Fig. 12a. Fundus photo of a normal human retina.(189K jpeg image)

Fig. 12b. Fundus photo of a patient with retinitis pigmentosa. (59 K jpeg image).

ERGs recorded from a representative normal subject (Fig. 12a) and from a patient with retinitis pigmentosa (RP) (Fig. 12b) using the above methodology are illustrated in figure 13. The scotopic blue and red ERG traces are 200 milliseconds and the other traces are 100 milliseconds. The vertical calibration is 100 microvolts. The low bandpass limit was 0.1 Hz and the upper 1 KHz. When dim stimuli are used such as an intensity series starting with low intensity white or dim scotopic red and blue flashes it is important that the low bandpass be less than 1 Hz. The slow b-wave initiated by dim stimuli will be attenuated if a low bandpass is not used.

The first two responses are scotopically matched blue and red ERGs. The blue flash was dim enough that no a-wave can be discerned in a normal patient leaving only the rod-dominated slower b-wave. The red flash is bright enough that oscillations can be observed just after the a-wave. Bright white flash in the dark produces the largest amplitude ERG. The 30 Hz flicker illustrates the response of the rapidly recovering cones, and the photopic response is representative of a normal response with the more sensitive rods bleached by background illumination. Oscillatory potentials on the ascending b-wave are seen in responses to moderate-high intensity white flashes and in response to red, yellow, and green flashes (Fig. 13).

This particular case of retinitis pigmentosa (RP) was selected because the individual was tested early in the onset of retinitis pigmentosa, as a young adult when she still had remnants of a cone ERG. As in most cases of retinitis pigmentosa, the rods are affected most severely as evidenced by the extinguished response to the blue flash. Although it may take some imagination, some of those "squiggles" in the first half of the response to red flashes are remnants of photopic cone physiology. There are also remnants of cone physiology in the responses to bright white flash in the dark, 30 Hz flicker and photopic white flash. In many individuals with RP the electrophysiological progression is more severe with all ERGs extinguished, similar in appearance to the response to scotopic dim blue flash. Both scotopic and photopic b-wave peak implicit times are usually prolonged. Almost always it is impossible to record oscillatory potentials.

Early in the clinical onset of RP, with the exception of severe expressions such as Leber's congenital amaurosis or X-linked RP (Fig. 14), there are recordable ERGs at least to bright photopic stimuli. Some individuals with dominantly inherited RP maintain recordable ERGs throughout most of their lives. I have tested over 100 members of one extended family with dominantly inherited RP. Some of the affected members showed no ERG changes until their mid-teens. Expression of RP in all forms of inheritance varies considerably even between siblings. Female carriers of the X-linked form can show fundus changes and somewhat abnormal ERGs.

Fig. 14. Fundus photo of patient with carrier X-linked retinitis pigmentosa.(189K jpeg image)

Fig. 15. Fundus photo of a patient with paravenous retinitis pigmentosa. (59 K jpeg image).

Atypical cases of RP are common. There are occasional cases of RP without the usual pigment changes in the fundus (retinitis pigmentosa sine pigmento). Often these cases represent early stages of the disease. Sector retinitis pigmentosa usually results in a subnormal ERG proportional to the area of retina involved. Paravenous retinitis pigmentosa (Fig. 15) is associated with a poor ERG most of the time but again, similar to sector RP, the ERG may be attenuated proportional to the extent of retinal involvement.

RP is seen as a component of a number of syndromes with variability in expression. A common syndrome is Usher's. Usher's syndrome is congenital deafness plus RP. Usher's syndrome may comprise over 20% of RP cases not associated with other syndromes (Boughman and Fishman, 1983).

Myotonic dystrophy (MD) can show ocular changes similar to RP (Fig. 16). Even without fundus changes the ERG in MD patients is usually moderately affected like that seen in early dominantly inherited RP (Creel et al. 1985). It is interesting to note that minimally affected individuals without neurological symptoms usually have significant attenuation of their dim flash scotopic ERG b-wave amplitudes. Thus the ERG can be used to identify the minimally affected parent with MD (Fig. 16, the mother) in cases where neither parent of a child with myotonic dystrophy exhibits neurological symptoms.

