Podcasts about faan

"I think we really need to push more of our oncology nurses to get into elected and appointed positions. So often we're looking at health positions to get involved in, and those are wonderful. We need nurses as secretaries of health, but there are others. We as nurses understand higher education. We understand environment. We understand energy. So I think we look broadly at, what are positions we can get in? Let's have more nurses run for state legislative offices, for our House of Representatives, for the U.S. Senate," ONS member Barbara Damron, PhD, LHD, RN, FAAN, told Ryne Wilson, DNP, RN, OCN®, CNE, ONS member and member of the ONS 50th anniversary committee, during a conversation about the future of oncology nursing advocacy and health policy. Wilson spoke with Damron and ONS member Janice Phillips, PhD, RN, CENP, FADLN, FAAN, about how ONS has advanced advocacy and policy efforts over the past 50 years and its approaches for the future. 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 229: How Advocacy Can Shape Your Nursing Career ONS Voice articles: Oncology Nurses Take to Capitol Hill to Advocate for Cancer Care Priorities Our Unified Voices Can Improve Cancer Survivorship Care With Voices Amplified by ONS, Oncology Nurses Speak Out for Patients and the Profession on Capitol Hill NOBC Partnerships Advance Nurses' Placements on Local and National Boards Nursing Leadership Has Space for You and Your Goals ONS courses: Advocacy 101: Making a Difference Board Leadership: Nurses in Governance Oncology Nursing Forum articles: Nurses on Boards: My Experience on the Moonshot Strengthening Oncology Nursing by Using Research to Inform Politics and Policy ONS Center for Advocacy and Health Policy Current ONS position statements Connie Henke Yarbro Oncology Nursing History Center Campaign for Tobacco-Free Kids Cancer Moonshot National Cancer Policy Forum National Council of State Boards of Nursing APRN Roundtable National Patient Advocate Foundation Nurses on Boards Coalition One Voice Against Cancer Patient Quality of Life Coalition Robert Wood Johnson Foundation Health Policy Fellows 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 Phillips: "I think that there are so many pressing issues, but I'm going to start with any kind of threats or legislation that's poised to take away safety-net resources. It's really going to set us back because we all know that, particularly for minorities and certain other underserved populations, they have experienced poor cancer outcomes for a variety of reasons, variety of socioeconomic reasons, lack of access to quality screening resources—you name it. When you take away those safety net resources and take away resources for people who are already underserved, uninsured, or underinsured, it also jeopardizes their ability to get proper screening, get proper follow-up, have access to state of the art cancer services. I think the lack of affordability of health care is a problem that continues to challenge us, whether you on Medicaid or whether you have limited insurance." TS 10:16 Damron: "Because ONS is so grounded in science and research—we're not just a clinical organization; we're grounded in scholarship, science, research, and publication—we're able to take this vast network of strong clinicians [and combine it] with amazing scientists. … We've had some amazing scientists come out of ONS; some of the leading nurse scientists of all time were also oncology nurses. So by combining this, we're able to make a difference at the state and federal level. So the advocacy work that I've been involved in, state and federal levels, really involved working with the ONS staff involved with advocacy and those scientists and clinicians who brought that expertise." TS 18:19 Phillips: "I think expanding the work around multiculturalism in oncology will always be important. Are there any new partnerships or avenues that ONS can reach out to or explore? Maybe there are other specialty organizations or groups—and not always necessarily nursing— because as we think about the determinants of health, we think about things like health and all policies. Maybe there are other disciplines or other specialties that we need to embrace as we launch our agendas." TS 23:28 Damron: "As nurses, just our basic nursing training, we get these skills—we see a problem, we identify the problem, we assess what we're going to do about it, we do it, and then we evaluate what we did. Does that work or not? That's how you make policy. So we were all trained in this. Then what you bring on top of that are oncology nursing experience, whether it's clinical, whether it's research, whether it's teaching, practice, etc. Those continue to refine those skills that are basic to us as nurses. We have this built-in skill set, and we need to own it and understand it." TS 30:25

In this episode, editor in chief Joseph E. Safdieh, MD, FAAN, highlights articles about how monoclonal antibodies revolutionized neurologic treatment, why pregabalin link to increased heart failure, and a combined therapy that slows progression in primary progressive aphasia.

In today's episode, we had the pleasure of speaking with Sikander Ailawadhi, MD, and Beth Faiman, PhD, MS, APN-BC, BMTCN, AOCN, FAAN, FAPO, about the potential clinical implications of the phase 3 IRAKLIA (NCT05405166) and phase 2 IZALCO (NCT05704049) studies, which investigated the use of isatuximab-irfc (Sarclisa) administered via an on-body delivery system in patients with relapsed/refractory multiple myeloma. Ailawadhi is a consultant in the Division of Hematology/Oncology in the Department of Internal Medicine, a consultant in the Department of Cancer Biology, and a professor of medicine at Mayo Clinic in Jacksonville, Florida. Faiman is a nurse practitioner in the Multiple Myeloma Program at Cleveland Clinic in Ohio. In our exclusive interview, Ailawadhi and Faiman discussed the rationale for efforts to bring isatuximab on-body injectors into the clinic, key patient-reported outcome findings from these studies, and how these findings may one day influence therapy administration across the broader multiple myeloma treatment paradigm.

* Add FAAN to Anita's creds after Oct. 18.Guests: Anita Rich, DNP, RN, CHFN, CDCES, FAAN, and Jane DeMeis.Related resources:PCNA CKM tools and resources: https://pcna.net/resources/patient-education/patient-information/cardiovascular-kidney-metabolic-syndrome-resources/ 2025 ACC Expert Consensus Statement on Medical Weight Mgmt for Optimization of CV Health: https://www.jacc.org/doi/10.1016/j.jacc.2025.05.024 Adiponectin, Leptin and CV Disorders: (https://www.ahajournals.org/doi/10.1161/CIRCRESAHA.120.314458Racial and Ethnic Disparities in Adult Obesity in the US: https://www.cdc.gov/pcd/issues/2019/18_0579.htmCardiometabolic Syndrome: A Global Health Issue: https://www.uspharmacist.com/article/cardiometabolic-syndrome-a-global-health-issueTaking Aim At Belly Fat: https://www.health.harvard.edu/newsletter_article/taking-aim-at-belly-fatGender Disparities in People Living with Obesity: https://pubmed.ncbi.nlm.nih.gov/34526743/ Systematic review and meta-analysis suggests obesity predicts onset of CKD: https://www.sciencedirect.com/science/article/pii/S0085253816307529AHA Weight-Loss Strategies for Prevention and Treatment of Hypertension: https://pubmed.ncbi.nlm.nih.gov/34538096/ Renal Fat Accumulation Assessed by MRI or CT and Metabolic Disorders: https://pmc.ncbi.nlm.nih.gov/articles/PMC12194363/See Privacy Policy at https://art19.com/privacy and California Privacy Notice at https://art19.com/privacy#do-not-sell-my-info.

