DIP Episode 87 - USMLE Step 1 Neuro Review 1

Okay, welcome. My name is Divine. I am a PGOI-1 transitional year as in that's I'm going into a biology. This will be the 87th episode of the Divine Intervention Podcast. This is actually coming exactly four days after our first year anniversary. So our first year anniversary is technically on the 14th of March and we had 86 episodes in that one year. So I really, really hope I can bid that number in this new I guess divine intervention podcast year. But big thanks to everyone that has been listening and I thank God everything has been going pretty smoothly and if you have any suggestions for improvement please feel free to send them my way. But in today's episode I am going to start a new step one topic. We're going to be talking about a neurology. That's like a Nebulous chapter in first state. So we're gonna try to break it down over a series of podcasts. So this will be the very first one and I have some slides and I'll go over some questions but I'll use those questions to cover certain bits of information. So the first slide. So we have a 35 year old female with a pass medical history of Hashimoto's thyroiditis. Presented a chief complaint of blurry vision in her left eye. H&T exam is positive for 20 over 200 vision in the left eye, but 20 over 25 vision in the right eye. She deniespin in the involved eye. Two years ago she had a three week episode of left arm weakness that resolved with high doses of prednisone. So what's your diagnosis? Right.

So hopefully this is streaming a lot like multiple sclerosis with optic neuritis. Right. Remember they have lesions and separated in space and time. And I'll talk about these things as we're proceeding to this podcast and also like in future podcasts. Right. And I mean the pathophys is basically you are it's almost like an autoimmune destruction of a person's excuse me. It's an autoimmune destruction basically for persons like oligodine for sites. And then and again I'll say some more stuff about this but I just want to answer the questions first. And then what is your diagnosis in a patient that recently had a viral operator infection? But presents with bilateral lower extremity weakness that has progressively gotten worse over the last three days. And let's assume that this bilateral lower extremity weakness is ascending. Right. This is more giomba re syndrome. Right. And remember the pathophys involves again. It's sort of kind of like an autoimmune destruction or attack against like your schwan cells. And I will give you some more details on this. I mean sometimes you can attack like my lean proteins and there's molecular mimicry and all that stuff. But that's my basic surface answer for now. I'll go deeper on giomba re syndrome and multiple sclerosis down the line. And then what are the two major parts of the nervous system? Right. So obviously the central and peripheral nervous system and big big thing central nervous system for the most part comes from the neuro tube.

Okay. Well the peripheral nervous system for the most part comes from the neuro crest. So let's say a few more things about this. Right. So let's sort of break this down a little. Right. So we know that the central I mean the nervous system obviously there's central nervous system that again for the most part is like the brain and spinal cord comes from the neuro tube. And then we have the peripheral nervous system that is for the most part like you know like derived from neuro crest includes like cranial nerves like one through 12. Subtract cranial nerve two from that equation. I'll talk about why in a bit. And then also like those nerves that sort of come off the spinal cord right so your spinal nerves those are also part of the those are part of the peripheral nervous system. Now the thing is as you'll see later right neuro crest gives rise to your peripheral nervous system gives rise to your spinal nerves. But the thing is the neuro crests are derivatives are things that are very high you'll talk really no first step one. Right. So things like your odontoblasts they come from neuro crest. All the post ganglionic cells in your autonomic nervous system come from neuro crest. Right.

So say for example like like you see pathetic nervous system remember we have pre and post ganglionic in your parasympathetic system we have pre and post ganglionic those post ganglionic cells they actually all come from the neuro crest all your cranial nerves with the exception of cranial nerve to the come from the diencephaline they all come from neuro crest right. So again these are all high yield things to know remember your the chromatin cells of your genometallia your genometallia is basically like a modified post ganglionic sympathetic neuron it also comes from neuro crest. Now and obviously right as we have a central nervous system we should have cells that might donate the neurons in the central nervous system at least the axons in the central nervous system and then we should also have a different cell type that might donate the axons in the peripheral nervous system.

The thing that does this job in the central nervous system is your oligodanger site okay and the thing is one oligodanger site can might donate multiple axons okay that's actually a very high yield thing to know for exams so all the axons that constitute like your corticospinal tract your your corticobalbert tract all these tracks that are all like descending coming from the brain those tracks those axons they are all mylineithed by oligodanger sites and then in the peripheral nervous system the analogous cell is the schwan cell the schwan cell might limits only one single axon okay the schwan cell might limits only one single axon so again very high yield to know those for your tests right and we know that along those axons those either the schwan cell or the oligodanger site be sort of might donate certain sections they don't might need the entire axon no you don't want that right because remember fat is not super good for conducting electricity so you have my lineation at different spots along the axon but there are spots along the axon that don't have my lineation right those are your nodes of Ranveer remember those nodes of Ranveer contain like Votage Gated Sodium channels and one high yield thing you kind of want to know there is that those nodes of Ranveer the concentration of the Votage Gated Sodium channels is probably what matters the most because the thing is if you don't have a high concentration of Votage Gated Sodium channels and they are kind of like spread out along the axon that is where you can begin to get into trouble right so take for example if a person has like multiple sclerosis right and they are basically having troubles with my lineation instead of those Votage Gated Sodium channels to be all like locked in in the nodes of Ranveer those sort of be spread around the axon and that basically shots of solitary conduction so you have like slower

