Lecture: Approach to the Patient With Unilateral Optic Disc Swelling

Dr. Golnik: Well, greetings, everyone. Thanks for joining the Orbis webinar on July 16th, might have the same date, maybe not with time changes. And this is on unilateral optic disc swelling. And today because instead of one speaker we have four participants, myself, Karl Golnik, I’m a neuro-ophthalmologist and professor at the Barrow Institute Phoenix, Arizona. Jay, would you introduce yourself?

Dr. Patel: Nice to meet everyone, I’m Jay Patel, as at the Barrow Neurological Institute in Phoenix, Arizona.

Olufunmilola.

I’m Olufunmilola Ogun from Ibadan, Nigeria. I practice general and neuro-ophthalmology.

Mario?

Hi, I’m Mario Perez.

Dr. Golnik: Okay. Good. Our objectives for this webinar are several. When we’re done, you should be able to describe the approach to the patient with unilateral optic disc swelling. Be able to list the differential diagnosis, and be able to list signs and symptoms that help differentiate the various potential etiologies of the disc swelling. And here’s the plan. So, I’m going to present a case, fairly briefly, just in a moment. And then I’ll ask if there are further questions from the panelists to sort out what could be going on. Then the panelists will provide each of their individual differential diagnosis. We’ll talk then about the diagnosis — or I’ll ask about the diagnostic approach. What sort of tests might be ordered to help sort these things out. And then there will be three short talks about the most common entities that we think could result in this patient presentation. Finally, conclusions and questions. Finally, a question and answer option for all of the participants and you can put questions in there any time you want. I don’t think we’re gonna get to them until towards the end. But feel free to — feel free to put in questions or write them down or whatever and we’ll try to answer as many as we can, time permitting. So, with that, we’ll move on to — whoops, sorry. The case. So, that’s the — here we go. So, this is a 48-year-old woman. Complaining of painless, blurry vision in the left eye for the last two days. Her past ocular history is only remarkable for mild myopia. Her past medical history for hypertension. Her family history for hypertension and a stroke in her father. Social history, she says that she has one to two alcoholic drinks per week, but does not use tobacco or any illicit drugs. Her exam, she’s 20/20, 6/6 in the right eye, 20/80, or 6/24 in the left eye, the eye in question. And Ishihara are r plates, 11/11, 4611 in the left. There’s a 2 + left defect. Visual fields normal on the right, but sort of just generally depressed. Not a particular pattern of a visual field, but it’s clearly abnormal. Her motility exam, external exams, exams are all normal. And her fundus looks like this on the left. On the right, she has a normal fundus, normal disc. And so, I’ll let you look at that and the participants look at that. The panelists have seen this case up to this point in the past. So, they’ve had a chance to take a look at it. So, this is the fundus appearance. So, I think I’m gonna leave that photo up while I ask the panelists about other questions or things they may want to know about the case. And I’m gonna ask the panelists to just give me one question at a time because I don’t want one panelist to answer all the questions and then not give an opportunity for the other panelists. So, why don’t we start — we’ll see. I’ve got my photos in a row here, is there a question about the patient that I haven’t given answers to?

Dr. Ogun: Any headache or jaw pain?

Dr. Golnik: There is no headache or jaw pain. Denies issues with chewing at this time. Jay?

Does she notice these symptoms upon awakening?

Somewhere during the day, she woke up — something didn’t seem right, and started covering each eye. Oh, clearly it’s my left eye. Mario.

Dr. Perez: And the contralateral part?

Dr. Golnik: I did say the fundus is normal. That is .1. Funmi?

Yes, any similar event like this in the past?

This is not. She denies any other visual issues other than the glasses and no episodes of visual loss. Jay?

Dr. Patel: What time does she take her blood pressure medications typically?

Dr. Golnik: One in the morning and one in the evening, before bed. Mario?

Dr. Perez: Any family members with visual loss?

Dr. Golnik: There’s no family history of anything like this. Several of her family members wear glasses, but as far as she knows, none of her family members have had a significant, sudden change in vision.

Dr. Ogun: Do I go ahead?

Dr. Golnik: Yes, sorry. Go ahead.

Dr. Ogun: I know that her blood pressure is said to have been controlled, but is there a recent change to blood pressure medications? What exactly was a blood pressure?

Dr. Golnik: I don’t have her blood pressure, honestly. She says she thinks it is under control. At least in the US, a lot of patients have a home blood pressure monitoring thing. She doesn’t check it at home. It hasn’t been checked for a good eight months at this point. So, of course, we should have checked it in the clinic. Now I can tell you in my current practice, everybody gets their blood pressure checked by the technician before we see them. But this is not a patient from the older practice. We didn’t do that routinely. Jay?

Dr. Patel: Subtle proptosis on exam?

Dr. Golnik: No, we didn’t think there was any proptosis or any other external findings. Mario?

Dr. Perez: Signs? Like fever? Rash?

Dr. Golnik: Denies any sort of fever. She has not had any rashes. Good questions. I think for the audience who may not understand yet why we’re asking those questions, the talks that come up I think will explain those things. I debated whether we should talk about that. But I think that will come up when we have our three short talks as to why these questions — but I hope the audience is getting an appreciation for, you know, you don’t just ask the patient what’s wrong. I lost vision two days ago and then start the exam. There are a lot of things you want to ask about that may be relevant and you will see why they’re relevant when things come up.

Dr. Ogun: My last question would be does she have any pets, like cats?

Dr. Golnik: She does have a cat.

Dr. Ogun: Okay. And if she’s been scratched or injured recently.

Dr. Golnik: She doesn’t really remember any scratches in particular, but she does have a cat.

Dr. Ogun: Okay.

Dr. Golnik: Jay?

Dr. Patel: Any recent travel or illness prior to this development?

Dr. Golnik: The last illness she can remember was a viral thing, but it was about a year ago about. That’s two questions. And so, no recent — no recent illnesses and she does not have a fever, she doesn’t think. She’s feeling completely fine. She’s worried about the vision problem. And she’s had no international travel. I would say no one’s asked me, is she from the United States. She is from the United States. Of course, it’s my patient. But that might be relevant. So, she is from the US. And she’s — she literacies in the midwest, in Ohio, United States. And hasn’t really had any significant travel. Any significant travel. Mario?

Dr. Perez: She eats a raw food or unpasteurized dairy?

Dr. Golnik: Oh, raw food.

Dr. Perez: Raw food.

Dr. Golnik: She denies eating any raw food. That’s not super-common in the midwest. Denies eating any raw food. Further questions?

Dr. Ogun: The only thing I want to know, has the vision changed in the lath two days or gotten worse?

Dr. Golnik: It hasn’t changed in the last two days. No big changes either way. Jay.

Dr. Patel: What’s her body habitus?