Military-connected children face unique challenges and stressors, such as frequent relocations and  parental deployments, which may be overlooked in civilian clinical settings but can significantly impact their physical and mental health. In this episode, we are joined by Alicia Gill Rossiter DNP, APRN, FNP, PPCNP-BC, FAANP, FAAN  and Catherine G. Ling, PhD FNP-BC CNE FAANP to discuss the physical,  psychological, and behavioral health issues unique to military-connected children and the importance of identifying these children in civilian clinical settings to provide culturally competent care. They highlight the I Serve 2: A Pocketcard for Healthcare Providers Caring for Military Children© pocket card as a valuable tool that empowers nurses and advanced practice clinicians to identify these children, helping make these "hidden heroes" visible and better supported. To access the I Serve 2 Pocketcard for Healthcare Providers Caring for Military Children© and the Serving on the Homefront Pocketcard  for Caring for Military Spouses, Partners, and Caregivers© as well as resources on how to use them in your practice, please go to www.missionvalorhealth.com. This website will be available starting on November 10, 2025. Transcript ------------ Vancouver Coastal Health is hiring nurses in British Columbia. Experience the beauty and lifestyle of Canada's West Coast and join a team that's dedicated to caring for patients and for each other. Visit www.vch.ca/international-nurses

Stephen Grootes speaks to Faan van der Walt, Founder and Executive Director at WeBuyCars, about the JSE-listed company’s profit warning that sent its share price tumbling 14%, wiping out R2.76 billion in market value. In other Interviews: Stephen Grootes speaks to Old Mutual CEO Jurie Strydom as the Group unveils its refreshed strategy at its 2025 Capital Markets Day. The Money Show is a podcast hosted by well-known journalist and radio presenter, Stephen Grootes. He explores the latest economic trends, business developments, investment opportunities, and personal finance strategies. Each episode features engaging conversations with top newsmakers, industry experts, financial advisors, entrepreneurs, and politicians, offering you thought-provoking insights to navigate the ever-changing financial landscape.    Thank you for listening to a podcast from The Money Show Listen live Primedia+ weekdays from 18:00 and 20:00 (SA Time) to The Money Show with Stephen Grootes broadcast on 702 https://buff.ly/gk3y0Kj and CapeTalk https://buff.ly/NnFM3Nk For more from the show, go to https://buff.ly/7QpH0jY or find all the catch-up podcasts here https://buff.ly/PlhvUVe Subscribe to The Money Show Daily Newsletter and the Weekly Business Wrap here https://buff.ly/v5mfetc The Money Show is brought to you by Absa     Follow us on social media   702 on Facebook: https://www.facebook.com/TalkRadio702 702 on TikTok: https://www.tiktok.com/@talkradio702 702 on Instagram: https://www.instagram.com/talkradio702/ 702 on X: https://x.com/CapeTalk 702 on YouTube: https://www.youtube.com/@radio702   CapeTalk on Facebook: https://www.facebook.com/CapeTalk CapeTalk on TikTok: https://www.tiktok.com/@capetalk CapeTalk on Instagram: https://www.instagram.com/ CapeTalk on X: https://x.com/Radio702 CapeTalk on YouTube: https://www.youtube.com/@CapeTalk567 See omnystudio.com/listener for privacy information.

Faan van der Walt, uitvoerende hoof van WeBuyCars, gesels oor hul handelsverklaring wat vandag bekend gemaak is, en die aandeelprys se reaksie daarop. Volg RSG Geldsake op Twitter

Stephen Grootes speaks to Faan van der Walt, Founder and Executive Director at WeBuyCars, about the JSE-listed company’s trading update that sent its share price tumbling 14%, wiping out R2.76 billion in market value. The stock slid despite guidance of up to a 17% rise in core headline earnings to R958 million for FY2025, as earnings per share are expected to grow just 0.8% to 6% - weighed down by share dilution from recent capital raises The Money Show is a podcast hosted by well-known journalist and radio presenter, Stephen Grootes. He explores the latest economic trends, business developments, investment opportunities, and personal finance strategies. Each episode features engaging conversations with top newsmakers, industry experts, financial advisors, entrepreneurs, and politicians, offering you thought-provoking insights to navigate the ever-changing financial landscape.    Thank you for listening to a podcast from The Money Show Listen live Primedia+ weekdays from 18:00 and 20:00 (SA Time) to The Money Show with Stephen Grootes broadcast on 702 https://buff.ly/gk3y0Kj and CapeTalk https://buff.ly/NnFM3Nk For more from the show, go to https://buff.ly/7QpH0jY or find all the catch-up podcasts here https://buff.ly/PlhvUVe Subscribe to The Money Show Daily Newsletter and the Weekly Business Wrap here https://buff.ly/v5mfetc The Money Show is brought to you by Absa     Follow us on social media   702 on Facebook: https://www.facebook.com/TalkRadio702 702 on TikTok: https://www.tiktok.com/@talkradio702 702 on Instagram: https://www.instagram.com/talkradio702/ 702 on X: https://x.com/CapeTalk 702 on YouTube: https://www.youtube.com/@radio702   CapeTalk on Facebook: https://www.facebook.com/CapeTalk CapeTalk on TikTok: https://www.tiktok.com/@capetalk CapeTalk on Instagram: https://www.instagram.com/ CapeTalk on X: https://x.com/Radio702 CapeTalk on YouTube: https://www.youtube.com/@CapeTalk567 See omnystudio.com/listener for privacy information.

Faan van der Walt – CEO, WeBuyCars SAfm Market Update - Podcasts and live stream

Tehillah Niselow speaks to Faan van der Walt, CEO at WeBuyCars See omnystudio.com/listener for privacy information.

Aging is a story of adaptation, strength, and possibility. In this SEE YOU NOW Insight, from Episode 50: Owning Your Aging, nurse, researcher, and philosopher Sarah L. Szanton, PhD, ANP, FAAN shares the story of CAPABLE, Community Aging in Place, Advancing Better Living for Elders, a nurse-led program that helps older adults maintain independence and dignity by pairing home visits from a nurse and occupational therapist with simple, low-cost home modifications.  By focusing on what people want and need to do, like bathing, cooking, or walking to the mailbox, CAPABLE helps participants cut disability in half, boost confidence, and dramatically reduce healthcare costs. Through small, smart changes, Szanton reveals how prevention, creativity, and respect for individual goals can transform lives and redefine what it means to age well.  To listen to this Insight clip's full episode visit SEE YOU NOW Podcast Episode 50: Owning Your Aging at APPLE, SPOTIFY, YOUTUBE, or at your favorite streaming platform. For more information on the podcast bundles visit ANA's Innovation Website at https://www.nursingworld.org/practice-policy/innovation/education.  Have questions or feedback for the SEE YOU NOW team?  Future episode ideas? Contact us at hello@seeyounowpodcast.com.  

