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PubMed1997

Postpolio muscular dysfunction: relationships between muscle energy metabolism, subjective symptoms, magnetic resonance imaging, electromyography, and muscle strength.

Eleven patients with previous polio were studied. The concentration of energy-related metabolites and energy charge was measured from the vastus lateralis muscle, as was isometric muscle strength of knee extension. Cross-sectional area of the quadriceps femoris muscle was calculated from magnetic resonance imaging. Reinnervation was studied using macroelectromyography. Muscle weakness, pain, and newly acquired muscle weakness in the legs was estimated by the patients. The findings in the legs in which the patients experienced new loss of muscle function were compared with the stable legs. There were no significant differences between these groups in any of the objectively measured variables. Only hip pain correlated with new loss of muscle function. Creatine phosphate was decreased in 5 patients. The symptoms and subjective muscle strength did not correlate with any of the objective measurements. There were no significant relationships between energy-related metabolites and postpolio symptoms.

Adult↗
PubMed1997

[Acute respiratory insufficiency revealing myasthenia gravis: apropos of 3 cases].

BACKGROUND: Myasthenia gravis is usually revealed by a ptosis or a diplopia. A respiratory muscle weakness often occurs during the course but an acute respiratory failure as initial feature is unusual. CASE REPORTS: Three girls, aged 8, 10 and 14 years, were hospitalised in an intensive care unit, along a 15 year-period, for an acute respiratory distress. The first two children suffered from skeletal and bulbar muscle weakness. The third, admitted with the diagnosis of unexplained pneumonia, was complaining of skeletal and bulbar muscle weakness for the last 18 months. Myasthenia gravis was confirmed with electromyography, and detection of the acetylcholine-receptors antibodies in all three cases. CONCLUSION: Any unexplained acute respiratory distress must lead to search for skeletal and bulbar muscle weakness, specially after muscular exercise or at the end of day, manifestations which characterize myasthenia gravis.

Acute Disease↗
PubMed1986

Susceptibility to murine experimental autoallergic myasthenia gravis: the role of antibody specificity.

To examine the differing susceptibility of C57BL/6J and C3H/HeJ mice to experimental autoallergic myasthenia gravis (EAMG), we have compared the pathogenicity of sera from the two strains. Mice were immunized with acetylcholine receptor from T. californica and muscle weakness assessed as the time mice were capable of running on an exercise drum following the administration of a sub-lethal dose of D-tubocurarine. 16 of 20 C57BL/6J and only 4 of 19 C3H/HeJ mice developed muscle weakness. However, anti-AChR antibody titres were similar in both strains. The effect of transfer of pooled immune sera from each strain to naive recipients was therefore compared. Transfer of pooled C57BL/6J sera to naive C3H/HeJ and C57BL/6J mice produced significant muscle weakness (P less than 0.001 & P less than 0.001 respectively). Transfer of pooled C3H/HeJ sera did not produce statistically significant muscle weakness in either strain. It is concluded that differences in disease susceptibility result from differences in antibody specificities of the major antibody populations, rather than differences in total antibody amounts or other factors.

Acetylcholine↗
PubMed2002

Amyopathic dermatomyositis: retrospective review of 37 cases.

Criteria for diagnosis of amyopathic dermatomyositis vary, and the prognosis is not clear. Our purpose was to investigate prognosis regarding progression to myositis and associated malignancy. We reviewed the medical records of patients with dermatomyositis evaluated at our institution from 1976 to 1994. Of 746 patients with dermatomyositis, 37 (5%) with the amyopathic subtype were divided into 3 groups: group 1 (73%), no subjective or objective evidence of myopathy; group 2 (13%), no subjective muscle weakness but abnormalities detected by objective tests; group 3 (13%), subjective muscle weakness but no objective evidence of myopathy. Follow-up was conducted by means of a mailed questionnaire. For 25 patients, follow-up of 1 to 17 years after diagnosis showed muscle weakness in 2 patients in group 1 within 5 years after diagnosis. Five patients (13%) had associated malignancies. Of 7 (19%) patients with disease onset before the age of 18 years, none had progression to myopathy. Although it presents with cutaneous lesions indistinguishable from those of classic dermatomyositis, amyopathic dermatomyositis is a distinct entity. In most patients, amyopathic dermatomyositis does not progress to myopathy. Prognosis appears favorable, but malignancy may develop.

Adolescent↗
PubMed2001

Simulations of foot stability during gait characteristic of ankle dorsiflexor weakness in the elderly.

