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Relevant bibliographies by topics / Myasthenic

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Academic literature on the topic 'Myasthenic'

Author: Grafiati

Published: 4 June 2021

Last updated: 17 February 2022

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Journal articles on the topic "Myasthenic"

1

van Lunteren, Erik, Michelle Moyer, and Henry J. Kaminski. "Adverse effects of myasthenia gravis on rat phrenic diaphragm contractile performance." Journal of Applied Physiology 97, no. 3 (September 2004): 895–901. http://dx.doi.org/10.1152/japplphysiol.01266.2003.

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Myasthenia gravis has variable effects on the respiratory system, ranging from no abnormalities to life-threatening respiratory failure. Studies characterized diaphragm muscle contractile performance in rat autoimmune myasthenia gravis. Rats received monoclonal antibody that recognizes acetylcholine receptor determinants (or inactive antibody); 3 days later, phrenic nerve and diaphragm were studied in vitro. Myasthenic rats segregated into two groups, those with normal vs. impaired limb muscle function when tested in intact animals (“mild” and “severe” myasthenic). Baseline diaphragm twitch force was reduced for both severe ( P < 0.01) and mild ( P < 0.05) myasthenic compared with control animals (twitch force: normal 1,352 ± 140, mild myasthenic 672 ± 99, severe myasthenic 687 ± 74 g/cm2). However, only severe myasthenic diaphragm had impaired diaphragm endurance, based on significantly ( P < 0.05) accelerated rate of peak force decline during the initial period of stimulation (0.02 + 0.02, 0.03 ± 0.01, and 0.09 ± 0.01%/pulse for normal, mild myasthenic, and severe myasthenic, respectively, during continuous stimulation) and intratrain fatigue (up to 30.5 ± 7.4% intratrain force drop in severe myasthenic vs. none in normal and mild myasthenic, P < 0.01). Furthermore, compared with continuous stimulation, intermittent stimulation had a protective effect on force of severe myasthenic diaphragm (force after 2,000 pulses was 31.4 ± 2.0% of initial during intermittent stimulation vs. 13.0 ± 2.1% of initial during continuous stimulation, P < 0.01) but not on normal diaphragm. These data indicate that baseline force and fatigue may be affected to different extents by varying severity of myasthenia gravis and furthermore provide a mechanism by which alterations in breathing pattern may worsen respiratory muscle function in neuromuscular diseases.

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Saraiva, Paulo A. P., José Lamartine de Assis, and Paulo E. Marchiori. "Evaluation of the respiratory function in myasthenia gravis: an important tool for clinical feature and diagnosis of the disease." Arquivos de Neuro-Psiquiatria 54, no. 4 (December 1996): 601–7. http://dx.doi.org/10.1590/s0004-282x1996000400009.

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Myasthenic gravis may affect both inspiratory and expiratory muscles. Respiratory involvement occurred in almost all patients with myasthenia gravis in all clinical forms of the disease: 332 lung function tests done in 324 myasthenic patients without respiratory symptoms (age 34.6 ± 18.3 years) were examined. Lung volumes analysis showed that all the patients of both sexes with generalized or ocular myasthenia gravis showed "myasthenic pattern". Male patients with "ocular" form only presented the "myasthenic pattern" with lung impairment and had, from the lung function point of view, a more benign behaviour. Female patients with the "ocular" form exhibited a behaviour of respiratory variables similar to that of the generalized form. It was not observed modification of the variables that suggested obstruction of the higher airways. The "myasthenic pattern" was rarely observed in other neuromuscular diseases, except in patients with laryngeal stenosis.

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Kruglyakov, N. M., D. G. Levitova, G. I. Bagzhanov, K. K. Gubarev, S. S. Ochkin, O. V. Parinov, S. S. Petrikov, K. A. Popugaev, and A. S. Samoilov. "Application of the Technique of Extracorporeal Membrane Oxygenation in a Patient With Respiratory Distress Syndrome Associated With Myasthenia Gravis." Russian Sklifosovsky Journal "Emergency Medical Care" 10, no. 2 (August 24, 2021): 393–400. http://dx.doi.org/10.23934/2223-9022-2021-10-2-393-400.

