Neurology Minute
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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New Resident Guide to Stroke Alerts - Part 2
06/05/2026
New Resident Guide to Stroke Alerts - Part 2
In part two of this series, Dr. Andy Southerland and Dr. Dan Ackerman discuss a few rapid‑fire concepts from the 2026 guidelines, focusing on what is new and how emerging data may shape patient care. Show transcript: Dr. Andy Southerland: Hello, everyone. This is Andy Southerland from the University of Virginia. And for today's Neurology Minute, I'm speaking with my friend and colleague, Dan Ackerman, Chief of Neurology and Director of Stroke at St. Luke's University Health System. We've been speaking in the main neurology podcast on tips for updated clinical practice related to the 2026 American Heart Association guidelines for the early management of patients with acute ischemic stroke. I'm going to hit Dan with a few rapid fire concepts that were touched on the guidelines that I think are new or provide some new insights, new based on the data and to how we treat patients. So Dan, you ready for it? Rapid fire, acute stroke treatment decision making? Dr. Dan Ackerman: Absolutely. Hit me. Dr. Andy Southerland: All right, Dan. I'm a resident going to my first stroke alert on July one this year and I've got a patient coming in, they're having disabling stroke symptoms and they're, in every other way, eligible to receive thrombolysis, but they have a history of paroxysmal atrial fibrillation. They are on apixaban and they took a dose of that apixaban. They forgot to take one yesterday, but they took one the day before, had the evening before. And so 36 hours ago, they took a dose of their apixaban. So based on previous dogma, I think prior guidelines might've said if it's within that 48 hour window, that's a relative contraindication of thrombolysis. What, say, you based on the new guidelines and then how do they inform us about making that decision? Dr. Dan Ackerman: I would actually say the new guidelines are a little bit more aligned with what you just said. You mentioned it as a relative contraindication to thrombolysis. I think before these guidelines came out, a lot of people would've said, "No, that is a strict contraindication to thrombolysis." And a lot of folks would run a stroke code or a stroke lid a little slower knowing that, hey, this person is on, whether it's apixaban, rivaroxaban, edoxaban, dabigatran, et cetera, any of these direct oral anticoagulants and say, "Well, no, we know that person's not a candidate for thrombolytics." Well, no, the newer guidelines would suggest that that is a relative contraindication, not a strict contraindication. And when we look back at studies on this, it has not been suggested that there is a big contribution in terms of exactly how long ago that last dose was. Was it two hours ago, 12 hours ago, 20 hours ago? And there has not been shown to be a clear benefit of testing for factor Xa activity levels, bleeding time and the like. So the guidelines do suggest that, hey, we need more data on this. It's not to, say, that this is 100% perfectly fine. Remember, that's a relative contraindication, so it's still a risk benefit discussion, but studies have not shown an increased risk for hemorrhagic complications in patients who have had recent DOAC exposure who receive IV thrombolysis otherwise according to the guidelines. So I would tend to offer it in that situation and make sure that we document what drugs someone's on, how long ago was their last dose, all of this kind of information in addition to what we might normally otherwise get down. Dr. Andy Southerland: Does that change, Dan, if they took the DOAC in the last 24 hours or even 12 hours? They took it last night, and they're presenting in the morning with their stroke-like symptoms? Dr. Dan Ackerman: The guideline just suggests less than 48 hours, and the data, to my knowledge, doesn't really delineate, at this point, any particular timeframe where we would say, no, there's a cutoff there at two hours or eight hours or 12 hours. So at this point, I would not use that as a way to decide not to offer thrombolysis based on that timeframe. Dr. Andy Southerland: Fair enough. I think that's very reasonable. And I think, again, it's always a good conversation to have either with your attending, if you're that resident on July 1, but particularly with the patient and their family on the risk-benefit of what we know based on the data. Well, that's all the time we have for this Neurology Minute. We hope this discussion will continue to help everyone out there in the hyperacute management of patients with acute ischemic stroke, making those difficult treatment decisions. Good luck.
