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  • Radiographic Evaluation of Normal Pressure Hydrocephalus With Dr. Aaron Switzer
     Normal pressure hydrocephalus (NPH) is a clinical syndrome of gait abnormality, cognitive impairment, and urinary incontinence. Evaluation of CSF dynamics, patterns of fludeoxyglucose (FDG) uptake, and patterns of brain stiffness may aid in the evaluation of challenging cases that lack typical clinical and structural radiographic features. In this episode, Katie Grouse, MD, FAAN, speaks with Aaron Switzer, MD, MSc, author of the article “Radiographic Evaluation of Normal Pressure Hydrocephalus” in the Continuum® June 2025 Disorders of CSF Dynamics issue. Dr. Grouse is a Continuum® Audio interviewer and a clinical assistant professor at the University of California San Francisco in San Francisco, California. Dr. Switzer is a clinical assistant professor of neurology in the department of clinical neurosciences at the University of Calgary in Calgary, Alberta, Canada. Additional Resources Read the article: Radiographic Evaluation of Normal Pressure Hydrocephalus Subscribe to Continuum®: shop.lww.com/Continuum Earn CME (available only to AAN members): continpub.com/AudioCME Continuum® Aloud (verbatim audio-book style recordings of articles available only to Continuum® subscribers): continpub.com/Aloud More about the American Academy of Neurology: aan.com Social Media facebook.com/continuumcme @ContinuumAAN Full episode transcript available here Dr Jones: This is Dr Lyell Jones, Editor-in-Chief of Continuum. Thank you for listening to Continuum Audio. Be sure to visit the links in the episode notes for information about earning CME, subscribing to the journal, and exclusive access to interviews not featured on the podcast. Dr Grouse: This is Dr Katie Grouse. Today I'm interviewing Dr Aaron Switzer about his article on radiographic evaluation of normal pressure hydrocephalus, which he wrote with Dr Patrice Cogswell. This article appears in the June 2025 Continuum issue on disorders of CSF dynamics. Welcome to the podcast, and please introduce yourself to our audience. Dr. Switzer: Thanks so much for having me, Katie. I'm a neurologist that's working up in Calgary, Alberta, Canada, and I have a special interest in normal pressure hydrocephalus. So, I'm very happy to be here today to talk about the radiographic evaluation of NPH. Dr Grouse: I'm so excited to have you here today. It was really wonderful to read your article. I learned a lot on a topic that is not something that I frequently evaluate in my clinic. So, it's really just a pleasure to have you here to talk about this topic. So, I'd love to start by asking, what is the key message that you hope for neurologists who read your article to take away from it? Dr. Switzer: The diagnosis of NPH can be very difficult, just given the clinical heterogeneity in terms of how people present and what their images look like. And so, I'd like readers to know that detailed review of the patient's imaging can be very helpful to identify those that will clinically improve with shunt surgery. Dr Grouse: There's another really great article in this edition of Continuum that does a really great job delving into the clinical history and exam findings of NPH. So, I don't want to get into that topic necessarily today. However, I'd love to hear how you approach a case of a hypothetical patient, say, where you're suspicious of NPH based on the history and exam. I'd love to talk over how you approach the imaging findings when you obtain an MRI of the brain, as well as any follow-up imaging or testing that you generally recommend. Dr. Switzer: So, I break my approach down into three parts. First, I want to try to identify ventriculomegaly and any signs that would support that, and specifically those that are found in NPH. Secondly, I want to look for any alternative pathology or evidence of alternative pathology to explain the patient's symptoms. And then also evaluate any contraindications for shunt surgery. For the first one, usually I start with measuring Evans index to make sure that it's elevated, but then I want to measure one of the other four measurements that are described in the article, such as posterior colossal angle zed-Evans index---or z-Evans index for the American listeners---to see if there's any other features that can support normal pressure hydrocephalus. It's very important to identify whether there are features of disproportionately enlarged subarachnoid space hydrocephalus, or DESH, which can help identify patients who may respond to shunt surgery. And then if it's really a cloudy clinical picture, it's complicated, it's difficult to know, I would usually go through the full evaluation of the iNPH radscale to calculate a score in order to determine the likelihood that this patient has NPH. So, the second part of my evaluation is to rule out evidence of any alternative pathology to suggest another cause for the patient's symptoms, such as neurodegeneration or cerebrovascular disease. And then the third part of my evaluation is to look for any potential contraindications for shunt surgery, the main one being cerebral microbleed count, as a very high count has been associated with the hemorrhagic complications following shunt surgery. Dr Grouse: You mentioned about your use of the various scales to calculate for NPH, and your article does a great job laying them out and where they can be helpful. Are there any of these scales that can be reasonably relied on to predict the presence of NPH and responsiveness to shunt placement? Dr. Switzer: I think the first thing to acknowledge is that predicting shunt response is still a big problem that is not fully solved in NPH. So, there is not one single imaging feature, or even combination of imaging features, that can reliably predict shunt response. But in my view and in my practice, it's identifying DESH, I think, is really important---so, the disproportionately enlarged subarachnoid space hydrocephalus---as well as measuring the posterior colossal angle. I find those two features to be the most specific. Dr Grouse: Now you mentioned the concept of the NPH subtypes, and while this may be something that many of our listeners are familiar with, I suspect that, like myself when I was reading this article, there are many who maybe have not been keeping up to date on these various subtypes. Could you briefly tell us more about these NPH subtypes? Dr. Switzer: Sure. The Japanese guidelines for NPH have subdivided NPH into three different main categories. So that would be idiopathic, delayed onset congenital, and secondary normal pressure hydrocephalus. And so, I think the first to talk about would be the secondary NPH. We're probably all more familiar with that. That's any sort of pathology that could lead to disruption in CSF dynamics. These are things like, you know, a slow-growing tumor that is obstructing CSF flow or a widespread meningeal process that's reducing absorption of CSF, for instance. So, identifying these can be important because it may offer an alternative treatment for what you're seeing in the patient. The second important one is delayed onset congenital. And when you see an image of one of these subtypes, it's going to be pretty different than the NPH because the ventricles are going to be much larger, the sulcal enfacement is going to be more diffuse. Clinically, you may see that the patients have a higher head circumference. So, the second subtype to know about would be the delayed onset congenital normal pressure hydrocephalus. And when you see an image of one of these subtypes, it's going to be a little different than the imaging of NPH because the ventricles are going to be much larger, the sulcal enfacement is going to be more diffuse. And there are two specific subtypes that I'd like you to know about. The first would be long-standing overt ventriculomegaly of adulthood, or LOVA. And the second would be panventriculomegaly with a wide foramen of magendie and large discernomagna, which is quite a mouthful, so we just call it PAVUM. The importance of identifying these subtypes is that they may be amenable to different types of treatment. For instance, LOVA can be associated with aqueductal stenosis. So, these patients can get better when you treat them with an endoscopic third ventriculostomy, and then you don't need to move ahead with a shunt surgery. And then finally with idiopathic, that's mainly what we're talking about in this article with all of the imaging features. I think the important part about this is that you can have the features of DESH, or you can not have the features of DESH. The way to really define that would be how the patient would respond to a large-volume tap or a lumbar drain in order to define whether they have this idiopathic NPH. Dr Grouse: That's really helpful. And for those of our listeners who are so inclined, there is a wonderful diagram that lays out all these subtypes that you can take a look at. I encourage you to familiarize yourself with these different subtypes. Now it was really interesting to read in your article about some of the older techniques that we used quite some time ago for diagnosing normal pressure hydrocephalus that thankfully we're no longer using, including isotope encephalography and radionuclide cisternography. It certainly made me grateful for how we've come in our diagnostic tools for NPH. What do you think the biggest breakthrough in diagnostic tools that are now clinically available are? Dr. Switzer: You know, definitely the advent of structural imaging was very important for the evaluation of NPH, and specifically the identification of disproportionately enlarged subarachnoid space hydrocephalus, or DESH, in the late nineties has been very helpful for increasing the specificity of diagnosis in NPH. But some of the newer technologies that have become available would be phase-contrast MRI to measure the CSF flow rate through the aqueduct has been very helpful, as well as high spatial resolution T2 imaging to actually image the ventricular system and look for any evidence of expansion of the ventricles or obstruction of CSF flow. Dr Grouse: Regarding the scales that you had referenced earlier, do you think that we can look forward to more of these scales being automatically calculated and reported by various software techniques and radiographic interpretation techniques that are available or going to be available? Dr. Switzer: Definitely yes. And some of these techniques are already in development and used in research settings, and most of them are directed towards automatically detecting the features of DESH. So, that's the high convexity tight sulci, the focally enlarged sulci, and the enlarged Sylvian fissures. And separating the CSF from the brain tissue can help you determine where CSF flow is abnormal throughout the brain and give you a more accurate picture of CSF dynamics. And this, of course, is all automated. So, I do think that's something to keep an eye out for in the future. Dr Grouse: I wanted to ask a little more about the CSF flow dynamics, which I think may be new to a lot of our listeners, or certainly something that we've only more recently become familiar with. Can you tell us more about these advances and how we can apply this information to our evaluations for NPH? Dr. Switzer: So currently, only the two-dimensional phase contrast MRI technique is available on a clinical basis in most centers. This will measure the actual flow rate through the cerebral aqueduct. And so, in NPH, this can be elevated. So that can be a good supporting marker for NPH. In the future, we can look forward to other techniques that will actually look at three-dimensional or volume changes over time and this could give us a more accurate picture of aberrations and CSF dynamics. Dr Grouse: Well, definitely something to look forward to. And on the topic of other sort of more cutting-edge or, I think, less commonly-used technologies, you also mentioned some other imaging modalities, including diffusion imaging, intrathecal gadolinium imaging, nuclear medicine studies, MR