All right, good morning. So everybody excited, bright and eye-wishing tail, ready to learn about how to get nerves. All right, so today we're going back to the Grand Tetons. And so, for those of you, I don't know, I see nice suits here. Who are you guys? Hi, Nathan in there. For the path? Ah, welcome. Where people wear a suit if it's more than one suit. I thought we were going to upgrade it. The shame of these guys is that they show up with at least a tie on or something. All right, so what we do is I've got a captive audience here, so I get to show people my travel fly. This is always fun for me and not for you guys. And so this is the brain trust for the Astros cataract clinical committee meeting. And so we had a meeting in Jackson. And so we showed up the first morning now. This is not planned, but you can see how great minds think alike. So this is the uniform for the cataract clinical committee from Astros. And so we got to take a picture of this because we all showed up wearing the same thing. So what was fun was that as part of this retreat, you know, we get to do some fun stuff in the afternoon. And so there's a, it's called the Teton Raptor Center. And basically these guys have domesticated raptors. So they bring them around so you can look at them. So this is a peregrine falcon, which, you know, is a pretty good predator. Then they brought a golden eagle. And so if you look at these guys, you know, their wings are tucked in, but they've got about a five-foot wingspan and some serious claws. And I mean, there's just some serious, serious raptors. And so the fun thing is, is they got them there and the people from the center, of course you give them a donation, of course, but they will come and they'll talk about what they do and how they rescue these birds and try to eventually rehabilitate them and train them and go back to the wild. And so if you look at them, it's a pretty majestic looking bird right there. And so they're all over around the Grand Teton. You'll see falcons, you'll see eagles, both bald and golden. So I thought I'd just show you guys some of these guys. It's very rare you get to set a foot away from a golden eagle. All right, so today we're going to talk about optic nerve. So this is what the optic nerve looks like as we're looking in. And you can see the nice, sharp edge, non-elevated, non-congested, reasonable color. As you're looking in, vessels, arteries coming out, vinyls going in. Okay, let's start with Ashley. Ashley, what stigma are we using here? A tricol. And how can you say it's a tricol? I don't think my way is the best way but just because of the colors. Well, exactly. So what do you remember now? Now the third color for tricol never shows up in any of these pictures. But in any event, it stains connected tissue blue and it stains tranquil tissue red or pink. So if you look, here's the optic nerve itself. And then it's got the connected tissue around it that is stained this blue color. Okay? So my analogy to the optic nerve is that I think of the optic nerve as a fiber optic cable. And so each axon, as it leaves that ganglion cell, goes through the laminar fibrosis and then out into the optic nerve. And once it gets posterior to the laminar fibrosis, it becomes myelinated. So it's a single fiber optic cable and it's got a little plastic around it. It's got myelin around it. Then these columns of axons, they form bundles with these little piocepti in between them. And those are the fiber optic bundles that you see when the fiber optic cable is there. Then the whole thing is shoved into the ground, but you can't put those fiber optic cables in the ground. So you have to put a steel cable around it, a steel round tube around it, and that's the optic nerve sheet. And so if you think of it as like a fiber optic cable in the ground, that's how you can remember it. So each axon is myelinated just posterior to laminar fibrosis. The levels of axons have these little piocepti in between them, and then the whole thing is surrounded by the optic nerve. So here we see, I'm not going to get a better picture than that. It's like 30 years old now. I'll take it. And remind me guys, when you get a retinoblastoma, you know with a good optic nerve, I'm going to take a better picture. But here's the optic nerve sheet. And so remember, this is the second cranial nerve. And so it's got similar surroundings to the brain hands. So you've got the dural sheath around it, the optic nerve sheet. And then you've got the arachnoid granulation, subarachnoid space, and then the pia mater, forming these little individual columns. Okay, Becca, what are these two structures? Central retinal artery. Exactly. So if you remember from last week, central retinal artery and vein, they share this common adventitial sheath. So thickening of that artery, arterial sclerosis, actually pushes on the vein next to it and can cause vein occlusion. And here's a close-up. This is the optic nerve sheet. These are these arachnoid granulations, subarachnoid space.  And here you can see the longitudinal. Okay, now there are some cells that live in between these columns here. But you see the little blue cell bodies. So Jason, what are some of the cells that live in there? There's... Okay, well, in the piocepts, they're mostly on the outside. They're more in that subarachnoid or arachnoid space. So they don't usually live inside the prank of that cell. What are the cells that produce the myelin? So the libidendrocyte. The libidendrocyte. So that myelin's got to come from somewhere. So some of these blue nuclei are a libidendrocyte. But there are also astrocytes that live in there. And that's important because you look at what tumors can affect the nerve. You don't get tumors of the nerve itself. You get tumors of the cells that are in the nerve. And so you get libidendrocyte. You get astrocytes that live in there. And here we can see again, central retinal artery. Central retinal vein. You're there apart. And then as you get closer and closer, the optic nerve can eventually come together. All right, so Chris, what are we seeing here? A funnest photo of the right eye with some kind of myopic changes around the optic nerve. Tilted disc. You look closer. So first glance you may say that's a myopic change, but I would say it's a little bit different than that. You definitely got this crescent of white around it. Right. I mean it looks like it, from the photo looks like a tilted disc, but I know that you're trying to lead me to something else. Here's the outline of the disc itself. Right. So that's actually a very small disc. Yeah, it's a hypoplastic disc. Exactly. This is a hypoplastic disc. So the way you tell us apart, myopic discs are big. Right. You still have that temporal crescent, but myopic discs are large. They're not small. They're larger discs. Whereas if you look right here, you can see this is a small disc, but this is a hypoplastic disc. It's kind of the opposite. Right. So what do you worry about in these patients? So cranial nerve, I mean not cranial nerve, central nerve or central nervous system abnormalities, mainly central or midline abnormalities. Okay. And if this is inherited, how is it inherited? Usually autosomal dominant. Exactly. So autosomal dominant. So it's interesting. I saw a teenager was referring in my outside of town, which is for funny looking discs. And we looked in there, hypoplastic discs. And so we asked the mom, do you mind if I take a look at you and turn up mommy Alan too? Oftentimes though, if these are just isolated to the eye, they do not cause problems. And so they're really not, and really these are more at risk for like, just giving up your ophthalmology, as far as I know. And so oftentimes these are just benign looking discs, but this is a hypoplastic optic disc. Okay. Tara, what do we see in here? This is what is below the right eye. I think that maybe like an optic nerve coloboma. Exactly. What does coloboma mean? Anybody? A failure of fusion of the embryonic tissue. It is, but... Oh, there's a Greek. Somebody look it up. Of course. What languages have come from? Okay. Maybe Greek or something. From the Greeks. So look it up. Coloboma. Look it up. Look it up. So. But exactly. This is indeed an optic nerve coloboma. So Eileen was onto something. Look at the location where it is. So it's usually these colobomas are inferior. So, Tara, why would an optic nerve coloboma be inferior? Because of the formation of the embryologically. That's where it failed to form. Okay. So how does that happen? What happens embryologically that allows these colobomas to form here inferiorly at the optic nerve? I'm not sure. Okay. So remember when that optic vesicle, it poaches out from the primitive neuroactoderm and then it imaginates. Well, on the inferior part, those vessels, those hyaluronic vessels come in and feed that as it's growing. But when it starts to seal off, that globe will seal at the equator. And then it'll be like a zipper that you're going both directions. So start from the equator and go back to the optic nerve and anterior to the iris. So when you get a defect in the closure of that fissure, that's when you get a coloboma. And so, optic nerve is the posterior part of that fissure. So you get an optic nerve coloboma. The anterior component of that would be what? Something on the lens council. Even more anterior than that? The other iris. Exactly. So those iris colobomas are the same thing. They're inferiorly there and they're kind of the anterior most location of that in rheologic fissure that's not fusing. Now, this is the ultimate kind of coloboma I call it. I named, what does this one call? This is named. This has got this name to it.  This is named after the flower, the morning glory. And so if you think of it, morning glory flower, it's like a trumpet horn. Okay, did we find coloboma? I had a question. Yes. So the difference between optic nerve and coloboma and pathologic? We're getting to that. Yes, hold that question. But it's highly debated. Some people think that they're related and some people think that they aren't. Exactly. And they're still debating on exactly what leaks out from a coloboma, too. So that's where we're coming to that. So this is a morning glory flower and if you think of it, it looks like a trumpet horn. And so when you go back to that optic nerve morning glory syndrome, it's like the ultimate coloboma.  