Podcasts about Continuum

Approximately 20% of African Americans experienced a mental health condition over the past year, and 5% had a serious mental illness. Where do you turn for help when a loved one experiences a mental health crisis? We talk with mental health professionals about the continuum of care available in Norfolk, and what you need to know to help those you love.

October 27, 2025Today's episode is a simple grounding practice using imagery and sound. Sometimes (like always) we just need to get out of our heads and back into our bodies and souls. We will assess where we are on the continuum of groundedness. Our reading for today is an excerpt from the poem Remember fromJoy Harjo, a Native American U.S. Poet Laureate from the Muscogee Nation.Remember, Joy HarjoRemember the sky that you were born under, know each of the star's stories.Remember the moon, know who she is.Remember the sun's birth at dawn, that is the strongest point of time. Remember sundownand the giving away to night.Remember your birth, how your mother struggledto give you form and breath. You are evidence ofher life, and her mother's, and hers.Remember your father. He is your life, also.Remember the earth whose skin you are:red earth, black earth, yellow earth, white earthbrown earth, we are earth.Remember the plants, trees, animal life who all have theirtribes, their families, their histories, too. Talk to them,listen to them. They are alive poems.Remember the wind. Remember her voice. She knows theorigin of this universe.Remember you are all people and all people are you.Remember you are this universe and this universe is you.Remember all is in motion, is growing, is you.Remember language comes from this.Remember the dance language is, that life is.Remember.https://www.joyharjo.com/Photo by Merri J on Unsplash

Send us a text 45 minutes of Ep 258 - 2 hour special, I'm diving deep into the real life monsters in this Halloween Episode. I start with Real Housewives of Salt Lake City and deliver some serious gossip that I promised you about the latest drama on Season 6 Ep 6 unfolding with the cast. I break down the current storylines and give you my insider take on what's really happening behind the scenes in Salt Lake with Bronwyn's felonies, Lisa Barlow take down and Mary Cosby's demons, but then I shift gears into something much darker. I've just finished reading Virginia Giuffre's new book, Nobody's Girl and I'm breaking down the most shocking revelations about her experiences with Jeffrey Epstein and Ghislaine Maxwell. I walk you through how Ghislaine first approached Virginia when she was just sixteen years old working at the Mar-a-Lago spa, how she was groomed and manipulated into Epstein's world, and the disturbing details about his properties from El Brillo Way mansion to Zorro Ranch to his infamous island Little St. James. I also expose what's happening now with Sarah Kellen, one of Epstein's alleged accomplices who's living in luxury at the Continuum in Miami while victims demand justice. I reveal details about Epstein's background from Virginia's perspective, his time teaching at the Dalton School sleeping with girls for grades, his connections to Bear Stearns, and his calculated methods of control. There are shocking revelations about Prince Andrew, Donald Trump, George Clooney and the web of powerful people in Epstein's orbit that you won't want to miss. We learn about all Virginia's abuse from a child to when she meets Epstein. This is only the first part of the book, so we're just getting started with Virginia's full testimony. Full episode here: https://www.patreon.com/cw/DishingDramaWithDanaWilkey

In this episode, Nona Boss from Florida joins the show at the Ozark Mountain Bigfoot Conference camp out to share her riveting encounters with Bigfoot. Nonna recounts her initial interest sparked by Leonard Nimoy's show 'In Search Of', leading to a life of extraordinary sightings. She details her first Bigfoot encounter in 1986 while snake hunting in the Everglades, a later peaceful daylight sighting in 2022, and other intriguing experiences, including a terrifying rock-throwing incident and mysterious missing time in the North Georgia Mountains.Throughout, Nona discusses the complexities of Bigfoot research, the connection between Bigfoot and other paranormal phenomena, and her balanced perspective between flesh-and-blood and high strangeness theories.The Nonna Boss YouTube ChannelGet Our FREE NewsletterGet Brian's Books Leave Us A VoicemailVisit Our WebsiteSupport Our Sponsors00:00 Welcome and Introduction 00:20 First Encounter with Bigfoot 03:43 Son's Experience and Family Investigation 06:14 Daytime Sighting and Reflection 08:08 Analyzing the Nighttime Sighting 14:32 Exploring Other Experiences 18:13 The Mysterious Wet Rocks Incident 18:51 A Chilly Hike in Coal Creek 19:51 Interactive Tree Knocking 20:40 The Wall of Fear 22:17 A Strange Encounter in North Georgia Mountains 25:33 Missing Time and UFO Theories 30:12 Reflecting on Bigfoot Experiences 31:37 Exploring the Continuum of Phenomena 34:23 The NBO YouTube ChannelBecome a supporter of this podcast: https://www.spreaker.com/podcast/sasquatch-odyssey--4839697/support.

Dr. Katie Krulisky talks with Dr. Rosemary Dray-Spira about trends in prenatal exposure to antiseizure medications over the past decade, according to medication safety profiles. Read the related article in Neurology®.  Read the related North American Antiepileptic Drug Pregnancy Registry.  Read the related Continuum article.  Disclosures can be found at Neurology.org.      

In this podcast, experts Tina Cascone, MD, PhD; Christina Baik, MD, MPH; and David Planchard, MD, PhD discuss data-driven treatment for EGFR-mutant non-small cell lung cancer.

