Podcasts about nmosd

Krissy Dilger of SRNA hosted Dr. Benjamin Greenberg of UT Southwestern to share updates on the Q Study, a Phase 1 trial assessing the safety and feasibility of transplanting human glial restricted progenitor cells into the spinal cord of people who have been diagnosed with transverse myelitis (TM). Dr. Greenberg cautioned the audience against stem cell tourism [00:03:03]. He described the decades-long development of the cell line and safety monitoring for this study [00:01:35]. He reported no safety signals prompting a trial pause and noted the FDA-approved expansion of eligibility from non-ambulatory participants to those who can walk with assistance, while efficacy results were not yet being shared [00:08:31]. Finally, Dr. Greenberg outlined potential next steps, including Phase 2 studies and expanded populations (e.g., MOGAD and NMOSD diagnoses), as well as future targets [00:17:02].Benjamin M. Greenberg, MD, MHS is a Professor and the Cain Denius Scholar in Mobility Disorders in the Department of Neurology [https://utswmed.org/why-utsw/departments/neurology/] at UT Southwestern Medical Center in Dallas, Texas. He currently serves as the Vice Chair of Translational Research and Strategic Initiatives for the Department of Neurology. He is also the interim Director of the Multiple Sclerosis Center [https://utswmed.org/locations/aston/multiple-sclerosis-and-neuroimmunology-clinic/] and the Director of the Neurosciences Clinical Research Center. In addition, he serves as Director of the Transverse Myelitis and Neuromyelitis Optica Program and the Pediatric Demyelinating Disease Program at Children's Medical Center [https://www.childrens.com/specialties-services/specialty-centers-and-programs/neurology/demyelinating-disease-program].Dr. Greenberg earned his medical degree at Baylor College of Medicine before completing an internal medicine internship at Chicago's Rush Presbyterian-St. Luke's Medical Center. He performed his neurology residency at the Johns Hopkins School of Medicine. He also holds an M.H.S. in molecular microbiology and immunology from the Bloomberg School of Public Health, as well as a bachelor's degree in the history of medicine – both from Johns Hopkins. Prior to his recruitment to UT Southwestern in 2009, Dr. Greenberg was on the faculty of the Johns Hopkins Division of Neuroimmunology, serving as the Director of the Encephalitis Center and Co-Director of the nation's first dedicated Transverse Myelitis Center.Dr. Greenberg splits his clinical time between adult and pediatric patients at William P. Clements Jr. and Zale Lipshy University Hospitals, Parkland, and Children's Medical Center. His research focuses on better diagnosing, prognosticating, and treating demyelinating diseases and nervous system infections. He also coordinates clinical trials to evaluate new treatments to prevent neurologic damage and restore function to affected patients.00:00 Welcome and Guest Intro01:35 Origins of Q Study02:46 Getting Cells Into Cord04:49 Phase One Trial Design06:31 Safety and Efficacy Measures08:31 Eligibility Expanded Criteria11:39 Screening and Selection14:05 Travel and Site Logistics15:15 Early Safety Findings17:02 Next Steps After Phase One19:01 Beyond Idiopathic Myelitis23:07 Damage Differences by Disease25:20 Optic Nerve and Brain Targets27:29 Expected Outcomes and Vision28:58 Final Thanks

In the second part of this series, Dr. Justin Abbatemarco and Dr. Paulus Rommer discuss how to apply these study results into clinical practice.  Show citation:  Vietzen H, Kühner LM, Berger SM, et al. Epstein-Barr Virus Antibodies to Differentiate Multiple Sclerosis From Other Neuroinflammatory Diseases. JAMA Neurol. Published online March 9, 2026. doi:10.1001/jamaneurol.2026.0240  Show transcript: Dr. Justin Abbatemarco: Hello and welcome back. This is Justin Abbatemarco, and we're finishing up our interview with Paulus Rommer on his article on JAMA Neurology, Epstein-Barr Virus Antibodies that differentiate multiple sclerosis from other Neuroinflammatory Diseases. Paulus, can we talk about how we would apply your results into clinical practice right now? Dr. Paulus Rommer: The persistent high apnea antibody responses are a hallmark of multiple sclerosis. And in our micro center study, we found that the singular measurement is not sufficient to differentiate multiple sclerosis from other related disorders like MOGAD or NMOSD, but it's the repeated high levels over time. We see them in about 95% of our MS patients, but really rarely in MOGAD or NMOSD. So this persistent high levels is a good factor, with a high accuracy, to really diagnose multiple sclerosis and to differentiate them from MOGOD or NMOSD. Dr. Justin Abbatemarco: I think these are really helpful and I think a little more evolution in how we interpret these on individual patient level, like we talked about in the podcast, but more to come. Paulus, thank you again for all your work on this topic for coming on and we're excited to have you back in the future. Dr. Paulus Rommer: Thank you.   

Krissy Dilger of SRNA spoke with Matt Rathbun and Charlotte Engebrecht from the University of Rochester Center for Health and Technology about the Neuromyelitis Optica Spectrum Disorder-Health Index (NMOSD-HI) study, which aims to develop and validate an NMOSD-specific patient-reported outcome survey for use in clinical trials and routine care [02:25]. They explained that existing measures are often adapted from multiple sclerosis and may not reflect NMOSD patients' unique experiences [04:38]. They shared phase one insights from interviews with 15 individuals showing multi-system impacts [09:51]. They described eligibility for the current anonymous survey (adults 18+ with NMOSD, aquaporin-4 positive or negative, in the US, Canada, EU, UK, or Australia) and noted prior participants can join later phases [13:22]. You can learn more about the study here:https://redcap.link/nmo-hiQuestions can be sent to Matt and Charlotte:Matthew_Rathbun@urmc.rochester.eduCharlotte_Engebrecht@urmc.rochester.eduMatt Rathbun, BA, graduated from Nazareth University in May of 2025 and is currently pursuing his Master of Public Health degree at Nazareth University. At the University of Rochester Center for Health + Technology (CHeT), he works as a Human Subject Research Specialist, where he coordinates translational research studies focused on the lived experiences of individuals living with rare diseases. This work supports the development and validation of disease-specific PRO measures that capture aspects of disease burden most meaningful to patients. Matt's interests center on strengthening the relevance, inclusivity, and equity of clinical research. He aims to ensure that clinical research more accurately reflects the real-world impact of disease on patients' lives. He also works to advance more equitable and patient-centered approaches to treatment evaluation in rare disease communities.Charlotte Engebrecht, BS, is a graduate of Hobart and William Smith Colleges and a current Master of Science in Clinical Investigations student at the University of Rochester. She serves as a Clinical Trials Project Specialist at the University of Rochester Center for Health + Technology (CHeT), where her work centers on the development and validation of patient-reported outcome (PRO) measures for rare diseases. Charlotte conducts research that is grounded in a commitment to elevating the patient voice as a central pillar of clinical research. Patient-reported outcomes offer critical insight into how diseases and treatments truly impact daily life. She is particularly passionate about ensuring that these perspectives are not only included, but prioritized, in the design and evaluation of clinical trials. Her work focuses on rare diseases, with a specific interest in neuromyelitis optica spectrum disorder (NMOSD), where traditional clinical endpoints often fail to capture the full burden of illness. By integrating patient-centered measurement tools into therapeutic development, Charlotte aims to advance more meaningful and responsive approaches to evaluating new treatments.00:00 Welcome02:25 Study Overview04:38 Why Patient Voices Matter06:16 How the Study Works08:29 Who Can Participate09:51 Phase One Findings13:22 Join the Survey15:43 Wrap Up

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

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

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

In this SRNA "Ask the Expert" episode moderated by Krissy Dilger, Dr. John Chen of the Mayo Clinic answered audience questions about MOG antibody disease (MOGAD). He discussed diagnosis and the importance of titers and live cell-based assays given possible false positives [00:02:42]. Dr. Chen reviewed acute management with early high-dose steroids, prolonged tapers, and escalation to plasma exchange for severe or steroid-refractory attacks, as well as evolving long-term options including IVIG/subcutaneous IG and IL-6 blockade [00:04:14]. Audience questions covered relapse prediction, vision recovery timelines, fatigue, pregnancy, heredity, symptom interpretation, and whether to stop immunotherapy when antibodies become undetectable [00:12:13]. Finally, Dr. Chen described current and upcoming research, including a trial that is currently enrolling participants, and future prospects for optic nerve regeneration while cautioning against unproven stem cell clinics [00:41:37].John J. Chen, MD, PhD attended the University of Virginia for his undergraduate and combined MD/PhD degrees and completed his Ophthalmology residency and Neuro-Ophthalmology fellowship training at the University of Iowa. He then took a position at the Mayo Clinic in 2014 where he specializes in Neuro-Ophthalmology. Currently, he serves as a Consultant and Professor of Ophthalmology and Neurology, and Neuro-Ophthalmology Fellowship Director at the Mayo Clinic. Among Dr. Chen's awards and honors are the AAO Senior Achievement Award, Top Doctors in Minnesota, the Heed Fellowship, Real World Ophthalmology Inspiring Academic Leader Award, Ophthalmology Teacher of the Year Award four times leading to induction to the Educators Hall of Fame, and the Mayo Clinic Distinguished Educator Award – awarded to the top educator at Mayo Clinic in Rochester. He is an Associate Editor for Ophthalmology and the Journal of Neuro-Ophthalmology, has authored more than 250 peer-reviewed publications, and focuses his research on ophthalmic imaging, idiopathic intracranial hypertension, and optic neuritis, particularly NMOSD and MOG antibody–associated disease.00:00 Welcome and Introductions01:08 What Is MOGAD?02:42 Causes and Triggers03:23 How MOGAD Is Diagnosed04:14 Acute Attack Treatments06:35 Steroid Side Effects08:13 Testing During Treatment09:09 Long Term Therapies12:13 Interpreting MOG Positivity16:51 Eye Symptoms and Vision Fluctuations20:12 Antibody Titers and Severity21:19 Relapse Risk After First Attack23:09 Seizures and Encephalitis24:17 Vision Recovery After Optic Neuritis25:13 Acute Treatment Window25:57 Hereditary Risk Questions26:35 Stopping Azathioprine Safely29:56 Managing Post Attack Pain30:16 Steroids IVIG and Plasma Exchange32:08 Infections as Triggers33:01 Retesting MOG Antibodies35:01 Fatigue and Workup36:23 Prognosis and Life Expectancy37:45 Tinnitus and Brain Pressure39:05 Pediatric and Pregnancy Concerns41:37 Trials and Future Regeneration46:05 Research Resources and Wrap Up

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.

Die EMSP Conference 2026 ist eines der wichtigsten Events für Menschen mit Multipler Sklerose (MS), NMOSD und MOGAD – und du kannst kostenlos online teilnehmen. Auch wenn die Konferenz dieses Jahr in Berlin stattfindet, sind die Plätze vor Ort bereits ausgebucht. Umso besser: Du kannst alle Inhalte ganz bequem von zu Hause aus verfolgen und erhältst Zugang zu den neuesten Erkenntnissen aus Forschung, Versorgung und Patientenperspektive. Das diesjährige Thema:

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.

