DIP Episode 311 - The Clutch CSF Findings and Brain Imaging USMLE Podcast (for Step 1-3)

Okay, welcome. My name is Divine. This is episode 311 of the Divine Intervention Podcast. And this podcast I'm going to be describing, in fact I'm going to call this the Clutch CSF Find-Ints, Slash, Brain, and Spine Image and Podcast. Again I'm not going to be using any pictures here. I'm going to be describing the Find-Ints. I think one point I want to be going ahead and establish is that on MBME exams, image-in is not absolutely like many times you can get the question right from just reading the description in the Q-step. I'll say at least in my experience working with students and also taking these exams. About 90% of the images you see on exams are not absolutely necessary. So today basically I'm going to be focusing a lot on the brain, on the spine, on the neck. And again this is a very high-yout podcast, right? You're going to be getting a bunch of questions right from this podcast on your exams. Now one thing I want to say I want to throw a plug in. If you're taking the USMELIS-1 CK-1 CK-3 exams any time soon, at least if you're taking each one, I do have the courses coming up. So I have a 20-hour comprehensive course. I'll first have 2 CK-1 CK-3s from the 26th to the 29th of this month. It's from 11 a.m. to 4 p.m. Pacific Standard Time each day. And then on the 25th we have a 2.5 hour MBME test-taking strategies class again. Lots of people have taken these courses. They've done really well on the exams.

I think the highest score I've had on a present in my course is something just on the tweed. And if you want more information just shoot me an email through the website and I'll give you some more details. We basically cover PEEDS, Surgery, Internal Medicine, OBGY, Neurosyck, the 2020 November changes, Bios stats, ethics. And also the step one material that is migrating from step one to step 2, 2, 3, I cover those as well. So from ecology and things like that, I do cover. And then for those that don't have the luxury of being able to attend 4 days because they have rotations or whatever, in June I have the course. The same 20-hour course is the same cost but I'm compressing it into 2 days. It's on the 18th and 19th of June. And then I have the, so it's basically like 6 to 10 a.m., 1 to 4 p.m. and 6 to 8 p.m. Pacific Standard Time for those 2 days. And then the Thursday before I have the test-taking strategies class from like 3 to 5 p.m. Pacific Time. So that'll be like 6 to 8 30 Eastern Time. So people should have like rough schedules, should be able to attend. So again if you're interested in any of those who should be an email and I'll give you some more details. Okay, so let's maybe start with the CSF Finance first. So what is your expected CSF Finance in a person that had like an operating infection like 2 weeks ago. And now the person is beginning to have like leg weakness.

Well I would hope first of you saying that old divine sounds like this person has a Guillembury syndrome. When the person has Guillembury syndrome, what are you looking for in the person's brain? In their CSF if you do a lumber puncture. I would hope you're saying old divine. I expect to see this thing called albino cytologic dissociation. Again the newer in beam exams they're not very big on buzzwords. So unfortunately what they're going to do for you is they're going to give you CSF studies. You're going to see that in the present CSF. They tell you that you see like 3 or 4 plus protein like a ton of protein. And then you see like 0 to 3 red blood I mean white blood cells per high power field. Right. There is no agreement between the number of white blood cells you're seeing on protein. Usually whenever there is high protein in your CSF you're going to have a high number of white blood cells. If you don't see that that's albino cytologic dissociation albino referring to protein psych Dominic cell. Right. There is no agreement between those two numbers. That's what you find in Guillembury syndrome. Now what if you check the CSF of a person that has like a 30 year old African American female. That you know they tell you that oh she had visual difficulty. Like 2 weeks ago that resolved without treatment right if you see that I hope you're thinking of multiple sclerosis. Right.

When people have multiple sclerosis remember typically on in beam exams we're going to find oligoclonal bands in their CSF. So if you look at your CSF you're going to find oligoclonal bands is just a bunch of band of different antibodies. Usually I G G right that again I kind of markers of inflammation into persons as central nervous system. And one thing I want to say remember of all the cranial nerves that are affected on general the cranial that's affected in MS is cranial to right remember. Multiple sclerosis is a central D malini 18 disease unlike Guillembury syndrome that's a peripheral D malini 18 disease. So because it's a central D malini 18 disease on all your cranial nerves actually happen to derive from your peripheral nervous system. MS only affects one cranial nerve and that one cranial nerve is cranial to right the optic nerve the optic nerve is derived from the dying cephalon right. It's not derived from the neural crest all your cranial nerves are derived from neural crest cells with the exception of cranial to right. So that's why again Guillembury does usually cause cranial nerve deficits MS does the only cranial nerve affected by MS is is cranial to the optic nerve right optic nerve is for example.

And then what are the CSF findings you'd expect in a person that has bacteria meningitis well that's pretty easy right so the opening pressures are going to be high right and you'll have a lucositis right so they're going to have an increase in white blood cells. But because it's a bacterial infection what can a white blood cell would be I hope you're seeing divine it's going to be neutrophils it's going to be neutrophils so neutrophils will be increased right and they'll also have increased protein right so they'll have increased protein and decreased glucose. They'll have increased white blood cells and again it will be neutrophils and then the open pressures will be elevated right but if it's viral meningitis viral meningitis everything is roughly normal right so their CSF open pressures will be roughly normal. They're protein amounts will be roughly normal they'll have an increase in white blood cells it won't be much but those white blood cells will be lymphocytes that's very high to know you'll be lymphocytes right and their glucose will just be. A little bit decrease nothing too big there now what if we're dealing with a fungal meningitis fungal meningitis is pretty much identical to about German meningitis the only difference is the white blood cells that are elevated will be lymphocytes right so they'll have an increase of open pressure they'll have.

They'll have decreased glucose they'll have increased white blood cells again it will be lymphocytes and they'll have increased protein. Now how about TB meningitis for Brazil's TB meningitis it's actually going to be identical to fungal meningitis they'll have increased CSF open pressures decreased glucose increased protein right and they'll have an increase in white blood cells even if TB you know my co-bacterial tuberculosis is a. Bacterial infection it's your. Sell me it's your lymphocytes that help you deal with that although if a person has TB and you biopsy the part of the body that had TB what is the most likely sell you would find out hope you're saying oh divine the most likely sell a fine will be a macro feature right you'll find a micro feature because micro features help you maintain those granadomas most specifically those epithelioid micro features.

