Vitreal pathogenic role in optic pit foveolar retinoschisis and central serous chorioretinopathy

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Abstract
To expand on current theories concerning the vitreal-induced mechanism underlying the development of foveolar retinoschisis and macular sensory detachments associated with optic nerve head pits. To propose the notion that vitreal traction may contribute to the pathogenesis of serous detachments in central serous chorioretinopathy (CSC). We describe two patients, one with macular retinoschisis and the other with central serous detachment. The first patient, a 45-year-old Hispanic female, presented with a temporally located optic nerve head pit, foveolar retinoschisis and schisis retinal spaces extending to the surrounding macula and to the disc. The second patient, a 43-year-old Haitian male, developed a central serous retinal detachment OS with decreased visual acuity one day following in-office administration of Apraclonidine (0.5 per cent Iopidine, Alcon) and Dorzolamide-Timolol Maleate (Cosopt, Merck) to lower elevated intraocular pressure (IOP). Macular retinal pigment mottling and epiretinal membrane sheen OU had been observed on his initial visit. Visual acuity improved within a three-day period with resolution of the serous detachment. We suggest that the persistence of Cloquet's canal may permit fluid leakage into the proximal vitreous in cases of congenital optic nerve head pits. Tangential vitreal traction may promote the opening of a fistula at the optic pit and additionally thrust vitreal fluid into the pit and retinal space inducing the formation of schisis spaces, foveolar-schisis and underlying sensory serous detachment. We question whether a reduction in vitreous volume, induced by initial administration of anti-glaucoma medications, may contribute to the development and/or recurrence of central serous choroidopathy in predisposed individuals.