Lecture: Using OCT as an Approach to Diagnose Glaucomatous and Other Optic Neuropathies

>> Ladies and gentlemen, good morning, good afternoon, good evening. Thanks for inviting me to this talk about using OCT as an approach to diagnose glaucomatous and other optic neuropathies. I’m Christian Mardin and I work as an ophthalmologist at the University Hospital of Erlangen. My outline today, is just to introduce the OCT toolbox and the role of the retinal ganglion cell layer. We talk about the appearance of glaucomas. Other optic neuropathies and in the end, we will discuss disc swelling. When we have to deal with patients with optic neuropathy we have these three types. Glaucomatous optic disc atrophy, a simple optic disc atrophy and a swollen disc. Still, by diagnosing these patients we know that there are many shades of gray in between them and sometimes it’s difficult to say by the appearance what’s the reason behind it. And you need for that many examinations and we will discuss today this topic by using our OCT toolbox. Optical tomography, we are able to measure the width of the neuro retinal rim and compare to the normative database. We are able to measure retinal nerve fiber thickness around the optic disc and compare it to a normative database. If the patients are in a normal range, then they are in green here in this diagram. If they’re yellow, they are borderline. 95 percent tile. And if they’re pathologic, they are in red. The same we can do for the retinal ganglion cell layer thickness in the macula with a scan of the acute scan of the macula, we’re able to assess the thickness of the gangly on cell layer and compare it to the normative database with this deviation map. In the future we will apply OCT angiography to the macula and peri optic area in order to design where the damage is, what kind of damage do we encounter. Let’s talk a little more about the deviation maps of the macula. This is quite an interesting tool, especially the differential diagnosis for optic neuropathies. And the thickness of the ganglion cell of the retinal nerve fiber layer and the plexiform layer is compared to the normative database and again in green, normative values. In yellow, suspect. And at 99 percentile in red for pathological layers. Again, in the center, we get readings in this wheel diagram with the mean thickness of the ganglion cells in the center. But we are able to exploit the whole image to see where topographically we have a problem, for example, here, with the ganglion cells. When we think about ganglion cells, we have to think how their axons go further. This is quite an interesting story when we discuss optic neuropathies. We encounter two types, mostly two types of ganglion cells. In the center are the so-called P cells. And these cells project to the lateral geniculate nucleus in the — cellular layer. To the center of our optic disc. And a little more to the periphery of the macula, we find the so-called M cells. And they project to the — cellular layers of the geniculate nucleus. And this is quite important to keep in mind if we encounter different neurological diseases. When we look more in detail in the center and do an over-law with our deviation maps of the macula, we are able to see pronouncing of the ganglion cells and are able by correlating it with the region of atrophy to say which kind of ganglion cells might be damaged and get a hint towards the underlying disease. For example, we know from the literature, from this very nice paper that for example, in Parkinson’s disease, we found, we find an atrophy of the central P cells more likely. In Alzheimer’s disease we’re more likely to encounter a loss of the M cells and therefore, the region of ganglion cell atrophy may be different between those two degenerative diseases in neurology. But, to begin with, we encounter firs our glaucoma patient. The glaucomatous optic atrophy is the optic atrophy most often seen in our everyday life. It’s quite easy to diagnose because during the disease, we have an enlargement of our optic cup. A loss of rim. And the rim keeps the same color as the healthy rim. In contrast to the simple optic atrophy. The loss of rim is flanked with a loss of retinal nerve fiber layer thickness. In this case it’s the typical place of first loss of axons and rim that is temporally inferior sector of the optic disc. And in this case, we see 52-year-old female patient with a thinned rim all flagged in red. We see the thinning of the, the pronounced thinning of the nerve fiber layer with the red sector here. With the B scan we can see the nerve fiber layer that is very important to look at because the B scan has a lot of information for us, we will discuss that later. Of course, we have to check for segmentation errors before we trust this mathematic evaluation. When we look in the ganglion cell layer of this glaucoma patient, we realize