Podcasts about Continuum

In this episode, Lyell K. Jones Jr, MD, FAAN, speaks with Michael S. Okun, MD, FAAN, who served as the guest editor of the August 2025 Movement Disorders issue. They provide a preview of the issue, which publishes on August 1, 2025. 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. Okun is the director at Norman Fixel Institute for Neurological Diseases and distinguished professor of neurology at University of Florida in Gainesville, Florida. Additional Resources Read the issue: continuum.aan.com Subscribe to Continuum®: shop.lww.com/Continuum 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 Guest: @MichaelOkun Full episode transcript available here: Dr Jones: Our ability to move through the world is one of the essential functions of our nervous system. Gross movements like walking ranging down to fine movements with our eyes and our hands, our ability to create and coordinate movement is something many of us take for granted. So what do we do when those movements stop working as we intend? Today I have the opportunity to speak with one of the world's leading experts on movement disorders, Dr Michael Okun, about the latest issue of Continuum on Movement Disorders. 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 subscribing to the journal, listening to verbatim recordings of the articles, and exclusive access to interviews not featured on the podcast. Dr Jones: This is Dr Lyle Jones, Editor-in-Chief of Continuum: Lifelong Learning in Neurology. Today, I'm interviewing Dr Michael Okun, who is Continuum's guest editor for our latest issue on movement disorders. Dr Okun is the Adelaide Lackner Distinguished Professor of Neurology at the University of Florida in Gainesville, where he's also the director of the Norman Fixel Institute for Neurological Diseases. Dr Okun, welcome, and thank you for joining us today. Why don't you introduce yourselves to our listeners?  Dr Okun: It's great to be here today. And I'm a neurologist. Everybody who knows me knows I'm pretty simple. I believe the patient's the sun and we should always orbit around the person with disease, and so that's how I look at my practice. And I know we always participate in a lot of research, and I've got a research lab and all those things. But to me, it's always the patients and the families first. So, it'll be great to have that discussion today.  Dr Jones: Yeah, thank you for that, Dr Oaken. Obviously, movement disorders is a huge part of our field of neurology. There are many highly prevalent conditions that fit into this category that most of our listeners will be familiar with: idiopathic Parkinson's disease, essential tremor, tic disorders and so on. And having worked with trainees for a long time, it's one of the areas that I see a lot of trainees gravitate to movement disorders. And I think it's in part because of the prevalence; I think it's in part because of the diversity of the specialty with treatment options and DBS and Botox. But it's also the centrality of the neurologic exam, right? That's- the clinical examination of the patient is so fundamental. And we'll cover a lot of topics today with some questions that I have for you about biomarkers and new developments in the field. But is that your sense too, that people are drawn to just the old-fashioned, essential focus on the neurologic encounter and the neurologic exam? Dr Okun: I believe that is one of the draws to the field of movement. I think that you have neurologists from all over the world that are really interested and fascinated with what things look like. And when you see something that's a little bit, you know, off the normal road or off the normal beaten path… and we are always curious. And so, I got into movement disorders, I think, accidentally; I think even as a child, I was looking at people who had abnormal movements and tremors and I was very fascinated as to why those things happened and what's going on in the brain. And, you know, what are the symptoms and the signs. And then later on, even as my own career developed, that black bag was so great as a neurologist. I mean, it makes us so much more powerful than any of the other clinicians---at least in my biased opinion---out on the wards and out in the clinic. And, you know, knowing the signs and the symptoms, knowing how to do a neurological examination and really walking through the phenomenology, what people look like, you know, which is different than the geno- you know, the genotypes, what the genes are. What people look like is so much more important as clinicians. And so, I think that movement disorders is just the specialty for that, at least in my opinion. Dr Jones: And it helps bring it back to the patient. And that's something that I saw coming through the articles in this issue. And let's get right to it. You've had a chance to review all these articles on all these different topics across the entire field of movement disorders. As you look at that survey of the field, Dr Okun, what do you think is the most exciting recent development for patients with movement disorders?  Dr Okun: I think that when you look across all of the different specialties, what you're seeing is a shift. And the shift is that, you know, a lot of people used to talk in our generation about neurology being one of these “diagnose and adios” specialties. You make the diagnosis and there's nothing that you can do, you know, about these diseases. And boy, that has changed. I mean, we have really blown it out of the water. And when you look at the topics and what people are writing about now and the Continuum issue, and we compare that the last several Continuum issues on movement disorders, we just keep accumulating a knowledge base about what these things look like and how we can treat them. And when we start thinking about, you know, all of the emergence of the autoimmune disorders and identifying the right one and getting something that's quite treatable. Back in my day, and in your day, Lyle, we saw these things and we didn't know what they were. And now we have antibodies, now we can identify them, we can pin them down, and we can treat many of them and really change people's lives. And so, I'm really impressed at what I see in changes in identification of autoimmune disorders, of channelopathies and some of the more rare things, but I'm also impressed with just the fundamental principles of how we're teaching people to be better clinicians in diseases like Parkinson's, Huntington's, ataxia, and Tourette. And so, my enthusiasm for this issue of Continuum is both on, you know, the cutting edge of what we're seeing based on the identification on our exams, what we can do for these people, but also the emergence of how we're shifting and providing much better care across a continuum for folks with basal ganglia diseases. Dr Jones: Yeah, I appreciate that perspective, Dr Okun. One of the common themes that I saw in the issue was with these new developments, right, when you have new tools like new diagnostic biomarker tools, is the question of if and when and how to integrate those into daily clinical practice, right? So, we've had imaging biomarkers for a while, DAT scans, etc. For patients with idiopathic Parkinson disease, one of the things that I hear a lot of discussion and controversy about are the seed amplification assays as diagnostic biomarkers. What can you tell us about those? Are those ready for routine clinical use yet?  Dr Okun: I think the main bottom-line point for folks that are out there trying to practice neurology, either in general clinics or even in specialty clinics, is to know that there is this movement toward, can we biologically classify a disease? One of the things that has, you know, really accelerated that effort has been the development of these seed amplification assays, which---in short for people who are listening---are basically, we “shake and bake” these things. You know? We shake them for like 20 hours and we use these prionlike proteins, and we learn from diseases like prion disease how to kind of tag these things and then see, do they have degenerative properties? And in the case of Parkinson's disease, we're able to do this with synuclein. That is the idea of a seed amplification assay. We're able to use this to see, hey, is there synuclein present or not in this sample? And people are looking at things like cerebrospinal fluid, they're looking at things like blood and saliva, and they're finding it. The challenge here is that, remember- and one of the things that's great about this issue of Continuum is, remember, there are a whole bunch of different synucleinopathies. So, Dr Jones, it isn't just Parkinson's disease. So, you've got Parkinson's disease, you've got Lewy body, you know, and dementia with Lewy bodies. You've got, you know, multiple system atrophy is within that synucleinopathy, you know, group primary autonomic failure… so not just Parkinson's disease. And so, I think we have to tap the brakes as clinicians and just say, we are where we are. We are moving in that direction. And remember that a seed amplification assay gives you some information, but it doesn't give you all the information. It doesn't forgive you looking at a person over time, examining them in your clinic, seeing how they progress, seeing their response to dopamine- and by the way, several of these genes that are associated with Parkinson; and there's, you know, less than 20% of Parkinson is genetic, but several of these genes, in a solid third---and in some cases, in some series, even more---miss the synuclein assay, misses, you know, the presence of a disease like Parkinson's disease. And so, we have to be careful in how we interpret it. And I think we're more likely to see over time a gemish: we're going to smush together all this information. We're going to get better with MRIs. And so, we're actually doing much better with MRIs and AI-based intelligence. We've got DAT scans, we've got synuclein assays. But more than anything, everybody listening out there, you can still examine the person and examine them over time and see how they do over time and see how they do with dopamine. And that is still a really, really solid way to do this. The synuclein assays are probably going to be ready for prime time more in choosing and enriching clinical trials populations first. And you know, we're probably 5, 10 years behind where Alzheimer's is right now. So, we'll get there at some point, but it's not going to be a silver bullet. I think we're looking at these are going to be things that are going to be interpreted in the context for a clinician of our examination and in the context of where the field is and what you're trying to use the information for. Dr Jones: Thank you for that. And I think that's the general gestalt I got from the articles and what I hear from my colleagues. And I think we've seen this in other domains of neurology, right? We have the specificity and sensitivity issues with the biomarkers, but we also have the high prevalence of copathology, right? People can have multiple different neurodegenerative problems, and I think it gets back to that clinical context, like you said, following the patient longitudinally. That was a theme that came out in the idiopathic Parkinson disease article. And while we're on Parkinson disease, you know, the first description of that was what, more than two hundred years ago. And I think we're still thinking about the pathophysiology of that disorder. We understand risk factors, and I think many of our listeners would be familiar with those. But as far as the actual cause, you know, there's been discussion in recent years about, is there a role of the gut microbiome? Is this a prionopathic disorder? What's your take on all of that?  Dr Okun: Yeah, so it's a great question. It's a super-hot area right now of Parkinson. And I kind of take this, you know, apart in a couple of different ways. First of all, when we think about Parkinson disease, we have to think upstream. Like, what are the cause and causes? Okay? So, Parkinson is not one disease, okay? And even within the genes, there's a bunch of different genes that cause it. But then we have to look and say, well, if that's less than 20% depending on who's counting, then 80% don't have a single piece of DNA that's closely associated with this syndrome. And so, what are we missing with environment and other factors? We need to understand not what happens at the end of the process, not necessarily when synuclein is clumping- and by the way, there's a lot of synuclein in the brains normally, and there's a lot of Tau in people's brains who have Parkinson as well. We don't know what we don't know, Dr Jones. And so when we begin to think about this disease, we've got to look upstream. We've got to start to think, where do things really start? Okay? We've got to stop looking at it as probably a single disease or disorder, and it's a circuit disorder. And then as we begin to develop and follow people along that pathway and continuum, we're going to realize that it's not a one-size-fits-all equation when we're trying to look at Parkinson. By the way, for people listening, we only spend two to three cents out of every dollar on prevention. Wouldn't prevention be the best cure, right? Like, if we were thinking about this disease. And so that's something that we should be, you know, thinking about. And then the other is the Global Burden of Disease study. You know, when we wrote about this in a book called Ending Parkinson's Disease, it looked like Parkinson's was going to double by 2035. The new numbers tell us it's almost double to the level that we expected in 2035 in this last series of numbers. So, it's actually growing much faster. We have to ask why? Why is it growing faster? And then we have lots of folks, and even within these issues here within Continuum, people are beginning to talk about maybe these environmental things that might be blind spots. Is it starting in our nose? Is it starting in our gut? And then we get to the gut question. And the gut question is, if we look at the microbiomes of people with Parkinson, there does seem to be, in a group of folks with Parkinson, a Parkinson microbiome. Not in everyone, but if you look at it in composite, there seems to be some clues there. We see changes in Lactobacillus, we see some bacteria going up that are good, some bacteria going down, you know, that are bad. And we see flipping around, and that can change as we put people on probiotics and we try to do fecal microbiota transplantations- which, by the way, the data so far has not been positive in Parkinson's. Doesn't mean we might not get there at some point, but I think the main point here is that as we move into the AI generation, there are just millions and millions and millions of organisms within your gut. And it's going to take more than just our eyes and just our regular arithmetic. You and I probably know how to do arithmetic really well, but this is, like, going to be a much bigger problem for computers that are way smarter than our brains to start to look and say, well, we see the bacteria is up here. That's a good bacteria, that's a good thing or it's down with this bacteria or this phage or there's a relationship or proportion that's changing. And so, we're not quite there. And so, I always tell people---and you know, we talk about the sum in the issue---microbiomes aren't quite ready for prime time yet. And so be careful, because you could tweak the system and you might actually end up worse than before you started. So, we don't know what we don't know on this issue.  Dr Jones: And that's a great point. And one of the themes they're reading between the lines is, we will continue to work on understanding the bio-pathophysiology, but we can't wait until that day to start managing the risk factors and treating patients, which I think is a good point. And if we pivot to treatment here a little bit, you know, one of the exciting areas of movement disorders---and really neurology broadly, I think movement disorders has led the field in many ways---is bioelectronic therapy, or what one of my colleagues taught me is “electroceutical therapy”, which I think is a wonderful term. Dr Okun, when our listeners are hearing about the latest in deep brain stimulation in patients who have movement disorders, what should they know? What are the latest developments in that area with devices? Dr Okun: Yeah. So, they should know that things are moving rapidly in the field of putting electricity into the brain. And we're way past the era where we thought putting a little bit of electricity was snake oil. We know we can actually drive these circuits, and we know that many of these disorders---and actually, probably all of the disorders within this issue of Continuum---are all circuit disorders. And so, you can drive the circuit by modulating the circuit. And it's turned out to be quite robust with therapies like deep brain stimulation. Now, we're seeing uses of deep brain stimulation across multiple of these disorders now. So, for example, you may think of it in Parkinson's disease, but now we're also seeing people use it to help in cases where you need to palliate very severe and bothersome chorea and Huntington's disease, we're seeing it move along in Tourette syndrome. We of course have seen this for various hyperkinetic disorders and dystonias. And so, the main thing for clinicians to realize when dealing with neuromodulation is, take a deep breath because it can be overwhelming. We have a lot of different devices in the marketplace and no matter how many different devices we have in the marketplace, the most important thing is that we get the leads. You know, where we're stimulating into the right location. It's like real estate: location, location, location, whether you've got a lead that can steer left, right, up, down and do all of these things. Second, if you're feeling overwhelmed because there are so many devices and so many settings, especially as we put these leads in and they have all sorts of different, you know, nodes on them and you can steer this way and that way, you are not alone. Everybody is feeling that way now. And we're beginning to see AI solutions to that that are going to merge together with imaging, and then we're moving toward an era of, you know, should I say things like robotic programming, where it's going to be actually so complicated as we move forward that we're going to have to automate these systems. There's no way to get this and scale this for all of the locales within the United States, but within the entire world of people that need these types of devices and these therapies. And so, it's moving rapidly. It's overwhelming. The most important thing is choosing the right person. Okay? For this, with multidisciplinary teams, getting the lead in the right place. And then all these other little bells and whistles, they're like sculpting. So, if you think of a sculpture, you kind of get that sculpture almost there. You know, those little adds are helping to maybe make the eyes come out a little more or the facial expression a little bit better. There's little bits of sculpting. But if you're feeling overwhelmed by it, everybody is. And then also remember that we're starting to move towards some trials here that are in their early stages. And a lot of times when we start, we need more failures to get to our successes. So, we're seeing trials of people looking at, like, oligo therapies and protein therapies. We're seeing CRISPR gene therapies in the laboratory. And we should have a zero tolerance for errors with CRISPR, okay? we still have issues with CRISPR in the laboratory and which ones we apply it to and with animals. But it's still pretty exciting when we're starting to see some of these therapies move forward. We're going to see gene therapies, and then the other thing we're going to see are nano-therapies. And remember, smaller can be better. It can slip across the blood brain barrier, you have very good surface area-to-volume ratios, and we can uncage drugs by shining things like focused ultrasound beams or magnets or heat onto these particles to turn them on or off. And so, we're seeing a great change in the field there. And then also, I should mention: pumps are coming and they're here. We're getting pumps like we have for diabetes and neurology. It's very exciting. It's going to be overwhelming as everybody tries to learn how to do this. So again, if you're feeling overwhelmed, so am I. Okay? But you know, pumps underneath the skin for dopamine, pumps underneath the skin for apomorphine. And that may apply to other disorders and not just Parkinson as we move along, what we put into those therapies. So, we're seeing that age come forward. And then making lesions from outside the brain with focused ultrasound, we're starting to get better at that. Precision is less coming from outside the brain; complications are also less. And as we learn how to do that better, that also can provide more options for folks. So, a lot of things to read about in this issue of Continuum and a lot of really interesting and beyond, I would say, you know, the horizon as to where we're headed.  Dr Jones: Thank you for that. And it is a lot. It can be overwhelming, which I guess is maybe a good reason to read the issue, right? I think that's a great place to end and encourage our listeners to pick up the issue. And Dr Okun, I want to thank you for joining us today. Thank you for such a great discussion on movement disorders. I learned a lot. I'm sure our listeners will as well, given the importance of the topic, your leadership in the field over many years. I'm grateful that you have put this issue together. So, thank you. And you're a busy person. I don't know how we talked you into doing this, but I'm really glad that we did.  Dr Okun: Well, it's been my honor. And I just want to point out that the whole authorship panel that agreed to write these articles, they did all the work. I'm just a talking head here, you know, telling you what they did, but they're writing, and the people that are in the field are really, you know, leading and helping us to understand, and have really put it together in a way that's kind of helped us to be better clinicians and to impact more lives. So, I want to thank the group of authors, and thank you, Dr Jones. Dr Jones: Again, we've been speaking with Dr Michael Okun, guest editor of Continuum's most recent issue on movement disorders. 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. Thank you for listening to Continuum Audio.

Freunde zu supporten, bedeutet auch, ihnen einen Safe Space zu bieten. Ilija ist dankbar für seine Freundin Laura, bei der er sich sicher fühlt. Eine Soziologin und ein Psychologe sagen: Reflexion und Privilegien-Check sind wichtig für gute Allys.**********Ihr hört: Gesprächspartner: Ilija, hat als queere Person in Laura eine Ally gefunden Gesprächspartnerin: Janine Dieckmann, Sozialpsychologin am Institut für Demokratie und Zivilgesellschaft in Jena, forscht zu Allyship Gesprächspartnerin: Tobias Herrmann-Schwarz, klinischer Psychologe, hat sich auf die Beratung queerer Menschen spezialisiert Autor und Host: Przemek Żuk Redaktion: Ivy Nortey, Stefan Krombach, Nina Bust-Bartels Produktion: Susanne Beyer**********Quellen:Namer, Y. et al. (2024). Intersectional Challenges to Cohesion? On Marginalization in an Inclusive Society. Campus Verlag, Frankfurt am Main.Pereira-Jorge, I. et al. (2025). Organizational norms and gender identity contexts shape when pronoun-sharing is perceived as disingenuous allyship: Evidence of a normative eclipsing effect. Journal of Experimental Social Psychology, 120.Knott-Fayle, G., Kehler, M., & Gough, B. (2023). Navigating allyship: straight and queer male athlete's accounts of building alliances. NORMA, 19(2), 80–95.Pietri, E.S. et al. (2024). A framework for understanding effective allyship. Nat Rev Psychol 3, 686–700.Cumming-Potvin, W. (2023). LGBTQA+ allies and activism: past, present and future perspectives. Continuum, 38(3), 338–352.**********Mehr zum Thema bei Deutschlandfunk Nova:Das queere ABC – Teil 1: "Niemand in der Community sagt 'divers'"Allyship: So werden Männer gute Verbündete für FrauenQueer auf dem Land: Wie wir unsere Community finden**********Den Artikel zum Stück findet ihr hier.**********Ihr könnt uns auch auf diesen Kanälen folgen: TikTok und Instagram .**********Meldet euch!Ihr könnt das Team von Facts & Feelings über Whatsapp erreichen.Uns interessiert: Was beschäftigt euch? Habt ihr ein Thema, über das wir unbedingt in der Sendung und im Podcast sprechen sollen?Schickt uns eine Sprachnachricht oder schreibt uns per 0160-91360852 oder an factsundfeelings@deutschlandradio.de.Wichtig: Wenn ihr diese Nummer speichert und uns eine Nachricht schickt, akzeptiert ihr unsere Regeln zum Datenschutz und bei Whatsapp die Datenschutzrichtlinien von Whatsapp.

What is the Church of the SubGenius?What if parody could be sacred? This video explores the Church of the SubGenius—a surreal blend of satire, esotericism, and counterculture. Discover the origins of “Bob” Dobbs, the mystery of Slack, and how this invented religion both mocks and mirrors spiritual belief. Drawing from academic research on contemporary religion, occultism, and pop culture, this episode unpacks one of the most bizarre and thought-provoking movements of our time. Is it a joke, a faith, or something in between? Watch to find out.CONNECT & SUPPORT

SUPPORT THIS PODCAST!Join PatreonGet some merch~~~~FEATURED SONGREC – “Rhythm 77” (from KITE TO CAMDEN)This week's PODFAST is the return of Quick Takes from the Continuum, but with a twist. I usually give overviews of new albums, but it's been hard finding complete albums worth talking about. Instead, I'm doing a midyear check-in on my 2025 playlist. I do one every year, and this year it's called “2025alive”. You're gonna hear about a TON of new music, from both new and legacy acts, as well as some old music I discovered this year that deserves mention. It's already pretty damn robust & eclectic, and I guarantee you'll be surprised more than once.It's only on Spotify. If enough people request it, I'll recreate it on YouTube. Nick's 2025alive PLAYLISTAnything from my playlist that sparks your interest? Anything you're already listening to? Anything I missed? Anyone remember the fruity drink that inspired my playlist name? Discuss dammit!~~~~*intro music credit: REC - "You Make Me Wanna" (from RECcollection: The Best of REC 2007-2020)