Now what if a person comes in with the worst headache of their lives right and they tell you that this person has you know really really bad headache has no core agility and this headache and no core gg is started like 30 minutes ago obviously that's a sub-rock night hemorrhage we know that when people have a sub-rock night hemorrhage the very first thing you're going to do is you're going to do a non-conheads CT you're going to do a non-contrast CT scan of the head is going to be if it's neck if it shows you blood you're done but if he doesn't show you anything you're not done right you need to do a number of punch on you check their CSF when you check their CSF I really hope you're saying oh divine. These people CSF I'm going to be looking for Zanctochromy I'm going to be looking for Zanctochromy right so you're going to find your red blood cells within those people's CSF now what is the classic CSF finding a person that has a major depressive disorder on in the mix sense well we know that when people are depressed there's this monomy theory of depression that people that are depressed they tend to have low levels of nirvana of dopamine and of serotonin.

So the key thing you want to keep out the back of your mind here is that if you check these people CSF you will find lower than normal amounts of nirvana and dopamine and serotonin that's why many of the drugs we give are meant to boost the levels of these agents in the CSF but one actually high yield want to know is cortisol cortisol is actually going to be increased in the CSF of people that have major depressive disorder because they are always stressed right so because you're always stressed you're going to find increased levels of cortisol in their CSF having that increased level of level having those increased levels of cortisol in the CSF is also pathomomonic for present the hospital.

So that's something you want to keep at the back of your mind for for example now what if a person has narcolepsy on mbms right again it will be a person that you know they fall asleep during the day they fall asleep at the will you probably have no weight which tells you that or this person doesn't have obstructive sleep acne or anything weird like that if you see stuff like that what are you expecting in the CSF although hope you're seeing you're going to have decreased levels of a protein called orexin another name for this orexin protein remember that you're going to have a lot of blood cells in the CSF and you're going to have a lot of blood cells in the CSF and you're going to have a lot of blood cells in the CSF and you're going to have a lot of blood cells in the CSF and you're going to have a lot of blood cells in the CSF and you're going to have a lot of blood cells in the CSF and you're going to have a lot of blood cells in the CSF and you're going to have a lot of blood cells in the CSF and you're going to have a lot of blood cells in the CSF and you're going to have a lot of blood cells in the CSF and you're going to have a lot of blood cells in the CSF and you're going to have a lot of blood cells in the CSF and you're going to have a lot of blood cells in the CSF and you're going to have a lot of blood cells in the CSF and you're going to have a lot of blood cells in the CSF and you're going to have a lot of blood cells in the CSF and you're going to have a lot of blood cells in the CSF and you're going to have a lot of blood cells in the CSF and you're going to have a lot of blood cells in the CSF and you're going to have a lot of blood cells in the CSF and you're going to have a lot of blood cells in the CSF and you're going to have a lot of blood cells in the CSF and you're going to have a lot of blood cells in the CSF and you're going to have a lot

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oing to have a lot of blood cells in the CSF and you're going to have a lot of blood cells in the CSF and you're going to have a lot of blood cells in the CSF and you're going to have a lot of blood cells in the CSF and you're going to have a lot of blood cells in the CSF and you're going to have a lot of blood cells in the CSF and you're going to have a lot of blood cells in the CSF and you're going to have a lot of blood cells in the CSF and you're going to have a lot of blood cells in the CSF and you're going to have a lot of blood cells in the CSF and you're going to have a lot of blood cells in the CSF and you're going to have a lot of blood cells in the CSF and you're going to have a lot of blood cells in the CSF and you're going to have a lot of blood cells in the CSF and you're going to have a lot of blood cells in the CSF and you're going to have a lot of blood cells in the CSF and you're going to have a lot of blood cells in the CSF and you're going to have a lot of blood cells in the CSF and you're going to have a lot of blood cells in the CSF and you're going to have a lot of blood cells in the CSF So I think if you kind of understand those CSF findings have discussed you should be in pretty good shape for your exam so let's just jump straight into the brain and you can find it so you may notice I'm trying to get a little aggressive here with how quickly I'm covering the material because I feel like this podcast can go really long if I'm not careful So what if they give you a question about some guy he's like a 35 year old guy and for the last three months you've been having these really bad headaches in the morning and then they tell you that oh you get a CT scan of the head or even an MRI and then you notice a mass that is either parisagetal or you notice a mass that is right underneath the burrow So it's like outside of the brain matter itself and they

tell you that you see like thickening and enhancement of the dura matter in the proximity of the mass If you see stuff like that I want you to think about it in jama remember in jama in general has a dura tail So they won't say oh a person has a brain mass with a dura tail and put an answer in jama no that's too easy right They're going to tell you that you see thickening and enhancement of the dura in the region around this mass If you see stuff like that then you want to think about I mean in jama Now what if they tell you that prenatal ultrasound you know you have a baby the baby is still in utero and you get a prenatal ultrasound and you notice an increase in the no coltranslucency that's pretty easy right that's either going to be Down syndrome right or that's either that's probably going to be Edward syndrome so down and Edwards associated with an increase in no coltranslucency on an emb Mix M Now what if you're getting like a prenatal ultrasound and you detail you that the frontal bones you notice a loss of convexity that's the buzzword A loss of convexity in fact the presence from toe bones you can see looks like a lemon on imaging if you see stuff like that on a prenatal ultrasound If you see stuff like that just stop reading the question the person the child has spina bifida on an mbmi right the child has spina bifida remember there are many kinds of spina bifida And then what if you see ringing enhancing lesions in the brain of a HIV patient what should you be thinking about Well I hope you're going to see all the vine is probably toxoplasmosis or you could be a primary cn-eslam form Remember the way you handle those ringing enhancing lesions in brains of HIV patients first things first you're going to assume it's toxoplasmosis So you're going to go ahead and treat them for toxop by giving them like pyramidamine and sulfodizing If they get better it will sta

