Lecture: Pertinent Pupillary Problems

This lecture will cover the pupillary examination, relative afferent pupillary defect, and the differential diagnosis of anisocoria. Videos will be used to illustrate all pertinent pupillary abnormalities.

Lecturer: Dr. Karl Golnik


(To translate please select your language to the right of this page)

DR KARL GOLNIK: Today’s topic is on pertinent pupillary problems. And I hope that during the course of the webinar, we learn a number of things, including the parasympathetic and sympathetic pupillary pathway anatomy, which will probably be a review for most of you. You’ll be able to identify a relative afferent pupillary defect when we’re done. And list the differential diagnosis of anisocoria. So as an outline, we’re gonna start briefly with the anatomy, to make sure that everybody’s on the same page. Move on to the pupil examination. Talk about relative afferent pupillary defects, and then finally, about the differential diagnosis and approach to the patient with anisocoria. So I’m gonna start with a question. And I’m gonna — this is one of these polling questions. And you should be able to see the poll in a moment. But I want you to look at this video, and I’m gonna give you a multiple choice question as to what you think this patient has. And so you can see the choices, and you can see the exam. I’m going to open the poll. And so you would simply click on your answer that you think the person has. And I’m doing this to sort of get a feel for the audience, and to see what you all know about pupils. Or at least about some pupils. So that I can help gauge the rest of my talk and make sure I’m on about the right level. So you will be able to see the results of this poll. Of course, it is anonymous. And I’m gonna give you a few more seconds. We have about half of you have voted at this point. So if you’re going to vote, I’ll give you 10 more seconds. And we’ll see what the audience says. And I’m going to end the poll, and you should be able to see. So certainly the majority of you are absolutely correct. This is a right relative afferent pupillary defect. And I’m going to get back into the screen, so you can see — and we’ll talk, of course, more about this, but as we swing the light from the left pupil to the right, the right pupil dilates. When we swing it back, the left pupil constricts. So this is a right relative afferent pupillary defect. And we’ll of course be talking about this in more detail, but again, I just wanted a page. Very good to the 78% of you who got that correct. So I’m not a big believer in rote memorization, but I think anatomy is one of those things that if you can know the anatomy, you will probably be able to figure out most other things. So the afferent anatomy is, by way of review — of course, light comes in, focus onto the retina, the retina generates the signal, the signal goes down the optic nerve, there’s a decussation in the chiasm, and then a second decussation in the posterior commissure. Prior to that, there’s a synapse in the pretectal nucleus, and then the second decussation in the posterior commissure, leading to the third nerve nucleus. The subnucleus related to the parasympathetics is called the Edinger-Westphal nucleus. The efferent pathway coming back from the brain to the eye is then, of course, the third nerve. It’s called the fascicle while it is in the brain stem. It’s not really a nerve until it comes out of the brain stem, and then the parasympathetics travel with the third nerve and branch off in the branch of the inferior oblique muscle and finally going on their own to the ciliary ganglion, which is located in the general — the inferolateral portion of the orbit. And then onward, as the short posterior ciliary nerves from the ciliary ganglion to the iris sphincter, and to the ciliary body. So here is an example of the consensual light response, and you’ll see that as you shine the light in one pupil, that pupil constricts. We call that the direct response. And then the other pupil constricts. That’s the consensual response. So ignore the eye where the light is being introduced, and look at the other pupil. And, of course, this is a normal consensual light response. Hopefully everyone is able to see this. I’m told that this webinar will be recorded, so if you need to go back and look for any of these things, you should be able to. So the normal consensual light response. And the anatomic basis for this, in two words, is simply the double decussation. So here in the circles are the two decussations, so this means when you shine a light in one eye, by the time that signal gets back to your third nerve nucleus, it is decussated twice. So both third nerve nuclei get the same signal. Both pupils react symmetrically. The consensual light response. So if you understand this anatomy, you’ll understand a lot about the pupils. Now, the other bit of the anatomy, of course, other than the iris sphincter muscle — we have the iris dilator muscle, and that’s controlled by the sympathetic anatomy. And I showed the schematic here. And you can see that the sympathetics start up in the hypothalamus, travel, as I tell my patients — have a kind of a wacky course. Traveling down the brain stem, down the spinal cord, ’til about the level of C7 to T1, also known as the ciliospinal center of Budge or Budge-Waller. And then they exit the spinal cord at that point, synapse, travel back up — or go over the top of the lung first, and then back up the carotid artery, and in fact travel within the wall of the internal carotid artery, up towards the angle of the jaw, where they synapse for the last time in the superior cervical ganglion, which is right about here. Those postganglionic sympathetic fibers then travel up along the internal carotid artery into the cavernous sinus for a short time. These fibers travel with the 6th nerve, the abducens nerve, prior to jumping over to V1 of the trigeminal nerve, and then onward to both the pupil dilator muscle, the Muller’s muscle, one of the weak elevators of the upper lid, and also to a muscle in the lower lid, also known as Horner’s muscle. And when there’s a problem with the sympathetics, you might see something that looks like this. Where there is a slight ptosis, because of Muller’s muscle not getting the correct innervation. And relative miosis. And we’ll talk more about this when we talk about anisocoria, and the differential diagnosis. So that’s the relevant anatomy. And hopefully that’s a review. Everyone has known that and committed it to memory. We’re gonna move on briefly to the examination, before getting on with abnormalities. So as far as the examination goes, I think there are four main things that we look for. The shape, size, reactivity, and then something that I call the fellow travelers. And the shape usually is round. I usually don’t write round. I don’t like PERLA, if you are familiar with that. Pupils are equal and reactive to light and accommodation. If the pupils are not round, however, it should be noted. Probably the easiest way to do this is to draw a circle that represents the iris, and then draw the shape of the pupil. So that the pupil may be slit-like, in this alligator or crocodile, or it may also be — although it’s round in the bottom picture, it’s not centered. So I would simply draw that for the record. The size, I think, is important. I mean, I don’t care too much if you say the pupils are 3 millimeters and I say the pupils are 4 millimeters, but I do care if you say that one is 3 and one is 3.5 or one is 3 and one is 4. And you can see in the bottom photo here a very obvious anisocoria, a much larger pupil on the right than the left. The top patient also has anisocoria. The left pupil is slightly larger than the right. Both of these degrees of anisocoria need to be noted, and that will become evident as we talk about the differential diagnosis of difference in size of the pupils. Reactivity can be graded in many different ways. I don’t care too much how you do it. I think you have to have your own internal mechanism for doing this. So if you’re gonna use a trace, mild, moderate, or brisk, you know that if you