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Results for “Muscle Weakness”

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At least 613 records · Page 34Linked to original sources

PubMed2001

A mutation in alpha-tropomyosin(slow) affects muscle strength, maturation and hypertrophy in a mouse model for nemaline myopathy.

Nemaline myopathy is a hereditary disease of skeletal muscle defined by a distinct pathology of electron-dense accumulations within the sarcomeric units called rods, muscle weakness and, in most cases, a slow oxidative (type 1) fiber predominance. We generated a transgenic mouse model to study this disorder by expressing an autosomal dominant mutant of alpha-tropomyosin(slow) previously identified in a human cohort. Rods were found in all muscles, but to varying extents which did not correlate with the amount of mutant protein present. In addition, a pathological feature not commonly associated with this disorder, cytoplasmic bodies, was found in the mouse and subsequently identified in human samples. Muscle weakness is a major feature of this disease and was examined with respect to fiber composition, degree of rod-containing fibers, fiber mechanics and fiber diameter. Hypertrophy of fast, glycolytic (type 2B) fibers was apparent at 2 months of age. Muscle weakness was apparent in mice at 5-6 months of age, mimicking the late onset observed in humans with this mutation. The late onset did not correlate with observed changes in fiber type and rod pathology. Rather, the onset of muscle weakness correlates with an age-related decrease in fiber diameter and suggests that early onset is prevented by hypertrophy of fast, glycolytic fibers. We suggest that the clinical phenotype is precipitated by a failure of the hypertrophy to persist and therefore compensate for muscle weakness.

Amino Acid Substitution↗

PubMed1982

Hypokalemic myopathy associated with 17 alpha-hydroxylase deficiency: a case report.

We studied a patient with hypokalemic myopathy associated with 17 alpha-hydroxylase deficiency. An 18-year-old high school student, who appeared to be a girl with poorly developed secondary sex characteristics, had generalized muscle weakness. The cause of muscle weakness proved to be hypokalemic myopathy confirmed by clinical findings and muscle biopsy. Endocrinologic study demonstrated 17 alpha-hydroxylase deficiency with male pseudohermaphroditism. The metabolic abnormality of this patient was corrected by the administration of glucocorticoid. The possibility of this rare disease has to be considered when we examine a patient who has hypokalemic myopathy associated with hypogonadism.

Adolescent↗

PubMed2001

Respiratory complications related to bulbar dysfunction in motor neuron disease.

Bulbar dysfunction resulting from corticobulbar pathway or brainstem neuron degeneration is one of the most important clinical problems encountered in motor neuron disease (MND) and contributes to various respiratory complications which are major causes of morbidity and mortality. Chronic malnutrition as a consequence of bulbar muscle weakness may have a considerable bearing on respiratory muscle function and survival. Abnormalities of the control and strength of the laryngeal and pharyngeal muscles may cause upper airway obstruction increasing resistance to airflow. Bulbar muscle weakness prevents adequate peak cough flows to clear airway debris. Dysphagia can lead to aspiration of microorganisms, food and liquids and hence pneumonia. MND patients with bulbar involvement commonly display an abnormal respiratory pattern during swallow characterized by inspiration after swallow, prolonged swallow apnoea and multiple swallows per bolus. Volitional respiratory function tests such as forced vital capacity can be inaccurate in patients with bulbofacial weakness and/or impaired volitional respiratory control. Bulbar muscle weakness with abundant secretions may increase the risk of aspiration and make successful non-invasive assisted ventilation more difficult. We conclude that an evaluation of bulbar dysfunction is an essential element in the assessment of respiratory dysfunction in MND.

Bulbar Palsy, Progressive↗

PubMed1999

Exploration of paretic gait by differential loading in normals.

