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COURSE CODE: C-8367
Clinical Decision Making I: Visual Field
Interpretation
30
11/07/08 CET
Revision of the visual
pathways
The anatomy of the sensory visual
system is described here very briefly,
and reference to a detailed text is
strongly recommended 1,2.
The optic nerve head (ONH) so
readily discerned by ophthalmoscopy
is considered the reference location to
which features are related from an
anatomical or structural perspective.
However, from a functional
perspective, when assessing the visual
fields, its projected representative, the
blind spot takes a minor role. Instead,
the fovea and fixation with its
significant representation at the cortical
level becomes the key reference locus.
The inverted visual representation
that is generated by the optical system
focussing light entering the eye, is
maintained throughout the visual
system. Lesions temporal to the fovea
give rise to nasal visual field defects
whilst those superior to the fovea or
involving superior-originating fibres at
any point along the pathway produce
inferior visual field loss.
The ganglion fibres originating from
the innermost layer of the retina tend to
group themselves by regions according
to their origin relative to the fovea. The
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Shirley Ann Hancock PhD, BSc (Hons), MCOptom
Visual field assessment provides a measure of the neural pathway integrity
from eye to visual cortex. Certain patterns of visual field defect are associated
with damage to specific regions of this pathway. Inaccurate test results can
compromise interpretation leading to potentially serious consequences for
diagnosis and ultimately the management decisions for that patient.
macula fibres nasal to the fovea decussate (cross-over) to the opposite
(maculo-papilla bundle), follow a side of the brain tissue en route to each
direct course across the retinal surface occipital lobe. Axons from retinal
to turn down through the ONH at its ganglion cells nasal to the fovea, which
temporal border. They form the core of carry information from the temporal
the optic nerve with axons from the visual field, cross the midline to join
superior retina uppermost and those axons from the temporal retinal
from the inferior half of the retina, ganglion cells, that do not cross in the
beneath them. Those macula fibres chiasm. Together these form the optic
temporal to the fovea arch around the tracts. Once again the division of the
maculo-papilla bundle to enter the fibres from each half of the retina is
supero-temporal and infero-temporal through the fovea as represented in the
ONH boundaries. Fibres arising nasal field of view by the point of fixation.
to the optic disc travel radially directly The blind spot falls entirely within the
to the nasal side of the ONH. The ONH temporal field.
forms the intraocular portion of the The fibres leaving the optic chiasm
optic nerve. Beyond this region the 1.2 course posterio-laterally to synapse in
million afferent nerve fibres travel a the lateral geniculate nucleus (LGN),
further 25-30mm intraorbitally, passing where they retain a well-defined
via the optic foramen to the optic canal laminar organisation. The crossed
in the orbital wall to emerge into the fibres terminate in layers 1,4 and 6
intracranial section. The optic nerve whilst the uncrossed ipsilateral fibres
travel for another approximately 10mm synapse in layers 2, 3 and 5. The
to reach the chiasm.3 macula fibres occupy a proportionally
The term, ‘chiasm’ is derived from large area within this structure. The
the Greek letter chi that describes the LGN is quite small and it is unusual for
shape of the neural tissue at the region a lesion to involve the nucleus alone
where the optic nerves from each eye without encroaching on the optic tract
converge. It is about 4mm thick and on or radiations either side of it.
average 10-12mm wide by 8mm in Upon leaving the LGN, the upper
length. At the chiasm approximately fibres of the optic radiations take a
half of the nerve fibres from each eye relatively direct course backwards,
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spreading in a broad fan through the

parietal lobe to terminate in the
occipital visual cortex. The lower fibres
initially loop forward towards the
anterior pole of the temporal lobe to
form Meyers Loop, before turning back
to join the lower part of the optic
radiations at the occipital pole.
31
Guidance in choosing an
appropriate test

11/07/08 CET
strategy/program
To interpret visual field plots one needs
knowledge of the visual pathways. An
appreciation of the skill, or arguably
the art, employed supervising a visual
field test particularly under less than
favourable conditions should also be
expressed.
The human visual system is poor at
estimating absolute magnitude of light
intensity but remarkably good at
perceiving contrast. This facility is
evaluated when a visual field test is
performed. By measuring the
differential light sensitivity to a
stimulus against a standardised,
constantly illuminated background,
one can obtain an estimate of the
threshold for detection at a given
retinal location.
The choice of visual field test
depends on the degree of detail
required and the patients’ ability to co-
operate. One of the most valuable < Figure 1
techniques to master is confrontation Typical printout from Automated Static Threshold Perimetry
testing, particularly in suspected
neurological disease. Confrontation characteristic of parietal lobe lesions. interpolation of the visual field is
testing being both rapid and simple Testing the macula area with an Amsler introduced in the post-test processing.
should always precede any more Chart is useful for rapidly screening the Manual perimetry has been considered
detailed attempts with more central 20° of the visual field, despite superior to automated perimetry for
sophisticated automated static or sensitivity being relatively low. neurological fields, but recent studies
manual kinetic perimetry. For those Automated perimeters that include have found the Swedish Interactive
patients too poorly, whether mentally the Humphrey Visual field analysers Thresholding Algorithms (SITA) to be
or physically, this test can be most and Henson perimeters are less comparable 4,5.
