DIP Episode 46 - Neurology Clerkship Shelf Review Part 3

Okay, welcome. My name is Devine. I am a PGOI1 resident. Today we will be going through the 46th episode of the Devine Intervention Podcasts. And this will be the third installation of a Neurologic Fellowship Show for you. This is just a pickup from yesterday pretty much. So again, I'll try to go through some Neurology material and hopefully by the end of the series, you should have a fairly thorough review for the Neurologic Fellowship. And I apologize, it's not like one big video like I did for the other clerkships. I just really don't have the recording equipment. That's one. I was able to obtain that from my school back in the day. And I also don't have like two hours to just record stuff because I'm currently on rotations as a PGOI1. So that makes things a little difficult. So I have to sort of break things up into bits and pieces. But overall, you should get the whole same message just in smaller chunks. So let's get started. So the first slide says, a child is not doing well in school. His teacher often observes him staring into space with no awareness of his surroundings. So this is a child. This is a pediatric question. So what's your diagnosis? So obviously this is an upsand seizure. Don't forget that on EE Gs. You find the three hertz spike and like you find like three basically just look for the buzzword three hertz. And the way you treat this is with Ethosoxamide. Ethosoxamide is actually a calcium channel blocker.

But more specifically, it's a tea type calcium channel blocker. Okay. And again, upsand seizures will be something that I'll show up in a kid on your exam. It's not going to show up in another adopt. So always look at age ranges on tests. So especially on the MBA meetings, they're usually pretty helpful in dealing eating. What's going on? Now, second question. A 55 year old female presents with a six month history of filling like the room is spinning around her that last for about three days at a time. She also had difficulty here in at home. So she has hearing loss. She has a feeling of the room spinning. She also complains of a ringing sound in her ear. So that's tenet us. So what's your diagnosis? Well, I really hope you're sort of putting together the triad here. It's all like vertigo. Tenet us, which is ringing in the ears and hearing loss. Okay. It's actually a sensory neural hearing loss. That's pretty classic for man ears disease. Okay. And the dietary modification that at least helps in man ears disease is like eating like a low salt diet. In terms of pharmacologic management, you can try to calm down like the the vertiginous symptoms by giving anti-cholinergic agents, right? So like scopolamine or mechlezine or even benadure, right? So diphenhydramine. That can help with the nausea and the vertigo. Alternatively, you could also give diuretics. Diuretics, some people actually respond pretty well to diuretics with man ears disease.

But if you want definitive treatment, you actually have to oblique the eighth cranial nerve. Okay. You essentially do that by injecting gentomising into the ear. Remember, gentomising is a 30th inhibitor. It's bacterial side. It's an amino glycoside. Aminoglycosides are auto toxic. So you can use that auto toxic effect to just oblique the eighth cranial nerve. And that can essentially resolve man ears disease. The only problem is the patient will also have a permanent sensor in your ear here and loss with that. And the pathophysiology behind man ears disease is kind of shaky. But the buzzword you kind of want to remember for exams is something known as endolemphatic hydrops. Okay. Endolemphatic hydrops. And endolemphatic hydrops, right? It just means that oh, so think of hydrops, right? So if something is hydropic, it means it's swelling. Right. So sort of think of this in the context of like poor absorption of endolemph in the ear. Okay. And that classically causes like increased endolemphatic pressures. And that can create the clinical presentation of man ears disease. Right. So if you tell your patient, it even has a like a feeling of fullness in their ear or something again. You really want to think about man ears disease. Well, classically, in exam questions, they will give you the other triad of vertical tinnitus and hearing loss. Okay. And just a quick word on some of these vestibular disorders because they're kind of hard to tell apart.

