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Query: UMLS:C0015672 (fatigue)
51,768 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

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 medium-chain acyl-CoA dehydrogenase (MCAD) deficiency of mitochondrial beta oxidation has been identified in a nine-year old boy with a very bland course and easy fatigue as the main symptom. Repeated low frequency stimulation test and EMG for excluding a myasthenia gravis, and screening for urinary organic acid excretion were helpful for the diagnosis. The EMG test at the m. trapezius by stimulation of the n. accessorius showed an extreme decrease of muscle power down to 49%. After i.v. injection of Edrophonium the loss of power of 20% was still significant, so that we could exclude a myasthenia gravis, but we had found signs of a generalised defect in cell chemistry. The diagnosis could be confirmed by a positive 3-phenylpropionic acid-test and moleculargenetic proof of the Adenine to Guanine mutation at position 985 in the MCAD cDNA (G985) with the polymerase chain reaction. The incidence of this organic aciduria is probably 1:60,000 in Germany, but with more attention to this disease and diagnosis of cases with bland courses the incidence will be higher. The MCAD-defect should be considered in the differential diagnosis of patients with Reye syndrome-like encephalopathies, non-ketotic hypoglycaemia or sudden unexpected deaths in infancy.
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PMID:[Acyl coenzyme A dehydrogenase deficiency of medium-chain fatty acids in a 9-year-old boy with adymia. A rare mitochondrial cytopathy which may be more common than previously assumed]. 177 46

The response of eye movements to edrophonium is easily missed by clinical observation alone. Binocular horizontal ten degree saccades were recorded by infrared oculography, whilst the vision of one eye was occluded, before and after fatigue repeated intravenous injection of dilute edrophonium, and fatigue induced during anticholinesterase inhibition by intravenous edrophonium, in 26 patients with diplopia or ptosis of uncertain aetiology. The most reliable criterion of a positive response was an increase in the amplitude of the saccades of the fixating eye by 10% or more after each of several injections of dilute edrophonium. The response was positive in 13 patients and was difficult to observe clinically when the responses of the saccades of the eyes moving conjugately were unequal and when the patient presented with ptosis and no diplopia. Edrophonium infrared oculography proved to be a sensitive test for weakness due to the neuromuscular junction defect of myasthenia gravis affecting extraocular muscles.
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PMID:Edrophonium test in myasthenia: quantitative oculography. 358 98

Disabling generalized fatigue and muscle fatiguability are common features of post-poliomyelitis syndrome (PPS). In 17 fatigued PPS patients, we measured jitter on stimulation single-fiber electromyography (S-SFEMG) for at least 3.5 min before and after i.v. injection of 10 mg edrophonium. We observed reduction in jitter (defined as a significant difference in jitter means before and after edrophonium, unpaired t-test P < 0.05) in 7 patients, no change in 8, and a significant increase in 2 patients. Blinded to their edrophonium results, the 17 patients were treated with pyridostigmine 180 mg/day for 1 month, with a subjective improvement of fatigue in 9 patients, and with a significant reduction in mean Hare fatigue scores in the entire group of 17 patients (pre = 2.71, and post = 1.71; Wilcoxan signed rank sum test, P < 0.05). Edrophonium-induced reduction of jitter on S-SFEMG was significantly associated with pyridostigmine-induced subjective improvement of fatigue (Fisher's exact test, P < 0.04). A significant reduction in fatigue with pyridostigmine was observed only in the 7 patients who experienced a significant reduction in jitter with edrophonium (Wilcoxan signed rank sum test, P = 0.03). In addition, the 9 pyridostigmine responders experienced a significant reduction in jitter means pre- and post-edrophonium (100% vs. 88%, Bonferroni corrected, P < 0.01). We conclude that neuromuscular transmission as measured by jitter on S-SFEMG can improve with edrophonium in a proportion of PPS patients, and that generalized fatigue and muscle fatiguability in some patients with PPS may be due to anticholinesterase-responsive NMJ transmission defects.
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PMID:Anticholinesterase-responsive neuromuscular junction transmission defects in post-poliomyelitis fatigue. 838 88