Neurology Minute

In this lab update, Dr. Stacey Clardy discusses the latest information on chronic wasting disease. 

In part two of this series, Dr. Aaron Zelikovich discusses the clinical implications for patients with HSV encephalitis.  Show citation:  Solomon T, Hooper C, Easton A, et al. Safety and efficacy of adjunct dexamethasone in adults with herpes simplex virus encephalitis in the UK (DexEnceph): a multicentre, observer-blind, randomised, phase 3, controlled trial. Lancet Neurol. 2026;25(2):136-146. doi:10.1016/S1474-4422(25)00454-5 

Dr. Greg Cooper and Dr. Kerry Sheets discuss how hearing aid use affects cognition and the risk of dementia in older adults with hearing impairment.  Show citations: Cribb L, Moreno-Betancur M, Pase MP, et al. Treating Hearing Loss With Hearing Aids for the Prevention of Cognitive Decline and Dementia. Neurology. 2026;106(3):e214572. doi:10.1212/WNL.0000000000214572  Show transcript: Dr. Greg Cooper: Hi, this is Greg Cooper. I just finished interviewing Kerry Sheets for this week's Neurology Podcast. For today's Neurology Minute, I'm hoping you can tell us the main points of your paper. Dr. Kerry Sheets: The central message of our paper is that hearing aid use in adults aged 70 years or older with hearing impairment may reduce dementia risk over 7 years. Results for the impact of hearing aid use on cognitive decline were less. Dr. Greg Cooper: Well, thank you for that summary and for all of your work on this topic. Please check out this week's podcast to hear the full interview and read the full article published in Neurology: Treating Hearing Loss with Hearing Aids for the Prevention of Cognitive Decline and Dementia. 

Dr. Jessica Ailani and Dr. Richard Lipton discuss future advancements in headache medicine.  Show transcript:  Dr. Jessica Ailani:  Hello and welcome to the Neurology Minute. I'm Jessica Ilani from Georgetown Headache Center in Washington, DC. In the neurology podcast with Richard Lipton from the Montefiore Headache Center, we'll be discussing the latest clinical trials in headache medicine, where our field is going, where it's been, and you'll get lots of great advice on thinking through a clinical trial, what the advances have been, where their pitfalls have been, and really how to think of both positive and negative trials. So Richard, what are you most looking forward to when it comes to new treatment targets within headache? Dr. Richard Lipton:  First, let me say that I'm sure most know about the eight CGRP targeted treatments have been approved for migraine, both as acute and preventive treatments. And it's very clear that those treatments have had incredible benefits for our patients and have really improved headache practice. There's another neuropeptide target also targeted by monoclonal antibodies called PACAP or pituitary adenolyte cyclase activating polypeptide. This peptide is also a potent vasodilator involved in pain signaling like CGRP. While CGRP is primarily linked to sensory pathways, PACAP is found in parasympathetic ganglia. And for that reason, it may have a special role in headaches associated with cranial autonomic symptoms. And that includes both migraine, which commonly has cranial autonomic symptoms and also cluster headache. There's a recent randomized trial published in New England Journal showing that a monoclonal antibody targeting PACAP reduced monthly migraine day frequency and was beneficial in people who failed to respond to CGRP inhibitors. So that's at least one area that I'm hopeful about. Dr. Jessica Ailani:  So Richard, thank you so much. I hope you have a few moments and listen to our full podcast that'll tell you a lot more about the future of headache medicine. 

In part one of this series, Dr. Aaron Zelikovich discusses the trial design and primary results.  Show citation:  Solomon T, Hooper C, Easton A, et al. Safety and efficacy of adjunct dexamethasone in adults with herpes simplex virus encephalitis in the UK (DexEnceph): a multicentre, observer-blind, randomised, phase 3, controlled trial. Lancet Neurol. 2026;25(2):136-146. doi:10.1016/S1474-4422(25)00454-5  Show transcript:  Dr. Aaron Zelikovich:  Welcome to today's Neurology Minute. My name is Aaron Zelikovich. I'm a neuromuscular specialist at Lenox Hill Hospital in New York City. Today, we'll discuss part one of a three-part series reviewing a recent article titled Safety and Efficacy of Adjunct Dexamethasone in Adults with Herpes Simplex Virus Encephalitis in the United Kingdom (DexEnceph) Study, a multicenter observer-blind randomized phase three control trial published in Lancet Neurology. In the first episode, we'll focus on the trial design and primary results. In part two, we'll discuss the clinical implications for patients with HSV encephalitis, and in part three, discuss the outcomes seen across the trial during and after an acute infection. Overall, the study found that adjunct dexamethasone did not improve outcomes in patients with CSF-confirmed HSV encephalitis. But importantly, it also did not worsen outcomes. Prior research that was non-randomized and retrospective of 45 patients with HSV encephalitis found that patients did not receive corticosteroids had worse outcomes. A different randomized trial looking at dexamethasone and HSV encephalitis was only able to recruit 41 patients and was stopped prematurely due to the lack of recruitment. Prior to the study, there was no clear evidence that adjunct steroids with acyclovir improved outcomes in HSV encephalitis. The Dex and phase three randomized clinical trial performed in the United Kingdom at 53 hospitals recruited patients from 2016 to 2022. They screened over 1,400 patients of which only 94, or 6%, were enrolled. Patients were randomized to either acyclovir only or acyclovir and intravenous dexamethasone. In order to be randomized, patients had to have a febrile illness with new onset seizure or new focal neurological sign or altered mental status as well as a positive HSV type one or two PCR from the CSF. The primary outcome for this study was the Wechsler Memory Scale Type Four Auditory Memory Index Score which was collected at 26 weeks. It had a range of 40, which is the worst outcome, to a range of 160 which was considered normal. 81 patients were included in the modified intention-to-treat analysis. Of the 13 patients, six were lost to follow-up, and seven withdrew consent. There were 39 patients in the dexamethasone group and 42 in the acyclovir-only group in the final analysis. The primary outcome of the Wechsler Memory Scale had similar scores in both groups. 71 in the dexamethasone group and 69 in the control group with a P value of 0.76. The safety profile was similar in both groups, and there were no additional safety signals found in the dexamethasone-treated group. At 26 weeks, there were 12 deaths from HSV encephalitis, six from each group, as well as a similar time to discharge between both cohorts. The DexEnceph clinical trial did not show any clear clinical benefit for dexamethasone with regards to clinical outcomes but also didn't show any increased safety concerns compared to only acyclovir. In part two, we will discuss the implications of this trial in patients with undifferentiated encephalitis and the role that steroids play in patients that HSV encephalitis is suspected. Thank you so much, and have a wonderful day.   

In the second part of this series, Dr. Tesha Monteith and Dr. Jennifer Robblee discuss updates to the emergency room recommendations for the acute treatment of migraines.  Show citations:  Robblee J, Minen MT, Friedman BW, Cortel-LeBlanc MA, Cortel-LeBlanc A, Orr SL. 2025 Guideline Update to Acute Treatment of Migraine for Adults in the Emergency Department: The American Headache Society Evidence Assessment of Parenteral Pharmacotherapies. Headache. 2026;66(1):53-76. doi:10.1111/head.70016 Robblee J, Khan FA, Marmura MJ, et al. Reaching International Consensus on the Definition of Refractory Migraine Using the Delphi Method. Cephalalgia. 2025;45(9):3331024251367767. doi:10.1177/03331024251367767 Show transcript:  Dr. Tesha Monteith:   Hi, this is Tesha Monteith with the Neurology Minute. I've just been speaking with Jennifer Robblee about her exciting work, defining refractory migraine with an international consensus, as well as her work with the American Headache Society on a guideline update for parental pharmacotherapies for migraine in the emergency department. So Jennifer, we've just been chatting on the podcast about all the great work out of the American Headache Society, updating the emergency room recommendations for acute treatment of migraine. Can you give a summary of those findings? Dr. Jennifer Robblee:  We looked at all of the new data for randomized control trials in the emergency room. We found 26 new trials, and several of those were actually a class one study that we felt had a low risk of bias. And from that, we applied the grading. So we actually have two grade A medications where it is that you must offer, of course, to the appropriate patient. And that's prochlorperazine IV, and greater occipital nerve blocks. Now, there's also a grade A must not offer, and that's IV hydromorphone. Then we have some grade B, which is should offer, and that's dexketoprofen, ketorolac, metaclopramide, sumatriptan subcutaneous, and supraorbital nerve blocks. So really exciting that we have lots of things that we can now say we have pretty good evidence or very good evidence to offer them to our patients. Dr. Tesha Monteith:  Great. It's always nice to see this update based on evidence. Dr. Jennifer Robblee:  Yes, I think it's so important, because right now when we see patients, and I'm sure you get this all the time, they come back, say they were in the emergency room for a severe headache and they got a migraine cocktail. And you're like, "Do you know what you were given?" And they say, "I don't know. I was just told it's a migraine cocktail." And as you know, that mean many, many different things. And when you are able to pull the records, it is many, many different things that a migraine cocktail can mean. So I'm hoping that this can start to standardize what we're actually giving our patients as we await more trials in the future that might start to tell us what that combo of treatments really should be. For right now, these at least tell us what individual treatments have the best evidence. Dr. Tesha Monteith:  Thanks so much, Jennifer.  

In this episode, Dr. Jason Crowell reviews the March 9th Capitol Hill Report discussing the AAN's advocacy priorities for 2026. Stay updated with what's happening on the hill by visiting aan.com/chr.  Learn how you can get involved with AAN advocacy.  Show transcript:  Dr. Jason Crowell: Hey, this is Jason Crowell. Thanks for listening to today's Neurology Minute. Today, we have an advocacy update from the AAN's Capitol Hill Report. The AAN has come out with its top advocacy priorities for 2026, and the first is access to care which includes affordable prescription drug prices, telehealth, and adequate coverage policies. Neurological conditions can require expensive specialty drugs as we know, so the AAN supports policies that ensure prescription medications are accessible to patients. Related to this priority, the Center for Medicare and Medicaid Innovation recently announced the GLOBE and GUARD models, two proposed mandatory drug pricing models that would make manufacturers pay rebates if their drug prices exceed global benchmarks. The AAN has responded to these proposals with recommendations to avoid unintended access issues. It's also important to make telehealth flexibilities permanent for Medicare beneficiaries, and the AAN has been lobbying for the CONNECT for Healthcare Act to do that. The second top priority is reducing regulatory and administrative burdens, like prior authorization and step therapy which we're familiar with. This is a longtime problem for physicians who spend a lot of time each week. We deal with these processes and we'd rather be treating patients, as you know. A new Medicare initiative called the WISeR Model establishes new prior authorization requirements for some medical services, and while it doesn't directly affect neurology, the AAN and other organizations are pushing back and closely monitoring for future similar models. Next is the neurology workforce. This includes making sure Medicare reimbursement for neurological services is enough to maintain a practice, as well as supporting wellness and immigration policy to allow international medical graduates to practice in the US. Related to this priority, the AAN has been pushing for a permanent inflationary update to the Medicare Physician Fee Schedule and to end the schedule's outdated budget neutrality requirement that ends up causing cuts to reimbursement each year. The final priority is neuroscience research and brain health. There have been a lot of threats to research funding recently, and the AAN has been lobbying for NIH and NINDS funding that includes the BRAIN Initiative, an important program that's led to neurology breakthroughs. It's set to lose a big part of this funding at the end of the year when funding from the 21st Century Cures Act expires. So the AAN has been asking Congress to help make up the gap through appropriation spending. There's much more in this week's Capitol Hill Report, and this is available on aan.com/chr, and for our US members, you can also find this Capitol Hill Report in your inbox. So check it out to learn more. 