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Myasthenia gravis is an autoimmune neuromuscular disease characterized by pathologically rapid fatigue of striated muscles [1]. The main symptom of myasthenia gravis is the presence of pathological muscle weakness with involvement of the ocular, bulbar and skeletal muscles in the pathological process. The provoking factors for the development of myasthenia gravis can be infectious diseases, surgery, drugs [2, 3]. The main danger is represented by myasthenic and cholinergic crises, which are characterized by a severe course and high mortality; therefore, the problems of treating myasthenia gravis are still of high medical and social significance. The prevalence of myasthenia gravis is 17.5–20.3 per 100 thousand population, and the number of patients is increasing by 5–10% annually [4, 5]. In recent years, there has been a steady increase in morbidity with an increase in age over 50 years [6, 7]. Myasthenia gravis is a serious disease with a high mortality rate of up to 30–40% [3]. There are difficulties in the early differential diagnosis of muscle weakness in patients with respiratory failure between myasthenia gravis, myasthenic syndrome and critical illness polyneuropathy. These difficulties and insufficient awareness of patients and doctors of various specialties about myasthenia gravis can lead to the choice of the wrong treatment tactics and the development of myasthenic crisis, which is manifested by respiratory failure, requiring respiratory support. The progression of respiratory failure against the background of myasthenic crisis may require the use of extracorporeal membrane oxygenation (ECMO).It is necessary to expand the differential diagnosis of muscle weakness in a patient during the period of resolution of respiratory failure, allowing to move away from compulsory respiratory support, termination of ECMO.

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Schroeter, Michael, Günther Thayssen, and Julia Kaiser. "Myasthenia Gravis – Exacerbation and Crisis." Neurology International Open 02, no. 01 (January 2018): E10—E15. http://dx.doi.org/10.1055/s-0043-118441.

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AbstractMyasthenic exacerbation and crisis are most critical incidences in myasthenia gravis. Even nowadays myasthenic crisis is a life-threatening condition, with a lethality of 2–3%. We review means of avoiding myasthenic exacerbation and crisis, elaborate on red flags and how to establish highly-active therapy in a timely manner. This includes the reasonable use of cholinesterase inhibitors, immunoadsorption or plasma exchange, as well as immunoglobulins and steroids. Immunosuppressive agents and monoclonal antibody therapy add to the therapeutic options.Intensive care of myasthenic patients includes the management of dysphagia and delirium. Importantly, the perioperative management of patients undergoing thymectomy and weaning are specific challenges in the treatment of myasthenic patients in the ICU.Establishing timely consequent immunosuppression and treatment of myasthenic patients in specialized outpatient centres help to avoid repetitive exacerbations and crises.

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5

Job, Anand, R. Raman, and C. Gnanamuthu. "Laryngeal stridor in myasthenia gravis." Journal of Laryngology & Otology 106, no. 7 (July 1992): 633–34. http://dx.doi.org/10.1017/s0022215100120390.

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AbstractTwo patients with laryngeal stridor secondary to myasthenia gravis are reported. The cause of bilateral abductor weakness in myasthenia is discussed; anticipation of the stridor in myasthenic patients is highlighted.

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Anand, Uttara Swati, Stalin Viswanathan, and Jayanthi Arulneyam. "Pulmonary Edema in Myasthenic Crisis." Case Reports in Critical Care 2013 (2013): 1–3. http://dx.doi.org/10.1155/2013/863620.

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We report a previously asymptomatic 50-year-old lady who came with myasthenic crisis as initial presentation of myasthenia gravis. She developed pulmonary edema following intravenous immunoglobulin administration and had ischemic changes in ECG and left ventricular dysfunction on echocardiography. She improved with diuretics, dobutamine, and fluid restriction alone. This is the first report in English-language medical literature describing the association between myasthenic crisis and likely takotsubo cardiomyopathy-related pulmonary edema following intravenous immunoglobulin administration.

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Itoh, Hironori, Keizo Shibata, Masahiro Yoshida, and Ken Yamamoto. "Neuromuscular Monitoring at the Orbicularis Oculi May Overestimate the Blockade in Myasthenic Patients." Anesthesiology 93, no. 5 (November 1, 2000): 1194–97. http://dx.doi.org/10.1097/00000542-200011000-00010.