With the increase in the public's attention to all aspects of brain health, neurologists need to understand their role in raising awareness, advocating for preventive strategies, and promoting brain health for all. To achieve brain health equity, neurologists must integrate culturally sensitive care approaches, develop adapted assessment tools, improve professional and public educational materials, and continually innovate interventions to meet the diverse needs of our communities. In this BONUS episode, Casey Albin, MD, speaks with Daniel José Correa, MD, MSc, FAAN and Rana R. Said, MD, FAAN, coauthors of the article “Bridging the Gap Between Brain Health Guidelines and Real-world Implementation” in the Continuum® June 2025 Disorders of CSF Dynamics issue. Dr. Albin is a Continuum® Audio interviewer, associate editor of media engagement, and an assistant professor of neurology and neurosurgery at Emory University School of Medicine in Atlanta, Georgia. Dr. Correa is the associate dean for community engagement and outreach and an associate professor of neurology at the Albert Einstein College of Medicine Division of Clinical Neurophysiology in the Saul Korey Department of Neurology at the Montefiore Medical Center, New York, New York. Dr. Said is a professor of pediatrics and neurology, the director of education, and an associate clinical chief in the division of pediatric neurology at the University of Texas Southwest Medical Center in Dallas, Texas. Additional Resources Read the article: Bridging the Gap Between Brain Health Guidelines and Real-world Implementation Subscribe to Continuum®: shop.lww.com/Continuum 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: @caseyalbin Guests: @NeuroDrCorrea, @RanaSaidMD Full episode transcript available here Dr Jones: This is Dr Lyell Jones, Editor-in-Chief of Continuum. This exclusive Continuum Audio interview is available only to you, our subscribers. We hope you enjoy it. Thank you for listening. Dr Albin: Hi all, this is Dr Casey Albin. Today I'm interviewing Dr Daniel Correa and Dr Rana Said about their article on bridging the gap between brain health guidelines and real-world implementation, which they wrote with Dr Justin Jordan. This article appears in the June 2025 Continuum issue on disorders of CSF dynamics. Thank you both so much for joining us. I'd love to just start by having you guys introduce yourselves to our listeners. Rana, do you mind going first? Dr Said: Yeah, sure. Thanks, Casey. So, my name is Rana Said. I'm a professor of pediatrics and neurology at the University of Texas Southwestern Medical Center in Dallas. Most of my practice is pediatric epilepsy. I'm also the associate clinical chief and the director of education for our division. And in my newer role, I am the vice chair of the Brain Health Committee for the American Academy of Neurology. Dr Albin: Absolutely. So just the right person to talk about this. And Daniel, some of our listeners may know you already from the Brain and Life podcast, but please introduce yourself again. Dr Correa: Thank you so much, Casey for including us and then highlighting this article. So yes, as you said, I'm the editor and the cohost for the Brain and Life podcast. I do also work with Rana and all the great members of the Brain Health Initiative and committee within the AAN, but in my day-to-day at my institution, I'm an associate professor of neurology at the Albert Einstein College of Medicine in the Montefiore Health System. I do a mix of general neurology and epilepsy and with a portion of my time, I also work as an associate Dean at the Albert Einstein College of Medicine, supporting students and trainees with community engagement and outreach activities. Dr Albin: Excellent. Thank you guys both so much for taking the time to be here. You know, brain health has really become this core mission of the AAN. Many listeners probably know that it's actually even part of the AAN's mission statement, which is to enhance member career fulfillment and promote brain health for all. And I think a lot of us have this kind of, like, vague idea about what brain health is, but I'd love to just start by having a shared mental model. So, Rana, can you tell us what do you mean when you talk about brain health? Dr Said: Yeah, thanks for asking that question. And, you know, even as a group, we really took quite a while to solidify, like, what does that even mean? Really, the concept is that we're shifting from a disease-focused model, which we see whatever disorder comes in our doors, to a preventative approach, recognizing that there's a tremendous interconnectedness between our physical health, our mental health, cognitive and social health, you know, maintaining our optimal brain function. And another very important part of this is that it's across the entire lifespan. So hopefully that sort of solidifies how we are thinking about brain health. Dr Albin: Right. Daniel, anything else to add to that? Dr Correa: One thing I've really liked about this, you know, the evolution of the 2023 definition from the AAN is its highlight on it being a continuous state. We're not only just talking about prevention of injury and a neurologic condition, but then really optimizing our own health and our ability to engage in our communities afterwards, and that there's always an opportunity for improvement of our brain health. Dr Albin: I love that. And I really felt like in this article, you walked us through some tangible pillars that support the development and maintenance of this lifelong process of maintaining and developing brain health. And so, Daniel, I was wondering, you know, we could take probably the entire time just to talk about the five pillars that support brain health. But can you give us a pretty brief overview of what those are that you outlined in this article? Dr Correa: I mean, this was one of the biggest challenges and really bundling all the possibilities and the evidence that's out there and just getting a sense of practical movement forward. So, there are many organizations and groups out there that have formed pillars, whether we're calling them seven or eight, you know, the exact number can vary, but just to have something to stand on and move forward. We've bundled one of them as physical and sleep health. So really encouraging towards levels of activity and not taking it as, oh, that there's a set- you know, there are recommendations out there for amount of activity, but really looking at, can we challenge people to just start growing and moving forward at their current ability? Can we challenge people to look at their sleep health, see if there's an aspect to improve, and then reassess with time? We particularly highlight the importance of mental health, whether it's before a neurologic condition or a brain injury occurs or addressing the mental health comorbidities that may come along with neurologic conditions. Then there's of course the thing that everyone thinks about, I think, with brain health in terms of is cognitive health. And you know, I think that's the first place that really enters either our own minds or as we are observers of our elder individuals in our family. And more and more there has been the highlight on the need for social interconnectedness, community purpose. And this is what we include as a pillar of social health. And then across all types of neurologic potential injuries is really focusing on the area of brain injury. And so, I think the area that we've often been focused as neurologists, but also thinking of both the prevention along with the management of the condition or the injury after it occurs. Dr Albin: Rana, anything else to add to that? That's a fantastic overview. Dr Said: Daniel, thank you for- I mean, you just set it up so beautifully. I think the other thing that maybe would be important for people to understand is that as we're talking through a lot of these, these are individual. These sound like very individual-basis factors. But as part of the full conversation, we also have to understand that there are some factors that are not based on the individual, and then that leads to some of the other initiatives that we'll be talking about at the community and policy levels. So, for example, if an individual is living in an area with high air pollution. Yes, we want them to be healthy and exercise and sleep, but how do we modify those factors? What about lead leaching from our aging pipes or even infectious diseases? So, I think that outside of our pillars, this is sort of the next step is to understand what is also at large in our communities. Dr Albin: That's a really awesome point. I love that the article really does shine through and that there are these individual factors, and then there there's social factors, there's policy factors. I want to start just with that individual because I think so many of our patients probably know, like, stress management, exercise, sleep, all of that stuff is really important. But when I was reading your article, what was not so obvious to me was, what's the role that we as neurologists should play in advocating? And really more importantly, like, how should we do that? And again, it struck me that there are these kind of two issues at play. And one is that what Daniel was saying that, you know, a lot of our patients are coming because they have a problem, right? We are used to operating in this disease-based care, and there's just limited time, competing clinical demands. If they're not coming to talk about prevention, how do we bring that in? And so Rana, maybe I'll start with you just for that question, you know, for the patients who are seeing us with a disease complaint or they're coming for the management of a problem, how are you organizing this at the bedside to kind of factor in a little bit about that preventative brain health? Dr Said: You know, I think the most important thing at the bedside is, one, really identifying the modifiable risk factors. These have been well studied, we understand them. Hypertension, diabetes, smoking, weight management. And we know that these definitely are correlative. So is it our role just to talk about stroke, or should we talk about, how are you managing your blood pressure? Health education, if there was one major cornerstone, is elevating health literacy for everyone and understanding that patients value clear and concise information about brain health, about modifiable risk factors. And the corollary to that, of course, are what are the resources and services? I completely understand---I'm a practicing clinician---the constraints that we have at the bedside, be it in the hospital or in our clinics. And so being the source of information, how are we referring our families and individuals to social workers, community health worker support, and really partnering with them, food banks, injury prevention programs, patient advocacy organizations? I think those are really ways that we can meet the impacts that we're looking at the bedside that can feel very tangible and practical. Dr Albin: That's really excellent advice. And so, I'd like to ask a follow-up question. With your knowledge of this, trying to get more multidisciplinary buy-in from your clinic so that you really have the support to get these services that are so critically important. And how do you do that? Dr Said: Yeah, I think it's, one, being a champion. So, what does a champion mean? It means that somebody has to decide this is really important. And I think we all realize that we're not the only ones in the room who care about this. We're all in this, and we all care about it. But how do we champion it and carry it through? And so that's the first. Second you find your partnerships: your social workers, your case managers, your other colleagues. And then what is the first-level entry thing that you can do? So for example, I'm a pediatric epileptologist. One of the things we know is that in pediatric epilepsy, depression and anxiety are very strong comorbidities. So, before we get to the point where a child is in distress, every single one of our epilepsy patients who walks in the door over the age of twelve has an age-appropriate screener that is given to them in both English and Spanish. And we assess it and we determine stratifying risk. And then we have our social workers on the back end and we decide, is this a child who needs resources? Is this a child who needs to be walked to the emergency room, escorted? And anything in between. And I think that that was a just a very tangible example of, every single person can do this and ask about it. And through the development of dot phrases and clear protocols, it works really well. Dr Albin: I love that, the way that you're just being mindful. At every step of the way, we can help people towards this lifelong brain health. And Daniel, you work with an adult population. So I wonder, what are your tips for bringing this to a different patient population? Dr Correa: Well, I think---adult or child---one thing that we often are aware of with so many of the other things that we're doing in bedside or clinic room counseling, but we don't necessarily think of in this context of brain health, is, remember all the people in the room. So, at the bedside, whether it's in the ICU, discharge counseling, the initial admission, the whole family is often involved and really concerned about the active issue. But you can look for opportunities- we often try to counsel and support families about the importance of their own sleep and rest and highlighting it not just as being there for their family member, but highlighting it to them as a measure of their own improvement of their brain health. So, looking at ways where, one, I try to find, is there something I can do to support and educate the whole family about their brain health? And then- and with an epilepsy, or in many other situations, I try to look for one comorbidity that might be a pillar of brain health to address that maybe I wasn't already thinking. And then I consider, is there an additional thing that they wouldn't naturally connect to their epilepsy or their headaches that I can bring in for them to work on? You know, we can't often give people twelve different things to work on, and they'd just feel like, okay like, you have no realistic understanding of my life. But if we can just highlight on one, and remind them that there can be many more ways to improve their health and to follow up either with us as their neurologist or their future primary care doctors to address those additional needs. Again, I would really highlight the importance of a multidisciplinary approach and looking for opportunities. We've too often, I feel, relied on primary care as being the first line for addressing unmet social health needs. We know that so many people, once they have a neurologic condition or the potential, even, of a neurologic condition, they're concerned about dementia or something, they may view us, as their neurologist, as their most important provider. And if they don't have the resource of time and money to show up at other doctors, we may be the first one they're coming to. And so, tapping into your institution's resources and finding out, are there things that are available to the primary care services that for some reason we're not able to get on the inpatient side or the outpatient side? Referring to social workers and care workers and showing that our patients have an independent need, that they're not somehow getting captured by the primary care doctors. Dr Albin: I really love that. I think that we- just being more invested and just being ready to step into that role is really important. I was noticing in this article, you really call that being a brain health ambassador, being really mindful, and I will direct all of our listeners to Figure 3, which really captures what practitioners can do both at the bedside, within their local community, and even at the professional society level, to really advocate for policies that promote brain wellness. Rana, at the very beginning of this conversation, you noted, you know, this is not just an individual problem. This really is something that is a component of our policy and the structure of our local communities. I really loved in the article, there's a humility that this cannot be just a person-by-person bedside approach, that this is a little bit determined by the social determinants of health. And so, Rana, can you walk us through a little bit of what are the social determinants of health, and why are these so crucially important when we think about brain health for all? Dr Said: Yeah, social determinants of health are a really key factor that it looks at, what are the health factors that are environmental; for example, that are not directly like what your blood pressure is, what, you know, what your BMI is, that definitely impact our health outcomes. So, these include environmental things like where people are born, where they live, where they learn, work, play, worship, and age. It encompasses factors like your socioeconomic status, your education, the neighborhoods where you are living, definitely healthcare access. And then all of this is in a social and community context. We know that the impact of social determinants of health on brain health are profound for the entire lifespan and that- so, for example, if someone is from a disadvantaged background or that leads to chronic stress, they can have limited access to healthcare. They can have greater risk of exposure to, let's say, environmental toxins, and all of that will shape how their brain health is. Violence, for example. And so, as we think about how we're going to target and enhance brain health, we really have to understand that these are vulnerable populations, special high-risk populations, that often have a disproportionate burden of neurologic disorders. And by identifying them and then developing targeted interventions, it promotes health equity. And it really has to be done in looking at culturally- ethnocultural-sensitive healthcare education resources, thinking about culturally sensitive or adaptive assessment tools that work for different populations so that these guidelines that we have, that we've already identified as being so valuable, can be equitably applied, which is one crucial component of reducing brain health risk factors. And lastly, at the neighborhood level, this is where we really rely on our partnerships with community partners who really understand their constituents and they understand how to have the special conversations, how to enhance brain health through resource utilization. And so, this is another plug for policy and resources. Dr Albin: I love that. And thinking about the neighborhood and the policy levels and all the things that we have to do. Daniel, I'd like to ask you, is there anything else you would add? Dr Correa: Yeah, you know, so I really wanted to come back to this thing is that often and unfortunately, in the beginning understanding of social determinants of health, they're thought of as a positive or a negative factor, and often really negative. These are just facts. They're aspects about our community, our society, and some of them may be at the individual level. They're not at fault of any individual or community, or even our society. They're just the realities. And when someone has a factor that may predict a health disparity or an unmet social need---I wanted to come back to that concept and that term---one or two positive factors that are social determinants of health for that individual are unmet social needs. It's a point of promise. It's a potential to be addressed. And seeking ways to connect them with community services, social work, caregivers, these are ways where- that we can remove a barrier to, so that the possibility of the recommendations that we're used to doing, giving recommendations about medications and management, can be fully appreciated for that person. And the other aspect is, like brain health, this is a continuous state. The social determinants of health may be different for the child, the parent, and the elderly family member in the household, and there might be some that are shared across them. And when one of those individuals has a new medical illness or a new condition, a stroke, and now has a mobility limitation, that may change a social determinant of health for that person or for anyone else in the family, the other people now becoming caregivers. We're used to this. And for someone after a stroke or traumatic brain injury, now they have mobility changes. And so, we work on addressing those. But thinking on how those things now become a barrier for engaging with community and accessing things, something as simple as their pharmacy. Dr Albin: I hear a lot of “this is a fluid situation,” but there's hope here because these are places that we can intervene and that we can really champion brain health throughout this fluid situation. Which kind of brings me to what we're going to close out with, which is, I'm going to have you do a little thought exercise, which is that you find a magic lamp and a genie comes out. And we'll call this the brain health genie. The genie says that they are going to grant you one wish for the betterment of brain health. Daniel, I'll start with you. What is the one thing that you think could really move the needle on promoting and maintaining brain health? Dr Correa: I will jump on nutrition and food access. If we could somehow get rid of food insecurity and have access to whole and fresh foods for everyone, and people could go back to looking at opportunities from their ancestral and cultural experiences to cook and make whole-food recipes from their own cultures. Using something like the Mediterranean diet and the mind diet as a framework, but not looking at those as cultural barriers that we somehow all have to eat a certain way. So, I think that would really be the place I would go to first that would improve all of our brain health. Dr Albin: I love that. So, wholesome eating. Rana, how about you? One magic wish. Dr Said: I think traumatic brain injury prevention. I think it's so- it feels so within our reach, and it just always is so heart-hurting when you think that wearing helmets, using seatbelts, practicing safety in sports, gun safety---because we know unfortunately that in pediatric patients, firearm injury is the leading cause of traumatic brain injury. In our older patients, fall reduction. If we could figure out how to really disseminate the need for preventative measures, get everyone really on board, I think this is- the genie wouldn't have to work too hard to make that one come true. Dr Albin: I love that. As a neurointensivist, I definitely feel that TBI prevention. We could talk about this all day long. I really wish we had a longer bit of time, but I really would direct all of our listeners to this fantastic article where you give really practical advice. And so again, today I've been interviewing Drs Daniel Correa and Rana Said about their article on bridging the gap between brain health guidelines and real-world implementation, written with Dr Justin Jordan. This article appears in the most recent issue of Continuum on the disorders of CSF dynamics. Be sure to check out Continuum Audio episodes from this and other issues. And thank you so much for our listeners for joining us today. Dr Monteith: This is Dr Teshamae Monteith, Associate Editor of Continuum Audio. We hope you've enjoyed this subscriber-exclusive interview. Thank you for listening.

0:00 Intro6:54 Ghost Town PCVR30:37 Astro Bot36:45 Death Stranding Luke Ross VR Mod45:07 Wipeout Omega Collection50:22 Stray UEVR1:00:38 Synapse1:07:30 Zombie Army VR PCVR1:12:44 Escaping Wonderland PCVR1:20:18 Bridge Constructor Studio PCVR1:22:41 Space Docker VR1:23:32 Squirrel with a Gun UEVR1:27:41 Pools VR1:29:19 Starship Troopers Continuum1:31:18 Witchblood1:32:26 Walkabout Crystal Lair1:32:58 Hidden Memories of the Gardens Between Demo1:34:48 Vitriol Demo1:35:24 Upcoming GamesJustin's YouTube channel: www.youtube.com/mamefanAlex's YouTube channel: www.youtube.com/virtualinsiderNick's YouTube Channel: www.youtube.com/BuffaloPinballVR Gaming Podcast on YT: www.youtube.com/@vrgamingpodcastVR Gaming Podcast Discord link: https://discord.gg/Kbg44ADPD2Justin's email: mamefanyt@gmail.comIf you'd like to donate, Paypal: https://paypal.me/mamefanVenmo: @Justin-Davis-1030

