Chronic headaches that are constant and unrelenting, especially in young women, should prompt consideration of systemic vasculitis like Takayasu arteritis, which can cause carotid intimal hyperplasia and aortic involvement; the key diagnostic question is 'when was your last good day?' to distinguish primary headache syndromes (which have good days) from secondary causes (which are continuous).
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May 8, 2026 VMR with Rabih & Manaswini - chronic headachesAdded:
Oops. Sorry.
All right, y'all. Happy Friday. You know what this means? Uh, this means I get to hang out with a legend in the world of CP solvers, and that is the one and only Manusweeni. Um, I don't think she needs an introduction at all. I vividly remember you're bursting on the scene mere months ago, Manoseni, and you've climbed to the heights to be one of the leaders of this space. Um, and you know, my favorite thing about Monosini is uh is the fact that she has probably the biggest smile under the sun. Um, but don't let that fool you. She can be a very very sneaky case presenter with that smile on her face. She makes people absolutely bamboozled and sweat quite a bit um in our uh behind the scene rapid fire sessions where she takes you into the heat of the battle on a patient who's sick or complicated or that's a convoluted story. So u I'm so excited to get to discuss with you. I think we'll we'll miss you quite a bit when you get very very busy. So I think it's the perfect timing to celebrate what you've accomplished and to transition to you learning from patients in real time. So I'll hand you the mic to say hello and then we'll introduce everybody else who's making the session happen.
>> Hello everyone. Hi Dr. Rabi. I'm so excited today. I've been waiting for this day for so long. Uh, and I just want to say I'll keep it short and I just want to say that every session, every moment, spending it with you and with the academy is an absolute blessing. And I'm just here to like bask your radiance and your um, enigmatic aura today and learn from you. So, I'm super excited.
>> Oh my gosh, you have so many fancy words. I barely understood it. O wow, look at that vocabulary. Oh, amazing.
[laughter] So nice of you, Anna, sweetie. We have a very very special guest to uh to honor this occasion. Our first time case presenter Gata. I'll hand you the mic.
Tell us a little bit about yourself, please.
>> Uh hi. Thank you guys for having me. My name is Harata McKenzie. Um I'm a second year going on thirdyear medical student at uh UMKC in Kansas City, Missouri. So >> I'm so sorry for butchering your uh your name. Can you pronounce it one more?
>> No, it's okay. Um the G sounds like an H, so it's hard.
>> I see. Gotcha. Gotcha. That's so cool.
Wow. you are jumping into the um biggest inflection point in medical training.
How is that? You're I missed what you said. Are you in the middle of that transition now or of second to third?
>> Yeah.
>> Yeah, I'm in the middle of it. I'm on my first like core rotation right now.
Pediatrics. So >> Oh, cool.
>> That is awesome. You know, uh it is my dream whenever we have people in the beginning of their clinical years to hop in and present cases. What What inspired you to pop on up here and present a case? Um, it was a mentor attending. Um, she, this is a patient that I've seen with her.
>> She recommended that present.
>> Yeah, that's awesome. I'm so glad you're getting to do that. What do you like to do outside of medicine?
>> Um, I teach swim lessons. I enjoyed swimming. Um, I like baking. Um, I feel like medicine has kind of taken my hobbies a little bit >> dry. I like reading too when I can, but >> yeah, I think it's, you know, I think uh my hobby is medicine to be honest, though I I I love to do some other things. Uh and enjoy the delightful baking of a couple of family members of mine after a nice swim. So, I think we have that in common. That's really cool.
Do you have a sense of what you want to do?
>> Um kind of. I like internal medicine.
I'm I really like pediatrics, so it's kind of making me like think about it, but I also like critical care, too. So, >> amazing. Yeah, we have uh a medical student colleague of yours in New York um named Jillian who has a very similar tension between medicine uh and pediatrics. Um so yeah, it's a it's it's not an easy decision to make, but I think you have plenty of time to make it. Um well, very excited for your case.
We got to uh shed the spotlight on the people who are anchoring the session, beginning of course with our scribe king, Lucas. Mike to you, my friend.
>> Hey guys, [laughter] what's up Lucas? subscribing. Um, yeah, that's it. [laughter] >> Oh, thank you, Lucas. And Glenn is doing more today. Mike, Mike to you, Glenn.
>> Uh, hello everyone. Yeah, I'm glad I'm doing teaching today. Excited for um think I'm pronouncing it well.
>> Yeah.
>> Yeah. Yeah. Um, nothing much for me. um just studying and it's getting u winter here so >> I can tell >> you're bundled up there. That's awesome.
