Podcasts about Continuum

In the Star Trek: Voyager episode Q2, Q drops by Voyager for a surprise visit, and he brings Q with him. No, not himself… the other Q. His son. This junior Q is every bit as powerful, unpredictable, and exasperating as his old man, with none of the charm (yet). When the Continuum threatens to de-Q him permanently, it's up to Aunt Kathy to teach Q some responsibility before he's stuck living as an amoeba or worse, a teenager. Mission Log wrangles Q, Q, and more Q in Q2. Hosted by John Champion and Norman Lao MISSION LOG SURVEY: Take the survey NOW and you could win rare, original TOS film cells! Offer ends October 10, 2025. Welcome to Mission Log, a Roddenberry Entertainment podcast, where we explore the Star Trek universe one episode at a time. Each week, Mission Log examines a single episode of Star Trek, diving into its ethical subtext, metaphors, and cultural significance. From the show's most iconic moments to its hidden gems, we analyze what makes Star Trek one of the greatest science fiction sagas of all time. In every episode of Mission Log we… Recap the story and analyze key moments. Discuss the morals, messages, and meanings of the dilemmas presented. Debate whether the episode holds up and if the themes are still relevant. Join the Conversation: For as little as $1 a month, you can gain access to our exclusive Discord Community! There, we continue the discussion with dedicated channels and  weekly video chats with the hosts. Become a member of our Patreon today! https://www.Patreon.com/MissionLog SPECIAL THANKS the supporters of this week's show: Chris Garis, Julie Miller, Stuart, Michael Park, Paul Shadwell, Matt Esposito, Alan Simonis, Mike Richards, David Takechi, Mike Schiable, VADM Erickson, and Lars Seme Thanks to all of our Patreon Supporters https://www.missionlogpodcast.com/sponsors/ Want to share your thoughts on an upcoming episode? Email us at MissionLog@Roddenberry.com for a chance to be featured during the episode. Follow us on Social Media: INSTAGRAM https://www.instagram.com/RoddenberryEntertainment THREADS https://www.threads.net/@roddenberrypodcasts FACEBOOK https://www.facebook.com/MissionLogPod Did you know we're on YouTube? Find the video versions of your favorite shows like Mission Log: Prodigy, The Orville, as well as exclusive content only available on YouTube. Subscribe now:  https://www.youtube.com/@RoddenberryEntertainment?sub_confirmation=1 Our shows are part of the Roddenberry Entertainment family. For more great shows and to learn more about how we live the legacy of Gene Roddenberry, creator of Star Trek, follow us here: RODDENBERRY PODCASTS https://www.instagram.com/roddenberrypodcasts RODDENBERRY ENTERTAINMENT https://www.instagram.com/roddenberryofficial THE RODDENBERRY FOUNDATION https://www.instagram.com/theroddenberryfoundation   THIS EPISODE IS SPONSORED BY: Listeners like you - Support Mission Log on Patreon for early access to shows and the Mission Log Discord! Subscribe and Stay Updated: Never miss an episode! Subscribe on your preferred podcast player, leave a review, and join Mission Log on the journey of weekly deep dives into the Star Trek universe. Technical Director - Earl Green Producer - John Champion Associate Producer - Jessica Lynn Verdi Executive Producer - Eugene “Rod” Roddenberry Roddenberry Entertainment | All Rights Reserved

In today's episode I chat with Dr Daniela Aiello, a registered osteopath specialising in pregnancy and postpartum care at Bulleen Osteopathy in Melbourne's northern suburbs. Daniela brings over two decades of experience treating pregnant and postpartum women, combined with her personal journey as a mother of two (aged 14 and 11) and founder of Continuum, a compression wear brand designed specifically for women during pregnancy and postpartum recovery. This episode serves as an essential guide for expectant mothers, doulas, and midwives seeking to understand the most common musculoskeletal complaints during pregnancy and the fourth trimester. Today's sponsor - iL Tutto iL Tutto design nursery furniture that's as stylish as it is supportive. Their Trend Collection has already given parents the award-winning Frankie and Louie Nursery Chairs in our signature teddy-fleece. And now, we're so excited to welcome Louie in Corduroy — a brand new textured fabric available in three colours: Taupe, Green Olive, and Coconut.Corduroy brings a modern, tactile finish to the nursery, while Louie delivers the comfort parents love — with plush cushioning, smooth gliding, and thoughtful design for every feed, cuddle, and nap-time story.To celebrate, we're giving Australian Birth Stories listeners an exclusive discount:Use the code BIRTHSTORIES20 at checkout to receive 20% off your iL Tutto order, but hurry — this offer ends 12th October 2025.Shop the collection now at iltutto.com.au Hosted on Acast. See acast.com/privacy for more information.

Functional movement disorders are a common clinical concern for neurologists. The principle of “rule-in” diagnosis, which involves demonstrating the difference between voluntary and automatic movement, can be carried through to explanation, triage, and evidence-based multidisciplinary rehabilitation therapy. In this episode, Gordon Smith, MD, FAAN speaks Jon Stone, PhD, MB, ChB, FRCP, an author of the article “Multidisciplinary Treatment for Functional Movement Disorder” in the Continuum® August 2025 Movement Disorders 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. Stone is a consultant neurologist and honorary professor of neurology at the Centre for Clinical Brain Sciences at the University of Edinburgh in Edinburgh, United Kingdom. Additional Resources Read the article: Multidisciplinary Treatment for Functional Movement Disorder 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: @gordonsmithMD Guest: @jonstoneneuro 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 Smith: Hello, this is Dr Gordon Smith. Today I've got the great pleasure of interviewing Dr Johnstone about his article on the multidisciplinary treatment for functional neurologic disorder, which he wrote with Dr Alan Carson. This article will appear in the August 2025 Continuum issue on movement disorders. I will say, Jon, that as a Continuum Audio interviewer, I usually take the interviews that come my way, and I'm happy about it. I learn something every time. They're all a lot of fun. But there have been two instances where I go out and actively seek to interview someone, and you are one of them. So, I'm super excited that they allowed me to talk with you today. For those of our listeners who understand or are familiar with FND, Dr Stone is a true luminary and a leader in this, both in clinical care and research. He's also a true humanist. And I have a bit of a bias here, but he was the first awardee of the Ted Burns Humanism in Neurology award, which is a real honor and reflective of your great work. So welcome to the podcast, Jon. Maybe you can introduce yourself to our audience. Dr Stone: Well, thank you so much, Gordon. It was such a pleasure to get that award, the Ted Burns Award, because Ted was such a great character. I think the spirit of his podcasts is seen in the spirit of these podcasts as well. So, I'm a neurologist in Edinburgh in Scotland. I'm from England originally. I'm very much a general neurologist still. I still work full-time. I do general neurology, acute neurology, and I do two FND clinics a week. I have a research group with Alan Carson, who you mentioned; a very clinical research group, and we've been doing that for about 25 years. Dr Smith: I really want to hear more about your clinical approach and how you run the clinic, but I wonder if it would be helpful for you to maybe provide a definition. What's the definition of a functional movement disorder? I mean, I think all of us see these patients, but it's actually nice to have a definition. Dr Stone: You know, that's one of the hardest things to do in any paper on FND. And I'm involved with the FND society, and we're trying to get together a definition. It's very hard to get an overarching definition. But from a movement disorder point of view, I think you're looking at a disorder where there is an impairment of voluntary movement, where you can demonstrate that there is an automatic movement, which is normal in the same movement. I mean, that's a very clumsy way of saying it. Ultimately, it's a disorder that's defined by the clinical features it has; a bit like saying, what is migraine? You know? Or, what is MS? You know, it's very hard to actually say that in a sentence. I think these are disorders of brain function at a very broad level, and particularly with FND disorders, of a sort of higher control of voluntary movement, I would say. Dr Smith: There's so many pearls in this article and others that you've written. One that I really like is that this isn't a diagnosis of exclusion, that this is an affirmative diagnosis that have clear diagnostic signs. And I wonder if you can talk a little bit about the diagnostic process, arriving at an FND diagnosis for a patient. Dr Stone: I think this is probably the most important sort of “switch-around” in the last fifteen, twenty years since I've been involved. It's not new information. You know, all of these diagnostic signs were well known in the 19th century; and in fact, many of them were described then as well. But they were kind of lost knowledge, so that by the time we got to the late nineties, this area---which was called conversion disorder then---it was written down. This is a diagnosis of exclusion that you make when you've ruled everything out. But in fact, we have lots of rule in signs, which I hope most listeners are familiar with. So, if you've got someone with a functional tremor, you would do a tremor entrainment test where you do rhythmic movements of your thumb and forefinger, ask the patient to copy them. It's very important that they copy you rather than make their own movements. And see if their tremor stops briefly, or perhaps entrains to the same rhythm that you're making, or perhaps they just can't make the movement. That might be one example. There's many examples for limb weakness and dystonia. There's a whole lot of stuff to learn there, basically, clinical skills. Dr Smith: You make a really interesting point early on in your article about the importance of the neurological assessment as part of the treatment of the patient. I wonder if you could talk to our listeners about that. Dr Stone: So, I think, you know, there's a perception that- certainly, there was a perception that that the neurologist is there to make a diagnosis. When I was training, the neurologist was there to tell the patient that they didn't have the kind of neurological problem and to go somewhere else. But in fact, that treatment process, when it goes well, I think begins from the moment you greet the patient in the waiting room, shake their hand, look at them. Things like asking the patient about all their symptoms, being the first doctor who's ever been interested in their, you know, horrendous exhaustion or their dizziness. You know, questions that many patients are aware that doctors often aren't very interested in. These are therapeutic opportunities, you know, as well as just taking the history that enable the patient to feel relaxed. They start thinking, oh, this person's actually interested in me. They're more likely to listen to what you've got to say if they get that feeling off you. So, I'd spend a lot of time going through physical symptoms. I go through time asking the patient what they do, and the patients will often tell you what they don't do. They say, I used to do this, I used to go running. Okay, you need to know that, but what do they actually do? Because that's such valuable information for their treatment plan. You know, they list a whole lot of TV shows that they really enjoy, they're probably not depressed. So that's kind of useful information. I also spend a lot of time talking to them about what they think is wrong. Be careful, that they can annoy patients, you know. Well, I've come to you because you're going to tell me what's wrong. But what sort of ideas had you had about what was wrong? I need to know so that I can deal with those ideas that you've had. Is there a particular reason that you're in my clinic today? Were you sent here? Was it your idea? Are there particular treatments that you think would really help you? These all set the scene for what's going to come later in terms of your explanation. And, more importantly, your triaging of the patient. Is this somebody where it's the right time to be embarking on treatment, which is a question we don't always ask yourself, I think. Dr Smith: That's a really great point and kind of segues to my next question, which is- you talked a little bit about this, right? Generally speaking, we have come up with this is a likely diagnosis earlier, midway through the encounter. And you talked a little bit about how to frame the encounter, knowing what's coming up. And then what's coming up is sharing with the patient our opinion. In your article, you point out this should be no different than telling someone they have Parkinson's disease, for instance. What pearls do you have and what pitfalls do you have in how to give the diagnosis? And, you know, a lot of us really weren't trained to do this. What's the right way, and what are the most common land mines that folks step on when they're trying to share this information with patients? Dr Stone: I've been thinking about this for a long time, and I've come to the conclusion that all we need to do with this disorder is stop being weird. What goes wrong? The main pitfall is that people think, oh God, this is FND, this is something a bit weird. It's in a different box to all of the other things and I have to do something weird. And people end up blurting out things like, well, your scan was normal or, you haven't got epilepsy or, you haven't got Parkinson's disease. That's not what you normally do. It's weird. What you normally do is you take a deep breath and you say, I'm sorry to tell you've got Parkinson's disease or, you have this type of dystonia. That's what you normally say. If you follow the normal- what goes wrong is that people don't follow the normal rules. The patient picks up on this. What's going on here? This doctor's telling me what I don't have and then they're starting to talk about some reason why I've got this, like stress, even though I don't- haven't been told what it is yet. You do the normal rules, give it a name, a name that you're comfortable with, preferably as specific as possible: functional tremor, functional dystonia. And then do what you normally do, which is explain to the patient why you think it's this. So, if someone's got Parkinson's, you say, I think you've got Parkinson's because I noticed that you're walking very slowly and you've got a tremor. And these are typical features of Parkinson. And so, you're talking about the features. This is where I think it's the most useful thing that you can do. And the thing that I do when it goes really well and it's gone badly somewhere else, the thing I probably do best, what was most useful, is showing the patient their signs. I don't know if you do that, Gordon, but it's maybe not something that we're used to doing. Dr Smith: Wait, maybe you can talk more about that, and maybe, perhaps, give an example? Talk about how that impacts treatment. I was really impressed about the approach to physical therapy, and treatment of patients really leverages the physical examination findings that we're all well-trained to look for. So maybe explore that a little bit. Dr Stone: Yeah, I think absolutely it does. And I think we've been evolving these thoughts over the last ten or fifteen years. But I started, you know, maybe about twenty years ago, started to show people their tremor entrainment tests. Or their Hoover sign, for example; if you don't know Hoover sign, weakness of hip extension, that comes back to normal when the person's flexing their normal leg, their normal hip. These are sort of diagnostic tricks that we had. Ahen I started writing articles about FND, various senior neurologists said to me, are you sure you should write this stuff down? Patients will find out. I wrote an article with Marc Edwards called “Trick or Treat in Neurology” about fifteen years ago to say that actually, although they're they might seem like tricks, there really are treats for patients because you're bringing the diagnosis into the clinic room. It's not about the normal scan. You can have FND and MS. It's not about the normal scan. It's about what you're seeing in front of you. If you show that patient, yes, you can't move your leg. The more you try, the worse it gets. I can see that. But look, lift up your other leg. Let me show you. Can you see now how strong your leg is? It's such a powerful way of communicating to the patient what's wrong with them diagnostically, giving them that confidence. What it's also doing is showing them the potential for improvement. It's giving them some hope, which they badly need. And, as we'll perhaps talk about, the physio treatment uses that as well because we have to use a different kind of physio for many forms of functional movement disorder, which relies on just glimpsing these little moments of normal function and promoting them, promoting the automatic movement, squashing down that abnormal pattern of voluntary movement that people have got with FND. Dr Smith: So, maybe we can talk about that now. You know, I've got a bunch of other questions to ask you about mechanism and stuff, but let's talk about the approach to physical therapy because it's such a good lead-in and I always worry that our physical therapists aren't knowledgeable about this. So, maybe some examples, you have some really great ones in the article. And then words of wisdom for us as we're engaging physical therapists who may not be familiar with FND, how to kind of build that competency and relationship with the therapist with whom you work. Dr Stone: Some of the stuff is the same. Some of the rehabilitation ideas are similar, thinking about boom and bust activity, which is very common in these patients, or grading activity. That's similar, but some of them are really different. So, if you have a patient with a stroke, the physiotherapist might be very used to getting that person to think and look at their leg to try and help them move, which is part of their rehabilitation. In FND, that makes things worse. That's what's happening in Hoover sign and tremor entrainment sign. Attention towards the limb is making it worse. But if the patient's on board with the diagnosis and understands it, they'll also see what you need to do, then, in the physio is actively use distraction in a very transparent way and say to the patient, look, I think if I get you to do that movement, and I'll film you, I think your movement's going to look better. Wouldn't that be great if we could demonstrate that? And the patient says, yeah, that would be great. We're kind of actively using distraction. We're doing things that would seem a bit strange for someone with other forms of movement disorder. So, the patients, for example, with functional gait disorders who you discover can jog quite well on a treadmill. In fact, that's another diagnostic test. Or they can walk backwards, or they can dance or pretend that they're ice skating, and they have much more fluid movements because their ice skating program in their brain is not corrupted, but their normal walking program is. So, can you then turn ice skating or jogging into normal walking? It's not that complicated, I think. The basic ideas are pretty simple, but it does require some creativity from whoever's doing the therapy because you have to use what the patient's into. So, if the patient used to be a dancer- we had a patient who was a, she was really into ballet dancing. Her ballet was great, but her walking was terrible. So, they used ballet to help her walk again. And that's incredibly satisfying for the therapist as well. So, if you have a therapist who's not sure, there are consensus recommendations. There are videos. One really good success often makes a therapist want to do that again and think, oh, that's interesting. I really helped that patient get better. Dr Smith: For a long time, this has been framed as a mental health issue, conversion disorder, and maybe we can talk a little bit about early life of trauma as a risk factor. But, you know, listening to you talk, it sounds like a brain network problem. Even the word “functional”, to me, it seems a little judgmental. I don't know if this is the best term, but is this really a network problem? Dr Stone: The word “functional”, for most neurologists, sounds judgmental because of what you associate it with. If you think about what the word actually is, it's- it does what it says on the tin. There's a disordered brain function. I mean, it's not a great word. It's the least worst term, in my view. And yes, of course it's a brain network problem, because what other organ is it going to be? You know, that's gone wrong? When software brains go wrong, they go wrong in networks. But I think we have to be careful not to swing that pendulum too far to the other side because the problem here, when we say asking the question, is this a mental health problem or a neurological one, we're just asking the wrong question. We're asking a question that makes no sense. However you try and answer that, you're going to get a stupid answer because the question doesn't make sense. We shouldn't have those categories. It's one organ. And what's so fascinating about FND---and I hope what can incite your sort of curiosity about it---is this disorder which defies this categorization. You see some patients with it, they say, oh, they've got a brain network disorder. Then you meet another patient who was sexually abused for five years by their uncle when they were nine, between nine and fourteen; they developed an incredibly strong dissociative threat response into that experience. They have crippling anxiety, PTSD, interpersonal problems, and their FND is sort of somehow a part of that; part of that experience that they've had. So, to ignore that or to deny or dismiss psychological, psychiatric aspects, is just as bad and just as much a mistake as to dismiss the kind of neurological aspects as well. Dr Smith: I wonder if this would be a good time to go back and talk a little bit about a concept that I found really interesting, and that is FND as a prodromal syndrome before a different neurological problem. So, for instance, FND prodromal to Parkinson's disease. Can you talk to us a little bit about that? I mean, obviously I was familiar with the fact that patients who have nonepileptic seizurelike events often have epileptic seizures, but the idea of FND ahead of Parkinson's was new to me. Dr Stone: So, this is definitely a thing that happens. It's interesting because previously, perhaps, if you saw someone who was referred with a functional tremor---this has happened to me and my colleagues. They send me some with a functional tremor. By the time I see them, it's obvious they've got Parkinson's because it's been a little gap. But it turns out that the diagnosis of functional tremor was wrong. It was just that they've developed that in the prodrome of Parkinson's disease. And if you think about it, it's what you'd expect, really, especially with Parkinson's disease. We know people develop anxiety in the prodrome of Parkinson's for ten, fifteen years before it's part of the prodrome. Anxiety is a very strong risk factor for FND, and they're already developing abnormalities in their brain predisposing them to tremor. So, you put those two things together, why wouldn't people get FND? It is interesting to think about how that's the opposite of seizures, because most people with comorbidity of functional seizures and epilepsy, 99% of the time the epilepsy came first. They had the experience of an epileptic seizure, which is frightening, which evokes strong threat response and has somehow then led to a recapitulation of that experience in a functional seizure. So yeah, it's really interesting how these disorders overlap. We're seeing something similar in early MS where, I think, there's a slight excess of functional symptoms; but as the disease progresses, they often become less, actually. Dr Smith: What is the prognosis with the types of physical therapy? And we haven't really talked about psychological therapy, but what's the success rate? And then what's the relapse rate or risk? Dr Stone: Well, it does depend who they're seeing, because I think---as you said---you're finding difficult to get people in your institution who you feel are comfortable with this. Well, that's a real problem. You know, you want your therapists to know about this condition, so that matters. But I think with a team with a multidisciplinary approach, which might include psychological therapy, physio, OT, I think the message is you can get really good outcomes. You don't want to oversell this to patients, because these treatments are not that good yet. You can get spectacular outcomes. And of course, people always show the videos of those. But in published studies, what you're seeing is that most studies of- case series of rehabilitation, people generally improve. And I think it's reasonable to say to a patient, that we have these treatments, there's a good chance it's going to help you. I can't guarantee it's going to help you. It's going to take a lot of work and this is something we have to do together. So, this is not something you're going to do to the patient, they're going to do it with you. Which is why it's so important to find out, hey, do they agree with you with the diagnosis? And check they do. And is it the right time? It's like when someone needs to lose weight or change any sort of behavior that they've just become ingrained. It's not easy to do. So, I don't know if that helps answer the question. Dr Smith: No, that's great. And you actually got right where I was wanting to go next, which is the idea of timing and acceptance. You brought this up earlier on, right? So, sometimes patients are excited and accepting of having an affirmative diagnosis, but sometimes there's some resistance. How do you manage the situation where you're making this diagnosis, but a patient's resistant to it? Maybe they're fixating on a different disease they think they have, or for whatever reason. How do you handle that in terms of initiating therapy of the overall diagnostic process? Dr Stone: We should, you know, respect people's rights to have whatever views they want about what's wrong with them. And I don't see my job as- I'm not there to change everyone's mind, but I think my job is to present the information to them in a kind of neutral way and say, look, here it is. This is what I think. My experience is, if you do that, most people are willing to listen. There are a few who are not, but most people are. And most of the time when it goes wrong, I have to say it's us and not the patients. But I think you do need to find out if they can have some hope. You can't do rehabilitation without hope, really. That's what you're looking for. I sometimes say to patients, where are you at with this? You know, I know this is a really hard thing to get your head around, you've never heard of it before. It's your own brain going wrong. I know that's weird. How much do you agree with it on a scale of naught to ten? Are you ten like completely agreeing, zero definitely don't? I might say, are you about a three? You know, just to make it easy for them to say, no, I really don't agree with you. Patients are often reluctant to tell you exactly what they're thinking. So, make it easy for them to disagree and then see where they're at. If they're about seven, say, that's good. But you know, it'd be great if you were nine or ten because this is going to be hard. It's painful and difficult, and you need to know that you're not damaging your body. Those sort of conversations are helpful. And even more importantly, is it the right time? Because again, if you explore that with people, if a single mother with four kids and, you know, huge debts and- you know, it's going to be very difficult for them to engage with rehab. So, you have to be realistic about whether it's the right time, too; but keep that hope going regardless. Dr Smith: So, Jon, there's so many things I want to talk to you about, but maybe rather than let me drive it, let me ask you, what's the most important thing that our listeners need to know that I haven't asked you about? Dr Stone: Oh God. I think when people come and visit me, they sometimes, let's go and see this guy who does a lot of FND, and surely, it'll be so easy for him, you know? And I think some of the feedback I've had from visitors is, it's been helpful to watch, to see that it's difficult for me too. You know, this is quite hard work. Patients have lots of things to talk about. Often you don't have enough time to do it in. It's a complicated scenario that you're unravelling. So, it's okay if you find it difficult work. Personally, I think it's very rewarding work, and it's worth doing. It's worth spending the time. I think you only need to have a few patients where they've improved. And sometimes that encounter with the neurologist made a huge difference. Think about whether that is worth it. You know, if you do that with five patients and one or two of them have that amazing, really good response, well, that's probably worth it. It's worth getting out of bed in the morning. I think reflecting on, is this something you want to do and put time and effort into, is worthwhile because I recognize it is challenging at times, and that's okay. Dr Smith: That's a great number needed to treat, five or six. Dr Stone: Exactly. I think it's probably less than that, but… Dr Smith: You're being conservative. Dr Stone: I think deliberately pessimistic; but I think it's more like two or three, yeah. Dr Smith: Let me ask one other question. There's so much more for our listeners in the article. This should be required reading, in my opinion. I think that of most Continuum, but this, I really truly mean it. But I think you've probably inspired a lot of listeners, right? What's the next step? We have a general or comprehensive neurologist working in a community practice who's inspired and wants to engage in the proactive care of the FND patients they see. What's the next step or advice you have for them as they embark on this? It strikes me, like- and I think you said this in the article, it's hard work and it's hard to do by yourself. So, what's the advice for someone to kind of get started? Dr Stone: Yeah, find some friends pretty quick. Though, yeah, your own enthusiasm can take you a long way, you know, especially with we've got much better resources than we have. But it can only take you so far. It's really particularly important, I think, to find somebody, a psychiatrist or psychologist, you can share patients with and have help with. In Edinburgh, that's been very important. I've done all this work with the neuropsychiatrist, Alan Carson. It might be difficult to do that, but just find someone, send them an easy patient, talk to them, teach them some of this stuff about how to manage FND. It turns out it's not that different to what they're already doing. You know, the management of functional seizures, for example, is- or episodic functional movement disorders is very close to managing panic disorder in terms of the principles. If you know a bit about that, you can encourage people around you. And then therapists just love seeing these patients. So, yeah, you can build up slowly, but don't- try not to do it all on your own, I would say. There's a risk of burnout there. Dr Smith: Well, Dr Stone, thank you. You don't disappoint. This has really been a fantastic conversation. I really very much appreciate it. Dr Stone: That's great, Gordon. Thanks so much for your time, yeah. Dr Smith: Well, listeners, again, today I've had the great pleasure of interviewing Dr Jon Stone about his article on the multidisciplinary treatment for functional neurologic disorder, which he wrote with Dr Alan Carson. This article appears in the August 2025 Continuum issue on movement disorders. Please be sure to check out Continuum Audio episodes from this and other issues. And listeners, thank you once again 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.

