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Query: UMLS:C0015672 (fatigue)
 51,768 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

We measured saccadic peak velocities in 8 patients with myasthenia gravis, 9 patients with proven nonmyasthenic ocular palsies, and 3 controls. Patients followed a target moving to and from primary position at 1-second intervals for 8 minutes. We measured the amplitudes and velocities of centrifugal saccades at the start of the task, after 3 minutes of the task (fatigue) and 1 minute after receiving IV edrophonium. The effects of fatigue, though prominent in some myasthenic patients, did not distinguish between the groups. However, edrophonium increased saccadic peak velocities in myasthenic patients but decreased them in both controls and nonmyasthenic patients. Analysis of saccades by amplitude bins showed that these changes in peak velocity reflected shifts in the velocity-amplitude relationship.
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PMID:Effects of edrophonium on saccadic velocity in normal subjects and myasthenic and nonmyasthenic ocular palsies. 794 91

We have previously shown that the amplitudes of motor evoked potentials (MEPs) elicited by transcranial magnetic stimulation (TMS) were transiently decreased after exercise, indicating fatigue of motor pathways in the central nervous system. The responsible mechanism is apparently decreased efficiency in the generation of the descending volleys in the motor cortex. We also noted a progressive decrement in amplitude from the first to the fourth MEP. To further clarify the mechanism of this phenomenon, 5 subjects were studied with TMS delivered at the rates of 0.1, 0.15, 0.3, 1, 3, and 6 Hz. The effect was best demonstrated at 0.3 Hz, and occurred after both isometric and isotonic exercise. Three of the subjects also had 0.3-Hz percutaneous electrical stimulation of the brainstem, and a decrement in MEP amplitude did not occur. Further, the delivery of TMS during muscle contraction after muscle fatigue failed to produce a decrement. The results are similar to those found at the neuromuscular junction in myasthenia gravis and are consistent with a reduced safety factor of cortical synaptic transmission in central nervous system fatigue.
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PMID:Central fatigue as revealed by postexercise decrement of motor evoked potentials. 800 95

Eleven patients with mild or moderate myasthenia gravis (MG) were subjected to a strength training program of 27 to 30 sessions during ten weeks. Voluntary maximal muscle force and the degree of fatigue during repetitive maximal isometric muscle contractions were measured in three muscle groups. The subjects did not experience any subjective discomfort or any adverse effect on their MG due to the training. A 23% increase of the maximal voluntary muscle force in knee extension in the trained side was found, compared to 4% in the untrained side (p < 0.05). Only small changes were noted regarding maximal muscle force in elbow flexion and extension or in any of the muscle groups in the fatigue test. Physical training can be carried out safely in mild MG and provides some improvement of muscle force.
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PMID:Physical training effects in myasthenia gravis. 823 58

Most patients with neuromuscular disease develop muscle weakness, including the ventilatory muscles leading to respiratory difficulty and, at times, respiratory insufficiency. We studied the effect of ventilatory muscle training on the ventilatory function and capacity of patients with various types of neuromuscular disease. The ambulatory patients were divided into three major groups. Group I (n = 6) patients with motor neuron disease (MND), such as amyotrophic latera sclerosis; Group II (n = 11) patients with myoneural junction disease (MNJ), such as myasthenia gravis and: Group III (n = 7) patients with muscle diseases such as progressive muscular disease. Patients were evaluated for their neuromuscular diagnosis and status of the disease. A complete physical examination and the various neuromuscular tests were performed. A complete respiratory evaluation was applied: pulmonary function tests (PFT), maximum inspiratory pressure (MIP). Patients then started ventilatory muscle training by resistive breathing, as a prophylactic treatment, for 10 min, three times daily, with a resistance which would induce fatigue. All tests were repeated every six weeks, and the results were as follow: forced vital capacity (FVC) changed from 38.8 +/- 12.3 to 53.2 +/- 9.6% (NS) of predicted value in group I, from 49.8 +/- 8.7 to 66.1 +/- 7.5% (p < 0.002) in group II, and from 47.0 +/- 7.5 to 53.3 +/- 7.6% (p < 0.04) in group III. Forced expiratory volume in one second (FEV1) was 34.8 +/- 11.0, 46.3 +/- 5, and 45.1 +/- 9% for the three groups, respectively, and did not change with training.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:The effect of ventilatory muscle training on respiratory function and capacity in ambulatory and bed-ridden patients with neuromuscular disease. 825 74

