Spence and the producer of radio's outstanding theater of thrills the master of mystery and adventure William M. Rubison. There is an old definition which describes the theater as a plank on two barrels and a passion Analogously we might describe radio drama as a microphone a voice and a story Tonight we have all three and little else Little else is needed when the voice belongs to an actor of the statue of Herbert Marshall We present him without supporting players without sound effects and no more than the usual musical crimmings His voice is all that's needed to strike terror to your heart So send the more impressionable small children out of the room dim the lights settle back and listen as Mr. Marshall stars in A. M. Burridge's chilling story the wax work Which begins in just a moment Here's Frankie Lane. I never feel like singing with a bad cold So I take wonderful four-way cold tablets to relieve my cold misery fast right Tests of four leading cold tablets proved four way fastest acting of all Amazing four-way starts in minutes to relieve aches pains headache reduce fever calm upset stomach also Overcomes irregularity. So when you catch cold take my advice take four-way cold tablets It's the fast way to relieve those nasty cold miseries and feel better quickly four-way 29 and 59 cents Here's a word about another fine product of Grove Laboratories to get rid of embarrassing dandruff in three minutes change to Fitch dandruff Remover shampoo three minutes with Fitch regularly is guaranteed to keep unsightly dandruff away forever Apply Fitch before wetting hair rub in one minute add water lather one minute then rinse one minute Every trace of dandruff goes down the drain three minutes with Fitch and embarrassing dandruff's gone At the same time Fitch can brighten hair up to 35 percent get Fitch dandruff remover shampoo today and now The wax work starring mr. Herbert Marshall a tale well calculated to keep you in Suspense uniform attendance of Melanie's wax works were ushering the last travelers through the exit The manager sat in his office interviewing Raymond Houston a young journalist Somewhat down in his luck The manager was speaking It used to be said years ago But madam two sewers would give a man a hundred pounds for sleeping alone in the chamber of horrors I hope you don't think that we have made any such often as to use and By the way, what is your paper? I'm Freelancing at present forever. I should find no difficulty in getting the story printed the morning echo would use it like a shot a night with Maddeners murderers Very well, Mr. Houston That was warn you it's no small ordeal that you're proposing to undertake. I Oh, and I shouldn't care to take it on I Should hate having to spend the night alone and the murderers then Why well Those wax works represent the lowest and most appalling types of humanity There are a lot of spheres and places on prison and if you are susceptible to atmosphere I warn you that you are in for a very uncomfortable night Houston had known that from the moment the idea had first occurred to him He's so sick and at the prospect But here was a chance not to be missed The price of a special story in the morning echo Besides if he wrote the story well, it might lead to an offer of regular employment The manager smiled and rose Well, I think the rest of the people must have gone by now. Oh One condition I'm afraid I must impose on you. I must ask you not to smoke We had a fire scared on there this evening. I don't know who gave the alarm, but whoever it was was a false one Fortunately, there were very few people down there at the time or there might have been a panic And now if you're ready I'll take you down to the murderers den in a moment. We continue with the second act of Here comes Elmer Blurt world's lowest pressure salesman Nobody home.  Would you doc?  Yeah, but That's right, you know, you don't have to sell me on the 59 rambler first in economy first in sales gains And no wonder rambler has the best of both big car room small car economy.  You don't remember it's got quite an idea with that personalized comfort independently adjustable front seats adjustable headrests easiest parking and handling in America On that 59 rambler is so terrific. It makes you want to put your foot right down on the accelerator Oh That didn't hurt did it oh gosh well occur. No, that's my lower plate. You've been drilling Rambler continues to pass car after car and sales in state after state Rambler now outsells all but two other makes come see why dry of the success car at your rambler dealers and now Starring mr. Herbert Marshall act to love the wax work in in Mariner's wax works was an area an uncomfortable chamber The chamber whose atmosphere invited its visitors to speak and whispers The wax work murderers stood on low pedestals recent notoriety rubbed justice shoulders with the old favorites Sertel the murderer of we're stood as a frozen in the act of making a shop window gesture to young bywaters There was the floor the poor half-baked little snob who killed for games so that he might hate the gentleman Within a few yards with him set mrs. Thompson that heretic romanticist and to appreciate British middle-class making hood Charles peace the only member of the vile company Sneered across The manager pointed out several more interesting of these unholy notabilities That's um, that's Crippen.  Have a good look at him. This is our star He's the only one of the bunch that hasn't been hanged The figure which Houston indicated was out of a small slight man not much more than five feet in height It wore little wax from stashes large spectacles and an opera cake There was something so exaggeratedly French in its appearance that it reminded Houston of a stage caricature He could not have said precisely why the mile-looking face seemed to him so repellent Who is he? That said the manager is doctor word that Houston shook his head darkfully. I I think I've heard the name, but I forget in connection with what No, you would remember better if you were a Frenchman a little while back that man was the terror of Paris He carries on his work of healing by day and no fruit cutting by night He killed for the sheer devilish pleasure it gave him to kill And always in the same way With the razor But at last he left the clue behind him which set the police upon his track But he was too clever for them when he realized that the coils were closing about him. He mysteriously disappeared And ever since the police of every civilized country been looking for him However, there's no doubt that he managed to do away with himself and by some means which has prevented his body coming to light. I I Don't like him at all. What eyes he's got Yes, this figures a little masterpiece You find the eyes bite into you Well, that's excellent realism then for bird death practiced mesmerism and was supposed to hypnotize his victims before dispatching them Indeed had he not done so it is impossible to see how some smaller man could have accomplished his ghastly work There were never any signs of a struggle. I thought I saw him move You will have more than one optical illusion before the night's out. I expect sir I'm sorry. I can't give you any more light, but all the lights are already on For obvious reasons we keep this place as do me as possible Well Good night, Mr. Houston the manager had provided an arm chair for Houston who immediately turned it so this back Was towards the effort here of dr. Waddett For some undefined reason he liked dr. Waddett a great deal less than his companions The dim unwavering light filled in the rows of figures Which was so uncannily like human beings of the silence and the stillness seen unnatural and even ghastly He missed the sound of breathing the rustling clothes The hundred and one minute noises one hears when even the deepest silence has fallen upon a crowd And the air was as stagnant as water at the bottom of the standing pond Must be like this at the bottom of the sea he thought He faced the sinister figures boldly enough They were only wax works So long as he let that thought dominate all others. He promised himself that all would be well It did not however save him long from the discomfort occasion by the wax and stare of dr. Waddett Which he knew was directed upon him from behind The eyes of the little Frenchman's effigy haunted and tormented him and he etched for the desire to turn and look At last the compulsion was too great and he threw his chair around And look behind him The image of the dreadful little doctor seemed to stand out with a queer prominence He was fringed before the parody of mildness But some fiendishly skilled craftsman had managed to convey in wax met the eyes for an agonized second and Turned again to face the other direction He is only a wax work like the rest of you. You are all only wax works They were only wax works. Yes, but wax works don't move Not that he had seen the least movement anywhere, but it struck him that in the moment or two when he had looked behind him there Had been the least subtle change in the grouping of the figures in front Crippin for instance seemed to have turned a degree to the left All thought you some perhaps the illusion was due to the fact that he had not returned his chair to his exact original position He had never seen nor heard a movement But it was as if some sixth sense had made him aware of one He looked straight into the vapid countenance of LeFloy which smiled vacantly back as if to say it wasn't I Of course, it wasn't he or any of them It was his own nerves or was it He swung around quickly To encounter the mild but belches Then without warning he jerked his head back to stare straight at Crippin He nearly caught Crippin that time You'd better be careful Crippin and all the rest of you. I do see one of you move. I'll smash you to pieces. Do you hear? This would not do This distinctly would not do These