On this episode of Mission Matters,⁠ Adam Torres⁠ interviews ⁠Paul Barry⁠, Ikigai Whisperer at Dreaming for a Living. Paul shares the inspiration behind his new comedy-magic show Continuum, weaving together storytelling, illusion, and the Japanese philosophy of Ikigai to help audiences rediscover purpose and joy. Get tickets to the show at The Illusion Magic Lounge in Santa Monica on October 1st and 2nd ⁠here⁠. Follow Adam on Instagram at ⁠https://www.instagram.com/askadamtorres/⁠ for up to date information on book releases and tour schedule. Apply to be a guest on our podcast: ⁠https://missionmatters.lpages.co/podcastguest/⁠ Visit our website: ⁠https://missionmatters.com/⁠ More FREE content from Mission Matters here: ⁠https://linktr.ee/missionmattersmedia⁠ Learn more about your ad choices. Visit podcastchoices.com/adchoices

On this episode of Mission Matters, Adam Torres interviews Paul Barry, Ikigai Whisperer at Dreaming for a Living. Paul shares the inspiration behind his new comedy-magic show Continuum, weaving together storytelling, illusion, and the Japanese philosophy of Ikigai to help audiences rediscover purpose and joy. Get tickets to the show at The Illusion Magic Lounge in Santa Monica on October 1st and 2nd here. Follow Adam on Instagram at https://www.instagram.com/askadamtorres/ for up to date information on book releases and tour schedule. Apply to be a guest on our podcast: https://missionmatters.lpages.co/podcastguest/ Visit our website: https://missionmatters.com/ More FREE content from Mission Matters here: https://linktr.ee/missionmattersmedia Learn more about your ad choices. Visit podcastchoices.com/adchoices

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Paroxysmal movement disorders refer to a group of highly heterogeneous disorders that present with attacks of involuntary movements without loss of consciousness. These disorders demonstrate considerable and ever-expanding genetic and clinical heterogeneity, so an accurate clinical diagnosis has key therapeutic implications. In this episode, Kait Nevel, MD, speaks with Abhimanyu Mahajan, MD, MHS, FAAN, author of the article “Paroxysmal Movement Disorders” in the Continuum® August 2025 Movement Disorders issue. Dr. Nevel is a Continuum® Audio interviewer and a neurologist and neuro-oncologist at Indiana University School of Medicine in Indianapolis, Indiana. Dr. Mahajan is an assistant professor of neurology and rehabilitation medicine at the James J. and Joan A. Gardner Family Center for Parkinson's Disease and Movement Disorders at the University of Cincinnati in Cincinnati, Ohio. Additional Resources Read the article: Paroxysmal Movement Disorders 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 Guest: @MahajanMD Full episode transcript available here Dr Jones: This is Doctor 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 Kait Nevel. Today I'm interviewing doctor Abhi Mahajan about his article on diagnosis and management of paroxysmal movement disorders, which appears in the August 2025 Continuum issue on movement disorders. Abhi, welcome to the podcast and please introduce yourself to the audience. Dr Mahajan: Thank you, Kait. Thank you for inviting me. My name is Abhi Mahajan. I'm an assistant professor of neurology and rehabilitation medicine at the University of Cincinnati in Cincinnati, Ohio. I'm happy to be here. Dr Nevel: Wonderful. Well, I'm really excited to talk to you about your article today on this very interesting and unique set of movement disorders. So, before we get into your article a little bit more, I think just kind of the set the stage for the discussion so that we're all on the same page. Could you start us off with some definitions? What are paroxysmal movement disorders? And generally, how do we start to kind of categorize these in our minds? Dr Mahajan: So, the term paroxysmal movement disorders refers to a group of highly heterogeneous disorders. These may present with attacks of involuntary movements, commonly a combination of dystonia and chorea, or ataxia, or both. These movements are typically without loss of consciousness and may follow, may follow, so with or without known triggers. In terms of the classification, these have been classified in a number of ways. Classically, these have been classified based on the trigger. So, if the paroxysmal movement disorder follows activity, these are called kinesigenic, paroxysmal, kinesigenic dyskinesia. If they are not followed by activity, they're called non kinesigenic dyskinesia and then if they've followed prolonged activity or exercise they're called paroxysmal exercise induced dyskinesia. There's a separate but related group of protogynous movement disorders called episodic attacks here that can have their own triggers. Initially this was the classification that was said. Subsequent classifications have placed their focus on the ideology of these attacks that could be familiar or acquired and of course understanding of familiar or genetic causes of paroxysmal movement disorders keeps on expanding and so on and so forth. And more recently, response to pharmacotherapy and specific clinical features have also been introduced into the classification. Dr Nevel: Great, thank you for that. Can you share with us what you think is the most important takeaway from your article for the practicing neurologist? Dr Mahajan: Absolutely. I think it's important to recognize that everything that looks and sounds bizarre should not be dismissed as malingering. Such hyperkinetic and again in quotations, “bizarre movements”. They may appear functional to the untrained eye or the lazy eye. These movements can be diagnosed. Paroxysmal movement disorders can be diagnosed with a good clinical history and exam and may be treated with a lot of success with medications that are readily available and cheap. So, you can actually make a huge amount of difference to your patients' lives by practicing old-school neurology. Dr Nevel: That's great, thank you so much for that. I can imagine that scenario does come up where somebody is thought to have a functional neurological disorder but really has a proximal movement disorder. You mentioned that in your article, how it's important to distinguish between these two, how there can be similarities at times. Do you mind giving us a little bit more in terms of how do we differentiate between functional neurologic disorder and paroxysmal movement disorder? Dr Mahajan: So clinical differentiation of functional neurological disorder from paroxysmal movement disorders, of course it's really important as a management is completely different, but it can be quite challenging. There's certainly an overlap. So, there can be an overlap with presentation, with phenomenology. Paroxysmal nature is common to both of them. In addition, FND and PMD's may commonly share triggers, whether they are movement, physical exercise. Other triggers include emotional stimuli, even touch or auditory stimuli. What makes it even more challenging is that FND's may coexist with other neurological disorders, including paroxysmal movement disorders. However, there are certain specific phenom phenotypic differences that have been reported. So specific presentations, for example the paroxysms may look different. Each paroxysm may look different in functional neurological disorders, specific phenotypes like paroxysmal akinesia. So, these are long duration episodes with eyes closed. Certain kinds of paroxysmal hyperkinesia with ataxia and dystonia have been reported. Of course. More commonly we see PNES of paroxysmal nonepileptic spells or seizures that may be considered paroxysmal movement disorders but represent completely different etiology which is FND. Within the world of movement disorders, functional jerks may resemble propiospinal myoclonus which is a completely different entity. Overall, there are certain things that help separate functional movement disorders from paroxysmal movement disorders, such as an acute onset variable and inconsistent phenomenology. They can be suggestibility, distractibility, entrainment, the use of an EMG may show a B-potential (Bereitschaftspotential) preceding the movement in patients with FND. So, all of these cues are really helpful. Dr Nevel: Great, thanks. When you're seeing a patient who's reporting to these paroxysmal uncontrollable movements, what kind of features of their story really tips you off that this might be a proximal movement disorder? Dr Mahajan: Often these patients have been diagnosed with functional neurological disorders and they come to us. But for me, whenever the patient and or the family talk about episodic movements, I think about these. Honestly, we must be aware that there is a possibility that the movements that the patients are reporting that you may not see in clinic. Maybe there are obvious movement disorders. Specifically, there's certain clues that you should always ask for in the history, for example, ask for the age of onset, a description of movements. Patients typically have videos or families have videos. You may not be able to see them in clinic. The regularity of frequency of these movements, how long the attacks are, is there any family history of or not? On the basis of triggers, whether, as I mentioned before, do these follow exercise? Prolonged exercise? Or neither of the above? What is the presentation in between attacks, which I think is a very important clinical clue. Your examination may be limited to videos, but it's important not just to examine the video which represents the patient during an attack, but in between attacks. That is important. And of course, I suspect we'll get to the treatment, but the treatment can follow just this part, the history and physical exam. It may be refined with further testing, including genetic testing. Dr Nevel: Great. On the note of genetic testing, when you do suspect a diagnosis of paroxysmal movement disorder, what are some key points for the provider to be aware of about genetic testing? How do we go about that? I know that there are lots of different options for genetic testing and it gets complicated. What do you suggest? Dr Mahajan: Traditionally, things were a little bit easier, right, because we had a couple of genes that have been associated with the robust movement disorders. So, genetic testing included single gene testing, testing for PRRT2 followed by SLC2A. And if these were negative, you said, well, this is not a genetic ideology for paroxysmal movement disorders. Of course, with time that has changed. There's an increase in known genes and variants. There is increased genetic entropy. So, the same genetic mutation may present with many phenotypes and different genetic mutations may present with the similar phenotype. Single gene testing is not a high yield approach. Overall genetic investigations for paroxysmal movement disorders use next generation sequencing or whole exome sequence panels which allow for sequencing of multiple genes simultaneously. The reported diagnostic yield with let's say next generation sequencing is around 35 to 50 percent. Specific labs at centers have developed their own panels which may improve the yield of course. In children, microarray may be considered, especially the presentation includes epilepsy or intellectual disability because copy number variations may not be detected by a whole exome sequencing or next generation sequencing. Overall, I will tell you that I'm certainly not an expert in genetics, so whenever you're considering genetic testing, if possible, please utilize the expertise of a genetic counsellor. Families want to know, especially as an understanding of the molecular underpinnings and knowledge about associated mutations or variations keeps on expanding. We need to incorporate their expertise. A variant of unknown significance, which is quite a common result with genetic testing, may not be a variant of unknown significance next year may be reclassified as pathogenic. So, this is extremely important. Dr Nevel: Yeah. That's such a good point. Thank you. And you just mentioned that there are some genetic mutations that can lead to multiple different phenotypes. Seemingly similar phenotypes can be associated with various genetic mutations. What's our understanding of that? Do we have an understanding of that? Why there is this seeming disconnect at times between the specific genetic mutation and the phenotype? Dr Mahajan: That is a tough question to answer for all paroxysmal movement disorders because the answer may be specific to a specific mutation. I think a great example is the CACNA1A mutation. It is a common cause of episodic ataxia type 2. Depending on when the patient presents, you can have a whole gamut of clinical presentations. So, if the patient is 1 year old, the patient can present with epileptic encephalopathy. Two to 5 years, it can be benign paroxysmal torticollis of infancy. Five to 10 years, can present with learning difficulties with absence epilepsy and then of course later, greater than 10 years, with episodic ataxia (type) 2 hemiplegic migraine and then a presentation with progressive ataxia and hemiplegic migraines has also been reported. So not just episodic progressive form of ataxia has also been reported. I think overall these disorders are very rare. They are even more infrequently diagnosed than their prevalence. As such, the point that different genetic mutations present with different phenotypes, or the same genetic mutation I may present with different phenotypes could also represent this part. Understanding of the clinical presentation is really incomplete and forever growing. There's a new case report or case series every other month, which makes this a little bit challenging, but that's all the more reason for learning about them and for constant vigilance for patients who show up to our clinic. Dr Nevel: Yeah, absolutely. What is our current understanding of the associated pathophysiology of these conditions and the pathophysiology relating to the genetics? And then how does that relate to the treatment of these conditions? Dr Mahajan: So, a number of different disease mechanisms have been proposed. Traditionally, these were all thought to be ion channelopathies, but a number of different processes have been proposed now. So, depending on the genetic mutation that you talk about. So certain mutations can involve ion channels such as CACMA1A, ATP1A3. It can involve solute carriers, synaptic vesicle fusion, energy metabolism such as ECHS1, synthesis of neurotransmitters such as GCH1. So, there are multiple processes that may be involved. I think overall for the practicing clinician such as me, I think there is a greater need for us to understand the underlying genetics and associated phenotypes and the molecular mechanisms specifically because these can actually influence treatment decisions, right? So, you mentioned that specific genetic testing understanding of the underlying molecular mechanism can influence specific treatments. As an example, a patient presenting with proximal nocturnal dyskinesia with mutation in the ADCY5 gene may respond beautifully to caffeine. Other examples if you have SLC2A1, so gluc-1 (glucose transporter type 1) mutation, a ketogenic diet may work really well. If you have PDHA1 mutation that may respond to thiamine and so on and so forth. There are certain patients where paroxysmal movement disorders are highly disabling and you may consider deep brain stimulation. That's another reason why it may be important to understand genetic mutations because there is literature on response to DBS with certain mutations versus others. Helps like counselling for patients and families, and of course introduces time, effort, and money spent in additional testing. Dr Nevel: Other than genetic testing, what other diagnostic work up do you consider when you're evaluating patients with a suspected paroxysmal movement disorder? Are there specific things in the history or on exam that would prompt you to do certain testing to look for perhaps other things in your differential when you're first evaluating a patient? Dr Mahajan: In this article, I provide a flow chart that helps me assess these patients as well. I think overall the history taking and neurological exam outside of these paroxysms is really important. So, the clinical exam in between these episodic events, for example, for history, specific examples include, well, when do these paroxysms happen? Do they happen or are they precipitated with meals that might indicate that there's something to do with glucose metabolism? Do they follow exercise? So, a specific example is in Moyamoya disease, they can be limb shaking that follows exercise. So, which gives you a clue to what the etiology could be. Of course, family history is important, but again, talking about the exam in between episodes, you know, this is actually a great point because out– we've talked about genetics, we've talked about idiopathic paroxysmal movement disorders, –but a number of these disorders are because of acquired causes. Well, of course it's important because acquired causes such as autoimmune causes, so multiple sclerosis, ADEM, lupus, LGI1, all of these NMDAR, I mentioned Moyamoya disease and metabolic causes. Of course, you can consider FND as under-acquired as well. But all of these causes have very different treatments and they have very different prognosis. So, I think it's extremely important for us to look into the history with a fine comb and then examine these patients in between these episodes and keep our mind open about acquired causes as well. Dr Nevel: When you evaluate these patients, are you routinely ordering vascular imaging and autoimmune kind of serologies and things like that to evaluate for these other acquired causes or it does it really just depend on the clinical presentation of the patient? Dr Mahajan: It mostly depends on the clinical presentation. I mean, if the exam is let's say completely normal, there are no other risk factors in a thirty year old, then you know, with a normal exam, normal history, no other risk factors. I may not order an MRI of the brain. But if the patient is 55 or 60 (years) with vascular risk factors, then you have to be mindful that this could be a TIA. If the patient has let's say in the 30s and in between these episodes too has basically has a sequel of these paroxysms, then you may want to consider autoimmune. I think the understanding of paraneoplastic, even autoimmune disorders, is expanding as well. So, you know the pattern matters. So, if all of this is subacute started a few months ago, then I have a low threshold for ordering testing for autoimmune and paraneoplastic ideology is simply because it makes such a huge difference in terms of how you approach the treatment and the long-term prognosis. Dr Nevel: Yeah, absolutely. What do you find most challenging about the management of patients with paroxysmal movement disorders? And then also what is most rewarding? Dr Mahajan: I think the answer to both those questions is, is the same. The first thing is there's so much advancement in what we know and how we understand these disorders so regularly that it's really hard to keep on track. Even for this article, it took me a few months to write this article, and between the time and I started and when I ended, there were new papers to include new case reports, case series, right? So, these are rare disorders. So most of our understanding for these disorders comes from case reports and case series, and it's in a constant state of advancement. I think that is the most challenging part, but it's also the most interesting part as well. I think the challenging and interesting part is the heterogeneity of presentation as well. These can involve just one part of your body, your entire body can present with paroxysmal events, with multiple different phenomenologies and they might change over time. So overall, it's highly rewarding to diagnose such patients in clinic. As I said before, you can make a sizeable difference with the medication which is usually inexpensive, which is obviously a great point to mention these days in our health system. But with anti-seizure drugs, you can put the right diagnosis, you can make a huge difference. I just wanted to make a point that this is not minimizing in any way the validity or the importance of diagnosing patients with functional neurological disorders correctly. Both of them are as organic. The importance is the treatment is completely different. So, if you're diagnosing somebody with FND and they do have FND and they get cognitive behavioral therapy and they get better, that's fantastic. But if somebody has paroxysmal movement disorders and they undergo cognitive behavioral therapy and they're not doing well, that doesn't help anybody. Dr Nevel: One hundred percent. As providers, obviously we all want to help our patients and having the correct diagnosis, you know, is the first step. What is most interesting to you about paroxysmal movement disorders? Dr Mahajan: So outside of the above, there are some unanswered questions that I find very interesting. Specifically, the overlap with epilepsy is very interesting, including shared genes, the episodic nature, presence of triggers, therapeutic response to anti-seizure drugs. All of this I think deserves further study. In the clinic, you may find that epilepsy and prognosis for movement disorders may occur in the same individual or in a family. Episodic ataxia has been associated with seizures. Traditionally this dichotomy of an ictal focus. If it's cortical then it's epilepsy, if it's subcortical then it's prognosis for movement disorders. This is thought to be overly simplistic. There can be co-occurrence of seizures and paroxysmal movement disorders in the same patient and that has led to this continuum between these two that has been proposed. This is something that needs to be looked into in more detail. Our colleagues in Epilepsy may scoff this, but there's concept of basal ganglia epilepsy manifesting as paroxysmal movement disorders was proposed in the past. And there was this case report that was published out of Italy where there was ictal discharge from the supplementary sensory motor cortex with a concomitant discharge from the ipsilateral coordinate nucleus in a patient with paroxysmal kinesigenic cardioarthidosis. So again, you know, basal ganglia epilepsy, no matter what you call it, the idea is that there is a clear overlap between these two conditions. And I think that is fascinating. Dr Nevel: Really interesting stuff. Well, thank you so much for chatting with me today. Dr Mahajan: Thank you, Kait. And thank you to the Continuum for inviting me to write this article and for this chance to speak about it. I'm excited about how it turned out, and I hope readers enjoy it as well. Dr Nevel: Today again, I've been interviewing doctor Abhi Mahajan about his article on diagnosis and management of paroxysmal movement disorders, which appears in the August 2025 Continuum issue on movement disorders. I encourage all of our listeners to be sure to check out the Continuum Audio episodes from this and other issues. As always, please read the Continuum articles where you can find a lot more information than what we were able to cover in our discussion today. And thank you for our listeners for joining today. And thank you, Abhi, so much for sharing your knowledge with 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.

“As ONS continues to look ahead, its commitment to shaping the future of oncology nursing remains unwavering. ONS is proactively developing the tools, capabilities, and strategies needed to support oncology nurses in a rapidly evolving healthcare landscape. ONS will continue to set the standard, ensuring that oncology nurses are equipped with clinical expertise, collaborative skills, technology proficiency, and mentorship necessary to thrive,” Diane Barber, PhD, APRN, ANP-BC, AOCNP®, FAANP, FAAN, member of the ONS 50th anniversary committee, said regarding the continuously changing roles of oncology nurses. Barber spoke with ONS members Danelle Johnston, MSN, RN, HON-ONN-CG, OCN®, RuthAnn Gordon, MSN, RN, FNP-BC, OCN®, Tamika Turner, DNP, NP-C, AOCNP®, and Bertie Fields, MS, RN, about their experience in nursing roles in navigation, clinical trials, advanced practice, and the pharmaceutical industry and how these roles have evolved and may change in the future. The advertising messages in this episode are paid for by Natera. ONS is solely responsible for the criteria, objectives, content, quality, and scientific integrity of its programs and publications. Music Credit: “Fireflies and Stardust” by Kevin MacLeod Licensed under Creative Commons by Attribution 3.0  Episode Notes  This episode is not eligible for NCPD. ONS Podcast™ episodes: ONS 50th anniversary series Episode 331: DNP and PhD Collaboration Strategies to Help Advance Oncology Care Episode 312: Virtual Nursing in Health Care Episode 304: Nursing Roles in FDA: The Drug Labeling and Package Insert Process Episode 302: Patient Navigation Eliminates Disparities in Cancer Care Episode 284: How AI Is Influencing Cancer Care and Oncology Nursing Episode 119: What Will the Future of Cancer Care Look Like in 2029? ONS Voice articles: Leadership Is the Foundational Competency for Oncology Nursing in 2029 New Technology Tools Help Oncology APRNs Improve Patient Outcomes Oncology Nurses Drive Discovery in Cancer Clinical Research The Oncology Nurse's Role in Interprofessional Collaboration in Clinical Research What the New CMS Reimbursement for Principal Illness Navigation Means for Oncology Nurses ONS books: Manual for Clinical Trials Nursing (third edition) Oncology Nurse Navigation: Delivering Patient-Centered Care Across the Continuum (third edition) ONS competencies: Oncology Clinical Nurse Specialist Competencies Oncology Clinical Research Nurse Competencies Oncology Nurse Generalist Competencies Oncology Nurse Navigator Competencies Oncology Nurse Practitioner Competencies ONS course: Professional Practice for the Advanced Practice Registered Nurse Clinical Journal of Oncology Nursing articles: How Do I Evolve as a Research Nurse Practitioner? Incorporating Nurse Navigation to Improve Cancer Survivorship Care Plan Delivery Oncology Nurse Practitioner Competencies: Defining Best Practices in the Oncology Setting ONS Learning Libraries: Clinical Trials Nurse Navigation Connie Henke Yarbro Oncology Nursing History Center American Cancer Society National Navigation Roundtable To discuss the information in this episode with other oncology nurses, visit the ONS Communities. To find resources for creating an ONS Podcast club in your chapter or nursing community, visit the ONS Podcast Library. To provide feedback or otherwise reach ONS about the podcast, email pubONSVoice@ons.org. Highlights From This Episode Johnston: “In the early years, navigation programs varied widely. We had minimal technology, no standardized training, and often tracked our work on spreadsheets and narrative notes. The broader healthcare team didn't always understand navigation, so educating colleagues in defining our role was essential. Today, navigation is becoming a well-established specialty. It's recognized by the Commission on Cancer, supported by [Centers for Medicare and Medicaid Services] reimbursement codes, and integrated across diverse care settings. It's backed by evidence, standardized training, and emerging technologies that improve both patient care and program sustainability. I'm proud to have witnessed and contributed to the incredible evolution, and I'm excited for what's next in advancing navigation to better support patients and families.” TS 6:20 Gordon: “When I was first introduced to the [clinical trial nurse] role, there weren't published competencies in order to learn the role or any real standardization of the role. And so when you worked in clinical trials, you kind of picked up things from the providers, from the other investigators on how you should operationalize the role. We've seen that evolve. We've seen ONS develop competencies, ONS come out with the clinical trial nursing manual. And our organization has been able to use those tools to standardize the practice of the clinical trial nurse across our institution. So we take those competencies, and they are the foundation of our program. And we've been able to build our program over the last decade, mostly by the use of the tools that ONS has and the ability to share knowledge.” TS 14:22 Fields: “For nurses, many of my colleagues are going on to get master's in things other than nursing. They're getting master's in public health. They're getting master's in business. I have a colleague who is in [information technology], and so we should not limit ourselves. We should expand ourselves. And the more varied degrees that we have, we are more viable candidates for positions. I was never a clinical nurse specialist, even though that was my goal, but I have done above and beyond what I ever anticipated that I would do. And there are so many more new degrees for us to make us viable in this changing environment.” TS 28:30 Turner: “It is vital that the current generation of oncology nurse practitioners take the lead to mentor the next generation. The next generation needs to be educated regarding the importance of oncology nurse practitioners, filling those critical gaps in health care by caring for patients in rural areas and those areas where healthcare resources are scarce. Technology should be utilized to bring oncology care—for example, office visits, imaging, and treatments—closer to those areas where patients live further away or have difficulty accessing transportation and health care. This will provide continuity of care.” TS 32:42

