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Social determinants of health, including housing, food access, insurance status, and structural inequities, significantly influence stroke prevention, recovery, and long term outcomes. These factors affect biological risk, treatment adherence, and disparities in care, even when traditional clinical measures are addressed. This episode highlights practical strategies for integrating screening, leveraging multidisciplinary teams, and identifying opportunities for advocacy to improve patient outcomes. In this episode, Teshamae Monteith, MD, FAAN, speaks with Nneka L. Ifejika, MD, MPH, author of the article "Social Determinants of Health and Their Impacts on Stroke Prevention and Outcomes" in the Continuum® June 2026 Cerebrovascular Disease 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. Ifejika is an adjunct professor of physical medicine and rehabilitation at UT Southwestern Medical Center in Dallas, Texas, and the chief scientific officer of the Division of Academics at Ochsner Health System in New Orleans, Louisiana. Additional Resources Read the article: Social Determinants of Health and Their Impacts on Stroke Prevention and Outcomes 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 Monteith: Two patients have the same stroke, but when they return, they have very different outcomes. We can look into some of their comorbidities, but something we don't spend enough time talking about is the social determinants of health. Stay tuned to this discussion. I promise you, you'll become a better neurologist. Dr Jones: This is Dr. Lyell Jones, Editor-in-Chief of Continuum. Thank you for listening to Continuum Audio. Be sure to visit the links in the episode notes for information about earning CME, subscribing to the journal, and exclusive access to interviews not featured on the podcast. Dr Monteith: This is Dr. Teshamae Monteith. Today I'm interviewing Dr. Nneka Ifejika about her article on social determinants of health and their impacts on stroke prevention and outcomes. This article appears in the June 2026 Continuum issue on cerebrovascular disease. How are you? Welcome to our podcast. Dr Ifejika: Thanks for having me. I'm doing great. Dr Monteith: Great. So, can you introduce yourself to our audience? Dr Ifejika: Sure. I'm Dr. Nneka Ifejika. I am the Chief Scientific Officer of Ochsner Health System in New Orleans, Louisiana. But I'm also a cerebrovascular rehabilitation doctor. I've been practicing for about nineteen years, and am happy and honored to be a contributor to this Continuum Neurology article. It's a really important topic. Dr Monteith: Great. So, what got you into this field, first of all? Dr Ifejika: Well, I was deciding between PM&R and neurology, and I was putting in both match lists. And I thought about it and I leaned toward PM&R, but stroke still had a grasp on my heart and my mind. And so, after I finished my residency, I joined the UT Houston stroke team, and I did a, thankfully did a two-year fellowship and became cross-trained in stroke as well as physical medicine rehab. So, I am a jack of both trades. Dr Monteith: So, you got your way in a way. Dr Ifejika: I did. Dr Monteith: You know, we have a lot of learners that are listening, so it's always, uh, nice for them to be inspired, I think, by people's career paths. So why don't we talk about the objectives of your article? Dr Ifejika: Sure. So, one of the most important things that we wanted to do was make sure that medical students, residents, faculty, and fellows understood the impact of social determinants of health on stroke recovery and stroke rehabilitation. It's not as simple as you have hypertension, hyperlipidemia, we're going to manage your stroke risk factors. Oh, you had an ischemic stroke. You presented in time for the window. We're going to give you endovascular therapy and then modified Rankin scale at hospital discharge in ninety days. No, no, no. The stroke survivor and their caregivers and their family have a lot more to deal with outside of what we look at during the acute stroke hospitalization and post-acute rehabilitation. Things like, can they afford the medication that we're prescribing? Antiplatelet agents or anticoagulation can be extremely expensive. Do they have housing insecurity? Is there food insecurity? What's going on behind the scenes that we are not addressing that can directly impact the admission rate and the readmission rate after we take care of a stroke survivor? Dr Monteith: I love the article because you took a real deep dive into social determinants of health, what they are, why they matter, and what we can do about them. And so why don't we talk a little bit about the NINDS framework for social determinants of health? I think many of us might not be familiar with the framework per se. Dr Ifejika: So, the framework consists of multiple domains specifically that relate to social determinants of health that were published in Neurology a couple of years ago. So, I do hope that people who are hearing this recording actually read them. There are interpersonal domains, there are classic medical domains, there are indeterminate domains, and there are six total domains. And health domains are the last domain. So, things like when it comes to housing insecurity, food insecurity, that's a domain of social determinants of health. When it comes to chronic racism, when it comes to biases that patients experience, those actually impact outcomes. So, there are six separate indices that we're going to get into in detail and how we address them as clinicians, whether it be at the medical student level, resident level, faculty level, to integrate the social determinants of health in our care plans, because we could be doing a much better job. And I think it'll be really important from the interpersonal perspective when we really relate to our patients and their families that we ask these questions. For example, if we're prescribing someone to have treatment for their diabetes mellitus and ha- and, and be taking insulin, if they have housing insecurity and they're in a homeless shelter, they have to leave the homeless shelter during the day. So, what happens to the insulin that we prescribe? These are variables that we are not considering on a regular basis, but they directly relate to compliance. Dr Monteith: Great. So that was one thing I wanted to bring up. We're very good at measuring blood pressure and trying to determine, uh, the association between stroke outcomes and things that we can measure, glucose, lipids, blood pressure. What is the evidence for social determinants of health and stroke outcome? Dr Ifejika: The evidence is growing, and there have been many publications that have come out that are, are going to be highlighted in this article related to structural determinants of health inequities, like structural racism, as well as disparities related to ethnicity and race. There's geographical disparities. For example, a lot of patients are, are primarily concerned about rural versus urban, whether you have access to different post-acute rehabilitation, whether you have access to secondary stroke prevention because you simply don't have the transportation from a, a rural area to get to a drugstore to get things available to you. Social status. There are actually publication related to socioeconomic status and the concerns when it comes to air pollution. So particulate matter 2.5, we know that that has a direct impact on stroke outcomes and health overall, but we don't really think about it as a structural determinant of health inequity. There's several multiple layers of research that have gone on specifically that have been cited in the literature that relate directly to social determinants of health and how we can address them moving forward. Dr Monteith: And what I found interesting in your article in that you gave at least a few examples where social factors like income, education were controlled for, and maybe in large part it is, but even when you control for some of these very obvious social risk factors, you still have inequities. Dr Ifejika: Absolutely. And I think it was really important to show that we had strong peer review evidence behind this, as it wasn't just something that we were creating or hypothesizing about. There have been studies that have been done over this over decades of time, showing the impacts of social determinants of health on outcomes. But the question and concern that we have is we know this growing body of literature continues to expand. What are we doing about it when it comes to education of the future generations of providers who will be caring for this population? Dr Monteith: Before we get into how, you know, what we're going to do about that, let's just kind of put that link, cause the evidence is there. How does it drive biology? Dr Ifejika: It's a great question. So, for example, particulate matter 2.5 in air pollution has been shown to have an existing impact on hypertension, raising your blood pressure. So that's a direct effect of a social determinant of health related to socioeconomic status because people who live in areas with higher air pollution are... They're not green spaces. They live near highways. Those are areas that unfortunately are also impacted by food deserts. Food deserts, if you're not able to get fresh fruits, vegetables, whole foods, increases your risk of developing diabetes, hyperlipidemia, also increases your sodium intake, again, increasing hypertension. These things are all connected to biological determinants. It's just that we're not asking about them necessarily within the social history when we're taking people into the hospital, but they have direct effects. Dr Monteith: Great. Neurologists tend to be busy and, you know, we're... have all of these things that we're being asked to do and chart and click and all of that stuff. And so how can we more readily integrate screening for social determinants of health and that conversation into the work we do? We recognize it's important. We recognize it's an important risk factor. There's a lot of these determinants. So, what is a good way to do so? And I, I know that in the paper you've, you've given different roles to different team players, so I want you to talk about that too, but just kind of even a regular routine office visit. Walk us through a way we can more easily integrate that kind of conversation. Dr Ifejika: It's an excellent question, and what I've recommended that we do in a standard office visit is utilize the time before the visit to send out screeners. So, for example, usually with an electronic medical record, you can send documents before the visit even starts, where people can check off whether they have any concerns regarding housing, food insecurity. They can check out their location of where they live, whether they live near a highway or not near a highway. It's specifically related to socioeconomic status. We can ask about insurance status, whether they have insurance, insured versus uninsured, but then also types of insurance, whether they have Medicaid insurance versus Medicare insurance. Then even drilling even further, type of Medicare insurance, Medicare Advantage versus traditional Medicare, cause all of those things actually play a role in this. Dr Ifejika: And evaluate these things and don't take time during your office visit. Send these screeners out beforehand. Have them be assimilated by your medical staff. Make sure you're utilizing every resource that you have at your disposal to help streamline things, so by the time the person comes in for the visit, you've primed the pump. You have this information already in your hands at your fingertips cause it was sent out in advance, and you have your medical staff already have an understanding of. If they didn't fill it out electronically, give it to them in the lobby. Make sure they have a handwritten copy in the lobby so that when they come into the office visit, you have the information at your fingertips. Dr Monteith: Are there any particular resources that you recommend for those types of screeners? Dr Ifejika: What I've used in the past, if you have patient-reported outcomes, so the PROMIS instruments, that's a good start. It doesn't get into the details of housing insecurity, food insecurity, but it's a good start to help prime questions and to start the conversation during your office visit. In my clinics, I do a PROMIS 27 on every patient, as well as a PHQ-9 for depression on everyone. And then I collect data longitudinally, and I can always drill down on factors that I noticed that could become a problem moving forward. Dr Monteith: Yeah. And then also in your article, you spoke a bit about this impact from the acute presentation in the hospital to rehab. Dr Ifejika: Yeah. Dr Monteith: So why don't you talk about these different entry points where we can really engage our patients and try and help reduce their burden? Dr Ifejika: Sure. So, healthcare can be quite fragmented, and the stroke patient, stroke survivor, and their family member have no grasp of that. They've had a stroke, and they may be going from the ER to the ICU to the stroke unit to the floor to the rehab unit, and we see it as multiple levels of care, multiple types of providers. They see it as one hospital. And the concern that we have is, at those branch points, things get dropped, and we have the opportunity to pick things up at those branch points. So, during the acute care hospitalization-Primarily, that's the establishment of what has happened, how we're gonna treat it, what are the variables that we can control for right now to address those determinants of health moving forward, and to specifically looking at whether they were taking medications before, whether they could afford medications before, what that looks like at hospital discharge. Is there any duplication of medications? If a person is taking Coreg and you prescribe metoprolol, but they still have the Coreg at home, should we have really prescribed the metoprolol? We're just spending money that they may have concerns when it comes to access to care and the cost of these prescriptions. So, it's the responsibility of the acute care physician to kind of look at that. Those are subtle things that we think are subtle, but they add up quickly for the family when it comes to having one group of medications that's the same class and having to buy another type. When it comes to post-acute rehabilitation, it's really an important time to screen for whether the caregiver can handle what's occurring. So specifically, if the caregiver is already burning out and the average length of stay for a stroke patient is five days and they've come to rehab for two weeks, what's gonna happen in the next two years or the next four years? So, during the post-acute rehabilitation phase, it's time to kind of look at that and drill down on those kind of questions. Also, the levels of care, Dr Ifejika: it's really important to look at other levels of rehabilitation, so skilled nursing facilities, making sure people have access to that if they need to, if the caregiver is burned out and they don't have the ability to go straight home. Because acute inpatient rehab, the goal of it afterwards, is to go straight home. It's not to go to another facility. So, you need to have that screener in place when it comes to whether the family can take care of this person, and whether the family can do it in an effective way to prevent them being readmitted. Dr Monteith: Great. I also like that you spoke about kind of the team approach and different roles, both for screening and for intervention, both being very important, especially the intervention. And so why don't you give us a few examples how the team could break up the responsibility and how also for the intervention component that can be done. Dr Ifejika: Sure. So, I broke up the team into several levels. So, the team medically is the medical student, resident, and faculty physician. However, the team also includes the support staff, so your case manager, your social worker, the therapist, physical therapy, occupational therapy, speech therapy, the pastoral services, all these members of the team. You know, sometimes as physicians, we don't read those notes. There's a lot of information in the notes from social work, care coordination, and the therapist. They get down to subtleties cause they're asking questions, for example, "What kind of equipment do you have at home? How many stairs do you have at home? What level of house do you have, one story, two story? If you live in an apartment, do you have an elevator access?" That's important for someone with hemiparesis. When it comes to medications, when it comes to insurance status, when it comes to your ability to have the mechanisms to pay for care as an outpatient, social workers are required to ask these questions cause they have to figure out resources for the patient and their family to help facilitate improved outcomes. So, they have to ask questions regarding these tasks. The concerns are, do we read what they're saying? So, it's really important to interact with them, and if it's not something that you're looking at in the chart, cause we're all so tied to our computers, find where they are in the hospital. Walk by their office and have a chat. Run your list with them, especially for people who you're concerned have vulnerabilities, and make sure that you're setting an example for your medical students with your faculty doing so. If you're looking at it from the medical student, resident, faculty perspective, medical students, listen. This is your opportunity to really contribute to the team as well as learn about social determinants of health and research in their fields. You are the boots on the ground for the medical team. You are the ones who should be priming the pump and asking these questions of the family members. We're sending you into the rooms to do a history and physical. Social determinants of health should be a part of your history and physical, and you should be taking what we're saying in this article and asking these questions and tying it into your resident. Now, the resident is the work person of the hospital. We all know this. Things run through the resident. Things run through the fellow. It's really important that they have this information in a manner that is negotiable. The list keeps getting longer, and a resident doesn't need to be overburdened. It needs to be synthesized in a manner that can help facilitate the resident being able to act as well as communicate any concerns to the faculty. And at the faculty level, we are the voices that can affect change. So, if there's any concerns when it comes to advocacy, research, making sure that people are accessing care in a way that makes sense, particularly when it comes to the ability for us to galvanize change on a national level, that's kind of our job. Dr Monteith: Great, and so let's talk about intervention. What are things that, let's say, the neurologist can do to deal with some of these social factors? Dr Ifejika: From the neurology perspective, I think it's really important to identify missed opportunities and making sure that we address them. For example, the conversations around the ability to have access to care related to insurance versus no insurance. There are many, many ways that neurologists are able to advocate for a person being able to get to Medicare insurance, particularly in the outpatient setting. When we see patients in clinic, it takes two years, them, to qualify for Medicare, two years at a minimum. But there's a gap there that can be filled by us making sure that we document what's happened, contact their providers, facilitate communication with their employers, if they're employees, they can get some short-term disability benefits to help bridge that gap prior to receiving Medicare insurance. It behooves us to do this because if we do not, they fall into the gap and they get readmitted and they're back on service anyway. So, what's important is the outpatient that we really kind of focus on things that we can impact and things like insurance and getting people transitioned from having employer-based insurance versus getting to Medicare is a really important way that we can effect change in a, in a way that's viable and, and replicable. So, in the outpatient setting, neurologists have a wonderful opportunity to effect change in social determinants of health. When it comes to employed persons, who had a stroke transitioning to Medicare, it takes two years to do so. So, in the outpatient clinic, if you have an employed person, make sure that you fill out their short-term disability benefits forms, their long-term disability benefits form. Bridge the gap. Get that information to their employer so they can maintain constant coverage. Because if they do not, if they have to choose between refilling medications and putting food on the table, they're going to choose putting food on the table, and that's going to directly impact their outcomes if they're not taking the medication that we recommend. Dr Monteith: I think that's a great point. I mean, there's a lot that we can do, and in some ways, it may not take that much to document and to be able to ask the questions and to include some of that information into the assessment and plan is really a, a great idea. Dr Ifejika: And you know, if we don't bring these things up and have these conversations, it doesn't get addressed. And that's why I'm very, very thankful that I had the opportunity to do so, cause this is a part of what I do all day. I think that if I wasn't integrating these kind of conversations into my practice, I wouldn't have the ability to share these tips and these abilities to move things forward in a manner that will be constructive for our field overall and for our patients. Dr Monteith: And towards the end of the article, you brought up something I think we don't see in many articles, and that's the role of advocacy and getting involved in health policy. So, can you talk a little bit about that? Dr Ifejika: You know, it's really important to facilitate change when you see that there are things that need to be changed. And the best way to do that is through advocacy at the local or state or federal level. A lot of these variables that we're dealing with can be addressed through legal changes. I'll give you an example. End-stage renal disease, if you have immediate hemodialysis and you have that requirement upon hospital discharge, you qualify for Medicare immediately. Immediately. Before you even leave the hospital. Why wouldn't something be similar for a stroke? Well, the reason why is because there was a level of advocacy that came around end-stage renal disease and a member of Congress's wife had hemodialysis requirements. And so, a law was passed to make sure Medicare covered it immediately after hospital discharge. So, it requires advocacy in some significant ways to get things done, but we have the bandwidth to do this. We take care of a population that has some of the highest rates of preventable disability. That's not going away. We need to make sure that we're effecting change for this group to make sure that they have the best possible outcomes they can experience. Dr Monteith: So, any final messages for our listeners? Dr Ifejika: I look forward to hearing everyone's feedback about our issue. I am thankful for the opportunity to talk about, address, and write about this important topic, and look forward to everyone's feedback. Dr Monteith: Well, thank you so much for being on our podcast. It was a really wonderful summary and we had a very thorough conversation, but you didn't give away too much, so I think they're going to have to read the article. Dr Ifejika: You're going to have to read the article. And we want medical students, residents, fellows, faculty, all of our ancillary staff within the hospitals, please read this article. We really appreciate it. Dr Monteith: Again today, I've been interviewing Dr. Nneka Ifejika about her article on social determinants of health and their impacts on stroke prevention and outcomes. This article appears in the June 2026 Continuum issue on cerebrovascular disease. 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.

DescriptionIn this episode of Perfect Prey, I'm joined by Ann Burgess, pioneering forensic nurse, researcher, educator, and author of Expert Witness. Ann's groundbreaking work transformed how professionals understand trauma, victimization, sexual violence, and offender behavior. Her research has influenced criminal investigations, forensic psychology, victim advocacy, and some of the most well-known criminal cases in modern history.Together, we explore the long-term impact of trauma, why victims are so often disbelieved, and how systems continue to fail those who come forward. Ann shares insights from decades of work studying victims, offenders, serial violence, child abuse, and the psychology of coercion and control. We also discuss institutional betrayal, trauma responses in children and adults, family court failures, pornography, grooming, and what it takes to create meaningful change within systems that were never designed to fully protect victims.What we coverAnn Burgess's pioneering work in victimology and forensic nursingHow trauma impacts behavior across the lifespanWhy victims are often disbelieved by systems and institutionsInstitutional betrayal and systemic failuresCoercive control, fear, and psychological abuseTrauma responses in children and adolescentsChild sexual abuse and delayed disclosureFamily court, victim credibility, and expert testimonyThe role of pornography and grooming in abusive behaviorThe Menendez case and evolving understandings of traumaWhy trauma-informed education is critical for professionalsHow offender thinking patterns develop and escalateWhy listenIf you are a survivor, clinician, attorney, advocate, educator, or protective parent, this episode offers a rare opportunity to hear from one of the most influential voices in trauma and victim research.Ann Burgess's work helped shape how we understand trauma today. Her insights illuminate why victims respond the way they do, why systems often misunderstand those responses, and why meaningful reform requires us to listen more closely to survivors' experiences.Guest BioAnn Burgess, DNSc, APRN, FAAN is an internationally recognized forensic nurse, researcher, educator, and author. She is a professor at Boston College and has spent decades studying trauma, victimization, sexual violence, serial offenders, and forensic mental health.Ann's groundbreaking research on rape trauma syndrome helped transform the understanding of victim responses to sexual assault. She has consulted with the FBI's Behavioral Science Unit, contributed to offender profiling research, and served as an expert witness in numerous high-profile cases.She is the author of several books, including Expert Witness, which chronicles her work at the intersection of trauma, criminal behavior, and justice.Connect with Ann BurgessBook: Expert Witnesshttps://www.amazon.com/stores/Ann-W.-Burgess/author/B0H13DQXPP?ref=sr_ntt_srch_lnk_3&qid=1780604748&sr=1-3&shoppingPortalEnabled=true&ccs_id=9489809f-1ae4-4998-b8db-a0cbcc536d23Boston College Faculty Profile: https://www.bc.eduConnect with Dr. ChristineProtective Parenting Program: https://www.coercivecontrolconsulting.com/services/for-parents/Dr. C's Community: https://go.drcocchiola.com/innercirclecommunityOfficial site: https://www.coercivecontrolconsulting.com/YouTube: https://www.youtube.com/@DrCocchiola-coercivecontrol/videosTikTok: https://www.tiktok.com/@dr.c_coercivecontrolInstagram: https://www.instagram.com/dr.cocchiola_coercivecontrol/TEDxTalks: https://www.youtube.com/watch?v=gp2qByKOue4&t=24sBooks:https://url-shortener.me/c/FramedBookhttps://url-shortener.me/c/EveryMomentOfEveryDayIf this episode landed for you, please share it with someone who needs to hear it, subscribe for more trauma-informed conversations, and consider leaving a review — it helps other survivors find validation and safety.— Dr. Christine Cocchiola & Ann Burgess

Could you imagine working in a rural location where access is truly a lifeline for people? Today's guest is April Erickson, DNP, CRNA, an ​Alaska ​based ​nurse ​anesthesiologist ​and ​anesthesia ​medical ​director ​with ​more ​than ​15 ​years ​of ​experience ​in ​rural ​independent ​practice. Sharon and guest host Jackie Rowles, DNP, MBA, MA, CRNA, ANP-BC, NSPM-C, FNAP, FAANA, FAAN, sit down with April to discuss frontier medicine, independent practice, leadership, and what it truly means to provide care where access is critical but not guaranteed. Here's some of what you'll hear in this episode:

In this episode, editor in chief Joseph E. Safdieh, MD, FAAN, highlights articles about a link between higher meat and slower cognitive decline in APOE34/44 carriers, the geographic distribution of research funding, and how artificial intelligence is reshaping neurology.

