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 685 records · Page 38Linked to original sources

PubMed1997

Common patterns of clinical motor dysfunction.

An upper motor neuron syndrome often leads to the development of stereotypical patterns of deformity secondary to agonist muscle weakness, antagonist muscle spasticity and changes in the rheologic (stiffness) properties of spastic muscles. Identification of the spastic muscles that contribute to deformity across a joint allows therapeutic denervation to be implemented with the maximum likelihood of success. Identifying responsible muscles can be complex, since many muscles may cross the joint involved, and not all muscles with the potential to cause deformity will be spastic. Strategies including polyelectromyography and diagnostic blocks with local anesthetics can be used to test hypotheses regarding the deformity, providing information for more long-term denervation. In this review, we discuss frequently observed patterns of deformity associated with problematic spasticity, paresis, contracture, and impaired voluntary motor control.

Diagnosis, Differential↗

PubMed1990

[A case of polymyositis associated with chronic active hepatitis].

A case of polymyositis associated with chronic active hepatitis was reported. A 53-year-old man, who had no previous history of blood transfusion nor hepatitis, noticed proximal dominant muscle weakness on January 29, 1985. He was admitted to Kyoto National Hospital on February 7, and laboratory studies disclosed the elevation of serum enzyme levels; creatine kinase (CK) 9845 IU/L (normal 54-263), glutamate oxaloacetate transaminase (GOT) 834 IU/L (9-31), glutamate pyruvate transaminase (GPT) 491 IU/L (4-34), lactate dehydrogenase (LDH) 2135 IU/L (248-464). Also serum gamma globulin was high (1.8 g/dl) and LE-like cell was found. The diagnosis of polymyositis was made and prednisolone therapy (60 mg/day) was started on February 23. The elevated serum enzymes decreased gradually, but severe muscle weakness persisted for about one month. On April 3, he was admitted to our hospital. Physical examination revealed moderate proximal dominant muscle weakness without skin eruption, jaundice or hepatosplenomegaly. The serum enzymes were still high; CK 1826, GOT 173, GPT 232 (GOT less than GPT), LDH 1548. However, alkaline phosphatase (ALP) and bilirubin were normal. Hepatitis B surface antigen (HBsAg) was not detected. Antinuclear antibody was positive. The electromyogram study showed myopathic change, and the muscle biopsy demonstrated myopathic change and cell infiltration, compatible with polymyositis. These results suggested liver dysfunction associated with polymyositis. Prednisolone therapy was continued and muscle weakness decreased. From December, 1985, serum enzymes (CK, GOT, GPT, LDH) elevated again and muscle weakness also slightly increased. Anti-smooth muscle antibody was positive. It was suggested that both polymyositis and liver dysfunction deteriorated.(ABSTRACT TRUNCATED AT 250 WORDS)

Autoantibodies↗

PubMed2003

Muscle-derived stem cells: potential for muscle regeneration.

Duchenne muscular dystrophy (DMD) is a devastating X-linked muscle disease characterized by progressive muscle weakness caused by the lack of dystrophin expression at the sarcolemma of muscle fibers. Although various approaches to delivering dystrophin in dystrophic muscle have been investigated extensively (e.g., cell and gene therapy), there is still no treatment that alleviates the muscle weakness in this common inherited muscle disease. The transplantation of myoblasts can enable transient delivery of dystrophin and improve the strength of injected dystrophic muscle, but this approach has various limitations, including immune rejection, poor cellular survival rates, and the limited spread of the injected cells. The isolation of muscle cells that can overcome these limitations would enhance the success of myoblast transplantation significantly. The efficiency of cell transplantation might be improved through the use of stem cells, which display unique features, including (1) self-renewal with production of progeny, (2) appearance early in development and persistence throughout life, and (3) long-term proliferation and multipotency. For these reasons, the development of muscle stem cells for use in transplantation or gene transfer (ex vivo approach) as treatment for patients with muscle disorders has become more attractive in the past few years. In this paper, we review the current knowledge regarding the isolation and characterization of stem cells isolated from skeletal muscle by highlighting their biological features and their relationship to satellite cells as well as other populations of stem cells derived from other tissues. We also describe the remarkable ability of stem cells to regenerate skeletal muscle and their potential use to alleviate the muscle weakness associated with DMD.

