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Journal articles on the topic 'Myasthenic'

Author: Grafiati

Published: 4 June 2021

Last updated: 17 February 2022

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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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2

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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3

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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4

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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6

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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7

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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8

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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9

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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10

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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11

Kostera-Pruszczyk, A. "Myasthenia gravis and myasthenic syndromes." European Journal of Paediatric Neurology 12 (May 2008): S17. http://dx.doi.org/10.1016/s1090-3798(08)70056-4.

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12

Karachunski, P. "CONGENITAL MYASTHENIC SYNDROMES AND MYASTHENIA." Neuromuscular Disorders 28 (October 2018): S47. http://dx.doi.org/10.1016/j.nmd.2018.06.084.

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13

García Erro, M., E. Cavassa, J. Muntadas, M. Pauni, and G. Vázquez. "CONGENITAL MYASTHENIC SYNDROMES AND MYASTHENIA." Neuromuscular Disorders 28 (October 2018): S47—S48. http://dx.doi.org/10.1016/j.nmd.2018.06.085.

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14

Rugiero, M., V. Salutto, V. Alvarez, M. Bettini, N. Genco, and C. Mazia. "CONGENITAL MYASTHENIC SYNDROMES AND MYASTHENIA." Neuromuscular Disorders 28 (October 2018): S48. http://dx.doi.org/10.1016/j.nmd.2018.06.086.

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15

de Meel, R., K. Keene, M. Tannemaat, and J. Verschuuren. "CONGENITAL MYASTHENIC SYNDROMES AND MYASTHENIA." Neuromuscular Disorders 28 (October 2018): S48. http://dx.doi.org/10.1016/j.nmd.2018.06.087.

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16

Vajsar, J., H. Katzberg, H. Qashqari, N. Chrestian, and I. Narang. "CONGENITAL MYASTHENIC SYNDROMES AND MYASTHENIA." Neuromuscular Disorders 28 (October 2018): S48. http://dx.doi.org/10.1016/j.nmd.2018.06.088.

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17

Rugiero, M., M. Bettini, F. Silveira, F. Sosa Albacete, and S. Christiansen. "CONGENITAL MYASTHENIC SYNDROMES AND MYASTHENIA." Neuromuscular Disorders 28 (October 2018): S48—S49. http://dx.doi.org/10.1016/j.nmd.2018.06.089.

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18

Ho, S., J. So, and D. Bae. "CONGENITAL MYASTHENIC SYNDROMES AND MYASTHENIA." Neuromuscular Disorders 28 (October 2018): S49. http://dx.doi.org/10.1016/j.nmd.2018.06.090.

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19

So, J., S. Ho, and D. Bae. "CONGENITAL MYASTHENIC SYNDROMES AND MYASTHENIA." Neuromuscular Disorders 28 (October 2018): S49. http://dx.doi.org/10.1016/j.nmd.2018.06.091.

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20

Louet, E., S. Misdrahi, C. Orblin Bedos, S. Birnbaum, JR Hogrel, P. Portero, B. Clair, et al. "CONGENITAL MYASTHENIC SYNDROMES AND MYASTHENIA." Neuromuscular Disorders 28 (October 2018): S49. http://dx.doi.org/10.1016/j.nmd.2018.06.092.

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21

Zhang, Y., R. Ban, H. Liu, C. Pu, and Q. Shi. "CONGENITAL MYASTHENIC SYNDROMES AND MYASTHENIA." Neuromuscular Disorders 28 (October 2018): S49—S50. http://dx.doi.org/10.1016/j.nmd.2018.06.093.

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22

Eymard, B., D. Sternberg, M. Mayer, T. Stojkovic, E. Fournier, S. Nicole, A. Behin, et al. "CONGENITAL MYASTHENIC SYNDROMES AND MYASTHENIA." Neuromuscular Disorders 28 (October 2018): S50. http://dx.doi.org/10.1016/j.nmd.2018.06.094.

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23

Shen, X., D. Selcen, J. Brengman, S. Shen, H. Durmus, V. Preethish-Kumar, A. Yuceyar, et al. "CONGENITAL MYASTHENIC SYNDROMES AND MYASTHENIA." Neuromuscular Disorders 28 (October 2018): S50. http://dx.doi.org/10.1016/j.nmd.2018.06.095.

