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Results for “Muscle Weakness”

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PubMed1997

Muscle weakness, paralysis, and atrophy after human cervical spinal cord injury.

Muscle weakness and failure of central motor drive were assessed in triceps brachii muscles of individuals with chronic cervical spinal cord injury (SCI) and able-bodied controls. Electrical stimuli were applied to the radial nerve during rest and during triceps submaximal and maximal voluntary contractions (MVCs). The mean forces and integrated EMGs generated by SCI subjects during MVCs were significantly less than those produced by controls (P < 0.01), with 74 and 71% of muscles generating <10% control force and EMG, respectively. There was an inverse linear relationship between the evoked and voluntary forces (n = 32 muscles of SCI subjects) which, when extrapolated to zero evoked force, also showed significant whole muscle weakness for SCI compared to control subjects (P < 0. 01). Severe muscle atrophy was revealed which might reflect disuse and/or muscle denervation subsequent to motoneuron loss. Many triceps muscles of SCI subjects showed no force occlusion (n = 41) or were impossible to stimulate selectively (n = 61). Force was always evoked when the radial nerve was stimulated during MVCs of SCI subjects. The force elicited by single magnetic shocks applied to the motor cortex at Cz' during voluntary contractions of SCI subjects was also inversely related to the voluntary triceps force exerted (n = 18), but usually no force could be elicited during MVCs. Thus central motor drive was probably maximal to these muscles, and the force evoked during MVCs by below-lesion stimulation must come from activation of paralyzed muscle. SCI subjects also had significantly longer mean central nervous system (CNS) conduction times to triceps (P < 0.01) suggesting that the measured deficits reflect CNS rather than peripheral nervous system factors. Thus, the weak voluntary strength of these partially paralyzed muscles is not due to submaximal excitation of higher CNS centers, but results mainly from reduction of this input to triceps motoneurons.

Adult↗

PubMed2002

Serum muscle enzymes, muscle pathology and clinical muscle weakness: correlation in Thai patients with polymyositis/dermatomyositis.

The clinical correlation between serum muscle enzymes, muscle pathology and muscle weakness was studied in 100 Thai patients (22 males and 78 females) with polymyositis (PM) and dermatomyositis (DM). Their mean +/- SD age and duration of disease were 45.0 +/- 13.9 years and 6.3 + 13.4 months, respectively. There was idiopathic PM in 37 cases, idiopathic DM in 13, PM/DM associated with malignancy in 5 and PM associated with connective tissue disease in 45. Serum muscle enzymes including creatine phosphokinase, lactate dehydrogenase and aspartate aminotransferase were elevated in 87 per cent, 92 per cent, and 82 per cent of cases, respectively. Abnormal electromyographic findings that were compatible with inflammatory myopathy were found in 76 per cent of cases. Seventy-seven per cent had an abnormal muscle biopsy that was consistent with polymyositis. There was a significant correlation between serum muscle enzymes and muscle pathology (p < 0.01). The degree of muscle weakness correlated better with the degree of muscle destruction (p = 0.01) than the degree of muscle inflammation (p = 0.03). The erythrocyte sedimentation rate showed no correlation with serum muscle enzymes, muscle pathology or muscle weakness.

Adult↗

PubMed1989

Cutaneous changes of dermatomyositis precede muscle weakness.

A retrospective review of 50 patients with dermatomyositis was performed to determine the temporal relationship between onset of muscle weakness and skin involvement. We found that cutaneous changes sometimes preceded muscle weakness more than a year before the onset of muscle weakness. These findings suggest that the characteristic dermatomyositis eruption without muscle weakness should not preclude a diagnosis of dermatomyositis, and these cases should be carefully followed.

Dermatomyositis↗

PubMed2005

Proposed model of botulinum toxin-induced muscle weakness in the rabbit.

