DIP Episode 211 - USMLE Step 2CK Rapid Review Series 32

Okay, welcome. My name is Divine, I'm a resident. This is episode 211 of the Divine Intervention Podcasts. And in this podcast, I'll be continuing the Rapid Review series for the US Emily Step 2 CK exam. This will actually be Rapid Review Series 32. This podcast is going to be a really short podcast, but it's going to be a really high-year podcast because it's one of those things that people tend to get wrong on exams. It's actually going to be neuro-focused, right? But I don't want people to keep making these kinds of mistakes on exams. Like these are like five, six easy points on a test, right? But people tend to get the stuff wrong. So let's just get through it. And really the focus of today's podcast is just going to be on like some common brain lesions, okay? Like some common brain lesions. Just again, things people tend to kind of like forget after Step 1 and not do it with a Wendy and Contrary on Step 2 CK. Now, the thing is, if for example, I mean, it's kind of dovetails of some stuff I mentioned in the previous podcast, right? But I want to make it a little more comprehensive and see some more things here, right? So what if they give you a question about a patient that has trouble forming new memories? What part of the brain is all screwed up? Well, I would really hope you're telling me about the hippocampus, right? The thing is, if they don't put hippocampus, then they will likely put like temporal lobe.

What in general, the hippocampus is a very important key component of the temporal lobe. So if you're having trouble with making new memories like an anterior grade amnesia, that's a hippocampal lesion, right? And that's something that happens in the temporal lobe. And then also remember, if the temporal lobe doesn't work, right? The person will likely get some kind of renegies aphasia, right? Renegies aphasia. And one thing I think as you go ahead and point out, right? Like this brookas versus renegies and stuff. There's one thing your friends at the MBM love to capitalize on people think for whatever reason that if you injure the temporal lobe on either side or the frontal lobe on either side, you can get a brookas official renegies aphasia. That is actually not true. I'll say that right now. That is not true. Right? The thing is, if you have a lesion, like an, and it's going to be like an MC stroke, right? On an MBM example, because we think about the homonculus, the middle cerebral artery covers with the brookas and the renegies area of the brain. It's actually going to be a lesion on the dominant hemisphere, right? So say, for example, you're a right-handed person. If you're a right-handed person, that means your left hemisphere is the dominant hemisphere. So when you have like a lesion, like in the left MCA, that's what will cause a brookas aphasia and a renegies aphasia.

And I really hope that you understand the differences between a brookas and a renegies aphasia, right? Like a brookas aphasia is going to be like the non-fluent aphasia, right? And it's almost like the person has like a motor aphasia. And the reason it's almost like a motor aphasia is because remember that the pre-central gyres, like the brookas areas around the pre-central gyres, winky areas are around the post-central gyres. I remember that the pre-central gyres is model. The post-central gyres is sensory, right? So the thing is, when people have the brookas aphasia, it's a non-fluent aphasia, right? Those people also tend to have like dysaphria and they also tend to have impaired repetition, but their comprehension is per se. Okay? And again, if they want to be like super, super, super specific, right? Like the actual part of the brain that causes brookas aphasia is like the inferior frontal gyres. Okay? And again, remember, it's in the dominant cerebral hemispheres. So if you're right handed person, that's going to be your left cerebral hemispheres, right? And then when he's aphasia, right? He's a fluent aphasia. So these people have good speech. They're not going to have dysaphria. They're still going to have problems with repetition, right? But the thing is their comprehension is all screwed up. Okay? So this is when he's aphasia, is a fluent aphasia, brookas aphasia is a non-fluent aphasia. Okay?

And again, these are problems in the dominant hemisphere for that respective individual, right? And then I guess another key area where your friends at the NBA, we love to test this dominant versus non-dominant stuff is when you're talking about like the Pridal Loop, right? So for example, what if they give you a question about a patient and this patient is neglecting one side of the world, like putting makeup on only one side of your face, they have like a proxy, like they can't tell one finger apart from the other, then what what Pridal Loop has been screwed up? Is it the dominant Pridal Loop or the non-dominant Pridal Loop? Well, I'll really hope you're telling me that it's the non-dominant Pridal Loop, right? So whenever you see a person have like a hemispational neglect, that's a non-dominant Pridal Loop Legion, right? But on the flip side ready, if a person has a dominant Pridal Loop Legion, right? That will be the person who have like again, the aphasis that I've kind of talked about like the brookas, the wrenikis, right? But they will also have problems like a graphia, a calculea, so they'll have trouble like doing math, they'll have trouble doing graphs, you'll have trouble writing, right? In fact, that's something that's actually known as Gersmann syndrome, right? So Gersmann from Momestik is probably a German term, but it's G-E-R-S-T, M-A-D-O-N, Gersmann syndrome, okay?

