Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0015672 (fatigue)
 51,768 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Monoclonal IgG gammopathy of the lambda light-chain type was detected in a 51-year-old woman who had unexplained fever, muscle fatigue, and myalgia. One year later, myasthenia gravis was diagnosed. There was no evidence of myelomatosis or other malignancy. On the assumption that her M-component (gammopathic paraprotein) was related to myasthenia, she was treated with melphalan and cyclophosphamide, but her clinical condition was not improved. Despite therapeutic trials of other agents and a time course of 6 years, the quantity of the M-component remained unchanged. Serum AChR antibody activity was not located in the paraprotein peak. The findings do not support a relationship between the M-component and myasthenia gravis.
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PMID:Myasthenia gravis and monoclonal IgG gammopathy. 10 88

After discussion of the modern concepts of pathophysiology of ocular myasthenia the ocular symptoms such as ptosis and eye muscle palsies are discussed. As important diagnostic sign the Simpson lid fatigue test before and after application of Tensilon is described. For diagnosis of myasthenic eye muscle palsies electrooculography has a special significance especially in connection with the application of Edrophonium, which normalizes myasthenic hypometric saccades and transforms them even in hypermetric saccades. In doubtful cases of eye muscle palsies the electromyogram of the affected muscle in connection with the Edrophonium-test is extremely valuable. With regard to modern treatment apart from cholinesterase inhibitors (Pyridostigmine, Neostigmine) thymectomy, the application of corticosteroids, ACTH and especially also immune suppressive drugs (Imurel etc.) is discussed. Of great significance in ocular myasthenia is the local application of cholinesterase inhibitors like Eserine, Prostigmin or Phospholine Iodide.
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PMID:[Diagnosis and treatment of ocular myasthenia (author's transl)]. 20 42

The behavior of the stapedius reflex was examined by means of the Z0-70 Madsen electroacoustic bridge in 41 patients (aged 9-73) with myasthenia gravis. A higher stapedius reflex threshold (90-130 db) at normal hearing was found in 66% of the cases. In 46.3% of the cases, an increased fatigue of the stapedius muscle was observed, as characterized by the lowering of the amplitude or the disappearance of the reflex after several successively repeated recordings. The examination of stapedius muscle fatigqu may be helpful indiagnosing early forms of myasthenia, in following the results of therapy for the disease, as well as in assessing the efficiency of antimyasthenic drugs.
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PMID:[The value of stapedius reflex examinations in patients with myasthenia gravis (author's transl)]. 66 94

In the past 25 years, we have studied 73 cases of Myasthenia. 19 of these have had 24 pregnancies. We confirm the results that are given in the literature (15). Pregnancy does not trigger off Myasthenia. The action of pregnancy on Myasthenia is variable and there is an equal chance of worsening, improvement or a stationary state of the condition. All the same, patients who are well stabilised and have been for some time do not become worse. Worsening, when it does happen, happens especially in the first trimester of the pregnancy and calls for precise observation of the patient in order to regulate the treatment. Myasthenia has no direct or indirect action on the fetus and the pregnancy is not disturbed. Labour can be normal but the second stage often has to be aided because of the patient's muscle tiredness. In labour and particularly in the second stage an acute crisis can occur with difficulty in breathing. For this it is necessary to have an anaesthetist present who can resuscitate the patient and if necessary give respiratory aid by ventilation. Curare and like substances are absoultely contra-indicated if general anaesthesia is required. Transitory neonatal Myasthenia is rare, but the severity of the respiratory complications can be such that is should be sought for routinely and if there is the slightest doubt the newborn should be transferred to the special care neonatal unit.
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PMID:[Myasthenia and pregnancy (author's transl)]. 74 45

A collection of symptoms and signs indistinguishable from ocular myasthenia can be caused by an intracranial mass. We illustrate this condition with the case of an adolescent girl with neurofibromatosis type 1 and a dorsal midbrain astrocytoma. At presentation, she had fatigable ptosis, upgaze paresis, and a positive "lid twitch" sign. Radiation therapy resulted in marked reduction of her signs, confirming that the muscle fatigue was central in origin. We discuss the possible mechanisms of this central fatigability.
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PMID:Midbrain myasthenia: fatigable ptosis, 'lid twitch' sign, and ophthalmoparesis from a dorsal midbrain glioma. 156 51

