Pract Neurol 2009; 9: 324–334
Assess and interpret the visual
fields at the bedside
S A Cooper
, R A Metcalfe
Specialist Registrar in Neurology,
Institute of Neurological Sciences,
Southern General Hospital,
Glasgow, UK
Consultant Neurologist, Institute
of Neurological Sciences, Southern
General Hospital, Glasgow, UK
Correspondence to:
Dr R Metcalfe,
Institute of Neurological Sciences,
Southern General Hospital, 1345
Govan Road, Glasgow G51 4TF, UK;
Understanding and applying a bedside visual field assessment is an important
skill for the neurologist. By appreciating some basic anatomical and
physiological principles it is possible to target the examination appropriately,
thus gaining important diagnostic information with the minimum of fuss.
Specific patterns of visual loss are caused by damage at various sites within
the visual pathway. This review focuses on techniques that can be used at the
bedside to identify common visual field defects and cites examples by dividing
the visual system into its component parts. We urge the use of an
appropriately sized red pin and berate the well worn ‘‘waggling finger’’
he process of converting the photons
that stimulate retinal rods and cones
into our perception of a three-dimen-
sional full colour environment is an
extraordinary feat of evolutionary engineer-
ing. The foveate human visual system is
adapted to provide both high quality central
colour vision and sensitive movement detec-
tion. The basic ‘‘camera’’ functions are
enhanced by a sophisticated eye movement
system which provides image stabilisation,
gaze shift and binocularity too. These produce
the benefits of depth perception, acuity and
colour vision. Most people of course take their
vision for granted but ‘‘you don’t know what
you’ve got ‘til it’s gone’’.
Moreover, even
transient visual loss is frequently a frighten-
ing experience for patients. Many fear that
they will go blind and this can both amplify
and distort perceptions.
In this article, we will discuss the ‘‘bedside’’
assessment of the visual fields and their
importance in both the localisation of disease
and the identification of its absence. Not
everything of course fits into the typical
patterns that we describe but we hope that
this article may at least whet the appetite to
know more. In order to understand how
particular defects in the area seen by a
fixating eye can occur, first it is important to
know something of the organisation of the
visual sensory system.
The functional organisation of the visual
sensory system begins at the retina (fig 1)
which has an inner layer—the neural retina—
that contains the 95 million or so light sensitive
receptor cells, or rods (responsible for vision in
dim light) and cones (for fine detail and colour
The distribution of visual function
across the retina is not uniform. The highest
concentration of cones is in the central macular
area, the fovea. The neural retina also contains
the retinal ganglion cells whose axons pass
across the surface of the retina, collect in a
bundle at the optic disc and leave the eye to
form the optic nerve. These cells can be divided
into two main populations: M and P (relating to
the layers of the lateral geniculate nucleus to
which they project (M=magnocellular and
P =parvocellular)). M cells function to detect
324 Practical Neurology
motion and contrast sensitivity whereas P cells
deal with fine spatial detail and colour vision.
As a result of the convex lens in the eye, objects
that stimulate the nasal retina are located in
the temporal visual field and those that
stimulate the inferior retina are located in the
superior visual field.
More than 90% of retinal nerve fibres arise
from the macula to form the papillomacular
bundle passing to the optic nerve, taking up
its central core (fig 2).
Lesions of this bundle
(either in the retina or in the optic nerve
head) produce central or centrocaecal scoto-
mas (ie, a central scotoma that connects with
the physiological blind spot) (fig 3).
Retinal nerve fibres temporal to the
macula must arc above or below the
papillomacular bundle to enter the optic disc.
Lesions of these arcuate bundles produce
arcuate scotomas (fig 4). Nasal fibres pass
directly to the nasal border of the disc.
Lesions of the nasal retinal axons cause
temporal field defects.
Optic nerve
Once in the optic nerve, the macular fibres
move to a central position with the superior
retinal fibres above and the inferior retinal
fibres below. Temporal and nasal fibres retain
these positions within the optic nerve.
Figure 1
The visual pathway (taken from Trobe J,
The neurology of vision, with
permission from Oxford University
Press Inc
Using a small red pin is the best way to
test visual fields at the bedside.