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 patients with heart failure, remote hemodynamic monitoring can identify health changes long before symptoms appear, contributing to slower disease progression, improved patient outcomes, and reduced rehospitalizations. Learn more about current and future technology that can support better patient health, and the role of nurses in patient education and monitoring. Guests: Linda Park, PhD, MS, FNP-BC, FAAN, FAHA, FPCNA, and Eryn Bryant, MSN, APRN-CNP, FPCNA.PCNA Heart Failure Tools: https://pcna.net/health-topics/heart-failure/Tele-HF study: https://www.jacc.org/doi/10.1016/j.jchf.2015.07.017 CHAMPION Trial (CMEMs after CRT): Pulmonary Artery Pressure-Guided Management of Patients With Heart Failure and Reduced Ejection Fraction https://www.acc.org/latest-in-cardiology/clinical-trials/2015/12/29/12/44/championJournal of American College of Cardiology paper, Remote Monitoring and Heart Failure Scientific Statement: https://www.jacc.org/doi/10.1016/j.jacc.2023.04.010 European Society of Cardiology consensus statement: https://doi.org/10.1093/eurheartjsupp/suae116BMAD trial: BMAD Trial: Wearable Remote Monitor Reduces Hospital Readmission Risk in HF Patients - American College of Cardiology: https://www.acc.org/Latest-in-Cardiology/Articles/2023/03/01/22/45/mon-830am-bmad-acc-2023 GUIDE-HF trial (CMEMS, Lancet): Haemodynamic-guided management of heart failure (GUIDE-HF): a randomised controlled trial - The Lancet: https://www.thelancet.com/journals/lancet/article/PIIS0140-6736(21)01754-2/abstractESCAPE trial (using RHC / pulm art pressures to guide therapy during ADHF: Evaluation study of congestive heart failure and pulmonary artery catheterization effectiveness: the ESCAPE trial - PubMed: https://pubmed.ncbi.nlm.nih.gov/16204662/MONITOR-HF trial (improved QOL and functional status w/ CMEMs): Remote haemodynamic monitoring of pulmonary artery pressures in patients with chronic heart failure (MONITOR-HF): a randomised clinical trial - The Lancet: https://www.thelancet.com/journals/lancet/article/PIIS0140-6736(23)00923-6/abstract MONITOR-HF: Pulmonary artery pressure monitoring in chronic heart failure: effects across clinically relevant subgroups in the MONITOR-HF trial | European Heart Journal | Oxford Academic: https://academic.oup.com/eurheartj/article/45/32/2954/7668040MONITOR-HF (summary in ACC): Remote Hemodynamic Monitoring of Pulmonary Artery Pressures in Patients With Chronic Heart Failure - American College of Cardiology: https://www.acc.org/Latest-in-Cardiology/Clinical-Trials/2023/07/18/17/21/monitor-hfHeartLogic: HeartLogic Multisensor Algorithm Identifies Patients During Periods of Significantly Increased Risk of Heart Failure Events: https://www.ahajournals.org/doi/10.1161/CIRCHEARTFAILURE.117.004669SCALE-HF-1 Trial (bodyport scale to predict worsening HF trends): Use of a Cardiac Scale to Predict Heart Failure Events: Design of SCALE-HF 1 | Circulation: Heart Failure: https://www.ahajournals.org/doi/10.1161/CIRCHEARTFAILURE.122.010012See Privacy Policy at https://art19.com/privacy and California Privacy Notice at https://art19.com/privacy#do-not-sell-my-info.

“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

In this episode, editor in chief Joseph E. Safdieh, MD, FAAN, highlights articles about a PET radiotracer that shows intranasally delivered insulin enters the brain, GLP-1s and dementia risk in people with Type 2 diabetes, and how exposure to green space may reduce the risk of neurodevelopmental delays in children.

Pioneer, MacArthur Fellow, and nurse-midwife Ruth Watson Lubic, EdD, RN, CNM, FAAN, FACNM opened the nation's first freestanding birth center in 1975, challenging a system where women often had little voice in their own maternity care. In this SEE YOU NOW Insight, she reflects on the movement that grew from one center in New York City to more than 350 across the country, and the transformational power of centering families in childbirth.  To listen to this Insight clip's full episode visit SEE YOU NOW Podcast Episode 6: Empowering Childbirth at APPLE, SPOTIFY, YouTube, or at your favorite streaming platform. For more information on the podcast bundles, visit ANA's Innovation Website at https://www.nursingworld.org/practice-policy/innovation/education.  Have questions or feedback for the SEE YOU NOW team?  Future episode ideas? Contact us at hello@seeyounowpodcast.com.     

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.

Host Nelba Márquez-Greene, Yale School of Public Health Community Scholar, is joined by "The Relentless School Nurse," Robin Cogan, MEd, RN, NCSN, FNASN, FAAN. Cogan is in her 25th year as a school nurse in the Camden City School District in New Jersey. She discusses how her family experienced multiple mass shootings seven decades and multiple generations apart, the critical role of school nurses in public health, and the overlaps between COVID safety and gun safety in schools.   Cogan also teaches the next generation of school nurses and is an inaugural member of Brady United's newest advocacy arm, This Is Our Lane. In her blog, "The Relentless School Nurse," she addresses critical issues, including firearm violence prevention, health equity, and school nursing advocacy.

In this episode, Nursing Economic$ Editor Dr. Donna Nickitas talks with Kimberly J. Harper, CEO Emeritus and Executive Consultant for the Indiana Center for Nursing, and Board Chair Emeritus of the Nurses on Boards Coalition in Indianapolis, Indiana, along with Dr. Cole Edmonson, the CEO of the Nurses on Boards Coalition in Dallas, Texas.Kimberly J. Harper, MS, RN, FAAN, is CEO Emeritus and Executive Consultant for the Indiana Center for Nursing, and Board Chair Emeritus of the Nurses on Boards Coalition in Indianapolis, Indiana.  Cole Edmonson, DNP, RN, FAAN, is the CEO of the Nurses on Boards Coalition in Dallas, Texas.  Donna M. Nickitas, PhD, RN, NEA-BC, CNE, FAAN, is Dean and Professor of the Rutgers School of Nursing, in Camden, New Jersey, and the Editor of Nursing Economic$.© Jannetti Publications, Inc.All rights reserved. No portion of this podcast may be used without written permission.To learn more about Nursing Economic$, visit http://www.nursingeconomics.net Visit our new JPI journal platform at www.jannettipublications.comMusical selections by Scott Holmes.http://www.scottholmesmusic.com

In this episode, editor in chief Joseph E. Safdieh, MD, FAAN, highlights articles about pegivirus's potential role in Parkinson's disease pathology, the impact of GLP-1 receptor agonistst on idiopathic intracranial hypertension, and the geographic spread of epilepsy specialists.