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New Resident Guide to Stroke Alerts - Part 1
06/04/2026
New Resident Guide to Stroke Alerts - Part 1
In part one of this series, Dr. Andy Southerland and Dr. Dan Ackerman discuss what stands out in the latest thrombolysis guidelines, how these decisions are applied in stroke center practice, and how to educate residents and fellows on incorporating new evidence into treatment choices. Show transcript: Dr. Andy Southerland: Hi. This is Andy Southerland from the University of Virginia, and for today's Neurology Minute, I'm speaking with my friend and colleague, Dan Ackerman, Chief of Neurology and Director of Stroke at St. Luke's University Health System. I've been speaking with Dan on the main neurology podcast regarding updates to acute stroke treatment related to the 2026 American Heart Association guidelines that came out in late January of this year on the early management of patients with acute ischemic stroke. For our episode today, we might focus our discussion around thrombolytic therapy thrombolysis, which is at the core of what we do as acute stroke neurologists when it comes to treatment decision-making. So maybe as a first prompt, Dan, when you look at these guidelines, what stands out to you as you're thinking about how you practice, how you all are practicing at your stroke center, and then specifically how we educate our residents, our fellows on what they need to know, particularly the newness of it when it comes to making thrombolysis treatment decisions? Dr. Dan Ackerman: With all the discussions we've had in the past, there have been a lot of specifics about certain studies and how they might affect practice, but this guideline really opened up a lot and gave us an opportunity to do things in a way that makes really good clinical sense and really brings a lot of practices that have now become common at some centers into the fore so that we can get that information out to everyone and make sure everyone has that same really high level of stroke care everywhere they go. I think the first thing that stands out to me is what did not change. And want to reinforce that, particularly for people who are just getting into this, stroke alert is a screening tool, not a severity score. It's not like an MI alert where you do an EKG and you see the tombstone wave and you say, "Oh, there's an MI and we're taking them to treatment." This is a screening tool, so it is meant to be highly sensitive at the cost of being specific. At our shop for a long time now, we have initiated stroke alert for anyone who presents either within 24 hours of acute onset of neurologic symptoms or has an unknown onset of acute neurologic symptoms and they are still symptomatic to some degree at the time of their presentation, and that's it. We don't make any other statements about how severe something is or what kinds of symptoms someone necessarily has to have. We purposely keep it as broad as possible, again, because we're trying to screen. And the other thing that has not changed, time is still brain. So with all of these different nuances on how we can treat patients and who might be candidates for intervention, it is still a matter of understanding these guidelines, applying our best evidence, but doing it as quickly as possible to make sure that we are rescuing as much of that ischemic penumbra as we possibly can. Now, aside from that, in terms of what stands out that is different, I think one of the early things for me are the recommendations for extended time window for IV thrombolysis. So when you look at the original studies, we understand that when you get out beyond four and a half hours, if you just take all-comers, the risk is going to start to outweigh the benefit. But that doesn't mean there's zero benefit or that no one would receive benefit, but it's a question of, well, how do we cherry-pick those patients who may still receive benefit? And there are a few real specifics in the guideline that help us figure that out. One is for patients who have an unknown time of onset, but they're within four and a half hours of symptom discovery. And for those patients, they would suggest that doing a stat MRI and comparing a DWI lesion with the corresponding area flare to determine if you see DWI hyper-intensity and the flare image is nice and normal, that would suggest that stroke is young enough that it may still be appropriate to treat that patient. But we would also say for folks who have salvageable ischemic penumbra, so again, brain at risk that is not core yet, who either awoke with stroke symptoms within nine hours from the midpoint of sleep or, and this is the kicker, are within four and a half to nine hours from last known well. So in other words, they may have been symptomatic already for more than four and a half hours. If those patients have an appropriate ischemic penumbra, it may be reasonable to treat them with IV thrombolysis to improve functional outcomes. Dr. Andy Southerland: Well, that's all for this Neurology Minute. We hope this vibrant conversation will help all those who are out looking to make the best treatment decisions for their patients, both based on established evidence and most recent evidence in our new guidelines.
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Understanding Rett Syndrome - Part 3
06/03/2026
Understanding Rett Syndrome - Part 3
In the third episode of this series, Dr. Stacey Clardy discusses treatment options and ongoing management. Show transcript: Dr. Stacey Clardy: This is The Neurology Minute. I'm Stacey Clardy from the Salt Lake City VA at the University of Utah. This is the third episode today in our four-part series on Rett syndrome, and we're going to talk about treatment options and ongoing management. There is still no curative therapy for Rett syndrome and management remains largely supportive and multidisciplinary. But there is now an FDA-approved treatment, trofinetide, for adults and children two years of age and older with Rett syndrome. Trofinetide is a synthetic analog of glypromate. It's thought to modulate neuroinflammation and synaptic function, right? Because Rett syndrome involves difficulty with synaptic function. Clinical trials demonstrated improvements in some of the core Rett symptoms, but of course, as always, treatment decisions are going to require an individualized discussion, particularly given some common adverse effects such as diarrhea and vomiting. Beyond disease-specific therapy, management remains symptom driven. Given that epilepsy is common and may be refractory, careful EEG correlations are often necessary. Of course, the breathing abnormalities like hyperventilation and apnea are fairly characteristic and can fluctuate over time so need to be monitored, and gastrointestinal dysfunction, nutritional challenges, other sleep disturbances, and scoliosis require ongoing monitoring and intervention when relevant. Rehabilitation therapies, physical, occupational, and speech, are foundational throughout life. A key principle here is anticipatory management, right? Many of the complications, like cardiac conduction abnormalities and bone health issues, can be identified early and addressed early with better outcomes when Rett syndrome patients have coordinated care. That's it for today. Be sure to listen to the other Neurology Minute episodes in this series on Rett syndrome, and check back for our next and final episode, where we will cover care team essentials and multidisciplinary management. I'm Stacey Clardy for the minute.