lks with if they don't get better there was a primary cn-eslam form So you're going to do a brain biopsy of some sorts to roll out a primary cn-eslam form Now what if they give you a question about a patient again having headache for the last three months worse in the mornings And then you get like a city of the head and you notice like a calcified mass in the frontal lobe Notice the lobe itself it's not in any other lobe it's in the frontal lobe that calcified mass in the frontal lobe If you see that you want to think about an oligodendro glion on an mbmi sometimes you see that it's a frontal lobe mass with coarse calcifications COAR SE with coarse calcifications if you see stuff like that I want you to think about an oligodendro glion And then what if they give you a question about a patient and they tell you that this patient has been having here in difficulty And you'll find a mass at the cerebellum pontine angle on image and on brain imaging So you see a mass at the cerebellum pontine angle and they tell you that it's protruding into the internal calacoustic meyras If you see that I would hope you're seeing divine this is very likely some kind of schwannoma Remember schwannomas sometimes are called acoustic neuromas and when you have them bilaterally or even unilaterally One of the first things you want to think about on an mbmi exam is the person having neurofibromatosis type 2 Remember that's an autism or dominant disorder the mutation is in chromosome 22 And sometimes on mbmi is very nice they will see that they see a mass at the cerebellum pontine angle That has an ice cream cone shape if you see an ice cream cone shape mass at the cerebellum pontine angle So you want you to think about a schwannoma and acoustic neuroma on your exam But if you give you a question about the person having a cerebellum pontine angle mass And you notice that there is no schwannom

a or acoustic neuroma as an answer Then on mbmi exams you want to go ahead and pick the answer that says meninjou Meninjou must at the second most common cerebellum pontine angle mass on mbmi exams Now what if they give you a question about a patient that is an immigrant for the past 4-5 days As we have severe headaches, really high fever, no cordiality And then they tell you that you obtain the image of the brain and you notice that there is enhancement at the base of the brain at the skull base If you see stuff like that I really hope you are saying oh divine This person likely has some sort of TB meningitis Okay now what if they give you a question about like an 11 year old female And they tell you that she is forgetting to turn off the stove, blah blah blah blah blah Right?

And they tell you that oh the obtain the image of the brain And you notice that the corded nuclei on both sides are markedly enlarged If you see that I would hope you are thinking about something called hydrocephalus X-Vaco So Vaco is spelled as VACO hydrocephalus X-Vaco That's a pretty common finding people that have Alzheimer's because they have a lot of cerebellum atrophy Right? So that hydrocephalus X-Vaco looks like the lateral ventricles are huge Actually, sorry did I say dilation of the corded? Forgive me on that, not dilation of the corded, dilation of the lateral ventricles So you see that lateral ventricle dilation, if you see that that's what's called hydrocephalus X-Vaco The cerebro cortex is shrinking so the lateral ventricles look bigger in comparison That's a high-o thing to know for exams Now, one other thing your friends at the MVM you love to do is they like to give you Hydrocephalus questions and ask you to ask to see if you can look a lies delusion Many people tend to struggle with this stuff, but to be honest with you You don't have to struggle with any of this on exams Right?

You just need to ask yourself what is dilated Because if you remember this principle whenever there is an obstruction somewhere Remember, by the way, obstructive hydrocephalus is also called a non-communicating hydrocephalus Whenever there is an obstruction anywhere in the body, you're going to have a build-up of fluid proximal to the obstruction You're going to have no build-up of fluided distal to the obstruction So if you give you an in-me-me-me question, you notice that the persons lateral ventricles are the only things that are dilated And that's what they give you in the Q-stem In this person likely has a stenosis of the interventricular foramen of Monroe Because remember, the two lateral ventricles drain into the interventricular foramen of Monroe Before you go towards the third ventricle Now, if you notice that, oh wow, this person's third ventricle is dilated This person's third ventricle is dilated And you notice that lateral ventricles are also dilated Then that tells you that this person likely has some kind of mid-brain problem They have like aqueductos stenosis The subbral aqueductos silvia is stenosed So because of that, the person's third ventricles and the lateral ventricles will be dilated Another classic way, again, I know this is a brain-imaging podcast But I guess I can throw in a plug for posterior urethral valves versus vesico-uriterral reflux This is something that many met students for again, unfortunately, it reasons You don't get right on exams And remember, vesico-uriterral reflux It's a problem in the urethers, right?

The urethers are proximal to the bladder So those people, the only thing you see on imaging is hydronephrocess The bladder will not be distended But when a person has posterior urethral valves, right? Urethral, u-r-e-t-h-r-a-l It's the urethral that's affected Urethral comes distal to the bladder So these people in addition to having hydronephrocess, they will also have bladder distension Because the problem is distal to the bladder So hopefully that really helps And usually you're going to do some kind of voiding cystoid urethral grap Some kind of cystoid urethral grap to make the diagnosis in those people You can even do a retrograde urethral grap, also remember A retrograde urethral grap in an acute case, right? Obviously posterior urethral valves, vesico-uriterral reflux, these are not acute problems These are chronic problems But the classic acute situation, so an end-bim exam, where you perform a urethral grap urethral grap Right? We'll likely be in the setting of a person that has blood at the urethral medias In the setting of a trauma, that's an acute circumstance But another one, maybe if a person has a scurdo hematoma For a person who has a hematoma of the scurdo, right?

You always want to perform some kind of urethral grap urethral grap To see what in the world is happening to help you plan your surgical repair And then, what if they give you a question about a patient that, you know, They were playing some game, they were hitting the head by a bat The past time for a bat came back, finished the game, and now they are like some lends, right? That's pretty easy, right? That's an acute urethral hematoma When a person has an acute urethral hematoma, what are you supposed to see on image it? Well, if you don't know the contrast-head CT Remember, the reason you, for strokes, you first do a non-contrast-head CT is because blood will basically serve as its own contrast So if you see contrast, their hands bend in the brain, you don't want to be seen Is this blood or is this the contrast that gave this person? So you do a non-conhead CT for an epidural hematoma, right? Classically, that's going to be, you're going to see a lendsheet, it's going to be a hyperdense Lensheet lesion on brain imaging, right? Lensheet lesion on brain imaging But contrast, that was sub-dural hematomas, right? Subdural hematomas on nbim exams usually presents as a child abuse case, right? Where you're abuse in a child, where you can show up in an alcoholic Because remember, as an alcoholic, alcohol causes a presence When you take alcohol over a long period of time It actually causes the presence bring to atrophy, right?