elastography, for example. Are any of these modalities particularly promising for NPH evaluations, in your opinion? Do you think any of these will become more popularly used? Dr. Switzer: Yes, I think that diffusion tract imaging and MR elastography are probably the ones to keep your eye out for. They're a little more widely applicable because you just need an MR scanner to acquire the images. It's not invasive like the other techniques mentioned. So, I think it's going to be a lot easier to implement into clinical practice on a wide scale. So, those would be the ones that I would look out for in the future. Dr Grouse: Well, that's really exciting to hear about some of these techniques that are coming that may help us even more with our evaluation. Now on that note, I want to talk a little bit more about how we approach the evaluation and, in your opinion, some of the biggest pitfalls in the evaluation of NPH that you've found in your career. Dr. Switzer: I think there are three of note that I'd like to mention. The first would be overinterpreting the Evans index. So, just because an image shows that there's an elevated Evans index does not necessarily mean that NPH is present. So that's where looking for other corroborating evidence and looking for the clinical features is really important in the evaluation. Second would be misidentifying the focally enlarged sulci as atrophy because when you're looking at a brain with these blebs of CSF space in different parts of the brain, you may want to associate that to neurodegeneration, but that's not necessarily the case. And there are ways to distinguish between the two, and I think that's another common pitfall. And then third would be in regards to the CSF flow rate through the aqueduct. And so, an elevated CSF flow is suggestive of NPH, but the absence of that does not necessarily rule NPH out. So that's another one to be mindful of. Dr Grouse: That's really helpful. And then on the flip side, any tips or tricks or clinical pearls you can share with us that you found to be really helpful for the evaluation of NPH? Dr. Switzer: One thing that I found really helpful is to look for previous imaging, to look if there were features of NPH at that time, and if so, have they evolved over time; because we know that in idiopathic normal pressure hydrocephalus, especially in the dash phenotype, the ventricles can become larger and the effacement of the sulci at the convexity can become more striking over time. And this could be a helpful tool to identify how long that's been there and if it fits with the clinical history. So that's something that I find very helpful. Dr Grouse: Absolutely. When I read that point in your article, I thought that was really helpful and, in fact, I'm guessing something that a lot of us probably aren't doing. And yet many of our patients for one reason or other, probably have had imaging five, ten years prior to their time of evaluation that could be really helpful to look back at to see that evolution. Dr. Switzer: Yes, absolutely. Dr Grouse: It's been such a pleasure to read your article and talk with you about this today. Certainly a very important and helpful topic for, I'm sure, many of our listeners. Dr. Switzer: Thank you so much for having me. Dr Grouse: Again, today I've been interviewing Dr Aaron Switzer about his article on radiographic evaluation of normal pressure hydrocephalus, which he wrote with Dr Patrice Cogswell. This article appears in the most recent issue of Continuum on disorders of CSF dynamics. Be sure to check out Continuum Audio episodes from this and other issues, and thank you to our listeners for joining today. Dr Monteith: This is Dr Teshamae Monteith, Associate Editor of Continuum Audio. If you've enjoyed this episode, you'll love the journal, which is full of in-depth and clinically relevant information important for neurology practitioners. Use the link in the episode notes to learn more and subscribe. AAN members, you can get CME for listening to this interview by completing the evaluation at continpub.com/audioCME. Thank you for listening to Continuum Audio.
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  • Clinical Features and Diagnosis of Normal Pressure Hydrocephalus with Dr. Abhay Moghekar
    Normal pressure hydrocephalus (NPH) is a clinical syndrome characterized by the triad of gait apraxia, cognitive impairment, and bladder dysfunction in the radiographic context of ventriculomegaly and normal intracranial pressure. Accurate diagnosis requires consideration of clinical and imaging signs, complemented by tests to exclude common mimics. In this episode, Lyell Jones, MD, FAAN speaks with Abhay R. Moghekar, MBBS, author of the article “Clinical Features and Diagnosis of Normal Pressure Hydrocephalus” in the Continuum® June 2025 Disorders of CSF Dynamics issue. Dr. Jones is the editor-in-chief of Continuum: Lifelong Learning in Neurology® and is a professor of neurology at Mayo Clinic in Rochester, Minnesota. Dr. Moghekar is an associate professor of neurology at Johns Hopkins University School of Medicine in Baltimore, Maryland. Additional Resources Read the article: Clinical Features and Diagnosis of Normal Pressure Hydrocephalus Subscribe to Continuum®: shop.lww.com/Continuum Earn CME (available only to AAN members): continpub.com/AudioCME Continuum® Aloud (verbatim audio-book style recordings of articles available only to Continuum® subscribers): continpub.com/Aloud More about the American Academy of Neurology: aan.com Social Media facebook.com/continuumcme @ContinuumAAN Host: @LyellJ Full episode transcript available here Dr Jones: This is Dr Lyell Jones, Editor-in-Chief of Continuum. Thank you for listening to Continuum Audio. Be sure to visit the links in the episode notes for information about earning CME, subscribing to the journal, and exclusive access to interviews not featured on the podcast. Dr Jones: This is Dr Lyell Jones, Editor-in-Chief of Continuum: Lifelong Learning in Neurology. Today I'm interviewing Dr Abhay Moghekar, who recently authored an article on the clinical features and diagnosis of normal pressure hydrocephalus for our first-ever issue of Continuum dedicated to disorders of CSF dynamics. Dr Moghekar is an associate professor of neurology and the research director of the Cerebrospinal Fluid Center at Johns Hopkins University in Baltimore, Maryland. Dr Moghekar, welcome, and thank you for joining us today. Why don't you introduce yourself to our listeners? Dr Moghekar: Thank you, Dr Jones. I'm Abhay Moghekar. I'm a neurologist at Hopkins, and I specialize in seeing patients with CSF disorders, of which normal pressure hydrocephalus happens to be the most common. Dr Jones: And let's get right to it. I think most of our listeners who are neurologists in practice have encountered normal pressure hydrocephalus, or NPH; and it's a challenging disorder for all the reasons that you outline in your really outstanding article. If you were going to think of one single most important message to our listeners about recognizing patients with NPH, what would that be? Dr Moghekar: I think I would say there are two important messages. One is that the triad is not sufficient to make the diagnosis, and the triad is not necessary to make the diagnosis. You know these three elements of the triad: cognitive problems, gait problems, bladder control problems are so common in the elderly that if you pick 10 people out in the community that have this triad, it's unlikely that even one of them has true NPH. On the other hand, you don't need all three elements of the triad to make the diagnosis because the order of symptoms matters. Often patients develop gait dysfunction first, then cognitive dysfunction, and then urinary incontinence. If you wait for all three elements of the triad to be present, it may be too late to offer them any clear benefit. And hence, you know, it's neither sufficient nor necessary to make the diagnosis. Dr Jones: That's a really great point. I think most of our listeners are familiar with the fact that, you know, we're taught these classic triads or pentads or whatever, and they're rarely all present. In a way, it's maybe a useful prompt, but it could be distracting or misleading, even in a way, in terms of recognizing the patient. So what clues do you use, Dr Moghekar, to really think that a patient may have NPH? Dr Moghekar: So, there are two important aspects about gait dysfunction. Say somebody comes in with all three elements of the triad. You want to know two things. Which came first? If gate impairment precedes cognitive impairment, it's still very likely that NPH is in the differential. And of the two, which are more- relatively more affected? So, if somebody has very severe dementia and they have a little bit of gait problems, NPH is not as likely. So, is gait affected earlier than cognitive dysfunction, and is it affected to a more severe degree than cognitive dysfunction? And those two things clue me in to the possibility of NPH. You still obviously need to get imaging to make sure that they have large ventricles. One of the problems with imaging is large ventricles are present in so many different patients. Normal aging causes large ventricles. Obviously, many neurodegenerative disorders because of cerebral atrophy will cause large ventricles. And there's an often-used metric called as the events index, which is the ratio of the bitemporal horns- of the frontal horns of the lateral ventricles compared to the maximum diameter of the skull at that level. And if that ratio is more than 0.3, it's often used as a de facto measure of ventriculomegaly. What we've increasingly realized is that this ratio changes with age. And there's an excellent study that used the ADNI database that looked at how this ratio changes by age and sex. So, in fact, we now know that an 85-year-old woman who has an events index of 0.37 which would be considered ventriculomegaly is actually normal for age and sex. So, we need to start adopting these more modern age- and sex-appropriate age cutoffs of ventriculomegaly so as not to overcall everybody with big ventricles as having possible NPH. Dr Jones: That's very helpful. And I do want to come back to this challenge that we've seen in our field of overdiagnosis and underdiagnosis. But I think most of us are familiar with the concept of how hydrocephalus could cause neurologic deficits. But what's the latest on the mechanism of NPH? Why do some patients get this and others don't? Dr Moghekar: Very good question. I don't think we know for sure. And it for a long time we thought it was a plumbing issue. Right? And that's why shunts work. People thought it was impaired CSF absorption, but multiple studies have shown that not to be true. It's likely a combination of impaired cerebral blood flow, biomechanical factors like compliance, and even congenital factors that play a role in the pathogenesis of NPH. And yes, while putting in shunts likely drains CSF, putting in a shunt also definitely changes the compliance of the brain and affects blood flow to the subcortical regions of the brain. So, there are likely multiple mechanisms by which shunts benefit, and hence it's very likely that there's no single explanation for the pathogenesis of NPH. Dr Jones: We explored this in a recent Continuum issue on dementia. Many patients who have cognitive impairment have co-pathologies, multiple different causes. I was interested to read in your article about the genetic risk profile for NPH. It's not something I'd ever really considered in a disorder that is predominantly seen in older patients. Tell us a little more about those genetic risks. Dr Moghekar: Yeah, everyone is aware of the role genetics plays in congenital hydrocephalus, but until recently we were not aware that certain genetic factors may also be relevant to adult-onset normal pressure hydrocephalus. We've suspected this for a long time because nearly half of our patients who come to us to see us in clinic with NPH have head circumferences that are more than 90th percentile for height. And you know, that clearly indicates that this started shortly at the time