judge a pupil as being mildly reactive, then the next time you see that patient and you look at their pupils, you can say — yeah, that’s how I would grade mild. You have an internal sort of a control as to what you would call it. Your mild could possibly be my moderate. I don’t think that’s a big deal. And then something I’d call the fellow travelers. So fellow travelers mean if there’s a problem with the size and the pupils, if there’s anisocoria, what do you really need to look really closely at, other than the pupils? And certainly you need to look closely at the eyelids, because of the anatomy we just discussed. So if someone has a third nerve palsy, like our patient on the top picture, then there could be complete or very significant to very mild ptosis, depending on how bad the third nerve palsy is, and that’s very obvious. In the photo in the center, you’ll see the dramatic anisocoria, but you’ll notice that there’s also ptosis on the left. It’s not very obvious. So if it’s not obvious, when there’s anisocoria, pull out your ruler, and measure the interpalpebral distance, the distance from the center of the eyelash margin in the upper lid to the center of the eyelash margin in the lower lid. In this patient, there’s gonna be a millimeter, maybe a millimeter and a half of ptosis and miosis, which is crucially important. In the bottom photo, we see the other fellow traveler, other than the eyelid position, and that is eye movement. Some ocular motility. And this patient, of course, is trying to look to the left. This is the same patient that you see in the upper photo, who has the very marked anisocoria. And also the ptosis. But you’ll see that this eye does not have any adduction, and, in fact, if we showed you the rest of the eye movements, you would see that there’s no elevation or depression in somebody with a third nerve palsy. Excuse me. So it’s important to note, whenever there’s anisocoria, look closely at eyelids and eye movements. And this is the anatomy that we just discussed, that I probably don’t need to reiterate. All right. So let’s move on to abnormalities that we’re looking for. And really, when it comes to pupils, there’s two main things that we’re gonna be looking at from a neuro-ophthalmologic standpoint. The first is the relative afferent pupillary defect. Also known as the Marcus Gunn pupil. And the second is the various causes of anisocoria. And so this is the video that we saw earlier, that I had you vote on. Of the Marcus Gunn pupil. I often ask my residents — who were those guys, Marcus Gunn, anyway? And the answer is it was one guy. Marcus Gunn. And basically a Marcus Gunn pupil — I prefer the term relative afferent pupillary defect. Why? Because Marcus Gunn is just an eponym. Relative afferent pupillary defect is a description of actually what’s occurring, why this person is having this pupillary abnormality. There’s a problem, relative problem, with the afferent pathway. So the definition I put here in the box in white — one pupil dilates and the other constricts. Now, really, they’re both dilating. It’s just hard to see that when the light is shown, in this case, in the right eye. You can’t really see the left pupil. Both are dilating. When you swing the light back, both are constricting. Why? Because in this patient, with a moderate right relative afferent pupillary defect, more light is getting back to this person’s brain when you shine the light in the left pupil. And so there’s more of a response. When you shine the light in the right pupil, there’s less response getting back to the brain, and the pupil doesn’t constrict as much. It does constrict. When you look at the direct response — you see? This person’s pupils are PERLA. They’re equal and reactive to light and accommodation. But there’s still a big problem. And that’s why I don’t like the term PERLA. People will often use it to mean that the pupils are fine. This patient’s pupils are PERLA, and there is a moderate relative afferent pupillary defect. And this is just our photos on the left — a schematic — not a schematic. Our photos of this happening. So you see the black arrow. This is the normal resting state of the pupils. In the next frame down, you can see the light is being introduced into the right pupil. It’s being swung over to the left. You’ll notice that the left pupil — when you do that, the left pupil gets larger. They both get larger, because there’s less light getting back on the left than the right. You swing the light back in the bottom frame, and both get smaller. And so that simply means that in this case, there’s a left relative afferent pupillary defect. And more light is getting back on the right side than the left. So there’s more signal getting back to the brain stem when you shine the light in the right eye than the left. That is the basis of a relative afferent pupillary defect. Now, what do you need to test for a relative afferent pupillary defect? Well, I should mention, of course, that whenever you’re checking pupils, you want to have a room hopefully that you can have relatively dim illumination. Not pitch black, but not really bright sunlight, if possible. Mostly because you want the pupils to be bigger, so that you can see a better reaction of the pupils. So you want the room to be dark or dark-ish. You want a bright light. Now, that does not mean you want your indirect ophthalmoscope set on stun. You want it bright. Moderately bright. A penlight that’s weak is probably not good enough. A muscle light would be good enough. You want them to have a fixation target. So you don’t just say look straight ahead or I’m gonna look at your pupils. I always throw up something like the 20/400 or — depending on where you are — like a 6/36 or bigger than that E, or a target, or have them look at something at the end of the room that will fix their accommodation. You don’t want them looking at your light or looking at you. You want them looking at something in the distance that they can focus on. Of course, you need the patient. I’ve had a little box here that popped in that says no tech. So in the United States, at least, and even in my group, my retina specialist partners — oftentimes they have a technician, who is not an MD, who has some training in looking at pupils, check the pupils, and then dilate the pupils. Obviously, once you dilate both pupils, you no longer can tell if there’s a relative afferent pupillary defect. So if there is a potential neurologic problem or unexplained loss of vision, don’t delegate checking the pupils and checking for a relative afferent pupillary defect to your technician. On the right, I’ve got pictures of two different sets of filters. And these are really just the same thing as camera filters. You can see that on the top, the circles there — those are individual filters. On the right is something called the filter bar. Now, the filter bar is available from an ophthalmic supply kind of a place. What you can do with the filters is measure, quantitate, a relative afferent pupillary defect. And it’s fairly simple. You simply identify the patient has a relative afferent pupillary defect. You then place the filters in front of the good eye, and swing the light. So when you put the filters in front of the good eye, not as much light gets through. And what you do is you swing the light, and you increase the strength of the filter, until you neutralize the relative afferent pupillary defect. In other words, you increase the strength of the filter, until you no longer see a relative afferent pupillary defect. And when you do that, you simply read off the strength. So it’s usually expressed in log units. So 1 log would be 10 times less light. So in this way, you can measure. Now, I mention this not because I use these all the time. When I was a resident in training, my neuro-ophthalmologist asked us to measure every patient’s relative afferent pupillary defect. When I became a fellow, and doing just neuro-ophthalmology, my mentor said — what are you doing with those filters? They either have one or they don’t. Put those away. So I mention it mostly not because I advocate using them routinely. But you might read articles in journals where they talk about log unit relative afferent pupillary defects. That’s simply a way to measure them. The smaller the log unit — 0.3 would be a very mild APD. A 1.5 log unit relative afferent pupillary defect would be at least moderate. Okay. Now, this is another question. It’s a little tougher one, perhaps. And I’m gonna give you a polling option here. Let me go ahead and give you that polling option. Okay. So you should now be seeing the options for the answer. And I’m gonna let you watch this a little bit. And you’ll see the light being swung from side to side. And the question is: Is this a small right relative afferent pupillary defect, a small left relative afferent pupillary defect, or these are just normal pupils? And I’m hearing a number — seeing, actually — a number of responses. I’m gonna give you another 10 or so seconds. We’ve got almost half the people voting. All right. 