In this episode, Lyell K. Jones Jr, MD, FAAN, speaks with Cheryl Bushnell, MD, MHS, who served as the guest editor of the June 2026 Cerebrovascular Disease issue. They provide a preview of the issue, which publishes on June 3, 2026. Dr. Jones is the editor-in-chief of Continuum: Lifelong Learning in Neurology® and is a professor of neurology at Mayo Clinic in Rochester, Minnesota. Dr. Bushnell is a Professor of Neurology and Director of the Center for Transformative Stroke Care at Wake Forest University School of Medicine in Winston-Salem, North Carolina. Additional Resources Read the issue: continuum.aan.com Subscribe to Continuum®: shop.lww.com/Continuum Continuum® Aloud (verbatim audio-book style recordings of articles available only to Continuum® subscribers): continpub.com/Aloud More about the American Academy of Neurology: aan.com Social Media facebook.com/continuumcme @ContinuumAAN Host: @LyellJ Guest: @CBushnellMD  Full episode transcript available here Dr Jones: One of the core tenets of our field is that we learn neurology one stroke at a time. But what do we have to learn about preventing them altogether? The science of stroke prevention, acute treatment, and recovery are evolving rapidly, and it's hard to keep up. Today, we're speaking with Dr. Cheryl Bushnell, guest editor of our latest Continuum issue on Cerebrovascular Disease, to discuss these topics and much more.  Dr Jones: This is Dr. Lyell Jones, editor-in-chief of Continuum. Thank you for listening to Continuum Audio. Be sure to visit the links in the episode notes for information about subscribing to the journal, listening to verbatim recordings of the articles, and exclusive access to interviews not featured on the podcast.  Dr Jones: This is Dr. Lyell Jones, editor-in-chief of Continuum: Lifelong Learning in Neurology. Today, I'm interviewing Dr. Cheryl Bushnell, who is Continuum's guest editor for our latest issue on Cerebrovascular Disease. Dr. Bushnell is a professor of neurology and the director of the Center for Transformative Stroke Care at the Wake Forest University School of Medicine in Winston-Salem, North Carolina, where she specializes in the care of stroke patients and their social and functional determinants of recovery and health, and is an internationally recognized expert on those topics. Dr. Bushnell, welcome. Thank you for joining us today. Why don't you introduce yourself to our listeners?  Dr Bushnell: Absolutely. Thank you for the invitation. It's really an honor to be here. So, as you mentioned, I am the director of the Center for Transformative Stroke Care at Wake Forest. It's a really fun transition for me to be involved with different care models for stroke, and I think a lot of the Continuum topics are directly relevant to some of the things that I'm doing now as an administrator and sort of a facilitator of new research. So, thanks again for having me.  Dr Jones: Yeah, and, and you have a wonderful perspective, and we're gonna pull that out today in our interview questions, and I'm looking forward to sharing that with our listeners. But before we get to the questions, we're gonna start off today's podcast with another Continuum Audio trivia question for our listeners. Anticoagulation has played a critical role in secondary ischemic stroke prevention for a long time now. While direct oral anticoagulants have taken on a greater role in the treatment of prevention of stroke, there are still some use cases for vitamin K antagonists like warfarin. The trivia question for our listeners is this: How was warfarin discovered, and how did it get its name? Stick around and we'll share the answer to that question toward the end of our interview today. So, Dr. Bushnell, let's get right to it. You alluded to your various roles, and your leadership in the field has been exemplary. The interventions for acute ischemic stroke have really exploded over the last decade or so, and they get a lot of attention and discussion, but prevention and recovery are just as important in the care of these patients. Tell us a little more about how you approached this issue, about the article topics you chose, etc.  Dr Bushnell: Well, once I was chosen to lead the guest editorship, I wanted to come up with a group of topics that were maybe a little bit different from previous issues. So, I kind of looked at the previous issues and saw, as you said, an emphasis on acute stroke, and that's really important because it has been evolving. But my thought was, how about what happens to patients after they get the intervention and they're discharged home? And because a lot of trainees may not get to see these patients ever again, or it's months before they might see them, or if they're readmitted, which is what we don't want to see, but that certainly is a lot of the exposure is in the inpatient setting. So, I thought I would kind of transport the education into the outpatient and transitional setting, as well as prevention, not only secondary, but primary prevention, with an emphasis on brain health. Some of the populations that may not get as much attention. So, sex differences, stroke in women, pregnancy, the transitions of care, and also the emphasis on holistic view of patients and their challenges, which includes the non-medical factors that drive health, otherwise known as social determinants of health.  Dr Jones: I appreciate that perspective, and obviously th-this is an area of your deep expertise, and it's great to have an issue that really digs into some of those topics a little more deeply. As an educator, I'm really glad you mentioned that about the trainee's perspective. You know, especially junior neurology trainees that are in the hospital all the time. They're seeing patients in the middle of a cerebrovascular catastrophe. But there's a long tail of recovery, right? And they'll get to see that in continuity clinic, but it's a good message to share from an evidence and, um, experiential perspective in the issue. So, appreciate that perspective. You've just read all these articles and edited them. Was there anything that you ran across that was a surprise to you?  Dr Bushnell: Well, I personally chose a lot of the authors based on my knowledge of their work. So, I wouldn't say that it was completely surprising, but I do think that I was just genuinely impressed with the quality of the writing and the synthesis of information. I just was incredibly proud of the work that these co-authors have put together. I'd say that that was-- it wasn't surprising so much as just a sense of pride that I had with the product that's coming out. But of course, there have been some new trials that had to be incorporated at the last minute, some of which were presented at the International Stroke Conference just a few weeks ago.  Dr Jones: Yeah. We try to be as up-to-date as we can, and I will completely agree with you. We have some really good writers in our field, and it's really just a pleasure when you read an article that's by an expert, and it's a joy to read. I can tell you it's one of the best parts of this job, and you get to learn a lot. I think one of the more challenging scenarios that I hear about from colleagues in recent years has been optimal management of patients with asymptomatic extracranial atherosclerosis. The pivotal trials that inform how we manage those patients were from a long time ago, decades ago, predating a lot of the more intensive medical management tools that we have today. In that scenario, Dr. Bushnell, what's the latest on that, and what should our listeners know?  Dr Bushnell: Well, obviously, the CREST 2 trial has been long awaited. It's been going on for over ten years, I believe. Of course, it's, uh, two different trials all in one, the carotid stenting and angioplasty versus intensive medical management. And of course, each of the carotid vascularization arms of the trial also had intensive medical management. And then the other trial is the carotid endarterectomy as the form of revascularization. And it interestingly did not show any benefit of carotid endarterectomy compared to intensive medical management. But of course, the somewhat surprising result was that carotid angioplasty and stenting truly was superior, although it was a small number of events in the trial overall. But that stenting plus intensive medical management was somewhat better than intensive medical management alone. And I think stenting has come a long way in terms of safety, and so I think that's been part of the evolution of the field. I do wanna say that I'm a huge fan of the intensive medical management, and I think that what the protocol does in terms of blood pressure management, cholesterol management is very much above and beyond what's done in private practice even. And the health coaching for all the other things related to diabetes and weight loss and smoking cessation and physical activity, that is what we need to be doing to actually decrease the risk of stroke, and I think that it's very effective. I can't say enough about the design of the study for that reason, that everyone gets the intensive medical management, and then you just layer on the type of revascularization on top of it. So, I wouldn't have been surprised if this was a completely negative trial overall. They just happened to have some better outcomes in the stenting arm.  Dr Jones: I recall a few years ago when the series of endovascular therapy trials for acute stroke came out, and I think there was a, a period of time where the field had to adapt to that. I wonder what you think about with the CREST 2 findings on stenting. I mean, is that gonna be a big change? Because obviously atherosclerosis is highly prevalent. Is that gonna be a big change? Is the field ready for that? How much adjustment do we have in store?  Dr Bushnell: I'm not sure it's gonna be a really big change. If you read the editorial that accompanied the trial in the New England Journal, just a few patients in either direction would have changed the outcome. I kind of look at it as an absolute difference that's relatively small. So, I'm not sure that it will have a huge impact on the field. I do think that the specialists who insert the stents may have some differences of opinion of who should be stented and who shouldn't. Because I think, you know, all of the specialists who do procedures were involved with the trial. But I would say there's a larger percentage of vascular surgeons who were involved, and so I'd say they may have a change of their practice. And neurologists may not even get involved at all.  Dr Jones: Right.  Dr Bushnell: That was one of the challenges for getting patients in the trial is that, you know, not all of us see the asymptomatic carotid stenosis, that they tend to get referred to vascular surgery. So, I think maybe in a corner of the practices of vascular surgeons is where you might see the differences.  Dr Jones: Your point about the way the trial was designed or the trials were designed, that intensive medical management is really important, and we have huge gaps in that. In our specialty, it's, you know, we have probably an opportunity in primary care even to address that. And that leads me to my next question. You know, given your perspective and your expertise, what do you think is the biggest practice gap in the care of patients with stroke or with cerebrovascular disease of any kind?  Dr Bushnell: I think by far the biggest gap is transitions of care and access to follow-up in a specialty clinic after discharge and continuous secondary prevention. We only call it secondary prevention because it happened to come after a stroke, but I really feel like we should just focus on prevention and call it that. There are a lot of people who are trying to kind of, get us away from primary versus secondary prevention. And, and Mitch Elkind is phenomenal and had a beautiful chapter weaving in prevention and brain health. So, I highly recommend that people, if they don't read any other chapters of the Continuum to read his, because I think that it's getting to your point about where the gaps are, and I think prevention is the biggest one. I think we could do so much more in models of care to ensure that there is a pathway once patients are discharged. We have no quality metrics. We have no measurement of how well people are doing after they're discharged. We have all of these fancy things and sophisticated acute treatments, but all of those are for naught if somebody goes home and they fall and they have a severe head injury or hip fracture because they weren't properly supervised or they didn't have the help that they needed at home. So, you got me on my soapbox here for a second, but that is definitely what I see as the gap.  Dr Jones: That's an important soapbox, an important gap, and obviously, if it was a simple problem, we could solve it. But it's obviously something that education is a valuable tool for that, and that's part of why we are including so much content in this issue of Continuum. So, if we put that aside as a gap that we would love to close, when you look into the near future or distant future, Dr. Bushnell, and what's the next big thing on the horizon? New interventions, new prevention tools, or something else entirely? What do you think?  Dr Bushnell: There are two things that I would mention. One is sort of the new category of anticoagulants, antithrombotics, the factor XIa inhibitors. We had an amazing presentation of the oceanic stroke trial at the International Stroke Conference, and this is probably going to be a game changer for the arsenal of antithrombotic therapies that we can offer to patients that do not have a reason for anticoagulation. So, they, they don't have atrial fibrillation, for example, or something else that requires anticoagulation. And so, the factor XI, asundexian, is the drug that they used in that trial. The safety profile is pretty amazing. There was very little bleeding complications and a great benefit in those patients with some degree of atherosclerosis, but, you know, of course, not enough to require carotid revascularization, but then also, um, small vessel disease and cryptogenic stroke. I think those are the three categories of patients, and that's a lot of the strokes that we see all benefited from this new drug. So, I think that's gonna be exciting. There, of course, it has to go through the FDA approval process, and so it might take a little bit of time before that's on the market, and we don't know how much it's gonna cost, but I think it is a, a major breakthrough. And of course, there are other similar medications in that category that are coming. And then I think the other thing is the emphasis on brain health and lifestyle factors and the things that we can do to prevent stroke and dementia because they are the same, essentially. Those are really important. And when we have someone in the hospital with a stroke or a TIA in particular, it's a great teaching opportunity for those patients to say, "Hey, here's what you can do to protect your brain." These are things that we always tell people to prevent a stroke, but just think about it as protecting your brain and keeping your brain as healthy as possible.  Dr Jones: That's a great message, and one that you get to share with patients directly. You're joining us today for this interview. You're on stroke service, so you're actively involved in caring for patients with stroke. What in your practice is the most rewarding aspect of caring for these patients? What is it that you find most rewarding?  Dr Bushnell: I've been involved in a clinical trial that has focused on managing blood pressure and also coaching and other aspects of stroke recovery. I think that has probably been the most rewarding aspect of my career. Until I was involved with this trial, I didn't necessarily do intensive blood pressure monitoring, but I'm seeing the benefits of having data from home, what those blood pressures are over a span of time. I see the immediate or intermediate effects of the blood pressure medication changes that I've made, and I see how the patients respond. So, I have to say that this is not part of usual practice, but I think it should be. And I think it's been incredible from the perspective of a neurologist who is really intensively trying to make the patients' lives better. And it's not just what I do, it's what the health coaches do as part of this intervention. And again, very similar to intensive medical management. So, I, I feel like I've been living it in a slightly different setting than in the CREST 2 trials. But there are other trials that have used the intensive medical management as approach as well. But I would say that's the most rewarding. I've seen people who've lost weight, who are physically fit, who are able to get off of blood pressure medications practically by the end of six months, and that's amazing. And then they continue doing it because they see the benefits.  Dr Jones: You've had a front row seat to a lot of that. That's really got to feel rewarding.  Dr Bushnell: It is, absolutely.  Dr Jones: You know, when you put it that way, it makes me want to go home and check my blood pressure, which I haven't done in a while. But I think that's a message to all of our listeners that we do have plenty of opportunity for risk factor optimization and following the evidence that has been generated and is being generated. Huge opportunity, not only at the population level, but I think the, um, individual patient level too. Okay, so now we're back to our Continuum Audio trivia question, and I'll repeat it for our listeners. How was warfarin discovered, and how did it get its name? Dr. Bushnell and I were talking about this earlier, so I'll just go ahead and share the answer. So, in the early 20th century in the U.S. Midwest, there were epidemics of a hemorrhagic disease in cattle, of all places, and this was eventually traced to moldy cattle feed that was made from sweet clover. And in 1940, researchers at the University of Wisconsin discovered that the anticoagulant in the sweet clover was a compound that was later synthesized for therapeutic use in 1954 as warfarin. And the name came from, uh, the support for the research. The research support came from the Wisconsin Alumni Research Foundation, or WARF, and the end of the word came from the underlying compound, which was coumarin. So that was a little bit of trivia that I had never heard. It's not in the issue, everyone, so you're getting something extra here on the podcast. But been using the drug forever. It still has its uses, even though it's become less advantageous than some of the newer agents. But-- And of course, Dr. Bushnell already knew that when I brought it up, but I just thought that was an interesting bit of history. Well, Dr. Bushnell, thank you for joining us. Thank you for such a great conversation about the latest in cerebrovascular disease. I learned a lot today. I learned a lot in reading these wonderful articles. I hope our listeners learned a lot today as well. I'm really grateful for your hard work on the issue, which I think will come in handy for junior readers and subscribers, as well as our more experienced neurologists as well. Sometimes it's hard to keep up with a rapidly changing subspecialty of our field. So, thank you for joining us today.  Dr Bushnell: Thank you for having me. It's been my pleasure.  Dr Jones: Again, today we've been speaking with Dr. Cheryl Bushnell, guest editor of Continuum's most recent issue on cerebrovascular disease. Please check it out, and thank you to our listeners for joining today.  Dr Monteith: This is Dr. Teshamae Monteith, Associate Editor of Continuum Audio. If you've enjoyed this episode, you'll love the journal, which is full of in-depth and clinically relevant information important for neurology practitioners. Use the link in the episode notes to learn more and subscribe. Thank you for listening to Continuum Audio.

Leading health experts have declared 2026 the Year of the Brain, and for good reason. Scientists are making exciting breakthroughs in understanding the body's command center, from prevention to diagnosis and treatment of neurological disorders. The brain enables us to think, see, learn, move, feel emotions and connect with our fellow humans, so keeping it healthy is essential at every stage of life. For a refresher on all that the brain does for us—and how to keep it performing at its best—we're joined by Dr. Anna Hohler, Director of Neurology for Northwell Health's Westchester Region. Dr. Hohler shares insights on brain development and milestones, and explains how exercise, good nutrition, adequate sleep and stress relief work together to support a healthy brain. She also shares simple strategies—some that may surprise you—that you can use to keep your brain healthy and strong for years to come.    The Takeaway We want to hear from you! Please complete our survey: 1199SEIUBenefits.org/member-feedback. Drop us a line at our social media channels: Facebook// Instagram // YouTube. Get started on your health journey by making an appointment with your primary care physician to know your numbers: 1199SEIUBenefits.org/healthyrelationships Get to know your numbers at 1199SEIUBenefits.org/healthyhearts. Relieve stress with mindfulness classes at 1199SEIUBenefits.org/healthyminds. Find healthy recipes and meal-prep tips at 1199SEIUBenefits.org/food-as-medicine. Visit the Healthy Living Resource Center for wellness tips, information and resources: 1199SEIUBenefits.org/healthyliving. Get inspired by fellow members through our Members' Voices series: 1199SEIUBenefits.org/healthyliving/membervoices. Stop by our Benefits Channel to join webinars on building healthy meals, managing stress and more: 1199SEIUBenefits.org/videos. Visit our YouTube channel to view a wide collection of healthy living videos: youtube.com/@1199SEIUBenefitFunds/playlists. Sample our wellness classes to exercise body and mind: 1199SEIUBenefits.org/wellnessevents.   Guest Bio Anna DePold Hohler, MD, FAAN, is a distinguished neurologist, researcher and educator who recently joined Northwell Health to lead and enhance neurology services for its Westchester Region, as well as launch a new virtual neurology program across the 28-hospital system. An internationally recognized expert in movement disorders, she is deeply involved in research furthering novel therapies to treat Parkinson's disease. Dr. Hohler began her career in the U.S. Army, serving for eight years and achieving the rank of major.   

In this episode of HPNA Palliative Perspective, we're joined by Betty Ferrell—Editor of the Journal of Hospice & Palliative Nursing (JHPN), nurse, and internationally recognized researcher. As the leader of the End-of-Life Nursing Education Consortium, she brings a unique perspective shaped by decades of connection with hospice and palliative care nurses across the U.S. and around the world.  Now in her 49th year in nursing—beginning in oncology and entering hospice as it emerged in the United States—Dr. Ferrell reflects on the remarkable growth of the field and where we stand today.  At the heart of this conversation is the idea of a “professional home.” Drawing on the foundational work of pioneers like Florence Wald and Cicely Saunders, she highlights the enduring importance of interprofessional, whole-person care—and the need to stay grounded in those values as the field evolves.  In a time that can feel complex and demanding, this episode offers a clear message: you don't have to do this work alone. Finding your people, building community, and staying connected—through colleagues and organizations like the Hospice and Palliative Nurses Association—are essential to sustaining both practice and purpose.  A thoughtful and reassuring conversation about belonging, connection, and the future of hospice and palliative nursing.      Betty Ferrell, RN, PhD, MA, CHPN®, FAAN, FPCN® Betty Ferrell, RN, PhD, MA, CHPN®, FAAN, FPCN® has been in nursing for 48 years and has focused her clinical expertise and research in pain management, quality of life, and palliative care. Dr. Ferrell is the Director of Nursing Research & Education and a Professor at the City of Hope Medical Center in Duarte, California. She is a Fellow of the American Academy of Nursing and she has over 500 publications in peer-reviewed journals and texts. She is Principal Investigator of the “End-of-Life Nursing Education Consortium (ELNEC)” project. She directs several other funded projects related to palliative care in cancer centers and QOL issues. Dr. Ferrell was Co-Chairperson of the National Consensus Project for Quality Palliative Care. Dr. Ferrell completed a Masters degree in Theology, Ethics and Culture from Claremont Graduate University in 2007. She has authored 12 books including the Oxford Textbook of Palliative Nursing (5th Edition, 2019) published by Oxford University Press. She is co-author of the text, The Nature of Suffering and the Goals of Nursing published by Oxford University Press (2nd Ed, 2023) and Making Health Care Whole: Integrating Spirituality into Patient Care (Templeton Press, 2010). In 2013 Dr. Ferrell was named one of the 30 Visionaries in the field by the American Academy of Hospice and Palliative Medicine. In 2019 she was elected a member of the National Academy of Medicine. In 2021 Dr. Ferrell received the Oncology Nursing Society Lifetime Achievement Award and she was inducted as a “Living Legend” by the American Academy of Nursing   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.

Photo by Patty Brito on Unsplash The U.S. healthcare system is in crisis. COVID strained health care organizations and stressed healthcare workers; and it seems that we've not yet recovered from that nightmare. We're unlikely to see the system recover in the short term and it may take a lot longer, as the Trump Administration and Congress make cuts to tax credits for health insurance, Medicaid, and other health programs. The leaders of healthcare organizations are focused on the bottom line to survive but some exceptional healthcare administrators are also focused on supporting their staff, particularly nurses who provide the bulk of care. They know that you can't have quality healthcare with good outcomes if you don't address employee satisfaction. But what does this work look like? How do healthcare organizations such as hospitals ensure that nurses and other healthcare workers are provided with the support they need to be able to do their jobs well and feel joy in their practice? The American Nurses Credentialing Center has looked at this for nurses and has an initiative called Pathway to Excellence that focuses on how organizations can create positive practice environments that empower and engage staff, and recognizes the organizations that do create such environments. HealthCetera host Diana J. Mason, PhD, RN, talked about this work with Christine Pabico, RN, PhD, FAAN, Senior Director of the Pathway to Excellence Program for the American Nurses Credentialing Center. This interview first aired on HealthCetera in the Catskills on WIOX Radio on April 29, 2026. The post Providing Nurses & Other Healthcare Workers with Support appeared first on HealthCetera.

Photo by Meg Sanchez on Unsplash Summer is upon us and, even in spring, people are enjoying the outdoors after a rough winter. But the sunny days are notinnocuous. Public health nurse and HealthCetera Correspondent Barbara Glickstein, MPH, RN, FAAN, who worked for a time in adermatologist's office many years ago and continues to pay attention to issues related to skin cancer, talked with HealthCetera host Diana Mason, PhD, RN, FAAN, about this important topic, including the Trump Administration’s Health and Human Services Secretary Robert F. Kennedy, Jr.’s removal of a proposal that would have banned the use of indoor tanning beds by children. This interview first aired on HealthCetera in the Catskills on WIOX Radio on May 13, 2026. The post The Importance of Skin Cancer Awareness appeared first on HealthCetera.

Photo by Igor Omilaev on Unsplash Artificial intelligence (AI) is already upending our world. It's being used in health care in a variety of ways, including for interpreting x-rays and other imaging, flagging potential concerns that a clinician may overlook, and supporting diagnostic decision-making. There have been suggestions that robots and AI could even replace nurses. Needless to say, there are a lot of concerns within the nursing community about how AI is used in health care. In recognition of these concerns, the American Academy of Nursing issued a position statement on Artificial Intelligence in Health Care. HealthCetera host Diana J. Mason, RN, PhD, FAAN, discussed this position statement with  Debra Barksdale, RN, PhD, FAAN, president of the Academy and Dean of the University of North Carolina at Greensboro School of Nursing. This interview first aired on HealthCetera in the Catskills on WIOC Radio on April 15, 2026. The post AI and Healthcare appeared first on HealthCetera.

Photo by Reproductive Health Supplies Coalition on Unsplash In June of 2022 in the case of Dobbs v. Jackson Women's Health Organization, the Supreme Court overruled Roe v.Wade on the basis that access to abortion is a state issue. Since that decision, some states have passed laws restricting or banning altogether women's access to abortion. But the Food and Drug Administration approved the distribution of Mifepristone for medical abortions without an in-person visit as a safe practice. Louisiana filed a lawsuit against the FDA for this action and at the end of April 2026, the Fifth Circuit Court of Appeals ruled in favor of Louisiana, restricting women's access to the drug in states that have banned abortions. On May 4th, the Supreme Court ordered a halt to stopping access to the drug until May 11th so that both sides could respond and the court could consider the issue more fully. HealthCetera host Diana Mason, PhD, RN, FAAN, discussed the case of Louisiana v. the FDA and the Fifth Circuit Court of Appeal's ruling with Anna Beernstein, principal federal policy advisor for the Guttmacher Institute, a research and policy organization committed to advancing sexual and reproductive health and rights worldwide. This interview first aired on HealthCetera in the Catskills on WIOX Radio on May 6, 2026. The post The Fifth Circuit Court of Appeals & Women’s Health appeared first on HealthCetera.

Brian Maher is the Assemblyman for NY's 101st Assembly district that includes parts of Orange, Ulster, Sullivan, and Delaware Counties. Assemblyman Maher is in the Navy reserves and was activated and deployed last year. He remains deployed and his chief of staff, Meghan Hurlburt, is carrying forth with representing him and his positions in the Assembly and the communities he represents. HealthCetera host Diana Mason, RN, PhD, FAAN, talked with Hurlburt about Assemblyman Maher’s positions on several issues that are before the New York State legislature in the 2026 session. This interview first aired on HealthCetera in the Catskills on WIOX Radio on May 6, 2026. The post Interviewing Meghan Hurlburt about Assemblyman Brian Maher appeared first on HealthCetera.

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 NCPD/ILNA information, and to apply for credit, please visit us at PeerView.com/FJB865. NCPD/ILNA credit will be available until May 25, 2027.“Off-the-Shelf” Choices in RRMM: Oncology Nurse Guidance on Delivering Quality Care With BCMA and Non-BCMA Immunotherapy 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 educational activity is supported by an independent medical education grant from GSK.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 NCPD/ILNA information, and to apply for credit, please visit us at PeerView.com/FJB865. NCPD/ILNA credit will be available until May 25, 2027.“Off-the-Shelf” Choices in RRMM: Oncology Nurse Guidance on Delivering Quality Care With BCMA and Non-BCMA Immunotherapy 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 educational activity is supported by an independent medical education grant from GSK.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 NCPD/ILNA information, and to apply for credit, please visit us at PeerView.com/FJB865. NCPD/ILNA credit will be available until May 25, 2027.“Off-the-Shelf” Choices in RRMM: Oncology Nurse Guidance on Delivering Quality Care With BCMA and Non-BCMA Immunotherapy 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 educational activity is supported by an independent medical education grant from GSK.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 NCPD/ILNA information, and to apply for credit, please visit us at PeerView.com/FJB865. NCPD/ILNA credit will be available until May 25, 2027.“Off-the-Shelf” Choices in RRMM: Oncology Nurse Guidance on Delivering Quality Care With BCMA and Non-BCMA Immunotherapy 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 educational activity is supported by an independent medical education grant from GSK.Disclosure information is available at the beginning of the video presentation.

When blood collects in the skull outside the brain and below the outermost layer of tissue surrounding the brain (dura), a subdural hematoma results. This may occur due to head trauma when it is called an acute subdural hematoma. Chronic subdural hematomas may occur due to aging and the increased fragility of blood vessels. The pooled blood may resolve on its own or may require surgical intervention as development of a subdural hematoma can be a life-threatening condition. Symptoms of subdural hematoma can include headache, confusion, change in behavior, dizziness, nausea and vomiting, lethargy or excessive drowsiness, weakness, apathy, and seizures. Subdural hematomas are generally diagnosed by CT scan or MRI imaging. Ashkan Mowla, MD, FAHA, FAAN, is neuro-interventional surgeon at the Pacific Neuroscience Institute® (PNI). He specializes in minimally invasive endovascular procedures to treat conditions and diseases of the brain and spine, including stroke, brain aneurysm, brain and spine arteriovenous malformation and fistula and carotid and intracranial disease. Accepting new patients: 424-212-5361

This episode features Prof. Rihua Xie from Guangdong Medical University (China) and Dr. Yuhang Zhang from Peking University First Hospital (China), speaking about vaginal microbiota transfer (VMT) and how it may affect neurodevelopment in newborn infants born by Cesarean section. Compared with vaginally delivered infants, C-section delivered infants have altered microbial exposures. VMT has been proposed as a way to ‘restore' the microbiota of these infants to more closely resemble that of vaginally-born infants. A recent study by Prof. Xie and Dr. Zhang showed that the order and timing of early microbial colonization of the infant is important. They found that VMT could establish a vaginal-like skin microbiota in infants born by C-section, with two particular bacterial species that were higher after VMT. These two species led to the production of metabolites that combined on the newborn's skin to synthesize an important lipid, which was positively correlated with neurodevelopment scores at three and six months. Subsequent mouse model work showed how this lipid could reach the brain. In the future, safety and standardization of VMT will be important priorities in this research area. Prof. Xie and Dr. Zhang emphasized that their work needs to be replicated in larger cohorts, with the eventual goal of engineering bacteria to create a probiotic intervention that delivers neurodevelopmental benefits to C-section born infants. Episode abbreviations and links: The research by Prof. Xie and Dr. Zhang demonstrating how a VMT intervention alters the skin microbiota of newborns, with a mechanistic link to neurodevelopment: Vaginal microbiota transfer ameliorates cesarean-associated neurodevelopmental deficits in mice via N-bc2S1P synthesis on neonatal skin About Prof. Rihua Xie: Dr. Ri-hua Xie (RN, PhD, FAAN) is Professor, Principal Investigator, and Chief Nurse at the School of Nursing, Southern Medical University, and the Affiliated Foshan Women and Children Hospital, Guangdong Medical University, China. Dr. Xie is widely recognized for her expertise in maternal and infant health as a clinician, researcher, and supervisor. She has published more than 90 peer-reviewed papers and 11 nursing textbooks and has received 12 competitive research grants from institutions in China and Canada. In addition to her academic work, Dr. Xie is actively engaged in community and public health service, including breastfeeding promotion and frontline support during the COVID-19 pandemic. Her research focuses on perinatal epidemiology, maternal and child health, and microbiome science, with a particular emphasis on the effects of vaginal microbiota transfer (VMT) on the microbiota composition and health outcomes of cesarean-delivered infants. About Dr. Yuhang Zhang: Yuhang Zhang, PhD in Pharmacology, is an Associate Professor and Principal Investigator at Peking University First Hospital. He received his MD-PhD from Capital Medical University and was a visiting scholar at McGill University, Canada. Dr. Zhang's research focuses on gut microbiome, probiotics, and microbial metabolism in metabolic diseases, who has published over 20 peer‑reviewed papers as first or corresponding author in journals including Gastroenterology, Journal of Hepatology, and Nature Communications, cited >1,000 times. He has led 9 grants, including the National Natural Science Foundation of China, who was selected for the Beijing Association for Science and Technology Young Talent Program (2022) and the China Association for Science and Technology Young Talent Program (2025). The research of Dr. Zhang focuses on the integrated systems pharmacology, multiomics and microbiome‑host interactions to develop precision medicine.

In this episode, Jill Hoggard Green, PhD, RN, FAAN, Trustee for The Joint Commision, Joint Commision International and Health Catalyst, discusses the lasting impact of COVID-19, the importance of balancing financial priorities with clinical innovation, and strategies for supporting and developing the next generation of healthcare leaders and caregivers.

In this episode, Jill Hoggard Green, PhD, RN, FAAN, Member of Joint Commission's Board of Commissioners and is chair of Joint Commission Resources' Board of Directors, discusses the lasting impact of COVID-19, the importance of balancing financial priorities with clinical innovation, and strategies for supporting and developing the next generation of healthcare leaders and caregivers.

In this episode, editor in chief Joseph E. Safdieh, MD, FAAN, highlights articles about a new selective dopamine agonist for people with Parkinson's disease, the use of artificial intelligence in preparing journal manuscripts, and caffeinated coffee's role in reducing dementia risk.

