What is the visual pathway and why do lesions give predictable defects?
The visual pathway runs from the retina → optic nerve → optic chiasm → optic tract → lateral geniculate nucleus (LGN) → optic radiations → primary visual cortex (Brodmann area 17) along the calcarine fissure. All along this route fibres keep a strict retinotopic order, so the shape of a field defect tells you where the lesion is.
- Optic nerve — about 1.2 million retinal ganglion cell axons from one eye; it is a CNS white-matter tract.
- Optic chiasm — lies in the suprasellar cistern above the pituitary and below the hypothalamus. Nasal retinal fibres (which see the temporal field) cross; temporal fibres stay on the same side. About 53–57% of fibres cross.
- Optic tract — each tract carries the opposite half of the visual field from both eyes. Most fibres end in the LGN; collaterals go to the pretectal nuclei (pupillary reflex), superior colliculus and suprachiasmatic nucleus.
- LGN — a six-layered thalamic relay.
- Optic radiations — inferior fibres (Meyer loop) sweep through the temporal lobe and carry the superior field; superior fibres run through the parietal lobe and carry the inferior field.
- Visual cortex — the upper bank of the calcarine fissure represents the inferior field; the lower bank the superior field.
Which visual field defect results from a lesion at each site?
| Site of lesion | Field defect | Classic causes | Pupil |
|---|---|---|---|
| Optic nerve (one side) | Ipsilateral monocular blindness; or central / cecocentral scotoma | Optic neuritis, ischaemic optic neuropathy, compression; toxic (ethambutol, methanol) | RAPD in the affected eye |
| Junction of optic nerve and chiasm | Junctional scotoma — central scotoma in one eye + (usually superior) temporal defect in the other | Parasellar tumours | — |
| Optic chiasm (central) | Bitemporal hemianopia (heteronymous) | Pituitary adenoma (commonest), craniopharyngioma, suprasellar meningioma, ACom aneurysm | — |
| Chiasm (both lateral edges) | Binasal hemianopia (rare) | Bilateral ICA aneurysms, advanced glaucoma, atherosclerosis | — |
| Optic tract | Contralateral incongruous homonymous hemianopia | Stroke, tumour, trauma | Contralateral RAPD; Wernicke hemianopic pupil |
| LGN (anterior choroidal territory) | Homonymous wedge-shaped defects above and below the horizontal meridian | Anterior choroidal artery infarct | No RAPD |
| Meyer loop (temporal radiation) | Contralateral superior quadrantanopia — 'pie in the sky' | Temporal lobe tumour, MCA infarct, temporal lobectomy | Normal |
| Parietal radiation | Contralateral inferior quadrantanopia — 'pie on the floor' | Parietal infarct, tumour, trauma | Normal |
| Occipital cortex | Contralateral congruous homonymous hemianopia with macular sparing | Posterior cerebral artery infarct | Normal |
Why does a pituitary adenoma cause bitemporal hemianopia?
The crossing nasal fibres sit in the body of the chiasm, directly above the sella. A tumour growing up out of the sella presses on them first. Because nasal retina sees the temporal field, both temporal half-fields are lost — bitemporal hemianopia, a heteronymous defect. Central vision is usually retained — StatPearls notes the central 110–120 degrees of field remains intact — so patients lose peripheral vision on both sides, and complete defects also disturb binocular vision.
- Pituitary adenomas are the most frequently encountered cause of bitemporal hemianopia; visual impairment from suprasellar extension occurs in about 40–60% of patients with pituitary adenoma.
- Because they compress the chiasm from below, they hit the inferior nasal fibres first → the defect usually begins in the superior temporal quadrants ('upper outer first').
- Craniopharyngioma — a sellar/suprasellar tumour with a bimodal age peak (5–14 and 50–74 years for the adamantinomatous type, which calcifies); it causes visual field loss, raised ICP and endocrine deficits.
- Pituitary apoplexy — sudden headache, ophthalmoplegia and bitemporal hemianopia.
