Visual pathway
Visual pathway: field defects, pupillary reflexes and their lesions
Visual pathway for FCPS Part 1: retina to visual cortex, the field defect at each site, blood supply, pupillary light and accommodation reflexes. Covers chiasmal compression by pituitary tumours, Meyer's loop, macular sparing, RAPD, Argyll Robertson and Adie pupils.
The pathway and the rule of inversion
| Stage | Structure | Key fact |
|---|---|---|
| 1 | Retina: photoreceptors, bipolar cells, ganglion cells | Ganglion cell axons form the optic nerve |
| 2 | Optic nerve | Carries all fibres from one eye |
| 3 | Optic chiasm | Nasal retinal fibres (temporal fields) cross; temporal fibres stay on their own side |
| 4 | Optic tract | Carries the opposite visual field from both eyes; pupillary fibres leave here for the pretectal nucleus |
| 5 | Lateral geniculate body (thalamus) | Where most optic tract fibres end |
| 6 | Optic radiation | Lower fibres loop forward through the temporal lobe (Meyer's loop); upper fibres run through the parietal lobe |
| 7 | Primary visual cortex (area 17) | Banks of the calcarine sulcus; upper bank (cuneus) gets the lower field, lower bank (lingual gyrus) the upper field |
- The image is inverted on the retina: upper retina sees the lower field, nasal retina sees the temporal field. So each hemisphere sees the opposite half of the visual world.
- Meyer's loop carries lower retinal fibres, which represent the upper visual field; parietal fibres carry upper retinal fibres, the lower field.
Lesions and field defects
| Site | Field defect | Typical cause |
|---|---|---|
| Optic nerve | Ipsilateral monocular blindness; central scotoma in optic neuritis | Optic neuritis (MS), ischaemic optic neuropathy, trauma |
| Chiasm, centre | Bitemporal hemianopia | Pituitary macroadenoma growing upwards (upper quadrants first), craniopharyngioma from above (lower quadrants first), meningioma |
| Chiasm, both lateral edges | Binasal hemianopia (rare) | Bilateral ICA atheroma or aneurysms |
| Optic tract | Contralateral homonymous hemianopia, incongruous | Tumour, anterior choroidal infarct |
| Meyer's loop (temporal) | Contralateral superior homonymous quadrantanopia | Temporal tumour, abscess, MCA inferior division stroke |
| Parietal radiation | Contralateral inferior homonymous quadrantanopia | Parietal tumour or stroke |
| Occipital cortex | Contralateral homonymous hemianopia with macular sparing, congruous | PCA stroke, occipital trauma |
| Both occipital lobes | Cortical blindness with normal pupils; Anton syndrome (denial) | Bilateral PCA infarcts, top-of-basilar |
- Any lesion behind the chiasm gives a homonymous defect on the opposite side: the right optic tract lesion causes a left homonymous hemianopia.
- Pituitary tumours that reach the chiasm include prolactinomas and GH-secreting adenomas (acromegaly: enlarging hands, feet and jaw) and, after bilateral adrenalectomy for Cushing disease, ACTH tumours with skin pigmentation (Nelson syndrome). Upward growth hits the chiasm; lateral growth enters the cavernous sinus (III, IV, VI, V1).
- Homonymous hemianopia with hemiplegia and hemisensory loss on the same side indicates a large lesion in the opposite hemisphere involving the internal capsule and optic radiation (MCA or anterior choroidal territory).
Why the macula is spared
- The macula is represented at the occipital pole, which receives blood from both the PCA (calcarine branch) and MCA collaterals. A PCA occlusion therefore leaves central vision intact. Macular sparing localises the lesion to the cortex, not the tract.
- Macular cortex is also very large, so a partial lesion rarely removes all of it.
Blood supply of the visual pathway
| Part | Artery |
|---|---|
| Inner retina | Central retinal artery (ophthalmic) |
| Outer retina (photoreceptors) | Choroidal circulation (posterior ciliary arteries) |
| Optic nerve head | Short posterior ciliary arteries |
| Chiasm | Branches of ICA, ACA and anterior communicating |
| Optic tract and LGB | Anterior choroidal artery and PCA |
| Optic radiation | MCA (deep branches) and PCA |
| Visual cortex | PCA (calcarine), MCA at the pole |
Pupillary light reflex
| Limb | Pathway |
|---|---|
| Afferent | Retina, optic nerve, chiasm, optic tract, then pretectal nucleus (bypassing the LGB) |
| Centre | Each pretectal nucleus projects to both Edinger–Westphal nuclei |
| Efferent | Oculomotor nerve, ciliary ganglion, short ciliary nerves, sphincter pupillae |
- Because each pretectal nucleus feeds both sides, light in one eye constricts both pupils (consensual reflex).
