|Year : 1961 | Volume
| Issue : 1 | Page : 1-19
Electroretinography-diagnostic and prognostic evaluation
MGM Medical College, Indore, India
|Date of Web Publication||29-Mar-2008|
R P Dhanda
MGM Medical College, Indore
Source of Support: None, Conflict of Interest: None
|How to cite this article:|
Dhanda R P. Electroretinography-diagnostic and prognostic evaluation. Indian J Ophthalmol 1961;9:1-19
|How to cite this URL:|
Dhanda R P. Electroretinography-diagnostic and prognostic evaluation. Indian J Ophthalmol [serial online] 1961 [cited 2021 May 14];9:1-19. Available from: https://www.ijo.in/text.asp?1961/9/1/1/39674
To this society and to the Scientific Committee charged with carrying out the wishes of Mr. Adenwala, I give my thanks. It is an honour for me that you found me worthy of the award. I accept it with gratitude not for me but for the Institution and all the people who gave me opportunity for this useful work and joined me in this arduous task. I wish to take this opportunity to pay tribute to the man to whom I have special reasons to feel grateful, the man who made electroretinography for the first time feasible in this country. The Chris: of Central India as we call him, Prof. S. K. Mukherji permitted me unhindered access to the Cardiology Department with only one Cardiograph machine then. It is typically great of him because he did this knowing fully well that one electroretinogram can do more damage to the machine than a roo cardiograms. And thus the first successful electroretinogram in India was recorded on 17th September 1952. My gratefulness to the Indian Council of Medical Research is no less because it is the grants of ICMR which helped me tread the path of clectroretinography for years till I grew up with it, and today we are a founder member on the International Society, of Clinical ERG. I am particularly conscious of the help received from our colleague Dr. Sepaha and a row of research assistants ever since 1953. Unichern Laboratories gave timely help more than once.
I believe that on this occasion I am also given licence to drift away and, therefore, before I start my talk on subject proper, as an academic research worker, I may dwell for a while on the limitations, and prospects of research in this country.
Research has been described as a catalogue of mistakes, but mistakes from which we are duty bound to profit. However, to do an original and intricate research in India has its own problems to solve. Ample funds, freedom of action, availability of equipment and dependable assistant colleagues and above all peace of mind so necessary at serious research arc just the things so rarely available. More over the basic concept of research is so variedly understood that even collection of statistical data, report of a few odd clinical cases is a part of research with some. A clinical Ophthalmologist in this country as everywhere earns more than his bread and butter from cataracts alone while a research worker is always struggling with his work and his pocket. This reminds me of a story of the hen and the pig. As they were walking on the street, the hen and the pig noticed that in every luncheon room people were eating ham and eggs. The hen suggested to the pig that they both go into the business together. The pig demurred on the premise that for the hen the work was routine (to lay eggs) but for him it was a sacrifice (to provide the ham) and many people do think that the clinical worker is a lucky hen and a research worker a pig and so the paucity of research workers specially in this country. A research worker is like a philosopher who has his own accentricities and how many of us are prepared to tolerate it? An organisation like I.C.M.R. is probably the only source of inspiration to some but it has its own limitations. Tolerance, encouragement, appreciation, forbearance, envy not jealousy, facilities not obstructions, faith not doubts at our personal levels are what we can contribute by. We are after all travelers in the land of Serendipity whether our voyages take us to laboratories or to the clinic. And with that I pass on to the subject proper.
My first paper on ERG read at Aligarh probably aroused only curiosity. My second attempt at Bangalore, I thought created interest and I had hoped after the conference at Indore that I should soon be no longer alone in India to walk the path of Electro-Tetinography. The task of every research worker is to take and transmit the torch and I am still hoping that there should be many such torch bearers, ERG being within easy practicable means in any Medical College in India. I am reading this oration with a conviction that all of you are by now actively interested in the subject.
Electrical potential accompanies activity in any nervous clement, retina is no exception. The fact that the retina produces an electrical potential in response to photic stimulation, which can be detected and recorded, has been known for many years.
