Lecture: Anterior Ischemic Optic Neuropathy: Arteric vs. Non-Arteritic

>> Hi, all, my name is Tais Estrela. I’m a physician at Harvard University. I’m talking today from Boston on this snowy day. I would like to thank Cybersight for the invitation and I’m happy to talk about this topic that is common in my clinical practice. I’m from Harvard University and I’m an ophthalmologist. Most of my practice is neuro-ophthalmology and strabismus. So, let’s start talking about this topic. First, I have no financial disclosures relevant for this topic. And I want to start by telling you a story. This is what we see here in our practice. This should give you a background here in Boston, Harvard, we have an emergency 24/7 that attends to patients from all of New England and that includes new ham shire. We have a 60 year-old woman with acute painless vision loss. She had systemic hypertension and type two diabetes. This is the visual field. Usually they report a black cloud when they wake up and when you check the fundus exam, we see this optic nerve is swollen. Unilateral. Only one eye. In this case was the left eye. You see here there is this extensive swelling, more pronounced superior that match the inferior defect in the visual field. And you have some hemorrhage around the disc. So we are consulted a lot for cases like that. Another situation is also 60 year-old woman with acute painless vision loss but this patient also reports she is having a temporal headaches for about maybe 3 months. When we ask, she also has jaw pain and unintentional weight loss. She has poly myalgia rheumatica that she is followed with rheumatology. This patient presents are vision loss. It’s more superior but extending to the inferior field. And it’s also optic nerve swollen. These two case are anterior ischemic optic neuropathy. What we call AION. One is arteritic is caused by inflammation in the arteries and the other is not related to inflammation. So the goal from this lecture today is to understand the pathophysiology of this condition, the anterior ischemic optic neuropathy and try to differentiate the nonarteritic and the art, the AAION. And also to discuss the management strategies. Because these vary between these conditions. So just to go back and what is ischemic optic neuropathy? It’s when you have most commonly acute vision loss that is secondary to insufficient blood flow to the optic nerve. Sometimes we say to the patients, try to explain, it’s like a stroke at the optic nerve. When there is no blood flow. This causes reduced perfusion that can be limited to the optic nerve head. These are anterior ischemic optic neuropathy or posterior, affecting the whole bulbar portion. The lack of blood flow leads to axonal injury and optic nerve dysfunction and vision loss with the visual field defect. Let’s review the vascularization of the optic nerve. This helps to understand the conditions. So basically from the internal carotid we have the ophthalmic artery. The ophthalmic artery gives a branch that’s the central retinal artery. And this is a short posterior ciliary artery. This short posterior ciliary artery goes very close to the laminar portion and pre-laminar portion of the optic nerve head, the one that we see when we do the fundus exam. You see you have these very little ventriculares that form circles of Zinn-Haller. This is — lack of blood flow because they have this very thin anastomosis. Here is another picture. Here shows the central retinal artery that gives all the vascularization for the sclera, the choroid and the retina. The short ciliary artery. And posterior, we have this Pial vasculature that you also, they come from the ophthalmic artery and give supply for the bulbar portion of the optic nerve. We have the optic nerve head from the pre-laminar and laminar posterior ciliary arteries and the retro bulbar portion. Both from internal carotid ophthalmic artery. The option of head is the circle of Zinn-Haller. It’s the watershed zone that is around the anastomosis. The posterior portion is — the posterior — has intense blood loss with like no blood pressure and then they can have posterior ischemic optic neuropathy. We will start talking about the arteritic one. Why this matters, we call the most common cause of arteritic anterior ischemic optic neuropathy is giant cell arteritis. And it’s the most common systemic vasculitis in adults over 50 years old. This can lead to preventable permanent vision loss that for elderly patients can be very impairing. And it can become bilateral within days if you don’t treat. The clinical diagnosis is from the — prevent vision loss. If you suspect, we say treat. You can investigate and you have some time to confirm the diagnosis. So let’s talk about giant cell arteritis. Usually affects people, like older than 50 years and I have seen patients, like, really 50 years, 49 years old. It’s