informative. It can reveal the presence operator dependent than for the Static testing, whereby the stimuli
of a constricted field or altitudinal, manually operated Goldmann are presented at specific locations and
quadrant or hemifield defect (see perimeter. The tested locations are their brightness is varied are relatively
definitions later). standardised and provide a high level sensitive to shallow depressions of the
By employing simultaneous testing of quantitative data that allows visual field where there are flat almost
of opposite quadrants it is possible to statistical analysis and facilitates data equally sensitive areas. Kinetic testing
detect asymmetric subtle relative storage and transfer of information. is more useful in regions whose
visual field defects or ‘extinction’. The They can be tedious to perform sensitivity sharply changes between
latter phenomenon occurs when a irrespective of age, even with the adjacent areas. Goldmann perimetry
target is missed in an affected benefit of the newer interactive employs primarily a kinetic technique
hemifield only when both hemifield algorithms. There are limited choices to plot boundaries of isopters (points
are tested simultaneously and is to test speeds and a degree of joined together by a drawn line with
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< Figure 2
Schematic of visual pathway. Letters A-J correspond to pairs of VF plots in Figure 3
equal levels of estimated sensitivity)
and scotomas (depressed areas of
sensitivity) by moving a visual
stimulus from a non-seeing to a seeing
region. Additional static testing is then
used to verify the regions within a
given isopter and as catch trials to
reveal false positive, negative and
fixation losses.
Supra-threshold testing until the
newer thresholding algorithms were
developed was considered the least
time consuming. The stimuli
brightness selected is chosen such that
subtle shallow defects are unlikely to
be revealed. By using multiple
stimulus patterns the test duration can
be further reduced. Threshold testing,
on the other hand, uses single stimuli
testing and an estimation of the
threshold based on ‘frequency-of-
seeing’ characteristics. Greater detail of
defect depth and extent is possible
when using a thresholding system.
The choice of programme for visual
field assessment is dependent on the
suspected lesion. Generally, central
visual field programmes are considered
adequate to reveal the majority of
visual field defects that one is likely to
encounter arising from intracranial
lesions, including those at the optic
chiasm or optic tract. There are
17:11 Page 32
however some exceptions that involve
only the peripheral retinal fibres, the
temporal crescent represented region of
the occipital lobe or associated with a
stato-kinetic dissociation. Peripheral
visual field programmes should be
undertaken if doubt exists over the
results of a central VF programme
when neurological disease is
suspected.
Should a group of 2 or 3 points (a
‘cluster’) at the edge of a 24° visual
field examination be abnormal then
one should consider repeat testing and
include a peripheral plot. Similarly, if
fixation and visual acuity are
reasonable good, but visual field
abnormalities are extensive and
threaten the 5-10° region, then
selecting a specific macula programme
with greater sampling of locations close
to fixation would reveal the risks to
vision. The results are then interpreted
both qualitatively for patterns of visual
field abnormality and quantitatively in
terms of depth or degree of damage.
Determination of test
reliability
Sources of error can be broadly
categorised into those arising during
the test period and those introduced
in the subsequent analysis and
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By the subjective nature of a visual
field test, the results can be profoundly
affected should the test operator take
insufficient care. It is they who generally
provide initial instruction and a brief
explanation of why the test is being
performed and its relevance to the
patients’ management. Although the
patient may claim to have done a similar
test previously, one should repeat the
instructions and consider running a
demonstration programme to familiarise
each person with the test. This allows
for retinal adaptation and overcomes
some of the apprehension that many
experience when faced with the
demands of formal perimetry.
Unless functional vision for driving or
mobility purposes is being evaluated,
the non-test eye should be appropriately
occluded. Fixation should be directed to
a single point to ensure steady fixation,
with the patient alert and mentally
competent.
The blind spot, temporal to fixation,
represents the projection into visual
space of the ONH, nasal to the fovea,
where the ganglion cell axons exit at the
back of the eye. It produces a small,
physiological, absolute scotoma. If
fixation is not maintained the blind spot
is less likely to be plottable and the
credibility of the visual field test
evidence derived from the rest of the
procedure is brought into doubt.
A comfortable, correctly aligned set-
up for the patient should be established
and maintained. Gentle encouragement
at appropriate intervals may be required
to optimise a relaxed yet attentive
attitude. During the course of the test,
the operator should seek to minimise
fixation losses, by monitoring eye and
head movements visually, alerting
patients to poor stability and replotting
the blind spot position if incorrectly
identified by the subroutines that most
modern automated perimeters use. Brief
rests can be incorporated within and
between the test of each eye and the
patient should be encouraged to blink
naturally during the test sequence,
without the perceived fear that stimuli
may be missed to the detriment of their
test result. The test may need to be
restarted, repeated or even aborted if the
operator judges the results being
generated to be significantly unreliable.
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The printout provides clues to the
reliability of the test results. Comments
made by the patient or by the operator
documented at the time of the test are
invaluable when considering the true
value of the information generated.
Patients may admit to having seen
repeated stimuli to which they had not
responded. They may have been
distracted mentally by anxiety, their ill
health, or extraneous noises. The test
duration reported on the printout does
not account exclusive for rest periods,
that may, by necessity, have been
frequent albeit brief.
Upon receiving the completed test
results, several points need to be
< Figure 3
Schematic paired sets of visual field plots for selected pathway locations
17:11 Page 33
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checked to establish their authenticity.