There are a number of central nervous system syndromes with RP-like ocular involvement. Prominent among these are the mucopolysaccharidoses such as the Hurler, Scheie and Hunter syndromes, which often have abnormal ERGs early in the disease. Another group is the neuronal ceroid lipofuscinoses such as Batten's disease which have abnormal ERGs, usually attenuated b-waves.

There are syndromes that may include retinitis pigmentosa. The following list summarizes many of these syndromes:

Albers-Schonberg syndrome (osteopetrosis): ERG often abnormal

Alport's syndrome: ERG normal or subnormal

Alstrom's syndrome: ERG abnormal

Ataxia with isolated vitamin E deficiency (AVED) and RP: ERG abnormal

Bassen-Kornzweig syndrome (a-beta-lipoproteinemia): ERG abnormal

Cockayne's syndrome: ERG often abnormal

Cystinosis: ERG abnormal in older children

Flynn-Ard syndrome: ERG sometimes abnormal

Friedreich's ataxia: ERG sometimes abnormal

Hallervorden-Spatz syndrome: ERG often abnormal

Infantile phytanic acid storage disease: ERG usually abnormal

Jeune's syndrome: ERG usually abnormal

Joubert's syndrome: ERG abnormal

Kearn's-Sayres syndrome: ERG some abnormal

Laurence-Moon-Bardet-Biedl syndrome: ERG usually abnormal

Methlmalonic aciduria with homocystinuria: ERG some abnormal

Mucopolysaccharidoses:

Hurler; Scheie; Hunter: ERG often has b-wave attenuation

Myotonic dystrophy: ERG abnormal, dim scotopic ERGs

Neuronal ceroid lipofuscinosis:

Haltia-Sanavouri; Jansky-Bielschowsky; Batten's: ERG often has b-wave attenuation

Neuropathy ataxia and retinitis pigmentosa (NARP): ERG abnormal

Refsum's disease : ERG often abnormal

Saldino-Merzbacher syndrome: ERG usually abnormal

Spinocerebellar atrophy Type 7 (SPA7): ERG abnormal

Usher's syndrome: ERG abnormal

Zellweger's syndrome: ERG usually abnormal

In the differential diagnosis of retinitis pigmentosa there are a number of disorders in which the ERG can be used to distinguish the correct diagnosis. Pigment in the retina is prominent in many infectious diseases and may not solely be an indication of retinitis pigmentosa. Syphilis, particularly the congenital form, can mimic the fundus appearance of RP (Fig. 17) but the ERG is usually normal or only slightly subnormal.

Fig. 17. Fundus photo of patient with syphilis.(189K jpeg image)

Fig. 18. Fundus photo of patient with rubella. (59 K jpeg image).

Rubella and viral infections such as mumps, measles, and herpes can produce pigment changes in the retina (Fig. 18). These ERGs are usually normal.

Stationary rod dystrophies

Congenital stationary night blindness (CSNB) is found in several forms. Although rare, CSNB is more often seen in the form with a normal appearing retina and may be inherited in any fashion. Within this form are two types. Type 1 have an abnormal dim scotopic ERGs but the bright flash ERG maintains oscillatory potentials on the ascending limb of the b-wave. Type 2 (Fig. 19) has a very abnormal dim scotopic ERG and the bright flash scotopic ERG has a large a-wave and no b-wave (Fig. 20). Oscillatory potentials are also missing.

Fig. 19. Fundus photo of patient with CSNB Type 2.(189K jpeg image)

Fig. 20. ERGs in a patient with CSNB Type 2. (59 K jpeg image).

