Podcast
Neurology Minute
Hosted by American Academy of Neurology · EN
The Neurology Minute podcast delivers a brief daily summary of what you need to know in the field of neurology, the latest science focused on the brain, and timely topics explored by leading neurologists and neuroscientists. From the American Academy of Neurology and hosted by Stacey Clardy, MD, Ph.D., FAAN, with contributions by experts from the Neurology journals, Neurology Today, Continuum, and more.
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Episodes
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Association of Changes in Activity Patterns With Brain Atrophy and Disability Progression in People With MS
2d ago00:01:00Tap to summarizeDr. Alex Menze and Dr. Kathryn C. Fitzgerald discuss using accelerometry to detect subtle, longitudinal changes in disability in people with multiple sclerosis and how these changes relate to brain atrophy and disability progression. Show citation: Fitzgerald KC, Sanjayan M, Dewey BE, et al. Association of Changes in Activity Patterns With Brain Atrophy and Disability Progression in People With Multiple Sclerosis. Neurology. 2026;106(7):e214678. doi:10.1212/WNL.0000000000214678 Show transcript: Dr. Alexander Menze: Hi, this is Alexander Menze. I just finished interviewing Kate Fitzgerald for the Neurology Podcast. For today's Neurology Minute, Kate, I'm hoping you can tell us the main points of your paper. Dr. Kathryn C. Fitzgerald: So we followed 238 people with MS who are 40 or older for over three years and they wore risk-worn accelerometers roughly every three months and had regular clinical assessments and brain MRI. And what we found was that changes in activity patterns over time at the individual level were associated with subsequent changes in disability worsening and brain volume loss, particularly in the deep gray matter and thalamus. Dr. Alexander Menze: Thank you very much. Be sure to download this week's podcast to hear our full interview.
Transcribe →Clinical Heterogeneity and Candidate Biomarkers in POLG-Related Mitochondrial Disease - Part 2
3d ago00:02:07Tap to summarizeIn the second part of this series, Dr. Katie Krulisky and Dr. Cristina Domínguez-González explore the most effective approach to evaluating suspected mitochondrial disease. Show citation: Bermejo-Guerrero L, Restrepo-Vera JL, Martin-Jimenez P, et al. Clinical Heterogeneity and Candidate Biomarkers in POLG-Related Mitochondrial Disease. Neurol Genet. 2026;12(2):e200365. Published 2026 Mar 10. doi:10.1212/NXG.0000000000200365 Show transcript: Dr. Katie Krulisky: This is The Neurology Minute. This is the second part of our series. I'm Katie Krulisky from the University of Utah and I'm here with Cristina Domínguez-González from the 12th of October University Hospital and its affiliated health research institute in Madrid, Spain. We've just recorded a full podcast on our paper, Clinical Heterogeneity and Candidate Biomarkers in POLG-related Mitochondrial Disease, which has been published in Neurology Genetics. Cristina, for The Minute, what's the most practical way to work up suspected mitochondrial disease today? Dr. Cristina Domínguez-González: In practice, everything starts with the clinical picture. Recognizing the pattern, whether it's a combination of features or a more subtle isolated presentation, is what should first raise suspicion. From there, you decide the next step. Targeted genetic testing if the phenotype is well-defined, grow their sequencing if it is less clear or more complex. Biomarkers can also be very helpful. GDF15, Growth Differentiation Factor 15, is markedly elevated in many mitochondrial diseases and can support the suspicion. In myopathies in particular, it is especially useful because of its high negative predictive value helping to rule out a mitochondrial cause when levels are not elevated. And finally, muscle biopsy still has a role. It can provide important information in selected cases, particularly in adults or when genetic results are inconclusive, both for diagnosis and also to guide further studies. Dr. Katie Krulisky: Thank you. That's super helpful. And for more on mitochondrial diseases and POLG-related disorders, have a listen to the full neurology podcast. Again, I'm Katie Krulisky from the University of Utah with Cristina Domínguez-González from the 12th of October University Hospital and its affiliated health research institute in Madrid, Spain.
