Podcasts about Translational research

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. Benjamin Greenberg of the UT Southwestern Medical Center. He outlined his translational research, including 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) [05:49]. He also described research on immune-remodeling therapies for NMO aimed at reducing long-term immunosuppression. Dr. Greenberg illustrated multidisciplinary care at UT Southwestern and Children's Medical Center, emphasized options for second opinions and clinician-to-clinician remote consultation, and shared hopes for nervous system repair trials and curative immune therapies [07:18]. You can view Dr. Benjamin Greenberg's medical profile here:https://utswmed.org/doctors/benjamin-greenberg/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 Intro01:41 Path to Neurology03:50 Why Neuroimmunology05:49 Research Focus and Trials07:18 Clinic Team and Referrals10:31 Self Care and Hobbies12:17 How the Clinic Can Help14:16 Hope for Future Therapies15:56 Wrap Up

In this episode, we talk with Dr. Nicholas Theodosakis, MD, PhD. Dr. Theodosakis is a physician scientist at Massachusetts General Hospital who completed his MD/PhD at Yale School of Medicine before going on to pursue a combined dermatology residency and research fellowship at the Harvard Combined Dermatology Residency Program. Today, Dr. Theodosakis tells us about his path to dermatology, what it looks like to have a career as a physician scientist and interesting recent findings from his lab that impact our understanding of the skin. Dr. Theodosakis also discusses opportunities for students to work in his research lab. We wrap up with general advice for students interested in research as well as building an application for the field of dermatology. We hope you enjoy!If you enjoyed this episode, please share it with other students interested in dermatology!Learn More:Educational links: Dr. Theodosakis research: https://pubmed.ncbi.nlm.nih.gov/41446198/Email: NTHEODOSAKIS@MGH.HARVARD.EDU---DIGA Instagram: @derminterestToday's Host, George: @georgepapadeas---For questions, comments, or future episode suggestions, please reach out to us via email at derminterestpod@gmail.com ---District Four by Kevin MacLeodLink: https://incompetech.filmmusic.io/song/3662-district-four**License: https://filmmusic.io/standard-license**---

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

HIV research is one of the clearest examples of molecular biology in action. In this Mol Bio Minutes episode, Dr. Ryan Jeep walks through how fundamental molecular techniques power everything from detection to drug resistance studies to cure-focused research. Ryan begins with HIV biology and detection, explaining how qRT-PCR enables highly sensitive viral load measurement. These assays not only detection strategies but also support research to monitor treatment efficacy and viral rebound. From there, he moves into drug resistance, describing how sequencing, RT-PCR, and cloning strategies help researchers map resistance-associated mutations. By generating recombinant reporter viruses and measuring infectivity against different drugs, scientists can better understand treatment failure and move toward more personalized therapeutic strategies. Finally, Ryan explores cutting-edge cure research, including CRISPR-Cas9 approaches aimed at either disabling integrated viral genomes or engineering HIV-resistant immune cells. Across all three areas one theme remains constant: PCR, sequencing, and cloning form the technological backbone of HIV research. As these tools continue to evolve, so too does the potential to improve outcomes and one day eliminate the virus entirely. Since recording this episode, Ryan has joined KBI Biopharma as a Scientist l in their Formulation Development Group. Helpful resources and links: Access Stanford University's HIV Drug Resistance Database. Visit International AIDS Society's Towards an HIV Cure site, which includes resources.  Access Thermo Fisher PCR resources and products. Learn about RT-qPCR, which is relevant to HIV research.  Explore the cloning technologies referenced in this episode.  Subscribe to get future episodes as they drop and if you like what you're hearing we hope you'll share a review or recommend the series to a colleague.  Visit the Invitrogen School of Molecular Biology to access helpful molecular biology resources and educational content, and please share this resource with anyone you know working in molecular biology. For Research Use Only. Not for use in diagnostic procedures.

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.

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.

At the 3rd Biennial Miami Precision Medicine Conference, CancerNetwork® spoke with a variety of researchers and clinicians who presented on different topics regarding the use of targeted therapies across several cancer types. Faculty from the University of Miami Sylvester Comprehensive Cancer Center shared key advances and ongoing initiatives across pancreatic cancer, sarcomas, genitourinary malignancies, and other diseases.First, Jashodeep Datta, MD, an associate professor of surgery, a co-leader of the Gastrointestinal Site Disease Group, an associate director of Translational Research, and Sylvester Pancreatic Cancer Research Institute DiMare Family Endowed Chair in Immunotherapy, discussed his presentation on overcoming a historical “moratorium” associated with immunotherapy in pancreatic cancer. Based on recent data, he noted that current goals include analyzing distinct subpopulations of patients who respond to immunotherapy and understanding the biology of why they respond to inform the design of novel therapeutic approaches. Looking towards the future, Datta described how mRNA vaccines may play a larger role in advancing personalized patient care.Next, Steven Bialick, DO, a gastrointestinal and sarcoma and connective tissue medical oncologist, spoke about his presentation on diagnosing and treating patients with sarcomas. He highlighted how markers like microsatellite instability-high status may help identify patients who are suitable candidates to receive immunotherapies like pembrolizumab (Keytruda). Overall, he emphasized the practice of thorough molecular testing to help navigate a treatment landscape that has “changed so dramatically” over the years. Finally, Jaime Merchan, MD, director of the Phase 1 Program and a tenured professor of medicine at the University of Miami Miller School of Medicine, talked about his presentation on the development of novel targeted therapies in genitourinary malignancies, which included bladder and kidney cancers. He described strategies for using new HIF-2⍺ inhibitors alongside therapeutic standards like tyrosine kinase inhibitors. Additionally, he detailed how other investigational drug classes, including oncolytic viruses and T-cell engagers, may fit into the treatment paradigm for these genitourinary cancers. References Datta J. Mission impossible? Strategies for precision immunotherapy in pancreatic cancer. Presented at the 3rd Biennial Miami Precision Medicine Conference; April 11-12, 2026; Fort Lauderdale, FL. Bialick S. Precision oncology in the diagnosis and management of sarcoma patients. Presented at the 3rd Biennial Miami Precision Medicine Conference; April 11-12, 2026; Fort Lauderdale, FL. Merchan J. Genitourinary cancers: bladder and kidney. Presented at the 3rd Biennial Miami Precision Medicine Conference; April 11-12, 2026; Fort Lauderdale, FL.

Järvinen-Seppo discusses how translational research is advancing understanding of early allergic disease, from maternal antibodies to global collaborations shaping the future of prevention and care. Timestamps: 00:57 – Research scope  03:49 – Maternal antibodies  07:34 – Integrating new evidence  09:17 – International coordination  10:37 – Emerging areas

In this special “Ask the Expert” collaboration between The MOG Project and SRNA, Julia Lefelar and Dr. GG deFiebre welcomed Dr. Benjamin Greenberg of UT Southwestern, who answered questions from the audience. Dr. Greenberg reviewed major advances in MOG antibody disease research and diagnostic criteria [00:05:06]. He discussed efforts to predict relapse risk using sustained antibody positivity, demographic and clinical models, and immune-cell profiling studies [00:07:55]. Dr. Greenberg detailed controversies around low-positive antibody titers and how cell-based assays and dilution thresholds affect specificity [00:21:38]. He outlined concepts and progress in tolerance-inducing approaches such as Tregs and CAR T therapy, described differences from B-cell–depleting drugs like rituximab [00:26:32] Finally, Dr. Greenberg highlighted the satralizumab meteoroid trial and the ongoing cosMOG study of rozanolixizumab, emphasizing community engagement, registries, surveys, and trial participation to accelerate access and potential curative strategies [00:38:36]. You can learn more about The MOG Project here:https://mogproject.org/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 Welcome01:44 Hosts and Guest Intro05:06 Research Buckets Overview07:55 Predicting Relapse Risk11:46 Tregs and Immune Brakes17:40 Attack Severity and Relapse19:24 MOGAD Criteria Updates21:38 Titers Explained Simply26:32 Targeting MOG Antibodies29:11 CAR T and Immune Reset32:39 When Criteria Changes33:52 Tolerance Research Boom34:48 From Animals to Trials37:17 Community Drives Progress38:36 Meteoroid and cosMOG Clinical Trials41:39 How These Drugs Work44:02 FDA Approval and Access45:49 Insurance Switch Concerns48:39 Rituximab Dosing Debate52:41 Why Antibodies Develop54:18 Future Attack Patterns55:47 CAR T Versus Rituximab57:10 Lab Research and Support01:00:51 Hope for a Cure01:02:14 Closing and Resources

On this episode of SurgOnc Today, Flavio Rocha, Professor and Division Head of Surgical Oncology at OHSU Knight Cancer Institute, leads a discussion about engagement of surgeons in the National Clinical Trials Network cooperative groups with Sepideh Gholami, Associate Professor and Director of Translational Research in Surgical Oncology at Northwell Health, and Michael Lowe, Associate Professor and Director of the Melanoma Program at Winship Cancer Institute of Emory University. They discuss the impact that surgeons can have on the design and implementation of NCI-sponsored clinical trials and offer insights on ways for surgeons to engage with the cooperative groups.

This episode originally aired on December 2nd, 2021. Drs. Julie Bastarache and Katie Wick sit down to discuss non-invasive sampling of the lungs in translational research.

In this episode, Robert A. Figlin, MD, FACP, Steven Spielberg Family Chair in Hematology Oncology and Interim Director of Cedars-Sinai Cancer and the Samuel Oschin Comprehensive Cancer Institute, discusses aligning cancer strategy with system priorities, embedding research into clinical care, and building innovative, patient centered models to improve access and outcomes across the continuum.

In this episode, Robert A. Figlin, MD, FACP, Steven Spielberg Family Chair in Hematology Oncology and Interim Director of Cedars-Sinai Cancer and the Samuel Oschin Comprehensive Cancer Institute, discusses aligning cancer strategy with system priorities, embedding research into clinical care, and building innovative, patient centered models to improve access and outcomes across the continuum.

In this powerful episode, we sit down with Dr. Joe Zundell — aka “Cancer Daddy” — for a wide-ranging conversation on cancer science, early detection, and what's actually moving the field forward. We cover: • Multi-cancer early detection (MCED) testing and the promise of liquid biopsies • Accuracy, limitations, and clinical decision-making • Metabolic vulnerabilities in cancer (Warburg effect, glutamine dependence) • Epigenetics and tumor biology • Immunotherapy, targeted therapies, and radiopharmaceuticals • Translational research and the bench-to-bedside gap • Drug resistance and evolutionary pressure in cancer treatment • Personalized risk reduction and prevention strategies We also get very personal in this episode — discussing loss, integrity in academia, career pivots, and what truly drives Dr. Zundell's mission in cancer research. This is an honest, science-first, and deeply human conversation about cancer, prevention, innovation, and responsibility in modern medicine. Coach Vinny Email: vinny@balancedbodies.io Instagram: vinnyrusso_balancedbodies Facebook: Vinny Russo Dr. Eryn Email: dr.eryn@balancedbodies.io Instagram: dr.eryn_balancedbodies Facebook: Eryn Stansfield Dr. Joe Zundell Email: drjoezundell@gmail.com Instagram: dr.joezundell LEGION 20% OFF CODE Go to https://legionathletics.com/ and use the code RUSSO for 20% off your order!

Guest: Dr. Thomas E. Van Dyke, DDS, PhDShow Notes:Your mouth does far more than help you chew; it may be quietly shaping your risk for heart disease, diabetes, and chronic inflammation. In this episode, we explore the powerful (and often overlooked) connection between gum health and whole-body health.You'll learn how everyday habits like brushing, flossing, smoking, and diet choices can influence inflammation throughout the body. We break down what science really says about gum disease, cardiovascular risk, blood sugar control, and the oral microbiome, plus which small changes can make an outsized impact over time.If you care about heart health, diabetes prevention, or lowering inflammation naturally, this episode will change how you think about oral care.Guest Bio:Dr. Van Dyke is Sr. Vice President for Clinical and Translational Research, and Senior Member of Staff, ADA Forsyth Institute in Somerville, MA; he received his D.D.S. from Case Western Reserve University; his Master's, Periodontics Certificate, and Ph.D., State University of NY at Buffalo; he is a Diplomate of the American Board of Periodontology. He is internationally recognized for his work on inflammation in periodontal disease and other systemic conditions. He has  500+ original publications. Quote:“The keyword of the day is maintaining homeostasis. You want to maintain the balance that we have in the oral cavity that is compatible with health in the individual.”Question of the Day:Have you ever considered how your oral health could affect your heart? After today, what's one step you could change or add to your oral hygiene routine?On This Episode You Will Learn:How gum disease and oral inflammation can increase the risk of heart disease, diabetes, and other chronic conditions.Why inflammation, not just bacteria, is the key link between oral health and whole-body health.Which daily habits matter most for protecting your gums, including brushing, flossing, smoking cessation, and diet.How nutrition choices, such as omega-3s, ultra-processed foods, and sugary drinks, affect your oral microbiome and inflammation levels.One small change you can start today that can make a meaningful difference for both your oral health and your heart.Connect with Yumlish!Yumlish Website: YumlishYumlish on Instagram: @yumlish_Yumlish on Facebook: YumlishYumlish on Twitter: @yumlish_Yumlish on LinkedIn: YumlishConnect with Thomas E. Van Dyke!Website URL: www.forsyth.org