CSNB with retinal lesions is quite rare. Oguchi's disease is CSNB with an unusual golden to rust coloration of the fundus that is reversed with long dark adaptation. This is called Mizuo's sign and requires 2-3 hours of dark adaptation. The ERG resembles CSNB Type 2 with no b-wave although cases have been reported that the ERG returns to normal after hours of dark adaptation. Another rare form of night blindness is stationary albipunctate degeneration also referred to as fundus albipunctata. This disorder includes stationary night blindness with white dots scattered throughout the fundus. The ERG b-wave is attenuated but returns to normal after long dark adaptation. A third form is Kandori's syndrome characterized by large irregular hyperfluorescent flecks in the peripheral and central retina. In Nyctalopia the ERG is similarly affected as in stationary albipunctate degeneration.

Other retinal atrophies

The bright flash ERG b-wave is selectively attenuated in:

Juvenile retinoschisis

Coat's disease

Central retinal vein occlusion and central retinal artery occlusion

Myotonic dystrophy

Congenital stationary night blindness Type 2

Oguchi's disease

Lipopigment storage diseases (Batten's disease)

Choroideremia represents an X-linked diffuse atrophy of the choroid and pigment epithelium. In its mature form the fundus appearance is white to yellow-white with some small islands of choroid (Fig. 21). Carriers are asymptomatic except for more subtle peripheral fundus abnormalities (Fig. 22). ERGs are usually abnormal.

Fig. 21. Fundus photo of patient with Choroideremia.(189K jpeg image)

Fig. 22. Fundus photo of a patient with X-linked choroideremia carrier. (59 K jpeg image).

Gyrate atrophy (Fig. 23) is a recessively inherited atrophy of the pigment epithelium and choroid caused by a deficient mitochondrial enzyme ornithine aminotransferase (OAT).

Gyrate atrophy is less extensive than choroideremia and the fundus usually shows scalloped borders to degenerative areas (Fig. 23). ERGs are abnormal and progressly deteriorate according to the extent of degeneration of retinal pigment.

X-linked juvenile retinoschisis is a splitting or schisis in the central retina with a characteristic fundus appearance (Fig. 24). These patients have poor acuity. The ERG has a specific abnormality showing a normal a-wave but no b-wave. It is a negative ERG (Fig. 24). The picture is similar to that recorded in central retinal artery occlusion and Congenital Stationary Night Blindness Type 2.

Patients with Creutzfeldt-Jakob disease (CJD) can also show selective loss of the b-wave (Katz et al. 2000).

Except for some retinal dystrophies such as patients with severe retinitis pigmentosa or Leber's congenital amaurosis, most retinal disorders produce reduced, "graded" amplitude attenuation of the ERG as we have seen in the above cases.

However, a few disorders result in a completely extinguished ERG. They include the following:

1) Leber's congenital amaurosis

2) Severe retinitis pigmentosa

3) Retinal aplasia

4) Total detachment of retina

5) Ophthalmic artery occlusion

Leber's congenital amaurosis unfortunately presents with significant visual loss in the first year after birth. The fundus usually has a salt and pepper appearance. The ERGs are usually unrecordable.

8. The ERG in cone dystrophies.

In contrast to retinitis pigmentosa, the ERGs of a patient with a cone dystrophy exhibit good rod b-waves that are just slower. However, the early "cone" portion (b_x) of the scotopic red flash ERG is missing. The scotopic bright white ERG is fairly normal in appearance but with slow implicit times. The 30 Hz flicker and photopic white ERGs dependent upon cones are very poor. Cone dystrophies are inherited in all forms and include poor color vision and poor acuity. The most common fundus findings are a "bullseye" appearance or diffuse pigmentation in the macular area (Fig. 25). Many patients have nystagmus and photophobia. Cone-rod dystrophy appears to involve only cones early in the disease, but the ERGs usually show attenuated rod physiology after a while (Fig. 26).

Fig. 25. Fundus photo of patient with cone dystrophy.(189K jpeg image)

Fig. 26. ERGs in a patient with cone dystrophy. (59 K jpeg image).