- The pathway leaves before the LGB, so pupils react normally in cortical blindness and in lesions of the radiation.
- Relative afferent pupillary defect (Marcus Gunn): on the swinging torch test both pupils dilate when the light moves to the affected eye; caused by optic nerve disease or extensive retinal damage, never by cataract.
- Argyll Robertson pupil (neurosyphilis, diabetes): small, irregular pupils that constrict to near but not to light (light–near dissociation, a pretectal lesion).
- Holmes–Adie pupil: large pupil with slow, sustained constriction to near, from ciliary ganglion damage, in young women with absent tendon reflexes.
Accommodation and papilloedema
- Near reflex: convergence (medial recti), pupil constriction and lens thickening from ciliary muscle contraction relaxing the zonules. It involves the visual cortex and the Edinger–Westphal nucleus.
- Papilloedema (raised intracranial pressure) is bilateral disc swelling with an enlarged blind spot; acuity is preserved until late. Optic neuritis causes painful eye movement, reduced acuity, a central scotoma and impaired colour vision.
Optic neuritis and MS relapses
- Optic neuritis is often the first event of multiple sclerosis. A disabling MS relapse (after excluding infection) is treated with high-dose methylprednisolone for a short course: it speeds recovery but does not change long-term disability.
- Heat or fever can temporarily bring back old symptoms (Uhthoff phenomenon).
- WHO blindness: visual acuity below 3/60 in the better eye, or a field under 10 degrees, with best correction.
Remember Nasal fibres cross; behind the chiasm every defect is homonymous and opposite; temporal is the upper quadrant, parietal the lower.
Exam trap A lesion of the right optic tract causes a left, not right, homonymous hemianopia.
Exam trap Normal pupil reactions in a blind patient point to the occipital cortex, because the light reflex leaves before the LGB.
How FCPS asks about this
- Pituitary macroadenoma growing upwards: bitemporal hemianopia, upper quadrants first.
- Left temporal lobe tumour in Meyer's loop: right superior homonymous quadrantanopia.
- Parietal lesion of the radiation: contralateral inferior quadrantanopia.
- PCA stroke with central vision preserved: dual MCA supply to the macular cortex.
- Most optic tract fibres end in: the lateral geniculate body.
- Pupils that accommodate but do not react to light: Argyll Robertson (neurosyphilis).
- MS relapse with disabling weakness: short course of high-dose methylprednisolone.
Test yourself on this topic
5 of the 15 questions in our bank on this topic. Choose an answer to see why every option is right or wrong.
Light shone in the left eye makes both pupils constrict, but light shone in the right eye causes no constriction of either pupil. Where is the lesion?
Answer: Right optic nerve
The afferent limb of the light reflex is the optic nerve; impulses reach the pretectal nuclei and both Edinger–Westphal nuclei, so each eye's light drives both pupils. The efferent limb is parasympathetic fibres in the oculomotor nerve via the ciliary ganglion. If light in the right eye moves neither pupil while light in the left moves both, the right afferent pathway is damaged.
Light reflex
- Afferent: optic nerve
- Centre: pretectal, Edinger–Westphal
- Efferent: III via ciliary ganglion
- Afferent lesion: both pupils fail from that eye
Remember Afferent fault: eye cannot see the light; efferent fault: pupil cannot move.
Exam trap A partial afferent defect shows as a relative afferent pupillary defect on the swinging light test.
Why the other options are wrong
- Right oculomotor nerve Would leave the right pupil fixed whichever eye is lit.
- Left optic nerve Light in the left eye would then fail.
- Left oculomotor nerve Would leave the left pupil fixed whichever eye is lit.
- Right ciliary ganglion Right pupil would not constrict either way.
A man with a left homonymous hemianopia after a right occipital infarct has normal direct and consensual pupil reflexes in both eyes. Why are the reflexes preserved?
Answer: Pupil fibres leave the tract before the geniculate
The afferent fibres for the pupillary light reflex travel in the optic nerve, chiasm and optic tract, but leave the tract before the lateral geniculate body and pass through the brachium of the superior colliculus to the pretectal nuclei. These project bilaterally to the Edinger–Westphal nuclei. Lesions of the lateral geniculate body, optic radiation or visual cortex therefore cause field loss with normal pupil reflexes, whereas an optic tract lesion can produce a relative afferent pupillary defect.