Pediatric neuropalliative medicine is an emerging area of subspecialty practice that emphasizes the human experience elements of serious neurologic illness. Child neurologists care daily for patients who can benefit from the communication strategies and management practices central to pediatric neuropalliative medicine, whether at the primary or subspecialty level. In this episode, Gordon Smith, MD, FAAN, speaks with Lauren Treat, MD, author of the article "Neuropalliative Medicine in Pediatric Neurology" in the Continuum® December 2025 Neuropalliative Care 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. Treat is an associate professor in the divisions of child neurology and palliative medicine at the University of Colorado School of Medicine in Aurora, Colorado. Additional Resources Read the article: Neuropalliative Medicine in Pediatric 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: @gordonsmithMD Full episode transcript available here Dr Jones: This is Dr Lyell Jones, Editor-in-Chief of Continuum. Thank you for listening to Continuum Audio. Be sure to visit the links in the episode notes for information about earning CME, subscribing to the journal, and exclusive access to interviews not featured on the podcast. Dr Smith: This is Gordon Smith. Today I've got the great pleasure of interviewing my good friend Dr Lauren Treat about her article on neuropalliative medicine in pediatric neurology practice. This article appears in the December 2025 Continuum issue on neuropalliative care. Lauren, welcome to the Continuum podcast, and maybe you can introduce yourself to our listeners. Dr Treat: Such a delight to be here, Gordon. Thank you. I am a pediatric neurologist and palliative medicine doctor at the University of Colorado, Children's Hospital Colorado, and I am practicing in both areas. I do general child neurology, and I also run a pediatric neuropalliative medicine clinic. So, I'm happy to be here to talk about it. Dr Smith: And, truth in advertising, I tried very hard to get Dr Treat to move to VC to work with me. And I haven't given up yet. I'm looking forward to the conversation. And Lauren, I wonder- one, I'm really excited about this issue, by the way. This is the second podcast I've done. And I'd like to ask the same question I asked of David Oliver, who's amazing. What a great article and conversation we had. And that question is, can you define palliative care? I think a lot of people think of it as, like, end-of-life care or things like that. And is the definition a little different in the pediatric space than it is in the adult space? Dr Treat: Such a great place to start, Gordon. I absolutely think that there are nuances that are very important in pediatrics. And we especially acknowledge in pediatrics that there is a very longitudinal component of this. And even moreso, I think, then in adult neuropalliative medicine, in pediatrics, we are seeing people=even prenatally or early in their first hours and days of life, and walking with them on a journey that might last days or weeks, but might last years or decades. And so, there is this sense that we are going to come alongside them and be part of the ups and the downs. So yes, neuropalliative medicine is a kind of medicine that is a very natural partner to where neurology is in its current field. We're doing a lot of exciting things with modifying diseases, diagnosing things early, and we have a very high reliance on the things that we can measure in medicine. And not all things can be measured that are worthwhile about one's quality of life. A family very poignantly told me very recently, making sure someone stays alive is different from making sure they have a life. And that's what neuropalliative medicine is about. Dr Smith: Well, great summary, and I definitely want to follow up on several aspects of that, but there's one point I was really curious about as I've been thinking about this, you know, these are really exciting times and neurology in general and in child neurology in particular. And we've got all of these exciting new therapies. And as you know, I'm a neuromuscular person, so it's hard not to think back on SMA and not be super excited. And so, I wonder about the impact of these positive developments on the practice of neuropalliative care in kids. You know, I'm just thinking, you know, you mentioned it's a journey with ups and downs. And I wonder, the complexity of that must be really interesting. And I bet your job looks different now than it did seven or eight years ago. Dr Treat: That's absolutely true. I will self-reference here one of the figures in the paper. Figure 2 in my section is about those trajectories, about how these journeys can have lots of ups and downs and whether this person had a normal health status to begin with or whether they started out life with a lot of challenges. Those ups and downs inherently involve a lot of uncertainty. And that's where palliative medicine shines. Not because we have the answer---everyone would love for us to have the answer---but because we consider ourselves uncertainty specialists in the way that we have to figure out what do we know, what can we ground ourselves in, and how can we continue to move forward even if we don't have all the answers? That is a particular aspect of neurology that is incredibly challenging for families and clinicians, and it can't stand as a barrier to moving forward and trying to figure out what's best for this child, what's best for this family. What do we know to be true about them as people, and how can we integrate that with all of the quantitative measures that we know and love in neurology? Dr Smith: So, I love the comment about prognostication, and this really ties into positive uncertainty or negative undercertainty in terms of therapeutic development. I wonder if you can talk a little bit about your approach to prognostication, particularly in a highly fluid situation. And are there pearls and pitfalls that our listeners should consider when they're discussing prognosis for children, particularly maybe young children who have severe neurological problems? Dr Treat: It's such a pivotal issue, a central issue, to child neurology practice. Again, because we are often meeting people very, very early on in their journey---earlier than we ever have before, sometimes, because of this opportunity to have a diagnosis, you know, prenatally or genetically or whatever else it is---sometimes we are seeing the very early signs of something as compared to previously where we wouldn't have a diagnosis until something was in its more kind of full-blown state. This idea of having a spectrum and giving people the range of possible outcomes is absolutely still what we need to do. However, we need to add on another skill on top of that in helping people anchor into what feels like the most likely situation and what the milestones are going to be in the near future, about how we're going to walk this journey and what we'll be on the lookout for that will help us branch into those different areas of the map down the road. Dr Smith: So, I wonder if we can go back to the framework you mentioned, two answers ago, I think? You and the article, you know, provide four different types of situations kind of based on temporal progression. I wonder if maybe the best way of approaching is to give an example and how that impacts your thoughts of how you manage a particular situation. Dr Treat: Absolutely. So, this figure in particular is helpful in multiple ways. One is to just give a visual of what these disease trajectories are doing, because we're doing that when and we take a history from a patient. But actually, to put it into an external visual for yourself, for your team, but also perhaps for the family can be really powerful. It helps you contextualize the episode of care in which you're meeting the family right now. And it also helps, sometimes, provide some sense of alignment or point out some discrepancies about how you're viewing that child's health and quality of life as compared to how the family might be viewing it. And so, if you say, you know, it sounds like during those five years before we met, you were up here, and now we find ourselves down here, and we're kind of in the middle of the range of where I've seen this person's health status be. Do I have that right? Families feel really seen when you do that and when you can get it accurately. And it also invites a dialogue between the two parties to be able to say, well, maybe I would adjust this. I think we had good health or good quality of life in this season. But you're right, it's getting harder. It's kind of that "show, don't tell" approach of bringing together all the facts to put together the relative position of where we are now in the context of everything they've been through. Dr Smith: You know, I wonder if you could talk a little bit more about the differences between palliative care and adult patients and in children? Dr Treat: Absolutely. One of the key features in pediatrics is this kind of overriding sense of an out-of-order event in the family's life. Children are not supposed to have illness. Children are not supposed to have disability. Children are not supposed to die before their parents. And that layer of tragedy is incredibly heavy and pervasive. It's not every encounter that you have in child neurology, but it does kind of permeate some of the conversations that neurologists have with their patients, especially patients who have serious neurological disease. So that could be things like epileptic encephalopathies, birth injuries, other traumatic brain injuries down the line. In the paper, I'd go through many different categories of the types of conditions that are eligible for pediatric neuropalliative medicine, that kind of support. When we think about that layer of tragedy in the relation to where we're meeting these families, they deserve extra support, not just to think about the medicines and the treatments, but also, what can we hope for? How can we give this child the best possible life in whatever circumstance that they're in? How can we show up in whatever medical decision-making circumstances present themselves to us and feel like we've done right by this child? It's a complex task, and pediatric neural palliative medicine is evolving to be able to be in those spaces with families in a very meaningful way. Dr Smith: So, of course, one of the differences is the, you know, very important role of parents in the situation, right? Obviously, parents are involved in adult palliative care issues and family is very important. But I wonder if you can talk about specific considerations given the parent-child relationship? Dr Treat: So, pediatric neuropalliative medicine really helps facilitate discussions not just about, again, those things that we have data on, but also about what is meaningful and foundational for those families. What's possible at home, what's possible in the community. In pediatrics, parents are making decisions on behalf of their child, often as a dyad, and I don't think this gets enough attention. We know from adult literature that making decisions on behalf of someone else is different from making decisions on behalf of oneself. We call this proxy decision-making. And proxies are more likely to be conservative on behalf of someone else than they are on behalf of themselves, and they're also more likely to overestimate the tolerability of a medical intervention. So, they might say, I wouldn't want this, or, I wouldn't accept this risk on behalf of myself, or, I don't think I'd want to have to persevere through something, but on behalf of this other person, I think they can do it or I will help them through it or something else like this, or, I can't accept the risk on behalf of them. So that's not good or bad. That's just different about making a decision on behalf of oneself as compared to making a decision on behalf of someone else. When there's two people trying to be proxies on behalf of a third person, on behalf of a child, that's a really, really complex task, and it deserves support. And so, pediatric neural palliative medicine can function, then, as this neutral space, as this kind of almost coaching opportunity alongside the other medical doctors to give parents an opportunity when their minds are calm---not in the heat of the moment---to talk about how they see their child, how they've shown up themselves, what they've seen go well, what they've struggled with. And how,, then we can feel prepared for future decision making times, future high-stress encounters, about what will be important to ground them in those moments, even though we can't predict fully what those circumstances might be. Dr Smith: It sounds, you know, from talking to you and having read the article, that these sorts of issues evolve over time, right? And you have commented on this already from your very first answer. And you do describe a framework for how parents think---their mental model, I guess---of, you know, a child with a serious illness. And this sounds like appreciation of that's really important in providing care. Maybe you can talk us through that topic? Dr Treat: I refer to this concept of prognostic awareness in all of the conversations that we have with families. So, what I mean by prognostic awareness is the degree of insight that an individual has about what's currently happening with their child and what may happen in the future regarding the disease and/or the complications. And when we meet people early on in their journey, often their prognostic awareness, that sense of insight about what's going on, can be limited because it requires lived experience to build. Oftentimes time is a factor in that, we gain more lived experience over time, but it's not just time that goes into building that. It's often having a child who has a complication. Sometimes it's experiencing a hospitalization. That transfer from a cognitive understanding of what's going on, from a lived experience about what's going on, really amplifies that prognostic awareness, and it changes season by season in terms of what that family is going through and what they're willing to tolerate. Dr Smith: You introduced a new term for me, which is hyper-capableism. Can you talk about that? I found that really interesting and, you know, it reminds me a lot of the epiphanies that we've had about coma and coma prognosis. So, what's hyper-capableism? Dr Treat: Yes. In neurology, we have to be very aware of our views on ableism, on understanding how we prognosticate in relation to what we value about our abilities. And hyper-capableism refers to someone who feels very competent both cognitively and from a motor standpoint and fosters that sense of value around those two aspects to a high degree. I'm referencing that in the article with regard to medicine, because medicine, the rigors of training, the rigors of practice, require that someone has mental and motor fortitude. That neurology practice and medical practice in general can breed this attitude around the value of skills in both of those areas. And we have to be careful in order to give our patients and families the best care, to not overly project our values and our sense of what's good and bad in the world regarding ableism. Impairments can look different in different social contexts. And when the social context doesn't support an impairment, that's where people struggle. That's where people have stigma. And I think there's a lot of work that we can do in society at large to help improve accommodations for impairment so that we have less ableism in society. Dr Smith: Another term that I found really interesting kind of going back to parents is the "good parent identity." Maybe you can talk about that? Dr Treat: Good parent identity, good parent narrative, is something that is inherent to the journey when you're trying to take care of and make decisions on behalf of a child. And whether you're in a medical context or outside of a medical context, all parents have this either explicit or implicit sense of themselves about what it means to do right by their child. This comes up very poignantly in complex medical conditions because there are so many narratives about what parents ought to do on behalf of their child, and some of those roles can be in tension with one another. It's a whole lot of verbs that often fall under that identity. It's about being able to love and support and take good care of and make good decisions on behalf of someone. But it's also about protecting them from harm and treating their pain and being able to respond to them and know their cues and know these details about them. And you can't, sometimes, do multiple of those things at once. You can't give them as much safety and health as possible and also protect them from pain and suffering when they have a serious illness, when they need care in the hospital that might require a treatment that might be invasive or burdensome to them. And so, trying to be a good parent in the face of not being able to fulfill all those different verbs or ideas about what a good parent might do is a big task. And it can help to make it an explicit part of the conversation about what that family feels like their good parent roles might be in a particular situation. Dr Smith: I want to shift a little bit, Lauren, that's a really great answer. And just, you know, listening to you, your language and your tongue is incredibly positive, which is exciting. But, you know, you have talked about up and downs, and I wanted you to comment on a quote. I actually wrote it down, I'm going to read it to you, because you mentioned this early on in your article: "the heavy emotional and psychological impacts of bearing witness to suffering as a child neurologist." I think all of us, no matter how excited we are about all the therapeutic development, see patients who are suffering. And it's hard when it's a child and you're seeing a family. I wonder if you could talk a little bit about that comment and how you balance that. You're clearly- you're energized in your career, but you do have to bear witness to suffering. Dr Treat: You're right. Child neurologists do incredible work, it's an incredible, exciting field, and there are a lot of challenges that we see people face. And we see it impacts their lives in really intense ways over the course of time. We bear witness to marriages that fall apart. We bear witness to families that lose jobs or have to transition big pieces of their identity in order to care for their children. And that impacts us. And we hold the collective weight of the things that we are trying to improve but sometimes feel less efficacious than we hoped that we could around some of these aspects of people's lives. And so, pediatric neuropalliative medicine is also about supporting colleagues and being able to talk to colleagues about how the care of the patients and the really real effort that we exert on their behalf and the caring that we have in our hearts for them, how that matters. Even if the outcome doesn't change, it's something that matters for our work and for our connections with these families. It's really important. Dr Smith: I wonder, maybe we can end by learning a little bit about your journey? And maybe this is your opportunity to- I know we have students and residents who listen to us, and junior faculty. I think neuropalliative care is obviously an important issue. There's a whole Continuum issue on it---no pun intended---but what was your journey, and maybe what's your pitch? Dr Treat: I'm just going to give a little bit of a snippet from a poem by Andrea Gibson, who's a poet, that I think speaks really clearly to this. They say a difficult life is not less worth living than a gentle one. Joy is simply easier to carry than sorrow. I think that sums these things up really well, that we find a lot of meaning in the work that we do. And it's not that it's easier or harder, it's just that these things all matter. I'm going to speak now, Gordon, to your question about how I got to my journey. When I went into pediatrics and then neuro in my training, I have always loved the brain. It's always been so crucial to what I wanted to do and how I wanted to be in the world. And when I was in my training, I saw that a lot of the really impactful conversations that we were having felt like we left something out. It felt like we couldn't talk about some of the anticipated struggles that we would anticipate on a human level. We could talk about the rate and the volume of the G tube, but we couldn't talk about how this was going to impact a mother's sense of being able to nourish and bond and care for their child because we didn't have answers for those things. And as I went on in my journey, I realized that even if we don't have answers, it's still important for us to acknowledge those things and talk about them and be there for our patients in those conversations. Dr Smith: Well, Lauren, what a great way to end, and what a wonderful conversation, and what a great article. Congratulations and thank you. Dr Treat: Thank you, Gordon. It was a pleasure to be here. Dr Smith: Again today, I've been interviewing Dr Lauren Treat about her really great article on neuropalliative medicine in pediatric neurology practice. This article appears in the December 2025 Continuum issue on neuropalliative care. Be sure to check out Continuum Audio episodes from this issue and other issues. And thanks again 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.

Send us a textIn episode #170 we spoke with researcher Dr. David Church about:The crucial role of muscle protein synthesis in endurance athletesThe role of essential amino acids on muscle growth and recoveryThe impact of sleep deprivation on muscle recovery and performance.Dr. David Church, the Director of the Center for Translational Research in Aging & Longevity at University of Arkansas for Medical Sciences, College of Medicine. Dr. Church obtained his bachelor's degree in exercise science and biochemistry from DePauw University where he played football and baseball. He was an athletic performance intern at Baylor University where he studied exercise and nutritional biochemistry. He obtained his PhD from the University of Central Florida with a focus on enhancing human performance through exercise and nutrition and completed his post-doctoral fellowship in stable-isotope tracer methodology under the mentorship of Drs. Robert R. Wolfe and Arny Ferrando. He has led multiple trials investigating energy restriction in healthy and clinical populations including two active trials on individuals prescribed GLP-1RA's. He has been recognized for his work with the Nutrition Research Achievement Award from the National Strength and Conditioning Society, the Vernon Young International Award for Amino Acid Research from the American Society for Nutrition, and a Fellow of the International Society of Sports Nutrition.Please note that this podcast is created strictly for educational purposes and should never be used for medical diagnosis or treatment.Follow Dr. Church:InstagramWebMentioned:Dr. Dan MooreDr. Mikkel OxfeldtSleep studies:pmc.ncbi.nlm.nih.gov/articles/PMC7785053/pmc.ncbi.nlm.nih.gov/articles/PMC6917985/Dr. Shiloah KviatkovskyDr. Keith Barr, NR episode 82, collagenWhey Protein IsolateEssential Amino AcidsDr. Heather LeidyMORE NR Save 10% on our website with code NEWPOD10 Apply to work with us, click here: https://nutritional-revolution.com/ Follow us @nutritionalrevolution Save 20% on supplements at our trusted online source: https://us.fullscript.com/welcome/kchannell Join Nutritional Revolution's The Feed Club to get $20 off with an additional $20 Feed credit drop every 90 days.: https://thefeed.com/teams/nutritional-revolution If you're interested in sponsoring Nutritional Revolution Podcast, shoot us an email at nutritionalrev@gmail.com.

On-site on the sidelines of JP Morgan Healthcare conference in San Francisco this year, pharmaphorum editor-in-chief Jonah Comstock sat down with Andrew Beck, co-founder and CEO at PathAI. The conversation covers what PathAI has been up to lately in AI within diagnostics in pathology, explores what's been discussed on the ground at the conference, and also touches upon equality and access to precision diagnostics. Additionally, Beck notes the company's work in prospective clinical trials in life sciences, as well as co-partnering with pharma. Having seen an over 10 x growth of adoption of their technology in 2025, Beck also discusses advances in the MASH field. Listen to this and other conversations from JPM2026 here. You can listen to episode 240 of the pharmaphorum podcast in the player below, download the episode to your computer, or find it - and subscribe to the rest of the series – on Apple Podcasts, Spotify, Overcast, Pocket Casts, Podbean, and pretty much wherever else you download your other podcasts from.

This is Part 3 of a conversation with Lucy Butler of River Haven Animal Sanctuary, and Dr Stephanie Jones and her grad student, Sofia Abuin Dr. Jones graduated with her PhD in Behavior Analysis from West Virginia University in 2021. Her primary research focuses on effects of implementer errors that occur during well-established behavioral treatments. To meet this aim, she conducts laboratory and applied research with the aim of supporting development of robust behavioral interventions. She started teaching and conducting research at Salve Regina University in 2021 and is the principal investigator for the Translational Research and Applied Intervention Lab. IN PART 1 we talked about the common links between teaching people and working with animals. We talked about coercion, control, and most importantly about empathy. In part 2 Stephanie described a pilot study she and her colleagues set up at the River Haven Animal Sanctuary. Shaping can be incredibly challenging to teach well. Often people refer to the science and the art of training. What Stephanie and her colleague Michael Yencha wanted to investigate is what makes up the “art” part of training? Is there a way to tease this apart so it becomes less mystery and more approachable through science? Stephanie began by describing the shaping procedures they used with the goats at River Haven. In one context the criteria was changed when the goat had successfully met the current criterion three times in a row. In the second context a latency component was added. The goat had to meet the criterion within a certain time period which was determined by the goat's own previous performance. I described the metaphor of shaping from the wide versus the narrow end of the funnel and what it means to shape using narrow end of the funnel thinking. In Part 3 Stephanie reminded us that the goal of this research was to help new trainers shape well. That was the reason for the latency criterion. They were using it to judge when to shift criteria. They weren't looking at any other aspects of shaping. They weren't looking at the details of the reinforcement strategy or the set up of the environment. They weren't saying those elements aren't important, but they wanted to focus on this one component and give it a good rule. The question was how do you get robust interventions that aren't influenced by implementor errors? Even in art there is technique. If you give people this rule, does that mean learners will be better off because shapers are able to minimize exposure to extinction without even needing to know what it means to minimize exposure to extinction? Can new trainers shape well even when they are lacking experience and a broad theoretical background?

Finding Science in the Art of Training This is Part 2 of a conversation with Lucy Butler of River Haven Animal Sanctuary, and Dr Stephanie Jones and her grad student, Sofia Abuin Dr. Jones graduated with her PhD in Behavior Analysis from West Virginia University in 2021. Her primary research focuses on effects of implementer errors that occur during well-established behavioral treatments. To meet this aim, she conducts laboratory and applied research with the aim of supporting development of robust behavioral interventions. She started teaching and conducting research at Salve Regina University in 2021 and is the principal investigator for the Translational Research and Applied Intervention Lab. Through her lab, she supports research engagement of students at the undergraduate, master's, and doctoral training levels. She publishes in and reviews for several peer-reviewed behavior-analytic journals, such as the Journal of Applied Behavior Analysis and Education and Treatment of Children. Good training is very much emphasizes the importance of taking the time to build a relationship with the individuals you're interacting with. We modeled that in Part One. Dominique and I were meeting Stephanie and Sophia for the first time in this recording. So I instead of jumping straight in to the study Stephanie and her collegues conducted at River Haven, in Part One we began by talking about control, and even more about empathy. In this episode Stephanie describes a pilot study she and her collegues from Salve Regina University set up at the River Haven Animal Sanctuary. Shaping can be incredibly challenging to teach well. Often people refer to the science and the art of training. What Stephanie and her colleague Michael Yencha wanted to investigate is what makes up the “art” part of training? Is there a way to tease this apart so it becomes less mystery and more approachable through science?

