No use of MRI, MRA or CTA, echo for strokes.

[Neurologo]

2018 ASA/AHA guidelines made a very controversial recommendation in their laudable effort to avoid wasting medical resources in tests and labs that are not proven effective. They decided against routine use of MRI brain, CTA or MRA, echocardiogram, prolonged cardiac monitoring or even lipid panel in managing strokes. This is obviously hotly debatable, but I wanted to see how this is being received in your institutions. My biggest problem is that it is very difficult to narrow down the most likely etiology of strokes and most appropriate Rx without these studies.

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[cerebral edema]

Ridiculous

 

[typhoonegator]

What do you think they should have said? I'm friends with many of the authors so I'd be glad to forward your concerns.

 

[neglect]

2018 ASA/AHA guidelines made a very controversial recommendation in their laudable effort to avoid wasting medical resources in tests and labs that are not proven effective. They decided against routine use of MRI brain, CTA or MRA, echocardiogram, prolonged cardiac monitoring or even lipid panel in managing strokes. This is obviously hotly debatable, but I wanted to see how this is being received in your institutions. My biggest problem is that it is very difficult to narrow down the most likely etiology of strokes and most appropriate Rx without these studies.

Can you quote the offending passages?

MRI, CTA and MRA very much ARE overutilized and nearly NEVER change management. Residents seem dumbfounded that one can diagnose and treat stroke without a positive MRI, and that some strokes have negative MRIs, and that a stroke-in-the-young work up is perhaps not useful in a 70 year old with HTN and DM. You ever been called by an eager resident who asks “what are we going to do now that the MRI shows stroke” in a patient who was admitted from the ER FOR stroke?

Also, if one’s approach is minimal, can you speculate how many more patients over, say, 70 would have a change in management for routine stroke prevention? Assume no ICA stenosis, EKG no A fib, no large thrombus or cardiac source on echo. We’re left with BP, statin, anti-plts, diet and exercise. I’m personally for judicious and selective intracranial vessel evals and Holter monitors, but why should they be used every time? There are very real risks to keeping these folks longer in the hospital, over-testing and getting false positives, which begat more testing. And CTA is TOTALLY overutilized in the ER with no hope of changing management in those with no symptoms or mild symptoms who will never have LVO and are too good to go to cath anyway.

Thankfully we have no institutional approaches. We have well trained neurologists who bring guidelines and data to real patients.

 

[Neurologo]

Never say never and never say always. Certainly there are cases when some of these tests are not needed. Keep in mind that the authors themselves admitted that there was a strong disagreement even among themselves and that this remains controversial as neurologists continue to hotly debate. I will list why these tests are important and often critical in assessing the etiology of stroke and formulating best treatment plan.

MRI: Small scattered embolic strokes are often not visible even on repeat CT several days later. CT may show one infarct making you think that it was due to the carotid stenosis or small vessel. But what if MRI also showed diffuse tiny embolic infarcts in multiple territories? Often we find old infarcts that patients themselves did not know about. They can be moderate sizes and not always those small lacunes. The location and characteristics of these old infarcts can help determine the etiology of current stroke. GRE or SWAN may lead to finding venous thrombosis rather than arterial. Microhemorrhages and cerebral amyloid angiopathy (CAA) are often only visible on GRE or SWAN. If I see CAA, the #2 most common cause of spontaneous ICH, I become more cautious with any antithrombotic agents, and sometimes the patient and I may even decide against any. Fat emboli often only seen on MRI.

MRA/CTA: Stroke is a rare opportunity for patients to have a vessel imaging. Personally I think everyone should get one of these at least once in our lives before the age of 60; but I digress. For patients with acute strokes, I look for the followings: significant intracranial stenosis >50% makes me give dual antiplatelet for 90 days instead of one. Ipsilateral carotid critical stenosis leads to an urgent CEA (Day 3-14). Patent vessels reinforce my suspicion of cardioembolism. Often we find incidental aneurysms large enough and in a risky location to require a closer follow up. Other related vascular abnormalities are discovered, such as Moyamoya or occluded ICA or a large ascending aortic thrombus or segmental narrowings suspicious of RCVS or vasculitis. These drastically change my treatment plan. Vascular anomaly can tell us the actual path that embolism took different from the typically suspected direction such as PCAs supplied solely by ICAs, the artery of Percheron, vertebral artery terminating in PICA, etc. Cerebral venous thrombosis or dissecdtion may be found instead.

Echo: PFO with atrial septal aneurysm, left atrial dilation, very low LV EF, vegetation, LV thrombus.

Lipid: I am not too particular about this although it does help me feel better to give lower dose of atorvastatin if LDL is already 40-70. I would go more with the degree of atheroslcerosis seen on MRA/CTA.

These are some of the more common reasons why I would order these tests, and they do change my treatment plan for secondary stroke prevention. Without these tests and careful analysis, what is the use of neurologists for stroke? ED team can give tPA and call for thrombectomy. IM hospitalists can tell stroke patients to just keep taking their aspirin, statin and control BP and DM and hope for the best. By advocating over simplication of stroke assessment and management, the ASA/AHA have inadvertently made the role of neurologists, especially stroke specialists, dispensible. I don't know about you but I would not want to miss most of the above conditions listed. And that will also scare non-neurologists from arguing that they can handle strokes just fine.

 

[Neurologo]

Ridiculous

Who is ridiculous? The guideline or my view? And why?

 

[TUGM]

I agree with what Neurologo has said above in terms of determining etiology of stroke. Not every stroke has to be worked up with such vigor, though - sometimes the etiology is extremely clear, and that guides prevention itself.