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Shunting for Idiopathic Normal Pressure Hydrocephalus
06/02/2026
Shunting for Idiopathic Normal Pressure Hydrocephalus
Dr. Margarita Fedorova discusses the effectiveness of shunting for idiopathic normal pressure hydrocephalus. Show citation: Luciano MG, Williams MA, Hamilton MG, et al. A Randomized Trial of Shunting for Idiopathic Normal-Pressure Hydrocephalus. N Engl J Med. 2025;393(22):2198-2209. doi: Show transcript: Dr. Margarita Fedorova: Welcome to Neurology Minute. My name is Margarita Fedorova and I'm a neurology resident at the Cleveland Clinic. Today we're reviewing a randomized trial that provides high quality evidence for treatment we've been using for decades, shunting for idiopathic normal pressure hydrocephalus. The PENS trial, a placebo controlled effectiveness and iNPH shunting trial was published in the New England Journal of Medicine in December 2025 by Luciano and colleagues. This international multicenter study enrolled 99 patients across the United States candidate in Sweden. While idiopathic normal pressure hydrocephalus or iNPH is characterized by triad of gait impairment, cognitive decline in urinary continence, these findings can be non-specific and we mass factor in radiological findings too. Furthermore, while CSF shunting has long been the standard treatment, its effectiveness has never been rigorously confirmed in a large well-powered randomized trial. In this trial, patients with a clinical improvement in gait velocity after temporary CSF drainage were deemed eligible for shunting and randomizing the trial. What makes this trial particularly elegant is its blending strategy. All 99 participants underwent the same surgical procedure with the same commercially available programmable shunt valve. After surgery, the valve was set either to an open functioning position or to a high resistance placebo setting. Neither patients nor assessors knew who had a working shunt. This is about as close to a true double-blind design as neurosurgery can get. The primary outcome was changing gait velocity at three months. The open shunt group improved by 0.23 meters per second on average, while the placebo group showed essentially no change in 0.03 meters per second. That's a treatment difference of 0.21 meters per second, both statistically significant and clinically meaningful. To put that in perspective, a change of 0.10 meters per second is considered the threshold for substantial meaningful change in the elderly. 80% of the open shunt group exceeded that threshold compared to only 24% of the placebo group. The Tenet scale, which measures gait imbalance, also showed significant improvement in the open shunt group. However, screening measures for good condition using the MoCA scale and bladder symptoms did not reach significance at three months, though tertiary outcomes for cognitive testing, quality of life and functional independence tended in favor of shunting. Importantly, falls were more common in the placebo group at 46% compared to 25% in the open shunt group. This is a meaningful safety signal given how dangerous falls are in older adults. There were also real risks with active shunting. Subdural hematomas occurred in 12% of the open shunt group versus 2% of placebo and three even required surgical intervention. Positional headaches from low CSF pressure were more common in the open shunt group at 59% versus 28%. The good news is that the adjustable valve allowed non-invasive management of many of these complications. While this trial gives us reasons to be cautiously optimistic about shunting for appropriately selected iNPH patients, it's worth noting that we only have evidence for improvement in gait and follow-up is only three months. Longer-term data is still being collected so we don't know yet how durable these benefits are. If you want to read more, please find the paper by Mark G. Luciano, et al. It's titled A Randomized Trial of Shunting for Idiopathic Normal Pressure Hydrocephalus published in the New England Journal of Medicine in December 2025. That's your neurology menu for today. Keep exploring and we'll see you next time.