Falls are common among the elderly and often cause injuries. They most frequently occut during walking and are associated with the chronic deterioration in neuromuscular and sensory systems, as well as with ankle dorsiflexor muscular weakness and lowered endurance of these muscles to fatigue. In the present study, a three-dimensional (3-D) finite element model of the structure of the foot was utilized to determine the effects of ankle dorsiflexor muscle weakness on the structural stability of the foot and, consequently, on the risk of falls during gait. The medial-lateral tendency of instability of the foot during gait in such conditions of weakness was analyzed by means of this model to identify the most important muscles used in controlling foot stability in affected individuals. The values of the eccentricity of the center of pressure under the heel during foot placement were used to indicate the degree of foot stability. The computational analysis indicated that it is the tibialis anterior muscle's weakness that dramatically decreases foot stability. Clinical investigation is now needed to correlate the significance of tibialis anterior muscle weakness with other known risk factors affecting the tendency to falls among the elderly, e.g., deterioration of sensory abilities. Rehabilitation practitioners and physical therapists may apply the present analytic approach to evaluate the stability of a foot before treatment and compare the predicted with the actual therapeutic results in terms of optimization of foot-ground pressure.

Accidental Falls↗
PubMed1994

Acute idiopathic axonal neuropathy (AIAN): a clinical and electrophysiological observation.

Twenty patients (M:F 15:5) with electrophysiological evidence of predominant axonal lesion and fulfilling clinical criteria for Guillain Barré Syndrome were observed during a period of 6 years (1985-1990). Their mean age was 27.5 years (range 5-55). Seven patients had antecedent febrile illness. Peak motor deficit was reached at a mean period of 6.5 days (range 2-21 days). All the patients had distal muscle weakness out of proportion to proximal muscle weakness. Facial paresis (13 patients), bulbar palsy (2), respiratory failure (1), sensory deficits (7) and dysautonomia (1) were other salient features. CSF analysis revealed albumino-cytological dissociation in 12 patients. One patient died and in the remaining patients the recovery was delayed and incomplete. Presence of predominant distal muscle wasting and weakness, low amplitude CMAP or inexcitable nerves, absence of conduction block or significant temporal dispersion, normal or only slightly reduced conduction velocity and evidence of poor recovery suggest that the primary pathology in these patients may be axonal degeneration. These cases may represent a distinct entity and need to be differentiated from the more commonly observed acute idiopathic demyelinating neuropathy.

Acute Disease↗
PubMed1999

Superimposed single impulse and pulse train electrical stimulation: A quantitative assessment during submaximal isometric knee extension in young, healthy men.

Superimposed electrical stimulation techniques can be used to detect central activation failure (CAF), defined as incomplete central nervous system recruitment, suboptimal activation of motor units, or both. The purpose of this study was to evaluate superimposed electrical stimulation techniques to be used to detect CAF during isometric knee extension. We performed three sets of experiments and compared the torque increments from transcutaneous electrical stimulation with: (i) single impulses of different amplitudes (100 V, 150 V, and 200 V) and a pulse train of 100 Hz (100 V, 100 ms); (ii) pulse trains (100 Hz, 100 V) of different lengths (100 ms, 200 ms, and 300 ms); and (iii) pulse trains (100 Hz, 100 ms) of different amplitudes (50 V, 100 V, 150 V, and 200 V). Stimulation was evaluated at submaximal (80% of MVC) isometric knee extension in 24 healthy young men using a Biodex isokinetic dynamometer. Electrodes were placed over the rectus femoris muscle and all stimulation impulses were monophasic, rectangular waves of 0.2-ms duration. Pulse train stimulation at 100 V always elicited a torque increment, whereas single impulse stimulation, even at 200 V, only caused a torque increment in about half of the trials. For each subject, the pulse train generated a significantly larger torque increment than for any of the three single impulses. There was no significant difference in torque increment between the three pulse trains of different lengths. Pulse trains at 150 V and 200 V generated significantly larger torque increments than at 50 V and 100 V. High-frequency maximal train stimulation may thus improve the detection of CAF during isometric knee extension. Detection of CAF may be important in the clinical assessment of muscle weakness, investigating the mechanisms underlying muscle weakness, and evaluating potential therapeutic strategies.

Adult↗
PubMed1992

Combined enzyme defect of mitochondrial fatty acid oxidation.