5 seconds. 4, 3, 2, 1. Okay. I’m gonna close the poll. And I’m going to share the results. Okay. So you should be able to see the results. The majority, 56%, said there’s a small right relative afferent pupillary defect. A small percent said the opposite. Small left. And then about a third thought the pupils were normal. So let’s — I’m gonna get rid of the sharing here. And let’s look at the video. So I think the important thing — and of course, the first patient we saw, it’s fairly easy. This person’s a bit tougher. But what I want you to do is look at the initial reaction when you swing that light. And when you swing the light, every time the left pupil gets a bit smaller, and the right pupil either does nothing or comes up a little bit. Down, nothing. Down… So this person has a small right relative afferent pupillary defect. And so this is where it can get kind of tough. Now… I will say that sometimes I will look at pupils and say I’m not sure. Maybe there’s a trace relative afferent pupillary defect. So I would hope that most of you would at least look at this person and say — I’m not sure. Now, you might, then, say to the patient: Is the light brighter in this eye or this eye? Brighter in the left or brighter in the right? If it’s worth a dollar of light in one eye, how much is it worth in the other? Now, the problem with that is, of course, you’ve then taken a very hopefully objective test and made it very subjective, and as we all know, patients will say the darndest things, and sometimes I’ll ask people who I know have a relative afferent pupillary defect on one side, and because it’s their bad eye, they think the light should be brighter, so they’ll tell me it’s brighter in that eye, even though there’s clearly a relative afferent pupillary defect. So I try not to ask people. Sometimes I do, if I think it’s close, and I think the person’s a reliable person. But you look at that initial reaction. The pupil gurus also will say that once you swing that light about four times, if you’re not sure, go to part of the rest of your exam and come back in a few minutes. Because you can affect the system by shining that light in the eyes too much. You can bleach out one retina more than the other. And I think we’ll talk about that. That can even create a little relative afferent pupillary defect. So it can be tough. And if I do write — and sometimes I’ll write question — trace afferent pupillary defect. What do I do? I’ll go back at the rest of the measures of function of the optic nerve. Look closely at visual acuity. Look closely at automated computerized perimetry. Look at the optic disc. Look at color vision. I look at all those things. And perhaps optic neuropathies will be a topic of a future webinar. Okay. So a couple of nuances. A nuance basically means some fine points about relative afferent pupillary defects. The R is for relative. So the implications of this is that the presence of a relative afferent pupillary defect doesn’t mean that the other side is normal. In other words, if I damage one of your optic nerves 75% and I damage the other optic nerve 25%, you have a bilateral optic neuropathy. But you’re gonna have a relative afferent pupillary defect on the side with more damage. So the fact that there’s an APD on one side doesn’t mean the other side’s normal. Sometimes my residents assume — oh, look closely at the eye with the APD. The other side, there’s none. It doesn’t mean that the other optic nerve is okay. The second implication for this is that there will be no relative afferent pupillary defect if the damage is symmetric. That means if I damage both of your optic nerves 50%, there will be no relative afferent pupillary defect. That doesn’t mean you’re normal. Once in a while, my residents will see one of my follow-up patients who’s had a problem in one eye in the past, documented relative afferent pupillary defect, that is persistent and will be there forever. But what happens? They come in with a new symptom in the other eye, and the resident comes out of the room and says — oh, good news. Their relative afferent pupillary defect went away! And I said — well, no, that’s not good news. It’s canceled. Now they have a bilateral optic neuropathy, and there’s no longer a relative afferent pupillary defect. So that’s nuance, fine point, number one. And here’s a good example of a patient who had no relative afferent pupillary defect. You can see both optic nerves coming back from the globes in this very large — what turned out to be a huge pituitary tumor, affecting both optic nerves symmetrically. So no relative afferent pupillary defect. But big problem. The second fine point or nuance is that you only need one working pupil to tell if there’s a relative afferent pupillary defect. So let’s look at these pupils. You can quickly see that when you shine the light, indicated by the arrow, in the right eye, the right pupil constricts nicely. There is no consensual response. You shine the light in the left side, and there is no direct response. So immediately you know this pupil does not work. The left pupil does not work. You do not look at that pupil. But you still swing the light. So what happens when you swing the light? You swing the light from the right eye to the left eye. You watch the right pupil. It gets bigger. Why? Because not as much light is getting back to the brain on the left side. You swing the light back to the right side, the right pupil gets smaller, because more light is getting back to the brain. So there is indeed a left relative afferent pupillary defect. Now, you also have to figure out what the heck is going on with that left pupil, because the left pupil doesn’t work, and there is obvious anisocoria, and the next question, other than — there’s a left relative afferent pupillary defect — is what else is going on with that left pupil. So a left relative afferent pupillary defect. You might hear the term reverse afferent pupillary defect. I hate that term. It’s confusing. People don’t know what it means. I don’t use the term “reverse”. Just call it like it is. This person has a left relative afferent pupillary defect. And here is the same thing in a video. This person has a third nerve palsy on the left. I have to hold the eyelid open. You can see the eye is turned out. But watch the pupil. So left pupil doesn’t work, because they have a third nerve palsy. But watch the right pupil. Every time I swing the light to the right pupil — let me show that again — it gets small. It’s hard to see, but it gets big when I shine it in the left eye. Why? More light is getting to the brain when you shine the light on the right than on the left. So not only is there a left third nerve palsy — there’s a left second nerve palsy in optic neuropathy. So what about some more causes of relative afferent pupillary defects? Typically we think about optic nerve, and maybe some big retinal problem. But there are some other things that might cause small relative afferent pupillary defects. So amblyopia can cause a small APD. Monocular occlusion. A classic story — my resident sees a patient of mine, who’s patching one eye, because of double vision. They go in to see the patient, they ask the patient to take the patch off, they look at