Lecturer: Dr. Thomas Ciulla, Indiana University School of Medicine
During this Live Lecture, the basics behind retinal OCT are reviewed, followed by normal anatomic correlations and then OCT assessment of retinal conditions. Finally, structure-function correlations are discussed.
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DR CIULLA: And I will be speaking on optical coherence tomography, or OCT, for clinicians. Well, as many of you know, OCT is non-contact and non-invasive. It provides micron resolution of the retina and optic nerve. It provides cross sectional studies of the retina, and correlates very well with retinal histology. The first paper on OCT was by Huang and others in 1991, and the first in vivo studies of the human retina occurred in 1993. OCT was originally based on the Michaelson interferometer. And basically if you look at the right portion of the slide, you see that when two waves are in phase, and you add them, the combined wave form is larger. And on the far right, when two waves are 180 degrees out of phase and they’re combined, you can form a line. They nullify each other. So with that in mind, on the left, you can see that when you have a coherent light source, and it passes through this half-silvered mirror, the path between the mirrors at each extreme and the center determine how the waveforms arrive back at the detector. And the distance will result in either a combined or… A combined waveform that’s additive or nullifies each other. And this provides a basic signal through which OCT pictures can be formed. So if you substitute the mirrors with this setup here, you can see in the upper right we have this tissue that is retina tissue being scanned, and we have the scanning reference mirror in the midright. And we know where this scanning reference mirror is, as it moves back and forth. So with that in mind, the computer can then analyze the signals, to derive an image. So that’s the basis behind time domain OCT. The reference mirror moves, and that’s a slower process. Whereas in spectral domain or Fourier domain OCT, the reference mirror is stationary, and the interference is detected by a special interferogram, requiring Fourier transformation. This is much more rapid and provides sharper and clearer images. So once again, this is a schematic comparing the time domain OCT and the Fourier domain OCT. And once again, the scanning mirror, the reference mirror moves at a known speed and distance in the time domain OCT. And in the Fourier domain OCT, the reference mirror is stationary. Well, how does that work? So each scan is simply an A scan, and the computer will sample various parts of the tissue. And in this case, we’re showing a line. So each A scan is summed to form a B scan, that we’re all familiar with. When all these A scans are combined in one image, the image has a resolving power of about 10 microns vertically, and about 20 microns horizontally. And these are the different OCTs that have been available over the years. And you can see in the lower left, this OCT 1 was one of the first models, with the lowest resolution. OCT 3 provided better resolution. And nowadays, we’re using Spectralis OCT, which is perhaps one of the most popular units here in the United States. And we can see a very fine resolution. As many of you are aware, the system involves a fundus viewing unit with the interferometric unit, computer display, control panel, and printer. Basically the patient sits comfortably and is asked to look at a target in the system. They’re discouraged to blink. And this is a very rapid image acquisition. The scan protocol types involve a line, as I just alluded to, but also we can have circles or radial scans. The line simply scans in a single straight line, and the length of the line can be changed, as well as the scan angle. So this is a typical macular horizontal line scan, shown with this arrow. The circle scans in basically a circle, instead of a line. So in the case of the optic nerve, we can look at the retinal nerve fiber layer thickness around the optic nerve, by scanning in a circle around the optic nerve. One of the more common macular scans involve these six radial line scans in a star pattern, centered at the fovea. There are various protocols. There can be these fast scan protocols, which reduce the time needed for multiple scans. And most currently, the raster scan. So these are multiple lines in a rectangle. Similar to a television set. That it scans across, very rapidly, line by line. This is a typical raster scan. And you can see that the scans would go back and forth in this fashion. And then providing this printout with a horizontal and vertical cut, denoted by the white and yellow. These can be used to perform various types of scans. The three most common posterior segment scans involve a macular scan, an optic disc scan, and a glaucoma retinal nerve fiber layer thickness analysis scan. Anterior segment scans can also be performed of the angle and cornea. However, we’re not gonna cover that today. First, the macular scan. This is a typical normal foveal profile. You can see there’s a slight depression in the center of the retina. This is a typical printout. You’ll see the horizontal cut in this section, and a vertical cut in that section. They’re both centered on the fovea. And we have both a two-dimensional