In SRNA's Ask the Expert episode moderated by Krissy Dilger, Dr. Elena Grebenciucova described neuromyelitis optica spectrum disorder (NMOSD) symptoms including optic neuritis, transverse myelitis, brainstem syndromes, and intractable hiccups [00:01:05]. She outlined diagnostic evaluation using MRI and correct blood-based antibody testing (preferably cell-based assays), common diagnostic pitfalls, and the need to rule out infections before immunosuppressive treatment [07:08]. Dr. Grebenciucova reviewed urgent relapse management with IV steroids and early plasma exchange, side effects, long-term preventive therapies (FDA-approved and off-label) [14:02]. Finally, she answered community questions on supplements, chronic optic neuritis, rehab appeals, pain/spasticity, pregnancy planning, long-term treatment duration, mental health, seronegative syndromes, follow-up frequency, and recovery expectations [25:22].Elena Grebenciucova, MD completed neurology residency at the University of Chicago in Chicago, Illinois. Dr. Grebenciucova has been interested in autoimmune disorders of the central nervous system, including rare neuroimmune disorders, since medical school. After residency, she completed a neuroimmunology Fellowship under the mentorship of Dr. Brenda Banwell and Joseph Berger at the Perelman School of Medicine of The University of Pennsylvania. Currently she is an assistant professor of Neurology (MS/Neuroimmunology) and neurological infections at Northwestern University in Chicago, Illinois, and she runs the Transverse Myelitis Center there. Dr Grebenciucova sees patients with rare autoimmune conditions including NMOSD, MOGAD, transverse myelitis, and autoimmune encephalitis.00:00 Welcome and Introduction01:05 What Is NMOSD?01:59 Symptoms and Relapse Signs03:27 What Causes NMOSD?07:08 How NMOSD Is Diagnosed10:09 Key Tests and Pitfalls14:02 Acute Attack Treatment17:18 Steroid Side Effects22:19 Long-Term Therapies Worldwide25:22 Community Questions, Beginning with Vitamins27:40 Optic Neuritis Breakthroughs28:47 Chronic Optic Nerve Inflammation29:19 Winning Insurance Appeals31:23 Waist Band Pain and Spasticity34:04 Pregnancy and Family Planning37:40 Stopping Long-Term Treatment39:40 Long-Term Side Effects43:04 Mood and Personality Changes49:47 Trials for Seronegative NMOSD52:55 Follow Up Visit Schedule55:34 Relapse Recovery Timeline58:02 Closing

In dieser Episode dreht sich alles um die Neuromyelitis-optica-Spektrum-Erkrankung (NMOSD) – eine seltene, aber oft schwer verlaufende Autoimmunerkrankung des zentralen Nervensystems. Im Interview spricht Luis Alfonso Zarco Montero, Neurologe und Neuroimmunologe aus Kolumbien, über aktuelle Therapie-Fortschritte, die Bedeutung einer frühen Diagnose und darüber, warum NMOSD klar von Multipler Sklerose unterschieden werden muss. Wir sprechen über typische Symptome, den Krankheitsverlauf, moderne monoklonale Antikörpertherapien, Herausforderungen beim Zugang zu Behandlungen und einen Ausblick auf personalisierte Therapien der Zukunft.

BIG ANNOUNCEMENT! Beginning January 5, 2026, SRNA is bringing all five of our podcast series together into a single, unified podcast channel called “SRNA Soundwaves.” This means that all episodes of "Ask the Expert, ABCs of MOGAD, ABCs of NMOSD, ADEM Academy, and Community Meets Clinic" - past and present - will now be found in one feed on Apple Podcasts, Spotify, and other podcast streaming platforms.What this means for you: If you are already subscribed to our "Ask the Expert" series, you will automatically be subscribed to "SRNA Soundwaves" once the merge happens on January 5th. If you are subscribed to "ABCs of MOGAD, ABCs of NMOSD, ADEM Academy, or Community Meets Clinic," make sure to subscribe to "Ask the Expert," which will be renamed “SRNA Soundwaves” on January 5th, to continue to get new episodes in your feed. You can subscribe here: https://creators.spotify.com/pod/profile/srna-ask-the-expert/We hope this change helps our community navigate our educational content more easily and enjoy a smoother, more organized podcast experience. If you have questions about the upcoming change, please email: podcast@wearesrna.org

SRNA's Krissy Dilger was joined by Dr. Hamza Coban to discuss neuromyelitis optica spectrum disorder (NMOSD) relapses. They discussed distinguishing between true relapses, pseudo relapses, and Uhthoff's phenomenon. Dr. Coban discussed the importance of early diagnosis and prompt treatment to prevent severe and debilitating symptoms. He described various treatments to prevent relapses. He also talked about the timing of relapses and when to consider switching therapies.

In this episode of "ABCs of NMOSD," host Landy Thomas, joined by Doug Newby, Heather Dawn Newbie, and Caitlyn Flickinger, discussed the impact of NMOSD on romantic relationships. The guests shared their personal experiences with relationships and how they manage living with NMOSD [00:02:27]. They also addressed how they met, support each other during treatment, and the importance of understanding and patience in relationships [00:09:37]. Finally, they provided advice on dating with a chronic illness and the significance of self-love and finding a supportive partner [00:35:06].Johnney (Doug) Newby lived most of his life in Colorado, only moving recently to Pennsylvania in the last year. Doug has a background in criminal justice and worked as a security guard the last few years in Colorado. Doug became symptomatic more than ten years ago with neuromyelitis optica spectrum disorder (NMOSD) spending many weeks in and out of hospitals with transverse myelitis (TM) and optic neuritis (ON). Doug is newly married to Heather ,who is also an NMO patient, and they're making a life together in Pennsylvania along with their dog, Bailey and their cats.Heather Dawn Newby has lived most of her life in Pennsylvania. After earning her bachelor's degree in Environmental Science and her master's degree in Environmental Studies, she returned home to her family's dairy farm where she utilized her degree focusing on sustainable agriculture. Heather also spent two summer seasons working in Alaska with the Fish and Wildlife Department focusing on sustainable fisheries. Heather first became symptomatic for neuromyelitis optica spectrum disorder (NMOSD) around 2004 and has since lost a good deal of her vision, but she is doing well otherwise. Heather is newly married to Doug, a fellow NMOSD patient, and they are creating a life together in Pennsylvania along with their dog, Bailey and their cats.Caitlyn Flickinger is a care partner to Landy Thomas, her fiancée, who has NMOSD. Starting college at only 14 years of age, Caitlyn is pursuing her bachelor's degree in political science, with minors in sociology and business. A prolific writer, Caitlyn spends most of her free time writing sci-fi books and letters to her soon-to-be wife, dreaming of one day breaking into the industry and getting her work published and in the hands of readers. Caitlyn also serves as president of the UCF student club she and Landy helped establish, called Epoch: A Minecraft SMP.00:00 Introduction and Guest Bios02:27 Meet Doug and Heather Newbie06:22 Meet Landy Thomas and Caitlyn Flickinger09:37 Doug and Heather's Love Story14:46 Landy and Caitlyn's Love Story20:00 Living with NMOSD25:50 Navigating Relationships with NMOSD26:38 Commitment and Understanding29:47 Challenges and Support35:06 Dating Inside and Outside of the Community47:00 Advice for NMOSD Patients on Dating55:17 Final Thoughts and Encouragement

Welcome to the NeurologyLive® Mind Moments® podcast. Tune in to hear leaders in neurology sound off on topics that impact your clinical practice. In this episode, "ECTRIMS 2025 Meeting Highlights and Clinical Takeaways," Daniel Ontaneda, MD, PhD, neurologist at Cleveland Clinic's Mellen Center for MS, shared his reflections from the 2025 ECTRIMS Congress, held September 24-26, in Barcelona, Spain. He discussed the significance of the updated MS diagnostic criteria, which generated immediate research applications and clinician discussion early in the meeting. Ontaneda also highlighted the growing emphasis on precision medicine and individualized treatment approaches, including extended-interval dosing strategies for B-cell therapies. In addition, he reviewed new therapeutic developments such as BTK inhibitors, CAR-T therapies, and remyelination research, noting both promising and disappointing data. Finally, he spoke on how ECTRIMS continues to expand beyond MS, with more presentations dedicated to NMOSD, MOGAD, and other autoimmune neurological conditions, reflecting the evolving landscape of neuroimmunology. Looking for more Multiple Sclerosis discussion? Check out the NeurologyLive® Multiple Sclerosis clinical focus page. Episode Breakdown: 1:00 – Overall impressions of ECTRIMS 2025, highlighting diagnostic updates, precision medicine, and late-breaking trial results 4:10 – Expanding focus on individualized care, especially interval-adjusted dosing strategies for B-cell therapies 7:50 – Neurology News Minute 9:50 – Insights on emerging therapeutic approaches including BTK inhibitors, CAR-T therapies, and remyelination strategies 14:35 – Growing attention toward NMOSD, MOGAD, and other autoimmune conditions within neuroimmunology discussions The stories featured in this week's Neurology News Minute, which will give you quick updates on the following developments in neurology, are further detailed here: EMA Approves Semaglutide as First GLP-1 RA for Cardiovascular, Stroke-Related Benefits Del-Zota Reverses Duchenne Disease Progression in 1-Year Trial Update MDA and PPMD Release Consensus Guidelines for Safe and Equitable Use of Gene Therapy in Duchenne Thanks for listening to the NeurologyLive® Mind Moments® podcast. To support the show, be sure to rate, review, and subscribe wherever you listen to podcasts. For more neurology news and expert-driven content, visit neurologylive.com.

Direct from Barcelona, listen to Alvaro Cobo Calvo from the Multiple Sclerosis Center of Catalonia (Cemcat) and host Brett Drummond discuss the highlights of ECTRIMS 2025 Pre-Day, which is focused on specialised topics in MS and related neuroinflammatory autoimmune diseases such as MOGAD and NMOSD.

The "Community Meets Clinic" podcast series introduces clinicians and healthcare personnel specializing in rare neuroimmune disorders. In this episode, Krissy Dilger moderated a discussion with Dr. Shuvro Roy of the University of Washington and Dr. Catherine Otten of Seattle Children's Hospital. Dr. Otten elaborated on her work with child neurology and pediatric neuroinflammatory disorders, while Dr. Roy discussed his research interests and the complexities of neuroimmunology [00:06:03]. They shared insights into their multidisciplinary clinic teams and how new patients can expect to be integrated into their care systems [00:11:01]. Both doctors highlighted the promising future of treatments for rare neuroimmunologic disorders and shared how they personally manage the emotional toll of their work [00:17:41]. You can view their medical profiles here:https://www.uwmedicine.org/bios/shuvro-royhttps://www.seattlechildrens.org/directory/catherine-ellyn-otten/Shuvro Roy, MD is an Assistant Professor of Neurology at the University of Washington, specializing in neuroimmunology, with a specific focus on multiple sclerosis (MS) and related neuroimmunologic disorders. He is Co-Director of the UW SRNA Center of Excellence for Rare Neuroimmune disorders. He is also a core teaching faculty member for the UW Medicine Multiple Sclerosis Center's fellowship program, contributing to clinical education and research initiatives like the ECHO MS program in collaboration with the National MS Society. Dr. Roy is actively engaged in projects aimed at improving access to care, addressing healthcare disparities, and enhancing patient safety for individuals living with MS and related conditions. He has co-authored recent research articles in medical journals on a variety of topics, including studies on stiff person syndrome, encephalomyelitis, MOG-antibody disorder, and multiple sclerosis treatment protocols. Dr. Roy is dedicated to helping his patients thrive amid challenging, lifelong neurological conditions.Catherine E. Otten, MD is a Clinical Associate Professor of Neurology at the University of Washington in the Neurology Department, specializing in child neurology and pediatric neuroinflammatory disorders. Dr. Otten is the Neuroimmunology Medical Director at Seattle Children's Hospital where she runs subspecialty programs for patients with rare neuroimmune conditions. She is board-certified in Pediatrics and Neurology. She leads the Pediatric Neuroimmunology clinic serving patients with multiple sclerosis, MOGAD, NMOSD, transverse myelitis, optic neuritis, acute flaccid myelitis, and other neuroimmune conditions. Dr. Otten co-leads the Inflammatory Brain Disorders Clinic, a multidisciplinary hub serving patients with autoimmune encephalitis, autoinflammatory disease, and other forms of brain inflammation. Her work extends across Alaska, where she has provided care in outreach clinics in rural Alaskan communities for the past decade. Her academic work includes collaboration with CDC as a consultant on acute flaccid myelitis, as well as published work on autoimmune encephalitis, demyelinating disease, and other neuroimmune conditions. She is committed to the care of pediatric patients with neuroinflammatory diseases and their families across the Pacific Northwest.00:00 Introduction02:01 Journey into Neurology and Neuroimmunology06:03 Research and Clinical Interests11:01 Multidisciplinary Clinic Teams17:41 Self-Care and Wellness25:04 Future of Rare Neuro Immune Disorders27:57 Conclusion and Final Thoughts