A young girl presented with recurrent episodes of muscle weakness culminating in a severe attack of generalized muscle weakness. In the muscle mitochondria from the patient there was an abnormal pattern of intermediates of beta-oxidation with an accumulation of 3-hydroxyacyl- and 2-enoyl-CoA and carnitine esters, and 3-oxoacylcarnitines. There was low activity of long-chain 3-hydroxyacyl-CoA dehydrogenase in mitochondria from all tissues. The activity of long-chain 2-enoyl-CoA hydratase was low in muscle mitochondria and 3-oxoacyl-CoA thiolase activity measured with 3-oxohexadecanoyl-CoA as substrate was low in fibroblast, muscle, and cardiac mitochondria but only partial deficiency was present when the activity was measured with 3-oxooctanoyl-CoA. The activity of the long-chain 3-hydroxyacyl-CoA dehydrogenase and long-chain 3-oxoacyl-CoA thiolase in fibroblasts from the patient's parents was intermediate between those of controls and the patient. The patient has a combined defect of the long-chain 3-hydroxyacyl-CoA dehydrogenase, long-chain 3-oxoacyl-CoA thiolase, and long-chain 2-enoyl-CoA hydratase which appears to be inherited in an autosomal recessive manner. This suggests there is a multifunctional enzyme catalyzing these activities in human mitochondria and that this enzyme is deficient in our patient.

3-Hydroxyacyl CoA Dehydrogenases↗
PubMed2006

[Association of coeliac disease and myasthenia gravis].

Coeliac disease is a malabsorption syndrome induced by the gluten-containing cereals leading to the damage of small intestinal mucosa. A case of a young woman is presented whose coeliac disease became overt in the puerperium. Despite strict adherence to gluten-free diet, her muscle weakness affecting several muscle regions persisted. Following a diagnostic work-up covering numerous co-disciplines, the diagnosis of myasthenia gravis was set up underlying her muscle symptoms. After the thorough review of the corresponding literature, the authors could not find any case report on the association of coeliac disease with myasthenia gravis.

Adult↗
PubMed1989

Respiratory complications and their management in motor neuron disease.

Although respiratory insufficiency is common in the advanced stages of motor neuron disease, some patients may develop distressing respiratory symptoms early in the course of the disease or even present with respiratory failure or arrest. We describe 14 patients with motor neuron disease who were considered for respiratory support; 11 received such support and all derived significant symptomatic improvement without distressing prolongation of life. Of the 8 patients with typical features of amyotrophic lateral sclerosis, 7 had predominant diaphragm weakness and 1 generalized respiratory muscle weakness; 7 received negative pressure ventilation by cuirass which improved both the quality of sleep and exercise tolerance. Three patients with predominantly bulbar disease had nocturnal apnoea or hypoventilation. Two received no support. One, who also developed diaphragm weakness, was treated by a cuirass, continuous positive airway pressure (CPAP), and later nocturnal intermittent positive pressure ventilation (IPPV). Three patients with progressive muscular atrophy had predominant diaphragm weakness or nocturnal apnoea. These patients received nocturnal CPAP, cuirass or IPPV with symptomatic benefit. This series shows that some patients with motor neuron disease, mainly those with symptoms due to respiratory muscle weakness in the absence of severe bulbar impairment, derive symptomatic benefit from supported ventilation.

Adult↗
PubMed1999

Spinal muscular atrophy.

Spinal muscular atrophy is a common cause of disability in childhood and is characterized by weakness and wasting of voluntary muscle. It is frequently fatal. The gene for this disorder has been identified as the SMN gene and is part of a highly complex duplicated region of chromosome 5 that is subject to a high rate of gene deletion and gene conversion. The severity of muscle weakness correlates with the amount of full-length SMN protein produced. Molecular genetic studies support a model in which patients are compound heterozygotes of deleted and converted alleles that predicts a progressively decreasing amount of protein product with severity of muscle weakness. The function of SMN is beginning to be understood and it appears to be involved in ribonucleoprotein biogenesis and thus indirectly in post-transcriptional processing of mRNA. There are theoretical grounds for motor neurons having a cell-specific vulnerability to disturbances of mRNA processing and transport and these are briefly reviewed.

Animals↗
PubMed2002

Vitamin D deficiency, muscle function, and falls in elderly people.