Dr. Halley Alexander and Dr. Abel Sandmann discuss seizure rates and risk factors in patients with cerebral cavernous malformations (CCMs) during long-term follow-up without CCM intervention.  Show citation:  Sandmann ACA, Vandertop WP, White PM, Verbaan D, Coutinho JM, Al-Shahi Salman R. Seizures and Epilepsy in Patients With Untreated Cerebral Cavernous Malformations: A Prospective, Population-Based Cohort Study. Neurology. 2025;105(11):e214387. doi:10.1212/WNL.0000000000214387  Show transcript:  Dr. Halley Alexander: Hi, this is Halley Alexander with today's Neurology Minute. I'm here with Abel Sandmann from Amsterdam University Medical Center, and we just finished recording a full-length podcast about some exciting findings related to cerebral cavernous malformations and the risk of seizures and epilepsy. Abel, can you give our listeners a rundown of the most exciting findings and how it can change practice? Dr. Abel Sandmann:  In our paper, we show that patients with a cerebral cavernous malformation who have a first unprovoked seizure should be diagnosed with epilepsy and considered for anti-seizure medication, as most of them achieve long-term seizure freedom with medical therapy alone. These findings are based on a prospective population-based cohort study in which we analyze long-term follow-up and assess the rates and risk factors for: one, a first-ever epileptic seizure; two, seizure recurrence to evaluate the updated ILAE definition of epilepsy; and three, seizure freedom over two years and five years among patients with epilepsy. We found that among patients who had never experienced a seizure before, the 10-year risk of a first-ever seizure was only 6%. This supports current recommendations against prophylactic anti-seizure medication in patients who are incidentally diagnosed with a cerebral cavernous malformation. However, following a first unprovoked seizure, the 10-year risk of recurrence was 80%, which exceeds the 60% threshold defined by the ILAE. This justifies diagnosing epilepsy after the first and provoked seizure in this population. Given that the risk of recurrence was lower in patients treated with anti-seizure medication after the first seizure, this supports early initiation of therapy, although these treatment analyses were non-randomized and should be interpreted cautiously. Most patients who met the definition of epilepsy became two year and five years seizure-free with medical management alone. But some patients with cerebral cavernous malformations develop medically intractable seizures and might benefit from surgical treatments. Dr. Halley Alexander: Excellent. Thank you so much, Abel. You can find the full-length podcast, which is available now on the Neurology Podcast, or you can also find the full article in Neurology at neurology.org, or in the December 2025 print issue. As always, thanks for tuning in for today's Neurology Minute.   

In part one of this series, Dr. Tesha Monteith and Dr. Jennifer Robblee discuss an international consensus definition for refractory migraine and why clearer criteria are needed.  Show citations: Robblee J, Minen MT, Friedman BW, Cortel-LeBlanc MA, Cortel-LeBlanc A, Orr SL. 2025 Guideline Update to Acute Treatment of Migraine for Adults in the Emergency Department: The American Headache Society Evidence Assessment of Parenteral Pharmacotherapies. Headache. 2026;66(1):53-76. doi:10.1111/head.70016 Robblee J, Khan FA, Marmura MJ, et al. Reaching International Consensus on the Definition of Refractory Migraine Using the Delphi Method. Cephalalgia. 2025;45(9):3331024251367767. doi:10.1177/03331024251367767 Show transcript:  Dr. Tesha Monteith: Hi, this is Tesha Monteith with the Neurology Minute. I've just been speaking with Jennifer Robblee about her exciting work defining refractory migraine with an international consensus, as well as her work with the American Headache Society on a guideline update for parental pharmacotherapies for migraine in the emergency department. Hi, Jennifer. Thanks again for coming on our Neurology Minute. Dr. Jennifer Robblee: Thank you so much for having me. I'm delighted to be here. Dr. Tesha Monteith: You've done a lot of work in the area of refractory migraine. Why don't you tell us why you felt there need to be clarification on the definition? Dr. Jennifer Robblee: Well, this is a patient population that I'm really passionate about. There's not enough research out there. We don't really know who these patients are, why they're not responding to treatment, and we don't know how to help them because we have no guidelines, obviously, since they're refractory to what we use for treating. So I thought it was really good to get an international group to standardize our definition and hopefully help move the research forward. Dr. Tesha Monteith: Why don't you tell us a little bit about the consensus definition Dr. Jennifer Robblee: So we came up with an international consensus definition for refractory migraine that was laid out the same way that migraine is, say, laid out in the ICHD-3 diagnostic manual, if you want to call it that. So we have different criteria on. So criterion A basically allowed for it to be episodic or chronic migraine. Criterion B had three subcriteria, so you needed to have at least two out of three of severe to very severe disability and/or a constant background headache and/or at least eight monthly migraine days. Criterion C was about the lack of response to treatment. And basically it says that you needed to have failure of all medication categories, and there is an extra one for an other in case any new treatments emerge before the diagnostic criteria get updated. And what we considered a, quote, unquote, failure was that you did not have a 50% improvement in monthly migraine days, or you had intolerable side effects, or you had an absolute contraindication. There is a caveat that you need to have at least four true lack of efficacies. And then the CGRP monoclonal antibody or gepant category and the onabotulinumtoxin toxin category both had to be a true lack of response. And of course, there's a criterion B to say that this should not be from another diagnosis. Dr. Tesha Monteith: Thanks so much, Jennifer.

Dr. Stacey Clardy reviews biotin deficiency and biotin-related lab interference. Show transcript:  Dr. Stacey Clardy: Hi, this is Stacey Clardy from the Salt Lake City VA and the University of Utah, and I'm back with you for another lab minute. Today, let's talk about Biotin or vitamin B7, because the Biotin story in neurology has two very different aspects. The first is a real deficiency, which is uncommon, but clinically really important. And the second is the modern problem of biotin supplementation that's quietly wrecking our lab interpretation. So first, true biotin deficiency in adults is less common, but it can look like a multi-system neurologic syndrome. The classic teaching is dermatitis and alopecia, so keep those in your mind. But neurologists end up seeing the downstream features. So lethargy, depression, paresthesias and sometimes ataxia. Now, in infants and children, the bigger higher stakes entity is biotinidase deficiency, which is fortunately screened in many newborn programs in the US. Untreated, it can produce seizures, developmental delay, optic atrophy, and hearing loss. And the key point is that these neurologic injuries can be prevented if biotin is started early enough. Also, remember, there are numerous reports now in the literature of it mimicking the clinical and radiological features of neuromyelitis optica spectrum disorder or multiple sclerosis. So if you have one of those diagnoses and you're not quite sure that it's right, keep biotinidase deficiency in the back of your mind. Now, what most of us clinicians are living with is the biotin supplement era. So high dose biotin, taken by a lot of people, either knowingly or unknowingly, can interfere with biotin streptavidin immunoassay platforms. And the direction of error depends on the assay design, but the practical pitfalls are simple. You can be handed a lab pattern that screams something like hyperthyroidism or other endocrine pathology, and it can actually be purely analytical artifact. Thyroid testing is the most common example, and troponin and other assays can also be affected depending on the assay platform. So a common clinical misstep is to treat the lab burnout rather than the patient. So if your patient symptoms don't match this new endocrine emergency that the lab appears to be showing, ask, are they taking biotin? This is commonly in hair and nail supplements or buried in the myriad ingredients of another fix all supplement. So you need to find out if it's in any of those. The easiest thing is to say, tell me all of the supplements and the brands you're taking. And then I usually do a quick internet search right there to find out if biotin's in there. And so the lowest friction fix is generally to repeat the test after holding biotin for an appropriate interval. At least a week is usually a safe time to guess about. The key is coordination with the laboratory. Not every lab behaves the same and some systems now actually have evolved mitigations, which is quite helpful. So that's the biotin update. So remember, biotin deficiency is treatable and sometimes urgent. And also, biotin supplementation is now a common lab confounder that can trigger avoidable diagnostic and therapeutic errors. Thanks for spending a few minutes with me. This is Stacey Clardy, and that's your lab minute.  

In this episode, Dr. Stacey Clardy reviews the February 23rd Capitol Hill Report, recapping key takeaways from Neurology on the Hill. Stay updated with what's happening on the hill by visiting aan.com/chr.  Learn how you can get involved with AAN advocacy.  Show transcript:  Dr. Stacey Clardy: Hi, this is Stacey Clardy with today's Neurology Minute. It's an advocacy update from the AAN's Capitol Hill Report. More than 200 AAN members came to Washington, DC, last week for the AAN's annual advocacy fly-in, Neurology on the Hill. As you probably know, this is the annual chance for neurologists to get some face-to-face time with members of Congress or their aides in the US right on Capitol Hill. AAN members had three asks for this year's event. We did cover them last week individually on the Neurology Minute, so have a listen if you want more detail, but I'll review them quickly.  First, we asked for a permanent inflationary update to physician reimbursement based on the Medicare Economic Index and to raise the outdated budget neutrality triggers in the Medicare physician fee schedule. Under the current system, the AAN needs to ask Congress nearly every year to fix a proposed cut to physician payment under Medicare, so it's time for a better solution. The second ask, AAN members requested their legislators to co-sponsor the Connect for Health Act in the US. This legislation would support patient access to care by making those old COVID era telehealth flexibilities now permanent rather than requiring repeated extensions. And the need to make these flexibilities permanent was especially clear in the US during the 2025 government shutdown when Medicare recipients' access to telehealth lapsed for about 45 days. And finally, the third ask was for the BRAIN Initiative at the National Institutes of Health, it's a very important program funding basic research into the brain and it's losing a key funding stream that was previously provided through the 21st Century Cures Act, so the AAN members asked their legislators to close the gap by supporting $468 million in funding for the BRAIN Initiative in 2027. If you didn't go to Neurology on the Hill but want to support these causes, check the AAN's Advocacy Action Center, and you could contact your representative that way. Outside of DC news, a number of state legislators are considering bills that positively or negatively affect neurology. The AAN has weighed in on several of those bills with advocacy letters. The bills it supported include later school start times in Pennsylvania, restricting AI prior authorization denials in Florida and Hawaii, mandating coverage for telehealth services in Massachusetts, and reducing prior authorization burdens in Arizona and Kansas. The AAN opposed a New York bill, however, that would give chiropractors the ability to evaluate and diagnose neuromusculoskeletal conditions and provide consultation advice and recommendations on neurology. So you can find links and more in the Capitol Hill Report. It's available on aan.com/CHR, that's short for Capitol Hill Report, and in US members' email inboxes. That's it for this time. Thanks. I'm Stacey Clardy for The Minute. 

In the March episode of the President's Spotlight, Dr. Jason Crowell and Dr. Natalia Rost share key updates and strategic insights for the upcoming April meeting in Chicago.  Stay informed by watching the President's Spotlight video.   Show transcript:  Dr. Jason Crowell: Hey, this is Jason Crowell. Thanks for listening to today's Neurology Minute. Once again, this month, we have Natalia Rost joining us, the president of the AAN for her presidential spotlight. Natalia, the sun is starting to come out. The flowers are starting to bloom. Spring is here. What is going on with the academy? What would you like to tell us about this month? Dr. Natalia Rost: These are exciting times indeed. Our annual meeting is just one month away. And so I'm looking forward to all of us coming together to learn, share ideas, and to connect. And this year, the world's largest neurology event is even larger. And I like to say it's my meeting of 15,000 friends. Dr. Jason Crowell: Terrific. For those who are listening today who haven't heard about the annual meeting, what would you like for them to know about it? Dr. Natalia Rost: Well, so the meeting takes place April 18th through 22nd in Chicago and online. And like so many, I love Chicago. It's a world-class city. It's a major travel hub and making it easy for many of us to attend. And we're expecting presentations of more than 3,500 abstracts. It's a new record for our meeting. Registration is also trending ahead of previous years, so now is the time to make your plans. Dr. Jason Crowell: And what would you say are the three things that you look forward to the most every year at the meeting? Dr. Natalia Rost: Well, first of all, the Sunday of this meeting, April 19th, is our research day, which will focus on advancing neuroscience and the AAN's renewed commitment to research funding we talked about last month. It includes my presidential plenary, which is titled Neuroscience at the Crossroads, and which will feature interactive panels of seasoned neuroscience leaders and clinician scientists who are right in the midst of their exciting careers. We will have our research hub to take part in many opportunities to support our high quality research program, so that's going to be great. Another highlight is a celebration of the extraordinary accomplishments of Dr. Walter Koroshetz, the immediate past NINDS director, and a phenomenal neurologist who is our 2026 President's Award winner and who will join us at the Presidential Plenary. This is going to be a very special and spirited event. And also, I'm excited to debut the new Brain Hub this year. I hope folks will stop by. Along with that, we have a special museum exhibit and reception for the Neurology Journal's 75th anniversary. I sure will be stopping by both. Dr. Jason Crowell: I would say that people in the world of medicine often misunderestimate just how much fun neurologists can be. What fun is planned for the annual meeting this year? Dr. Natalia Rost: Oh yeah, we're on it. As always, we will have our celebrated annual meeting party on Sunday night. This year, the entire Griffin Museum of Science and Industry will be hours to explore while you enjoy your food, drinks, and conversation with colleagues. Dr. Jason Crowell: And for our listeners, where can they learn more about the annual meeting and all the details? Dr. Natalia Rost: Please register now at aan.com/am. This is an annual meeting you won't want to miss, so join me with everything neurology premier event has to offer. Dr. Jason Crowell: Terrific. Natalia, thanks so much. Looking forward to Chicago.  