Dr. Golnik: Like many midwest earners, she is 20 to 30 pounds overweight at least. Mario?:

Dr. Perez: I would like to know about — going into the woods or what does she like to do?

Dr. Golnik: Well, she lives near the woods. She lives in kind of a rural area. And she does do sort of walks with her — well, not with her dog, her cat. She does do walks in the woods. Kind of on a, you know, kind of a regular basis. Any other — there are actually a few questions. I think we have time. Do any of the panelists have any further questions?

Dr. Ogun: Does she snore while she sleeps?

Dr. Golnik: Let me see if she snores or not. Her significant other isn’t there and she says she doesn’t snore. I would say the same thing, and my wife says I snore a lot. It’s indetermined whether she snores. She doesn’t think she does. But that’s all I know.

Dr. Ogun: Okay. Thank you.

Dr. Golnik: I think we have time. I’m just gonna take a look at the questions in the Q&A and just see. So, one attendee asked, is there any history of cancer? That’s a good question, I think. The answer is no. There’s no history of cancer. Let’s see. Pain on eye movements? No. There’s no pain of any sort. No pain in general. Or pain on eye movements. Let’s see. There’s a question about medication. She’s just taking the blood pressure medication. Oh, her eye pressures are 16 in each eye. So, normal eye pressures. And so, there’s a question about obstructive sleep apnea which we’ve talked just briefly about a moment ago. So, there’s no history of sleep apnea. Good question. And there’s no — we don’t really know whether she snores or not. And perhaps we can talk about that. Any optic disc drusen? Not in this eye. And not the other eye. That’s not really a question. I’m gonna skip over that. But let me just see. So, a doctor said, question neuroretinitis. Well, there’s no macular star of exudate now. Let’s see. Any history of phosphines as the vision proves. No phosphines. We talked about the vision. There’s sort of a generalized depression of the visual field centrally. There’s not really any particular pattern other than that. Thyroid’s okay. No oral contraceptives. So, we haven’t talked about the evaluation. There was a comment about blood testing and so on. We haven’t talked about that yet. We’re going to. No headaches. Okay. I think we’ll move on from this question, then. But thank you, participants, for all those good questions. Okay. So, that’s the case. Let me just move forward on my slides. We talked about questions from panelists. So, let me just start in a different order. So, Mario, just, you know, briefly, it doesn’t have to be an exhaustive differential diagnosis. What are you thinking here at this point about what are the possibilities, maybe, I don’t know, more or less from most to least likely?

Dr. Perez: Okay. I think the main — so, differential diagnosis must be ischemic. I would also would like to find out if there could be the inflammatory or infectious.

Dr. Golnik: Part this webinar from the participants, we tried to get panelists from around the world. Nigeria, Latin America, the US. Well, is it any different? Depending where you literacy in the world, is the differential diagnosis different? It may not be. But that’s one of the sort of things we want to see. Is the differential different? Jay. What are your thoughts? And you can include the three things we’re ultimately going to talk about.

Dr. Patel: I definitely agree with Dr. Perez, Mario, and it’s definitely considering the blood pressure and risk. And you have to consider the with the anterior disc edema, doesn’t necessarily have to be painful. But the colors are down as you can see. And typically it’s proportional. It’s consideration. Neuroretinitis, and we know that it occurs two to three weeks later. That could be a possibility with her cat. Less likely, but things to consider, syphilis always, and papilledema. Number five and six. And optic nerve glioma, and we don’t see the optic ciliary shunt that occurs later, and lastly, edema. That port.

Dr. Golnik: Certainly the latter part of your list are pretty rare. I’ve probably seen one or two malignant nerve gliomas in my career of 35 years. That’s a pretty rare thing. Getting from the common to the really less common things. But all things reasonable to think about. What about you, Funmi?

Dr. Ogun: With this patient, considering her age, and the fact that she has blood pressure issues. Think first of ischemic neuropathy. Specifically non-arthritic. She doesn’t have features suggestive of vasculitis and inflammation of the vessels which could give us some headache and — then my second consideration would be because of her age, I would want to make sure that this is not an optic neuritis. But she doesn’t have pain with eye movement. Then another consideration would be inflammatory or infectious optic neuritis. We know that something like cat scratch disease would give a granuloma. That would look pale and swollen on the disc. But doesn’t have history of injury from her cat. She does have a cat. She doesn’t have any fever. Another thing that I would consider also in this patient would be, well, the list has been exhaustive, really. The last thing, then, was would be something like syphilis. It’s a possibility. I don’t know if she’s immunosuppressed for any reason, but there has been an increase in syphilis. That tends to give what people would call a neuroretinitis. She doesn’t have a macular — but start up with optic nerve swelling. Thank you.

Dr. Golnik: Okay. There were a couple of comments in the Q&A. One is could this be MS? I think MS would be very, very, very unlikely because of that significant degree of disc swelling, so let me just go backwards for a second. In the optic neuritis treatment trial, which is based in North America. So, be careful applying those results wherever you live. But in the optic nerve, no patients who developed MS had hemorrhage or severe disc swelling. So, that would be to me a big clue that this — I’m really not gonna be thinking about MS. Jay mentioned MOG, which some of you may have not have ever heard of, but we’re gonna cover that in his talk. So, that’s my line oligodendrocyte disease. That’s covered. And the differential, vary with infectious, maybe TB, of course, depending where you live. We’ll hear about infectious optic neuropathies from Dr. Perez regarding that, because that’s an important point and in part why I pointed out that she lives in the United States. In part. Someone provided a list of NAION, AAION, hypertensive retinopathy, pretty unusual for someone to have unilateral big time disc swelling and a relative pupillary defect from hypertension, which is systemic. I don’t think I’ve ever seen that. Increased intracranial pressure. Jay mentioned, again, although it is possible to have unilateral papilledema, number one, I’ve never seen that kind of asymmetric. This is big-time disc swelling on one side, nothing on the other. I have seen a grade or two difference between the eyes kind of a thing. And the history is not right. I mean, people with papilledema don’t have sudden central loss of vision. That’s probably not. Central vein obstruction. It certainly can cause significant optic disc swelling. It would be a little unusual to have it be 20/80 and 624 and have an APD. Usually you’re gonna see a lot of vascular tortuosity. There’s maybe some dilation of these veins. Interesting. Let me see if there’s anything else. Acute chronic vascular — hypertension is chronic — yeah, unlikely. If you had retinal arterial occlusions, whitening in the retina. Usually not the disc swelling. See if there’s anything else here. Space occupying. So, Jay sort of mentioned, there could be a tumor. I guess it is important to say that if there is a compressive optic neuropathy, the compression has to be occurring in the orbit. If there’s an intracranial tumor, a meningioma. You do not get optic disc swelling from an intracranial compressive lesion. Unless there’s high intracranial pressure and you have papilledema on top of it. It would be unusual to cause the history. But maybe washing the face and covering one eye and suddenly noticed her vision was bad two days ago. Maybe. Stranger things have happened. And we all know there could be a sudden realization of loss of vision because one eye is covered. I saw, looking at the time here. I saw a patient some years ago, a college student, who was being evaluated for impotence. And so, we got a prolactin level and they got an MRI and a big pituitary tumor. Endocrinologist said how is your vision, it’s fine. Came in, checked the vision in the right eye, 20/20, 6/6, and covered the right eye, I can’t see the chart. He was legally blind. Even though they asked him. This was a college student. Never know. A few other comments, disc drusen. Certainly not pseudopapilledema. Sarcoid. That could do this. Good thought. Maybe depending on where you live. But sarcoid could clearly cause this appearance. And someone asked, this is first noticed 48 hours prior to her evaluation. Okay. I’m gonna move on, then, with the webinar. But great comments. And so, panelists, what diagnostic evaluation — let me just see. I don’t want one person to give all the answers. Funmi, what are you gonna order? Start with your first thought. If you want to list a bunch of blood tests, that’s okay. Just give me in general. Or maybe you want to order something else on the exam, I don’t know. But tell me what you want. What are you gonna do with this person, maybe now.