that the ganglion cells are thinned in the area where the axons have offspring. We see the pronunciation of the inferior hemi field, the superior hemifield starts to have a problem but the inferior hemifield is most damaged. And we see that the ganglion cells are thinned in the area beyond the 99 percentile. So this is very exact information. We don’t get by ophthalmoscopy. It’s easy to correlate the visual field of our patient who has a defect in the upper hemifield, very close to the center. Nicely correlating to the ganglion cell loss in the inferior sector. When we do an overlay with OCT angiography, we easily appreciate the loss of vessel density in the area where the inner layers of the retinal structure and retinal thickness is loss its nerve fiber layer and ganglion cell layer. When the glaucoma continues and progresses and when we have nearly total optic atrophy, then we have ganglion cell loss in the area in the superior and inferior hemifield. There’s a very nice paper from New York in IOVS from 2023 showing how the ganglion cell layer loss in glaucoma slowly progresses. Typically, we have to look at the vulnerability zones defined in the temporal inferior and superior sector where we see the first loss of axons and the ganglion cells are thinned a little more to the periphery in the upper and lower hemifield. And then with progressive disease, these zones are — less axon loss moving towards the macular papillary bundle and the loss of ganglion cells then start to move to the center as it is nicely imaged here in this graph from the paper. And this is a typical change which is rather typical for glaucoma disease. Gives us an idea and a differential diagnosis for other optic neuropathies. The reason may be that the pours of our upper and lower part of the — have the largest holes and perhaps the mechanical vulnerability is larger than on the temporal and nasal side. We have to remember that in glaucoma, the popular macular bundle is the last structure to be thinned and lost. But there are also qualitative changes we find in our B scans or infrared scans. We see nicely the loss of nerve fiber layer as a darker area in contrast to the healthy nerve fibers on the infrared picture. We encounter a splitting of the nerve fiber layer with interaction of the vitreous body and limiting membrane. You have a Swiss cheese like change of disease. Retinal nerve fiber layer that can cause an artificial thickening. We have the thinning of the nerve fiber layer and when you look a little closer, you will realize the reflectivity is loss in the diseased areas. When you have a progressive disease, you will encounter this acquired pits, defects. Interestingly when you look at the inner nuclear layer of the macula, you will realize there are changes in the area where the ganglion cells above with the red arrow, are a little bit thinned. This is quite an interesting change which is not typical for glaucoma but is also found in other diseases as you can see from this nice article from Wolff. All kinds of different optic neuropathies with changes that may appear. We see them quite often in patients with multiple sclerosis. This leads us to the other optic neuropathies we can see in our everyday clinical work. So again, an example and this is something to make you a little bit think about the case. This is a 70-year-old man who was under topical glaucoma therapy and sent to us to get glaucoma surgery. This was the appearance of the optic disc. This was the visual field of our patient. And I will share with you the OCT examination. You see the thinning of the rim. You see here the thinning of the ganglion cells in the macula area. And the changes in the retinal thickness. So I would like to ask, which statement is incorrect? So incorrect? First rim loss superiorly found? Second visual field defect inferiorly. GCL thinning superiorly. Or this is a typical glaucoma? Which answer would be the incorrect answer? I would like to cooperate and give me your opinion. So the ballot is open now. And yes, the incorrect answer, the majority is right again. It’s not a typical glaucoma. That’s correct. When you look at, close look at the optic disc, the failure of the rim is not typical for glaucoma. That’s the first thing. Let’s continue. We see the failure of the superior optic disc respecting the horizontal line. We see the angiography immediately — when the patient was taken to the ward. We see the darkness of fluorescein uptake in the upper part of the optic disc. Reminds us of the — circle of the optic test and anastomosis of the vessels. This fits nicely to a patient having an anterior ischemic optic neuropathy and not glaucoma. So the majority was right again. We continue with our next case. When you look at the visual fields, everybody of you will realize this is not quite normal. When you look at the optic disc of our patient — just a moment, I