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Related Concept Videos

Myasthenia Gravis: Overview and Treatment01:20

Myasthenia Gravis: Overview and Treatment

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Myasthenia gravis is a neuromuscular transmission disorder characterized by weakness and increased fatigability of skeletal muscles. It is an autoimmune disease affecting approximately one in 2000 people, where antibodies against the α1 subunit of nicotinic acetylcholine receptors are produced.
These antibodies interfere with the function of the nicotinic receptors in three ways: by binding to the receptor and disrupting acetylcholine binding; by causing cross-linking of receptors which...
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Myasthenia Gravis: Diagnostic Tests01:15

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Myasthenia gravis is an autoimmune condition affecting neuromuscular transmission, causing generalized weakness in skeletal muscles. Initial diagnoses rely on patients' signs, symptoms, and medical history. The challenge lies in distinguishing myasthenia from other muscular dystrophies. An important diagnostic feature is the significant improvement of symptoms after administering anticholinesterase inhibitors.
The edrophonium test is a diagnostic tool for myasthenia gravis. It involves...
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Disorders of the Skeletal Muscle01:28

Disorders of the Skeletal Muscle

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The clinical conditions affecting the skeletal muscle tissue are broadly categorized as musculoskeletal and neuromuscular disorders.
Musculoskeletal disorders
Musculoskeletal disorders involve injuries and conditions affecting the skeletal muscles and associated connective tissues. These disorders can arise from acute biomechanical stresses or chronic overuse and can occur across different age groups. Common injuries include sprains, fractures, and muscular strains, often resulting from...
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Chemical Synapses01:26

Chemical Synapses

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Chemical synapses are specialized sites between two neurons or between a neuron and a non-neuronal cell like a muscle, glandular or sensory cell.
Because chemical synapses depend on the release of neurotransmitter molecules from synaptic vesicles to pass on their signal, there is an approximately one millisecond delay between when the axon potential reaches the presynaptic terminal and when the neurotransmitter leads to opening of postsynaptic ion channels. Additionally, this signaling is...
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Chemical Synapses01:26

Chemical Synapses

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Chemical synapses are specialized sites between two neurons or between a neuron and a non-neuronal cell like a muscle, glandular or sensory cell.
Because chemical synapses depend on the release of neurotransmitter molecules from synaptic vesicles to pass on their signal, there is an approximately one millisecond delay between when the axon potential reaches the presynaptic terminal and when the neurotransmitter leads to opening of postsynaptic ion channels. Additionally, this signaling is...
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Muscle Contraction01:10

Muscle Contraction

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In skeletal muscles, acetylcholine is released by nerve terminals at the motor endplate—the point of synaptic communication between motor neurons and muscle fibers. The binding of acetylcholine to its receptors on the sarcolemma allows entry of sodium ions into the cell and triggers an action potential in the muscle cell. Thus, electrical signals from the brain are transmitted to the muscle. Subsequently, the enzyme acetylcholinesterase breaks down acetylcholine to prevent excessive...
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Antigenic Liposomes for Generation of Disease-specific Antibodies
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[Myasthenia gravis].

Wolfgang Müllges1, Guido Stoll2

  • 1Neurologische Klinik, Universitätsklinikum Würzburg, Josef Schneider Str. 11, 97080, Würzburg, Deutschland. Muellges_W@ukw.de.

Der Nervenarzt
|September 21, 2019
PubMed
Summary
This summary is machine-generated.

Myasthenia gravis is an autoimmune condition affecting neuromuscular junctions. Treatments range from symptom management to immunosuppression, with new options like eculizumab offering hope for refractory cases.

Keywords:
EculizumabImmunotherapyMyasthenic crisisPlasma exchangeThymus

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Area of Science:

  • Neurology
  • Immunology
  • Autoimmune Diseases

Background:

  • Myasthenia gravis (MG) is an autoimmune disorder targeting the neuromuscular junction.
  • Antibodies against acetylcholine receptors (AChR) disrupt cholinergic transmission, causing fatigue and muscle weakness.
  • The thymus is implicated in AChR antibody-positive MG, sometimes linked to thymoma.

Purpose of the Study:

  • To review current and emerging treatment strategies for myasthenia gravis subtypes.
  • To highlight advancements in managing ocular and generalized MG.
  • To discuss novel therapies for patients unresponsive to standard immunosuppression.

Main Methods:

  • Review of basic and advanced treatment options for MG.
  • Inclusion of emergency treatments like plasma exchange and immunoglobulins for myasthenic crisis.
  • Discussion of newly approved therapies such as complement inhibitors.

Main Results:

  • Ocular MG typically managed with acetylcholinesterase inhibitors.
  • Generalized MG necessitates long-term immunosuppression.
  • Eculizumab offers a new therapeutic avenue for refractory AChR antibody-positive MG.

Conclusions:

  • MG treatment is tailored to disease subtype and severity.
  • Advances in understanding MG pathophysiology are driving new treatment approvals.
  • Complement inhibition represents a significant addition to the MG treatment landscape.