DIP Episode 19 - Neurology Shelf Review Part 1

Welcome, my name is divine. I am a fourth-year medical student. In today's episode of the divine intervention podcast We're gonna be talking about neurology and this is primarily for people that are thinking a third-year neurology shelf or those that studying neurology for step one or step two CK We'll do this in parts because if I were to do one for review, it will take many many hours So let's begin So the first question talks about a brain tumor that can present with a loss of vertical gaze, okay So obviously the thing I'm going after here is a pinealoma, okay, remember This can present as parynotes syndrome Basically remember that the pineal gland is low-key thread if you look at the brain stem It's located superior to the superior coliculus and the superior coliculus is the vertical congegase gase center So whenever you have a pinealoma a mass that's compressing the superior coliculus You will get into problems with vertical congegase Okay, next question 13-month-old child with a history of hypopigmented macules presents with seizures So what's the diagnosis? What are the EEG findings and how is this treated? Okay, so this kid Let's assume this kid has actually spots, okay? There are the hypopigmented macules you find on the skin in tuberous sclerosis So the seizure syndrome that has a very strong association with tuberous sclerosis is something known as West syndrome Every now and then you see people refer to it as an infantile spasm, okay?

The classic EEG finding you want to be aware of you don't need to know how to spot it We need to recognize the buzzword is a hypsiridmia, okay? And it's treated with ACTH It's an unusual answer. That's why they love it on exams or you could also use an anti-peleptic drug known as vagabatrin, okay? It's a GABA-urgic agent Okay, next question So this is a fairly long one the most common primary brain tumor in kids I'll talk about a mandolublastoma, pandemoma, cranioferin, geoma, GBM, acoustic neuromas And some other stuff. So I guess let's just talk about it right now then So basically the most common primary brain tumor in kids is a pylucytic astrocytoma, okay? So because it's an astrocytoma right to And astrocytes are kind of glial cell the marker is GFAP glial fibrillary acetic protein, okay? And the classic finding on histology has things known as rosin thal fibers. I'll encourage you to look up a picture of this They're like pinkish like you'll synophilic fibers. They're sort of shaped like coxcrus And then a mandolublastoma the common location on exams is the cerebellum, okay?

And the associated histologic finding is a homerite rosette In fact, I would encourage you to do a google search for the forming types of rosettes and pathology It leaves out like the different kinds of rosettes like pandemoma rosettes, homerite rosettes, perivascular pseudo rosettes and stuff like that And tells you the tumors that they are associated with although I also mentioned that here, okay? So homerite rosettes are classically associated with pedloblastomas and usually growing the cerebellum vernis on exams Now anapendimoma on exams usually presents as hydrocephalus, okay? Because it may green the ventricleus system or like the central canal of the spinal cord, okay? And on histology you may find um Perivascular pseudo rosettes or ependomal rosettes, okay? I can do that google search. I just mentioned For craniofarinjomas they love to see if you can Tie this in with embryology they are classically derived from a structural and as rocky spouch, okay? And on imaging if they tell you that the kid presenting with like seizures or visual problems They do like some kind of brain imaging you see calcifications You can pretty much stop reading the question and know that they're getting you to think of a craniofarinjoma, okay?

It may present with bytemporal hemionapsia right because it can compress the optic chiasm And it may also present with signs of hypopituitarism right so like deficiencies of the anterior pituitary hormone because it can compress the pituitary gland or the pituitary stock now GBM right so glioblastoma multiformin. It's the most common primary brain tumor in adults Although remember that match to the brain at the most common cause of brain cancers in In adults usually like they're usually like Multiple masses of they're usually like very well circumscribed or you find them at like the blood brain barrier The gray white junction, okay? Those are classic formats But the most common brain tumor that arises from the brain itself is glioblastoma Multiforme, okay? And the classic presentation on imaging. They even describe this in a question. They may say It's a butterfly shaped mass that crosses the corpus calusum and it has this has like a ton of edema and central no creuses That's the big buzzword you're looking for central no creuses of imaging You really want to think about GBM with that, okay? And again because it's an astrocytoma in fact Neurosurgeons call this a stage four astrocytoma right the tumor marker is a GFAP Now for bilateral acoustic neuromas. It's basically a kind of shuanoma classically involves cranio nerve eight um The big tumor marker you want to be aware of they love this a lot of exams is S100, okay?