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Background In most publications about myasthenia, monitoring neuromuscular blockade during anesthesia is recommended. In healthy patients, the relation of blockade between muscles has been established, but there is little information about the relation in myasthenic patients. Our objective was to investigate whether the relation between the orbicularis oculi and adductor pollicis muscles is the same in healthy patients and myasthenic patients. Methods After anesthesia was induced with 4-6 mg/kg thiopental and 2 microg/kg fentanyl, followed by 2% sevoflurane and 60% nitrous oxide in oxygen, 10 healthy patients and 10 myasthenic patients received 0. 025 and 0.01 mg/kg vecuronium, respectively. Neuromuscular monitoring was performed with use of accelerometry at the orbicularis oculi and the adductor pollicis muscles by stimulating the temporal branch of the facial nerve and the ulnar nerve. Results The relation of blockade between these two muscles was not the same in healthy patients and myasthenic patients: in healthy patients, the maximum neuromuscular blockade with 0.025 mg/kg vecuronium was less in the orbicularis oculi than in the adductor pollicis (median 72% vs. 91%; P < 0.05); in contrast, in myasthenic patients, the blockade with 0.01 mg/kg vecuronium was greater in the orbicularis oculi than in the adductor pollicis (median 96% vs. 62%; P < 0.05). Conclusion Neuromuscular monitoring at the orbicularis oculi may overestimate blockade in myasthenic patients. Extubation must be performed when the muscle most sensitive to neuromuscular blocking agents is recovered. Therefore, neuromuscular monitoring at the orbicularis oculi is recommended to avoid persistent neuromuscular blockade in patients with myasthenia gravis.

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Zaloum, A., JR Falet, A. Elkrief, and C. Chalk. "P.022 Myasthenia gravis following dabrafenib and trametinib for metastatic melanoma." Canadian Journal of Neurological Sciences / Journal Canadien des Sciences Neurologiques 46, s1 (June 2019): S19. http://dx.doi.org/10.1017/cjn.2019.122.

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Background: Inhibitors of BRAF and MEK, enzymes in the mitogen-activated protein kinase (MAPK) pathway, are now widely used in the treatment of metastatic melanoma. We report a case of acetylcholine receptor (AChR) antibody-positive myasthenia gravis developing after exposure to dabrafenib, a BRAF inhibitor, and trametinib, a MEK inhibitor. Methods: A 68-year-old man presented with dysarthria, dysphagia, cough, dyspnea, and fever. Examination revealed fatigable ptosis and proximal muscle weakness. He had started dabrafenib and trametinib for metastatic melanoma two weeks prior. He was diagnosed with myasthenia gravis and superimposed aspiration pneumonia. AChR antibodies were positive. Dabrafenib and trametinib were stopped. He improved rapidly with pyridostigmine alone, and remained free of myasthenic symptoms for the next two months. Another course of dabrafenib and trametinib was given, and seven weeks later, his myasthenic symptoms recurred. Pyridostigmine produced only partial improvement, and treatment with intravenous immunoglobulin and prednisone was initiated. Results: We are unaware of prior reports of an association between BRAF/MEK inhibitors and seropositive myasthenia gravis. The development of myasthenic symptoms twice after BRAF/MEK inhibitor exposure suggests that the association is more than coincidental. Conclusions: Myasthenia gravis may be a complication of treatment of melanoma with dabrafenib and trametinib. The mechanism by which this occurs is unknown.

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Souza, Paulo Victor Sgobbi de, Gabriel Novaes de Rezende Batistella, Valéria Cavalcante Lino, Wladimir Bocca Vieira de Rezende Pinto, Marcelo Annes, and Acary Souza Bulle Oliveira. "Clinical and genetic basis of congenital myasthenic syndromes." Arquivos de Neuro-Psiquiatria 74, no. 9 (September 2016): 750–60. http://dx.doi.org/10.1590/0004-282x20160106.

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ABSTRACT Neuromuscular junction disorders represent a wide group of neurological diseases characterized by weakness, fatigability and variable degrees of appendicular, ocular and bulbar musculature involvement. Its main group of disorders includes autoimmune conditions, such as autoimmune acquired myasthenia gravis and Lambert-Eaton syndrome. However, an important group of diseases include congenital myasthenic syndromes with a genetic and sometimes hereditary basis that resemble and mimick many of the classic myasthenia neurological manifestations, but also have different presentations, which makes them a complex clinical, therapeutic and diagnostic challenge for most clinicians. We conducted a wide review of congenital myasthenic syndromes in their clinical, genetic and therapeutic aspects.