An inadequate serum vitamin D status is commonly seen in elderly people as the result of various risk factors interacting in this population. Apart from the well-known effects on bone metabolism, this condition is also associated with muscle weakness, predominantly of the proximal muscle groups. Muscle weakness below a certain threshold affects functional ability and mobility, which puts an elderly person at increased risk of falling and fractures. Therefore, we wanted to determine the rationale behind vitamin D supplementation in elderly people to preserve and possibly improve muscle strength and subsequently functional ability. From experimental studies it was found that vitamin D metabolites directly influence muscle cell maturation and functioning through a vitamin D receptor. Vitamin D supplementation in vitamin D-deficient, elderly people improved muscle strength, walking distance, and functional ability and resulted in a reduction in falls and non-vertebral fractures. In healthy elderly people, muscle strength declined with age and was not prevented by vitamin D supplementation. In contrast,severe comorbidity might affect muscle strength in such a way that restoration of a good vitamin D status has a limited effect on functional ability. Additional research is needed to further clarify to what extent vitamin D supplementation can preserve muscle strength and prevent falls and fractures in elderly people.

Accidental Falls↗
PubMed1990

[A manifesting carrier of Duchenne muscular dystrophy presenting mosaic distribution of dystrophin negative and positive muscle fibers].

A 25-year-old female patient with an approximate 10-year-history of slowly progressive muscle weakness was diagnosed as a manifesting carrier of Duchenne muscular dystrophy (DMD) because her muscle biopsy showed scattered fibers with no dystrophin on immunohistochemical staining. She had no family history of neuromuscular disorders. She was in good health until about 14 years of age, when she developed muscle weakness and atrophy of the extremities with slow aggravation. On admission at the age of 25 years, she had asymmetrical muscle atrophy in the lower extremities; the left femur, right femur, left crus, and right crus measured 36.0, 40.5, 31.5, and 35.5 cm in circumference, respectively. However, the muscle weakness of the extremities was symmetrical with no laterality, and the proximal muscles in the lower extremities were predominantly affected to 3+/5 MMT test. She walked with a mild wadding manner and stood up with Gower' maneuver. Deep tendon reflexes of the extremities were almost normoactive with no pathologic reflexes. As to laboratory findings, serum enzymes of muscular origin were elevated; GOT was 44 IU/l, GPT 60 IU/l, LDH 829 IU/l, CK 4238 IU/l, and aldolase 31 SL units. The electromyogram showed myopathic changes mixed with some neurogenic components. Peripheral nerve conduction velocity was normal. A computed tomography of the skeletal muscles showed more marked atrophy and lower density in the left lower extremity than in the right. The biopsied left gastrocnemius muscle demonstrated a marked variation in fiber size with some necrotic and regenerating fibers. On immunohistochemical stain with anti-dystrophin antibody, the dystrophin negative fibers were scattered among positive fibers in a mosaic distribution.

Adult↗
PubMed1998

Peripheral skeletal muscles and exercise performance in patients with chronic obstructive pulmonary disease.

Impaired exercise capacity is a common finding in chronic obstructive pulmonary disease (COPD) patients. This reduction is not a simple consequence of airflow limitation. Peripheral muscle weakness, deconditioning and impaired gas exchange, were recognized as important contributors to exercise intolerance. In this overview, the contribution of peripheral muscle function and muscle training to exercise performance is discussed by means of three questions: 1) Is peripheral muscle dysfunction contributing to exercise limitation in COPD? 2) How do we measure peripheral muscle function? 3) Are peripheral muscle training modalities effective? At present, there is substantial evidence for peripheral muscle dysfunction. Both reduced force generating capacity as well as impaired muscle metabolism were observed and these findings contributed substantially to the reduced exercise capacity in COPD. Peripheral muscle strength measurements are feasible with mechanical or electronic devices and revealed muscle weakness in COPD patients. However, this weakness is not uniform for all muscle groups. Upper arm and leg muscles were more affected than hand muscles. This may, at least in part, be related to differences in the levels of inactivity between leg and hand muscles. In addition, muscle weakness is associated with impaired exercise capacity and symptoms of increased exertion during exercise. Endurance exercise training, i.e. cycling and treadmill walking, improved exercise capacity and was associated with alterations in muscle metabolism. Strength training of peripheral muscles showed increases in submaximal exercise performance and quality of life measures. These improvements were observed independently of the degree of airflow obstruction. The optimal training regimen (strength or endurance), and the muscle groups to be trained, remain to be determined.

Exercise↗
PubMed1983

The clinical presentation of hypothyroid myopathy and its relationship to abnormalities in structure and function of skeletal muscle.

