Floaters and the quality of life.

c t h P p t a o m a i N 1976, DR ERNST WYNDER, FOUNDING PRESIDENT OF THE American Health Foundation and founding editor of the journal Preventive Medicine, stated that “It should be the function of medicine to help people die young . . . as late in life as possible.” However, medicine in general, and phthalmology in specific, are disease-oriented disciplines. In he former case, this is due to the fact that “Disease is a living xperience for the man of flesh and bone. In contrast, health s a disembodied concept. It stimulates no emotional response ecause it is an inhuman, fleshless abstraction” (René Jules ubos, The Silliman Lectures, Yale, 1965). As ophthalmolgists, we are trained to evaluate eyes by seeking evidence of isease using biomicroscopy and ophthalmoscopy, as well as ith diagnostic testing. When we rule out pathology by these odalities, we advise patients that they are free of disease. uch advice is apparently a frustrating and unfulfilling expeience for patients with “floaters.” From their point of view, he consulting ophthalmologist who sought evidence of isease and found none has nonetheless failed to address their ealth and quality-of-life issues. In youth, vitreous is a solid and clear gel filling the enter of the eye, firmly attached to the retina. The xquisite transparency of vitreous allows unhindered transission of light to the retina for photoreception. Other than “exogenous” sources, such as hemorrhage and inflammation, there are 2 main causes of the entopic phenomenon called “floaters,” which result from light scattering by structures within the vitreous body and/or at the posterior vitreous cortex. Although devoid of liquid during infancy, the vitreous body begins to liquefy in childhood due to molecular rearrangement of the constituent macromolecules hyaluronan and collagen. Part of this molecular alteration involves cross-linking and aggregation of vitreous collagen fibrils. If advanced, fibrillar aggregation can cause sufficient interference of photon transmission to induce chronic and progressive floaters. In myopia, the process of vitreous gel liquefaction and fibrillar aggregation appears to be accelerated, a manifestation of myopic vitreopathy. Concurrent with vitreous gel liquefaction, there is weakening of vitreoretinal adhesion. When both processes advance in tandem to a critical threshold, there is eparation of the posterior vitreous cortex from the retina, erhaps initially only in the perifoveal region. Displace-