Dr. Tesha Monteith and Dr. Patricia Pozo-Rosich discuss the latest advancements in headache medicine, focusing on key research findings from 2025.  Show transcript: Dr. Tesha Monteith: Hi, this is Tesha Monteith with the Neurology Minute. Welcome to our 2026 Headache Medicine Series. I've just been speaking with Patricia Pozo-Rosich about all of the exciting advances in headache medicine in 2025. For a minute, why don't you summarize some of the key advances in headache medicine research? Dr. Patricia Pozo-Rosich: I think that we have good news in headache. We are currently phase two trials for two or three different compounds, anti-part two, packup and new toxins. So we are actually, I think, excited to find out the phase 2B trial results and phase three. So well, that's something that I think is worth mentioning. Then I think it is important to remember that we have new data coming from real world evidence with long-term use of anti CGRP therapies. We also have data that shows that anti CGRP therapies are useful for patients with migraine and major depressive disorder, as well as as children. Finally, I think that it is very important to remind everyone that there are new papers on practice recommendations around the world on how we have to treat our patients with migraine, and that is related both to the acute and preventive therapies. And finally, couple of position statements that have been written by the International Hague Society that strive to improve the quality of how migraine individuals are treated, and that really conveys a paradigm shift where we probably should be starting preventive therapy sooner than later. Dr. Tesha Monteith: Great. Thank you so much for that quick summary. And please check out the Full Headache Medicine series. I appreciate talking to you, Patricia, and look forward to discussing more highlights next time. Dr. Patricia Pozo-Rosich: Thank you, Tisha. See you very soon. Dr. Tesha Monteith: And thank you for listening to the Neurology Minutes.

In part two of the series, Dr. Andy Southerland and Dr. Seemant Chaturvedi break down key takeaways from the OCEANIC‑STROKE trial.  Show citation:  Read more about the OCEANIC-STROKE trial.  Show transcript:  Dr. Andy Southerland:  Hello everyone. This is Andy Southerland from the University of Virginia. For today's Neurology Minute, I've just been speaking with my colleague, Seemant Chaturvedi from the University of Maryland, about exciting trials presented at this year's 2026 International Stroke Conference from the American Heart Association, American Stroke Association. And the one we want to discuss for today's Neurology Minute in brief was the OCEANIC-STROKE trial. This was a very large international trial looking at the use of a novel antithrombotic agent, a Factor XI inhibitor, compared to placebo as an adjunct to our traditional antiplatelet therapies for secondary stroke prevention. And it was received with quite a bit of excitement. So Seemant, tell us in brief, what did we learn from OCEANIC-STROKE? Dr. Seemant Chaturvedi:  One new class of agents, which is being tested are the Factor XIa inhibitors. And this has a unique mechanism of action, and it's believed that it can reduce thrombotic events without causing an increase in bleeding, which would be truly a major breakthrough. And so in OCEANIC-STROKE, over 12,000 patients were enrolled with either stroke or high-risk TIA within 72 hours of the last event. And the trial found that patients who had fairly mild strokes with a median NIH score of two, that when you add the asundexian 50 milligrams per day on top of either dual antiplatelet or single antiplatelet therapy, that there was an improved outcome and reduction in stroke with asundexian. There was a 2.2% absolute reduction in ischemic stroke, 26% in relative terms. Stroke, MI, and vascular death was also reduced with asundexian, as was disabling stroke. An exciting finding was that major bleeding was not increased with asundexian. And so this confirmed the preclinical hypothesis. And so I think this was a significant result in terms of reducing recurrent ischemic stroke without increasing bleeding. And so I think we eagerly await the full publication, and I think it could be applicable to many of the patients that we see in our clinical practice. Dr. Andy Southerland:  So asundexian, folks, you'll hear more about this as the drug hopefully comes on the market and we see the full primary publication of this OCEANIC-STROKE trial, but exciting nonetheless to have a possible new treatment to help us reduce the risk of recurrent stroke for our patients. So Seemant, thanks so much again for joining us for today's Neurology Minute. And I encourage all of our listeners, as always, to listen to the full podcast interview ain The Neurology Podcast. Seemant, thanks for joining us. Dr. Seemant Chaturvedi:  My pleasure.  

In part on of this series, Dr. Andy Southerland and Dr. Seemant Chaturvedi discuss two trials highlighted at the 2026 International Stroke Conference.  Show citation:  Read more about the CHOICE-2 trial.  Show transcript:  Dr. Andy Southerland: Hello everyone. This is Andy Southerland. And for this week's Neurology Minute, I have just been speaking once again with my colleague, Seemant Chaturvedi, about his impressions from this year's 2026 American Heart Association, American Stroke Association International Stroke Conference. We've discussed a number of the very exciting pivotal trials presented at this year's meeting that occurred just a couple of weeks ago. But for the minute today, we want to just highlight two that were represented as late breaking trials in the world of acute stroke treatment. And the first was OPTION, which was a trial looking at extended window thrombolysis patients between four and a half and 24 hours. And the second was in the use of thrombolysis as an adjunct local treatment in patients receiving thrombectomy. So Seemant, to the best of your ability in our brief snippet today, what were the main highlights from these studies? Dr. Seemant Chaturvedi: In the OPTION trial, 570 patients were enrolled from China, and these were patients in the four and a half to 24 hour window with no evidence of large vessel occlusion. And they had a mismatch present at baseline imaging, median NIH score was seven. And when the tenecteplase was administered in this select group of patients, there was improvement in the excellent outcome of about 44% with tenecteplase and 34% with placebo. And there was a slight increase in hemorrhage of about 3%, but no increase in mortality. The second trial, CHOICE-2, also looked at thrombolysis, but it looked at local intraarterial thrombolysis following thrombectomy. And they enrolled patients with a median NIH score of 15 and the patients were enrolled from Spain and they gave a local TPA versus placebo following successful thrombectomy. And they also reported improved outcomes with about 57.5 having an excellent outcome with intraarterial TPA compared to 43% with placebo. There was slightly increased mortality in the TPA group, but this didn't seem to be explained by intracerebral hemorrhage. And so I think both of these were very intriguing and they add some complexity to acute stroke treatment. And so primary stroke centers and comprehensive stroke centers need to discuss the results with their teams and see if they want to embrace these treatment options. Dr. Andy Southerland: Fantastic, Seemant. So bottom line is thrombolysis is much more than it used to be in that very narrow time window and that very narrow indication. There are now patients who may benefit in that extended time window, and it's also being shown to have benefit in cases in which we get incomplete reperfusion with our traditional mechanical thrombectomy. So take that and run with it. Hopefully we can apply it to our stroke systems of care and help patients. Thank you again, Seemant for being with us on today's Neurology Minute. Seek out the full interview and also the primary publications as well.  

In part four of this series, Dr. Tesha Monteith explores the true potential of AI integration in medical education.  Show transcript:  Dr. Tesha Monteith: Hi. This is Tesha Monteith with the Neurology Minute. I've been speaking with Roy Strowd, Jeff Ratliff, and Justin Abbatemarco about the use of AI in neurology education for the neurology podcast. My take is that we're just getting started with this stuff, including the true potential of AI integration in medical education. In my regular work, I used AI to generate clinical case vignettes that help trainees practice diagnostic reasoning, and also to create patient images that better reflect the cultural diversity of our neurology population. Beyond content creation, AI has helped me evaluate my curriculum by identifying gaps and strengths to better train fellows and residents. I've even used it as a tool to help me frame feedback, highlighting strengths, identifying areas for growth, and to provide a more forward-looking feedback approach. AI still needs work. It should be monitored and scrutinized, and it certainly can't replace us, but it can provide meaningful augmentation of how we teach and how our learners develop. This is Tesha Monteith. Thank you for listening to the Neurology Minute.

In part two of this series, Dr. Justin Abbatemarco, Dr. Marjo S. van der Knaap, and Romy J. van Voorst discuss the patient management card and how patients should use it.  Show citation: and Clinical Management of Vanishing White Matter. Neurology. 2025;105(11):e214320. doi:10.1212/WNL.0000000000214320  Show transcript:  Dr. Justin Abbatemarco: Hello and welcome back. This is Justin Abbatemarco here with Romy J. van Voorst and Dr. Marjo S. van der Knaap. After discussing her article, Published Neurology Consensus Base Expert Recommendation for Diagnosis and Clinical Management of Vanishing White Matter Disease. Romy, I really want to talk with you about the patient management card. What inspired you to create that in this publication, and how should patients use that? Romy J. van Voorst:  So what the main motivation was of the study was actually a previous study that we did before. And in this study, we looked at the impact of any short matter on unaffected family members. And we found out that actually many family members encountered clinicians that were unfamiliar with its disease or disease-specific management. And during interviews, we saw that there was an urgent need for moral harmonization of care and also symptom management because families felt like they are left alone with just their child and no guidance on how to go further. And we wrote these recommendations to help families better understand the diagnostic and care process so they can also participate in informed decision-making. So they can understand what kind of preventive measures they can take and whether or not this interferes, for example, with quality of life goals. So there are a lot of different recommendations families can take home with. Dr. Justin Abbatemarco:  Marjo, anything else you want to add there? Dr. Marjo S. van der Knaap:  Yeah, I think the management card also helps because they have a physical card when they go to consultation or to emergency room that they can hand over. It's an official publication. It's developed by the Finishing WebMetter Expert Consortium in combination with other experts in combination with patient advocates and representatives. And so it's really a sort of a guidance that cannot be denied. So it has some authority to it. Dr. Justin Abbatemarco:  But I think it's a theme that applies to many neurological diseases, and addressing that. You do it really practically. And I agree, giving something more tangible for patients to present, especially to non-neurologists to help them give some guidance. It's an idea that we need to think about in clinic all the time on how we're interacting and supporting caregivers and when they're interfacing with the medical community at large. So I love what you guys have done here and to make us think about this more broadly. Thanks again for all your time and your work on this topic. Dr. Marjo S. van der Knaap:  Thank you for having us. 

Dr. Andy Southerland and Dr. Shyam Prabhakaran explain the significance of these guidelines and why they are important.  Show citation:  Prabhakaran S, Gonzalez NR, Zachrison KS, et al. 2026 Guideline for the Early Management of Patients With Acute Ischemic Stroke: A Guideline From the American Heart Association/American Stroke Association. Stroke. Published online January 26, 2026. doi:10.1161/STR.0000000000000513  Show transcript:  Dr. Andy Southerland: Hello everyone. This is Andy Southerland from the University of Virginia. And for this week's Neurology Minute, I've just been speaking with my colleague, Shyam Prabhakaran, from the University of Chicago, who was the Chair of the 2026 AHA/ASA guidelines for the early management of patients with Acute Ischemic stroke published in the January 2026 online version of the journal, Stroke. So Shyam, in our brief Neurology Minute today, why don't you just give a plea about why these guidelines are so important? Dr. Shyam Prabhakaran: Thanks, Andy. These guidelines are the first guidelines since 2019, so a lot has happened. So when you look at these guidelines, you'll see a lot of new recommendations. In fact, I think the majority have been revised in some way or another. And I'd point to the actual guideline document, which is in the journal Stroke online January '26, and the print version will be for the March edition of the journal Stroke. In addition to that, I'd say because you want to have interpretability and ease of practice, there are a bunch of derivatives on the AHA website that are very useful. They include case studies, they include figures and workflows that could be really useful for you to have these conversations. And there's even a slide deck that was prepared by our AHA ambassadors. There are these young whippersnappers that did a great job putting together a slide deck for anyone to use. They can use that to have conversations locally or anywhere they want. I encourage people, read the guidelines, but then also use the derivative products that people spent a lot of time on developing. Dr. Andy Southerland: Thank you, Shyam. I think that's a great message from the Chair of the writing group, that when you look at these guidelines, they can seem daunting. But the way you all have provided all these additional resources and analogs for people to interpret it and apply it in their own stroke centers and practice, I think folks definitely will be running out to do that, just to seek out the full guideline, and let's apply all this great new evidence to better care for our patients. So Shyam, thanks again for joining us for this week's Neurology Minute. 