around this window. You always have to keep this in mind. If you see a patient that comes with painless vision loss, it’s mandatory to ask systems about GCA. You have to ask — you need to do a review of system to investigate GCA. GCA is predominant in women and common in our region here, more common in Caucasian patients. Overlap of 40 to 60 percent with polymyalgia rheumatica. If the patient has this, you have to turn on the lights and put up the red flag. What is GCA? Inflammation of medium and large arteries caused by the CD 4T cell activation. The IL6 is very involved in the inflammation and the inflammation of the vessel wall cause intimal hyperplasia and close the lumen. As we see in the picture, the lumen is very narrow, when you do a biopsy, you can identify large cells triggered by the CD 4 activation. GCA can affect the posterior ciliary arteries as well the central retinal artery. Both, they have this medium wall that is the site of the inflammation. And these can cause completely central artery retinal occlusion or ischemic optic neuropathy. The clinical presentation is vision loss, but when you review of systems, the patient also has headache that’s usually long standing. They have scalp tenderness. Not always they say tender, they say when I touch here it’s painful. Sometimes they report they have jaw pain. Not always the patient says I have jaw pain. Sometimes they can’t think this is related to the tooth or sometimes TMJ. But you have to ask, do you have any difficulty chewing? Do you feel tired chewing? Some patients report, oh, I don’t feel tired or pain but I have — to have a big bite. They can have an overlap with poly myalgia rheumatica and sometimes they have constitutional symptoms like weight loss. They can report intentional weight loss and this should be a red flag. In terms of ocular symptoms, they can present as Amaurosis Fugax, brief transient vision loss. Given narrow and reduced blood flow. When it’s not completely occluded, you don’t see anything and then the blood flow goes back. They can report with sudden vision loss in the case of AION or present are double vision because this inflammation can affect not only the arteries, the posterior ciliary arteries and the central retinal artery but also the arteries that irrigate the cranial nerve 3, 6, 4 and these can cause cranial nerve palsy. This can cause strokes. And the patient can present sometimes with double vision. So when you have a patient with vision loss, you have to ask, do you have headaches? Scalp tenderness, jaw claudication? These are questions that we need to review for GCA. When you see the presentation, they usually present with this pale optic nerve swelling. That is because of lack of blood flow. As I mentioned with the visual field defects, that can be extensive sometimes. What additional tests can help? Here is a very nice paper, I posted the reference below that talks about the signs of choroidal ischemic and other retinal times. Sometimes you don’t only look at the optic nerve. GCA can involve the central retinal artery and the short ciliary artery. You can find signs of retinal ischemic. There is edema here in the layers of the retina. Sometimes if you order a flourescent angiogram or ICG, you can see the lack of blood flow, the delay of blood flow in the choroids and retina. In G and H we see choroidal hypoperfusion. When you have these signs you’re really concerned about GCA and you should treat the patient. Usually, when the patient presents at the emergency with vision loss, the process is, you have this patient with vision loss and optic nerve swelling. It’s over 60 years old. The first thing you do is order labs. There are two very important markers for GCA. One is ESR and the other is CRP. The CRP is more sensitive. The platelet numbers can help. Usually the patients have thrombocytosis. If the disease is chronic, you can see anemia. And often the ESR is very high. But importantly ESR does not rule out GCA. And it’s important to remember there is correction for age when you check if the ECR is elevated over here at the corner. So the gold standard for diagnosis, this patient presented, you have elevated ESR and CHP. Before anything you treat. After treatment you have a window of two weeks to do the biopsy. Don’t delay treatment waiting to confirm diagnosis. Sometimes you can’t do the biopsy right away so we usually treat and then the patient has the temporal artery biopsy within one week, ten days. This is the gold standard. You can find the granulomatous inflammation and when you find the giant cells is like pathognomonic of this inflammation. The other diagnosis modality is ultrasound where you can see the halo sign that shows the narrowing of the lumen of the artery. Usually you do ultrasound in both temporal arteries. And ultrasound as any other ultrasound is operator dependent. If you are in a place