In this episode of the SRNA "Ask the Expert" podcast moderated by Dr. GG deFiebre, Dr. Kyle Blackburn and Dr. Benjamin Greenberg discussed the need for updated diagnostic criteria for myelitis. Dr. Blackburn explained the term myelitis and the importance of precise terminologies for accurate diagnoses and research [00:05:10]. Dr. Greenberg elaborated on the advancements in testing and understanding of associated disorders like NMOSD and MOGAD since 2002 [00:11:10]. Both experts stated that the shift from "transverse myelitis" to "myelitis" will aid future research, treatments, and patient care [00:17:27]. They reassured patients that these changes would essentially refine their care but not alter it dramatically [00:23:40]. They encouraged patients to stay informed and communicate with their healthcare providers about these updates [00:28:58].Kyle Blackburn, MD is an Assistant Professor in the Department of Neurology at UT Southwestern Medical Center in Dallas, Texas. He specializes in neuroimmunology and has clinical interests in antibody-mediated neurologic disorders, including autoimmune encephalitis, epilepsy, and ataxias; neurologic complications of cancers, including paraneoplastic disorders and checkpoint inhibitor/CAR T-cell toxicity; and demyelinating disorders, including sarcoidosis, neuromyelitis optica, myelin oligodendrocyte glycoprotein (MOG)-associated disease, and multiple sclerosis. Dr. Blackburn earned his medical degree at the University of Kentucky College of Medicine. He performed his residency in adult neurology at UT Southwestern, serving his final year as Chief Resident, and stayed to complete a fellowship in neuroimmunology, during which he earned the James T. Lubin Clinician Scientist Award from the Siegel Rare Neuroimmune Association (SRNA). He joined the UT Southwestern faculty in 2020.Benjamin M. Greenberg, M.D., M.H.S. is a Professor and the Cain Denius Scholar in Mobility Disorders in the Department of Neurology at UT Southwestern Medical Center in Dallas, Texas. He currently serves as the Vice Chair of Translational Research and Strategic Initiatives for the Department of Neurology. He is also the interim Director of the Multiple Sclerosis Center and the Director of the Neurosciences Clinical Research Center. In addition, he serves as Director of the Transverse Myelitis and Neuromyelitis Optica Program and the Pediatric Demyelinating Disease Program at Children's Medical Center.Dr. Greenberg earned his medical degree at Baylor College of Medicine before completing an internal medicine internship at Chicago's Rush Presbyterian-St. Luke's Medical Center. He performed his neurology residency at the Johns Hopkins School of Medicine. He also holds an M.H.S. in molecular microbiology and immunology from the Bloomberg School of Public Health, as well as a bachelor's degree in the history of medicine – both from Johns Hopkins. Prior to his recruitment to UT Southwestern in 2009, Dr. Greenberg was on the faculty of the Johns Hopkins Division of Neuroimmunology, serving as the Director of the Encephalitis Center and Co-Director of the nation's first dedicated Transverse Myelitis Center.Dr. Greenberg splits his clinical time between adult and pediatric patients at William P. Clements Jr. and Zale Lipshy University Hospitals, Parkland, and Children's Medical Center. His research focuses on better diagnosing, prognosticating, and treating demyelinating diseases and nervous system infections. He also coordinates clinical trials to evaluate new treatments to prevent neurologic damage and restore function to affected patients. 00:00 Introduction00:58 Overview of Myelitis and Diagnostic Criteria02:57 Historical Context and Importance of Updated Criteria05:10 Challenges with Current Terminology11:10 Changes in Understanding and Diagnostic Approaches17:27 Implications for Patients and Clinical Practice23:40 Impact on Research and Future Directions28:58 Patient Advocacy31:17 Conclusion

Dr. Justin Abbatemarco discusses updates around treatments in AQP4+ NMOSD.  Show references: https://pubmed.ncbi.nlm.nih.gov/38760098/ https://www.neurology.org/doi/10.1212/NXI.0000000000200071  

Victoria Jackson, the founder of No Makeup Makeup, was the first person to sell beauty via an infomercial. From there she built a makeup empire, became a medical trailblazer, and established a charitable foundation that helps fund research for neuromyelitis optica spectrum disorder (NMOSD). We talk to Victoria about her start in makeup, her thoughts on social selling and beauty today, what she loves about QVC, her bookstore, and, most importantly, how she tackles challenges and works through fear and anxiety to stay positive.Episode recap: fatmascara.com/blog/victoria-jacksonProducts mentioned in this episode: shopmy.us/collections/1578970 Sponsor links & discount codes: fatmascara.com/sponsorsPrivate Facebook Group: Fat Mascara Raising a WandTikTok & Instagram: @fatmascara, @jenn_edit, @jessicamatlin + contributors @garrettmunce, @missjuleeSubmit a "Raise A Wand" product recommendation: text us or leave a voicemail at 646-481-8182 or email info@fatmascara.com Become a member at https://plus.acast.com/s/fatmascara. Hosted on Acast. See acast.com/privacy for more information.

The "Community Meets Clinic" podcast series introduces clinicians and healthcare personnel specializing in rare neuroimmune disorders. In this episode hosted by Krissy Dilger of SRNA, we meet Dr. Michael Levy, a clinician from Massachusetts General Hospital. Dr. Levy is the Research Director of the Division of Neuroimmunology and Neuroinfectious Disease at Mass General and an Associate Professor at Harvard Medical School. He shared his journey into the field of neuroimmunology, discussed his research on the causes of MS, NMOSD, and MOGAD, and provided insights into the multidisciplinary clinic team at Mass General [01:27]. The episode also touched on the importance of understanding and reeducating the immune system to improve patient outcomes [15:22]. You can view the medical profile of Dr. Levy here:https://doctors.massgeneralbrigham.org/provider/michael-levy/1090088Michael Levy, MD, PhD is a recognized neurologist with over 15 years of clinical and research expertise in rare neuroimmunological disorders. He established the Neuroimmunology Clinic and Research Laboratory at Massachusetts General Hospital and is the Research Director in the Division of Neuroimmunology and Neuroinfectious Disease. Previously, Dr. Levy was on the faculty at Johns Hopkins University and was the founding Director of their Neuromyelitis Optica Clinic.Clinically, Dr. Levy cares for patients with MOG antibody disease (MOGAD), neuromyelitis optica spectrum disorder (NMOSD), and idiopathic transverse myelitis (TM). Dr. Levy is also the principal investigator (PI) on numerous patient studies and drug trials for new and improved treatments for these disorders. In 2022, Dr. Levy became the lead principal investigator for the two worldwide clinical trials in MOG antibody disease.In the lab, Dr. Levy's research focuses on the development of animal models of NMO and MOG with the goal of tolerization as a sustainable long-term treatment. Dr. Levy has more than 200 peer-reviewed research articles, reviews and editorials, and 3 patents covering NMO tolerization therapy, TM diagnostics, and stem cell regeneration approaches.00:00 Introduction00:54 Meet Dr. Michael Levy01:27 Dr. Levy's Journey into Neuroimmunology04:50 Research Focus and Discoveries08:54 Clinic Operations at Mass General12:12 Self-Care and Professional Fulfillment15:22 Future of Neuroimmunology16:52 Closing Remarks

"I thought my job was to save my daughter, but I realized my job was to show her how to live with strength and resilience." – Dr. Maggie Kang   We extend our sincere gratitude to our sponsor for this episode, Gebauer PainEase®. We are pleased to provide more information about this product, and we invite you to learn more by visiting their website. In this powerful episode, Dr. Maggie Kang shares her deeply personal journey as a physician and a mother navigating her daughter's rare disease diagnosis, Neuromyelitis Optica Spectrum Disorder (NMOSD). She discusses the emotional and medical challenges she faced, her transition into advocacy, and how she now supports families through life coaching. In an insightful conversation, Katie and Maggie explore the complexities of grief, resilience, and advocacy. Maggie opens up about the difficult moments in her daughter's diagnosis, how she learned to trust her instincts, and the importance of both self-care and community in the rare disease journey. Together, they discuss the emotional weight of parenting a child with a chronic illness and the ways families can empower themselves in the healthcare system.  What You'll Take Away from This Episode:

In this episode of "Ask the Expert," Dr. Eoin Flanagan joined Dr. GG deFiebre of SRNA. Dr. Flanagan explained how immunosuppressive medications impact the immune system and the efficacy of vaccines [00:02:45]. He discussed the primary concerns and risks of vaccinating individuals on these therapies, including avoiding live vaccines and the need for additional booster doses [00:04:52]. Dr. Flanagan also talked about the recommended vaccines for those with conditions like NMOSD or MOGAD, and underlined the importance of getting vaccinated to prevent severe infections [00:09:40]. He addressed common misconceptions and emphasized the role of healthcare providers in educating and supporting their patients regarding vaccinations [00:15:32].Eoin Flanagan, MB, BCh is a Professor of Neurology and Consultant in the departments of Neurology and Laboratory Medicine and Pathology at the Mayo Clinic (Rochester, MN). He completed his medical school training at University College Dublin in Ireland in 2005. He did a medical residency in Ireland and then completed neurology residency, fellowships in neuroimmunology and a masters in clinical and translational science at Mayo Clinic (Rochester, MN). He works in the Autoimmune Neurology and Multiple Sclerosis Clinics and the Neuroimmunology Laboratory at the Mayo Clinic. His clinical expertise and research are focused on inflammatory myelopathies and their imaging patterns, myelin oligodendrocyte glycoprotein (MOG) antibody associated disorder, neuromyelitis optica spectrum disorders, autoimmune encephalitis, paraneoplastic neurologic disorders, and multiple sclerosis. He is principal investigator on an NIH RO1 grant studying MOG antibody associated disorder.00:00 Introduction 00:47 Understanding Immunosuppressants and Vaccines01:28 Primary Concerns with Vaccinating Immunosuppressed Patients02:30 Recommended Vaccines for Immunosuppressed Patients07:11 Timing and Effectiveness of Vaccinations08:21 Measuring Vaccine Response09:24 Addressing Missed Doses and Safety Considerations16:41 Public Health Implications and Patient Advocacy17:56 Advice for Vaccine-Hesitant Patients19:06 Healthcare Providers' Role in Vaccination20:03 Conclusion and Final Thoughts

In the "ABCs of NMOSD" episode, Landy Thomas of SRNA was joined by Heather Dawn Sowalla and Dr. Meghan Beier to discuss post-diagnosis body dysmorphia in NMOSD patients [00:00:12]. Heather shared her misdiagnosis journey, the impact of steroids, and her coping mechanisms [00:06:24]. Dr. Beier highlighted the importance of finding a supportive community and suggested strategies for managing new identities and body perception [00:08:02]. Both emphasized the significance of connecting with others and seeking professional help to navigate these challenges [00:11:25].Heather Sowalla has lived most of her life in Pennsylvania. After earning her bachelor's degree in Environmental Science and her master's degree in Environmental Studies, she returned home to her family's dairy farm where she utilized her degree focusing on sustainable agriculture. Heather also spent two summer seasons working in Alaska with the Fish and Wildlife Department focusing on sustainable fisheries. Heather first became symptomatic for NMOSD around 2004 and has since lost a good deal of her vision, but she is doing well otherwise. Heather is newly engaged to Doug, a fellow NMOSD patient, and they plan on creating a life together in Vintondale, Pennsylvania.Meghan Beier, PhD is on faculty at Johns Hopkins and is a Health and Rehabilitation Psychologist specializing in multiple sclerosis at the Rowan Center for Behavioral Medicine. Dr. Beier completed her PhD in Clinical Psychology, Health Emphasis, from Yeshiva University then completed a postdoctoral fellowship, funded by the National MS Society, at the University of Washington where she focused on the rehabilitation, cognition, and mental health of individuals living with MS.Dr. Beier has been featured in well-known publications such as the New York Times, People Magazine, and Psychology Today. She is an internationally invited keynote speaker and also an active consultant and speaker for organizations such as National MS Society, Can Do Multiple Sclerosis, and more. Dr. Beier's research interests include neuropsychological outcomes for individuals living with MS; cognitive rehabilitation; and behavioral approaches to wellness. She continues to remain active in research as an adjunct faculty member of Johns Hopkins University School of Medicine.Dr. Beier's passion for improving care for people living with challenging medical conditions led her to create Find Empathy, which provides a free directory of mental health providers that specialize in working with medical populations. Find Empathy also provides continuing education for mental health professionals focused on how best to serve those living with or affected by life altering illnesses.https://www.nationalmssociety.org/https://cando-ms.org/https://scholar.google.com/citations?user=KUPu4O4AAAAJ&hl=enhttps://findempathy.com/https://findempathy.com/learn/00:00 Introduction01:10 Meet the Guests: Heather Sawala and Dr. Megan Beier03:26 Heather's Diagnosis Journey05:04 Dr. Beier's Work and Find Empathy08:02 Discussion on Post-Diagnosis Body Dysmorphia11:25 Coping Strategies and Personal Experiences24:57 Advice for Newly Diagnosed Patients33:18 Final Thoughts and Resources