Osteoarthritic patients show only a weak association between radiographic signs of joint disease and joint pain and disability. Conversely, muscle weakness is one of the earliest and most common symptoms of patients with osteoarthritis (OA). However, while many experimental models of osteoarthritis include a component of muscular weakness, no model has isolated this factor satisfactorily. Therefore, the purpose of this study was to develop and validate an experimental animal model of muscle weakness for future use in the study of OA. Botulinum Type-A toxin (BTX-A) was uni-laterally injected into the quadriceps musculature of New Zealand white rabbits (3.5 units/kg). Isometric knee extensor torque at a range of knee angles and stimulation frequencies, and quadriceps muscle mass, were quantified for control animals, and at one- and six-months post-repeated injections, in both, the experimental and the contralateral hindlimb. Ground reaction forces were measured in all animals while hopping across two force platforms. Isometric knee extension torque and quadriceps muscle mass was systematically decreased in the experimental hindlimb. Vertical ground reaction forces in the push off phase of hopping were also decreased in the experimental compared to control hindlimbs. We conclude that BTX-A injection into the rabbit musculature creates functional and absolute muscle weakness in a reproducible manner. Therefore, this model may be used to systematically study the possible effects of muscle weakness on joint degeneration, either as an isolated intervention, or in combination with other interventions (anterior cruciate ligament transection, meniscectomy) known to create knee joint degeneration.

Animals↗

PubMed2002

Respiratory and limb muscle weakness induced by tumor necrosis factor-alpha: involvement of muscle myofilaments.

The respiratory and limb skeletal muscles become weakened in sepsis, congestive heart failure, and other inflammatory diseases. A potential mediator of muscle weakness is tumor necrosis factor (TNF)-alpha, a cytokine that can stimulate muscle wasting and also can induce contractile dysfunction without overt catabolism. This study addressed the latter process. Murine diaphragm and limb muscle (flexor digitorum brevis [FDB]) preparations were used to determine the relative sensitivities of these muscles to TNF-alpha. Intact muscle fibers were isolated from FDB and microinjected with indo-1 to measure changes in sarcoplasmic calcium regulation. We found that TNF-alpha depressed tetanic force of the diaphragm and FDB to comparable degrees across a range of stimulus frequencies. In isolated muscle fibers, TNF-alpha decreased tetanic force without altering tetanic calcium transients or resting calcium levels. We conclude that (1) TNF-alpha compromises contractile function of diaphragm and limb muscle similarly, and (2) TNF-alpha decreases force by blunting the response of muscle myofilaments to calcium activation.

Actin Cytoskeleton↗

PubMed1998

[A patient with an ACTH-releasing thymic carcinoid tumor presenting with proximal muscle weakness].

We report a 36-year-old man with proximal dominant muscle weakness, thymic tumor, diabetes mellitus, hypokalemia, and increased levels of plasma ACTH and cortisol. The diagnosis of carcinoid tumor was made on the basis of pathological findings in the biopsied specimen of the thymic tumor. The proximal muscle weakness was considered to be due to steroid myopathy resulting from the overproduction of cortisol from the adrenal glands induced by the ectopic ACTH secreted by the thymic carcinoid tumor. Although thymoma in frequently associated with myasthenia gravis, we should also consider carcinoid tumors in patients with a thymic tumor presenting with a proximal muscle weakness.

Adrenocorticotropic Hormone↗

PubMed1987

Flow-volume loop changes reflecting respiratory muscle weakness in chronic neuromuscular disorders.

In order to identify the changes in pulmonary function and in the flow-volume loop due to respiratory muscle weakness, two groups of 10 nonsmokers with stable, chronic neuromuscular disease but without respiratory symptoms were studied: one without (Group 1) and one with (Group 2) respiratory muscle weakness as assessed by measurement of maximal static inspiratory and expiratory pressures. In Group 1, pulmonary function was normal except for increased ratio of one-second forced expiratory volume to forced vital capacity and forced expiratory flow at 25 to 75 percent forced vital capacity, which may reflect increased elastic lung recoil. Group 2 had mild volume restriction, appropriate for the degree of respiratory muscle weakness, and reduced inspiratory and expiratory flow rates. Pulmonary function was significantly more disturbed in Group 2 than in Group 1, and correlated well with maximal static inspiratory and expiratory pressures. Analysis of the flow-volume loop configuration revealed that four parameters describing effort-dependent portions were significantly related to maximal static inspiratory pressure and maximal static expiratory pressure. These parameters were peak expiratory flow, the slope of the ascending limb of the maximal expiratory curve, a drop of forced expiratory flow near residual volume, and forced inspiratory flow at 50 percent of vital capacity. A flow-volume loop score obtained from these four parameters was significantly higher in Group 2 than in Group 1 (2.8 +/- 1.03 versus 1.1 +/- 1.37; p less than 0.01). A flow-volume loop score of 2 or more had 80 percent specificity and 90 percent sensitivity in predicting respiratory muscle weakness in these patients with chronic neuromuscular disease. These data suggest that sensitive assessment of the flow-volume loop configuration as part of routine pulmonary function testing may help to suspect and identify respiratory muscle weakness.

