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Inflammatory and autoimmune axonal neuropathies can cause rapidly progressive weakness, sensory loss, and pain, but recognizing treatable cases can be challenging. In this episode, Dr. Qihua Fan discusses key clinical patterns, diagnostic strategies, and common mimics of inflammatory axonal neuropathies, emphasizing the importance of careful follow-up and realistic treatment goals. Learn how electrodiagnostic studies, biomarkers, pathology, and emerging imaging techniques can help guide diagnosis, monitor disease activity, and assess treatment response. In this episode, Teshamae Monteith, MD, FAAN, speaks with Qihua Fan, MD, author of the article "Inflammatory and Autoimmune Axonal Neuropathies" in the Continuum® October 2026 Peripheral Nerve and Motor Neuron Disorders issue. Dr. Monteith is the associate editor of Continuum® Audio and an associate professor of clinical neurology at the University of Miami Miller School of Medicine in Miami, Florida. Dr. Fan is a neuromuscular specialist, neuromuscular medicine fellowship director, and director of the ALS Clinic at Virginia Commonwealth University in Richmond, Virginia. Additional Resources Read the article: Inflammatory and Autoimmune Axonal Neuropathies Subscribe to Continuum®: shop.lww.com/Continuum Earn CME (available only to AAN members): continpub.com/AudioCME Continuum® Aloud (verbatim audio-book style recordings of articles available only to Continuum® subscribers): continpub.com/Aloud More about the American Academy of Neurology: aan.com Social Media facebook.com/continuumcme @ContinuumAAN Host: @headacheMD Full episode transcript available here Dr. Monteith: A patient presents with rapidly progressive weakness, sensory loss, and severe neuropathic pain. Is this an inflammatory neuropathy requiring urgent treatment, or a mimic that could lead to a misdiagnosis? Today, we'll discuss how to recognize inflammatory and autoimmune axonal neuropathies, navigate the diagnostic workup, and apply emerging advances in biomarkers, imaging, and treatment.   Dr. Jones: This is Dr. Lyell Jones, Editor-in-Chief of Continuum. This exclusive Continuum audio interview is available only to you, our subscribers. After listening, you can get CME by going to continpub.com/audiocme. We hope you enjoy the interview.   Dr. Monteith: This is Dr. Teshamae Monteith. Today, I'm interviewing Dr. Qihua Fan about her article on inflammatory and autoimmune axonal neuropathies. This article appears in the October 2026 Continuum issue on peripheral nerve and motor neuron disorders. Welcome to our podcast. How are you?   Dr. Fan: Good. Thank you so much for having me.   Dr. Monteith: Please introduce yourself to our audience.   Dr. Fan: My name is Qihua Fan. I'm an Assistant Professor in Neuromuscular Medicine at Virginia Commonwealth University in Richmond, Virginia. It's nice to be here.   Dr. Monteith: And what got you interested in this field?   Dr. Fan: I was very lucky to meet a lot of brilliant thinkers along the way and a lot of really great role models. I was really blown away by how they're able to take a lot of different pieces of data. So, for example, meeting somebody in the emergency room and then doing their exam and doing their electrodiagnostics, then their pathology, and putting it all together and kind of seeing them from end-to-end care. They taught me how to think about things in a different way, and I've been hooked ever since.   Dr. Monteith: Cool. And so, what were the goals of your article?   Dr. Fan: The goals of this article was to try and pull out a couple of pearls in kind of approaching inflammatory axonal neuropathies. I think one of the trickiest things in axonal neuropathy management is we don't want to miss the treatable, reversible etiologies. But when we get it, it takes so much patience to not rush into judging whether or not we're successful, just because nerve recovery and axonal processes take such a long time. And so, we have to be used to kind of sitting there and waiting for 3 to 6 months to see if we're even on the right track. So, the biggest takeaway that I want folks to get out of this, is that stability is the goal in axonal inflammatory axonal neuropathies, and to be patient and to be creative about the modalities that we're using to see if our treatments are working.   Dr. Monteith: Why don't you help our listeners understand, as a group, how do you describe autoimmune axonal neuropathies?   Dr. Fan: So, a couple of principles in diagnosing and recognizing immune and inflammatory-mediated axonal neuropathies. One is that the tempo typically tends to be subacute. Number two, is you need to be able to recognize the typical patterns in which they'll present. So, the most common textbook one is the mononeuritis multiplex, subacute stepwise progression. That will coalesce over time into another pattern, asymmetric axonal polyneuropathy. A third pattern is sensory ataxia or sensory neuropathy or neuronopathy. And a fourth pattern is, it's a mouthful, it's radiculoplexus or plexus syndromes. So that will be similar to your diabetic amyotrophy. And then your exam electrodiagnostics should be working together to confirm that pattern. So, once you have that pattern recognized, then you're looking for labs, electrodiagnostics, pathology, and then treatment responsiveness to help support that hypothesis every step along the way.   