The personal data (Figure 1, A)
should be scanned to confirm the
patient’s full name, their date of birth
(including correctly stated year), how
recent the test. If the test duration
stated was longer than expected for that
test strategy, it is worth verifying that
appropriate rest periods were given
and the eye to which it relates.
Significant alterations to pupil size
can lead to diffuse visual field changes,
so pupil diameter should have been
recorded if the patient was known to be
using miotic or mydriatic eyedrops. An
alternative fixation target may have
been chosen if severe foveal damage
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had obscured the view of the default
fixation target. A refractive error
correction should have been chosen
appropriate to the test distance to
compensate for significant ametropia,
including astigmatism and presbyopia.
The operator should always verify that
the lenses chosen are single vision, full
aperture, correctly powered and 33
aligned, and do not ‘steam-up’ or get
touched during the test. If contact
11/07/08 CET
lenses were worn for the test, one needs
to ensure that suitable ‘over’ correction
was chosen. Presbyopia corrective
contact lens designs are becoming more
common. Inappropriately corrected
refractive error can produce an
enlarged blind spot, diffuse field
depression and a more negative Mean
Deviation index.
Modern perimeters generally provide
some form of reliability indices (Fig.1,
B). These commonly include a measure
of fixation losses, false positive and
false negative responses. High fixation
losses suggest poor eye or head
fixation. Other causes include
inadequate occlusion of non-tested eye,
poor BS localisation, and poor
response button control. Whether the
index is a true representation of
fixation stability can be corroborated
by comments documented by the test
operator from their direct visual
observation at the time of the test. If an
automated fixation monitor has been
disabled, ‘zero fixation losses’ may not
necessarily represent excellent
fixation. False positive responses are
generally associated with anticipation
(‘trigger happy’) which can lead to a
more positive Mean Deviation index
and high Pattern Deviation values.
False negative errors can be attributed
to fatigue (health related or disturbed
sleep patterns), but are also known to
be present in patients with early onset
of visual loss, developing a relative
scotoma and demonstrating varying
visual response, or who already have
visual field defects that are progressing.
The time between testing for each eye
should be noted. Adequate but not
excessive rest should have been
provided and the previously occluded
eye given sufficient time to re-adapt to
the background illumination. This can
be particularly pertinent if delayed
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Sectoranopia
Temporal lobe
optic radiations
Parietal lobe
optic radiations
Inferior Altitudinal
Hemianopic
Any postchiasmal lesion
< Figure 4
Visual Field Defect (VFD) Decision Tree
retinal adaptation is likely to be a factor
for example, in those with rod/cone
dystrophies.
Goldmann visual field plots,
similarly should include the patient
name, date of birth, date of test,
selected eye, refractive correction used
and the stimuli characteristics
employed. It is assumed that the
instrument has been adequately
maintained and is calibrated regularly.
Generally the blind spot position/size
and at least three isopters are
presented, having been selected to
demonstrate the location, depth and
extent of any significant variation in
the visual field. As with contour lines
on an Ordinance Survey map, the
closeness of the isopters to each other
indicates the rate of change in
sensitivity and the gradient of a
17:11 Page 34
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Is VFD bitemporal?
Recheck
1. Other eye for subtle
incongruous homonymous VFB
2. Poor px co-operation
3. Does this correlate with
fundoscopy?
Bilateral
ON disease
Is VFD binasal?
or Disc
Drusen?
Inferior
chiasm
Ischaemic
Glaucoma?
optic neuropathy?
Possible causes: Possible causes:
Bilateral Diabetic PRP Bilateral ARMD Check ophthalmoscopy
Bilateral RP Bilateral Glaucoma
Bilateral retinoschisis Bilateral Choroiditis
boundary. It is good practice that each the test sequence. The threshold values
of the isopters is annotated, in addition are a function of the instrument
to colour codes that indicate the dynamic range of contrast between
stimuli characteristics from which they stimuli and the background
were derived. Subsequent evaluation illuminance. Small defects can be
of the raw threshold values (Fig. 1, D) missed should they lie between the test
in an automated perimetric printout, locations.
their associated age-corrected (Fig. 1, The Total Deviation grid (Fig. 1, E)
E), pattern corrected (Fig. 1, F) and provides pointwise age-corrected
probability-derived plots (Fig. 1, G) numerical values of the estimated
depends upon the overall impression threshold. Comparisons across the
of reliability that is given. horizontal and vertical meridia can alert
Grayscale plots (Fig. 1, C), despite one to potential abnormalities. The
their immediacy of visual field Pattern Deviation (Fig. 1, F) filters out
representation can be misleading. They the presumed diffuse sensitivity
have a limited palette of gray scale tone depression to highlight potential
and regions between test locations regions of focal depressed function.
undergo interpolation. The numeric These are statistically analysed to
grid provides an estimate of patient generate the probability plots (Fig. 1, G)
visual sensitivity in terms of decibel as to the likelihood of the estimated
values at locations determined during values indicative of normal function.