Dr. Ogun: The first thing I want to look at is her blood pressure. She says it’s controlled, but it’s not checked in eight months.

Dr. Golnik: Let me tell you — I can’t remember — her blood pressure was normal. Jay, what next are you gonna do? That’s the first thing you can do. Get a blood pressure in the clinic.

Dr. Ogun: Yes, very easy, non-invasive.

Dr. Patel: I completely agree with Dr. Ogun. Because her age is 48, and it’s a condition of patients a little bit older. Can, of course, be seen in the 40s and 30s. Because of this, I would get an MRI, of brain and Orbis. Specifically with fat saturation, looking at the entirety of the optic nerve.

Dr. Golnik: And presumably looking for enhancement of the nerve and/or maybe we already talked about how MS would be unlikely. But typically in this setting, you would be getting an MRI thinking about are there periventricular plaques, depending on where you live in the world. Okay. Imaging. Mario.

Dr. Perez: Visual field.

Dr. Golnik: I didn’t have a visual field. It was depressed centrally. You can ask for something else.

Dr. Perez: Protein, CBC.

Dr. Golnik: CBC, sed rates, protein, those were all normal. Funmi?

Dr. Ogun: I would like to check fasting blood sugar, hemoglobin A1c, fasting lipids.

Dr. Golnik: Vascular risk factors. Those are all normal, too. Jay.Le

Dr. Patel: I would check what’s a CDS1 panel or —

Dr. Golnik: Neuromyelitis, and MOG, hear about that in the short talk. Those who were sent, we don’t know these results yet. There’s something else. Oh, Mario?

Dr. Perez: Check for syphilis.

Dr. Golnik: Throw that in with the other blood tests. Would anybody else like to do testing in the office? I’m guessing specifically, would you want to order an OCT.

Dr. Ogun: OCT would be very good. Ultrasound of the optic nerve. Looking for —

Dr. Golnik: Right. Look for Barry Drusen or the OCT. And one of them asked — there aren’t any visible. That doesn’t necessarily mean — OCT which is better than ultrasound and depending on how you are with the ultrasound. In the OCT, what is — is there anything you’re maybe looking for in the OCT in particular? Other than Drusen?

Dr. Patel: The PLEX from layer, which would be helpful. Could be evolved into a macular later. Could be helpful.

Dr. Golnik: Fluid on the retina — could be right. All right. Let’s see. All right. So, that would sort of be at least the initial evaluation, I think. Let me just — I’m just gonna quickly take a look at the question and answer part of this. Hold on a second. Let me just see. So, okay. Right. So, someone mentions Bartonella, otherwise the same stuff that we’ve talked about. Someone mentions chest X-ray which would get at the sarcoid, presumably, and maybe TB test. No problem with ocular motilities. The MRI was — someone asked about the MRI results. It was normal opinion MRI was normal. No nerve enhancement, interestingly. Ophthalmodynamometry. That’s something I haven’t thought of for a long time. Angiogram, that would be reasonable, I suppose. Lyme testing, thyroid function test. I don’t know. I don’t think I’d order a thyroid function test. The person has no external signs of thyroid eye disease. Having a compressive optic neuropathy from thyroid eye disease without extra ocular motility problems or significant exophthalmos would be, I hate to say impossible. but I’m gonna. Anyway. And HIV. So, someone mentioned. And maybe depending on where you live in the world, maybe that would be a good test. There is a relative — for people. Okay. All right. Very good. So, let’s — hold on. So, what we’re gonna do — I’m switching the order around from what you’re seeing here a little bit. But what we’re gonna do is have three short talks on these three entities. Which at least probably in most parts of the world, these three things or entities within these three things would be the — we think are probably the most common. Certainly if I see a hundred patients with unilateral optic disc swelling and loss of vision, it’s probably gonna be in one of these three categories. We thought we would provide information on each of these. We’re going to start with Dr. Ogun with non-arteritic anterior ischemic neuropathy. I’m going to stop sharing my screen so is she can share her screen. And I think you should be able to share your screen now, Funmi.