Limb-girdle muscular dystrophies (LGMDs) encompass a group of genetically heterogeneous skeletal muscle disorders. There has been an explosion of newly identified LGMD subtypes in the past decade, and results from preclinical studies and early-stage clinical trials of genetic therapies are promising for future disease-specific treatments. In this episode, Gordon Smith, MD, FAAN, speaks with Teerin Liewluck, MD, FAAN, FANA, author of the article “Limb-Girdle Muscular Dystrophies” in the Continuum® October 2025 Muscle and Neuromuscular Junction 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. Liewluck is a professor of neurology at the Division of Neuromuscular Medicine and Muscle Pathology Laboratory at Mayo Clinic College of Medicine in Rochester, Minnesota. Additional Resources Read the article: Limb-Girdle Muscular Dystrophies Subscribe to Continuum®: shop.lww.com/Continuum Earn CME (available only to AAN members): continpub.com/AudioCME Continuum® Aloud (verbatim audio-book style recordings of articles available only to Continuum® subscribers): continpub.com/Aloud More about the American Academy of Neurology: aan.com Social Media facebook.com/continuumcme @ContinuumAAN Host: @gordonsmithMD Guest: @TLiewluck 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 Smith: This is Dr Gordon Smith with Continuum Audio. Today I'm interviewing Dr Teerin Liewluck, a good friend of mine at the Mayo Clinic, about his article on the limb girdle muscular dystrophies. This article appears in the October 2025 Continuum issue on muscle and neuromuscular junction disorders, a topic that is near and dear to my heart. Teerin, welcome to the podcast, and maybe you can introduce yourself to our listeners. Dr Liewluck: Thank you very much, Gordon, and I want to say hi to all the Continuum fans. So, I'm Dr Teerin Liewluck, I'm the professor of neurology at Mayo Clinic in Rochester, Minnesota. So, my practice focus on all aspects of muscle diseases, both acquired and genetic myopathies. Glad to be here. Dr Smith: I just had the great pleasure of seeing you at a seminar in Houston where you talked about this topic. And so, I'm really primed for this conversation, which I'm very excited about. I find this topic a little hard, and I'm hoping I can learn more from you. And I wonder if, as we get started, recognizing many of our listeners are not in practices focused purely on muscle disease, maybe you can provide some context about why this is important for folks doing general neurology or even general neuromuscular medicine? Why do they need to know about this? Dr Liewluck: Yes, certainly. So, I would say limb girdle muscular dystrophy probably the most complex category of subgroup of muscle diseases because, by itself, it includes thirty-four different subtypes, and the number's still expanding. So, each subtype is very rare. But if you group together, it really have significant number of patients, and these patients present with proximal weakness, very high CK, and these are common patients that can show up in the neurology clinic. So, I think it's very important even for general neurologists to pick up what subtle clues that may lead to the diagnosis because if we are able to provide correct diagnosis for the patients, that's very important for patient management. Dr Smith: So, I wonder if maybe we can talk a little bit about the phenotype, Terran. I mean, your article does a great job of going over the great diversity. And you know, I think many of us here, you know, limb girdle muscular dystrophy and we think of limb girdle weakness, but the phenotypic spectrum is bananas, right? Rhabdomyolysis, limb girdle distal myopathy. I mean, when should our listeners suspect LGMD? Dr Liewluck: Yes, I think by the definition to all the LGMD patients will have limb girdle of proximal weakness and very high CK. So, these are common phenotypes among thirty-four different subtypes. But if it did take into details, they have some subtle differences. In the article, what I try to simplify all these different subtypes that we can categorize at least half of them into three main group that each group the underlying defect sharing among those subtypes and also translate into similar muscles and extra muscular manifestations. You will learn that some of the limb girdle muscular dystrophy may present with rhabdomyolysis. And we typically think of this as metabolic myopathies. But if you have a rhabdomyolysis patient, the CK remain elevated even after the acute episode, that's the key that we need to think this could be LGMD. That's for an example. Dr Smith: So, I wonder if maybe we can start there. I was going to go in a different direction, but this is a good transition. It's easy to see the opportunity to get confused between LGMD or, in that case, a metabolic myopathy or other acquired myopathies. And I think particularly adult neurologists are more accustomed to seeing acquired muscle disease. Are there particular clues that, or pearls that adult neurologists seeing patients with muscle disease can use to recognize when they should be thinking about LGMD given the diverse phenotype? Dr Liewluck: Yes. What I always tell the patient is that there are more than a hundred different types of muscle diseases, but we can easily divide into groups: acquired and genetic or hereditary. So, the acquired disease is when you encounter the patients who present with acute or subacute cause of the weakness, relatively rapidly progressive. But on the opposite, if you encounter the patient who present with a much more slowly progressive cause of weakness over several months or years, you may need to think about genetic disease of the muscle with also including limb-girdle muscular dystrophy. The detailed exam to be able to distinguish between each type of muscular dystrophy. For example, if proximal weakness, certainly limb girdle muscular dystrophy. If a patient has facial weakness, scapular winking, so you would think about facial scapular hematoma dystrophy. So, the slowly progressive cause of weakness, proximal pattern of weakness, CK elevation, should be the point when you think about LGMD. Dr Smith: So, I have a question about diagnostic evaluation. I had a meeting with one of my colleagues, Qihua Fan, who's a great peripheral nerve expert, who also does neuromuscular pathology. And we were talking about how the pathology field has changed so much over the last ten years, and we're doing obviously fewer muscle biopsies. Our way of diagnosing them has changed a lot with the evolution of genetic testing. What's your diagnostic approach? Do you go right to genetic testing? Do you do targeted testing based on phenotype? What words of wisdom do you have there? Dr Liewluck: Yes, so, I mean, being a muscle pathologist myself, it is fair to say that the utility of muscle biopsies when you encounter a patient with suspects that limb girdle muscular dystrophy have reduced over the year. For example, we used to have like fifteen, seventeen hundred muscle biopsies a year; now we do only thirteen hundred biopsies a year. Yes, as you pointed out, the first step in my practice if I suspect LGMD is to go with genetic testing. And I would prefer the last gene panel that not only include the LGMD, but also include all other genetic muscle disease as well as the conjunctive myopic syndrome, because the phenotype can be somehow difficult to distinguish in certain patients. Dr Smith: So, do you ever get a muscle biopsy, Teerin? I mean you obviously do; only thirteen hundred. Holy cow, that's a lot. So, let me reframe my question. When do you get a muscle biopsy in these patients? Dr Liewluck: Muscle biopsy still is present in LGMD patients, it's just we don't use it at the first-tier diagnostic test anymore. So, we typically do it in selected cases after the genetic testing in those that came back inconclusive. As you know, you may run into the variant of unknown significance. You may use the muscle biopsy to see, is there any histopathology or abnormal protein Western blot that may further support the heterogenicity of the VUS. So, we still do it, but it typically comes after genetic testing and only in the selected cases that have inconclusive results or negative genetic testing. Dr Smith: I'd like to ask a question regarding serologic testing for autoantibodies. I refer to a really great case in your article. There are several of them, but this is a patient, a FKRP patient, who was originally thought to have dermatomyositis based on a low-titer ME2 antibody. You guys figured out the correct diagnosis. We send a lot of antibody panels out. Wonder if you have any wisdom, pearls, pitfalls, for how to interpret antibody tests in patients with chronic myopathies? We send a lot of them. And that's the sort of population where we need to be thinking about limb-girdle muscular dystrophies. It's a great case for those, which I hope is everyone who read your article in detail. What do you have to say about that? Dr Liewluck: Yes, so myositis antibodies, we already revolutionized a few of muscle diseases. I recall when I finished my fellowship thirteen years ago, so we don't really have much muscle myositis antibodies to check. But now the panel is expanded. But again, the antibodies alone cannot lead to diagnosis. You need to go back to your clinical. You need to make sure the clinical antibodies findings are matched. For example, if the key that- if the myocytes specific antibodies present only at the low positive title, it's more often to be false positive. So, you need to look carefully back in the patient, the group of phenotypes, and when in doubt we need to do muscle biopsies. Now on the opposite end, the other group of the antibody is the one for necrotizing autoimmune myopathy; or, the other name, immune-mediated necrotizing myopathy. This is the new group that we have learned only just recently that some patients may present as a typical presentation. I mean, when even thinking about the whole testing autoimmune myopathy, we think about those that present with some acute rapidly progressive weakness, maybe has history of sudden exposures. But we have some patients that present with very slowly progressive weakness like muscular dystrophies. So now in my practice, if I encounter a patient I suspect LGMD, in addition to doing genetic testing for LGMD, I also test for necrotizing doing with myopathy antibodies at the same time. And we typically get antibody back within what, a week or two, but projected testing would take a few months. Dr Smith: Yeah. And I guess maybe you could talk a little bit about pitfalls and interpretation of genetic tests, right? I think you have another case in your article, and I've certainly seen this, where a patient is misdiagnosed as having a genetic myopathy, LGMD, based on, let's say, just a misinterpretation of the genetic testing, right? So, I think we need to think of it on both sides. And I like the fact that the clinical aspects of diagnosis really are first and foremost most important. But maybe you can talk about wisdom in terms of interpretation of the genetic panel?  Dr Liewluck:Yes. So genetic testing, I think, is a complex issue, particularly for interpretation. And if you're not familiar with this, it's probably best to have your colleagues in genetics that help looking at this together. So, I think the common scenario we encounter is that in those dystrophies that are autosomal recessive, so we expect that the patient needs to have two abnormal copies of the genes to cause the disease. And if patients have only one abnormal copy, they are just a carrier. And commonly we see patients refer to us as much as dystrophy is by having only one abnormal copy. If they are a carrier, they should not have the weakness from that gene abnormality. So, this would be the principle that we really need to adhere. And if you run into those cases, then maybe you need to broaden your differential diagnosis. Dr Smith: I want to go back to the clinical phenomenology, and I've got a admission to make to you, Teerin. And I find it really hard to keep track of these disorders at, you know, thirty-four and climbing a lot of overlap, and it's hard to remember them. And I'm glad that I'm now going to have a Continuum article I can go to and look at the really great tables to sort things out. I'm curious whether you have all these top of mind? Do you have to look at the table too? And how should people who are seeing these patients organize their thoughts about it? I mean, is it important that you memorize all thirty-four plus disorders? How can you group them? What's your overall approach to that? Dr Liewluck: I need to admit that I've not memorize all twenty-four different subtypes, but I think what I triy to do even in my real-life practice is group it all together if you can. For example, I think that the biggest group of these LGMD is what we call alpha-dystroglycanopathies. So, this include already ten different subtypes of recessive LGMD. So alpha-dystroglycan is the core of the dystrophin-associated glycoprotein complex. And it's heavy glycosylated protein. So, the effect in ten different genes can affect the glycosylation or the process of adding sugar chain to this alpha-dystroglycan. And they have similar features in terms of the phenotype. They present with proximal weakness, calf pseudohypertrophy, very high CK, some may have recurrent rhabdomyolysis, and cardiac and rhythmic involvement are very common. This is one major group. Now the second group is the limb-girdle muscular dystrophy due to defective membrane repair, which includes two subtypes is the different and on dopamine five. The common feature in this group is that the weakness can be asymmetric and despite proximal weakness, they can have calf atrophy. On muscle biopsy sometimes you can see a myeloid on the muscle tissues. And the third group is the sarcoglycanopathy, which includes four different subtypes, and the presentation can look like we share. For the rest, sometimes go back to the table. Dr Smith: Thank you for that. And it prompts another question that I always wonder about. Do you have any theories about why such variability in the muscle groups that are involved? I mean, you just brought up dystroglycanopathy, for instance, as something that can cause a very distal predominant myopathy; others do not. Do we at this point now have an understanding given the better genetics that we have on this and work going on in therapeutic development, which I want to get to in a minute, that provides any insight why certain muscle groups are more affected? Dr Liewluck: Very good question, Gordon. And I would say the first question that led me interested in muscle disease---and this happened probably back in 2000 when I just finished medical school---is why, why, why? Why does muscle disease tend to affect proximal muscles? I thought by now, twenty-five years later, we'd have the answer. I don't. I think this, you don't know clearly why muscle diseases, some affect proximal, some affect distal. But the hypothesis is, and probably my personal hypothesis is, that maybe certain proteins may express more in certain muscles and that may affect different phenotypes. But, I mean, dysferlin has very good examples that can confuse us because some patients present with distal weakness, some patients present with proximal weakness, that's by the same gene defect. And in this patient, when we look at the MRI in detail, actually the patterns of fatty replacements in muscle are the same. Even patient who present clinically as a proximal or distal weakness, the imaging studies show the same finding. Bottom line, we don't know. Dr Smith: Yeah, who knew it could be so complex? Teerin, you brought up a really great point that I wanted to ask about, which is muscle MRI scan, right? We're now seeing studies that are doing very broad MR imaging. Do you use some muscle MRI very frequently in your clinical evaluation of these patients? And if so, how? Dr Liewluck: Maybe I don't use it as much as I could, but the most common scenario I use in this setting is when I have the genetic testing come back with the VUS. So, we look at each VUS, each gene in detail. And if anything is suspicious, what I do typically go back to the literature to see if that gene defect in particular has any common pattern of muscle involvement on the MRI. And if there is, I use MRI as one of the two to try to see if I can escalate the pathogenicity of that VUS. Dr Smith: And a VUS is a “Variant of Unknown Significance,” for our listeners. I'm proud that I remember that as a geneticist. These are exciting times in neurology in general, but particularly in an inherited muscle disease. And we're seeing a lot of therapeutic development, a lot going on in Duchenne now. What's the latest in terms of disease-modifying therapeutics and gene therapies in LGMD? Dr Liewluck: Yes. So, there are several precritical and early-phase critical trials for gene therapy for the common lymphoma of muscular dystrophies. For example, the sarcoglycanopathies, and they also have some biochemical therapy that arepossible for the LGMD to FKRP. But there are many things that I expect probably will come into the picture broader or later phase of critical tryouts, and hopefully we have something to offer for the patients similar to patients with Duchenne muscular dystrophy. Dr Smith: What haven't we talked about, I mean, holy cow? There's so much in your article. What's one thing we haven't talked about that our listeners need to hear? Dr Liewluck: Good questions. So, I think we covered all, but often we get patients with proximal weakness and high CK, and they all got labeled as having limb-girdlemuscular dystrophy. What I want to stress is that proximal weakness and high CK is a common feature for muscle diseases, so they need to think broad, need to think about all possibilities. Particularly don't want to miss something treatable. Chronic, slowly progressive cause, as I mentioned earlier, we think more about muscle dystrophy, but at the cranial range, we know that rare patients with necrotic autonomyopathy and present with limb good of weakness at a slowly progressive cost. So, make sure you think about these two when suspecting that LGMD patient diabetic testing has come back inconclusive. Dr Smith: Well, that's very helpful. And fortunately, there's several other articles in this issue of Continuum that help people think through this issue more broadly. Teerin, you certainly don't disappoint. I enjoyed listening to you about a month ago, and I enjoyed reading your article a great deal and enjoy talking to you even more. Thank you very much. Dr Liewluck: Thank you very much, Gordon. Dr Smith: Again, today I've been interviewing Dr Teerin Liewluck about his article on limb-girdle muscular dystrophy, which appears in the October 2025 Continuum issue on muscle and neuromuscular junction disorders. Please be sure to check out Continuum Audio episodes for this and other issues. And thanks to our listeners for joining today. Dr Monteith: This is Dr Teshamae Monteith, Associate Editor of Continuum Audio. If you've enjoyed this episode, you'll love the journal, which is full of in-depth and clinically relevant information important for neurology practitioners. Use the link in the episode notes to learn more and subscribe. AAN members, you can get CME for listening to this interview by completing the evaluation at continpub.com/audioCME. Thank you for listening to Continuum Audio.

