The easiest way to screen for defects of visual field is simply to ask the patient to cover each eye in turn and to notice whether there is any part of their vision missing, this will detect most field defects.
If a field defect is suspected then it can by confirmed by confrontation.
I have created the following YouTube video which is 10 minutes long and goes into some detail regarding visual fields. The following excerpt goes straight in at 7mins 40s to the part of the video showing how to examine to confrontation. You could drag the slider back to the beginning to watch the whole video, and I have added the full transcript below.
Our field of vision is the total area we are able to see, and is the combination of the individual visual fields of our 2 eyes. When looking straight ahead a normal field extends about 60 degrees up, 75 degrees down, 60 degrees nasally and an impressive 110 degrees temporally. The overlapping areas represent binocular vision, where depth perception or stereopsis is possible.
The shape of the field of each eye is rather like the shape of a pair of sunglasses. For simplicity the field of each eye can be documented as an oval shape, with the visual field of the right eye drawn on the right side of the page and the left eye on the left side. This is as if the patient is looking out through the page you have in front of you. For example a patient who could not see below the horizon from his right eye would be documented like this, with the dark area representing the area the patient is unable to see. You should notice that this is different from how you would record a scar on the right side of a patients face, where the drawing would be as if the patient was sitting in front of you. This reversal of sides when recording visual fields can cause confusion, so remember that fields are drawn the wrong way round, compared with the rest of the notes, and make sure you label them accordingly. This is a right inferior altitudinal defect.
The visual pathway is the wiring from the eye to brain, with the destination being the primary visual cortex in the occipital lobes, also known as the striate cortex. Damage along this pathway causes characteristic field defects. This pathway starts in the eye with the rod and cone photoreceptors in the retina. These synapse via bipolar cells with the ganglion cells of the retinal nerve fibre layer. These unmyelinated fibres pass into the optic disc and become myelinated as they become the optic nerves. We all have a small blind spot or scotoma corresponding to the optic disc which lacks photoreceptors. This physiological scotoma is slightly to the side or temporal to the centre of our vision.
Damage to the macula area of retina causes loss of central vision or central scotoma, seen most commonly in age related macular degeneration or AMD. An Amsler grid is a simple 5mm grid pattern, where the patient attempts to fix at the central dot from about 30cm with each eye in turn. These can be useful to identify and monitor central scotoma.
A new or changing central scotoma or indeed distortion of central vision may indicate treatable Wet AMD, and should be seen promtly by an eye specialist. Damage to the nerve fibres as they pass through the optic disc is seen in glaucoma. These defects cause an arcuate scotoma which follows the pattern of the nerve fibre layer. Here an upper nerve fibre layer defect causes a lower arcuate scotoma. Later this can extend to an upper or lower altitudinal defect, then complete loss of peripheral field and finally blindness. Identification of early glaucoma field defects can allow treatment to delay or prevent this progression, and preserve vision. As well as the visual field, assessment of glaucoma features the appearance of the optic disc, the Intraocular Pressure and the medical history.
The optic nerve function can be affected in many ways, for example in thyroid eye disease it can be compressed, In optic neuritis it can be inflamed and in Giant cell arteritis it can be ischaemic. These may cause various shapes of field defect such as an altitudinal defect or a mixed field defect which does not respect the horizontal or vertical midline. These causes mentioned can affect one or both eyes at the same time.
The optic chiasm is named after the greek letter chi or X. At this crossing the signal from each eye is split in two, with the nasal retinal fibres crossing sides, while the temporal retinal fibres stay on the same side. The effect of this selective crossing is that the vision corresponding to the left hand field of view is supplied to the right hand side of the brain, with the right visual field going to the left brain. So the right brain controls the left hand, and the right brain sees the left field of vision from both eyes. Compression of the chiasm, most commonly by a pituitary tumour can cause a bitemporal hemianopia, with only the crossing fibres are affected. In the early stages these field defects may be missed, sometimes for years. In practice these defects are neither complete nor symmetrical.
Beyond the chiasm is the optic tract which terminates in the lateral geniculate nucleus in the thalamus. From here fibres fan out into the optic radiations which synapse in the striate cortex. Defects beyond the chiasm, the so-called retrochiasmal pathway, cause homonymous defects, meaning a similar area of the field is affected in both the eyes. It is important to note that the vertical midline is never crossed.