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24

Estephan, E., A. Zambon, P. Marchiori, A. Silva, C. Moreno, U. Reed, A. Töpf, H. Lochmüller, and E. Zanoteli. "CONGENITAL MYASTHENIC SYNDROMES AND MYASTHENIA." Neuromuscular Disorders 28 (October 2018): S50. http://dx.doi.org/10.1016/j.nmd.2018.06.096.

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25

Coppens, S., G. Glibert, and N. Deconinck. "CONGENITAL MYASTHENIC SYNDROMES AND MYASTHENIA." Neuromuscular Disorders 28 (October 2018): S51. http://dx.doi.org/10.1016/j.nmd.2018.06.097.

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26

Gidaro, T., L. Vandenbrande, E. Malfatti, C. Labasse, P. Carlier, N. Romero, L. Servais, and J. Böhm. "CONGENITAL MYASTHENIC SYNDROMES AND MYASTHENIA." Neuromuscular Disorders 28 (October 2018): S51. http://dx.doi.org/10.1016/j.nmd.2018.06.098.

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27

Jonsrud, C., P. Aden, G. Hansen, M. Mork, B. Nygård, T. Popperud, M. Rasmussen, N. Songstad, K. Ørstavik, and T. Fagerheim. "CONGENITAL MYASTHENIC SYNDROMES AND MYASTHENIA." Neuromuscular Disorders 28 (October 2018): S51. http://dx.doi.org/10.1016/j.nmd.2018.06.099.

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28

Rodriguez Cruz, P., J. Palace, and D. Beeson. "CONGENITAL MYASTHENIC SYNDROMES AND MYASTHENIA." Neuromuscular Disorders 28 (October 2018): S51—S52. http://dx.doi.org/10.1016/j.nmd.2018.06.100.

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29

Balaraju, S., A. Töpf, P. Veeramani, S. Vengalil, K. Polavarapu, S. Nashi, J. Kirschner, R. Horvath, N. Atchayaram, and H. Lochmüller. "CONGENITAL MYASTHENIC SYNDROMES AND MYASTHENIA." Neuromuscular Disorders 28 (October 2018): S52. http://dx.doi.org/10.1016/j.nmd.2018.06.101.

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30

Munell, F., D. Gomez-Andrés, L. Costa Comellas, A. Macaya, M. Gratacós, M. Dusl, J. Senderek, and H. Lochmüller. "CONGENITAL MYASTHENIC SYNDROMES AND MYASTHENIA." Neuromuscular Disorders 28 (October 2018): S52. http://dx.doi.org/10.1016/j.nmd.2018.06.102.

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31

Selby, V., G. Ramdharry, M. Hanna, and F. Muntoni. "CONGENITAL MYASTHENIC SYNDROMES AND MYASTHENIA." Neuromuscular Disorders 28 (October 2018): S52. http://dx.doi.org/10.1016/j.nmd.2018.06.103.

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32

Vacca, Vincent M. "Myasthenia gravis and myasthenic crisis." Nursing Critical Care 12, no. 5 (September 2017): 38–46. http://dx.doi.org/10.1097/01.ccn.0000521932.75838.5c.

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33

Sanders, Donald B. "Myasthenia gravis and myasthenic disorders." Annals of Neurology 48, no. 5 (November 2000): 820. http://dx.doi.org/10.1002/1531-8249(200011)48:5<820::aid-ana24>3.0.co;2-q.

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34

Antozzi, C. "Myasthenia gravis and myasthenic syndrome." Neurological Sciences 24 (October 1, 2003): s260—s263. http://dx.doi.org/10.1007/s10072-003-0091-5.

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35

Lobzin, S. V., M. G. Sokolova, V. A. Shavurov, and A. A. Zuev. "EMERGENCY CARE OF CRISIS CONDITIONS IN MYASTHENIA GRAVIS." EMERGENCY MEDICAL CARE 20, no. 2 (June 4, 2019): 25–30. http://dx.doi.org/10.24884/2072-6716-2019-20-2-25-30.