Animals↗

PubMed1987

Proximal weakness of the extremities as main feature of amyloid myopathy.

Two patients with muscle weakness caused by amyloid myopathy are described. Characteristic features such as pseudohypertrophy and abnormal firmness, and tumours of muscles were absent. It is suggested that muscle weakness in amyloid myopathy is caused by layers of amyloid covering muscle fibres. In middle aged or elderly patients with proximal muscle weakness the diagnosis of amyloid myopathy should be considered.

Aged↗

PubMed1996

Reduction in thigh muscle cross-sectional area and strength in a 4-year follow-up in late polio.

OBJECTIVE: To study changes in cross-sectional thigh muscle area and muscle strength in late polio subjects over a 4-year period. DESIGN: Longitudinal study of a cohort of polio survivors, comparing subjects who acknowledge (unstable) with those who do not acknowledge (stable) new muscle weakness. SETTING: University hospital. SUBJECTS: Eighteen subjects (6 men, 12 women) with polio-myelitis sequelae (39 to 46 years of age) were studied on two occasions 4 years apart; the first examination was 37 to 44 years after onset of polio. Subjects were recruited through hospital registers, newspaper advertisement, and a patient organization. OUTCOME MEASUREMENTS: Thigh muscle and intermuscular and intramuscular adipose tissue (AT) cross-sectional areas were measured by computed tomography. Isometric muscle strength for knee extension and flexion was measured using a Kin-Com dynamometer. RESULTS: Cross-sectional muscle area decreased on average 1.3 +/- 3.6 cm2 (1.4%, p < .05); the intermuscular and intramuscular AT area increased 1.8 +/- 3.4 cm2 (12.1%, p < .05). When divided by legs in which subjects reported (unstable) or did not report (unstable) or did not report (stable) increased muscle weakness, unstable legs showed significant reduction (p < .05) in muscle area, whereas stable legs did not. Estimated total thigh muscle strength decreased 7.8% +/- 2.9% (p < .01), with a significant (p < .001) reduction in unstable legs (13.4% +/- 4.3%) but not in stable legs. The reduction in strength appears to be greater than the reduction in cross-sectional muscle area, but there is still a significant correlation (r = .44, p < .05). CONCLUSION: The present results demonstrate not only progress of muscle weakness, but also of muscle atrophy in postpolio subjects.

Adipose Tissue↗

PubMed1999

[Subacute motor neuronopathy associated with myasthenia gravis and thymoma].

We reported a 63-year-old woman, suffered from myasthenia gravis with thymoma who later developed subacute motor neuronopathy after thymectomy. She noticed distally dominant muscle weakness and atrophy of bilateral upper extremities without sensory loss 4 month after thymomectomy. Her muscle weakness did not improve by intravenous administration of anti-cholinesterase (Tensilon test). Electrophysiological examinations showed no decremental response of examined muscles during repetitive nerve stimulation, nor motor nerve conduction block nor demyelination of affected peripheral nerves. Laboratory study demonstrated positive anti-acetylcholine receptor, anti-nuclear and SS-A antibodies. On immunohistochemistry, the patient's sera positively stained human and rat anterior horn cell cytoplasm as well as axoplasm of spinal white matter and root nerve axon, suggesting the presence of anti-axon antibody, possibly against neurofilament or tubulin components. The biopsied muscle specimen showed neurogenic muscle changes, but with no evidence of vasculitis nor cellular infiltration. Therapeutic trial of plasmapheresis was effective for her muscle weakness. Further recovery of weakness and muscle atrophy of hand muscles was obtained by combined therapy of intravenous and oral corticosteroid administration and plasmapheresis. These clinical, electrophysiological and histological findings suggested that antibodies against neuronal component might be responsible for her motor neuronopathy associated with myasthenia gravis. The findings of our case study may support the idea that some cases of motor neuron disease are caused by auto-immune mechanism.

