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Relevant bibliographies by topics / Lambert-Eaton Myasthenic Syndrome

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Academic literature on the topic 'Lambert-Eaton Myasthenic Syndrome'

Author: Grafiati

Published: 4 June 2021

Last updated: 1 February 2022

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Journal articles on the topic "Lambert-Eaton Myasthenic Syndrome"

1

Kesner, Vita G., Shin J. Oh, Mazen M. Dimachkie, and Richard J. Barohn. "Lambert-Eaton Myasthenic Syndrome." Neurologic Clinics 36, no. 2 (May 2018): 379–94. http://dx.doi.org/10.1016/j.ncl.2018.01.008.

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Katirji, Basfhar. "Lambert-Eaton Myasthenic Syndrome." Journal of Clinical Neuromuscular Disease 1, no. 3 (March 2000): 134–36. http://dx.doi.org/10.1097/00131402-200003000-00004.

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Young, Jeffery D., and Jacqueline A. Leavitt. "Lambert–Eaton Myasthenic Syndrome." Journal of Neuro-Ophthalmology 36, no. 1 (March 2016): 20–22. http://dx.doi.org/10.1097/wno.0000000000000258.

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D'Amour, M., G. Gariepy, and J. Braidy. "Lambert-Eaton myasthenic syndrome." Canadian Medical Association Journal 176, no. 1 (December 13, 2006): 37. http://dx.doi.org/10.1503/cmaj.060767.

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Mareska, Michael, and Laurie Gutmann. "Lambert-Eaton Myasthenic Syndrome." Seminars in Neurology 24, no. 02 (July 15, 2004): 149–53. http://dx.doi.org/10.1055/s-2004-830900.

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6

Newsom-Davis, J. "Lambert-Eaton Myasthenic Syndrome." Revue Neurologique 160, no. 2 (February 2004): 177–80. http://dx.doi.org/10.1016/s0035-3787(04)70888-7.

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Titulaer, Maarten J., and Jan J. G. M. Verschuuren. "Lambert-Eaton Myasthenic Syndrome." Annals of the New York Academy of Sciences 1132, no. 1 (June 2008): 129–34. http://dx.doi.org/10.1196/annals.1405.030.

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Petty, R. "Lambert-Eaton myasthenic syndrome." Case Reports 2009, jan27 1 (February 2, 2009): bcr0920080914. http://dx.doi.org/10.1136/bcr.09.2008.0914.

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9

SANDERS, DONALD B. "Lambert-Eaton Myasthenic Syndrome." Annals of the New York Academy of Sciences 998, no. 1 (September 2003): 500–508. http://dx.doi.org/10.1196/annals.1254.065.

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Chiang, Yi Zhen, Kian Tjon Tan, and Ian K. Hart. "Lambert–Eaton myasthenic syndrome." British Journal of Hospital Medicine 70, no. 3 (March 2009): 168–69. http://dx.doi.org/10.12968/hmed.2009.70.3.40574.

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Dissertations / Theses on the topic "Lambert-Eaton Myasthenic Syndrome"

1

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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Maddison, Paul. "A quantitative study of the immune-mediated neuromuscular disorders of acquired neuromyotonia and Lambert-Eaton myasthenic syndrome." Thesis, University of Newcastle Upon Tyne, 1998. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.285378.

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3

Duffield, Michael. "Comparison of the expression pattern of voltage-gated calcium channel subunits and Lambert-Eaton myasthenic syndrome autoantibodies in the mouse colon /." Adelaide, 1999. http://web4.library.adelaide.edu.au/theses/09SB/09sbd857.pdf.

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4

von, Rosch Anthony Stanislav Wierzbicki. "The isolation and characterisation of the genes coding for the calcium channel affected by Lambert-Eaton myasthenic syndrome antibodies in NG108-15 cells." Thesis, University of Oxford, 1992. https://ora.ox.ac.uk/objects/uuid:096b02c9-8c80-4f82-8d4c-8ed2ca59aa2e.

