 Over the next week or so, I'm going to talk about electrophysiology. I'm going to start today with electro-rhythmograms and electro-ocular grams if we get that far. Well, since 1791, they've known that electricity was involved in bodily function and really in the last 150 years or so ago, starting about 1850, they started to develop the membrane theory and that the electrophysiology and chemical exchange across membranes were the basis of function. But as far as functional practical use in allophthalmology, the use of electro-rhythmograms, eye-electricity, well, electro-ocular grams dates to about 1960 for first publications, but for electro-rhythmograms, really just in my lifetime, the last 70 years or so, and basically with the advent of computers. Some pioneers were using electrophysiology in the late 1940s and 1950s, but the common use of electrophysiology dates to the 1960s when you could actually buy computers. Since 1865, we've known the basic waves involved in electro-rhythmogram, which that sheet I passed out summarizes the basics of the electro-rhythmogram. One of the most common questions is, what are the basis of the A in the B waves? As I mentioned a minute ago, the standard ERG has just been in the last 20 or 30 years. This is the basic ERG. Whenever you have a brief change of illumination, such as having your photo taken with a flash, you get an electro-rhythmogram similar to the handout like pictured in this slide. The rods and cones respond to the flash of light, producing a response that is initiated in 18 nanoseconds, followed by a approximately twice as big B wave, which reflects the mid-retina, a combination of all of the contributions from the mid-retina, the biggest cell of which is the Mueller cell, but it's a combination of the Mueller cells, the horizontal cells, the amicron cells, the glial cells. It's a combination of all of them, and if you mess with any of them, you're going to affect the B wave. There are approximately 35 known transmitters in the retina, and you mess with any of them, so it really is an extension to the brain, because you mess with any of those chemicals due to, say, just a whole-body metabolic disturbance, particularly if it involves the liver, you're going to see changes in the electro-rhythmogram. Again, A wave, initial negativity, B wave, the following positivity, and the C wave, a slow positive wave generated by the pigment epithelium. Very few labs use anything but the A wave and the B wave. The C wave is not as reliable in diseases and so just labs that specialize in the C wave use it clinically. This was drawn by me at my desk with a pen about 40 years ago, where it's really an impossible wave, but it shows all of the possible components except for the early receptor component. So if you have a light that's not a flash but stays on for a while, you get initially the A and the B wave, and then the slow C wave, and then when the light goes off, you get the off wave and the D wave. As I said, only the first components are evaluated 99% of the time in the clinical electrophysiology. Ragnar Granit won Nobel Prize in Physiology in 1967 for isolating the different functions of the of the electro-rhythmogram. This is repetitive with the earlier slide. The early receptor potential is a potential that can be recorded that appears and is over in the first two milliseconds. So if you looked at the very early first two milliseconds when a flash of light goes off, you get an early receptor potential. These also are not used commonly clinically because they're not reliable in what you record and are difficult to apply clinically. Also, you can't use a metal to record these because the responses occur so quickly that with a flash of light you get a photovoltaic effect with if metals involved in the recording from the eye. I'll show you later the kind of electrodes you have to use for that. A wave, B wave. We know the origin of these, which I've already alluded to. The origin of the A wave, this is an early drawing from Helga Kolb, which she's the originator and chief editor of WebVision. If you guys didn't know that, do most of you know who Helga Kolb is? No? She's an emeritus here. You what? Where did you see her? At her house. Oh, what she did. She's responsible for the. She was somewhat offended. Oh, yeah. Well, rightfully so, really, that if you're in ophthalmology, Helga Kolb received emeritus awards from the Academy of Ophthalmology and from our vote. She's responsible for the microanatomy of most of the mid-retinal cells. And also when she was about 21 years old or 20 years old, she was a co-author of the first EOG paper with Arden in London. So she's got a long history. The origin of the B wave then is the next step, first rods and cones. And then the mid-retina, this proceeds into the mid-retina. And again, as I mentioned earlier, the mid-retina B wave is a combination of all of these cells, commonly used in the United States, although people are starting to skew towards using disposable electrodes where it's required in some countries, such as Great Britain, since the transmission of Kreuzfeld-Yakov disease, Med-Cal, about, wow, how long has it been ago now? 17, 18 years ago. Since that occurred, Great Britain doesn't allow you to reuse anything because of what I consider paranoia. But they don't use anything but disposable. So they don't use speculum contacts like I use here that we clean. I use the Burian speculum