A lesion located posterior to the lateral geniculate nucleus would most likely not cause an afferent pupillary defect.

• A. Cause an afferent pupillary defect
• B. Not cause an afferent pupillary defect
• C. Always cause color vision loss
• D. Only affect peripheral vision

Answer: (B)

The key idea is that an afferent pupillary defect (APD) reflects a disruption of the afferent limb of the pupillary light reflex up to the pretectal area. The reflex relies on retinal input reaching the pretectum and then signaling the Edinger–Westphal nucleus to constrict the pupil. Importantly, a lot of the retinal input that drives the reflex reaches the pretectum via pathways that do not require the lateral geniculate nucleus (LGN). So a lesion behind the LGN—in the optic radiations or occipital cortex—typically spares the reflex. You can have impaired conscious vision in the corresponding visual field while the direct and consensual pupillary light responses remain intact.

In other words, posterior-to-LGN damage can disrupt what you perceive but not the reflex that constricts the pupil in response to light. Color vision loss depends on involvement of specific color-processing areas and is not an automatic consequence of a posterior LGN lesion, and cortical damage can affect central vision as well as peripheral, so neither of those outcomes is as reliably predicted as the lack of an APD.