In the acute setting, we always end up getting vessel imaging anyway... maybe this is institutionally dependent, but sometimes I've seen strokes that present with low NIHSS, but still with an LVO. Anything can happen, I suppose. A stroke presenting outside the acute window can be treated differently.

Guidelines are just that - they are a general method of approaching a specific disease process based on the evidence we have, but each patient is different and their specific story should guide their workup and treatment. Also, our understanding of neurological diseases continues to evolve at a rapid pace so, in my humble opinion, guidelines will continue to change dramatically over the upcoming years

 

[neglect]

Never say never and never say always.

Yes, which is why I said "MRI, CTA and MRA very much ARE overutilized and nearly NEVER change management." Sorry, I think my all caps reduced the nearly, which I agree is important.

We're quibbling about things and I'm sure we agree more than disagree. But this is fun, and permit me to challenge some of your points, no disrespect.

MRI is the most objectionable part of stroke mgmt to me because I see far too many residents and even neurologists turning their brain off, allowing the MRI to make the diagnosis. So there's danger with overutilization. And I think some of your cases actually make this point for me.

MRI: Small scattered embolic strokes are often not visible even on repeat CT several days later. CT may show one infarct making you think that it was due to the carotid stenosis or small vessel. But what if MRI also showed diffuse tiny embolic infarcts in multiple territories?

Then you still don't know if the ICA accounted for some of them. If the ICA is >70%, then the risk/benefit is between NASCET (a lot of benefit) and perhaps closer to ACAS (none or slight). This is 1/1000 cases BTW. Old strokes, commonly seen on head CT (another danger of the MRI is it allows radiologists to give bad readings on head CTs), require max medical therapy. Venous clots are their own problem and should be imaged and worked up robustly. Microhemes, absent severe HTN/DM or cardiac surg, are due to AD (brain makes amyloid, blood vessels do not). Because all the trials looking at coumadin, asa, plavix included them (they didn't know better), you can too. Would never hold at least anti-plts or if you have a good reason to give full A/C, do so in the setting of microhemes. Again, here we see the danger of too much information. A fat emboli, like the artery of Percheron and bigfoot, is a myth told to scare medical students.

Yes, ICA's should be evaluated. But in >80, not sure I'm ready to dictate that every person get an intracranial MRA for the rare folks who will get 90 days of dual anti-plts rather than 30. You're only doing this because SAMMPRIS did it and it worked out better than expected for the medical wing. How about pushing exercise? I'm all for stroke in the young and stroke in the youngish workups. You will find Moya Moya, odd segmental narrowing, RVCS and dissections. But not in the >80 crown. And not in the >70 with typical RF's.

Concur with echos, although I think we should appreciate the rarity of making a change from anti-plts to A/C.

And I think lipids are the easiest thing in the world to check, statins save so many lives, that not doing so is crazy.

These are some of the more common reasons why I would order these tests, and they do change my treatment plan for secondary stroke prevention. Without these tests and careful analysis, what is the use of neurologists for stroke? ED team can give tPA and call for thrombectomy. IM hospitalists can tell stroke patients to just keep taking their aspirin, statin and control BP and DM and hope for the best. By advocating over simplication of stroke assessment and management, the ASA/AHA have inadvertently made the role of neurologists, especially stroke specialists, dispensible. I don't know about you but I would not want to miss most of the above conditions listed. And that will also scare non-neurologists from arguing that they can handle strokes just fine.

I really value the ER docs. I think they are the most amazing doctors, period. But they have 20 patients at a time. When I'm called for a stroke code, I have one patient. I totally disagree that they can give tPA. Perhaps some can. IM hospitalists: same thing, but have you spoken to many? Many cannot diagnose stroke, and will either overutilize terribly (how many folks you see who get a combination of CTA/MRA/US?), or underutiilze terribly ("can I send this TIA home?" not mentioning that will be doing so without ICA imaging.)

As a stroke guy, I don't see you actually needing to protect your turf at all! The Duning Kruger effect is two sided. What you take to be simple, after years of thought and practice, is not (and the more famous side is that for the incompetent what seems simple without any thought, is also not). But as a stroke guy you know that, what, 99% of strokes would be fine with minimal workups, and no frills medical protection.

I agree with what Neurologo has said above in terms of determining etiology of stroke. Not every stroke has to be worked up with such vigor, though - sometimes the etiology is extremely clear, and that guides prevention itself.

In the acute setting, we always end up getting vessel imaging anyway... maybe this is institutionally dependent, but sometimes I've seen strokes that present with low NIHSS, but still with an LVO. Anything can happen, I suppose. A stroke presenting outside the acute window can be treated differently.

Guidelines are just that - they are a general method of approaching a specific disease process based on the evidence we have, but each patient is different and their specific story should guide their workup and treatment. Also, our understanding of neurological diseases continues to evolve at a rapid pace so, in my humble opinion, guidelines will continue to change dramatically over the upcoming years

Exactly. That's our job.

 

[Neurologo]

A fat emboli, like the artery of Percheron and bigfoot, is a myth told to scare medical students.
QUOTE]

You are joking, right? This week alone I saw two cases of cerebral fat emboli in young trauma patients. As usual CTs were negative.

Importance of the artery of Percheron is not to falsely assume multiple bilateral embolisms when you see infarcts in the bilateral thalami.

My point was there are many details that will be missed on CT but only seen on MRI which would change our treatment plan. You focus on microhemorrhages but my point of being cautious with antithrombotics is with CAA not microhemorrhage.

You accept what you see on MRI and sort out what truly matters from the insignificant findings. If you believe there was a stroke, especially the brainstem strokes, but MRI is negative, you go with your clinical assessment. Never say MRI "ruled out" stroke.