Autoantibodies↗

PubMed2004

Treatment in myotonia and periodic paralysis.

The myotonic disorders, including the myotonic dystrophies (myotonic dystrophy type 1, DM1; myotonic dystrophy type 2, DM2/PROMM/PDM), the muscle channelopathies or non-dystrophic myotonias (chloride, sodium, calcium and potassium channelopathies) are all characterized by myotonia and muscle weakness despite different pathophysiology involved in these disorders. Myotonia may affect the eye, facial and jaw muscles as well as the hands and legs. It may be painful and disabling. Muscle weakness may be episodical as in the paralytic attacks of the sodium and calcium channelopathies or culminate in permanent muscle weakness as in the calcium channelopathies and some sodium channelopathies associated to specific point mutations. The severity of myotonia may fluctuate in the myotonic dystrophies, but weakness is usually fixed, affecting neck flexors, facial and jaw muscles as well as proximal and distal muscles of the limbs. Despite the recent progress in molecular genetics the precise mechanisms responsible for myotonia and weakness are not fully understood and there is no standardized treatment strategy. We present a review of selected treatment trials in the myotonic disorders and the muscle channelopathies, and discuss our experience in the treatment of myotonia and muscle weakness, with reference to the limits and advantages of treatment trials in this field.

Biopsy↗

PubMed2000

Mechanism of CO(2) retention in patients with neuromuscular disease.

BACKGROUND: In many studies of patients with muscle weakness, chronic hypercapnia has appeared to be out of proportion to the severity of muscle disease, indicating that factors other than muscle weakness are involved in CO(2) retention. In patients with COPD, the unbalanced inspiratory muscle loading-to-strength ratio is thought to trigger the signal for the integrated response that leads to rapid and shallow breathing and eventually to chronic hypercapnia. This mechanism, although postulated, has not yet been assessed in patients with muscular dystrophy. SUBJECTS: Twenty consecutive patients (mean age, 47.6 years; range, 23 to 67 years) were studied: 11 patients with limb-girdle dystrophy, 3 with Duchenne muscular dystrophy, 1 with Charcot-Marie-Tooth syndrome, 1 with Becker muscular dystrophy, 1 with myotonic dystrophy, 1 with facioscapulohumeral dystrophy, and 2 with amyotrophic lateral sclerosis, without any respiratory complaints. Seventeen normal subjects matched for age and sex were studied as a control group. METHODS: Routine spirometry and arterial blood gases, maximal inspiratory and expiratory muscle pressures (MIP and MEP, respectively), and pleural pressure during maximal sniff test (Pplsn), were measured. Mechanical characteristics of the lung were assessed by evaluating lung resistance (RL) and dynamic elastance (Eldyn). Eldyn was assessed as absolute value and as percent of Pplsn; Eldyn (%Pplsn) indicates the elastic load per unit of inspiratory muscle force. Breathing pattern was assessed in terms of time (inspiratory time [TI]; respiratory frequency [Rf]) and volume (tidal volume [VT]) components of the respiratory cycle. RESULTS: A rapid shallow breathing pattern, as indicated by a greater Rf/VT ratio and a lower TI, was found in study patients compared to control subjects. Eldyn was greater in study patients, while MIP, MEP, and Pplsn were lower. PaCO(2) inversely related to VT, TI, and Pplsn (p = 0.012, p = 0.019, and p = 0.002, respectively), whereas it was directly related to Rf, Rf/VT, Eldyn, and Eldyn (%Pplsn) (p < 0.004 to p < 0.0001). Also Eldyn (%Pplsn) inversely related to TI, and the latter positively related to VT. In other words, increase in Eldyn (%Pplsn) was associated with decrease in TI, and the latter was associated with lower VT and greater PaCO(2). Mechanical and breathing pattern variables were introduced in a stepwise multiple regression that selected Eldyn (%Pplsn) (p < 0.0001; r(2) = 0.62) as a unique independent predictor of PaCO(2). CONCLUSIONS: The present study shows that in patients with neuromuscular disease, elastic load and respiratory muscle weakness are responsible for a rapid and shallow breathing pattern leading to chronic CO(2) retention.

