Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0029089 (ophthalmoplegia)
3,338 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The most common causes of internuclear ophthalmoplegia (INO) are multiple sclerosis and vascular disease of the brain stem. Rarer causes are tumor, Arnold-Chiari malformation, and syphilis. Myasthenia gravis has, on occasion, presented with ocular abnormalities indistinguishable from INO. A case is described of bilateral INO of brief duration following head trauma. There were no other brain-stem abnormalities. This brings to 11 the number of reported patients in whom head trauma precipitated this abnormality.
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PMID:Internuclear ophthalmoplegia following head injury. Case report. 47 39

A 70-year-old man with known vascular disease, who had bilateral internuclear ophthalmoplegia, and an 18-month-old girl with a long-term variable esotropia culminating in a postinfectious oculopharyngeal neuropathy both responded with a positive edrophonium chloride (Tensilon) test, strongly suggesting the diagnosis of myasthenia gravis. Both subsequently received maintenance doses of neostigmine methylsulfate (Prostigmin).
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PMID:Ocular myasthenia gravis mimicking pseudointernuclear ophthalmoplegia and variable esotropia. 48 61

Myasthenia gravis developed in two children at 2 and 3 years of age respectively. Minimal improvement followed chronic oral administration of cholinesterase inhibitors. Patient 1 had ptosis and ophthalmoplegia but no clinical or electromyographic involvement of muscles of the extremities, although a quadriceps muscle biopsy revealed lymphorrhages. Patient 2 had progressive generalized myasthenia for 3 1/2 years. Both children were given a 3-month course of prednisone followed by thymectomy. They both are in remission, 12 and 8 months after thymectomy, with only minimal residual ocular weakness, but this weakness is much more responsive to anticholinesterase drugs than before thymectomy. Long-term administration of steroids, with the attendant complication of growth retardation, is avoided.
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PMID:Effective treatment of infantile myasthenia gravis by combined prednisone and thymectomy. 55 63

The purpose of this report is to alert the ophthalmologist and neurologist to the fact that intermittent ocular symptoms may herald the onset of chronic progressive external ophthalmoplegia and therefore resemble the weakness produced by myasthenia gravis. In addition, chronic progressive external ophthalmoplegia may complicate the course of Charcot-Marie-Tooth disease.
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PMID:Charcot-Marie-Tooth disease mimicking ocular myasthenia gravis. 69 78

Until such time as results of more rigorous studies are available, the morbidity rates for thyroid dysfunction cited here must suffice. The 1955 to 1956 outpatient "incidence" for England and Wales was 1.1 per 1,000 for thyrotoxicosis and 1.7 per 1,000 for myxedema (18). United States in-patient "incidence" for 1971 was 0.16 per 1,000 for thyrotoxicosis and 0.13 per 1,000 for myxedema (25). The 1935 to 1967 average annual incidence of Graves' disease for females in Olmsted County, Minnesota, was 30.5 per 100,000 (10). Well over 50% of hyperthyroid patients have clinical evidence of mild or moderate muscle weakness. Usually this weakness is proximal, and electro-myography and muscle biopsy confirm the existence of myopathic process (Table 11). Severe muscular weakness of acute onset is relatively rare and is encountered in approximately 1% of hyperthyroid patients (11,17,40). Ophthalmoplegia and psychosis are reported 4% and 2% of patients, respectively (17). Myasthenia gravis, although well publicized, is estimated to occur in less than 1% of patients (3,30). TPP is virtually nonexistent in the West; in the Orient it is reported in 2 to 8% of hyperthyroid patients and is 20 to 60 times more frequent in the hyperthyroid male than in the hyperthyroid female (Table 12). The neurologic symptomatology of myxedema is more extensive, and agreement among the various series is poor. The only unselected series addressing itself to neuromuscular manifestations of myxedema that is suitable for citation is that of Scarpalezos et al. (36). This comprehensive study was done without apparent patient selection, and it reported 2% of patients with definite carpal tunnel syndrome, 6% with myopathy, and 18% with polyneuropathy (Table 13). Reported percentages of hypothyroid patients found to have neurologic manifestations of cerebellar dysfunction are extremely diverse: ataxic gait was reported in 5 to 32% (6,7,12,27) of patients and dysdiadochokinesia in 6 to 52% (7,12,27). Psychosis is encountered in 2 to 5% (6,14,17,27,39) of myxedematous patients, memory loss in 23 to 55% (6,14,27), and coma in less than 1% (27).
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PMID:Neurologic complications of thyroid dysfunction. 74 45