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Recent Updates in Central Retinal Artery Occlusions
06/01/2026
Recent Updates in Central Retinal Artery Occlusions
Dr. Casandra MacLeod discusses central retinal artery occlusions, recent trials, and those anticipated in the future. Show citation: Préterre C, Gaultier A, Obadia M, et al. Intravenous alteplase versus oral aspirin for acute central retinal artery occlusion within 4·5 h of severe vision loss (THEIA): a multicentre, double-dummy, patient-blinded and assessor-blinded, randomised, controlled, phase 3 trial. Lancet Neurol. 2025;24(11):909-919. doi: Poli S, Grohmann C, Wenzel DA, et al. Early REperfusion therapy with intravenous alteplase for recovery of VISION in acute central retinal artery occlusion (REVISION): Study protocol of a phase III trial. Int J Stroke. 2024;19(7):823-829. doi: Ryan SJ, Jørstad ØK, Skjelland M, et al. A Randomized Trial of Tenecteplase in Acute Central Retinal Artery Occlusion. N Engl J Med. 2026;394(5):442-450. doi: Show transcript: Dr. Casandra MacLeod Hello, this is Casandra MacLeod, a neurology resident at Cleveland Clinic with today's Neurology Minute. Today we will be discussing central retinal artery occlusions, or CRAOs, and the recent trials that have come out and even those further on the horizon. The 2026 American Heart Association and American Stroke Association guidelines for the early management of patients with acute ischemic stroke were recently published and in them highlight the uncertainty around the treatment of acute CRAOs with intravenous thrombolysis, even when the patient presents within four and a half hours and is otherwise eligible. These guidelines come after two recent trials, which we will further discuss. The thrombolysis in patients with acute central retinal artery occlusion, or the THEIA trial, was published in the November issue of Lancet Neurology. This multicenter trial out of France randomized 70 patients with acute CRAOs presented within four and a half hours of time from last known well to either receive IV alteplase and oral placebo or IV placebo and oral aspirin. While safety measures showed no symptomatic hemorrhage event, although they did have one asymptomatic intracerebral hemorrhage occur, the primary outcomes, which included visual acuity improvement at one month, showed some evidence for a trend of improved acuity in the IV thrombolytic group at 66% compared to 48 in the aspirin group, it did not reach significant. And now more recently, the Tenecteplase in central retinal artery occlusion study, or TenCRAOs, was published in the January 2026 issue of The New England Journal of Medicine. TenCRAOs was a six European country multicenter trial that randomized 78 patients with CRAOs all presenting within four and a half hours of time from last known well to either receive IV Tenecteplase or aspirin, both with placebo-matching as in THEIA. The primary outcomes of TenCRAOs also included visual acuity at one month, but unfortunately this trial also did not show [inaudible 00:02:07]. They showed 20% in the IV TNK group compared to 24% in aspirin. And additionally, there was one fatal intracerebral hemorrhage in the TNK group that should be considered. Overall, the AHA and ASA guidelines state the usefulness of treatment with intravenous thrombolysis is uncertain. And this is based largely on these studies as neither trial showed improved visual recovery. Although both of these trials are underpowered, leading many to believe that the jury is still out on the use of IV thrombolytics in CRAOs. But importantly, stay on the lookout for one last trial. The early reperfusion therapy with intravenous alteplase for recovery of vision and acute central retinal artery occlusion, or the Revision trial, is actively recruiting. Revision is similar in design as THEIA, but with a goal of up to 422 total patients for a goal of a well-powered study to guide decision making.
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Prion Disease Clinical Trial NN112
05/29/2026
Prion Disease Clinical Trial NN112
Dr. Gregg Day and Drs. Sonia Vallabh and Eric Minikel discuss scientific insights and the future of prion disease treatment, highlighting the importance of early diagnosis, personalized medicine, and hope for affected families. Learn about the . Learn more about the . Show transcript: Dr. Gregg Day: This is Gregg Day with Neurology Minute. I've just been speaking with Eric Minikel and Sonia Vallabh, a husband and wife team at the heart of the PRiSM trial, a first-in-human study of a prion protein-lowering, divalent, small-interfering RNA for patients with symptomatic prion disease. Eric and Sonia, could you provide us with a brief overview of the PRiSM trial and what this first-in-human study seeks to accomplish? Dr. Eric Minikel: The PRiSM trial is testing a short interfering RNA designed to bind the RNA that encodes the prion protein. That is the protein that causes Prion disease. We are at the heart of what causes this disease. Through doing this, we hope to make prion disease a treatable and preventable condition. We both want to stabilize symptomatic patients and prevent the disease in people who are at genetic risk. This is a personal mission for us. Sonia is a carrier of a prion disease mutation that she inherited from her mother who died of prion disease, and we, along the way, aspire to be a different kind of sponsor. We want to create our own clinical data that are shareable learnings for the entire field. Dr. Gregg Day: This is Gregg Day with Neurology Minute. Thanks for listening.
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Headache Medicine Highlights from the 2026 AAN Annual Meeting - Part 2
05/28/2026
Headache Medicine Highlights from the 2026 AAN Annual Meeting - Part 2
In the second episode of this series, Dr. Tesha Monteith and Dr. Peter Goadsby discuss the prediction of treatment responses for personalized medicine. Show transcript: Dr. Tesha Monteith: Hi, this is Tesha Monteith with The Neurology Minute. Today I'm speaking with Peter Goadsby from the Division of Biomedical Sciences at King Abdullah University of Science and Technology about key trends in headache medicine and some of the most impactful research presented at the AAN annual meeting. Can you talk a little bit about prediction of treatment response for personalized medicine? Dr. Peter Goadsby I hope that AI gives us some direction. I haven't seen anything yet, but I don't think we've done enough with it to make it stunning yet. I think that the AI systems ... I'd love to know, for example ... I've been using triptans for 30 years and apart from using sumatriptan first when [inaudible 00:00:51] had a triptan simply because it's the commonest triptan, which is generally what I do, that's a pretty naff rule when you think about it. I'd like to think that AI systems could work out where we should be going in terms of acute therapy, preventive therapy, whether there are particular red flags or amber flags you might say in a person's broad history. I don't think we've got there yet, but I actually think we will get there. I think we'll be surprised and we'll learn things about the biology of the disorder and about the pharmacology of these medicines, which must have subtle differences because we all see people who respond to one and don't respond to another, and you sort of scratch your head, but you're happy that it happens. Dr. Tesha Monteith: I agree with you, and I think the future is really bright for headache medicine and the potential of AI to move the needle. Peter, thank you again for joining us and sharing your insights. I really appreciate you being on. This is Tesha Monteith. Thank you for listening to The Neurology Minute.