Dr. Monteith: Why don't you tell us a little bit about some of the areas that you're most excited about in terms of latest developments in the field?   Dr. Fan: Yeah. So, I think a lot of us are seeing the role of neurofilament light chain entering into our practice, and I think this has been a huge game changer in the area of inflammatory axonal neuropathies in particular. I'll give an example. So, if we see a new vasculitic neuropathy, right, somebody who is dropping nerves left, right, and center, and you see a very precipitous decline, you want to do everything you can to try and stabilize that. But the most satisfying short-term thing that we can achieve in the past was just stability, so that they stop losing nerves, they stop progressing in terms of their weakness, stop progressing in terms of their sensory loss, but they still have a lot of pain, and it's very challenging to manage. But with the development and commercialization of neurofilament, we're able to kind of demonstrate a normalization in a very quantifiable way to say, "Hey, look, we were burning through nerve very quickly before, and now this is a data point that can help support our treatment decision to say, yes, we're on the right track."   Dr. Monteith: Great. Maybe you can speak a little bit more about the approach to the evaluation. I read in your article that two key areas is determining the subtype and then the extent of nerve injury.   Dr. Fan: Right. So, it's a little bit of pattern recognition, and we talk about four different common presentation patterns. The classic one that we get taught is the mononeuritis multiplex subacute stepwise progression. But a lot of times, once the inflammation has been there for long enough, we've picked off enough nerves that the pattern has coalesced into a more length-dependent pattern. Typically, there's a little bit of asymmetry, and so that's the second pattern, is an asymmetric sensory motor polyneuropathy. The third type is a sensory ataxia. Somebody's coming in, their balance is way off, they can't do fine motor tasks, but there's not much other cerebellar findings, but their sensory examination is shot. And then the fourth type is an LRPN. So, this is much more like your diabetic amyotrophy phenotype is, is one example, and a lot of times that will be monophasic. So those are kind of the four patterns that can commonly present as inflammatory axonal neuropathies.   Dr. Fan: Once you think that this might be inflammatory or axonal in etiology, you want to kind of gather data points and see if it's treatment responsive. And so, when you're thinking about autoimmune or inflammatory etiologies, you want to look for biomarkers, for example, pathology to say, "Yes, there are inflammatory infiltrates that are attacking the nerve." One of the most surprising and clinically important findings that I learned about this when I was a fellow, is that you can see inflammation on pathology in conditions that are not immune-mediated neuropathies. So, for example, even in diabetic neuropathy, you can find a dusting of perivascular inflammation on pathology, and that creates a very confusing interpretive picture because inflammation on biopsy doesn't automatically establish that this is an immune-driven problem or that immunotherapy will be helpful. So, the key takeaway is that the pathology alone is not enough. You still have to demonstrate that the disease is biologically active and that it's treatment responsive over time. So, you can confirm inflammatory neuropathy on pathology, but you need to show that you can alter the disease course, that it's treatment responsive, and you can't just go off of seeing inflammatory cells under a microscope.   Dr. Monteith: So how do you pivot away from that?   Dr. Fan: So that's why you have to build in multiple levels of confirmation. So, you have the pattern recognition to say, "Hey, I think this is, this might be an inflammatory neuropathy." Number two, I still look for the pathology for confirmation. I find it and then say, "Okay, if this is true inflammatory neuropathy, it should respond to treatment over time on exam, on biomarkers, on functional assessments, in the way that axonal neuropathy is expected to respond." So, you have to follow the exam over time, follow your biomarkers, and see if things are mapping out the way that you expect it to.   Dr. Monteith: Great. So, you gave some nice pearls in the article about ways to elicit temporal progression, and the ext

Diabetic neuropathy is more than a disorder of numbness and pain in the feet. In this episode, Dr. Vera Fridman discusses diabetic neuropathy as a complex, multisystem condition, highlighting the importance of recognizing autonomic involvement, identifying high-risk patients early, and addressing factors that influence progression. Learn practical strategies for screening, prevention, symptom management, and recognizing when symptoms may suggest an alternative diagnosis. In this episode, Kait Nevel, MD, speaks with Vera Fridman, MD, author of the article "Diabetic Neuropathies" in the Continuum® October 2026 Peripheral Nerve and Motor Neuron Disorders issue. Dr. Nevel is a Continuum® Audio interviewer and a neurologist and neuro-oncologist at Indiana University School of Medicine in Indianapolis, Indiana. Dr. Fridman is an Associate Professor of Neurology and Neuromuscular Medicine Fellowship Director at the University of Colorado in Aurora, Colorado. Additional Resources Read the article: Diabetic Neuropathies Subscribe to Continuum®: shop.lww.com/Continuum Earn CME (available only to AAN members): continpub.com/AudioCME Continuum® Aloud (verbatim audio-book style recordings of articles available only to Continuum® subscribers): continpub.com/Aloud More about the American Academy of Neurology: aan.com Social Media facebook.com/continuumcme @ContinuumAAN Host: @IUneurodocmom Full episode transcript available here Dr. Nevel: Diabetic neuropathy affects millions of people, but in our neurology clinics, are we thinking about it too narrowly? In this clinic, Dr. Vera Fridman emphasizes that diabetic neuropathy is not simply a disease of the feet, revealing it instead as a complex neurologic syndrome with consequences that reach far beyond numbness and pain.   