325 Cooper, Metcalfe
Lesions of the optic nerve tend to produce
several different patterns of visual field
abnormality depending on whether the lesion
is in the anterior, middle or posterior portions.
A good example of disease affecting the
anterior optic nerve (the optic nerve head) is
ischaemic optic neuropathy. The middle
portion is often affected by demyelinating
optic neuritis and the posterior optic nerve
may be compressed by an enlarging pituitary
tumour. The optic chiasm is usually situated
directly above the pituitary gland but in about
15% it is ‘‘pre-fixed’’, meaning that it is fixed
anterior to the pituitary gland. When the
chiasm is ‘‘post-fixed’’ (posterior to the
pituitary) then a pituitary tumour may directly
compress the optic nerves or the junction
between the optic nerves and the chiasm
causing either monocular field loss or a
‘‘junctional scotoma’’ which will be discussed
later. Anterior pathologies tend to respect the
horizontal meridian (including arcuate
defects), lesions of the mid portion of the
nerve cause central scotomas, and those
involving the posterior portion close to the
optic chiasm often show some respect to the
vertical meridian.
Optic chiasm, tract and radiation
At the optic chiasm, the visual system
becomes functionally divided by a vertical
meridian through fixation. Visual information
from the left hemifields of both eyes now
continues through the visual pathway
towards the right occipital cortex (and vice
versa with the right hemifields). The crossed
nasal fibres once joined with uncrossed
temporal fibres proceed as the optic tract.
These fibres in the optic tract then pass to the
lateral geniculate nucleus of the thalamus
where crossed and uncrossed retinal fibres
are organised into retinotopic pairs (retino-
topy refers to the projection of an image onto
a part of the visual cortex in a way that
preserves the spatial relations of the image
on the retina). From the lateral geniculate
nucleus the optic radiations pass posteriorly
to the visual cortex. Nerve fibres originating
from the superior retina (ie, lower visual field)
travel directly to the visual cortex through the
parietal lobe while those from the inferior
retina (superior visual field) pass through the
temporal lobe initially anteriorly and laterally.
Homonymous quadrantanopias may thus be a
feature of lesions of the optic radiations.
Visual cortex
The primary visual cortex lies along the superior
and inferior sides of the calcarine fissure. It
contains a large macular projection area in the
occipital pole (with peripheral optic tract fibres
terminating more anteriorly). The occipital pole
in particular has a rich anastamotic network
between the terminal branches of the middle
cerebral and posterior cerebral arteries.
Activation of the primary visual cortex results
in distribution of visual information into
temporal, parietal and frontal lobes with
increasing visual specialisation (colour, motion)
and decreasing retinotopy. Broadly, a division
into dorsal (parietal) and ventral (temporal)
streams can be made but although this has
some relevance to visual field assessment (for
example, the use of static or moving targets
and simultaneous stimulation) detailed discus-
sion is beyond the scope of this article.
The visual field is the area seen by the steadily
fixating eye and as such it is a slightly
Figure 3
Centrocaecal scotomas.
Figure 2
The course of the retinal nerve fibres
towards the optic nerve
1 =papillomacular bundle, 2 =superior
and inferior arcuate bundles, 3 =nasal
bundle (taken from Trobe J, The
neurology of vision, with permission
from Oxford University Press Inc
326 Practical Neurology
artificial construct. Traquair described it as
‘‘an island of vision surrounded by a sea of
The central peak of this island
(fig 5) corresponds to the fovea (the centre of
the retina where there is the highest
concentration of cones) and is typically the
area of highest sensitivity. Central field
representation greatly dominates all levels
of the visual pathway, including the visual
In practice, nearly all of the patho-
logical abnormalities fall within this central
area (ie, virtually all visual field defects are
detected within 20–30u of fixation).
Defects in the visual field may be relative
or absolute. Large and dense visual field
defects are easily identified but for the
detection of small or relative defects, the
choice of test is crucial. This applies in
particular to confrontation tests at the bed-
side. Formal perimetry with either Goldmann
or Humphrey perimeters requires trained
operators and relatively expensive equipment
and we will not discuss these here.
