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At least 19 recordsLinked to original sources
PubMed2002

Electromyographic assessment of back muscle weakness and muscle composition: reliability and validity issues.

OBJECTIVE: To assess the reliability and construct validity of various electromyographic indices developed to assess back muscle weakness and muscle fiber composition. DESIGN: A prospective study with repeated measures performed on 3 days along with comparisons of groups presenting different back strength and/or back muscle fiber composition. SETTING: A biomechanics laboratory within a rehabilitation center. PARTICIPANTS: Forty male volunteers (20 healthy, 20 with chronic low back pain) were assessed on 3 different days to assess reliability and to make group comparisons. Thirteen healthy women were also assessed once to obtain a third group with known lower strength and different back muscle fiber composition. INTERVENTIONS: Not applicable. MAIN OUTCOME MEASURES: Surface electromyography was recorded for 4 pairs of homologous back muscles while the subjects performed, on a dynamometer, static trunk extension efforts. Electromyographic parameters were computed to assess muscle weakness and muscle fiber composition. The reliability of the data collected across the 3 sessions and comparisons between groups were determined. RESULTS: Electromyographic parameters generally showed good to excellent reliability, but were insensitive to differences in back muscle strength and did not appear to be related to muscle composition. Some trends were observed in the electromyographic parameters across the force levels, but the large interindividual variability impeded statistical comparisons. CONCLUSIONS: The assessment of muscle weakness and muscle fiber composition through electromyographic analysis does not appear feasible, at least on an individual basis, for the muscles of the back.

Adult↗
PubMed2005

Evaluation of the patient with muscle weakness.

Muscle weakness is a common complaint among patients presenting to family physicians. Diagnosis begins with a patient history distinguishing weakness from fatigue or asthenia, separate conditions with different etiologies that can coexist with, or be confused for, weakness. The pattern and severity of weakness, associated symptoms, medication use, and family history help the physician determine whether the cause of a patient's weakness is infectious, neurologic, endocrine, inflammatory, rheumatologic, genetic, metabolic, electrolyte-induced, or drug-induced. In the physical examination, the physician should objectively document the patient's loss of strength, conduct a neurologic survey, and search for patterns of weakness and extramuscular involvement. If a specific cause of weakness is suspected, the appropriate laboratory or radiologic studies should be performed. Otherwise, electromyography is indicated to confirm the presence of a myopathy or to evaluate for a neuropathy or a disease of the neuromuscular junction. If the diagnosis remains unclear, the examiner should pursue a tiered progression of laboratory studies. Physicians should begin with blood chemistries and a thyroid-stimulating hormone assay to evaluate for electrolyte and endocrine causes, then progress to creatine kinase level, erythrocyte sedimentation rate, and antinuclear antibody assays to evaluate for rheumatologic, inflammatory, genetic, and metabolic causes. Finally, many myopathies require a biopsy for diagnosis. Pathologic evaluation of the muscle tissue specimen focuses on histologic, histochemical, electron microscopic, biochemical, and genetic analyses; advances in technique have made a definitive diagnosis possible for many myopathies.

Adult↗
PubMed2004

Muscle weakness after muscle relaxants: an audit of clinical practice.

Residual muscle weakness after general anaesthesia, assessed using handgrip strength, was audited in a teaching hospital. The relationships between residual weakness, the use of muscle relaxants and patient characteristics were examined. Handgrip strength was measured preoperatively, one hour postoperatively and one day postoperatively using a hand dynamometer in 151 patients having general anaesthesia. Forty-nine patients received no muscle relaxant, 34 patients received vecuronium and 68 received rocuronium. Patients were managed by their anaesthetist according to that anaesthetist's clinical choice. All patients who received muscle relaxants received neostigmine. One hour postoperatively, there was a decline in handgrip strength of 16% for the no relaxant group, 24% for vecuronium and 29% for rocuronium. The degree of weakness for the relaxant groups was unrelated to age (P=0.89) but was strongly influenced by the patient's sex. Almost all of the increased weakness with relaxants was found in the female patients. The mean decline in handgrip strength in the male patients who received either vecuronium or rocuronium was similar to that seen when relaxants had not been used (P=0.40). One hour postoperatively, female patients showed a marked decrease in handgrip strength after both vecuronium and rocuronium (32% and 34% respectively, combined P=0.01). These results suggest that in usual clinical practice at our institution, female patients are more likely to have residual weakness after muscle relaxants.

Age Factors↗
PubMed2000

[A case of sarcoid myopathy presenting muscle pain and muscle weakness and with muscle MRI abnormality].

