Some degree of nuclear sclerosis and yellowing is normal in adult patients past middle age. In general, this condition interferes only minimally with visual function. An excessive amount of light scattering and yellowing is called a nuclear cataract, which causes a central opacity (Fig 5-2). The ophthalmologist can evaluate the degree of increased color and of opacification by using a slit-lamp biomicroscope and by examining the red reflex with the pupil dilated.
Nuclear cataracts tend to progress slowly. Although they are usually bilateral, they may be asymmetric. Nuclear cataracts typically cause greater impairment of distance vision than of near vision. In the early stages, the progressive hardening of the lens nucleus frequently causes an increase in the refractive index of the lens and thus a myopic shift in refraction (lenticular myopia). In hyperopic eyes, the myopic shift enables otherwise presbyopic individuals to read without spectacles, a condition referred to as second sight. Occasionally, the abrupt change in refractive index between the sclerotic nucleus (or other lens opacities) and the lens cortex can cause monocular diplopia. Progressive yellowing or browning of the lens causes poor hue discrimination, especially at the blue end of the visible light spectrum. Photopic retinal function may decrease with advanced nuclear cataract. In very advanced cases, the lens nucleus becomes opaque and brown and is called a brunescent nuclear cataract.
Histopathologically, the nucleus in nuclear cataract is difficult to distinguish from the nucleus of normal, aged lenses. Investigations by electron microscopy have identified an increased number of lamellar membrane whorls in some nuclear cataracts. The degree to which protein aggregates or these membrane modifications contribute to the increased light scattering of nuclear cataracts is unclear.