where people are very well trained, it’s valid to do. If not, I would say temporal artery biopsy. And you also investigate if there is other involvement when you confirm diagnosis. So usually rheumatology you’ll be ordering the CTA, the MRI or pet CT to see if there is large cell involvement. It affects medium and large artery sites — vessels. About ultrasound, for who is interested. This has been largely used in Europe. Here, we have a connection with rheumatology. So sometimes we perform — if this is positive, it’s fine: But if it’s negative, does not rule out. And this because the sensitivity varies by study and operator as I mentioned. Just giving some data about comparing with clinical diagnosis, the sensitivity is about 70 to 80 percent. Not very high for this dangerous condition. And comparing to the pathologic confirmation studies that use the temporal artery biopsy as the gold standard, the sensitivity is 60 to 75 percent. This mean ifs you have a negative exam in the ultrasound, does not rule out GCA. Now, the specificity is high. It’s 80 to 95 percent. Especially if you have a bilateral halo sign it’s 100%. If it’s a positive test, you can trust. But negative, you should still go and perform the temporal artery biopsy. Now, the MRI, advances in MRI and now it’s very thin cut, you can find some signs of GCA in the MRI and this can help the diagnosis especially in patients that doesn’t want to have a temporal artery biopsy or sometimes they can arrive with more significant pain and you do the MRI anyways to rule out optic neuritis. The MRI can show some important signs that can guide you towards a diagnosis of GCA. What you see, you can see some enhancement of the vessel wall. This is called secondary inflammation. And sometimes this can affect the ophthalmic artery. Sometimes you see this in the aorta. That is why you do an MRA and CTA. It’s best detected with high resolution, we call it black blood MRI and with fat suppression. So you can really delineate the arteries and see the vessel enhancement as the white arrow is showing here. You have circumferential wall thickening. The other important thing that an MRI can show that gives you like — towards the diagnosis of GCA is some patients can have signs of perineuritis secondary to ischemic. This is important, you see in this picture, they have some fat enhancement. Here perineuritis. When you see a patient with bilateral perineuritis, you don’t think first GCA: You want to rule out other conditions. But we have recently many, a couple patients, a good number that the diagnosis was based on MRI findings and a lot of them had signs of perineuritis. In terms of treatment, this is very important. If you have a patient that you did the review of systems, very suspicious of GCA, the first thing you do is treat. You check the — elevated but don’t delay treatment. You treat and you need high dose of IV steroids. It cannot be oral. It needs to be IV. This is because you want to make sure that you deplete all receptors and keep all inflammation low quickly to prevent vision loss on the other side. Here retreat with IV steroids. The patient comes to receive the infusion. This can be arranged to have this at home. One thing that is important is these patients are usually old, elderly, and we have to be caseous because they can have side effects from the high dose. After they get the IV steroids, we start oral steroids in a dose that is usually 1 mg per kg. To be honest, we usually like to start with 100 mg. We had a couple case that has recurrence of inflammation or the symptoms when we changed the IV dose to 60. If the patient can tolerate, 100 mg. Then use low taper down. Monitoring the ESR and CRP. It should go down and it will go down if the treatment is effective. If the patient does not have visual symptoms. Sometimes the patient says I have a temporal hydrophobic, I have jaw claudication. The inflammatory markers are elevated but does not have vision loss or double vision, then you can start with high dose of oral, 1 mg per kg. Importantly, you have a window to do the biopsy that’s about two weeks from the studies that show you can still find the signs of inflammation in patients that have been receiving steroids. So don’t delay treatment waiting for that: Now, after the high dose, use low tapered. You have to make sure you work together with the PCP or rheumatology to monitor glucose. Some patients can develop systemic hypertension or have uncontrolled blood pressure secondary to the high dose of steroids and bone protection with vitamin D and calcium. Now the other, the good thing that really changed the management of GCA was the introduction of the IL6 inhibitors. The commercial name is docilizumab. This is a steroid sparing drug that is used for GCA with very good results. Most of my patients, I start the IL6 inhibitor and they stay with this medication