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.

In this special behind-the-scenes episode of Transmission Interrupted, host Jill Morgan gathers the core Education & Training Team from NETEC to pull back the curtain on how they create timely and practical resources for healthcare professionals facing special pathogens. Join Jill, along with Sharon Vanairsdale Carrasco (Director of Education), Benjamin Mattson and Jason Noble (Instructional Designers), Michael Konomos (Medical Illustrator), and Britton Clark (Project Manager), for an engaging conversation about what it takes to turn expert-driven knowledge into accessible, actionable training.Hear how the team prioritizes urgent topics, adapts to ever-changing demands, and keeps materials up-to-date and user-focused. Get insider perspectives on the collaborative process, the creative use of medical illustration, and how NETEC strives to meet healthcare workers where they are. Whether you're an educator, clinician, or just curious about emergency preparedness and infection control, this episode offers an inspiring look into the power of teamwork and the importance of supporting frontline staff with the best education possible.Have suggestions for future content or resources? The team wants to hear from you! Contact NETEC at info@netec.org.Tune in, subscribe, and join the conversation. Visit Transmission Interrupted on the web at netec.org/podcast.GuestsSharon Carrasco DNP, APRN, ACNS-BC, ANP-C, CEN, FAEN, FAAN, FNAPNETEC, Director of Education and TrainingBritton Clark PMP, MPHNETEC Project Manager, Education & TrainingProject Management Professional (PMP)Michael Konomos MS, CMINETEC Medical Illustrator and Visual DesignerBenjamin Mattson M.S.EdNETEC Instructional DesignerJason Noble BA, BFANETEC Instructional DesignerHostJill Morgan, RNEmory Healthcare, Atlanta, GAJill Morgan is a registered nurse and a subject matter expert in personal protective equipment (PPE) for NETEC. For 35 years, Jill has been an emergency department and critical care nurse, and now splits her time between education for NETEC and clinical research, most of it centering around infection prevention and personal protective equipment. She is a member of the Association for Professionals in Infection Control and Epidemiology (APIC), ASTM International, and the Association for the Advancement of Medical Instrumentation (AAMI).ResourcesTransmission Interrupted: netec.org/podcastNETEC Resource Library: repository.netecweb.orgNETEC YouTube: YouTube.com/thenetecNETEC eLearning Center: courses.netec.orgAbout NETECA Partnership for PreparednessThe National Emerging Special Pathogens Training and Education Center's mission is to set the gold standard for special pathogen preparedness and response across health systems in the U.S. with the goals of driving best practices, closing knowledge gaps, and developing innovative resources.Our vision is a sustainable infrastructure and culture of readiness for managing suspected and confirmed special pathogen incidents across the United States public health and health care delivery systems.For more information visit NETEC on the web at

Global issues that impact cardiovascular health include access to, and continuity of, care for migrant workers, as well as rising temperatures in both rural and urban environments. Nurse Practitioner and researcher Daniel Smith, PhD, AGPCNP-BC, CNE, FAAN, shares strategies to help improve cardiovascular disease prevention and management to help every patient everywhere have improved outcomes.Related resources:Global Cardiovascular Nursing Leadership Forum: gcnlf.netCE course: https://pcna.net/course/rural-and-environment-health-a-cross-roads/See Privacy Policy at https://art19.com/privacy and California Privacy Notice at https://art19.com/privacy#do-not-sell-my-info.

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.

Episode Resources:LEAD Guideline (4th Edition)Mobile Guideline SeriesKnowledge-to-Action Framework - Registered Nurses' Association of Ontario (RNAO)PAD National Action Plan - American Heart AssociationGet With the Guidelines - American Heart Association2024 LEAD Guideline Executive Summary - Journal of Wound, Ostomy, and Continence Nursing (JWOCN®)ECRI Guidelines TrustWorld Federation of Vascular SocietiesInternational Working Group on the Diabetic Foot (IWGDF)WOCNext® Conference SessionsWOCN Society Document Library: Wound Resources About the Speaker:Phyllis Bonham, PhD, MSN, RN, CWOCN, DPNAP, FAAN, brings nearly 60 years of nursing experience, with more than 50 years dedicated to wound, ostomy, and continence (WOC) care in clinical, academic, administrative, and research roles. She developed and directed the WOCN® Society–Accredited Wound Care Education Program at MUSC for 17 years and is widely recognized as a speaker, educator, and published author in peer-reviewed journals and textbooks on lower-extremity arterial disease (LEAD) and wound management.Since 2000, Dr. Bonham has played a leading role on WOCN Society Clinical Guideline Task Forces, contributing to the development and updates of 13 evidence-based guidelines addressing wounds from LEAD, lower extremity venous disease (LEVD), diabetes/neuropathy, and pressure injuries. She has chaired the Wound Guidelines Task Force since 2012 and served as a primary author for the 2024 LEAD guideline update, as well as co-author of multiple executive summaries published in the Journal of Wound, Ostomy, and Continence Nursing (JWOCN®).Her service to the WOCN Society includes leadership as President-Elect (2007–2009), President (2009–2011), and Past President (2011–2012), as well as roles as Clinical Editor (2011–2017), Co-Section Editor for wound research for JWOCN, and faculty for the Wound Treatment Associate (WTA®) Program Committee.Editing and post-production work for this episode was provided by The Podcast Consultant.

“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

In this SEE YOU NOW Insight, nurse leaders Gaurdia Banister, PhD, RN, NEA-BC, FAAN, and Hiyam Nadel, MBA, CCG RN, share how the Ether Dome Challenge at Massachusetts General Hospital is using open innovation to surface frontline solutions and strengthen care delivery. Against a backdrop of persistent nurse staffing shortages and a global talent emergency, they show how including every role group in innovation, and ensuring leadership engagement, communication, and follow-through, creates a culture where staff feel heard, valued, and supported. Innovation, they remind us, isn't just about solving problems; it's about caring for patients and caregivers, and building strong systems for the future.      To listen to this Insight clip's full episode visit SEE YOU NOW Podcast Episode 77: Fostering a Culture of Inquiry at APPLE, SPOTIFY, or YOUTUBE or at your favorite streaming platform. For more information on the podcast bundles visit ANA's Innovation Website at https://www.nursingworld.org/practice-policy/innovation/education.  Have questions or feedback for the SEE YOU NOW team?  Future episode ideas? Contact us at hello@seeyounowpodcast.com.  