So your brain just gets smaller But on volume of the ear, your skull does not atrophy, so your brain is at atrophys So if that happens, the person is going to, you know, You have like this smaller brain, bobbin around in a fixed-sized box AKA the skull of the cranium So you can tear the bridging veins if you're doing that And as you tear those bridging veins, that's going to cause a sub-dural hematoma And that one is usually not like super acutement, like an epidural It can be like for the past like five or six days The person has just not been feeling right They'll tell you that they are kind of slow, they're kind of forgetful, and things of that nature And again, it will be either a child abuse situation, an alcoholic situation, or an old person Because again, as a person gets older, their brain unfortunately may get smaller And then, what if they give you a question about, And again, remember in a sub-dural hematoma, it's going to be a crescent-shaped hematoma, right? It's going to be a crescent-shaped hematoma And what if they give you a question about a child that's losing motorbiles, stones, has all these upper motor neurons and thums And they have like hypoinitramia, metabolic acidosis, and hyperchylemia If you see that, I really hope you're saying, oh, this person likely has a adrenalin-lucodistrophy So what would you likely find on brain-in-aging? You'll find a bilateral muscle, right?

You have like bilateral white matter de-mylineation in a very okayed If you see that, I want you to think about a adrenalin-lucodistrophy on your exam Now, again, what is the classic finding you'd expect on imaging in a person that's an alcoholic I hope you're seeing o-divine on imaging I would likely find again just global ultrrophy of the cerebral cortex And if a person has any keys in cephalopathy, you can remember it's a triad, right? They'll be confused You'll have like an estagmas that's indicative of the ophthalmoplesia And you'll have it taxia. If you put all those things together, what's the classic CSA finding in those folks? I hope you're seeing o-divine. I mean, not CSA, brain-in-aging finding I hope you're seeing o-divine, I would likely find like hemorrhagic infarctions, right? Andorrhagic infarctions of the mammillary bodies, right? Andorrhagic infarctions of the mammillary bodies And then, what if they give you a question about a person that has like an irregular, again, it'll be like a guy in his 50s or it can even be a young person, then his 50s, heading for the last three months, be getting the weak hem up from bed, right? And then they tell you that brain-in-aging, right? Usually it'll be a brain MRI. Let me tell you this. If you suspect any brain tumor or something, always get an MRI. An MRI is just going to give you much better information than a CT scan, that's for sure.

So they tell you that, oh, on imaging of the brain and MRI of the brain, you see like an irregular, so you'll be an MRI with contrast. You see any irregular, like ring and Hansen lesion that is extending across the corpus calusa. You see stuff like that. I want you to think about glublastoma motiformi, right? I want you to think about GBM, right? Glublastoma motiformi. Typically, it's going to be a mass that crosses that it has some kind of interaction on an embankment exams, where the corpus calusa. And it usually contains like necrosis, so you can see that it contains large areas of necrosis, right? And then you'll see it has visogenic edema, right? There's just a lot of fluid around it. And the person will have like acute like symptoms, right? If you see stuff like that, I want you to think about glublastoma motiformi, right? Now, what if they give you a question about like a woman in her 30s? And you notice that, they tell you that, oh, she, you notice demilination around the ventricles, right? Demilination around the ventricles. If you see stuff like that, I want you to think about like a periventricular demilination. I want you to think about multiple sclerosis. Now, let's talk about the same ventricle. What if you see calcifications around the ventricle in a newborn? And this newborn may have like sensorinear here in loss, may have microcephaly, may have like PTK on the face, the trunk, right? That's like the blueberry muffin rash.

If you see stuff like that, I'll hope you're seeing o-divine. This child likely has some kind of congenital CMV, right? Now, what if they give you a question about a patient that has a very severe headache in December, comes to the emergency room, is friends bring him to the emergency room, and they tell you that oil was grilling because the temperatures were really cooled outside. If you see that, I'll hope you're seeing o-divine. This sounds a no-for-look like carbon monoxide poisoning, right? Carbon monoxide poisoning. When you have carbon monoxide poisoning, what's the classic brain imaging finding? I hope you're seeing o-divine who likely see bilateral hyperintensities in the global spallidus, right? So you see bilateral hyperintensities in the global spallidus and imaging in a person that has carbon monoxide poisoning. Remember, for that, you're going to check their caboxidium o-glubin levels, right? And give them hyperbariac oxygen, like, you know, 100% oxygen. Now, what if they give you a question about a child, and they tell you that on imaging, you'll find an enhancing cystic lesion in the posterior fossa. And that that lesion is effacing the fourth ventricle. It's effacing the fourth ventricle. If you see this, and they don't give you much else beyond that, again, it's a posterior fossa mass. I want you to think about something called a pylocytic astrocytone, right? I want you an exam to think about a pylocytic astrocytone.

If you don't see this as an answer, then you can people to pick in the answer that says medulublastoma. Now, one thing I'll see that's going to hide you to know about medulublastoma is it loves to metastasize through the ventricles into the central canal of the spinal cord, right? So it does this thing called drop metastasis. That's very high to know for purposes of exams. Now, what if they give you a question about, like, a child, and they tell you that this child has a cerebellar mass, right? And this mass is calcified, right? It's a smooth cystic cerebellar mass with calcified. And let's see if this child's hematocritis is like 80% or something crazy high like that. If you see that, that's pretty easy, right? That's hemangoblastoma. Remember, hemangoblastoma is associated with one hipol endow. That's like another somodominant disorder. It's a problem with chromosome 3, right? So those kids, they tend to get like hemangoblastomas, they tend to get like renocell carcinomas, right? By lateral clear serenosella, no carcinomas, and they can get many other kinds of problems, unfortunately. And then they can even get pancreatic like cysts, but that's probably beyond the scum of our discussion. So again, calcified mass cerebellar, kid, easy, that's a hemangoblastoma. Now, what if they give you a question about an enhanced mass within the ventricle in a person that has hydrocephalus? Well, I hope you're seeing that, oh, divine, this is an appendimoma, right?