Dr. Ogun: Okay. Okay. So how would I spot a case of non-arthritic anterior ischemic optic neuropathy? Quick points to note. From the case history, a 48-year-old female, painless, blurry vision. Sudden onset, two days. She’s hypertensive. She says she’s controlled, but there’s a strong family history of hypertension and stroke. These are strong risk factors. She doesn’t have much else in her systemic history. But we know that she has reduction in vision, reduction in color vision, an RA PD which shows that the optic nerve has a problem and then she has depressed fields. So, this is her fundus picture. And so, I just tried to highlight the little aspects of her history that stand out to me. So, the fact that she’s 48. She’s under 50. She has a unilateral, pain less vision loss of, you know, very short duration. And she has evidence of optic nerve dysfunction. And she has a pale, as we can see here, swollen disc with some splinter hemorrhages around the disc. Showing a lot of congestion and impairment of the flow there. So, again, something that was interesting was the fact that she has this medical history pointing to hypertension. So, my question is this. Non-arteritic ischemic optic neuropathy or not? What is it? It is an impairment of the blood supply to the most anterior part of the optic nerve, which is called the optic nerve head. And that’s the disc that we see on fundoscopy. And arises from the impairment of flow of the short posterior ciliary arteries shown here. There are two sets of blood vessels that supply the optic nerve. These show posterior ciliary arteries are supplied. The optic nerve head. And then the blood vessels, branches from the ophthalmic artery that comes from the internal Carofit. There are two types. There’s the arteritic, and the non-arteritic. The arteritic is associated with inflammation of middle to large-caliber blood vessels and common in older patients. In this patient, I’m considering more of the non-arthritic, which is — which is my first consideration in this patient. So, I have a polling question here. Which of these is not a risk factor for non-arteritic anterior ischemic optic neuropathy. Encourage everyone to vote. There is five options. The age, female sex, the use of the new drug Ozempic. Hypertension. Snoring. Which you can get from the history. And I’m not sure if — okay. Good. We have votes here. Remember the question which of these is not a risk factor? Not? So, we have to look at the questions here. So, age under 50 I would say is a risk factor. So, unfortunately about 34% of people didn’t read my question right. Okay. About 90% think that Ozempic is not a risk factor. 6% say hypertension is not a risk factor. We have a mixed bag here. Very good. I’ll close this and just go to my next slide. It’s actually female sex. Okay? And what are the risk factors? So, we’ve — there’s a very large study that looked at all the studies that has been done on non-arteritic anterior ischemic optic neuropathy, and while some people felt that, you know, females and males have an equal proportion, a good number of the studies actually found that it’s found more commonly in male patients. So, male gender is actually a risk factors rather than female. It’s very common, actually, in patients below the age of 50 compared to the other form, which is arteritic. That is commoner in patients over 50. Usually the elderly range. 60 years, 70 years. And present just like this. Hypertension, hyperlipidemia, diabetes, coronary heart disease. All risk factors. Obstructive sleep apnea, present with the history of snoring. Usually the patient wouldn’t know this. The patient’s significant other might complain of this. So, patient is reported to be snoring. And then there are some other risk factors like risk factors for clotting. Like deficiency of factor 5, which is a clotting factor. And new medication. So, medications for weight loss. And diabetes. The new injectables, semaglutide, Ozempic, no randomized control trials, but there are case reports. As well as medications, Sildenafil, also used for erectile dysfunction. Again, in this patient, when you look at the age, she’s 48 years. So, I want to tell you, when you’re looking at a patient and you’re thinking about NA-AION, think age. 50/50. Is this patient belove or below 50? Below 50, you want to think of NAION, take it higher on your differential risk and look for microvascular risk factors. Not that it appears in patients over 50. But that’s not likely to be the arteritic type. And associated with vasculitis. This is hypertension. There’s a strong family history of hypertension and stroke. So, NA-ION is a possibility. The patient also has the clinical signs of optic neuropathy. So, the next polling question. Looking at the fundoscopy of this function, what are the characteristic signs in a patient that might have NA, or non-arteritic ischemic optic neuropathy. Flame shaped hemorrhages, pallor of the optic disc, swelling, sheathing — in the affected eye. Would you be looking for that? And in the other eye, would you be concerned whether you notice a small cup disc ratio. Please vote.

Dr. Golnik: It looks like this should be a select any of these, doesn’t it?

Dr. Ogun: Except.

Dr. Golnik: Sorry, got ya.

Dr. Ogun: Except. You have to let the odd man out. Four of these things belong together. Okay. Good. I was just singing Sesame Street. Okay. So, good. We have also a mixed bag here. But very good. It seems like almost 40% of us have noticed the odd man out. Sheathing of retina blood vessels which would point to vasculitis. So, in non-arteritic ischemic optic nerve, we will not be expected to see signs of vasculitis which would be characterized by blood vessels. However, yes. We do look at the disc of the other eye to look for signs of what’s called the disc at risk. I don’t know if you can see what I’ve written here. Let me just move these pictures here. So, a smaller vertical disc ratio is — it’s highly correlated with non-arteritic anterior ischemic optic neuropathy. In this study, that was done by Gonzalez et al., it looked at what are the factors? Is it the size of the disc? Is it the disc diameter or the disc issue? And of all these, the most significant finding there was a small vertical cop to disc ratio in the fellow eye. You can get information from the individual or, you know, the eye that is affected, but you can also get some helpful information in the other eye. Because a very small disc ratio, what we call a crowded disc, is a risk factor for ischemic optic neuropathy. You can see some signs in the contralateral eye. We have other signs of non-arteritic anterior ischemic optic neuropathy. And one is what we call the relative papillary defect. I’m not sure if you have seen this before, but when you do the pupil reactions, you look at the direct response and the consensual response. When you stimulate the good eye, it stimulates both pupils to constrict. Whether you come back to the affected eye with an rAPD, that eye cannot sustain the constriction because of the impaired optic nerve function and then the pupil begins to dilate. As you can see in the left eye of this patient. This is not the patient that presented to Dr. Golnik. But that’s what an rAPD looks like. And patients can present with any kind of field defect. Commonly the books will talk about what is called an attitudinal defect. Swelling of one optic nerve head or the other much more than the other. So, you could have a superior swelling. And that would give you an inferior altitudinal field defect like in this picture. Or a swelling, then you can have a superior depression of the field. And as in this case, that Dr. Golnik mentioned, the entire field might be just depressed. And then, of course, when you look at the disc, we expect to see swelling. There would be blurring of the disc mergings, there might be some little hemorrhages at the edge. Flame-shaped hemorrhages and the disc is swollen. So, you look for these signs. And if you see them, of course, you do don’t expect to see sheathing of the blood vessels as you would see in vasculitis. You don’t expect to see round hemorrhages in other parts of the retina.

Dr. Golnik: About one minute, okay?

Dr. Ogun: I think this is my last slide. Screen the patient for evidence of small vessel disease. All these microvascular risk factors. And we mentioned the tests already. The other thing I mentioned about the vision, sometimes you have a patient that develops a sudden vision loss. It gets worse over a few days to a maximum within one to one week. About a few days to one week. And that’s because sometimes the swelling increases. Some patients after about a few weeks to a month or two months the vision is either restored, it can get better, it can get worse, or it can stay the same. And that’s roughly the case in about one-third of each of the patients. And, of course, always look at the contralateral disc. And so, the take home points are sudden painless vision loss that’s unilateral. And associated with signs of optic neuropathy like poor color vision, sluggish pupil with an afferent. In a patient who is less than 50 years old, should generate the impression of the possible non-arteritic anterior ischemic optic neuropathy. Examine the patient for microvascular risk factors and always look at the contralateral disc for the issue. And look at the vasculitis by doing the sed rate with the ESR is very high in vasculitis, and the C reactive protein which is also elevated. And that would exclude that.

Dr. Golnik: If you could stop sharing your slides and why don’t — who did we say — Jay was going to go next. Share your slides. While he’s doing that I give a talk and reviewed information on the GLP-1 agonists and NAION. So far there have been about six big data studies. Three showed an increased risk and three did not. And just on Monday of this week, two days ago, the American Academy of Ophthalmology and the Neuro-ophthalmology Society came out with a statement. Because the European group came out with a statement saying if the person is on a GLP-1 agonist, and has an AION they should stop medication. They came out and said, no. We don’t agree with that. It needs to be a case-by-case basis. There needs to be a discussion with all of the care providers of that patient because sometimes these medicines are life-changing and important. They’re not just used for weight loss, of course, but for diabetes, too. So, there is — there is still debate. I don’t think they were really — we don’t really have an answer yet. I’m not a big fan of big data studies, honestly. I know how badly I code things. And so, I don’t know. I think I just wanted to say that so that people don’t start telling everyone don’t use these medications. They are life altering for some people. Okay. So, now — so, that’s certainly one of the possibilities. NAION. We heard about it. Let’s hear about optic neuritis from Dr. Patel.