OBJECTIVE: To determine if the gait patterns of artificially loaded healthy subjects resemble those of patients with weak ambulatory muscles. DESIGN: The gaits of artificially loaded healthy subjects and their controls were compared with the gaits of amputees and paretic patients, using analysis of variance. BACKGROUND: Muscle weakness due to paresis or limb amputation results in a misrelation between muscle power and body weight borne during ambulation. When body weight is increased by artificial loading of a normal subject, a misrelation between muscle strength and body weight results. METHODS: The gaits of paretic patients and artificially loaded normal subjects were recorded in the laboratory, by means of foot-switches. Stride length and stride frequency were used to calculate stride ratio which was used to compare the different gaits. RESULTS: Mean stride ratios of paraparetics, peroneal paretics and healthy subjects who carried load in the hand showed no statistically significant difference, while the ratio for hemiparetics differed significantly from the value for the artificially loaded healthy subjects. Below-knee amputees had a similar stride ratio to normal subjects who carried load on the ankles, while the above-knee stride ratio differed significantly from ankle-loaded normal subjects. CONCLUSION: Paraparetic and peroneal paretic gaits were approximated by the gaits of normal subjects who carried artificial load in the hand while the below-knee amputee gait was mimicked by normal subjects who carried load on the ankles. The two models of artificial loading could not generate any semblance with hemiparetic and above-knee gaits.

Adult↗

PubMed1992

[A case of myasthenia gravis complicated by cyclic thrombocytopenia].

A 47-year-old woman with myasthenia gravis for last 11 years was admitted because of relapsed muscle weakness, hypermenorrhea and thrombocytopenia. Physical and neurological examinations revealed diplopia, proximal muscle weakness and purpuras on the left arm and bilateral legs. Repeated hematological examinations revealed cyclic fluctuation of platelet counts which spontaneously changed from the nadir levels of 12-27 x 10(3)/microliters to the peak levels of 150-400 x 10(3)/microliters. The platelet count reached a nadir at the onset of menstruation. Platelet-associated IgG (PAIgG) was within normal level when platelet count was at an increasing phase. Survival time of autologous platelets was normal when platelet count was at an increasing phase. Megakaryocytes in the bone marrow were apparently normal at the nadir phase. The patient's serum obtained at the nadir of platelet count significantly suppressed megakaryocyte colony forming unit (Meg-CFU) formation in comparison with that after the stabilization of platelet count, suggesting that this cyclic thrombocytopenia was secondary to cyclic hypoproduction of megakaryocytes caused by a suppressive factor. On the other hand muscle weakness showed no cyclic fluctuation. Administration of 60 mg/day prednisolone stabilized the platelet count at about 280 x 10(3)/microliters, abolished hypermenorrhea and gradually improved muscle weakness. These findings suggested autoimmune mechanism in the production of a Meg-CFU-suppressive factor might be involved in the pathogenesis of thrombocytopenia.

Female↗

PubMed1996

Acute brachial neuropathy--electrophysiological study and clinical profile.

Acute brachial neuropathy (ABN) is a rare disease, characterized by an acute or subacute onset of pain followed by weakness of shoulder or arm muscles without trauma or traction injury. So the diagnosis of this clinical entity is not easy. The purpose of this study was to analyze retrospectively the ABN in 14 cases focusing on the clinical profile and to evaluate the effectiveness of electrophysiologic study in diagnosis of ABN with a new result helpful in localizing a brachial plexus disorder. The most helpful electrophysiologic data of ABN in my patients seemed to be abnormalities of low amplitude, abnormal right to left difference of compound motor action potentials (CMAPs) and sensory nerve action potentials (SNAPs) in axillary nerve, ulnar or median nerves. Results of nerve conduction velocity, terminal and F-wave latency were not as useful. But the electromyogram was most helpful in localization of upper or lower plexus lesions and cervical radiculopathy. The most striking clinical feature of ABN was the rapid onset of pain followed by the development of muscle weakness of shoulder girdle after a variable period or within four days. In contrast to other reports, intrinsic hand muscle weakness was observed in 3 cases with sensory changes in ulnar nerve distribution. The cervical radiculopathies (C5-C7 roots) were simultaneously combined with ipsilateral axillary neuropathy in 3 cases. In this study, decreased amplitude, abnormal right to left difference of SNAPs and CMAPs, and neurogenic EMG findings with normal data of NCV, terminal and F-wave latencies suggest that the pathology of ABN might not be a demyelinating process, but axonopathy.