Other dystrophies are the flecked retina disorders, such as fundus flavimaculatus (Fig. 27) and Stargardt's disease. The retinas display an abnormal accumulation of lipofuscin. The ERG in these disorders is normal except in very late stages where it may become slightly subnormal.

Fig. 27 Fundus photo of patient with fundus flavimaculatus. (59 K jpeg image)

9. ERGs in retinal vascular disease.

Vascular occlusions such as central retinal artery thrombosis produce a characteristic avascular appearance to select areas of the fundus (Fig. 28a) and an ERG with no b-wave (Fig. 28b). Ophthalmic artery occlusions usually result in unrecordable ERGs.

Fig. 28a. Fundus photo of patient with central retinal artery occlusion.(189K jpeg image)

Fig. 28b. ERGs in a patient with central retinal artery occlusion. (59 K jpeg image).

10. Foreign bodies and Trauma

The ERG is useful to assess cases of retinal foreign bodies and trauma to estimate the extent of retinal dysfunction. Foreign bodies affect retinal function depending on the extent of tearing of the retina, the location and composition of the object.

Fig. 29 Fundus photo of a patient with a hole in the retina caused by a metallic foreign body. (59 K jpeg image)

A small piece of stainless steel or plastic outside the macula may have a minor affect on the retina. However a piece of copper or iron (Fig. 29) would likely have deleterious affects within a few weeks (Figs. 30a and 30b). In general if b-wave amplitudes are reduced 50% or greater compared to the fellow eye, it is unlikely that the retinal physiology will recover unless the foreign body is removed.

Fig. 30a. The effect of the foreign body on the ERG waveform.(189K jpeg image)

Fig. 30b. The effect of the foreign body on the ERG waveform some weeks later. (59 K jpeg image).

The ERG can be used to estimate the extent of functional retina in cases of retinal detachment. An interesting case is shown in figures 31a and 31b. The patient had a small retinal detachment of the macular area in one eye (Fig. 31a, arrows point to circle of detachment). With the new techniques of optical coherence tomography (OCT) which gives an optical image like a vertical section plane, the detached portion of the retina in the foveal and macular area can be clearly seen, in comparison to the normal attached macular area in the fellow eye. In general ERG b-wave amplitudes correspond to the amount of attached healthy retina, although the detached retina may function for some time.

Fig. 31a. Fundus photo of a patient with a retinal detachment at the fovea and macula in one eye.(189K jpeg image)

Fig. 31b. Optical coherence tomography (OCT) images of the patients normal macula and of the retina in the other eye with the macular detachment. (59 K jpeg image).

11. Drug toxicities.

A number of drugs given in high doses or for long periods of time can produce retinal degeneration with pigmentary changes. Traditional culprits are thioridazine (Mellaril), chlorpromazine (Thorazine) and the antimalarial, chloroquine. These are drugs usually taken at high dosages for many years and can end up damaging the retina and producing a retinopathy. Chloroquine retinopathy shows as a characteristic "bullseye" appearance of the macula (Fig. 32). The ERGs become abnormal in these cases (Fig. 33).

Fig. 32. Fundus photo of patient with chloroquine retinopathy.(189K jpeg image)

Fig. 33. ERGs in a patient with chloroquine retinopathy. (59 K jpeg image).

Hydroxychloroquine (Plaquenil) is usually less disruptive to the retina than chloroquine, but ERG changes can still occur. Other drugs can end up being accidentally toxic to the retina. Cis-platinum used to treat brain tumors sometimes reaches ophthalmic vascularization (Fig. 34) and causes a reduction in ERG waveform in the affected eye (OD in this case) (Fig. 35).

Fig. 34 Fundus photo of patient with OD cis-platinum toxicity. (59 K jpeg image)

Fig. 35 ERGs in a patient with OD cis-platinum toxicity. (59 K jpeg image)

An interesting case was seen in our clinic, where an intranasal steroid injection affected the retina of the patient's right eye (OD) only. The fundus photo shows a cherry red spot in the macula (Fig. 36). The ERG response was diminished in size particularly following dim scotopic flashes (Fig. 37).

