The absence of receptive elements in the optic disc accounts for the normal blind spot. The normal optic disc varies in color, being paler in infants and in blond individuals. The ganglion cell axons normally acquire their myelin sheaths after penetration of the lamina cribrosa, but they sometimes do so in their intraretinal course, as they approach the disc. These myelinated fibers adjacent to the disc appear as white patches with fine-feathered edges and are a normal variant, not to be confused with optic disc edema or retinal ischemia.
If there is a lesion in one optic nerve, a light stimulus to the affected eye will have no effect on the pupil of either eye, although the ipsilateral pupil will still constrict consensually, that is, in response to a light stimulus from the normal eye. This phenomenon is termed a relative afferent pupillary defect (the Marcus Gunn pupil).
In the optic chiasm, the fibers derived from the nasal half of each retina decussate and continue in the optic tract with the uncrossed temporal fibers of the other eye (Figs. 12-2 and 12-4). Thus, interruption of the left optic tract causes a right hemianopic defect in each eye, that is, a homonymous (left nasal and right temporal) field defect (see Fig. 12-2D). In partial tract lesions, the visual defects in the two eyes may not be congruent, as the tract fibers are not evenly admixed. Lesions at the junction of the optic nerve and chiasm, generally compressive in nature, may cause a small contralateral superotemporal quadrantic defect in addition to the expected central scotoma in the ipsilateral eye (“junctional scotoma,” Fig. 12-2B). It had been thought for many decades to result from compression of Wilbrand knee, a bundle of fibers that turn back into the contralateral optic nerve before crossing in the chiasm, but it has since been related by Horton that the very existence of the bundle is merely an artifact of long-term monocular enucleation.
The optic chiasm lies just above the pituitary gland and also forms part of the anterior wall of the third ventricle; hence, the crossing fibers may be compressed from below by a pituitary tumor, a meningioma of the tuberculum sellae, or an aneurysm, and from above by a dilated third ventricle or craniopharyngioma. The resulting field defect is bitemporal (“bitemporal hemianopia”; Fig. 12-2C). In albinism, there is an abnormality of chiasmatic decussation, in which a majority of the fibers cross to the other side because of a defect in melanin signaling that normally contributes to patterning of the chiasm.
From the retina, there is a point-to-point projection to the lateral geniculate nucleus and from there, to the calcarine cortex of the occipital lobe. For purposes of description of the visual fields, each retina and macula are divided into a temporal and nasal half by a vertical line passing through the fovea. A horizontal line represented roughly by the junction of the superior and inferior retinal vascular arcades also passes through the fovea and divides each half of the retina and macula into upper and lower quadrants. Visual field defects are always described from the patient’s view (nasal, temporal, superior, inferior) rather than of the retinal defect or the examiner’s perspective. The retinal image of an object in the visual field is inverted and reversed from right to left, like the image on the film of a camera. Thus the left visual field of each eye is represented in the opposite half of each retina, with the upper part of the field represented in the lower part of the retina (Figs. 12-2 and 12-4). Figure 12-5 illustrates the retinal projections to the geniculate nuclei and occipital cortex.