conduction of neural impulses and that is part of the pathophysiology behind some of the problems that are observed in multiple sclerosis so multiple sclerosis right we know that it's essentially a disorder that affects that affects derivatives of the central nervous system right so all those tracks remember those tracks start from like the brain they start from like the cerebral cortex so if you start from the cerebral cortex it should make sense that those things should all be neural tube derived right so like your corticospinal tract for example so anything that's coming from your neural tube right from your central nervous system you know automatically it's my lineathe by oligodendrocytes and because multiple sclerosis is central the myelinating problem you have oligodendrocyte problems so those tracks will begin to have issues right so for example people those people have like low extremity weakness or per extremity weakness bloody bloody bloody blood right because the acotico spinal tract is basically not well myelinated if you notice people with multiple sclerosis in fact like this example like giving this question right be tend to have optic neuritis the reason they tend to have optic neuritis is because cranial nerve to the optic nerve is actually one of those rare nerves one of those cranial nerves in fact I will say probably the only cranial nerve that is not derived from neurocrest so all your other cranial nerves are derived from neurocrest right because remember your cranial nerves are effectively the second order neurons in your corticobalbert tract the first if you wanted to say define this is your confusing me a little let me explain for a bit the thing is if you look at your corticospinal tract right corticospinal starts in the cerebral cortex and is going towards the spinal cord right so the first order neurons in your corticospinal tract start in t

he pre-central gyres of the cerebral cortex those are your first other neurons those first other neurons they are derived from neurocube okay but your corticospinal tract fibers they ultimately go to the ventral horn of the spinal cord those alpha-modo neurons that you find in the ventral horn of your spinal cord guess where they are derived from they actually derive from neurocrest okay that's your corticospinal tract so the first order neurons neuro tube no issues there but the second other neurons which are the ventral horn alpha-modo neurons they are all derived from neurocrest cells so same thing with the corticobalbert tract the thing is your corticospinal tract is like the like the cerebral cortex controlling those alpha-modo neurons your corticobalbert tract is your cerebral cortex controlling your cranial nerves okay so think of your cranial nerves as like a fancy schmancy kind of second order neuron so your fancy schmancy cranial nerves actually derive from neurocrest you may say divine this looks like I promise it's not low yield it is actually very high yield to understand these things for your example so your cranial nerves are derived from neurocrest okay with the exception of cranial nerve two cranial nerve two your optic nerve is actually derived from the your optic nerve is actually derived from the from the diencephaline okay it's actually derived from the from the diencephaline so that's again a high yield thing you sort of want to keep at the back of your mind for examples so so where was I initially so okay so this is why patients with multiple sclerosis they actually tend to get issues with the optic nerve because the optic nerve believe it or not the axons of the optic nerve I actually mylineated bioligo danger sites because again they're derived from the central nervous system neuro tube okay you know I'm spending time on this but it's very imp

ortant to understand that for your exams and remember right the boss phrase you associate with a ms is like oh they have lesion separated in space and time of course they have lesion separated in time because like the lesion tend to come and go they're not like super persistent although that's not entirely true but for step one purposes that's that should be enough but they also have lesion separated in space and by that what people usually mean is that they can have sensory symptoms or they can have motor symptoms alternatively lesion separated in space can also be that they are lead like the issues they have are not symmetric right so it's rare to find it's like they don't have like their two legs give out at the same time no today they may have like right low extremity weakness to more they may have like left upper extremity weakness right so they have those lesions sort of like separate it in different parts of the nervous system okay so again those are high your things you want to know but contrast our giomberis syndrome right so giomberis syndrome is like a peripheral dimilinitin disorder it's usually after like a viral respiratory infection or after like a GI tract infection classically on exams think about a Campino-bacterge in junei with a bloody diarrhea right although that is now being emphasized on the usml is because they know that everyone has memorized that piece of information so giomberis syndrome is more of a pns dimilinitin disorder so it's more of a shwan cell problem okay and i will tell you this for the purposes of the usml think of giomberis syndrome as a model problem okay there are almost always never sensory deficits in giomberis syndrome on the usml that's a very high your thing to know from ms it's different ms they can have sensory and model issues no problems but giomberis syndrome they tend to have only model issues on the usml is right

