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Peer-reviewedCC BY-NC-NDJournal of Clinical and Diagnostic Research

Bilateral Vision Loss due to Fulminant Hypertensive Optic Neuropathy Mimicking Cortical Blindness in a Patient with Co-existing Vestibular Schwannoma: A Case Report

  1. 1Assistant Professor, Department of Ophthalmology, Dr. DY Patil University, Pune, Maharashtra, India.
  2. 2Resident, Department of Ophthalmology, Dr. DY Patil University, Pune, Maharashtra, India.

Abstract

Malignant hypertension is a hypertensive emergency characterised by acute target-organ damage involving the cardiovascular, renal, neurological and ocular systems. Although hypertensive retinopathy is a well-recognised manifestation of malignant hypertension, profound bilateral visual loss secondary to hypertensive optic neuropathy is exceedingly rare and may mimic cortical blindness, posing a significant diagnostic challenge. Here, the authors report a case of a 66-year-old male with poorly controlled systemic hypertension who presented with sudden painless bilateral visual loss progressing to no perception of light in both eyes. Fundus examination revealed bilateral grade 4 hypertensive retinopathy with marked optic disc oedema. Pupillary reactions were sluggish but preserved without a relative afferent pupillary defect. Optical coherence tomography demonstrated relatively preserved retinal architecture, whereas Magnetic Resonance Imaging (MRI) revealed a vestibular schwannoma without occipital lobe involvement or diffusion restriction, effectively excluding cortical causes of blindness. The patient was managed as a hypertensive emergency with gradual blood pressure reduction. At one-month follow-up, visual acuity improved to finger counting at one foot in both eyes with mild reduction in optic disc oedema. This case highlights the importance of clinicoradiological correlation in patients presenting with profound bilateral visual loss and emphasises the diagnostic limitations of relative afferent pupillary defect in bilateral symmetric optic nerve disease.

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BibTeX
@article{chaturvedi2026bilateral,
  title = {{Bilateral Vision Loss due to Fulminant Hypertensive Optic Neuropathy Mimicking Cortical Blindness in a Patient with Co-existing Vestibular Schwannoma: A Case Report}},
  author = {Naina Chaturvedi and Rohan Jagadish and Kritika Aggarwal and Sai Hari Chandana and Gautami Ramesh Laturkar},
  journal = {Journal of Clinical and Diagnostic Research},
  year = {2026},
  month = nov,
  doi = {10.7860/jcdr/2026/89882.24688},
  url = {https://doi.org/10.7860/jcdr/2026/89882.24688},
  note = {CC BY-NC-ND},
}
RIS
TY  - JOUR
TI  - Bilateral Vision Loss due to Fulminant Hypertensive Optic Neuropathy Mimicking Cortical Blindness in a Patient with Co-existing Vestibular Schwannoma: A Case Report
AU  - Naina Chaturvedi
AU  - Rohan Jagadish
AU  - Kritika Aggarwal
AU  - Sai Hari Chandana
AU  - Gautami Ramesh Laturkar
PY  - 2026
DA  - 2026/11/04
JO  - Journal of Clinical and Diagnostic Research
DO  - 10.7860/jcdr/2026/89882.24688
UR  - https://doi.org/10.7860/jcdr/2026/89882.24688
AB  - Malignant hypertension is a hypertensive emergency characterised by acute target-organ damage involving the cardiovascular, renal, neurological and ocular systems. Although hypertensive retinopathy is a well-recognised manifestation of malignant hypertension, profound bilateral visual loss secondary to hypertensive optic neuropathy is exceedingly rare and may mimic cortical blindness, posing a significant diagnostic challenge. Here, the authors report a case of a 66-year-old male with poorly controlled systemic hypertension who presented with sudden painless bilateral visual loss progressing to no perception of light in both eyes. Fundus examination revealed bilateral grade 4 hypertensive retinopathy with marked optic disc oedema. Pupillary reactions were sluggish but preserved without a relative afferent pupillary defect. Optical coherence tomography demonstrated relatively preserved retinal architecture, whereas Magnetic Resonance Imaging (MRI) revealed a vestibular schwannoma without occipital lobe involvement or diffusion restriction, effectively excluding cortical causes of blindness. The patient was managed as a hypertensive emergency with gradual blood pressure reduction. At one-month follow-up, visual acuity improved to finger counting at one foot in both eyes with mild reduction in optic disc oedema. This case highlights the importance of clinicoradiological correlation in patients presenting with profound bilateral visual loss and emphasises the diagnostic limitations of relative afferent pupillary defect in bilateral symmetric optic nerve disease.
SN  - 2249-782X
SN  - 0973-709X
ER  -