Electro-physiology

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Electro-physiology
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Electro-oculogram (EOG)

• 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

• 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

• 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 gt170 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

• 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

• 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)

• 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

• 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

• 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)

• 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

• 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

• 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

• Furthermore, when taken in conjunction with the
  full-field 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)

• 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

• 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 sub-clinical
  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

• 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.