and again it's usually an ascending paralysis starts distally and moves more proximally right and i mean at some point people giomberis syndrome if they're not treated on time they may require intubation because remember the frenic nerve is a peripheral nerve right so they could scrub the frenic nerve and then their diaphragms don't work as well anymore and then they're going to like respiratory failure right so again those little things here and there that you definitely want to know you definitely want to know for for your exam so i think that is all i want to say here so i'm just going to go ahead and jump to the next question so the next question is a matching game and again it's sort of kind of uh going to be like this where basically i give questions i'll answer them but after i answer them i'll sort of give like my reasoning and explain and then do some teaching right so matching game so it says giving the following parameters what is the most likely diagnosis right so the first one says increase the acetylcholinesteris increased alpha-fidloprotein and increased amniotic fluid index well if you see this increased amniotic fluid index is basically like mbmi code word for polyhydram meals okay if you see that on an exam i really hope you're thinking about and then cipherly okay because remember your swallowing centers are gone and if your swallowing center is gone you'll be able to swallow your pests in utero so you'll basically have polyhydram meals okay and i'll explain why the acetylcholinesteris and the afpi are increased now next question says increase acetylcholinesteris increased alpha-fidloprotein amniotic fluid index is not increased so this is actually more like spina bifida like the super bad form of spina bifida where like in fact this is not a meningocel this is not a myelum meningocel this is not spina bifida occultor this is like spina bifida where

like literally the spinal cord is hanging out outside the body it's not covered by like your meninges or anything like that there's a super bad spina bifida in fact some people call it like spina bifida i believe it like my myeluschises or something like that okay it's like super bad spina bifida but again your swallowing centers in your brain right it's not in your spinal cord so because it's more of a spinal cord defect these kids will not have polyhydram meals because they can swallow just fine now whatever person has normal fp normal acetylcholinesteris and they have like a tough tough hair on the lower back this is more of this is more of spina bifida occultor in fact spina bifida occultor many people classified as a neuro tube defect it is technically not a neuro tube defect and you see why in a bit now next one says increase alpha-fiddle protein normal acetylcholinesteris levels and it's associated with here two malformations i really really hope you're thinking about like a myelome meningocel some people call it meningome myelosell same thing especially lombus sacromylo meningocel doodas associated with the chiaritumal formations and i'll talk about the chiaritumal formations in a short while now next one increased alpha-fiddle protein normal acetylcholinesteris levels not as a chiaritumal formations whether there's a chiaritumal formation then that tells you that there should be a chiaritumal formation and again i'll explain all this shortly and then uh final one says increased afp ventral protruding structures on phidolotrosound this is probably more like gastroschisis right so you can see gastroschisis gastroschisis because now this idea literally just popped into my mind right so gastroschisis gastro a part of your GI tract scaris protruding out of the body not covered by a membrane okay not covered by a membrane remember that super bad um spina bifida i

just talked about that they call it spina bifida with myelosechisis myelose stands for spinal cord schesis means you're hanging out outside the body but you're not sealed by a membrane okay that's why that's super bad spina bifida with myelosechisis actually has increased levels of acetylcholinesteris because really if you're dura or it should be i guess a little more specific if your arachnoid is covering um the spinal cord is covering like neural elements cssf will not leak again this is a simplified explanation but it should be more than ample for your u smls cssf will not leak and guess what if cssf does not leak you will not have um uh you will not have elevations in your in your acetylcholinesteris okay so again high yield to kind of to kind of understand that so uh so myelosechisis spinal cord outside the body not covered versus gastroschisis GI tract outside the body not covered another thing that would also be responsible for the final answer i have here is um um what is it called um on follow seal although remember that is sealed by a peritoneal membrane although that is not sealed by skin so because it's not sealed by skin which is a derivative of an ectoderm your alpha-fidil protein levels will be high so let's talk about these topics real quick right so the thing is um i'll have an embryology podcast in the future but remember um that in the formation of the neuro tube um we sort of go through certain processes in fact i will encourage you to maybe go to the next slide um and let's talk through those processes right so the thing is your nervous system comes from ectoderm simple as that right your ectoderm and the thing is it's ectoderm like on the dorsal surface of your body okay kind of important to know that ectoderm on the dorsal surface of the body right uh because if you notice i've been saying oh neuro tube defects causing crease AFP but gastroschis

is and on follow seal causing crease AFP the thing is some of these neuro tube defects um think of them where as like dorsal body wall defects basically if you ever have a body wall defect your alpha-fidil protein will rise okay um but you can have dorsal body wall defects like your neuro tube defects or you can have ventral body wall defects like gastroschisis and on follow seal okay so that's kind of like they're all one of the same one and the same thing is just or is it the front of your body that's a ventral body wall defect is the back of your body that's a dorsal body wall defect so we have ectoderm again on the dorsal side of the uh faith person in utero um and then you'll have something called a neuro plate no one really cares much about that but the thing is the neuro plate invaginates and when that neuro plate invaginates right uh you form something called a neuro groove right groove is like a valley right so you have the neuro groove and then on either side of that neuro groove you have neuro folds and the thing is the most uh think of them as like the outermost parts of those neuro folds um are basically a future neuro crest please excuse these boxes over um some of the letters i try to sneak this from one note but these text boxes kept popping up i know i could pull off those text boxes in an older episode of um office but i can't necessarily do it now so i'll try and figure it out for hopefully the next up podcast because for these neuro podcasts i probably have to do a lot of drawing uh just because of the way neuro is unfortunately so so we have the future neuro crest right and then the thing is this neuro groove will ultimately close to form a tube okay so remember it's a tube so that tube has a hollow on the inside that hollow on the inside will ultimately become like the ventricle okay and also like the central canal of the spinal cord so we have t

