 When I come to things that you guys have seen on tests, this is something that you brought up after class yesterday. Like, hey, more or something. He said, it would have been more advantageous if I'd have spent a little time on when I was talking about the Chittokagashi syndrome and Prater-Willi and those syndromes as a sort of a review to you guys and like all the characteristics of Albinism where I glossed over them thinking, oh, this isn't, you know, this isn't ERGs. Let's move on to the, or Albinism, let's move on to the next thing. So if you see something you've seen, raise your paw. Before I do visually evoke potentials, I'm gonna spend just five or 10 minutes on EOGs because it's something you need to know about even though they're used very rarely. I would say I don't do more than two a month and all of these are on potential best patients so you need to know about it. And as genetics gets more and more common, it will become less and less useful. There's a real good paper that just came out, oh, maybe a month ago. In fact, it doesn't even have page numbers because it's an e-publication and it'll be in Retina. First off, there's named Khan and they looked at 120-something best patients and oh, the exceptions are incredible about the, you know, the locus they found for some that like, oh, this isn't best but it is best, or it looks like best, that kind of a thing. I'll be adding that to my chapter on web vision when I redo it in the next few months. So EOGs are not the same as electoretina grams even though they're both generated in the retina, the sources of the generation are different. The source of the generation of the EOG is an interaction between the pigment epithelium. The pigment epithelium is the main actual generator of the potential but the light rise of the EOG when a person is exposed to the light after being in the dark for 10 or 15 minutes, the light rise is dependent upon interaction between the pigment epithelium and the mid retina. So both of them have to be intact. It's not an evoked potential like electoretina gram is. There's a standing potential about two to five millivolts between the retinal pigment epithelium and the mid retina that is cornea positive at the outside of the eye. Here's a graphic that shows this. So you can think of the eye as a little battery with the cornea positive in the retinal area negative at the back. So if you place electrodes near the inner and outer canthus like so and then a person wiggles their eyes left and right, this will produce a potential swing that will give you that voltage. Before I go any further, a little bit of, to me, interesting history, being older than dirt, I knew the guy that named this was named Elwyn Marg. Unusual name, he named the EOG in 1951 but it wasn't introduced as a clinical test until 1962 by Jeffrey Arden in London. And so the ratio I'm gonna talk about is called the Arden ratio. Is that something that they refer to in your books as Arden, he's still alive by the way. And he authors one of the chapters in web vision. He'd be at least 85. And those of you that know Helga Kolb's name, the editor of web vision, Helga Kolb was a co-author when she was 21 years old on the first clinical EOG paper in 1962 with Arden, small world. So if you place electrodes on the face like so, they're usually always recorded bilaterally and my experience of having done them for 40 years, I've never seen a difference between the eyes. This is Gail McNeil. Gail used to be, what are the texts, the texts that's orthoptic texts, tech here, years and years ago. But she has a lot of money and last time I saw her, a chauffeur was dropping off a dance. She now lives in this, I think Scottsdale. But she's a model for all my contact lenses. So a Gansfeld like so is used like for recording ERGs. Patient puts their chin in the chin rest and usually use a forehead bar to keep their head stationary and you pre-train them to not move their head and only move their eyes and to look at the LEDs when they alternate left and right. So they're inside the globe, the right one comes on, then the left one comes on, then the right one comes on, then the left one comes on. 10 second sample is taken about each minute depending on the program you're using but it's very close to 10 seconds each minute for a period of 10 to 15 minutes in the dark. So you get a baseline, here's 10 seconds of eyes swinging back and forth every couple of seconds just in room lighting. And then after you're put in the dark, everybody, the voltage goes down a little bit. Everybody, whether you have pathology and you're retina at all, everybody in the dark, the voltage goes down maybe 20%. And then when you turn the lights on, it approximately doubles in size for most people. That approximately is any ratio greater than about 1.8, so almost double or greater is normal. Ratios of 1.7 or below are considered abnormal. That is comparing the low in the dark, excuse me, the low in the dark between how big in the light, that's the ardent ratio. So it's usually a number of like 2.3, 2.4. A young adolescent female will give you ratios of three or four. This thing will be twice as big as that. The young, the adolescent female has the biggest electrophysiology in all electrophysiology. Women are just better, you guys can attest to that. Ratio of the amplitudes of how big is that voltage across the eye when you compare the low in the dark to the greatest rise. So the low in the dark is hit after about eight to 10 minutes and similarly, the high in the light is hit about between eight and 12 minutes, usually before 10 minutes. So if you've tracked it and printed out, here are two eyes of a normal person I tested in the last year here. So in the dark, the voltage goes down like so and then stays stable after about eight or nine minutes and if you would carry this out for even 15 minutes. Some programs go a full 15 minutes, the one we use just goes 12. 