year-old boy who had suffered from severe schizophrenia for 8 years developed myasthenia gravis. Both disorders were treated simultaneously and successfully with neostigmine bromide. The authors suggest that these two disorders may in some cases be part of the same disease process and urge that physicians consider this possibility in patients with severe emotional problems and muscle weakness.
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PMID:Coexisting childhood schizophrenia and myasthenia gravis treated successfully with neostigmine bromide. 90 Feb 86

During the summer and fall of 1973, a few horses, goats, and cattle in the Napa Valley of California became intoxicated by bromide via the ingestion of volunteer oat hay that had been cut from a field treated with methyl bromide, a soil fumigant. The bromide content of the hay ranged from 6,00 to 8,400 ppm. Signs of intoxication were lethargy, weakness, and ataxia. Animals experimentally fed the contaminated hay developed signs of intoxication between the 7th and 9th days.
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PMID:Bromide intoxication of horses, goats, and cattle. 90 90

Symptoms as an important sign of the effects of methyl bromide were studied in 56 male workers (37 currently exposed and 19 previously exposed) in a methyl bromide factory. The workers were 18 to 62 yr of age (mean age: 41) and were exposed from 1 to 25 yr (mean: 7 yr). They were compared to 56 age-matched referents with a standardized questionnaire. The results of pairwise comparison of the symptoms of the age-matched pairs of exposed and referent subjects showed that the occurrence of dizziness, numbness, paresthesia and weakness of extremities, nightmares, fatigue and dry and scaly skin was statistically significantly higher among the workers than among the referents. When the symptoms during the work shift (acute symptoms) were compared, irritation symptoms such as itching, bullae or reddish swollen hands and runny noses with nasal irritation were reported significantly more often in the exposed groups. The correlation of the symptoms among the exposed workers suggested that chronic symptoms are closely related to acute irritation symptoms and exposure duration. The results suggest that symptom inquiry is useful for detecting the possible effects of exposure to methyl bromide.
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PMID:Symptoms among workers with long-term exposure to methyl bromide. An epidemiological study. 165 69

In therapy lasting between 8 and 79 (means = 31) months 22 epileptic dogs had been unsuccessfully treated with phenobarbital and/or primidone. Both drugs had been administered in their maximum dosages. In an add-on therapy, these dogs were given potassium bromide at a rate of 17 to 58 mg/kg daily for a period of 7 to 61 (means = 21) months. We could quantitatively evaluate the seizure data from 19 of the dogs: four became free of seizures; seven showed a greater than 50% reduction in seizure frequency; in two dogs, the seizures were reduced by greater than 50% but the number of seizure-days by less than 50%; in the remaining six dogs the therapy was unsuccessful. We achieved the best therapeutic results in animals that suffered only grand mal seizures. Grand mal in addition to other types of seizures and tonic seizures were affected to a lesser extent if at all. At the beginning of the therapy we saw temporary side effects--weakness in the hind limbs and sedation; these were temporary and dependent on the dosage. Serum concentrations differed even with the same dosage among individual dogs. The therapeutic range of bromide serum concentration was from 0.7 to 2.0 mg/ml. Most of the animals tolerated concentrations up to 1.5 mg/ml quite well. To begin an add-on therapy with potassium bromide we would recommend a daily dose of 30 to 40 mg/kg. During treatment, the dose should be determined for each individual dog.
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PMID:[Effectiveness of bromide in therapy resistant epilepsy of dogs]. 194 87

In one hospital over a 15-month period, four out of nine patients ventilated for acute severe asthma developed acute hydrocortisone myopathy. All patients had received less than 1.0 g day-1 hydrocortisone. Affected patients had severe generalized weakness which recovered over 1-6 weeks. When myopathic and unaffected subjects were compared, there was no clearcut difference with respect to age, sex, types of drug used, serum potassium levels, duration of ventilation and muscle paralysis, total dose of vecuronium bromide, or mean daily doses of hydrocortisone. The main difference between the two groups was in the total doses of hydrocortisone. The myopathic patients all received greater than 5.0 g hydrocortisone (range 5.4-10.2 g) and the others less than 4.0 g (range 0.9-3.5 g). The possibility that neuromuscular blockade might predispose to the development of myopathy is discussed. Hydrocortisone myopathy can occur when less than 1.0 g day-1 is used, and even with as little as 5.4 g given over 6 days.
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PMID:Risk factors for hydrocortisone myopathy in acute severe asthma. 227 93