he neuro tube closure right but the thing is the closing is like a stage closure right so i sort of think of it like a surgeon like surgeons they are certain surgeries where like they do things in stages they don't just do everything at once right they do like stage closure or fascia or whatever right same thing here right you have like a stage closure of the neuro tube the thing is the middle part of the neuro tube closes first it's kind of weird right but that's just how it happens the middle part closes fast and then you keep going and then your cranial part or your rostral part closes second and then your quadcopart closes third right and the thing is again remember your neuro crest is kind of excluded from this neuro tube so because it's excluded it's not like kept in the family it can wander and go anywhere in the body that it wants to that's why literally wonders to like goes to adrenal gland sets up shop in the medulla becomes chromafint cells stuff like that and the thing is overline all of this i mean like you don't have your spinal processes like literally sticking out of your body the reason that is is because the remaining nectarium right sort of covered over covered over your spinal processes so you don't have those things as sticking out okay so you need that nectarium to cover things over if nectarium does not cover things over that is a body wall defect and if you have a body wall defect guess what happens your AFP goes up okay but again remember a body wall defect is not the same thing as an open neuro tube defect it is when your body wall is exposed like basically nectarium does not cover things over that is where you get into elevated AFP okay but if you're dura and you're acnoid and what not covering over your neuro elements then acetylcholine estrus is not gonna leak out that's why acetylcholine estrus is more like elevations and like amniotic fl

uid acetylcholine estrus is more specific for neuro tube defect versus elevations in AFP if you can be elevated for like many reasons right down syndrome gastroscheses on follow say whatever okay so it's again these are subtle points but the thing is sometimes it's these subtle points that really helps you to ultimately understand in certain bits of information as you'll see in the next in the next slide we will for sure we will for sure talk about talk about these things so so I think I've covered most of what I want to say there right so again just to summarize right so your nervous system comes from ectoderm right and again remember ectoderm is one of those three germ layers right that initially starts from the process of gastro lesion where you from like ectoderm endoderm misoderm right so ectoderm forms your entire nervous system but the thing is don't forget though your misoderms sort of kind of contributes right so it's like if you want your neuro tube to form right it needs to receive signals right someone needs to tell it okay neuro tube time to form the thing that does that is actually notocard and notocard it's actually like floridly high yield to know for exams that it is derived from misoderm okay that sonic hedgehog business that you probably learned about in embryology sort of kind of related to the notocard which is from misoderm which again induces the ectoderm to go ahead and form the neuro tube right and again remember you go through neuroplate first that invaginate you from the neuro grooves we have the neuro crest on the outermost portions of those neuro folds and then you close you have a stitched closure right you have like middle first and then rostral second and then cordal third okay remember that your neuro crest cells can migrate and do a lot of wonderful things so if so let's talk I guess let's say some more things about this staged closur

e right so what if your rostral neuro tube fails to close right so like your rostral neuro pore doesn't close if it doesn't close that's what creates an encephaly right so basically these people like most of their brain abro of the brain stem is is really not there right so and remember your swallowing center is sort of kind of part of your cerebral cortex so because they can swallow they will have polyhydramneus and because right I mean literally like whatever is left of the brain is exposed is not covered by ectoderm right that is sort of kind of like a body wall defect so they're AFPOBI well think about it if your cerebral cortex is not there what is also not there right the pia and arachnoid and whatever that overlies your cerebral cortex will obviously not be there so if those things are not there guess what happens your CFF leak and if CFF leaks your acetylcholinesis levels and the amniotic fluid will be high okay now what if your codon neuro pore fails to close your codon neuro pore what if it what if it fails to close so the thing is how do I put this okay let's put it this way so let's say your codon neuro pore fails to close and there's no ectoderm overline it and your meninges your spinal cord basically like your spinal it's almost like anencephaly but in a lower part of the body so it's like literally like there actually no meninges covering your spinal cord your spinal cord is literally like left out to hang out to dry outside your body right so obviously you have a body wall defect because your spinal cord is hanging out so your AFPOBI and because your spinal cord is hanging out not necessarily covered by meninges right you are cerebral colinesis level in the maternal amniotic fluid will also be elevated but these people will not have polyhydram meals so they are not amniotic fluid index should be normal okay because again they can swallow just just fine