From the history of electroretinography it is evident how long and difficult the way was from the first recognition of retinal action currents by Holmgren (1865) till the first attempt to carry out Clinical Electro-retinography by Karpe (1947). A detailed historical review and analysis of the principles of electroretinography have been best elucidated in the Book "Sensory Mechanism of Retina" by Granit (1947). The most comprehensive treatise up-to-date is by Karpe (1945) who is the father of Clinical Electroretinography. Another very useful monogram is "O fysiologii a pathologii Lidskeho electroretinogramu" by Vanysek (1954).
| Electroretinogram|| |
An clectroretinogram is the resultant record of an electrical potential developed from the retina and produced as a result of stimulation by a flash or flashes of light, and is a composite response of the retina as a whole. It is the summation result of two opposite potentials, the small initial negative and the big positive, with a few after effects.
A Diagramatic representation is shown below:
It is called a SCOTOPIC ELECTRORETINOGRAM when recorded from a dark adapted eye, the retina being stimulated with illuminations of 80 lux the stimulii being repeated at an interval of 15 seconds. In the scotopic electroretinogram the negative a-wave is usually obscured by the main positive b-wave and the stimulii of short illumination used, do not permit the development of d-wave. A scotopic electroretinogram is thus measured in terms of the height of b-wave which represents the functioning capacity of the rod system of the retina as a whole. In human studies, scotopic electroretinography has been widely practised in conditions like Vitamin-A deficiency, retinitis pigmentosa and allied diseases and detachment of retina. All of my work so far is on scotopic electroretinography.
PHOTOPIC ELECTRORETINOGRAM is a record from a moderately light adapted retina stimulated by an intense flash stimulus, the initial light adaptation avoiding the rod response element of the electroretinogram. A distinctly prominent a-wave is found in 72% of photopic electroretinograms (Vanysek.) The main positive x-wave corresponding to the b-wave of a scotopic electroretinogram is of a relatively smaller amplitude, which could be explained by the smaller number of cones in the retina as compared to the number of rod cells, an electroretinogram after all, being the summation response of the retinal elements.
Photopic electroretinography can also be studied by colour stimulii e.g. the red colour to which the cone system of the human retina is most sensitive. This SPECTRO-ELECTRORETINOGRAPHY completely excludes the response from the rod cells and thus it may become a useful tool in electroretinography hitherto not covered by those who have adopted the Karpe method.
In contrast to the above described single flash records, another intricate method and more accurate in its results, is what is called FLICKER ELECTRORETINO GRAPHY. Adrian (1945) first practised flicker electroretinography on normal subjects. Flicker electroretinography will be particularly useful for cone function test. Wadensten (1956) has observed that flicker ERG may be distinctly altered even though the single flash photopic ERG be quite normal.
As to the origin of this electrical potential, Granit has suggested the origin of the negative part of the ERG in the conducting layer of retina and that of the positive part in the bipolar cell layer. These observations are however, still in a hypothetical stage.
| Method of Recording|| |
I presume that having yourself seen the actual procedure at the time of Indore Conference it is no longer a matter of curiosity for most of you. To be brief, therefore I shall only be content to state that the following equipment is necessary.
- A contact lens electrode for the cornea.
- An indifferent electrode for the forehead or the temple.
- An amplifier for recording the resultant potential.
- A lux-meter to standardise the illumination; and
- An adjustable source of light controlled by a timer switch.
| Amplifier|| |
The most easily available machine in India is a monobeam Unit. In fact, all my work of last 82 years has been done on a Sanborn cardiograph. The advantages of bi-beam machine like the Swedish ERG amplifier or an EEG machine is the simultaneously binocular recording which would be distinct advantage for comparative study and for recording spectro electroretinography and flicker electroretinography. To all these old techniques have been added a myriad of electronic gadgets but whichever machine is used, the principle remains the same, that the cornea is treated as positive pole and the forehead or the temple as the negative pole.
