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PubMed1987

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↗
PubMedDate not supplied

Distribution of muscle weakness in patients with stable chronic obstructive pulmonary disease.

PURPOSE: The authors determined the degree of respiratory and peripheral muscle weakness in patients with moderate to severe chronic obstructive pulmonary disease (COPD). Differences in severity of muscle weakness among muscle groups may provide treatment options, such as selective muscle training, to adapt the exercise prescription in pulmonary rehabilitation programs. In addition, this information may add to the knowledge on the mechanisms of muscle weakness. METHODS: Respiratory and peripheral muscle force were quantified in 22 healthy elderly subjects and 40 consecutive COPD patients (forced expiratory volume in 1 second, percent of predicted value [% pred] 41 +/- 19; transfer factor for carbon monoxide, % pred 47 +/- 26) admitted to a pulmonary rehabilitation program. Lung function, diffusing capacity, isometric force of four peripheral muscle groups (handgrip, elbow flexion, shoulder abduction, and knee extension), neck flexion force, and maximal inspiratory and expiratory pressures were measured. RESULTS: Patients had reduced respiratory muscle strength (mean 64% of control subjects' value [% control]) and peripheral muscle strength (mean 75% control) compared to normal subjects. Inspiratory muscle strength (59 +/- 18% control) was significantly lower than expiratory muscle strength (69 +/- 25% control) and peripheral muscle strength (P < 0.01). Neck flexion force (80 +/- 19% control) was better preserved than maximal inspiratory pressure and shoulder abduction force (70 +/- 15% control, P < 0.01). Handgrip force (78 +/- 16% control) and elbow flexion force (78 +/- 14% control) were significantly less affected than shoulder abduction force (70 +/- 15% control, P < 0.01). Finally, shoulder abduction force and knee-extension force (72 +/- 24% control) were not significantly different. CONCLUSIONS: Muscle weakness in stable COPD patients does not affect all muscles to a similar extent. Inspiratory muscle force is affected more than peripheral muscle force, whereas proximal upper limb muscle strength was impaired more than distal upper limb muscle strength.

Aged↗
PubMed2003

Clinical spectrum of muscle weakness in human West Nile virus infection.

Poliomyelitis has recently been identified as a cause of muscle weakness in patients with West Nile virus (WNV) infection. However, the clinical spectrum of WNV-associated weakness has not been described. We reviewed data on 13 patients with WNV infection. Patients with muscle weakness were classified into one of three distinct groups based on clinical features. Group 1 comprised five patients who developed acute flaccid paralysis, four with meningoencephalitis and one without fever or other signs of infection. Paralysis was asymmetric, and involved from one to four limbs in individual patients. Electrodiagnostic studies confirmed involvement of anterior horn cells or motor axons. Group 2 involved two patients without meningoencephalitis who developed severe but reversible muscle weakness that recovered completely within weeks. Muscle weakness involved both lower limbs in one patient and one upper limb in the other. Group 3 consisted of two patients who experienced subjective weakness and disabling fatigue, but had no objective muscle weakness on examination. In addition to the three distinct groups, two other patients developed exaggerated weakness in the distribution of preexisting lower motor neuron dysfunction. We conclude that the clinical spectrum of WNV-associated muscle weakness ranges from acute flaccid paralysis, with or without fever or meningoencephalitis, to disabling fatigue. Also, preexisting dysfunction may predispose anterior horn cells to additional injury from WNV. Awareness of this spectrum will help to avoid erroneous diagnoses and inappropriate treatment.

Acute Disease↗
PubMed1994

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↗
PubMed1989

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↗
PubMed1995

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↗
PubMed2004

Ultrasound imaging distinguishes between normal and weak muscle.