okay but before I talk about the other neuro tube defects I think it probably is instructive to sort of just dovetail and discuss one thinner real quick right and the thing that I sort of kind of want to discuss real quick is the whole concept of a vertebral arch right so the thing is in embryology right so you have your vertebral bodies you don't know what a vertebral body is the thing is the vertebral body a neural arch or some people call it like a vertebral arch sort of grows out from it right and the thing is a vertebral arch I will encourage you maybe look up a picture of this online I probably have drawn a picture but I don't really have time for that I need to get to other things soon but basically your vertebral arch is made up of two laminate so just sort of think of it as like a triangle your neural arch of vertebral arch envision it as a triangle so this is me trying to describe what I should have drawn right think of it as a triangle we have like those two sides I mean think of two sides as the laminate okay so like like individual lamina so like two individual lamina deform two sides of the triangle and then sort of think of your spinos process as forming the third part the third leg of that triangle so the thing is if you have problems with that process of forming a vertebral arch that is where you can actually begin to get into trouble right so for example if if say for example right those two lamina form but the spinos process does not form over it then you essentially have like two like two legs of a triangle but you don't have the third leg of that triangle so because you have two legs that's why that cordon neural tube defect for the most part they are called spina bifida right by fit by means two so you have two legs of that triangle that is sticking out the third part is not necessarily showing up as it should to sort of complete the triangle th

at constitutes your your neural your neural arch so let's sort of talk about these neuro tube defects and stages right so I've talked about the first one where you have the the spina bifida with myloscisis right where basically the spinal cord is literally hanging out outside the body that's bad AFP is up as it local ineseris is up and that's actually the least common thankfully right I mean that's obviously like obviously like pretty bad right it's like the list common and that's actually an example of an open neuro tube defect because again the spinal cord is hanging out okay and it's not covered by meninges that's an open neuro tube defect now if you have issues that revolve more around you forming that vertebral arch that neural arch right that's more of like a booney defect that begins to open up arvenus for things to sort of like gual of the abnormal place okay so again let me explain this if that neural arch does not form right you can have things still stay in the abnormal place like your spinal cord stays in its normal place you may ingest in the normal place with that you have no issues right it's like your ectoderm will form normally because there's nothing that has like honey fed out of that vertebral arch out of that neural arch and you're fine that'll be spina bifida right because there's nothing taking the place of that ectoderm so normal ectoderm just goes and forms over it right but let's take things up a notch what if through that because the third leg of that triangle did not form some of your meninges decided to sort of hernitha through the place where your spinal process should have been if meninges hernitha guess what happens you have something known as meningocel and because something has taken the space that should ordinarily have been taken by ectoderm ectoderm does not overlap that defect and the person has meningocel and because ectoderm did

not cover over the defect that person will have increased levels of alpha-fiddle protein okay but let's take things up a notch even more what if you have your meninges sticking out through that spinoff process basically your spinoff process is nowhere should be so you have your meninges sort of sticking out and then in addition to that you have your spinal cord also sticking out right but still covered over by meninges again those things have taken spots that should have been taken by ectoderm so ectoderm does not overlap the defect so guess what happens the person also has has an increase in AFB but the thing is meninges are still covering the spinal cord just fine so the levels of um um um um um um um um um um um um um um um um um um um um um um um um um um um um um um um um um um um um um um um um um um um um um um um um um um um um um um um um um um um um um um um um um um um um um um um um um um um um um um um um um um um um um um um um um um um um um um um um um um um um um um um um um um um um um um um um um um um um um um um um um um um um um um um um um um um um um um um um um um um um um um um um um um um um um um um um um um um um um um um um um um um um um um um um um um um um um um um um um um um um um um um um um um um um um um um um um um um um um um um um um um um um um um um um um um um um um um um um um um um um um um um um um um um um um um um um um um um um um um um um um um um um um um um um um um um um um um um um um um um um um um um um um um um um um um um um um um um um um um um um um um um um um um um um um um um um um um um um um um um um um um um um um um um um um um um um um um um um um um um um um um um um um um um um um um um um um um um um um um um um um um um um um um um um um um um um um um um um um um um um um um um um um um um um um um um um um um um um um um um um um um um um um um um um um um um um um um um um um um um um um um u

m um um um um um um um um um um um um um um um um um um um um um um um um um um um um um um um um um um um um um um um um um um um um um um um um um um um um um um um um um um um um um um um um um um um um um um um um um um um um um um um um um um um um um um um um um um um um um um um um um um um um um um um um um um um um um um um um um um um um um um um um um um um um um um um um um um um um um um um um um um um um um um um um um um um um um um um um um um um um um um um um um um um um um um um um um um um um um um um um um um um um um um um um um um um um um um um um um um um um um um um um um um um um um um um um um um um um um um um um um um um um um um um um um um um um um um um um um um um um um um um um um um um um um um um um um um um um um um um um um um um um um um um um um um um um um um um um um um um um um um um um um um um um um um um um um um um um um um um um um um um um um um um um um um um um um um um um um um um um um um um um um um um um um um um um um um um um um um um um um um um um um um um um um um um um um um um um um um um um um um um um um um um um um um um um um um um um um um um um um um um um um um um um um um um um um um um um um um um um um um um um um um um um um um um um um um um um um um um um um um um um um um um um um um um um um um um um um um um um um um um um um um um um um um um um um um um um um um um um um um um um um um um um um um um um um um um um um um um um um um um um um um um um um um um um um um um um um um um um um um um um um um um um um um um um um um um um um um um um um um um um um um um um um um um um um um um um um um um um um um um um um um um um um um um um um um um um um um um um um um um um um um um um um um um um um um um um um um um um um um um um um um um um um um um um um um um um um um um um um um um um um um um um um um um um um um um um um um um um um um um um um um um um um um um um um um um um um

um um um um um um um um um um um um um um um um um um um um um um um um um um um um um um um um um um um um um um um um um um um um um um um um um um um um um um um um um um um um um Bom, let's up the ante or not, right?

