To see the other types of publications on this topic, follow the link: Lambert-Eaton.
Books on the topic 'Lambert-Eaton'
Create a spot-on reference in APA, MLA, Chicago, Harvard, and other styles
Consult the top 18 books for your research on the topic 'Lambert-Eaton.'
Next to every source in the list of references, there is an 'Add to bibliography' button. Press on it, and we will generate automatically the bibliographic reference to the chosen work in the citation style you need: APA, MLA, Harvard, Chicago, Vancouver, etc.
You can also download the full text of the academic publication as pdf and read online its abstract whenever available in the metadata.
Browse books on a wide variety of disciplines and organise your bibliography correctly.
1
Jones, Dominic. Antibodies against the voltage-gated calcium channel in Lambert-Eaton myasthenic syndrome. Oxford: Oxford Brookes University, 2000.
Find full text
2
Miller, Aaron E., and Teresa M. DeAngelis. Lambert-Eaton Myasthenia Syndrome. Oxford University Press, 2013. http://dx.doi.org/10.1093/med/9780199732920.003.0023.
Full textAbstract:
Lambert-Eaton myasthenia syndrome (LEMS) is an autoimmune-mediated disorder of the neuromuscular junction, which involves autoantibodies to voltage-gated calcium channels on the presynaptic membrane. In this chapter, we discuss the characteristic clinical features of LEMS, its electrophysiological distinction from MG, as well as its paraneoplastic presentation. We also review the immunotherapeutic management options in cases with severe weakness and those refractory to tumor removal.
3
P, Lisak Robert, ed. Handbook of myasthenia gravis and myasthenic syndromes. New York: M. Dekker, 1994.
Find full text
4
Katirji, Bashar. Case 21. Edited by Bashar Katirji. Oxford University Press, 2018. http://dx.doi.org/10.1093/med/9780190603434.003.0025.
Full textAbstract:
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.
5
Kaplan, Tamara, and Tracey Milligan. Neuromuscular Junction Disease (DRAFT). Oxford University Press, 2018. http://dx.doi.org/10.1093/med/9780190650261.003.0015.
Full textAbstract:
The video in this chapter explores neuromuscular junction disease. It outlines the steps in neuromuscular transmission, as well as the symptoms, causes, and treatments for Myasthenia Gravis, and Lambert Eaton Syndrome
6
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.
Full textAbstract:
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.
7
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.
Full textAbstract:
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).
8
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.
Full textAbstract:
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.
9
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.
Full textAbstract:
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.
10
Katirji, Bashar. Case 24. Edited by Bashar Katirji. Oxford University Press, 2018. http://dx.doi.org/10.1093/med/9780190603434.003.0028.
Full textAbstract:
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.
11
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.
Full textAbstract:
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.
12
Cohen, Jeffrey A., Justin J. Mowchun, Victoria H. Lawson, and Nathaniel M. Robbins. A 72-Year-Old Female with Facial Weakness and Droopy Eyelids. Oxford University Press, 2016. http://dx.doi.org/10.1093/med/9780190491901.003.0030.
Full textAbstract:
Fatigable weakness is the hallmark of myasthenia gravis (MG). It may present with false localizing signs leading to an itinal incorrect diagnosis of a brainstem stroke. MRI scanning of the brain with specific sequences can rule out the diagnosis of stroke. Differential diagnosis of MG may also include also motor neuron disease. Electromyography is very helpful in confirming the diagnosis of motor neuron disease. The two major diseases of the neuromuscular junction are MG and Lambert-Eaton syndrome (LEMS). A table presents the differing characteristics of each. LEMS can be associated with malignancy and MG with thyoma. Laboratory examinations have greatly assisted in differentiating these two conditions. There is specific antibody testing for each condition. Repetitive stimulation and single fiber electromyography also improve diagnostic acumen.
13
Sanders, Donald B. Clinical aspects of neuromuscular junction disorders. Oxford University Press, 2016. http://dx.doi.org/10.1093/med/9780199688395.003.0023.
Full textAbstract:
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.
14
Pitt, Matthew. Pathophysiological associations in paediatric neuromuscular junction disorders. Oxford University Press, 2017. http://dx.doi.org/10.1093/med/9780198754596.003.0010.
Full textAbstract:
Myasthenia can be caused by acquired or autoimmune conditions and other conditions resulting from genetic abnormalities of the proteins in the neuromuscular junction. The clinical clues to diagnosis in the paediatric population are highlighted in this chapter. Among these are sudden death, episodic apnoea, stridor, association with myopathy, and limb-girdle weakness presentation. Acquired disorders of the neuromuscular junction occur, such as infantile botulism, tick paralysis, and persistence of neuromuscular blocking agents. Some patterns of abnormality are seen in the neurophysiological findings, the most notable of which is a repetitive compound muscle action potential at low rates of stimulation. Decrement only seen after long-duration, high-frequency repetitive nerve stimulation is described in choline acetyltransferase (CHAT) abnormalities. DOK7 myasthenia may demonstrate patchy abnormalities of jitter and this is described along with the profound increment of the high-frequency repetitive nerve stimulation in Lambert–Eaton syndrome.
15
Kuwabara, Satoshi. Neuromuscular junction disorders. Oxford University Press, 2015. http://dx.doi.org/10.1093/med/9780199658602.003.0014.
Full textAbstract:
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.
16
Cohen, Jeffrey A., Justin J. Mowchun, Victoria H. Lawson, and Nathaniel M. Robbins. Peripheral Nerve and Muscle Disease. Oxford University Press, 2016. http://dx.doi.org/10.1093/med/9780190491901.001.0001.
Full textAbstract:
Peripheral Nerve and Muscle Disease uses a case-based approach to cover common and important topics in the diagnosis and treatment of neuromuscular disorders. Neuromuscular cases are always challenging. This is because even with nerve conduction studies and electromyography diagnostic certainty can still be difficult. Even with recent advances in serologic and genetic testing diagnostic certainty may be elusive. Each chapter provides an overview of the approach to the problem in question followed by a discussion of the diagnosis, key points to remember, and selected references for further reading. For this edition, new cases include Lambert-Eaton syndrome, botulism, facioscapulohumeral muscular dystrophy, and several types of neuropathy. Peripheral Nerve and Muscle Disease is an engaging collection of thought-provoking cases that clinicians can use when they encounter difficult patients on the ward or in the clinic. The volume is also a self-assessment tool that tests the reader’s ability to answer the question “What do I do now?”
17
Katirji, Bashar. Specialized Electrodiagnostic Studies. Edited by Bashar Katirji. Oxford University Press, 2018. http://dx.doi.org/10.1093/med/9780190603434.003.0003.
Full textAbstract:
In addition to nerve conduction nerve studies and needle EMG, the clinical EMG study include more specialized examinations Some of the tests, such as the F waves and H reflexes are now often used as part of the routine nerve conduction studies. Others are utilized for specific indications: Repetitive nerve stimulation and single fiber EMG are used predominantly in patients with suspected neuromuscular junction disorders such as myasthenia gravis, Lambert-Eaton myasthenic syndrome or botulism; the blink reflexes are used in patients with disorders of the facial and trigeminal nerves as well as brainstem conditions. This chapter covers the late responses, including the F waves, H reflexes and blink reflexes and their applications in the diagnosis of peripheral nerve disorders. This is a followed by a discussion of the basic concepts of slow and rapid repetitive nerve stimulation and single fiber EMG, as well as their applications in the diagnosis of neuromuscular junction disorders.
18
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.
Full textAbstract:
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.