Dr. Patel: Can you see my slides okay?

Dr. Golnik: Yes.

Dr. Patel: Yes, my talk is on optic neuritis, no disclosures. And briefly, terminology, etiology, epidemiology, clinical presentation and testing and management and prognosis. So, I have a polling question here. Hopefully you guys can see this. This says which of the following is true about optic neuritis? One, majority of patients will present with optic disc edema. The presence of an arcuate scotoma or altitudinal field defect excludes optic neuritis. All patients with suspected optic — all patients can optic neuritis will ultimately require some form of long-term immunotherapy a patient can have optic neuritis without a detectable rAPD. 32% say that they will present with optic disc edema. And a patient can have optic neuritis without a detectable rAPD, and hopefully a good mix. Hopefully informative.

First to talk about terminology. Optic neuritis, whether we think about that, it’s a term to think about inflammation of the optic nerve as we know. With the swollen disc, more specifics would be a papillitis, and with the normal appearing optic nerve, refer to the retrobulbar optic neuritis. You can see on the left, this is an example of a patient who basically this is a normal, you know, fundus photograph. This was a patient that had retrobulbar optic neuritis. And on the right, the remarkable disc swelling that we can see in MOG-type of optic neuritis, which I’ll get to. Which is briefly for the terminology. This is a pie chart, adapted from Dr. Neil Miller’s presentation on the various causes of optic neuritis. It’s a good schematic that shows on the legend that you can see that idiopathic and MS make the vast majority of optic neuritis that we typically see. About 85%. A smaller subsect, about 10% NMO and MOG, and the protein, 4% being systemic, infectious and autoimmune. Like mentioned by the audience members, and drug-related, et cetera. And so, optic neuritis as a whole is more common in North America and Europe rather than Asia. And annual incidence varies, but one to five per 100,000. And typically 20 to 50 years of age, and females, a higher predilection than males. I put an asterisk, this doesn’t hold true. There’s no major gender predilection. And whether we think of NMO, lower in Caucasians and higher in Asian, African, or south American descent. And seen in patients over 60. Similar thing, less common in Caucasians and more common in Asians, Hispanics and African descent. There was a nice study that was conducted globally, published in 2021, looked at aggregate data from 2008 to 2021. Of course, the caveats is this did use diagnostic coding. Some countries don’t have access to testing. They’re using different assays. Keeping that in mind, nonetheless, this is a fairly useful diagram to look at. We can see with idiopathic and MS, it’s North American countries in Europe that we see this predominate as far as MS. We see this a lot in our part of the world. And when we look at here with NMO, as you can appreciate, we see in the far east countries and South America is where it predominates. It doesn’t mean that it doesn’t occur in the other countries. But these are the most predominant. And you can see far east is where it tends to predominant. And it’s scattered throughout. And we see it in the US as well. So, how do these patients present? They have an acute onset of central vision loss. It really can be any pattern of field loss. And they had reduced color vision, which is often proportional to the visual acuity. And have an rAPD, and astutely, unless there’s a bilateral or previous optic neuropathy in the fellow eye, will not see. 90% of patients will have the pain in or around the eye, and particularly with eye movements as the sheathe is irritated. Visual acuity is no light perception. And one-third of patients with demyelinating optic neuritis may have mild optic disc edema. And this is a nice diagram. The top three, things that we typically entertain when thinking about demyelinating optic neuritis. In the first panel, NOS and NOG. And you can see it more common, and the bilateral, that’s more common in MOG, still definitely seen in NMO. Disc edema, that’s the reason we entertain in the differential of 85%. The visual acuity, NMO often has a poor prognosis. The numbers further acute and chronic visual acuity, poor. Longitudinal extensive, but think of the chiasma involvement, any of NMO. And anterior involvement, think of MOG. And so, going guard. What does the imaging look like? You’ll get the I meaning. This is a nice schematic, and you can see the anterior enhancement, short segment, and characteristics of MS. And see it longitudinally extensive and fat stranding. And NMO, notice how the chiasm is involved. And this is an image showing chiasm involvement, and the point of that is to think about that and ask some of those other questions of any weakness, numbness, bowel, bladder. That can help you formulate your differential. Here is MOG, good example of the fat stranding you might see. Other things can cause fat stranding, but MOG comes to mind for this. What do we order? We would think of MRI brain and orbits with and without. You want to specify your center fat suppression. And look at the optic nerve ins it entirety. And, of course, this will be in conjunction probably with the neurology colleagues with the workup. And check MOG andAQP4, cell-based as I recommended. And the suspicious for the optic neuritis. And you can consider syphilis, ACE, and CT — pending your clinical suspicion. And don’t need to do a lumbar puncture unless you have quote, unquote, terms that are supplanted, and typical and atypical, immunocompromised, severe optic disc edema. Bilateral, or any diagnostic uncertainty. Then certainly lumbar puncture would be included to exclude inflammatory and infectious causes. Use the terms typical, atypical. And neural literature renders this obsolete. When I say typical, I’m referring to MS or idiopathic. And most common in the US. And atypical, what we know from typical, following the optic neuritis treatment trial, they did 250 milligrams QID for three days. We do one gram per day monitoring them. And followed by oral prednisone taper. And do 50 milligram tablets of 25 tablets per day for three to five days followed by oral taper. For NMO, IV Solu-Medrol for five to seven days. And be primed or think about PLEX, done concomitantly, plasma exchange. And require immune know therapy as you can see. And do recognize that immune owe modulatory therapy can worsen NMO. And don’t need to start the long-term therapy, 50% of the time could be monophasic. How do they fair? They may worsen over 7 to 14 days and then improve typically over 2 to 3 months and oftentimes improve even up to one year. 90% of patients as we know in the treatment trial improve to 20/40 at 6 months, but may still notice washed out colors, Uhthoff phenomenon, et cetera. The reoccurrence rate is about 35%, and the question comes up, will I develop MS, so on and so forth. A lot of this is determined by the presence of lesions. In a typical, this is MOG coming together, some patients develop this entity of CRI-ON as you may have read or heart about. And taper and get worse, this can be associated with MOG, prognosis is often poor. And MOG has a good recovery, rather. And, of course, then we do have to think about that other 4% that we talked about with I know Dr. Perez will talk in a little more detail. But certainly various viral agents are known to cause optic nerve — optic disc edema, vision loss. Syphilis, Lyme, TB, meningitis, post-vaccine, sarcoid. And learning more that GFAP and others are tried. And so on and so forth. Relevant to think about. And with that, I would like to thank my co-presenters, Dr. Golnik, and all of you folks for listening in.