It is nearly impossible to have a direct evidence that the carotid stenosis, occluded ICA, lipohyalinosis, AFib or hypercoagulability actually caused the stroke. But we can surmise the most likely etiology to direct the treatment plan accordingly. To do this we often need these images. If we say these are not needed since the treatment and outcome will be the same anyway, then we are making ourselves unimportant and replaceable. My point on ED and IM hospitalists was that they are NOT able to properly handle strokes precisely due to their inability to properly analyze these data.

Guidelines are simply just that. No need to follow them like the ten commandments. But this particular conclusion they made is just too controversial. They should have just emphasized more judicious use of images and labs and end it there or say perhaps for advanced ages >80. I listed some of the important or critical conditions that can be missed by not doing these tests.

 

[cerebral edema]

Who is ridiculous? The guideline or my view? And why?

I work as a neurohospitalist in the stroke belt. CTA and MRI very frequently change management and should be obtained, when able.

 

[TUGM]

You are joking, right? This week alone I saw two cases of cerebral fat emboli in young trauma patients. As usual CTs were negative.

Importance of the artery of Percheron is not to falsely assume multiple bilateral embolisms when you see infarcts in the bilateral thalami.

My point was there are many details that will be missed on CT but only seen on MRI which would change our treatment plan. You focus on microhemorrhages but my point of being cautious with antithrombotics is with CAA not microhemorrhage.

You accept what you see on MRI and sort out what truly matters from the insignificant findings. If you believe there was a stroke, especially the brainstem strokes, but MRI is negative, you go with your clinical assessment. Never say MRI "ruled out" stroke.

It is nearly impossible to have a direct evidence that the carotid stenosis, occluded ICA, lipohyalinosis, AFib or hypercoagulability actually caused the stroke. But we can surmise the most likely etiology to direct the treatment plan accordingly. To do this we often need these images. If we say these are not needed since the treatment and outcome will be the same anyway, then we are making ourselves unimportant and replaceable. My point on ED and IM hospitalists was that they are NOT able to properly handle strokes precisely due to their inability to properly analyze these data.

Guidelines are simply just that. No need to follow them like the ten commandments. But this particular conclusion they made is just too controversial. They should have just emphasized more judicious use of images and labs and end it there or say perhaps for advanced ages >80. I listed some of the important or critical conditions that can be missed by not doing these tests.

Just out of curiosity, would you suggest withholding anti platelet agents in a patient with new acute ischemic stroke if they had evidence of CAA? Since CAA is a diagnosis really made at autopsy, you would evaluate CAA based on evidence of micro bleeds in a cortical distribution on GRE/SWI?

 

[NeurologyHopeful2018]

How are neurologist going to earn a liveable income without getting the chance to bill for these tests?

 

[Postictal Raiden]

How are neurologist going to earn a liveable income without getting the chance to bill for these tests?

Someone correct me if I'm wrong. I was under the impression that you don't make money off ordering tests. Sure, you make money from having the patient to come back for a return visit to discuss the findings, but you don't get paid for ordering the test/study.

 

[neglect]

You are joking, right? This week alone I saw two cases of cerebral fat emboli in young trauma patients. As usual CTs were negative.

Importance of the artery of Percheron is not to falsely assume multiple bilateral embolisms when you see infarcts in the bilateral thalami.

It is possible that I was joking by comparing fat emboli and the artery of Percheron to Bigfoot. It is also possible I was using humor to try to concede the point. Relax.

All these cases are very rare. Having a young trauma patient with a stroke raises many possible etiologies which should be worked up to the hilt. Check, we’re on the same page.

Here’s where we differ: a 80 yo woman with sudden onset of aphasia and right sided weakness who improves to minor speech problem and mild right drift. No tPA due to time. She has a background of obesity, DM, HTN, and is sedentary. Head CT neg. ICA clean, echo neg. I”m probably fine with her going home with no further testing, focusing on stroke risk reduction. If there’s something weird in her story or medical history, I’ll reserve further testing. But in that case, other than quibbling about anti-plts, a maximal worked up is more likely going to lead to an incidentaloma or false + than data that will change my thinking and treatment plan.

The think about guidelines is that they put one in a bind. Legally they become the standard of care. The joint comissions and stroke accrediation people see if hospitals are abiding by them. So they have to be written to account for folks in Montana who might not have the resources, and for folks who tend towards minimization like me, and for patients like a 30 year old s/p MVA and a 90 year old going to hospice.

My point was there are many details that will be missed on CT but only seen on MRI which would change our treatment plan. You focus on microhemorrhages but my point of being cautious with antithrombotics is with CAA not microhemorrhage.

Now you’re going to get amyloid imaging on these patients? (Humor alert). The vast majority of your >85 patients have some degree of CAA. We agree on the rest.

Someone correct me if I'm wrong. I was under the impression that you don't make money off ordering tests. Sure, you make money from having the patient to come back for a return visit to discuss the findings, but you don't get paid for ordering the test/study.

You do if you own the machines. But bundled payments

It is very important to keep the idea of downstream revenue in mind when negotiating with hospital systems. The admins will never tell you, but the average neurologist beings in more than 1 mil in revenue a year in pharm fees, imaging, BW, etc. A stroke guy likely brings in way more by feeding endovascular, getting patients in and out, and ordering amyloid PET scans. It is pretty easy to bring in over 400K in direct billing for professional services. If you’re not private, then remember this when dealing with the non-patient facing admin who negotiates your salary.

 

[Postictal Raiden]

.



