Visual Pathway Simulator
Localisation from the retina to the occipital cortex. Click a station on the pathway diagram and the simulator shows the visual field defect that lesion produces — not as an abstract perimetry chart, but drawn over a real scene the way the patient would see it, with soft defect edges and macular sparing where macular sparing belongs.
Each hemisphere-specific station can be lesioned on either side, and the optic radiations split into a Meyer loop (temporal) and a parietal variant, because the two produce opposite quadrantanopias. The classic teaching rules fall straight out of it: a prechiasmal lesion is monocular, the chiasm is bitemporal, and anything retrochiasmal is homonymous and more congruous the further back it sits.
Stations along the pathway (7)
Retina
Anatomy. The retina is the light-sensitive neural tissue lining the back of the eye. Photoreceptors (rods and cones) transduce light into electrical signals relayed through bipolar and ganglion cells. Ganglion cell axons converge at the optic disc to form the optic nerve.
Function. Phototransduction and initial visual signal processing. The nasal retina captures the temporal visual field, and the temporal retina captures the nasal visual field.
Clinical correlation. The classic retinal presentation is a central scotoma from macular disease (e.g. age-related macular degeneration, central serous retinopathy) — the macula occupies central fixation, so macular disease is felt as a blind or distorted patch straight ahead with peripheral vision intact. Other retinal patterns exist (central retinal artery occlusion causes complete monocular loss, branch retinal artery occlusion causes an altitudinal defect), but they all follow the retina's own vascular or structural anatomy rather than respecting the vertical midline the way a chiasmal or retrochiasmal lesion does.
- A monocular field defect confined to one eye (not a bilateral, midline-respecting hemianopic pattern) localizes to the retina or optic nerve — anything past the chiasm affects both eyes.
- A central scotoma with metamorphopsia (straight lines look wavy) points to macular disease, e.g. age-related macular degeneration or central serous retinopathy — test with an Amsler grid.
- Central retinal artery occlusion is the retinal lesion that instead causes sudden, painless, COMPLETE monocular vision loss, with a cherry-red spot on fundoscopy — a different pattern from macular scotoma.
Optic Nerve
Anatomy. Each optic nerve carries roughly 1.2 million ganglion cell axons from one retina toward the chiasm. Once it leaves the eye it is myelinated by oligodendrocytes rather than Schwann cells, making it part of the CNS and vulnerable to demyelinating disease.
Function. Transmits all visual information from one eye toward the chiasm. Because it carries fibers from only one eye, any defect from an optic nerve lesion is strictly monocular — and ipsilateral: a left optic nerve lesion affects the left eye, not the right.
Clinical correlation. Because every ganglion cell axon from one eye funnels through this single trunk, a significant optic nerve lesion tends to cause more complete, uniform vision loss in that eye — up to total monocular blindness — rather than the discrete, circumscribed defect typical of focal retinal disease. A relative afferent pupillary defect (RAPD) accompanies it. Partial optic nerve lesions (e.g. early optic neuritis) can instead produce a central scotoma, altitudinal defect, or diffuse dimming, but complete or near-complete monocular loss is the hallmark, exam-defining presentation.
- Optic neuritis (classically an early presentation of multiple sclerosis) causes subacute monocular vision loss with pain on eye movement, and can progress to near-complete loss in that eye.
- A relative afferent pupillary defect (RAPD / Marcus Gunn pupil) is the hallmark exam finding of a unilateral optic nerve lesion.
- Unlike retinal disease, optic nerve disease often disproportionately affects color vision (red desaturation) and contrast sensitivity relative to visual acuity.
Optic Chiasm
Anatomy. The optic chiasm sits just above the pituitary gland. Nasal retinal fibers from each eye — which carry the TEMPORAL visual field — decussate here to join the contralateral optic tract, while temporal retinal fibers continue uncrossed.
Function. Combines information from both eyes so that each optic tract downstream carries the full contralateral half of the visual field from BOTH eyes.
Clinical correlation. A midline chiasmal lesion — classically a pituitary adenoma — compresses the crossing nasal fibers from both eyes, producing bitemporal hemianopia: loss of the outer (temporal) field on both sides, with the central, binocularly-overlapping field preserved.
- Pituitary adenoma is the classic cause; craniopharyngioma (arising above the chiasm) can produce a similar but often inferior-predominant bitemporal defect.
- Because pituitary tumors grow from below, the defect often starts as a superior bitemporal quadrantanopia before progressing to a full bitemporal hemianopia.
