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a
f
e
Fig. 31.6 Illustration of various components and analysis of mfERG responses. (a) Field view of extracted
mfERG responses represented in a ring pattern used for
calculating ring ratios. The colour of the responses corresponds to specic zonal rings. For example, at the 0–2°
level, the response from the fovea is depicted in red. At the
2–5° level, the responses are represented in green.
Similarly, the 5–10, 10–15, and> 15° regions from the
xation area are shown in yellow, blue, and grey, respectively. (b) Responses were obtained from each quadrant of
the retina. (c) Summation of coded responses within a
specic region. (d) True response and noise levels, where
coloured histograms represent the true response (per rings
g
d
h
or quadrants) and the black region at the bottom indicates
the amount of generated noise. (e) Individual components
of N1, P1, and N2 responses are displayed in amplitudes
based on the region of interest (by ring or quadrant). (f)
Composite view presenting the responses along with scalar values, compared with age-matched controls and
colour-coded (green: within normal range, warm colours
towards red indicating reduced response compared to normal). (g) Merged responses overlaid on a fundus image,
known as the retina view. (h) Three-dimensional view of
response density providing insights into sensitivity. These
visual representations aid in analysing and interpreting
mfERG data for assessing retinal function
Artefacts can arise from the patient (eye
movements, muscle, etc.) or environmental factors (electrical contamination due to induced or
inherent line frequency noise) and should be
minimised to obtain a satisfactory signal: noise
ratio. Therefore, available systems often provide options to lter out noise or artefacts, and
repeating the test is recommended if the artefact values exceed a certain level. In general, it
is best practice to determine the source of artefacts and eliminate these at the source instead
of ltering. Testing should never routinely be
performed using a 50/60 Hz line frequency
notch lter; it should be remembered that line
frequency artefact is often the rst sign of electrode problems, alerting the technician to
intervene.
31.3.2.4 Artefacts
Several artefacts can impact the mfERG recordings. [Fig. 31.7] These include line frequency
interference, eye movements, eccentric xation,
positioning errors, central peak artefact, and
waveform distortions. Careful inspection of trace
arrays is crucial for correctly identifying and
interpreting these artefacts. Reports should mention all recording issues that could impact reliability and interpretation, such as media opacities,
pseudophakia, refractive correction problems,
blocked view, unstable xation, and frequent
blinking. Repeat recordings, using monocular
xation or adjusted trial frames, may be necessary to rule out artefactual causes of abnormal
mfERG results. [34].
31.3.2.5 Interpretation ofData
Interpreting mfERG test results involves careful
analysis and comparison with normative data;
each laboratory should establish its normative
values. The main components (N1, P1, and N2)
can be evaluated, but many investigators focus on
P1; amplitude and peak time values are measured
and compared against age-matched controls.
Reporting should include demographic details,
visual acuity, pupil status, noise level, compliance, and protocol. Normative data can be pro-
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A. R. Hathibelagal et al.
Fig. 31.7 Examples of artefacts and their impact on
mfERG results. (a) Sloping effect observed in the test
result, indicating improper xation during the procedure.
Eccentric xation can lead to trace arrays and topographic
3-D plots that exhibit central depression or a “sloping”
appearance, characterised by low signals on one side and
high signals on the other. (b) A case demonstrating no
xation, resulting in erratic and unreliable responses. (c)
Test results are affected by loosely connected electrodes,
leading to distorted waveforms and unreliable data. (d)
vided in a tabular format if an available option on
the equipment is used.
31.3.2.6 Clinical Applications
ofMultifocal ERG
[Table 31.4]
Eye gaze tracker at the bottom indicates intermittent eye
movement, which can introduce artefacts and affect the
accuracy of the results. (e) Positioning errors or rim artefacts observed in the test result causing localised irregularities in the response pattern. The trial frame’s rim
obstructed the view, causing a reduction in the eccentric
superior responses. (f) Excessive blink artefacts affect the
test result, characterised by abrupt disturbances in the
waveform due to blinking during the recording
a small signal, technical factors are important,
but when given due consideration, test-retest and
trial-to-trial variability are like full-eld
ERG.Practitioners should perform testing per the
ISCEV Standard recommendations. A minimum
of 100 averages per trial will be needed and usually far more in patients with signicant disease.