This is an appendimoma. Remember, the appendimol cells are the things that give rise to CSF. And some famous on exams in ECD referred to as a toothpaste-like tumor within the ventricles. It's been within the fourth ventricle for some reason. Appendimomas, they love to like squeeze tumor cells through the medial forimenogeondi and the lateral forimeno of luscha, right? So that's why they're called toothpaste tumors. It was like they are squeezing the tumor out as like a toothpaste from those forimeno. So that's how you know for for exams. And then, what if they give you a question about a heterogeneous enhanced mass in the brain of like some HIV patients with no central and crosses? They tell you that, oh, it's an enhanced mass is heterogeneous, so you're like, oh, I hope this is not GBM. But then they tell you in the Q StM that there is no central and crosses in a HIV patient. If you see stuff like that, I really, really want you to think about a primary CNS lymphoma. Right? Think about a primary CNS lymphoma. Now, what if they give you a question about like a supicella mass in a child, right? So it's above the cellotrasticity is supicella. And then they tell you that this mass contains a complex cystic structure. And it has a lot of coarse calcifications. If you see that, what are you thinking about? Well, I hope you're saying, oh, divine. This person likely has some kind of... Chrinofarinjoma. Right?

Remember, these chinofarinjomas sometimes on exams in the CDM refer to us Adamantinomadas, chinofarinjoma. Right? And these things, they can lick this blue oil fluid. Right? And they can compress the optic chiasm and cause a bite temporal heteronymous, no homonymous. Bite temporal heteronymous, hemianopsy, essentially tonal vision. And then, what if they give you a question about a patient that has like skin, like a 19 year old male, he has skin hyperpigmentation, and they tell you that you obtain an MRI. And that MRI shows an enhancing mass. And enhancing mass that is proximal to the optic chiasm, right? And enhancing mass that is proximal to the optic chiasm. If you see this, I really hope you're saying, oh, divine. This person likely has some kind of optic nerve glioma. Right? Remember, the optic nerve, and this person obviously has like neurofibromatosis of some sort. Right? So remember, these optic nerve gliomas have an association with... These optic nerve gliomas, again, they have an association with neurofibromatosis, especially like NF, NF, and NF. Remember, that's an autosomodominant disorder. It's a problem with chromosome 17 on nb-emixemps. Right? So again, remember, the optic nerve comes before the chiasm. And then after the chiasm, you have the optic radiation. Right? So you see a mass before the optic chiasm, proximal to the optic chiasm as I described on image. And I want you to think about a person having an optic nerve glioma.

Now, what if they give you a question about a person and you know, it's a child, and they tell you that this child, you know, they give you like imaging, brain imaging. And you notice like multiple like well circumscribed litigations in the cranium of the child. If you see that, what should you be thinking about? Right? So if you see that, I would really hope you're saying, oh, divine, this person likely has longer hand cell histiosytosis. If you see like almost like just these little holes in the child's like skull, litigations, the world circumscribed. Think about longer hand cell histiosytosis. Remember, that's associated with burbec granules. Right? Those tenish-shaped rachet granules on biopsy. Okay. Now, what if they give you a question about, and then they tell you that, oh, we have this patient that has double vision when they're trying to like climb upstairs. Or whatever. Right? And they tell you that, oh, when you tell them to look up, they are unable to look up. And then they tell you that imaging shows like an enhanced mass above the tectum. Right? Above the tectum. Right? And again, this patient that has this vertical giznepropia. If you see stuff like this, I want you to think about a pineyloma. Right? I want you to think about a pineyloma. Remember, the very cool conjugate giznep is the superior colliculus. Right? It's the superior colliculus. So the thing is, the pineal gland is just above the superior colliculus.

The pineal gland, as you may say, is superior to the superior colliculus. So if a patient has a pineyloma, that can compress the superior colliculus. And the person can essentially have a vertical giznepalsey. Right? That was called parynotes syndrome on an embini. And remember, you can also get parynotes syndrome not just from parynolomans on embinis. You can get them from like a germinoma or a teratoma. Teratomas and germinomas, they absolutely love to grow. Right? They absolutely love to grow around the pineylo gland area. Right? And also, if you're looking for a vascular cause of parynotes syndrome on your exam, you want to think about like some kind of infarction of the superior serabella artery. The superior serabella artery is the blood supply. It is the blood supply to the superior colliculus. So easy would remember that the superior is match. So people can definitely get some problems there if you infarct that. You basically infarct the superior colliculus and your vertical conjugate giznepalsey. Or be begun. Now, what if they give you a question about like HIV patients? And the presence of the cd 4 comes like 10 or 15, something like super super low. And in detail, you have an e-symmetric multifocal white-moderal legions in the brain. Right? If you see that, right? Multifocal white-moderal legions, right? Then you're thinking about some kind of dimi-lineating problem, probably like from, especially with this low cd 4 count, think about the gc virus, right?

Think about a pml progressive multifocal luchensifalopathy. Right? Progressive multifocal luchensifalopathy. Remember, this is also associated with this drug called a nautilizumab. Nautilizumab is a monoclonal antibody against integrates. I believe it's alpha-point integrates that use to treat multiple sclerosis. It's associated with a relatively high risk. Or for currents of progressive multifocal luchensifalopathy. Progressive multifocal luchensifalopathy. Now, what if they give you a question about like a child? And they tell you that this child on imaging, like a chest for a neck CT, you'll find a mass that is inferior to the mylohyoid muscle. So inferior to the mylohyoid muscle. And then they tell you that this neck imaging shows again this midline cystic structure, right? And it enhances peripherally. That's actually very high autonone. So midline cystic structure and it enhances peripherally. If you see this, I really, really want you to think about a phyroglosodoxis. I really want you to think about a phyroglosodoxis. Remember, it's from the back of the tongue, right, from the foreman's seeker. So the phyroglosodoxis, you see this cystic mass that enhances peripherally, right, on imaging. If you see that, I want you to think about a phyroglosodoxis. Again, it will be inferior to the to your mylohyoid. But what if they tell you that you see this similar cystic lesion, but it's at the angle of one of the mandibles, right?

Again, if it's at the angle of the mandible, they're pretty much telling you that, oh, this thing is lateral. This thing is not midline, right? So it will be at the angle of the mandible. And then it will be, sometimes it can be like posterior to the submandibular gland, or it can be anterior to the stenoclydomostoid muscle, right? So I'll say it again, posterior to the submandibular gland, anterior to the stenoclydomostoid, muscle, right? If you see stuff like that, and they tell you that, oh, you know, again, your single cystic mass is lateral to the midline, and it does not, or if it does, maybe very minimal, like peripheral enhancement, if it does not, and you see, like, again, no peripheral enhancement, I want you to think about. I really want you to think about a brinkel cleft cyst. Remember, in a thyrglyso-doxis, your thyrglyso-doxis obliterate, that's an endogromal structure. But in a brinkel cleft cyst, your second to your fourth fine gel grooves or clefts, filter obliterate, right? Filter obliterate, right? So you did not obliterate those seconds or third fine gel grooves or clefts, which are ectoderm derived, right? So that tells you that you want to brinkel cleft cyst. Now, what if they give you a question about a patient that is hearing voices? What is the likely, you know, schizophrenia, basically? What is the likely CSF finding? I mean, not CSF, breathing machine finding. I hope you're seeing all the fine.