Chronic Disease↗

PubMed2005

Frequency and length-dependent effects of Botulinum toxin-induced muscle weakness.

While the pathogenesis of Botulinum toxin type A (BTX-A)-induced muscle weakness has been systematically researched, little is known about the effects of motor fibre paralysis on the mechanical properties of skeletal muscle. Here, the long-term effect of BTX-A injection on the force-length and force-frequency properties of rabbit knee extensors is investigated. BTX-A-induced muscle weakness was greater at short compared to long muscle lengths and at low compared to high stimulation frequencies four weeks following intervention. Therefore, we conclude that the paralysing effects of BTX-A are not uniform, and must be considered in biomechanical models of musculoskeletal rehabilitation in which BTX-A is used therapeutically, as for example in patients with cerebral palsy. Although the present results could be explained through a variety of mechanisms, this study does not allow for drawing firm conclusions about the length and frequency-dependent effects of BTX-A.

Animals↗

PubMed1996

Muscle weakness in mechanically ventilated patients with severe asthma.

Patients who undergo mechanical ventilation for severe asthma are at risk of developing diffuse muscle weakness because of acute myopathy. The relative importance of corticosteroids and neuromuscular paralysis in causing the myopathy is controversial, and it is uncertain whether the chemical structure of the drug used to induce paralysis influences the risk of myopathy. Using a retrospective cohort study design, we evaluated 107 consecutive episodes of mechanical ventilation for severe asthma to assess (1) the incidence of clinically significant weakness in patients treated with corticosteroids alone versus corticosteroids with neuromuscular paralysis, (2) the influence of the duration of paralysis on the incidence of muscle weakness, and (3) the relative risk of weakness in patients paralyzed with the nonsteroidal drug atracurium versus an aminosteroid paralytic agent (pancuronium, vecuronium). The use of corticosteroids and a neuromuscular blocking agent was associated with a much higher incidence of muscle weakness as compared with the use of corticosteroids alone (20 of 69 versus O of 38, p < 0.001). The 20 weak patients were paralyzed significantly longer than the 49 patients who received a neuromuscular blocking agent without subsequent weakness (3.4 +/- 2.4 versus 0.6 +/- 0.7 d, p < 0.001). Eighteen of the 20 weak patients had been paralyzed for more than 24 h. The incidence of weakness was not reduced when paralysis was achieved with atracurium as opposed to an aminosteroid neuromuscular blocking agent. In conclusion, corticosteroid-treated patients with severe asthma who undergo prolonged neuromuscular paralysis are at significant risk for the development of muscle weakness, and the risk of weakness is not reduced by use of atracurium.

Acute Disease↗

PubMed1996

[Nine cases of debrancher deficiency (glycogen storage disease type III) presenting muscle weakness--study on clinicobiochemical analysis].

In nine patients aged 3 to 45 years with glycogen storage disease type III (GSD III) presenting muscle weakness, the clinical manifestations and biochemical subtype-classifications based on organ specificity or enzymatic varieties of debrancher enzyme were analyzed. All the patients developed muscle weakness since childhood. Five patients who showed muscle weakness beginning from childhood became apparently progressive during adult life. Cardiac involvements were noticed in six patients. Eight patients were diagnosed as having type IIIa and one type IIId. Our results suggest that progressive muscle weakness and cardiac symptoms are not rare in GSD III patients, especially in the patients with enzyme deficiency in muscle tissue as well as liver. Hence we recommend to measure debrancher activity in muscle tissue in order to predict the clinical prognosis of the patients with GSD III.

1,4-alpha-Glucan Branching Enzyme↗

PubMed1990

Correlation between tests of muscle involvement and clinical muscle weakness in polymyositis and dermatomyositis.

A correlation study was performed on the degree of muscle weakness in 36 patients with dermatomyositis and 69 with polymyositis in relation to muscle biopsy findings, electromyography (EMG) abnormalities, and serum concentrations of creatine kinase (CK), aspartate aminotransferase (AST) and alanine aminotransferase (ALT) enzymes. Statistically significant correlations were found between muscle weakness and EMG results in patients with polymyositis, and between muscle weakness and serum CK and AST levels in dermatomyositis. As expected, correlations were found between the results of the three enzyme determinations in both groups of patients.

Alanine Transaminase↗

PubMed1997

Characterization of satellite cells derived from chickens with the low score normal (LSN) muscle weakness.

