Podcasts about jama neurology

Most of us are familiar with the idea that you need to take 10 thousand steps per day to stay healthy but getting to this magic number is not that easy. The 10,000-step target first became popular in Japan in the 1960s. A clockmaker capitalising on people's new interest in fitness following the 1964 Tokyo Olympic Games made a pedometer with a name that, when written in Japanese characters, resembled a walking man and coincidentally translated as “10,000-steps metre.” A study of over 78,000 people in the UK between 2013 and 2015 using wearable trackers was published in the journals JAMA Internal Medicine and JAMA Neurology. Where did we get the number 10 thousand from? Does that mean that we do not need to take 10 steps? So how many steps should I be aiming for per day? In under 3 minutes, we answer your questions! To listen to the last episodes, you can click here: ⁠⁠⁠Can you eat eggs everyday?⁠⁠⁠ ⁠⁠⁠What is Lucky Girl syndrome, this new method that is all the rage on Tik Tok?⁠⁠⁠ ⁠⁠⁠Which type of wine is best for your health?⁠⁠⁠ A podcast written and realised by Amber Minogue. First broadcast: 19/1/2023 Learn more about your ad choices. Visit megaphone.fm/adchoices

When you quit drinking, you expect the hard part to be over, but sometimes, the brain finds a new outlet for the same addictive patterns. In this episode, Sara opens up about her personal experience with transfer addictions - how her addictive tendencies shifted from alcohol to food tracking, sugar, and weed, and what she learned about herself in the process. Through stories, science, and self-compassion, Sara breaks down: What transfer addiction (or cross-addiction) actually is Why our brains latch onto new sources of dopamine when we remove alcohol How dopamine depletion and reward substitution keep us chasing “the buzz” Why it's normal to experience new compulsions in early sobriety and how to move through them 7 powerful ways to heal the void and rebuild balance in recovery You'll also hear Sara share research-backed insights on dopamine regulation, neuroplasticity, and the incentive sensitization theory, explaining why we crave even when we no longer enjoy the thing we're craving. Whether your new obsession is sugar, scrolling, or staying “in control,” this episode reminds you that awareness is the first step toward freedom. 00:00 Introduction and Personal Journey 01:16 Understanding Transfer Addictions 03:36 Promoting the 30-Day Alcohol-Free Challenge 04:43 Realizing Transfer Addictions 07:40 Defining Transfer Addiction 10:40 The Science Behind Addiction 20:27 Recognizing and Managing Transfer Addictions 22:06 Practical Tools for Overcoming Addictions 26:02 Conclusion and Final Thoughts  

Send us Fan MailThis episode unpacks what "probable CTE" actually means — where the term comes from, what the science can and can't currently tell us, and why a single case (former Socceroos captain Paul Wade) has reignited debate about diagnosing a disease that's only ever been confirmed after death. It walks through the genuine case for and against using this label in living patients, and why the language we use around it matters.Note: This episode is for educational purposes only and is not medical advice or a diagnostic tool. While I've done my best to accurately interpret the cited journal articles, please read the original sources yourself for full context before drawing conclusions. 06:00 - Segment One: What Chronic Traumatic Encephalopathy Actually Is 09:45 - Segment Two: Why You Can't Diagnose It in the Living — Yet 12:00 - Segment Three: "Probable CTE" — Where the Term Actually Comes From 17:09 - Segment Four: Why This Topic Divides Even the Experts — The Dose-Response Problem 21:30 - Segment Five: The Case For Diagnosing Probable CTE in Living Patients 24:00 - Segment Six: The Case Against — Or At Least, the Case for Caution 29:27 - Segment Seven: Why the Words We Use Actually Matter 32:50 - Segment Eight: Where This Leaves Us  Episode — Reference List1. Martland, H.S. Punch drunk. Journal of the American Medical Association. 1928;91(15):1103–1107.2. McKee, A.C., Cairns, N.J., Dickson, D.W., et al. The first NINDS/NIBIB consensus meeting to define neuropathological criteria for the diagnosis of chronic traumatic encephalopathy. Acta Neuropathologica. 2016;131(1):75–86.3. Bieniek, K.F., Cairns, N.J., Crary, J.F., et al. The second NINDS/NIBIB consensus meeting to define neuropathological criteria for the diagnosis of chronic traumatic encephalopathy. Journal of Neuropathology & Experimental Neurology. 2021;80(3):210–219.4. Mez, J., Daneshvar, D.H., Kiernan, P.T., et al. Clinicopathological evaluation of chronic traumatic encephalopathy in players of American football. JAMA. 2017;318(4):360–370.5. Montenigro, P.H., Baugh, C.M., Daneshvar, D.H., et al. Clinical subtypes of chronic traumatic encephalopathy: literature review and proposed research diagnostic criteria for traumatic encephalopathy syndrome. Alzheimer's Research & Therapy. 2014;6(5):68.6. Cantu, R.C., Budson, A.E. Management of chronic traumatic encephalopathy. Expert Review of Neurotherapeutics. 2019;19(10):1015–1023.7. Katz, D.I., Bernick, C., Dodick, D.W., et al. National Institute of Neurological Disorders and Stroke consensus diagnostic criteria for traumatic encephalopathy syndrome. Neurology. 2021;96(18):848–863.8. Dickstein, D.L., Pullman, M.Y., Fernandez, C., et al. Cerebral [18F]T807/AV1451 retention pattern in clinically probable CTE resembles pathognomonic distribution of CTE tauopathy. Translational Psychiatry. 2016;6(9):e900.9. Arena, J.D., Stewart, W., Schneider, A.L.C., et al. Performance of traumatic encephalopathy syndrome criteria in identifying individuals with chronic traumatic encephalopathy. Nature Medicine. 2026;32:2037–2046.10. Iverson, G.L., Gardner, A.J. Risk for misdiagnosing chronic traumatic encephalopathy in men with anger control problems. Frontiers in Neurology. 2020;11:739.11. Iverson, G.L., Gardner, A.J. Risk of misdiagnosing chronic traumatic encephalopathy in men with depression. Journal of Neuropsychiatry and Clinical Neurosciences. 2020;32(2):139–146.12. Iverson, G.L., Gardner, A.J. Symptoms of traumatic encephalopathy syndrome are common in the United States general population. Brain Communications. 2021;3(1):fcab001.13. Grashow, R., Weisskopf, M.G., Baggish, A., et al. Premortem chronic traumatic encephalopathy diagnoses in professional football. Annals of Neurology. 2020;88(1):106–112.14. Eagle, S.R., et al. Interaction of medical conditions and football exposures associated with premortem chronic traumatic encephalopathy diagnosis in former professional American football players. Sports Medicine. 2024;54:743–752.15. Stewart, W., Buckland, M.E., McInnes, K., et al. Primum non nocere: a call for balance when reporting on CTE. Lancet Neurology. 2019;18(3):231–233.16. Hazrati, L-N., Schwab, N. Embracing the unknown in the diagnosis of traumatic encephalopathy syndrome. Neurology. 2021;96(18):835–836.17. McKee, A.C., et al. Chronic traumatic encephalopathy (CTE): criteria for neuropathological diagnosis and relationship to repetitive head impacts. Acta Neuropathologica. 2023;145(4):371–394.18. Atherton, K., Han, X., Chung, J., et al. Association of APOE genotypes and chronic traumatic encephalopathy. JAMA Neurology. 2022;79(8):787–796.19. SBS News. Former Socceroo becomes first Australian footballer to share probable CTE diagnosis. July 2026.20. beIN SPORTS. Former Socceroos captain reveals probable CTE diagnosis. July 22, 2026.21. The Washington Post. Ex-Socceroos captain Paul Wade says he has probable CTE, urges no heading for junior players. July 22, 2026.

Interview with Kelly G. Gwathmey, MD, author of Efficacy and Safety of Gefurulimab in Generalized Myasthenia Gravis: The PREVAIL Phase 3 Randomized Clinical Trial. Hosted by Cynthia E. Armand, MD. Related Content: Efficacy and Safety of Gefurulimab in Generalized Myasthenia Gravis Gefurulimab—The First Effective Nanobody in Myasthenia Gravis Therapy

Most of us are familiar with the idea that you need to take 10 thousand steps per day to stay healthy but getting to this magic number is not that easy. The 10,000-step target first became popular in Japan in the 1960s. A clockmaker capitalising on people's new interest in fitness following the 1964 Tokyo Olympic Games made a pedometer with a name that, when written in Japanese characters, resembled a walking man and coincidentally translated as “10,000-steps metre.” A study of over 78,000 people in the UK between 2013 and 2015 using wearable trackers was published in the journals JAMA Internal Medicine and JAMA Neurology. Where did we get the number 10 thousand from? Does that mean that we do not need to take 10 steps? So how many steps should I be aiming for per day? In under 3 minutes, we answer your questions! To listen to the last episodes, you can click here: ⁠⁠Can you eat eggs everyday?⁠⁠ ⁠⁠What is Lucky Girl syndrome, this new method that is all the rage on Tik Tok?⁠⁠ ⁠⁠Which type of wine is best for your health?⁠⁠ A podcast written and realised by Amber Minogue. First broadcast: 19/1/2023 Learn more about your ad choices. Visit megaphone.fm/adchoices