In this episode, editor in chief Joseph E. Safdieh, MD, FAAN, highlights articles about the relationship between income, “food deserts,” and stroke risk; why staying active may reduce cognitive decline in patients with Parkinson's disease; and how initiating rimegepant for migraine could help reduce opioid and butalbital use. 

John skips leg day, Alison skips art day, and Liz skips opinions. An uncorrected transcript of this episode is available here. Please email your letters of comment to comment@octothorpecast.uk, join our Facebook group, and tag @OctothorpeCast (on Bluesky or on Mastodon) when you post about the show on social media. Content warnings this episode: None Letters of comment Alan Fleming & David Bamford (email) Eastercon 2027: Unconfined in Glasgow Christopher J Garcia (email) Doug Faunt (Facebook) Fredrik Coulter (Facebook) Jake Casella Brookins (email) Jesi Lipp (Facebook) Meg MacDonald (Facebook) Paul Weimer (Bluesky) Raj (Bluesky) Sari Polvinen (email) Shi Lala (Facebook) Next episode, we are going to watch Dredd! 2025 Worldcon: Seattle Seattle apologised after we recorded The Hugo Awards longlist is now out! Donald E Eastlake III at the MPC 2026 Worldcon: LAcon V in Los Angeles ‪Weyodi OldBear‬: first post, second post Apology from the chair 2027 Worldcon: Montréal Old bid site Jeph Jacques's Questionable Content Picks John: FlickFleet Eurydice Games Alison: Slay the Spire again Liz: Luminous by Sylvia Park “More Real Than Him” Credits Cover art: “Inside Coverage” by Arthur Thomson Alt text: An abstract, geometric figure stands, their torso through a panel which has various trailing wires. There is a radio or walkie talkie on the floor and a textured background which is also geometric. The words “Octothorpe 143” appear at the top, “Walt Willis” appear at the right, and “Inside Coverage” appear at the bottom. Explanation: This is a previously unused piece of art by Atom (Arthur Thomson), originally intended for a Walt Willis column in Hyphen that never happened. Alison wants to use it as an Octothorpe cover to make Atom eligible for Best Fanzine Cover in the FAAn awards. Except, you know, not. Theme music: “Surf Shimmy” by Kevin MacLeod (CC BY 4.0)

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.

Episode Resources:WOCNext Abstract DetailsAbstract Author ResourcesePoster InformationPrevious Accepted AbstractsAbstracts in JWOCN® Online SupplementInterested in an abstract mentor? Email abstracts@wocn.orgAbout the Speaker:Donna Bliss, PhD, RN, FGSA, FAAN, WOCNF, is a Professor, Chair of the Adult and Gerontological Health Cooperative, and School of Nursing Foundation Professor of Nursing Research at the University of Minnesota School of Nursing, Minneapolis, MN. She has 25 years of funded research and 125+ publications and presentations about assessing, preventing, and managing fecal incontinence and incontinence associated skin damage. She is a forerunner in investigating disparities in skin damage and assessing dark skin. Donna is an active member of the WOCN® Society and is the 202-2026 WOCNext® Abstract Chair. During the WOCNext 2023 event, Donna was awarded the Barbara Braden Future is Bright Award and was also inducted into the inaugural class of the WOCN Fellow Program.Editing and post-production work for this episode was provided by The Podcast Consultant.

This content has been developed for healthcare professionals only. Patients who seek health information should consult with their physician or relevant patient advocacy groups.For the full presentation, downloadable Practice Aids, slides, and complete CME/MOC/AAPA information, and to apply for credit, please visit us at PeerView.com/PXM865. CME/MOC/AAPA credit will be available until August 26, 2026.From Migraine Recognition to Relief: Improving Outcomes With Patient-Centered CGRP Antagonist Strategies In support of improving patient care, PVI, PeerView Institute for Medical Education, is jointly accredited by the Accreditation Council for Continuing Medical Education (ACCME), the Accreditation Council for Pharmacy Education (ACPE), and the American Nurses Credentialing Center (ANCC), to provide continuing education for the healthcare team.SupportThis activity is supported by an educational grant from Pfizer.Disclosure information is available at the beginning of the video presentation.

This content has been developed for healthcare professionals only. Patients who seek health information should consult with their physician or relevant patient advocacy groups.For the full presentation, downloadable Practice Aids, slides, and complete CME/MOC/AAPA information, and to apply for credit, please visit us at PeerView.com/PXM865. CME/MOC/AAPA credit will be available until August 26, 2026.From Migraine Recognition to Relief: Improving Outcomes With Patient-Centered CGRP Antagonist Strategies In support of improving patient care, PVI, PeerView Institute for Medical Education, is jointly accredited by the Accreditation Council for Continuing Medical Education (ACCME), the Accreditation Council for Pharmacy Education (ACPE), and the American Nurses Credentialing Center (ANCC), to provide continuing education for the healthcare team.SupportThis activity is supported by an educational grant from Pfizer.Disclosure information is available at the beginning of the video presentation.

This content has been developed for healthcare professionals only. Patients who seek health information should consult with their physician or relevant patient advocacy groups.For the full presentation, downloadable Practice Aids, slides, and complete CME/MOC/AAPA information, and to apply for credit, please visit us at PeerView.com/PXM865. CME/MOC/AAPA credit will be available until August 26, 2026.From Migraine Recognition to Relief: Improving Outcomes With Patient-Centered CGRP Antagonist Strategies In support of improving patient care, PVI, PeerView Institute for Medical Education, is jointly accredited by the Accreditation Council for Continuing Medical Education (ACCME), the Accreditation Council for Pharmacy Education (ACPE), and the American Nurses Credentialing Center (ANCC), to provide continuing education for the healthcare team.SupportThis activity is supported by an educational grant from Pfizer.Disclosure information is available at the beginning of the video presentation.

This content has been developed for healthcare professionals only. Patients who seek health information should consult with their physician or relevant patient advocacy groups.For the full presentation, downloadable Practice Aids, slides, and complete CME/MOC/AAPA information, and to apply for credit, please visit us at PeerView.com/PXM865. CME/MOC/AAPA credit will be available until August 26, 2026.From Migraine Recognition to Relief: Improving Outcomes With Patient-Centered CGRP Antagonist Strategies In support of improving patient care, PVI, PeerView Institute for Medical Education, is jointly accredited by the Accreditation Council for Continuing Medical Education (ACCME), the Accreditation Council for Pharmacy Education (ACPE), and the American Nurses Credentialing Center (ANCC), to provide continuing education for the healthcare team.SupportThis activity is supported by an educational grant from Pfizer.Disclosure information is available at the beginning of the video presentation.