Myogenic satellite cell clones were established from the pectoralis major muscle of chickens with the low score normal (LSN) muscle weakness and controls. The percentage of cells which attached to substrata and began to proliferate was higher for the control line than the LSN line (55% vs 30%). Furthermore, of those clones which initiated growth, 63% of the control cells and only 32% of the LSN cells proliferated to confluence in 25 cm2 tissue culture flasks. Proliferation rates were significantly lower with LSN satellite cells than with controls (p < 0.05). LSN satellite cells were less responsive to the mitogenic effects of chicken serum (p < 0.05) and differentiation rates were lower compared with controls (p < 0.05). There was a greater (p < 0.05) number of insulin-like growth factor receptors on LSN satellite cells compared with controls. The IGF receptor binding affinities (Kds) between the two cell lines were similar (p > 0.05). The results suggest that a defect in satellite cell physiology may contribute to the skeletal muscle weakness seen in the LSN line.

Animals↗

PubMed1989

[Muscle weakness and intolerance to exercise in mitochondrial myopathies].

Muscle weakness and intolerance to exercise are two of the main features commonly shown by patients affected by mitochondrial myopathies. In order to obtain an objective and quantitative evaluation of muscle weakness and endurance, we studied an evaluation protocol devoted to the assessment of 1) muscle strength by the isokinetic ergometer and 2) the metabolic aspects of exercise by means of Maximal Oxygen Consumption and endurance by a Steady State Submaximal exercise evaluation. The protocol has been applied to the study of patients affected by mitochondrial diseases and proved to be a reliable method to quantitate the defect in the oxidation pathways, either before or during the therapeutic follow-up.

Humans↗

PubMed2005

Skeletal muscle weakness in patients with sarcoidosis and its relationship with exercise intolerance and reduced health status.

BACKGROUND: Skeletal muscle weakness is assumed to be present in patients with sarcoidosis but has never been reported in a consecutive group of patients. Moreover, its relationship with previously observed exercise intolerance and reduced health status has never been studied in these patients. METHODS: Pulmonary function, skeletal and respiratory muscle forces, peak and functional exercise capacity, health status, and the circulating levels of inflammatory and anabolic markers were determined in 25 patients with sarcoidosis who complained of fatigue (15 men) and in 21 healthy subjects (13 men). RESULTS: Patients with sarcoidosis had lower respiratory and skeletal muscle forces, reduced exercise capacity and health status, higher anxiety and depression scores, and higher circulating levels of tumour necrosis factor-alpha than healthy subjects (all p< or =0.01). Its soluble receptor p75 tended to be higher (p=0.04). Circulating levels of interleukin (IL)-6, IL-8, insulin-like growth factor I and its binding protein 3 were not significantly different between the two groups. Skeletal muscle weakness was related to exercise intolerance, depression, and reduced health status in patients with sarcoidosis, irrespective of age, sex, body weight and height (p< or =0.05). Quadriceps peak torque was inversely related to fatigue but not to the circulating levels of inflammatory or anabolic markers. The mean daily dose of corticosteroids received in the 6 month period before testing was related to quadriceps peak torque only in patients who received oral corticosteroids. CONCLUSION: Skeletal muscle weakness occurs in patients with sarcoidosis who complain of fatigue and is associated with reduced health status and exercise intolerance.

Adult↗

PubMedDate not supplied

Isolated progressive muscle weakness with tubular aggregates.

We report 2 isolated cases of slowly progressive muscle weakness in which tubular aggregates in muscle biopsy were found as the major pathological feature. Tubular aggregates were present in both types of fibers. Electron microscopy revealed the accumulation of double-walled tubular structures in dense subsarcolemmal locations or in smaller amounts within the myofibrils, close to cytoplasmic organelles. Myopathy with tubular aggregates is believed to form a distinct clinico-pathological entity with 3 well-distinguished clinical groups. The cases reported herein would fall into the group of sporadic isolated progressive muscle weakness of which only 3 other cases have been previously described.

Adult↗

PubMed2026

Targeted long-read genomic and epigenomic profiling enhances timely comprehensive variant discovery in hypotonia and muscle weakness.