So what if we say that you know through that spot where the spineless process should have been as a constituent of your vertebral arch meninges herniage through that defect. If meninges herniage through that defect, that's called a meningocel but because those meninges that take in the space that should have been taken by ectoderm, ectoderm has no ability to cover over that defect. So because ectoderm does not cover over that defect, those kids will have elevations in their AFP but they will not have elevations in their acetylcholinesterase because that acetylcholinesterase is elevated if you have a CSF leak and that CSF leak happens if you're dura or if you want to be a little more specific, your arachnoid does not cover your spinal cord. Now let's up the ante up even more, right? Um what if your meninges and your actual spinal cord are herniating through that region that should have been taken over by your spinal processes, that's what's known as a myelomeminingocel, okay or a meningomilo cell, whatever doesn't matter, okay? Um again that would take up the spot that should have been taken up by ectoderm to cover cover over the defect. So ectoderm does not cover over the defect. So guess what your AFP goes up and then your acetylcholinesterase actually does not go up, okay?

The acetylcholinesterase does not go up and my reasoning behind that is because even if your spinal cord and your meninges have herniated out, your spinal cord is still covered over by the meninges like your dura or arachnoid and pier, okay? So you don't have CSF leaks technically and if you don't have CSF leaks, guess what does not happen? You do not have, um, you do not have, um, elevations in the amniotic fluid acetylcholinesterase again, that is super, super, super, super, super high yield to know for exams. You may not necessarily need to know it but the thing is it's high yield to understand, right? And the thing is if you really think about it, if your friends at the MBM you wanted to be mean, they could very easily put the matching game questions that I put, like sort of make it like an arrow sort of question on your test, right? And the thing is this is where you then see who really understands this neuro tube defect and who really does not understand these neuro tube defect? Because everyone has memorized like some basic things like oh, AFP is up, acetylcholinesterase is up. The thing is it's not every neuro tube defect that is associated with elevations in your acetylcholinesterase that's just the fact of life, right? So again, that is specifically why I put this question. So sort of bring out and buttress these points. So you really understand, you really understand them.

So, um, so I think that's really all, I mean, I guess I could summarize because I have, I even have like a neuro defect algorithm, right? So I say is your AFP elevated. If the answer to that is, um, no, right? Then that tells you that you have nobody or defect, right? So everything is covered over nicely by a term. It could also mean that you have spina befidolcotum, right? And again, I've explained the reasoning behind that, right? But if your AFP is elevated, it could mean one of two things. It could mean that you have a ventral, it could actually mean many things, okay? But just to dumb down this discussion, let's say it could mean you could have like ventral body wall defect like gastroschesis. And I'm following you remember again, I'm following still is sealed by peritoneum. Gastroschesis is not. Although I'm following still tends to be as real more like congenital defects than gastroschesis, but that's a different discussion. But another reason your AFP could be elevated could be from a dose of body wall defect. So defecting the back, right? Now, the thing is I divide those dose of body wall defects into open neuro tube defects where you have increases in your amniotic fluid acetylcholinesteris and closed neuro tube defects where you do not have increases in your amniotic fluid acetylcholinesteris. Okay? And another of the open neuro tube defect, the next question you ask yourself is, do they have polyhydramios?

If they do, they could say polyhydramios on the NBM, they could try to mess with your head by putting, oh, an increase in the amniotic fluid index, right? Because remember your friends at the NBM, if they run out of ways to test things, they can just begin to change like the words, right? So for example, they could do things like instead of saying like some homo bodies they can put laminated calcifications, those are classic things they don't exempt, right? So polyhydramios increased amniotic fluid index mean one and the same thing, okay? If you see that, that's an encephaly. Remember, the assualoincenter is gone. And then contrast that with no polyhydramios if they have like increases in AFP and acetylcholinesteris, think more about like the super severe spina bifida. So spina bifida with myeloschesis, okay? Now, if you're thinking about closed neuro tube defects, the acetylcholinesteris is not elevated, it's not basically normal in both of these problems, but you could have like this cystic expansion that contains only meninges, that's a meningo cell, okay? Or you can have this cystic expansion. In fact, sometimes people call this like spina bifida okay? You have this like expansion that contains like humaninjes and you're like legit spinal cord, okay? That's a meningo myelosch. Remember, the word myelosch literally stands for spinal cord, okay? And remember that lombus, lombus sacral myelomininocelus have an association with with the chiarityum alformations.