A visual field assessment should, like all
elements of the neurological diagnosis, be a
targeted procedure, and we hope the clinician
has a fair idea of what might be going on
from the history alone and so know what to
expect and what to examine. Pertinent
questions include:
N What is the time course of the visual loss
(eg, an acute onset suggests a vascular
cause, progression over days followed by
a plateau and then recovery is the rule for
demyelinating optic neuritis, and a stead-
ily progressive course is more in keeping
with a compression)? The patient who
suddenly notices a defect that may have
been present for some time, when, say an
insect flies into the other (good) eye does
imply that the pathology is anterior to
the chiasm, and except in the most
unobservant, usually suggests an insid-
ious onset of visual loss.
N Is the visual loss monocular or binocular
(has the patient tried covering one eye?)
and is the defect homonymous (ie, loss of
vision on the same side of the visual field
in both eyes) in which case the pathology
is retrochiasmal? Many patients with
homonymous visual loss attribute their
visual problems to the eye with the
temporal field defect. It is useful in such
circumstances, particularly if the distur-
bance was transient, to ask the patient
what they can or could see (eg, is or was
one half of faces missing, etc)? If so, this
is not consistent with monocular loss and
indicates a homonymous field defect
N Is there pain, which may point to an
inflammatory aetiology affecting the
optic nerve?
N Are there symptoms of raised intracranial
pressure (including visual obscurations)?
N Are there additional symptoms (eg,
double vision or those suggesting a focal
cortical disorder)?
The initial examination should include docu-
menting the uncorrected and corrected visual
acuity (important to know if the patient can see
the targets used for field examination) and
colour vision (with Ishihara test plates) which
provides useful additional information on
optic nerve function and underlying colour
Figure 5
The hill or island of vision, as described
by Traquair. The higher the ‘‘hill’’ the
greater the visual sensitivity (taken
from Scott GI, Traquair’s clinical
with permission).
Figure 4
Inferior arcuate scotoma, typical of
327 Cooper, Metcalfe
blindness which may influence the use of a
red pin for field testing.
Confrontation testing of visual
The examination performed should be tailored
to the particular clinical problem. For example,
in the case of monocular visual loss asso-
ciated with painful eye movement, one would
look for a central scotoma to a red pin. If a
patient has papilloedema, extra time should
be spent examining for an enlarged blind
spot. Clearly, when considering retrochiasmal
pathology, looking for homonymous field
defects is paramount.
Start any confrontation testing of the
visual fields by asking the patient, viewing
with both eyes, to describe any visual loss
when looking at the examiner’s face and then
to count (one or two) fingers in each of the
four quadrants in each eye. Follow this by
individual and then bilateral simultaneous
stimulation of the superior and inferior
quadrants. This is a quick way of picking up
homonymous hemianopias and attentional
field defects and neglect but cannot, of course,
be expected to detect monocular or even
chiasmal defects (because this is a binocular
test it cannot necessarily pick up bitemporal
defects because of the overlap between the
visual fields in both eyes—a large enough target
in the temporal field of one eye might be seen
in the nasal field of the other eye).
The most sensitive method of detecting
visual field defects by confrontation is to use
a small (ideally 5 mm) red pin (this has a
sensitivity of 73% compared with automated
perimetry) (table 1). A ‘‘kinetic to finger’’ (ie,
waggling finger) test to assess for field
defects in the same study had a sensitivity
of only 40%, while a 20 mm white pin was
48% sensitive.
Assess each eye in turn, and
move the target slowly in from the periphery
while asking the patient when the colour red
becomes detectable rather than when they
first can see the pin; they will initially see it as
black at the periphery where there are no
colour sensitive cones. The same target
should then be presented statically to multi-
ple points within the central red field (usually
representing about 20–30u). A red pin, by
stimulating fewer cones than a white pin,
detects more subtle defects. Although white
pins are easier to find than red pins in a local
shop, they can be painted red or ordered from
If a chiasm defect is suspected, then
careful comparison of colour perception
across the vertical meridian in each eye is
important. The simultaneous presentation of
two identical red pins on either side of the
vertical meridian both above and then below
the horizontal meridian is a sensitive method
of doing this.