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Benatar, M. "Myasthenia Gravis and Myasthenic Disorders." Neurology 81, no. 1 (July 1, 2013): 99. http://dx.doi.org/10.1212/wnl.0b013e318297ef4d.

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Dissertations / Theses on the topic "Myasthenic"

1

Carr, A. S. "An epidemiological study of myasthenia gravis and congenital myasthenic syndromes in Northern Ireland." Thesis, Queen's University Belfast, 2012. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.546021.

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Abdelgany, Amr. "Gene therapy for congenital myasthenic syndromes." Thesis, University of Oxford, 2005. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.441062.

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Finlayson, Sarah E. "Congenital myasthenic syndromes : current diagnostic and therapeutic aspects." Thesis, University of Oxford, 2014. http://ora.ox.ac.uk/objects/uuid:5e08ab86-8a20-48b3-86b9-683eb8b2c6e4.

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Zoltowska, Katarzyna Marta. "Novel pathogenic mechanisms of myasthenic disorders and potential therapeutic approaches." Thesis, University of Oxford, 2014. http://ora.ox.ac.uk/objects/uuid:e817f50a-0318-4944-bf67-773af523c4c3.

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Congenital myasthenic syndrome (CMS) and myasthenia gravis (MG) are, respectively, inherited or autoimmunological disorders caused by aberrant neuromuscular transmission, which manifests as fatiguable muscle weakness. A novel subtype of CMS, resulting from mutations in GFPT1 and characterised by a limb girdle pattern of muscle weakness, has been described. The gene encodes L glutamine:D fructose-6-phosphate amidotransferase 1 (GFAT1) – a key rate limiting enzyme in the hexosamine biosynthetic pathway, providing building blocks for glycosylation of proteins and lipids. The research focused on the molecular bases of the CMS resulting from mutations in the ubiquitously expressed gene, but with symptoms largely restricted to the neuromuscular junction (NMJ). The work has established a link between the NMJ and GFPT1 CMS by demonstrating that the AChR cell surface is decreased in GFPT1 patient muscle cells and in GFPT1-silenced cell lines. The decrease is likely to be caused by reduced steady-state levels of individual AChR α, δ and ε, but not β, subunits. To optimise treatment for myasthenic disorders, a comparative in vivo trial of therapy with pyridostigmine bromide and salbutamol sulphate, and pyridostigmine bromide alone, was conducted. Supplementation of the AChE inhibitor-based therapy with the β2-adrenergic receptor agonist had a beneficial effect. This offers promise for more effective treatments for CMS and MG affected individuals. Molecular causes of MG were also investigated. The search for novel antibody targets was conducted with the use of a designed cell-based assay for the detection of anti COLQ autoimmunoglobulins in MG patient sera. The antibodies were detected in 24 out of 418 analysed samples, but their pathogenicity has not been determined.

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Cheung, Jonathan Yu. "Pathogenic mechanisms of RAPSN mutations in congenital myasthenic syndromes." Thesis, University of Oxford, 2015. https://ora.ox.ac.uk/objects/uuid:c343ca03-563e-4b4a-9e35-aac09bfc5ea7.

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Rapsyn is essential for clustering acetylcholine receptors (AChR) at the neuromuscular junction (NMJ). Congenital myasthenic syndrome (CMS) due to RAPSN mutations compromises neuromuscular transmission through a deficiency of AChR at the NMJ. RAPSN-CMS is autosomal recessive, and most patients harbour a common mutation p.Asn88Lys. A definitive genetic diagnosis for patients who do not carry the p.Asn88Lys allele can be challenging. In this thesis 10 novel variants in RAPSN are shown to impair AChR clustering in vitro, and are thus defined as pathogenic. The properties of RAPSN mutations p.Val45M, p.Asn88Lys, p.Arg91Leu and p.Ala153Thr were studied and were found to be diverse, though common mechanisms were found to underlie the AChR deficiency. The mutations reduce the stability of rapsyn and the stability of AChR-rapsyn clusters formed on cultured myotubes. A unique missense mutation in the AChR d-subunit encoding gene, p.Glu381Lys, phenotypically mimics RAPSN-CMS, and investigations revealed that this mutation also causes instability of the AChR clusters. Salbutamol, a medication that is believed to stabilise NMJ, has recently been found to benefit AChR deficiency patients when used in combination with pyridostigmine. However, the mode of action of salbutamol at the NMJ is undefined. A pilot study was performed to evaluate the efficacy and mechanism of salbutamol therapy in a mouse model of AChR deficiency. Methodologies were established for the analysis of the effects of salbutamol and will provide the basis for a more detailed study of its beneficial action in disorders of neuromuscular transmission.

