Figure 6.

Thalamic defects caused by the misrouting of retinal fibers at the optic chiasm. (a) In primates, nasal RGC axons (red) cross the midline at the optic chiasm while temporal RGC axons (green) extend ipsilaterally, projecting toward the lateral geniculate nucleus and then the visual cortex, maintaining the strict retinotopic segregation of the visual field. (b) In achiasmatic individuals, nasal RGC axons fail to decussate adequately at the chiasm, instead projecting ipsilaterally toward the lateral geniculate nuclei together with temporal RGC axons. (c) In albinism, ipsilaterally destined temporal RGC axons erroneously decussate and project contralaterally at the optic chiasm. In both of these conditions, the corresponding visual field is a complete (achiasmatic) or partial (albinism) mirror inversion of the representation in each hemisphere, creating an incongruent representation that results in a lack of binocular vision and nystagmus. The abnormal visual input perceived in achiasmia or albinism does not induce topographic reorganizations of the thalamocortical projections. Reorganization of local intracortical architecture in the cortex rather underlies the ability to cope with abnormal visual inputs derived from axonal misrouting at the chiasm. N = nasal retina; T = temporal retina.