for about one year. I had only one patient that has recurrence in vision loss in the other eye while on this medication. But this is not very often and you have only few reports in literature. So it’s a very effective drug. Here, just remember, GCA is a systemic disease. As neuro ophthalmologists we see the anterior ischemic optic neuropathy but we can have a more extensive disease with CRAO, the central retinal artery occlusion. And it’s a more severe blindness. You can also have a stroke that effects the vertebral bro basilar arteries and aortic aneurysm or dissection if it affects the major vessels. You treat and work closely with rheumatology to prevent the systemic complications. To close up here the GCA, just always think about GCA in patients over 50 years old that present with anterior ischemic optic neuropathy. Always interrogate about headaches, jaw claudication, vision symptoms. If you have a suspicion, treat as GCA. Jaw claudication is highly specific and needs to sometimes have to ask the patient. They do not come to you saying that. Because they associate it with TMJ and problems with the teeth. So ask. Remember to order CRP and ESR. I can tell a briefcase. Once we had a patient with GCA. We thought was not GCA. The patient came back very quickly with vision los in the other eye. These patients have high risk of losing vision in the other eye. It’s better to treat and then investigate than miss. Don’t forget it’s a systemic disease. Now I would like to show you a case. So keep this in your memory and to show you how these patients present to us. This is a 72-year-old woman that presents with acute vision loss in the right eye. She started noticing some headache and allodynia in the scalp weeks prior. She had 10 pounds unintentional weight loss and mild discomfort after prolonged chewing. This is because it affects the arteries that — the chewing muscles. So there is weakness, jaw claudication. By the absence of low blood flow to the muscles. As you see in the pictures on the right eye, you have this pale optic nerve swelling. In the left eye the optic nerve is normal. Here, the visual fields for this patient. In the right eye, you see this visual field defect. Just to show you, this visual field defects can vary and can progress. Sometimes they start — and they go — depression within the first few days and weeks. And this patient now — we’re going to a question to see if you really own this topic. What is next. So this patient is at the ED, has vision loss in the right eye with pale swelling. What do you want to do next? You have here a few, No. 1, treat with steroids. No. 2, check ESR and CRP. No. 3, MRI. No. 4, temporal artery biopsy. Let’s give you a few seconds. All right. Perfect. I see here that most people mentioned treat with steroids. That’s correct. If you have time, you can check ESR and CRP. So the second most answer here was check ESR and CRP. But this patient is like highly suspicious of GCA. If the patient is waiting for the blood to be drawn, you don’t need to wait for the ESR and CRP, you treat right away while you wait. Do not change the ESR and CRP just because you gave one dose. If you have a high suspicion, you treat with the steroids. This patient had normal platelets but CRP is 31, elevated. And ESR is highly elevated. So this is a classic GCA. Patient losing vision. This patient was treated first and then we checked the ESR and CRP and one week later we’re able to obtain the temporal artery biopsy that shows the granulomatous arteritis with these giant cells. Confirmed diagnosis. Now, I want to show another case. This case is very interesting because when I was a fellow and so I really was involved in the care of this patient. The patient is 85 year-old man that reports cloudily vision in the right eye for three days. The patient denies any pain. Only cloudy vision and no other associated symptoms. We interrogate about GCA symptoms and everything was negative. Medical history. The patient was super healthy. No major systemic risk factors. The vision was central vision was good. The color vision was good which is surprising. But he has this APD in the right eye, the eye that has vision loss. Here are the visual fields. Probably the left eye had low reliability. And just a rim artifact. In the affected eye you see generalized depression. This is the fundus exam. So the patient had this swelling but also had some hemorrhage here. But interesting for this patient, platelets, ESR and CRP, everything was normal. So this patient was seen by an attending that felt this patient was old, 84 years old and there was no symptoms for GCA and the labs were all normal. So it was felt that perhaps this was NION even though looking back at the pictures this is a pale — swelling. Then when I found the patient, I first saw this patient was the follow up visit three weeks later. The patient