The article “Angle-closure glaucoma–Simpler answers to complex mechanisms: LXVI Edward Jackson Memorial Lecture” by Harry A Quigley introduces a new concept of dynamic physiological features precipitating acute angle closure in susceptible individuals with static anatomic factors. This answers many issues related to the pathogenesis of glaucoma in general and angle-closure glaucoma in particular.
The possible mechanism of reduced exchange of extracellular fluid with the aqueous as suggested by Quigley, citing the difference in iris connective tissue histologic studies in angle-closure eyes, is understandable in diseased eyes. In eyes affected by acute angle closure, the damage caused by acute rise in intraocular pressure (IOP) results in higher density of collagen in the stromal tissue and damage to the stroma. This is a result of the increased IOP rather than the cause, initiating the process of angle closure. In addition, the irideal stroma as a percentage of iris tissue is negligible compared to the other constituents, like the iris vasculature, muscles and nervous tissue, and pigmented epithelium. It is logical to propose that increased vascular resistance could be the reason why reduced loss of irideal volume and area in persons with a tendency to develop vascular resistance leads to reduced irideal contraction and thus ability to lose volume and area as recorded by Quigley. The time taken to lose the volume/area of iris (ie, 10 seconds, as shown in the article) also is in favor of a vascular phenomenon as opposed to losing extracellular fluid, which theoretically is a more rapid process. It has been reported that vascular deficits (such as vascular resistance) may contribute to the initiation and progression of glaucoma. The drug trials with calcium channel blockers in normal-tension glaucoma have shown beneficial effect in reducing vascular resistance, which consequently increases the optic disc blood flow. Quigley has felt that choroidal expansion is inappropriately regulated in angle-closure glaucoma. It is probably attributable to unstable vasomotor tone in susceptible people. The author has highlighted the role of choroidal expansion in secondary angle closure attributable to varied conditions wherein the vascular component is an integral part. In all the conditions mentioned by the author vascular compromise is an essential factor. The extracellular fluid accumulation resulting in increased irideal volume and choroidal expansion in angle-closure glaucoma can be explained well if reduction of vascular resistance is considered as a factor initiating and compromising the angle closure, leading to increased IOP.