Electrooculogram

All content on Eyewiki is protected by copyright law and the Terms of Service. This content may not be reproduced, copied, or put into any artificial intelligence program, including large language and generative AI models, without permission from the Academy.

Article initiated by:

Hema L. Ramkumar, MD

All contributors:

Hema L. Ramkumar, MD, Vinay A. Shah M.D., Koushik Tripathy, MD (AIIMS), Zachary Koretz, MD, MPH, Robert A Hyde, MD, PhD, Jennifer I Lim MD, Peter A.Karth, MD

Assigned editor:

Robert A Hyde, MD, PhD

Review:

Assigned status Up to Date

 by Robert A Hyde, MD, PhD on April 29, 2024.

add
Contributing Editors:	add

Definition

The electroocoulogram (EOG) is an elecrophysiologic test that measures the existing resting electrical potential between the cornea and Bruch's membrane. The mean transepithelial voltage of bovine Retinal pigment epithelium is 6 millivolts (mV). 

History

The EOG was described and named by Elwin Marg in 1951. Clinical applications were described first by Geoffrey Arden in 1962, who realized that the most valuable information was the comparison of the amplitudes under light and dark-adapted states (the Arden ratio).

Testing process

The patient should be dilated. The amount of light passing through the pupils is measured in a unit called Trolands (the product of luminance (cd/m2) and pupil area (mm²)). Thus the pupillary diameter may change the needed luminance for the same effect on the retina.

The patient should be in stable indoor lighting for at least 30 min before the test. Strong retinal illumination including retinal imaging (fluorescein angiogram, fundus photography and others) and indirect ophthalmoscopy should be avoided during this period.

The patient is told to remain still other than moving his/her eyes back and forth. Four recording skin electrodes (silver-silver chloride or gold-disk) are placed at the medial and lateral canthi of both eyes, and the grounding electrode is placed on the forehead. 

Principle of EOG

The difference of electrical potential of the anterior and posterior part of the eyeball is called the standing potential. Standing potential indirectly measures the transepithelial potential (TEP) of the retinal pigment epithelium (RPE). TEP is the difference of membrane potential of basolateral and apical membranes of RPE.

The standing potential may be determined in 2 ways:

• EOG- determines function of outer retina and RPE. It has positive waveform in light and negative waveform in dark. It is recorded during 15 min of dark adaptation and 15 min of light adaptation. During 15 min of dark adaptation the standing potential usually reaches a minimum level (dark trough/DT) at 10-15 min. During 15 min of light adaptation the standing potential achieves the highest value at 7-12 min called a light peak/LP. The LP results from increased free intracellular calcium released from the endoplasmic reticulum. The role of bestrophin of endoplasmic reticulum and L type calcium channel of basolateral membrane is crucial in this. The increased intracellular calcium opens the 'Calcium dependent light peak chloride channels' of the basolateral membrane through which negative chloride ions are extruded from the RPE and the RPE depolarizes in light.

• Fast Oscillations (FO)- Is an optional additional test performed using alternate 1 min dark and light periods. It has negative waveform in light and positive waveform in dark. This opposite waveform compared to EOG is related to different mechanism of FO and shorter dark and light periods. At the onset of light, there is a decrease in potassium levels at the subretinal space. This creates a strong outward hyperpolarising potassium current from the apical membrane of RPE which results in the c wave of electroretinogram. The chloride channels at the basolateral membrane (CFTR) of RPE may have important role in the generation of the FO, which may be reduced in cystic fibrosis. The wave form of FO is sinusoidal compared to the EOG which has a shape of plateau after post hoc DC restoration by digital integration,
  

Components of the EOG

The light-insensitive component accounts for the dark trough and is dependent on the integrity of the retinal pigment epithelium (RPE) as well as the cornea, lens, and ciliary body. The light-sensitive component is the slow light rise of the EOG and is generated by the depolarization of the basal membrane of the RPE.

Reporting of EOG

According to the 2017 ISCEV standards, the report of EOG should include

• Light peak: dark trough ratio (this terminology is preferred over conventional Arden ratio)
• Amplitude of dark trough (mv)
• Time from the start of light phase to light peak (when present)
• type of adapting light source
• pupil size
• Difficulties/deviation from protocol including patient compliance, inconsistent eye movements

Interpretation of Results

The Arden ratio, the ratio of the Light peak (Lp) to dark trough (Dt) is used to determine the normalcy of the results.

An Arden ratio of 1.80 or greater is normal, 1.65 to 1.80 is subnormal, and < 1.65 is significantly subnormal.

The EOG in Retinal Disorders

The EOG is abnormal in:

• Best vitelliform macular dystrophy (early stage) and in carriers
• Stargardt macular dystrophy (advanced stage)
• Pattern dystrophies (normal or modestly subnormal)
• Membranoproliferative glomerulonephritis with electron dense material deposition in the choriocapillaris (normal or subnormal)
• Ectodermal dysplasia, ectrodactyly, and macular dystrophy, EEM syndrome (markedly reduced)
• Retinitis pigmentosa and rod-cone dystrophies
• Acquired cone and cone-rod dystrophies 
• Oguchi disease
• Fundus Albipunctatus (no notable light rise with dark adaptation of 15 minutes)
• Choroideremia
• Gyrate atrophy
• Diffuse choroidal atrophy
• Diffuse chronic chorioretinal inflammation
• Hypertensive retinopathy
• Retinal detachment
• Silicone oil exposure during retinal detachment repair surgery, even 4 mo after removal
• Chloroquine and hydroxychloroquine toxicity
• Didanosine use (can be reversible after stopping therapy)
• Desferrioxamine
• Diabetes, worsening with the duration of diabetes
• Retained intraocular iron particles (siderosis bulbi)
• Progressive high myopia
• Choroidal malignant melanoma

The EOG is normal in:

• Dominantly inherited drusen of Bruch's membrane
• Congenital achromatopsia
• Progressive diffuse cone dystrophy
• Autosomal recessive and X-linked recessive congenital stationary nyctalopia
• Carotid occlusive disease
• Optic nerve disease

Drugs that reduce systemic standing potential

• IV 20% mannitol (reduced by 43%)   hyperosmolarity-induced response
• IV 500 mg acetazolamide
• Timolol

Conditions that increased systemic standing potential

• Retinal hypoxia
• Silicone oil exposure and removal
  

Conclusions

In some cases, EOG is a very useful tool in diagnosing hereditary macular diseases. It is most classically used in the confirmation of Best Disease. Understanding the disease states that affect the EOG make it easier to interpret the results. In conjunction with an ERG, it can be useful in diagnosing various progressive retinal disorders.