It is fairly common to see clinicians bring a
waggling finger in from the periphery but this
dramatically reduces the test sensitivity (see
above) in the peripheral field and fails entirely
Figure 6
Bilaterally enlarged blind spots, often
observed in papilloedema.
TABLE 1 Comparison of techniques used to analyse visual fields
Method of visual
field analysis Advantages Disadvantages
Confrontation methods
(binocular face
description and
quandrant finger
counting, red pin)
Relatively quick and
easy, always available,
cheap, can be performed
at the bedside
Less sensitive than other
methods, more difficult to
compare results over time
(kinetic) perimetry
Sensitive. Good for
monitoring defects over
time. Can asses for
patient reliability
Requires a skilled
operator; subject to
interoperator variability.
(static) perimetry
Sensitive, good for
monitoring defects over
time, can assess for
patient reliability
Requires significant
concentration, may
produce artefacts if test
conditions not correct (eg,
spectacle rims).
Impossible with sick
328 Practical Neurology
to assess the central fields. This technique
should not be used.
There are a number of different patterns of
visual field defects which we will consider in
relation to the anatomical structures affected
by pathology (table 2). Generally speaking,
lesions of the retina, optic nerve, optic chiasm
and visual pathways conform to a limited set of
N altitudinal field defect
N central scotoma
N arcuate field defect
N hemianopia (homonymous or bitemporal)
N quadrantanopia (homonymous or bitem-
N wedge shaped field defect
N blind spot enlargement
The retina
Diseases of the retina can cause a variety of
visual field defects but usually there is visible
disease when viewing the retina with the
ophthalmoscope. Macular lesions produce
central (at fixation) scotomas that spare the
periphery. These are mostly caused by
ophthalmological disorders and a full discus-
sion of retinal disease is beyond the scope of
this review.
The optic nerve
Lesions at the optic disc typically produce
visual defects which emerge from the blind
spot and often respect the horizontal mer-
With papilloedema, central and arcuate
scotomas may be seen, and in chronic
papilloedema inferior nasal defects are not
infrequent. Generally the field defects are
worse nasally than temporally where some
Figure 7
An (inferior) altitudinal field loss typical
of ischaemic optic neuropathy.
Figure 8
A central scotoma affecting the right
329 Cooper, Metcalfe
vision may remain before progression to
complete blindness. The increase in blind spot
size in papilloedema is thought to be due to
compression, detachment and displacement
of the peripapillary retina or the elevation of
that part of the retina by subretinal fluid
(fig 6).
The neuronal swelling in papilloedema
is more extensive in the peripheral than the
central optic nerve accounting for the addi-
tional constriction of the visual field (as all
fibres carrying information from the periph-
eral field enter the edge of the optic disc).
Minor enlargement of the blind spot is
difficult to identify by bedside testing; formal
perimetry is needed both in this situation and
when sequential assessments are required to
follow the progress of papilloedema.
When the anterior portion of the optic
nerve (including the optic nerve head) is
involved in a disease process, the defect
usually respects the horizontal meridian. This
is termed an ‘‘altitudinal’’ field loss. Ischaemic
optic neuropathy typically produces an infer-
ior defect (fig 7). It is postulated that
impairment of posterior ciliary artery perfu-
sion is responsible
because the ciliary arteries
supply a vascular anastamosis known as the
circle of Zinn-Haller, which may have distinct
upper and lower zones thus providing an
anatomical basis for the altitudinal visual field
defect observed in two-thirds of reported
Lesions at the optic disc may also produce
defects which extend from the blind spot to
the temporal periphery.
Glaucoma also affects the anterior optic
nerve but typically causes arcuate defects,
and these too respect the horizontal meridian
(fig 4).
As the optic disc has no retinal photo-
receptors it forms the blind spot (a physio-
logical absolute scotoma) in the visual field. A
central scotoma occurring in the absence of
macular disease is the hallmark of a lesion
involving the optic nerve (fig 8).
Defects are usually, but not always,
monocular; hereditary optic atrophies and
toxic/nutritional neuropathies are bilateral
and optic neuritis may be bilateral and
simultaneous (eg, in neuromyelitis optica).
