Visual pathway
16 named structures.
Draft — not yet clinically reviewed. The structure of this map is checked automatically, but its wording has not been fact-checked against a textbook. Do not rely on it for an exam answer yet.
Hover or tab a structure to trace what it connects to. Some structures reveal further branches.
Clinical detail
- Temporal hemiretinaNasal field of same eyeRod degeneration (retinitis pigmentosa)
- Nasal hemiretinaTemporal field of same eyeLoss of the crossing nasal fibres of both eyes at the chiasm
- Macula and papillomacular bundleCentral scotomaMacular disease (age-related macular degeneration, macular hole, macular oedema)
- Optic nerve (CN II)Monocular loss RAPDComplete lesion of one optic nerve (trauma, compression, severe neuritis)4 questions
- Optic disc (optic nerve head)Enlarged blind spotRaised intracranial pressure transmitted along both nerve sheaths (papilloedema)
- Optic chiasmBitemporal hemianopiaPituitary macroadenoma extending up through the diaphragma sellae to compress the chiasm from below2 questions
- Optic tractIncongruous homonymous Contralateral RAPDLesion of one optic tract (uncal herniation, anterior choroidal artery infarct, tumour, demyelination)
- Lateral geniculate nucleusSectoranopiaInfarction of the LGN (anterior choroidal or lateral posterior choroidal artery)
- Pretectal (olivary pretectal) nucleusLight-near dissociationAfferent lesion anywhere from retina to optic tract (e.g. optic neuritis)1 question
- Superior colliculusDestruction of V1 with intact retinotectal pathway1 question
- Suprachiasmatic nucleusLoss of rods and cones with surviving ganglion cells
- Meyer's loop (temporal optic radiation)Superior quadrantanopiaTemporal lobe lesion: tumour, inferior-division MCA infarct, anterior temporal lobectomy for epilepsy
- Parietal (superior) optic radiationInferior quadrantanopiaParietal lobe lesion (superior-division MCA infarct, tumour)
- Edinger-Westphal nucleus and oculomotor parasympathetic fibresFixed dilated pupilPosterior communicating artery aneurysm or uncal herniation compressing the oculomotor nerve1 question
- Primary visual cortex (V1, striate cortex)Congruous hemianopia Macular sparingPosterior cerebral artery infarct of one occipital lobe2 questions
- Ciliary ganglion and sphincter pupillaeTonic pupilPostganglionic denervation of the ciliary ganglion (Holmes-Adie tonic pupil), typically a young woman1 question
Common questions
Why does a chiasmal lesion produce a bitemporal hemianopia rather than blindness of one eye?
Only the nasal-retinal fibres cross in the chiasm, and the nasal retina of each eye sees the temporal field. A midline lesion therefore removes the temporal field of both eyes while the uncrossed temporal-retinal fibres, which carry each eye's nasal field, pass by intact. A pituitary adenoma pushing up from below hits the inferior nasal fibres first, so the superior temporal quadrants go first; a craniopharyngioma from above starts with the inferior quadrants.
How do I tell an optic tract lesion from an occipital lobe lesion when both give a contralateral homonymous hemianopia?
A tract lesion is incongruous (the defect differs between the two eyes), gives a mild RAPD in the contralateral eye because the pupillary fibres are still travelling with the tract, and shows no macular sparing. An occipital lesion is congruous, spares the macula after a posterior cerebral artery stroke because the occipital pole has middle cerebral collateral supply, and leaves the pupils entirely normal because the reflex fibres left the pathway before the geniculate.
Why is the pupillary light reflex preserved in cortical blindness?
The afferent limb leaves the optic tract through the brachium of the superior colliculus to the pretectal nucleus, then reaches the Edinger-Westphal nuclei bilaterally through the posterior commissure. It never passes through the lateral geniculate nucleus, optic radiation or striate cortex, so bilateral occipital infarction abolishes vision but leaves both direct and consensual reflexes intact, which is the key bedside clue against a functional or ocular cause.
Why does an optic nerve lesion cause a relative afferent pupillary defect but not unequal pupils?
Each pretectal nucleus projects to both Edinger-Westphal nuclei, so whatever light reaches the midbrain from either eye constricts both pupils equally. A damaged optic nerve delivers less afferent signal, so when the torch swings to that eye both pupils dilate relative to their response to the good eye, but at rest the two pupils remain the same size. Anisocoria therefore always means an efferent (CN III, ciliary ganglion or sympathetic) problem, never a purely afferent one.
Which quadrant is lost with a temporal lobe lesion and which with a parietal lesion?
Meyer's loop in the temporal lobe carries fibres from the inferior retina, which sees the superior visual field, so a temporal lesion gives a contralateral superior homonymous quadrantanopia ('pie in the sky'). The parietal radiation carries the superior retina and therefore the inferior field, giving a contralateral inferior quadrantanopia ('pie on the floor'). The same rule applies in V1: the lingual gyrus below the calcarine sulcus holds the superior field and the cuneus above it the inferior field.
Why is the pupil involved early in a compressive third-nerve palsy but spared in a diabetic one?
The preganglionic parasympathetic fibres from the Edinger-Westphal nucleus run superficially on the dorsomedial surface of the oculomotor nerve. External compression by a posterior communicating artery aneurysm or a herniating uncus crushes them first, producing a fixed dilated pupil that demands urgent imaging. Microvascular ischaemia in diabetes or hypertension damages the core of the nerve where the vasa nervorum run, so the eye is ptotic and immobile but the pupil reacts normally.