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Issop, Yasmin. "A GFPT1 deficient mouse model of congenital myasthenic syndrome." Thesis, University of Newcastle upon Tyne, 2017. http://hdl.handle.net/10443/3902.

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Congenital myasthenic syndromes (CMS) are inherited disorders characterised by fatigable muscle weakness resulting from impaired transmission at the neuromuscular junction (NMJ). CMS occur due to mutations in genes encoding proteins responsible for maintaining the structure and function of the NMJ. Glutamine-fructose-6-phosphate transaminase 1 (GFPT1) is the rate-limiting enzyme in the hexosamine biosynthetic pathway which yields precursors required for protein and lipid glycosylation. Mutations in GFPT1 and genes downstream of this pathway are pathogenic for CMS. One hypothesis is that hypoglycosylation of NMJ proteins results in defective neurotransmission. The aim of this study is to generate and characterise a GFPT1 deficient mouse model of CMS. One of the challenges we face is the viability of Gfpt1 knockout mice. Here we generate a novel muscle-specific GFPT1 knockout mouse model using Cre/loxP technology. We demonstrate that a deficiency of GFPT1 in muscle only, is sufficient for causing a CMS phenotype. Our model recapitulates many aspects of the phenotype observed in patients with GFPT1-related CMS. Mutant mice display early changes in the morphology of postsynaptic components of the NMJ, which are accompanied by presynaptic alterations. They later develop a myopathic phenotype and formation of tubular aggregates. We further identify proteins in skeletal muscle that are differentially regulated because of GFPT1 deficiency. Our data demonstrates a critical role for GFPT1 in the development of the NMJ, neurotransmission, and skeletal muscle integrity. The muscle-specific GFPT1 deficient mouse model allows us to investigate the implications of not only GFPT1 mutations, but may also give us an insight into the pathophysiological consequences of mutations in genes downstream of GFPT1, which also result in hypoglycosylation. This model has the potential to enhance our understanding of current drug therapies, and to drive forward the development of new compounds which can be implemented in the clinic.

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Chaouch, Amina. "The clinical and genetic characteristics of congenital myasthenic syndromes." Thesis, University of Newcastle upon Tyne, 2014. http://hdl.handle.net/10443/2748.

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Congenital myasthenic syndromes (CMS) are inherited disorders in which the safety margin of the neuromuscular transmission is compromised. The clinical hallmark of CMS is fatigable weakness. To date, nineteen genes have been implicated in causing this disorder, with most mutations located in postsynaptic proteins. Nevertheless, a great proportion of patients remains with no molecular diagnosis and cannot therefore access optimum therapy. In this thesis, each topic is summarized in one chapter that corresponds to one or part of a selected journal publication, or a book chapter. Chapter 1 is dedicated to the review of our current understanding of the different CMS subgroups based on their underlying molecular defects. Chapter 2 focuses on the methodology used to acquire the data described in the subsequent chapters. Chapter 3 reports on the mutation distribution, clinical features and genotype phenotype correlation of CMS patients referred to one of the largest CMS diagnostic centres worldwide. The phenotype genotype correlation and response to treatment in specific CMS subgroups are refined in chapters 4 and 5, including slow channel CMS and GFPT1 associated CMS respectively. Chapter 6 focuses on the selection strategy of an undiagnosed CMS cohort for whole exome sequencing and reports on the candidate variants identified. Finally, in chapter 7 and 8, detailed clinical and biological data are shown to demonstrate the pathogenicity of novel AGRN and SLC25A1 mutations identified using next generation sequencing.

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Childs, Lisbeth Ann. "The effects of myasthenic serum on skeletal muscle cells in culture." Thesis, University of Bath, 1985. https://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.484407.