So when you look in there, you see that this is in focus here, but this is all blurry because that's actually moving away from you. This is called a morning glory syndrome. You see that there's very little, you know, active fibers going in there. So you get a significant visual loss from these morning glory anomalies. All right, speaking of which, we're going to skip to Rhys. So Rhys, what are we looking at right here? Optic nerve pit. Exactly. There it is. And so I'd like to show you guys the obvious. I probably shouldn't do that because that's so obvious even these guys interviewing me. Well, maybe they wouldn't work, but you never know. But this is an optic nerve pit and so it's pretty obvious here. You know, maybe one of the interns could pick it up. I would figure that out. But this is an optic nerve pit and what's the biggest problem with an optic nerve pit in terms of vision? Distant attachments. And how do they occur? I mean, so you did an indentation of the retina into that pit and then it just comes up right over that. All right, so indeed, here is an optic nerve pit. There's optic nerve pit and you see part of the retina almost dipping into that, but the reason that people have this vision is you actually get fluid leaking under the retina. And so some people would argue, they'll say it's CSF fluid leaking. Other people say, no, it's something different and they talk about how you're out of gas and there's a big argument about exactly what happens. But bottom line is when you get an optic nerve pit you can get leakage of fluid from the optic nerve under the retina to the macula. So if you think about that, how do you usually get rid of that? Well, you could laser up it.  And so it's going to be, you guys are way too young, but in your history books, which I don't teach you anymore, there was this war called Vietnam. And in Vietnam, these generals would get up there and they would say, well, we bomb the village to save it. So you get these Viet Cong and infiltrate into the village. So what would the U.S. do? They bomb the hell out of it so they destroy the whole village, but we got rid of the Viet Cong and so it's the same thing here and so if you were to laser that, yeah, you'd get rid of the fluid but you'd kill the retina. And so these are tough to treat. Some people have dug for trectomies and tried to put gas in there and push it back and others have tried to do some light laser in that area, but these are tough to seal off because the fluid leaks out and goes underneath the macula. All right, now we're going to go back. Lee, what are we seeing here? And that's not, you know, a picture that Joa took. I mean, this is actually in focus. Exactly. So you can see that that white in there almost looks like kind of a giant cotton wool spot. That's actually myelination and so remember, those axons normally don't become myelinated until they cross through the lamina fibrosis and so sometimes you can get myelination that jumps the lamina fibrosis and hits the retina. Usually these are congenital and so the optic nerve is interesting. When the nerve grows, the nerve fibers themselves grow from that optic cup back to the chiasm but the myelination goes opposite so the myelination later in embryology comes from the chiasm forward and then it stops at the lamina fibrosis but sometimes it jumps and you get these. Now, do these cause visual problems? They can. Yeah, so you can kind of get an enlargement of the blind spot or maybe a little focal defect because they will, the fibers are still working okay but that myelination will block some of the transmission underneath and much like a giant cotton wool spot would. There's people that increase risk at all of like a, you know, that would come from that. Usually not. Usually it's a separate, it's a separate entity so I'm not sure why, you know, just once they jump and start growing they don't have a chance of growing even more but they don't so these people aren't going to increase risk for that. So I'm supposed to say, sorry, to make you say more, Steve, good question. There you go, very good. Sorry, I'm not slipping here. I didn't bring trophies for everybody today. That's a good question. Actually, that's what you say when you don't know the answer to it and you're intended to go, that's a good question. And then if you don't know then you say, why don't you look that out and go back to us? That way you don't have to flip Steve's answer. No, as far as I know that's not related to like, you know, astrocytomas or whatever it is like that. Alright, Nico, what do we see in here?  Exactly, so you see this bumpiness here and so at first glance and again, you may get these referred in. I've got these referred in from outside ERs before.  If you look carefully, you'll see there's these little deposits here and these are drusen. Now the tricky ones are when the drusen are buried. So if they're down deep or you can't quite see them, that optic nerve head looks elevated and can you have bilateral drusen?  Now, sometimes, you know, if you look at them, they're pretty blatant here. This is a bilateral drusen but you can see them pretty well here and even here on these different, on these bilateral drusen. So you see the drusen. What are optic nerve drusen comprised of? Calcium. Okay. So there you can see that's a severe one and that's even one with atrophy there and that's just kind of showing you these buried drusen, how they're harder to see. So there's calcium in them and so what does that mean if you were to do a CT scan? Palloidum. Yeah. So look at the drusen right here and so if you were to do a CT scan they light up but what's an easier thing you can do in the clinic besides send them to a CT scan? Exactly. So if you think about how ultrasound works when sound waves hit something thickly calcified they really bounce off hard and so if you put a B scan on these and you find the shadow of the optic nerve you'll see a bright spike right in that area and even if you turn the game down the eye starts to disappear and then there still be that area of the calcification there so you can diagnose these with a B scan. They are even early on and so the ultrasound is a good way if you've got some deep drusen you look in there and you say I think there might be drusen I don't think this is papillodema you can just grab a B scan put it on there and you'll be able to tell if there's any calcium there because if it's truly papillodema there'll be no calcium or no lesions there at all so very important to tell and so you can actually even do it with a CT scan because that's a better one you can see bilateral here bilateral drusen. How come one of those was white? Yeah that was great. Good question I like to show that to Chris Davidson that's funny I never thought of it it's like this one's white and that one's not and it's the same it should be the same scan so I'm not sure maybe it's silicone in there and because it kills that completely that's funny all this time I'm looking at drusen and I never even noticed that Good pick up Is that a squirrel on there too? Yeah Believe it or not these are older people and have you ever seen old people where they've got that calcified place where the muscle inserts anteriorly?  Drusen You can but even more than that they'll often get nerve fiber layer effects sometimes when these nerve fiber layer bundles are coming over the drusen you can actually get the big ones with disruption so Brad Kanz at one time was doing serial visual fields on these patients through the years and I think he did show that as the drusen get bigger and bigger you can get these little focal nerve fiber layer visual defects you can see right here here's some drusen here and drusen here and this nerve is being a little bit more atrophic a little bit more atrophic these are further along Alright what are we seeing right here Chris? This looks like optic nerve head, Eva and I'm glad you said it that way because they love on normal boards to ask you about this and so you'll say papillodema and then the examiner goes like this because by definition what is papillodema? Is it bilateral optic nerve swollen from the cranial pressure? Exactly for pressure increases so you never say papillodema looking at one nerve when you're on normal boards you say this is a swollen optic nerve and then they say what's the differential diagnosis and then you can say well if it's bilateral and the pressure is high it can be papillodema if it's due to congestion you know or something in the nerve itself but if you look you can see that the edges of that nerve are irregular you've got some flame hemorrhages here you've got some dilation of the vein cells so this is classic optic nerve swelling and if it's bilateral there's a pressure we call it papillodema there's a severe one again this would be one you know even a student would recognize something one of the applicants would recognize so definitely papillodema lots of flame hemorrhages elevated disc engorgement of the vessels and so this is what it looks like so remember from a few weeks ago we showed you the glaucoma changes where you get that excavation and that cupping this is the opposite and so when you look at this you actually get swelling here of the nerve so it poaches out from the nerve you have engorgement of the vessels and you've also got hemorrhages on the anterior surface and boy this is dying here wrapping up the new battery here but so you can see hemorrhages on the surface there and so this is optic nerve swelling or papillodema if we're by that on this is actually the laminocrobrosa gets bowed forward so it's almost like that pressure pushes it forward and so you get forward bowing of the laminocrobrosa in this optic nerve swelling alright what are we seeing right here Joe up well if you look right here this is interesting because this is more focal swelling so if you look carefully look at superiorly it looks like that optic nerve is swollen superiorly but inferiorly you know down here it's not quite as swollen up here it's more swollen so what's your differential diagnosis here let's say this is unilateral okay well no but no when you think of a segmental you know optic nerve swelling you want to start looking at broad categories of the etiology so what are a couple of broad categories that could cause this let's take a step back even more how about ischemia alright so when you look at a focal a nerve and there's some focal swelling in that nerve you want to look at various areas you could have ischemia what's that okay no so you want to start to develop a differential diagnosis and that's what's important and when you see focal swelling like this now Ashley let's say this is a 20 year old essentially optic neuritis exactly so you worry about optic neuritis optic neuritis in the acute phase can give you some segmental swelling of the disc it's more posteriorly so you often