Visual Field Defects & Pathway Lesions

The single most "localisable" topic in neuro-ophthalmology: a defect on perimetry tells you exactly where the lesion sits along the visual pathway. Master the rule of the chiasm (decussation of nasal fibres) and congruity, and almost every PYQ falls into place. These notes walk the pathway anteriorly → posteriorly and map each lesion to its field defect.

The visual pathway — anatomy you must own

Light from a point in space hits the opposite half of each retina (object in the temporal field → nasal retina; object in nasal field → temporal retina). The brain therefore sees the world "crossed". Tracking fibres from retina to cortex:

Retinal ganglion cells → optic nerve → optic chiasm → optic tract → lateral geniculate body (LGB) → optic radiations → primary visual (striate, calcarine) cortex — Brodmann area 17.

Key decussation rule: at the chiasm, only the NASAL retinal fibres cross; temporal fibres stay ipsilateral. Because the nasal retina sees the temporal field, crossing fibres carry temporal field information. This is why central chiasmal lesions knock out both temporal fields (bitemporal hemianopia).

Segment	Fibres carried	Side of field represented
Optic nerve	All fibres of one eye	Entire field of that eye (monocular)
Chiasm (centre)	Crossing nasal fibres of both eyes	Both temporal fields
Optic tract	Temporal fibres (same side) + nasal fibres (opposite)	Contralateral half-field of both eyes
LGB / radiation / cortex	Same homonymous arrangement	Contralateral homonymous half-field

High-yield: The chiasm is the watershed. Anterior to the chiasm = monocular defect (one eye only). At the chiasm = bitemporal (heteronymous) defect. Posterior to the chiasm = homonymous defect (same side of field in both eyes).

Defining the vocabulary

• Hemianopia — loss of half the field.
• Quadrantanopia — loss of one quadrant.
• Homonymous — same side of field affected in both eyes (e.g. right field of right eye + right field of left eye) → always retrochiasmal.
• Heteronymous — opposite sides affected (bitemporal or binasal) → chiasmal.
• Congruous — the two eyes' defects are identical in shape/extent → lesion is far posterior (closer to cortex).
• Incongruous — the two defects differ → lesion is more anterior (optic tract).
• Macular sparing — central few degrees preserved despite hemianopia → occipital cortex lesion.

High-yield: The more posterior the retrochiasmal lesion, the more congruous the defect. Occipital cortex = perfectly congruous; optic tract = most incongruous.

Lesion-by-lesion localisation (anterior → posterior)

1. Optic nerve lesion → total monocular field loss

A complete optic nerve lesion blinds that eye entirely. Partial lesions give a central scotoma (optic/retrobulbar neuritis — classically multiple sclerosis), centrocaecal scotoma (toxic/nutritional — tobacco-alcohol amblyopia, B12, methanol, ethambutol), or altitudinal defect respecting the horizontal meridian (anterior ischaemic optic neuropathy, AION).

High-yield: A defect respecting the horizontal midline (altitudinal) = optic nerve head ischaemia (AION). A defect respecting the vertical midline = chiasmal or retrochiasmal.

A lesion at the junction of optic nerve and chiasm produces the classic junctional scotoma: ipsilateral central scotoma + contralateral superotemporal field defect — due to involvement of the inferonasal crossing fibres that loop anteriorly into the opposite optic nerve (historically "Wilbrand's knee"). Highly localising to a parasellar mass.

2. Chiasmal lesion → bitemporal hemianopia

Central compression splits the crossing nasal fibres → bitemporal hemianopia respecting the vertical midline. The classic cause is a pituitary adenoma growing upward from below, so the defect begins in the upper temporal quadrants and progresses inferiorly.

Direction of compression	Cause	Field pattern
From below (pushes up)	Pituitary adenoma	Bitemporal, upper quadrants first
From above (pushes down)	Craniopharyngioma, suprasellar meningioma	Bitemporal, lower quadrants first
Lateral pressure on uncrossed fibres	Posterior communicating / ICA aneurysm, distended 3rd ventricle	Binasal hemianopia (rare)

High-yield: Pituitary adenoma → bitemporal hemianopia, superior quadrants affected first (tumour grows up from the sella). Craniopharyngioma → bitemporal but inferior quadrants first.

3. Optic tract lesion → incongruous homonymous hemianopia

Beyond the chiasm, fibres serving the contralateral half-field of both eyes travel together. A right optic tract lesion → left homonymous hemianopia. Because fibre sorting is incomplete here, the defect is incongruous. Two extra clues:

• Contralateral relative afferent pupillary defect (RAPD) without visual acuity loss — more crossed (nasal) fibres are damaged.
• Bow-tie / band atrophy of the contralateral optic disc on long-standing lesions.