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Rat muscle cells were grown in culture for use as an experimental model in which to study the myolytic effects of myasthenic serum in vitro. Use was made of a procedure which depends upon the selective uptake of tritium-labelled carnitine by cultured myotubes, loss of which can be monitored following cytolytic damage. The studies demonstrated that heat-inactivated myasthenic serum samples caused myotube-specific lysis in a manner that was dependent on the addition of complement. The concentration and activity of the complement source was shown to be a major factor in detecting myotoxicity. Using optimised assay conditions, a myotoxicity study was carried out using a range of normal and myasthenic serum samples. In the presence of guinea-pig complement, heat-inactivated serum samples from 9 out of 13 myasthenic patients showed clear rnyotoxicity in contrast to 0 out of 12 normal controls and 0 out of 6 polymyositis patients. Neither heat-inactivated sera alone nor guinea-pig complement alone showed myotoxicity. A further study defined new conditions under which previously 'non-toxic' myasthenic serum samples demonstrated myotoxicity. Removal of anti-AChR antibodies from a myasthenic serum sample by affinity absorption led to a loss of complement-mediated myotoxicity. Finally, studies were carried out in which IgG or IgG depleted of subclass 3, was purified from myasthenic serum samples and tested for complement-mediated myotoxicity. The IgG fractions caused myotoxicity in a similar manner to the whole serum. The studies were extended to human foetal muscle cells in culture which were shown to be less mature than the cultured rat muscle cells in this study. Attempts were made to define optimal growth conditions for the human foetal muscle cells vitro but these were inconclusive. Comparable complement-mediated myotoxicity by myasthenic serum towards human muscle cultures was not shown. However, manipulation of assay conditions resulted in clear myotoxicity by the 2 myasthenic serum samples tested, relative to normal controls. The results gained from this work support the suggestion that complement-mediated cell damage, initiated by anti-AChR antibodies, may contribute to post-synaptic membrane degeneration in myasthenia gravis.

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Nichols, Philip Paul. "Transcriptional regulation of the human nicotinic acetylcholine receptor." Thesis, University of Oxford, 1999. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.326016.

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Pinto, Ashwin. "Specificity of autoantibodies in Lambert-Eaton myasthenic syndrome for neuronal calcium channels." Thesis, University of Oxford, 2000. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.342539.

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Books on the topic "Myasthenic"

1

Jones, Dominic. Antibodies against the voltage-gated calcium channel in Lambert-Eaton myasthenic syndrome. Oxford: Oxford Brookes University, 2000.

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2

Baets, M. H. De, 1950-, Oosterhuis, Henricus Josephus Gerardus Hubertus., and Toyka K. V. 1945-, eds. Myasthenia gravis. Basel: Karger, 1988.

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3

Christadoss, Premkumar, ed. Myasthenia Gravis. Dordrecht: Springer Netherlands, 2000. http://dx.doi.org/10.1007/978-94-011-4060-7.

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Giovanni, Giacalone. Contributo della pranoterapia nella myasthenia gravis =: Pranotherapy help in the myasthenia gravis. Vercelli: Edizioni G. & G., 1986.

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service), SpringerLink (Online, ed. Myasthenia Gravis and Related Disorders. Totowa, NJ: Humana Press, 2009.

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6

Kaminski, Henry J. Myasthenia Gravis and Related Disorders. Totowa, NJ: Humana Press, 2009. http://dx.doi.org/10.1007/978-1-59745-156-7.

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Kaminski, Henry J., ed. Myasthenia Gravis and Related Disorders. Totowa, NJ: Humana Press, 2003. http://dx.doi.org/10.1007/978-1-59259-341-5.

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Kaminski, Henry J., and Linda L. Kusner, eds. Myasthenia Gravis and Related Disorders. Cham: Springer International Publishing, 2018. http://dx.doi.org/10.1007/978-3-319-73585-6.

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Kaminski, Henry J. Myasthenia Gravis and Related Disorders. New Jersey: Humana Press, 2002. http://dx.doi.org/10.1385/1592593410.

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Giacalone, Giovanni. Pranotherapy help in the myasthenia gravis. Vercelli: [s.n.], 1986.

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Book chapters on the topic "Myasthenic"

1

Swash, Michael, and Martin S. Schwartz. "Myasthenia Gravis and Other Myasthenic Syndromes." In Neuromuscular Diseases, 257–83. London: Springer London, 1997. http://dx.doi.org/10.1007/978-1-4471-3834-1_12.

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2

Swash, Michael, and Martin Schwartz. "Myasthenia Gravis and Other Myasthenic Syndromes." In Neuromuscular Diseases, 229–50. London: Springer London, 1988. http://dx.doi.org/10.1007/978-1-4471-3526-5_12.