12 minutes in the dark and then you turn the lights on, the first testing, nothing happens and then it shoots up like this and as soon as they peek out and start to come down you can end the test cause you're, that's it. You don't need to keep running them in time, you're not gonna get any gain. So what happens here, if you kept testing them this would just come back down to this baseline over the next five or 10 minutes. So there's the two eyes in an individual. This is a best disease patient tested here in the last six months. So you get the same phenomena, if it goes down a little in the dark and then you turn the light on and you don't get a light rise, usually any greater than 1.5, some of them are as low as 1.1 like they hardly increase at all. So best disease in adult vetelepharm dystrophy are associated with normal ERG but abnormal EOG, it's the only disease and that's what makes it peculiar. These two disease states are the only two that give you normal ERG and abnormal EOG. Yes, Ferguson? Yeah, you're using a globe, yeah. Right, I don't know of a way to do focal EOGs and I've never seen that question addressed in the literature, you could try searching for it. I've never run across the answer to that accidentally. In best disease in the textbooks, it's considered an absolute, it's not an absolute. There are no absolutes in the universe and they say if you throw your body into a brick wall for infinity, sometime the molecules will all match and you'll pass through. But in general, best disease especially at the younger stage when you're making the diagnosis is normal ERG, abnormal EOG. When they get older and the disease progresses, you will also start to see abnormalities in the ERG. In adult vetelepharm dystrophy, even though they look, just you can't tell them apart in the progression when you look at the OCT progression that I'm gonna show you in a couple of minutes. You can't tell them apart but the number of adult vetelepharm dystrophies that show the normal ERG and abnormal is spotty. It's not consistent. These are the only two I know of that are characteristic for that, for almost all retinal disorders, abnormal ERG and abnormal EOG. So in the early days, 50 years ago, they tried various things, which is better, in the early days, it was thought that drug toxicities were maybe a little more sensitive using detecting drug toxic, a little more sensitive with EOGs but that would fit because you get things like the accumulation of drugs and the pigment epithelium and stuff but still the ERG because it has so many other parameters where you're looking at rods and cones and light and dark and everything is the more sensitive test. So an EOG, except for research purposes, is pretty much a waste of time unless you're working with adult vetelepharm dystrophies or best and I can see even just in a handful of years that this will be all genetic when the speed of the genetic feedback comes and stuff. So as you guys are familiar, both diseases are due to a buildup of lipofusion and a breakdown of the retinal pigment between the outer retina and the retinal pigment epithelium and I'm gonna run through that there's just so much variability which you guys have probably already seen as you pass through retina. This is a rare one here just a few months ago, a five year old, this was the fundus. I've never seen anyone this young and a confirmed best at five years old and he was just classic. Some others, this is the classic sunny side egg looking. Veteleformin means egg-like, a yellow egg-like. You only catch them at this phase if you're lucky. Usually they're past this phase and you get them in the scrambled egg category but let me run through a few here. Here's the progression. This is actually an adult veteleform but the sequence I've been told does not differ between best if you know otherwise, tell me. So here's a progression a couple of years ago, 2011 of a woman, I think she was about 50 and passing through the sunny side egg stage and then the breakdown to the scrambled egg stage. Scrambled egg stage, more bests. I show you these just to appreciate that it's so much as dependent upon when you get to see them at diagnostic stages. I've seen undiagnosed bests that are 40 years old, not adult veteleform dystrophy, that undiagnosed that they have a history, like a phone book and they had never been correctly diagnosed and people have been looking at them since they were teenagers, autofluorescence. So adult veteleform dystrophy, the difference is not much. The difference is age of onset but the progression is usually quite similar. Dominantly inherited juvenile onset, abnormal EOG, EOG normal or mildly abnormal, so it varies quite a bit. I think in the last year of the maybe dozen or so that I've tested, one of the adults was abnormal. Now, do you remember any coming through that were tested? Potential adult veteleform dystrophies that you guys also got an EOG? We haven't done it. Yeah, well, no, I know there's not. One every couple of weeks is the most I see. I don't remember. In this paper I mentioned that came