the pupils, and they say — oh my gosh, Dr. Golnik missed a relative afferent pupillary defect in the other eye! In the good eye! And they come out. They tell me — oh, by the way, you missed this finding. And I go back in 10 minutes later. The patient is now light-adapted, and there’s no longer a small relative afferent pupillary defect. And I say — you idiot. There’s no APD. I could have sworn there was. So I explain to them what’s happened. So monocular occlusion can do it. Big time anisocoria. Not 1 millimeter, 2 millimeters, 3 millimeters. Huge anisocoria. Why? Because the pupil, the aperture, the area, is pi R², right? So a huge pupil, compared to the other side, is gonna let in a bit more light. And you can see a very small APD. Really dense blood in the eye. So an 8-ball hyphema — that means the front of the eye filled up with blood. Excuse me. A vitreal hemorrhage that is very dense, that does not allow you to see details of the fundus, might cause a small APD, but those sorts of things — if there’s more than a small APD, you’ve got to look for other problems. Cataracts don’t do it. There are some reports of really dense cataracts causing a contralateral relative afferent pupillary defect. Contralateral. So the implication here is if there’s anything more than a small APD in any of these conditions, you need to look for other causes of relative afferent pupillary defects. So, in summary, the R is for relative. Bilateral, symmetric optic nerve damage doesn’t result in an APD. You only need one working pupil. Watch the pupil that works. The other pupil is not telling you anything. And a small APD can be seen in some of these other conditions that we talked about, but only small. Anything more than small — look for other causes. Look for an optic nerve problem. Okay. So that’s what I have to say about relative afferent pupillary defects, and I can tell that some questions were being typed in. I’m gonna wait ’til the end to try to answer the questions, and I’m gonna move on to our second big topic of anisocoria. So this is not an exhaustive list of causes, but this is sort of the six things that are probably by far the most common things I’m gonna see in somebody with anisocoria. And it’s pretty straightforward, once you know sort of — these are the things you’re looking for. The first step is, of course, how does the pupil — how do the pupils react to light? If there’s a normal light reaction, then it may be physiologic. Which means there’s just a normal difference in the size of the pupils. Or it could be Horner syndrome. If there’s an abnormal light reaction, you’re left with a few more choices. It could be an Adie’s tonic pupil, third nerve palsy, could be pharmacologic, or could be iris sphincter damage. And we’re gonna talk about each of these entities. We’ll start with this side of the flowchart. The normal light reaction. So here’s a young woman. This is actually — she came in with her husband. They were newlyweds. She’d gotten married a couple weeks earlier, and the night after her wedding night, she noticed anisocoria. And that’s why she was sent to me. She said — oh, this is new. I’m not sure what happened my wedding night, but this is the result. My pupils are different sizes. And her husband was sitting in the corner with his chin down. He wouldn’t look me in the eye. And I looked at the pupils, and they both reacted symmetrically. There were no fellow travelers. Her lids were normal. Her eye movements were normal. And I said… You know, this looks a lot like normal anisocoria. Normal meaning this is just the way your pupils are. She said — are you kidding me? I’ve got light blue eyes. I put makeup on every day. You don’t think I would have noticed this? And I said — well, let’s do a FAT scan. Family album tomography. Let’s look at old photographies. She said I don’t have any old photos. But I know this is new. I said — how about your driver’s license? So she pulled out her driver’s license, which had a photo. Not a very good one. And I used my 20-diopter lens and a muscle light, magnified it up, sure enough, there it was. I showed it to her, and she said… Huh. I said… When was this photo taken? She said — oh, two years ago. And I said… Well, you see, there it was. And her husband picked up his head, smiled at me, and she looked at him and she said — why didn’t you notice that before? And he put his head back down. Not sure what happened to them. So this is an example of physiologic or normal anisocoria. By far the most common scenario that you’re going to see anisocoria. And in fact, in one study done some years ago, they took photographs and measured with a computer. They chose 0.3 millimeters, more than 0.3, as anisocoria. Pretty small, but something they thought you could see with the naked eye. And they found that indeed one in nine patients have physiologic anisocoria. So that means that for every nine patients you see, you should be documenting physiologic anisocoria. When you look at the pupils in the light versus the dark, there’s about the same degree of anisocoria. So you can see both pupils are larger in the dark, on the bottom right. There’s about the same degree of anisocoria. Try to look at old photographs. I recently had a 40-year-old anesthesiologist, a woman who came in with a sudden onset of anisocoria. She had about 1 millimeter of anisocoria. And I said — you know, we went through the exam, and I said — boy, it looks, like, normal. It looks physiologic. And she said… Are you kidding me? I’m an anesthesiologist. I would have noticed this. I said — humor me. Go home. Look at some photos. And she called me and said — sure enough. There’s a photo from 20 years ago, plain as day. It’s been there. I just never noticed it. And the other thing to say about physiologic is that it can come and go. It doesn’t have to be there 100% of the time. All right. So this is another polling slide. And I’m going to give you — let me open the poll. Let’s see. Let me find the poll here. No, it doesn’t let me do that. Hold on. One sec. I’m gonna go backwards and see if it will… Poll three. Oh, I didn’t… I skipped poll three. Sorry about that. I’m not sure where my poll three slide was. Okay. Here’s poll four. So I’m gonna launch the poll, and then I’m gonna try to… Okay. So you should be able to see the poll slide and questions. And this is a 55-year-old woman. She was in the emergency room, just because she had this car accident. She had some neck pain. It wasn’t terrible. And she wanted to go home, basically. And they said — well, we noticed something about your pupils. They’re not the same size. And we think you need to see an ophthalmologist.. Let me try to play that again. There we go. We want one of our ophthalmologists to come over and check you out. And she was kind of upset, because she felt fine. She just wanted to go home. Thought she had a little whiplash kind of an injury. And you can see that her pupils both react. And you can see the pupil exam. So I’m letting you vote here. Hopefully everybody’s voting. I’m collecting the votes. Let me see if I can play that one more time without doing that. And one more time. I’ve got about — almost 2/3 of you voted. Okay. I’m gonna close the poll. All right. 