And the thing is if you see bilateral acoustic neuromas on an exam the first big thing you really want to think of is a neurofibromatosis type two Okay, and these tumors they are almost almost always at the cerebellum pointing angle, okay? In fact, if you get an exam question that says the most common tumor found at the CP angle, okay? Is a is an acoustic neuroma, okay? The second most common will be a mengeoma, okay? now So that sort of leads to a next question right so parasadero mass along the folk cerebride Really want to think about a mengeoma, okay? So they usually shop at convexities in the cerebral cortex like the folk cerebride for example, okay? The classic histological finding is a samoma body, okay? Remember samoma bodies are common in mengeomas and They are common in papillary thyroid cancer and they also common in a serosacist adenocarcinomas of the ovary, okay? So those are your high-yield samoma body associations instead of want to take away so And if they don't put samoma body on your exam, they may try to trip you up with the buzzword laminated calcification Okay, that's a classic mbamie strategy to take what you know and just put in a different language, okay? So just be mindful of that now the calcified mass in a kid that crosses the midline That'll be a neuroblastoma, okay? They try to trip you up on exams by getting you to different sheathes from Wilms tumor, okay?

So Wilms tumor is usually unilateral and does not cross the midline and neuroblastoma usually does cross the midline And it almost always has calcifications on abdominal imaging. That's what will tilt you away from a Wilms tumor Now the neuroblastoma it's a neuro tumor right so you could also find it in the posterior Mediastinum, okay? Remember that for these exams they love you to know what Kind of tumors are rising in the anterior medius thinum or the posterior medius thinum and stuff like that, okay? So neuro tumors in general like the neuroblastoma can arise in the posterior medius thinum The anterior medius thinum is more like thymomas and teratomas, okay? Your terributees Now a neuroblastomas they do have an association with neurofibromatosis type one, okay? And they also have an association with a weird syndrome known as Beckwith with a men syndrome Beckwith with a men syndrome Now Beckwith with a men syndrome. It's one of those things that you see people get wrong quite often on exams And the big thing you just want to remember here are the associations right so neuroblastoma is one Beckwith with a men association Another high-yield association is overgrowth of one side of the body, right? So it's like The buzz where there is hemie hypertrophy where one side of the body is bigger than the other Another association with Beckwith with a men syndrome is hypo glycemic seizure in a newborn, okay?

Because BW syndrome is associated with hyperplasia of the beta cells of the pancreatic i-let So they produce a ton of insulin which can severely lower their blood neonates block glucose levels and precipitate seizures So that's another association you want to know and also Welmstrummer is also associated with Beckwith with a men syndrome one more tumor is a hepatoblastoma right so if they present a question where um You see a right-up quadrant mass in a neonate and they have some of these other BW syndrome findings Think of a hepatoblastoma, okay? It's a mass in the liver Now tumor with a Friday appearance That's more legal danger glioma On exams it'll almost certainly be in the frontal lobe Uh hemangioblastoma is a brain tumor that produces hypo, okay? So if they give you a person that has like signs of increased i-c-p headaches like chronic headaches and They tell you that the patient has a hematochrid of like I don't like 60 percent something like super high Think of polycythemia from hemangioblastoma and The thing is these tumors they have an association with the one-hipole lindale syndrome VHL, okay? And usually they try to treat them because they can actually cause a life threatening hemorrhage In the central nervous system because they are hypervascular Okay, so now we're done with this one.