In this inspiring episode of It Happened To Me, hosts Cathy and Beth sit down with Alex Brito, a remarkable advocate in the rare disease community and one of the first 100 individuals diagnosed with neuromyelitis optica spectrum disorder (NMOSD). NMOSD is a rare neurological disease that affects an estimated 6,000 Americans, causing severe and unpredictable relapses that can lead to vision loss, chronic pain, and paralysis. Alex shares her journey, from the challenges of misdiagnosis and temporary paralysis to her empowering outlook on life with NMOSD—she affectionately refers to the condition as “her bestie.” Alex's dedication to advocating for individuals with disabilities is evident in her work teaching adaptive technology to those with vision loss. Her incredible resilience is matched by her active lifestyle, which includes powerlifting and earning the distinction of being the first blind woman to achieve a yellow belt in Krav Maga. Listeners will also learn about Alexion's short film, Rare Connections in NMOSD (Accessible Version), which highlights Alex's story and helps raise awareness about this rare disease. Key Takeaways: What is NMOSD, its symptoms, and the challenges in diagnosing this rare condition. Alex's personal journey with NMOSD, including vision loss, paralysis, and finding strength in adversity. The importance of adaptive technology and how Alex empowers individuals with vision loss. Alex's inspiring accomplishments as a powerlifter and martial artist. Insights into Alexion's short film Rare Connections in NMOSD and its impact on awareness and advocacy. Resources Mentioned in This Episode: Watch Alexion's short film, Rare Connections in NMOSD here Alex mentioned using JAWS, a screen reading program for those with vision difficulties Support organizations for NMOSD that Alex recommends in the episode are The Guthy-Jackson Foundation and The Sumaria Foundation Learn more about NMOSD through the organization NMOSD Won't Stop Me  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. 

E435 Alex Brito has Neuromyelitis optica spectrum disorder (NMOSD), a rare condition that targets the central nervous system. It can cause vision loss, chronic pain, and paralysis. Despite challenges—including an initial misdiagnosis, blindness and temporary paralysis, Alex helps others with disabilities and teaches adaptive technology to those with vision loss. She's also the first blind […]

In this episode, our guest, Tamar (Tay-mar) Thompson with us, the Head of Corporate Affairs at Alexion, AstraZeneca Rare Disease. With over 20 years of experience in healthcare, Tamar leads global corporate efforts in policy and advocacy. She recently has been showcasing Alexion's new short film, Rare Connections in NMOSD where she underscores the need to raise awareness of NMOSD, a rare neurological disease, to help reduce the time to diagnosis and advance care. A dedicated advocate for health equity, Tamar continues to highlight the unmet needs of the rare disease community.TopicsNeuromyelitis optica spectrum disorder (NMOSD): diagnosis, prevalence/incidence, overview of symptoms, and why it's so important to raise awareness of rare diseasesRare Connections in NMOSD and why Alexion created this first-of-its-kind short filmWhat Alexion is doing to help improve equity and health outcomes for people living with rare diseasesUnveiling Connections: The Story Behind Alexion's Groundbreaking Film on NMOSD• Bridging the Gap: Confronting the Diagnostic and Care Challenges in Rare Diseases• Left Behind: Addressing Health Equity for the Rare Disease Community• Global Voices: How Alexion Shapes Policy to Transform Rare Disease Care• Driven by Purpose: Alexion's Journey to Champion Rare Disease AdvocacyGuest - Tamar ThompsonLinkedIn: - https://www.linkedin.com/company/alexion-pharmaceuticals/- https://www.linkedin.com/in/tamarthompson/Facebook: https://www.facebook.com/AlexionPharmaceuticalsInc/Twitter/X: https://x.com/alexionpharma?lang=eYouTubehttps://www.youtube.com/@alexionpharmaceuticalsinc.3357Rare Connections Film: https://youtu.be/cfnE7cxfY3s?si=zozSq2NZK8kb2i6kRare Connections Film (Accessible Version): https://youtu.be/dwKpZQSZuZ0?si=77UN5QaRJNuM2rnmHost - Hillary Blackburn, PharmD, MBAwww.hillaryblackburn.comhttps://www.linkedin.com/in/hillary-blackburn-67a92421/ @talktoyourpharmacist for Instagram and Facebook ★ Support this podcast on Patreon ★

In this "Ask the Expert" episode titled, "Women's Health within Neuroimmunology," Dr. Sonia Singh joined Krissy Dilger of SRNA to share women's health concerns within the context of neuroimmunology, focusing on issues like fertility and pregnancy for those with rare neuroimmune disorders [00:01:20]. Dr. Singh discussed how certain conditions, such as neuromyelitis optica spectrum disorder (NMOSD) and autoimmune encephalitis, and medications could impact fertility [00:03:45]. They also explored the increased risks of relapse during and after pregnancy and the importance of coordinated care between neurologists and obstetricians [00:07:10]. Dr. Singh emphasized the importance of teamwork during pregnancy to ensure optimal outcomes for both mother and child [00:21:45]. Sonia Kaur Singh, MD is a Neurologist and Assistant Professor of Neurology at Medical University of South Carolina (MUSC), Charleston who specializes in Neuroimmunology. Dr. Singh obtained her medical degree from Kasturba Medical College, Mangalore in Southern India. After graduation, she worked with dementia specialists in India studying dementia in culturally and linguistically diverse populations. She completed her neurology residency at University of Texas Health Science Center Houston (UTHealth Houston) in the Texas Medical Center. During residency, she was involved with innovative learning strategies including a structural competency curriculum and graduated with the prestigious Frank Yatsu Award for Excellence in Clinical Neurology. After residency, she completed a one-year fellowship in Multiple Sclerosis and Neuroimmunology from UTHealth Houston where she was actively involved in medical education and clinical trials. Dr. Singh has a special interest in women's health and cognition in neuroimmune conditions.

Drs. Justin Abbatemarco, Marius Ringelstein, and Ilya Ayzenberg discuss a new class of complement inhibitors that we're using in NMOSD. Show reference: https://www.neurology.org/doi/full/10.1212/WNL.0000000000209888

Dr. Justin Abbatemarco talks with Drs. Marius Ringelstein and Ilya Ayzenberg about the effectiveness and safety of Eculizumab in routine clinical care. Read the related article in Neurology. Disclosures can be found at Neurology.org.

In the "ABCs of NMOSD" episode titled, "Managing the Dread of Relapse," Landy Thomas of SRNA was joined by Heather Dawn Sowalla. Heather shared her journey with neuromyelitis optica spectrum disorder (NMOSD) [00:01:54] and discussed the fear of relapse associated with the condition [00:14:04]. She described how long-term misdiagnosis and numerous flares impacted her life and mental health [00:16:02]. She shared coping strategies and emphasized the importance of a supportive community and the advancements in NMO treatment [00:25:49]. Finally, Heather encouraged those newly diagnosed to seek a doctor they connect with and lean on the community for support [00:34:12].Heather Sowalla has lived most of her life in Pennsylvania. After earning her Bachelors degree in Environmental Science and her Masters degree in Environmental Studies, she returned home to her families dairy farm where she utilized her degree focusing on sustainable agriculture. Heather also spent two summer seasons working in Alaska with the Fish and Wildlife Department focusing on sustainable fisheries. Heather first became symptomatic for NMOSD around 2004 and has since lost a good deal of her vision, but she is doing well otherwise. Heather is newly engaged to Doug, a fellow NMOSD patient, and they plan on creating a life together in Vintondale, Pennsylvania.

In the “ABCs of NMOSD” episode titled, “Social Reintegration Following an NMOSD Diagnosis,” Landy Thomas of SRNA and Kim Jackson-Matthews discussed social reintegration following an NMOSD diagnosis [00:00:14]. Kim shared her diagnosis story, including the onset of symptoms and the challenges she faced [00:04:42]. They talked about the emotional impact of the disease, how it changed Kim's life, and her strategies for maintaining a social life despite her condition [00:22:34]. Kim also offered advice for others dealing with NMOSD on how to stay connected and live their best life [01:19:17].Kim Jackson-Matthews, a past Continuity Director with KCBS-FM / Jack93.1 radio station, is well known in the rare patient community for being an advocate for Neuromyelitis Optica Spectrum Disorder, NMOSD. Her passion for helping people with rare diseases and those in underrepresented areas along with her personal experience with chronic disease has leveraged her as the Diversity, Equity, Inclusion and Accessibility Liaison with the Guthy-Jackson Charitable Foundation. As a 2nd degree Black Belt in Taekwondo, she is very passionate about health and wellness. For over twenty-five years Kim has been a licensed Personal Fitness Trainer whose focus is to educate and motivate people to, “Just Keep Moving!” Kim has held the office of Co-Chair of the Physical and Mental Health Committee as a member of Delta Sigma Theta Sorority, Inc. Los Angeles Alumnae Chapter and was excited to spread the word about NMOSD during their Self-Care Summit: Seven Days of DeltaCare now on YouTube. Kim has gone to Washington, DC for Rare Disease Week on Capitol Hill with RDLA to speak to state stakeholders. She will continue to use her voice to advocate for those who can't do so for themselves.https://www.youtube.com/playlist?list=PLOLU7_4RDHZlPqQq42qkHaFkmwFWcTVyU

This bonus episode of Continuum Audio features Continuum Aloud, a program of verbatim audiobook-style recordings of Continuum articles. In this episode, Dr. Michael Grasso reads the NMOSD and MOGAD article from the August 2024 issue on Autoimmune Neurology.  This article is open access until December 2, 2024. Read it here. Continuum Aloud is available to Continuum subscribers at the article level on ContinuumJournal.com or on the AAN's Online Learning Center at continpub.com/Aloud. For more information on subscribing to the journal visit shop.lww.com/continuum.