5, 4, 3, 2, 1. And good. Okay. A few of you got your votes in. Let’s see what people say. I’m gonna share the results. Okay. So about half the people said a right Horner syndrome. Which is indeed what she does have. So let’s look at this video. About 23% said left APD. About 26% physiologic. Okay. So let’s look at this video. Okay. So clearly she’s got anisocoria. The left pupil is larger than the right. She does not have really obvious ptosis, but if you measure, you’ll see that she indeed has a difference in her lid fissure. She’s got at least a millimeter difference in the lid fissure. So she has relative ptosis and miosis. There’s no relative afferent pupillary defect. Now, I’m not showing you that too well, but there’s no APD. So she has a right Horner syndrome. Whoops. And you’ll remember the anatomy — which I tell my patients — this can be a problem anywhere from your head to your lung, as the anatomy goes down the spinal cord, out through C7, T1, over the top of the lung, back up the internal carotid artery, for a short time, with the 6th nerve. Then the 5th nerve to the dilator muscle and Muller’s muscle in the upper lid. So Horner’s syndrome is a problem somewhere along that chain. Now, this is a photo in the upper right from actually a magazine, from many years ago. Being a good neuro-ophthalmologist, I immediately noticed the anisocoria. She also has slight ptosis, relative ptosis, on the left, as compared to the right. Here’s a little bit more obvious ptosis in the bottom left. And the key thing here to separate this from physiologic — which I didn’t show you in the video — is to turn the lights off or dim the lights significantly. And you should see an accentuation of the anisocoria. Why? Because the normal iris dilator muscle in this case on the left is not working well. The right is working. So there’s more. Unlike physiologic. More anisocoria in the dark than in the light. Something else you can look for is called dilation lag. So let’s look at a video. And look at the pupils. Pretty subtle Horner’s on the left. Now watch as the lights go out. Eventually. You’ll see the right pupil — look how much anisocoria. Big time. Watch as time goes by. This is real time. The left pupil gradually gets some bigger. So that as 15, 20, 25 seconds go by, there’s less anisocoria now. Look at how subtle this Horner’s is. Tiny ptosis. Tiny anisocoria. Yet this could be life threatening. So initially big time anisocoria. So this is called dilation lag. Some people think this is pathognomonic for Horner’s. You don’t have to see it, but if you do see it, it’s Horner’s syndrome. So many of you most likely — I don’t know for sure — don’t have cocaine drops to use. I do. Our pharmacy makes them for me to use for this condition. You can use apraclonidine to confirm. Hopefully if you don’t have any drops, you’re gonna just look and clinically you’re gonna make the diagnosis. You can use hydroxyamphetamine, which is even tougher to get, at least in the US, to localize. So the cocaine inhibits the reuptake of norepinephrine, so it will accentuate the anisocoria. Apraclonidine is a weak agonist, and it works on the principle of denervation supersensitivity. Probably more than we need to go into here. Hydroxyamphetamine causes the release of stored norepinephrine. So if there’s a problem that is postganglionic, and these fibers are dead, there is no stored norepinephrine. So you put the hydroxyamphetamine in, and nothing happens. On the other hand, if the problem is preganglionic, somewhere between the superior cervical ganglion and back up to the brain, then these postganglions are filled with norepinephrine. You put in the hydroxyamphetamine, it’s all released, and the pupil gets big. There is some controversy as to whether — who cares? Just get the imaging studies that are appropriate, and look at the whole system. There are differences in what might cause pre versus postganglionic Horner’s. In general, postganglionic Horner’s are usually gonna be more of a benign problem. We worry about things like lung cancer. Pretty rare — at least for this to be — present in this way in the United States, in this day and age. But internal carotid artery dissections we worry a lot about. And the reason we worry about them is they can kill you, and the woman in the emergency room, the video I showed you, had an internal carotid artery dissection. So she had a little tear in the inner wall of her carotid artery. That allowed blood to dissect between the layers, which then caused a narrowing of the lumen of the artery, and either no blood flow to the brain on this side, or very slow, stagnant blood flow. And what can happen is that, if the blood flow is stagnant and slow, blood clots form. Travel to your brain. And can kill you. Or perhaps make you paralyzed forever. Here’s an axial image of her MRI. It was read, by the way, as normal. Here is her left internal carotid artery, with a normal flow void. Here is her right internal carotid artery, with the so-called crescent moon sign. This is clotted blood in the wall of the artery. This is a sign on MRI. You would of course get an MRA as well. But this is a sign on MRI of carotid artery dissection. So if there is anisocoria, and you look at the pupils, and they both react well, then you need to decide: Is it physiologic? Or is it Horner’s? Using the test that we just discussed. Let’s move to the other side of our flow sheet. If the pupil does not react well. So here’s a patient whose coworker notes that the pupils are not the same size. Oh my God. And the patient is asymptomatic. Let me show you a video of a pupil. It’s not her pupil, but it’s someone with the same problem. And… Ah-ha. I have a question slide. Let me see if I can find… Okay. Here is the poll. It’s coming up nicely. Let me open up the polling for you to see the choices here. All right. So you see the choices. So what’s happening here is the lights are — the person here is looking at a near target, and there has to be — read the near card. I’ll let this video loop. And now the person has to look towards the end of the room. You can see what happens when they do that. And… Okay. Again, this is the patient looking at the near card. And looking towards the end of the room. Now, let’s look at the light response. Okay. So the lights are gonna go off and then on. Watch what happens when the lights turn on. Here they go off. And you can see what happens with the light response. And the near response. So is this a relative afferent pupillary defect? Is this an Adie tonic pupil? Is this a third nerve palsy? Is this pharmacologic dilation? And I have people voting. Doing a pretty good job. Got more than half. I’ll give you another 10 seconds. 9, 8, 7, 6, 5, 4, 3, 2, 1. Okay. I’m going to close the poll. And share the results. Okay. So very good. Most of you, 84%, got the correct answer. Which is the Adie tonic pupil. Let’s get out of there. So what we’re seeing here are a number of things. Number one, we see sectoral contraction right here. And in general, a poor light reaction. We see a good 360-degree near reaction. So this is pupillary light near dissociation. And when the person looks towards the end of the room, we see a slow — some might say tonic — redilation of the pupil. That’s how this pupil got its name. From the slow tonic redilation, compared to other things that cause light near dissociation, which might be a different webinar, that don’t cause a slow topic redilation. So the correct answer is Adie tonic pupil. Whoops. So this is a postganglionic parasympathetic problem. There’s no ptosis or ophthalmoplegia, because the problem is somewhere at the ciliary ganglion or onward. So this is after these fibers have already left the third nerve. So it’s an isolated pupil problem. The pupil is usually big, although over decades it can become actually the smaller of the two pupils. Although it’ll never react to light like it used to. There may be or may not be segmental iris contraction. There should be slow tonic redilation. And then light near dissociation. This is usually idiopathic, and there is no big evaluation for this in general. You want to make sure there are no other orbital signs, of course. But most patients with this — there’s no diagnostic testing done. You can prove that it’s an Adie’s pupil by using weak pilocarpine. So we know that 1% pilocarpine, a strong agonist, will constrict your pupils. But a weak one won’t, unless you have an Adie tonic pupil. Because of denervation supersensitivity. So in a patient with denervation supersensitivity, the pupil is supersensitive to this weak solution, and now the Adie’s pupil is actually the smaller of the two pupils. So you can do this. I haven’t had to do this in quite some time, because if you see all the findings, in the US, at least, we have a saying that goes like this. If it looks like a duck and quacks like a duck and walks like a duck, it’s a duck. Here’s a patient with double vision for two weeks. I’m trying to show you the pupils. He’s got dark brown irises. You can see there is anisocoria. I hope you can see. And that left