We're going to find enlargement of the person's alladrom, and the a third, and the a third, and the a third, and the triophols. Okay. Now, what if they give you a question about a patient that has no originality and stuff? And they tell you that, or bringing it into your notice that there's a lot of... There's a lot of hyper-density or increased signal intensity from the... From the temporal loop, if you see that, I would really hope you're saying, oh, divine, this person probably has some kind of herpes and cephalitis, right? Herpes and cephalitis, herpes and cephalitis. Although, remember, you're going to find like, increase the tension of the temporal loop. In the person that has a seizure, right? So that's another association, because why is that? Well, most seizures tend to arise from the temporal loop. And then, what if they give you a question about a patient? And they tell you the experience having gradual hearing loss, and they tell you that they get a CT of the neck and the head. And let's say they tell you that, oh, you know, the CT shows like a soft tissue mass, right? So CT shows like a soft tissue mass. How would you put this on an exam? So you see like a soft tissue mass. And they tell you that, oh, this soft tissue mass has completely faced the person's... Orcicles, like the amalus, the anincus, and the ST Ps.

If you see something like this, in fact, something they say that, oh, there is a pacification of the mastoid air cells, so mess up your head and get you the big mastoid. The mastoid air is remembered as an acute problem. These people that have been having this problem for a long period of time, right? So you see a soft tissue mass, grown within the middle ear, neck CT, right? And you notice like, complete or, you know, near completely faced end of the ossecles of the ears, the middle ears, only think about a colistia tumor. Remember, those people need surgery, because that carotene debris, the debris can cause like just permanent problems in terms of conductive hearing loss, since you're pretty much destroying the ossecles of the head. Now, what if they give you a question about a patient, and they tell you that, oh, it's a woman in her 30s, and she comes into the emergency room, because for the last 24 hours she's been having severe eye pain and severe blurry vision in that eye. And they tell you that MRI of the brain shows increased signal intensity around the optic nerve, right? If you see stuff like this, right? Again, if you notice, even if you don't know the... Whatever the image is, and I'm describing, these are women in her 30s, right? They're probably thinking about some kind of optic nerve, right? They're probably thinking about some kind of optic nerve. Remember, you treat that with high dose IV-colicosteros. If not, those people can get permanently blind, right?

Again, it's going to be funny. People that have multiple sclerosis. And again, usually on in-beaming exams, people that have MS, they're going to be females in their 30s, but they can be... They're going to be older, they can definitely be older than that. Now, what if they give you a question about... A young child, they tell you that, oh, they obtain a non-contrast CT in a young child. And they tell you that, oh, in one of the eyes, you see chorus calcifications, like chorus calcifications in the eyes, in the retina. If you see that, I really hope you're saying, oh, the brain in this child likely has some kind of retinoblastoma. Remember, that's an RBG mutation, and it's all the zoom-on dominance in heritins, and unfortunately, these kids, right? They have a very high risk of contracting of developing an osteosarcoma. Sometimes they call osteosarcoma, osteogenics, or coma, on in-beaming exams. And then, what if they give you a question about... Actually, what are the contents of the carotid's sheath? This is something that many people seem to forget for some reason for in-beaming exams. It's very high, you know. The carotid's sheath actually contains the internal carotid artery. It contains the internal drug loving, and it contains... So it contains the common carotid artery, not internal carotid, sorry. The common carotid artery, the internal drug loving, and the vigospere, that's greener than 10, the all-round-throw-the-carotid sheath.

The reason you need to know that is they love to give questions on in-beaming exams, where let's see if you're placing a central line in a joggerloving, right? And then they say, oh, which of the full instructions is most likely to be injured in the close area, right? Is it going to be the common carotid artery? It's going to be the greener of 10, right? Exactly. That's why you do need to know the contents of the carotid sheath, okay? The contents of the carotid sheath. Now, what if they give you a question about a patient that was born at 28 weeks, like very premature, and they tell you that he has been the necure for a long time? I think they tell you that they get like... They get like imaging of the child, like brain imaging, and you notice cut out calcifications in both eyes in that child. That was born prematurely. If you see this, especially the child that has received prolonged oxygen therapy, I want you to think about right, nopathy of prematurity, right? Right, nopathy of prematurity on an ambient exam. And then what if they give you a question about, you know, like CT of the spine, right? Again, usually for a person who has a brain or a spinal cord problem, you usually want to do some kind of MRI. That's usually better. But sometimes you can do CT that's fine, right? So let's say you perform a CT of the spine.

And you notice that there's, you know, in an IV drug user, they start describing to you that, oh, there is a loss of disc space height, there's a region of the end plate, there's bone destruction, and a person has back pain. Again, an IV drug user wants to think about osteomyelitis, right? Remember, osteomyelitis, the most common cause of osteomyelitis, is going to be stuff, it's going to be staphoreus. It's going to be staphoreus. But if you see like a similar presentation, right, you know, in like an immigrant or a TSE agent, so that has a lot of foreign, you know, like immigrant exposure, right? And they tell you that the discs are spirit. So this is a very important thing to know. The interval interval, interval, the discs for this pathology, we're going to talk about, they're scared, right? I mean, so it's not scared if you're a spirit, they're a spirit, right? Because this is a 3 TB meningi, TB osteomyelitis. So remember, TB osteomyelitis in the spine can cause parts disease. So the person will have like, the person will have like a version of the end please, bone destruction, but you will not have anything with the disc space height, right? The interval, the disc will be spirit. Because the thing is TB actually does not have these proteolytic enzymes to break down the substance that constitutes the, that constitutes the, the interval, the discs. So that's something I ought to know for exams, right?

