Jove
Visualize
Contact Us
JoVE
x logofacebook logolinkedin logoyoutube logo
ABOUT JoVE
OverviewLeadershipBlogJoVE Help Center
AUTHORS
Publishing ProcessEditorial BoardScope & PoliciesPeer ReviewFAQSubmit
LIBRARIANS
TestimonialsSubscriptionsAccessResourcesLibrary Advisory BoardFAQ
RESEARCH
JoVE JournalMethods CollectionsJoVE Encyclopedia of ExperimentsArchive
EDUCATION
JoVE CoreJoVE BusinessJoVE Science EducationJoVE Lab ManualFaculty Resource CenterFaculty Site
Terms & Conditions of Use
Privacy Policy
Policies

Related Concept Videos

Myasthenia Gravis ll: Pathophysiology01:22

Myasthenia Gravis ll: Pathophysiology

The disease process of myasthenia gravis begins at the neuromuscular junction, where antibodies attack key proteins needed for muscle activation. This immune reaction weakens signal transmission, leading to the characteristic muscle fatigue and weakness that define the condition.Immune-Mediated DamageIn most individuals, antibodies target acetylcholine receptors (AChRs) on the postsynaptic membrane of muscle cells. By blocking acetylcholine binding, these antibodies prevent the nerve signal...
Myasthenia Gravis: Diagnostic Tests01:15

Myasthenia Gravis: Diagnostic Tests

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...
Skeletal Muscle Relaxants: Adverse Effects01:21

Skeletal Muscle Relaxants: Adverse Effects

Skeletal muscle relaxants are widely used for muscle paralysis and relieving pain following any muscle injury or stiffness. However, depending on the drug type, they can have adverse effects that range from mild to severe. Usually, nondepolarizing neuromuscular blockers have minimal side effects. For example, drugs like d-tubocurarine, cisatracurium, and rocuronium cause hypotension, whereas drugs like baclofen, when stopped abruptly, can lead to the recurrence of spastic conditions.
Unlike...
Disorders of the Skeletal Muscle01:28

Disorders of the Skeletal Muscle

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...
Myasthenia Gravis: Overview and Treatment01:20

Myasthenia Gravis: Overview and Treatment

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 leads...
Alterations in Muscle Tone lll01:11

Alterations in Muscle Tone lll

Rigidity and myotonia are distinct abnormalities of muscle tone that affect resistance and relaxation during movement. Although both involve altered muscle contraction, they arise from different neurological and muscular mechanisms.CharacteristicsRigidity is characterized by uniform resistance to passive movement across the entire range, independent of speed, affecting flexors and extensors equally. It may appear as lead-pipe rigidity (smooth, constant resistance) or cogwheel rigidity...

You might also read

Related Articles

Articles linked to this work by shared authors, journal, and citation graph.

Sort by
Same author

Precision Medicine in Neurodegeneration with Brain Iron Accumulation (NBIA) Disorders: An Update on Emerging Treatments.

Movement disorders clinical practice·2026
Same author

[Rare hereditary and acquired diseases with parkinson's syndrome].

Fortschritte der Neurologie-Psychiatrie·2026
Same author

Transitional Life Events in Friedreich Ataxia: Differential Age at Onset Perspectives.

Cerebellum (London, England)·2026
Same author

Cerebellar cognitive-affective syndrome in Friedreich Ataxia.

Journal of neurology·2026
Same author

A Patient-Reported Outcome Measure of Communication Difficulties in Friedreich Ataxia: COMATAX.

Cerebellum (London, England)·2026
Same author

Synaptophysin autoantibodies mediate synaptic dysfunction in cerebellar ataxia.

Cell reports. Medicine·2026

Related Experiment Video

Updated: Jul 2, 2026

Detection of Anti-MDA5 Autoantibodies Using HeLa Cells and Immunocytochemistry with Light Microscopy
10:55

Detection of Anti-MDA5 Autoantibodies Using HeLa Cells and Immunocytochemistry with Light Microscopy

Published on: October 31, 2025

Drug-induced myopathies.

Thomas Klopstock1

  • 1Friedrich-Baur-Institute, Department of Neurology, Ludwig-Maximilians-University, Munich, Germany. Thomas.Klopstock@med.uni-muenchen.de

Current Opinion in Neurology
|September 5, 2008
PubMed
Summary

Drug-induced myopathies, including statin and antiretroviral cases, require careful risk-benefit assessment. Coenzyme Q supplementation for statin myopathy lacks conclusive evidence, and genetic factors are key for future prevention.

Related Experiment Videos

Last Updated: Jul 2, 2026

Detection of Anti-MDA5 Autoantibodies Using HeLa Cells and Immunocytochemistry with Light Microscopy
10:55

Detection of Anti-MDA5 Autoantibodies Using HeLa Cells and Immunocytochemistry with Light Microscopy

Published on: October 31, 2025

Area of Science:

  • Pharmacology
  • Toxicology
  • Neurology

Background:

  • Drug-induced muscle disorders are significant causes of morbidity.
  • Understanding the risk-benefit profile of implicated drugs is crucial.
  • Recent advances focus on statin and antiretroviral drug-induced myopathies.

Purpose of the Study:

  • To review recent advances in statin- and antiretroviral-induced myopathies.
  • To highlight less common drug-induced myotoxic disorders.
  • To discuss the role of coenzyme Q in statin myopathy.

Main Methods:

  • Literature review of recent advances in drug-induced myopathies.
  • Analysis of findings on coenzyme Q supplementation in statin myopathy.
  • Discussion of drug-induced dermatomyositis, tendinopathy, and rhabdomyolysis.

Main Results:

  • Coenzyme Q reduction in statin myopathy is debated; supplementation trials show conflicting results.
  • Highly active antiretroviral therapy shifts morbidity towards drug-induced issues in HIV.
  • Recent findings include drug-induced dermatomyositis, tendinopathy, and rhabdomyolysis.

Conclusions:

  • Statin myotoxicity can often be prevented by managing drug-drug interactions; avoid unnecessary statin withdrawal for minor myalgias.
  • Further large-scale trials are needed to confirm coenzyme Q efficacy for statin myopathy.
  • Identifying genetic risk factors is essential for future pharmacogenomic research into myotoxicity.