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Understanding Rett Syndrome - Part 2
05/27/2026
Understanding Rett Syndrome - Part 2
In the second episode of a four-part series on Rett syndrome, Dr. Stacey Clardy discusses the importance of early referrals, particularly during the regression phase. 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. This is the second episode in a four-part series on Rett syndrome. Today, let's discuss when to refer and specifically early referral is absolutely critical in Rett syndrome, particularly during the regression phase. Any child, most often a girl with previously acquired developmental milestones who begins to lose language or lose purposeful hand use or develops stereotyped hand movements should prompt urgent neurologic evaluation. This would be referral to pediatric neurology, of course, and this should not wait for genetic confirmation. Early involvement of pediatric neurology allows for diagnostic clarification, anticipatory guidance, and coordination of care across systems. The genetic testing, typically with MECP2 sequencing and deletion or duplication analysis, this should be pursued early and if initial testing is negative but suspicion remains high, expanding that genetic evaluation is warranted. And beyond neurology, early engagement with developmental services, speech, occupational, and physical therapy should start before even a definitive diagnosis is necessarily established. Rett syndrome is a multi-system disorder. So a care team is going to monitor for common comorbidities. This is not just epilepsy, but also gastrointestinal dysfunction, breathing abnormalities, and orthopedic complications. When delayed referrals occur, it's often due to attribution of regression to more common developmental conditions. Be sure to listen to the other Neurology Minute episodes in this series. We'll be back next time for our third episode, and we'll cover treatment options and ongoing management.
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Lower Risk of Dementia with AS01-Adjuvanted Vaccination Against Shingles and Respiratory Syncytial Virus Infections
05/26/2026
Lower Risk of Dementia with AS01-Adjuvanted Vaccination Against Shingles and Respiratory Syncytial Virus Infections
Dr. Margarita Fedorova discusses whether a vaccine ingredient is quietly protecting the brain. Show citation: Taquet M, Todd JA, Harrison PJ. Lower risk of dementia with AS01-adjuvanted vaccination against shingles and respiratory syncytial virus infections. NPJ Vaccines. 2025;10(1):130. Published 2025 Jun 25. doi: Show transcript: Dr. Margarita Fedorova: Welcome to Neurology Minute. My name is Margarita Fedorova, and I'm a neurology resident at the Cleveland Clinic. Today we're exploring a study that raises a compelling question. Could a vaccine ingredient be quietly protecting the brain? A recent study by Taquet et al., published in npj Vaccines in 2025, investigated whether vaccination with an AS01-adjuvanted vaccine is associated with a lower risk of dementia. You might know it as the immune-boosting ingredient in Shingrix, the shingles vaccine, and Arexvy, the new RSV vaccine. We already know from prior work that the Shingrix vaccine was associated with a reduced risk of dementia, but the question this paper asks is why. Is it because preventing shingles itself protects the brain, or is there something specific about the adjuvant that's doing the work? To answer this, the researchers used a large US electronic health record database comparing over 35,000 people who received the AS01-adjuvanted RSV vaccine, over 100,000 who received the AS01-adjuvanted shingles vaccine and over 78,000 who received both. Each matched against individuals who got the seasonal flu vaccine instead. The findings were interesting. People who received the RSV vaccine had a 29% lower risk of new dementia diagnosis over the following 18 months. Those who received the shingles vaccine had an 18% increase in time without dementia, and those who received both had a 37% increase in dementia-free time. Here's a key insight. Both vaccines target completely different viruses, but both contain the same adjuvant. The fact that a similar protective signal was seen with both suggests the benefit may not be about which virus is prevented, and it may be about the AS01 itself. Why might an adjuvant protect the brain? AS01 contains two active components, monophosphoryl lipid A, known as MPL, and QS21. Together they activate macrophages and dendritic cells, triggering cascade that includes a production of interferon gamma. In animal models, stimulation of a receptor called toll-like receptor 4, which MPL activates, has been shown to reduce Alzheimer's-like pathology. The authors also point out that the protective effect appears within just a few months of vaccination, which is hard to explain purely by prevented infections and may point instead to a direct immunological mechanism. Very important caveat. This is an observational study, not a randomized trial, so we can't prove causation. There was also uncertainty about which brand of RSV vaccines some patients received, which could affect the strength of the AS01-specific conclusion. And with all of the dementia studies, it's unclear whether the vaccines prevent dementia or delay its onset. Though even a delay would be clinically meaningful given how few tools we have. What does this mean for clinical practice? For now, it doesn't change your vaccination recommendations. Both Shingrix and Arexvy already indicated in appropriate patients for the primary purposes, but it adds an intriguing possible benefit when counseling patients who ask about vaccines. And it opens the door to a genuinely exciting question. If AS01 has neuroprotective properties, could it be studied in a therapeutic target in its own right? That's the Neurology Minute for today. Keep exploring and we'll see you next time. If you want to read more, please find the paper by Maxime Taquet, et al., titled Lower Risk of Dementia with AS01-Adjuvanted Vaccination Against Shingles and Respiratory Syncytial Virus Infections, published in npj Vaccines in June 2025.