out, it's an E publication right now in Retina but should appear any month now. First author, Kahn, KAHN, they looked over 120 and they found recessively inherited, everything's possible. So more is discussed in web vision and keep that in mind for a resource. Trying to get something to go away here. Ah, no, go away. God, it's so easy. Now I get into Photoshop. Let's try this. Okay, let's talk about visually evoked potential. They gave that little handout. That waveform is the classic waveform of the most commonly used visually evoked potential. That is the pattern reversal visually evoked potential. It's important that you choose the right stimulus depending on the pathology you're looking for. For example, I'll address this in a few minutes. You cannot use pattern reversal with any patient that has nystagmus because the pattern reversal because of the quote apparent movement to pattern reversal, it just exacerbates their nystagmus and so they can't focus and you will be guaranteed an abnormal visually evoked potential. I remember a patient that was sent from Cal, that was worked up in California that ended up a degree patient and the history was optic nerve disease, abnormal visually evoked potential. Well, the idiots had only done a pattern reversal visually evoked potential on them. And it wasn't optic nerve disease. It was nystagmus. So the 10, 20 international electrode placements system you may or may not have been exposed to when you pass through neurology. It's the agreed upon international system of where electrodes should be placed for EEGs. And the south view of the northbound human, the occipital pole, these electrode locations are used to record visually evoked potential. It's not in my opinion, not necessary to do anything but the central unless you're looking for albinism. Why I'll get into in the next couple of minutes. There, even the majority probably of labs put an array across the back of the head thinking they're gonna lateralize pathology. Not, these three locations are most commonly used in both neurology and ophthalmology for tapping the information from the occipital pole. The Indian is the bump going up the back of the head, the large bump. The placement of these electrodes is 10% of that distance to the nasion, the bridge of the nose here. And in anybody in this room, it'll be about three to four centimeters. So you don't have to get out the tape measure to do it. Feel the back of the head, go up what you think is about three or four centimeters. And I adjust that based on the size of the head. You know, if it's a nine-year-old, I don't go up more than three centimeters. If it's a Samoan football player, and he's got a head the size of a basketball, I go up four centimeters or more. This is the reason to me, the main reason that you can't lateralize pathology. These are sections of functional MRIs. This person was viewing a checked pattern that appeared three times a second. And this is the areas of excitation in the functional MRIs, with the red being the greatest excitation, and the purple and blue being the least in excitation. First of all, note the asymmetry. Particularly look at these slices. The asymmetry of the hot area. Sometimes the hot area is buried down three or four centimeters between the walls and that. This is why, in my opinion, you cannot lateralize pathology. You can lateralize pathology best based on your other information. Visual fields, if you have scanning information, history of the individual. This is an interesting, this is a paper, this is interesting. This is the functional areas for combining MRI and EEG, showing the hottest areas in the brain in different planes. When you get to the walls that face each other between the hemispheres, down in between the hemispheres, if you have good symmetry, you not only cannot lateralize, you get cancellation, electrical cancellation across the walls, and you will actually get false lateralization. That what you, what you appears from the visually evoked potential information across the head might give you opposite of what you're expecting because of the electrical interaction. As soon as those fields leave the occipital pole and get down into the sulci, forget it. But the visually evoked potential is really good at telling you are the pathways working normally between the retina and the visual pole. These are the multifocal visually evoked potentials. You can see in this a little bit polarity reversal. If you look at the upper and lower fields and these potentials, they almost reverse in polarity. Look at this one versus this one. That's the electrical phenomenon I'm talking about. All evoked potentials, auditory, somatosensory and visual come from EEG. The EEG was first described in 1929 by a German named Hans Berger. And within just a couple of years, it was being recorded routinely both in Europe and the United States and Canada. And one of the things that if you would observe an EEG, like when they're doing photic driving to check for epilepsy, you can see, you can see when there's a flash of light presented, you can see the evoked potential like this one. You don't always see it because it depends on which way the EEG is going. If the EEG happens to be coming down when the evoked potential is supposed to be coming up, you won't see it. That's why it takes an average of across time to pull the EEG, pull out of the EEG the visually evoked potential. So all evoked potentials, a stimulus is presented such as a flash of light or a pattern appearing