Careful assessment and individualized care, provided by a skilled multidisciplinary care team, are emphasized in the holistic approach to neuropalliative care, which considers physical, psychological, social, spiritual, and existential aspects for people with neuromuscular diseases. In this episode, Gordon Smith, MD, FAAN, speaks with David J. Oliver, PhD, FRCP, FRCGP, FEAN, author of the article "Neuropalliative Care in Neuromuscular Disorders" in the Continuum® December 2025 Neuropalliative Care 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. Oliver is an honorary professor of Tizard Centre at the University of Kent in Canterbury, United Kingdom. Additional Resources Read the article: Neuropalliative Care in Neuromuscular Disorders Subscribe to Continuum®: shop.lww.com/Continuum Earn CME (available only to AAN members): continpub.com/AudioCME Continuum® Aloud (verbatim audio-book style recordings of articles available only to Continuum® subscribers): continpub.com/Aloud More about the American Academy of Neurology: aan.com Social Media facebook.com/continuumcme @ContinuumAAN Host: @gordonsmithMD Full episode transcript available here Dr Jones: This is Dr Lyell Jones, Editor-in-Chief of Continuum. Thank you for listening to Continuum Audio. Be sure to visit the links in the episode notes for information about earning CME, subscribing to the journal, and exclusive access to interviews not featured on the podcast. Dr Smith: Hello, this is Dr Gordon Smith. Today I've got the great pleasure of interviewing Dr David Oliver about his article on neuropalliative care and neuromuscular disorders, which appears in the December 2025 Continuum issue on neuropalliative care. David, welcome to the Continuum podcast, and please introduce yourself to our audience. Dr Oliver: Thank you. It's a pleasure and a privilege to be here. I'm a retired consultant in palliative medicine in the UK. I worked at the Wisdom Hospice in Rochester for over thirty years, and I'm also an honorary professor at the University of Kent in Canterbury in the UK. I've had a long interest in palliative care in neurological diseases. Hopefully we can talk about a bit later. Dr Smith: I really look forward to learning a little bit more about your path and experiences. But I wonder if, before we get into the meat of neuropalliative care with a focus on neuromuscular, if maybe you can kind of set the stage by just defining palliative care. I mean, my experience is that people think of this in different ways, and a lot of folks think- hear palliative care, and they immediately go to end-of-life care or comfort care. So, what- how should we think about maybe the discipline of palliative care or neuropalliative care? Dr Oliver: I see palliative care as very much responding to people's needs, whether that's physical needs, psychological needs, social or spiritual or existential. So, it can be much earlier in the disease progression. And I think particularly for neurological diseases, early involvement may be very important. Dr Smith: That was actually going to be my first substantive question, really, was when to begin the conversation and what does that look like and how does it evolve over time. You have a really great figure in the article that kind of emphasizes the various stages within a patient's journey that, you know, palliative care can become involved. But I wonder if you could use ALS as a good example and describe what that looks like from when a patient is first diagnosed with ALS through their course? Dr Oliver: I think particularly in ALS at the beginning, soon after diagnosis, someone may have a lot of distress and a lot of questions that they need answering. This is a disease they've not had any contact with before. And they don't understand what's going on, they don't understand the disease. So, there may be a great need to have the opportunity to talk about the disease, what may happen, what is happening, how it's going to affect them and their family. As think time goes on, there may be later they develop swallowing problems, and that will need to be talking about a feeding tube and gastrostomy. And again, there may be a lot of issues for the person and their family. As they deteriorate, they may have respiratory problems and need to have discussion about ventilatory support, either by PAP, noninvasive ventilation, or even tracheostomy. And again, I think that's a big issue that needs wide discussion. And then it may be at the final few months of the disease, where they are deteriorating, that they may have increased needs, and their families may have those needs after the death. And I think often families bereaved from someone with a neurological disease such as ALS need a great deal of support, having many mixed emotions. There may be a feeling of relief that they're not involved in that caring, but then a feeling of guilt that they shouldn't be having those feelings. So, I think that can happen over a period of… what with ALS it may be two, three, four years, but it may be similar changes over time with any patient with a neurological disease. It may be ten or fifteen years with Parkinson's or five to ten years with a progressive supranuclear palsy, but there'll be this similar need to look at palliative care during their disease progression. Dr Smith: So, I'm curious at the time of diagnosis of ALS, how far out in the future do you provide information? So a specific question would be, do you talk about end-of-life management? In my experience, ALS patients are sometimes interested in knowing about that. Or do you really focus on what's in front of you in the next three to six months, for instance? Dr Oliver: I think it's both. Obviously, we need to talk about the next three to six months, but often giving patients the opportunity to talk about what's going to happen in the future, what may happen at the end of life, I think is important. And I think a disease like ALS, if they look it up on the Internet, they may have a lot of very distressing entries there. There's a lot about how distressing dying with ALS is. And actually confront those and discuss those issues early is really important. Dr Smith: So of course, the other thing that comes up immediately with an ALS diagnosis---or, for that matter, with any other neurodegenerative problem---is prognosis. Do you have guidance and how our listeners who are giving a diagnosis of ALS or similar disorder should approach the prognostication discussion? Dr Oliver: It's often very difficult. Certainly in the UK, people may have- be a year into their disease from their first symptoms before they're diagnosed, and I've seen figures, that's similar across the world. So, people may be actually quite way through their disease progression, but I do think we have to remember that the figures show that at five years, 25% of people are still alive, and 5 to 10% are still alive at ten years. We mustn't say you are going to die in the next two or three years, because that may not be so. And I think to have the vagueness but also the opportunity to talk, that we are talking of a deterioration over time and we don't know how that will be for you. I always stress how individual I think ALS is for patients. Dr Smith: One of the other concepts that is familiar with anyone who does ALS and clearly comes through in your article---which is really outstanding, by the way. So, thank you and congratulations for that---is the importance of multidisciplinary teams. Can you talk a little bit about how neuropalliative care sits within a multidisciplinary care model? Dr Oliver: I think the care should be multidisciplinary. Certainly in the UK, we recommended multidisciplinary team care for ALS in particular, from the time of diagnosis. And I think palliative care should be part of that multidisciplinary team. It may be a member of the team who has that palliative care experience or someone with specialist experience. Because I think the important thing is that everyone caring for someone with ALS or other neuromuscular diseases should be providing palliative care to some extent: listening to people, discussing their goals, managing their symptoms. And a specialist may only be needed if those are more complicated or particularly difficult. So, I think it is that the team needs to work together to support people and their families. So, looking at the physical aspects where the physiotherapist or occupational therapist may be very important, the psychologicals are a counsellor or psychologist. The social aspects, most of our patients are part of wider families, and we need to be looking at supporting their carers and within their family as well as the person. And so that may involve social work and other professionals. And the spiritual, the why me, their fears about the future, may involve a spiritual counsellor or a chaplain or, if appropriate, a religious leader appropriate to that- for that person. So, I think it is that wider care provided by the team. Dr Smith: I'm just reflecting on, again, your earlier answers about the Continuum of neuropalliative care. Knowing your patient is super valuable here. So, having come to know someone through their disease course must pay dividends as you get to some of these harder questions that come up later during the disease progression. Dr Oliver: I think that's the very important use of palliative care from early on in the diagnosis. It's much easier to talk about, perhaps, the existential fears of someone while they can still talk openly. To do that through a communication aid can be very difficult. To talk about someone's fear of death through a communication aid is really very, very difficult. The multidisciplinary team, I think, works well if all the members are talking together. So that perhaps the speech therapist has been to see someone and has noticed their breathing is more difficult, comes back and talks to the doctor and the physiotherapist. The social worker notices the speech is more difficult and comes back and speaks to the speech therapist. So, I think that sort of team where people are working very closely together can really optimize the care. And as you said, knowing the person, and for them to know you and to trust you, I think that's important. Those first times that people meet is so important in establishing trust. And if you only meet people when they're very disabled and perhaps not able to communicate very easily, that's really difficult. Dr Smith: I think you're reading my mind, actually, because I was really interested in talking about communication. And you mentioned a few times in your article about voice banking, which is likely to be a new concept for many of our listeners. And I would imagine the spectrum of tools that are becoming available for augmented communication for patients who have ALS or other disorders that impair speech must be impressive. I wonder if you could give us an update on what the state of the art is in terms of approaching communication. Dr Oliver: Well, I think we all remember Stephen Hawking, the professor from Cambridge, who had a very robotic voice which wasn't his. Now people may have their own voice on a communication aid. I think the use of whether it's a mobile phone or iPad, other computer systems, can actually turn what someone types into their own voice. And voice banking is much easier than it used to be. Only a few years ago, someone would have to read for an hour or two hours so the computer could pick up all the different aspects of their voice. Now it's a few minutes. And it has been even- I've known that people have taken their answer phone off a telephone and used that to produce a voice that is very, very near to the person. So that when someone does type out, the voice that comes out will be very similar to their own. I remember one video of someone who'd done this and they called their dog, and the dog just jumped into the air when he suddenly heard his master's voice for the first time in several months. So, I think it's very dramatic and very helpful for the person, who no longer feels a robot, but also for their family that can recognize their father, their husband, their wife's speech again. Dr Smith: Very humanizing, isn't it? Dr Oliver: There is a stigma of having the robotic voice. And if we can remove that stigma and someone can feel more normal, that would be our aim. Dr Smith: As you've alluded to, and for the large majority---really all of our ALS patients, barring something unexpected---we end up in preparing for death and preparing for end of life. I wonder what advice you have in that process, managing fear of death and working with our patients as they approach the end of their journey. Dr Oliver: I think the most important thing is listening and trying to find what their particular concerns are. And as I said earlier, they may have understood from what they've read in books or the Internet that the death from ALS is very distressing. However, I think we can say there are several studies now from various countries where people have looked at what happens at the end of life for people with ALS. Choking to death, being very distressed, are very, very rare if the symptoms are managed effectively beforehand, preparations are made so that perhaps medication can be given quickly if someone does develop some distress so that it doesn't become a distressing crisis. So, I think we can say that distress at the end of life with ALS is unusual, and probably no different to any other disease group. It's important to make sure that people realize that with good symptom control, with good palliative care, there is a very small risk of choking or of great distress at the end of life. Dr Smith: Now, I would imagine many patients have multiple different types of fear of death; one, process, what's the pain and experience going to be like? But there's also being dead, you know, fear of the end of life. And then this gets into comments you made earlier about spirituality and psychology. How do you- what's your experience in handling that? Because that's a harder problem, it seems, to really provide concrete advice about. Dr Oliver: Yeah. And so, I think it's always important to know when someone says they're frightened of the future, to check whether it is the dying process or after death. I've got no answer for what's going to happen afterwards, but I can listen to what someone may have in their past, their concerns, their experience. You know, is their experience of someone dying their memories of someone screaming in pain in an upstairs bedroom while they were a child? Was their grandfather died? Trying to find out what particular things may be really a problem to them and that we can try and address. But others, we can't answer what's going to happen after death. If someone is particularly wanting to look at that, I think that may be involving a spiritual advisor or their local spiritual/religious leader. But often I think it's just listening and understanding where they are. Dr Smith: So, you brought up bereavement earlier and you discussed it in the article. In my experience is that oftentimes the families are very, very impacted by the journey of ALS. And while ALS patients are remarkably resilient, it's a huge burden on family, loved ones, and their community. Can you talk a bit about the role of palliative care in the bereavement process, maybe preparing for bereavement and then after the loss of their loved one? Dr Oliver: Throughout the disease progression, we need to be supporting the carers as much as we are the patient. They are very much involved. As you said, the burden of care may be quite profound and very difficult for them. So, it's listening, supporting them, finding out what their particular concerns are. Are they frightened about what's going to happen at the end of life as well? Are they concerned of how they're going to cope or how the person's going to cope? And then after the death, it's allowing them to talk about what's happened and how they are feeling now, cause I think having had that enormous input in care, then suddenly everything stops. And also, the support systems they've had for perhaps months of the carers coming in, the doctor, the nurse, the physiotherapist, everyone coming in, they all stop coming. So, their whole social system suddenly stops and becomes much reduced. And I'm afraid certainly in the UK if someone is bereaved, they may not have the contact with their friends and family because they're afraid to come and see them. So, they may become quite isolated and reduced in what they can do. So, I think it's allowing them to discuss what has happened. And I think that's as important sometimes for members of the multidisciplinary team, because we as doctors, nurses and the wider team will also have some aspects of bereavement as we face not seeing that person who we've looked after for many years and perhaps in quite an intensive way. So, we need to be looking at how we support ourselves. And I think that's another important role of the multidisciplinary team. I always remember in our team, sometimes I would say, I find this person really difficult to cope with. And the rest of the people around the team would go have a sigh of relief because they felt the same, but they didn't like to say. And once we could talk about it, we could support each other and work out what we could do to help us help the patient in the most effective way. Dr Smith: Well, David, I think that's a great point to end on. I think you've done a really great job of capturing why someone would want to be a palliative care specialist or be involved in palliative care, because one of the themes throughout this conversation is the very significant personal and care impact that you have on patients and families. So, I really appreciate your sharing your wisdom. I really encourage all of our listeners to check out the article, it's really outstanding. I wonder if maybe you might just briefly tell us a little bit about how you got into this space? It's obviously one for which you have a great deal of passion and wisdom. How did you end up where you are? Dr Oliver: I became interested in palliative care as a medical student, and actually I trained as a family doctor, but I went to Saint Christopher's Hospice following that. I had actually had contact with them while I was a medical student, so I worked Saint Christopher's Hospice in South London when Dame Cecily Saunders was still working there. And at that time Christopher's had sixty-two beds, and at least eight of those beds were reserved for people with ALS or other neurological diseases. And I became very involved in one or two patients and their care. And Dame Sicily Saunders asked me to write something on ALS for their bookshelf that they had on the education area. So, I wrote, I think, four drafts. I went from sort of C minus to just about passable on the fourth draft. And that became my big interest in particularly ALS, and as time went on, in other neurological diseases. When I went to the Wisdom Hospice as a consultant, I was very keen to carry on looking after people with ALS, and we involved ourselves with other neurological patients. That's how I got started. Having that interest, listening to patients, documenting what we did became important as a way of showing how palliative care could have a big role in neurological disease. And over the years, I've been pressing again and again for the early involvement of palliative care in neurological diseases. And I think that is so important so that there can be a proper holistic assessment of people, that they can build up the trust in their carers and in the multidisciplinary team so that they can live as positively as possible. And as a result of that, that their death will be without distress and with their family with them. Dr Smith: Well, David, you've convinced and inspired me, and I'm confident you have our listeners as well. Thank you so much for a really informative, enjoyable, inspiring conversation. Dr Oliver: Thank you for inviting me. Dr Smith: Again, today I've been interviewing Dr David Oliver about his article on neuropalliative care and neuromuscular disorders, which appears in the December 2025 Continuum issue on neuropalliative care. Be sure to check out Continuum Audio episodes from this and other issues, and thanks to our listeners for joining us today. Dr Monteith: This is Dr Teshamae Monteith, Associate Editor of Continuum Audio. If you've enjoyed this episode, you'll love the journal, which is full of in-depth and clinically relevant information important for neurology practitioners. Use the link in the episode notes to learn more and subscribe. AAN members, you can get CME for listening to this interview by completing the evaluation at continpub.com/audioCME. Thank you for listening to Continuum Audio.

This is Part One of a conversation with Lucy Butler of River Haven Animal Sanctuary, Dr Stephanie Jones and her grad student, Sofia Abuin Dr. Jones is new to Equiosity. She graduated with her PhD in Behavior Analysis from West Virginia University in 2021. Her primary research focuses on effects of implementer errors that occur during well-established behavioral treatments. To meet this aim, she conducts laboratory and applied research with the aim of supporting development of robust behavioral interventions. She started teaching and conducting research at Salve Regina University in 2021 and is the principal investigator for the Translational Research and Applied Intervention Lab. Through her lab, she supports research engagement of students at the undergraduate, master's, and doctoral training levels. She publishes in and reviews for several peer-reviewed behavior-analytic journals, such as the Journal of Applied Behavior Analysis and Education and Treatment of Children. Good training is very much emphasizes the importance of taking the time to build a relationship with the individuals you're interacting with. We modeled that in Part One. Dominique and I were meeting Stephanie and Sophia for the first time in this recording. So instead of jumping straight in to the study Stephanie and her collegues conducted at River Haven, we began by talking about coercion, control, and even more about empathy.

From Discovery to Delivery: Charting Progress in Gynecologic Oncology, hosted by Ursula A. Matulonis, MD, brings expert insights into the most recent breakthroughs, evolving standards, and emerging therapies across gynecologic cancers. Dr Matulonis is chief of the Division of Gynecologic Oncology and the Brock-Wilcon Family Chair at the Dana-Farber Cancer Institute and a professor of medicine at Harvard Medical School, both in Boston, Massachusetts. In this episode, Dr Matulonis sat down with guest Panagiotis (Panos) A. Konstantinopoulos, MD, PhD, to discuss the different subtypes of endometrial cancer and treatment developments for this disease. Dr Konstantinopoulos is the director of Translational Research in the Division of Gynecologic Oncology, the director of the Mellen and Eisenson Family Center for BRCA and Related Genes, and the Velma Eisenson Chair for Clinical and Translational Research at Dana-Farber Cancer Institute; as well as a professor of medicine at Harvard Medical School. Drs Matulonis and Konstantinopoulos explained that patients with mismatch repair–deficient (dMMR) tumors substantially benefit from a decreased risk of progression or death when immunotherapy is added to standard therapy. They noted that immunotherapy appears important for the management of dMMR tumors, even those in earlier stages or in patients who have no measurable disease remaining after surgery. For MMR-proficient (pMMR) tumors, Drs Matulonis and Konstantinopoulos highlighted that PD-1 blockade combined with chemotherapy improves survival vs chemotherapy alone, but that this benefit is not as substantial as that seen in dMMR disease. Crucially, they reported that if a pMMR tumor has no measurable disease after surgery, adding immune checkpoint blockade does not appear beneficial. They stated that tailored treatment approaches are key for managing pMMR disease subtypes. They added that hormonal therapy may be used upfront for slow-growing, estrogen receptor–positive metastatic disease. They continued by saying that DNA damage and replication stress are critical targets, particularly in p53-mutated tumors, like uterine serous cancers. Furthermore, they stressed that although the antibody-drug conjugate fam-trastuzumab deruxtecan-nxki (Enhertu) is highly effective in HER2-positive tumors, treatment with this agent requires monitoring for toxicities, including interstitial lung disease and decreased ejection fraction.

How This Is Building Me, hosted by world-renowned oncologist D. Ross Camidge, MD, PhD, is a podcast focused on the highs and lows, ups and downs of all those involved with cancer, cancer medicine, and cancer science across the full spectrum of life's experiences. In this episode, Dr Camidge sat down with Gideon Blumenthal, MD, vice president of Clinical Development Oncology at Merck in Silver Spring, Maryland. Drs Camidge and Blumenthal discussed Dr Blumenthal's experience serving on both sides of the oncology regulatory divide. Though initially leaning toward humanities during his education, he pursued a career in medicine. During medical school, he shifted his focus from neuroscience to oncology due to the field's high unmet need, fascinating drug development pathways, and the intensity of patient interaction. He chose to complete his hematology and oncology fellowship at the National Cancer Institute to immerse himself in translational oncology and drug development. Before joining industry, Dr Blumenthal also spent several years working for the FDA. He started there as a medical officer, focusing on all facets of drug development, from ethics and manufacturing to trial design and biostatistics. He emphasized that success at the FDA involves both approving effective agents and identifying drugs that do not work, maintaining transparency through venues like the public Oncologic Drug Advisory Committee meetings. He used FDA data to conduct independent meta-research, such as analyzing the correlation between response rates and overall survival in lung cancer. His proudest achievement at the FDA was helping to establish the Oncology Center of Excellence, which unified drug development reviews across different centers within the agency. Dr Blumenthal left the FDA in early 2020, seeking to gain direct experience in developing new therapeutics. Joining Merck, he first worked in regulatory affairs, navigating international regulations in addition to US filing procedures, which are typically prioritized in oncology. He later transitioned into clinical development, and currently focuses on new assets as Merck evolves its pipeline beyond pembrolizumab (Keytruda). Dr Blumenthal concluded that he is excited by the future of oncology, anticipating radical changes driven by new modalities and advanced biomarkers like artificial intelligence–driven digital pathology.

