Masked Myasthenia Gravis

Weisman, Sydney J.

doi:10.1001/jama.1949.62910130001008

Cited by 17 publications

(3 citation statements)

References 3 publications

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“…26 Approximately one-third to one-half of patients may have no obvious cause for their myasthenic crisis. 6,8 Numerous medications may exacerbate MG, including quinidine, 27 procainamide, 28 b-adrenergic antagonists, 29 calcium channel antagonists (verapamil, nifedipine, felodipine), [30][31][32] magnesium, 33 antibiotics (ampicillin, gentamicin, streptomycin, polymyxin, ciprofloxacin, erythromycin), [34][35][36][37][38] phenytoin, 39 gabapentin, 40 methimazole, 41 a-interferon, 42 and contrast media. 43 These medications should be used cautiously in myasthenic patients, especially after surgery.…”

Section: Precipitants Of Myasthenic Crisismentioning

confidence: 99%

Myasthenic Crisis

Wendell

Levine²

2011

The Neurohospitalist

183

193

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Myasthenic crisis is a complication of myasthenia gravis characterized by worsening of muscle weakness, resulting in respiratory failure that requires intubation and mechanical ventilation. Advances in critical care have improved the mortality rate associated with myasthenic crisis. This article reviews the epidemiology of myasthenic crisis and discusses patient evaluation. Therapeutic options including mechanical ventilation and pharmacological and surgical treatments are also discussed.

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Section: Precipitants Of Myasthenic Crisismentioning

confidence: 99%

Myasthenic Crisis

Wendell

Levine²

2011

The Neurohospitalist

183

193

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“…Aside from antimicrobial drugs, the class Ia antiarrhythmic drug quinidine (and its stereoisomer quinine) have been observed to transiently worsen neuromuscular weakness in patients with MG (Weisman, 1949). Somewhat paradoxically at first sight, while deteriorating MG, quinidine represents an effective therapeutic option in (slow channel) CMS (Lee et al, 2018).…”

Section: Presumed (Combined) Pre-and Postsynaptic Effectsmentioning

confidence: 99%

Pathomechanisms and Clinical Implications of Myasthenic Syndromes Exacerbated and Induced by Medical Treatments

Krenn

Grisold

Wohlfarth

et al. 2020

Front. Mol. Neurosci.

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Myasthenic syndromes are typically characterized by muscle weakness and increased fatigability due to an impaired transmission at the neuromuscular junction (NMJ). Most cases are caused by acquired autoimmune conditions such as myasthenia gravis (MG), typically with antibodies against the acetylcholine receptor (AChR). Different drugs are among the major factors that may complicate pre-existing autoimmune myasthenic conditions by further impairing transmission at the NMJ. Some clinical observations are substantiated by experimental data, indicating that presynaptic, postsynaptic or more complex pathomechanisms at the NMJ may be involved, depending on the individual compound. Most robust data exist for the risks associated with some antibiotics (e.g., aminoglycosides, ketolides, fluoroquinolones) and cardiovascular medications (e.g., class Ia antiarrhythmics, beta blockers). Apart from primarily autoimmune-mediated disorders of the NMJ, de novo myasthenic manifestations may also be triggered by medical treatments that induce an autoimmune reaction. Most notably, there is growing evidence that the immune checkpoint inhibitors (ICI), a modern class of drugs to treat various malignancies, represent a relevant risk factor to develop severe and progressive medication-induced myasthenia via an immune-mediated mechanism. From a clinical perspective, it is of utmost importance for the treating physicians to be aware of such adverse treatment effects and their consequences. In this article, we aim to summarize existing evidence regarding the key molecular and immunological mechanisms as well as the clinical implications of medication-aggravated and medication-induced myasthenic syndromes.

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“…234 Drug-induced disturbances of neuromuscular transmission usually resemble naturally occurring myasthenia gravis, with prominent extraocular muscle weakness and ptosis, and variable degrees of facial, bulbar, and generalized muscle weakness. Respiratory weakness may occur early and be severe.…”

Section: Disorders Characterized By Presynaptic Abnormalitymentioning

confidence: 99%

Disorders of neuromuscular transmission other than myasthenia gravis

Swift

1981

Muscle and Nerve

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Disorders of neuromuscular transmission in humans are caused by a wide variety of agents including systemic diseases, drugs, environmental toxins, animal envenomation, cations, and hormones. Some are genetically determined. Many are of known etiology. All such disorders interfere with one or more events in the sequence whereby a nerve impulse excites a muscle action potential. In many disorders of neuromuscular transmission, abnormal fatigue occurs, and some cases respond dramatically to treatment. Investigation of the microphysiology, microanatomy, and pharmacology of both normal and diseased neuromuscular junctions has increased our knowledge of these disorders.

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Masked Myasthenia Gravis

Cited by 17 publications

References 3 publications

Myasthenic Crisis

Myasthenic Crisis

Pathomechanisms and Clinical Implications of Myasthenic Syndromes Exacerbated and Induced by Medical Treatments

Disorders of neuromuscular transmission other than myasthenia gravis

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