An electroretinogram can be successfully recorded in over 9o% subjects under local surface anaesthesia in most but a general anaesthesia is necessary below the age of 7 years. The picture below' will recall to you the simple procedure of recording the electroretinogram.
| Evolution of Electroretinogram|| |
The electrical response from the human retina is not fully developed at birth and remains sub-normal till the child reaches the stage of adolescence. Zetterstrom (1951) studied 30 prematurely born children and noted that electroretinogram appears after a considerable longer time than in children born at full-term and also that it is directly related to the weight of the child. The ERG is thus indicative of the maturity and development of the' infant's retina. Horsten and Winkelman (1960) on the basis of investigations in two litters of pups in relation to histological development of retina however concluded that an ERG could also be expected to be present and could be recorded with high intensity stimulii after an adequate dark adaptation even in prematurely born infants.
While studying full term new-born infants, Zetterstrom further observed that a small potential can be recorded by the third day of life. The amplitude increases and varies from .2o to .30 mV. at the age of I year. Response to flicker stimulii after infancy is however found to rise more rapidly so much so that at the age of 8 weeks it is comparable to that recorded in adults.
At the other end of the life span, ERG again tends to be subnormal even though there is no ocular pathology (Karpe 1950). This is probably due to the vascular changes in the retina leading to diminished nutrition and relative anoxoemia,
| Electroretinography in Normal Human Beings|| |
Findings reported in next table are based on studies at this ERG unit covering a large variety of normal Indians in different age groups.
Electroretinography in normal Indians in different age groups:
The height of `b' or `x'-wave representing the electrical response of the retina however varies from individual to individual within a certain range e.g., in case of adults, scotopic response from 0.25 mV. to 0.45 mV. is treated as normal ERG (Dhanda 1955) . Where the response is less than 0.25 mV, it is called a subnormal ERG and when it is more than 0.45 mV. it is called a supernormal ERG.
The next figure [Figure - 3],[Figure - 4] shows a few typical normal records.
| Clinical Electroretinography|| |
Clinical application of electroretinography is being rapidly extended into newer aspects so much so that electroretinography workers have even a passport for intrusion into the romaine of general medicine. The following is the list of conditions where electroretinography has been -considered a useful clinical tool in the diagnositic and prognostic aids to ophthalmology.
- vitamin A deficiency and xerosis.
- retinitis pigmentosa and allied diseases e.g.
(a) Congenital Night Blindness.
(b) Oguchi's Disease.
(c) Retinitis punctate albicans.
- detachment of retina.
- systematic and retinal vascular conditions.
- macular disease,
I shall now discuss important observations on scotopic electroretinography in some of these conditions.
| Vitamin-A Deficiency|| |
Why this subject was the first to he taken up for electroretinography, specially in a country like India, should be easy to understand. Electroretinography has been studied in cases of xerosis, night-blindness and keratomalacia. During these investigations, simultaneous estimation of vitamin-A by antimonytrichloride method was also done and has helped fresh orientation of this deficiency syndrome, Dhanda (1955).
(a) E. R. G. in cases of xerosis alone:- 41 eyes of 28 cases of xerosis were studied in detail and [Table - 2] below gives a summary of observations. The figures in brackets indicate findings in normals of similar age groups
The average b-potential of 16 eyes of II adults with very good co-operation and xerotic patches of more than mm. in diameter was 0.290 mV., the average vitamin-A content of 8 of these persons being 103 I. U . per 100 c.c. of plasma.
The average b-potential of 25 eyes of 17 children below the age of 15 years, again with the same grade of xerosis, was however 0.201, mV., the average vitamin-A content being 28 I.U. per 100 c.c. of plasma. Under the age of 7 years, the ERG was extinguished in 5.
A nearly normal electroretinograrn in adults with xerosis alone, is an interesting finding. The interest is fur. ther heightened by a normal content of vitamin-A of the blood, in such cases. This raises a pertinent question whether a primary xerosis in the absence of any other conjunctival pathology is a direct result of Vitamin-A deficiency or some other indirect manifestation. This mystery, is further heightened by poor response of xerotic patches in adults to vitamin-A administration. For example in a 2o-year-old person who had typical Bitot's spots for three years and had taken 6o injections of Massive-A (Unichem), the xerotic patch remained unchanged. Interestingly enough his ERG was also normal.
In children however, xerosis, if untreated, soon results in night blindness. But so long as there is no nightblindness, the b-potential and the vitamin-A content are only slightly subnormal-Dhanda 4956).
Some typical ERGS in xerosis are shown below [Figure - 5].