Pregnancy is certainly an option open to patients with myasthenia gravis. Preconceptional counseling is the ideal, with the goal of discontinuing or reducing corticosteroid medications in patients requiring those agents. Alterations in physiology will require ongoing and careful assessment of the pregnant myasthenic or cholinergic crises. Antenatal testing for fetal well-being may be difficult to interpret. A small number of fetuses with fetal myasthenia gravis will be diagnosed by ultrasound. Attempts may be made to decrease the amount of circulating antibody crossing to the fetus. Interventions may include starting or increasing corticosteroid therapy, therapy with azathioprine, or plasmapheresis. Thymectomy is usually not performed during pregnancy. The intrapartum period will increase fatigue in the mother and may precipitate a myasthenic crisis. Epidural anesthesia is currently the agent of choice for decreasing pain and fatigue. An outlet forceps or vacuum delivery will shorten the second stage of labor in those patients who are unable to push repetitively. Cesarean delivery is preferably avoided in those patients at risk for pulmonary and thrombo-embolic complications. Narcotic and sedative medications may be used in the presence of careful and continuous assessment; they may increase respiratory and muscular symptoms. The postpartum period may be associated with an increase in exacerbations. Support services may help to eliminate or to reduce potent stressors during this time. Medication dosages may need to be adjusted as the mother's body returns to her prepregnant state. Transient, neonatal myasthenia is seen in up to 21% of maternal myasthenic cases, even in those patients with no detectable circulating antibody.
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PMID:Myasthenia gravis and pregnancy. 833 87

Fatigue mechanisms in normal intercostal muscle and muscle from patients with myasthenia gravis (MG) were evaluated by monitoring the compound muscle action potential (CMAP) and tetanic tension responses to repetitive nerve or muscle stimulation in vitro. When fatigue was induced by nerve stimulation at 30 Hz for 0.5 s every 2.5 s, about half of the original tension decreased after 30 min in normal muscle and 5 min in MG muscle. Analysis of the changes in area of CMAPs and tension indicated that impairment of neuromuscular transmission, muscle membrane excitation, and excitation-contraction (E-C) coupling and contractility accounted for 40%, 29%, and 31% of fatigue in normal muscle, and 83%, 0%, and 17% of fatigue in MG muscle. When fatigue was induced by muscle stimulation at 30 Hz, tension declined by a quarter after 30 min in normal muscle, but by a half after 17 min in MG muscle. Impairment of muscle membrane excitation and E-C coupling and contractility accounted for 58% and 42% of fatigue in normal muscle, and 22% and 78% of fatigue in MG muscle. Thus, fatigue of normal muscle is caused by impairment of at least four processes, and enhanced fatigue of MG muscle is caused by greater impairment of neuromuscular transmission, E-C coupling, and contractility.
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PMID:Mechanisms of fatigue in normal intercostal muscle and muscle from patients with myasthenia gravis. 835 22

A forty-nine-year-old female patient, complaining of swallowing difficulties and general fatigue, was admitted to the first hospital of Nippon Medical School. At the age of 32, she was operated on for the removal of a well encapsulated non-invasive thymoma. Since then, she had been well till the age of 46, when chest X-ray films showed a recurrent thymoma which was excised together with the complete thymic tissues. One year later, she developed myasthenia gravis (MG) with a ptotic right upper eyelid and general fatigue. Subsequently, she was placed on medication. After 21 months, however, she died of myasthenic crisis in spite of vigorous respiratory and nutritional support. The autopsy revealed a small residual thymoma on the left lung, and systemic atrophy of the skeletal muscles. In this paper, the mechanism of post-thymectomy MG and the recurrence of non-invasive thymoma are discussed.
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PMID:A case report of post-thymectomy myasthenia gravis with residual thymoma. 837 Jul 17