In part one of this two-part series, Dr. Justin Abbatemarco, Dr. Marjo S. van der Knaap, and Romy J. van Voorst discuss vanishing white matter disease, focusing on the clinical and MRI findings that would prompt the consideration of genetic testing.  Show citation: van Voorst RJ, Schoenmakers DH, Bonkowsky JL, et al. Consensus-Based Expert Recommendations for Diagnosis and Clinical Management of Vanishing White Matter. Neurology. 2025;105(11):e214320. doi:10.1212/WNL.0000000000214320  Show transcript:  Justin Abbatemarco: Hello and welcome. This is Justin Abbatemarco here with Romy J. van Voorst and Marjo S. van der Knaap. After discussing their article published in Neurology, Consensus-Based Expert Recommendation for Diagnosis and Clinical Management of Vanishing White Matter. They both work for Amsterdam University Medical Center in the Netherlands. And we're going to have a two-part episode dissecting maybe two elements of this paper. Marjo, maybe we could start here and just talking about what vanishing white matter disease is and what in the clinic and MRI findings would make us go towards a genetic testing. Dr. Marjo S. van der Knaap:  There are two things about vanishing white matter that matter most to families, and one is the stress sensitivity. So any type of physical stress, like fever, viral infection, anything may cause a rapid decline and you never know when it comes. And that brings me to the second item that's very difficult and painful for families. And that's the unpredictability. You never know when a disease is going to hit and then your child is going to go down. So you really need the support of neurologists who know about this disease and help you go through this situation. Dr. Justin Abbatemarco: Right. And this paper serves as a great resource for folks that if they have a patient in clinic like this, medications to avoid, how to manage those stress responses. And so it's a really helpful publication to have there. And then I think another message we talked a lot about on the podcast was the importance of genetic testing when patients aren't fitting a typical bucket and this specific disease has unique characteristics. I think the cystic appearance of the MRI, which you do a great job highlighting, would really lead us down that road. So I think it's all really helpful and it gives us some ways to start in clinic with patients and our caregivers. So thank you. Come back and join us for the second part of The Neurology Minute episode where we're going to talk about the patient management. 

In the final episode of this three-part series, Dr. Stacey Clardy and Max Goldman talk about telehealth.  Stay updated with everything related to Neurology on the Hill. Show transcript:  Dr. Stacey Clardy: Hi, this is Stacey Clardy, and today we're wrapping up our three-part series covering the Top Advocacy Issues for Neurology on the Hill 2026 in Washington, DC. This is the event where many neurologists fly in from all over the country to meet with our elected representatives to discuss the issues of the most importance to our patients, and to allow us to continue to take good quality care of our neurology patients. We have again back with us, Max Goldman. He's the Director of Congressional Affairs from the AAN Legislative Team. Max, we covered Medicare, we covered neuroscience research in the Brain Initiative. The third and final issue is telehealth. What do we need to accomplish on telehealth in Washington, DC this year? Max Goldman: The telehealth flexibilities provided with the COVID-19 public health emergency have been so important to providing neurological care to patients across the country. However, what we saw during the government shutdown at the end of 2025 was a lapse in those flexibilities, which caused a huge amount of panic, of uncertainty for both our members, the AAN, who are providing care, and patients who relied on care through telehealth from their neurologist. That can't happen again. These flexibilities have been extended short-term basis for one year, two year, a couple of months, and what we need now is a permanent extension of these flexibilities so they can't lapse again, and our patients know they can access the care they need. What we're doing at Neurology on the Hill is going to ask our members of Congress to co-sponsor the Connect for Health Act. This bill would permanently extend telehealth flexibilities, including a full extension of protection of audio-only visits, which is important for folks in areas without great broadband or access to internet. This would just be a really good bill. It's got a lot of momentum this year, and we're hopeful that this will finally make telehealth a permanent part of neurological care going forward. Dr. Stacey Clardy: So important. I certainly know out here in Utah where we cover several rural states, this has really been a lifeline to our patients. To learn more about this issue and the other issues being discussed at Neurology on the Hill, you can go to AAN.com and click on advocacy. Thanks for listening, and thank you Max, for representing us in DC.   

In the second installment of this three-part series, Dr. Stacey Clardy and Max Goldman discuss neuroscience research and the BRAIN Initiative.  Stay updated with everything related to Neurology on the Hill. Show transcript:  Dr. Stacey Clardy:  Hi, this is Stacey Clardy. We are going to continue with our three-part series today about the top advocacy issues covered at Neurology on the Hill 2026 in Washington, DC. Again, as many of you know, this is the AAN's annual advocacy fly-in event. Neurologists come from all over the US to Washington and meet with elected representatives to discuss issues of high importance to allow us to continue providing high-quality care to patients in the US with neurological diseases. In the first minute, we discuss the topic of Medicare, and I have with me again, Max Goldman, director of Congressional Affairs from the AAN legislative team, to talk to us about issue number two, which is neuroscience research, and specifically the BRAIN Initiative. Max, what are we going to discuss about neuroscience research? What do we need to happen in order to continue doing high-quality research? Max Goldman: So, this one is so important, and there's this wonderful program at the NIH called The BRAIN Initiative. This was founded in 2013, really reinforced in 2016 with the 21st Century Cures Act. It's just funding for basic research into how the brain works, right? And the idea behind this is that if we can understand how the brain works, we can find the next generation of treatment or cures for neurological conditions, psychiatric conditions, and issues that go through the brain. This year, we are in a precarious position. Mandatory funding for this program is expiring, and so we're going to lose a lot of money and a lot of opportunities to provide more grants to people to figure out how the brain works. So, what we are doing on Neurology on the Hill is we're asking members of Congress to support $468 million in funding in fiscal year 2027 for the BRAIN Initiative, so we can keep up the good work and keep working towards the next generation of treatments and cures for neurological conditions. Dr. Stacey Clardy: So important. Thank you, Max. To learn more about this issue and the other two issues, you can go to AAN.com. Click on advocacy. And stick with us for the third Neurology Minute, where we will get to the final issue to be discussed, telehealth. 

In the first part of this three-part series, Dr. Stacey Clardy and Max Goldman discuss the state of Medicare in 2026. Stay updated with everything related to Neurology on the Hill. Show transcript: Dr. Stacey Clardy: Hi, this is Stacey Clardy. Today, we're going to start the first of a three-part series about the top advocacy issues at Neurology on the Hill 2026 in Washington, DC. As many of you know, this is the AAN's Annual Advocacy fly-in event in the US, where neurologists come to Washington and meet with our elected representatives to discuss the issues that are important for all of us in the US to continue providing high-quality care to patients with neurological diseases. Every year in preparation for this event, the AAN selects a few issues to focus on with our lawmakers, and we're going to cover those in a three-minute series. We have Max Goldman, the Director of Congressional Affairs from the AAN Legislative Team, to give us the details. Max, the first topic that will be covered at Neurology on the Hill this year is Medicare. What do we need to know about the state of Medicare in 2026? Max Goldman: Thank you so much for having me. As many of you know, the way the Medicare physician fee schedule works and the way that you all are reimbursed for the care you provide patients across the country has been broken for several years. We have this cycle of indiscriminate cuts that keeps happening, where the CMS will present a fee schedule, it'll have a cut for you all, then we have to go to Congress to beg for them to fix the cut. This year, we are talking to Congress about a structural reform that they can make, so we don't have to do that anymore, and the reimbursement that you all receive is commensurate with cost of actually providing care. This year we're going to ask for two things. We're going to ask for them to adjust the triggers to the budget neutrality requirement in the fee schedule, meaning that CMS can make some more changes to the fee schedule without requiring cuts to everyone's reimbursement, and we're going to request that they provide a permanent inflationary adjustment to physician reimbursement so that the reimbursement you get is in track with the cost of providing care in any given year. Dr. Stacey Clardy: Thanks for that summary. Here's hoping to get some traction on that. To learn more about this issue, you can go to aan.com and click on advocacy. And in the upcoming two minutes, we are going to discuss the other issues being brought to Congress at Neurology on the Hill. Thank you for listening to today's Neurology Minute. 

Dr. Alex Menze and Dr. Divyanshu Dubey discuss the clinical insights into autoimmune nodopathies, particularly focusing on CASPR1 and CASPR1/CNTN1-complex-IgG.  Show citation:  Paramasivan NK, Basal E, LaFrance-Corey RG, et al. Clinical Insights Into CASPR1 and CASPR1/Contactin-1 Complex Autoimmune Nodopathies. Neurology. 2026;106(5):e214403. doi:10.1212/WNL.0000000000214403 Show transcript:  Dr. Alexander Menze: Hi, this is Alexander Menze. I just finished interviewing Divyanshu Dubey for the Neurology podcast. For today's Neurology Minute, I'm hoping you can tell us the main points of your paper. Dr. Divyanshu Dubey: Our paper talks about a rare form of autoimmune neuropathy associated with antibodies, CASPR1, as well as CASPR1/Contactin-1 complex IgG. These patients present with similar to CIDP, IDP, but tend to have more rapid progression, often a lot of sensory features preceding motor deficits including sensory ataxia in the contact and CASPR complex cases and presence of neuropathic pain in some of the CASPR1 cases. These patients, similar to other neuropathies are refractory to IVIg, but respond relatively well to rituximab.  Dr. Alexander Menze: Thank you. Be sure to download this week's podcast to hear our full interview.  

Dr. Halley Alexander and Dr. Alissa M. D'Gama discuss genetic testing for infantile epilepsies.  Show citation:  Nguyen JNH, Lachgar-Ruiz M, Higginbotham EJ, et al. Diagnostic Yield of Comprehensive Reanalysis After Nondiagnostic Short-Read Genome Sequencing in Infants With Unexplained Epilepsy. Neurology. 2026;106(6):e214645. doi:10.1212/WNL.0000000000214645  Show transcript:  Dr. Halley Alexander:  Hi, this is Halley Alexander with today's Neurology Minute, and I'm here with Dr. Alissa D'Gama from Boston Children's Hospital and Harvard Medical School, and we just finished recording a full-length podcast about some exciting new work in genetic testing for infantile onset epilepsies. Alissa, can you tell us what you found briefly and why it's important for neurology care? Dr. Alissa D'Gama:  Infantile epilepsies are relatively common, and they're associated with substantial burden of disease, and we know that identifying underlying genetic causes can impact clinical care. It's important for emerging precision therapies. But even after genome sequencing, which is the most comprehensive clinical genetic testing currently available, most infants remain genetically unsolved. And so what we did was take that genome sequencing data and reanalyze it for a cohort of infants who had unexplained non-acquired epilepsy and non-diagnostic genome sequencing, and in about 5% of cases, our reanalysis was able to identify a genetic diagnosis, and all of these diagnoses had impact on clinical care for their infants and their families. In some cases, we could incorporate new information, either new clinical information about the patient or new scientific methods or information about disease associations, and in other cases, we were able to incorporate new analysis methods to identify variants. And so our findings suggest that implementing reanalysis for infants or any individual with epilepsy within a year or two of non-diagnostic testing may be useful. Dr. Halley Alexander:  Thank you so much, and you can find a lot more details by listening to the full-length podcast, which is available now on the Neurology podcast, and you can find the full article in the March 10th issue of Neurology or online at neurology.org. As always, thanks for tuning in for today's Neurology Minute. 