(b) ERG in xerosis with night blindness:-[Table - 3] below, summarises the results of studies in 6o eyes of patients of xerosis with night blindness.
Of the 19 eyes of patients above the age of 15 yrs. the electroretinogram was completely extinguished in 13; 5 eyes had a potential of less than 0.05 mV., and only one eye had a potential of 0.125 mV. The group had an average Vitamin-A content of 33 i.u. / 100 c.c. plasma.
Among the children night blindness associated with xerosis is a very common clinical feature. Of the to eyes of six children between the ages of 7-15 years, the electroretinogram was completely extinguished in all except three and even these had b-potentials of 0.058, 0.065 and 0.10 mV. only. While 30 eyes of those below the age of 7 years, the electroretinogram was completely extinguished in all but 3, the b-potential of these 3 being below 0.05 mV. The average vitamin-A content done in 14 of these children was 15 LU. per 100 c.c. In one child (D.B.), 10 years of age, with xerosis and night blindness, chemical analysis revealed complete absence of vitamin-A in the blood.
In general therefore, either the electroretinogram teas extinguished or the b-potential was extremely small. Treatment of these children resulted in rapid disappearance of night blindness while the return of the clectroretinogram to normal was comparatively slower, xerotic patches taking still longer to disappear.
Tracings above show some typical case records of cases of xerosis with night blindness before and after treatment.
During the development of vitamin-A deficiency syndrome a stage must come when three things happen simultaneously. The patient develops night blindness, the ERG get-, suddenly and completely extinguished and the vitamin-A level in blood falls to an absolute minimum threshold, On the basis of Biochemical analysis of blood at this stage, it is suggested that this threshold level of vitamin-A in blood must be very low indeed, and has been found to be about 20 i.u./100 c.c. plasma in children and a little higher in adults.
To explain the relation of xerosis and night blindness to vitamin-A dificiency, I suggest that vitamin-A deficiency affects two distinct groups of epithelial structures at different stages. One stage mainly affects the surface: ' ectoderma-causing Xerosis-conjunctive, keratomalacia and dermatosis while a different aspect of vitamin-A deficiency affects the neural ectoderm causing night blindness. The former is further supported by the ERGS of extreme dcficiency cases, of keratomalacia shown in the figure, [Figure - 7] in both of which a good electrical retinal potential has been recorded.
May I therefore suggest that xerosis is not a direct result of vitamin A deficiency but is probably an indirect manifestation of an intermediate factor, the deficiency of which upsets the metabolism or utilisation of vitamin-A. The specific nature of this however cannot be deducted from these investigations but it certainly opens up a new field of biochemical research of an interesting nature.
Incidentally these investigations also throw an interesting light on the pathogenesis of night blindness. The degeneration of the retina as a whole in retinitis pigmentosa, resulting in an extinguished electroretinogram, is too well known. However, observations submitted above show that an electroretinogram can be completely extinguished even though the retina may be structurally normal, and only functionally affected as in the case of vitamin-A deficiency. That structural changes in the retina are not necessary for an electroretinogram to be extinguished is also proved by the observation that a retina which has lost its electric response completely may regain fully under treatment with vitamin-A. This leads to the conclusion that no organic change is necessary for the electroretinogram to be extinguished and that an electrorctinogram represents the functioning capacity of the retina, rather than being related to its structural pathology.
| Retinitis Pigmentosa and Allied Conditions|| |
The early and complete extinction of electroretinogram in retinitis Pigmentosa (Karpe 1947) has become an established diagnostic feature. This in fact was the first proved clinical application of scotopic electroretinography by Karpe's method. This should be easy to understand because retinitis pigmentosa is a generalised pathology selectively of the rod system of the retina and it is these cells which are selectively and primarily affected in this disease. Riggs (1954) reported complete absence of the response in cases of congenital night blindness, again for the same reasons. Krill & L har (1959) further emphasised the value of ERG in pigmentary degeneration. They reported extinguished records in 16 out of 19 cases of primary pigmentary degeneration but found normal or moderately subnormal patterns in 10 cases of secondary pigmentary degeneration. 18 cases of retinitis Pigmentosa have been studied at this electroretinographv unit. An early and completely extinguished response in cases of primary pigmentary degeneration of retina as compared to cases of chorioretinitis with a subnormal but distinctly present b-pot, is a significant observation. I suggest that scotopic eiectroretinography could be a method of very important differential diagnosis in such cases where clinically it may otherwise be difficult to do so.