You do if you own the machines. But bundled payments

It is very important to keep the idea of downstream revenue in mind when negotiating with hospital systems. The admins will never tell you, but the average neurologist beings in more than 1 mil in revenue a year in pharm fees, imaging, BW, etc. A stroke guy likely brings in way more by feeding endovascular, getting patients in and out, and ordering amyloid PET scans. It is pretty easy to bring in over 400K in direct billing for professional services. If you’re not private, then remember this when dealing with the non-patient facing admin who negotiates your salary.

Good to know.

Would it be legal for a group of neurologists to own an MRI and scan their own pts?

 

[Neurologo]

Just out of curiosity, would you suggest withholding anti platelet agents in a patient with new acute ischemic stroke if they had evidence of CAA? Since CAA is a diagnosis really made at autopsy, you would evaluate CAA based on evidence of micro bleeds in a cortical distribution on GRE/SWI?

If you think about how they came up with an epidemiological data saying CAA is the second most common cause of spontaneous ICH behind ruptured aneurysm, you will see that the diagnosis of CAA does not need to wait until death and autopsy. By the time of our death in old age, most of us may have some degree of CAA making such conclusion meaningless. GRE/SWAN and T1/T2 are good enough to distinguish between microhemorrhages due to HTN, small vesell disease or trauma vs. high altitude cerebral edema (difficult to tell from trauma) vs. fat embolism vs. cavernoma vs. neurocysticercosis vs. CAA.

And the risk of hemorrhage with CAA appears to be real. I only saw maybe 2-3 cases so far, but talking with guys who have been practicing for decades, I see that they are much more afraid of it than I. Whether to use antiplatelet or not depends on the number and size of CAA lesions, the recurrent stroke risk and the risk tolerance of patients and families. Seeing CAA on MRI certainly help me to at least alert them about it so that they are not surprised when they come back with an hemorrhage or accuse me of not informing them.

And to reply to Neglect, No, I don't order MRI to look for CAA. It is an unexpected bonus finding that help me formulate the optimal treatment plan. And I've seen plenty of 80-95 yr old MRIs with no visible CAA.

 

[deathmerchant]

I agree with @Neurologo : MRI, vessel imaging and ECHO do change management in a significant minority of patients (much more than many other unnecessary testing and treatment in Neurology, and Medicine in general). Also that no one can be sure clinically in which patients it will be important. Hence, we have to obtain these tests in most patients with obvious exceptions as stated above. That should be the standard of care. Is the standard of care for everyone worth it for some greater good?- that might be a separate debate.
If it was my family, I would want all these tests.

 

[warchild]

Here’s where we differ: a 80 yo woman with sudden onset of aphasia and right sided weakness who improves to minor speech problem and mild right drift. No tPA due to time. She has a background of obesity, DM, HTN, and is sedentary. Head CT neg. ICA clean, echo neg. I”m probably fine with her going home with no further testing, focusing on stroke risk reduction. If there’s something weird in her story or medical history, I’ll reserve further testing. But in that case, other than quibbling about anti-plts, a maximal worked up is more likely going to lead to an incidentaloma or false + than data that will change my thinking and treatment plan.
.

I disagree -you're dealing with an embolic event (atheroembolic vs cardioembolic LVO with distal embolization) and her next event could be fatal or completely debilitating. Distinguishing these etiologies can reduce her stroke risk by ~60% (anticoagulation) rather than ~20% (aspirin alone), which I feel is enough to warrant expedited work-up prior to discharge (vessel imaging and MRI, consider long term cardiac monitoring on discharge), especially since the risk of recurrent stroke is highest in the first 1-2 weeks. I guess if she had a small vessel syndrome and your CT suggested diffuse WM disease or you had an old MRI, you could defer the work-up to outpatient. Or if she had afib and needed anticoagulation regardless. And embolic strokes are a majority of patients (70%) vs small vessel (20%). If the ESUS trials find that NOACs are as safe as aspirin, then maybe we can minimize our inpatient work-up, but so far this has not been the case. These new guidelines seem to take the minimal approach to stroke management from a public health perspective and neglect the "precision medicine" movement that validates the existence of stroke specialists or even adequately trained neurologists.

 

[Groy]

By advocating over simplication of stroke assessment and management, the ASA/AHA have inadvertently made the role of neurologists, especially stroke specialists, dispensible.

This was the first thing that came to my mind when I read this report. Suggesting an explicit reduction in usage of that many diagnostic tools for stroke on the grounds that they are not effective seems like risky business, especially in acute cases.

What does this type thinking spell for the future of stroke specialists, if anything? If the process of stroke diagnosis becomes so algorithmic that the EM docs and hospitalists have it covered, what becomes of stroke docs?

 

[neglect]

Good to know.

Would it be legal for a group of neurologists to own an MRI and scan their own pts?

Yes! But the finances suck. In house revenue streams from EEG and infusions are the way to go. DM me for why MRI is not good and what others are good if you’re interested.

And to reply to Neglect, No, I don't order MRI to look for CAA. It is an unexpected bonus finding that help me formulate the optimal treatment plan. And I've seen plenty of 80-95 yr old MRIs with no visible CAA.

Yikes. No evidence of CAA on MRI =/= freedom from CAA. You know the MRI doesn’t ‘see’ CAA, but the microhemes that occur with amyloid, right? And you know that this beta amyloid causes Alzheimer’s. And you know that half of those >85 have AD and thus by definition will have amyloid. And only 5-10% of AD people will NOT have CAA. Here’s a good review: Cerebral amyloid angiopathy in the aetiology and immunotherapy of Alzheimer disease

So you’re giving tPA to these folks, only about 1/50 (of all comers) is suffering a fatal bleed. There is no data I’m aware of regarding selection or risk stratification for full a/c, or dual anti-plts in the setting of CAA with micro bleeds. But if you have some, I’ll take a look.

