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Related Concept Videos

Myasthenia Gravis: Diagnostic Tests01:15

Myasthenia Gravis: Diagnostic Tests

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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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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.
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Satellite Stem Cells and Muscular Dystrophy01:21

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Satellite stem cells or myosatellite cells are quiescent stem cells that Alexander Mauro first identified in 1961. These cells are located between the sarcolemma, the plasma membrane of muscle fibers, and the basal lamina, the connective tissue sheath covering it. These mononucleated cells are activated in response to muscle injury, can transform into myoblasts, and may form or repair muscle fibers. Myosatellite cells can provide additional myonuclei for muscle regeneration or return to a...
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Cross-bridge Cycle01:26

Cross-bridge Cycle

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As muscle contracts, the overlap between the thin and thick filaments increases, decreasing the length of the sarcomere—the contractile unit of the muscle—using energy in the form of ATP. At the molecular level, this is a cyclic, multistep process that involves binding and hydrolysis of ATP, and movement of actin by myosin.
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Long-term Potentiation01:35

Long-term Potentiation

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Long-term potentiation, or LTP, is one of the ways by which synaptic plasticity—changes in the strength of chemical synapses—can occur in the brain. LTP is the process of synaptic strengthening that occurs over time between pre- and postsynaptic neuronal connections. The synaptic strengthening of LTP works in opposition to the synaptic weakening of long-term depression (LTD) and together are the main mechanisms that underlie learning and memory.
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Related Experiment Video

Updated: Jun 20, 2025

In Vivo Electrophysiological Measurement of Compound Muscle Action Potential from the Forelimbs in Mouse Models of Motor Neuron Degeneration
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Late-onset myopathies.

Emmanuelle Salort-Campana1,2, Shahram Attarian1,2

  • 1Neuromuscular Reference Center PACARARE, La Timone Hospital University, Marseille.

Current Opinion in Neurology
|July 17, 2024
PubMed
Summary
This summary is machine-generated.

Late-onset myopathies (LOM) can stem from genetic causes, not just acquired conditions. Early diagnosis of genetic LOM, like facioscapulohumeral muscular dystrophy, is crucial for effective management.

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Area of Science:

  • Neurology
  • Genetics
  • Internal Medicine

Background:

  • Late-onset myopathies (LOM) are muscle diseases diagnosed after age 50.
  • While often acquired, genetic factors can also cause LOM, sometimes with atypical presentations.

Purpose of the Study:

  • To review recent evidence on diagnosing LOM, with a focus on genetic etiologies.
  • To highlight key genetic causes and diagnostic indicators for LOM.

Main Methods:

  • Literature review of recent studies on LOM diagnosis.
  • Analysis of clinical features suggestive of genetic LOM.
  • Summary of differential diagnoses for LOM.

Main Results:

  • Facioscapulohumeral muscular dystrophy (FSHD) can present late with atypical symptoms.
  • Metabolic myopathies, including late-onset multiple acyl-CoA dehydrogenase deficiency (MADD), are treatable LOM causes.
  • MADD shows significant improvement with riboflavin supplementation.

Conclusions:

  • Inclusion body myositis is the most common LOM.
  • Myotonic dystrophy type 2, FSHD, and oculopharyngeal muscular dystrophy are frequent genetic LOM causes.
  • Clinical examination findings can guide the diagnosis of genetic LOM.