or disappearing on a screen or an auditory click in the ear or somatosensory stimulation of the medial or peripheral tibial nerve. And then a computer grabs the set time after that stimulus, such as these windows and adds one to the next to the next to the next to the next. In the case of a visually evoked potential in a child that has a thin skull in just five flashes, you can see the visually evoked potential. Whereas in an adult with a thicker skull, it might take 20 or so before you start to see it and then it smooths out over the next minute. These stimuli are all used even today other than this mirror system that I'll talk about historically. But in the beginning, a strobe flash was used and in the beginning and the beginning went up until the mid sixties, EEG recording was used. So you had the EEG recording on paper and then from the amplifiers that was put into a little computer that was dedicated to be able to average. And these started to appear in the early 1960s, which is when I got into it. And computers that did the whole thing didn't come out until the seventies. And still they weren't programmable. They had no keyboards or anything like that. They just, the earliest computers, and they were wonderful. Not all of these choices. It had start, stop, print. Loved it. So in the beginning, a strobe flash was used such as photic driving in EEG, the old grass stimulators, what I started with like this. And then pattern flash appeared. Then pattern reversal was invented in the mid 1970s by a guy named Martin Halliday at Queen Square in London. And I visited his lab beginning about, first time maybe 77, and he had two Kodak slide projectors with camera shutters in front of them. And he had one that produced a check of one pattern and then the other one produced the check opposite. And by using the camera shutters, he could make it appear to reverse by back projecting it onto a screen. It was really neat. And they put into the TVs didn't come until early 1980s. So in the beginning, the strobe flash was used. Then beginning the late 1960s, people started putting patterns on top of the flash. It was a pattern flash. It didn't reverse. And then the pattern reversal came up. So you'd see this, and then this, and then this, and then this. And so this is what is still used today, pattern reversal produced on a television screen. Martin Halliday's old slide system produced sharper, bigger evoked potentials because you can change a pattern much quicker with a camera shutter than you can with a TV screen. Because a TV screen is based on the line frequency. So 16.66 milliseconds is as fast as you could change it. Whereas Halliday's system could change it in like a thousandth of a second. It was neat. Normal pattern reversal VEP looks like this, like the handout. Probably anyone in this room would give you this kind of a form. And that's the great thing about pattern reversal. You get the same potential from every body that's normal. Whereas any other stimulation, flash, pattern flash, pattern onset, all of those, you get more reflection of the individual idiosyncrasies of the individual. Development of the visually evoked potential. At 22 weeks, you get very sparse embryonic 22 weeks. Early cones. And then more development postnatal five days. And then the development when you get old with the cone packing. Cone packing yields up to 2020 vision measured by VEPs by six months of age. Preferential looking indicates 2060 by six months of age. So physiologically, it seems like the system is capable of 2020 vision within six months. But perceptually, there's a little lag behind. The main difference in visually evoked potentials is the myelination of the optic pathways. This was a patient I recorded during one of the exams under anesthesia over at primary a few months ago. So the visually evoked potential of an infant, baby, only a few months old, will be very slow. So this is the quote P100 out here at about 240 milliseconds. And what happens over the next five years as the system myelinates, this P100 just marches back to left of the middle of the screen. So it just goes, it just month by month by month, it would just come back faster and faster. So that by school age, by kindergarten or first grade, the VEP just looks like that of an adult. Did you, can you? Yeah, so like the question that we always get on tasks is for you to sweep VEP? Yeah, sweep the sinusoidal VEPs, yeah. Can you talk about that? Sweep VEPs are produced at a fast rate. So it gives you a sinusoidal waveform. I know there's at least one company that's out there. All they wanna do is sell you. They don't care if it helps patients. Their sales pitch is, this is what you can bill for. Run it on everybody and bill. So we don't have. We don't, I don't do it, yeah. It can be used, there's nothing wrong with it, but it, you can get information from it, but it's more obscure than the information. What kind of questions do they ask you? They always say to add in things is to use sweep VEPs. Yeah, they do that. But you can do the same thing with the pattern, but that doesn't get you out of the fact you have to answer the question. What do they wanna know? Yes, no? Can you? Yes, you can. The visually evoked potential, either the sweep or the transient, where transient means that the rate is no more than about three per second. So the evoked potential can completely recover before the next one is presented. Whereas sweep is usually at a fast rate and you can do that, but it can't do any