Intracerebral hemorrhage carries high morbidity and mortality, but growing evidence highlights meaningful opportunities for prevention, risk reduction, and long-term recovery. This episode covers key strategies, including blood pressure management, interpretation of neuroimaging markers, and individualized decisions around antithrombotic therapy. It also emphasizes the prolonged recovery timeline and the importance of a holistic, patient-centered approach to improving outcomes. In this episode, Casey S. Albin, MD, FAAN, speaks with Wendy C. Ziai, MD, and Vishank A. Shah, MD, coauthors of the article "Intracerebral Hemorrhage" in the Continuum® June 2026 Cerebrovascular Disease issue. Dr. Albin is a Continuum® Audio interviewer, associate editor of media engagement, and an assistant professor of neurology and neurosurgery at Emory University School of Medicine in Atlanta, Georgia. Dr. Ziai is a professor of neurology and critical care medicine at Johns Hopkins University School of Medicine in Baltimore, Maryland. Dr. Shah is an assistant professor of neurology and critical care medicine at Johns Hopkins University School of Medicine in Baltimore, Maryland. Additional Resources Read the article: Intracerebral Hemorrhage Subscribe to Continuum®: shop.lww.com/Continuum Earn CME (available only to AAN members): continpub.com/AudioCME Continuum® Aloud (verbatim audio-book style recordings of articles available only to Continuum® subscribers): continpub.com/Aloud More about the American Academy of Neurology: aan.com Social Media facebook.com/continuumcme @ContinuumAAN Host: @caseyalbin Guest: @VishankShah3 Full episode transcript available here Dr Albin: A patient has suffered an intracerebral hemorrhage. They're taken to the neuro ICU, and they fortunately survive. But the journey does not end there. In fact, in some ways, the journey has just begun. Join us today as we unpack holistic care for ICH patients.  Dr Jones: This is Dr. Lyell Jones, Editor-in-Chief of Continuum. Thank you for listening to Continuum Audio. Be sure to visit the links in the episode notes for information about earning CME, subscribing to the journal, and exclusive access to interviews not featured on the podcast.  Dr Albin: Hello to our audience. This is Dr. Casey Albin. Today, I'm interviewing Dr. Wendy Ziai and Dr. Vishank Shah about their article on intracerebral hemorrhage. This article appears in the April 2026 Continuum issue on cerebrovascular disease. Welcome to the podcast. I am so delighted that both of you are joining. To begin, let's just do a brief introduction of who you are and, and a little bit of how you got interested in the topic.  Dr Ziai: Hi, I'm Wendy Ziai. Thank you for having me on this podcast. I am a professor of neurology at Johns Hopkins. I am a neurointensivist, and I think I got primarily interested in this topic through clinical trials that I have been a part of since my fellowship days.  Dr Shah: Hi, everyone. I'm, uh, Vishank Shah. I am also, uh, very thankful for being invited to be a part of this podcast. I'm also a neurointensivist at Hopkins and the fellowship program director here for neurocritical care, and I'm interested in recovery after ICH, and that's why I'm a part of this work.  Dr Albin: Welcome to you both. It is such a treat for me to get to interview fellow neurointensivist, particularly those who have such a wealth of experience. So, I am delighted to dive into this. All right. So, to set the stage for our audience, intracerebral hemorrhage has long been approached with pessimism. But your article really highlights that there are meaningful advantages in prevention and risk stratification and long-term recovery for these patients. Though you both are neurointensivist, this article really emphasizes primary prevention and the holistic long-term care for the survivors. And so, to begin, Dr. Shah, can you just lay out a little bit for our listeners the scope of intracerebral hemorrhage and its community impact?  Dr Shah: Yeah. So, you know, ICH is the second most common type of stroke. There are more than three million new cases of ICH globally each year, and it accounts for thirty percent of all stroke types, but it is the one that has the highest mortality, with more than forty to fifty percent of the patients dying in the first thirty days, and then continued long-term impact on both functional as well as outcomes, as well as survivorship after the early period. And it also disproportionately impacts lower socioeconomic, and then minority races like Blacks, Asians, as well as Hispanic ethnicity. And so, there's a lot of work that needs to be done to reduce the burden of this disease.  Dr Albin: Absolutely. I mean, these can really be devastating for families, and I really am appreciative of your highlighting that there's a lot of disparities, and there's a lot of work to be done to really increase equity to these patients. I think a lot of this goes into really the AAN's focus on brain health and trying to improve some of what we're doing to maintain brain health. And I really wanted to kind of drill down on this because for ICH, there's a lot that can be done upfront as we think about how do we counsel patients who may walk into the office about strategies to prevent ever becoming an intracerebral hemorrhage patient. So, Dr. Shah, can you walk us through a little bit about what neurologists in the community need to be doing to make sure that no one ends up with us in the neurointensive care unit?  Dr Shah: Yeah, sure. So, I think, you know, one of the most important risk factors is, of course, hypertension and long-standing uncontrolled hypertension. And so really recognizing the need for early onset screening with regular blood pressure monitoring at a very early age, particularly in the races that I discussed earlier. And then I think another big part, obesity, metabolic syndrome, and type two diabetes. And I think there's a lot of interesting new work that with the GLP-1 agonist, you know, in a large multicenter cohort studies showing that patients receiving these had a significantly lower reduction risk of ICH. And so, this might be a really important part that, you know, clinicians need to start increasingly recognizing and using in their practice. And then, of course, other risk factors that are common include smoking, diet high in sodium, exposure to air pollution, both indoor as well as outdoor. And so, mitigating all of these risk factors can also reduce the burden of ICH.  Dr Albin: Absolutely. And I really want to highlight that hypertension plays such an important role and that we as neurointensivist, as community neurologists, really need to be creative about ways that we can help people meet those blood pressure target and meeting people in the community where they are, making sure that they're not suffering from side effects from their medication that would prevent them from sticking with it long term. Dr. Ziai, anything else to add about what we can do in the community?  Dr Ziai: So, we really want to emphasize, even in the acute phase, that patients moving forward need to have targeted interventions to reduce blood pressure, smoking, enhance their physical activity, have a diet that is high in fruits and vegetables and low in alcohol and salt, and then promoting weight loss, of course.  Dr Albin: And Dr. Ziai, I'm gonna ask you a little bit about one of the things that maybe not all of our listeners have heard about is this APOE2, APOE4 genetic risk for intracerebral hemorrhage. What's going on there and, and should clinicians be testing for that? Dr Ziai: That's a great question, and it is not one that we currently test people for at least acute ICH presentation. APOE2 and A4- E4 alleles, these give patients a two to three times higher risk of ICH by increasing cerebral amyloid deposition. And if you happen to have APOE2 carrier ship status, then along with other risk factors like white matter disease and vascular risk factors, these predict the onset of new microbleeds even during very short follow-up periods of about two years. And as we know, having cerebral microbleeds are associated with an increased risk of all strokes, ischemic and ICH, but they are one of many MRI markers of small vessel disease, which along with cortical superficial siderosis, does significantly increase future ICH risk. And so even in people who've never had an ICH, if they happen to have an MRI, it may be reasonable to look at the MRI and incorporate this burden of small vessel disease, and especially these hemorrhagic markers into, uh, decision-making about interventions.  Dr Albin: That's a really excellent point. And so, I think that your article did a really beautiful job of thinking holistically about the patient, incorporating clinical markers of their risk for having ICH, but also those radiographic markers. I'm just gonna ask you to summarize those again one more time because not everyone will be familiar with these. So, when you're looking at an MRI, what are the things that you're particularly clued in on that would increase the patient's risk of future ICH?  Dr Ziai: In the past, what we're looking for really is markers of cerebral amyloid angiopathy, which significantly increase a person's risk for lobar hemorrhage in particular. And so, we have a set of criteria called the Boston Criteria, and there's a new version of these, version 2.0. And these, um, incorporate a number of imaging markers that provide a very high sensitivity and specificity to diagnose CAA after an ICH. But even if someone's never had an ICH, and they evaluate that risk-benefit ratio for different cardiovascular prevention strategies. And so, the markers that we're specifically interested in are, of course, microbleeds. But not just having microbleeds, but are they lobar or are they deep? Lobar having a higher risk for lobar ICH. How many microbleeds are there? Is it greater than five, or is it just one or two? Also, cortical superficial siderosis is a marker, a hemorrhagic marker, that does portend a significant increased risk of recurrent ICH, along with having a lobar ICH. And now we have these new markers, which are the white matter hyperintensity multi spot pattern, which requires these hyperintensities on flare imaging in the subcortical area, having greater than at least ten of these multi spots, and also having enlarged perivascular spaces in the centrum semiovale, and having at least twenty of those. And finally, white matter hyperintensities, which can be measured with the physica score or just by visualizing them. We can look at white matter hyperintensities as well as being a measure of small vessel disease.  Dr Albin: Got it. And so just to summarize, we're looking for small vessel disease markers because that puts our patients at higher risk of ongoing future bleeds. And then we're also looking for markers of particularly small vessel disease that's caused by cerebral amyloid angiopathy, which again, because it's having that protein deposition, that puts the patient at risk of those leptomeningeal very small vessels, putting the patient at risk of lobar ICH. Just confirming I've summarized this all correctly.  Dr Ziai: Yes. That was perfect.  Dr Albin: Amazing. Dr. Shah, I'm gonna go back to you. Let's say we have a patient. Let's say this is a sixty-five-year-old man who comes in and they want follow-up and they're... And you're trying to think about they've had an ICH in the past, and they are also at risk for ischemic disease. Let's say they, they have hypertension, they've had a smoking history. They have some risk for ischemic events. And you're trying to think about how do you balance those. Let's say the patient needs to be on aspirin but does have some of those high-risk features on their MRI. Is there any guidance on how we think through preventing them from having a recurrent bleed if they're a high-risk patient, also preventing them from having an ischemic event, which they might be at high risk for as well?  Dr Shah: Yes. So, I think, you know, the first step is of course trying to understand what was the type of bleed. I think that has a very important role, like you mentioned. If it's a lobar hemorrhage versus a deep hemorrhage, the risk of recurrent ICH and ischemic events is very variable. So lobar hemorrhages, there's obviously a higher risk of recurrent hemorrhage events, whereas deep hemorrhage is actually at or behaves sort of like small vessel ischemic strokes and have a higher risk of recurrent arterial ischemic events. So that distinction in itself can help you gauge which patients would be safe and would benefit from these therapies. To begin, and of course, looking for some of these markers on MRI that were mentioned by Dr. Ziai for recurrence of hemorrhage risk. In terms of antiplatelet, the, there is a lot more data now to guide treatment, and we have the RESTART as well as the ESTART trial that showed that starting an, a single antiplatelet after intracerebral hemorrhage did not increase the risk of hemorrhage recurrence. They were very variable in the timing when aspirin was started, and so that remains still a question about what is the safest time point to start aspirin. For example, in the ESTART trial, they started them very early, within the first three days, whereas in  the RESTART it was all the way up to two months after the hemorrhage. And so... But in general, the risk of recurrent ICH was very low with a single antiplatelet agent. And so, if it's needed for ischemic prevention, it's relatively safe broadly across all types of hemorrhages.  Dr Ziai: Yeah. I would just mention that there was also a subgroup analysis of the RESTART trial using MRI. And so, this more than likely included patients with CAA, since 40% of the hemorrhages were lobar in that study, and therefore seeing that there was no increased risk of recurrent ICH in RESTART, it is thought that putting patients back on their antiplatelet therapy is safe.  Dr Albin: That's a really huge takeaway pearl for our listeners, that regardless of whether it's a lobar bleed or a deep bleed, if there is a strong indication, you know, this is not just, oh, because someone gave them aspirin 81, but truly that there is a reason that they need to be on a single antiplatelet agent, it probably benefits them to be on that agent, and there's good data that there's not a huge increase in risk. Summarizing all of that?  Dr Ziai: Great.  Dr Albin: Now, things are gonna get a little bit tricky here, because what if the patient, what if they need to be on dual antiplatelet therapy? Or what if they need to be on anticoagulation? Dr. Ziai, I'll, I'll throw that to you. How do you tackle that patient population?  Dr Ziai: Yeah, the safety of dual antiplatelet therapy hasn't really been studied in patients who've had a prior ICH. Although, in people who've had previous strokes, putting them on dual antiplatelets doesn't seem to increase the risk of ICH, but it does increase extracranial hemorrhage. And so there may be other reasons not to put patients on dual antiplatelet agents. Patients who have cancer and also cardiovascular or cerebrovascular disease, putting them on dual antiplatelet therapy does seem to increase the risk for intracranial hemorrhage. So, I think there is enough of a bias against DAPT therapy in patients who have had an ICH that we would not recommend DAPT for patients with a prior ICH.  Dr Albin: Absolutely. And, and then what about, let's say they have atrial fibrillation, and you know that they have a high CHA2DS2-VASc score, and they are at very high risk of ischemic events, but they've also had a prior intracerebral hemorrhage. Walk us through a little bit, how should we approach that patient? Dr. Ziai, I'm gonna start with you again.  Dr Ziai: Sure. So again, looking at the MRI, which all patients with ICH should have nowadays. If patients do have these hemorrhagic findings, a lobar ICH, evidence of CSS, cortical superficial siderosis, especially if it's disseminated, and also lobar microbleeds, especially if there are greater than five, if they're multiple, then anticoagulation should really be avoided in those patients.  Dr Albin: Absolutely. So, I'm really hearing that when we have a patient with ICH, it is just critically important that we understand is this a hypertensive bleed or is this a lobar bleed that is probably related to cerebral amyloid angiopathy? And getting to that distinction is going to play a major role in our deciding whether or not the patient can be on DAPT or can be on anticoagulation. And then what are some of the strategies for patients that you're referring them to if they really cannot tolerate being on anticoagulation, but they have atrial fibrillation, and they do need some sort of ischemic stroke prevention?  Dr Shah: There's still a lot of controversy, even in non-lobar hemorrhages, about resuming anticoagulation and when that would be safe. HAF trial, there was a reduction in ischemic stroke recurrence, uh, but a significantly higher increase in hemorrhage recurrences. I think that trial included both deep and lobar hemorrhages. So, we still need more data, and I think the ASPIRE trial and maybe a meta-analysis would answer that eventually. But in the meantime, if a, specifically for lobar hemorrhages, which are, uh, thought to be CAA related, if they, uh, and the patient has AFib, you know, where anticoagulation would be contraindicated, a watchman device or, you know, AFib ablation may be some of the other strategies that can be looked into for those patients specifically.  Dr Albin: Right. I think that's a really important point to emphasize, that we don't just don't give up and say, "Oh, you're not a candidate for anticoagulation," but we really reach out to our cardiovascular friends and say, "Hey, what other procedures can you offer that will minimize the risk of recurrence?" You know, we don't want them to have an ischemic event, but we also know long-term that there would be a real risk of anticoagulation. Just reminder to our listeners that there are new procedures, and our cardiology colleagues are always doing new trials and new devices, and so we should really leverage their expertise here. I am in the final minutes gonna just switch gears a little bit from talking about sort of the nitty-gritty of secondary ischemic prevention and secondary hemorrhagic stroke prevention and thinking about there has been this degree of pessimism around ICH patients, and that, you know, they have a much more severe outcome than our patients with ischemic strokes. I think that that is probably a myth that we need to do some debunking around, and I think maybe we need to reframe in terms of thinking about just the trajectory. So, Dr. Shah, walk us through a little bit about what we can expect about the recovery trajectory in ICH compared to those patients who have an ischemic stroke. Dr Shah: Yes. From some newer data and studies, it is becoming clear that recovery after ICH is much slower than we expect. In general, for ischemic stroke, recovery is measured within the first few weeks to up to 90 days. But in ICH, we now know that patients can keep recovering all the way up to six months and even beyond. In general, from just a, a study of heart recovery that occurs after ischemic stroke, there's a steep recovery in the first seven days, and then sort of after that, patients still continue to recover, but it, it starts plateauing where up to 90 days. Whereas with ICH, there is not much recovery in the first 7 to 30 days, but after that, there is a recovery that occurs significantly between day 30 and day 180, and then some patients continue to recover all the way up to one year. The more severe the hemorrhage, the slower the recovery, but there's still some evidence to suggest that even severe hemorrhage patients can recover all the way up to one year out and beyond. This is, of course, in terms of functional recovery.  Dr Albin: I think that's a really important point for our audience. Many of the listeners are residents, they're fellows, they're seeing these patients in the hospital, and they may not see a whole lot of improvement over even 30 days. But to keep in mind that just because the patient has not had a dramatic recovery within that first month that they may be in the ICU and then on the floor does not mean that that patient will never have recovery, and that we reset our expectations that recovery is possible, it's just gonna be slower. And I think that that's not only important for the healthcare team to take in mind, but also for patients and their families to know there is hope here. It's just gonna be slower. Dr. Ziai, looking ahead, what developments in this are you most excited about that you think will move the needle for care for the long-term outcomes and the prevention for these patients? What's ahead in, in ICH?  Dr Ziai: Yeah, I think the research that's going on is very exciting at the moment. We just saw the presentation at the World Stroke Organization conference in the fall of the TRIDENT trial, Triple therapy prevention of Recurrent intracerebral Disease events, meaning strokes. And these investigators found that a single pill, a fixed dose of three blood pressure-lowering agents actually was successful in significantly reducing the risk of recurrent stroke in patients who have had a history of ICH and have just normal or low-grade hypertension. So rather than having patients on multiple antihypertensive agents, it may be possible to have them on a single pill, and may dramatically reduce their stroke risk. So that's exciting. There is also a trial ongoing, ASPIRING, testing whether antiplatelet monotherapy after 24 hours only can reduce the risk of all serious vascular events in ICH survivors. So very early antiplatelets. The SATURN trial, we didn't talk about statins yet, but it is comparing continuation versus discontinuation of statin therapy in ICH patients. And then we have ongoing epidemiological studies that are really needed to understand this interaction between the cardiovascular prevention strategies, the antithrombotic use, the blood pressure targets, and these high-risk neuroimaging markers for ICH. And I think that's gonna be key, personalizing the interventions for these patients.  Dr Albin: So, I love that. And what I'm hearing is that it's really important to think about the personalized approach as well as how do we simplify things. We know that blood pressure control is critically important to the primary and secondary prevention of ICH, but we have to make it easy for patients to do so. Dr. Shah, I want to end with kind of understanding, you know, this was an unusual topic for neurointensivists to talk about. This was really about prevention. It was about long-term survivorship. It was about not what's happening in the neuro ICU. How did you guys get interested in sort of that aspect of care?  Dr Shah: Yeah, so that's a great question. Dr. Ziai has been my mentor since I was in fellowship, so now about eight years that I've been working with her, and this was a project that I started in fellowship with under her mentorship, looking at long-term recovery in ICH patients, and specifically severe patients. Happy that work has received a lot of recognition. It was published in JAMA Neurology. We looked at patients with severe intracerebral and intraventricular hemorrhage, those that survived with an mRS of four and five at day 30, and what happened to them over the course of the year. There was really not much data on recovery after ICH. And we were very surprised to see that up to 40% of patients that were an mRS of four and five, so really, really severely disabled at day 30, recovered to an mRS of zero to three by one year. About one-third of that group that recovered actually achieved functional independence with an mRS of zero to two, which was very surprising, really breaking the myths around the pessimism with ICH. We found that a lot of the baseline comorbidities like diabetes, white matter disease, as well as what happens to them during the acute hospitalization, were adding all of that information to the severity of the hemorrhage significantly improved our ability to predict long-term recovery after ICH. And so that's kind of how we got interested in this work, looking at how factors in the care that we provide in the ICU, as well as what the patients come in with, how all of that could be modified to promote recovery in these patients that are often been forgotten.  Dr Albin: I think that there's one takeaway to our listeners is that this is really a place where there's a lot of hope for recovery, and that the nihilism that has really surrounded ICH is a thing of the past, and we have to move forward with thinking about how do we proactively impact the recovery and counsel the patients and give them hope. Because just as your research shows, there really is the ability that they can attain that functional independence, which is absolutely astounding. It's really amazing. Again, today I've been interviewing Dr. Wendy Ziai and Dr. Vishank Shah about their article on intracerebral hemorrhage. This article appears in the April 2026 Continuum issue on cerebrovascular disease. Please be sure to check out Continuum Audio episodes from this and other issues. Please go and check out. They have a wonderful article with lots of tables and figures, so much data. And again, thank you to our listeners for joining us today. Thank you, Dr. Ziai and Dr. Shah.  Dr Ziai: Thanks very much.  Dr Shah: Thank you.   Dr Monteith: This is Dr. Teshamae Monteith, Associate Editor of Continuum Audio. If you've enjoyed this episode, you'll love the journal, which is full of in-depth and clinically relevant information important for neurology practitioners. Use the link in the episode notes to learn more and subscribe. AAN members, you can get CME for listening to this interview by completing the evaluation at continpub.com/audioCME. Thank you for listening to Continuum Audio.