Awareness of the specific clinical and MRI features associated with AQP4-NMOSD and MOGAD and the limitations of currently available antibody testing assays is crucial for a correct diagnosis and differentiation from MS. Growing availability of effective treatment options will lead to personalized therapies and improved outcomes. In this episode, Gordon Smith, MD, FAAN speaks with Elia Sechi, MD, author of the article “NMOSD and MOGAD,” in the Continuum August 2024 Autoimmune Neurology issue. Dr. Smith is a Continuum® Audio interviewer and 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. Sechi is a neurology consultant in the neurology unit of the Department of Medical, Surgical and Experimental Sciences at the University Hospital of Sassari in Sassari, Italy. Additional Resources Read the article: NMOSD and MOGAD Subscribe to Continuum: shop.lww.com/Continuum Earn CME (available only to AAN members): continpub.com/AudioCME Continuum® Aloud (verbatim audio-book style recordings of articles available only to Continuum® subscribers): continpub.com/Aloud More about the American Academy of Neurology: aan.com Social Media facebook.com/continuumcme @ContinuumAAN Host: @gordonsmithMD Guest: @EliaSechi 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 Smith: Hello. This is Dr Gordon Smith. Today, I've got the great pleasure of interviewing Dr Elia Sechi about his article on aquaporin-4 antibody-positive NMOSD and MOGAD, which appears in the August 2024 Continuum issue on autoimmune neurology. Dr Sechi, before we dig into this really exciting topic about NMOSD and MOGAD, perhaps you can tell our listeners a little bit about yourself, where you practice, how you got interested in this topic.   Dr Sechi: Hi, Dr Smith, and thank you for having me. So, my story begins here in Italy, actually - I did my med school and residency in neurology at the University Hospital of Sassari here in Sardinia. And after residency, I was lucky enough to be accepted at the Mayo Clinic in Rochester, Minnesota for a research fellowship - and that's where I spent the next three-and-a-half years, approximately. My fellowship was focused on autoimmune neurology, specifically demyelinating diseases of the CNS associated with antibodies – so, of course, NMOSD and MOGAD mostly, but also myelitis, MS, and autoimmune encephalitis – so, there's where I built most of my expertise in the field. And then, it was at the beginning of the pandemic (of the COVID pandemic) that I came back here to Italy to practice. And now, I work mostly as a neurohospitalist, and I also have my subspecialty outpatient service for patients with autoimmune neurological diseases.   Dr Smith: I wonder if you might just give us a minute or two about what it was like training in Mayo? I went to medical school there, and, you know, at the time, I thought that was just normal healthcare and normal training, and, you know, it was only later that I realized how amazing that was. I mean, this is where aquaporin-4 was discovered - I mean, what was that like? It must have been really cool training there with that team.   Dr Sechi: Yeah. You know, it's the temple of autoimmune neurology. It's fantastic. It's a great environment, very stimulating. You know, I think the great strength is that they see many patients with rare diseases, so, you get really confident with MRI features and clinical features with the history of the diseases, and this is important to recognize the typical features and differentiate from MS to do a good differential. And, of course, you know, the team is fantastic - superstars in the field. It's very, very stimulating. So, it's something that I definitely recommend. It was a fantastic experience.   Dr Smith: Well, you know what's great is, I don't know if you follow sports, but, you know, like, in the United States and college football, people refer to Gator Nation – right, these are all people who are fans of the Florida Gators. Or, maybe it's AC Milan nation in Italy. I don't want to get there (Roma, whatever), but there are all these people who've trained at Mayo, and, uh, what's great is it's a small world, right? So, I'm super excited to meet you and talk about this, because - I'm going to add you to my Rolodex, because when I see these patients (I'm a neuromuscular guy, but I do a fair bit of inpatient time), I'm always calling a small number of people, so I'm really pleased to meet you so I can put you on speed dial and ask you questions about these patients. I wonder if, maybe, we can begin? You know, in our preparatory discussions, I shared that I just came off our hospital service, and we had several of these patients, you know, where we were thinking about NMO or MOGAD as a cause for their problem - and I wonder if you just have any pearls or pitfalls in when we should suspect this, right? Most of us recognize bilateral optic neuritis, longitudinally extensive myelitis - we need to be thinking about these. Any pearls or pitfalls for when we should or should not be looking for these disorders?   Dr Sechi: Yeah, I think this is a great question. I think the first thing to pay attention is the phenotype. So, the clinical MRI phenotype that are typically associated with NMOSD and MOGAD, they are quite characteristic - and it's important to be aware of those phenotypes and how they differ from MS, because in my experience, one of the common misinterpretation (misconception) in clinical practice is just to test for AQP-4 and MOG antibodies in any patient with new-onset demyelinating disease of the CNS, even if it's typical MS. And, this is quite wrong, because MS is way more common in clinical practice - it's sixty, eighty times more common than NMO and MOGAD - and so, if you test all those patients without filter (indiscriminately) for antibodies, you increase the risk of false positivity exponentially, even if you have a highly specific test. So, first of all, I think it's good to select the right patients to test. As you said, patients with LTM, extensive involvement of the optic nerves on MRI, ADEM - there's also patients with cortical encephalitis phenotype (which is a rare phenotype of MOGAD), but not definitely good to test the typical MS patients. This is the first thing.   Dr Smith: Yeah, I mean, that's an issue in all of neurology, isn't it, right? I mean, it's an issue in sort of just sending, you know, the Mayo panel, the autoimmune encephalitis panels - you need to select patients carefully, but I think this attention to prior probability is something that we need to really focus on in multiple areas. So, I wonder if you might expand a little bit on assays. I do a lot of work in myasthenia and I know which labs do a really good job with, you know, acetylcholine receptor antibody testing and those that maybe do not, and there are different methodologies for testing - do you have any wisdom in terms of how to select a lab, what to look for, and how to interpret the results you see based on the particular assay that's being used?    Dr Sechi: Yeah, that's a critical point. I agree. And especially if you work in myasthenia, you're very well aware of the differences between different assays, and nowadays, most of the high-quality assays are cell-based assays (either fixed or live) - it's the same in myasthenia, and people need to pay attention to some of the less-specific assays. Let's say ELISA, for instance - testing AQP-4 and MOG antibodies with ELISA is quite dangerous, because the risk of false positivity is quite high. So, it's good to know what assays to trust most and also good to know what's the right specimen to send for antibody test. For instance, with AQP-4, we know that serum testing is recommended only, and the CSF doesn't add much, but with MOG, we know that approximately 10% of patients have an isolated positivity in the CSF, which is interesting, because it means that when you have a patient with a strong diagnostic suspicion as a phenotype that is highly suggestive for MOGAD and the serum testing is negative, you may consider testing the CSF to increase your sensitivity. So, this is very important.   Dr Smith: So, I have a question for you that may seem a little naïve, but I bet other people are thinking it - can you tell us why it is that these disorders affect optic nerve and spinal cord preferentially? And I think, for NMO, the whole area postrema thing seems awfully specific to me. What's the deal? Why are these areas preferentially affected by these antibody-mediated disorders?   Dr Sechi: This is a tough question. For NMO, we know, probably, there is higher expression of some of the isoforms. Let's say there is a higher density of AQP-4 molecules that target the most affected regions - so, of course, AQP-4 is preferentially expressed in the subependymal regions around the ventricles and in the spinal cord and optic nerves, but you may have, also, solutions along the cortical spinal tracts in case of the brain involvement. The area postrema is kind of a different explanation, because there is a sort of permeability - increased permeability - of the blood-brain barrier there. So, there are several factors in MOGAD - this is not very clear, so, this is a great topic to study in the future, I think.   Dr Smith: This is a really interesting area, and one that's really benefited by significant therapeutic development. I wonder if you might look a little bit in the future and tell us, maybe, the agent, or perhaps the target, that you're most excited about therapeutically that's coming down the road these days?   Dr Sechi: There are trials ongoing for MOGAD, which is the real need in terms of treatment, because for NMO, we already have three, four drugs that have been approved and which efficacy have been demonstrated by randomized clinical trials, and those are B-cell depleting agents, IL-6 inhibitors, and complement inhibitors. For MOGAD, this is still a gray zone, because the optimal treatment strategies remains to be defined. There are ongoing trials that are quite promising on IL-6 inhibitors and the inhibitors of the neonatal Fc receptor (which is also used in myasthenia gravis as you know). And something that seems to be quite effective - a good option for long-term treatment in these patients and relapse prevention - is also the periodic administration of IVIG (intravenous immunoglobulin), which is a nice option, for instance, in the children where you want to avoid immunosuppressants of other types. So, I think IL-6 is going to show to be very effective in the end. We'll see. We'll see.   Dr Smith: So, I wonder if I might just give you a vignette and get your thoughts about, kind of, acute management, right? I just took care of a patient who had a longitudinally extensive myelitis and she was essentially paraplegic and actually came in progressing fairly rapidly, and we, of course, started her on IV methylprednisolone, sent off the proper diagnostic testing - the question I have is, how quickly do you advance therapy and go to IVIG or plasma exchange when you're encountering these, right? It takes, you know, I think the turnaround time is, you know, often about a week to get these tests back (at least several days) - I mean, should we be going very quickly to plasma exchange in someone who has a severe phenotype? Is it okay to do three to five days of IV methylprednisolone and wait for the results to come back? What's the right approach?   Dr Sechi: I think this is a great question, actually. You know, management of the acute attacks probably is the most important thing, you know, to allow a good recovery, and I think timing of PLEX administration should be very short - so, the threshold for PLEX should be low, especially when the attack is severe, and this has to be done regardless of antibody testing results, which is typically not available before one or two weeks (at least a year in Italy), I think, in many hospitals. So, I think the risk-benefit ratio of administering PLEX is in favor of treatment in these patients, because the side effects (the potential side effects) are very rare and can be prevented. Some diseases, they can mimic NMO or MOGAD - they're very rare, and they can really worsen with PLEX. As an example, we can say spinal cord infarction can worsen, maybe, because of hypotension due to PLEX. Or some very rare infections, like one case, a bad case of intramedullary spinal cord abscess that looked really similar to an AQP-4 IgG-related LTM - and it was bad, because the patient had no fever, no signs of infection, the CSF culture was negative initially, so we ended up doing a biopsy after failure of PLEX and steroids. So, it is recommended to start within the first three to five days, preferentially, in severe cases, and this is great for the outcome of the patient, so, I do recommend PLEX as a second treatment option. And I'm not sure about IVIG acutely. There is some data on MOG, but it's still controversial - it works a lot when PLEX fails, but it can be considered after PLEX, of course. And there are some very rare patients that do not improve, even after IV methylprednisolone, PLEX, or IVIG, and so, you need to consider some rescue therapies. In those patients, it's kind of complicated, because there are some options, like IL-6 inhibitors seem to be quite effective and quite fast-acting for MOGAD attacks, and also eculizumab and complement inhibitors can be an option in patients with AQP-4 - but maybe less in patients with MOG. So, these are the possibilities (very quickly).   Dr Smith: So, you mentioned FcRn inhibitors a moment ago, and I wonder, do you see a future where - and I think you were mentioning them as maybe more chronic therapy? Correct me if I'm wrong.   Dr Sechi: Yeah, yeah.   Dr Smith: Do you foresee a role for these agents in acute management? I mean, there are some that, you know, very quickly lower immunoglobulin levels, though just looking out in the future, you think that these sort of infusion therapies that we think about chronic therapy (you mentioned, you know, complement inhibitors) are going to be useful in acute management?   Dr Sechi: Yeah, it depends. It's a good option to try. I'm not sure about the time to action. It's very dependent on that, because IL-6 inhibitors and complement inhibitors are very fast-acting (I think they can be effective already within twelve hours, 24 hours, which is good), but it's reasonable that, also, Fc inhibitors can be an alternative in the future. As far as I know, there is not much in the literature, but it's good to try in the future in case, acutely.   Dr Smith: Well, exciting times indeed. Elia, thank you so much for a great discussion. I thoroughly enjoyed this. I look forward to visiting you soon, and I want to congratulate you on a really great article that's very interesting and very clinically useful.   Dr Sechi: Well, thank you, Dr Smith. This is my pleasure, and thank you for great questions. I had a great time and hope the readers of Continuum will like the article and the nice figures we have put together. So, thank you, thank you very much.   Dr Smith: Well, again, congratulations. And for our listeners today, I've been interviewing Dr Elia Sechi, whose article on aquaporin-4 antibody-positive NMOSD and MOGAD appears in the most recent issue of Continuum, which is on autoimmune neurology. It's a very exciting issue. Please check out Continuum Audio episodes from this and other issues of Continuum. And thanks to you all 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 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.

The spinal cord serves as the main communication highway between the brain and body. Did you know that 80% of people with multiple sclerosis have spinal cord lesions on MRI? These lesions can disrupt specific neural pathways, leading to common MS symptoms like numbness, weakness, impaired coordination, balance issues, bladder problems, constipation, and sexual dysfunction. For instance, damage to the corticospinal tract on one side of the spinal cord can weaken an arm or leg. A remarkable autopsy study revealed that nearly 90% of people with MS still had active inflammation in the spinal cord. This finding brings new hope for potential treatments, even for older and progressive MS patients. Advances in imaging technology, including more powerful MRI scanners (3 Tesla and higher), are enhancing our ability to see inside the spinal cord, which is as thin as a pinky finger. Improved spinal cord imaging is driving the development of new therapies in clinical trials and helping identify those at risk for worsening disability, ultimately guiding better treatment decisions. Barry Singer MD, Director of The MS Center for Innovations in Care, interviews: Gabriele De Luca MD DPhil, Professor of Clinical Neurology and Experimental Neuropathology, University of Oxford, United Kingdom Bruce Cree MD PhD, Professor of Neurology at University of California, San Francisco School of Medicine

Autoimmune neurology is a rapidly evolving subspecialty that focuses on neurologic disorders with atypical immune responses. In this episode, Aaron Berkowitz, MD, PhD FAAN, speaks with Sean J. Pittock, MD, an author of the article “Overview and Diagnostic Approach in Autoimmune Neurology,” in the Continuum August 2024 Autoimmune Neurology issue. Dr. Berkowitz is a Continuum® Audio interviewer and professor of neurology at the University of California San Francisco, Department of Neurology and a neurohospitalist, general neurologist, and a clinician educator at the San Francisco VA Medical Center and San Francisco General Hospital in San Francisco, California. Dr. Pittock is the director for the Center for Multiple Sclerosis and Autoimmune Neurology at Mayo Clinic in Rochester, Minnesota. Additional Resources Read the article: Overview and Diagnostic Approach in Autoimmune Neurology 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 Transcript Full 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 Berkowitz: This is Dr Aaron Berkowitz, and today, I'm interviewing Dr Sean Pittock about his article, “Introduction to Autoimmune Neurology and Diagnostic Approach”, which he wrote with his colleague, Dr Andrew McKeon. This article is a part of the August 2024 Continuum issue on autoimmune neurology. Welcome to the podcast, Dr Pittock. Could you introduce yourself to our audience?    Dr Pittock: Well, thank you very much, Dr Berkowitz. So, yeah, I'm a neurologist at the Mayo Clinic. I direct the neuroimmunology laboratory with Dr McKeon and Dr Mills here, and I have also been very much involved in the autoimmune neurology section at the American Academy of Neurology.    Dr Berkowitz: So, many of you probably know Dr Pittock - or if you don't know, you've certainly diagnosed diseases that he has described and written about, and so it's a real honor to get to talk to you today and pick your brain a little bit about some of these complex diseases. So, autoimmune neurology is certainly one of the most exciting subspecialties of our field. I feel like when I talk to students and they ask me to make a case for why they should consider neurology as a career, I tell them, “Of course, I have many reasons I love neurology”, but one thing I mention is that, although many other fields of medicine may have made incredible advances as far as treatments, I can't think of too many other fields outside neurology where entirely new diseases have been described since I've been in training and come out of training - and many of those have been in your field of autoimmune neurology. I can think of cases where I've heard you or one of your colleagues on a neurology podcast describing a new antibody, new disease, and a few weeks later, we see that disease and give a patient a diagnosis that had been elusive from other physicians and hospitals. It's a very exciting, gratifying area. It's also daunting, like, every time I go to the AAN and hear one of your colleagues, there's a new disease, and we realize, “Oops! Was I missing that?” or, “Am I going to see this?” And so, hoping to pick your brain a bit today about some of the key concepts and how to keep them in mind so our listeners can recognize, diagnose, and treat these conditions, even if they can't remember every single antibody in your article and all the new ones you and your colleagues will probably discover between now and when this, um, podcast is released. So, before we get into some of the important clinical aspects of these conditions, could you just lay out sort of the broad breaststrokes, the lay of the land of cell-mediated versus antibody-mediated paraneoplastic versus nonparaneoplastic cell surface versus intracellular - how can we sort of organize this area in our minds?    Dr Pittock: Yeah. It's complex, and it's really an evolving story. But the importance, really, from the perspective of the reader and the perspective of the clinician is that we're talking about disorders where we can actually do something - we can actually impact patients.  And we think about the concept of stopping and restoring in neurology now. We're talking about disorders where we have the potential to stop these inflammatory immune-mediated disorders and, potentially, by stopping early, we may be able to restore function - so, a really important new and evolving field in neurology, because you don't want to miss these conditions. Trying to get your head around the complexity of these entities is difficult, but what we've done in this chapter is, really, to try and lay the groundwork for the following chapters, but provide somewhat of a simplistic approach, but a practical approach that really, I think, can help clinicians. So, the way I think of it, a lot of autoimmune neurology really has stemmed from the discovery of antibodies that cause neurological disease, and the examples of those would be going back to myasthenia gravis (with antibodies to the acetylcholine receptor), going back to Lambert-Eaton syndrome. And then, you know, even if you go back to the older traditional paraneoplastic disorders (the Hu, the Ri, the Yo), at the end of the day, you really have two essential entities, if you want to be very simple. The first is disorders that are caused by an antibody, and the second are disorders where the antibodies you detect are not causing the disorder, but they're telling you that there's predominantly a cellular or T-cell mediated attack of the nervous system. And I think thinking about the diseases in those kind of simple terms helps us when we think about what would be the best treatment to use in these types of cases.   Dr Berkowitz: Fantastic. I think that's very helpful. And just to make sure it's clear in the minds of our listeners when we're dividing into these sort of causative antibodies versus antibodies that might be, uh (I don't know if I'm using the word properly), but, sort of epiphenomena (or they're present, but they're not causative) as you said, can you just give some examples of the ones on either side and how making this distinction helps us in practice?    Dr Pittock: Yes. So, antibodies that are causative of disease - I think, you know, the one that I've done a lot of work on is in neuromyelitis optica, where you have antibodies that are targeting a water channel that sits on an astrocyte, and so it causes NMOSD, or what we consider an autoimmune astrocytopathy. And we know that when the antibody binds to the target, many things can happen. So, when aquaporin-4 antibodies bind to aquaporin-4, they can do a lot of things. They can cause internalization, they can activate complement that results in the killing of the cell - but there can be other situations. For example, when NMDA-receptor antibodies bind to the NMDA receptor, then a variety of different things can occur different to water channel autoimmunity - where, for example, the receptor (the NMDA receptor) is downregulated off the cell surface, and that results, to some extent, in the neuropsychiatric phenomenon that we see in NMDA-receptor autoimmunity. And, obviously, when you have a situation where the antibodies are causing the disease, removal of those antibodies, or the reduction in the production of those antibodies, is going to help patients. Now, on the other side, we have antibodies that we detect in the blood or in the spinal fluid, and those antibodies are targeting proteins that are inside the cell - so those antibodies we don't consider as being pathogenic. Now, remember, there are sometimes situations where proteins that are inside the cell occasionally can be available for antibodies to bind at certain situations. So, for example, in the synapse, amphiphysin or the septins, may at times become available. And so, sometimes, there are targets or antibodies that are somewhat in between those two simplistic concepts. But when we're talking about antibodies that are targeting proteins on the inside of the cell, remember that antibodies don't just suddenly occur. There's a whole process of presentation of target antigen at the lymph node, and then both a T- and a B-cell response. The B-cell response potentially produces the antibodies but also triggers and stimulates T-cells, and those T-cells then go on to cause the disease. And those T-cells are very problematic, because those classical paraneoplastic and the newer ones we've described (and many have described) - these are associated with quite severe neurological disability, and they're very, very difficult to treat. And if you ask me, “Where is the holy grail of autoimmune neurology therapeutic research?” It's in trying to actually figure out ways of treating the predominantly T-cell mediated paraneoplastic and autoimmune neurological disorders. We're making great headway in terms of the treatments of the antibody-mediated neurological disorders.   Dr Berkowitz: That's a helpful overview. So, sticking with this framework, you mentioned as sort of the “causative antibody” category and the antibodies that are predominantly for intracellular antigens, but not believed to be causative - I want to make sure I'm understanding this correctly and we can convey it to our listeners - I believe you said in your paper, then, that the antibodies that are predominantly causative are more likely to be associated with conditions that are very treatable, as compared to the intracellular antibodies that are not thought to be causative, as you just said the disability can be irrecoverable or very hard to treat. And I believe another theme in your paper that you brought out is the antibodies that tend to be causative tend to be cell surface and tend to be less likely to be associated with underlying cancer (although not a perfect rule), and the intracellular antigens more commonly associated with cancer in those cases to look very hard for a cancer before giving up. Are those themes that I understand them from your paper properly, or anything else to add there?    Dr Pittock: Yes, I think that that's exactly the message that we were trying to get across, so that's good news that you've picked up on the themes. I think, yeah, in simple terms, remember that when a cytotoxic T-cell identifies the peptide that its T-cell receptor will target, the ultimate outcome is poor, all right? T-cells are like the marines - they don't mess around. Once they find their target, they eliminate that target, and so, it's really difficult to treat those types of diseases if you get them late. And most patients with cytotoxic T-cell mediated paraneoplastic neurological disorders, oftentimes, by the time they get to a center of excellence, the boat has left the dock in many respects - in other words, it's too late. So, you know, I will often see patients, for example, with progressive cerebellar degeneration (say, in the context of Purkinje cell autoantibody type 1 antibodies and a breast cancer), and if those patients are in a wheelchair at the time that I see them, there's very, very little that we can do. So, you really want to try and get that patient into the office, you know, when they're using a cane (or not), and then, potentially, you have the opportunity - using very aggressive immunosuppressive medications - to make a difference. And that is quite different to other scenarios, where, for example, if you have NMDA-receptor encephalitis - as many of the readers will know, this is a condition that is very treatable, and most patients do very well, because the antibodies, they're disrupting function, but they're not killing the neuron, as we see in those more aggressive, paraneoplastic cytotoxic T-cell mediated diseases.   Dr Berkowitz: Also, in terms of searching for an underlying cancer, another theme in your paper as I understood (but want to make sure I'm understanding and conveying to our listeners and hear your thoughts), that the cell surface and treatable antibody-mediated syndromes, as you mentioned (NMO, NMDA) tend to be less associated with underlying cancers (although can be), whereas the intracellular antigens, um, a much higher percentage of those patients are going to end up having underlying cancers. Is that correct, or any notable exceptions to be aware of in that framework?    Dr Pittock: Yeah, I think the major exception to the rule for the antibodies that are targeting intracellular antigens is the GAD65 antibody story. We generally don't consider the stiff person syndrome, cerebellar ataxia, or other autoimmune neurological disorders associated with very high levels of GAD65 antibodies - those are generally not paraneoplastic. And then there are always exceptions on both sides. You know, one of the benefits of understanding the implications of certain antibodies is trying to understand, you know, what is the likelihood of identifying a malignancy, which antibodies are high-risk antibodies (in other words, high-risk paraneoplastological disorders), and which are low risk in terms of cancer? And, you know, age and the demographic of the individual is often important, because we know, for example, with NMDA-receptor antibodies, the frequency of ovarian teratoma varies with the age of the patient.   Dr Berkowitz: Fantastic. And we encourage our listeners to read your articles – certainly, some very helpful tables and figures that help to elucidate some of these broad distinctions Dr Pittock is making - but just to summarize for the antibody-related part of autoimmune neurology, we have one category of cell-surface antibodies and another of intracellular antibodies. Both can cause very severe and varied neurologic presentations, but the cell surface tend to be more treatable, less likely to be associated with the underlying cancer, and the intracellular less treatable, more likely to be associated with the underlying cancer - but, as with everything in neurology and medicine, exceptions on both sides. Is that a fair aerial view of some of the details we've discussed so far, Dr Pittock?    Dr Pittock: Yeah, I think so. I mean, I also think that, you know, not only, at least, for the antibody-mediated disorders (you know, as we discussed) we have drugs that will reduce the production of those antibodies, but we're also learning a lot more about the cytokine and chemokine signatures of these disorders. For example, NMO, water-channel antibody-mediated diseases are associated with elevated levels of IL-6. We know, for example, in LGI1 encephalitis and other encephalitides, that IL-6 also is elevated at the time of that encephalitic process. And so, the potential to target IL-6 with, you know, drugs that inhibit IL-6 and the IL-6 receptor, these potentially have, you know, a role to play in the management of these types of patients - whereas in the T-cell mediated disorders, you know, no advance has been made in the treatment of those conditions, I would say, in over 50 years. So, for example, the standard of treatment is steroids and then drugs that impact the bone marrow, and so we really haven't moved forward in that respect. And that, I think, is an area that really needs drive and enthusiastic out-of-the-box thinking so that we can try to get better treatments for those patients.   Dr Berkowitz: This has been a helpful overview. I look to dive into some of the scenarios that frontline practitioners will be facing thinking about these diseases. An important point you make in your article is that autoimmune and antibody-mediated neurologic syndromes can affect any level of the neuraxis. Even just our discussion so far, you've talked about anti-NMDA receptor encephalitis, you've talked about myasthenia gravis (that's at the neuromuscular junction), you've talked about paraneoplastic cerebellar degeneration - there can be an “itis” of any of our neurologic structures and that “itis” can be antibody-mediated. So, one of the key messages you give us is, one, that these are sort of in the differential diagnosis for any presenting neurologic syndrome, and, two, sort of one of the key features of the history, really, to keep in mind (since we could be anywhere along the neuraxis) is the subacute presentation when this should really sort of be top of mind in our differential diagnosis - so, many of these patients are going to be mystery cases at the outset. And one striking element you bring out in the paper is that, sometimes, the MRI, CSF, electrophysiology studies may be normal or nonspecifically abnormal, and although it's very helpful when we can send these antibody panels out, in some cases, resources are limited or institutions have certain thresholds before you can send these out (because neurologists love to send them in). Sometimes, they are not necessarily appropriate. So, love to hear your thoughts on when we should be sending these panels. What are some clues? Um we have a subacute neurologic presentation at any level of the neuraxis, and when it's not anti-NMDA receptor encephalitis, that is sort of a clear phenotype in many cases. How you would approach a patient, maybe, where the MRI is either normal or borderline abnormal (or people are squinting at the medial temporal lobe and saying, “Maybe they're a little brighter than normal”), CSF is maybe normal or nonspecifically, um, and the protein is a little high, but no cells? What clues do you use to say, you know, “These are the patients where we should be digging deep into antibody panels and making sure these are sent and not miss this diagnosis?”    Dr Pittock: Well, thank you. That's a good question. So, I think, you know, first of all, these are complex cases. So, the patient is sitting in front of you and you're trying to figure out, first of all, Is this a hardware or a software problem? Are we definitively dealing with an encephalitis or an organic neurological entity that's immune-mediated? And, you know, the way I think of it is, for me, you see a patient, it's a twenty-five-piece jigsaw puzzle and you've got two pieces, and you're trying to say, “Well, if I step back and look at those two pieces, do I have any sense of where we're going with this patient?” So, the first thing you need to do is to collect data, both the clinical story that the patient tells you (and I think you make the good point that that subacute onset is really a big clue), but subacute onset, also fluctuating course, sometimes, can be important. The history of the patient - you know, Is the patient somebody who has a known history of autoimmune disease? Because we know that patients that have thyroid autoimmunity are more likely to have diabetes, they're more likely to have gastrointestinal motility or dysmotility, they're more likely to have a variety of different immune-mediated conditions. So, is there a family history or a personal history of autoimmunity? Is the patient at high risk for malignancy? Are there clues that this potentially could be a tumor-initiated immune process affecting the nervous system? The neurological exam also is extremely important because, again, that helps you, first of all, kind of define and get some objectivity around what you're dealing with. So, does the patient have hyperreflexia? Are there signs that there is neurological involvement? And then, really, what I think we need to do is to try and frame the predominant neurological presentation. So, what is the major issue? Because a lot of these patients will have multiple complaints, multiple symptoms, and it's very important to try and identify the major presentation. And that's important, because the neural autoantibody tests are now presentation-defined - in other words, they're built around the neurological presentation, because the old approach of just doing, apparently, a plastic evaluation is gone, because we've got to a stage where we have now so many neural antibodies, you can't test every single neural antibody. So, if you're suspecting that there may be an autoimmune neurological component, then you really need to think about what would be the most appropriate comprehensive evaluation I need to do for this patient. So, for example, if a patient comes in with a subacute-onset encephalopathy, you're probably going to want the autoimmune encephalitis evaluation, and then you have to pick whether it's going to be serum or spinal fluid - and as we outlined in the paper, there are certain antibodies that are better detected in serum versus spinal fluid. So, for example, in adults over the age of 50, LGI1 is much more accurately detected in serum than spinal fluid, and the absolute opposite is true for NMDA-receptor antibody detection. One of the most important components of the neurological evaluation is the spinal fluid, but actually looking at the white cell count - and in fact, sometimes, it's quite interesting to me that I'll often see patients referred with a diagnosis of encephalitis and autoimmune encephalitis, and yet they haven't had a spinal fluid examination. So, the presence of a white cell count, you know, greater than five is hugely helpful - it's like two pieces of that twenty-five-piece jigsaw, because that really tells you that there is something inflammatory going on. And now, in terms of imaging, you're right - some patients will have normal MRI. And if you really do think that there's evidence of - you know, for example, you do an MRI, but you're getting a good sense that there's a temporal lobe seizure occurring, MRI looks normal, the EEG shows some abnormalities in the mesial temporal area - you know, considering additional imaging modalities (like PET scan of the brain), I think, is reasonable. We know that in NMDA-receptor encephalitis cases, 30% of patients will have normal MRI but they'll often have abnormalities on the PET scans. So, I think, what we do is we try to gather data and gather information that allows us to add in pieces of that jigsaw so that, eventually, after we've done this evaluation, we can see now we have ten pieces. If we step back, we say, “Yes, now we know what this condition is”, and then we essentially plan out the therapeutic approach dependent on what we've found. In terms of identification of underlying malignancy, you know, different people have different approaches. Our approach generally has been to try to get a PET-CT scan of the body as our first go-to test, because, actually, we found that CT chest abdomen and pelvis really actually delivers the same amount of radiation - and from a cost perspective, it's about the same - and we have found that PET-CTs really do provide a higher sensitivity for cancer detection.   Dr Berkowitz: Perfect. A lot of very helpful clinical pearls there. So, in closing, Dr Pittock, I've learned a lot from you today. I'm sure our listeners will as well. What does the future hold in this field? What's coming down the pipeline? What are we going to be learning from you and your colleagues that are going to help us take care of patients with these diseases going forward?    Dr Pittock: Well, thank you, Dr Berkowitz, for that question. I think the future is very bright and very exciting, and, hopefully, some of the more junior members will be enthused by this Continuum series, and, hopefully, we'll go into this area. So, let's talk about the future. The future, I think, is going to be of great interest. Firstly, there's going to be continued discovery of novel biomarkers, and the reasons for that is because of the technical and technological advances we've seen. So, for example, there have been many, many antibodies discovered by us and others that have been discovered on the basis of, for example, phage technology. In fact, the Kelch 11 biomarker discovery in collaboration with UCSF and our group was done on the basis of Joe DeRisi and Michael Wilson's phage approach. And we're actually using that now at Mayo Clinic, and we've discovered about three or four new antibodies just in the last couple of years using this technology (and that here is led by John Mills and Div Dubey). And then, we're also going to see, I think, the evolution of protoarrays much more in biomarker discovery, so, we'll have more antibodies, and again, I think, generally, those antibodies will fall into the two categories we kind of described - so, you know, in terms of the approach to those conditions, maybe not so much change. I do think, though, that the introduction and the utility of comprehensive cytokine and chemokine analysis in the future will assist us in making diagnoses of seronegative encephalitis, but also potentially will direct therapy. So, for example, cytokine A is elevated - maybe that would be a potential target for therapy that's available for these patients with rare and potentially very disabling disorders. Then, when we look at the cytotoxic T-cell mediated disorders, I think the major areas of advance are going to be in better understanding the immunophenotype of cytotoxic T-cell mediated diseases, and then the potential development of tolerization strategies using the specific targets, those specific epitope targets that are involved in paraneoplastic and nonparaneoplastic diseases, and seeing if we can vaccinate patients, but move that immune response into more of a tolerogenic immune response rather than a cytotoxic killing response. And then I think, lastly, we're going to see a dramatic revolution in CAR-T therapeutic approaches to these types of disorders moving forward - and not just, you know, CAR-T therapies that are targeting, you know, CD19 or CD20, but CAR-Ts that are actually personalized and developed so that they can target the specific B- and T-cells in an individual patient and actually do a very fine removal of that autoimmune pathologic process that I think would have significant benefit for patients not only in stopping progression, but also in significantly reducing the potential of side effects - so, a much more targeted approach. So, that's where I think the next ten years is going to be. I think it's very exciting. It's going to require the collaboration of neurologists with, you know, immunologists, hematologists, you know, across the board. So, a very exciting future, I think, for this field.    Dr Berkowitz: Exciting, indeed. And we have learned so much from you and your colleagues at the Mayo Clinic about these conditions, and I definitely encourage our listeners to read your article on this phenomenal issue that really gives us a modern, up-to-date overview of this field and what's coming down the pipeline. So, a real honor to get to speak with you, pick your brain about some of the clinical elements, pitfalls and challenges, and also hear about some of the exciting signs. Thank you so much, Dr Pittock, for joining me today on Continuum Audio.   Dr Pittock: Thank you very much.    Dr Berkowitz: Again, today, I've been interviewing Dr Sean Pittock, whose article with Dr Andrew McKeon on an introduction to autoimmune neurology and diagnostic approach appears in the most recent issue of Continuum on autoimmune neurology. Be sure to check out Continuum Audio episodes from this and other issues. And thank you so much to our listeners for joining us today.    Dr 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.