Well, thank you so much for having on.
All right, Har, we're ready whenever you are. Take it away, please.
>> Uh yeah, I can start with the chief concern. Um, it is a 29year-old female with chronic headaches.
>> Dr. Have you been you're muted.
>> Oh my gosh. Oh, thank you. I was just commenting on your neuropilia.
Um, Hana, did you did you intend to stop here or did I cut you off?
>> Um, I can continue. I'm not sure if you'd like me to give like a HPI as well.
>> Whatever you had planned. We don't want to disrupt your flow. If you had planned to stop here, that's great. If not, we can go.
>> Whatever you >> Okay, go for it. Go for it.
>> Okay, so this is a 29-year-old Somali woman. She's presenting to the clinic for establishing care. Um, she's been waking up with headaches since she was very young. Um, she describes them as occipital in location. They radiate to her posterior neck. Um, and they're relieved by NSAIDs. She takes them um almost daily. Um, and then the headaches consistently return in the evenings. Um, and she has associated shoulder pain due to muscle tension. Um, she denies vision changes, dizziness, numbness, tingling.
Um, and she's also reporting some superficial kind of like neck throat tenderness that's located more in the upper neck, more prominent on the left side. Um, and this had started a year prior to this visit. Um, the pain is not affected by swallowing or neck movement.
Um, she's not having any dysphasia. Um she's not reporting any ticardia, anxiety, tremors, weight loss, weight gain, cold intolerance, or fatigue.
Kind of hard to believe that you're just beginning your clinical exposure. That was a really crystal clear uh you really bringing the patient to life, a very clear imagination of what's going on. So yeah, Monasi, what what are you thinking so far?
>> Hi Orata, welcome. Such a beautiful presentation. Um so I first of all this is a young female who's been presenting with chronic headaches and it's great to hear that she has uh when I think of headaches and how we have taught us it's um either there's a dysfunction or an impending dysfunction. So I'm glad to see that she does not have a dysfunction like bluring of vision or um like a weakness in one of the limb. But uh this has been going on for so long. Uh so I'm so curious to know if there's any um impending dysfunction but there um we don't see it because it's chronic and also does she have an underlying vulnerability like um in HIV or like a congenital um infection uh before she was um curious to see her um birth history and um but also if we just focus on what we're seeing at the moment um it's seen on waking up but it's in the hospital. So I remember that waking up um might mean that it might involve the frontal uh region of the brain but then we're seeing oipital um headaches that are radiating. So curious to know how um if there's any um so localizing it what is the disease where is the disease and why so what is it it might where might it be it might be um anywhere from um like uh the nerve root or it could be something involving the the structures in the brain like the ventricles or how we have taught us um ventricles, parenima, um meninges or um the vascule. But here I think what I would be focusing on is um the ventricles and it's been going on for so long. So curious to know her previous imaging. Uh but also there might be some compression. Uh so o in overall is it like a substance or a structure and I think I'm leaning towards structure at the moment. Uh but still there might be um curious to see if there's any variation um and would love to hear what you think.
>> Yeah. I know. I think I think your thoughts are spot on. And I think just to recreate the tension that you might feel just in a one short month if you were in a similar situation sitting across this person, you might have to ask yourself like how how extensive do you do a workup for somebody who has had longstanding headaches? Because a real life question will be um what is the real life question would be the following. Essentially, the vast majority of people who have long-standing headaches without consequences um have a primary headache syndrome. And essentially what a primary headache syndrome is is the reason that your head hurts is there's a dysfunction in the um irregulatory systems of sensation and that you really your head shouldn't hurt. It's not hurting for any good reason. Um and so what have you picked up on this case if anything that pushes you to say, "Hey, I'm not diagnosing a primary headache syndrome and I'm more specific about a secondary one." What do you think that might be?
>> Yeah, absolutely. Is it um systemic versus the brain? I think the most concerning one for me is um there's some throat tenderness.
>> Uh >> yeah, >> returns in the evenings and comes in the morning. So the variation perhaps >> and yeah, what do you think Dr. Abi?
Yeah, I think it's a difficult situation, man, cuz you have to ask yourself if you get CTS and MRIs and people who have migraines or tension headaches or cluster headaches, you're probably going to be uh overburdening the health care system. And I think when somebody has such a longstanding headache, the chances that they have menitis is zero. The chances that they have uh glyobblastoma multififor as I presented to you all, zero. So I think the longer the headache lasts, the more and more you have to be uh judicious in your diagnostic testing.
But there's one characteristic feature of primary headache syndromes that appears to be absent in this case which is a primary headache syndrome does not affect you every single day for your life.
