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 51,768 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Myasthenia gravis is a disorder characterized by weakness and fatigue of voluntary muscles. The muscular disorder is generalized in 85% and confined to extraocular muscles in 15% of patients. The disease is graded based on pattern and severity of muscular involvement. Myasthenia gravis is an autoimmune disease which leads to a reduction of the number of acetylcholine receptors (Ach-R) at the muscular motor endplate. This results in less receptors available for stimulation, lower amplitude stimulations, less muscle fiber activation, and the resultant clinical findings of weakness in the affected muscles. The work-up and treatment of this disease originated from an understanding of its pathogenesis. Diagnostic tests include use of anticholinesterase agents (tensilon test), curare test, repetitive nerve stimulation, Ach-R antibody assay, and single fiber electromyography. Medical therapy includes use of anticholinesterase agents, immunotherapy, and plasmapheresis.
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PMID:Myasthenia gravis: clinical features, pathogenesis, evaluation, and medical management. 993 Jul 11

To evaluate the weight reducing effect of fluoxetine on steroid-induced obesity, we conducted an open, clinical intervention study of 20-40 mg/day fluoxetine, 24 weeks duration. Thirteen myasthenia gravis, overweight, long-term steroid-treated patients [age: 31-59, body mass index (BMI): 29-54 kg/m2] were included. Measurements of weight, BMI, and routine laboratory tests, were undertaken at baseline, 12 and 24 weeks. Muscle strength and fatigue parameters were assessed at 4 week intervals. Fluoxetine induced mean weight loss of 7.7+/-2.6 kg and 10.3+/-2.9 kg over a period of 12 and 24 weeks respectively, (P<0.05). Mean BMI decreased from 35.8 to 32.2 kg/m2 over the study period. No significant side effects were noted. We conclude that patients suffering from steroid-induced obesity respond to fluoxetine treatment of overweight by significant weight loss.
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PMID:Fluoxetine treatment for weight reduction in steroid-induced obesity: a pilot study in myasthenia gravis patients. 1008 36

Plasma exchange (PE) has been one of the most powerful treatments for patients with myasthenia gravis (MG) since Pinching et al. reported its clinical usefulness in 1976, despite the need for supplemental human plasma. However, new apheresis techniques, e.g., plasma adsorption (PA) and double filtration plasmapheresis (DFPP), which do not need human plasma, were developed and have been introduced for clinical use in MG. We compared the effects of these plasma purification therapies in patients with MG and found that DFPP improved such subjective symptoms as chest compression and general fatigue better than PA while both of them could decrease the serum level of acetylcholine receptor (AChR) antibodies and relieve objective muscle weakness to a similar degree. It may be that DFPP can remove some circulating pathogenic factors other than AChR antibodies more efficiently than PA.
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PMID:Comparative study of clinical effects between plasma adsorption and double filtration plasmapheresis in patients with myasthenia gravis. 1022 28

Failure to induce and maintain remission in severe exacerbations of myasthenia gravis (MG), despite optimal care, is a common problem. We evaluated the efficacy and safety of high-dose intravenous immunoglobulin (IVIg) therapy in an open-label study of 10 patients with severe generalized myasthenia and an acute deterioration unresponsive to conventional therapy including high-dose corticosteroids, cyclosporine, and azathioprine. Intravenous Ig at a loading dose of 400 mg/kg was administered daily for 5 consecutive days, with maintenance IVIg treatment at a dose of 400 mg/kg, once every 6 weeks. Significant improvement occurred in all patients, beginning at 6 +/- 2 days of treatment as measured by the Osserman scale, fatigue variables, muscle strength, and respiratory function tests. No side effects were observed during induction of remission. Further IVIg treatments were highly efficacious in maintaining the remission. The severity of the disease decreased by 2.5 +/- 0.8 grades of the Osserman scale over a period of 1 year (P <0.001), in parallel with reduction of immunosuppressive therapy as well as a decrease in acetylcholine receptor antibody titers (P < 0.01). Intravenous Ig therapy seems to be highly potent for inducing rapid improvement in refractory myasthenia during acute deterioration as well as for maintaining remission.
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PMID:Immunoglobulin treatment in refractory Myasthenia gravis. 1071 66

Myasthenia gravis (MG) is a neuromuscular disorder that affects skeletal muscles, in particular, the extraocular muscles. Response variability is a hallmark sign. Detailed findings are described in a patient with MG in which the presenting sign was accommodative insufficiency. Objective accommodative findings were recorded 3 years before the onset of myasthenia, soon after the initial diagnosis was made, and then after the treatment commenced with pyridostigmine. In addition, clinical measurements were obtained periodically at different times of the day for various binocular motor functions, including near point of convergence, phoria, fusional and accommodative amplitudes, and relative accommodation. The disease adversely affected all accommodative and vergence findings, with fatigue being the primary disturbance. The therapeutic administration of pyridostigmine improved static measurements of accommodation and vergence and reduced asthenopia. The objective dynamic measurements of accommodation, vergence, and versions were less affected. These findings provide a clear demonstration that both intrinsic and extrinsic ocular muscles may be affected in the prepresbyopic myasthenic patient.
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PMID:Accommodative and vergence findings in ocular myasthenia: a case analysis. 1113 Jul 61

