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Muscle weakness in osteoarthritis.

Muscle has an integral role in the structure and function of joints. Evidence for muscle weakness in osteoarthritis of the knee exists and is not fully explained by the effects of aging. Weakness is associated with pain and disability. The temporal relationship requires further study, but preliminary evidence for a causative role is emerging. Muscle weakness can be assessed in various ways. Voluntary measures of strength are affected by degree of effort. In osteoarthritic patients, as in other patient groups, effort may be influenced by pain and psychologic outlook. Techniques to estimate muscle activation are available but have yet to be fully explored in osteoarthritis. Quadriceps exercises increases strength and may have beneficial effects on pain and function. The long-term benefits of exercise for therapy and possible prevention of osteoarthritis are not yet known. This is an exciting area of research, and it is anticipated that more findings will emerge in the near future.

Aging

Respiratory muscle activity and oxygenation during sleep in patients with muscle weakness.

Patients with respiratory muscle weakness show nocturnal hypoventilation, with oxygen desaturation particularly during rapid eye movement (REM) sleep, but evidence in individuals with isolated bilateral diaphragmatic paresis (BDP) is conflicting. The effect of sleep on relative activity of the different respiratory muscles of such patients and, consequently, the precise mechanisms causing desaturation have not been clarified. We have studied eight patients, four with generalized muscle weakness and four with isolated BDP during nocturnal sleep with measurements including oxygen saturation and surface electromyographic (EMG) activity of various respiratory muscle groups. Nocturnal oxygenation correlated inversely with postural fall in vital capacity, an index of diaphragmatic strength. During REM sleep, hypopnoea and desaturation occurred particularly during periods of rapid eye movements (phasic REM sleep). In most subjects, such events were "central" in type and associated with marked suppression of intercostal muscle activity, but two subjects had recurrent desaturation due to "obstructive" hypopnoea and/or apnoea. Expiratory activity of the external oblique muscle was present whilst awake and during non-rapid eye movement (NREM) sleep in seven of the eight subjects in the semirecumbent posture. This probably represents an "accessory inspiratory" effect, which aids passive caudal diaphragmatic motion as the abdominal muscles relax at the onset of inspiration. Expiratory abdominal muscle activity was suppressed in phasic REM sleep, suggesting that loss of this "accessory inspiratory" effect may contribute to "central" hypopnoea. We conclude that, in patients with muscle weakness, nocturnal oxygenation correlates with diaphragmatic strength.(ABSTRACT TRUNCATED AT 250 WORDS)

Electromyography

Muscle weakness in osteomalacia.

The muscle weakness that frequently accompanies osteomalacia and rickets may arise from a variety of causes. Particularly in patients with muscle weakness, identification of the metabolic disorder is important, since effective treatment is often possible.

Calcium

Determinants of respiratory muscle weakness in stable chronic neuromuscular disorders.

In neuromuscular disease, the precise relationship between general and respiratory muscle weakness is at present unclear. That relationship and the influence on respiratory muscle strength of such factors as type and duration of neuromuscular disease, distribution of general muscle weakness, and nutritional status were studied in 30 patients with stable chronic neuromuscular disease not presenting with respiratory symptoms. The degree of general muscle weakness was assessed by clinical examination of the strength of 17 muscle groups, yielding a general muscle strength index. The degree of respiratory muscle weakness was assessed by measuring maximal static inspiratory and expiratory mouth pressures. Maximal inspiratory (mean +/- SD: 68 +/- 28 percent predicted) and expiratory (66 +/- 29 percent predicted) mouth pressures were frequently reduced, but did not correlate with general muscle strength. The ability to estimate the degree of respiratory muscle weakness improved to some extent when the type of neuromuscular disease and the distribution of general muscle weakness were taken into account: thus, maximal expiratory mouth pressure was significantly lower (p less than 0.05) in myopathy than in polyneuropathy, and in proximal than in distal muscle weakness. Duration of neuromuscular disease and nutritional status did not influence respiratory muscle strength. It is concluded that in stable chronic neuromuscular disease, respiratory muscle involvement depends on a complexity of factors, in particular the type of neuromuscular disease and the distribution, rather than the degree, of general muscle weakness. In the individual patient, however, only direct measurement of maximal inspiratory and expiratory mouth pressures allows accurate assessment of respiratory muscle strength. These tests ought to complement neurologic examination.