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The article presents an analysis of current data on emergency management of crises in patients with myasthenia gravis, which is supplemented by our own observations of 892 patients with myasthenia gravis. A follow-up study was conducted, which helped us to assess the frequency, nature and course of crises in patients with myasthenia gravis, taking into account the form of the disease, sex and age of patients. It was found that crises were observed in 154 (17.4%) patients, these conditions were significantly more often registered at the age of 20 to 40 and in the first three years of the disease. Myasthenic crises 149 (96.9%) prevailed among the crises and were registered mainly in patients with generalized and pharyngeal-facial myasthenia. Based on long-term follow-up of patients and assessment of the results of emergency management of myasthenic crises we have presented an optimal scheme for prescription of anticholinesterase medicines as a part of combined therapy of crises of varying severity.

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36

Ashjazadeh, Nahid, Maryam Sharifian Dorche, Soheila Zareifar, Masood Nomovi, and Amirhossein Sharian Dorche. "Rare Coexistence of Myasthenia Gravis and Lambert-Eaton Myasthenic Syndrome with Adenocarcinoma of the Bladder: A Case Report." Internal Medicine and Medical Investigation Journal 2, no. 4 (October 5, 2017): 171. http://dx.doi.org/10.24200/imminv.v2i4.71.

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Abstract Introduction: The coexistence of myasthenia gravis and Lambert-Eaton myasthenic syndrome (LEMS) is very rare.Case report: Herein we report an 82 year old man a known case of adenocarcinoma of bladder who came with ptosis in left eye, diplopia, and dysphagia, weakness of both lower extremities and autonomic dysfunction. According to history, physical examination and para clinical work ups coexisting of myasthenia gravis and LEMS was diagnosed.Discussion: our patient is the first patient with Overlap myasthenic syndrome on the base of adenocarcinoma of bladder. The purpose of this case report is to emphasize on this fact that a patient with LEMS should be evaluate carefully for detecting underlying malignancies. Although in the most cases the origin is lung, extra pulmonary origin such as urinary system should be evaluate carefully too.

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37

Ciafaloni, Emma. "Myasthenia Gravis and Congenital Myasthenic Syndromes." CONTINUUM: Lifelong Learning in Neurology 25, no. 6 (December 2019): 1767–84. http://dx.doi.org/10.1212/con.0000000000000800.

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38

Sharp, H. R., A. Degrip, D. B. Mitchell, and A. Heller. "Bulbar presentations of myasthenia gravis in the elderly patient." Journal of Laryngology & Otology 115, no. 1 (January 2001): 1–3. http://dx.doi.org/10.1258/0022215011906740.

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We report on three cases of patients whose primary symptoms of myasthenia gravis were related to the upper aerodigestive tract. Symptoms had been present unrecognized in all patients for up to three years, and one patient subsequently developed a myasthenic crisis. We highlight the clinical features of myasthenia gravis to allow its prompt recognition in patients presenting to the ENT surgeon or physician.

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39

Ho, Stacey, and Antonio Liu. "A Co-Occurrence of Serologically Proven Myasthenia Gravis and Pharyngeal-Cervical-Brachial Variant of Guillain-Barré Syndrome." Case Reports in Neurological Medicine 2019 (April 8, 2019): 1–3. http://dx.doi.org/10.1155/2019/4695010.

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We report on a co-occurrence case of ocular myasthenia gravis with exacerbation leading to myasthenic crisis in addition to pharyngeal-cervical-brachial variant of Guillain–Barré syndrome in a patient with severe oropharyngeal dysphagia and acute respiratory failure.

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40

Garcia, Catherine R., Jessica N. Cox, and John L. Villano. "Myasthenia gravis and Guillain-Barré syndrome adverse events with immune checkpoint inhibitors." Journal of Clinical Oncology 36, no. 5_suppl (February 10, 2018): 37. http://dx.doi.org/10.1200/jco.2018.36.5_suppl.37.