So again, your dominant Pridal Loop will be like an essentially like a left, your left Pridal Loop, so it'll be a left MCA Legion that will give rise to those problems, your non-dominant Pridal Loop will be a right MCA Legion that gives rise to those kinds of problems, so please, please, please make sure that you understand exactly what I just mentioned, right? And then if a person has a cortical blindness, what part of the brain is all screwed up? Well, I would really hope you're telling me that the person will have like a Legion to the occipital loop, right? Basically, like the things I'm going to be talking about in this podcast are big picture things, but they are big picture things that seem to evaporate from people's minds after they take step one, right? But they are high-youtu-no for step two, CK, and unfortunately step three, right? So the thing is that person has cortical blindness because remember your primary visual cortex is in the occipital loop, right? So if you scrub the occipital loop, then the person is going to get into, going to get into trouble with blindness, right? So and remember also if you have like an occipital loop Legion, obviously you have a homonymous hemi anopsia, right? You have a homonymous hemi anopsia, and some of you may be wondering, divine, what do you mean by homonymous hemi anopsia? Well, homonymous hemi anopsia means you lose the same visual field in both eyes, right?

So it's like you're losing the right visual field in the right eye and the right visual field in the left eye, right? So whenever you have an occipital loop Legion, basically any Legion that's distal to the optic chiasm will cause a contralateral, homonymous hemi anopsia, say that again will cause a contralateral, homonymous hemi anopsia, right? So say for example, your left occipital loop is all screwed up, you're going to lose the right visual field in both eyes, right? So it's going to be a contralateral, right? And it's going to be a homonymous hemi anopsia, homonymous homo means like the same, right? So if you're losing the right visual field in the right eye and the right visual field in the left eye, that's a homonymous hemi anopsia, right? But think about it, if you have a Legion at the level of the optic chiasm, you have a heteronimus hemi anopsia, right? What do I mean by heteronimus hemi anopsia? It means you're losing two different visual fields in both eyes, right? So for example, if you have a compression at the optic chiasm, say for example from a prolactinoma or a craniofarygeoma, the person will lose the right visual field in the right eye and the left visual field in the left eye, right? So notice it's not like we're losing the right visual field in both eyes or the left visual field in both eyes, no, we're just losing the right visual field in the right eye, the left visual field in the left eye, right?

So that's what's typically known as a bite temporal hemi anopsia aka tunnel vision. Sometimes people call it again bilateral heteronimus hemi anopsia, right? So heteronimus means like heterogenous, right? So that means things are different, okay? Again, that's something you want to make sure you know for exams, right? And then if for example they give you a question about a patient and this patient, which I've again I've kind of talked about this already, right? If a patient has their eyes deviating towards the side of a lesion, right? I hope you're telling me that that's a frontal eye field lesion. If a person has their eyes deviating away from the side of, that's a cortical problem obviously, right? If a person has the eyes deviating away from the side of the lesion, I'll really hope that you're telling me that oh this person has a PPR-F lesion, right? Like a lesion of the paramedian, pontin reticular formation and already describe the mechanisms behind that in like literally the podcast I mean yesterday, right? And then what if they give you a question about a patient and this patient is you know has like executive dysfunction, cannot balance their checks anymore, they have like contralateral like opomodonioron signs, right? They have like the babinsky, they have like a pronator drift and you know they just kind of become disinhibited and start doing like inappropriate things, right? If you see those kinds of things, what lobe of the brain is all screwed up?

I really hope you're telling me that it's the frontal lobe, right? It's the frontal lobe. Remember this is floorly high up to now. The frontal lobe, right, controls executive function, right? Controls executive function. So when people have issues with the frontal lobe, remember the frontal lobe, right, is essentially like mostly mono, in fact it's probably almost entirely like mono activity for your brain, right? So those people become disinhibited, right? They will become like apathetic, you can't get much from them, right? It's almost like having like a flat effect, right? They'll have like they will have trouble like with executive tasks, right? And those people, right, like they will begin to do things that are inappropriate and because the corticospinal tract starts in the cortex, right? They'll have contralateral opomodonioron symptoms, right? So like they'll have like hyperreflexia. So let's say it's like the right frontal lobe that's screwed up. They'll have like left-sided hyperreflexia. They'll have like a left positive babinski, like an outgoing babinski. They'll have like a predator drift and all that stuff, right? So the thing is you want to keep that at the back of your mind with the frontal lobe. One thing I think I want to say with the frontal lobe is please, please, please, please, please, please, do not forget that when a person has a frontal lobe problem, okay?