This content has been developed for healthcare professionals only. Patients who seek health information should consult with their physician or relevant patient advocacy groups.For the full presentation, downloadable Practice Aids, slides, and complete CME/MOC/AAPA information, and to apply for credit, please visit us at PeerView.com/PXM865. CME/MOC/AAPA credit will be available until August 26, 2026.From Migraine Recognition to Relief: Improving Outcomes With Patient-Centered CGRP Antagonist Strategies In support of improving patient care, PVI, PeerView Institute for Medical Education, is jointly accredited by the Accreditation Council for Continuing Medical Education (ACCME), the Accreditation Council for Pharmacy Education (ACPE), and the American Nurses Credentialing Center (ANCC), to provide continuing education for the healthcare team.SupportThis activity is supported by an educational grant from Pfizer.Disclosure information is available at the beginning of the video presentation.

This content has been developed for healthcare professionals only. Patients who seek health information should consult with their physician or relevant patient advocacy groups.For the full presentation, downloadable Practice Aids, slides, and complete CME/MOC/AAPA information, and to apply for credit, please visit us at PeerView.com/PXM865. CME/MOC/AAPA credit will be available until August 26, 2026.From Migraine Recognition to Relief: Improving Outcomes With Patient-Centered CGRP Antagonist Strategies In support of improving patient care, PVI, PeerView Institute for Medical Education, is jointly accredited by the Accreditation Council for Continuing Medical Education (ACCME), the Accreditation Council for Pharmacy Education (ACPE), and the American Nurses Credentialing Center (ANCC), to provide continuing education for the healthcare team.SupportThis activity is supported by an educational grant from Pfizer.Disclosure information is available at the beginning of the video presentation.

This content has been developed for healthcare professionals only. Patients who seek health information should consult with their physician or relevant patient advocacy groups.For the full presentation, downloadable Practice Aids, slides, and complete CME/MOC/AAPA information, and to apply for credit, please visit us at PeerView.com/PXM865. CME/MOC/AAPA credit will be available until August 26, 2026.From Migraine Recognition to Relief: Improving Outcomes With Patient-Centered CGRP Antagonist Strategies In support of improving patient care, PVI, PeerView Institute for Medical Education, is jointly accredited by the Accreditation Council for Continuing Medical Education (ACCME), the Accreditation Council for Pharmacy Education (ACPE), and the American Nurses Credentialing Center (ANCC), to provide continuing education for the healthcare team.SupportThis activity is supported by an educational grant from Pfizer.Disclosure information is available at the beginning of the video presentation.

Grief is more than just an emotional experience. It rewires the brain, changes how the body functions, and challenges us spiritually. Learn how to transform it with our guest Phil Cohen. https://bit.ly/42j06ZsHow Do We Break the Grip of Grief?Phil Cohen returns this week with a chat about how grief impacts the mind, body and spirit and what we can do to help support healing in each. We explored how grief is more than just an emotional experience. It rewires the brain, changes how the body functions, and shakes our spiritual foundation. Phil works to bring hope and clarity to something that often feels overwhelming and isolating. Remember that grief does not need to break us and that there are ways to carry grief that make life meaningful again. In this Episode:03:10 - Road Trip to Idaho: Kootenay Legends, Frog Eye Salad05:23 -  How Grief Impacts the mind, body and spirit, with Phil Cohen09:04 - Why Don't I Feel Like Myself After a Loss? Learn What Changes Happen with Grief13:40 - Actions you Can Take to Adapt to the Pain of Grief19:31 - Guilt with Grief - Do we Need that Sense of Control?25:47 - Why Sitting Alone is Harmful29:26 - The Triad to Break the Grief Physiological Impact: Movement, Focus, and Words We Say44:38 - A Tribute to Andrea Gibson, by D.L. White49:41 - OutroSupport the showGet show notes and resources at our website: every1dies.org. Facebook | Instagram | YouTube | mail@every1dies.org

In this episode, editor in chief Joseph E. Safdieh, MD, FAAN, highlights articles about a promising blood test to distinguish Parkinson's disease from dementia with Lewy bodies, how CAR T-cell therapies are showing potential for patients with glioblastoma, and a new wireless electroencephalogram device that can even monitor young children with epilepsy.

