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Relevant bibliographies by topics / Neuromuscular autoimmune disease

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Academic literature on the topic 'Neuromuscular autoimmune disease'

Author: Grafiati

Published: 4 June 2021

Last updated: 6 February 2022

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Journal articles on the topic "Neuromuscular autoimmune disease"

1

Parry, Garth, and Terry Heiman-Patterson. "Pregnancy and Autoimmune Neuromuscular Disease." Seminars in Neurology 8, no. 03 (September 1988): 197–204. http://dx.doi.org/10.1055/s-2008-1041378.

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Tanovska, Nikolina, Gabriela Novotni, Slobodanka Sazdova-Burneska, Igor Kuzmanovski, Bojan Boshkovski, Goran Kondov, Marija Jovanovski-Srceva, Anita Kokareva, and Rozalinda Isjanovska. "Myasthenia Gravis and Associated Diseases." Open Access Macedonian Journal of Medical Sciences 6, no. 3 (March 5, 2018): 472–78. http://dx.doi.org/10.3889/oamjms.2018.110.

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BACKGROUND: Myasthenia gravis (MG) is an autoimmune disease caused by the action of specific antibodies to the postsynaptic membrane of the neuromuscular junction, leading to impaired neuromuscular transmission. Patients with MG have an increased incidence of other autoimmune diseases.AIM: to determine the presence of other associated diseases in patients with MG.METHOD: A group of 127 patients with MG followed in 10 years period, in which the presence of other associated diseases has been analysed.RESULTS: The sex ratio is in favour of the female sex, the average age of the initial manifestation of the disease is less than 50 years, 65.4% of the patients with MG have another disease. 15.0% patients have associated another autoimmune disease. Thyroid disease is the most common associated with MG, rarely rheumatoid arthritis (RA), systemic lupus erythematosus (SLE) and other autoimmune diseases. Other diseases include hypertension, heart disease, diabetes, respiratory diseases, dyslipidemia. 10.2% of the patients are diagnosed with extrathymic tumours of various origins.CONCLUSION: Associated diseases are common in patients with MG, drawing attention to the possible common basis for their coexistence, as well as their impact on the intensity and treatment of the disease.

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Bichuetti, Denis Bernardi, Tatiane Martins de Barros, Enedina Maria Lobato Oliveira, Marcelo Annes, and Alberto Alain Gabbai. "Demyelinating disease in patients with myasthenia gravis." Arquivos de Neuro-Psiquiatria 66, no. 1 (March 2008): 5–7. http://dx.doi.org/10.1590/s0004-282x2008000100002.

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Myasthenia gravis (MG) is an autoimmune disease characterized by fluctuating muscle weakness, caused by impaired neuromuscular transmission. Patients with MG can present other autoimmune diseases in association, commonly hypo or hyperthyroidism. The association of MG to demyelinating disease is rare and has been described before. We report on three Brazilian patients with MG that presented distinct demyelinating diseases, two monophasic and one recurrent neuromyelitis optica, several years after the diagnosis of MG, and discuss their clinical courses.

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Levinson, Arnold I., Decheng Song, Glen Gaulton, and Yi Zheng. "The Intrathymic Pathogenesis of Myasthenia Gravis." Clinical and Developmental Immunology 11, no. 3-4 (2004): 215–20. http://dx.doi.org/10.1080/17402520400001769.

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The thymus is considered to play an important role in the pathogenesis of Myasthenia gravis, an autoimmune disease characterized by antibody-mediated skeletal muscle weakness. However, its role is yet to be defined. The studies described herein summarize our efforts to determine how intrathymic expression of the neuromuscular type of acetylcholine (ACh) receptors is involved in the immunopathogenesis of this autoimmune disease. We review the work characterizing the expression of neuromuscular ACh receptors in the thymus and advance a new hypothesis that examines the intrathymic expression of this autoantigen in disease pathogenesis.