One thing that will classically happen is they can have like reemergence of like reflexes that are lost when the person is like super, super young, right? That's one thing that can happen. And they're one of the high your frontal lobe association for in-beaming exemptions. If they give you a question about a person that has a brain tumor in the frontal lobe and it's calcified, right? And they may even tell you that oh, they biopsy the mass and they notice that it has like a fried egg appearance on histology. If you see that, I would really hope you're thinking about analigo dendroglioma, okay? I'll say that again, analigo dendroglioma. So frontal lobe mass, it's calcified, right? On histology has a fried egg appearance that's an oligo dendroglioma on an endgame exempt, right? And then what if they give you a question about a person that you know just has like tremors or they have like choriform movements or they have, you know, they're kind of like, yeah, I'll just say like just in general tremors for a person has tremors, what kind of problems you want to think about? I would really hope you're thinking about just in general a basal ganglia problem, okay? A basal ganglia problem when a person has a lot of tremors, right? And then if a person, for example, or it loses like all motor function on just one side of the body is like, man, this person's left side, like the operand lower extremities, motor function is just completely gone.

If you see that, I would really hope you're thinking about a lesion to the internal capsule, most specifically the posterior limb of the internal capsule, right? The person likely has like rupture of a baryanurism. In fact, many times it's called a shakobushard microorganism, right? Usually from hypertension, right? So you have like a shakobushard microorganism of the lenticular striad artery with that ruptures, right? You'll essentially infarct, you'll have a hemorrhagic infarction of the posterior limb of the internal capsule, and that can absolutely, absolutely, absolutely cause those things where you see like those clean cuts, right? Even like a pure sensory, like a pure sensory, like stroke, right? Again, that's almost always from a problem in the at the level of the internal capsule, right? And again, lenticular striad arteries and the thing is the biggest risk factor for that presentation is actually hypertension. That's a very common NV Me exam question that you want to keep at the back of your mind, right? And then obviously for a person who has a lesion of the substantiate Niagara, right? They will get like these Parkinsonian symptoms. And if you see like Parkinsonian symptoms in a young person on an NV Me exam, you want to think about two potential pathologies, right? If it's a psych question, the person probably took like improperly cooked like heroin, right?

So they have like MPTP damage of the substantiate Niagara, so they have like a permanent early in life Parkinsonism, right? Alternatively, and it's usually like a very sudden onset Parkinsonism, right? And then also think of Wilson's disease. When you see a person that has Parkinsonian like symptoms and then they have like some psych issues like depression or schizophrenia, like symptoms going on. And usually they'll have like liver problems as well. Think about Wilson's disease. Remember, Wilson's disease, right? Like that copper can deposit in the bisocanglia and it can begin to cause Parkinsonian like symptoms, right? And then obviously if you have a question about a person that's you know is having trouble like with being a roused, right? I would hope you're thinking more along the lines of like an issue at the level of the reticule activating system, right? Remember, it's an activating system, right? So it's something it's actually in the midbrain, right? That's why if people have like midbrain injury, it'll be those people essentially become comatose, right? Like it'll be very hard to kind of like rouse those people from from sleep and whatnot, right? They'll just be completely comatose. And then there's this thing that most of you probably learned maybe like in med school like your first or second year. But usually you won't even find it in like a step one resource or step two CK resource or step three resource, but they love to test this on exams.

Is this whole thing called like the red nucleus, right? The red nucleus. The thing is the red nucleus, right? I think of it as like a defining part of the brain. And why do I call it a defining part of the brain? The thing is if you have, if we like if you as you study for the USMLE exams, you probably heard of these terms, the corticate and deseribrate posturing, right? You've probably heard of the terms, the corticate and deseribrate posturing. The thing is when a person has deseribrate posturing, it means that their problems are below the level of the red nucleus in the midbrain. Whenever you see a person have the corticate posturing, it means that they have problems above the level of the red nucleus. And again, like I said, the red nucleus is found in the midbrain, right? Basically, when you think and I'll encourage you to probably look up pictures of this, but the corticate posturing essentially, it's a person that's lying completely straight. And then they have like their two fists kind of clenched towards their chests, right? And just like giving people that mental image, it's just much easier to remember than to say this is flexed, this is extended, this, no, no, no, no, no, I'm not going to do that to you, right? So the corticate posturing, that's a problem above the level of the red nucleus. And an easy way to remember that is the corticate, right? Your cortex is literally above the red nucleus, right?

