Visual Field Defects Explorer

What are visual field defects?

A visual field defect is a part of the visual field where sight is missing or dimmed. The visual field is everything one eye can see while it looks at a fixed point, and the shape of a defect is set by where the visual pathway is damaged, because the pathway sorts its fibres by the part of the field they carry. One rule explains every defect in this explorer: right half of each retina → right optic tract → left half of the visual field, and the same with left and right swapped.

Three consequences follow, and they are the first thing to look for on any field chart. A defect in one eye only comes from a lesion in front of the optic chiasm, on the same side. A defect in the outer half of both fields comes from the chiasm itself. A defect on the same side of the field in both eyes, a homonymous defect, comes from a lesion behind the chiasm, on the opposite side of the brain.

How the visual pathway is wired

The lens projects an inverted and reversed image onto the retina, so the temporal half of each eye’s field, the half nearer the temple, falls on the nasal half of its retina, and the upper field falls on the lower retina. A vertical line through the fovea divides each retina into nasal and temporal halves, and the axons of its ganglion cells leave the eye together in the optic nerve. Each fibre in the diagram stands for many such axons, each carrying the action potentials the action potential simulator builds from sodium and potassium currents.

At the optic chiasm, which lies just above the pituitary gland, the fibres from the nasal half of each retina cross to the other side. They are about 53 percent of each nerve, in the counts of Kupfer, Chumbley and Downer (1967). The temporal fibres stay on their own side, along the outer edges of the chiasm. Behind it, each optic tract therefore carries the temporal fibres of its own eye and the nasal fibres of the other, and between them those see the opposite half of the world.

Most tract fibres end in the lateral geniculate nucleus of the thalamus, which has six layers: crossed fibres end in layers 1, 4 and 6 and uncrossed fibres in layers 2, 3 and 5. A small share leaves the tract before the nucleus for the pretectal area of the midbrain, which drives the pupil reflexes. From the nucleus the optic radiation fans out to the occipital lobe. Fibres from the lower retina, which carry the upper field, first loop forward around the temporal horn of the lateral ventricle into the temporal lobe: this is Meyer’s loop. Fibres from the upper retina, carrying the lower field, run back more directly through the parietal lobe.

The primary visual cortex, V1, lines the calcarine sulcus on the inner surface of the occipital lobe. Its upper bank, the cuneus, receives the lower field and its lower bank, the lingual gyrus, the upper field, while the macula is mapped at the occipital pole and given far more cortex than its size suggests. The brain explorer has the optic nerves, chiasm, tracts and both geniculate bodies as 3D models, and the head and neck explorer shows the chiasm in place above the pituitary fossa of the skull.

Using the explorer

Choose a lesion site from the list, or tap one of the small rings on the diagram. With the diagram focused, the up and down arrow keys move the lesion along the pathway, from the optic nerve back to the cortex, and the left and right arrow keys move it to that side. The diagram looks down on the head from above with the nose at the top, so the patient’s left is on the left. A red bar marks the lesion, or red shading on the geniculate nucleus or the cortex, and each fibre it cuts is drawn dashed beyond the cut, because past that point it carries nothing.

The two circles are the visual fields, drawn as the patient sees them: the left eye’s field on the left with its temporal half on the left, and the right eye’s field on the right with its temporal half on the right. Each shows the central 30°, the region an automated perimeter usually tests, with rings at 10° and 20°, and anything lost is hatched. The dark oval about 15° into each temporal field and 1.5° below the horizontal is the normal blind spot, where the optic disc has no photoreceptors. It is roughly 5.5° wide and 7.5° high, and because it is always on the temporal side it tells you which eye a chart belongs to.

Colour the fibres by half of the field to watch the sorting at the chiasm: everything carrying the left half of the world is one colour, and after the chiasm all of it is in the right hemisphere. Colour them by eye to see that every tract carries both eyes. The readouts name the defect and its pattern, and the panel under the diagram says which fibres are cut, why, and what usually causes a lesion there.

Worked example: a lesion at the centre of the chiasm

The explorer opens with a lesion at the centre of the chiasm, the defect a pituitary tumour is known for.

• Light from the left eye’s temporal field lands on its nasal retina, and those fibres cross: left temporal field → left nasal retina → crosses.
• The same is true of the right eye, whose crossing fibres pass through the same point the other way: right temporal field → right nasal retina → crosses.
• A midline lesion cuts only the crossing fibres. In the drawing that is 4 of 8 fibre groups, the nasal ones, and in a real chiasm it is about 53% of each optic nerve.
• Each eye keeps the half of its field that its temporal retina serves, the nasal half, and loses the temporal half: the readouts give Temporal half for both eyes.
• The two eyes have lost opposite halves, so the defect is heteronymous, and its name is Bitemporal hemianopia.

Each blind spot, 15° into the temporal field, now sits inside the defect. With both eyes open, each eye’s surviving nasal half covers the half of the central field that the other eye has lost, which is one reason a bitemporal hemianopia can go unnoticed until the eyes are tested one at a time. A real pituitary tumour also rarely cuts so cleanly: pressing from below, it reaches the lower crossing fibres first, which serve the upper field, so the loss usually begins in the upper temporal quadrants and spreads downwards.

Visual field defects by lesion site

The table gives the defect from each right-sided lesion, taken from the same model the explorer draws with. A left-sided lesion gives the mirror image.