tells everything is fine, my vision did not change but the head and neck zone, everything went dark for a few seconds in my left eye. I thought it was a stroke and went to a hospital close to me. I asked the patient, do you have any jaw pain. He said no. Any weakness or weight loss? No. The wife remind him, you could not finish your hot dog. Yes, I don’t have pain but I cannot finish my meals. Then, when I check his visit, I went to the chart to see what happens in that ED visit where they did a stroke work up and the CRP was 26.5. Just remember this patient first presented with vision loss with no symptoms and no inflammatory markers. Was not treated because it was felt it was nonarteritic. And then the patient goes home and has transient vision los in the other eye, thinks about stroke and goes to the ED and this is what it was. The ED doctors did not think about GCA and sent him home. When he came to our follow up, he had jaw ache and elevated CRP with transient vision loss. We ordered a biopsy. The biopsy was three weeks later, shows the arteritis. This patient could have lost vision in the left eye. Thankfully he didn’t lose. Sometimes this pale optic nerve that was there since the beginning, looking back, this patient should had been treated for GCA. And maybe had the biopsy. Thankfully he did not lose vision in the other eye but he could have. So your threshold to treat needs to be very low for GCA. And if the patients are elderly, 84, manage with the PCP but make sure you treat the patient. You cannot miss a GCA. This is not a case of giant cellular arteritis. This patient was thought to be nonarteritic. What is nonarteritic ischemic optic neuropathy. How these patients can have this ischemia. It’s the most common cause of optic neuropathy in patients over 50 years old. It’s acute. The incidence is not very common, 2 to 10 per 100,000. But a lot of patients, there is an under-diagnosis. So the incidence may be higher. Most commonly like a GCA is unilateral at presentation but there is a risk of — also affects the fellow eye in the first five years after the first case that is 15 to 25 percent. So it’s a significant risk. Simultaneous bilateral cases are rare. I have seen a cup thal were short or sequential within a few weeks but not exactly simultaneous bilateral. So the pathophysiology is you have the infarction of the optic nerve head. Basically that short ciliary artery and the Zinn-Haller is a region that is very susceptible for lack of blood flow. This, if you have this impairment, if the outer regulation of these arteries, or if you have a nocturnal hypertension, that is another hypothesis. Or if you have this already, the anatomical risk factor, you have this very narrow optic canal with a crowded nerve, you are susceptible to have NION. If there are other things involved but the anatomical factor and impaired autoregulation are mainly involved in the pathophysiology of the disease. So we always think about the disc at risk. Patients that have crowded optic nerve, narrow optic nerve canal, this may be a structural predisposition to ischemia. If you add to this uncontrolled diabetes, systemic hypertension, you may have this lack of blood flow and it usually occurs when you’re around 50. And you end up having this ischemia at the optic nerve head. Because these are anatomical risk factors, it can affect the fellow eye. That is why there is a high risk of affecting the fellow eye. Sorry, one second. Let’s go back here and just — here. Systemic and ocular risk factors: You have this area that is susceptible to ischemia and if you add hypertension, diabetes, hyperlipidemia, sleep apnea or smoking or the optic disc drusen you’re more likely to have a lack of blood flow. In young patients you can see NAION. I have a couple young patients like 14 years old and this is secondary to the optic drusen that can compress and narrow and cause impairment of the blood flow at this level. So usually, a lot of people around the United States, they tend to order EDIOCT to investigate for drusen. In young patients with NAION. You want to see if this patient has drusen. This does not change the treatment or prognosis but can explain to the patient and also assess the risk for the fellow eye. Now, about medications and this is important. Medications associated with ANION. The PDE5 inhibitors are high. Amiodarone, interferon alpha. There is not confirmation but there is a lot of discussion in the literature about the possible role of nighttime anti-hypertensive medications. You don’t want to nocturnal hypertension the patients but there are cardiovascular benefits of taking this medication at night. Because this has not been established, a connection, a causality, you measure the risks and benefits. What is more important. And most recently, the GLP1 agonist drugs for diabetes and largely used for weight loss like Ozempic, for