Let's jump to the next question So recent viral illness plus vertical plus tenitis Hopefully this gets you thinking of labyrinthitis Not the way they could frame this on an exam is as a vestibular arthritis, okay? So if you basically see a person that has like vertiginous symptoms They have to not like ringing in the ears and they recently had a viral infection or some kind of Prespiratory infection the first thing you want to think about on an exam is labyrinthitis, okay? And then if they tell you the person has the feeling like the room is spinning and this feeling comes when they change positions uh You really want to think about bppv bppv stands for b9 proxysmal positional vertigo, okay? So it's a positional vertigo, right? So as they change position they have a Trigrin of that feeling like the room is spinning around them and another classic thing they put on exams is that the person when you're doing a provocative maneuver to make the diagnosis like the dix hall pike maneuver they have an astagmas As that test is being conducted, okay? If you want to treat this You basically try to do maneuvers that displays the ortholets in the semi-secular canals that are triggering the symptoms Some of these maneuvers is like the epi maneuver There's there's some month maneuver There's another one that's like probably offers like zero yield for exams I believe it's called the brand deroff maneuver, okay?

But those are different ways you can try to displace the otoconia if you may into the right spot so that the symptoms are relieved Okay, next question Anastasia over the medial thigh and weakness in thigh abduction So anesthesia over the medial thigh and weakness in thigh abduction. This is an obturator nerve injury, okay? Those classically are extra L2 to 4, okay? Is this one of those weird neurological complains that are tied to like a specific nerve that they love you to know for for shelf exams And then an asthesia over the lateral thigh is classic injury to the lateral femoral cutaneous nerve, right? So that kind of makes sense right lateral femoral because the femur the femur is around the thigh area, right? So that's an easy way to remember that Now next question Seven-year-old kid with ataxia hypertrophic cardiomyopathy and low extremity hyporeflexia, okay? So what's the diagnosis? What's the genetic pathophysiology? How's this inherited? I would actually say some special things there and then what's the most common cause of death in these kids and how can this be treated? so This child has a phridraxy ataxia, okay? The classic presentation is a kit with ataxia, okay?

With cardiac problems usually from hypertrophic cardiomyopathy and also low extremity weakness because they have destruction of the posterior columns of the spinal cord So don't like what you'll find in a phytamine B12 deficiency So this kid has phridraxy ataxia The mechanism of inheritance is autosomal recessive, okay? The thing is they love To test the mechanism of inheritance because this is one of those tri-neucleothide repeat disorders that does not have autosomal dominant inheritance, okay? Most, that was same general most tri-neucleothide repeat disorders have autosomal dominant inheritance but there are certain exceptions like phridraxy ataxia, phridraxy ataxia has autosomal recessive inheritance, okay? So they love to test that because it's unusual The associated mutation is a GAAA tri-neucleothide repeat that basically causes a loss of function mutation in the phytaxine gene on chromosome 9 and When you have this loss of function mutation, you have reduced levels of phytaxine The thing is phytaxine I think of it as an iron binding protein So think of it if you don't have if you have a deficiency of a protein that binds iron iron can run a mock and cause a lot of problems It can cause like problems in the cerebellum that's how you get the ataxia You can cause some problems in the heart from oxidative damage That's how you get the hypertrophic cardiomyopathy potentially, okay?

So associate phridraxy ataxia with GAA tri-neucleothide repeat Rosomal recessive inheritance ataxia low extremity weakness, okay? And the cardiac problems like hypertrophic cardiomyopathy in a kid, okay? The most common cause of death in this kid's actually is Is a congestive heart failure from the hypertrophic cardiomyopathy and certain arrhythmias that he commonly get and I mean you can try treating the heart failure with a bitter blocker But most of these kids ultimately are succumb to the illness unfortunately Okay, so let's jump to the next question So 35-year-old female with a BMI of 35 with visual difficulty and severe intermeat and headaches, okay? She takes tetracycline for acne ding ding ding So for the scopic exam is consistent with papilladema. What's the diagnosis? What kind of diagnostic testing would you want to do? How is this managed pharmacologically? What other things could you do lifestyle changes surgery blah blah blah so let's talk about this right? So young female With visual difficulty on a very high BMI Hopefully that gets you thinking of pseudo tumor cerebride Another name for this condition is idiopathic intracranial hypertension, okay? Now if these patients present usually the first step in management is to get a fondoscopic exam, okay? Classically you'll find a papilladema so you're like hmm papilladema So this person potentially has increased ICP so the next thing you jump to is to then get a head CT, okay?