Dr. Golnik: Thanks very much, Jay. Very nice, comprehensive review of optic neuritis, which is becoming an increasingly difficult entity to try to characterize with all these new discoveries. I would just say one thing about the optic — the MRI and the enhancement. Although most people with optic neuritis have enhancement of the nerve, you do not have to have enhancement. I have plenty of patients, the radiologist says no enhancement, no optic neuritis. It’s a clinical diagnosis. If there’s enhancement that helps you, but if there’s no enhancement, it doesn’t mean there can be no optic neuritis. Start sharing your slides, Mario. And you saw the pie chart from, that would be the US experience, 80 plus, if you did that same pie chart in China, it would be very different. NMO would be a big part of the chart as you pointed out with the other slides. Very good. Mario, go ahead. Finish the short talks on optic neuropathies. You’re muted, Mario.

Dr. Perez: Okay. Let’s start with the question for the audience. The proper clinical diagnosis of infectious optic neuropathies is based on — A, epidemiological data, B, clinical history of the patient, C, systemic symptoms and signs, or D, pattern of ocular involvement, and E, all of the above. I’ll give you a few seconds to think about .

All right. All of them are important when we are thinking about infectious optic neuropathy. Okay. Infectious ocular neuropathy typically caused atypical optic neuritis in the patient. They have different forms of optic neuropathy. The severity of the visual impairment can vary and there is no proper clinical presentation of an infectious optic neuropathy. The clinical diagnosis is based on epidemiological data. It depends on where you practice. It depends on what is common in the region where you are. For example, in Colombia, I’m thinking of an infectious optic neuropathy, rule out syphilis, TB, toxoplasma. It depends on the clinical history of the patient. If the patient can have, for example, HIV, if the HIV infection is well-controlled or not. Because it is not well-controlled. We must rule out less typical microorganisms. It depends on the systemic symptoms and signs. Those systemic symptoms and signs can help you to guide yourself into the diagnosis to rule out what is common in your area. And it depends on the pattern of ocular involvement. Resultant ischemia, edema, and inflammation may co-exist with the inflammation of the optic nerve. The clinician must maintain a high index of suspicion depending on where you are as I mentioned before. It is partnered with colleagues providing pulmonary, otolaryngology, and infectious disease expertise to facilitate your diagnosis. We have, too, learned how to collaborate with other colleagues. So, if you’re suspecting an infectious optic neuropathy, you have to question as your patient about the travel history. It is because it may vary — your diagnosis may get a little bit more ample if the patient has done to certain areas with endemic diseases. Ask the patient for systemic involvement if other symptoms like fever, and look for a neurological environment. And always ask for the immune status of that patient. Look for HIV — a concomitant HIV infection. There is not an autonomic pattern of nerve involvement in any optic neuropathy. So, you kind of guide a diagnosis depending upon the compromise of the optic nerve. But always look for additional ophthalmological findings like retinitis, vitreous formation, that can guide you to an infectious disease. And look for the inflammation, especially in immunocompromised patients because they can get you to life threatening infections like —

What to look for in the patients? It will depend on what are you suspecting and what is more common in your area. You can ask for CBC, a set rate, serological testing, blood cultures, PCR, antibody assessment in aqueous humor, tuberculin, CT or MRI. It depends on what you are suspecting in your patient. Let’s see two cases. For example, this is a 28-year-old male that had sudden profound visual loss in the right eye without ocular pain one month prior to consultation. There was no relevant past medical history. He has visual acuity of CF on his right eye and 20/20 on his left eye. Has right rAPD. And what’s normal in the right eye. And this is the appearance of his fundus. He has optic disc edema as you can see in the right eye, and fundus in the left eye. A central disc scotoma on the right eye. And you can see has an inflammation of the — edema of the layer. And he has a decrease in the cell layer in the right eye. But when we check for the macular positive, we can see this. We can granular RPE that we cannot see in the control of the eye. And these are the lesions when we see — when we check the — so, it’s layered in the macular OCT. So, we have edema with these lesions in the RP consistent with posterior retinitis. And you can see a mild vitreous eye for which we have vitreitis with retinopathy. And this edema do make — you have to think about — it was positive. He has R PR reactive in 64 dilutions and positive FTA-ABS. This patient was treated for ocular — a second example is this 23-year-old female. With rapidly progressive visual loss in the right eye with pain with eye movement in that eye. From the MRI we can see this hyperintense — hyper-intensity consistent with perineuritis. And check the fundus, she has this retinal lesion, fluffy lesion, very close to the optic nerve. And he has positivity of IDG for toxoplasma. And we are informed yet, this is very, very common. It’s a very common cause of neuritis. And so, always guide yourself by the behavior in your region and your suspicion when you’re thinking about optic nerve — optic neuritis.

