gms | German Medical Science

Presbyopia, the age-related loss of the ability to focus on near objects, is the most common ocular affliction affecting every human being from the early 40s on. Presbyopia is universally attributed to progressive hardening and stiffening of the eye’s crystalline lens, so that despite ciliary muscle (CM) contraction and zonular relaxation, the lens progressively loses the ability to ‘sphericize’ and thereby enable focus on near objects. Rhesus monkeys and humans have an accommodative apparatus that is functionally and anatomically essentially identical, and they both develop presbyopia on the same time scale relative to life span.

Loss of accommodative amplitude starts early in life – late teen-age in humans and comparable age (given the 2.5/1 life span ratio) in monkeys, yet the CM retains its structural, biochemical, neuromuscular and contractile properties throughout most of life. However, imaging the CM during accommodative effort (Edinger-Westphal nucleus electrical stimulation in monkeys, topical pilocarpine eye drops in humans) reveals that forward/inward CM movement is progressively diminished.

Primary open angle glaucoma (POAG) and its variants, is a pressure-related optic neuropathy beginning at about the same time that the last vestiges of accommodation are lost, and is the world’s most common cause of irreversible visual loss and blindness.

Detailed ultrasound biomicroscopic and scanning electron microscopic imaging reveal that the CM movement is restricted by its posterior tendinous attachments to the elastic lamina of Bruch’s membrane, and thence the choroid and the elastic ring around the optic nerve head, and thereby to the lamina cribrosa. Fundus photography and optical flow analysis of retinal landmarks reveals that tissue movement decreases with age and with proximity to the optic nerve head, which is the center of the centrifugal movement. The CM’s progressively isometric contraction produces progressively more centrifugal force on the optic nerve head. This, coupled with posteriorly directed vitreous fluid and fibrillary movement indicating a pressure gradient and likely a pressure spike at the optic nerve head, point to altered pressure, stretch and overall force at the optic nerve head with age and with every accommodative effort. Coupled with even a small age-related increase in intraocular pressure these changes may play a role in the development of glaucomatous optic neuropathy, first seen at the age (40–50 yrs.) when the last remnant of accommodative amplitude disappears.

Are presbyopia and glaucoma two diseases with one pathophysiology?