map and a three-dimensional map. We have the internal limiting membrane contour, and the RPE contour. And finally, we have these various segments with thickness denoted in microns. The most commonly used parameter is the central subfield thickness. Which is here. This slide shows the retinal anatomy, compared to OCT. We all know that the vitreous is black in the top of the image. The fovea is this normal depression. We can see — we know this is a horizontal cut, because we can see the retinal nerve fiber layer here, with the maculopapular bundle denoted with this NFL. Beneath the fovea, we can see the ellipsoid zone. And we can see the external limiting membrane. The internal limiting membrane is on the surface of the retina. The RPE is this orange line. And the choroid and choroidal vasculature is shown at the bottom of the scan. This is a more highly resolved image. It’s really quite a beautiful image of the retinal anatomy. And once again, just to orient everybody, we see the fovea. It’s this depression. Again, the papillomacular bundle, the nerve fiber layer of the papillomacular bundle. One of the most important microanatomy lines shown on this OCT is this ellipsoid zone. And that’s denoted by this line here. We’ll go into that in more detail in a moment, but that’s a very important feature of these high resolution OCT scans. Because this actually correlates with function. We’ll go over that in more detail in a moment. I should also add that many of the cases I’m gonna cover tonight are covered in a download that’s available for free, which will provide more detail on some of the concepts we’re reviewing today. So back to the ellipsoid zone. The ellipsoid zone is this mitochondrial rich area of the rods and cones. And when the rods and cones are aligned, these mitochondrial rich areas will form that line we just saw. When the rods and cones are misaligned, the ellipsoid zone will be disrupted on the OCT. And once again, that correlates with vision. In addition, OCT has some very special correlations with fluorescein angiography. Fluorescein angiographies are very sensitive, but not very specific. And they do provide size and extent information on the X and Y axis. But the OCT gives us depth on the Z axis, telling us what layers of the retina are affected by pathology. So here’s an example of a RAP lesion. We can see this RAP lesion here, with some hemorrhage. And then we see a pigment epithelial detachment, as well as some surrounding subretinal fluid, which is denoted by the hard exudates. On the fluorescein angiogram, there’s pooling of dye in the pigment epithelial detachment, and on the OCT, we see this pigment epithelial detachment as this elevation, and we see some cystoid edema as well. The optic disc scan can be very helpful, especially in glaucoma. We’ll have… This will provide a disc diameter, as well as a cup diameter. And another common scan is the retinal nerve fiber layer thickness scan. There’s various protocols. And a typical printout is shown here. And again, this is done in a circle. And the thickness of the retinal nerve fiber layer is denoted by this black line. The green is normal. So when there’s thinning of the retinal nerve fiber layer, this black line will dip into the yellow or red, showing that there’s thinning. And although it’s not very resolved in this slide, not only will it reveal thinning, but it will reveal where on the optic nerve thinning typically — thinning is occurring. It can be very helpful for assessment of glaucoma progression. Next I’m gonna review some of the clinical applications of the posterior segment scan. And we’re gonna start on the retinal inner surface and work our way posteriorly to the RPE and choroid. So first we’ll cover vitreomacular disorders. Many of you have seen macular hole, denoted with this black arrow. This is a right eye. Here’s the optic nerve, the blood vessels, and the macular hole here. This slide shows macular hole in both the time domain versus spectral domain OCT system. The spectral domain OCT image is shown in the lower portion of the slide. We can see there’s much greater resolution. We see this inner segment/outer segment line, which I was calling the ellipsoid zone, but another name for that is the IS/OS line. We can see a break in that, obviously, at the edges of the macular hole. Macular holes are caused by vitreomacular traction. So this is a high resolution OCT. We have the optic nerve here. This is a horizontal cross section through the fovea. We see the posterior hyaloid is attached at the optic nerve. And attached at the fovea. But causing some traction, some anterior-posterior traction. So we have this vitreomacular traction, which is shown with this distortion of the fovea. And also, incidentally, there’s optic nerve drusen, which are these irregularities on the RPE. This slide shows the evolution of a macular hole. We can see this normal foveal contour in the upper portion of the slide. And then we have some vitreomacular traction, with an adhesion at the foveal center, causing some anterior-posterior traction and distortion of the foveal pit. And as the traction progresses, we can see ultimately a macular hole is formed. And we have some intraretinal cysts, when there’s chronicity. This is a small hole. Macular holes evolve through various phases, which we’ll cover in a little