SEARCH · PubMed Health

Results for “Muscle Weakness”

Explore indexed PubMed citations for clinical trials, systematic reviews and public health research. Read source abstracts and follow each citation to its original PubMed record.

Quote a phrase for an exact phrase match. Source license links do not imply unrestricted reuse.

At least 1,099 records · Page 61Linked to original sources

PubMed2003

Corticosteroids and skeletal muscle function in cystic fibrosis.

Patients with cystic fibrosis (CF) have reduced peripheral muscle strength. We tested the hypothesis that steroid treatment contributes to muscle weakness in adults with CF. Twenty-three stable CF patients were studied. Measurements included knee extensor (KE), knee flexor (KF), elbow flexor (EF), handgrip (HG), expiratory (Pemax), and inspiratory (Pimax) muscle strengths. Spirometry, body mass index (BMI), and days spent in hospital over the preceding 12 mo (DH) were also measured. Average daily dose of prednisolone over the preceding 12 mo (ADD) was 5.1 mg/day. Pearson's correlation analysis revealed that ADD correlated significantly with skeletal muscle strengths (KF%, r = -0.63, P < 0.01) with the exception of HG%. These findings are independent of age, BMI, pulmonary function, and DH. Multiple-regression analysis revealed that ADD was the most significant predictor of all measures of skeletal muscle function except HG%. It was independently responsible for 54% of the variance in Pimax%, for 46% of the variance in Pemax%, for 45% of the variance in KE%, for 39% of the variance in KF%, and for 41% of the variance in EF%. Concomitant medications (e.g., theophylline) were shown to have no causative effect. Corticosteroids contribute to the skeletal muscle weakness seen in CF patients. The correlation of proximal muscle strength, but not HG strength, with steroid dosage further supports a cause-effect relationship.

Administration, Oral↗

PubMed1999

Post-operative effects on insulin resistance and specific tension of single human skeletal muscle fibres.

Surgery and accidental trauma are associated with a transient period of insulin resistance, substrate catabolism and muscle weakness. In the present study, we evaluated the changes in the force-generating capacity of chemically skinned single muscle fibres following abdominal surgery. Biopsies of the m. vastus lateralis were obtained in three patients 1 day before and 3 or 6 days after surgery. Part of the biopsy was frozen for histochemical analysis of the fibre cross-sectional area (FCSA) and myofibrillar protein content, and another part was used for single-fibre contractile measurements. All patients developed insulin resistance following surgery. The maximum velocity of unloaded shortening of single muscle fibres did not change following surgery. The FCSA did not decrease after surgery, as determined either from histochemical sections or from single fibres measured at a fixed sarcomere length of 2.76+/-0.09 microm (mean+/-S.D.). Further, the force-generating capacity of the single fibres, measured as maximal Ca(2+)-activated force (P(0)) or as P(0) normalized to FCSA (specific tension), remained unchanged, as did the myofibrillar protein content of the muscle. In conclusion, the muscle weakness associated with post-operative insulin resistance is not related to a decreased specific tension or a loss of myofibrillar proteins. Other potential cellular mechanisms underlying post-operative weakness are discussed.

Abdomen↗

PubMed1999

Muscle dysfunction in the intensive care unit.

Muscle weakness, particularly impairment of the respiratory muscles, is a frequent abnormality in ICU patients. This is more relevant in some clinical situations--for example, in weaning patients from mechanical ventilation. Intensive care procedures that are designed to "rest" respiratory muscles, such as mechanical ventilation, may also contribute to impaired muscle function. Pharmacologic administration of glucocorticoids, several antibiotics, NMB agents, and so on has the potential to cause untoward effects. The development of myopathy and prolonged paresis has been increasingly recognized after prolonged use of these drugs in the ICU. Pathophysiologic changes in the nerve, muscle, or neuromuscular junction associated with the patient's underlying condition may also play a role in the development of impaired function. The assessment of muscle function is difficult and inaccurate. The techniques developed have a poor predictive value because of the difficulty in making the measurements in uncooperative patients and the lack of standardization. Furthermore, it is likely that some voluntary maneuvers underestimate muscle strength. Invasive procedures such as phrenic nerve stimulation or EMG recording are also of limited value.

Female↗

PubMed1994

Inclusion body myositis: clinical, morphological, physiological and laboratory findings in 18 cases.