Adult↗

PubMed1998

Expiratory muscle function in amyotrophic lateral sclerosis.

Few data exist concerning expiratory muscle function in amyotrophic lateral sclerosis (ALS). We studied 26 patients with ALS (16 with respiratory symptoms and 10 without) and measured the maximal static expiratory mouth pressure (MEP), the gastric pressure during a maximal cough (Cough Pga), and the gastric pressure after magnetic stimulation of the lower thoracic nerve roots (Tw Pga). These measurements were related to the ability to generate transient supramaximal flow during a cough (cough spikes), to arterialized capillary blood gases, and to inspiratory muscle strength. Vocal cord motion was examined endoscopically in 11 of the 16 symptomatic patients. Expiratory muscle weakness was related to inability to generate cough spikes with a threshold effect such that spikes were absent for Cough Pga < 50 cm H2O (p = 0.009) or Tw Pga < 7 cm H2O (p = 0.006) and was usually associated with inspiratory muscle weakness. However, in multivariate analysis, PaCO2 was only significantly associated with the maximal sniff esophageal pressure (p = 0.02). Symptomatic patients had significantly lower inspiratory muscle strength, whereas, of the expiratory muscle tests, only Tw Pga was significantly lower (p = 0.0009) in symptomatic patients. Abnormal vocal cord motion was observed in two of the 11 patients examined. We conclude that abdominal muscle weakness in ALS, when substantial, results in an inability to generate transient supramaximal flow during a cough. However, the primary determinant of both ventilatory failure and respiratory symptoms seems to be inspiratory muscle weakness.

Adult↗

PubMed2005

Non-invasive assessment of respiratory muscle strength in patients with previous poliomyelitis.

UNLABELLED: In patients with poliomyelitis, respiratory failure requiring ventilatory support may occur during the acute illness. Some patients continue to require long-term nocturnal ventilatory support; others are weaned but subsequently require support because of a late deterioration in ventilatory function. OBJECTIVES: To assess the sensitivity of sniff nasal inspiratory pressure (SNIP) to post-poliomyelitis respiratory muscle weakness and to assess the relationship between the respiratory muscle strength and the need for ventilatory support in patients with previous poliomyelitis (post-polio patients). METHODS: Respiratory muscle strength was measured in 50 post-polio patients. Tests included forced vital capacity (FVC), maximum inspiratory and expiratory pressures (MIP and MEP), and SNIP. RESULTS: Twenty-one patients used non-invasive nocturnal ventilatory support (NIV group) compared to 29 on no support (non-NIV group). The percentage predicted FVC was significantly lower in the NIV group compared to the non-NIV group (P=0.01). Similarly, the percentage predicted MIP was significantly lower in NIV group (P=0.007). Low SNIP values (both absolute value and percentage predicted) were associated with the need for ventilatory support (P<0.001). Of the patients requiring no support, those who had been ventilated during the acute episode of poliomyelitis had a significantly lower SNIP than those who had never been ventilated (P=0.04). CONCLUSIONS: Post-polio patients who are currently on nocturnal ventilation have significantly lower FVC, MIP and SNIP compared to currently non-ventilated patients. Non-ventilated patients who were ventilated during the acute episode of poliomyelitis have significantly weaker respiratory muscle strength than patients who were never ventilated. This study indicates that SNIP is more sensitive to post-polio respiratory muscle weakness than other non-invasive tests. Thus measurement of SNIP is a valuable tool for monitoring the progression of respiratory muscle weakness due to previous poliomyelitis and this can be applied to other neuromuscular disorders.

