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Episode Notes

Source / episode info

  • Episode: 516
  • Title: Divine Intervention Episode 516: The Floridly HY Brain Tumor Podcast (for Step 1-3, lots of integrations)
  • Published: 2024-02-28
  • Source: Episode page

One-liner

This episode provides a comprehensive review of brain tumor pathology and clinical presentations, emphasizing anatomical localization (super/infra-tentorial), key syndromes (FAP, VHL, Tuberous Sclerosis), differential diagnosis based on histology (Rosenthal fibers vs. Homerite rosettes), and complex physiological integrations like CSF flow obstruction patterns.

High-yield summary

  • Clinical Presentation: The classic triad of a brain tumor is progressively worsening headaches (worse in the morning/supine position), nausea, vomiting, and seizures, often accompanied by signs of increased ICP (e.g., papilledema).
  • Anatomical Localization: In adults, most tumors are super-tentorial; in children, most tumors are infratentorial (cerebellum). The major exception is the craniopharyngeal junction.
  • Tumor Differentiation: Meningiomas are extraaxial masses derived from the dura/meninges; Glioblastomas and Ependymomas are intraaxial masses growing within brain parenchyma.
  • Pediatric Tumors: Pylocytic astrocytoma (most common, benign) is typically cerebellar; Medulloblastoma (most common malignant) is highly metastatic via CSF pathways ("drop metastasis") and often presents with obstructive hydrocephalus.
  • Syndromes & Associations: NF2 triad includes bilateral schwannomas/acoustic neuromas and meningiomas. VHL syndrome links hemangioblastomas to hypertension, polycythemia, and renal cell carcinoma.
  • Hydrocephalus Patterns: Obstructive (non-communicating) hydrocephalus requires identifying the point of obstruction: Medulloblastoma/Ependymoma obstruct the 4th ventricle; Pineocytoma compresses the cerebral aqueduct.

Learning objectives

  • Differentiate between intraaxial and extraaxial brain tumors based on their anatomical origin.
  • Correlate specific clinical syndromes (e.g., VHL, FAP) with associated primary CNS malignancies.
  • Analyze CSF flow dynamics to determine the location of obstruction in non-communicating hydrocephalus.
  • Identify key histological features (e.g., Rosenthal fibers, Homerite rosettes, pseudorosettes) for common brain tumors.
  • Understand the hormonal axis disruptions caused by pituitary adenomas and apoplexy.

Board exam buzzwords

ConditionKey FindingAssociationBoard Exam Tip
MeningiomaCalcifications (sammoma bodies); Extraaxial locationFemale predominance; Radiation historyAlways remember meningiomas are derived from the dura, making them extraaxial.
MedulloblastomaHomerite rosettes; Synaptophysin positiveCerebellum; Obstructive hydrocephalus ("drop metastasis")The most common malignant pediatric brain tumor and a key cause of obstructive hydrocephalus.
Pylocytic AstrocytomaRosenthal fibers; GFAP positiveCerebellum; Benign/Slow-growingMost common primary benign pediatric brain tumor.
HemangioblastomaCalcifications; Polycythemia, HypertensionVHL disease; CerebellumHigh blood pressure and polycythemia are key clues pointing to this diagnosis in the setting of a cerebellar mass.

Rapid review table

TopicKey PointContextExam Relevance
Intraaxial vs. ExtraaxialIntraaxial = within parenchyma; Extraaxial = adjacent to meninges/dura.Meningioma is extraaxial; GBM is intraaxial.A common source of confusion on exams; knowing the origin dictates the diagnosis.
Hydrocephalus PatternsNon-communicating (Obstructive) vs. Communicating.Obstruction site determines which ventricles are dilated (proximal to obstruction).Requires detailed knowledge of CSF flow pathways and anatomical landmarks.
Pediatric Brain TumorsPylocytic Astrocytoma (Benign, Cerebellum); Medulloblastoma (Malignant, Cerebellum)The distinction between benign/malignant is critical for prognosis and metastatic potential.Always ask: Is the tumor malignant? If yes, think medulloblastoma.
Pituitary AdenomasProlactinoma; Hypogonadotropic hypogonadismHigh prolactin suppresses GnRH release from the hypothalamus.Understanding the hormonal axis failure (GnRH -> FSH/LH) is key to diagnosis and treatment.

Board-speak -> diagnosis

Board-speak / Vignette phraseDiagnosis / ConceptWhy it fits
A child with a cerebellar mass, history of ataxia, and elevated hematocrit/hypertension.Hemangioblastoma (VHL association)VHL syndrome causes hemangioblastomas, typically in the cerebellum, leading to polycythemia and secondary hypertension.
An adult patient presenting with an extraaxial mass adjacent to the falx cerebri, often calcified.MeningiomaMeningiomas are derived from the meninges (extraaxial) and frequently occur along dural attachments like the falx or tentorium.
A pediatric brain tumor causing non-communicating hydrocephalus that dilates the lateral ventricles, third ventricle, cerebral aqueduct, AND fourth ventricle.Medulloblastoma / EpendymomaThese tumors obstruct the 4th ventricle (the common drainage point), leading to proximal dilation of all upstream structures.
A patient with a history of radiation exposure to the head and neck presenting with a thyroid mass.Papillary Thyroid CarcinomaRadiation is a known risk factor for PTC, which often presents as a neck mass.
A pituitary adenoma causing hypogonadotropic hypogonadism and bilateral breast discharge.Prolactinoma (MEN1)High prolactin levels suppress GnRH production, leading to low FSH/LH and secondary amenorrhea/galactorrhea.
An adult with an intraaxial brain mass showing necrosis, hemorrhage, and associated with a GFAP marker.Glioblastoma Multiforme (GBM)GBM is the most common primary malignant adult brain tumor; it is highly aggressive, necrotic, and often marked by GFAP expression.

Differential diagnosis / distinguishing features

Pediatric Cerebellar Tumors

Key FeaturesDistinguishing FindingsNext Step
Pylocytic AstrocytomaLow-grade, slow growth; Rosenthal fibers; GFAP positive.Observation/Aspiration if stable; Biopsy for confirmation.
MedulloblastomaHigh-grade, highly metastatic ("drop metastasis"); Homerite rosettes; Synaptophysin positive.Staging workup (CSF analysis); Neurosurgical resection.

Pituitary Adenomas

Key FeaturesDistinguishing FindingsNext Step
ProlactinomaCauses hypogonadotropic hypogonadism, galactorrhea, amenorrhea.Dopamine agonists (Cabergoline/Bromocriptine).
Pituitary ApoplexyAcute presentation; Severe headache, visual changes, low cortisol/ACTH.High-dose steroids and replacement therapy (Hydrocortisone + Levothyroxine).

Management pearls

  • Increased ICP Management: Treat the underlying mass first. If symptoms are severe, osmotic agents (Mannitol) or hypertonic saline may be used.
  • Meningioma Treatment: Generally managed with observation unless symptomatic; resection is performed if causing neurological deficits or hemorrhage.
  • GBM Chemo: Use nitrosoarials ( Lomustine, Semustine, Camustine ) due to their ability to cross the blood-brain barrier better than many other agents.
  • Pituitary Adenoma Treatment: First line for prolactinomas is a dopamine agonist (Cabergoline preferred over Bromocriptine).

Don't miss

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Intraaxial vs. Extraaxial: This distinction is critical; meningiomas are extraaxial, while GBM and ependymomas are intraaxial.
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CSF Flow Dynamics: Remember that obstruction at the 4th ventricle (e.g., medulloblastoma) will dilate all upstream structures (lateral ventricles -> third ventricle -> cerebral aqueduct -> fourth ventricle).
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Pediatric Malignancy Gradient: Pylocytic astrocytomas are typically benign, while medulloblastomas are highly malignant and metastatic.
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Pituitary Apoplexy Replacement: Always replace both glucocorticoids (Hydrocortisone) AND thyroid hormone (Levothyroxine), as the pituitary failure affects multiple axes.