Welcome to Episode 50 of the HPNA Palliative Perspective podcast—a meaningful milestone, and one that gave us pause to reflect on the incredible leaders who've shaped the hospice and palliative care space. In early conversations about this episode, we considered dedicating it to Betty Ferrell, a visionary in the field and the longtime Editor-in-Chief of JHPN, the Journal of Hospice and Palliative Nursing.  But, in true Betty fashion, those close to her reminded us she prefers to stay out of the spotlight. So instead, we're honoring her legacy in a way we think she'd appreciate: by celebrating the educators.  In this episode, we're shining a light on the hospice and palliative nurse educators featured in an upcoming issue of JHPN—innovators who are creating new programs and pushing boundaries in their Schools of Nursing to bring both primary and specialty palliative care to the forefront of nursing education. Their work is not only advancing the field but also shaping the future of compassionate care.  Join Andra Davis, PhD, MN, RN, and Megan Lippe, PhD, MSN, RN, ANEF, FPCN®, FAAN—guest editors of the November issue of JHPN—as they share powerful insights on preparing the next generation of nurses in hospice and palliative care. Educating future nurses requires more than just a solid curriculum—it demands mentorship, creativity, and a deep, ongoing commitment. In this episode, we explore why palliative care is no longer a “nice to have,” but a necessity in nursing education. From shifts in accreditation standards to real-world bedside challenges, Drs. Davis and Lippe discuss the essential role faculty and mentors play in helping students navigate the emotional, clinical, and human complexities of whole person care. We also explore how practicing nurses can be part of this movement—supporting learners and strengthening the future of compassionate care.   Podcast Notes/Links  JPHN Article, releasing in Nov— https://journals.lww.com/jhpn/pages/default.aspx   Betty Ferrell, speaking at HPNA Annual Conference, link  Scope, Standards and Competencies for the Hospice & Palliative RN & APRN, link  The Corner https://www.aacnnursing.org/elnec/elnec-faculty-corner      Megan Lippe, PhD, MSN, RN, ANEF, FPCN®, FAAN Dr. Lippe is Associate Professor with tenure at the University of Texas Health San Antonio and a national leader in palliative nursing education. Her work focuses on educational innovation, simulation, interprofessional collaboration, and social justice. She serves as a co-investigator for the End of Life Nursing Education Consortium (ELNEC), helping advance palliative care education in nursing programs across the country. She has co-authored several key works in the field of palliative care, including undergraduate and graduate palliative care competence statements endorsed by the American Association of Colleges of Nursing (CARES and G-CARES, respectively), ELNEC Undergraduate/New Graduate and ELNEC Graduate online curricula, and the scopes section of the new Hospice and Palliative Nurses Association (HPNA) Scopes, Standards, and Competencies for Hospice and Palliative Registered Nurses (RNs) and Advanced Practice Registered Nurses (APRNs). In collaboration with colleagues, she has conducted research that led to the development of new tools to assess palliative care curriculum, self-competence, and knowledge among nursing students and entry-level nurses. Honors include 2019 Cambia Sojourns Scholar, 2017 ELNEC Award, and 2019 HPNA New Investigator Award. She is a fellow of the American Academy of Nursing, the Academy of Nursing Education and of Palliative Care Nursing by HPNA.      Andra Davis, PhD, MN, RN Is an Associate Professor of Nursing at the University of Portland, where she teaches across both undergraduate and graduate programs. She is a co-investigator with the End-of-Life Nursing Education Consortium (ELNEC) and brings extensive clinical expertise in cancer symptom management, palliative care, and primary palliative nursing education. Dr. Davis's research centers on strengthening palliative care education, including revising national competency guidelines and developing outcome measures for undergraduate nursing programs. She is recognized for her leadership at regional and national levels in advancing the integration of palliative care into nursing curricula. Internationally, she collaborates with nursing colleagues in Thailand that expand access to palliative education, research, and caregiver wellbeing. Her scholarship also contributes to the evidence base for nurse-led, evidence-informed symptom management guides for patients undergoing cancer treatment.   Brett Snodgrass, DNP, FNP-C, ACHPN®, FAANP Dr. Brett Snodgrass has been a registered nurse for 28 years and a Family Nurse Practitioner for 18 years, practicing in multiple settings, including family practice, urgent care, emergency departments, administration, chronic pain and palliative medicine. She is currently the Operations Director for Palliative Medicine at Baptist Health Systems in Memphis, TN. She is board certified with the American Academy of Nurse Practitioners. She is also a Fellow of the American Association of Nurse Practitioners and an Advanced Certified Hospice and Palliative Nurse. She completed a Doctorate of Nursing Practice at the University of Alabama – Huntsville. She is a nationally recognized nurse practitioner speaker and teacher. Brett is a chronic pain expert, working for more than 20 years with chronic pain and palliative patients in a variety of settings. She is honored to be the HPNA 2025 podcast host. She is married with two daughters, two son in laws, one grandson, and now an empty nest cat. She and her family are actively involved in their church and she is an avid reader.  

The dynamics of AFib and Heart Failure often lead to patients navigating both diseases simultaneously. Learn how to apply effective strategies for management, including team-based care, shared decision-making, addressing adherance barriers, and more, in this conversation with Kathy Wood, PhD, RN, FAHA, FAAN, and Eryn Bryant, MSN, APRN-CNP, FPCNA.PCNA Resources:Atrial Fibrillation:https://pcna.net/health-topics/atrial-fibrillation/ Heart Failure: https://pcna.net/health-topics/heart-failure/EAST-AF NET-4 Trial: acc.org/Latest-in-Cardiology/Clinical-Trials/2020/08/28/16/16/EAST-AFNET-4AFFIRM Trial: https://pubmed.ncbi.nlm.nih.gov/12466506/ See Privacy Policy at https://art19.com/privacy and California Privacy Notice at https://art19.com/privacy#do-not-sell-my-info.

In this special edition episode, recorded live at the ASCO Annual Meeting, hosts Shikha Jain, MD, and Edward Kim, MD, honor Healio's 2025 Disruptive Innovators for their positive disruption in the field of hematology/oncology, and for pushing the status quo to improve clinical practice.  •    Welcome to the fourth annual Healio Disruptive Innovator Awards in hematology/oncology. 1:00 •    VK Gadi, MD PhD, presents the Health Equity Award. 3:56 •    The Health Equity Award winner, Ana Velázquez Mañana, MD, makes a speech. 6:00 •    Morgan Collier presents the Woman Disruptor of the Year Award. 7:38 •    Betty S. Pace, MD, accepts the Woman Disruptor of the Year Award. 9:19 •    The Social Media Influencer Award, presented by Eleonora Teplinsky, MD. 11:53 •    Amani Jambhekar, MD, also known as @ajvictorymd on Instagram and TikTok, accepts the Social Media Influencer Award. 13:13 •    Brenda M. Nevidjon, MSN, RN, FAAN, presents the Advanced Practice Trailblazer Award. 14:40 •    Ashley Leak Bryant, PhD, RN, OCN, FAAN, delivers her acceptance speech for the Advanced Practice Trailblazer Award. 16:19 •    Kamal Jethwani, MD, MPH, presents the Patient Voice Award. 18:44 •    Founder Kimberly Richardson, MA, accepts the Patient Voice Award for the Black Cancer Collaborative. 20:44 •    Healio's chief content officer, Joan-Marie Stiglich, ELS, presents the NextGen Disruptor Award to Nazli Dizman, MD. 22:22 •    The Clinical Innovation Award goes to UNC Lineberger Comprehensive Cancer Center for their at-home symptom reporting, led by Ethan Basch, MD, MSc. 24:18 •    Hope S. Rugo, MD, wins the Lifetime Disruptor Award. 26:48 •    The Industry Breakthrough Award goes to Breyanzi (lisocabtagene maraleucel, or liso-cel) from Bristol Myers Squibb. 30:57 •    On behalf of Bristol Myers Squibb, Amy Corrao, MSN, NP-C, accepts the Industry Breakthrough Award. 32:33 •    Thanks to all of the winners, nominees and sponsors! 35:39 •    Thanks for listening. 36:21 We'd love to hear from you! Send your comments/questions to Dr. Jain at oncologyoverdrive@healio.com. Follow Healio on X and LinkedIn: @HemOncToday and https://www.linkedin.com/company/hemonctoday/. Follow Dr. Jain on X: @ShikhaJainMD. Read the full coverage from Healio's Disruptive Innovators here.

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.

In this episode, editor in chief Joseph E. Safdieh, MD, FAAN, highlights articles about whether small fiber neuropathy is an autoimmune disorder; Merit Cudkowicz, MD, MSc, FAAN, recipient of this year's AAN Lifetime Achievement Award for Clinically Relevant Research; and how neurologist couples pursue work-life balance.