In part three of this series, Dr. Jeff Ratliff discusses how access to information is not the same as clinical confidence. Show transcript:  Dr. Jeff Ratliff:  Hi, this is Jeff Ratliff from Thomas Jefferson University, and this is your Neurology Minute. I'm back again with a Neurology Minute episode to complement the podcast discussion I had with Roy Strowd, Justin Abbatemarco, and Tesha Monteith on the topic of technology-driven shifts in neurology education. In the episode, we touched on podcasting, AI-based learning, and social media on neurology education as a panel discussion. While there is still tremendous utility and promise and excitement around these tools, I think it's still helpful for us all to remember that access to information is not the same as clinical confidence. With tools like podcasts, learners can hear expert discussions on their commute or review topics in new interactive formats. With AI tools, learners can simulate talking to patients with a multitude of neurologic conditions. These digital tools can provide answers at hours, and our learners fingertips much more readily than even recent years. But as we watch the explosion of these tools impact, we must keep in mind the value of bedside clinical teaching. As teachers, as educators, there's still a great impact we can have by watching a resident examine a patient with ataxia, or coaching them through a difficult conversation with a patient. We can still help them teach the skill of reasoning through their clinical encounters in real time so that they can remember to ask that key history question, or to add in that critical exam maneuver. So, as impressive and impactful the latest and greatest teaching tool may be, I encourage you all not to shy away from going back to the bedside with the student, the resident, or fellow working with you today. Thanks for listening to the Neurology Minute. We'll see you next time.

In part two of this series, Dr. Jeff Ratliff discusses the expanding role of AI and digital tools in neurology education, emphasizing the importance of verifying information and developing source literacy.  Show transcript:  Dr. Jeff Ratliff: Hi, this is Jeff Ratliff from Thomas Jefferson University, and this is your Neurology Minute. I recently recorded a podcast episode with Roy Stroud, Justin Abadamarko, and Tisha Monteith, where we discussed the growing impact of technology in neurology education. In this episode, we touched on podcasting, AI-based learning and social media in neurology education, all as a panel discussion. As an accompaniment to that conversation, we're releasing a series of Neurology Minute episodes, exploring those tools. Today I want to focus an important caution, verification. With increasing use of digital tools, AI or otherwise. The need for caution and verification of sources is even more important. Large language models and other AI tools are very frequently used by trainees at all levels. To summarize topics, generate explanations, and even draft a differential diagnosis. But as you all know, the outputs of these tools can be efficient and really impressive, but we need to keep in mind that potential issues with reliability. While less and less common, these tools may hallucinate producing information that sounds authoritative and sounds correct, but it's actually outdated or maybe even unsupported by evidence. So for those of us teaching at the bedside or in clinic, this means we have a responsibility to help our learners develop literacy towards AI and other digital tools. We have to be critics of our sources. As neurologists, we can role model asking questions like, where did this information come from and how do we verify it, and did you read the study that they cited? We encourage trainees to trace these claims back to the primary literature or to pull up guidelines or other trusted review sources just as we do in our own practice. I don't want to pour water on the AI enthusiasm. The truth is still that AI education tools can be a powerful adjunct for learning, but we should treat it like an assistant, not a supervisor. It's useful, it's fast, but it's still in need of our own supervision. Please tune into our podcast discussion to hear more about the rapidly changing landscape of neurology education. Meanwhile, thanks for listening to the Neurology Minute.   

In part two of this series, Dr. Tesha Monteith and Dr. Andrew Hershey discuss appropriate treatment strategies to prevent migraines in children and adolescents. Show citation:  Hershey AD, Szperka CL, Barbanti P, et al. Fremanezumab in Children and Adolescents with Episodic Migraine. N Engl J Med. 2026;394(3):243-252. doi:10.1056/NEJMoa2504546  Show transcript:  Dr. Tesha Monteith: This is Tesha Monteith with the Neurology Minute. I'm back with Andrew Hershey, professor of Pediatrics and Director of the Division of Neurology at Cincinnati Children's and the Children's Headache Center. This is part two of our discussion on his paper published in the New England Journal of Medicine, fremanezumab in Children and Adolescents with Episodic Migraine. Andrew, now that we have fremanezumab approved for prevention of episodic migraine in children and adolescents, and we have a number of other devices and treatments for patients that can be used as part of FDA-approved treatment or even off-label, can you discuss an appropriate treatment paradigm to prevent migraine? Dr. Andrew Hershey: I think the first and foremost part of the paradigm is to identify the disease, so recognition that headaches are a component of the disease migraine, so you have headaches attacks due to migraine is an essential part. Many of the children, adolescents and their families are unaware that that is even what they're having, and clarifying the etiology actually goes a long way. One of my former mentors, Dr. Prensky, always said that 50% of kids get better from just seeing a child neurologist, and I think it's that clarification of the diagnosis. Second to that, you need to provide a very adequate acute treatment as well as what's probably even more essential than anything else is healthy lifestyle habits. So regular eating, drinking, sleeping, and exercise. And then finally, if the headache is causing severe disability or frequent headaches or interfering with the child's school, home or social life, the prevention medications may need to be added. And this is where the fremanezumab, or if you prefer devices, devices can be used for both the acute and preventive treatment. Dr. Tesha Monteith: Well, thank you for the summary, and congratulations again on your paper. Dr. Andrew Hershey: Thank you. Dr. Tesha Monteith: Do check out the full podcast for more details about the paper and treatment of migraine in children and adolescents. This is Tesha Monteith. Thank you for listening to the Neurology Minute.

Dr. Greg Cooper and Dr. David G. Coughlin discuss the role of αSyn-SAAs in diagnosing DBL and their relationship with Alzheimer's disease biomarkers.  Show citation: Coughlin DG, Jain L, Khrestian M, et al. CSF α-Synuclein Seed Amplification Assays and Alzheimer Disease Biomarkers in Dementia With Lewy Bodies: Presentation and Progression. Neurology. 2025;105(12):e214346. doi:10.1212/WNL.0000000000214346 Show transcript:  Dr. Greg Cooper: Hi, this is Dr. Greg Cooper. I just finished interviewing Dr. David Coughlin for this week's Neurology Podcast. For today's Neurology Minute, I'm hoping you can tell us the main points of your paper. Dr. David Coughlin: The main points of this paper in my mind is that α-Synuclein seed amplification assays from cerebrospinal fluid samples is useful in confirming the presence of synuclein pathology in people with clinically suspected dementia with Lewy bodies. But also that, for people who have synuclein positivity, that the presence of Alzheimer's disease mixed pathology is associated with a worse cognitive progression over time. Dr. Greg Cooper: Thank you Dr. Coughlin, for that summary and for all of your work on this topic. Please check out this week's podcast to hear the full interview and read the full article published in Neurology, CSF α-Synuclein Seed Amplification Assays and Alzheimer's Disease Biomarkers in Dementia with Lewy Bodies. Thank you.

In part one of this two-part series, Dr. Tesha Monteith and Dr. Andrew Hershey summarize findings from the SPACE trial evaluating fremanezumab in adolescents and children with migraine. Show citation: Hershey AD, Szperka CL, Barbanti P, et al. Fremanezumab in Children and Adolescents with Episodic Migraine. N Engl J Med. 2026;394(3):243-252. doi:10.1056/NEJMoa2504546  Show transcript:  Dr. Tesha Monteith: Hi, this is Tesha Monteith with the Neurology Minute. I'm here with Andrew Hershey, Professor of Pediatrics and Director of the Division of Neurology at Cincinnati Children's and the Children's Headache Center. We're here talking about his new paper published in the New England Journal of Medicine, Fremanezumab in Children and Adolescents with Episodic Migraine. Andrew, thank you for being on our Neurology Minutes. Dr. Andrew Hershey: Thank you for inviting me. Dr. Tesha Monteith: Can you summarize the findings of the space trial investigating Fremanezumab for adolescents and children with migraine? Dr. Andrew Hershey: This is one of the four monoclonal antibodies against CGRP, or it's this receptor that had been proven effective for adults. And it's the first one, the formazepam, that's been able to report its effectiveness in children and adolescents with less than 15 headache days per month. This study looked at over 200 children adolescents that were in a double-blinded randomized placebo controlled study. And reached its primary, as well as its secondary endpoint of a reduction compared to placebo. And the number of attacks of migraine per month, as well as a greater than 50% reduction in the number of headache attacks per month, with minimal to no side effects, the most notable side effect being injection site erythema. Dr. Tesha Monteith: Great. Thank you so much for providing that update. Do check out the full podcast for more details about his paper and the treatment of migraine in children and adolescents. This is Tesha Monteith. Thank you for listening to the Neurology Minute.  

In this episode, Dr. Andy Southerland reviews the February 9 Capitol Hill Report, highlighting state-level advocacy efforts. Stay updated with what's happening on the hill by visiting aan.com/chr.  Learn how you can get involved with AAN advocacy.   

In the February episode of the President's Spotlight, Dr. Jason Crowell and Dr. Natalia Rost discuss the AAN's Research Program.  Stay informed by watching the President's Spotlight video. 

In the final episode of this series, Casey Kozak discusses functional sensory loss.  Show citation: Sonoo M. Abductor sign: a reliable new sign to detect unilateral non-organic paresis of the lower limb. J Neurol Neurosurg Psychiatry. 2004;75(1):121-125.  Show transcript: Welcome back to Neurology Minute. My name is Casey Kozak, and today we're finishing our discussion of functional neurological disorder and physical exam findings. We're going to now turn to functional sensory loss. But first, it's important to acknowledge that the subjective nature of sensory symptoms means that our physical exam tests will be less reliable than those used for functional weakness or movement disorders. Therefore, it's especially important that we as physicians listen carefully to the symptoms our patients are describing and remain aware of the potential for biases such as suggestion, when taking our histories. Nevertheless, there is certainly utility in physical exam tests as positive findings are present in many patients. We're going to discuss a few of these findings. The first is midline splitting, meaning that the patient's sensory loss has a clear edge at the midline of the body. For example, a patient may describe total sensory loss on the right side of their body, including their face, arm, and leg.  And on testing, their sensory loss resolves in exactly the middle of their trunk. This is an unusual finding for sensory loss caused by central lesions, as the trunk is typically spared. The one exception to this rule, however, are thalamic lesions, which may be caused by stroke or mass effect, for example. While midline splitting is not a sensitive finding, it has a relatively high specificity if present. The second finding is splitting a vibration sense. This time, you will use your tuning fork to measure vibratory sensation across a bone that crosses midline, such as the frontal bone or the sternum. The sensation should be the same across the entire bone as vibration is perceived throughout bone conduction. Splitting a vibration, meaning there is loss of vibratory sensation on the numb side of the body is consistent with functional sensory loss because it defies its principle. Unlike midline splitting, however, splitting a vibration sense has been found to have a much lower specificity in testing. Finally, sensory deficits may be precisely demarcated by anatomical borders, such as the shoulder or the groin, which is incongruent with peripheral nerve distributions. Beyond these examples, there are many more findings that can suggest FND in patients experiencing motor, sensory, or even visual, gait, or cognitive symptoms. Functional neurological disorder is a challenging disorder, though our understanding of it is improving. If you haven't yet, I highly encourage you to check out the seven-part Neurology Minute series on FND by Jon Stone and Gabriela Gilmour, focusing on recent advances in diagnosis and treatment. With that, thank you for joining us. 