4. LGB / radiation → quadrant patterns

After the LGB the radiations split:

• Temporal (Meyer's) loop carries superior field fibres → temporal lobe lesion → superior quadrantanopia = "pie in the sky."
• Parietal radiation carries inferior field fibres → parietal lobe lesion → inferior quadrantanopia = "pie on the floor."

High-yield: PITS — Parietal = Inferior defect; Temporal = Superior defect. Temporal "pie in the sky" superior quadrantanopia is a favourite single-best-answer stem (often with associated formed visual hallucinations or amnesia).

Stepwise localisation flow: Monocular? → optic nerve. → Bitemporal? → chiasm. → Homonymous + incongruous + RAPD? → optic tract. → Homonymous superior quadrant? → temporal lobe. → Homonymous inferior quadrant? → parietal lobe. → Homonymous, congruous, macula spared? → occipital cortex.

5. Occipital (striate) cortex → congruous homonymous hemianopia with macular sparing

The calcarine cortex is supplied mainly by the posterior cerebral artery (PCA), with the occipital pole (macular representation) receiving collateral supply from the middle cerebral artery. Hence a PCA infarct → congruous homonymous hemianopia with MACULAR SPARING.

Additional cortical patterns:

• Tip of occipital pole lesion → congruous homonymous (central) scotoma — macular fibres only.
• Anterior calcarine lesion → contralateral temporal crescent (monocular) loss — the unpaired peripheral temporal field.
• Bilateral occipital infarcts → cortical blindness; if pupils react and the patient denies blindness = Anton syndrome (visual anosognosia). Riddoch phenomenon = perception of moving but not static objects in a "blind" hemifield.

High-yield: Macular sparing = occipital cortex (PCA territory) lesion — the give-away that the lesion is at the very back of the brain. Normal pupillary reflexes are preserved in all retrochiasmal lesions (the afferent pupillary pathway leaves before the LGB at the brachium).

Quick reference: lesion ↔ defect

Site	Field defect	Classic cause
Optic nerve (complete)	Total monocular blindness + RAPD	Trauma, severe optic neuritis
Optic nerve (partial)	Central / centrocaecal / altitudinal scotoma	MS, toxic, AION
Nerve–chiasm junction	Junctional scotoma	Pituitary/parasellar tumour
Mid-chiasm	Bitemporal hemianopia	Pituitary adenoma
Optic tract	Incongruous homonymous hemianopia + contralateral RAPD	Tumour, demyelination
Temporal radiation (Meyer)	Superior homonymous quadrantanopia (pie in the sky)	Temporal lobe tumour/stroke
Parietal radiation	Inferior homonymous quadrantanopia (pie on the floor)	Parietal lesion
Complete radiation	Complete homonymous hemianopia	MCA infarct
Occipital cortex	Congruous homonymous hemianopia, macular sparing	PCA infarct
Occipital pole	Congruous homonymous central scotoma	Trauma, watershed infarct
Bilateral occipital	Cortical blindness ± Anton syndrome	Bilateral PCA, eclampsia/PRES

Diagnosis & investigation of choice

Field testing: The gold standard for quantifying defects is automated static perimetry — Humphrey Field Analyzer (commonly the 30-2 / 24-2 programme). Goldmann (kinetic) perimetry is preferred for very advanced/peripheral fields and uncooperative patients. Confrontation testing is the quick bedside screen. Always plot both eyes to judge congruity and which side of the vertical midline is respected.

Imaging: Once a defect localises to a site, MRI brain with contrast is the investigation of choice (MRI of the orbits/optic nerve for anterior lesions; dedicated pituitary/sellar MRI for bitemporal hemianopia). CT is reserved for acute haemorrhage/trauma or when MRI is contraindicated.

Additional: OCT of the retinal nerve fibre layer shows band ("bow-tie") atrophy in chronic chiasmal/tract lesions; VEP for optic neuritis; endocrine panel (prolactin, GH, ACTH/cortisol) for pituitary lesions.

High-yield: Bitemporal hemianopia on confrontation → next step is MRI of the pituitary/sella, plus serum prolactin (prolactinoma is the commonest secretory adenoma). A prolactinoma is the one pituitary tumour with a medical drug of choice.