In otherwise healthy people without rip-roaring HTN/DM/cocaine use, seeing MH’s = CAA. The classic finding of MH's NOT due to CAA is location in the cerebellum.

I disagree -you're dealing with an embolic event (atheroembolic vs cardioembolic LVO with distal embolization) and her next event could be fatal or completely debilitating. Distinguishing these etiologies can reduce her stroke risk by ~60% (anticoagulation) rather than ~20% (aspirin alone), which I feel is enough to warrant expedited work-up prior to discharge (vessel imaging and MRI, consider long term cardiac monitoring on discharge), especially since the risk of recurrent stroke is highest in the first 1-2 weeks. I guess if she had a small vessel syndrome and your CT suggested diffuse WM disease or you had an old MRI, you could defer the work-up to outpatient. Or if she had afib and needed anticoagulation regardless. And embolic strokes are a majority of patients (70%) vs small vessel (20%). If the ESUS trials find that NOACs are as safe as aspirin, then maybe we can minimize our inpatient work-up, but so far this has not been the case. These new guidelines seem to take the minimal approach to stroke management from a public health perspective and neglect the "precision medicine" movement that validates the existence of stroke specialists or even adequately trained neurologists.

So how does MRI help you distinguish? It was already established that she did not have a small vessel syndrome based on history (the danger of over-reliance on imaging is that we forget the fundamentals). And everything else is exactly right. If she has a fib, then you're going to use a/c. If she has echo evidence of thrombogenesis, then you will have that conversation. NOACs are nowhere close to being as safe as aspirin, and I concur that these trials MAY very much alter 2018 management. But that's why we do trials, because we don't know it all. When these trials are done, if they show benefit, then in the absence of A fib, would want to adhere to their protocol: if cardioembolic "look" and clean vascular WU with MRA, and no A Fib, then use Xarelto.

Precision medicine is nonsense and magical thinking at this time with regard to stroke mgmt. Sure, in cancer. But in stroke, we can now lump many different stroke etiologies into the same mgmt: aspirin, statin, BP, diet, exercise.

 

[deathmerchant]

Yikes. No evidence of CAA on MRI =/= freedom from CAA. You know the MRI doesn’t ‘see’ CAA, but the microhemes that occur with amyloid, right? And you know that this beta amyloid causes Alzheimer’s. And you know that half of those >85 have AD and thus by definition will have amyloid. And only 5-10% of AD people will NOT have CAA. Here’s a good review: Cerebral amyloid angiopathy in the aetiology and immunotherapy of Alzheimer disease

So you’re giving tPA to these folks, only about 1/50 (of all comers) is suffering a fatal bleed. There is no data I’m aware of regarding selection or risk stratification for full a/c, or dual anti-plts in the setting of CAA with micro bleeds. But if you have some, I’ll take a look.

In otherwise healthy people without rip-roaring HTN/DM/cocaine use, seeing MH’s = CAA. The classic finding of MH's NOT due to CAA is location in the cerebellum.

1. CAA Has shown to be associated with higher risk of bleeding with anti platelet, anti-thrombotic and anticoagulation. There is more and more evidence accumulating every year( many reports/series). Instead of playing the odds- I personally would like to know and make a slightly more precise attempt at treatment and in addition, also hope to learn about various outcomes. No one is thinking magically that this is precision medicine- its far from it, but its a step closer to it.
Also, presence of Beta amyloid =/ Alzheimer's. It is just 'Present' in a significant number of patients with AD. We are nowhere near causality. It is present in 30% of normal people >85. And absent in 10% of AD patients. So may be there are people who have amyloid and have MH and many who don't.

Point being- I am more concerned about MH rather than presence of amyloid or CAA.
Yes, you are right- there is no (Level 1) data yet- but as I too am not crazy about precision medicine and would use clinical judgement and logic until we have enough data.

So how does MRI help you distinguish? It was already established that she did not have a small vessel syndrome based on history (the danger of over-reliance on imaging is that we forget the fundamentals). And everything else is exactly right. If she has a fib, then you're going to use a/c. If she has echo evidence of thrombogenesis, then you will have that conversation. NOACs are nowhere close to being as safe as aspirin, and I concur that these trials MAY very much alter 2018 management. But that's why we do trials, because we don't know it all. When these trials are done, if they show benefit, then in the absence of A fib, would want to adhere to their protocol: if cardioembolic "look" and clean vascular WU with MRA, and no A Fib, then use Xarelto.

As much as I would like to believe otherwise, there is no person who can distinguish the clinical symptoms with a certainty more than MRI(May be there are some people!). History and Exam has high specificity but much lower sensitivity than MRI. Our knowledge of the brain keeps changing and I would want to use fundamentals + Imaging; instead of just one of those. The number of stroke mimics getting tpa is increasing insanely( upto 30% in some centers) and one would think people should move towards more frequent/faster MRI and MRI based tpa protocols!! (Again here comes the debate of resource utilization, which I believe in)
And again there are many more etiologies other than Afib. ECHO helps to make a diagnosis of PAFib and other cardioembolic etiologies and if absent, makes one look for other causes.

 

[neglect]

Also, presence of Beta amyloid =/ Alzheimer's. It is just 'Present' in a significant number of patients with AD. We are nowhere near causality. It is present in 30% of normal people >85. And absent in 10% of AD patients. So may be there are people who have amyloid and have MH and many who don't.