don't see anything in the disc but if you do you can get some focal swelling there what's another let's say this is a 70 year old AI1 exactly so anterior ischemic optic neuropathy so you want to start thinking of what could happen and so when you're looking at someone and they're young and you've got a little thema here in their eye they say oh my eye suddenly went blurry and it hurts when I move you start thinking of things like optic neuritis if you have a 70 year old male and he's a smoker and he's overweight and he's got high blood pressure medicine he comes in and he says you know I woke up this morning and half my vision is gone then again that could be something like this so this could be an ischemic optic neuropathy AI1 if you're an ischemic optic neuropathy all right Becca what is this we're showing but why would I be showing you this it looks like possibly a climb in there so what are we looking at first I'm guessing it's the central retinal artery so it is it's an artery except we usually don't unless the person dies we don't give pieces of central retinal artery what artery do we actually that's probably the temporal artery exactly this is a temporal artery biopsy seen in cross section why would we be taking the biopsy of the temporal artery if you were concerned for GCA exactly so when you see someone who's got ischemic optic neuropathy one of the things you don't want to miss is you don't want to miss an auretic form now most of the male AI1 are not inflammatory they're not auretic they're you get arteriosclerosis and you get this little posterior ciliary artery just blocking off but you don't want to miss a case of what's called gynecologist or you don't want to miss the cranial lobinus inflammation of those arteries because that can cause people to lose vision in both times and so you'll do a superficial temporal artery biopsy why because you can take that out without harming anything so you're always going to find a case report somewhere where someone's circle of closed off and the superficial temporal artery is feeding it I mean that's like one in several million and so you can pretty much remove these safely without causing any harm and then we can look at it and see if there's any inflammation now do you see inflammation on this one yeah and so we don't see any here and so you look at a temporal artery and cross-section there's the lumen and it's got some red blood cells in here's the intima that actually looks pretty good so this I want this artery right now this guy's not been to crowd burgers or moochies you know he's drumming cheeseburgers and cheese steaks you know and so pretty good looking intima and then this little squiggly line is the internal elastic lamina you see that's completely intact so I like to say what does that look like do you ever see those satellite pictures of the Mississippi River when it's like flooding Iowa every spring and you know it goes back and forth and it's got completely intact and then the adamant tissue around that no inflammatory cells what do we see right here Jason this looks quite alright so we start in the middle what do you make of the lumen it's very narrow very narrow suspicion is severe arteriosclerosis this is lots and lots of cheeseburgers you know and pastrami and all that other good stuff so markedly thickened intima look at the pretty much white you can't even see the muscular media here and then the adamant tissue is surrounded by this cuff of blue so this is a positive temporary biopsy and you can see that when you get this you're at real risk for the arteries completely closing off so you really have to treat these with steroids right away so if you see a patient and there's a high suspicion for temporal arthritis you can set him up for the biopsy but if you wait for the biopsy results and to give him the steroids they can actually lose vision not only in that but in the other eye so start them on steroids now and then do the biopsy within 7 to 10 days and then you'll see if you need to keep them on there my pet peeve is you get the guys you know that are referring from the outside they say oh we think this is temporal arthritis what do they do they give them so then the patient gets a septic necrosis so they're here where they get crazy from the penis and they say well do they still need to be on it so then we do the biopsy and then you see an artery that you say well is it yield-arter arthritis because the inflammation's calm down and you try to figure it out so the key is if you're going to put somebody on steroids maybe for a long time you got to have a diagnosis and so so long as you do the biopsy first because you want to prevent that and what do we look at right here Jason so we see a lot of giant cell giant cell that's the name giant cell arthritis so you can see the giant cell that's there and so you don't have to have giant cells necessarily you can just have lymphocytes maybe some epithelioid cells but it's called giant cell arthritis and here we can see this is that and they ran into complications they want to know is this giant cell arthritis and if you look there's a little bit of thickening of the intima there's a little bit of destruction of the internalized deployment and over here look the muscular media's gone from that area so this is what we call a healed arthritis so this is one that's been on steroids for a while and you do it but we don't want to make the diagnosis because you need to know what you're treating if you're going to put somebody on steroids alright so we're looking here Chris what do we see in here so it's a fairly so there's a little bit of edema there super old nasally and then it's fairly kind of white disc yeah so this is what could this be giant cell arthritis yeah it could be or it could even be AION could be and maybe this is not quite acute because you see a little bit of power in the air and a little bit of swelling and this is what happens when you get an AION be it arthritic or not this is the optic nerve and if you look right here it's just wiped out I mean you look at that here's some normal nerve down here but you look in this area and it's just wiped out and so what happens is it's those little posterior ciliary arteries which feed much of the optic nerve head that block off with either AION or arthritic AION and then you can get the optic nerve pretty much wiped out alright boy again I keep showing you guys these swollen discs you know here's another one Tara anything different about this one I mean it kinda looks like more like you know 360 diffusely elevated so again if it's unilateral instead of binaural so it's not you know increased intracranial pressure so what's your differential if it's unilateral like AION exactly so it could be ischemic AION could be optic nerve it could be inflammatory again so it could be an optic neuritis could be increased pressure from a tumor blocking it off or something so you always want to keep that in the back of your mind when you're looking at things and we look at this one and let's say that person was 20 and they have this piece of the nerve right here exactly segmental demyelination so here's that normal nerve myelinated here's some segmental demyelination so what would cause that? multiple sclerosis exactly optic neuritis and the most common thing of course is multiple sclerosis so you guys gotta be aware I'm sure that the neurologist really pounded in your head about the trials that were done and how you use your steroids and how you do IV and then go to oral and it's very interesting that study because people used to give patients kind of a moderate dose of oral steroids and it turned out that actually makes things worse and so when you see people coming in with this acute neuritis you gotta blast them with the high dose of IV steroids and then taper the oral steroids and not only does it make the neuritis heal quicker but it actually it may not prevent MS but it certainly will delay MS for up to a couple of years afterwards so kind of important that you treat them right away with the high dose steroids but if you don't you could get this segmental demyelination so this is optic neuritis and this patient did have MS and here you can see kind of a longitudinal view again this area right over here a segmental area of demyelination of the optic nerve seen sagittal now what happens in the long run on any of these lesions Eileen yeah if you look right here there's the optic nerve sheath there's the PM look how big that optic nerve space is and it's not that there's fluid in there pushing it out it's that the optic nerve is shrunk and so anything that can damage it ischemic, inflammatory, compressive, whatever eventually those axons can start dying off and then you get shrinkage this isn't a trophic optic nerve this is an end stage how long does it take when you've had say an acute ischemic episode of the nerve for that nerve to turn pale yeah weeks at least maybe even months and so when you guys are looking in there saying well that nerve looks pretty good that can't be ischemic now because it takes a while for those axons to really die off and for that nerve to turn white and pale so it could be weeks maybe even a couple of months after an event for the nerve to turn pale and eventually it gets a trophic alright Lee what are we seeing here what else are you seeing when you look here again because I know you don't have depth perception in a flat picture we're here look how full that superior sulcus is and you know that's the normal side so when you see it by that our picture the first thing you gotta do is say jeez which eye is abnormal so you're looking here saying which of those two is abnormal but if you look right here look at that sulcus how it's full up there and you almost get the idea that that eye is pushing out something's behind it pushing it out how old is this patient I would guess yeah so they're an adolescent they probably think she was like 10 and so you've got this unilateral kind of proctotic eye there's a fullness somewhere behind it it looks like it's sticking out and then you look in and you see this what are you seeing here exactly are they people call these coradal folds so what are the causes of coradal folds okay and where would the mass be located usually anywhere in the orbit or a particular place in the orbit okay which place you did answer the question you credit for that yeah which particular place so what I'm getting at you have to sometimes play guess what the the person thinking but a mass within the muscle cone behind the eye pushing forward can give you these coradal folds yeah I was taught that you know coradal