bit more detail next. I want to point out… We have resolution of the macular hole on E. This is a postsurgical repair. And often in postsurgical repair, there’s often some slight irregularity in the fovea, which is quite typical. And patients typically see quite well with this. So on to the evolution. A stage 1 macular hole involves a foveal detachment, shown here. We can see on this OCT some vitreomacular traction. Here’s the posterior hyaloid attaching at the fovea. And coming up here. Causing some anterior-posterior traction, resulting in a foveal detachment. Again, stage 1. Stage 2 is a small eccentric hole, so we have the foveal detachment, and just the very beginnings of a macular hole. We can see the vitreomacular traction coming down here, and causing some interior-posterior traction. Hence this dehiscence in the foveal region. Stage three is a larger macular hole. There’s no vitreous detachment here. We can see that the hyaloid is still attached to the edge of the macular hole. The edges are rolled up, and show cystoid changes as well. Now on to macular pucker. It’s very typical. A quite severe macular pucker. It’s a right eye. Here’s the optic nerve. The blood vessels. And we can see this macular pucker as this white collagenous scar, overlying the fovea. It’s drawing in the blood vessels, and hence they’re distorted. This is an OCT cross section. And once again, you can see the macular pucker, which is shown here. And it’s causing some tangential traction on the fovea. This is a more severe case of macular pucker, with retinoschisis. This patient has had chronic macular pucker. We can see the macular pucker denoted by this line here. There’s severe distortion of the foveal architecture. And then we have this splitting of the macula itself, the retinoschisis. And this is generally a poor prognostic sign. Another common finding with macular pucker is a pseudohole, which is shown here. Again, we can see the macular pucker. Causing some anterior-posterior traction. And then if you were to examine this patient, you might see this thinning in the center, in the fovea, and maybe even mistake it for a macular hole. But OCT will confirm that it is a pseudohole. These patients typically have good vision. Much better vision than patients with macular hole. Here’s a more severe case of macular pucker with a pseudohole, and there’s quite severe distortion of the fovea, as well as thickening. Another variation is macular pucker with severe vitreomacular traction. So once again, we can see the posterior hyaloid attaching to the macular pucker, and causing very severe anterior-posterior traction, with great distortion of the fovea. This patient would have a very poor vision. So that covers vitreomacular disorders, and some of the more common OCT findings, with these disorders. Next I’m gonna talk about intraretinal disorders. First, branch retinal artery occlusions with retinal ischemia can show on OCT. So in this case, we can see the patient’s had an inferior branch retinal artery occlusion. And it’s been chronic, because there’s thinning of the bottom half of the… Macula. And on the vertical cross section, it’s quite apparent. As denoted by this red arrow. Again, quite apparent on the three-dimensional map. Macular edema is often denoted by intraretinal areas of decreased reflectivity and retinal thickening. There’s round, optically clear regions within the neurosensory retina, which is quite apparent on this cross section. This is a typical case of macular edema with cystoid features. Again, another case of macular edema. This one just happens to be diabetic macular edema. And we can see that there’s atrophy related to these prior laser scars. Another form of macular edema is macular telangiectasia. This is a case of macular telangiectasia type 1. It’s affecting the patient’s right eye. The left eye is normal, which is quite typical in type 1 macular telangiectasia. We can see in the fluorescein angiogram these abnormal telangiectatic vessels, which are often temporal to the fovea, and on the OCT, we see this very distinctly temporal edema. This is in contrast to macular telangiectasia type 2, in which there’s bilateral telangiectatic vessels, shown on this fluorescein angiogram. And we can see typical subtle bitemporal changes, which stain on the late frames of the fluorescein angiogram. In macular telangiectasia type 2, we have these pseudocysts. So there’s these optically clear areas without thickening of the fovea. This is a typical pseudocyst. And this is quite typical of macular telangiectasia type 2. Next on to some subretinal disorders. Macular detachment in particular. This is a common scenario, a classic scenario, of central serous retinopathy, affecting a patient’s left eye. We can see in the left eye there’s the optic nerve and the blood vessels. And this subretinal fluid can be seen by this ring. Which can be seen on exam as well. On the fluorescein angiogram, we have this classic but less common smokestack pattern. And then on OCT, this very typical, fairly symmetric subretinal fluid. This is another case of a macular detachment, caused by optic pit-related subretinal fluid. This patient has had laser treatment. We can see this atrophy denoted by the blue from the laser around the optic nerve. And then thickening on the map denoted by the red. On cross section, we