Neurology Minute

The Neurology Minute podcast delivers a brief daily summary of what you need to know in the field of neurology, the latest science focused on the brain, and timely topics explored by leading neurologists and neuroscientists. From the American Academy of Neurology and hosted by Stacey Clardy, MD, Ph.D., FAAN, with contributions by experts from the Neurology journals, Neurology Today, Continuum, and more.

How Non-Traditional Educational Formats are Reshaping Neurology Training - Part 3 02/18/2026

How Non-Traditional Educational Formats are Reshaping Neurology Training - Part 3 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. /episode/index/show/neurologyminute/id/40153090

How Non-Traditional Educational Formats are Reshaping Neurology Training - Part 2 02/17/2026

How Non-Traditional Educational Formats are Reshaping Neurology Training - Part 2 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 Strowd, Justin Abbatemarco, and Tesha 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. /episode/index/show/neurologyminute/id/40139940

Fremanezumab in Children and Adolescents with Episodic Migraine - Part 2 02/16/2026

Fremanezumab in Children and Adolescents with Episodic Migraine - Part 2 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: 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. /episode/index/show/neurologyminute/id/40124915

CSF α-Synuclein Seed Amplification Assays and Alzheimer's Disease Biomarkers 02/13/2026

Fremanezumab in Children and Adolescents with Episodic Migraine - Part 1 02/12/2026

Fremanezumab in Children and Adolescents with Episodic Migraine - Part 1 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: 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. /episode/index/show/neurologyminute/id/40080830

February 9, 2026 Capitol Hill Report: State Advocacy Update 02/11/2026

February 2026 President Spotlight: Expanding the AAN’s Fundraising for Research Grants 02/10/2026

Understanding Physical Exam Findings Associated With FND - Part 4 02/09/2026

Understanding Physical Exam Findings Associated With FND - Part 4 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. . 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. /episode/index/show/neurologyminute/id/40047380

How Non-Traditional Educational Formats are Reshaping Neurology Training - Part 1 02/06/2026

How Non-Traditional Educational Formats are Reshaping Neurology Training - Part 1 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. /episode/index/show/neurologyminute/id/40021015

Physician as Patient Series - Stroke and Cancer Survivor 02/05/2026

Physician as Patient Series - Stroke and Cancer Survivor 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. /episode/index/show/neurologyminute/id/39987455

Rethinking How We Evaluate Small Fiber Neuropathy 02/04/2026

Rethinking How We Evaluate Small Fiber Neuropathy 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 . 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: 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. /episode/index/show/neurologyminute/id/39987405

Understanding Physical Exam Findings Associated With FND - Part 3 02/03/2026

Understanding Physical Exam Findings Associated With FND - Part 3 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. . 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. /episode/index/show/neurologyminute/id/39981900

US Burden of Disorders Affecting the Nervous System - Part 2 02/02/2026

US Burden of Disorders Affecting the Nervous System - Part 2 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: 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. /episode/index/show/neurologyminute/id/39967735

CGRP-Targeted Migraine Therapies in Patients With Vascular Risk Factors or Stroke 01/30/2026

CGRP-Targeted Migraine Therapies in Patients With Vascular Risk Factors or Stroke 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: 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. /episode/index/show/neurologyminute/id/39938210

US Burden of Disorders Affecting the Nervous System - Part 1 01/29/2026

US Burden of Disorders Affecting the Nervous System - Part 1 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: 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. /episode/index/show/neurologyminute/id/39926885

Understanding Physical Exam Findings Associated With FND - Part 2 01/28/2026

Understanding Physical Exam Findings Associated With FND - Part 2 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. /episode/index/show/neurologyminute/id/39903275

Understanding Physical Exam Findings Associated With FND - Part 1 01/27/2026

Understanding Physical Exam Findings Associated With FND - Part 1 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. /episode/index/show/neurologyminute/id/39900610

Environmental Toxicants and Parkinson Disease 01/26/2026

Environmental Toxicants and Parkinson Disease 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: 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. /episode/index/show/neurologyminute/id/39888570

Updates in Non-Arteritic Ischemic Optic Neuropathy - Part 2 01/23/2026

Updates in Non-Arteritic Ischemic Optic Neuropathy - Part 2 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. /episode/index/show/neurologyminute/id/39838685