Retrobulbar disorders of the optic nerve (eg,
optic neuritis, toxic neuropathies) especially
depress the function of the central core of the
nerve which carries fibres from the macula
region (the papillomacular bundle) and so
disease here causes a central scotoma (seen
to some extent in over 90% of patients
with demyelinating optic neuritis
). Central
scotomas are classic in demyelinating optic
Figure 9
(A) A junctional scotoma, caused by a
lesion at the junction of the right optic
nerve and chiasm. (B) The ‘‘junctional
scotoma of Traquair’’,
a less frequently
observed visual field defect.
Figure 10
In bitemporal hemianopia there is a
blind field beyond fixation (horizontal
lines) with dotted areas indicating
monocular fields.
330 Practical Neurology
neuritis but a broader spectrum of patterns
commonly occurs, including diffuse defects
(ie, generalised depression of the entire
central 30u of the visual field) and focal
When a central field defect is found in one
eye it is important to carefully examine the
field of the other eye in case there is a
junctional scotoma caused by compression at
the meeting point of the optic nerve and
chiasm (fig 9A, and see below).
The optic chiasm
The essential feature of visual field defects
caused by damage to the optic chiasm is
some form of bitemporal field defect with
considerable variations on this depending on
the exact site of the lesion. The lesions are
usually insidiously progressive as most are the
result of slow growing tumours, commonly
pituitary adenomas, but craniopharyngiomas
and meningiomas also occur.
Junctional scotomas
Pathology at the anterior angle of the chiasm
(ie, where the optic nerves join) causes a
‘‘junctional’’ scotoma because of separation
of nasal crossed and temporal uncrossed
fibres. What this means in practice is that
small lesions may damage only the crossing
fibres of the ipsilateral eye and can encroach
on the ipsilateral optic nerve causing varying
degrees of field defect. The contralateral field
defect (caused by damage to the crossing
fibres) may be overlooked unless the ‘‘normal’’
eye is carefully tested. So, a junctional lesion
consists of a central scotoma in one eye with
temporal (often superior) field loss in the
other eye (fig 9A). The way in which the
contralateral fibres are damaged is attributed
to a structure known as ‘‘Wilbrand’s knee’’
where there is an anterior extension of these
fibres into the affected optic nerve. This
anatomical explanation has been challenged
but, as Trobe points out, ‘‘the clinical entity
Figure 11
Tilted optic discs (taken from Williams
Figure 12
Macular sparing, as seen with retinitis
pigmentosa or glaucoma. Bilateral
macular sparing occipital infarcts
usually do not produce perfect circles
because the lesions on the two sides
are of different sizes—hence there is
usually a subtle ‘‘step’’. Functional
visual loss is also a common cause of
this constricted field.
331 Cooper, Metcalfe
Identifying junctional scotomas is
important because it localises anterior chias-
mal lesions. Less common is the ‘‘junctional
scotoma of Traquair’’ (fig 9B) also caused by
compression in a similar anatomical location
but where only crossing nasal fibres are
affected, producing a small temporal quad-
rantanopic scotoma.
Damage to the body of the optic
A bitemporal field defect (albeit sometimes
quadrantic) is usually seen. Other symptoms
may relate to problems with depth perception
(eg, threading a needle). Figure 10 shows how
a bitemporal field defect can cause blindness
beyond a fixation point.
Other conditions that may mimic chiasmal
field defects include congenitally tilted discs,
nasal sector retinitis pigentosa and papilloe-
dema with greatly enlarged blind spots. The
first is a condition where the superotemporal
optic disc is elevated and the inferonasal disc
displaced posteriorly leading to an oval-
shaped obliquely orientated disc (fig 11).
Patients often have myopic astigmatism and
can present with a bitemporal hemianopia
Figure 14
A spiralling kinetic visual field, typical of functional visual loss.
Figure 13
An example of crossing isopters from kinetic perimetry whereby the patient fails to report seeing a target brighter than one they have already seen. These fields are also
very irregular in outline which again points to an inconsistent responder.
332 Practical Neurology
suggesting a chiasmal syndrome. In these
patients, however, the hemianopia is typically
incomplete, does not respect the vertical
meridian and is confined primarily to the
superior quadrants.