A boy aged five and a girl aged one year suffering from myasthenia gravis are described. Both cases had respiratory complications and were treated erroneously until their ptosis was noticed and the diagnosis of myasthenia gravis confirmed. The etiology, types, symptomatology, and treatment of the diseases are described. Attention of the pediatric ophthalmologists is called to the fact that they should consider myasthenia gravis in the differential diagnosis of ptosis and external ophthalmoplegia.
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PMID:Childhood myasthenia gravis. 92 39

Deficient abduction can be due to both innervational deficiencies and/or mechanical restrictions. Innervational deficiencies include lateral rectus weakness or paralysis, myasthenia gravis, progressive external ophthalmoplegia nd Duane's syndrome with aberrant innervation to the lateral rectus muscle. Mechanical causes include restrictions on the medial side of the globe (a tight medical rectus due to endocrine ophthalmopathy, a contractured medial rectus muscle as a result of a lateral rectus paralysis, excessive resection of the medial rectus muscle, scarring and hemorrhage due to multiple previous operations upon the medial rectus), as well as a posteriorly inserted lateral rectus. This latter condition may result from a traumatically disinserted lateral rectus muscle, an excessively recessed lateral rectus muscle or a lateral rectus that has slipped from its attachment following strabismus surgery. Insufficient force for full abduction is caused by posterior insertion of the lateral rectus. The diagnosis of these various conditions is considered with reference to the forced duction, force generation and saccadic velocity tests. The treatment of these different causes of abduction deficiency is discussed noting that the approach to treatment depends upon the etiology of the abduction deficiency.
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PMID:The diagnosis and treatment of abduction deficiencies. 93 51

Rapid eye movements, having high velocity and low amplitude, are described in 11 patients with myasthenia gravis. These movements occur with various degrees of ophthalmoplegia. To distinguish them from the somewhat similar lid-twitch phenomenon, they are called quiver movements. We believed that their presence is pathognomonic of myasthenia and results from a differential involvement of the two myoneural mechanisms that are peculiar to the extraocular muscles.
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PMID:Rapid eye movements in myasthenia gravis. I. Clinical observations. 93 89

Voluntary saccades were studied by electro-oculography in ten patients with myasthenia gravis (MG) and in eight patients with other types of ophthalmoplegia. Despite limited range of eye movements, maximum velocities of 20 degree and 40 degree saccades in patients with MG were not significantly different from those in normal individuals, whereas maximum velocities in patients with other types of ophthalmoplegia were significantly decreased. In some myasthenic patients, small amplitude saccades were hypermetric and had high velocities, appearing clinically as "quiver" movements characteristic of MG. In MG the preservation of saccades with high initial velocities, even in the presence of severe ophthalmoplegia, suggests that muscle fibers generating rapid movements during saccades (twitch fibers) can be relatively spared when muscle fibers responsible for maintenance of excentric gaze (tonic fibers) are severely affected.
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PMID:Rapid eye movements in myasthenia gravis. II. Electro-oculographic analysis. 96 56

Two brothers with congenital myasthenia gravis are described. In both, ptosis and ophthalmoplegia responded poorly to oral anticholinesterase therapy and to thymectomy. The brothers had two different HLA haplotypes and neither had the HLA-A1-B8-DW3 haplotypes which are commonly associated with myathenia gravis in adult-onset cases.
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PMID:Congenital myasthenia gravis: clinical and HLA studies in two brothers. 101 Oct 24


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