Dr. Golnik: Thank you. Very good, Mario. Thank you very much. So, we’ve heard about the three sort of either entities or categories of entities that would be the most likely things. We mentioned earlier some very unusual things. We’re not — this was really meant to try to get you thinking about the most common stuff that you’re gonna see. Most of those other things probably gonna be diagnosed by a neuro-ophthalmologist if you have one. I’m gonna just share my screen again. Hold on. Is that — oh. Hold on. I see what I did. Sorry. I just got to get back into show mode here. Sorry. It’s giving me a hassle here. Share… there we go. Okay. So, we heard that the very nice short three talks. So, this is a polling question for the audience about our case. So, if we can put this poll up, this is not the poll, but yeah. So, what do you think the diagnosis is for this case? After hearing all those talks, after the discussion, and questions and answers, do you think it’s optic neuritis? Do you think it’s NAION? Or do you think it’s infectious optic neuropathy? And I’m going to ask our host, once we get the answer to this question, I’m gonna ask this question again in a couple minutes. So, get rid of, you know, if that’s possible for the host. I want to ask the same question after divulging a little more information. All right. So, interesting. So, the majority — or yeah. The majority of people think it’s NAION. And then kind of evenly split between optic neuritis. And I think that’s part of the point is that sometimes it’s hard to know. We just — we said earlier that the MRI was normal. No enhancement. Well, maybe that means it’s NAION and not infectious or optic neuritis. But you can have the infectious and without enhancement. We talked about NAION. Well, she’s got risk factors. I would say that certainly you can clearly a fair percentage of people get NAION under the age of 50. That said, probably not age 20. That would be pretty unusual. But, you know, in the mid-30s to 40s, certainly, that’s common. I don’t want people to go away thinking that NAION is uncommon over 50. It is still certainly common over 50. But then you have to think about giant cell arteritis, depending on where you are in the world, it may be more common. And infectious optic neuropathy. No other signs or symptoms of a systemic infection. Let me just move on. Here’s our patient, and again, this fundus photograph is from two days after her symptoms. She had a big evaluation. It included pretty much everything the staff — not staff — the participants mentioned in that. So, a number of blood tests were sent at that time. Ultimately, the blood test — a blood test did become positive. I won’t say what it was. But I can tell you when she came back in a few days, she looked like this. Now, and so what I would like to do if possible for the host. I don’t know if it’s possible because we didn’t discuss this in advance. Is it possible to show that same question that I just asked the audience again? There we go. So, does that change your tune? Do you think that — what do you think of the diagnosis is now based on this six day follow-up visit that you’re having with the patient? Does that change your thought about what the diagnosis is? And remember the other thing is that although there is a disc at risk in the other eye, that is important because if there wasn’t, you would say it can’t be NAION. Did doesn’t mean it is NAION Because it is a disc at risk. Okay. We have changed a fair number of people’s minds appropriately so. This is as one of the participants pointed out early on before they saw this, as Jay pointed out in his talk, sometimes — and you can kind of see if you look here… even if you can imagine. There is a little elevation. There’s a little fluid in the retina. It’s too soon for that exudate to coalescence into this nice star of what we call neuroretinitis. So, early on, you may not see the star. And OCT will show you all this fluid. Now, potentially anything that causes huge disc swelling could cause a star. Potentially. But it’s rare. I mean, I don’t think I’ve ever seen a complete star in NAION. But there are reports. So, it doesn’t mean if there’s exudate in the macula, it can’t be something else. But certainly if you think you see it, you’ve got to be thinking infectious. Infectious, infectious. And in the United States, we are thinking syphilis, but thinking cat scratch. And the point is although she had a cat. And if you want to be even more specific, a kitten. It’s more common with getting scratched by a kitten. But people don’t always remember that they got scratched. You got a cat. It’s there every day. And it’s there, I don’t remember. And in fact, you don’t actually have to be scratched by a cat. It can be spread by a flea on a cat. So, if your cat has a flea and the flea bites you, you can get it. This is not common necessarily in all parts of the world. But the point is you should be thinking infectious if you see this. But you may not see it early on. If you see this patient within a day or two. So, let me just — I’m gonna — I think — I will not have any more — I want to just summarize — summary. Okay. So, I think the points that I make. And then open up to questions and then we’ll see if there are questions. So, if you have questions, I know there are some in the chat or in the question and answer right now. We’ll get to those in a second. Let me see if there’s anything else I wanted to say. I think that in general when we see unilateral optic disc swelling, we talked about the three most common sort of scenarios and then the subgroups. As Mario said, depends on where you live, right? I never see a lot of those entities that were on his flowchart list of things. So, depending on where you live, things are gonna be common. If you live in India, tuberculosis is gonna be a lot more common than in the United States. So, I think that’s the main point with infectious things. Of course, if there are other signs, fever, you know, systemic symptoms of infection, that’s relevant. For NAION, all the points that Funmi made about, you know, check the other disc. Is there a disc at risk? If there is, that doesn’t mean it isn’t NAION. But if it’s not a disc at risk we think long and hard. The most important factor is that crowded, congested disc. As far as the optic neuritis goes these days, I mean, really our management of optic neuritis has changed over the last decade or so, we have a blood test for MOG, we didn’t have that before. Now we do. And that’s changing how we manage these patients, as Jay said. And, you know, if someone’s presenting with their first episode of optic neuritis, you don’t know what they have. What kind of — and even if you’re sure it’s optic neuritis, they have pain on eye movement. And even though they didn’t have an infectious optic nerve problem. Not everyone has pain. 8% didn’t. And 8% of a really common thing still is — you’re gonna see it. I think that’s sort of what I have to say about the summaries. Let’s go to the — do any of the panelists have any other thing that I left out they want to say? Or Jay, go ahead?

Dr. Patel: Yeah, excellent point. I agree. You don’t have to have contrasting, you can still have an optic neuritis. And in addition, they may have T2C, that’s hyper-intensity seen on the optic nerve, correlated for optic neuritis. It’s a caveat to recall, T2 signal is not specific. Seen in any of the optic neuro-optics, glaucomatous, et cetera. And keep that in mind looking at the MRI, T2 signal doesn’t always mean optic neuritis.

Dr. Golnik: And did you mention the perineural enhancement?

Dr. Patel: Yeah, the fat straining and perineuritis.

Dr. Golnik: A third of the time, you can see the perineural enhancement. Enhancement of the optic nerve sheathe, which you tend to not see in other entities, you might see infectious, but other types of optic neuritis. I’m going to the question and sort them out. There’s a question about lupus neuritis. Could this not also have palish unilateral swelling? I’ve never seen a case in 35 years. I think it’s pretty darn rare to be lupus. I’ve seen a lot of patients misdiagnosed as having lupus. But I don’t think I have seen lupus optic neuritis. I’m not sure about that answer. Does anyone have experience on the panel with lupus optic neuritis. That’s how rare it is. Yeah. Okay. Funmi, there’s a question when you say, vertical cup to disc ratio, are you saying that the contralateral eye is higher cup to disc ratio being vertical than horizontal?

Dr. Ogun: No, talking about vertical cup to disc ratio, it’s possible to measure vertically as well as horizontally. And it’s generally in ophthalmology, it’s the vertical that we tend to align with. Because superior and inferior nerve fiber layers of the rim are thickest in that region. If you start noticing any increase in that diameter, that means you are losing that nerve fiber layer. That makes what makes that more important. But the disc at risk is generally a cup to disc ratio, vertical cup to disc ratio less than 0.3. In this case, it was 0.1. But as we can see, this patient generally had the diagnosis to the last possible minute.

Dr. Golnik: Yeah, sorry I did that.

Dr. Ogun: A nice case.

Dr. Golnik: Then a question, assuming we’re talking about NAION, is the altitudinal field defect more common my superior or inferior?

Dr. Ogun: A patient can choose to have more swelling of either the superior — but in the books, I tend to see that people talk about more superior nerve swelling. So, inferior altitudinal defects, you may expect maybe more.

Dr. Golnik: I think I see more commonly inferior. But you can’t rule out NAION with superior defect. In my experience, inferior is more common than superior. There’s a question about statins. The use of statins in NAION?

Dr. Ogun: NAION, you see, if patients have hyperlipidemia, which can cause anterior ischemic optic neuropathy, then they could — they may be placed on statins to treat it. But I haven’t seen any of the literature talking about statins being a course of NAION.

Dr. Golnik: Or using statins. I don’t think there’s any evidence base to recommend statins in the use of NAION. It is part of the syndrome. Yeah.

Dr. Ogun: You need it.