figures grouped around him were only dummies made of wax and so does They stood there for the entertainment of morbid sightseers and orange-sucking trippers It was no good He knew the effigy of Dr. Woodette was staring at him He could feel the two places where the gaze of those piercing eyes pressed into his back He turned halfway And tried to steal the glance at the figure But instead he felt himself world around to face those dreadful hypnotic eyes You moved Yes, you did. You moved. I saw you you moved Then he sat quite still Staring straight before him like a man found frozen in the arctic snarls Dr. Woodette's movements were leisurely He stepped off the pedestal of the missing girl of a lady alighting from the bus and Then quietly sat down on the edge facing him Once where I miss you Something tells me that you are nervous My dear sir have no illusions I'm not one of these contemptible effigies miraculously come to life. I Am In a moment we continue with the third act of With no danger of acid rebound sometimes caused by harsh alkalizers always carry tums 10 cents Three roll pack a quarter new tums six roll pack with free metal carrier 49 cents and now Starring mr. Herbert Marshall staring at the mile little murder You could see He could not move a muscle And he could not tear his eyes away from dr. Woodette's hypnotic eyes The doctor continued in his easy manner the circumstances have made it desirable that I should live in England I Was close to this building this evening when I saw a policeman regarding me Little too curiously I Guess that he intended to follow and perhaps ask me embarrassing questions So I mingle with the crowd and came in here a Coin bought my admission to the chamber in which we now meet and an inspiration showed me a certain means of escape I Raised a cry of fire and when all the fools had rushed to the stairs I stripped my effigy of the cape which you behold me wary Donned it hid my effigy under the platform at the back and took its place on the pedestal The manager's description of me which I had the embarrassment of being compelled to over here Was biased but not Altogether inaccurate Clearly I am not dead although it is as well that the world think I am His account of my hobby which I have indulged for years Although through necessity less frequently of late was in the main true For you see the world is divided between collectors and non-collectors Was a non-collectors we are not concerned the collectors Collect anything according to their individual tastes from money to cigarette cars from Mouths to matchboxes Collect fruits pause again and regarded Houston search with interest mingled with disfavor Appraised to the chance which brought us together tonight, and perhaps it would seem ungrateful to complain From motives of personal safety my activities have been somewhat curtailed of late And I'm glad of this opportunity of gratifying my somewhat unusual whim But you have a skinny nexa If you will overlook a personal remark I should never have selected you from choice. I like men with thick necks Sick red necks fumble in an inside pocket and took out something which he tested against the wet forefinger And then proceeded to pass gently to and fro across the palm of his left hand This is a little French razor The blade you observe is very narrow They do not cut very deep But deep enough in just one little moment you will see for yourself I shall ask you the little civil question of all two light barbers Does the razor suit you sir? He rose up at a minute of but menacing figure of evil And approached Houston with a silent fertile step of a hunting panther You will have the goodness to raise your chin a little Thank you And a little more just a little more. I think merci Merci monsieur Merci Merci Chamber was a thick skylight of frosted glass which by day lit in a fume sickly and filtered rays from the floor above After sunrise these began to mingle with a subdued light from the electric bulbs And this mingles illumination added a certain gas thinness to a scene which needed no additional touch of horror The waxwork figures stood epithetically in their places Waiting to be admired or executed by the crowds who were presently wonder Fearfully among them in their midst Houston sat still Leading far back in his frivol chair His chin was up tilted as if it were waiting to receive attention from a barber And although there was not a scratch upon his throats nor anywhere upon his body He still watched the dead man unenotment He did not move Nor was he capable of motion But then after all He was only a waxwork starred in William and Robeson's production of the waxwork Written by A. M. Burridge and adapted for radio by meldinelli In a moment a word about next week's story of suspense Do you have trouble getting your husband to talk frankly about the intimate and important things in your married life? All too often a husband's reluctance to talk about sex money or the children can destroy a happy marriage Be sure to read one woman's real life solution to this problem in the new march issue of mccall's magazine Now at your favorite newsstand in all you'll find more than 40 exciting features in this big new issue of mccalls Read 15 practical down-to-earth ideas on how you can earn an extra thousand dollars this year by doing just a few hours work each week Learn debbie reynolds side of the strange divorce story that wrecked hollywood's ideal marriage And see many full color photos previewing the newest styles and hairdos that women will be wearing this spring Don't miss the fascinating march issue of mccalls with more than 40 exciting features for you and your family Buy the new march mccalls at all new stands now Listen Listen again next week when we return with myron mccormick in madman of manhattan Another tale well calculated to keep you in Suspense News follows then have gun will travel on the cbs radio network


Please subscribe to this YouTube channel mentor talk and do press bell button for notifications. Well, this is about times of today where technology and virtual events have become an essence or I would even say a compulsive choice. I'm talking about webinars and individual recorded talks, lectures and discourses, post COVID or lockdown times, let's say. For a webinar or video talk, you need to follow the following guidelines. I will be talking in a very concise manner in this final lecture, more like bullet points because this is more about technical specifications. First, sit straight with body, not curving, tilting, bending or turning. In video, it looks very clumsy and distracts the viewer if the talker or speaker is constantly shaking his body or moving his body, let's say. But you can certainly move your arms and hands in sync with your script as this is part of body language. Second, there should be no background noise. Not even fan or aircon noise should be there when you are speaking. Microphones are tuned to catch background noise more prominently, I have noticed. This is why there are noise cancellation features in most recording devices. The background noise suppresses the primary voice of the speaker. So be mindful of that. Point three, room where you are seated should have no echo. So therefore look to record your talk in a room which is properly stuffed with wooden furniture or books etc. as they are natural sound balances and absorbers. It gives a good supporting acoustic atmosphere. Find a lot of wood, wooden furniture in a room where you are intending to speak from. Fourth point, use a background behind you which is contrast to your attire and costume. Use a library background, some art oriented background or absolutely plain white wall that can also do. Point five, video should cover just upper part of your body meaning starting from little below the chest. You do not have to be visible from waist and up. You have to be visible from somewhere from here as I am visible. Point six, if possible use a collar mic like I am using or otherwise use a camera, laptop or a mobile phone inbuilt mic that will also do provided you are speaking a little louder. You have to speak louder than in case of inbuilt mics. I will prefer you to use mobile phone as a recording device using the inside screen face camera. Keep it closer so that audio visual is of good quality. Point seven, the video settings should be horizontal, not vertical as is in Instagram TV. You have to have use horizontal settings. Point eight, do not take long pauses while you are talking because there is paucity of duration available for video. Point nine, video talk of yours should be less than three minutes, preferably I would say two minutes, 20 seconds or 30 seconds at the most. Two minutes, 20 seconds or two minutes, 30 seconds, definitely less than three minutes. Point 10, your talking script should be in the range of 200 to 220 words then you will be able to timeline your duration well. So your script should be 200 to 220 words. Point 11, you may see the sample videos on the mentor talk YouTube channel. Point 12, mentor talk is a YouTube channel. It is an initiative of the law and public policy think tank Goman bind HTO, in short GBHTO. Next point, I think it's point 13, mentor talk videos focus on topics related to law, public policy and any social or social economic issues. So you can choose to speak on any of these issues and subjects. Point 14, the content of videos should not be political and should should only contain objective views of yours opinions and analysis. Point 15, the videos are widely shared at all social media platforms, you know, YouTube, Facebook, Twitter, blogger, Tumblr, Mix, LinkedIn and many more mediums. I don't remember all of these. So thank you and hope you found the series of four lectures on successful public speaking useful. Look forward to having your video contributions as well. Stay safe and thank you. Mentor talk and do press bell button for notifications.