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Kopishinskaya, S. V., N. O. Zharinova, I. A. Velichko, N. G. Zhukova, V. V. Bucev, I. V. Korobejnikov, A. A. Gasanova, A. S. Arakelyan, O. V. Petruchik, and A. N. Payudis. "Basic principles for the management of neurological patients during the COVID-19 pandemic." Neuromuscular Diseases 10, no. 1 (June 3, 2020): 31–42. http://dx.doi.org/10.17650/2222-8721-2020-10-1-31-42.

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In a COVID-19 pandemic, a neurologist needs to be able to assess the risks of virus infection in patients with individual neurological diseases. The review presents categories of risk groups from the Association of British Neurologists for neuromuscular diseases, multiple sclerosis and other autoimmune diseases of the central nervous system, stroke, epilepsy and Parkinson’s disease. The risk of infection and the management of patients with neuromuscular diseases are analyzed in detail. The use of multiple sclerosis disease modifying drugs, the treatment of stroke patients are discussed. The data from the international guidelines for the management of patients with epilepsy and Parkinson’s disease are presented.

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Jacob, Saiju. "Myasthenia Gravis – A Review of Current Therapeutic Options." European Neurological Review 13, no. 2 (2018): 86. http://dx.doi.org/10.17925/enr.2018.13.2.86.

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Myasthenia gravis (MG) is an autoimmune disorder that leads to skeletal muscle weakness and fatigue. The autoimmune attack is caused by autoantibodies against the acetylcholine postsynaptic receptors at the neuromuscular junction of skeletal muscles. However, other antigenic targets that are components of the neuromuscular junction have also been implicated in the pathogenesis of MG. The current standard of care is immunosuppressive therapy; however, many existing therapeutic options have not been validated for use in MG in large randomised controlled trials. Furthermore, around 10% of patients with generalised MG are refractory to treatment. The complement system is involved in numerous inflammatory, neurodegenerative and autoimmune diseases, and is a key factor in the pathogenesis of acetylcholine receptor antibody-related MG. Targeting complement and other components involved in the underlying pathogenesis of the disease may provide useful treatment options, particularly for refractory patients.

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Herbert, Megan K., Judith Stammen-Vogelzangs, Marcel M. Verbeek, Anke Rietveld, Ingrid E. Lundberg, Hector Chinoy, Janine A. Lamb, et al. "Disease specificity of autoantibodies to cytosolic 5′-nucleotidase 1A in sporadic inclusion body myositis versus known autoimmune diseases." Annals of the Rheumatic Diseases 75, no. 4 (February 24, 2015): 696–701. http://dx.doi.org/10.1136/annrheumdis-2014-206691.

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ObjectivesThe diagnosis of inclusion body myositis (IBM) can be challenging as it can be difficult to clinically distinguish from other forms of myositis, particularly polymyositis (PM). Recent studies have shown frequent presence of autoantibodies directed against cytosolic 5′-nucleotidase 1A (cN-1A) in patients with IBM. We therefore, examined the autoantigenicity and disease specificity of major epitopes of cN-1A in patients with sporadic IBM compared with healthy and disease controls.MethodsSerum samples obtained from patients with IBM (n=238), PM and dermatomyositis (DM) (n=185), other autoimmune diseases (n=246), other neuromuscular diseases (n=93) and healthy controls (n=35) were analysed for the presence of autoantibodies using immunodominant cN-1A peptide ELISAs.ResultsAutoantibodies directed against major epitopes of cN-1A were frequent in patients with IBM (37%) but not in PM, DM or non-autoimmune neuromuscular diseases (<5%). Anti-cN-1A reactivity was also observed in some other autoimmune diseases, particularly Sjögren's syndrome (SjS; 36%) and systemic lupus erythematosus (SLE; 20%).ConclusionsIn summary, we found frequent anti-cN-1A autoantibodies in sera from patients with IBM. Heterogeneity in reactivity with the three immunodominant epitopes indicates that serological assays should not be limited to a distinct epitope region. The similar reactivities observed for SjS and SLE demonstrate the need to further investigate whether distinct IBM-specific epitopes exist.