Fig. 36. Fundus photo of patient with steroid retinopathy.(189K jpeg image)

Fig. 37. ERGs in a patient with steroid retinopathy. (59 K jpeg image).

Talc retinopathy is also seen occasionally (Fig. 38). Again the global ERG is attenuated in such cases (Fig. 39).

Fig. 38. Fundus photo of patient with talc retinopathy.(189K jpeg image)

Fig. 39. ERGs in a patient with talc retinopathy. (59 K jpeg image).

12. Systemic disorders and the ERG.

Systemic metabolic disorders are reflected in retinal physiology. Liver and kidney disease and drugs that affect those organ systems, usually reduce ERG b-wave amplitudes, particularly in scotopic dim flash ERGs. For example, deferoxamine, an iron chelating drug used to reduce iron overload, can be toxic to the retina. This is reflected in reduced a- and b-waves of the ERG (Fig. 40).

Fig. 40. Deferoxamine toxity affects on the ERG.(59 K jpeg image)

13. The multifocal ERG mfERG.

A limitation of the traditional global or full-field ERG is that the recording is a massed potential from the whole retina. Unless 20% or more of the retina is affected with a diseased state the ERGs are usually normal. In other words a legally blind person with macular degeneration, enlarged blind spot or other central scotomas will have normal global ERGs.

The most important development in the ERG field in recent years is the multifocal ERG recording system (Bearse and Sutter, 1996). This system allows assessment of ERG activity in small areas of retinal dysfunction. With this method one can record mfERGs from hundreds of small retinal areas (100 um) simultaneously in less than 10 minutes per eye (Marmor et al., 2003). A bipolar Burian speculum contact is usually used to record ERGs from the cornea from a dilated eye. Scotomas of only a couple of millimeters in diameter can be mapped and extent of retinal dysfunction quantified very accurately.

Below are the mfERGs of a patient tested at the Moran Eye Center (Figs. 41b and 42). The patient is an elderly woman with macular degeneration. The fundus photograph of another patient with age related macular degeneration (AMD) is seen in Figure 41a. In Figure 41b are 103 multifocal ERGs from approximately the central 50 degrees of retinal field. In Figure 42 are the b-wave voltages from these 103 locations transformed into a 3-D color plot. The lower far right (Fig. 42) shows a plot of a normal patient for comparison. The top color transformation is the difference between the patient's multifocal ERGs and a normal group, which points out the worst areas of retinal function. Colors reflect standard deviations (S.D.) from average ERG amplitudes. These plots can be rotated from 3-D to 2-D so that they resemble visual field plots.

Fig. 41a. Fundas photograph of a patient with age related macular degeneration.(189K jpeg image)

Fig. 41b. Multifocal ERG recordings in a patient with age related macular degeneration (AMD). (59 K jpeg image).

A second example shows the mfERGs of an adult female with big blind spot syndrome. She is thought to have lost vision due to a viral infection, which came out of the optic nerve head exaggerating the blind spot 15-20 degrees inferiorly (Fig. 43). Multifocal ERGs show attenuation in amplitudes in the affected area close to the macula compared to a normal person's plot (Fig. 43).

Fig. 42. Multifocal ERG recordings transformed into 3-D maps of the macular area in a patient with AMD compared to a normal patient.(189K jpeg image)

Fig. 43. Multifocal ERG recordings transformed into the 3-D map of the fovea and optic nerve side in a patient with an enlarged blindspot. (59 K jpeg image).

The mfERG method is a very reliable test and really helps in following the progression of a macular (or other limited retinal area) disorders.