folds that means there's like a tumor in them so you should be really worried it turns out that's really not true when people look at a bunch of patients with coradal folds it turns out the most common cause is actually just a hyper-opic eye that's kind of flat on the posterior surface you know we used to get excited about these we said oh my god we have border CT scan right away and it turns out you know a hyper-opic eye that's kind of flat can give you coradal folds too so it doesn't necessarily mean a tumor but if you do have a mass it means a mass in the muscle cone all right so this is what happens if you and this is a little over exposed but this is what happens if a mass that's in that muscle cone long enough and causes problems this is a totally atrophic optic nerves you get total atrophic nerve all right so we're looking at the scan here and what are we seeing in the scan so there's a mass right behind the globe exactly so what do you worry about if that was indeed a 10 year old and that was this girl scan okay exactly so you worry about an optic nerve glioma and so what cells do the gliomas arise from astrocytes and so when you look at astrocytomas anywhere in the central nervous system they're graded from grade one the most benign to grade four the most malignant what are the optic nerve gliomas usually uh-huh what astrocytoma grade grade one exactly and so people used to call these juvenile pylocytic gliomas that means hairlike and I'll show you the path why they came up with that but the key thing is these are the benign now Brandon they're growing in the optic nerve they can cause a lot of damage to the nerve and if they go back into the chiasm they can cause damage to the other eye but these don't metastasize they don't spread they're a low grade a grade one astrocytoma and here we can see one that's been removed here's the nerve here's the sheath above it and then you can see this big fusiform enlargement within the nerve itself so these astrocytes are inside the nerve and they're growing into the nerve and here you can see an eye that's been removed and you see this glioma behind it alright so an eco you can see this is why we call this pylocytic or hairlike you know pathologists spend a lot of time in a poorly ventilated basement room sleeping formula and so sometimes see things that maybe other people don't quite say really but in any event you look at this you can see where you've got these spindly cells on here and what people would call a hairlike now there is a feature on here that's real commonly seen in these optic nerve baleons what am I talking about here right there so there's these like isonophilic material the big ones the patient products are these rosenthal exactly these are called rosenthal fibers and so these are characteristically seen in these low grade astrocytomas you get these little pink isonophilic cytoplasmic conclusions and there's a close up of one and they call these rosenthal fibers so you've got this low grade astrocytoma rosenthal fibers now the one thing I want you to remember is if you have a particular tumor that's out of the normal age group in the optic nerve those could be more aggressive so you have a glioma in a kid that's usually a grade one an older adult which is really uncommon those can be aggressive and so you've got to remember if you're outside that normal age range then they behave differently but in a kid with an optic nerve astrocytoma glioma like this these are usually low grade now promise what do you do you cut the nerve out again you kill the vision you let it grow what does it do it kills the vision you radiate these well some people say yeah radiation really helps others say that kills the nerve anyway so you're pretty much stuck can I ask how often do you see optic nerve biopsies specimens very rare very rare because often we go by the scans and you'll see when we talk about these in orbit conference Chris Davidson has really nice scans that can allow us to differentiate these but we do I've seen biopsies on occasion they're very rare that you see them the one problem is if you have what you think is a astrocytoma and you do superficial and you just get the sheath itself you can often get a little reaction to the meninges overlying it but almost looks like a meningioma so you gotta be really careful when you read those superficial optic nerve biopsies you don't over call it this is what I mean by that this is an optic nerve glioma here and you see it's growing inside the nerve squeezing that nerve down but overlying it you get this reactive meningioma proliferation that wasn't a planted question and so you can get this reactive meningio change overlying it so someone does just a biopsy of that and say oh my god it's a meningioma that shouldn't happen in a 10 year old and so you can get this reactive meningioma proliferation but underlying it here's that tidalcytic astrocytoma under here with this reactive proliferation of meningioma overlying it so you gotta be really careful when you do a biopsy that you get this is a glioma with astrocytoma proliferation of the meningophenyl cells Chris what are we seeing here so it's like a propotic right eye with subcutaneous hemorrhage probably you hear that alright so you worry about again something behind that eye pushing it back now the other thing you can say is you can say that this is probably a little Greek or Italian lady because they've got the mustache you are allowed to make fun of your own kind so I'm pretty comfortable with that so I thought it was normal when your grandma would kiss you when you were kid you'd get that little pickle from the mustache so she could also be Greek alright so what are we seeing here Chris what more specifically I'm showing one feature here that's a little funny from an early call that it's a shut it's a shut I mean so if you think about it if something squeezes the optic nerve slowly slowly go and lesion squeezes it it starts getting you can get these shut vessels almost like you get in a central retinal vein occlusion where you can get some shut vessels at the optic nerve and so this is a some more ice cream what is this showing it's like a fusiform lesion on the right talking nerve running parallel with the nerve yeah so what we call this fusiform because it's not in the nerve you know tapering and then growing and tapering it looks like there's something around the nerve and so radiologists they don't sniff form on but they sit in the dark too and so they're pretty better hallucinating and so what it means is there's a nerve in the center and then there's like some thickened tissue around it and so they call this the tram track sign and this is of course the ultimate example of that huge tumor that is pinching on the optic nerve in the center and so what kind of tumor is this meningiomy exactly so I showed you those pictures of those reactive meninges but this is truly like squamous cells they have this pink cytoplasm you see the nucleus with conchromatone and nucleolide there and this is what they look like so if you look at that they almost look like squamous cells and again like squamous cells they often form worlds but in these menygothelial cells when they start to grow you will get these concentric concretions of calcium and hyaline what do we call those somomobodies and how does that spell yeah so there's a double M in there but it's a PS somoma and so somomobodies and these are these concentric calcified concretions that are in there and they almost look like the little squamous worlds that you get in a squamous cell so they look kind of similar when you look at they originate from the arachnoid subarachnoid space now sometimes they can come from meninges senoid wing and come out they can come from the menygothelial cells there and go back and so they can start from any one of those different areas kind of like a astrocytoma these aren't really malignant cells that metastasize but again if you're squeezing the optic nerve you can cause a lot of damage students it's tough to go in there and try to peel these guys off because once you do you kill the blood supply to the other side and you can have a re-put-together sagittal scan here Rhys they pull this mass behind the eye alright so another intraconal mass so we've talked about stuff that can come from that intraconal area around the optic nerve we have gliomas we have meningiomas what else can grow there that's but what else so what other actually there's one other one that may not be coming from the nerve itself or from the little nerves kind of adjacent to it schwannomas so you can even get schwannomas in the intraconal space not common but you can get them in there and now what is the classification that we do for schwannomas a pathological classification exactly so for once there's a pathologist who like wasn't an Austrian or something so an antony named the cell top and there's antony A and antony B characteristic proliferation for the schwannomas so which one is this one this is antony A so it looks vesicular so it kind of looks like you ever see flocks of birds how they kind of sweep together and so that's what this looks like it looks like a big flock of birds sweeping together so this is the antony A running acid and all that around them so I don't think there's a difference prognostically these are very rare but you can get schwannomas within the cone that can't affect the optic nerves okay so say goodbye to the grand ketones and sir so that's coming from the adjacent nerve not the actual optic nerve exactly usually it doesn't come from the optic nerve itself there's little nerves that kind of run around it too but it can't come the grand ketone the middle one has had glaciers on here for you know since the last ice age receded and over the last 20 years those glaciers have receded so much because of you know global warming which is a plot from the Chinese to you know hobble our industries but for some reason that plot that false thing has caused all sadly just in the years since I used to go up there on high call all the time the glaciers are just melting away in another couple decades of record heat you're not going to have any glaciers up on the grand anymore just be bare rock in August alright so with that political aside that I had to speak in there next week we'll be in orbit so know your orbit because there's lots of stuff in the orbit


Snapshots from 1998. A season of greatness. On July 3rd, Andy Pettit threw a now unheard of total of 144 pitches in a complete game win over the Orioles at the stadium. It was one of 16 regular season wins for Pettit during that magical year.