see both subretinal fluid and intraretinal fluid. Next, on to some findings and cases involving some of the deeper layers. The photoreceptors, the ellipsoid zone, and the RPE. So once again, very important concept for this lecture is the ellipsoid zone. And once again, it’s this mitochondrial rich portion of the photoreceptors. When these are lined up properly, we’ll have that distinct line I pointed out earlier. And this typically correlates with good function. When there’s disruption of the ellipsoid zone, visual acuity often is decreased, and/or a scotoma could be present. This is the same slide I showed earlier, but just to stress the ellipsoid zone here. External limiting membrane. And the interdigitating zone, sitting on top of the RPE Bruch’s complex. The interdigitation zone is that zone where the tips of the rods are interdigitating with the RPE microvilli. This is a patient with Plaquenil toxicity. And we can see quite distinctly in the patient’s right eye, in the OCT, there’s intact ellipsoid zone underlying the fovea, but the ellipsoid zone is disrupted, surrounding the fovea. So this intact ellipsoid zone centrally, with absent ellipsoid zone around it, is often called the flying saucer sign, because it looks like a flying saucer. This is another interesting case, a patient of mine, actually, who had a macular laser injury. It affected the right eye. We can see the left eye here for normal comparison. And the ellipsoid zone is quite intact in the left eye. But in the right eye, we have this disruption of the ellipsoid zone. Interestingly enough, the patient’s vision was decreased, with a scotoma, symptomatically. But by week 6, we can see the ellipsoid zone is starting to reappear. Not quite as distinct as in the fellow left eye, for comparison, but it is trying to repair, improve, and this correlated with improving symptoms in the patient. This is another patient, who had solar retinopathy, staring at the sun. They had both disruption of the ellipsoid zone and deeper interdigitation zone. We can see the symmetric foveal punctate RPE disruption on the color photos. On the angiogram, we see staining. And on the OCT, once again, disruption of the ellipsoid zone and interdigitation zone. And finally, a patient with cone dystrophy. We can see the typical bull’s eye pattern on the color photos. It shows up more distinctly on the fluorescein angiogram. And on the OCT, the ellipsoid zone and deeper layers are disrupted. There’s some retention of the ellipsoid zone centrally, in this right eye. Incidentally, the patient has mild macular pucker. Now on to even deeper layers. The RPE and choroid. This is a patient with choroidal folds. It can be quite subtle on the color photos. I believe you can see them radiating horizontally through the fovea in the right eye. They’re quite distinct on the fluorescein angiogram. And they’re distinct on the OCT as well. What’s quite interesting: On these horizontal cuts, oftentimes you’ll miss them. So the vertical cuts will cut right through them, and we’ll see these undulating deeper layers. This is a patient with adult-onset foveal vitelliform dystrophy. We have the symmetric pigment clumping in the fovea. These patients are often sent in with a diagnosis of macular degeneration, but notice that there’s no drusen typical of macular degeneration. These patients are middle aged. And they’re often just minimally symptomatic. They may complain of some difficulty reading, some slight metamorphopsia. Oftentimes their visual acuity is fairly well preserved. On the OCT, we have this typical dome-like elevation that’s symmetric. Underlying each fovea. And on fluorescein angiogram, in this panel, there’s no leakage. So that’s quite typical of this disorder. These patients do not require treatment unless they develop a secondary choroidal neovascular membrane. Another disorder that we don’t as commonly see in the United States as in Asia is polypoidal choroidal vasculopathy. We can see this lesion in the maculopapular bundle in this right eye, surrounded by hemorrhage. And on the OCT, we have this very distinct inverted U lesion, which often denotes a polyp. And then there’s adjacent subretinal fluid, very typical of this disorder. These patients often don’t respond as well to anti-VEGF therapy as typical age-related macular degeneration. And often will require photodynamic therapy for best results. Now on to macular degeneration. These are typical drusen. We can see this undulation from the drusen, in the fovea, on this high resolution OCT. We can also see it on this spectral domain OCT. Another common feature in dry macular degeneration is geographic atrophy. We can see this increased signal penetration into the choroid. What’s interesting here is we do have ellipsoid zone and external limiting membrane, which disappear. Which is quite typical in geographic atrophy. And we have this increased signal penetration, which is quite distinct, denoted up here. The RP layer is very attenuated. Oftentimes with geographic atrophy, we’ll have this pseudocyst. This does not contain typical fluid, as in cystoid edema. It often is thought to contain waste products of this entire process. These are important to recognize, because these are often mistaken for cystoid edema and are often treated unnecessarily. In neovascular macular degeneration, we have