Sorry, total whiff. Amyloid causes Alzheimer’s disease. No amyloid, no Alzheimer’s. And, worse, the data currently support an idea of + amyloid just being Alzheimer’s.

How do we know? PSEN mutations for one, and every single autosomal dominant mutation that gives rise to AD in the 40s and 50s increases beta-amyloid generation. This includes the famous Mrs. Deter, Dr. Alzheimer’s case report. This dovetails with Trisomy 21, with 150% lifelong ‘load’ of beta-amyloid c/w wild type.

So we were no-where near causality until these mutations were discovered, or if one doesn’t know about them. Now we are in causal territory.

But wait, I’m not even done yet! Combine this with the Icelandic mutation, which protects against amyloidogenesis by giving a natural and lifelong bace-inhibitor. Combine it with tau mutations that do NOT cause AD, but cause specific FTD/PSP tauopathies. Combine it with the APOE4 data showing decreased proteinolysis of amyloid with APOE4 and increased risk of the disease. Combine it with the epidemiology of risk of amyloid exponentially rising starting at, say, 30 (and 20 if you have APOE44). Then 15-20 years later an epidemiologic nightmarish rise of the disease.

So this data is impossible to ignore. The horrible failures in the field may be due to timing, delivery, dose, and targets. Still, these give one pause, everything else supports the amyloid hypothesis.

Amyloid is present in many folks with normal cognition. Check in on them in 10-20 years. It isn’t the fall that kills you, ha ha, but the landing. And this is a very long fall. You find HIV virus, they don’t have AIDS - yet, get it?

Absent in 10% of AD patients? Misdiagnoses occur, is that what you’re talking about here? Or never mind.

 

[deathmerchant]

Sorry, total whiff. Amyloid causes Alzheimer’s disease. No amyloid, no Alzheimer’s. And, worse, the data currently support an idea of + amyloid just being Alzheimer’s.

.

I don't know how we got into AD debate from stroke, but "Amyloid is not the cause of Alzheimer's". it is associated/it could be substrate/indirect culprit etc.
It has not been proven, not even close. it is a hypothesis that is failing everyday. The day someone comes up with a definitive evidence and causality- that person will win the Nobel prize. There is so much data questioning this hypothesis. It was reinforced by the recent Drug trials that definitively decreased amyloid in the brain with no change in the disease or its progression. There are so many studies- Ill just plug in the first one that shows up on pub med.(I agree there is data on both sides though)

Is Beta-Amyloid Accumulation a Cause or Consequence of Alzheimer’s Disease?

Another logical fallacy - That 10% number is derived after extrapolation of numbers. It is just similar to saying 90% people with AD have amyloid. 90% people with amyloid do not get biopsies. I actually think, more people diagnosed with AD now and esp in the past, actually had other diagnoses which we didn't know abt then and we keep finding.
And all the points you are making for causality don't fit the Koch's postulates of causality.

 

[neglect]

I don't know how we got into AD debate from stroke, but "Amyloid is not the cause of Alzheimer's". it is associated/it could be substrate/indirect culprit etc.
It has not been proven, not even close. it is a hypothesis that is failing everyday. The day someone comes up with a definitive evidence and causality- that person will win the Nobel prize. There is so much data questioning this hypothesis. It was reinforced by the recent Drug trials that definitively decreased amyloid in the brain with no change in the disease or its progression. There are so many studies- Ill just plug in the first one that shows up on pub med.(I agree there is data on both sides though)

Is Beta-Amyloid Accumulation a Cause or Consequence of Alzheimer’s Disease?

Another logical fallacy - That 10% number is derived after extrapolation of numbers. It is just similar to saying 90% people with AD have amyloid. 90% people with amyloid do not get biopsies. I actually think, more people diagnosed with AD now and esp in the past, actually had other diagnoses which we didn't know abt then and we keep finding.
And all the points you are making for causality don't fit the Koch's postulates of causality.

So that was clarifying. I’m speaking to someone who thinks we prove scientific hypotheses. Consider suing your college and consider learning Popper.

Explain why the Icelandic mutation (you’ll have to look it up first) protects against Alzheimer’s disease, since you are fond of Koch’s postulates. Or don’t.

 

[deathmerchant]

So that was clarifying. I’m speaking to someone who thinks we prove scientific hypotheses. Consider suing your college and consider learning Popper.

Explain why the Icelandic mutation (you’ll have to look it up first) protects against Alzheimer’s disease, since you are fond of Koch’s postulates. Or don’t.

(Ignoring personal remarks)- Yes One does Try to prove scientific hypothesis in the hopes of bringing them closer to actual Laws of nature. I don't expect everyone to think that way. I already conceded that there is evidence on both sides, hence take everything with a grain of salt. I understand the presence of confirmation bias and others in my and your arguments. I will be more than happy once someone proves that hypothesis definitively. But I wouldn't let anyone get away with a statement that is unequivocally true, on a semi-public platform.

 

[neglect]

(Ignoring personal remarks)- Yes One does Try to prove scientific hypothesis in the hopes of bringing them closer to actual Laws of nature. I don't expect everyone to think that way. I already conceded that there is evidence on both sides, hence take everything with a grain of salt. I understand the presence of confirmation bias and others in my and your arguments. I will be more than happy once someone proves that hypothesis definitively. But I wouldn't let anyone get away with a statement that is unequivocally true, on a semi-public platform.

No, one cannot prove hypotheses or theories. Other people do not think in your way because you are thinking poorly and adopted a primitive, pre-scientific mindset that many of us try to avoid. Start here: Scientific theory - Wikipedia

You may have misundertood my second paragraph. I tried to formulate it better here: Explain why the Icelandic mutation protects against Alzheimer’s disease without relying on the amyloid hypothesis. Or don’t bother replying (this is actually the part you might have missed).