Good morning to you. Welcome back. This is Why In The Morning. My name is Ram Aguco, because we apologize for the technical glitch a few moments ago, but of course this conversation continues right here on Why In The Morning. And of course keep talking to us. The hashtag is Why In The Morning at Ram Aguco and at Y254 Channel. That's where you can engage with us. Because we value your feedback, let us know where you're watching us from and I shall sample your comments a bit later on during this morning conversation. So as I had mentioned earlier on, we want to talk about matters concerning building our skillset in mechatronics. And we want to find out what mechatronics is all about and how best you can be able to harness these particular skills here right here on Why In The Morning. Before we went on that particular break, we had a conversation with a particular set of students that managed to go to the world skills competition that took place in Namibia. And of course particularly these skills were meant to showcase the skills of our Kenyan students in regards to the skills and institutions that they are in the world skills Africa Swakup Mood 2022. So world skills Kenya participated in this event and of course we were represented as a country in Namibia and I am with the different set of students today. To my far right I am with Victoria Wanjiko, 2nd runner up mechatronics and also next to me Magoi Maxwell also 2nd runner up in the area of mechatronics. Karibuni Sana. And of course let me start with you Maxwell. We are talking about mechatronics and it may appear to be a big terminology for some. What is mechatronics all about? So mechatronics, mechatronics is a multidisciplinary course. It combines the traditional mechanical engineering, electrical engineering and computer science. It came about trying to meet the skills required in the current technological developments. See there are new technologies that are emerging that require certain skills and the traditional engineering courses that we had didn't match the required skills for certain areas of industries. So you're trying to keep yourself updated with the changing times in technology. Yes. Okay.  Mechatronics is a combination of 3 engineering courses that is electrical, mechanical and programming. You can give her your mark. Yes. Yes. Yes. All right. Yes. Mechatronics is a combination of 3 engineering courses that is mechanical, electrical and programming. And then it is as we move, as the industrial world evolves, we move with it. So we are coming to a place where we are replacing the normal workers with automation. All right. And of course this is in regards to how we can be able to fuse all of them at the same time. They make electronic, mechanical and engineering. I believe that's the terminology. Let me come back to you. I think your mic has been sorted out. All right. So the hammock is good. All right. Thank you.  Oh yeah. Right? Yeah. How was it there? During the competition, actually the first date was really tense because it's the first time you're competing in such an environment. Yeah. And because it's a new environment, we didn't know what to expect. We didn't know how our competitors from other countries would behave. It was really tense, but in the coming, the next day until the competition ended, I think it became more familiar with the equipment and everything. I think it was fun after that. It was fun after that? Yeah. But Katonix, how was it for you going to Namibia? It was a nice experience that I can say. It was still the first time for the both of you? Yeah, it was the first time. It was a nice experience. But I could learn new things that you didn't know. Yeah. And it was a learning experience. But for many, you have mentioned this a bit earlier on. We look at mechanics or mechatronics as a man's kind of a thing. Not a man's kind of a business. Yes. Have you received such sentiments from people? It's challenging. For us, he's doing mechatronics. I'm the industry mechatronics. It is a duo system. It was introduced by the Germans. It is 50-50. 50% you are in school, 50% you are in industry. So, we can get discriminated by men in industry. We will soon see that machines will prevent mechatronics from pushing apenas. Players will tell and there will be all sorts of things. So you look at mechatronics. It's kinda different. Stuff like this, it's in the books more. we go through a system when it was introduced in 2020 we get through the reading, so you can see how we would get into our classes Right now you have practical sessions and when you go to the industry and you have some practical lessons twice a week then you are into school three days a week So is this a form of gender discrimination and gender bias? How have you managed to go above and beyond these kinds of discriminations? See you try to prove them wrong. Kwa kwa ambia kwa ambia no. This is my skill. Una kata. Or asmua onkinshumgumu. Asgo kwa asmau. Ia wana oka demo. See aki sama di samawa. Aki sama di samawa. Lakini, siun, halan baadu. Jugu kwen na pala kutumu atumu? Wana. Going to Namibia. S� kwa kwa hatu kwa kwenago Waveko? Sama b sizesu na kona? Kwa bagu na kenya na flagi? Kwa wana na kwa bagu na kwa wana na kwa kwa kwa nanku? Kwa bisha kwa wana na kwa bagu na kwa kwa karimapu na kwa? Kwa bisha kwa kwa bisha kwa kwa kwa arikufu na kwa? I believe we are going to get a few photos that are going to be displayed in a bit so once the photos are ready just let me know these and then we can just take a look at how it was but let me come to you What are your thoughts in regards to this skill of mechatronics because there is this perception that it's not something that people need to go to school to learn you know the people who just go and they want to do furniture in the hood Okay so obviously there's those people that will prefer to learn from themselves and it's okay up to some point but I think learning for yourself it brings a lot of challenges with it because such a heavy cost it requires a lot of equipments and a lot of equipments and supports and doing that but I don't think you can manage Before you continue I'm seeing the photos are coming up on the screen this is you Ya that's us with the team leader What is that device that I'm seeing on the table there Okay that's a simplification of an automated system like in traditional manufacturing systems there's like a lot of people working on the same thing like there's someone moving past from here someone controlling this and that but I think for what we built is a system that only requires one person or even sometimes nobody to run it just runs by itself That whole piece is it the whole thing from head to toe it looks like yoyote Ya the whole thing You built it Ya you have to build it from scratch From scratch Ya and then you have to program it to do certain things Let's go back to the previous picture this one here So I'm looking at the wiring and the cabling system and the technology there How did you come by all this particular idea and putting them all up together Yes to you Ya so many creativity and your mind the brains That is a robotic arm Now we came to the industry You see like example if you go to the industry Let me use Coca Cola We came to Coca Cola See that there is someone who is feeling the juice It is the machine that is feeling If you cut a certain level in the same image and then it goes to the next So that Ya yoyote Ya yoyote Like that you pick once something from one place to another Then the process continues Okay You thought on that How did you come up with this particular idea Was this something you carried on there in Namibia Ya so during the compression you are given certain instructions And certain pieces And equipment that you are supposed to use Then it's up to you to come up with the best way Of how to combine the equipment and all the electronics The wiring and tubing and everything To come up with your own system So I think it's purely your imagination Your imagination and from the knowledge that you had from school And the training that you had before going to Namibia I think it was just purely You had to come up with something I think this country Do you think we need more of this in Kenya? Ya Ya sure because most of the manufacturing in Kenya Medium Kenya is more of an importing country than an exporting country And for us to reach that economical milestone That we desperately need We need to manufacture stuff in Kenya Locally in Kenya And bringing mechatronics engineering And systems like this It will help in improving Proving the manufacturing capabilities of Kenya And we do not necessarily Have to depend on western nation countries To help us setting up the systems Because in Kenya we have the skills to build such things So is this the day of the event? Ya, that's after the event Or this after? Ya after the event After the closing ceremony Ya? The closing ceremony The closing ceremony Ya I'm seeing your team leaders They are Shrada, Joseph and Oxyrenmy Just the four competitors Hey Wow I cut off 40 parts Interesting How did it feel? You day in the event Was it your recognition And second on yourself For mechatronics? Ya And I hope for the best But it was nice Bado Since it was the first time to compete in such a skill And we don't have those facilities Those machines in our country So we tried Ya, I believe you did It's not easy to come Second runs up It's not easy on that particular day Apani, this is I believe this is you Ya You look at the vizganis That's the same machine Ya, the same machine Ya, that's the same machine Same day The last day The very last task And this? That's me Same thing? Looks like a CPU or computer The wiring of the system Ya It has a brain, a controller It's like a PC But a PC That was developed specifically For industries Because industries have high conditions High temperatures And all of that So they have to develop A certain controller That meets the needs Wow And what is the feature For that particular device Now that you've managed to make it up Is it Is it still going to be Something that you are going to Build up on, work on