example, a GLP1 agonist have been involved and discussed as potential correlation with NAION. So the presentation of NION is acute monocular vision loss. Readily affects both eyes at the same time. Usually it’s not as pale. And tends to have hemorrhage. Can vary degree. Sometimes it’s localized and sometimes more diffuse swelling. If it’s more diffuse you may have vision loss. If you have vision loss you have the relative afferent pupillary defect. Hyperemia of the optic nerve. And altitudinal visual field defect and sometimes you see progression to a more generalized defect that affects central vision. It can vary. I have had patients with minimum defect and patients with generalized depression in both eyes secondary to NION. Management strategies and I know a lot of people ask about steroids. There is only one famous study checking the use of steroids and showed that steroids can help to reduce the swelling faster. However, does not change visual outcome. So here, I can tell talking from our group that’s the Harvard neuro ophthalmology service. We have ten ophthalmologist, I have one colleague that treats patients with steroids. I have treated once, a young patient with bilateral NION and severe vision loss. I treated, did not change anything. But sometimes it’s not wrong to treat if you want to try something. It’s the only thing that has been, at least, studied. But we don’t do this routinely for patients with NION. We always check any signs and any suspicion for giant cell arteritis and then we would treat. The management is to control vascular risk factors. So we make sure to contact the PCP and cardiologist to monitor blood sugar, blood pressure. In patients sometimes we investigate lipid — and we recommend to treat with CPAP. And related to GLP1 agonist because we have a lot of patients, a lot, is everything about risks and benefits. If the patient has an option to change the medication for another diabetic medication, we would say, talk with your PCP and change. Because especially in severe case of vision loss, you don’t want to lose vision in the other eye. But it’s very important to highlight that we don’t have a causality related to that. And prognosis, most of the case the vision is stabilized within a few weeks. I usually tell the patients when the swelling is gone, we know this will be the visual field. It doesn’t progress once the swelling resolved and this usually happens within 6 weeks. Some patients can have some improvement of visual field but this is not very common. Most common they have persistent visual field defect. And recurrence in the same eye is also uncommon. This possibly because after you have loss of optic nerve fibers you reduce the crowdedness of the optic nerve canal and it’s less likely to cause pressure on the small vessels. Let’s show a quays here. We’re getting to the end of this talk. We have a 46 year-old man with painless vision loss in the left eye. Systemic hypertension and no diabetes. He was not taking his medication correctly. This is the visual field: It’s more — altitudinal superior defect in the left eye. And here is the fundus exam. In the right eye, there is a very tiny small optic nerve, very crowded, barely see the cupping. In the left eye you see the swelling, hyperemic. But no visible hemorrhage. This is one thing that I always do, I check the other eye to see how the optic nerve looks like. If there is a disc at risk. The OCT of this patient is at the beginning we don’t have a lot of — it’s quite useless you have the OCT because the swelling is bad. So this just confirms that it’s swelling. Most of the case, this GCA was not present. It’s more like a segmentation error because of the swelling and the quality of the image. But usually after a couple of weeks you see the GCC loss. Additional testing. This is important because this patient was 46 years old. He is young and only has systemic hypertension. For young patients I do a more extensive work up to make sure it’s nothing else. If there is any pain you do neural imaging. Make sure this is not optic neuritis. You order ANCA or ANA to see if there is other vasculitis. He is not the age for GCA but you order the GRP and CSR anyways. In the fall, we have a lot of cases of Lyme and that is associated with ischemic optic neuropathy. One thing that is very important, syphilis serology. We have in the United States, an increased number of syphilis case. And we have encountered a couple of patients that presented as a NION but it was syphilis. These patients need to be treated. So the OCT three months later, this is not three months later, sorry. I was supposed to show 3 months later where there was a decrease of the thickness. So the swelling goes down. And then you’re able to see the GCC. The OCT can be helpful in case of NION to check the retina. So you can see if there is any signs of retinal ischemia