Adult↗

PubMed2005

Limb muscle dysfunction in COPD: effects of muscle wasting and exercise training.

PURPOSE: Lower-limb muscle weakness has often been reported in COPD, and contributes to exercise intolerance. Controversial information is available regarding upper-limb muscle adaptations and the influence of muscle wasting on muscle weakness. We investigated leg and arm muscle function in 59 stable COPD patients (GOLD stage III) with preserved fat-free mass (FFM) and in 28 patients with reduced FFM relative to age- and sex-matched healthy control subjects and studied the effects of 8 wk of whole-body exercise training. METHODS: FFM was measured with bioelectrical impedance analysis. Isokinetic quadriceps (F-leg) and biceps strength (F-arm), as well as quadriceps (E-leg) and biceps endurance (E-arm) were determined with a Biodex dynamometer. Exercise training consisted of cycle ergometry, treadmill walking, weight training, and gymnastics during 5 d.wk. RESULTS: F-leg (76.2 +/- 3.6 vs 118.2 +/- 6.3 N.m, P < 0.001) and F-arm (25.6 +/- 1.3 vs 38.1 +/- 2.1 N.m, P < 0.001) were significantly and similarly reduced in the COPD patient group compared with controls. Also, E-leg (-2.13 +/- 0.12 vs -1.61 +/- 0.11, P < 0.01), but not E-arm (-2.72 +/- 0.11 and -2.47 +/- 0.13 NS), was decreased in patients. F-leg (62.4 +/- 4.3 vs 82.8 +/- 4.7 N.m, P < 0.01), but not F-arm or muscle endurance, was reduced in FFM-depleted compared with non-FFM-depleted patients. Whereas after training F-leg and E-leg significantly increased by 20% in the whole COPD group, biceps muscle function remained unchanged. CONCLUSION: Lower- and upper-limb muscle dysfunction was observed in COPD patients, irrespective of the presence of FFM depletion. Generalized muscle weakness suggests systemic muscular involvement, although the preserved arm endurance and the poor response of arm performance to exercise training is indicative for intrinsic differences in muscular adaptations between leg and arm muscles.

Case-Control Studies↗

PubMed2000

[Muscle involvement of Stormorken's syndrome].

We described two patients, a mother and daughter, of Stormorken's syndrome. The syndrome is characterized clinically by autosomal dominant inheritance, congenital miosis, thrombocytopenia, asplenia and muscle weakness. Both patients had bleeding tendency, ichthyosis of arms, and muscle weakness. The daughter additionally had short stature (146 cm), low body weight (32 kg) and muscle cramp. Neurological findings of the patients included migraine-like headache, cognitive dysfunction, limitation of upward and lateral gaze, and amydriasis. Femoral muscle MRI of the daughter demonstrated decreased volume with patchy high intensity areas in the hamstrings. A muscle biopsy from the daughter showed myogenic changes with muscle fiber necrosis and regeneration, variation in fiber size, tubular aggregates in approximately 5% of fibers, and fibrous tissue proliferation. Dystrophin, dystrophin-associated proteins and dysferlin were normally expressed. Although both patients had elevated creatine kinase levels and generalized muscle wasting, muscle weakness was mild with slow progression. A certain membrane defect in the platelet and muscle fiber might be responsible for the pathogenesis of this syndrome.

Adult↗

PubMed1995

Histopathologic and MRI findings in hypokalemic myopathy induced by glycyrrhizin.