Establishing that the vertical meridian forms
the central border of the temporal defect is key
to distinguishing chiasmal pathology from
other defects that may mimic this.
Retrochiasmal lesions
Any lesion posterior to the chiasm produces a
homonymous defect. The exception is a defect
in the temporal periphery of the eye contra-
lateral to a lesion of the anterior-most occipital
lobe known as a ‘‘monocular crescent’’.
The optic tract
As only the contralateral hemifield is
represented in the optic tract then visual
field defects are homonymous. Partial
lesions cause contralateral homonymous
defects but these may be incongruous (ie,
defects are differing in shape and depth in
each eye). There is a trend for more
congruent homonymous hemianopias with
lesions situated more posteriorly in the
visual pathway but 50% of optic tract
lesions produced congruent field defects in
one study.
The optic radiations
Superior homonymous quadrantic field
defects (‘‘pie in the sky’’) may result from
lesions located in the temporal (Meyer’s) loop
of the optic radiation. The defect is usually,
but not always, incongruous. If the optic
radiation involved is in the parietal lobe, then
a homonymous hemianopia usually results
(often denser in the inferior quadrant). There
are frequently other symptoms and signs of
cerebral damage specific to the location of
the pathology.
The occipital cortex
Focal lesions of the occipital cortex produce
homonymous, contralateral visual hemifield
defects which are highly congruent. A lesion
at the posterior pole of the visual cortex will
produce a homonymous, paracentral hemi-
anopic scotoma. Such defects involve the
central 5–10u of vision and may spare the
remainder of the visual field if the rest of
the striate cortex is normal. Alternatively, a
TABLE 2 Some visual field defects and their more typical causes
Field defect Localisation Seen in
Arcuate scotoma Optic nerve, retinal
nerve fibre layer
Glaucoma, papilloedema,
optic neuritis, ischaemic optic
neuropathy, optic disc drusen,
branch retinal artery
Altitudinal field loss Optic nerve, retinal
nerve fibre layer
Ischaemic optic neuropathy,
optic neuritis
Central scotoma Macula, optic nerve,
retinal nerve fibre
Macular lesions, optic
neuritis, ischaemic and other
optic neuropathies
Optic nerve, retinal
nerve fibre layer
Toxic/nutritional optic
constriction and
enlarged blind spot
Optic nerve, retina Papilloedema, optic disc
Bitemporal Optic chiasm Disease of the optic chiasm
(usually adjacent tumour)
Homonymous Retrochiasmal (ie,
optic tract, lateral
geniculate body,
optic radiations,
visual cortex)
Strokes, tumours, etc, of the
structures listed
Quadrantanopia Optic radiation Strokes, tumours, etc
Tunnel vision Retina, occipital
cortex (with macular
Advanced retinitis
pigmentosa, vascular disease
of the occipital cortex,
functional visual loss
The visual pathway consists of the retinas, optic nerves, optic chiasm, optic
tracts, optic radiations and visual cortex; lesions in each area cause distinct
patterns of visual loss.
The organisation of the retinal nerve fibre layer and the subsequent
arrangement in the optic nerve head gives rise to arcuate defects, central/
centrocaecal scotomas or temporal defects depending on the site of the lesion.
Lesions of the optic nerve may result in several different field defects
depending on whether the anterior, middle or posterior portion of the nerve is
affected; a central scotoma localises the pathology to the optic nerve.
At the chiasm vision becomes functionally divided by a vertical meridian.
Posterior to the chiasm visual field defects are homonymous (ie, involving
the same hemifield in each eye).
Targeting the examination is important; beginning with asking for a
description of the examiner’s face and then quadrant finger counting is
A red pin is the most sensitive tool for assessing the visual fields at the
333 Cooper, Metcalfe
homonymous hemianopia with ‘‘macular spar-
ing’’ occurs with occipital lesions that spare the
posterolateral striate cortex (fig 12). Partial
lesions are frequently observed. In order to
qualify as macular sparing, at least 5u of the
macular field must be spared in both eyes on
the side of the hemianopia (but this can be an
artefact if the patient shifts fixation).