14. The Electrooculogram EOG.

The electrooculogram measures the potential that exists between the cornea and Bruch's membrane at the back of the eye. The potential produces a dipole field with the cornea approximately 5 millivolts positive compared to the back of the eye, in a normally illuminated room. Although the origin of the EOG is the pigment epithelium of the retina, the light rise of the potential requires both a normal pigment epithelium and normal mid-retinal function. Elwin Marg named the electrooculogram in 1951 and Geoffrey Arden (Arden et al. 1962) developed the first clinical application. With the cornea constantly positive, movement of the eye produces a shift of this electrical potential. By attaching skin electrodes on both sides of an an eye (Fig. 44) the potential can be measured by having the subject move his or her eyes horizontally a set distance (Fig. 45). The eyes are usually dilated. Skin electrodes are attached near the lateral and medial canthus of each eye (Fig. 44). A ground electrode is attached usually to either the forehead or earlobe. It is helpful, but not necessary, that the patient have a chin rest to reduce head movement. Either inside a Ganzfeld, or on a screen in front of the patient, small red fixation lights are place 30 degrees apart (Fig. 46). The distance the lights are separated is not critical for routine testing. Any set distance subtending from 20-40 degrees of visual angle is satisfactory.

Fig. 44. Placement of the electrodes for recording an EOG.(189K jpeg image)

Fig. 45. How the EOG potential is measured as the eyes turn towards and away from the skin electrodes. (59 K jpeg image).

The patient should be light adapted such as in an well-illuminated room, and their eyes dilated. After the electrodes are attached the procedure is explained and the patient asked to practice several times while baseline data are recorded. The procedure is simply that the patient keeps his or her head still while moving the eyes back and forth alternating between the two red lights. The movement of the eyes produces a voltage swing of approximately 5 millivolts between the electrodes on each side of the eye, which is charted on graph paper or stored in the memory of a computer.

Fig. 46. Ganzfeld used for stimulating the EOG waveform.(59 K jpeg image)

Below are 10-second periods of eye movement back and forth between two red LED lights placed 30 degrees apart inside a Ganzfeld (Fig. 47).

Fig. 47. Light adapted pre-EOG, dark adaptation phase and light-rise phase.(59 K jpeg image)

After training the patient in the eye movements, the lights are turned off. About every minute a sample of eye movement is taken as the patient is asked to look back and forth between the two lights (Fig. 47). Some laboratories have the patients move their eyes the entire testing period. After 15 minutes the lights are turned on and the patient is again asked about once a minute to move his or her eyes back and forth for about 10 seconds. The top of Figure 48 shows segments of eye movement that have been cut from 10 second samples from a normal person. The chart (Fig. 48) graphs the change in voltage in the eye through 15 minutes of dark adaptation and 15 minutes of bright light. Typically the voltage becomes a little smaller in the dark reaching its lowest potential after about 8-12 minutes, the so-called "dark trough." When the lights are turned on the potential rises, the light rise, reaching its peak in about 10 minutes. When the size of the "light peak" is compared to the "dark trough" the relative size should be about 2:1 or greater (Fig. 48). A light/dark ratio of less than about 1.7 is considered abnormal. Figure 49 shows an abnormal response recorded from a patient with Best's disease.

Fig. 48. Normal EOG recording.(189K jpeg image)

Fig. 49. EOG from a patient with Best's disease. (59 K jpeg image).

The EOG is redundant with the ERG in most retinal disorders. Retinal diseases producing an abnormal EOG will usually have an abnormal ERG which is the better test for analysis of scotopic and photopic measures. The most common use of the EOG is to confirm Best's disease. Best's vitelliform macular dystrophy and variants of this disease are usually identified by the appearance of a retinal lesion resembling an egg yolk early in the disease (Fig. 50). In vitelliform macular dystrophy (Fig. 51) the ERG will be normal but the EOG will be abnormal.

Fig. 50. Fundus photo in Best's disease.(189K jpeg image)

Fig. 51. Fundus in Adult viteliform dystrophy. (59 K jpeg image).

15. References.

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Boughman, JA and Fishman, GA (1983) A genetic analysis of retinitis pigmentosa. Brit. J. Ophthalmol. 67: 449-454.