better job than you can do or a good pediatric ophthalmologist can do at estimating it, estimating the visual acuity. Yeah, Ferguson? So it's true. Uh-huh, yeah. The, the location of the generators is not known that well, those first slides that I showed you and there's tremendous inner, individually. The P100 is generated from about all of my hand here like this. Yeah, beginning from below, below the Indian up to the top of the head. And then the negativity is just the preceding and following voltage swing that takes place. And they don't know the origin of them like they do for ERGs where we know the A wave comes in the rods and cones and the B wave comes from the mid-retina and the C wave comes from the pigment epithelium. And I think the D wave is the off-response of on and off bipolar cells. They don't know that about VEPs. VEPs are best to estimate and quantify the integrity of the pathways. I don't know if this is answering your question, but. Well, it sort of does peak at 75 milliseconds. Right. And at 75 milliseconds, it's probably. 90 or something. And then the P100 peak, which I'll show you in MS, is if it's delayed two standard deviations, which is about six milliseconds. So if you get beyond about 112 in a person over age of seven or so, if you get past 112, then it probably is reflecting true pathology. Latency, no, but also amplitude. Yeah, amplitude is usually reflects more, usually. There are no absolutes. Usually reflects pressure on the pathways like hydrocephalus, pituitary tumor, or such. So the analogy I use when I'm explaining to parents is the optic nerve is like a water hose going from the faucet, your eyeball, around the house to a sprinkler in the backyard that's your occipital pole. And the question is, is somebody along the line getting cute and stepping on the hose? And that's what tumors usually do. So you get a reduction in amplitude and that can be quantified. I'm gonna show, let me progress and I'll show you a series that might answer those questions. So if you look at P100s in groups that included, doesn't have the numbers in these groups, but there were about 10 or 20 in each of these age groups and you get just this progression that the biggest difference, look at the standard deviation, the biggest difference when you get over 65 is not really the mean times, but the standard deviation because the two times in life that things vary the most in visually evoked potentials and well, not so much in ERGs, but in visually evoked potentials is the variation in maturation those first three or four years and then after 50 or 60. And there's even greater variation in how people age. You've all seen this as patients, I once, I've made a lot of mistakes assuming the relationship between patients between individuals that I see and one time there were a couple and they were about the same age but their wife looked so bad from her illness he looked like at least his mother, at least his mother and I made that assumption. And the woman told her husband to hit me. But you know you see people who are 60, 70, 80 years old some of them look like 60, 70, 80 and some look like 90, 100, 110. Here's a scattergram of those peak 100. So the biggest variation is in the development, preschool age, this only goes back to about six. And then things tighten up through young adulthood and then again when you get over 70 the spread gets at least as big and this probably the spread will get even bigger in this group when you get to 80, 90, 100. Well it's yeah and over general health, yeah it's not really demyelination as much as it is just aging cell loss breakdown of your body. Something that most of you are probably 28 by now, close or close, the studies of hundreds of people indicate you are at peak here in your adolescence as far as speed things stay the same but by age 28 you start dying as far as visual function. It's all over at 28. From then on it's just a slide. Merry Christmas. Okay, besides pattern reversal pattern onset offset is the stimulus of choice in any patient with nystagmus because of the fact pattern reversal exacerbates nystagmus. So if your patient comes in with any etiology of nystagmus pattern onset which is pattern comes blank screen pattern comes on pattern goes off pattern comes on pattern goes off. So this is what the stimulus is like. So you use this for whether it's idiopathic nystagmus or an albino pattern onset VPs are best for poor fixation, poor acuity. Eye movement disorders, nystagmus, malingering and deliberate de-focusing which is not an issue in adults. We lose the ability to deliberately de-focus. You don't get many children that are malingerers that know enough to deliberately de-focus so I probably should drop that one but I leave it so I can point out that adults can't deliberately de-focus. Again, this is progression. This is upside down the P100s but it shows the progression from this number of people in each group with the average age of this. So even though it goes down a little bit in amplitude there's no statistical difference till at least 55 or 60 and that's mostly due to variation. How are we doing on time? Oh, good. Okay, sweep VPs that stimulate lines or bars of different widths and also by using different sizes of checks either way you can estimate acuity. The biggest fastest VEP will be produced by the image, the patient, the smallest image a person can see sharply. So for all of you with your best corrected vision it would be a small check like a quarter inch check at a meter. That