In fact, I should probably go ahead and talk about those chiarimalfomations. In fact, you know what? Let me just go ahead and do it now. So those chiarimalfomations, basically, their problems where your cerebellum herniates downward into the foreman magnum, okay? Remember your cerebellum has multiple parts, right? You have like your cerebellum tonsils that are a little more lateral, you have your cerebellum vermess that's a little more like in the midline, okay? So the thing is if it's your cerebellum tonsils that are herniating, that are herniating downward through the foreman magnum, that's a chiari-1 malformation. In fact, it's actually the most common kind of chiarimalfomation and usually this tends to not be super clinically significant for the most part. Although this chiari-1 malformations can actually be associated with like a syringomalia, okay? So that's something to sort of keep at the back of your mind. Now, if you have your cerebellum vermess instead being the thing that's herniating downwards, that's more of a chiari-2 malformation. And the thing is because your cerebellum vermess is like kind of central, especially in the posterior fossa, it's more prone to sort of like blocking your fourth ventricle. So the thing is your chiari-2 malformation or your anal chiari-2 malformation for the most part tends to be more associated with hydrocephalus. And I mean if you want to be more exact, a non-communicated or an obstructive hydrocephalus, okay?

So these people could have hydrocephalus that they could have increasing intracurial pressures. And remember that this is the one that is also associated with a lombus sacral myelomaningo cell. And then I guess another one that occasionally confuses people is like a dandelwalker malformation. Basically the thing that happens here is like, remember the way CSF flows, right? So it starts in the two lateral ventricles. Remember, the reason you have two lateral ventricles is because you have two cerebral hemispheres, right? So you have two cerebral hemispheres. So each one should have a lateral ventricle. And then from the two lateral ventricles, you send things through the interventricular foramen of monorail and then go to the third ventricle. And then from the third ventricle, you go to the cerebral aqueduct of silvios, which is a part of the midbrain, part of the mesencephalon. And then from the cerebral aqueduct of silvios, you go to the fourth ventricle, right? And then the fourth ventricle drains into the subracnoid through the arachnoid granulations into the subracnoid space through like the midline foramen of magendi. And then the lateral foramen of luska. Remember magendi has an m, median has an m. Luska has an l, lateral has an l, okay? So there are two foramenes of luska and one foramen of magendi.

And the thing is if you actually have like a congenital obstruction of like the foramen of magendi or the foramen of luska, you can actually basically have like a lot of csf backing up in the, in the fourth ventricle in utero. And if that csf begins to back up, your fourth ventricle will essentially dilute and that can cause like really, really bad hydrosophilus. I mean this will be an obvious example of again another like non-communicating or you can say obstructive hydrosophilus, okay? That's more of the dandy walkers syndrome is like a cystic expansion of the, of the fourth ventricle. And again, usually arises because your foramen of magendi or your lateral foramen of luska, just congenitally do not open, okay? And then you get into trouble. And I guess so that I can know that I'm pretty set from a neuroinbrilogy standpoint. I guess I can also discuss holopers and cipheli, right? So again, remember if your, remember I said that you have two cerebral hemispheres, right? I mean, they are separated by the foxes cerebride, which is like a drool of fort. If those, normally those cerebral hemispheres they start out as one unit and then they separate. If they don't separate, you have like one big cortex. That's what's known as holopers and cipheli, okay? It's very common actually in trisomy 13, yeah trisomy 13, that's like I believe that's a patose syndrome, okay? So it's just a patose syndrome, the pain in where you come from in the world. That's holopers and cipheli.

Those kids tend to have like clefle, clef palette and all that, all that badness. So I said that of the carry malformations, right? I said that carry one is more common and tends to be less symptomatic than carry two. And if you're looking at those like auto neuro tube defects, right? So I said like, if you're looking at those codon neuro tube defects, right? So like, Spina Bifida, my last case is the least common codon neuro tube defect. Actually, the most common codon neuro tube defect is Spina Bifida, or Cota, right? We'll just have that tough tough here. Nothing is anything out. Ectrodom covers over the spinal cord just fine, and then we're left with two. Between the last two, between like a meningocel and a myelome meningocel, the worst one actually, myelome meningocel is actually more common than meningocel, okay? So that's something to know. I guess another thing I could also talk about is, man, this is something that will probably take me like a minute. So remember that neuro tube, right? So I said that neuro tube forms, forms, um, um, your neuro tube forms, your brain and your spinal cord, right? So it's actually the more rostral or the more cranial part of your neuro tube that forms the brain. The more codal portions form the, um, the more codal portions form the spinal cord, okay? And the thing is, that more rostral portion, right? It sort of breaks up into like vesicles.