Tics are movements or sounds that are quick, recurrent, and nonrhythmic. They fluctuate over time and can be involuntary or semivoluntary. Although behavioral therapy remains the first-line treatment, modifications to comprehensive behavioral intervention have been developed to make treatment more accessible. In this episode, Casey Albin, MD, speaks with Jessica Frey, MD, author of the article “Tourette Syndrome and Tic Disorders” in the Continuum® August 2025 Movement Disorders 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. Frey is an assistant professor of neurology, Movement Disorders Fellowship Program Director, and Neurology Student Clerkship Director at the Rockefeller Neuroscience Institute in the department of neurology at West Virginia University in Morgantown, West Virginia. Additional Resources Read the article: Tourette Syndrome and Tic Disorders 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 Transcript 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 all, this is Dr Casey Albin. Today I'm interviewing Dr Jessica Frey about her article Tourette Syndrome and Tic Disorders, which appears in the August 2025 Continuum issue on movement disorders. Dr Frey, thank you so much for being here, and welcome to the podcast. I'd love for you to briefly introduce yourself to our audience. Dr Frey: Thank you for having me here today. My name is Jessica Frey, and I am a movement disorder specialist at West Virginia University. I'm also the movement disorder fellowship director, as well as the neurology clerkship student director. Dr Albin: Dr. Frey, I feel like this was one of the things I actually had no exposure to as a resident. For trainees that kind of want to get a better understanding of how these are managed, what kind of counseling you do, what kind of interventions you're using, how can they get a little bit more exposure? Dr Frey: That's a great question, and I actually had a similar experience to you. I did not see that many patients with Tourette syndrome while I was in my residency training. I got a lot more exposure during my fellowship training, and that's when I actually fell in love with that patient population, caring for them, seeing them be successful. I think it depends on the program that you're in. During the pediatric neurology rotation might be your best bet to getting exposure to patients with Tourette syndrome, since a lot of them are going to be diagnosed when they're quite young, and sometimes they'll even continue to follow through young adulthood in the pediatric neurology clinic. However, up to 20% of patients with Tourette syndrome will have persistent tics during adulthood. And so, I think it is important for neurology trainees to understand how to manage them, understand what resources are out there. So, if you have an interest in that, absolutely try to follow either in the pediatric neurology department, or if you have a movement disorder program that has a Tourette clinic or has a movement disorder specialist who has an interest in Tourette syndrome, definitely try to hang out with them. Get to know that patient population, and educate yourself as much as you're able to educate the patients as well. Dr Albin: Yeah, I think that's fantastic advice. You wrote a fantastic article, and it covers a lot of ground. And I think let's start at some of the basics. When I think of Tourette syndrome and tics, I think of Tourette syndrome having tics, but maybe not all patients who have tics have Tourette syndrome. And so, I was wondering, A, if you could confirm that's true; and then could you tell us a little bit about some of the diagnostic criteria for each of these conditions? Dr Frey: Sure. So, a tic is a phenomenological description. So basically, what you're seeing is a description of a motor or phonic tic, which is a particular type of movement disorder. Tourette syndrome is a very specific diagnosis, and the diagnostic criteria for Tourette syndrome at this point in time is that you need to have had at least one phonic tic and two or more motor tics over the course of at least a year before the age of eighteen. Dr Albin: Got it. So, there's certainly more specific and a lot more criteria for having Tourette syndrome. I was struck in reading your article how many myths there are surrounding Tourette syndrome and tic disorders kind of in general. What's known about the pathophysiology of Tourette syndrome, and what are some common misconceptions about patients who have this disorder? Dr Frey: Yeah, so I think that's a really excellent question because for so many years, Tourette syndrome and tic disorders in general were thought to be psychogenic in origin, even dating back to when they were first described. The history of Tourette syndrome is quite interesting in that, when Tourette---who, you know, it's named after---was working with Charcot, a lot of the initial descriptors were of actual case reports of patients who had more psychogenic descriptions, and eventually they became known as tic disorders as well. It wasn't until the discovery of Haldol and using Haldol as a treatment for tic disorders that people started to change their perception and say, okay, maybe there is actually a neurologic basis for Tourette syndrome. So, in terms of the pathophysiology, it's not completely known, but what we do know about it, we think that there is some sort of hyperactivity in the corticostriatal-thalamocortical circuits. And we think that because of this hyperactivity, it leads to the hyperactive movement disorder. We think similar circuitry is involved in conditions like OCD, or obsessive compulsive disorder; as well as ADHD, or attention deficit hyperactivity disorder. And because of that, we actually do tend to see an overlap between all three of these conditions in both individuals and families. Dr Albin: And hearing all of that, does this all come back to, sort of, dopamine and, sort of, behavioral motivation, or is it different than that? Dr Frey: It's probably more complex than just dopamine, but there is the thought that dopamine does play a role. And even one of the hypotheses regarding the pathophysiology is actually that these tics might start as habits, and then when the habits become more common, they actually reshape the dopaminergic pathways. And each time a tic occurs, there's a little bit of a dopaminergic reward. And so over time, that reshapes those hyperactive pathways and changes the actual circuitry of the brain, leading it to be not just a habit but part of their neurologic makeup. Dr Albin: It's fascinating to hear how that actually might play into our neural circuitry and, over time, rewire our brain. Fascinating. I mean, this is just so interesting how movement disorders play into such behavioral regulation and some comorbid conditions like ADHD and OCD. I thought it would be really helpful, maybe, to our listeners to kind of think through a case that I suspect is becoming more common. So, if it's okay with you, I'll present sort of a hypothetical. Dr Frey: Absolutely. Dr Albin: This is a father bringing in his seventeen-year-old daughter. She's coming into the clinic because she's been demonstrating, over the past four to six weeks, some jerking movement in her right arm. And it's happened multiple times a day. And it was a pretty sudden onset. She had not had any movement like this before, and then several weeks ago, started moving the right hand. And then it became even more disruptive: her right leg was involved, she had some scrunching her face. This is all happening at a time where she was dealing with some stress, maybe a little bit of applications around college that she was having a lot of anxiety about. How do you sort of approach this case if this is someone who comes to your office? Dr Frey: Sure. So, I think the first thing that you want to get is a good solid history, trying to understand, what is the origin of these abnormal movements and what led to the abnormal movements. Now, a key thing here is that in Tourette syndrome, and most physiologic tic syndromes, there's a pretty early onset. So, in Tourette syndrome, the expected age of onset is between the ages of five and seven years old. So, to have kind of acute new abnormal movements as a seventeen-year-old would be very unusual for a new-onset diagnosis of Tourette syndrome. However, there's a couple of things from the history that could help you. One would be, were there ever tics in the past? Because sometimes, when you think retrospectively, a lot of these patients might have had a simple eye-blinking tic or a coughing tic when they were a child. And perhaps they did have Tourette syndrome, a very mild case of it. But because the tics were never that pronounced, they never went to see anyone about it and it was never known that they had Tourette syndrome in the first place. If there is no history like that and the movements are completely new, out of the blue, of course you want to rule out anything acute that could be going on that could be causing that. Looking at the phenomenology of the movements can also be very helpful. When you're looking at abnormal tic movements, you would expect most cases of something like Tourette syndrome to occur first in the midline and go in a rostrocoidal distribution. So, you mostly see things happening with eye blinking, throat clearing, sniffling, neck snapping. These are some of the immediate tics that start to happen. We also usually start to see simple tics, as opposed to complex tics, at the beginning. Now, over the course of time, many patients do develop more complex tics that might involve the arms or the extremities, but that would be unusual to see this as a presenting feature of new-onset Tourette syndrome. Dr Albin: Got it. So, I'm hearing that the history really matters and that sometimes, like those, like, first-onset seizures, I imagine as a neurointensivist, we see a lot of patients who've had seizures who think that they're presenting the first time. And then we go back and we say, well, actually they have had some abnormal movements at night. Sounds like it's very similar with these movement disorders where you have to really go back and ask, well, was there some sniffling? Did they go through a phase where they were grunting frequently? Because I can imagine that many children make those behaviors, and that it may not have registered as something that was cause for concern. Dr Frey: Absolutely. Dr Albin: And then the other thing I heard from you was that the phenomenology really matters and that there is a typical presentation, starting from sort of the face and working the way down. And that can be really helpful. But in this case, the family is quite clear. No, no, no. She's never had movements like this before. This is- nothing like this. We promise you, did not go through a phase where she was coughing or blinking, or, this is all totally new. And the phenomenology, they say, no, no, she did not start with blinking. It definitely started in the arm and then progressed in its complex movements. So, knowing that about her, how does that sort of shape how you move forward with the diagnosis? Dr Frey: Yeah. So, really good question. And this is something that I think really peaked during the Covid-19 pandemic. We saw an influx of patients, especially teenage girls or young adult girls, who basically would come in and have these new, acute-onset, abnormal movements. We weren't sure what to call them initially. There was some discussion of calling them “explosive tic disorder” and things like that. A lot of these actually looked very similar to psychogenic nonepileptic seizures, where they would come into the emergency department and have many abnormal movements that were so severe, that they were having a “tic attack” and couldn't stop the abnormal movements from occurring. And we saw so many of these cases during the Covid-19 pandemic that it eventually became known as a distinctive diagnostic criteria with the name of “functional ticlike behavior”, or FTLB. When we think about functional ticlike behavior, we think that these tics are driven more by anxiety and stress. A lot of times, the backstory of these patients, they were in a very stressful situation, and that's when the abnormal movement started. So, a very similar kind of backstory to patients that might develop psychogenic nonepileptic seizures. These tics were popularized, for lack of a better term, via social media during the Covid-19 pandemic. One article is out there that even has called these functional ticlike behaviors as “a pandemic within a pandemic”, because there was such a strong showing of ticlike behavior in the clinics during the Covid-19 pandemic. Although social media was thought to play a big role in these functional ticlike behaviors, we think that there's probably a little bit more complexity and nuance to why these functional ticlike behaviors develop. There is probably a little bit of a genetic predisposition. There's probably some other psychosocial factors at play. And when we see cases like this, the best thing that you can do is educate your patients about the differences between functional ticlike behaviors and tics that we see associated with conditions like Tourette syndrome. And then the best types of treatments that we have seen thus far are treating any underlying stressors, if any of those exist, as well as cognitive behavioral therapy has been shown to be somewhat helpful. As the Covid-19 pandemic has wound down, we have actually seen a lot less cases in our clinic. And one reason we think is less stressors, less uncertainty for the future, which we think was a driving precipitant of some of these cases. But it also is not as popularized in the media as well. There were a lot of TikTok users in particular, which lent itself to the name “TikTok tic”. These videos are not as viewed or not as popular as they were during the Covid-19 pandemic. One reason being that because we are not all relegated to our homes, constantly looking to online sources of information---just in general, we have kind of not been on the Internet as much as we were during the Covid-19 pandemic---as a society as a whole. Dr Albin: This is really fascinating how the environmental milieu, for lack of a better word, like, really influenced how patients were experiencing, sort of, functional neurologic disorders. In your article you describe really these three baskets of primary tic---which can then be a part of Tourette syndrome---,functional ticlike behaviors---which really were a unique manifestation of stress and anxiety specifically during the Covid-19 pandemic---, and then tics as a manifestation of some either different underlying etiology or medication side effect. So, when do you get concerned about that secondary etiology? Dr Frey: So secondary tics can occur in a variety of instances. I think some of the more common examples would be in genetic disorders. So, Huntington's disease is a really good example. I think we all associate chorea with Huntington's disease. That's probably the most commonly associated phenomenology that we see with Huntington's disease. But we can see a variety of movement disorders in Huntington's, and one of them is tics. So, when we see tics in association with other types of movement disorders, we should be thinking about a possible genetic etiology. If we see tics in association with other neurologic symptoms, such as seizures or cognitive changes, we should be thinking that this is something besides a primary tic disorder. You also mentioned medication use, and it's really important to think about tardive tics. I know we often think about tardive dyskinesia, and the first kind of phenomenology that jumps into our brain is usually chorea because it's those abnormal lip movements, finger movements, toe movements that we see after a patient has been on, for example, an antipsychotic or an antiemetic that has antidopaminergic properties. However, we can see a variety of abnormal movement disorders that occur secondary to antidopaminergic medications, especially after abrupt withdrawal of these antidopaminergic medications. And tics are one of them. There have been cases reported where people that have tardive tics will still report that they have a premonitory urge, as well as a sense of relief after their tics. So, it actually can seem very similar to Tourette syndrome and the tics that people with Tourette syndrome experience on a regular basis. The key here is that the treatment might differ because if it's due to an antidopaminergic medication or abrupt withdrawal of that antidopaminergic medication, you might need to treat it a little bit differently than you would otherwise. Dr Albin: I love that you bring in, it's not just looking at their specific movement disorder that they may be coming to clinic with, that tic disorder, but are there other movement disorders? Has there been a change in their medication history? Have they had cognitive changes? So really emphasizing the importance of that complete and comprehensive neurologic history, neurologic physical exam, to really get the complete picture so that it's not honing in on, oh, this is a primary tic. That's all there is to it, because it could be so much more. I know we're getting close to sort of the end of our time together, but I really wanted to switch to end on talking about treatment. And your article does such a beautiful job of talking about behavioral interventions and really exciting new medical interventions. But I would like to, if you don't mind, have you focus on, what behavioral counseling and what education do you provide for patients and their families? Because I imagine that the neurologist plays a really important role in educating the patient and their family about these disorders. Dr Frey: Absolutely. When we think about treatment, one of the most important things you can do for patients with Tourette syndrome or other primary tic disorders is educate them. This remains true whether it's a primary tic disorder that we see in Tourette syndrome or the functional ticlike behavior that we've discussed here. A lot of times, because there is such a stigma against people with tic disorders and Tourette syndrome, when they hear that they have Tourette syndrome or they are diagnosed with that, sometimes that can be an upsetting diagnosis. And sometimes you have to take time explaining what exactly that means and debunking a lot of the myths that go along with the stigmas associated with Tourette syndrome. I think a lot of times people are under the false assumption that people with Tourette syndrome cannot lead normal lives and cannot hold down jobs and cannot be productive members of society. None of that is true. Most of my patients have great lives, good quality of life, and are able to go about their day-to-day life without any major issues. And one of the reasons for that is we do have a lot of great treatment options available. Another important stigma to break down is that people with tic disorders are doing this for attention or doing this because they are trying to get something from someone else. That is absolutely false. We do think that the tics themselves are semivolitional because people with Tourette syndrome have some degree of control over their tics. They can suppress them for a period of time. But a lot of people with tic disorders and Tourette syndrome will describe their tics as if you're trying to hold onto a sneeze. And you can imagine how uncomfortable it is to hold in a sneeze. We're all able to do it for a period of time, but it's much easier to just allow that sneeze to occur. And a lot of times that's what they are experiencing, too. So, although there is some degree of control, it's not complete control, and they're certainly not doing these tics on purpose or for attention. So that's another important myth to debunk when you're counseling patients and their families. I think the dynamic between young patients that are presenting with their parents or guardians, sometimes that dynamic is a little bit challenging because another faulty assumption is that parents feel they are responsible for having this happen to their child. There used to be a really strong sense that parents were responsible for the tics that occurred in their children, and that is also absolutely not true. Parenting has nothing to do with having the tics or not. We know that this is a neurodevelopmental disorder. The brain is indeed wired differently and it's important to counsel that with the parents, too, so that they understand what tools they need to be successful for their children as well. Dr Albin: I love that. So, it's a lot of partnership with patients and their families. I really like that this is just a wire different, and I hope over time that working together we as neurologists can help break down some of that stigmatization for these patients. This has been an absolutely phenomenal discussion. I have so enjoyed learning from your article. For the listeners out there, there are some really phenomenal tables that go into sort of how to approach this from the office perspective, how to approach it from the treatment perspective. So, thank you again, Dr Jessica Frey, for your article on Tourette syndrome and tic disorders, which appears in the August 2025 Continuum issue on movement disorders. Be sure to check out Continuum Audio episodes from this and other issues, and thank you so much to our listeners for joining us today. Dr Frey: Thank you 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.

Dans ce 12e épisode de cette saison 2, nous écoutons Amani, originaire de République démocratique du Congo, qui livre un récit puissant et épique. Orpheline, elle devient en situation de prostitution à 18 ans pour nourrir son petit frère et gagner de l'argent. Après 10 ans, elle doit fuir le pays enceinte, avec sa première fille, car elle est menacée. Commence un parcours migratoire qui la conduit en Turquie et en Grèce, Obligée d'avoir recours à la prostitution, victime de conjoints proxénètes et "clients" prostitueurs, elle subit de multiples violences avant de parvenir, avec un courage immense à s'enfuir avec ses filles? Arrivée en France, elle se retrouve dans une ville de région, où en attente de soutien social, elle envisage à nouveau la prostitution, jusqu'à rencontrer le Mouvement du Nid. Elle a tout au long de son parcours fait preuve d'un courage immense, elle exprime des sentiments complexes vis-à-vis de la prostitution, et prend conscience de la résistance farouche qu'elle a toujours développée face aux violences masculines. Tout entière tournée vers le bien être de ses filles, aujourd'hui elle veut aussi parler pour elle même et pour dire aux autres que si c'était à refaire, elle ne le referait pas. Et qu'elle ne le souhaite "même pas à son pire ennemi", comme vous pourrez l'entendre dans le prochain épisode, qui sera diffusé à partir du 30 septembre.Si vous souhaitez soutenir financièrement La Vie en Rouge, contactez-nous à l'adresse lavieenrougelepodcast@gmail.comLa Vie en Rouge, un podcast conçu et réalisé par des femmes ayant connu la prostitutionHébergé par Ausha. Visitez ausha.co/politique-de-confidentialite pour plus d'informations.

What happens when Italian folk traditions cross the Atlantic? This video explores how Italian witchcraft, especially the healing practice of Segnature, has been reimagined, reinvented, and often misrepresented in the United States. From Leland's Aradia to Wicca-inspired “Stregheria,” we'll look at how Italian-American communities blended folklore, Catholic devotion, and Pagan spirituality to create new forms of practice. But are these the same as the vernacular traditions in Italy, or something entirely different?This video is a recording of the paper I presented at the World Congress of the International Association for the History of Religions, held at Jagiellonian University in Kraków, Poland.Join me as we unpack the myths, the reinventions, and the cultural translations behind Italian witchcraft in America.CONNECT & SUPPORT