Palliative care in multiple sclerosis spans the disease course, from early screening and support after diagnosis to symptom management and quality‑of‑life optimization in midstage disease, and end‑of‑life care in advanced MS. This episode outlines a staged approach to palliative care, highlights the roles of neurology and primary care teams, and discusses tools such as patient‑reported outcomes and symptom scales to support ongoing assessment of patients and care partners. In this episode, Katie Grouse, MD, FAAN, speaks with Penelope Smyth, MD, FRCPC and Janis M. Miyasaki, MD, MEd, FRCPC, coauthors of the article "Palliative Care in Multiple Sclerosis" in the Continuum® April 2026 Multiple Sclerosis and Related 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. Smyth is the director of the Division of Neurology in the Department of Medicine at the University of Alberta in Edmonton, Alberta, Canada. Dr. Miyasaki is a professor in the Division of Neurology in the Department of Medicine at the University of Alberta and the zone clinical department head for Clinical Neurosciences at Alberta Health Services in Edmonton, Alberta, Canada. Additional Resources Read the article: Palliative Care in Multiple Sclerosis 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 Grouse: With the new treatments for MS, people might be saying palliative care is not relevant at all. It's about giving up hope and hopelessness. But this article covers why palliative care is important for your patients and families throughout their illness trajectory. 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 Drs Penelope Smyth and Janis Miyasaki about their article on palliative care in multiple sclerosis, which appears in the April 2026 Continuum issue on multiple sclerosis. Welcome to the podcast, and please introduce yourselves to our audience.  Dr Smyth: Thank you, Katie. I'm Penny Smyth. I am a neurologist at the University of Alberta, a professor in neurology, and a clinical multiple sclerosis specialist.  Dr Miyasaki: Hi, Katie. Thanks for having us. I'm Janis Miyasaki. I am a movement disorder neurologist primarily who also provides neuropalliative care at the University of Alberta in Edmonton, Canada.  Dr Grouse: It's so great having you today to talk with us about your article. I thought this article was really a wonderful take on the topic. I learned a lot, and I'm really hoping all of our listeners will take advantage of this article and take advantage of all the learning they can get from reading about this topic. So, I wanted to start with a more general question, which is, what is the key message from this article that you're hoping your readers will take away?  Dr Smyth: In terms of key takeaways, I think it's our hope that neurologists will come away from reading this article with, really, an expanded understanding of what palliative care is and how that might be applicable to them in their care for their patients with MS along a continuum of treating people with MS, that there can be components of palliative care and strategies that can be integrated early after diagnosis in, really, anywhere along the continuum of caring for people with MS. We've called that kind of mid-stage. And then there are particular needs for people with MS and their care partners in late-stage or severe MS and end of life that might require different palliative care strategies. I think we kind of have maybe a bit of a bias sometimes in thinking of palliative care as more directed towards those that are near end-of-life. But in fact, it's a much expanded concept.  Dr Miyasaki: And I'll just add that we also discuss a palliative approach, that palliative care skills and philosophies can be used by generalists---in this case, neurologists who are providing care to people with MS---and that adopting certain skills and communication techniques can help us better address our patients' and their families' symptoms. And also to keep in mind that for most people with neurologic illness, the unit of care is not only the patient, but it's the patient and the family, however that family looks.  Dr Grouse: Now, Penny, I'm curious, how are early-stage and mid-stage multiple sclerosis palliative care strategies different from, say, a typical evaluation and counseling that a neurologist would give, say, an MS specialist or even a general neurologist?  Dr Smyth: Thank you, Katie. That's a great question, and something that actually I learned in writing this piece with Janice and from her as a neuropalliative care expert. I think in terms of early strategies around palliative care that can be helpful to the general neurologist in their office, palliative care is about holistic support for patients and their care providers spiritually, emotionally, physically. There are components of palliative care and symptom management and making sure that the patient is at the center of the care, as well as support for their care partners with their holistic approach of relief of suffering as well as offering hope. When I started this piece, I was thinking that many of us neurologists, I think, often informally utilize many of these components already when we're dealing with patients early on after diagnosis in terms of communication, counseling, and education; going through their fear of an uncertain future; spiritual well-being; and then connecting them with supports for adaptive coping strategies. And then as well in mid-stage, which is really around what we can do in symptom management and improving quality of life, with screening tools and patient-reported outcome measures. However, I have to say that there are many unmet needs for people with MS and their care partners that they identify that are clearly not being met by us neurologists in this day and age. So even though we may be incorporating some of these strategies, I don't think we're meeting the mark all the time and hitting the target, especially in our busy office practices, in various ways. Dr Grouse: Given that, at a high level, what are some important early-stage MS palliative care concepts that we should be keeping in mind when we are counseling patients in these stages of the disease? Dr Miyasaki: An important concept to keep in mind for neurologists dealing with early-stage MS patients is that for us, we feel successful that we have made a diagnosis. And yet for the patient, it is taking away that hope. Maybe it's not MS. Maybe I just have a numb hand and it's gonna go away. And for us to appreciate that while we make this diagnosis multiple times a week---or, for MS specialists multiple times a day---for this person, it is the first time, the first experience, and it shakes their entire foundation of who they are as a person, how they will perform all the tasks and roles that they have in society, in their professional lives, in their family structures, and in their close, intimate relationships. As physicians, we may be overwhelmed by acknowledging that. I feel that it's important for us to understand the needs that our patients have and to allow them to have their feelings. You know, feelings can feel messy and time-consuming, and yet when we fully see our patients, I feel that this is the best of medicine. And it certainly is, in terms of palliative care, the principle that we seek. We accept all of the patient, the joy and the sorrow, the anger and the frustration. We accept it all, and we try to determine what will serve this person who is suffering in front of us now.  Dr Smyth: There's another piece to this, which came up as Janice and I were writing together. We were talking about offering a prognosis to a patient as to how they would do, and this was something that I thought deeply about, because I said, we always communicate how uncertain the prognosis is and how we can't predict the future. And then she said to me, well, what about offering a roadmap to a person with MS soon after diagnosis as to how you're gonna determine how they do over the next couple of years? Which are really important years in terms of determining how patients are doing on their disease-modifying therapies, whether they're having progression or not, and things. It's a pivotal time. So, if you can offer a roadmap to a person with MS and say, look, this is when we will be following you up. This is how we will be following you with MRI and biomarkers if you have that available, and this is how we will determine how responsive you are and then how we move forward from there. Dr Grouse: Really important concepts. And the roadmap certainly makes a lot of sense to me and something that, apart from just being useful to the patient for so many reasons to help set expectations, you know, is useful for us to better partner with the patient so they understand this is sort of how we do things and everyone's sort of expectations are met. So, I think those sound like really great goals and things to keep in mind. Now, we talked about early-stage MS palliative care concepts. How does that change as you get into the mid-stage of the disease?  Dr Smyth: Yeah. So, this is reflecting the fact that the course of MS is so different and the experience of MS is so different person to person. And so, what do we do as neurologists when we follow these people long-term over years and decades of living with their MS as their needs evolve, as their symptoms evolve, and as their disability evolves? Well, really, this is about the time of getting into, what are the symptoms that they're struggling with, what are the causes of their suffering at various points? And then how do we identify that, maybe with use of patient-reported outcome measures, screening scales, things like that. And then how do we direct symptomatic management to the specific symptoms that are causing distress to the patient? As well as trying to improve their quality of life in various ways, treating their comorbidities, making sure to check on exercise, healthy living, and that kind of thing.  Dr Grouse: Now getting into, I think, topics that we're more used to thinking about when we think about palliative care: a lot of us, I think, are really unsure of the right time to discuss advanced care directives in the course of multiple sclerosis, and I think that's not helped by the fact that many of us are just, in general, not terribly comfortable talking about those types of things in general. What is your advice to questions like this?  Dr Smyth: And this is something that, again, Janice and I had to come together on, because there is no universal accepted time for when is the right time in multiple sclerosis to discuss advanced care directives and goals of care. And in fact, when they have looked at it in the literature, different things have come out. It has come out that neurologists can be uncomfortable discussing this. There's unique challenges to people with MS in that they have a diagnosis at a young age with an uncertain trajectory of how their course of disease is going to go. And many of these things lead care providers to be somewhat hesitant as to when is the right time, as well as, there were identified barriers within patients themselves as to when the right time might be to discuss. In that, you know, some of the coping strategies might be, as identified by some of the qualitative studies that have been done on this, around the fact that they would prefer to focus on the present rather than the future. In some studies expressed an ambivalence as to when they thought the right time might be, as well as some negative experiences that they might have had from providers trying to discuss these things in their previous experience. So, I went back to looking at the European guidelines for palliative care in MS, who suggested when a person might have severe MS---which they define as walking with bilateral aids for at least twenty meters or an EDSS of six or higher---or trigger-based, when there has been a change in the patient's status, when there's been a decline in some way or progression. Now, this is a little different, actually, than what we offer other people with neurologic diseases, and I don't know if that's the right answer. And this is where I'm going to turn it over to Janice, because I think we could learn something, as neurologists who treat people with MS, from our palliative care specialists.  Dr Miyasaki: I think of advanced care planning in a very different way. I think what a lot of the patients were expressing in the studies was that being asked about advanced care planning signaled to them in some way that they have reached this point in their illness where things aren't going so great and I anticipate that you may run into complications. Whereas in our movement disorder clinic, one of our fellows did a study looking at capacity for decision-making. And even in people who scored normally on the Montreal Cognitive Assessment, they had impairments in some of the domains of decision-making. And so, our philosophy in movement disorders at least---and some of our patients are quite young who have multiple system atrophy, they could be in their forties---we take the philosophy that everyone over the age of decision-making capacity, which is generally eighteen, should have some goals of care established. And how I introduce it in my clinic is, you know, for the young resident, you want the full-meal deal, because the likelihood of the resident surviving the ICU admission is very high. And then when we look at me, who… I am older, the likelihood of surviving an ICU admission is considerably lower. And so, the appropriate goals of care might be that I am willing to go to the ICU, and if things go well, then they can continue. But if things are not going well, they can have a discussion with my personal directive or power of attorney to talk about what the goals of care should be. And then the other aspect is sometimes having the conversation with family is really important because most of our families in hospital express an uncertainty. Am I doing the right thing? And they want to do the right thing for their loved ones. And most people actually say, if you ask them, I don't want to burden my family with making decisions that are going to tear at their hearts. So, then we can't actually make good informed decisions for our loved ones unless we have clear conversations. I think it does speak to our superstitious beliefs that if we talk about death, it's going to happen. But I hope the listeners will take my word for it, it really doesn't. And someone had a really good saying about the advanced directive. They're kind of like evening clothes. You should take them out every once in a while and make sure they still fit. And so, when you normalize it in this way, it helps people to just say, oh, yeah, it's once a year. Dr. Miyasaki is gonna ask me about how do I feel about those goals of care. And then it doesn't have this portent of, oh, I'm not doing well. Instead, it's just, this is what we should all be doing for our sake and for our family's sake.  Dr Smyth: Now, one thing that I have to add on to this is that it is important to try to establish advanced care directives before patients experience cognitive decline, because then that can make it a much more challenging conversation and brings nuances of challenge into the interactions, which, you know, are hard.  Dr Grouse: And Penny, I'm glad you brought that up, because I was really struck by that point too when reading this article, how easy it is to miss the subtle signs that cognitive changes are happening. I think it's just- it's a good kind of segue into that topic in general, but it is such an important link to, you know, making sure that you get those advanced directives at a time when the patient's really able to express and understand what they're talking to you about. Now, on the topic of the cognitive screenings, what's a good way to do this type of screening, and why is this type of screening so particularly important in the case of multiple sclerosis?  Dr Smyth: Yeah. Thank you, Katie. I think that it's important for our listeners to think about and recognize when we see our patients with MS because it is one of the invisible symptoms that people with MS can live with and may not be apparent on regular conversation in the office. So, it's important to deliberately ask about subjective challenges in cognition. Ask the partner about how they're doing in terms of their cognition in various ways. As well as asking them and exploring then, how are they doing in their professional roles if they're working or in their surroundings? How are they coping on a daily basis on a cognitive level in addition to a physical level? We know that cognitive issues are actually the biggest contributor for not working and are a huge driver of disability in MS in terms of functioning, even more than physical decline in many ways. So, it is important for us neurologists to keep top of mind and to think about and deliberately attend to. There are screening tests that we can do in the office. The easiest for us, which measures the verbal processing speed, is the SDMT test, which is a ninety-second test matching symbols and numbers. It's easy to do. You can train a MOA to do it before you see the patient and things like that, and it just gives you an idea as to where the patient is at. And usually they're having difficulties if they're greater than two standard deviations below the norm for their age, or if there's a significant drop of four or eight points, and that might signal to you that there might be more going on. You can explore it, and then if you do have this available, the ability to refer for neuropsychological testing if there's questions. But often we can't get it with the MoCA score, unfortunately.  Dr Grouse: Talking about all these concepts, I think they all sound great. I think a lot of us hearing this will naturally say, "Yes, these are absolutely things we should be incorporating in the care of these patients." What I wondered about was, certainly we're all very busy, it is really hard to find time for a lot of these things. We don't always have access to specialists who can help us with some of these conversations. How can we find time, and how can we work this into the care of our patients effectively and still make time for all the other things we have to talk about, and make sure that we're seeing all of our other patients and staying on time and all of those things?  Dr Miyasaki: Yes. I think that's the challenges of dealing with people who actually, over time, their care needs increase, is huge in neurology. I can't think of a single subspecialty where care actually gets easier. It's constantly getting harder. You know, having come from private practice, I completely understand my colleagues' challenges in the community. Some of the ways that other groups have managed this when they don't have government or university support in their center is actually to look at not-for-profits. There are a lot of not-for-profits that can help in terms of wayfinding for social services, explaining to the patients and the family what is available to them. And in fact, some of them can also provide some cognitive supports, as well as point them in the way of day programs. And many of them have very established caregiver support groups, as well as patient support groups for various stages of their illness. So, I think it requires for the individual or small or even a large group practice to be inventive, to look in your community and see what resources are available and free for your patients in order to establish that loose team without boundaries to help your patients. Of course, for those in academic centers, I know that times are tight for all of us, and if you haven't established a team, it is a challenge; and then learning how to write a business plan or a briefing note for your institution and to learn how to speak the love language of administrators, is really key to putting forward the needs of our patients. Which, compared to heart attack patients or hips and knees, they are very rare, and yet our patients can result in significant cost to the healthcare system. So, we do have an opportunity to make the case that putting a little bit of investment in the ambulatory setting can result in significant cost savings to the system when it comes to acute care hospitalization.  Dr Smyth: So, I was thinking, Janis, as you were talking about that, when you were talking about not-for-profit groups, it's really the MS societies in various countries that are very active in this and have a lot of resources available, especially for care partners.  Dr Grouse: Those are really great tips. Thank you for bringing those up as potential other resources we can take advantage of. I wanted to ask specifically about physician-assisted death and assisted suicide, which certainly does come up, especially in later-stage parts of the disease. How can palliative care specialists be helpful when patients do express interest in these types of interventions?  Dr Miyasaki: As you know, Katie, in Canada, we've had a legislative right to access to what we call medical assistance in dying. When the legislation passed, one of my other colleagues and I felt that these were the only conversations we were having with our patients. In all this experience, I have sort of developed in my mind a framework of people who are what we call MAID-curious. They want to know what their rights are and how it would look, when they feel the time is close, for them to exercise that right. And then there are those who are fearful of future suffering. And some of them may have a very unrealistic view of what the future will look like. And this may be in particular for multiple sclerosis because many of the public's view is based on what treatment was like thirty years ago. It may not be informed by more recent treatment where patients actually do quite well, and the majority never get to progressive MS. And so, to explore and be open to that request is the first thing that is important. And then if the person has unresolved symptoms that, traditionally, we can't care for, the palliative care specialist can be very helpful because they just have inventive ways of looking at things. They look at it outside the box, and they have a different toolkit available to them. I would not want all neurologists to just send all these patients requesting physician-assisted death to their palliative care colleagues. But I think for those who are having unaddressed symptoms, it can be very helpful. Certainly, if there is an acute event in the hospital, then this is a time of crisis. And often hospitals will have an in-hospital palliative care team who can come and speak to the patient about what is going on and address some of their needs. And I would also like to emphasize the importance of spiritual care, because for many of our patients, they are not just having the physical suffering, they are also having the spiritual suffering of hopelessness or of feeling that they are a burden or that they just are not seen because a lot of the symptoms in MS are invisible. To have that understanding by a spiritual care counselor is really helpful for the people to feel understood and to reduce some of that suffering.  Dr Grouse: That's a really great point, I think, to end on, and I think it really ties in a lot of the themes that we've been talking about today. Thank you so much for coming to talk with us today. It's been such a pleasure having you both here. Dr Smyth: Thank you. Dr Miyasaki: Thank you, Katie. Dr Grouse: Again, today I've been interviewing Drs Penelope Smyth and Janis Miyasaki about their article on palliative care in multiple sclerosis, which appears in the April 2026 Continuum issue on multiple sclerosis. Be sure to check out Continuum Audio episodes from this and other issues, and thank you to our listeners for joining today.  Dr Monteith: This is Dr. Teshamae Monteith, Associate Editor of Continuum Audio. If you've enjoyed this episode, you'll love the journal, which is full of in-depth and clinically relevant information important for neurology practitioners. Use the link in the episode notes to learn more and subscribe. AAN members, you can get CME for listening to this interview by completing the evaluation at continpub.com/audioCME. Thank you for listening to Continuum Audio.

In this episode of the Society of Critical Care Medicine (SCCM) Podcast, Diane C. McLaughlin, DNP, AGACNP-BC, CCRN, FNCS, FCCM, is joined by Aarti Sarwal, MD, FAAN, FNCS, RPNI, FCCM, and Brian L. Erstad, PharmD, FCCP, FASHP, MCCM, to discuss the 2026 guidelines for neuromuscular blockade in adult patients with acute respiratory distress syndrome. The guidelines, “Society of Critical Care Medicine Guidelines for the Administration of Neuromuscular Blockade in Adults With Acute Respiratory Distress Syndrome,” were published in the March issue of Critical Care Medicine. Drs. Sarwal and Erstad discuss how the evidence in two key trials, ACURASYS and PETAL-ROSE, has helped shape the recommendations provided in the SCCM guidelines. Despite how influential these trials were in shaping the recommendations, only conditional recommendations were made due to low or very low quality of evidence. The lack of evidence proved to be a driving factor in including a call to action in the guidelines. Future research priorities largely revolve around precision medicine and finding more patient-specific interventions to improve patient outcomes. Aarti Sarwal, MD, FAAN, FNCS, RPNI, FCCM, is a professor of neurology and the division chair of neurocritical care at Virginia Commonwealth University (VCU) School of Medicine in Richmond, Virginia, USA. She is also an associate editor of Critical Care Medicine, secretary of the American Society of Neuroimaging, and director of VCU-Wake Forest neuro-ultrasound courses. Brian L. Erstad, PharmD, FCCP, FASHP, MCCM, is a tenured professor and interim dean at the University of Arizona R. Ken Coit College of Pharmacy in Tucson, Arizona, USA. He is also a center investigator for the Center for Health Outcomes, a member of the BIO5 Institute and Comprehensive Center for Pain & Addiction and Pharmacoeconomics Research Center, and a codirector for the Arizona Clinical and Translational Research Graduate Certificate Program. Resources referenced in this podcast: Society of Critical Care Medicine Guidelines for the Administration of Neuromuscular Blockade in Adults With Acute Respiratory Distress Syndrome Early Neuromuscular Blockade in the Acute Respiratory Distress Syndrome Neuromuscular Blockers in Early Acute Respiratory Distress Syndrome

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Advances in immunotherapies for multiple sclerosis and related disorders have increased the risk of infections and raised important questions about vaccination efficacy. This episode reviews infection risks across treatment classes, emphasizes the importance of monitoring and patient education, and discusses optimal vaccine timing to preserve protective immune responses. In this episode, Aaron L. Berkowitz, MD, PhD, FAAN, speaks with Avindra Nath, MBBS, FAAN, coauthor of the article "Infection Risk and Vaccine Considerations in Multiple Sclerosis and Related Disorders" in the Continuum® April 2026 Multiple Sclerosis and Related Disorders issue. Dr. Berkowitz is a Continuum® Audio interviewer and a professor of neurology in the Department of Neurology at the University of California, San Francisco, in San Francisco, California. Dr. Nath is the chief of the Section of Infections of the Nervous System at the National Institute of Neurological Disorders and Stroke, National Institutes of Health, in Bethesda, Maryland Additional Resources Read the article: Infection Risk and Vaccine Considerations in Multiple Sclerosis and Related 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: @AaronLBerkowitz Full episode transcript available here Dr Berkowitz: Over the last decades, there has been a revolution in the treatment of multiple sclerosis, neuromyelitis optica spectrum disorder, and other immune-mediated neurologic conditions with countless new, highly effective medications. However, with every new treatment comes new risks; and in the case of immunomodulatory therapy, many of those risks relate to infection. Today, I have the privilege of talking with an expert on this topic, Dr Avindra Nath, about the infectious risks of treatments for multiple sclerosis and other immune-mediated neurologic disorders.  Dr Jones: This is Dr Lyell Jones, Editor-in-Chief of Continuum. Thank you for listening to Continuum Audio. Be sure to visit the links in the episode notes for information about earning CME, subscribing to the journal, and exclusive access to interviews not featured on the podcast.  Dr Berkowitz: This is Dr Aaron Berkowitz, and today I'm interviewing Dr Avi Nath about his article on vaccine considerations and infection risk in multiple sclerosis and related disorders, which he coauthored with Dr Amit Bar-Or. This article appears in the April 2026 Continuum issue on multiple sclerosis. Welcome to the podcast, Dr Nath, and could you please introduce yourself to our audience?  Dr Nath: Thanks very much for inviting me to this podcast. I'm absolutely delighted to have the opportunity to discuss our areas of interest and expertise related to infections and vaccinations for MS patients. My area has been studying the infections of the nervous system since the beginning of the AIDS pandemic, and over the years and decades, we've developed expertise related to various types of CNS infections. That includes ones that are developing in individuals who have immune compromise due to a variety of different reasons. Dr Berkowitz: Fantastic. Well, glad to have the opportunity to speak with you today. When I was in medical school---and you were my attending, actually, we were just reminiscing, which we probably think was not that long ago, but is now over twenty years ago---there were just two medications for MS, right? Beta interferon and glatiramer acetate. And now we have over a dozen, and it's amazing to think of all the progress in these last two decades, as well as for related diseases like NMO. I don't think we even had the aquaporin-four biomarker, right, when I was working with you as a med student in the early 2000s. Dr Nath: And that certainly dates me a lot.  Dr Berkowitz: Both of us.  Dr Nath: Yeah.  Dr Berkowitz: Of course, with all these new treatments, these have been amazing advances for our patients, right? But these come with new treatment-related risks to monitor for with the immunomodulatory medications for MS and related disorders. And one of those most important risks is that of infection. So, your article reviews the potential infectious complications of medications used to treat MS, NMO, etc, and also covers considerations related to thinking about vaccines in this patient population. So, as the MS treatment landscape grows, I can say as a general neurologist, keeping up with all these medications and what to screen for and what to worry about and when to vaccinate just becomes more challenging every year. And your article has so many helpful tables, some organized by medicine, some organized by- sorry, medication, some organized by infection, some by vaccines. So, this is gonna be a great resource for our providers to print out and tape up in their clinic rooms. We won't be able to get into all the depth and detail that you have in this article today, but I do want to focus on some of the key points here related to the common medications we use for MS and which infections to think about and which vaccine considerations we might need to keep in mind for these medications. But before we delve into the drugs, I just wanna ask you more broadly, you talk in the article about the challenge of patients with immune-mediated diseases who are on immunomodulatory therapy being at risk for both flares of their disease and for infections; and these infections can present somewhat atypically, right, in immunomodulated hosts, to maybe coin a term you can correct me on, because they can't mount the full inflammatory response. So how do you approach new symptoms in patients on these immunomodulatory medicines as far as distinguishing disease flare from a treatment-related infection?  Dr Nath: So, I have to say that although a lot of new treatments have come along for MS, and they've really, you know, improved the outcome tremendously and there are so many different options, it has also kept people like me relevant because they cause a lot of various types of infections, and so keeps me in business all the same. But just as you mentioned, there's so many of them, even I have difficulty keeping track of what does what. So, you do need to be able to refer back to published literature, and the tables, I hope, will be quite useful in that regard. You're absolutely right, and you can get new infections, you can get reactivation of existing infections, and you can get atypical presentations of various types of infections that you may not normally think of. So that presents multiple challenges to the treating physician. The other interesting thing about MS is, just as you mentioned, that you already have CNS lesions to begin with. Now, on top of it, you have an infection, so now how to sort out what is the existing disease and what is the infection, it can again become challenging. But one thing is for sure: all these infections are caused by an organism. So, what you really need to do is, the underlying diagnostic is to demonstrate the presence of the organism. Whether you demonstrate it depending on the infection in the spinal fluid or in the brain or, you know, some peripheral organ system, that is going to be key to making the diagnosis. So, all your clinical acumen is good, but that alone may not be sufficient. Dr Berkowitz: Very good. So, when you see a, a patient now who has a new neurologic symptom in the context of an immune-mediated disease who's on immunomodulatory therapy, what goes through your mind? Are you thinking this disease and this drug, and sort of what are the infections, and does the syndrome match? Or are you thinking, you know, you can't always rely on the imaging to distinguish between, say, a flare of an MS and PML because white matter lesions could look similar? How do you sort of approach this scenario when it comes up?  Dr Nath: So, you're right. You have to keep an open mind so that even though you know some infections are more likely to occur with certain types of medications, that doesn't mean that others cannot occur. So, I think when you first see the patient, you should not jump to conclusions, but rather have an open mind. But yes, for example, your patient is on natalizumab, the chances of PML are going to be high. It's a very interesting drug. It does not cause immune compromise in the periphery, but what it's doing is preventing these cells from getting into the brain. So, because then it's acting at the blood-brain barrier. So that means that organisms that are already present in the brain have an opportunity to get reactivated. Turns out you don't have a lot of organisms in the brain, except JC virus seems to be one of them that does somehow, in some individuals, manage to reside out there. And so that can get reactivated. It can get reactivated in the periphery and then enter the brain, too. So, where the very specific mutations have to occur in that virus in order to take residence in the brain. That would be a suspicion that you might have, and MRI can be useful in, again, helping you think about that possibility. If you have typical lesions involving the U fibers, they're demyelinating, usually you do not have much edema around them because patient is immune compromised, but certainly within the brain in these individuals. And so, then you need to demonstrate the organism. The demonstration of the organism should be in the spinal fluid and not in the blood because in the virus, it can-- is reservoir in the kidneys and in the lymph nodes, and periodically it'll shed into the blood. Detection of the organism in the blood can be a false positive, but in the spinal fluid, it shouldn't be there unless you have an infection. Or if you cause a traumatic tap, I guess, if a patient is viremic, that's a possibility, but those are extremely rare. So at least for PML, that's the way that you would diagnose it. Now, you can develop, for example, if an individual is on fingolimod, you can get a wide variety of infections. Here it's a totally different type of mechanism of action. Here the cells are trapped within the lymph nodes, so that means now your entire periphery is immune compromised, right?  So here you can get viral infections, bacterial infections, fungal infections. So here, if a patient presents with new neurological symptoms, you have to have a really open mind for all these possibilities. Now, let's say a patient was on dimethyl fumarate, and dimethyl fumarate causes neutropenia early on. So here you have to worry about an individual developing bacterial infections, so latent tuberculosis or bacterial meningitis can occur in these individuals. That's something to keep in mind. It's not that other infections cannot occur with dimethyl fumarate, you can see PML and other things too, but the chances of bacterial infections are greater. So, you got to make sure that you draw all the cultures for that purpose. Similarly, if you're on a complement inhibitor, like a C5 inhibitor or the thing that I could use in NMO, there are the chances of meningococcal meningitis. So, these patients, you need to prevaccinate them before you start these kinds of treatments and look for that possibility. When you suspect bacterial infections, particularly acute bacterial meningitis, there time is of essence. Also, in some of the acute viral infections, for example---herpes encephalitis is another one---you have to be so careful, and if you suspect any of them, even if they're with possibly atypical manifestations, you treat first and then diagnose later, and draw all your cultures, whatever you need to, and just treat them. And these infections can also cause cerebral edema, so one has to be careful about doing spinal taps in these individuals. You want some kind of neuroimaging before you do them. In the days when we didn't have neuroimaging, we used to say, "Okay, if your patient has focal neurological signs or is comatose, you don't do it." But these days, you can get imaging very quickly and very easily. All the-- Because of our stroke management, we've learned how to do them so quickly. So, I think there's little excuse not to do imaging and prevent herniation from occurring.  Dr Berkowitz: That's very helpful. So, using the information we know about the drug, and we're going to rapid-fire review some of that in a bit to know what infections the patient is susceptible to, but acknowledging that any patient can get any infection, right? Whether they're on particular medications or not. And then if you're not sure, based on the neuroimaging, which as you said, is helpful, but not always helpful in distinguishing between infections and flares or, as you said, in the case of meningitis, encephalitis, early on at least, especially in immunocompromised or immunomodulated, quote unquote, patient might not see the typical imaging. So really, when safe, getting CSF or cultures, PCRs, and other infectious studies too is really gonna be the definitive diagnostic maneuver here. Is that fair summary across the board?  Dr Nath: I think you said that absolutely right. And you summarized that correctly. And, you know, thing about infection, a lot of neurological diseases are, you know, diagnosed by clinical acumen, like your Parkinson's and Alzheimer's and others. Think about infections is caused by an organism, demonstrate the organism, right? That should be your goal. It doesn't mean that clinical acumen is not important, but here you have an opportunity to demonstrate the organism, so you should depend upon that.  Dr Berkowitz: Okay. Well, you gave us a nice segue by talking about some of the infections to worry about with some of the medications. So what I'd like to do now for the sort of second half of our interview here is to go through some of the more common medications used for MS, and if we have time, for NMO, and just sort of go kind of rapid fire here, and for each medication, if you can tell us the kind of top infectious concerns and whether when to consider them or what screening needs to take place before or during administration of the medication, and then any vaccine considerations we should be aware of. Some of these will obviously be quite short depending on the medicine. So, going back to the two medications I alluded to earlier that were the only ones in play when you and I last saw each other on the wards when I was a medical student, beta interferon, glatiramer acetate, any infections or vaccine considerations with these medications?  Dr Nath: No, I think they're probably your safest medications now as far as immunomodulatory therapies are concerned. These two, and IVIG, if you ever use them, are probably the safest, do not require any vaccine considerations, per se. Dr Berkowitz: Perfect. Okay. So, moving on to fingolimod and others in the sphingosine-one phosphate receptor modulator family, what are the infectious considerations? Any prescreening or vaccination considerations?  Dr Nath: I think all your patients should be prescreened for antibodies to JC virus, because there is a risk for PML, and those who are positive should be closely monitored. So, it's not an absolute contraindication for using these medications, but they just require closer monitoring. With this class of drugs, PML is of consideration. Also, these varicella-zoster virus infection, yeah, with that you can develop zoster encephalitis or myelitis. It can present with motor symptoms as well, which can be atypical. You don't usually see them otherwise in immune-competent individuals. So, varicella-zoster, sometimes you can develop encephalitis, also vasculitis with varicella-zoster, so one has to be careful. So, getting the shingles vaccine can be actually very helpful to prevent these things. And then some patients can even develop herpes simplex encephalitis also, and that can be extremely atypical. So, they don't- they can involve the basal ganglia, can involve the brain stem and cerebellum. So again, your index of suspicion should be very high. Interestingly, although HSV encephalitis has been associated with NMDA receptor encephalitis, those reports of NMDA receptor encephalitis have not been published yet with NMS patients. Not sure why, maybe they just have been missed. But that doesn't seem to be a major concern. And then there are a whole host of other infections that can occur with this class of drugs, and that can include toxo; fungal infections, particularly crypto. There's a case report of histoplasmosis; hepatitis virus, particularly hepatitis C; and then the poxvirus is a good example. You can get molluscum contagiosum; warts with papillomavirus; you can get atypical mycobacteria; and even Kaposi sarcoma, which is HHV8. So, there's a huge variety of infections with the sphingosine one phosphate receptor modulators.  Dr Berkowitz: And any- aside from screening for JC virus before initiating these, any- and then continuing to monitor for JC antibody index, any other considerations as far as labs to send, monitoring before or on the drug or vaccine considerations for patients on fingolimod and the others in this category, siponimod, etcetera?  Dr Nath: Yeah, there are a lot of things to consider. All the details are really available in the chapter if you look at them. But briefly, all the things that one could potentially vaccinate patients for, all these infections I mentioned, one should do so. The timing is critical so that if you can do it before treatment, I think, before starting treatment, that is absolutely important. And you got to give them at least, you know, two to three weeks for these vaccines to take effect before starting your medication. If your patient already arrives on a medication, then you got to play this game of you know, before the next dose, give them again two to three weeks before the next dose and start vaccinating them and get all the vaccines in. Broadly, about the things to worry about the vaccines are you have live vaccines, and you've got the inactivated vaccines or the subunit vaccines. You have to be careful with live vaccines, because if your patient is immunocompromised, that virus can sometimes itself cause harm. For example, you know, yellow fever is one, and there you can develop encephalitis from it. Measles, mumps, rubella, these are all live vaccines. Now, the good thing is that a lot of us have been immunized very early in childhood, but that may not be the case any longer. And so, these things, one has to be very careful with when you're giving live vaccines, that we want to avoid them as much as possible, and individuals are gonna be immune-compromised. But all the others, meningococcus, for example, you should- the HPV vaccines, the varicella zoster vaccines, all these things, you've got to pre-vaccinate and make sure that they have an antibody response to them before starting immunocompromising therapy. Dr Berkowitz: Perfect. Okay, moving on to some of the other orals. What infectious and/or vaccine considerations do we have with teriflunomide?  Dr Nath: Okay, yeah. Teriflunomide is a very interesting drug. It's relatively safe. There is concern about the possibility of varicella zoster infection, people have reported that, and also tuberculosis. But PML is extremely rare, if not at all, and we haven't seen herpes encephalitis quite yet.  Dr Berkowitz: Got it. How about dimethyl fumarate? Dr Nath: Yeah. So dimethyl fumarate is... as I mentioned earlier, it's interesting because it causes this neutropenia. It's transient, but it occurs early on, and these patients can be at risk of PML, although small. They can develop varicella zoster virus infection, herpes encephalitis, and also fungal infections. For example, cryptococcal infection has been reported with dimethyl fumarate. Dr Berkowitz: Okay. We've spoken a bit about natalizumab and PML, and you have extensive information on this in your article, and I'll defer the reader to that. But for natalizumab, what are the key points every neurologist should know about natalizumab and PML as far as from the practical perspective, screening, frequency of screening, when to worry, when to not use natalizumab at all in the first place based on what you find in your screening for JC virus? What are the key points every neurologist should know?  Dr Nath: Uh, yes. You bring up an important point, and that is all patients should be monitored for JC virus. If they're JC virus-negative, so that's your most ideal patient to go on natalizumab, but that doesn't mean they cannot get infected with the virus. In fact, there's an interesting study claiming that, you know, patients, when they get these infusions, they're all sitting in the same room getting infused. Some have JC virus, some don't have JC virus, and so there's the potential that we may be aiding the transmission here in some way or another. The virus is an interesting one. It comes out in urine, and then it's spread through oral contamination, gets into the tonsils, and then spreads from there to your marrow and resides in the kidney and the marrow, as well as the lymph nodes, forever. So, you, you have to monitor these patients to see that during the course, even if they're negative, they could turn out positive. So, every six months or a year, an antibody test should be done on all patients irrespective. If a patient already has antibodies, that's not an absolute contraindication. It just means you've got to monitor them closely for development of new symptoms, and if, whenever there are new symptoms, don't just assume this is due to MS, but just make sure the MRI is done with and without contrast. The- and if there's still a suspicion, that you do a CSF evaluation for JC virus. Just detecting, looking for JC virus in the blood, a rising titer is another thing that can help you. And so, the titer is also important. And the reason you have rising titers is it means that there's an infection that's already occurred in the brain, and the immune system is reacting to that infection by increasing titers. But that alone is not sufficient to make the diagnosis. You still- that gives you an index of suspicion. You've got to then do the MRI and the spinal tap to, you know, be absolutely certain. So, each patient is a little bit different, so the way you monitor them is going to depend on where they are. You know, if they've had prior immunomodulatory therapy before starting natalizumab, or if they're on natalizumab for more than two years, then the chances of PML are much greater, so you may want to monitor them more closely. Uh, they never had any prior immunomodulatory therapy, you're just starting natalizumab, maybe once a year is sufficient. So, I think you've got to tailor it depending on what your risks are for each patient. Dr Berkowitz: Perfect. That's very helpful. And again, you write extensively about PML and natalizumab and PML considerations in your article. So, for a more detailed and in-depth discussion of what we just discussed, definitely hope readers will take a look at your article. Okay. Last but not least---certainly not least, 'cause we're using these probably, it seems, the most commonly in many places I've worked---rituximab, ocrelizumab are B-cell therapies for MS. What are some of the infectious and vaccine considerations related to these infusion medications?  Dr Nath: So, there's concern for PML with anti-B-cell therapies also, maybe not to the same degree as natalizumab, but the same principles should be applied. A lot of people think that these are relatively safe. I don't think so. I think we see enough number of patients on B-cell therapies with PML. So, I would use the same caution because these infections are... you know, can be fatal. So, one should be very careful, even with anti-B-cell therapies. And just with natalizumab, you also have the risk of VZV infection causing shingles. HSV1 has been reported, but there's another interesting complication that has been reported with anti-B-cell therapies, and that is severe West Nile encephalitis. And as mosquitoes-borne diseases are getting more and more prevalent, and we're seeing West Nile cases erupting every summer, I think one's got to be, you know, very cognizant of the fact that this can occur. These patients should take precautions to prevent mosquito bites from occurring and not expose themselves to areas where they could be at risk for it. Unfortunately, there is no vaccine for it and no specific treatment for West Nile. So, all one can do is use prevention strategies for mosquito bites.  Dr Berkowitz: Yeah, I'm glad you mentioned that. I think the only really truly severe neuroinvasive cases I've seen of West Nile virus have indeed been in patients who were being treated with B-cell therapy. Not, if I'm remembering correctly, for immune-mediated disease, but for a lymphoma, so probably other confounding factors there. But yeah, it's a disease we learn about and think about, but I've only seen the most severe cases in patients who had abnormal immune systems, so I'm glad you flagged that. This has been a very helpful discussion, and I've learned a lot from you. I learned a lot from your article, just as I did when you were my attending some 20-something years ago on the wards when I was a medical student. So, it's good to continue learning from you through your writing and research, and today from getting to talk to you again. I encourage our readers to read your article and to bookmark those tables for when these considerations come up for your patients on these immunomodulatory therapies and you're wondering which infections to worry about and how to manage vaccines in this patient population. So again, today I've been interviewing Dr. Avi Nath about his article on vaccine considerations and infection risk in multiple sclerosis and related disorders, which he wrote with Dr. Amit Bar-Or. This article appears in the April 2026 Continuum issue on multiple sclerosis. Be sure to check out Continuum Audio episodes from this and other issues, and thank you again to our listeners for joining today.  Dr Nath: Thank you so much, Aaron, for that wonderful interview, and I'm extremely proud of all your accomplishments over the last 20 years. You've done an amazing job, and it was such a pleasure to see you and to be able to do this interview with you. Thank you again.  Dr Berkowitz: Thanks. That means a lot. I never would have imagined- we won't say 20, how many, but 20-something years ago as the medical student looking up to you and all your expertise on these infections and all of your research that led to so much of our understanding on these, that I would find myself interviewing you two decades later. So, for all the students listening, you never know where you'll end up, but I appreciate your very kind words.  Dr Nath: That's what we hope for all our students. Thank you so much.  Dr Berkowitz: Thanks again.  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 the increase in neurology residency matches this year, the risk of dementia in people with Type 1 diabetes, and the role of neurologists in the public health conversation.

