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)

Weakness or stiffness of key posture muscles can cause much of the disability seen in elderly patients. Too much tension and too little exercise greatly increase the natural loss of muscular fitness with age. A systematic program of exercise, stressing relaxation and stretching of tight muscles and strenghthening of weak muscles, can improve physical fitness. The program must be tailored to the patient, starting with relaxation and gentle limbering exercises and proceeding ultimately to vigorous muscle-stretching exercises. Muscle aches and pain from tension and muscle imbalance are to be expected. Relaxation relieves tension pain, and strengthening weak muscles and stretching tight muscles will correct muscle imbalance. To prevent acute muscle spasm, the patient should avoid excessive exertion and increase exercise intensity gradually.
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PMID:Reconditioning aging muscles. 14 91

We report a 22-year-old very thin man, who showed various symptoms and signs of oculoskeletal muscle weakness, episodes of myalgia, prolonged diarrhea, severe myopia, perceptive deafness, electrocardiographic and electroencephalographic abnormalities, and endocrinological abnormality. The onset was at about 3 months of age and a positive family history was strongly suggested. The light-microscopic, histochemical and electron-microscopic findings showed abnormal mitochondria not only in the skeletal muscle, but also in liver cells. From the clinical as well as morphological points of view, this case was suspected to be one of congenital oculoskeletal myopathy probably due to an unidentified systemic metabolic disorder.
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PMID:Congenital oculoskeletal myopathy with abnormal muscle and liver mitochondria. 17 34

14 subjects with influenza or echovirus infection, all suffering myalgia, and 9 subjects with mumps, in whom this symptom was lacking, were investigated with single fibre electromyography (EMG) in the acute phase and during convalescence to reveal a possible disturbance in neuromuscular transmission. In both groups about the same percentage of the potential pairs studied showed abnormal transmission characteristics in the acute phase. Two weeks after the acute infection, this percentage had decreased significantly in the group with myalgia, whilst in the non-myalgia group it was still at the same level. However, on both occasions of investigation and in both groups the percentages were substantially greater than those recorded in healthy individuals. This study demonstrates that acute febrile infections may adversely affect neuromuscular transmission in previously healthy human subjects. The effects observed might offer an explanation to the accentuated muscular weakness in association with infections in patients with an already low safety margion of neuromuscular transmission, e.g. in myasthenia gravis.
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PMID:Distubed neuromuscular transmission in viral infections. 19 96

Forty-one children with dermatomyositis who were treated with corticosteroids and who have been followed over a period of 15 years have been presented. Progressive proximal muscle weakness was seen in all and 60% had muscle pain. The skin rash considered classic for dermatomyositis was seen in 33 children at the time of diagnosis. Elevation of serum muscle enzymes, electromyographic abnormalities, and muscle biopsy evidence of acute myositis were of confirmatory diagnostic value. The course of the disease in this study group has reconfirmed the efficacy of adrenal corticosteroid treatment in conjunction with an individualized physical therapy program and consistent followup. Prognosis for life and minimal functional disability has been good. There have been 3 deaths recorded in this series, only one of which was certain in its relationship to dermatomyositis.
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PMID:Dermatomyositis in the pediatric patient. 26 8

Five years following jejunoileal intestinal bypass surgery for obesity, a patient developed debilitating weakness and muscle pain. Osteomalacia was suspected clinically by radiographic and laboratory abnormalities and confirmed by bone biopsy. Malabsorption was documented as well as secondary hyperparathyroidism. Successful treatment of this syndrome with vitamin D and calcium identified a medically reversible disorder which obviated the need for surgical reanastomosis.
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PMID:Osteomalacia and weakness complicating jejunoileal bypass. 43 11

Myoglobinuria has a variety of causes, ranging from trauma to heavy exercise. Symptoms usually consist of myalgia and muscle weakness; dark, bloody-looking urine may be noted. Myoglobin can be identified by readily available laboratory techniques. Acute renal failure can be a dangerous consequence of myoglobinuria but, with rapid recognition and strict monitoring, the prognosis in most cases is good.
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PMID:Myoglobinuria. 48 22

A hyperthyroid patient treated with methimazole for three weeks developed proximal muscle weakness, myalgia, arthralgia, and fever, and thyrotoxic myopathy was diagnosed. The signs and symptoms spontaneously abated when antithyroid medication was discontinued. This case identified a complication of thionamide treatment mimicking thyrotoxic myopathy and points to the therapeutic necessity of making such a differentiation.
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PMID:Pseudothyrotoxic myopathy: a complication of thionamide therapy in hyperthyroidism. 50 96

A case of the rare systemic capillary leak syndrome (SCLS) is described. The patient suffered 9 attacks with muscle pain, weakness and profuse sweating. He showed increased Hct values up to 79 percent and a decreasing plasma volume to about 50 percent of normal. During the attacks the patient was in a state of shock and BP was unmeasurable. Studies with 131I-labelled albumin during attack showed an increased transcapillary escape rate to about 20 percent/hour, compared to 6 percent when he was without symptoms. A monoclonal IgG with a constant concentration of about 5g/l was found. Studies of the complement system during attack showed low C4 values, disproportions among the C1 subcomponents and C1r-C1s-C1IA complexes, suggesting a complement activation via the classic pathway. Hereditary angio-edema was excluded by normal C1IA values. The complement activation might be part of the pathogenesis of the increased macromolecular permeability in this syndrome. A short review of cases described earlier is given.
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PMID:Systemic capillary leak syndrome with monoclonal IgG and complement alterations. A case report on an episodic syndrome. 52 42

Four school children, aged 6 to 9 years, had acute postinfectious myositis. The prodromal illness usually involved the upper respiratory tract, but gastrointestinal symptoms were also seen. Fever and nonspecific malaise were characteristic. After cessation of the illness, myalgia involved the calves and thighs. Arm and neck muscles were less frequently affected. Weakness was less marked than muscle pain. Serum creatine phosphokinase (CPK) was markedly increased in all cases. Myalgia and CPK levels subsided in less than a week, although one child was not back to normal for 4 weeks. Two children had electromyography, and patchy myopathic changes were found. Viral studies were not helpful in any of the cases.
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PMID:Benign acute childhood myositis. 57 38

The case histories of 70 patients with typical motor neuron disease (MND) have been analysed to ascertain the natural history of the disease in Australia. The place of birth and residence during life of each patient has been sought to determine whether there is any 'clustering' of patients in the State of New South Wales. The mean age of onset was 55 years and mean duration of life from onset was 3 years 5 months. These figures are comparable with those from the USA and UK and Japan although the onset in Australia was later and the duration longer. The case history of 1 patient who is still living 38 years after the onset of the disease is described as there is no longer survival time recorded in the literature to our knowledge. Attention is drawn to muscle aches and cramps mentioned spontaneously by 27 of the 70 patients. These symptoms occurred at the onset of MND and often correlated with the site of onset of weakness. Weight loss averaged 1.6lb (0.7kg) per month in those patients in whom weight was recorded. The CSF protein was greater than 45mg/100ml, ranging up to 110mg/100ml, in 9 of 37 patients. The place of residence of patients bore no relation to known areas of increased manganese in the soil, and there was no evidence of 'clustering' of cases.
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PMID:Motor neuron disease in Australia (State of New South Wales). 61 8


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