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

The neuromuscular block of myasthenia gravis has the characteristics of an antidepolarizing (competitive block), similar to that produced by d-tubocurarine in normal subjects: progressive decrease in muscle action potentials evoked by two or more nerve stimuli, posttetanic facilitation, posttetanic fatigue, inhibition of the depolarizing action of acetylcholine (ACh) or anticholinesterase compounds, and reversal of the block by ACh or anticholinesterase compounds. In myasthenic patients spontaneously recurring negative discharges were more difficult to locate in the end-plate zone than in normal subjects, suggesting that the number or density of functioning end plates may be reduced. The threshold dose of intra-arterial ACh that increased electrical activity was higher than in normal subjects; the duration of the increased electrical activity was briefer, and was followed by more depression of negative discharges than in normal subjects and by a greater increase in the threshold dose of ACh. These results indicate that the end-plate zone of myasthenic patients is less responsive than that of normal subjects to the excitatory action of ACh, and may be more readily desensitized by ACh. In both myasthenic patients and normal subjects the intra-arterial injection of ACh produced a prompt transient decrease in evoked potentials, attributable to depolarization of the end plates, followed by recovery (and in myasthenic patients by repair), and then by a more prolonged late decrease in evoked potentials, attributable to desensitization of the end plates to transmitter. This prompt depressant effect of ACh on evoked potentials was less in myasthenic patients than in normal subjects, and the late depressant effect of ACh was greater. In myasthenic patients the late block produced by ACh had the characteristics of an antidepolarizing (competitive) type of block, including inhibition of the depolarizing action of ACh and reversibility by ACh or neostigmine, while in normal subjects the characteristics were those of a depolarizing (noncompetitive) type of block, including little or no inhibition of the depolarizing action of ACh and lack of reversal by ACh or neostigmine. The differences between the late depressant action of ACh in myasthenic patients and normal subjects resembled differences in the effect of other depolarizing compounds, such as choline, succinylcholine, and decamethonium, and are best explained by differences in behavior of the postsynaptic receptor. The disease appears to be due to the presence of abnormal forms of receptor or to abnormal responses of receptor to the transmitter. The predominance of one or other form of receptor may determine the clinical state of the myasthenic patient and his response to anticholinesterase medication.
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PMID:Characteristics and mechanism of neuromuscular block in myasthenia gravis. 18 86

The effect of dibutyryl 3',5'-cyclic monophosphate (D-cAMP) on the neuromuscular transmission was studied in a patient with myasthenia gravis during anesthesia. D-cAMP caused a slight increase in single twitch tension, and an initial transient decrease in tension which resulted from the trains of 2 Hz stimuli disappeared after D-cAMP. The finding of the present study suggests that D-cAMP has an anti-fatigue effect in patients with myasthenia gravis.
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PMID:Effect of dibutyryl cyclic AMP on neuromuscular transmission in myasthenia gravis. 18 50

Rabbits were immunized versus either an acetylcholinesterase- or a cholinergic receptor-rich fraction isolated from the electric organ of Torpedo marmorata. In both groups of animals we obtained a production of specific antibodies detected by immunodiffusion without cross reaction for the two antigens. Only rabbits immunized with the receptor-rich fraction developed a progressive flaccid paralysis, which affected first the leg muscles, progressively the neck muscles and eventually the respiratory muscles. The paralysis lasted in several animals up to 20 days. Eserine reversed the paralysis only in the first days but was ineffective in the "chronic" stage of the disease. In these animals high frequency stimulation of sciatic nerve induced a rapid failure of the responses of the anterior tibialis muscle while the muscle responded normally to a direct stimulation. A period of rest allowed a complete recovery of the muscle from fatigue. Tetani did not evoke the post-tetanic potentiation. Abnormalities, such as lymphocytic infiltration, fibers atrophy and necrosis, smearing and widening of Z line were sometimes present in muscles of Cho-R-immunized rabbits. In ACh-E immunized animals the neuromuscular transmission and the muscle morphology were similar to that of normal animals. Glycogen, ATP, cytochrome C oxidase, phosphorylases and acetylcholinesterase did not change significantly in the muscles of the immunized animals, while a large increase of cholineacetyltransferase activity was present. Red blood cell acetylcholinesterase showed a particularly high activity in ACh-E-immunized animals. The autoimmune paralysis induced in Cho-R-immunized rabbits may be a useful experimental model for further studies on human myasthenia gravis.
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PMID:Immunization of rabbits with secific components of postsynaptic membrane. Acetylcholinesterase and cholinergic receptor. 18 67

