AT the root of the clinical phenomena to be described, lies a singular haemodynamic arrangement to be found in the central retinal vein. Within a space of a.few millimetres, the pressure in this vessel drops from around 20 mm. Hg at the optic disc, to levels ranging from zero in the upright position, to 10 mm. in recumbency. The examination of the vein, however, reveals no special device whereby this high-pressure gradient is maintained. After entering the nerve-head, the vein traverses the lamina cribrosa and then maintains its central position within the optic nerve for a further distance of a'few millimetres. The lamina cribrosa, being able to withstand these pres- sure differences, is the only structure in the course of the central retinal vein capable of acting as a"throttle" device to maintain this pressure gradient. Being unyielding within this pressure range, the interstices of the lamina cannot be anything but fixed in size. Poiseuille's formula would suggest that, in order to bring about a 50 per cent. reduction of pressure after emission through the lamina cribrosa, the diameter of the vein would have to be reduced by only some 16 per cent. In keeping with this inferred "throttle" action of the lamina cribrosa are the observations that, in cats and dogs, pressure variations in the perioptic subarachnoid space below 18 mm. Hg failed to affect the pressure of the central retinal vein at the nerve-head The conclusion that the pressure gradient within the retinal vein is maintained by a high "flow resistance" is inescapable, though for the purpose of the thesis to be presented, its precise topology is immaterial.
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Simon Behrman (1962) studied this question.
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