Histopathologic studies and magnetic resonance images of the leg muscles were conducted in two patients with glycyrrhizin-induced hypokalemic myopathy (GHM). Muscle biopsy showed myopathic changes and vacuolated fibers with light microscopy, and dilatation of the sarcoplasmic reticulum, various types of vacuoles and myofibrillar degeneration with electron microscopy. High signal intensities in T2-weighted images obtained during severe muscle weakness were widely distributed in the leg muscles, especially the pretibial and soleus muscles. These high signal intensities disappeared after full recovery of muscle weakness. We suggest that high signal intensity in T2-weighted images can be seen and correspond to histopathologic changes in the muscles of GHM patients.

Adrenal Cortex Hormones↗

PubMed1999

Fiber atrophy, but not changes in acetylcholine receptor expression, contributes to the muscle dysfunction after immobilization.

OBJECTIVES: Muscle weakness associated with critical illness can be due to the illness itself, immobilization associated with it, and/or to concomitant use of drugs that affect neuromuscular transmission. This study investigated the contribution of immobilization per se to the muscle dysfunction, as well as the associated morphologic and biochemical changes. DESIGN: Prospective, laboratory study. SETTING: Hospital research laboratory. SUBJECTS: Adult, male, Sprague-Dawley rats, weighing 200 to 250 g, were randomly allocated to three experimental groups, depending on the duration (7, 14, or 28 days) of limb immobilization (n = 9 to 11 per group) or sham immobilization (n = 5 to 6 per group). INTERVENTIONS: Chronic, unilateral immobilization (disuse) of the tibialis cranialis muscle was produced by fixing the knee and ankle joints at 90 degrees flexion. The contralateral unimmobilized leg and a separate group of sham-immobilized legs served as controls. MEASUREMENTS AND MAIN RESULTS: After 7, 14, or 28 days of disuse of the tibialis muscles, the peak isometric twitch (Pt) and tetanic (Po) tensions, as well as fatigability during 5 secs of nerve stimulation at 50, 100, and 150 Hz, were measured simultaneously in situ in the immobilized group and in its contralateral control, and in the sham-immobilized group and in its contralateral control. Muscle fiber and endplate morphologies were determined by histochemical methods; membrane acetylcholine receptors (AChRs) were determined by 125I alpha-bungarotoxin assay; and the level of expression of AChR subunit transcripts was determined by reverse transcriptase-polymerase chain reaction. Immobilization reduced Pt, Po, fatigability, muscle mass, and fiber cross-sectional area (p<.001 vs. controls), but did not decrease tension per unit muscle mass, fiber oxidative capacity, or motor endplate size. Muscle mass correlated with fiber cross-sectional area. Changes in fiber cross-sectional area accounted for 23% and 46% (p< or =.043) of the variability in Pt and Po, respectively. Pt and Po correlated poorly with total AChR protein and expression of epsilon- and gamma-subunit messenger RNA. CONCLUSION: To the extent that the immobilization model simulates the disuse-induced muscle dysfunction of critical illness, the results suggest that disuse per se may contribute to the muscle weakness, and that the muscle weakness is explained, almost exclusively, by the fiber atrophy and not by the qualitative or quantitative changes in AChR expression.

Analysis of Variance↗

PubMed1987

Respiratory insufficiency in adult-onset acid maltase deficiency.

Although the adult form of acid maltase deficiency is characterized by weakness of the limb girdle muscles, weakness of the respiratory muscles out of proportion to that of the limb muscles may make the diagnosis less obvious. We present four patients aged 35 to 57 with respiratory muscle weakness associated with signs of cor pulmonale and symptoms of alveolar hypoventilation. Each had symptoms of fatigue, hypersomnolence, morning headache, and orthopnea, the cause of which was misdiagnosed. The key to diagnosis was paradoxic abdominal motion on inspiration. This finding, consistent with diaphragmatic paralysis, led to neurologic evaluation, electromyographic examination, and muscle biopsy to confirm the diagnosis. The symptoms of alveolar hypoventilation were reversed with chronic nocturnal ventilation, which assisted in rehabilitating some patients.

Adult↗

PubMed2001

Muscle strength and motor function in children and adolescents with spinal muscular atrophy II and III.

