Neurology Minute

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 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...