Transcribe →Workplace Lactation in Neurology: Barriers and Opportunities - Part 2
4d ago00:01:48Tap to summarizeIn the last episode of the series, Dr. Stacey Clardy and Drs. Deborah Hall and Deborah Setter discuss some practical changes that can immediately improve lactation support in neurology workplaces. Show transcript: Dr. Stacey Clardy: This is the Neurology Minute. I'm Stacey Clardy from the Salt Lake City VA and the University of Utah. I've just had a fantastic in depth podcast discussion with Deborah Hall from Rush University and Deborah Setter from Olmsted Medical Center on their paper titled Workplace Lactation in Neurology: Barriers and Opportunities. You can find that in Neurology Clinical Practice. Deborah Hall, what are some practical changes that can immediately improve lactation support in neurology workplaces? Dr. Deborah Hall: One practical change that could be considered is to plan immediately when you know a provider will be going out on maternity leave. Prior to departure, you can plan what that schedule's going to look like when that provider returns. Ensure that they have those 30 minute breaks every two to three hours in their inpatient or outpatient schedule. Make sure that there's a space for them and have them go look at it that would be appropriate for their lactation breaks. You want to make sure they have that dedicated refrigerator for breast milk storage. And finally, make a plan for compensation. It's really important that they understand how their productivity targets and how compensation will be affected by the breaks that they will be taking. Dr. Stacey Clardy: Easy to make changes, right? And as we discuss in the full-length podcast, please everyone take a listen to this. This is something we can all improve on to support all of our colleagues in neurology. Please have a listen to the full-length podcast. We give you everything that you need to know to be a better support to your colleagues. Thanks so much, Deborah.
Transcribe →May 2026 President Spotlight: AAN Annual Meeting Update
5d ago00:03:33Tap to summarizeIn the May episode of the President's Spotlight, Dr. Jason Crowell and Dr. Natalia Rost provide a leadership perspective on the 2026 Annual Meeting. Stay informed by watching the President's Spotlight video. Show transcript: Dr. Jason Crowell: Hey, this is Jason Crowell with today's Neurology Minute. Once again, we have Natalia Rost joining us for our monthly check-in. Of course, Natalia is the president of the AAN. Natalia, thanks for joining us again this month. Dr. Natalia Rost: Hi, Jason. Dr. Jason Crowell: So what have you been up to since we last spoke a month ago? Dr. Natalia Rost: Well, as you know, we just came back from Chicago, where our 2026 AAN annual meeting took place, and of course, it's the largest gathering of neurologists and neuroscience professionals worldwide, so not a small feat. We welcome this time a record-breaking 16,000 plus participants in person in Chicago and online, representing 110 countries and all 50 states, what I call a microcosm of the global neurology community. It was amazing, and an opportunity to step back, reflect, and be reminded that progress in neurology happens not in isolation, but through our shared purpose and collaboration, and the energy and optimism coming out of this meeting is something I'm so proud of. Dr. Jason Crowell: I can only imagine what a whirlwind week that is for you. So now that it's past us and you reflect back, what stands out to you from the week? Dr. Natalia Rost: Well, it was clear during that meeting that we're advancing what comes next and that's why science and research was at the heart of the week and why sustained investment in discovery matters. I had the privilege of seeing colleagues modeling leadership in neurology, both on stage and behind the scenes and attendees engaged with cutting-edge science, shared insights across disciplines, and bringing those new insights and techniques home to their practices, institutions, and communities. Dr. Jason Crowell: Now, your presidential plenary at the meeting was about neuroscience at the crossroads. What would you say is the most urgent challenge facing our neurology community right now? Dr. Natalia Rost: You know, as a physician scientist myself, I'm focused on how to sustain progress at this moment of rapid scientific advancement. Our neurology community is gathering extraordinary volume of knowledge, but translating that momentum into durable impact requires continued commitment to research, workforce development and collaboration across disciplines are key topics. And I feel that this is a pivotal time for our field. Dr. Jason Crowell: And if I could ask you to just briefly take off your president hat for a moment, personally, what was your favorite thing about the week? Dr. Natalia Rost: What always been for me for over two decades now, the chance to come together as a community. I always say AAN is our home and the annual meeting is like one big homecoming for us. There's a unique energy that comes from being in the same space with colleagues from across neurology, sharing ideas, learning from each other, and just reconnecting with people who care deeply about this field, your colleagues. And while our work can be demanding, as we know on a day-to-day basis, the meeting helps remind us why we chose this profession and why it matters. Dr. Jason Crowell: And lastly, what would you say for anyone who was not able to make it to this homecoming in Chicago? Dr. Natalia Rost: We got you. We have great resources for those who weren't able to join live and you can get high-level highlights or diving into programming online. Access it all at theaan.com/am. Dr. Jason Crowell: Natalia, thanks so much. Dr. Natalia Rost: Thanks for having me.