Management / drug of choice (by cause)

• Prolactinoma — drug of choice is a dopamine agonist: cabergoline (preferred) or bromocriptine; shrinks tumour and restores fields without surgery in most cases.
• Non-functioning / other pituitary macroadenoma compressing chiasm — trans-sphenoidal surgical decompression is definitive; fields often recover if decompressed early.
• Optic neuritis (MS) — IV methylprednisolone speeds recovery (does not change final acuity); oral prednisolone alone is contraindicated (raises relapse rate — ONTT).
• AION (non-arteritic) — no proven effective therapy; control vascular risk factors. Arteritic AION (giant cell arteritis) — immediate high-dose systemic steroids to save the fellow eye; do not wait for biopsy.
• PCA infarct / homonymous hemianopia — acute stroke care, secondary prevention; visual rehabilitation, prism therapy, scanning training.
• Pituitary apoplexy (sudden headache + ophthalmoplegia + vision loss) — neurosurgical emergency; steroids + urgent decompression.

Complications

• Permanent field loss if compressive lesions are decompressed late (chiasmal optic atrophy).
• Homonymous hemianopia → loss of driving eligibility, reading difficulty (right HH disrupts reading left-to-right), hemispatial neglect (right parietal).
• Pituitary apoplexy → acute panhypopituitarism, adrenal crisis.
• Anton syndrome → patient endangers self by denying blindness.
• Untreated GCA → bilateral blindness within days.

Key differentials

• Functional (non-organic) visual loss — tubular/spiralling fields not respecting physiological rules; tunnel field that does not enlarge with distance.
• Retinitis pigmentosa — progressive ring/peripheral constriction with night blindness; bilateral but retinal, not pathway.
• Glaucoma — arcuate (Bjerrum) scotoma, nasal step, respecting the horizontal meridian — a retinal nerve fibre pattern, never the vertical midline.
• Papilloedema — enlarged blind spot, generalised constriction.
• Migraine aura — transient fortification spectra/scintillating scotoma that moves and resolves in <60 min.

High-yield: Defects respecting the VERTICAL midline = pathway (chiasmal/retrochiasmal) lesion. Defects respecting the HORIZONTAL midline = retinal/optic nerve (glaucoma, AION, BRVO). This one rule separates two whole classes of MCQ.

Recently asked / exam angle

• "Superior homonymous quadrantanopia — site of lesion?" → Temporal lobe (Meyer's loop). (PITS mnemonic.)
• "Congruous homonymous hemianopia with macular sparing — vascular territory?" → Posterior cerebral artery (occipital cortex).
• "Bitemporal hemianopia with upper quadrants first — most likely tumour?" → Pituitary adenoma (grows up from below). Inferior first → craniopharyngioma.
• "Incongruous homonymous hemianopia with contralateral RAPD" → Optic tract.
• "Junctional scotoma localises to?" → Optic nerve–chiasm junction (parasellar mass).
• "Patient denies blindness with bilateral occipital infarcts" → Anton syndrome.
• "Investigation of choice for bitemporal hemianopia" → MRI sella + serum prolactin; DOC for prolactinoma = cabergoline.
• "Defect respecting horizontal midline" → optic nerve head lesion (AION/altitudinal), not chiasm.
• Image-based perimetry printouts pairing both eyes are increasingly used — read which side of the vertical line is black and whether the two eyes match (congruity).

Rapid revision

• Only nasal retinal fibres cross at the chiasm → carry temporal field → central chiasm lesion = bitemporal hemianopia.
• Anterior to chiasm = monocular; at chiasm = bitemporal; behind chiasm = homonymous.
• More posterior the lesion → more congruous the homonymous defect; occipital = perfectly congruous.
• Optic tract = incongruous homonymous hemianopia + contralateral RAPD + bow-tie disc atrophy.
• PITS: Parietal → Inferior quadrantanopia (pie on the floor); Temporal → Superior quadrantanopia (pie in the sky).
• Macular sparing = occipital cortex (PCA) lesion; macula gets dual PCA + MCA supply.
• Pituitary adenoma → bitemporal, superior quadrants first; craniopharyngioma → inferior first.
• Vertical midline respected = pathway lesion; horizontal midline respected = retinal/optic-nerve (glaucoma, AION).
• Investigation of choice for a chiasmal defect = MRI sella; DOC for prolactinoma = cabergoline.
• Junctional scotoma (ipsilateral central + contralateral superotemporal) = optic nerve–chiasm junction lesion.
• Anton syndrome = denial of cortical blindness; Riddoch = movement seen in blind field.
• Pupillary light reflex is normal in all retrochiasmal lesions (afferent fibres exit before the LGB).