Clinical assessment for the presence of myopathy was performed in fifteen untreated hypothyroid patients. In many of these patients plasma creatine kinase (CK) activities, tests of skeletal muscle function and vastus lateralis needle biopsies were performed. Muscle symptoms were extremely common, occurring in thirteen patients. Proximal muscle weakness, preferentially affecting the legs, muscle pains or cramps and delayed tendon jerk relaxation represented the commonest features of hypothyroid myopathy. Detailed descriptions are given of patients with muscle hypertrophy, muscle atrophy and developmental failure to illustrate the wide clinical spectrum. If examination revealed signs of myopathy, in particular if there was delayed relaxation of tendon jerks, biochemically severe hypothyroidism (serum thyroxine less than 20 nmol/l) was likely (P less than 0.01). The latter was a frequent finding in six patients with serous effusions (P less than 0.01). This subgroup also had a mean plasma CK activity of 1339 IU/l compared to 679 IU/l (normal 10-120 IU/l) for the whole hypothyroid group, and all five patients in this subgroup in whom vastus lateralis needle biopsies were performed showed abnormalities. Quadriceps force measurements and ankle jerk relaxation times were more sensitive than clinical examination in detecting muscle weakness and delayed relaxation. A reduced maximum relation rate (MRR) of the quadriceps, vastus lateralis needle biopsy abnormalities, and myopathic features on electromyography were characteristic.

Adolescent↗
PubMed2005

Hypogonadism, quadriceps weakness, and exercise intolerance in chronic obstructive pulmonary disease.

RATIONALE: Circulating levels of testosterone and gonadotrophins of patients with chronic obstructive pulmonary disease (COPD) have never been compared with those of elderly men with normal pulmonary function. Moreover, the relationship of hypogonadism with quadriceps muscle weakness and exercise intolerance has been studied scarcely in men with COPD. OBJECTIVES: To compare circulating levels of hormones of the pituitary-gonadotrophic axis of men with COPD with those of age-matched control subjects. Moreover, to study the relationship of hypogonadism with quadriceps muscle force, 6-min walking distance, and systemic markers of inflammation in the patients. METHODS AND MEASUREMENTS: Circulating levels of follicle-stimulating hormone, luteinizing hormone, testosterone, and sex hormone-binding globulin were determined, and free testosterone was calculated in 78 patients (FEV1: 44 +/- 17% of the predicted values) and 21 control subjects. Moreover, quadriceps muscle force, 6-min walking distance, number of pack-yr, and systemic inflammation were determined. MAIN RESULTS: Follicle-stimulating hormone and luteinizing hormone were higher in the patients, whereas testosterone was lower (p < or = 0.05). The latter finding was also present in 48 non-steroid-using patients with normal blood gases. Low androgen status was significantly related to quadriceps muscle weakness (r = 0.48) and C-reactive protein (r = -0.39) in the patients, but not to exercise intolerance, the number of pack-yr, or increased circulating levels of interleukin 8 or soluble receptors of tumor necrosis factor alpha. CONCLUSIONS: In contrast to exercise intolerance, quadriceps muscle weakness is related to low circulating levels of testosterone in men with COPD.

Aged↗
PubMed2002

The paper grip test for screening on intrinsic muscle paralysis in the foot of leprosy patients.

Plantar intrinsic foot muscles provide structure to the foot during walking and thus regulate mechanical foot sole stresses. When paralyzed, for instance in leprosy patients with neuropathy of the distal part of the tibial nerve, there is a high prevalence of plantar ulceration and deformities, especially when muscle weakness goes together with loss of foot sole sensibility. These patients should get immediate care involving education, special footwear and reconstructive surgery before further foot impairment and deformity becomes manifest. Thus far, in leprosy patients little attention is paid to screening of plantar intrinsic muscles activity. This can be done with a new simple and non-invasive method, the Paper Grip Test (PGT). There are two variants for detecting intrinsic muscle weakness of the foot, PGT1 for the great toe and PGT2 for the combined lesser toes. In this study, 517 leprosy patients and 170 healthy volunteers were investigated with the PGT. Sensibility of the foot sole was tested by means of a 10 gram monofilament. Specificity to the PGT1 is found to be about 95.3% which is considered good for physical diagnostic tests. PGT2 is less specific than PGT1. Individual muscle power and understanding of the patient seems to influence the outcome of the test to a certain extent. Sensitivity can only be calculated when the diagnosis is confirmed by electromyography. Especially patients with anesthetic feet, females, older patients and patients with PN-, BB- or LL-types of leprosy appeared to have a higher prevalence of intrinsic foot muscle weakness. All results were analyzed by means of the bivariate Pearson correlation-analysis and proved to be statistically significant (p = < 0.05). It is concluded that the PGT1, more than the PGT2, is a useful screening test on the function of plantar intrinsic foot muscles in leprosy patients in hospitals and during fieldwork in developing countries.

Adult↗