It looks really like paradise here.  It's a different world here. Hi, I'm Lavi and this is Oli. We are attempting a new Guinness World Record to become the youngest pair to circumnavigate the globe by motorcycle. After riding 3,000 miles across Europe, we are now ready to explore the roads of North Africa. Click the subscribe button to follow our journey around the world and let the adventure begin. Day number 73 on our round the world trip. So we're here at a camping place in the town of Boushdor, camping right next to the ocean. We can hear it on the other side of this wall just behind us. We had a really nice sleep here because we had the nice sea breeze coming through our tent because we slept without the cover tonight and that was really, really nice and refreshing. We had like our sleeping bags to cuddle up with. That was really cool. So let me show you guys where we're headed today. Okay, so we are here in Boushdor and we are going to be continuing our way south on the Rud National One and we will go as far as we can go towards Dakhla. So the first place that we're going to be checking out is going to be a wild camper on the beach and that's about halfway from here to Dakhla. So we'll see how the place is and we'll see how we're feeling there. Otherwise, we can push on further and try and make our way even closer to Dakhla. So we'll see how we get on. So it's 112 miles to the first camp we will check out. It's already 11.30, so better hit the road. Let's go. Ready to hit the road. Yes, ready. Let's go. Time for lunch soon, hey? Look, there's the ocean front just over there. On our way. So we just left Boushdor. We just filled up on fuel. We bought some bread, we got some water. We got a couple of red bulls for the road and now we are back out into the desert road. Yeah, and it's a really pleasant day. It looks like that the sky opened up a little bit. It looks a little bit lighter than yesterday, not so dusty. The ocean is right next to us with a beautiful color. It's very nice, like this turkeys blue is so cool. Yeah, hopefully it's going to be less of a crazy ride like than yesterday. Yeah, let's pray for less wind. Yeah, because it can be pretty unforgiving here on the coast. Yeah. Oh, look. Ah. First you have the police control out of town and now you've got the camel control. Do you have your passport ready? Yeah, passports, Duane vehicle documents. There you go guys. Hi guys, it's okay? It's okay. Let us pass. Thank you guys. Okay, see you later. Yeah, merci, bon voyage. I think I heard one of them saying bon voyage. Bon voyage. Sometimes the signs are pretty accurate. So we stopped for a little lunch break. I just keep my helmet on actually because it's so windy. I would just take it off quickly to eat, but otherwise. So we try to hide here a little bit behind Bumblebee. Oh no, I just dropped all the cream cheese. We've got my cinnamon bread and I love this bread. Look, look, look. Yes. So we've got that. We've got our red balls. It's a beautiful lunch hiding behind the bike. It's beautiful. Bon appetit. All right, our Missummon cheese lunch is over and now it's time to make our way back to the main road, but I can't remember which way I went. So I'm just gonna go this way. Let's see which way to go.  Which way was it? This way. Yeah, I think to the left here. But yeah, I can tell you it is windy as hell. So it's not very easy to stop on the side of the road.  Yeah, a hand in the face. All right, around here. There we go. The highway of dreams. Nice. There we go. Smooth as hell. Yeah, very nice and smooth. So it's 230 at the moment, 26 degrees. And we have 55 miles left to the beach camp where we try to pitch our tent. But anyway, we have to go there, check it out. Maybe it's as windy and yeah, we have to see. Yeah, yeah. So I'm gonna get up to 60 miles an hour and then set up my cruise control. There we go. 60. And that's it. Yesterday I was sort of going faster, slower, faster, slower today. We decided let's just set it at 60 the whole time and just take it nice and easy, cruising down the highway. Oh, there's some camels. There's some more camels. Oh, nice. All right, cruising for the next hour. Let's go turn right here. Go down to the camp road as well. I hope it won't be that windy down there. Oh my God, we're kind of going right into the wind now. Yes. Whereas on the highway it was kind of going with us. Now we're just being smashed by it and you can really feel how strong the wind is. Oh my God. But the landscape here is super nice though. Yeah, it looks spectacular, yeah. So much more going on around. Yeah. So it looks like this road is kind of heading down to the coast here and just about see the ocean. Oh yes, that's nice. Nice, look, yeah, we're not going to be up on the cliff. It looks like we're heading down to the ocean. Wow, look at that. Yeah, that's a nice spot. There's a nice area here. Oh, look at these crumbling cliffs as well. Yes. Whoa. Right down to the beach. Wow. That's cool. That is cool. According to the GPS, the camping should be just up ahead. OK, let's maybe just ask. Look at this boat. So pretty much this road just goes down to the beach and then stops. Yes, yes. Whoa, nice. Salam. Salam. Wow, that's really cool. Hello. OK, we're going to go back to the Gendarmerie post just up ahead and we're going to ask them if it's all right to camp somewhere around here. OK, so that plan did not work out very well. Pretty much asked at the Gendarmerie post and he told us camping in the military zone. So yeah, they really went into us staying there and just told us no. And they said, we said, OK, what about any place south? And they said, oh, Dakhla. So basically they said, go to Dakhla. Seems to be the only option they've given us. So I've rooted to a place, a camping in Dakhla, but it's 107 miles. There's 107 miles to get over there to Dakhla. But that was a really beautiful bay at least, at least to come and stop and have a look. Yes. Anyway, we're going to go back to the Root Nacional 1 and keep driving south, I guess. OK, so we just turned off the Root Nacional and we are just about to start heading down the spit towards Dakhla. Looking on the map, it looks like this road is heading across to the spit and then it's about 20 miles down to Dakhla. But it looks like such a thin bit of land that's coming out. It looks super interesting on the map, so I can't wait to see it. It's now nearly 7 o'clock, so we started quite late because we weren't actually expecting to do a crazy long day. Oh, look at this. This is interesting. Yeah. Whoa.  That looks really cool. Yeah. But I am pretty tired now, especially after the long day yesterday and then didn't expect to do such a long day today. But we've ended up doing well. We're just coming up to 200 miles for the day. But it's all right. We're getting to the end now. But I think we're going to sleep pretty good tonight. Oh, sand on the road. Yeah, I've got some dunes encroaching. Whoa, look at this in front. Wow. That's crazy.  Yeah, it's absolutely crazy windy here. Yeah, it's always when we're heading west that we get this massive crosswind. Yeah. Well, we have hit the Dachler Spit. And you can see that this is the start of the inland bit of the sea. And this actually stretches for another 16 miles down here. And basically, I don't know if you can see on the map here, but we're on this little bit of land which is sticking all the way out for 16 miles. Yeah, but it looks so cool because this is like the kites of paradise here. Here are probably like about 20 kites out there. Wow. Everyone is having fun. Yeah, it looks really cool. It looks like a really cool place for kite surfing. Yeah, yeah, because they've got all the wind coming up and over. Yes, yes. And I think it's very flat as well. So it's perfect for learning, training. Yeah, wow, that's cool. It looks really like paradise here. Yeah, it's like we were in the middle of the desert. And then suddenly we come up and over around the corner.  People walking on the beach. People just, yeah, it's a different world here. Pretty cool. Yeah, it looks like there's a police control at the start of the spit. So we'll just turn the cameras off for a second. All is well with the police control. Just gave them our temporary import permit, passports. No worries on your way. So we're now heading further down into the spit. And we've got seven and a half miles until we reach the place that we're going to try and free camp. But this road heading down the spit is super busy. There's a lot of people trying to get down to Dakhla. I can tell you that. Yeah, I think it's a very popular place here. Yeah, definitely. Very busy and popular place.   Yeah. Yeah, this is the hotspot right here. Yeah. OK, we've come off the main road now. And we're heading down to the area where we're supposed to be camping or going to try and camp. It's like one mile down this little road. But there's a lot of development going on. This place was added quite a few years ago. So for all we know, it might be that people have developed the area by now. It looks like here in Dakhla, there's a lot of development going on. They're really trying to push this tourism thing. A lot of apartments and hotels and all kinds of stuff coming up.  Yeah, it's super crazy. Oh, look, yeah, totally blocked off. It looks like they're trying to build something along the seafront here or maybe down there. I mean, look at the place. It's a giant construction site. Yeah. I think that whatever was here before is not here anymore. OK, so the free camp looks like it's all under development that area. And I really don't think we'll be able to free camp there. So we've seen on Ioverland that there's another place, which is a paid camp. And it should be just up ahead. So we'll carry on to there. And then we'll go and check that place out, see if that's all right. Let's ask these guys. Yeah. OK. Salam. Salam. It's the camping here, Tarvata. Wait. Yep. OK, so run, so run. OK, so where this wall is. I think so. OK, let's check it out. Where's the entrance? I don't know. Maybe on this side? Oh, yeah, look, booty camping. Tarvata camping. OK. Tarvata camping. OK. See. Yeah, let's go and ask. OK, so. I'm going to go and get the passports. OK, OK, merci. So this one is 10 euro for the night. And they're just going to show us where to go now. Ah. Just going to give the passport, do the business. Looks like it's also a ranch. Whee. Right, OK, merci. Thank you. Chokran, thank you. Thank you very much. There we go. It's the place. Well. I love free camps, but I don't want to ride around any more. I think it's time for us to set up and get chilled. Yeah, I mean, it's quarter past 8 already. So I think it's time for it to finish. Let's set up camp. Good evening, guys. We made it, happy and alive. Just before dark as well, time kept going on and on. And we were looking around for a place. We were looking around for a wild camp. So it's 100 dirham for tonight. And just to pitch up the tent. Everything's pitched up here, as you can see. Yeah. Bumblebee, the tent. There's some horses over there. Yeah. Which is quite cool. So that's all right in the end. We didn't have much of a choice of where we could stay. We looked around. There's not much possibilities. So, you know, 10 euro a night it is for the tent. It's OK. It's OK. Yes. So we did about 211 miles, which is 340 kilometers. A very, very long day. Yeah, apart from yesterday, that was the longest day that we've done. So that's like two incredibly long days in a row. Wow. It's a lot of road. It's a lot of road. It's a lot of wind. And it's a lot of sand. But it's a lot of nice road as well. So that's it from us today. We hope you enjoyed the episode. If so, please give us a thumbs up. Subscribe to the channel. Share the video with your friends and family. Please, please, please. Comment below. We will see you next time.