Ataxia is a neurologic symptom that refers to incoordination of voluntary movement, typically causing gait dysfunction and imbalance. Genetic testing and counseling can be used to identify the type of ataxia and to assess the risk for unaffected family members. In this episode, Katie Grouse, MD, FAAN, speaks with Theresa A. Zesiewicz, MD, FAAN, author of the article “Ataxia” in the Continuum® August 2025 Movement Disorders 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. Zesiewicz is a professor of neurology and director at the University of South Florida Ataxia Research Center, and the medical director at the University of South Florida Movement Disorders Neuromodulation Center at the University of South Florida and at the James A. Haley Veteran's Hospital in Tampa, Florida. Additional Resources Read the article: Ataxia 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 Theresa Zesiewicz about her article on ataxia, which appears in the August 2025 Continuum issue on movement disorders. Welcome to the podcast, and please introduce yourself to our audience.  Dr Zesiewicz: Well, thank you, Dr Grouse. I'm Dr Theresa Zesiewicz, otherwise known as Dr Z, and I'm happy to be here. Dr Grouse: I have to say, I really enjoyed reading your article. It was a really great refresher for myself as a general neurologist on the topic of ataxia and a really great reminder on a great framework to approach diagnosis and management. But I wanted to start off by asking what you feel is the key message that you hope our listeners will take away from reading your article. Dr Zesiewicz: Yes, so, thanks. I think one of the key messages is that there has been an explosion and renaissance of genetic testing in the past 10 years that has really revolutionized the field of ataxia and has made diagnosis easier for us, more manageable, and hopefully will lead to treatments in the future. So, I think that's a major step forward for our field in terms of genetic techniques over the last 10 years, and even over the last 30 years. There's just been so many diseases that have been identified genetically. So, I think that's a really important take-home message. The other take-home message is that the first drug to treat Friedreich's ataxia, called omaveloxolone, came about about two years ago. This was also a really landmark discovery. As you know, a lot of these ataxias are very difficult to treat. Dr Grouse: Now pivoting back to thinking about the approach to diagnosis of ataxia, how does the timeline of the onset of ataxia symptoms inform your approach? Dr Zesiewicz: The timeline is important because ataxia can be acute, subacute or chronic in nature. And the timeline is important because, if it's acute, it may mean that the ataxia took place over seconds to hours. This may mean a toxic problem or a hypoxic problem. Whereas a chronic ataxia can occur over many years, and that can inform more of a neurodegenerative or more of a genetic etiology. So, taking a very detailed history on the patient is very important. Sometimes I ask them, what is the last time you remember that you walked normal? And that can be a wedding, that can be a graduation. Just some timeline, some point, that the patient actually walked correctly before they remember having to hold onto a railing or taking extra steps to make sure that they didn't fall down, that they didn't have imbalance. That sometimes that's a good way to ask the patient when is the last time they had a problem. And they can help you to try to figure out how long these symptoms have been going on. Dr Grouse: I really appreciate that advice. I will say that I agree, it can sometimes be really hard to get patients to really think back to when they really started to notice something was different. So, I like the idea of referencing back to a big event that may be more memorable to them. Now, given that framework of, you know, thinking through the timeline, could you walk us through your approach to the evaluation of a patient who presents to your clinic with that balance difficulties once you've established that? Dr Zesiewicz: Sure. So, the first thing is to determine whether the patient truly has ataxia. So, do they have imbalance? Do they have a wide base gait? That's very important because patients come in frequently to your clinic and they'll have balance problems, but they can have knee issues or hip issues, neuropathy, something like that. And sometimes what we say to the residents and the students is, usually ataxia or cerebellar symptoms go together with other problems, like ocular problems are really common in cerebellar syndromes. Or dysmetria, pass pointing, speech disorder like dysarthria. So, not only do you need to look at the gait, but you should look at the other symptoms surrounding the gait to see if you think that the patient actually has a cerebellar syndrome. Or do they have something like a vestibular ataxia which would have more vertigo? Or do they have a sensory ataxia, which would occur if a person closes his eyes or has more ataxia when he or she is in the dark? So, you have to think about what you're looking at is the cerebellar syndrome. And then once we look to see if the patient truly has a cerebellar syndrome, then we look at the age, we look at---as you said before, the timeline. Is this acute, subacute, or chronic? And usually I think of ataxia as falling into three categories. It's either acquired, it's either hereditary, or it's neurodegenerative. It can be hereditary. And if it's not hereditary, is it acquired, or is it something like a multiple system atrophy or a parkinsonism or something like that? So, we try to put that together and start to narrow down on the diagnosis, thinking about those parameters. Dr Grouse: That's really a helpful way to think through it. And it is true, it can get very complex when patients come in with balance difficulties. There's so many things you need to think about, but that is a great way to think about it. Of course, we know that most people who come in to the Movements Disorders clinic are getting MRI scans of their brains. But I'm curious, in which cases of patients with cerebellar ataxia do you find the MRI to be particularly helpful in the diagnosis? Dr Zesiewicz: So, an MRI can be very important. Not always, but- so, something like multiple system atrophy type C where you may see a hot cross bun sign or a pontine hyperintensity on the T2-weighted image, that would be helpful. But of course, that doesn't make the diagnosis. It's something that may help you with the diagnosis. In FXTAS, which is fragile X tremor/ataxia syndrome, the patient may have the middle cerebellar peduncle sign or the symmetric hyperintensity in the middle cerebellar peduncles, which is often visible but not always. Something like Wernicke's, where you see an abnormality of the mammillary bodies. Wilson's disease, which is quite rare, T2-weighted image may show hyperintensities in the putamen in something like Wilson's disease. Those are the main MRI abnormalities, I think, with ataxia. And then we look at the cerebellum itself. I mean, that seems self-evident, but if you look at a sagittal section of the MRI and you see just a really significant atrophy of the cerebellum, that's going to help you determine whether you really have a cerebellar syndrome. Dr Grouse: That's really encouraging to hear a good message for all of us who sometimes feel like maybe we're missing something. It's good to know that information can always come up down the line to make things more clear. Your article does a great review of spinal cerebellar ataxia, but I found it interesting learning about the more recently described syndrome of SCA 27B. Would you mind telling us more about that and other really common forms of SCA that's good to keep in mind? Dr Zesiewicz: Sure. So, there are now 49 types of spinal cerebellar ataxia that have been identified. The most common are the polyglutamine repeat diseases: so, spinocerebellar ataxia type 3 or type 2, type 6, are probably the most common. One of the most recent spinocerebellar ataxias to be genetically identified and clinically identified is spinocerebellar ataxia 27B. This is caused by a GAA expansion repeat in the first intron of the fibroblast growth factor on chromosome 13. And the symptoms do include ataxia, eye problems, downbeat nystagmus, other nystagmus, vertical, and diplopia. It appears to be a more common form of adult-onset ataxia, and probably more common than was originally thought. It may account for a substantial number of ataxias, like, a substantial percentage of ataxias that we didn't know about. So, this was really a amazing discovery on SCA 27B. Dr Grouse: Now a lot of us I think feel a little anxious when we think about genetic testing for ataxia simply because there's so many forms, things are changing quickly. Do you have a rule of thumb or a kind of a framework that we can think of as we approach how we should be thinking about getting genetic testing for the subset of patients? Dr Zesiewicz: Sure. And I think that this is where age comes into play a lot. So, if you have a child who's 10, 11, or 12 who's having balance problems in the schoolyard, does not have a history of ataxia in the family, the teachers are telling you that the child is not running correctly, they're having problems with physical education, that is someone who you would think about testing for Friedreich's ataxia. A preteen or a child, that would be one thing that would be important to test. When you talk to your patient, it's important to really take a detailed family history. Not just mom or dad, but ethnicity, grandparents, etc. And sometimes, once in a while, you come up with a known spinal cerebellar ataxia. Then you can just test for that. So, if a person is from Portugal or has Portugal background and they have ataxia and the parents had ataxia, you would think of spinal cerebellar ataxia type 3. Or if they're Brazilian, or if the person is from a certain area of Cuba and mom and dad had ataxia and that person has ataxia, you would think of spinal cerebellar ataxia type 2. Or if a person has ataxia and their parent had blindness or visual problems, you may be more likely to think of spinal cerebellar ataxia type 7, for example. If they have that---either they have a known genetic cause in in the family, first degree family, or they come from an area of the world in which we can pinpoint what type we think it is---you can go ahead and get those tests. If not, you can take an ataxia comprehensive panel. Many times now, if you take the panel and the panel is negative, it will reflex to the whole exome gene sequencing, where we're finding really unusual and more rare types of ataxia, which are very interesting. Spinal cerebellar ataxia type 32, spinal cerebellar ataxia type 36, I had a spinal cerebellar ataxia type 15. So, I think you should start with the age, then the family history, then where the person is from. And then, if none of those work out, you can get a comprehensive panel, and then go on to whole exome gene sequencing. Dr Grouse: That's really, really useful. Thank you so much for breaking that down in a really simple way that a lot of us can take with us. Pivoting a little bit now back towards different types of acquired ataxias, what are some typical lab tests that you recommend for that type of workup? Dr Zesiewicz: Again, if there's no genetic history and the person does not appear to have a neurodegenerative disease, we do test for acquired ataxias. Acquired ataxias can be complex. Many times, they are in the autoimmune family. So, what we start with are just basic labs like a CBC or a CMP, but then we tried to look at some of the other abnormalities that could cause ataxia. So, celiac disease, stiff person syndrome. So, you would look at anti-glutamic acid decarboxylase antibodies, Hashimoto's---so, antithyroglobulin antibodies or antithyroperoxidase antibodies would be helpful. You know, in a case of where the patients may have an underlying neoplasm, maybe even a paraneoplastic workup, such as an anti-Hu, anti-Yo, anti-Ri. A person has breast cancer, for example, you may want to take a paraneoplastic panel. I've been getting more of the anti-autoimmune encephalitis panels in some cases, that were- that are very interesting. And then, you know, things that sometimes we forget now like the syphilis test, thyroid-stimulating test, take a B12 and folate, for example. That would be important. Those are some of the labs. We just have on our electronic chart a group of acquired labs for ataxia. If we can't find any other reason, we just go ahead and try to get those. Dr Grouse: Now, I'm curious what you think is the most challenging aspect of diagnosing a patient with cerebellar ataxia? Dr Zesiewicz: So, for those of us who see many of these patients a day, some of the hardest patients are the ones that---regardless of the workup that we do, we've narrowed it down, it's not hereditary. You know, they've been through the whole exome gene sequencing and we've done the acquired ataxia workup. It doesn't appear to be that. And then we've looked for parkinsonism and neurodegenerative diseases, and it doesn't appear to be that either; like, the alpha-synuclein will be negative. Those are the toughest patients, where we think we've done everything and we still don't have the answer. So, I've had patients in whom I've taken care of family members years and years ago, they had a presumed diagnosis, and later on I've seen their children or other family members. And with the advent of the genetic tests that we have, like whole exome gene sequencing, we have now been able to give the patient and the family a definitive diagnosis that they didn't have 25 years ago. So, I would say don't give up hope. Retesting is important, and as science continues and we get more information and we make more landmark discoveries in genetics, you may be better able to diagnose the patient. Dr Grouse: I was wondering if you had any recommendations regarding either some tips and tricks, some pearls of wisdom you can impart to us regarding the work of ataxia, or conversely, any big pitfalls that you can help us avoid? I would love to hear about it. Dr Zesiewicz: Yeah, there's no easy way to treat or diagnose ataxia patients. I've always felt that the more patients you see- and sounds easy, but the more patients you see, the better you're going to become at it, and eventually things are going to fall into place. You'll begin to see similarities in patients, etc. I think it's important not only to make sure that a person has ataxia, but again, look at the other signs and symptoms that may point to ataxia that you'll see in a cerebellar syndrome. I think it's important to do a full neuroexam. If a person has spasticity, that may point you more towards a certain type of ataxia than if a person has no reflexes, for example, that we see in Friedreich's ataxia. Some of the ocular findings are very interesting as well. It's important to know if a person has a tremor. I've seen several Wilson's disease cases in my life with ataxia. They're very important. I think a full neuroexam and also a very detailed history would be very helpful. Dr Grouse: Tell us about some promising developments in the diagnosis and management of ataxia that we should be on the lookout for. Dr Zesiewicz: The first drug for Friedreich's ataxia was FDA-approved two years ago, which was an NRF2 activator, which was extremely exciting and promising. There are also several medications that are now in front of the FDA that may also be very promising and have gone through long clinical trials. There's a medication that's related to riluzole, which is a medication used for amyotrophic lateral sclerosis, that has been through about seven years of testing. That is before the FDA as well for spinal cerebellar ataxia. Friedreich's ataxia has now completed the first cardiac gene therapy program with AAV vectors, which- we're waiting for full results, but that's a cardiac test. But I would assume that in the future, neurological gene therapy is not far behind if we've already done cardiac gene therapy and Friedreich's ataxia. So, you know, some of these AAV vector-based genetic therapies may be very helpful, as well as ASO, antisense oligonucleotides, for example. And I think in the future, other things to think about are the CRISPR/Cas9 technology for potential treatment of ataxia. It is a very exciting time, and some major promising therapies have been realized in the past 2 to 3 years. Dr Grouse: Well, that's really exciting, and we'll all look forward to seeing these becoming more clinically applicable in the future. So, thank you so much for coming to talk with us today. Dr Zesiewicz: Thank you. Dr Grouse: Again, today I've been interviewing Dr Theresa Zesiewicz about her article on ataxia, which appears in the August 2025 Continuum issue on movement disorders. 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.

Skip The Queue is back for Season 7 and we're announcing some big changes! Get ready for new hosts, a fresh new look, weekly content and find out where you can catch us live at events to be part of the action.Skip the Queue is brought to you by Rubber Cheese, a digital agency that builds remarkable systems and websites for attractions that helps them increase their visitor numbers. Your host is Paul Marden  and Andy Povey.If you like what you hear, you can subscribe on iTunes, Spotify, and all the usual channels by searching Skip the Queue or visit our website SkiptheQueue.fm. Show references: Paul Marden The CEO of Rubber Cheese, Paul pairs two decades of digital expertise with a love of creative problem solving, making him the go-to guy for turning tricky tech into seamless guest journeys, all delivered with his trademark energy and wit.https://www.linkedin.com/in/pmarden/ Andy Povey The Co-CEO of Crowd Convert, Andy brings sharp insights, deep industry knowledge and notorious anecdotes from decades in attractions.https://www.linkedin.com/in/andypovey/  Transcriptions:  Paul Marden: Welcome to Skip the Queue, the podcast about the world's best visitor attractions and the people that work in them. I'm Paul Marden. Along with my co-hosts, Andy Povey and Sinead Kimberley, I spend my days working with ambitious attractions like theme parks, museums, galleries, and science centres to help them to attract more guests. In today's episode, Andy and I talk about what's coming up for Skip the Queue as we enter Season 7.Paul Marden: Seven seasons, hey? Good lord. How very exciting. We've had our summer holidays. We've had our little break, but there's no rest for the wicked, is there?Andy Povey: Absolutely not. You say it's a busman's holiday, really, isn't it?  Working in our industry.Paul Marden: I think it is, isn't it? Life has changed quite a lot for us recently, hasn't it? In the last few months, with the advent of Crowd Convert and Merac coming back to life again, we've been out on the road going everywhere, haven't we?Andy Povey: Absolutely everywhere. And I promise I'm not going to bitch about electric cars and charging.Andy Povey: That's the only thing I've found that annoys me more than a poor online ticketing experience.Paul Marden: Yeah, absolutely. So we have both been visiting lots of clients. It's been very exciting. But we've also both had our summer holidays. Which attraction is memorable for you from your recent holiday?Andy Povey: Do you know, there's so many. We took our girls to the longest named tourist attraction in the world, I think. Warner Brothers Studio Tour London, the making of Harry Potter. On their 11th birthday. Oh, how was that? We had a beautiful experience. They have this really smart trick there where if they note your birthday, they give you a badge that says, 'It's my birthday.'Andy Povey: It's modelled on the birthday cake that Hagrid gave Harry. So it's all completely in keeping and in theme. So my daughters were walking around with these and every member of staff we saw that saw the badge wished them happy birthday. The first member of staff that did it absolutely blew my girls' minds. They hadn't associated it with the badge that they were wearing and they thought that they were the most special people on the face of the earth.Andy Povey: Absolutely superb. And the experience itself is wonderful. So that was probably the most memorable. I did something else very recently that was a little bit unusual. So I'm a man in my 50s. I was a teenager, probably not even a teenager, a kid when Grease came out. And all my mates and all my friends raved about it, and I didn't go and see it. And I've been very proud of the fact that I've never seen Grease.Andy Povey: Until last weekend. When we went to the Secret Cinema showing of Grease in Battersea Park, wow, wow, what an experience. Live actors, live scenes with the film running in the background, the fairground sitting outside the auditorium, where the final set, if you've watched Grease ever, where they're in the fairground, went out there.Andy Povey: Such a fantastic experience. Really does make me wonder why we don't have more of our larger parks doing that kind of stuff in partnership with Secret Cinema. It would make you stay for the evening and really extend your day. Absolutely superb experience. So, if you get the opportunity to go and see it, please do.Paul Marden: How very cool.Andy Povey: Tell them Andy sent you, which will mean absolutely nothing.  How about you?Paul Marden: We recently went to Scotland. We spent a day, which was really not enough, in Edinburgh. And actually, as you're talking about the Harry Potter experience, we did a little Harry Potter thing because there is a graveyard, Greyfriars Bobby's graveyard.Paul Marden: It was the inspiration for many of the names in Harry Potter. And this graveyard was, I mean, it was chock full of every nationality of tourist you could possibly imagine, plus the three of us wandering around all trying to find Harry Potter themed gravestones. Yeah, so we found Tom Riddle's tombstone. We saw a McGonagall. Yeah, it was just, that was quite magical. But the thing that sticks in my head is we also visited the Real Mary King's Close. And when you walk along the Royal Mile, falling off the side of the Royal Mile are all of these tenement closes that three of them were capped over a couple of hundred years ago and completely forgotten about. Continuum attractions have turned them into an attraction that you can wander around. You get a guided tour of this time capsule of what life was like in a tenement block. In Edinburgh, it was rated last year as the best tourist attraction in Britain, according to TripAdvisor.Paul Marden: And it really, really was magical. It was such a fun visit. We were guided around by a tour guide in costume and in character the whole way around. And at the end of it, she introduced herself as coming from Philadelphia.Paul Marden: She was really really great guide, and I just loved it. I've seen them in the Rubber Cheese Survey for the last four years, and thought, 'What a funny name for an attraction? I wonder what that is?' And so, when I saw it, I had to go. I loved every minute of it, and it was brilliant.Andy Povey: I agree, it's a fantastic place. Did you see J. K. Rowling's handprints just around the corner?Paul Marden: No.Andy Povey: In the courtyard next to the entrance?Paul Marden: No, I didn't.Andy Povey: See, I think they were trying to do something like the Hollywood Walk of Fame, where there are famous people's handprints. I should have told you before. Is there something to go back for?Paul Marden: Oh, we'll definitely be going back. There was so much there in Edinburgh that we didn't get to see. You just couldn't do it in a day.Paul Marden: But so much fun. So much fun.Paul Marden: So we are into season seven. And just like the last few seasons, we've got lots of ideas, brimming with ideas, few changes. And we thought we would tease them for you here in this short non-episode, just to tell you about some of the things that are coming up. And yeah, shall we?Paul Marden: We'll talk about the first thing that you came up with, which was the move to weekly content.Andy Povey:  You're blaming me for this?Paul Marden: Absolutely. Absolutely.Andy Povey: I mean, the objective was to double the listenership of the podcast. And so you did that by doubling my work. And it seemed like it would be really, really easy to do that if we doubled the episodes.Andy Povey: So, yeah, we're going weekly. I'm sure we're going to have plenty to fill it. Because you look at all of the interesting stories we come across, the people that we talk to, the things that we want to talk about, and we end up editing and cutting things. So I'm convinced that we're going to have loads of really exciting things to talk about. We're also going to introduce a couple of different themes. So do you want to talk about the Millennium-funded projects?Paul Marden: Yes, so this is carrying on the theme that I started back at the back end of Season 6. When I spoke to another Edinburgh attraction, Dynamic Earth. They were a good example of a Millennium project that was obviously kicked off 25 years ago. And we had a lovely conversation about what has been the challenges, what has been the opportunities for them in the last 25 years, and what does the future look like? I'm off to the Association of Science and Discovery Centres conference next week. That episode will be out in a few weeks' time. And we're going to be talking a lot about science centres. and how they can thrive over the next 25 years. But we'll be talking to some other Millennium projects as well in the season ahead. So Charles Bishop from the National Space Centre, if you're listening, give me a call.Andy Povey: I'm going to try and hound you to appear on the podcast.Paul Marden: We've also, this is very self-indulgent, but we are going to be going through a little bit of a rebrand. The Skip the Queue brand has stayed the same for the six seasons. And our friends at Plaster Creative Communications have been working really hard. They're the only reason why we could possibly go weekly with our content because Emily and Sami are helping us to ramp up our content and working with us closely. But they've also helped us with our rebrand, which is also going to be an audio rebrand. So there's going to be some new audio tickling your ears coming up as well, which is very exciting.Andy Povey: It's not just the rebrand though, is it? Let's talk about the other things that we're going to be doing with Skip the Queue.Paul Marden: Yeah. Should we talk playbooks?Andy Povey: Absolutely. Tell me what it means.Paul Marden: So I, for a long time, thought that there was something that Skip the Queue could do because, you know. Yes, this is our baby, but it is a lot of hard work from across the industry that goes towards making the podcast the success that it is. And we're going to move that successful collaboration into a series of playbooks where we're bringing together people from across the industry to help guide attractions into... the state of the art and what's possible within the sector across a number of different subjects. And we're starting that with e-commerce. So we're currently collaborating with our friends at Stephen Spencer Associates and at Navigate. And we're producing the first in that playbook series all about what... What does it take to be able to build an amazing e-commerce experience for an attraction? How do you curate the products?Paul Marden: How do you come up with the ideas? How do you put the technology together? And then how do you get anybody to come and visit and buy from you? So that's very exciting.Andy Povey: So that's more of your gift shop. Retail e-commerce.Paul Marden: Absolutely. Absolutely. And there'll be room as well within the series for us to talk about other things as well. So we are completely open to ideas. So listeners, if you've got ideas of a playbook that you'd like to see, it could be about digital sustainability. It could be about ticketing. It could be about any aspect of operating an attraction. Come and tell us and come up with ideas of who we could work with and we'll put something together for you. So I think that's really exciting, and that will be coming out in a few weeks' time.Andy Povey: Very interesting. Look forward to that.Paul Marden: We were excited in Season 6 to break out of the four walls of our little dungeon offices, working via video conferencing and going out and about, weren't we? We absolutely loved visiting the NFAN Conference, ASDC.Paul Marden: We worked from the floor of so many different events, didn't we? And tried lots of formats. And we definitely, definitely want to do more of that. And there's an exciting turn because weekly isn't enough, is it?Andy Povey:  If you're going to do it, go big. Go big or go home.Paul Marden: We have been invited to the IAAPA Europe Conference Expo in Barcelona, no less. And we are going to be coming into your ears daily, not weekly, daily.Paul Marden: So we have got an amazing lineup of people that we are going to be talking to from the conference floor. But there's also so much time to fill. We don't know who we're going to talk to. We're going to be hitting the floor and just grabbing people, just like we did at NFAN. You'll be out, Andy, just hooking people. And we'll be talking to them. And we plan to do those interviews during the day, and Wenalyn and Steve, our long-suffering editorial and production team, will be working furiously through the night to publish the following morning.Andy Povey: Fantastic. So do we need to talk about our launch episode for Season 7?Paul Marden: Yes.Andy Povey: As this is just the trailer.Paul Marden: Yes. So in 29 minutes, I will be recording my launch episode. So I'm meeting with Massimiliano Freddi, who is the IAAPA board chairman. We're going to find out more about Massimiliano. Not only is he the first Italian chairman of IAAPA, which has been in existence for over 100 years, I believe. We are also going to find out about what he does in his day job and the attraction that he runs over in Italy. So that's a very exciting first episode. So we will be launching that episode 17th of September, and then we will be live from Barcelona starting on the 23rd and going out daily from there on for the rest of that week. I mean, what more could we want? Andy Povey: It's justification for the family for me going to Barcelona after just having returned from Menorca so daddy does a holiday work.Paul Marden: We've at least got to walk down Las Rambla and chat about the conference we can't just be within the expo location surely. A little vino tinto on.Andy Povey: I'm sure we will be at Tribudabo at what, in my experience, this is the third time I've been to IAAPA in Barcelona. But the opening night party in Tribudabo has always been one of the most fantastic events I've ever been to. The view over the city at night with rides and superb food, drink and entertainment going off behind you is just  out of this world.Paul Marden: But it's work just for anyone that's listening outside the door right now.Andy Povey: Very hard work for very important people.Paul Marden: Yes so we are still planning out the rest of season seven, obviously going weekly, lots of opportunities for us to talk to lots of people. If you've got ideas for themes or people that we could interview, we are absolutely all ears. So hit us up on LinkedIn, hello@SkiptheQueue.fm, or go to the website, skipthequeue.fm. Yeah, and you'll find all of our contact details and we'd love to hear from you with ideas of what we could do for the rest of this season. What would you find interesting? Apart from that, we're going to sign off. I've got an interview to go to in 25 minutes. We will be back with you on the 17th of September with our first episode and from IAAPA on the 23rd of September for the rest of that week.Andy Povey: You're going to be on IAAPA. Come and find us. Come and have a chat.Paul Marden: Looking forward to it.Paul Marden: Skip the Queue is brought to you by Rubber Cheese, the digital agency that creates amazing websites for ambitious visitor attractions.  The 2025 Visitor Attraction Website Survey is now LIVE! Dive into groundbreaking benchmarks for the industryGain a better understanding of how to achieve the highest conversion ratesExplore the "why" behind visitor attraction site performanceLearn the impact of website optimisation and visitor engagement on conversion ratesUncover key steps to enhance user experience for greater conversionsTake the Rubber Cheese Visitor Attraction Website Survey Report

Hi Listeners. I'd love to hear from you. Send an email to Janet@jesteinkamp. It is not possible to respond to your Fan Mail posts directly.Jealousy is a natural emotion, and still, it can complicate an already painful estrangement.In this thoughtful episode, Dr. Janet helps parents and adult children understand the role jealousy plays in their strained or fractured relationships.Parents, you're not alone in this. Estranged adult children also tell us they experience jealousy. But the experience for parents and adult children is different. What does jealousy have to do with estrangement? And pointedly, how can jealousy hinder our ability to establish healthy and respectful communication?Listen in to hear compassionate insights and consider practical examples. This episode offers tools to recognize, manage, and move through jealousy in healthy ways.Past episodes referenced in this conversation:The Continuum of EstrangementFriendly Advocate or Flying Monkey (Short)What is the Difference: Gaslighting vs ReframingSupport the showFor more information, please go to https://www.WhenOurAdultChildrenWalkAway.com to find resources, strategies and tips to prepare to repair! The continuum of estrangement discussed today can be found at https://www.togetherestranged.org/levels-of-estrangement. The stories, examples, reflections, and perspectives shared in this podcast are based on my professional work as an estrangement coach and my personal estrangement journey. Any examples, characters, or stories referenced are either drawn from my own lived experience or represent a composite of multiple real-life situations shared with me over time. The intention of this podcast is not to accuse, label, or defame any individual but to provide insight, validation, and support for those navigating the complexities of family estrangement. All opinions expressed are my own and are shared with you, the listener, from a place of healing and learning.

Between me and we: identity through cultural psychology. Episode 96 explores how cultural psychology shapes identity between me and we. Justine Gonzalez shares insights from Benedict & Kitayama with practical tools for self-discovery.