Welcome to MS Research Briefs, a new ECTRIMS podcast series delivering an expert guided tour of important new studies in multiple sclerosis research. In each episode, leading MS experts will take a small number of recently published studies and go beyond the headline findings – exploring what the research shows and how it may influence clinical practice and future discovery. In this inaugural episode, Prof. Alan Thompson and Prof. Olga Ciccarelli discuss two studies exploring how advanced MRI biomarkers and machine learning may transform the diagnosis and prognosis of multiple sclerosis. Featured Publications Paramagnetic Rim Lesions and Development of Clinical MS in Radiologically Isolated Syndrome.JAMA Neurology. 2026;83(3):250–258. Machine learning-based combination of the central vein sign, cortical lesions and paramagnetic rim lesions: a web-based tool for the diagnosis of multiple sclerosis.Brain Communications. 2026;8(2):fcag079. Discussed in this episode Can paramagnetic rim lesions identify individuals with radiologically isolated syndrome (RIS) who are most likely to develop clinical MS? Why do paramagnetic rim lesions appear to be stronger prognostic biomarkers while the central vein sign remains a powerful diagnostic biomarker? Can machine learning models combining MRI biomarkers outperform traditional dissemination-in-space criteria? What role might advanced MRI biomarkers play in future diagnostic criteria and treatment decisions? How close are we to AI-supported diagnosis and automated biomarker detection in routine clinical practice? As advanced MRI biomarkers move from research tools towards clinically meaningful decision-making, this episode explores one of the most important developments in contemporary MS research.