And then what's the most likely portion of a person's spine to infarct? Well, I hope you're seeing all the vine is probably going to be like the opera thoracic spine or the thoracolumbar spine. Remember, those ones, the anterior spinal artery for those regions, right? They are supplied by something called the order of a damcoids. The order of a damcoids comes off of the, the de-sendinial order. So the problem is if you're fixing a triple A, and you periodically, while you're fixing that triple A, you infarct the order of a damcoids, then the unfortunate thing that can happen is you can have infarction of the, not just the order, but of the order of a damcoids. So the present anterior spinal artery for the thoracic and the opera lumbar spine is gone, right? So that's something kind of high you to keep out the bulk of your mind for, for exams. So again, remember TB osteomyelitis does not affect the interintibural, interintibural discs. Now, what if they give you a question about a patient, you know, he's a 69-year old male, he has smoked two packs of cigarettes per day since he was 14. And then it comes out of severe abdominal pain, and then they tell you that, oh, they get like a, they tell you that, they get imaging, right? And you get imaging either like a CT scan or whatever. And you notice calcifications that are anterior to the vertebral bodies. Note this buzzword, calcifications that are anterior to the vertebral bodies.

If you see stuff like that, I want you to think about a ruptured triple-lay. So what's this imaging find in, right? Again, it's kind of around vertebral bodies, so I'm just going to include it in this brain-imaging thin. You're thinking of something called the drape de-order sign. Remember, if a person has a triple-lay, that aneurysm, right? Already has a lot of calcifications in front of it, inside it. So if the person, and you know that the aeurysm, stands like right in front of your vertebral bodies. So if your aeurysm explodes, your abdominal aeurysm explodes, the part of the wall of that aeurysm is going to like almost fall back on your vertebral bodies. So if you do imaging, you'll find, especially like sight imaging, you're going to find calcifications and tear to the vertebral bodies. Although you can also see it on like just perpendicular imaging. If you see stuff like that, I want you to think about a ruptured triple-lay, a ruptured abdominal aeurysm, right? And again, whenever you see a person with a history of like a woman in her 50s, and she's been having headaches for the last couple of weeks, and then you see multiple like lesions in the brain. That's going to be brain met. So remember brain met, some more common data, primary brain, malignancy. And what if they tell you that you're performing for a telescopic exam, and you notice a loss of disc margins, right? Like the optic disc margins are gone.

If you see that, that's idiopathy, intracranial hypertension, right? That's pretty classic four. Again, remember that was what was previously called a pseudo-tumor cerebral. And then I guess just to wrap things up here, let me just talk about some of the tear or tear or tear which is real quick, that's really a lot of an exam. I'm going to more detail on these in my neuro podcasts, right? My neuro podcasts follow the neuro shelf, they're super comprehensive. Remember, if a person infarcts the temporal lobe, what otter is implicated in that? That's the middle cerebral otter. Right? The temporal lobe is supplied by the middle cerebral. Your frontal lobes, right? I'm going to be supplied by the anterior cerebral otter. Right? But remember the part of your frontal lobe that deals with the brocus area, because it's lateral in the cortex. That's going to be middle cerebral otter, tear or tear as well. So if you see a person that has leg weakness, you're probably thinking more along the lines of the medial frontal lobe. That's something that you're going to see more with an anterior cerebral otter problem. Right? And if a person has like cortical blindness, that's pretty easy, right? Remember, your occipital lobe, that's where your visual center is. Right? So a person can have cortical blindness when they have a problem with the posterior cerebral otter, which is the primary blood supply of the occipital lobe.

And then remember, the posterior limb of the internal capsule where you have your cortical spinal track going through, that's supplied by the lenticular straight artery. Right? That's supplied by the lenticular straight artery. And then remember, your lateral medulla, right? It's supplied by your paica posterior inferior cerebral otter, although they can put vertebral artery as an answer, but if they put both, go with paica because it's more specific. Your medulla is supplied by the anterior spinal artery. That's a branch of vertebral otter. And if we go up to the ponds, your lateral ponds, right? You supply by your eica, your anterior inferior cerebral otter, where your medial ponds is supplied by your paramedian pond, teen arteries. Right? And remember, if a person has a problem with the basilar artery, that's going to cause a locked-in syndrome, right? Because the entire ponds will be infarcted, right? So all your esenin-d-sendipath is a kind of landlocked. The only thing those people will be able to do is to be able to blink their eyes pretty much on exams. And then we've talked about how the superior cerebral otter, right? We said that, is the thing that supplies the superior colliculus, and you can cause parino syndrome if you infarct it. And remember, the posterior colliculus artery, right? It runs alongside cranial 3. So whenever you have an aneurysm of p-com, that can compress cranial 3 and cause, like a down-and-out eye in things of that nature.

And also, obviously, uncle herniation can cause the same thing. Okay, so I think I'm going to go ahead and stop. Even if I am tired, I kind of need some rest. But as I do at the end of every podcast, I do offer limited one-on-one tutoring for... I say limited because my schedule now gets three full. So if you want to book with me, you're probably thinking more like three weeks or there about a head. But I do offer one-on-one tutoring for the Step 1 exams, the 2 CK Step 3 exams. Pretty clinical medical exams, 30-ish-elf exams. If you're preparing for residency applications, like an iris application, I work with people on those. Again, I've worked with tons of people that have tricky applications or a lot of red flags and all those things. I work with people in those circumstances, and I've really polished some people's applications. Again, I have residents in many disciplines all over the country. I mean, even specialties that like a deal traditionally doesn't match into like dermatology. I've worked with people that have overcome those odds and matched into those disciplines. So again, if that's something I'm interested in, just shoot me an email. And I'll be happy to give you some more information on the cost, my schedule and things of that nature. And I have these podcasts on the website, Divine Intervention Podcasts.com. If you subscribe to the website whenever I make a new podcast, you'll get an email notification.

But I also have these podcasts on Google podcasts, on Apple podcasts, on Spotify. And my videos have them on You Tube. I have a You Tube channel actually, Divine Intervention, USM Ly Podcasts and Videos. If you subscribe to that You Tube channel, again, that's where I put my videos. Now, a common question people say is Divine, I cannot see all 311 of your podcasts. The reason you can't see them is it's a Word Press role. I literally have no control over it. So the most recent 150 podcasts will show up on all these podcasts apps. But the ones from episode one, you'll have to go to the website to source them. You can download them there. You can listen to them from there. If you download them, then you can pretty much listen to them on, you know, double speed or whatever, on like VLC, media player, something, something of that sort. And then my life lesson of today is getting to the root of a problem. Getting to the root of a problem, right? This is going to be a short life lesson because this has been a lengthy podcast. Getting to the root of a problem. So what do I mean by that? I feel like many people, they have problems in their lives. They keep trying many different things. The problems never end up getting solved. Why? Because they are not getting to the root of that problem. You see certain people, they have this thought process that they did throw. Unfortunately, even some governments have this thought process that they did throw enough money at a problem.