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Lambert-Eaton myasthenic syndrome is a rare paraneoplastic and autoimmune disorder affecting the presynaptic voltage gated calcium channels at the neuromuscular junction. The aim of this project was to isolate the genes coding for the Î±1 and Î±2 subunits of the voltage-gated calcium channel from hybrid neuronal cell lines including NG108-15 whose potassium stimulated ⁴⁵Ca²⁺ flux is reduced by IgG from patients with Lambert-Eaton myasthenic syndrome. The cDNA libraries were constructed in Î»gt10 from NG108-15 mRNA and screened with PCR products derived from the rabbit skeletal muscle Î±1 and Î±2-Î´ genes. A 2230 bp portion of the NG108-15 Î±2-Î´ gene homologous to bp 1000- 3304 of the rabbit gene has been isolated and sequenced. This shows 48% homology to the amino acid sequence of the rabbit gene and 56% nucleotide homology with particular conservation of the C-tenninal domains. The NG108-l5 Î±2 mRNA is 8.5 kb long and was found in the N18TG2 mouse neuroblastoma cell line from which NG108-15 is derived and in mouse brain. Rabbit Î±2-Î´ gene PCR primers were used to screen a rodent tissue cDNA panel to detect highly homologous sequences by PCR amplification. These products were detected only in mouse brain and lung and in rat skeletal muscle. The mouse brain and lung product amino acid sequences were 87% homologous to the rabbit gene while the rat skeletal muscle product was 81% homologous and both differed significantly from the homologous region of the NG108-15 gene. This suggests that some of the diversity of voltage gated calcium channels arises from the expression of different Î±2-Î´ subunits within the 5 subunit VGCC complex as well as from diversity in the other subunits.

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5

Armbruster, Lena. "Lambert-Eaton Myasthenie Syndrom." Diss., lmu, 2010. http://nbn-resolving.de/urn:nbn:de:bvb:19-112592.

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Armbruster, Lena [Verfasser]. "Lambert-Eaton Myasthenie-Syndrom : klinische Übersicht über 25 Patienten in Deutschland und Reaktivität von 46 Patientenseren gegen Untergruppen des spannungsabhängigen Kalziumkanals / vorgelegt von Lena Armbruster." 2010. http://d-nb.info/1001149629/34.

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Books on the topic "Lambert-Eaton Myasthenic Syndrome"

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

P, Lisak Robert, ed. Handbook of myasthenia gravis and myasthenic syndromes. New York: M. Dekker, 1994.

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3

Nageshwaran, Sathiji, Heather C. Wilson, Anthony Dickenson, and David Ledingham. Disorders of muscle and neuromuscular junction. Oxford University Press, 2016. http://dx.doi.org/10.1093/med/9780199664368.003.0008.

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This chapter discusses the clinical features and evidence base for the pharmacological treatment of muscular disorders (inflammatory myopathies: polymyositis, dermatomyositis, and inclusion body myositis), mitochondrial myopathies, Duchenne muscular dystrophy (DMD), myotonic dystrophy, inherited neuromuscular channelopathies, non-dystrophic myotonias (myotonia congenita, paramyotonia congenita), periodic paralyses, acquired neuromyotonia (Isaac syndrome and Morvan syndrome), stiff person syndrome, and disorders of the neuromuscular junction (myasthenia gravis (MG), myasthenic crisis, and Lambert–Eaton myasthenic syndrome (LEMS).

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Katirji, Bashar. Case 21. Edited by Bashar Katirji. Oxford University Press, 2018. http://dx.doi.org/10.1093/med/9780190603434.003.0025.

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Lambert-Eaton myasthenic syndrome is a rare yet very important neuromuscular disorder that may be difficult to confirm if not considered in the differential diagnosis. It is often misdiagnosed as myasthenic gravis or other nonspecific neuromuscular disorder. The electrodiagnostic findings in Lambert-Eaton myasthenic syndrome continue to be the cornerstone of the diagnosis. This case outlines the clinical and electrodiagnostic features of a patient with this syndrome and highlights the findings on repetitive nerve stimulation. It also discusses the practical approach in the search for occult malignancy. The distinguishing features among the various neuromuscular junction disorders are emphasized.

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Sanders, Donald B. Clinical aspects of neuromuscular junction disorders. Oxford University Press, 2016. http://dx.doi.org/10.1093/med/9780199688395.003.0023.