Integration & clinical reasoning

  • VHL Syndrome Integration: The triad of VHL -> Hemangioblastoma -> Polycythemia/Hypertension is a classic high-yield association that links genetics, neuroanatomy, and cardiovascular physiology.
  • Radiation Exposure Integration: Historic radiation to the head/neck/chest increases risk for multiple cancers (PTC, Meningioma, Lymphoma), demonstrating how environmental factors affect cancer epidemiology.
  • Endocrine Axis Failure: Understanding the hypothalamic-pituitary axis failure in prolactinomas (suppression of GnRH) and pituitary apoplexy (destruction of gonadotrophs/corticotrophs) is essential for hormonal replacement therapy.

OMM / COMLEX integration

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For COMLEX: know these viscerosomatics / Chapman points, but don't let OMM distract from emergent diagnosis and management.
  • Emergency Management Priority: In any suspected acute intracranial process (e.g., pituitary apoplexy, severe ICP), standard emergency management (Airway/Breathing/Circulation, managing elevated ICP) takes absolute priority over OMT.
  • Pituitary Apoplexy: The clinical picture of sudden hypopituitarism following a mass requires immediate replacement therapy; this is an endocrine crisis requiring rapid stabilization before any advanced imaging or surgical planning.

Concept connections / cross-references

  • For detailed information on adrenal insufficiency management, see [ Episode 37 ].
  • For general principles of neuroanatomy and CSF flow, review the basic anatomy sections in [ Episode 12 ].
  • For understanding pituitary function and hormone axes, refer to endocrine reviews like those covered in [ Episode 45 ].

High-yield association table

ConditionAssociationMechanismClinical Significance
MeningiomaEstrogen/Progestin receptors; Calcification (sammoma bodies)Hormonal influence on growth; Dural attachment.Female predominance and characteristic calcifications are key diagnostic clues.
MedulloblastomaCSF pathways ("drop metastasis")High metastatic potential through cerebrospinal fluid.Causes non-communicating hydrocephalus and is the most common malignant pediatric brain tumor.
HemangioblastomaVon Hippel-Lindau (VHL) disease; PolycythemiaVHL causes renal/pancreatic lesions, leading to hemangioblastomas in the cerebellum.The triad of cerebellar mass + polycythemia + hypertension is highly suggestive.
PineocytomaParinaud Syndrome (Vertical Gaze Palsy)Compression of the superior colliculus by the tumor.A specific cranial nerve/visual pathway deficit that points directly to a pineal region lesion.

Key terms glossary

TermDefinitionContextExample
Extraaxial MassTumor originating from structures adjacent to the brain parenchyma (e.g., dura, arachnoid).Meningiomas are classically extraaxial masses.A tumor arising from the falx cerebri is considered extraaxial.
Intraaxial MassTumor growing within the actual brain tissue/parenchyma.GBM and Ependymoma are examples of intraaxial tumors.The majority of primary adult brain tumors are intraaxial.
Non-communicating HydrocephalusObstructive hydrocephalus; blockage of CSF flow at a specific point.Medulloblastoma obstructing the 4th ventricle.Dilation is seen proximal to the obstruction site.
Parinaud SyndromeVertical gaze palsy (inability to look vertically).Caused by compression of the superior colliculus, often by a pineocytoma.A classic sign pointing to a lesion in the pineal region.

Study optimization

TopicStudy ApproachPriorityResources
Brain Tumor Differential DiagnosisUse clinical clues (age, sex, syndrome) first; then use imaging/histology for confirmation.HighReview board-specific tables comparing tumor types and markers.
CSF Dynamics & HydrocephalusDraw the CSF flow pathway on paper; identify where an obstruction would cause dilation.Medium-HighPractice questions focusing on anatomical location of blockage (e.g., aqueduct stenosis vs. 4th ventricle mass).
Endocrine IntegrationLink pituitary/hypothalamic axis failure to specific symptoms and replacement therapies.HighReview the HPA, HPT, and HPG axes; memorize the required replacements for apoplexy.

Question pattern recognition

  • Pattern: Super-tentorial calcified mass in a child. -> Think Craniopharyngioma (most common super-tentorial pediatric tumor).
  • Pattern: Bilateral schwannomas/acoustic neuromas + Meningioma. -> Highly suggestive of Neurofibromatosis Type 2 (NF2).
  • Pattern: Brain mass causing vertical gaze palsy. -> Think Pineocytoma, which compresses the superior colliculus.

Test yourself

Common mistakes to avoid

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Mistake 1: Confusing Intraaxial vs. Extraaxial. Remember that meningiomas are extraaxial (dural origin), while GBM and ependymomas are intraaxial (parenchymal growth).
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Mistake 2: Misinterpreting Hydrocephalus Patterns. Do not assume all ventricles dilate equally; the pattern of dilation must be traced proximally from the point of obstruction.
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Mistake 3: Overlooking Syndromic Links. Never forget to check for associated syndromes (VHL, FAP, NF2) when presented with a cluster of findings (e.g., cerebellar mass + hypertension).

Common traps

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Trap 1: The "Most Common" Trap: While GBM is the most common adult primary brain tumor, Pylocytic Astrocytoma is the most common benign pediatric brain tumor.
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Trap 2: Pituitary Hormone Replacement: When treating pituitary apoplexy, remember to replace both glucocorticoids (Hydrocortisone) and thyroid hormone (Levothyroxine), as failure affects multiple axes.
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Trap 3: The "Fried Egg" Appearance: While GBM is often associated with GFAP/astrocytoma lineage, the fried egg appearance can also be seen in seminomas or teratomas; this requires careful correlation with clinical context and markers.

Original transcript with highlights

Original transcript with highlights

Welcome, my name is Divine. This is episode 516 of the Divine Intervention Podcasts. Into this podcast, I'm going to be addressing a topic that I'd like to call brain tumors. In fact, I guess I'll call this the clutch brain tumor podcast. This is one of these podcasts where there are two things that's going to help you. Number one is the presentation. Number two is the key facts to know. So presentation, key facts to know. And then every now and then, they kind of throw in some weird integration of the other. So I'm going to try to hit those as we go. So what if they give you a question about a patient? The tell you that is a 55 year old guy. And that for the last two or three months, he has been having severe progressively worsening headaches. And then you're told that over the last week he has vomited three or four times upon a weekening in the morning. And then you're told that it was brought to the emergency room because he had a generalized tonic chronic seizure that lasted for two minutes. If you see something like this, I hope you're saying divine. This is a brain tumor. And the thing is the way I frame the best way to understand that brain tumors is as follows. So I think the first thing you need to realize is that there is this thing, this. The first thing you need to realize is that the brain tumor is a brain tumor. And then you need to know that the brain tumor is a brain tumor. And then you need to know that the brain tumor is a brain tumor.

And then you need to know that the brain tumor is a brain tumor. And then you need to know that the brain tumor is a brain tumor. And then you need to know that the brain tumor is a brain tumor. And then you need to know that the brain tumor is a brain tumor. And then you need to know that the brain tumor is a brain tumor. And then you need to know that the brain tumor is a brain tumor. And then you need to know that the brain tumor is a brain tumor. And then you need to know that the brain tumor is a brain tumor. But that's a landmark that helps you define if a tumor is super-tentorial or if it is infertentorial. So if something is super-tentorial, that means it's above the ten-term cerebelli. If it's infertentorial, that means it's below the ten-term cerebelli. So generally in adults, most tumors are going to occur above the ten-term cerebelli. In adults, most brain tumors are going to be above the ten-term cerebelli. But in kids, most brain tumors are going to be below the ten-term cerebelli. Now, so that should tell you that, if I see a pediatric brain tumor on my exam, it's probably going to be somewhere in the cerebellum or below. It's just kind of simple, right? And think about this. I'm sure many of you have heard of pylocytic astrocytomas and metroloblastomas and all those things that I think are pending moments. Those things are all going to be infratentorial. There's one major exception to that role though. And that's the craniofarinjum.