pupil — you may have to take my word for it — that left pupil just doesn’t react as well to the light. So that’s the pupil problem. We’re of course going to look closely, because there’s anisocoria. We’re gonna look closely at the fellow travelers. He has a bit of ptosis on the left, and he has a problem with depression. It’s not normal. It depresses. And look at his adduction, compared to the other side. Not quite as good. And when he looks upward… Not as good. So he has a third nerve palsy. Now, does his eye move up and down and in? Yes. Does it look like a textbook? No. But things are not always gonna look textbook. This is a mild left third nerve palsy with pupil involvement. So the point of the slide is that a third nerve palsy may be obvious. The lid is shut. The eye doesn’t move up, down, or in. But it can be mild. This photo is from a patient with a third nerve palsy. She had no double vision, until you asked her to look up, and then she did. She was actually sent to me by a neurosurgeon who was wondering why the person was sent to her. And she indeed had anisocoria, and had an aneurysm pushing on her left third nerve. So I say here — the pupil exam will dictate your evaluation, in part. That’s because tumors and aneurysms tend to push on the third nerve. And cause third nerve palsies that you want to identify the cause. There’s some debate about whether every patient with a third nerve palsy should be imaged, and the imaging typically would be MRI and MRA, or CT and CTA. But you want to look at the blood vessels, obviously, to rule out an aneurysm. And here another patient with big time anisocoria. The right pupil doesn’t work either. The left pupil does. And there’s no relative afferent pupillary defect. And here we are, after 1% pilocarpine. 1%. So 1% pilocarpine will not constrict a pharmacologic pupil or a pupil that’s had a lot of sphincter damage. But you should be able to diagnose that with a slit lamp. But this patient, 30 minutes after 1% pilo, had no constriction of the right pupil. Now, let’s say that right pupil was a little bit smaller. Let’s say it was, instead of being 7 millimeters, it was 4Ms. After the pilo. That’s still pharmacologic. It’s still a pharmacologic blockade. If that pupil were big, because it was a third nerve palsy, because it was an Adie’s tonic pupil, you put in 1% pilo, and that pupil is gonna be as small as the contralateral pupil. If there’s a pharmacologic blockade, even partial, then the pupil won’t get as small. So a large dilated pupil. We do this all the time in clinic. Right? No ptosis. No ophthalmoplegia. No fellow travelers. I say here the lack of a history of something in the eye shouldn’t dissuade you. I’ve seen all sorts of bizarre stories. I had a woman recently who came in. It looked like a pharmacologic pupil. She’d already had MRI, MRA. Multiple blood tests. I don’t know how much they spent on her evaluation. It looked pharmacologic. I put in 1% pilocarpine. Nothing happened. I said — something had to have gotten in your eye. She denied it initially. Then she pulled a tube out of her pocket. It was a tube of atropine ointment. And I said — she said well, could this do it? And I said — well, yes. That could dilate your pupil for days. She said — oh. I said — where did you get that? She said — oh, they prescribed it for my horse’s eye problem, and my eye felt funny, so I thought maybe I’d put some in my eye. Why didn’t you tell anyone, before they spent $10,000 on your evaluation? I was embarrassed. So don’t let that dissuade you. One of the more common things I see are the scopolamine patches, the motion sickness patches, that go behind the ear. If you put that patch on and then rub your eye, guess what? You’ll have a pharmacologically dilated pupil. And then finally, iris sphincter damage. I’m trying to show you here this very diffuse damage to the iris. And this of course may render the pupil large and not working. So that would be the end of that differential. So in summary for the entire webinar, pertinent pupillary problems, as usual, you need to know some anatomy. So memorize that brief bit of the anatomy. RAPDs are crucial. You need to swing the light, you’ve got to swing the light. Remember the fine points that we talked about. Anisocoria should be fairly straightforward. You got about half a dozen possibilities, and you can narrow it down to either the physiologic in Horner’s, the normal light reaction, or to the abnormal light reaction, and the four entities we discussed. So… I am going to stop there and see if I can look at the questions and answers. Okay. So let me start with the first and try to work my way back, and see what we can get through here. So the question is — and I’m not sure if you can see these or not. How long should you hold the light on each side, when checking for the APD? I hold the light there… Wait a minute. Hopefully people are… Okay. Hopefully people are hearing this. I shine a light only for as long as it takes, really, for me to see that initial reaction. Because if you keep the light on the pupil for any length of time, a couple of things are gonna happen. One, the pupil is probably gonna bounce around a little bit and then confuse you. And two, if you hold the light on one pupil more than you hold the light on the other pupil, you can bleach out the retina and actually affect the system. You could create a small APD by shining the light persistently in one pupil longer than the other. So I hold the light very briefly, to look primarily at the initial reaction. Okay. Anonymous viewer asked: How do you grade the APD? So… Whoops. Sorry. I clicked the wrong button. How do you grade the APD? You know, you can grade it, of course, with the filters that I mentioned. I think it’s tough to grade the APD. And the reason I say that is, if you have a young person, like the person I showed you at the very beginning of the webinar, they had very reactive pupils. And they had what looked like a moderate APD. But I can tell you, if that person is 80 or 70, and their pupils are small, and their pupils don’t react well to light, you may look and say… Oh, there’s a small APD. But if you try to measure that with filters, you’re gonna say… Wow. This is way bigger than I thought. Why? Because the pupils are not that reactive. So, frankly, grading the APD, from my standpoint — I mean, I think it’s okay to grade it. It doesn’t really mean much. It doesn’t mean — oh, the person can’t see, if it’s a big APD, in a young person, versus what looks like a small APD in an older person. Because you can be fooled by the grade. And I think as one of my mentors said, either they have one or they don’t. And I think that’s pretty much true. So that would be my answer to that. Okay. Let me make sure I get to — I hope I’m doing this right. The next question is: How can the patients see the fixation target in a dark room? That’s a good question. Because, of course, in my dark room, the fixation target is an illuminated screen with a light. If you don’t have an illuminated screen, then I think I would darken the room enough that they can see a target. But you’ve got to fix their accommodation. And again, the room doesn’t have to be pitch black. It can be just somewhat dim. So I would say, if you don’t have an illuminated screen, then you need to have the room bright enough that hopefully they can see something at the end of the room. Otherwise their pupils can be bouncing around, because they’re accommodating. Let’s see. What is RAPD by reverse? So that is the video that I showed, where one pupil doesn’t react. So whenever someone talks about the reverse, they mean — hopefully, if they’re doing it right, or speaking about it the way it’s supposed to be spoken about — they are implying that that means that one pupil doesn’t react. And as soon as you determine that one pupil doesn’t react to light, direct or consensual, then you still swing the light, but you just look at the pupil that works. You swing the light. But look at the pupil that works. So if the pupil that works gets bigger every time you swing the light to the opposite side, and then smaller when you swing the light back to the