contact lens when I can. And little kids and in the OR and small eyes, I have to use others that I'll show you. This was invented at the University of Iowa in the early 50s by an ophthalmologist named Burian and a technician named Hanson. And the third generation of the Hansons are still making all of these for the world. It takes about six months to two years to get one. Two people make them by hand for the world. And I've known all three generations because I'm older than dirt. I started with grandpa that started the company in the 60s. And he died of old age. And then I went through the whole career of his son who was about my age and retired. And now I'm in the grandson who's in his mid-30s to 40. These are other kinds that are used around the world commonly. The upper left one is called the ERG jet. And it's a plano lens about 10 millimeters in diameter with a gold foil that touches the corny and picks up the electrical signal. On the right is one invented by Arden in London that's a piece of cassette tape with gold foil on one side. And you have droops in the lower lid and then you tape it to, you can see the piece of tape. Do I have a pointer? No, sorry. Piece of tape to the skin. I also occasionally have to use these in the operating room when there's severe trauma cases. And you can only get the eye open a millimeter or two and just barely get the eye open and stick it in there. Or in microphthalmia, the same when there's almost no eye, I'll just put it in there and then use a lot of BSS, balanced salt solution to help with the conduction. The lower left one is a carbon filament. You can't really see that you're also similar to the upper right and the lower right. You just pull out the lens and it's a carbon filament. It looks like a piece of black thread. The first of the time I got one, I thought it was a defect and I tried to pull it off. Like a thread they hadn't removed, like a piece of clothing that had an extra thread and that. But it's a carbon filament, not even an inch long. And occasionally I've used these for the same reason in extreme trauma cases, cases that are microphthalmia. Commonly used around the world now in disposables, the lower right one, it's called a DTL. It has these self adhering spots that are about the size of a dime. And between the two, there's a silver thread that's actually five strands that the total diameter is less than a human hair. And I use these on kids if they're below about nine or so just for comfort and occasionally also in trauma cases they're small eyes. So you just numb the eye, stick one on and then have them open widely and droop it in the lower lid. And the first time they blink, it goes to the lower lid margin. So why not use these all the time? They're noisy. Any kind of blink produces more muscle artifact than you're recording from the eye. So you have to record and throw away ERGs, record, throw away, record, throw away because if they blink while it's going off in the first 10th of a second or so you get more muscle artifact than the ERG. So they don't give you as cleaner response but I can see the day where everything will go to recording with only disposable. It's the price is the killer because even these others cost 10 to $15 a piece. So every testing you're throwing in the trash an hour later, 10 or $15. And like particularly with the DTL, if you screw up at all and like get a fold in the silver thread, don't keep it taut or it actually, it touches one of those self adhering little things, it's ruined. And you just take like taking a $10 bell out of your pocket and throw it in the trash. And no matter how good you are, that happens. Patients move, their eyelid catches it and it twists and stuff. Whereas the speculum, they cost now $1,200 a piece. But I have some I've used for 30 years. And way short of a year, you'll pay for one of those if you're throwing away or using $20 to $30 worth with every patient. And we do here 500 or more patients a year through the years. I've lost count. I don't know how many I've done, but somewhere in the 40, 50,000 patients through the years. So these are some of the types of disposable. Let's move on to important stuff. ERG jet, DTL silver, ardent gold foil. Until 30 years ago, most people used strobe lamps. This is the old strobe lamp that the similar models they use now in EEG recording for photic driving. And this is what I was trained to use 50 years ago. Patients were tested on an examining table lying down. And on an articulated arm was this strobe lamp and you would place it a measured distance from the eyes. And then for colors you would put filters over it. And this is how they were done. But now since the mid 80s, about 82, 84, you've been able to buy what they're called Gansfelds. Let's see if I've got one coming up here. A Gansfeld looks like a field machine. And Gansfeld is a German word that means whole field. So the patient sits with the chin and the chin rest, sometimes use the forehead bar, sometimes not. It's just important the face stays vertical. This is a really old model. I was the beta sight for this company and the serial number was 0002. It was the first one they let out of their R&D here. I had it for years and years. I got this about 1980. The modern version of these instead of strobe flashes are what these had was in the top of them, it had strobes. And how it changed colors was a filter tray would move on command so that a blue filter would