Craniofarinjum is a super-tentorial. But again, most adults, your tumors are going to be super-tentorial. So that tells you that these problems are probably going to be in the cortex. These problems are probably going to be in the cortex. And again, there are some things I would say you should associate some syndroms. They should associate with a person getting a brain tumor, some syndroms, some risk factors. Again, the thing is our friends at the NBM is they care a lot of our risk factors these days. Risk factors are no things you can just successfully ignore. So like for example, if they give you a question about a person that has a brain tumor and then they tell you that this person is like a 25-year-old male, 25-year-old male with a brain tumor, and then you're told that he has had colonoscopies for the past decade. And then they ask which of the following is the most important risk factor for this person's brain tumor? I'll hope you're saying, oh, divine, this is going to be an APC mutation. Again, the thing is the NBM is these days. Huge on integrations, huge on integrations because many people think of APC gene mutation and they just think of FAP, obviously, right? Familiar adenomirus polyposis. But again, you'll just be surprised. They give your brain cancer question and then they make it a risk factor question. And instead of even putting FAP, they just put APC mutation. You know, I'm sure many people have memorized that drug-course syndrome.

It's when you have an FAP mutation and you see these people getting a lot of brain tumors. But again, all these classic Bos words, Bos phrases, who FAP mutation plus brain tumor equals turtleneck syndrome. No, they're probably not going to put turtleneck syndrome as the answer. Because it's just something that you can find in every onky-deknone-to-monk kind. If you've just memorized that association is going to be there. But what do they do instead? They'll give you a question about a person. They have a brain tumor. They give you an image and you clearly see it's a brain tumor. And then they tell you that a person has had colonoscopies like every year, every two years, for like a decade. At a very young age of life, less than persons in their 20s. And they ask about the most important risk factor. And then you see an answer that says APC mutation. So just kind of be careful about that. Be able to make these kinds of integrations. You do that, you're preparing yourself beautifully for the exams that exist these days. So don't forget that family and other nomados polyposes is associated with people having brain tumors, especially the turtleneck syndrome variant. Another thing that can also be a zero brain tumors is just you being a woman, especially like many engeomers. Many engeomers, they have receptors that respond to many of these female hormones, like estrogen and progestin. Many engeomers, they have estrogen and progestin receptors.

So and shouldn't be so surprising that all these tumors are going to be most likely found in women. Although men can certainly get many engeomers as well. And then another association to keep in mind is they can give you a question about a person that has all these different brain tumors. Like meningiomas, schwanomas, especially those bilateral acoustic neuromas. If you see something like that and also a pendy momas, you want to think about neurofibromatosis type 2. Remember people that have NF2, they can absolutely get brain tumors. They can absolutely get brain tumors, especially meningiomas, schwanomas. Especially if you see a person that has a bilateral schwanoma, a bilateral acoustic neuroma, you certainly want to think about NF2. But also a pendy momas also found in NF2. And then they give you a question about a person that has brain tumors. And they tell you that this person has all these hypopegmented lesions on their skin. Then I hope you're thinking about tuberous sclerosis. Remember people that have tuberous sclerosis believe they're not, they can actually get astrocytomas in the brain. I'm going to say that again because it's very, very high yield to know for your exams. There's not something many resources mention, but it's actually kind of important to know for your test. But tuberous sclerosis has an association with astrocytomas in the brain. It wasn't a astrocytomas in the brain. So just going to keep these things at the back of your mind.

Or if they give you a question about a person that has, they tell you that this person is very hypertensive. And the tell you the person in your motorcrates is like super high, is like 75%. And we're told that this person has had multiple P Es, multiple DV Ts, or has had a minor cardiovascular infarction. And then they give you an image showing a brain tumor. In those circumstances, what should you be thinking about? And they'll say, oh, which of the four needs the most important risk factor for this person's condition? Again, I would hope you're thinking of like a chromosome 3 mutation. They can put it as an answer or they can put V-cell mutation. You know, just kind of keep those things at the back of your mind. So what's the deal there? Well, obviously I'm talking about a hemangioblastoma. Hemangioblastomas, and again, don't worry, we'll talk about the brain tumors. Just chill. I'm just kind of giving you some quick, I'm giving you like, this is like the introduction. We're going to the astro-termors. But hemangioblastomas have an association with Von Hippo Lendau. So I know your mind may be wondering, divine. Like, what's it with this high blood pressure? Multiple P Es, DV Ts, bloody, bloody, bloody. Well, let me explain. The thing is, Von Hippo Lendau, again, is a surreling hemangioblastomas. Hemangioblastomas tend to be in the cerebellum. They love to make Hippo in a perinoplastic fashion, so they can cause a polycythemia, a secondary polycythemia.

So when you have polycythemia, obviously your hematocritus is going to go up. Your ablote cell count is going to go up. Now, the thing is, think about this, it kind of goes back to, or sells law. When you have polycythemia, what happens to your blood viscosity? When your blood viscosity is going to increase. If your blood viscosity increases, what do you think is going to happen to your peripheral resistance? The peripheral resistance is going to go up. Like literally, your peripheral resistance, as many of you know, is directly related to your blood viscosity, is directly related to the length of the tube of the blood vessel, and universally related to the radius of the fourth power. So since the viscosity is going up, because your hematocritus is going up, then in those circumstances, your total peripheral resistance is going to go up. So it shouldn't be a surprise that people that have polycythemia should have hypertension. It just happened to be a relationship we see now with the Emanginal Blastomas. And they may wonder, divine, why are all these hyperquaglable problems? Or think about this. When a person has polycythemia, when your hematocritus is high, and your blood is viscous, is your blood going to flow fast? No, it's not going to flow fast. When something is viscous, it flows slow. I'm going to say that again. When something is viscous, it flows slow. When something flows slow, it means you have stasis.

And if you remember, Verkho's triad of hyperquaglability, number one is stasis. Number two is endothelial dysfunction. You have some kind of an endothelial dysfunction, at least that's part of Verkho's triad. So that's stasis. It's going to make you more hyperquaglable. I know someone may be like, do you mention Verkho's triad was the third part of the triad? Yes, there is stasis. There is endothelial dysfunction. And honestly, the third part of the triad is hyperquaglability. Which is kind of odd. That's kind of a catch-all for anything that makes you hyperquaglable. For example, you see people that have cancer. Cancer is make a person hyperquaglable. You see a person that has an euphoric syndrome where your p-naud antithromine is three in your urine. That's an anticoagulant protein. When you peel an anticoagulant protein, it's going to become hyperquaglable. Or let's see, you have some kind of genetic disease, like factor of five lighten, that makes you hyperquaglable. All those things are going to make you hyperquaglable. So again, just going to keep these general risk factors. And also, if a person has had previous radiotherapy, again, these are literally all different vignettes you can get on your exams. It's just going to be mindful of these things. If a person has had radiotherapy to the brain in the past, and you see a brain tumor, they only be thinking about them in angioma. In angioma, it's a straight-up prior brain radiation. So just going to keep that in mind.

If a person has had radiation to the head and neck, there are two cancers that... And these people can actually... three cancers that these people can get. Number one, is that they can get many angiomas from that. Number two, they give you a neck mass. You won't be thinking about a papillary thyroid cancer. Believe it or not, that is, in fact, the biggest risk factor for a papillary thyroid cancer. Priority of therapy to the head, neck, and chest. And they also think of lymphomas. That's going to be obviously chest mass. It's going to be in the anterior mediasis, or the middle mediasis, so just going to keep those at the back of your mind. And usually, when people have brain tumors, right, they're usually going to present with nasty headaches. It's going to be worse at night, because when you're sleeping at night, right, you're essentially putting like your... ... your supine. So it's like more blood is flowing back to your heart, more your brain's being better perfused. So that can slightly raise your IC Ps. If you have a spiss-occupied lesion, it's going to make things worse. Also, these people tend to have like really bad headaches when they wake up. But as they go through the headache, they recede, because again, all those pressures are kind of going down. And they know, forget that, at mean times, you'll have a lot of nausea, a lot of vomiting. They can have seizures, seizures, or very actually classic brain tumor presentation.