working side, there’s a relative afferent pupillary defect on the pupil that doesn’t work. On the other hand, if you swing the light from the pupil that works to the other side, and the pupil that works gets smaller, and then you swing the light back to the pupil that works, and it gets bigger, then there’s an afferent pupillary defect on the side of the pupil that works. I hope that makes any kind of sense. What does PERLA stand for? Pupils are equal and reactive to light. And the reason I hate that, PERLA, is that — and I’m not sure if that’s used in other countries — but it seems like in the US, it’s a phrase — they often add the A at the end, PERLA, for accommodation — a phrase that means I looked at the pupils and they were fine. The problem is that pupils can be PERLA, and there can be a relative afferent pupillary defect. So I discourage using that entirely. So I wonder, in the setting of a clinical exam… Hold on. It’s bouncing. I wonder, in the setting of a clinical exam, what is the priority of examining the pupil? Is it after or before other, with the slit lamp of the patient? We usually forget to test the pupil in the outpatient clinic, because we have no fixed sequence. I usually do it before I shine any other lights in the eye. Especially the slit lamp. Because, of course, that slit lamp is darn bright. Or usually it is. And you can affect the system. So my feeling would be as soon as the visual acuity is checked, I check the pupils. And so if you start — and we usually start with checking acuity. Second step is checking the pupils. Okay. Let’s see. Can Adie’s pupil patient have reading problems initially when she starts to read? Definitely. So remember, when this starts, and we didn’t talk about it in detail — this is a postganglionic parasympathetic problem. The ciliary body is out, initially. The ciliary body is out. And so people will have problems with accommodation. Now, you can quickly reassure them, in a sense, by holding up a +3 lens, and they’ll be able to read just fine. The good news is that, although the light reaction of the pupil does not usually get better — not usually — does not get better, the accommodation almost always does. And that gets to the reason we think that there is light near dissociation. So this gets a little more complicated, but the bottom line is that for every hundred postganglionic parasympathetic fibers, 97 go to the ciliary body. 3 go to the iris sphincter. Those postganglionic parasympathetic fibers regenerate in everybody. But what happens is… Usually 3 of the 97 fibers that used to go to the iris sphincter regenerate to the ciliary body. And 3 of the 97 fibers that used to go to the ciliary body go to the iris sphincter. So when you shine a light in the eye, if you could measure 3/97 accommodation, that’s what you would see. So the point is that the accommodation — it basically gets better. Now, obviously, if the patient’s got bad accommodation, because they’re of that age, then it won’t. But that’s the answer. So usually it takes a month or two for the accommodation to recover. But it usually does recover. Okay. Is it okay if someone age 61 with longstanding diabetes suffering third nerve palsy with pupillary involvement — and I don’t check her with a radiologic exam, because I simply think this is caused by a diabetic retinopathy? So the answer is… Clearly you can have — and I have had patients over the years — with diabetic thirds, even with a lot of pain, with pupillary involvement, with normal MRI/MRA, or CT/CTA, who have got diabetic microvascular third nerve palsies. In the United States, they’re gonna get imaged. Because of the pupil involvement and the wish to not run the risk of being sued if you’re wrong. So it’s a tough question to answer. I mean, I think the teaching certainly is — they should be imaged. Can it happen? It definitely can happen, that the pupil can be involved with a diabetic microvascular third nerve palsy. The next question is: What kind of filter do you use for relative afferent pupillary defect? You can buy… At a photography shop, at a camera shop, they sell filters for cameras. Those were the round filters I showed you. I personally have a set and I have not used them in a decade, because I don’t — I just don’t find it very useful. You can also buy — and I have no financial affiliation or association with Gulden Ophthalmics. They’re a company. Gulden. That sells that filter bar. Sort of like a prism bar. Could a relative afferent pupillary defect even happen if both eyes are normal? Well, so… The answer is it shouldn’t happen, if both eyes are normal. Now… As a fine point, the pupillomotor fibers branch off from the visual fibers in the brachium of the superior colliculus in the midbrain. If you had a lesion in the midbrain that affected those pupillomotor fibers, after they’ve separated from the visual fibers, which go on to the lateral geniculate body, you could have a relative afferent — a small relative afferent pupillary defect with no loss of vision. Because there’s a separation between the pupillomotor fibers and the visual fibers in that area. Okay, hold on. Total third nerve palsy with pupillary involvement. Is it an emergency? The answer is yes. In general, that is what we were just talking about.. Third nerve palsy. With pupillary involvement, you want to get urgent imaging to rule out the aneurysm, so you need not just an MRI or a CT. You need an MRA or a CTA. Can you see abnormal consensual reflex and no relative afferent pupillary defect? Sure. If the… If I pharmacologically dilate one of your pupils — there will be no consensual reflex, right? But there will also be no relative afferent pupillary defect. So anything that affects the efferent side of things — so it will cause a problem with the consensual reflex. And there will be no afferent pupillary defect. Should the other eye be occluded while performing the direct light reaction test? No. Can you explain reverse RAPD anatomically? Sure. It’s simply that… Hm. I think I’ve… I might have already explained this, but the bottom line is: It’s simply — again, I hate the term reverse APD, because it’s not really — it’s really — the best way to talk about it is I see a relative afferent pupillary defect by the reverse technique. So it’s not really a reverse APD. If there’s an APD on the left, and the left pupil doesn’t work, I’m going to swing the light and look at the right pupil. If I swing the light from the left to the right, and the right pupil constricts, and I swing the light back to left, and the right pupil gets big, there’s a left relative afferent pupillary defect. Now, you could say — I detected a left relative afferent pupillary defect by reverse technique. But I would avoid the term reverse APD. Personally, I wish that term had never been introduced anywhere by anybody. In one case, you talked about third nerve palsy, you mentioned the second nerve — that was simply in that video that I showed — I should have said — the second nerve, of course, was the optic nerve. That person was the one with the left third nerve palsy. And I was trying to demonstrate that they had a left relative afferent pupillary defect too, by the reverse technique. So I said there was a third nerve palsy, plus a second nerve palsy, which I meant — plus an optic neuropathy. So they had — cranial nerve II and III had been injured, actually, in that case, in a motor vehicle accident. Is it proper to measure the pupil with plus optics? Some autorefractive measures from one… To see the difference… I’m not familiar with plus optics. Unless that means — I know that right now there are some relative afferent pupillary defect machines that will detect relative afferent pupillary defects. But I’m not sure what that is. Is pediatric patient with pupil abnormality common? Well, of course, it depends what you mean by common. I tend to not see lots of kids, because we have a big children’s hospital, and seven pediatric ophthalmologists. I mean, it’s common obviously, if they have an optic nerve problem, it’s common. It’s gonna be present. But I’m not really sure how to answer that question. Pupil response in oculocutaneous