be placed in front of the strobe or a red filter or no filter or dimming filters. And that's how it worked. The modern ones that have existed about the last 12, 15 years, they're smaller. And also the flashes are produced by LEDs. So there's unlimited colors. You can produce as many colors as the TV can produce. Photopic is the secret medical term for light. And scotopic, the secret medical term for dark. And these equate to cones and rods. Separating rod and cone function by manipulating level of light adaptation, stimulus rate, stimulus intensity and color, you can pretty well separate rods and cones. A question, by the way, once things come up, if anybody sees that I've seen this question on a board question, remind me so that I can make sure and include it. In this is a question. Why is it that only cones can go fast? What is it about 30 Hertz? Y'all know that one? Only cones, like the old neuron function of relative refractory period, how fast can a neuron recover before it can re-fire? Only cones can recover quickly. They're not as sensitive, but they're faster and they recover more quickly. Rods cannot follow a flicker any faster at best to about 15 to 18 per second. It's as quick as it can recover. A healthy retina cones can respond and re-fire up to 80 100 per second because 30 per second is well above the threshold for rods commonly and in the international protocol, labs around the world use 30 Hertz. So if an eye can follow a 30 per second flicker, you know that as a group, the cones are healthy. You cannot use this to detect the X-linked male color blindness, but it's useful to detect cone dystrophies, cone rod dystrophies, et cetera. That is a question you'll see sometime. What is it about them? Wow, they can source, one of the reasons is they can source the chemicals multiple ways whereas rods can't. And I don't know the complete answer without researching it myself. One of the billions of things I've forgotten through the years. Along with the cell death that's going on rampantly right now, that you guys will be able to identify with in 40 years. You won't like it, believe me, you won't like it. I could think a decade ago. Also, stimulus intensity because there's about a three log difference between rods and cones insensitivity. Rods are three logs, a thousand fold more sensitive than cones. And then you can add to this dark and light adapting the patient. This is the summary of peak rod sensitivity and peak cone sensitivity if you grouped all three of the kinds of cones together. What color would you end up with? Tennis ball yellow, it's not an accident. Tennis ball yellow was not just a color people liked. It is the peak sensitivity of your cones combined in a daylight situation. It's the color the human eye can see best in daylight. Rods are not black, white receptors. They peak at 510 nanometers, which is a bluish green color. It's a color, not black, white. So if you use deep red filters, these numbers are based on a Kodak filter series called RATAM, W-R-A-T-T-E-N. They're filters you can buy from Kodak that are specifically certain color transmission. And in the olden days before LEDs, this is how what filters were added to the strobe flashes to produce the reds and the blues. So if you use a very deep red, a RATAM 26, it just nicks the cones. And if you use a dark blue, this 47 series, it just nicks the rod. So if you use these dimly, you can pretty much isolate rod and cone function. So when I test a patient, I start off with a really dim blue after 30 minutes dark adaptation. Then the next one is a really dim red. And then I move to the white flashes, dim getting brighter, which is the international protocol. Unfortunately, the international quote protocol does not include the blue and the red, even though it's quote recommended. A survey a year or so ago showed that less than 20% of the major labs in the world use the colored filters. They're missing a whole bunch of stuff. When you use different colors in light and dark, you get different looking responses. That's because by manipulating light and dark adaptation and the colors you use, you're gonna produce stimulation of different populations of cells. So if you use a bright white and a light adapted person in the upper left, you'll get a response that's fast, but not very big in amplitude. If you use the same flash in the dark upper right, you get a response that is slower, just look across time, but in true amplification, the one on the upper right is double or triple the size of the one on the left. If you isolate with a really dim blue response, you get a response that looks like on the lower left and then on the right, the scotopic red 30 minutes dark adaptation and dim red. The little quote BX that's halfway up the red response is a miniature version of the upper left response. You're getting just a tickle of your cones. When I'm recording a patient, I do the first one and then I do the second one. If the red one looks like the blue one, I say, how's your color vision? And they almost always say, not very good. Because if that little BX is missing, that little just tickle of the rod of the cones, then this is an early indication that you'll further evaluate later in the procedure. This is a 30 Hertz flicker. It's just two traces superimposed. That's the 10th of a second. In the normal eye, you get following like this. If it's nearly flat or very small in amplitude, this is associated with