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Myasthenia gravis historically has been associated with significant morbidity and mortality rates, and most of those afflicted either died of the disease or became greatly disabled. However, modern understanding of the pathogenesis of this disorder has led to several effective treatments which have transformed the prognosis of this disease greatly.
Myasthenia gravis (MG) is an autoimmune disease of neuromuscular transmission associated with the presence of anti-acetylcholine receptor antibodies (anti-AChR Ab). Current treatment of MG includes anti-cholinesterase drugs, thymectomy, corticosteroids, immunosuppressants and plasma exchange (PE). The use of intravenous immune globulin (IVIG) in MG was proposed 10 years ago. Published results of IVIG treatment are discussed and the need for a controlled study is emphasized.
Myasthenia gravis is characterized by variable ocular and skeletal muscle weakness. Peak incidence is in young women and older men. Thymomas are present in 30 percent of myasthenic patients over age 40. Binding of acetylcholine receptors by IgG antibodies may be the mechanism of the neuromuscular disorder. Repetitive nerve stimulation (Jolly test), provocative tests with quinine or curare and the edrophonium test (cholinesterase inhibition) are the diagnostic maneuvers employed.
Myasthenia gravis is described on the basis of both the physiological mechanisms of neuromuscular transmission and the current knowledge of the pathogenesis of the disease. The different laboratory tests in use are considered with regard to their diagnostic significance, in addition to the clinical features of the disease. Differential diagnosis has to include myasthenic syndromes of different origin, periodic paralysis, diseases of the peripheral motor neuron as well as certain myopathies.
Myasthenia gravis (MG) is an antibody-mediated muscle disease in which any skeletal muscle can be affected. MG may produce numerous symptoms and signs. To doctors and patients, it may seem like lung disease, stroke, heart disease, or the effects of emotional stress. This article explores the "territory" between MG and diseases of the heart and lungs as well as the other neuromuscular diseases.
Myasthenia gravis (MG) is an autoimmune neuromuscular disease, characterized by muscle weakness and electrophysiological abnormality. No treatment which would reliably induce permanent clinical remission of MG is yet available. The therapeutic efficacy and toxic effect of daunomycin (Dm), an antibiotic of the rhodomycin group, was evaluated in murine experimental autoimmune MG. Low dosage Dm treatment effectively prevented the development of muscle weakness and its associated electrophysiological abnormality, without inducing detectable toxicity and global immunosuppression.
Myasthenia gravis is a disorder that most commonly affects young adults but occasionally appears in the elderly. Muscle weakness and easy fatigability, particularly of the ocular muscles, are characteristic. Diagnosis is confirmed by electromyography and the edrophonium (Tensilon) test. The pathology results from inability of acetylcholine to gain access to receptor sites at the neuromuscular junction, possibly because of a blocking antibody produced by the thymus. Initial treatment (in the absence of a thymoma) consists of administration of an anticholinesterase drug. If that is ineffective, thymectomy and/or corticosteroids may be useful.
Myasthenia gravis (MG) is an acquired autoimmune disorder of neuromuscular transmission associated with a deficiency of acetylcholine receptor at the neuromuscular junction. Current therapeutic strategies are aimed at increasing the amount of acetylcholine at the neuromuscular junction or at addressing the abnormal immune response. Therapies influencing the immune response include thymectomy, corticosteroids, nonsteroidal immunosuppression, and plasmapheresis. Unfortunately, whether used alone or in combination the toxicities of these agents can be quite significant; thus, an agent with a distinct and more favorable side effect profile might be useful in MG. Intravenous immunoglobulin has such potential.
Myasthenia gravis is a relatively rare neurological disease that is associated with loss of the acetylcholine receptors that initiate muscle contraction. This results in muscle weakness, which can be life-threatening. The story of how both the physiological basis of the disease and the role of acetylcholine-receptor-specific antibodies were determined is a classic example of the application of basic science to clinical medicine, and it has provided a model for defining other antibody-mediated disorders of the peripheral and central nervous systems.
Myasthenia gravis (MG) classically presents with ocular, bulbar, and predominantly proximal muscle weakness. Isolated bulbar symptoms occur in less than 25% of cases and can mimic stroke (1-3). If left untreated, MG can lead to significant morbidity and mortality, including myasthenic crisis and recurrent aspiration pneumonia. We describe a case of a 68-year-old man who presented with isolated bulbar symptoms. We used a novel approach to diagnosis which included a videofluorographic swallow study with concomitant Tensilon (edrophonium) injection.