We experienced a 70-year-old female diagnosed as sarcoidosis. She complained bilateral femoral pain from 70-year-old. 3 months after the onset, she developed muscle weakness extending to her upper extremities with high fever of 38-39 degrees C. The erythema appeared at the right femoral region 4 months after the onset. She admitted to our hospital because of further evaluation. When she was admitted, she had tenderness on grasping the femoral muscles, proximal limb muscle weakness and Gowers' sign. On laboratory examination, CRP, aldorase, myoglobin, lysozyme were increased mildly. The EMG demonstrated a myogenic pattern. Muscle biopsy performed from the left quadriceps femoris muscle revealed non-caseating granuloma and muscle fiber necrosis. A diagnosis of muscle sarcoidosis was made from the biopsy findings and the clinical features. With oral prednisolone administration, muscle weakness and other clinical features improved gradually. On muscle MRI, multiple small high intensity areas were scattered in the femoral muscles. Muscle MRI is considered to be useful for differential diagnosis of muscle sarcoidosis.

Aged↗
PubMed2005

Acute botulinum toxin-induced muscle weakness in the anterior cruciate ligament-deficient rabbit.

We established botulinum type-A toxin (BTX-A) injections as a powerful tool to cause knee extensor weakness in New Zealand White (NZW) rabbits. The purpose of this study was to determine if BTX-A induced quadriceps weakness causes muscle dysfunction beyond that caused by anterior cruciate ligament (ACL) transection in the knee of NZW rabbits. Twenty animals were randomly divided into four study groups (n=5 each); uninjected controls, BTX-A injection alone, ACL transection alone, BTX-A injection and ACL transection combined. Isometric knee extensor torque, quadriceps muscle mass, and vertical and anterior-posterior ground reaction forces were measured four weeks post single (BTX-A and ACL), unilateral intervention. Muscle weakness, muscle atrophy and decrease in ground reaction forces were all significantly greater for the experimental compared to the untreated contralateral legs. BTX-A injection produced a greater deficit in quadriceps mass and knee extensor torque than ACL transection alone, but produced smaller deficits in the ground reaction forces. ACL transection superimposed on BTX-A injection did not change either knee extensor torque production or muscle mass. Together these results suggest that BTX-A injection causes great force and muscle mass deficits, and affects functional gait in a significant manner, but it has no measurable functional effect when superimposed on ACL transection, at least not in the acute protocol tested here. Hopefully, BTX-A injection for acutely enhancing the degree of muscle weakness in otherwise untreated animals, or in experimental models of osteoarthritis, will help in investigating the role of muscle weakness in joint degeneration.

Animals↗
PubMed1998

Distribution of muscle weakness of central and peripheral origin.

According to the established clinical tradition about the distribution of weakness, the ratios of flexor/extensor strength of patients with upper motor neuron lesions are expected to be relatively high for the elbow and wrist and low for the knee. To assess the diagnostic value of these patterns of weakness, muscle strength of 70 patients with limb weakness of central or peripheral origin was measured with a hand held dynamometer. The ratios of flexor/extensor strength at the knee, elbow, and wrist did not differ significantly between patients with central or peripheral origin of muscle weakness. The examination of tendon jerks proved to be of more value as a localising feature. The traditional notion about the distribution of weakness in upper motor neuron lesions may be explained by an intrinsically greater strength in antigravity muscles, together with the effects of hypertonia.

Adult↗
PubMed2000

Respiratory muscle weakness and respiratory muscle training in severely disabled multiple sclerosis patients.

OBJECTIVE: To evaluate the contribution of respiratory muscle weakness (part 1) and respiratory muscle training (part 2) to pulmonary function, cough efficacy, and functional status in patients with advanced multiple sclerosis (MS). DESIGN: Survey (part 1) and randomized controlled trial (part 2). SETTING: Rehabilitation center for MS. PATIENTS: Twenty-eight bedridden or wheelchair-bound MS patients (part 1); 18 patients were randomly assigned to a training group (n = 9) or a control group (n = 9) (part 2). INTERVENTION: The training group (part 2) performed three series of 15 contractions against an expiratory resistance (60% maximum expiratory pressure [PEmax]) two times a day, whereas the control group performed breathing exercises to enhance maximal inspirations. MAIN OUTCOME MEASURES: Forced vital capacity (FVC), inspiratory, and expiratory muscle strength (PImax and PEmax), neck flexion force (NFF), cough efficacy by means of the Pulmonary Index (PI), and functional status by means of the Extended Disability Status Scale (EDSS). RESULTS: Part 1 revealed a significantly reduced FVC (43% +/- 26% predicted), PEmax (18% +/- 8% predicted), and PImax (27% +/- 11% predicted), whereas NFF was only mildly reduced (93% +/- 26% predicted). The PI (median score, 10) and EDSS (median score, 8.5) were severely reduced. PEmax was significantly correlated to FVC, EDSS, and PI (r = .77, -.79, and -.47, respectively). In stepwise multiple regression analysis. PEmax was the only factor contributing to the explained variance in FVC (R2 = .60), whereas body weight (R2 = .41) was the only factor for the PI. In part 2, changes in PImax and PEmax tended to be higher in the training group (p = .06 and p = .07, respectively). The PI was significantly improved after 3 months of training compared with the control group (p < .05). After 6 months, the PI remained significantly better in the training group. CONCLUSIONS: Expiratory muscle strength was significantly reduced and related to FVC, cough efficacy, and functional status. Expiratory muscle training tended to enhance inspiratory and expiratory muscle strength. In addition, subjectively and objectively rated cough efficacy improved significantly and lasted for 3 months after training cessation.