The head CT will be stone-court normal and then you say okay I think this person has pseudo tumor cerebride So your next step after that will then be to get a lumbar puncture, okay? And on a lumbar puncture you classically see elevated opening pressures, okay? So it may be like more than 200 or 250 even up to 500 in some cases Okay, I believe the unit I'm using here will be centimeters of water So they have very high pressures on lumbar puncture and The way you actually treat I-I-H so idiopathic intracranial hypertension is to recommend weight loss, okay? You can also try to decrease the production of CSF with azulomide, okay? Remember as azulomide is a carbonic and hydrace inhibitor Alternatively you could also do zero lumbar punctures remember lumbar punctures are diagnostic and therapeutic of this disorder You can place a VP shunt, okay, to try to reduce Sertoshunt CSF to like the the GI tract for example You can also tell the patients to try to avoid triggers like vitamin E-DRV tips, right?

So like treatments for acne like isotric knowing or uh Antibiotic exactly right to your 30s inhibitors that are bacteria static like tetracycline uh, if they have like very bad visual difficulty that's like Sort of like getting them close to like being blind you can also do a surgical procedure known as an optic nerve fenestration you basically just Poke holes along the path of the optic nerve to relieve those pressures Okay, next question Management of an ischemic stroke Your initial imaging time window for TP administration Some contraindications to the administration of TPA Blood pressure management strategies in stroke settings, including the drugs that you could use to make that happen And then we'll talk about the concept of permissive hypertension in patients that That have ischemic strokes that are not going to get TPA. So for example, let's say we presented outside the time window So let's answer these questions, okay So uh in an ischemic stroke in general your first imaging test is a non-contrast Head CT, okay, because that helps you differentiate between an ischemic stroke and a hemorrhagic stroke, okay? You don't give contrast because contrast looks just like blood on CT Imaging so that would make the diagnosis of a hemorrhagic stroke very difficult, okay? So you perform a non-con head CT first, okay?

And then if it's negative you then get an MRI because an MRI is very sensitive for the detection of an ischemic stroke Okay, in general if the patient presents within three to four and a half hours of symptom onset It is safe and they don't have contraindications to the administration of TPA. You can go ahead and give those people TPA, okay? This is super low yield, but it may be a thin that shows up on an exam But you can actually go up to six hours if you can inject TPA directly into the involved vessel Now There are certain high yield contraindications to the administration of TPA or because again I mean if you give TPA to some people they can bleed out and die which is not ideal So certain high yield contraindications that things like a bleeding disorder, right? Or a person that has like GI bleeding or they had like recent brain surgery Or they're an anti-quagulation and the PTI NR is like super high So they're like over-quagulated In general for those people you want to go ahead and avoid TPA because the risks of like severe bleeding and death probably not worth the probably not worth the try And in general for a person has an ischemic stroke and they're not getting TPA, okay?

You can actually allow the blood pressures to run high so they can produce the brain Because in an ischemic stroke right to have some thin known as a cytotoxic edema That's a concept that's probably not very relevant to Discussions I'm gonna skip that although if you have any questions You're welcome to email me or look it up But basically they have cytotoxic edema so the brain is beginning to swell So they're intracranial pressures are increasing and that's for the decreasing brain profusion So you let the person's blood pressure run high In fact the cut of classically used is you can let the pressure run as high as a 220 Sestolic over 120 diastolic, okay, to keep the brain profused Although if a person is getting TPA you don't want those kinds of high pressures right so they don't bleed out and die In general your blood pressures have to be below 185 over 110 Okay, if you're gonna get TPA And if a patient has a hemorrhagic stroke right so not an ischemic stroke a hemorrhagic stroke And they have very high blood pressures or they have Some kind of hypertensive and cephalopathy you can try to lower the blood pressure with drugs like a labeta law Remember that's an alpha beta blocker on my trope or site Which is a powerful dilator of blood vessels You could alternatively use an acardi Pine my cardepine is a dihydroperidine calcium channel blocker Then um, I think that's all I want to see on this slide. Okay. Good.