after birth or soon afterwards. So, we've suspected for a long time that genetic factors play a role, but for a long time there were not enough large studies or well-conducted studies. But recently studies out of Japan and the US have shown mutations in genes like CF43 and CWH43 are disproportionately increased in patients with NPH. So, we are discovering increasingly that there are genetic factors that underlie even adult onset in patients. There are many more waiting to be discovered. Dr Jones: Really fascinating. And obviously getting more insight into the risk and mechanisms would be helpful in identifying these patients potentially earlier. And another thing that I learned in your article that I thought was really interesting, and maybe you can tell us more about it, is the association between normal pressure hydrocephalus and the observation of cervical spinal stenosis, many of whom require decompression. What's behind that association, do you think? Dr Moghekar: That's a very interesting study that was actually done at your institution, at Mayo Clinic, that showed this association. You know, as we all get older, you know, the incidence of cervical stenosis due to osteoarthritis goes up, but the incidence of significant, clinically significant cervical stenosis in the NPH population was much higher than what we would have expected. Whether this is merely an association in a vulnerable population or is it actually causal is not known and will need further study. Dr Jones: It's interesting to speculate, does that stenosis affect the flow of CSF and somehow predispose to a- again, maybe a partial degree for some patients? Dr Moghekar: Yeah, which goes back to the possible hydrodynamic theory of normal pressure hydrocephalus; you know, if it's obstructing normal CSF flow, you know, are the hydrodynamics affected in the brain that in turn could lead to the development of hydrocephalus. Dr Jones: One of the things I really enjoyed about your article, Abhay, was the very strong clinical focus, right? We can't just take an isolated biomarker or radiographic feature and rely on that, right? We really do need to have clinical suspicion, clinical judgment. And I think most of our listeners who've been in practice are familiar with the use and the importance of the large-volume lumbar puncture to determine who may have, and by exclusion not have, NPH, and then who might respond to CSF diversion. And I think those of us who have been in this situation are also familiar with the scenario where you think someone may have NPH and you do a large-volume lumbar puncture and they feel better, but you can't objectively see a difference. How do you make that test useful and objective in your practice? What do you do? Dr Moghekar: Yeah, it's a huge challenge in getting this objective assessment done carefully because you have to remember, you know, subconsciously you're telling the patients, I think you have NPH. I'm going to do this spinal tap, and if you walk better afterwards, you're going to get a shunt and you're going to be cured. And you can imagine the huge placebo response that can elicit in our subjects. So, we always like to see, definitely, did the patient subjectively feel better? Because yes, that's an important metric to consider because we want them to feel better. But we also wanted to be grounded in objective truths. And for that, we need to do different tests of speed, balance and endurance. Not everyone has the resources to do this, but I think it's important to test different domains. Just like for cognition, you know, we just don't test memory, right? We test executive function, language, visuospatial function. Similarly, walking is not just walking, right? It's gait speed, it's balance, and it's endurance. So, you need to ideally test at least most of these different domains for gait and you need to have some kind of clear criteria as to how are you going to define improvement. You know, is a 5% improvement, is a 10% improvement in gait, enough? Is 20%? Where is that cutoff? And as a field, we've not done a great job of coming up with standardized criteria for this. And it varies currently, the practice varies quite significantly from center to center at the current time. Dr Jones: So, one of the nice things you had in your article was helpful tips to be objective if you're in a lower-resource setting. For you, this isn't a common scenario that someone encounters in their practice as opposed to a center that maybe does a large volume of these. What are some relatively straightforward objective measures that a neurologist or someone else might use to determine if someone is improving after a large-volume LP? Dr Moghekar: Yeah, excellent question, Dr Jones, and very practically relevant too. So, you need to at least assess two of the domains that are most affected. One is speed and one is balance. You know, these patients fall ultimately, right, if you don't treat them correctly. In terms of speed, there are two very simple tests that anybody can do within a couple of minutes. One is the timed “up-and-go” test. It's a test that's even recommended by the CDC. It correlates very well with faults and disability and it can be done in any clinic. You just need about ten feet of space and a chair and a stopwatch, and it takes about a minute or slightly more to do that test. And there are objective age-associated norms for the timed up-and-go test, so it's easy to know if your patient is normal or not. The same thing goes for the 10-meter walk test. You do need a slightly longer walkway, but it's a fairly easy and well-standardized test. So, you can do one of those two; you don't need to do both of them. And for balance, you can do the 30-second “sit-to-stand”; and it's literally, again, 30 seconds. You need a chair, and you need somebody to watch the patient and see how many times they can sit up and stand up from a seated position. Then again, good normative data for that. If you want to be a little more sophisticated, you can do the 4-stage balance test. So, I think these are tests that don't add too much time to your daily assessment and can be done with even trained medical assistants in any clinic. And you don't need a trained physical therapist to do these assessments. Dr Jones: Very practical. And again, something that is pretty easily deployed, something we do before and then after the LP. I did see you mentioned in your article the dual timed up-and-go test where it's a simultaneous gait and executive function test. And I’ve got to be honest with you, Dr Moghekar, I was a little worried if I would pass that test, but that may be beyond the scope of our time today. Actually, how do you do that? How do you do the simultaneous cognitive assessment? Dr Moghekar: So, we asked them to count back from 100, subtracting 3. And we do it particularly in patients who are mildly impaired right? So, if they're already walking really good, but then you give them a cognitive stressor, you know, that will slow them down. So, we reserve it for patients who are high-performing. Dr Jones: That's fantastic. I'm probably aging myself a little here. I have noticed in my career, a little bit of a pendulum swing in terms of the recognition or acceptance of the prevalence of normal pressure hydrocephalus. I recall when I was a resident, many, many people that we saw in clinic had normal pressure hydrocephalus. Then it seemed for a while that it really faded into the background and was much less discussed and much less recognized and diagnosed, and less treated. And now that pendulum seems to have swung back the other way. What's behind that from your perspective? Dr Moghekar: It's an interesting backstory to all of this. When the first article about NPH was published in the Newman Journal of Medicine, it was actually a combined article with both neurologists and neurosurgeons on it. They did describe it as a treatable dementia. And what that did is it opened up the floodgates so that everybody with any kind of dementia started getting shunts left, right, and center. And back then, shunts were not programmable. There were no antibiotic impregnated catheters. So, the incidence of subdural hematomas and shunt-related infections was very high. In fact, one of our esteemed neurologists back then, Houston Merritt, wrote a scathing editorial that Victor and Adam should lose their professorships for writing such an article because the outcomes of these patients were so bad. So, for a very long period of time, neurologists stopped seeing these patients and stopped believing in NPH as a separate entity. And it became the domain of neurosurgeons for over two or three decades, until more recently when randomized trials started being done early on out of Europe. And now there's a big NIH study going on in the US, and these studies showed, in fact, that NPH exists as a true, distinct entity. And finally, neurologists have started getting more interested in the science and understanding the pathophysiology and taking care of these patients compared to the past. Dr Jones: That's really helpful context. And I guess that maybe isn't rare when you have a disorder that doesn't have a simple, straightforward biomarker and is complex in terms of the tests you need to do to support the diagnosis, and the treatment itself is somewhat invasive. So, when you talk to your patients, Dr Moghekar, and you've established the diagnosis and have recommended them for CSF diversion, what do you tell them? And the reason I ask is that you mentioned before we started recording, you had a patient who had a shunt placed and responded well, but continued to respond over time. Tell us a little bit more about what our patients can expect if they do have CSF diversion? Dr Moghekar: When we do the spinal tap and they meet our criteria for improvement and they go on to have a shunt, we tell them that we expect gait improvement definitely, but cognitive improvement may not happen in everyone depending on what time, you know, they showed up for their assessment and intervention. But we definitely expect gait improvement. And we tell them that the minimum gait improvement we can expect is the same degree of improvement they had after their large-volume lumbar puncture, but it can be even more. And as the brain remodels, as the hydrodynamics adapt to these shunts… so, we have patients who continue to improve one year, two years, and even three years into the course of the intervention. So, we’re, you know, hopeful. At the same time, we want to be realistic. This is the same population that's at risk for developing neurodegenerative disorders related to aging. So not a small fraction of our patients will also have Alzheimer's disease, for example, or go on to develop Lewy body dementia. And it's the role of the neurologist to pick up on these comorbid conditions. And that's why it's important for us to keep following these patients and not leave them just to the neurosurgeon to follow up. Dr Jones: And what a great note to end on, Dr Moghekar. And again, I want to thank you for joining us, and thank you for such a wonderful discussion and such a fantastic article on the clinical diagnosis of normal pressure hydrocephalus. I learned a lot reading the article, and I learned a lot more today just in the conversation with you. So, thank you for being with us. Dr Moghekar: Happy to do that, Dr Jones. It was a pleasure. Dr Jones: Again, we've been speaking with Dr Abhay Moghekar, author of a wonderful article on the clinical features and diagnosis of NPH in Continuum's first-ever issue dedicated to disorders of CSF dynamics. Please check it out. And thank you to our listeners for joining today. Dr Monteith: This is Dr Teshamae Monteith, Associate Editor of Continuum Audio. If you've enjoyed this episode, you'll love the journal, which is full of in-depth and clinically relevant information important for neurology practitioners. Use the link in the episode notes to learn more and subscribe. AAN members, you can get CME for listening to this interview by completing the evaluation at continpub.com/audioCME. Thank you for listening to Continuum Audio.