cone dystrophies and cone rod dystrophies. Acceleratory potentials are isolated from the responses by changing the filters that you use. It's a burst of four waves between about 17 and 42 milliseconds after the flash. If you go back and look at these, see the little oscillations on the ascending B wave on the top two traces? Those are the oscillatory potentials and you can isolate them by changing the filter settings. Oscillatory potentials are most associated with vascular disorders. So if you test a person at the right stage in diabetic retinopathy, you will get completely normal looking responses for everything but the oscillatory potentials because they're very sensitive to the vascular leaks that you get, for example. But also these will disappear in arterial or venous when the blood flow is compromised from the retina. Not used by everybody also. Development of the ERG. ERGs can be small the first couple of months, but generally most of you or all of you have been in the OR with me at primary. Basically, if they're old enough to be in the OR, the ERGs look like an adult ERG. How old is that? Well, that's what, well just, my record is a one day old that I've recorded ERGs from but mostly the kids are like the ones you would see Hoffman or the people see. They're usually at least a few months old unless they're born with cataracts like an old dog or something like that and there's a reason to examine them very early. As the bottom says, they can be small but you generally in a full term infant in the first couple of months it just looks normal. The voltages are normal, everything is normal. Anesthetic effects. Talking about the OR is that you need to work with the anesthesiologist, those that have been there with me have heard me say to the anesthesiologist, light anesthesia. The retina is pretty resistant to anesthesia because it's a very old, multi-million year old system but if you're doing also visually evoked potentials which I'll talk about next time which are not resistant because of they come from the cortex it's important you keep the anesthetic level down. Do you know about the use of oral glucose or sucrose in infants? Might be useful to you sometime in your careers. A CC of glucose or sucrose to a child under about 15 or 18 months is like morphine to us. I did a study about a decade ago I was one of the centers along with Harvard Children's that was testing a food supplement in premies. And we tested these little premies I used an instrument tray with a pillow on it and my gums felt like until 90 degrees down on their face. And you'd give these little few month old kids just a shot in the cheek of this stuff and 10 minutes later they're just and you put the speculum contact in their eye and they're just, and if it wears off you give them another CC and they oh, it's like somebody's shooting up. Very few things produce extinguished electro-retinograms. Retinal aplasia, total retinal detachment, labors congenital amaurosis and really severe expression of retinitis pigmentosa. That's about it. Everything else gives you a graded response. There are disorders that the B wave is particularly sensitive to. Ex-juvenile retinoschesis, you can read through them here and at the end there, not a patient that hopefully you're gonna see many of Kreuzfeld-Jakob disease. One of the first things affected is the eye. Similar to in multiple sclerosis, often you're the first person to see an early MS patient because usually the most common site of demyelination that is clinically apparent is optic neuritis. So that they come to you first. Well, also it would not be unusual for Kreuzfeld-Jakob to be the first contact with an ophthalmologist. We followed one patient where we, I mean, degree in Warner and Katz followed one patient that came in from, and we got to follow her to the whole stages where her only symptom was a little blurriness and four months later she was dead. From just appearing, came in like one of us and over the next four months went through 25 years of dementia. As I mentioned earlier, there are about 35 chemicals in the retina that might affect retinal physiology. An unusual example is transurethral resection of the prostate. Until the last few years, the previous 50 or 60 years, the irrigating solution for removal of the prostate was glycine. It was not unusual for a patient under spinal anesthesia during the procedure to say, why'd you turn the lights off? So you're in this OR looking at the ceiling, like looking at these lights here that you can hardly see and lights out. Glycine is an inhibitory transmitter that mainly affects amicone and bipolar cells. If during the procedure it was a long procedure or it was a large prostate that had to be worked on a long time so that the person absorbed some of the glycine and it hit the eye, it was like throwing an off switch. So I hung around the OR for over a year, pre-examining and post-examining patients that were selected because of having a large prostate and found a handful of patients that experienced this. And what you see is pre-glycine, what it knocks out are the oscillatory potentials and the 30 Hertz flicker. This is an example, not that you're gonna run into nowadays because they stopped using glycine. I don't know what they substituted with, but they stopped in a decade or so ago using glycine as the irrigating solution. It's just to show you how sensitive any, if you mess with any of those