Updates in Non-Arteritic Ischemic Optic Neuropathy - Part 1 01/22/2026

The Temporal Order of Genetic, Environmental, and Pathological Risk Factors in Parkinson Disease 01/21/2026

The Temporal Order of Genetic, Environmental, and Pathological Risk Factors in Parkinson Disease 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: 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. /episode/index/show/neurologyminute/id/39815475

Headache Medicine and Women's Health Series: Migraine Screening and ID Migraine Tool 01/20/2026

Headache Medicine and Women's Health Series: Migraine Screening and ID Migraine Tool 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: 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. /episode/index/show/neurologyminute/id/39800730

Neural Synaptic Vesicle Autoimmunity Following Aerosolized Porcine Neural Tissue Exposure - Part 2 01/19/2026

Neural Synaptic Vesicle Autoimmunity Following Aerosolized Porcine Neural Tissue Exposure - Part 2 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: 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. /episode/index/show/neurologyminute/id/39788900

Neural Synaptic Vesicle Autoimmunity Following Aerosolized Porcine Neural Tissue Exposure - Part 1 01/16/2026

Neural Synaptic Vesicle Autoimmunity Following Aerosolized Porcine Neural Tissue Exposure - Part 1 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: 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. /episode/index/show/neurologyminute/id/39759570

Monogenic Mimics of Neuroinflammatory Phenotypes in Children and Young Adults - Part 2 01/15/2026

Monogenic Mimics of Neuroinflammatory Phenotypes in Children and Young Adults - Part 2 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: 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. /episode/index/show/neurologyminute/id/39735020

Monogenic Mimics of Neuroinflammatory Phenotypes in Children and Young Adults - Part 2 01/15/2026

Using Neurofilament Light Chain in Clinical Practice 01/14/2026

Using Neurofilament Light Chain in Clinical Practice Dr. Aaron Zelikovich discusses the utility of neurofilament light chain as a serum biomarker in peripheral neuropathy. Show citation: Karam C. Clinical Utility of Serum Neurofilament Light Chain in Peripheral Neuropathy. Muscle Nerve. 2026;73(1):86-92. doi: 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 on the utility of neurofilament light chain as a serum biomarker in peripheral neuropathy. It has been studied in other neurological diseases like ALS and multiple sclerosis, as in the 2024 study by Robert Fox et al, which highlighted the limitations of serum neurofilament light chain in patients with multiple sclerosis, since the elevation was inconsistent and tended to occur weeks after MRI changes, and was really only found to be helpful in certain clinical situations. The study we highlight today is a single-center retrospective study that highlights the opportunities and limitations of using serum neurofilament light chain as a biomarker to monitor treatment response and peripheral neuropathy. Serum neurofilament light chain has been shown as an indicator of neuronal injury in both central and peripheral nervous system disease that has been associated with axonal injury or degeneration. It is now commercially available. The authors in this study provide a real-world single-center retrospective study that looked at various forms of peripheral neuropathy over 12 months. Patients had to be evaluated and meet criteria for peripheral neuropathy with either genetic testing, nerve conduction studies, and/or clinical exams. Neuropathies included TTR amyloid, vasculitis, CMT, CIDP, GBS, and anti-MAG neuropathy. Patients with TTR amyloid who were treatment naive and had elevated serum neurofilament light chain showed a reduction in neurofilament light chain levels with treatment. Additionally, patients with CIDP who were treatment naive with elevated serum neurofilament light chain also showed a reduction in neurofilament light chain levels with treatment. All patients with idiopathic peripheral neuropathy had normal serum neurofilament light chain levels. However, serum neurofilament light chain can vary in patients based on age, if they have diabetes, renal dysfunction, and body weight. And this makes it really challenging to interpret it in an isolated setting. Serum neurofilament light chain is a new biomarker for peripheral neuropathies. It can be a supplemental tool in the appropriate clinical context. Future studies are needed to identify its potential to be used as a treatment response biomarker in neuropathies like CADP, GBS, and TTR amyloid. Thank you so much, and have a wonderful day. /episode/index/show/neurologyminute/id/39732735

Headache Medicine and Women's Health Series: Overview of Menstrual Migraine 01/13/2026