In this episode of "ABCs of NMOSD," Landy Thomas of SRNA hosted a discussion about the experiences of men who are living with neuromyelitis optica spectrum disorder (NMOSD). Doug Kirby and Andrew Jopson shared their diagnosis journeys, highlighting the physical and emotional challenges they faced [00:04:20]. They delved into the impact of the disorder on their personal lives, careers, and relationships, offering advice to newly diagnosed men [00:17:24]. Finally, they emphasized the importance of support groups and looking towards the future with hope [00:32:28]. Doug Kirby has lived most of his life in Utah. After earning a degree in microbiology from BYU, he went to the University of Washington to gain his master's degree in environmental health science. Doug also spent two years in South Korea as a church missionary. He has been married to his wife, Holly, for 39 years, and they have 5 kids, all boys but the first four, and eight grandchildren. Doug spent the first ten years of his career in the environmental field working at two different hazardous waste disposal sites and then switched to information technology. During his career, Doug has been a developer and manager. He currently lives in Herriman, Utah where he and Holly are looking forward to retirement in a little over three years. Doug was diagnosed with NMOSD when he was 56 in 2017. His vision is fine, but he has some physical difficulties including numbness and trouble walking that he has learned to live with. Doug enjoys meeting with and learning from others who are going through similar challenges.Andrew Jopson is a PhD candidate at Johns Hopkins University, researching how Medicaid-funded long-term services and supports (LTSS) influence the care experiences of older adults with disabilities and their caregivers. His research, policy, and advocacy interests are motivated by his experience as a caregiver for his brother. He earned his BA at the University of California, Berkeley and MPH at the University of Washington (UW) in Seattle. Andrew was diagnosed with seronegative NMOSD, lupus, and Graves' Disease in 2022 following an attack and extended hospitalization. He is an aviation enthusiast who enjoys swimming, making people laugh, and reminding everyone that his chocolate chip cookies were awarded second place in the 2019 Washington State Fair.

This content has been developed for healthcare professionals only. Patients who seek health information should consult with their physician or relevant patient advocacy groups.For the full presentation, downloadable Practice Aids, slides, and complete CME information, and to apply for credit, please visit us at PeerView.com/HXG865. CME credit will be available until June 27, 2025.Mastering Diagnosis and Navigating the Sea of Targeted Treatments in NMOSD: Practical Guidance on Optimizing Patient Care In support of improving patient care, PVI, PeerView Institute for Medical Education, is jointly accredited by the Accreditation Council for Continuing Medical Education (ACCME), the Accreditation Council for Pharmacy Education (ACPE), and the American Nurses Credentialing Center (ANCC), to provide continuing education for the healthcare team.SupportThis activity is supported by an educational grant from Genentech, a member of the Roche Group.Disclosure information is available at the beginning of the video presentation.

Dr. Michael Levy joined Dr. GG deFiebre of SRNA for the “Ask the Expert” podcast episode titled "What is ULTOMIRIS?" Dr. Levy explained that ravulizumab (ULTOMIRIS) is the newest FDA-approved medication for neuromyelitis optica spectrum disorder (NMOSD), offering a longer dosing interval compared to eculizumab (Soliris) [00:01:08]. Dr. Levy discussed the mechanism of ULTOMIRIS, which blocks the complement system to prevent relapses in NMOSD and highlighted the importance of vaccinations and possible antibiotic use to prevent infections while on this medication [00:02:48]. He also noted that ULTOMIRIS is more affordable than Soliris and emphasized the need for insurance coverage to make it accessible to patients [00:16:39]. Michael Levy, MD, PhD is an Associate Professor of Neurology at Massachusetts General Hospital and Research Director of the Division of Neuroimmunology & Neuroinfectious Disease. He completed the MD/PhD program at Baylor College of Medicine with a focus on neuroscience. In 2009, Dr. Levy was appointed to the faculty as Assistant Professor at Johns Hopkins where he started the Neuromyelitis Optica Clinic and Research Laboratory and in 2019 he moved to the Massachusetts General Hospital and Harvard Medical School to develop the research program in neuroimmunology. Clinically, Dr. Levy specializes in taking care of patients with rare neuroimmunological diseases including neuromyelitis optica, transverse myelitis, MOG antibody disease, acute disseminated encephalomyelitis and optic neuritis. In addition to neuroimmunology clinics, Dr. Levy has a special interest in patients with superficial siderosis of the central nervous system. Dr. Levy is the principal investigator on several clinical studies and drug trials for all of these conditions. In the laboratory, Dr. Levy's research focuses on the development of animal models of neuromyelitis optica and transverse myelitis with the goal of tolerization as a sustainable long-term treatment.