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Disorders that primarily impair neuromuscular transmission (NMT) produce weakness that characteristically affects certain muscle groups and varies with activity. Acquired, autoimmune myasthenia gravis (MG) is the most common of these disorders. Much less common are genetic abnormalities of the neuromuscular junction (NMJ), the Lambert–Eaton myasthenic syndrome (LEMS), and toxic effects of various biological and chemical agents. The diagnosis of MG or LEMS is suspected from the history and clinical findings, and is confirmed in most patients by the presence of specific auto-antibodies. The precise diagnosis of most genetic myasthenic syndromes may require sophisticated DNA analysis. Impaired NMT can be confirmed in all of these conditions by repetitive nerve stimulation (RNS) testing and measuring the neuromuscular jitter. Treatment of MG requires selecting among several therapeutic options, taking into consideration the clinical characteristics of the individual patient. Treatment of LEMS and genetic myasthenic syndromes is more limited.

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Cohen, Jeffrey A., Justin J. Mowchun, Victoria H. Lawson, and Nathaniel M. Robbins. A 46-Year-Old Man with Double Vision and Proximal Leg Weakness. Oxford University Press, 2016. http://dx.doi.org/10.1093/med/9780190491901.003.0033.

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Lambert-Eaton myasthenic syndrome (LEMS) can be a difficult condition to diagnose. In this chapter, the clinical picture and characteristics are discussed. The pathophysiology is also reviewed. Features to distinguish LEMS from more common neuromuscular junction conditions such as myasthenia gravis are reviewed. We review features that distinguish between idiopathic and paraneoplastic forms, and we discuss the importance of tumor surveillance. Antibody testing and the correct electrodiagnostic strategy are presented. Treatment of LEMS is outlined.Lambert-Eaton syndrome (LES) is a difficult condition to diagnose. The unique clinical picture and its characteristics are discussed. This is especially true in the patient without a diagnois of cancer. Antibody testing and the correct electrodiagnostic strategy are presented. Treatment of LES is outlined.

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Katirji, Bashar. Electrodiagnostic Findings in Neuromuscular Disorders. Edited by Bashar Katirji. Oxford University Press, 2018. http://dx.doi.org/10.1093/med/9780190603434.003.0004.

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Neuromuscular disorders are often classified into four major categories: anterior horn cell disorders, peripheral neuropathies, neuromuscular junction disorders and myopathies. This chapter discusses the electrodiagnostic and clinical EMG findings in these various neuromuscular disorders. Peripheral neuropathies are subdivided into focal mononeuropathies, radiculopathies, plexopathies and generalized peripheral polyneuropathies. Focal peripheral nerve lesions and generalized peripheral polyneuropathies may be axonal or demyelinating, and manifest quite distinctly on nerve conduction studies. Neuromuscular junction disorders may be presynaptic, as seen with the Lambert-Eaton myasthenic syndrome, or postsynaptic, as seen with myasthenia gravis.

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Murray, E. Lee, and Veda V. Vedanarayanan. Neuromuscular Disorders. Edited by Karl E. Misulis and E. Lee Murray. Oxford University Press, 2017. http://dx.doi.org/10.1093/med/9780190259419.003.0021.

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The hospital neurologist may encounter neuromuscular disorders as known chronic conditions that are exacerbated by a hospital stay, be the principal reason for admission, or develop during a prolonged hospitalization. This chapter details the presentation, diagnosis, and management of conditions affecting the peripheral nerves and neuromuscular junction, such as myasthenia gravis, Lambert-Eaton (myasthenic) syndrome, botulism, and tick paralysis; as well as muscular weakness from various causes such as rhabdomyolysis, critical illness neuromyopathy, inflammatory myopathies, muscular dystrophies, periodic paralysis, and metabolic and endocrine myopathies. Also discussed are motoneuron degeneration, including amyotrophic lateral sclerosis and progressive muscle atrophy, and neuromuscular respiratory failure.

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Kuwabara, Satoshi. Neuromuscular junction disorders. Oxford University Press, 2015. http://dx.doi.org/10.1093/med/9780199658602.003.0014.

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Ten seminal papers on disorders of the neuromuscular junction are described, covering historical aspects, recent advances in immunological, biological, and genetic researches, and future perspectives. Early descriptions of myasthenia gravis (MG) date back to the seventeenth century, and MG acquired its name in the nineteenth century. The first symptomatic treatment with cholinesterase inhibitors was reported in 1934, leading to the development of modern immunological therapies. Following the discovery of anti-MuSK (muscle-specific tyrosine kinase) antibody in 2001, MG is currently classified into three categories: AChR-positive, MuSK-positive, and dual-seronegative. Lambert-Eaton myasthenic syndrome was recognized in 1956, followed by the discovery of antibodies to voltage-gated calcium channels in the pre-synaptic membrane, facilitating diagnosis and improving the understanding of the pathophysiological mechanisms. Since the late twentieth century, many types of congenital myasthenic syndromes with pre-synaptic, synaptic, and post-synaptic defects have been identified, and a classification based on molecular genetics is in evolution.