Childhood-onset hydrocephalus encompasses a wide range of disorders with varying clinical implications. There are numerous causes of symptomatic hydrocephalus in neonates, infants, and children, and each predicts the typical clinical course across the lifespan. Etiology and age of onset impact the lifelong management of individuals living with childhood-onset hydrocephalus. In this episode, Casey Albin, MD, speaks with Shenandoah Robinson, MD, FAANS, FAAP, FACS, author of the article “Childhood-onset Hydrocephalus” in the Continuum® June 2025 Disorders of CSF Dynamics issue. Dr. Albin is a Continuum® Audio interviewer, associate editor of media engagement, and an assistant professor of neurology and neurosurgery at Emory University School of Medicine in Atlanta, Georgia. Dr. Robinson is a professor of neurosurgery, neurology, and pediatrics at Johns Hopkins University School of Medicine in Baltimore, Maryland. Additional Resources Read the article: Childhood-onset 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: @caseyalbin 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 Albin: Hi, this is Dr Casey Albin. Today I'm interviewing Dr Shenandoah Robinson about her article on childhood onset hydrocephalus, which appears in the June 2025 Continuum issue on disorders of CSF dynamics. Dr Robinson, thank you so much for being here. Welcome to the podcast. I'd love to start by just having you briefly introduce yourself to our audience. Dr Robinson: I'm a pediatric neurosurgeon at Johns Hopkins, and I'm very fortunate to care for kids and children from the neonatal intensive care unit all the way up through young adulthood. And I have a strong interest in developing better treatments for hydrocephalus. Dr Albin: Absolutely. And this was a great article because I really do think that understanding how children with hydrocephalus are treated really does inform how we can care for them throughout the continuum of their lifespan. You know, I was shocked in reading your article about the scope of the problem for childhood onset hydrocephalus. Can you walk our listeners through what are the most common reasons why CSF diversion is needed in the pediatric population? Dr Robinson: For the United States, and Canada too, the most common reasons are spina bifida---so, a baby that's born with a myelomeningocele and then develops associated hydrocephalus---and then about equally as common is posthemorrhagic hydrocephalus of prematurity, congenital causes such as from aquaductal stenosis, and other genetic causes are less common. And then we also have kids that develop hydrocephalus after trauma or meningitis or tumors or other sort of acquired problems during childhood. Dr Albin: So, it's a really diverse and sort of heterogeneous causes that across sort of the, you know, the neonatal period all the way to, you know, young adulthood. And I'm sure that those etiologies really shift based on sort of the subgroup population that you're talking about. Dr Robinson: Yes, they definitely shift over time. Fortunately for our kids that are born with problems that raise concerns, such as myelomeningocele or if they're born preterm, they sort of declare themselves by the time they're a year old. So, if you're an adult provider, they should have defined themselves and it's unlikely that they will suddenly develop hydrocephalus as a teenager or older adult. Dr Albin: Totally makes sense. I think many of the listeners to this podcast are adult neurologists who are probably very familiar with external ventriculostomies for temporary CSF diversion, and with the more permanent ventricular peritoneal shines or ventricular atrial or plural shines that are needed when there's the need for permanent diversion. But you described in your article two procedures that provide temporary CSF diversion that I think many of our listeners are probably not as familiar with, which is the ventricular access devices and ventriculosubgaleal shunts. Can you briefly describe what those procedures provide? Who are the candidates for them? And then what complications neurologists may need to think about if they're consulted for comanagement in one of these complex patients? Dr Robinson: Well, the good thing is that if as an adult neurologist you encounter someone with, you know, residual tubing from one of these procedures, you are unlikely to need to do anything about it. So, we put in ventricular access device or ventriculosubgaleal shunts, usually in newborns or infants. And sometimes when they no longer need the device, we just leave it in because that saves them an extra surgery. So, if you encounter one later on, it's most likely you won't need to do anything. Often if the baby goes on to show that they need a permanent shunt, we go ahead and put in that permanent shunt. We may or may not go back and take out the reservoir or the subgaleal shunt. The reservoir and subgaleal shunts are often put in the frontal location. Sometimes we'll put the permanent shunt in the occipital location and just leave the residual tubing there. So, you're very unlikely to need to intervene with a reservoir or subgaleal shunt if you encounter an older child or adult with that left in. We use these in the small babies because the external ventricular drains that we're very familiar with have a very high complication rate in this population. In the adult ICU, you often see these, and maybe there's, you know, a few percent risk of infection. It actually heads into 20 to 25% in our preterm infants and other newborns that require one of these devices for drainage. So, we try not to use external ventricular drains like we use in older patients. We use the internalized device: either the ventricular reservoir with a little area for us to tap every day, every other day; or the ventriculosubgaleal shunt, which diverts the spinal fluid to a pocket in the scalp. So, we use these in preterm infants that are too tiny for a permanent shunt. And for some of our babies that are born, for example, with an omphalocele, that we can't use their peritoneal cavity and so we need some temporizing device to manage their CSF. Dr Albin: Totally makes sense. And so just to clarify, I mean, this is a tube that's placed into the ventricles of the brain and then it's tunneled into the subgaleal space and the collection, the CSF, just builds up there, like? Dr Robinson: Yeah. Dr Albin: And over time either, you know, the baby will learn how to account for that extra CSF, and then I guess it's just reabsorbed? Dr Robinson: Yeah. When it's present, though, it looks like maybe, I don't know if you're familiar with like a tissue expander. There is this bubble of fluid under the scalp, but it's prominent, it can be several centimeters in diameter. Dr Albin: Wow, that's just absolutely fascinating. And I don't think I've ever had the opportunity to see this in clinical practice. I've really learned quite a bit about this. I assume that these children are going to go on to get some sort of permanent diversion. And then, you know, over time, those permanent shunts do create a lot of problems. And so, I was hoping you could kind of walk us through, you know, what are some of the things that you're seeing that you're concerned about? And then if you've just inherited a patient who had a shunt placed at, say, a different institution, how do you go about figuring out what kind of shunt it is and if they're still dependent on it? Dr Robinson: There's a few things that, fortunately, technology is helping with. So, it is much easier now for patients to get their images uploaded to image-sharing software, and then we can download their images into our institutional software, which is very helpful. Another option is that we are strongly encouraging our families to use a app such as HydroAssist that's available from the Hydrocephalus Association. So that's an app that goes on your phone, and you can upload the images from an MRI or a CT scan or x-rays from a shunt series. And then that you can take if you're traveling and you have to go to emergency department or you're establishing care with a new provider, you can have your information right there and not be under stress to remember it. It also has areas so you can record the type of valve. And all of our valves have pluses and minuses, they all tend to malfunction a little bit. And they can be particularly helpful with different types of hydrocephalus. I really doubt that we're going to narrow down from the fifteen or so valves we have access to now. And so, recording your valve type, the manufacturer as well as the setting, is very helpful when you're transferring care or if you're traveling and then have to, unfortunately, stop in the emergency department. Dr Albin: Yeah, I thought that was a really great pearl that, like, families now are empowered to sort of take control of understanding sort of the devices that they have, the settings that they're using. And what an incredible thing for providers who are going to care for these patients who, you know, unfortunately do end up in centers that are not their primary center. The other challenge that I find… I practice as a neurointensivist, and sometimes patients come in and they have a history of being shunt dependent and they present with a neurologic change. And I think that we as neurologists can be a little quick to blame the shunt and want the shunt to be tapped. And I was really struck in reading this article about the complexity of shunt taps. And I was hoping, you know, can you kind of walk us through what's involved and maybe why we should have a little bit of a higher threshold before just saying, ah, just have the neurosurgeons tap the shunt. Like, it's not that straightforward. Dr Robinson: And it may depend on the population you're caring for. So, when I was at a different institution, we actually published that there's about a 5% complication rate from shunt taps. And that may be- that was in pediatric patients. And again, that may be population dependent, but you can introduce infection to a perfectly clean shunt by doing a shunt tap. You can also cause an acute shunt malfunction. So that's why we tend to prefer that only neurosurgeons are doing shunt taps for evaluation of a shunt malfunction. There are times that, for example, our patients who are getting intrathecal chemotherapy or something have a CSF access device like an Ommaya reservoir, and other providers may tap that reservoir to instill medicine. But that's different than an evaluation, like, you're talking about somebody with a neurological change. And so, it is possible that if somebody has small ventricles or something, if you tap that shunt, you can take a marginally functioning shunt and turn it into an acute proximal malfunction, which is an emergency. Dr Albin: Absolutely. I think that's a fantastic pearl for us to take away from this. It's just that heightened level. And kind of on the flip side of that, you know, and I really- I do feel for us when we're trying to kind of, you know, make a case that it's, it's not the shunt. Many of our shunted patients also have a lot of neurologic complexity, which I think you really talked upon in this article. I mean, these are patients who have developmental cognitive delays and that they have epilepsy and that they're at risk for, you know, complications from prematurity, since that's a very common reason that patients are getting shunts. But from your experience as a neurosurgeon, what are some of the features that make you particularly concerned about shnut malfunction? And how do you sort of evaluate these patients when they come in with that altered mental status? Dr Robinson: It is challenging, especially for our patients that have, you know, some intellectual delay or other difficulties that make it hard for them to give an accurate history. Problem is, if they're sick and lethargic, they may not remember the symptoms that they had when they were sick. But sometimes there's hopefully there's a family member present that does remember and can say, oh, no, this is what they look like when they have a viral illness. And this is different from when they have the shot malfunction, which was projectile emesis, not associated with a fever. It's rare to have a fever with a shunt malfunction, although shunt infection often presents with malfunction. So, it's not completely exclusionary. We often look at the imaging, but it's taking the whole picture together. Some of the common other diagnoses we see are severe constipation that can decrease the drainage from the shunt and even cause papilledema in some people. So, we look at that as well on the shunt series. It's very important to have the shunt series if you're concerned about shunt malfunction or- the shunt tubing is good. It tends to last maybe 20to 25 years before it starts to degrade. And so, you may have had a functioning shunt for decades and it worked well and you're very dependent on it, and then it breaks and you become ill. But on the flip side, we have patients that have had a broken shunt for years, they just didn't know about it. And we don't want to jump in and operate on them and then cause complexities. And so, it is a challenge to sort out. The simplest thing is obviously if they come in and their ventricles are significantly larger, and that goes along with a several-hour or a couple-day deterioration, that's a little more clear-cut. Dr Albin: Absolutely. And you talked about this shunt series. What other imaging- and, sort of maybe walk us through, what's involved in a shunt series, what are you looking at? And then what other imaging is sort of your preferred method for evaluating these patients? Dr Robinson: In adult patients, the shunt series is the x-ray from the entire shunt. And so, if they have an atrial shunt, that would be skull x-ray plus a chest x-ray; or the shunt ends in the perineal cavity, it goes to the perineum. And we're looking for continuity. We're looking for the- sometimes as people grow and age, the ventricular catheter can pull out of the ventricle. So, we're looking to make sure that the ventricular catheter is in an optimal position relative to the skull. We can also look at the valve setting to see the type of valve. So, that can also be helpful as well. And then in terms of additional imaging, a CT scan or an MRI is helpful. If you don't know what type of valve they have, they should not, ideally, go in the MRI scanner. We like to know what their setting is before they go in the MRI because we're going to have to reset the valve after they come out of the MRI if it's a programmable valve. Dr Albin: This is fantastic. I've heard several pearls. So, one is that with the shunt series, which, am I correct in understanding those are just plain X-rays? Dr Robinson: Yes. Dr Albin: Right. Then we can look for constipation, and that might be actually something really serious in a pediatric patient that could clue us in that they could actually be developing hydrocephalus or increased ICP just because of the abdominal pressure. And then that we need to be mindful of what are the stunt settings before we expose anyone to the MRI machine. Is that two good takeaways from all of this? Dr Robinson: Yes. And it's very rare that there'll be an MRI tech that will allow a patient with a valve in the MRI without knowing what it is. So, they have their job security that way. But yeah, if you're not sure, just go ahead and get the CT. Obviously, in our younger kids, we're trying to avoid CT scans. But if you're weighing off trying to decide if somebody has a shunt malfunction versus, you know, waiting 12 or 24 hours for an MRI, go ahead and get the CT. Dr Albin: Absolutely. I love it. Those are things I'm going to take with me for this. I have one more question about these shunts. So, every now and then, and I think you started to touch on this, we will get a shunt series and we'll see that the catheter is fractured. Do the patients develop little- like, a tract that continues to allow diversion even though the catheter is fractured? Dr Robinson: Yes. So, they can develop scar tissue around, and some people have more scar tissue than others. You'll even see that sometimes, say, the catheter has fractured and we'll take out that old fractured tubing and put in new tubing on the other side. But if you go and palpate their neck or chest, you'll still feel that tract is there because it calcifies along the tract. Some patients drain through that calcified tract for weeks or months without symptoms, and then it can occlude off. So, we don't consider it a reliable pathway. It's also not a reliable pathway if you're positioned prone in the OR. So some of our orthopedic colleagues, for example, if they go to do a spine fusion, we like to confirm that the shunt is working before you undergo that long anesthesia, but also that you're going to be positioned prone and you could potentially- you know, the pressure could occlude that track that normally is open. Dr Albin: This is fantastic. I feel like I've gotten everything I've ever wanted to know about shunts and all of their complications in this, which is, you know, this is really difficult. And I think that because we are not trained to put these in, sometimes we see them and we just say, oh, it's fractured that must be a malfunction. But it's good to know that sometimes those patients can drain through, you know, a sort of scarred-down tract, but that it may not be nearly as reliable as when they have the tubing in place. Another really good thing that I'm going to put in my back pocket for the next time I see a patient with a potential shunt malfunction. Dr Robinson: And we do have some patients that the tubing is fractured years ago and they don't need it repaired, and that totally can be challenging when they then transfer to your practice for follow-up care. We tend to follow those patients very closely, both our clinic visits as well as having them seen by ophthalmology. So, there are teenagers and young adults out there that have… their own system has recovered and they are no longer shunt-dependent; and they may have a broken shunt and not actually be using that track, but they usually have had fairly intensive follow up to prove that they're not shunt-dependent. And we still have a healthy respect there that, you know, if they start to get a headache, we're going to take that quite seriously as opposed to, you know, some of our shunt patients, about 10 to 20%, have chronic headaches that are not shunt-related. So, not everybody who has a headache and has a shunt has a shunt malfunction. It's tough. Dr Albin: This is really tough. That actually brings me to sort of the last clinical scenario that I was hoping we could get your perspective on. And I think this would be of great interest to neurologists, especially in the context that these children may develop headaches that have nothing to do with the shunt. I'd like to sort of give you this hypothetical case that I'm a neurologist seeing a patient in clinic and it's a teenager, maybe a young adult, and they had a shunt placed early in childhood. They've done really well. And they've come to me for management of a new headache. And, you know, as part of this workup, their primary care provider had ordered an MRI. And, you know, I look at the MRI, and I don't think that the ventricles look really enlarged. They don't look overdrained. Is having an MRI that looks pretty okay, is that enough to exonerate the shunt in this situation? Dr Robinson: In most cases it is. The one time that we don't see a substantial change in the ventricles is if we have a pseudocyst in the abdomen. The ventricles cannot enlarge initially, and then later on they might enlarge. So, we see that sometimes that somebody will come in and their ventricles will be stable in size, but we're still a little bit suspicious. They've got this persistent headache. They may have, you know, some emesis or loss of appetite, loss of activity, and a slower presentation than you would get with an acute proximal malfunction. We can check an abdominal ultrasound for them. And sometimes, even though the ventricles haven't changed in size, they still have a malfunction because they have that distal pseudocyst. One of the questions that we ask our patients when we're establishing care, in addition to what valve type they have and what sort of their shunt history or other interventions such as endoscopic third ventriculostomy, is to ask if their ventricles enlarge when they have a shunt malfunction. There is a small fraction where they do not. They kind of have a stiff brain, if you will. And so, it's good to know that. That's one of the key factors is asking somebody, do the ventricles enlarge when they have a malfunction? If they have enlarged in the past, they're likely to enlarge again if they have a malfunction. But again, it's not 100%. So, in peds, 20% of the time the ventricles don't enlarge. So, in adults, I'm not that- you know, I don't know what percentage it is, but it's something to consider that you can have a stable ventricular size and still have a shunt malfunction. So, if your clinical judgment, you're just kind of, like, still uneasy, you know, respect that and maybe do a little more workup. That's why we so much want patients to establish care with somebody, whether it's a neurologist or a neurosurgeon or other provider in some areas that have fewer neurospecialists, but to establish care so that you all know what a change is for that patient. That's really important. Dr Albin: That's fantastic. So, to summarize that, it's really important to understand the patient's baseline and how they presented with prior shunt complications, if they've had some. That if they're coming in with a new headache that we don't have a baseline, so, we should just have a heightened level of awareness that, like, the shunt has a start and it has an end. And even if the start of the shunt in the brain looks okay, there still could be the potential for complications in the abdomen. And maybe the third thing I heard from that is that we should look for GI symptoms and sort of be aware of when there could be a complication in the abdomen as well. Does that all sound about right? Dr Robinson: And especially for our kids with spina bifida and for posthemorrhagic hydrocephalus are now adults, because the preterm infants are prone to necrotizing enterocolitis. And they may not have had surgery for it, but they still may have adhesions and other things that predispose them to develop pseudocysts over time. And then our individuals with spina bifida often have various abdominal surgeries and other procedures to help them manage their bowel and bladder function. And so that can also create adhesions that then predisposes to pseudocysts. So, we do have a healthy respect for that. In addition, it used to be---because we have gotten a little better with shunts over time---it used to be, like, when I was in training that you heard, you know, if you haven't had a shunt malfunction for 10 or 15 years, you must- you may no longer be dependent. And that's not really true. There are some people who outgrow their need for shunt dependence, but not everyone does outgrow it. And so, you can be 15, 20 years without a shunt revision and still be shunt-dependent. Dr Albin: Those are fantastic pearls. I think most of them, walking away with this, like, a very healthy respect for the fact that these are complex patients, which the shunt is one component of sort of the things that can go wrong and that we have to have a really healthy respect and really detailed investigation and sort of take the big picture. I really like that. Dr Robinson: Yeah, I know. I think it's- there's a very strong push amongst pediatric neurosurgery and a lot of the related, our colleagues in other areas, to develop multidisciplinary transition clinics and lifespan programs for these patients to help keep everything else optimized so that they're not coming in, for example, with seizures. But then you have to figure out if this is a seizure or a shunt; you know, if we can keep them on track, if we can keep them healthy in all their other dimensions, it makes it safer for them in terms of their shunt malfunction. Dr Albin: Absolutely. I love that, and just the multidisciplinary preventative aspect of trying to keep these patients well. So important. Dr Robinson, I really would like to thank you for your time. We're getting towards the end of our time together. Are there any other points about the article that you just are anxious that leave the readers with, or should I just direct them back to the fantastic review that you've put together on this topic? Dr Robinson: No, I think that we covered a lot of the high points. I think one of the really exciting things for hydrocephalus is that there's a lot of investigations into other options besides shunts for certain populations. We are seeing less hydrocephalus now with the fetal repair of the myelomeningocele, which is great. And we're trying to make inroads into posthemorrhagic hydrocephalus as well. So, there are a lot of great things on the horizon and, you know, hopefully someday we won't have the need to have these discussions so much for shunts. Dr Albin: I love it. I think that's really important. And all of those points were touched on the article. And so, I really invite our listeners to go and check out the article, where you can see sort of, like, how this is evolving in real time. Thank you, Dr Robinson. Please go and check out the childhood-onset hydrocephalus article, which appears in the most recent issue of Continuum on the disorders of CSF dynamics. And be sure to check out Continuum Audio episodes from this and other issues. Thank you again to our listeners for joining us today. And thank you, Dr Robinson. Dr Robinson: Thanks for having me. 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.

Continuum was previously known as Molyworks, and we loved their crazy startup story with founder Chris Eonta. Now Rob Higby is the firm's CEO. With him, we discuss a more mature very different firm. We talk a lot about making aircraft, and aircraft MRO, which is a considerable opportunity but maybe not as easy as we think. Rob suggests that cargo aircraft could be a sweet spot for AM and gives us a lot of insight into an industry he worked in for years. Then we get into Continuum's future, its strategy, and what the company is doing to meet powder demand. What's the opportunity in reclaimed, recycled powder, and where is this part of the market headed?

Today, leaders from Sacramento County and the cities of Folsom and Sacramento, as well as the Continuum of Care gathered to strongly oppose Senate Bill 802 (Sacramento Area Housing and Homelessness Agency). Read More https://www.saccounty.gov/us/en/articles/2025-articles/local-leaders-oppose-sb-802.html

Jeff Halevy has lived many lives. After surviving a childhood brain tumor and living with undiagnosed PTSD, he poured himself into achievement – becoming an award-winning, multi-exit entrepreneur in health, wellness, and technology. He built businesses at the intersection of fitness and behavior change, served as a correspondent for NBC's Today Show, hosted the internationally syndicated Workout From Within with Jeff Halevy, and advised on Michelle Obama's “Let's Move!” campaign. Outwardly, he was thriving. Internally, he was struggling.The pressure to produce and the need to stay in motion became unsustainable. Jeff eventually hit a spiritual bottom that forced him to reassess how he was living – redefining how he channeled his energy and passion in a healthier, more sustainable way. Not long after that shift, tragedy struck: his wife died by suicide following severe mental health challenges compounded by postpartum, leaving Jeff to raise two young children alone.In this conversation, Jeff shares the pain and trauma that shaped him, the emotional cost of high achievement, and how fatherhood became the anchor that kept him grounded. He also reflects on how his journey – through undiagnosed trauma, success, loss, and recovery – inspired the founding of Continuum, where he now serves as founder and CEO. Continuum is a luxury wellness club that uses biometric data and AI to deliver individualized, precision-based wellness – with the mission to make the practice of wellness as precise and intentional as the practice of medicine.This episode is about trauma, sobriety, grief, and turning pain into purpose: how one man's healing journey became the blueprint for helping others.Topics include:Emergency brain surgery as a teenager and its lasting psychological impactLiving with undiagnosed PTSD while building a wellness careerWhen overachievement becomes survival – and how that is not sustainableLosing his wife to suicide and raising two infants aloneBuilding and exiting multiple companies in fitness and healthFounding Continuum: precision wellness through biometric data and AIHow Jeff has come to view success through the lens of fatherhood and being emotionally present For more information about Jeff's new wellness company, Continuum, please click here: ContinuumConnect with Zachttps://www.instagram.com/zwclark/https://www.linkedin.com/in/zac-c-746b96254/https://www.tiktok.com/@zacwclarkhttps://www.strava.com/athletes/55697553https://twitter.com/zacwclarkIf you or anyone you know is struggling, please do not hesitate to contact Release:(914) 588-6564releaserecovery.com@releaserecovery

Normal pressure hydrocephalus (NPH) is a pathologic condition whereby excess CSF is retained in and around the brain despite normal intracranial pressure. MRI-safe programmable shunt valves allow for fluid drainage adjustment based on patients' symptoms and radiographic images. Approximately 75% of patients with NPH improve after shunt surgery regardless of shunt type or location. In this episode, Aaron Berkowitz, MD, PhD, FAAN, speaks with Kaisorn L. Chaichana, MD, author of the article “Management of Normal Pressure Hydrocephalus” in the Continuum® June 2025 Disorders of CSF Dynamics issue. Dr. Berkowitz is a Continuum® Audio interviewer and a professor of neurology at the University of California San Francisco in the Department of Neurology in San Francisco, California. Dr. Chaichana is a professor of neurology in the department of neurological surgery at the Mayo Clinic in Jacksonville, Florida. Additional Resources Read the article: Management 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 Guest: @kchaichanamd 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 Berkowitz: This is Dr Aaron Berkowitz, and today I'm interviewing Dr Kaisorn Chaichana about his article on management of normal pressure hydrocephalus, which he wrote with Dr Jeremy Cutsforth-Gregory. The 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 Chaichana: Yeah, thank you for having me. I'm Kaisorn Chaichana. I'm a neurosurgeon at Mayo Clinic in Jacksonville, Florida. Part of my practice is doing hydrocephalus care, which includes shunts for patients with normal pressure hydrocephalus. Dr Berkowitz: Fantastic. Well, before we get into shunt considerations and NPH specifically, which I know is the focus of your article, I thought it would be a great opportunity for a neurologist to pick a neurosurgeon's brain a bit about shunts. So, to start, can you lay out for us the different types of shunts and shunt procedures, the advantages, disadvantages of each type of shunt, how you think about which shunt procedure should be used for which patient, that type of thing? Dr Chaichana: Yeah. So, there are different types of shunts, and the most common one that is used is called a ventricular peritoneal shunt. So, it has a ventricular catheter, it has a catheter that tunnels underneath the skin and it goes into the peritoneum where the fluid goes from the ventricular system into the peritoneum. Typically, the shunts are in the ventricle because that is the largest fluid-filled space in the brain. Other terminal areas include the atrium, which is really the jugular vein, and those are called ventricular atrial shunts. You can also have ventricular pleural shunts, which end in the pleural space and drain flui into the pleural space. Those are pretty much the most common ventricular shunts. There's also a lumboperitoneal shunt that drains from the lumbar spine, similar to a lumbar drain into the peritoneum. For the lumbar shunts, we don't typically have a lumbar pleural or lumbar atrial shunt just because of the pressure dynamics, because the lumbar spine is below the lung and as well as the atrium. And so, the drainage pattern is very different than ventricular peritoneal which is top to bottom. The most common shunt, why we use the ventricular peritoneal shunt the most, is because it has the most control. So, the peritoneum is set at a standard pressure in the intraabdominal pressure, whereas the ventricular atrial shunt depends on your venous return or venous pressure and your ventricular pleural shunt varies with inspiration and expiration. So, the easiest way for us to control the fluid, the ventricular system is through the ventricular peritoneal shunt. And that's why that's our most common shunt that we use. Dr Berkowitz: Fantastic. So, as you mention in the article, neurologists may be reluctant to offer a shunt to patients with NPH because many patients may not improve, or they improve only transiently; and out of fear of shunt complications. So, of course, as neurologists, we often only hear about a patient's shunt when there is a problem. So, we have this sort of biased view of seeing a lot of shunt malfunction and shunt infection. Of course, we might not see the patient if their shunt is working just fine. How common are these complications in practice, and how do you as a neurosurgeon weigh the risks against the often uncertain or transient benefits of a shunt in a patient with NPH who may be older and multiple medical comorbidities? How do you think about that and talk about it with patients? Dr Chaichana: When you hear about shunt complications, most of the shunt complications you hear about are typically in patients with congenital hydrocephalus. Those patients often require several shunt revisions just from either growing or the shunt stays in for a long time or the ventricular caliber is a lot less than some with normal pressure hydrocephalus. So, we don't really see a lot of complications with normal pressure hydrocephalus. So that shunt placement in these patients is typically pretty safe. The procedure's a relatively short procedure, around 30 minutes to 45 minutes to place a shunt, and we can control the pressure within the shunt setting so that we don't overdrain---which means too much fluid drains from the ventricular system---which can cause things like a subdural, which is probably the most common complication associated with normal pressure hydrocephalus. So, to obviate those risks, what we do is typically insert the shunt and then keep the shunt setting at a high setting. The higher the setting, the less it drains, and then we bring it slowly down based on the patient's symptoms to try to minimize the risk of this over drainage in the subdural hematoma while at the same time benefiting the patient. So, there's a concern for shunt in patients with normal pressure hydrocephalus. The concern or the complication risks are very low. The problem with normal pressure hydrocephalus, though, is that over time these patients benefit less and less from drainage or their disease process takes over. So, I do recommend placing this shunt as soon as possible just so that we can maximize their quality of life for that period of time. Dr Berkowitz: So, if I'm understanding you, then the risk of complication is more sort of due to the mechanical factors in patients with congenital hydrocephalus or sort of outgrowing the shunt, their pressure dynamics may be changing over time. And in your experience, an older patient with NPH, although they may have more medical comorbidities, the procedure itself is relatively quick and low-risk. And the actual complications due to mechanical factors, my understanding, are just much less common because the patient is obviously fully grown and they're getting one sort of procedure at one point in time and tend to need less revision, have less complication. Is that right? Dr Chaichana: Yeah, that's correct. The complication risk for normal hydrocephalus is a lot less than other types of hydrocephalus. Dr Berkowitz: That's helpful to know. While we're talking about some of these complications, let's say we're following a patient in neurology with NPH who has a shunt. What are some of the symptoms and signs of shunt malfunction or shunt infection? And what are the best studies to order to evaluate for these if we're concerned about them? Dr Chaichana: Yeah. So basically, for shunt malfunction, it's basically broken down into two categories. It's either overdrainage or underdrainage. So, underdrainage is where the shunt doesn't function enough. And so basically, they return to their state before the shunt was placed. So that could be worsening gait function, memory function, urinary incontinence are the typical symptoms we look for in patients with normal pressure hydrocephalus and underdrainage, or the shunt is not working. For patients that are having overdrainage, which is draining too much, the classic sign is typically headaches when they stand up. And the reason behind that is when there's overdrainage, there's less cerebrospinal fluid in their ventricular system, which means less intracranial pressure. So that when they stand up, the pressure differential between their head and the ground is more than when they're lying down. And because of that pressure differential, they usually have worsening headaches when standing up or sitting up. The other thing are severe headaches, which would be a sign of a subdural hematoma or focality in their neurological symptoms that could point to a subdural hematoma, such as weakness, numbness, speaking problems, depending on the hemisphere. How we work this up is, regardless if you're concerned about overdrainage or underdrainage, we usually start with a CAT scan or an MRI scan. Typically, we prefer a CAT scan because it's quicker, but the CAT scan will show us if the ventricular caliber is the same and/or the placement of the proximal catheter. So, what we look for when we see that CAT scan or that MRI to see the location of the proximal catheter to make sure it hasn't changed from any previous settings. And then we see the caliber of the ventricles. If the caliber of the ventricles is smaller, that could be a sign of overdrainage. If the caliber of the ventricles are larger, it could be a sign of underdrainage. The other thing we look for are subdural fluid collections or hydromas or subdural hematomas, which would be another sign of lower endocranial pressure, which would be a sign of overdrainage. So those are the biggest signs we look for, for underdrainage and overdrainage. Other things we can look for if we're concerned of the shunt is fractured, we do a shunt X-ray and what a shunt x-ray is is x-rays of the skull, the neck and the abdomen to see the catheter to make sure it's not kinked or fractured. If you're really concerned, you can't tell from the x-ray, another scan to order is a CT of the chest and abdomen and pelvis to look at the location of the catheter to make sure there's no brakes in the catheter, there's no fluid collections on the distal portion of the catheter, which would be a sign of shunt malfunction as well. Other tests that you can do to really exclude shunt malfunction is a shunt patency test, and what that is a nuclear medicine test where radionucleotide is injected into the valve and then the radionucleotide is traced over time or imaged through time to make sure that it's draining appropriately from the valve into the distal catheter into the peritoneum or the distal site. If there's a shunt malfunction that's not drainage, that radioisotope would remain stagnant either in the valve or in the catheter. There's overdrainage, we can't really tell, but there will be a quick drainage of the radioisotope. For shunt infection, we start with an imaging just to make sure there's not a shunt malfunction, and that usually requires cerebrospinal fluid to test. The cerebrospinal fluid can come from the valve itself, or it can come from other areas like the lumbar spine. If the lumbar spine is showing signs of shunt infection, then that usually means the shunt is infected. If the valve is aspirated with- at the bedside with a butterfly needle into the valve and that shows signs of shunt infection, that also could be a sign of infection. Dr Berkowitz: That's very helpful. You mentioned CT and shunt series. One question that often comes up when obtaining neuroimaging in patients with a shunt, who have NPH or otherwise, is whether we need to call you when we're doing an MRI to reprogram the shunt before or after. Is there a way we can know as a neurologists at the bedside or as patients carry a card, like with some devices where we know whether we have to call and bother our neurosurgery colleagues to get this MRI? Or if the radiology techs ask us, is this safe? And is the patient's shunt going to get turned off? How do we go about determining this? Dr Chaichana: Yeah, so unfortunately, a lot of patients don't carry a card. We typically offer a card when we do the shunt, but that card, there's two problems with it. One is it tells the model, but the second thing is it has to be updated any time the shunt is changed to a different setting. Oftentimes patients don't know that shunt setting, and often times they don't know that company brand that they use. There are different types of shunts with different types of settings. If there's ever concern as to what type of shunt they have, an x-ray is usually the best bet to see with a shunt series, or a skull x-ray. A lateral skull x-ray usually looks at the valve, and the valve has certain radio-dense markers that indicate what type of shunt it is. And that way you can call neurosurgery and we can always tell you what the shunt setting is before the MRI is done. Problem with an MRI scan if you do it without a shunt x-ray before is that you don't know the setting before unless the patient really knows or it's in the patient chart, and the MRI can need to change the setting. It doesn't usually turn it off, but it would change the setting, which would change the fluid dynamics within their ventricular system, which could lead to overdrainage or underdrainage. So, any time a patient needs MRI imaging, whether it's even the brain MRI, a spine MRI, or even abdominal MRI, really a shunt x-ray should be done just to see the shunt setting so that it could be returned to that setting after the MRI is done. Dr Berkowitz: So, the only way to know sort of what type of shunt it would be short of the patient knowing or the patient getting care at the same hospital where the shunt was placed and looking it up in the operative reports would be a skull film. That would then tell us what type of shunt is there and then the marking of the setting. And then we would be able to call our colleagues in neurosurgery and say, this patient is getting an MRI this is the setting, this is the type of shunt. And do we need to call you afterwards to come by and reprogram it? Is that right? Dr Chaichana: That's correct, yeah. Dr Berkowitz: Is there anything we would be able to see on there, or it's best we just- best we just call you and clarify? Dr Chaichana: The easiest thing to do is, when you get the skull x-ray, you can Google different types of shunts or search for different shunts, and they'll have markers that show the type of shunt it is as well as the setting that it's at. And just match it up with the picture. Dr Berkowitz: And as long as it's not a programmable shunt, there's no concern about doing the MRI. Is that right? Dr Chaichana: Correct. So, if it's a programmable shunt, even if it's MRI-compatible, we still like to get the setting before and make sure the setting after the MRI is the same. Nonprogrammable shunts can't be changed with MRI scans, and those don't need neurosurgery after the MRI scan, but it should be confirmed before the scan is done. Dr Berkowitz: Very helpful. Okay, so let's turn to NPH specifically. As you know, there's a lot of debate in the literature, some arguing, even, NPH might not even exist, some saying it's underdiagnosed. I think. I don't know if it was last year at our American Academy of Neurology conference or certainly in recent years, there was a pro and con debate of “we are underdiagnosing NPH” versus “we are overdiagnosing NPH.” What's your perspective as a neurosurgeon? What's the perspective in neurosurgery? Is this something we're underdiagnosing, and the times you shunt these patients you see miraculous results? Is this something that we're overdiagnosing, you get a lot of patients sent to that you think maybe won't benefit from a shunt? Or is it just really hard to say and some patients have shunt-responsive noncommunicating hydrocephalus of unclear etiology and either concurrent Parkinson's disease, Alzheimer's, cervical lumbar stenosis, neuropathy, vestibular problems, and all these other issues that play into multifactorial gait to sort of display a certain amount of the percentage of problem in a given patient or take overtime? What's your perspective if you're open to sharing it, or what's the perspective of neurosurgery? Is this debated as it is in neurology or this is just a standard thing you see and patients respond to shunt to some degree in some proportion of the time? And what are the sort of predictors you see in your experience? Dr Chaichana: Yeah, so, for me, I'd say it's too complicated for a neurosurgeon to evaluate. We rely on neurology to tell us whether or not they need a shunt. But I think the problem is, obviously, a part of the workout for at least the ones that I like to do, is that I want them to have a high-volume lumbar puncture with pre- and postgait analysis to see if there's really an objective measure of them improving. If they have an objective measure of improvement---and what's even better is that they have a subjective measure of improvement on top of the objective measure of improvement---then they benefit from a shunt. The problem is, some patients do benefit even though they don't have objective performance increases after a high-volume shunt. And those are the ones that make me the most worrisome to do the shunt, just because I don't like to do a procedure where there's no benefit for the patient. I do see, according to the literature as well, that there's around a 30 to 40%, even 50%, increase in gait function, even in patients that don't have large improvements following the high-volume lumbar puncture. And those are the most challenging patients for us as neurosurgeons because we'll put the shunt in, they say we're no better in terms of their gait, no better in terms of their urinary incontinence. We try to lower their shunt down to a certain setting and we're kind of stuck after that point. The good thing about NPH, though, is that, from the neurosurgery side, the shunt, like I said, is a pretty benign, low-risk procedure. So, we're not putting the patient through a very severe procedure to see if there's any benefit. So, in cases where we try to improve their quality of life in patients that don't have a benefit from high-volume lumbar puncture, we give them the odds of whether or not it's improving and say it might not improve. But because the procedure's minimally invasive, I think it's a good way to see if we can benefit their quality of life. Dr Berkowitz: Yeah, it's a very helpful perspective. Yeah, those are the most challenging cases on our side as well, right. If the patient- we think they may have NPH, or their gait and/or urinary and/or cognitive problems are- at least have a component of NPH that could be reversible, we certainly want to do the large volume lumbar puncture and/or consider a lumbar drain trial, all discussed in other articles and interviews for this issue of Continuum, But the really tough ones, as you said, there is this literature on patients who don't respond to the large-volume lumbar puncture for some reason but still may be shunt responsive. And despite all the imaging predictors and all the other ways we try to think about this, it's hard to know who's going to benefit. I think that's really a helpful perspective from your end that, as you say in the very beginning of your article, right, maybe there's a little bit too much fear of shunting on the neurology side because when we hear about shunts, it's often in the setting of complication. And so, we're not sort of getting the full spectrum of all the patients you shunt and you see who are doing just fine. They might not improve---the question is related to NPH---but at least they're not harmed by the shunt, and we're maybe overbiased and/or seeing a overly representative sample of negative shunt outcomes when they're actually not that common in practice. Is that a fair summary of your perspective? Dr Chaichana: Yeah, that's correct. So, I mean, complications can occur---and anytime you do a surgery, there are risks of complications---but I think they're relatively low for the benefit that we can help their quality of life. And the procedure's pretty short. So, the risk, it mostly outweighs the benefits in cases with normal pressure hydrocephalus. Dr Berkowitz: Very helpful perspective. So, well, thanks so much again. Today I've been interviewing Dr Kaisorn Chaichana about his article on management of normal pressure hydrocephalus, which he wrote with Dr Jeremy Cutsforth-Gregory. 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 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.