Join Dr. Mitzi and her amazing friends, Sumaira Ahmed and Dr. Michael Levy, as they dive into a Brainchat on NMOSD

This “MOGcast” edition of the “Ask the Expert” podcast series is a collaborative episode titled, “The Latest in Treatments from an Adult and Pediatric Perspective.” Dr. Elias Sotirchos and Dr. Grace Gombolay joined Julia Lefelar of The MOG Project and Dr. GG deFiebre of SRNA and answered questions from the online audience. Dr. Sotirchos and Dr. Gombolay reviewed acute treatments for MOG antibody disease (MOGAD) in adults and children and possible side effects [00:03:57]. Regarding preventative treatments, Dr. Sotirchos and Dr. Gombolay described the importance of shared decision-making with patients to consider factors like administration method, insurance coverage, and patient preferences [00:20:10]. They discussed ongoing clinical trials for MOGAD treatments and the hope for future FDA approval [00:51:38]. Finally, Dr. Gombolay highlighted the difficulties in accessing preventive medications for patients from certain demographic groups and ongoing efforts to improve access [00:56:35]. Elias Sotirchos, MD is a neurologist at Johns Hopkins Hospital in Baltimore, Maryland. He specializes in the diagnosis, management, and treatment of neuroimmunological disorders that involve the central nervous system, including multiple sclerosis (MS), neuromyelitis optica spectrum disorder (NMOSD), and myelin oligodendrocyte glycoprotein-immunoglobulin G (MOG-IgG)-associated disorder (MOGAD). His research focuses on developing and validating novel imaging and blood-based biomarkers of these conditions, and clinical trials of experimental therapeutic agents. Grace Gombolay, MD is a Pediatric Neurologist at Children's Healthcare of Atlanta and Assistant Professor at Emory University School of Medicine. Dr. Gombolay attended medical school at The Johns Hopkins School of Medicine, where she was awarded a yearlong position as a Howard Hughes Medical Institute–National Institutes of Health Research Scholar in basic immunology research. After finishing medical school, she completed a pediatric neurology residency at Massachusetts General Hospital. She then completed an additional year of fellowship training in pediatric neuroimmunology at Boston Children's Hospital, Brigham and Women's Hospital and Massachusetts General Hospital. Over the course of her career at Children's, Dr. Gombolay started the Pediatric Neuroimmunology and Multiple Sclerosis Clinic. This multidisciplinary clinic helps manage all aspects of patient care, including medical, psychological and school-related issues. Her goal is to have the clinic become part of multi-center collaborations for clinical care and research. Dr. Gombolay also serves as a part-time consultant for the Centers for Disease Control and Prevention (CDC), where she reviews cases related to surveillance of acute flaccid myelitis cases in the U.S.

The “Community Spotlight” edition of the “Ask the Expert” podcast series shares the stories of our community members. In this episode, titled, “Voices of SRNA Volunteers, Part 2,” Minaal Zahid and Doug Kirby joined Lydia Dubose of SRNA. Doug shared his journey with NMOSD, emphasizing the role of volunteers in providing support and education [00:01:49]. Minaal discussed her motivation to volunteer stemming from her brother's diagnosis of NMOSD [00:02:42]. Minaal and Doug delved into their volunteer activities, including organizing events and contributing to educational resources, highlighting the impact of volunteering on both personal growth and community support [00:07:13]. Minaal Zahid is an incoming neurodevelopmental disabilities resident physician whose journey in medicine was shaped by her family's history of autism and NMOSD. She witnessed firsthand the challenges her family faced in obtaining a diagnosis for her younger brother, who struggled with NMOSD symptoms for nearly a year before diagnosis, resulting in the unfortunate loss of vision in his left eye. Assuming the role of caretaker as the eldest daughter, Minaal was inspired to pursue a career in neurology to assist families facing similar struggles with neurological disorders. This pursuit led her to SRNA where she is excited to educate the general public and her colleagues about rare neuroimmune disorders and help enact policy changes to better serve patients with neurological disabilities. Doug Kirby has lived most of his life in Utah. After earning a degree in microbiology from BYU, he went to the University of Washington to gain his master's degree in environmental health science. Doug also spent two years in South Korea as a church missionary. He has been married to his wife Holly for 39 years, and they have 5 kids, all boys but the first four, and eight grandchildren. Doug spent the first ten years of his career in the environmental field working at two different hazardous waste disposal sites and then switched to information technology. During his career, Doug has been a developer and manager. He currently lives in Herriman, Utah where he and Holly are looking forward to retirement in a little over three years. Doug was diagnosed with NMOSD when he was 56 in 2017. His vision is fine, but he has some physical difficulties including numbness and trouble walking that he has learned to live with. Doug enjoys meeting with and learning from others who are going through similar challenges.

The “Community Spotlight” edition of the “Ask the Expert” podcast series shares the stories of our community members. In this episode, Alexandra Goulimi and Angela Jackson joined Lydia Dubose of SRNA share their backgrounds and how they got involved with volunteering for SRNA [00:01:43]. Alexandra and Angela discussed their experiences with rare neuroimmune disorders and the support they found through SRNA's programs [00:13:41]. They also shared what they hope to see in the future related to rare neuroimmune disorders and SRNA [00:22:53] and offered advice for anyone who might be interested in getting involved [00:30:51]. Alexandra Goulimi was born in 1969 and lived in Germany until she moved to Greece in 2011. She has a background in Human Resources Development and holds a master's degree in Sociology and a PhD in Communications. In 2009 Alexandra met the Human Design System and has been experimenting since then with making decisions guided by her body's intelligence. In 2017 Alexandra was diagnosed with NMOSD. It was challenging to meet the initial shock and deal with the symptoms. She has navigated her NMO-journey guided in her decisions by her intuitive response. Alexandra's experience of NMO has led her to a profound understanding and a deeper love of herself and life. Angela Jackson has been a member of a book club for 20 years. She is also a published author. Angela was a VP of Account Management working for a software company responsible for Customer Success. On February 27, 2019, she woke up with a numb left thigh. 12 hours later she was paralyzed from the waist down, diagnosed with idiopathic transverse myelitis, and hospitalized. Her lifestyle changed: acceptance of the diagnosis, therapy, limitations, working from home, depending on others... Moving forward with a positive outlook on life, Angela joined SRNA, serving as a Peer Connect Leader and hosting the first Houston, Texas Walk-Run-N-Roll. Angela has an awesome family. She is thankful for loving and supportive family and friends.

Dr. Rae Bacharach discusses the Neurology Today article, "How Long-Term Disability Progression Is Different in Neuromyelitis Optica and Myelin Oligodendrocyte Glycoprotein-antibody Associated Disease" by Susan Kreimer, available in the March 7th issue of Neurology Today or at neurologytoday.com.  Show References:  https://journals.lww.com/neurotodayonline/fulltext/2024/03070/how_long_term_disability_progression_is_different.3.aspx?WT.mc_id=HPxADx20100319xMP  https://onlinelibrary.wiley.com/doi/10.1002/ana.26858  This podcast is sponsored by argenx. Visit www.vyvgarthcp.com for more information.

The “Community Spotlight” edition of the “Ask the Expert” podcast series shares the stories of our community members. For this episode, Ilona Williams joined Lydia Dubose of SRNA to discuss her journey with neuromyelitis optica spectrum disorder (NMOSD). Ilona described her initial symptoms and the challenges she faced in receiving a correct diagnosis [00:01:22]. Despite experiencing skepticism and frustration, she persisted in seeking medical care and advocating for herself [00:02:38]. Eventually, after enduring significant health challenges, she was correctly diagnosed [00:12:07]. Despite ongoing symptoms and lifestyle adjustments, Ilona highlighted the importance of education, advocacy, and supportive communities in managing NMOSD [00:18:55] and mental health [00:37:56]. Ilona grew up as a military brat, spending most of her youth in Germany. She attended high school and community college in Maryland and has worked in Intellectual Property (IP) as a secretary and coordinator in two large international law firms over the last 25 yrs. Originally, she was diagnosed with transverse myelitis (TM) in 2006. Then, after additional issues and relapses, she was diagnosed with and treated for relapsing and remitting multiple sclerosis (MS). Finally, in 2018, Ilona was diagnosed with NMOSD AQP4+. In 2018 and 2019, she also battled breast cancer and was treated with radiation, chemotherapy, double mastectomy surgery, and complete hysterectomy. After five months of being transferred in and out of different hospitals and two years of very intensive speech therapy and physical therapy, she lives independently and on her own. Her mother is a great advocate and caretaker. She keeps Ilona motivated, strong, with her spirits up, and looking forward to every day. She's helped to motivate Ilona to become her own best advocate.

I get messages often from those with NMOSD that include so many great questions. This episode is dedicated to the effort of answering those questions as in depth as possible! { 3 Myths } About Autoimmune Disease Diet Protocol. Get it here—> www.taylorannmacey.com/3-myths-pod Schedule your FREE Set Your Custom Macros Call with me here: https://app.acuityscheduling.com/schedule.php?owner=18505613 Come hang out with me on Instagram! https://www.instagram.com/taylorannmacey/

Sumaira Ahmed is a force! Upon being diagnosed with a rare neuroimmune condition (Neuromyelitis optica spectrum disorder/ NMOSD, whose symptoms can include vision loss, paralysis, and weakness), Sumaira couldn't find the community she needed, so she went right ahead and launched a foundation (two months later!) to create that support for herself and patients around the world. The Sumaira Foundation has since advocated for patients, funded disease research, increased NMO awareness globally and truly been a game changer in the field. Hear how this young dancer and Bollywood aspirant (who was crowned the first Miss Bangladesh-USA) turned into a fearless non-profit leader and champion for patients suffering from this rare disease.Join me with the wonderful Sumaira - now on your favorite podcast app, Spotify or iTunes and please please take a second to rate us wherever you're listening so the voices of these inspiring women can be heard all over the world!SHOWNOTES FOR EPISODE 88:Read more about Sumaira's work at The Sumaira Foundation and connect with her and The Sumaira Foundation on InstagramInfinite Vision: How Aravind Became the World's Greatest Business Case for CompassionQuestions? Comments? Get in touch @theindianeditpodcast on Instagram ! Want to talk gardens? Follow me @readyourgardenSpecial thanks to Sudipta Biswas and the team @ Boon Castle / Flying Carpet Productions for audio post-production engineering!

Christine Ha, an award-winning blind chef and restauranteur, shares her experience grappling with neuromyelitis optica spectrum disorder (NMOSD). Facing relapses with the inability to walk and feed herself that challenged her independence, she leaned on the support from family and friends. As she lost her sight due to optic neuritis in both eyes, Ms. Ha had to embark on a journey of rediscovery in the kitchen, starting with the fundamentals. Winning MasterChef Season 3 marked a turning point, propelling her culinary career forward despite the obstacles posed by her disability.  NMOSD is an autoimmune disease in which an antibody attacks water channels on astrocyte cells in the optic nerves, spinal cord and sometimes the brain. Attacks or relapses can be devastating and incomplete recovery from attacks is typical. Like Ms. Ha, some people living with the condition can be misdiagnosed with multiple sclerosis. A blood test for the aquaporin-4 antibody is key to getting diagnosed correctly early. Since 2019, highly effective treatment options have been FDA-approved that reduce relapses by 77-94%. Barry Singer MD, Director of The MS Center for Innovations in Care, interviews: Christine Ha, "The Blind Cook".  Her first cookbook, Recipes from My Home Kitchen, was a New York Times best-seller. Ms. Ha's first restaurant in Houston, The Blind Goat, was named a semi-finalist for 2020 Best New Restaurant in America by the James Beard Foundation. She was also named a James Beard finalist for Best Chef in Texas in 2022. Michael Levy MD PhD, Associate Professor at Harvard Medical School and Director of the Neuroimmunology Clinic and Research Laboratory