Interview with Joseph T. Colonel, PhD, author Acoustic Analysis of Primary Care Patient–Clinician Conversations to Screen for Cognitive Impairment. Hosted by Cynthia E. Armand, MD. Related Content: Acoustic Analysis of Primary Care Patient–Clinician Conversations to Screen for Cognitive Impairment

In this episode of the NCS Podcast Hot Topics series, host Eric Lawson, MD, is joined by Adam Arthur, MD, neurosurgeon at the University of Tennessee and Semmes Murphey Clinic in Memphis, Tennessee, to discuss the article "Minimally Invasive Surgery Versus Medical Management Alone for Intracerebral Hemorrhage: The MIND Clinical Trial," published in JAMA Neurology. Their conversation explores the MIND trial's evaluation of minimally invasive hematoma evacuation compared with best medical management for patients with intracerebral hemorrhage. Dr. Arthur reviews the trial's design, primary outcomes and early termination, and explains how findings from the ENRICH trial influenced enrollment and feasibility considerations. He also explores key considerations such as the importance of hematoma location, evacuation thresholds and timing, while reflecting on what the trial's negative primary outcome may still reveal about the future of surgical intervention and more individualized approaches for ICH patients. The views expressed on the NCS Podcast are solely those of the hosts and guests and do not necessarily reflect the opinions or official positions of the Neurocritical Care Society. 

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

Interview with Alessandra Fanciulli, MD, PhD, and Eduardo de Pablo-Fernández, MD, PhD, authors of Phenoconversion in Pure Autonomic Failure: A Systematic Review and Meta-Analysis. Hosted by Cynthia E. Armand, MD. Related Content: Phenoconversion in Pure Autonomic Failure Pure Autonomic Failure and Central Synucleinopathy Risk

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:10.1001/jamaneurol.2026.0240  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. 

Dr. Justin Abbatemarco talks with Dr. Paulus Rommer about the evolving understanding of Epstein-Barr virus (EBV) and its role in multiple sclerosis (MS), including recent research on EBV antibodies as diagnostic markers and potential therapeutic targets.  Read the related article in JAMA Neurology.  Disclosures can be found at Neurology.org. 

Interview with Susan M. Landau, PhD, author of Brain Imaging Biomarkers and Cognitive Outcomes in a Multidomain Lifestyle Intervention: The POINTER Imaging Ancillary Study. Hosted by Cynthia E. Armand, MD. Related Content: Brain Imaging Biomarkers and Cognitive Outcomes in a Multidomain Lifestyle Intervention

Host Dr. Erica Bostick from the University of Rochester Medical Center Division of Adolescent Medicine chats with Dr. Stacy Sun, a double board-certified physician in obstetrics and gynecology and complex family planning at the University of Rochester, about misconceptions they hear from patients about contraception. Should patients get their hormone levels checked before starting a birth control method? What is emergency contraception and how does it work? Is it safe to use contraception to suppress the menstrual cycle? What do recent studies show about the Depo-Provera shot and the risk of meningioma? Listen to this episode to hear all about these common questions and more, and to get real examples of counseling tips from Dr. Bostick and Dr. Sun! Related Content:  CEI Line: 1-866-637-2342 https://ceitraining.org/ www.hivguidelines.org Curtis KM, Nguyen AT, Tepper NK, et al. U.S. Selected Practice Recommendations for Contraceptive Use, 2024. MMWR Recomm Rep 2024;73(No. RR-3):1–77. DOI: http://dx.doi.org/10.15585/mmwr.rr7303a1 Nguyen AT, Curtis KM, Tepper NK, et al. U.S. Medical Eligibility Criteria for Contraceptive Use, 2024. MMWR Recomm Rep 2024;73(No. RR-4):1–126. DOI: http://dx.doi.org/10.15585/mmwr.rr7304a1 Xiao T, Kumar P, Lobbous M, Yogi-Morren D, Soni P, Recinos PF, Kshettry VR. Depot Medroxyprogesterone Acetate and Risk of Meningioma in the US. JAMA Neurology. 2025;82(11):1094-1102. doi:10.1001/jamaneurol.2025.3011. Roland N, Neumann A, Hoisnard L, Duranteau L, Froelich S, Zureik M, Weill A. Use of progestogens and the risk of intracranial meningioma: national case-control study. BMJ. 2024;384:e078078. doi:10.1136/bmj-2023-078078

Interview with Hannes Vietzen, PhD, author of Epstein-Barr Virus Antibodies to Differentiate Multiple Sclerosis From Other Neuroinflammatory Diseases. Hosted by Cynthia E. Armand, MD. Related Content: Epstein-Barr Virus Antibodies to Differentiate Multiple Sclerosis From Other Neuroinflammatory Diseases