 

[deathmerchant]

I feel like this conversation is dropping below the intellectual/academic levels worthy of further discussion. So my last attempt -
Hypothesis =/theory =/law=/axiom (Not interchangeable: everyone knows the difference). So yes theories will stand without more evidence; hypothesis will Not (and you do continue to test for and against hypotheses). That is what the Amyloid/AD correlation is at this point. In addition, current theories can be superseded with better(more accurate) theories based on new knowledge/evidence.

Beta-amyloid and the Amyloid Hypothesis - Alzheimer's Association (why don't we just refer to the official AD associations' interpretation. Please just read the first 3 lines.)

And about your cherry picked Icelandic mutation; I will repeat as before, "There is evidence on both sides and causality has not been proven". It is the only statement I am trying to convey.
Im sorry to see that people these days are missing the healthy amount of skepticism needed for a scientific mindset and believing things blindly. Back to basics Sir. I am out.

 

[neglect]

I feel like this conversation is dropping below the intellectual/academic levels worthy of further discussion. So my last attempt -
Hypothesis =/theory =/law=/axiom (Not interchangeable: everyone knows the difference). So yes theories will stand without more evidence; hypothesis will Not (and you do continue to test for and against hypotheses). That is what the Amyloid/AD correlation is at this point. In addition, current theories can be superseded with better(more accurate) theories based on new knowledge/evidence.

Beta-amyloid and the Amyloid Hypothesis - Alzheimer's Association (why don't we just refer to the official AD associations' interpretation. Please just read the first 3 lines.)

And about your cherry picked Icelandic mutation; I will repeat as before, "There is evidence on both sides and causality has not been proven". It is the only statement I am trying to convey.
Im sorry to see that people these days are missing the healthy amount of skepticism needed for a scientific mindset and believing things blindly. Back to basics Sir. I am out.

Your conversation is dropping below any level. Not surprising given your simplistic notions of science. You have had ample chance to defend your position. All you had to to was explain the Icelandic mutation’s protective effects. You failed to do so. This was never cherry picked. I picked it because it is the latest evidence that gives fundamental support to and failed to falsify the amyloid hypothesis.

 

[Postictal Raiden]

Yes! But the finances suck. In house revenue streams from EEG and infusions are the way to go. DM me for why MRI is not good and what others are good if you’re interested.

Trying to PM you, but the system is not allowing me.

 

[Hank Rearden]

To circle back to the question from the original poster, Bill Powers is a minimalist, so perhaps no surprise with the new guidelines. If you go strictly by the clinical trial data, he's pretty much right. SPARCL for example tested 80mg atorvastatin so all stroke patients need this almost regardless of LDL level. WARCEF was somewhat equivocal, but most of us still feel strongly that stroke patients with low EF should be on coumadin. The minimalist workup with carotid duplex often misses intracranial athero - so I'm a proponent CTA or MRA, but not clear that putting these patients on dual antiplatelet is better than just single antiplatelet. I'm a fan of extended Holter monitoring either externally or with implanted loop recorder, but whether picking up more A-Fib in this manner and starting anti-coag truly reduces stroke risk has not been tested in a clinical trial (and probably never will because most of us would consider it unethical to withhold anticoag if we found A-Fib).

I think the bottom line is these new guidelines are not going to change practice much, at least not in the U.S.

 

[cerebral edema]

Well well what do we have here

 

[Whitetail]

Can you quote the offending passages?

MRI, CTA and MRA very much ARE overutilized and nearly NEVER change management. Residents seem dumbfounded that one can diagnose and treat stroke without a positive MRI, and that some strokes have negative MRIs, and that a stroke-in-the-young work up is perhaps not useful in a 70 year old with HTN and DM. You ever been called by an eager resident who asks “what are we going to do now that the MRI shows stroke” in a patient who was admitted from the ER FOR stroke?

Also, if one’s approach is minimal, can you speculate how many more patients over, say, 70 would have a change in management for routine stroke prevention? Assume no ICA stenosis, EKG no A fib, no large thrombus or cardiac source on echo. We’re left with BP, statin, anti-plts, diet and exercise. I’m personally for judicious and selective intracranial vessel evals and Holter monitors, but why should they be used every time? There are very real risks to keeping these folks longer in the hospital, over-testing and getting false positives, which begat more testing. And CTA is TOTALLY overutilized in the ER with no hope of changing management in those with no symptoms or mild symptoms who will never have LVO and are too good to go to cath anyway.

Thankfully we have no institutional approaches. We have well trained neurologists who bring guidelines and data to real patients.

+1

It’s amazing what a history and physical exam will reveal about a patient.

 

[JBabinski]

+1

It’s amazing what a history and physical exam will reveal about a patient.

yes this is true but the problem with guidelines like this is that insurance companies will follow these and some cases definitely need more extensive workup. as is the case in many things in medicine, in the real world there is more of a grey area. Some cases don't need a full extensive workup and others do. However, the ERs and hospitals want "protocols" of how to evaluate and treat every patient with a certain diagnosis (in this case ischemic stroke). But medicine is an art not a science and this cookie cutter approach certainly is not appropriate for every patient. Furthermore, if it was your family member, would you want the minimalist approach or the full workup? You have to balance that individual point of view vs. the population based view that these guidelines adhere to, which look more at cost, use of resources, etc.

 

[Neurologo]

+1

It’s amazing what a history and physical exam will reveal about a patient.