So let's jump to the next one So 17-year-old is brought to the eD by his daughter He reports a 15-minute episode an hour ago where he completely lost vision in one eye That has since resolved. So what is the next best step in management? What's the pharmacological management? What are the surgical strategies you could employ and what is the most important Modifiable risk factor for strobely love this stuff on the mb ME risk factors risk factors So let's answer this question. Okay, so this patient had a TIA okay Transient is gimmick attack. Okay If you want to be a little more specific he has something known as amorosis few gags Okay, the classic description on exempt is as a curtain coming down over the eye that causes like a painless loss of vision Okay, so in general for these patients you want to do a couple of things right? So you want to get some kind of brain imaging like a non-conhead CT first or an MR You could also get an MR if the non-conhead CT is negative You could get an eco cardiogram to detect cardiac cause of the vascular insult Alternatively, you could also get a corroded ultrasound with Doppler in fact. I will say on exams Um, the answer I would most likely go with Excuse me If I was asked about imaging in this patient population is a corroded ultrasound with Doppler Okay, because most TIA is a rise from like Like emblazum or like hyper-perfusion through the corroded arteries Okay, and classically you hear corroded a brewing with that.

Okay Now in general this patient You probably want to place them on aspirin. I'll see aspirin is like a safe answer in exams If they are intolerant to aspirin like they have like aspirin exacerbated respiratory disease Which was previously I believe called aspirin induced asthma you could consider giving them a clopidogra instead, okay Also on exams I will see a mix of aspirin and extended released diperidomal The drug name is like agronox could also be used that believe there's actually studies that have shown that a mixture of aspirin and diperidomal works better than aspirin alone um The only time I will see that giving a brain or some kind of anti-cogulan like wafring is right answer on exams Is if they tell you that oh an echocardiogram Reveals like some kind of valveulopthology and we predispose them to embolec phenomena Or they tell you that the person has an irregularly irregular rhythm on telemetry right so they have a fit for example That's probably the only time we're given an anti-cogulan like hyper-inol wafring is a reasonable answer choice on a test Okay, and in general, I mean there are some very specific criteria for these But the big thing I'll just say is if stenosis detected on On ultrasound or like CT angiography of the carotid Ottery is more than 70% in a guy. Okay, so in males and they're symptomatic You generally want to refer them for something known as a carotid in that erectomy, okay?

a carotid in that erectomy and The most important modifibolous factor for stroke is a hypertension, okay? Most important modifibolous factor for stroke is hypertension Okay now six-year-old male with difficulty walking plus using his arms to walk up his leg slash thighs Plus hypertrophy of the carotid by lateral so what's the diagnosis? How do you test for this? What's the genetic pathophysiology and how is this inherited? Okay, what's the elevated serum marker? How do you treat this? What's the most common cause of death? We'll talk about that and then we'll talk about a close causing disease Okay, so this kid has something on his gaur sign Okay, so that should tell you that they have doshing most kind of dystrophy Okay, in general the way you manage this is you want to check a creatine kinase first We usually be elevated, okay? Because those people's muscles are classically broken down, okay? And then the next thing you want to do is to do a disc check for a distrofinging mutation, okay? Um, don't be deceived by an answer choice that says to do a muscle biopsy on exams Uh, that is no longer the standard of care, okay? In general, you want to check a ck first as your first step, okay? And then the next thing you do is to uh, do DNA testin for the distrofin gen mutation, okay?

Uh, distrofin is actually a gene you find it on the excromosome and it connects the cytoskeleton of uh, myocybers right so like skeletal like muscle cells uh, to the extracellular matrix like the bizolaminate, okay? So if you have a complete like loss of function of that gene, right? Complete loss of distrofin you get into like a lot of muscular problems, okay? Um, in fact in the q-stem I described that oh the person's cows are big Uh, it's just a deposition of fat and fibrocess in the low extremity that causes that calf pseudo-hypactrophy that is classically associated with uh, the shins muscular distrofin And in general this disease uh, it's inherited in an x-linked recessive fashion So it's probably not a girl disease on exams, okay?