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Identification of the likely
location of a suspected
visual pathway lesion
One of the primary tasks is to determine
whether the lesion is intraocular
(IO) or intracranial (IC) 6. The IO lesion
needs ophthalmological investigation
whereas the IC lesion needs neurological
investigation. An inappropriate referral
can cause delay in management by
several weeks or even months. If a
patient describes a visual loss as being
‘missing’ it suggests a ‘Negative’ scotoma
that implies a neurological disease,
whereas a smear, smudge, cloud or veil
is classified as a ‘Positive’ scotoma and
implies a retinal disease or media
opacity.
Knowledge of the visual pathway
anatomy is required to differentiate
between specific VF patterns. One
should always check the VF from the
‘uninvolved’ eye for subtle defects even
when symptoms are unilateral (such as
in the case of a temporal defect in
junctional scotoma that could arise from
a chiasmal compressive lesion). (See
figures 2 and 3).
The key points to consider for each
aspect, pertaining to the relevant
ophthalmic and systemic factors, are a
careful and thorough history, the
reported symptoms and identified signs,
and any visual field results.
The principal points of history taking
in cases of impaired vision are, the type
of involvement, whether unilateral or
bilateral, the time course of vision
dysfunction/disturbance and any
associated symptoms.
The possible cause of visual field loss
implied by the speed of onset can only
be inferred according to how soon the
patient becomes aware of loss. In terms
of the presumed time course in which
the condition has developed, sudden
onset (within minutes) usually indicates
an ischaemic event (e.g. occlusion of
retinal vessels from emboli), whilst rapid
onset (over hours) is also characteristic
of ischaemic event, but at the level of the
optic nerve. Moderately rapid (days to
weeks) is likely to be ischaemia-related,
but can also be linked to inflammation.
Gradual progression over months are
found in lesions of toxic origin, whilst
slower progression of months to years is
17:12 Page 35
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suggestive of ‘compression’.
Associated symptoms can assist in
localisation though not wholly specific.
They can include ocular or orbital pain
(as in retrobulbar ON), diplopia,
hemiparesis, headaches, and in
extreme cases variable levels of
consciousness.
The ophthalmological or neuro-
ophthalmological examination, is
directed towards detecting, quantifying
and localising the region of vision loss.
Any visual field test should be
interpreted in context with the other
results arising from a full examination.
This should include a measure of
visual acuity, both best-corrected and
pinhole vision at distance and near
(line and single letter) and an
evaluation of the pupillary responses.
The aim is to detect a relative afferent
pupillary defect (RAPD), which is
characteristic of impaired optic nerve
conduction. The presence of an RAPD
is an extremely reliable and sensitive
indicator of asymmetric optic nerve
dysfunction. It is likely to accompany
any substantial lesion that decreases
ganglion cell output to the optic nerve,
for example severe age-related macular
degeneration, acute retrobulbar ON or
retinal detachment. It is derived from a
disparity between the direct and
consensual light responses in an
< Figure 5a and 5b
Set of Humphrey perimeter visual field printouts for MCQ number 8
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affected eye (not dealt with in this
article). The pupil on the abnormal side
appears to paradoxically dilate in
response to a light stimulus. An RAPD
becomes more apparent when the
ambient lighting is dimmed. It can be
detected in the presence of a total 3rd
nerve palsy, as only one active pupil is
necessary to detect an RAPD. Bilateral 35
optic neuropathies (if equally
impaired) may show no relative
11/07/08 CET
differences between the two pupil
responses and an RAPD may not be
detectable.
Careful direct monocular and
binocular slit lamp ophthamoscopy,
preferably through dilated pupils,
should establish whether a VFD arises
wholly or partially from a retinal or
anterior segment component. Optic
atrophy, if present, indicates damage to
the retinal ganglion cell, its cell body, or
axon up to its synapse at the LGN. It
can take 4-6 weeks from the time of
damage until it becomes apparent. The
resultant atrophy can be diffuse or
segmental. Acute retrobulbar ON is not
normally associated with a swollen
optic disc. Atrophy, though not
diagnostic in itself, demands
immediate referral for thorough
investigation as to its cause. A VA of
6/6 or better does not exclude the
possibility of significant VF loss. Optic
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< Figure 6a and 6b
Set of Humphrey perimeter visual field printouts for MCQ number 9
disc oedema results from impaired
axoplasmic transport that includes
raised intracranial pressure, ischaemia,
or inflammation. It is characterised by an
elevated ONH, indistinct disc borders,
venous and capillary dilation and
tortuosity, sometimes accompanied by
peripapillary haemorhages and
exudates. Bilateral optic disc swelling
needs urgent referral to a neuro-
ophthalmologist opinion as MRI
scanning may need to be arranged, even
in the absence of vision disturbance.
Beware of the ‘silent’ neuro-
ophthalmic patient presenting with
blurred vision (with or without reports
of loss of field). Confrontation field-
testing and RAPD evaluation (before
dilated fundoscopy) should always be
performed, and if either are abnormal or
the degree of vision loss is inconsistent
with the ocular examination, formal
perimetric testing is required.
The normal VF extends approximately
100 temporally, 60 nasally, 60 superiorly
and 75 inferiorly from fixation in each
eye7. Unilateral loss almost invariably
indicates an intraorbital lesion or one
anterior to the chiasm on the affected
side. Bilateral loss, can be indicative of
bilateral retinal or optic nerve origin,
chiasmal or retrochiasmal location.
There are several terms that are used to
describe the type of defect that may be
encountered with perimetry.
