Chapter 104
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The electro-oculogram (EOG) is an indirect measure of the standing potential of the eye.1 This standing potential exists because of a voltage difference between the inner and outer retina and is so oriented that the inner retina is positive with regard to the outer retina. The clinical EOG measures this change indirectly by placing electrodes on either side of the eye and having the person move the eyes back and forth over a specific distance. Thus, one electrode will become more positive than the other as the eye (here considered a dipole) moves back and forth (Fig. 1).

Fig. 1. Electro-oculogram (EOG) schematic. The eye can be considered a dipole with the anterior part relatively more positive than the posterior pole. EOG electrodes have been fixed to the outer and inner canthi of the left eye. On the left side of the diagram as the eye moves to the left, the outer canthal electrode (being closer to the positive pole of the eye) becomes more positive than the inner canthal electrode. Such a change in potential can then be recorded on a voltage meter. When the eye turns to the right, the inner canthal electrode then becomes positive and again a change in potential can be recorded but with opposite polarity. (Carr RE, Siegel IM: Visual Electrodiagnostic Testing. Baltimore: Williams & Wilkins, 1982)

The importance of the clinical measurement of the EOG lies in the fact that the amplitude of the response changes when certain luminance conditions are varied. Thus, if a patient is placed in darkness the potential will decrease, whereas if a bright light is turned on following dark adaptation the potential will increase.2

To obtain reproducible and comparable results, recommendations to standardize EOG testing have been made by the International Society of Clinical Electrophysiology of Vision (ISCEV).3 The reader should refer to this article for specific recommendations, but the essence of an EOG is as follows. After a preadaptation period of several minutes to acquaint the patient with the test, the lights are turned off for 15 minutes. Recordings for several saccades are made in the dark at 1-minute intervals. The lowest potential (dark trough) is reached in 8 to 12 minutes. A bright light is then turned on and recordings continue at 1-minute intervals with the potential increasing in amplitude until the highest point (light peak) is reached in 7 to 10 minutes. The ratio of the light peak to the dark trough is then calculated with normal being 165% or greater4 (Fig. 2).

Fig. 2. Graphic representation of the electro-oculogram (EOG) at various periods of adaptation. The black circles represent the average pen swing amplitude of several saccades taken at that period of time. Insert shows how an individual saccade might appear at certain time periods with a decrease in darkness and increase in light. The greatest EOG amplitude achieved in light (light peak) is divided by the lowest amplitude in the dark (dark trough) and the calculated ratio is expressed as a percent. (Carr RE, Siegel IM: Visual Electrodiagnostic Testing. Baltimore: Williams & Wilkins, 1982)

It should be noted that this test may be performed with either dilated or undilated pupils, but the amount of light used to induce a full EOG light rise will vary with the pupillary size. Because the EOG light rise is proportional to the amount of light entering the eye up to an asymptote, it is important to have the necessary luminance to obtain a maximal response. Failure to account for this explains many of the lower-than-normal responses reported in the older literature.

Each laboratory should establish its own set of standards and these should be obtained using the standardized protocol referred to previously.

This electrical response is generated by the retinal pigment epithelium (RPE) with the light peak generated by a depolarization of the basal portion of the RPE.5 To generate this potential, intact photoreceptors, which are apposed to the RPE, are necessary.2

In the clinical situation the EOG almost always parallels the electroretinogram (ERG). Thus, in retinitis pigmentosa a patient with an extinguished ERG will show little or no EOG light rise. This is likewise true of any disorder in which there is a generalized degeneration of most of the photoreceptor cells, including drug-induced retinal toxicity and diffuse chorioretinitis.

Although specific abnormalities in the ERG may be recorded in a number of other abnormalities, including congenital stationary night-blindness (CSNB), X-linked retinoschisis, and cone dystrophy, the normalcy or abnormalcy of the EOG is dependent on the total number of functioning photoreceptors in these cases. Thus, in most cases of CSNB, there is an abnormality in neural transmission in the bipolar cell region; the EOG would be normal because of normal functioning rods.6 The same is true in X-linked retinoschisis. In cone dystrophy, although there may be an absence of cones, the large number of functioning rods give a normal EOG.

