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An unusual mimic of intracranial hypertension
  1. Nejla Ghane1,
  2. Jorge C Kattah1,2,
  3. Brady Mannett1,
  4. Sang H Hong3
  1. 1Department of Neurology, College of Medicine at Peoria, University of Illinois Chicago, Peoria, Illinois, USA
  2. 2Department of Neurology, Illinois Neurological Institute, Peoria, Illinois, USA
  3. 3Ophthalmology, Medical College of Wisconsin, Milwaukee, Wisconsin, USA
  1. Correspondence to Dr Jorge C Kattah, Department of Neurology, Illinois Neurological Institute, Peoria, Illinois, USA; kattahj{at}

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Initial presentation

A 60-year-old man had a 2-week history of daily recurrent episodes of transient, painless vision loss, each lasting 3–5 s. He had attended ophthalmology for years because of intermittent diplopia, and a history of type 1 diabetes mellitus, primary open angle glaucoma, bilateral cataract surgery and Graves’ disease with subsequent hypothyroidism. In April 2021, he developed vision loss described as complete bilateral, non-simultaneous visual blackout prompted by left/right gaze. His vision returned to baseline on return to centre gaze. There was also a more persistent left visual field defect. Funduscopy identified asymmetric optic disc oedema. The right optic disc showed mild margin blurring with congestion, but with distinct optic disc vessels (Frisén grade 2). The left optic disc had more pronounced optic nerve swelling, indistinct peripapillary arterioles and microhaemorrhages (Frisén grade 3) (figure 1). Ophthalmology, therefore, referred him for emergency evaluation because of concern for permanent vision loss.

Figure 1

Digital fundus photography. (A,B) (pre treatment) Elevated right optic disc margins and the outline of the optic nerve head vessels (Frisén grade 2). The left optic nerve head is significantly elevated with indistinct optic nerve vasculature (Frisén grade 3). The patient also had retinal striae in the left eye (not shown). (C,D) (post-treatment) The optic disc oedema has resolved, leaving moderate pallor and greyish peripapillary changes.

1. Is this patient’s vision loss more appropriately classified as transient vascular obscurations or amaurosis fugax?

Transient visual obscurations are caused by episodes of reversible, decreased perfusion to the optic nerve, causing momentary complete vision loss. With binocular vision loss, the localisation can be bilateral in the optic nerves, optic chiasm or retrochiasmal areas. The pathophysiology of amaurosis fugax, a subset of transient visual obscurations, includes hypoperfusion secondary to obstruction or recurrent emboli involving the internal carotid or ophthalmic artery circulation, causing reversible ischaemia to the retina, …

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  • Contributors NG: Drafting/revision of the manuscript for content, including medical writing for content. BM: Major role in the acquisition of data. SHH: Drafting/revision of the manuscript for content, including medical writing for content. JCK: Drafting/revision of the manuscript for content, including medical writing for content, analysis or interpretation of data.

  • Funding The authors have not declared a specific grant for this research from any funding agency in the public, commercial or not-for-profit sectors.

  • Competing interests None declared.

  • Provenance and peer review Not commissioned; externally reviewed by Mark Lawden, Leicester, UK and Sui Wong, London, UK.

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