So if you have a problem above the red nucleus, that's the corticate posturing. And again, it's a person like essentially lying straight, okay? And then there are two fists, I kind of clenched towards the middle of their chest, right? That's the corticate posturing, right? Basically, your wrists, your fingers, those are flexed, your elbows are flexed as well, right? And then your legs are kind of like extended and rotated inward. On the flip side, the serivate posturing is a problem below the level of the red nucleus, okay? And basically, the thing that happens with the serivate posturing is the prison is just all stretched out, right? They're like all stretched out. They are elbows and their hands is kind of like off to the side, but their wrists are flexed, right? It's almost like having like a double-weather-step post, right? But everything is all extended. Elbows are extended, wrists, like everything is all extended, right? So again, I will encourage you to, I will encourage you to look up pictures of this online, right? And then obviously, if a prison has haunting, tin-stile symptoms, you can treat that to like an atrophy of the cortic nucleus, right? If a prison has like, they tell you that, oh, this prison has lost all motor function, right? The only thing the prison can do is to like wink their eyes, right? You want to think about like a locked-in syndrome under those circumstances.

Remember, there are two things that can cause locked-in syndrome, an MBM exams, right? You can get a vascular cause of locked-in syndrome. If for example, a prison has like a visual artery stroke, alternatively, you can also get like central pontine myelinalysis. Remember, the name has recently been changed to osmotic demyelination syndrome, where you fix hypoinitremia too quickly, right? Remember, the nomonic that from low to high, a prison's pont will die and from high to low, the prison's brains will blow, right? So when you fix hypoinitremia too quickly, you can get osmotic demyelination syndrome. If you fix hypoinitremia too quickly, you can get cerebral edema. Also, that similar also applies to hyperglycemia. So if they give you a question about a person that has like decay or HHNS, and then the person suddenly becomes comatose, right? If you see that kind of stuff on an MBM exam, then you will definitely want to think about, you know, like the person getting cerebral edema from fixing the hypochlycemia, like just a little too quickly, right? And then remember, if a person has, if a person has like, they tell you that a person has like vertical dyplopia, right? So like, like when you're walking up and downstairs, they have like double vision or, you know, basically like they see double in a very cool direction, you want to think about parinot syndrome. That's almost always from a pineyloma on an MBM exam, right?

Remember the pineyogland is superior to the superior collectulus, right? So if you have a pineyloma, that can compress the superior collectulus and cause a radical dyplopia. And then don't forget, right? If a person has like a lesion of the cerebellar veramis, so say for example, from like a medalloplastoma or a pylocytic astrosytoma of, from a hemangioblastoma, right? Those people have like, you know, like truncally taxia, right? So they'll have like a taxia like almost like in the middle of the body. Contrast that with people that have like a cerebella hemisphere lesion, right? Where do you have like, you know, like more of like the intention tremors, but you have more like limbatexia. And the thing is the limbatexia is going to be epsilon lateral to the lesion. I'll say that again, it's going to be epsilon lateral to the lesion. The thing is there are actually some decusations that happen, but it's actually two decusations. But the thing is that is beyond the scope of, if you're interested in that, you can email me, I can explain, but that's beyond the scope of this discussion. But basically whenever you have a cerebellar lesion, you'll have like epsilon lateral limbatexia, right? And then if they tell you that, oh, a person has like flailing movements of one arm, you want to think about like something called a hemibalismus, right? It's usually contralateral to the lesion, right?

So if you have like a left-softalamic nucleus lesion, you have like contralateral hemibalismus. So and also don't forget, like the most, if a person has like, if a person has like like a non-communicating hydrocephalus, aka an obstructive hydrocephalus, and you ask you like, what's the most common location in the ventricular system to give rise to those troubles? You absolutely want to think about the cerebellar quaddoctor of celvious, remember that's in the midbrain. And then if a person has a communicating hydrocephalus, right? You want to think more about a problem at the level of the arachnoid granulations, right? Where CsF is like, we're absorbed into the superior sagittal sinus, that's almost always like normal pressure hydrocephalus on an in-bim exam or from like meningitis or like malignancy that's growing at that at the level of those arachnoid granulations, right? And then don't forget that if a person has schizophrenia, right, they tend to have like enlargement of the lateral ventricle, if a person has Alzheimer's, right, you have like this function of the bison nucleus of minor, right? If a person has Alzheimer's, right, they can also have like this function of the enzyme, a colinacidl transfer is a chat, right? So again, these are just all high yield things you want to keep at the back of your mind, for example.