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Humoral Vaccine Responses and One-year Follow-up of Infants Potentially Exposed to Ocrelizumab During Pregnancy and Breastfeeding - Part 3
05/25/2026
Humoral Vaccine Responses and One-year Follow-up of Infants Potentially Exposed to Ocrelizumab During Pregnancy and Breastfeeding - Part 3
In the final episode of this series, Dr. Justin Abbatemarco and Dr. Ruth Dobson discuss navigating conversations with women and their families about potential ocrelizumab exposure during pregnancy and breastfeeding. Read more about this abstract on the . Show transcript: Dr. Justin Abbatemarco: Hello and welcome back. This is Justin Abbatemarco on our final episode with Ruth Dobson from Queen Mary University of London on our AAN annual meeting abstract humoral vaccine response and one year follow-up of infants potentially exposed to ocrelizumab during pregnancy and breastfeeding. Our previous two episodes, we've talked about this wider world of monoclonal antibodies during pregnancy and then we've talked about the data specifically around ocrelizumab. But Ruth, I think the million-dollar question is how do we approach this in clinical care? How can we talk to women and their families during this really exciting time and how do you employ this, especially within the MS space? Dr. Ruth Dobson: So it's a really exciting time for women in our families, but it can be really hard to talk about. And many of my patients have loads of anxieties about living with a chronic disease, thinking about pregnancy and breastfeeding, worrying about how to balance effective treatment against wanting not to cause any potential harm or risk to their child. A lot of this is actually about informed decision making and having those discussions and having the data to back up those discussions. What this data really helps us to do is have those discussions in a way that is meaningful for women so we can say, "Well, actually where you have received treatment up until the point of conception, we can see that babies are being born with normal B cell levels, that the drug is not causing long term effects to the best of our knowledge in your babies." And similarly, when people are thinking about restarting treatment postpartum, we know specifically in MS that the relapse risk is highest in those postpartum three months. So often people feel quite anxious about that and want to get on top of their disease, but don't want to forego breastfeeding for that. We are now in a situation where women no longer have to choose. We know that the drug doesn't get into breast milk. We can reassure them. Certainly in Europe, we've had a label change around CD20s now being safe for use in breastfeeding. So we can have that discussion and enable people to actually have that pregnancy and breastfeeding experience that they want to have without having to make compromises in the way that maybe people have previously. Dr. Justin Abbatemarco: I love that message because our messaging before was compromising. But now we can really have an informed discussion with patients and their families that MS does not define them and does not define their family planning needs. I love that idea about breastfeeding as well. I think that's a really anxious time. It's a really intimate moment that we as the medical community shouldn't dictate that we should allow that to be a time that the families get to choose on how they want to approach that. And so this data helps so much. Maybe we could just talk about that label change, how we could think about keeping up with our governing bodies and how they talk about these medications, because it's really challenging if a patient checks on the internet and sees something different from our FDA or other European governing bodies. How do you think through that? Dr. Ruth Dobson: Yeah, it's really hard and it creates lots of anxieties for patients. And I think even at the moment, the label washout is different across CD20 drugs. It's different between Europe and America. And that in itself causes anxiety. But in some ways that helps with those discussions to say, these labels, they're not always based in the kind of evidence that we need that's really helped us to recruit women studies to get people taking part in this research. And also in Europe, it shortened the washout period. These studies work in terms of changing that policy. I think that regulators are increasingly recognizing, certainly in Europe, class effects. They're increasingly recognizing the importance of including people considering pregnancy, lactating mothers in studies so that we can actually better answer these questions without having to wait eight, 10 years for these kind of data to come out before we can allow our patients to really partake in informed decision making. Dr. Justin Abbatemarco: And your work, work like it is so important for these conversations. So we'll hopefully have some really great discussions and be able to come back and have better conversations with patients because of it. So Ruth, thanks. Dr. Ruth Dobson: Thank you.
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Headache Medicine Highlights from the 2026 AAN Annual Meeting - Part 1
05/22/2026
Headache Medicine Highlights from the 2026 AAN Annual Meeting - Part 1
In the first part of this series, Dr. Tesha Monteith and Dr. Peter Goadsby discuss some major themes that emerged from the AAN Annual Meeting regarding headache medicine.