               0:00- Intro               1:00- Alex staying lean               2:00- Bodybuilders continuing to do the same thing year after year               10:00- Should you really care about going on PEDs at an older age?               13:30- Natural limitations               22:00- Wide Grip Pull Ups / Calisthenics               49:30- How Alex is training for Pull Up PRs

John Mee from Outhouse talks to PJ about the gaps in mental health support for Ireland's LGBTQ+ community—and how their groundbreaking ‘Continuum of Care' programme is saving lives long after the rainbow flags come down Hosted on Acast. See acast.com/privacy for more information.

10e émission de la 62e session...Cette semaine, on fait le plein de post-bop! En musique: Art Pepper sur l'album An Afternoon in Norway: The Kongsberg Concert (Elemental, 2025, enr. 1980); Jamale Davis sur l'album Run With The Hunted  (SteepleChase, 2024); CODE Quartet sur l'album CODE Red  (Justin Time, 2025); Jeremy Pelt sur l'album Woven  (HighNote, 2025); Nathan Ott Quartett sur l'album Continuum  (An:Bruch, 2025)...

 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.

Through the lens of Context, Contrast, and Continuum, I introduce a new mental model—one that honors nuance, invites integration, and transcends the binary habits that shape much of our perception. I like to call it the evolution of yin and yang symbol and it's very useful in everyday life. What do you think of the episode? Let's talk about it! Reach out on IG @lovingchallengers or send me a message megan@meganbhatia.com Learn more about the Loving Challengers Community click here!

Big thank you to actress and executive producer Rachel Nichols for coming on my show for an interview! Rachel Nichols talked about attending Columbia University, getting discovered by modeling agents in New York, and her audition for The Amityville Horror. She discussed Wes Bentley being protective of her while filming P2, having to face her fears of swimming underwater while filming Inside, and working with Nicholas Cage. She got into why Continuum ended at 4 seasons despite being a hit show, becoming an executive producer on Raze and Demigod, and getting injured while filming G.I. Joe: The Rise of Cobra. Rachel also spoke about the struggles Hollywood has been facing since the new administration took over, her charity work, and what she is currently working on next. Stay tuned! Follow Rachel Nichols on Instagram: @ticklenichols Follow me on Instagram and X: @thereelmax Website: https://maxcoughlan.com/index.html. Website live show streaming link: https://maxcoughlan.com/sports-and-hip-hop-with-dj-mad-max-live-stream.html. MAD MAX Radio on Live365: https://live365.com/station/MAD-MAX-Radio-a15096. Subscribe to my YouTube channel Sports and Hip Hop with DJ Mad Max: https://m.youtube.com/channel/UCE0107atIPV-mVm0M3UJyPg. Rachel Nichols on "Sports and Hip-Hop with DJ Mad Max" visual on YouTube: https://www.youtube.com/watch?v=CyBhRVkAafk. 

Join Justin as he chats with actor Tahmoh Penikett about growing up in the wilderness, his paranormal experiences, fatherhood, overcoming impostor syndrome, Battlestar Galactica, Trick 'r Treat, Supernatural, and more!Tahmoh Penikett bio:“Tahmoh Penikett (born May 20, 1975) is a Canadian actor. He is known for playing Karl "Helo" Agathon on SyFy's 2004 television series Battlestar Galactica and Paul Ballard in the Fox series Dollhouse. He has appeared in TV series Supernatural, the Showcase time travel show Continuum, and as the antagonist Darius in the 2006 racing video game Need for Speed: Carbon. “Intro and outro theme created by Wyrm. Support Wyrm by visiting the Serpents Sword Records bandcamp page (linked below):https://serpentsswordrecords.bandcamp.com/Monsters, Madness and Magic Official Website. Monsters, Madness and Magic on Linktree.Monsters, Madness and Magic on Instagram.Monsters, Madness and Magic on Facebook.Monsters, Madness and Magic on Twitter.

Layne and Jon take a look back at all that has come before in The Transformers: Continuum and then launch into the first proper ongoing series from IDW with The Transformers 1, both from 2009!

Layne and Jon take a look back at all that has come before in The Transformers: Continuum and then launch into the first proper ongoing series from IDW with The Transformers 1, both from 2009!

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.

This content has been developed for healthcare professionals only. Patients who seek health information should consult with their physician or relevant patient advocacy groups.For the full presentation, downloadable Practice Aids, slides, and complete CME/MOC/AAPA information, and to apply for credit, please visit us at PeerView.com/AWM865. CME/MOC/AAPA credit will be available until June 30, 2026.Strategies for Immunotherapy Success in NSCLC: How to Incorporate Modern ICI Platforms Across the Disease Continuum In support of improving patient care, this activity has been planned and implemented by PVI, PeerView Institute for Medical Education, and LUNGevity Foundation. PVI, PeerView Institute for Medical Education, is jointly accredited by the Accreditation Council for Continuing Medical Education (ACCME), the Accreditation Council for Pharmacy Education (ACPE), and the American Nurses Credentialing Center (ANCC), to provide continuing education for the healthcare team.SupportThis activity is supported through independent educational grants from Bristol Myers Squibb, Merck & Co., Inc., Rahway, NJ, USA, and Regeneron Pharmaceuticals, Inc.Disclosure information is available at the beginning of the video presentation.

This content has been developed for healthcare professionals only. Patients who seek health information should consult with their physician or relevant patient advocacy groups.For the full presentation, downloadable Practice Aids, slides, and complete CME/MOC/AAPA information, and to apply for credit, please visit us at PeerView.com/AWM865. CME/MOC/AAPA credit will be available until June 30, 2026.Strategies for Immunotherapy Success in NSCLC: How to Incorporate Modern ICI Platforms Across the Disease Continuum In support of improving patient care, this activity has been planned and implemented by PVI, PeerView Institute for Medical Education, and LUNGevity Foundation. PVI, PeerView Institute for Medical Education, is jointly accredited by the Accreditation Council for Continuing Medical Education (ACCME), the Accreditation Council for Pharmacy Education (ACPE), and the American Nurses Credentialing Center (ANCC), to provide continuing education for the healthcare team.SupportThis activity is supported through independent educational grants from Bristol Myers Squibb, Merck & Co., Inc., Rahway, NJ, USA, and Regeneron Pharmaceuticals, Inc.Disclosure information is available at the beginning of the video presentation.

This content has been developed for healthcare professionals only. Patients who seek health information should consult with their physician or relevant patient advocacy groups.For the full presentation, downloadable Practice Aids, slides, and complete CME/MOC/AAPA information, and to apply for credit, please visit us at PeerView.com/AWM865. CME/MOC/AAPA credit will be available until June 30, 2026.Strategies for Immunotherapy Success in NSCLC: How to Incorporate Modern ICI Platforms Across the Disease Continuum In support of improving patient care, this activity has been planned and implemented by PVI, PeerView Institute for Medical Education, and LUNGevity Foundation. PVI, PeerView Institute for Medical Education, is jointly accredited by the Accreditation Council for Continuing Medical Education (ACCME), the Accreditation Council for Pharmacy Education (ACPE), and the American Nurses Credentialing Center (ANCC), to provide continuing education for the healthcare team.SupportThis activity is supported through independent educational grants from Bristol Myers Squibb, Merck & Co., Inc., Rahway, NJ, USA, and Regeneron Pharmaceuticals, Inc.Disclosure information is available at the beginning of the video presentation.

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.

Rey walks us through the first part of David Austin Walsh's book Taking America Back, which is centered around Hart's career in the 1933-1953 period. Merwin was a "liminal figure of the US right-wing", able to meet the president in the White House, but also to work together with known fascist "crackpots" (Coughlin, G. L. K. Smith, Wesley Swift...). Subscribe to patreon.org/tenepod @tenepod.bsky.social  + x.com/tenepod

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.

Welcome, welcome, welcome to the Distraction Pieces Podcast with Scroobius Pip!This week Pip is joined by a long awaited guest and general acting legend, DOMHNALL GLEESON!Business first - if Percy Pigs want to come through and sponsor the podcast we're all on board (you're welcome Percy for the free plug btw

Sacramento County Board of Supervisors meeting, primarily focusing on grant allocations, and health initiatives.  A significant portion of the discussion revolves around the Transient Occupancy Tax (TOT) Grant program, with supervisors debating funding distribution to various non-profit organizations and expressing appreciation for their community work, particularly in literacy and homeless services. Another key theme is the state of sexually transmitted infections (STIs) in Sacramento County, highlighting high rates, prevention efforts, and the crucial role of the county's sexual health clinic, alongside concerns about potential federal funding cuts. The session concludes with board member comments, including a proposal to explore bringing the Continuum of Care model for homeless services back under county oversight.

660. The physical and emotional pain you have worked through is your gift to give to humanity and Joey Corona proves it. Joey Corona is a lifelong Meta Mover, Movement catalyst, motivator, and longevity expert. He holds a master's degree in Physical Education and Exercise Physiology from Florida International University (where he competed on the men's golf team) and a post-grad certification in Golf Biomechanics from the Chek institute and The Titleist Performance Institute. He recently added a bachelor's and master's degree in golf stroke engineering from The Golfing Machine. His golf accomplishments include the Illinois Junior college championship and the Chicago City Amateur Championship as well as 35 other titles. He is a devout Black Belt Martial Artist in Shotokan Karate. After grad school, Joey went to Sea with Norwegian Cruise Line as Onboard Fitness Director heading their Sports Afloat Program and traveling the World. While with NCL he interviewed over 500 professional athletes as NCL became the Official Cruise Line of the NFLPA, Major League Baseball, the PGA, NHL, AVP, NHL, NASCAR, and the NBA. After ships, he directed the "Sports Afloat" program from NCL's home offices. As a yoga teacher, he has attained E-RYT status, the highest credential of the Yoga Alliance. His students include Mel Brooks, Anne Bancroft, Alicia Silverstone, Vanessa Williams, Boris Becker, Vince Vaughn, Isaiah Thomas, and Gabrielle Anwar. Currently, he works with Olympic gold medal boxer Cool Hand Luke Campbell and World Middleweight Champion Vitaly Kopelynko. He was the official yoga teacher for the Michael Jordan Celebrity Golf Tournament at the Ocean Club in the Bahamas. And the creator of GolfYoga. The professional golfers that he has taught include Jim McLean, Erik Compton, Willy Pumarol, Veronica Felibert, Helen Alfredson, Charlotta Sorenstam, and Jill McGill. He was recently invited to teach at the National Yoga Journal Conference. Joey combines his quick wit, levity, command of anatomy and physiology, biomechanics, kinesiology, and his love of music into a sensational movement experience. He teaches his signature Yoga program exclusively in the Miami area at LaGorce Country Club, Trump National Doral Golf Resort and Spa, The Continuum, Fisher Island Spa, Anatomy @ 1220, and the Equinox Fitness Centers. He has appeared on The Today Show, Fox and Friends Live, Deco Drive and contributed articles for Fit Magazine, Golf for Women, and Shape. "There is absolutely no better human movement protocol Than Yoga. After 5000 years of testing, yoga has proven itself and is the finest longitudinal study of health science known to man. “Some people move Mountains, I move People!” Joey says about his passion for instructing Yoga.  

Simon Barry (Warrior Nun, Continuum) returns to the YVR Screen Scene Podcast to discuss his latest series. Bet – 10 episodes of which dropped on Netflix in May 2025 – draws its inspiration from the manga Kakegurai – Compulsive Gambler. The series tells the story of Yumeko (portrayed by Miku Martineau), a young woman who enrols in an exclusive boarding school to avenge the murder of her parents. This exclusive boarding school ain't Hogwarts: it's a cutthroat academy run by a powerful Student Council whose power structure is entirely based on gambling. Yumeko's prowess at gambling and her overarching revenge quest put her in the crosshairs of the Student Council and its formidable president, Kira – leading to a showdown that is both high-octane and deeply satisfying.Bet is at once a breath of fresh air and exactly what we've come to expect from Simon Barry: a wildly entertaining adventure set in an unexpected world about a whip-smart woman on a seemingly impossible quest. In this fascinating interview, Simon discusses his journey with Bet, what Miku Martineau brought to the pivotal role of Yumeko, his thoughts on AI, collaborating with director Jacquie Gould (Outlander, Obi-Wan Kenobi), Dennis Heaton's brain, and what he learned from Warrior Nun and its fans.Episode sponsor: Directors Guild Of Canada, BC District Council

Tiffany, Kelly and Steve talk about emotions associated with pediatric cancer diagnosis from the perspective of a pediatric cancer survivor, a pediatric cancer parent and a bereaved pediatric cancer parent. Reintroducing: Steve Garraty was lucky to be graduating high school. He was partying and living a lifestyle that wasn't sustainable. His priorities were upside down. He was running towards the edge of a cliff and unable to stop himself. Then God intervened. He heard the three dreaded words none of us ever want to hear: “You have cancer.”After embarking on chemotherapy and a year of hell, as all his friends headed off to college, he beat the cancer. He went from victim to victor, from asking “Why me” to “Why not me?” He ended up not only surviving but thriving.Today, Steve has been married for more than thirty years to his beautiful wife, Wendy. They have raised two incredible kids who have both graduated college and begun their own careers. Steve has had a successful career in sales and leadership. He's hired more than 250 people in his career. He's coached and developed more than a thousand sales contributors and sales leaders. He cares deeply about helping others and seeing others achieve success and accomplishing their goals.He views cancer as being the best thing to ever happen to him. It changed everything…for the better! He grew from his experience. It set the foundation to be a better husband, father, friend, and leader. He writes to share his experience to help others alter their perspective and view the glass as full!Steve resides in Tampa, Florida. He enjoys traveling, music, exercise, watching UGA football with his son, and spending as much time with family as possible.https://stevegarraty.com/https://www.instagram.com/stevegarratyauthor/If you want to donate to Gold Ribbon Kids: https://givebutter.com/gold-ribbon-kids-cancer-foundationto learn more go to:goldribbon-kids.orgnationalpcf.orgkgoddard@nationalpcf.org - Kellyinfo@goldribbon-kids.org - TiffanySupport the show

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.