chemicals, how it can be reflected in retinal physiology. Retinitis pigmentosa first described by Donders in 1857. As you guys know, huge variability in expression of retinitis pigmentosa. Different patients, different. Normals in the left column, retinitis pigmentosa on the right. Again, I cannot overemphasize the difference in expression. I have seen siblings that are as good as you can be with retinitis pigmentosa and the other one about as bad as you can be in siblings. So even people with the same gene pool can vary from one end to the other of the spectrum. I saw a pair of brothers that had Usher's syndrome and one had been at the school for the blind since preschool and wore a battery pack earphone. This huge thing, because he was almost completely deaf. His brother also, and he had no ERGs, flat. Everything looked like the upper right there. His brother was a graduate student in engineering at Stanford. His vision was good enough that he was an engineering student. You could see 2030, 2040 anyway. And all he wore was a little tiny earbud for his hearing and they were siblings. Typically, because retinitis pigmentosa is a rod cone dystrophy, you'll get no response or only the remnants of the cone physiology with the BX response when you use the dim blue and red. And then in the bright white, just get a tickle and then the 30 hertz and the photopic are present but smaller in amplitude and slower. Again, it depends on where you record. This was picked by me as a typical example of a person that didn't notice symptoms until they were, say, 15 or 20 years old and it was a woman that was tested that was about 20 years old. You can see this same severity in a five year old in an X-linked male with retinitis pigmentosa. In a patient with labor's congenital amaurosis right during an exam under anesthesia when they're only a year old or 15 months old and labor's this suspected because of nystagmus, you can see nothing except the upper right. And then on the other end, some people with dominantly inherited retinitis pigmentosa don't have ERGs this bad even when they're 30 or 40 years old. I've tested over 100 members of one extended family here in Utah where it was large LDS, mostly LDS family where some of them had 10 kids and five of them had it and some of them didn't notice any symptoms at all until they were 15 or 20 years old at least. There is a single year that people first notice problems if they have it mildly in the United States. 16, what happens at 16? Driving, driving. A question I developed 40 years ago was in suspicious patients. I said, if you're driving at night and someone's with you, do they see things before you? And they'll almost always say, or the worst case scenario was a woman that was more, she was more like 30 or 40. I said, do you have trouble seeing things at night like animals or things coming from the side? And she put her head down and she said, oh, I've hit a lot of animals. So 16 years old, another question I have is, if you're driving at night and someone's with you, do the people with you say a lot? There are, if you look at my website on, web vision on ERGs, it's more than a screen of disorders that retinitis pigmentosa can be associated with. Most of them really rare. These are some of the more common. Lawrence Moon-Bardae beetle. We see a new one every few months because being the only eye tertiary center around here. Extra digits, mental retardation, obesity. Remember, this was, this dates to even before the first Moran, so before 93. The mother looked like someone off the cover of 17 Magazine and the children looked like a couple of overweight moon-faced kids. And I was sent from ERG and I asked the mother, I said, so, how long have you known that they had, I just looked at them because like, what's wrong with this picture? And they'd never been diagnosed and they were like 12 and 14 years old because they lived somewhere in a rural community. This is just a sample of a pretty severely affected Lawrence Moon-Bardae beetle with retinitis pigmentosa. The articles say only 85, 90%, but I've never seen one without the RP. You can also see in retinitis pigmentosa effect in a carrier state. The mother's, their carriers are excellent that are reduced in amplitude. Just the opposite in the ERG is seen in cone dystrophy. Cone dystrophies are best detected with full-field ERGs. You would mistakenly think that, well, let's do multi, multi-focal, even, you know, that'll tell us, well, the thing is, you can't tell cone dystrophy from stargarts from any kind of central macular problems with a multi-focal ERG, but the full-field ERG, you can detect cone dystrophy better because you can separate the parts and compare how the people do on both the rod and cone physiology, because in spite of the fact that cones are 100% right at the foveola, still outside of the macular are 90% of the cones. They're everywhere. There's just a lot fewer as soon as you get about five degrees from the retina. In cone dystrophy, you get just the opposite effect. You get good but slower responses to the dim blue and the dim red and the bright white, but in the classic case, you'll get no flicker following or just a hint of, I've got these question marks, is that an A wave, is that a B wave? But again, can't overemphasize how much expression varies between individuals because people that you know have cone dystrophy from all the other parts of the exam and their performance on