Myasthenia gravis (MG) characteristically involves ocular, bulbar, and proximal extremity muscles. Distal extremity muscles are typically spared or less prominently involved. The authors performed a retrospective chart review of MG patients treated at two university-based neuromuscular clinics. From a total population of 236, nine patients (3%) had distal extremity weakness exceeding proximal weakness by at least one Medical Research Council grade during their illness. Hand muscles, particularly finger extensors, were involved more frequently than were distal leg and foot muscles.
Myasthenia gravis is an autoimmune disease where corticoids are the basis of therapy. They are taken for short periods in large amounts, as well as for prolonged periods in medium or small doses. The authors investigated in the described groups the effect of corticoids on bone tissue. They provided evidence of a significant effect on the diffraction pattern, geometrical arrangement of the apatite grid and ion changes in relation to the period of corticoid administration without significant clinical manifestations of osteoporosis, when respecting therapeutic principles.
Myasthenia gravis (MG) is a common neuromuscular disorder, however, voiding dysfunction in conjunction with MG is rare. A review of the literature yielded only 7 prior reports of such a combination. Most of the reported cases involved incontinence in males which developed after a transurethral resection of the prostate. Only 3 cases described de novo voiding dysfunction. We report a fourth patient. In all 4 cases of de novo dysfunction, the voiding problem either heralded a new diagnosis of MG or an exacerbation of the disease process. It is hypothesized that autonomic dysfunction in patients with MG might indicate a unique subset with a worse prognosis.
Myasthenia gravis (MG) is an autoimmune disease often associated with other autoimmune disorders. A case history of MG with a coexisting atypical megaloblastic anaemia with vitamin B12 deficiency and anti Intrinsic Factor (IF) antibodies, led to a study of humoral and cellular immunity to IF in 81 MG patients. Within this series, 3 other patients had a disturbed humoral and cellular immunity to IF. These 3 patients presented no other features of pernicious anaemia. The possible origins and significance of the anti IF antibodies in MG patients are discussed.
Myasthenia gravis (MG) represents the prototypic autoimmune disorder with well characterized immunopathology. Advances in the diagnosis and treatment of this neuromuscular transmission disorder have significantly improved the management of myasthenic patients. Unfortunately the currently available immunomodulating treatments have significant side effects and some patients do not tolerate them or adequately respond to them. Therefore the possibility of a new immunosuppressant agent that is safe, effective and has steroid-sparing effect is very appealing. Mycophenolate mofetil (MMF) has shown promising effects in MG patients in preliminary studies and is currently being studied in two prospective, randomized, double-blind, placebo controlled, multicenter trials to better establish its role in the treatment of MG.
Myasthenia gravis (MG) may in some patients, especially in those with a thymoma, involve the heart. Using an ELISA, we measured heart muscle antibodies in sera from 75 MG patients and in 173 control sera. Heart muscle antibodies were detected in 29/30 thymoma MG patients, in none of 30 young onset MG patients with thymic hyperplasia and in 7/15 late onset MG patients with thymic atrophy. Among the controls, four sera had a very low concentration of heart muscle antibodies. Absorption studies showed that the heart muscle antibodies cross-react with skeletal muscle, but are unrelated to acetylcholine receptor antibodies.
Myasthenia gravis, first described in 1672 by Sir Thomas Willis and named by Jolly in 1895, is clinically characterized by muscular weakness relieved by rest. The incidence rate is about 4/million/year, the prevalence in Norway is about 100/million. Anticholinesterase drugs, introduced by Mary Walker in 1934, are still the primary therapeutics. Since about 1960 the disease has been recognized as autoimmune. Circulating antibodies to the acetylcholine receptor of the neuromuscular synapse are detectable in greater than or equal to 85% of the patients. Hence thymectomy, plasmapheresis and immunosuppressant drugs are useful. The thymus is recognizably pathological in 75-80% of the cases. The thymic hormone thymopoietin stimulates thymocytes and T-cells, and directly blocks the acetylcholine receptor.
Myasthenia gravis (MG) is an autoimmune disorder of the neuromuscular junction that causes muscle weakness and fatigue. Fluctuating fatigue of skeletal muscles is the key clinical feature. Late-onset MG is more frequent in elderly men and is often misdiagnosed. While involvement of oropharyngeal musculature has been described with symptoms of dysphagia and slurred speech, the presence of fluctuating dysphonia as the first symptom of late-onset MG has not been emphasized. The case of an elderly man, who demonstrated voice changes and later swallowing impairment with weight loss, is reported. This case presentation of late-onset MG emphasizes that this form of the disease should be considered in the differential diagnosis of acute onset dysphonia in elderly persons.