this very typical fibrovascular pigment epithelial detachment. Shown here. And associated subretinal fluid. Other common elevations of the RPE include this serous pigment epithelial detachment. These do not always convey choroidal neovascularization. Sometimes they can occur due to impermeable and diseased Bruch’s membrane, with RPE pumping, but unable to pump across into the choroid. So fluid can develop. Oftentimes, however, they do denote occult choroidal neovascularization. And on the right, we have this hemorrhagic pigment epithelial detachment. We can see hemorrhage surrounding the edges of the lesion. And on the OCT, this typical appearance of a pigment epithelial detachment. This is a case of a central pigment epithelial detachment, with overlying subretinal fluid, which often denotes an active choroidal neovascular process. And this is a very typical retinal pigment epithelial tear. So we can see on the right we have an optic nerve, the blood vessels, and this area of atrophy, which is staining on the fluorescein angiogram, as well as this adjacent bunched-up RPE, which blocks the underlying choroidal flush. So when you see this hyperfluorescence with adjacent hypofluorescence, that’s very typical of an RPE tear. On the OCT, we can see this area of atrophy — again, this increased signal penetration into the choroid. And then there’s this adjacent scrolled and irregular RPE, which denotes the RPE tear with some retraction. In the fellow left eye, we see atrophy and drusen, which are staining. And again, on the OCT, drusen, with this irregular contour, and then this increased signal penetration in various portions, which correlate with geographic atrophy. This is a typical patient with neovascular AMD, showing both subretinal fluid and intraretinal fluid. Another important feature in neovascular AMD to recognize is outer retinal tubulation. This is an area of a clear lesion with this thick wall. Not to be confused with cystoid macular edema. These patients typically do not require treatment. This does not represent active leakage. This is another case. It’s a patient with bilateral geographic atrophy. We can see on this autofluorescence… I’m sorry. On this infrared image. And then we see this outer retinal tubulation, as well as increased signal penetration into the choroid. Incidentally, there’s this nerve fiber layer, which is thickened, in the papillomacular bundle. And finally I want to talk a little bit about scar formation in neovascular AMD. This is a patient with very severe scarring. It looks like I have some questions? Okay. Two questions. Number one: Regarding macular puckers, do you find baseline OCT can be predictive of how well the patient will do following surgical repair? That’s a very good question. And yes. As I alluded to earlier, with very severe macular pucker, patients who have, for example, very greatly distorted foveas, patients with macular schisis — those patients often do not do as well as patients with less severe disease. And another question: Are OCT and OCT-A substitutes for fluorescein angiography? This is an excellent question. I’m not going to go into OCT angiography, because that’s a lecture in its own right. But this is an evolving discussion. And I think it remains to be seen if OCT angiography will substitute fluorescein angiography. Although I’m not going to discuss OCT angiography in detail, I do want to remind everybody that OCT angiography is really just looking at flow, and does not convey leakage. Whereas fluorescein angiography does convey leakage. So that’s a key difference. I’m not sure how that will settle out in the future, in terms of whether OCT-A will substitute for fluorescein angiography. But certainly OCT-A is less invasive and it’s quicker. So I thank you both for those questions. Now back onto scar formation in neovascular AMD. Oh, one more question? What is the difference between a true and pseudocyst? Excellent question. I want to backtrack a little bit and mention that none of these are true cysts, because true cysts are aligned with an epithelium. But for purposes of OCT, we often call them cysts. In any case, a true cyst or true cystoid edema involves active leakage. So there would be serous fluid in that cystoid cavity. Whereas a pseudocyst would involve degenerating retinal elements. And does not convey active leakage. And that was the point behind showing outer retinal tubulations. So that’s a reason that should not be mistaken as a cystoid space, requiring intravitreal anti-VEGF injection, for example. Again, thank you. Excellent questions. So back onto neovascular AMD. This is a patient who has very advanced disciform scarring. It’s the right eye. Optic nerve, central fibrosis, surrounding atrophy and hemorrhage. We can see very severe staining on the fluorescein angiogram. I do not have… There we go. Okay. On the OCT, we have this highly reflective lesion, underlying the retina. This patient would have a very profound loss of vision. So we want to… We would like to prevent scar formation, because this is associated with poor vision. We’d like to identify some of the risk factors. So scar risk factors include classic choroidal neovascularization, thickening of the retina, thick subretinal fluid, and thick subretinal tissue. Here’s an excellent example of scar formation in the classic portion of this