In fact, if you see, I don't explain seizure. In a person that's over 50, on the USML exams, I would really, really hope you're thinking about that person having some kind of brain tumor. And then many times, they can also have signs and symptoms of increased IC Ps. So like, for example, they can have... ... they can have a papillodema and things of that nature. And in general, our friends on the MBA means when you have a brain tumor, ... you want to pick a diagnostic test. If I'm completely honest with you, you want to go to an MRI. Go ahead and get an MRI of the brain with contrast. It's just better than a CT of the brain, but again, if you don't see MRI as an answer, CT is fine. If they give you MRI and CT as answers, pick MRI. MRI is just better. MRI is literally just better. MRI is literally just better. And most brain tumors, how are we going to treat them? We're going to treat them with surgery or radiation or chemo. The thing is brain tumors, some have been nine, what mean a bad. And honestly, most brain tumors don't bother metastasizing. Because I just like to think of it as brain tumors know their bad. They know they're going to likely kill the person. So it's almost like they don't even bother a waste energy metastasizing. But on that whole concept of metastasis, again, I know you're like, ... it's not going into the specifics. No, this background will help you. And this background I'm giving is where a lot of your questions are going to be drawn from.

Again, I'm telling you the USM Ls are not super fucked based anymore. They're more reasoning based, an integration based. So listen and pay attention. So on the whole topic of metastasis, there is a brain tumor that has this nasty habit actually of metastasizing. And it's going to be a brain tumor in a child. It'll be a child that has strongly taxia. And this child will tell you that the alpha-sense of increased ICP. And then you see a mass in the veramis of the cerebellum. If you see that, I hope you're thinking about a middle-oblast tumors. A middle-oblast tumor. A middle-oblast tumors, they love to metastasize. And there's this concept of metastasis. A middle-oblast tumor is known as a drop metastasis. Drop metastasis. Drop metastasis. Drop metastasis. These drop metastasis, they... You basically have the tumor cells sitting through the CSF pathways. That's a high-o thing to know. Sitting through the CSF pathways, many times you're going to see them like on MRI in the spinal cord. If you're doing a neurology rotation or you're doing a neurosurgery rotation, that's like a classic lymph order for those are rotations. It's just something you want to keep at the back of your mind. Now, in terms of the reverse, I would encourage you to think of also metastasis from the body to the brain. So, most brain tumors you're going to see in a person are going to be straight up met. Many times it's going to be from lung cancer. Lung cancer is probably the most common...

it's not probably. It is the most common cancer that causes metastasis to the brain. So, that's something you want to know for your exams. Many times when you didn't with brain met, they're usually going to be at the gray-white matter interface. They're going to be well circumscribed. Sometimes you can see multiple lesions, something you want to keep at the back of your mind. And one other thing I think I want to mention is just in terms of epidemiology. Our friends at the MBM is kind of wanting to know in epidemiology with many of these things. So, don't forget that if you're looking at brain tumors, the most common primary adult brain tumor is going to be GBM, glioblastoma multi-phomine. Number two is going to be a meningioma. Number three is going to be an ependymoma. And then don't forget in terms of kids, the most common primary adult brain tumor in kids, think of a pylocytic astrocytoma. Basically a cerebellar astrocytoma. Sometimes they may not use that term pylocytic astrocytoma. They will just use cerebellar astrocytoma. And then think of number two being metroloblastoma. Just going to keep those at the back of your mind. So now that we've kind of hit those, let's start making some integration. So, number one, what if they give you a question about a patient that's in his 50s, and he has a brain mass, seizures, blah, blah, blah, blah. And literally they almost give you like no clues whatsoever.

But sometimes they can give you a clue, they can show you an MRI, and you see the middle of the brain, the middle of the cortex, you see a lot of black, a lot of white. What should you be thinking about? I hope you're saying divine, this is a glioblastoma. This is literally glioblastoma multifonial. So remember sometimes on the exam, it's not called in GBM, they'll call this a great force for cytoma. This is the most common primary brain tumor in adults. And the prognosis of this is pretty terrible. Most of this would have this 14 months or thereabouts, and they're gone. And it's pretty high you to know that the tumor marker, like for these brain cancers, many times it's important to know the tumor markers. So don't forget that GFEP is the tumor marker. So glioblary acidic protein, GFEP glioblary acidic protein is the tumor marker for glioblastomas. Remember that's also the tumor marker for pilot city gastrocytomas, which should make sense because the glioblastoma is a great force astrocytoma. So if it's an astrocytoma, it should make sense that any of that kind of astrocytoma probably has GFEP as a tumor marker, like a pilot acidic astrocytoma. So again, usually on imaging, you're going to see a lot of necrosis. That's a classic feature of GBM. You're going to see a lot of visogenic edema. You're going to see a lot of necrosis, a lot of bleeding, a lot of hemorrhage. And sometimes you can crush the corpus callosa. Again, those are the important things to know about GBM.

And again, one thing I guess I can say with brain tumors, in terms of treating brain tumors, you can treat them with chemo, one group of chemo drugs that you miss you on your exams. This is probably more for the step one, step three folks. They miss you on your exams with GBM. I want you to think of the nitrosoerius. There is this numonic that you probably remember from step one about putting some nitro in your Mustang. So drugs like lumustine, semustine, camustine, I think streptozocin is one of them. That's one that kind of breaks away from the mold. Those are your nitrosoerius. They are alkalinity agents, but they're very good at treating brain tumors. Why? Because they have this unique property of being able to cross the blood brain barrier better, than many of the other chemo drugs. Although for GBM, there's also this drug known as a Timosola mind. It's an alkalinity agent. It's very good for treating glueblastoma-motiforme as well. Alright, so let's move along. Now, what if they give you a question about a lady? That's a hint. And they tell you that she has been having headaches, seizures. And they show you brain imaging, and you see something that is close to the folk cerebride. Or they show you the tell you in the question that, oh, the image of the brain displays, or discloses a parasagetomas. When you see that, I hope you're saying divine, this is a meningioma. Right? Meningiomas, just keep in mind. So, you know, they love to grow parasagetally.

And there is one radiological term that our friends at the inbimmies can throw you for a little bit. So, is this whole concept of something being extra or intraaxial? A brain tumor that's intraaxial is within the brain panchema itself. Pretty much almost every brain tumor is intraaxial. Like, glueblastoma, it literally grows within the brain. That's an intraaxial tumor. I mean, injoma is derived from cells that are adjacent to the meningis. That's why it's called meningioma. So, it's actually pretty important. Don't forget this. I mean, injoma may touch the brain, but it's not part of the brain. It's an extraaxial mass. Please, I'm begging you. It's an extraaxial mass. This is a term that could easily confuse people on exams. Meningiomas are extraaxial. All right. So, again, as I've described already, meningiomas, usually be nine. Sometimes you'll notice that they have a dual tail. So, basically, they'll have like an attachment to the dura. And you'll notice that again, they are way more common in females. Why? Because, again, they have estrogen and progestin receptors. Now, don't forget that meningiomas, they have someoma bodies. Sometimes, you may see them referred to as laminated calcifications. You see a person that has a brain tumor to give you histology. You see something that is blue or pink and is like a whirl, like a circle. You absolutely want to think about meningioma. meningiomas are associated with someoma bodies.

So, I guess as a quick sidebar, what are the tumors, what are the cancers that are associated with someoma bodies? I've mentioned to already in this podcast. Number one, meningiomas. Number two, papillary thyroid cancer. Number two, and do you see that? Man, it's like kind of not surprising that, hmm. Historic radiotherapy to the head, neck, chest. Is a risk factor for papillary thyroid cancer. And historic brain radiation is a risk factor for meningioma. So, maybe they may be as an association, I don't know, but it's kind of interesting. Receive people having like radiation to the neck or chest or brain. And then they have meningiomas of papillary thyroid cancers. There's something you can keep in mind. And then, so meningiomas papillary thyroid cancers, don't forget the serocystatinocorsionomus of the ovaries. Serocystatinocorsionomus of the ovaries. And then, don't forget as well, isotheliomas. Isotheliomas also have someoma bodies on histology. Again, those things are also called laminated calcifications. And most times on the USML Es, this is for the step two, step three level. If a person has a meningioma and they are symptomatic, you don't have to treat, just watch it. But if you start having symptoms, you can resect it or you can do like radio surgery. Those are, I will say, probably the key things to know about meningiomas. But again, meningiomas, or again, they are not in drugs, they are not the right from brimperencoma.