So let me just try to be as obvious as possible in my descriptions of these. Right. So I've talked about man ears disease, right? Classically presents with vertical tinnitus and sensor in your hearing loss. Right. Now another one is BPPV, benign paroxysmal, positional vertical. This will probably come up in a little podcast, but I'll just talk about it right now. Basically, right, you have like displacement of the otoconia in the ear, right, classically in the posterior semi-secular canal. Right. So those people tend to have position of vertical. Right. So it's not like they're sitting still and they have vertical. If they have changes in position, that's where the vetigenus, that's when the vetigenus symptoms begin to show up. Right. And remember that these people do not have any kind of hearing loss. That's important to know. And remember that you can make the diagnosis with the Dixhole pipe maneuver and you can potentially treat this with the Epli maneuver. That's the most common answer you see on exams. So I've talked about man ears disease. I've talked about BPPV. Now the third one I want to talk about is vestibular neuronitis, okay, vestibular neuronitis. Classically, this shows up after a patient that's had like like a viral operator infection. And then they tell you that they have like just constant vertical. So it's not positional like BPPV, okay? This one is not positional. Like sitting still, they still have vertigenus symptoms.

They still feel like the room is spinning around them. And it's constant. It's pretty severe and it can last for these two weeks before it resolves on its own, okay? So it's not positional, okay? But it classically arises on exams after viral operator infections. And vestibular neuronitis is not very high yield. It is not associated with hearing loss. However, if the, if the, if the given exam question with it iscribed symptoms of vestibular neuronitis and then they tell you that the patient also has hearing loss, then think about labyrinthitis. Labyrinthitis is basically vestibular neuronitis plus hearing loss. So that's what I'm going to say about the vestibular disorders. I'll see some more stuff about them down the line. Now the next slide, hitting the head with a bat, passed out for less than 30 seconds, finished out the game, now presents with severe headache and some the lens, right? You've heard this horror story before, right? This is obviously an epidural hematoma, okay? And the diagnostic testing you want to do, right? You want to do a non-conhead CT. Remember, blood will serve as its own contrast. And on the non-contrast head CT, right? You obviously see the lens shaped hematoma, okay? For these patients, you obviously do not want to do a long-term puncture, right? Because if you do that, you will, let's just say you have a lot of problems with the legal system down the line, but basically you don't want to do that, right? So that they don't hurt you and die.

And the path of physiology, right? It's basically like if you have like a fracture of like the temporal bone, right? And you sort of transect the middle meningel artery. Remember, that's like a branch of the maxillary artery, which is the terminal branch of the external corroded artery, okay? So you basically last read the middle meningel artery and then you have an arterial bleed, okay? And it's above the duress and epidural hematoma, okay? And the way you treat this, you basically call your friendly neurosurgeon, see? So they can help you evacuate the hematoma if not this thing is a rapidly fetal. And in terms of reducing intracranial pressures, right? So there are many things that you can use to reduce intracranial pressures, right? So you can elevate the head of the bed to like 30 degrees. You can hyperventilate the patient, right? Because think about it. If a patient hyperventilates, the CO2 tension goes down, right? And when your CO2 tension goes down, that actually causes a cerebral viso-construction. So that sort of decreases blood flow to the brain, okay? In fact, that's actually the quickest means of reducing ICP. Very high, you'll to know that. Is the quickest acute means of reducing ICP? Hyperventilation, okay? Other things you can do, you can give right? So manitol, it's an osmotic diuretic, you can give acedazolo-migro, although a manitol is probably a better answer on tests. You can also place a VP shot, but that's more for like chronic management.

That's not something that's going to help you watching the acute in the acute phase. And so, there are hematomas, right? These classically show up in one of two people on test, right? So old person, probably taking warframe as heart falls, and then over the last couple of weeks, having like this bad dementia, sort of like acting out of it, right? Think about a subdual hematoma. And then another patient population, you also want to think about a subdual hematoma in his is an alcoholic, right? So alcoholics, right? They may have like, essentially like they have like sort of like a microcephaly from that alcoholism, right? So the brain's going to get shrinked and the box of the brain, which is the skulls, these the same size. So as that ball, the the brain keeps like jerking around in the in the skull. You can imagine that it potentially shear the bridge in veins that can cause a venous bleed, okay? So that's a subdual hematoma. And actually one of the last high occene areas is shaking baby syndrome. Shaking baby syndrome classically presents as a subdual hematoma on exams, okay? And remember again, it's from the rupture of the bridge in veins. It's a venous bleed, so it's a lower pressure bleed. The treatment is probably about the same as an epidural hematoma. And don't forget that it looks like a crescent on non-conscious head-city imaging. Okay, so next question. Super-tense muscles and a temperature of 105 after intubation.