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  • Treatment and Monitoring of Idiopathic Intracranial Hypertension With Drs. John Chen and Susan Mollan
    Idiopathic intracranial hypertension (IIH), a condition of increased intracranial pressure (ICP), causes debilitating headaches and, in some, visual loss. The visual defects are often in the periphery and not appreciated by the patient until advanced; therefore, monitoring visual function with serial examinations and visual fields is essential. In this episode, Kait Nevel, MD speaks with John J. Chen, MD, PhD, and Susan P. Mollan, MBChB, PhD, FRCOphth, authors of the article “Treatment and Monitoring of Idiopathic Intracranial Hypertension” in the Continuum® June 2025 Disorders of CSF Dynamics issue. Dr. Nevel is a Continuum® Audio interviewer and a neurologist and neuro-oncologist at Indiana University School of Medicine in Indianapolis, Indiana. Dr. Chen is a professor of ophthalmology and neurology at the Mayo Clinic in Rochester, Minnesota. Dr. Mollan is an honorary professor of metabolism and systems science in the department of neuro-ophthalmology at University Hospitals Birmingham in Birmingham, United Kingdom. Additional Resources Read the article: Treatment and Monitoring of Idiopathic Intracranial Hypertension Subscribe to Continuum®: shop.lww.com/Continuum Earn CME (available only to AAN members): continpub.com/AudioCME Continuum® Aloud (verbatim audio-book style recordings of articles available only to Continuum® subscribers): continpub.com/Aloud More about the American Academy of Neurology: aan.com Social Media facebook.com/continuumcme @ContinuumAAN Host: @IUneurodocmom Guests: @chenmayo, @DrMollan Full episode transcript available here Dr Jones: This is Dr Lyell Jones, Editor-in-Chief of Continuum. Thank you for listening to Continuum Audio. Be sure to visit the links in the episode notes for information about earning CME, subscribing to the journal, and exclusive access to interviews not featured on the podcast. Dr Nevel: Hello, this is Dr Kate Nevel. Today, I'm interviewing Drs John Chen and Susan Mollan about their article on treatment and monitoring of idiopathic intracranial hypertension, which appears in the June 2025 Continuum issue on disorders of CSF dynamics. Drs Chen and Mollan, welcome to the podcast. And please, could you introduce yourselves to the audience? Dr Chen: Hello, everyone. I'm John Chen, one of the neuro-ophthalmologists at the Mayo Clinic. Thanks for having us here. Dr Mollan: Yeah, it's great to be with you here. I'm Susan Mollan. I'm a consultant neuro-ophthalmologist in Birmingham, England. Dr Nevel: Wonderful. So great to have you both here today, and our listeners. To start us off, talking about your article, can you share with us what you think is the most important takeaway from your article for the practicing neurologist out there? Dr Chen: Yeah, so our article talked about the treatment and monitoring of IIH. And I think one takeaway point is, IIH is becoming much more prevalent now that there's this worldwide obesity epidemic with obesity having- essentially being the largest risk factor for IIH other than female. It's really important to monitor vision because vision loss is often peripheral vision loss at first, which the patient may be completely unaware of. And so, it's important to pair up with an ophthalmologist so you can monitor the papilledema of the visual fields and make sure they don't get permanent vision loss. And in the article, we also talk about- there's been changes in the treatment of severe IIH, where traditionally, we used VP shunts; but there's been a trend toward using more venous sinus stenting in addition to the traditional surgeries. Dr Nevel: Great, thank you. I think probably most of our listeners or a lot of neurologists out there have a pretty good understanding of kind of the basics of the IIH. But can you kind of just go over a few key characteristics of IIH, and maybe some things that are less commonly known or things that are maybe just been kind of better understood over the past decade, perhaps? Dr Mollan: Yes, certainly. I think, as Dr Chen said, it's because this condition is becoming more prevalent, people recognize it. I think it's- we like to go back to the diagnostic criteria so that we're making a very accurate diagnosis. So, the patients may come in to the emergency room with, say, papilledema that's been identified elsewhere or crashing headaches. And it's important to go through that sort of diagnostic pathway, taking a blood pressure, taking a full blood count to make sure the patient is anemic, and then moving forward with that confirmation of papilledema into urgent neuroimaging, whether it's CT or MRI, but including venography to exclude a venous sinus thrombosis. And then if you have no structural lesion that's causing the raised ICP, it's moving forward with your lumbar puncture and carefully checking those pressures. But the patients may not only have crashing headache, they often have pulsatile tinnitus and neck pain. I think some of the features that we're now recognizing is the systemic metabolic effects that are unique to IIH. And so, there's an increased risk of cardiometabolic disease that's over and above what is conferred by obesity. Also, our patients have a sort of maternal health burden where they get impaired fertility, gestational diabetes and preeclampsia. And there's also an associated mental health burden, amongst other things. So we're really starting to understand the spectrum of the disease a bit more. Dr Nevel: Yeah, thank you for that. And that really struck me in your article, how important it is to be aware of those things so that we're making sure that we're managing our whole patient and connecting them with the appropriate providers for some of those other issues that may be associated. For the practicing neurologist out there without all the neuro-ophthalmology equipment, if you will, what should our bedside exam focus on to help us get maybe an early but accurate picture of the patient's visual function when we suspect IIH to be at play, perhaps before they can get in with the neuro-ophthalmologist? Dr Chen: Yeah, I think at the bedside you can still check visual acuity and confrontational visual fields, you know, with finger counting. Of course, you have to know that those are, kind of, crude kind of ways of screening. With papilledema, oftentimes the visual acuity is intact. And the confrontational visual fields aren't as sensitive as automated perimetry. Another important thing will be to do your direct ophthalmoscope and look at the amount of papilledema. If it's grade one or two papilledema on the more mild side, it's actually not vision threatening. It's the higher degrees of papilledema that can cause rapid vision loss. And so, if you look in and you see grade one papilledema, obviously you need to do the full workup, the MRI, MRV, lumbar puncture. But in terms of rapidly getting to an ophthalmologist to screen for vision loss, it's not going to be as important because you're not going to have vision loss at that low grade. If you look in and you see this rip-roaring papilledema, grade five papilledema, that patient is going to be at very severe risk of vision loss. So, I think that exam, looking at the optic nerve can be very helpful. And of course, talking to the patient about symptoms; is there decreased vision Is there double vision from a sixth nerve palsy? Are there transient visual obscurations which would indicate at least a higher degree of papilledema? That'd be helpful as well. Dr Nevel: Great, thank you. And when the patient does get in with a neuro-ophthalmologist, you talk in your article and, of course, in clinical practice, how OCT testing is important to monitor in this condition. Can you provide for the listeners the definition of OCT and how it plays a role in monitoring patients with IIH? Dr Mollan: Sure. So, OCT is short for optical coherence tomography imaging, and really the eye has been at the forefront of OCT alone. Our sort of cardiology colleagues are catching up on the imaging of blood vessels. But what it allows us to do is give us really good cross-sectional, anatomical-level changes that we can see both in the retina and also at the optic nerve head. And it gives us some really good measurements. It's not so good at sort of saying, is this definitely papilledema or not? That sort of lower end of disc elevation. But it is very good at ruling out what we call the pseudopapilledema. So, things like drusens or these other little masses we find underneath the optic nerve head. But in terms of monitoring, because we can longitudinally take these images and the reproducibility is pretty good at the optic nerve head, it allows us to see whether there's direct changes: either the papilledema getting worse or the papilledema getting better at the optic nerve head. It also gives us some indication of what's going on in the ganglion cell layer complex. And that can be helpful when we're thinking about sort of looking at structure versus function. So, ophthalmologists in general, we love OCT; and we spend much more time nowadays looking at the OCT than we really do the back of the eye. And it's just become critical for patients with papilledema to be able to be very accurate from visit to visit to see what's changing. Dr Nevel: How do you determine how frequently somebody needs to see the neuro-ophthalmologist with IIH and how often they need that OCT evaluation? Dr Chen: Once the diagnosis of IIH is made, how often they need to be seen and how frequent they need to be seen depends on the degree of papilledema. And again, OCT is really nice. You can quantify it and then different providers can actually use the same OCT numbers, which is super helpful. But again, if it's grade three papilledema or higher, or article thickness of 200 or higher, I tend to follow them a little bit more closely, trying to treat them more aggressively. Try to get the papilledema down into a safer zone. If it's grade one or two papilledema, we see them less frequently. So, my first visit might be three months out. They come with grade five papilledema, I'm seeing them within a few days to make sure that's papilledema’s come down quickly because we're trying to decide, are they going to need surgery or not? Dr Nevel: Yeah, great. And that's a nice segue into talking a little bit about how we treat patients with IIH after the diagnosis is confirmed. And I'd like to just point out you have a very lovely figure in your article---Figure 5-6,---that I'd like to direct our listeners to read your article and check out that figure, which is kind of an algorithm on how we think about the various treatment options for patients who have IIH, which seems to rely a lot on the degree of