Visual Field Defects

A visual field defect is a loss of part of the usual field of vision, so it does not include blindness of either one eye or both. The lesion may be anywhere along the optic pathway; retina to ophthalmic cortex.

Central field loss occurs with:

• Macular degeneration
• Macular holes
• Cone dystrophies¹
• A number of rare conditions like Best's disease, Stargadt's disease and achromatopsia.

Peripheral field loss occurs with:

• Retinitis pigmentosa
• Hemianopia
• Chorioretinitis
• Glaucoma
• Retinal detachment
• Leber's optic atrophy

• Was the onset sudden, rapid or slow?
• Where is the field loss? It is often helpful to say to the patient, "If what you see is like a television screen then where is the bit that is missing?"
• Does it affect one eye or both? If the patient says that it affects only one eye it is worth asking him to close or cover the affected eye and to note again if there is any visual loss. If it is much more marked in one eye than the other the loss in the less affected eye may be overlooked.
• Does the visual defect look like a black spot, a blur or does the picture look normal?
  If the lesion is cortical the patient may fail to notice any defect. If the onset has been insidious it may also have gone unnoticed.
• Does the patient tend to bump into people or things? Has there been any damage to the car recently? Patients may continue to drive as they are oblivious of quite significant field loss. This can cause failure to judge parking, failure to negotiate obstacles or failure to notice other vehicles at road junctions. There may be remarkable lack of insight despite numerous claims on the insurance.

It is important to remember that the image is projected on to the retina upside down. Hence a lesion of the top right of the retina or in pathway beyond will cause a defect in the bottom left of the visual field. Traditionally a hat pin has been used to define the visual field. A red or a white head is used and it may be moved across the visual field to ascertain where it disappears and hence to define a scotoma.

Confrontation

This is a simple, but crude, method of assessing visual field loss. A normal field of vision is nearly 180º horizontally and about 120º in the vertical axis. The nasal fields of each eye show significant overlap.

• Sit about 50cms away from the patient, look at his nose and get him to look at yours.
• Move your fingers in from the side, wiggling them as they go, and ask him to tell you when he first sees your fingers.
• Use this to compare the patient's field of vision with your own.
• Peripheral vision is rods and they are most sensitive to movement.
• Repeat the process from above and below and possibly from the 4 corners.
• You can ask the patient to cover or close one eye and you close the one opposite.

If the patient lets his sight drift away from your nose bring him back. This way, by comparing the patient's field of vision with your own it is possible to get a very crude assessment of any visual field defect. More detailed assessment will probably be required and this will involve the services of an optometrist. There are a number of techniques used in specialist practice.
Various tools to examine the visual fields include:

• Lister and Goldmann perimeters; used to assess the whole field.
• Bjerrum screens are used to assess the 30° of central vision.
• Amsler grid charts are used to assess the 10° of central vision. They are used to screen for macular disease and optic nerve lesions. The chart is 10 x 10cm square with 5mm squares drawn on it and a dot in the middle. The chart is 30cm away and the patient is instructed to look at the central dot and report any distorted squares or wavy lines (metamorphopsia) or blank or dark areas (scotomata).

There are also many automated computerised perimeters to test visual fields.

Ophthalmoscope

Abnormalities of the retinal arteries or veins may be apparent, as may a retinal detachment. Lesions of diabetes or hypertension may be visible. The cupping of glaucoma may be seen.

• The visual image is projected through the lens onto the retina upside-down. The macula is responsible for central vision. Fibres from the macula feed into the temporal part of the optic nerve at the level of the retina, and gradually migrate to the central part of the optic nerve at the optic chiasm.
• The information from each eye is split at the chiasm, with the medial fibres (lateral visual field) crossing to the opposite side and the lateral fibres (nasal visual field) passing to the ipsilateral optic tract.
• Thus information from both eyes concerning the same part of the visual field pass to the same part of the visual cortex (left half of visual field in right optic tract) via the optic tract, geniculate body and optic radiation.

Lesions at the level of the retina

These affect one eye only.