Primary headache syndromes are transient discomforts that resolve.
So even though we know this disease has affected her for decades, what we have to establish is when the last time she had a day without a headache.
And if the answer is never, there's a problem.
If the answer was, you know, 3 days out of the week I'm fine, it's hard to imagine that you have introanial hypertension or a strategic lesion that gives you relief. Why would it just hide in a closet for a few days and then come back?
This is I I'll talk to you in the in the spirit of Kevin who's kind enough to turn his video on despite being so busy about real life medicine. Chronic diseases are the most common diseases we see and acuity hiding under a chronic disease is the most common cause of morbidity. Kevin's case last week was acute or subacute pancreatic cancer camouflaged by chronic constipation and psychiatric chronicity.
How do you sniff out a morbid underlying cause when it's camouflage and chronicity? You ask one question. When was your last good day?
And in patients with chronic back pain, they always have some good days. In patients with migraines, they always have some good days. In patients with constipation, they always have some good days.
If you have a pancreatic cancer, you're never going to have any good day.
If you have intracal hypertension, you're never not going to have any good day. So my only question for her now is when was your last good day? And I think that is allows you to gain a lot more momentum than otherwise. Now that question may not be asked understandably. So it's a difficult one, but in short, how do you how do you distinguish a primary benign headache syndrome from a secondary one? In most people, most people, it's that a secondary one, if let and given time, turns into something way more serious than a headache. It turns into weakness or paralysis or vomiting or nausea.
But here, for 20 years, it hasn't turned into anything. So, statistically speaking, this is a primary headache syndrome. She's coming into clinic, primary headache syndrome. But are there some mimics? Of course, what are those mimics? We'll probably talk about them.
Um, but how do you even know?
One key question. When was your last good day? And if somebody has a benign cause, chronic back pain, chronic constipation, um, chronic benign headaches, they have good days. If you have pathology, you're never going to have a good day. Any questions about that, Monosi?
Yeah, that's a wonderful thought.
>> All right, Harata, very very interesting case. I don't think we've discussed a 30 20 year headache on VMR ever. So excited to see what learning you bring. Give you the mic back.
[cough and clears throat] >> All right. So for her past medical history, [clears throat] her she has type class one obesity um and then those chronic headaches. Um for pregnancy history, she's G3 P3. Her first two were vaginal births. The last one was not on record. Um but um it was a viable pregnancy. Um she takes a leave in Tylenol, mostly just for those headaches. Uh for social history, she denies alcohol, tobacco, or recreational drug use. Um she does not work and she lives at home with her three kids and husband.
Um she doesn't report family history of any cardiovascular, autoimmune, endocrinologic issues. and she doesn't have any known allergies.
Um, and then I can talk to about like objective information. Uh, temperature is 98.7, heart rate is 94, blood pressure is 136 over 72, oxygen saturation is 98%.
Um, physical exam shows a wellappearing female. Uh, no tenderness to palpation of the neck and thyroid. Um, no cervical lymphatinopathy or thyrogaly. Uh she has full range of motion of the cervical spine. Uh neuroexam is non-focal. Cardio exam shows regular rain rhythm, no murmurss, normal profusion, and no lower extremity edema.
>> Incredible. It's going to be scary to see you as an MS4 like probably making the attending feel intimidated as to how skilled you are. This is unbelievable.
Um Monasini, what are you thinking with this data so far? What stood out to you?
>> Yeah. Um, awesome. Um, Harata. So, I see that she's only on Tylenol and the first thought is she's been having headaches for so long, but she's um I'm curious to know if she's tried getting um like profilaxis perhaps, but um she's only on Tylenol, which intrigues me. And um she's obese, so class one might be um yeah, she's pretty severely obese, I believe. And uh the first thought that came to my mind is um looking at the blood pressure >> [clears throat] >> uh causing the secondary uh if there is any um sympathetic um con constant sympathetic activation in the body. So why is there 136 over 72 and a 29 year old um might not have something that's more than 120 or 120 around 130. So there might be an underlying u substance um that might be chronically present um >> that is increasing her uh that is um remodeling her blood vessels >> u due to her obesity perhaps >> and we haven't gotten her BMI um yet um >> but yeah she's uh quite obese and that that was my first thought but her on her exam we see nothing going on so nothing happening externally but is there something brewing for so long and we might see it in the next allequat yeah >> um curious about that and um those were my thoughts Dr. What do you think?