choroidal neovascular membrane. Let me stop for a moment, because I believe we have some more questions. What is the difference between a true macular hole and a pseudohole, both clinically and on OCT? That’s an excellent question. A true macular hole involves a full thickness disruption of the fovea. And so since there is easily no fovea centrally, the patient will have a scotoma. A pseudohole involves typically macular pucker or an epiretinal membrane with distortion around the fovea. And gives the appearance of a hole, but is not a full thickness hole. And therefore the patient often has good vision. In many of those cases of a pseudohole, where patients have well preserved vision, and only a mild macular pucker, those patients can be observed. So this is an example of a patient that has both occult and classic choroidal neovascularization. We can see the classic portion as denoted by this black arrow, and the surrounding occult choroidal neovascularization in this right eye. This is the earlier frame of the angiogram, and on the later frame, we have this mild leakage. On OCT, we have this pigment epithelial detachment. And then later, several months later, we have this fibrosis forming in the fovea. And it only formed in the portion of the classic choroidal neovascular membrane, which is quite interesting. The occult portion did not lead to scarring. And we can see that on the OCT. Again, this pigment epithelial detachment, which is now flattened, but we see this area of scarring, again, correlating to the original area of the classic choroidal neovascular membrane. So this is an example of how classic choroidal neovascularization leads to scarring, which is bad, prognostically. And that leads to a very important finding, and that is a subretinal hyperreflective material. And that is shown by this black arrow. We can see this hyperreflective lesion between the retina and the RPE. This often correlates with classic choroidal neovascularization. Here’s another excellent example of a lesion. So this is tissue external to the photoreceptors and internal to the RPE and/or Bruch’s membrane. It’s thought to represent choroidal neovascular components, and correlates with type 1 or classic choroidal neovascularization. As we just mentioned, type 1 or classic choroidal neovascularization correlates with scarring. So therefore subretinal hyperreflective material can correlate with scarring. And that’s been extensively assessed by the CAT trials. Which found that subretinal hyperreflective material was common, that it correlates with a visual acuity. For example, if patients had none at baseline, they had a better result. They had 74 letters, on average, at the end of this trial, versus patients who had SHRM, or subretinal hyperreflective material, which had 10 letters less. Ellipsoid zone loss is associated with foveal subretinal hyperreflective material. And as I mentioned, ellipsoid zone also correlates with visual acuity. And finally, as I mentioned, scar is associated with SHRM. Patients with SHRM, a subretinal hyperreflective material, have a 70% risk of scar, versus patients without SHRM, who only have a 35% risk of scar. And finally, SHRM thickness measurements correlate with vision. The visual acuity is worse with increasing SHRM height and increasing SHRM width. We can see that the height of the SHRM can be measured here. So here’s a very nice OCT. We have this fibrovascular pigment epithelial detachment, with overlying SHRM. And then the retina is draped over this SHRM. We can see some cystoid macular edema. And once again, the SHRM correlates with classic choroidal neovascular membrane. I’m gonna stop there. We have a few more minutes for questions. How can we differentiate between polypoidal choroidal vasculopathy and central serous retinopathy on OCT? That’s an excellent question. Polypoidal choroidal vasculopathy will have — if you’re able to scan through a lesion, you’ll have that inverted U sign that I showed you, whereas central serous retinopathy typically just has subretinal fluid. As I mentioned, there is a free download of a paper we just wrote. It was actually a clinical case series of OCTs. And we go into this in more detail. So that’s available for your reference, which has more detailed explanations than what I can do here live. Another question: A simplified reference to learn OCT? Again, you can download the reference I mentioned on the Cybersight website. And that would be a good starting point. Of course, just looking at lots of OCTs will help. Next question: Is there a specific definition of SHRM? Yes. It’s hyperreflective material between the retina and the RPE. And then a question about hyperreflective material can be seen overlying choroidal melanoma… That I would not be 100% sure about. I would have to research that more. I didn’t really get into neoplasms in this lecture. However, choroidal melanoma can be associated with choroidal neovascularization. So I’m not sure if the SHRM would denote choroidal neovascularization in that situation or not. Any other questions? Well, I thank you very much for your attention. And once again, you can download the case series that we wrote up, which I think will be helpful, in terms of stressing some of the clinical features of the cases we reviewed tonight. Again, thank you for your attention.
June 27, 2017