The standard eld is usually ~150x 120, which
31.4 The Pattern ERG
measures central macular function; doubling the
stimulus size from 150 to 300 allows an objective
The pattern ERG is the retinal response to an isoluminant contrast reversing stimulus. In clinical
practice, it is usually a reversing black-and-white
checkerboard. It is a small signal compared to
full-eld ERGs, and computerised signal averaging is essential to obtain clinically usable data. As
measure of peripheral macular function. [38]
With a high contrast stimulus reversing at 4/s, the
waveform consists of two main components [Fig.
31.8]: a positive component at approximately
50ms, P50, and a larger negative component at
approximately 95 ms, N95. [39] A small early
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Table 31.4 Depicts clinical applications of multifocal ERG
Disorder Multifocal ERG changes
Glaucoma Some authors nd mfERG useful in glaucoma [33], but in general, PERG or
PhNR recording may be of more value
Drug toxicity mfERG is useful in determining central retinal involvement in suspected drug
toxicity. It can assist in long-term monitoring of disease progression or
improvement [35]
Age-related macular degeneration
(ARMD)
Diabetic retinopathy Some authors nd mfERG useful in diabetes, showing delayed timing in
Inherited retinal disease (IRD) Many patients with IRD have generalised retinal dysfunction, and the nature
Macular oedema mfERG may be unaffected in cystoid macular oedema as the elevated
Central serous Chorioretinopathy mfERG may help dene the extent and severity of the disorder
Retinal vascular disorders mfERG is used in conjunction with full-eld ERG and may be useful in
High myopia Many high myopes will show mfERG abnormalities, particularly in a
Neuro-ophthalmic disorders The presence of a normal mfERG, when it is clinically challenging to
The extent and severity of macular dysfunction in ARMD can be assessed
with mfERG.It provides insights into disease progression and response to
interventions. It can reveal localised areas with reduced amplitudes or
delayed implicit times that may not be evident in overall averaged results
(ash electroretinogram) [36]
retinal locations with vascular lesions and in some locations outside of
lesions. Amplitude remains relatively normal. It may reveal abnormalities in
people with diabetes without retinopathy [37]
of the disorder (rod-cone dystrophy, cone-rod dystrophy, etc.) may be dened
by the electrophysiological features. The mfERG can help quantify the
severity and spatial extent of macular involvement. For example, in “classical
retinitis pigmentosa (RP)” where the patient has very constricted visual elds
but normal Snellen visual acuity, full-eld ERGs may be virtually
undetectable, but PERGs or the central mfERG responses may be normal or
near-normal. Equally, the full-eld ERG is normal if dysfunction is conned
to the macula; in these cases, testing of macular function with PERG and/or
mfERG is essential to determine the nature and severity of macular
involvement. Such patients may have normal macular structure, and normal
macular optical coherence tomography (OCT) or fundus autouorescence
imaging should not be assumed to be normal macular function
photoreceptors are still capable of phototransduction, and thresholds may be
normal on microperimetry
branch artery occlusions in demonstrating the extent of dysfunction,
particularly after re-perfusion
peripapillary distribution
differentiate between macular or optic nerve dysfunction (both can have
delayed pattern VEP), PERG is preferred as it provides the retinal responses
to the same reversing checkerboard pattern used for evoking the pattern VEP,
and in addition, the N95 component indicates central retinal ganglion cell
function directly
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negative component, N35, can be seen at approximately 35 ms in most subjects. From clinical
practice [40], conrmed by pharmacological
blocking experiments [41], it has been established that N95 arises exclusively in the retinal
ganglion cells (RGCs). Much of P50 arises in the
RGCs, perhaps 70%, with the remainder arising
in pre-ganglionic structures that have not been
fully elucidated. From a clinical point of view,
P50 is generated via stimulation of the macular
photoreceptors and objectively reects the func-
tion of the macula. PERG measurement usually
focuses on the peak time and N35 trough-to-peak
amplitude for P50, and the amplitude of N95
measured from the peak of P50 to the trough of
N95. It is often difcult to accurately measure
N95 peak time as it is often broadened, and many
workers do not routinely address that parameter.
