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

Open Angle Glaucoma: Treatment01:27

Open Angle Glaucoma: Treatment

1.1K
In open-angle glaucoma, the iridocorneal angle remains open, but the trabecular meshwork becomes stiff, slowing down the outflow of aqueous humor. This causes a buildup of aqueous humor in the anterior chamber, leading to a sudden increase in intraocular pressure. The treatment for open-angle glaucoma focuses on reducing the elevated intraocular pressure by either decreasing the secretion of aqueous humor or increasing its outflow.
Drugs such as carbonic anhydrase inhibitors, α2- and...
1.1K
Angle Closure Glaucoma: Treatment01:28

Angle Closure Glaucoma: Treatment

1.7K
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...
1.7K
Glaucoma: Overview01:25

Glaucoma: Overview

1.7K
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...
1.7K

You might also read

Related Articles

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

Sort by
Same author

Spinal claudication due to myxopapillary ependymoma.

BMJ case reports·2025
Same author

Comparison of Chemotherapy Combined with Percutaneous Electroporation and Chemotherapy Alone in the Management of Locally Advanced Gallbladder Carcinoma (GBC): A Study Protocol.

Cardiovascular and interventional radiology·2024
Same author

Five-year analysis of neoadjuvant dabrafenib and trametinib for stage III melanoma.

Annals of oncology : official journal of the European Society for Medical Oncology·2024
Same author

Invited review: Shelf-stable dairy protein beverages-Scientific and technological aspects.

Journal of dairy science·2022
Same author

FDG-PET to predict long-term outcome from anti-PD-1 therapy in metastatic melanoma.

Annals of oncology : official journal of the European Society for Medical Oncology·2021
Same author

Dapsone-induced methaemoglobinaemia in leprosy: a close mimic of 'happy hypoxia' in the COVID-19 pandemic.

Journal of the European Academy of Dermatology and Venereology : JEADV·2021

Related Experiment Video

Updated: Apr 14, 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

1.6K

Neuroprotection for acute optic neuritis-Can it work?

R E Raftopoulos1, R Kapoor1

  • 1Institute of Neurology, Queen Square, London WC1N 3BG, United Kingdom.

Multiple Sclerosis and Related Disorders
|April 17, 2015
PubMed
Summary

Optic neuritis, a common MS symptom, involves inflammation and neuroaxonal loss. Early sodium channel blockade may protect nerves and improve vision recovery in multiple sclerosis (MS) relapses.

Keywords:
DisabilityMultiple sclerosisNeuroprotectionOptic neuritisSodium channel blockade

More Related Videos

Dynamic Visual Tests to Identify and Quantify Visual Damage and Repair Following Demyelination in Optic Neuritis Patients
12:23

Dynamic Visual Tests to Identify and Quantify Visual Damage and Repair Following Demyelination in Optic Neuritis Patients

Published on: April 14, 2014

14.7K
An Optic Nerve Crush Injury Murine Model to Study Retinal Ganglion Cell Survival
09:07

An Optic Nerve Crush Injury Murine Model to Study Retinal Ganglion Cell Survival

Published on: April 25, 2011

32.1K

Related Experiment Videos

Last Updated: Apr 14, 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

1.6K
Dynamic Visual Tests to Identify and Quantify Visual Damage and Repair Following Demyelination in Optic Neuritis Patients
12:23

Dynamic Visual Tests to Identify and Quantify Visual Damage and Repair Following Demyelination in Optic Neuritis Patients

Published on: April 14, 2014

14.7K
An Optic Nerve Crush Injury Murine Model to Study Retinal Ganglion Cell Survival
09:07

An Optic Nerve Crush Injury Murine Model to Study Retinal Ganglion Cell Survival

Published on: April 25, 2011

32.1K

Area of Science:

  • Neuroscience
  • Ophthalmology
  • Immunology

Background:

  • Optic neuritis is a frequent manifestation of multiple sclerosis (MS), characterized by inflammatory lesions in the optic nerve.
  • Corticosteroid treatment for MS relapses, including optic neuritis, has minimal impact on long-term visual recovery.
  • Neuroaxonal loss is a primary driver of permanent disability in MS, evidenced by imaging studies like optical coherence tomography (OCT) and MRI.

Purpose of the Study:

  • To investigate the potential of sodium channel blockade as a neuroprotective strategy in acute optic neuritis.
  • To evaluate the efficacy of phenytoin in preventing axonal loss and improving visual function following optic neuritis, a model for MS relapses.

Main Methods:

  • Utilizing optical coherence tomography (OCT) and magnetic resonance imaging (MRI) to quantify neuroaxonal volume loss in the optic nerve and retina.
  • Assessing the correlation between inflammation, axonal loss, and visual impairment.
  • Conducting a randomized placebo-controlled trial of phenytoin in patients with acute optic neuritis, with outcome measures timed to account for treatment and atrophy lag periods.

Main Results:

  • Excessive sodium ion accumulation within axons during inflammation contributes to axonal degeneration.
  • Partial blockade of sodium channels has shown promise in protecting against axonal loss and improving outcomes in experimental MS models.
  • Previous trials, like the lamotrigine study in secondary progressive MS, yielded mixed results but suggested potential benefits in walking speed and neurofilament levels.

Conclusions:

  • The pathophysiology of optic neuritis shares similarities with other MS relapses, suggesting that neuroprotective strategies may have broader applications.
  • Targeting sodium channels offers a potential therapeutic avenue to mitigate neuroaxonal damage and enhance recovery from MS-related optic nerve inflammation.
  • The ongoing phenytoin trial in acute optic neuritis aims to address limitations of previous studies and provide robust evidence for neuroprotection in early inflammatory lesions.