In this episode of PEM Currents: The Pediatric Emergency Medicine Podcast, we take a structured, evidence-based approach to the acute treatment of migraine in children and adolescents. From confirming the diagnosis and screening for concerning features to optimizing outpatient therapy and executing a protocolized emergency department strategy, this episode walks through what works. We review the role of NSAIDs and triptans, clarify how IV fluids and ketorolac fit into care, and provide a stepwise framework for dopamine antagonists, valproate bridge therapy, DHE protocols, steroids, discharge planning, and admission decisions. Practical dosing, reassessment timing, and family-centered communication strategies are emphasized throughout. Learning Objectives Recognize the clinical features of pediatric migraine and distinguish it from secondary causes of headache. Implement a stepwise, evidence-based emergency department approach to acute pediatric migraine, including appropriate medication selection and timing of reassessment. Develop safe discharge and follow-up plans by defining treatment endpoints, minimizing medication overuse, and identifying patients who require referral or inpatient management. References 1. Oskoui M, Pringsheim T, Holler-Managan Y, et al. Practice Guideline Update Summary: Acute Treatment of Migraine in Children and Adolescents: Report of the Guideline Development, Dissemination, and Implementation Subcommittee of the American Academy of Neurology and the American Headache Society. Neurology. 2019;93(11):487-499. doi:10.1212/WNL.0000000000008095. 2. Patterson-Gentile C, Szperka CL. The Changing Landscape of Pediatric Migraine Therapy: A Review. JAMA Neurology. 2018;75(7):881-887. doi:10.1001/jamaneurol.2018.0046. 3. Bachur RG, Monuteaux MC, Neuman MI. A Comparison of Acute Treatment Regimens for Migraine in the Emergency Department. Pediatrics. 2015;135(2):232-238. doi:10.1542/peds.2014-2432. 4. Ashina M. Migraine. The New England Journal of Medicine. 2020;383(19):1866-1876. doi:10.1056/NEJMra1915327. 5. Richer L, Billinghurst L, Linsdell MA, et al. Drugs for the Acute Treatment of Migraine in Children and Adolescents. The Cochrane Database of Systematic Reviews. 2016;4:CD005220. doi:10.1002/14651858.CD005220.pub2. Transcript This transcript was generated using Descript automated transcription software and has been reviewed and edited for accuracy by the episode's author. Edits were limited to correcting names, titles, medical terminology, and transcription errors. The content reflects the original spoken audio and was not substantively altered. And today we're gonna talk about the acute treatment of migraine headache in children and adolescents. This is bread and butter for the PED, requires precise diagnosis and evidence-based treatment. We're gonna talk about making that diagnosis, red flags, outpatient and ED treatment, as well as some second-line agents, admission decisions, and a whole lot more. So migraine in children is defined by three criteria, and at least five attacks lasting two to 72 hours. So you gotta have at least two of the following: pulsating or throbbing quality, moderate to severe intensity, aggravation by routine activity, and a unilateral location. Although in children, it's often bilateral, plus at least one of nausea or vomiting and photophobia and/or phonophobia. In children headaches are frequently bilateral, bifrontal, bitemporal. The duration might be shorter than adults, especially in kids under second or third grade. And you may have to infer whether or not they have photophobia from their behavior. Like does the child close their eyes or wanna go into a dark room? In the emergency department, we're often diagnosing based on pattern recognition plus exclusion of dangerous secondary causes. Or even more often than that, the patient comes in and says, I've got a migraine. Before I move on to treatments, let's talk about some red flags where you might wanna pause and not just jump to migraine therapy. And the mnemonic SNOOP can be helpful here. And it stands for S for systemic symptoms such as fevers, myalgia, weight loss, or another S, secondary risk factors such as an immune deficiency, cancer, pregnancy, N for neurologic signs, papilledema, focal deficit, confusion, seizures. O onset sudden, or thunderclap. Migraines are often a little more gradual than that. The other O is older age, or technically younger age too, younger than five years or older than 50. Hopefully those patients are not coming into the pediatric emergency department. And then pattern changes, these new symptoms in a previously stable pattern. Don't ignore that. And precipitants, you know, is it worse with Valsalva, position change, or under significant exertion? If these signs are present, you'll probably wanna take a pause and just not throw migraine treatment at the patient. If they're stable, MRI is the preferred imaging modality, but a very sick patient, it'd be okay to get a head CT. If you've got a normal neurologic exam, there's no red flags. Again, you don't need routine imaging for migraine headaches. So let's talk about treatment. So hopefully patients have actually started to treat their headache before they arrive in the emergency department. If they haven't, it's a good idea to have some triage protocols in place. So ibuprofen, 7.5 to 10 milligrams per kilogram, 10 milligrams per kilogram is superior to placebo and it's superior to acetaminophen at two hours. So that's what we would use. Early treatment's critical. So ideally within the first hour of onset. So that's why triage protocols help. We'll give kids 10 mg per kg of ibuprofen and like 30 ounces of Gatorade. Blue is often the first Gatorade choice, though that's not an evidence-based statement. You can also use naproxen, but most of the studies are on ibuprofen. If NSAIDs fail, many adolescents and some older children will be prescribed triptans. The best evidence currently supports sumatriptan plus naproxen or zolmitriptan nasal spray. Rizatriptan is FDA approved down to age six. Adolescents respond to these agents better than younger children, and the route matters. The nasal formulations help when nausea is prominent. Families should be counseled to treat early, use weight-appropriate dosing, and avoid using acute medications more than 10 days per month. Often patients will have already taken an NSAID and a triptan before they get to the ED, and that's where we get into the treatment of refractory migraine. Now this is most of the patients that I will see, and before we push medications, let's briefly review ED treatment goals. You either want the patient headache free. Back to their baseline or mild descending pain. So a pain score of one to three. If you don't reach one of those endpoints and it's not agreed upon with the patient and their family, you've not completed treatments. You should do a reassessment within one hour after each intervention. And let's face it, if you're not reassessing within an hour and defining treatment goals, you're not practicing protocolized migraine care. So in the emergency department, many of you may be familiar with the migraine cocktail. So what is that? In general, it's a dopaminergic agent such as prochlorperazine or metoclopramide plus ketorolac, plus IV fluids. Let's take a look at all three of those components and see if you can guess which one is actually the one that can abort the migraine. So fluids are commonly given in pediatric migraine, but they alone do not treat it. They're helpful. Many patients have been throwing up or a bit dehydrated, but there are small randomized trials that show essentially no meaningful pain reduction in patients that get IV fluids alone. Well, what about ketorolac? Toradol, like that's the first thing you give to a kid with a kidney stone, right? It does help, but it's really adjunctive. So the main first-line agents for refractory or status migrainosus in the emergency department are the dopamine antagonists, and the first-line treatment for most patients is prochlorperazine or Compazine. The dose is 0.15 milligram per kilogram IV. The max is 10 milligrams. This is the backbone of ED migraine care. And why do they work? Well, migraines aren't just some random vascular headache. This is an inherited disorder with central pain pathways gone awry. Dopamine plays a large role in that pain, nausea, hypersensitivity, amplification of symptoms and more that, frankly, I won't get into this podcast because molecules hurt my head. The dopamine antagonists treat the headache, they reduce the nausea, and they just tamp down this process. Overall, the response rates approach 85%. Some studies have suggested that the response rate is about 77% at an hour and 90% at three hours. If you add the ketorolac and IV fluids, you get your response rate up to about 93 to 94%. These agents really do work well together. There have been randomized trials comparing IV prochlorperazine versus ketorolac. 85% of prochlorperazine patients achieved headache relief versus only 55% of ketorolac patients. So ketorolac helps, but really it's the prochlorperazine. Metoclopramide, or Reglan, is used in a lot of centers as well. There are some smaller studies in children and adolescents that show that prochlorperazine is more effective, but if kids have an adverse reaction, more on that in a moment, or they prefer metoclopramide because they've responded to it in the past, it's okay to go with it as well. Right. So what does it actually look like when you give the migraine cocktail to a patient? I think it's important to explain to patients and families what to expect, and if this is a teenager, I'm talking to them directly. I mean, they're getting the medication first and foremost. I tell them that the most effective way to treat their headache is with an IV. This often causes lots of angst, even in older teenagers. The medication just does not get to the brain as effectively and fast enough if you take it by mouth. Many patients who get the dopaminergic agents, so prochlorperazine, will invariably feel jittery or anxious or like they gotta move or like they got ants in their pants. I tell them to expect this so they're not surprised and worried when it happens. I tell them that once they start feeling that way, it means the medicine is probably working. They need to hit the nurse button and we're gonna get them up and have them take a walk. This fixes it for the majority of patients just getting up and moving. In adult centers, even with the initial administration of the prochlorperazine or as sort of a reflexive response to any of those symptoms, they just give a slug of IV Benadryl. There's some studies in adolescents especially that this may decrease the effectiveness of the IV agents you're giving in the first place, and it may also increase return rates to the ED. So I will use IV diphenhydramine if getting up and moving around isn't working, or if the distress is significant, or if the patient clearly indicates they've needed it in the past. So if after the migraine cocktail, the patient has met their pain goals and the reassessment is favorable, they can go home to outpatient follow-up. How about if the headache got better, but not all the way? It's usually when the initial migraine cocktail didn't achieve the pain endpoints fully, like it helped partially. If the dopamine blockade didn't do anything, valproate is unlikely to rescue the case. And so valproate works on GABA and it stabilizes some of these pain processes, but the dopaminergic agent needs to have done something first for valproate to work. Per the most common protocol, you give an initial dose of IV valproate, then you discharge the patient home on Depakote ER. So oral valproic acid under 10 years old or under 50 kilograms, 250 milligrams PO twice a day for two weeks, or older than 10 or greater than 50 kilos, 500 milligrams twice a day for two weeks. This is the extended release and it's most helpful if you give the first oral dose in the emergency department. So that's why it's very important to build this protocol in advance. If you don't have IV valproate, then don't just give the patient oral valproate, and definitely don't prescribe an oral course for discharge. All right, well, what about DHE? Dihydroergotamine for refractory or status migrainosus? Generally, this is only given at pediatric centers where you have neurology coverage. It's contraindicated if you've had another dose of DHE within 14 days, or you've had any triptan of any sort within 24 hours, and you must obtain a pregnancy test in adolescent females before giving it. The dosing for less than 30 kilograms is 0.5 milligram. At least 30 kilograms is one milligram. You give 50% of the dose over three minutes, then the remaining 50% over 30 minutes. If this is gonna work, the patients are gonna start feeling wretched at first. They're gonna get very nauseous and they're gonna vomit. They're gonna have flushing, and you'll see transient hypertension. Most of that resolves within the hour in most centers. If you're committing to DHE, you're kind of bringing the patient into the hospital anyway, though some facilities will have DHE done in the emergency department with close outpatient follow-up. Either way, it's really best practice to involve child neurology if you're giving DHE. Alright, well what about steroids? They give those in grownups too, right? Steroids really only have a role for recurrence prevention in children. So for kids that have a history of returning within 72 hours for rebound headache, you can give dexamethasone 0.6 milligram per kilogram IV dose, the max of 10 milligrams. You do not discharge them home on a steroid prescription or a Medrol dose pack or something else, and this can cut the recurrence risk down a bit. There's other therapies out there like magnesium and ketamine. There's just not enough evidence there. And the purpose of this episode is to discuss the therapies that have good evidence behind them and should be part of protocols across the country. Some patients are unfortunately not responsive to emergency department therapy and need admission. The main inpatient therapy is the DHE protocol. If they're not DHE eligible, they haven't tolerated it well or it's unavailable, admission's unlikely to help them unless they just need some IV fluids to help them get back up on their feet. You should consult neurology if the headache goals are not met after maximizing ED therapy for advice. And we should definitely avoid opioids. They don't treat patients with migraines. They increase recurrence risk. They increase revisit rates. Again, the dopamine antagonist prochlorperazine, it's superior for sustained relief when families ask about them, and fortunately they're asking about opioids far less. We use medications that treat the migraine pain pathways and signaling. We don't just wanna mask the pain. All right, so that's all I've got on the acute management of migraine headaches, especially in the emergency department. Remember that migraine care in the ED should be protocolized and evidence-based. IV fluids are supportive. Prochlorperazine is the first line, or you can use metoclopramide as well. Ketorolac is an adjunctive therapy. Valproate is next line. If you've gotta escalate, and DHE is specialized therapy, you can start in the ED, but most of these patients are getting admitted. Dexamethasone or steroids in children can reduce recurrence risk, but they're not really part of the acute management. You should definitely define the endpoints and structurally and systematically reassess patients at an hour. The goal is to get them feeling better to a defined endpoint and to restore function. There is evidence-based pediatric emergency migraine care. You should understand that, plus how to explain why these agents are being given and some of the side effects to patients and families. I find that that approach increases your likelihood of buy-in and success. Alright, so that's it for this episode on the Acute Management of Migraine Headaches in Children and Adolescents. I hope you found it helpful and I can pretty much guarantee that you're gonna see a patient with a migraine on your next shift. If you've got any feedback or comments, send them my way. If you like this episode, leave a review on your favorite podcast site. It helps more people find the show. Or recommend it to a colleague. If there's other topics that you'd like to hear, send them my way for the Pediatric Emergency Medicine podcast. This has been Brad Sobolewski. See you next time.    