Creel, DJ, Crandall, AS and Ziter, FA (1985) Identification of minimal expressionof myotonic dystrophy using electroretinography. Electroencephalog. Clin. Neurophysiol. 61:229-235.

Creel, DJ, Wang, JM and Wong, KC (1987) Transient blindness associated with transurethral resection of the prostate. Arch. Ophthalmol. 105:1537-1539.

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Fishman, GA, Birch, DG, Holder, GE and Brigell, MG (2001) Ophthalmology Monograph 02: Electrophysiologic testing in disorders of the retina, optic nerve, and visual pathway. American Academy of Ophthalmology, 2nd Edition 2001.

Granit, R (1933) The components of the retinal action potential in mammals and their relation to the discharge in the optic nerve. J. Physiol. 77: 207-239.

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Katz, BJ, Warner, JEA, Digre, KB and Creel, DJ (2000) Selective loss of the electroretinogram b-wave in a patient with Creutzfeldt-Jakob Disease. J. Neuro-ophthal. 20:116-118.

Lawwill, T and Burian, HM (1966) A modification of the Burian-Allen contact-lens electrode for human electroretinography. Am. J. Ophthalmol. 61:1506-9.

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Marmor, MF and Hock, PA (1982) A practical method for c-wave recording in man. Doc. Ophthalmol. Proc. Ser. 31: 67-72.

Marmor, MF, Hood, DC, Keating, D, Kondo, M, Seeliger, MW and Miyake, Y. (2003) Guidelines for basic multifocal electroretinography (mfERG). Doc. Ophthalmol. 106: 105-115.

Marmor, MF and Zrenner, E (1993) Standard for clinical electro-oculography. Arch. Ophthalmol. 111: 601-604.

Marmor, MF and Zrenner, E. (1998) Standard for clinical electroretinography (1999 update). Doc. Ophthalmol.: 97:143-156

Miller, RF and Dowling, JE (1970) Intracellular responses of the Muller (glial) cells of mudpuppy retina: their relation to the b-wave of the electroretinogram. J. Neurophysiol. 33: 323-341.

Perlman, I (1983) Relationship between the amplitudes of the b wave and the a wave as a useful index for evaluating the electroretinogram. British J. Ophthalmol.: 67: 442-448.

Sieving, PA, Fishman, GA and Maggiano, J (1978) Corneal wick electrode for recording bright flash electroretinograms and early receptor potential. Arch. Ophthalmol. 96: 899-900.

Wachtmeister, L and Dowling, JE (1978) The oscillatory potentials of the mudpuppy retina. Invest . Ophthalmol. Vis. Sci. 17: 11-76-1188.

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The author Dr. Donnell Creel was born in Kansas City, Missouri. He attended the University of Hawaii and received his B.A and M.A. from the University of Missouri at Kansas City. His Ph.D. was in Neuropsychology from the University of Utah in 1969. Don's doctoral thesis and post doctoral research centered on abnormal decussation of retinal ganglion cell fibers at the optic chiasm in albino mammals. In the early 1970s he created a visual evoked potential test that detects this misrouting in human albinos. Later research demonstrated that melanin pigment in the inner ear is necessary for normal auditory function and that lack of pigment in albinos has consequences affecting normal cell development in the brainstem. Don has been in the Department of Ophthalmology, University of Utah Medical Center since 1980, and Director of Clinical Electrophysiology at the Moran Eye Center since its inception in 1993. Clinical research interests center around the application of visual and auditory evoked potentials and electroretinography.

[Introduction] [The electroretinogram ERG] [ERG recording electrodes] [Light stimulation for ERGs] [ERG recording methods] [Oscillatory potentials OPs] [ERGs in retinitis pigmentosa-like diseases] [The ERG in cone dystrophies] [ERGS in retinal vascular disease] [Foreign bodies and trauma] [Drug toxicities] [Systemic disorders and the ERG] [The multifocal ERG mfERG] [The electrooculogram EOG] [References] [Author]

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Updated: December 9, 2003