In part one of this series, Dr. Justin Abbatemarco explores how to effectively reach today's learners through podcasts and social media. Show transcript: Dr. Justin Abbatemarco: Hello and welcome. This is Justin Abbatemarco, and I just got done finishing an episode on non-traditional educational formats reshaping neurology training. I was joined by some really terrific teachers and faculty members, Roy Strowd, Jeff Ratliff and Tesha Monteith, and it was really great hearing from these different perspectives. On today's Neurology Minute, we really want to talk about how we can reach our learners in today's learning environment, and I think two themes emerged from our conversations, especially around podcasts and social media. You know, the example I always think about is when we get done learning in either the bedside or clinic rounding, and I try to share some articles with our learners, I find that if I send a bunch of PDFs or textbook chapters, it just doesn't resonate as well these days. And so trying to reach learners where they're at, and I think podcasts and social media feeds allow for this kind of asynchronous, really engaging learning style. It allows for them to listen at a time that's convenient for them, to get the information in a different way in some audio or audiovisual type ways, and to hear from experts around the world that maybe have a different voice and can resonate the message in a different way, which I find really powerful. I think the other part of this is that those social media feeds allow for a sense of community that is hard to replicate in a traditional classroom, and the ability for them to, again, listen to an expert in a less intimidating circumstance or a setting, and then to hear from other learners on questions they've had really resonates with folks. I would really encourage everyone to listen to the entire interview with the entire team. It was, again, great to hear from all the different experts on this topic, and I appreciate your time, and that's today's Neurology Minute.

Dr. Andy Southerland and Dr. Dipika Aggarwal discuss her remarkable journey as both a physician and a patient. After overcoming stage four colon cancer, she experienced a life‑altering stroke that reshaped her perspective.  Show transcript: Dr. Andy Southerland: Hello everyone. This is Andy Southerland and for this week's Neurology Minute, I've just been speaking with our colleague, Dipika Aggarwal, who's a clinical assistant professor of neurology at University of Kansas, who's been sharing her story for the Physician's Patient series from Cancer Survivorship and as a stroke survivor. And for the Neurology Minute, we wanted to share an important pearl that Dipika shared with me in her interview about stroke recovery and specifically about mental health outcomes after stroke. So Dipika, please, share with us for the Neurology Minute. Dr. Dipika Aggarwal: So yes, my biggest takeaway point from my own stroke experience was the neuropsychiatric complications that can happen as a risk from stroke. The most important ones being post-stroke depression, post-stroke anxiety. Even if the literature says that they can happen just for 30% of the cases, in reality, I think the incidence is more. But then they can affect quality of life of the stroke survivor, the recovery, and even in some cases can affect their mortality. So I think it is really important for healthcare providers, especially the neurologists, to ask their patients how they are doing mentally or emotionally. I think it is as important as checking their vitals during every visit. It is as important as that, because again, it can affect their recovery. Dr. Andy Southerland: Well, thank you, Dipika. I think it's a good message for all of us in the busyness of our clinics and seeing patients in rapid throughput in and out of the hospital with stroke to make sure that not only in those early days, but also all the way out in the continuum of their recovery, to continue to come back to their mental health recovery. And their personal recovery, as you've articulated, which is so critical to one stroke recovery. And for this and more, I really encourage our listeners, please listen to the entirety of this interview. You will come away with it being a better neurologist for your patients. I promise you that. And I'm truly grateful again to Dipika for joining us for this week's Neurology Minute.

Dr. Aaron Zelikovich discusses recent survey findings highlighting the wide variability in how clinicians evaluate and diagnose small fiber neuropathy. Fill out the Neurology® Clinical Practice Current survey.  Show citation:  Thawani S, Chan M, Ostendorf T, et al. How Well do We Evaluate Small Fiber Neuropathy?: A Survey of American Academy of Neurology Members. J Clin Neuromuscul Dis. 2025;26(4):184-195. Published 2025 Jun 2. doi:10.1097/CND.0000000000000502  Show transcript:  Dr. Aaron Zelikovich: Welcome to today's Neurology Minute. My name is Aaron Zelikovich, a neuromuscular specialist at Lenox Hill Hospital in New York City. Today, we will discuss a recent article, How Well Do We Evaluate Small Fiber Neuropathy? A survey of The American Academy of Neurology members, which evaluates small fiber neuropathy in clinical practice. The current landscape of evaluating and testing for small fiber neuropathy remains highly variable in regards to serum testing, skin biopsy, and nerve conduction studies. In this survey study, 800 members of The American Academy of Neurology were randomly selected and emailed a survey. 400 neuromuscular physicians and 400 non-neuromuscular physicians were selected. The overall response rate was 30% with half of the completed surveys coming from neuromuscular physicians. The most common overall initial blood work for this patient population was a CBC, vitamin B12, basic metabolic profile, TSH, and hemoglobin A1C. Other high yield blood tests included ESR, SPEP, immunofixation, and ANA. 70% of responders would also order a nerve conduction study as part of the initial workup. Second line evaluation had less consensus and included skin biopsies for intraepidermal nerve fiber density, hepatitis panel, HIV, and paraneoplastic testing. Responders noted that if the patient had acute onset of symptoms, had symptoms that were asymmetric, or being under 30 years old, they would order a more extensive workup. The authors discussed the importance of both clinical exam, history, and diagnostic workup in patients with symptoms compatible with small fiber neuropathy. They highlight that there is no current objective gold standard for a diagnosis of small fiber neuropathy. The current diagnostic recommendation by the AAN for distal symmetric polyneuropathy includes serum blood sampling for glucose, vitamin B12, SPEP, and immunofixation. Clinical practice in the diagnosis of small fiber neuropathy remains highly variable based on the provider and clinical context of the patient. Neurology Practice Current is currently accepting surveys on clinical practice patterns for patients with small fiber neuropathy. Please check out the link in today's Neurology Minute to complete the survey. Thank you and have a wonderful day. 

In part three of this four-part series, Casey Kozak discusses the hip abductor sign as an option for assessing weakness in the lower extremities.  Show citation: Sonoo M. Abductor sign: a reliable new sign to detect unilateral non-organic paresis of the lower limb. J Neurol Neurosurg Psychiatry. 2004;75(1):121-125.  Show transcript: Casey Kozak: Hello, this is Casey Kozak with Neurology Minute, and today we're returning to physical exam tests for functional neurological disorder. This episode will piggyback off our last focusing on Hoover's sign, now focusing on other signs of functional weakness. Besides Hoover's sign, another option for assessing lower extremity weakness is the hip abductor sign. Remember that AB-duction means to move away from midline. To perform this test, the patient will be laying on their back. You will then place your hands on the outside of both of their legs. First, you will test the weak leg by asking the patient to push their weak leg outwards in AB-duction against the resistance of your hand. The weak leg will give way easily. Next, you will test the non-affected leg by asking the patient again to push outwards against the resistance of your hand. In a patient with functional weakness, the weak leg may exhibit spontaneous recovery of strength and push outwards against your resting hand while the patient is trying to push their unaffected leg out. This is an automatic effort by the body to remain midline by engaging the opposite leg, and just like with Hoover's sign, this is based on the principle that the contralateral limb will produce an opposite movement pattern. However, in organic neurological weakness from neurodegeneration, stroke, or peripheral nerve damage, this isn't possible. Therefore, the hip abductor sign is positive if AB-duction of the unaffected leg against resistance causes improvement in the weaker leg's abductor strength. If you're a visual learner like me, don't worry. There's a great diagram for the hip abductor test in a paper by Masahiro Sonoo that we have linked to this episode. What if a patient has upper extremity weakness? In this case, you can test for drift without pronation. Ask the patient to hold their arms up as of holding a large tray. Then, ask the patient to close their eyes and shake their head no to add distraction to the test and remove visual sensory input. Watch what their arms do. In normal neurological screening examinations, we test for pronator drift, in which the upper motor neuron damage causes a weak arm to fall while the hand pronates or turns inwards. However, in functional arm weakness, you may find that the patient exhibits dramatic drooping of the affected arm without pronation. Keep in mind, however, that this test is not entirely specific, and a musculoskeletal injury to the shoulder, even a remote one, may cause drift alone. If you notice this, it's helpful to inquire about past shoulder injuries. Finally, in any affected body part, you can test for give-way weakness, in which there is a sudden loss of resistance after initial good strength, like a switch was turned off. This abrupt collapse is inconsistent with muscle weakness originating in the musculoskeletal system or a central lesion, and may support a diagnosis with FND. All right, this gives us plenty to practice with, so let's break again. Join us for the last episode of this series in which we'll discuss functional sensory loss. Until then, happy studying.  

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.

Dr. Tesha Monteith and Dr. Michael Eller discuss the implications of CGRP therapies in migraine treatment, particularly for patients with vascular risk factors or a history of stroke.  Show citation: Eller MT, Schwarzová K, Gufler L, et al. CGRP-Targeted Migraine Therapies in Patients With Vascular Risk Factors or Stroke: A Review. Neurology. 2025;105(2):e213852. doi:10.1212/WNL.0000000000213852  Show transcript:  Dr. Tesha Monteith: Hi, this is Tesha Monteith with the Neurology Minute. I've just been speaking with Michael Eller from the Department of Neurology Medical University of Innsbruck, Austria on the neurology podcast on his paper, CGRP Targeted Migraine Therapies in Patients with Vascular Risk Factors or Stroke: A Review. Hi, Michael. Dr. Michael Eller: Hello. Dr. Tesha Monteith: Why don't you summarize your general approach to use of CGRP targeted therapies in patients that might be at risk for vascular events when considering safety? Dr. Michael Eller: Yeah. About acute vascular events, we should stop CGLP targeted drugs immediately. When we come to post-stroke, we should reassess the necessity of these targeted treatments after recovery. We suggest a minimum of three months pause after ischemic stroke to allow early recovery and remodeling, and then restart only after individualized benefit risk review. In high-risk primary prevention, so no stroke yet, but elevated risk, if the patients are 65 years or older with established cardiovascular disease, we should prefer traditional preventives. And if CGLP targeted therapy is essential, we should consider Gepants cautiously due to their shorter half lives. We should avoid CGLP targeted treatments in small vessel disease, distal stenosis, Raynaud's phenomenon, and uncontrolled hypertension. For acute migraine treatment, we can consider gepants or ditans as alternatives to triptans and NSAIDs in relevant stroke risk or post-stroke patients, individualized to comorbidities. Dr. Tesha Monteith: Great. And we should say that the label updates include hypertension and Raynaud's phenomenon as potential vascular complications. Otherwise, these are more theoretical risks based on what we know about CGRP. Dr. Michael Eller: Yes, I totally agree because large studies did not show any elevated cardiovascular risk signals. And for post-marketing databases, we did not see any elevated cardiovascular risk so far. However, in pre-clinical settings, studies showed large infarct size in pretreated mice. Dr. Tesha Monteith: Great. Well, thank you again for doing this work. It was a phenomenal read and congratulations. Dr. Michael Eller: Thank you. Dr. Tesha Monteith: This is Tesha Monteith. Thank you for listening to the Neurology Minute.

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.

In part two of this four-part series, Casey Kozak discusses Hover's sign, the most well-known test for FND.  Show transcript:  Casey Kozak:  Welcome back to Neurology Minute. My name is Casey Kozak with Rutgers, and today we're continuing our examination of functional neurological disorder. That is physical examination. This episode is dedicated to Hoover's sign, probably the most well-known test for FND, and in my humble opinion, one of the most confusing maneuvers to learn. So today, we're going back to the origin using Dr. Charles Franklin Hoover's original description. Maybe you've heard of Hoover's Sign, but when do we use it? Hoover's sign is useful when a patient presents with one-sided lower extremity weakness, and FND is on the differential. Because the test relies on one healthy leg, you can't perform Hoover's test on a patient with total lower-body paralysis. Now, how to perform Hoover's test. First, have the patient lie on their back and place their hand under the heel of the patient's weak leg. Then ask the patient to raise their strong leg off the plane of the bed. What do you expect to happen? Dr. Hoover made the astute observation that muscular resistance offered by the leg on the bed will be pressed onto the bed with the same force which is exhibited in lifting the strong leg off the bed. This is based on the principle that when one limb flexes, the contralateral limb extends. In this way, the leg on the bed acts as a sort of counterbalance to assist the action of raising the other leg. Okay, but what does this mean for our examination? Well, if a patient's leg was paralyzed as the result of a stroke, for example, the patient would not be able to create that downward resistance. In a patient with functional leg weakness, however, this action is still possible. Therefore, Hoover's sign is present if the weak leg produces a downward force into the bed while the strong leg is lifted, which you will be able to feel as their heel pressing into your hand. So to summarize, you're looking for a down pressure from the patient's weak leg when you ask them to raise their unaffected leg. Time to break for some practice. Join us in our next episode when we'll look at some other helpful maneuvers for functional weakness. 