Body Mass Index↗
PubMed1997

Alterations in sarcomere structure, collagen organization, mitochondrial activity, and protein metabolism in the avian low score normal muscle weakness.

Skeletal muscle fibers are surrounded by an extracellular matrix. The extracellular matrix is composed of glycoproteins, collagen, and proteoglycans. Proteoglycans have been suggested to play an important functional role in tissue differentiation. However, an understanding of how the extracellular matrix affects skeletal muscle development and function is largely unknown. In the avian genetic muscle weakness, low score normal (LSN), a late embryonic increase in the expression of decorin is followed by a subsequent increase in collagen crosslinking. The sarcomere organization, collagen fibril diameter and organization were investigated using transmission electron microscopy. Measurements were made at 20 days of embryonic development and 6 weeks posthatch. These studies showed changes in sarcomere organization and deterioration of muscle fibril structure in the LSN pectoral muscle. In vitro satellite cell cultures were developed and assayed for mitochondrial activity, and protein synthesis and degradation. In these analyses, mitochondrial activity from LSN satellite cells was significantly higher than those from normal pectoral muscle satellite cells. Protein synthesis rates between the normal and LSN satellite cell-derived myotubes were similar, but protein degradation rates were higher in the LSN cultures. Based on the reported functions of decorin as a regulator of cell proliferation and collagen fibril organization, it is possible that the late embryonic increase in decorin may be influencing the alterations in LSN sarcomere and collagen organization.

Animals↗
PubMed1999

A second locus for autosomal dominant myopathy with proximal muscle weakness and early respiratory muscle involvement: a likely chromosomal locus on 2q21.

We recently mapped a locus for a new variant of autosomal dominant myopathy (Swedish families) with proximal muscle weakness, early respiratory muscle involvement, and unique muscle biopsy findings to chromosomal region 2q24-31. In this study, a French family with a similar clinical phenotype and pathology (muscle biopsy) was investigated to see whether the disease gene associated with the myopathy is mapped to the same region as the one in the Swedish families; however, chromosomal region 2q24-q31 was completely excluded. In order to localise the disease gene for the French family, a genome-wide scan was performed using polymorphic microsatellite markers. A maximum two-point lod score of 2.11 (the highest lod score that can be achieved in this family) was obtained for the markers in the region between D2S1272 and D2S1260, spanning 4 cM. This result suggests that the gene responsible for the French form is likely to be located on chromosome 2q21.

Chromosome Mapping↗
PubMed1997

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↗
PubMed1995

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↗
PubMed1976

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↗
PubMed2003

Distribution of extremity muscle weakness in myasthenia gravis: sparing of tibialis anterior muscle.

We evaluated the distribution of muscle weakness in 70 myasthenia gravis (MG) patients, using the MRC scale. Extensors in the upper extremities and proximal flexors in the lower extremities (LE) were found to be weak. Tibialis anterior muscle was rarely affected and only when there was substantial weakness in LE proximal muscles. Attention to this distribution may help in differentiating MG, particularly MG with only limb weakness, from muscular dystrophies.

Adolescent↗
PubMed1998

[Immobilizing muscle weakness accentuated in leg and proximal muscles].

A 54 year old waiter was referred to the hospital because of proximal muscle weakness, most pronounced in his legs, which progressed to an inability to stand or walk within weeks. Myopathy was diagnosed based on the muscle biopsy findings and myositis was ruled out by laboratory and biopsy results. Further investigations led us to exclude an endocrine cause, hypovitaminosis D, infectious myopathy or a paraneoplastic syndrome. Heteroanamnesis revealed severe alcoholism, lasting for more than 30 years. The presumed alcohol induced hepatopathy was confirmed by liver biopsy. There were no signs of an acute alcoholic myopathy, as the weakness had developed rather insidiously, there was no elevation of the CK serum level nor myoglobinuria and a type 2 fibre atrophy was found by muscle biopsy. As expected the weakness improved under abstention. Thus the final diagnosis of a chronic alcohol induced myopathy was established.