will get my curser again. Yes, you will see a very faint, not looking like glaucoma of course in the visual field with the defect to the upper left hemifield. Doesn’t look like glaucoma at all. This is a patient with a resection of a glioblastoma. This is the visual field and this is the rim and the nerve fiber layer thickness of our patient, not flagging too much pathology in the beginning. You’ll see the nerve fiber layer is quite thick. That is nice. When you look at the rim width, the optic nerve head, the measurements are in the normative range. And when we look at the nerve fiber layer and the cause of the disease, we see that the patient slowly changes. On the right-hand side, you see the change of the visual fields. Under follow-up examination, the follow-up examination is about three years. Here you have the ganglion cells in the beginning on the left-hand side. You see a thinning of the nasal ganglion cells. Look at the vertical orientation. On the right-hand side, on the right eye, the temporal ganglion cells don’t show too much. Then we continue at the time and you see that here the nasal defect becomes larger and the temporal defect also appears in the course of the follicular up examination. You will realize the defect grows larger in the follow-up. Although the tumor is stopped, doesn’t grow. You also see the visual field now, the horizontal midline is crossed and the visual field defects grow to the lower hemifield as the ganglion cells are showing to be lost in the upper hemifield also. It’s a very nice correlation, ganglion cells topography to visual field structure and function. So what we encounter here has been described a long time ago by Hoyt in this 1972 publication observing illumination of the fundus of young patients. And he encountered a defect in the right temporal optic tract. And here you lose the nasal fibers on the contralateral eye and the temporal fibers of the ipsilateral eye. And on the contralateral eye this reminds us of a bow tie and it’s called bow tie atrophy. This can be imaged now with OCT. More easily than just looking at the red free photographs. The trans-geniculate atrophy is something that was to be said impossible 30 years ago when I started my training in grownups. But now with OCT, it happens and there’s a nice overview about this topic in neurology. And the paper gives us a time perspective when to expect the first change in the macula. He tells us in the post geniculate lesions you have to wait five to six months to see the first thinning of the ganglion cells. And if the change, or the damage is more anterior, you have to wait four to six weeks to see something in the macula or the optic disc. We know the old rule — the optic disc happens to be seen after six weeks. So when you look into neurologic neuropathies of the optic nerve, you have to think of compressive lesions, ischemic lesions, inflammatory, and neuro degenerative loss of axons. We distinguish between so call ascendent and descendent atrophy. The ascendent takes more time to see on the photographs of the OCT examination. This very young patient, 35-years old. Has a chronic relapse in inflammatory optic neuropathy, called CRION. This patient experiences a rapid loss of vision and visual acuity. These are the visual fields. On the right-hand side the right-hand side and on the left, the left-hand side. And these are the optic disc photographs. You will appreciate a temporal failure of the optic disc with normal cupping. When we look in our OCT examination, strikingly we see a thinning of the nerve fiber layer in the pap low macular bundle showing this is neurologic and not glaucoma typically. We see a circular thinning of the ganglion cells in the upper and lower hemifield showing this red circle. This is a patient who has optic disc damage from another disease. It’s a toxic disease due to alcohol abuse. This patient shows us a slight thinning and thinning of the rim in the form of simple atrophy. Here we don’t encounter enlargement of the cupping but we see thinning of the flattening of the optic disc rim due to atrophy of the axons. The glial cells seem to be preserved. When you look at the nerve fiber layer thickness, you see a thinning of the nerve fiber layer in the borderline area temporally. The rest of the retinal nerve fiber layer is nicely preserved. When you look at the ganglion cells, we see again this red ring of ganglion cell loss on both eyes indicating something neurologic going on. And this is the thickness of the retinal nerve fiber layer, again. You will realize that the pattern is quite different from our ganglion cells of the red circle. When we look at the inner plexiform layer, you encounter the circle like atrophy of the ganglion cells in the red, flagging out, thinning of the ganglion cells beyond the 99 percentile. So I like to call this the red circle sign. When you encounter