In part one of this four-part series, Casey Kozak breaks down tremors observed during the physical examination of FND.  Show transcript:  Casey Kozak: Welcome back to Neurology Minute. This is Casey Kozak with Rutgers, and today we'll be discussing a very important and evolving topic, that is Functional Neurological Disorder, or FND. If you're a regular fan of the Minute, you'll have already heard a great miniseries on FND by Jon Stone and Gabriela Gilmour, which focuses on diagnosis and treatment. If you haven't listened yet, I encourage you to check it out. In this series, we're going to focus in on physical exam findings associated with FND to help you excel on the floors. Talking about the physical exam, it's important to keep in mind that FND looks different for every patient. However, some general characteristics of symptoms may include inconsistency, variability, selectivity of impairment, meaning mismatch of impairment with different tasks, distractibility, suggestibility, and incongruence with symptoms seen in other neurological disorders. Since tremors are one of the most common presentations of FND, we'll start there. Even while taking their history, you may notice features consistent with FND. And in fact, this is a great time to make natural observations of the patient and their symptoms. Unlike tremors associated with degenerative movement disorders like Parkinson's, functional tremors may exhibit variability of frequency and amplitude, especially during periods of shifted attention. You can further evaluate the tremor using the entrainment test. To perform the entrainment test, ask the patient to make a tapping motion. As the patient taps, look for a change in frequency in their tremor. The frequency of the tremor may begin to match the frequency of the patient's tapping. Any change in the tremor while the patient is tapping is considered a positive finding. Alternatively, you can also test the whack-a-mole sign. To elicit the whack-a-mole sign, the examiner holds down the tremulous body part while looking for the emergence of a tremor in a different body part. This finding is consistent with a functional tremor, as tremors related to neurodegenerative diseases do not jump limbs. Let's break now to practice. Join us again for our next episode where we will turn to functional weakness. See you then.

Dr. Margarita Fedorova discusses possible environmental exposures and their risk of Parkinson disease.  Show citation:  Dorsey ER, De Miranda BR, Hussain S, et al. Environmental toxicants and Parkinson's disease: recent evidence, risks, and prevention opportunities. Lancet Neurol. 2025;24(11):976-986. doi:10.1016/S1474-4422(25)00287-X  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 some information about possible environmental exposures and their risk of Parkinson disease. As we see in diagnose patients with Parkinson, they often want to know why they developed it and some emerging studies may offer insights. A recent personal view published in The Lancet Neurology by Ray Dorsey and colleagues in November 2025 examined associations between three environmental exposures and Parkinson's disease; pesticides, dry cleaning chemicals and air pollution. Since only five to 15% of Parkinson's cases have an identifiable genetic cause, environmental factors are an important area of investigation. Dorsey and colleagues describe studies showing that pesticide exposure is associated with Parkinson's risk. One example is Paraquat, an herbicide widely used in agriculture. It's banned in over 30 countries, but remains legal in the United States. In a population-based US study, residents living or working near areas where Paraquat was sprayed at twice the risk of developing Parkinson's, suggesting residential proximity alone may confer risk. Other pesticide exposures may show similar patterns. The organic chlorides, DGT and gildren are used in various agricultural areas. They're fat-soluble compounds that accumulate over decades. Postmortem studies found that when brains with lewd pathology and some studies suggest developmental exposure may increase risk of neurodegeneration years later. There have also been risks possibly associated with chemicals used in dry cleaning and metal degreasing. Trichloroethylene or TCE is one such chemical that was found in high amounts in the water at Camp Lejeune in North Carolina. A study of over 170,000 marines stationed there showed a 70% increase in risk of developing Parkinson's compared to marines at a non-contaminated base. What's particularly striking is the timing. Marines were exposed at an average age of 20 and the exposure lasted just over two years, yet disease manifested 34 years later. This suggests a long latency period between exposure and disease onset. TCE is also concerning because it evaporates from contaminated groundwater and can seep into buildings. As of 2000, 30% of US groundwater was contaminated with TCE. The third category of environmental exposure is air pollution. Studies from Canada, South Korea, Taiwan, and the UK show association between exposure to fine particular matter known as PM 2.5 in nitrogen dioxide with increased Parkinson's risk. These pollutants come from vehicle emissions, industrial sources, and combustion processes. The studies suggest that chronic exposure to these air pollutants may contribute to neurodegeneration through inflammatory and oxidative stress mechanisms. Unlike pesticides and dry cleaning chemicals, the magnitude of increased risk is often modest, typically ranging from one to 20%. However, the potential impact at large since almost everyone worldwide, 99% of people breathe on healthy air. For us as clinicians, this underscores the importance of taking detailed environmental histories. When patients ask, "Why me?" We can acknowledge that environmental exposures may have contributed to their disease. It's important to note that these studies show associations, but they don't confirm clear causation. Regardless, they may provide some answers to patients asking about the etiology of their Parkinson's or even the risks to others. That's your neurology minute for today. Keep exploring and we'll see you next time. If you want to read more, please find the paper by Ray Dorsey, titled Environmental Toxicants and Parkinson's Disease: Recent Evidence and Prevention Opportunities, published online in The Lancet Neurology in November 2025.

In the second episode of this two-part series, Drs. Justin Abbatemarco, Valérie Biousse, and Nancy J. Newman discuss the risk of non-arteritic ischemic optic neuropathy and how to counsel patients around GLP-1 medications.  Show transcript:  Dr. Justin Abbatemarco: Hello and welcome back. This is Justin Abbatemarco again with Valarie Biousse and Nancy Newman talking about non-arteritic ischemic optic neuropathy. I think the other major point that we had a discussion in the podcast was around the GLP-1 medications, which you mentioned have been truly life-changing for diabetes management and obesity. Can we talk about the risk of non-arteritic ischemic optic neuropathy and how you're counseling patients around this class of medications? Dr. Nancy J. Newman:  Absolutely. This is probably one of the most difficult things we are dealing with because it is something that is in process and progress right now. We don't have all the information yet, but it would appear that there is likely a small association of about slightly less than two times risk in patients who are taking these medications of having NAION with a resultant still very, very small overall risk. And it is not necessarily causal. This has prompted the European Medicines Agency to say that these patients should have their GLP-1 RAs stopped if they have NAION. Our own FDA and certainly the American Academy of Ophthalmology and the North American Neuro-Ophthalmology Society have not taken that step, but have suggested that this be shared decision-making, not only with the person who makes this diagnosis of an NAION in the patient, but with their primary care doctor or the provider who has felt that a GLP-1 receptor agonist is important for this patient's treatment and health. Dr. Justin Abbatemarco: More to come. We're going to have you back to have discussions as we learn more and better understand the disease and how we help our patients with both their diagnosis and treatment. Thank you so much for your time. 

In part one of this two-part series, Drs. Justin Abbatemarco, Valérie Biousse, and Nancy J. Newman discuss common myths around non-arteritic ischemic optic neuropathy (NAION). Show transcript:  Dr. Justin Abbatemarco: Hello and welcome. This is Justin Abbatemarco, and I just got done interviewing Valérie Biousse and Nancy Newman on all things around non-arteritic anterior ischemic optic neuropathy. I think one of my favorite takeaways from our interview were breaking some common myths around this disorder. Valérie and Nancy, could you maybe talk about one or two that you think are important that people should know are not true about this disease? Dr. Nancy J. Newman: So thing number one is that it's just another stroke of the eye. We know that it likely does have some vascular background to it, but the reality is it's not a stroke like neurologists know a stroke. You don't need to do an embolic workup. It has to do likely with the anatomy that a person is born with or that they acquire that crowds the front of their optic nerve. Secondly, thing number two, that it's a disease only of old people. I think that we know that you can be as young as age 11 and have this happen, mostly because you have a small, crowded optic nerve head. Thing number three, steroids really have not been proven to be helpful in this disorder and should likely not be used unless you are trying to decrease the optic nerve head edema, and the patient is insisting that they have some treatment. Dr. Justin Abbatemarco: So helpful. Please come back and check out the full podcast episodes where we dive into some of these elements in a little bit more detail.   

In part one of this two-part series, Drs. Justin Abbatemarco, Valérie Biousse, and Nancy J. Newman discuss common myths around non-arteritic ischemic optic neuropathy (NAION). Show transcript:  Dr. Justin Abbatemarco: Hello and welcome. This is Justin Abbatemarco, and I just got done interviewing Valérie Biousse and Nancy Newman on all things around non-arteritic anterior ischemic optic neuropathy. I think one of my favorite takeaways from our interview were breaking some common myths around this disorder. Valérie and Nancy, could you maybe talk about one or two that you think are important that people should know are not true about this disease? Dr. Nancy J. Newman: So thing number one is that it's just another stroke of the eye. We know that it likely does have some vascular background to it, but the reality is it's not a stroke like neurologists know a stroke. You don't need to do an embolic workup. It has to do likely with the anatomy that a person is born with or that they acquire that crowds the front of their optic nerve. Secondly, thing number two, that it's a disease only of old people. I think that we know that you can be as young as age 11 and have this happen, mostly because you have a small, crowded optic nerve head. Thing number three, steroids really have not been proven to be helpful in this disorder and should likely not be used unless you are trying to decrease the optic nerve head edema, and the patient is insisting that they have some treatment. Dr. Justin Abbatemarco: So helpful. Please come back and check out the full podcast episodes where we dive into some of these elements in a little bit more detail.   

Dr. Margarita Fedorova outlines how genetic, environmental, and pathological factors interact in Parkinson's disease and what this means for patient counseling.  Show citation:  Blauwendraat C, Morris HR, Van Keuren-Jensen K, Noyce AJ, Singleton AB. The temporal order of genetic, environmental, and pathological risk factors in Parkinson's disease: paving the way to prevention. Lancet Neurol. 2025;24(11):969-975. doi:10.1016/S1474-4422(25)00271-6  Show transcript:  Dr. Margarita Federova: Welcome to Neurology Minute. My name is Margarita Fedorova, and I'm a neurology resident at the Cleveland Clinic. Today we're exploring a framework for understanding how genetic, environmental, and pathological factors interact in Parkinson's disease and what this means for how we counsel our patients. A personal view paper by Blauwendraat and colleagues, published in The Lancet Neurology in September 2025, addresses a critical question. We've identified over 100 genetic loci for Parkinson's, but how do they act? The common saying is genetics loads the gun and environment pulls the trigger, but this paper suggests the relationship may be more complex. The key tool here is alpha-synuclein seeding amplification assays or SAAs. These detect misfolded alpha-synuclein protein in cerebrospinal fluid. Over 90% of Parkinson's patients test positive for misfolded alpha-synuclein using this assay. But here's what's notable. 2% to 16% of neurologically healthy older adults also test positive with prevalence increasing with age. This means there are more asymptomatic people with detectable alpha-synuclein pathology than people with actual Parkinson's disease. Most of these asymptomatic individuals will never develop symptoms. This raises an important question. What determines who converts to a disease and who doesn't? By integrating SAA results with genetic data, researchers can examine whether genetic factors drive initial protein misfolding or whether they modulate the response to pathology triggered by environmental or random events. Preliminary data suggests polygenic risk scores don't strongly associate with SAA positivity in healthy older adults. In other words, people with high genetic risk for Parkinson's aren't necessarily more likely to have misfolded alpha-synuclein if they're healthy. This suggests most Parkinson's genetic risk factors may not be causing initial misfolding. Instead, they may be determining what happens afterward, such as whether the pathology progresses to clinical disease. LRRK2 mutations support this model. About 33% of LRRK2 related Parkinson's patients are SAA-negative compared to only 7% in sporadic disease. This means many people with LRRK2 mutations develop Parkinson's without the typical alpha-synuclein pathology. LRRK2 mutations also show varied pathology. Sometimes alpha-synuclein, sometimes tau, sometimes neither. This suggests LRRK2 may modulate responses to different initiating events rather than directly causing protein misfolding. What does this mean for us as clinicians? Asymptomatic SAA-positive individuals could represent a window for intervention. If we can understand what protects them from converting to disease or what triggers that conversion, we could enable earlier identification of at risk individuals and potentially intervene before symptoms develop. The authors call for large scale studies using SAAs in older populations, combined with genetic analysis and longitudinal follow-up. By integrating pathological biomarkers with genetic and environmental data, we can better understand the temporal sequence of events in development of Parkinson's. This approach could fundamentally change how we think about disease prevention and early intervention, potentially allowing us to identify at risk individuals before symptoms appear and develop targeted prevention strategies. That's your neurology minute for today. Keep exploring, and we'll see you next time. If you want to read more, please find the paper by Cornelis Blauwendraat et al titled The Temporal Order of Genetic, Environmental and Pathological Risk Factors in Parkinson's Disease: Paving the Way to Prevention, published online in September 2025 in Lancet Neurology.

Dr. Tesha Monteith highlights the American Headache Society's position statement, which advocates for migraine screening in girls and women.  Show citation: Schwedt TJ, Starling AJ, Ailani J, et al. Routine migraine screening as a standard of care for Women's health: A position statement from the American Headache Society. Headache. Published online December 10, 2025. doi:10.1111/head.70023 Show transcript:  Dr. Tesha Monteith: Hi, this is Tesha Monteith with the Neurology Minute. Welcome back to our Women's Health and Headache Medicine series. Did you know the American Headache Society recently published a position statement to encourage screening for migraine in girls and women? The position statement was based on review of the literature to establish if migraine met standards for screening in subpopulations and to assess appropriate screening tools. The team achieved consensus, agreeing that migraine, due to its prevalence, morbidity, high cost, availability of screening methods and treatments, does meet criteria to justify screening for girls and women. The panel suggested that migraine should be screened annually as part of women's preventative care with tools like ID-Migraine. ID-Migraine is a self-administered three-question survey that has been validated in primary care settings. Patients answer yes or no to having the following with headache over the past three months. Patients are asked if headaches limited your ability to work, study, or do what they need to do on at least one day. You felt nauseated or sick to your stomach. Light bothered you a lot more than when you don't have headaches. Answering at least two of the three is positive for migraine. The panel acknowledged certain barriers, but they ultimately emphasize the overwhelming benefits of screening for migraine in women and children. Although the focus is for females, they recognize benefits in boys and men as well. Check out this position statement. It's a great read. This is Tesha Monteith. Thank you for listening to the Neurology Minute. 

In the final installment of this series, Dr. Justin Abbatemarco and Dr. Divyanshu Dubey discuss the latest findings and some non-occupational exposures.  Show citation:  Hinson SR, Gupta P, Paramasivan NK, et al. Neural synaptic vesicle autoimmunity following aerosolized porcine neural tissue exposure: insights into autoimmune inflammatory polyradiculoneuropathy. EBioMedicine. 2025;122:106053. doi:10.1016/j.ebiom.2025.106053 Show transcript:  Dr. Justin Abbatemarco:  Hello, and welcome back. This is Justin Abbatemarco. I'm here with Divyanshu Dubey, discussing his article, Neural Synaptic Vesicle Autoimmunity Following Aerosolized Porcine Neural Tissue Exposure: Insights Into Autoimmune Inflammatory Polyradiculoneuropathy. Div, maybe we could talk about non-occupational exposures? I think many of us don't see this cohort of patients commonly, but I really think this helps inform care, beyond just this specific occupational exposure. What did you guys find in your work? Dr. Divyanshu Dubey:  So, one of the inspirations for this study was driven by the phenotypic characterization of patients who were described in this 2010 paper, which is somewhat similar to some of the patients I currently see in my clinic who don't seem to meet GBS or CIDP criteria. But, based on their MRI findings, based on their CSF studies, the EMG nerve conduction studies, they seem to have this polyradiculoneuropathy presentation, often presenting with asymmetric disease onsets, starting on one leg and then sometimes transitioning to the other side. In some cases, even a non-length dependent pattern with sort of proximal cervical brachial nerve root plexus involvements, which don't really seem to have a blood test, or a biomarker right now. Currently, many of these cases are a diagnosis of exclusion. I was thinking if there's a biomarker that we can identify from this 2006 to 2008 unfortunate event, that might actually help us diagnose these patients. So, once we identified synaptophysin and GAP43 antibodies in the swine abattoir cohort, I went back to our storages of these patients with other inflammatory polyradiculoneuropathy, and found about 5% of these patients from a large cohort of close to 300 patients, did have these antibody biomarkers. Some of these patients had paraneoplastic trigger, where we had patients with neuroendocrine tumors, or hematological malignancies mounting a response to these antibodies. But a good chunk of these patients we did not truly understand, or know what the triggers were. That might be a potential for future studies, as we expand our cohort of these antibodies, as well as study further the phenotypic characterization of these cases. Dr. Justin Abbatemarco: Yeah, there's just so much there, really helping to inform future clinical care outside of this very specific occupational exposure. And then, as we talked about in the podcast, I think really helping to think through how neurological autoimmune diseases develop. So, just really exciting work. We really appreciate you coming on, sharing this. We're excited for how this evolves over the coming years. Dr. Divyanshu Dubey:  Thank you, Justin.  

In part one of this two-part series, Dr. Justin Abbatemarco and Dr. Divyanshu Dubey discuss the original patient cohort with occupational exposure, what motivated this line of research, and the key findings from the initial workup.  Show citation:  Hinson SR, Gupta P, Paramasivan NK, et al. Neural synaptic vesicle autoimmunity following aerosolized porcine neural tissue exposure: insights into autoimmune inflammatory polyradiculoneuropathy. EBioMedicine. 2025;122:106053. doi:10.1016/j.ebiom.2025.106053 Show transcript:  Dr. Justin Abbatemacro: Hello and welcome. This is Justin Abbatemacro. And I'm here with Divyanshu Dubey to discuss his article published in eBiomedicine, Neurosynaptic Vessel Autoimmunity Following Aerosolized Porcine Neural Tissue Exposure: Insight into Autoimmune Inflammatory Polyradicular Neuropathy. Dr. Justin Abbatemacro: Div is a professor of neurology at the Mayo Clinic, and we just finished our interview, which I would encourage everyone to check out. Div, maybe we could talk about the original cohort with this occupational exposure, what inspired you to do this work and then what did you find with that initial workup? Dr.  Divyanshu Dubey: As recounted in our paper, this story began in 2006 to 2008, when a group of swine abattoir workers developed a striking neurological syndrome. These people were previously healthy and suddenly developed severe neuropathic pain, tingling, and variable weakness. The localization stood out, these cases were initially identified by Dan Lachance, who characterized these patients having an autoimmune neuropathy, which was further phenotypically characterized by the work done by Dr. Dyck, calling these inflammatory polyradicular neuropathy based on their nerve root plexus and proximal nerve collisions. And interestingly, a lot of work done back then by Dr. Lennon showed these patients had a unique synaptic staining pattern suggesting there was an underlying antibody driving this disease process. So as I joined the neuroimmunology lab a few years ago, this was one of the areas I wanted to go back and study, not only to find this mystery biomarker which caused the disease in these patients, but also to try and understand how this can help. Dr. Justin Abbatemacro: Yeah. I think my takeaway is be curious, right? You hear the story, you see this pattern. Be curious and investigate, and it takes a team or a village to do it. Dr.  Divyanshu Dubey: 100%. So observation, communication between, as you said, a team or a village with like-minded, passionate individuals is one of the successes of many of our discoveries, not just this one in this biomarker space. Dr.  Divyanshu Dubey: So the technique we use for discovery of these biomarkers was called a phage display where we use the archive sera to test from these patients, the swine abattoir worker patients with autoimmune polyradicular neuropathy. And we ended up finding two dominant antigens, which was synaptophysin and GAP-43, which were present in majority of these cases. Dr. Justin Abbatemacro: Please come back and check out part two where we discuss the latest findings and maybe some non-occupational exposures. And check out the podcast. Thanks.  

In the second installment of this two-part series, Drs. Stacey Clardy, Ayush Gupta, and Kuntal Sen discuss the most practical testing approach to minimize both under‑ and over‑testing for these disorders. Show citation: Gupta A, Sahjwani D, Kahn I, Gombolay GY, Sen K. Monogenic Mimics of Neuroinflammatory Phenotypes in Children and Young Adults: An Evolving Landscape. Neurol Genet. 2025;11(6):e200326. Published 2025 Nov 25. doi:10.1212/NXG.0000000000200326 Show transcript:  Dr. Stacey Clardy: Hi, this is Stacey Clardy from the Salt Lake City VA in the University of Utah. For a two-part podcast series this week, I've been speaking with Ayush Gupta, from the University of Nebraska Medical Center, and Kuntal Sen, from Children's National Hospital in Washington, DC about monogenic disorders that mimic neuroinflammatory disease. There are a lot of them, and they are no doubt sitting in our clinics waiting to be recognized. Ayush, for the minute, once a neurologist starts suspecting one of these disorders, what's the most practical testing strategy to avoid both under and over-testing for these disorders? Dr. Ayush Gupta: I think the most practical strategy is to write down all the phenotypic symptoms that you think could be related, put that exact information into a genetic testing panel that will be suitable. Or, if possible, try to do a broader genetic testing such as whole genome sequencing, and make yourself equipped to be able to analyze the results that you get from the testing. Dr. Stacey Clardy: I hear you saying, at least when you're thinking about this, be a bit of a lumper. As we covered in the podcast, if we are going to pursue that genetic testing, it is absolutely critical that we share that list with the interpreting geneticist because that determines how they score variants and how they rate them as related or not. Please take a listen to that two-part podcast series, where we get into all these details. I walked away with a great framework on how to do better in terms of picking these disorders out. Again, the paper that accompanies the two-part podcast series is in Neurology Genetics. It's a comprehensive review and called Monogenic Mimics of Neuroinflammatory Phenotypes in Children and Young Adults in Evolving Landscape. Thank you, Ayush. Dr. Ayush Gupta: Thank you so much.

In the second installment of this two-part series, Drs. Stacey Clardy, Ayush Gupta, and Kuntal Sen discuss the most practical testing approach to minimize both under‑ and over‑testing for these disorders. Show citation: Gupta A, Sahjwani D, Kahn I, Gombolay GY, Sen K. Monogenic Mimics of Neuroinflammatory Phenotypes in Children and Young Adults: An Evolving Landscape. Neurol Genet. 2025;11(6):e200326. Published 2025 Nov 25. doi:10.1212/NXG.0000000000200326 Show transcript:  Dr. Stacey Clardy: Hi, this is Stacey Clardy from the Salt Lake City VA in the University of Utah. For a two-part podcast series this week, I've been speaking with Ayush Gupta, from the University of Nebraska Medical Center, and Kuntal Sen, from Children's National Hospital in Washington, DC about monogenic disorders that mimic neuroinflammatory disease. There are a lot of them, and they are no doubt sitting in our clinics waiting to be recognized. Ayush, for the minute, once a neurologist starts suspecting one of these disorders, what's the most practical testing strategy to avoid both under and over-testing for these disorders? Dr. Ayush Gupta: I think the most practical strategy is to write down all the phenotypic symptoms that you think could be related, put that exact information into a genetic testing panel that will be suitable. Or, if possible, try to do a broader genetic testing such as whole genome sequencing, and make yourself equipped to be able to analyze the results that you get from the testing. Dr. Stacey Clardy: I hear you saying, at least when you're thinking about this, be a bit of a lumper. As we covered in the podcast, if we are going to pursue that genetic testing, it is absolutely critical that we share that list with the interpreting geneticist because that determines how they score variants and how they rate them as related or not. Please take a listen to that two-part podcast series, where we get into all these details. I walked away with a great framework on how to do better in terms of picking these disorders out. Again, the paper that accompanies the two-part podcast series is in Neurology Genetics. It's a comprehensive review and called Monogenic Mimics of Neuroinflammatory Phenotypes in Children and Young Adults in Evolving Landscape. Thank you, Ayush. Dr. Ayush Gupta: Thank you so much.