Adult

Functional electrical stimulation treatment of postradiculopathy associated muscle weakness.

Eighteen chronic pain patients (CPPs) with postradiculopathy-associated muscle weakness were entered into a nonrandomized functional electrical stimulation (FES) clinical treatment study to determine if FES can improve postradiculopathy associated muscle weakness. Because of the clinical nature of the unit, the CPPs could not be denied treatments other than FES. To control for these other treatments, the CPPs were used as their own controls with two control conditions, ie, where possible, the contralateral probable normal muscle was used as a control (control 1) and; in a subgroup of CPPs (n = 6), FES treatment was initially withheld to the probable weak muscle (control 2). Strength was measured as isometric maximum voluntary contraction (IMVC) and was used as the outcome treatment variable. IMVC was measured in both the probable weak and contralateral probable normal muscles at entrance into the Pain Center, at beginning of FES treatment, at completion of FES treatment, and for the control 2 condition at the end of the non-FES treatment period. Statistical analyses of the IMVC strength results using the two control conditions indicated (1) both the FES-treated and untreated muscles increased significantly in IMVC strength, (2) improvement in IMVC strength for FES-treated muscles was significantly greater than for probable normal FES-untreated muscles and, (3) improvement in IMVC strength in FES-treated muscles was significantly greater during the FES-treatment period than during the non-FES treatment period. FES treatment of postradiculopathy-associated muscle weakness in CPPs seems to increase the strength of the probable weak muscle above the increase in strength provided by other concurrent treatments.(ABSTRACT TRUNCATED AT 250 WORDS)

Adult

Respiratory muscle weakness and fatigue.

Respiratory muscle weakness can result from a variety of neuromuscular disorders, and it is now possible to identify different patterns of weakness and quantify the extent of this weakness using reliable, sensitive tests of respiratory muscle strength. However the quantification of respiratory muscle 'fatigue' has proved more difficult, and it is now recognized that there is unlikely to be one single index of fatigue, rather a whole sequence of changes that occur in response to loading. It is likely that in practice, a close interplay between respiratory pump capacity, demands on the pump and more especially, adaptive changes in respiratory drive, protect the respiratory muscles from overt peripheral contractile failure, and that the fall in tension following prolonged muscular activity involves many different closely inter-related processes. Investigation of these processes is likely to be more rewarding than attempts to develop a single 'test of fatigue', and may lead to an improved understanding of the role of respiratory muscle dysfunction in ventilatory failure.

Fatigue

Dermatomyositis without muscle weakness. Long-term follow-up of 12 patients without systemic corticosteroids.

BACKGROUND AND DESIGN: We retrospectively studied 12 patients with dermatomyositis (DM) with at least one laboratory criterion of muscle involvement but without muscle weakness. We reported their outcome without systemic corticosteroid treatment and searched for distinctive baseline data and associated neoplasia among a group of 29 patients with classic DM. RESULTS: After a mean follow-up of 5.3 years, complete or partial skin improvement occurred in nine patients with DM without muscle weakness, and muscle enzyme levels were normalized in all. When compared with the classic DM group, no statistical differences were found for associated neoplasia or for any baseline data studied except, as expected, for muscle parameters. CONCLUSIONS: The lack of distinctive baseline data between DM without muscle weakness and classic DM suggests that there is a continuum from amyopathic to classic DM. However, DM without muscle weakness is a clinical entity with respect to favorable long-term prognosis. Unless frank muscle weakness develops, treatment with systemic corticosteroids can be avoided.

Adolescent

Preseason hamstring muscle weakness associated with hamstring muscle injury in Australian footballers.