- Patients often describe bumping into objects or people approaching from the side — the 'temporal island' phenomenon — rather than a clear blind spot.
Optic Tract
Anatomy. Each optic tract carries crossed fibers from the contralateral eye's nasal retina and uncrossed fibers from the ipsilateral eye's temporal retina — together representing the entire CONTRALATERAL half of the visual field from both eyes. It runs from the chiasm to the lateral geniculate nucleus (LGN).
Function. Relays the full contralateral visual hemifield, combined from both eyes, toward the thalamus.
Clinical correlation. A lesion of the left optic tract causes a right homonymous hemianopia, and vice versa. Because the crossed and uncrossed fiber populations are not perfectly matched in size at this level, the resulting hemianopia is often incongruous — the defect differs somewhat in shape between the two eyes.
- Optic tract lesions are often accompanied by a contralateral RAPD, since a disproportionate number of crossed (nasal) fibers are affected.
- Look for 'band' (bow-tie) optic atrophy on fundoscopy — nasal fibers from the contralateral eye and temporal fibers from the ipsilateral eye degenerate.
- Incongruous homonymous hemianopia points toward the optic tract; congruous (near-identical in both eyes) points toward the occipital cortex.
Lateral Geniculate Nucleus (LGN)
Anatomy. The LGN is a six-layered thalamic relay nucleus. Layers 2, 3, and 5 receive uncrossed (ipsilateral eye) input; layers 1, 4, and 6 receive crossed (contralateral eye) input — but every layer represents the same contralateral visual hemifield.
Function. Relays and performs initial processing of visual information from the optic tract on its way to the optic radiations.
Clinical correlation. Isolated LGN lesions are rare (usually vascular, from the anterior choroidal or lateral posterior choroidal arteries) and produce a homonymous hemianopia that is typically more congruous than an optic tract lesion, sometimes with a characteristic wedge- or sector-shaped defect.
- A distinctive horizontal sectoranopia (a wedge-shaped defect sparing a horizontal strip) can occur with LGN infarcts because of its unique dual blood supply.
- Isolated LGN lesions are uncommon — always consider the optic tract or radiations first when a homonymous hemianopia is found.
- Pupillary light reflex fibers branch off the optic tract BEFORE the LGN, so the pupillary response is typically preserved with an isolated LGN lesion.
Optic Radiations
Anatomy. The optic radiations carry fibers from the LGN to the occipital cortex. Inferior fibers — representing the SUPERIOR visual field — loop forward through the temporal lobe as Meyer's loop before traveling posteriorly; superior fibers — representing the INFERIOR visual field — take a more direct parietal route.
Function. Final white-matter relay of retinotopically organized visual information to the primary visual cortex.
Clinical correlation. Because the radiations split anatomically, temporal lobe lesions selectively damage Meyer's loop (inferior fibers), producing a contralateral superior quadrantanopia — the classic 'pie in the sky' defect. Parietal lobe lesions damage the superior fibers, producing a contralateral inferior quadrantanopia — 'pie on the floor.'
- Pie in the sky = temporal lobe (Meyer's loop). Pie on the floor = parietal lobe. Mnemonic 'PITS': Parietal → Inferior, Temporal → Superior.
- Temporal lobe lesions causing this pattern are often due to mesial temporal sclerosis or tumor, and may come with other temporal lobe signs (déjà vu, olfactory auras).
- Parietal lobe lesions can also cause optokinetic nystagmus asymmetry and, when the non-dominant hemisphere is involved, contralateral hemispatial neglect.
Occipital (Visual) Cortex
Anatomy. The primary visual cortex (V1) lies along the banks of the calcarine fissure in the occipital lobe. It is retinotopically organized, with the macula represented posteriorly at the occipital pole and peripheral field represented more anteriorly.
Function. Primary cortical processing of visual input — each hemisphere processes the contralateral visual hemifield.
Clinical correlation. Occipital lesions — most often posterior cerebral artery (PCA) infarction — cause a congruous homonymous hemianopia. Because the occipital pole (representing the macula) has a dual blood supply from both the PCA and MCA, central/macular vision is often spared even with a complete PCA territory infarct.
- Macular sparing strongly suggests an occipital (cortical) lesion rather than an optic tract or radiation lesion.
- Bilateral occipital infarcts ('top of the basilar' syndrome) can cause cortical blindness with preserved pupillary light reflexes, since the pupillary pathway diverges before the LGN/cortex.
- Congruity increases the further back along the pathway a lesion sits: incongruous → optic tract, congruous → occipital cortex.
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