Light reflex pathway
- Optic nerve, chiasm, optic tract
- Leaves before the LGB to pretectal nuclei
- Bilateral to Edinger–Westphal
- Cortical blindness: pupils still react
Remember Behind the geniculate, pupils are spared.
Exam trap Normal pupils with severe visual loss point to a lesion behind the lateral geniculate body.
Why the other options are wrong
- Pupil fibres travel in the optic radiation Pupil fibres do not enter the radiation.
- The light reflex is relayed in the occipital cortex The cortex is not part of the light reflex arc.
- Each optic tract carries pupil fibres to the pons The relay is in the pretectal midbrain, not the pons.
- The reflex needs only the oculomotor nerve The afferent limb is the optic pathway; both limbs are needed.
A 10-year-old boy with short stature and headaches has a calcified cystic mass above the sella pressing down on the optic chiasm. Which visual field defect is most likely to appear first?
Answer: Bitemporal inferior quadrantanopia
Craniopharyngioma arises from Rathke pouch remnants above the sella and compresses the chiasm from above. The crossing fibres from the upper nasal retina lie superiorly in the chiasm, and the upper retina sees the lower field, so the earliest loss is in the lower temporal quadrants. A pituitary adenoma pushes up from below, catching the inferior crossing fibres first and causing superior temporal loss. Calcification and short stature from growth hormone deficiency are typical of craniopharyngioma.
Chiasm: above or below
- Upper retina sees the lower field
- From above (craniopharyngioma): inferior temporal loss
- From below (pituitary): superior temporal loss
- Craniopharyngioma: calcified, child, short
Remember Pressure from above, field loss below.
Exam trap Both tumours eventually cause full bitemporal hemianopia; only the early pattern differs.
Why the other options are wrong
- Bitemporal superior quadrantanopia Typical of a pituitary adenoma pressing from below.
- Binasal hemianopia Would need pressure on both lateral sides of the chiasm.
- Right homonymous hemianopia Due to a lesion behind the chiasm.
- Central scotoma in one eye Typical of optic nerve disease, not chiasmal compression.
A pituitary macroadenoma grows upward under the optic chiasm. Which visual field defect usually appears first?
Answer: Bitemporal superior quadrantanopia
Crossing nasal retinal fibres carry the temporal fields. A tumour pushing up from below first compresses the inferior crossing fibres (from the inferior nasal retina), which serve the upper temporal fields, giving bitemporal superior quadrantanopia that progresses to full bitemporal hemianopia. A craniopharyngioma pressing from above affects the inferior quadrants first.
Chiasmal compression
- From below (pituitary): upper temporal first
- From above (craniopharyngioma): lower first
- Full: bitemporal hemianopia
- Crossing nasal fibres
Remember Pituitary pushes up: upper fields go first.
Exam trap Bitemporal loss is easily missed by patients until they bump into things.
Why the other options are wrong
- Bitemporal inferior quadrantanopia Typical of compression from above (craniopharyngioma).
- Binasal hemianopia Requires lateral compression of both sides.
- Right homonymous hemianopia Optic tract or radiation lesion.
- Central scotoma in one eye Optic nerve lesion.
A woman with multiple sclerosis has a new relapse with leg weakness over 5 days, affecting her walking. Infection is excluded. What short-term treatment speeds recovery?
Answer: High-dose methylprednisolone
Disabling MS relapses are treated with high-dose corticosteroids (IV or oral methylprednisolone for 3–5 days), which speed recovery but do not change long-term disability. Infection, especially UTI, should be excluded first because it can cause a pseudo-relapse. Long-term disease-modifying therapy reduces relapse frequency. Plasma exchange is reserved for severe relapses unresponsive to steroids.
MS relapse
- Exclude infection (UTI)
- Methylprednisolone 3–5 days
- Speeds recovery, not outcome
- Long-term DMT reduces relapses
Remember Disabling MS relapse: short high-dose steroids.
Exam trap Heat or fever can temporarily worsen old symptoms (Uhthoff phenomenon).
Why the other options are wrong
- Antibiotics No infection.
- Interferon started that day only Disease-modifying therapy is long-term, not for the relapse.
- Plasma exchange as first line Second line.
- Bed rest only Steroids speed recovery.
Where this sits in the CPSP syllabus
- Paper 1: Neuroanatomy, Visual pathway and lesions
- Medicine & Allied, Paper 2: Central nervous system, Visual pathway and lesions