this red circle time, you have to think of some neurological disease not related to glaucoma. So again, the patient who had to do a vitrectomy with Silikon oil for retinal detachment. A rather young patient we had to remove — the patient experienced vision loss. And first we thought we had optic atrophy. But here optic atrophy was not present in the patient both in the rim and the nerve fiber layer. When we looked in the ganglion cell layer, we see a thinning, circular thinning of the ganglion cells. This is unfortunately happening when you use a Silikon oil and you may encounter and even after removal of the Silikon oil, this patient does not gain vision which is very unhappy. This patient reports a reduced vision since two weeks after heavy lifting on the right-hand eye. On the left hand eye unfortunately is amblyopia. We got this visual field and you will appreciate the right hand side on the right and the left-hand side on the left. This patient shows a typical multiple sclerosis pattern. Atrophy of the rim, a little on the temporal side. Thinning of the nerve fiber layer. Pronounced temporally on both sides. And when we look a little closer in the bundle, you will realize that on the right-hand side, we have a problem. On the left-hand side, a little bit less with the central bundle of the papillomacular bundle. You would say, multiple sclerosis, it’s fine. So my question for you would be these four. Which statement is correct? Optic disc shows no sign of atrophy. Glaucomatous visual field loss typically. Bilateral red circle sign is positive. And all findings support a suspect multiple sclerosis. You should think of multiple sclerosis. Which of these four options is the most correct one? Please go to the ballot. I’m curious what you would say after this 20 minutes of the first lecture time. Which answer is correct. It’s a bilateral red circle sign. That is correct. And all findings support the suspect findings of multiple sclerosis. We thought the same. But of course, when you do the work up we don’t stop with the OCT toolbox, you do an MRI and CT scan of the brain. And interestingly enough, we found that the patient had a cranial far ring owe ma. A compressive disease mimicking the red circle sign of an MS patient. Therefore, this is the lesson that we learned from this patient, never fully trust the OCT. And all our toolbox but of course, you have to continue the check up of the patient by the book. And MRI scan in this case revealed this change of this compressive fibro meningioma. And we overlooked the vertebral orientation of the defect. So this patient has a defect on the left-hand side which has — should have us think of something in the crossing of both nerve fibers, of the optic, both optic nerve heads in the center and hypothesis is the first to think of all other tumors. In this case it was a crane owe far ring owe ma. And the neurosurgeons had to deal with the patient. When you have to do a rough differential diagnosis between glaucomatous and simple optic atrophy due to other neurological diseases, when you compare the nerve fiber layer with the rim width with the ganglion cell layer thickness, the numbers all should be normal, of course. This can sometimes be tricky with the rim width due to anatomic changes and variability of the optic nerve head. But when we go to glaucoma, there has to be some pathology in all three measurements. Nerve fiber layer, rim, and ganglion cells. But in the neurologic patients, when they have an optic disc failure first temporal and later the whole rim is atrophic and pale, we mostly encounter a pronounced loss of ganglion cell layer thickness in the macula layer of the OCT followed up by a nerve fiber layer thickness mostly on the temporal side. And most of the rim, unlike the glaucoma, is not much change. The rim becomes pale. The rim gets a little bit flattened but the cupping does not enlarge as it does in glaucoma. So by comparison of all three measurements you may get a hint which kind of disease you have to do. Especially in patients you would call a novel glaucoma patient. When we look at the thinning pattern of the ganglion cells we can differentiate roughly four types. One type is in glaucoma, found in glaucomas or Alzheimer’s disease. That’s the arcuate temporal orientation in the upper or lower hemifield in glaucoma of ganglion cell loss. Remember resembling a nautilus. When you have chiasmal problems or retro chiasmal problems, you have vertical orientation of visual field effect as a counter and vertical orientation of the ganglion cell layer thinning. Resembling a half-moon. When you have an anterior ischemic optic neuropathy, you may encounter a loss of perfusion in the upper or lower part of the optic disc leading to a thinning of the ganglion cells in the upper or lower hemifield like, resembling a sunset. And the fourth change is the red circle sign. You