which unfortunately happens to be the longest lecture of the whole series. So I'm gonna talk a lot about that today and I believe next week is orbit. And then it kind of starts going on to the center, so please look ahead at time and know what's to be expected. So the other tradition is, is you get the pleasure of seeing my travel slides. And historically what I've done is I've shown you slides from the previous ESCRS meeting, but because of the COVID and the fact that the ESCRS was a week before the AAO, I haven't been for three years. And so this is where ESCRS was this year. This is Milano. And unfortunately this was a decade ago. So this is the Duomo, the cathedral in the main square in Milano, inside of the cathedral. What's interesting is there are murals on the wall on both sides. Let's see if we've got, do we have our little player thing? Let's see if we've got our little player thing. Okay, so murals on both sides. Unfortunately the, people hasn't been spiffed up in a while, so it's really kind of hard to see them. But classic stained glass, vaulted ceilings.  So we're gonna, this is one of the popes. Popes is buried here in Duomo in Milano. Okay, we're gonna talk about the retina. Now, when you talk about the retina, we wanna get a few definitions in there. And so from the pathologist, the definition of the macula is what? Startin' to swing around, more than one layer of ganglion. Exactly, so the pathologist's definition of the macula is more than one ganglion cell layer. But that pretty much matches up the retina doctor's definition of the macula, which is the area pretty much temporal to the disc within the arcades. And so when we look at the retina, the retina has, I can't say anything right, I'm just pointing. So, what do retinas and ogres and onions have in common? Layers. Layers. All right, so we're gonna start with the layers. And so, as a pathologist, I look at the retina this way. When you have the anatomists and the research guys do it, they do it upside down. So, you have to kind of turn your head when we do the lecture. So, these are the layers. This is the vitreous on top. This is the core rate of the bottom. So, we're gonna start going through the layers. So, this is the vitreous. What layer is this? Isle. Internal limiting membrane. Next layer. Inner fiber layer. Inner fiber layer. Next, I can't see a thing here. Next layer. Ganglion cell layer. Ganglion cell layer. Next, inner plexiform. Inner plexiform. Next. Next. Outer plexiform. Outer plexiform. Next. Outer plexiform. Outer nuclear. Okay, and these are our receptors, and this is our PE. What is this? Coriocampillaris. Then we've got medium and large vessels of the coroid. All right, so we're gonna start again at the top. Internal limiting membrane. What forms that? Hopefully, it's a new result. It's not really a membrane. It's the foot plates of the muller cells, okay? And then, what I wanna do, you know what? Let's do a little bit differently. Let's trace a photon of light. It's a little bit easier to kind of understand the anatomy if you understand what cells do what. So, photon of light goes through the vitreous all the way through the retina. It hits the outer segments of the photoreceptors. It hyperpolarizes the membrane and switches the retinol, switches from Cystitrans, and you start to get a signal, and it goes from these photoreceptors to this cell body right there. What cell body is that? Exactly, and it lives where? The outer nuclear layer. All right, so then that signal goes through the axons of this photoreceptor cell body, and it synapses with what cell right here? Bipolar cell. Bipolar cell. All right, and the bipolar cell lives in the... Internuclear layer. Internuclear layer. All right, so then that goes out the axon of the bipolar cell, and it synapses right here with what cell? Ganglion cell. Ganglion cell, all right? And that ganglion cell lives in the... Ganglion cell. Ganglion cell layer, good. And then the axon of the ganglion cell layer goes out. Alarna fell to the LGM. All right, and where does it pass through to get there? Alarna fell. Yep. So trace that axon from that ganglion cell to where it synapses again. Okay, but where does it go to get there? There, this far apart. All right, so it goes out through the optic nerve, all the way out through the chiasm, then all the way back and finally at the lateral geniculate body, it synapses. So that's an incredibly long axon. And what it does is it allows any place along that long tube that axon to be disrupted to eventually lead to atrophy of that ganglion. So it's a very, very long one. All right, now, there is a layer in here, the inner nuclear layer, which is a very busy layer. So we already said there are bipolar cells in there. What other cells live there? Let's name one. Emercant cell, another one. Sorry? Horizontal cells. And the last one? Neural cells. Neural cells, all right. So, emercant and horizontal cells are the first line of processing of an image in the retina. And so those think about them, they're like octopuses. They send their tentacles out and they're horizontally oriented. And so they already start to touch multiple other cells and they already start processing going on. So there's already visual processing going on right there. And then the Mueller cell, we already said it sends its little fibers all the way to the internal limiting membrane. So the Mueller cell is kind of the scavenger support cell, if you will, and it pretty much goes almost the whole width of the retina. Okay, so everybody comfortable with the layers? All right, where are we now? What part of the retina are we in now? Exactly, so you look at the ganglion cell there, ganglion cell layer is multiple cell layers thicker, so we know we're in the macula. Now, when we look at the center of the macula, what is this area called? The phobia, and so if you think about it, that's the part of the eye that gives you your fine vision and you don't want to have those light waves coming all the way through all those layers of the retina. So the way the retina is designed to avoid that is you see it thins out markedly here in the center of the phobia so that that light reflects, that light ray, I mean, come all the way in, get those photoreceptors here. Now, the center of the phobia is very, very cone rich and because you want fine vision, one cone links up with one horizontal cell which links up with one ganglion cell. So because of that, there's a lot of ganglion cells there so they get stacked up on the side there so these fibers as they come out start to run, not vertically, but start to run obliquely to link with those. Now it's different in the peripheral retina. The peripheral retina's purpose is to give you side vision and to give you movement and other things and so in the periphery of the retina, up to a hundred rods may be linked up to a single ganglion cell. What does that do? That gives you summation. So if you've ever been out on a dark night and you see, boy, there's a little straight line way over here and then you look at it, it disappears because the rods all gather that up and do that and so that's important evolutionary wise because if there's a sabertooth tiger sneaking up on you to eat you, you wanna be able to see that and so that's what the periphery does but in the center, you wanna be able to see your fine detail and that's why they're all stacked up there. So if you look right here, you see the fibers here in this layer run almost obliquely. What do we call that layer? Henle's layer, so Henle's layer runs obliquely. Why is that layer important in the area right next to the center of the phobia? Exactly, so that's where edema, cystoid macular edema starts up. All right, so let's talk a little bit about diseases that can affect the retina. So what do we see in here in this, from this photo? What do you think could cause this? Believe it or not, even diabetes can cause pictures like this, so believe it or not, this was a patient who came in and we looked at it and we did all that differential diagnosis and then interestingly enough, the student with me at that time said, what's the blood pressure? And we went, gee, I don't know. We searched the entire clinic, eventually we found one of those things that goes on your arm that measures blood pressure and we did it and this patient was 200 over 100, literally. So went right to the ER, this is severe hypertensive retinopathy. Now, sometimes it'll look a little bit different and good evening, all right, good timing. So, what do we see in right here? And you see, they call this a star shape, starfish shape and so that really kind of tracks along Henley's layers, so you get kind of that star shape looking to it and so this is again a severe hypertensive retinopathy. If you look carefully, you see that that disc, instead of looking that kind of yellowish light pink it's more red and so the vessels on that disc are more dilated and in severe hypertensive retinopathy, you can even get papillodema and severe disc changes. So if you look right here, again, this is a patient with severe hypertensive retinopathy and you can see in addition to the hemorrhages, you can also see exudates here and you see edema of the optic nerve and it's a severe hypertensive retinopathy. All right, what are we seeing right here? So what causes this? All right, so what gives us the cherry red spot? Why don't we see that? That's from the... Sure, I find some. Exactly. So it's kind of like a window showing you when you have a central retinal artery occlusion that coroidal blood flow is still intact. So in the center of the fovea where the retina is really thinned out in that area, you can still see normal coroidal blood flow showing through yet the rest of the retina is ischemic. It's white, it's pale. This is a central retinal artery occlusion. So what are we seeing right here? Exactly. So this is where not the central retinal artery but one of the main four branches of the central retinal artery has been included. Now, when we look at occlusion of a central retinal artery or just arterial occlusion in general, traumatic or embolic? Usually embolic. Usually embolic. And so when you see either central retinal artery occlusion or a branch artery occlusion, you really need to work up the patient carefully for a source of that. That could be a blood clot. It could be cholesterol plaque. It could be coming from the carotids. It could become from the aortic arch. It could be even coming from the heart itself or one of the valves in the heart. So very important that you work this up because if clots are going to the eye, they could be going to the brain and elsewhere. All right. What are we looking at right here? What is this? This is the central retinal artery. So what's going on with this central retinal artery? So way too many crown burgers and moochies here. So this is a good old American diet. You can see a ton of cholesterol, lipid. Look at that artery. It is markedly narrowed.  