Or is it ready for usage? I think the main idea Behind the entire competition Was just building us It's like a prototype Of a system So after building it I think After the experience that you had In building the system Much skilled A big and better one Ya, big and better That can do a lot of manufacturing And stuff Does the size matter? Yes, it does matter Comparing to Ni niniu na manufacture Because There's different types Of products In manufacturing industries You find that there's Manufacturing, for example Chips In electronics That requires a smaller Sample of the machine But in developing every machinery You require very huge machines Ya Ulipea challenges Ga ni kwa ii kompetitia ni mulianda Uka face That you have managed to Come over Just a few challenges that you face What challenges do you face? Challenges The machines We are not familiar with them So it's our first time Ulipea machines stuff out Different You don't have such Stations In Kenya So kupa taiso parts Kwa zi combine it was challenging Kujoe inafaku nda And the connection Uki pata People from South Africa and Namibia They are familiar with those machines Since wana opanyanga Wana tumiyanga sana For their training It's time we brought those things to Kenya To relate as to kwa nazo pia It's good to relate to kwa nazo We get to learn more It's a fact that we don't have a particular Ya Do you think such an endeavor like this Ya, it can Since We are growing So as the industrial world is Involving Waki let us search machines Those industries in Yazina Is a more automated system Will come and buy Bado it a great employment to the youths Waki sooma As a pata job Challenges can be made In this whole competition I think The main challenge As she said Is familiarization with the equipments Most of the equipments That we use in mechatronics Are not available in Kenya Because even in our school I think it's two of them But it's just two For you to compete favorably With other countries like South Africa and Namibia And the rest You really have to invest heavily In the equipments And a lot of training and experts That we need to help us in the training So I think the main challenge was We are not familiar with the machines And I think that was the main challenge And how long did you take While you were there Because I'm trying to look at the duration You have to take to familiarize yourself With these machines How long did it take How long did it take It had to take you time It took time Because the competition It went for four days The first day you had to familiarize yourself With the machine Love to go through all the equipments And then in the second day That's when the competition started You're given five hours To do a certain task Assembling the session It took the entire four days But the first day you had to accomplish A certain task So the first day you do a certain task Then tomorrow you do a certain task So by the end of the competition Your system had to work It had to do something So these different tasks Are they meant to build one particular item Or are these tasks for different items It builds one complete product After the fourth days Those four days You are given two stations First day you have to assemble the first station It works completely The second day they have a station That day you do some changes And the fourth day still you do some changes On the sensation But it had to work as one And if you don't manage to finish it up On the first day You're still allowed to continue the second day Yeah you'll continue But you don't have time That's your task That's your siku If you don't finish the first day You have to continue the second day And then you have a second day Badu uta itabidi umalize It's basically the first task The second task depends on the first task So for the second task to work It must be the first And if you delay on the first day You've messed up in the one on seven Then you must have been challenging Yeah this is really challenging Let's look at the support that you got The support system that you have So again I come and support you In this whole period That I am a tisha Or I am going to encourage Or I am going to think about it Yes Most people would say My family Then my teacher And the Sponsors The Jaman Sponsors who are sponsoring us And still the FESTA and UNESCO people All right Support system I think the big support That I had was from my lecture And he was also an expert I think he was the one That encouraged me to like To work on Because sometimes we had to stay at school Until later night practicing Practicing Practicing They are building the machines And apart from Apart from my professor I think it's my family I had a very supportive family My sister My sister bugged me all the way From the beginning Because Only the training Only the training It took a lot of time A lot of time A lot of resources And I think My sister really helped me And also The government Without the government We wouldn't be here today Because they helped you to move there The sponsor The government UNESCO No I'm really interested in finding out The perception that Because we need to change the narrative And build The skillset in the country Do you know What is your take on the guys Let me start with you How youths perceive This particular area Of mechatronics And whether we are actually building This particular skillset Or from the Kenyan youth I think for most of the youth For most of the youth When it comes to engineering Or engineering in general It seems like a really hard A really hard course For me to say Course or a skill But as we see As time changes We have a new platform Where they can learn the skills For example Tiveta Before Mechatronics was only offered In universities as a degree But for the reason Tiveta started offering mechatronics In Tiveta And also polytechnics They are offering mechatronics So there are a lot of platforms Where you can learn Or you can gain the skill of mechatronics You don't necessarily have to go to university Polytechnic Most polytechnic Offer the course Tiveta And I think mechatronics For everyone And anyone can actually Yeah you can In terms of mechatronics Youths How are you building Youths in the Fawa Or change perception How are you going to change skills How are you going to make mechatronics Because you know You don't know You know what This skill See how are you You know If you don't know You have to learn it And if you don't know How are you going to change your perception Of youths How are you going to change skills How are you going to change skills Most youths I am a mechatronics Engineering In general I am those genius people I don't know how to manage It's not hard So you are an engineer Yeah I am a genius I am an OP See how I am It's just only you commit yourself Yes You can be a mechatronics And how about youths When you ready to pick up challenges For mechatronics See what Yeah You can say Like How much do you do I am an engineering How are you I am an industry mechatronics You can say See how much do you earn I am an engineer Unafanya kusngumu ya kushtua kijiji na kushtua. That is what they say. Raki ni singumu. You can still manage. You didn't pass. You can still do engineering at a lower level. Unaza pitaweyum tu menyali nda university. Unajaga 2 koses poli poli. Unaza pitaweyum tu poli poli. Unaza patawe kuna more skills Than that person went to do a degree and yet you have done either certificate or diploma or artisan in engineering. Unaza unaza from certificate level. Unaza unaza at artisan level. Okay. Then we upgrade certificate, diploma and degree. Alright. Anybody can do this course. Anybody. Upana. Nani unaza utaka ula ula utaka kupanya engineering. And you didn't pass. You still can do it. And you can make it. I want us to do this kind of a physician to close. Of course, I want us to wrap it up. And let me give it time to have a final word and let me start with you. Ongependa kuhambiya mayutsunini doors skills is is not that I If you have a skill, you can find a platform that values your skill, that is able to push you to the next level, and you can build your career out of that. So just finding what you like, what you are really good at, and the right platform. You can build your empire from that. You can build your empire from that. I love that. What I can say, baza zi apo enja wa support wa toto awo. If it's a girl, aki kuja kuambia na takapanya engineering, senza kum discriminator muambis jiyu, ka misi mamangud, hangi ni supportin muambia na takapanya engineering, hangi ni support singekua apa. So neza takapanya muambia, mischiana aki kuja kuambia, ama any gender of a child, aki kuja kuambia na takapanya e engineering, muambia ni supportin. So you don't know, ama you and your passion aki. Still, kuambia na takapanya kukini, muambia jiyu na geuza mila. We are still going with the time. We are not in the 19th century or in the 21st century. I love what I would like to tell a girl out there. What a man can do, a lady can do it even better. So engineering is not only for men. It is also for social media in case you want to follow me. You can follow me on Instagram. Me on Instagram you can follow me at Torishiku. That's understand. That is Victoria Majiko and Magoi Maxwell. Congratulations guys. I wish you guys the best. Keep doing what you're doing. I want to appear to change the industry and make electronics. We need most of this equipment in our garages. Tuziwa na kila paali. Nikiya na garia ngo paali na jiyu na komba, ni machine ni tahanl. Mituwa nuna kuandolaf, ni niruli nyuma ni nipatespana ali sahum. Thanks for coming. I appreciate it. Of course that is the end of this morning conversation right here. Why in the morning? And of course it's all about matters concerning training, skills training in mechatronics. I hope you've learned something. I have. Keep talking to us. The hashtag is why in the morning at Ram Aguko at Y254 Channel which is the official station handle. That is us to the end of this conversation and of course keep talking to us. We are taking a short break, a musical break but we'll be back to wrap these up in a bit.