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37 Background: Immune checkpoint inhibitors (ICI) have provided landmark breakthrough achieving success in prolonging survival in multiple cancer types. As a new class of therapy immune related serious adverse drug reactions (sADRs) have had limited reporting. This includes neurologic based, with reports limited to clinical trials and case-based. Ours is the largest database analysis to date reporting neurological adverse events after ICI therapy. Methods: We analyzed the FDA Adverse Event Reporting System (FAERS) database for pembrolizumab, atezolizumab, nivolumab, and ipilimumab two years prior their FDA approval to September 2017, to include all cases reported with Guillain-Barré syndrome (GBS), Myasthenia gravis, ocular myasthenia, and myasthenic syndrome after the usage of ICI. Results: A total 35,726 cases were reported in FAERS. We identified a total of 263 cases of which 121 (46%) were GBS, 112 (42.6%) myasthenia gravis, 22 myasthenic syndrome (8.4%), and 8 (3%) ocular myasthenia. The mean age in our study was 66 years, with 63% being male. The majority of the cases were reported in the United States (49%), followed by Japan (10%), France (6%), and Australia (5.7%). Over 30% of patients presented more than one significant symptom. Around 20% of these patients were taking more than one immune checkpoint inhibitor, combining ipilimumab with either nivolumab or pembrolizumab. A significantly higher proportion of patients with GBS taking more than one ICI (28.1%, p = 0.013). Nivolumab was the most common ICI in patients with myasthenia gravis, myasthenic syndrome, and ocular myasthenia, while ipilimumab was the most common in patients with GBS. Sixty four percent of these patients required hospitalization, 17% were reported as life threatening events, 7% resulted in disability, and 22% died. Conclusions: Neurological adverse events associated with ICI are relatively uncommon, but can have serious clinical consequences. Recognizing and detailing neurological immune syndromes in relation to ICI therapy are essential in the oncological and neurological practice due to the growing usage of these agents in cancer treatment.

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41

Cetin, Hakan, and Angela Vincent. "Pathogenic Mechanisms and Clinical Correlations in Autoimmune Myasthenic Syndromes." Seminars in Neurology 38, no. 03 (June 2018): 344–54. http://dx.doi.org/10.1055/s-0038-1660500.

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AbstractAutoimmune myasthenic syndromes are antibody-mediated disorders of the neuromuscular junction. Common antigenic targets are the acetylcholine receptor or muscle specific kinase (MuSK) in myasthenia gravis (MG) and the voltage-gated calcium channel in Lambert-Eaton myasthenic syndrome. There is evidence that antibodies directed against other antigens such as low-density lipoprotein receptor-related protein 4 (LRP4) are also involved in MG. The mechanisms by which various antibodies exert their pathogenic effect depend on the IgG subclass and also the epitope location on the antigens. These mechanisms are partly heterogeneous and include antigen degradation, complement activation, direct functional blocking, or disruption of protein–protein interactions. The neuromuscular junction is characterized by a structural and functional plasticity that is able to compensate for some of the neuromuscular junction defects. Here, we discuss the underlying pathogenic mechanisms of the different autoantibodies and correlate them with phenotypic features. The understanding of these elements should help guide the clinical management of patients with autoimmune myasthenic syndromes.

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Bonanni, Luca, Michele Dalla Vestra, Andrea Zancanaro, and Fabio Presotto. "Myasthenia Gravis following Low-Osmolality Iodinated Contrast Media." Case Reports in Radiology 2014 (2014): 1–2. http://dx.doi.org/10.1155/2014/963461.

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We describe the case of 79-year-old man admitted to our general hospital for a 6-week history of progressive dysphagia to solids and liquids associated with weight loss. To reach a diagnosis a total body CT scan with low-osmolality iodinate contrast agent was performed. Two hours later the patient developed an acute respiratory failure requiring orotracheal intubation and mechanical ventilation. The laboratory and neurological tests allow formulating the diagnosis of myasthenia gravis. In literature, other three case reports have associated myasthenic crisis with exposure to low-osmolality contrast media. This suggests being careful in administering low-osmolality contrast media in myasthenic patients.

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Finnis, Maria F., and Sandeep Jayawant. "Juvenile Myasthenia Gravis: A Paediatric Perspective." Autoimmune Diseases 2011 (2011): 1–7. http://dx.doi.org/10.4061/2011/404101.