The ERG below of cases of Primary Retinitis Pigmentosa and Secondary Chorioretinitis are typical of the series.
| Cataract|| |
In my studies, 56 eyes with different grades of lens opacity were investigated by electroretinography and [Table - 4] gives a summary of the observations in comparison with the findings in normal Indians of similar age groups.
The average b-potential of 30 eyes with mature cataract was 0.260 mV. and in 26 eyes with immature cataract, the average b-potential was 0.262 mV. as compared to .290 mV. in normals above the age of 40 years.
This suggests that b-potential may be reduced by the formation of cataract but more important to note is that a good amount of electric potential can be recorded in cases of mature cataract where the vision is reduced to hardly hand movement. This implies that even a very small amount of light passing through a nearly opaque lens and the spongy iris is enough to bring the retina to appreciable activity.
It is possible to assess the prognosis in most cases of cataract. Every one of us is however. conscious of the pitfalls. Ophthalmologists have therefore long sought more accurate means of testing retinal function specially in the presence of opaque media.
That electroretinography could be a means of determining the prognosis in doubtful cases is proved by the following interesting observations :
An extinguished electroretinogram in an eve with mature cataract was noted. The cataract was removed and a detachment of retina was discovered, which explained the loss of electrical response (the other eye was normal with b-pot. of 3o mV.) Another case with mature cataract with good perception and projection of light had extinguished electroretinogram. Secondary Retinitis Pigmentosa was discovered after cataract extraction and this further proves the prognostic utility of erectroretinography. In either case, an extinguished ERG was the only preoperative guide to poor prognosis.
| Glaucoma|| |
Glaucoma is another condition where Electroretinography may help in the explanation of those aspects of pathology, which it has still not been possible to understand and may also contribute towards the assessment of prognosis in certain circumstances. Venysek studied 35 Glaucomatous eyes and observed normal ERG in 24%, subnormal in 70% and supernormal in 6%. My studies of Glaucomatous eves comprised 45 cases, 19 with chronic Glaucoma, 5 with secondary Glaucoma and 21 of absolute Glaucoma. The next table gives the electrical response in relation to the degree of tension and the type of Glaucoma.
The presence of 0.218 mV. as the b-pot. in 19 cases of Chronic Glaucoma out of which all except one had a vision less than 6/6o and a fair amount to the extent of .135 mV. even in cases of Absolute Glaucoma with not even perception of light, is certainly an objective confirmation that loss of vision in Glaucoma is mainly due to the effect of raised tension directly on optic nerve rather than on retina. It is however not conceivable that pressure ranges between 50 & 90 mm. of Hg. would not impair the retinal function. Although the visual loss is due to the nerve head pressure, the subnormal character of ERG is retinal in origin. If that were not so, ERG should have remained unaffected. This is further supported by the commonly associated symptom of defective dark adaptation in early cases of Glaucoma which is again due to retinal dysfunction. It is. at the same time evident from the fair amount of electrical potential reported above that retina can stand prolonged and marked effect of raised intraocular tension and the bipolar cells of retina from which the + ve part of elect roretinogram is presumed to arise can continue to produce the electrical potential. Following typical case records will I am sure make it clearer.
| Detachment of Retina|| |
Jacobson (1958) and others have emphasised the utility of ERG as a prognostic aid more from the functional point of view than anatomical because in their investigations of 50 cases they have observed that in a case with subnormal preoperative ERG visual return cannot be more than 20/200 (6/6o) even though the retina may be completely reattached. Randhal (1957) also confirms the preoperative prognostic utility of electroretinography in detachment of retina. On the basis of study of 100 cases Karpe (1952) pointed out the significance of the subnormal response occasionally recorded in the other eye in which there was no detachment suggested predisposition to retinal detachment. I have studied II cases of primary detachment by scotopic electroretinography, and the above tracings show some typical records. [Figure - 10].