Lesions in front of the chiasm: one eye

In front of the chiasm each optic nerve carries one eye’s fibres and no others, so a complete optic nerve lesion blinds that eye and leaves the other untouched. The pupils then show a relative afferent pupillary defect: both constrict when light is shone in the good eye, and both dilate when the light swings to the blind one. Most optic nerve disease is partial, though, and optic neuritis typically leaves a central scotoma, an island of lost vision at fixation, rather than a blind eye.

The uncrossed fibres run along the outer edges of the chiasm, so pressure from one side, classically from an aneurysm or a hardened internal carotid artery, cuts that eye’s temporal fibres alone and gives a nasal hemianopia in that eye. Pressure on both edges at once gives a binasal hemianopia, which is rare; most binasal defects come from disease of the eye or the optic disc instead. A lesion where one optic nerve meets the chiasm can catch that nerve and the crossing fibres from the other eye together, giving a central scotoma in one eye and an upper temporal defect in the other: the junctional scotoma.

Lesions behind the chiasm: homonymous defects

Behind the chiasm a lesion on one side takes the same half of the field from both eyes, on the opposite side. What changes from front to back is how much of that half goes and how alike the two eyes’ defects are.

• Optic tract. A complete lesion gives a contralateral homonymous hemianopia that splits the macula. Partial tract lesions are usually incongruous, with differently shaped defects in the two eyes, and because the pupil fibres still run in the tract, the eye opposite the lesion, which loses the larger temporal half, may show a relative afferent pupillary defect.
• Lateral geniculate nucleus. A complete lesion gives the same hemianopia. Partial ones give wedge-shaped sectoranopias, whose shape depends on which of the nucleus’s two arteries, the anterior or the lateral posterior choroidal, is blocked.
• Meyer’s loop. A temporal lobe lesion takes the upper quadrant on the opposite side in both eyes, the ‘pie in the sky’ defect. It is a familiar result of anterior temporal lobectomy for epilepsy.
• Parietal optic radiation. A parietal lesion takes the lower quadrant on the opposite side, the ‘pie on the floor’. A larger lesion that reaches the whole radiation gives a complete hemianopia.
• Primary visual cortex. Usually damaged by a posterior cerebral artery stroke, it gives a congruous homonymous hemianopia, often with the macula spared. A lesion of the occipital pole alone gives a central homonymous scotoma instead, and damage to both occipital lobes gives cortical blindness with normal pupil reactions.

From the lateral geniculate nucleus back the pupil reflexes are normal, because the pupil fibres have already left for the midbrain.

Why the macula is spared

Most occipital strokes are in the territory of the posterior cerebral artery, but the occipital pole, where the macula is mapped, is often also supplied by branches of the middle cerebral artery and survives. The explorer spares a central disc of 5° radius, a modelling choice inside the range seen in patients. On the plotted field that island is small: (5/30)² = 1/36 of the disc, so the spared half is ½ × 1/36 = 1/72, about 1.4% of the field. Yet it holds fixation and the central vision used for reading and for recognising faces, which is why sparing matters so much to the patient. A narrow strip of apparent sparing can also be an artefact of the eye drifting towards the blind side during testing, so on its own it does not prove the macula is spared.

Congruity: how alike the two eyes’ defects are

A homonymous defect is congruous when the two eyes’ defects have the same shape and size, and incongruous when they differ. Congruity increases from front to back. In the optic tract the fibres from matching points of the two retinae are not yet side by side, so a partial lesion catches them unequally; in the radiation and the cortex they lie together, so even a small occipital lesion punches matching holes in both fields. The explorer draws complete lesions, which match exactly wherever they are; the rule is about the partial lesions patients actually have.

What this model leaves out

• Partial and relative defects. Every lesion here is complete and absolute. Real ones are usually partial, ragged at the edges and often only dim the field, which perimetry records as reduced sensitivity rather than blindness.
• The far periphery. Only the central 30° is drawn. The whole field reaches much further, furthest on the temporal side, and its outermost temporal crescent, seen by one eye only, is mapped at the front of the calcarine cortex, so an occipital lesion can spare it.
• Disease of the eye. Glaucoma, retinal detachment and macular disease have patterns of their own, such as arcuate defects and central scotomas, which respect the horizontal meridian or no meridian at all.
• Progression. A growing tumour changes the field over months, and the order in which the quadrants go is a clue to where it presses, which a single complete lesion cannot show.
• Testing itself. Bedside confrontation testing misses many defects that formal perimetry finds, so a normal result does not rule one out. The sensitivity and specificity visualiser shows what a test of modest sensitivity does to the chance of missing a real defect.
• Diagnosis. This is a teaching diagram. Real fields are read with the history, the other eye, the optic discs and imaging.

Common mistakes

• Drawing the fields as the examiner sees them. Field charts are always drawn as the patient sees them, so the right eye’s temporal half is on the right of its chart.
• Mixing up the retina and the field. The nasal retina sees the temporal field, so “nasal fibres cross” means that the fibres serving the temporal fields cross.
• Naming a homonymous defect after the lesion. A left optic tract lesion gives a right homonymous hemianopia: defects are named for the half of the field that is lost.
• Swapping the quadrantanopias. Meyer’s loop, in the temporal lobe, carries the upper field, so a temporal lesion takes the upper quadrant and a parietal one the lower.
• Expecting macular sparing everywhere. Sparing points to the occipital cortex. A complete optic tract lesion splits the field right through fixation.
• Treating hemianopia and hemianopsia as different. They are two spellings of the same thing, and so are quadrantanopia and quadrantanopsia.