Transcribe →Clinical Heterogeneity and Candidate Biomarkers in POLG-Related Mitochondrial Disease - Part 1
1w ago00:01:48Tap to summarizeIn part one of this series, Dr. Katie Krulisky and Dr. Cristina Domínguez-González discuss when a neurologist should start thinking about mitochondrial disease. Show citation: Bermejo-Guerrero L, Restrepo-Vera JL, Martin-Jimenez P, et al. Clinical Heterogeneity and Candidate Biomarkers in POLG-Related Mitochondrial Disease. Neurol Genet. 2026;12(2):e200365. Published 2026 Mar 10. doi:10.1212/NXG.0000000000200365 Show transcript: Dr. Katie Krulisky: This is The Neurology Minute, and this will be a two-part series. I've had the pleasure of speaking with Cristina Domínguez-González from the 12th of October University Hospital and its affiliated Health Research Institute in Madrid, Spain. I'm Katie Krulisky from the University of Utah. We've just recorded a full podcast on our paper, Clinical Heterogeneity and Candidate Biomarkers and POLG-related Mitochondrial Disease, which has been published in Neurology Genetics. So for our first minute, Cristina, when should a neurologist start thinking about mitochondrial disease? Dr. Cristina Domínguez-González: Mitochondrial diseases are among the most common inherited neurological disorders. Think of them whenever you see compatible features like ptosis ophthalmoplegia, polyneuropathy, ataxia or myopathy, especially when they occur in combination. But even when these features appear in isolation, mitochondrial disease should still be part of the differential. This is particularly important because many patients do not present with a full classical picture, especially in early the disease course. In practice, this means maintaining a low threshold to consider mitochondrial disease, even in a typical presentations. Dr. Katie Krulisky: Thank you so much. And for more information on mitochondrial disease and POLG-related disorders, do listen to the full neurology podcast. Again, I'm Katie Krulisky from the University of Utah with Cristina Domínguez-González from the 12th of October University Hospital and its affiliated Health Research Institute in Madrid, Spain.
Transcribe →Workplace Lactation in Neurology: Barriers and Opportunities - Part 1
1w ago00:01:32Tap to summarizeIn the first episode of this series, Dr. Stacey Clardy, along with Drs. Deborah Hall and Deborah Setter, discusses the most overlooked barrier to effective lactation support in neurology today. Show citation: Hall D, Setter D, Ullrich N, et al. Clinical Workplace Lactation in Neurology: Barriers and Opportunities. Neurol Clin Pract. 2026;16 (3) e200611. Published 2026 Apr 17. doi:10.1212/CPJ.0000000000200611 Show transcript: Dr. Stacey Clardy: This is the Neurology Minute. I'm Stacey Clardy from the Salt Lake City VA in the University of Utah. I've just had a great discussion with Deborah Hall and Deborah Setter about their paper, Workplace Lactation in Neurology: Barriers and Opportunities. Deborah Setter, my question for you for the minute is what is the most overlooked barrier or barriers to effective lactation support in neurology today? Dr. Deborah Setter: I think the biggest barrier is that lactation is a knowledge gap for neurologists. I was surprised to find out that a lactating person needs a 20 to 30-minute break every two to three hours to maintain their milk supply, prevent complications of insufficient milk expression, and to meet their personal lactation goals. Dr. Stacey Clardy: Awareness is key. I admit that I didn't even know the details surrounding the federal law in the United States regarding this as well. There is so much more in our full podcast discussion, so please take a listen. This is essential listening for all of us in neurology to help our field do better and to support our colleagues. Thanks so much, Deborah.