>> Yeah, I think you've identified the key piece of history to study. Um, I think importantly, uh, whenever you're getting a history, you want to make sure that that history lines up on exam and we're lining up with that she doesn't have any consequences so far. So, your eyes now have confirmed that, which is great. Um, but I think it's very very important for all of us to have a rich understanding of how a high BMI overlaps with chronic headaches.
So, Manosini, if you were to do the exercise of removing yourself from this case and practicing schema building, so what do you think of the overlap between obesity and headaches? What crosses your mind in that domain?
>> Um, awesome. So um so I think that if the if someone is obese it might um like the amount of fat in the first thought that came to my mind is the amount of fat in your neck that's compressing the >> um airways and then that's decrease in the amount of oxygen um reaching your brain or like um causing like increase in carbon dioxide and um headaches and that sort. Um another thing is um underlying Cushings.
So I divide the bucket again. Um obesity to headache. Uh whether there's any um infection I I wouldn't think about that.
>> Um but um endocrine causes like um probably uh Cushings uh increased AC um I'm thinking there's hypothyroid might cause it. Um >> but I don't think so. Um and then um >> um we after endocrine I would think about >> I don't think any autoimmune obesity is there but um or if there's a malignancy underlying malignancy that's causing the obesity like ACT release and that's causing the headache that's that's >> this is so much fun to do this with you because as Krishna said literally Krishna said Kushings is a genius idea and um you know what's really impressive about skill set is, you know, you haven't even started intern year yet.
And then you have the you have the equinimity to compose yourself in a public audience and kind of think creatively about something you've clearly have thoughts about, but you probably haven't done this random thought experiment before, right? But what we did was true. What I thought was genius wasn't the endocrine hypothesis because I think those are actually really, really interesting, but they're rare, right? And I know you know that. But what was genius in my opinion was that you actually uncovered the pathway physiology of all common forms of the overlap of obesity and headache with one simple word, neck crowding. And you're absolutely right. Neck crowding can result in two things.
Uh I'm leaning in because I find this really interesting. the neck crowding.
The most common cause is obstructive sleep apnea as the as the uh impact of uh obesity on the airway, especially at night when the airway is relaxed. And so OSA is a very very very common cause of lifelong headaches if not treated.
But man, we need do you know what other structures can be compressed in the neck that can affect the brain?
Now this will be genius squared if you get it but why not try thinking what else in the neck is really important to the brain apart from the >> airway the uh the blood vessels.
>> Yes. Yes. Pseudo tumor cerebri or idiopathic intraanial hypertension is a complex disease that is in small part driven by elevated filling pressures of the jugular vein that impair the drainage of the cerebral veins which creates this vicious cycle of reabsorption of CSF causing intraanial hypertension.
The most common mimic of primary headache syndromes are those of gentle compression here, the airway or the neck. And when Herata was presenting this case, I thought it was going to get really, really, really interesting if the BMI was normal.
But now that it's not, you have two of the most common mimics of primary headache syndromes, which is strategic, gentle, slow compression. Not here, but here.
And the compression here is so diffuse and so slow that it's not manifest here.
It's manifest here.
And so yeah, I think um any situation like this you have to ask the question does the patient have OSA and does the patient have idio idiopathic intracal hypertension and uh uh we'll let the case proceed just for time management sake but I'm curious just to keep authentic to base rate what do you think is more common osa or ih Dr. by orders of magnitude. So now that you're generating this hypothesis, it's really important to go back to the patient and ask an OSA review of systems. There's a really nice questionnaire that you can Google called stop bang. It's an it's essentially an acronym for asking targeted questions about OSA and I encourage all of you to review that. It's really good to have that in your back pocket. So let's see where Herata takes us next. But I think the as you aptly identified the obesity is the key clue here to pursue. And um uh while there may be underlying drivers of the BMI like endocrinopathies, the common causes of obesity and uh uh headaches are compression here, airway more than veins. All right, Har, thank you for this really intriguing case. I'm curious what you have next for us.
>> Okay. Um so uh at the end of this visit she was sent home with amryptalene.
There was higher concern for like possible primary headache and then in terms of like working up the throat pain and for just general adult health examination um an apo A1C lipid panel CMP as well as a TSH were obtained. Um and all of these things came back within normal limits.