Scotomas represent a focal area of
17:12 Page 36
depressed sensitivity either relative
(dependent on the perimeter used) or
absolute (to any level of stimulus),
surrounded by normal sensitivity. When
the scotoma involves fixation, as often
found with age-related maculopathy, it is
termed ‘central’. If it also involves the
maculopapillae bundle as found in toxic
optic neuropathies, or congenital optic
disc pits associated with central serous
detachments, a centrocaecal scotoma can
develop. A paracentral scotoma adjacent
to, but not involving, fixation is typical
of early glaucoma. Arcuate patterns that
can extend to the nasal boundary where
a nasal step due to the asymmetry of
sensitivity across the horizontal
meridian, often arise from glaucomatous
visual field progression are associated
with damage to the retinal nerve fibre
bundles at the optic disc poles. They can
also be associated with ischaemic optic
neuropathy or congenital disc drusen.
Congruency describes the similarity in
the shape of visual field loss or
conversely the visual field preservation
between each eye. Generally, the greater
the similarity or congruency, the more
posteriorly located the lesion. Both
anatomical and psychophysical
variability, however, confounds its
diagnostic value. The degree of
congruency is not only dependent on the
visual field region involved but also the
causative agent. An infarct to a cerebral
vessel is generally associated with well-
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defined boundaries, whilst the
disorganised behaviour of tumour tissue
can involve more diverse regions.
Altitudinal defects respect the
horizontal meridian, involving either
pair of superior or inferior quadrants
(Figure 3 A). They are typical of
ischaemic optic neuropathies or a hemi-
retinal vascular occlusion, though they
can very rarely be due to bilateral
symmetrical lesions of the visual cortex.
Hemianopia describes a defect
involving the complete right or left half
of the visual field. Quadrantanopic
defects predominantly involve one of the
four quadrants. ‘Heteronymous’
hemianopia refers to opposite halves for
each eye as in bitemporal hemianopia.
‘Homonymous’ defects affect the same
side for each eye, characteristic of
retrochiasmal lesions. A complete
homonymous hemianopia is non-
localising. The entire hemifield being
involved confounds attempts to
differentiate between the likely
retrochiasmal location that a visual
pathway lesion has occupied.
Homonymous visual field loss can be
perceived by the patient as monocular
loss to the eye of the affected hemifield
until examined.
A centrocaecal scotoma in one eye
accompanied by a superior temporal
quadrantanopia in the other eye, termed
a ‘junctional’ scotoma, is suggestive of a
prechiasmal lesion close to where the
optic nerve meets the chiasm (Figure 3
C).
By far the most common cause of
chiasmal disorders is compression by a
tumour in the region of the pituitary
gland, but rare non-compressive causes
including infection, inflammation, and
ischaemia and toxicity are encountered.
About 10mm directly below the chiasm
lies the sella turcica, a depression in the
sphenoid bone that supports the
pituitary gland. Significant enlargement,
with suprasellar extension of pituitary
tissue, is therefore necessary before it is
likely to be associated with any field
defects. Suprasellar masses infrequently
cause raised intracranial pressure and
optic atrophy occurs late in chiasmal
lesions. The extent of the defect does not
always correlate with the magnitude of
the tumour since the damage to the fibres
can be both due to direct and indirect
interference.
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Chiasmal Lesions, whether arising
from the pituitary gland itself or the
surrounding tissue, are rarely
accompanied by the classic, complete
bitemporal field loss (Figure 3 D). They
more commonly present with an optic
neuropathy and a varied pattern of field
defect, in one or both eyes, due to
compression of more than one structure.
They tend to fall into four basic groups;
from above, from beneath, from the
antero-lateral or postero-lateral direction
depending on the direction the lesion
impinges on the chiasm. Chiasmal
lesions can produce an RAPD though
they tend to be more subtle than those
arising from a lesion of the optic nerve.
Anatomical variation in chiasm
location and pathological variation in
tumour growth pattern leads to diversity
in the visual field defect presentation
and confounds precise interpretation.
Bitemporal hemianopias may be
confined to the central visual fields
particularly in lesions compressing the
posterior portion of the chiasm. A
bitemporal hemianopia which respects
the vertical meridian that is
predominantly superior strongly suggest
compression from beneath, for example
a pituitary adenoma whilst one biased
inferiorly suggests a craniopharyngioma,
exerting force from above. These latter,
slow growing tumours, occur in all age
groups, but particularly children.
Binasal visual field loss is much more
likely to be caused by optic nerve
damage, such as glaucoma since the
temporal retinal fibres do not merge and
are likely to only be simultaneously
involved if there is bilateral eye lesions.
Retrochiasmal Lesions (affecting the
optic tract, lateral geniculate body, optic
radiation) cause a partial or complete
homonymous hemianopia. Pure optic
tract or LGN lesions are rare. They can be
distinguished from lesions of the optic
tract by the absence of an RAPD. The
most common cause is cerebrovascular
disease, and although brain tissue
malignancy, inflammation, infection or
arteriovenous malformations are rare,
neuroimaging is necessary to exclude
these possibilities in all patients with
homonymous visual field defects.
Three types of VFD have been
attributed to LGN lesions, and each can
be accompanied by optic atrophy 8, 9, 10.
An incongruous homonymous
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hemianopia, a congruous sectoral
hemianopia that crosses the horizontal
meridian and sparing of this sector but
damage to the upper and lower sections.