A medical expert's opinion had to be given on five patients complaining about temporary visual disturbances. 1. Haze caused by keratoconjunctivitis sicca; 2. changing refraction related to diabetes; 3. phosphenes in a paralyzed monoculus; 4. double vision with fatigue in myasthenia; 5. presumed elevation of the risk for accidents in congenital nystagmus. The loss of earning capacity in these cases should be calculated as the mean of the earning capacity during the phases of least and maximal disturbance, if it is not yet included in the loss caused by additional stationary defects. Psychological adaptation to or an additional disturbance by the disease has to be considered and may justify a higher loss of earning capacity.
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PMID:[Temporary vision disorders, accentuated by deficient illness adjustment]. 175 76

The diagnosis of myasthenia gravis is usually confirmed by a Tensilon test, which can be complicated by cholinergic side effects that include cardiopulmonary arrest. An alternative, the Sleep test, based on the characteristic of myasthenia that symptoms and signs worsen with fatigue and improve after a period of rest, is safe, moderately sensitive, and specific. The diagnosis of myasthenia can be confirmed by observing resolution of ptosis or ophthalmoparesis immediately after a 30-minute period of sleep; the reappearance of the myasthenic signs over the next 30 seconds to 5 minutes adds further confirmation.
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PMID:The sleep test for myasthenia gravis. A safe alternative to Tensilon. 183 52

In patients with myasthenia gravis, vigorous exercise and electric stimulation produce weakness that is usually reversed by rest. We describe a case of persistent weakness in a 31-year-old woman with myasthenia gravis following therapeutic electric stimulation. She was injured in an automobile accident, with cervical and lumbar muscle strain diagnosed by a local emergency room physician. She consulted a chiropractor two days later because her symptoms had not abated. The chiropractic treatment of short-wave diathermy, high-voltage electric stimulation and spinal manipulation continued thrice weekly for six weeks. She then presented to her neurologist, complaining of persistent fatigue, weakness, increased diplopia, cervical and occipital pain, and disrupted sleep. Neck weakness had developed since her last visit. She was admitted to the hospital for evaluation. Neurologic exam showed no other abnormality of strength, sensation, or reflexes. The exacerbation of myasthenia responded to prednisone and increased pyridostigmine. After two months she required only her preinjury dose of pyridostigmine (60 mg q.d. p.r.n.) to prevent diplopia or fatigue, and her strength was normal. Repeated electrically induced muscle contraction is suspected of causing this exacerbation of myasthenia gravis.
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PMID:Exacerbation of a case of myasthenia gravis during therapeutic electric stimulation. 349 64

Ocular myasthenia is a special form of general myasthenia gravis characterized by unilateral or bilateral ptosis and eye muscle pareses of distinct variability, depending on the time of day and the state of fatigue of the patient. Most important for diagnosis is the Tensilon test, which can, however, produce negative results. In such cases a combination of the Tensilon test with electromyography is indispensable. In ocular myasthenia there is not always an increase in the antibody titer against acetylcholine receptors in the blood. The treatment of ocular myasthenia is based on the application of cholinesterase inhibitors. The drug of choice is Mestinon; however, the reaction of the eye muscles to this drug is often unsatisfactory. Local application of cholinesterase inhibitors in the form of Eserine, Prostigmin etc. is an additional important therapy. Also in ocular myasthenia the modern treatment with Cortisone (alternate-day therapy with 100 mg Prednisone every second day) has proved very useful. Another possible method of interfering with the immunological systems of myasthenia is immunosuppression with Azathioprin or Cyclophosphamide. The pathognomonic significance of the thymus in the autoimmune process of myasthenia gravis is demonstrated by the good results obtained by thymectomy, which can also be performed successfully in ocular myasthenia, not only in young patients in whom the condition is severe, but also in older patients in whom it is chronic. Often, the therapeutic measures mentioned have to be tested one after another or in combination in order to achieve an optimal therapeutic effect.
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PMID:[Ocular myasthenia]. 399 98

An account is given of four cases of myasthenia gravis in the dog. All animals showed fatigue, and considerably reduced tolerance to exercise. Recovery followed rest or treatment with neostigmine. Three animals, two of which are still alive, had dilatation of the oesophagus. The fourth eventually died from an aortic body tumour. The occurrence of myasthenia in the dog may be of value in elucidating the cause of the disease in man.
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PMID:Myasthenia gravis in the dog. 424 23


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