Myasthenia gravis (MG) was diagnosed in four cats--one had an apparently congenital form and three had the acquired autoimmune form. All four cats were examined because of episodes of weakness including gait abnormalities, voice change, neck ventroflexion, and regurgitation. Palpebral reflexes were absent in all cats. Administration of edrophonium chloride resulted in transient resolution of clinical signs in all four cats. Three cats were tested for the presence of serum autoantibodies against acetylcholine receptor (AChR) by radioimmunoassay. Two cats with acquired MG had anti-AChR antibody titers of 10.5 and 96.8 nmol/l (normal, less than or equal to 0.03 nmol/l). Antibodies were not detected in the cat with presumptive congenital MG. All four cats were treated with pyridostigmine bromide. Two cats with acquired MG were euthanatized because of clinical deterioration. The third cat with acquired MG has been asymptomatic since 2 months after diagnosis. The cat with presumed congenital MG is alive 3 years after diagnosis.
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PMID:Myasthenia gravis in the cat. 322 61

We describe pathological alterations at the light microscopical and ultrastructural level of motor end plates and muscle fibres in 2 critically ill patients with generalized muscular atrophy and weakness. Axonal degeneration of intramuscular nerve fibres was not conspicuous. The sural nerve in one patient showed only minor abnormalities. There was a marked atrophy of type 1 and especially type 2 muscle fibres. Nodal and ultraterminal nerve sprouts were seen in both biopsies. Motor end plates showed features of regeneration. They were enlarged in one patient. This patient was treated for a prolonged period with vecuronium bromide. Pharmacological denervation may explain the presence of fibrillation potentials, and, partially, of the histological abnormalities. Another factor which must be considered is inhibition of neuromuscular transmission by antibiotics. In addition to disuse atrophy and a minor degree of axonal neuropathy, the production of muscle proteolytic factors may be involved in the rapidly occurring massive loss of muscle fibre size in critically ill patients.
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PMID:Histological investigations of muscle atrophy and end plates in two critically ill patients with generalized weakness. 322 32

We investigated the breathing patterns of 17 subjects anesthetized with enflurane before and after partial muscle paralysis produced by pancuronium bromide. In the face of significant muscle weakness produced by pancuronium, breathing patterns are characterized by decreases in both tidal volume and respiratory frequency. The decreased tidal volume corresponded to the decrease in occlusion pressure, indicating that the decreased tidal volume results solely from a decreased contractile force of the respiratory muscles. The decreased respiratory frequency was due to prolongation of both inspiratory and expiratory time without changing the ratio of the inspiratory time to the total breath time. Withdrawal of phasic vagal influence by airway occlusion before partial muscle paralysis revealed that an active Breuer-Hering inflation reflex was operative in only 8 of all 17 subjects. Since the contribution of the Breuer-Hering inflation reflex alone does not seem to account for the consistent decrease in respiratory frequency, some other mechanisms modulating respiratory frequency might be involved in the characteristic breathing patterns during partial muscle paralysis under enflurane anesthesia.
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PMID:Breathing pattern of anesthetized humans during pancuronium-induced partial paralysis. 335 69

The influence of tonic inspiratory muscle activity on the relaxation characteristics of the chest wall, rib cage (RC), and abdominal wall (ABW) has been investigated in four highly trained subjects. Chest wall shape and volume were estimated with magnetometers. Pleural pressure (Pes) and abdominal pressure were measured with esophageal and gastric balloons, respectively. Subjects were seated reclining 30 degrees from upright, and respiratory muscle weakness was produced by pancuronium bromide until RC inspiratory capacity was decreased to 60% of control. Only minor changes were observed for Konno-Mead relaxation characteristics (RC vs. ABW) between control and paralysis. Similarly, although RC relaxation curves (RC vs. Pes) during paralysis were significantly different from control (P less than 0.05), the changes were small and not consistent. The differences between paralysis-induced changes in resting end-expiratory position of the chest wall and helium-dilution functional residual capacity (FRC) suggested changes in volume of blood within the chest wall. We conclude that 1) although tonic inspiratory activity of chest wall muscles exists, it does not significantly affect the chest wall relaxation characteristics in trained subjects; 2) submaximal paralysis produced by pancuronium bromide is likely to modify either spinal attitude or the distribution of blood between extremities and the thorax; these effects may account for the changes in FRC in other studies.
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PMID:Effects of paralysis with pancuronium on chest wall statics in awake humans. 399 28


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