In this episode, Adam interviews the researcher behind SecretMilitaryTechnology.com — a digital investigator using custom AI systems to uncover the hidden connections between plasma physics, classified propulsion programs, and black-budget funding networks.Through advanced open-source intelligence (OSINT) and AI-driven analysis, he has mapped a stunning continuity of research — from the 1977 Los Alamos thermonuclear experiments to Boeing's alleged Compact Fusion Reactor (CFR) tests, and even to Jeffrey Epstein's strange intersection with frontier physics.We walk through four core documents from his site:Epstein, Plasma Physics Nexus Analysis — how Epstein's “Confronting Gravity” workshop may have linked plasma and fusion experts.Boeing CFR Orb Test Analysis — evidence of classified plasma containment systems hidden within Next Generation Air Dominance (NGAD).1977 Los Alamos Controlled Thermonuclear Research Report — a Cold War rootline for today's fusion-propulsion experiments.CIA P2 Memo — how compartmentalized funding channels keep advanced physics hidden under intelligence cover.Together, these form a picture of a continuing plasma research lineage—one that may have evolved into today's secret propulsion programs and UAP encounters.At the end, we also discuss the controversy with Ashton Forbes, the importance of open peer review, and how AI itself might become the ultimate disclosure tool.Explore the documents: SecretMilitaryTechnology.comFollow on X: https://x.com/MilitarySolved

