Clinically and pathologically there are two kinds of posterior subcapsular cataracts: vacuolar-lacy and solid plaque. Vacuolar opacities occur in senile, diabetic, retinitis pigmentosa, steroid, and secondary cataracts (Elschnig pearls). Plaque opacities occur in congenital polar, myotonic dystrophy, and Turner syndrome (chromosome XO) cataracts. The vacuolar opacities tend to be more superficial (closer to the posterior capsule), whereas the plaque opacities are generally slightly deeper (more cortical). The vacuolar opacities show cellular proliferation of aberrantly migrated lens epithelial cells in the posterior pole which have added damage to the cataract by secretion of basement membrane, intra- and extra-cellular filaments, and release of cytolytic lysozymes causing liquefaction and necrosis. The plaque opacities are acellular. Both types of cataracts show breakdown of lens fibres into rounded up disorganized globules and some membranous whorls. The liquefied vacuolar opacity is more readily removed by extracapsular cataract extraction, but the retention of nucleated lens epithelial cells in the vacuolar type of opacity is the source of a secondary cataract or Hirchberg-Elschnig pearls which require a discussion or membranectomy to clear the visual axis. This article will review the salient features in the histopathology (light and electron microscopy) and morphology of PSC and amalgamate the findings reported by several investigators (Eshagian and Streeten, 1975; Eshagian, March, Goossens, and Rafferty, 1978, 1978; Eshagian, Rafferty, and Goossens, 1980, 1981; Eshagian, Rafferty, Goossens, and March, 1979; 1980; Streeten and Eshagian, 1978).