Levetiracetam - Part 2 01/12/2026

Levetiracetam - Part 2 In the second part of this series, Dr. Neishay Ayub discusses levetiracetam and one of its most common side effects, irritability. Show citations: Abou-Khalil B. Levetiracetam in the treatment of epilepsy. Neuropsychiatr Dis Treat. 2008;4(3):507-523. doi: Löscher W, Gillard M, Sands ZA, Kaminski RM, Klitgaard H. Synaptic Vesicle Glycoprotein 2A Ligands in the Treatment of Epilepsy and Beyond. CNS Drugs. 2016;30(11):1055-1077. doi: Rogawski MA. Brivaracetam: a rational drug discovery success story. Br J Pharmacol. 2008;154(8):1555-1557. doi: Ulloa CM, Towfigh A, Safdieh J. Review of levetiracetam, with a focus on the extended release formulation, as adjuvant therapy in controlling partial-onset seizures. Neuropsychiatr Dis Treat. 2009;5:467-476. doi: Wu PP, Cao BR, Tian FY, Gao ZB. Development of SV2A Ligands for Epilepsy Treatment: A Review of Levetiracetam, Brivaracetam, and Padsevonil. Neurosci Bull. 2024;40(5):594-608. doi: Mahmoud A, Tabassum S, Al Enazi S, et al. Amelioration of Levetiracetam-Induced Behavioral Side Effects by Pyridoxine. A Randomized Double Blind Controlled Study. Pediatr Neurol. 2021;119:15-21. doi: Major P, Greenberg E, Khan A, Thiele EA. Pyridoxine supplementation for the treatment of levetiracetam-induced behavior side effects in children: preliminary results. Epilepsy Behav. 2008;13(3):557-559. doi: Romoli M, Perucca E, Sen A. Pyridoxine supplementation for levetiracetam-related neuropsychiatric adverse events: A systematic review. Epilepsy Behav. 2020;103(Pt A):106861. doi: Show transcript: Dr. Neishay Ayub: Hello, my name is Neishay Ayub, and today we will be discussing levetiracetam and one of its most common side effects, irritability. While levetiracetam can be remarkably helpful for patients, behavioral adverse effects were noted in post-marketing analysis and open-label studies in adult and pediatric patients. For this, physicians started using vitamin B6 supplementation, particularly in the pediatric populations. Why would physicians use B6? Well, low vitamin B6 has been associated with neuropsychiatric disorders, which could be related to the fact that vitamin B6 is an essential co-factor for several neurotransmitters that affect mood and behavior, such as serotonin, dopamine, and GABA. There is an epilepsy syndrome associated with vitamin B6 deficiency. And vitamin B6 deficiency is seen with enzyme-inducing anti-seizure medications, although levetiracetam is not an enzyme-inducing seizure medication. These are some of the possibilities as to why vitamin B6 supplementation was initially explored. Some initial anecdotal evidence and case reports were suggested that it was helpful in reducing behavioral side effects and the need to discontinue levetiracetam. There was a meta-analysis reviewing pyridoxine use, which included 11 case reports and retrospective studies, as well as one prospective study, case-control study, which was not placebo controlled. While evidence was suggestive of a benefit, the quality of the evidence was poor due to selection, reporting, and assessment biases. Overall, the authors recommended a larger randomized, controlled, double-blind trial with adequate statistical power, well-defined eligibility criteria and standardized assessment tools to evaluate B6 efficacy in treating levetiracetam-induced irritability. Since then, there was one small randomized, controlled, double-blind study involving 105 children for whom neuropsychiatric adverse effects were noted after levetiracetam was introduced. Children were randomized to receive a therapeutic dose of pyridoxine, which was 10 to 15 milligrams per kilogram per day, up to 200 milligrams, or a homeopathic dose of 0.5 milligrams per kilogram per day. They were scored on a behavioral checklist and monitored for up to six months. While there was a reduction in behavioral symptoms reported in the therapeutic pyridoxine group, there was no validated assessment tools used, and there was an absence of a true placebo group. Lastly, there are a few studies reporting on adverse effects of B6 toxicity, which is possible, but it's typically seen at higher daily doses, although something to keep in mind if considering B6 supplementation. In summary, while there has been a clinical practice of prescribing pyridoxine at 50 to 100 milligrams as a low-cost, well-tolerated adjunctive supplement, there may be a modest benefit for some patients, but the overall efficacy for the treatment of neuropsychiatric side effects for levetiracetam remain unclear, and more evidence is needed. /episode/index/show/neurologyminute/id/39704375

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