The optic radiations are also called the geniculo-calcarine tract. Damage to this tract occurs most commonly due to stroke and can cause quadrantanopia or hemianopia depending upon lesion size. Temporal lobe lesions cause superior quadrantanopia, or pie in the sky, and may have associated complex partial seizures, memory problems or Wernicke’s aphasia if dominant hemisphere. Parietal lobe lesions cause inferior quadrantic defects or pie on the floor, with possible associated sensory disturbances and Gerstmanns and aphasic syndromes if dominant hemisphere.
Homonymous hemianopia and quadrantanopia most commonly arise from occipital strokes affecting the striate cortex. Posterior cerebral artery infarcts with intact middle cerebral collateral perfusion may cause so-called macula sparing, where the hemianopia spares the central vision.
Visual inattention is common in stroke patients and may mimic or accompany homonymous hemianopia. With visual inattention the visual pathway may be intact, but the patient fails to notice the vision on the affected side. This can be demonstrated by offering the patient simultaneous bilateral stimuli.
So how should visual fields be assessed? Well this depends upon the context of the examination. So far we have looked at field defects as being absolute, they are either present or absent. In practice the visual field is like and island of vision, with the centre of the vision being most sensitive. This means a small or dim target can be detected centrally just as easily as a bright or large target peripherally. Accurately mapping the shape of this island of field allows for early detection of problems, and to demonstrate changes over time. Two machines are in common use in the UK to assist with this, first is the humphrey field analyzer, second is the goldmann visual field. Both machines sit the persons face inside a bowl of uniform light.
The humphrey machine typically only measures the central 24 or 30 degrees of field. This makes it unsuitable for early detection of compression of the optic chiasm. One eye is covered while the other fixates upon a central target. Lights of various brightness are shown across a grid pattern within the bowl until the threshold for detection of the light is established at each point. When the person sees the light flash, they press a button. The results are printed as a numeric value for the sensitivity at each point, and then represented as a grey-scale picture to aid interpretation. This is typically used for screening and monitoring of glaucoma. Here is a normal Humphrey field, while here is an arcuate defect in glaucoma. This is termed static threshold perimetry as the stimuli are shown in fixed grid positions to establish the threshold at each point.
In contrast the Goldmann Field is kinetic threshold perimetry, where the light stimulus is moved in towards the centre of vision until it is detected. The patient again fixes the tested eye upon a central light target, while this time an examiner manually brings lights towards the centre of vision until it is detected. These points are then plotted into isopters like contour lines on a map. By repeating with differcnt light brightness or size the ‘shape’ of the field is plotted. The goldmann field can be measured out to 90 degrees, and is most commonly used to monitor neurological field changes. For example before and after treatment of a pituitary tumour.
Finally we have field testing to confrontation. In an asymptomatic individual I think this should be a brief screening examination taking a few seconds. I check central vision, four quadrants and temporal field. If they are a possible stroke patient, begin by checking for inattention.
First ask the patient cover one eye and look at my face. Then ask them to tell you if any part of the vision is missing. If the patient thinks it is all present, then usually they have normal fields. If they cannot see part of your face, then use an amsler grid to check their central vision for distortion and scotoma. Patients may use this grid to monitor their central vision at home.
Next the four quadrants. Again with one eye covered. Ask a patient to look you in the eye and tell you if they can see your finger wiggling in each quadrant. If they cannot see part, then it can be mapped out more carefully with a red hat pin, particularly noticing whether it crosses the horizontal or vertical midline. Finally, for peripheral field I ask a patient whether they can see a finger wiggle at 90 degrees to each eye, about 5cm away.
Of course more detailed examination is possible, but I think the most likely reason to miss a field problem is not because of a brief examination, but because the fields are not examined at all.
So lets wrap up.
Central loss of field is most common in macular degeneration, and should be assessed by and eye specialist, urgently if recent in onset. Field defects which respect the horizontal midline arise from the eye or optic nerve. Causes include glaucoma, branch retinal vein occlusion, optic neuritis, optic nerve ischaemia. They should be assessed by an eye specialist. Field defects which respect the vertical midline may arise from the optic chiasm and beyond. Causes include stroke and brain tumours. Humphrey field testing is routinely used to screen and monitor glaucoma, while goldmann testing may be used in neurological field defects.
Examination to confrontation can be done quickly, so that it need not be missed out of any routine neurological or ophthalmological assessment