that made you change your mind and think about GCA or intra-retinal deposits that are suspicious for syphilis. GLP1 agonists have been a hot topic. This paper was published in JAMA and I’m a coauthor that shows increased risk of NION in patients that were taking semaglutide medication. The GLP1 agonist. This paper was receiving more citations between 2024 and 2025 among all papers. So I would recommend you to read. This paper has — I can tell, we did a careful manual short review. We had large data calculating this risk and all patients had their charts checked. This is important because a lot of papers that use large data, they are based on ICD codes. And there is no ICD code for NION itself. We have ischemic optic neuropathy. So when you use this kind of data search to find this, it’s not very reliable. And this paper we did a manual review. They found the risk lower than our risk. And I can tell that last month we have another publication of a meta analysis also questioning that. But I think now we are running a couple of studies here at Harvard including animal models that shows, we’re trying to find the explanation why these patients are susceptible to have NION. And, hopefully, we have more results to share and more publications to share with you. So if you have any questions about this topic, I’m happy to answer. Just to finalize, let’s see the major difference, what we learned today between NION and arteritic ischemic optic neuropathy. NION there is edema and the swelling is hyperemic and the AAION is pale. So the vision loss of NION can vary but usually less severe than GCA. I showed you two cases. Systemic symptoms NION, they are not there but you should check. And with GCA, you find the systemic symptoms most commonly and most specifically the jaw pain so ask for that. ESR and CRP ordered for anybody. They will be normal in NION and elevated in GCA. Just go back to the first case there, we talk about this painless vision loss in a patient with systemic symptoms and hypertension and diabetes. This case here is a NION case. You see that it was hyperemic swelling with this flame hemorrhage. In the second case where the patient had temporal headaches, jaw pain, weight loss and poly myalgia rheumatica, pale optical swelling, this is a GCA case. And I’d like to thank you and here is my email if you want to contact for any questions related to how — from how is the neurology practice or questions about NION or studied that you’re interested to participate. Here is my email. Let’s go to the Q&A questions here. We have a couple of questions. There are so many questions. We’ll see what the first one, we have here I may be wrong to pronounce the last name, but — what do you think about correlation between high ICP and NION? This is an interesting question. There is not very high in the literature about that. What you can say is in patients that have high ICP, they can have this prolonged swelling. If you have this congestion of the optic nerve long standing, you can end up with ischemic optic neuropathy. I have seen two patients and this led to a very high discussion. Then I have another question. What is anterior ischemic optic neuropathy and what causes the reduced blood flow? It can be secondary to the inflammation in the artery. And these reduce the blood flow, or can be secondary to medications or structural — an anatomical risk factor that can lead to reduced blood flow at the optic nerve head. And if you don’t have blood flow, even for a few minutes, the optic nerve will suffer injury causing vision loss. I see a couple of questions that I hope I answered during the talk. There is another question that says is there an [inaudible] for the biopsy. We have the ultrasound that is not as sensitive as the biopsy. But can be used. But really depends on the management. The training of the operator. One of my patients underwent cataract surgery, postop vision is 20/20 and one week later an episode of NION where the vision dropped to 2100. This is a coincidence or could the cataract surgery promote a NION episode? That’s a good question and there are a couple studies looking at that. There was a known association but this was a long time ago when cataract surgery was not phaco and the patient had a lot of intraocular pressure during surgery. So before the patient was more susceptible to have changes in the blood flow of the optic nerve head secondary to the intraocular change in pressure during the procedure. So nowadays, with phaco, usually the procedure is much faster and the pressure is more stable. Can be that this patient and especially if it was one week later, I would say that’s a coincidence. But if it was a few days later, could be there is some change in pressure, not caused the NION itself but led to changes in the perfusion of the optic nerve. I hope I replied that answer well. I have here, Deborah Hage. She