Acute Disease↗

PubMed1994

Assessment of ventilatory function in patients with neuromuscular disease.

In early phases of neuromuscular disease, patients are either free of respiratory symptoms or have exertional dyspnea not explained by obvious obstructive or restrictive lung disease. Physical examination may be negative because generalized muscle weakness does not correlate with the degree of respiratory muscle involvement. When the diaphragm is involved, one may detect the absence of outward excursion during inspiration or even paradoxic inward inspiratory movement of the abdomen on one side. A substantial loss of respiratory muscle strength is typically accompanied by little or no change in spirometry or arterial blood gas composition. Other characteristics are moderate loss of maximal voluntary ventilation and an increase in residual volume, yet PImax and PEmax may be as low as 50% of the predicted value. In more advanced neuromuscular disease, patients may have severe symptoms if the onset is acute or subacute; however, patients with chronic advanced generalized muscle weakness do not exercise and, therefore, may not be breathless. Many patients with advanced neuromuscular disease present with daytime somnolence as a manifestation of a sleep-related breathing disorder. Physical examination may reveal generalized muscle weakness and difficulty with speech or swallowing. Signs specific to respiratory involvement include tachypnea, use of neck inspiratory muscles and abdominal expiratory muscles, and loss of chest-abdomen synchrony. Sometimes paradoxic bilateral inward movement of the abdomen with inspiration is overt. Patients may be unable to cough effectively, have scoliosis, and lack a gag reflex. At this advanced stage, PImax and PEmax are lower than 50% of the predicted value, and the vital capacity is reduced. Maximal voluntary ventilation increases, and residual volume increases further. Patients may not yet exhibit CO2 retention during the day and may even have a low PaCO3. A sleep study may reveal significant hypopneas with severe desaturation and hypercapnia, especially during REM sleep. It is important to be aware that overt ventilatory failure can occur abruptly and that measurement of arterial blood gas composition is not a reliable indicator of this danger. Therefore, it is critically important to heed clinical phenomena, such as increasing dyspnea and tachypnea, and symptoms of sleep disturbance, such as morning headache and daytime somnolence. Physicians should make serial measurements of VC and respiratory muscle strength in patients considered to be at risk for further deterioration.(ABSTRACT TRUNCATED AT 400 WORDS)

Female↗

PubMed2002

Possible pathogenic mechanisms in inflammatory myopathies.

The limitations associated with the different approaches into the pathogenesis of the IIM have resulted in incomplete knowledge of disease mechanisms in myositis. In most research, in which muscle tissue was used to study the different aspects of disease, biopsies with inflammatory infiltrates have been selected. Although inflammatory cell infiltrates are a characteristic feature of myositis, selecting patients with inflammatory cell infiltrates for investigations naturally introduces a selection bias. Only a few studies have been published on patients without inflammatory infiltrates but with muscle weakness, and few studies have included follow-up biopsies after different therapies. The heterogeneity of the population of patients with myositis is another limitation of the studies of pathogenic mechanisms. Although most studies classify patients according to the Bohan and Peter criteria [118, 119], some studies used histopathologic criteria [6], and only a few studies included characterization with myositis-specific autoantibodies. Because myositis-specific autoantibodies are often associated with certain clinical profiles, classification according to autoantibody profiles could be important to define differences in the pathogenesis of different phenotypes [3]. From available data on pathogenic mechanisms it is evident that cellular and humoral immune responses are involved in disease mechanisms of myositis, but whether there is a muscle-specific immune response cannot be answered by current studies. It is likely that other mechanisms are important for development of muscle weakness, including metabolic disturbances, and muscle weakness could be caused by different mechanisms in different IIM subsets or in patients in different phases of the disease. There could be early changes, which reversibly affect the metabolism, and later, irreversible changes, that could be dependent on muscle fiber damage and replacement of muscle tissue by connective tissue and fat. Current findings suggest that cytokines, which are produced in muscle tissue from different cell sources including inflammatory cells, endothelial cells, and muscle fibers, could affect muscle function. Careful follow-up studies, including the effect of therapies targeting different molecules on molecular expression in muscle tissue, are likely to increase our knowledge on disease mechanisms. A better understanding of which molecules and mechanisms affect muscle function is likely to lead to improved, less toxic therapies in patients with myositis. Many possible target molecules for blocking therapies, especially the proinflammatory cytokines IL-1 and TNF-alpha, have been identified and should be studied in appropriate clinical settings given the currently poor outcomes of many patients with IIM.