In this episode, Vera and Renae explore bulimorexia—a term used for people who oscillate between restriction and binge/purge behaviors—and how this mixed pattern might help explain stubborn relapse rates across eating disorders and food addiction. Dr. Norton shares her clinical lens on risks (medical and psychological), why some traditional programs may miss the mark, and what a holistic, skills-based, harm-reduction treatment can look like (family involvement, gentle re-feeding, DBT/EMDR, food quality, and relapse prevention). Note: Some views expressed are the guest's opinions and experience. This episode is educational and not medical advice. Please consult your care team. What we cover Defining “bulimorexia”: alternating restriction with binge/purge; how it differs from anorexia nervosa and bulimia nervosa; why it's easier to hide than classic anorexia. Continuum vs. categories: where binge eating disorder fits; overlap with food addiction. Why relapse is common: risks of aggressive refeeding; short-stay residential models; lack of individualized care; missing family systems support. Medical risks (high-level): cardiac arrhythmias and hypotension, esophageal tears/GERD, laxative misuse and constipation, electrolyte disturbance, kidney strain, dental/enamel erosion, parotid swelling, menstrual disruption and fertility concerns. Psychological load: anxiety/OCD traits, depression, social avoidance; the “addiction to restricting” and the short-term ‘high' of hunger. Treatment principles Dr. Norton uses: Gentle, stepwise re-feeding (small, frequent meals; stabilize blood sugar; avoid triggering extremes). Skills over meal plans (shop, prep, and eat whole foods; mindful interoception). DBT for arousal regulation, plus EMDR and trauma work as indicated. Family-based involvement (Maudsley-style boundaries and support). Movement re-entry: slow, safe progression; curbing compulsive exercise. Relapse prevention: strong parent/caregiver alignment, food routines, anxiety skills, and ongoing monitoring. Contested terrain: ultra-processed food, additives, and differing regulations by region; the guest's emphasis on “clean/organic” sourcing. Intermittent fasting cautions: for restrict-prone folks, it can mask restriction; prefer regular, structured eating. What recovery can look like: decreased self-hatred, restored relationships, school/work re-engagement, and more flexible functioning. Resources from the guest: forthcoming book Below the Radar: What They're Not Telling You About Your Food; wellness tools she finds helpful. Suggested chapter markers 00:00 Welcome & guest intro 02:20 What is “bulimorexia”? How it differs from AN/BN 10:55 Why relapse stays high; critique of standard programs 18:30 Medical complications: heart, GI, dental, endocrine 28:15 Psychological patterns: anxiety, OCD traits, depression 34:40 Treatment pillars: re-feeding, DBT/EMDR, family work 45:05 Food quality and UPFs: guest's perspective & debate 53:10 Intermittent fasting cautions; safe movement 58:20 Relapse prevention & outcomes 1:04:10 Advice to clinicians, families, and society 1:08:00 What's next for Dr. Norton & closing Key takeaways (listener-friendly) Mixed patterns (restricting and binge/purge) may be under-recognized and can carry high medical risk. Slow, individualized re-feeding plus emotion-regulation skills (DBT) and family involvement improve safety and engagement. If you're prone to restriction, consistent meals beat fasting. Recovery gains include less self-hatred, more connection, and functional life goals—progress over perfection. Sensitive content note This episode discusses eating-disorder behaviors (restriction, purging, laxatives, insulin manipulation) and medical complications. Please use discretion and support. Links & mentions Dr. Renae Norton — Norton Wellness Institute / Mind, Weight & Wellness Pro Book (forthcoming): Below the Radar: What They're Not Telling You About Your Food Maudsley/Family-Based Treatment (FBT) overview DBT skills resources (distress tolerance, emotion regulation, interpersonal effectiveness) If you need help now: NEDA (US), BEAT (UK), local crisis lines, or your clinician. For clinicians Screen for mixed presentations (restrict + purge), including non-vomit purging (laxatives, insulin manipulation). Prioritize medical monitoring (vitals, electrolytes) during re-feeding; avoid one-size-fits-all calorie jumps. Integrate DBT skills, caregiver coaching, and regular eating structure; track arousal and urge patterns.   The content of our show is educational only. It does not supplement or supersede your healthcareprovider's professional relationship and direction. Always seek the advice of your physician or other qualified mental health providers with any questions you may have regarding a medical condition, substance use disorder, or mental health concern.

Chorea describes involuntary movements that are random, abrupt, and unpredictable, flowing from one body part to another. The most common cause of genetic chorea in adults is Huntington disease, which requires comprehensive, multidisciplinary care as well as support for care partners, who may themselves be diagnosed with the disease. In this episode, Aaron Berkowitz, MD, PhD FAAN speaks with Kathryn P. L. Moore, MD, MSc, author of the article “Huntington Disease and Chorea” in the Continuum® August 2025 Movement Disorders 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. Moore is an assistant professor and director of the Parkinson's Disease and Movement Disorders Fellowship in the department of neurology at Duke University in Durham, North Carolina. Additional Resources Read the article: Huntington Disease and Chorea 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: @AaronLBerkowitz Guest: @KatiePMooreMD 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 with Continuum Audio, and today I'm interviewing Dr Kathryn Moore about her article on diagnosis and management of Huntington disease and chorea, which appears in the August 2025 Continuum issue on movement disorders. Welcome to the podcast, Dr Moore. Could you please introduce yourself to our audience? Dr Moore: Yeah, thank you so much. I'm so excited to be here. I'm Dr Moore. I'm an assistant professor of neurology at Duke University, where I work as a movement disorder specialist. I run our fellowship there and help with our residency program as well. So, I'm excited to speak with our listeners about chorea today. Dr Berkowitz: Fantastic. And we're excited to talk to you about chorea. So, as a general neurologist myself, I only see chorea pretty rarely compared to other movement disorders like tremor, myoclonus, maybe the occasional tic disorder. And like anything I don't see very often, I always have to look up the differential diagnosis and how to evaluate a patient with chorea. So, I was so glad to read your article. And next time I see a patient with chorea, I know I'll be referring to your article as a great reference to have a framework for how to approach it. I hope our readers will look at all these helpful tables on differential diagnosis based on distribution of chorea in the body, potential etiologies, time course of onset and evolution, associated drug-induced causes, what tests to send. So, I highly recommend our listeners read the article. Keep those tables handy for when a patient comes in with chorea. I'm excited to pick your brain about some of these topics today. First, how do you go about distinguishing chorea from other hyperkinetic movement disorders when you see a patient that you think might have chorea? Dr Moore: One of the wonderful things about being a movement disorder specialist is we spend a lot of time looking at movements and training our brain to make these distinctions. The things that I would be looking out for chorea is involuntary, uncontrolled movements that appear to be brief and flowing from one part of the body to another. So, if you can watch a patient and predict what movements they're going to do, this probably isn't chorea. And it should be flowing from one part of the body to another. So, not staying just in one part of the body or having sustained movements. It can be difficult to distinguish between a tic or dystonia or myoclonus. Those things tend to be more predictable and repetitive than the chorea, which tends to be really random and can look like dancing. Dr Berkowitz: That's very helpful. So, once you've decided the patient has chorea, what's your framework for thinking about the differential diagnosis of the cause of the patient's chorea? Dr Moore: Well, that could be really challenging. The differential for chorea is very broad, and so the two things that I tend to use are age of the patient and acuity of onset. And so, if you're thinking about acute onset of chorea, you're really looking at a structural lesion like a stroke or a systemic issue like infection, hyperglycemia, etc. Where a gradually progressive chorea tends to be genetic in nature. When you're thinking about the difference between a child and an adult, the most common cause of chorea in a child is Sydenham's chorea. And actually, the most common cause of chorea that I tend to see is Parkinson's disease medication. So, if anybody's seen dyskinesia in Parkinson's disease, you've seen chorea. But it's those two things that I'm using, the age of the patient and the acuity. Somewhere in the middle, though---so, if you have subacute onset of chorea---it's important to remember to think about autoimmune conditions or paraneoplastic conditions because these are treatable. Dr Berkowitz: That's very helpful. So, like in any chief concern in neurology, we're using the context like the age and then the time course. And then a number of other helpful points in your article about the distribution of chorea in the body. Any comments you'd like to make about- we have this very helpful table that I thought was very interesting. So, you really get deep into the nuances of chorea and the movement disorder specialist expert level. Are there any aspects of parts of the body affected by chorea or distribution of chorea across the body that help you hone your differential diagnosis? Dr Moore: Certainly. I think where the chorea is located in the body can be helpful, but not as helpful as other conditions where you're localizing a lesion or that sort of thing. Because you can have a systemic cause of chorea that causes a hemichorea; that you can have hyperglycemia causing a hemichorea, or even Sydenham's chorea being a hemichorea. But things that we think about, if the forehead is involved, I would think about Huntington's disease, although this is not pathognomonic. And if it's involving the face or the mouth, you can think about neuroacanthocytosis or, more commonly, tardive dyskinesia. Hemichorea would make me think about some of those systemic issues like hyperglycemia, Sydenham's chorea, those sorts of things, but I would rely more on the historical context and the acuity of presentation than the distribution itself. Dr Berkowitz: Got it. That's very helpful. So those can be helpful features, but not sort of specific for any particular condition. Dr Moore: Exactly. Dr Berkowitz: Yeah, I often see forehead chorea mentioned as sort of specific to Huntington's disease. Since I don't see much Huntington's disease myself, what does forehead chorea look like? What is the forehead doing? How do you recognize that there is chorea of the forehead? It's just sort of hard for me to imagine what it would look like. Dr Moore: It's really tricky. I think seeing the eyebrows go up and down or the brows furrow in an unpredictable way is really what we're looking for. And that can be hard if you're having a conversation. My forehead is certainly animated as we're talking about one of my favorite topics here. One of the tricks that I use with the fellows is to observe the forehead from the side, and there you can see the undulation of the forehead muscles. And that can be helpful as you're looking for these things. I think where it's most helpful to use the forehead is if you're trying to determine if someone with a psychiatric history has tardive dyskinesia or Huntington's disease, because there can be quite a lot of overlap there. And unfortunately, patients can have both conditions. And so, using the forehead movement can be helpful to maybe direct further testing for Huntington's disease. Dr Berkowitz: Oh, wow, that's a very helpful pearl. So, if you see, sort of, diffuse chorea throughout the body and the forehead is involved, to my understanding it may be less specific. But in the context of wondering, is the neuropsychiatric condition and movement disorder related by an underlying cause in the case of seeing orofacial dyskinesias, is the relationship a drug having caused a tardive dyskinesia or is the whole underlying process Huntington's, the absence of forehead might push you a little more towards tardive dyskinesia, presuming there is an appropriate implicated drug and the presence of forehead chorea would really clue you in more to Huntington's. Did I understand that pearl? Dr Moore: That's exactly right, and I'm glad you brought up the point about making sure, if you're considering tardive dyskinesia, that there has been an appropriate drug exposure. Because without that you can't make that diagnosis. Dr Berkowitz: That's a very helpful and interesting pearl, looking at the forehead from the side. That is a movement disorders pearl for sure. Sort of not just looking at the forehead from one angle and trying to figure out what it's doing, but going to look at the patient in profile and trying to sort it out. I love that. Okay. So, based on the differential diagnosis you would have crafted based on whether this is sort of acute, subacute, chronic, the age of the patient, whether it's unilateral, bilateral, which parts of the body. How do you go about the initial evaluation in terms of laboratory testing, imaging, etc.? Dr Moore: Well, certainly in an acute-onset patient, you're going to get a number of labs---and that's listed out for you in the paper---and consider imaging as well, looking for an infarct. One thing our learners will know is that sort of the typical answer to what's the infarct causing hemichorea would be the subthalamic nucleus. But really, those infarcts can be almost anywhere. There are case reports for infarcts in a wide variety of places in the brain leading to hemichorea. So, I think some general blood work and an MRI of the brain is a good place to start. For someone who has a more chronic course of the development of chorea, there are certain labs that I would get---and an MRI, because if you get an MRI and there's heavy metal deposition or other disease, structurally, that indicates a certain condition, that can help you pretty considerably. But otherwise, I'm looking for inflammatory markers, heavy metals, HIV, some general other things that are outlined, to help make sure that I'm not missing something that's treatable before I go down the route of genetic testing. And we may talk about this in a little bit, but if you start out with genetic testing and then you sort of have to back up and do more systemic testing, that can be very disjointed when it comes to good patient care. Dr Berkowitz: That's very helpful. So yeah, if it's acute, obviously this is the most straightforward scenario, acute and unilateral. We're imagining something lesional, as you said, either a stroke or---not sort of sudden, but fast, but not sudden---you might think of another structural lesion. Toxoplasmosis, right, has an affinity for the basal ganglia if you were seeing this in a patient who is immunocompromised. But in a case that, probably as you alluded to, sort of what we would see most commonly in practice, those still relatively rare, sort of subacute to chronic symmetric chorea. There's a long list of tests that are recommended. In your article and in other texts, I've read lupus testing, anti-phospholipid antibodies… but the list is long. I'll refer readers to your article. Out of curiosity as a specialist, how often do you see any of these labs come back revealing any underlying diagnosis in a patient who's otherwise healthy and just has developed chorea and comes to you with that chief concern? I feel like I've sent that mega-workup a few times; I'm obviously a general neurologist, but not nearly as many times as you have been. It's- I can't remember a time where something has come up, maybe an ANA one to forty or something like this that we don't think is relevant. But in your practice, how often do you end up finding a reversible cause in the laboratory testing versus ending up starting to go down the genetic testing route, which we'll talk about in a moment? Dr Moore: It's not common, but it is important that we capture these things. Because for a lot of those laboratory tests, there are treatments that are available, or other health implications if those come back positive. So, the case I think of is a polycythemia vera patient who had diffused subacute onset chorea and was able to be treated, was temporarily managed with medication for her chorea, and as her PV improved, she was able to come off those medications. As I was alluding to before---and I'm sure we'll talk about genetic testing---if you test for HD and it's negative, do you go down the route of additional expensive genetic testing, or do you then circle back and go, oops, I missed this treatable condition? As we talk about genetic testing as well, getting HD testing is a pretty involved process. And so, we want to make sure we are checking all those boxes before we move forward. So, it's not common, but we do catch some treatable conditions, and that's really important not to miss. Dr Berkowitz: That's very interesting. So, you diagnosed that polycythemia vera by blood smear, is that how you make the diagnosis? Dr Moore: Yes. Dr Berkowitz: And is that a once-in-a-career-so-far type of thing, or does that happen time to time? Dr Moore: For me, that's a once-so-far, but I don't doubt that I'll see it again. Dr Berkowitz: Great. And how about lupus and some of these other things we look for in the absence of other systemic features? Have you picked up any of these or heard of colleagues picking up something on laboratory testing? They said, oh, this patient came in for a referral for genetic testing, negative Huntington's disease. And good news, we found polycythemia vera; good news, we found undiagnosed lupus and we reversed it. I'm just curious, epidemiologically, seeing these long lists and not having the subspecialty practice that you do, how often you find a reversible cause like we do for neuropathy all the time, right? Oh, it's diabetes, it's B12---maybe not reversible, but preventing progression---or reversible dementia work up. You get so excited when you find low B12 and you replete the patient's B12, and they get better when they had been concerned they were developing an irreversible condition. How often does one in your subspecialty find a reversible cause on that initial mega-lab screen? Dr Moore: I think it's really uncommon, and maybe the folks that do are caught by someone else that never make it to Huntington's clinic, but I don't tend to see those cases. There are, of course, case reports and well-described in the literature about lupus and movement disorders and things of that nature, but that doesn't come to our clinic on a regular basis for sure. Dr Berkowitz: Got it. That's helpful to hear. Well, we've alluded to genetic testing a number of times now, so let's go ahead and talk about it. A lot of your article focuses on Huntington disease, and I was thinking about---in the course of our medical training in medical school, and then neurology residency, for those of us who don't become movement disorder experts like yourself---we learn a lot about Huntington disease. That's sort of the disease that causes chorea, until we later learned there are a whole number of diseases, not just the reversible causes we've been talking about, but a number of genetic diseases which you expertly reviewing your article. So, what are some of the red flags that suggest to you that a patient with chronically progressive chorea---and whom you're concerned for Huntington's or another genetic cause---what are some things you notice about the history, about the exam, the symptoms, the signs, the syndrome, that suggest to you that, actually, this one looks like it might not turn out to be HD. I think this patient might have something else. And as you have alluded to, how do you approach this? Do you send HD testing, wait for it to come back, and then go forward? Are there genetic panels for certain genetic causes of chorea? Do you skip just a whole exome sequencing, or will you miss some of the trinucleotide repeat conditions? How do you approach this in practice? Dr Moore: I'll try to tackle all that. One thing I will say is that a lot of patients with chorea, regardless of the cause, can look very similar to one another. So, if you're looking at chronic onset chorea, perhaps with some neuropsychiatric features, I'm going to most often think about HD because that's the most common cause. Certainly, as we mentioned before, if there's a lot of tongue protrusion, I would think about the acanthocytic conditions, neurocanthocytosis and McCloud syndrome. But generally in those conditions, we're looking at HD as the most likely cause. Certainly, if there is epilepsy or some other syndromic types of things going on, I may think more broadly. But it's important to know that while HD, as you mentioned, is the cause of chorea, many of our patients will have parkinsonism, tics, dystonia, a whole host of other movement phenomenologies. So, that wouldn't dissuade me from thinking about HD. When we think about the kind of patients that you're describing, upwards of 95% of those people will have Huntington's disease. And the process for genetic testing is fairly involved. The Huntington's Disease Society of America has organized a set of recommendations for providers to go about the process of genetic testing in a safe and supportive way for patients and their families. And so that's referred to in the article because it really is important and was devised by patients and families that are affected by this disease. And so, when we're thinking about genetic testing for HD, if I reveal that you have HD, this potentially affects your children and your parents and your siblings. You can have a lot of implications for the lives and health and finances of your family members. We also know that there is high suicidality in patients with HD, in patients who are at risk for HD; and there's even a higher risk of suicidality in patients who are at risk but test negative for HD. So, we do recommend a supportive environment for these patients and their families. And so, for presymptomatic patients or patients who are at risk and don't have chorea, this involves making sure we have, sort of, our ducks in a row, as it were, when we think about life insurance, and, do you have somebody supportive to be with you through this journey of genetic testing, no matter what the results are? So, oftentimes I'll say to folks, you know, there's this 20-page policy that I encourage you to look at, but there are Huntington's Disease Centers of Excellence across the country that are happy to help you with that process, to make sure that the patients are well supported. This is an individual genetic test because, as you mentioned, it is a CAG repeat disorder. And unfortunately, there is no chorea panel. So, if an HD test comes back negative, what we'll do then is think about what's called the HD phenocopies. As I mentioned before, some of these patients who look like they have HD will have a negative HD test. And so, what do you do then? Well, there's a handful of phenocopies---so, other genetic mutations that cause a very similar presentation. And so, we try to be smart, since there's not a panel, we try to be smart about how we choose which test to do next. So, for instance, there's a condition called DRPLA that is present in an African-American family here in my area, in North Carolina, as well as in Japan. And so, if someone comes from those backgrounds, we may decide that that's the next test that we're going to do. If they are white European descent, we may consider a different genetic test; or if they're sub-Saharan African, we may choose a different one from that. However, even if you do a really thorough job, all those blood tests, all those genetic tests, you will occasionally get patients that you can't find a diagnosis for. And so, it's important to know even when you do a good job, you may still not find the answer. And so, I think trying to do things with this complex of the presentation in a systematic way for yourself so you're not missing something. So, going back to our answer about, how do I look at lupus and polycythemia vera and all of that, to think about it in a systematic way. That when you get to the end and you say, well, I don't have an answer, you know you've tried. Dr Berkowitz: That's very helpful to hear your approach to these challenging scenarios, and also how to approach the potential challenging diagnosis for patients and their families getting this diagnosis, particularly in the presymptomatic phase. And your article touches on this with a lot of nuance and thoughtfulness. So, I encourage our listeners to have a read of that section as well. So, last here, just briefly in our final moments, you discuss in your article the various symptomatic treatments for chorea. We won't have time to go into all the details of all the many treatments you discussed, but just briefly, how do you decide which medication to start in an individual patient with chorea for symptomatic management? What are some of the considerations related to the underlying condition, potential side effect profiles of the particular medications, or any other considerations just broadly, generally, as you think about choosing one of the many medications that can be used to treat chorea? Dr Moore: Certainly. So, there is a group of FDA-approved medications, VMAT2 inhibitors, that we can choose from, or the off-label use of neuroleptics. And so, there's a lot of things that go into that. Some of that is insurance and cost and that sort of thing, and that can play a role. Others are side effects. So, for the VMAT2 inhibitors, they all do have a black box warning from the FDA about suicidality. And so, if a patient does struggle with mental health, has a history of suicidality, psychiatric admissions for that sort of thing, then I would be more cautious about using that medication. All patients are counseled about that, as are their families, to help us give them good support. So, the neuroleptics do not tend to have that side effect and can help with mood as well as the chorea and can be helpful in that way. And some of them, of course, will have beneficial side effects. So, olanzapine may help with appetite, which can be important in this disease. So, the big considerations would be the black box warning and suicidality, as well as, are we trying to just treat chorea or are we treating chorea and neuropsychiatric issues? Dr Berkowitz: Fantastic. Thank you for that overview. And again, for our listeners, there's a lot more detail about all of these medications, how they work, how they're used in different patient populations, their side effects, etc, to be reviewed in your excellent article. Again, today, I've been interviewing Dr Kathryn Moore about her article on diagnosis and management of Huntington's disease in chorea, which appears in the August 2025 Continuum issue on movement disorders. Be sure to check out Continuum Audio episodes from this and other issues. And thank you so much to our listeners for joining today. And thank you again, Dr Moore. Dr Moore: 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.

Patients with opioid use disorder (OUD) present to the hospital setting for a variety of reasons, so emergency and inpatient pharmacists increasingly need to have a working knowledge of OUD, its treatment modalities, and other factors that affect the management of these patients. This podcast will discuss aspects of care from presentation to discharge, dispel common misconceptions about the management of OUD and acute pain, and promote a standardized approach to care of an often-marginalized population of patients. The information presented during the podcast reflects solely the opinions of the presenter. The information and materials are not, and are not intended as, a comprehensive source of drug information on this topic. The contents of the podcast have not been reviewed by ASHP, and should neither be interpreted as the official policies of ASHP, nor an endorsement of any product(s), nor should they be considered as a substitute for the professional judgment of the pharmacist or physician.

This episode of Simply Feedback features an insightful conversation with Cathleen Swody, PhD, an executive coach and organizational psychologist. As the co-author of The Leadership Continuum, Cathleen shares her sharp insights from two decades of shaping leaders and teams that thrive. From a pivotal personal experience receiving feedback to practical strategies for managers, Cathleen discusses how to shift from reactive to intentional leadership. She introduces the core idea behind her book's framework, explaining why flexing your leadership style is essential in today's fast-paced environment. She also provides guidance on how to avoid common pitfalls, such as the temptation to go on autopilot, and how to use feedback to identify when your current approach isn't working.If you're a leader aiming to be more intentional, foster better team engagement, and create a culture where feedback drives success, this episode is filled with actionable advice and valuable perspectives.

Episode SummaryIn this episode, Ali welcomes Jo Cobbett - movement facilitator, artist, and poet - for a rich conversation about the transformative power of embodied movement. Jo shares her experiences navigating personal and community challenges, including the aftermath of wildfires, and how dance and somatic practices offer healing and connection, to self and community.Together, they explore the importance of presence, curiosity, and intention in reclaiming body intelligence. Other topics explored are inhibition, learning from the outside rather than the inside, and finding answers through movement. Jo discusses her approach to creating inclusive, supportive spaces where people of all backgrounds can rediscover themselves through movement. The episode offers inspiration for embracing change, building community, and finding body brilliance in every stage of life.FOR MORE ALI MEZEY:ALI - WebsiteALI - LinkTreeFOR MORE JO COBBETT:https://www.movinground.com/https://www.facebook.com/jobcobbettBIO:Jo Cobbett is a devotee and lover of wonder - crafting windows into profound self-encounters and discovering beauty throughout life's journey. Her primary portals are embodied movement and visual art, inviting play, curiosity, and existential dialogue with the world. Jo is directly engaged in life through nurturing family and creating spaces for self-exploration, expressed via her visual art, streamed poetry, and embodied movement offerings. Developing alongside her earlier partnership with Michael Mullen Skelton, Jo has been leading classes and workshops for over 30 years in Los Angeles and around the globe.She trained in bodywork at Esalen Institute, studied 5Rhythms with Gabrielle Roth, Soul Motion with Vinn Arjuna Martí, and Open Floor with Kathy Altman, Lori Saltzman, and Andrea Juhan, among others. Her practice has been further deepened through improvisation and creative play with Paula Shaw, Camille Maurine, and Ruth Zaporah.A primary influence in her life has been her training and collaboration with Susan Harper in Continuum Montage. Her ongoing inspiration also comes through Laura Sirkin‑Brown, and a lifelong conversation with nature — the whispers of wind, the flow of water, and the subtle intelligence of embodied movement.Jo honors countless teachers encountered along the way and remains continuously inspired — including by Ali Mezey, whose presence and insights have enriched her path.OTHER RESOURCES, LINKS AND INSPIRATIONS: Michael Molin-Skelton — Conscious Dance/Soul Motion“A few things that I hold sacred; the love of my life Anneli, the miracle of that love, Jaylan, resilience, friends that cherish and challenge me, integrity, dancing alone, dancing with you, transparency, love.”Esalen Institute -  A historic retreat center in Big Sur, California, focused on human potential and somatic practices.Five Rhythms® with Gabrielle Roth – A dynamic movement practice founded by Gabrielle Roth exploring flow, staccato, chaos, lyrical, and stillness.Soul Motion® with Vinn Arjuna Martí  –  A conscious dance practice rooted in presence, relational awareness, and creative expression.Open Floor with Kathy Altman, Lori Saltzman, and Andrea Juhan - A movement meditation practice designed for personal healing and collective connection.Improvisation with Paula Shaw, Camille Maurine, and Ruth Zaporah - Explorations in expressive arts, performance, and authentic movement.Susan Harper & Continuum Montage - Susan Harper is a Continuum teacher who developed Continuum Montage, blending movement, breath, and sound to deepen somatic awareness.Yakov & Susannah Darling Khan - Founders of Movement Medicine, a conscious dance practice integrating shamanic, therapeutic, and artistic paths.Emilie Conrad, Founder of Continuum MovementAndrea JuhanPaula ShawCamille Maurine Laura Sirkin-Brown  Anna Halprin - Pioneer in postmodern dance and healing movement practices; creator of the Life/Art Process.Baba Olatunji - Nigerian drummer and educator who popularized African drumming in the West; known for *Drums of Passion*.Rupert Sheldrake - Biologist and author known for his theories on morphic resonance and collective memory fields.Dancing in the Streets: A History of Collective Joy by Barbara Ehrenreich - A cultural and historical study of how communal dance and celebration have shaped human history.Ecstatic Dance - A global movement community offering conscious, freeform dance events with no talking, alcohol, or shoes.Let There Be Light by Jacques Lusseyran - Memoir of a blind French resistance fighter exploring inner vision and resilience.[From time to time, a word or phrase goes wonky. Please forgive my wandering wifi.]