asks if you have started a patient on steroids and they are negative, how quickly can you wean the steroids? This is a very good question because we do this a lot. Sometimes we treat. Really depends on when is the biopsy. Usually say if you’re waiting five day of high dose steroids you can just stop. Over five days if the patient had a biopsy within two weeks, you can do a quick taper just going to like a half dose every two days. And you’ll be fine. You should not stop if the patient is on steroids for more than five days. Another one here, can OCT and visual field testing help to differentiate AAION for NION? I would say yes, not so much the visual field because NION can very from very extensive visual field defect to — defect. And sometimes we have only a small defect. So visual field not as much but OCT, yes. If you see signs of retinal ischemia, it’s most likely this is a GCA and you should investigate. The OCT, yes, you should perform a OCT retina in these patients. There is another question, Kajal. For how long we need to continue prednisolone? The IV, we use IV steroids for three days. And then we transition to oral steroids, like prednisone in high dose, start with 100 and reducing every, like week to ten days to 20 mg lower. And usually, we keep this medication about like over 18 weeks until the patient is on the oral medication. If the patient doesn’t transition to the IL6 inhibitors, sometimes you keep the patient at dose for longer. Keep the patient on a dose for a year, just checking ESR and CRP. Most cases you send the patient to rheumatology to consider the IL6 inhibitors that have less side effects than steroids and we need to keep the patient on the steroids until this medication starts being effective. That takes a couple of weeks. Dr. Abbas asks, if we start steroids before TAB if it has any effects on diagnosis or biopsy results? As I mentioned in the talk, it can. If it’s over two weeks. I can tell that I had a couple of patients that had biopsy after ten days and there were some scared biopsy. So they perhaps had inflammation in the past. So I would say you do the biopsy as soon as you can within one week it’s not really a factor. So you can trust the biopsy. After two weeks, definitely, it would not be worth to try because you can have a lot of false negative results but try also do within one week. But by literature it’s within two weeks you can have and still find signs of inflammation even if the patient is on steroids. How long will the oral 100 mg of steroids last? I usually keep 100 at least for a week. Then I go for 80 mg. After 80 mg, I go a little longer keeping every two weeks. Another question here for Michael. How about GCA in hypertensive and diabetic patients? We can see and you have a lot of problems of monitoring the glucose when you have this high dose of steroids. I usually, I communicate, I send a message to PCP or endocrinologist to manage the patient very closely. I had patients that had terrible complications with the diabetes. Another question, can steroids cause glaucoma. There are patients that have glaucoma and they are steroid responsive. And they can have increased intraocular pressure when they have a high dose. I had a patient yesterday that had that. If the patient has glaucoma, you have to make sure you have a close follow up to monitor IOP and sometimes you have to adjust the intraocular lowering medications. I had to do this yesterday in one of my patients. CIO, that’s the one for cherry head spot. Yes. The CIO is when you have the central artery occlusion that can be caused by GCA or from emboli. Why you have the cherry red spot is when you close the central artery, you have ischemia of almost everything, the optic nerve and retina but you can — the fovea region has also vascularization through the choroid. So that region can continue receiving some blood flow and it’s pink when it’s in the fundus photo. Let me see another question here. We have time for one more question. It’s from Yadif. How do you manage the patient during FA. We have technicians that do that. We try to do the FA as soon as we can, especially when we have suspicious of GCA. We ask the technician to inject and start counting from the affected eye. We do a video or pictures every 2 seconds to see if we can see the signs of hyperperfusion and this is mostly important at the beginning of the test. We usually can see delay of perfusion, the first 25 seconds are the most important to find this choroidal hyperperfusion. All right. I’m sorry there are so many questions and I didn’t have time to reply to all. But we’re reaching the end of the talk. If you have a super important question that I was not able to reply and you really want the answer, you can email and I will do my best to reply. Thank you for your attendance, this was great. And thank you, Cybersight, for having me here today.