So obviously, right, you should hopefully think about this as malignant hypothermia, okay? Remember the pathophysiology involves mutations in the dihydroperidine receptor and the ryanodine receptor. In fact, these are actually autosomal dominant inherited, okay? So dihydroperidine receptor, ryanodine receptor. And basically, by having all those problems, you have an increased extrusion of calcium from the sacroplasmic reticulum into the cytosol of skeletal muscle. And when you have that, you have like a hypercontractile state, you generate a ton of heat, right? And that can cause super elevated, that can cause super elevated body temperatures, okay? So this is malignant hypothermia, autosomal dominant inheritance, okay? And the way you treat this, you actually treat it with downtruling, right? So I just said that remember the ryanodine receptor is a, is basically like, think of it, think of the ryanodine and the dihydroperidine receptors as being like calcium channel conduits if you may. So if you know that you have a problem where your calcium channels are not functioning well, well, it should make sense that you should give a calcium channel blocker, like downtruling. Dantruling is, think of it as like a ryanodine receptor antagonist, it's a calcium channel blocker that basically prevents the release of calcium from the sacroplasmic reticulum. And that helps in treating the symptoms of, helps in treating the symptoms of malignant hypothermia.

And if a patient has malignant hypothermia, right, they could potentially have like muscle necrosis, right? So if you actually think about it, remember potassium is primarily an intracellular ion. So when a cells begin to die like muscle cells, they can extrude a lot of potassium into the serum. And that potassium, right? First, so you obviously have a hyperkalemia, that hyperkalemia will first manifest as picked T waves, okay? If the potassium keeps going up and you don't do anything to treat it, you then begin to have white QRS complexes. If nothing happens, right? So if it's not caught at that point, you keep going, you basically form like a sine wave EKG. And then after that, you're going to a system, which is obviously a bad outcome, right? And remember, right? If a patient has hyperkalemia, the first thing you do to stabilize the myocardium is to give calcium glucone, right? And then after that, you can give like insulin, that increases the activity of the sodium potassium ATP is pump. So you dump, you begin to get redistribute potassium from the extracellular environment to the intracellular environment, right? Or you can give a bit of a, again, it's like a bit around, right? That can also drive potassium into cells. Another thing you could also do is to give sodium bicarp, right? So remember, sodium bicarp can create a metabolic alkalosis, okay? When you create a metabolic alkalosis in the blood, right? You draw hydrogen ions out of cells.

To maintain electronic neutrality, as those hydrogen ions are coming out, potassium goes in reverse. So again, that also leads to potassium into the extracellular environment, sorry. And then another thing you can do is you can give Kx-lit, right? So Kx-lit makes K exit out of your body, okay? So Kx-lit actually helps you get rid of potassium. You could also give like ferozomide, right? So it's a lube diuretic, has hyperkalemia as a side effect. So you basically use the potassium-wisting function of lube diuretics to help you get rid of some potassium. And then if a patient has malignant hyperthermia, right? And they have glyvide creatinine, right? Hopefully you're thinking about ruptum analysis, okay? So basically the muscle cells that have died, the myoglobin goes and clogs up the kidneys. Obviously the way you treat that is you just do like vigorous hydration, vigorous diuresis to just wash away that myoglobin. Now, same presentation. So super tense muscles, high temperature blah, blah, blah. But this is after studying flufena zine. Hopefully you remember that flufena zine is first generation high potency typical anti-psychotic. So this is obviously in your leptic malignant syndrome, okay? treatment is the same, right? You can give dantrulline. Well, actually you have other options here. You can actually also give a dopamine agonist like bromo cryptine or carbureguline.