Myasthenia gravis is a neuromuscular, autoimmune, and acquired disturbance characterized by weakness and fatigue of skeletal muscles. During the past two decades, remarkable progress has been made in the understanding of myasthenia gravis, and the new knowledge has been applied directly to the clinical diagnosis and treatment of this formerly severe disease. Myasthenia gravis is undoubtedly the most thoroughly understood of all human autoimmune diseases and has served as a model for the elucidation of mechanisms underlying other autoimmune disorders. In this review we mention the most important physiopathological aspects and its application in the clinic practice.
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PMID:[Pathogenesis of myasthenia gravis]. 1081 14

A patient with painful neuropathy developed ocular, facial, and masticatory weakness and fatigue after 3 months of gabapentin (GBP) treatment (400 mg/day). An elevated level of serum acetylcholine receptor antibodies (AChR-Ab) was detected. The patient recovered following pyridostigmine therapy and withdrawal of GBP and, 2 years later, is practically asymptomatic despite positive AChR-Ab. Because of this clinical observation, we gave 150 mg/kg GBP to rats with experimental autoimmune myasthenia gravis (EAMG). Repetitive nerve stimulation at 3-Hz was performed, and the 5th/1st amplitude ratio was used to calculate the decremental response. In all EAMG rats, GBP induced a transient, abnormal decrement (7-20%) 90 to 240 min after administration. No decrement was induced by GBP in normal rats. Thus, GBP aggravates the decrement in EAMG. The mechanism involved in the hitherto unreported possible unmasking of myasthenia gravis (MG) by GBP is unknown. Gabapentin should be used with caution in this disease.
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PMID:Gabapentin may be hazardous in myasthenia gravis. 1091 56

We report a patient with myasthenia gravis (MG) who had marked clinical benefit in response to treatment with mycophenolate mofetil as documented by serial quantitative measures of strength and muscle fatigue. Our patient had experienced either adverse side effects or a suboptimal response to the usual immunosuppressive agents used in MG. Mycophenolate mofetil was used in combination with cyclosporine and prednisone and allowed for significant reductions in dosage of these immunosuppressants. We conclude that mycophenolate mofetil deserves further study as a therapeutic agent in MG. In particular, its role as a steroid-sparing agent and as a drug to be used in combination immunotherapy in more severe or refractory cases of MG should be investigated.
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PMID:Treatment of myasthenia gravis with mycophenolate mofetil: a case report. 1091 71

We have examined fatigue in myasthenia gravis (MG) by administering a measure of cognitive and physical fatigue to patients and control subjects before and after administration of a lengthy cognitive battery. Subjects also completed a scale that assessed the impact of fatigue on physical, social, and cognitive function. Results of the study revealed that MG patients experience significantly more cognitive and physical fatigue than do control subjects, and the patients' perceptions of both cognitive and physical fatigue increased significantly following completion of demanding cognitive work. Control subjects reported no significant change in fatigue. Furthermore, MG patients reported that fatigue produced mild to moderate effects on cognitive and social function and moderate effects on physical function. Results from this study indicate that cognitive fatigue is an important symptom of MG and that fatigue produces pervasive impairments in important aspects of patients' lives. Additional studies are needed to understand the neurobehavioral determinants of cognitive fatigue in this population.
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PMID:Fatigue and its impact on patients with myasthenia gravis. 1095 43

The neuromuscular junction is the target of a variety of autoimmune, neurotoxic and genetic disorders, most of which result in muscle weakness. Most of the diseases, and many neurotoxins, target the ion channels that are essential for neuromuscular transmission. Myasthenia gravis is an acquired autoimmune disease caused in the majority of patients by antibodies to the acetylcholine receptor, a ligand-gated ion channel. The antibodies lead to loss of acetylcholine receptor, reduced efficiency of neuromuscular transmission and muscle weakness and fatigue. Placental transfer of these antibodies in women with myasthenia can cause fetal or neonatal weakness and occasionally severe deformities. Lambert Eaton myasthenic syndrome and acquired neuromyotonia are caused by antibodies to voltage-gated calcium or potassium channels, respectively. In the rare acquired neuromyotonia, reduced repolarization of the nerve terminal leads to spontaneous and repetitive muscle activity. In each of these disorders, the antibodies are detected by immunoprecipitation of the relevant ion channel labelled with radioactive neurotoxins. Genetic disorders of neuromuscular transmission are due mainly to mutations in the genes for the acetylcholine receptor. These conditions show recessive or dominant inheritance and result in either loss of receptors or altered kinetics of acetylcholine receptor channel properties. Study of these conditions has greatly increased our understanding of synaptic function and of disease aetiology.
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PMID:Molecular targets for autoimmune and genetic disorders of neuromuscular transmission. 1108 82


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