There are many treatment options for people with relapsing MS. Patients should be carefully monitored to assess treatment response, and a change in treatment approach should be considered if safety concerns emerge. In this episode, Teshamae Monteith, MD, FAAN, speaks with Ellen M. Mowry, MD, MCR, and Daniel Ontaneda, MD, PhD, coauthors of the article "Treatment of Multiple Sclerosis" in the Continuum® April 2026 Multiple Sclerosis and Related 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. Mowry is the director of the Multiple Sclerosis Experimental Therapeutics Program and a professor of neurology at The Johns Hopkins University School of Medicine in Baltimore, Maryland. Dr. Ontaneda is the director of research at the Mellen Center for Multiple Sclerosis and a professor of neurology at the Cleveland Clinic Lerner College of Medicine of Case Western Reserve University in Cleveland, Ohio. Additional Resources Read the article: Treatment of Multiple Sclerosis Subscribe to Continuum®: shop.lww.com/Continuum Earn CME (available only to AAN members): continpub.com/AudioCME Continuum® Aloud (verbatim audio-book style recordings of articles available only to Continuum® subscribers): continpub.com/Aloud More about the American Academy of Neurology: aan.com Social Media facebook.com/continuumcme @ContinuumAAN Host: @headacheMD Guest: @EllenMowryMD Full episode transcript available here Dr. Monteith: There are so many new treatment strategies for multiple sclerosis, which is a blessing, but it does come with the complexity of really just trying to nail down the approach. I just got finished talking to Drs Ellen Mowry and Daniel Ontaneda about their article on treatment of multiple sclerosis. We discussed relapses, weighing escalation versus early high-effective treatment and progressive disease. This is a must-listen-to podcast. I hope you enjoy it as much as I enjoyed talking to them.  Dr. Jones: This is Dr. Lyell Jones, Editor-in-Chief of Continuum. Thank you for listening to Continuum Audio. Be sure to visit the links in the episode notes for information about earning CME, subscribing to the journal, and exclusive access to interviews not featured on the podcast. Dr. Monteith: This is Dr. Teshamae Monteith. Today, I'm interviewing Ds Ellen Mowry and Daniel Ontaneda about their article on treatment of multiple sclerosis, which they wrote with Dr. Darin Okuda. This article appears in the April 2026 Continuum issue on multiple sclerosis. Welcome, both of you. How are you?  Dr. Mowry: Great. And thank you so much for having us.  Dr. Monteith: Absolutely. So, why don't you both introduce yourself?  Dr. Ontaneda: All right. My name is Daniel Ontaneda. I'm a neurologist at the Cleveland Clinic. I spend the majority of my time doing research, but I still dedicate about a day a week to seeing people with MS in clinic.  Dr. Mowry: I'm Ellen Mowry. I'm also a neurologist, but practice at the Johns Hopkins University. And similar to Dan, I mostly work on research, but also have an active clinical care component, taking care of people with MS.  Dr. Monteith: Well, thank both of you for writing this article and being on our podcast. I assume you guys have probably known each other for quite a while now.  Dr. Mowry: Yes. Dr. Ontaneda: Yes. Dr. Monteith: What inspired you to get into multiple sclerosis research and then clinical care?  Dr. Ontaneda: I always loved neurology, and I think a lot of us who go into neurology are attracted to the complexity of the human brain and how the nervous system works. But what really hit home to me was a family member of mine who had multiple sclerosis, and he was being treated in a time where we really didn't have super effective disease-modifying medications. And so, as I went through my medical career, I always kind of kept an eye on what was happening with multiple sclerosis, and I started my training at a time where it was really flourishing in terms of the medications available, so that's what inspired me to go into MS. It's a disease that we can definitely treat, and you can change outcomes for people. So, that was it.  Dr. Monteith: Yeah, that personal experience can be very impactful.  Dr. Mowry: My journey started, actually, because I was thinking about whether I wanted to be a physician at all, and I happened to land, just after high school, a position with a neurologist who happened to mostly focus on multiple sclerosis and taking care of folks with multiple sclerosis. And by the end of the summer, I knew I wanted to go to med school and I wanted to be a neurologist and I wanted to work with people with MS. I thought I would be a clinician exclusively, but I think as time went on and I started to hear the consistent questions that people I served were asking in the clinic and realizing that those questions could be turned into research projects that could address their concerns, I moved more and more towards research. Dr. Monteith: Great. There are a lot of really detailed information in the article, so I think that research mind is very useful, and I see that in the writing. Why don't we talk about the goal of the article? Dr. Ontaneda: So, I think the goal of the article was to set out kind of what the large view of what treatment for multiple sclerosis looks like. And, you know, many times we divide the treatment of multiple sclerosis into these large pillars, and I think that's what we did in the article. The first was, you know, what do you do with a person who has an MS attack or relapse? The second is, what medications do we use to treat the relapsing forms of multiple sclerosis where there is a lot of acute inflammation, focal inflammatory lesions that are occurring? And then the final one is, what do you do with individuals who have a more progressive form of the disease where they're accruing disability slowly and gradually? Dr. Monteith: And what were some of the main points? Dr. Mowry: Dr. Okuda provided a really nice section on the treatment of acute relapses in multiple sclerosis, and it's important to understand what we talk about when we are saying "relapse". For people with MS, many symptoms can fluctuate and occur and then get better over time, and sometimes people with MS use the same term of "relapse" to describe those symptom fluctuations. As neurologists, when we're thinking about relapse, we're really trying to think about symptoms that can be attributed to new focal inflammatory events somewhere in the central nervous system. Typically, these are accompanied---if you were to get an MRI at the same time---by a new lesion or MS spot, as I like to call them, on MRI scan. And so, it's important to distinguish when somebody is talking about symptoms, whether they are true new symptoms that could be mapped to a place in the central nervous system. Because alternatively, a lot of people who've had attacks or relapses in the past can have what we call pseudo-relapses, and these are essentially recrudescence of old symptoms, typically in a similar pattern as what had occurred in the past. And these can be brought out by things like fever or infection, sometimes stress. And pseudo-relapses are not thought to be due to new development of immune system-induced injury and therefore would be less likely to respond to treatment; and in fact, treatment may be contraindicated for those events. We also talked a little bit in that article about how relapses are treated, talking about the use of high-dose steroids for true new relapses, but also kind of cautioning that those are not necessarily free of concerns, especially if you have a pseudo-relapse or there could be an infection going on. And that ultimately, the decision as to whether to treat a relapse really is a shared decision-making because it's thought that although the steroids can speed up recovery from a relapse, they may not have a major impact on ultimate recovery. And so, a lot of the shared decision-making comes in here because for a mild relapse, you might choose to forego a course of high-dose steroids.  Dr. Monteith: Daniel, any other main points?  Dr. Ontaneda: Yeah. On the side of treating relapses, I think one of the other things that probably has changed a lot, at least during the course of my training, is that in the past, whenever we had identified a relapse, as Dr. Mowry has clearly defined, we would typically treat with intravenous high-dose corticosteroids, typically with methylprednisolone. And that was kind of our go-to. We would either do it in an infusion center or we would set it up with home care. And I think one of the things that our field learned over, I would say, the last five or ten years is there's an abundance of studies that show that you can give that same dose of methylprednisolone. Rather than giving it IV, you can give it orally. No pun intended, as I tell my patients, a lot of pills to swallow because we use fifty-milligram prednisone pills, and they have to take 1,250 a day. The pharmacy always pushes back on that many pills, but really the advantage of being able to take steroids orally that way for three to five days is really, I think, one, better for people with MS because they can do it in the comfort of their own home, and two, I think also when you look at the costs associated with that treatment, it is the most cost-effective option. Dr. Monteith: And what are some of the latest developments that you're really excited about that weren't in the article?  Dr. Mowry: A lot of the article focused on the approach to treatment of people with what we've traditionally called relapsing/remitting multiple sclerosis. So, this is the kind of MS that traditionally presents with a relapse or an attack initially, although some of that nomenclature is changing, actually. And the article focused a lot on the strategies surrounding treatment of somebody with newly diagnosed relapsing MS, and thinking about this vast number of disease-modifying therapies that are available to people with MS and their clinicians, and how to think about the strategy with respect to largely centered around the efficacy class of the medication, whether people should take an approach of using a higher-efficacy therapy---meaning a medicine that in clinical trials was more likely on average to suppress relapses as well as new lesions---or whether there's still a good argument for the case of using an escalation approach, using some of the more modest efficacy medications that also probably in general have lower risks, monitoring for response to treatment and changing if the medication isn't working. And so, there's still a lot of debate in the field, I would say, even though many people have moved towards a one-size-fits-all kind of approach. I think there's still a lot of debate in the field about the evidence underlying that. And, you know, full disclosure, Dr. Ontaneda and I are each running parallel and very complementary clinical trial programs to address this very question, the results of which should be available within the next year, year and a half.  Dr. Monteith: Well, we can't wait that long. Give me some clinical pearls to how we initiate these modifying therapies. Like, what are the pearls that we need to have in our mind?  Dr. Ontaneda: Yeah. I think when we think about starting the disease-modifying therapy in an individual who has an active form of multiple sclerosis, I think, you know, one of the cornerstones I would say of making that decision is shared decision-making. I think we tend to sit down with the patient and analyze the data that we have at hand, what we know about their multiple sclerosis, and we use several factors to inform how likely we think their disease is gonna be active or potentially might not respond to the initial treatment you give. And we look heavily at the MRI. The MRI is really a useful marker because it shows us, one, how many lesions a person might have---both, you know, where those lesions are and also kind of the amount of lesions. Lesions, certainly, that are in the spinal cord, a very large burden of diseases. A lot of active lesions, which we determine by the presence of contrast-enhancing lesions, really helps us inform on disease severity. I would say that was our number one tool that we use to decide and help us decide how we think that person's MS is gonna do over time. And then the second thing that we put into the equation also is, you know, how well do we think this person is going to tolerate our medications? All our disease-modifying medications act through suppression of the immune system, and we know that that carries some risks associated with it. Some of those risks are stuff like infections. Some of those can be simple infections that really don't have major consequences, but some of them can be quite serious, including the need for hospitalizations or prolonged antibiotic treatment courses. And so, we also look at what, you know, the underlying risk of a person has for infection. This kind of is determined by, one, A, how many infections they've had up to date, and also how much disability they had. I would say in our average patient who when we see them, they're probably typically pretty young, in their twenties, thirties, forties, they typically don't have a lot of infectious risks. And therefore, I think there's kind of a move to saying, "Well, actually their risk of infections is quite low." And we put that together with, you know, also what the preference of the patient might want. So, do they prefer to take a pill, for example? Do they prefer a medication where they receive that via infusion every six months and they don't really have to think about it? There are some people that don't like going into a hospital, and they might prefer an injection type of those medications. And so, after a complex discussion of all those factors, we take into consideration how much risk the patient wants to take as well, and we come up with a rational choice of a couple of medication options. So, I think it's challenging sometimes because we have over two dozen medications. There's the risk of you saying, "There are these twenty-four medications, you can pick one." And I think our job as neurologists is to kind of pare those down, talk about, in a person like yourself, these are the two or three medications that I would recommend using. Why don't you review them? And then we bring them back, and we kind of make a final decision with, one of the key factors that I think is important to remind people is that you're gonna start this medication, and we are gonna monitor to make sure it's working. We're gonna monitor to make sure you're tolerating it well. And although it's an important, the first decision you make, I think one key theme that we tell people is, we can revise our strategy whenever we like. We just have to think about it and do it in a way that we think is gonna make sure that their MS is under the best control. And then we think about the ultimate goal of treatment, which, in multiple sclerosis, is the absence of any attacks and also the absence of any new lesions on MRI. And that's where whether you are offering more of the high-effective medications or more moderate- or low-efficacy medications, that's where there's a little bit of controversy still in our field, and that's what our trials are trying to answer.  Dr. Monteith: Excellent. So now we've selected a particular option- and I love those points with shared decision-making, using the MRI to guide and then kind of risk tolerance related to infection. But now a patient's still having relapses, and I know the goal is zero, but, you know, there's some margin. What are the pearls to advance to more high-efficacy therapies?  Dr. Mowry: Yeah, that's a great question. Dr. Ontaneda in the article actually talked about the literature surrounding monitoring for breakthrough disease and when to say this much is too much, and there's actually not a definite right answer. It's clear that more active disease early in the course is probably more of concern than, say, developing, you know, a new spot in your fifties or something to that effect. So, different people have different thresholds. I know at our center, we tend to be pretty on top of making changes for breakthrough disease. So, what we typically do is reimage people about six months after they start a medication to establish a new baseline. And sometimes, because of delays in starting or because the medications take a while to kick in, there might be a new spot or two. So, if that's the case, I really only get concerned if the spots are also taking up the dye or enhancing to indicate they're really quite recent, and I think, "Ugh, that's not something I'd like to see six months after starting a medication." And so that otherwise is sort of the reference scan, moving forward, to evaluate the medication, and I have a very low threshold for changing, particularly if somebody is on a moderate-efficacy therapy. To me, I think, well, our goal of trying the moderate efficacy therapy is essentially to see if we could get away with a medicine that is probably, on average, safer and that will still work for your MS. But if the answer is no, I personally don't like to stick around too much on them. One caveat I would say is that if somebody develops what appears to be a new lesion or spot on higher-efficacy therapy, before presuming that that new area of activity is a definite new MS event, I always like to rethink carefully, did I get the diagnosis correct? Or could this be an early infection such as, you know, progressive multifocal leukoencephalopathy in people on natalizumab in particular? Because I see breakthrough activity so rarely in people on higher-efficacy therapies that I just like to rethink my diagnosis and the differential prior to making switches to, typically, another higher-efficacy therapy in that case. But that, again, is a little bit of shared decision-making. It's sometimes contextual. If a person is using a self-administered medication and they have a little breakthrough, sometimes you can solicit some history, saying, "Oh, I actually kind of stopped taking it for a few weeks because something was going on, and I really want to retry." And that's very reasonable as well. Dan, do you have any other thoughts?  Dr. Ontaneda: No, I think I agree. That's really close to how I practice myself as well, and the majority of people at my center. I think that we are learning that when you start a treatment, many times---depending on how deeply you look---you can find evidence of ongoing disease, and that's something that we struggle with. It's almost like we have tools to treat inflammation in terms of new MS lesions and new relapses. And so, when those are present, it's pretty clear that you probably have to switch medication. I think a slightly trickier issue is when, for example, you have a person who might be stable. They don't have an attack. But you notice that they're worsening, and they tell you they're worsening. I think our ability and tools for that is a little bit harder, and we recognize that that can actually happen fairly early in the disease. And that's why we're trying to rethink this mantra that we've had for many years, where we kind of divide MS up into relapsing and progressive, and we see people develop progressive MS 10 to 15 years after they've had a relapsing form of the disease. So, I think that's just a reality of clinical practice. And we don't have as many tools to treat that gradual worsening, which is kind of what the rest of our article spent some time talking about. Dr. Monteith: You've also written about the clinical trial long-term extension studies. And what are the few points that you take away from the emergence of these types of publications over the past few years? Dr. Mowry: Yeah, well, long-term extension studies can be really helpful to understand whether the findings that are evidenced during the randomized portion of trials themselves continue into a longer term. And for people with MS, understanding these data can be really helpful because, particularly when we're looking for impact of a given treatment or a strategy on disability worsening, often it takes longer than the short-term portion of the trial to truly understand if the medication or strategy has an impact on insidious worsening that Dan is speaking about. Many trials have demonstrated a short-term benefit, but we think a lot of times that benefit is probably because of the reduction in relapses, which sometimes leave a permanent mark on neurologic function. But the extension studies are trying to understand a little bit more about whether the effect on disability worsening is sustained, and also to look a little bit more deeply at long-term safety, especially when it comes to medications that do increase the risk of infection. The caveats, though, in interpreting those types of studies are that people drop out, and so probably the people who drop out of those studies are really different. They may be either less disabled and they think, "Oh, you know, I'm done. I feel good." Or potentially more disabled and they think, "Ugh, I have more things to do I've got to take care of. What's going on?" And so that kind of dropout can produce some bias in interpreting the results. Dan, any other thoughts?  Dr. Ontaneda: No, I think that's spot on. I mean, I think that when we're trying to decide on what general philosophy to use, right? Like, you're seeing a patient for the first time. They've recently been diagnosed with MS, and you have... you know, I kind of bin them into three options. You can start a low-efficacy, a moderate, or a high-efficacy medication. And the first piece of information you could use is clinical trials, and Dr Mowry very clearly identified why some of that data might be a little bit biased and isn't, you know, completely applicable to the patient who's in front of you. The second thing that we might look at is observational data, and there's a wealth of observational data that shows that, in general, people on higher-efficacy medications tend to do better over time. But one of the challenges we have is that there's always biases related to those observational study designs. And so, I think you have to interpret them with a little bit of caution because there are reasons people start specific medications in people. And when you look at them in a purely observational study, even if you do some fancy way of addressing those biases, such as propensity, there always is the possibility of some residual bias. You know, that's part of the reason why we're doing the trials that Dr Mowry described, because we really need kind of long-term evidence to show that these medications actually can affect disability ten, twelve years after started. And I think pragmatic clinical trials, like the ones we're running, are really gonna be the key to answer those questions. We all have our favorite approaches right now, but I think that the data to actually demonstrate what's best for people with MS is really needed.  Dr. Monteith: Great, and there's so much in this article. I mean, we didn't even touch on radiological isolated syndrome, monitoring MS therapeutically, and treatment of progressive MS. Any final take-home points?  Dr. Ontaneda: Yeah. Maybe I will touch a little bit on the side of progressive MS, because it has been, you know, the MS that we historically have not been able to treat as much. So, we described there's over two dozen therapies approved for relapsing forms of MS. For purely progressive forms of MS that don't have any evidence of activity, we really only have one approved therapy, and it appears that that therapy actually does work through active inflammation anyway. And in the article, we highlighted examples of studies that have been negative, but also some recent examples of studies that have been positive, specifically with a new class of medication called BTKI, or Bruton tyrosine kinase inhibitors. We just recently heard of a second molecule that also had positive results in this realm. So, we're excited that, you know, in the next four to five years-  Dr. Monteith: I'm sorry. Can you just go ahead and say what that molecule...You're leaving people hanging.  Dr. Ontaneda: One molecule is tolebrutinib, which already has a positive study in secondary progressive MS in individuals without activity. And then the second compound that has been studied with positive trial results, we only have summary results from that, is a medication called fenobrutinib. And we think these two compounds that are part of a single class, the hope is that maybe they can address some of that gradual worsening that occurs in MS. And then the question comes whether we should use those from the get-go or if we should just use them later. So, a whole sort of variety of different questions. But I think important to call out for clinicians that this area where we had no available treatments for so many years might be changing.  Dr. Monteith: Well, thank you both. I really loved this conversation. I learned a lot listening to both of you, and I look forward to your clinical trial results.  Dr. Mowry: Thank you so much for having us. Dr. Ontaneda: Thanks so much. It was our pleasure. Dr. Monteith: Again, today I've been interviewing Doctors Ellen Mowry and Daniel Ontaneda about their article on treatment of multiple sclerosis, which they wrote with Dr. Darin Okuda. This article appears in the April 2026 Continuum issue on multiple sclerosis. 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.

Today's podcast features an interview with Casey Balio, PhD, research assistant professor at the East Tennessee State University Center for Rural Health and Research, and Betty Bekemeier, PhD, MPH, RN, FAAN, director of the Northwest Center for Public Health Practice. They share new insights about the rural public health workforce from their recent article published in the Journal of Public Health Management & Practice. The transcript and a list of resources and organizations mentioned in the episode can be found at: https://www.ruralhealthinfo.org/podcast/public-health-workforce-may-2026 Exploring Rural Health is an RHIhub podcast.