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Katirji, Bashar. Case 24. Edited by Bashar Katirji. Oxford University Press, 2018. http://dx.doi.org/10.1093/med/9780190603434.003.0028.

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Botulism is an extremely rare neuromuscular disorder, caused by botulinum toxin which is produced by the anaerobic bacteria Clostridium botulinum. It has several forms: classic foodborne, infantile, wound, intestinal, and iatrogenic forms. The presentation is often acute and severe but may be occasionally subacute and moderate. The diagnosis may be difficult and requires a high index of suspicion. This case presents an adult with classic foodborne botulism and highlights the clinical and electrodiagnostic findings that distinguish this disorder from other neuromuscular junction disorders including myasthenia gravis and Lambert-Eaton myasthenic syndrome. Specifically, the findings on repetitive nerve stimulation are discussed and distinguished from the results seen in other neuromuscular junction disorders.

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Book chapters on the topic "Lambert-Eaton Myasthenic Syndrome"

1

Lang, Bethan. "Lambert-Eaton Myasthenic Syndrome." In Diagnostic Criteria in Autoimmune Diseases, 413–16. Totowa, NJ: Humana Press, 2008. http://dx.doi.org/10.1007/978-1-60327-285-8_75.

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Pourmand, Rahman. "Lambert-Eaton Myasthenic Syndrome." In Frontiers of Neurology and Neuroscience, 120–25. Basel: KARGER, 2009. http://dx.doi.org/10.1159/000212373.

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3

Nicolle, Michael W. "Lambert-Eaton Myasthenic Syndrome." In Neuromuscular Disorders, 134–41. Oxford, UK: Wiley-Blackwell, 2011. http://dx.doi.org/10.1002/9781119973331.ch18.

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4

Kerty, Emilia. "Lambert-Eaton myasthenic syndrome." In International Neurology, 527–28. Chichester, UK: John Wiley & Sons, Ltd, 2016. http://dx.doi.org/10.1002/9781118777329.ch129.

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5

Leung, Alexander K. C., William Lane M. Robson, Carsten Büning, Johann Ockenga, Janine Büttner, Hartmut Schmidt, Antonio V. Delgado-Escueta, et al. "Lambert Eaton Myasthenic Syndrome." In Encyclopedia of Molecular Mechanisms of Disease, 1137–38. Berlin, Heidelberg: Springer Berlin Heidelberg, 2009. http://dx.doi.org/10.1007/978-3-540-29676-8_1014.

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6

Benatar, Michael. "Lambert-Eaton Myasthenic Syndrome." In Neuromuscular Disease, 337–49. Totowa, NJ: Humana Press, 2006. http://dx.doi.org/10.1007/978-1-59745-106-2_18.

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Verschuuren, Jan J. G. M., Maarten J. Titulaer, and Paul Maddison. "Lambert-Eaton Myasthenic Syndrome." In Neuromuscular Disorders in Clinical Practice, 1089–99. New York, NY: Springer New York, 2013. http://dx.doi.org/10.1007/978-1-4614-6567-6_49.

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8

Khadilkar, Satish V., Rakhil S. Yadav, and Bhagyadhan A. Patel. "Lambert–Eaton Myasthenic Syndrome." In Neuromuscular Disorders, 261–72. Singapore: Springer Singapore, 2017. http://dx.doi.org/10.1007/978-981-10-5361-0_23.

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9

Wirtz, Paul W., Maarten J. Titulaer, and Jan J. G. M. Verschuuren. "The Lambert-Eaton Myasthenic Syndrome." In Pathologies of Calcium Channels, 189–204. Berlin, Heidelberg: Springer Berlin Heidelberg, 2013. http://dx.doi.org/10.1007/978-3-642-40282-1_10.

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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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Conference papers on the topic "Lambert-Eaton Myasthenic Syndrome"

1

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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2

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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