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Fig. 31.8 The normal PERG
31.4.1 Clinical Applications
The PERG in clinical practice is usually combined with full-eld ERG and/or pattern VEP.
Retinal Diseases: The ERG assesses global
retinal function (the peripheral retina), and the
PERG assesses the degree of macular involvement. This enables the distinction between macular dystrophy, cone dystrophy, and cone-rod
dystrophy in a patient with clinically abnormal
appearing macula. For example, primary macular
dysfunction is characterised by a normal ERG
and an abnormal PERG, a common combination
in ABCA4 retinopathy (Stargardt-fundus avimaculatus; (Fig. 31.9). As described above, the
full-eld ERG is of prognostic value in ABCA4
disease, which is not necessarily progressive, and
the PERG helps delineate the extent and severity
of macular involvement. Indeed, it can demonstrate early macular involvement at a stage when
fundus examination may not reveal a signicant
abnormality.
Patients with rod-cone dystrophy (RP) may
have spared central retinal function, and in such
cases, the PERG may be normal even when the
ERG is almost undetectable. Further, the objective index of macular function provided by the
PERG can demonstrate early central retinal
abnormalities before the symptoms or signs of
macular involvement appear (Fig.31.10).
A. R. Hathibelagal et al.
Optic Nerve Diseases. The clinical distinction
between maculopathy and optic neuropathy can
be difcult as both are associated with reduced
visual acuity, a central visual eld defect, and
may have a relative afferent pupillary defect. A
delayed pattern VEP is very common in people
with macular dysfunction [40] and must never in
itself be considered to indicate optic nerve disease. The ability of the PERG to detect macular
dysfunction, even in the presence of normal macular anatomy, or to demonstrate retinal ganglion
cell dysfunction directly makes it an invaluable
adjunct to the PVEP in assessing people with suspected or possible optic nerve dysfunction. The
P50 component is affected in macular disease,
whereas a delayed PVEP with a normal PERG or
a PERG with a normal P50 but N95 component
reduction indicates optic nerve disease. Providing
the patient can maintain reasonably good xation, even an eye with no light perception from
optic nerve disease will have a detectable pattern
ERG; it is a macular disease that is associated
with an undetectable PERG. There is eventual
P50 involvement with increasing severity of retinal ganglion cell dysfunction. There would be
some P50 amplitude reduction (never extinction),
which is usually associated with a shortening of
P50 peak time. The shortening reects the exposure of the contribution to P50 of pre-ganglionic
structures by the loss of the ganglion cell-derived
N95 component. Some clinical PERG examples
are shown in Fig.31.11.
The PERG is also important in primary retinal
ganglion cell disease such as Leber Hereditary
Optic Neuropathy (LHON) or Kjer type dominantly inherited optic atrophy (DOA; OPA1 variant). Figure 31.12 data are from an LHON
patient.
The delayed VEP in primary retinal disease
can be distinguished from optic neuropathy using
the PERG (Fig.31.13).