Eighteen consecutive patients with inclusion body myositis (IBM) were studied. The mean age of onset of symptoms was 60 years. A typical clinical pattern with insidious onset of muscle weakness in knee extensors and finger flexors combined with dysphagia was observed. Serial measurements of the maximal voluntary muscle strength revealed a mean loss of muscle strength of 1.4% per month. Two of the cases had common variable immunodeficiency, and three cases had reduced levels of the IgG3 subclass. Treatment with prednisone resulted in a temporary improvement of muscle function in three patients. No positive effect of azathioprine or cyclosporine A could be documented. The results show that IBM may be associated with immunodeficiency, and that prednisone treatment may temporarily improve the clinical signs. The results from our studies on the progression of the muscle weakness may provide basis for future studies on treatment of IBM.

Adrenal Cortex Hormones↗

PubMed1999

Dominant-inherited hypokalemic periodic paralysis in a large Chinese family.

Familial hypokalemic periodic paralysis (HoPP) is a rare condition among Chinese. We studied a large Chinese family (48 members in six generations) with dominant-inherited HoPP, using incidental tracing of family history of a proband who presented with the typical features of HoPP. Fifteen family members were found to have the disease. We found the familial type of HoPP to differ from the sporadic type in Taiwan, in that the familial type has an equal gender distribution, earlier onset of paralytic attacks, and more severe clinical features in both frequency and extent. When these patients were compared with Caucasian families, the common features were the involvement of the respiratory and the bulbar muscles, and the eye muscles in Chinese patients. Cold-induced attacks and permanent muscle weakness were not common in Chinese subjects. Age and history of paralytic attacks were not the major determinants for the development of permanent muscle weakness. Two family members died during attacks because of severe involvement of the respiratory and bulbar muscles.

Adult↗

PubMed2000

Mechanisms of toxicity, clinical features, and management of acute chlorophenoxy herbicide poisoning: a review.

INTRODUCTION: Chlorophenoxy herbicides are used widely for the control of broad-leaved weeds. They exhibit a variety of mechanisms of toxicity including dose-dependent cell membrane damage, uncoupling of oxidative phosphorylation, and disruption of acetylcoenzyme A metabolism. Between January 1962 and January 1999, 66 cases of chlorophenoxy herbicide poisoning following ingestion were reported in the literature. FEATURES FOLLOWING INGESTION: Adjuvants in the formulations may have contributed to some of the features observed. Vomiting, abdominal pain, diarrhea, and, occasionally, gastrointestinal hemorrhage were early effects. When present, hypotension was predominantly due to intravascular volume loss, although vasodilation and direct myocardial toxicity may have contributed in some cases. Neurotoxic features included coma, hypertonia, hyperreflexia, ataxia, nystagmus, miosis, hallucinations, convulsions, fasciculation, and paralysis. Hypoventilation occurred not infrequently, usually in association with central nervous system depression, but respiratory muscle weakness was a factor in the development of respiratory failure in some patients. Myopathic symptoms including limb muscle weakness, loss of tendon reflexes, and myotonia were observed and increased creatine kinase activity was noted in some cases. Other clinical features reported included metabolic acidosis, rhabdomyolysis, renal failure, increased aminotransferase activities, pyrexia, and hyperventilation. Twenty-two of 66 patients died. FEATURES FOLLOWING DERMAL AND INHALATIONAL EXPOSURE: Substantial dermal or inhalational 2,4-dichlorophenoxyacetic acid exposure has occasionally led to systemic features but no such reports have been published in the last 20 years and no fatalities have been reported at any time. Substantial dermal exposure has been reported to cause mild gastrointestinal irritation after a latent period followed by progressive mixed sensory-motor peripheral neuropathy. Mild, transient gastrointestinal and peripheral neuromuscular symptoms have also occurred after occupational inhalation exposure, with or without dermal exposure. MANAGEMENT: In addition to supportive care, alkaline diuresis to enhance herbicide elimination should be considered in all seriously poisoned patients. Limited clinical data suggest that hemodialysis produces similar herbicide clearance to alkaline diuresis without the need for urine pH manipulation and the administration of substantial amounts of intravenous fluid in an already compromised patient. CONCLUSIONS: While chlorophenoxy herbicide poisoning is uncommon, ingestion of a chlorophenoxy herbicide can result in serious and sometimes fatal sequelae. In severe cases of poisoning, alkaline diuresis or hemodialysis to increase herbicide elimination should be considered.

2,4-Dichlorophenoxyacetic Acid↗

PubMed1987

Sleep in restrictive lung disease.