Alternatively, you can give a benzodiazepine like lorazapem, for example, that can also help in in your leptic malignant syndrome. Now, last part of this question says history of depression. So potentially a patient taking SSR Is and then treatment for stuff where it's bacteria or so that's like maybe like ligny solid if you may or migraines, right? So maybe like so much ruptum, which is a serotonin receptor agonist, okay? Detail you that this patient presents with high fever, diarrhea and clonus, clonus, right? So hopefully this gets you thinking about serotonin syndrome, okay? Remember, you don't want to combine two serotonergic agents, not a good idea, right? So history of depression, right? So think about SSR Is, SNR Is, M-E-O-I-C-C-A-S, right? Stuff where it's bacteria, think about ligny solid, remember ligny solid, yes, it's a 50-S inhibitor and it covers MRSA and vancomycin resistant interococcus, but it also has weak mononamine oxidase inhibiting activity, so you can actually boost your levels of serotonin and trigger serotonin syndrome. And then don't forget your triptans that are used for the treatment of migraines, okay? They are serotonin receptor agonists, so they can also trigger serotonin syndrome when combined with another serotonergic agent. And then don't forget from my discussion of Parkinson's disease yesterday, right? Like your MEOB inhibitors, like cellulogenin or esagenin, can also trigger similar symptoms or your MDMA, right?

X-D-C, it's a serotonergic agent, it can also trigger those problems, okay? So those patients the present high fever is diarrhea, so you're thinking about serotonin syndrome. Usually you give a benzodiazepine and supportive care, and that's usually fine, but on exams one commonly sought after answer is super heptidine. Super heptidine is an anti-histamine with powerful serotonin receptor blocking activity, so it's actually used quite commonly to treat serotonin syndrome. Now next question says tremors, six hours after the successful completion of a triple air repair in a business executive, right? This is obviously this person begins to go into alcohol withdrawal, right? And basically your prevention is you give benzos, right? You can give like if a patient is actively seasoned from like the lyrium tremors, you obviously give the person a short actin benzone like lorazapam, right? But if you're trying to like profile acts, you can actually give a long actin benzodiazepine, like the trade name is Lebrem. What's the real name? Clodazapoxide. Clodazapoxide is a longer actin benzodiazepine that can be used to profile acts classically, it's used like in the COA protocol. You'll learn about this when you become a resident to sort of prevent the lyrium tremors, okay? Now the next part of this question is tremors after studying in DAPA-MIDE, right? So what is end-dAPA-MIDE? End-dAPA-MIDE is a thiozydhyretic.

So in DAPA-MIDE, it's a thiozydhyretic and then they tell you that a patient has tremors after studying this drug and they tell you that they have a history of episodes where they spend tons of money and jump into severe depression, right? So this is like, oh, this person is manic and this person is depressive, right? So hopefully you're thinking about bipolar disorder and you're thinking of lithium as the treatment. So the thing is diuretics classically can actually raise a person's lithium levels and that can cause that can cause lithium toxicity. One of the tell-tale signs on exams of lithium toxicity is tremors, okay? So that's one high-ealthing you want to keep in mind and really like there are many things that can cause lithium toxicity and people always say, oh come on, divine, how am I supposed to remember all this stuff? Well, let me give you one general principle. If you can organize, if you can think of the scenario you get on a test in the context of this principle, you should be able to resolve answers to the most of these questions, almost 100% of the time. So here's the principle. The principle is anything that ultimately causes an activation of your reigning and your tensing out-dosterone system will increase lithium toxicity and I'll give you some quick pathophysiology on that, right? So basically, if your reigning and your tensing out-dosterone system is revved up, you'll ultimately at some point in the cycle, make out those two.

If you go to the principle cell of the nephron, out-dosterone causes an increased reabsorption of sodium, right? Through that in-ex-channel at the principle cell. If you go back to college chemistry, remember that sodium is a group one element? Lithium is also a group one element. So if your reigning and your tensing out-dosterone system is revved up, your dose-dron levels are high, that in-ex-channel is working better than normal, reabsorbing a ton of sodium. You can also kind of like just equalize that you could also be reabsorbing a lot of lithium at the same time, right? So you boost your lithium levels and you get into trouble. So anything that activates your reigning and your tensing system, like being volume-deplicated, for example, if you're thinking of diuretic, can make a person have elevated lithium levels and you can get into trouble? Endsense, right? Endsense also activates the reigning and your tensing system, right? Because if you take an end-set, you inhibit cycloxygenase, so you make less prostaglandins. And if you make less prostaglandins, you have less dilution of the afrin arterial. And if the afrin arterial is not diluted, your afrin arterial will be hypoperfused, those will make your GG cells get mad and then they begin to secret a ton of reigning. And then that kicks starts the whole cascade. Okay, so next slide. Child presents with bulging fontanels and some nullets.