Biochemist Lingyin Li survived breast cancer at just 30 and now works to harness the human immune system to fight cancers that have long evaded treatment. T cells, she says, are powerful cancer killers, but they can be oblivious. She and her lab colleagues have discovered a masking enzyme that squelches the immune system's “danger signals” and are now developing drugs to block that enzyme. She likens her work to an arms race between cancer and immunotherapy. “The cancers are not getting smarter, but we are,” Li tells host Russ Altman on this episode of Stanford Engineering's The Future of Everything podcast.Have a question for Russ? Send it our way in writing or via voice memo, and it might be featured on an upcoming episode. Please introduce yourself, let us know where you're listening from, and share your question. You can send questions to thefutureofeverything@stanford.edu.Episode Reference Links:Stanford Profile: Lingyin LiConnect With Us:Episode Transcripts >>> The Future of Everything WebsiteConnect with Russ >>> Threads / Bluesky / MastodonConnect with School of Engineering >>> Twitter/X / Instagram / LinkedIn / FacebookChapters:(00:00:00) IntroductionRuss Altman introduces guest Lingyin Li, a professor of biochemistry at Stanford University.(00:03:38) Research MotivationLingyin explains how her breast cancer diagnosis inspired her research.(00:04:31) How T-Cells WorkT-cell mechanisms and why they struggle to reach solid tumors.(00:05:38) Immune System OverviewInnate and adaptive immunity and how mutations make cancer recognizable.(00:07:28) Awakening the Immune SystemEfforts to stimulate innate immune cells to detect and expose tumors.(00:10:54) The Cancer SignalDiscovery of cancer-derived DNA signals that alert the immune system.(00:13:01) Cancer's Evasion MechanismHow tumors destroy immune signals to hide from detection.(00:14:26) ENPP1 EnzymeIdentification of ENPP1 as the enzyme enabling immune evasion.(00:15:22) Balancing Immunity and SafetyRole of ENPP1 in autoimmunity and the challenge of targeting it safely.(00:19:30) ENPP1 InhibitorsDevelopment of molecules to block ENPP1 and enhance immune signaling.(00:24:55) Preclinical FindingsThe promising results against aggressive solid tumors in animal studies(00:28:05) From Lab to ClinicThe progress toward FDA approval and preparation for human testing.(00:31:04) Future In a MinuteRapid-fire Q&A: innovation, collaboration, and the outlook for cancer treatment.(00:33:14) Conclusion Connect With Us:Episode Transcripts >>> The Future of Everything WebsiteConnect with Russ >>> Threads / Bluesky / MastodonConnect with School of Engineering >>>Twitter/X / Instagram / LinkedIn / Facebook Hosted by Simplecast, an AdsWizz company. See pcm.adswizz.com for information about our collection and use of personal data for advertising.

In this episode of Speaking of Mol Bio, Dr. Andre Ghetti, CEO of AnaBios, offers a deep dive into the world of translational preclinical research. AnaBios is redefining early human insights by using ethically sourced, functional human tissues and cells to generate actionable data before compounds ever enter clinical trials. Ghetti walks us through the company's approach of offering human-relevant safety and efficacy data, validating drug targets, and supporting everything from small startups to major pharma groups.We learn how AnaBios engages with clients to customize assays, especially in high-need areas like non-opioid pain therapies, fibrosis, and cardiac safety, and how they use a blend of standardized and novel functional assays, some of which required building their own hardware. He also discusses their integration of RT-PCR, RNA-seq, and calcium imaging, including genetically encoded sensors to monitor neuronal activity at scale.From their use of machine learning to analyze massive data sets, to collaborations with the FDA, to their unique ability to preserve tissue viability across the U.S., AnaBios offers a powerful glimpse into the future of translational biology. Dr. Ghetti also shares advice for young scientists and reflects on what's next for AnaBios, including oncology and stem-cell model integration. Subscribe to get future episodes as they drop and if you like what you're hearing we hope you'll share a review or recommend the series to a colleague.  Visit the Invitrogen School of Molecular Biology to access helpful molecular biology resources and educational content, and please share this resource with anyone you know working in molecular biology. For Research Use Only. Not for use in diagnostic procedures.

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

Welcome to this insightful episode of Behaviour Speak, where we speak with the inspiring Jaime Santana, founder of Santana Behavioural Services in Toronto. Join us as Jaime shares his journey as a dedicated behaviour analyst, exploring the challenges and triumphs of working with adults with developmental disabilities. Discover how Jaime's passion for empowering change and building independence has shaped his approach to ABA, particularly through the use of Acceptance and Commitment Training (ACT). Plus, get a sneak peek into the upcoming ONTABA 2025 conference. Register for ONTABACON 2025 now! https://behaviorlive.com/conferences/ontaba/registration Use the code BxSpeak10 to get 10% off your registration Watch on YouTube: https://youtu.be/Uy_e7qzRLWs Continuing Education Credits (https://www.cbiconsultants.com/shop) BACB: 1.0 Learning IBAO:  1.0  ABA Topics QABA: 1.0 General CBA:    1.0 Learning  Follow us! Instagram: https://www.instagram.com/behaviourspeak/ LinkedIn:  https://www.linkedin.com/in/behaviourspeak/ Contact: Email: jsantana@santanabehavioural.ca Website https://www.santanabehavioural.ca LinkedIn https://www.linkedin.com/in/jaime-santana-563320153/ Links:  ONTABA https://ontaba.org/join-ontaba/ Shining Through Centre https://www.shiningthrough.ca/ Brock University https://brocku.ca/programs/graduate/mads/ Behaviour Speak Episodes Featuring Guests from Ontario  Get 75% off CEUs for these Episodes until the end of ONTABACON 2025 on November 7th! Episode 11: The Treatment of Life Threatening Pica wiht Louis Busch https://www.behaviourspeak.com/e/episode-11-the-treatment-of-life-threatening-pica-with-louis-busch-bst-abs-hc-med-bcba/ Episode 13: Behaviour Analysis and Psychotropic Medication with Dr. Alison Cox https://www.behaviourspeak.com/e/episode-13-behaviour-analysis-and-psychotropic-medication-with-alison-cox-phd-bcba-d/ Episode 20: Consulting in Group Homes Using ACT with Monica Peters https://www.behaviourspeak.com/e/episode-20-consulting-in-group-homes-using-act-with-monica-peters-mads-bcba/ Episode 24 Autistic Self Advocacy with Michau Van Speyk and Philip Lerner https://www.behaviourspeak.com/e/episode-24-autistic-self-advocacy-with-michau-van-speyk-and-philip-lerner/ Episode 27 Translational Research, DiGeorge Syndrome, and a Little Dash of Metacontingencies with Dr. Val Saini https://www.behaviourspeak.com/e/episode-27-translational-research-digeorge-syndrome-and-a-little-dash-of-metacontingencies-with-valdeep-saini-phd-bcba-d/ Episode 34: Neurodiversity, ADHD, and ODD with Ameila Bowler https://www.behaviourspeak.com/e/episode-34-neurodiversity-adhd-and-odd-with-amelia-bowler-mads-bcba/ Episode 100: Self Determination and Self Advocacy with Brooke Myers https://www.behaviourspeak.com/e/episode-100-self-determination-and-self-advocacy-with-brooke-myers-ma-bcba/ Episode 136: From Bias to Balance: Antiracism in Behaviour Analysis wth Dr. Sonia Levy https://www.behaviourspeak.com/e/episode-136-from-bias-to-balance-antiracism-in-behavior-analysis-with-sonia-levy-phd-bcba/ Episode 186: Culturo Behaviour Science: A Primer with Dr. Albert Malkin https://www.behaviourspeak.com/e/episode-186-culturo-behavior-science-a-primer-with-dr-traci-cihon-dr-kyosuke-kazaoka-and-dr-albert-malkin/ Episode 228: The Nubian Egyptian Behaviour Analyst with Nehal Siam https://www.behaviourspeak.com/e/episode-228-the-nubian-egyptian-behaviour-analyst-with-nehal-siam-mped-bcba-rba-ont/    

Functional movement disorders are a common clinical concern for neurologists. The principle of “rule-in” diagnosis, which involves demonstrating the difference between voluntary and automatic movement, can be carried through to explanation, triage, and evidence-based multidisciplinary rehabilitation therapy. In this episode, Gordon Smith, MD, FAAN speaks Jon Stone, PhD, MB, ChB, FRCP, an author of the article “Multidisciplinary Treatment for Functional Movement Disorder” in the Continuum® August 2025 Movement Disorders issue. Dr. Smith is a Continuum® Audio interviewer and a professor and chair of neurology at Kenneth and Dianne Wright Distinguished Chair in Clinical and Translational Research at Virginia Commonwealth University in Richmond, Virginia. Dr. Stone is a consultant neurologist and honorary professor of neurology at the Centre for Clinical Brain Sciences at the University of Edinburgh in Edinburgh, United Kingdom. Additional Resources Read the article: Multidisciplinary Treatment for Functional Movement Disorder Subscribe to Continuum®: shop.lww.com/Continuum Continuum® Aloud (verbatim audio-book style recordings of articles available only to Continuum® subscribers): continpub.com/Aloud More about the American Academy of Neurology: aan.com Social Media facebook.com/continuumcme @ContinuumAAN Host: @gordonsmithMD Guest: @jonstoneneuro Full episode transcript available here Dr Jones: This is Dr Lyell Jones, Editor-in-Chief of Continuum. This exclusive Continuum Audio interview is available only to you, our subscribers. We hope you enjoy it. Thank you for listening. Dr Smith: Hello, this is Dr Gordon Smith. Today I've got the great pleasure of interviewing Dr Johnstone about his article on the multidisciplinary treatment for functional neurologic disorder, which he wrote with Dr Alan Carson. This article will appear in the August 2025 Continuum issue on movement disorders. I will say, Jon, that as a Continuum Audio interviewer, I usually take the interviews that come my way, and I'm happy about it. I learn something every time. They're all a lot of fun. But there have been two instances where I go out and actively seek to interview someone, and you are one of them. So, I'm super excited that they allowed me to talk with you today. For those of our listeners who understand or are familiar with FND, Dr Stone is a true luminary and a leader in this, both in clinical care and research. He's also a true humanist. And I have a bit of a bias here, but he was the first awardee of the Ted Burns Humanism in Neurology award, which is a real honor and reflective of your great work. So welcome to the podcast, Jon. Maybe you can introduce yourself to our audience. Dr Stone: Well, thank you so much, Gordon. It was such a pleasure to get that award, the Ted Burns Award, because Ted was such a great character. I think the spirit of his podcasts is seen in the spirit of these podcasts as well. So, I'm a neurologist in Edinburgh in Scotland. I'm from England originally. I'm very much a general neurologist still. I still work full-time. I do general neurology, acute neurology, and I do two FND clinics a week. I have a research group with Alan Carson, who you mentioned; a very clinical research group, and we've been doing that for about 25 years. Dr Smith: I really want to hear more about your clinical approach and how you run the clinic, but I wonder if it would be helpful for you to maybe provide a definition. What's the definition of a functional movement disorder? I mean, I think all of us see these patients, but it's actually nice to have a definition. Dr Stone: You know, that's one of the hardest things to do in any paper on FND. And I'm involved with the FND society, and we're trying to get together a definition. It's very hard to get an overarching definition. But from a movement disorder point of view, I think you're looking at a disorder where there is an impairment of voluntary movement, where you can demonstrate that there is an automatic movement, which is normal in the same movement. I mean, that's a very clumsy way of saying it. Ultimately, it's a disorder that's defined by the clinical features it has; a bit like saying, what is migraine? You know? Or, what is MS? You know, it's very hard to actually say that in a sentence. I think these are disorders of brain function at a very broad level, and particularly with FND disorders, of a sort of higher control of voluntary movement, I would say. Dr Smith: There's so many pearls in this article and others that you've written. One that I really like is that this isn't a diagnosis of exclusion, that this is an affirmative diagnosis that have clear diagnostic signs. And I wonder if you can talk a little bit about the diagnostic process, arriving at an FND diagnosis for a patient. Dr Stone: I think this is probably the most important sort of “switch-around” in the last fifteen, twenty years since I've been involved. It's not new information. You know, all of these diagnostic signs were well known in the 19th century; and in fact, many of them were described then as well. But they were kind of lost knowledge, so that by the time we got to the late nineties, this area---which was called conversion disorder then---it was written down. This is a diagnosis of exclusion that you make when you've ruled everything out. But in fact, we have lots of rule in signs, which I hope most listeners are familiar with. So, if you've got someone with a functional tremor, you would do a tremor entrainment test where you do rhythmic movements of your thumb and forefinger, ask the patient to copy them. It's very important that they copy you rather than make their own movements. And see if their tremor stops briefly, or perhaps entrains to the same rhythm that you're making, or perhaps they just can't make the movement. That might be one example. There's many examples for limb weakness and dystonia. There's a whole lot of stuff to learn there, basically, clinical skills. Dr Smith: You make a really interesting point early on in your article about the importance of the neurological assessment as part of the treatment of the patient. I wonder if you could talk to our listeners about that. Dr Stone: So, I think, you know, there's a perception that- certainly, there was a perception that that the neurologist is there to make a diagnosis. When I was training, the neurologist was there to tell the patient that they didn't have the kind of neurological problem and to go somewhere else. But in fact, that treatment process, when it goes well, I think begins from the moment you greet the patient in the waiting room, shake their hand, look at them. Things like asking the patient about all their symptoms, being the first doctor who's ever been interested in their, you know, horrendous exhaustion or their dizziness. You know, questions that many patients are aware that doctors often aren't very interested in. These are therapeutic opportunities, you know, as well as just taking the history that enable the patient to feel relaxed. They start thinking, oh, this person's actually interested in me. They're more likely to listen to what you've got to say if they get that feeling off you. So, I'd spend a lot of time going through physical symptoms. I go through time asking the patient what they do, and the patients will often tell you what they don't do. They say, I used to do this, I used to go running. Okay, you need to know that, but what do they actually do? Because that's such valuable information for their treatment plan. You know, they list a whole lot of TV shows that they really enjoy, they're probably not depressed. So that's kind of useful information. I also spend a lot of time talking to them about what they think is wrong. Be careful, that they can annoy patients, you know. Well, I've come to you because you're going to tell me what's wrong. But what sort of ideas had you had about what was wrong? I need to know so that I can deal with those ideas that you've had. Is there a particular reason that you're in my clinic today? Were you sent here? Was it your idea? Are there particular treatments that you think would really help you? These all set the scene for what's going to come later in terms of your explanation. And, more importantly, your triaging of the patient. Is this somebody where it's the right time to be embarking on treatment, which is a question we don't always ask yourself, I think. Dr Smith: That's a really great point and kind of segues to my next question, which is- you talked a little bit about this, right? Generally speaking, we have come up with this is a likely diagnosis earlier, midway through the encounter. And you talked a little bit about how to frame the encounter, knowing what's coming up. And then what's coming up is sharing with the patient our opinion. In your article, you point out this should be no different than telling someone they have Parkinson's disease, for instance. What pearls do you have and what pitfalls do you have in how to give the diagnosis? And, you know, a lot of us really weren't trained to do this. What's the right way, and what are the most common land mines that folks step on when they're trying to share this information with patients? Dr Stone: I've been thinking about this for a long time, and I've come to the conclusion that all we need to do with this disorder is stop being weird. What goes wrong? The main pitfall is that people think, oh God, this is FND, this is something a bit weird. It's in a different box to all of the other things and I have to do something weird. And people end up blurting out things like, well, your scan was normal or, you haven't got epilepsy or, you haven't got Parkinson's disease. That's not what you normally do. It's weird. What you normally do is you take a deep breath and you say, I'm sorry to tell you've got Parkinson's disease or, you have this type of dystonia. That's what you normally say. If you follow the normal- what goes wrong is that people don't follow the normal rules. The patient picks up on this. What's going on here? This doctor's telling me what I don't have and then they're starting to talk about some reason why I've got this, like stress, even though I don't- haven't been told what it is yet. You do the normal rules, give it a name, a name that you're comfortable with, preferably as specific as possible: functional tremor, functional dystonia. And then do what you normally do, which is explain to the patient why you think it's this. So, if someone's got Parkinson's, you say, I think you've got Parkinson's because I noticed that you're walking very slowly and you've got a tremor. And these are typical features of Parkinson. And so, you're talking about the features. This is where I think it's the most useful thing that you can do. And the thing that I do when it goes really well and it's gone badly somewhere else, the thing I probably do best, what was most useful, is showing the patient their signs. I don't know if you do that, Gordon, but it's maybe not something that we're used to doing. Dr Smith: Wait, maybe you can talk more about that, and maybe, perhaps, give an example? Talk about how that impacts treatment. I was really impressed about the approach to physical therapy, and treatment of patients really leverages the physical examination findings that we're all well-trained to look for. So maybe explore that a little bit. Dr Stone: Yeah, I think absolutely it does. And I think we've been evolving these thoughts over the last ten or fifteen years. But I started, you know, maybe about twenty years ago, started to show people their tremor entrainment tests. Or their Hoover sign, for example; if you don't know Hoover sign, weakness of hip extension, that comes back to normal when the person's flexing their normal leg, their normal hip. These are sort of diagnostic tricks that we had. Ahen I started writing articles about FND, various senior neurologists said to me, are you sure you should write this stuff down? Patients will find out. I wrote an article with Marc Edwards called “Trick or Treat in Neurology” about fifteen years ago to say that actually, although they're they might seem like tricks, there really are treats for patients because you're bringing the diagnosis into the clinic room. It's not about the normal scan. You can have FND and MS. It's not about the normal scan. It's about what you're seeing in front of you. If you show that patient, yes, you can't move your leg. The more you try, the worse it gets. I can see that. But look, lift up your other leg. Let me show you. Can you see now how strong your leg is? It's such a powerful way of communicating to the patient what's wrong with them diagnostically, giving them that confidence. What it's also doing is showing them the potential for improvement. It's giving them some hope, which they badly need. And, as we'll perhaps talk about, the physio treatment uses that as well because we have to use a different kind of physio for many forms of functional movement disorder, which relies on just glimpsing these little moments of normal function and promoting them, promoting the automatic movement, squashing down that abnormal pattern of voluntary movement that people have got with FND. Dr Smith: So, maybe we can talk about that now. You know, I've got a bunch of other questions to ask you about mechanism and stuff, but let's talk about the approach to physical therapy because it's such a good lead-in and I always worry that our physical therapists aren't knowledgeable about this. So, maybe some examples, you have some really great ones in the article. And then words of wisdom for us as we're engaging physical therapists who may not be familiar with FND, how to kind of build that competency and relationship with the therapist with whom you work. Dr Stone: Some of the stuff is the same. Some of the rehabilitation ideas are similar, thinking about boom and bust activity, which is very common in these patients, or grading activity. That's similar, but some of them are really different. So, if you have a patient with a stroke, the physiotherapist might be very used to getting that person to think and look at their leg to try and help them move, which is part of their rehabilitation. In FND, that makes things worse. That's what's happening in Hoover sign and tremor entrainment sign. Attention towards the limb is making it worse. But if the patient's on board with the diagnosis and understands it, they'll also see what you need to do, then, in the physio is actively use distraction in a very transparent way and say to the patient, look, I think if I get you to do that movement, and I'll film you, I think your movement's going to look better. Wouldn't that be great if we could demonstrate that? And the patient says, yeah, that would be great. We're kind of actively using distraction. We're doing things that would seem a bit strange for someone with other forms of movement disorder. So, the patients, for example, with functional gait disorders who you discover can jog quite well on a treadmill. In fact, that's another diagnostic test. Or they can walk backwards, or they can dance or pretend that they're ice skating, and they have much more fluid movements because their ice skating program in their brain is not corrupted, but their normal walking program is. So, can you then turn ice skating or jogging into normal walking? It's not that complicated, I think. The basic ideas are pretty simple, but it does require some creativity from whoever's doing the therapy because you have to use what the patient's into. So, if the patient used to be a dancer- we had a patient who was a, she was really into ballet dancing. Her ballet was great, but her walking was terrible. So, they used ballet to help her walk again. And that's incredibly satisfying for the therapist as well. So, if you have a therapist who's not sure, there are consensus recommendations. There are videos. One really good success often makes a therapist want to do that again and think, oh, that's interesting. I really helped that patient get better. Dr Smith: For a long time, this has been framed as a mental health issue, conversion disorder, and maybe we can talk a little bit about early life of trauma as a risk factor. But, you know, listening to you talk, it sounds like a brain network problem. Even the word “functional”, to me, it seems a little judgmental. I don't know if this is the best term, but is this really a network problem? Dr Stone: The word “functional”, for most neurologists, sounds judgmental because of what you associate it with. If you think about what the word actually is, it's- it does what it says on the tin. There's a disordered brain function. I mean, it's not a great word. It's the least worst term, in my view. And yes, of course it's a brain network problem, because what other organ is it going to be? You know, that's gone wrong? When software brains go wrong, they go wrong in networks. But I think we have to be careful not to swing that pendulum too far to the other side because the problem here, when we say asking the question, is this a mental health problem or a neurological one, we're just asking the wrong question. We're asking a question that makes no sense. However you try and answer that, you're going to get a stupid answer because the question doesn't make sense. We shouldn't have those categories. It's one organ. And what's so fascinating about FND---and I hope what can incite your sort of curiosity about it---is this disorder which defies this categorization. You see some patients with it, they say, oh, they've got a brain network disorder. Then you meet another patient who was sexually abused for five years by their uncle when they were nine, between nine and fourteen; they developed an incredibly strong dissociative threat response into that experience. They have crippling anxiety, PTSD, interpersonal problems, and their FND is sort of somehow a part of that; part of that experience that they've had. So, to ignore that or to deny or dismiss psychological, psychiatric aspects, is just as bad and just as much a mistake as to dismiss the kind of neurological aspects as well. Dr Smith: I wonder if this would be a good time to go back and talk a little bit about a concept that I found really interesting, and that is FND as a prodromal syndrome before a different neurological problem. So, for instance, FND prodromal to Parkinson's disease. Can you talk to us a little bit about that? I mean, obviously I was familiar with the fact that patients who have nonepileptic seizurelike events often have epileptic seizures, but the idea of FND ahead of Parkinson's was new to me. Dr Stone: So, this is definitely a thing that happens. It's interesting because previously, perhaps, if you saw someone who was referred with a functional tremor---this has happened to me and my colleagues. They send me some with a functional tremor. By the time I see them, it's obvious they've got Parkinson's because it's been a little gap. But it turns out that the diagnosis of functional tremor was wrong. It was just that they've developed that in the prodrome of Parkinson's disease. And if you think about it, it's what you'd expect, really, especially with Parkinson's disease. We know people develop anxiety in the prodrome of Parkinson's for ten, fifteen years before it's part of the prodrome. Anxiety is a very strong risk factor for FND, and they're already developing abnormalities in their brain predisposing them to tremor. So, you put those two things together, why wouldn't people get FND? It is interesting to think about how that's the opposite of seizures, because most people with comorbidity of functional seizures and epilepsy, 99% of the time the epilepsy came first. They had the experience of an epileptic seizure, which is frightening, which evokes strong threat response and has somehow then led to a recapitulation of that experience in a functional seizure. So yeah, it's really interesting how these disorders overlap. We're seeing something similar in early MS where, I think, there's a slight excess of functional symptoms; but as the disease progresses, they often become less, actually. Dr Smith: What is the prognosis with the types of physical therapy? And we haven't really talked about psychological therapy, but what's the success rate? And then what's the relapse rate or risk? Dr Stone: Well, it does depend who they're seeing, because I think---as you said---you're finding difficult to get people in your institution who you feel are comfortable with this. Well, that's a real problem. You know, you want your therapists to know about this condition, so that matters. But I think with a team with a multidisciplinary approach, which might include psychological therapy, physio, OT, I think the message is you can get really good outcomes. You don't want to oversell this to patients, because these treatments are not that good yet. You can get spectacular outcomes. And of course, people always show the videos of those. But in published studies, what you're seeing is that most studies of- case series of rehabilitation, people generally improve. And I think it's reasonable to say to a patient, that we have these treatments, there's a good chance it's going to help you. I can't guarantee it's going to help you. It's going to take a lot of work and this is something we have to do together. So, this is not something you're going to do to the patient, they're going to do it with you. Which is why it's so important to find out, hey, do they agree with you with the diagnosis? And check they do. And is it the right time? It's like when someone needs to lose weight or change any sort of behavior that they've just become ingrained. It's not easy to do. So, I don't know if that helps answer the question. Dr Smith: No, that's great. And you actually got right where I was wanting to go next, which is the idea of timing and acceptance. You brought this up earlier on, right? So, sometimes patients are excited and accepting of having an affirmative diagnosis, but sometimes there's some resistance. How do you manage the situation where you're making this diagnosis, but a patient's resistant to it? Maybe they're fixating on a different disease they think they have, or for whatever reason. How do you handle that in terms of initiating therapy of the overall diagnostic process? Dr Stone: We should, you know, respect people's rights to have whatever views they want about what's wrong with them. And I don't see my job as- I'm not there to change everyone's mind, but I think my job is to present the information to them in a kind of neutral way and say, look, here it is. This is what I think. My experience is, if you do that, most people are willing to listen. There are a few who are not, but most people are. And most of the time when it goes wrong, I have to say it's us and not the patients. But I think you do need to find out if they can have some hope. You can't do rehabilitation without hope, really. That's what you're looking for. I sometimes say to patients, where are you at with this? You know, I know this is a really hard thing to get your head around, you've never heard of it before. It's your own brain going wrong. I know that's weird. How much do you agree with it on a scale of naught to ten? Are you ten like completely agreeing, zero definitely don't? I might say, are you about a three? You know, just to make it easy for them to say, no, I really don't agree with you. Patients are often reluctant to tell you exactly what they're thinking. So, make it easy for them to disagree and then see where they're at. If they're about seven, say, that's good. But you know, it'd be great if you were nine or ten because this is going to be hard. It's painful and difficult, and you need to know that you're not damaging your body. Those sort of conversations are helpful. And even more importantly, is it the right time? Because again, if you explore that with people, if a single mother with four kids and, you know, huge debts and- you know, it's going to be very difficult for them to engage with rehab. So, you have to be realistic about whether it's the right time, too; but keep that hope going regardless. Dr Smith: So, Jon, there's so many things I want to talk to you about, but maybe rather than let me drive it, let me ask you, what's the most important thing that our listeners need to know that I haven't asked you about? Dr Stone: Oh God. I think when people come and visit me, they sometimes, let's go and see this guy who does a lot of FND, and surely, it'll be so easy for him, you know? And I think some of the feedback I've had from visitors is, it's been helpful to watch, to see that it's difficult for me too. You know, this is quite hard work. Patients have lots of things to talk about. Often you don't have enough time to do it in. It's a complicated scenario that you're unravelling. So, it's okay if you find it difficult work. Personally, I think it's very rewarding work, and it's worth doing. It's worth spending the time. I think you only need to have a few patients where they've improved. And sometimes that encounter with the neurologist made a huge difference. Think about whether that is worth it. You know, if you do that with five patients and one or two of them have that amazing, really good response, well, that's probably worth it. It's worth getting out of bed in the morning. I think reflecting on, is this something you want to do and put time and effort into, is worthwhile because I recognize it is challenging at times, and that's okay. Dr Smith: That's a great number needed to treat, five or six. Dr Stone: Exactly. I think it's probably less than that, but… Dr Smith: You're being conservative. Dr Stone: I think deliberately pessimistic; but I think it's more like two or three, yeah. Dr Smith: Let me ask one other question. There's so much more for our listeners in the article. This should be required reading, in my opinion. I think that of most Continuum, but this, I really truly mean it. But I think you've probably inspired a lot of listeners, right? What's the next step? We have a general or comprehensive neurologist working in a community practice who's inspired and wants to engage in the proactive care of the FND patients they see. What's the next step or advice you have for them as they embark on this? It strikes me, like- and I think you said this in the article, it's hard work and it's hard to do by yourself. So, what's the advice for someone to kind of get started? Dr Stone: Yeah, find some friends pretty quick. Though, yeah, your own enthusiasm can take you a long way, you know, especially with we've got much better resources than we have. But it can only take you so far. It's really particularly important, I think, to find somebody, a psychiatrist or psychologist, you can share patients with and have help with. In Edinburgh, that's been very important. I've done all this work with the neuropsychiatrist, Alan Carson. It might be difficult to do that, but just find someone, send them an easy patient, talk to them, teach them some of this stuff about how to manage FND. It turns out it's not that different to what they're already doing. You know, the management of functional seizures, for example, is- or episodic functional movement disorders is very close to managing panic disorder in terms of the principles. If you know a bit about that, you can encourage people around you. And then therapists just love seeing these patients. So, yeah, you can build up slowly, but don't- try not to do it all on your own, I would say. There's a risk of burnout there. Dr Smith: Well, Dr Stone, thank you. You don't disappoint. This has really been a fantastic conversation. I really very much appreciate it. Dr Stone: That's great, Gordon. Thanks so much for your time, yeah. Dr Smith: Well, listeners, again, today I've had the great pleasure of interviewing Dr Jon Stone about his article on the multidisciplinary treatment for functional neurologic disorder, which he wrote with Dr Alan Carson. This article appears in the August 2025 Continuum issue on movement disorders. Please be sure to check out Continuum Audio episodes from this and other issues. And listeners, thank you once again for joining us today. Dr Monteith: This is Dr Teshamae Monteith, Associate Editor of Continuum Audio. We hope you've enjoyed this subscriber-exclusive interview. Thank you for listening.