Muscle may suffer from a number of diseases or disorders, some being fatal to humans and animals. Their management or treatment depends on correct diagnosis. Although no single method may be used to identify all diseases, recognition depends on the following diagnostic procedures: (1) history and clinical examination, (2) blood biochemistry, (3) electromyography, (4) muscle biopsy, (5) nuclear magnetic resonance, (6) measurement of muscle cross-sectional area, (7) tests of muscle function, (8) provocation tests, and (9) studies on protein turnover. One or all of these procedures may prove helpful in diagnosis, but even then identification of the disorder may not be possible. Nevertheless, each of these procedures can provide useful information. Among the most common diseases in muscle are the muscular dystrophies, in which the newly identified muscle protein dystrophin is either absent or present at less than normal amounts in both Duchenne and Becker's muscular dystrophy. Although the identification of dystrophin represents a major breakthrough, treatment has not progressed to the experimental stage. Other major diseases of muscle include the inflammatory myopathies and neuropathies. Atrophy and hypertrophy of muscle and the relationship of aging, exercise, and fatigue all add to our understanding of the behavior of normal and abnormal muscle. Some other interesting related diseases and disorders of muscle include myasthenia gravis, muscular dysgenesis, and myclonus. Disorders of energy metabolism include those caused by abnormal glycolysis (Von Gierke's, Pompe's, Cori-Forbes, Andersen's, McArdle's, Hers', and Tauri's diseases) and by the acquired diseases of glycolysis (disorders of mitochondrial oxidation). Still other diseases associated with abnormal energy metabolism include lipid-related disorders (carnitine and carnitine palmitoyl-transferase deficiencies) and myotonic syndromes (myotonia congenita, paramyotonia congenita, hypokalemic and hyperkalemic periodic paralysis, and malignant hyperexia). Diseases of the connective tissues discussed include those of nutritional origin (scurvy, lathyrism, starvation, and protein deficiency), the genetic diseases (dermatosparaxis, Ehlers-Danlos syndrome, osteogenesis imperfecta, Marfan syndrome, homocystinuria, alcaptonuria, epidermolysis bullosa, rheumatoid arthritis in humans, polyarthritis in swine, Aleutian disease of mink, and the several types of systemic lupus erythematosus) and the acquired diseases of connective tissues (abnormal calcification, systemic sclerosis, interstitial lung disease, hepatic fibrosis, and carcinomas of the connective tissues). Several of the diseases of connective tissues may prove to be useful models for determining the relationship of collagen to meat tenderness and its other physical properties. Several other promising models for studying the nutrition-related disorders and the quality-related characteristics of meat are also reviewed.
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PMID:Diseases and disorders of muscle. 839 47

Myasthenia gravis should be entertained as a possible diagnosis in any patient who presents with muscle weakness or visual disturbance. The most common symptom is exacerbation of muscle fatigue with repeated use of the muscle and improvement with rest. Several inexpensive diagnostic tests for myasthenia gravis that can be performed by primary care physicians are available. Standard therapy in most cases is early thymectomy, followed by a highly individualized medication program that usually includes the anticholinesterase drug pyridostigmine bromide (Mestinon, Regonol). Corticosteroids and other immunosuppressive agents (usually azathioprine [Imuran]) may be added or substituted if response to anticholinesterase therapy is inadequate. Although myasthenia gravis is a chronic disease, it can be well controlled in most patients, provided they comply with treatment. Patient education is therefore essential.
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PMID:Myasthenia gravis. Diagnostic methods and control measures for a chronic disease. 841 29

A 52-year-old woman had a 14-year history of stridor attacks. Pulmonary function tests revealed reversible airway obstruction, and bronchial asthma was diagnosed. She also has bilateral ptosis, diplopia, and moderate weakness of all four limbs; a positive edrophonium test confirmed the diagnosis of myasthenia gravis. Although the parasympathetic system plays an important role in the regulation of bronchial tone, in this patient the edrophonium test did not provoke an asthmatic attack or exacerbate pulmonary function, except for increases in sputum production and in frequency of cough. The general weakness was usually worse in the afternoon. The decrease in grip strength and the shortening of arm elevation time also occurred after asthma attacks, which means that general muscle fatigue was caused by the work of breathing. Furthermore, dyspnea increased and pulmonary function worsened when an anti-cholinesterase inhibitor was discontinued, probably because of respiratory muscle weakness. Accordingly, the clinical status of bronchial asthma seemed to change in parallel with that of the myasthenia gravis.
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PMID:[Bronchial asthma complicated by myasthenia gravis]. 869 67


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