albino patients is always deceiving. Can you share your experience? I think my experience is that I don’t have a lot of experience. But I don’t think that there should be… I mean, I think when you’re checking either for anisocoria or for relative afferent pupillary defects, you should be able to detect them. But I must say I don’t have lot of experience with that particular situation. How can we define pupillary status in case of bilateral optic atrophy? How we term the pupil status? So if someone has bilateral optic atrophy, if there is asymmetric damage to the optic nerves, then there will be a relative afferent pupillary defect. If there is symmetric damage to the optic nerves, there will be no relative afferent pupillary defect, and I will simply say I think there’s a bilateral optic neuropathy, because there’s bilateral optic atrophy. But, of course, because it’s symmetric, I don’t see a relative afferent pupillary defect. Is there any pupillary abnormality common in — I believe CP is meant to be cerebral palsy in the child. Not that I know of, no. What other than microvascular can spare the pupil in third nerve palsy? So that’s an interesting question, because there is some debate right now, and there is a paper published that basically says: Gee, you know, you certainly can have a tumor or an aneurysm push on your third nerve and cause pupillary sparing. In other words, if you have a mild third nerve palsy, and there’s no pupil involvement, well, maybe the aneurysm or the tumor just hasn’t pushed hard enough yet. So clearly this rule of the pupil is really filled with lots of exceptions. So if I see a patient with a third nerve palsy, and we’ll probably do this in a subsequent webinar — we’re talking about doing a comprehensive neuro-ophthalmology webinar series, for those of you interested — but if I see a patient with a third nerve palsy, and it’s not complete — in other words, the lid’s not completely shut, and the eye has some movement, up and down and in toward the nose — all bets are off on the pupil. And that’s a whole different scenario. Those people are much more likely to get imaged. Or at least to be seen very soon. Like, in the next couple of days. To make sure the pupil doesn’t become involved. Now, a complete third nerve palsy, complete, lid is shut, eye doesn’t move up or down or in, with pupil-sparing — other than microvascular, that would be really unusual, to have pupil sparing. You could put in the differential myasthenia gravis. Because that’s always in the differential if the pupil is not involved. That would be pretty unlikely, but that would be in the differential. Should you always use white light? The answer is I always use white light. Never use some other color. Do we see an RAPD in albinism? I don’t believe so, although I don’t see lots of albinism, as I mentioned. Unless, of course, there’s some reason to have an optic neuropathy. Can we have a patient with no pupillary involvement in third nerve palsy? Yes. So in the setting of — that we just mentioned — of a microvascular diabetic hypertensive, I routinely see no pupillary involvement. Let’s see. Hold on. Apart from optic neuropathies, please give us other causes of moderate to severe. So the main cause of a moderate to severe APD other than optic neuropathy is gonna be a retina problem. So if there’s a big — if you have a total retinal attachment, if you’ve got a central retinal artery occlusion. If it’s a subtle retinal problem, there should be at most a small relative afferent pupillary defect. But those really, other than — optic nerve and retina are the things that are gonna give you big APDs. Dilation post-blunt trauma — the sphincter is normal. Can this recovery spontaneously? If not, treatment? So the answer is yeah. So certainly, if we see this thing, and I didn’t mention it, called dramatic mydriasis, where the iris, in a sense, is stunned, hopefully. There’s not gonna be permanent iris sphincter damage. I think that — clearly those patients initially are gonna be followed. You’re gonna look for any other fellow travelers, and hopefully, the pupil is gonna recover from whatever. And I’m not sure we know for sure what causes it. But hopefully it’s gonna recover, over some hours, days, weeks, kind of ballpark. If it doesn’t recover, then there’s probably been iris sphincter damage. And there’s not really much to do about it. Depending on the patient’s age, you know, we could, if the person ultimately needs cataract surgery, you could do, you know, a baseball stitch, a stitch to make the pupil smaller, but that wouldn’t be recommended if person is phakic, without cataract. Let’s see here. A couple more. what’s the next step, after finding a relative afferent pupillary defect? Ah-ha. Well, then, of course, the question is: You know, let’s assume you’ve looked at the fundus and the fundus is completely normal. Or let’s say there’s optic disc swelling. It’s not some big retinal problems. You’ve ruled out those other things that can cause small APDs, like dense blood and amblyopia, that kind of stuff. Well, then you’re gonna have to look for a cause of an optic neuropathy, and that’s gonna be a whole nother webinar. But the bottom line is: It depends on what you think is going on. Why is there an optic neuropathy present? That can take some hours to answer. How sensitive is a relative afferent pupillary defect in the diagnosis of early suspicious glaucomatous optic nerve changes? Well, probably… I’m gonna say not as sensitive as other measures, because, you know, usually glaucoma is fairly symmetric. And so oftentimes you don’t see a relative afferent pupillary defect in glaucoma, even when it’s more advanced, because it’s symmetric. But if it’s asymmetric, you’re gonna see a small APD. But I would think that would be a pretty insensitive way, compared to the other measures that we have. One of my patients was using atropine for 14 days, and during the time, while the pupils were dilated, I was doing panretinal photocoagulation. Suddenly her pupil constricted. What happened? That is a good question. I don’t know. You know, panretinal photocoagulation can cause an Adie-type pupil by affecting the short posterior ciliary nerves, as they travel in the wall of the eye. In the sclera. So rarely I will see a patient, after heavy PRP, who develops what looks like an Adie’s tonic pupil. Now, this is sort of the opposite of that. So, you know, I really don’t know. Maybe… I don’t know. It would be total conjecture. Maybe you caused some sort of overaction of those… But even then, I would think the atropine would blockade it. So I don’t have a good explanation for that, and I’ve never heard of it. What are the fellow travelers in the pupil exam? So primarily the fellow travelers are the lid and the motility. Because the third nerve and the sympathetics and what those nerves innervate, other than the pupils, and those are the primary fellow travelers. Obviously you’re gonna do a good eye exam on anybody. But those are the things you really want to pay close attention to. All right. I think this is the last question. Do you dilate pupils on the same day when the patient’s had severe blunt trauma? So it depends. I mean, if the person is in the intensive care unit, and the neurosurgeons tell me — hey, this person might herniate, and we need to monitor their pupils. They’re unconscious. We need to monitor their pupils for that eventuality. Then the answer is we don’t. That’s about the only time we would not, I think, you’re talking about severe blunt trauma, like to the head. Okay. I think I’m at the end of the questions. And I know that we’re about 15 minutes over time. So I thank everybody for participating, and like I said, stay tuned. We may have further — try to do some sort of a comprehensive neuro-ophthalmology series of webinars on Cybersight. And I’m going to sign off here. I think, I hope, that everyone enjoyed it, and have a good morning, evening, or night, depending on what time it is where you are. Thank you.

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August 16, 2016

Last Updated: October 31, 2022

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