Spontaneous intracranial hypotension reflects a disruption of the normal continuous production, circulation, and reabsorption of CSF. Diagnosis requires the recognition of common and uncommon presentations, careful selection and scrutiny of brain and spine imaging, and, frequently, referral to specialist centers.  In this episode, Gordon Smith, MD, FAAN speaks with Jill C. Rau, MD, PhD, author of the article “Clinical Features and Diagnosis of Spontaneous Intracranial Hypotension” in the Continuum® June 2025 Disorders of CSF Dynamics issue. Dr. Smith is a Continuum® Audio interviewer and a professor and chair of neurology at Kenneth and Dianne Wright Distinguished Chair in Clinical and Translational Research at Virginia Commonwealth University in Richmond, Virginia. Dr. Rau is an assistant professor of clinical neurology at the University of Arizona, School of Medicine-Phoenix in Phoenix, Arizona. Additional Resources Read the article: continuumjournal.com 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: @gordonsmithMD Full episode transcript available here Interview with Jill Rau, MD 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 Smith: This is Dr Gordon Smith. Today I'm interviewing Dr Jill Rau about her article on clinical features and diagnosis of spontaneous intracranial hypotension, which she wrote with Dr Jeremy Cutsworth-Gregory from the Mayo Clinic. This article appears in the 2025 Continuum issue on disorders of CSF dynamics. I'm really excited to welcome you to the Continuum podcast. Maybe you can start by just telling our listeners a little bit about yourself? Dr Rau: Hi, thanks for having me. I'm really honored to be here, and I really enjoyed writing the paper with Dr Cutsforth-Gregory. I hope you guys enjoy it. I am the director of headache medicine at the Baba Bay Neuroscience Institute at Honor Health in Scottsdale, Arizona. I'm also currently the chair of the special interest group in CSF Dynamics at the American Headache Society, and I've had a special interest in this field since I first watched Dr Linda Gray speak at a conference where she talked about spinal CSF leaks and their different presentations. And they were so different than what I had been taught in residency. They're not just the post-LP headache. They have such a wide variety of presentations and how devastating they can be, and how much impact there is on someone's life when you find it and fix it. And I've been super interested in the field and involved in research since that time. And, yeah. Love it. Dr Smith: Well, thanks for sharing your story. And as I reflected on our conversation ahead of time and have been thinking about this issue… this is a cool topic, and every time I read one of these manuscripts and have the opportunity to speak with one of the authors, I learn a ton, because this was something that wasn't even on the radar when I trained back in the 1800's. So, really looking forward to the conversation. I wonder if you could really briefly just summarize or remind for everyone the normal physiology about CSF dynamics, you know, production, absorption, and so forth? Dr Rau: So, the CSF is the fluid that surrounds the brain and the spinal cord, and it's contained by the dura, which is like a canvas or a sac that covers that whole brain and spinal cord. And within the ventricles of the brain, the choroid plexus produce CSF. It's constantly producing and then being reabsorbed by the arachnoid granulations and pushed into the venous space, the cerebral sinuses, venous sinuses. And also some absorption and push into the lymphatics that we've just learned about in the past year. This is kind of new data coming out, so always learning more and more about CSF, but we know that it bathes the brain and the spinal cord, helps keep some buoyancy of the brain as well as pushing nutrients in and pulling out metabolic waste. And it sort of keeps the brain in the state of homeostasis that's happy. And so, when there's a disruption of that flow and the amount of fluid there, that disrupts that, that can cause lots of different symptoms and problems for people. Dr Smith: One of the many new things I learned is that even the name of this---spontaneous intracranial hypotension---is misleading. And I think this is clinically relevant, as we'll probably get to in a moment, but can you talk a little bit about this? Is this really like a pressure disorder or a volume disorder? Dr Rau: Yeah. It's almost certainly a volume disorder. We do see in some people that they have low pressure, and it's still part of the diagnostic criteria. But it's there because if you have a low pressure, if you measure an opening pressure and it's below six, if you're measuring it in the spine in the right place, then you have indication that there's low volume. But there's over 50% of people's opening pressure who have a spinal CSF leak, have all the symptoms and can be fixed. So, they have normal pressure in 50% of the people. So, it is an inaccurate term, hypotension, but it was originally discovered because of the thought that it was a low-pressure situation. Some of the findings would suggest low pressure, but ultimately, we are pretty sure it's a low-volume condition. Dr Smith: Another new thing that I learned that really blew me away is how bad this can be. I did a podcast with Mark Burish about cluster, and I was reminded many cluster patients are pushed to the point of suicidal ideation or committing suicide by the severity of pain. And this sounds like for many patients it's equally severe. Can you maybe paint a picture for our listeners why this is so clinically important? Dr Rau: A large number of people, even people who are known to have leaks because they've had them before or they've releaked, they have a lot of brain fog and cognitive impairment. They often have severe headaches when they're upright. So, orthostatic headache is probably the number one most common symptom, and those headaches are one of the worst headaches out there. When people stand up, their fluid is not supporting the brain and there's an intense amount of pain. And so, they spend a large portion of their lives horizontal. And there's associated symptoms with that, it's not just headache pain and brain fog. There's neck pain. There's often subsequent disorders that accompany this, like partial orthostatic tachycardia syndrome. We don't know if that's because of deconditioning or an actual sequela of the disease, but it's a frequent comorbidity. We have patients that have extreme dizziness with their symptoms, but many patients are limited to hours, if that, upright per day, combined, total. And so they live their lives, often, just in the dark, lots of photophobia, sensitive to the light, really unable to function. It's also very hard to find and so underrecognized that a lot of patients, especially if they don't have that really clinical symptom of orthostatic headache. So, it's often missed. So, they're just debilitated. You know, treatments don't work because it's not a migraine and it's not a typical headache. It's a mechanical issue as well as a metabolic issue and not found, not a lot helps it. Dr Smith: So, you know, I have always thought about this as really primarily an orthostatic symptom. I wonder if you can talk about the complexity of this; in particular, kind of how this evolves over time, because it's not quite that simple. And maybe in doing so, you can give our listeners some pearls on when they should be thinking about this disorder? Dr Rau: A large portion of people do have headache with spinal CSF leak, in particular, spontaneous intracranial hypertension- hypotension, excuse me. And that's something to be thought about, is that there are spontaneous conditions where people have either rupture of the dural sac, or an erosion of the dural sac, or a development of a connection between the dura and the venous system. And that is taking away or allowing CSF to escape. In these instances that patients have spontaneous, there may be a different presentation than if they have, like, a postdural puncture or a chronic traumatic or iatrogenic leak. And we're not sure of that yet, but we're looking into that. Still, the largest presentation is headache, and orthostatic headache is very dominant in the headache realm. But over time, patients' brains can compensate for that lack of CSF and start overproducing---or at least we think that's probably what's happening. And you may see a reduction in the orthostatic symptoms over time, and you may see an improvement in the radiographic findings. So, there are some interesting papers that have been published that look at these changes over time, and we do see that sometimes within that first three to four months; this is the most common time to see that change. Other patients may worsen. You may actually see someone going from looking sort of normal radiographically to developing more of a SIH-type of picture on the brain. And so it's not predictable which patients have gone from orthostatic to improvement or the other way around, both radiographically and clinically. So, it can be quite difficult to tell. So, for me, if I have a patient that comes to me and they're struggling with headache… if it's orthostatic, very clearly orthostatic: I lay down, I get considerably better or my headache completely goes away. And then when I stand up, it comes on relatively quickly, within an hour. And sometimes it's a worsening-throughout-the-day type of thing, it's lowest in the morning and it worsens throughout the day. These are the times that it's most obvious to think about CSF leak. Especially if that headache onset relatively suddenly, if it onset after a small trauma. Like I've had patients that say, you know, I was doing yoga and I did some twists and I felt kind of a pop. And then I've had this headache that is horrible when I'm upright but is better when I lay down ever since, you know, since that time. That's kind of a very classic presentation of spinal CSF leak or spontaneous intracranial hypotension. Maybe a less common presentation would be someone who comes to you, they've had a persistent headache for a couple years, they kind of remember it started in March of a couple years ago, but they don't know. Maybe it's, you know, it's a little better when they lay down. It may be a little worse when they're up moving around, but so is migraine, and it's a migrainous headache. But they've tried every migraine drug you can think of. Nothing is responding, nothing helps. I'm always looking at patients who are new daily, persistent headaches and patients who aren't responding to meds even if it's not new daily, but they have just barely any response. I will always go back and examine their brain imaging and get full spine to make sure I'm not missing. And you can never be 100% sure, but it's always good to consider those patients to the best of your ability, if that- have that in the back of your mind. Dr Smith: So obviously, goes without saying, this is something people need to have on their radar and think about. And then we'll talk more about diagnostic tools here in a second. But how common is this? If you're a headache doc, you see a lot of patients who have intractable headaches. And how often do you see this in your headache practice? Now you're- this is your thing, so probably a little more than others, but, you know, how common will someone who sees a lot of headache encounter these patients? Dr Rau: If you see a lot of headache, I mean, currently the thought is it's about 5 in 100,000. That was from a study before we were finding CSF venous fistulas. I think a lot of us think it's more common than that, but it's not super common. We don't have good estimates, but I would guess between 5 and 10 for 100,000 persons, not “persons who come to a tertiary headache clinic with intractable headaches”. So, it's hard to gauge how frequent it is, but I would say it's considerably more frequent than we currently think it is. There's still a group of people with orthostatic headaches that we can't find leaks on; that, once you treat other things that can cause or look for other things that can cause orthostatic headaches. So, there may be even still a pathophysiology out there that is still a leak type. Before 2014, we didn't even know about CSF venous fistulas. And now here we are; like, 50% of them are CSF venous fistulas. So, you know, we're still in a huge learning curve right now. Dr Smith: So, I definitely want to talk about the fistulas in a second. But before moving on, one of the things that I found really interesting is the wide spectrum of clinical phenotype. And we obviously don't have a lot of time to get into all of these different ones, but the one that I was hoping you might talk about---and there's a really great case, and you're on bunch of great case, a great case of this---is brain sagging dementia, not a term I've used before. Can you really briefly just tell our listeners about that, because that's a really interesting story and a great case in your article? Dr Rau: Yeah. So, brain sag dementia is a… almost like an extreme version of a spontaneous intracranial hypotension. Where there is clear brain sag in the imaging---so that's helpful---but the patients present kind of like a frontotemporal dementia. And when this was first started to being determined, you could turn the patient into Trendelenburg, and sometimes they would improve. There are some practitioners that have introduced fluid into the thecal sac and had temporary improvement. Patching has improvement, then they leak again, sometimes  not. But the clinical changes with this have been pretty tremendous to be able to identify that that's a real thing. And in some cases, out of Cedars Sinai, you know, who does a lot of the best research in this, they've had lots of cases where they can't find the leak, but there's clear brain sag that fits with our clinical picture of CSF leaks. So, we're on a learning curve. But yeah, this- they really present. They have disinhibition and cognitive impairment that is very similar to frontotemporal dementia. Dr Smith: Well, so let's talk about what causes this. You mentioned CSF venous fistulas. I mean, that was reported now just over a decade ago, it's pretty amazing. That accounts for about half of cases, if I understand correctly. What are the other causes? And then we'll talk more about therapy in a minute, but what causes this? Dr Rau: So, within the realm of spontaneous, you know, we say it's spontaneous. But the spontaneous cases we account for, they can be tears in the dura, which are usually sort of lateral tears in the dura. They can be little places that rubbed a hole, often on an osteophyte from the spine. They can come from these spinal diverticuli. So, I always describe it to my patients like those balls that have mesh and squishy, and you squeeze them in the- through the mesh, there's the extra little bubbling out. If you think of like the dura bubbling, out in some cases, through the framing of the spine, right where the spinal nerve roots come out, they should poke out like wires from the dura. But in many cases they poke out with this extra dura surrounding them, and we call that spinal diverticuli. And if you imagine like the weakening of where you squeeze that, you know, balloon through your fingers, in those locations, that's a very common place to find a CSF leak, and you can imagine that the integrity of the dura there may be less than it would be if it were not being expanded in that direction. And that's often the most common place we see these CSF venous fistulas. So, you can get minor traumas; like I said, it can be spontaneous, like someone just develops a leak one day. It can be rubbed off, and it can be a development of a connection between the dura and the venous system. There are also iatrogenic causes, but we don't consider them spontaneous. But when you're considering your patients for spontaneous cases, you should consider if they've ever had chronic---even long, long time ago---had any spinal implementation, procedures near the spine, spinal injections, LPs in the past, and especially women who've had epidurals in pregnancy. Dr Smith: All right, so we see a patient, positional severe headache, who meets the clinical criteria. Next step, MRI scan? Dr Rau: Yeah. So, the first thing is always to get the brain MRI with and without contrast. Most places will have a SIH or a spinal CSF leak protocol, but you should get contrast because one of the most pathognomonic findings on brain MRI is that smooth diffuse dural enhancement. And that's a really fantastic thing when you find it, because it's kind of a slam dunk. If you find it, then you will see other findings. It almost never exists alone. But if you see that, it's pretty much a spinal CSF leak. But you're also looking for subdural collections, any indication of brain sag. We do have these new algorithms that have come out in the past couple of years that are helpful. They're not exclusionary---you can have negative findings on the brain and still have spinal CSF leak---but the brain MRI is extremely helpful. If it's positive for the findings, it really does help you nudge you in the direction of further investigations and treatments. Dr Smith: And what about those further investigations and treatments, right? So, you see that there's findings consistent with low pressure, and I guess I should say low intracranial CSF volume. Be that as it may, what's the next step after that? Dr Rau: Depends on where you are and what you can do. I almost always will get a full spine MRI: so, C spine, T spine, and L spine separately. Not, you know, we don't want it all in one picture, because we want to get the full view. And you want to get that with at least T2 highly- heavily T2 weighted with fat saturation in at least the sagittal and axial planes. It's really helpful if you can get it in the coronal planes, but we have to have- often have good talks with your radiologist to get the coronal plane. I spoke about the spinal diverticuli earlier, and I want to clarify a little bit of something. The coronal image will show those really nicely. It's interesting, but 44% of people have those. So just having the spinal diverticuli does not indicate that you have a leak. But if you have a lot of those, there may be more likelihood of having leak than if you don't have any of those. So, I will get all of those and I will look at them myself, but I've been looking at them myself for a long time. But a lot of radiologists in community hospitals, especially not- nonneuroradiologists, but even neuroradiologists, this isn't something that's that everybody's been educated about, and we've been learning so much about it so rapidly in the past ten years. It's not easy to do and it's often missed. And if it's not protocoled properly, the fat saturation's not there, it's very hard to see… you can have a leak and not see it. Even the best people, like- it's not always something that's visible. And these CSF venous fistulas that we talked about are never visible on normal MRI imaging. Nonetheless, I will run those because if I can find a leak---and 90% of the ones that are found on MRI imaging are in the thoracic spine. So that's where I spend the most of my time looking. But if you find it, that's another thing to take to your team to say, hey, look, here it is, let's try and do this, or, let's try and do that, or, I've got more evidence. And there are other findings on the spine; not just the leak, but other findings, sometimes, you can see on spine that maybe help you push you towards, yes, this is probably a leak versus not. Dr Smith: So, your article has a lot of great examples and detail about kind of advanced imaging to, like, find the fistula and what not. I guess I'm thinking most of our listeners are probably practicing in a location where they don't have a team that really focuses on that. So, let's say we do the imaging of the spine and you don't find a clear cause. Is the next step to just do a blood patch? Do you send them to someone like you? What's the practical next step? Dr Rau: Yeah, if your- regardless of whether you find a leak or not, if your clinical acumen is such that you think this patient has a leak or I've treated them for everything else and it's not working and I have at least a high enough suspicion that I think the risk of getting a patch is lower than the benefit that if they got a patch and it worked, I do send my patients for non-directed blood patches, because it currently does take a long time to get them to a center that can do CT myelograms or any kind of advanced imaging to look for sort of a CSF venous fistula or to get treated outside of a nondirected patch. You know, sometimes nondirected patches are beneficial for patients, and there's some good papers out there that sort of explain the low risks of doing these if done properly versus the extreme benefit for patients when it works. And, I mean, I can't tell you how many people come in and tell me how their lives are changed because they finally got a blood patch. And sometimes it works. And it's life-changing for those people. You know, they go back to work. They can interact with their kids again. Before, they didn't know what was wrong, just had this headache that started. So it's worth doing if you have a strong clinical suspicion. Dr Smith: Yeah. I mean, that was great. And, you know, to go back to where we began, this is severe. It's something like 60% of patients with this problem have thought about suicide, right? And you take this patient and cure the problem. I feel really empowered having read the article and talked to you today. And so, I'm ready to go out and look for this. Thank you so much for a really engaging conversation. This has been terrific. Dr Rau: Thank you. I appreciate it. I enjoyed being here. Dr Smith: Again, today I've been interviewing Dr Jill Rau about her article on clinical features and diagnosis of spontaneous intracranial hypotension---which I guess I should say hypovolemia after having talked to you---which she wrote with Dr Jeremy Cutsworth-Gregory. This article appears in the most recent issue of Continuum on disorders of CSF dynamics. Please be sure to check out Continuum Audio episodes from this really interesting issue and other interesting issues. And thank you, our listeners, again for listening to 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.

Sponsored By AdCirrus ERP, your trusted partner for cloud ERP solutions. Learn more at adcirruserp.com.Meet Jim MayerWith over two decades of experience in the manufacturing industry, Jim Mayer is a recognized leader, storyteller, and advocate for the transformative power of connection. As the founder of The Manufacturing Connector, Jim has built a platform that strengthens the industry through innovative content, leadership development, and community-building initiatives. His work inspires collaboration, empowers emergingleaders, and celebrates the human side of manufacturing.A passionate advocate of manufacturing, Jim is dedicated to amplifying the voices of industry leaders and sharing the values and innovations that drive the sector forward. Through his leadership programs, live events, and thought-provoking media, Jim equips professionals with the tools and insights they need to thrive in a rapidly changing landscape.Known for his authenticity, humility, and innate curiosity, Jim is a sought-after speaker who engages audiences with his unique ability to connect people to ideas, opportunities, and each other. His commitment to fostering meaningful growth and innovation continues to shape the future of manufacturing and elevate its culture.Connect with Jason!The Manufacturing ConnectorLinkedIn​​Manufacturing Culture PodcastLead the Change Tour 2025jim.mayer@themfgconnector.com  (480)532-2717Highlights00:00 The Power of Body Language04:22 Introducing Jim Mayer: A Leader in Manufacturing09:00 Jim Mayer on Leadership in Manufacturing17:45 The Leadership Development Continuum25:36 The Importance of Culture in Manufacturing26:45 Understanding Organizational Culture28:28 The Impact of Hiring for Culture30:03 Defining Buzzwords and Values30:58 Marketing and Culture Alignment35:57 Challenges in Mergers and Acquisitions40:56 The Importance of Intentional Culture Building41:36 Fun Facts and Personal StoriesConnect with the Broads!Connect with Lori on LinkedIn and visit www.keystoneclick.com for your strategic digital marketing needs! Connect with Kris on LinkedIn and visit www.genalpha.com for OEM and aftermarket digital solutions!Connect with Erin on LinkedIn!

With the Old Tent City encampment set for closure early next week, is Metro's “Housing First” strategy being followed? Executive producer Whitney Pastorek sits down with Homelessness Planning Council chair Kennetha Patterson and writer/community organizer Mike Lacy, who say they have significant concerns about the Office of Homeless Services, the outside organizations tasked with overseeing supportive housing sites like Strobel House, and how Nashville's Continuum of Care is being impacted as a result. Read Mike Lacy's “Housing Last: The Rodeway to Nowhere” report here. Watch the music video for Daniel Holmes' original song referenced in the episode here. Want some more City Cast Nashville news? Then make sure to sign up for our Hey Nashville newsletter.  Follow us @citycastnashville You can also text us or leave a voicemail at: 615-200-6392 Interested in advertising with City Cast? Find more info HERE.

How many questions is too many?You know that asking effective questions is key to helping others solve problems and unlocking improvement, but can you ask too many questions?Yes! And when you do so, you actually hinder progress, not enable it.In this episode, I share one of the most common mistakes leaders and coaches alike make when learning to Break the Telling Habit® and moving from “telling” to “asking”. It's a crucial shift to stop being the expert with all the answers, but when you overpivot to only asking, you can leave the person you're intending to support feeling frustrated and stuck. Coaching for improvement isn't just about inquiry—it's about navigating what I call the “Coaching Continuum”—knowing when to provide open support for problem-solving and when to step in with direction.And importantly, always keeping the problem-solving responsibility with the person you are coaching.YOU'LL LEARN:When and how to switch between directive coaching and open coachingThe Coaching Continuum and how to maintain the ownership of problem-solving with the actual problem ownerThree key steps to navigate the Coaching Continuum effectivelyA leader or coach's role in overseeing the problem-solving process, whether using an A3 report or another improvement methodThe importance of embracing struggle in the learning process and allowing time for responseTune in to learn how to navigate this continuum and become a more effective Transformational Improvement Coach!IMPORTANT LINKS:Full episode show notes with links to other episodes and resources: ChainOfLearning.com/44Check out my website for resources and ways to work with me KBJAnderson.comFollow me on LinkedIn: linkedin.com/in/kbjandersonDownload my FREE KATALYST™ Change Leader Self-Assessment: KBJAnderson.com/katalyst Learn more about the role of leader as coach: Learning to Lead, Leading to LearnTIMESTAMPS FOR THIS EPISODE:02:59 Navigating the coaching continuum 03:59 A brief explanation of the coaching continuum to be a more helpful coach05:32 The 3 key steps to effectively navigate the coaching continuum05:43 Step 1: Understand their thinking to know whether open coaching or directive guidance is needed07:12 Step 2: Get comfortable with struggle08:26 When to pivot from open coaching to directive coaching8:37 How to label your actions to clarify your intention11:01 Step 3: Today's not the only day, follow up with a coaching process question to encourage learning11:27 Benefit of asking a process question to understand next steps13:32 A leader's role in developing an  A3 report and owning the thinking process not the thinking15:13 Why coaching and leadership is situational15:35 Steps to make a plan for effective coaching15:42 Step 1: Ask a question before immediately jumping in15:54 Step 2: Give an example how you might approach the problem16:15 Step 3: The next step to take and what to expect

Extended School Year (ESY) services can raise nuanced questions for IEP teams and special education professionals. On this episode of the Lozano Smith Podcast, host Aly R. Bivins talks with Roxana E. Khan and Erin Frazor about how ESY differs from summer school, the legal requirements under the IDEA, and how to make sound, individualized decisions. They round out the conversation by highlighting common pitfalls and offering practical tips to ensure compliance, including the importance of clear documentation. Show Notes & References 2:10 – ESY (Extended School Year services) vs. Summer School 2:52  – FAPE (Free Appropriate Public Education) and ESY 3:40 – Endrew F. v. Douglas County School District Re-1, 137 S. Ct. 988 (Client News Brief 12 - March 2017) 5:54 – Common ESY issues and questions 8:18 – How to determine eligibility for ESY 8:45 – Regression/Recoupment Analysis applied in California 10:14 – Three other standards determined by the courts 14:08 – What to provide during ESY 21:21 – When to make ESY determination 25:10 – Determining ESY eligibility for incoming students with less available information 28:01 – Litigation regarding ESY 34:17 – Does ESY only apply during the summer? 37:14 – Does the IDEA speak to Least Restrictive Environment (LRE) in relation to ESY? 38:45 – M.C. by & through S.B. v. Los Angeles Unified School District (C.D. Cal., Aug. 9, 2023) Case No. 2:20-CV-09127-CBM-E, 2023 WL 11066079 40:07 – Continuum of ESY placement options   For more information on the topics discussed in this podcast, please visit our website at: www.lozanosmith.com/podcast.