Three patients with myasthenia gravis demonstrated a distinctive sign of orbicularis fatigue. After momentary opposition on gentle sustained lid closure, the lid margins separated, resulting in widening of the palpebral fissure and scleral exposure. The patient thus appeared to "peek" at the examiner. The "peek" sign was not observed in 200 control patients and in 49 of 50 patients with facial weakness secondary to a spectrum of neuromuscular disorders. Three of 25 patients with myasthenia gravis displayed this sign, and in one patient it was the major diagnostic finding. The presence of the "peek" sign suggests the diagnosis of myasthenia gravis.
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PMID:Orbicularis fatigue: the 'peek' sign of myasthenia gravis. 42 81

Myasthenia gravis is a neuromuscular disease of insidious onset, characterized by weakness and fatigability of voluntary muscles. Most patients present with symptoms relating to the head and neck and thus may be seen first by the otolaryngologist. Predominant symptoms may be ocular (ptosis or diplopia) or related to fatigue of the oropharyngeal or laryngeal musculature (dysarthria, dysphonia, or dysphagia). Alleviation of muscular weakness and fatigability after administration of anticholinesterase drugs is pathognomonic of myasthenia gravis.
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PMID:The otolaryngologic presentation of myasthenia gravis. 44 37

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

Myasthenia gravis is a rare disease with unique clinical features. These include (1) progressive fatigue on exertion, most evident clinically in the muscles of the head and neck (2) a definite relationship of the disease to the thyroid, parathyroid and thymus glands. A hypothesis is advanced with correlates these facts on the basis of a common embryologic origin of these glands and the branchial arch muscles. A corollary is that the muscles of the head and neck differ from the somatic musculature in some as-yet-unidentified manner, for example, pharmacologically. A plea is made for comparative studies between the two.
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PMID:Myasthenia gravis: An embryologic and phylogenetic perspective. 93 7

Maximum velocity and amplitude of repetitive ( 1-per-second) 30 degrees saccadic eye movements were quantitatively assessed for 4 minutes before and after intravenous edrophonium chloride as a diagnostic test for myasthenia gravis. Atropine was given initially to suppress muscarinic side effects. Eye movements were recorded by electrooculography and a digital computer identified saccadic eye movements and plotted amplitude-velocity relationships. When compared with control subjects, eleven of twelve patients with proven MG had a significant increase in saccade amplitude and/or maximum velocity after edrophonium chloride. Only three of twelve proven MG patients had clinically apparent extraocular muscle weakness. The initial period of fatigue improved the sensitivity of the test in those patients who began with normal saccade amplitude and maximum velocity. Two of the patients with positive saccade fatigue tests had no change in optokinetic nystagmus amplitude before and after edrophonium chloride. It is concluded that, quantitative assessment of repetitive large angle saccades before and after edrophonium chloride is a sensitive test for extraocular muscle involvement in MG.
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PMID:Saccade fatigue and response to edrophonium for the diagnosis of myasthenia gravis. 106 99

In myasthenia gravis (MG) a typical decrementing response is frequently revealed with repetitive stimulation (RS) in clinically unaffected muscles. However, RS is unlikely to give normal results in weak muscles. In two of our patients we found a normal response in clinically affected muscles. However, a decrementing response surprisingly appeared after the administration of anticholinesterase drugs. A possible explanation for this apparently paradoxical effect is as follows: some junctions are already blocked at rest, whereas others function normally both at rest and during RS. As a consequence, the initial compound muscle action potential (CMAP) is reduced in amplitude and shows no further decrement on RS. Anticholinesterase drugs reverse some blocks, therefore causing the CMAP increase in amplitude. However, these labile junctions are more prone than normal to synaptic fatigue, so a decrementing response is produced on RS. This behavior, though not frequently encountered, can account for some negative results of RS in MG.
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PMID:Repetitive stimulation in myasthenia gravis: decrementing response revealed by anticholinesterase drugs. 168 68


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