Interview with Emanuele Cerulli Irelli, MD, PhD, author of Comparative Effectiveness of Brivaracetam, Cenobamate,Lacosamide, and Perampanel in Focal Epilepsy. Hosted by Cynthia E. Armand, MD. Related Content: Comparative Effectiveness of Brivaracetam, Cenobamate, Lacosamide, and Perampanel in Focal Epilepsy

In the second episode of this two-part series, Dr. Stacey Clardy and Dr. John Ney discuss why deaths from neurologic conditions are decreasing, but disability is rising, and what this shift means for future care.  Show citation:  Ney JP, Steinmetz JD, Anderson-Benge E, et al. US Burden of Disorders Affecting the Nervous System: From the Global Burden of Disease 2021 Study. JAMA Neurol. 2026;83(1):20-34. doi:10.1001/jamaneurol.2025.4470  Show transcript:  Dr. Stacey Clardy: Hi, this is Stacey Clardy from the Salt Lake City VA and the University of Utah. I've been talking with John Ney from Yale about why neurologic disease now represents the top source of disability in the United States. John, for the minute, deaths from neurologic conditions are declining overall, right? But disability is increasing. So what does that shift mean for how we, the health system, should be planning for neurologic care? Dr. John Ney: I would say overall, both deaths and disability are increasing as a function of greater life expectancy in the population and, then relative to 1990, a greater increase in population of 50 million individuals came into the US either through birth or immigration during that time. So both of those are going up when we actually look by adjusting for age and per 100,000 individuals, both are actually going down, but not at a rate that we would like. So I think there's a lot more work to do. Dr. Stacey Clardy: Understood. Amongst our growing population, neurologic disability is still the leading cause and not less of a problem. For more details, we really get into the specifics and break this down by states even, take a listen to the full-length neurology podcast. And also check out the paper, it is packed with all of the data. It's in JAMA Neurology. It's titled: US Burden of Disorders Affecting the Nervous System from the Global Burden of Disease 2021 study.

In part one of this two-part series, Dr. Stacey Clardy and Dr. John Ney break down the key message neurologists need to understand from this update and offer guidance on how to clearly convey it to patients. Show citation:  Ney JP, Steinmetz JD, Anderson-Benge E, et al. US Burden of Disorders Affecting the Nervous System: From the Global Burden of Disease 2021 Study. JAMA Neurol. 2026;83(1):20-34. doi:10.1001/jamaneurol.2025.4470  Show transcript:  Dr. Stacey Clardy: Hi, this is Stacey Clardy from the Salt Lake City VA in the University of Utah. I've been talking with John Ney from Yale about a global burden of disease analysis showing that disorders affecting nervous system health are the leading cause of disability in the United States. This is probably not too surprising to any neurologist, but very important that they rigorously went through to prove what we experience in clinics. So John, for the Minute, when neurologists do hear it though, when they hear it out loud that more than half of the US population is affected by neurologic conditions, we're still a little skeptical. That's one in two, right? What's the single most important thing we need to understand about how that number was calculated and how to communicate it to our patients and our communities? Dr. John Ney: It's not just the sum of all conditions added up and then translated into the entire population. It's really looking at unique persons with a condition affecting the nervous system. And certainly our top two are tension type headache and migraine, but then we also get into diabetic neuropathy with 17 million individuals, stroke and Alzheimer's with six million and five million respectively. So individuals, unique persons may have more than one of these conditions, but 180 million or more persons in the United States or 54% of the population actually has at least one of these conditions. Dr. Stacey Clardy: So important that we understand this, these numbers. This matters to our patients when we're explaining it to them. Sometimes they feel alone, but this really also matters when we're talking about what we need for our patients as neurologists, more research, more resources. If you want to learn more, listen to the full-length podcast. We get into the discussion, even breaking it down by states and conditions, and a bit more of the health economics and what informs these numbers. And also check out the paper in JAMA Neurology. It's titled US Burden of Disorders Affecting the Nervous System from the Global Burden of Disease 2021 Study.

10,000 – that's the magic number of steps often recommended for a healthy lifestyle. With recent research looking into whether that number is an accurate benchmark for health, could the number of steps taken per day have an impact on brain health and, specifically, cognitive decline? That's precisely what a new study from Harvard Medical School and Mass General Brigham sought to examine, looking at how physical activity, specifically step count, impacted cognitive decline for those living with Alzheimer's disease. Dr. Bri Breidenbach and Sarah Lose join the podcast to break down the results of this new study, as well as share what current research says about the effect of other kinds of physical activity, such as different intensity exercises, on the brain and Alzheimer's progression. Guests: Bri Breidenbach, PhD, scientist, exercise physiologist, Okonkwo Lab, and Sarah Lose, MS, research program manager, exercise physiologist, Okonkwo Lab, UW School of Medicine and Public Health   Show Notes Read the study, “Physical activity as a modifiable risk factor in preclinical Alzheimer's disease,” published by the journal Nature Medicine on their website. Learn more about Dr. Breidenbach and Sarah Lose's work on the Okonkwo Lab website. Read “Association of Daily Step Count and Intensity With Incident Dementia in 78 430 Adults Living in the UK,” mentioned by Dr. Breidenbach at 12:01, on JAMA Neurology's website. Listen to Sarah Lose's previous episode, “Building the Brain: Finding the Cognitive Benefits of Physical Activity,” on our website. Learn more about physical activity and the six pillars of brain health on our website. Complete the Dementia Matters Feedback Survey to let us know what our show is doing well and how we can improve in the New Year! This anonymous survey is estimated to take about 5 minutes to complete and is open to all.   Connect with us Find transcripts and more at our website. Email Dementia Matters: dementiamatters@medicine.wisc.edu Follow us on Facebook and Twitter. Subscribe to the Wisconsin Alzheimer's Disease Research Center's e-newsletter. Enjoy Dementia Matters? Consider making a gift to the Dementia Matters fund through the UW Initiative to End Alzheimer's. All donations go toward outreach and production.