Autoimmunity↗

PubMed2006

Multifocal motor neuropathy with conduction block: Distribution of demyelination and axonal degeneration.

OBJECTIVE: Multifocal motor neuropathy with conduction block (MMN) is an immune-mediated neuropathy, characterized by progressive muscle weakness. Although demyelination is regarded as the underlying pathophysiologic mechanism of MMN, recently, it was reported that different pathophysiologic mechanisms were responsible for disease in the upper and lower limbs. Specifically, demyelination in the upper limbs and axonal loss in the lower limbs. Consequently, the aim of the present study was to assess, through clinical neurophysiology studies, whether different pathophysiologic mechanisms were occurring in the upper and lower extremities. Furthermore, we wanted to investigate whether the presence of conduction block (CB) correlated with axonal degeneration (AD), and to determine the electrophysiological abnormalities that correlate with muscle weakness. METHODS: We reviewed medical records of 18 patients with MMN for clinical features (using the Medical Research Council score and Guys Neurology Disability Scale) and neurophysiologic abnormalities (CB, AD prolongation of distal motor and F-wave latencies, and reduction of conduction velocity in the demyelinating range). RESULTS: Electrophysiological abnormalities deemed specific of demyelination were non-significantly different in the upper and lower extremities. The presence of axonal degeneration correlated significantly with conduction block (odds ratio 10.4, 95% CI 4.2-25.6), and both parameters correlated with muscle weakness (P<0.01). CONCLUSION: Our study suggests that the same pathophysiologic process occurs in the upper and lower extremity nerves. Moreover, one pathophysiologic process may be responsible for the development of CB and AD, and therefore muscle weakness. SIGNIFICANCE: The present study has established that both AD and CB occur in MMN, irrespective of extremity, and both correlate with muscle weakness.

Action Potentials↗

PubMedDate not supplied

[A case of limb-girdle type myasthenia gravis in whom rheumatoid arthritis appeared immediately after thymectomy].

We report a 48-year-old female who presented limb-girdle type myasthenia gravis with inflammatory lung lesions and rheumatoid arthritis. She demonstrated a rapidly progressive muscle weakness of extremities. Neurological examination revealed facial muscle weakness, and proximal dominant limb muscle atrophy and weakness. Ptosis, ophthalmoplegia, and bulbar palsy were not observed. The edrophonium test and serum anti-acetylcholine receptor antibody were positive. The repetitive nerve stimulation showed 55% waning in the thenar muscles. From these findings, she was diagnosed as having myasthenia gravis. Plain chest X-P and body CT showed tumor-like lesions in the lung. Lung biopsy revealed the infiltration of lymphocytes. These lesions decreased in size after thymectomy and corticosteroid administration. Immediately after thymectomy, she began to have morning stiffness with pain and swelling of the finger and knee joints. RAHA test, which was negative before thymectomy, became highly positive. These findings were consistent with rheumatoid arthritis. In this patient, thymus probably played a role to suppress the development of rheumatoid arthritis.

Arthritis, Rheumatoid↗

PubMed1989

Weakness in patients with hemiparesis.

Clinical and experimental results are reviewed concerning muscle weakness in patients with hemiparesis after a stroke. The discussion includes the important role that alterations in the physiology of motor units, notably changes in firing rates and muscle fiber atrophy, play in the manifestation of muscle weakness. This role is compared with the lesser role that spasticity (defined as hyperactive stretch reflexes) of the antagonist muscle group appears to play in determining the weakness of agonist muscles. The contribution of other factors that result in mechanical restraint of the agonist by the antagonist (e.g., passive mechanical properties and inappropriate cocontraction) is discussed relative to muscle weakness in patients with hemiparesis.

