Visual Field Defects

The visual field is the portion of the subject's surroundings that can be seen at any one time.¹ The normal extent of field of vision is 50°superiorly, 60°nasally, 70°inferiorly and 90° temporally. 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.

There are many causes of visual field loss. Some more common ones are included here.

Central field loss occurs with:

• Optic neuropathy
• Macular degeneration
• Macular holes
• Cone dystrophies²
• A number of rare conditions like Best's disease, Stargardt's disease and achromatopsia.

Peripheral field loss occurs with:

• Retinitis pigmentosa
• 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 them 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.
  Looking for evidence of 'asymptomatic' visual field loss.
  
  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.
• Are there associated neurological or ophthalmic symptoms?

Visual acuity tests the eye's greatest power of resolution whereas visual field testing measures the peripheral sensitivity. It is important to remember that the image is projected on to the retina upside down and inverted. 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. Assessing for visual field defects can be via:

• Screening tests (easily carried out in a surgery) which include confrontational visual field testing and use of an Amsler grid.
• Quantitative measurements using manual or automated perimetry (need specialist equipment).

Terms which may be encountered include:³

• Visual field defect - a portion of visual field missing. This may be central (e.g. optic disc or nerve problem) or peripheral (along the visual pathways from the optic chiasm back).
• Scotoma - this is a type of visual field defect. It is a defect surrounded by normal visual field.
  • Relative scotoma - an area where objects of low luminance cannot be seen but larger or brighter ones can.
  • Absolute scotoma - nothing can be seen at all within that area.
• Hemianopia - binocular visual defect in each eye's hemifield.
  • Bitemporal hemianopia - the two halves lost are on the outside of each eye's peripheral vision, effectively creating a central visual tunnel.
  • Homonymous hemianopia - the two halves lost are on the corresponding area of visual field in both eyes, i.e. either the left or the right half of the visual field.
  • Altitudinal hemianopia - refers to the dividing line between loss and sight being horizontal rather than vertical, with visual loss either above or below the line.
  • Quadrantanopia - is an incomplete hemianopia referring to a quarter of the schematic 'pie' of visual field loss.
  • Sectoral defect - is also an incomplete hemianopia.

Confrontation visual field testing

This is a simple (but approximate) method of assessing visual field loss. It is a qualitative measurement but is a good starting point and can easily be carried out in the surgery. 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.

• Sit about 50 cms away from the patient, look at his nose and get the patient to look at yours.
• Starting at the top outer quadrant, move your fingers (or the pin) in from the side, wiggling them as they go, and ask the patient to tell you when they first see your fingers and, as you move towards the centre, whether they disappear. Peripheral vision tests rods and they are most sensitive to movement.
• Repeat the process in each quadrant and for each eye separately.
• If you detect a defect, re-examine that area and define it further.
• You can ask the patient to cover or close one eye and you close the one opposite.

Difficulties

• The most common is the patient's (or your) eye drifting away from the nose target. If this is happening, gently remind them throughout the test to keep fixing on your nose.
• This technique compares the patient's visual field with yours, so it does assume normal examiner visual fields!
• Visual fields in infants can be crudely assessed by making use of their involuntary fixational reflexes. First get the child's attention in a frontal gaze and while the child is watching your face, silently bring an interesting toy in from the periphery. This is a tricky process and eyes cannot be tested individually but, if you can manage it, valuable information will be gained.

Amsler grid testing

This assesses the central 10° the visual field. It detects central and paracentral scotomas. See our separate record on Examination of the Eye (go to 'Macular function' under 'Examination of function' heading) for details on performing this easy test.

Other examinations in a GP surgery

Visual field defects may stem from neurological or ophthalmic problems. Depending on what the history and findings so far suggest, a full neurological examination or further examination of the eye may be warranted. For the latter, examination of the function of the optic nerve (visual acuity, relative afferent pupillary defect, colour impairment and brightness sensitivity). Fundoscopy is a very important aspect of assessing the patient with a suspected visual field defect.

To find details on how to test the optic nerve and use an ophthalmoscope, refer to the above-mentioned separate record Examination of the Eye.

Quantitative measurements

There are a number of techniques used in specialist practice. They fall into one of two categories: static or kinetic perimetry.

Static perimetry

This is the most commonly used assessment. An 'on/off' light signal is presented throughout the patient's potential visual field and the patient clicks every time they see the signal. These automated machines can assess various amounts of the visual field (10° to full field).

These are sensitive tests but are difficult to perform in that the patient has to be able to understand the instructions and respond appropriately. The tests may take time and can be very tiring for the patient. Thus, frail individuals who may tire easily, patients unable to sit still for long or unable to follow the instructions will get unreliable results. Even if the patient can follow what is going on, a temporary loss of concentration can affect the results. Pupil size, refractive error and artefacts (drooping eyelid, thick spectacles' rim) may also affect the result if not taken into consideration. To some extent, this can be detected by the machine but if the defect is very subtle, it may take a few readings to confirm its presence.

Humphries' (and to a lesser extent, Henson's) machines are most commonly used.

Kinetic perimetry

This presents a moving stimulus from a non-seeing area to a seeing area. It is repeated at various points around the clock and a mark is made as soon as the point is seen. These points are then joined by a line (an isoptre). The process is repeated with a point of lesser luminescence and another isoptre is created. Thus, a number of isoptres are plotted and you have a chart of the maximal peripheral vision for each (decreasing) level of brightness.

The most commonly used kinetic test is Goldmann perimetry. It tends to be used for more neurological conditions, although not exclusively so. It is also used where there is suspicion of functional rather than organic problems as a characteristic pattern of spiralling isoptres may be seen. Goldmann perimetry also has its limits and can be affected by ptosis, refractive errors, tremor and inadequate operator skills.

Having elicited a visual defect, the patient needs referring on for further confirmation of the defect and investigation. However, you may find the following useful for your own investigative work.

Visual pathway⁴

• The visual image is projected through the lens on to 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 passes 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.
• Age-related macular degeneration which 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.⁵ Vigabatrin can cause field defects in up to 40% of those who take it.⁶

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, e.g. meningioma).

Lesions at the chiasm

These classically produce a bitemporal hemianopia.

• If they spread up from below, for example, 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 produce congruous homonymous macular defect, e.g. blunt injury to occiput.
• Lesions of the intermediate visual cortex produce a homonymous arc scotoma, with sparing of both macula 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.