There's like primary vesicles, there's three of those, and in those primary vesicles, bring down even further to secondary vesicles, and there's five of those. Basically, like the first primary vesicle forms two things, the third primary vesicle forms two things, the second primary vesicle does not form any other thing, okay? The first primary vesicle is like your forebrain, that's like your, um, your, uh, prosensophalon, right? Um, and, um, from your prosensophalon, right? You form, um, like the talin-sephalon, that essentially includes like your, you know, both of your saber, hermispheres, um, your two lateral ventricles are sort of like those hollows inside that tube, right? Um, those essentially, um, all come from the, um, from the talin-sephalon, the talin-sephalon, is a derivative of your, of your prosensophalon. And then another derivative, right? So the other secondary vesicle that comes from your prosensophalon is your dian-sephalon, right? And your dian-sephalon, um, uh, your dian-sephalon basically forms everything that has like thalamus in his name, right? So like your pineal gland, uh, technically your pineal gland is called like the epithalamus, is right from the dian-sephalon, your hypothalamus, right? That basically controls your autonomic nervous system and like all pretty much every endocrine functioning your body for the most part, okay? Now you know there's no entire literature, uh, come from the dian-sephalon, um, uh, your sub thalamus, right?

We'll talk about the sub thalamic nucleus when we get to like basal ganglia and all that weird secutory, um, those all come from the dian-sephalon, so don't forget cranial nerve two, super high yield to know this, the optic nerve comes from the dian-sephalon, okay? It is the only cranial nerve that is derived from the central nervous system, the other cranial nerves, guess what? We are derived from the peripheral nervous system, so we are derived from neurocrest cells, again, super high yield to know that for exams. And for the most part your dian-sephalon control contains the third ventricle, okay? And then the second, uh, primary vesicle, right? Um, is your mesencephalon? Your mesencephalon, um, um, um, your mesencephalon basically forms your midbrain, okay? And your mesencephalon, right? Doesn't develop even further into like secondary vesicles, just is mesencephalon, has midbrain, and doesn't have a part of the ventricle in it, just has the cerebral aqueduct of, uh, of the cell of the cell of the cell of the cell of the cell of the cell of the cell of the cell of the rhombus and cephalon, these rights to two secondary vesicles. Those two secondary vesicles are your mesen, are your, sorry, are your mesencephalon and your mesencephalon. Your mesencephalon includes, so contains a T, basically, your ponsence cerebellum, and then your mesencephalon is your medulla, okay? Um, and basically those two things like your contain like the fourth, uh, your fourth ventricle.

So, um, I think with that, I think I'm probably gonna go ahead and stop, and again, as I always mentioned, I do offer one on one tutoring for the USMLS Step 1, 2 CK, 2 CS, and 3 exams, um, and then, I offered tutoring for like the preclinical medical exams, the 30th shelf exams, and weirdly for organic chemistry, and also for the internal medicine, an infreland exam, and the internal medicine board exams. So, I do offer, I do, um, I do actually offer tutoring for those, and then I've been on, and the admissions committee of like a top three medical school, um, so I prepare ear applications for med students trying to become residents, and then I'm kept applications for college students trying to become med students. Um, I do like interview prep, I do, I help with like editing personal statements, preparing applications, checking them, presenting your strengths in like the best way possible. So those are things I'll do. So if you know anyone that needs any of those things by any chance, uh, let me know. But I really hope you got something from this podcast, um, if you have any questions, let me know. Nero will be a pretty long series of podcasts, because Nero is literally 10% of first aid. Um, so I'll see you in the next podcast. Have a wonderful rest of the day, and God bless you. See you next time. Thanks.

Oligodendrocytes myelinate multiple axons in the CNS; Schwann cells typically myelinate only one axon in the PNS.

Cranial Nerve II (Optic nerve). All other C Ns are generally derived from the neural crest.

Elevated Acetylcholinesterase (A ChE) AND Polyhydramnios/Increased Amniotic Fluid Index.

Any failure of the ectoderm to cover a defect (e.g., Gastroschisis, Spina Bifida).

Myelomeningocelesis has normal A ChE because the spinal cord is still covered by its own meninges (dura/arachnoid), preventing CSF leak.

Prosencphalon, Diencephalon, and Mesencphalon.

Ectoderm.

Postganglionic autonomic neurons; Odontoblasts; Most peripheral nerves/cranial nerves (except CN II).

Alpha-fetoprotein (AFP) and Acetylcholinesterase (A ChE).

Spina Bifida Occulta/Tinea; Often asymptomatic or presenting with minor bony defects without neural elements exposed.

Diencephalon (derived from Prosencphalon).

Chiari I involves tonsils herniating; Chiari II involves the cerebellum vermis herniating.

Ectoderm.

Postganglionic autonomic neurons; Odontoblasts; Most peripheral nerves/cranial nerves (except CN II).

Alpha-fetoprotein (AFP) and Acetylcholinesterase (A ChE).

Spina Bifida Occulta/Tinea; Often asymptomatic or presenting with minor bony defects without neural elements exposed.

Diencephalon (derived from Prosencphalon).

Chiari I involves tonsils herniating; Chiari II involves the cerebellum vermis herniating.