would be the biggest one. If you're 2050, 2100 or worse it might be closer to a three quarter inch check and on and on. So by using multiple check sizes or multiple sweep stimulation of different widths of lines you can estimate acuity. But again I emphasize even though it's a question a good pediatric ophthalmologist can do as good or better with their testing. Most of you as you rotate through PEADS you're gonna see exams under anesthesia. This is one taken next door at primary with the goggles I use which inside as an array of 15 LEDs made to be bright enough to go through closed lids. They're quite irritating when I use them in clinic. Little kids don't like it at all. Oops, looks like so inside. There's really neat, a company is supposed to give me one but they've been dragging their feet and dragging their feet. Hopefully I'll get it. It has a head on it smaller than a softball between a baseball and a softball and it has a cup system around it similar to this kind of a thing but oval. So it's made to place over the eye so you can monocularly stimulate and you can produce any of the colors like you do in a full field ERG and dark adapt and use dim blue and dim red and everything. So I'm hoping to get one of those that I'll start using in the OR so we can do a little bit more, a better job at rod and cone isolation in the exams under anesthesia. Whereas this you have no choice but these red LEDs. Okay, let's talk about optic neuritis in a series of different kinds of patients and what happens in the visually rock potentials. The classic optic neuritis patient is one eye showing demyelination first, the other eye usually comes along at a later date but not necessarily no absolutes but usually one nerve precedes the other so you get slowing of the quote P100 and not much amplitude change at all. This is the diagnostic stage when you're seeing the MS patient for the first time who's 25 or 30 or 35 years old. As people progress you'll get amplitude loss and also if you would follow that patient and do VEPs every two or three or four or five years for the rest of their life you would see with the demyelination as the demyelination proceeds you would see that P100 go 110, 120, 125, 130, 135 so that the 60 year old classic MS patients that P100 might be 160 and once you get a lot of demyelination roughly in years these are not, these are just thrown out at you, I don't know what this study says, like 40, 50 years old beyond you'll start seeing significant amplitude loss. Yes? Usually, yeah, yeah, usually. Although 99% of decisions are made about either the amplitude or the speed of the P100 peak in the pattern reversal. Here's just some more, here's bilateral pretty symmetrical but both slow. Later stage, optic neuritis patient starting to lose some amplitude. If you show me the visually evoked potential of a MS patient with optic neuritis versus a neurofibromatosis type one patient they look the same. You get the same slowing but for different reasons. Roughly similar to you lose your B wave and ERG from both classic congenital stationary night blindness and retinal schesis but the reason is complete or the etiology is completely different. Essentially all neurofibromatosis type one patients have slow VEPs by school age whether or not they develop the gliomas. So something else is going on metabolically producing a slow VEP look that looks like optic neuritis. So this is a neurofibromatosis patient, slow. Just same as what a MS optic neuritis patient would look like. Okay, this is initial VEP on a child. Pretty happy. This is two, three years later. This patient had bilateral gliomas. Four years later. This is the procedure mostly from compression produced by the gliomas. Sorgazan. Standard deviation is about six or seven depending on the lab. Why it varies is people use different brightnesses of televisions. They place the patient different distances. There's no standard. Some people place the patients just half a meter away some a meter away, rarely more than a meter. And the field is different. So that some use just some use a 14 inch quote TV. Some use a 27 inch TV. When you change parameters like that different people use different room lighting. It will affect the standard deviation. So about six or seven. So 112 or so is pretty definitive that it's pathology if you get slowing to that. Of course you don't know what that person was when they got out of high school. I would like that on everybody. Then there's no question because many women their normal P100 is 95. And so a number of 104 or 105, 106, 107 that would be considered well slow but still, I bet if you knew what their VEPs were like when they were 18 and not now that you were tested as a potential MS patient when they're 30 but we don't have that. Okay let's move through. So I'm just gonna go through some different disorders so you can see some of the applications of visually low potentials. Pale nerves, what the VEP is useful for it's not that you can't make the diagnosis of a pale nerve it will quantitate the degree of dysfunction for you. How bad is it? Cause some nerves can look terrible and still have pretty good function and vice versa. Some can be borderline and be quite dysfunctional. Orbital mass, both sides affected. One side no VEP at all. Do I have the follow up? Here's that same patient after decompression. So you get a much better on the basically unaffected side and the return of some kind of VEP there. So you can follow progression. Some of the neurosurgeons