The latter two patterns result from
occlusion of the lateral choroidal artery
or ischaemia of the anterior choroidal
artery, a branch of the internal carotid,
respectively (Figure 3 F & E).
Partial homonymous hemianopias can
be categorised in terms of their degree of
congruity, whether predominantly in the
superior or inferior field or whether
accompanied by macular sparing.
‘Macular sparing’, whereby the
hemifield defect includes preserved
central 3-5 vision, suggests a posterior
cerebral artery stroke with middle
cerebral artery support, akin to the role
of a cilio-retinal artery in maintaining
vision in central retinal artery occlusion.
It is diagnostic of an occipital lobe
lesion, being rarely encountered with
lesions anterior to the visual cortex
(Figure 3 J). A homonymous hemianopia
that does not spare the fovea, causing
‘Macular splitting’ has less localising
value.
A predominantly superior
homonymous quadrantanopic field
defect (‘pie-in-the-sky’) may be due to a
temporal lobe lesion that impinges on
the inferior bundle of nerve fibres that
form the optic radiations (Figure 3 H).
An inferior defect (pie-on-the-floor) can
arise from a parietal lobe lesion
< Figure 7a and 7b
Set of Humphrey perimeter visual field printouts for MCQ number 10
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interfering with the superior optic
radiations (Figure 3 G). Parietal lesions
typically present with additional
neurological deficits that confound
formal perimetry and may only be
inferred from confrontation testing.
Quadrant VFD that respects both the
horizontal and vertical meridian is likely
to be located along the calcarine fissure
at the cortex. 37
Lesions that occur at the Occipital
Primary Visual Cortex potentially retain
11/07/08 CET
good visual acuity, particularly with
distance vision but may have more
difficulty with near vision if the text is
large or enlarged. Generally the lesion is
not associated with optic atrophy unless
associated with raised intracranial
pressure. The pupil reactions are
typically normal. The visual field defects
are highly congruous. There may be
additional neurological disturbances
including hallucinations, alexia and loss
of colour perception.
Rarely, if a lesion should damage the
tip of one occipital lobe, the patient may
complain of reading difficulties (despite
no apparent macular abnormality) and
Amsler grid testing or a central 10-2
threshold programme with Humphrey
automated perimetry may reveal a small
homonymous paracentral scotoma
(Figure 3 l). The causes are primarily
vascular, with occlusion along the
posterior cerebral artery, or ischaemia
caused by a cardiac embolus,
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characteristic of a malingering cause.

The more common causes are:
• End stage glaucoma that is associated
with extensive optic disc cupping
• Retinitis Pigmentosa, accompanied by
retinal pigment clumping, disc pallor
and attenuation of the retinal arteries
• Extensive panretinal photocoagulation
in proliferative diabetic retinopathy
38 • Chronic Pailloedema with swollen or
pale optic discs
• Chorioretinitis with widespread
11/07/08 CET

retinal pigment disturbance or

functional loss
• Bilateral occipital lobe infarcts with
macular sparing supported by the
relevant history, neurological condition
and neuroimaging
• Functional loss due to hysteria or
malingering.

< Figure 8a and 8b
Set of Goldmann perimeter visual field printouts for MCQ number 11
vertebrobasilar occlusive disease,
arteriovenous malformations or in some
cases following cervical manipulations
that injure the vertebral arteries. Other
causes are primary and secondary
tumours or trauma.
Arguably, some of the most difficult
cases to diagnose are those that produce
a tunnel vision field defect11 (Figure 3 B).
One should differentiate between the
‘true’ funnel type of constricted visual
field loss where the breadth of the defect
changes with the distance at which the
test is performed and the tunnel vision
that remains the same angular subtense
for different test distances, that is
Selection of salient
observations to support
referral decision
Each referral should include the date,
full name of referring optometrist, their
practice address and contact telephone
number and the patients’ GP details in
block capital letters. The full details of
the patient, including their date of birth,
NHS number (if known) and a contact
telephone number should be provided.
The referral should be supported by a
salient history, to include the prime
complaint, its duration, whether
constant, intermittent, progressive or
stationary and the time of onset.
A list of current medication may also
prove useful (if known). If additional
neurological signs are observed, that
could include any or all of the following;
headaches, nausea/vomiting, loss or
impaired consciousness, unsteady gait,
speech or hearing impairment,
hemiparesis; then they need stating.
Test results should included a
measure of the current visual acuity and
previous visual acuity (if known),
indications as to the presence or absence
of RAPD, and a summary of the
ophthalmoscopic findings. If formal
perimetry or merely confrontation has
been undertaken, the type of visual field
defect, its repeatability and reliability
should be shown. The reason for the
referral, a provisional diagnosis and an
indication of its urgency, should be
clearly stated. (Figure 4).
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< Figure 9a and 9b
Set of Humphrey perimeter visual field
printouts for MCQ number 12
Recommendations for
referral prioritisation
There is a wide range of causes of
binocular visual field defects. Some are
sight and life threatening and it is not
easy to differentiate from those that are
not, without further investigations, such
as neuro-imaging. In general terms, all
those suspected of having a neurological
feature need urgent investigation. A
young patient, particularly if
symptomatic, needs a more urgent
referral than an elderly asymptomatic
patient. A suspected bitemporal
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hemianopia needs urgent same day
referral as the sooner the cause is
identified the greater the chance of any
visual recovery.