And you treat with steroids, steroids in pro-survivol somewhat Although that's to a very limited extent uh, you also try to like give these kids like very solid like high-calorie nutrition And most of them unfortunately die from uh, like respiratory failure or like cardiac failure when the muscular dystrophy begins to involve their, their own organs I mean they're their cardiac and uh, like uh, like the muscles that control respiration like the phrenic, I mean like the diaphragm for example Uh, the close causing disease here is a becker muscular dystrophy They tend to lift to their fifties, they tend to not have intellectual disability And the part, it's also a dystrophy in gen mutation also x-linked recessive inheritance But usually these kids uh, don't have a complete loss of dystrophy, okay? They have like a pretty severe loss but they still have like some dystrophy activity Good, so let's jump to the next question Confusion plus of thermoplegia I'll say this of thermoplegia on exams it classically presents as an astagnus, okay? plus a taxi right so like walking like you just uh, uh, took too much boost, okay? In a chronic alcoholic, right? So uh, this should hopefully get you thinking of when he keys uh, syndrome, okay? It's a triad on exams, right? You won't say oh, a patient walks in with confusion of thermoplegia and anitaxia No, then I'm gonna do that.

They're gonna describe a person like staggering the exam room and they feel you perform a fundoscopic exam or some kind of i exam and they detect my stagmus and then they they'll probably pose the question to the person like oh where are you and they can save their, I don't know like in Mars or something ridiculous, okay? You sort of need to put all that together to know that it's renecise and cephalopathy, okay? And if you add on to all the symptoms where they're like making stuff up that's known as a confabulation or they're uh, having amnesia they're beginning to forget stuff, okay? They have progressed to coarsacops psychosis. In general, renecise syndrome is reversible but coarsacops is not and the classic image and finding in these uh, the sodders, right? because it's a spectrum like where any keys all the way up to coarsacops, you if you do like bring imaging you'll usually usually an MRI, you'll find a hemorrhagic in fact of the manillary bodies, okay? And the deficient vitamin here is vitamin B1, okay? Thiamine and no, I don't think this has exactly been proven but there are many schools of thought out there that believe that some of the findings you get in this disease are from problems with proper function of transketolies. Remember transketolies is one of the big enzymes, it's probably the rich limiting enzyme of the non-oxidated phase of the pentose phosphate pathway also known as the hexose one of phosphate shunt, okay?

So they believe it's problems with transketolies because transketolies uses that have been B1 of thiamine as a cofactor that causes many of the problems you observe in where any key coarsacoff syndrome. And in general your treatment here is an IV thiamine, okay? Good, next question. A classic presentation on myestheniographies, right? So the way myestheniographies presents is usually a female in her 30s to 50s, okay? presents with a diplopia that's worse by the end of the day like like double vision or she says that oh she has like her eyes drop, she finds it difficult to keep her eyelids up by the end of the day or difficulty swallowing, that's another classic presentation or they have like some kind of weird speech, okay? If you see all those things, young female and it gets worse the more you test it think about myestheniographies, okay? If you want to compare and contrast this with Lambert etymisthenic syndrome, Lambert etymisthenic syndrome usually shows up more in older individuals, right? So people in their 70s, classic inhibitions that have a small cell lung cancer, okay? And the thing is Lambert etymisthenic syndrome actually gets better when you keep testing the muscle function because as you as you may know the pathophysiology involves the formation of autoantibodies against pristineaptic, voltage gated, calcium channels, okay?