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Myasthenia gravis (MG) is an autoimmune disease in which antibodies are directed against the postsynaptic membrane of the neuromuscular junction, resulting in muscle weakness and fatigability. Juvenile myasthenia gravis (JMG) is a rare condition of childhood and has many clinical features that are distinct from adult MG. Prepubertal children in particular have a higher prevalence of isolated ocular symptoms, lower frequency of acetylcholine receptor antibodies, and a higher probability of achieving remission. Diagnosis in young children can be complicated by the need to differentiate from congenital myasthenic syndromes, which do not have an autoimmune basis. Treatment commonly includes anticholinesterases, corticosteroids with or without steroid-sparing agents, and newer immune modulating agents. Plasma exchange and intravenous immunoglobulin (IVIG) are effective in preparation for surgery and in treatment of myasthenic crisis. Thymectomy increases remission rates. Diagnosis and management of children with JMG should take account of their developmental needs, natural history of the condition, and side-effect profiles of treatment options.

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Matthews, Harrison J., Apisadaporn Thambundit, and Brandon R. Allen. "Anti-MuSK-Positive Myasthenic Crisis in a 7-Year-Old Female." Case Reports in Emergency Medicine 2017 (2017): 1–3. http://dx.doi.org/10.1155/2017/8762302.

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A seven-year-old African American female with anti-MuSK-positive Juvenile Myasthenia Gravis collapsed while at school from progressively worsening weakness and dyspnea. On initial emergency department presentation, she required 15 liters per minute of supplemental oxygen to maintain oxygen saturation above 92%. Initial pulmonary function tests and venous blood gas led to the decision to place her on noninvasive positive pressure ventilation (NPPV) with BiPAP in the emergency department. Due to worsening hypercarbia, she later required mechanical intubation in the PICU and underwent IVIG therapy followed by plasmapheresis in order to achieve a stable discharge from the hospital. A respiratory virus panel PCR was positive for influenza A, influenza B, and rhinovirus, likely precipitating the respiratory failure and myasthenic crisis in this seven-year-old patient. Given the rarity of this condition, this case report is to provide further education to the clinician managing severe, prepubertal Juvenile Myasthenia Gravis and myasthenic crisis.

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De Haes, Ann, Johannes H. Proost, Mark H. De Baets, Maurice H. W. Stassen, Martin C. Houwertjes, and J. Mark K. H. Wierda. "Pharmacokinetic–Pharmacodynamic Modeling of Rocuronium in Case of a Decreased Number of Acetylcholine Receptors." Anesthesiology 98, no. 1 (January 1, 2003): 133–42. http://dx.doi.org/10.1097/00000542-200301000-00022.

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Background In myasthenic patients, the sensitivity for nondepolarizing relaxants is increased and the time course of effect is prolonged due to a reduced number of functional acetylcholine receptors at the neuromuscular junction. The authors investigated both the performance of the link model proposed by Sheiner and a pharmacodynamic-pharmacokinetic model taking into account the number of unbound acetylcholine receptors in myasthenic pigs. Methods After obtaining the approval of the Animal Experiments Committee of their institution, the authors studied eight myasthenic pigs and eight control pigs. Myasthenia gravis was induced by injecting Torpedo acetylcholine receptors in weeks 1 and 4. On the day of the experiments, the pigs were anesthetized and intubated, and the appropriate muscles and nerves were prepared for the measurements. Rocuronium was administered by infusion to reach 90% twitch height block. Arterial blood was sampled during onset and offset of effect, and the plasma concentration of rocuronium was measured with high-performance liquid chromatography. Plasma concentration-time effect data were analyzed using two different pharmacokinetic-pharmacodynamic models, the link model according to Sheiner and a pharmacokinetic-pharmacodynamic model taking into account the unbound receptor concentration. Muscles were removed after the experiment for laboratory analysis of the acetylcholine receptor concentration. Results All eight pigs of the myasthenic group developed clinical signs of myasthenia gravis (muscle weakness) and showed increased sensitivity toward rocuronium. Pharmacokinetic modeling revealed no significant differences between myasthenic and control pigs. In pharmacokinetic-pharmacodynamic analysis, visual inspection as well as the Akaike Information Criterion (3,605 3,769) and the residual SD (3.2 3.6%) revealed a better fit for the unbound receptor model in myasthenic animals compared to the Sheiner model. Pharmacokinetic-pharmacodynamic analysis with the unbound receptor model demonstrated a decreased EC50 of 0.27 micro m (ranging from 0.17 to 0.59 micro m) compared to 2.71 micro m (ranging from 2.42 to 4.43 micro m) in control animals. The results of the Sheiner pharmacokinetic-pharmacodynamic analysis were in the same range. Both the laboratory analysis and pharmacokinetic-pharmacodynamic modeling showed a decrease in receptor concentration of more than 75%. Conclusion Both the Sheiner model and the unbound receptor model may be used to fit plasma concentration-effect data of rocuronium in pigs. The unbound receptor concentration model, however, can explain the observed differences in the time course of effect, based on receptor concentration.