How do you tell an optic tract lesion from an occipital lesion?
| Feature | Optic tract lesion | Occipital cortex lesion |
|---|---|---|
| Field defect | Contralateral homonymous hemianopia | Contralateral homonymous hemianopia |
| Congruity | Incongruous (defects differ between eyes) | Congruous (nearly identical in both eyes) |
| Macula | Split | Often spared |
| Pupil | RAPD in the contralateral eye; Wernicke hemianopic pupil | Normal — lesions behind the LGN do not cause RAPD |
| Optic disc (late) | Bow-tie atrophy of the contralateral disc can develop | Normal |
| Usual cause | Tumour, trauma, demyelination | PCA infarct |
Why incongruous in front, congruous behind? Fibres from corresponding points of the two retinas are not yet perfectly lined up in the optic tract; they come together progressively towards the cortex. So StatPearls: if the defect in the two eyes is not similar, the lesion is usually anterior; if it is identical, the lesion is likely posterior, including the occipital lobe.
Why macular sparing? The occipital pole, where the macula is represented, often receives a dual blood supply — the posterior cerebral artery plus collateral branches of the middle cerebral artery. When the PCA is occluded, the macular cortex can stay perfused, so central vision survives. This is why macular-sparing homonymous hemianopia is especially typical of stroke.
What are the RAPD and the Wernicke hemianopic pupil?
The relative afferent pupillary defect (RAPD, Marcus Gunn pupil) is detected with the swinging flashlight test. Light in the normal eye constricts both pupils; when the light is swung quickly to the affected eye, both pupils dilate, because the damaged eye sends a weaker afferent signal. The efferent pathway (CN III) is intact, so both pupils always behave together.
- Common causes: optic neuritis, ischaemic optic neuropathy, glaucoma, retinal detachment, central retinal artery or vein occlusion.
- Less common: lesions of the chiasm, optic tract (contralateral RAPD) or pretectal region.
- Lesions posterior to the LGN do not cause an RAPD — the pupillary fibres have already left for the pretectal nuclei.
- Trap: a dense cataract can create a small contralateral RAPD through light scatter.
The Wernicke hemianopic pupil belongs to optic tract lesions: light shone onto the functioning half of the retina produces a pupillary constriction, but light shone onto the blind half gives a reduced or absent response, because the afferent pupillary fibres in the damaged tract are interrupted. A lesion of the radiations or cortex leaves the pupil reflex normal.
What field defects come from the retina and optic nerve?
| Defect | Meaning | Typical cause |
|---|---|---|
| Central scotoma | Loss of fixation, periphery preserved — macular or papillomacular fibres | Optic neuritis, nutritional/toxic optic neuropathy, hereditary optic neuropathy, macular disease |
| Cecocentral scotoma | Extends from fixation to the blind spot (papillomacular bundle) | Ethambutol, methanol, vigabatrin; nutritional deficiency; mitochondrial optic neuropathy |
| Enlarged blind spot | The normal blind spot (~15° temporal to fixation) is bigger | Papilloedema, optic disc oedema |
| Arcuate (Bjerrum) scotoma, nasal step | Nerve fibre bundle loss respecting the horizontal meridian | Glaucoma |
| Transient monocular loss (amaurosis fugax) | Curtain-like temporary loss | Retinal emboli, carotid stenosis, giant cell arteritis |
What causes homonymous hemianopia and how is it assessed?
In adults, stroke accounts for about 70% (69.7%) of homonymous hemianopia; in children, tumours (39%), cerebrovascular disease (25%) and trauma (19%) lead. Lesions most often involve the occipital lobe, then the optic radiations and optic tract. About half of patients with post-stroke hemianopia improve spontaneously within the first month.
- Confrontation fields at the bedside, then automated perimetry (Humphrey 24-2 or 30-2) or Goldmann perimetry to map the defect and judge congruity.
- Swinging flashlight test for an RAPD.
- Fundoscopy — disc pallor, papilloedema, optic atrophy.
- MRI brain (and of the sella for a bitemporal defect); urgent imaging following stroke protocols if the deficit is acute.
- Pituitary hormone profile when a sellar mass is found.