Transcribe →Maintenance Immunotherapy in MOGAD: Early Steroid Benefit, Dose Thresholds, and Disability Risk - Part 3
1w ago00:03:05Tap to summarizeIn the last episode of this series, Dr. Justin Abbatemarco and Dr. Benjamin P. Trewin discuss how to apply this data into clinical practice. Read more about this abstract on the AAN website. Show transcript: Dr. Justin Abbatemarco: Hello, and welcome back. This is Justin Abbatemarco and I'm joined by Benjamin Trewin where we're reviewing top abstracts from the AAN annual meeting in Chicago. Today we're talking about his abstract maintenance immunotherapy and MOGAD, early steroid benefit, dose thresholds, and disability risk. Ben, we've done this really great job of dissecting the data, steroids, non-steroidal agents. How do you think about the treating MOGAD cases in clinic though? How do you try to put this data and the data we've talked about into clinical practice? Dr. Benjamin P. Trewin: It's obviously a very good and actionable question, and our research has always tried to focus on these dilemmas facing the clinician at the bedside. And so the way that we think about this is, of course, we try to come up with some rules or some guidelines to treat all patients, as that's the most effective way of giving the message, but we need to acknowledge there is variation within MOGAD patients. There are people with low relapsing propensity who will take a very long time to relapse. You'll need to follow them for a long time. And there are ones with high relapsing propensity. So some of our previous work, we actually reviewed thousands of MOGAD patients in the literature and found that if you follow them for more than five years, over 70% actually relapse. It's just a matter of following them. So acknowledging this variation in the patients is important, but at the same time, the guideline we would probably endorse based on our research is that all patients with MOGAD after a first attack should be treated with oral corticosteroid taper, including at least five months of 12.5 milligrams per day oral corticosteroids. Now, how does that work in practice? Well, you would probably start them, and I say probably here because we don't have the strength of evidence for the very start of the course and the very end. But what did we do? Well, we start them at about one milligram per kilogram. And over probably about two to three weeks, you can bring them down to about 12.5 milligrams per day, or in children, 0.16 milligram per kilogram per day. And then you'll do that four or five months. And then over two or three weeks after that, you would step them down. Of course, you want to be careful that you don't have any adrenal issues. You would want to go slow enough for that. But at the same time, you don't want to prolong the course too long and put yourself at risk of side effects. Dr. Justin Abbatemarco: I think that's really helpful and practical. And you don't need these huge doses, it looks like, to treat these patients well and trying to really be mindful of those side effects that are truly dose dependent. And then yeah, we have some really great data. We need some randomized data to help us inform next steps, but this retrospective data, we're starting to put together this picture around B-cell depleting IVIG like we talked about. So super helpful. Ben, really excited to see you at the annual meeting. And yeah, thank you for your time and expertise.
Transcribe →Maintenance Immunotherapy in MOGAD: Early Steroid Benefit, Dose Thresholds, and Disability Risk - Part 2
2w ago00:05:24Tap to summarizeIn the second episode of this series, Dr. Justin Abbatemarco and Dr. Benjamin P. Trewin discuss what was found in non-steroidal maintenance therapies. Read more about this abstract on the AAN website. Show transcript: Dr. Justin Abbatemarco: Hello and welcome back. This is Justin Abbatemarco from the Cleveland Clinic. And we're joined by Ben Trewin on his abstract maintenance immunotherapy and MOGAD, early steroid benefit, dose thresholds and disability risk. Ben, in our first episode we really talked about corticosteroids, but your paper and abstract looked at other therapies. What did you find in those non-steroidal maintenance therapies? Dr. Benjamin Trewin: In addition to looking at oral corticosteroid therapies, we also looked at B-cell depleting therapies, namely rituximab and ocrelizumab, and intravenous immunoglobulin and steroid-sparing therapies, namely azathioprine and mycophenolate predominantly, I suppose a couple on methotrexate. Now, what we found, it's important to note that we were able to tease apart the effects of all these drugs with our Cox proportional hazard model chops up, follow up into distinct intervals with different combinations and permutations of these medications and their different doses in a more granular way than is allowed by previous techniques like incident rate ratios when we compare pre and post annualized relapse rate, and we think this is a strength of the study. With this methodological strength, we were able to see that steroid-sparing therapies, despite 334 patient years of data, do not appear to have any independent benefit with respect to time to next relapse. The estimate of effect there was 1.06. And then for time to confirm sustained disability, there was also no confidence signal, the confidence interval being 0.15 to 1.4, that it actually prevented any disability despite a wealth of data, which I think is an important thing to note. And I think previous studies, particularly looking with incident rate ratios, have been a little more optimistic with that. And I think there might be misattributing some of the benefit of concomitant steroids to the steroid-sparers, but it's more complex than that, of course. And then with respect to B-cell depleting therapies, we did have 48 of 261 patients