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3

Oette, Mark, Marvin J. Stone, Hendrik P. N. Scholl, Peter Charbel Issa, Monika Fleckenstein, Steffen Schmitz-Valckenberg, Frank G. Holz, et al. "Myasthenic Syndrome." In Encyclopedia of Molecular Mechanisms of Disease, 1395. Berlin, Heidelberg: Springer Berlin Heidelberg, 2009. http://dx.doi.org/10.1007/978-3-540-29676-8_9280.

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Janjua, Nazli, and Stephan A. Mayer. "Myasthenic Crisis." In Critical Care Neurology and Neurosurgery, 469–80. Totowa, NJ: Humana Press, 2004. http://dx.doi.org/10.1007/978-1-59259-660-7_26.

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5

Bensard, Denis D., Philip F. Stahel, Jorge Cerdá, Babak Sarani, Sajid Shahul, Daniel Talmor, Peter M. Hammer, et al. "Myasthenic Crisis." In Encyclopedia of Intensive Care Medicine, 1478. Berlin, Heidelberg: Springer Berlin Heidelberg, 2012. http://dx.doi.org/10.1007/978-3-642-00418-6_1910.

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Toyka, Klaus V., Wolfgang Müllges, and Daniel F. Hanley. "Myasthenia gravis and Lambert-Eaton Myasthenic Syndrome." In Neurocritical Care, 807–15. Berlin, Heidelberg: Springer Berlin Heidelberg, 1994. http://dx.doi.org/10.1007/978-3-642-87602-8_71.

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7

Muley, Suraj A., and Christopher M. Gomez. "Congenital Myasthenic Syndromes." In Myasthenia Gravis and Related Disorders, 309–26. Totowa, NJ: Humana Press, 2003. http://dx.doi.org/10.1007/978-1-59259-341-5_14.

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Beeson, David. "Congenital Myasthenic Syndromes." In Myasthenia Gravis and Related Disorders, 251–74. Cham: Springer International Publishing, 2018. http://dx.doi.org/10.1007/978-3-319-73585-6_16.

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Kaminski, Henry J., and Robert L. Ruff. "The Myasthenic Syndromes." In Molecular Biology of Membrane Transport Disorders, 565–93. Boston, MA: Springer US, 1996. http://dx.doi.org/10.1007/978-1-4613-1143-0_28.

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Engel, A. G., K. Ohno, and A. A. Stans. "Congenital Myasthenic Syndromes." In Monographs in Clinical Neuroscience, 96–112. Basel: KARGER, 2000. http://dx.doi.org/10.1159/000061631.

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Conference papers on the topic "Myasthenic"

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Pickens, A. W., and M. C. Miles. "Nivolumab Toxicity: Myasthenic Crisis and Myocarditis." In American Thoracic Society 2019 International Conference, May 17-22, 2019 - Dallas, TX. American Thoracic Society, 2019. http://dx.doi.org/10.1164/ajrccm-conference.2019.199.1_meetingabstracts.a4837.

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Ashhurst, Jasmine, Rami Haddad, and Rob Zielinski. "062 Pembrolizumab induced lambert-eaton myasthenic syndrome." In ANZAN Annual Scientific Meeting 2021 Abstracts. BMJ Publishing Group Ltd, 2021. http://dx.doi.org/10.1136/bmjno-2021-anzan.62.

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Lochmüller, H. "Update on inherited neuromuscular transmission disorders (congenital myasthenic syndromes)." In 24. Kongress des Medizinisch-Wissenschaftlichen Beirates der Deutschen Gesellschaft für Muskelkranke (DGM) e.V. Georg Thieme Verlag KG, 2019. http://dx.doi.org/10.1055/s-0039-1684994.

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Rizzo, A. N., A. Gupta, P. Hume, and T. M. Bull. "Lambert Eaton Myasthenic Syndrome Presenting as Hypoventilation-Induced Right Heart Dysfunction." In American Thoracic Society 2020 International Conference, May 15-20, 2020 - Philadelphia, PA. American Thoracic Society, 2020. http://dx.doi.org/10.1164/ajrccm-conference.2020.201.1_meetingabstracts.a3768.