may see in patients with MS, LHON, Parkinson’s disease, and other diseases. I have shown you also toxic diseases. Showing the typical circle shaped atrophy of the ganglion cells. Beyond the 99 percentile, flecked out in red in the deviation maps and therefore it’s called a red circle sign. So the last chapter we would like to discuss together is disc swelling. Disc swelling is not as easy to diagnose as one would think. Of course, we have to first think with disc swelling, do we have a loss of vision or do not have a loss of vision. Do we have a loss of visual field or not a loss of visual field. You can’t use ophthalmoscopy and OCT only. You always have to use the visual field which is very helpful. And all the other diagnostic tools you may have going to MRI and all the neighbors, neurologists, larynology, you have to ask and do a cooperation with them in order to deal with the patient. The first idea you get from this kind of examination. Let’s look at the first patient with a so-called swollen disc. This patient is rather easy because it’s an elderly patient and you easily appreciate with fundoscopy already the Drusen. But the work flow in many places is that you first get the OCT, you have not — the pupil yet. You don’t get a picture of the optic disc and then you need an interpretation of the OCT. This can be sometimes misleading. When you look at the optic disc, you appreciate the Drusen and you see the highly reflective area in the B scan. When you look at these optic discs with the OCT, with rim width measurements, the rim is ridiculously thickened. You will encounter the superficial Drusen with dark center and a little hyperreflective surface. Then the diagnosis is rather easy. When you look at the retinal nerve fiber layer, you may encounter a thinned layer in complicated Drusen, in combination with visual field defects. This is in contrast with the rim which is super normal. And the nerve fiber layer is thinned. And most often when we look at the BMO area opening, reading, and the area, the area is much smaller than normal. The normal BMO area is around .8 square mm and this patient had .7 square mm because the Drusen discs are most often small discs. This patient had a diffuse loss of ganglion cells not respecting the midline horizontally or vertically in both eyes. It’s a crazy pattern of atrophy. Therefore, the visual field defects also have a very crazy pattern. This pattern doesn’t fit to all the cases we have discussed up to now. Respecting the horizontal or the vertical line. And when you do an overlay, you flip the ganglion cell layer image and you get a nice correlation upside down with the visual field defects. This is a young woman we saw six weeks ago with idiopathic cranial hypertension. 45 cm water was the opening pressure of the cerebral spinal fluid. The vision was full. 90 degree visual was fine. And 30 degree visual field with the octopus, you realized the enlargement of the blind spot. A typical finding of papilledema where the visual field in the beginning is good and the visual acuity is normal. You see a flattening of the high. Sis. When we look at the OCT scans, you will appreciate the pattern lines, wrinkling on the flank of the disc edema. This does not happen in very small discs. You don’t encounter this sign in patients with Drusen. But if the disc is really swollen from inflammation, to hypertension or ischemia, when you encounter these pattern lines you see the small wrinkles of the flank of the optic disc. You can perform a star scan and a volume scan of the disc. You don’t do this scan in order to do the diagnosis seen by your eyes but for the follow up examination it’s useful to see whether the patient responds to therapy by flattening of the disc, by reduction of the optic disc edema or not. Of course, you take — to measure the swelling. Nowadays the cause of the disease, OCT has a higher resolution than [indiscernible] This is a patient encountering a change of the volume of the optic disc. And this change and this volume scan can easily be shown by the volume measurements and topography of the optic disc. Here the OCT is very helpful. Also showing us very small steps of change. When you look at the star scan, you will realize in this graphic, how under therapy, this flattening of the optic disc takes place. And we always combine this with a surface scan of the nerve fiber layer because sometimes you encounter a loss of nerve fiber layer thickness and here in this event-based analysis, you see the topographic image change of the retinal nerve fiber layer in the course of the therapy of this patient. In this case with acetazolamide and lumbar puncture. When you have disc swelling and beginning optic atrophy, then something is wrong. Especially when you look at the optic disc and you have this Frisen’s sign. Enlarged capillaries at the optic disc. This must let you think of