exposed, which is reasonable, but not quite enough to get the signal we're looking for. However, we found something quite interesting, because when we compared the Liverpool data to the Australasian data, the two big study groups involved, we saw that it wasn't quite as effective in Liverpool as it was in Australasia in this subgroup analysis. And so we dug a little deeper, as one should, and found that the dosing is actually different. And in Australasia, we have a tendency to just give two grams of rituximab up front, or 600 milligrams of ocrelizumab. And then six-monthly, you give a gram of rituximab without fail, without trying to watch the B cells or trying to muck around with doses in any way. And when we looked at that, the threshold dosing, as we termed it, as compared to below threshold dosing, there actually was weak evidence at a PVA of 0.08 that threshold dosing is superior to below threshold dosing. And that needs to be reproduced, but I think that was an important signal. And finally, I would say IVIG, of course, has some very strong data in this area. And I think it's important from this study at least to remain a little agnostic on that as we only had 31 patients on IVIG, and so I absolutely wouldn't say it's not effective. I would say unfortunately, we had insufficient data to make any big claims about that. Dr. Justin Abbatemarco: I think some really great data to help pick apart here and help inform practice. I think your point about looking at the previous literature and trying to tease apart these steroid-sparing agents, that corticosteroids they're not uniformly addressed, and so it's difficult to think about at those previous data points, so I appreciate that. And then this dose response to the B-cell therapies, there's been questions in the literature, because I think we've gotten a lot of mixed results on B-cell therapies. And so this to me is one of the larger studies that really help answer this question that maybe B-cell therapies are effective and maybe we need to be a little more sensitive to dose, which is the same theme we saw on IVIG. IVIG, maybe at higher doses, could be more effective for MOGAD. What do you think about that comparison? Dr. Benjamin Trewin: I like where you're going with that because we're quite interested in these dose responses as we introduce this 12.5 milligram per day oral corticosteroid dose or 0.16 milligrams per kilograms per day in kid. And so we're quite interested. And, of course, that work by Dr. Chen and Dr. Mariner has revealed that IVIG also has quite a sensitive dose threshold there at one gram every four weeks. And we followed that precinct because that research was so strong. So it's nice to feel like we're building on previous studies and then perhaps even detecting another dose threshold with respect to rituximab. And I must say, it was a little bit of a surprise, we came in and saw why is the Liverpool data moving that way and the other one moving this way? So it was a nice data-driven evolution of our multi-variable model. Dr. Justin Abbatemarco: So helpful. And I'll ask everyone to come back for the final episode, where we try to put this all together. We're going to put Ben on the spot and really understand how he approaches these cases in clinical practice. Ben, thank you. Dr. Benjamin Trewin: Thanks very much, Justin.
Transcribe →Epstein-Barr Virus Antibodies to Differentiate MS From Other Neuroinflammatory Diseases - Part 2
2w ago00:01:35Tap to summarizeIn the second part of this series, Dr. Justin Abbatemarco and Dr. Paulus Rommer discuss how to apply these study results into clinical practice. Show citation: Vietzen H, Kühner LM, Berger SM, et al. Epstein-Barr Virus Antibodies to Differentiate Multiple Sclerosis From Other Neuroinflammatory Diseases. JAMA Neurol. Published online March 9, 2026. doi:10.1001/jamaneurol.2026.0240 Show transcript: Dr. Justin Abbatemarco: Hello and welcome back. This is Justin Abbatemarco, and we're finishing up our interview with Paulus Rommer on his article on JAMA Neurology, Epstein-Barr Virus Antibodies that differentiate multiple sclerosis from other Neuroinflammatory Diseases. Paulus, can we talk about how we would apply your results into clinical practice right now? Dr. Paulus Rommer: The persistent high apnea antibody responses are a hallmark of multiple sclerosis. And in our micro center study, we found that the singular measurement is not sufficient to differentiate multiple sclerosis from other related disorders like MOGAD or NMOSD, but it's the repeated high levels over time. We see them in about 95% of our MS patients, but really rarely in MOGAD or NMOSD. So this persistent high levels is a good factor, with a high accuracy, to really diagnose multiple sclerosis and to differentiate them from MOGOD or NMOSD. Dr. Justin Abbatemarco: I think these are really helpful and I think a little more evolution in how we interpret these on individual patient level, like we talked about in the podcast, but more to come. Paulus, thank you again for all your work on this topic for coming on and we're excited to have you back in the future. Dr. Paulus Rommer: Thank you.
Transcribe →Clinical Reasoning Series: A 70-Year-Old Man With Systemic Illness Related Strokes Refractory to Medical Treatment Managed With Intracranial Stent
2w ago00:02:10Tap to summarizeDr. Zohaib Siddiqi and Dr. Laurence Poirier discuss a complex stroke case associated with systemic vasculitis, highlighting diagnostic challenges and management strategies, including the role of endovascular therapy. Show citation: Poirier L, Brissette V, Shamy MCF, Maxwell JP, Drake B, Fahed R. Clinical Reasoning: A 70-Year-Old Man With Systemic Illness Related Strokes Refractory to Medical Treatment Managed With Intracranial Stent. Neurology. 2025;104(1):e210068. doi:10.1212/WNL.0000000000210068
Transcribe →