The pattern ERG is of great clinical value in
the objective assessment of macular function and
retinal ganglion cell function. It is fundamental to
the accurate clinical interpretation of a pattern
VEP delay as delay in the VEP is non-specic,
and major delay can occur due to macular dysfunction. [40] The PERG is also of value in glau-
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Fig. 31.9 Electrophysiology in Group 1 ABCA4 retinopathy. A patient with bilaterally reduced visual acuity
due to ABCA4 retinopathy (Stardgardt disease). All full-
a
b
Fig. 31.10 Use of PERG in retinitis pigmentosa (rodcone dystrophy). Data from two patients with retinitis pigmentosa (a, b). The ERGs in each patient show marked
generalised impairment of retinal photoreceptor function,
severe for patient b (please note amplitude calibrations).
The appearances in patient b suggest that most, if not all,
of the ERGs are arising in the small residual cone population. The 150 and 300 PERGs from patient a are normal,
showing the expected doubling in P50 amplitude in the
eld ERGs from each eye are normal. The standard eld
PERG is bilaterally undetectable, but the large eld
PERG, although subnormal, is present
300 eld response relative to the 150 response. Patient b
shows a detectable standard 150 eld response, but there is
only minimal increase with the large eld stimulus, conrming that function has been lost between 150 and 300
eccentricity. Please compare the above ndings in ABCA4
disease (Fig. 31.9), where the 300 eld response is preserved, albeit subnormal, but the 150 eld response is
undetectable
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Fig. 31.11 Longstanding optic nerve disease. These data
are from a patient with an optic nerve glioma. The right
eye (RE) pattern VEP is undetectable. Right eye ash
VEP is delayed and markedly subnormal. Both standard
(150) and large eld (300) pattern ERGs show a good P50
component but with a shortening of P50 peak time in
keeping with marked retrograde degeneration of the retinal ganglion cells. All left eye (LE) ndings are normal
Fig. 31.12 Leber Hereditary Optic Neuropathy. VEP and
PERGs from a teenage patient with a 16-month history of
LHON. Pattern VEPs are bilaterally undetectable. Flash
VEPs are profoundly subnormal and of the altered waveform, precluding accurate component identication. Both
standard and large eld (150 and 300) PERGs show signicant N95 component reduction. Note there is a mild effect
on P50 amplitude and a marked shortening of P50 peak
time, in keeping with severe retinal ganglion cell
dysfunction
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Fig. 31.13 Electrophysiological ndings in a patient
with reduced left visual acuity and a relative afferent
pupillary defect initially thought to be secondary to optic
nerve disease. Neuroimaging could not assign a cause. All
right eye (RE) ndings were normal. There are clear pattern VEP and ash VEP abnormalities from the left eye
(both delayed and reduced), but PERGs indicate marked
left macular dysfunction as a cause of the delayed pattern
VEPs. Right eye ERGs are unremarkable; in the left eye
coma, where ganglion cell-related N95
abnormalities can occur, but in which VEP delays
are uncommon and usually minor. [42] Further,
while most optic nerve disorders are associated
with N95 loss, acute demyelinating optic neuritis
can show P50 abnormalities, suggesting that
macular involvement may contribute to the acute
visual loss [43], and they may possibly be prognostic for the degree of visual acuity recovery.
[40] It is also important to realise that as a contrast response requiring the optics of the eye to be
preserved, media opacities and refractive error.
Multifocal ERGs, which are luminance responses,
are used in conjunction with PERGs as the two
tests provide complementary information.
31.5 Other Tests
(LE), the DA 0.01 response is subnormal—loss of rod
system sensitivity; the DA red ash lacks a discernible
cone component; the bright ash a- and b-waves are subnormal, with additional delay, conrming the rod system
defect to have a photoreceptor origin; and cone ERGs are
markedly delayed and subnormal. The ndings, therefore,
indicate generalised left retinal photoreceptor dysfunction, with cones more affected than rods, with PERGs
showing global left macular involvement
protocols for recording the activity of shortwavelength cones. It is beyond the remit of this
chapter to address these in detail, and the reader
is referred to the ISCEV website for further
details (www.iscev.org). In addition, the reader is
referred to two main documents that address the
clinical issues. ( [7, 44]).