The aim of this study was to quantify isometric muscle strength and motor function in children and adolescents with spinal muscular atrophy (SMA) and to analyse the impact of reduced muscle strength on motor function. Six children and adolescents with SMA II and eight with SMA IlI were assessed regarding isometric muscle strength and motor function. Isometric muscle strength was tested with a myometer and the values obtained were compared with normative data. Motor function was videotaped and 20 movements were scored according to a three-point scale. All of the assessed children and adolescents with SMA II and SMA III showed reduced muscle strength, but there were great differences within the group. The typical pattern of muscle weakness in SMA, with proximal weakness greater than distal and the lower limbs more affected than the upper, was also seen in these children. The muscle weakness affected motor function in all assessed children. Walking, transfer from lying or sitting to the standing position and stair-climbing were possible in some of the children, despite marked reduction of muscle strength. The study increases our knowledge concerning the degree of muscle weakness in children with SMA and the impact of muscle weakness on motor function. The results increase our possibilities of understanding the prerequisites for everyday life in these children and planning therapeutic interventions. Repeated assessments with the methods used in this study may be used to monitor the course of the disease and to evaluate the efficacy of treatment.

Activities of Daily Living↗

PubMed2000

[Polymyositis with marked paravertebral muscle atrophy in patients with primary biliary cirrhosis].

We reported two patients with polymyositis (PM) associated with primary biliary cirrhosis (PBC) who noticed head-drop as the incipient symptom. Muscle computed tomography showed marked hypodensity in the paravertebral muscles as compared with limb muscles. Patient 1, a 48-year-old female, was admitted in our hospital for the examination because of her neck and proximal limb muscle weakness, increasing fatigability, and abnormal serum liver and muscle enzyme levels. She felt her throat was so dry at age 39, and she noticed weight loss at age 41 and head-drop at age 42. A diagnosis of PM was made from symmetrical proximal limb muscle weakness, elevated creatine kinase (CK) level, and the electromyographic and muscle biopsy findings. Her illness was also diagnosed as PBC because of the increased serum alkaline phosphatase and IgM immunoglobulin levels, and liver biopsy findings. The anticentromere antibody titer was positive, though the antimitochondrial antibody titer negative. The HLA typing was DR 4, DR 8, DR53, DQ 4, DQ 6, DRB 1 (0405/0803). She was placed on 60 mg of prednisolone/day for PM and 300 mg of ursodeoxycholic acid/day for PBC. Patient 2, a 49-year-old female, presented with proximal limb muscle weakness and head-drop. Serum CK, alkaline phosphatase and IgM immunoglobulin levels were increased. The antimitochondrial antibody titer was positive. She began to have 60 mg of prednisolone/day, and 50 mg of azatioprine/day and 300 mg of ursodeoxycholic acid/day were subsequently added. PM associated with PBC seems to be rare, because only 21 cases have been described in literature. In those patients, marked paravertebral muscle atrophy has never been described. Further study is necessary to examine whether or not the preferential paravertebral muscle involvement is a striking and diagnostic finding for PM with PBC.

Atrophy↗

PubMed1982

Concepts of multiple congenital contractures (arthrogryposis) in man and animals.

This is a concept of multiple congenital contractures, based upon clinical experience with the malformation and available literature, leading to a conception of the multiple categories of etiology, which cause neuropathic or myopathic muscle weakness or limb immobilization. The muscle weakness and imbalance of muscle power around the joints elicits a physiological compensatory collagenic response, which replaces atrophied muscle fibers with connective tissue and thickens the joint capsule sufficiently to result in prenatal fixation of limb segments at the joint.

Animals↗

PubMed2004

Hypothyroidism presenting as Hoffman's syndrome.

Muscle weakness, stiffness and delayed tendon jerk relaxation are usual features of hypothyroidism while muscle hypertrophy, myoedema and wasting are occasionally seen. A 60-year-old male, who presented with proximal muscle weakness and muscle hypertrophy has been reported here. Thyroid function tests, electromyogram and muscle biopsy established the diagnosis of thyroid myopathy with Hoffman's syndrome.