presence of papilledema and the presence of vision disturbance. Could you maybe walk us through a little bit about how you think about the different treatment options for patients with IIH and when more urgent surgical intervention might be indicated? Dr Mollan: Yeah, sure. We always find it quite hard in any medical specialty to write these kind of flow diagrams because it's really an individual we're looking at. But these are kind of what we’d say is “broad brushstrokes” into those patients that we worry about, sort of, red disease in those patients, more amber disease. Now obviously, even those patients that may not have severe papilledema, they may have crashing headaches. So, they may be an urgent referral themselves because of that. And so, it's nice to try and work out which end of the spectrum you're working with. If we think of the papilledema, Dr Chen's already laid out the sort of lower end of the prison's scale---our grades one, our grades two---that we're less anxious about. And those patients, we would definitely be having discussions about medical management, which includes acetazolamide therapy; but also thinking about weight management. And it may well be that we talk a little bit further about weight management, but I think it's helpful to sort of coach those conversations after you've made a definite diagnosis. And then laying out the risk that's caused, potentially, the IIH in an individual. And then having a sort of open conversation with them about what changes they can have in their lifestyle alongside thinking about medical therapy. There’s some patients with very low levels of papilledema that we decide not to put on medicines initially. As patients progress up that papilledema grade, we're definitely thinking about medical therapy. And our first line from the IIH treatment trial would be using acetazolamide, but we need to be thinking about using appropriate dosing. So, a lot of the patients that I see can be sent to me with very low doses that may be inappropriate for that person. In the IIHTT they used up to four grams daily in a divided dose. And you do need to counsel your patients when you're putting them on acetazolamide because of the side effects. You've got quite a nice table in this article about the side effects. I think if you get the patient on board, that they understand that they will experience side effects, that is helpful because they will expect it, and then possibly tolerate it a bit better. Moving through to that area where we're more anxious, that visual-threatening papilledema. As Dr Chen said, it's sort of like you look in and it's sort of “blood and thunder” in there. And you need to be getting on and encouraging the ophthalmologist to get a formal assessment of the visual field. It's very difficult to determine exactly the level at which- and we talk about the mean deviation in a lot of our research studies. But in general, it's a combination of things: the patient's journey to get to you, their symptoms, what's going on with the visual field, but what's also happening at the OCT. So, we look in and we see that fluid is seeping towards the fovea. We get very anxious, and those patients may not even have enough time for a rapid escalation of acetazolamide. It may well be at the first presentation, which we would term, like, fulminant; that we'd be thinking about surgical intervention. And I think before I stop, the other thing to say is, the surgical landscape is really changing. So, we're having some good studies coming out in terms of stenting. And so, there is a sort of bracket where it may well be that we are thinking about neuroradiological intervention in an earlier case. They may not quite be at that visual-threatening stage, but they may be resistant to medical treatments. Dr Nevel: Thank you for that. What do you think is a potential pitfall or a mistake to avoid, if you will, in the management of patients with IIH? Dr Chen: I think it's- in terms of pitfalls, I think the potential pitfalls I've seen are essentially patients where we don't necessarily create a good patient physician relationship. Where they don't have buy-ins on the treatment, they don't have buy-ins to come back, and they're lost to follow-up. And these patients can be dangerous, because they could have vision threatening papilledema and if not getting the appropriate treatment---and if they're not monitoring the vision---this can lead to poor outcomes. So, I've definitely seen that happen. As Dr Mollan said, you really have to tell them about the side effects from the medications. If you just take acetazolamide, letting them know the paresthesias and the changes in taste and some of these other side effects, they're going to immediately stop the medication. Again, and these medications do work, proven in the IIH treatment trial. So again, I think that patient-physician relationship is very important to make sure they have appropriate follow up. Dr Nevel: The topic of weight loss in this patient population can be tricky, and I know I talked with Susie in a prior interview about how to approach this topic with our patients in a sensitive and compassionate manner. Once this topic is broached, I find many patients are looking for advice on strategies for weight loss, or potentially medications or other interventions. How do you prioritize or think about the different weight loss strategies or treatments with your patients, and how do you think about the way that you recommend these different treatments or not? Dr Mollan: Yeah. I think that's a really great question because we sort of stray here into a specialty that we have not been trained in. One thing I definitely ask my patients: if they've been on a weight loss journey before, and what's worked for them and what's not worked for them. And within our different healthcare systems, we have access to different tiers of weight management approaches. But for the person sitting in front of me, that possibly there may be a long journey to access more professional care, it's about understanding. iIs there things that are free, such as, we have some apps in the National Health Service which are weight management applications where they can actually just start putting in their calories, their daily calorie intake. And those apps can be quite helpful and guiding in terms of targeting areas, but also informing the patient of what types of foods to avoid in their diet and what types of foods to include in their diet. And with some of the programs that are completely complementary, they also sometimes add on things about exercise. But I think it is a really difficult thing to manage as, say, an ophthalmologist or a neurologist, mainly because it's not our area of expertise. And I think we've all got to find, in our local hospitals and healthcare systems, those pathways where the patients may be able to access nutritional support, and sort of behavioral lifestyle therapy support, all the way through to the new medications for weight loss; and also for some people, bariatric surgery pathways. It's a tricky topic. Dr Nevel: So how should we counsel our patients about what to expect in the future in terms of visual outcomes? Dr Chen: I think a lot of that depends on the degree of papilledema when they present. If a patient comes in with grade five papilledema, that fulminant IIH that Dr Mollan had mentioned, these patients can have very severe vision loss. And even if we treat them very aggressively with high-dose medications and urgent surgical interventions, sometimes they can have permanent vision loss. And so, we counsel them that, you know, there's a strong chance that they're going to have a good amount of vision loss. But some patients, we're very surprised and we get a lot of vision back. So, we kind of set expectations, but we're cautiously optimistic that we can get vision back. If a patient presents with more mild papilledema like grade one or two papilledema, they're most likely not going to have any permanent vision loss as long as we're treating them, we're monitoring their vision, they're coming to their follow-ups. They tend to do very well from a vision perspective. Dr Nevel: That's great, thank you. And you know, ties into what you said earlier about really making sure that, you know, we create good- as with any patient, but good physician-patient relationships so that they, you know, trust us and they come to follow up so we can really monitor their vision appropriately. What do you think is going on in research in this area that's exciting? What do you think one of the next breakthroughs or thing that we need to understand the most about treatment and monitoring of IIH? Dr Chen: I think surgically, venous sinus stenting is going to probably take over the bulk of surgeries. We still need that randomized clinical trial, but we have some amazing outcomes with venous sinus stenting. And there's many efforts on randomized clinical trials for venous sinus stenting. So we'll have those results soon. From a medical standpoint, Dr Mollan can actually say, actually, more about this. Dr Mollan: I completely agree. The GLP-1 receptor agonists, the twofold prong approach: one is the weight loss where these patients, you know, have significant weight loss to put their disease into remission; and the other side of it is whether certain GLP-1s have the ability to reduce intracranial pressure. So, a phase 2 study that we undertook here in Birmingham did show that we were able to reduce intracranial pressure, but we don't think it's a class effect. So, I think the sort of big breakthrough will be looking at novel therapies like xenotide and other drugs that, say, work on the proximal kidney tubule. Are they able to reduce intracranial pressure directly? And I think we are on the cusp of a real breakthrough for this disease. Dr Nevel: Great. Thank you so much for chatting with me today. And I really learned a lot, appreciated the opportunity. I hope our listeners learned something today, too. So again, today I've been interviewing Drs John Chen and Susan Mollan about their article on treatment and monitoring of idiopathic intracranial hypertension, which appears in the most recent issue of Continuum on disorders of CSF dynamics. Be sure to check out Continuum Audio episodes from this and other issues. And thank you to our listeners for joining us today. Dr Monteith: This is Dr Teshamae Monteith, Associate Editor of Continuum Audio. If you've enjoyed this episode, you'll love the journal, which is full of in-depth and clinically relevant information important for neurology practitioners. Use the link in the episode notes to learn more and subscribe. AAN members, you can get CME for listening to this interview by completing the evaluation at continpub.com/audioCME. Thank you for listening to Continuum Audio.