Dr. Jones: This is Dr. Lyell Jones, Editor-in-Chief of Continuum. Thank you for listening to Continuum Audio. Be sure to visit the links in the episode notes for information about earning CME, subscribing to the journal, and exclusive access to interviews not featured on the podcast.   Dr. Nevel: Hello, this is Dr. Kate Nevel. Today, I'm interviewing Dr. Vera Fridman about her article on diabetic neuropathies. This article appears in the October 2026 Continuum issue on peripheral nerve and motor neuron disorders. Vera, welcome to the podcast, and please introduce yourself to the audience.   Dr. Fridman: Hello, it's great to be here. I'm Vera Fridman, and I'm located at the University of Colorado Medical Center. I'm a neuromuscular neurologist with focus on neuropathy clinically and in my research, and it's great to join you.   Dr. Nevel: Wonderful. Looking forward to talking to you about your article and learning more. So, I always like to start these interviews with the question, what is the most important takeaway from your article for the practicing neurologist?   Dr. Fridman: I think to me, in thinking about this article and writing it, the most important message and take-home is that we need to start thinking about diabetes-associated nerve injury as a complex disorder that's multisystemic. So rather than sort of just focusing on the peripheral nerve involvement we're used to seeing at the bedside, to really start taking that early clinical presentation of numbness or tingling as a warning sign, as a heralding sign of something that is widespread, complex, systemic, the way we might think about other multi-organ systemic disorders.   Dr. Nevel: Great. And that leads me into my next question, because you really do emphasize that throughout your article, all the different ways that this kind of more systemic diabetic nerve injury can impact a person and affect their morbidity and even their mortality. So, can you tell us a little bit more about this more widespread diabetic nerve injury beyond the kind of classic diabetic peripheral neuropathy that maybe we think of as neurologists?   Dr. Fridman: Yeah, I think the idea here is that we have nerves innervating a lot of different organs, and they are also not siloed. They're interfacing with other parts of our biology, vasculature, you know, the impact of inflammation. All of these things are converging, and they are complicated. And so clinically, when I think about diabetic neuropathy associated with systemic injury, I think about cardiac autonomic neuropathy, about gastrointestinal and urogenital neuropathies, and that these symptoms can be really diverse, and they can be nebulous. And so, in seeing someone who just says, "I have a little bit of numbness and tingling in my toes," I think the clinician has to sort of force themselves to imagine that there's all this asymptomatic disruption in the person's presentation that they have to dig for to understand better.   Dr. Nevel: What else should we be asking to kind of delve deeper to investigate or identify a more widespread diabetic nerve injury?   Dr. Fridman: When I think about what sort of trainees and early clinicians miss, like when I see histories come from people who haven't been thinking about diabetic neuropathy for a long time, it's usually the autonomic that's missing. Do you have lightheadedness? Have you noticed decreased or increased sweating? Do you get full easily with meals, what we call early satiety? Patients don't know that word. Do you have sexual dysfunction? That's an enormously important question because it can actually herald that there's more widespread neuropathy, more severe neuropathy, and that there's autonomic involvement or potentially vascular involvement. So those are the ones that I see missed. And then the others would be related to the risk of ulceration. What is your foot care approach? Have you had ulcers in the past? I think a lot of people don't realize that having had an ulcer, even if it happened some time ago and healed, is a major risk factor for recurrent ulceration. You're going to pay attention differently to that patient. And then the other question that doesn't necessarily relate to symptoms, but I think is hugely important to ask is, what are your barriers to caring for your diabetes and for yourself? What is getting in the way of those preventative measures, which are really the only really reliable preventative things we can do, right? Like, we don't have good treatments for this disease. So why can't you exercise? What are some of the reasons why you can't? Really in a non-judgmental, guilt-free way, because we know diabetes increases the barrier to these things substantially, and that patients are struggling just to get through their day. So, I think understanding those obstacles early in the therapeutic relationship is where you can make the most impact.   