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Gajdos, P. "Contribution of intravenous immunoglobulins to the treatment of myasthenia." Neurology Bulletin XXXIII, no. 1-2 (May 15, 2001): 114–15. http://dx.doi.org/10.17816/nb79794.

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Mizrachi, Tehila, Livnat Brill, Malcolm Rabie, Yoram Nevo, Yakov Fellig, Mayan Zur, Dimitrios Karussis, Oded Abramsky, Talma Brenner, and Adi Vaknin-Dembinsky. "NMO-IgG and AQP4 Peptide Can Induce Aggravation of EAMG and Immune-Mediated Muscle Weakness." Journal of Immunology Research 2018 (2018): 1–10. http://dx.doi.org/10.1155/2018/5389282.

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Neuromyelitis optica (NMO) and myasthenia gravis (MG) are autoimmune diseases mediated by autoantibodies against either aquaporin 4 (AQP4) or acetylcholine receptor (AChR), respectively. Recently, we and others have reported an increased prevalence of NMO in patients with MG. To verify whether coexisting autoimmune disease may exacerbate experimental autoimmune MG, we tested whether active immunization with AQP4 peptides or passive transfer of NMO-Ig can affect the severity of EAMG. Injection of either AQP4 peptide or NMO-Ig to EAMG or to naive mice caused increased fatigability and aggravation of EAMG symptoms as expressed by augmented muscle weakness (but not paralysis), decremental response to repetitive nerve stimulation, increased neuromuscular jitter, and aberration of immune responses. Thus, our study shows increased disease severity in EAMG mice following immunization with the NMO autoantigen AQP4 or by NMO-Ig, mediated by augmented inflammatory response. This can explain exacerbation or increased susceptibility of patients with one autoimmune disease to develop additional autoimmune syndrome.

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Chirileanu, Ruxanda Dana, Mihaela Simu, Cecilia Rosca, Raluca Tudor, and Patricia Jurca. "TRANSVERSE MYELITIS IN A MYASTHENIA GRAVIS PATIENT. A CASE PRESENTATION." Romanian Journal of Neurology 15, no. 1 (March 31, 2016): 44–47. http://dx.doi.org/10.37897/rjn.2016.1.7.

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Myasthenia gravis (MG) is an autoimmune disease caused by the presence of immunoglobulin G (IgG)1 and IgG3 complement activating antibodies against the nicotinic acetylcholine receptor, which affects the neuromuscular junction leading to fluctuating muscle weakness due to impaired neuromuscular transmission. The association of MG and demyelinating diseases is rare, but it has been described before and it could be part of an unspecific immune activation, due to genetic susceptibility or it could just happen randomly. Demyelinating diseases (DD) in MG patients can occur as monophasic events (myelitis, optic neuritis, acute disseminated encephalomyelitis) or recurrent diseases (multiple sclerosis, recurrent transverse myelitis) and since the incidence of DD is higher in MG patients than in general population this association could be part of an autoimmune syndrome or genetically induced. We present the case of a 30 year old woman who presented with an unspecific onset of MG and after 5 months was readmitted to our unit with transverse myelitis (with negative aquaporin 4 antibodies) which regressed after 5 days of combined intravenous corticotherapy and immunoglobulin treatment.

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Dissertations / Theses on the topic "Neuromuscular autoimmune disease"

1

Tang, Teresa. "Effects of plasmas from seronegative myasthenia gravis patients on the function of skeletal muscle nicotinic acetylcholine receptor." Thesis, University of Oxford, 2001. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.365322.

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Books on the topic "Neuromuscular autoimmune disease"

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R, Hohlfeld, ed. Immunology of neuromuscular disease. Dordrecht: Kluwer Academic Publishers, 1994.

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Hamel, Johanna, and Emma Ciafaloni. Neuromuscular Diseases. Edited by Emma Ciafaloni, Cheryl Bushnell, and Loralei L. Thornburg. Oxford University Press, 2018. http://dx.doi.org/10.1093/med/9780190667351.003.0024.