Edema↗

PubMed1998

Measurement of sniff nasal and diaphragm twitch mouth pressure in patients.

BACKGROUND: Inspiratory muscle weakness is a recognised cause of unexplained dyspnoea. It may be suggested by the finding of a low static inspiratory mouth pressure (MIP), but MIP is a difficult test to perform, with a wide normal range; a low MIP may also occur if the patient has not properly performed the manoeuvre. Further investigation conventionally requires balloon catheters to obtain oesophageal (Poes) and transdiaphragmatic pressure (Pdi) during sniffs or phrenic nerve stimulation. Two non-invasive tests of inspiratory muscle strength have recently been described--nasal pressure during a maximal sniff (Sn Pnas) and mouth pressure during magnetic stimulation of the phrenic nerves (Tw Pmo). The use of these two tests in combination might identify patients without inspiratory muscle weakness who are unable to produce a satisfactory MIP< therefore avoiding the need for investigation with balloon catheters. METHODS: Thirty consecutive patients with clinically suspected inspiratory muscle weakness and a low MIP underwent both conventional (Sn Poes and Tw Pdi) and non-invasive testing (Sn Pnas and Tw Pmo). Weakness was considered to be excluded by a Sn Poes of > or = 80 cm H20 or a Tw Pdi of > or = 20 cm H20. The limit values used to test the hypothesis were Sn Pnas > or = 70 cm H20 or Tw Pmo > or = 12 cm H20. RESULTS: Inspiratory muscle weakness was excluded in 17 of the 30 patients. Fifteen of these would have been identified using Sn Pnas and Tw Pmo, with better results when the two tests were combined. The cut off values selected for Sn Pnas and Tw Pmo were shown by ROC plots to indicate normal strength conservatively, avoiding failure to detect mild degrees of weakness. No patient with global weakness was considered normal by Sn Pnas or Tw Pmo. CONCLUSIONS: In most patients with normal inspiratory strength and a low MIP, Tw Pmo and Sn Pnas used in combination can reliably exclude global inspiratory muscle weakness, reducing the number of patients who need testing with balloon catheters.

Adult↗

PubMed1985

Rehabilitation of conversion paralysis.

Three patients referred for rehabilitation of brachial plexus lesions and two referred with leg weakness associated with sciatica were found to have conversion paralysis. The diagnosis was made by demonstrating normal motor nerve conduction to the clinically weak muscles. The weakness was treated by intensive physical rehabilitation with complete and sustained recovery in all cases.

Adult↗

PubMed2000

Physiotherapy as an adjuvant to the surgical treatment of anterior chest wall deformities: a necessity? A prospective descriptive study in 21 patients.

PURPOSE: The authors postulated that physiotherapy as an adjuvant to the surgical treatment of anterior chest wall deformities is only indicated if specific abnormalities can be found that could be corrected by physiotherapy. The purpose of this study is to investigate whether such abnormalities can be found and to evaluate their course during a postoperative period of 18 months. METHODS: Twenty-one patients, 16 with pectus excavatum and 5 with pectus carinatum, were evaluated 6 weeks before and 6 weeks, 6 months, and 18 months after surgical correction. Postural impairments, spinal mobility and curvature, muscle strength, and muscle length were evaluated. RESULTS: Preoperatively, poor posture was seen in 10 patients, nonstructural scoliosis in 11, and abdominal muscle weakness in 4 patients. None of the patients had restriction of spinal mobility or shortened pectoral muscles. Six weeks after surgery, poor posture was seen in 9, nonstructural scoliosis in 11, and abdominal muscle weakness in 10 patients. The authors found a higher percentage of recovery for abdominal muscle weakness than for poor posture (90% versus 33%, respectively). CONCLUSIONS: The authors found preoperative postural impairments in 52% of their patients, in patients with pectus carinatum as well as in patients with pectus excavatum. In patients without postural impairments, physiotherapy is not necessary, with the exception of postoperative pulmonary care.

Abdominal Muscles↗