In honor of Nurses Month, this episode explores the unique power of nurses, grounded in trust, human connection, and frontline insight, and how that power can shape care, leadership, equity, and policy in today's health care system. Joining us for this discussion is Jennifer S. Mensik Kennedy, PhD, MBA, RN, NEA-BC, FAAN, a nationally recognized nursing leader and the 38th president of the American Nurses Association, where she advocates on behalf of the nation's 5.5 million registered nurses. The conversation weaves together advocacy, technology, burnout, and purpose, ultimately calling for health care leaders to take concrete action to protect nurses and fully realize their impact. Transcript

Indigenous maternal health is in a critical state, but we can change that.Learn why 93% of pregnancy-related deaths in these communities are preventable. Explore the healthcare gaps for First Nations and how restorative midwifery is working to save lives.  https://bit.ly/4uncumOWhat You'll Learn:The 93% Preventability Gap: While 87% of all U.S. maternal deaths are preventable, that number rises to 93% for Native American and Alaska Native populations, signaling a critical failure in the care pipeline.The Postpartum "Blind Spot": 68% of pregnancy-related deaths occur between one week and one year after birth. Most of these happen after 43 days postpartum, a period when many mothers lose insurance or clinical support. Leading Causes are Treatable: Mental health conditions and infections are the top underlying causes. These are highly manageable when caught early, yet they often go unnoticed in "medical deserts." The Power of Advocacy: Learn why every mother should explicitly state, "I was pregnant within the last year," to every healthcare provider they see to trigger appropriate clinical protocols.Restoring Traditions: How Indigenous-led midwifery and the Momnibus Act are working to dismantle systemic bias and return to culturally safe birthing practices.#MaternalHealth #NativeHealth #PublicHealth #PostpartumCare #HealthEquity #HearHer #MaternalMortality #WomensHealth #IndigenousHealth #HealthcareAccess #CDCSupport the showConnect with Us: Email our Host: mail@every1dies.org  Website: https://every1dies.org: Find show notes, links and expanded resources Follow Us: Facebook | Instagram | YouTube  

Although rare, recognizing NMOSD is crucial for improving patient outcomes through correct diagnostic and treatment approaches. Reports of atypical forms and increasing knowledge of clinical, imaging, and laboratory-specific features are fundamental for the accurate recognition of this condition. Research on targeted therapies and biomarkers measuring and predicting disease activity will improve NMOSD management. In this episode, Gordon Smith, MD, FAAN, speaks with Sara Mariotto, MD, PhD, coauthor of the article "Neuromyelitis Optica Spectrum Disorder" in the Continuum® April 2026 Multiple Sclerosis and Related 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. Mariotto is a neurologist in the Neurology Unit in the Department of Neurosciences, Biomedicine, and Movement Sciences at the University of Verona in Verona, Italy. Additional Resources Read the article: Neuromyelitis Optica Spectrum Disorder Subscribe to Continuum®: shop.lww.com/Continuum Earn CME (available only to AAN members): continpub.com/AudioCME Continuum® Aloud (verbatim audio-book style recordings of articles available only to Continuum® subscribers): continpub.com/Aloud More about the American Academy of Neurology: aan.com Social Media facebook.com/continuumcme @ContinuumAAN Host: @GordonSmithMD Full episode transcript available here Dr Smith: Neurology is an increasingly therapeutic specialty, and across many of our subspecialty areas, lots of new drugs are being approved. Are you interested in learning more about a historically disabling disorder for which we now have a spectrum of new therapies that, if used appropriately and promptly in the right clinical situation, promise to dramatically improve patient outcomes? If so, keep listening. My name's Dr Gordon Smith. Today I'll be talking with Dr Sara Mariotto about her article on neuromyelitis optica spectrum disorder or NMOSD, which she wrote with Dr Romain Marignier. This article appears in the April 2026 Continuum issue on multiple sclerosis.  Dr Jones: This is Dr Lyell Jones, Editor-in-Chief of Continuum. Thank you for listening to Continuum Audio. Be sure to visit the links in the episode notes for information about earning CME, subscribing to the journal, and exclusive access to interviews not featured on the podcast.  Dr Smith: This is Dr Gordon Smith. Today, I'm interviewing Dr Sara Mariotto about her article on neuromyelitis optica spectrum disorder or NMOSD, which she wrote with Dr Romain Marignier. This article appears in the April 2026 Continuum issue on multiple sclerosis. Sara, welcome to the podcast, and maybe you can start by introducing yourself to our audience.  Dr Mariotto: Yes. Thanks, Gordon. I'm Sara Mariotto. I'm a neurologist, and I work at the Neurology Unit, University of Verona, where I do both clinical diagnosis and research into neuroimmunology---so, in particular, autoimmune encephalitis, NMOSD, and MOGAD.  Dr Smith: Well, this is a super exciting area. Whenever I hear about NMOSD, I think of one specific patient I had, and I always think of her when I come across something like your article, which is really fantastic. So, before we dive into the details, I wonder if maybe you can just explain to our listeners who aren't up to speed on what NMOSD is, what the disorder is, and maybe why it's so important that all of our listeners learn how to recognize it quickly and get people started on therapy.  Dr Mariotto: Yes, sure. So, neuromyelitis optica is an inflammatory autoimmune CNS disorder usually associated with aquaporin-4 antibodies, although there are a few cases, around 10%, who can be antibody-negative. And I think it's very much important to have in mind this disease and recognize it because it can be severe, as you pointed out; can present with very severe optic neuritis, myelitis, the brain stem, or area postrema syndrome. So, it can be really severe, affect quite young people around 40 years of age---although it can affect also the pediatric population and elderly people---and, importantly, it can be treated. It's very much important to treat this patient in the acute stage very quickly with steroids or plasma exchange in addition, and then to start a chronic treatment. So, we have treatment for this condition. So, it's very much important to, to recognize it quickly and treat the patient properly.  Dr Smith: So, I wonder if we can talk a little bit about the diagnostic criteria and boundaries of NMOSD, right? So, someone who comes in with bilateral op- severe long segment optic neuritis or long segment myelitis, we think about it. But what are the boundaries? Should we be looking for this, for instance, in someone who comes in with a unilateral optic neuritis or looks like typical multiple sclerosis? Is it important to get aquaporin-4 antibodies in those patients? What do the diagnostic criteria say about this?  Dr Mariotto: So, I wouldn't test aquaporin-4 antibodies in all patients with demyelinating conditions because although aquaporin-4 antibody assay is very specific, as for all assay and all antibody testing---also for MOG antibodies, for example---some false positive results can come out. So, I would suggest to test aquaporin-4 antibodies not in typical MS cases but in those who could be suggestive for not being MS, so in all those cases with atypical optic neuritis and myelitis or other syndromes. For those cases, it's important to test aquaporin-4 antibodies, but I wouldn't test them in all typical, classical MS cases. As I said, it's quite specific, the assay, so it's uncommon to have false positive results, but it can be.  Dr Smith: Serum, CSF, both?  Dr Mariotto: So, for aquaporin-4 antibodies, they're usually present in serum. They can be positive also in the CSF. And there are a few reports of isolated CSF positivity. But if we analyze larger samples volume, then it becomes clear that isolated CSF positivity is so, so rare that it's not recommended to test them in the CSF when serum is negative. So, for aquaporin-4 antibodies, the recommended matrix of testing is serum, which is different for MOG, which is not the topic of our article but is important to mention because MOG antibodies should be tested in serum and CSF. But aquaporin-4, I would recommend to test serum.  Dr Smith: What are the boundaries between MOGAD and NMOSD? And you talked about the differential testing of antibodies, which I was going to ask about. But when should we think of NMOSD relative to MOG? Dr Mariotto: Yeah. There are aspects which are the one mentioned in the criteria, highly suggestive for NMOSD. But the clinical spectrum can be similar to that of MOGAD. Usually, although there are some clinical aspect---like, for example cortical encephalitis or ADEM, which is more typical for MOGAD, or others like area postrema syndrome, which are more typical of NMOSD. The spectrum can be similar among the two conditions, so that's why in our clinical experience, usually they ask both aquaporin-4 and MOG antibodies in patients. It's- for experts, it can be easy to differentiate the two conditions, but for nonexperts can not be so easy.  Dr Smith: Can you define area postrema syndrome? I think not all of our listeners see that every day.  Dr Mariotto: Yeah, sure. This is a syndrome which is highly suggestive of NMOSD. That's why I mention it. And it's characterized by nausea, vomiting, hiccups are known as the syndrome. And it is very, very suggestive because of the expression of aquaporin-4 in that area of NMOSD. That's why I strongly recommend for all patients who comes out to have this syndrome to test for aquaporin-4 antibodies. MOGAD is hardly ever positive for that, so I think that whenever you see a patient with that syndrome, you should think about NMOSD.  Dr Smith: I'm just curious, aquaporin-4 is a water channel, which is kind of an interesting concept. Our conversation, I really want to make sure we give clinically important information to folks, but it's so curious to me at least, how does this actually result in a inflammatory demyelinating syndrome? For a simple neuromuscular guy, what's the immunopathogenesis of this?  Dr Mariotto: Yeah, the immunopathogenesis is quite complicated, as in all CNS disorders. And of course, aquaporin-4 antibodies are the main focus, but they are not the only one. As you said, aquaporin-4 antibodies have a target, this water channel, which is at the basis of the disease, and they are produced by the interplay between T cells, B cells, and plasma cells. But then also eosinophils, macrophages, cytokines, and chemokines are involved, enter the CNS, and then another important component is complement, which is highly activated in this disease. At the end, we have astrocyte damage because astrocytes are the main target of the disease, but also axon and myelin are involved. So, it's a quite complex pathogenesis based on the antibodies, but not only on that.  Dr Smith: And this will become important when we start talking about treatment. There seems to be a recurring theme of long segment demyelination, right? Optic neuritis is typically a large percentage of the length of the optic nerve, and obviously the myelitis se- more than three segments. Do you see other long segment areas of CNS demyelination, corpus callosum or things like that? Any ideas why that is, if that's true?  Dr Mariotto: Of note, this is quite interesting because usually when we have NMOSD, we have a longitudinal involvement, especially of the optic nerve and spinal cord, while brain lesions are quite different. Like, we usually do not have the typical Dawsen fingers-like lesions that we have in MS, for example, or the classical periventricular or subcortical extensive lesions that we can see and we have in mind when we think about MS. In some cases with NMOSD, the brain is completely negative, so we do not see anything. And Dawsen lesion's quite suggestive of NMOSD. So, you're right. I mean, this is related partially to the expression of aquaporin-4, and that's why we have this typical involvement also for area postrema, for example, and maybe also our other examples of clinical aspect that we can see in these conditions. But it's basically linked with the expression of aquaporin-4, which is the main target of the disease. And that's why usually the brain doesn't show so much involvement as we can see in MS, for example.  Dr Smith: I was actually really interested in some of the unusual manifestations or phenotypes, and I don't want to get into arcadia, really, but which of these should our listeners be familiar with that would really suggest that they should be thinking about NMOSD beyond the area postrema and other features that we've already talked about that are part of the core criteria?  Dr Mariotto: Yeah. I mean, I think that the encephalic syndromes or also ADEM, which is most typical of MOGAD but can be observed also in NMOSD or PRES, for example, are syndromes that can be considered in patients with NMOSD. There are the typical ones, which are the ones showed in the criteria, but whenever we have a brainstem involvement or, like, these encephalic syndromes or also PRES, we should think about NMOSD also.  Dr Smith: Another area I was interested in are red flags. In your article, you talk about red flags that might suggest an alternative diagnosis, right? And then this presumably is particularly important in seronegative patients, which 10% is not a reasonably high number, I suppose. What are red flags we should be thinking about for some other diagnosis?  Dr Mariotto: Yeah. I would here mention two very important red flags. The first one is a very hyperacute onset. Usually these conditions, these inflammatory conditions have a subacute onset, so whenever you have a very, very acute onset, you should think about something else. This can occur sometimes also in NMOSD, but hardly ever occur. Like, a very acute myelitis, the first thing we should think about is a vascular origin, for example, with a lot of pain and not about NMOSD, although sometimes the differential diagnosis is not so easy. The second thing is a progression independently of relapses, which hardly ever occur in NMOSD. Usually in NMOSD, we have the onset, and then we have a relapsing disease course. That's why we have to treat patients always and not to stop treatment. But we do not have progression in the meanwhile, while we can have, for example, this in MS. Same thing is for MOGAD. So, these are two things that I think is very much important to keep in mind.  Dr Smith: I want to pivot to talk about treatment because that's been super exciting. But rumor has it there are new diagnostic criteria coming for NMOSD in the next year. I bet you know a bit about those. Can you give our listeners any indication about kind of where the puck is going on this? Not so much what the criteria are specifically, but what sort of diagnostic challenges are the new criteria going to help us with once they come out?  Dr Mariotto: Yeah. So basically, we are working on that, so you will read them in the next future. This is the good point of the conversation on the new criteria. And we work a lot on the definition, on the new definition and nomenclature of NMOSD; on the definition of seronegative NMOSD, which is also quite tricky; and then on the assay we should use to test aquaporin-4 antibodies, and also on potentially new syndromes which should be included into the main feature of the disease. But hopefully you will read about this very soon.  Dr Smith: Looking forward to it. And Continuum Audio listeners, you heard it here first, so thank you. Let's pivot to treatment. This has been super exciting, and I wonder if the way to approach this is to start with acute management and then sort of chronic management. Would that make sense?  Dr Mariotto: Sure.  Dr Smith: Let's say I go on service on Friday, and I have a patient who comes in with positive aquaporin-4 and bilateral optic neuritis. What's the acute approach to managing that patient?  Dr Mariotto: So, the first approach is to administer intravenous steroids, but I would not wait to escalate to plasma exchange. There is quite good evidence that we should treat the patient with additional plasma exchange very quickly, and every day of delay of plasma exchange can cause increased disability. So, we should treat patients with steroids first, and then if we are not satisfied by the recovery, soon start with a plasma exchange. There is also some evidence, although less, for IVIG, but it's important to try to treat them very quickly, even if it's Friday, you know, there is the weekend and so on. But I think it's very much important to start with steroids after excluding other infectious causes or so on, and then to start quickly with plasma exchange. The main problem could be that we do not have the results of the antibody yet.  Dr Smith: Right. So, let me ask that question. You know, let's say my patient comes in on Friday, and clinical syndrome that really looks like NMOSD, and we're waiting for the aquaporin-4. There are many places where it's hard to get plasma exchange over weekends. And so, in that setting, are you better off doing the steroids over the weekend then PLEX on Monday, or should we just give IVIG because maybe it's as good as PLEX? What's your advice there? I'm trying to get ready for Friday because I know one's coming in.  Dr Mariotto: That's true, that's true. Usually they come on Friday or Saturday. I think it's acceptable to have three days of steroids and see how the patient improves, and then after three days to start with plasma exchange. Actually, we have a very good improvement if we start between three and five days after onset. So, I think waiting for three days is acceptable just because we can see if the steroids work properly or not, and then we can quickly start to plasma exchange. But I would not wait, like, 10 days, you know, before starting with a plasma exchange, and I would not wait for antibody results.  Dr Smith: Got it. Super helpful. And I'm actually not joking around, I learned recently that I have a reputation among our residents for having lots of optic neuritis when I'm on service, which I think is sort of karmic justice for being a peripheral nerve expert. But let me ask another question. So, let's say we do that, and the patient gets three or five days of pulse methylprednisolone and five courses of PLEX, and they're not doing well. Do you then just move right along into another agent B cell depletion therapy? I mean, what's your next step in escalation in the acute setting?  Dr Mariotto: I would for sure start to, as you said, with steroids, plasma exchange, and in case IVIG, and then quickly move to chronic treatment. And for patients who are not recovering well, I would think of something which has a quick effect so we can really start treating patients very quickly. There are different options. And all over the world, there are different rules for using immunosuppression in NMOSD. Like in Italy, for example, it's different from US or other countries, Germany, for example. There are different approved treatments and different rules of using them before or after rituximab, for example. We all know that there are treatments approved for NMOSD all over the world. But in some countries, like for example in Italy, we should use rituximab first, and then if it doesn't work, escalate to the approved treatment. I know in the US it's different. But anyway, for a patient who does not improve quickly, I would start with something which has a quick effect on the disease.  Dr Smith: And then rituximab versus inebilizumab, you know, CD20, CD19, what's your advice there? Is one preferable to the other, you know, if we have options to do either?  Dr Mariotto: Yeah. So, between rituximab and inebilizumab, we know that the target, well, is different, but is anyway B cells, so CD19 and CD20. With CD19, we can affect both plasma blast, plasma cells, and B cells. That's why the target is broader. And of note, this is an approved drug, while rituximab is, in most countries, used as off-label treatment.  Dr Smith: So inebilizumab would probably be preferable if we're able to do that.  Dr Mariotto: Unfortunately, there are not so many studies comparing rituximab with the approved drug, which is, of course, a pity, but that's the case. While we have clinical trials for all the approved drugs, and although the trials were designed differently, as we mentioned in the Continuum paper, we can argue something of the comparison between the approved drugs. But it is not so clear the comparison between rituximab and the new drugs, which is also something that we should work on.  Dr Smith: And then for chronic suppressive management, what other options are there?  Dr Mariotto: So, in addition to B cells, target can be interleukin-6, as we know with tocilizumab or satralizumab, and then complement with eculizumab. These drugs are both based on the pathogenesis of the disease. That's why we also discuss it in the paper, which shows a clear involvement of complement, and among cytokines of interleukin-6. So, targeting these made clear that could improve the disease quite well, and that's why they designed some clinical trials on these drugs, which are now approved, as we said, for NMOSD.  Dr Smith: Wow, so many options, and a lot of questions, but limited time. Let me just ask a couple of more. I see a lot of myasthenia patients, and there's a lot of variability, as you know, in patients with myasthenia, the extent to which complement is an important mechanism versus other, you know, important mechanisms. To what extent is response to a complement inhibitor kind of uniform across NMOSD? Or there's some patients who just don't respond to a complement inhibitor and others that respond really well. And then just, I'll just give my second question out is, you know, what about combination therapies for patients who have particularly challenging NMOSD?  Dr Mariotto: So usually these patients have a terrific response to complement inhibitors, and this is also shown by the clinical trials where we saw how eculizumab have a very impressive effect on the disease. And also, maybe this is also your experience, a very quick effect. So that's why there are also thoughts on using it in a very acute stage of the disease. That was what I was thinking about before. But then it has a very huge effect on complement, which is a major factor involved in the pathogenesis of NMOSD also in the chronic disease stage, and that's what also we see from clinical trials. Usually, we prefer to switch treatment from one to another and not to combine them. Of course, in very difficult cases, this can be considered, but the recommendation is to switch from one of these approved drugs to the other, or from rituximab to one of the approved drugs, and try to find out the best for our patient before combining them. Dr Smith: The complement inhibitor trials are breathtaking, at least for me. If I'm trying to convince students to go into neurology, I'll say, "Take a look at that paper," because anyone who claims that we're "diagnose and adios" is so wrong. It's so exciting. So, at a high level, this must have fundamentally changed outcomes for patients. I mean, it's still a difficult disease, but what is the kind of prognosis for that patient I described who comes in, gets the therapy you talked about? What does their long-term outcome look like in this modern therapeutic environment? Dr Mariotto: So, NMOSD is almost always a relapsing disease. That's why, as we mentioned, we have to treat patients always. But the prognosis changes a lot since we were also able to use all these drugs for the disease. So, the prognosis changes if we recognize it properly and early, and if we treat NMOSD properly with immunosuppressives. So, whatever we choose it's important to start it quickly, and this is the only way that we have to improve the prognosis of this disease. We have very active cases, but we have also cases who responds quite well to this immunosuppressive treatment, since now we have, as mentioned, these ones which are very impressive and show incredible results. So, the prognosis of the disease change in the last year, thanks also to the improvement of the diagnosis and of the treatment choices for the disease.  Dr Smith: I'm just... I- maybe my last question, you know, just at a personal level, not only for you as an expert who's caring for these patients, but in the patient community, this must have been a pretty exciting period of time, right? I mean, these, these drugs are coming fast and furious, and what a change. What's the kind of zeitgeist in the community, both your professional community and amongst the patient community about where we are? Dr Mariotto: Yeah, you're right. The last years were defined the years of NMOSD and also MOGAD because we had finally approved drugs which is relevant for all the disease that we treat and changed the landscape of the disease for clinicians, but also for patients. And we have more than one, as we said, so we have more options that we can also discuss with patients to try to choose the best one in terms of activity, but also route of administration or time. Some years ago, we just had rituximab, which is not approved in most of the countries, and now we have different approved drugs. And we improved the diagnosis of the disease thanks to the availability of live cell-based assay. And then we are working a lot also on biomarkers like GFAP, for example, which has been shown to be a very attractive biomarker able to mark disease activity and maybe also prognosis on this disease. So, you're right. I mean, in the last years, the landscape of NMOSD changed a lot.  Dr Smith: Sara, thank you so much for talking with me. I could keep going for another half an hour, but I would be in trouble with my editor, so I think we probably need to wrap it up. But thank you so much. This has been very informative.  Dr Mariotto: My pleasure. Dr Smith: Mine too. Thank you. Again, today I've been interviewing Dr Sara Mariotto about her article on NMOSD, which she wrote with Dr Romain Marignier. This article appears in the April 2026 issue of Continuum on multiple sclerosis. Be sure to check out Continuum Audio episodes from this and other issues, and thanks to you, our listeners, for joining us today. Dr Monteith: This is Dr Teshamae Monteith, Associate Editor of Continuum Audio. If you've enjoyed this episode, you'll love the journal, which is full of in-depth and clinically relevant information important for neurology practitioners. Use the link in the episode notes to learn more and subscribe. AAN members, you can get CME for listening to this interview by completing the evaluation at continpub.com/audioCME. Thank you for listening to Continuum Audio.

The "Community Meets Clinic" podcast series introduces clinicians and healthcare personnel specializing in rare neuroimmune disorders. In this episode hosted by Krissy Dilger of SRNA, we met Dr. Grace Gombolay and Dr. Varun Kannan, both from Emory University and Children's Healthcare of Atlanta, designated Centers of Excellence in Rare Neuroimmune Disorders. Dr. Kannan discussed learning alongside families as conditions like MOG antibody disease emerged clinically and his focus on tailoring treatment and supporting clinical trials in a field with few approved therapies [03:37]. Dr. Gombolay outlined her research on biomarker development, a Children's biobank, advanced MRI collaborations, and participation in the Network of Pediatric MS Centers covering disorders such as MOGAD, NMOSD, optic neuritis, ADEM, and TM [06:36]. They described their multidisciplinary clinic team, highlighted home infusions and telemedicine to reduce burden, and shared personal self-care strategies [10:22]. Dr. Gombolay and Dr. Kannan expressed hope for more trials, remyelination, prevention, and earlier diagnosis aided by AI prompts [20:43].You can view Dr. Grace Gombolay's medical profile here:https://www.choa.org/doctors/grace-gombolayYou can view Dr. Varun Kannan's medical profile here:https://www.choa.org/doctors/varun-kannanGrace Gombolay, MD, MSc, FAAN is an Associate Professor at Emory University and Director of the Pediatric Neuroimmunology and Multiple Sclerosis Clinic at Children's Healthcare of Atlanta. Her research interest involves biomarker development in pediatric neuroinflammatory diseases including autoimmune encephalitis, multiple sclerosis, MOGAD, and NMOSD.Varun Kannan, MD graduated from Emory University School of Medicine in 2017. He then completed child neurology residency in 2022, followed by pediatric neuroimmunology and multiple sclerosis fellowship at Baylor College of Medicine and Texas Children's Hospital in 2023. He returned to Emory and Children's Healthcare of Atlanta in 2023, where he has worked closely with Dr. Grace Gombolay in the neuroimmunology program. He is interested in clinical research regarding severe/relapsing forms of rare neuroimmune disorders including autoimmune encephalitis and MOGAD. He is currently involved in multiple upcoming phase 3 clinical trials exploring new disease modifying treatments for pediatric rare neuroimmune disorders. He is also passionate about medical education and is currently one of the Associate Program Directors for the Emory child neurology residency.00:00 Welcome01:56 Dr. Grace Gombolay's Journey03:37 Dr. Varun Kannan's Path05:06 Kannan's Research Focus06:36 Biomarkers and Biobank10:22 Clinic Team and Care13:44 Self Care and Balance16:15 Children's Healthcare of Atlanta20:43 Hopeful Future Ahead24:49 Closing

This week's episode of the Brain & Life Podcast was recorded live at the American Academy of Neurology's Annual Meeting in 2025! Hosts Dr. Daniel Correa and Dr. Katy Peters were joined by Joel Salinas, MD, MBA, MSc, FAAN, Andrea Lendaris, MD, MS, Andrew M. Southerland, MD, FAAN, and Eric J. Seachrist, MD to share what it's like living and practicing neurology with their own neurological condition(s) and neurodiverse perspectives, and explore how their experiences serve as a window into the patient and community perspective.   Brain & Life Articles Mentioned Neurology® Podcast Switching Roles: A Neuro-oncologist Reflects on his Own Experience with a Brain Tumor We want to hear from you! Have a question or want to hear a topic featured on the Brain & Life Podcast? ·       Record a voicemail at 612-928-6206 ·       Email us at BLpodcast@brainandlife.org   Social Media Hosts: Dr. Daniel Correa @neurodrcorrea; Dr. Katy Peters @KatyPetersMDPhD