Um and then once the TSH came back normal, um a thyroid ultrasound was recommended to further work up the neck pain. Um and the thyroid ultrasound showed normal gland size and structure, but it did find abnormal intimal hyperplasia of the corateeds. Um and because of this, um they ended up doing corateed Doppler as well. and that showed bilateral corateed intimal hyperplasia um which was out of proportion with age and history um described as abnormal moderate intimal hyperplasia of her internal external and common corateed um resulting in diffuse luminal narrowing set >> very interesting thanks Ra yeah um monos this case went uh and followed an incidental finding to an interesting uh observation of the karate how are you thinking about this what do you Um yes Dr. Abby this is so interesting ora um so we see moderate intimal hyperplasia and you um astutely suspected it as well um and I am it's we see that she's a 29 year old and there's intimal hyperplasia of internal external and common corroted arteries. So it's at the artery and um we don't see any atherosclerosis. She's young. So we see the problem in the vessel itself. So I'm curious to know what caused the hyperplasia like why is it um hypoplastic? So is there um an infiltrative pathology or is there a um um there's hyperlasia because of remodeling from an a substance or is there an autoimmune cause that's going on or um is there a vasculitis involved?
Um curious to know what you think Dr. Abby.
>> Yeah I think Moni I just ask you one follow question. Do you feel like this finding uh readily explains her headaches or are you creating this in your note a separate problem? What are you inclined to do? Lump it into headache or keep it separate for now?
>> Um awesome. Yeah. So I am thinking of keeping it separate for now because I don't see how I'm able to link the two.
But curious to learn from you.
>> Yeah. I mean I think uh genius and genius and genius you're right. You have to be careful. The simple reason to keep this as separate is you found it by luck alone. And you have to be careful. You might have gotten really really lucky or you might have gotten distracted.
Now the distraction may be of clinical significance, but it's it's maybe a complete distraction, right? And so I think this case is teaching us a lot of things. One, we don't know that she doesn't have a primary headache syndrome. She easily could have a primary headache syndrome if we had if you and I will only know this if we ask her with confidence when she has relief from her headaches. And if she says, you know, I have these headaches, I have many good days. Then it it becomes plausible that her headache is a separate thing and then we got lucky and found something in her neck that doesn't seem to be causing her problems right now, but potentially could allow us to intervene earlier before she develops problems from this. So I like you have now two separate problems. headache, concern for secondary headache syndromes potentially related to obesity.
However, response to emitalene and further interviewing may help us clarify the legitimacy of these concerns.
Problem number two, corateed intimal hyperplasia.
And you translated that that intimal hyperplasia into exactly what it should be. This is a disease of the blood vessel wall.
So Manosini again let's practice base rate and remove yourself from this case.
What do you think is the most common cause of a blood vessel wall disease in general all comers? What do you think?
>> Um I was my reflex thought was hypertension but that's not a blood vessel disease.
So um >> blood vessel wall think about wall >> keroted artery disease um atherosclerosis >> yes by far and away it's so intuitive that we forget and manosini we would not be interested in this finding at all if she was 70 because we would immediately conclude that she has atheroscerotic disease of a blood vessel All and Harata is such an astute presenter because she told us two things. She told us this is out of proportion to her age. Well, why would it be proportion to her age in the first place? Atheroscerosis.
But she did something else. She snuck in an A1C, a lipid profile to tell you, hey, this is not aththeroscerosis in a young person.
This is a sneaky setup for an aloquat for us to actually look at this and be like, oh, she's too young for aththeroscerosis and even if she's not too young, she doesn't have the risk factors for it because she doesn't have hyper lipidmia, diabetes, and nor hypertension. So, she's telling us that she has a nonathoscerotic blood vessel wall issue.
And that is the only time you start to solve a blood vessel wall issue when you prove it's non-athoscotic because otherwise you're completely wasting your time. Can you imagine every time a cardiologist casts somebody and sees an LD wall thickening with plaque and they have to do a work up for vasculitis and vasculopathy the healthare system would be bankrupt. It happens so commonly.
So now we have to think what's causing it and you said the right words. Is this a vasculitis or a vasculopathy?
So I'm curious how do you how do you think you can go about making that distinction between a vasculitis and a vasculopathy? What do you think?
>> Um yes Dr. Abby I'm not sure I'm not 100% sure about this but I think associated systemic symptoms like fever or weight loss or >> Yeah that would be vas >> exactly you're trying to figure out the itis and vasculitis is inflammation. So a follow-up question for you. What do you think is the most sensitive test and of all tests, history, exam, labs? What do you think is the most sensitive test that is present in all people of any inflammation of any kind? What do you think?
>> Um yes, Dr. Abby. Um, so I think it's the inflammatory markers though I'm not um, we have constantly learned how it doesn't have a very good positive predictive value, but >> but negative predictive value is through the roof. It's really So if her ESR and CRP are high, she could still have a vasculopathy with a little bit of inflammation, but if they're negative, she has a vascularity. So the ESR CRP is very, very helpful in trying to figure out is it vasculitis for vascularity if it's negative. So yeah, I think we have a lot more to go in this case, but I think um this we have two problems. Not ready to put them together yet. They might be combined for sure. And the question now is since this is not aoscerosis, is this uh a vasculitis or a vasculopathy?