“It started out by doing a kind of a white paper that we called Imperatives for Quality Cancer Care. Ellen Stovall, our CEO [of the National Coalition for Cancer Survivorship] at the time, gave this report to Dr. Richard Klausner, who was the head of National Cancer Institute at the time. He called Ellen immediately and said, ‘Why are we not doing something about this?' Within one year, we had the Office of Cancer Survivorship at NCI,” ONS member Susan Leigh, BSN, RN, told ONS member Ruth Van Gerpen, MS, RN-BC, APRN-CNS, AOCNS®, PMGT-BC, member of the ONS 50th anniversary committee, during a conversation about her involvement in cancer survivorship advocacy. Van Gerpen also spoke with ONS members Deborah Mayer, PhD, RN, AOCN®, FAAN, and Timiya S. Nolan, PhD, APRN-CNP, ANP-BC, about the history and future of cancer survivorship. 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: Episode 201: Which Survivorship Care Model Is Right for Your Patient? Episode 91: The Seasons of Survivorship Episode 49: The Cancer Survivorship Conundrum ONS Voice article: Our Unified Voices Can Improve Cancer Survivorship Care ONS book: Oncology Nurse Navigation: Delivering Patient-Centered Care Across the Continuum (third edition) ONS course: Essentials in Survivorship Care for the Advanced Practice Provider Clinical Journal of Oncology Nursing articles: Incorporating Nurse Navigation to Improve Cancer Survivorship Care Plan Delivery Survivorship Care: More Than Checking a Box The Missing Piece of Survivorship: Cancer Prevention Oncology Nursing Forum articles: Patient Perceptions of Survivorship Care Plans: A Mixed-Methods Evaluation Survivorship Care Plans: Health Actions Taken and Satisfaction After Use ONS Survivorship Learning Library Rehabilitation of People With Cancer: Position Statement from the Association of Rehabilitation Nurses (ARN) and endorsed by the Oncology Nursing Society Connie Henke Yarbro Oncology Nursing History Center American Cancer Society Survivorship resources Cancer Survivors Network Cancer Nation (formerly National Coalition for Cancer Survivorship) Cancer Survival Toolbox Imperatives for Quality Cancer Care: Access, Advocacy, Action, and Accountability (white paper) National Cancer Survivors Day Foundation New England Journal of Medicine article: Seasons of Survival: Reflections of a Physician With Cancer by Fitzhugh Mullan 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 Leigh: “Another way that [National Coalition of Cancer Survivorship] got very involved with looking at how we keep this information coming and how we really share care with our outside physicians is the development of survivorship care plans. And then we also hoped that we would see more survivorship clinics by now. But between trying to get people to develop care plans and clinics, it's been like pulling teeth. It has been very difficult. And a lot of this struggle to get this going has been, first of all, there isn't enough money to do this. There isn't enough time for immediate staff to take these on, and we just don't have enough staff as it is now. And survivorship is not a moneymaker, so it's just something that has to be done kind of on the side.” TS 11:54 Mayer: “When I became ONS president in the '80s—I was the fourth ONS president—we were given a cancer grant to do something with our presidency. And that was when I really wanted to bring attention to rehabilitation as a means to address cancer survivorship issues because we had a very ‘treat 'em and street 'em' attitude. We gave you your treatment, and we sent you home, and you had to figure out the rest. And there wasn't a lot of knowledge or support to help you put your life back together again afterwards. And so in that process, it was an interdisciplinary group of professionals that tried to come up with what was an appropriate position statement because ONS was just starting to do position statements. And so we developed a first position statement on cancer rehabilitation to address survivorship issues in like 1987 to '89.” TS 17:15 Mayer: “When I went back to school for my PhD, I did my dissertation on health behaviors of cancer survivors and realizing the huge gap in the care that they were getting for anything other than their cancer. We were still focused on their tumor and on treating their tumor. But we were missing the picture that if the cancer didn't kill them, their heart disease would, and they would develop diabetes and other things. … But as people started living longer and longer, we were missing all these other chronic illnesses that would contribute to their quality of life and overall lifespan. So my dissertation put me on a different path, and I think the second part of my career was really focusing on instead of just relieving suffering and the quality of life issues, really looking at cancer care delivery and how we could do a better job of doing the team of teams that people needed to have their issues addressed.” TS 19:34 Nolan: “I ended up having my first permanent role on a hematology-oncology unit at the University of Alabama at Birmingham. And there, I literally saw patients who were fighting for their lives. And despite the severity of their illness, they wanted more than just survival. They wanted to have meaning. They wanted to have dignity. They wanted to have impact with the time that they had left, whatever it was. And so those experiences planted a seed in me. And that seed was that cancer care must extend beyond treatment and we need to embrace, really, quality of life.” TS 23:31 Leigh: “I was not the researcher. I was not the major writer. I was not the identifier of a lot of the risk factors. But I spread the seed. I took all that information from different sources and shared that with all of the audiences that I spoke to. So I was called a seed spreader, kind of the Johnny Appleseed of oncology nursing at that particular time. And then once we saw academia step in and say, ‘We need to get good data about what's going on here,' … then my stories and stories from survivors started decreasing and the presentations were given more from the academic standpoint.” TS 34:41 Nolan: “I really believe in community, academic, government, and industry approaches to survivorship as well. We can no longer operate in silos. We really need to learn how to walk across the aisle, build bridges as we can so that we can do this work together because we know that communities bring lived wisdom and context. And academicians bring the research and the ability to create the evidence. The government brings policy and public health infrastructure, and certainly industry brings innovation and scalability. But also in this new paradigm that we find ourselves in, the industry may also bring the dollars to be able to help us to do even more work.” TS 43:45

Send us a text with your feedback from this session! Session 158 (World Congress - Dublin): Human Performance and Manual Therapy: A ContinuumMichael Higgins sits down to discuss the continuum of human performance and what the World Congress event is all about: learning, sharing and connecting. Michael is the Athletic Training Program Director at the University of Virginia. His two interactive workshops at WC 13 are: "Optimizing Squat Mechanics for Rehabilitation Success" and "Thoracic Manual Therapy for Neck and Shoulder Pain". 