Restrictive lung disease patients exhibit a wide range of breathing and oxygenation abnormalities during sleep. The combination of degree of restriction, whether it is intrapulmonary or extrapulmonary, and confounding factors, such as obesity, age, and sex, will ultimately determine the degree of disturbed nocturnal physiology. The sleep literature is still sparse in most restrictive diseases. For patients with interstitial lung disease, the role of nocturnal oxygen in chronic established fibrosis, and also in acute alveolitis (e.g., farmer's lung, bird fancier's lung, etc.), has not been addressed. As fibrotic lung disease progresses, the degree of nocturnal desaturation and breathing dysrhythmias will progress. Changes in sleep architecture are likely related to the progression of the disease, but this is not known with certainty. Long-term evaluation of sleep and breathing in interstitial lung disease will give further insight into whether or not sleep changes are primary or secondary events. For kyphoscoliosis patients, again, we need more information on sleep as the thoracic deformity changes. In addition, the use of drugs (acetazolomide, medroxyprogesterone, and almitrine) and/or nasal CPAP to treat nocturnal desaturation needs to be assessed in a controlled fashion. In neuromuscular disease, the dynamics of gas exchange and sleep structure need to be defined in a larger group of patients. Factors such as degree of muscle weakness, degree of underlying lung diseases, and medications must be taken into consideration. Nocturnal hypoxemia may cause muscle weakness and fatigue, which in time, could cause more nocturnal hypoventilation and further hypoxemia. Supplemental nocturnal oxygen should be evaluated in this population.

Female↗

PubMed2004

Acute effect of oral steroids on muscle function in chronic obstructive pulmonary disease.

Prospective data to support the hypothesis that corticosteroids are a significant cause of muscle weakness in patients with chronic obstructive pulmonary disease (COPD) are lacking. The authors studied respiratory and quadriceps muscle function, using both volitional techniques and magnetic nerve stimulation, as well as measuring metabolic parameters during incremental cycle ergometry, in 25 stable COPD patients. The forced expiratory volume in one second was 37.6 +/- 21.4% predicted, before and after a 2-week course of o.d. prednisolone 30 mg. Quadriceps strength was also assessed in 15 control patients on two occasions. Only two patients met the British Thoracic Society definition of steroid responsiveness. There was no change either in sniff transdiaphragmatic pressure (pre: 96.8 +/- 19.7 cmH2O; post: 98.6 +/- 22.4 cmH2O) or in twitch transdiaphragmatic pressure elicited by bilateral anterolateral magnetic phrenic-nerve stimulation (pre: 16.8 +/- 9.1 cmH2O; post: 17.9 +/- 10 cmH2O). Quadriceps twitch force did not change significantly either in the steroid group (pre: 9.5 +/- 3.1 kg; post: 8.9 +/- 3.7 kg) or in the control patients (pre: 8.1 +/- 2.7 kg; post: 7.9 +/- 2.2 kg). There were no changes in either peak or isotime ventilatory and metabolic parameters during exercise. In conclusion, in stable patients with chronic obstructive pulmonary disease, a 2-week course of 30 mg prednisolone daily does not cause significant skeletal muscle dysfunction or alter metabolic parameters during exercise.

Adrenal Cortex Hormones↗

PubMed2004

Poisoning due to chlorophenoxy herbicides.

Chlorophenoxy herbicides are used widely for the control of broad-leaved weeds. They exhibit a variety of mechanisms of toxicity including dose-dependent cell membrane damage, uncoupling of oxidative phosphorylation and disruption of acetylcoenzyme A metabolism. Following ingestion, vomiting, abdominal pain, diarrhoea and, occasionally, gastrointestinal haemorrhage are early effects. Hypotension, which is common, is due predominantly to intravascular volume loss, although vasodilation and direct myocardial toxicity may also contribute. Coma, hypertonia, hyperreflexia, ataxia, nystagmus, miosis, hallucinations, convulsions, fasciculation and paralysis may then ensue. Hypoventilation is commonly secondary to CNS depression, but respiratory muscle weakness is a factor in the development of respiratory failure in some patients. Myopathic symptoms including limb muscle weakness, loss of tendon reflexes, myotonia and increased creatine kinase activity have been observed. Metabolic acidosis, rhabdomyolysis, renal failure, increased aminotransferase activities, pyrexia and hyperventilation have been reported. Substantial dermal exposure to 2,4-dichlorophenoxy acetic acid (2,4-D) has led occasionally to systemic features including mild gastrointestinal irritation and progressive mixed sensorimotor peripheral neuropathy. Mild, transient gastrointestinal and peripheral neuromuscular symptoms have occurred after occupational inhalation exposure. In addition to supportive care, urine alkalinization with high-flow urine output will enhance herbicide elimination and should be considered in all seriously poisoned patients. Haemodialysis produces similar herbicide clearances to urine alkalinization without the need for urine pH manipulation and the administration of substantial amounts of intravenous fluid in an already compromised patient.

