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)

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

Ocular myasthenia can mimic central disorders of eye movements. We compared horizontal saccades in two patients with myasthenia gravis who presented as pseudo-internuclear ophthalmoplegia (pseudo-INO), two patients with true INO due to multiple sclerosis (MS), and five healthy subjects. In myasthenics, peak velocity of horizontal saccades was similar to, or greater than, controls; in MS patients, adducting saccades were slower than controls. Differences between the peak velocity of abducting and adducting eyes for each saccade were similar to controls for myasthenic pseudo-INO, but greater than controls for true INO. Using the technique of phase-plane analysis, in which eye velocity is plotted against eye position, we found that initial components of abducting and adducting saccades in the myasthenics were as conjugate as controls, even though later components of myasthenic saccades were highly and variably disjunctive. Conversely, phase planes of saccades in true INO showed disjunctive early components of abducting and adducting saccades. Two hypotheses have been offered to account for preservation of fast saccades despite reduced range of eye movements in ocular myasthenia. The first is intrasaccadic neuromuscular fatigue, which is variable over time. Our finding that initial components of saccades were consistently conjugate in the myasthenics gives support to a second hypothesis: selective sparing of pale global fibers, which are important for generating highspeed eye movements, and which are unique amongst extraocular fibers in possessing well developed synaptic folding.
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PMID:Ocular myasthenia revisited: insights from pseudo-internuclear ophthalmoplegia. 1771 27

Ocular myasthenia is a form of myasthenia gravis in which weakness is restricted to the ocular muscles and may produce significant visual disability. Patients present with fluctuating ptosis, diplopia, or a combination of both. Examination may show any type of ocular motility deficit ranging from isolated muscle palsy to complete ophthalmoplegia. Cogan lid twitch, enhanced ptosis, peek sign, and saccadic fatigue are specific examination findings that support the clinical diagnosis of myasthenia gravis. Confirmation of the diagnosis is challenging with autoantibody serology, and repetitive nerve stimulation studies are often negative.
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PMID:Ocular Myasthenia. 2965 47

Ocular myasthenia gravis and orbital metastases have overlapping symptoms but divergent diagnostic and treatment strategies. Here, we present a 58-year-old female, with a 20-year history of advanced metastatic breast cancer, who presented to the neurology clinic with fatigue, muscle weakness, bilateral ptosis, and diplopia that worsened throughout the day. While the initial presentation was consistent with ocular myasthenia gravis, a subsequent evaluation revealed bilateral metastatic lesions of breast origin within the orbits. This case highlights the variable nature of metastatic disease and underscores the importance of a comprehensive neoplastic workup in patients with new-onset symptomatology and a prior history of advanced cancer despite purported remission status.
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PMID:Bilateral Orbital Metastases Masquerading as Ocular Myasthenia Gravis: A Case Report and Review of the Literature. 3278 50