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Gogovska, L., R. Ljapcev, M. Polenakovic, L. Stojkovski, M. Popovska, and L. Grcevska. "Plasmaexchange in the Treatment of Myasthenia Gravis Associated with Thymoma." International Journal of Artificial Organs 26, no. 2 (February 2003): 170–73. http://dx.doi.org/10.1177/039139880302600212.

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Background All patients with thymomatous Myasthenia Gravis (MG) should undergo early and total thymectomy, but controversy abounds in the choice of chronic immunosuppressive agents. The value of plasmaexchange (PE) in MG has been clearly estabilshed in preoperative preparation and treatment of myasthenic crisis. Whether PE may be used in the chronic long-term therapy of patients with thymomatous MG in addition to conventional immunosuppressive agents and cholinesterase inhibitors is yet to be answered. Case history We present a 40-year old woman with an 11 year history of MG. Thymectomy was done during the first year of the disease and the histopathologic finding was thymoma. To sustain clinical remission after thymectomy she continued with immunosuppression with methylprednisolone and cyclosporin A (or azathioprine) in addition to cholinesterase inhibitors. Despite the almost continuous immunosuppression, the disease course continued with fluctuating myasthenic weakness which few times progressed to myasthenic crisis requiring mechanical ventilation. During myasthenic crisis we performed 6–8 plasmapheresis at 2–3 day intervals in addition to conventional immunosuppressive therapy. The disease rapidly worsened in January 2000 and we started with intermittent plasmapheresis (3–6 procedures at 2–3 day intervals, every 6–8 weeks) in order to sustain remission. With this therapeutic protocol, during 20 months follow-up we managed to prevent myasthenic crisis and to avoid ventilatory support. Conclusions Plasmaexchange could be used as a successful and safe therapeutic tool in chronic long-term therapy in addition to conventional immunosuppressive agents to sustain remission in patients with MG. This is particularly important in the treatment of patients with thymomatous MG because they have an increased frequency of myasthenic crisis and often respond poorly an to immunosuppression with steroids or other immunosuppressants.

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Varma, AnoopRanjan. "What kills a myasthenic? Myasthenia or otherwise." Neurology India 65, no. 3 (2017): 525. http://dx.doi.org/10.4103/neuroindia.ni_350_17.

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Sanders, Donald B., and Jeffrey T. Guptill. "Myasthenia Gravis and Lambert-Eaton Myasthenic Syndrome." CONTINUUM: Lifelong Learning in Neurology 20 (October 2014): 1413–25. http://dx.doi.org/10.1212/01.con.0000455873.30438.9b.

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Dineen, Jennifer M., and Steven A. Greenberg. "Myasthenis Gravis or Lambert-Eaton Myasthenic Syndrome?" American Journal of Physical Medicine & Rehabilitation 94, no. 2 (February 2015): e20-e21. http://dx.doi.org/10.1097/phm.0000000000000176.

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Zajicek, J. "Handbook of Myasthenia Gravis and Myasthenic Syndromes." Journal of Neurology, Neurosurgery & Psychiatry 58, no. 6 (June 1, 1995): 766. http://dx.doi.org/10.1136/jnnp.58.6.766.

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