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Inflammation, Limbic White Matter, and Symptoms After Repetitive Head Impacts in Retired Football Players
05/21/2026
Inflammation, Limbic White Matter, and Symptoms After Repetitive Head Impacts in Retired Football Players
Dr. Alex Menze and Dr. Breton Asken discuss the long-term impacts of repetitive head impacts in football players, focusing on inflammation, brain microstructure, and cognitive decline. Show citation: Emanuel OM, Miner AE, Lee SY, et al. Inflammation, Limbic White Matter Microstructure, and Clinical Symptoms in Retired American Football Players With Repetitive Head Impacts. Neurology. 2026;106(6):e214646. doi:
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Understanding Rett Syndrome - Part 1
05/20/2026
Understanding Rett Syndrome - Part 1
In the first episode of a four-part series, Dr. Stacey Clardy discusses the diagnosis and clinical presentation of Rett syndrome.
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Humoral Vaccine Responses and One-year Follow-up of Infants Potentially Exposed to Ocrelizumab During Pregnancy and Breastfeeding - Part 2
05/19/2026
Humoral Vaccine Responses and One-year Follow-up of Infants Potentially Exposed to Ocrelizumab During Pregnancy and Breastfeeding - Part 2
In part two of this series, Dr. Justin Abbatemarco and Dr. Ruth Dobson discuss the main findings of this study. Read more about this abstract on the .
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Humoral Vaccine Responses and One-year Follow-up of Infants Potentially Exposed to Ocrelizumab During Pregnancy and Breastfeeding - Part 1
05/18/2026
Humoral Vaccine Responses and One-year Follow-up of Infants Potentially Exposed to Ocrelizumab During Pregnancy and Breastfeeding - Part 1
In part one of this series, Dr. Justin Abbatemarco and Dr. Ruth Dobson discuss current evidence on monoclonal antibodies in pregnancy and breastfeeding and prior understanding of CD20 therapies. Read more about this abstract on the .
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Updates Regarding Radiation Necrosis - Part 1
05/15/2026
Updates Regarding Radiation Necrosis - Part 1
Dr. Justin Abbatemarco and Dr. Kait Nevel discuss tips and tricks for managing radiation necrosis in hospitals and outpatient settings. Show transcript: Dr. Justin Abbatemarco: Hello, and welcome. This is Justin Abbatemarco, and I just finished interviewing Kate Neville about radiation necrosis following radiosurgery. Kait is a neuro-oncologist at Indiana University. Kait, maybe we could just start with what this entity looks like and some tips and tricks on how we can manage in that hospital or in the outpatient setting when we were picking this up. Dr. Kait Nevel: Yeah. Radiation necrosis can present in a variety of ways. People with radiation necrosis can be completely asymptomatic. In fact, most patients with radiation necrosis are asymptomatic. But symptoms can include things like headaches, seizures, and then focal neurologic deficits related to where the radiation necrosis is located. Imaging-wise, radiation necrosis typically looks like necrotic enhancing lesion as the name implies. Typically, we look at certain anatomical characteristics on standard MRI like vague enhancement along the edges, et cetera, but perfusion can be very helpful including cerebral blood volume, which is typically low in cases of radiation necrosis and high in cases of tumor progression. But this is a really big challenge in neuro-oncology, and differentiating radiographically between tumor and radiation injury. Dr. Justin Abbatemarco: I would encourage people to listen to podcast. We talked a little bit about medications, how to dose dexamethasone and others, and how we think through that. So please jump on and take a listen, and then join us back for the next Neurology Minute. We're going to talk about some evidence for supplement use in this disease. So Kait, thank you. Dr. Kait Nevel: Great. Thank you.
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Association of Changes in Activity Patterns With Brain Atrophy and Disability Progression in People With MS
05/14/2026
Association of Changes in Activity Patterns With Brain Atrophy and Disability Progression in People With MS
Dr. 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: 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.
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Clinical Heterogeneity and Candidate Biomarkers in POLG-Related Mitochondrial Disease - Part 2
05/13/2026
Clinical Heterogeneity and Candidate Biomarkers in POLG-Related Mitochondrial Disease - Part 2
In 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: 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.
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Workplace Lactation in Neurology: Barriers and Opportunities - Part 2
05/12/2026
Workplace Lactation in Neurology: Barriers and Opportunities - Part 2
In 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.
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May 2026 President Spotlight: AAN Annual Meeting Update
05/11/2026
May 2026 President Spotlight: AAN Annual Meeting Update
In 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 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.
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Clinical Heterogeneity and Candidate Biomarkers in POLG-Related Mitochondrial Disease - Part 1
05/08/2026
Clinical Heterogeneity and Candidate Biomarkers in POLG-Related Mitochondrial Disease - Part 1
In 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: 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.
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Workplace Lactation in Neurology: Barriers and Opportunities - Part 1
05/07/2026
Workplace Lactation in Neurology: Barriers and Opportunities - Part 1
In 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: 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.