Two topics are covered in this episode: (1) how parents with lived experience of nonsuicidal self-injury (NSSI) can navigate conversations with their children about their own scarring and wounds, and (2) how parents (with or without lived experience) can navigate conversations about self-injury with their young adult children when they turn 18. Dr. Whitlock is emerita research faculty at Cornell University, a former Associate Director of the Bronfenbrenner Center for Translational Research, and the founder and director of the Self-Injury & Recovery Resources (SIRR) research program, which serves as one of the best and most comprehensive collations of online resources about self-injury: www.selfinjury.bctr.cornell.edu. It is a go-to resource for parents, therapists, friends, family members, schools, other caring adults, the media, and individuals with lived experience of self-injury. Dr. Whitlock is also Senior Advisor for The JED Foundation. To learn more about The JED Foundation, visit https://www.jedfoundation.org/.Below is some of the work referenced in this episode:Whitlock, J., & Lloyd-Richardson, E. E. (2019). Healing self-injury: A compassionate guide for parents and other loved ones. Oxford University Press.Taliaferro, L. A., Jang, S. T., Westers, N. J., Muehlenkamp, J. J., Whitlock, J. L., & McMorris, B. J. (2020). Associations between connections to parents and friends and non-suicidal self-injury among adolescents: The mediating role of developmental assets. Clinical Child Psychology and Psychiatry, 25(2), 359-371.Kibitov, A. A., & Mazo, G. E. (2023). Genetics and epigenetics of nonsuicidal self-injury: A narrative review. Russian Journal of Genetics, 59(12), 1265-1276.Dawkins, J., Hasking, P., & Boyes, M. (2021). Knowledge of parental nonsuicidal self-injury in young people who self-injure: The mediating role of outcome expectancies. Journal of Family Studies, 27(4), 479–490.Want to have a bigger role on the podcast?:Should you or someone you know be interviewed on the podcast? We want to know! Please fill out this Google doc form, and we will be in touch with more details if it's a good fit.Want to hear your question and have it answered on the podcast? Please send an audio clip of your question (60 seconds or less) to @DocWesters on Instagram or Twitter/X, or email us at thepsychologyofselfinjury@gmail.comWant to be involved in research? Send us a message at thepsychologyofselfinjury@gmail.com and we will see if we can match you to an active study.Want to interact with us through comments and polls? You can on Spotify!Follow Dr. Westers on Instagram and Twitter/X (@DocWesters). To join ISSS, visit itriples.org and follow ISSS on Facebook and Twitter/X (@ITripleS).The Psychology of Self-Injury podcast has been rated as one of the "10 Best Self Harm Podcasts" and "20 Best Clinical Psychology Podcasts" by Feedspot  and one of the Top 100 Psychology Podcasts by Goodpods. It has also been featured in Audible's "Best Mental Health Podcasts to Defy Stigma and Begin to Heal."

Save 20% on all Nuzest Products WORLDWIDE with the code MIKKIPEDIA at www.nuzest.co.nz, www.nuzest.com.au or www.nuzest.comThis week on the podcast Mikki speaks to Prof Arny Ferrando about his work in protein, essential amino acids, protein timing, aging, anabolic resistance, and how to optimise muscle retention and fat loss.Arny Ferrando is a Professor of Geriatrics at the University of Arkansas for Medical Sciences (UAMS), where he co-directs the Center for Translational Research in Aging & Longevity (CTRAL) and holds the position of Wes Smith Distinguished Chair in Geriatrics for Longevity, Health Promotion and Frailty Prevention.His research deploys stable isotope techniques to dissect muscle protein metabolism under stress—from spaceflight, burn injury, joint arthroplasty, renal and heart failure, to aging and surgical recovery. He pioneers nutritional, pharmacological, and exercise-based strategies to counteract muscle wasting and functional decline.After earning a Ph.D. in Nutrition & Physiology from Florida State University, he conducted postdoctoral work at NASA's Johnson Space Center. He served as a U.S. Army pilot and armor officer, retiring as Lieutenant Colonel. He's driven by a lifelong athletic spirit: from West Point gymnast to powerlifter, bodybuilder, masters track athlete, and now Krav Maga instructor.He drives multiple research programs funded by NIH, the U.S. Army, and industry, and since 2023 holds a Visiting Senior Research Scientist appointment at IHMC, extending his work to human performance in extreme environments.https://www.ihmc.us/groups/arny-ferrando/ Curranz Supplement: Use code MIKKIPEDIA to get 20% off your first order - go to www.curranz.co.nz  or www.curranz.co.uk to order yours Contact Mikki:https://mikkiwilliden.com/https://www.facebook.com/mikkiwillidennutritionhttps://www.instagram.com/mikkiwilliden/https://linktr.ee/mikkiwilliden

In today's episode, we spoke with Scott Kopetz, MD, PhD, FACP, about the use of circulating tumor DNA (ctDNA) in patients with colorectal cancer (CRC). Dr Kopetz is the deputy chair for Translational Research and a professor in the Department of Gastrointestinal (GI) Medical Oncology in the Division of Cancer Medicine, as well as the leader of the Department of Cancer Center Support Grant in the GI Program, the TRACTION medical director in the Division of Therapeutics Discovery, and the associate vice president for Translational Integration at The University of Texas MD Anderson Cancer Center in Houston, Texas. In our conversation, Dr Kopetz discussed the high positive predictive value of ctDNA assays, which indicate disease presence when positive. He emphasized  clinical trials that have shown strong prognostic implications with this type of assay, as well as study findings that demonstrated that ctDNA results could reduce chemotherapy use without compromising efficacy. Additionally, he noted the potential significance of ongoing trials that are exploring the use of ctDNA to guide therapy. Overall, he explained that ctDNA testing is becoming a standard in clinical practice for colorectal cancer. 

A new study, published in JDR Clinical & Translational Research and based on data from 4,400 children, has found a link between tooth loss and bullying among adolescents. Senior author of the study, Associate Professor Ankur Singh from the University of Sydney, highlights the psychological effects of tooth decay. Based on official figures showing that 24 per cent of children suffer from decay in their adult teeth, the study is calling for stronger government support to provide free dental care for children and adolescents.

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

In this episode of Onc Now, host Jonathan Sackier is joined by Jean Abraham, Professor of Precision Breast Cancer Medicine at the University of Cambridge, to delve into the future of integrated cancer medicine, the evolving role of clinical trials, and how precision oncology is redefining outcomes for patients with breast cancer across the UK.  Timestamps  00:00 – Introduction  01:28 – Quickfire round  09:50 – Cambridge institutes for precision medicine  12:53 – Predictive/prognostic tools in breast cancer  15:33 – The future of breast cancer clinical trials  18:34 – Integrating genomic data  22:31 – Addressing cost barriers  24:22 – How AI is transforming breast cancer care  28:08 – Why oncology?  30:04 – A message to non-oncologists  31:54 – Abraham's three wishes for healthcare  

Please Support the Podcast: If you are enjoying, do me a small favour which helps a lot - subscribe and leave a review on your preferred podcast platform. Your support helps us bring valuable conversations like this one to a wider audience. Today I sit down with Martijn Arns, a biological psychologist at the forefront of applied neuroscience, to discuss the advancements and challenges in psychiatry. We delve into his pioneering research on brain biomarkers, the promising applications of brain stimulation techniques like Transcranial Magnetic Stimulation (TMS), and how lifestyle factors may influence conditions such as ADHD. Martijn also shares cutting-edge insights into the role of heart-brain coupling and the potential impact of psychedelics in mental health treatment, offering a glimpse into the future of personalised and stratified psychiatry. What You'll Learn: Understanding Biological vs. Clinical Psychology: Martijn explains the focus of biological psychology in studying brain activity rather than engaging in traditional talk therapy. The Role of Biomarkers in Psychiatry: Discover the challenges of seeking biological signatures for psychiatric conditions. Understand why a biomarker-driven psychiatry might be theoretically impossible due to clinical impairment and situational variables. Innovations in Brain Stimulation: Explore the mechanisms and applications of TMS for treating depression and other psychiatric disorders. Learn about the groundbreaking use of heart rate to optimise TMS targeting, enhancing treatment effectiveness. Lifestyle Factors and ADHD: Understand the significant role sleep and sunlight exposure play in ADHD symptoms. Consider the implications of lifestyle interventions in managing and reducing ADHD diagnoses. The Exciting Future of Psychiatric Treatments: Dive into how psychedelics might transform therapeutic approaches with their profound effects in combination with therapy. Reflect on the potential shift from daily medication to periodic brain stimulation treatments. Key Takeaways: Psychiatry is evolving, with innovations in neuroscience paving the way for more personalised and effective treatments. There's a growing recognition of the importance of lifestyle factors, like sleep and sunlight exposure, in influencing mental health conditions, especially ADHD. Advancements like TMS offer hope, showing potential even where conventional treatments have failed. Future therapies may focus more on brain stimulation and targeted interventions rather than a one-size-fits-all medication approach. Resources: For more insights and updates on cutting-edge neuroscience research, visit Brain Clinics at brainclinics.com. Connect with Martijn Arns on LinkedIn to follow his latest work in applied neuroscience. Share this episode with someone who might benefit from these insights—understanding and innovation in psychiatric treatment are vital as we move towards a future of tailored mental health care. 00:40 Biological vs. Clinical Psychology 01:38 Journey Through Academia and Early Career 04:04 Starting Brain Clinics and Translational Research 06:48 Challenges in Psychiatric Diagnosis 16:20 Stratified Psychiatry and Biomarkers 27:26 Transcranial Magnetic Stimulation (TMS) 31:25 Ethical Considerations in TMS Treatment 32:40 Future of Brain Stimulation Treatments 33:34 Personal Experiences with TMS and Psychedelics 34:23 TMS Applications Beyond Depression 36:02 Innovations in TMS Targeting 37:21 Heart-Brain Coupling and TMS 40:18 Exploring the Vagus Nerve and Depression 47:39 Sleep's Role in ADHD 55:59 Lifestyle Factors and ADHD 01:00:34 Exciting Ventures in Brain Research See omnystudio.com/listener for privacy information.