Welcome to Part 2 of my catch-up with Annie Schuessler Zam. If you haven't already, I recommend starting with Part 1: A Continuum of Connection: Parent-Child Relationships, Caregiving, and Self-Healing. I consider Annie as a case study in remaining open to possibility. She embodies a fearlessness that we all possess but often shy away from activating. Courageousness is scary, after all.  GUEST BIO Annie Schuessler Zam (she/they) is a therapist turned healer and the host of the Rebel Therapist™ podcast. She helps people who are estranged from a parent or caregiver who want to heal trauma and live their most beautiful lives. *** Join the Group Practice (R)evolution! GPR is a new platform and podcast series offering insights from owners, employees, and experts, and resources to support this wildly ambitious vision for the future. For a limited time, podcast listeners can get a full year of membership for only $19.99 by using the discount code PODCAST.  Visit: https://tinyurl.com/GPRPodcast and click on “have a coupon” and enter PODCAST to enjoy all the perks of Group Practice (R)evolution for a year!  Get Support! Earn CEs! Care in Chaos: https://tinyurl.com/CareInChaosRec Bridging Heart and Practice: https://tinyurl.com/TheSarahsOnlineSupe  SUPPORT THE SHOW Conversations With a Wounded Healer Merch Join our Patreon for gifts & perks Shop our Bookshop.org store and support local booksellers Share a rating & review on Apple Podcasts *** Let's be friends! You can find me in the following places… Website Facebook @headheartbiztherapy Instagram @headheartbiztherapy

Progressive supranuclear palsy and corticobasal syndrome are closely related neurodegenerative disorders that present with progressive parkinsonism and multiple other features that overlap clinically and neuropathologically. Early recognition is critical to provide appropriate treatment and supportive care. In this episode, Teshamae Monteith, MD, FAAN speaks with Nikolaus R. McFarland, MD, PhD, FAAN, author of the article “Progressive Supranuclear Palsy and Corticobasal Syndrome” in the Continuum® August 2025 Movement Disorders 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. McFarland is an associate professor of neurology at the University of Florida College of Medicine at the Norman Fixel Institute for Neurological Diseases in Gainesville, Florida. Additional Resources  Read the article: Progressive Supranuclear Palsy and Corticobasal Syndrome 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: Hi, this is Dr Teshamae Monteith. Today I'm interviewing Dr Nikolaus McFarland about his article on progressive supranuclear palsy and cortical basilar syndrome, which appears in the August 2025 Continuum issue on movement disorders. Welcome, how are you? Dr Farland: I'm great. Thank you for inviting me to do this. This is a great opportunity. I had fun putting this article together, and it's part of my passion. Dr Monteith: Yes, I know that. You sit on the board with me in the Florida Society of Neurology and I've seen your lectures. You're very passionate about this. And so why don't you first start off with introducing yourself, and then tell us just a little bit about what got you interested in this field. Dr Farland: I'm Dr Nicholas McFarlane. I'm an associate professor at the University of Florida, and I work at the Norman Fixel Institute for Neurological Diseases. I am a director of a number of different centers. So, I actually direct the cure PSP Center of Care and the MSA Center of Excellence at the University of Florida; I also direct the Huntington's clinic there as well. But for many years my focus has been on atypical parkinsonisms. And, you know, I've treated these patients for years, and one of my focuses is actually these patients who suffer from progressive supranuclear palsy and corticobasal syndrome. So that's kind of what this review is all about. Dr Monteith: You probably were born excited, but I want to know what got you interested in this in particular? Dr Farland: So, what got me interested in this in particular was really the disease and the challenges that's involved in it. So, Parkinson's disease is pretty common, and we see a lot of that in our clinic. Yet many times, roughly about 10 to 15% of my patients present with these atypical disorders. And they're quite fascinating. They present in different ways. They're fairly uncommon. They're complex disorders that progress fairly rapidly, and they have multiple different features. They're sort of exciting to see clinically as a neurologist. I think they're really interesting from an academic standpoint, but also in the standpoint of really trying to bring together sort of a team. We have built a multidisciplinary team here at the University of Florida to take care of these patients. They require a number of folks on that team to take care of them. And so, what's exciting, really, is the challenge of treating these patients. There are very limited numbers of therapies that are available, and the current therapies that we have often really aren't great and over time they fail. And so, part of the challenge is actually doing research. And so, there's actually a lot of new research that's been going on in this field. Recently, there's been some revisions to the clinical criteria to help diagnose these disorders. So, that's really what's exciting. The field is really moving forward fairly rapidly with a number of new diagnostics, therapeutics coming out. And hopefully we can make a real difference for these patients. And so that's what really got me into this field, the challenge of trying to treat these patients, help them, advocate for them and make them better. Dr Monteith: And so, tell me what the essential points of this article. Dr Farland: So, the essential points, really, of this article is: number one, you know, just to recognize the new clinical criteria for both PSP and corticobasal syndrome, the diagnosis for these disorders or the phenotypic spectrum has really expanded over the years. So, we now recognize many different phenotypes of these disorders, and the diagnosis has gotten fairly complicated. And so, one of the goals of this article was to review those new diagnostic criteria and the different phenotypic ways these diseases present. I wanted to discuss, also, some of the neuropathology and clinicopathological overlap that's occurred in these diseases as well as some of the new diagnostic tests that are available. That's definitely growing. Some of the new studies that are out, in terms of research and clinical trials. And then wanted to review some of the approaches for treatment for neurologists. Particularly, we're hoping that, you know, this article educates folks. If you're a general neurologist, we're hoping that recognizing these diseases early on will prompt you to refer these patients to specialty clinics or movement disorder specialists early on so they can get appropriate care, confirm your diagnosis, as well as get them involved in trials if they are available. Dr Monteith: And how has the clinical criteria for PSP and cortical basilar syndrome changed? Dr Farland: I think I already mentioned there's been an evolution of the clinical criteria for PSP. There's new diagnostic criteria that were recently published, and it recognizes the multiple clinical phenotypes and the spectrum of the disease that's out there, which is much broader than we thought about. Corticobasal clinical criteria are the Dr Armstrong criteria from 2013. They have not been updated, but they are in the works of being updated. But it does recognize the classic presentation of corticobasal syndrome, plus a frontal executive predominant and then a variant that actually overlaps with PSP. So, there's a lot more overlap in these two diseases than we originally recognized. Dr Monteith: And so, you spoke a bit about FTD spectrum. So why don't you tell us a little bit about what that is? I know you mentioned multiple phenotypes. Dr Farland: What I really want to say is that both PSP and corticobasal syndrome, they're relatively rare, and what- sort of as to common features, they both are progressive Parkinson disorders, but they have variable features. While they're commonly associated with Parkinson's, they also fit within this frontotemporal lobar spectrum, having features that overlap both clinically and neuropathologically. I just want folks to understand that overlap. One of this pathological overlap here is the predominant Tau pathology in the brain, an increasing recognology- recognition of sort of the pathological heterogeneity within these disorders. So, there's an initial description, a classic of PSP, as Richardson syndrome. But now we recognize there are lots of different features to it and there are different ways it presents, and there's definitely a lot of clinical pathological overlap. Dr Monteith: Why don't we just talk about some red flags for PSP? Dr Farland: Yeah, sure. So, some of the red flags for PSP and even corticobasal syndrome are: number one is rapid progression with early onset of falls, gait difficulty, falling typically backwards, early speech and swallow problems that are more prominent than you see in Parkinson's disease, as well as eye gaze issues. So, ocular motor features, particularly vertical gaze palsy. In particular what we talk about is the supranuclear gaze palsy, and one of the most sensitive features that we've seen with these is downgaze limitation or slowed downgaze, and eventually a full vertical gaze palsy and followed supranuclear gaze palsy. So, there's some of the red flags that we see. So, while we think about the lack of response to levodopa frequently as something that's a red flag for Parkinson's, there are many times that we see Parkinson's patients, and about a quarter of them don't really respond. There's some features that don't respond to levodopa that may not be so specific, but also can be helpful in this disease. Dr Monteith: And what about the red flags for cortical basilar syndrome? Dr Farland: So, for cortical basilar syndrome, some of the red flags again are this rapidly depressive syndrome tends to be, at least in its classical present presentation, more asymmetric in its presentation of parkinsonism, with features including things like dystonic features, okay? For limb dystonia and apraxias---so, inability to do a learned behavior. One of those red flags is a patient who comes in and says, my hand doesn't work anymore, which is something extremely uncommon that you hear in Parkinson's disease. Most of those patients will present, say, I might have a tremor, but they very rarely will tell you that I can't use my hand. So look out for that sign. Dr Monteith: And let's talk a little bit about some of the advances in the fields you mentioned, evolving biomarker and imaging capacities. So, how are these advances useful in helping us understand these conditions, especially when there's so much heterogeneity? Dr Farland: I might start by talking a little bit about some of the clinical criteria that have advanced. Why don't we start there and just discuss some of the advances? I think in PSP, I think, originally we had both probable and possible diagnoses of PSP, and the diagnostic criteria were basically focused on what was what's called “classical PSP” or “Richardson syndrome”. But now we recognize that there are multiple phenotypes. There's an overlap with Parkinsonism that's slower in progression and morphs into PSP, the classical form. There's a frontal behavioral variant where patients present with that frontal behavioral kind of thing. There's a speech-language variant that can overlap with PSP. So they have prominent speech language, potentially even apraxia speech. So, recognition of these different phenotypes is sort of a new thing in this field. There's even overlap with cortical basal syndrome and PSP, and we note that the pathology can overlap as well. So, I think that's one of the things that have changed over time. And these were- recently came out in 2017 in a new publication in the Movement Disorders Society. So, in terms of diagnostic tests as well---and there's been quite a bit of evolution---really still to date, our best diagnostic test is imaging. MRI is really one of our best tests currently. Currently blood tests, spinal fluid, there's new biomarkers in terms of skin… they're still in the research phase and not necessarily very specific yet. So, we rely heavily on imaging still; and for PSP, what we're looking for largely are changes in the brain stem, and particularly focused on the midbrain. So disproportionate midbrain atrophy compared to the pons and the rest of the midbrain is a fairly specific intensive sign for PSP. Whereas in MSA we see more of a pontine atrophy compared to the midbrain. So that can be really helpful, and there are lots of different new measurements that can be done. PET scans are also being used as well. And there are new PET markers, but they still remain kind of research-based, but are becoming more and more prevalent and may be available soon for potential use. Although there's some overlap with PET tracers with Alzheimer's disease and different Tau isoforms. So, something to be wary about, but we will be seeing some of these soon coming out as well. More kind of up-to-date things include things like the spinal fluid as well as even some of the skin biopsies. And I think we've heard some word of recent studies that have come out that potentially in the very near future we might actually have some Tau protein tests that we can look at Tau either in spinal fluid or even in a skin biopsy. But again, still remains research-based and, we still need more information as to whether these tests can be reproducible and how sensitive or specific they are. Dr Monteith: It sounds like, when really approaching these patients, still, it's a lot of back to the history, back to the clinical and some basic imaging that we should be able to identify to distinguish these types of patients, and we're not quite where we need to be yet for biomarker. Dr Farland: I totally agree with you. I think it starts, really, with the clinical exam and that's our main focus here; and understanding some of the new clinical criteria which are more sensitive, but also specific, too. And they're really useful to look at. So, I think reviewing those; patients do progress, following them over time can be really useful. And then for diagnosis, getting imaging if you suspect a patient has an atypical presentation of parkinsonism, to look for signs or features that might be specific for these different disorders. Dr Monteith: Why don't we take a typical case, a typical patient that you would see in clinic, and walk us through the thought process---especially, maybe they presented somewhat early---and the different treatment approaches to helping the patient, and of course their family. Dr Farland: Yeah, sure. So, a typical patient might be someone who comes in with, like, a three year history of progressive gait problems and falling. And let's say the patient says, I'm falling backwards frequently. They may have had, like, a rib fracture, or they hit their head once, and they're describing some speech issues as well. Now they're relying on a walker and family members saying they rarely let them be by themselves. And there may be some slowing of their cognitive function and maybe a bit of withdrawal. So that's a typical patient. So, the approach here is really, what are some of the red flags? I think already you hear a red flag of a rapidly progressive disease. So, Parkinson's disease patients rarely have frequent falls within the first five years. So, this is within three years or less. You're already hearing early onset of gait problems and falling, and particularly falling backwards rather than forwards as often Parkinson's disease patients do. You're hearing early speech problems and maybe a subtle hint of cognitive slowing and some withdrawal. So, a lot of things that sort of are red flags. So, our approach really would be examining this patient really closely. Okay? We'd be listening to the history, looking at the patient. One thing is that some of these patients come in, they may be in a wheelchair already. That's a red flag for us. If they're wearing sunglasses---sometimes we see that patients, they have photosensitivity and they're in a chair and they're wearing sunglasses---you take the glasses off and you look at their face and they have that sort of a facial stare to them---not just the masked face, but the stare---and their eyes really aren't moving. So, another kind of clue, maybe this is probably something atypical, particularly PSP is what I'm thinking about. So, the approach is really, do a thorough exam. I always recommend looking at eye movements and starting with volitional saccades, not giving them a target necessarily, but asking them to look up and then look down. And then particularly look at the speed of downgaze and whether they actually have full versions down, are able to do that. That's probably your most sensitive test for a patient who has PSP. Not the upgaze, which can be- upgaze impairment in older patients can be nonspecific. So, look for that down gaze. So, if I can get out one message, that's one thing that can be easily done and examined fairly quickly for diagnosis of these patients. And then just look for signs of rigidity, bradykinesia, maybe even some myelopraxia, and then look at their gait carefully so that there's a high suspicion. Again, if there's some atypical features, imaging is really important. So, my next step would be probably getting an MRI to evaluate whether- do they have brain somatrophy or other widespread atrophy or other signs? You need to think about your differential diagnosis for some of these patients as well. So, common things are common; vascular disease, you can't have vascular parkinsonism or even signs of NPH. Both of those can present with progressive gait difficulty and falls. So, the gait may look more like Parkinson's rather than ataxic gait that we see in classic PSP, but still they have early gait issues, and that can be a mimicker of PSP, So looking for both of those things in your imaging. Think about sort of autoimmune potentially causes. So, if they have a really rapid progressive cause, there are some rare autoimmune things. There have been recent reports of things like IgLON5, although there's limited cases, but we're doing more screening for some of those autoimmune causes. And then even some infectious causes like Whipples, that are rarely present like this. Okay? And have other signs and features. Dr Monteith: So, let's say you diagnose this patient with PSP and you're assessing the patients to see how you can improve their quality of life. So, what are some potential symptomatic managements that will help our patient? Dr Farland: I recommend for most all of these patients… while the literature indicates that many patients with PSP, and especially corticobasal syndrome, don't respond well to levodopa. So, the classic treatment for parkinsonism. However, we all recommend a trial of levodopa. These patients may respond partially to doses of levodopa, and we try to push the doses a bit higher. So, the recommended trial is usually a dose up to roughly 1000 milligrams of levodopa per day. And give it some time, at least two, if not actually three months of a trial. If not well-tolerated, you can back off. If there's no response at all or no improvement, then slowly back off and taper patients off and ask them to tell you whether they feel like they're actually worsening. So, many patients, sometimes, don't recognize the improvements, or family members don't recognize it until we actually taper them back off. And they may end up saying there are some other things that even recognize. Even some nonmotor benefits can be seen with levodopa. In some cases, we do keep them on levodopa, but levodopa's our best therapy for this. Dopamine agonists, MAO inhibitors, have all been sort of tried and they've been studied, but often don't really help or fail to help benefit these patients and could be fraught with some other side effects. I think many people do also turn to Amantadine as a treatment for Parkinson's, gait problems, freezing, if you see it in these disorders. Yet Amantadine is fraught with issues of side effects, including cognitive issues, and I think is not well-tolerated. But there are the rare patient who actually does respond to this or claims they respond to this. By and large, these patients relentlessly progress, unfortunately. So, beside treatment of other symptoms, I think it's really important to recognize that they require supportive cares and therapy. So, starting those early on and getting your allied healthcares kind of involved. So that includes people like physical, occupational therapy for the gait issues, the falls, occupational therapy for doing daily activities. Speech language pathology can be really a critical player for these because of the early speech and language issues, as well as swallow difficulties. Swallow is compared quickly in these patients. And so, we do recommend the screening evaluation, then often following patients either every six- or even annually, at least, with a swallow evaluation. And we recommend the fluoroscopic-guided kind of modified barium swallow for these patients.  Dr Monteith: And how does that differ if, let's say, the patient had cortical basilar syndrome? What are some of the symptomatic treatments that would be high on your consideration? Dr Farland: So actually, these patients also have a very similar approach, and they often have some overlapping features. Maybe a little bit of difference in terms of the level of apraxia and some dystonic features that you see in corticobasal syndrome. So, as I mentioned earlier that these patients have a more typ- when they present, typically have a more asymmetric presentation. And one of the biggest issues is this limb apraxia. They may have abnormal movements as well as, like, the alien limb-type phenomena as well. So, the focus of therapy, while similar in the sense we focus on the parkinsonism, I do always try levodopa and try to ramp up the doses to see if it benefits. It does often fail, but it's definitely worth trying. The other focus of these patients is trying to treat symptoms. Dystonia, those features… in some cases, we can help; if it's painful or uncomfortable, muscle relaxants can be used. If it's vocal, things like Botox can be really helpful. Often times it is more palliative than actually restorative in terms of function, but still can be really helpful for patients who ask about pain and discomfort and trying to treat. And then of course, again, the focus on our supportive care. We need to build that network and build that team of folks, the therapists, the physical, occupational, and the speech therapist to help them. If they have language problems---like either in PSP or corticobasal---I'll also include my request to a speech language pathologist to work on cognitive function. That's a special, additional thing you have to ask for and then specifically request when you make a referral to a speech language pathologist. Dr Monteith: That is so important. I think keeping the simulation, keeping the social support, and I would probably guess that you would also include screening for sleep and mood disorder. Dr Farland: Absolutely. Mood disorders are really big in these diseases. Patients are suffering terribly. You do hear about labile mood in both of these diseases, particularly PSP; and even what's called pseudobulbar palsy, where the mood is not always congruent with the affect. So they may laugh or cry inappropriately, and particularly the crying can be very disturbing to family and caregivers to see that. And so, treating those things can be really important. So always asking about the mood issues. Depression in particular is something that we're very sensitive about, and there is a higher incidence of suicidal ideations. Asking about that and feeling and making sure that they are in a safe environment can be really important. Dr Monteith: Thank you so much. Dr Farland: Thank you. Dr Monteith: Today I've been interviewing Dr Nikolaus McFarland about his article on progressive supranuclear palsy and cortical basilar syndrome, which appears in the August 2025 Continuum issue on movement disorders. 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.

Shout out to all the folks who continue to show up for themselves. Lending physical and emotional support to others is easy. Extending that same amount of empathy and reliability to ourselves? Ugh, no. That's why many of us abandon our healing work just as things start to challenge us. But the muck is where we need to be if we have any hope of growing into a true expression of self. Annie Schuessler Zam, a therapist-turned-healer and host of the Rebel Therapist™ podcast, personifies the life-long practice of showing up for oneself. So, when she asked if she could return to the show to discuss her recent healing experiences, I was all in! Our conversation recalls the quintessential premise of this show: that sharing stories of personal healing is integral and transformational to the changes we hope to make in the professional realm and beyond.  GUEST BIO Annie Schuessler Zam (she/they) is a therapist turned healer and the host of the Rebel Therapist podcast. She helps people who are estranged from a parent or caregiver who want to heal trauma and live their most beautiful lives. Join the Group Practice (R)evolution! GPR is a new platform and podcast series offering insights from owners, employees, and experts, and resources to support this wildly ambitious vision for the future. For a limited time, podcast listeners can get a full year of membership for only $19.99 by using the discount code PODCAST.  Visit: https://tinyurl.com/GPRPodcast and click on “have a coupon” and enter PODCAST to enjoy all the perks of Group Practice (R)evolution for a year!  Get Support! Earn CEs! Care in Chaos: https://tinyurl.com/CareInChaosRec Bridging Heart and Practice: https://tinyurl.com/TheSarahsOnlineSupe  SUPPORT THE SHOW Conversations With a Wounded Healer Merch Join our Patreon for gifts & perks Shop our Bookshop.org store and support local booksellers Share a rating & review on Apple Podcasts *** Let's be friends! You can find me in the following places… Website Facebook @headheartbiztherapy Instagram @headheartbiztherapy