Hi all, Salvatore here. I'm coming to today with an atypical video. It's a video about how to manufacture grievance and enforce academic intolerance, and it's based on my own personal experience. In fact, an experience I had today. Today, I received a letter today, Australia time, that is, it was, I guess, December 4th in the US, December 5th here in Australia, addressed to the editorial board of the International Review of Modern Sociology. Now, I do sit on the editorial board of the International Review of Modern Sociology. It is a rather obscure sociology journal. I've been on the editorial board for some 20 years, and I don't think I've even heard from the publishers in the last 10 years, but luckily, I found myself receiving this letter, and I say luckily because it gave me an insight into this whole anti-Hindutva madness that I've heard about, and I've recently been involved with, but which, well, at the time I got involved with the International Review of Modern Sociology, I had no idea about it. I'd never heard of Hindutva 10 or 15 years ago. Okay, now, of course, everyone now is aware of the Dispandling Global Hindutva Conference, the notorious conference from 2021, with all these letters of support from various organizations, including terrorist organizations, which I think is very funny that they include them on their list, and very typical academic conference, right, in which you give fact sheets on the RSS, and you tell people how to respond to being trolled by Hindutva activists, and you hear all the amazing, you know, all the universities involved with it, co-sponsors. I mean, this is a, well, anyway, let's go to the letter I received. I received a letter today. addressed to the editorial board, and this letter was about an article recently published in the International Review of Modern Sociology, Global Hinduphobia Construed, Constructed, and Unleashed from the West by a scholar named Lavanya Vemsani. Now, I had never, I've since looked her up. She seems a perfectly respectable academic, but I had never before heard of her. I hadn't read this article, but I did go ahead and read this article when I received this letter as a member of the editorial board. It was my duty. Now, the article, this letter, makes several very serious allegations.  Okay, well, I mean errors and citations are pretty much par for the course for an academic paper. Okay, worse, this article also contains numerous inaccurate factual claims, and distorts and misrepresents the scholarship of other scholars. That sounds serious, something I should look into as a member of the editorial board. And finally, some of these distortions falsely and irresponsibly attribute shocking views to other scholars, which is potentially libelous. Oh, well, I might get sued as a member of the editorial board. They're shocked, shocked to find that the journal's peer review process did not catch these multiple errors, and they go on to tell me about, you know, our processes on the editorial board. Okay, thank you. Okay, then they offer evidence that the paper presents a narrow one-sided view of historical events and contemporary protests. Well, if it really did that, it would be a pretty typical academic paper. And now here, the works of several scholars mentioned in this publication, so a one-sided view of the works of the scholars, and they go on to say, you know, they go on to very virtuously opine. We live in a politically charged climate where scholars bear great responsibility not to exacerbate forms of majoritarian oppression and bigotry, and to examine political claims and ideology with care and nuance. And so, of course, we would expect these undersigned academics to examine political claims with care and nuance. And who are these people?  These are both senior academics, Eaton and Hatcher, and Northwestern, and there we go, Rutgers University. So I'll let you be the judge of the reputations of these scholars, but they all are establishment scholars, and they all do have, you know, established positions at major American universities. So let's look into their claims.  Here's the article they are unhappy with. Global Hinduphobia, construed, constructed, and unleashed from the West, a kind of, you know, third-world scholarship that most of us in the social sciences tend to be sympathetic to. So let's take a look at it. Let's see what they say about it. So here is their analysis. This comes from the undersigned, the six good professors. So first, the first problem with this article, distortions of the scholarship of other authors, an inaccurate citation. So false references to Richard Eaton's work. Well, let's check what Vemsani says about Richard Eaton. We'll go to her article, and let's actually just search for Eaton and where Eaton is mentioned. All right. Eaton is mentioned claiming that Hinduism is not a religion, or Hinduism is only called such in the 15th century. And there are a list of three references, one of which is Eaton. Eaton may or may not have said this. I don't know. But numerous theses and books have been written noting that India did not have developed cities. Did Eaton claim that? Honestly, I don't know. And denying temple desecration and genocidal work. So these are claims that Eaton did things. Now, I don't know if Eaton actually said those things. When I go to the review, it says none of the works attributed to Professor Eaton are listed in the bibliographical references at the end. And that is, in fact, true. I searched, of course, and, you know, I'm sorry, Professor Vemsani, but, you know, you're a passionate author, but you are not a very good, a very good compiler of citations. Your reference list does not include Eaton at all. What's more, your reference, the reference list here isn't even an alphabetical order.  Then, you know, then it starts again with B. So there's a second, you know, starts a second time. This is not a high quality citation list. It looks like two citation lists squeezed together. That said, it doesn't sound like anything really terrible is said about Eaton. I mean, maybe the claims are right, maybe the claims are wrong, but they're pretty much par for the course. Eaton should probably be pleased that someone bothered to cite him. I certainly would be. No one's ever cited me correctly, but I'm always thrilled when they cite me. Okay, and a other scholar's name is misspelled. Well, again, you know, hardly something that I would be concerned about. It doesn't rise to the level of, you know, distortions of scholarship. Now, did Eaton actually say those things? They say he has not denied Temple desecration, but he has placed them in the longer history of state building and political formation. Now, you know, what did she say about it? Well, you know, doesn't seem like she says he denied Temple desecration and genocidal wars. Well, there might be a little bit of academic argument there. I don't know what the truth is. It's pretty subtle if it exists at all. Strangely, the six good professors criticizing this paper say that, in fact, two of the three works citing Eaton are impossible because he published nothing in 1990 and 1991. Now, I found that an unlikely claim. This is a very highly published author, so I downloaded his CV. And, you know, sure enough, on his own CV from the University of Arizona website, I looked for what he published. Well, there you go in his list of, this is a list of his own. I'm going to scroll, scroll, scroll, scroll, scroll to show you what this is. This is a list of book chapters that he has published and, well, turns out he published an article in the Women's Studies Encyclopedia when in 1991. All right. He also had a book banned, but let's forget that for a minute. So he had this published. Now, what about 1990? Did he have a book chapter published in 1990? Oh, there we go. Human Settlement and Collelation in the Sunderbond. So, again, I don't know who's right and who's wrong. I'm not going to do a full review of Eaton's works to see. The claims that are being made here, that these citations are impossible, well, that's clearly wrong. I could write a letter back to them saying, the claims you've made in your letter are clearly mendacious. After all, Eaton's own CV shows this. If I were so uncivil, I could do that. But of course that would be ridiculous. Now, the suggestion is that, you know, Vemsami does not engage with Eaton's claims. And look, I've been cited, well, a couple of thousand times and almost always it's just a long list of citations. And it mentions that, you know, Salvatore Bobonis is one of the people who said certain things and half the time it has it backwards. I'm not defending that. I'm just saying that to give me, let's see, one, two, three, four paragraphs in order to say that someone's work doesn't say what they've been cited to say. Well, if the work had been cited to say something really horrific, all right, you want to deny it. But these are pretty anodying claims being made about Eaton. Eaton suggested that India did not have developed cities until the arrival of Islamic invaders. I don't know if that's true. Actually, this is one that the authors of this letter don't deny. They simply deny that he denied temple desecration and genocidal wars against Hindus. Well, you know, is this sloppy citation? Absolutely sloppy citation. Does this warrant a letter to the editorial board saying that we should withdraw the article? I think that's a bit extreme. Okay, then we go on to Distorted References to Brian Hatcher's work. Now, this is the only, I believe the only citation of Hatcher in the whole article. And let's get it. Hatcher, all right. And I think that's the only one. Yep, only one. So Hatcher's only cited once in this entire article. All Hatcher is cited as saying is that Hatcher penned an essay that was purported to be evil since it was quoted by an evil fox. Now, that doesn't seem defamatory. Again, I don't know if it's right or wrong. What doesn't strike me as really something I would write a letter to an editorial board authored by myself and five of my colleagues saying that this article should be withdrawn because how dare they say that I penned an essay saying that a fox was evil. Again, maybe right, maybe wrong. I'm not defending it. I haven't gone into it in detail, but it does seem a bit over the top. They're saying that they got the year wrong, but of course there are many ways to get articles online and often the year doesn't match up with what was given in a particular reference. Now, to complain about this one sentence in the Vemsani article, we have one, two, three, four paragraphs. Well, that seems a bit extreme. So if we take the first half of this letter, the first half of this letter pretty much comes down to Vemsani's citation was sloppy. All right, Vemsani's citation was sloppy. You know, slap on the wrist. Please don't do it again. The rest of this letter is a really serious part, buried farther down in the letter, but the really serious part falls apart when you start looking at it. So the author of Vemsani, the author of Global Hinduphobia, claimed that the first Hinduphobia in North America began in the 1880s. Now, that would seem to be a pretty anodyne statement. After all, we know there was a lot of Hinduphobia when Vivekananda gave his Chicago speech in the 1890s. So we really want to question that there was Hinduphobia in America in the 1880s. Well, they want to question it because they accuse her of calling Sikhs and Muslims. Oh, and also Hindus. They accuse her of claiming that Hinduphobia, they're appropriating the Hinduphobia that was directed at Muslims and Sikhs as well as Hindus. Now, again, they're going to give me half a page trying to deny. They're not actually denying that there was Hinduphobia. They're not even denying that she was correct. They're saying that the evidence she gave showing that there was Hinduphobia in the 1880s was not proper evidence, although they seem to be open to the idea that there probably was other evidence that there was Hinduphobia in the 1880s. Okay, well, that's a bizarre claim. All right, then we get into the more serious ones about the Roma. So Vemsani does appropriate Roma as Hindus. Now, that's not very surprising since Roma are widely acknowledged to have originated in India. So if we search for Roma in the article, she says that Hindus were not aware of atrocities. So here we have historical atrocities against Hindus are not recorded. Okay, that's a reasonably reasonable and reasonably correct claim. Hence Hindus were not aware, but one of the groups subject to genocidal treatment during the Second World War were the Roma. Who were the largest Hindu groups subjected to various humiliation for centuries before? Now the question here is, is she appropriating the experience of Roma people who died in the Holocaust? Now, this is something we could debate whether Roma are Hindu, whether there's a broad conception of Hindu that includes Roma who are not practicing religious Hindus, or should Roma be considered an Indian origin people who are not Hindu? That would probably be the majority view. But again, she doesn't seem to be in some, she's not denying the Holocaust. She's not doing anything terribly bad about Roma. I mean, this is an academic disagreement over the status of Roma. Okay, reasonable enough. But they're saying calling them Hindus without basis and denies the unique Roma cultural religious identity. In other words, she is somehow herself committing a cultural genocide against Roma by appropriating them as Hindu. Well, that seems a bit far-fetched, but you know, there you go. And again, we have a couple more paragraphs. Now they claim that the reason she's doing this is to help Vemsani make a sinister link between modern scholarship on Hinduism and Nazi propaganda. In other words, she is effectively suggesting that attacking Hindus is Nazi propaganda.  