Microangioarchitecture of optic papilla

Two hundred postmortem normal human eyes of 100 cases were studied by four methods to investigate the microangioarchitecture of the optic papilla. The following results have been obtained. The Zinn's circle is important to the blood supply of the optic papilla. It gives off tributaries to the papillar prelaminar and laminar layers and pial vessel network at the retrolaminar portion. The blood supply of the prelaminar layer comes directly from the branches of the short posterior ciliary arteries and Zinn's circle, while the choroidal vessels contribute only a few branches to this area. The above two results are not consistent with Hayreh's idea. Between the central retinal artery system and short posterior ciliary artery system, there are anastomoses at the pial vessel network and in the optic nerve at the retrolaminar portion, but none is found, obviously, in the intraocular portion of the optic nerve. The microangioarchitecture of the optic papilla is accommodated to the nerve in which it resides. The most superficial vessels are radiating, those in the prelaminar and laminar layers are lamellar, and those in the retrolaminar portion are an interwoven network. The caliber of the capillary at the prelaminar and laminar layers is the narrowest, therefore, an ischemic change easily takes place right here.     

Hemorrhagic complications in drusen of the optic papilla

A case of optic disc drusen complicated by retinal hemorrhages similar to those seen in central retinal vein occlusion is presented. While haemorrhagic complications of optic disc drusen are rare, three types have been described: small disk haemorrhages, vitreous haemorrhages and deep peripapillary haemorrhages. This clinical aspect of the haemorrhagic retinopathy presented in this paper has rarely been described; the pathogenesis of this lesion can be attributed to a progressive compression by the drusen on the central vein in the optic disk, causing a venous stasis retinopathy. Since it is impossible to remove the cause of the venous compression, the prognosis of this clinical form is always poor. Finally, the author emphasizes the need to consider this rare complication of drusen of the optic disk, especially in young patients with no systemic pathology who present this ophthalmoscopic picture, in order to avoid useless, time consuming tests and ineffective therapies.     

Unilateral infiltration of the optic papilla in chronic lymphatic leukemia

This paper reports the clinical history of a 72-year-old woman in whom unilateral papilledema was the only organic manifestation of chronic lymphatic leukemia. In the light of the laboratory parameters direct leukemic infiltration of the optic disk was diagnosed by fundus examination and fluorescein angiography. Combined cytostatic therapy bed to a considerable improvement in the patient's clinical condition.     

Pits of the optic papilla in large optic nerve papillae. Papillometric characteristics in 15 eyes

Fifteen optic nerve heads with pits measured by optic disk planimetry according to Littmann and Jaeger's method were significantly larger than previously determined normal optic nerve heads. Their area measured 4.84 +/- 1.42 mm2 (2.77-8.02 mm2), their horizontal diameter 2.42 +/- 0.42 mm (1.76-3.38 mm) and their vertical diameter 2.53 +/- 0.30 mm (1.14-3.06 mm). The quotients of minimum to maximum diameter and the angle between the maximum diameter and the horizontal line were similar to those in normal optic disks. Because of their enlarged area but normal form this pathologic entity forms a subunit of macrodisks. The pits were located in 14 optic disks on the temporal side on average 100 degrees from the upper disk pole, and in two optic disks on the nasal side about 85 degrees from the upper pole. In two cases they were double and in one bilateral. Their area and number were significantly correlated (p less than 0.001 and p less than 0.05) to the area of the optic disk. With increasing optic nerve head size the optic cup was less excavated. The largest optic disk seen in this study did not have one at all. There might be a stepless continuation from normal-sized optic disks to macrodisks with physiologic macrocups and to optic nerve heads with pits. These represent a maximum extreme in the spectrum of optic disk anomalies and diseases associated with optic nerve head size.     

Effect of carbogen breathing and acetazolamide on optic disc PO2

PURPOSE: Acetazolamide was previously shown to increase optic disc partial pressure of oxygen (PO(2)). The study was conducted to evaluate optic disc PO(2) variations during normoxia, hyperoxia (100% O(2)), and carbogen breathing (95% O(2), 5% CO(2)), before and after intravenous administration of acetazolamide. METHODS: PO(2) measurements were obtained at intervascular areas of the optic disc in nine anesthetized minipigs using oxygen-sensitive microelectrodes (10-microm tip diameter) placed at <50 microm from the optic disc. PO(2) was measured continuously during 10 minutes under normoxia, hyperoxia, or carbogen breathing. Oxygen measurements were repeated under these conditions after intravenous injection of acetazolamide (500-mg bolus). RESULTS: In hyperoxia, optic disc PO(2) increased moderately (DeltaPO(2) = 4.81 +/- 1.16 mm Hg (mean +/- SD; 24%; P < 0.001) after a much larger increase in systemic PaO(2). Carbogen breathing induced a significant increase in both systemic PaO(2) and PaCO(2), which resulted in a large increase in optic disc PO(2) (DeltaPO(2) = 13.17 +/- 2.18 mm Hg; 67%; P < 0.001). Acetazolamide induced a slow and progressive increase in both systemic PaCO(2) and optic disc PO(2) (30 minutes DeltaPO(2) = 4.24 +/- 2.45 mm Hg; 24%; P < 0.04). However, it was when carbogen was simultaneously administered that optic disc PO(2) increased most substantially (DeltaPO(2) = 18.91 +/- 5.23 mm Hg; 90%; P < 0.002). CONCLUSIONS: Carbogen breathing increases optic disc Po(2) significantly in minipigs, more than hyperoxia. The association of acetazolamide injection with carbogen breathing could induce an additional increase in optic disc PO(2) through the effect of higher systemic PaCO(2).