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  • Clinical Features and Diagnosis of Idiopathic Intracranial Hypertension With Dr. Aileen Antonio
    Idiopathic intracranial hypertension (IIH) is characterized by symptoms and signs of unexplained elevated intracranial pressure (ICP) in an alert and awake patient. The condition has potentially devastating effects on vision, headache burden, increased cardiovascular disease risk, sleep disturbance, and depression.  In this episode, Teshamae Monteith, MD, FAAN speaks with Aileen A. Antonio, MD, FAAN, author of the article “Clinical Features and Diagnosis of Idiopathic Intracranial Hypertension” in the Continuum® June 2025 Disorders of CSF Dynamics issue. Dr. Monteith is the associate editor of Continuum® Audio and an associate professor of clinical neurology at the University of Miami Miller School of Medicine in Miami, Florida. Dr. Antonio is an associate program director of the Hauenstein Neurosciences Residency Program at Trinity Health Grand Rapids and an assistant clinical professor at the Michigan State University College of Osteopathic Medicine in Lansang, Michigan. Additional Resources Read the article: Clinical Features and Diagnosis of Idiopathic Intracranial Hypertension Subscribe to Continuum®: shop.lww.com/Continuum Earn CME (available only to AAN members): continpub.com/AudioCME Continuum® Aloud (verbatim audio-book style recordings of articles available only to Continuum® subscribers): continpub.com/Aloud More about the American Academy of Neurology: aan.com Social Media facebook.com/continuumcme @ContinuumAAN Host: @headacheMD Guest: @aiee_antonio Full episode transcript available here Dr Jones: This is Dr Lyell Jones, Editor-in-Chief of Continuum. Thank you for listening to Continuum Audio. Be sure to visit the links in the episode notes for information about earning CME, subscribing to the journal, and exclusive access to interviews not featured on the podcast. Dr Monteith: Hi, this is Dr Teshamae Monteith. Today I'm interviewing Dr Aileen Antonio about her article on clinical features and diagnosis of idiopathic intracranial hypertension, which appears in the June 2025 Continuum issue on disorders of CSF dynamics.  Hi, how are you? Dr Antonio: Hi, good afternoon. Dr Monteith: Thank you for being on the podcast. Dr Antonio: Thank you for inviting me, and it's such an honor to write for the Continuum. Dr Monteith: So why don't you start off with introducing yourself? Dr Antonio: So as mentioned, I'm Aileen Antonio. I am a neuro-ophthalmologist, dually trained in both ophthalmology and neurology. I'm practicing in Grand Rapids, Michigan Trinity Health, and I'm also the associate program director for our neurology residency program. Dr Monteith: So, it sounds like the residents get a lot of neuro-ophthalmology by chance in your curriculum. Dr Antonio: For sure. They do get fed that a lot. Dr Monteith: So why don't you tell me what the objective of your article was? Dr Antonio: Yes. So idiopathic intracranial hypertension, or IIH, is a condition where there's increased intracranial pressure, but without an obvious cause. And with this article, we want our readers---and our listeners right now---to recognize that the typical symptoms and learning about the IIH diagnostic criteria are key to avoiding errors, overdiagnosis, or sometimes even misdiagnosis or underdiagnosis. Thus, we help make the most of our healthcare resources. Early diagnosis and management are crucial to prevent disability from intractable headaches or even vision loss, and it's also important to know when to refer the patients to the appropriate specialists early on. Dr Monteith: So, it sounds like your central points are really getting that diagnosis early and managing the patients and knowing how to triage patients to reduce morbidity and complications. Is that correct? Dr Antonio: That is correct and very succinct, yes. Dr Monteith: And so, are there any more recent advances in the diagnosis of IIH? Dr Antonio: Yes. And one of the tools that we've been using is what we call the optical coherence tomography. A lot of people, neurologists, physicians, PCP, ER doctors; how many among those physicians are well-versed in doing an eye exam, looking at the optic disc? And this is a great tool because it is noninvasive, it is high resolution imaging technique that allows us to look at the optic nerve without even dilating the eye. And we can measure that retinal nerve fiber layer, or RNFL; and that helps us quantify the swelling that is visible or inherent in that optic nerve. And we can even follow that and monitor that over time. So, this gives us another way of looking at their vision and getting that insight as to how healthy is their vision still, along with the other formal visual tests that we do, including perimetry or visual field testing. And then all of these help in catching potentially early changes, early worsening, that may happen; and then we can intervene more easily. Dr Monteith: Great. So, it sounds like there's a lot of benefits to this newer technology for our patients. Dr Antonio: That is correct. Dr Monteith: So, I read in the article about the increased incidence of IIH, and I have to say that I completely agree with you because I'm seeing so much of it in my clinic, even as a headache specialist. And I had a talk with a colleague who said that the incidence of SIH and IIH are similar. And I was like, there's no way. Because I see, I can see several people with IIH just in one day. That's not uncommon. So, tell me what your thoughts are on the incidence, the rising incidence of IIH; and we understand that it's the condition associated with obesity, but it sounds like you have some other underlying drivers of this problem. Dr Antonio: Yes, that is correct. So, as you mentioned, IIH tends to affect women of childbearing age with obesity. And it's interesting because as you've seen that trend, we see more of these IIH cases recently, which seem to correlate with that rising rate of obesity. And the other thing, too, is that this trend can readily add to the burden of managing IIH, because not only are we dealing with the headaches or the potential loss of vision, but also it adds to the burden of healthcare costs because of the other potential comorbidities that may come with it, like cardiovascular risk factors, PCOS, and sleep apnea. Dr Monteith: So why don't we just talk about the diagnosis of IIH? Dr Antonio: IIH, idiopathic intracranial hypertension, is also called pseudotumor cerebri.  It’s essentially a condition where a person experiences increased intracranial pressure, but without any obvious cause. And the tricky part is that the patients, they're usually fully awake and alert. So, there's no obvious tumor, brain tumor or injury that causes the increased ICP. It's really, really important to rule out other conditions that might cause these similar symptoms; again, like brain tumors or even the cerebral venous sinus thrombosis. Many patients will have headaches or visual disturbances like transient visual obscurations---we call them TVOs---or double vision or diplopia. The diplopia is usually related to a sixth nerve palsy or an abducens palsy. Some may also experience some back pain or what we call pulsatile tinnitus, which is that pulse synchronous ringing in their ears. The biggest sign that we see in the clinic would be that papilledema; and papilledema is a term that we only use, specifically use, for those optic nerve edema changes that is only associated with increased intracranial pressure. So, performing of endoscopy and good eye exam is crucial in these patients. We usually use the modified Dandy criteria to diagnose IIH. And again, I cannot emphasize too much that it's really important to rule out other secondary causes to that increased intracranial pressure. So, after that thorough neurologic and eye evaluation with neuroimaging, we do a lumbar puncture to measure the opening pressure and to analyze the cerebrospinal fluid. Dr Monteith: One thing I learned from your article, really just kind of seeing all of the symptoms that you mentioned, the radicular pain, but also- and I think I've seen some papers on this, the cognitive dysfunction associated with IIH. So, it's a broader symptom complex I think than people realize. Dr Antonio: That is correct. Dr Monteith: So, you mentioned TVOs. Tell me, you know, if I was a patient, how would you try and elicit that from me? Dr Antonio: So, I would usually just ask the patient, while you're sitting down just watching TV---some of my patients are even driving as this happens---they would suddenly have these episodes of blacking out of vision, graying out of vision, vision loss, or blurred vision that would just happen, from seconds to less than a minute, usually. And they can happen in one eye or the other eye or both eyes, and even multiple times a day. I had a patient, it was happening 50 times a day for her. It's important to note that there is no pain associated with it most of the time. The other thing too is that it's different from the aura that patients with migraines would have, because those auras are usually scintillating and would have what we call the positive phenomena: the flashing lights, the iridescence, and even the fortification that they see in their vision. So definitely TVOs are not the migraine auras. Sometimes the TVOs can also be triggered by sudden changes in head positions or even a change in posture, like standing up quickly. The difference, though, between that and, like, the graying out of vision or the tunneling vision associated with orthostatic hypotension, is that the orthostatic hypotension would also have that feeling of lightheadedness and dizziness that would come with it. Dr Monteith: Great. So, if someone feels lightheaded, less likely to be a TVO if they're bending down and they have that grain of vision. Dr Antonio: That is correct. Dr Monteith: Definitely see patients like that in clinic. And if they have fluoride IIH, I'm like, I'll call it a TVO; if they don't, I’m like, it's probably more likely to be dizziness-related. And then we also have patient migraines that have blurriness that's nonspecific, not necessarily associated with aura. But I think in those patients, it's usually not seconds long, it's usually probably longer episodes of blurriness. Would you agree there, or…? Dr Antonio: I would agree there, and usually the visual aura would precede the headache that is very characteristic of their migraine, very stereotypical for their migraines. And then it would dissipate slowly over time as well. With TVOs, they're brisk and would not last, usually, more than a minute. Dr Monteith: So, why don't we talk about routine imaging? Obviously, ordering an MRI, and I read also getting an MRV is important. Dr Antonio: It is very important because, one: I would say IIH is also a diagnosis of exclusion. We need to make sure that the increased ICP is not because of a brain tumor or not because of cerebral venous sinus thrombosis. So, it's important to get the MRI of the brain as well as the MRV of the head. Dr Monteith: Do you do that for all patients’ MRV, and how often do you add on an orbital study? Dr Antonio: I usually do not add on an orbital study because it's not really going to change my management at that point. I really get that MRI of the brain. Now the MRV, for most of my patients, I would order it already just because the population that I see, I don't want to lose them. And sometimes it's that follow-up, and that is the difficult part; and it's an easy add on to the study that I'm going to order. Again, it depends with the patient population that you have as well, and of course the other symptoms that may come with it. Dr Monteith: So, why don't we talk a little bit about CSF reading and how these set values, because we get people that have readings of 250 millimeters of water quite frequently and very nonspecific, questionable IIH. And so, talk to me about the set value. Dr Antonio: Right. So, the modified Dandy criteria has shown that, again, we consider intracranial pressure to be elevated for adults if it's above 250 millimeters water; and then for kids if it's above 280 millimeters of water. Knowing that these are taken in the left lateral decubitus position, and assuming also that the patients were awake and not sedated during the measurement of the CSF pressure. The important thing to know about that is, sometimes when we get LPs under fluoroscopy or under sedation, then these can cause false elevation because of the hypercapnia that elevated carbon dioxide, and then the hypoventilation that happens when a patient is under sedation. Dr Monteith: You know, sometimes you see people with opening pressures a little bit higher than 25 and they're asymptomatic. Well, the problem with these opening pressure values is that they can vary somewhat even across the day. People around 25, you can be normal, have no symptoms, and have opening pressure around 25- or 250; and so, I'm just asking about your approach to the CSF values. Dr Antonio: So again, at the end of the day, what's important is putting everything together. It's the gestalt of how we look at the patient. I actually had an attending tell me that there is no patient that read the medical textbook. So, the, the important thing, again, is putting everything together. And what I've also seen is that some patients would tell me, oh, I had an opening pressure of 50. Does that mean I'm in a dire situation? And they're so worried and they just attach to numbers. And for me, what's important would be, what are your symptoms? Is your headache, right, really bad, intractable? Number two: are you losing vision, or are you at that cusp where your optic nerve swelling or papilledema is so severe that it may soon lead to vision loss? So, putting all of these together and then getting the neuroimaging, getting the LP. I tell my residents it's like icing on the cake. We know already what we're dealing with, but then when we get that confirmation of that number… and sometimes it's borderline, but this is the art of neurology. This is the art of medicine and putting everything together and making sure that we care and manage it accordingly. Dr Monteith: Let's talk a little bit about IIH without papilledema. Dr Antonio: So, let's backtrack. So, when a patient will fit most of the modified Dandy criteria for IIH, but they don't have the papilledema or they don't have abducens palsy, the diagnosis then becomes tricky. And in these kinds of cases, Dr Friedman and her colleagues, when they did research on this, suggested that we might consider the diagnosis of IIH. And she calls this idiopathic intracranial hypertension without papilledema, IIHWOP. They say that if they meet the other criteria for modified Dandy but show at least three typical findings on MRI---so that flattening of the posterior globe, the tortuosity of the optic nerves, the empty sella or the partially empty sella, and even the narrowing of the transverse venous sinuses---so if you have three of these, then potentially you can call these cases as idiopathic intracranial hypertension without papilledema. Dr Monteith: Plus, the opening pressure elevation. I think that's key, right? Getting that as well. Dr Antonio: Yes. Sometimes IIHWOP may still be a gray area. It's a debate even among neuro-ophthalmologists, and I bet even among the headache specialists. Dr Monteith: Well, I know that I've had some of these conversations, and it's clear that people think this is very much overdiagnosed. So, that's why I wanted to plug in the LP with that as well. Dr Antonio: Right. And again, we have not seen yet whether is, this a spectrum, right? Of that same disease just manifesting differently, or are they just sharing a same pathway and then diverging? But what I want to emphasize also is that the treatment trials that we've had for IIH do not include IIHWOP patients. Dr Monteith: That is an important one. So why don't you wrap this up and tell our listeners what you want them to know? Now's the time. Dr Antonio: So, the- again, with IIH, with idiopathic intracranial hypertension, what is important is that we diagnose these patients early. And I think that some of the issues that come into play in dealing with these patients with IIH is that, one: we may have anchoring bias. Just because we see a female with obesity, of reproductive age, with intractable headaches, it does not always mean that what we're dealing with is IIH. The other thing, too, is that your tools are already available to you in your clinic in diagnosing IIH, short of the opening pressure when you get the lumbar puncture. And I need to emphasize the importance of doing your own fundoscopy and looking for that papilledema in these patients who present to you with intractable headaches or abducens palsy. What I want people to remember is that idiopathic intracranial hypertension is not optic nerve sheath distension. So, these are the stuff that you see on neuroimaging incidentally, not because you sent them, because they have papilledema, or because they have new headaches and other symptoms like that. And the important thing is doing your exam and looking at your patients. Dr Monteith: Today, I've been interviewing Dr Aileen Antonio about her article on clinical features and diagnosis of idiopathic intracranial hypertension, which appears in the most recent issue of Continuum on disorders of CSF dynamics. Be sure to check out Continuum Audio episodes from this and other issues, and thank you to our listeners for joining today. Thank you again. Dr Antonio: Thank you. Dr Monteith: This is Dr Teshamae Monteith, Associate Editor of Continuum Audio. If you've enjoyed this episode, you'll love the journal, which is full of in-depth and clinically relevant information important for neurology practitioners. Use the link in the episode notes to learn more and subscribe. AAN members, you can get CME for listening to this interview by completing the evaluation at continpub.com/audioCME. Thank you for listening to Continuum Audio.