They are derived from cells that are adjacent to the, your adjacent to your dura. And it's fucked some things, you see them called the arachnoid cells, the arachnoid cells. And then another brim tumor of pretty much this cost already. You see a person, they tell you that, ooh, you see, they have a, it's going to be in a child, they have a cerebellum mass. Although it could also be in an adult, they have a cerebellum mass. And they have very high hematocrate, hypertension or whatnot. And obviously, want to think about a hemangioblastoma. Now, hemangioblastomas, right, they are obviously derived from blood vessels. That's why they're called hemangioblastomas. Again, they have that V-chial association for hipolindal. That's a nozomodominant disease, chromosome three. Those people tend to have like bilateral renal cell carcinomas. They can have pancreatic cancers, they can have hemangioblastomas. Think about those things for V-chial. So, hemangioblastomas, they produce hipo, they're almost always going to be in the cerebellum on your exams. Okay, they're almost always going to be in the cerebellum on your exams. And typically on imaging, they're going to contain some calcifications. Again, they can make an arrow question out of this. Your hipo is going to be high, your hematocrate is going to be high, your blood pressure is going to be high. Your afterload is going to be high. Remember, after a systemic vascular resistance, a kind of similar.

I've explained that the blood vessel is up. So, your SVR is up, I've proved out, it's cells long. So, SVR is going to be high. Just kind of keep that at the back of your mind. Again, they can easily make arrow questions from these things. Again, these things tend to contain calcifications on imaging. Okay, what if they give you a question about an adult, headaches, seizures, they tell you that, you know, brain imaging demonstrates a tumor, and they tell you that it's in the frontal lobe, contains calcifications. That's pretty straightforward. That's an oligodendroglio. Remember, oligodendroglio is the aderai from oligodendrocytes. oligodendrocytes are the cells that might need stuff in your central nervous system. And remember, your oligodendrocytes get away from the neuro tube. Your oligodendrocytes are the right from the neuro tube. Your oligodendrocytes, this is not like a glitch in the podcast. I'm repeating this because this is a high yield. oligodendrocytes are the right from neuro tube. They might need cells within the central nervous system. Schwann cells are the right from the neurocress cells. They might need cells in the peripheral nervous system. Okay, just kind of keep that at the back of your mind. That's an important factor to know for your exam. So, what are you going to see on the image? Again, these things are calcified. What are you going to see on the histology? These things have that fried egg appearance. They have that fried egg appearance.

So, you'll see like the nucleus in the middle. And then you'll see like a lot of white around the nucleus. So, it kind of looks like a fried egg. Looks like a fried egg. Remember that fried egg appearance? We don't only find that in oligodendroglio. We also find those in seminomers. And we find them in this terminomas, I believe. So, seminomers, this terminomas, oligodendroglio. Have that fried egg appearance. Again, that's pretty high to know for, for exams. And then, this group, what if they give you a question about like a woman in her 30s? And she has been having bilateral, you know, breast discharge. They tell you that she has like two sons. One is five, one is seven. Hedics, seizures. If you see that, I don't do you think I'll have a pituitary adenoma. I don't do you think I'll have a pituitary adenoma. Right? Remember, pituitary adenomas, the most common kind is going to be a prolectinoma. And I guess we're kind of talking about that. Let's not forget that prolectinomas. That's what we know with MEN1. It's an OZOMO dominant disorder. And those people tend to have parathyroid problems, primary hyperparathyroidism. That's the most common presentation. They tend to have pituitary adenomas, like prolectinomas being the most common. And they tend to have a pancreatic neuroendocrine tumors like insulinomas, glucagonomas, zollinger-elicin syndrome, things of that nature. So, these pituitary adenomas, prolectinomas are probably the most common kind.

Prolectinomas are probably the most common kind. And sorry, I just don't want to forget. I know I said that the most common cancer to make that the size of the brain is long cancer. Remember, number two is breast cancer, actually. So, number one is long cancer. Number two is breast cancer. Number three is melanoma. That's just something I want to keep out the back of your mind for, for example. Okay, let's go back to prolectinomas. So, prolectinomas, you produce a lot of prolectin. So, again, there are many things they can throw out here with prolectinomas. Like you're going to see the Bialectoria, canachomasia. You're going to see those bilateral discharge from the breast. Many things they can test. Remember, those things can compress the optic chiasm. And the person will have like a bytemporal hemianopsia. They can also give you a question about the pressing being infertile. And they can ask about the mechanism behind the infertility, the mechanism behind the infertility. And the person that has a prolectinoma is hypogonadotropic hypogonadism. Hypogonadotropic hypogonadism. Why? What's the mechanism there? Well, productin suppresses generic production. So, if your generic production is suppressed, your generic will be low. Your FSHL is will be low. And your ACTH, I mean, your estrogen production will be low as well. So, the person's gonadotrophs will stop working. The things that make FSHLH and your gonad is not going to be stimulated.

So, it's going to be a hypogonadotropic hypogonadism. Again, I know that many people are like, oh, the brain tumor podcast, but man, I've been talking about a lot of things that are not related to brain tumors. Yes, these are all integrations. That's how I like to structure these podcasts. Because it's just way more useful for you that way for your exam. So, hypogonadotropic hypogonadism, they can even give you a bone mineral density question. In a person that has a prolectinoma, what's going to be true of the bone mineral density? It's going to be decreased. Because again, if you're not making generic, you're not making FSHLH, you're not making estrogen. Then you're not getting that estrogen protective effect from bones. Remember that whole business resource, osteoportagric? I've kind of talked about that in many, many podcasts. And don't forget, in males, they can have decreased libido, also in females as well. So, how are we going to treat these prolectinomas? Well, you're going to give a dopamine agonist, like bromo-cryptin or carburegoline. If they make you pick between both, big carburegoline, carburegoline is just probably a little better than bromo-cryptin. And I think it doesn't have as many problems as bromo-cryptin. So, just going to keep that in mind. The first line treatment for prolectinomas is going to be a dopamine agonist, like bromo-cryptin or carburegoline. The second line treatment is going to be resection, transphenoidal resection.

That's the Bosrille Misi on your exams. That's the Bosrille Misi on your exams. And if they give you a question about a person that has a pituitary adenoma, and they tell you that, hmm, this person has this sodium onset severe headache, and they tell you that, you know, around the pituitary sea a lot of white, like increase radio density. And the person you're told, maybe days later, they are already very low. Their cortisol is extremely low. They tell you that, you know, this person is hypoglycemic. Then I want you to think of pituitary appleplexi, actually. So pituitary appleplexi, many times you're going to see this in people that have pituitary adenomas. And then they have like a hemorrhagic stroke of the pituitary, associated with those pituitary adenomas. You know, I have hemorrhagic stroke is going to cause like this sodium hypopituitaryism. So you're going to notice these people are going to become hypothyroid because they are making TSH. They're going to develop adrenaline and soficiency because they are making an CTH. And usually the symptoms that are going to come to the limelight with those people are. The hypothyroid symptoms and the adrenaline and soficiency symptoms. So most times on the exam, don't be afraid to, if you want to treat a person that has pituitary appleplexi, it's not a horrible idea to treat them with lethal thyroxae and hydrochloridesone. So basically give them thyroid hormone replacement therapy.

And so thyroid hormone replacement therapy and cortisol replacement therapy. Do you remember hydrochloridesone does not just have cortisol like effects. It doesn't just have glauquocoricoid like effects. It also has some mineral coericoid like effects. So it hits those things. So again, if a person is being treated for hypothyroidism and they ask you to give them drugs, live a thyroxan and hydrochloridesone. That's where it's out on your exams. Again, mineral resources don't talk about this stuff but it probably suits you pretty high ill to know for your exams. And if this person is infertile, if a person that has pituitary appleplexi is infertile, what do you want to use to promote their fertility? Well, I'll hope you're saying, hmm, divine. I think I'm going to give this person a continuous, I mean, sorry. Positile looper light. Positile looper light. And but looper light is a generic analog. When you give it an opositile fashion, that should promote the HPG axis. But let me ask you this. So again, this is, you know, this is actually a good small segue here. I want to discuss something. Just related to what I just said. So I just literally made a mistake right now. But let's use this mistake as a teaching point. So I just said that if a person has pituitary appleplexi causing hypopitrytoryzm, they got to be on a level of thyroxin, they got to be on hydrochlorid zone. And then I said, ooh, if you're trying to get pregnant, you should give them Positile looper light.