The News With Courtney: Bobcats and tabletop fire warnings // Anne Gross, PhD, RN, FAAN, Senior Vice President of Patient Care Services // Almost halfway to $1 million (which becomes 2 thanks to Rob Hale!) raised! //

Live from Fenway for the 23rd annual Jimmy Fund Radio-Telethon! // Our guy Rob Hale promises a 1 MILLION dollar match for donations! // Greg's old man "non sports" lead: the Yankees are interested in Bregman // Bill O'Brien joins, challenges Belichick to UNC vs. BC at Gillette! // Sam Kennedy joins, talks road woes, last leg playoff push // 17 year old cancer survivor Christian Mayo joins with his mom Debbie // Courtney is curious if Greg had anything to do with Nantucket bomb threats // They Said It: The Sox carry on Marcello Mayer-less for the rest of the year // Wiggy says Maye's success rides on how well Stephon Diggs plays // The News With Courtney: Bobcats and tabletop fire warnings // Anne Gross, PhD, RN, FAAN, Senior Vice President of Patient Care Services // Almost halfway to $1 million (which becomes 2 thanks to Rob Hale!) raised! //

Anne Gross, PhD, RN, FAAN, Senior Vice President of Patient Care Services, Chief Nursing Officer, Ning Zhao Chair of Nursing, Dana-Farber Cancer Institute ● Anne is responsible for adult and pediatric nursing across all care sites at Dana-Farber, The Phyllis F. Cantor Center for Research in Nursing and Patient Care Services, and the Center for Clinical and Professional Development. She also oversees a variety of other clinical services, patient and family programs, and Volunteer Services. ● Since joining Dana-Farber in 2002, she has led implementations of a primary nursing care model and a residency training program for newly licensed nurses and has secured funding for programs and research to support inclusion, diversity and equity, positive practice environments, and self-care and renewal programs. She also is involved in committees, boards, and initiatives nationally and internationally and is a Fellow in the American Academy of Nursing.

“At least some of the answer to these issues of compassion fatigue and burnout have to do making our practice environments the very, very best they can be so that nurses and other clinicians can really connect and care for patients in the ways that they want to be able to do that—and the patients need them to be able to do. I think there's a lot that is here already and will be coming, and I feel pretty optimistic about it,” ONS member Anne Gross, PhD, RN, NEA-BC, FAAN, senior vice president for patient care services and chief nursing officer at Dana-Farber Cancer Institute in Boston, MA, told ONS member Christine Ladd, MSN, RN, OCN®, NE-BC, member of the ONS 50th anniversary committee, during a conversation about burnout and compassion fatigue in oncology nursing. Ladd spoke with Gross and ONS member Tracy Gosselin, PhD, RN, NEA-BC, AOCN®, FAAN, senior vice president and chief nursing executive at Memorial Sloan Kettering Cancer Center in New York, NY, about the history of nurse well-being and how nurses and health systems are approaching it today. 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 315: Processing Grief as an Oncology Nurse Episode 292: What We Need to Do to Retain Today's Oncology Nursing Workforce Episode 291: Build a Sense of Belonging for Nurses and Patients Episode 264: Stop the Stressors and Improve Your Mental Health as a Nurse Episode 246: Create a Culture of Safety: Fair and Just Culture Episode 160: Build Innovative Staff Education Tools and Resources ONS Voice articles: Critical Event Debriefings Can Reduce Oncology Nurses' Risk of Compassion Fatigue and Burnout ONS Chapters and DNP Candidates Combine Forces to Support Oncology Nurse Well-Being Step Out of Reality With Virtual Breaks to Support Your Wellness at Work Clinical Journal of Oncology Nursing articles: Burnout and Well-Being: Evaluating Perceptions in Bone Marrow Transplantation Nurses Using a Mindfulness Application Engaging Nurse Residents Through Poetry Strategies to Mitigate Moral Distress in Oncology Nursing ONS Nurse Well-Being Learning Library ONS Communities ONS Chapters Connie Henke Yarbro Oncology Nursing History Center Oncology Nursing Foundation Resiliency Resources 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 Gross: “I was on an oncology unit early in practice. And just like today, we were dealing with very sick patients. We were dealing with death and dying. We were administering very toxic treatments and really pushing a field forward in oncology. So there were similar challenges, but I think different from today. There weren't the kind of resources; there wasn't the body of work that's been done today around compassion fatigue and burnout, work-life balance, and things like that. There was not that body of literature and science like there is today. And so there was more of a grassroots kind of support building in the clinical environment that I think I experienced.” TS 2:35 Gosselin: “I think there's also a piece when we think about nurses in the work we do—we also have families. We have aging parents and children. And sometimes that burnout is multifactorial in that we have family obligations and other obligations that make it really hard. And for some people, they say work is their escape from some of that. Yet it's all hard to balance sometimes.” TS 8:09 Gosselin: “It's this question that people like Anne, myself, other chief nurses are saying. If we add this new technology, what are we going to take away? Do we need another alarm to ring to the phone or to their badge? How much can you ask people to do and not be distracted when they're at point of care delivering patient care? Technology should never be a distractor, nor should it tell us how to practice. The technologies we have today—I'm like, ‘Wow, I wish I had that when I started my career.' And yet there's also a double-edged sword to that. I think we have to balance when we think about care and care delivery.” TS 16:36 Gross: “There are so many resources, first of all, that ONS provides to all of us at all levels and in all points in our career and our path from novice to experts. And the needs, though, are the same. Whether you're a novice nurse or whether you're a very experienced nurse, you need to continue to learn and to get new information, and ONS is an incredible resource for that. … As I think both of us keep alluding to and emphasizing here, you also need that connection to other people. And that's what ONS provides—that opportunity to get connected to other people that might be working in some other part of the country or other part of the world but is dealing with similar things that you're dealing with. So it provides that opportunity, and then it also provides an opportunity to get involved. I think when you can get involved and be part of solving a problem, it doesn't then control you and you won't feel defeated by it.” TS 22:24

For many years, it was rare to see a new CRNA grad get a 1099 opportunity, but that's been changing over the past decade. This new generation of CRNAs looks at work differently than previous generations and 1099 fits their lifestyle needs much better. So what do you really need to know if you are choosing between traditional W2 employment and the increasingly popular 1099 pathway? Kevin and Larry welcome on Beyond the Mask hosts Jeremy Stanley, EA, CFP®, AIF® and Sharon Pearce, DNP, CRNA, FAANA, FAAN to talk tax advantages, income potential and career flexibility. Here's some of what we discuss in this episode: