Podcasts about related disorders

Balancing disease control with pregnancy and neonatal considerations in people with neuroinflammatory disease throughout the family planning, pregnancy, and postpartum periods is crucial. Modern treatment paradigms enable women to safely become pregnant and breastfeed alongside effective disease management. Shared decision making is an important part of this process. In this episode, Kait Nevel, MD, speaks with Ruth Dobson, MD and Kerstin Hellwig, MD, authors of the article "Family Planning in Neuroinflammatory Disease" in the Continuum® April 2026 Multiple Sclerosis and Related Disorders issue. Dr. Nevel is a Continuum® Audio interviewer and a neurologist and neuro-oncologist at Indiana University School of Medicine in Indianapolis, Indiana. Dr. Dobson is a professor in the Centre for Preventive Neurology at the Wolfson Institute of Population Health, Queen Mary University of London, and a consultant neurologist in the Department of Neurology at the Royal London Hospital, Barts Health NHS Trust, in London, United Kingdom. Dr. Hellwig is a professor in the Department of Neurology at Katholisches Klinikum, Ruhr‑Universität Bochum, in Bochum, Germany. Additional Resources Read the article: Family Planning in Neuroinflammatory Disease Subscribe to Continuum®: shop.lww.com/Continuum Earn CME (available only to AAN members): continpub.com/AudioCME Continuum® Aloud (verbatim audio-book style recordings of articles available only to Continuum® subscribers): continpub.com/Aloud More about the American Academy of Neurology: aan.com Social Media facebook.com/continuumcme @ContinuumAAN Host: @IUneurodocmom Guest: @drruthdobson Full episode transcript available here

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.

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.

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.

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.

In this episode, I sit down with Licensed Clinical Social Worker Sebastian Washburn to talk about anxiety disorders and panic disorder. We break down what anxiety actually is, what's happening in your body during a panic attack, and how you can begin to heal.⸻

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.

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.

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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.

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.

Are you working hard, caring deeply, and still feeling like it's not enough? You're not alone, and this episode is for you. This week, Molly and Clarissa sit down with Dr. Ellen Hendriksen, clinical psychologist, core faculty at the Center for Anxiety and Related Disorders at Boston University, and author of How to Be Enough and How to Be Yourself. Ellen brings warmth, science, and radical compassion to one of the most common, and most quietly painful, struggles in recovery: perfectionism. In this conversation, we explore:

All Home Care Matters and our host, Lance A. Slatton were honored to welcome Dr. Dale V. Atkins as guest to the show.   About Dr. Dale V. Atkins:   Dale V. Atkins, Ph.D., is a licensed psychologist and educator with more than forty-five years of experience working with individuals, couples, and families. Dr. Atkins consults domestically and internationally. She conducts seminars and retreats for health and educational institutions, executives and employees of major corporations, and government agencies in matters related to the fields of psychology, sociology, education, and communication.   She practices, teaches, and consults in the field of Alzheimer's and Related Disorders with a focus on prevention as well as patient and caregiver wellness and resilience. She emphasizes the benefits of intergenerational relationships in families and communities. Dr. Atkins values opportunities to share everyday human stories with those in the health care field. She is the author of eight books; most recently, The Turquoise Butterfly, (her first children's book), chapters, articles, and journals for popular and professional audiences.   For 22 years Dr. Atkins was a recurring guest expert on NBC's "Today" show.   Dr. Atkins is an active volunteer in her community. She and her dog are a certified dog therapy team who have participated in school readers' programs as well as visitation programs at day and residential facilities for people who have Alzheimer's. She is a member of several non-profit boards whose focus is literacy, tolerance, women's health and wellness, child protection, hospital leadership, and community action.   An engaged citizen, she has received multiple recognitions for her community service and leadership.   Dr. Atkins has two children and six grandchildren. She has private practice in NYC and lives in CT, where she is often found outdoors.

Do you spend way too much time checking yourself in the mirror? Fixating on flaws that nobody else seems to notice? Canceling plans because you feel like you look "off" that day? You're not alone, and this isn't about vanity—this is about a real struggle that deserves understanding. Today we're diving into Body Dysmorphic Disorder (BDD) and how it shows up in eating disorder recovery. The statistics are eye-opening: while only 1 in 50 people in the general population experience BDD, 25-40% of people with eating disorders also struggle with body dysmorphic disorder. In this episode, you'll discover: What Body Dysmorphic Disorder actually is (beyond occasional insecurity) The shocking connection between eating disorders and BDD Real client story: How BDD stole years of living from a successful VP 6 practical tools to break free from obsessive body thoughts Why "your body is an instrument, not an ornament" How to practice body neutrality when body positivity feels impossible The difference between healthy awareness and destructive obsession This goes beyond the mirror—it's about reclaiming the mental energy that's been stolen from you and learning to live present in your own life. THE EYE-OPENING STATISTICS 1 in 50 people in general population experience Body Dysmorphic Disorder 25-40% of people with eating disorders also struggle with BDD This means: If you're struggling with disordered eating, there's a much higher chance you're also dealing with body dysmorphic disorder. WHAT IS BODY DYSMORPHIC DISORDER? BDD is classified in the DSM-5 under Obsessive Compulsive and Related Disorders. It's when thoughts about your appearance become all-consuming—when they start stealing your joy and limiting your life. This isn't about vanity. This is about genuine struggle that deserves compassion and understanding. Common signs include: Spending hours checking your appearance in mirrors Constantly comparing yourself to others (especially on social media) Avoiding social settings because you're convinced everyone is staring Taking dozens of photos from different angles to "capture what you really look like" Canceling plans when you feel you look "off" Fixating on specific body parts (face, stomach, skin, weight) CLIENT STORY: ELLA'S BREAKTHROUGH Ella was a VP at her company—successful, married, two kids. From the outside, everything looked perfect. But inside, she was crumbling. Ella spent hours fixating on what she perceived as facial asymmetry and "hating her stomach." She would: Cancel plans if her appearance didn't feel right Take dozens of selfies from different angles Hibernate in loose clothing when her stomach wasn't "flat enough" Miss out on living because she was trapped in the obsession The truth: When I looked at Ella, I saw an amazingly beautiful and confident woman. The things she fixated on weren't visible to me or anyone else in her life. Six months later, Ella shared: "For the first time in years, I went to my daughter's birthday party and I didn't think about my appearance. I was just there. I was present. I laughed, and I played and I connected. This is what living feels like." 6 TOOLS TO BREAK FREE FROM BODY OBSESSION 1. Practice Awareness Notice when you're engaging in checking behaviors Observe with compassion: "I notice I'm having thoughts right now" Technique: Set a timer when getting ready—when it goes off, walk away from the mirror no matter what 2. Challenge the Distortion Question absolute thoughts: "Everyone notices this about me" or "I look disgusting" Exercise: Write how you'd respond if your best friend shared the same concerns Remember: "Our minds distort our mirrors" 3. Reduce Comparison (Eliminate If Possible) Studies show increased social media correlates with worse BDD symptoms Action: Go on a social media detox or unfollow triggering accounts Replace scrolling time with something that feeds your soul 4. Redirect Your Focus Create a list of activities that fully engage your mind Have this list ready BEFORE the thoughts hit Examples: Reading, puzzles, nature walks, calling a friend 5. Practice Body Neutrality Focus on what your body can DO rather than how it looks "Can your legs carry you through the day? Can your arms hug people you love?" Remember: Your body is an instrument, not an ornament 6. Seek Help and Support BDD responds well to treatments like Cognitive Behavioral Therapy (CBT) Working with specialists in body image issues makes an enormous difference You don't have to heal from this alone THE TRUTH ABOUT YOUR BODY Your body was never meant to be your life's work. It was meant to champion you in doing your life's purpose and your life's work. You only have one precious life. You deserve to: Be present and laugh without wondering how your face looks Eat cake without worrying about your stomach afterward Connect deeply without background noise of how others view you Live without the mental prison of appearance obsession KEY QUOTES

Top of 2025 // One of Our Most Engaged Episodes of 2025In our world, emotional distress seems to be increasing. So, can we integrate biblical principles, evidence-based insights from psychology, and spiritual practices to help us master our emotions rather than allowing our emotions to master us? In this week's conversation on FrontStage BackStage, host Jason Daye is joined by Dr. Kevin Chapman. Kevin is a licensed clinical psychologist and the Founder and Director of the Kentucky Center for Anxiety and Related Disorders. He leads the Sound Mind Ministries and hosts The Sound Mind Show on YouTube. His most recent book is entitled Mastering Our Emotions. Together, Kevin and Jason have a hope-filled conversation about how we can master our emotions through biblical principles and the power of Christ. Kevin also touches on some of the realities and some of the misconceptions about negative emotions and gives us practical ways that we, as ministry leaders, can help others overcome negative emotions through the power of Christ.Dig deeper into this conversation: Find the free Weekly Toolkit, including the Ministry Leaders Growth Guide, all resource links, and more at http://PastorServe.org/networkSome key takeaways from this conversation:Kevin Chapman on the connection between faith, intentionality, and the power of transformation that reaches both the heart and mind: "By partnering with the Holy Spirit and confronting those emotions, you're literally reprogramming your brain."Kevin Chapman on the importance of analyzing and understanding the broader aspects of emotions rather than solely experiencing or describing how they feel: "Focus on the features of emotions, not just the feelings of emotions."Kevin Chapman on the important role emotions play in guiding us through life and our spiritual journey: "Our emotions are meant to help us navigate our world, even to serve God, but we have to learn to regulate them."----------------Looking to dig more deeply into this topic and conversation? FrontStage BackStage is much more than another church leadership show, it is a complete resource to help you and your ministry leaders grow. Every week we go the extra mile and create a free toolkit so you and your ministry team can dive deeper into the topic that is discussed.Visit http://PastorServe.org/network to find the Weekly Toolkit, including the Ministry Leaders Growth Guide. Our team pulls key insights and quotes from every conversation with our guests. We also create engaging questions for you and your team to consider and process, providing space for you to reflect on how each episode's topic relates to your unique church context. Use these questions in your staff meetings, or other settings, to guide your conversation as you invest in the growth of your ministry leaders. Love well, live well, & lead well Complimentary Coaching Session for Pastors http://PastorServe.org/freesession Follow PastorServe LinkedIn | Twitter | Instagram | FacebookConnect with Jason Daye LinkedIn | Instagram...

We're re-releasing one of our most popular episodes, an important conversation with Wolfram syndrome expert Dr. Fumi Urano.   We're bringing this episode back in honor of Diabetic Eye Disease Month, and because it's the perfect follow-up to our last episode featuring Dr. Rachel Hyman and our very own co-host Cathy Gildenhorn as guests. Their experiences with the milder, adult-onset variant of Wolfram syndrome sparked so much interest, we knew this episode needed another moment in the spotlight. You'll hear Cathy interview Dr. Urano, her lead physician, about symptoms, diagnosis, and promising research underway to help people with rare neurodegenerative disorders like Wolfram syndrome.   We are thrilled to have Dr. Fumihiko Urano on “It Happened To Me” as he is our co-host Cathy's lead doctor, for her variant of the rare disease, Wolfram Syndrome.    Fumihiko “Fumi” Urano, MD, Ph.D., is a Physician and Medical Researcher specializing in Wolfram syndrome, characterized by juvenile-onset diabetes, vision loss, and neurodegeneration. Dr. Urano is a Professor of Medicine and Pathology & Immunology, an attending physician at Endocrinology Genetics Clinic, and currently holds Samuel E. Schechter Endowed Professorship in Medicine at Washington University Medical Center, St. Louis, USA. Dr. Urano is a driving force in the study of Wolfram syndrome and Related Disorders, including WFS1-related disorders/Wolfram-like disorders. As the Director of the Wolfram Syndrome and Related Disorders Clinic and Study at Washington University Medical Center, Dr. Urano has been leading the clinical, translational, and interventional studies of Wolfram syndrome and Related disorders. Dr. Urano's collaboration with colleagues at the medical center and around the world has allowed him to develop cutting-edge treatments for this disease, including gene therapy and regenerative therapy.    Learn more on their Wolfram syndrome website, wolframsyndrome.wustl.edu. If you want to reach out directly you can contact the Research Nurse Coordinator Stacy Hurst, RN, CDE by calling 314-747-3294 or emailing shurst@wustl.edu.    During the episode Dr. Urano mentioned two episodes of “It Happened To Me”: during this episode. The first was our interview with Dr. Gladstone in Episode 5. He also gave a shoutout to our conversation with Stephanie Snow Gebel (Snow Foundation) in Episode 9.    Stay tuned for the next new episode of “It Happened To Me”! In the meantime, you can listen to our previous episodes on Apple Podcasts, Spotify, streaming on the website, or any other podcast player by searching, “It Happened To Me”.    “It Happened To Me” is created and hosted by Cathy Gildenhorn and Beth Glassman. DNA Today's Kira Dineen is our executive producer and marketing lead. Amanda Andreoli is our associate producer. Ashlyn Enokian is our graphic designer.   See what else we are up to on Twitter, Instagram, Facebook, YouTube and our website, ItHappenedToMePod.com. Questions/inquiries can be sent to ItHappenedToMePod@gmail.com.

Don't miss this inspirational episode with Dr. E, a family practice physician with a specialty in pediatric anxiety and depression.  Dr. E has four children. Her second child, Sophie, has Selective Mutism, a mental health condition where a person can't talk in certain situations because of fear and anxiety. Dr. E says she knew something was off when Sophie was about 3 1/2 years old.  Sophie was super talkative at home, but became a different person when she was out of the house. Advocating for her daughter sent Dr. E on a quest to find Sophie the right help.  After several different diagnoses and even accusations of child abuse, Dr. E set out to figure out for herself what Sophie was battling. Through her research and work, Dr. E found the diagnosis of Selective Mutism and founded the Selective Mutism Association (https://www.selectivemutism.org/). Dr. E then created the Social Communication Anxiety Treatment (S-CAT) and the Selective Mutism Anxiety and Related Disorders Treatment Center (Smart Center) (https://selectivemutismcenter.org/), where thousands of people worldwide overcome Selective Mutism. Dr. E emphasizes the importance of parents trusting their guts, and how critical it is to be your child's advocate. Dr. E concludes the episode by talking about the book Sophie wrote called Unspoken Words (https://www.amazon.com/Unspoken-Words-Childs-Selective-Mutism/dp/1467982598) at age 13. Sophie went to college and medical school and is now married and expecting her first child. Dr. E also hosts a podcast called Unspoken Words (https://podcasts.apple.com/us/podcast/unspoken-words-a-selective-mutism-podcast-by-dr/id1621959774?i=1000732656789)

Come to a Dehoarding Accountability Zoom Session: http://www.overcomecompulsivehoarding.co.uk/ticket Subscribe to the podcast: https://www.overcomecompulsivehoarding.co.uk/subscribe Podcast show notes, links and transcript: http://www.overcomecompulsivehoarding.co.uk/  Why is it so hard to deal with uncertainty, and what does that have to do with hoarding? This week I'm joined by Dr Jan Eppingstall to unpack how our brains handle ambiguity, why fear of making mistakes can keep us stuck, and how intolerance of uncertainty feeds into hoarding behaviours. We break down practical ways to build up your tolerance for not knowing and share some strategies that might actually make a difference. Uncertainty and Its Challenges Definition and context of uncertainty Evolutionary reasons for discomfort with uncertainty (Selfish Brain Theory) Contrast between historical resource scarcity and modern abundance Our minds' outdated ways of managing uncertainty Cognitive Closure What is cognitive closure? Difference between cognitive closure (psychological need for definite answers) and “closure” in pop culture (emotional resolution) How it relates to need for certainty in present/future, not just past events The creation of cognitive closure measurement scales by researchers Factors influencing need for cognitive closure: Personality traits: Conscientiousness, neuroticism (now called emotionality), openness to experience, extroversion Trauma history and its effects on the nervous system Neurodivergence (with emphasis on autism and “sticky thinking”) Combination of personality, trauma, and neurodivergence Intolerance of Uncertainty Psychological definition of intolerance of uncertainty Negative cognitive bias: How it affects perception and response Manifestations in people experiencing uncertainty as distress Its direct relevance to hoarding behaviours The Link Between Hoarding Disorder and Intolerance of Uncertainty Research findings: intolerance of uncertainty as a predictor of hoarding symptom severity Usefulness in early intervention strategies intolerance of uncertainty as a transdiagnostic factor (across anxiety, some depression, and other mental health conditions) How heightened anxiety sensitivity in hoarding perpetuates avoidance Experiential avoidance in hoarding (saving and acquiring behaviours) Connection between maladaptive behaviours and intolerance of uncertainty Fear of Making Mistakes and Perfectionism Common fears of mistakes in hoarding (disposing, acquiring, putting things away) Perfectionism's role (fear of failure, not wasting) All-or-nothing thinking and rigid decision-making rules Paralysing effect of avoidance due to fear of mistakes Not making a decision as a potential mistake itself Interaction and reinforcement between perfectionism and intolerance of uncertainty Comorbidity and Severity Research on multiple diagnoses: More than half of psychiatric patients have more than one diagnosis Diagnostic challenges and overlapping criteria How comorbidity compounds issues: More symptoms and more complexity Higher intolerance of uncertainty linked with more severe hoarding, especially when other conditions are present Impact on treatment difficulty intolerance of uncertainty's Impact on Acquiring and Discarding Behaviours How acquiring reduces fear of missing out and future needs Difficulty discarding as protection against future regret Shame around mistake-making Common inner questions: Future use, responsibility, relationships More complexity leading to more avoidance Nuances in intolerance of uncertainty and Hoarding Study on sub-factors of uncertainty: Factor 1: Negative self-referential implications (linked to hoarding severity) Factor 2: Perception of uncertainty as unfair (not linked) Internal vs. external perspectives on uncertainty Relevance of anxiety-driven self-criticism Changing Relationship to Uncertainty: Curiosity and Reframing Rilke's quote on “loving the questions” Transforming approach from fear to curiosity Curiosity as a therapeutic tool Creativity in imagining alternatives and solutions Relevance of loss aversion and cognitive biases Modern Life and Uncertainty Intolerance Research linking increased use of technology (instant answers) to rising intolerance of uncertainty Smartphone/information overload and decreased tolerance “muscle” Relevance to hoarding (desire for backups, information saving) Example: IMDb, screenshots, saving digital info Treatment Strategies Cognitive Behavioural Therapy (CBT) effects on intolerance of uncertainty in anxiety Acceptance and Commitment Therapy (ACT) and exposure-based methods: Pros and cons Importance of a therapist experienced in error-related distress and uncertainty Key skills: Observing distress, sitting with uncomfortable feelings, gradual exposure Self-help approaches: Reframing mistakes as learning Practicing self-compassion Values-based decision-making Systematic exposure to small errors Gradually breaking rigid rules (e.g., waste, tidiness) Recognising individual differences and seeking appropriate support Embracing Mistakes and Humanity Learning from therapist/client anecdotes Cultural expectations around perfectionism vs. real human messiness How mistakes can be positive or even entertaining Letting go of the need for perfection The Four Cs for Managing Uncertainty From Elizabeth Weingarten: Curiosity, Conversation, Community, Commitment How to foster each: Curiosity: Approach with questions and exploration Conversation: Discuss uncertainties with trusted people Community: Build social support Commitment: Dedication to exploring questions and knowing when to let go Links Hillman, S. R. HOARDING DISORDER AND Intolerance of Uncertainty, Anxiety Sensitivity and Distress Tolerance in Hoarding Disorder Compared to OCD and Healthy Controls - Shemariah R. Hillman; Claire L. Lomax; Nadeen Khaleel; Theresa R. Smith; James D. Gregory Baldwin, P. A Multimethod Examination of Vulnerability in Hoarding, UNSW Sydney, 2016. https://doi.org/10.26190/UNSWORKS/19156 Castriotta, N.; Dozier, M. E.; Taylor, C. T.; Mayes, T.; Ayers, C. R. Intolerance of Uncertainty in Hoarding Disorder. Journal of Obsessive-Compulsive and Related Disorders 2019, 21, 97–101. https://doi.org/10.1016/j.jocrd.2018.11.005 Exploring Humanity's Relationship to Uncertainty with Elizabeth Weingarten  Podcast ep 49: Sitting with discomfort: distress tolerance and hoarding – How unconscious distress avoidance might be worsening your problems Podcast ep 190: What if we forgive ourselves, but now we know better, we do better? Choosing compassion over shame in hoarding disorder Podcast ep 182: What are “towards and away moves” and what on earth do they have to do with hoarding recovery? With Dr Jan Eppingstall Podcast ep 127: Overcoming overspending with Paige Pritchard, Money Coach Come to a Dehoarding Accountability Zoom session: Accountability Booking Form Dr Jan Eppingstall at Stuffology https://www.facebook.com/stuffologyconsulting/ https://twitter.com/stuff_ology https://www.instagram.com/stuff_ology/ Dr Jan Eppingstall on Pinterest Website: Overcome Compulsive Hoarding Become a Dehoarding Darling Submit a topic for the podcast to cover Questions to ask when dehoarding: https://www.overcomecompulsivehoarding.co.uk/podquestions Instagram: @thathoarderpodcast Twitter: @ThatHoarder Mastodon: @ThatHoarder@mastodon.online TikTok: @thathoarderpodcast Facebook: Overcome Compulsive Hoarding with That Hoarder Pinterest: That Hoarder YouTube: Overcome Compulsive Hoarding with That Hoarder Reddit: Overcome Compulsive Hoarding with That Hoarder subreddit Help out: Support this project Sponsor the podcast Subscribe to the podcast Subscribe to the podcast here

Our guest this week is Peter Gerhardt of Rich Hill Park, NJ who is executive director at EPIC Schools located in Paramus, NJ, author of dozens of publications and books, an internationally recognized Autism expert and outspoken advocate for the disability community.Peter has three degrees from Rutgers University: a BA in Psychology, an EdM in Special Education, and a PhD in Education Psychology and Special Education. He has dedicated his life to researching Autism and serving the disability community.  He has developed workshops and given hundreds of presentations domestically and internationally.  Some of his publications include: Make it Meaningful: Creating Programs that Matter into Adulthood for Learners with Autism and Related Disorders (2024).Handbook of Quality of Life for Individuals with Autism Spectrum Disorder. Autism and Child Psychopathology Series (2022).Transition to Adulthood for Adolescents and Young Adults with Autism: Can We Improve Outcomes? (2022) Social Skill and Adaptive Behavior Intervention with Learners with Autism (2013). Peter also served as a consultant for the widely respected documentary In A Different Key (2021) co-producers: Caren Zucker, John Donovan & Ray Conley with music by Wynston Marsalis.Given the scope of Peter's work we decided to split his interview into two parts. This is part #2. Show Links:Phone – (210) 576-0600Email – PGerhardt@epicschool.orgLinkedIn –  https://www.linkedin.com/in/peter-gerhardt-112a4b29/Website - https://www.epicschool.org/Organization for Autism Research (OAR) - https://researchautism.org/Books – - Make it Meaningful: Creating Programs that Matter into Adulthood for Learners with Autism and Related Disorders - Handbook of Quality of Life for Individuals with Autism Spectrum Disorder. Autism and Child Psychopathology Series - Publication- Transition to Adulthood for Adolescents and Young Adults  with Autism: Can We Improve Outcomes?. Movie – https://www.inadifferentkeythemovie.com/Special Fathers Network -SFN is a dad to dad mentoring program for fathers raising children with special needs. Many of the 800+ SFN Mentor Fathers, who are raising kids with special needs, have said: "I wish there was something like this when we first received our child's diagnosis. I felt so isolated.  There was no one within my family, at work, at church or within my friend group who understood or could relate to what I was going through."SFN Mentor Fathers share their experiences with younger dads closer to the beginning of their journey raising a child with the same or similar special needs. The SFN Mentor Fathers do NOT offer legal or medical advice, that is what lawyers and doctors do. They simply share their experiences and how they have made the most of challenging situations.Check out the 21CD YouTube Channel with dozens of videos on topics relevant to dads raising children with special needs - https://www.youtube.com/channel/UCzDFCvQimWNEb158ll6Q4cA/videosPlease support the SFN. Click here to donate: https://21stcenturydads.org/donate/Special Fathers Network: https://21stcenturydads.org/  SFN Mastermind Group - https://21stcenturydads.org/sfn-mastermind-group/

Our guest this week is Peter Gerhardt of Rich Hill Park, NJ who is executive director at EPIC Schools located in Paramus, NJ, author of dozens of publications and books, an internationally recognized Autism expert and outspoken advocate for the disability community.Peter has three degrees from Rutgers University: a BA in Psychology, an EdM in Special Education, and a PhD in Education Psychology and Special Education. He has dedicated his life to researching Autism and serving the disability community.  He has developed workshops and given hundreds of presentations domestically and internationally.  Some of his publications include: Make it Meaningful: Creating Programs that Matter into Adulthood for Learners with Autism and Related Disorders (2024).Handbook of Quality of Life for Individuals with Autism Spectrum Disorder. Autism and Child Psychopathology Series (2022).Transition to Adulthood for Adolescents and Young Adults with Autism: Can We Improve Outcomes? (2022) Social Skill and Adaptive Behavior Intervention with Learners with Autism (2013). Peter also served as a consultant for the widely respected documentary In A Different Key (2021) co-producers: Caren Zucker, John Donovan & Ray Conley with music by Wynston Marsalis.Given the scope of Peter's work we decided to split his interview into two parts. This is part #1. Show Links:Phone – (210) 576-0600Email – PGerhardt@epicschool.orgLinkedIn –  https://www.linkedin.com/in/peter-gerhardt-112a4b29/Website - https://www.epicschool.org/Organization for Autism Research (OAR) - https://researchautism.org/Books – - Make it Meaningful: Creating Programs that Matter into Adulthood for Learners with Autism and Related Disorders - Handbook of Quality of Life for Individuals with Autism Spectrum Disorder. Autism and Child Psychopathology Series - Publication- Transition to Adulthood for Adolescents and Young Adults  with Autism: Can We Improve Outcomes?. Movie – https://www.inadifferentkeythemovie.com/Special Fathers Network -SFN is a dad to dad mentoring program for fathers raising children with special needs. Many of the 800+ SFN Mentor Fathers, who are raising kids with special needs, have said: "I wish there was something like this when we first received our child's diagnosis. I felt so isolated.  There was no one within my family, at work, at church or within my friend group who understood or could relate to what I was going through."SFN Mentor Fathers share their experiences with younger dads closer to the beginning of their journey raising a child with the same or similar special needs. The SFN Mentor Fathers do NOT offer legal or medical advice, that is what lawyers and doctors do. They simply share their experiences and how they have made the most of challenging situations.Check out the 21CD YouTube Channel with dozens of videos on topics relevant to dads raising children with special needs - https://www.youtube.com/channel/UCzDFCvQimWNEb158ll6Q4cA/videosPlease support the SFN. Click here to donate: https://21stcenturydads.org/donate/Special Fathers Network: https://21stcenturydads.org/  SFN Mastermind Group - https://21stcenturydads.org/sfn-mastermind-group/

Welcome to Dr. M's Women and Children First, where we dive into the latest insights on health and wellness for women and children. Today, we're honored to have Dr. Peter Rowe, a world-renowned expert from Johns Hopkins University, joining us to unravel the complexities of chronic fatigue.  Dr. Peter Rowe is a Professor of Pediatrics at the Johns Hopkins University School of Medicine. He is the inaugural Sunshine Natural Wellbeing Foundation Professor of Chronic Fatigue and Related Disorders and serves as the Director of the Chronic Fatigue Clinic at Johns Hopkins Children's Center. His areas of clinical expertise include chronic fatigue syndrome and other disorders characterized by fatigue and orthostatic intolerance. Dr. Rowe and his colleagues were the first to describe the relationship between chronic fatigue syndrome (CFS) and treatable orthostatic intolerance syndromes, as well as the association between Ehlers-Danlos syndrome and CFS. In this episode, Dr. Rowe and I dive deep into CFS and long Covid for both the parent and the clinician. We set the stage for a better understanding of this complex disorder in order to encourage earlier diagnosis and better therapy. From its impact on daily life to cutting-edge approaches for management, Dr. Rowe brings decades of expertise to help us understand this challenging condition.  Please Enjoy, Dr. M  

Attention-deficit/hyperactivity disorder (ADHD) was once thought of as a condition that affects only children. The belief was that children would grow out of it, but research has shown that the condition often persists throughout life. In fact, ADHD is the second most prevalent psychiatric disorder in adults, but many misconceptions still exist about it. On this episode, host Sara Frueh is joined by David Goodman, an assistant professor at Johns Hopkins University School of Medicine and director of the Adult Attention Deficit Disorder Center of Maryland. Goodman has treated adults with ADHD for over 40 years. Goodman explains how ADHD affects adults, the complexities in how it's diagnosed and treated, and open questions for research in the field. Resources: Visit the Adult Attention Deficit Disorder Center of Maryland's website to learn more about adult ADHD, and find links to more of David Goodman's research, interviews, and publications. The American Professional Society of ADHD and Related Disorders will release guidelines for diagnosis and treatment of ADHD in late 2025. Check out their website to learn more. Read the New York Times article “Have We Been Thinking About ADHD All Wrong?,” which was discussed during the podcast episode.

In honor of Mental Health Awareness Month and Military Appreciation Month, we're rekindling our interview with Olympian Samantha Schultz, former modern pentathlete and member of the US Army World Class Athlete Program. Samantha realized her goal of becoming an Olympian--but then after Tokyo 2020, she discovered underlying mental health issues, including an eating disorder, that turned her life upside down. In early 2024, Samantha shared her journey with us and how she's working toward better mental health. Follow Samantha on Instagram and YouTube!   If you're struggling with mental health, finding the right support can help you get on a better path. In the US, anyone can call or text 988, the suicide and mental health crisis hotline. Resources for eating disorders include: National Eating Disorder Association: https://www.nationaleatingdisorders.org/ National Alliance for Eating Disorders: https://www.allianceforeatingdisorders.com/ The Bulimia Project  https://bulimia.com/ National Association of Anorexia Nervosa and Related Disorders: https://anad.org/ and helpline: 1-888-375-7767   For a transcript of this episode, please visit http://flamealivepod.com.   Thanks so much for listening, and until next time, keep the flame alive! *** Keep the Flame Alive: The Olympics and Paralympics Fan Podcast with hosts Jill Jaracz & Alison Brown. New episodes released every week, and daily during the Olympics and Paralympics.   Support the show: http://flamealivepod.com/support Bookshop.org store: https://bookshop.org/shop/flamealivepod Become a patron and get bonus content: http://www.patreon.com/flamealivepod Buy merch here: https://flamealivepod.dashery.com Hang out with us online: Facebook: https://www.facebook.com/flamealivepod Insta: http://www.instagram.com/flamealivepod Facebook Group: hhttps://www.facebook.com/groups/flamealivepod Newsletter: Sign up at https://flamealivepod.substack.com/subscribe VM/Text: (208) FLAME-IT / (208) 352-6348        

This week I'm talking with Dr. Maggie Sibley, a clinical psychologist and professor at the University of Washington School of Medicine. Dr. Sibley has spent over two decades studying ADHD, and is author or co-author of over 120 research papers on the topic. And she is the author of Parent-Teen Therapy for Executive Function Deficits and ADHD: Building Skills and Motivation. So recently, when I was working on the newsletter for the show, I came across an article about ADHD titled "Study describes fluctuations, remissions seen with ADHD,” and that felt like it was worth investigating more. While reading through the paper that was linked into the article I got to thinking, “hey, I'd love to ask some more questions about the findings in this paper,” and it occurred to me, hey, I can just reach out to the author of the paper for a conversation on the podcast. And so that's what today's show is all about, we dig into that paper, titled “Characteristics and Predictors of Fluctuating Attention-Deficit/Hyperactivity Disorder in the Multimodal Treatment of ADHD (MTA) Study” that looks into symptom fluctuation based on the a review of the Multimodal Treatment of ADHD (MTA) Study. We talk about how ADHD symptoms don't just disappear but actually tend to fluctuate — a lot more than many researchers expected. We also dive into why having more going on in life might actually make your ADHD symptoms less severe (or how that's just one interpretation of the results), how motivation works for us, and what it means to find your own “sweet spot” of structure. Plus, we get into the upcoming diagnostic guidelines for adult ADHD from the American Professional Society for ADHD and Related Disorders. This is definitely an episode you don't want to miss if you really enjoy the sciency side of things. Start Freedom today! Use code ADHD40 to get them 40% off a Freedom Yearly premium subscription! Listen to the Climbing the Walls podcast here! If you'd life to follow along on the show notes page you can find that at HackingYourADHD.com/222 YouTube Channel My Patreon This Episode's Top Tips ADHD symptoms don't always follow a straight decline or improvement. Symptoms can often fluctuate, sometimes improving for years and then intensifying again. Expect waves, not a straight line, and don't blame yourself when experiencing higher-than-normal symptoms. When you're in a phase where ADHD feels more manageable, that's a great time to try and take on more meaningful responsibilities — like work, school, or parenting — that can help create external structure and reinforce good patterns. While having more life demands (like a busy schedule, work responsibilities, or kids) can improve ADHD functioning by creating natural urgency and external motivators, it's also important to make sure it doesn't tip into overload. Not all clinicians are trained to recognize ADHD in adults, especially when childhood histories are murky. If your concerns are dismissed, it's okay — and important — to seek out a more knowledgeable provider. And on that note, look out for updated diagnostic and treatment guidelines for adult ADHD from APSARD (American Professional Society for ADHD and Related Disorders). While these guidelines won't change any of the diagnostic criteria in the DSM, they will help give clinicians clearer, evidence-based advice on how to apply them when evaluating ADHD in adults. 

Dr. Kevin Chapman is a licensed clinical psychologist. Dr. Chapman is the director at the Kentucky Center for Anxiety and Related Disorders.  He specializes in Cognitive Behavioral Therapy.  Kevin received his doctorate from the University of Louisville.  He completed his undergraduate at Centre College. He was also a 2 sport athlete in track and football.  Author of "Mastering Our Emotions: Biblical Principles for Emotional Health. 5:18 God's Word To Write The Books 7:20 God Working Through You 9:34 The Truth Of Anger 11:48 The Difference Between Anger And Sadness 16:04 The Importance Of Grieving Then Morning 18:51 The Old Covenant Mentality  21:37 Big Misconception That Everything Will Be Different Now 24:58 Satan's Affect On Our Thinking 27:33 The Power Of Shame 30:13 Addition And Emotions Are Inseparable 32:29 The Bravery Of Small Talk 36:58 The Fruit Of The Spirit 39:50 New Book Activating Joy 46:27 Implementing New Skills To Become A Better Person Don't forget you can also follow Dr. Rob Bell on Twitter or Instagram.  Follow At:  Twitter @drrobbell Instagram @drrobbell Download Your Daily Focus Road Map! https://drrobbell.com/ If you enjoyed this episode on Mental Toughness, please subscribe and leave a review! Dr. Rob Bell

Can we master our emotions? Is that healthy? Are emotions a gift from God, or part of our sinful reality? That's what we are talking about today. Dr. Kevin Chapman is a licensed clinical psychologist with a specialty in cognitive behavioral therapy. He is the founder and director of the Kentucky Center for Anxiety and Related Disorders. He leads Sound Mind Ministries and hosts The Sound Mind Show (YouTube). And he just release Mastering Our Emotions: Biblical Principles for Emotional Health.  Join Attaching to God Learning Cohort: Quieting an Anxious and Avoidant Faith.Starting Nov. 12 (2024), with the live calls on Tuesdays, 2:30pm-3:30pm (EST). Link: https://www.embodiedfaith.life/attaching-to-god-cohortStay Connected: Check out our Attaching to God 6-Week Learning Cohort. Join the Embodied Faith community to stay connected and get posts, episodes, & resources. Support the podcast with a one-time or regular gift (to keep this ad-free without breaking the Holsclaw's bank).

In this episode, we review the high-yield topic of⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠ ⁠⁠⁠⁠Somatic Symptom and Related Disorders⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠ ⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠from the Psychiatry section.Follow⁠⁠ ⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠Medbullets⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠ on social media:Facebook: www.facebook.com/medbulletsInstagram: www.instagram.com/medbulletsofficialTwitter: www.twitter.com/medbullets

We're running a survey to see how podcasts help women with ADHD learn about mental health and health-related topics. Make your voice heard today.We're back with another episode from our Hyperfocus field trip to San Diego. While we were at the APSARD (American Professional Society of ADHD and Related Disorders) conference, one of the talks that really piqued our interest was on genetics and neurodevelopmental disorders, including ADHD. Genetic science is tough to understand. And, as you'll hear in this interview, we had a lot to learn and a lot of questions. Is ADHD genetic? And if it is, what does that mean for people who have it? What does it mean for treatment? Luckily, Dr. Anne Arnett, a scientist at Boston Children's Hospital and assistant professor of pediatrics at Harvard Medical school, was kind enough to brave a chilly, windy outdoor recording. In this conversation, she help us understand more about what we know (and what we don't) about ADHD and genetics. Related resourcesVideo: Dyscalculia, dyslexia, and geneticsCan genetic testing help me find the right ADHD medication?Is ADHD hereditary?ADHD runs in the family (Michelle's story)The Arnett Lab at Boston Children's HospitalTimestamps(2:01) Is ADHD genetic?(8:28) Genetic vs. environmental factors and ADHD co-morbidities(11:50) What does the latest research mean for people with ADHD?(13:55) Is there genetic testing for ADHD?(18:56) Why bother with early detection?  (21:44) Anne's goals for her researchFor a transcript and more resources, visit the Hyperfocus page on Understood.We'd love to hear from you. Email us at hyperfocus@understood.org. Understood is a nonprofit organization dedicated to empowering people with learning and thinking differences, like ADHD and dyslexia. If you want to help us continue this work, donate at understood.org/give

Trinity researchers have developed a new gamified mobile health (mHealth) app designed to help people with Multiple Sclerosis (MS) manage fatigue, one of the most common and debilitating symptoms of the disease. The research - led by Dr Guido Giunti, Adjunct Professor, School of Medicine, Trinity College Dublin and Associate Professor of Digital Health at the University of Oulu, Finland, and researchers from the University of Oulu and Oulu University Hospital - evaluated the feasibility, usability, and impact of the app, named, More Stamina over a 60-day period. The study, which highlights the potential of the app, is published in the journal Multiple Sclerosis and Related Disorders today. "Fatigue is an invisible but life-altering symptom of MS," said Dr. Guido Giunti, Adjunct Professor, School of Medicine, Trinity College Dublin and leader of the More Stamina project. "Managing it requires more than just medication. More Stamina gives people the tools to understand their energy levels, take control of their day, and communicate their needs more effectively." The study followed 20 participants from Oulu University Hospital in Finland, who used the app daily for two months. Key Findings Users became more aware of their fatigue patterns, enabling them to plan their days more effectively. Higher engagement correlated with increased self-awareness, particularly among those with more severe fatigue. The app helped facilitate discussions with family members and healthcare providers, improving mutual understanding of fatigue's impact. Usability improved over time, though some users found data entry cognitively demanding, indicating areas for refinement. An Evidence-Driven Digital Health Solution More Stamina helps users track their daily activities and energy expenditure using "Stamina Credits", a gamified approach that visualizes energy use and helps users make informed decisions about their daily plans. Unlike many digital health solutions, More Stamina stands out for its research-driven approach at every stage, from identifying patient needs to design, prototyping, development, and testing. Each phase has been accompanied by peer-reviewed research, creating a transparent scientific trail for a mobile health solution. Bringing Digital Health into MS Care Fatigue affects up to 80% of MS patients and has a profound impact on their quality of life. Managing fatigue is challenging, as it involves physical, cognitive, and emotional factors, often leaving patients feeling exhausted, misunderstood, and unsupported. While digital health solutions have been increasingly proposed to help manage chronic conditions like MS, few have been rigorously evaluated to ensure their effectiveness and real-world impact. Neurologists at Oulu University Hospital emphasize the potential of such solutions in complementing traditional MS care. While the study confirmed that More Stamina is a feasible and acceptable tool, researchers emphasize that larger and longer-term studies are needed to evaluate its full clinical impact. The team is now exploring ways to integrate More Stamina into broader MS care strategies. Professor Minna Isomursu, University of Oulu, said: "Digital health solutions are only as good as their foundation. We worked with real patients and healthcare professionals from the start to build something truly useful. That is key to creating tools that people actually find useful in their daily lives." Empowering Patients and Strengthening Family Dialogue One of the unexpected yet powerful outcomes of the study was the role More Stamina played in facilitating conversations between MS patients and their families. Many participants reported that sharing their fatigue patterns with loved ones helped them feel understood and supported. More Stamina's development was not just about technology, it was about people. Active participation from patient representatives was key to ensuring that the app addressed real-life challenges. Tonja Molin-Juusti...

Earlier this year, Hyperfocus took a field trip to San Diego for an ADHD conference called APSARD, which stands for the American Professional Society of ADHD and Related Disorders (quite a mouthful).A conference of ADHD professionals might not sound fascinating, but it was — and we learned a ton. But there was one person and one talk I really wanted to find: A keynote speech about how ADHD affects women's bodies by Dr. Sandra Kooij. What Sandra is doing is something so sensible and radical: Looking at ADHD as a whole-body issue. Digging into how it can affect women's hormones, our health, and especially our hearts. I find Sandra's research fascinating and was thrilled when she agreed to sit down for a conversation with me. We didn't waste any time and quickly set up a makeshift studio for this week's episode of Hyperfocus. Also, a quick note on the audio this week: We had to record this episode outside the conference hotel, on a bustling patio full of ADHD professionals and some noisy birds. So, please forgive the extraneous sounds. Related resourcesMissUnderstood: The ADHD in Women ChannelDid my ADHD make me more likely to have postpartum depression?ADHD Powerbank: Sandra's video platformThe Head, Heart, Hormones foundation (in dutch with translations) Prevalence of hormone-related mood disorder symptoms in women with ADHD The heart health and ADHD connectionTimestamps(4:07) Swedish registry study data on diseases in people with ADHD(7:06) ADHD and hormones  (13:56) Cardiovascular disease in women(20:21) Talking to your doctor about diseases related to ADHDFor a transcript of this episode and more resources, visit the Hyperfocus page on Understood.org.We'd love to hear from you. Email us at hyperfocus@understood.org Understood is a nonprofit organization dedicated to empowering people with learning and thinking differences, like ADHD and dyslexia. If you want to help us continue this work, donate at understood.org/give

Today we've got another necessary conversation for so many of us — we're talking with Dr. Ellen Hendriksen about her new book How to Be Enough: Self-Acceptance for Self-Critics and Perfectionists, which came out January 7. It turns out, perhaps not surprisingly, that feeling a lack of enoughness is a widespread problem, and Ellen's book taught me so much about perfectionism — including that I apparently am one, even though I never would have thought that of myself. Perfectionism, as Ellen writes, can be used for good — it can help us have high standards, a strong work ethic, reliability, and a deep care of others — but it can also be used for ill, especially when it comes to our relationship with ourselves. Today on the show we explore the link between perfectionism and never feeling good enough; we talk about clinical perfectionism and where it stems from; how to stop putting our self-worth in the wrong places; seven shifts we can take to feel more enough; and so much more. Ellen has a Ph.D. from UCLA and completed her training at Harvard Medical School; she is a clinical psychologist at Boston University's Center for Anxiety and Related Disorders and, in addition to How to Be Enough, she also wrote How to Be Yourself: Quiet Your Inner Critic and Rise Above Social Anxiety. You might have seen her work everywhere from The New York Times to The Washington Post, BBC News, New York Magazine, Harvard Business Review, Psychology Today, Scientific American, The Guardian, Goop, O: The Oprah Magazine, and more, and she's here to help us stop being so hard on ourselves already.  How to Be Enough: Self-Acceptance for Self-Critics and Perfectionists by Dr. Ellen Hendriksen

In our world, emotional distress seems to be increasing. So, can we integrate biblical principles, evidence-based insights from psychology, and spiritual practices to help us master our emotions rather than allowing our emotions to master us? In this week's conversation on FrontStage BackStage, host Jason Daye is joined by Dr. Kevin Chapman. Kevin is a licensed clinical psychologist and the Founder and Director of the Kentucky Center for Anxiety and Related Disorders. He leads the Sound Mind Ministries and hosts The Sound Mind Show on YouTube. His most recent book is entitled Mastering Our Emotions. Together, Kevin and Jason have a hope-filled conversation about how we can master our emotions through biblical principles and the power of Christ. Kevin also touches on some of the realities and some of the misconceptions about negative emotions and gives us practical ways that we, as ministry leaders, can help others overcome negative emotions through the power of Christ.Dig deeper into this conversation: Find the free Weekly Toolkit, including the Ministry Leaders Growth Guide, all resource links, and more, at http://PastorServe.org/networkSome key takeaways from this conversation:Kevin Chapman on the connection between faith, intentionality, and the power of transformation that reaches both the heart and mind: "By partnering with the Holy Spirit and confronting those emotions, you're literally reprogramming your brain."Kevin Chapman on the importance of analyzing and understanding the broader aspects of emotions rather than solely experiencing or describing how they feel: "Focus on the features of emotions, not just the feelings of emotions."Kevin Chapman on the important role emotions play in guiding us through life and our spiritual journey: "Our emotions are meant to help us navigate our world, even to serve God, but we have to learn to regulate them."----------------Looking to dig more deeply into this topic and conversation? FrontStage BackStage is much more than another church leadership show, it is a complete resource to help you and your ministry leaders grow. Every week we go the extra mile and create a free toolkit so you and your ministry team can dive deeper into the topic that is discussed.Visit http://PastorServe.org/network to find the Weekly Toolkit, including the Ministry Leaders Growth Guide. Our team pulls key insights and quotes from every conversation with our guests. We also create engaging questions for you and your team to consider and process, providing space for you to reflect on how each episode's topic relates to your unique church context. Use these questions in your staff meetings, or other settings, to guide your conversation as you invest in the growth of your ministry leaders. Love well, live well, & lead well Complimentary Coaching Session for Pastors http://PastorServe.org/freesession Follow PastorServe LinkedIn | Twitter | Instagram | FacebookConnect with Jason Daye LinkedIn | Instagram...

High standards, attention to detail, and self-control are invaluable qualities at work. They're also aspects of perfectionism, something to which many high achievers credit much of their success. But Ellen Hendriksen, clinical psychologist at Boston University's Center for Anxiety and Related Disorders, says being your own worst critic can also lead to constant dissatisfaction at work and alienation from coworkers. Her new book is How to Be Enough: Self-Acceptance for Self-Critics and Perfectionists. Drawing on her own research, clinical work, and personal experience as a perfectionist, she explains where perfectionism comes from and how it affects teams. Hendriksen shares how not to be so hard on yourself—while still keeping your high standards.

Dr. Ellen Hendriksen is an author, anxiety specialist, and clinical psychologist at Boston University's Center for Anxiety and Related Disorders. Her work has been featured in the NY Times, Washington Post, Harvard Business Review, among others. Dr. Hendriksen will help you calm your anxiety and be your authentic self. Her most recent book, How to Be Enough: Self-Acceptance for Self-Critics and Perfectionists, is a clear and compassionate guide to help you be good to yourself. She is also the author of How to Be Yourself: Quiet Your Inner Critic and Rise Above Social Anxiety. For my podcast listeners, get your FREE copy of my Launch Your Dare 12-week Playbook - the perfect kickstart to your 2025 transformation! Here's what you need to do RIGHT NOW: Head over to www.idareyoupod.com and grab your copy of the Launch Your Dare 12-week Playbook. Don't wait - your future self will thank you! Connect with Ellen: www.ellenhendriksen.com Substack: How to Be Good to Yourself When You're Hard on Yourself Instagram: @ellen_hendriksen

At airports all over the world, luggage gets lost – sometimes forever. So, what happens to it? It can't sit there in baggage claim forever. Well, in the U.S. a lot of the lost luggage makes it way to a place in Alabama and the contents of that luggage can be yours for a price. Listen as I explain. https://www.unclaimedbaggage.com You have heard people say, “Happiness is a state of mind.” But it also might be a state of body. There is some wonderful news about how what you do with your body can significantly affect your level of happiness. In fact, your body is constantly sending messages to your brain about what it is experiencing which in turn affects what you think and how you feel. This is according to my guest, Janice Kaplan. She is a journalist and former editor of Parade magazine – and she is author of the book What Your Body Knows About Happiness (https://amzn.to/49XpSFj) It appears that a lot of people walk around with a nagging sense they aren't good enough – that they are not living up to their potential, that they should be doing better. If that sounds familiar, you need to hear my guest, Ellen Hendriksen. She is a clinical psychologist at Boston University's Center for Anxiety and Related Disorders whose work has been featured in The New York Times, The Washington Post, and Psychology Today, among others. She is here to reveal some fascinating insight into how feeling like you are not good enough is really a form of perfectionism. And she has some great suggestions to help anyone break free of all that self-criticism. Ellen is the author of How to Be Enough: Self-Acceptance for Self-Critics and Perfectionists (https://amzn.to/49YfIo6). Most of us accumulate a lot of receipts. For every purchase, there is a receipt. Often, we feel compelled to keep them but is that really necessary? Listen as I reveal which receipts to hold on to and which ones you can toss out. https://www.lifehack.org/articles/featured/receipts-which-to-keep-and-which-to-pitch.html PLEASE SUPPORT OUR SPONSORS!!! SHOPIFY:  "Established in 2025". Has a nice ring to it, doesn't it? Sign up for a $1 per-month trial period at https://Shopify.com/sysk . Go to SHOPIFY.com/sysk to grow your business! HERS: Hers is changing women's healthcare by providing access to GLP-1 weekly injections with the same active ingredient as Ozempic and Wegovy, as well as oral medication kits. Start your free online visit today at https://forhers.com/sysk Learn more about your ad choices. Visit megaphone.fm/adchoices

In this episode, we review the high-yield topic of ⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠Somatic Symptom and Related Disorders⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠ ⁠⁠⁠⁠⁠⁠⁠⁠from the Psychiatry section at ⁠⁠⁠⁠⁠⁠Medbullets.com⁠⁠⁠⁠⁠⁠ Follow ⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠Medbullets⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠ on social media: Facebook: www.facebook.com/medbullets Instagram: www.instagram.com/medbulletsofficial Twitter: www.twitter.com/medbullets Linkedin: https://www.linkedin.com/company/medbullets

Orofacial pain comprises many disorders with different etiologies and pathophysiologies. A multidisciplinary approach combining medication, physical therapy, and procedural and psychological strategies is essential in treating patients with orofacial pain. In this episode, Teshamae Monteith, MD, FAAN, speaks with Meredith Barad, MD; Marcela Romero-Reyes, DDS, PhD, authors of the article “Orofacial Pain,” in the Continuum® October 2024 Pain Management in Neurology 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. Barad is a clinical associate professor of anesthesiology, perioperative and pain medicine, and neurology and neurological sciences and codirector of the Stanford Facial Pain Program at Stanford Medicine in Stanford, California. Dr. Romero-Reyes is a clinical professor and director of the Brotman Facial Pain Clinic and Department of Neural and Pain Sciences at the University of Maryland in Baltimore, Maryland. Additional Resources Read the article: Orofacial Pain 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 @ContinuumAAN Host: @headacheMD Guest: @meredith_barad facebook.com/continuumcme Full episode transcript available here Dr Jones: This is Dr Lyell Jones, Editor-in-Chief of Continuum, the premier topic-based neurology clinical review and CME journal from the American Academy of Neurology. Thank you for joining us on Continuum Audio, which features conversations with Continuum 's guest editors and authors who are the leading experts in their fields. Subscribers to the Continuum Journal can read the full article or listen to verbatim recordings of the article and have access to exclusive interviews not featured on the podcast. Please visit the link in the episode notes for more information on the article, subscribing to the journal, and how to get CME. Dr Monteith: This is Dr Teshamae Monteith, associate editor of Continuum Audio. Today I'm interviewing Drs Meredith Barad and Marcela Romero-Reyes about their article on oralfacial pain, which appears in the October 2024 Continuum issue on pain management and neurology. Welcome to the podcast, ladies. How are you?  Dr Barad: Excellent.  Dr Romero-Reyes: Fine, happy to be here.  Dr Monteith: I am so happy to see you. I mean, I think both of you I've known for like ten years. Dr Romero-Reyes: Yeah.  Dr Barad: Yes.  Dr Monteith: So why don't you introduce yourselves? While I know you, our audience, some of them, may not know you.  Dr Romero-Reyes: I'm Dr Marcella Romero Reyes. I am a neuropathial pain specialist, clinical professor, and director of the Provident Special Pain Clinic here in the University of Maryland School of Dentist. Dr Monteith: Excellent.  Dr Barad: My name is Meredith Barad. I'm a clinical associate professor at Stanford and I work- I'm the codirector of our headache and facial pain clinic in the Stanford pain management clinic. Dr Monteith: Well, first of all, thank you for writing this article. It is extremely detailed and up-to-date and very informative. And in neurology, I think we don't get enough pain management. I'm interested in both of your backgrounds and, you know, what led you even to become an expert in this area? And both of you have complementary areas. I think we can see in the quality of this article. But why don't we start with you, Dr Romero-Reyes? Dr Romero-Reyes: Well, for me to get interested in orofacial pain, I will say more than an interest was like a calling that I wanted to take care of this patient population. So, as you know, my background is dentistry and at that time I was very interested in patients with complex medical issues. And was the time I was- I started to be interested in temporomandibular disorders. But what really picked completely my attention was the first time I saw a patient with trigeminal neuralgia. This was my last year in dental school. This patient already had, like, almost a full upper quadrant of teeth extracted where pain was not resolved. So when the patient came to us and I did my exam and, you know, and I triggered the pain, the sharp shoot electrical pain, that really broke my heart. And I took an x-ray and I didn't find anything that will explain it was something wrong until I talked to my professor and he said, no, this is medical. There's nothing wrong with it, with that tooth and needs to be, you know, followed with proper management and medication. And for me, that was like, wow, what a proper diagnosis and proper management can take care of these of these patients. And when the patient got better, that really said, oh, you know, I want to do this.  Dr Monteith: That's a crazy story. It's always that last patient of the day.  Dr Romero-Reyes: And you know, think about it, at least in dentistry at that time, I learned about trigeminal neuralgia from a book, right, my classes. But when you see the patient, this is it. That completely, you know, made me say yes, I want to study this.  Dr Monteith: Yeah. And unfortunately, that's not an uncommon scenario where patients with trigeminal neuralgia get, you know, their extractions and pain can sometimes be more complicated. What about you, Dr Barad? Dr Barad: Well, I guess I'm sort of like the opposite. So as a neurologist and a trained pain physician, I saw a lot of patients with neuralgic pain and headache pain, but I also saw many patients who would say, I have TMJ. And as, as Dr Romero has educated us, that's like saying I have shoulder or I have knee. But I quickly realized that I needed to work with a multidisciplinary team to really understand more about orofacial pain. It's not just neuralgic. There are other ideologies. And so that's how we started working together and that's how we practice in our clinic at Stanford. Dr Monteith: So, why don't you tell us about the objectives of this article? Dr Barad: I think our objectives were to help the neurologist broaden the differential diagnosis on facial pain to encompass below the nose, the oral cavity, the temporal mandibular joint. And to just think more broadly about facial pain and to understand some of the more recent diagnostic criteria that have been developed for facial pain and to- how to diagnose properly and how to begin treatment for some of the other conditions that are non-neurologic.  Dr Romero-Reyes: And I think I will ask about what Dr Barad say that also to bring awareness to the neurologist about the vast classification of oral facial pain disorder, craniofacial and orofacial. I think that was also a key thing too. And also, to show how well we can work together, you know, the multi-disciplinary management that is indicated for these cases. Dr Monteith: Cool. And you mentioned some of the new diagnostic criteria. I want to talk just briefly about the new international classification of orofacial pain, ICOP. When did that come out and what was the process there in really fine-tuning the diagnosis of orofacial pain disorders? Dr Romero-Reyes: So, in 2019 the orofacial head pain especially interest group of the International Association for the Study of Pain, the International Network for Orofacial Pain and Related Disorders methodology and the American Academy of Orofacial Pain and the International Headache Society. They partnered together to develop to develop this international classification of orofacial pain. And these, I think- it's such a great effort, you know, all the main people doing pain about this area, and goes very well together with the international classification of headache disorders. So, for example, you know, some disorders that International Classification of Headache Disorders doesn't present such as and the ICOP, International Classification of Orofacial Pain, presents, like the persistent idiopathic dental Viola pain. You have it in the ICOP. It's not, you know, mentioned in the in the International Classification of Headache Disorders, as well as, also we have the- I think it's item number five, the orofacial representations headache disorder or primary headache disorder. The ICOP gives you a nice, clean diagnostic criteria.  Dr Monteith: So, I guess I would ask Dr Barad with this classification in mind, how useful is it in neurology practice? And I know obviously you see patients with pain, but how useful even in managing patients with headache? Dr Barad: I think it's great because I've had a lot of dentists and ENT doctors who have started referring patients to me because they've realized that they've increased their awareness about orofacial pain and realized that pain in the sinuses, for example, accompanied by light sensitivity and sound sensitivity and rhinorrhea, may not be a recurrent monthly sinus infection. And so that kind of broadens our awareness of these of these disorders. And it's been, it's brought new patients into my clinic that we can help and treat. So that's been exciting.  Dr Monteith: And what about in the world of dentistry? Obviously, I think people in orofacial pain worlds are highly attuned to this, but I would hope this would hopefully have been disseminated into dentists and regular practice at C patients with trigeminal neuralgia. Dr Romero-Reyes: Going back for the, what you were discussing about the ICOP. So, it's what we're trying now as a new specialty. Well that we have been for the last four years, but finally in 2020 we have been recognized by the American Mental Association to disseminate this knowledge. But also, you know, can you imagine in in the realm in orofacial pain or dentistry have a patient with this recurrent pain, phonophobia, photophobia, throbbing dental pain is throbbing, but it's nothing wrong with your tooth. And that did they tell you that actually you have an orofacial or facial migraine or a neurovascular or facial pain. How crazy, right? And that is managed with migraines therapy. So it really, you know, to make you think like that. Wow, so these weird tooth things that used to come every week or these with facial pain, it's nothing to deal with, you know, with my teeth or any structure, you know, inside my mouth. Dr Barad: It sounds to me like what you're saying is that we've, this has encouraged patient education as well, not only interdisciplinary education, but really helping provide an explanation for the patient about what is going on with them. So rather than just getting sent away to another tertiary specialist, the patient is getting a more robust understanding of what's going on.  Dr Romero-Reyes: And going back to what you were saying about trigeminal neuralgia, you know, at least in dentistry also we're teaching now a new awareness like for two things, right? What about from the neurology setting? The patient has captured electrical pain. The trigger is intraoral. If it's pain inside your mouth, the first practitioner you're going to see who will be maybe the dentist that the dentist knows that could be a possibility of a disorder that doesn't deal with teeth, but also, it's important and we discussed that in our paper. What about that actually that weird trigger actually, it's not a general. What about if it's a cracked tooth has that singing sensation too. So, you see, it's two ways; one, to teach dentist to learn about this disorder and you know, we have learned, but you know, it's much more awareness now that this is great that, you know, these disorders you're not going to treat with dental procedures. Right? It's medical and vice versa, that the neurologist also has the awareness that oh, central trigger. Have you gone to the to the dentist? Have you checked that out? Dr Monteith: So what should neurologist know about dental sources of pain? Dr Barad: Well, maybe they should read the paper?  Dr Romero-Reyes: Yeah. Yeah, you need to read the paper. Yeah.  Dr Monteith: Top three, don't treat this with gabapentin.  Dr Romero-Reyes: Like well, dental pain is not going to be resolved with gabapentin. That would need to make a diagnosis if and you know it's that examination that come comes with a radiographic evidence that shows that maybe could be a cavity or could be a problem. You know in the in the practical tissues of the tooth that is given a symptomatology. Not only dental could be a lot of different disorders inside there now that can produce pain that also the readers can check our paper and learn about and see the wonderful interesting pictures that we have added there. Dr Monteith: Yeah. And so why don't we talk a little bit about TMD disorders and what is the new thinking around these conditions? Dr Romero-Reyes: Well, I will say for the last decade, maybe a little bit more has been a change in the evidence. They evidence based understanding of the theologia pathophysiologist and for mandibular disorders. Imagine that what's the shift in the in the paradigm that in dentistry prevails for a long, long time. That is that really focus and I will call it the pathological mechanistic point of view. What I mean by that I was focusing your bite, your occlusion, how the relation between in your maxilla mandible. That was the only issues that would create in temporomandibular disorders. So now we know that temporomandibular disorders are complex, are multifactorial and you need to understand them and see them within a biopsychosocial framework. And this dictate the main way to management for the primary way that we start will be conservative, reversible and basing evidence that the best evidence available that we have. Dr Monteith: And what about for trigeminal neuralgia? Is there newer kind of classification around trigeminal neuralgia? and what are some key points that we should consider when diagnosing these patients and treating these patients, Dr Barad?  Dr Barad: There haven't been any new diagnostic criteria, but I would say that there's been an increased awareness that classical trigeminal neuralgia is more likely than not related to neurovascular compression or we should say, maybe I should say neurovascular contact or compression. There is a developing grading system of that. That's an evolution as we speak. I think it's an exciting time for facial neuralgia because it's opened the door for us to look at other neuralgia also as vascular compressions and to think about how we can treat them with decompression or possibly with peripheral nerve stimulation or medicine or Botox. Or who knows what's the future is going to hold? But it is I think a change in the way we are thinking about the definition of neuralgia of, of trigeminal neuralgia in that is caused by a compression which is different than other neuralgia in other parts of the body. I should, I just want to classify there's about maybe ten twelve percent of people who present with classical trigeminal neuralgia who there is not evidence on imaging of a vascular contact or compression. But the majority of cases do seem to have some somewhere in the spectrum from contact to compression.  Dr Monteith: Even contact I find to be a bit vague sometimes say, well, thanks for letting me know that they're touching. But and then some of the neurosurgeons have different perspective when you open the patient up. So, I didn't know about the grading.  Dr Barad: Yeah, I think you've hit on it exactly like that is a big problem in the field right now. How do we understand what patients will be the best patients for surgery? And it used to be that you have the classical trigeminal neurologist symptomology plus some imaging that shows something versus nothing. And now we're getting into parsing out the imaging and trying to understand who's the best candidate for that with the imaging.  Dr Monteith: Dr Romero, anything to add?  Dr Romero-Reyes: No, that I agree about that, you know, and I think now maybe for the patients that I have seen with that, because under partial pain settings, sometimes we're the ones that, oh, actually what you have is trigeminal neuralgia idea, you know, so we start to have our small disciplinary management, but you know, when they come out, I already have an MRI doctor, but, and they say that these are compression, but what degree? And some patients that they don't have symptoms can have a compression. And I'm thinking maybe right that later on when we have more time and maybe nicer imaging, we're going to really find out or if it's the development angle is the measurement has some other characteristics, who knows. So, I think for trigeminal neuralgia, the things is still evolving, right? For our understanding. I have to help us to make a more- I will not say definitive diagnosis, but maybe some parameters will change in the future. Dr Monteith: So now we have a lot of people listening, international folks listening, and they always want some treatment, a tip, some clinical tips. So, can you give us a little bit of clinical insight to how to treat patients with trigeminal neuralgia and when you're seeing patients for second and third opinions, what might you see that may explain why their pain is not well controlled? We all get into interdisciplinary care, but in terms of pharmacology? Dr Barad: I think people are a little reluctant to use some of these medications that neuromodulating medications because, in general, it's an older population and they're rightly worried about falls and dizziness and confusion and low sodium. And so, I think they hesitate to go to the doses that are needed to help with pain control. So, a lot of our, my initial management is gingerly and gently titrating that to try to get to see if we can get control of the pain. Dr Monteith: Dr Romero?  Dr Romero-Reyes: I could add, for example, one thing that I in the realm of facial pain addition to pharmacology. Let's say that we have a patient with that intraoral trigger and we were able to localize that intraoral trigger. Sometimes we can even also use topical medication. And in the topical medication we can use, for example, an anticonvulsant, let's say gabapentin, oxcarbazepine for example, to add in the cream. And we use, we call it a neurosensory stent in my looks like a Nygard, but it's not a Nygard that can cover that area. So, the patient can add that cream very delimited in that area. And that helps, you know, can help with the pain sometimes. What we can find is that, at least in my, in my experience, and that when we add a topical, maybe we don't need to increase as much. The systemic medication, of course, depends from case to case.  Dr Monteith: So those are two great tips. Not being afraid to push those doses up in a safe manner and maybe with monitoring as well as of maybe utilizing more topicals. And I think we could probably hear a lot more from you on topicals at some other point. But thank you also for the table. I think it's, it's really nice the way all the treatments are laid out. So what other cranial neuralgia advances have there been? Dr Barad: I would say the main advancements have been in applying the knowledge that neurosurgeons have learned from microvascular decompression of the trigeminal nerve, to the glossopharyngeal nerve, to the geniculate nerve, and really trying to optimize imaging and optimize neurosurgical techniques to try to treat these neuralgias. If the patient has failed medicine, if the patient is a good candidate for surgery and if the patient desires that. Dr Monteith: Great. So now let's talk about multidisciplinary approaches. I know both of you are big fans of that, and you may do things a little bit differently at your institution, especially with your background. So maybe Dr Romero, do you want to tell us about your experience? And then we'll have Dr Brad. Dr Romero-Reyes: But in my experience from study management, let's say depend, of course, also the started we're talking about. But let's say for example about temporomandibular disorders, you know that for TMD is one of these overlapping pain conditions and we know that TMD is common with primary headache disorders, especially migraine. So, if we're able to utilize, you know, the expertise of neurologist specializing headache. With me, for example, or a facial pain person that is that is helping you manage a patient with this comorbidity. This is super effective because we know the presence of TMD in a migraineur can help the disorder to, to progress some more chronic form. So, you see, this is super important and effective to provide, you know, optimal care for the patient. For example, in the patients that I do see with neuralgias, like in addition to trigeminal neuralgia, let's say nervous intermediates neuralgia, that sometimes they can come to me like, oh, the pain is in my ear and my EMT or, or I think maybe it's my TMJ and for the pain is charged shooting inside the ear doesn't follow the for the diagnosis of temporomandibular disorders. And I can maybe help the patient to get a proper imaging or already penalize it with a neurologist to make sure. And maybe at least my way will be maybe I'm the one that can catch those disorders and help, you know, the patient to go for the next step. Dr Barad: I think Marcella, Dr Romero-Reyes, hit on a nice point that maybe this group is not as familiar with and that is that temporal mandibular dysfunction TMD is a, is one of the disorders that we call chronic overlapping pain conditions or COCPs. And those include headache. it's not, it's not specified fibromyalgia, irritable bowel syndrome, chronic pelvic pain and several other chronic pain syndromes. And they suggest a central sensitization to one's pain. And the way that we treat centrally sensitized pain is not just through medications, it's in a biopsychosocial framework because we see much higher rates of depression and anxiety in this group. And so, using a pain psychologist to help the patient develop coping strategies to help them manage their pain, using a physical therapist to help them learn this, the stretching exercises and using medications to help with not only with their pain syndrome, but also sometimes with their psych comorbidities. And then additionally, procedures sometimes play a role in the process to help usually turn down the pain. Interestingly, when we look at trigeminal neuralgia, we see much less overlapping pain disorders. It's much rarer to see somebody with TN who has other COCPs or the kind of chronic levels of depression and anxiety that we see in these patients. So, the approach is very different, and I think it requires the use of a multidisciplinary team to help guide the treatment pathways for these patients. Dr Monteith: Today, I've been interviewing Drs Meredith Barad and Marcelo Romero-Reyes, whose article on orofacial pain appears in the most recent issue of Continuum on pain management and neurology. 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 this 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.

Comments or feedback? Send us a text!Compulsive reassurance seeking can be a challenging issue for both clients and therapists to manage. Clients are often highly adept—sometimes knowingly, sometimes unknowingly—at eliciting excessive reassurance from therapists and family members. At the same time, resisting the urge to seek reassurance can feel nearly impossible for clients. In this episode, Amanda Petrik-Gardner, LCPC, joins us to discuss core themes from her new book, "The Compulsive Reassurance Workbook". Our conversation covers:What compulsive reassurance seeking is and its significance across various mental health presentations.Differentiating between normal reassurance seeking and compulsive reassurance seeking.Common triggers that lead to compulsive reassurance seeking.The importance of distress tolerance in managing reassurance-seeking behaviors.Mental health disorders that are more susceptible to compulsive reassurance-seeking behaviors.he cycle of reassurance seeking and how it perpetuates anxiety.Avoiding the use of clinical interventions (e.g., a thought record) as a safety behavior.Key components of the reassurance-seeking cycle.Effective metaphors for psychoeducation.Guidance for family members on navigating this specific challenge.Treating compulsive reassurance seeking in complex situations (e.g., trauma, pandemics, checking the accuracy of completed tasks).The role of “extinction bursts” in exposure-based work.Relapse prevention and normalizing setbacks.Understanding when to approach versus step back from a feared stimulus.Managing dysfunctional beliefs about worry.Feedback or comments?  Email us at: oicbtpodcast@gmail.comAmanda Petrik-Gardner, LCPC specializes in the treatment of Obsessive Compulsive and Related Disorders. Amanda is the creator of the OCD Exposure Coloring Books and The Compulsive Reassurance Workbook, now available on Amazon. Amanda is on the board for OCD Kansas, an affiliate of the IOCDF (International OCD Foundation) and the president of the Kansas Counseling Association. She has completed the Behavioral Therapy Training Institute through the IOCDF and the Professional Training Institute through the TLC Foundation for BFRBs. Amanda currently provides Teletherapy to the states of Kansas, Colorado, Nebraska, Missouri, Michigan, Maine, Arizona and Florida.https://www.amandalcpc.com

Drs. Peter Gerhardt and Shanna Bahry join me to talk about a range of topics centering around supporting adults with ASD and related disabilities. They are the authors of the new book, Make it Meaningful: Creating Programs that Matter into Adulthood for Learners with Autism Spectrum and Related Disorders. In this conversation, we talk about how ABA services are skewed towards younger populations, how programming for younger learners might look different if practitioners knew more about the unique needs of adult service recipients, risk aversion and other barriers to promoting independence, their 'wishlist' of skills that they'd like to see all adults with disabilities learn, having difficult conversations with parents, and lots more. Of course we discuss their book, the resources their book provides, and how these resources relate to other functional skills curricula that are out there... such as Essential for Living. You're also going to want to stay tuned for the entire conversation, because we close with some fantastic advice for just about everyone in this field. Here are links to some of the resources discussed in this episode: Where to get more info on the book, Make it Meaningful. Meaningful Hope ABA. The Epic School. Dr. Bahry on LinkedIn. Dr. Gerhardt on LinkedIn. Essential for Living. Bannerman et al. (1990). Balancing the right to habilitation with the right to personal liberties: The rights of people with Developmental Disabilities to eat too many doughnuts and take a nap. Rubin (2018). The Happiness Project, Tenth Anniversary Edition: Or, Why I Spent a Year Trying to Sing in the Morning, Clean My Closets, Fight Right, Read Aristotle, and Generally Have More Fun. This podcast is brought to you by the following: ACE Approved CEUs from .... Behavioral Observations. That's right, get your CEUs while driving (maybe even this episode!), walking your dog, doing the dishes, or whatever else you might have going on, all while learning from your favorite podcast guests! The 2024 Stone Soup Conference! Behavior Analysis' premier online event is taking place on October 25th. Come hear from pod faves including Drs. John Austin, Lina Slim, Jim Moore, and many others! 8.5 Learning CEUs are available, and when you use the promo code PODCAST24, that comes out to less than 8 bucks per credit. Learn more here! The Behavioral Toolbox. thebehavioraltoolbox.com is a new education and training site that my colleagues Anika Costa and Dr. Paulie Gavoni and I have been working on for over two years. We have two courses available: our first course, Ready, Set, Consult! and our newly released course, When Not to FBA: 5 Quick Strategies for Improving Behavior in Classrooms. Behavior University. Their mission is to provide university quality professional development for the busy Behavior Analyst. Learn about their CEU offerings, including their 8-hour Supervision Course, as well as their RBT offerings over at behavioruniversity.com/observations. Don't forget to use the coupon code, PODCAST to save at checkout!

"Vintage Offbeat" continues with our very first episode, from June 13, 2022. ORIGINAL DESCRIPTION: We all know office parties can be a drag, but for some, they can be more than uncomfortable. Recently, a court awarded a man who suffers from an anxiety disorder $450,000 for being subjected to an unwanted office party. Why do some people dismiss mental health issues such as anxiety, and why are some boundaries not respected? To find out, host Mike Rogers spoke with Dr. Kevin Chapman, founder and director of the Kentucky Center for Anxiety and Related Disorders.

Did you know there is a psychological approach to treating OCD that DOESN'T focus on preventing compulsions?To mark OCD Awareness Week, I am joined by Amanda Petrik-Gardner, a licensed clinical professional counsellor specializing in inference-based CBT (iCBT). We discuss the principles of iCBT, which differs from the traditional exposure and response prevention (ERP) approach. Instead, iCBT focuses on the reasoning process behind obsessional doubts rather than stopping compulsions. Our conversation highlights the concept of inferential confusion and the feared possible self, aiming to restore trust in the individual's real self. The conversation provides insights into the practical aspects of iCBT therapy, valuable insights into this purely cognitive approach that seeks to resolve the roots of obsessive doubt.  Highlights of the episode include:03:10 What is iCBT?04:02 Core Concepts of iCBT07:30 Research and Evidence for iCBT09:03 Inferential Confusion Explained12:39 Components Leading to Inferential Confusion18:34 The Feared Possible SelfThis week's guest:Amanda Petrik-Gardner, LCPC, LPC, LIMHP specialises in the treatment of Obsessive Compulsive and Related Disorders. Amanda is the creator of the OCD Exposure Colouring Books and The Compulsive Reassurance Workbook. Amanda currWhat did you think of this episode?More free downloads and resources to support your mental health and wellbeing: https://www.harleyclinical.co.uk/free-mental-health-downloadable-guidesJoin our email list for more mental health tips: https://mailchi.mp/harleyclinical/newsletter-sign-upFor private psychology services and therapy in person (London/Hertfordshire) or online, please visit Harley Clinical Psychology.*****************Subscribe to Dr Liz's YouTube channelFollow Harley Clinical on InstagramFollow Dr Liz White on InstagramFollow Dr Liz White on TikTok*****************DISCLAIMER - The Hello Therapy podcast and the information provided by Dr Liz White (DClinPsy, CPsychol, AFBPsS, CSci, HCPC reg.), is solely intended for informational and educational purposes and does not constitute personalised advice. Please reach out to your GP or a mental health professional if you need support.

Host Paul Bryson, MD, MBA is joined by a special guest for today's episode, as Eileen Meehan from Dysphonia International shares her journey. Listen to learn more about this condition and the latest innovations in treatment.

Clarissa W. Ong is a postdoctoral associate at the Center for Anxiety and Related Disorders at Boston University. She has done extensive research on perfectionism, OCD, hoarding disorder, and therapies such as Acceptance and Commitment Therapy (ACT) and process-based therapy. She recently authored The Anxious Perfectionist: How to Manage Perfectionism - a deep dive into how perfectionism aggravates anxiety, stress, and overall mental health.  In this episode we talk about: ◾️ What defines perfectionism ◾️ How perfectionism becomes a root problem for anxiety ◾️ Processing perfectionism through ACT Find Clarissa here: poislab.com Find Zach here: zachwesterbeck.com @zach_westerbeck The POIS Lab at the University of Toledo and Personalized Mental Health Lab at Southern Illinois University are researching the effects of two self-help interventions that aim to help people cope with problematic perfectionism. To learn more about participating in the study, please visit https://bit.ly/goodenoughstudy.  This podcast is made possible by NOCD. NOCD offers effective, affordable, and convenient OCD therapy. NOCD therapists are trained in Exposure Response Prevention, or ERP, therapy, the gold standard treatment for OCD. With NOCD, you can do virtual, live face-to-face video sessions with one of their licensed, specialty-trained therapists, and they accept most major 2insurance plans. If your insurance isn't covered, mention discount code ZACH100 for a special $100 rate for the next two months. To find out more about NOCD, visit zachwesterbeck.com/virtual-ocd-therapy/ to book a free 15-minute call. Zach Westerbeck is not a licensed medical professional. Zach Westerbeck is not trained in diagnosing psychological or medical conditions. Zach Westerbeck is not a substitute for medical care or medical advice. If you require assistance with any mental health or medical issue, please contact your health care provider for any medical care or medical advice. Zach Westerbeck makes no guarantees of any kind that the information or services provided by Zach Westerbeck will improve the client's situation. This podcast should not be considered medical advice. Please seek professional assistance from a licensed professional. Zach Westerbeck (https://zachwesterbeck.com/virtual-ocd-therapy/) Virtual OCD Therapy - Zach Westerbeck I've partnered with NOCD to bring you effective, affordable and convenient OCD therapy.

Text Dr. Lenz any feedback or questions Understanding ADHD in Women: Insights from ExpertsThis episode delves into the complex recognition and treatment of ADHD in girls and women. It features discussions from a recent American Professional Society for ADHD and Related Disorders conference, emphasizing the stigmatization and challenges in diagnosing ADHD in female patients. The episode explores the interplay between ADHD and conditions like chronic pain, chronic fatigue syndrome, fibromyalgia, and the impact of hormonal fluctuations on ADHD symptoms. Guest expert Dr. Littman shares insights on the high correlation between ADHD and negative outcomes such as suicidality, self-harm, early mortality, eating disorders, and overall lower quality of life in women. She also shares the connection between ADHD and abortion. It also covers the misdiagnosis and misunderstanding of ADHD in women, stressing the importance of awareness and tailored treatment to improve life quality.00:00 Opening Remarks a00:12 Exploring ADHD: Insights from the XR Conference01:01  Introduction and Mission01:28 ADHD Recognition and Misdiagnosis: A Deep Dive05:19 The Impact of Hormones on ADHD and Pain09:27 Addressing ADHD: Personal Stories and Clinical Insights22:17 The Importance of Support and Understanding ADHD27:14 Conclusion Support the Show.A Fibromyalgia Starter Pack, which is a great companion to the book Conquering Your Fibromyalgia, is now available. Dr. Michael Lenz practices general pediatrics and internal medicine primary care, seeing patients from infants through adults. In addition, he also will see patients with fibromyalgia and related problems and patients interested in lifestyle medicine and clinical lipidology. To learn more, go to ConquringYourFibromyalgia.com. Remember that while Dr. Lenz is a medical doctor, he is not your doctor. All of your signs and symptoms should be discussed with your own physician. He aims to weave the best of conventional medicine with lifestyle medicine to help people with chronic health conditions live their best lives possible. Dr. Lenz hopes that the podcast, book, blog, and website serve as a trusted resource and starting point on your journey of learning to live better with fibromyalgia and related illnesses.

