Retinitis Pigmentosa MCQ — NEET PG Practice Question | NEETPGAI
Retinitis Pigmentosa
medium
eye Ophthalmology
A 28-year-old man presents with progressive night blindness over the past 5 years and gradual constriction of his visual fields. Fundoscopic examination reveals the characteristic findings shown in the diagram. The structure marked **A** (bone-spicule pigmentation in the mid-periphery) represents migration of which cell type into the neurosensory retina, and what is the underlying pathophysiological process driving this migration?
A. Retinal astrocytes undergoing reactive gliosis in response to increased intraocular pressure
B. Retinal pigment epithelial cells migrating along perivascular spaces secondary to photoreceptor degeneration and loss of metabolic support
C. Microglial cells infiltrating the retina as part of an autoimmune response against cone photoreceptor antigens
D. Müller glial cells proliferating in response to inflammatory cytokines released by dying rod cells
Explanation
Why option 1 is right
The bone-spicule pigmentation characteristic of retinitis pigmentosa results from migration of retinal pigment epithelial (RPE) cells into the neurosensory retina along perivascular spaces. This migration occurs secondary to progressive rod and cone photoreceptor degeneration, which reduces metabolic demand and disrupts the normal RPE-photoreceptor relationship. The RPE cells, no longer anchored by viable photoreceptors, migrate along blood vessels and appear as dark, bone-spicule-like deposits in the mid-periphery—a hallmark of the classic fundus triad of RP. This is the pathognomonic finding that defines the structural changes in RP (AAO BCSC Section 12, 2024).
Why each distractor is wrong
Option 2 (Müller glial cells): While Müller cells do undergo reactive gliosis in RP (contributing to waxy pallor of the optic disc), they do not migrate to form bone-spicule pigmentation. The pigmentation is specifically from RPE cells, not glial cells.
Option 3 (Microglial cells): Retinitis pigmentosa is a primary photoreceptor dystrophy, not an autoimmune disease. Although microglial activation occurs secondarily in RP, it does not produce the characteristic bone-spicule pattern. This confuses secondary inflammation with the primary RPE migration.
Option 4 (Retinal astrocytes): Astrocytic gliosis contributes to optic disc pallor (structure B), not bone-spicule pigmentation. Additionally, RP is not driven by elevated intraocular pressure; it is a hereditary photoreceptor dystrophy.
High-YieldNEET PG
Bone-spicule pigmentation in RP = RPE cell migration along perivascular spaces due to loss of photoreceptor support; this is the first component of the classic fundus triad.
AAO BCSC Section 12: Retina and Vitreous (2024)
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