• Retinal detachment and occlusion of blood vessels at a level smaller than the central retinal artery or vein, give defects with boundaries in the horizontal meridian.
• Chronic glaucoma is associated with raised intraocular pressure that damages the optic nerve starting with the peripheral fibres. If it is left unchecked the peripheral part of the vision is lost and tunnel vision develops (like looking down a tube although with an insidious onset the patient may be remarkably unaware of considerable field loss).
• Retinal detachment tends to be fairly rapid in onset. It may follow trauma or there may be predisposing factors. It may be preceded by floaters and flashes before what the patient describes as "a curtain" coming across the visual field. A crescentic red or orange slip of detachment may be apparent at the periphery of the retina.
• Central retinal artery occlusion tends to be a sudden and complete loss of vision in one eye but if occlusion is at the level of one of the 4 arteries to the retina there will be loss of just a quadrant of field. The affected area will look pale and poorly supplied with blood vessels. 1 of the 4 arteries will not be seen.
• Central retinal vein occlusion presents in a fairly similar way to arterial occlusion but the retina looks very different. Haemorrhages are scattered throughout the fundus in a typical blood-storm pattern with cotton-wool spots. With less complete blockage sparse scattered haemorrhages occur.
• Senile macular degeneration is often called just macular degeneration or age-related macular degeneration to avoid the word senile. It affects the macular area and the periphery is spared until very late.

Drugs can cause disturbance of vision; chloroquine can cause a classic bull's eye maculopathy affecting the centre of the field. The Amsler grid can be used as a screening tool.³ Vigabatrin can cause field defects in up to 40% of those who take it.⁴

Lesions before the chiasm

These will produce a field deficit in the ipsilateral eye. Field defects from damage to the optic nerve tend to be central, asymmetrical and unilateral. Visual acuity is often affected.
Consider optic neuritis or optic atrophy. Lesions just before the chiasm can also produce a small defect in the upper temporal field of the other eye as the decussating fibres loop back into the optic nerve after crossing (anterior chiasmal syndrome - eg meningioma).

Lesions at the chiasm

These classically produce a bitemporal hemianopia.

• If they spread up from below e.g. pituitary tumours, the defect is worse in the upper field.
• If the tumour spreads down from above e.g. craniopharyngioma, the lesion is worse in the lower quadrants.

Lesions of the optic chiasm may show a phenomenon where two identical coloured objects are shown to one eye in the two vertical halves of the visual field, but one appears to be brighter and sharper than the other. For example, with a right hemianopia the left hemifield is brighter than the right.

Lesions after the chiasm

These produce homonymous field defects; a lesion in the right optic tract produces left visual field defect. Fibres in the optic tracts gradually rotate until the fibres reach the geniculate body, so lesions in the tract before geniculate body may produce incongruous defects.

• Lesions in the main optic radiation or optic peduncle cause complete (left or right) homonymous hemianopia without macular sparing. This is seen in stroke and middle cerebral artery lesions.
• Lesions in the temporal radiation cause congruous upper quadrantic homonymous hemianopia commonly with macular sparing e.g. tumours.
• Lesions in the parietal radiation (rare) cause inferior quadrantic homonymous hemianopia without macular sparing.
• Lesions in the anterior visual cortex (common) produce a contralateral homonymous hemianopia with macular sparing e.g. posterior cerebral artery occlusion.
• Lesions in the macular cortex produces congruous homonymous macular defect e.g. blunt injury to occiput.
• Lesions of the intermediate visual cortex produces a homonymous arc scotoma, with sparing of both macular and periphery. This is seen in a distal posterior cerebral artery occlusion.

Occipital lobe lesions

• If both occipital lobes are injured then the patient is in a state of cortical blindness. The patient is unable to process visual information and behaves in a similar fashion to someone who suffers a peripheral blindness. However, some patients deny their blindness and attempt to behave as if they have vision. This state of denial of cortical blindness is called Anton's Syndrome.
• Lesion of the primary visual perception area of the right or left occipital lobe will produce a clear loss of visual perception from the contralateral visual field. Patients are usually aware of the deficit and do not neglect that side of the visual field.
• Ventral Stream damage; this area is involved with recognition, and damage here does not tend to produce visual field defects.