Now, again, is there some way you could make that seem to stick? I mean, if I look for Nazi in this article. She does suggest that the steps of Nazi propaganda are replicated in the documents and comments included in the Dismantling Global Hindutva Conference. All right, well, if we look at the Dismantling Global Hindutva Conference, I could see that there are all these associations being mobilized to promote or to isolate a group of people. That's maybe a bit of a stretch. She also mentions the poster for the conference, somehow reminding people of anti-Jewish propaganda from the 1930s. Well, that's not so much of a stretch. I mean, it is kind of a socialist realist sort of poster. We see these RSS members, clearly people dressed as RSS, giving an RSS salute, being uprooted with a hammer. I mean, the claw of the hammer is literally uprooting RSS volunteers from the soil, presumably the soil of India. They're colored saffron, so they are being associated with Hinduism, and they're being uprooted by presumably people of ostentatiously different colors. We have two right hands on the claw of the hammer, which turns into a pencil. Now, I think it's probably going too far to call this Nazi-like poster. On the other hand, is this a typical academic conference?  I mean, this is certainly no ordinary academic conference. So, you know, a little too far on both sides, perhaps, but maybe not so too far on Vemsani's side. Now, they disagree with her characterization of the Hali against Hindutva celebrations, and fair enough, they disagree, but people disagree on lots of things. If I go again to where she actually wrote about that, there are debates on Hindutva versus Hindu, and she said that this has reared its ugly head in the form of Hali against Hindutva or Diwali against Hindutva organized on campuses across the United States. She acknowledges that such distinctions do not exist. Well, fine, that's her opinion. Others may disagree. But to say that she's somehow doing something inappropriate, or she even acknowledges explicitly here that Hinduism constitutes multiple practices. Again, it seems like, you know, fine, they disagree with her, but there's nothing really evil in the paper that I can see. Then she goes on to make the point. Some disgruntled politicians with support from academics and activists have made it their mission to propagate this misconstrued, divisive narrative as the progressive representation of India, blaming all Hindus who do not subscribe to this divisive narrative as Hindutva, or worse, sometimes referring to them as Hindu extremists and Hindu fanatics, even though it is utterly senseless to link religion and violence. Well, that sounds like a perfectly liberal, reasonable response to what she perceives rightly or wrongly as hatred directed against her and her community. All right, well, let's return to the review. They take issue with the fact that Vemsami claims that Hindutva as a term only means Hindunas. Now, again, this is something that is highly contested in India. Fine, she can feel this way in a paper. The fact that they feel differently is not something that really constitutes an issue for the editorial board of the journal. She calls the Hindus of India indigenous. Well, again, are the Hindus of India indigenous? Well, by one way of looking at it, absolutely yes. You could look at it a different way, but, again, that's a matter for opinion and for legitimate academic debate. The authors, the six authors of this letter seem to imply that she is somehow maligning indigenous people just as she has maligned, in their view, Roma people by appropriating these narratives. Okay, then we get to the final conclusion. Vemsami's essay also includes multiple unsighted claims. These are highly damaging to the scholars in question, and that's the basis for suggesting that we, the editorial board, might face the legal penalties of... And this goes back to the accusations of defamation and slander, but really all we have here is some sloppy citation. I mean, when I go through all of these many claims, all I come up with, and this is eight pages of claims, all I come up with is some sloppy citation errors and academic differences. Now, if I go to the paper itself, I can find much more serious issues that need to be discussed. So let's go to what the author actually says. First, she says there are a few important points I would like to stress before proceeding with my examination of Indian studies and Hindu studies and the rise of Hindu phobia. This examination is not focused on any individual academic, but on the general trend of partial examination of Hinduism noted in the academia, not very good English there, which can be generally traced to the colonial beginnings of Indic studies. In other words, although she has cited these authors, two of the authors who are writing the complaint letter, she has cited them, she has potentially miscited them, she has not attacked them. In fact, she has stressed that she is not attacking them. They've only been cited in passing as part of the background of this study. Okay, let me go a little further down to page 13. Let's see if I can get there a little more quickly. And here we go. Now, what has she experienced? She experienced, in June 2019, she had a call for papers for her own association, the American Academy of Indic Studies, an annual conference. She just posted an announcement of this conference on the ListServe Indology list. What did she get? She got the association and the scholars associated with it being canceled. People called them Hindutvaists, and the association pulled down their announcement. Okay, they went to another mailing list for South Asian studies. She shared her call for papers on another list. And again, it was called down, closed down. They weren't allowed to discuss it on the list. Now, if anyone is showing intolerance, it's not Vemsani. Now, Vemsani may disagree with the authors of this letter. She clearly seems to disagree with the authors of this letter. They disagree with her. Now, I would have no problem with the authors of this letter writing an article. Like, if they wrote to this journal and they said, we would like a right to reply. We would like to write our own article in which we provide a rebuttal. Well, fair enough, we academics do that all the time. But to write to the editorial board is akin to what was done to Vemsani on the mailing list. That is, it was an explicit effort to shut her down. They're not trying to disagree with her in a civil way in open academic debate. They're trying to shut her down. They're trying to shut her down by going to an editorial board who are composed of people, you know, me just three years ago. I would have had no idea what any of this meant. And we would have seen this letter from six well-credentialed scholars at top universities saying that you have an article in your journal that is a travesty for all these reasons. And the bizarre tactic is instead of foregrounding with any actual allegations. I mean, if there were serious allegations, they should be foregrounded. I mean, if there were serious allegations of problems to this paper that meant it had to be pulled off the website, it had to be unpublished. Distortions of scholarship, right? If there was something truly awful in this paper, you wouldn't lead off with your number one claim is, oh yeah, these articles aren't in the bibliography. These articles aren't in the bibliography is a typographical error. This hardly rises to the level of, you know, shut down this author. But, you know, a typical member of an editorial board who's not studying this sort of thing, knows nothing about these arguments, has never heard of the dismantling global Hindutva movement, just wants a simple, easy life on the editorial board. You know, we might have called for the article to be withdrawn just so that we wouldn't have any trouble. Now, that is distasteful tactic. It's not only distasteful tactic. It is clearly a tactic that is organized, that is organized to shut down debate. I mean, six scholars, four of whom aren't even mentioned in the article, being so angry about a paper in an obscure journal. I mean, an international review of modern sociology. Look, I know I'm on the editorial board, but this is a pretty darn obscure journal. I mean, if I search for it, you know, international review of modern sociology, you can see that I've searched for it before. Okay, I can find it, but it's a pretty obscure Indian journal. This is not, I mean, they don't even have their information posted here. It's not from a major, you know, it's not published by a major publisher. You know, even their website still has the Spring 2015 edition up as its graphic. I've never even, even though I'm on the editorial board, I've never heard of serials, publications, PVT limited, you know, to take an article in a truly obscure academic journal. Written by, and again, you know, no offense to my colleague Lavanya Vemsani, but you know, Shawnee State University is not a major university. What we see is six scholars at major research universities ganging up to beat up on and vilify a, let's face it, you know, a scholar from a developing country who takes a non-western, subaltern perspective in an obscure Indian journal that probably no one reads. This article would probably never be heard of had I not made. No, I mean, I'm sorry to my own heart if I had not made this video. So yeah, this is the manufacturer of grievance. They couldn't possibly, these six people could possibly have been so upset by this article that it required an eight page letter in response to the journal. What they are doing is they're trying to shut down anybody, anybody who disagrees with them. And I would be willing to bet. And please, if you're out there and you're listening to this, yeah, send me an email. I would be willing to bet they have done this to dozens of similar articles. But anytime someone publishes something that questions their dominance of the field, they're going out to get her no matter if she's female, no matter if she's subaltern, no matter if she's at a small college, you know, they are not there to protect the defenseless. They are there to attack the defenseless in order to assert their own dominance of the field. Look, this is how academia works. This is how peer review works. This is how academic intolerance works. Sorry for such a long video. Thanks for listening. And if you want to talk to me more about it, please do email me. I'm always happy to talk to people. Thank you.