As artificial intelligence (AI) tools become increasingly mainstream, they can potentially transform neurology clinical practice by improving patient care and reducing clinician workload. Critically evaluating these AI tools for clinical practice is important for successful implementation. In this episode, Katie Grouse, MD, FAAN speaks with Peter Hadar, MD, MS, coauthor of the article “Clinical Applications of Artificial Intelligence in Neurology Practice” in the Continuum® April 2025 Neuro-ophthalmology 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. Hadar is an instructor of neurology at Harvard Medical School and an attending physician at the Massachusetts General Hospital in Boston, Massachusetts. Additional Resources Read the article: Clinical Applications of Artificial Intelligence in Neurology Practice Subscribe to Continuum®: shop.lww.com/Continuum 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 Guest: @PeterNHadar 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 subscribing to the journal, listening to verbatim recordings of the articles, and exclusive access to interviews not featured on the podcast. Dr Grouse: This is Dr Katie Grouse. Today I'm interviewing Dr Peter Hadar about his article on clinical applications of artificial intelligence in neurology practice, which he wrote with Dr Lydia Moura. This article appears in the April 2025 Continuum issue on neuro-ophthalmology. Welcome to the podcast, and please introduce yourself to our audience. Dr Hadar: Hi, thanks for having me on, Katie. My name is Dr Peter Hadar. I'm currently an instructor over at Mass General Hospital, Harvard Medical School, and I'm excited to talk more about AI and how it's going to change our world, hopefully for the better. Dr Grouse: We're so excited to have you. The application of AI in clinical practice is such an exciting and rapidly developing topic, and I'm so pleased to have you here to talk about your article, which I found to be absolutely fascinating. To start, I'd like to hear what you hope will be the key takeaway from your article with our listeners. Dr Hadar: Yeah, thank you. The main point of the article is that AI in medicine is a tool. It's a wonderful tool that we should be cautiously optimistic about. But the important thing is for doctors, providers to be advocates on their behalf and on behalf of their patients for the appropriate use of this tool, because there are promises and pitfalls just with any tool. And I think in the article we detail a couple ways that it can be used in diagnostics, in clinical documentation, in the workflow, all ways that can really help providers. But sometimes the devil is in the details. So, we get into that as well. Dr Grouse: How did you become interested in AI and its application, specifically in the practice of neurology? Dr Hadar: When I was a kid, as most neurologists are, I was- I nerded out on a lot of sci-fi books, and I was really into Isaac Asimov and some of his robotics, which kind of talks about the philosophy of AI and how AI will be integrated in the future. As I got into neurology, I started doing research neurology and a lot of folks, if you're familiar with AI and machine learning, statistics can overlap a lot with machine learning. So slowly but surely, I started using statistical methods, machine learning methods, in some of my neurology research and kind of what brought me to where I am today. Dr Grouse: And thinking about and talking about AI, could you briefly summarize a few important terms that we might be talking about, such as artificial intelligence, generative AI, machine learning, etcetera? Dr Hadar: It's a little difficult, because some of these terms are nebulous and some of these terms are used in the lay public differently than other folks would use it. But in general, artificial intelligence is kind of the ability of machines or computers to communicate independently. It's similar to as humans would do so. And there are kind of different levels of AI. There's this very hard AI where people are worried about with kind of terminator-full ability to replicate a human, effectively. And there are other forms of narrow AI, which are actually more of what we're talking about today, and where it's very kind of specific, task-based applications of machine learning in which even if it's very complex, the AI tools, the machine learning tools are able to give you a result. And just some other terms, I guess out there. You hear a lot about generative AI. There's a lot of these companies and different algorithms that incorporate generative AI, and that usually kind of creates something, kind of from scratch, based on a lot of data. So, it can create pictures, it can create new text if you just ask it. Other terms that can be used are natural language processing, which is a big part of some of the hospital records. When AI tools read hospital records and can summarize something, if it can translate things. So, it turns human speech into these results that you look for. And I guess other terms like large language models are something that also have come into prominence and they rely a lot on natural language processing, being able to understand human speech, interpret it and come up with the results that you want. Dr Grouse: Thank you, that's really helpful. Building on that, what are some of the current clinical applications of AI that we may already be using in our neurologic practice and may not even be aware that that's what that is? Dr Hadar: It depends on which medical record system you use, but a very common one are some of the clinical alerts that people might get, although some of them are pretty basic and they can say, you know, if the sodium is this level, you get an alert. But sometimes they do incorporate fancier machine learning tools to say, here's a red flag. You really should think about contacting the patient about this. And we can talk about it as well. It might encourage burnout with all the different flags. So, it's not a perfect tool. But these sorts of things, typically in the setting of alerts, are the most common use. Sorry, and another one is in folks who do stroke, there are a lot of stroke algorithms with imaging that can help detect where the strokes occur. And that's a heavy machine learning field of image processing, image analysis for rapid detection of stroke. Dr Grouse: That's really interesting. I think my understanding is that AI has been used specifically for radiology interpretation applications for some time now. Is that right? Dr Hadar: In some ways. Actually, my background is in neuroimaging analysis, and we've been doing a lot of it. I've been doing it for years. There's still a lot of room to go, but it's really getting there in some ways. My suspicion is that in the coming years, it's going to be similar to how anesthesiologists at one point were actively bagging people in the fifties, and then you develop machines that can kind of do it for you. At some point there's going to be a prelim radiology read that is not just done by the resident or fellow, but is done by the machine. And then another radiologist would double check it and make sure. And I think that's going to happen in our lifetime. Dr Grouse: Wow, that's absolutely fascinating. What are some potential applications of AI in neurologic practice that may be most high-yield to improve patient care, patient access, and even reduce physician burnout? Dr Hadar: These are separate sort of questions, but they're all sort of interlinked. I think one of the big aspects of patient care in the last few years, especially with the electronic medical record, is patients have become much more their own advocates and we focus a lot more on patient autonomy. So, they are reaching out to providers outside of appointments. This can kind of lead to physician burnout. You have to answer all these messages through the electronic medical record. And so having, effectively, digital twins of yourself, AI version of yourself, that can answer the questions for the patient on your off times is one of the things that can definitely help with patient care. In terms of access, I think another aspect is having integrated workflows. So, being able to schedule patients efficiently, effectively, where more difficult patients automatically get one-hour appointments, patients who have fewer medical difficulties might get shorter appointments. That's another big improvement. Then finally, in terms of physician burnout, having ambient intelligence where notes can be written on your behalf and you just need to double-check them after allows you to really have a much better relationship with the patients. You can actually talk with them one on one and just focus on kind of the holistic care of the patient. And I think that's- being less of a cog in the machine and focusing on your role as a healer would be actually very helpful with the implementation of some of these AI tools. Dr Grouse: You mentioned ambient technology and specifically ambient documentation. And certainly, this is an area that I feel a lot of excitement about from many physicians, a lot of anticipation to be able to have access to this technology. And you mentioned already some of the potential benefits. What are some of the potential… the big wins, but then also potential drawbacks of ambient documentation? Dr Hadar: Just to kind of summarize, the ambient intelligence idea is using kind of an environmental AI system that, without being very obtrusive, just is able to record, able to detect language and process it, usually into notes. So, effectively like an AI scribe that is not actually in the appointment. So, the clear one is that---and I've seen this as well in my practice---it's very difficult to really engage with the patient and truly listen to what they're saying and form that relationship when you're behind a computer and behind a desk. And having that one-on-one interaction where you just focus on the patient, learn everything, and basically someone else takes notes for you is a very helpful component of it. Some of the drawbacks, though, some of it has to do with the existing technology. It's still not at the stage where it can do everything. It can have errors in writing down the medication, writing down the exact doses. It can't really, at this point, detect some of the apprehensions and some of the nonverbal cues that patients and providers may kind of state. Then there's also the big one where a lot of these are still done by startups and other companies where privacy may be an issue, and a lot of patients may feel very uncomfortable with having ambient intelligence tools introduced into their clinical visit, having a machine basically come between the doctor and the patient. But I think that over time these apprehensions will lessen. A lot of the security will improve and be strengthened, and I think that it's going to be incorporated a lot more into clinical practice. Dr Grouse: Yeah, well, we'll all be really excited to see how that technology develops. It certainly seems like it has a lot of promise. You mentioned in your article a lot about how AI can be used to improve screening for patients for certain types of conditions, and that certainly seems like an obvious win. But as I was reading the article, I couldn't help but worry that, at least in the short term, these tools could translate into more work for busy neurologists and more demand for access, which is, you know, already, you know, big problems in our field. How can tools like these, such as, like, for instance, the AI fundoscopic screening for vascular cognitive risk factors help without adding to these existing burdens? Dr Hadar: It's a very good point. And I think it's one of the central points of why we wanted to write the article is that these AI in medicine, it's, it's a tool like any other. And just like when the electronic medical record came into being, a lot of folks thought that this was going to save a lot of time. And you know, some people would say that it actually worsened things in a way. And when you use these diagnostic screening tools, there is an improvement in efficiency, there is an improvement in patient care. But it's important that doctors, patients advocate for this to be value-based and not revenue-based, necessarily. And it doesn't mean that suddenly the appointments are shorter, that now physicians have to see twice as many patients and then patients just have less of a relationship with their provider. So, it's important to just be able to integrate these tools in an appropriate way in which the provider and the patient both benefit. Dr Grouse: You mentioned earlier about the digital twin. Certainly, in your article you mentioned, you know, that idea along with the idea of the potential of development of virtual chatbot visits or in-person visits with a robot neurologist. And I read all this with equal parts, I think excitement, but horror and and fear. Can you tell us more about what these concepts are, and how far are we from seeing technology like this in our clinics, and maybe even, what are the risks we need to be thinking about with these? Dr Hadar: Yeah. So, I mean, I definitely think that we will see implementation of some of these tools in our lifetime. I'm not sure if we're going to have a full walking, talking robot doing some of the clinical visits. But I do think that, especially as we start doing a lot more virtual visits, it is very easy to imagine that there will be some sort of video AI doctor that can serve as, effectively, a digital twin of me or someone else, that can see patients and diagnose them. The idea behind the digital twin is that it's kind of like an AI version of yourself. So, while you only see one patient, an AI twin can go and see two or three other patients. They could also, if the patients send you messages, can respond to those messages in a way that you would, based on your training and that sort of thing. So, it allows for the ability to be in multiple places at once. One of the risks of this is, I guess, overreliance on the technology, where if you just say, we're just going to have a chatbot do everything for us and then not look at the results, you really run the risk of the chatbot just recommending really bad things. And there is training to be had. Maybe in fifty years the chatbot will be at the same level as a physician, but there's still a lot of room for improvement. I personally, I think that my suspicion as to where things will go are for very simple visits in the future and in our lifetime. If someone is having a cold or something like that and it goes to their primary care physician, a chatbot or something like that may be of really beneficial use. And it'll help segment out the different groups of simple diagnosis, simple treatments can be seen by these robots, these AI, these machine learning tools; and some of the more complex ones, at least for the early implementation of this will be seen by more specialized providers like neurologists and subspecialist neurologists too. Dr Grouse: That certainly seems reasonable, and it does seem that the more simple algorithmic things are always where these technologies will start, but it'll be interesting to see where things can go with more complex areas. Now I wanted to switch gears a little bit in the article- and I thought this was really important because I see it as being certainly one of the bigger drawbacks of AI, is that despite the many benefits of artificial intelligence, AI can unfortunately perpetuate systemic bias. And I'm wondering if you could tell us a little bit more about how this happened? Dr Hadar: I know I'm beating a dead horse on this, but AI is a tool like any other. And the problem with it is that what you put in is very similar to what you get out. And there's this idea in computer science of “garbage in, garbage out”. If you include a lot of data that has a lot of systemic biases already in the data, you're going to get results that perpetuate these things. So, for instance, if in dermatologic practices, if you just had a data set that included people of one skin color or one race and you attempted to train a model that would be able to detect skin cancer lesions, that model may not be easily applicable to people of other races, other ethnicities, other skin colors. And that can be very damaging for care. And it can actually really, really hurt the treatments for a lot of the patients. So that is one of the, kind of, main components of the systemic biases in AI. The way we mitigate them is by being aware of it and actually implementing, I guess, really hard stops on a lot of these tools before they get into practice. Being sure, did your data set include this breakdown of sex and gender, of race and ethnicity? So that the stuff you have in the AI tool is not just a very narrow, focused application, but can be generalized to a large population, not just of one community, one ethnic group, racial group, one country, but can really be generalized throughout the world for many patients. Dr Grouse: The first step is being aware of it, and hopefully these models will be built thoughtfully to help mitigate this as much as possible. I wanted to ask as well, another concern about AI is the safety of private data. And I'm wondering, as we're starting to do things like use ambient documentation, AI scribe, and other types of technologies like this, what can we tell our patients who are concerned about the safety of their personal data collected via these programs, particularly when they're being stored or used with outside companies that aren't even in our own electronic medical records system? Dr Hadar: Yeah, it's a very good question, and I think it's one of the major limitations of the current implementation of AI into clinical practice, because we still don't really have great standards---medical standards, at least---for storing this data, how to analyze this data. And my suspicion is that at some point in the future, we're going to need to have a HIPAA compliance that's going to be updated for the 21st century, that will incorporate the appropriate use of these tools, the appropriate use of these data storage, of data storage beyond just PHI. Because there's a lot more that goes into it. I would say that the important thing for how to implement this, and for patients to be aware of, is being very clear and very open with informed consent. If you're using a company that isn't really transparent about their data security and their data sharing practices, that needs to be clearly stated to the patient. If their data is going to be shared with other people, reanalyzed in a different way, many patients will potentially consider not participating in an AI implementation in clinic. And I think the other key thing is that this should be, at least initially, an opt-in approach as opposed to an opt-out approach. So patients really have- can really decide and have an informed opinion about whether or not they want to participate in the AI implementation in medicine. Dr Grouse: Well, thank you so much for explaining that. And it does certainly sound like there's a lot of development that's going to happen in that space as we are learning more about this and the use of it becomes more prevalent. Now, I also wanted to ask, another good point that you made in your article---and I don't think comes up enough in this area, but likely will as we're using it more---AI has a cost, and some of that cost is just the high amount of data and computational processing needed to use it, as well as the effects on the environment from all this energy usage. Given this drawback of AI, how can we think about potential costs versus the benefits, the more widespread use of this technology? Or how should we be thinking about it? Dr Hadar: It's part of a balance of the costs and benefits, effectively, is that AI---and just to kind of name some of them, when you have these larger data centers that are storing all this data, it requires a lot of energy consumption. It requires actually a lot of water to cool these things because they get really hot. So, these are some of the key environmental factors. And at this point, it's not as extreme as it could be, but you can imagine, as the world transitions towards an AI future, these data centers will become huge, massive, require a lot of energy. And as long as we still use a lot of nonrenewable resources to power our world, our civilization, I think this is going to be very difficult. It's going to allow for more carbon in the atmosphere, potentially more climate change. So, being very clear about using sustainable practices for AI usage, whether it be having data centers specifically use renewable resources, have clear water management guidelines, that sort of thing will allow for AI to grow, but in a sustainable way that doesn't damage our planet. In terms of the financial costs… so, AI is not free. However, on a given computer, if you want to run some basic AI analysis, you can definitely do it on any laptop you have and sometimes even on your phone. But for some of these larger models, kind of the ones that we're talking about in the medical field, it really requires a lot of computational power. And this stuff can be very expensive and can get very expensive very quickly, as anyone who's used any of these web service providers can attest to. So, it's very important to be clear-eyed about problems with implementation because some of these costs can be very prohibitive. You can run thousands and you can quickly rack up a lot of money for some very basic analysis if you want to do it in a very rapid way, in a very effective way. Dr Grouse: That's a great overview. You know, something that I think we're all going to be having to think about a lot more as we're incorporating these technologies. So, important conversations I hope we're all having, and in our institutions as we're making these decisions. I wanted to ask, certainly, as some of our listeners who may be still in the training process are hearing you talk about this and are really excited about AI and implementation of technology in medicine, what would you recommend to people who want to pursue a career in this area as you have done? Dr Hadar: So, I think one of the important things for trainees to understand are, there are different ways that they can incorporate AI into their lives going forward as they become more seasoned doctors. There are clinical ways, there are research ways, there are educational ways. A lot of the research ways, I'm one of the researchers, you can definitely incorporate AI. You can learn online. You can learn through books about how to use machine learning tools to do your analysis, and it can be very helpful. But I think one of the things that is lacking is a clinician who can traverse both the AI and patient care fields and be able to introduce AI in a very effective way that really provides value to the patients and improves the care of patients. So that means if a hospital system that a trainee is eventually part of wants to implement ambient technology, it's important for physicians to understand the risks, the benefits, how they may need to adapt to this. And to really advocate and say, just because we have this ambient technology doesn't mean now we see fifty different patients, and then you're stuck with the same issue of a worse patient-provider relationship. One of the reasons I got into medicine was to have that patient-provider interaction to not only be kind of a cog in the hospital machine, but to really take on a role as a healer and a physician. And one of the benefits of these AI tools is that in putting the machine in medicine, you can also put the humanity back in medicine at times. And I think that's a key component that trainees need to take to heart. Dr Grouse: I really appreciate you going into that, and sounds like there's certainly need. Hoping some of our listeners today will consider careers in pursuing AI and other types of technologies in medicine. I really appreciate you coming to talk with us today. I think this is just such a fascinating topic and an area that everybody's really excited about, and hoping that we'll be seeing more of this in our lives and hopefully improving our clinical practice. Thank you so much for talking to us about your article on AI in clinical neurology. It was a fascinating topic and I learned a lot. Dr Hadar: Thank you very much. I really appreciate the conversation, and I hope that trainees, physicians, and others will gain a lot and really help our patients through this. Dr Grouse: So again, today I've been interviewing Dr Peter Hadar about his article on clinical applications of artificial intelligence in neurology practice, which he wrote with Dr Lydia Moura. This article appears in the most recent issue of Continuum on neuro-ophthalmology. 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. Thank you for listening to Continuum Audio.

Neuro-ophthalmic deficits significantly impair quality of life by limiting participation in employment, educational, and recreational activities. Low-vision occupational therapy can improve cognition and mental health by helping patients adjust to visual disturbances. In this episode, Katie Grouse, MD, FAAN, speaks with Sachin Kedar, MD, FAAN, author of the article “Symptomatic Treatment of Neuro-ophthalmic Visual Disturbances” in the Continuum® April 2025 Neuro-ophthalmology 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. Kedar is the Cyrus H Stoner professor of ophthalmology and a professor of neurology at Emory University School of Medicine in Atlanta, Georgia. Additional Resources Read the article: Symptomatic Treatment of Neuro-ophthalmic Visual Disturbances 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 Guest: @AIIMS1992 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 Sachin Kedar about his article on symptomatic treatment of neuro-ophthalmic visual disturbances, which appears in the April 2025 Continuum issue on neuro-ophthalmology. Welcome to the podcast, and please introduce yourself to our audience. Dr Kedar: Thank you, Katie. This is Sachin Kedar. I'm a neuro-ophthalmologist at Emory University, and I've been doing this for more than fifteen years now. I trained in both neurology and ophthalmology, with a fellowship in neuro-ophthalmology in between. It's a pleasure to be here. Dr Grouse: Well, we are so happy to have you, and I'm just so excited to be discussing this article with you, which I found to be a real treasure trove of useful clinical information on a topic that many find isn't covered enough in their neurologic training. I strongly recommend all of our listeners who work with patients with visual disturbances to check this out. I wanted to start by asking you what you hope will be the main takeaway from this article for our listeners? Dr Kedar: The most important takeaway from this article is, just keep vision on your radar when you are evaluating your patients with neurological disorders. Have a list of a few symptoms, do a basic screening vision, and ask patients about how their vision is impacting the quality of life. Things like activities of daily living, hobbies, whether they can cook, dress, ambulate, drive, read, interact with others. It is very important for us to do so because vision can be impacted by a lot of neurological diseases. Dr Grouse: What in the article do you think would come as the biggest surprise to our listeners? Dr Kedar: The fact that impairment of vision can magnify and amplify neurological deficits in a lot of what we think of as core neurological disorders should come as a surprise to most of the audience. Dr Grouse: On that note, I think it's probably helpful if you could remind us about the types of visual disturbances we should be thinking about and screening for in our patients? Dr Kedar: Patients who have neurological diseases can have a whole host of visual deficits. The simplest ones are deficits of central vision. They can have problems with their visual field. They can have abnormalities of color vision or even contrast sensitivity. A lot of our patients also complain of light sensitivity, eyes feeling tired when they're doing their usual stuff. Some of our patients can have double vision, they can have shaky vision, which leads to their sense of imbalance and maybe a fall risk to them. Dr Grouse: It's really helpful to think about all the different aspects in which vision can be affected, not just sort of the classic loss of vision. Now, your article also serves as a really important reminder, which you alluded to earlier, about how impactful visual disturbances can be on daily activities. Could you elaborate a little further on this, and particularly the various domains that can be affected when there are visual disturbances present? Dr Kedar: So, when I look at how visual disturbances affect quality of life, I look at two broad categories. One is activities of basic daily living. These would be things like, are you able to cook? Are you able to ambulate not just in your home, but in your neighborhood? Are you able to drive to your doctor's appointment or to visit with your family? Are you able to dress yourself appropriately? Are you able to visualize the clothing and choose them appropriately? And then the second category is recreational activities. Are you able to read? Are you able to watch television? Are you able to visit the theatre? Are you able to travel? Are you able to participate in group activities, be it with your family or be it with your social group? It is very important for us to ask our patients if they have problems doing any of this because it really can adversely impact the quality of life. Dr Grouse: I think, certainly with all the things we try to get through talking with our patients, this may not be something that we do spend a lot of time on. So, I think it's it is a good reminder that when we can, being able to ask about these are going to be really important and help us hit on a lot of other things we may not even realize or know to ask about. Now, I was really struck when I was reading your article by the meta-analysis that you had quoted that had showed 47% higher risk of developing dementia among the visually impaired compared to those without visual impairments. Should we be doing more in-depth visual testing on all of our patients with cognitive symptoms? Dr Kedar: This is actually the most interesting part of this article, and kind of hones in on the importance of vision in neurological disorders. Now I want to clarify that patients with visual disorders, it's not a causative influence on dementia, but if you have a patient with an underlying cognitive disorder, any kind of visual disturbance will significantly make it worse. And this has been shown in several studies, both in the neurologic and in the ophthalmological literature. So, I quoted one of the big meta-analysis over there, but studies have clearly shown that if you have these patients and treat them for their visual deficits, their cognitive indices can actually significantly improve. To answer your question, I would say a neurologist should include basic vision screening as part of every single evaluation. Now, I know it's a hard thing in, you know, these days when we are literally running on the hamster wheel, but I can assure you that it won't take you more than 2 to 3 minutes of your time to do this basic screening; in fact, you can have one of your assistants included as part of the vital signs assessment. What are these basic screening tools? Measure the visual acuity for both near and distance. Check and see if their visual field's off with the confrontation. Look at their eye movements. Are they able to move their eyes in all directions? Are the eyes stable when they're trying to fixate on a particular point? I think if you can do these basic things, you will have achieved quite a bit. Dr Grouse: That's really helpful, and thanks for going through some of the standard, or really, you know, solid basic foundation of visual testing we should be thinking about doing. I wanted to move on to some more details about the visual disturbances. You made an excellent point that there are many types of primary ophthalmologic conditions that can cause visual disturbances that we should keep in mind. So maybe not things that we think about a lot on a day-to-day basis, but, you know, are still there and very common. What are some of the most common ones, and when should we be referring them to see an ophthalmologist? Dr Kedar: So, it depends on the age group of your patient population. Now, the majority of us are adult neurologists, and so the kinds of ophthalmic conditions that we see in this population is going to be different from the pediatric age group. So in the adult population, we might see patients with uncorrected refractive error, presbyopia, patients who have cataracts creep on them, they may have glaucoma, they may have macular degeneration, and these tend to have a slightly higher incidence in the older age group. Now for those of us who are taking care of the younger population, uncorrected refractive errors, strabismus and amblyopia tend to be fairly common causes of visual deprivation in this age group. What I would encourage all of our neurologists is, make sure that your patients get a basic eye examination at least once a year. Just like you want them to go to their primary care and get an annual maintenance visit, everybody should go to the ophthalmologist or the optometrist and get a basic examination. And, if you're resourceful enough, have your patients bring a copy of that assessment. Whether it is normal or there's some abnormality, it is going to help you in the management. Dr Grouse: Absolutely. I think that's a great piece of advice, to think of it almost, like, them seeing their primary care doctor, which of course we offer encourage our patients to do, thinking of this as another very important piece of standard primary care. If a patient comes to you reporting difficulty reading due to possible visual disturbances, I'm curious, can you walk us through how you would approach this evaluation? Dr Kedar: It is not a very common presenting complaint of our patients, even in the neuro-ophthalmology clinic. It's a very rare patient that I see who comes and says, I cannot read or, I have difficulty reading. Most of the patients will come saying, oh, I cannot see. And then you have to dig in to find out, what does that actually mean? What can you not see? Is it a problem in your driving? Is it a problem in your reading? Or is it a problem that occurs at all times? Now you asked me, how do you approach this evaluation? One of the things that all of us, whether we are neurologists, ophthalmologists, or neuro-ophthalmologists, forget to do is to actually have the patient read a paragraph, a sentence, when they are in clinic. And that will give you a lot of ideas about what might actually be going wrong with the patient. Now, as far as how do I approach this evaluation, I will do a basic screening examination to make sure that their visual acuity is good for both distance and near. A lot of us tend to do either distance or near and we will miss the other parameter. You want to do a basic confrontation visual field to make sure that they do not have any subtle deficits that's impacting their ability to read. Examine the eye movements, do a fundoscopic examination. Now, once you've done this basic screening, as a neurologist, you already have some idea of whether your patient has a lesion along the visual pathways. If you suspect that this is a problem with, say, the visual pathways, ask your ophthalmology colleague to do a formal visual field assessment, and that'll pick up subtle deficits of central visual field. And lastly, don't forget higher visual function testing or cortical visual function testing. So basically, you're looking for neglect, phenomenon, or simultanagnosia, all of which tends to have an impact on reading. So, in the manuscript I have a schema of how you can approach a patient with reading difficulties, and in that ischemia you will see categories of where things can go wrong during the process of reading. And if you can approach your patient systematically through one of those domains, there's a fairly good chance that you'll be able to pick up a problem. Dr Grouse: Going a little further on to when you do identify problems with loss of central or peripheral vision, what are some strategies for symptomatic management of these types of visual disturbances? Dr Kedar: As a neurologist, if you pick up a problem with the vision, you have to send this patient to an eye care provider. The vast majority of people who have visual disturbances, it's from an eye disease. You know, as I alluded to earlier, it can be something as simple as uncorrected refractive error, and that can be fixed easily. A lot of patients in our older age group will have dry eye syndrome, which means they are unable to adequately lubricate the surface of the eye, and as a result, it degrades the quality of their vision. So, they tend to get intermittent episodes of blurred vision, or they tend to get glare. They tend to get various forms of optical aberration. Patients can have cataracts, patients can have glaucoma or macular degeneration. And in all of those instances, the goal is to treat the underlying disease, optimize the vision, and then see what the residual deficit is. By and large, if a patient has a problem with the central vision, then magnification will help them for activities that they perform at near; say, reading. Now for patients with peripheral vision problem, it's a different entity altogether. Again, once you've identified what the underlying cause is, your first goal is to treat it. So, for example, if your patient has glaucoma, which is affecting peripheral vision, you're going to treat glaucoma to make sure that the visual field does not progress. Now a lot of what happens after that is rehabilitation, and that is always geared towards the specific activities that are affected. Is it reading? Is it ambulating? Is it watching television? Is it driving? And then you can advise as a neurologist, you can advise your occupational therapist or low vision specialist and say, hey, my patient is not able to do this particular activity. Can we help them? Dr Grouse: Moving on from that, I wanted to also hit on your approach when patients have disorders of ocular motility. What are some things you can do for symptomatic management of that? Dr Kedar: So, patients with ocular motility can have two separate symptoms. Two, you know, two disabling symptoms, as they would call it. One is double vision and the other is oscillopsia, or the feeling or the visualization of the environment moving in response to your eyes not being able to stay still. Typically, you would see this in nystagmus. Now, let's start with diplopia. Diplopia is a fairly common presenting complaint for neurologists, ophthalmologists, and the neuro-ophthalmologist. The first aspect in the management of diplopia is to differentiate between monocular diplopia and binocular diplopia. Now, monocular diplopia is when the double vision persists even after covering one eye. And that is never a neurological issue. It's almost always an ophthalmic problem, which means the patient will then have to be assessed by an eye care provider to identify what's causing it. And again, refractive error, cataracts, opacities, they can do it. Now, if the patient is able to see single vision by covering one eye at a time, that's binocular diplopia. Now, in patients with binocular diplopia in the very early stages of the disease, the standard treatment regimen is just monocular occlusion. Cover one eye, the diplopia goes away, and then give it time to improve on its own. So, this is what we would typically do in a patient with, say, acute sixth nerve palsy or fourth nerve palsy or third nerve palsy, maybe expect spontaneous improvement in a few months. Now if the double vision does not improve and persists long term, then the neuro-ophthalmologist or the ophthalmologist will monitor the amount of deviation to see if it fluctuates or if it stays the same. So, what are the treatment options that we have in a patient who absolutely refuses any intervention or is not a candidate for any intervention? Monocular occlusion still remains the viable option. Now, patients who have stable ocular deviation can benefit from using prisms in their glasses, or they can be sent to a surgeon to have a strabismus surgery that can realign their eyes. So, again, a broad answer, but there are options available that we can use. Dr Grouse: Thank you for that overview. I think that's just really helpful to keep in mind as we're working with these patients and thinking about what their options are. And then finally, I wanted to touch on patients with higher-order vision processing and attention difficulties. What are some strategies for them? Dr Kedar: These are frankly the most difficult patients that I get to manage in my clinic, simply because there is no effective therapies for managing them. In fact, I think neurologists are far better at this than ophthalmologists or even neuro-ophthalmologists. In patients with attentional disorders, everything boils down to the underlying cause, whether you can treat it or whether it is a slowly progressive, you know, condition, such as from neurodegenerative diseases. And that tailors our goals towards therapy. The primary goal is for safety. A lot of these patients who have visual disturbances from vision processing or attention, they are at accident and fall risk. They have problems with social interactions. And, importantly, there is a gap of understanding of what's going on, not just from their side but also from the family's side. So, I tend to approach these patients from a safety perspective and social interaction perspective. Now, I have a table listed in the manuscript which will go into details of what the specific things are. But in a nutshell, if your patient has neglect in a specific part of the visual field, they have accident risk on that side. Simple things like walking through a doorway, they can hurt their shoulders or their knees when they bang into the wall on that side because they are unable to judge what's on the other side. Another example would be a patient who has simultanagnosia or a downgaze policy, such as from progressive super nuclear policy. They are unable to look down fast enough, or they are simply unable to look down and appreciate things that are on the floor, and so they can trip and fall. Walking downstairs is also not a huge risk because they are unable to judge distances as they walk down. A lot of what we see in these patients are things that we have to advise occupational therapists and help them improve these safety parameters at home. Another thing that we often forget is patients can inadvertently cause a social incident when they tend to ignore people on their affected side. So, if there is a family gathering, they tend to consistently ignore a group of people who are sitting on the affected side as opposed to the other side. And I've had more than a few patients who've come and said that, I may have offended some of my friends and family. In those instances, it's always helpful when they are in clinic to demonstrate to the family how this can be awkward and how this can be mitigated. So, having everybody sit on one side is a useful strategy. Advise your family and friends before a gathering that, hey, this may happen. And it is not because it is deliberate, but it's because of the medical condition. And that goes a lot, you know, further in helping our patients come out of social isolation because they are also afraid of offending people, you know. And they can also participate socially, and it can overall improve their quality of life. Dr Grouse: That's a really helpful tip, and something I'll keep in mind with my patients with neglect and visual field cuts. Thank you so much for coming to talk with us today. Your article has been so helpful, and I urge everybody listening today to take a look. Dr Kedar: Thank you, Katie. It was wonderful talking to you. Dr Grouse: I've been interviewing Dr Sachin Kedar about his article on symptomatic treatment of neuro-ophthalmic visual disturbances, which appears in the most recent issue of Continuum on neuro-ophthalmology. 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.