Familiarity with the clinical, MRI, CSF, and serologic features of MOGAD can help neurologists recognize this condition in clinical practice. Awareness of the utility and pitfalls of the MOG antibody test is critical. The current therapeutic approach is guided by retrospective studies and the application of immunotherapies used in other autoimmune neurologic disorders. In this episode, Gordon Smith, MD, FAAN, speaks with Eoin P. Flanagan, MBBCh, coauthor of the article "Myelin Oligodendrocyte Glycoprotein Antibody–Associated Disease" in the Continuum® April 2026 Multiple Sclerosis and Related 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. Flanagan is a professor of neurology and the division chair of the Division of Multiple Sclerosis and Autoimmune Neurology in the Department of Neurology at Mayo Clinic in Rochester, Minnesota. Additional Resources Read the article: Myelin Oligodendrocyte Glycoprotein Antibody–Associated Disease Subscribe to Continuum®: shop.lww.com/Continuum Earn CME (available only to AAN members): continpub.com/AudioCME Continuum® Aloud (verbatim audio-book style recordings of articles available only to Continuum® subscribers): continpub.com/Aloud More about the American Academy of Neurology: aan.com Social Media facebook.com/continuumcme @ContinuumAAN Host: @GordonSmithMD Full episode transcript available here Dr Smith: So, what neurological disorder can cause bilateral optic neuritis, transverse myelitis, ADEM, or can mimic acute flaccid myelitis, intracranial hypertension, viral encephalitis, or cause seizures? Sounds like the great imitator, perhaps. If you want to know and learn more about this syndrome and how you can treat it---and it is very treatable---keep listening. My name is Gordon Smith, and today I have the great opportunity to talk with Dr Eoin Flanagan from the Mayo Clinic on his article on myelin oligodendrocyte glycoprotein antibody associated disease, or MOGAD, which is in the April 2026 issue of Continuum on Multiple Sclerosis and Related Disorders.  Dr Jones: This is Dr Lyell Jones, Editor-in-Chief of Continuum. Thank you for listening to Continuum Audio. Be sure to visit the links in the episode notes for information about earning CME, subscribing to the journal, and exclusive access to interviews not featured on the podcast. Dr Smith: This is Dr Gordon Smith. Today I'm interviewing Dr Eoin Flanagan about his article on myelin oligodendrocyte glycoprotein associated disease, or MOGAD, which appears in the April 2026 Continuum issue on multiple sclerosis and related disorders. Eoin, welcome to the podcast, and please introduce yourself to our audience.  Dr Flanagan: Yeah, thanks so much. I'm Eoin Flanagan. I'm a neurologist at the Mayo Clinic. I'm originally from Ireland. I work in the neuroimmunology lab at the Mayo Clinic, and work and see patients with MS, MOG, and autoimmune disorders here in Rochester, Minnesota.  Dr Smith: Your article is super interesting, I think, and this has been a really rapidly evolving area over the last, you know, many years. We have many more antibodies, and MOG is something that's been around for a while, but we've certainly learned a lot more about it. This is a topic that I think will be familiar to most of our listeners, but I wonder if maybe you can just begin by laying the foundation. Like, what is MOG? What's its typical presentation?   Dr Flanagan: So, MOG is a protein on the surface of the oligodendrocyte or its CNS myelin, and it was always of interest as a potential antibody target, and initially it was investigated in multiple sclerosis. But subsequently, we recognized that the antibodies to MOG have a specific syndrome, of which about a quarter of patients are pediatric and then the remainder are adults. And they can present with a variety of syndromes, probably most commonly optic neuritis, but also acute disseminated encephalomyelitis, or ADEM. Transverse myelitis can also occur, and then some other unusual brain and brainstem cerebellar syndromes can also occur.   Dr Smith: I was really impressed in the very broad phenotypic spectrum of MOG. We'll talk more about that, of course. But I wonder if maybe you can tell us when we should be ordering MOG antibody? Given this broad variability, does anyone who has a CNS demyelinating disease need a MOG assay, only specific phenotypes? What guidance do you have for our listeners?   Dr Flanagan: Yeah. It's a great question. So, I think you have to be a little bit careful because the MOG antibody test is a little bit sticky. So sometimes we can see some low-positive false positives. So, we don't wanna order it in every single patient with classical MS. So, I suppose we'll start with who not to order it in. I think it's also a very optic nerve- and optic neuritis-central disease, so I think you really need to be considering this in a patient with optic neuritis who does not have lesions in the brain suggestive of multiple sclerosis. And then we think about some of the features: if the lesion, the enhancement along the optic nerve is long, if it's bilateral, if there's a lot of optic disc edema accompanying that, we tend to think about MOG antibodies. And then children with demyelinating disease, MOG is over-represented in that cohort, so it accounts for about a third of those. So, if you have a child with CNS demyelinating disease, particularly if they're under twelve, with ADEM presentations or other presentations, you probably want to be ordering the MOG antibody test. And then a longitudinally extensive transverse myelitis in adults, certain types of cerebral phenotypes that we can get into, you would want to consider ordering MOG antibodies too.   Dr Smith: Now, you point out in the article that it's really important that laboratories use the cell-based assay for MOG as opposed to an ELISA, for instance. Is this something folks need to be very attentive to, or are all of the commercial laboratories now using a cell-based assay?   Dr Flanagan: Yeah. I think all of the commercial labs are using cell-based assays, so we don't really get into much of an issue. There are some differences between serum and CSF, so really, serum is the optimal sample to order. There is also some differences between the live cell-based assay and the fixed cell-based assay, where the live cell-based assay may have some advantages in terms of sensitivity. And then CSF is kind of still under evaluation about its role in the condition. So in general, it's a serum test. And then we have to remember that the antibody tends to be highest at the onset, and then it goes down over time. So, if you delay your testing or you're testing a patient long after the condition, it can go negative, for example. So it tends to be highest both around the relapses and particularly at the onset of the condition.   Dr Smith: You mentioned earlier that the test is sticky, which I take to mean that there is some risk for low-titer false positives. How do you navigate that situation? When should we be suspicious about a false positive?   Dr Flanagan: Yeah. I think there's some very useful features that can help you. You know, the main differential diagnosis is going to be multiple sclerosis, particularly in the US, in regions of the northern US where MS is particularly common. So, you really wanna be making sure that if you get a positive result, low positive, that it's not multiple sclerosis. And some of the best discriminating features are CSF oligoclonal bands. They're about 85% in MS and about 15% in MOG, so an easy number to remember, 85 and 15. And then the lesions in MOG, the brain lesions, tend to disappear over time. So, if you have the advantage of that follow-up MRI a year down the line, about 70% of lesions in MOGAD will resolve, while in MS, as we know, the term means multiple scars, so the MS lesions tend to persist over time. So, they are two quite useful features that can help discriminate.   Dr Smith: And how about specific phenotypes or areas of involvement or imaging abnormalities that suggest MOG? One of the things I found really interesting in your article is there are a host of different syndromes that I think had largely been previously described, many of them, that became clear later that these were really tied to MOG antibodies. Presumably, that's helpful in interpreting the antibody assay in that patients who have, perhaps, a borderline low titer, for instance, but have a very typical phenotype are more likely to have MOG than those who have a more clearly MS-type phenotype.   Dr Flanagan: Yeah, absolutely right. Yes. So, there's certain phenotypes that we don't tend to see with MS. The acute disseminated encephalomyelitis, or ADEM, is one that's particularly common in children. And about half of people that have ADEM will be positive for the MOG antibody. So that's a syndrome you need to look out for, which would be often in children, encephalopathy, and they would have multifocal white matter lesions, sometimes involving the gray matter. A second syndrome that was an interesting discovery from a Japanese group was this unilateral cerebral cortical encephalitis, where patients can have this swelling and T2 hyperintensity, often just on one side of the brain. And it's in the cortex, and some of those patients won't have any white matter lesions. And in that situation, it's important to order the MOG antibody, and that seems to be a specific phenotype of MOGAD. But sometimes people don't think about it because the white matter is not involved. So, if you see these patients, they often present with seizures, sometimes they even have fever accompanied by it. And if you see those patients and see this radiological feature, then you really want to consider ordering the MOG antibody too.   Dr Smith: Yeah, I found that really interesting. And I- actually, my next question is perhaps a good follow-up on that, is, what are the diagnostic pitfalls? You give a lot of examples of situations and I think some cases where it's easy to get tripped up and misdiagnose someone who has MOG with another fairly common neurological problem.   Dr Flanagan: Yeah, I think some of the things that can help you when you're determining if the MOG is a true positive or false positive is the level of the antibodies. The super high titers, if it's a clear positive or very strong positive, the likelihood is that that is much more likely to be MOGAD than those low positives just above the cutoff. So that can be useful to help you discriminate from false positives. Those lesions, again, if all the lesions persist over time, that's going to be more suggestive of multiple sclerosis. Other diagnostic pitfalls, I suppose, if it's a syndrome that's not really associated with MOG, like peripheral neuropathy or other syndromes where we'll see some case reports, but usually I would be very cautious about those kind of presentations. So usually, having the antibody at a high level, and then also if they've had other symptoms suggestive of MOGAD, like if a patient has had recurrent optic neuritis and then they have an unusual brain syndrome, or they start out with an unusual brain syndrome and then have recurrent optic neuritis. You know, there are situations that make it more likely if they're having other typical phenotypes of the MOGAD where we can kind of expand the spectrum, but we have to be careful.   Dr Smith: I was really curious about the dynamic imaging findings. And you point this out both in terms of the resolution of imaging findings, but also in that patients who have an acute MOG syndrome often have very rapid evolution of the imaging abnormalities. I'm just curious, you know, why is that, and what do you make of it? Does it have a mechanistic implication, do you think?   Dr Flanagan: I don't think we know for sure. I think there's probably a lot more happening than we see on MRIs sometimes. What sometimes can happen in about 10% of patients is the initial MRI can be normal. We don't tend to see that with multiple sclerosis or NMOSD. Then what we see is it evolving over time. So, at that time, if you do a CSF, you'll often see inflammation, but we don't see the lesions. Now, that might be because the MRI is not very good at picking up cortical involvement. That can be difficult to see in MRI. Or there could be other factors. It could be a functional effect on the MOG but without frank demyelination yet, for example. Or there could be edema that you- myelin edema that you can't see as a lesion yet on MRI. But we do see that if you repeat the MRI, sometimes it'll change a lot. So, you may go from one or two lesions on the first MRI to twenty lesions on the second MRI a week later. So, it does tend to change a lot. And then over time, those lesions also resolve. So, what I say is if it's a very suspicious situation---like a child comes in with new-onset encephalitis, has inflammatory CSF---you might wanna consider repeating that MRI down the line and seeing if it's changing. And then over time, you know, a repeat MRI a year after the onset when there's brain or spinal cord lesions can be very helpful just to make sure you're on the right track, because lots of those lesions will then disappear, and that's a very clear discriminator from multiple sclerosis.   Dr Smith: Yeah, thanks. I mean, I was wondering the same thing about whether that particular feature might imply, you know, a functional abnormality as opposed to more of a structural abnormality. So probably a lot more to learn as we move forward. There are now consensus diagnostic criteria that were published a couple of years ago. I think you've already touched on kind of the general approach, but do you want to speak to those? I found your summary pretty helpful.   Dr Flanagan: Yeah, I think that those criteria are quite useful. They have three main parts to them. The first part is having a characteristic clinical syndrome. So, we talked about ADEM, we talked about cerebral cortical encephalitis, transverse myelitis that's often longitudinally extensive, and optic neuritis being the main syndromes, but sometimes other brainstem or cerebellar involvement can be seen. And then the second part is having a positive MOG antibody. And then there's some caveats there. So, if you have a high positive, then you don't really need any additional supportive criteria. On the other hand, if you're low positive, to get at those sticky antibodies that make sure it's not a false positive, you need some additional supportive clinical or MRI criteria. Or if you're only positive in CSF, you need that additional criteria. You also need to be negative for the aquaporin-4 antibody, because they can overlap clinically. And some of those supportive criteria are things that we talked about a little bit earlier, longer lesions within the optic nerve, bilateral involvement, involvement of the nerve sheath or optic disc edema. This is a situation, MOG antibody disease, where your fundoscope is useful and looking in the back of the eye and seeing swelling, because we don't tend to see that quite as often. It's less common in multiple sclerosis, but we often see prominent edema in MOGAD. And then in the spinal cord, the lesions tend to be central in the cord. Sometimes they form this H sign where it's restricted to the gray matter, and they tend to be longer, sometimes involving the conus. Patients will often have neurogenic bowel or bladder. And then in the brain, deep gray involvement, those large lesions along the cortex with swelling are some of the typical features. And then the final step is exclusion of another diagnosis. Just like with any test that we do in neurology, our final step is going to be to put that into context. So that's just a normal thing that we will always do when we get a group of test results back that we don't know what it means. We have to put it into context. So, make sure it's not multiple sclerosis, everything else does not look like multiple sclerosis, and then you can be on your way to make a diagnosis.   Dr Smith: Definitely encourage listeners to read your article. I guess I say that with every time I- or with everyone I talk to for Continuum Audio, but the images are really fantastic and the cases are fantastic. So, everything you've described is well-illustrated, including really nice schematic sort of diagrams that help differentiate NMO from MOG and MS. So, if you like MRI scans and good imaging frameworks, then this is the article for you.   Dr Flanagan: I think that's true, and the other thing is that the imaging is quite helpful because it takes a while for that antibody to come back. We're lucky at Mayo Clinic, if you work here, it, it comes back faster for you. But for many places, that time of sending it in, so a lot of times you don't know right away. So, looking at scrutinizing that MRI can be very helpful to guide you on your way and to know what you're dealing with and how to approach both the acute treatment and plans to have potentially a steroid taper after the acute treatment and those kind of things that can help guide you in that regard.   Dr Smith: Yeah. So, let's talk about treatment. You know, what's your approach to treating a patient who has an acute demyelinating syndrome related to MOG?   Dr Flanagan: So similar to other things, MOG is very steroid responsive. So, we use high-dose IV methylprednisolone in adults. That would be one gram IV for five days. And then we also will sometimes use oral steroids, twelve hundred and fifty milligrams. That's a bit of a hassle because it's twenty-five fifty-milligram tablets, it doesn't come in a larger tablet version. But it's very helpful to patients because they can get started on it right away. You don't have to set up an infusion center. So, we have used those oral steroids often in people who don't have access to an infusion center, are not in the hospital. And particularly as it's often optic neuritis, some of those patients are seen in the outpatient setting, so we can get in with treatment quickly. In patients where it's more severe, it doesn't recover quickly with steroids, then we would consider escalating to plasma exchange as our second-line treatment, and there's some retrospective data that suggests that plasma exchange can be useful. That's gonna be particularly for those people who don't have that quick response to steroids, or maybe more severe phenotypes like that brain involvement with ADEM or cerebral cortical encephalitis, where those patients might be in the hospital and quite unwell. I will say, we might get on to this, that sometimes MOG can be very, very severe and even fulminant, where there can be increased intracranial pressure, and these patients can be in the ICU, and it can be life-threatening. And so, it's really important to treat those patients aggressively, and some patients have even required hemicraniectomy or additional treatment. Sometimes IL-6 blocking medications have been used in that situation. So, monitoring and treating increased intracranial pressure in those rare patients, probably 2 or 3% that have the very severe attack, is important.   Dr Smith: I think one of the things I found interesting, and then I'd love to get your feedback on this, is that most patients with MOG seem to have a very readily treatable disorder that's monophasic, right? You treat them with steroids, and they do well. On the other extreme, there are these patients that have a much more malignant presentation, and there are some that sound like they benefit from prophylactic or some chronic therapy. What's your approach, right? In MS, we do serial scans to monitor, and obviously, our patients are on, you know, chronic disease-modifying therapy. How do you decide when you're going to provide some sort of prophylactic therapy? How do you monitor it? How long do you continue it?   Dr Flanagan: That's a great point. We don't know for sure yet, but I think for the most part, our approach has been if the patient has a single episode, they recover well from that episode. So, if that's optic neuritis, they're back to twenty/twenty vision. They have recovered well. We don't tend to use chronic maintenance immunotherapy. Sometimes after the first attack, we'll do a little bit of a slow taper, maybe over four, six weeks. We have done longer than that. And then we won't place them on any long-term treatment, because it's about 50% of patients that may have a monophasic disease, so we don't want to treat all those people who are destined never to have another relapse. On the other hand, if a patient had a very severe episode, they're in the ICU, they're intubated, some of those patients then afterwards we will start them at least temporarily on an attack prevention medication for at least a few years to get them through. Some patients will be very fearful of future relapses in that situation. Or if they don't recover well, if they're blind in one eye after an episode and then their other eye is vulnerable, or they're left with some residual deficits neurologically from a myelitis, then we would often sometimes put those patients after the first attack. But most of the time, we're gonna wait and see if they get that second attack, and then once they have the second attack, that is when we would consider a steroid-sparing medication. But I will say that there's no proven medications. We don't have any clinical trial data available yet. So some of those patients with relapsing disease, we'll either try to enroll them in a clinical trial, or we'll use an off-label treatment to try and manage their disease based on what we've learned from neuromyelitis optica or from multiple sclerosis. A few different options seem to be better, and we can maybe get into that too.   Dr Smith: Yeah, let's go there. So, what options are there? You mentioned in more fulminant disease IL-6 inhibitors, and by that I assume you mean tocilizumab, but what are the options when you want to use prophylactic therapy?   Dr Flanagan: So, that tocilizumab can be beneficial in the very acute situation, in that malignant situation. But also as an attack prevention treatment, the IL-6 blockers seem to- some of the retrospective data seems to look like it works reasonably well, so we work and see if we can get that approved. Another medication that can work well is IVIG or subcutaneous immunoglobulin as a maintenance treatment, so we would sometimes give that, like, at least one gram per kilogram once a month. The benefit of that is it doesn't lower your immune system, so there's some advantages there, particularly in people who may be more prone to infections, older people. So, we'll sometimes use that. But we do get into a lot of challenges with insurance coverage, and it can be difficult to get these approved by insurance because we only have retrospective data out there. So then for some patients, if they're in a region where there's a clinical trial available, we might try to enroll them in a clinical trial. And there are some clinical trials underway now, so hopefully in the future we'll be able to have some FDA-approved medications that can have some Class 1 data that we can follow. Because it's hard when you're just following retrospective data or anecdotal reports, it's a little bit difficult to know exactly how well you're doing with your treatments.   Dr Smith: Well, Eoin, I wonder if we could finish up by just looking into the future, right? I mean, it sounds like a fun patient population to take care of because you've got lots of great therapies and can have a durable impact. But sure would be nice to have more evidence-based therapies and an FDA approval. What trials are going on? What's the future look like?   Dr Flanagan: Yep. So, there's some trials going on in the- a couple of worldwide trials. One is on an FCRN blocker called rozanolixizumab, which is kind of like a plasma exchange-type treatment which removes your antibodies, and it's a weekly subcutaneous treatment where adults are enrolled. And the second one is called satralizumab, which is another IL-6 blocking medication. And again, that one's given once monthly under the skin. And the trial for that also includes children down to age eighteen, so for adolescents, too, that can be an option. There are trials, I believe, in Asia for tocilizumab too, and there's one starting in Australia for rituximab. So, the good news is that we're going to have some really good data down the line for lots of different agents, and we'll be able to figure out which treatments work. And this will be really of great benefit to our patients when we get that Class 1 data to kind of guide us on what we should be using and really build on the success of some of the other conditions like neuromyelitis optica spectrum disorder, where we now have four or five approved, medications that work very well.   Dr Smith: Well, Eoin, thank you. This is a great conversation. I will say that it... the topic that I was a little intimidated about. I'm a simple peripheral nerve guy, as you know. But I think moreso than any other Continuum article I've read recently, I'm, like, loaded for bear. I can't wait to go back on the inpatient service and look for some MOG patients, because your article really left me feeling kind of prepared to think through this in a clinical setting. So, thank you for the conversation, and congratulations on a really wonderful piece for Continuum.   Dr Flanagan: Yeah, thanks so much. Always a great honor to be involved in the Continuum, and thanks to all the readers out there.   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 the academic job market for fellowship graduates, the challenges of today's complex neuromuscular therapies, and the changes made in a new stroke guideline.

Adult‑onset leukodystrophies, though rare, can closely mimic MS on both clinical presentation and neuroimaging, posing a significant diagnostic challenge. This episode highlights key clinical and radiologic red flags that can help distinguish these disorders from MS, preventing misdiagnosis and avoiding inappropriate treatment while enabling timely genetic counseling and targeted therapies. In this episode, Teshamae Monteith, MD, FAAN, speaks with Roberta La Piana, MD, PhD, coauthor of the article "Adult-Onset Leukodystrophies Mimicking Multiple Sclerosis" in the Continuum® April 2026 Multiple Sclerosis and Related 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. La Piana is an associate professor in the Department of Neurology and Neurosurgery at the Montreal Neurological Institute, McGill University, and an associate member of the Department of Diagnostic Radiology at McGill University in Montreal, Quebec, Canada. Additional Resources Read the article: Adult-Onset Leukodystrophies Mimicking Multiple Sclerosis 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 Monteith: You just saw a patient in clinic. And you're clear, the diagnosis is multiple sclerosis. Not everything fits, but it kind of looks like multiple sclerosis. You see the patient back years later. There're some treatment issues, the patient's not responding to treatment, and things look different. Have you thought about a genetic inherited problem like leukodystrophy or a genetic white matter disorder? Listen to this podcast. We're going to help you figure it out. Dr Jones: This is Dr Lyell Jones, Editor-in-Chief of Continuum. Thank you for listening to Continuum Audio. Be sure to visit the links in the episode notes for information about earning CME, subscribing to the journal, and exclusive access to interviews not featured on the podcast. Dr Monteith: This is Dr Teshamae Monteith. Today I'm interviewing Dr Roberta La Piana about her article on adult-onset leukodystrophies mimicking multiple sclerosis, which she wrote with Dr Gabrielle Macaron. This article appears in the April 2026 Continuum issue on multiple sclerosis. Welcome to our podcast.  Dr La Piana: Thank you. Thank you for having me.  Dr Monteith: Absolutely. Why don't we start off with you introducing yourself? Dr La Piana: So, my name is Roberta La Piana. I'm a pediatric neurologist. I trained in Italy, I did my medical school, I did my residency in pediatric neurology there. And then I moved here to Montreal, to the Montreal Neurological Institute, to do a PhD in neuroscience. And that's where I specialized in adult-onset genetic white matter diseases. And after my PhD, I was recruited as an assistant professor here. So, that's where I got into this field.  Dr Monteith: This big field, highly specialized; lots of disorders, but highly specialized. And what got you into this? Neuroscience is huge. So, was it a mentor, or…?  Dr La Piana: No, actually, it was because of my background, because I trained as a pediatric neurologist and I loved the genetic white matter disorders in the pediatric population. So, when I came to the Montreal Neurological Institute, initially it was mainly to have a better expertise in imaging. And being at an adult neurology institute, I started seeing patients with adult genetic white matter diseases, and I was immediately fascinated by how different they were from their pediatric counterparts. Because in pediatric genetic white matter diseases, pediatric leukodystrophies look very diffuse, look very confluentous, so it's difficult to mistake them. But in adults, in the adult forms, I was initially driven by how often they can be misdiagnosed as multiple sclerosis or as other acquired white matter disorders. So that's why I got really interested in in this field.  Dr Monteith: You're, like, literally the perfect person for this discussion.  Dr La Piana: I'm not sure- *laughs* Dr Monteith: Why don't we start off with what your objectives were when writing this article? Dr La Piana: With writing this article, the goal is what I have been, actually, doing for the past ten years or so. So, really try to get more attention into the field because of the high rate of potential misdiagnosis of patients. So, that's exactly the reason why I really would like to raise the interest of neurologists for these disorders, because they are not considered enough in the differential diagnosis of patients, of adult patients presenting with white matter disorders. They are considered rare---which are, they are rare, definitely. But collectively, while each single form is rare, collectively they are not as rare. So- and thus, the risk of misdiagnosis and the potential impact of misdiagnosis on them with, you know, you can imagine giving patients inappropriate treatment or missing the possibility of a prenatal genetic diagnosis is so high that I really would like people to keep these disorders in the differential.  Dr Monteith: And it sounds like more than ever, this is really important because some of the newer developments in the field. Dr La Piana: Yes. Specifically, we have now tools that will allow to diagnose these patients quite quickly. All the genetic techniques that are available nowadays can really, with one single shot, we can now sequence hundreds of genes so we can have a quicker diagnosis. And this thing was impossible up until ten years ago. So that's definitely the first huge improvement that makes these disorders now easily diagnosed. Dr Monteith: Yeah. So why don't we talk a little bit about how common is this misdiagnosis for these rare subtypes? Dr La Piana: Yeah, the misdiagnosis, it depends on the cohorts. Generally speaking, I would say that the rate of that misdiagnosis for these forms is up to 25% or even more in some other cohorts. And it really depends on the forms. Like, there are clearly some forms, especially those that present with multifocal white matter diseases, that present with nonspecific clinical presentations like migraines, image---and especially for female patients, and for which migraine is so common, having multifocal with other abnormalities is so common, the rate of diagnosis increases even further. So, these are all things that we need to keep in mind. I know these are rare, but still, we need to always have them on the back of our minds.  Dr Monteith: Are there any particular disorders that are more often misdiagnosed? And you spoke about progressive forms of multiple sclerosis being a common kind of misdiagnosis.  Dr La Piana: Yeah. So, there are definitely forms that are more commonly misdiagnosed. And these are those that, as I probably repeated already too many times, is the word multifocal, which is key. So, all those genetic white matter disorders that present with multifocal white matter abnormalities are not initially considered as genetic. So, I'm thinking about all of the leukovasculopathies, so, the small vessel diseases which are genetic in origin. For example, CADASIL; for example, the disorders related to collagen-4; so, the COL4 A1 or A2-related disorders. Those are clearly more commonly misdiagnosed initially. Another big group, unfortunately, is the CSF1R-related disorders. I know I'm saying a lot of gene names, but due to the fact that they start with multifocal abnormalities and they start with quite nonspecific, slowly progressive symptoms, the rate of misdiagnosis is definitely higher. Dr Monteith: And can you discuss some of the clinical challenges when seeing patients that might lead to this misdiagnosis?  Dr La Piana: There are multiple clinical challenges. One is definitely the presence of nonspecific or initially mild clinical symptoms that sometimes don't raise initially the red flag of something, degenerative or progressive or genetic. One category that I would mention are psychiatric disturbances, especially in the form of depression, anxiety, or apathy. This is quite common in patients with some forms of genetic white matter disorders, and they are initially misdirected to psychiatrists and taken care in that domain. But it's only when some even mild neurological symptoms like a gait disturbance or hyperreflexia, or we had patients with, like, a urinary incontinence. It's only at that time, but maybe years have passed meanwhile, that these patients are finally referred to the neurologist Dr Monteith: You spoke about some of these clinical symptoms. Can you give us some other clinical red flags?  Dr La Piana: Well, some other clinical red flags can be, for example, the extraneurological involvement. So, we have patients where- and there's a reason immediately to some specific disorders. For example, infertility. The presence of infertility in a female patient with white matter disorders should immediately form the consideration of the specific genetic white matter diseases that are associated with these forms. And this is not something that neurologists tend to ask about in the collection of the clinical history. And this is something that can make the difference and can accelerate the diagnosis.  Dr Monteith: What are some other things? I mean, I know we can think about treatment, lack of a common treatment response, maybe, to steroids. You gave a great example of optic neuritis, for example. Give us some other things that we should say, hey, this doesn't fit the picture. Red flag.  Dr La Piana: In this case, I think we want to talk more about the specific misdiagnosis of MS. Because these patients are often misdiagnosed with MS, but they might sometimes be misdiagnosed with other forms of acquired white matter diseases. When we consider MS, definitely the presence of being treatment resistant: so, patients that are not responsive to the common MS-targeting treatment should be always a red flag. The evolution as well. So, for example, the presence of a more slowly progressive course is another red flag. The presence of optic neuritis. Sometimes it's tricky because it's not common in the genetic white matter disorders, it's used as a criterion to orient correctly towards a multiple sclerosis. But we need to keep in mind that there are forms, genetic forms, especially the mitochondrial forms, that can present with optic neuritis and are really at the overlap with the multiple sclerosis spectrum. Then, if we want to move forward beyond the clinical side and go into the laboratory, of course a negative lumbar puncture with no oligoclonal bands should be a major red flag. Dr Monteith: What about some of the radiographic features?  Dr La Piana: So, the radiographic features is something we are really working on in the field, especially with the new criteria used in MS. So, for example the paramagnetic rim lesions or the central vein sign, they are considered the specific forms. But it's true- and don't have an answer for that. I want to be clear, but it's true that they haven't been assessed yet extensively in patients with genetic white matter disorders. Anecdotally, I can say, because I have already reported this at conferences, that we have seen patients with genetic white matter conditions reaching a threshold for a central vein sign that can be considered diagnostic for MS. And we have seen that in some patients. Again, no study has been carried out extensively to date, but I think we should consider that with a grain of salt. But yeah, the paramagnetic rim in lesions is probably more accurate to distinguish between genetic and acquired white matter disorders.  Dr Monteith: And what about some of the genetic white matter disorders that mimic MS? You spoke about things like CADASIL; what are other things that we should keep in the back of our mind? And you have great charts, to our listeners, and they're going to have to review those charts, because they're excellent. I think maybe they need to find a way to make that a little bookmark you walk around with on the ward. But what are some other conditions that kind of commonly mischaracterized?  Dr La Piana: Two of the main groups are the one that you mentioned. So, leukovasculopathy is- so, CADASIL, is definitely one of the most common misdiagnoses of MS. And the presence, as we said, of some clinical features like migraine, especially when it's complicated migraine with visual aura, we all know that. But especially in the context of a positive family history for either a psychiatry condition or migraine as well, or strokes, these are all factors that should prompt the consideration of these disorders in the differential of a patient with white matter disorders. Another category are definitely mitochondrial disorders, which I think are more neglected than others because we don't think about mitochondrial disorders when we see white matter disease; we tend to consider that mitochondrial disorders are a problem of the gray matter, but they are not. There are white matter diseases that have definitely mitochondrial. And the third category are probably microgliocytes, which are represented by the CSF1R-related disorder. And this is also something that is clearly quite prevalent, relatively prevalent, in the field of genetic white matter disorders misdiagnosed as MS.  Dr Monteith: Yeah. Why don't we go through some of the, kind of, key history, you know, some of the key questions you would ask in the history to try and differentiate? You mentioned kind of subtle symptoms, longstanding progressive symptoms. I know things that we look at like relapsing/remitting and some trigger factors can actually be associated with some of these genetic disorders. So how do you approach a patient? What are some of the key questions? You talked about family history and you talked about medical history, but why don't you kind of give us a nice way to kind of hone in on to the patient? Dr La Piana: There are a couple of questions that we usually ask. I should make a disclaimer, though, that I work very closely with the MS clinics, so we are ready to receive patients that are prescreened. So, these are already patients that people working on acquired white matter disorders feel like they are atypical, so they want our opinion. But usually, there are two groups of questions that we always ask. One is about the family history. And by saying family history, I really dig into the family history. I don't just want to know whether there are family members with neurological disorders. I ask specifically about migraine. I ask specifically about infertility issues. I ask specifically about psychiatric issues. These three things are always on the top of my mind when asking about family history. The other thing is a family history for neurodevelopmental disorder, because you know that some people might not remember that some genetic white matter diseases can present at different ages. So, in the same family, there might be cases with a pediatric-onset leukodystrophy, and that can manifest at a later age in other family members. So, this is something that we always explore. In terms of the clinical history, one question that I recommend always to ask is really about more subtle symptoms. So, for example, many of our patients present with progressive balance problems or progressive mobility issues that have been going on for a while. So, we always ask how they were when they were in their teenage years, for instance. And it's frequent that they say, actually, I was a bit clumsy. Actually, I was not the first being picked in school at phys-ed sports. And these are all interesting aspects. Maybe they are totally incidental, and sometimes they suggest that there was probably something going on for a long time. The other thing is the presence, for example, of learning difficulties. Again, these are things that are subtle but testify that there was probably a process that was more longstanding. Dr Monteith:  You talked about things like rim lesions. Are there other types of sequences that might be useful to better characterize demyelinating diseases that are genetic in origin? I assume higher levels of MRI might be better at differentiating.  Dr La Piana: Yeah. So, in the clinical setting, there are a couple of sequences that are very useful. One is the diffusion, because as opposed to multiple sclerosis, the presence of persistently restricted areas of diffusion can point immediately towards some genetic white matter diseases. One is CSF1R-related disorders. But there are also some other, more rare tremor and ataxia syndrome that present with persistent areas of restricted diffusion as well as others. The presence of calcification. So, adding an SWI, susceptibility weighted imaging, to check not just for calcifications that can immediately orient towards some disorders, but can also identify areas of microhemorrhages that, if we are going back to the leukovasculopathies, to the genetic leukovasculopathies, can tell us that we are on the right track for excluding those type of diseases. Basically, these are the two that are available in every scanner without even going into fancy, more advanced techniques. Dr Monteith: I was going to ask you that question, how often should we think about this next-generation sequencing when you're kind of on the fence, allowing for some negative results to come back in the abundance of caution?  Dr La Piana: The problem with the panel, of course, is that you run a panel and you don't know what's coming back. So, then having to deal with variants of unknown significance in genes, then you have to deal with them, and then you have to deal with results that maybe are not as black or white as you would expect initially. So, I'll answer to your question when to do that, our recommendation would be to do that every time you are presented with a patient that presents those atypical features that we summarized in the paper, and that basically raise multiple red flags for an atypical white matter disease that is not multiple sclerosis. And then what to do when you have results? I still believe that having access, of course, to genetic counselors, to neurogeneticists, is critical, but also having access and being in contact with the network of people working on this. Because we are a network; we put the website address on the paper of the white matter rounds because this is an international network that we built over the years, and we connect monthly, on a monthly basis, with meetings to discuss exactly this type of patient. So, we are all learning together, and it's very frequent that people ask us to present cases at the white matter rounds because they have a presented with unusual or atypical genetic findings and they want the opinion of experts.  Dr Monteith: Great. Well, I'm really glad that resource is available. And I'm also really glad that you wrote that article with your colleague. Thank you so much. Dr La Piana: Thank you so much, Tesha.   Dr Monteith: Today I have been interviewing Dr Roberta La Piana about her article on adult-onset leukodystrophies mimicking multiple sclerosis, which she wrote with Dr Gabrielle Macaron. This article appears in the April 2026 Continuum issue on multiple sclerosis. 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.