An ERG being the summation and composite response of retina as a whole, it is evident that the electrical response of such a retina would be directly proportional to the amount and duration of detachment and the functioning vitality of the retina. Electroretinography is thus the only dependable preoperative guide as to the postoperative prognosis in a particular case of detachment of retina.
| Systemic & Retinal Vascular Conditions|| |
That the blood circulation in the eye is of decisive importance for the type and the shape of the electroretinogram, has been established ever since physiologists started to record and study the action, potentials of retina.
Occlusion of the arterial blood flow has been used by Granit (1933) as a means of study of the components of the electroretinogram, Henken (1954) was the first to publish and report consistant and interesting changes in ERG by bringing about sudden and marked changes in blood pressure in animals.
An electroretinogram after all represents the functioning capacity of the retina as a whole and any local vascular disturbance may have a profound effect on this electrical potential. Similarly systemic vascular hypertension associated with arterial attenuation and consequent anoxacmic condition of the retina may thus appreciably alter the electroretinogram. I therefore, undertook this newer aspect of clinical electroretinography with the purpose to study ERG changes in benign and malignant hypertension and if possible to diagnose subclinical malignant hypertension or in other words to try to detect as to which cases of benign malignant hypertension before retinopathy has become clinically apparent hypertension are likely to go on to or before gross biochemcal changes in blood have taken place.
Till the time of writing this paper, 61 cases of benign hypertension and r6 cases of malignant hypertension have been studied. All cases with grade IV retinopathy have been labelled, as malignant hypertension and grade I, II and III as benign hypertension
The first significant observation which is quite apparent from this table is the increasing number of subnormal responses as the gravity of hypertension increases on the basis of the grades of retinopathy. While in a series of 64 normals of comparable age the b-pot. was subnormal only in 250, the percentage in hypertension cases increased from 56% to 6% in the first three grades of benign hypertension and it rapidly increased to 75% in cases of malignant hypertension. More than double the incidence of subnormal response even in benign grades of hypertension is highly suggestive of the anoxemic condition of the retina. Follow up of these cases during the last 5 years has provided some very interesting information. Of the 26 cases of benign hypertension with normal or supernormal ERG, only one is reported to have died while others improved with treatment. On the other hand among the other 35 cases out of 61 with subnormal ERG, 9 who could be followed up reported no improvement. 4 are known to have died during this follow up period. One of these cases is pointedly interesting indeed. Mr. G. age 4o yrs. male with 13. P. 220/140 Retinopathy grade-I. Blood urea 24 mg. First ERG recorded on 23-3-6o the response was 282 mV. The second ERG on 19-5-6o, the b-potential fell down to 123 mV. and the patient died on 26-5-60, so that a falling b-potential could be of serious prognostic value.
Of the 16 cases of malignant hypertension, all except 3 had markedly subnormal ERG, 10 of the 13 cases with subnormal ERG are known to have died during the follow-up period. Of the 3 cases with a normal or supernormal ERG, S. R. 43 years male. Blood urea 25 mg. B.P. 220/140 grade IV retinopathly. The b-pot. at the first examination. 480 fell down to .287 three months later and the patient died another month after wards. Similarly L.B. 30 years, female on first examination had B.P. 240/140. Blood urea 22 mg. retinopathy grade II but the b-potential was only .095 mV. Re-examination 4 months later, the blood urea rose to 8o mg., retinopathv grade III and b-potential was .065 mV. and a third examination on 21-6-58 the retinopathv changed to grade IV and b-potential .069 mV. So that at the first examination except the markedly subnormal ERG there was no other clinical evidence of seriousness of the disease.
These individual cases and the group of others with subnormal ERG might therefore be the cases of subclinical malignant hypertension. If that be true it is highly indicative that a subnormal ERG in an otherwise clinically benign hypertension is suggestive of oncoming malignancy.