Hamstring muscle strain is the most prevalent injury in Australian Rules Football, accounting for 16% of playing time missed as a result of injury. Thirty-seven professional footballers from an Australian Football League team had preseason measurements of hamstring and quadriceps muscle concentric peak torque at 60, 180, and 300 deg/sec measured on a Cybex 340 dynamometer. Players were studied prospectively throughout the 1995 season. During that time, six players sustained clinically diagnosed hamstring muscle injuries that caused them to miss match-playing time. The injured hamstring muscles were all weaker than in the opposite leg in absolute values and hamstring-to-quadriceps muscle ratios. According to our t-test results, hamstring muscle injury was significantly associated with a low hamstring-to-quadriceps muscle peak torque ratio at 60 deg/sec on the injured side and a low hamstring muscle side-to-side peak torque ratio at 60 deg/sec. Flexibility (as measured by the sit-and-reach test) did not correlate with injury. Discriminant-function analysis using the two significant ratio variables resulted in a canonical correlation with injury of 0.4594 and correctly classified legs into injury groups with 77.4% success. These results indicate that preseason isokinetic testing of professional Australian Rules footballers can identify players at risk of developing hamstring muscle strains.

Adult

Wheat kernel ingestion protects from progression of muscle weakness in mdx mice, an animal model of Duchenne muscular dystrophy.

A simple, reproducible test was used to quantify muscle weakness in mdx mice, an animal model of Duchenne muscular dystrophy. The effect of bedding on wheat kernels and of dietary supplementation of alpha-tocopherol on the progression of muscle weakness was investigated in mdx mice. When measured during the first 200 d of life, mdx mice developed muscle weakness, irrespective of bedding and diet. When kept on wood shavings and fed a conventional rodent diet, mdx mice showed progressive muscle weakness over the consecutive 200 d, and eventually showed a significant weight loss during the next 200-d observation period. Progression of muscle weakness and weight loss were almost completely prevented in mdx mice that were kept on wheat kernel bedding. In contrast, only incomplete maintenance of muscle strength and body weight was observed in mdx mice kept on wood shavings and fed the alpha-tocopherol-supplemented diet. It is concluded from these experiments that a component of wheat kernels other than alpha-tocopherol is essential to prevent the progression of muscle weakness in mdx mice.

Aging

Negative affect, pain and disability in osteoarthritis patients: the mediating role of muscle weakness.

Negative affect has been shown to be associated with high levels of pain and disability in osteoarthritis (OA) patients. As an explanation of this association, it was hypothesized that muscle weakness is a mediating factor between negative affect, pain and disability. Accordingly, negative affect enhances the patient's tendency to avoid pain-related activities; a low activity level induces muscle weakness, instability of joints and thus pain and disability. This theory leads to the prediction that the association between negative affect, pain and disability is most pronounced in patients with weak muscles. The prediction was tested in a study on patients with OA of the hip and/or knee. Regarding disability (but not pain), the prediction was confirmed. This study indicates that muscle weakness is a mediating factor between negative affect and disability in OA-patients.

Adaptation, Psychological

Inspiratory muscle weakness in chronic heart failure: role of nutrition and electrolyte status and systemic myopathy.

Inspiratory muscle weakness has been demonstrated in ambulatory, stable chronic heart failure (CHF) and may contribute to dyspnea during daily living. However, the mechanisms underlying this weakness are unknown. Malnutrition and electrolyte depletion are recognized complications of CHF that may impair skeletal muscle function, and limb muscle weakness and myopathic changes have also been demonstrated in CHF. We examined whether nutrition and electrolyte status contribute to the reduced skeletal muscle strength and whether inspiratory muscle weakness in CHF is part of general skeletal muscle weakness. We measured maximum inspiratory and expiratory mouth pressures as indices of respiratory muscle strength, maximum hand-grip strength as an index of limb muscle strength, anthropometric indices, serum albumin, and total lymphocyte count as indices of nutritional status, and serum electrolytes in 15 stable patients with chronic cardiac pump failure who had no evidence of primary lung disease, and in 15 age-and-sex-matched healthy controls. As compared with the matched controls, the CHF patients had reduced inspiratory muscle strength (p < 0.0025), but their expiratory and limb muscle strength were not significantly reduced. CHF patients were not malnourished; they were heavier than matched controls because of increased body fat (p < 0.05). Serum sodium was significantly lower in the CHF patients than in the controls (p < 0.01), but was within the normal range in both groups.(ABSTRACT TRUNCATED AT 250 WORDS)

Age Factors

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

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

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

[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

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