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

Antiarrhythmic Drugs: Class III Agents as Potassium Channel Blockers01:12

Antiarrhythmic Drugs: Class III Agents as Potassium Channel Blockers

1.9K
Class III antiarrhythmic drugs are a group of medications that can prolong action potentials in the heart. They achieve this by blocking potassium channels or enhancing inward currents from sodium channels. However, these drugs have a unique property of "reverse use-dependence," which is most pronounced at slower heart rates and can lead to torsades de pointes—a specific type of arrhythmia. However, it is essential to note that excessive QT interval prolongation—a measure of...
1.9K
Local Anesthetics: Adverse Effects01:12

Local Anesthetics: Adverse Effects

758
While local anesthetics are generally safe and well-tolerated, they can occasionally cause adverse effects that vary in severity. Local anesthetics can induce toxicity at two distinct levels. They can either produce local effects through direct contact with the neural elements or be absorbed into the bloodstream from the injection site, leading to systemic effects.
Once absorbed into the systemic circulation, local anesthetics can affect the organs that depend on the functioning of sodium...
758
Antiarrhythmic Drugs: Class IV Agents as Calcium Channel Blockers01:20

Antiarrhythmic Drugs: Class IV Agents as Calcium Channel Blockers

1.6K
Class IV antiarrhythmic drugs, such as verapamil and diltiazem, block calcium channels. They primarily affect the heart, slowing the conduction in calcium-dependent tissues like the SA and AV nodes. These drugs manage reentrant supraventricular tachycardia (SVT) and reduce ventricular rate in atrial flutter/fibrillation.
Verapamil, a calcium channel blocker, inhibits calcium movement across myocardial cell membranes and vascular smooth muscle. This results in the dilation of coronary and...
1.6K
Antiarrhythmic Drugs: Class I Agents as Sodium Channel Blockers01:22

Antiarrhythmic Drugs: Class I Agents as Sodium Channel Blockers

2.8K
Class I antiarrhythmic drugs are used to treat various types of arrhythmias or irregular heart rhythms. These drugs block the sodium (Na+) channels in the cardiac cells, thereby affecting the movement of electrical impulses across the heart. Class I antiarrhythmic drugs are divided into three subgroups: Class IA, Class IB, and Class IC, each with distinct mechanisms of action and effects on the heart.
Class 1A Antiarrhythmic Drugs: These drugs work by moderately blocking sodium channels,...
2.8K
Angle Closure Glaucoma: Treatment01:28

Angle Closure Glaucoma: Treatment

1.2K
Angle-closure glaucoma, or closed-angle glaucoma, is an eye condition where the iris bulges out and blocks the iridocorneal angle, resulting in a buildup of aqueous humor and increased intraocular pressure. Immediate medical attention is necessary due to the sudden onset of symptoms. The treatment for angle-closure glaucoma includes short-term and long-term approaches. Short-term treatment involves using eye drops like pilocarpine to lower intraocular pressure by increasing aqueous humor...
1.2K
Glaucoma: Overview01:25

Glaucoma: Overview

1.3K
Glaucoma is an eye condition characterized by increased intraocular pressure that damages the retina and optic nerve, leading to irreversible blindness if left untreated. The human eye has various components, including the cornea, iris, pupil, lens, and optic nerve. Aqueous humor is secreted by the epithelium of the ciliary body in the posterior chamber and flows through the trabecular meshwork and canal of Schlemm, maintaining normal intraocular pressure. The trabecular meshwork and the canal...
1.3K

You might also read

Related Articles

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

Sort by
Same author

Inclusive Search for Anomalous Single-Photon Production in MicroBooNE.

Physical review letters·2026
Same author

First Search for Dark Sector e^{+}e^{-} Explanations of the MiniBooNE Anomaly at MicroBooNE.

Physical review letters·2026
Same author

Black Hole Spectroscopy and Tests of General Relativity with GW250114.

Physical review letters·2026
Same author

First Measurement of Charged-Current Muon-Neutrino-Induced K^{+} Production on Argon Using the MicroBooNE Detector.

Physical review letters·2026
Same author

GW250114: Testing Hawking's Area Law and the Kerr Nature of Black Holes.

Physical review letters·2025
Same author

Search for an Anomalous Production of Charged-Current ν_{e} Interactions without Visible Pions across Multiple Kinematic Observables in MicroBooNE.

Physical review letters·2025

Related Experiment Video

Updated: Jan 18, 2026

A Surgical Approach for Optic Nerve Crush in a Rabbit Model
06:15

A Surgical Approach for Optic Nerve Crush in a Rabbit Model

Published on: July 8, 2025

1.2K

[Amiodarone-induced optic neuropathy: A rare side effect].

R Arcani1, M Pellerey1, F Rouby2

  • 1Service de médecine interne, gériatrie et thérapeutique, hôpital de la Timone, Aix-Marseille université, AP-HM, 264, rue Saint-Pierre 13385 Marseille, France.

La Revue De Medecine Interne
|September 29, 2019
PubMed
Summary

Bilateral papilledema can indicate serious conditions, but drug side effects are an important cause. This case highlights amiodarone-induced toxic optic neuropathy, emphasizing the need for awareness in patients using this medication.

Keywords:
AmiodaroneNeuropathie optiqueOptic neuropathyPapillary diseaseToxicityToxicitéŒdème papillaire

More Related Videos

The Rodent Model of Nonarteritic Anterior Ischemic Optic Neuropathy rNAION
06:49

The Rodent Model of Nonarteritic Anterior Ischemic Optic Neuropathy rNAION

Published on: November 20, 2016

9.4K
Rat Model of Photochemically-Induced Posterior Ischemic Optic Neuropathy
14:54

Rat Model of Photochemically-Induced Posterior Ischemic Optic Neuropathy

Published on: November 29, 2015

9.0K

Related Experiment Videos

Last Updated: Jan 18, 2026

A Surgical Approach for Optic Nerve Crush in a Rabbit Model
06:15

A Surgical Approach for Optic Nerve Crush in a Rabbit Model

Published on: July 8, 2025

1.2K
The Rodent Model of Nonarteritic Anterior Ischemic Optic Neuropathy rNAION
06:49

The Rodent Model of Nonarteritic Anterior Ischemic Optic Neuropathy rNAION

Published on: November 20, 2016

9.4K
Rat Model of Photochemically-Induced Posterior Ischemic Optic Neuropathy
14:54

Rat Model of Photochemically-Induced Posterior Ischemic Optic Neuropathy

Published on: November 29, 2015

9.0K

Area of Science:

  • Ophthalmology
  • Neurology
  • Cardiology

Background:

  • Bilateral papilledema necessitates urgent evaluation for intracranial hypertension and arteritic ischemic neuropathy.
  • Drug-induced ophthalmological side effects, though often overlooked, can manifest severely and bilaterally.

Observation:

  • An 80-year-old female presented with bilateral papilledema and reduced visual acuity.
  • Intracranial hypertension, arteritic/non-arteritic ischemic optic neuropathy, and inflammatory causes were excluded.

Findings:

  • The patient was diagnosed with toxic optic neuropathy.
  • Bilateral edematous optic neuropathy is an identified, albeit uncommon, side effect of amiodarone therapy.

Implications:

  • This case underscores the importance of considering amiodarone as a potential cause of toxic optic neuropathy.
  • Increased awareness is crucial given the widespread use of amiodarone for cardiac conditions.