Cerebrovascular Disorders↗

PubMed2002

Altered ryanodine receptor function in central core disease: leaky or uncoupled Ca(2+) release channels?

Central core disease (CCD) is an autosomal-dominant human congenital myopathy that is associated with at least 22 different mutations in the skeletal muscle isoform of ryanodine receptor (RyR1). CCD mutations in RyR1 have been proposed to lead to the formation of sarcoplasmic reticulum (SR) Ca(2+) release channels that are excessively leaky to Ca(2+). Although some of the CCD mutations in RyR1 may indeed result in leaky SR Ca(2+) release channels, the leaky-channel hypothesis may not represent the only mechanism for muscle weakness in this disorder. The presence of an alternate mechanism of muscle weakness in CCD is supported by the observation that muscle cells expressing a CCD mutation in the putative pore-forming segment of RyR1 (I4898T) exhibit a functional uncoupling of SR Ca(2+) release from sarcolemmal depolarization. These observations cannot be explained by the leaky-channel hypothesis and indicate that muscle weakness in some forms of CCD arises from an alternate and completely unexpected mechanism, termed "excitation-contraction uncoupling."

Calcium↗

PubMed2002

Avoidance of activity and disability in patients with osteoarthritis of the knee: the mediating role of muscle strength.

OBJECTIVE: Avoidance of activity is hypothesized to lead to muscle weakness and consequently, to physical disability. This study was undertaken to validate the avoidance model by providing evidence for the mediating role of muscle weakness in the relationship between avoidance of activity and physical disability in patients with osteoarthritis (OA) of the knee. METHODS: Data on avoidance of activity, observed physical disability, and muscle strength of the knee in 107 patients with knee OA were analyzed. A series of regression analyses was performed to establish the mediating role of muscle weakness. First, the effect of avoidance of activity on the level of disability was assessed. Next, the relationship between avoidance of activity and muscle strength was established. Finally, the mediating role of muscle strength could be established if the effect of avoidance of activity on disability decreased when muscle strength was taken into account. RESULTS: Initially, avoidance of activity accounted for 21.5% of variance in disability. Avoidance of activity also accounted for 3.9% of variance in muscle strength. After muscle strength was taken into account, the variance in disability accounted for by avoidance of activity was reduced from 21.5% to 15.7%. Thus, the criteria for establishing the mediating role of muscle strength were met. CONCLUSION: The results of this study provide evidence for the mediating role of muscle weakness in the relationship between avoidance of activity and disability in patients with knee OA.

Aged↗

PubMedDate not supplied

Testing of an Index of Pulmonary Dysfunction in Multiple Sclerosis.

The reliability and validity of an Index of Pulmonary Dysfunction in Multiple Sclerosis (Index) comprised of four readily assessed clinical signs was studied. Forty patients with MS performed pulmonary function testing and underwent clinical evaluation to determine whether or not the Index correctly identified those patients with pulmonary dysfunction. The Index correctly predicted the presence or absence of significant respiratory muscle weakness (defined as Pemax less than 50% of predicted) in 32 (80%) of the subjects. All subjects who had normal expiratory muscle strength (Pemax greater than or equal to 80% of predicted) were correctly classified by the Index; however, not all patients with isolated expiratory muscle weakness were correctly identified. Test-retest reliability, interrater reliability (Spearman rho coefficients of 0.87 and 0.94, respectively), and internal consistency (alpha = .83) of the Index were acceptable. Index scores were not associated with changes in any other PFT results except residual volume, which increased with the severity of respiratory muscle weakness. The Index has acceptable validity and reliability for use in clinical practice to identify those neurological patients with expiratory muscle weakness.

Adult↗