In this episode of the Epigenetics Podcast, we talked with Sarah Teichmann from the University of Cambridge about the Human Cell Atlas. In the Interview we explore Sarah Teichmann's impressive career trajectory, covering her current role as Chair of Stem Cell Medicine at the Cambridge Stem Cell Institute and Vice President of Translational Research at GlaxoSmithKline. Professor Teichmann explains her unique dual appointments, a rare arrangement that allows her to bridge academia and industry effectively. As the conversation shifts focus to computational biology, she takes us on a historical journey from her PhD work at the MRC Laboratory of Molecular Biology to the present advancements driven by next-generation sequencing and artificial intelligence methods. Professor Teichmann emphasizes that the landscape of biological research has evolved significantly, particularly in the realm of data-driven methodologies. The conversation then transitions seamlessly into her pivotal role in advancing single-cell genomics, where she discusses the motivation behind using single-cell RNA sequencing methods in her research on T cells. This technique offered unmatched insights compared to bulk sequencing techniques, allowing for a more detailed understanding of cell states and their complex interactions within tissues. A highlight of the episode is Professor Teichmann's insights on the Human Cell Atlas project, which she co-founded in 2017. She elaborates on the ambitious vision to map all human cells, likening the endeavor to the Human Genome Project. Through the atlas, researchers aim to create a detailed reference map that facilitates a deeper understanding of human health and disease. Professor Teichmann shares the collaborative efforts that led to its inception and the importance of international cooperation in scientific research. The discussion culminates with an exploration of the biggest scientific findings thus far from the Human Cell Atlas. Among the revelations, she notes the astounding complexity and diversity of cell types identified, particularly within the immune system, and the unexpected locations of certain cell types during human development. She also highlights significant discoveries related to COVID-19, demonstrating the immediate real-world impact of their work.   References https://www.humancellatlas.org The Human Cell Atlas: towards a first draft atlas Kock, K. H., Tan, L. M., Han, K. Y., Ando, Y., Jevapatarakul, D., Chatterjee, A., Lin, Q. X. X., Buyamin, E. V., Sonthalia, R., Rajagopalan, D., Tomofuji, Y., Sankaran, S., Park, M. S., Abe, M., Chantaraamporn, J., Furukawa, S., Ghosh, S., Inoue, G., Kojima, M., Kouno, T., … Prabhakar, S. (2025). Asian diversity in human immune cells. Cell, 188(8), 2288–2306.e24. https://doi.org/10.1016/j.cell.2025.02.017   Related Episodes The Discovery of Genomic Imprinting (Azim Surani)   Contact Epigenetics Podcast on Mastodon Epigenetics Podcast on Bluesky Dr. Stefan Dillinger on LinkedIn Active Motif on LinkedIn Active Motif on Bluesky Email: podcast@activemotif.com

This is a really exciting conversation with Dr. Davide D'Amico from Timeline, where we're taking a closer look at Urolithin A and heart health. It should come as no surprise that this mitochondrial wonderkin of a nutrient is showing promise here—especially when you consider that 40% of the heart's weight is mitochondria. That's an extraordinary factoid, and one that really shifts how we think about aging in the cardiovascular system. What's particularly compelling in this new preclinical research is that restoring mitochondrial function may do more than just improve ejection fraction. It may also have ripple effects on other hallmarks of aging—like chronic inflammation, cellular stress signaling, and impaired autophagy. I'm thrilled Timeline is continuing to invest in both preclinical and clinical research on this front—and yes, I'm totally nerding out over what they're up to. ~DrK Check out the show notes at https://www.drkarafitzgerald.com/fxmed-podcast/ for the full list of links and resources. GUEST DETAILS Davide D'Amico, PhD: Director of Discovery and Translational Research at Timeline. With over 15 years of experience in mitochondrial and aging biology, he contributed to developing Urolithin A as a science-backed, clinically validated nutritional product to enhance mitochondrial and muscle health. THANKS TO OUR SPONSOR Timeline: http://Timeline.com/kara10 Email: care@timeline.com EXCLUSIVE OFFER FOR NEW FRONTIERS LISTENERS Mitopure is making impressive strides for cellular health and longevity. Get 10% off your first order at http://Timeline.com/kara10 with code Kara10. CONNECT with DrKF Want more? Join our newsletter here: https://www.drkarafitzgerald.com/newsletter/ Or take our pop quiz and test your BioAge! https://www.drkarafitzgerald.com/bioagequiz YouTube: https://tinyurl.com/hjpc8daz Instagram: https://www.instagram.com/drkarafitzgerald/ Facebook: https://www.facebook.com/DrKaraFitzgerald/ DrKF Clinic: Patient consults with DrKF physicians including Younger You Concierge: https://tinyurl.com/yx4fjhkb Younger You book: https://tinyurl.com/mr4d9tym Better Broths and Healing Tonics book: https://tinyurl.com/3644mrfw

In this deeply informative solosode, Dr. Mike Belkowski guides listeners through a comprehensive exploration of mitochondrial function and its profound connection to aging and longevity. Kicking off with a brief reflection on recent guest episodes and a teaser about an upcoming podcast rebrand, Mike then dives into a newly released scientific article from Cell Communication and Signaling titled “Mitochondrial Dysfunction in the Regulation of Aging and Aging-Related Diseases.”   Mike reads and unpacks dense but crucial sections from the paper, including:   The Structure and Function of MitochondriaHe outlines the intricacies of the electron transport chain, supercomplexes, and mitochondrial DNA, emphasizing their roles in energy production, oxidative stress, and aging. Key Cellular Processes Affected by MitochondriaTopics covered include metabolic regulation, calcium and ROS homeostasis, mitochondrial biogenesis, and autophagy, tying them all back to aging and degenerative diseases. Modulating Mitochondrial Function to Slow AgingMike highlights emerging research on mitochondrial nutrients (like CoQ10, alpha-lipoic acid, carnitine), lifestyle interventions (exercise, diet, intermittent fasting), and breakthrough therapies such as mitochondrial transfer and replacement therapies.     He also introduces BioLight's new supplement, BioBlue Fountain of Youth, emphasizing its inclusion of methylene blue or leucomethylene blue, urolithin A, adaptogenic mushrooms, shilajit, and PQQ—all aimed at mitochondrial optimization.   The episode wraps with a powerful message: movement is medicine. Exercise remains the most accessible and potent strategy to boost mitochondrial health naturally. Mike encourages listeners to stay active, get sunlight, engage in red light therapy, and embrace the mitochondrial lifestyle. If you found the information in today's episode particularly interesting and/or compelling, please share it with a family member, friend, colleague and/or anyone that you think could benefit and be illuminated by this knowledge. Sharing is caring :)As always, light up your health! - Key Quotes from Dr. Mike Belkowski: ​​“The mitochondrial space is going to be blown up in the next couple decades for sure… it's going to become a much larger, well-adopted aspect of health and wellness.” ​​“You don't want these dysfunctional cells or these dysfunctional mitochondria to linger around… you want them to be recycled and turned into new, healthy cells.”​“Exercise is the best way to have your endogenous program of mitogenesis running.” - Key points: 00:00 – Introduction: Mitochondrial Focus and Podcast Evolution 02:14 – Podcast Rebrand Announcement & Mitochondrial Mission 03:15 – Review of Article: Mitochondrial Dysfunction in Aging 04:09 – Structure of the Mitochondria: A Deep Dive 06:15 – Electron Transport Chain & Supercomplexes Explained 10:05 – Mitochondrial DNA, Genome, and Gene Expression 11:18 – New BioBlue Supplement Overview and Key Ingredients 14:01 – Mitochondrial Functions: Metabolism, Apoptosis, and Energy 16:29 – Calcium Homeostasis & ROS Generation 20:11 – Antioxidant Defense Systems in Mitochondria 22:15 – Overview of Remaining Sections in the Research Article 25:18 – Targeting Mitochondria to Slow Aging: Introduction 27:13 – Nutrients That Modulate Mitochondrial Function 29:29 – Hormetic Stress, Resilience, and Mitochondrial Biogenesis 31:22 – Calcium Modulators and Mitochondrial Stability 32:01 – Exercise as the Ultimate Mitochondrial Booster 35:03 – Exercise vs. Caloric Restriction in Mitochondrial Health 36:30 – Mitochondria-Supportive Diets and Nutrients 39:12 – Mitochondrial Therapy and Replacement Explained 42:18 – Mitochondrial Replacement for Age-Related Decline 44:17 – Cross-Tissue Mitochondrial Signaling in Aging 45:41 – Translational Research in Mitochondrial Therapeutics 49:08 – Future of Mitochondrial Medicine and Final Thoughts - Save 25% when you Subscribe & Save to a BioBundle!For a BioBundle, you choose: 1.) Any one BioBlue supplement(BioBlue, BioBlue (SR), BioBlue Leuco, BioBlue Calm, BioBlue Capsules or BioBlue Leuco Capsules)2.) Any one BioC60 supplement (Regular or Concentrated)   The BioBundle automatically saves you 15% on both of the supplements you choose. You save an additional 10% by choosing to Subscribe & Save to that BioBundle.   The 25% savings is passed along for every monthly delivery of your BioBundle. No discount code necessary! Discount automatically applied at checkout.   Shop BioBundle by clicking here! - Dr. Mike's #1 recommendations: Water products: Water & Wellness Grounding products: Earthing.com EMF-mitigating products: Somavedic Blue light-blocking glasses: Ra Optics - Stay up-to-date on social media: Dr. Mike Belkowski: Instagram LinkedIn   BioLight: Website Instagram Facebook