“Recovery isn't a pause — it's part of the plan.” In this global edition of Performance Talk, Dr. Jo Brown joins Dr. Ewell Gordon to break down the clinical-performance continuum, why individualized recovery matters, and how elite athletes can stay consistently healthy and competition-ready. If you're a coach, clinician, or athlete, this episode will change how you think about performance. #PerformanceTalk #SportsScience #AthleteHealth #TrainingIQ #HumanPerformance #RecoveryMatters

In Muay Thai, you must dig deep, but do you know when to push your limits, and when to ease off to level up?Are you the “More!” type… or the “Too Much!” type?Over the years—training myself and coaching fighters around the world—I've spotted a pattern.We all live on a sliding scale when it comes to challenge.And that scale moves.Push the edge regularly, and your capacity rises.But let it slide for too long? It drops. Fast.What challenged you six months ago might not touch the sides today.Or worse—what used to be easy now feels hard again, because you've unknowingly slid backward.You're always moving on the scale.The question is: which direction?KEY MOMENTSFollow along using these quick timestamps:00:00 Go Hard or Go Home?00:38 The Challenge Level – Sliding Scale01:04 Are You the “More!” Type… or the “Too Much!” Type?01:16 Train Hard… But Redefine What “Hard” Actually Means01:51 So… Where Are You On the Continuum?02:13 Be Brutally Honest02:28 Further Videos...Further notes and resources at https://heatrick.com/2025/05/16/dig-deep-but-know-your-edge-understand-the-moving-scale/You'll find the "How Much Muay Thai Training Do You Really Need?" episode here: https://youtu.be/7a0s6qW5m6w

This content has been developed for healthcare professionals only. Patients who seek health information should consult with their physician or relevant patient advocacy groups.For the full presentation, downloadable Practice Aids, slides, and complete CME/AAPA/IPCE information, and to apply for credit, please visit us at PeerView.com/EMS865. CME/AAPA/IPCE credit will be available until May 5, 2026.Bridging Gaps, Shaping Lifelong NF1 Care: Team Strategies & Management Choices With MEK Inhibitors Across the Pediatric-to-Adult Care Continuum In support of improving patient care, this activity has been planned and implemented by PVI, PeerView Institute for Medical Education, and American Neurological Association. PVI, PeerView Institute for Medical Education, is jointly accredited by the Accreditation Council for Continuing Medical Education (ACCME), the Accreditation Council for Pharmacy Education (ACPE), and the American Nurses Credentialing Center (ANCC), to provide continuing education for the healthcare team.SupportThis activity is supported by independent medical education grants from Alexion Pharmaceuticals and SpringWorks Therapeutics, Inc.Disclosure information is available at the beginning of the video presentation.

This content has been developed for healthcare professionals only. Patients who seek health information should consult with their physician or relevant patient advocacy groups.For the full presentation, downloadable Practice Aids, slides, and complete CME/AAPA/IPCE information, and to apply for credit, please visit us at PeerView.com/EMS865. CME/AAPA/IPCE credit will be available until May 5, 2026.Bridging Gaps, Shaping Lifelong NF1 Care: Team Strategies & Management Choices With MEK Inhibitors Across the Pediatric-to-Adult Care Continuum In support of improving patient care, this activity has been planned and implemented by PVI, PeerView Institute for Medical Education, and American Neurological Association. PVI, PeerView Institute for Medical Education, is jointly accredited by the Accreditation Council for Continuing Medical Education (ACCME), the Accreditation Council for Pharmacy Education (ACPE), and the American Nurses Credentialing Center (ANCC), to provide continuing education for the healthcare team.SupportThis activity is supported by independent medical education grants from Alexion Pharmaceuticals and SpringWorks Therapeutics, Inc.Disclosure information is available at the beginning of the video presentation.

Dysfunction of the supranuclear ocular motor pathways typically causes highly localizable deficits. With sophisticated neuroimaging, it is critical to better understand structure-function relationships and precisely localize pathology within the brain. In this episode, Lyell K. Jones Jr, MD, FAAN, speaks with Gregory P. Van Stavern, MD, author of the article “Supranuclear Disorders of Eye Movements” in the Continuum® April 2025 Neuro-ophthalmology 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. Van Stavern is the Robert C. Drews professor of ophthalmology and visual sciences at Washington University in St Louis, Missouri. Additional Resources Read the article: Internuclear and Supranuclear Disorders of Eye Movements 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 Gregory Van Stavern, who recently authored an article on intranuclear and supranuclear disorders of eye movements for our latest Continuum issue on neuro-ophthalmology. Dr Van Stavern is the Robert C Drews professor of ophthalmology and visual sciences at Washington University in Saint Louis. Dr Van Stavern, welcome, and thank you for joining us today. Why don't you introduce yourself to our audience? Dr Van Stavern: Hi, my name is Gregory Van Stavern. I'm a neuro-ophthalmologist located in Saint Louis, and I'm pleased to be on this show today. Dr Jones: We appreciate you being here, and obviously, any discussion of the visual system is worthwhile. The visual system is important. It's how most of us and most of our patients navigate the world. Roughly 40% of the brain---you can correct me if I'm wrong---is in some way assigned to our visual system. But it's not just about the sensory experience, right? The afferent visual processing. We also have motor systems of control that align our vision and allow us to accurately direct our vision to visual targets of interest. The circuitry is complex, which I think is intimidating to many of us. It's much easier to see a diagram of that than to describe it on a podcast. But I think this is a good opportunity for us to talk about the ocular motor exam and how it helps us localize lesions and, and better understand diagnoses for certain disorders. So, let's get right to it, Dr Van Stavern. If you had from your article, which is outstanding, a single most important message for our listeners about recognizing or treating patients with ocular motor disorders, what would that message be? Dr Van Stavern: Well, I think if we can basically zoom out a little to the big picture, I think it really emphasizes the continuing importance of the examination. History as well, but the examination. I was reading an article the other day that was essentially downplaying the importance of the physical examination in the modern era with modern imaging techniques and technology. But for neurology, and especially neuro-ophthalmology, the history and the examination should still drive clinical decision-making. And doing a careful assessment of the ocular motor system should be able to tell you exactly where the lesion is located, because it's very easy to order a brain MRI, but the MRI is, like Forrest Gump might say, it's like a box of chocolates. You never know what you're going to find. You may find a lot of things, but because you've done the history and the examination, you can see if whatever lesion is uncovered by the MRI is the lesion that explains what's going on with the patient. So even today, even with the most modern imaging techniques we have, it is still really important to know what you're looking for. And that's where the oculomotor examination can be very helpful. Dr Jones: I did not have Forrest Gump on my bingo card today, Dr Van Stavern, but that's a really good analogy, right? If you order the MRI, you don't know what you're going to get. And then- and if you don't have a really well-formed question, then sometimes you get misleading information, right?  Dr Van Stavern: Exactly. Dr Jones: We'll get into some technology here in a minute, because I think that's relevant for this discussion. I think most of our listeners are going to agree with us that the exam is important in neuro-ophthalmology, and neurology broadly. So, I think you have some sympathetic listeners there. Again, the point of the exam is to localize and then lead to a diagnosis that we can help patients with. When you think about neurologic disorders where the ocular motor exam helps you get to the right diagnosis, obviously disorders of eye movements, but sometimes it's a clue to a broader neurologic syndrome. And you have some nice discussions in your article about the ocular motor clues to Parkinson disease or to progressive supranuclear palsy. Tell us a little more about that. In your practice, which neurologic disorders do you find the ocular motor exam being most helpful? Dr Van Stavern: Well, just a very brief digression. So, I started off being an ophthalmology resident, and I do two years of ophthalmology and then switch to neurology. And during neurology residency, I was debating which subspecialty to go into, and I realized that neuro-ophthalmology touches every other subspecialty in neurology. And it goes back to the fact that the visual system is so pervasive and widely distributed throughout the brain. So, if you have a neurologic disease, there is a very good chance it is going to affect vision, maybe in a minor way or a major way. That's why careful assessment of the visual system, and particularly the oculomotor system, is really helpful for many neurologic diseases. Neuromuscular disease, obviously, myasthenia gravis and certain myopathies affect the eye movements. Neurodegenerative diseases, in particular Parkinson's disease and parkinsonian conditions, often affect the eye movements. And in particular, when you're trying to differentiate, is this classic Parkinson's disease? Or is this progressive supranuclear palsy? Is it some broad spectrum multisystem atrophy? The differences between the eye movement disorders, even allowing for the fact that there's overlap, can really help point in one direction to the other, and again, prevent unnecessary testing, unnecessary treatment, and so on. Dr Jones: Very good. And I think, to follow on a thread from that concept with patients who have movement disorders, in my practice, seeing older patients who have a little bit of restriction of vertical gaze is not that uncommon. And it's more common in patients who have idiopathic Parkinson disease. And then we use that part of the exam to help us screen patients for other neurodegenerative syndromes like progressive nuclear- supranuclear palsy. So, do you have any tips for our listeners to- how to look at, maybe, vertical gaze and say, this is maybe a normal age-related degree of change. This is something that might suggest idiopathic Parkinson disease. Or maybe something a little more progressive and sinister like progressive super nuclear palsy? Dr Van Stavern: Well, I think part of the issue- and it's harder to do this without the visual aspect. One of my colleagues always likes to say for a neurologist, the eye movement exam begins and ends with the neurology benediction, just doing the sign of the cross and checking the eye movements. And that's a good place to start. But I think it's important to remember that all you're looking at is smooth pursuit and range of eye movements, and there's much more to the oculomotor examination than that. There's other aspects of eye movement. Looking at saccades can be really helpful; in particular, classically, saccadic movements are selectively abnormal in PSP versus Parkinson's with progressive supranuclear palsy. Saccades, which are essentially rapid movements of the eyes---up and down, in this case---are going to be affected in downward gaze. So, the patient is going to have more difficulty initiating downward saccades, slower saccades, and less range of movement of saccades in downgaze. Whereas in Parkinson's, it's classically upward eye movements and upgaze. So, I think that's something you won't be able to see if you're just doing, looking at, you know, your classic, look at your eye movements, which are just assessing, smooth pursuit. Looking carefully at the eye movements during fixation can be helpful. Another aspect of many parkinsonian conditions is saccadic intrusions, where there's quick movements or saccades of the eye that are interrupting fixation. Much, much more common in PSP than in Parkinson's disease. The saccadic intrusions are what we call square-wave jerks because of what they look like. Eye movement recordings are much larger amplitude in PSP and other multisystem atrophy diseases than with Parkinson's. And none of these are perfect differentiators, but the constellation of those findings, a patient with slow downwards saccades, very large amplitude, and frequent saccadic intrusions might point you more towards this being PSP rather than Parkinson's. Dr Jones: That's a great pearl, thinking about the saccades in addition to the smooth pursuit. So, thank you for that. And you mentioned eye movement measurements. I think it's simultaneously impressive and a little scary that my phone can tell when I'm looking at it within a few degrees of visual attention. So, I imagine there are automated tools to analyze eye movement. Tell us, what's the state of the art there, and what should our listeners be aware of in terms of tools that are available and what they can and can't do? Dr Van Stavern: Well, I could tell you, I mean, I see neuro-ophthalmic patients with eye movement disorders every day and we do not have any automated tools for eye movement. We have a ton of imaging techniques for imaging the optic nerve and the retina in different ways, but we don't routinely employ eye movement recording devices. The only time we usually do that is in somebody where we suspect they have a central or peripheral vestibular disease and we send them for vestibular testing, for eye movement recordings. There is interest in using- I know, again, sort of another digression, but if you're looking at the HINTS technique, which is described in the chapter to differentiate central from peripheral disease, which is a very easy, useful way to differentiate central from peripheral or peripheral vestibular disease. And again, in the acute setting, is this a stroke or not a stroke? Is it the brain or is it the inner ear? Part of the problem is that if you're deploying this widespread, the people who are doing it may not be sufficiently good enough at doing the test to differentiate, is a positive or negative test? And that's where some people have started introducing this into the emergency room, these eye movement recording devices, to give the- using, potentially, AI and algorithms to help the emergency room physicians say, all right, this looks like a stroke, we need to admit the patient, get an MRI and so on, versus, this is vestibular neuritis or an inner ear problem, treat them symptomatically, follow up as an outpatient. That has not yet been widely employed. It's a similar way that a lot of institutions are having fundus photography and OCT devices placed in the emergency room to aid the emergency room physician for patients who present with acute vision issues. So, I think that could be the future. It probably would be something that would be AI-assisted or AI-driven. But I can tell you at least at our institution and most of the ones I know of, it is not routinely employed yet. Dr Jones: So maybe on the horizon, AI kind of facilitated tools for eye movement disorder interpretation, but it's not ready for prime time yet. Is that a fair summary? Dr Van Stavern: In my opinion, yes. Dr Jones: Good to know. This has struck me every time I've read about ocular motor anatomy and ocular motor disorders, whether they're supranuclear or intranuclear disorders. The anatomy is complex, the circuitry is very complicated. Which means I learn it and then I forget it and then I relearn it. But some of the anatomy isn't even fully understood yet. This is a very complex real estate in the brainstem. Why do you think the neurophysiology and neuroanatomy is not fully clarified yet? And is there anything on the horizon that might clarify some of this anatomy? Dr Van Stavern: The very first time I encountered this topic as an ophthalmology resident and later as a neurology resident, I just couldn't understand how anyone could really understand all of the circuitry involved. And there is a lot of circuitry that is involved in us simply having clear, single binocular vision with the afferent and efferent system working in concert. Even in arch. In my chapter, when you look at the anatomy and physiology of the smooth pursuit system or the vertical gaze pathways, there's a lot of, I'll admit it, there's a lot of hand waving and we don't completely understand it. I think a lot of it has to do with, in the old days, a lot of the anatomy was based on lesions, you know, lesion this area either experimentally or clinically. And that's how you would determine, this is what this region of the brain is responsible for. Although we've gotten more sophisticated with better imaging, with functional connectivity MRI and so on, all of those have limitations. And that's why I still don't think we completely understand all the way this information is integrated and synthesized, and, to get even more big level and esoteric, how this makes its way into our conscious mind. And that has to do with self-awareness and consciousness, which is a whole other kettle of fish. It's just really complicated. I think when I'm at least talking to other neurologists and residents, I try to keep it as simple as possible from a clinical standpoint. If you see someone with an eye movement problem, try to see if you can localize it to which level you're dealing with. Is it a muscle problem? Is it neuromuscular junction? Is it nerve? Is it nucleus? Is it supranuclear? If you can put it at even one of those two levels, you have eliminated huge territories of neurologic real estate, and that will definitely help you target and tailor your workup. So, again, you're not costing the patient in the healthcare system hundreds of thousands of dollars. Dr Jones: Great points in there. And I think, you know, if we can't get it down to the rostral interstitial nucleus of the medial longitudinal fasciculus, if we can get it to the brainstem, I think that's obviously- that's helpful in its own right. And I imagine, Dr Van Stavern, managing patients with persistent ocular motor disorders is a challenge. We take foveation for granted, right, when we can create these single cortical images. And I imagine it's important for daily function and difficult for patients who lose that ability to maintain their ocular alignment. What are some of the clinical tools that you use in your practice that our listeners should be aware of to help patients that have a persistent supranuclear disorder of ocular movement? Dr Van Stavern: Well, I think you tailor your treatment to the symptoms, and if it's directly due to underlying condition, obviously you treat the underlying condition. If they have sixth nerve palsy because of a skull base tumor, obviously you treat the skull base tumor. But from a practical standpoint, I think it depends on what the symptom is, what's causing it, and how much it's affecting their quality of life. And everyone is really different. Some patients have higher levels of tolerance for blurred vision and double vision. For things- for patients who have double vision, depending upon the underlying cause we can sometimes use prisms and glasses. Prisms are simply- a lot of people just think prism is this, like, mystical word that means a lot. It's simply just an optical device that bends light. So, it essentially bends light to allow the eyes- basically, the image to fall on the fovea in both eyes. And whether the prisms help or not is partly dependent upon how large the misalignment is. If somebody has a large degree of misalignment, you're not going to fix that with prism. The amount of prism you'd need to bend the light enough to land on the fovea in both eyes would cause so much blur and distortion that it would essentially be a glorified patch. So, for small ranges of misalignment, prisms are often very helpful, that we can paste over glasses or grind into glasses. For larger degrees of misalignment that- let's say it is due to some skull base tumor or brain stem lesion that is not going to get better, then eye muscle surgery is a very effective option. We usually like to give people a long enough period of time to make sure there's no change before proceeding with eye muscle surgery. Dr Jones: Very helpful. So, prisms will help to a limited extent with misalignment, and then surgery is always an option if it's persistent. That's a good pearl for, I think, our listeners to take away. Dr Van Stavern: And even in those circumstances, even prisms and eye muscle surgery, the goal is primarily to cause single binocular vision and primary gaze at near. Even in those cases, even with the best results, patients are still going to have double vision, eccentric gaze. For most people, that's not a big issue, but we have had a few patients… I had a couple of patients who were truck drivers who were really bothered by the fact that when they look to the left, let's say because it's a 4th nerve palsy on the right, they have double vision. I had a patient who was a golfer who was really, really unhappy with that. Most people are okay with that, but it all depends upon the individual patient and what they use their vision for. Dr Jones: That's a great point. There's not enough neurologists in the world. I know for a fact there are not enough neuro-ophthalmologists in the world, right? There's just not many people that have that dual expertise. You mentioned that you started with ophthalmology and then did neurology training. What do you think the pipeline looks like for neuro-ophthalmology? Do you see growing interest in this among trainees, or unchanged? What are your thoughts about that? Dr Van Stavern: No, that's a continuing discussion we're having within our own field about how to attract more residents into neuro-ophthalmology. And there's been a huge shift. In the past, this was primarily ophthalmology-driven. Most neuro-ophthalmologists were trained in ophthalmology initially before doing a fellowship. The last twenty years, it switched. Now there's an almost 50/50 division between neurologists and ophthalmologists, as more neurologists have become more interested. This is probably a topic more for the ophthalmology equivalent of Continuum. One of the perceptions is this is not a surgical subspecialty, so a lot of ophthalmology residents are disincentivized to pursue it. So, we have tried to change that. You can do neuro-ophthalmology and do eye muscle surgery or general ophthalmology. I think it really depends upon whether you have exposure to a neuro-ophthalmologist during your neurology residency. If you do not have any exposure to neuro-ophthalmology, this field will always seem mysterious, a huge black box, something intimidating, and something that is not appealing to a neurologist. I and most of my colleagues make sure to include neurology residents in our clinic so they at least have exposure to it. Dr Jones: That's a great point. If you never see it, it's hard to envision yourself in that practice. So, a little bit of a self-fulfilling prophecy. If you don't have neuro-ophthalmologists, it's hard to expose that practice to trainees. Dr Van Stavern: And we're also trying; I mean, we make sure to include medical students, bring them to our meetings, present research to try to get them interested in this field at a very early stage. Dr Jones: Dr Van Stavern, great discussion, very helpful. I want to thank you for joining us today. I want to thank you for not just a great podcast, but also just a wonderful article on ocular motor disorders, supranuclear and intranuclear. I learned a lot, and hopefully our listeners did too. Dr Van Stavern: Well, thanks. I really appreciate doing this. And I love Continuum. I learn something new every time I get another issue. Dr Jones: Well, thanks for reading it. And I'll tell you as the editor of Continuum, I learn a lot reading these articles. So, it's really a joy to get to read, up to the minute, cutting-edge clinical content for neurology. Again, we've been speaking with Dr Gregory Van Stavern, author of a fantastic article on intranuclear and supranuclear disorders of eye movements in Continuum's most recent issue on neuro-ophthalmology. 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.