something which is growing in the orbit or the apex of the orbit. In this case, this patient suffered from meningioma. You see the swelling of the optic disc. The cause of this tumor, the optic disc atrophy became complete. Swelling always goes down and the optic disc becomes pale. This change can easily be visualized with OCT and can be measured at any point you want to. Or you can get a volume if you do an optic disc volume measurement. So if you have a compressive descending atrophy of the optic disc after papilledema. It may end up like this. With defects of the retinal nerve fiber layer. This in contrast is the healthy eye with the normal measurement of the nerve fiber layer in the course of the disease. Unilateral disc disease with vision loss, you always rule out a tumor. This patient as we have shown add an optic nerve meningioma. And there was an MRI scan and contrast enhanced in the anterior part and then the atrophy in the part of the tumor. And we are able to see the inner part on the optic disc with OCT. So this is a patient, 68 years old. Acute vision loss left, and suspect anterior ischemic optic neuropathy. There was an event on the right-hand side and can now acutely, with a swollen optic disc and visual field loss, on his former better eye here. When we look, again, in our rim measurement, the rim looks nice on the right-hand side. On the left-hand side with the acute swelling, we see an enlarged rim width. And also, an enlarged reading for the thickness of the nerve fiber layer. On the older right side, we see already the optic atrophy pronounced in the superior hemifield corresponding to the paleness of the disc. And here the ganglion cell ins the superior part are lost and here we have the beginning thinning of the ganglion cells and the nerve fiber layers are thickened by the edema. But if you encounter this image you have to always think of brain tumor. It cannot always be the second eye but it can be also a foster Kennedy syndrome with large tumor of the brain leading to atrophy of the first disc and later onto a disc swelling due to elevated cerebral spinal fluid pressure. And then you have a similar picture as in our ischemic optic neuropathy patients but the visual fields may then be different. So myelinated nerve fibers look dangerous but they’re harmless. They cause a thickening of the nerve fiber layer, too. Leber’s optic neuropathy starts with the swelling of the disc leading to a fast pale — of the disc and fast visual loss as in this young patient. This patient encountered a rapid vision loss, we first thought of MS or CRION inflammatory change. But the analysis of the mitochondrial DNA reveals Leber’s optic neuropathy. A fiber layer thickens with OCT over time, and you have to think about Leber’s disease or an aggressive inflammatory disease like CRION. In the end the patient lost a lot of nerve fibers and visual field. So you can differentiate without the dominant optic neuropathy not being as aggressive in nerve fiber loss as Leber’s as it has been shown by this publication. When you have disc swelling, you have a thickening of the rim, a thickening of the nerve fiber. You have to think of papillitis, disc edema, AION or myelinated retinal nerve fiber. You have to look at the visual field and acuity. If the nerve is thickened and the nerve fiber is thinned you may have complicated Drusen. In GCL thickness may help. Visual acuity, visual field and echography and MRI. OCT never stands alone, as helpful as it might be in this talk. To close my talk, I have a last question for you. I’m demonstrating a young patient, 18-year-old girl. 98 kg. 185 cm height. Full vision. Headache two weeks. Was referred to neurologist for check up to rule out papilledema. Unfortunately, the discs were rather swollen. And I have the question for you now, this is bilateral papilledema. Normal nerve fiber layer in OCT. Idiopathic cranial hypertension. Or typical normal visual field. Which statement is the most correct in this case? So this patient has all the features of idiopathic cranial hypertension. Normal visual field is also right. The wrong thing is that the patient doesn’t have bilateral papilledema. Although it looks like that. When we got the patient to work up, we realized that the patient was hyperopic, under corrected. Learning hard for two weeks reading a lot of books and got headache. So this is the differential diagnosis for disc edema and could be misleading. In this patient everything was done. MRI, spinal fluid tap. And then she saw the ophthalmologist. Unfortunately, this was the wrong road. And also in our B scan, we didn’t see a flying bat sign. So everything was normal. So with this last minute, I would like to say thank you for your attention. I have shown how you can apply OCT examination, the toolbox on your optic nerve diseases. I have also shown you that OCT is not everything. Only