In contrast to nuclear cataracts, cortical cataracts are associated with the local disruption of the structure of mature fiber cells. Once membrane integrity is compromised, essential metabolites are lost from the affected cells. This loss leads to extensive protein oxidation and precipitation. Cortical cataracts are usually bilateral but are often asymmetric. Their effect on visual function varies greatly, depending on the location of the opacification relative to the visual axis. A common symptom of cortical cataracts is glare from intense focal light sources, such as car headlights. Monocular diplopia may also result. Cortical cataracts vary greatly in their rate of progression; some cortical opacities remain unchanged for prolonged periods, whereas others progress rapidly.
The first signs of cortical cataract formation visible with the slit-lamp biomicroscope are vacuoles and water clefts in the anterior or posterior cortex (Fig 5-3). The cortical lamellae may be separated by fluid. Wedge-shaped opacities (often called cortical spokes or cuneiform opacities) form near the periphery of the lens, with the pointed end of the opacities oriented toward the center (Fig 5-4). Since these peripheral opacities occur in fiber cells that extend from the posterior to the anterior sutures, they affect only the central regions of the fiber cells. In the initial stages of the cataract, affected fiber cells remain clear at their anterior and posterior ends. The cortical spokes appear as white opacities when viewed with the slit-lamp biomicroscope and as dark shadows when viewed on retroillumination. The wedge-shaped opacities may spread to adjacent fiber cells and along the length of affected fibers, causing the degree of opacity to increase and extend toward the visual axis. When the entire cortex from the capsule to the nucleus becomes white and opaque, the cataract is said to be mature (Fig 5-5). In mature opacities, the lens takes up water, swelling to become an intumescent cortical cataract.
A hypermature cataract occurs when degenerated cortical material leaks through the lens capsule, leaving the capsule wrinkled and shrunken (Fig 5-6). A morgagnian cataract occurs when further liquefaction of the cortex allows free movement of the nucleus within the capsular bag (Fig 5-7).
Histopathologically, cortical cataracts are characterized by local swelling and disruption of the lens fiber cells. Globules of eosinophilic material (morgagnian globules) are observed in slitlike spaces between lens fibers.