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Myasthenia gravis is an acquired autoimmune disorder characterized by weakness of skeletal muscle, which often affects women in the childbearing age. A number of questions arise when a woman with myasthenia gravis plans to become pregnant or presents with pregnancy, as myasthenia can affect the pregnancy, delivery and the fetus. In addition, the pregnancy can affect the course of myasthenia and worsening of the disease during pregnancy may require treatment modifications. Therefore supportive counseling, ideally preceding conception, is indicated, focusing on issues of fertility, treatment optimization and drug safety, risks of worsening of symptoms during pregnancy and delivery. Counseling on possible effects on the infant should be discussed, as such as neonatal myasthenia gravis, a treatable and transient disease. Patients with myasthenia gravis may require more intensive monitoring and care, and should be supported by a multidisciplinary team involving the obstetrician, anesthesiologist, and neurologist.

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Abrams, Gary M. Parathyroid, Adrenal, Gonadal, and Pituitary Disease. Oxford University Press, 2017. http://dx.doi.org/10.1093/med/9780199937837.003.0187.

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Endocrine disorders can cause diverse changes in cognition and affect as well as changes in neuromuscular function that may simulate primary neurologic disease, and they generally require a specialized endocrine workup to make a diagnosis. For example, hypoparathyroidism, which may be congenital (e.g., DiGeorge syndrome or Kearns-Sayre syndrome) or disease-acquired (e.g., autoimmune hypoparathyroidism) can present as neuromuscular irritability or tetany due to hypocalcemia, the most distinctive features, which may manifest as carpopedal spasm or laryngospasm. Primary hyperparathyroidism is the most common cause of hypercalcemia and is usually due to oversecretion of PTH by a solitary adenoma of the parathyroid glands. This chapter covers most common primary endocrine disorders that can present as neurological disorders.

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Leung, Doris G. Other Proven and Putative Autoimmune Disorders of the Peripheral Nervous System. Oxford University Press, 2017. http://dx.doi.org/10.1093/med/9780199937837.003.0098.

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Myasthenia gravis is in most cases an autoimmune disorder of the neuromuscular junction in which antibodies are directed at nicotinic acetylcholine receptors or other synaptic proteins, such as the MusK protein that is involved in the formation of the formation and maturation of the motor endplate. Less commonly, myasthenia gravis can result from antibodies directed to presynaptic calcium channels as a side effect of paraneoplastic antibodies (Lambert-Eaton syndrome) or from a developmental paucity of acetylcholine receptors in the neonatal form of the disease. Treatment is usually a combination of aceetylcoholinesterase inhibitors such as pyridostigmine to prolong the life of acetylcholine released at the neuromuscular junction and/or drugs such as corticosteroids aimed at reducing inflammation.

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(Editor), Mark A. Agius, David P. Richman (Editor), Robert H. Fairclough (Editor), and Ricardo A. Maselli (Editor), eds. Myasthenia Gravis and Related Disorders: Biochemical Basis for Disease of the Neuromuscular Junction (Annals of the New York Academy of Sciences, V. 998). New York Academy of Sciences, 2003.

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Reddy, Ugan, and Nicholas Hirsch. Diagnosis, assessment, and management of myasthenia gravis and paramyasthenic syndromes. Oxford University Press, 2016. http://dx.doi.org/10.1093/med/9780199600830.003.0244.