Depo-Provera was approved in 1992 by U.S. regulators. About 1 in 4 sexually active women in the United States have used the shot at some point, according to the U.S. Centers for Disease Control and Prevention (CDC). Meningiomas are common intracranial tumors with a female predominance. In fact, they are the most common primary brain tumor in women, with an incidence of approximately 12.76 per 100,000 in the general female population. The vast majority of these tumors are benign (World Health Organization [WHO] grade 1) while 15% to 20% of these tumors can behave atypically (WHO grade 2) and rarely, in 1% to 2% of cases, these tumors can be malignant (WHO grade 3). We covered the relationship between Depo-Provera, as a contraceptive agent, and brain meningiomas back in March 2024. With the increase in data, the ACOG released a patient centered counseling tool titled, “Counseling Patients on Birth Control Injection and Meningioma”. The most recent update on this story comes from the FDA, which has granted a medication label change to Depo-Provera (Pfizer) warning of this association. Even though association does not prove causation, the association between depo and meningiomas seems strong (with new data from the US). Does this warning extend to other progestins? Listen in for details. 1. https://podcasts.apple.com/us/podcast/dr-chapas-obgyn-clinical-pearls/id1412385746?i=10006508795722. ACOG's “Counseling Patients on Birth Control Injection and Meningioma” 3. https://www.statnews.com/pharmalot/2025/12/17/fda-pfizer-contraception-cancer-preemption-depoprovera/4. Xiao T, Kumar P, Lobbous M, et al. Depot Medroxyprogesterone Acetate and Risk of Meningioma in the US. JAMA Neurology. 2025;82(11):1094-1102. doi:10.1001/jamaneurol.2025.3011.5. de Dios E, Näslund O, Choudhry M, et al.Prevalence and Symptoms of Incidental Meningiomas: A Population-Based Study.Acta Neurochirurgica. 2025;167(1):98. doi:10.1007/s00701-025-06506-7.6. Schaff LR, Mellinghoff IK.Glioblastoma and Other Primary Brain Malignancies in Adults: A Review. JAMA. 2023;329(7):574-587. doi:10.1001/jama.2023.0023.7. BMJ 2024; 384 doi: https://doi.org/10.1136/bmj-2023-078078 (Published 27 March 2024) Cite this as: BMJ 2024;384:e078078

Interview with John P. Ney, MD, MPH, author of US Burden of Disorders Affecting the Nervous System: From the Global Burden of Disease 2021 Study. Hosted by Cynthia E. Armand, MD. Related Content: US Burden of Disorders Affecting the Nervous System

What if one side of your body suddenly stopped moving — and your doctor said, “It's a migraine”?Hemiplegic migraines are rare, disorienting, and often confused with strokes. They challenge everything you think you know about how your brain, body, and energy connect.In this episode of Migraine Heroes Podcast, hosted by Diane Ducarme, we explore the science and the story behind this rare form of migraine — one that blurs the line between neurology and mystery. Together, we look at how the body can temporarily lose its flow, and how to gently help it find its rhythm again.In this episode, you'll learn:

Ready to finally break free from alcohol—and stop the cycle of numbing? Start your journey today with the Refresh & Reboot: 30 Day Alcohol-Free Challenge. This self-paced program gives you daily guidance, mindset tools, and video support from Sara to help you thrive through your first 30 days without alcohol. Podcast listeners get 20% off with code PODCAST20 at checkout.

Interview with Helen Kim, PhD, author of Risk of Future Hemorrhage From Unruptured Brain Arteriovenous Malformations: The Multicenter Arteriovenous Malformation Research Study (MARS). Hosted by Cynthia E. Armand, MD. Related Content: Risk of Future Hemorrhage From Unruptured Brain Arteriovenous Malformations

Send comments and feedbackSomatic genetic epilepsies arise from mutations that occur early in fetal development. They are usually only detectable by genetic sequencing of tissue. For these epilepsies, the timing of the mutation is key: For example, research has shown that focal cortical dysplasia type IIB and hemimegaloencephaly are genetically the same disease, but arise from somatic mutations at different developmental time points. This relatively new area of research is discussed by Dr. Alina Ivaniuk and Dr. Christian Bosselmann.Resources:Analysis of 1,386 epileptogenic brain lesions reveals association with DYRK1A and EGFR (Nature Communications 2024 - C. Bosselmann et al.)Neocortical development and epilepsy: Insights from focal cortical dysplasia and brain tumours (The Lancet Neurology 2021 - I. Blumcke et al.)Contribution of somatic Ras/Raf/Mitogen-activated protein kinase variants in the hippocampus in drug-resistant mesial temporal lobe epilepsy (JAMA Neurology 2023 - S. Khoshkhoo et al.)Somatic mosaicism and neurodevelopmental disease (Nature Neuroscience 2018 - AM D'Gama and CA Walsh)BRAF somatic mutation contributes to intrinsic epileptogenicity in pediatric brain tumors (Nature Medicine 2018 - HY Koh et al.)SLC35A2 loss-of-function variants affect glycomic signatures, neuronal fate and network dynamics (Brain 2025 - D Lai et al.)Precise detection of low-level somatic mutation in resected epilepsy brain tissue (Acta Neuropathologica 2019 - NS Sim et al.)Toward a better definition of focal cortical dysplasia: An iterative histopathological and genetic agreement trial (Epilepsia 2021 - I Blumcke et al.)Seizure outcome and use of antiepileptic drugs after epilepsy surgery according to histopathological diagnosis: A retrospective multicentre cohort study (The Lancet Neurology 2020 - HJ Lamberink et al.) Sharp Waves episodes are meant for informational purposes only, and not as clinical or medical advice.Let us know how we're doing: podcast@ilae.org.The International League Against Epilepsy is the world's preeminent association of health professionals and scientists, working toward a world where no person's life is limited by epilepsy. Visit us on Facebook, Instagram, and LinkedIn.

Delaying diagnosis of parkinsonism can mean delaying care. In a study recently published in JAMA Neurology, David Vaillancourt, PhD, and colleagues tested the ability of an AI model to differentiate between Parkinson disease and other neurodegenerative disorders when paired with MRI. He joins JAMA and JAMA+ AI Associate Editor Yulin Hswen, ScD, MPH to discuss. Related Content: A Large Proportion of Parkinson Disease Diagnoses Are Wrong—Here's How AI Could Help Automated Imaging Differentiation for Parkinsonism

Interview with Colin P. Derdeyn, MD, author of Intravenous Argatroban or Eptifibatide in Patients Undergoing Mechanical Thrombectomy: A Subgroup Analysis of the MOST Randomized Clinical Trial. Hosted by Cynthia E. Armand, MD. Related Content: Intravenous Argatroban or Eptifibatide in Patients Undergoing Mechanical Thrombectomy

To subscribe to our podcast and YouTube channel visit: https://www.youtube.com/@davisphinneyfdn/podcasts This episode of the Parkinon's Podcast features the full, unedited audio from a Live Well Today Webinar. During this live webinar, Dr. Corcos, Professor of Physical Therapy and Human Movement Sciences, shared insights from decades of research focused on the benefits of exercise for people with Parkinson's. Listen in as Dr. Corcos discusses the latest findings in Parkinson's exercise science and offers practical takeaways for incorporating effective movement strategies into everyday life.  Some links discussed in this webinar: SPARX Phase 2 Trial--https://jamanetwork.com/journals/jamaneurology/fullarticle/2664948 Dr. Corcos' Exercise Advice Article--https://journals.sagepub.com/doi/10.3233/JPD-230277 Cardio Pulmonary Exercise Test Article-https://journals.sagepub.com/doi/10.1177/1877718X251330814 Industrial Chemicals and Parkinson's Blog-- https://davisphinneyfoundation.org/industrial-chemicals-pesticides-and-parkinsons/ Climbing and Parkinson's Blog-- https://davisphinneyfoundation.org/stay-moving-with-parkinsons-tai-chi-ping-pong-and-rock-climbing/ ---- Speaker Bio Daniel Corcos, PhD Professor of Physical Therapy & Human Movement Sciences  Daniel Corcos obtained his PhD in Motor Control from the University of Oregon after obtaining his Master's Degree in Psychology. The primary research interests of Dr. Corcos are aimed at helping people with Parkinson's disease improve their quality of life, improve their mobility and cognition, and slow down the rate at which their disease progresses. Integrating neuroscience and expertise in conducting clinical trials, the research of Dr. Corcos focuses on interventions (such as resistance exercise, endurance exercise, stretching and balance training) that aim to reduce the symptoms of the disease and delay the rate at which the disease progresses. Within this context, Dr. Corcos uses exercise interventions whose dose (frequency, intensity, time and type) can be precisely controlled to achieve these goals and thereby develops and integrates laboratory-based interventions that people with Parkinson's disease can employ in their local community. His current research, published in JAMA Neurology suggests that high intensity endurance slows down the rate at which Parkinson's disease progresses. These findings have been covered in the New York Times and the general press world-wide. Dr. Corcos lectures nationally and internationally to physicians, neuroscientists, and people with the disease on the benefits of exercise for those with Parkinson's disease.

Interview with Dennis J. Rivet II, MD, author of GLP-1 Receptor Agonists in Idiopathic Intracranial Hypertension. Hosted by Cynthia E. Armand, MD. Related Content: GLP-1 Receptor Agonists in Idiopathic Intracranial Hypertension

Most of us are familiar with the idea that you need to take 10 thousand steps per day to stay healthy but getting to this magic number is not that easy. The 10,000-step target first became popular in Japan in the 1960s. A clockmaker capitalising on people's new interest in fitness following the 1964 Tokyo Olympic Games made a pedometer with a name that, when written in Japanese characters, resembled a walking man and coincidentally translated as “10,000-steps metre.” A study of over 78,000 people in the UK between 2013 and 2015 using wearable trackers was published in the journals JAMA Internal Medicine and JAMA Neurology. Where did we get the number 10 thousand from? Does that mean that we do not need to take 10 steps? So how many steps should I be aiming for per day? In under 3 minutes, we answer your questions! To listen to the last episodes, you can click here: ⁠Can you eat eggs everyday?⁠ ⁠What is Lucky Girl syndrome, this new method that is all the rage on Tik Tok?⁠ ⁠Which type of wine is best for your health?⁠ A podcast written and realised by Amber Minogue. First broadcast: 19/1/2023 Learn more about your ad choices. Visit megaphone.fm/adchoices