Functional visual field loss
Tests of the visual fields, either by confronta-
tion or especially using perimetry, may be
helpful in highlighting inconsistencies char-
acteristic of functional field defects (figs 13,
14). Observing someone navigating around an
unfamiliar environment with ease and then
struggling to observe large bright targets on
formal testing also helps. It is often suggested
that, in this situation, it is helpful to test the
visual fields at, for example, 1 m and 2 m. The
concept is that in functional field loss the
patient will maintain an equally constricted
field at a greater distance while the normal
field might be expected to enlarge. However,
this technique does not recognise that in
moving further away the angle subtended by
the target at the retina diminishes and its
luminance is reduced which may counteract
any field enlargement. The technique can be
useful using tangent (Bjerrum) screen testing
at 1 and 2 m with appropriately sized targets
but in practice we do not find this helpful,
preferring to rely on the general principles
The visual pathway is complex but lesions
along its course cause visual field defects that
conform to certain patterns. Simple techni-
ques make it possible to select a bedside
examination appropriate to the clinical situa-
tion to aid localisation of the lesion. Lesions
anterior to the chiasm may cause a variety of
(usually but not exclusively) monocular
defects. The classical bitemporal hemianopia
of chiasmal compression may start as a subtle
alteration of red perception across the vertical
meridian. Retrochiasmal defects are homon-
ymous. Armed with a grasp of the funda-
mental principles outlined above and a red
pin, we hope that bedside visual field testing
will become a more frequently performed and
better understood aspect of the neurological
This article was reviewed by Christian Lueck,
Canberra, Australia.
Competing interests: None.
Provenance and peer review: Commissioned;
externally peer reviewed.
1. Mitchell J. Big yellow taxi. On: Ladies of the canyon.
Warner Bros Records, 1970.
2. Rizzo JF. Embryology, anatomy and physiology of
the afferent visual system. In: Miller NR, Newman
NJ, eds. Walsh and Hoyt’s clinical neuro-
ophthalmology, 6th Edn. Philadelphia: Lippincott,
Williams and Wilkins, 2005:9.
3. Spector RH. Visual fields. In: Walker KH, Hall DW,
Hurst WJ, eds. Clinical methods: history,
examination and laboratory investigations, 3rd
Edn. Boston: Butterworths, 1990:116.
4. Scott GI. Clinical perimetry introductory. In: Scott
GI, ed. Traquair’s clinical perimetry, 7th Edn.
London: Henry Kimpton, 1957:1.
5. Pandit RJ, Gales K, Griffiths PG. Effectiveness of
testing visual fields by confrontation. Lancet
6. Zimmerman LE. Histology and general pathology of
the optic nerve: Symposium on diseases of the
optic nerve. Trans Am Acad Ophthalmol
Otolaryngol 1956;60:14–30.
7. Friedman DI. Papilloedema. In: Miller NR, Newman
NJ, eds. Walsh and Hoyt’s clinical neuro-
ophthalmology, 6th Edn. Philadelphia: Lippincott,
Williams and Wilkins, 2005:257.
8. Arnold AC. Ischaemic optic neuropathy. In: Miller
NR, , Newman NJ, eds. Walsh and Hoyt’s clinical
neuro-ophthalmology, 6th Edn. Philadelphia:
Lippincott, Williams and Wilkins, 2005:358–9.
9. Arnold AC. Ischaemic optic neuropathy. In:
Miller NR, Newman NJ, eds. Walsh and Hoyt’s clinical
neuro-ophthalmology, 6th Edn. Philadelphia:
Lippincott, Williams and Wilkins, 2005:357.
10. Marshall D. Ocular manifestations of multiple
sclerosis and relationship to retrobulbar neuritis.
Trans Am Ophthalmol Soc 1950;48:487–525.
11. Keltner JL, Johnson CA, Spurr JO, et al. Comparison
of central and peripheral visual field properties in
the Optic Neuritis Treatment Trial. Am J Ophthalmol
12. Trobe J. Visual fields. In: Trobe J, ed. The neurology
of vision. Oxford: Oxford University Press,
13. Williams A. The tilted disc syndrome. Pract Neurol
14. Kedar S, Zhang X, Lynn MJ, et al. Congruency in
homonymous hemianopia. Am J Ophthalmol
334 Practical Neurology