Abstract
Purpose: :
Optic nerve loss in glaucoma may result in intraocular pressure induced biomechanical deformation of the load bearing structures of the optic disc (lamina cribosa, peripapillary retina) that can be shown by OCT. We postulate that intracranial hypertension causes elevated pressure transmission in the subarachnoid space outside to inside the globe, which can cause a similar alteration of the optic disc. Although, the degree and direction of the deformation will differ from those observed in glaucoma.
Methods: :
We compared OCT optic nerve findings in patients with papilledema due to intracranial hypertension to disc edema due to optic neuritis and non-arteritic anterior ischemic optic neuropathy (conditions without intracranial hypertension). We measured the angle of the retinal pigment epithelium/Bruch’s membrane (RPE/BM) at its temporal and nasal rim relative to the surrounding retina.
Results: :
In 6/12 patients with papilledema the RPE/BM rim was deflected anteriorly (5-15 degrees) where 0/9 NAION and 1/5 optic neuritis optic discs had this finding. The 1 case in optic neuritis had MRI evidence of inflammation extending to the sclera. The anterior angulation did not correlate with the amount of optic disc edema or nerve fiber layer thickening. Three of the six with papilledema with anteriorly displaced RPE/BM rims underwent procedures that reduced the intracranial pressure. This resulted in a reversal in the RPE/BM angulations (0 to -10 degrees, outward) and reduction in total RNFL thickening (424 to 72, 407 to 88, 319 to 181, 304 to 153, 293 to 118, 457 to 231µ).
Conclusions: :
The RPE/BM appears to be displaced more anteriorly by elevation in the optic nerve subarachnoid pressure and is not a function of the degree of optic disc swelling. This feature may aid in determining the cause of optic disc edema and in following the course of pressure lowering treatments.
Keywords: optic disc • imaging methods (CT, FA, ICG, MRI, OCT, RTA, SLO, ultrasound) • neuro-ophthalmology: optic nerve