gives you a hint in addition to ophthalmoscopy. In the end you have to decide which other examinations you have to do. I hope you learned a little bit from that talk and I’m very looking forward to your questions. Thank you very much. So I have opened now the questions and answers and I would like to start answering the questions. How we predict visual field pattern. Flip the macula ganglion cell, yes. That’s how you do it and you can correlate the visual field defects with the ganglion cell layer loss. And astonishingly, this works quite good. Another question was, oh, many now coming in. What is the isn’t rule. The inferior part of the rim is the thickness followed by the superior part followed by the nasal. And the thinnest part is the temporal side. If the inferior rim becomes thinner, the superior part when you have beginning glaucoma — the visual fields still work and one of the major achievements — Is it normal to have a linear or vertical CDR zero. Yes. In very small disc, you don’t have cupping. So it’s zero. If these discs start with glaucoma, they have a beginning cupping but this can already be pathologic. Which study has the most sensitivity in early glaucoma. I’m a little more — oriented and it’s the nerve fiber measurement followed by the visual field examination. Sit normal to have no optic disc edema, no vision loss, absolutely nothing but a CDR zero in a 30-year-old female. Yes, I think the last patient answered this question. In hyper optics you may encounter exactly this situation. If the patient has in our case, had an under-correction and reads a lot, gets headaches and this very much resembles papilledema due to elevated intracranial pressure, then you get a problem. Will EHOH present the same on OCT as vitamin deficiency. This is an interesting question and I left out exactly this case because a vitamin A deficiency you have a normal ganglion cell layer thickness. You have the problem in the periphery, in the layer of the photoreceptors. And the outer nuclear layer. The whole retina thins but the ganglion cells are more normal than the outer areas and you can distinguish these patients from other optic neuropathies and by supplementation of vitamin A, the thickness gain becomes normal again. And the patients gain their vision again if it’s not been a very long time of a deficiency. What is the explanation there is ganglion cell loss but normal retinal nerve fiber layer, like in red circle disease? Before, I would think of something pathologic, I would check the segmentation. And I’m unhappy to say that in very shallow foveas, you may encounter red circle sign as a false positive. So before thinking of something neurologic where the red circle sign appears before nerve fiber loss, I would always check the B scan. The role of IOP and optic nerve head disease. I think the question hints towards other neuropathies and glaucoma. In glaucoma we know we have a low IOP. In other optic neuropathies, there is no evidence for that whether lowering the optic — the IOP has a good effect on the progression of the disease. What we do, but that’s off label, what we do in patients with complicated disc Drusen where you see to do nothing, we give alpha agonist in order to preserve a little bit the nerve fiber layer and lower the pressure in other words to help the patient. But there is no evidence for that at all. The abbreviation for BMO and MRW is membrane opening base, minimum rim width. That’s a specialty. And this name was coined. It’s rather complicated. But it sounds for omitting based. This is diagnosed by the device. The opening of the — membrane. Then you take the shortest distance to the limited membrane and then you have the reading and the measurement of the rim and therefore, it’s followed by MRW. It’s rather difficult to pronounce every time I have my talks. How do you investigate a normal tension in glaucoma suspect? We do the normal workup you do for glaucoma. Apply the OCT toolbox not to encounter a red circle sign. What we always do is CT or MRI scan of the brain in order to rule out a midline tumor. It has been shown in some publications that you may encounter a five percent midline tumor. Therefore, in these patients we always perform this kind of imaging. Next question is, most ganglion cell thickness reduced only in glaucoma. No it’s reduced in all optic neuropathies just the pattern is different as I showed in one of my slides. If we don’t have perimetry, can we rely on the — tests. You can do a confrontation test which is a very rough test. But then I would more rely on my OCT. And on the appearance of the optic nerve head in a dilated pupil situation. Pupillary reaction will be affected in optic neuritis? Yes, it is. One very early sign in optic neuritis is the afferent pupillary reaction. And most MRI scans reveal something but not always. If we suspect optic neuritis, then optic disc