2,4,5-Trichlorophenoxyacetic Acid↗

PubMed2000

Muscle function assessment in children.

Assessment of muscle function has a range of applications, including appraisal of the presence and severity of muscle weakness and fatigability, examination of the effectiveness of intervention programmes and development and monitoring of training programmes. Muscle function assessment is routinely performed in rehabilitation, physical education, coaching and research. Procedures have been extensively examined in adults, but not in children. The aim of this review is to bring to the forefront the issue of paediatric muscle function assessment. Objective methods of muscle function assessment are critically analysed with specific attention to the issues of applicability, validity and reliability. Each of the methods reviewed (isokinetic dynamometry, hand-held dynamometry, field tests, and standard weights equipment) has its limitations. All procedures have been occasionally studied for validity and reliability and optimal procedures have yet to be identified. Methodological limits can be generalized to the type and speed of activation, standardization of procedures, subject familiarization, gravity and size and psychological influences. It is important for administrators of muscle function tests to be aware of the various factors that can both influence and confound interpretation. It was concluded that muscle function assessment in children requires significant further investigation. Although there is a wide range of procedures available, there is limited and equivocal research proving validity and reliability. Widespread use of the most valid and reliable methods is encouraged. Future research directions are also considered.

Adolescent↗

PubMed1993

Successful treatment of refractory polymyositis with pulse intravenous cyclophosphamide and low-dose weekly oral methotrexate therapy.

A 36-year-old woman gradually developed dysphagia and muscle weakness of the lower extremities. Diagnosis of polymyositis was given from elevation of serum creatine kinase and pathological findings of a muscle biopsy. Despite oral prednisolone and intravenous pulse methylprednisolone therapy, her muscle weakness persisted, and then pulse intravenous cyclophosphamide (IVCY) therapy was initiated and repeated five times in total, which resulted in significant improvement in muscle strength. Thereafter, weekly administration of methotrexate at low dosage further normalized the serum creatine kinase level. We may conclude that IVCY and low-dose weekly methotrexate together could be an alternative in refractory polymyositis.

Administration, Oral↗

PubMed1995

Evaluation of muscle diseases using artificial neural network analysis of 31P MR spectroscopy data.

Dermatomyositis is an autoimmune disease characterized by an erythematous rash and severe muscle weakness. 31P Magnetic resonance spectroscopy (MRS) provides quantitative data for longitudinal monitoring of disease status and responses to immunosuppressive therapy. A disease variant, amyopathic dermatomyositis, presents with a typical rash but no clinical muscle weakness. However, metabolic abnormalities in the oxidative capacity of muscles of amyopathic patients during exercise were detected with 31P MRS. Because MRS provided the best quantitative data for evaluating dermatomyositis, the 31P metabolic parameters derived from the MR spectra were further processed using an artificial neural network (XERION). The neural network analyses provided additional clinical information from the weighted correlations of multiple 31P parameters, namely, inorganic phosphate, phosphocreatine, ATP, phosphodiesters, and selected ratios. This investigation analyzes the relative importance of the various metabolic parameters for accurate patient characterization and provides insights into the pathogenesis of the disease.

Adenosine Triphosphate↗

PubMed2002

Concomitant dermatomyositis and myasthenia gravis presenting with respiratory insufficiency.

We report a 28-year-old woman with a history of chronic immune-mediated hepatitis, in whom the simultaneous manifestation of dermatomyositis and myasthenia gravis resulted in severe neck extensor weakness and subacute respiratory insufficiency, followed by proximal muscle weakness and external ophthalmoplegia. Radiological signs of a thymoma were absent. The distinguishing clinical, electrophysiological, and biopsy findings are discussed. We suggest that an underlying immunoregulatory disorder was present, explaining the occurrence of three rare immune-mediated diseases in one patient.

Adult↗

PubMed1988

Muscle strengthening through high-resistance weight training in patients with neuromuscular disorders.