All righty. Uh you're crushing it. It's amazing to see the progress you're making. Uh all right, Harat Mike to you.
What do you have next for us?
Okay. So after uh this imaging was obtained, she was brought back into the clinic for repeat examination.
Um so cardiovascular examination showed uh low rumbling systolic murmur in the aortic region uh bilateral corateed brewy tachicardia and diminished radial pulses graded as one plus bilaterally. And um when we tried to obtain blood pressure, we were not able to with um different machines and manually um different providers. So that was interesting.
>> And then [laughter] yeah, pleased. Were you panicking when you heard this?
>> Yeah, I was [laughter] very strange.
>> Very strange.
>> Um and then at that same visit, we got some inflammatory um markers. She had elevated ESR at 60, elevated CRP at 43 or 43.8. Yeah. And then we also got um ANA antibodies and autoimmune panel and those were negative.
>> Amazing. Awesome. Well, R, I think you're uh setting us up for a really rich conversation. I think it's about time that we put our thoughts together in a breakout room. So, I'm gonna pause the recording.
>> Yes, we are. All right. What do you think about us? what you guys talk about.
>> Awesome. Um so um so the first thought is that um thinking about is is it's a vessel issue. So is it is the is it is I'm sorry is the vessel um only in the um the issue is the issue only in the kotids or is it um elsewhere as well involving the other vessels? Um so would be curious to see what's on a CT angography of the brain and also of if there's any associated stenosis. Uh and we're seeing how that there's a a murmur that's radiating to the keroted. So again um it's that's a physical a clinical sign that we see uh that we that we've already confirmed on Doppler.
And uh I think the other important um points are thinking about stenosis again and MR um also MR angography to see if there's involvement of um the subclavian because we see that there's diminished radial pulses and that's not something we would often see. Uh but also it's it's amazing that we got the um blood pressure before and we're not seeing it now. So um I think it's been brewing for a long time and uh also curious to see what the renal vessels look like. So what do you think doctor?
>> Yeah, I think you're you know you're teaching us a very important lesson which is whenever whenever you define vascular disease you have to understand the extent of it and I think we made a lot of progress. Let's just make list where the disease is involved. So we know it's involved in the in the bilateral karate. Um, if you were to enumerate what other locations you believe the disease might be, where do you think it is?
>> Uh, I'm thinking the subclavian vessels because there's radial pulse >> and there's also um, but her CMP is normal. I was initially thinking it might involve the renal vascule and then thinking about um to get the anchors as well. Yeah. Okay. So you so you're confident that it's subclavian. You're wondering about kidney.
And I will tell you there is a finding here that tells you what the diagnosis is.
Um and that finding is her murmur. And oh sorry maybe Herata I misunderstood. I I thought I heard that she has a rumbling diastolic murmur at the aortic position but I I I don't see that on the board. So I might have hallucinated that. You mind reminding us what her cardiovascular exam was?
Yeah, it was rumbling systolic murmur in the aortic region.
>> Systolic.
>> Yeah, >> I see. Interesting. Okay. All right.
Thank you so much. Oh, yeah. I see it down there. Sorry about that. Um Um So, Manini, what do you think about the murmur here?
Um so murmur we usually see murmurss if there's a valvular pathology or the structures associated with u before it or after it.
>> Um so if we do a TTE and um see that there's she's a 29year-old and it's systolic. So does she have a bicuspid aortic valve >> or is there um uh if in terms of the aorta is there a stenosis there or like hypertrophy of the vessels and then but then we see that it's being radiated to the kerotids. So I think that gives us a clue that the murmur is um present because of senosis of the kerotids. These are my thoughts. Curious to know what you think. We said the key word aorta.
The stakes are now high.
A vasculopathy in the corateed or vasculitis in the corateed. It's okay.
You got the aorta involved. Now the reason the aorta is an emergency that's a lie. It's not an emergency.
It's an urgent thing is because aortic disease can extend into the coronaries and the patients with aortic involvement can now start to have coronary involvement and the aortic involvement can affect the aortic valve. So if we don't have proof that the aorta is involved, but if you have a murmur in the aortic position, you worry that the aortic valve is involved. And with the aortic valve is involved, you worry that there is a relationship between this entity and the aorta.
Um there are no no zero large vessel vasculopathies.
None.
There are some vasculopathies like marfans and aeros danlos that have a propensity to the uh aorta but they often have prominent other findings especially cutaneous ones.
So here the fact that she has an elevated ESR and CRP is supporting of a hypothesis that you should already generate which is to ask when you think the aorta is involved you have to prioritize a vasculitis and the reason for that is that the number of vasculopathies that affect the aorta are essentially zero.
those that do have prominent extra aortic findings but more importantly do not result in chronic stenotic aortic disease and now this is like really really far-fetched so moni this is a reflection for you to study when you're an R3 uh not pre-inter year but just to put it out there for people to digest and to stretch all of us when you have a vasculopathy affecting the aorta what tends to happen is you have aortic dilation and an aortic opathy as a result of really large aorta or aortic dissections.
Here the problem that we're solving is cyenotic vasculopathy as evidenced by the poor flow and a stenotic aortic disease is a vasculitis until proven otherwise and then you have these inflammatory markers.
So what can you think of as a vasculitis that involves the aorta? What thoughts do you have?
>> U yes Dr. this is a large vessel that's involved.
So I'm thinking of um it could the Takayasu is my biggest um um thought here but I have also learned that GCA can present anywhere and she has a headache and um and age is never something we should focus on if we have other systemic signatures that point otherwise. And uh also thinking of uh actually I wanted to get an RPR as well to see um if to rule out um Kogan syndrome perhaps. um but or pan but takayaso is the most important um one and yeah >> you know the most important finding here is that you potentially have aortic involvement or coronary involvement in this disease process which is very very morbid and the problem that you're trying to solve is a chronic vasculitis that involves likely involves the aorta and at that point in a young uh healthy woman takasu becomes your default diagnosis and the question is what else can mimic it and there are very very few mimics uh quite honestly ly of a chronic smoldering isolated vasculitis without any extravascular clues and so I think the next step is to image it and understand it better um which I think u would be really important implications for this patient are enormous um so for the sake of time let's hand the mic back to you Herata this alipquot really pushed things forward thank you >> uh yeah so we got a CT angiogram and it showed a mild Mild circumferential neural thickening and mild narrowing of the entire right common corateed artery. Severe neural thickening. Severe circumferential narrowing of the left common corateed artery just past the origin with high-grade stenosis and occlusion of the proximal left subclavian artery. Left common corateed artery, left internal corateed artery, proximal left vertebral artery and left cavernous paracenoid in ICI internal corateed artery.
Um I can continue and give the diagnosis that we came to.
>> Yeah.
>> Yeah. Maybe. Yeah. I think why don't you just take us home? I think for the sake of time.
>> Okay.
>> Yeah. Um so based on this imaging, our physical exam and lab studies, we diagnosed her with takayasu arteritis.
So >> keep going. Tell us more. What did you think? How did how did you treat her?
>> Yeah. So she after the CT um results were reviewed, she was admitted to the hospital and started on highdose steroids and antiplatlet therapy. Um and then after she was um discharged, she was also seen for follow-up in the rheatology clinic and started on hum and then aspirin for secondary prevention. And then she after getting treated, she reported improvement in the neck pain and in the headaches. Um she got an echo cardiogram that showed no valvular heart disease, ejection fraction of 60 to 65%.
Um as discussed her blood pressure was um controlled um no neurological deficits. Um no evidence of impaired renal function. She also got um a whole body PET scan that showed um no pathologically increased glycolytic activity in head, neck, chest, abdomen, pelvis, and msk.
Um so no evidence of like severe complications at that point.
>> Incredible. I I'm I'm genuinely in awe of your ability to tell this story with u two years of clinical exposure under your belt. It's um really really impressive. It doesn't come for free.
It's the product of a tremendous amount of hard work. And there are very very few people who had as much exposure to medicine as you are who are um comfortable enough to turn a camera on and present in a public audience, let alone do so with such high quality. So thank you. I'm really curious, what did you learn from this experience? Where would this case live in your mind? Yeah, I mean I think at this point in my learning, I've been really trying to work on like keeping my differential broad and not having like an anchoring bias. Um, and so like based on her initial presentation, I think I would have just kind of thought she has a primary kind of like you guys were talking about a primary headache thing.
Um, she didn't have any like headache red flag symptoms, which is something I always think about like no vision changes, dizziness, weakness. Um, and like you said, the headaches were chronic. She didn't like report any changes in severity or character.
Um, her neuroexam was unremarkable.
And then also the fact that the mtryptalene helped with the headaches um would have really convinced me that they were just kind of migraines. And then I also saw someone in the chat talking about um like the fact that she's been using NSAIDs daily, so there's probably could be a rebound effect. Um, but I think that this case really taught me to like think a little harder, look a little further into things because this is something that it's probably good that we didn't miss that she has a systemic vasculitis. Um, so thankfully my attending looked further into it. Um, and like you kind of talked a bit through it like think about the anatomy of like the area and what could be um, wrong. So we kind of thought about the thyroid. Um and then of course the kurateed is like a area that you don't want to miss if there's something wrong going on with the corateeds. Um and so yeah that was really what I learned from this case.
>> I think your learning is very digestible and actionable. I completely agree with you. I think the question that will uh lives long in this case is are our first two problems headache and vasculitis are they linked and I think the most definitive way to to suspect that they are is the fact that you treated her for her vasculitis and her headaches dramatically improved as you mentioned at the end and I think when you realize how much headache is a feature of giant cell arteritis in older adults and you ask well why why wouldn't it be a feature of takayas and the only difference really is the the vessel involvement and here I figure the probability of her having intraranial or perranial vessel involvement seems to be very high. And so I think um Manosini said from the very get-go that a systemic disease is unlikely to be causing her headaches. And I think you can use this case as a reminder of how uh that is a universal truth only if you've done a complete survey of the rest of the system. And sometimes uh the complete survey is usually obvious. Um and in this case it became very obvious when you couldn't measure a blood pressure that she had a systemic component to her disease. But you can use Takayas as a great mimicker of how subtle the systemic disease can be. Um so yeah I think this is a absolutely fascinating journey. I really appreciate you bringing in herein. What are your thoughts and reflections?
uh such a fantastic presentation and a case harata. Thank you so much for bringing it and uh thank you so much Dr. Abby. This was u the best experience ever and um I think there's so much to reflect on and learn. Um we had another case of Takayasu and that the patient there presented with transient loss of consciousness and this headache and I think my biggest learning is to always keep systemic symptoms in mind and keep a broad differential as possible and it's so important to do the survey you spoke of because the man management changes and then um that I think that would make a huge difference. So thank you so much.
>> Yeah the thanks is all to you. It was really cool to see how uh sharp and shrewd your reasoning was throughout the whole journey and uh yeah from headache primary versus secondary from obesity and overlap with headaches to vasculitis versus vasculopathy and then to the ultimate diagnosis you were uh yeah I think I was like two steps behind you quite frankly so I'm glad I was able to keep up. Um alrighty the moment is here Glenn Mike to you for the teaching points.
Uh thank you man for the great uh discussion. Um I think one important learning for me in this choice case and um I think you mentioned that thank you for that as the caring bias. I think in this case that's important to to not think this is a primary headache just because of the the response. um just um going ahead with investigation was uh very helpful and yeah uh going over to the teaching points we started with chronic headaches um I wanted to know whether it's primary secondary um and the what we used to to differentiate the two was the is it transate and is it resolving so because it was constant throughout u it could the a primary headache. Um um and also the the response to amitryptin that um increase the likelihood that this could be a primary headache. Uh and also we we then talked about headaches and obesity.
So that um we talked of endocrine causes and also the fact that um obesity can cause obstruction of some structures in the neck. So thinking of if it obstruct the blood vessels there you think of sud tumor cerebria which can increase the the venous pressures and the the um the neck which can increase the the ICP um that can happen and also the arthraxia itself can cause chronic headaches um and then there's an interesting finding of the um carat inal hypoplasia which is what could be unrelated to the headaches.
um as most commonly caused by athosclerosis. patient didn't have those risk factors but um uh we we then um investigated for vasculitis was a clue for that since the patient um can be having at that age and um in the end we found that the patient has takitis um which was interesting um diagnosis based how the the the patient presented initially. So thank you for attending this interesting case and also Lucas for scribing and everyone in the in the chat for all your inputs. Uh it was a brilliant presentation.
>> It may be cold uh Glenn but uh you came in very hot with incredible teaching points. It's unreal to think about what all of you are accomplishing uh uh as uh people who are early in your training.
It's unreal. every single person involved here um is in the beginning of their medical journey and I'm the old fart who gets to hang out with you all.
Although I look young, people think I my mom tells me, "Oh, you and your sister have a baby face." It's true. Um it's so so cool to see uh how bright the future is for medicine. All of you involved, thank you. And a big big thank you to LRA for saving my butt. And uh I hear I just saw that Kevin was promoting the book while I was gone. So big fist bump to you, Kevin. I didn't hear any of it.
U but really really appreciate you doing that. All right, guys. Have a great I see you.
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