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  • Radiographic Evaluation of Spontaneous Intracranial Hypotension With Dr. Ajay Madhavan
    Recently, sophisticated myelographic techniques to precisely subtype and localize CSF leaks have been developed and refined. These techniques improve the detection of various types of CSF leaks thereby enabling targeted therapies. In this episode, Katie Grouse, MD, FAAN, speaks with Ajay A. Madhavan, MD, author of the article “Radiographic Evaluation of Spontaneous Intracranial Hypotension” in the Continuum® June 2025 Disorders of CSF Dynamics issue. Dr. Grouse is a Continuum® Audio interviewer and a clinical assistant professor at the University of California San Francisco in San Francisco, California. Dr. Madhavan is assistant professor of radiology at the Mayo Clinic in Rochester, Minnesota. Additional Resources Read the article: Radiographic Evaluation of Spontaneous Intracranial Hypotension Subscribe to Continuum®: shop.lww.com/Continuum Earn CME (available only to AAN members): continpub.com/AudioCME Continuum® Aloud (verbatim audio-book style recordings of articles available only to Continuum® subscribers): continpub.com/Aloud More about the American Academy of Neurology: aan.com Social Media facebook.com/continuumcme @ContinuumAAN Full episode transcript available here Dr Jones:  This is Dr Lyell Jones, Editor-in-Chief of Continuum. Thank you for listening to Continuum Audio. Be sure to visit the links in the episode notes for information about earning CME, subscribing to the journal, and exclusive access to interviews not featured on the podcast. Dr Grouse:  This is Dr Katie Grouse. Today I'm interviewing Dr Ajay Madhavan about his article on Radiographic Evaluation of Spontaneous Intracranial Hypotension, which he wrote with Dr Levi Chazen. This article appears in the June 2025 Continuum issue on disorders of CSF dynamics. Welcome to the podcast, and please introduce yourself to our audience. Dr Madhavan:  Hi, thanks a lot, Katie. Yeah, so I’m Ajay Madhaven. I'm a neuroradiologist at the Mayo Clinic in Rochester, Minnesota. I did all my training here, so, I've been here for a long time. And I have a lot of interest in spinal CSF leaks, and I do a lot of that work. And so I'm really excited to be talking about this article with you. Dr Grouse:  I'm really excited too. And in fact, it's such a pleasure to have you here talking today on this topic. I know a lot's changed in this field, and I'm sure many of our listeners are really interested in learning about the developments and imaging techniques to improve detection and treatment of CSF leaks, especially since maybe we've learned about this in training. I want to start by asking you what you think is the most important takeaway from your article. Dr Madhavan:  Yeah, that's a great question. I think---and you kind of already alluded to it---I think the main thing is, I hope people recognize that this field has really changed a lot in the last five to ten years, through a lot of multi-institutional collaboration and also collaboration between different specialties. We've learned a lot about different types of spinal CSF leaks, how we can recognize the disease, particularly the types of myelography that we need to be using to accurately localize and treat these leaks. Those are the things that have really evolved in the last five to ten years, and they've really helped us improve these patients’ lives. Dr Grouse:  Can you remind us of the different common types of spinal leaks that can cause spontaneous intracranial hypotension? Dr Madhavan:  Yeah, so there are a number of different spinal CSF leaks, types, and I would say the three most common ones that really most people should try to be aware of and cognizant of are: first, ventral dural tears. So those are, like, just physical holes in the dura. And they're usually caused by little bone spurs that come from the vertebral columns. So, they're often patients who have some degenerative changes in their spine. And those are really very common. Another type of spinal CSF leak that we commonly see is a lateral dural tear. So that's like the same thing in a slightly different location. So instead of being in the front, it's off to the side of the dura laterally. And so, it's also just a hole in the dura. And then the third and most recently discovered type of spinal CSF leak is a CSF-venous fistula. So those are direct connections between the subarachnoid space and little paraspinal vein. And it took us a long time to even realize that this was a real pathology. But now that it's been recognized, we've found that this is actually quite common. So those three types of leaks are probably the three most common that we see. And there's certainly others out there, but I would say over 90% of them fall into one of those three categories. Dr Grouse:  That's a great review, thank you. Just as another quick review, as we talk more about this topic, can you remind us of some of the most common or typical brain imaging findings that you'll see in cases of spontaneous intracranial hypotension? Dr Madhavan:  Yeah, absolutely. So, when you do a brain MRI in a patient who has spontaneous intracranial hypotension, you will usually, though not always, see typical brain MRI abnormalities. And I kind of think of those as falling into three different categories. So, the first one I think of is dural enhancement or thickening. So that's enlargement or engorgement of the dura, the pachymeninges, and enhancement on postgadolinium imaging. So, that's kind of the first category. The second is that, when you lose spinal fluid volume, other things often expand to take up the space. So, for example, you can get distension or enlargement of the dural venous sinuses, and sometimes you can also get subdural food collections or hematomas. They can arise spontaneously. And I kind of think of those as, you know, you, you've lost the cerebrospinal fluid volume and something else is kind of filling up the space. And then the third category is called brain sagging. And that's a constellation of findings where the posterior fossa structures and the pituitary gland in the cell have become abnormal because you've lost the fluid that normally cushions those structures and causes them to float up. For example, the brain stem will sag down, the distance between the mammillary body and the ponds may become reduced. The suprasellar cistern space may be reduced such that the optic chiasm becomes very close to the pituitary gland, and the prepontine cistern may also become reduced in size. And there are various measurements that can be used to determine whether something is subtly abnormal. But just generally speaking, those are really the three categories of brain MRI abnormalities you'll see. Dr Grouse:  That was a great review. And of course, I think in many times when we are thinking about or suspecting this diagnosis, we may be lucky to find those imaging findings to reinforce a diagnosis. Because as it turns out, after reading your article, I was really surprised to find out that in as many as 19% of cases we actually see normal brain imaging, which really was a surprise to me, I have to say. And I think that this really encompasses why spontaneous intercranial hypotension is such a difficult diagnosis to make. I think a lot of us struggle with how far to take the workup when, you know, spontaneous intercranial hypotension is clinically suspected, but multiple imaging studies are normal. Do you have any guidance on how to approach these more difficult cases? Dr Madhavan:  So, that's a really good question. And you know, it's- as you can imagine, that's a topic that comes up in most meetings where people discuss this, and it's been a continued challenge. And so, like you said, about 19 or 20% of patients who have this disease can have a, a normal brain MRI. And we've tried to do some work to figure out why that is and how we can identify patients who still have the disease. And I can just provide, I guess, some tips that have helped me in my clinical practice. One thing is, if I ever see a patient with a normal brain MRI where this disease is clinically suspected---for example, maybe they have orthostatic headaches or other very typical symptoms and we don't know why, but their brain MRI is normal---the first thing I do is I try to look back at their old imaging. So many times, these patients who present to us at Mayo, who, when we do their MRI scan here, their brain MRI looks normal… if you really look back at imaging that they've had done elsewhere---maybe even two to three years prior---at the time their symptoms started, they actually had some abnormalities. So, I might see that a patient, two years ago, had dural enhancement that spontaneously resolved; but now they still have symptoms of SIH and they may still have a CSF leak that we can find and treat, but their brain MRI has, for whatever reason, normalized. So, I always start by looking back at old imaging, and I found that to be very helpful. The other thing is, if you see a patient with a normal brain MRI, it's also important to look at their spine MRI because that can provide clues that might suggest that they could still have a spinal CSF leak. And the two things I look for on the spine MRI: one, if there's any extradural CSF. So, spinal fluid outside of where it's supposed to be within the confines of the subarachnoid space. And you know, really, if you see extradural CSF, you know they probably have a spinal fluid leak somewhere. Even if their brain MRI is normal, that just gives you the information that there is a dural tear probably somewhere. And so, in those patients we’ll definitely still proceed to myelography or other testing, even if they have a normal brain MRI. And then the last thing I look for is whether or not they have prominent meningeal diverticula. Patients with CSF venous fistulas almost always have one or more prominent diverticula on their spine along the nerve root sleeves. And that's probably because most of these fistulas come from nerve root sleeve diverticula. We don't completely understand the pathogenesis of CSF venous fistulas, but they're clearly associated with meningeal diverticula. So, if I see a patient who has a normal brain MRI, but I see on their spine MRI that they have many meningeal diverticula that are relatively prominent, that makes me more inclined to be a little bit more aggressive in doing myelography to find a CSF leak. And then I look at other demographic features, too. So, for example, elevated BMI and older age are associated with CSF venous fistulas. So, that can help you determine whether or not it's warranted to go on to more advanced imaging, too. So those are all just a variety of different things that we've used to help us. Dr Grouse:  Thank you for sharing that. I wanted to go on to say that, you know, reading your article, of course, as you mentioned, you alluded to the fact there's lots of new imaging modalities out there. It was very illuminating and just an excellent resource for the options that exist and when they're useful. You did a great job summarizing it. And I encourage our readers to check out your article, to refresh themselves, update themselves on what's happened in this space. And of