"Cancer and environmental disasters in particular, but the worsening of our environment, are really things that are great equalizers. And we recognize that we're all kind of in this world together. We can really face these issues on a more human level. I think always recognizing that if we look at something, we think, 'Well, that doesn't relate to me or that problem is it really isn't my problem'—it sure is," ONS member Margaret "Peggy" Rosenzweig, PhD, CRNP-C, AOCNP®, FAAN, ONS scholar-in-residence and distinguished service professor of nursing and Nancy Glunt Hoffman Chair in Oncology Nursing at the University of Pittsburgh School of Nursing in Pennsylvania told Jaime Weimer, MSN, RN, AGCNS-BS, AOCNS®, manager of oncology nursing practice at ONS, during a conversation about the effects of the environment on cancer care and outcomes. Music Credit: "Fireflies and Stardust" by Kevin MacLeod Licensed under Creative Commons by Attribution 3.0  Earn 0.75 contact hours of nursing continuing professional development (NCPD) by listening to the full recording and completing an evaluation at courses.ons.org by April 10, 2027. The planners and faculty for this episode have no relevant financial relationships with ineligible companies to disclose. ONS is accredited as a provider of nursing continuing professional development by the American Nurses Credentialing Center's Commission on Accreditation. Learning outcome: Nurses caring for people with cancer require knowledge to recognize and address how environmental factors influence cancer care delivery, patient outcomes, and workforce resilience. Episode Notes  Complete this evaluation for free NCPD. ONS Podcast™ episodes: Episode 190: The Environment, Cancer, and Nurses' Role in Advocating for Climate Change Episode 107: Social Determinants Lead to Unequal Access to Health Care ONS Voice articles: Most Oncology Nurses Want to Address Climate Change but Don't Know How to Start Here's How the Environment Affects Cancer Care—and What Oncology Nurses Can Do About It Climate Change Is Contributing to the Cancer Burden, and Nurses Must Take Action Clinical Journal of Oncology Nursing articles: Oncology Nurses' Awareness, Concern, Motivations, and Behaviors Related to Climate Change and Health Environmental Risk Factors: The Role of Oncology Nurses in Assessing and Reducing the Risk for Exposure Oncology Nursing Forum articles: Research Priorities of the Oncology Nursing Society: 2024–2027 The Impact of Climate Change Across the Cancer Control Continuum: Key Considerations for Oncology Nurses (ONS white paper) ONS Huddle Card: Environmental Health and Climate Change ONS Congress® session: The Impact of Climate Change on Patient Care Supportive Care in Cancer article: Climate Disasters and Oncology Care: A Systematic Review of Effects on Patients, Healthcare Professionals, and Health Systems What If We Get It Right? by Ayana Elizabeth Johnson The Cancer–Climate Connection: Environmental Drivers of Cancer in the Climate Era (webinar by AnnMarie L. Walton) 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 "The process of establishing these research priorities usually happens every three or so years. And there's a lot of preliminary work of talking to multiple parties of interest regarding what they believe the research priorities are, what nurses are seeing in clinics and in the community, and really multiple opinions regarding where the direction of research for ONS should go. And we heard this time—loud and clear—from researchers, from nurses in clinics and in communities, from scholars, and multiple other interested parties, that the environment in a very broad context was very much a concern and specifically a concern for impact on cancer care delivery, quality, and outcomes." TS 1:49 "You can take some cancer outcome data and you can take patient data related to home address or zip code or even larger geographic areas and kind of do correlational studies to see 'Does one impact the other?' … There's been a lot of those in the literature. But they are very helpful because they're starting to define this idea that beyond the idea of just demographics—gender, age, race—that the whole concept of neighborhood and the influences of the neighborhood do impact cancer outcomes. And that's where we're seeing the sort of explosion in literature across multiple malignancies, stages of cancer, and across multiple questions—specific kinds of outcomes, everything from quality of life to tumor progression." TS 8:43 "There is growing literature around how cancer delivery can be better prepared for climate-related disasters. … There's a good article by Pamela Ginex that was published in Supportive Care in Cancer talking about climate disasters and oncology care. And that was really a systematic review looking at published literature and starting to classify where are the disruptions and how could we think about that from a research perspective. They ended up saying there are these patient-level outcome disruptions that of course include treatment disruption but also include this inability to communicate with the oncology care team, which is quite distressing. And there's a workforce disruption because there are very distressed clinicians who are experiencing the same climate-related disaster in their own lives and feeling like they are torn between their commitment to work and their commitment to family." TS 13:25 "After all these years in oncology nursing, I am convinced that we have to get the consideration of neighborhood. I think we do have to get back to the neighborhood level in order to boost the resilience of communities against cancer throughout the cancer trajectory." TS 31:53 "Let's take some of this to the community and boost the community in that way. I really feel like we have to think about just boots on the ground outside of the cancer center, instead of just documenting disparities or even doing interventional work, but still within our little ivory towers." TS 34:21 "You see the work of many in looking at the specific environmental risks to nurses through the toxic chemicals to which were exposed. But then thinking about the people who aren't as protected as nurses and the environmental workers, who are usually contracted out or not in unions, who don't have some of the same protections that nurses or other healthcare workers might have, and they are exposed to the chemicals without proper training or sometimes without protection. All of these things are very much worthy of an oncology nursing voice elevating these questions and saying, 'How can we study this? How can we best mitigate some of these risks?' Oncology nursing—we have to use our respect and good name in elevating all of these questions." TS 35:39

Novel MRI biomarkers, including cortical lesions, the central vein sign, and paramagnetic rim lesions, are highly specific for MS and can aid diagnosis in select clinical scenarios, particularly early in the disease course or in atypical presentations. When used with appropriate MRI sequences, these markers can improve diagnostic sensitivity while helping prevent misdiagnosis. In this episode, Casey Albin, MD, speaks with Jiwon Oh, MD, PhD, FRCPC, FAAN, author of the article "Diagnostic Neuroimaging Biomarkers for Multiple Sclerosis" in the Continuum® April 2026 Multiple Sclerosis and Related 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. Oh is the medical director of the Barlo Multiple Sclerosis Program at St. Michael's Hospital and an associate professor at the University of Toronto in Toronto, Ontario, Canada. Additional Resources Read the article: Diagnostic Neuroimaging Biomarkers for Multiple Sclerosis 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 Albin: Spend any time in a neurology conference, and you are certain to hear about the new central vein sign, which, as I learn, is not actually all that new. But have you heard about cortical lesions or these paramagnetic rim lesions? Because today I have the privilege of talking to Dr Jiwon Oh about her article, and we're going to unpack all these new biomarkers in MS. 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 Jiwon Oh about her article on diagnostic neuroimaging biomarkers for Multiple Sclerosis, which appears in the April 2026 Continuum issue on multiple sclerosis. Welcome to the podcast. Thank you so much for being here. I'd love to start by having you introduce yourself to our listeners.  Dr Oh: Thanks, Casey. Hi, everybody. My name is Jiwon Oh and I'm a neurologist, mainly an MS specialist at Saint Michael's Hospital at the University of Toronto, and I'm the medical director of our MS program. Dr Albin: And you have written a really fantastic article that dives deep into some of the nitty gritty about these new diagnostic biomarkers that we find on the MRI that we're getting for our patients with multiple sclerosis. And I think we are going to get into a lot of that nitty gritty. How do we look for them? How do they improve our diagnostic specificity? This is really come a long way in shaping the advances for multiple sclerosis. And I'd kind of like to just start with the big picture. Like why do we need these more specific biomarkers?  Dr Oh: This set of diagnostic criteria in MS, it's actually a huge change in the field, and particularly for people like me who are really interested in developing new MRI measures, we're really, really excited because it's actually the first time since MRI was officially incorporated into the MS Diagnostic criteria, which was way back in 2001. It's the first time that we've actually been able to get newer, more advanced imaging measures beyond just simply detecting, new T2 lesions in the MS diagnostic criteria. So, it's a big moment in the field, and many of us are really excited about it in terms of why we need some of these newer, more specific imaging measures. Well, you know, diagnostic criteria always evolve over time for any disease state, and MS is one that we've recognized over the years. By the time someone actually presents with typical clinical symptoms and has diagnosed, whatever has been happening from a patho-biological standpoint has been happening probably for almost 5 to 10 years before that individual actually presents. And so, because of this recognition in the field and the fact that we're recognizing how important it is to first diagnose MS and then treat MS earlier and earlier, because we know that early treatment helps prevent more clinical outcomes. Diagnostic criteria over time have become much more permissive, meaning that we're doing everything that we can to try to facilitate a diagnosis of MS when we know that someone biologically has MS. But the problem with making diagnostic criteria more permissive, and it's obviously a good thing because you want to capture as many people with MS as early on as possible. The problem with making it permissive is there is this terrible risk of misdiagnosis. As clinicians, we all think we never make mistakes. But it turns out when you actually do studies, you do. And even at MS specialty centers, when studies have been done, 10% to 20% of people with MS are misdiagnosed. So, this is exactly why we need in diagnostic criteria that really help to facilitate a diagnosis. We need things that help us prevent misdiagnosis as well. And these are these specific imaging measures that have now been incorporated into the diagnostic criteria in many settings that will help to facilitate a diagnosis. But the really big perk is if you use them, you can help to prevent misdiagnosis as well.  Dr Albin: Yeah, that really shone through in your article that this was such a big step in towards being more specific about who were diagnosing. Also capturing more people, right? Trying to get those people that we, we don't want to miss because of all the things you say, you know, that allows them to accumulate more disability, have worse outcomes. Early diagnosis is so important. But I really did take away from your article just how critical these are and sharping our diagnostic acumen. And so just to jump right in, and you describe these three new biomarkers, these cortical lesions the central vein sign and paramagnetic rim lesions. And so just to kick things off let's start with cortical lesions I sort of conceptualize multiple sclerosis a disease of white matter. So, what's going on here?  Dr Oh: Yes. MS classically has always been described as a white matter disease. But it turns out when you look at brain and spinal cord tissue, as well as when you use kind of better sequences to actually look for lesions in the gray matter, it actually turns out there's a ton of lesions in the gray matter as well. And in fact, what's interesting is that regardless of whether it's the cortex or the deep gray matter, it's lesions within these areas that seem to have the highest relevance for clinical disability in MS. So, all this to say, of course, MS is a lesion that does affect white matter, but it also affects gray matter a lot. And maybe pathology within the gray matter is even more relevant to clinical disability. So, this is why we're really interested in being able to develop methods using MRI to more accurately visualize the gray matter, particularly the cortex, as well as deep gray matter structures like the thalamus. I should add the caveat that cortical lesions were actually included in the 2017 diagnostic criteria revisions, but they were included together with juxtacortical lesions, which are a typical area that MS lesions form. And so, this imaging measure, despite the fact that it is relatively novel and we consider it advanced, it hasn't been used that much only because it's not that easy to detect lesions within the cortex. And reasons for this include that you usually need higher field magnet platforms. And so, the typical clinical MRI scanners that are available kind of widely, regardless of whether you're at an academic center or a community center, are 1.5 Tesla magnets. And cortical lesions are actually really difficult to detect on those typical scanners. But when you get to like, say, three Tesla or seven Tesla, they're a lot easier to detect. But obviously that's a big hindrance to widespread use. And then you actually need very specialized sequences to adequately visualize cortical lesions. And these are not sequences that are usually collected for clinical purposes. So, it kind of requires convincing your radiologists that you need this additional sequence. And then it actually takes a lot of time and training to be able to adequately, accurately detect cortical lesions. So, despite the fact that it's actually very useful when you do have the appropriate MRI sequences and scanners to detect cortical lesions, even though they were incorporated into the 2017 criteria outside of specialty centers, they're not actually widely used. But when you do have the appropriate sequences, cortical lesions are actually pretty specific for MS. So, very helpful for a diagnosis in certain settings. But there's all these practical limitations that have really limited its widespread use. Dr Albin: That is a beautiful summary. So, it sounds like once we kind of get up to speed in terms of like the protocols for this, having the magnet strength for this, this will be really a game changer in terms of increasing the specificity and also maybe finding things that impact patient's clinical presentation and therefore quite meaningful. But it sounds like for most of us, this is probably not something that they're going to be adopting right away. Is that a fair assessment?  Dr Oh: Yes. And you know, they were included in the last diagnostic criteria revisions. And it really hasn't changed things very much, only because of these difficulties with, you know, requiring higher field magnet strengths and these specialized sequences and then needing training to kind of figure out how you can adequately detect cortical lesions. Dr Albin: Totally. So, the other thing we've heard a lot about, and I have to say, I was in the AAN fall conference not too long ago, and this came up quite a bit, was the central vein sign and the fascination with that, because it tells us a lot about the MS pathophysiology and again, increasing that specificity. And it seems like maybe this is one that we can more easily adopt in clinical practice. So, tell our listeners about what that is, how they detect it. How many do you need to find?  Dr Oh: Sure. And so, this is one of the imaging measures I'm really excited about. So, the central vein sign heard about it recently. And probably in the last ten years particularly in the MS field we're talking about it all the time. But just wanted to emphasize that the central vein sign is not something that is new. Even back in the 1800s, when Charcot described MS lesions in these ancient textbooks, he actually very clearly described that MS lesions form around the central vein. And that makes sense, because we know that these waves of peripherally mediated inflammation somehow get through the blood-brain barrier and cause this cascade of events leading to inflammation in the brain and spinal cord, which is what MS is. But we know that B cells in T cells require veins to get into the central nervous system. And so, it's no surprise, really, that MS lesions form around veins. And so, this is something that's been known pathologically. But the reason we're so excited about it now is because we actually have good enough iron-sensitive MRI sequences that allow us to see a central vein when it is present within a white matter lesion. As a neurologist, we know that there's probably hundreds and hundreds of different things that can cause white matter lesions in the brain. But when you use an appropriate iron-sensitive sequence and you see that many of them, if not most of them, actually have visible central veins, that tells you that this person very likely has MS. And so that's why we're so excited about it, because there have been many studies done in the last ten years. In fact, so much evidence generated in the last ten years that there have been I think it's now four systematic reviews and meta analyzes. Looking at the diagnostic properties of the central vein sign. And, you know, it turns out that when you look at people with MS, most of them have a pretty high proportion of white matter lesions that have visible central veins. And there's a lot of questions about, you know, how to best use the central vein sign. But when 40% or more of the white matter lesions that you see have visible central veins, then the likelihood of a diagnosis of MS is very high. So, this is why we're so excited about it in the MS field because it's a really useful diagnostic tool. You know, again when you have appropriate ion sensitive sequences, if you see someone with white matter lesions and you see that 40% or more of them have visible central veins, this tells you that this person very likely has MS.  Dr Albin: So, Dr Oh, I hear you say, you know, 40% of the lesions. Does that mean the neuro radiologist needs to look at every single lesion and then count how many have the central veins, or is there an easier way to do this? Dr Oh: Great question. Casey, there is definitely an easier way because our neuro radiologists would not be our friends anymore if we made them look at every white matter lesion and make sure that 40% of them had the central vein sign. So, because it's so time-consuming to use that 40% threshold, there's an easier criterion that has actually made it into the diagnostic criteria. And it's called Select Six. And what this means is when you have more than ten lesions, as long as you show that six of them have a visible central vein, you just have to count six with the central vein. Then you're done. So that means you're Select Six positive or central veins nine positive. However, if you have ten or fewer lesions, as long as you show that more than 50% of them show a visible central vein, then you are select six positive, and then you're done. So, as you can see, it's a much simpler criterion to apply, and it seems to perform almost as well as that 40% threshold, which is why that is the criterion that's made it into the new diagnostic criteria.  Dr Albin: Perfect. I love that we definitely do not want to make enemies with our neuro radiology colleagues, but yet they do so much for us. So perfect. I'm glad that we can, make their jobs a little easier without losing any specificity there, or just losing a touch of specificity there. All right. If I am working with a, you know, in a center that maybe doesn't do this all the time, am I just getting a run of the mill SWI sequence? Do I need to ask my radiologist for a special sequence? Or is this just, you know, you can get it from the typical array of what our patients are getting.  Dr Oh: You know, SWI is a widely available commercial sequence that's iron-sensitive, the ones that are typically commercially available, they can detect central veins, but there actually are little tweaks that you can do to make it a little more optimal. With the recent diagnostic criteria publication, which was, led by Xavier Montalban and recently published in Lancet Neurology. There's actually a companion MRI paper that was led by Frederick Barkov and Danny Wright. And the reason I'm specifically citing those papers is in that companion MRI paper, there's a table that has kind of optimal sequence parameters that you can use even with a conventional SWI sequence, to try to best detect the central vein sign. And then there's a wide range of different iron-sensitive sequences, and SWI is one of them, but the one that seems to have emerged as most sensitive to detect the central vein sign is something called the 3D T2*-EPI sequence. But the bottom line is there's a whole bunch of different iron-sensitive sequences that you can use, little tweaks that you can do to make them optimal, to be able to visualize central veins when they're present within white matter lesions. Dr Albin: Incredible. So like partner with your neuro radiologist, there is a great sounds like a field guide almost to this. So, it makes it easy to pick up in your standard of care so that you can make sure that you are detecting them at the optimal level to see that more specific diagnostic biomarker.  Dr Oh: Yes. And you know, in contrast to what we were talking about with cortical lesions, you can actually detect central veins when you use these iron-sensitive sequences at any field magnet. So even at 1.5 Tesla, particularly when you use contrast, which is often given with the diagnostic scan anyway, you can very easily detect a central vein. So that's a huge benefit because it allows for widespread use. As long as you work with your radiologist to get the right iron-sensitive sequences in.  Dr Albin: Yeah, that's incredible. I mean, I think that it really will be practice-changing. And then the last one that I think was honestly new to me, I feel like I had heard a lot about the central vein sign, but the whole new to me term was this paramagnetic rim lesion. So, what does that tell us about the underlying biology of MS? And are there any other things that might also have this finding that we should sort of be aware of? And how specific is it?  Dr Oh: You know, the central vein sign is kind of the main, really new imaging measure that's made it into every part of the MS diagnostic criteria. And then together with that paramagnetic rim lesions or we call them PRL or pearls for short, they've made it as well, but in a much more limited way only because there's not as much evidence that has accumulated over time to support the diagnostic utility of pearls. But first of all, what are pearls? So, people in the MS field are really excited about pearls, because we know that they capture a subset of what we call chronic active lesions. So, MS lesions will form acutely and over time, some of them will become inactive. And then some of them are chronic active lesions, meaning that they have this rim of activated microglia around them. Over time, they continue to slowly expand. And it's almost like this slow burn. And the reason why we focus a lot on chronic active lesions is because we know that they're a driver of progressive disease biology and MS, meaning that in people who have progressive MS or who have pretty severe disability, global disability or cognitive disability, we know that they have a high burden of pearls. And so that's why there's so much excitement in MS about being able to image chronic active lesions. It's because we're always looking for an imaging measure that allows us to accurately predict progression or to, measure progression over time. So that's why there's so much excitement in MS about pearls. But as kind of an added bonus, it turns out pearls are also really specific for MS. And so, when you use the same iron-sensitive sequences, by the way, that's used to detect the central vein sign when you use appropriate iron‑sensitive sequence. And if you see that someone has a pearl, the likelihood of a diagnosis of MS is very high. The one exception to that is Susac syndrome, where pearls have been observed. But other than that, with many other white matter diseases like neuro rheumatology disease, NMOSD, MOGAD, you really don't see pearls. And so, this is why it's made it into the new diagnostic criteria. In contrast to the central vein sign, though, not everybody with MS has a pearl, so the sensitivity isn't as high. However, it's really, really specific in the range of, you know, 90 to 95%. So, this is why it's been added as, an imaging measure in certain settings. It can help facilitate a diagnosis. But the real utility, again, is when you use it, it helps you to prevent misdiagnosis.  Dr Albin: It's fantastic. And hearing you talk about that, this one stands out to me as a biomarker that not only helps increase our diagnostic specificity, but also may really inform if the patient has having progression despite the treatment they're on, that this could play a role in helping you say, look, there probably is something that we need to switch because we can still see this ongoing progression. Dr Oh: Yes. And especially in this new era of treatment in MS. I think, you know, MS as a field, we've been so fortunate to have so many treatments emerge over the years that mainly target relapsing disease. But we hopefully, in the next little while, in short order, I hope we'll have treatments that target these progressive disease biologies. And so, not only is it helpful as a diagnostic marker, but there's a lot of evidence accumulating, showing that it may have a lot of prognostic value and will also help guide treatment decisions, exactly as you said.  Dr Albin: It truly does sound like it's a great time to be an MS doctor there. So, so many new advances in the field. There is so much more that we can do for these patients in our limited time left. I'd love to ask you, what is it that you're most excited about now with the change in the biomarkers, the change in the treatment, what makes you really excited to be a doctor specializing in MS right now? Dr Oh: I feel like we're on the brink of a new era of treatment. I think, you know, in the last two decades, MS care has changed so dramatically. I remember, you know, way back when, as a medical student, when I did my first neurology elective, this was when the first treatments for MS were emerging. And the prognosis that we were talking to patients about at that time is like night and day compared to what we talk to them about now. But we're going to do even better in the next couple of years. And so, there's a number of new treatments that hopefully will be approved soon that, for the first time, have shown an effect in clinical trials where it seems to be decreasing progression that is independent of relapsing activity. And that's really the greatest unmet treatment need that we have. And it seems like we might have some therapies on the horizon that can actually target that aspect of progression. It's really exciting, and even more that we're going to be able to do for our patients to completely change the way, we look at and the way we treat MS in the years to come.  Dr Albin: Dr Oh, this has just been fantastic. To all of our listeners, I really want to point you to the article because obviously, as an imaging biomarker article, there are so many beautiful images. There are great examples. There are some fantastic cases that show how applying these new biomarkers can help get you to the right diagnosis. This is truly a tour de force of how imaging has really shifted the care that we provide patients with MS, and so please go and check it out. It is one that you do not want to miss. And again, today I've been interviewing Dr Jiwon Oh about her article on diagnostic neuroimaging biomarkers for multiple sclerosis, which appears in the April 2026 Continuum issue on multiple sclerosis. Thank you again, Dr Oh, this has just been such a delight.  Dr Oh: Thank you for having me on the show, Casey, and look forward to people reading the article. 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.

Advanced practice providers are a growing part of the healthcare workforce, but many organizations aren't necessarily seeing the productivity gains they expected. On today's episode, we examine new Kaufman Hall insights on why traditional physician-APP models often underperform, and how redesigning team roles, incentives, and compensation could yield better outcomes for clinicians and patients alike. Bonnie Proulx, DNP, APRN, PNP-BC, FAAN, Senior Vice President with Kaufman Hall and a member of the firm's Physician Enterprise practice, joins the podcast to explain more. You can read Bonnie's blog post here. This interview first aired on Monday, January 26, 2026. Hosted on Acast. See acast.com/privacy for more information.

Send us Fan MailWhat if the “behavior problems” we see in people living with dementia are actually signs of pain?Host Dana Rampolla speaks with Barbara Resnick, PhD, RN, CRNP, FAAN, FAANP, Distinguished University Professor and associate dean of research at the University of Maryland School of Nursing who is an expert in aging and long-term care, about how pain often goes unrecognized in people with dementia. Because they may struggle to communicate discomfort, pain can show up as agitation, withdrawal, resistance to care, or sudden changes in appetite and engagement. These behaviors are sometimes misunderstood and treated with sedating medications instead of addressing the root cause.Resnick explains what caregivers and clinicians should watch for, from facial expressions and lashing out to subtle shifts in participation and mood. Health care professionals can learn more about pain management in long-term care settings in this Clinical Practice Guide co-authored by Resnick: https://www.jamda.com/article/S1525-8610(21)00911-7/fulltextChapters00:00 Pain Without Words00:28 Meet Dr. Resnick02:36 Why Pain Gets Missed06:15 The Vicious Cycle07:28 Signs to Watch For08:55 Find the Root Cause10:40 Guidelines in Nursing Homes11:37 Non-Drug Pain Relief15:36 Questions for Care Teams17:30 Key Takeaways19:06 Why She Does This Work20:55 NIH Study in Practice22:56 Closing CreditsListen to The UMB Pulse on Apple, Spotify, Amazon Music, and wherever you like to listen. The UMB Pulse is also now on YouTube.Visit our website at umaryland.edu/pulse or email us at umbpulse@umaryland.edu.

In this episode, editor in chief Joseph E. Safdieh, MD, FAAN, highlights articles about acetaminophen use during pregnancy, the link between air pollution and motor neuron disease risk, and the use of fremanezumab for pediatric migraine.

In this episode of The Nurse Practitioner Podcast, Julia Rogers, DNP, APRN, CNS, FNP-BC, FAANP, FAAN; Tracie Kirkland, PhD, DNP, ANP-BC, PPCNP-BC, PNP-BC, FAANP, FAAN; and Cheryl Thaxton, DNP, APRN, CPNP, FNP-BC, CHPPN, ACUE, FPCN, FAANP, FAAN discuss DNP-PhD preparation.