What is the most likely region of stenosis responsible for the presenting hydrosophilus? This is just a factoid you need to know. The cerebral acuduct of sylvia, remember that's a part of the midbrain, that's the most common region of stenosis in a patient that has like a congenital hydrosophilus. Okay, next question. 70-year-old female that is forgetful. She staggers into the exam room. Okay, so she's forgetful. She staggers into the exam room. So she has dementia. Well, let's see, she has dementia. Staggers into the exam room. Okay, sort of create a mental picture of a person, stagger into an exam room. And then they tell you she has a history of recurrent perino sores from urinary and continents. So this patient is wet. This patient is wacky and this patient is wobbly. What does this sound like? Well, I hope you're thinking about a normal pressure hydrosophilus. Okay, so these people write hydrosophilus. That tells you that you have to probably obtain some kind of brain imaging. Okay, you obtain brain imaging and you will see like enlarged ventricles. You're like, that's not good, right? So you see signs of hydrosophilus on imaging. But if you actually do a lumber puncturing these patients, you actually will not detect elevated CSF pressures. That's why it's called normal pressure hydrosophilus. Okay, and really the way you treat this on tests is you can do like a VP shot, ventriculo, peritoneal shunt. That's basically the most common treatment that you see on exams.

Now next question, tuberosclerosis, right? So this is autosomodominant inheritance. Okay, remember it's basically the pathophysiology involves like two genes. One is called TSC1 and the other is called TSC2. If I'm not mistaken, I believe TSC1 calls for protein known as hemartin. And if I'm not mistaken, I believe TSC2 calls for protein known as tuberin. So if you have mutations in hemartin and tuberin, those actually tumor suppressor genes. So if you have mutations in tumor suppressor genes, you can sort of imagine that tumors will no longer be suppressed. So tumors will start growing everywhere, right? For example, in the brain, you can have sub-ependental tumors growing, right? They're usually like calcified masses in the brain. In the kidneys, you can have tumors growing, right? Classically, they're angiomyolipomas, right? So angiomyolipomas. So it contains fat, muscle and blood vessels, right? So renal angiomyolipomas, they're classic tumors and tuberous sclerosis. In terms of cardiac findings, right? Hopefully you're thinking about the cardiac ruptum ayoma, okay? And then in the skin, right? You're hopefully thinking about the hypopigmented macules, right? So those are your Ashley spots.

Please do not confuse your Ashley spots, which are hypopigmented macules, that are classically associated with tuberous sclerosis, with caffeine-lase spots, which are hyper-pigmented macules, that are classically found in the context of neurofibromatosis, or I guess some fanconeanemia, okay? So don't mix those things up. And remember that patients with tuberous sclerosis, right? They tend to have like performment or retardition, well, I should use that terminology. Profound in telekto-disability, okay? That's the appropriate term. So I apologize for that. And classically, when they hit six months of age on mbim exams, they can tell you, they can be easily describe a child with T.S. And they tell you that the child wakes up and his hands begin to like vibrate and he has like general eye seizures. That should make you think about infantile spasms, okay? That's also known as West Syndrome. And that seizure, it's actually, they love to test it on exams because the treatment is unusual. You actually treat it with ACTH, right? So like Adrenal quadricotropic hormone, you can also use a drug known as a Vi-gaba-train. Vi-gaba-train has like Gaba-urgic activity. It's an anti-segeum-medication. Alternatively, you can also use steroids, okay? And don't forget that infantile spasms has. So she did with hypsi-rhythmias on the classic pattern. It's like a chaotic pattern on EEG. I would encourage you to look up a picture of this, looks super bizarre. It's called the hypsi-rhythmi.

That's the classic EEG finding in an infantile spasim. Okay. Now next slide. Mom has a history of inconsistent condom use. Okay, that's not good. She delivers a stillborn fetus with no brain. Okay, that's not great either. So this mom's baby has an encephal, right? So no brain. So you, and the pathophysiology, right, is basically your your anterior, your anterior, basically your neuro tube does not close anterior. Let me think about this for a second. Sorry, I have to think about this, giving this practically from memory. So you have failed cranial closure of your anterior of your neuro pores. So that is how you get an encephal. Okay, so you don't develop a brain. So you have no swallowing center. So classically, these kids have polyhydramnos. That's a classic OB-GYN shelf question. And I guess some other quick spinal disruptisms you want to keep in mind. So you want to think of things like spinal bifida or cauter. So that's where you have like a congenital absence of the spinal processes. And I mean, you won't see like meninges or neural tissue hernating through the defect. In fact, you may not see any like clinical signs on physical exam, right? But like in the lumbar sacral area, usually it's around like L5 S1. You find like a dimple or like a point one stain or like a tuft of hair. Okay, those are pretty classic. Usually it doesn't require any kind of treatment and those kids are fine. Another high yield of spinal dysraphism to know is a meningocel, right?

So like basically you have like hernation of like meningial tissue and CSF. Okay, it's usually through a defect in the spine. Okay, and there is a Boswart pathophysiology actually want to commit to memory for exams. Okay, the Boswart pathophysiology is a failure of fusion of the posterior neural arch. Failure of fusion of the posterior neural arch, that's something you sort of want to commit to memory. And again, it usually shows up mostly in the lumbar sacral area. These kids may have like a hydrocephalus. Okay, and generally for this, you have to do like some kind of neurosurgical intervention. And if you intervene neurosurgetly, these kids usually do pretty well. And then the worst one is myelomanin-gousille. Okay, this is basically where you have like hernation of meninges and like CNS tissue through like a defect in the spine. Okay, and again, this arises because your neuro tubes did not close. And remember, folic acid deficiencies, right? Deficiency of folic is like a big risk factor for a neuro tube defect, but notice I'm using the term spinal dysphysine. Your friends at the MDME, right? One thing they classically do to people on tests is they think what you know and give it like a different term. Okay, just to sort of mess with your head. I mean, you probably know this example, I cite all the time like, oh, like some of these being like laminate calcifications. Well, neuro tube defect, think of that as a spinal dysphysine. It's basically one and the same thing.

Okay, so myelomanin-gousille, one big, high-o thing I want to remember is that if a patient has a lombus sacral myelomanin-gousille, it's associated with a chiaritumal formation. Okay, lombus sacral myelomanin-gousille have an association with chiaritumal formations. Lock down that concept in your mind. It's a classically tested exam concept. And many times these kids, I mean, they survive, but they tend to have some relatively serious neurologic deficits. So that's my take on the spinal dysphysine. Okay, and if you have a neuro tube defect, aka spinal dysphysine, you have an elevated maternal serum AFP, right? You can also have like elevated levels of cidoculin esterase in the in the amniotic fluid. That's just something to keep in mind. And while we're on this topic of elevated maternal serum AFP, if you see an exam question where the where child, where like you do like the quad screen and the maternal serum AFP is decreased, well, hopefully you're thinking about Down syndrome. Okay, Down syndrome. Now, your chiarimal formations, right? There's type 1 and type 2 chiarimal formations. In a type 1 chiarimal formation, it's one thing that herniates through the foreman magna, right? So in that, in this case, it's the cerebellatonsum. So those are the things that herniate in a chiarimal formation. But in a chiaritumal formation, you have two things herniate in. Okay, you have the cerebellatonsum, and then you have the cerebellat verbiage.

Okay, and again, don't forget that a type 2 chiarimal formation is associated with a lumbus sacral myelomaningo cell. A type 1 chiarimal formation is associated with a syringomalia. So classically it presents with hydrocephalus. Okay, so remember like syringo, like just remember that I in syringo as a one to help you remember that syringomalia is associated with chiarim 1 mow formation. Okay, and then again, chiaritum lumbus sacral myelomaningo cell. Notice I'm repeating this over and over again. I'm not repeating it for funsies, I'm repeating it because it's super high-yodontes. Now, be to have deficiency. I remember that it's classically associated with a subacute combined degeneration of the cord. So you basically knock out your quadricoster, your lateral quadricoster spinal tract, and your dorsal columns. So your dorsal column medial lumbus sacral system. So you have problems with like vibration, touch, and perception, and you also have opomodonuran findings. I believe in a little podcast that I'll talk about those spinal cord pathologies. And B12, if you want to differentiate it from fully deficiency, right? So we know that B12 and fully are both involved in homo-system metabolism. So your levels of homo-system behind both doesn't matter, right? And you can get a macrositic or omega-lodlastic anemia with both, right? But remember that methylmalano co-A mutase that converts methylmalano co-A to succino co-A, okay? Use this vitamin B12 as a co-factor.