course, we can't summarize them all today, but I was wondering if you could possibly walk us through a hypothetical case of a patient who comes in with a history very suspicious for SIH? How would you approach this patient? Say you have gotten imaging that suggested that there is a spinal fluid leak and now you have to figure out where it is. Dr Madhavan:  Yeah. So, you know, I think the most typical scenario it'll be a patient who has been seen by one of my excellent neurology colleagues and they've done a brain MRI and they've made the diagnosis through a combination of clinical information and brain MRI finding. And then the next thing we'll do always is, we'll obtain a spine MRI. So, I think of the purpose of the spine MRI as to determine what type of spinal fluid leak they have. On the spine MRI, if you see extradural CSF, those patients essentially always will have a dural tear. And it may be a ventral dural tear or a lateral dural tear. But if you see extradural CSF, that is pretty much what they have. And conversely, if you don't see extradural CSF---if you just see, for example, many meningeal diverticula, but you don't see anything else particularly abnormal---most of those patients have a CSF venous fistula, just common things being common. So I use the spine MRI to determine what type of leak they have. And then the next thing I think about is, okay, I'm going to do a myelogram on this patient. How do I want to position them? Because it turns out that positioning is probably the most important factor for finding these spinal fluid leaks. You have to have the patient positioned correctly to find the leak that you're trying to localize. And so, if I suspect they have a ventral dural tear, I will always position those patients prone for their myelogram. And I might do one of many different types of myelograms. And, you know, the article talks about things like digital subtraction myelography and dynamic CT myelography. And you can find any of these leaks with any of those techniques, but you just have to have the patient positioned correctly. So, if I think I have a ventral dural tear, I’ll put them prone for the myelogram. If I think they have a lateral dural tear, I'll put them in the cubitus position for the myelogram. And also, if they- if I think they have a CSF-venous fistula, I'll also put them in the decubitus position. Obviously if you're putting them in the decubitus position, you have to decide whether it's going to be left or right side down. So that may require a two-day exam. Sometimes you don't have to; in many cases, we're able to just do everything in one day. But those are all the different factors I think about when I'm trying to determine how I'm going to work those patients up further. So, I really use the spine MRI chiefly to think about what type of leak they're going to have and how I'm going to plan the myelogram. Dr Grouse:  That's really great. And it's, I think, really nice to emphasize how much the positioning matters in all this, which I think is not something we've been classically taught as far as the diagnosis of spinal leaks. Another thing I'm really interested in your opinion on is, you talked a lot about how to optimize and what can make you successful at diagnosis. I'm curious what you think one of the easiest mistakes to make or, you know, that we should hopefully avoid when treating patients with this disease. Dr Madhavan:  Yeah. And I think, you know, one other thing that's been discussed a lot in this topic… you know, we've talked about the patients with a normal brain MRI. Another barrier or challenge particularly with CSF-venous fistulas is, sometimes they can be very subtle on imaging. So, it's not always you see it very definitive CSF-venous fistula where you can say, like, there's no question, that's a fistula. There are many times where we do a good-quality myelogram and we see something that looks, like, possible for a CSF venous fistula, or probable. If I had to put a number on it, maybe there's a 50 to 70% chance of real. So, in those cases, we end up wondering, like, should we treat this suspected leak? And I think one common mistake  or one thing that needs to be looked at further is, how do we handle these patients where we don't know whether the fistula is real or not? That's usually something where I will have a discussion with the patient, and I'm usually just very upfront with him about my interpretation of the imaging. I'll just tell them, we did a good-quality myelogram. You did a great job. We got good images. I don't see anything definitive, but I see this thing that I think has maybe a 60% chance of being real. And then I'll confer with one of my neurology colleagues and we'll decide whether it's worth treating that or not. And we'll just be very upfront with a patient about whether- about the likelihood of its success and what their long-term prognosis is. And oftentimes we let them make the decision. But I think that remains to be one of the big challenges is, how do we treat these patients who have suspected leaks that are not definitive on imaging. Dr Grouse:  That sounds absolutely like an important area where there can be problems, so I appreciate that insight. I'm interested what you think in your article would come as the biggest surprise to our listeners who may not have kept up as much with all of the changes that have happened in recent years? Dr Madhavan:  One of the things that was certainly, at least, a surprise to me as I was going through my training and learning about this topic is how diverse myelography has really become. You know, when I was a radiology resident, I learned about myelography as this thing that we've been doing for 30 to 40 years. And historically we've used myelograms just to look for degenerative changes: disc bulges, you know, disc herniations and things like that. Now that MRI is more prevalent, we don't use it as much, but it has turned out that it has a very big role in patients with spinal fluid leaks. Furthermore, something that I've learned is just how diverse these different types of myelograms have become. It used to kind of be just that a myelogram is a myelogram is a myelogram, but now we have different types of positioning, different types of equipment that we use. We vary the timing between contrast injection and imaging to optimize success for finding spinal fluid leaks. So, I think many times I talk to people who may not be as familiar with this field and they're surprised at just how diverse that has become and how sophisticated some of the various myelographic techniques have become and how much that really makes a difference in being able to accurately diagnose these patients. Dr Grouse:  Well, I can say it was a surprise to me. Even as someone who does treat quite a few patients with this condition, I was surprised to see the breadth of different options that have become available. And then kind of a follow-up to that, what do you think the current area of controversy is in this area of diagnosis and treatment? Dr Madhavan:  The biggest ones are ones you've sort of already alluded to. So, one big one is, how far do we go in patients who have a normal brain MRI who still have a clinical suspicion of the disease? And sometimes it's really hard, because sometimes you will find patients who clinically have a very strong case for having spontaneous intracranial hypotension. You look at them, they have very acute-onset orthostatic headaches. There's no better explanation for their symptoms that we know of. And it's hard to know what to do with those patients, because some of them want to continue to undergo diagnostic workup, but you can only do so many myelograms and you can only do so much with this diagnostic workup that requires some radiation dose before it becomes very challenging. That's a major point of just, I guess, ongoing research as to what can we do better for that subset of patients. Fortunately, it's not all of them, it's a subset of them, but I think we could help those patients better in the future as we learn more about the disease. So that's one. And the other one is treating these equivocal findings, like I discussed.  And where should our threshold be to treat a patient, and what type of treatment should we do in patients where we don't know whether a leak is real? Should we just do a very noninvasive- relatively noninvasive blood patch? Do we do an embolization where we're leaving a foreign body there? Is it worth sending those patients to surgery? Those are all unanswered questions and things that continue to spark ongoing debate. Dr Grouse:  Do you think that there's going to be any new big breakthroughs, or even, do you know of any big developments on the horizon that we should be keeping our eyes out for? Dr Madhavan:  You know, I think for me the biggest thing is, imaging is dramatically improving. We talked a little bit about photon counting detector CT in our article, and that's one of the newest and best techniques for imaging these patients because it has very, very high resolution, it has a lower radiation dose, it has allowed us to find leaks that we were not able to find before. And there are other high-resolution modalities that are emerging and becoming more accessible to things like cone beam CT which we do in addition to digital subtraction myelography. And on top of that, we've started to use AI-based tools to make images look a lot better. So, there are various AI algorithms that have come out that allow us to remove artifacts from imaging. They help us image patients with a bigger body habitus better without running into a lot of imaging artifacts. They help us reduce noise in imaging. They can just give us better-quality images and aid us in the diagnosis. For me as a radiologist, those are some of the most exciting things. We're finding less invasive ways with less radiation to better diagnose these patients with just better-quality imaging. Dr Grouse:  Well, that is definitely something to be excited about. So, I just want to thank you so much for talking with us today. It's been such an interesting, informative discussion and a real privilege to talk with you about this important topic. Dr Madhavan:  Yeah, thanks so much. I really appreciate the time to talk with you, and I look forward to seeing the article out there and hopefully getting some interesting questions. Dr Grouse:  Again, today I've been interviewing Dr Ajay Madhavan about his article on Radiographic Evaluation of Spontaneous Intracranial Hypotension, which he wrote with Dr Levi Chasen. This article appears in the most recent issue of Continuum on disorders of CSF dynamics. Be sure to check out Continuum Audio episodes from this and other issues, and thank you to our listeners for joining today. Dr Monteith: This is Dr Teshamae Monteith, Associate Editor of Continuum Audio. If you've enjoyed this episode, you'll love the journal, which is full of in-depth and clinically relevant information important for neurology practitioners. Use the link in the episode notes to learn more and subscribe. AAN members, you can get CME for listening to this interview by completing the evaluation at continpub.com/audioCME. Thank you for listening to Continuum Audio.
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