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Electro-physiology
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Electro-oculogram
(EOG)
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Conventional electro-oculography (the
EOG slow oscillation) records the light
induced rise in ocular standing potential
following a period of dark adaptation.
This reflects the rise in the potential
across the retinal pigment epithelium
(RPE) resulting from the progressive
depolarisation of the basal membrane of
the RPE which occurs in response to
light adaptation. The clinical value of the
EOG, and a reliable method for its
measurement, were developed in the
early 1960s by Arden's group
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Recording methods
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To record the EOG, surface electrodes are positioned
at the medial and outer canthi of each eye. After a
short period of pre-adaptation, the patient, usually
seated at a Ganzfeld bowl with two light emitting
diodes (LEDs) to provide fixation lights, performs fixed
excursion lateral eye movements of approximately 30
degrees for 15-20 minutes during dark adaptation.
During this time the standing potential, reflected in the
amplitude of the signal measured between the lateral
and outer canthus electrodes in relation to the eye
movements, will usually reach a minimum value, the
Dark Trough. The background light of the Ganzfeld is
then switched on to create a full-field photopic
environment, and the patient continues to make the
same lateral movements during light adaptation until
the gradual increase in standing potential which occurs
has reached a maximum, usually at 7-10 minutes - the
Light Peak.
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Normal results
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The value of the amplitude of the
Light Peak divided by the Dark
Trough expressed as a percentage
is known as the Arden index, and
will be >170% in a normal subject.
A normal EOG requires a normally
functioning RPE and a normally
functioning rod population with the
retina in contact with the RPE.
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Clinical uses
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In most diseases an abnormality of the
EOG light rise reflects demise or
dysfunction of the (rod) photoreceptors,
but can also indicate primary RPE
disease. The EOG is of principal value in
Best disease (vitelliform macular
dystrophy), where loss of the EOG light
rise is accompanied by a normal ERG; in
most other diseases, loss of the EOG
light rise is usually accompanied by an
abnormal rod ERG.
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Full field
electroretinogram (ERG
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The ERG measures the mass
response of the whole retina,
reflects photoreceptor and inner
nuclear layer retinal function, and
allows separate functional
assessment of the photopic and
scotopic systems
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Full field
electroretinogram (ERG)
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The leading edge of the a-wave of the
scotopic ERG arises from
hyperpolarisation of the (rod)
photoreceptors. The b-wave is probably
generated by Muller cells in response to
changes in extracellular potassium
consequent upon depolarisation of the
ON-bipolar cells. There is recent
evidence that the hyperpolarising bipolar
cells may have a role in "shaping" the
photopic cone b-wave.
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Recording methods
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The ERG protocols now commonly adopted in
most respectable laboratories include the
recommendations by ISCEV, the ISCEV
Standard ERG. This specifies the brightness of a
"standard flash", and requires that the response
to this flash (the mixed rod-cone maximal
response), and to the same flash attenuated by
2.5 log units of neutral density filter (the scotopic
rod response) be recorded under full dark
adaptation, and that following light adaptation
photopic transient and flicker ERGs be recorded.
30 Hz is usually used for the flicker ERG. In
addition to the presence of a rod-saturating
background in the Ganzfeld, the rods have poor
temporal resolution and cannot respond to a 30
Hz flicker.
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Clinical Uses
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In general, diseases that affect photoreceptor function will
cause a-wave reduction accompanied by reduction in the
amplitude of the b-wave, whereas diseases that have a
maximal effect post-phototransductionally will give a
"negative" ERG, so called because the overall waveform is
dominated by the negative a-wave and where there is relative
loss of the post-receptorally derived b-wave.
Generalised retinal degenerations, the retinitis pigmentosa
(RP) type conditions, will tend to give overall reduction of the
ERG usually accompanied by changes in implicit time. The
ERG may be extinguished in severe disease.
Restricted disease, such as sector RP or retinal detachment,
will tend to give amplitude reduction but no change in implicit
time.
Causes of a "negative" ERG include: central retinal artery
occlusion, where the a-wave sparing reflects the preservation
of photoreceptor function due to intact choroidal circulation,
X-linked retinoschisis, X-linked congenital stationary night
blindness, quinine toxicity, melanoma associated retinopathy
and others.
