Abstract
Compression in the lamina cribrosa is discussed as a reason for central retinal vein occlusion. Radial optic neurotomy should release the pressure and increase venous blood outflow. In a clinical trial 27 eyes with central retinal vein occlusion (22 eyes with clinical ischaemia, 5 eyes with continuous disc oedema and visual acuity below 4/10) underwent surgical decompression by vitrectomy and radial optic neurotomy. During surgery the intravenous pressure in the central vein was tested by infusion dynamometry before and right next to the incision. Follow up-time minimally was 1.5 years. Infusion dynamometry demonstrated a decrease of the central vein pressure right next to the incision in all eyes. In 17/22 eyes with ischaemic type of occlusion 6 weeks after surgery the relative afferent pupillary defect was lowered significantly and no growth of neovascularisations occurred. 5 eyes with persistence of the afferent pupillary defect received laser/cryocoagulation because of neovascularisations. After surgery visual acuity improved in 20/27 eyes and remained unchanged in 4/27 eyes. As complications we saw small subretinal haemorrhages at the neurotomy site (5/27), vitreous haemorrhages (7/27), hypotonia and choroidal detachment (1/27) and segmental visual field loss (14/27). The results of infusion dynamometry strongly support the hypothesis of a postulated compression of the central retinal vein in the lamina cribrosa. Functional results of radial optic neurotomy are superior to those of the natural course of ischaemic retinal vein occlusion in the literature, but visual field defects in association with the neurotomy site seem to be a serious side-effect of this therapeutic approach.
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