The problem will fix itself. It's not going to fix itself, right? There are many problems in life that are not fixed with money. Or if you need to fix with money, they are fixed when you solve, you use that money to fix the underlying issue. Right? So you see some people, they're like, okay, I'm going to start doing 2000 Anki cards a day. But you notice their scores are not going up because they've not fixed it on the list. Because they've not fixed it on the line issue. Right? So many times in life, we go through problems. We keep trying, trying, trying, working hard, but not working smart. Right? You need to fix it on the line problem. If a person has an addiction, again, certain times you see people, they are trying to fix that addiction by like, okay, I will brute force, quote, ter ki ba ba ba ba ba ba. But then they've not fixed it on the line issue, which is their mind. Right? Many battles that people face in life, to be honest with you. Many problems that people face in mind, even in the way people take tests is in their mind. They just have maladaptive thinking patterns. I mean, like many people have worked with that have improved their scores. Again, they just had a certain odd, wrong thought pattern on endemic exams. And then you modify that and then the problem faces itself. So before you jump around trying to solve a problem, ask yourself, what's the underlying cause? It's almost like you're trying to find the path of physiology behind the problem. Right?

Go to the source of that problem. Stop fixing the symptoms of the problem. Right? If you're just fixing the symptoms, right? Oh, okay, let me fix the symptom. You are not really solving anything. That problem is going to come back in a big back form. Right? And one thing that people don't realize is when a problem, when you notice a problem initially, don't wait. Keep fix, like fix that problem when it's small, not when it's big and will destroy you. I see this occasionally in my church that problems are like little kids. Well, what is one thing you can count on for little kids? Little kids, they grow. A problem that is not fixed when it's small will eventually become some kind of emergency. Right? You've got to fix a problem early. Right? If not, that thing can destroy your person. Right? If you notice, many addictions that a person has is not that, or they just stumbled upon that addiction and they have it. No, they've had it for years for decades. Right? But when it was like a minor problem, they didn't deal with it. And I guess maybe one other thing I'll say as a, as a corollary to that is, if you know something is not good, don't start it. That's the thing to be honest with you. I actually don't keep many commitments. I don't. Before I make a commitment, I think about it long and hard. I don't make many commitments. I don't. I don't. Before I start certain things, I think about it like, oh, like a TV show that I want to watch.

Ask myself, hmm, what is it with this TV show? What is the sketch behind this TV show? Right? It is a TV show. I know that, you know, shows things that I know will take my mind in all sorts of wrong directions. Then I don't start it. Doesn't matter how awesome the TV show is or whatever. Right? Again, this is just all ideas of personal discipline. Right? You know what you want in life. There are some people that, a certain addiction that they've gone into and that addiction has held them down for years, is something that started from an innocent TV show they watched. Already may have seen a scene or something weird. Again, they just let them down just wrong directions for the long call. So again, I'll encourage you, if all you start something, just evaluate it. Right? Think with the end in mind. Right? Some people are very reactive. Be proactive. When you're making commitments, when you're about to do something, evaluate it ahead of time before jumping into it. Right? There's even a part of the Bible that says that, foolish people, they see trouble and they just walk straight through it. And obviously, trouble is going to come upon them. But the people that are righteous and wise, they look ahead, they see trouble and they take cover. Right? Take cover. Don't just jump into problems. Learn from the experiences of other people. Right? Like, don't just say, oh, I'll just take one step, two steps, two steps, whatever, and see what happens. See where the chips fall. No. Right?

Even that term of, who less see where the night sticks also, less see where the wind sticks us, I hate those terms. Because those are terms of people that are reactive. Not people that are proactive. Right? You need to plan for things. You need to plan for things. How am I going to build student loans? How am I going to study for a step point? You need to have a solid plan. Look at the experiences of people that have been successful in something. And try to get advice from them. Right? That's why you see many times, I write all these ready posts. Right? Oh, how to study for this? How to do this? How to do that? Or those of people still email me, even if I've answered those questions like 500 times. You know, that's an exaggeration, obviously. But again, right? Like, go ahead and check. Check these things. Look at the experiences of people that are knowledgeable in something. And then don't make those same mistakes. That's the whole mark of a person that is proactive. Right? Not a person that waits until the problem shows up before they start reacting to it. So hopefully you found this to be helpful. Thank you so much for listening. Again, sorry, this podcast is a little wrong. But it's a super high-end podcast. There's a probably discussed like 70 or 80 different conditions that show up on in-beaming exams with this. But again, I brought in some images and some CSF correlates. So thank you for listening. I'll see you next time. God bless you. Thank you.

Albino cytologic dissociation (high protein, normal WBC count).

Cranial Nerve II (Optic nerve), because it is derived from the diencephalon, not the neural crest.

High opening pressure, increased WBC count dominated by neutrophils, increased protein, and decreased glucose.

Lymphocytes (even though it is technically a bacterial infection).

A ruptured abdominal aortic aneurysm (AAA), known as the "drape de-order sign."

Enlarged lateral ventricles due to cerebral cortex atrophy (e.g., in Alzheimer's disease).

Bacterial has high neutrophils, low glucose, and high protein; Viral/Fungal have lymphocytes, normal-to-high protein, and near-normal glucose.

Pineyloma (or Germinoma/Teratoma).

A crescent-shaped collection of blood over the surface of the brain.

Common Carotid Artery, Internal Jugular Vein, and Vagus nerve.

Staphylococcus aureus.

Thyroglossal duct cyst (or thyroglossa).

Bacterial has high neutrophils, low glucose, and high protein; Viral/Fungal have lymphocytes, normal-to-high protein, and near-normal glucose.

Pineyloma (or Germinoma/Teratoma).

A crescent-shaped collection of blood over the surface of the brain.

Common Carotid Artery, Internal Jugular Vein, and Vagus nerve.

Staphylococcus aureus.

Thyroglossal duct cyst (or thyroglossa).