color vision still can have some graded response. So say the 30 hertz and the photopic B wave would be maybe only half amplitude. So there's big expression differences. I mentioned earlier, compromising the vasculature supplied to the retina affects the electroretina gram, central retinal artery occlusion, central retinal artery occlusion. You're not, I'm not telling you to memorize these just to show you the different ways that can be expressed in different applications of the electroretina gram. Bane occlusion, this can be a question also. I don't know if anybody's ever seen it. More affected, so the B wave. B wave is more affected and our cilatory potentials are more affected. But again, I can't, there was a guy that gave a talk here, it's been over a year ago and he was talking about the clinical expression diagnosis and then when they got the genetics. Everything, like people that look like classic retinitis pigmentosa, but the gene turned out to be stargards. Just crazy stuff. In general, when you get areas of the retina that have different compromised vascularization or different proportions detached, in general the B wave amplitudes reflect the total amount of area that's affected. Stargards disease. Do they use fundus flavimaculatus at all down days? You ever hear it even? No, it was used pretty commonly 30 years ago. Classically stargards, Jerry Fishman in Chicago, he has a four stage classification. It's basically teens 20s, 30s, 40s is what it comes down to the stage for. And in the first two stages, the ERGs are completely normal. In the third stage, you might see a little bit and then the late stages, most people after 40, that's when the ERGs affected. But again, you see everything. I saw a 17 year old in the last year that had the ERG of a typical stargards that'd be 50 years old, severely affected. Running through some stargards. You can also have some bad looking retinas that have normal ERGs such as a rubella retina. A Cardi syndrome has gotten to see any of these. We see them as EUAs with Hoffman and usually with Hoffman maybe once or twice a year. This is taken by Scott Larson a couple of years ago, before he went back to Iowa. This one is another one, not from here. Full field ERGs can be used to detect some retinal toxicity, but in general, they're not as sensitive as the multifocal electroretinograms. Chloroquine is still commonly used in the rest of the world for malaria arthritis, lupus, and some dermatological inflammations. If you take it long enough, you're doomed because you have a cumulative effect that can't be avoided. Hydroxychloroquine, commonly Plaquanil, is not the case and I've seen more than a handful of people that have taken it for 25 years and still have the ERGs of a teenager. But some, because of individual physiologic effects, some are affected after, if they're not affected right the first, some are affected after a decade or so. That's why it's important to keep repeating them. In my personal opinion, I think of people are clean for the first couple of years and they don't change the dose, that there's no reason to submit them to ERGs every year until they've been on it for a decade or something like that. In fact, the international protocol which I disagree with says just check them once early and then on again. I think that's a mistake because I've seen patients that are clean in the first few months but if they're particularly susceptible to it, you'll see a problem in a year or so. Classic cases back, again, 30, 40 years ago when it was the commonly used, the only choice, we'd see patients all the time with the classic ring scatoma. And here's a person that's affected with the chloroquine just responses are slower, lower amplitude, a little bit more of effect of the cones because of more of them being near the center. But if they get to this stage, there's no help in them. That's the great thing about multifocal electro-retinograms. It'll pick it up a year or more before a patient would notice anything clinically. This one is, I don't know how commonly it's used. I don't get sent these patients very often. I bet it's more common, they should be sent but they're not. The guy that used to send them to me retired and I don't think I've seen anybody on depheroxamine for the last, it's an iron-key-lating drug that can be toxic to the retina that's used in internal medicine. Amplitude, again, let's get through these more quickly. Steroid toxicity, this was an unusual case of a ENT injection, too high and got the ophthalmic vasculature. So they had one good eye on the left, really good eye on the left and then the affected eye on the right. This is a mystery patient that came through here a year or so ago. I don't know if any of you were involved with it. It was an over 80-year-old male, had successful IOL surgery, but his vision right after that dropped from 2025 to 2050 and he complained of poor night vision. It's one of my few gets ever, that something that went through a handful of ophthalmologists and his general physician and they missed what the problem was. When I saw his ERGs, these were his ERGs, even though these go up, those upper left one, that's just baseline shift. He really had no ERGs to the dim flash stimuli, but his cone physiology was almost normal. The last two on the bottom there were almost normal. And up there on the upper right, that's a bright flash one. All that you see is the early BX, component. When