So this is where the central retinal artery and the central retinal vein come into the retina together in the optic nerve head. So the other thing I want you to see as you can see this very arteriosclerotic artery shares a common adventitial sheath with that vein. And so arteriosclerosis is the most common cause of central retinal artery occlusion. Also arteriosclerosis is the most common cause of central retinal vein occlusion because that artery kind of pushes on the vein next to the complete stasis of the vein occlusion. And what are we looking at right here? Looks like it's just swollen in a retina. Okay, care to rephrase. So it looks like the R-N-F-L is very swollen and retinal layers are kind of hard to differentiate. So I wouldn't use the word swollen. I would use the word absent. And so what you're seeing right here is you're not so much seeing swelling here. But look, that ganglion cell layer is pretty much gone. And you look at that big inner nuclear layer, all that's left is just the outer third of it. And so this shows nicely where the blood supply of the retina comes from. The outer retina gets its blood supply from the coroid, the outer third. So the outer nuclear layer and just part of the inner nuclear layer, they get their blood supply from the coroid. They're still intact. The inner two-thirds of the retina gets its blood supply from the central retinal artery. It's totally wiped out. And so in this part, I wouldn't use swollen. I would use absent. And so you're just looking at retina that's been wiped out the inner two-thirds from the central retinal artery occlusion. Question? Yes? Is there an exact layer where you can say the one-third starts with the two-thirds here? Not really. It's just it's a rough estimate because it's different in each person. But roughly you can say that about the outer third of the inner nuclear layer is from the coroid and the inner two-thirds is from the central retinal artery. Was it really? Yeah. Well, I'm glad. I think it's the outer nuclear layer is like the watershed layer. Yeah. So that's interesting how they do that on OCAPs because I find that OCAPs, they literally want to separate wheat from chaff. And so there's lots of chaff and not much wheat in people taking that exam. So they can ask some really obscure questions. All right, what are we seeing here? So I love that term blood and thunder. I don't know what that means, but I don't know what thunder means. There's a lot of blood. So blood and thunder, if you look, all four quadrants are affected. You see that the venials are really dilated here. There's blood everywhere. So central retinal vein inclusion. And again, we said that's caused by arteriosclerosis, causing stasis in that vein. So central vein inclusion. Central vein inclusion is thrombotic, not embolic. Now, what is this right here? I think it's a similar case, but you know what I'm saying. All right, so this is a branch retinal vein inclusion. And you can see a few little cotton wool spots on here. Now, where do those usually occur, those branch retinal vein inclusions? Exactly. So when you've got an arteriosclerotic arterial, and the vein crosses over at that thick, again, arteriosclerotic arterial presses on that vein, gives you stasis. And so oftentimes when you see these branch retinal vein inclusions, it's at a crossing point where the vein crosses over the arterial. And this is an eye cut in half, sagittally. And you can see hemorrhages from the optic nerve all the way to the aurocerot, all four quadrants, in central retinal vein inclusion. And now you can see, this is blood everywhere, and ischemic damage, because you do get ischemia, you get background damage to the retina diffusely from the central retinal vein inclusion. All right, what are we seeing here? So some of the things you can see are a lot of exotides, I'm not going to say this in some sense, and varying types of hemorrhages. There's several flame hemorrhages. So what's the difference? No, that was good.  What gives you dot hemorrhages? So much of hemorrhages. And then deeper, maybe like the dot hemorrhage. Okay, so if you think about it, remember that nerve fiber layer, it comes out and then it runs parallel to the surface of the retina. So if you get superficial hemorrhages, they spread out along that surface. And so we call these flame hemorrhages. Whereas if you get deeper hemorrhages, they tend to be more localized, and those will be the dot lot hemorrhages. And you know, we've got lots of exudates. What is this right here? Cotton wool spot. Cotton wool spot, all right? Let's keep going. What causes a cotton wool spot? Ischemia, I mean, it can be in fission, but certainly localized ischemia. But again, it's of the RNFL. So if you look at this, the reason people call them cotton wool spots, they look like little pieces of cotton kind of on the surface of the retina instead of deep inside the retina. All right, so we're looking at a special preparation of the vessels, the capillaries in the retina. What do we look at at right here? All right, so these little micro aneurysms, these are the first sign of diabetic damage to the retina. So the parasites tend to drop out. So when you get ischemia from diabetic retinopathy, the parasites are the first ones to drop out. And then the little capillary wall weakens and you get these little micro aneurysms starting to pooch out. And then you get leakage of blood and you also get exudate. And so this is exudate in the macula. Now this exudate tends to be very lipid rich. It tends to have a lot of yellow in it. And so you can see a lot of lipid here in the macula from the leakage. And this is what it looks like when you look at a pethanol. This is exudate right here. And so it's lipid rich, it's protein rich. It's just serum basically leaking out. Eventually a lot of the serum gets reabsorbed but a lot of the lipid leaves get left over. So this is hard exudate here in the retina, especially in the macula. Now what do we look at at right here? Some of your seven cotton spots. Exactly, so we're seeing lots of cotton oil spots. Again, they look very superficial. They look like fluffy pieces of cotton on the surface of the retina. And then we look at them and what are we seeing right here? Exactly, so this is caused by a focal ischemic, eventually infarct in the nerve fiber layer, the ganglion cell layer, the superficial retina. So you see this very, very swollen area. And if you look at this at higher power, these are ganglion cells here and they are very swollen from the ischemia.  But if you were to track that, do a multifocal ERG, you could actually find areas where they've dropped out. So you can see swelling from the ischemia acutely and then eventually that goes down. So cotton oil spots, focal ischemia. What are we seeing right here? Exactly, so this is neovascularization where? Else, so it's funny that somebody was non-imaginative. So you have neovascularization of the disc and then the other 90% of the retina, if you call it NVE, neovascularization elsewhere. So this is neovascularization elsewhere. And then of course this is? Neovascularization of the disc. NVD, and so we call this the medusas, look. Remember medusa from mythology who had the snakes coming out of her head? That's what this looks like. You've got all these dilated vessels in the optic nerve head. Now, it's very interesting when people first got lasers. There was a xenon arc laser that came out in the 1970s and these things were amazing.  It's very powerful laser. So people said, hey, why don't we treat these and shrink the blood vessels and cure neovascularization? So they took the xenon laser and they blasted the blood vessels right on the optic nerve head. Well, what that did is that caused huge loss of nerve fiber layer coming in and huge damage. But at the same time they found people with neovascularization elsewhere. They blasted it with a xenon laser. And what happened is not only would that neovascularization perfectly go away but on the central disc would go away. So what does that tell you about the cause of the neovascularization on the disc? Yeah, so it's from mediators put out by ischemia and that's the key thing. So VEGF is one of them. And so one of the things you can do is you can treat the peripheral retina with laser, decrease the load of ischemic factors coming out and the neovascularization goes away. Of course, now we've got anti-VEGF injections that we can do which again, decrease those blood vessels. And so it's chronic ischemia that causes the NVD of the disc. And what can happen if you don't treat this? Exactly, so hard to see where this is because of all the hemorrhage but this is along the arcade. So you can get not only chronic hemorrhage but you can get fibrosis. So you really want to treat the diabetic retinopathy before you get to some of these end stages. And of course the ultimate end stage of NVD is, all right, so what kind of hemorrhage is this? So it's a pre-retinal hemorrhage and when you've got a pre-retinal hemorrhage it's kind of between the surface of the retina and the vitreous, you get what's called a boat shape. And so you see it's flat on top and then it's kind of curved on the bottom so you get this pre-retinal boat shaped hemorrhage. So again, that's a sign of bleeding from neovascularization. So again, you want to try to prevent this from happening. What's another result of ischemia? You can get neovascularization of the iris and the ingus. So this is neovascularization that even an intern would recognize. So it's called rubeosoceridus or neovascularization. We used to call this ropeosis, you know, it's a group of blood vessels on there but the problem is, is if you let this neovascularization grow unchecked on the iris it can cause some issues. What are we seeing right here? All right, so you can see that that retinal pigment, I'm sorry, the iris pigment epithelium has been pulled around the corner and look at all those little blood vessels on the surface of the iris. And so as you get that neovascularization growing it contracts, it can pull the pigment epithelium of the iris around the corner. So you end up getting this picture. And what else can this do if you've got neovascularization in the iris? You can get PIS, you can close off the ankle, you can get lacyvaculization and thickening of the visumum. So what does PIS stand for? Perforolantereal scenicia. Exactly, so you get scenicia, you get iris sticking to the peripheral cornea and the anterior chamber angles clear back here. So you get blockage and then severe neovascular glaucoma if you don't treat this. And this is what you already said, as you get lacyvaculization of the pigment epithelium of the iris sticking to the diabetes. Does that represent a certain stage like the lacyvaculization? Yeah, that's usually a later stage. Like PDR. Yep, it's a very late stage where you've got significant proliferation. What else does diabetes do? So it causes a little thickening. And what stain is this? Acid. Okay, so I apologize for you guys. Normally I give you the basic lecture first. Sorry, but. So the PIS stain stands for basic membrane and this nicely shows that the basic membrane of the ciliary body gets thickened.  