That third point I mentioned is wrong. Is wrong. Literally as I was seeing it out with my mouth, I'm like, hmm, divine. That doesn't make physiologic sense. So let's talk about this. So why will Positile and then we'll talk about the real treatment? Why will Positile looper light be a bad idea in these people? If you have hypopitrytoryzm, you give a person Positile looper light. Why will that not be effective to help these people get pregnant? Hmm. Okay. So let's talk about the pathophys. So number one, looper light is a generic analog. When you give it an Positile fashion, it promotes the HPG access. When you give it in a continuous fashion, it shuts down the HPG access. So if you give looper light in a Positile fashion, giving generic, it's supposed to stimulate your gonadotrophs in your anterior pituitary to make ACTH and, I mean, to make FSH and LH. Well, let me ask you this. If you have pituitary papal plexi and your anterior pituitary is gone, are you going to be able to respond to Positile looper light? No, you will not respond. You literally do not have the gonadotrophs to respond. And if your gonadotrophs are not responding, then you're not going to be making any FSH or LH to stimulate your gonads. So actually, how should you treat infertility in a person that has hypopitritors and, like, pituitary papal plexi? Well, you want to give that person actual gonadotrophins. You want to give them synthetic gonadotrophins.

Because by giving those gonadotrophins, you're pretty much replacing FSH and LH activity. So those gonadotrophins you give, they're going to stimulate the person, it's gone out. And that's going to promote fertility. So again, I'm glad, honestly, that I need this mistake. But I think it shows you the importance of actually understanding things instead of just blind memorization. Because if you notice in this, as I was saying it, I was like, define this makes absolutely no sense. Let's back up here. Let's think about this. So the thing is, many times if you have understanding, you'll notice that you can wiggle your way to the right answer on many USM-Liquestions. That's just the honest truth. So there's something you want to keep at the back of your mind as you're studying. Again, like, understanding and obtaining you, bit memorization every single time. That's the truth. There are very few times where I'm like, man, memorization is probably the better course of action here. So there's something to kind of keep at the back of your mind. Now, remember with regards to pituitary denomas, so we've talked about proteinomas. Let's not forget the high dose dexamethasone suppression test with Cushing's disease. Remember, Cushing's disease is a pituitary denuma that literally is making a ton of ACTH. So obviously that's going to be an ACTH dependent cause of Cushing's syndrome.

So the person's ACTH will be high, they'll have skin hyperpigmentation because of the increase in AC from opiumelano-cortin. So you're just going to keep that at the back of your mind as you're studying for your exams. And then, if they give you a question about a person that has bilateral hearing loss, that's pretty straightforward. That's a bilateral acoustic neuroma. That's a schwanoma. One of the cool things about this, don't forget S100 positive. These tumors are S100 positive. And we tend to find them at the cerebellopontin angle. And if you're trying to get you to find a location, because again, that cerebellopontin angle is in every on-key deck known to mankind. So what is one other way they can test this? They can say, where would you find this? And you notice that cerebellopontin angle is not an answer. But they just happen to be an answer that says internal acoustic meedus or internal auditory meedus. That's another location in my Cushing's exams. And typically on the exams, the cranial nerve that's going to be compressed by a schwanoma is going to be cranial nerve 8, your vestibulo-coclear nerve. So that's why those people can have hearing loss. They can have hearing loss, they can have tenitis, and things like that. And again, many times you're going to resect this or you can do like radio-sertory. I think like the gamma knife or something like that, from non-meas seeking, maybe what you use for these folks.

So just going to keep these things at the back of your mind as you prepare for your exams. And then, what if they give you a question about a child? And they tell you that this child has a brain tumor, and that this child has a bite temporal hemianopsy. If you see something like that, I want you to think of a cranial fire in Juma. The cranial fire in Juma is the... Pretty much I will say like probably the only or the very important, super-tentorial brain tumor you'll find in kids. Most pediatric brain tumors are below the tentarium cerebelli, as I described earlier on. So think of cranial fire in Juma's. They love to test this one within biology. These things that arrive from... There are many ways they can test this. They can call it raffkey spouch. They arrive from surface sector, they arrive from the roof of the mouth. And these things tend to contain calcifications. So if you see a super-tentorial calcified mass in a child, you want to think about a cranial fire in Juma. And these tumors grossly tend to have a lot of cholesterol crystals. That's why sometimes they're told... They're told that, ooh, they have like motor oil fluid. It's not real motor oil. You can be doing your oil changes from your cranial fire in Juma, but just something you can keep in mind. Right? Some of you can keep in mind. So again, don't forget, in rheological origin, raffkey spouch, roof of the mouth, or a lectorum, or aectoder. Okay? Just kind of keep that at the back of your mind.

And again, they usually contain calcified gaseous. Now, one thing I want to mention is... The pediatric brain tumors, especially like astrocytoma, the pailosidic astrocytomas, the medallol astomas. They love to be in the cerebellum. And our friends at the NBNEAS, they can try to ask you to rein the cerebellum based on the clinical presentation that is supply for your exams. So they can tell you that the person has truncally taxia. In the question, or they can tell you that, oh, the person has peripheral taxia in the question. By giving you the kind of etaxia, you should be able to deduce precisely where in the cerebellum that tumor is. If they have truncally taxia, your trunk is the middle of you. So it should tell you that the problem is probably coming from the middle of the cerebellum. That's the vernis. But if they have peripheral taxia, then your periphery is on the external of you. So that tumor is probably coming from the external of the cerebellum, from the wings of the cerebellum. There's going to be the para vernis. There's going to be the para vernis. It's going to be the para vernis. So remember, pailosidic astrocytoma is the most common primary brain tumor in kids. And usually, you're going to see some kind of etaxia. Usually, you're going to see some kind of etaxia. Again, GFEP is the tumor marker. It's going to meet the integrations with that already.

And again, the critical thing to know about histology with these things is that you're going to see rosenthal fibers. Let me tell you that, oh, histological examination shows pink cox-screw-like fibers. If you see that, you want to think about a pailosidic astrocytoma. Those things are called rosenthal fibers. Rosenthal fibers. Rosenthal fibers. And again, they're going to be in the posterior forza. Again, if something is in cerebellum, it's in the posterior forza. Again, I'm just trying to orient to it all these terms. So when you're reading these questions, you know exactly what you're dealing with. And again, it's a kind of astrocytoma. It's a low-grade astrocytoma. And then again, the drop metastasis, when we've talked about already, that's going to be a metaloid blastoma. So let me make a quick point here, too. Make sure you kind of understand this. The most common primary pediatric brain tumor is a pailosidic astrocytoma. The most common primary pediatric brain tumor is a pailosidic astrocytoma. But the most common primary malignant, so if something is malignant, it means it spreads. Most common primary malignant pediatric brain tumor is a metaloid blastoma. Pailosidic astrocytomas basically do not spread. But metaloid blastomas absolutely spread. Remember that whole phenomenon of going through the CSF-5 ways, drop metastasis to the spinal cord. So again, typically they're going to be in the cerebellum.

And they can cause this thing we call non-communicating hydrocephalus. Remember, whenever you see the terminal communicating hydrocephalus, they love to use this communicating terms. Because again, it's just a way to see people actually understand what's going on. A non-communicating hydrocephalus means that it's an obstructive hydrocephalus. It's an actual obstruction to the flow of CSF. So obviously if your CSF flow is being obstructed, then you're going to notice that this person's going to have signs and symptoms of increased ICP. So metaloid blastomas and ependymomas are famous for causing a non-communicating, which we call an obstructive hydrocephalus. So you can see headaches, pplidema, things of that nature. And again, remember, histologically, what are you going to see with a metaloid blastoma? You're going to see these homerite rosettes. You're going to see those homerite rosettes. Remember, homerite rosettes are not only found in metaloid blastomas, they also found in neuroblastomas. Remember, neuroblastomas have talked about them in previous podcasts. It's going to be an abdominal mass that is calcified and crosses the midlining kits. Now remember that metaloid blastomas, again, you know, just like OGFEP is like a marker for polycytocytomas. Don't forget that synaptophysin, synaptophysin, SN, sorry, syneap TOPHYSIN, synaptophysin. I was positive in blue to have metaloid blastomas.