BACKGROUND: Identifying the genetic basis of hypotonia and muscle weakness is critical for patient management and family counseling. However, diagnosis is often hindered by diverse genomic alterations, including repeat expansions, structural variants (SVs), and methylation defects. Standard-of-care testing, largely based on short-read sequencing, is limited in its ability to detect this heterogeneous variation landscape, leaving many patients undiagnosed or requiring lengthy sequential testing. Long-read sequencing represents a promising solution. However, its application as a first-tier diagnostic assay for hypotonia remains unexplored. METHODS: We retrospectively analyzed 227 patients with hypotonia to assess diagnostic yield, time-to-diagnosis, and costs associated with standard-of-care testing. A long-read whole-genome sequencing (LR-WGS) workflow with targeted analysis of hypotonia-associated genes was developed to detect and prioritize pathogenic SNVs, SVs, and CNVs, repeat expansions, and methylation changes at key disease loci. The workflow was validated in a reference-positive cohort with known diagnoses (n = 15) and applied to an unsolved cohort (n = 14). Variant interpretation followed ACMG guidelines and was confirmed with orthogonal methods. RESULTS: Standard-of-care testing achieved a diagnostic yield of 42% with an average time-to-diagnosis of 68.7 days; however, 30% of diagnosed patients experienced significant delays (average 169 days) due to sequential testing. The LR-WGS based approach identified all known pathogenic variants in the positive cohort, including SMN1 deletions, methylation defects at 15q11.2/Prader-Willi locus, FMR1 repeat expansions, and sequence and copy-number variants in > 100 genes underlying myopathies and muscular dystrophies. The targeted long-read pipeline reduced prioritized variant calls by 97.9-99.9% and, in the unsolved cohort, yielded one definitive diagnosis (de novo COL6A3 deletion) and one possible diagnosis (aberrant methylation and copy number at POMK), for an additional 14% yield. Among patients diagnosed after sequential testing (n = 29), LR-WGS is expected to reduce time-to-diagnosis by ~ 85% and decrease cumulative diagnostic delays, with projected healthcare cost savings of $396,000-439,000. Across the entire 227 patient cohort, LR-WGS is anticipated to reduce testing costs by 6.5%, yielding an average savings of $105 per patient. CONCLUSIONS: LR-WGS enables comprehensive discovery of genomic and epigenomic variants in hypotonia and muscle weakness, improving diagnostic yield, shortening diagnostic timelines, and reducing costs compared with current standard-of-care testing.

Humans↗

PubMed1989

Nocturnal rocking bed therapy: improvement in sleep fragmentation in patients with respiratory muscle weakness.

Three patients with respiratory muscle weakness developed sleep fragmentation due to nonobstructive apnea and hypopnea. In two patients in whom inspiratory muscle electromyogram was recorded, the apneas and hypopneas were terminated only by arousal and excessive recruitment of accessory muscles. Nocturnal rocking bed ventilatory support resulted in immediate improvement in sleep fragmentation and inhibited arousal-associated phasic accessory muscle activation, resulting in improvement in daytime hypercapnia and subjective sleepiness. Sleep fragmentation may occur more commonly than generally appreciated in neuromuscular disease patients who are independent of daytime ventilatory support. The use of nocturnal rocking bed is an effective noninvasive method of reversing sleep fragmentation and daytime sequelae when obstructive apnea is absent.

Adult↗

PubMed1984

Effect of diet on human muscle weakness following prolonged exercise.

The effect of altering muscle glycogen on the ability of skeletal muscle to generate voluntary and electrically evoked isometric force following prolonged exercise has been investigated in five healthy male subjects. Measurements from the triceps surae were made at rest, and before and after prolonged exercise (uphill walking) at approximately 75% VO2 max in low muscle glycogen (low CHO) and high muscle glycogen (high CHO) conditions. The results showed that before exercise there was no change in maximal twitch tension (Pto), maximal tetanic tension at frequencies of 10 (Po10), 20 (Po20) and 50 HZ (Po50), and maximal voluntary contraction (MVC) in low and high CHO compared with normal. The loss of force during a 2 min electrically evoked "fatigue test" at rest was found to be higher (p less than 0.05) in low CHO and lower (p less than 0.05) in high CHO than normal. Following the prolonged exercise, muscle weakness was produced in both low and high CHO conditions, but was found to be significantly greater in the low CHO condition for the measurements of Po10 (P less than 0.01), Po20 (p less than 0.05) and MVC (p less than 0.05). It is concluded that changes in muscle glycogen alone do not alter the isometric force generating capacity of human muscle, but when combined with prolonged exercise low muscle glycogen enhances exercise-induced muscle weakness.

Adult↗