In this episode, Lyell K. Jones Jr, MD, FAAN, speaks with Andrew J. Solomon, MD, FAAN, who served as the guest editor of the April 2026 Multiple Sclerosis and Related Disorders issue. They provide a preview of the issue, which publishes on April 2, 2026. Dr. Jones is the editor-in-chief of Continuum: Lifelong Learning in Neurology® and is a professor of neurology at Mayo Clinic in Rochester, Minnesota. Dr. Solomon is the Division Chief of Multiple Sclerosis and a Professor in the Larner College of Medicine at the University of Vermont in Burlington, Vermont. Additional Resources Read the issue: continuum.aan.com Subscribe to Continuum®: shop.lww.com/Continuum Continuum® Aloud (verbatim audio-book style recordings of articles available only to Continuum® subscribers): continpub.com/Aloud More about the American Academy of Neurology: aan.com Social Media facebook.com/continuumcme @ContinuumAAN Host: @LyellJ Full episode transcript available here Dr Jones: It's been more than 150 years since Jean-Martin Charcot first described the disease that we now know as multiple sclerosis. Since then, the tools we have to diagnose and treat this disorder have expanded enormously. So why are the diagnostic criteria for MS. still evolving? Today we're speaking with Dr Andrew Solomon, guest editor of our latest issue of Continuum on MS and related disorders. To learn more about this question and much more. Dr Jones: This is Dr Lyell Jones, editor in chief of Continuum. Thank you for listening to Continuum Audio. Be sure to visit the links in the episode notes for information about subscribing to the journal, listening to verbatim recordings of the articles, and exclusive access to interviews not featured on the podcast. Dr Jones: This is Dr Lyell Jones, editor in chief of Continuum, Lifelong Learning in Neurology. Today I'm interviewing Dr Andrew Solomon, who is Continuums guest editor for our latest issue of Continuum on multiple sclerosis and related disorders. Dr Solomon is a professor of neurological sciences at the University of Vermont, where he also serves as the division chief of multiple sclerosis. Dr Solomon is an internationally recognized authority on MS, particularly on the diagnostic approach to this complex disorder. Dr Solomon, welcome. Thank you for joining us today. Why don't you introduce yourself to our listeners?  Dr Solomon: Hi, everyone. This is Andy Solomon. It's a pleasure to be here with you. And I feel honored to have helped this collaborative effort that created this important tool for trainees and clinicians in practice, the Continuum issue on multiple sclerosis and related disorders.  Dr Jones: Obviously, we're grateful that you've taken us on. A lot has happened in the world of MS and other neuroinflammatory disorders in the last few years, so lots to update. But as we've done over the last few podcasts, I'm going to start off the interview today, Dr Solomon, with a trivia question. And then we'll come back at the end of the podcast and give the answer. So, the trivia question is this. There are now more than 20 drugs approved by the FDA for the treatment of MS. What was the first disease-modifying therapy approved for MS? And when was it approved? So, don't answer because I know you know the answer. But we'll come back to it at the end of the interview. And our listeners can think about that question. So, let's get right to it. As many of our listeners know, the diagnostic criteria for MS. were recently revised. And you were involved with that revision. So, you're the perfect person to ask what were the major changes in the 2024 McDonald criteria, and why did we need to update them in the first place? Dr Solomon: I'm very excited about the 2024 McDonald criteria, and it was an honor to be part of that process that resulted in that manuscript. When we revise the diagnostic criteria for MS usually it's driven by accumulating data that suggests some changes or revisions might help us diagnose patients either earlier or with more accuracy. And that's certainly the case with this criteria. There was accumulating data that suggested some particular changes were important. You know, there's a lot of expert opinion involved as well. You know, there's many experts who are involved in the collaborative decisions that go into these revisions. And some of the changes in our field also pushed some of the revisions to where maybe there's not as much evidence, but where we felt it would improve care for patients with MS. This criteria, I would argue, is probably one of the most substantial revisions in over 20 years. There's multiple changes that are potentially impactful for the diagnosis of MS. Some very important changes involve the incorporation of new paraclinical tools that we can use to assess the visual pathway, as well as, imaging tools that provide high specificity for MS that we can use to substitute or dissemination in time, for instance, as well as other tools that may allow us to diagnose patients earlier than we would have in prior criteria.  There's also some opportunities with the new criteria to potentially provide access in regions where some tools are more available than others. For instance, the incorporation of Kappa Free Light Chains as a substitute for oligoclonal bands may open up opportunities in regions where expertise for oligoclonal band testing are not available. That's a very qualitative test, whereas Kappa Free Light Chain index is more quantitative, less expensive and may allow CSF testing to be performed to aid the diagnosis of MS in some regions where it wasn't available previously. This criteria provides multiple pathways to the diagnosis of MS, many more than we've had in prior criteria. So, it's important to emphasize that while there's all these new tools and changes that have been incorporated, not every pathway needs to be available where you practice. What it incorporates as flexibility. It is a bit more complex looking at all of these different possibilities, but the point is this flexibility allows clinicians or providers to diagnose MS early with high accuracy based on the tools they have available. Dr Jones: I think it will be a learning curve, right? I think any time we make a change in how clinicians get accustomed to approaching a diagnosis of a disorder, it will take some time for folks to incorporate it. And I see what you mean about the complexity, but I think that's a really great point, that emphasizing the different pathways to the diagnosis is really a strength of the revision, right? Dr Solomon: I agree, I think, you know, in other disorders, particularly if you think about rheumatologic disorders, systemic rheumatologic disorders or inflammatory disorders, where over time we've not had very highly specific and sensitive biomarkers. And we've incorporated a variety of clinical and prior clinical findings, testing, laboratory testing and biopsy and other things to confirm a diagnosis. These approaches to these disorders are sort of a checklist. And I think that clinicians became familiar with that approach and were able to make diagnoses accurately this way. And I think of the new criteria in a similar way. It's not quite amenable to a checklist, but the pathways are sort of simplified with multiple options. Hopefully, using the figures, clinicians can look at the paper and see what tools they have available to help them confirm a diagnosis of MS. I think it's really important to emphasize that the diagnostic criteria for MS still does not discriminate MS from other disorders. Everyone who's listening here, you do, the clinicians do. So, to enter the diagnostic criteria and these pathways, we first have to feel confident that the patient has a clinical presentation and an MRI presentation or MRI findings that are highly suggestive of MS. That aspect of the criteria hasn't changed since, the Schumacher criteria in the 1960s. This concept of no better explanation. So, we still need to know what's typical for MS. And we need to know what signs or symptoms or findings are that might suggest another disorder, because the criteria are really only validated and tested in patients who have these presentations to start with that are typical for MS. A major change in this particular criteria is that we can now diagnose patients who are asymptomatic. Previously just called radiological isolated syndrome. Not every patient with an MRI finding concerning for MS and now being diagnosed with MS. There's other features that, must be present, but even more than before, knowing what the typical appearance of MRI lesions suggestive of MS, it is even more critical now than it was before, because in those patients who have either no symptoms or a nonspecific presentation, if we have an MRI that's highly convincing for MS and some other prior clinical findings, we can make the diagnosis. But we first need to know with some confidence what that MRI should look like.  Dr Jones: So, there is a little circularity when we do these diagnostic criteria. I think our listeners who see patients will be reassured that the clinician is still in the loop. We haven't been automated out of the process yet.  Dr Solomon: We need a highly sensitive and specific biomarker or a set of biomarkers for MS.  We're getting closer with some of these advanced imaging findings like central vein sign and paramagnetic rim lesions. But not every patient can be diagnosed with those. And they're not required for the diagnostic criteria. In lieu of a highly sensitive and specific test. Our clinical acumen, for what we find a neurologic exam. And what we see on imaging in particular, is quite critical for ensuring that the criteria perform as well as we hope they will. Dr Jones: So, you've had the opportunity, the vantage point, to review all of these articles covering a wide variety of topics, MS, other neuroinflammatory disorders like aquaporin‑4–positive neuromyelitis optica spectrum disorder (NMOSD), myelin oligodendrocyte glycoprotein antibody-associated disease, MOGAD. Anything that surprised you in these articles as you were reading through them?  Dr Solomon: I think maybe for listeners, what may be surprising to some of them is that despite guidelines surrounding the use of some of our disease modifying therapies in pregnancy and breastfeeding that are published by regulatory authorities in the United States or Europe or other places, we are making other decisions for patients based on the data we have, the best data we have. Thinking about family planning is really important for us with patients who are newly diagnosed with MS, as well as through the course of their disease. This is a conversation we should be having shortly after diagnosis, because there are strategies we can take to minimize the risk of exposure of DMT around conception and to make plans for how we're going to think about DMT surrounding breastfeeding, to ensure the health of mom and the baby, and reduce risks as much as we can with the knowledge we have. I think in medicine it's quite common for us to use medications off label, right? I mean, so medications are often FDA approved for one indication. And in neurology, for instance, we find a lot of medications after their approval were quite effective for migraine prophylaxis for instance. Right? And so, it's not unusual for us to prescribe medications beyond the label. And I'm not suggesting that we necessarily ignore the advice of our regulatory authorities. But sometimes the data is accumulating really fast around some of these therapies after they're approved. Sometimes we can look towards experts and how we can navigate pregnancy and breastfeeding in MS. Dr Jones: I think that's a great point about the importance of family planning and having to use judgment. I do want to highlight to our listeners and our subscribers a fantastic article in the issue on family planning and MS and other neuroinflammatory disorders. This was written by Dr Ruth Dobson and Dr Kersten Hellwig, and I think it covers a lot of that gray area where we have to use our clinical judgment to manage these diseases in the absence of a regulatory approval. And I think, again, that's an important gap that the issue fills. And really, that's just a wonderfully written article that I think is a must-read. So, we cover lots of topics in this issue. And one of them is again a relatively newly characterized disorder, MOGAD. What's the latest in the world of MOGAD, what should our listeners be aware of? Dr Solomon: I agree, I think we're in an exciting time in CNS inflammatory disease. And this is a recently described disorder. You know, and the diagnostic criteria now is only a few years old. So, I think importantly, readers should be aware of the diagnostic criteria. This is something that, really will help us distinguish this disorder from NO spectrum disorder and MS. There's a key overlap between the MS diagnostic criteria and MOGAD. Two decades ago we saw a pediatric MS included somewhat atypical presentations like bilateral optic neuritis or acute disseminated encephalomyelitis. And we had caveats in our approaches to pediatric presentations of presumed MS, suggesting that there could be something very different than adult MS. Subsequently, we've realized that pediatric MS presents quite similarly to adult MS in terms of its clinical syndromes and MRI appearance, and many of those pediatric patients who had initially been diagnosed with MS and MOGAD. MOGAD is actually probably more common demyelinating syndrome in patients who are under 12 years old. So, the MS diagnostic criteria requires testing for MOG-IgG with a good assay, a cell-based assay, any patient being evaluated under the age of 12 or with a demyelinating syndrome to avoid misdiagnosis.  Dr Jones: Thanks for that. Obviously, MOGAD is one of several disorders that have been more recently characterized and, something that our readers need to be familiar with, and there's plenty of updates within the issue on that and other topics. Okay. So now back to our Continuum audio trivia question. And just to remind our listeners, there are now more than 20 drugs approved by the FDA for the treatment of MS. What was the first disease-modifying therapy approved for MS? And when was it approved? Dr Solomon, do you want to take the honors and answer the question?  Dr Solomon: Sure. It was way back in 1993. You had to get on a wait list, I believe, initially to get on it. There was some sort of lottery, and it was Betaseron.  Dr Jones: Betaseron in 1993, was the first disease-modifying therapy approved by the FDA for the treatment of MS. It just shows how much water under the bridge we've had since then. 1993 was also the first year of the Jurassic Park series of movies. It was the biggest movie of the year, the song of the year in 1993 was "I Will Always Love You" by Whitney Houston. It was also the year you can tell that I look back into 1993 to see what else happened. It was also the first year the World Wide Web became publicly available, which is it kind of puts brackets on the era or the epoch of MS disease modifying therapy. And finally, the Super Bowl champs that year were the Dallas Cowboys, who unfortunately, have not had much luck in Super Bowls since the 1990s. Maybe they will have more opportunities like we've seen with MS therapeutics. So, Dr Solomon, I want to thank you for joining us today. I want to thank you for such a wonderful discussion of the latest in MS. I think the updated diagnostic criteria are really going to be critical for our listeners to understand and incorporate into their practice. Really grateful for your leadership of the issue, putting together a really stellar group of experts for all of our articles and grateful for your time today. Thank you for joining us.  Dr Solomon: Thanks so much for having me. Thank all the other listeners out there for joining us as well. I'm really excited about this issue of Continuum.  Dr Jones: Again, we've been speaking with Dr Andrew Solomon, guest editor of Continuums most recent issue on multiple sclerosis and related disorders. Please check it out. And thank you to our listeners for joining today. Dr Monteith: This is Dr Teshamae Monteith, associate editor of Continuum Audio. If you've enjoyed this episode, you'll love the Journal, which is full of in-depth and clinically relevant information important for neurology practitioners. Use the link in the episode notes to learn more and subscribe. Thank you for listening to Continuum Audio.

Omari Richins, MPH of Public Health Careers podcast talks with Dr. Lisa Carter-Bawa, PhD, MPH, APRN, ANP-C, FAAN, FSBM. In this conversation, Dr. Lisa Carter-Bawa shares her journey as a cancer prevention scientist and nurse practitioner, discussing her multiracial identity, the importance of community engagement in public health, and her philosophy of leadership. She emphasizes the need for a return to one's authentic self rather than reinvention, the impact of stigma in healthcare, and the significance of trust in patient-provider relationships. Dr. Carter-Bawa also highlights her work in cancer prevention research and the integration of behavioral science into public health leadership. In this conversation, Dr. Lisa Carter-Bawa shares her journey from nursing to becoming a leader in public health and behavioral science. She discusses the importance of understanding the barriers to health screenings, particularly lung cancer screening, and emphasizes the need for awareness and education in communities. Dr. Carter-Bawa highlights her commitment to continuous learning and the role of informatics in public health. She reflects on her experiences as a leader in spaces not traditionally designed for her and the importance of community engagement in research. The conversation concludes with insights on the cost of leadership and the importance of self-acceptance.

Welcome to Perimenopause WTF!, brought to you by ⁠Perry⁠—the #1 perimenopause app and education space. The Perry Academy was created for

Neurologic complications of substance use may be the first symptoms that lead patients with substance use disorders to seek care. Neurologists have a key role in identifying patients with substance use disorders and connecting them to treatment. In this episode, Lyell K. Jones Jr, MD, FAAN, speaks with Adeline L. Goss, MD, author of the article "Neurologic Complications of Drug and Alcohol Use" in the Continuum® February 2026 Neurology of Systemic Disease issue. Dr. Jones is the editor-in-chief of Continuum: Lifelong Learning in Neurology® and is a professor of neurology at Mayo Clinic in Rochester, Minnesota. Dr. Goss is a neurohospitalist and associate chief of neurology for Highland Hospital in Oakland, California. Additional Resources Read the article: Neurologic Complications of Drug and Alcohol Use Subscribe to Continuum®: shop.lww.com/Continuum Earn CME (available only to AAN members): continpub.com/AudioCME Continuum® Aloud (verbatim audio-book style recordings of articles available only to Continuum® subscribers): continpub.com/Aloud More about the American Academy of Neurology: aan.com Social Media facebook.com/continuumcme @ContinuumAAN Host: @LyellJ Full episode transcript available here Dr Jones: A big part of neurology is solving mysteries. Patients can show up with all kinds of mysterious symptoms. Sometimes the diagnosis comes from within, some internal disruption of neurophysiology. But sometimes the problem is a complication of drug or alcohol use. Today we have the pleasure of speaking with Dr Adeline Goss, who recently authored an article for Continuum on this exact problem, a topic all neurologists need to be familiar with. Dr Jones: This is Dr Lyell Jones, Editor-in-Chief of Continuum. Thank you for listening to Continuum Audio. Be sure to visit the links in the episode notes for information about earning CME, subscribing to the journal, and exclusive access to interviews not featured on the podcast. Dr Jones: This is Dr Lyell Jones, Editor-in-Chief of Continuum: Lifelong Learning in Neurology. Today I'm interviewing Dr Adeline Goss, who recently authored an article on the neurologic complications of drug and alcohol use for our latest issue of Continuum on the neurology of systemic disease. Dr Goss is a neurohospitalist and the associate chief of neurology at Highland Hospital in Oakland, California. She's also an accomplished writer, broadcaster and podcaster. Dr Goss, welcome, and thank you for joining us today. Why don't you introduce yourself to our listeners? Dr Goss: Great to speak with you, Dr Jones. Yes, I'm Adeline. I also go by Addie Goss. Dr Jones: So, before we get into the discussion, we're going to start off today with something fairly new to the podcast, the Continuum Audio trivia question. So, we all know that alcohol and other substances have many potential complications in that use of these substances fluctuates over time. But this one stood out to me from your article, Dr Goss, just for the sheer size of the change. So, for our listeners, here's the question. Accidental exposures to what substance increased a whopping 1,375% between 2017 and 2021? I'll read that again. Accidental exposures to what substance increased 1,375% between 2017 and 2021? So, stick around to the end of our interview for the answer. And let's get right to it, Dr Goss. If you had a single most important message to our listeners from your article, what would it be? Dr Goss: Well, I mean, many of us went into neurology because of the way that neurologic illnesses can be life-changing for patients. And I work as a neurohospitalist at a public hospital in Oakland, California. Many of my patients are admitted for neurologic conditions related to substance use. And when I see my patients later in the discharge clinic, many tell me that the last day that they used meth or the last day they used cocaine, the last day they smoked, was the day they had their stroke or whatever they came into the hospital for. I think the most important message is that hospitalization for a neurologic condition related to substance use can interrupt use patterns, can motivate change. And therefore, as neurologists, we really have an opportunity to connect to our patients and connect our patients to substance use treatment and make a dramatic difference in people's lives in this regard. Dr Jones: I think that's a fantastic point. I enjoyed a point you made in your article---and I can't remember exactly how you phrased it, I won't say it as well---that you think of the syndromes through which alcohol and drug exposures can present. Those syndromes almost always could end up of other primary neurologic disorders. So, put a different way, when a patient presents with a neurologic problem, most of the time an exposure could be on the differential.  And so, we really do have a responsibility as neurologists to be familiar with these. Dr Goss: To be familiar with these and to know how to connect patients to resources to try to get treatment. Dr Jones: Totally agree. And you touched on the public health aspect of this. It's really hard to talk about drug or alcohol use without acknowledging the public health impact particularly of opioids, which has been a crisis for most of this century. Right? And I think most of our listeners will be familiar with the rapid rise in opioid-related deaths. But there might be a glimmer of optimism there. Is what I've seen true, that opioid-related deaths may have plateaued? Dr Goss: So, yes, it's true that opioid-related deaths, overdose deaths in general, have begun to decline, actually, since 2023. And that's in part because overdose deaths really surged early on in the Covid-19 pandemic, in the setting of all of the social disruption, reduced access to services, and social isolation that occurred with the pandemic. But there were really multiple factors there. So, as you mentioned, there was this really rapid rise in illicitly manufactured fentanyl. Fentanyl became a major driver in overdose deaths starting in the mid-2010s. And by the late 2010s, it overtook heroin and prescription opioids as drivers of overdose deaths. And then this just collided with the pandemic in 2020, causing skyrocketing deaths. So, as we know as neurologists, fentanyl is more potent, it's shorter-acting, and it's also cheaper than heroin. It can cost as little as 50 cents or a dollar a pill. Thankfully, as services have rebooted and also as naloxone has become more widely distributed, there has begun to be a decline in opioid overdose-related deaths. So, we're relying on provisional data from the CDC for the most recent years, but that shows about a 24% decline in annual overdose deaths, comparing late 2023 to late 2024. And that's real. That comes out to 70 lives saved per day. Unfortunately, deaths still remain above prepandemic levels, and we're still talking about 87,000 drug overdoses per year. So, I would agree, a glimmer of hope. But we're still seeing overdose as the leading cause of death among young Americans aged 18 to 44. And there's a very long way to go. Dr Jones: 23% is a big number, and that is certainly exciting to think about, but we're still above that long-term secular trend. So, hopefully whatever is happening to bring that down, hopefully it continues. And we talk a lot about- appropriately, we talk a lot about opioid exposures and some of the neurologic presentations of opioid use and toxicity, but alcohol use disorder is the most common substance use disorder, correct? I learned that from your article. And it has been for some time, and it has well-known acute and chronic toxicities. But I think many of us have been taught something of a myth in the acute treatment of patients who may have thiamin deficiency or Wernicke's encephalopathy. Can you tell us a little more about that? Dr Goss: Yeah, sure. So, boy, what is my favorite vitamin? As a neurologist, I think thiamin is my favorite vitamin. Thiamin is a cofactor in- for several enzymes that are involved in glucose catabolism. And it's necessary to synthesize myelin and several neurotransmitters. And as we know, alcohol use disorder leads to reduced nutritional intake and impaired digestion and absorption of nutrients. And this can lead to deficiencies in water-soluble B vitamins, including thiamin, as well as trace elements. The thing about thiamin is that thiamin deficiency often appears first, because the body's stores of thiamin deplete in about 4 to 6 weeks. You know, we're traditionally taught if a patient presents with symptoms concerning for Wernicke's encephalopathy, that if they're also hypoglycemic or just in general, we have to get glucose into them first, because we don't want to tax these thiamin-dependent glucose catabolism pathways. But really, there's no reported case of a single glucose bolus precipitating some dramatic symptomatic thiamin deficiency. It's thought that harm would come potentially from prolonged carbohydrate administration without thiamin. And so, if a patient in front of you is both thiamin deficient and hypoglycemic, you just treat both. You treat both emergently. But it doesn't really matter in what order you do so. Dr Jones: That's good to know that doing the right thing for the patient can involve using either of those in whatever order. And I agree with you, I don't think I've ever hurt anybody by giving them thiamin. It's an easy one to miss and an important one to remember in the right context. And speaking of, and I think a lot about in your article, Dr Goss, I can see a neurologist seeing a patient in the emergency department or in the hospital or even in the clinic thinking about the wonderful points in your article. But we know that when alcohol or substance use enters our mind on the differential, the next impulse is to test for it. And we also know there are pitfalls of drug screening, doing urine drug screens, etc. How do you approach testing when you think about a potential drug-related complication in their differential? Dr Goss: So, like most people, I would start with a urine drug screen for any patient who's presenting with a possible toxidrome or some substance-related neurological presentation. These urine drug screens, they're rapid, they're inexpensive, they're immunoassays for traditional drugs and their metabolites. So, usually amphetamines, cocaine, opiates, plus/minus cannabis. But I think the first thing to note is that they miss entire categories of drugs, and not just drugs that are not in that list. They miss synthetic opioids, including fentanyl. One group is keeping track of this number. So, I have an update for mid-2025. And that's that 30% of U.S. ED overdose encounters as of mid-2025 included fentanyl testing. Only 30% for patients who are presenting with an overdose syndrome. Dr Jones: And that's for one of the most widely used synthetic opioids. So that's really a striking number. Dr Goss: Yeah, one of the most widely used and one with the greatest rate of complications. So, states can make a difference here. In 2022, California passed a law requiring fentanyl testing on hospital urine drug screens and several states have followed. And so that number is rising, the rate of testing for fentanyl. But that's just a really key thing to know, that that one is often missed. Other just important pitfalls, the timing of the urine drug screen matters because for most substances, it only picks up the drug within 24 to 72 hours after the last use. With amphetamines and cocaine going out a couple more days after that, especially in patients who use repeatedly. And then also, notably, there's a risk of false positives. This is especially true with amphetamine use, and beta blockers are one of the drugs that can lead to false positives on an amphetamine test, on a urine drug screen. So, I'll share that I've had several patients who have presented with intracerebral hemorrhage and who tested positive on the emergency department's urine drug screen and who adamantly stated that they do not use amphetamines, they've never used amphetamines, and they didn't ingest anything that could have contained amphetamines. And when we did serum confirmatory testing, in fact, their amphetamine testing was negative, and all those patients had received esmelol or the labetalol in the ED to treat their blood pressure related to their ICH. So false positives can occur with, you know, other medications like decongestants and certain antidepressants. But beta blockers are a key one to know. And then finally, there are just a number of things outside of that short list of substances that I mentioned, including a huge range of novel psychoactive substances that would not be tested for on a standard urine drug screen. And for those, you'd require serum testing, or at some large academic centers or specialty toxicology labs, you can actually do liquid chromatography high-resolution mass spectrometry, with- which is basically unbiased testing for any substance that's present in the patient sample. So, I guess, you know, you asked about my approach. Start with the urine drug screen, but there's no substitute for good history-taking and close examination of your patient's general examination, not just their neurologic presentation. And if patients are presenting with a toxidrome that I would expect would show up on a urine drug screen but it's negative, there are other confirmatory tests that can be sent, although they're often send-out labs and come back in a very delayed fashion. Dr Jones: So, in other words, it's complicated, which usually means it's humbling. And if I'm understanding it correctly, there's the risk of the false positive on the urine drug screen. And then there's the risk of the false negative if we think we're screening for something that might not even be on that initial screen. So, that's a wonderful reminder that these are clinical diagnoses and we have to keep our clinician hats on while we're thinking about how to establish these diagnoses or exclude them. So, back to opioids, Dr Gross. There are some really peculiar neurologic syndromes associated with opioid overdose. Tell us a little about those. Dr Goss: Well, I mean, some of these were described first with heroin. So, we can start with the one that almost anybody has heard of, heroin-associated spongiform leukoencephalopathy, which we know is associated with a practice known as "chasing the dragon," which is inhaling vapors of heroin heated on foil. But we know now that this syndrome can occur with other opioids, including fentanyl. The clinical features are, you know, apathy, cerebellar signs, quadriparesis, parkinsonism, myoclonus, and some patients progress to coma or even death. But on MRI you're seeing, you know, these confluence symmetric white matter diffusion restriction and T2 hyperintensities in the cerebellar white matter and the posterior limb of the internal capsule that spare the subcortical U-fibers. So, you know, I think this is kind of the classic example of something that's symmetric, that has a very obvious and interesting MRI pattern. But as time is passing, we're seeing more and more similar types of syndromes of leukoencephalopathies, but with different clinical presentations and MRI characteristics. So, another of these is CHANTER syndrome. This is an opioid overdose-related presentation where people have stupor and coma. And on the MRI there, you see bilateral symmetric diffusion restriction in the cerebellar cortex, in the hippocampi, in the basal ganglia. And it spares the cerebral cortex. And notably in these cases, patients can progress to cerebellar edema, to obstructive hydrocephalus. And some require suboccipital craniotomy. I had a week recently at Highland Hospital, where I work, where we had two of these cases in the same week, in just a community hospital. And there's a similar syndrome in children known as POUNCE syndrome with profound cerebellar edema, and many patients require posterior decompression. So that's another different distribution of findings with a different outcome. Fortunately, there's a milder sort of phenotype of opioid-associated amnestic syndrome, is what it's been described, where there's primarily DWI changes in the hippocampi and the globus pallidus. So, patients primarily present with an amnestic syndrome, mostly anterograde amnesia. Seeing these in practice, I'm not sure that patients always fall into one bucket or another. But in general, you'll see some degree of symmetric diffusion restriction or symmetric white matter changes that clearly point to a toxic presentation, a toxic syndrome, as opposed to pure anoxia, for example. And it's important to know that because from a prognostic standpoint, anoxic brain injury, which can occur after cardiac arrest and after opioid overdose, can look different than some of these syndromes. Finally, heroin has been associated with myelopathy, but also that's been reported on with fentanyl. So, I think some of these conditions got their reputation from heroin. But as fentanyl has proliferated---and prior to that as prescription opioid, you know, misuse had proliferated---we're seeing similar syndromes with all of the opiates. Dr Jones: And I think it's a good case in point that you can have multifocal disease and it be a manifestation of an intoxication, and I think that's a really good reminder that we have to have many of these syndromes in our differential, we have to be aware of them, otherwise we might miss them or attribute them to another mechanism. Dr Goss, our last issue of Continuum that was dedicated to the neurology of systemic disease came out in 2023, and here we are in 2026 publishing our latest issue, including your article and this podcast. Since 2023, have there been any emerging patterns or novel agents of abuse or misuse out there? Dr Goss: The short answer is yes, and I would say the reason is just the supply is moving at more and more rapid speed. The relationship between the internet and drug supply has really informed what's out there at any given moment. So, the turnover in the market can change in weeks, not in years. And there's all of this distribution through social media and encrypted apps. And then manufacturers are kind of continuously tweaking chemical structures to evade law enforcement. In the process of researching this article, I came across some, I mean, really wild examples. To be clear, these are not- not all these are common substances, but I think the general phenomenon should be known that people can walk into a vape shop or walk into a gas station or meander around online and buy some really weird stuff. So, in 2024, there was this nationwide recall of a product called Diamond Shrooms that was sold online and in smoke and vape shops, and this was billed as, like, a hemp and mushroom mixture. But it led to multiple- I mean, over 100 cases of seizures and agitation and depressed consciousness and a few possible deaths. And when the contents were analyzed, they included psilocybin analogs and pregabalin. I mean, some weird stuff. And so, those have been pulled. But people are constantly inventing and marketing these different substances. I think another example… we all know about nitrous oxide and its association with B12 myopathy. But the use of nitrous oxide has really changed. Companies are selling large canisters online and in vape shops, and they're flavored, like, in blue raspberry flavor. And unfortunately, there's been a rise of nitrous among youth. So, we're seeing not just increased cases of myelopathy, but also a 2025 study in JAMA found a spike in deaths attributed to actual nitrous oxide overdose. And so nitrous, I think, had not been that commonly used a few years ago, but has become more common in the last couple of years. A final one I'll just mention is ketamine. So, ketamine has certainly appeared in reviews of neurological syndromes related to substance use for a long time, and it's also been studied and used off-label for mood disorders in outpatient infusion clinics for some time. But in the pandemic, there was an expansion in telemedicine, as we know, and an associated proliferation of teleclinics that were prescribing very frequent, even daily oral and lozenge and nasal formulations of ketamine, which has led to increased rates of misuse. So, you know, acutely, the syndrome associated with ketamine intoxication is very brief. And often by the time people come to the emergency department, their symptoms have already worn off. But long-term, frequent use of ketamine is really still being studied. There seems to be an association with persistent neuropsychiatric effects like cognitive impairment, psychosis, persistent depressive symptoms. And so, you know, I think it's just important to realize that while the list of substances may look pretty similar to 2023, the use patterns, the distribution patterns are continuing to change. It's hard to keep up. And while alcohol and opioids and stimulants are by far the most common substances that a neurologist is going to encounter in daily practice, there's this ever-expanding range of possible substances that can trigger neurologic syndromes, both acute and chronic. Dr Jones: And I think that might be the best possible plug to read your article, because it is evolving and we have to stay on top of it. And we really can't be complacent with it. So, thank you for that update. Okay, back to our trivia question. Accidental exposures to what substance increased a whopping 1,375% between 2017 and 2021? Dr Goss, what do you think? Dr Goss: That was THC-infused edibles. Specifically, these would be THC-infused substances that are often marketed as looking like candy or snacks or cereal. Exactly what a kid might want to get their hands on. And unfortunately, accidental cannabis exposures in children under age five went up by 1,375% between 2017 and 2021, and 600 of those patients required critical care admission. Dr Jones: Yeah. So, just a mind-blowing number, and obviously something for us to be on the lookout for, especially if you see children in your practice and someone comes in with CNS depression or stupor, it's one to not miss. So that was something I learned in reading your article, among many other things. And Dr Goss, I want to thank you for joining us. I want to thank you for such a great discussion. I learned a lot from reading your article, I learned a lot just from our conversation today, and I suspect our readers and our listeners will too. Dr Goss: What a pleasure. Thank you so much, Dr Jones. Dr Jones: Again, we've been speaking with Dr Adeline Gross, author of a fantastic article on neurologic complications of drug and alcohol use in our latest issue of Continuum on the neurology of systemic disease. Please check it out, and thank you to our listeners for joining us today. Dr Monteith: This is Dr Teshamae Monteith, Associate Editor of Continuum Audio. If you've enjoyed this episode, you'll love the journal, which is full of in-depth and clinically relevant information important for neurology practitioners. Use the link in the episode notes to learn more and subscribe. AAN members, you can get CME for listening to this interview by completing the evaluation at continpub.com/audioCME. Thank you for listening to Continuum Audio.

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