And then ependymomas usually is probably going to present with signs and symptoms of increased IC Ps. If they show you any kind of brain tumor within the ventricles. So this one is not going to be on the cerebellum, it's going to be within the ventricles, especially in the fourth ventricle. Again, this is a classic question emission step one. But you can give you an ependymoma and you can ask what's the most common location. And you'll put third ventricle, a lot of ventricles, fourth ventricle, arachnoid granulations, spinal cord, yada yada yada. If you see something like this, I want you to think of ependymomas being in the fourth ventricle. That's the most common location. So they can cause again an obstructive or we can call that a non-communicating hydrocephalus. Now what is one weird unique factoid to know about ependymomas? I said that, oh, they're going to be in the fourth ventricle in kids. Most times ependymomas are going to be in kids on your exams. But is there a kind of a weird place where you may find ependymomas in adults on your exams? Especially, and many times they can give you this adult having a lot of radical apathy, symptoms, a lot of neuromodoneurin symptoms like ear reflexia or hyperreflexia, sadrulanesthesia, blah, blah, blah, blah. Especially when you see developed gradually over time in an adult, don't forget about an ependymoma. Ependymomas love with the spinal cord. What part of the spinal cord? The corda equina.

In adults, that's something again, they don't find many resources, but pretty high up to know for you exams. Ependymomas in adults, they love to go after the corda equina. They love to go after the corda equina. Now what are you going to see on histology in a person that has an ependymoma? The critical thing to keep in mind is that you're going to see perivascular sugar resets. So please don't confuse your resets. Medulla blastomas are associated with homeritore resets. Ependymomas are associated with perivascular. So you're going to see blood vessels around pseudo resets, perivascular, pseudo resets, perivascular, pseudo resets. Now what if they give you a question about a person that has a brain tumor? And you tell them to look up and they can't. You tell them to look up and they can't. You tell them to look up and they can't. What should you be thinking about? What should you be thinking about? I hope you're saying, ooh, divine. This is a pineyloma. A pineyloma is a brain mass that can cause parinote syndrome. Basically, these people, if you see a person that has a brain tumor and they have a conjugate gase paulzy, you want to think about a pineyloma. Why? Because the pineal gland is superior to the superior collectulus. The pineal gland is literally just above the superior collectulus. So if you have a pineyloma, the thing that's going to happen is it can compress the superior collectulus. And the superior collectulus is your vertical conjugate gase center.

So if you compress it, you're not going to be able to look. You're going to have a vertical conjugate gase paulzy. Another thing you may also see with these pineylomas. And I guess, let's make a little extra integration here. So I said that we call it a parinote syndrome, right? Where you have a vertical conjugate gase paulzy. Remember, if you have a superior cerebellar artery stroke, you can also have parinote syndrome. Because the superior cerebellar artery supplies blood to the superior collectulus. So that's like an ischemic cause of parinote syndrome. That's an ischemic cause of parinote syndrome. And again, I've talked about some brain tumors that can cause an obstructive or non-communicating hydrocephalus. I talked about medalloblastumas. They can compress the fourth ventricle. I talked about epinodymomas. They grow within the fourth ventricle. Now, don't forget these pineylomas. You can actually compress the cerebral aqueduct. The cerebral aqueduct of selvius. Remember, the cerebral aqueduct is one of those things that drains CSF. Remember, you have your lateral ventricles. And in those lateral ventricles drain through the interventricular foramen of monorool to the third ventricle. And then your third ventricle drains through the cerebral aqueduct of selvius to the fourth ventricle. And then your fourth ventricle is going to drain laterally to the two lateral foramen of lusica and the one median foramen of magendi.

So again, I can already see our friends at the MDM Es making you work out the location of the obstruction in a pressing that has a non-communicating or an obstructive hydrocephalus. Just based on what is distended. Remember, when you have an obstruction, the stuff before the obstruction that's proximal to the obstruction will be occluded. The stuff that's distilled to the obstruction will be not distended. So if a pressing has a medalloblastoma, those things obstruct the fourth ventricle. So you're going to see dilation of your cerebral aqueduct of your third ventricle, of your foramen of monorool and of your lateral ventricles as well. But, and also your fourth ventricle may be distended actually. In fact, I'm going to chalk this, I'm going to throw this thing. Your fourth ventricle will be distended as well. If you have something occluding the fourth ventricle, your fourth ventricle will be distended. So, your fourth ventricle, cerebral aqueduct, third ventricle and foramen of monorool and your lateral ventricles will all be distended in a medalloblastoma, one in an appendimoma. But, in a pressing that has a panelloma that's compressing the cerebral aqueduct, your fourth ventricle will not be distended. So you should not see what fourth ventricle distension in a panelloma.

The only things that should be distended should be your lateral ventricles, your ventricle fermentant of monorool, your interventricular foramen of monorool and your third ventricle, that's it, that's it, that's it, that's it. And I guess this noncommunicating hydrocephalus with the cerebral aqueduct, don't forget that if you see a newborn with hydrocephalus and they tell you, what was the most likely location of obstruction in the child's CSF pathway that's causing that noncommunicating hydrocephalus? I want you to think of the cerebral aqueduct, there's this thing called aqueductose stenosis, it's one of the most common causes, especially if you see it on an MBME exam in a newborn that has like hydrocephalus and it's noncommunicating, I want you to think of aqueductose stenosis, I really want you to think about aqueductose stenosis. And in these panellomas, they also have these nasty habit of producing HCG, so you can cause percotious puberty as well, they can cause percotious puberty. Because remember, HCG has somewhat similar effects as some of these gonadotropes, because remember, they are not very different structurally, so you can have a similar receptor-like effects, so something you want to keep at the back of your mind, something you want to keep at the back of your mind. Alright, now, what if they give you a question about a person that has HIV and they have like brain lesion, if you see this, think of a CNS lymphoma, right?

Don't forget that HIV has an association with a primary CNS lymphoma, that's obviously a kind of brain lesion. And these CNS lymphomas, again, usually going to be a sort of HIV, but don't forget that EBV, EBV has a very, very solid association with CNS lymphomas, okay? Just something you want to keep at the back of your mind. And remember, leukemias love to spread. In fact, let me tell you this, the most common kind of brain malignancies metastasis, okay? The most common kind of brain malignancies is just metastasis from elsewhere. It's just metastasis from elsewhere. And again, I said, long is number one, breast is number two, melanoma is number three, kidneys, probably number four, and stuff from your GI tract is number five. But one thing I want to mention with this whole metastasis business, this is a very high olfactory to know for your exams. I'm telling you this guys, please call me this to remember for your exams. When people have leukemias, when people have leukemias, typically one part of your workup has to be CSF studies. In fact, leukemias have a predilection for the spinal cord. They love to go to the spinal cord. So that's why many times people get intrathecal chemotherapy, intrathecal chemotherapy, intrathecal chemotherapy for that precise reason. Just make sure you kill off the tumor cells within the spinal cord.

Again, I'm telling you this, it will be that one question you see on your exam, you don't expect it, and you'd be like, man, I remember there was some podcast divine need where he talked about this random thing from nowhere. I know I'm talking about this random thing from nowhere. So make sure you know this stuff for your exams. So I think I'm going to stop here. This podcast has gone on for a long enough, but I think this has been a very comprehensive review of all the brain tumors and pretty much most of the classic integrations with these brain tumors. If you like the way it presents things from a clinical perspective and explain pathophase and whatnot, then I think you'll be interested in my review courses. This course is applied to step one or the way to step three. I have a class studying on Friday actually. So 25 hours step one course is over zoom. It's going to be in the evenings. Basically is for booting step one or complex one or if you're taking step two or step three complex two or three, you have a poor foundation. Because again, those foundations, these step one foundations are now tested heavily on the leader, you see the step to the step three. The class is going to be perfect for you. And then you know within the month of March, I have a testing strategies class of a bio stats class of social sciences and ethics class. I made a separate podcast where I talked about those classes. Those classes are not lectures at all by any stretch.