Recent developments in electrophysiology
include the use of hand-held stimulators and
recording devices that have a valuable role in
screening and some clinical applications. These
can be very useful for recording at the bedside, in
intensive care, etc. and may provide a rapid
assessment for retinal screening in a paediatric
patient. Such devices will likely expand in the
future, but at the time of writing, these are unable
to perform a comprehensive range of tests and
are, therefore, limited in application.
The ISCEV Standard recommendations are
intended as minimum standards, and additional
testing may be needed to make an accurate diagnosis. Examples of some of these renements
have been noted, such as the dark-adapted red
ash, additional large eld for PERG, extended
dark adaptation in RDH5 variant testing, etc.
ISCEV publishes “extended protocols” that
include long-duration stimulation to separate the
function of the on- and off-pathways and
31.6 Conclusion
Electrophysiological recording provides objective, non-invasive functional data. This short
review has addressed some of the basics of acquisition and interpretation. All data should be
obtained in consideration of existing International
Standards, with the recognition that as minimum
standards, the data may not be sufcient to make
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A. R. Hathibelagal et al.
an accurate diagnosis in all circumstances.
Additional testing may be needed. It is usually
the integration of the different test protocols
available to the electrophysiologist that enables
an accurate diagnosis, but the importance of a
comprehensive clinical history cannot be underestimated. The data should always be placed in
full clinical context, with the origins of the signals identied and the abnormalities observed
related to the presumed underlying pathophysiology. Electrophysiology aims to answer clinical
questions, and a complete knowledge of the tests
helps choose the appropriate tests to answer those
questions.
Funding Hyderabad Eye Research Foundation.
Disclosure None.
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The Visual Evoked Potential
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OliverR.Marmoy
32.1 Introduction
The visual evoked potential (VEP) was one of the
rst time-locked electroencephalographic potentials recorded in humans. Seminal works rst
demonstrated that a series of positive and negative
potentials could be recorded from the human
scalp following ash stimulation, demonstrating
the recording of a ash VEP for the rst time.
Along with technological developments in visual
display units (VDUs), the VEP to structured stimuli (i.e., patterns, gratings) was soon developed.
These were found to have more reproducible and
predictable waveforms than that produced to ash
stimuli. Following its conception, the pattern VEP
has subsequently been used in assessment visual
pathway dysfunction, particularly for optic nerve
disease. Much of its application was used to dis-
cover “clinically silent” lesions of the optic nerve
in patients with demyelinating disease [1].
However, it is now known that the pattern VEP
can be affected in a range of conditions affecting
the visual apparatus from the macula to the primary visual cortex, and the ash VEP is less sensitive in the disorders of the visual pathway. As
such, the clinical practice encourages the complementary use of the pattern and ash VEPs with a
pattern electroretinogram (PERG) or full-eld
electroretinogram (FFERG) [2]. These allied
electrophysiological tests provide specicity in
the locus of visual pathway dysfunction and complement normal or abnormal VEP ndings.
The VEP can often be overlooked in clinical
practice, yet it provides a unique and valuable
addition to ophthalmic diagnoses in the modern
age. The pattern VEP can be used in disease monitoring, outcome measurements in clinical trials,
or estimation of vision levels in people unable to
comply with subjective testing. In the era of
genetic testing, phenotyping, and novel treatments or therapies for eye disease, the VEP will
likely provide an objective functional measure of
the visual pathway.
O. R. Marmoy (*)
Great Ormond Street Hospital for Children NHS
Foundation Trust , London, UK
GOS-ICH University College London, London, UK
e-mail: o.marmoy@nhs.net
© The Author(s), under exclusive license to Springer Nature Singapore Pte Ltd. 2024
T. Das, P. Satgunam (eds.), Ophthalmic Diagnostics, https://doi.org/10.1007/978-981-97-0138-4_32
32.2 Technology
Recording the VEP requires two major technological considerations: the recording equipment
and stimuli to elicit a visually evoked response.
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