Delaying diagnosis of parkinsonism can mean delaying care. In a study recently published in JAMA Neurology, David Vaillancourt, PhD, and colleagues tested the ability of an AI model to differentiate between Parkinson disease and other neurodegenerative disorders when paired with MRI. He joins JAMA and JAMA+ AI Associate Editor Yulin Hswen, ScD, MPH to discuss. Related Content: A Large Proportion of Parkinson Disease Diagnoses Are Wrong—Here's How AI Could Help Automated Imaging Differentiation for Parkinsonism

Interview with Manuel Comabella, MD, author of Prognostic Factors for Multiple Sclerosis Symptoms in Radiologically Isolated Syndrome. Hosted by Cynthia E. Armand, MD. Related Content: Prognostic Factors for Multiple Sclerosis Symptoms in Radiologically Isolated Syndrome

Interview with Richard B. Lipton, MD, author of Fremanezumab for the Treatment of Patients With Migraine and Comorbid Major Depressive Disorder. Hosted by Cynthia E. Armand, MD. Related Content: Fremanezumab for the Treatment of Patients With Migraine and Comorbid Major Depressive Disorder

While large retailers may weather the storm, independent businesses are struggling to absorb rising costs tied to new trade policies. "CBS Mornings" hears from one Los Angeles entrepreneur facing tough choices. Lori Vallow Daybell was in an Arizona court Monday to represent herself in a trial involving the killing of her fourth husband, Charles Vallow, in 2019. In her opening statement, Vallow said the evidence will show it was self defense, but prosecutors argued she conspired with her brother to kill Vallow, who had filed for divorce, to collect a $1 million life insurance policy. Two new studies in JAMA Neurology show some diabetes and popular weight loss drugs could help to protect against dementia. CBS News medical contributor Dr. Celine Gounder joins "CBS Mornings" to explain what researchers found. The Florida Gators won their first NCAA basketball title since 2007. Will Richard, who hit four three-pointers in the first half, speaks about the big win, what he'll remember from this season and the next steps in his career. Deja Kelly has turned her platform into a personal brand, but she says having the right support system — from a financial advisor to her "momager" — is key to staying grounded in the new NIL economy. With just days to go before liftoff, Gayle King gets a surprise sendoff on "CBS Mornings" from friends and famous faces including Tom Hanks, William Shatner, Bill Nye and Megan Rapinoe. Nearly a decade since her last Broadway role, Idina Menzel is back, this time climbing through midair as a grieving mother who finds healing and hope in California's redwood forest. To learn more about listener data and our privacy practices visit: https://www.audacyinc.com/privacy-policy Learn more about your ad choices. Visit https://podcastchoices.com/adchoices

Interview with Steven J. Warach, MD, PhD, author of Optimal Delay Time to Initiate Anticoagulation After Ischemic Stroke in Atrial Fibrillation: A Pragmatic, Response-Adaptive Randomized Clinical Trial. Hosted by Cynthia E. Armand, MD. Related Content: Optimal Delay Time to Initiate Anticoagulation After Ischemic Stroke in Atrial Fibrillation

Interview with David J. Seiffge, MD, author of Location and Timing of Recurrent, Nontraumatic Intracerebral Hemorrhage. Hosted by Cynthia E. Armand, MD. Related Content: Location and Timing of Recurrent, Nontraumatic Intracerebral Hemorrhage

As the earth continues to get warmer and we see record high temperatures across the globe, scientists tell us that this pattern is going to continue and be more common. Higher temperatures, more frequently has led to more heat strokes and other conditions when people aren't prepared for this situation.  Additionally, people with neurodegenerative diseases like Parkinson's are at greater risk for heat related complications, A recent article published in JAMA Neurology, describes the issue, what to look for, and how we, as individuals and community, can help to prevent people from heat related complications. It was co-written by my guest today, Indu Subramanian, MD, a neurologist and movement disorders researcher at the University of California, Los Angeles (UCLA), and Al Saad, MD, a neurologist with expertise in climate change at the University of Colorado. With summer around the corner, this is a great time to prepare for the heat and work with your healthcare team on a plan to prevent any heat related issues. We as a community need to look out for our neighbors, friends and family. Our neighbors   may be isolated or scared if they have Parkinson's diseasae or are older. As a community, we should come together to identify people who may need our help during a difficult situation such as heatwaves and higher temperatures, especially in areas in the world where they are not prepared to assist. We should keep in touch, check in, offer some water.   Learn all about how to prepare, provent, find help as well as recognizing the symptoms of heatstroke on this episode of the Parkinson's Experience. https://www.parkinsonsecrets.com/  https://parkinsonsnewstoday.com/news/heat-intolerance-rising-parkinsons-risk-climbing-temperatures/ https://www.uclahealth.org/providers/indu-subramanian https://www.dbsandme.com/en.html  

Interview with Wei-Hsuan Lo-Ciganic, PhD, author of Cardiovascular Safety of Anti-CGRP Monoclonal Antibodies in Older Adults or Adults With Disability With Migraine. Hosted by Cynthia E. Armand, MD. Related Content: Cardiovascular Safety of Anti-CGRP Monoclonal Antibodies in Older Adults or Adults With Disability With Migraine

Most of us are familiar with the idea that you need to take 10 thousand steps per day to stay healthy but getting to this magic number is not that easy. The 10,000-step target first became popular in Japan in the 1960s. A clockmaker capitalising on people's new interest in fitness following the 1964 Tokyo Olympic Games made a pedometer with a name that, when written in Japanese characters, resembled a walking man and coincidentally translated as “10,000-steps metre.” A study of over 78,000 people in the UK between 2013 and 2015 using wearable trackers was published in the journals JAMA Internal Medicine and JAMA Neurology. Where did we get the number 10 thousand from? Does that mean that we do not need to take 10 steps? So how many steps should I be aiming for per day? In under 3 minutes, we answer your questions! To listen to the last episodes, you can click here: Can you eat eggs everyday? What is Lucky Girl syndrome, this new method that is all the rage on Tik Tok? Which type of wine is best for your health? A podcast written and realised by Amber Minogue. First broadcast: 19/1/2023 Learn more about your ad choices. Visit megaphone.fm/adchoices

Interview with Jordan L. Schultz, PharmD, author of β-Blocker Use and Delayed Onset and Progression of Huntington Disease. Hosted by Cynthia E. Armand, MD. Related Content: β-Blocker Use and Delayed Onset and Progression of Huntington Disease

Interview with Giovanni B. Frisoni, MD, author of Alzheimer Disease as a Clinical-Biological Construct—An International Working Group Recommendation. Hosted by Cynthia E. Armand, MD. Related Content: Alzheimer Disease as a Clinical-Biological Construct—An International Working Group Recommendation

A recent practice guideline provides updated evidence-based conclusions and recommendations regarding in utero effects of anti-seizure medications and folic acid supplementation on the prevalence of major congenital malformations, adverse perinatal outcomes, and neurodevelopmental outcomes. Dr. Parthvi Ravat interviewed Dr. Alison Pack about the guideline, which was produced by the American Academy of Neurology, American Epilepsy Society, and Society for Maternal-Fetal Medicine.Review the practice guideline: Teratogenesis, perinatal, and neurodevelopmental outcomes after in utero exposure to antiseizure medication (Neurology, May 2024)Other studies mentioned in the episode: Risk of major congenital malformations and exposure to antiseizure medication monotherapy (JAMA Neurology, March 2024) Sharp Waves episodes are meant for informational purposes only, and not as clinical or medical advice.Let us know how we're doing: podcast@ilae.org.The International League Against Epilepsy is the world's preeminent association of health professionals and scientists, working toward a world where no person's life is limited by epilepsy. Visit us on Facebook, X (Twitter), Instagram, and LinkedIn.

Interview with Rachel Grashow, PhD, MS, and Aaron L. Baggish, MD, authors of Perceived Chronic Traumatic Encephalopathy and Suicidality in Former Professional Football Players. Hosted by Cynthia E. Armand, MD. In the US, you can call, text, or chat 988, the Suicide and Crisis Lifeline. Related Content: Perceived Chronic Traumatic Encephalopathy and Suicidality in Former Professional Football Players

Dr. Gregg Day talks with Dr. Sebastian Palmqvist about the use of blood biomarkers to streamline the diagnostic workup and treatment of Alzheimer disease. Read the related article in JAMA Neurology. Disclosures can be found at Neurology.org.

Interview with Peter Vajkoczy, MD, author of Localized Nicardipine Release Implants for Prevention of Vasospasm After Aneurysmal Subarachnoid Hemorrhage: A Randomized Clinical Trial. Hosted by Cynthia E. Armand, MD. Related Content: Localized Nicardipine Release Implants for Prevention of Vasospasm After Aneurysmal Subarachnoid Hemorrhage

Dr. Matthew Barrett talks with Dr. Michael S. Okun about the caution and deliberation needed in understanding Parkinson disease biomarkers. Read the related viewpoint piece in JAMA Neurology. Disclosures can be found at Neurology.org.

Interview with Allison W. Willis, MD, MS, author of Direct-Acting Oral Anticoagulants and Antiseizure Medications for Atrial Fibrillation and Epilepsy and Risk of Thromboembolic Events. Hosted by Cynthia E. Armand, MD. Related Content: Direct-Acting Oral Anticoagulants and Antiseizure Medications for Atrial Fibrillation and Epilepsy and Risk of Thromboembolic Events

Dr. Deanna Saylor talks with Drs. Gretchen Birbeck and Melody Asukile about ways to improve global collaboration among neurologists. Read the related article in JAMA Neurology. Disclosures can be found at Neurology.org.