The only disorder in which a grossly abnormal EOG is found in the presence of a normal ERG is in the dominantly inherited disorder of Best's disease (vitelliform macular dystrophy).7 All patients with true Best's disease have an abnormal EOG with ratios invariably below 135% (Fig. 3). As is true of all autosomal dominant disorders there is a wide range of expressivity; thus, an individual who has the gene may show no fundus abnormalities yet has an abnormal EOG.8 Thus, this test serves as an electrophysiologic marker in this disorder and is important in assessing family members, as well as individuals with an atypical retinal picture (Figs. 4 and 5).

Fig. 3. Best's disease. A. Electro-oculogram (EOG) of a patient with Best's disease showing only baseline oscillations. B. EOG from a normal patient in the same family.

Fig. 4. Best's disease. A classic vitelliform lesion and fluorescein angiogram. The fluorescein test shows that the pigment epithelium is intact.

Fig. 5. Three different patients with Best's disease showing the remarkable range of changes that can occur. A. Subretinal neovascular membrane. B. Atrophic central retinal pigment epithelium (RPE) loss and several soft extramacular vitelliform lesions. C. Punctate drusen-like changes in foveal-parafoveal area.

The group of disorders known as pattern dystrophies of the RPE9 and the autosomal dominant disease foveomacular dystrophy10 have been reported to have reduced EOGs in some cases, but the number of exceptions make this test less helpful in these disorders than in Best's disease.

A normal EOG is likewise important to rule out Best's disease in certain patients who may present with a vitelliform lesion. These disorders, which are usually an atypical presentation of a macular degeneration (pseudovitelliform degeneration), have a normal EOG; this finding eliminates the necessity of examining other family members.

A number of studies have shown a yet unexplained abnormality of the EOG, which may be clinically useful.11 Patients with malignant melanoma of the choroid show a markedly reduced EOG in the affected eye as compared with the normal fellow eye. Although there seems to be no relationship between the size of the melanoma and the EOG ratio, there is a relationship between location and EOG ratio; those in the posterior pole have a greater EOG loss than more peripheral tumors.

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1. Arden GB, Kelsey JH: Changes produced by light in the standing potential of the human eye. J Physiol 161:189, 1962

2. Arden GB, Barrada A, Kelsey JH: New clinical test of retinal function based upon the standing potential of the eye. Br J Ophthalmol 46:449, 1962

3. Marmor MF, Zrenner E: Standard for clinical electro-oculography. Doc Ophthalmol 85:115, 1993

4. Adams A: The normal electrooculogram (EOG). Acta Ophthalmol 51(Suppl):551, 1973

5. Steinberg RH, Linsenmeier RA, Griff ER: Three light-evoked responses of the retinal pigment epithelium. Vis Res 23:1315, 1983

6. Carr RE, Ripps H, Siegel JM et al: Rhodopsin and the electrical activity of the retina in congenital night blindness. Invest Ophthalmol 5:497, 1966

7. Deutman AF: Electro-oculography in families with vitelliform dystrophy of the fovea. Arch Ophthalmol 81:305, 1969

8. Giuffre G, Lordolo G: Vitelliform dystrophy and pattern dystrophy of the retinal pigment epithelium: Concomitant presence in a family. Br J Ophthalmol 70:526, 1986

9. Marmor MF: Dystrophies of the retinal pigment epithelium. In Zinn KM, Marmor F (eds): The Retinal Pigment Epithelium. Cambridge: Harvard University Press, 1979:424–453

10. Gass JDM: A clinicopathologic study of a peculiar foveomacular dystrophy. Trans Am Ophthalmol Soc 72:139, 1974

11. Dawson WW: Malignant melanoma. In Heckenlively JR, Arden GB (eds): Principles and Practice of Clinical Electrophysiology of Vision. St. Louis: Mosby-Year Book, 1991:643–645

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