It is not acceptable to send a patient to
an acute referral centre without an
arranged appointment. Should a patient
present with a condition that warrants an
emergency referral the centre to which the
referral is directed should be informed
and appropriate advice or guidance
sought. Suspected serious, purely
intraocular conditions require same day
referral to an eye casualty unit,
ophthalmic outpatient clinic or an
Accident and Emergency Unit, dependent
on the local services available. Suspected
serious intracranial conditions with or
without an intraocular component require
referral to an Accident and Emergency
Unit. This is for guidance only as there
may be guidelines, in place, according to
the local arrangements.
S.U.P.E.R Summary Points
(adapted from Pane, Burdon
and Miller ) 12
Suspect the possibility of a serious
intraorbital/cranial disease when a
patient presents with a vision or eye
complaint.
Understand and use the knowledge of the
visual pathway to formulate a systematic
series of questions and investigations.
Perform a thorough and careful
examination including a full history,
ocular examination, confrontation test,
RAPD evaluation and formal perimetry.
Evaluate the visual field results for
reliability and correlate with other
evidence for unilaterality or bilaterality.
Refer to a neuro-ophthalmologist
with appropriate urgency if the
examination leads one to suspect a non-
ocular cause for a visual disturbance.
Acknowledgements
Thanks for invaluable assistance with
this article to Mike Burdon, Neuro-
ophthalmologist at Selly Oak Hospital,
Birmingham and Dr Leon Davies, Aston
University, Birmingham.
About the author
Shirley Ann Hancock PhD, BSc (Hons),
MCOptom, is a Principal Optometrist
based at the Heart of England NHS
Foundation Trust, Birmingham
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Heartlands Hospital with special interests
in ophthalmic imaging and perimetry.
References
1. Harrington DO, Drake MV (1990) The
Visual Fields. Text and Atlas of Clinical
Perimetry.The C.V Mosby Company, St.
Louis, USA
2. Rowe F (2006) Visual Fields via the
Visual Pathway. Blackwell Publishing 39
Ltd.
3. Kanski J (2003) Clinical
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ophthalmology: A Systematic Approach,
5th edition. London, Butterworth-
Heinemann.
4. Szamdry G, Biousse V, Newman NJ
(2202) Can Swedish Interactive
Thresholding Algorithm Fast preimetry
be used as an alternative to Goldmann
perimetry in neuro-ophthalmic practice?
Archives of ophthalmology 120: 1162-
1173
5. Wall M, Punke SG, Stickney TL,
Brito CF, Witbrow KR, Kardon RH (2001)
SITA Standard in optic neuropathies and
hemianopias: A comparison with Full
Threshold testing. Investigative
Ophthalmology & Visual Science 42:
528-537
6. Farris B K (1991) The Basics of
Neuro-Ophthalmology. Mosby Year Book
7. Douglas RA (1999) Automated
Static Perimetry (second edition) Mosby
International Limited.
8. Rosen ES, Eustace P, Thompson
HS, Cumming HJK (1998) Neuro-
Ophthalmology. Mosby International
Limited.
9. Martin TJ, Corbet JJ (2000)
Neuro-ophthalmology: The Requisites
in Ophthalmology Mosby International
Limited.
10. Walsh T J (1997) Neuro-
Ophthalmology Clinical Signs and
Symptoms. 4th Edition. Williams
and Wilkins.
11. Kline LB, Arnold AC,
Eggenberger E, Forozan R, Golnik
KC, Rizzo III JF, Shaw HE (2007)
Basic & Clinical Science Course:
Neuro-Ophthalmology Section 5 2007-
2008. American Academy of
Ophthalmology.
12. Pane A, Burdon M A and
Miller N R (2006) The Neuro-
Ophthalmology Survival Guide. Mosby
Elsevier Limited.
http://www.academy.org.uk/tutorials/
pathway.htm
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Module questions Course code: c-8367

Please note, there is only one correct answer. Enter online or by form provided
An answer return form is included in this issue. It should be completed and returned to CET initiatives (c-8367)
OT, Ten Alps plc, 9 Savoy Street, London WC2E 7HR by August 13 2008.
1. Which of these statements is true? 7. Which of these statements about post-chiasmal lesions is true?
radiations
(a) (Figureemploys
Goldmann perimetry 3 G). both aParietal automated
kinetic and static technique. perimetry mayreactions
(a) Pupil reveal are a
normal Extensive
in lesions of panretinal
the LGN. photocoagulation
lesions typically
(b) In automated present
perimetry the backgroundwith illuminationsmall homonymous
is varied according paracentral
(b) A macula in proliferative
splitting homonymous diabetic
hemianopia indicates retinopathy
an occipital
to the testing programme. lobe lesion.
additional neurological deficits that scotoma (Figure 3 l). The causes are Chronic Pailloedema with swollen or
(c) Kinetic perimetry is more reproducible than static perimetry. (c) A contralateral, homonymous, inferior quadrantanopia arises from
40 confound
(d) End stage formal perimetry
glaucomatous and
visual field lossmay
can only primarily
be monitored byvascular, with damageocclusion pale
to the inferior fibres optic
of the discs Chorioretinitis with
optic radiations.