But those who haven't heard it. So when I was a pre-residency fellow doing ophthalmic pathology with Dave Apple, he said they want some slides to put on board. So pick out some good slides and send them to him. So pick out some good ones and send them to him. So I sent him this slide. And sure enough, when I took OCAPS as a senior resident, my slide was on there and I said, oh wow, thickened basement membrane, diabetes, man, this is great, I'm so smart. And then the question said, A, a patient with this picture would have a urinary creatinine clearance of, B, a perineal nerve velocity of, and so they love two part questions on OCAPS.  You know it's decreased, but what is the number? What is the perineal nerve velocity? So even though it was my picture, I still don't think I got the question right. So I always remember diabetes, thickened ciliary body, basement membrane, and this can pop up occasionally. All right, what the heck is this? So these are laser spots. All right, so those are laser spots. So the idea again is we treat the peripheral retina to decrease the ischemic load to then make the neovascularization go away. You do not zap the vessels directly when you do this. Here's a laser spot. Now it's an argon laser usually. And what it does is it's absorbed by the RPE. You can see that in this laser spot, that RPE is just cooked. The toriel capillaris is sealed off. You get atrophy of the retina overlying it, and then of course you've got no more on both sides. So you decrease the load of ischemic retina and the periphery in order to save the center vision and save the center part of the retina.  Load for these vulnerable vessels. There's kind of an edge where there's a fence called the CFET. So it's called the CFET. So what do you see this in? What entities? All right, so right now if they'd be maturity, you could see this in a non-perfused area where it's just dark, of course, and getting in and then this CFET neovascularization. Again, this happens to be a patient with sickle cell. So when you have sickle cell, you get a lot of sickling of those RBCs.  So this is a patient with sickle cell. And this is a trypsin digest showing this lumpy, bumpy, knobby vasculature from chronic damage from sickle cell. So we don't see a lot of sickle cell in Utah. We just don't have a lot of African-American patients. We saw a ton of this in Chicago, but it just depends. But you always want to keep this in mind, especially when you've got an African-American patient with some funny peripheral vascular changes. You really want to take a good history and make sure that they don't have sickle cell. All right, what do we see in right here? Exactly, so that's a macular hole. And this is the picture. What the heck is that thing in there, coming out of the hole? Exactly, sorry, I put that in once in a while to see if you guys actually look at these pictures. So if the patient has trouble fixating, they sometimes put a rod in there. So that's a fixation rod showing you that. But there's a nice close-up of a full-thickness macular hole. Of course, this is what kind of a scan? OCT. OCT, and you can see not only is there a full-thickness hole, but what else can happen with these macular holes? Ultimately, the ventroregal tractions will get attached to them. Okay, well, that's what can ultimately happen, but that's not on this picture. What else is this picture showing? It's a edema as well. Edema, exactly. So there's a little bit of edema next to this. So oftentimes you'll have a full-thickness hole, but you'll have a rim of some thickening of the cornea due to edema. So the idea now, especially with these really high-resolution OCTs we have nowadays, we want to pick these up where there's traction early on before it forms a full-thickness hole. And so we will often try to catch these early where we treat them before it causes that. And then, pathologically, you can see that here's a full-thickness hole, it's in the center of the macular, the ganglion cell there, multiple cell there, it's thick. Look at the edema now, it looks just like the OCT. Edema next to the full-thickness hole is macular. All right, what do we see in here? So, a little bit more, it looks like the OCT. And what's the hint that tells you it might be an ERM? These vessels, it's like someone has kind of grabbed them and pulled them in a little bit. And so that's the subtle sign of an epiretinal membrane. Now this is not so subtle. Again, in turn, pick this up. You can see a severe epiretinal membrane with wrinkles. And so epiretinal membrane, think of it as a cellophane membrane on the surface of the macula. And then think of it as crinkling up like cellophane does and it can cause that kind of a change. And red-free photos show this nicely. This is a red-free photo. See the straightening of the vessels? And you can see this epiretinal membrane right here on the surface of the retina. This kind of shows you, again, the OCT shows it nicely, all OCT after it. You can see, again, the membrane on the surface of the macula. And this is what it looks like pathologically. You basically get this corrugated appearance. This irregular wrinkling. And so what happens is astrocytes, which live inside the retina, you don't think of them, but there are some in there, they will gain access to the surface of the retina and then they'll start proliferating and making this epiretinal membrane. All right, what are we seeing right here? All right, what are drusen? Exactly. So we look at a drusen. Some people even call it intra-RPE. So this is a good place to talk a little bit about Brooks membrane. Now, normally, I would talk about this when I choose the normal anatomy and just this morning I forgot. So what are the layers of Brooks membrane? It's a five-layered sandwich. Good, so it's a five-layer sandwich, Brooks membrane. And so you think about it, it's like those turkey sandwiches you get at a bad restaurant where you have bread, which is the basement membrane on both sides, and you have two layers of really fibrous, collagenous turkey, and then a layer of elastic tissue, which is the cheese. So you've got cheese, two layers of collagenous turkey, two layers of bread. So it's a five-layered sandwich. So technically, if you talk about drusen, they are under the basement membrane of the RPE, but on top of the collagenous layer. So technically, they're intra-RPE. So here they are. And you alluded, Ali alluded to the fact that these are kind of waste products of the RPE building up. So if you think about it, the RPE is a very, very busy layer. What does the RPE do? What are some of its functions? Okay, how does it do that? Okay, so now Brooks membrane does not stop transfer of stuff. And so the coreo-capillaris is very porous. Materials come out of the coreo-capillaris. The outer retinal junctions that are kind of the outer blood retinal barrier is actually the RPE. So the RPE has tight junctions in it. So fluid doesn't just flow passively. It flows actively. And so you get transformation of nutrients coming from the coreo-capillaris into the outer retina, which is extremely metabolically active. What else does the RPE do? I don't know. I just said that. I just said that, yeah, absorbs. All right, so it will actually, it's got pigment in it, so it absorbs light. And so it helps to decrease glare. So if you have an albino patient, man, light really bothers them. But normally the rest of us, we've got that RPE that absorbs some of the light so we don't get so much glare. What else is the RPE? All right, so it's kind of like a recycling factory, if you think of it. So those outer segments of the rods and cones, they eventually slough off. The RPE takes them. It re-esterifies them. It makes them like new. And then it puts them back out into the retina. So it really has a, you know, a really rebuilds. It has a recycling. So if you could imagine over the years that just a lot of that stuff builds up in there. You get a lot of lipofusins and pigment, a lot of breakdown products. And eventually it overwhelms that cell. It starts spitting them out and forms these drusen, which are the first sign of age-related macular degeneration. What is this? It's a giant drusen. And so you can get small, so-called hard drusen. You can get large, so-called soft drusen. So sometimes these drusen can be really big and it causes disruption of the overlying RPE layer. And eventually you can get, you know, the loss of the photoreceptors there. And then you get the loss of vision from macular degeneration. Here you can see a lot of drusen and you can see the RPE changes starting from macular degeneration. Now, these are what we call confluent drusen. It's your drusen all along here. So you get a lot of soft drusen kind of linked together and you get loss of RPE overlying them in significant loss of central vision. So what's happening right here? This is a fondest photo of the up-to-high. What else do you see? It's kind of subtle in this picture. You see kind of drusen throughout. But believe it or not, right here, I'll outline that the RPE in this area has been completely wiped out. It's a little bit of pigment on the edges. This is what we call geographic atrophy. So when you get significant enough changes from majorly macular degeneration, the RPE gets completely wiped out and you get what's called geographic atrophy. So this is what it looks like. Here's Brooke's membrane right here. You look right here, the RPE has been completely wiped out and therefore the retina overlying it has got no, you know, none of the RPE functions taking care of it so it gets wiped out. So this is what's called the end stage of geographic atrophy. And so this is macular degeneration. Unfortunately, we don't have good treatments for this yet. What do we see in right here? Oh, I'm sorry, question. Yes. We're like pseudo-drusen or reticular drusen that are above the RPE. Do they, does that not interfere with its function and transport everything? It does also. Yep. So they're kind of like, think of reticular pseudo-drusen as they kind of like do the same kind of damage that drusen do. All right, well, we're