Basically this podcast, I just wanted to focus mainly on like neuro anatomical associations that are very high yield and very commonly tested on the USMELIS. And as I do at the end of every podcast, I do offer one or one to iterate for step one, two CK, two CSTEP 3, preclinical medical exams, 30-ishelf exams, if you're a medicine resident, I do offer the EBIM board exam and internal medicine training exam. And also if you're a college student and a student for like the MCAT, right? For like Gen CAM, O-CAM, physics, biochemistology, physiology, I do offer all those subjects. And I also do these booster courses for the USMELIS, right? So it's like 15 hours for step two CK and step three, it's like 20 hours for step one. Again, the vast majority of people have done this with they've found it to be like super super super helpful. Basically in those courses, it's one on one, I review like the high yield things that you need to know for each and every for each and every exam. And again, many people have found out to be super super helpful and they were like, hmm, divine. I got a lot of questions right on my exam because of this little time we spent together one on one, kind of reviewing the most notes. It's rapid fire and it's Q&A, but again, it's very effective. And then there's this online private study group thing that I again, I'll likely be studying a few days.

Basically, it will just be like a group of, like, you know, a bunch of people like maybe like just some numbering like the low tens of people, right? Where it will probably be over zoom, right? And we'll have like a theme like a cardiology theme or an endocrinology theme for like either step one or two CK, even two C.S. or step three, we review those things, right? In a very quick, sustained higher fashion, I will also give people the opportunity to answer questions. Each person will just be a nominofy, right? So just look out for more details on that if you're interested. Reach out to me through the website or you can send me an email, a divine intervention podcast with an Saviend at gmail.com. And then another thing I want to say is if you're like a met student applying to residency, so like an era's application or a collection of the applying to Met School, so like an Amcass application, I'd offer like one on one, I guess I can call it like coaching or you can maybe call it consulting where like I work with you on like editing your personal statements, editing your applications, doing more interviews, rec letters, stuff like that. Again, the vast majority of people have worked with have pretty much all much of their first choices. And again, I also have like admissions committee experience at a top two Met School for a year, right? So again, I have a ton of experience reviewing people's applications.

So if this is something you're interested in, just reach out to me and I'll be happy to point you in the right direction. So have a wonderful rest of your day. God bless you. I'll see you in the next podcast. Thank you.

The hippocampus (a component of the temporal lobe).

Anterior grade amnesia.

The dominant hemisphere (e.g., left hemisphere for right-handers).

Broca's is non-fluent/motor; comprehension is intact. Wernicke's is fluent but nonsensical; comprehension is impaired.

The non-dominant (right) parietal loop.

Gerstmann syndrome.

Distal to the optic chiasm (in the occipital lobe/visual cortex).

A "fried egg" appearance.

Frontal lobe; leads to disinhibition, apathy, and contralateral opisthotonus symptoms (e.g., positive Babinski).

Bitemporal/Heteronymous hemianopsia ("tunnel vision").

Parinaud syndrome; usually due to pinealoma compressing the superior colliculus.

Vascular cause (e.g., pons stroke) or Osmotic Demyelination Syndrome (ODS).

The cerebellar aqueduct of Sylvius (midbrain).

Pure motor or pure sensory stroke; Hypertension.

Acetylcholine (due to ChAT deficiency/loss of basal nucleus of Meyn function).

Frontal lobe; leads to disinhibition, apathy, and contralateral opisthotonus symptoms (e.g., positive Babinski).

Bitemporal/Heteronymous hemianopsia ("tunnel vision").

Parinaud syndrome; usually due to pinealoma compressing the superior colliculus.

Vascular cause (e.g., pons stroke) or Osmotic Demyelination Syndrome (ODS).

The cerebellar aqueduct of Sylvius (midbrain).

Pure motor or pure sensory stroke; Hypertension.

Acetylcholine (due to ChAT deficiency/loss of basal nucleus of Meyn function).