So when you form those autoantibodies they attack that pristineaptic voltage gated calcium channel, you don't have the entry of calcium that causes the exosytosis and release of acetylcholine from vesicles at the neuromuscular junction, so you can run into muscle fatigue, okay? But if you keep working out that muscle, you begin to recruit more calcium to that voltage gated calcium channel and you can outcompete the abrant autoantibodies and you could potentially relieve the symptoms, right? So Lambert etymisthenic syndrome gets better with use, okay? But myestheniographies gets worse with use, okay? Now the pathophysiology of myestheniographies, right? It's the formation of autoantibodies against the nicotinic acetylcholine receptor, okay? So that's why you get the muscle weakness because you're not getting acetylcholine activity, okay? And the way you diagnose this the solder in general is you perform a test for the antiacetylcholine receptor antibodies, okay? In fact that's currently the standard of care, okay? So be careful on exams with picking an adrophonium test, that's no longer the standard of care. The first line diagnostic test for my astheniographies is to check the serum for antiacetylcholine receptor antibodies, okay? But if you don't see that as an optional exam, then you can pick the tensileant test, okay?

Where your administrative reformion, adrophonium is an acetylcholine esterase inhibitor, so by inhibiting acetylcholine esterase, your levels of acetylcholine go up and those outcompete the bad antibodies, okay? And in general, you treat my astheniographies with pyridolstigmin, pyridolstigmin helps you get rid of my astheniographies, okay? Pyridolstigmin is an acetylcholine esterase inhibitor, so it boosts your acetylcholine levels and that can outcompete the bad antibodies that you'll find on the surface of the nicotinic acetylcholine receptor and that could potentially relieve symptoms, okay? The associated new plasm with myastheniographies is a thymoma, okay? Classically shows up as an anterior medius-tinal mass, okay? So if they give you an exam question where a person has a myastheniographies, one answer choice, actually, after you've made the diagnosis, maybe to get a chest CT scan, okay? To look for a thymoma, okay? Before you start like pharmacological treatment, because there are some people where their myastheniographies could actually remit with the removal of the thymus, okay? So just keep that in mind, okay? Next question. Now, so where's the lesion? What's the occluded artery, right? So loss of pain and temperature on the left face, okay? Loss of pain and temperature on the right side of the body, okay? Absend gag reflex, right? So that's like crinonerv 9 or 10 territory, okay? And then vertigo, so that's potentially crinonerv 8 territory, okay?

And then these person also has toses and meiosis on the left, okay? So they have like an Ipsilateral Horner syndrome, okay? So let's explain the pathophysiology here, okay? So let's localize the lesion, right? This is one of the reasons I love neurology, localizing lesions. You don't need to do some expensive testing, just need to sort of like use your brain to make the diagnosis. So this patient has lost pain and temperature on the left face, okay? So this patient potentially has involvement of the trigeminal nerve, right? That the part of the trigeminal nerve that contains control, sorry, pain and temperature sensation for the face. Remember it's Ipsilateral innervation, okay? The person has lost pain and temperature on the right side of the body, right? So they may have involvement of the spinal thalamic tract. Remember the spinal thalamic tract runs in the lateral, not medium, lateral brinstem, okay? And it causes control lateral symptoms because remember your spinal thalamic tract decusates at the level of the anterior white comission in the spinal cord before it ascends in the brinstem. And then so control lateral symptoms. So if you have symptoms on the right, you probably have the lesion on the left, okay? You have an absent guard reflex, that's cranial nine slash ten gone, okay? That's medulla, okay? Remember your cranial nerves and where they line the brinstem, right? cranial nerves, nine through twelve, lined a medulla, okay? Ready to go, cranial eight, right?

So cranial eight, that's like medulla-ish ponds territory, okay? And then toses and meiosis on the left, okay? So honor syndrome, right? So an involvement of the cervical sympathetic tract, okay, that goes all the way to the superior cervical ganglia, that controls dilution of the pupial. That's a part of the sympathetic nervous system, okay? Honor syndrome lesions are usually epsilon-adural, okay? I remember that those fibers that control the sympathetic nervous system innervation of the eye run in the lateral brinstem as well, okay? So if you put all these things together, you can sort of imagine that this person has a lateral medullary syndrome, okay? In fact, if I'm not mistaken, this is known as Wallenberg's syndrome and the artery that's probably involved here is the posterior inferior cerebellar artery, okay? Your paika, okay? Because it supplies the lateral medulla, okay? The lateral medulla. Now, if a patient has right-sided paralysis and tongue deviation to the left, okay? Again, tongue deviation to the left, okay? That's a cranial 12 lesion, okay? Remember that the hypoglossal nerve runs in the medulla, okay? Medulla, okay? So this is a medulla-recentral. And the reason we have the right-sided paralysis is that we have involvement of the corticospinal tract. Remember the corticospinal tract, it decusates at the level of the medulla repair amids and it runs in the medulla, not lateral medulla, brinstem, okay?