These comments however carry such a great responsibility that I am anxious to continue the follow up further so that by the time of International Congress in Delhi I may be able to produce more concrete evidence.
| Malingering|| |
On the basis of what has already been said a complete extinction of a scotopic ERG in cases of night blindness and an equally complete absence of response to colour stimuli in cases of colour blindness can be a dependable and valuable objective test for detecting malingerers who feign the symptoms of total colour blindness or night blindness. It is precisely in such patients with a normal fundus and functional complaints that the electroretinogram is of a major diagnostic value.
| Macular Diseases|| |
I am reminded of a query 3 years back by Professor Tulsidas if electroretinography could help in detecting senile macular disease so commonly associated with cataract and equally commonly unpredictable because neither a peep into the fundus is possible nor the pupillary reaction a dependable guide in these cases. I may not have had an answer to Prof Tulsidas then but the very fact that I have something to say now is an ample indication of the rapid progress of electroretinography in recent times. It would be apparent that the scotopic electroretinogram as practised by Karpe and by me will not be adequately indicative of the extent of macular diseases which is predominently a cone pathology rather than a rod. A case of extensive macular disease with gross visual disability but a good electrical response will be seen in the last figure. Although a photopic electroretinogram may be a more dependable macular function test, it should again be realised that these cones in this area are only a small fraction of a total of 7 million cones distributed all over the retina, so that even a gross macular damage may detract only a few microvolts from the total photopic response of the retina as a whole.
Flicker sensation and colour perception being the special functions of the macular area, Flicker electroretinography and spectro-stimulus electroretinography have been studied on patients of macular disease with more dependable results. Jacobson and others (1956) using red light stimulus in single flash photopic electroretinography in 24 cases of senile macular degeneration invarably found extinguished response to red stimulus even though white light stimulus resulted in an amplitude of appreciable size in most of cases. Goodman and Iser (Y956) in their observations with flicker electroretinography have also reported distinctly subnormal results with red stimulus as compared to white stimulus in the practice of flicker electroretinography. Red stimulus photopic ERG and flicker electroretinography are therefore suggested as possible tests for macular function in cases of cataract.
| Miscellaneous|| |
Having discussed the material of investigations of a few selected groups of ophthalmic diseases studied at this ERG Unit, I shall now present to you an assortment of miscellaneous conditions which were incidentally studied by electroretinography during the 8½ years of the working of this electroretinography unit at the M. G. M. Medical College, Indore. I am presenting the assortment because electroretinography has to go a long way not only in ophthalmology but even in neuromedicine. Some results are interesting indeed and I shall refer to them as I show to you the slides of the following conditions.
- Amblyopia:-R. S. 20 Yrs. (m) with good vision in right eye and established amblyopia due to high myopia in left eye had an average b.-pot of 190mV. in the amblyopic eye as compared to .300mV. in better eye suggesting that the subnormal response is due to impaired functioning of retina.
- Embolism Central Retinal Artery:- J. B. 23 Yrs. (f) ERG was recorded 48 hours after attack of Embolism Central Retinal Artery right eye with not even perception of light vision. A supernormal ERG response of o.50 mV. is suggestive that the retinal elements function was in unstable stage. The response a week later however became subnormal, i.e. .150mV. If further follow up had been possible, one would expect even an extinguished ERG at still later stage.
- Primary Optic Atrophy :- NE. C.L. 25 Yrs., (male), the vision was reduced to perception of light in both eyes. A good electrical response of .25mV. is clearly suggestive that function can continue even when the conducting nural element is in a degenerative stage, both being presumably independent of each other.
- Optic Neuritis:- E. 19 Yrs. old girl was a very interesting case who came to us with a typical optic neuritis, vision reduced in both eyes to finger counting two feet. An ERG showed a b-pot. of .200mV. The vision after treatment improved to 6/9 both eyes and the b-pot. at this stage was .225mV. This again indicates the functioning independence of the cellular and. conducting elements of the visual pathways.
And now before I end, I must submit that as means of clinical investigations, ELECTRORETINOGRAPHY HAS ITS OWN LIMITATIONS too e.g., it is not possible to record the potential from any particular area of the retina. It is also not possible to determine which particular layer of retina is affected. The variability in the resultant response is another major handicap. Different potentials have been recorded from the same patient, same eye and from the same sitting of examination and that is why it is best to take into consideration at least ro to 12 records in determining the average electrical response of the retina. Serious difficulty may arise from the false potentials which may distort the electroretinogram. These false potentials may be caused by blinks, by eye movements, by loose contacts, by emotion, by defect in equipment and even by electrical disturbances from beyond the examination room. It should be appreciated that no single method of recording is without its drawbacks. I venture to say that electroretinographic examinations of pathological states of the eye cannot be confined to a single record or a single method but should include results obtained under various conditions of adaptation and various techniques of stimulation. Only in this way will it be possible to take into account all the complicated laws of retinal activities.