Facioscapulohumeral muscular dystrophy (FSHD) is one of the most common forms of muscular dystrophy, affecting individuals across the lifespan with variable severity. Advances in genetic understanding and therapeutic development have led to an era of promising disease-modifying strategies. In this episode, Katie Grouse, MD FAAN, speaks with Renatta N. Knox, MD, PhD, author of the article “Facioscapulohumeral Muscular Dystrophy” in the Continuum® October 2025 Muscle and Neuromuscular Junction 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. Knox is an assistant professor of neurology in the Division of Pediatric Neurology and Neuromuscular Section at Washington University School of Medicine in St. Louis, Missouri. Additional Resources Read the article: Facioscapulohumeral Muscular Dystrophy 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 Renatta Knox about her article on fascioscapulohumeral muscular dystrophy, which appears in the October 2025 Continuum issue on muscle and neuromuscular junction disorders. Welcome to the podcast, and please introduce yourself to our audience. Dr Knox: Hi Katie, thank you so much for the invitation for the audio interview. I'm looking forward to our conversation. As she mentioned, my name is Renata Knox. It's a pleasure to be here today. Dr Grouse: I'd like to start by asking, what is the key message that you hope your readers will take from your article? Dr Knox: I would say two things. The first is an appreciation and understanding of the unique genetic mechanism that leads to FSHD. And the second is the really exciting therapy landscape that we find ourselves in. So, we're hopeful that there will actually be disease-modifying therapies for FSHD soon. Dr Grouse: We're really looking forward to learning more about that. Now, before we get to that piece, could you just remind us of the clinical manifestations and features that are specific to FSHD? Dr Knox: So, one of the most unique things about FSHD that we see clinically is the pattern of weakness. So, one of the first features is that it's asymmetric. And then there are certain muscle groups that typically are affected, and that's partly where the name comes from. So, we see effects in the face, the limbs, the trunk; and so, those are some of the unique features that we see clinically. Dr Grouse: I'd love it if you could walk us through how you approach diagnosing a patient who presents with proximal weakness where FSHD is in your differential. Dr Knox: Yeah, it's a really great question. So, I would say it depends. So, I actually focus on FSHD in my clinical practice. So, many times patients are referred to me because there's a very high suspicion or there's a known family history of FSHD. So, that's one category of cases. I would say the other category of case is where it's, as you said, maybe more proximal weakness more broadly. Someone that's before me who has a known family history, they really have some of the characteristic physical features---which I'm pretty attuned to, as this is, you know, part of my subspecialty---I'll actually go directly to FSHD genetic testing. And that is one of the unique features of this disease, that the next-generation sequencing panels that are typically used for some of our other muscle diseases, FSHD is not captured on those. So, we actually have to send targeted testing for FSHD to diagnose it. So, that is one category where, again, I have a very high suspicion either based on their clinical presentation and/or a known family history, then I will actually go directly to FSHD-targeted genetic testing. In the second case, where it is one of the conditions that I'm considering among others, I will do more broad testing. So, I will get a CK level to see if there's evidence of muscle breakdown. I'll likely also do one of the next-generation sequencing panels that we have access to, which will allow us to identify, potentially, one to two hundred potential muscle diseases. And then again, if FSHD is higher on my differential in that second group of patients, then I will also send targeted FSHD-specific testing. Dr Grouse: That's really helpful. And I'm wondering if you have any thoughts about common pitfalls that you've seen when providers are trying to work this up? Dr Knox: I don't know if I would say pitfalls. I think I would acknowledge that it's challenging. My subspecialty training in neuromuscular medicine and also gene therapy. And so FSHD is pretty high on my radar. But I would say in neurology in general---and then, you know, the general medical population---,it really isn't something that many people are seeing. So, I would say what patients will communicate to us sometimes is some frustration that maybe it took time to make the diagnosis, but I just have a deep understanding that it's not something that is on many people's radars. And I think, again, it's tricky because it's not picked up on these next-generation sequencing panels, which many of us can send pretty easily. It will be missed. And I will say the biggest pitfall is, again, if you're not thinking about it and you don't send that testing, you actually- it's very difficult to diagnose it. Dr Grouse: Thank you so much for highlighting that. I think there are many people who are not aware that those different panels really aren't picking that up and that they have to test specifically. So, I think that's a great thing for all of us to keep in mind. Are there any tips or tricks to the diagnosis, other than the genetic issues that you mentioned, that sometimes can really bring this diagnosis to the forefront? Dr Knox: I think things that really tip me off to having a higher suspicion for FSHD is facial weakness that we can detect on our exam. Scapular winging---again, there's a small subset of disorders which can impact that. Someone who's presenting with foot drop, you know, with facial weakness, I think definitely about FSHD more. Also, clinically, kind of the presentation or things that they're beginning to have difficulty with is a tip-off. So, if someone is an athlete, like, they're a volleyball player or basketball player and they say, oh, I'm having difficulties, you know, with movements that require them to elevate their arm, which can be a sign of the shoulder weakness that we classically see. Or someone who says, oh, I'm having a harder time shampooing my hair or combing my hair. So those can be tip-offs again, which are basically referencing the type of weakness that they have. Another feature of FSHD which isn't necessarily as broadly appreciated is that pain and fatigue are very common. So, if someone is coming in and saying, actually, I also have a significant amount of fatigue as well or a lot of pain, that's something that can tip me off to it. Hearing loss is something that we can also see in up to 20% of patients with FSHD. So, if they are having those symptoms or saying they're ringing in their ears, these are some things that will make me begin to think about it more. Dr Grouse: Oh, really helpful. I also found it really fascinating reading some of the very FSHD-specific clinical signs, some interesting- some diagrams and pictures as well, that are very specific to the pattern of weakness that develops in FSHD. So, I encourage our listeners to check that out. But are there any highlights from those little clinical pearls that you'd like to point out? Dr Knox: I think the poly-hill sign---so, these are these literal hills that we can see in the shoulders of patients with FSHD---is pretty classic. Popeye arms, which is this older term that we still use that has to do with which muscle groups are preserved versus those that have atrophy. So that's a common feature. And then I would say, really, the asymmetry is something that is a unique feature in FSHD. And again, we did our best to provide good representative images. So again, as you mentioned, Katie, I would really encourage people to look at those images and then think about cases that they may have seen and how similar they are so they can begin to recognize those signs as well. Dr Grouse: Now going back to the genetic topic, the complex genetic underpinnings of FSHD are really well-explained in your article; and again, worth taking a look at to remind ourselves of everything that's of that pathology. Now, I was wondering though, if you could give us a brief overview of how we should approach genetic testing in a suspected case of FSHD? You mentioned some specific panels, but it does sound like there's some more complexity to it as well. Dr Knox: Yes, and I'll just kind of briefly explain that complexity. Part of the thing that we're detecting in the genetic testing is the repeat number. And so, we're actually looking for a contraction in a repeat number. So, not an expansion, which were typical for some of the diseases that we think about, the trinucleotide repeat disorders. And this is why it's not captured in the next-generation sequencing panels, because they do not currently have the ability to do that. And so, again, what the type of testing that I do really depends on my suspicion. So again, if my suspicion is very high for FSHD---they have a family history, they have the classic features---then I will actually go directly to an FSHD-specific testing, which is available from various sources. If, again, it's among different things that I'm thinking about, I will get a CK lab. I typically will also send a next-generation sequencing panel specific for muscle diseases, perhaps muscular dystrophy; again, depending on what I'm thinking about. And then I will also send in a specific FSHD genetic test as well. People are beginning to use whole-genome sequencing, which is capturing some of our true nucleotide repeat disorders and becoming more comprehensive. So, my hope is that as that becomes more standard of care---like, whole-exome sequencing can be gotten pretty routinely now---that it may be easier for us to make some of these diagnoses. Dr Grouse: Well, that's really helpful, and thanks for that overview. Now another thing that you mentioned that I thought was really interesting in your article was that patients with, you know, history of FSHD, perhaps in the family, who are pregnant and want to screen for this disease would not be able to use sort of the more common screening tests like cell-free DNA testing and may have to go to other means to do that. What is generally their route to this type of testing? Dr Knox: Yeah, great question, and really important question for family planning purposes, and it definitely comes up in clinical practice. And so again, because of the unique genetics of FSHD, you actually have to do invasive genetic testing currently to be able to test it. And so that's, you know, amnio or chorio, and then send it to a lab that can perform, again, FSHD-specific testing on the samples that are presented. And there are obviously labs that are capable of doing that and centers that are capable of doing that, but it is not picked up on the cell-free DNA panels that are being very routinely used. You or your provider has to be thinking about it to send that specific testing, similar to our patients that come into clinic and have not yet been diagnosed. Dr Grouse: Once you have the diagnosis, what are our options for therapy? I think it sounds like at this current time, it looks to be mostly supportive. What are some of the supportive care options we should keep in mind? Dr Knox: Yes, so that is definitely accurate. Care today is supportive, but again, we're very excited about the clinical trial and therapy landscape for FSHD. So, I work very closely with my physical therapy colleagues that are in clinic with me. So, we work very closely with physical and occupational therapists to help with supportive measures, adaptive measures, doing assessments, helping our patients to be able to move and exercise safely and effectively. As I mentioned, pain is very common in FSHD and so we can treat that with medications. The most common medication that we use to treat for pain in FSHD are NSAIDs. And then other than that it's really, you know, supportive measures. Do they need to see other subspecialists? There are some surgical options. Those are used very rarely to help with some of the scapular weakness, but typically it's physical therapy, occupational therapy, supportive devices. We treat the pain as we're able to, and then we work with other subspecialists to screen, monitor and support our patients to the best of our ability. Dr Grouse: Well, without further ado, I'd love to hear more about what's coming down the pipeline in clinical trials. What can we look forward to seeing, hopefully, in future years to treat these patients? Dr Knox: Yes. And so, this is actually what got me interested in the neuromuscle space in general is that, because we now for many years have known the genetic cause of many of these disorders as well as some of the underlying mechanisms, we can actually use advances in therapeutics to do what we call targeted therapies. So, rather than treating symptoms or indirect methods or doing kind of broad drug screens---which, again, still do take place and still do have their place---we actually can target mechanisms directly. And so, we know that the underlying biology of FSHD is due to this protein called DUX4 being expressed when it should not be. So, it's what we call a toxic gain of function. And so, the targeted way to address this is to suppress DUX4 expression. And so, kind of broadly speaking, what we're really excited about are a couple of products that are currently in clinical trials right now that actually caused DUX4 suppression to be suppressed. And again, these are targeted pathways. And so, again, the hope is that by doing that, we can hopefully slow the progression of the disease, potentially stop progression of the disease, and potentially reverse. Again, we don't know if that might be possible, but that is one of the hopes. Dr Grouse: Well, that's really exciting, and I know we're all looking forward to more coming down the pipeline soon, and hopefully more things that can really offer some exciting treatments for our patients with this condition. Now, a little more deep-dive into our patients who are diagnosed. You've reviewed some of the treatments currently available and hopefully may someday soon be available. Are there other things that we should be keeping in mind in this population? For instance, screenings that we should be doing for other extramuscular manifestations that we need to be thinking about? Dr Knox: I will answer that question two ways. I think something that's very important to acknowledge is the impact that these diagnoses and these conditions have on our patient practically, psychologically. One of the other unique features of FSHD is, it's autosomal-dominant. So, if it is in a family, you can have many family members who are affected, but the variability is very high. And so, you can have in the same family someone who is wheelchair-dependent, and someone else in the family with the same underlying genetics who has no signs or symptoms or is very mildly affected. And that is something that is definitely challenging for our families and patients to navigate if they're very different than their family members with the same condition. And just navigating the world with a condition that, you know, can be physically debilitating and cause changes to what they're able to do or not able to do, progression is something that's very difficult to handle. So, I think that's one set of things. And we try our best, you know, with my team and my other colleagues in the space, to support our families and patients in the best way that we can. Secondly, there is very important screening that needs to be done for this condition. So, one of the things- and the current guidelines which are actually being updated, the last update was in 2015 is all patients that undergo pulmonary function testing or PFTs. And so that's something we do at baseline and we do at least annually in my practice. Young kids who are presenting very early or patients with certain genetics that we know are more predisposed to extra muscular manifestations, we recommend screening for hearing, which is one of the manifestations, and ophthalmologic exam to look for retinovascular changes, which is one of the manifestations as well. Those are the more common ones that are typically done. There's also some evidence in pediatric patients with very severe manifestations that there may be some cognitive impacts, learning impacts. And so, that is something we're also thinking about screening and supporting our patients in that way. And again, we typically work with these patients in a multidisciplinary team depending on what manifestations and the degrees to which they're impacted by the disorder. Dr Grouse: Thank you so much for that answer. I think a lot of us forget sometimes when we get really focused on what can we do now, that we forget to kind of stop and reflect on sort of the more holistic approach. How is this affecting the patient? How is this affecting the patient's family dynamic, and what other ways are they going through life with this condition that we need to be thinking about? So, I appreciate you bringing that up. I wanted to ask, sort of based on what you're talking about and what you mentioned already, you happened to mention that what initially drew you that to this work was your interest in some of the really exciting breakthroughs in the field. Well, was there anything else that drew you to, specifically, congenital neuromuscular diseases, and FSHD in particular? Dr Knox: I'm a physician scientist by training, and so I would describe myself also as a molecular biologist. So, I love getting into the nitty gritties of disease mechanisms, what genes are doing in bodies, how they function. And so, as I mentioned earlier, in the neuromuscle space, we've known for many years the genetic cause of many of these disorders and have done great, you know, mechanistic work to kind of define why we see the disease. And then now we're at this intersection of that knowledge marrying with these really novel therapeutic approaches, gene therapy approaches, being able to intersect and then in very creative ways actually target diseases very directly. And so, I would say it really is the combination of those two things. FSHD has a really fascinating unique biology, which again, we encourage everyone to read about more in the article. That really drew me to it. I'm very interested in gene regulation, transcription. This is one of the underlying mechanisms that is gone awry in the disorder, and then that being married to advances in therapeutics. So, you could wed those two pieces of information and actually meaningfully impact patient 's lives. And again, that's the real privilege and honor to witness is how these therapies can transform lives. And I saw it happened with this one case for this one disorder when I was a resident where there was no treatment. Young children, unfortunately, would not survive the disease. And then I saw the therapy come be in development and literally change the trajectory. And this is what we're very hopeful for in the FSHD space, that wedding, this wonderful basic science research, translational research, companies working together to develop these therapies that can transform lives. It is just so beautiful to witness and see, and it's something that I get to do. You know, it's a part of my job, so it's a real privilege. Dr Grouse: Well, I have to say, it's really inspiring hearing you talk about it. And I imagine that many neurologists-in-training who are listening to this may be inspired as well and may be convinced to go into this field for that very reason. So, thank you so much for sharing all of this information with us today. I learned a lot, and I think all of our listeners have too. Dr Knox: Thank you. It's really been a pleasure. Dr Grouse: Again, today I've been interviewing Dr Renatta Knox about her article on fascioscapulohumeral muscular dystrophy, which appears in the October 2025 Continuum issue on muscle and neuromuscular junction 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.