Dr. Golnik: Dr. Funmi mentioned briefly about rAPD causing superior and inferior visual field defect? I missed that part. What was the reasoning?

Dr. Ogun: No, what I was saying about rAPD, it’s a sign of optic nerve dysfunction. When there’s a differential activity of the optic nerve between the two eyes, then you expect to see a relevant afferent pupillary defect. It’s relevant to the function of the other eye. And that is not to say that you cannot have, you know, depressed function of both eyes. In which case you will not see the relative afferent — you will know there is defect because the pupils will be sluggish in both eyes. The only thing I mentioned about visual fields after the rAPD was that it is a possible sign of the ischemic optic neuropathy. I mentioned that you look out for poor vision, look out for poor color vision. Look out for an rAPD. Look out for that pale swollen disc. Who you do the fields, you might be able to identify a field defect, which could be anything. But more commonly is described as a field defect. Especially if there’s differential swelling of that disc and the swelling is more superiorly.

Dr. Golnik: Okay. Jay, you talked a little bit about rAPD and unilateral optic neuropathy. I think there’s some confusion in the questions. Can we have no rAPD and unilateral optic neuropathy, and what is the mechanism?

Dr. Patel: Yeah, definitely. When you see an rAPD. Just like Dr. Ogun mentioned, imply unilateral or — they can have bilateral involvement, in which case you wouldn’t see an rAPD. Doesn’t differentiate the ophthalmology, but looking at the pupillary responses and recognizing could there be a — and looking at the contralateral fellow eye.

Dr. Golnik: You think the point is, if there’s a normal point on one side and optic on the other side, should be — if it’s really mild, maybe a really small afferent pupillary defect, but did should be. If the other eye nerve is normal. There is no mechanism that there would not be. This is for Mario. How do you differentiate this diagnosis from toxo at early stage? I’m assuming he is meaning Bartonella, I guess.

Dr. Perez: I guess if it’s not possible to differentiate shade at the early stage with a high confidence. But lesions are related only with mild if not vitreous inflammation. Local vitreous inflammation. These retinal lesions are not as you say, a high incidence of — on the other hand, toxoplasmosis causes a very, very high inflammatory local inflammatory reaction in the vitreous. And that differentiation in the inflammatory statute of the vitreous can guide you or can help you to differentiate between Bartonella and toxoplasma.

Dr. Golnik: And blood testing, ultimately. But in clinic.

Dr. Perez: Yes, in clinic.

Dr. Golnik: Is the absence of rAPD possible with NAION or optic neuritis? Only with nerve damage. Otherwise see a relevant pipe Lilian. The star on the fundus imaging after eight days. Was that avoidable? No. That star was the exudate — we think — the exudate, the fluid was all there. But that star was when exudate coalescences in the nerve fiber layer of Henley, get the star appearance. The fluid is reabsorbed, the exudate is more evident in clumps. That’s how I look at it. I don’t know if there’s proof of that. But as best as we know, it’s not preventable. What does the stars seen — by definition, if you see a swollen nerve and there’s a star of exudate, we call that neuroretinitis. Neuroretinitis is not a diagnosis. Just like optic disc swelling is not a diagnosis. The question is why do you have optic disc swell something it has a differential in the United States it’s usually either post-viral or cat scratch. Bartonella henselae. And in other infectious, and you can see what looks like knew retinitis in Papilledema, you can swill fluid and exudate into the retina and end up with what looks like neuroretinitis. I saw a kid years ago, sent to me, bilateral neuroretinitis and they had a venous thymus thrombosis and increased intracranial pressure in papilledema. Anyone have any experience for trying oral prednisone? Although studies showed no benefits. Well, I could tell you, my — the meta analysis have shown that steroids have no benefit. For a while, I was offering people steroids. And this was probably 15 — 10 to 15 years ago based on one study that was a bad study. I said, well, there’s some data, you present with visual acuity worse than 20/60, it might be a benefit. It’s all anecdotal. I had nobody who had any significant improvement in vision really on the steroids. So, I don’t know. In my talks on NAION, I basically say, there is no proven treatment, still, no evidence-based treatment for NAION. One patient — or someone asked, how did the patient respond to treatment? So, Bartonella henselae, there are no randomized controlled trials. Years ago, and I have a funny story, maybe I’ll tell, there aren’t a lot of questions. My group were the first group to publish the cause of cat scratch disease. Back in the 1990s, sorry, I know many of you probably weren’t born yet. On our examinations, the American Board of Ophthalmology exam, the case with that picture, they asked what bacteria caused this? And the answer was Afipia felis, a bacteria in cats. But then someone by the name of Diane Hensel, a microbiologist, discovered the bacteria that causes cat scratch. And back then, they called it Rochalimaea henselae. They have done away, it’s part of the family of Bartonellaceae. And it’s that henselae, after Hensel. I called the CDC, are you testing for this. They sent in the blood and sent a letter back, yeah, it’s positive. Hey, by the way, we have four patients from around the country that have been sent in with positive tests. Do you want the names and of the doctors? So, we got together, as the group of doctors and published the first paper on Rochalimaea henselae. It was thought to be self-limiting. It goes away like a cold. Now we not bacteria and know the antibiotics that can kill the bacteria. And also published a paper some years later, not everyone with cat scratch has good recovery of vision. Although in general people have good recovery. Most people, if they know there’s an infection and there’s an antibiotic to kill it. We do use antibiotics, there’s didn’t ones, ciprofloxacin, not in kids. And isoniazid, and she was treated with antibiotics. There’s a question, do you give some steroids at the same time? For syphilis, you can give steroids concurrently and the visual recovery can be better because you’re getting rid of the bacteria with the antibiotic and getting rid of the inflammation which can cause damage with the steroids. So, she did well. Do we include toxo igg-igm as part of a workup aside Bartonella for neuroretinitis? Mario, you would in your world?

Dr. Perez: We do, actually. toxoplasmosis is very, very common in Colombia and Brazil. So, we always, always check for toxoplasmosis in our patients.

Dr. Golnik perform I think it depends again —

Dr. Perez: Depends on where you are. It will depend on where you practice.

Dr. Golnik: All right. Okay. We are just about out of time. One last question. How about steroid the for prevention of full NAION when you incidentally find a disc swelling in a regular control visit with a patient where there’s nothing to answer your question? I would not. But there’s no evidence for steroid use in any form of NAION. So, all right. Well, listen. We are at end of our allotted time. I would really like to thank my panelists, Dr.S Patel, Perez, and Ogun, for their excellent comments and talks. I hope everyone learned something. And we’ll see you somewhere around the world at some meeting I’m at. Say hello, please. I love it when people come up, and say I saw your webinars on Orbis or your course. Please say hello. I love that. Everyone else, have a good rest of your day. In my world, it’s 7:30 a.m. So, wherever you are, have a good rest of the day and thanks, everybody, for participating.