EFFECTS OF TRANSIENT INDUCED ELEVATION OF THE INTRA-OCULAR PRESSURE ON THE VISUAL FIELD.

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THE cavernous atrophy of the optic nervehead and the visual field loss characteristic of the progressive glaucomatous process are thought to be due to an upset of balance between the intra-ocular pressure (I.O.P.) and the arteriocapillary pressure in the network supplying the optic nervehead. Which of these factors is primarily or predominantly responsible for this imbalance and for the pathogenesis of the impaired visual function is still under dispute. Clinically the degree of loss of visual field does not vary proportionally with the level of the I.O.P. in each case. Furthermore, the factors known to influence the glaucomatous process, such as the age of the patient or the state of the systemic and retinal circulation, do not explain why some eyes continue to lose visual field with a and almost hydrodynamic conditions, while others can withstand a high pressure with little or no damage. This fact became evident soon after the application of tonometry, and the low tension glaucoma described as a separate clinical entity is to-day accepted as no more than an extreme example of a high sensitivity of the optic nerve to the I.O.P., so that even a statistically normal produces damage to the optic nerve. The most valid concept relating these facts is that the primary event in chronic simple glaucoma is a functional vascular dyscrasia of the capillary bed of the eye as a whole, leading to structural changes in the vessel walls and to tissue sclerosis. This process affects in different degree the structures responsible for the production and outflow of the aqueous humour as well as the optic nerve. Therefore if the complication of a raised I.O.P. is added to the sclerosis of the optic nervehead, excavation of the optic disc will run on apace (Duke-Elder, 1957, 1962). Studies focused especially on the circulation of the optic nervehead led to the following more or less widely accepted conclusions: