Idiopathic intracranial hypertension

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I like this; but if you're really ready for a challenge then come down here to the United States Capital of Old People and try it on these turbo calcified seniors with Grade 8 kyphoscoliosis.

I don't even bother anymore.

Or South Texas where the average BMI is 32.

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I like this; but if you're really ready for a challenge then come down here to the United States Capital of Old People and try it on these turbo calcified seniors with Grade 8 kyphoscoliosis.

I don't even bother anymore.

and the Grade 4B spondylosis.
 
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Dude. Same same here.
I've "buried the needle" so many times and not yet hit bone.
I recall a pt when I was in SC. She needed an LP. I made an attempt. That didn't go anywhere. Had to call rads, who took her over and did it under fluoro. The rads called me back after - he said he used the longest needle they had, and it resembled a harpoon. He told me that it started to bow a bit, because it was so long. And, he hubbed the needle, and, just BARELY got the CSF.
 
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I like this; but if you're really ready for a challenge then come down here to the United States Capital of Old People and try it on these turbo calcified seniors with Grade 8 kyphoscoliosis.

I don't even bother anymore.

Have you ever tried L3/4 or L2/3? It's safe in older folks and I've found I meet a lot less resistance and a lot more success.
 
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Have you ever tried L3/4 or L2/3? It's safe in older folks and I've found I meet a lot less resistance and a lot more success.

I turned a whole ALF into pincushions.

EDIT: a sizable (lol) portion of these old fatties are so corpulent and immobile that there's no finding their hips. May as well poke and pray.
 
I like this; but if you're really ready for a challenge then come down here to the United States Capital of Old People and try it on these turbo calcified seniors with Grade 8 kyphoscoliosis.

I don't even bother anymore.

True US does nothing for calcifications everywhere and no doubt hardware everywhere, dating from multiple different decades

Then you ask "well even if you had a SAH would coiling or open neurosurgical resection REALLY be within your goals of care"
 
True US does nothing for calcifications everywhere and no doubt hardware everywhere, dating from multiple different decades

Then you ask "well even if you had a SAH would coiling or open neurosurgical resection REALLY be within your goals of care"

To be clear, I have IR do it and use my time more wisely.
 
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God's honest truth, brother, that's lame sauce. Hell, any rads sub has to do general work to keep going. IR does not live on interventional alone.

You know what? You're right; I was unclear in my response. We have IR folks who work regular D-Rad shifts and will do LPs in a heartbeat. However, we have a "flight" of D-rads who will balk at anything, including reading MRIs after hours.

No joke. I can the MRI, but Dr. D-Rad won't after 9pm if it's one of that clutch.
 
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I'm always late to these threads. I can't remember the last time I LP'd someone hunting for pseudotumor. I did a lot in residency and maybe for a couple of years afterwards but most of the time these people do fine with close neuro f/u. Occasionally, I might start diamox if my clinical suspicion is high. They've got to have serious vision loss or a cranial nerve palsy to make me break out the LP tray... It's just not emergent most of the time.
 
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We follow the 6 h rule. If CT is negative, we don't pursue LP unless Hct <30%, seizure, syncope, abnormal exam or primary neck pain. I order a CTA practically always though, unless I'm dealing with a young patient, in whom I pursue an MRI after a negative CT. I would also tap someone with a negative 6 h CT and an aneurysm, just to maintain my sanity and ability to sleep. I think CTA is also justifiable from the angle of dissections presenting as a thunderclap headache. You would probably pick up most of the cerebral venous thrombosis as well.

But I have question about head shaking. Some colleagues seem to employ it haphazardly to any patient with a dizziness complaint. I can't blame them, since many sources are very vague on the type of scenario calling for head shakes. I've only found this being broached in the article "Diagnosing Patients With Acute-Onset Persistent Dizziness" from the journal "Annals of Emergency Medicine". They say to use head impulse testing only if you detect a spontaneous nystagmus, because otherwise you will end up with only positive (including false-positive) results. The rationale being, that without spontaneous nystagmus it cannot be a vestibular neuritis and vestibular neuritis is pretty much the only condition in which you would get a negative test result. The only problem is, I can't find any source corroborating this line of reasoning. What do you do in these cases?
 
We follow the 6 h rule. If CT is negative, we don't pursue LP unless Hct <30%, seizure, syncope, abnormal exam or primary neck pain. I order a CTA practically always though, unless I'm dealing with a young patient, in whom I pursue an MRI after a negative CT. I would also tap someone with a negative 6 h CT and an aneurysm, just to maintain my sanity and ability to sleep. I think CTA is also justifiable from the angle of dissections presenting as a thunderclap headache. You would probably pick up most of the cerebral venous thrombosis as well.

But I have question about head shaking. Some colleagues seem to employ it haphazardly to any patient with a dizziness complaint. I can't blame them, since many sources are very vague on the type of scenario calling for head shakes. I've only found this being broached in the article "Diagnosing Patients With Acute-Onset Persistent Dizziness" from the journal "Annals of Emergency Medicine". They say to use head impulse testing only if you detect a spontaneous nystagmus, because otherwise you will end up with only positive (including false-positive) results. The rationale being, that without spontaneous nystagmus it cannot be a vestibular neuritis and vestibular neuritis is pretty much the only condition in which you would get a negative test result. The only problem is, I can't find any source corroborating this line of reasoning. What do you do in these cases?

I’m not going to comment on the first half because we clearly work in different places. I have to send csf to an outside lab to have it read, (I have no idea why this is any different than any other cell count/gram stain but whatever) so I basically just committed to transfer if I lp. Similarly if I ordered that many mris there would be a discussion with admin.

However the head shaking thing is ridiculous. I use a dix halpike in peripheral vertigo for lateral nystagmus, but 100% of the patients would tell me they were dizzy if I just had them shake their head. It’s a combination of the power of suggestion, patients wanting to play up symptoms to be taken seriously (ironically does the opposite here), and the fact that none of the worst disease processes seem to follow the bs “rules” we make up. Don’t use this to rule out anything important.

If it’s theatre for the obvious negative patient, which is admittedly 1/3 of what we do, then that’s fine.
 
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I’m not going to comment on the first half because we clearly work in different places. I have to send csf to an outside lab to have it read, (I have no idea why this is any different than any other cell count/gram stain but whatever) so I basically just committed to transfer if I lp. Similarly if I ordered that many mris there would be a discussion with admin.

However the head shaking thing is ridiculous. I use a dix halpike in peripheral vertigo for lateral nystagmus, but 100% of the patients would tell me they were dizzy if I just had them shake their head. It’s a combination of the power of suggestion, patients wanting to play up symptoms to be taken seriously (ironically does the opposite here), and the fact that none of the worst disease processes seem to follow the bs “rules” we make up. Don’t use this to rule out anything important.

If it’s theatre for the obvious negative patient, which is admittedly 1/3 of what we do, then that’s fine.

That's odd. I thought the cell counts were performed on a urinalysis machine?
 
However the head shaking thing is ridiculous. I use a dix halpike in peripheral vertigo for lateral nystagmus, but 100% of the patients would tell me they were dizzy if I just had them shake their head. It’s a combination of the power of suggestion, patients wanting to play up symptoms to be taken seriously (ironically does the opposite here), and the fact that none of the worst disease processes seem to follow the bs “rules” we make up. Don’t use this to rule out anything important.

If it’s theatre for the obvious negative patient, which is admittedly 1/3 of what we do, then that’s fine.

Thank you for the reply, but I think you may have misunderstood the nature of head shake/ head impulse test! It has nothing to do with how the patient feels! I suggest you watch this video on the topic, perhaps it will make you a convert as well. I find the HiNTS exam (of course in conjuction with the whole neurological) to be very powerful in differentiating between vestibular neuritis and a CNS event.
 
Thank you for the reply, but I think you may have misunderstood the nature of head shake/ head impulse test! It has nothing to do with how the patient feels! I suggest you watch this video on the topic, perhaps it will make you a convert as well. I find the HiNTS exam (of course in conjuction with the whole neurological) to be very powerful in differentiating between vestibular neuritis and a CNS event.


I personally find the HINTS (HiNTS, hInTs, HiNtS) exam useless, and I believe the data backs me up

 
I personally find the HINTS (HiNTS, hInTs, HiNtS) exam useless, and I believe the data backs me up


I bet it's the other way around...the data says it's ER doctors shouldn't use it, so therefore I don't use it.

In any event...our cohort of dizzy patients are largely grandmas...and SNAP! there goes their neck.

SNAP!

That's why I don't use HINTS.

Actually...I do two out of the three. Vertical skew and nystagmus are disgustingly easy to do and I can teach my 14 yo son how to do vertical skew
 
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Thank you for the reply, but I think you may have misunderstood the nature of head shake/ head impulse test! It has nothing to do with how the patient feels! I suggest you watch this video on the topic, perhaps it will make you a convert as well. I find the HiNTS exam (of course in conjuction with the whole neurological) to be very powerful in differentiating between vestibular neuritis and a CNS event.


I know what a hints exam is. You didn’t say head impulse testing, you said shaking, which is different. Some of our pas will have the patient shake their head side to side and ask if that makes it worse, which is in my opinion a worthless test.

I used to believe in the hints exam, but repeated trials have found it’s not nearly as good outside the hands of a trained neuro-ophthalmologist, which I am not. Interestingly, I think even other neuro-ophthalmologists have had difficulty reproducing the results of the trials by the guy who brought it in vogue.

There are a lot of problems with using it in the ed: patient has to be actively symptomatic, you have to do it regularly to be any good at it, and no one is going to spare me if I do it wrong. Posterior stroke is a really easy diagnosis to miss, I use hints to help convince me it’s there, but I don’t use it to prove to me it’s not.

Edit: noted that you did say head impulse test the second time, which I misread. My bas
 
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That's odd. I thought the cell counts were performed on a urinalysis machine?

I thought so too. I find it very confusing, as it seems like cell count per field should be a similar test regardless of the body fluid. Similarly, it’s not like a gram stain is some difficult test or any different than staining results from a blood culture.

My guess is they aren’t accredited to do more detailed testing I wouldn’t care about anyway, but have decided they don’t want the liability of giving firm answers on this because they don’t do it often. I don’t really know though, as I’ve seen way smaller hospitals keep the initial portion in house
 
Better question is --> TPA for a clinical posterior stroke within the window? I say yes, limited evidence of harm, and persistent vertigo is quite disabling.
 
Better question is --> TPA for a clinical posterior stroke within the window? I say yes, limited evidence of harm, and persistent vertigo is quite disabling.

I would respond that there's also limited evidence of benefit, and a tpa-induced posterior fossa bleed is likely to be fatal. I"m curious, do you have any studies you could point me to on the long-term outcomes of cerebellar stroke? I've always had the impression that the vertigo and disequilibrium improve substantially, but I could certainly be wrong.
 
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Better question is --> TPA for a clinical posterior stroke within the window? I say yes, limited evidence of harm, and persistent vertigo is quite disabling.

numerous harms....main ones being 6% bleeding
We are giving a drug for an indication that has not been studied. tPa probably doesn’t work as shown by 10+ studies, and if it does work we still don’t have a good idea who that cohort is.
It’s cowboy medicine giving tPA for isolated vertigo. It’s not defensible.
It’s not your problem that the NIH stroke scale is terrible for posterior circulation strokes.
 
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I would respond that there's also limited evidence of benefit, and a tpa-induced posterior fossa bleed is likely to be fatal. I"m curious, do you have any studies you could point me to on the long-term outcomes of cerebellar stroke? I've always had the impression that the vertigo and disequilibrium improve substantially, but I could certainly be wrong.

you are not, they do usually improve substantially.
 
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I distinctly recall on my neuro rotation a 3rd generation neurologist telling me he gave basically zero shyts about cerebellar infarctions, telling me in a matter of days to weeks that part of the brain recovers remarkably well, much better than cortex. He said this while we had a cerebellar stroke patient on the floor with a pretty cool unilateral epic fail of finger nose testing that rapidly improved.
 
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numerous harms....main ones being 6% bleeding
We are giving a drug for an indication that has not been studied. tPa probably doesn’t work as shown by 10+ studies, and if it does work we still don’t have a good idea who that cohort is.
It’s cowboy medicine giving tPA for isolated vertigo. It’s not defensible.
It’s not your problem that the NIH stroke scale is terrible for posterior circulation strokes.

I'd hardly say it's not defensible, there is no data for an increased risk of bleed in the posterior fossa (it sort of 'logically' makes sense, but it's not a supported statement), in fact the data we do have suggests posterior strokes have a lower risk of bleed (1) than anterior strokes, and the same, favorable, outcomes with IV thrombolysis. Which, regardless of whether you believe the TPA data or not, it is supported by multiple professional societies, including the major ones in our specialty. It's a grey area, and is one that most neurologists that I have spoken with will defend giving TPA, and likely testify against not giving TPA. All of this makes evaluating and treating acute vestibular syndrome incredibly challenging, especially given that MRIs miss a frustratingly high number of posterior strokes in the first 24 hours. Basically I just pray that all dizzy patients have had symptoms for 5 hours.


1. Sarikaya H, Arnold M, Engelter ST, Lyrer PA, Mattle HP, Georgiadis D, Bonati LH, Fluri F, Fischer U, Findling O, Ballinari P, Baumgartner RW. Outcomes of intravenous thrombolysis in posterior versus anterior circulation stroke. Stroke. 2011 Sep;42(9):2498-502. doi: 10.1161/STROKEAHA.110.607614. Epub 2011 Jul 21. PMID: 21778443.
 
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Dude, next time link to the study, rather than putting in a citation...

It's not the risk of a bleed in the posterior fossa, it's the consequence.

Also, asking whether or not they have good functional outcomes after TPA is missing the point. The questions is whether or not administration of TPA improves the functional outcomes. Most stroke mimics will have a good functional outcome after TPA.

I've had neurologists recommend TPA for isolated paresthesia before. Thankfully, most patients will decline after a discussion of risks/benefits.
 
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OK homey. Did you read the paper or even part of it? The average NIH score for those with PCS in the study was 9. What is the average NIH score for those with just vertigo? Above you wrote “clinical posterior circulation stroke” and I would also give tPA if it is supported by current standard protocols. If someone had an NIH score of 9, whether it’s anterior or posterior, if they are eligible for tPA and agree to it then I would give it.

however you also wrote that vertigo is disabling....and the implication is that you would give tPA for someone who just had vertigo. Their NIH stroke scale for isolated vertigo is 0, maybe 1 for ocular movements depending on presentation. That would be giving a drug for which there is no current guideline
 
TPA for posterior circulation stroke just feels bad haha. it's like burning your house down to deal with some ants
 
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First of all: I'm NOT advocating for tPA to treat isolated vertigo.

However, there are some reasons to think we underestimate the importance of the cerebellum. It may be that, because we're bad at describing things like proprioception that we fail to appreciate deficits when the "little brain" is injured.

At least that's what some smart folks think: https://www.cell.com/neuron/fulltext/S0896-6273(18)30898-5
 
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I've always been interested in vestibulopathic pts and regularly incorporate HINTS. However, the following two articles on Annals from a Dr. Edlow was probably the best two articles on vestibular syndromes that I've read in the past 10 years. I thought it was brilliant. I'm attaching below. Give it a read if you've got some time.
 

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I've always been interested in vestibulopathic pts and regularly incorporate HINTS. However, the following two articles on Annals from a Dr. Edlow was probably the best two articles on vestibular syndromes that I've read in the past 10 years. I thought it was brilliant. I'm attaching below. Give it a read if you've got some time.
this is the kinda stuff I still come to SDN for.
 
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Better question is --> TPA for a clinical posterior stroke within the window? I say yes, limited evidence of harm, and persistent vertigo is quite disabling.

I get that clinically it makes sense, IF tPA works for anterior ischemic CVAs (and that's debatable, but the current SOC is that "yes it works, yes let's give it") then it should work for posterior ischemic CVA as the pathophysiology is the same. That being said, where is the evidence? The evidence for tPA is based on studies that only enrolled predominately anterior vessel symptoms (as evinced by the NIH). We don't really know how much vertigo specifically improves controlling for and without tPA administration.
 
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I've always been interested in vestibulopathic pts and regularly incorporate HINTS. However, the following two articles on Annals from a Dr. Edlow was probably the best two articles on vestibular syndromes that I've read in the past 10 years. I thought it was brilliant. I'm attaching below. Give it a read if you've got some time.

I think I'm stupid. I've read these in the past and I don't understand them.
I also think I don't even know when someone has labrynythitis, vestibular neuritis, BPPV, menieres, I just know it's peripheral vertigo.
I need to go back to med school.
 
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I think I'm stupid. I've read these in the past and I don't understand them.
I also think I don't even know when someone has labrynythitis, vestibular neuritis, BPPV, menieres, I just know it's peripheral vertigo.
I need to go back to med school.

No, it's just that you've been thinking about it wrong. Vertigo becomes clear when you become your own gold standard.

What you need to do is to become so well-versed in vestibular, brainstem and cerebellar neuroanatomy that you can expound on it with such labyrinthine circumlocutions as to verbally induce vertigo in anyone who tries to disagree with you. Then you become the ultimate arbiter of vertigo!

You call it BPPV but the patient doesn't respond to an Eply's? Their semi-circular canals must be malformed - it's the patient's fault!
You call it central vertigo, but the MRI's negative for stroke? MRI is insensitive for posterior CVA - it's the machine's fault!
You call it Meniere's but a follow up MRI shows a cerebellar stroke? Well either that was a false positive or the CVA happened after you saw the patient and before follow up. Because you're the gold standard, it was NOT your fault. It couldn't be!
 
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Diagnostic criteria for IIH (modified Dandy Criteria:

1. Symptoms of increased ICP: headache, nausea, pulsatile tinnitus (whooshing sound), transient visual obscurations (blackouts of vision when bending over or Valsalva), etc.

2. Signs of increased ICP: papilledema, CN VI palsy. Any other localizing findings on neuro exam exclude the diagnosis of IIH

3. Negative MRI (and ideally MRV) for tumor, venous sinus thrombosis, etc. Flattening of posterior globe and empty sella are non-specific findings

4. Opening pressure >= 25 cm H2O (>= 28 cm H2O in children)

5. negative CSF composition

It looks like you’ve met criteria for 1, 3, 4, 5. I would call neuro or ophtho for dilated eye exam. Ideally she would also be discharged on Diamox with education on weight loss (most important modifiable risk factor!) and follow up as outpatient for serial dilated exams and visual field testing
 
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Thanks I have referred for both as it’s and out patient :)
 
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