So if you have B12 deficiency, you have a methylmalonic acidemia. So you have an evaded level, so methylmalonic acid. Okay, so final question today. So, caffeine-olate spots plus brown pigments in the axilla. Plus tuber-like skin growth. Plus episodic headache and severe hypertension, right? So this is neurofibromatosis type one, okay? Remember it's associta ocafio-li spots. Those are hyper-pigmented lesions on the skin. Brown pigments on the axilla. tuber-like skin growth, right? So those are the neurofibromas. Episodic headache and severe hypertension actually it's pretty high you to know that NF1 is associated with a few chromosidomers. And the common amelignancy they get, right? So they can get like optic nerve gliomas. In fact, that's probably one of the most common tumors in neurofibromatosis type one. That's why you have to screen these patients commonly. You need to screen them fairly frequently for these optic nerve gliomas, right? So that's a cranial tumor. The common ear malignancy, they tend to get, they tend to get acoustic neuromas, especially like neurofibromatosis type two, okay? They tend to get bilateral acoustic neuromas, right? Those are also known as vestibular schwanomas. And on exams, right? Those classically show up at the cerebellopontine angle, okay? In fact, acoustic neuromas, very high you to know this. They have the most common CNS mass at the cerebellopontine angle. I think the second most common, if I'm not mistaken, is ameligngiaoma.

And then the iris finding, right? So these are the lich nodules. Those are just hematomas in the iris. And then NF1 or neurofibromatosis in general is associated with with meningiomas, okay? So if they tell you like, oh, some of my buddies from a brain biopsy in this patient population, they are getting you to think about a meningioma, okay? Remember, meningiomas classically on MD Ns, they shop like parasagetally on a brain imaging, okay? And the mechanism of inheritance of neurofibromatosis, like many other neurocutaneous disorders, like tuberculosis, is autosomodominant, okay? And the gene mutation, right? NF1, it's like chromosome 17. I believe the gene is known as a neurofibromin. And then NF2 is on chromosome 22. So NF2, chromosome 22, NF1 17. 17 has a one in it. That, NF2, I believe it's like a merlin gene mutation, okay? So that's what I'm going to stop with today. I hope you've had a great day. I am certainly having a great one on my surgery rotation. I wish you all the best and I will see you in the next podcast. God bless and talk to you all later. Enjoy your day.

Vertigo, Tinnitus (ringing in ears), and Sensorineural Hearing Loss.

BPPV causes positional vertigo triggered by changes in head position; Ménière's causes constant/episodic vertigo regardless of position.

Vestibular neuritis involves only vertigo (no hearing loss); Labyrinthitis includes both vertigo AND hearing loss.

Chronic anticoagulation use (old age) or alcoholism/brain atrophy; they cause venous bleeding due to stretching of bridging veins.

It acts as a ryanodine receptor antagonist, preventing excessive calcium release from the sarcoplasmic reticulum into skeletal muscle cytosol.

Hypsarrhythmias (a chaotic pattern).

Myelomeningocele, especially sacral, is classically associated with Chiari malformation Type 2.

Absence seizures (specifically generalized absence seizures), targeting the 3 Hz spike pattern on EEG.

The eighth cranial nerve; Gentamicin is an aminoglycoside.

TSC1 and TSC2.

Calcium Gluconate.

Spina Bifida Occulta (or generally, spinal dysraphism).

NF1 is associated with Café-au-lait spots and Lisch nodules; NF2 is classically associated with bilateral acoustic neuromas.

Vitamin B12 deficiency.

Absence seizures (specifically generalized absence seizures), targeting the 3 Hz spike pattern on EEG.

The eighth cranial nerve; Gentamicin is an aminoglycoside.

TSC1 and TSC2.

Calcium Gluconate.

Spina Bifida Occulta (or generally, spinal dysraphism).

NF1 is associated with Café-au-lait spots and Lisch nodules; NF2 is classically associated with bilateral acoustic neuromas.

Vitamin B12 deficiency.