75 yr old right-handed lady, nonsmoker, with a transient R lower face droop and R arm numbness lasting only 15 minutes. She also had a mild L frontal headaches without visual aura. No longer symptomatic. MRI brain negative for an acute stroke. BP at target range. LDL 90. TTE unremarkable. Neuro exam intact the next morning. You send her home with ASA or plavix, a statin and a follow up appointment. You let go of costly vessel images. You feel good for being cost effective. You even wonder if it were all just due to migraine.

Three days later she returns as a stroke alert for global aphasia and R hemiparalysis. This time you are forced to do CTA head & neck. It turns out she has had a critical stenosis due to ulcerated soft plaque in the proximal L ICA with a pinhole flow but now with a new large thrombus occluding the L M1.

What is the magic evaluation or history taking skill we can all use to distinguish who needs CTA/MRA and who doesn't?

The above example was one of "typical" cases I see daily. I did order CTA on the first admission, and she was started on IV heparin drip and an ASA followed by a L CEA successfully 3 days later. She went home without a stroke. I could not hear any "bruit" on the L carotid on my first exam.

 

[neglect]

75 yr old right-handed lady, nonsmoker, with a transient R lower face droop and R arm numbness lasting only 15 minutes. She also had a mild L frontal headaches without visual aura. No longer symptomatic. MRI brain negative for an acute stroke. BP at target range. LDL 90. TTE unremarkable. Neuro exam intact the next morning. You send her home with ASA or plavix, a statin and a follow up appointment. You let go of costly vessel images. You feel good for being cost effective. You even wonder if it were all just due to migraine.

Three days later she returns as a stroke alert for global aphasia and R hemiparalysis. This time you are forced to do CTA head & neck. It turns out she has had a critical stenosis due to ulcerated soft plaque in the proximal L ICA with a pinhole flow but now with a new large thrombus occluding the L M1.

What is the magic evaluation or history taking skill we can all use to distinguish who needs CTA/MRA and who doesn't?

The above example was one of "typical" cases I see daily. I did order CTA on the first admission, and she was started on IV heparin drip and an ASA followed by a L CEA successfully 3 days later. She went home without a stroke. I could not hear any "bruit" on the L carotid on my first exam.

Unwittingly you’ve very much affirmed what the underutilizes are saying: do NOT rely on imaging to diagnose TIAs! Costly vessel images? Cartotid ultrasound is cheap. MRA of neck is fairly cheap. Do NOT let any stroke leave your hospital without neck imaging! Yield is low, but if you miss it, as you point out, catastrophic.

I think the point we’re trying to make is don’t get hypercoag panels and TEE’s on this patient.

 

[RenegadeSynapse]

Bill Powers was my chairman for residency and was in large part responsible for teaching me stroke neurology. There was never any debate about carotid imaging; you did not leave the ER or hospital without it. If you couldn't get US, you got an MRA or CTA (less common). When I read the stroke recs, they read like my stroke training in residency.

 

[neglect]

I feel like this conversation is dropping below the intellectual/academic levels worthy of further discussion. So my last attempt -
Hypothesis =/theory =/law=/axiom (Not interchangeable: everyone knows the difference). So yes theories will stand without more evidence; hypothesis will Not (and you do continue to test for and against hypotheses). That is what the Amyloid/AD correlation is at this point. In addition, current theories can be superseded with better(more accurate) theories based on new knowledge/evidence.

Beta-amyloid and the Amyloid Hypothesis - Alzheimer's Association (why don't we just refer to the official AD associations' interpretation. Please just read the first 3 lines.)

And about your cherry picked Icelandic mutation; I will repeat as before, "There is evidence on both sides and causality has not been proven". It is the only statement I am trying to convey.
Im sorry to see that people these days are missing the healthy amount of skepticism needed for a scientific mindset and believing things blindly. Back to basics Sir. I am out.

This happened: Eisai-Biogen to Advance Alzheimer's Drug, Provide Fresh Hope. 80% clearance of amyloid and 30% reduction in progression.

Edit: I should have said clearance of amyloid in 81% of subjects via PET vis read.

 

[cerebral edema]

This happened: Eisai-Biogen to Advance Alzheimer's Drug, Provide Fresh Hope. 80% clearance of amyloid and 30% reduction in progression.

Edit: I should have said clearance of amyloid in 81% of subjects via PET vis read.

There’s new evidence that the dominant approach to Alzheimer’s may be completely wrong

 

[neglect]

There’s new evidence that the dominant approach to Alzheimer’s may be completely wrong

 

[neglect]

There’s an interesting JAMA article about overutilization: Excessive Resource Utilization

This case analysis brings up some germane points about our culture of overutilization. I wish this would get talked about more often. You can’t make up for shoddy care, poor thinking, problematic decision making with more tests and more consults. The residents I see seem to disbelieve this. Sadly they become attendings and the culture shifts.

 

[deathmerchant]

View attachment 238583

@neglect @cerebral edema. Its good to see a positive study! I will definitely look forward to further results.
Although, there are 2 negative studies for every positive amyloid study- in basic science and clinical studies (and drug trials). Honestly, its time to start shifting focus on other mechanisms and other hypothesis too !!

 

[neglect]

@neglect @cerebral edema. Its good to see a positive study! I will definitely look forward to further results.
Although, there are 2 negative studies for every positive amyloid study- in basic science and clinical studies (and drug trials). Honestly, its time to start shifting focus on other mechanisms and other hypothesis too !!

There are several anti-tau antibodies in trials now. Having a diverse approach is the best one. Even if we remove all the amyloid, these folks still progress. Still waiting for full data set from Eisai.