They're pretty much all clinical scenarios. And I use those exam style questions to go over the concepts, teach you pathophase and help you understand the material. And then I also offer one on one tutoring and also help with your applications and more interviews and whatnot. And I have this podcast on the major apps Apple Google Spotify, I have a You Tube channel you can check out. And then I also have another website called divine intervention life lessons.com. From a biblical perspective every week, I post two podcasts roughly where I discuss a life lesson. Many people have listened to those podcasts and found those to be helpful. There's actually an Apple podcast associated with that. So thank you for listening to me today. I will see you in episode 517. For people going through the match, I wish all the best and I pray and trust God for you that you match at your desired spot. I'll give you peace and go train. But it's exciting and we show the best. So see you in episode 517. And again, thank you to everyone listening to those podcasts. I really appreciate it. So a lot of work making this podcast. So I certainly appreciate people listening to it. So God bless you. A wonderful day. Bye for now. Thank you.

Practice questions — USMLE style

Question 1 — Pediatrics/Neurosurgery

A 4-year-old boy is brought to the emergency department with progressive vomiting, lethargy, and signs of increased intracranial pressure (ICP). Imaging reveals a mass in the cerebellum. The child has a history suggestive of cerebellar ataxia. Biopsy confirms a highly malignant tumor that exhibits "drop metastasis" through the cerebrospinal fluid (CSF) pathways into the spinal cord. Which of the following is the most likely diagnosis?

  • A) Pilocytic astrocytoma
  • B) Meningioma
  • C) Medulloblastoma
  • D) Craniopharyngioma
  • E) Oligodendroglioma

Answer: C. The key features pointing to medulloblastoma are its high malignancy, typical location in the cerebellum (or vermis), and the classic pattern of "drop metastasis" through CSF pathways. Pilocytic astrocytomas are typically benign and do not exhibit this aggressive metastatic pattern. Medulloblastomas are known for their ability to spread via the CSF, which is a critical high-yield point on board exams.

Question 2 — Neurology/Pathology

A 35-year-old woman presents with a slowly enlarging mass arising from the dura mater adjacent to the falx cerebri. Physical examination and imaging reveal the mass contains characteristic laminated calcifications (soma bodies). Histological analysis confirms the tumor is derived from arachnoid cells. Which of the following statements best describes this tumor?

  • A) It is an intraaxial tumor, meaning it grows within the brain parenchyma itself.
  • B) Its primary risk factor is exposure to ionizing radiation in childhood.
  • C) It is typically associated with a history of bilateral acoustic neuromas and NF2.
  • D) It is an extraaxial mass derived from the meninges.
  • E) The most common tumor marker for this condition is GFAP.

Answer: D. Meningiomas are classically described as extraaxial masses because they originate from cells adjacent to the dura mater, not within the brain parenchyma (which would make them intraaxial). While NF2 and bilateral acoustic neuromas are associated with schwannomas (a different tumor type), meningiomas are characterized by their dural origin.

Question 3 — Endocrinology/Neurosurgery

A 40-year-old woman presents with headaches, fatigue, and signs of hypogonadism. Imaging reveals a pituitary adenoma compressing the optic chiasm. Laboratory tests show elevated ACTH levels and hyperpigmentation of the skin, consistent with Cushing's syndrome. Which initial management strategy is most appropriate?

  • A) Administering dopamine agonists (e.g., cabergoline) to suppress prolactin secretion.
  • B) Initiating high-dose glucocorticoid replacement therapy to manage adrenal insufficiency.
  • C) Performing transsphenoidal resection of the tumor, followed by replacement hormone therapy.
  • D) Treating with a somatostatin analog to reduce pituitary gland size.
  • E) Administering synthetic gonadotropins (FSH/LH) to stimulate the HPG axis.

Answer: C. The patient presents with signs of hypopituitarism due to a mass, and the elevated ACTH suggests an ACTH-dependent cause (like Cushing's disease). While replacement therapy is necessary for adrenal insufficiency, the primary treatment for most pituitary adenomas causing compression symptoms or hormone excess is surgical resection. If the tumor was specifically a prolactinoma, dopamine agonists would be first-line; however, given the hyperpigmentation and elevated ACTH, surgery remains paramount, followed by appropriate replacement hormones (glucocorticoids, thyroid hormone).

Question 4 — Neurology/Neuroanatomy

A patient presents with signs of non-communicating hydrocephalus. Imaging reveals dilation of the lateral ventricles, third ventricle, and interventricular foramen of Monro, but the fourth ventricle itself is not distended. The clinical presentation suggests a mass lesion in the suprasellar region that compresses the cerebral aqueduct. Which tumor type is most likely responsible for this specific pattern of obstruction?

  • A) Medulloblastoma
  • B) Ependymoma
  • C) Pineocytoma
  • D) Craniopharyngioma
  • E) Hemangioblastoma

Answer: C. This question tests knowledge of CSF flow dynamics and anatomical compression. The cerebral aqueduct is the narrowest point connecting the third and fourth ventricles. A mass compressing this specific structure (like a pineocytoma, which often arises near the superior colliculus/pineal gland) will cause dilation proximal to the obstruction (lateral ventricles $\rightarrow$ third ventricle), but it will not allow CSF to fill or distend the space distal to the obstruction (the fourth ventricle). Medulloblastomas and ependymomas, conversely, typically obstruct the fourth ventricle itself.

Quick fire review

What is the most common primary adult brain tumor?

Glioblastoma multiforme (GBM).

Which type of mass is considered an extraaxial mass, derived from the meninges?

Meningioma.

What specific constellation of findings suggests NF2?

Bilateral acoustic neuromas and/or meningiomas.

What are the key features of a patient presenting with signs of increased ICP due to a brain tumor?

Headache worse at night or upon waking, vomiting, seizures, papilledema.

Which specific type of metastasis is characteristic of medulloblastoma?

Drop metastasis (tumor cells passing through CSF pathways).

What are the key components of Von Hippel-Lindau syndrome associated with brain tumors?

Hemangioblastomas in the cerebellum, polycythemia, and hypertension.

What is the most common primary pediatric brain tumor?

Pilocytic astrocytoma (often found in the cerebellum).

What are the characteristic histological findings of oligodendroglioma?

Fried egg appearance; calcification is common.

Which pituitary adenoma is often associated with MEN1 syndrome and requires dopamine agonists for treatment?

Prolactinoma.

Name two tumors that can cause non-communicating (obstructive) hydrocephalus, and what are their respective locations/mechanisms?

Medulloblastoma (obstructing the fourth ventricle); Ependymoma (growing within the fourth ventricle).

What is the key difference between an intraaxial and extraaxial brain tumor?

Intraaxial tumors grow within the brain parenchyma; Extraaxial tumors are adjacent to the meninges/dura.

Which specific type of headache pattern suggests a pineocytoma?

Parinaud syndrome (vertical gaze palsy) due to compression of the superior colliculus.

Quick recall / Anki-style questions

What is the most common primary pediatric brain tumor?

Pilocytic astrocytoma (often found in the cerebellum).

What are the characteristic histological findings of oligodendroglioma?

Fried egg appearance; calcification is common.

Which pituitary adenoma is often associated with MEN1 syndrome and requires dopamine agonists for treatment?

Prolactinoma.

Name two tumors that can cause non-communicating (obstructive) hydrocephalus, and what are their respective locations/mechanisms?

Medulloblastoma (obstructing the fourth ventricle); Ependymoma (growing within the fourth ventricle).

What is the key difference between an intraaxial and extraaxial brain tumor?

Intraaxial tumors grow within the brain parenchyma; Extraaxial tumors are adjacent to the meninges/dura.

Which specific type of headache pattern suggests a pineocytoma?

Parinaud syndrome (vertical gaze palsy) due to compression of the superior colliculus.