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Visual Field Defects
Visual Field Defects
Aetiology
There are many causes of visual field loss. Some more common ones are included here.
Central field loss results from degeneration of the fovea and occurs with:
History
The following need to be established:
Remember that the image on the retina is upside down and inverted. Hence, a lesion of the top right of the retina
or in the 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 (specialist equipment is needed).
Central or peripheral
Loss may be central/foveal (eg, an optic disc or nerve problem) or peripheral (along the visual pathways from the
optic chiasm back).
Scotoma
This is a defect surrounded by normal visual field. It may begin as a gradual enlargement of the blind spot and
may pass unnoticed by the patient until quite large.
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
This is a 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 the visual field in
both eyes, ie either the left or the right half of the visual field.
Altitudinal hemianopia - the dividing line between loss and sight is horizontal, with visual loss either
above or below the line.
Quadrantanopia - this is an incomplete hemianopia referring to a quarter of the schematic 'pie' of
visual field loss.
Sectoral defect - this is another term for incomplete hemianopia.
Sit approximately 1 metre from the patient, facing the patient. Make sure that they have the acuity to
see the intended target. Remove the patient's glasses if worn, as the rims get in the way.
Look at the patient's nose and ask the patient to look at yours.
Test each eye separately; cover the other eye. You can ask the patient to cover or close one eye and
you close the eye opposite.
Make sure the target is equidistant between you and the patient.
Starting at the top outer quadrant, move the target object (eg, fingers or hatpin) in from the side and
ask the patient to tell you when they first see the object and, as you move towards the centre, whether
they disappear.
Repeat the process in each quadrant and for each eye separately.
If you detect a defect, re-examine that area and define it further.
Assess the blind spot (if you can't find it, then it's probably not enlarged).
Repeat for the fellow eye.
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Then systematically assess:
Pupils and optic nerve function (visual acuity, relative afferent pupillary defect, colour
impairment and brightness sensitivity).
Fundus.
Neurological examination (if a systemic problem is suspected).
Difficulties
The most common is the patient's (or your) eye drifting away from the nose. You may need to remind
them throughout the test to keep fixing on your nose.
This technique compares the patient's visual field with yours, so it assumes normal examiner visual
fields.
Visual fields in infants can be crudely assessed by making use of their involuntary fixational reflexes.
First the child's attention is held in a frontal gaze; then, while the child is watching the examiner's face,
the examiner silently brings an interesting toy in from the periphery. This is difficult to do well and eyes
cannot be tested individually.
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: they take time and can be very tiring for the patient. Frailer
patients who may tire easily, patients unable to sit still for long or those unable to follow the instructions will deliver
unreliable results. Even a temporary loss of concentration can affect the results. Pupil size, refractive error and
artefacts (drooping eyelid, spectacle rim) may also affect the result if not taken into consideration.
Kinetic perimetry
This is based on presenting a moving stimulus from a non-seeing area to a seeing area. It is repeated at various
points around a 'clock-face' chart of the field of vision; 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 to produce a chart showing maximal peripheral vision
for each (decreasing) level of brightness.
The most commonly used kinetic test is called Goldmann's perimetry. It tends to be used for neurological
conditions. It is also used where there is suspicion of functional rather than organic problems, when a
characteristic pattern of spiralling isoptres may be seen. Goldmann's perimetry can be affected by ptosis,
refractive errors, tremor and inadequate operator skills.
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Interpretation
Understanding the pathological process relating to visual field defects requires an understanding of the
anatomical arrangement of the visual pathway.
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.
Retinal detachment tends to be fairly rapid in onset. It may be preceded by floaters and flashes before
the patient notices 'a curtain' coming across the visual field. A crescentic reddish slip of detachment
may be apparent at the periphery of the retina.
Centralretinal 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 four 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.
Centralretinal vein occlusion presents in a fairly similar way to arterial occlusion but the retina looks
hyperaemic. Haemorrhages are scattered throughout the fundus in a typical blood-storm pattern with
cotton-wool spots. With incomplete blockage, sparse scattered haemorrhages occur.
Age-related macular degeneration affects the macular area; the periphery is spared until very late.
Drugs can cause disturbance of visual fields. This tends to be bilateral - eg:
Chloroquine can cause a classic bull's-eye maculopathy affecting the centre of the field [5] .
Vigabatrin can cause field defects in up to 40% of those who take it [6] .
Optic neuritis.
Optic atrophy.
Glaucoma.
Trauma (incomplete damage, transection or blunt trauma).
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).
If they spread up from below (for example, pituitary tumours), the defect is worse in the upper field.
If they spread down from above (for example, craniopharyngioma), the lesion is worse in the lower
quadrants.
Lesions at the optic chiasm may show a phenomenon where two identical coloured objects are shown to one
eye in the left and right 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 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 upper quadrantic homonymous hemianopia, commonly with
macular sparing - eg, tumours.
Lesions in the parietal radiation cause inferior quadrantic homonymous hemianopia without macular
sparing.
Lesions in the anterior visual cortex (common) produce a contralateral homonymous hemianopia with
macular sparing - eg, posterior cerebral artery occlusion.
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Lesions in the macular cortex produce homonymous macular defect - eg, blunt injury to the occiput.
Lesions of the intermediate visual cortex produce an homonymous arc scotoma, with sparing of both
macula and periphery. This is seen in a distal posterior cerebral artery occlusion.
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