OBJECTIVE: To determine whether real-time ultrasound imaging can provide quantitative data that distinguish pathologic from healthy muscle and that correlate with strength measures. DESIGN: Nonrandomized matched-pair, repeated-measures design. SETTING: Ultrasound imaging laboratory, rehabilitation medicine department, government research hospital. PARTICIPANTS: Nine patients with stable active or inactive myositis, stratified into 3 groups based on their 10-point manual muscle test (MMT) scores, and 9 age- and gender-matched controls. INTERVENTIONS: Maximal isometric contraction of the rectus femoris muscle in 2 knee-flexion positions (60 degrees, 90 degrees ) during simultaneous ultrasound imaging and muscle force dynamometry. MAIN OUTCOME MEASURES: Changes of the rectus femoris muscle in horizontal (X) and vertical (Y) diameters between relaxed and contracted states, and muscle force measurements. RESULTS: The X diameters decreased and the Y diameters increased during isometric contraction in all participants. For each group, average changes in cross-sectional diameters were consistently higher in controls than in patients. Patients with MMT less than 8 differed significantly from controls in both X and Y dimensions. A moderately strong correlation was found between muscle force and the Y diameter during contraction at 60 degrees (r =.78) and 90 degrees (r =.67) knee-flexion angles. CONCLUSIONS: Ultrasonography provided a quantitative measure of change between relaxed and contracted state of muscle, which correlated with muscle force. Ultrasound identified significant differences in cross-sectional diameters between the myopathic and normal muscles sampled and may be useful for measuring muscle response to drug and exercise therapy.

Adult↗
PubMedDate not supplied

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↗
PubMed2004

Muscle weakness and foot deformities in diabetes: relationship to neuropathy and foot ulceration in caucasian diabetic men.

OBJECTIVE: To examine the relationships among muscle weakness, foot deformities, and peroneal and tibial nerve conduction velocity in diabetic and nondiabetic men. RESEARCH DESIGN AND METHODS: A neuropathic and foot evaluation was undertaken in 10 nondiabetic control subjects (group C) and in 36 consecutive diabetic patients attending Diabetes Centre clinics, including 10 diabetic control subjects (group D), 15 diabetic neuropathic patients (group DN), and 11 diabetic patients with a history of ulceration (group DU). Neuropathy was defined as a peroneal motor nerve conduction <40 m/s. Muscle weakness was assessed in seven intrinsic and seven extrinsic muscles of the foot using a semiquantitative score (max score per muscle = 3). Foot deformities were assessed using a foot deformity score (max score = 3). A higher score indicated increased muscle weakness or more severe foot deformities. Muscle weakness and foot deformities were assessed without prior knowledge of patient and neuropathy status. RESULTS: Peroneal and tibial nerve conduction velocity were associated with weakness in muscles innervated by, respectively, the peroneal and tibial nerve (r = -0.70 and r = -0.51, P < 0.01) and foot deformities (r = -0.60 and r = -0.59, P < 0.001). The DN and DU groups had more weakness in intrinsic and extrinsic muscles compared with the C and D groups. Muscles innervated by the tibial nerve had a greater proportional muscle weakness than those innervated by the peroneal nerve in the DN and DU groups. The DN and DU patients had more foot deformities (median food deformity score [interquartile range]) (3 [2-3] and 2 [2-3]) compared with D and C patients (0 [0-0.75] and 0 [0-0]). CONCLUSIONS: Important relationships have been shown between motor nerve conduction deficit and muscle weakness; however, it is still not clear whether abnormal nerve function, leading to a decrease in muscle strength, could be responsible for the development of foot deformities.

Diabetic Foot↗
PubMed1996

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↗
PubMed2003

Cross-bridge mechanisms of muscle weakness in multiple sclerosis.