there. What is this? Yeah, so you can see, blowing the inferior back, maybe a little hemorrhage there, it looks elevated, I want to go to the front of the reflex. And then you can see like a darker, deeper, greenish-grayish color, which makes me think that there's sub-retinal fluid there. Yeah, so when you see this dark greenish color, not only is it sub-retinal, but it's actually sub-RPE. So this is a sign of neovascularization. It can be under the, you know, under the retinobit can also be under the RPE. And when it's green like this, the RPE is still overlying. And so this is neovascularization from age-related macular degeneration. And this is a nice picture. I had to copy this because I didn't have a pretty picture like this, but here's the coroid. Here's the overlying retina. Here's some fibrosis going on here, gliosis. And here's a break in Brooks membrane and you see the neovascularization coming through, going underneath the RPE. So you not only get hemorrhage, but you also get fibrosis from the wet macular degeneration. This is a severe one. This is sub-retinal when it's red and kind of sub-RPE when it's green or black. So this is a severe neovascular membrane underneath the bacula. You can see right here, here's an area of a focal neovascularization with fibrosis. So you'll start to get fibrosis underlying this. Here's a close-up. Sub-retinal fibrosis, RPE broken up and a few little tiny vessels right in here. So neovascular, fibrodech membrane underlying the macular for mutilated macular degeneration. This is a severe one. We used to call this a disciform scar which is a dense, thick, fibrodech scar underlying the retina. This is the end stage of neovascular age-related macular degeneration. All right, what are we looking at right here? So there's a fundus nodus, scarring, focal spots around the macular, as well as around the retina itself, kind of consists of potentially some disciform scars, but it's still fine. So some scarring in the retina, but what are these lesions? They're away from the retina and they're round and fairly distinct. This is a tip-off for something else that can cause neovascularization of the macular. Not disciform scarring. Well, it can cause disciform scarring, but in age-related macular degeneration, you don't have these peripheral lesions. What entity can you have peripheral lesions along with the macular lesion? Isn't that the case of plasmusis? Exactly, so now you have to put the P in front of it. The P stands for presumed ocular histoplasmosis because we often don't find living bugs in there, but you can find evidence of previous histoplasmosis infection and these are called the punched-out lesions. And so they call them punched-out because they're focal and they're like punched-out lesions in the periphery and then eventually you can get some neovascularization and some scarring in the macular. So this is presumed ocular histoplasmosis. What are we seeing right here? Yeah, you kind of see some elevation here and so you would be really suspicious that something's going on in here. And so we do a fluorescing angiogram. Remember what those were? Do you guys still do fluorescing angiograms? I know we had the, we call the Foursing Angiogram Conference, it's mostly OCDs, but you can do a Foursing Angiogram and you have this picture. What is this show? It shows a lot of things in the statement practice. All right, so if you remember, we showed you Henley's layer that goes out leakly. So when you get leakage in the area around the phobia, that fluid tends to track along Henley's layer and they call this kind of a flower petal distribution. So this is cystoid macular edema. And this shows it pathologically. Remember we said it's in Henley's layer or in the outer plexiform layer right here and here you see exudate here and here. Here's the outer nuclear layer, inner nuclear layer, and it's right there in Henley's layer. There's the ganglion cell layer, multiple cell layers thick. So this is cystoid macular edema. All right, what do we see in here? So this is what, yeah, gosh, I don't know if we can turn those lights down a little bit. My view is so much better than this. I'm sorry, we've got, I don't know, that helps a little bit. This is one where you kind of have to use your imagination and looking at this pattern. So I apologize, this shows up much better on my picture than up there. This is a bullseye maculopathy. So if you look, you can see some modeling of RPE here and then a more red outline around it. So this is called the bullseye maculopathy. Now, what are some entities that can cause bullseye maculopathy? Sometimes some of the psychiatric meds can cause this too, but most common one that you may be seeing patients in clinic to rule out is plaquanil toxicity. And so you obviously don't wanna let it get to this point. You wanna recognize it sooner. And nowadays, we can do macular OCT, we can do central visual fields and patients who've been on plaquanil to make sure they don't get to this point where you get this bullseye maculopathy. This is the fluorescein angiogram.  And this shows the bullseye pattern much nicer when you do the fluorescein. So bullseye maculopathy. What do we see in right here? This looks like angioid streaks. Oh, all right. So again, almost kind of like deeper medusa snake heads. And so these are what we call angioid streaks right here. What are angioid streaks? Brakes and brooks member. Exactly. So their focal breaks in brooks member. Now, why would I be showing you a picture of somebody's neck? I'd actually just love to do this.  Exactly. So they call this a pluck chicken look.   And so you can see the skin, this is a patient with pseudosanthoma elastocone. And it's a connective tissue disorder and therefore it affects brooks membrane. So you can get these angioid streaks and they can sometimes allow neovascularization to form. So they're important that you recognize those. What are we looking at right here? Exactly. So this picture kind of shows you pretty much all the findings of an advanced retinitis pigmentosa because you get wiping out of the retina, you get a pale optic nerve, you get the vessels markedly attenuated. And then as you go out to the periphery, they call this the bony spigula pigment. And so what happens is the RPE gets disrupted and then the pigment will track along the blood vessels. That's why you get that bony spigula. The pigment is released from the damaged RPE and then it'll almost diffuse out along the blood vessels. And there's the blood vessels there with the pigment on it. And so that's what you get in retinitis pigmentosa. And again, the retina guys will talk to you about the various genetics and all the other factors involved. But pathologically, the final common denominator is that the retinopigment of the feeling gets wiped out, the retina itself gets atrophied and then you get the pigment along the blood vessels forming the bony spigulas. What do we see in right here? This is the yellowish elevation of the Bermuda cycle. Yeah, so it kind of looks like, we like to tell people it looks like an egg yolk. So if a teleformed dystrophy or there's a type of a teleformed dystrophy, best dystrophy that can look like this. So you see that egg yolk underneath the retina in the center. And you can see this fateliform lesion is actually underneath the RPE right here forming the yellow form maculopathy lesion. Okay, what do we see in right here? So people call these pieceiform, pieceiform literally means fish-like. And so if you think about Nelso goldfish, you know, crackers that you eat, it kind of looks like, kind of, again. You know, people sometimes you wonder how they describe these bits called pieceiform. So you see these little tiny changes here. And so this is consistent with, you said it, Stargardt's disease, okay? Or fundus flavium aculata. And so this is characterized by deposition of lipofucin into the RPE right here. So it's lipofucin rich and can disturb the macula also, but then can cause these peripheral lesions, Stargardt's disease. What do we see in right here? We really see very many vestibules. So I'm gonna see if there's any vitritus. Exactly, so this is a vitritus.  This is vitritus. So what are some of the things you think about in vitritus, okay? So when you think about it, when you see this kind of vitritus picture, you wanna make classification.  So one mailbox says inflammatory, one mailbox says infectious. There's a third mailbox you wanna always keep in mind when you see a vitritus. Exactly, so you've got what your retinal lymphoma can present as a vitritus. And so those are kind of the three categories you always wanna keep in mind when you see a picture like this. And this shows you kind of the path on this. This was that, maybe had that picture five years ago. So what do we see in here? What do we think the diagnosis is here? This was toxa. And so when you have toxa acutely, you get the headlight and the fog, you get a vitro retinal inflammation. And then eventually when it settles down, you get this heavy pigmentation with these white lacunae where the RPE's been totally wiped out in this area. And so this is a previous toxoplasmosis that's not actively infected. When you look at it pathologically, you can see the RPE gets totally wiped out in this area. I think we can go up on the end. This is an ocular toxoplasmosis. All right, what do we see in here? So when you see a patient like this, they call this again maybe the ketchup or the pizza look to it. And so this could be CMV. And then we look and when you look at the retina itself, you can get intra-retinal, I mean intra-nuclear and intracytoplasmic inclusions. So you get these swollen retina cells. And so this can occur in people who are immunocompromised. We used to see it in people with HIV before we had triple therapy. But even people who have undergone bone marrow transplants or are being treated for a systemic cancers can get CMV retinitis flaring up. All right, so we say goodbye. We've made it. We say goodbye to the glomo and melano. Next time I believe it's orbit. I don't know, but please look and see. So please read that section of the BCS ahead of time. And we'll go ahead and do that. And then we're just gonna, you guys have me for the next seven Tuesday mornings at seven a.m. Oh, we've got exactly two minutes. Questions? Was it the future of toxoplasmoplasmosis? Was that the funnest photo of the rest? You know, I can't put anything by you guys. This is a nucleated globe that was doing it. So that's why it looks that way. So this is actually a globe that's been cut. That's what allowed us to have that path picture. Yeah, a good pickup. How's a good pickup there? So you get the gold star for the day. That was a good pickup. All right, any other questions?