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Pattern electroretinogram (PERG)
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The pattern electroretinogram (PERG)
assesses the retinal response to a
structured non-luminance stimulus such
as a reversing black and white
checkerboard. It provides useful
information in the distinction between
optic nerve disease and macular disease
in patients with poor central visual acuity.
This recording has a much lower
amplitude than the full-field ERG, and
signal extraction using computer
averaging is necessary.
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Normal tracings
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The PERG consists of two main
components, P50 and N95, with
N95 and much, but not all, of P50
probably arising in relation to
central inner retina (ganglion cell).
Analysis of the PERG concentrates
on the latency and amplitude of
P50, measured from the N35
trough, and the amplitude of N95
measured from the peak of P50.
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Clinical uses
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A normal P50 component suggests a normally
functioning macula, and macular dysfunction will
reduce or extinguish this component, usually with
concomitant reduction or extinction of N95. Disease of
the ganglion cells, either primary such as dominant
optic atrophy (DOA), or secondary due to retrograde
degeneration from an optic nerve insult, may result in
specific loss of the N95 component with sparing of
P50. This allows a distinction between optic nerve
disease and macular disease. In severe optic
nerve/ganglion cell disease, there will probably be
involvement of the P50 component, but this will not be
extinguished even if the pattern VEP is abolished.
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Clinical uses
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Furthermore, when taken in conjunction with the fullfield ERG, the PERG permits a distinction between
macular dystrophy and cone or cone-rod dystrophy in
the patient with an abnormal macula on
ophthalmoscopy; in disease confined to the macula the
PERG is abnormal but the ERG is unaffected. It should
be remembered that a normal retinal or macular
appearance does not necessarily imply normal
function. Although there has been only limited
application of the PERG to date, it is possible that
changes in the PERG may assist in the early detection
of central dysfunction in patients with retinal dystrophy
and normal visual acuity. This may have prognostic
implications.
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Visual evoked cortical
potential (VEP or VECP)
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Introduction
The VEP can be elicited by various
stimuli, usually pattern reversal, pattern
appearance or diffuse flash. Pattern
appearance, also known as onset/offset
is where a contrast pattern appears from
a uniform background of identical mean
luminance, is present for a short period,
and then disappears. In clinical practice
the reversing checkerboard is perhaps
the most common and useful stimulus,
but pattern appearance and diffuse flash
both have their uses.
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Clinical uses
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The pioneering work of Halliday's group in the
1970s demonstrated not only that the pattern
reversal VEP was delayed in patients with
demyelinating optic neuritis, and that delay
remained following resolution of the clinical
symptoms, but also that patients with multiple
sclerosis could show delayed VEP from eyes
with no signs or symptoms of optic nerve
disease, i.e. the VEP was able to detect subclinical demyelination. It soon became apparent
that the VEP was a sensitive indicator of optic
nerve dysfunction, but that the delay found in
association with optic nerve demyelination was
not pathognomonic, and that delays could also
occur in compression, vitamin B12 deficiency etc.
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Clinical uses
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Ischaemic optic neuropathy may produce amplitude reduction
without latency delay. The abnormal distribution of the VEP
across the scalp in chiasmal dysfunction was also first
described by Halliday's group; single channel mid-line
recording may fail to detect chiasmal involvement. It should
be noted that delayed VEPs are commonplace in relation to
macular dysfunction and a delayed VEP cannot in itself be
regarded as an indicator of optic nerve dysfunction. The
additional information provided by PERG may be crucial to
the accurate interpretation of an abnormal pattern VEP. There
is also an abnormal distribution of the pattern appearance
VEP in association with the intra-cranial misrouting of ocular
albinism where the majority of fibres from each eye
decussate to the contralateral hemisphere. VEPs, together
with the other electrophysiological tests, are of crucial
importance in the diagnosis of non-organic or "functional"
visual loss, which may reflect psychological disturbance or
malingering. In such cases there are normal
electrophysiological findings in association with symptoms
which should suggest otherwise.
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