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Diseases that affect the neuromuscular junction (NMJ) interfere with normal nerve transmission and cause weakness of voluntary muscles. The two most commonly encountered are acquired myasthenia gravis (MG) and the Lambert–Eaton myasthenic syndrome (LEMS). Acquired MG is an autoimmune disease in which antibodies are directed towards receptors at the NMJ. In 85% of patients, IgG antibodies against the postsynaptic acetylcholine receptor (AChR) are found (seropositive MG). The thymus gland appears to be involved in the production of these which cause an increase rate of degradation of AChR resulting in a decreased receptor density resulting in a reduced postsynaptic end-plate potential following motor nerve stimulation and leading to muscle weakness. Although all voluntary muscles can be affected, ocular, bulbar, respiratory, and proximal limb weakness predominates. In the majority of seronegative patients, an antibody directed towards a NMJ protein called muscle specific tyrosine kinase (MUSK) is found. Anti-MUSK MG is characterized by severe bulbar and respiratory muscle weakness. Diagnosis of MG requires a high degree of clinical suspicion coupled with pharmacological and electrophysiological testing, and detection of the various causative antibodies. Treatment of MG involves enhancing neuromuscular transmission with long-acting anticholinesterase agents and immunosuppression. Acute exacerbations are treated with either plasma exchange or intravenous immunoglobulin. Myasthenic crisis is associated with severe muscle weakness that necessitates tracheal intubation and mechanical ventilation. LEMS is an autoimmune disease in which IgG antibodies are directed towards the pre-synaptic voltage-gated calcium channels at the NMJ. It is often associated with malignant disease (usually small cell carcinoma of the lung). Autonomic dysfunction is prominent and patients show abnormal responses to neuromuscular blocking drugs.

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Rosenfeld, Myrna R., Maarten J. Titulaer, and Josep Dalmau. Overview. Oxford University Press, 2017. http://dx.doi.org/10.1093/med/9780199937837.003.0142.

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The chapter reviews a diversity of neurologic syndromes that are either proven or putatively autoimmune. The disorders affect all levels of the nervous system from neuromuscular junction, autonomic nervous system, spinal cord, brain, to retina. The pathologic substrates underlying the neurologic dysfunction are varied and include vasculitis (Behçets, Susac’s), encephalitis (NMDA receptor encephalitis), channelopathies (myasthenia, LEMS) and even an inflammatory granulomatous disease (neuro-sarcoid). The resulting syndromes cover myriad aspects of clinical neurology and neuropsychiatry. The understanding of and continued identification of autoimmune neurologic disorders is a very active area. With time some of these disorders may be moved to other sections while new disorders will join the autoimmune list. In this chapter we briefly review the emergence of the field of autoimmunity as it relates to the nervous system and make note of some of the open questions that remain.

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Rahman, Pourmand, ed. Immune-mediated neuromuscular diseases. Basel: Karger, 2009.

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Forsyth, Rob, and Richard Newton. Specific conditions. Oxford University Press, 2017. http://dx.doi.org/10.1093/med/9780198784449.003.0004.

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This chapter adopts a systematic approach to common diagnoses in paediatric neurology, aetiologies, management to include investigation and treatment, and outcome. For each condition current knowledge on cause and underlying biology is summarized. A rational approach to investigation and treatment is summarized for each topic. These include: acquired brain injury; autoimmune and autoinflammatory disease of the CNS; cerebral palsy and neurodisability which covers feeding, communication, special senses, and respiratory disease; demyelinating disease; epilepsy including its impact on daily life; non-epileptic paroxysmal phenomena; functional illness, illness behaviour; headache; hydrocephalus; spina bifida and related disorders; idiopathic intracranial hypertension; infection of the CNS; congenital infection; mitochondrial disease; movement disorders; neuromuscular disease which covers neuropathy, anterior horn cell disease, and myasthenic syndromes; neurocutaneous syndromes; neurodegenerative conditions; late presentations of metabolic disease; neurotransmitter disorders; sleep disorders; stroke and intracerebral haemorrhage; tumours of the CNS; and vitamin-responsive disorders.

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Bielekova, Bibiana, Gary Birnbaum, and Robert P. Lisak, eds. Neuroimmunology. Oxford University Press, 2019. http://dx.doi.org/10.1093/med/9780190050801.001.0001.