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Henrich, Maria, Burcin Ceylan, Adela Marina, Angela Abicht, Heike Kölbel, and Ulrike Schara. "P 409. The Noonan’s Syndrome as a Differential Diagnosis of a Congenital Myasthenic Syndrome." In Abstracts of the 44th Annual Meeting of the Society for Neuropediatrics. Georg Thieme Verlag KG, 2018. http://dx.doi.org/10.1055/s-0038-1675966.

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Moreno, FJ García, MS Pernia Lopez, and M. Sanjurjo Saez. "3PC-027 Amifampridine and pyridostigmine hard capsules for treatment of congenital myasthenic syndromes: a case report." In Abstract Book, 23rd EAHP Congress, 21st–23rd March 2018, Gothenburg, Sweden. British Medical Journal Publishing Group, 2018. http://dx.doi.org/10.1136/ejhpharm-2018-eahpconf.79.

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Wu, D., D. Condit, and J. C. Nascimento. "Pembrolizumab Induced Myasthenia Gravis." In American Thoracic Society 2021 International Conference, May 14-19, 2021 - San Diego, CA. American Thoracic Society, 2021. http://dx.doi.org/10.1164/ajrccm-conference.2021.203.1_meetingabstracts.a2408.

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Malladi, S., A. Aburahma, L. Rashdan, and K. Ranabhat. "The Many Faces of Myasthenia Gravis." In American Thoracic Society 2019 International Conference, May 17-22, 2019 - Dallas, TX. American Thoracic Society, 2019. http://dx.doi.org/10.1164/ajrccm-conference.2019.199.1_meetingabstracts.a2296.

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Liang, T., M. I. Boulos, B. J. Murray, S. Krishnan, H. Katzberg, and K. Umapathy. "Detection of myasthenia gravis using electrooculography signals." In 2016 38th Annual International Conference of the IEEE Engineering in Medicine and Biology Society (EMBC). IEEE, 2016. http://dx.doi.org/10.1109/embc.2016.7590845.

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Ceylan, Kenan Can, Seyda Ors Kaya, Ozgur Ozturk, Yasar Zorlu, and Muhtesem Gedizlioglu. "Minimally Invasive Thymectomy in Non-Thymomatous Myasthenia Gravis Cases." In ERS International Congress 2017 abstracts. European Respiratory Society, 2017. http://dx.doi.org/10.1183/1393003.congress-2017.pa2056.

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Reports on the topic "Myasthenic"

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Asenova, Asya, and Veneta Bojinova. Juvenile Myasthenia Gravis - Clinical Course and Serologic Tests. "Prof. Marin Drinov" Publishing House of Bulgarian Academy of Sciences, December 2020. http://dx.doi.org/10.7546/crabs.2020.12.17.

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Xie, Rongfang, Liting Liu, Ruiqi Wang, and Chunhua Huang. Traditional Chinese medicine for Myasthenia gravis: study protocol for a network meta-analysis. INPLASY - International Platform of Registered Systematic Review and Meta-analysis Protocols, June 2020. http://dx.doi.org/10.37766/inplasy2020.6.0049.

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Huang, Chunhua, Rongfang Xie, Liting Liu, and Ruiqi Wang. Efficacy and safety of Buzhong-Yiqi Decoction for Myasthenia gravis：study protocol for a systematic review. INPLASY - International Platform of Registered Systematic Review and Meta-analysis Protocols, May 2020. http://dx.doi.org/10.37766/inplasy2020.5.0080.

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Peng, Yuxuan, Lu Li, Yuting Pan, Bibo Lu, Qing Ye, Min He, Weiyin Chen, and Xueping Yang. External treatment of Traditional Chinese Medicine for myasthenia gravis: a protocol for systematic review and meta-analysis. INPLASY - International Platform of Registered Systematic Review and Meta-analysis Protocols, January 2021. http://dx.doi.org/10.37766/inplasy2021.1.0083.

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Li, Lu, Jiachun Lu, BiBo Lu, Yuxuan Peng, Yuting Pan, Qing Ye, Min He, et al. Tonifying Spleen and Replenishing Kidney method of Traditional Chinese Medicine for myasthenia gravis: a protocol for systematic review and meta-analysis. INPLASY - International Platform of Registered Systematic Review and Meta-analysis Protocols, January 2021. http://dx.doi.org/10.37766/inplasy2021.1.0097.

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Surgery to remove the thymus gland improves weakness for people with myasthenia gravis. National Institute for Health Research, October 2016. http://dx.doi.org/10.3310/signal-000310.

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