This episode is brought to you by Timeline, LMNT, and Strong Coffee Company. ESPN personality and producer Anne-Marie Anderson joins us to unravel the intricate dance between fear and failure. Anne-Marie sheds light on how fear, often perceived as a daunting obstacle, can actually be a stepping stone to courage and growth. In this episode, we challenge the traditional notions of failure by reimagining it as valuable data, a tool for learning and evolving. Through personal anecdotes and stories of renowned athletes like Michael Jordan and Kobe Bryant, she underscores how setbacks are not the end but merely redirections on the path to greatness. Follow Anne Marie @annemarieandersontv Follow Chase @chase_chewning ----- In this episode we discuss... (00:00) Overcoming Fear and Embracing Failure (12:08) Why You Need Trusted Advisors (22:07) How to Use Failure as Datapoints (28:13) Optimizing Relationships & Failure (38:07) Cultivating Audacity (45:35) Prioritizing Important Over Urgent Tasks (51:49) Personal Lessons From Failure and Success (58:43) The Relationship Between Fear and Generosity (01:07:57) Personal Growth Means Taking Responsibility  (01:13:43) Ever Forward ----- Episode resources: Save 10% on MitoPure mitochondrial revitalizer with code EVERFORWARD at https://www.Timeline.com  Get a FREE electrolyte variety pack with any purchase at https://www.DrinkLMNT.com/everforward  Save 15% on organic coffee and lattes with code CHASE at https://www.StrongCoffeeCompany.com  Watch and subscribe on YouTube Learn more at AnneMarieAnderson.com

Double vision is a symptom often experienced by patients with neurologic disease. An organized systematic approach to evaluating patients with diplopia needs a foundational understanding of the neuroanatomy and examination of eye movements and ocular alignment. In this episode, Teshamae Monteith, MD, FAAN, speaks with Devin Mackay, MD, FAAN, author of the article “Approach to Diplopia” in the Continuum® April 2025 Neuro-ophthalmology 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. Mackay is an associate professor of neurology, ophthalmology, and clinical neurosurgery at Indiana University School of Medicine in Indianapolis, Indiana. Additional Resources Read the article: Approach to Diplopia 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 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: This is Dr Teshamae Monteith. Today I'm interviewing Dr Devin Mackay about his article on approach to diplopia, which appears in the April 2025 Continuum issue on neuro-ophthalmology. Welcome to the podcast. How are you? Dr Mackay: Thank you. It's great to be here. Dr Monteith: Congratulations on your article. Dr Mackay: Thank you. I appreciate that. Dr Monteith: Why don't you start off with introducing yourself to our audience? Dr Mackay: So, yeah, my name is Devin Mackay. I'm a neuro-ophthalmologist at Indiana University. I did my residency at what was used to be known as the Partners Healthcare Program in Boston, and I did a fellowship in neuro-ophthalmology in Atlanta. And I've been in practice now for about ten years. Dr Monteith: Oh, wow. Okay. Tell us a little bit about your goals when you were writing the chapter. Dr Mackay: So, my goal with the approach to double vision was really to demystify double vision. I think double vision is something that as trainees, and even as faculty members and practicing neurologists, we really get intimidated by, I think. And it really helps to have a way to approach it that demystifies it and allows us to localize, just like we do with so many other problems in neurology. Dr Monteith: I love that, demystification. So why don't you tell us what got you interested in neuro-ophthalmology? Dr Mackay: Yeah, so neuro-ophthalmology I stumbled on during a rotation during residency. We rotated in different subspecialties of neurology and I did neuro-ophthalmology, and I was just amazed by the exam and how intricate it was, the value of neuroanatomy and localization, the ability to take a complicated problem and kind of approach it as a diagnostic specialist and really unravel the layers of it to make it better. To, you know, figure out what the problem is and make it better. Dr Monteith: Okay, so you had a calling, clearly. Dr Mackay: I sure did. Dr Monteith: You talked about latest developments in neuro-ophthalmology as it relates to diplopia. Why don't you share that with our listeners? Dr Mackay: Yeah. So, you know, double vision is something that's really been around since the beginning of time, essentially. So that part hasn't really changed a lot, but there are some changes that have happened in how we approach double vision. Probably one of the bigger ones has been, we used to teach that with a, you know, patient over the age of fifty with vascular risk factors who had a cranial nerve palsy of cranial nerves 3, 4, or 6, we used to automatically assume that was a microvascular palsy and we just wouldn't do any more testing and we'd just, you know, wait to see how they did. And it turns out we're missing some patients who have significant pathologies, sometimes, with that approach. And so, we've really shifted our teaching with that to emphasize that it's a lot easier to get an MRI, for example, than it ever has been. And it can be important to make sure we're not missing important pathology in patients, even if they have vascular risk factors over the age of fifty and they just have a cranial nerve 3, 4, or 6 palsy. So that's been one change. Dr Monteith: Interesting. And why don't you tell us a little bit about the essential points that you want to get across in the article? Dr Mackay: Yeah. So, I think one is to have a systematic approach to double vision. And a lot of that really revolves around localization. And it even begins with the history that we take from the patients. There's lots of interesting things we can ask about double vision from the patient. For example, the most important thing you can ever ask someone with double vision is, does it go away when you cover either eye? And that really helps us figure out the first question for us as neurologists, which is, is it neurologic or non-neurologic? If it's still there when covering one eye, then it is not neurologic and that's usually a problem for an ophthalmologist to sort out. So that's really number one. And then if it is binocular double vision, then we get into details about, is it horizontal or vertical misalignment? Is it- what makes it better and worse? Is there an associated ptosis or other symptoms? And based on all of that, we can really localize the abnormality with the double vision and get into details about further testing if needed, and so forth. I also love that that approach really reduces our need to rely on things like neuroimaging sometimes when we may not need it, or on other tests. So, I think it really helps us be more efficient and really take better care of patients. Dr Monteith: So definitely that cover/uncover test, top thing there. Your approach- and you mentioned, are you really getting that history, and are there any other kind of key factors when you're approaching diplopia before getting into some of the details? Dr Mackay: Yeah, that's a good question. I think also having some basics of how to examine the patient, because double vision is such a challenging thing. A lot of us aren't as familiar with the exam toolkit, so to speak, of what you would do with a patient with double vision. And so, I go over in the article a bit about a Maddox rod, which is a handy little tool that I always keep in my pocket of my lab coat. It allows you to assign a red line to one eye and a light to the other eye, and you can see if the eyes line up or not. And you don't need any other special equipment, you just need the light in that Maddox rod. That really helps us understand a lot about the pattern of misalignment, which is really important for evaluating double vision. So, for example, if someone has a right 6th nerve palsy, I'll expect a horizontal misalignment of the eyes that worsens when the patient looks to the right and improves when they look to the left. And especially if it's a partial palsy, it's not always easy to see that just by looking at their eye movements. And having a way to really measure the eye alignment and figure out, is it worse or better in certain directions, is really essential to localization, I think, in a lot of cases. Dr Monteith: You caught me. I skipped over that Maddox rod part, even though you spent a lot of time talking about Maddox rods. Kind of skipped over it. So, you're saying that I need one. Dr Mackay: Everyone needs one. I've converted some of our residents here to carry one with them. And yeah, I realize it's a daunting tool at first, but when you have a patient with double vision and their eye movements look normal, I feel like a lot of neurologists are- kind of, their hands seem like they're tied and they're like, oh, I don't know, I don't know what to do at this point. And if you can get some more details with a simple object like that, it can really change things. Dr Monteith: So, we've got to talk to the AAN store and make sure that they have enough of these, because now there's going to be lots of… Dr Mackay: We're going to sell out on Amazon today now because of this podcast. Dr Monteith: Cyber Monday. So, let's talk about the H pattern. And I didn't know it had the- well, yeah, I guess the official name is “H pattern.” In medical school, I mean, that's what I learned. But as a resident and, you know, certainly as an attendee, I see people doing all sorts of things. You're pro-H pattern, but are there other patterns that you also respect? Dr Mackay: It depends on what you're looking for, I think. The reason I like the H pattern is because you get to look at upgaze and downgaze in two different directions. So, you get to look at upgaze and downgaze when looking to the left, and up- and downgaze when looking to the right. And the reason that matters is because vertical movements of the eyes are actually controlled by different eye muscles depending on whether the eye is adducted toward the nose or abducted away from the nose. And so that's why I love the H pattern, is because it allows you to see that. If you just have them look up and down with just a cross pattern, for example, then you really lose that specificity of looking at both the adduction and abduction aspects. So, it's not wrong to do it another way with, like, the cross, for example, but I just think there are some cases where we'll be missing some information, and sometimes that can actually make a difference. Dr Monteith: Well, there you have it. Let's talk a little bit about eliciting diplopia during the neurologic exam. What other things should we be looking out for? Dr Mackay: So, in terms of eliciting diplopia, it really starts with the exam and again, figuring out, are we covering one eye? And figuring out, is this patient still having double vision? It's tricky because sometimes the patients won't even know the answer to that question or they've never done it, they've never covered one eye. And so, if that's the case, I really make them do it in the office with me and it's like, okay, well, are we having double vision right now? Well, great, okay, we are, then we're going to figure this out right now. And we cover one eye and say, is it still double? And that way we can really figure out, are we monocular or binocular? That's always step one. And then if we've established that it's binocular diplopia, then that's when we get into the other details that I mentioned before. And then as far as other things to look for, we're always in tune to other things that are going on in terms of symptoms, like ptosis, or if there's bulbar weakness, or some sensory change or motor problem that seems to be associated with it. Obviously, those will give us clues in the localization as well. Dr Monteith: And what about ocular malalignment? Dr Mackay: Yeah. So ocular malalignment, really, the cardinal symptom of that is going to be double vision. And so, if a patient has a misalignment of the eyes and they don't have double vision, then usually that means either we're wrong and they don't have double vision, or they do have double vision and they, you know, haven't said it correctly. Or it could be that the vision is poor in one eye. Sometimes that can happen. Or, some patients were actually born with an eye misalignment and their brain has learned in a way to kind of tune out or not allow the proper development of vision in one eye. And so that's also known as amblyopia, also known as the lazy eye, some people call it. But that finding can also make someone not experience double vision. But otherwise, if someone's had normal vision kind of throughout their life, they'll usually be pretty aware of when they first notice double vision. It'll be an obvious event for them in in most cases. Dr Monteith: And then the Cogan lid twitch? Dr Mackay: Oh yes, the Cogan lid twitch. So, the Cogan lid twitch is a feature of myasthenia gravis. The way you elicit it is, you have the patient look down. I'm not sure there's a standardization for how long; you want to have it long enough that you're resting the levator muscle, which is the muscle that pulls the upper lid open. And so, you rest that by having them look down for… I usually do about ten or fifteen seconds. And then I have them look up to looking straight forward. And you want to pay careful attention to their lid position as their eye settles in that straight-forward position. What will happen with a Cogan's lid twitch is, the lid will overshoot, and then it'll come back down and settle into its, kind of, proper position. And what we think is happening there is, it's almost like a little mini “rest test” in a way, where you're resting that muscle just long enough to allow some of the neurotransmission to recover. You get a normal contraction of the muscle, but it fades very quickly and comes back down. And that's experienced as a twitch. Dr Monteith: So, the patient can feel it. And it's something you can see? Dr Mackay: Yeah, the patient may not feel it as much. It's usually it's going to be something that the clinician can see if they're looking for it. And I would say that's one of the physical exam findings that can be a hallmark of myasthenia gravis, but certainly not the only one. Some others that we often look for are fatigable ptosis with sustained upgaze. You have the patient look up for a prolonged time and you'll see the lid droop down. So that can be one. Ice pack test is very popular nowadays, and it has pretty good sensitivity and specificity for myasthenia. So, you keep an ice pack over the closed eyes for two minutes and you compare the lid position before and after the ice pack test. And in the vast majority of myasthenia patients, if they have ptosis, the ptosis will have resolved, or at least significantly improved, in those patients. And yet one more sign is, if you find the patient's eye with ptosis and you lift open the eye manually, you'll often see that the other eyelid and the other eye will lower down. So, I'm not sure there's a name for that, but that can be a helpful sign as well. Dr Monteith: Since you're going through some of these, kind of, key features of different neurologic disease, why don't you tell us about a few others? Dr Mackay: Yeah, so another I mentioned in the in the article is measurement of levator function, which is really a test of eyelid strength. And so, that can be helpful if we have- someone has ptosis, or we're not sure if they have ptosis and we're trying to evaluate that to see if it's linked to the double vision, because that really changes the differential if ptosis is part of the clinical situation. So, the way that's measured is you have a patient look down as far as they can. And you get out a little ruler---I usually use a millimeter ruler---and I set the zero of the ruler at the upper lid margin when they're looking down. So, I hold the ruler there, and then I ask the patient to look up as far as they can without moving their head. Where the lid position stops of the upper lid is the new point on the ruler. And so, you measure that and see how much that is. And so, a normal patient may have a value somewhere between, I don't know, twelve or thirteen millimeters up to seventeen or eighteen millimeters, probably, in most cases. Especially if there is an asymmetric lid position, if you find that the levator function is symmetric, then it tells you that the muscle is working fine and that the ptosis is not from the muscle. So then the ptosis may be from dehiscence of the lid margin from the muscle. And so, that's a really common cause of ptosis, and that's often age-related or trauma-related. And we can dismiss that as being part of the symptom constellation of double vision. So, it can be really helpful to clarify, is this a muscle problem, which you'd expect with myasthenia or a third nerve palsy, or is this a mechanical problem with the lid, which is non-neurologic and really should be dismissed? So that can be a really helpful exam tool. Dr Monteith: So, you're just now getting into a little localization. So why don't we kind of start from the most proximal pistol with localization. Give us a little bit of tips. I know they just got to read your article, but give us a few tips. Dr Mackay: So, in terms of most proximal causes, there are supranuclear causes of ocular misalignment. For example, a skew deviation would qualify as that. Anything that's happening from some deficient input before you get to the cranial nerve nuclei, that we would consider supranuclear. So, we also see that with things like progressive supranuclear policy and certain other conditions. And then there can be lesions of the cranial nerve nuclei themselves. So, cranial nerves 3, 4, and 6 all have nuclei, and if they're lesioned they will cause double vision in specific patterns. And then there's also another subgroup, which is known as intranuclear problems with eye alignment. And so, the most common of that is going to be intranuclear ophthalmoplegia. And so that's very common in patients with demyelinating disorders, or it can also happen with strokes and tumors and other causes. And then there's infranuclear problems, which are from the cranial nerve nuclei out, and so those would be the cranial nerves themselves. So that's where your microvascular palsies, any tumor pressing on the nerve in those locations can cause palsies like that, any inflammatory disorder along that course. Then as we get more distal, we get into the orbit, we have the neuromuscular junction---so, the connection between the nerve and the muscle. And of course, that's our myasthenia gravis. And there are rare causes, things like botulinum and tick borne illnesses and certain other things that are more rare. And then, of course, we get to the muscle itself, and there can be different muscular dystrophies, different things like myositis or inflammatory disorders of the orbit or even physical trauma. So, if a patient, you know, had a trauma in trapping an extraocular muscle, that can be a localization. So really, anywhere along that pathway you can have double vision. So, I love to approach it from that perspective to help narrow down the diagnostic possibilities. Dr Monteith: Okay, just like everything? Dr Mackay: Just like all of the rest of the neurology. See, it's not that scary. Dr Monteith: You know, and so, yeah. And then you do a lot more than, you know, a few cranial nerves, right? Dr Mackay: Right. That's right. There's a lot more to double vision than that. I think as neurologists, we get lost if it's not a cranial nerve palsy, we're like, oh, I don't know what this is. And if it's not myasthenia, not a cranial nerve palsy. But it's worth also considering that there are ophthalmologic causes of someone having double vision that we often don't consider. So maybe someone who was born with strabismus, or maybe they have a little bit of a tendency toward an eye misalignment that their brain compensates, for and then it decompensates someday and that now they have a little bit of double vision intermittently, so that those can be causes to consider as well. Dr Monteith: Yeah, well, we'll just have to, you know, request those records from forty years ago. No problem. Dr Mackay: That's right. Dr Monteith: Why don't you also give us a little bit of tip when we're on the wards and we want to teach either a medical student or a resident, or if it's a resident listening, may want to teach a junior resident and seem like a star when approaching a patient with diplopia. Give us some teaching pearls. Dr Mackay: Yeah. So, I would love people teaching more about this at the bedside. I'd say probably the first thing to do would be to equip yourself by recognizing what some of the pertinent questions are to ask someone with double vision. Those things would include, is the double vision worse when looking in a certain direction? Does the double vision go away or not when you cover one eye? What happens when you tilt your head one direction or the other? Is it intermittent or constant? What makes it better? What makes it worse? Those kinds of things can really help us narrow down the possibilities. And then the other thing would be to equip yourself with some tools for examining. And it doesn't have to be physical tools. These can actually be things like, you mentioned the cross-cover test or cover/uncover test. That's described in the article. And I think knowing how to do that properly, knowing how to examine the eye movements properly and how to check for subtle things like a subtle intranuclear ophthalmoplegia, which is also mentioned in the article, being familiar with those things can be a really useful exercise in allowing you to teach others later on. Dr Monteith: Cool. Why don't you tell us about some of the things you're most excited about in the field? Dr Mackay: One of the things about our subspecialty for so long is we really haven't had big data with, you know, big trials and all these things that all the stroke people have. And that's starting to change slowly. There's been, for example, the idiopathic intracranial hypertension treatment trial that was published back in, I think it was 2014. You know, of course we had the optic neuritis treatment trial, back a few decades ago now. Some of the exciting ones coming up, there's going to be a randomized controlled trial looking at different treatments for idiopathic intracranial hypertension that are surgically based. So, for example, comparing venous sinus stenting with optic nerve sheath fenestration. And so, figuring out, is there a best practice for surgical intervention for patients with IIH? So, we're starting to have more trials like that now than I think we've had in the past. And so, it's exciting to get to have an evidence base for some of the things that we recommend and do. Dr Monteith: And what about some of the treatment for diplopia? Like prisms, and where are we with some of that? Dr Mackay: Yeah, great. So, it's a pretty simple concept, but still kind of difficult in practice. I kind of say there are four different ways to treat double vision: you can ignore it, you can patch or cover one eye, you can treat with prisms, and you can treat with eye muscle surgery. And so, those are the main ways other than, of course, treating the underlying disorder if there's a disorder causing double vision. So those are the main ways to treat. In terms of knowing if someone's going to be a candidate for prism therapy, we also have to remember that prisms are really going to be most helpful for when someone's looking straight forward. So, we need to make sure that their double vision is happening when they look straight forward. So, for example, if they're only having double vision looking to the left or to the right, that patient may not benefit from prisms as much as someone who is having double vision when they look straight forward. So that's one thing I look for. And then strabismus surgery is something to be considered if someone is not tolerating prisms and they're not helping and their eye alignment is stable. So, if you think about it, if someone's eye alignment is changing a lot, you're probably not going to want to do surgery for that patient because it's going to keep changing after surgery. And so, if someone's eye alignment is stable for six months or more and they're not getting the benefit they'd like from prisms, then maybe referral to a strabismus surgeon might be something to consider. Dr Monteith: Great. And then, I guess another question is just popping up in my head selfishly. What are your thoughts about patients that get referrals for exercises? Say they have, like, a convergence efficiency or something causing diplopia, maybe after a concussion. Maybe there's not a lot of evidence, but what is your take on exercising? Dr Mackay: Yeah, excellent question. So, there actually is evidence for exercises for convergence insufficiency. So, we know that those do work. Now where exercises are probably not as helpful, or at least not- there isn't an evidence base for them, is really with just about every other kind of eye misalignment in adults. We hear a lot about eye movement therapies for concussion and barely any other acquired misalignment of the eyes as well. And really, the evidence really hasn't shown us that that's helpful; again, with the exception being convergence insufficiency. So, we know that an office-based vision therapy type program for convergence insufficiency does work, but of course it's kind of inconvenient. It can cost money that may or may not be covered by insurance. And so, there are difficulties even with doing that. And so, I often recommend that patients with convergence insufficiency at least try something called pencil push-ups, where they take a pencil at arm's length and they bring it in and exercise that convergence ability. You know, that's a cheap, easy way to try to treat that initially. So yeah, there can be some limited utility for eye muscle exercises in certain conditions. Dr Monteith: My one example. I was- it was fuzzy, but in a different way. So, what do you do for fun? I mean, it sounds like you like to see a lot of eyeballs? Dr Mackay: I do. I like to see a lot of eyeballs. Dr Monteith: When you're not doing these things, what do you do for fun? Dr Mackay: So, people ask me what my hobbies are, and I laugh because my hobby is actually raising children. Dr Monteith: Oh, okay! Dr Mackay: So, my wife and I have eight kids- Dr Monteith: Oh, wow! Dr Mackay: Ages three to thirteen. So, kind of doesn't allow me to have other things right now. I'm sure I'll have more hobbies later on, but no, I really love my kids. And I- they give me plenty to do. There's no shortage of- in fact, they were really, they were really excited about this podcast today. They're so excited that Dad gets to be on a podcast, and so I'm going to have to show this to them later. They're going to be thrilled about it. Dr Monteith: Excellent. Well, thank you so much for being on the podcast. Dr Mackay: Thank you. It's been my pleasure. Dr Monteith: Again, today I've been interviewing Dr Devin Mackay about his article on approach to diplopia, which appears in the most recent issue of Continuum on neuro-ophthalmology. 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.

In this episode of [Podcast Name], we explore how to be a Gospel-centered teacher who faithfully handles God's Word, based on 2 Timothy 2:14–19. Building on Paul's powerful imagery of the soldier, athlete, and farmer, we focus today on the next crucial metaphor: the Unashamed Workman.Paul reminds Timothy—and every Christian teacher—that ministry is not about speculation or worldly trends, but about faithfully transmitting the truths of the Gospel through diligent and accurate teaching. Repetition and faithfulness are key (see 2 Peter 1:12–15).

Folx-- we've heard the cries from our mother's daughters and done an album by old sexy blue eyes (use google AI and it will confirm that he has blue eyes, famously) John Mayer. Our podcast is a wonderland is a thing I would say if I was a hack, which is why I bravely did not. Also up for discussion: When in the World is Carmen Thanksgivingo, no one on earth can eat American foods because they aren't safe to consume, and is this 98 degrees because its a wall a Mountain Goat could stand on. Hosted on Acast. See acast.com/privacy for more information.

In the aftermath of the time phone's energy burst, mind-blowing reunions abound. For more great shows and to listen early and ad-free, visit GZMshows.com Learn more about your ad choices. Visit megaphone.fm/adchoices