This episode is a very special one because, thanks to one of my guests, we are going to hear from somebody who I assumed I had missed my chance of getting to appear on this podcast. Let me explain. Tony Ursano of Insurance Advisory Partners is someone I have interviewed many times over the past 20 years. In fact I first met Tony when he was working at Willis during the thirteen-year reign of our second guest. Tony has recently executed quite a coup – that's because he has managed to convince industry legend and former Willis CEO Joe Plumeri to come and work with him at Insurance Advisory Partners. I'll let Joe and Tony do the talking, but I'll just say you are in for a treat. Many of us in the insurance industry, particularly when we get to a certain age, tend to get nostalgic about an unspecified past era when there were so many more strong characters working in the sector than there are now and then we complain that these days things aren't quite the same. Well, Joe Plumeri is exactly the kind of person that people my age tend to think of when they make that complaint Of course Joe is a senior executive with a glittering multi-decade career, spanning a broad spectrum of financial services, but he is also a complete original and a natural speaker and great motivator. One of his strongest skills is the ability to express often very complex ideas in simple terms that large numbers of people can quickly comprehend and get behind. He is always original and he is always direct. There are no grey areas. This discussion examines the prospects for M&A and consolidation all the way through the insurance value chain, from carriers of all sizes and specialisms to mega brokers, MGAs and even hybrid carriers. You'll leave this discussion incredibly well informed and in no doubt what Tony and Joe think are going to happen – but there'll be a little bit extra – you will have met an industry legend and heard his unique perspective along the way. LINKS: We thank our naming sponsor AdvantageGo: https://www.advantagego.com

