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Updated: Jun 27, 2025

Dynamic Visual Tests to Identify and Quantify Visual Damage and Repair Following Demyelination in Optic Neuritis Patients
Published on: April 14, 2014
Optociliary shunt vessels in multiple sclerosis
Sana Nadeem1, Aasma Nudrat Zafar2
1Department of Ophthalmology, Foundation University Medical College and Fauji Foundation Hospital, Rawalpindi, Pakistan.
Background/Introduction:
Optociliary shunt vessels develop as a result of chronic retinal venous obstruction. Optic neuritis has never been reported as a causative influence.
Objective:
To determine whether optic neuritis predisposes to the development of optociliary shunts in patients with multiple sclerosis.
Cases:
This case series follows two patients with multiple sclerosis from August 1st, 2019 to April 24th, 2024, who developed optociliary shunt vessels after attacks of optic neuritis. A 43-year-old female presented with left visual loss and bilateral superior optociliary shunt vessels. Perimetry showed bilateral peripheral visual field loss. Optical coherence tomography showed bilateral retinal thinning and ganglion cell complex loss. Optical coherence tomography angiography showed reduced capillary density bilaterally. We investigated her and eventually diagnosed her with multiple sclerosis. The second, a 49-year-old female, developed right-sided optociliary shunt vessels after an episode of neuroretinitis. Perimetry revealed bilateral central scotomata; optical coherence tomography showed disc and retinal nerve fiber layer edema, and serous retinal detachment; later, ganglion cell complex loss; and reduced capillary density on optical coherence tomography angiography. Neuroimaging revealed demyelination in both, leading to a diagnosis of multiple sclerosis, and therapy was instituted.
Conclusions:
We hypothesize, that demyelinating optic neuritis due to multiple sclerosis causes chronic retinal hypoperfusion, leading to subsequent optociliary shunt development in affected eyes. Our case series reveals that eyes with optic neuritis, both previous episodes and fresh cases, can contribute to sufficient retinal vein hypoperfusion to cause the development of optociliary shunts, which should be reported in the literature.
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