appearance can be normal. The patient has decreased visual acuity. Macula scan should be normal in that case. And then afferent pupillary reaction deficit is a very low-tech sign. When glaucoma, the concentration should be more on the nerve ganglion fiber cell or the — diagnose of OCT. My favorite is still the retinal nerve fiber layer. And for differential diagnosis or when I’m not sure whether it’s really something wrong the nerve fiber layer, not in OCT, I take the ganglion cells. If the ganglion cells are completely normal, then I have my doubts whether the nerve fiber layer is really thin. Does the red circle sign mean neurological base. The red circle sign is a hint towards it. You have to check your B scans where the segmentation anatomy is okay and perform of course the visual field testing. Normal tension glaucoma and other optic neuropathies. Well, normal tension glaucoma does not have elevated IOP. But the optic disc behaves the same way as all glaucoma optic discs and follows quite a different pattern than our other optic neuropathies. A disc at risk is a very small disc. These discs tend to have an anterior scanning optic neuropathy. They may have a Drusen and therefore they have the risk for ischemic events. Another question, what if the visual field has — distributed field defects what would be the problem? If you have diffuse effects, I would first think of optical problem like lens opacities. Can OCT detect antituberculosis drugs. Yes, quite nicely. By taking a measurement of the nerve fiber layer. If you have the opportunity of the ganglion cell layer. And together with the central visual acuity, that’s quite nice examination. When you have temporal nerve fiber layer thinning, I always look at the ganglion cell layer and rim width and look whether, of course, look at the optic disc in order to find out a temporal paling of the optic disc. Ganglion cells may decrease with diabetic neuropathy. Here it’s easier to differentiate from glaucoma because glaucoma has the vulnerability zones in the temporal, superior, and inferior part of the disc. But other optic neuropathies can be tricky. Will blood sugar levels affect nerve fiber layer thickness and ganglion cell thickness in the long run. You will end up with high sugar levels in diabetic retinopathy leading at the end after edema to a thinning. High myopia, a tricky topic. All the normative databases stop at minus 6 diopters. And at the moment, we are taking part in a project with — in order to extend the range of the normative database in myopia. Concerning the literature, the literature says that the ganglion cell layer may be more reliable than the nerve fiber layer in diagnosing a glaucoma patient. And OCTA is a little more reliable. But don’t forget that when you do a macula scan for OCTA or ganglion cells you have to have a very good image quality and if you have a staphyloma on the posterior pole of the eye, it’s very difficult for a good segmentation. And then in my place, we end up again with imaging of the optic discs with a disc photograph doing visual field measuring the IOP as we did 30 years ago. The causes for optic disc swelling can be inflammatory, they can be ischemic. Elevated cranial pressure, of course. And swelling due to tumor compression. There are many different reasons for that. Let’s look, we still have 2 minutes. When can we find OCT changes in retro bulbar neuritis. In the early face when there is no disc change, you might already find very faint red circle sign. That is our experience in our place. But this red circle sign already correlates with a slight loss of central vision. And this sign is earlier in MS than nerve fiber layer thinning. And OCTA changes are even more early here. For OCTA changes you need a very good image and a very reliable machine to measure it. The normative values for rim width are about in the mean 350 microns up and down. You will see in the literature where this normative database was published by an international cooperation group. If the patient has a normal IOP, how to interpret nerve fiber layer thickness and loss of ganglion cells. If the readings are normal, I would monitor the patient. The patient has some kind of risk like positive family history. If the patient is pathologic, I would start with therapy. It’s very individually different. Augmented disc atrophy in the beginning, as I know, they have no disc swelling. They start with atrophy and that is in contrast to Leber’s optic neuropathy in the beginning. So I think the time so far is up. We have, we had about 530 spectators. Thank you for your interest. Thank you for all of the questions for discussion. And I hope you could get a few bits of new knowledge from this 45-minute talk. It’s 1 past 4:00. I would like to say goodbye to you and have a good morning, afternoon, or evening, wherever you are in the world. Thank you very much. Bye bye.