Multiple system atrophy is a rare, sporadic, adult-onset, progressive, and fatal neurodegenerative disease. Accurate and early diagnosis remains challenging because it presents with a variable combination of symptoms across the autonomic, extrapyramidal, cerebellar, and pyramidal systems. Advances in brain imaging, molecular biomarker research, and efforts to develop disease-modifying agents have shown promise to improve diagnosis and treatment. In this episode, Casey Albin, MD speaks with Tao Xie, MD, PhD, author of the article “Multiple System Atrophy” in the Continuum® August 2025 Movement Disorders 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. Xie is director of the Movement Disorder Program, chief of the Neurodegenerative Disease Section in the department of neurology at the University of Chicago Medicine in Chicago, Illinois. Additional Resources Read the article: Multiple System Atrophy 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: Hello everyone, this is Dr Casey Albin. Today I'm interviewing Dr Tao Xie about his article on diagnosis and management of multiple system atrophy, which appears in the August 2025 Continuum issue on movement disorders. Welcome to the podcast, and please introduce yourself to our audience. Dr Xie: Thank you so much, Dr Albin. My name is Tao Xie, and sometimes people also call me Tao Z. I'm a mood disorder neurologist, professor of neurology at the University of Chicago. I'm also in charge of the mood disorder program here, and I'm the section chief in the neurodegenerative disease in the Department of Neurology at the University of Chicago Medicine. Thank you for having me, Dr Albin and Dr Okun and the American Academy of Neurology. This is a great honor and pleasure to be involved in this education session. Dr Albin: We are delighted to have you, and thank you so much for the thoughtful approach to the diagnosis and management. I really want to encourage our listeners to check out this article. You know, one of the things that you emphasize is multiple system atrophy is a fairly rare condition. And I suspect that clinicians and trainees who even have a fair amount of exposure to movement disorders may not have encountered that many cases. And so, I was hoping that you could just start us off and walk us through what defines multiple system atrophy, and then maybe a little bit about how it's different from some of the more commonly encountered movement disorders. Dr Xie: This is a really good question, Dr Albin. Indeed, MSA---multisystem atrophy----is a rare disease. It is sporadic, adult-onset, progressive, fatal neurodegenerative disease. By the name MSA, multisystem atrophy. Clinically, it will present with multiple symptoms and signs involving multiple systems, including symptoms of autonomic dysfunction and symptoms of parkinsonism, which is polyresponsive to the levodopa treatment; and the symptom of cerebellar ataxia, and symptom of spasticity and other motor and nonmotor symptoms. And you may be wondering, what is the cause- underlying cause of these symptoms? Anatomically, we can find the area in the basal ganglia striatonigral system, particularly in the putamen and also in the cerebellar pontine inferior, all of the nuclear area and the specific area involved in the autonomic system in the brain stem and spinal cord: all become smaller. We call it atrophy. Because of the atrophy in this area, they are responsible for the symptom of parkinsonism if it is involved in the putamen and the cerebral ataxia, if it's involved in the pons and cerebral peduncle and the cerebellum. And all other area, if it's involved in the autonomic system can cause autonomic symptoms as well. So that's why we call it multisystem atrophy. And then what's the underlying cellular and subcellular pathological, a hallmark that is in fact caused by misfolded alpha-synuclein aggregate in the oligodontia site known as GCI---glial cytoplasmic increasing bodies---in the cells, and sometimes it can also be found in the neuronal cell as well in those areas, as mentioned, which causes the symptom. But clinically, the patient may not present all the symptoms at the same time. So, based on the predominant clinical symptom, if it's mainly levodopa, polyresponsive parkinsonism, then we call it MSAP. If it's mainly cerebellar ataxia, then we call it MSAC. But whether we call it MSP or MSC, they all got to have autonomic dysfunction. And also as the disease progresses, they can also present both phenotypes together. We call that mixed cerebellar ataxia and parkinsonism in the advanced stage of the disease. So, it is really a complicated disease. The complexity and the similarity to other mood disorders, including parkinsonism and the cerebellar ataxia, make it really difficult sometimes, particularly at the early stages of disease, to differentiate one from the other. So, that was challenging not only for other professionals, general neurologists and even for some movement disorder specialists, that could be difficult particularly if you aim to make an accurate and early diagnosis. Dr Albin: Absolutely. That is such a wealth of knowledge here. And I'm going to distill it just a little bit just to make sure that I understand this right. There is alpha-synuclein depositions, and it's really more widespread than one would see maybe in just Parkinson's disease. And with this, you are having patients present with maybe one of two subtypes of their clinical manifestations, either with a Parkinson's-predominant movement disorder pattern or a cerebellar ataxia type movement disorder pattern. Or maybe even mixed, which really, you know, we have to make things quite complicated, but they are all unified and having this shared importance of autonomic features to the diagnosis. Have I got that all sort of correct? Dr Xie: Correct. You really summarize well. Dr Albin: Fantastic. I mean, this is quite a complicated disease. I would pose to you sort of a case, and I imagine this is quite common to what you see in your clinic. And let's say, you know, a seventy-year-old woman comes to your clinic because she has had rigidity and poor balance. And she's had several falls already, almost always from ground level. And her family tells you she's quite woozy whenever she gets up from the chair and she tends to kind of fall over. But they noticed that she's been stiff,and they've actually brought her to their primary care doctor and he thought that she had Parkinson's disease. So, she started levodopa, but they're coming to you because they think that she probably needs a higher dose. It's just not working out very well for her. So how would you sort of take that history and sort of comb through some of the features that might make you more concerned that the patient actually has undiagnosed multiple systems atrophy? Dr Xie: This is a great case, because we oftentimes can encounter similar cases like this in the clinic. First of all, based on the history you described, it sounds like an atypical parkinsonism based on the slowness, rigidity, stiffness; and particularly the early onset of falls, which is very unusual for typical Parkinson disease. It occurs too early. If its loss of balance, postural instability, and fall occurred within three years of disease onset---usually the motor symptom onset---then it raises a red flag to suspect this must be some atypical Parkinson disorders, including multiple system atrophy. Particularly, pou also mentioned that the patient is poorly responsive to their levodopa therapy, which is very unusual because for Parkinson disease, idiopathic Parkinson disease, we typically expect patients would have a great response to the levodopa, particularly in the first 5 to 7 years. So to put it all together, this could be atypical parkinsonism, and I could not rule out the possibility of MSA. Then I need to check more about other symptoms including autonomic dysfunction, such as orthostatic hypertension, which is a blood pressure drop when the patient stands up from a lying-down position, or other autonomic dysfunctions such as urinary incontinence or severe urinary retention. So, in the meantime, I also have to put the other atypical Parkinson disorder on the differential diagnosis, such as PSP---progressive supranuclear palsy---and the DLBD---dementia with Lewy body disease.---Bear this in mind. So, I want to get more history and more thorough bedside assessment to rule in or rule out my diagnosis and differential diagnosis. Dr Albin: That's super helpful. So, looking for early falls, the prominence of autonomic dysfunction, and then that poor levodopa responsiveness while continuing to sort of keep a very broad differential diagnosis? Dr Xie: Correct. Dr Albin: One of the things that I just have to ask, because I so taken by this, is that you say in the article that some of these patients actually have preservation of smell. In medical school, we always learn that our Parkinson's disease patients kind of had that early loss of smell. Do you find that to be clinically relevant? Is that- does that anecdotally help? Dr Xie: This is a very interesting point because we know that the loss of smelling function is a risk effect, a prodromal effect, for the future development of Parkinson disease. But it is not the case for MSA. Strange enough, based on the literature and the studies, it is not common for the patient with MSA to present with anosmia. Some of the patients may have mild to moderate hyposmia, but not to the degree of anosmia. So, this is why even in the more recent diagnosis criteria, the MDS criteria published 2022, it even put the presence of anosmia in the exclusion criteria. So, highlight the importance of the smell function, which is well-preserved for the majority in MSA, into that category. So, this is a really interesting point and very important for us, particularly clinicians, to know the difference in the hyposmia, anosmia between the- we call it the PD, and the dementia Lewy bodies versus MSA. Dr Albin: Fascinating. And just such a cool little tidbit to take with us. So, the family, you know, you're talking to them and they say, oh yes, she has had several fainting episodes and we keep taking her to the primary care doctor because she's had urinary incontinence, and they thought maybe she had urinary tract infections. We've been dealing with that. And you're sort of thinking, hm, this is all kind of coming together, but I imagine it is still quite difficult to make this diagnosis based on history and physical alone. Walk our listeners through sort of how you're using MRI and DAT scan and maybe even some other biomarkers to help sort of solidify that diagnosis. Dr Xie: Yeah, that's a wonderful question. Yeah. First of all, UTI is very common for patients with MSA because of urinary retention, which puts them into a high risk of developing frequent UTI. That, for some patients, could be the very initial presentation of symptoms. In this case, if we check, we say UTI is not present or UTI is present but we treat it, then we check the blood pressure and we do find also hypertension---according to new diagnosis criteria, starting drop is 20mm mercury, but that's- the blood pressure drop is ten within three minutes. And also, in the meantime the patients present persistent urinary incontinence even after UTI was treated. And then the suspicion for MS is really high right at this point. But if you want increased certainty and a comfortable level on your diagnosis, then we also need to look at the brain MRI mark. This is a required according to the most recent MDS diagnosis criteria. The presence of the MRI marker typical for MSA is needed for the diagnosis of clinically established MSA, which holds the highest specificity in the clinical diagnosis. So then, we have- we're back to your question. We do need to look at the brain MRI to see whether evidence suggestive of atrophy around the putamen area, around the cerebellar pontine inferior olive area, is present or not. Dr Albin: Absolutely. That's super helpful. And I think clinicians will really take that to sort of helping to build a case and maybe recognizing some of this atypical Parkinson's disease as a different disease entity. Are there any other biomarkers in the pipeline that you're excited about that may give us even more clarity on this diagnosis? Dr Xie: Oh, yeah. This is a very exciting area. In terms of biomarker for the brain imaging, particularly brain MRI, in fact, today there's a landmark paper just published in the Java Neurology using AI, artificial intelligence or machine learning aid, diagnoses a patient with parkinsonism including Parkinson's disease, MSA, and PSP, with very high diagnostic accuracy ranging from 96% to 98%. And some of the cases even were standard for autopsy, with pathological verification at a very high accurate rate of 93.9%. This is quite amazing and can really open new diagnosis tools for us to diagnose this difficult disease; not only in an area with a bunch of mood disorder experts, but also in the rural area, in the area really in need of mood disorder experts. They can provide tremendous help to provide accurate, early diagnosis. Dr Albin: That's fantastic and I love that, increasing the access to this accurate diagnosis. What can't artificial intelligence do for us? That's just incredible. Dr Xie: And also, you know, this is just one example of how the brain biomarker can help us. Theres other---a fluid biomarker, molecular diagnostic tools, is also available. Just to give you an example, one thing we know over the past couple years is skin biopsy. Through the immunofluorescent reaction, we can detect whether the hallmark of abnormally folded, misfolded, and the phosphorate, the alpha-synuclein aggregate can be found just by this little pinch of skin biopsy. Even more advanced, there's another diagnosis tool we call the SAA, we call the seizure amplification assay, that can even help us to differentiate MSA from other alpha-synucleinopathy, including Parkinson disease and dementia with Lewy bodies. If we get a little sample from CSF, spinal cerebral fluids, even though this is probably still at the early stage, a lot of developments still ongoing, but this, this really shows you how exciting this area is now. We're really in a fast forward-moving path now. Dr Albin: It's really incredible. So, lots coming down the track in, sort of, MRI, but also with CSF diagnosis and skin biopsies. Really hoping that we can hone in some of those tools as they become more and more validated to make this diagnosis. Is that right? Dr Xie: Correct. Dr Albin: Amazing. We can talk all day about how you manage these in the clinic, and I really am going to direct our listeners to go and read your fantastic article, because you do such an elegant job talking about how this takes place in a multidisciplinary setting, if at all possible. But as a neurointensivist, I was telling you, we have so much trouble in the hospital. We have A-lines, and we have the ability to get rapid KUBs to look at Ilias, and we can have many people as lots of diagnosis, and we still have a lot of trouble treating autonomiclike symptoms. Really, really difficult. And so, I just wanted to kind of pick your brain, and I'll start with just the one of orthostatic hypotension. What are some of the tips that you have for, you know, clinicians that are dealing with this? Because I imagine that this is quite difficult to do without patients. Dr Xie: Exactly. This is indeed a very difficult symptom to deal with, particularly at an outpatient setting. But nowadays with the availability of more medication---to give an example, to treat patients with orthostatic hypertension, we have not only midodrine for the cortisol, we also have droxidopa and several others as well. And so, we have more tools at hand to treat the patient with orthostatic hypertension. But I think the key thing here, particularly for us to the patient at the outpatient setting: we need to educate the patient's family well about the natural history of the disease course. And we also need to tell them what's the indication and the potential side effect profile of any medication we prescribe to them so that they can understand what to expect and what to watch for. And in the meantime, we also need to keep really effective and timely communication channels, make sure that the treating physician and our team can be reached at any time when the patient and family need us so that we can be closely monitoring, their response, and also monitoring potential side effects as well to keep up the quality of care in that way. Dr Albin: Yeah, I imagine that that open communication plays a huge role in just making sure that patients are adapting to their symptoms, understanding that they can reach out if they have refractory symptoms, and that- I imagine this takes a lot of fine tuning over time. Dr Xie: Correct. Dr Albin: Well, this has just been such a delight to get to talk to you. I really feel like we could dive even deeper, but I know for the sake of time we have to kind of close out. Are there any final points that you wanted to share with our listeners before we end the interview? Dr Xie: I think for the patients, I want them to know that nowadays with advances in science and technology, particularly given a sample of rapid development in the diagnostic tools and the multidisciplinary and multisystemic approach to treatment, nowadays we can make an early and accurate diagnosis of the MSA, and also, we can provide better treatment. Even though so far it is still symptomatically, mainly, but in the near future we hope we can also discover disease-modifying treatment which can slow down, even pause or prevent the disease from happening. And for the treating physician and care team professionals, I just want them to know that you can make a difference and greatly help the patient and the family through your dedicated care and also through your active learning and innovative research. You can make a difference. Dr Albin: That's amazing and lots of hope for these patients. Right now, you can provide really great care to take care of them, make an early and accurate diagnosis; but on the horizon, there are really several things that are going to move the field forward, which is just so exciting. Again today, I've been really greatly honored and privileged to be able to talk to Dr Tao Xie about his article on diagnosis and management of multiple system atrophy, which appears in the August 2025 Continuum issue on movement disorders. Be sure to check out Continuum Audio episodes for this and other issues. And thank you again to our listeners for joining us today. Dr Xie: Thank you so much 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.

We previously released this episode on December 18, 2024. We're excited to revisit some key ideas before we dive into fresh, exciting topics soon. In this episode, Ethan Nash introduces the Challenge-Competency Continuum, a framework for understanding how stress impacts employee productivity. Picture an upside-down “U” with productivity on the y-axis and stress on the x-axis. Too little stress leaves employees unmotivated; too much stress overwhelms them. Peak productivity? It's right in the middle. The key to finding that balance, Nash says, ask your employees. Ethan dives into how understanding where someone lands on the continuum—how “challenged” and “competent” they feel—can help managers make smarter decisions. With the right insights, leaders can fine-tune workloads, reduce unnecessary stress, and unlock their team's full potential. To get our Effective and Enjoyable Meetings Guidebook, send a note to contact@nashconsulting.com. Text the word “LEADING” to 66866 to be added to Nash Consulting's monthly newsletter. Just practical management skills and tips. And just once a month. Pinky swear.

Essential tremor is the most common movement disorder, although it is often misdiagnosed. A careful history and clinical examination for other neurologic findings, such as bradykinesia, dystonia, or evidence of peripheral neuropathy, can reveal potential alternative etiologies. Knowledge about epidemiology and associated health outcomes is important for counseling and monitoring for physical impairment and disability. In this episode, Lyell Jones, MD, FAAN, speaks with Ludy C. Shih, MD, MMSc, FAAN, author of the article “Essential Tremor” in the Continuum® August 2025 Movement Disorders 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. Shih is clinical director of the Parkinson's Disease and Movement Disorders Center at Beth Israel Deaconess Medical Center in Boston, Massachusetts. Additional Resources Read the article: Essential Tremor 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: @ludyshihmd 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 Ludy Shih, who recently authored an article on essential tremor for our latest issue of Continuum on movement disorders. Dr Shih is an associate professor of neurology at Harvard Medical School and the clinical director of the Parkinson's Disease and Movement Disorder Center at Beth Israel Deaconess Medical Center in Boston. Dr Shih, welcome, and thank you for joining us today. Why don't you introduce yourself to our listeners? Dr Shih: Thank you, Dr Jones, for having me. It's a real pleasure to be here on the podcast with you. I'm a neurologist, I trained in movement disorders fellowship, and I currently see patients and conduct clinical research. We offer a variety of treatments and diagnostic tests for our patients with movement disorders. And I have developed this interest, a clinical research interest in essential tremor. Dr Jones: And so, as an expert in essential tremor, the perfect person to write such a really spectacular article. And I can't wait for our listeners to hear more about it and our subscribers to read it. And let's get right to it. If you had, Dr Shih, a single most important message for our listeners about caring for patients with essential tremor, what would that message be? Dr Shih: Yeah, I think the takeaway that I've learned over the years is that people with essential tremor do develop quite a few other symptoms. And although we propose that essential tremor is this pure tremor disorder, they can experience a lot of different comorbidities. Now, there is some debate as to whether that is expected for essential tremor or is this some part of another syndrome, which we may talk about later in the interview. But the fact of the matter is, it's not a benign condition and people do experience some disability from it. Dr Jones: And I think that speaks to how the name of this disorder has evolved over time. right? You point out in your article, it used to be called benign essential tremor or benign familial tremor. But it's really not so straightforward as it. And fairly frequently these symptoms, the patient's tremor, can be functionally limiting, correct? Dr Shih: That is correct. In fact, the reason I probably started getting interested in essential tremor was because our center had been doing a lot of deep brain stimulation for essential tremor, which is remarkably effective, especially for tremor that reaches an amplitude that really no oral medication is going to satisfyingly treat. And if you have enough upper limb disability from this very large-amplitude tremor, a surgical option may make a lot of sense for a lot of patients. And yet, how did they get to that point? Do they continue to progress? These were the sort of interesting questions that got raised in my mind as I started to treat these folks. Dr Jones: We'll come back to treatment in just a minute here, because there are many options, and it sounds like the options are expanding. To start with the diagnosis- I mean, this is an extraordinarily common disorder. As you point out, it is the most common movement disorder in the US and maybe the world, and yet it seems to be underrecognized and frequently misdiagnosed. Why do you think that is? Dr Shih: Great question. It's been pretty consistent, with several case series over the decades showing a fairly high rate of quote/unquote “misdiagnosis.” And I think it speaks to two things, probably. One is that once someone sees a postural and kinetic tremor of the arms, immediately they think of essential tremor because it is quite common. But there's a whole host of things that it could actually be. And the biggest one that we also have to factor in is also the heterogeneity of the presentation of Parkinson's disease. Many people, and I think increasingly now these days, can present with not a whole lot of the other symptoms, but may present with an atypical tremor. And it becomes actually a little hard to sort out, well, do they have enough of these other symptoms for me to suspect Parkinson's, or is the nature of their tremor suspicious enough that it would just be so unusual that this stays essential tremor and doesn't eventually develop into Parkinson's disease? And I think those are the questions that we all still grapple with from time to time in some of our clinics. Dr Jones: Probably some other things related to it with, you know, our understanding of the pathophysiology and the availability of tests. And I do want to come back to those questions here in just a minute, but, you know, just the nomenclature of this disorder… I think our clinical listeners are familiar with our tendency in medicine to use words like essential or idiopathic to describe disorders or phenomena where we don't understand the precise underlying mechanism. When I'm working with our trainees, I call these “job-security terms” because it sounds less humbling than “you have a tremor and we don't know what causes it,” right? So, your article does a really nice job outlining the absence of a clear monogenic or Mendelian mechanism for essential tremor. Do you think we'll ever have a eureka moment in neurology for this disorder and maybe give it a different name? Dr Shih: It's a great question. I think as we're learning with a lot of our neurologic diseases---and including, I would even say, Parkinson's disease, to which ET gets compared to a lot---there's already now so much more known complexity to something that has a very specific idea and concept in people's minds. So, I tend to think we'll still be in an area where we'll have a lot of different causes of tremor, but I'm hopeful that we'll uncover some new mechanisms for which treating or addressing that mechanism would take care of the tremor in a way that we haven't been able to make as much progress on in the last few decades as maybe we would have thought given all the advances in in technology. Dr Jones: That's very helpful, and we'll be hopeful for that series of discoveries that lead us to that point. I think many of our listeners will be familiar with the utility---and, I think, even for most insurance companies, approval---for DAT scans to discriminate between essential tremor and Parkinsonian disorders. What about lab work? Are there any other disorders that you commonly screen for in patients who you suspect may have essential tremor? Dr Shih: Yeah, it's a great question. And I think, you know, I'm always mindful that what I'm seeing in my clinic may not always be representative of what's seen in the community or out in practice. I'll give an example. You know, most of the time when people come to the academic Medical Center, they're thinking, gosh, I've tried this or that. I've been on these medicines for the last ten years. But I've had essential tremor for twenty years. We get to benefit a little bit from all that history that's been laid down. And so, it's not as likely you're going to misdiagnose it. But once in a while, you'll get someone with tremor that just started a month ago or just started, you know, 2 or 3 months ago. And you have to still be thinking, well, I've got to get out of the specialist clinic mindset, and think, well, what else really could this be? And so, while it's true for everybody, moreso in those cases, in those recent onset cases, you really got to be looking for things like medications, electrolyte abnormalities, and new-onset thyroid disorder, for example, thyroid toxicosis. Dr Jones: Very helpful. And your article has a wonderful list of the conditions to consider, including the medications that might be used for those conditions that might result or unmask a tremor of a different cause. And I think being open-minded and not anchoring on essential tremor just because it's common, I think is a is a key point here. And another feature in your article that I really enjoyed was your step-by-step approach to tremor. What are those steps? Dr Shih: Well, I think you know first of all, tremor is such common terminology that even lay people, patients, nonclinicians will use the word “tremor.” And so, it can be tempting when the notes on your schedule says referred for tremor to sort of immediately jump to that. I think the first step is, is it tremor? And that's really something that the clinician first has to decide. And I think that's a really important step. A lot of things can look superficially like tremor, and you shouldn't even assume that another clinician knows what tremor looks like as opposed to, say, myoclonus. Or for example a tremor of the mouth; well, it actually could be orolingual or orobuccal dyskinesia, as in tardive dyskinesia. And another one that tremor can look like is ataxia. And so, I think- while they sound obvious to most neurologists, perhaps, I think that---especially in the area of myoclonus, where it can be quite repetitive, quite small amplitude in some conditions---it can really resemble a tremor. And so, there are examples of these where making that first decision of whether it's a tremor or not can really be a good sort of time-out to make sure you're going down the right path to begin with. And I think what's helpful is to think about some of the clinical definitions of a tremor. And tremor is really rhythmic, it's oscillatory. You should see an agonist and antagonist muscle group moving back and forth, to and fro. And then it's involuntary. And so, I think these descriptors can really help; and to help isolate, if you can describe it in your note, you can probably be more convinced that you're dealing with the tremor. The second step that I would encourage people to really consider: you've established it's a tremor. The most important part exam now becomes, really, the nontremor part of the exam. And it should be really comprehensive to think of what else could be accompanying this, because that's really how we make diagnosis of other things besides essential tremor. There really should be a minimum of evidence of parkinsonism, dystonia, neuropathy, ataxia- and the ataxia could be either from a peripheral or central nervous system etiology. Those are the big four or five things that, you know, I'm very keen to look for and will look pretty much in the head, neck, the axial sort of musculature, as well as the limbs. And I think this is very helpful in terms of identifying cases which turn out to have either, say, well, Parkinson's or even a typical Parkinson disorder; or even a genetic disorder, maybe even something like a fragile X tremor ataxia syndrome; or even a spinal cerebellar ataxia. These cases are rare, but I think if you uncover just enough ataxia, for example, that really shouldn't be there in a person, let's say, who's younger and also doesn't have a long history of tremor; you should be more suspicious that this is not essential tremor that you're dealing with. And then the last thing is, once you've identified the tremor and you're trying to establish, well, what should be done about the tremor, you really have to say what kind of tremor it is so that you can follow it, so you can convey to other people really what the disability is coming from the tremor and how severe the tremor is. So, I think an example of this is, often in the clinic, people will have their patients extend their arms and hands and kind of say, oh, it's an essential tremor, and that's kind of the end of the exam. But it doesn't give you the flavor. Sometimes you'll have a patient come in and have a fairly minimal postural tremor, but then you go out, take those extra few seconds to go grab a cup of water or two cups of water and have them pour or drink. And now all of a sudden you see this tremor is quite large-amplitude and very disabling. Now you have a better appreciation of what you really need to do for this patient, and it might not be present with just these very simple maneuvers that you have at bedside without props and items. And then the severity of it; you know, we're so used to saying mild, moderate, severe. I think what we've done in the Tremor Research Group to use and develop the Essential Tremor Rating Assessment Scale is to get people used to trying to estimate what size the tremor is. And you can do that by taking a ruler or developing a sense of what 1 centimeter, 2 centimeters, 3 centimeters looks like. I think it'd be tremendously helpful too, it's very easy and quick to convey severity in a given patient. Dr Jones: I appreciate you, you know, having a patient-centered approach to the- how this is affecting them and being quantitative in the assessment of the tremor. And that's a great segue to a key question that I run into and I think others run into, which is when to initiate therapy? You know, if you see a patient who, let's say they have a mild tremor or, you know, something that quantitatively is on the mild end of the spectrum, and you have, you know, a series of options… from a medication perspective, you have to say, well, when does this across that threshold of being more likely to benefit the patient than to harm the patient? How do you approach that question? What's your threshold for starting medication? Dr Shih: Yeah. You know, sometimes I will ask, because---and I know this sounds like a strange question---because I feel like my patients will come for a couple of different reasons. Sometimes it's usually one over the other. I think people can get concerned about a symptom of a tremor. So, I actually will ask them, was your goal to just get a sense for what this tremor is caused by? I understand that many people who develop tremor might be concerned it might be something like Parkinson's disease. Or is this also a tremor that is bothering you in day-to-day life? And often you will hear the former. No, I just wanted to get checked out and make sure you don't think it's Parkinson's. It doesn't bother me enough that I want to take medication. They're quite happy with that. And then the second scenario is more the, yeah, no, it bothers me and it's embarrassing. And that's a very common answer you may hear, may be embarrassing, people are noticing. It's funny in that many people with essential tremor don't come to see a doctor or even the neurologist for many years. And they will put up with it for a very long time. And they've adopted all sorts of compensatory strategies, and they've just been able to handle themselves very admirably with this, in some cases, very severe tremor. So, for some of them, it'll take a lot to come to the doctor, and then it becomes clear. They said, I think I'm at the point where I need to do something about this tremor. And so, I think those three buckets are often sort of where my patients fall into. And I think asking them directly will give you a sense of that. But you know, it can be a nice time to try some as-needed doses of something like Propranolol, or if it's something that you know that they're going to need something on day-to-day to get control of the tremor over time, there are other options for that as well. Dr Jones: Seems like a perfect scenario for shared decision-making. Is it bothersome enough to the patient to try the therapy? And I like that suggestion. That's a nice pearl that you could start with an a- needed beta blocker, right, with Propranolol. And this is a question that I think many of us struggle with as well. If you've followed a patient with essential tremor for some time and you've tried different medications and they've either lost effectiveness or have intolerable adverse effects, what is your threshold for referring a patient for at least considering a surgical neurostimulator therapy for their essential tremor? Dr Shih: Yeah, so surgical therapies for tremor have been around for a long time now, since 1997, which was when it was approved by the FDA for essential tremor and Parkinson tremor. And then obviously since then, we have a couple more options in the focus ultrasound thalamotomy, which is a lesioning technique. When you have been on several tremor medications, the list gets smaller and smaller. It- and then chance of likely satisfying benefit from some of these medications can be small and small as you pass through the first and second line agents and these would be the Propranolol and the primidone. And as you say, quite a few patients- it's estimated between 30 to 50% of these patients end up not tolerating these first two medications and end up discontinuing them. Some portion of that might also be due to the fact that some of our patients who have been living with essential tremor for decades now, to the point that their tremor is getting worse, are also getting older. And so, polypharmacy and/or some of the potential side effects of beta blockers and anticonvulsants like primidone may be harder to bear in an older adult. And then as you talk about in the article, there's some level of evidence for topiramate, and then from there a number of anticonvulsants or benzos, which have even weaker evidence for them. It's a personal decision. As I tell folks, look, this is not going to likely extend your life or save your life, but it's a quality of life issue. And of course, if there are other things going on in life that need to be taken care of and they need that kind of care and attention, then, you know, you don't need to be adding this to your plate. But if you are in the position where those other things are actually okay, but quality of life is really affected by your being unable to use your upper limbs in the way that you would like to… A lot of people's hobbies and applications are upper limb-based, and enjoying those things is really important. Then I think that this is something- a conversation that we begin and we begin by talking about yes, there are some risks involved, but fortunately this is the data we have on it, which is a fairly extensive experience in terms of this is the risk of, you know, surgery-related side effects. This is the risk of if you're having stimulation from DBS stimulation-related side effects, which can be adjustable. It's interesting, I was talking with colleagues, you know, after focused ultrasound thalamotomy was approved. That really led more people to come to the clinic and start having these discussions, because that seemed like a very the different sort of approach where hardware wasn't needed, but it was still a surgery. And so, it began that conversation again for a bunch of people to say, you know, what could I do? What could I tolerate? What would I accept in terms of risk and potential benefit? Dr Jones: Well, I think that's a great overview of a disorder where, you know, I think the neurologist's role is really indispensable. Right? I mean, you have to have this conversation not just once, this is a conversation that you have over time. And again, I really want to refer our listeners to this article. It's just a fantastic overview of a common disorder, but one where I think there are probably gaps where we can improve care. And Dr Shih, I want to thank you for joining us, and thank you for such a great discussion on essential tremor. I learned a lot from your article, and I learned even more from the interview today. I suspect our readers and listeners will too. Dr Shih: Well, thank you again for the invitation and the opportunity to kind of spread the word on this really common condition. Dr Jones: Again, we've been speaking with Dr Ludy Shih, author of a fantastic article on essential tremor in Continuum's latest 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. 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.