I saw this, it reminded me of a patient that I'd seen of Bernstein's a year or two before that had liver disease and it had most, the resection of most of his small bowel and he was on the transplant list for liver disease. And so I asked the guy, I said, tell me more about what was going on when you're, and the thing is, particularly the wife, blamed Dr. Olson for this eye disease because it coincided with his cataract surgery. So she was telling everybody that Randy ruined his eyes. Well, at the same time, after I quizzed him, but at the same time as he had his cataract surgery, he had seen on television, I saw the same thing, a guy on the CBS Evening News Medical Report said, there's no reason to take multivitamins as long as you're eating halfway decently, like if you're at least eating at McDonald's and have a salad every once in a while. So the guy quit taking his multivitamin. And I said, well, what else about? She says, well, I've only got, they tell me I've only got about a meter of my small intestine left. And so after seeing this, he had been through Randy and Randy had sent him to Bradcats and Bradcats sent him for an ERG and I suggested to Dr. Katz, I says, get a vitamin A level on this guy. And he got a vitamin A on it and it was like 0.006 or something like that. Because he had quit taking his multivitamin, which had been getting him through with his vitamin A, but he had no vitamin A. And so they put him on vitamin A supplements for one month. And this is his ERG one month later. Let's go back again. Here's his ERG, take a look at all of those upper ones. And here's the ERG only one month later. He returned to really normal range for an 80 plus year old and he still had a little bit more recovery to do. And it was just vitamin A deficiency. And his vision returned within a month to 2025. Again, just an example of how the eye and the electrophysiology can affect and reflect what's going on in the body, particularly if it's a system like the liver that's so important for the physiology of rod and cone cell function. These are just interesting, I'll stop there, interesting. Talcum powder, which is commonly used to cut cocaine, gets clogged in the micro vasculature. There's the ERG. Retinoschesis, this can be a question that people have seen on boards. There's two disorders that most reflect the sensitivity of the B wave in this, in, or one is schesis, what's anyone know of the other? Congenital stationary night blindness. CSNB, their ERGs look the same for different chemical reasons. So here's schesis. So in classic juvenile retinal schesis, the B wave will be gone. You have a super normal A wave and then little or no B wave because the generator of the B wave is the mid retina. How are we doing on time? What time? It's 74. Okay. The other is Congenital stationary night blindness, CSNB is for a completely different reason, for a transmission reason between the receptors and the bipolar cells of a handful of different causes, you get no B wave. There are different kinds in the classic which is called type two, you get no B wave and the others you get graded B waves. In this type, Schubert-Bornschein type, you get no B wave, poracuity, myopia, nystagmus, and it's X length on XP-11. This is the kind of response you get. The rigs form, you get A and B wave amplitudes reduced. It's on a different gene, 15 Q 22. This is enhanced S cone Goldman-Favre syndrome, also a form of Congenital stationary night blindness, also on a different gene. Fundus albifunctatus, another disorder, on several different loci, has a very interesting fundus appearance. Isn't that neat? That wasn't taken here. I forget the name of the guy. Nice guy retired now, but a photographer that both Paula Morris and Jim Gilman knew and he gave me permission to use it. Yeah, it's also in the revision chapter. Agucci disease, never seen one, but it's one that they like you to know. I don't know why. You might like them, you're never gonna see one either. I've not ever seen one. That they dark adapt, but it takes about two hours. And during that period of time, the fundus changes from this rust color to normal over the period of a couple of hours. Again, a form of poor night vision. So you've got all these different forms of congenital stationary night blindness on at least all of these loci, which they will probably add to every six months for the next years. The ERG can also be used to show the graded effect of trauma to the eye or a foreign body in the eye. If the foreign body is the iron or copper, the prognosis is very poor about retinal physiology. If it's nylon, if it's stainless steel, sometimes you can leave it alone. A general rule, this is one that shows a patient across time post-injury, not much difference between the eyes. But over the period of the next couple of months, so this is soon after the foreign body was found in the eye. Over a period of a couple of months, the amplitude started to go down. A general rule is if the electrophysiology compared to the fellow eye goes down as much as 50%, you just need to go in and get it, even if you don't want to, if its location is such that you would like to leave it alone. If it reduces down 50% or less, probably the toxicity will continue and you're bitter off to make the decision to go ahead and get it. I'll leave this for next time and I'll talk about multifocal electro-retinograms and then swing into visually evoked potentials next time.