It would thus appear that to study the physiology and pathology of electroretinography in even greater details we may have to specialise in the speciality of electroretinography. This wider conception of the pathology of electroretinogram may lead to the recognition of many aspects which arc at present still unknown or not clearly understood.
A comprehensive study of an eye by electroretinography could therefore include, the following methods of examinations:
i) recording of a scotopic electroretinogram after 5 minutes and 30 minutes dark adaptation.
ii) recording a single flash photopic electroretinogram with white and red light stimulii.
iii) recording the reaction of retina to flicker stimulation again with white and red stimulii and
iv) determining the flicker fusion frequency.
Though I have devoted much time and considerable efforts to this work till the conclusion of this report, I am aware of still being at the very begining, I have to admit that much of what seems to be clear might be everted and much will have to be explained. My enthusiasm should not cloud your vision because I am seeing electroretinography through glasses more deeply tinted than even the ones used by Professor Cooper four years ago. The biggest reward of my efforts would be the springing up of more and more centres of electroretinography in India and nobody will be more happy than me to see my observations improved upon or even proved wring because 'science, like life, is ever changing and ever advancing.
| Summary|| |
- The Physiological aspects of Electroretinography are discussed.
- ERG response in normal Indians of different age groups is reported.
- Results of ERG studies in different clinical conditions have been studied and reported.
- Utility of ERG as diagnostic and prognostic aid in Ophthalmology has been discussed and emphasised.
| References|| |
Adrian, E. D. (1945) J. of Physiol. 104, 84.
Dhanda, R. P. (1955) J.I.M.A. 25, 396.
Dhanda, R. P. (1955) A.M.A. Arch. Ophth. 54, 841.
Dhanda, R. P. (1956) I.J. Ped. 23, 349.
Goodman & Iser. (1956) Am. J. Ophth. 42, 212.
Granit, R. (1947)-''Sensory mechanism of the Retina" Oxford Univ. Press pub. : 1-191.
Horsten, G. P. & Winkelman, J.E. (1960) A.M.A. Arch. Ophth. 63, 232.
Henkes, H.E. (1954) A.M.A. Arch. Ophth. 51, 42.
Holmgren, F. (1865) Upsala Lak Foren Forh, 1, 177.
Jacobson, J. H.; Basar, D.; Kornzweig, A. L.; (1959) Ana. J. Ophth. 42, 199.
Jacobson, J. H.; Basar, D.; Carrol, J.; Stephens, G.; and Safir, A.; (1958) A.M.A. Arch. Ophth 59, 515.
Karpe, G. (1947) Acta. Ophth. Suppl. 24, 1-116
Karpe, G. (1950) Acta. Ophth. 28, 301.
Karpe, G. (1951) Acta. Ophth. 29, 113.
Karpe, G. and Randahl, I. (1952) Acta. Ophth. 30, 303.
Krill, A. E. & Iser. G. (1959) Am. J. Ophth. 47, 649.
Randhal, I. (1957) A.M.A. Arch. 0phth. 57, 566.
Riggs, L. A. (1954) Am. J. Ophth. 38, 70.
Vanysek, M, J. (1954)-"O fysiologii a pathologic lidskeho electroretinogram"-Nase Vojsko pub.-1-211.
Wadensten, L, (1956) Acta, Ophth. 34, 311.
Zettcrstrom, B. (1951) Acta. Ophth. 29, 295.
[Figure - 1], [Figure - 2], [Figure - 3], [Figure - 4], [Figure - 5], [Figure - 6], [Figure - 7], [Figure - 8], [Figure - 9], [Figure - 10], [Figure - 11]
[Table - 1], [Table - 2], [Table - 3], [Table - 4], [Table - 5], [Table - 6]