Dr. Alessio Fasano, who is considered the world's leading expert in celiac disease and gluten-related disorders, returns for his second appearance on STEM-Talk. Although just 2 million Americans have celiac disease, an estimated 20 million Americans suffer from gluten sensitivity. Alessio is a professor and director of the Mucosal Immunology and Biology Research Center at Massachusetts General Hospital. In addition to celiac disease and gluten-related disorders, Alessio's research is also focused on the microbiome, intestinal permeability and autoimmune disorders, which he discussed in his first interview on STEM-Talk, episode 20. Since Alessio's first appearance on STEM-Talk in 2016, he has published two books, “Gluten Freedom” and “Gut Feelings: The Microbiome and Our Health,” which we discuss in today's interview. We also talk to Alessio about an exciting new project that's bringing together an international consortium of researchers and scientists for a long-term study that will follow infants who are genetically at risk of developing celiac. Alessio is a researcher and physician who wears many hats. He is the director of the Center for Celiac Research and Treatment and chief of the Division of Pediatric Gastroenterology and Nutrition at Mass General Hospital. He also is a professor of pediatrics at Harvard Medical School and a professor of nutrition at Harvard's T.H. Chan School of Public Health. Show notes: [00:03:58] Marcas opens the interview welcoming Alessio back to STEM-Talk, mentioning that since his last appearance he has written two books: Gluten Freedom and Gut Feelings: The Microbiome and Our Health. Marcas asks Alessio how he became interested in pediatrics and gastroenterology. [00:05:42] Ken mentions that Alessio moved to the U.S. in the 1990s and spent 20 years in Maryland at the Center for Vaccine Development in Baltimore. Ken goes on to mention that while Alessio was there, he founded The Center for Celiac Research in 1996, and in 2003, Alessio accepted an offer to join Massachusetts General Hospital. Ken asks how that move came about. [00:08:53] Marcas asks about Alessio's early career working on cholera, where he discovered the zonula occuldens toxin, the bacteria that causes cholera. Marcas asks Alessio to talk about this finding and the insights he gleaned from it. [00:16:03] Ken asks about Alessio's discovery of zonulin, which is the molecule that modulates gut permeability in humans. Ken asks Alessio to share how this discovery led him to investigate celiac disease, which is triggered by gluten. [00:20:25] Ken asks Alessio what his thoughts are on why the medical community, historically, has not taken celiac disease seriously. [00:24:08] Marcas mentions that as we age, there is evidence that the gut becomes leakier, which is highly related to chronic inflammation. Marcas asks Alessio whether this happens to the gut over time due to diet and lifestyle rather than the typical aging process. [00:28:45] Ken mentions that there has been an increase in the diagnosis of celiac disease. Ken asks Alessio if that is due to an actual increase in the prevalence of the disease, or is it tied to a growing appreciation that clinicians have now for the disease? [00:29:32] Marcas mentions that Alessio's book, Gluten Freedom, which he co-authored with his colleague Susie Flaherty, was referred to by the Celiac Disease Foundation as “a must have,” and “an excellent reference for those with gluten related disorders.” Marcas asks Alessio about this reception to his book. [00:31:24] Marcas mentions that the only viable treatment for individuals with celiac disease has been a gluten-free diet, with pharmaceutical companies having had little interest until recently in investigating the disease. Now there are more than 20 drug therapies in development for celiac. Marcas asks Alessio about the progress being made to develop pharmacological interventions for celiac.

It's Wildcard Wednesday!(Still on sabbatical, so here's a classic episode for you, originally a Self-Brain Surgery Saturday operation!)Every week, we'll learn a specific neuroscience operation you can master to change your mind and change your life. Today, we learn the basics, and we start with Self-brain surgery tip #19:“There is almost nothing outside you that will help in any kind of lasting way, unless you are waiting for a donor organ.” - Anne Lamott in her book Almost EverythingReal help comes from within, from the Spirit inside us! See John 14:26-27Learning how your brain works helps you see how to manage it in a healthier way. Here's five self-brain surgery techniques to help you change your mind and change your life.Leave a voicemail with your question or comment!Five Ways You Can Support this show:Pray for us!Subscribe, like, and share it with your friends! (We even have a YouTube channel!)Leave reviews and comments wherever you listen to podcasts!You can become a paid partner of the podcast and get special bonus episodes and lots more content by clicking here. Visit one of our affiliate partners and consider using their products (we use them every day):Improve your gut health, immune system, and protect your brain with Pique!Other Helpful Links:Click here to access the Hope Is the First Dose playlist of hopeful, healing songs!Be sure to check out my new book, Hope Is the First Dose!Here's a free 5-day Bible study on YouVersion/BibleApp based on my new book!Sign up for my weekly Self-Brain Surgery Newsletter here!All recent episodes with transcripts are available here! (00:03) - Introduction and Recap of Appearance on 700 Club (03:28) - Introduction to Self-Brain Surgery Tip Number 19 (07:41) - The Importance of Mental Health in Patient Care (09:27) - Understanding the Role of Neurochemistry in Happiness (11:16) - The Cost of Depression and Related Disorders (14:01) - Neuroscience Validates the Power of Mind over Brain (17:05) - Recognizing and managing negative thoughts (19:18) - Thinking about thoughts and questioning their validity (22:11) - Overcoming a bad attitude and its impact on happiness (25:12) - Letting go of regrets and living in the past (27:00) - Severing Sick Synapses (29:06) - Drain Your Doubts and Fill Up Your Faith (36:04) - Introduction and Book Promotion

To claim educational credit, please follow the link to the show notes. In a special episode, we discuss a complex, rare disease, fibrodysplasia ossificans progressiva, or FOP. Host Aaron Lohr talks with three guests: Eileen M. Shore, PhD, Cali and Weldon Research Professor in FOP and co-director of the Center for Research in FOP and Related Disorders at the University of Pennsylvania School of Medicine; Elisabeth Marelise W. Eekhoff, MD, PhD, endocrinologist, principal investigator, and medical specialist at Amsterdam University Medical Center in the Netherlands; and Michelle Davis, executive director of the International Fibrodysplasia Ossificans Progressiva Association. This episode is certified for 0.5 American Medical Association Physician’s Recognition Award (AMA PRA) Category 1™ credits and 0.5 American Board of Internal Medicine Maintenance of Certification (ABIM MOC) points. If you want those credits and points, you will have to browse to the Endocrine Society’s Center for Learning, take a pre-test, listen to this episode there, then take a post-test. This episode is supported by an educational grant from Ipsen Biopharmaceuticals Inc. Show notes, including link to the Center for Learning, are available at https://www.endocrine.org/podcast/enp84-fibrodysplasia-ossificans-progressiva — for helpful links or to hear more podcast episodes, visit https://www.endocrine.org/podcast

Dr. Monnica Williams is a professor at the University of Ottawa, where she holds the Canada Research Chair in mental health disparities. Her research is focused on mental health, race, racism and novel approaches to treatment. In this conversation, she is sharing about her research and tips for healing racial trauma based on the latest research.She also offers a call to action for players in the psychedelic space to improve diversity at all levels. We also discuss what a culturally informed psychedelic experience looks like, and what to look for in a guide if you're looking to heal racial trauma. This conversation offers support and hope for those who have been harmed by racial trauma. It also offers insights and language for those who aspire to be allies.Dr. Monnica T. Williams is a board-certified licensed clinical psychologist and Professor at the University of Ottawa in the School of Psychology, where she is the Canada Research Chair in Mental Health Disparities. She is also the Clinical Director of the Behavioral Wellness Clinics in Connecticut and Ottawa, where she provides supervision and training to clinicians for empirically-supported treatments. Prior to her move to Canada, Dr. Williams was on the faculty of the University of Pennsylvania Medical School (2007-2011); the University of Louisville in Psychological and Brain Sciences (2011-2016), where she served as the Director of the Center for Mental Health Disparities; and the University of Connecticut (2016-2019), where she had appointments in both Psychological Science and Psychiatry. Dr. Williams' research focuses on BIPOC mental health, culture, and psychopathology, and she has published over 200 scientific articles on these topics. Current projects include the assessment of race-based trauma, barriers to treatment in OCD, improving cultural competence in the delivery of mental health care services, and interventions to reduce racism. This includes prior work as a PI in a multisite study of MDMA-assisted psychotherapy for PTSD for people of color. She also gives diversity trainings nationally for clinical psychology programs, scientific conferences, and community organizations.Through the Kentucky Psychological Association (KPA), Dr. Williams served as the diversity delegate to Washington DC for the American Psychological Association (APA) State Leadership Conference for two consecutive years. She has served as the African American SIG leader for Association of Behavioral and Cognitive Therapies (ABCT), and currently is Chair of their Academic Training & Education Standards (ATES). She serves as an Associate Editor of Behavior Therapy. She also serves on the editorial board of Cognitive Behaviour Therapy, Canadian Psychology, International Journal of Mental Health, Journal of Psychedelic Studies, the Journal of Obsessive Compulsive and Related Disorders and the Cognitive Behavioural Therapist. She is a member of the Scientific Advisory Board of the International OCD Foundation and co-founded their Diversity Council. Her work has been featured in all major US and Canadian media outlets, including NPR, CBS, CTV, Huffington Post, and the New York Times.Topics Covered:What is racial trauma?Tools and research approaches that are applied to understand racial traumaTreatments developed for racial trauma by Dr. Williams, including psychedelicsCommunity and group work versus individual treatment for racial traumaDr. Williams' psychedelics for racial trauma research findingsIdeal set and setting when using psychedelics for healing racial traumaHow to vet your psychedelic guide for this workA culturally informed psychedelic experienceIntegrating a psychedelic experience when healing racial traumaIntentional steps the psychedelic space can take to diversifyShow Links:Apply for 1:1 Coaching with LanaWhere to find Dr. Monnica Williams:https://www.instagram.com/drmonnica/www.monnicawilliams.comDeliberate Practice in Psychedelic Assisted Therapy [book]Support Dr. Williams' research at mentalhealthdisparities.org Want more Modern Psychedelics?Instagram | YouTube | Web | Facebook Inspired to transform your life from the inside out, and integrate higher consciousness in your day to day life?Explore 1:1 Coaching with Lana or Apply Now This episode was produced in collaboration with FWI Media. Check out their beautiful work! Please support the show and leave a review if this episode sparked something within. FREEBIES to support your journey DISCLAIMER: Modern Psychedelics does not endorse or support the illegal consumption of any substances. This show is meant for entertainment purposes only. Modern Psychedelics does not sell or promote the sale of any illegal substances. The thoughts, views and opinions on this show should not be taken as life advice, medicinal advice, or therapeutic guidance.

This week Zorba and Karl discuss how your protein needs change as you age, and they talk about cannabis-related disorders and toxic effects. Plus, they share a delicious recipe for One pot taco soup.

This week Zorba and Karl discuss how your protein needs change as you age, and they talk about cannabis-related disorders and toxic effects. Plus, they share a delicious recipe for One pot taco soup.