only Goldmann
be inferred from
visual field testingconfrontation along the posterior (d) cerebral
Lesions artery, or optic
of the anterior widespread retinal than those
radiations are more congruous pigment
testing. Quadrant VFD that respects ischaemia caused by involving
a the posterior radiations.
cardiac disturbance or functional loss. Bilateral
11/07/08 CET

2. In non-arteritic anterior ischaemic optic neuropathy, which of these

both statements
the horizontal
is true? and vertical embolus, vertebrobasilar 8. At whatocclusive
level of the visualoccipital
pathway does lobe infarcts
the lesion with
that gives rise to macular
the
meridian is likely
(a) It typically causes an toinferior
be located
altitudinalalong
field defect.disease, arteriovenous pair malformations sparingin Figure
of visual field plots illustrated supported by likely
5a and b most the lie? relevant
the Visual loss usually
(b) calcarine develops
fissure at over
the2-3cortex.
days. or in some cases (a) Retina or Optic
following nerve
cervical history, neurological condition and
(c) Visual acuity improves with time. (b) Chiasm or Optic Tract
Lesions that occur at the Occipital
(d) It usually causes a centrocaecal type field defect.
manipulations that injure the vertebral
(c) LGN or Optic radiations
neuroimaging Functional loss due to
Primary Visual Cortex potentially arteries. Other causes (d) are primary
Visual Cortex and hysteria or malingering.
3. Which
retain good of these
visual statements
acuity, is true? Acute retrobulbar
particularly ON is usually tumours
secondary or trauma.
with associated
distance with:vision but may have Arguably, some of 9.theAtmost
(a) An altitudinal field defect.
what level Selection of salient
of the visual pathway does the lesion that gives rise to this
difficult
pair of visual field plots illustrated in Figure 6a and b most likely lie?
more difficulty
(b) Normal with near vision if the cases to diagnose(a) are
pupil reactions. Retinathose
or Optic that
nerve observations to support
text
(c) is large or
A swollen opticenlarged.
disc. Generally the produce a tunnel vision field or
(b) Chiasm defect 11
Optic Tract referral decision
(d) Painison not
lesion eye movements.
associated with optic (Figure 3 B). One should (c) LGN differentiate
or Optic radiations Each referral should include the date,
(d) Visual Cortex
atrophy
4. Whichunless
of these associated
statements about with raised
the LGN is true? between the ‘true’ funnel type of full name of referring optometrist, their
intracranial pressure.
(a) The LGN is supplied The cerebral
by the anterior pupilartery.constricted visual field 10. At loss
whatwhere thevisualpractice
level of the address
pathway does andthat
the lesion contact
gives risetelephone
to this
(b) The LGNare
reactions receives input fromnormal.
typically both eyes. The breadth of the defect changes pair of visual
with field plots illustrated
the numberinand Figurethe
7a and b most likely
patients’ lie?
GP details in
(c) Pure optic tract or LGN lesions are relatively common. (a) Retina or Optic nerve
visual field
(d) The most common defects
cause of anare highly
LGN lesion distance at which the
is malignancy. (b) test or Optic Tract block capital letters. The full details of
is performed
Chiasm
congruous. There may be additional and the tunnel vision (c) that remains
LGN or the the patient, including their date of
Optic radiations
5. Which of these
neurological statements aboutincluding
disturbances an RAPD is false?same angular subtense (d) for
Visual Cortex test
different birth, NHS number (if known) and a
(a) It may be associated with normal visual acuity.
hallucinations, alexia and loss
(b) It can be quantified using a neutral density filter.
of distances, that is characteristic of a contact telephone number should be
11. At what level of the visual pathway does the lesion that gives rise to this
colour
(c) Opticperception.
nerve disordersRarely, if a lesion
can be differentiated malingering
from retinal cause. Thepair
disorders purely more common
of visual provided.
field plots illustrated in FigureThe
8a andreferral should
b most likely lie? be
should based on its findings.
damage the tip of one occipital causes are: (a) Retina or Optic nerve supported by a salient history, to
(d) It can
lobe, thebepatient
detected inmay the presence
complainof a totalof 3rd nerveEnd
palsy.stage glaucoma (b)that
Chiasm or Optic Tract include the prime complaint, its
is associated
(c) LGN or Optic rad iations
reading
6. Which ofdifficulties
these statements (despite
about chiasmalno lesionswith
is true? extensive optic cupping duration,
discCortex
(d) Visual whether constant,
apparent
(a) Bitemporalmacular
hemianopias abnormality)
always involve the and Retinitis
peripheral Pigmentosa, accompanied by intermittent, progressive or stationary
visual fields.
(b) Opticgrid
Amsler atrophy is an early
testing or sign of chiasmal
a ’central 10-2involvement.
retinal pigment clumping, 12. Whatdisc do the pallor
visual field plots
and illustrated
the timein of Figure 9a and
onset. Ablist
demonstrate?
of current
(c) Suprasellar masses are often associated with papilloedema. (a) Congruity
threshold programme with Humphrey
(d) In a child, an inferior bitemporal hemianopia suggests and attenuation of the retinal arteries.
(b) Preservation of foveal function medication may also prove useful (if
craniopharyngioma. (c) Fatigue
(d) Hemianopia

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