Platypus Revenge plays along to Stargate Continuum. Steve The Mad Drummer, Harry Weinberg, Hank Maiorino, Ammone Swinbank and DJMAGIKCLOWNS

This episode recorded live at the Becker's Hospital Review 15th Annual Meeting features Stephanie Martinez, Executive Director and Associate Chief Nursing Officer for the Care Continuum, Boston Medical Center Health System. She shares how multidisciplinary efforts to reduce length of stay improved care systemwide, and discusses the importance of supporting an evolving nursing workforce through retention strategies and shared decision-making.

Parkinson disease is a neurodegenerative movement disorder that is increasing in prevalence as the population ages. The symptoms and rate of progression are clinically heterogenous, and medical management is focused on the individual needs of the patient. In this episode, Kait Nevel MD, speaks with Ashley Rawls, MD, MS, author of the article “Parkinson Disease” in the Continuum® August 2025 Movement Disorders issue. Dr. Nevel is a Continuum® Audio interviewer and a neurologist and neuro-oncologist at Indiana University School of Medicine in Indianapolis, Indiana. Dr. Rawls is an assistant professor at the University of Florida Health, Department of Neurology at the Norman Fixel Institute for Neurological Diseases in Gainesville, Florida Additional Resources Read the article:  Parkinson Disease 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 Guest: @DrRawlsMoveMD 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 Kait Nevel. Today I'm interviewing Dr Ashley Rawls about her article on Parkinson disease, which appears in the August 2025 Continuum issue on movement disorders. Ashley, welcome to the podcast, and please introduce yourself to the audience. Dr Rawls: Thank you, Kait. Hello everyone, my name is Dr Ashley Rawls. I am a movement disorder specialist at the University of Florida Fixel Institute for Neurologic Diseases in Gainesville, Florida. It's a pleasure to be here. Dr Nevel: Awesome. To start us off talking about your article, can you share what you think is the most important takeaway for the practicing neurologist? Dr Rawls: Yes. I would say that my most important takeaway for this article is that Parkinson disease remains a clinical diagnosis. I think the field has really been advancing and trying to find a biomarker to help with diagnosis through ancillary testing. For example, with the dopamine transporter, the DAT scan, an alpha-synuclein skin biopsy, an alpha-synuclein amplification assay that can happen in blood and CSF. However, I think it's so critical to make sure that you have a very strong history and a very thorough physical exam and use those biomarkers or other testing to help with, kind of, bolstering your thoughts on what's going on with the patient. Dr Nevel: Great. And I can't wait to talk a little bit more about the ancillary testing and how you use that. Before we get to that, can you review with us some of the components of the clinical diagnosis of Parkinson disease? Dr Rawls: Yes. So, when I think about a person that comes in that might have a neurodegenerative disease, I think about two different features, mainly: both motor and Manon motor. So, for my motor features, I'm thinking about resting tremor, bradykinesia---which is fullness of movement with decrement over time---rigidity, and then a specific gait disturbance, a Parkinsonian gait, involving stooped posture, decreased arm swing. They can also have reemergent tremor while walking if they do have tremor as part of their disease process, and also in-block turning as they are walking down the hallway. So, those are my motor features that I look for. So now, when we're talking about a specific diagnosis of Parkinson disease, the one motor feature that you need to have is bradykinesia. The reason why I make sure to speak about bradykinesia, which is slowness of movement with decrement over time, is because people can still have Parkinson disease without having tremor, a resting tremor. So even though that's one of the core cardinal features that most of us will be able to notice very readily, you don't have to necessarily have a resting tremor to be diagnosed with Parkinson' disease. When I talk about nonmotor features, those are going to be the three, particularly the prodromal features that can occur even ten years before people have motor features, can be very prominent early on in the disease process. For example, hyposmia or anosmia for decrease or lack of sense of smell. Another one that we really look for is going to be RBD, or rapid eye movement behavior disorder; or REM behavior disorder, the person acting out their dreams, calling out, flailing their limbs, hitting their bed partner. And then the other one is going to be severe constipation. So those three prodromal nonmotor symptoms of hyposmia/anosmia, RBD or REM behavior disorder, and severe constipation can also make me concerned as a red flag that there is a sort of neurodegenerative issue like a Parkinson disease that may be going on with the patient. Dr Nevel: Great, thank you so much for that overview. While we're talking about the diagnosis, do you mind kind of going back to what you mentioned in the beginning and talking about the ancillary tests that sometimes are used to kind of help, again, bolster that diagnosis of Parkinson disease? You know, like the DAT or the alpha-synuclein skin biopsy. When should we be using those? Should we be getting these on everyone? And what scenarios should we really consider doing one of those tests? Dr Rawls: The scenario in which I would order one of the ancillary testing, particularly like a DAT scan or a skin biopsy, looking for alpha-synuclein is going to be when there are potential red flags or a little bit of confusion in regard to the history and physical that I need to have a little bit more clarification on. For example, if I have a patient that has a history of using dopamine blocking agents, for example, for severe depression; or they have a history of cancer diagnosis and they've been on a dopamine agent like metoclopramide; those I want to be mindful because if they're coming in to see me and they're having the symptoms of Parkinsonism---which is going to be resting tremor, bradykinesia rigidity, or gait disturbance---I need to try to figure out is it potentially due to a medication effect, particularly if they're still on the dopamine blockade medication, or is it something where they're actually having a neurodegenerative illness underneath it, like a Parkinson disease? The other situation that would make me order a DAT skin or a skin biopsy is going to be someone who is coming in that maybe has elements of essential tremor, they have more of a postural or an intention tremor that's very flapping and larger amplitude, and maybe have some mild symptoms and Parkinsonism that might be difficult to distinguish between other musculoskeletal things like arthritis, other imbalance issues from, you know, hip problems or knee problems and what have you. Then I might say, okay, let's see if there is some sort of neurodegeneration underneath this; that may be- that there could be, you know, potentially two elements like a central tremor and Parkinson disease going on. Or is this someone who actually really has Parkinson disease, but there's other factors that are kind of playing into that. Dr Nevel: Great, thank you for that. Gosh, things have really changed over the past fifteen years or so where we have this ancillary testing that we're able to use more, because what you read in the textbook isn't always what you see in clinic. And as you described, there are patients who… it's not as clear cut, and these tests can be helpful. Could you tell us more about the levodopa challenge test? How is this useful in clinical practice? And what are some key points that we should know about when utilizing this strategy for patients who we think have Parkinson disease? Dr Rawls: So, before we had all this ancillary testing with the DAT scan, the skin biopsy, the alpha-synuclein amplification assay, many times if you had a suspicion that a person that had Parkinson disease, but you weren't entirely sure, you would say, hey, listen, let us give you back the dopamine that your body may be missing and see if you have an improvement, in particular in your motor symptom. So, when I talk with my patients, I say, listen, I might have a strong suspicion that you have Parkinson disease. Doing a levodopa trial can not only be diagnostic, but also can be therapeutic as well. So, with this levodopa trial, what I end up doing is saying, okay, we're going to start the medication at a low dose because we are looking to see if you have improvement in three of the main cardinal motor symptoms. Obviously, tremor is much easier for us to see if it gets better. It's very obvious on exam, and the patients are more readily able to see it. Whereas stiffness and slowness is much harder to quantify and try to figure out. Am I stiff and slow because of potential muscle tightness from Parkinson disease, or is it something that's more of a musculoskeletal issue? So, I will tell persons, okay, we're looking for improvement in these three cardinal motor symptoms, and things that we're looking for is getting into and out of a car, into and out of a chair, turning over in bed, seeing how do we navigate ourselves in our daily lives? I give people the example of going through the grocery store, going through a busy airport. Are we able to move better and respond better to different changes in our environment which can give us a better clue of if our stiffness and slowness in particular are being improved with the medication? The other part of this is talking about potential side effects of the carbidopa- of the levodopa in particular. One big thing that I think limits people initially is going to be the nausea, vomiting, potential GI upset when starting this medication initially. So, oftentimes I will find people coming in, oh, you know, my outside doctor started me immediately on one tab of carbidopa/levodopa three times per day. I got nauseous, I threw up, and I never took the medication again. So often times I will start low and go slow because once someone throws up my medication, they are not going to want to take it again---with good reason. So, often times I will ask the patient, hey listen, are you very sensitive to medications? If you are very sensitive, we might start one tablet per day for a week, one tablet twice a day, and then go up until we get to two tablets three times a day if we're talking about carbidopa/levodopa. If someone is not as sensitive then I might go up a little bit quicker. What do we mean when we talk about 600 milligrams per day? So usually, the amount that I use is carbidopa/levodopa, 25/100; so, 100 milligrams being the levodopa portion. Many people just start off at 1 tab 3 times a day, which gives you 300 milligrams of levodopa, and they say, oh, it didn't work, I must not have Parkinson or something else. Well, it just may have been that we did not give an adequate trial and adequate dose to the person. Now if they're not able to tolerate the medication because of the side effects, that's something different. But if they don't have side effects and don't notice a difference, there is room to increase the carbidopa/levodopa or the levodopa replacement that you are using so that you can give it, you know, a very good try to see, is it actually improving resting tremor, bradykinesia and rigidity? Dr Nevel: Yeah, great. Thanks for that. When you diagnose a patient with Parkinson disease, how do you counsel that patient? How do you break that difficult news? And how do you counsel them on what to expect in the future and goals of treatment? I know that's a lot in that question, but it also is a lot that you do in one visit, oftentimes, or at least introduce these kind of concepts to patients in a single visit. Dr Rawls: One thing that I think is helpful for me is trying to understand where the patients and their families are when they come in. Because some of the patients come in and have no prior inkling that they may have a neurodegenerative illness like Parkinson disease. Some of my patients come in and say, I'm here for a second opinion for Parkinson disease. So, then I have an idea of where we are in regard to potential understanding of how to start the conversation going forward. If it is someone who is coming in and has not heard about Parkinson disease, or their family has not been made aware that that's the one reason why they're coming to see a movement disorder specialist, then I will start at the beginning After we finish our history, do a very thorough physical exam, I will talk about things that I heard in the history and that I see on the physical exam that make me concerned for a disease like Parkinson disease. I make sure to tell them where I'm getting my criteria from and not just start off, I think you have Parkinson, here's your medication. I think that's very jarring when you're talking with patients and their families, particularly if they had no idea that this could be a potential diagnosis on the table. Like I said, I will start off with recounting, this is what I've heard in your history that makes me concerned. This is what I've seen on your physical exam that makes me concerned. And I think you have Parkinson disease and here is why. And I'll tell them about the tenants like we discussed about Parkinson disease, both the motor and nonmotor symptoms that we see. So that's kind of the first part is, I make sure to lay it out and then open the room up for some questions and clarification. The other portion of this is that, when I'm talking about counseling the patient, I say, we do not expect Parkinson disease to decrease your lifespan. However, over time, our persons, because it is a neurodegenerative illnesses will accumulate deficits over time. So, more stiffness, more slowness, more walking problems. They may, if they have tremor, the tremor may become worse. If they don't have tremor, they might develop tremor in the future. If we're talking about the nonmotor symptoms that we talk about, the main ones are going to be issues with urinary problems, issues with bowels, and then the other thing is going to be neuropsychiatric issues like anxiety and depression. And those things become more prominent, usually, the nonmotor symptoms later on in the disease process, and then also cognitive impairment as well. I really want to make sure that they have the information that I'm seeing, and if there's anything that they want to correct on their end, as in they're saying, oh wait, well, actually I noticed something else, then that's usually when that comes out around kind of the wrapping-up portion of the visit. So, I think that's really important to, one, be very clear in what I am seeing and if there's red flags, and then tell them, okay this is not going to shorten your lifespan. However, over time, we do have other issues and problems that will arise and we can support you as best as we can through that. The one thing I also been very open with people about is- because our patients will say, is there anything I can do? What can be done? Is there any medication to slow down or stop things? And I let people know that unfortunately, right now there's not an intervention that slows down, stops, or reverses disease progression, with the exception of exercise. Consistent exercise has been found to help to slow down disease progression, okay? And also, it can help to release the dopamine already being made innately in the brain. And also, it can help with our cardiovascular health in the big thing: being balanced. Core strength, quadricep strength. So that's also something that people can work on that they should. And I let people know that exercise is as important as the medications themselves. Dr Nevel: Absolutely. And it's incredible how much they incorporate exercise into their daily lives and get active, people who weren't active before their diagnosis, and how much that can help. One question that I think patients sometimes ask is, when they understand how carbidopa/levodopa works and what the expectations are for that medication, that it's not a disease-modifying medication, but that it can help with their symptoms. And then they kind of hear, well as time goes on, they need higher doses or, you know, it doesn't control their motor symptoms as well. They'll say, okay well, is it better to wait then? Should I wait to start carbidopa/levodopa? Like in my mind, I'm only maybe going to get X amount of time from carbidopa/levodopa. So, I'd rather wait to start it than start it now. What do you say to them and how do you counsel them through that? Dr Rawls: So that is a common question that I do get with my patients. So, I tell people, I'm here for you. And it really depends on how you feel at this time. Because you have to weigh the risks and benefits of the medication itself. If someone who's very, very mild decides to take the medication, they feel nauseous, they're just going to say, hey, listen, it's not for me right now. I don't feel like I need it, and then stop, which is with definitely within their right. But what I always counsel patients as well is to say, the dopamine-producing neurons in the substantia nigra are starting to die over time. That is why we are getting the signs and symptoms of Parkinson disease. At some point, your brain is not going to produce enough dopamine that is needed for you to move when you want to move and not move when you don't want to move. Okay? Giving you at least the motor symptoms of Parkinson disease. With this, it's not that the medication stops working, it's just that you need more dopamine to help replace the dopamine that's being lost. However, the dopamine that you are taking or levodopa that you're taking orally is not going to be released as consistently as it is in your brain on demand and shut off when you don't need it. Hence the reason we get more motor fluctuations. Also, potential side effects in the medication like orthostatic hypertension, hallucinations, impulse control disorders. Because you're having to take more escalating doses, those side effects can become more prominent and also lead us to have to balance between the side effects and the medication itself. So, it's not that the medication does not work, your body needs more of it. Some people will say, oh, well, I want to wait, and I say, that's completely fine. However, my cutoff is basically saying, if you are finding that you, as the person who's afflicted is not able to get up in the morning like you want to, you're avoiding going to walk your dog or working in your garden, you know, because you feel stiff and feel slow; you're avoiding, you know, going out to the community, having lunch with your friends or your family because you're embarrassed by your tremor; this is something that is keeping you from living your life. And that's the time that we need to strongly consider starting the medications. So, a person afflicted will accumulate deficits. However, it's how much the deficits are going to affect you. So, if it's really affecting your life, we have tools and ways to help mitigate that. Dr Nevel: Yeah, absolutely. Are there any aspects of Parkinson disease management that you feel are maybe underrecognized or perhaps underutilized? In other words, you know, are there things that we the listeners should be maybe more aware of or think about offering or recommending to our patients that you think maybe aren't as much as they could be? Dr Rawls: I will say the nonmotor symptoms---in particular the neuropsychiatric symptoms with the anxiety and depression, usually later on disease process but also can be earlier as well---I think that is going to be something that is recognized but maybe undertreated in a lot of our patient population. I think part of that is also the fluctuations in dopamine that are occurring naturally in the person, but also, our patients, oftentimes with their medication regimen, really have to be on the ball taking the medication. If they're even 15 minutes late, 10 minutes late, 5 minutes late, we're now off, and now we're waiting for it to kick in. And so that can cause a lot of anxiousness even throughout the day. And then knowing that slowly over time that they're going to accumulate these motor and nonmotor deficits can definitely be problematic as well. There is obvious reason for this underlying potential anxiety and depression. And while we do talk about that and bring that up, sometimes patients will say, oh well, I don't think it's a problem right now. I don't have to mess with this. But usually at some point it does become an issue that usually the family members will bring up and saying, hey, you know, my loved one is very anxious. Or I've noticed that they're just really disengaged from what's going on in their lives and they are not talking as much, they're not going out as much. Again, that could be a combination of depression/anxiety, but it also can be a physical- a combination of, I'm not physically able to do these things, or, they're much more difficult for me to initiate doing these activities. I always want to be mindful. If my patients come in and they already have a diagnosis of depression or anxiety and they're already being treated by a mental health counselor, provider, or a psychiatrist, then I will work with providers so that we can try to optimize their medication regimen. The other thing is, well, if this is the first time that they're really being seen by someone and talking about their anxiety and depression, then oftentimes I will have them go back to their primary care and see if maybe an SSRI or SNRI will be helpful to try to help with the neuropsychiatric symptoms they may be experiencing. So that's one big one. Another one that I think that might be a little bit underappreciated is going to be drooling. Sometimes I'll come in and see my patients and notice some drooling that's happening with the mouth being open, not being able to initiate the swallowing reflex consistently throughout the day. Or they may be patting their face a lot with a napkin or a towel and then bringing that up and bringing it to light. Oh yeah. I have a lot of drooling while I'm awake. It's on my shirt. It's embarrassing. I feel like it's a little bit too much for me or my family. We have to put a bib on because I'm just drooling all throughout the day. That can really be uncomfortable and cause skin breakdown. It can also be socially embarrassing. So, there are some tools that I talk to people about with drooling. One thing I start with is going to be using sugar-free gum or candy while the person is awake to help initiate the swallow reflex, and sometimes that's all that's needed. There are other agents that can be used---like glycopyrrolate, sublingual atropine drops, and scopolamine patches---that can help with decreasing saliva production. But there can be side effects of making the entire body feel dry, and then also potential cardiac arrhythmias. If those are not helpful or they're contraindicated with the patient, another thing is going to be botulinum toxin injections. So those can be done on the parotid and salivary glands to decrease the amount of saliva that's being produced. So oftentimes people will come to me, because I'm also a botulinum toxin injector. I've been sent by some of my colleagues to inject our persons that have significant sialorrhea. Dr Nevel: Wonderful. Well, thank you so much for chatting with me today about your article. Again, today I've been interviewing Dr Ashley Rawls about her article on Parkinson disease, which appears in the August 2025 Continuum issue on movement disorders. Be sure to check out Continuum Audio episodes from this and other issues. And thank you to our listeners for joining today. And thank you, Ashley, for sharing all your knowledge with us today. Dr Rawls: Thank you, Kate, I appreciate your time. And have a great day, everyone. Dr Monteith: This is Dr Teshmae 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.

Vzpomenete si ještě na časy, kdy měl Microsoft sen, že dobude svět mobilů? Continuum smartphony s Windows 10 Mobile po připojení k doku proměnily na téměř plnohodnotný počítač. Tenhle koncept během pár let shořel i s mobilní strategií. Připomínám nám ale éru, kdy byl operační systém součástí velkých plánů Microsoftu.Windows 10 oslavily 29. července své desáté narozeniny. Při té příležitosti vzpomínáme na zajímavé funkce, které přinesly. Z těch úspěšných můžeme jmenovat Hello, tmavý režim, Edge či virtuální plochy. Ty neúspěšné nám minimálně připomínají, že Desítky za sebou zanechají nesmazatelnou historickou stopu.Jedenáctky budou brzy jedinými běžně podporovanými Windows, protože podpora Windows 10 skončí v říjnu. Domácnosti za určitých podmínek mohou přijímat bezpečnostní aktualizace o rok déle. Pokud máte kompatibilní počítač, můžete zdarma upgradovat na Windows 11. S trochou vůle to jde i neoficiálně.01:16 – 10. narozeniny Windows 1005:52 – Konec dotekové nadvlády16:30 – Hello!20:30 – Smrt Internet Exploreru24:13 – Ohořelé ambice34:04 – Jak řešit konec podpory

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

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?

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.

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 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!

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!

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.

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

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

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

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