The effects of weight training on muscle performance were quantified by measuring (1) maximum force (muscle strength), (2) force-time integral--area under force-time plot during 60 seconds of sustained maximum force (work done), and (3) fatigue index--percentage reduction in maximum force. Subjects included 16 patients with gradually progressive neuromuscular disorders. The muscle strength of these patients ranged from 2% to 75% normal before the program. For patients with markedly to moderately weak muscles, maximum force increased by 80% +/- 48%, force-time integral increased by 132% +/- 93%, and mean fatigue index was significantly reduced from 53% +/- 18% to 34% +/- 7.7% during the study period. Severely weak muscles (less than 10% normal strength) generally did not improve. High-resistance weight training can significantly increase muscle performance of patients with neuromuscular disease if disease progression is slow and initial muscle strength is greater than 15% normal.

Adult↗

PubMed2000

Congenital myotonic dystrophy: report of paternal transmission.

A female neonate born to a healthy mother was hospitalized because of enlargement of the lateral ventricles, muscle weakness, irregular respiration, and poor sucking. Characteristic facial appearance such as high forehead and carp mouth were noted. The father had mild manifestations of adult type myotonic dystrophy, including muscle weakness of the extremities, percussion myotonia and atrophy of the facial muscles. PCR analysis and southern blot analysis revealed that CTG repeats in the myotonic dystrophy gene of the infant and the father were about 1000 and 400, respectively. This is a rare case showing paternally transmitted congenital myotonic dystrophy and seems to be the first report describing a neonate.

Brain↗

PubMed1999

Skewed X-inactivation in a manifesting carrier of X-linked myotubular myopathy and in her non-manifesting carrier mother.

X-linked recessive myotubular myopathy (XLMTM) is a muscle disorder usually affecting newborn males. In the majority of cases, muscle weakness and hypotonia lead to a rapid demise at neonatal age. The responsible MTM1 gene is located in proximal Xq28. Heterozygous carriers are described as being asymptomatic but, in a few cases, mild facial weakness has been reported. We report a family in which a 39-year old female showed severe progressive muscle weakness. XLMTM was initially diagnosed in the male offspring of one of the patient's sisters. The patient, one of her sisters, and their mother were heterozygous carriers for a common MTM1 gene mutation. We found an extremely skewed X-inactivation pattern in the patient and, in the opposite direction, in her non-manifesting carrier mother, thus explaining her normal phenotype and indicating a possible inheritance of skewed X-inactivation. Linkage analysis excluded a possible involvement of the XIST locus at Xq13.

Adult↗

PubMed1988

Sudden deafness in a man with thyrotoxic hypokalemic periodic paralysis.

We treated a 32-year-old man with hearing loss in the right ear followed by severe muscle weakness of the extremities. When admitted to hospital by ambulance, the serum potassium level was 1.5 mEq/L. The muscle weakness was improved following administration of potassium chloride but the hearing impairment continued. Hearing level of the right ear was extremely impaired at the level of 60-105 dB, while hearing in the left ear was fairly normal. Spontaneous nystagmus was also present. The triiodothyronine level was 290 ng/dl, thyroxine 14.4 micrograms/dl, thyroid stimulating hormone (TSH) 0.84 microU/ml, and the anti-TSH-receptor antibody was positive. Attaining an enthyroid state, the patient was discharged on 80th hospital day with the continuous medication of Methimazole. This is a very rare case of sudden deafness complicated by hypokalemic paralytic attacks. Circulatory insufficiency and electrolytes imbalance in the right inner ear was assumed to have caused the deafness.

Adult↗

PubMed2002

Recent advances in the understanding of skeletal muscle fatigue.

Prolonged or repeated contractions of skeletal muscles lead to impaired muscle function, fatigue develops. Fatigue may be caused by factors within the muscle cells (peripheral fatigue) and diminished activation from the central nervous system (central fatigue). The relative importance of peripheral central fatigue depends on the type of physical activity. Central fatigue may be more prominent in elderly subjects. Increased concentration of inorganic phosphate seems to be of major importance for acute peripheral fatigue. There is frequently a long-lasting depression of force production after fatiguing muscle activity, especially at low stimulation frequencies. This low-frequency fatigue seems to be due to "structural" changes in proteins involved in intracellular Ca handling. Contractions in which the muscle is stretched (eccentric contractions) cause muscle weakness and damage. The initial defect induced by eccentric contractions is overstretched sarcomeres, but these appear to cause localized membrane tears that subsequently contribute to muscle weakness and damage.

Aging↗