So that's potentially why we have right-sided paralysis because they have the lesion prior to the pyramidal decussion, okay? And the artery that's probably involved here is the anterior spinal artery, okay? Remember the anterior spinal artery, supplies the anterior to thirds of the spinal cord, but it also supplies the medulla medulla, okay? So let's jump to the next question. Now, 35-year-old African-American presents with a three-day history of eye pain, okay? Fundoscopic exam is notable for congenital artery fema and meiosis. CBC is notable for increased ACE levels and a calcium of 12.9, okay? And let me also tell you that this African-American female has has shortness of breath and I tell you that oh she has a chest x-ray finding of bilateral hyalur lymphadenopathy. Hopefully this tells you that this patient has sacroidosis, okay? And the thing with sacroidosis is that it usually presents with like many problems, right? So you can present with like the respiratory difficulty, you can present with the classic eye finding, right? So like eye pain, that's an optic neuritis. And the classic presentation of that is you have eye pain and like an afferent popularity faith and you can see that the person's eye is like red and it hurts as the person tries to move your eye, okay? If you see that think about optic neuritis has a classic association with sacroidosis also has a classic association with with osteosolid disease multiple sclerosis, okay? Multiple sclerosis, okay?

Now next question, 35-year-old female with tremors in her hands bilaterally that are worsened by stretching of by stretching out her hand, okay? So what's the diagnosis, right? So what if I give you the other information that it gets better when she takes alcohol, okay? Hopefully that should get you thinking of an essential tremor, a benign essential tremor, okay? In general, these things are usually familiar actually, they actually associated with autozomo dominant inheritance and you want to be able to differentiate this from Parkinson's disease, okay? Benign essential tremors usually symmetric, Parkinson's disease tremors are usually asymmetric, okay? The benign essential tremors, the tremors are worsened by activity, the tremors you find and the resting tremors you find in Parkinson's disease actually made better with activity, okay? And in general, the way you treat a benign essential tremor is with a beta blocker like proprenolol or barbiturite, like primidone, remember, barbiturites increase the duration of opening of chloride channel, so they cause hyperpolarization of neurons. So you can use primidone, it's first line or you can use proprenolol, non-selective beta blocker, okay? So blocks both beta one and two receptors, that's also first line as well, okay? So that's where I'm going to stop today. We'll continue with this in a different podcast and I wish you all the best on whatever exam.

If you have any questions, feel free to drop me a line and have a wonderful day and God bless. Thank you.

Parinaud's syndrome (loss of vertical gaze).

Hypsiridmia.

Medulloblastoma.

Neuroblastoma (differentiates from Wilms tumor which is usually unilateral).

Papilledema on fundoscopic exam and elevated opening pressure on lumbar puncture.

Hypertension.

Dix-Hallpike maneuver; nystagmus.

Homerite rosettes (histology) and cerebellum (common location).

Neuroblastoma.

Confusion, Ataxia, Oculomotor abnormalities (ophthalmoplegia).

MG gets worse with use; LEMS gets better with use.

Neurofibromatosis Type 2 (NF2).

Essential Tremor.

Antiacetylcholine receptor antibodies in serum; Tensilon test (if antibody testing is unavailable).

Homerite rosettes (histology) and cerebellum (common location).

Neuroblastoma.

Confusion, Ataxia, Oculomotor abnormalities (ophthalmoplegia).

MG gets worse with use; LEMS gets better with use.

Neurofibromatosis Type 2 (NF2).

Essential Tremor.

Antiacetylcholine receptor antibodies in serum; Tensilon test (if antibody testing is unavailable).