This video is sponsored by One Football. One Football's app makes it easy to keep up to date with transfer news, scores and stats all in the one place. To download the One Football app, click the link in the description. The app is free. Silver's Blues falter once more at his old stomping ground. There's a lot of talk around this game in terms of the press. Michael Silver returned to Warford after what is still a disputed claim over the last year.  Michael Silver was able to motivate the players in the same way Troy Dini said that aggression would do. Looking at the team before the game, a lot of people would have said that Michael Silver had a good foundation to build off after last week against a good performance against Madden City, against the younger players coming into the team in Kenny. David's captain and they had a chance to stake more of a place and build on what people thought was a good performance last week. But instead he changes it and tinkers with the team once again, bringing Richardson and Guilfe back into the team after benching them against City. He went for like a diamond in midfield with Gomez, Ghana, Tom and Guilfe with Guilfe and Tom kind of swapping that forward attack and roll every nine again. Tom kept his place as captain, interestingly Kenny stayed and obviously Richardson came back in dropping those two wingers and going quite a narrow play. Funnily enough it was a similar kind of way to Warford lined up. Looking into the game itself those first 45 minutes really lacked quality on both sides. I didn't see too much from Everton or from Warford really, both teams struggling to get any quality on the ball. We looked poor on crosses 10 minutes in I would have said, which was typically a cumin trait in years gone by with set pieces being our biggest hurdle of time recently. But we did, we looked about, without Pickford's forehead save, those first open in 10 minutes they kind of saved this. Towson had a chance and then Shelf followed shortly after by Guilfe hitting the crossbar, easy to forget though. In a game like this they had a couple of chances like that but it was easily buried in amongst the poor performance that came. Especially in the second half. Right on the start of that second half a very astute Warford manager brings Andre Grey on when they win a free kick as Denny gives one away on the edge of a box. Danger signs, alarm bells ring. Funnily enough we actually deal with that free kick pretty well. We're able to deal with it following the free kick and then an open play and obviously it comes off the corner. And there's an issue towards the end of the game as we clearly see with Zimmer and the referee over whether Pickford got a touch there which led to the corner. Regardless of that fact to switch off in the way that they did after dealing well with the set piece which has been our biggest stumbling block over the last few weeks is just unforgivable. They just completely switch off from open play. Really easy to see everybody along that back line, everybody from Ghana who has come back well on the team along that back forward just switch off. It's an easy goal for Grey just brought on in the 65th minute. That's kind of in between two changes by Michael Silva. He brought Walcott on for Gomez which permues me and a lot of fans I think seeing as Walcott wasn't great last week, wasn't great the week before and hasn't really done much the replaced loopman in the team. I think a lot of people agree. Bernard comes on for Richardison in the 63th minute just after that goal goes in. Again a little surprisingly I think a lot of people would have liked to see Richardison and Bernard on those wings. Towards the end of that game as we were trying to get an equaliser Walcott again just didn't offer too much going forward. I think a lot of some people said that they thought they had a good game, that Man City game and a lot of people didn't as well. I was surprised for one anyway. Later on that game in terms of substitutions there wasn't really too much. In those last few minutes we had two chances. Then you hit off the crossbar the second time in the game. Optimus would say that we were unlucky maybe not to score two of those goals. But it's followed quite quickly by a sitter. A missing of a sitter by Don La Cavaloon just brought off the bench. Fresh legs, fresh mindset, couldn't finish, not good enough. It just summed up what we have in the striker role but ultimately it sums up that game for us. Obviously there was an issue at the end of the game with Zuma and the referee. As we mentioned Zuma feeling that the corner that had been gifted before Watford's only goal in the 64th minute was incorrect. But ultimately we couldn't keep her cool from open play. That's why we gave the goal away and then Zuma couldn't keep us cool at the end of the game. And we've been wanting for people to have a go at the referee to really call them on some decisions being made. But he couldn't keep us cool at the end of the game and ultimately we can't use somebody who has been good for us. Or has at least been relatively solid at the back and we probably would have used. I would prefer to replace Keane with Zuma with Mina to be honest for the next few weeks. I'm hoping obviously he's going to come in. Marco Silva didn't stay on that touch line very long. He shot down the tunnel but I would imagine a difficult day for him coming back to his old club. Football and why he's not able to compete or at least not being able to win the game. There was a lot of stigma around Silva in terms of his ability at Everton, in terms of his ability at Watford, in terms of the way that things ended between him and his former club when Everton came in for him last year. There's some bigger questions to be asked here. It's a really poor run of form and it's been particularly bad. For the last three years we come to this point in the year, end of January, start of February. And we hit a crisis point. David Squires did it really well in his cartoon a few weeks ago in The Guardian. We get to this point every year and we hit a crisis point for the last three years. And rightly so, it's not been the right level. Don't get me wrong. It's not been the standard. It's not been the results. It's not been the team. It's not been the attitude that we wanted Everton Football Club. But something told me a few weeks ago that after everything in the last three years, after the mega round of managers that we've had being topped off by Aladise last, and we can see how bad it could really get if we keep going along that way. I think there's more patience from fans this year. I certainly thought of a few, maybe after the Huddersfield game. I certainly thought then that there was more patience from the fans than the media were letting on. There was an understanding that we need stability. There was an understanding that there's somebody more at the helm of the ship in terms of Marcel Brands. But how long has that patience gone to last? I think a lot of fans want, of course we want them to succeed. Of course we want them to turn it around. Of course we want this team to be his team. And we want them to play the way we want Everton to play. And we want them to win games like that. But at what point do you give him too much time? At what point do we waste time? We've already wasted it three times in a row now. We've made the wrong decision since this money has come in from Mashiri. And obviously the stories have come out about Bielsa, about replacements being eyed up. Ultimately as fans I think we want a bit of comment whether it be from Brands for the board. I think there is a split start to grow in terms of people wanting Silva out or not. For me personally it's a difficult one. I think stability is massive for us now. I would hate to see us do what we've done for the last three years and what we know damages us. And what I think ultimately damages the squad further is just chopping and changing managerial staff. This group of players is turning in the... The group of players has had the same number of managers as teams that I would have looked at a few years ago, mid-table teams. Hoping when Martinez was sacked when we first got that money that that's not what would happen with us. Ultimately that's not the case. Ultimately I don't know whether Silva's good enough. The results certainly suggest that he's not. I mean the results haven't been there. The performances haven't been there. And I think if it had been slightly better there would be more patients coming from the Everton fans. But it's pretty dire, it's pretty awful. It's worrying that he had so many players brought in part of the season and he's still not being able to perform with him. It's not even like Galladais last year having two players. It's really difficult. Ultimately for me I think we still need to give them a little bit of time. I think it would certainly buy time for the manager, the coaching staff and relieve some of the Everton fans would be a comment from Marcel Brands, a comment from the board. They understand that it's not good enough. But we've seen this entrenchment happen over the last few years when the alarm bells start ringing and things start going wrong. It's just really not good enough. Beyond that it was a really dross game to go to Warford and for them to have all the comments that they had mid-week from Tridenti from the fans and ultimately show that Silva wasn't good enough twice this year to play them, not beat them. Really not good. I think that's Silva has started. Our opinion of Silva has changed over the last few weeks.  Stability is the main thing that we need at Everton Football Club but whether that's with or without Silva means you have to be seen. Let us know what you think in the comments below.