Dr. Shaalan Beg and Dr. Kristen Ciombor discuss practice-changing studies in GI cancers and other novel treatment approaches that were presented at the 2025 ASCO Annual Meeting. Transcript Dr. Shaalan Beg: Hello, I'm Dr. Shaalan Beg, welcoming you to the ASCO Daily News Podcast. I'm a medical oncologist and an adjunct associate professor at UT Southwestern Medical Center in Dallas, Texas. There were some remarkable advances in gastrointestinal cancers that were presented at the 2025 ASCO Annual Meeting, and I'm delighted to be joined by Dr. Kristen Ciombor to discuss some exciting GI data. Dr. Ciombor is the Ingram Associate Professor of Cancer Research and a co-leader of Translational Research and the Interventional Oncology Research Program at the Vanderbilt Ingram Cancer Center. Our full disclosures are available in the transcript of this episode. Dr. Ciombor, it's great to have you on the podcast today. Dr. Kristen Ciombor: Thanks, Dr Beg. It's great to be here. Dr. Shaalan Beg: Alright, let's kick it off. Big year for GI cancers. We'll start off with LBA1. This was the ATOMIC study sponsored by NCI and the National Clinical Trials Network (NCTN) and the Alliance group. This is a randomized study of standard chemotherapy alone or combined with atezolizumab as adjuvant therapy for stage III mismatch repair deficient colorectal cancer. Dr. Kristen Ciombor: I think this study was really definitely practice-changing, as you can tell because it was a Plenary. But I do have some concerns in terms of how we're actually going to implement this and whether this is the final answer in this disease subtype. So, as you said, the patients were enrolled with stage III resected mismatch repair deficient colon cancer, and then they were randomized to either modified FOLFOX6 with or without atezolizumab. And that's where it starts to become interesting because not many of us give FOLFOX for 6 months like was done in this study. Obviously, the study was done over many years, so that was part of that answer, but also the patients received atezolizumab for a total of 12 months. So the question, I think, that comes from this abstract is, is this practical and is this the final answer? I do think that this is practice-changing, and I will be talking to my patients with resected mismatch repair deficient colon cancer about FOLFOX plus atezolizumab. I think the big question is, do these patients need chemotherapy? And can we do a neoadjuvant approach instead? And that's where we don't have all the answers yet. Dr. Shaalan Beg: Yeah, but it has been great to see immunotherapy make its way into the adjuvant space after having made such a big impact in the metastatic space, but still some unanswered questions in terms of the need for chemotherapy and then the duration of therapy, which I guess we'll have to stay tuned in for the next couple of years to to get a lot of those questions answered. Dr. Kristen Ciombor: Yeah, but a big congratulations to the study team, to the NCTN, the NCI. I mean, this is really a great example of federally funded research that needs to continue. So, great job by the study team. The DFS 10% difference is really very large and certainly a practice-changing study. Dr. Shaalan Beg: Yeah, and and sticking with colon cancer, and and this another federally funded study, but this time funded by a Canadian cancer clinical trials group was LBA3510. This is the CHALLENGE study. It's a randomized phase 3 trial of the impact of a structured exercise program on disease-free survival for stage III or high-risk stage II colon cancer. This study got a lot of buzz, a lot of mainstream press coverage, and a lot of discussions on what that means for us for the patients who we're going to be seeing next week in our clinic. What was your takeaway? Dr. Kristen Ciombor: Yeah, this is a really interesting study, and I was so glad to see it presented because this partially answers one of the questions that patients always have for us in clinic, right? You know, once they've completed their standard chemotherapy and surgery, what else can they do to help prevent recurrence? And so we've always known and sort of extrapolated that healthy lifestyle habits are good, but now we have data, particularly in these patients. Most of them were stage III colon cancer patients, those had high-risk stage II cancer. And basically, the goal was to increase their physical activity by at least 10 MET hours per week. So, my big question, of course, as I came into this presentation was, “Okay, what does that mean exactly? How does that translate to real life?” And really what the author presented and explained was that basically most patients could hit their target by adding a 45- to 60-minute brisk walk 3 to 4 times a week. So I think this is very approachable.  Now, in the confines of the study, this was a structured exercise program, so it wasn't just patients doing this on their own. But I do think kind of extrapolating from that, that this is very achievable for most patients. And not only did this prevent recurrence of their prior cancer, but actually the rate of new primary cancer diagnoses, was less, which is really interesting, especially in the breast and prostate cancer. So this was a really interesting, and I think practice-changing study as well, especially given that this is something that most patients can do. Dr. Shaalan Beg: Yeah, and there was a lot of discussion in the hallways after the presentation in terms of how this really changes our existing practice because most folks already recommend exercise as a way for improving outcomes in cancer patients. So we've already been doing that. Now we have some data on how much it can impact the benefit. But there was some discussion about what the actual degree of impact was. There was a drop-off rate in terms of how long folks were able to stick with this exercise regimen. But you've seen this in clinic when someone have their surgery, they have their chemotherapy, they've been so intimately involved with the oncology world, with the oncology practice, and they somehow feel that they're being let loose into this mean, angry world without any guidance and they're looking for something to do. “What more can I do in terms of my lifestyle?” And then here we have very solid data, as solid as can be for an intervention like exercise, showing that there is an impact and you can give a prescription for exercise when someone wraps up their chemotherapy for colon cancer, thanks to the study. Dr. Kristen Ciombor: Yeah. It was a great study. Dr. Shaalan Beg: Moving to gastroesophageal cancer, another late-breaking abstract. This is LBA5. The MATTERHORN trial was a phase 3 trial of durvalumab plus FLOT for resectable GE junction and gastric cancer. And again, another area where immunotherapy has made an impact, and here we're seeing it move closer for earlier-stage disease. What was your take-home for the MATTERHORN trial? Dr. Kristen Ciombor: Yeah, so this study looked at neoadjuvant perioperative durvalumab plus our current standard chemotherapy of FLOT versus placebo plus FLOT. And this was a large study, almost 1,000 patients were randomized. And the primary endpoint was event-free survival, and it was definitely met in favor of the D + FLOT arm, as Dr. Klempner discussed after Dr Janjigian's presentation. I do think there are still some unanswered questions here. Overall survival is not yet mature, so we do have to wait and see how that shakes out. But it's very interesting and kind of is reflective of what, as you said, we're looking at earlier and earlier lines of therapy, particularly with immunotherapy, in these GI cancer spaces. So it makes a lot of sense to test this and and to look at this. So the toxicity was pretty similar to what we would expect. Primary endpoint was met, but again, we'll have to wait and see what the survival data looks like. Dr. Shaalan Beg: Yeah, and in oncology, we know, especially for treatment that does add additional cost, it does add additional potential toxicity that we want to see that overall survival nudged. I did see some polls on social media asking folks whether their practices changed from this, and I think the results were favoring adding durvalumab for this group of patients but understanding that there are caveats to the addition of treatments and the eventual FDA approval in that indication as well. Dr. Kristen Ciombor: Exactly. I completely agree with that. Dr. Shaalan Beg: All right. How about we stick with gastroesophageal cancer? LBA4002 was trastuzumab deruxtecan versus ramucirumab plus paclitaxel for second-line treatment in HER2-positive unresectable or metastatic gastric cancer or GE junction cancer. This was the DESTINY-Gastric04 study. And again, antibody-drug conjugates making a big impact across different diseases. And here we have more data in the HER2-positive gastric cancer space. Your thoughts on this study? Dr. Kristen Ciombor: Yeah, so this is a really important space in gastroesophageal cancer because the HER2 positivity rate is fairly high as compared to some of our other tumor types. So, I do think one of the important things was that patients did have biopsy confirmation of HER2 status, which was very important, and then they were randomized to either T-DXd versus the kind of second-line standard of ramucirumab-paclitaxel. So this was a great practical study and really answers a question that we had for a while in terms of does anti-HER2 therapy in the second-line really impact and improve survival. So we did see a statistically significant improvement favoring T-DXd. I do think it's always important to look at toxicity, though, too. And there was about almost 14% rate of interstitial lung disease, which of course is the most feared toxicity from some of these antibody-drug conjugates, especially T-DXd. So I do think it's important to keep that in mind, but this is definitely a great addition to the armamentarium for these HER2-positive patients. Dr. Shaalan Beg: And pancreas cancer was on the stage after a very long time with a positive clinical trial. This is Abstract 4006. These were preliminary results from a phase 2 study of elraglusib in combination with gemcitabine/nab-paclitaxel versus gemcitabine/nab-paclitaxel alone for previously untreated metastatic pancreas cancer. This is a frontline clinical trial of gemcitabine/nab-paclitaxel plus/minus the study drug. There were other cohorts in this study as well, but they reported the results of their part 3B arm. And great to see some activity in the pancreas space. And your thoughts? Dr. Kristen Ciombor: Yeah, we definitely need better treatments in pancreas cancer. This was a very welcome presentation to see. The elraglusib is an inhibitor of GSK-3beta, and it's thought that that mediates drug resistance and EMT. And so this is, I think, a perfect setting to test this drug. So patients basically were randomized. Patients with metastatic pancreas cancer were randomized 2: 1 to gemcitabine/nab-paclitaxel plus or minus this elraglusib. So, what we saw was that overall survival was better with the addition of this new drug. And overall, not only the 1-year overall survival, but also median overall survival.  The thing that was interesting, though, was that we saw that the overall survival rates were 9.3 months with the combination versus 7.2 months with just gemcitabine/nab-paclitaxel. And that's a little bit lower than we've seen in other studies. So, not sure what was going on there. Was it the patients that were a bit sicker? Was it a patient selection, you know, thing? I'm not really sure how to explain that so much. Also, the toxicity profile was much higher in terms of visual impairment, with over 60% of patients being treated with the combination versus 9% with gemcitabine/nab-paclitaxel. So these were mild, grade 1 and 2, but still something to be cautious about. Dr. Shaalan Beg: And especially with this being a phase 2 trial, making sure that in a larger study we're able to better evaluate the toxicity and see if the control arm in the larger confirmatory study performs differently will be really important before this compound makes it to the clinic in our space. But very exciting to see these kinds of results for pancreas adenocarcinoma. Dr. Kristen Ciombor: Yeah. Dr. Shaalan Beg: We've talked, it seems, a couple of times on this podcast about the BREAKWATER clinical trial. We did hear PFS and updated OS data, updated overall survival data on first-line encorafenib plus cetuximab plus modified FOLFOX6 for BRAF-mutated colorectal cancer. This was LBA3500. And eagerly anticipated results – we have all previously heard the progression-free survival results – but here we heard updated overall survival results, and very well-received study it seemed from the audience that time. So what are your takeaways on the updated results for BREAKWATER? Dr. Kristen Ciombor: In my opinion, this was one of the most practice-confirming studies. As you mentioned, we've already seen some of the preliminary data of BREAKWATER at prior meetings. But really what was particularly impactful for me was the median overall survival with the BREAKWATER regimen. So, again, patients received FOLFOX, encorafenib cetuximab in the first line if they had BRAF-mutated V600E-mutated colorectal cancer. And the median PFS was 12.8 months, which was actually really remarkable in this traditionally very aggressive, poor prognosis subtype of tumors. So, by seeing a median overall survival of 30.3 months was just incredible, in my opinion. Just a few years ago, that was considered the median overall survival for all comers for metastatic colorectal cancer. And we know the median overall survival was more in the less than 12 months range for BRAF. So this was incredibly impactful, and I think should be absolutely practice-changing for anyone who is eligible for this regimen.  I think again, where the practice meets the study is what's kind of important to think about too, how long did patients get FOLFOX, and certainly it adds toxicity to add a BRAF-targeted regimen on top of FOLFOX already. So, one of the other interesting things about the study, though, was that even though it didn't complete treatment, they actually did look at encorafenib/cetuximab alone and in the first line without chemotherapy. And those preliminary results actually looked okay, especially for patients who might not be able to tolerate chemotherapy, which we certainly see in practice. So, overall, definitely more data. And I agree that it's certainly practice-changing. Dr. Shaalan Beg: And it completely, as you mentioned, changes the outlook for a person who's diagnosed with BRAF-mutated metastatic colon cancer today versus even 7 or 8 years ago. Dr. Kristen Ciombor: And we're seeing this over and over in other subtypes too, but how you choose to treat the patient up front really matters. So really giving the right regimen up front is the key here. Dr. Shaalan Beg: And along the same lines, Abstract 3501 wanted to answer the question on whether people with MSI-high metastatic colorectal cancer need double checkpoint inhibitor therapy or is single therapy enough. So this [CheckMate-8HW] study compared nivo plus ipi with nivo alone, nivo monotherapy for MSI-high metastatic colorectal cancer. And we've known that both of these are fairly active regimens, but we also know the chance of immune-related adverse events is significantly higher with combination therapy. So this was a much-needed study for this group of patients. And what were your takeaways here? Dr. Kristen Ciombor: This, of course, has been really nivo-ipi in the first-line MSI-high metastatic colorectal cancer is now a standard of care. And not everybody is eligible for it, and there could be reasons, toxicity reasons, and other things too. But as we've been seeing for the last couple of years, immunotherapy clearly beats chemo in this space. And now looking at doublet versus single immunotherapy treatment in the first line, I think really nivo-ipi does beat out monotherapy. I will say, however, there is a caveat in that we still haven't seen the nivo-ipi versus nivo in the first line. So what has been presented thus far has been across all lines of therapy, and that does muddy the waters a little bit. So definitely looking forward and and we've asked this many times and based on the statistical plan and and what not, you know, we just haven't seen that data yet. But I do think it's becoming increasingly important to consider doublet immunotherapy for these patients as long as there are no contraindications. With the again, with the caveat that we have to have these toxicity discussions in the clinic with patients because many patients can tolerate it, you know, this regimen fairly well, but there can be very severe toxicities. So, I think an informed discussion should really be had with each patient before moving forward. Dr. Shaalan Beg: Yeah, informed decision, making them aware of the potential of real significant toxicities, immune-related toxicities with double therapy. But I am curious in your practice, how often do you see people choosing doublet therapy as frontline? Dr. Kristen Ciombor: So patients are really savvy, and a lot of times they've heard this data before or have come across it in patient advocacy groups and other things, and it's really nice to be able to have that conversation of the risk versus benefit. So I will say not all of my patients choose doublet, and many of them are still cured with immunotherapy monotherapy. So the big question there is, will we ever understand who actually needs the doublet versus who can still be cured or have very good long-term outcomes with just the single agent? And that has not been answered yet. Dr. Shaalan Beg: What a great point. So the last abstract I was hoping we could talk about is POD1UM-303 or the INTERAACT2 subgroup analysis and impact of delayed retifanlimab treatment for patients with squamous cell carcinoma of the anal canal. What were your thoughts here? Dr. Kristen Ciombor: This was a study, actually we saw at ESMO, we saw the primary data at ESMO last year, and this was an update with some exploratory analyses. But this was really an important study because once again, we're looking at immunotherapy in later lines of therapy. That's how we started looking at and investigating immunotherapy, and now we're moving it up and up in the treatment course. So this was a study of carboplatin/paclitaxel plus or minus retifanlimab. Actually it was retifanlimab versus placebo. And it was a positive study, as we heard last year. This actually led to FDA approval of this regimen last month, just before ASCO, and it has now been incorporated in the NCCN guidelines as the preferred first-line option.  So what I thought was important from the additional data presented at ASCO was looking at the different subgroups, it did not appear that patients with liver mets or not had different outcomes. So that was really good to see because sometimes in colon cancer we see that immunotherapy doesn't work as well when patients have liver mets. And interestingly, because we use immunotherapy in anal cancer without any biomarkers, unlike with colon cancer or some of the other tumor types, also the authors looked at PD-L1 status, and it did look like maybe patients did a little bit better if they had higher PD-L1 expression, but patients still could benefit even if they were PD-L1 negative. So that was important, I think, and we will continue to see further data come out from this study. I want to mention also that EA2176 just completed accrual, so that was carbo-taxol plus or minus nivolumab. And so we should be seeing that data sometime soon, which will hopefully also confirm the ongoing role for immunotherapy in the first-line setting for anal cancer. Dr. Shaalan Beg: That was a fantastic review. Thank you, Dr Ciombor. Thanks for sharing your valuable insights with us today on the ASCO Daily News Podcast. Dr. Kristen Ciombor: Thanks for having me here. Dr. Shaalan Beg: And thank you to our listeners for your time today. You will find links to the abstracts discussed today in the transcript of this episode. And if you value the insights that you hear on the podcast, please take a moment to rate, review, and subscribe, wherever you get your podcasts. Disclaimer: The purpose of this podcast is to educate and to inform. This is not a substitute for professional medical care and is not intended for use in the diagnosis or treatment of individual conditions. Guests on this podcast express their own opinions, experience, and conclusions. Guest statements on the podcast do not express the opinions of ASCO. The mention of any product, service, organization, activity, or therapy should not be construed as an ASCO endorsement. More on today's speakers:   Dr. Shaalan Beg  @ShaalanBeg  Dr. Kristen Ciombor @KristenCiombor Follow ASCO on social media:    @ASCO on Twitter   @ASCO on BlueSky  ASCO on Facebook    ASCO on LinkedIn    Disclosures:   Dr. Shaalan Beg:   Consulting or Advisory Role: Ipsen, Cancer Commons, Foundation Medicine, Science37, Nant Health, Lindus Health Speakers' Bureau: Sirtex Research Funding (Inst.): Delfi Diagnostics, Universal Diagnostics, Freenome Dr. Kristen Ciombor: Consulting or Advisory Role: Pfizer, Incyte, Exelixis, Bayer, ALX Oncology, Tempus, Agenus, Taiho Oncology, Merck, BeiGene Research Funding (Inst.): Pfizer, Boston Biomedical, MedImmune, Onyx, Bayer, Boehringer Ingelheim, Bristol-Myers Squibb, Merck, Novartis, Incyte, Amgen, Sanofi, Bristol-Myers Squibb, Array BioPharma, Incyte, Daiichi Sankyo, Nucana, Abbvie, Merck, Pfizer/Calthera, Genentech, Seagen, Syndax Travel, Accommodations, Expenses: Incyte, Tempus

Cory grew up in Maine and after spending time as a sea kayak guide and a ski instructor, found his way to biology and laboratory research. Currently a Postdoctoral Researcher in the Haller Lab at MDI Biological Laboratory, Cory is interested in the cell biology of kidney vascularization and uses renal organoids and zebrafish to investigate how we may, one day, be able to rebuild the kidney and develop non-donor solutions to kidney transplantation.Cory was one of the 5 Minute Genius™ speakers at this past year's Maine Science Festival; you can see his talk on our YouTube channel.This conversation was recorded in May 2025. ~~~~~The Maine Science Podcast is a production of the Maine Discovery Museum. It is recorded at Discovery Studios, at the Maine Discovery Museum, in Bangor, ME. The Maine Science Podcast is hosted and executive produced by Kate Dickerson; edited and produced by Scott Loiselle. The Discover Maine theme was composed and performed by Nick Parker. To support our work: https://www.mainediscoverymuseum.org/donate. Find us online:Maine Discovery MuseumMaine Discovery Museum on social media: Facebook Instagram LinkedIn Bluesky Maine Science Festival on social media: Facebook Instagram LinkedInMaine Science Podcast on social media: Facebook Instagram © 2025 Maine Discovery Museum

On today's show we're excited to welcome Rick Peng, the Innovation Hub Manager and Digital Licensing Professional at Memorial Sloan Kettering Cancer Center. We talk about how your organization can build an outside-in, external innovation program to deliver outsized results. Rick breaks down the secret sauce of the MSK Innovation Hub, an accelerator program designed to encourage collaborations between Memorial Sloan Kettering Cancer Center and digital health companies, focused on the diagnosis, treatment, and care of cancer patients. We discuss their new Innovation Hub Challenge focused on AI Drug Discovery – and why the access to data sets, is a key unlock for ai driven solutions.

