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Archetypal Visual Field Analysis of Patients With Chronic Leber Hereditary Optic Neuropathy in Relation to Visual Recovery.

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Updated: May 16, 2026

Full-Circle Cauterization of Limbal Vascular Plexus for Surgically Induced Glaucoma in Rodents
10:10

Full-Circle Cauterization of Limbal Vascular Plexus for Surgically Induced Glaucoma in Rodents

Published on: February 15, 2022

Bilateral vision loss responsive to corticosteroids.

Michele D Lee1, Brian J Song, Jeffrey G Odel

  • 1Department of Ophthalmology, Harkness Eye Institute, Columbia University, New York, New York, USA.

Survey of Ophthalmology
|November 17, 2012
PubMed
Summary
This summary is machine-generated.

A patient initially suspected of having Leber hereditary optic neuropathy experienced recurrent vision loss. Subsequent neurological symptoms confirmed a diagnosis of multiple sclerosis, highlighting diagnostic challenges in optic neuropathies.

Keywords:
Autoimmune optic neuropathyLeber hereditary optic neuropathy (LHON)chronic relapsing inflammatory optic neuropathy (CRION)multiple sclerosisoptic neuritissteroid complicationssteroid responsive optic neuropathy

Related Experiment Videos

Last Updated: May 16, 2026

Full-Circle Cauterization of Limbal Vascular Plexus for Surgically Induced Glaucoma in Rodents
10:10

Full-Circle Cauterization of Limbal Vascular Plexus for Surgically Induced Glaucoma in Rodents

Published on: February 15, 2022

Area of Science:

  • Neuro-ophthalmology
  • Neuroimmunology
  • Demyelinating Diseases

Background:

  • Optic neuropathies can present with vision loss and may be steroid-responsive.
  • Differentiating between inherited and autoimmune optic neuropathies is crucial for accurate diagnosis and treatment.
  • Leber hereditary optic neuropathy (LHON) is a genetic mitochondrial disease causing vision loss.

Observation:

  • A 48-year-old woman presented with painless, bilateral vision loss, initially responding to steroids.
  • Diagnosis was complicated by a positive Leber hereditary optic neuropathy screen and negative demyelinating disease workup.
  • The patient developed new neurological deficits including leg weakness and sensory loss.

Findings:

  • The patient's initial presentation mimicked steroid-dependent optic neuropathies.
  • Development of white matter and spinal cord lesions, along with neurological deficits, indicated a broader neurological process.
  • The final diagnosis shifted to multiple sclerosis after initial considerations of optic neuropathies.

Implications:

  • This case underscores the importance of considering multiple sclerosis in patients with recurrent optic neuropathy, even with atypical presentations.
  • Diagnostic delays can occur when initial symptoms overlap with other conditions like Leber hereditary optic neuropathy.
  • Comprehensive neurological evaluation is essential for patients with unexplained or relapsing optic nerve dysfunction.