In this episode of The Founder Spirit, Krista Kim, an ultra-contemporary artist known for her work exploring the concept of digital consciousness, shares her journey of exploring the intersection of art, technology, and meditation. Krista shares her pioneering approach to digital consciousness, emphasizing how art can serve as a meditative experience that fosters harmony between humanity and technology. She also discusses the profound impact of meditation on her creative process, illustrating how it fuels her artistic vision and innovation. Through her work, such as the Continuum project, Krista advocates for the role of artists in shaping digital culture and promoting mental wellness. How does Krista harness the power of consciousness with technology to create healing and sublime experiences in the metaverse? TUNE IN to this conversation & find out. Don't forget to subscribe and support us on Patreon!For detailed transcript and show notes, please visit TheFounderSpirit.com.Also follow us on: - LinkedIn: https://www.linkedin.com/company/TheFounderSpirit- Instagram:  https://www.instagram.com/TheFounderSpirit- YouTube:  https://www.youtube.com/@TheFounderSpirit- Facebook:  https://www.facebook.com/TheFounderSpirit- X:  https://twitter.com/founder_spiritIf this podcast has been beneficial or valuable to you, feel free to become a patron and support us on Patreon.com, that is P-A-T-R-E-O-N.com/TheFounderSpirit.As always, you can find us on Apple, YouTube and Spotify, as well as social media and our website at TheFounderSpirit.com.The Founder Spirit podcast is proud to be a partner of the Villars Institute, a non-profit foundation focused on accelerating the transition to a net-zero economy and restoring planetary health.About This Podcast:Whether you are an entrepreneur, a mid-career professional or someone who's just starting out in life, The Founder Spirit podcast is for you!In this podcast series, we'll be interviewing exceptional individuals from all over the world with the founder spirit, ranging from social entrepreneurs, tech founders, to philanthropists, elite athletes, and more. Together, we'll uncover not only how they manage to succeed in face of multiple challenges, but also who they are as people and their human story.So TUNE IN & be inspired by stories from their life journey!

In this episode, Rabbi Joshua checks in on day 9 of the government shutdown to highlight how this will potentially begin to affect the most vulnerable in our country, and how the current budget proposal includes sweeping cuts to the Continuum of Care funding for housing. In addition, he shares some thoughts from recent books on homelessness and poverty, including a clip from scholar Matthew Desmond. Listen and share!National Alliance to End HomelessnessMatthew Desmond on The Jon Stewart ShowClosing music: Eric Claptonhttps://friendsindeedpas.org

Funeral industry updates include Texas legal rulings, a new Before I Die Festival, and growing collaboration in end-of-life care. Click here for complete show notes.  

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.

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 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