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This book provides clinical and supporting scientific background on a diverse group of neurological disorders in an expanding field of neurology, that of neuroimmunology. It includes chapters on multiple sclerosis and related disorders in adults and children, neuromyelitis optica spectrum disorder, Guillain-Barré syndrome, chronic inflammatory deymyelinating polyradiculoneuropathy and variants, immune-mediated disorders of the neuromuscular junction, inflammatory myopathies, paraneoplastic disorders and autoimmune encephalitities, and neurologic manifestations of systemic immune-mediated diseases. In addition there is an introductory chapter dealing with basic of immunology and another on mechanisms of action of therapies used in neuroimmunologic disorders. The clinical chapters cover epidemiology, pathology, pathogenesis, and pathophysiology of the different diseases along with clinical presentation, diagnostic testing, differential diagnosis, and treatment.

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Book chapters on the topic "Neuromuscular autoimmune disease"

1

Hohlfeld, R., and A. G. Engel. "Autoimmune diseases of muscle." In Immunology of Neuromuscular Disease, 235–53. Dordrecht: Springer Netherlands, 1994. http://dx.doi.org/10.1007/978-94-011-1422-6_9.

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Linington, C. "Autoimmune-mediated models of peripheral nerve disease." In Immunology of Neuromuscular Disease, 123–45. Dordrecht: Springer Netherlands, 1994. http://dx.doi.org/10.1007/978-94-011-1422-6_5.

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Krolick, K. A., P. A. Thompson, T. E. Zoda, S. Mohan, R. J. Barohn, and T. M. Yeh. "Immunological factors that influence disease severity in experimental autoimmune myasthenia gravis." In Immunology of Neuromuscular Disease, 209–33. Dordrecht: Springer Netherlands, 1994. http://dx.doi.org/10.1007/978-94-011-1422-6_8.

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Nyberg-Hansen, Rolf, and Leif Gjerstad. "Disorders of Neuromuscular Transmission." In Immunopharmacology in Autoimmune Diseases and Transplantation, 325–33. Boston, MA: Springer US, 1992. http://dx.doi.org/10.1007/978-1-4899-1167-4_25.

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Bansal, Vibhav K., and Matthew N. Meriggioli. "Immunotherapy in the Treatment of Autoimmune Neuromuscular Diseases." In Neuromuscular Disorders in Clinical Practice, 341–62. New York, NY: Springer New York, 2013. http://dx.doi.org/10.1007/978-1-4614-6567-6_17.

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Miller, Dery, Jenny Joseph, and Rocio Garcia-Santibanez. "Autoimmune Diseases of the Neuromuscular Junction: Myasthenia Gravis and Lambert-Eaton Myasthenic Syndrome." In Neuroimmunology, 309–20. Cham: Springer International Publishing, 2021. http://dx.doi.org/10.1007/978-3-030-61883-4_19.

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Agius, Mark A., David P. Richman, and Angela Vincent. "Specific Antibodies in the Diagnosis and Management of Autoimmune Disorders of Neuromuscular Transmission and Related Diseases." In Myasthenia Gravis and Related Disorders, 177–96. Totowa, NJ: Humana Press, 2003. http://dx.doi.org/10.1007/978-1-59259-341-5_8.

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Cao, Michelangelo, and Angela Vincent. "Autoantibody Testing in the Diagnosis and Management of Autoimmune Disorders of Neuromuscular Transmission and Related Diseases." In Myasthenia Gravis and Related Disorders, 153–68. Cham: Springer International Publishing, 2018. http://dx.doi.org/10.1007/978-3-319-73585-6_10.

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Agius, Mark A., David P. Richman, and Angela Vincent. "Autoantibody Testing in the Diagnosis and Management of Autoimmune Disorders of Neuromuscular Transmission and Related Diseases." In Myasthenia Gravis and Related Disorders, 143–56. Totowa, NJ: Humana Press, 2008. http://dx.doi.org/10.1007/978-1-59745-156-7_9.

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"Autoimmune diseases of the neuromuscular junction and other disorders of the motor unit." In Autoimmune Neurological Disease, 257–303. Cambridge University Press, 1995. http://dx.doi.org/10.1017/cbo9780511526916.011.

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