Alcoholism↗
PubMed2002

Effect of pattern and severity of respiratory muscle weakness on carbon monoxide gas transfer and lung volumes.

In clinical practice, an elevated carbon monoxide (CO) transfer coefficient (KCO) and restrictive ventilatory defect are taken as features of respiratory muscle weakness (RMW). However, the authors hypothesised that both pattern and severity of RMW effect gas transfer and lung volumes. Measurements of CO transfer and lung volumes were performed in patients with isolated diaphragm weakness (n=10), inspiratory muscle weakness (n=12), combined inspiratory and expiratory muscle weakness (n=5) and healthy controls (n=6). Patients with diaphragm weakness and inspiratory muscle weakness had reduced total lung capacity (TLC) (83.6% predicted and 68.9% pred, respectively), functional residual capacity (FRC) (83.9% pred and 83.6% pred) and transfer factor of the lung for CO (TL,CO) (86.2% pred and 66.2% pred) with increased KCO (114.1% pred and 130.2% pred). Patients with combined inspiratory and expiratory muscle weakness had reduced TLC (80.9% pred) but increased FRC (109.9% pred) and RV (157.4% pred) with decreased TL,CO (58.0% pred) and KCO (85.5% pred). In patients with diaphragm weakness, the increase in carbon monoxide transfer coefficient was similar to that of normal subjects when alveolar volume was reduced. However, the increase in carbon monoxide transfer coefficient in inspiratory muscle weakness was often less than expected, while in combined inspiratory and expiratory muscle weakness, the carbon monoxide transfer coefficient was normal/reduced despite further reductions in alveolar volume, which may indicate subtle abnormalities of the lung parenchyma or pulmonary vasculature. Thus, this study demonstrates the limitations of using carbon monoxide transfer coefficient in the diagnosis of respiratory muscle weakness, particularly if no account is taken of the alveolar volume at which the carbon monoxide transfer coefficient is made.

Adult↗
PubMed1997

Development of degenerative muscle weakness by chronic administration of beta,beta'-iminodipropionitrile in the drinking water to rats: a model for motorneuropathy.

Progressive muscle weakness accompanied by progressive muscle atrophy was investigated in rats administered beta,beta'-iminodipropionitrile (IDPN) chronically in the drinking water. Spontaneous running wheel activity declined slowly and reached a constant low level before postural muscle weakness was apparent. The rats being offered IDPN in the drinking water showed definite postural muscle weakness about 25 weeks after first being given IDPN, and muscle strength declined gradually throughout the remainder of the experiment (to 66 weeks). Flaccid paralysis became apparent in the hind limbs in the later stages of the experiment. Neurogenic muscle atrophy, measured by group atrophy of the muscle fibers, also progressed slowly, almost in parallel with the loss of muscle strength. At the end of the experiment, muscle weight of the gastrocnemius had decreased to about 20% that of control [F(2, 12) = 40.4, p < 0.05]. Plasma creatinine in the rats given IDPN in the drinking water for 66 weeks was significantly elevated over that of controls [F(2, 12) = 20.1, p < 0.05]. On the other hand, in rats given IDPN intraperitoneally, postural muscle weakness and muscle atrophy were less apparent, and plasma creatinine was normal. However, in these animals, abnormal behaviors, such as hyperexcitement, circling, and choreic movement (ECC syndrome), were apparent. These results suggest that the present model, which administers IDPN chronically in the drinking water ad lib and does not show involuntary movements and ECC syndrome, is of potential importance for investigation of chronic diseases of progressive muscle weakness with progressive muscle atrophy, and for assessing the efficacy of drugs and therapies for treating chronic neuromuscular diseases.

Animals↗
PubMed1997

Segmental distribution of muscle weakness in SMA III: implications for deterioration in muscle strength with time.

We examined 26 spinal muscular atrophy type III (SMA III) patients with SMNt deletions, searching for possible segmental distribution of muscle weakness. In those with disease duration of < or = 11 years, the weakest muscles were upper lumbar innervated ones in the lower extremities. In the upper extremities, early involvement of triceps muscle suggested the possibility of lower cervical (C7) onset. Electrophysiologically, weaker muscles had a more severe reduction in the recruitment pattern, particularly in the lower extremities. However, severe reduction in recruitment was sometimes also observed in clinically strong muscles. In patients with disease duration of > or = 16 years and regardless of disease duration, in those with disease onset at < or = 3 years of age, weakness and severe electrophysiological changes were more widespread. These findings may suggest a progression in muscle weakness with time. When compared to 12 patients with Becker muscular dystrophy (BMD), early stage SMA III with weak iliopsoas-strong gluteus maximus stood in contrast to BMD with weak gluteus maximus-strong iliopsoas.

Adolescent↗