will send me patients prior to say pituitary adenoma surgery. Some don't and so you see the progression. Some I only see afterwards so I don't know what the baseline was before. Neuroblastoma, orbital fracture left. Pale optic nerve, pale optic nerve again. Yes yeah I know pale optic nerve but this again quantitate the degree of dysfunction. The Thambutile nerve toxicity. This was about a 30 something year old patient of Dr. Katz. Slowing like so you couldn't tell these from optic neuritis but you know from the history what's going on. So these are symptomatic all evoked potentials are symptomatic but not diagnostic. You have to, they have to be considered within the rest of your exam history scanning et cetera. Meningeal tuberculosis again slowing again. You can't tell these from optic neuritis or neurofibromatosis. The Cardi syndrome. I don't know why, why do we see so many Cardi syndromes here? Cause it's such a rare disorder. We see in a Cardi, I see a Cardi just with Hoffman every six months or so. Is it in the water or something? Almost all are females. It's thought to be a rare dominant mutation of the X chromosome and thought lethal to normal XY males. Some Klinefelters males will have it. But it's so rare that you don't have to worry about that. So they show this leucane cune. This was a series taken in the OR, not really sharp but done hand held by Scott Larson when he was here. And here's the VEP on this one. One eye, what makes such a, cause the expression is bilateral but it can be quite variable. So if the expression affects the optic nerve head or central macular area, that's when you'll get the real bad VEPs. Multifocal VEPs. Multifocal VEPs give you a evoked potential as if you divided the optic nerve into 100 over 100 channels. So you might pick up abnormalities that aren't apparent from just the gross overall optic nerve. Our system that hopefully we're gonna get in the next week or so will be like this and what will be new for us is currently, those of you, most of you I think have seen a multifocal, you get that external view of the eye. The new system we're supposed to get by pushing the arrow keys, it'll give you the fundus view. And the advantage of that will be those patients that have AMD or central macular scatomas, instead of them trying to fixate on an X the size of a pencil and hope that they can see the middle somewhere or interpolate the middle somewhere, will be able to focus the pattern onto their fovea and just tell them to stay still. Most systems, only one company has that, the guy who invented multifocal VEPs and ERGs. Most systems have a system like this where the patient looks at a wide screen and has a chin rest for both multifocal ERGs, which is this pattern is a multifocal ERG, multifocal ERGs and multifocal VEPs. The pattern for the VEP is not this hexagon pattern that blinks off and on, but a dart board that all of these blink off and on. And you end up with, these are normal multifocals. The red is the right, the blue is the left. This, the following series starts off with a severe episode of acute optic neuritis, which essentially obliterates all of the right VEPs followed by recovery. So the red is right, the blue are the good ones, the red are the poor during the acute phase. Next, over a period of two months, the amplitude recovered, but the time, the latency, peak latency remained. And then three months later, on the lower field, even the latency recovered, but it remained slower in the upper field. The schemic optic neuropathy, oops, shows the differences in this area. Optic nerve glioma, so it's more powerful, but don't even think about order, I hate doing them. They require four electrodes on the occipital pole that hopefully stay the same in their, how connected they are and everything and digging down through hair and placing those up to the nightmare. I just like run for my car when I hear them even talking about order, you know, multi-focal. Any questions? Oh, I'm glad you mentioned that. The question is, you know, what is the variation in amplitude? Because of the asymmetry of the brain and that one of those first slides I showed you of those functional MRIs, amplitude can't be considered definitively abnormal unless it's about 50% or greater because the back of the brain does not look like the drawings. The back of the brain looks like this. So the asymmetry in the occipital pole just anatomy is greater than the left and right of a face and you've all seen those where you take the half of a face of a person and replicate it and you're like, that's Tom Cruise that you don't recognize. So because of the natural asymmetry built into the idiosyncrasies of our anatomy, it's about 50% now. Yeah? I'm not sure if I understand. You're right. An after-matter. What's the mechanism that bullets with one side of the brain? The mass having a pressure effect even on the other nerve even though it was unilateral mainly, it would have pressure, for instance, in pituitary tumors in doing these for 40 years, actually 50 now, 50 years. I've only ever seen one that the VPs look symmetrical because there's always, there's some lateralization usually to the pressure. So if you have a mass on one side, just the spread of the pressure usually reaches the other nerve if it's a significant mass. And for the one side of the yellow, was that? I don't remember. Oh yeah, on the one, the bad one? The very first one. I don't remember. But you often see unilateral gliomas in these patients. Merry Christmas.