Vastus lateralis muscle biopsies were obtained from six individuals with multiple sclerosis (MS) having an Expanded Disability Status Score of 4.75 +/- 0.28, and from six age- and gender-matched individuals without MS. Biopsies from the MS group showed fewer fibers (31 +/- 4 vs. 46 +/- 4%) containing the type IIa myosin heavy chain (MHC) isoform exclusively. However, the percentage of fibers coexpressing type IIa and IIx MHC increased in direct proportion with MS disability status. The average unloaded shortening velocity of skinned fibers containing type I or IIa MHC did not differ between subject groups. Peak Ca(2+)-activated force was 11-13% lower in fibers from the MS group due to atrophy (type I and IIa fibers) and reduced specific force (type I fibers). Increasing intracellular inorganic phosphate (0-30 mM) or hydrogen ion (pH 7.0-6.2) reduced Ca(2+)-activated force in a manner that was independent of MS status. Thus, fibers from the MS group showed a subtle shift in fast MHC isoform coexpression and a modest reduction in cross-bridge number, density, or average force, with no change in maximal cross-bridge cycling rate or susceptibility to intracellular metabolites. These changes explain part of the muscle weakness and fatigue experienced by individuals with MS.

Adult↗
PubMed1998

Peripheral muscle weakness in patients with chronic obstructive pulmonary disease.

Peripheral muscle weakness is commonly found in patients with chronic obstructive pulmonary disease (COPD) and may play a role in reducing exercise capacity. The purposes of this study were to evaluate, in patients with COPD: (1) the relationship between muscle strength and cross-sectional area (CSA), (2) the distribution of peripheral muscle weakness, and (3) the relationship between muscle strength and the severity of lung disease. Thirty-four patients with COPD and 16 normal subjects of similar age and body mass index were evaluated. Compared with normal subjects, the strength of three muscle groups (p < 0.05) and the right thigh muscle CSA, evaluated by computed tomography (83.4 +/- 16.4 versus 109.6 +/- 15.6 cm2, p < 0.0001), were reduced in COPD. The quadriceps strength/thigh muscle CSA ratio was similar for the two groups. The reduction in quadriceps strength was proportionally greater than that of the shoulder girdle muscles (p < 0.05). Similar observations were made whether or not patients had been exposed to systemic corticosteroids in the 6-mo period preceding the study, although there was a tendency for the quadriceps strength/thigh muscle CSA ratio to be lower in patients who had received corticosteroids. In COPD, quadriceps strength and muscle CSA correlated positively with the FEV1 expressed in percentage of predicted value (r = 0.55 and r = 0. 66, respectively, p < 0.0005). In summary, the strength/muscle cross-sectional area ratio was not different between the two groups, suggesting that weakness in COPD is due to muscle atrophy. In COPD, the distribution of peripheral muscle weakness and the correlation between quadriceps strength and the degree of airflow obstruction suggests that chronic inactivity and muscle deconditioning are important factors in the loss in muscle mass and strength.

Aged↗
PubMed2004

Muscle weakness in a mouse model of nemaline myopathy can be reversed with exercise and reveals a novel myofiber repair mechanism.

Patients with the inherited muscle disease nemaline myopathy experience prolonged muscle weakness following periods of immobility. We have examined endurance exercise as a means of improving recovery following muscle inactivity in our alpha-tropomyosin(slow)(Met9Arg)-transgenic mouse model of nemaline myopathy. Physical inactivity, mimicked using a hindlimb immobilization protocol, resulted in fiber atrophy and severe muscle weakness. Following immobilization, the nemaline mice (NM) were weaker than WT mice but regained whole-body strength with exercise training. The disuse-induced weakness and the regain of strength with exercise in NM were associated with the respective formation and resolution of nemaline rods, suggesting a role for rods in muscle weakness. Muscles from NM did not show the typical features of muscle repair during chronic stretch-immobilization of the soleus muscle (regeneration occurred with relative lack of centralized nuclei). This indicates that the normal process of regeneration may be altered in nemaline myopathy and may contribute to poor recovery. In conclusion, endurance exercise can alleviate disuse-induced weakness in NM. The altered myofiber repair process in the nemaline mice may be a response to primary myofibrillar damage that occurs in nemaline myopathy and is distinct from the classical repair in muscular dystrophy resulting from plasma membrane defects.

Animals↗
PubMed1993

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↗
PubMed1995

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↗