While genetic testing has replaced muscle biopsy in the diagnosis of many genetic myopathies, clinical assessment and the integration of clinical and laboratory findings remain key elements for the diagnosis and treatment of muscle diseases. In this episode, Casey Albin, MD, speaks with Margherita Milone, MD, PhD, FAAN, FANA, author of the article “A Pattern Recognition Approach to Myopathy” in the Continuum® October 2025 Muscle and Neuromuscular Junction 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. Milone is a professor of neurology and the director of the Muscle Pathology Laboratory at Mayo Clinic College of Medicine and Science in Rochester, Minnesota. Additional Resources Read the article: A Pattern Recognition Approach to Myopathy 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, this is Dr Casey Albin. Today I'm interviewing Dr Margherita Milone on her article on a pattern recognition approach to myopathy, which appears in the October 2025 Continuum issue on muscle and neuromuscular junction disorders. Welcome to the podcast, Dr Milone. Thank you so much for joining us. I'll start off by having you introduce yourself to our listeners. Dr Milone: Hello Casey, thank you so much for this interview and for bringing the attention to the article on muscle diseases. So, I'm Margherita Milone. I'm one of the neuromuscular neurologists at Mayo Clinic in Rochester. I have been interested in muscle disorders since I was a neurology resident many years ago. Muscle diseases are the focus of my clinical practice and research interest. Dr Albin: Wonderful. Thank you so much. When I think about myopathies, I generally tend to think of three large buckets: the genetic myopathy, the inflammatory myopathies, and then the necrotizing myopathies. Is that a reasonable approach to conceptualizing these myopathies? Dr Milone: Yeah, the ideology of the myopathies can be quite broad. And yes, we have a large group of genetic muscle diseases, which are the most common. And then we have immune-mediated muscle diseases, which include inflammatory myopathies as well as some form of necrotizing myopathies. Then we have some metabolic myopathies, which could be acquired or could be genetic. And then there are muscle diseases that are due to toxins as well as to infection. Dr Albin: Wow. So, lots of different etiologies. And that really struck me about your article, is that these can present in really heterogeneous ways, and some of them don't really read the rule book. So, we have to have a really high level of suspicion, for someone who's coming in with weakness, to remember to think about a myopathy. One of the things that I like to do is try to take us through a little bit of a case to sort of walk us through how you would approach if someone comes in. So, let's say you get, you know, a forty-year-old woman, and she's presenting with several months of progressive weakness. And she says that even recently she's noted just a little bit of difficulty swallowing. It feels to her like things are getting stuck. What are some of the things when you are approaching the history that would help you tease this to a myopathy instead of so many other things that can cause a patient to be weak? Dr Milone: Yes. So, as you mentioned, people who have a muscle disease have the muscle weakness often, but the muscle weakness is not just specific for a muscle disease. Because you can have a mass weakness in somebody who has a neurogenic paralysis. The problem with diagnosis of muscle diseases is that patients with these disorders have a limited number of symptom and sign that does not match the large heterogeneity of the etiology. So, in someone who has weakness, that weakness could represent a muscle disease, could represent an anterior horn cell disease, could represent a defect of neuromuscular junction. The clinical history of weakness is not sufficient by itself to make you think about a muscle disease. You have to keep that in the differential diagnosis. But your examination will help in corroborating your suspicion of a muscle disease. Let's say if you have a patient, the patient that you described, with six months' history of progressive weakness, dysphagia, and that patient has normal reflexes, and the patient has no clinical evidence for muscle fatigability and no sensory loss, then the probability that that patient has a myopathy increases. Dr Albin: Ah, that's really helpful. I'm hearing a lot of it is actually the lack of other findings. In some ways it's asking, you know, have you experienced numbness and tingling? And if not, that's sort of eliminating that this might not be a neuropathy problem. And then again, that fatigability- obviously fatigability is not specific to a neuromuscular junction, but knowing that is a hallmark of myasthenia, the most common of neuromuscular disorders. Getting that off the table helps you say, okay, well, it's not a neuromuscular junction problem, perhaps. Now we have to think more about, is this a muscle problem itself? Are there any patterns that the patients describe? I have difficulty getting up from a chair, or I have difficulty brushing my hair. When I think of myopathies, I historically have thought of, sort of, more proximal weakness. Is that always true, or not so much? Dr Milone: Yeah. So, there are muscle diseases that involve predominantly proximal weakness. For example, the patient you mentioned earlier could have, for example, an autoimmune muscle disease, a necrotizing autoimmune myopathy; could have, perhaps, dermatomyositis if there are skin changes. But a patient with muscle disease can also present with a different pattern of weakness. So, myopathies can lead to this weakness, and foot drop myopathies can cause- can manifest with the weakness of the calf muscles. So, you may have a patient presenting to the clinic who has no the inability to stand on tiptoes, or you may have a patient who has just facial weakness, who has noted the difficulty sealing their lips on the glasses when they drink and experiencing some drooling in that setting, plus some hand weakness. So, the muscle involved in muscle diseases can vary depending on the underlying cause of the muscle disease. Dr Albin: That's really helpful. So, it really is really keeping an open mind and looking for some supporting features, whether it's bulbar involvement, extraocular eye muscle involvement; looking, you know, is it proximal, is it distal? And then remembering that any of those patterns can also be a muscle problem, even if sometimes we think of distal being more neuropathy and proximal myopathy. Really, there's a host of ranges for this. I really took that away from your article. This is, unfortunately, not just a neat way to box these. We really have to have that broad differential. Let me ask another question about your history. How often do you find that patients complain of, sort of, muscular cramping or muscle pain? And does that help you in terms of deciding what type of myopathy they may have? Dr Milone: Many patients with muscle disease have muscle pain. The muscle pain could signal a presence of inflammation in skeletal muscle, could be the result of overuse from a muscle that is not functioning normally. People who have myotonia experience muscle stiffness and muscle pain. Patients who have a metabolic myopathy usually have exercise-induced muscle pain. But, as we know, muscle pain is also very nonspecific, so we have to try to find out from the patient in what setting the pain specifically occurs. Dr Albin: That's really helpful. So, it's asking a little bit more details about the type of cramping that they have, the type of pain they may be experiencing, to help you refine that differential. Similarly, one of the things that I historically have always associated with myopathies is an elevation in the CK, or the creatinine kinase. How sensitive and specific is that, and how do you as the expert sort of take into account, you know, what their CK may be? Dr Milone: So, this is a very good point. And the elevation of creatine kinase can provide a clue that the patient has a muscle disease, but it is nonspecific for muscle disease because we know that elevation of creatine kinase can occur in the setting of a neurogenic process. For example, we can see elevation of the creatine kinase in patients who have ALS or in patients who have spinal muscular atrophy. And in these patients---for example, those with spinal muscular atrophy---the CK elevation can be also of significantly elevated up to a couple of thousand. Conversely, we can have muscle diseases where the CK elevation does not occur. Examples of these are some genetic muscle disease, but also some acquired muscle diseases. If we think of, for example, cases where inflammation in the muscle occurs in between muscle fibers, more in the interstitium of the muscle, that disease may not lead to significant elevation of the CK. Dr Albin: That's super helpful. So, I'm hearing you say CK may be helpful, but it's neither completely sensitive nor completely specific when we're thinking about myopathic disorders. Dr Milone: You are correct. Dr Albin: Great. So, coming back to our patients, you know, she says that she has this dysphasia. How do bulbar involvement or extraocular eye movement involvement, how do those help narrow your differential? And what sort of disorders are you thinking of for patients who may have that bulbar or extraocular muscle involvement? Dr Milone: Regarding dysphagia, that can occur in the setting of acquired myopathies relatively frequent; for example, in inclusion body myositis or in other forms of inflammatory myopathy. Your patient, I believe, was in their forties, so it's a little bit too young for inclusion body myositis. Involvement of the extraocular muscles is usually much more common in genetic muscle diseases and much less frequent in hereditary muscle disease. So, if there is involvement of the extraocular muscles, and if there is a dysphagia, and if there is a proximal weakness, you may think about oculopharyngeal muscular dystrophy, for example. But obviously, in a patient who has only six months of history, we have to pay attention of the degree of weakness the patient has developed since the symptom onset. Because if the degree of weakness is mild, yes, it could still be a genetic or could be an acquired disease. But if we have a patient who, in six months, from being normal became unable to climb stairs, then we worry much more about an acquired muscle disease. Dr Albin: That's really helpful. So, the time force of this is really important. And when you're trying to think about, do I put this in sort of a hereditary form of muscle disease, thinking more of an indolent core, something that's going to be slowly progressive versus one of those inflammatory or necrotizing pathologies, that's going to be a much more quick onset, rapidly progressive, Do I have that right? Dr Milone: In general, the statement is correct. They tend, acquired muscle disease, to have a faster course compared to a muscular dystrophy. But there are exceptions. There have been patients with immune mediated necrotizing myopathy who have been misdiagnosed as having limb-girdle muscular dystrophy just because the disease has been very slowly progressive, and vice versa. There may be some genetic muscle diseases that can present in a relatively fast way. And one of these is a lipid storage myopathy, where some patients may develop subacutely weakness, dysphagia, and even respiratory difficulties. Dr Albin: Again, I'm hearing you say that we really have to have an open mind that myopathies can present in a whole bunch of different ways with a bunch of different phenotypes. And so, keeping that in mind, once you suspect someone has a myopathy, looking at the testing from the EMG perspective and then maybe laboratory testing, how do you use that information to guide your work up? Dr Milone: The EMG has a crucial role in the diagnosis of muscle diseases. Because, as we said earlier, weakness could be the result of muscle disease or other form of neuromuscular disease. If the EMG study will show evidence of muscle disease supporting your diagnostic hypothesis, now you have to decide, is this an acquired muscle disease or is this a genetic muscle disease? If you think that, based on clinical history of, perhaps, subacute pores, it is more likely that the patient has an acquired muscle disease, then I would request a muscle biopsy. The muscle biopsy will look for structural abnormalities that could help in narrowing down the type of muscle disease that the patient has. Dr Albin: That's really helpful. When we're sending people to get muscle biopsies, are there any tips that you would give the listeners in terms of what site to biopsy or what site, maybe, not to biopsy? Dr Milone: This is a very important point. A muscle biopsy has the highest diagnostic yield if it's done in a muscle that is weak. And because muscle diseases can result in proximal or distal weakness, if your patient has distal weakness, you should really biopsy a distal muscle. However, we do not wish to biopsy a muscle that is too weak, because otherwise the biopsy sample will result just in fibrous and fatty connected tissue. So, we want to biopsy a muscle that has mild to moderate weakness. Dr Albin: Great. So, a little Goldilocks phenomenon: has to be some weak, but not too weak. You got to get just the right feature there. I love that. That's a really good pearl for our listeners to take. What about on the flip side? Let's say you don't think it's an acquired a muscular disease. How are you handling testing in that situation? Dr Milone: If you think the patient has a genetic muscle disease, you pay a lot of attention to the distribution of the weakness. Ask yourself, what is the best pattern that represent the patient's weakness? So, if I have a patient who has facial weakness, dysphagia, muscle cramping, and then on examination represent myotonia, then at that point we can go straight to a genetic test for myotonic dystrophy type one. Dr Albin: That's super helpful. Dr Milone: So, you request directly that generic test and wait for the result. If positive, you will have proof that your diagnostic hypothesis was correct. Dr Albin: You're using the genetic testing to confirm your hypothesis, not just sending a whole panel of them. You're really informing that testing based on the patient's pattern of weakness and the exam findings, and sometimes even the EMG findings as well. Is that correct? Dr Milone: You are correct, and ideally, yes. And this is true for certain muscle diseases. In addition to myotonic dystrophy type one, for example, if you have a patient who has fascial scapulohumeral muscular weakness, you can directly request a test for FSHD. So, the characterization of the clinical phenotype is crucial before selecting the genetic test for diagnosis. Dr Albin: Wonderful. Dr Milone: However, this is not always possible, because you may have a patient who has just a limb-girdle weakness, and the limb-girdle weakness can be limb-girdle muscular dystrophy. But we know that there are many, many types of limb-girdle muscular dystrophies. Therefore, the phenotype is not sufficient to request specific genetic tests for one specific form of a limb-girdle muscular dystrophy. And in those cases, more complex next-generation sequencing panels have a higher chance of providing the answer. Dr Albin: Got it, that makes sense. So, sometimes we're using a specific genetic test; sometimes, it is unfortunate that we just cannot narrow down to one disease that we might be looking for, and we may need a panel in that situation. Dr Milone: You are correct. Dr Albin: Fantastic. Well, as we wrap up, is there anything on the horizon for muscular disorders that you're really excited about? Dr Milone: Yes, there are a lot of exciting studies ongoing for gene therapy, gene editing. So, these studies are very promising for the treatment of genetic muscle disease, and I'm sure there will be therapists that will improve the patient's quality of life and the disease outcome. Dr Albin: It's really exciting. Well, thank you again. Today I've been interviewing Dr Margarita Malone on her article on a pattern recognition approach to myopathy, which appears in the October 2025 Continuum issue on muscle and neuromuscular junction disorders. Be sure to check out Continuum Audio episodes from this and other issues, and thank you to our listeners for joining us today. And thank you, Dr Milone. Dr Milone: Thank you, Casey. Very nice chatting with you about this. 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.

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.

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.

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.

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.

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.

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.

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