Spontaneous intracranial hypotension reflects a disruption of the normal continuous production, circulation, and reabsorption of CSF. Diagnosis requires the recognition of common and uncommon presentations, careful selection and scrutiny of brain and spine imaging, and, frequently, referral to specialist centers.  In this episode, Gordon Smith, MD, FAAN speaks with Jill C. Rau, MD, PhD, author of the article “Clinical Features and Diagnosis of Spontaneous Intracranial Hypotension” in the Continuum® June 2025 Disorders of CSF Dynamics 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. Rau is an assistant professor of clinical neurology at the University of Arizona, School of Medicine-Phoenix in Phoenix, Arizona. Additional Resources Read the article: continuumjournal.com 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 Interview with Jill Rau, MD 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 Jill Rau about her article on clinical features and diagnosis of spontaneous intracranial hypotension, which she wrote with Dr Jeremy Cutsworth-Gregory from the Mayo Clinic. This article appears in the 2025 Continuum issue on disorders of CSF dynamics. I'm really excited to welcome you to the Continuum podcast. Maybe you can start by just telling our listeners a little bit about yourself? Dr Rau: Hi, thanks for having me. I'm really honored to be here, and I really enjoyed writing the paper with Dr Cutsforth-Gregory. I hope you guys enjoy it. I am the director of headache medicine at the Baba Bay Neuroscience Institute at Honor Health in Scottsdale, Arizona. I'm also currently the chair of the special interest group in CSF Dynamics at the American Headache Society, and I've had a special interest in this field since I first watched Dr Linda Gray speak at a conference where she talked about spinal CSF leaks and their different presentations. And they were so different than what I had been taught in residency. They're not just the post-LP headache. They have such a wide variety of presentations and how devastating they can be, and how much impact there is on someone's life when you find it and fix it. And I've been super interested in the field and involved in research since that time. And, yeah. Love it. Dr Smith: Well, thanks for sharing your story. And as I reflected on our conversation ahead of time and have been thinking about this issue… this is a cool topic, and every time I read one of these manuscripts and have the opportunity to speak with one of the authors, I learn a ton, because this was something that wasn't even on the radar when I trained back in the 1800's. So, really looking forward to the conversation. I wonder if you could really briefly just summarize or remind for everyone the normal physiology about CSF dynamics, you know, production, absorption, and so forth? Dr Rau: So, the CSF is the fluid that surrounds the brain and the spinal cord, and it's contained by the dura, which is like a canvas or a sac that covers that whole brain and spinal cord. And within the ventricles of the brain, the choroid plexus produce CSF. It's constantly producing and then being reabsorbed by the arachnoid granulations and pushed into the venous space, the cerebral sinuses, venous sinuses. And also some absorption and push into the lymphatics that we've just learned about in the past year. This is kind of new data coming out, so always learning more and more about CSF, but we know that it bathes the brain and the spinal cord, helps keep some buoyancy of the brain as well as pushing nutrients in and pulling out metabolic waste. And it sort of keeps the brain in the state of homeostasis that's happy. And so, when there's a disruption of that flow and the amount of fluid there, that disrupts that, that can cause lots of different symptoms and problems for people. Dr Smith: One of the many new things I learned is that even the name of this---spontaneous intracranial hypotension---is misleading. And I think this is clinically relevant, as we'll probably get to in a moment, but can you talk a little bit about this? Is this really like a pressure disorder or a volume disorder? Dr Rau: Yeah. It's almost certainly a volume disorder. We do see in some people that they have low pressure, and it's still part of the diagnostic criteria. But it's there because if you have a low pressure, if you measure an opening pressure and it's below six, if you're measuring it in the spine in the right place, then you have indication that there's low volume. But there's over 50% of people's opening pressure who have a spinal CSF leak, have all the symptoms and can be fixed. So, they have normal pressure in 50% of the people. So, it is an inaccurate term, hypotension, but it was originally discovered because of the thought that it was a low-pressure situation. Some of the findings would suggest low pressure, but ultimately, we are pretty sure it's a low-volume condition. Dr Smith: Another new thing that I learned that really blew me away is how bad this can be. I did a podcast with Mark Burish about cluster, and I was reminded many cluster patients are pushed to the point of suicidal ideation or committing suicide by the severity of pain. And this sounds like for many patients it's equally severe. Can you maybe paint a picture for our listeners why this is so clinically important? Dr Rau: A large number of people, even people who are known to have leaks because they've had them before or they've releaked, they have a lot of brain fog and cognitive impairment. They often have severe headaches when they're upright. So, orthostatic headache is probably the number one most common symptom, and those headaches are one of the worst headaches out there. When people stand up, their fluid is not supporting the brain and there's an intense amount of pain. And so, they spend a large portion of their lives horizontal. And there's associated symptoms with that, it's not just headache pain and brain fog. There's neck pain. There's often subsequent disorders that accompany this, like partial orthostatic tachycardia syndrome. We don't know if that's because of deconditioning or an actual sequela of the disease, but it's a frequent comorbidity. We have patients that have extreme dizziness with their symptoms, but many patients are limited to hours, if that, upright per day, combined, total. And so they live their lives, often, just in the dark, lots of photophobia, sensitive to the light, really unable to function. It's also very hard to find and so underrecognized that a lot of patients, especially if they don't have that really clinical symptom of orthostatic headache. So, it's often missed. So, they're just debilitated. You know, treatments don't work because it's not a migraine and it's not a typical headache. It's a mechanical issue as well as a metabolic issue and not found, not a lot helps it. Dr Smith: So, you know, I have always thought about this as really primarily an orthostatic symptom. I wonder if you can talk about the complexity of this; in particular, kind of how this evolves over time, because it's not quite that simple. And maybe in doing so, you can give our listeners some pearls on when they should be thinking about this disorder? Dr Rau: A large portion of people do have headache with spinal CSF leak, in particular, spontaneous intracranial hypertension- hypotension, excuse me. And that's something to be thought about, is that there are spontaneous conditions where people have either rupture of the dural sac, or an erosion of the dural sac, or a development of a connection between the dura and the venous system. And that is taking away or allowing CSF to escape. In these instances that patients have spontaneous, there may be a different presentation than if they have, like, a postdural puncture or a chronic traumatic or iatrogenic leak. And we're not sure of that yet, but we're looking into that. Still, the largest presentation is headache, and orthostatic headache is very dominant in the headache realm. But over time, patients' brains can compensate for that lack of CSF and start overproducing---or at least we think that's probably what's happening. And you may see a reduction in the orthostatic symptoms over time, and you may see an improvement in the radiographic findings. So, there are some interesting papers that have been published that look at these changes over time, and we do see that sometimes within that first three to four months; this is the most common time to see that change. Other patients may worsen. You may actually see someone going from looking sort of normal radiographically to developing more of a SIH-type of picture on the brain. And so it's not predictable which patients have gone from orthostatic to improvement or the other way around, both radiographically and clinically. So, it can be quite difficult to tell. So, for me, if I have a patient that comes to me and they're struggling with headache… if it's orthostatic, very clearly orthostatic: I lay down, I get considerably better or my headache completely goes away. And then when I stand up, it comes on relatively quickly, within an hour. And sometimes it's a worsening-throughout-the-day type of thing, it's lowest in the morning and it worsens throughout the day. These are the times that it's most obvious to think about CSF leak. Especially if that headache onset relatively suddenly, if it onset after a small trauma. Like I've had patients that say, you know, I was doing yoga and I did some twists and I felt kind of a pop. And then I've had this headache that is horrible when I'm upright but is better when I lay down ever since, you know, since that time. That's kind of a very classic presentation of spinal CSF leak or spontaneous intracranial hypotension. Maybe a less common presentation would be someone who comes to you, they've had a persistent headache for a couple years, they kind of remember it started in March of a couple years ago, but they don't know. Maybe it's, you know, it's a little better when they lay down. It may be a little worse when they're up moving around, but so is migraine, and it's a migrainous headache. But they've tried every migraine drug you can think of. Nothing is responding, nothing helps. I'm always looking at patients who are new daily, persistent headaches and patients who aren't responding to meds even if it's not new daily, but they have just barely any response. I will always go back and examine their brain imaging and get full spine to make sure I'm not missing. And you can never be 100% sure, but it's always good to consider those patients to the best of your ability, if that- have that in the back of your mind. Dr Smith: So obviously, goes without saying, this is something people need to have on their radar and think about. And then we'll talk more about diagnostic tools here in a second. But how common is this? If you're a headache doc, you see a lot of patients who have intractable headaches. And how often do you see this in your headache practice? Now you're- this is your thing, so probably a little more than others, but, you know, how common will someone who sees a lot of headache encounter these patients? Dr Rau: If you see a lot of headache, I mean, currently the thought is it's about 5 in 100,000. That was from a study before we were finding CSF venous fistulas. I think a lot of us think it's more common than that, but it's not super common. We don't have good estimates, but I would guess between 5 and 10 for 100,000 persons, not “persons who come to a tertiary headache clinic with intractable headaches”. So, it's hard to gauge how frequent it is, but I would say it's considerably more frequent than we currently think it is. There's still a group of people with orthostatic headaches that we can't find leaks on; that, once you treat other things that can cause or look for other things that can cause orthostatic headaches. So, there may be even still a pathophysiology out there that is still a leak type. Before 2014, we didn't even know about CSF venous fistulas. And now here we are; like, 50% of them are CSF venous fistulas. So, you know, we're still in a huge learning curve right now. Dr Smith: So, I definitely want to talk about the fistulas in a second. But before moving on, one of the things that I found really interesting is the wide spectrum of clinical phenotype. And we obviously don't have a lot of time to get into all of these different ones, but the one that I was hoping you might talk about---and there's a really great case, and you're on bunch of great case, a great case of this---is brain sagging dementia, not a term I've used before. Can you really briefly just tell our listeners about that, because that's a really interesting story and a great case in your article? Dr Rau: Yeah. So, brain sag dementia is a… almost like an extreme version of a spontaneous intracranial hypotension. Where there is clear brain sag in the imaging---so that's helpful---but the patients present kind of like a frontotemporal dementia. And when this was first started to being determined, you could turn the patient into Trendelenburg, and sometimes they would improve. There are some practitioners that have introduced fluid into the thecal sac and had temporary improvement. Patching has improvement, then they leak again, sometimes  not. But the clinical changes with this have been pretty tremendous to be able to identify that that's a real thing. And in some cases, out of Cedars Sinai, you know, who does a lot of the best research in this, they've had lots of cases where they can't find the leak, but there's clear brain sag that fits with our clinical picture of CSF leaks. So, we're on a learning curve. But yeah, this- they really present. They have disinhibition and cognitive impairment that is very similar to frontotemporal dementia. Dr Smith: Well, so let's talk about what causes this. You mentioned CSF venous fistulas. I mean, that was reported now just over a decade ago, it's pretty amazing. That accounts for about half of cases, if I understand correctly. What are the other causes? And then we'll talk more about therapy in a minute, but what causes this? Dr Rau: So, within the realm of spontaneous, you know, we say it's spontaneous. But the spontaneous cases we account for, they can be tears in the dura, which are usually sort of lateral tears in the dura. They can be little places that rubbed a hole, often on an osteophyte from the spine. They can come from these spinal diverticuli. So, I always describe it to my patients like those balls that have mesh and squishy, and you squeeze them in the- through the mesh, there's the extra little bubbling out. If you think of like the dura bubbling, out in some cases, through the framing of the spine, right where the spinal nerve roots come out, they should poke out like wires from the dura. But in many cases they poke out with this extra dura surrounding them, and we call that spinal diverticuli. And if you imagine like the weakening of where you squeeze that, you know, balloon through your fingers, in those locations, that's a very common place to find a CSF leak, and you can imagine that the integrity of the dura there may be less than it would be if it were not being expanded in that direction. And that's often the most common place we see these CSF venous fistulas. So, you can get minor traumas; like I said, it can be spontaneous, like someone just develops a leak one day. It can be rubbed off, and it can be a development of a connection between the dura and the venous system. There are also iatrogenic causes, but we don't consider them spontaneous. But when you're considering your patients for spontaneous cases, you should consider if they've ever had chronic---even long, long time ago---had any spinal implementation, procedures near the spine, spinal injections, LPs in the past, and especially women who've had epidurals in pregnancy. Dr Smith: All right, so we see a patient, positional severe headache, who meets the clinical criteria. Next step, MRI scan? Dr Rau: Yeah. So, the first thing is always to get the brain MRI with and without contrast. Most places will have a SIH or a spinal CSF leak protocol, but you should get contrast because one of the most pathognomonic findings on brain MRI is that smooth diffuse dural enhancement. And that's a really fantastic thing when you find it, because it's kind of a slam dunk. If you find it, then you will see other findings. It almost never exists alone. But if you see that, it's pretty much a spinal CSF leak. But you're also looking for subdural collections, any indication of brain sag. We do have these new algorithms that have come out in the past couple of years that are helpful. They're not exclusionary---you can have negative findings on the brain and still have spinal CSF leak---but the brain MRI is extremely helpful. If it's positive for the findings, it really does help you nudge you in the direction of further investigations and treatments. Dr Smith: And what about those further investigations and treatments, right? So, you see that there's findings consistent with low pressure, and I guess I should say low intracranial CSF volume. Be that as it may, what's the next step after that? Dr Rau: Depends on where you are and what you can do. I almost always will get a full spine MRI: so, C spine, T spine, and L spine separately. Not, you know, we don't want it all in one picture, because we want to get the full view. And you want to get that with at least T2 highly- heavily T2 weighted with fat saturation in at least the sagittal and axial planes. It's really helpful if you can get it in the coronal planes, but we have to have- often have good talks with your radiologist to get the coronal plane. I spoke about the spinal diverticuli earlier, and I want to clarify a little bit of something. The coronal image will show those really nicely. It's interesting, but 44% of people have those. So just having the spinal diverticuli does not indicate that you have a leak. But if you have a lot of those, there may be more likelihood of having leak than if you don't have any of those. So, I will get all of those and I will look at them myself, but I've been looking at them myself for a long time. But a lot of radiologists in community hospitals, especially not- nonneuroradiologists, but even neuroradiologists, this isn't something that's that everybody's been educated about, and we've been learning so much about it so rapidly in the past ten years. It's not easy to do and it's often missed. And if it's not protocoled properly, the fat saturation's not there, it's very hard to see… you can have a leak and not see it. Even the best people, like- it's not always something that's visible. And these CSF venous fistulas that we talked about are never visible on normal MRI imaging. Nonetheless, I will run those because if I can find a leak---and 90% of the ones that are found on MRI imaging are in the thoracic spine. So that's where I spend the most of my time looking. But if you find it, that's another thing to take to your team to say, hey, look, here it is, let's try and do this, or, let's try and do that, or, I've got more evidence. And there are other findings on the spine; not just the leak, but other findings, sometimes, you can see on spine that maybe help you push you towards, yes, this is probably a leak versus not. Dr Smith: So, your article has a lot of great examples and detail about kind of advanced imaging to, like, find the fistula and what not. I guess I'm thinking most of our listeners are probably practicing in a location where they don't have a team that really focuses on that. So, let's say we do the imaging of the spine and you don't find a clear cause. Is the next step to just do a blood patch? Do you send them to someone like you? What's the practical next step? Dr Rau: Yeah, if your- regardless of whether you find a leak or not, if your clinical acumen is such that you think this patient has a leak or I've treated them for everything else and it's not working and I have at least a high enough suspicion that I think the risk of getting a patch is lower than the benefit that if they got a patch and it worked, I do send my patients for non-directed blood patches, because it currently does take a long time to get them to a center that can do CT myelograms or any kind of advanced imaging to look for sort of a CSF venous fistula or to get treated outside of a nondirected patch. You know, sometimes nondirected patches are beneficial for patients, and there's some good papers out there that sort of explain the low risks of doing these if done properly versus the extreme benefit for patients when it works. And, I mean, I can't tell you how many people come in and tell me how their lives are changed because they finally got a blood patch. And sometimes it works. And it's life-changing for those people. You know, they go back to work. They can interact with their kids again. Before, they didn't know what was wrong, just had this headache that started. So it's worth doing if you have a strong clinical suspicion. Dr Smith: Yeah. I mean, that was great. And, you know, to go back to where we began, this is severe. It's something like 60% of patients with this problem have thought about suicide, right? And you take this patient and cure the problem. I feel really empowered having read the article and talked to you today. And so, I'm ready to go out and look for this. Thank you so much for a really engaging conversation. This has been terrific. Dr Rau: Thank you. I appreciate it. I enjoyed being here. Dr Smith: Again, today I've been interviewing Dr Jill Rau about her article on clinical features and diagnosis of spontaneous intracranial hypotension---which I guess I should say hypovolemia after having talked to you---which she wrote with Dr Jeremy Cutsworth-Gregory. This article appears in the most recent issue of Continuum on disorders of CSF dynamics. Please be sure to check out Continuum Audio episodes from this really interesting issue and other interesting issues. And thank you, our listeners, again for listening to us today. Dr Monteith: This is Dr Teshamae Monteith, Associate Editor of Continuum Audio. If you've enjoyed this episode, you'll love the journal, which is full of in-depth and clinically relevant information important for neurology practitioners. Use the link in the episode notes to learn more and subscribe. AAN members, you can get CME for listening to this interview by completing the evaluation at continpub.com/audioCME. Thank you for listening to Continuum Audio.

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In this episode of SHE MD, Dr. Thaïs Aliabadi and Mary Alice Haney welcome melanoma specialist Dr. Omid Hamid. They explore the rising incidence of melanoma in young people, debunk common misconceptions, and discuss groundbreaking treatments. Dr. Hamid explains the different stages of melanoma and the revolutionary immunotherapy treatments that are changing patient outcomes. The hosts and guest discuss real-life cases, including those of celebrities Khloe Kardashian and Teddy Mellencamp, to illustrate the importance of awareness and regular skin checks. The conversation also touches on melanoma during pregnancy and genetic predisposition to the disease - learn why genetic testing is crucial, even without family history.Access more information about the podcast and additional expert health tips by visiting SHE MD Podcast and Ovii. Sponsors: Myriad: Knowing your family's history of cancer is the first step to understanding your own cancer risk and may qualify you for the MyRisk Hereditary Cancer Test with RiskScore hereditary cancer test. It's easy, accurate and covered by most insurers. Learn more at GetMyRisk.comCymbiotika: Go to Cymbiotikia.com/SHEMD for 20% off your order + free shipping today.Purely Elizabeth: Visit purelyelizabeth.com and use code SHEMD at checkout for 20% off. Purely Elizabeth. Taste the ObsessionEquip: To learn more about Equip treatment, visit equip.health/sobermomlife.Strivektin: Discover the Science Behind Great SkinDavid's Protein: David is giving my listeners an exclusive offer – buy four cartons and get the fifth free at davidprotein.com/shemdCure Hydration: Cure is offering 20% off your first order! Stay hydrated and feel your best by visiting curehydration.com/SHEMD and using promo code SHEMD at checkout. Dr. Omid Hamid's Key Takeaways:1. Reduce Sun Exposure: Limit time spent in direct sunlight, especially during peak hours. Use protective clothing, hats, and sunglasses to shield your skin from harmful UV rays.2. Schedule Regular Skin Checks: Schedule routine visits with a dermatologist for comprehensive skin examinations. Self-examine your skin monthly for any new or changing moles or lesions.3. Use Effective Sunscreen: Apply broad-spectrum sunscreen with at least SPF 30 daily, even on cloudy days. Reapply every two hours when outdoors, and after swimming or sweating.4. Get Genetic Testing Done: If you have a family history of melanoma or other cancers, consider genetic testing to assess your risk. Tests like the MYRIS can identify melanoma-related gene mutations.5. Avoid Tanning Beds: Steer clear of tanning beds, as they significantly increase the risk of developing melanoma and other skin cancers.6. Be Your Own Health Advocate: Stay informed about your health, ask questions, and seek second opinions if necessary. Advocate for yourself and your loved ones by being proactive about potential health concerns.In This Episode: (00:00) Intro: Melanoma Awareness Month(02:40) Dr. Omid Hamid: Melanoma specialist introduction(6:58) Surgery for melanoma explained(10:49) Immunotherapy revolutionizes melanoma treatment(14:57) Genetic testing for melanoma risk(23:25) Importance of advocating for yourself(32:22) Teddy Mellencamp's stage 4 melanoma journey(50:51) Hormonal changes and melanoma risk(57:00) Two key melanoma prevention tipsRESOURCES:Melanoma Research Alliance: https://www.curemelanoma.org/blog/omid-hamid-mdMelanoma Research Foundation https://melanoma.org/Myriad Genetics: https://myriad.com/ GUEST BIOGRAPHY:Omid Hamid, MD, is the Chief of the Translational Research and Immuno-Oncology Department at The Angeles Clinic and Research Institute and serves as the Co-Director of the Melanoma and Phase I Programs. Academic Title as Professor, Department of Medicine at Cedars-Sinai Medical Center. His areas of expertise include immunotherapy and Phase I drug development.Dr. Hamid has published extensively and has been at the forefront of the development of paradigm-shifting breakthroughs including BRAF/MEK targeted agents, AntiCTL4A, antiPD1, and PDL1 therapies. His current interests include new immunotherapeutic options for patients including bi-specific antibodies, Adoptive T-cell Therapy, and oncolytic therapies with a focus on combinatorial approaches resulting in potentially great patient benefit.See Privacy Policy at https://art19.com/privacy and California Privacy Notice at https://art19.com/privacy#do-not-sell-my-info.

Send us a textIn this episode of Causes or Cures, Dr. Eeks chats with Dr. Amir Baniassadi about how indoor temperature affects the aging brain.Dr. Baniassadi shares what we know so far about the relationship between temperature and cognitive function, and explores the theories behind how temperature might influence cognition as we age. He discusses the findings of his recent study on temperature and cognition, including what surprised his team most. He also touches on an earlier study he conducted on temperature and sleep, and offers practical tips for optimizing your home environment. Is there a “sweet spot” for room temperature that supports both clear thinking and better sleep?Dr. Baniassadi is an instructor of medicine at Harvard Medical School and a scientist at the Marcus Institute for Aging Research. His work focuses on the aging brain and how environmental factors affect health and well-being in older adults. He holds a PhD in Civil, Environmental, and Sustainable Engineering from Arizona State University and an undergraduate degree in Mechanical Engineering from the University of Tehran. He also completed postdoctoral training in Translational Research in Older Adults, as well as a fellowship at the Harvard Graduate School of Design.Learn more about his work here. You can contact Dr. Eeks at bloomingwellness.com.Follow Eeks on Instagram here.Or Facebook here.Or X.On Youtube.Or TikTok.SUBSCRIBE to her monthly newsletter here.Support the show

Today, Lisa G. is diving deep into the science of aging, longevity, and muscle health with a true pioneer—Dr. Robert Wolfe, Co-founder and Lead Scientist at The Amino Co. A former Harvard professor, Director of the Center for Translational Research in Aging and Longevity, and one of the most cited researchers in the field, Dr. Wolfe has published over 500 studies funded by NASA, the NIH, the Department of Defense, and even the Olympic Committee.

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Dr. Hunter Champion received his training in Cardiovascular Disease, Heart Failure and Transplant Cardiology at Johns Hopkins where he later directed the Bernard Laboratory for the Study of Cardiovascular Disease.  Thereafter he was recruited to the University of Pittsburgh to join the faculty of the Divisions of Pulmonary, Allergy and Critical Care Medicine and the Cardiovascular Institute as an Associate Professor of Medicine where he directed Translational Research for the University of Pittsburgh Vascular Medicine Institute. He is a Heart Failure trained specialist and a Pulmonary Hypertension trained specialist and treats patients with hypertension, coronary artery disease, heart rhythm issues, and valvular disease. Dr. Champion joins Mark Immelman on the #OntheMark podcast to introduce 5 lifestyle changes that are sure to lead to a healthier, happier existence - habits which will also set you on the path to better physical performance and, by extension, better golf. Dr Champions elaborates on: Healthy body movement High quality sleep Morning sunlight, fresh air and breathwork The practice of gratitude, and Healthier eating involving protein and green vegetables. He also talks about the 'mind-body connection', alcohol consumption, managing stress, hydration, dietary supplements, meditation, hot and cold water therapy and grounding. Download this podcast or watch it on YouTube - search and subscribe to Mark Immelman.  

Dr. Gee returns to the discussion of his involvement in a university report on the Black Community Experience at the University of Wisconsin–Madison. In episode 188 he discussed the upcoming report with UW-Madison Chancellor Jennifer Mnookin and now that the report is public, he is joined by fellow board members on the ad hoc committee. Dr. Angela Byers-Winston and Ray Allen discuss the difference between good intentions and intentionality, when it comes to identifying and creating real change? The ad hoc study group worked to present their critical findings and strategic recommendations aimed at addressing the long-standing challenges faced by Black students, faculty, and staff on university campus. They discuss the question, “What is the systemic inertia to follow through on the recommendations?” Hear the unfiltered conversation about the report conducted by the UW by those that served on the board. All three speak honestly about the process, offering what made them angry or frustrated, and the hopes they have for change. They talk about how creating programs only can't change the DEI issues, but it takes institutional and organizational change. Also, be sure to catch a double portion of the Black Ice Breakers segment. Dr. Angela Byars-Winston is a tenured faculty member in the Division of General Internal Medicine within the Department of Medicine. She is also the inaugural Chair of the University of Wisconsin Institute for Diversity Science, associate director in the Collaborative Center for Health Equity, and faculty lead in the Center for the Improvement of Mentored Experiences in Research. Dr. Byars-Winston has received numerous awards for her research on advancing diversity goals and mentorship in STEM fields. In 2011, Dr. Byars-Winston was selected as a Champion of Change by the White House through President Obama's Winning the Future initiative for her research efforts to diversify science fields. In 2022, she was the recipient of the Innovation in Mentorship Research award from the Association of Clinical and Translational Research. Dr. Byars-Winston chaired the National Academies of Sciences' 2019 consensus study report, The Science of Effective Mentorship in STEMM. She is an elected Fellow in the American Psychological Association and is currently an appointed member of the NIH National Advisory General Medical Sciences Council. Over a career spanning nearly 50 years, Ray Allen has worked at the John Deere Company and served in a number of leadership roles in state government, including Secretary of the Wisconsin Department of Workforce Development. He was elected to three terms on the Madison School Board from 1995 to 2004, has served as chair of the Madison Area Technical College Board, and is the former publisher and owner of weekly newspaper The Madison Times. In 2016 Allen was honored with the Outstanding Alumni of Color Award from the UW–Madison Division of Diversity, Equity & Educational Achievement. He currently serves on more than 10 corporate and community boards, including 100 Black Men, the Overture Center, UMOJA Magazine's board of directors, United Way of Dane County, American Red Cross, Downtown Madison Inc., and Madison College. Read the Report: Black Community Experience on the University of Wisconsin – Madison Campus- AD Hockey Study Group alexgee.com Support the Show: patreon.com/blacklikeme Join the Black Like Me Listener Community Facebook Group