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Maintenance Immunotherapy in MOGAD: Early Steroid Benefit, Dose Thresholds, and Disability Risk - Part 3
05/06/2026
Maintenance Immunotherapy in MOGAD: Early Steroid Benefit, Dose Thresholds, and Disability Risk - Part 3
In 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 . 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.
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Maintenance Immunotherapy in MOGAD: Early Steroid Benefit, Dose Thresholds, and Disability Risk - Part 2
05/05/2026
Maintenance Immunotherapy in MOGAD: Early Steroid Benefit, Dose Thresholds, and Disability Risk - Part 2
In 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 . 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.
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Epstein-Barr Virus Antibodies to Differentiate MS From Other Neuroinflammatory Diseases - Part 2
05/04/2026
Epstein-Barr Virus Antibodies to Differentiate MS From Other Neuroinflammatory Diseases - Part 2
In the second part of this series, Dr. Justin Abbatemarco and Dr. Paulus Rommer discuss how to apply these study results into clinical practice. Show citation: Vietzen H, Kühner LM, Berger SM, et al. Epstein-Barr Virus Antibodies to Differentiate Multiple Sclerosis From Other Neuroinflammatory Diseases. JAMA Neurol. Published online March 9, 2026. doi: 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.
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Clinical Reasoning Series: A 70-Year-Old Man With Systemic Illness Related Strokes Refractory to Medical Treatment Managed With Intracranial Stent
05/01/2026
Clinical Reasoning Series: A 70-Year-Old Man With Systemic Illness Related Strokes Refractory to Medical Treatment Managed With Intracranial Stent
Dr. 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:
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Epstein-Barr Virus Antibodies to Differentiate MS From Other Neuroinflammatory Diseases - Part 1
04/30/2026
Epstein-Barr Virus Antibodies to Differentiate MS From Other Neuroinflammatory Diseases - Part 1
In part one of this series, Dr. Justin Abbatemarco and Dr. Paulus Rommer discuss the relationship between Epstein-Barr virus and multiple sclerosis, as well as the questions that still remain unanswered. 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: Show transcript: Dr. Justin Abbatemarco: Hello and welcome. I just finished interviewing Paulus Rommer on his article published in JAMA Neurology, Epstein-Barr Virus Antibodies to Differentiate Multiple Sclerosis From Other Neuroinflammatory Diseases. Paulus, could we maybe talk about this relationship that we've understood about multiple sclerosis and Epstein-Barr virus? And maybe the points that still remain unanswered? Dr. Paulus Romme: There's a very long story behind this because in 1868, Pierre Marie, a student of Charcot was talking about that multiple sclerosis is a sequelae of an infection disorder. By this, we now know that there's a long story. There have been associations between infectious mononucleosis, EBV infection, multiple sclerosis. Also, the migration studies really fits very well in this. So there have been an association, but then, in 2022, there was the US Army study, Bjornevik and Ascherio, who really have shown that there is almost no multiple sclerosis without EBV infection. But still, we do not know why almost all of our patients have EBV infection, but only very small subset have multiple sclerosis. But this is very important to get a deeper understanding, but this is still unknown. Dr. Justin Abbatemarco: This story of EPV and multiple sclerosis continues to evolve. And your work, as we talked about on the podcast, has really helped inform that discussion as well. And we still need to understand, outside of the initiation of the disease, how it drives the pathophysiology years after that initial infection. But it's really helpful to understand this in the larger set and now maybe using it as a biomarker to help us with our other neuroinflammatory diseases, so we'll discuss that the next episode. Again, I was just speaking with Paulas Rommer on his article in JAMA Neurology, Epstein-Barr Virus Antibodies to Differentiate Multiple Sclerosis From Other Neuroinflammatory Diseases. Paulus, thank you.
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Maintenance Immunotherapy in MOGAD: Early Steroid Benefit, Dose Thresholds, and Disability Risk - Part 1
04/29/2026
Maintenance Immunotherapy in MOGAD: Early Steroid Benefit, Dose Thresholds, and Disability Risk - Part 1
In part one of this series, Dr. Justin Abbatemarco and Dr. Benjamin P. Trewin discuss the major findings from his work. Read more about this abstract on the .
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April 20, 2026 Capitol Hill Report: Neuroscience Research in FY2027
04/28/2026
April 20, 2026 Capitol Hill Report: Neuroscience Research in FY2027
In this episode, Dr. Jason Crowell discusses the Capitol Hill Report from April 20th, which provides updates on federal funding for neuroscience research in fiscal year 2027 (FY2027). Stay updated with what’s happening on the hill by visiting . Learn how you can get involved with .
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Navigating the Residency Application Process: Key Takeaways for Aspiring Neurologists
04/27/2026
Navigating the Residency Application Process: Key Takeaways for Aspiring Neurologists
Casey Kozak discusses the process of applying to neurology residency. This episode offers insights for applicants and for neurologists who guide and mentor the next generation of neurologists.
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