Dr. Nevel: Thanks for sharing that. Can you tell us a little bit more about cardiac autonomic neuropathy and why that's so important?   Dr. Fridman: Yeah, well, it's important because basically the largest driver of mortality and cardiac death in this population. And I think sometimes even with well-managed diabetes, we are sort of heartbroken to see patients who have gone on to have really terrible outcomes from cardiac autonomic involvement that we didn't necessarily know was there. The other reason it's so important is because it stays asymptomatic for a very long time. So, it's one of these sort of elephant in the room entities that if you don't ask about, you don't look for intentionally, you're just not gonna know, and the patient's not gonna know. They're gonna think they're lightheaded from their medication, which is a very reasonable postulation when someone's taking neuropathic pain medications and blood sugar is going up and down. But it may just be that there's autonomic disease underlying. The other reason it's important is because it's difficult to test for. So even if you have the awareness that you have to think about it and ask about it, it's not always clear to clinicians what they're supposed to do next if those symptoms are there or how to evaluate them. And so, I think for all those reasons, it's probably the most undetected complication, and it's hugely common, and in some cases preventable through aggressive management of disease. So, I think for all those reasons, it comes out as the one that we need to remind ourselves about.   Dr. Nevel: How do you evaluate for cardiac autonomic neuropathy in your clinic?   Dr. Fridman: That's a great question. I think I start really with the questions that will be included in this article of kind of these detailed questions about symptoms that they may not know come together as indicating autonomic disease. Then at the bedside, I do a quick heart rate screen to see if they have resting tachycardia. Unfortunately, resting tachycardia is a late manifestation of cardiac autonomic neuropathy, so once you see it, it's probably too late. The next thing is to just perform orthostatic vital signs in the clinic and trying to get in the habit of having the patient lying and sitting and standing and taking the time. And in a busy clinic, that's actually quite a big ask. But if you can get a medical assistant trained and ready to do it on most patients, that I think is really important. If I'm concerned about it, then an EKG, which obviously wouldn't necessarily happen in the same visit, can help look for heart rate variability. And then the next layer is really talking to their primary care about a cardiology referral, because at that point, I think neurologists need help. And that's the other, I think, salient message from my thinking about this field is that this is not something that one practitioner can take on alone, and there has to be a really strong multidisciplinary network, just like we would do for our other complex disorders.   Dr. Nevel: Yeah. Do you see in the future there being more multidisciplinary engagement between neurology and cardiology for these patients if this is such a difficult

Neuropathy can present in many ways beyond the classic pattern of numbness and tingling. In this episode, Dr. Reza Seyedsadjadi discusses a practical diagnostic approach, highlighting key clinical clues, electrodiagnostic findings, and the role of genetic testing and other specialized studies in identifying common and uncommon causes of neuropathy. In this episode, Casey S. Albin, MD, FAAN, speaks with Reza Sadjadi, MD, author of the article "The Diagnostic Approach to Neuropathy" in the Continuum® October 2026 Peripheral Nerve and Motor Neuron Disorders issue. Dr. Albin is a Continuum® Audio interviewer, associate editor of media engagement, and an assistant professor of neurology and neurosurgery at Emory University School of Medicine in Atlanta, Georgia. Dr. Sadjadi is an assistant professor of neurology at Harvard Medical School and Massachusetts General Hospital in Boston, Massachusetts. Additional Resources Read the article: The Diagnostic Approach to Neuropathy Subscribe to Continuum®: shop.lww.com/Continuum Earn CME (available only to AAN members): continpub.com/AudioCME Continuum® Aloud (verbatim audio-book style recordings of articles available only to Continuum® subscribers): continpub.com/Aloud More about the American Academy of Neurology: aan.com Social Media facebook.com/continuumcme @ContinuumAAN Host: @caseyalbin Full episode transcript available here Dr. Albin: The patient comes into your office with numbness and tingling, and it seems like it's probably a pretty straightforward neuropathy. But what about if it's not? Or what if the EMG and nerve conduction studies suggest something else? What if the patient is giving you extra clues about other symptoms where they feel ataxic or have systemic complications as well? All of those things may be part of a neuropathic picture. And today, we are so fortunate to talk to Dr. Seyedsadjadi about just this.   Dr. Jones: This is Dr. Lyell Jones, Editor-in-Chief of Continuum. Thank you for listening to Continuum Audio. Be sure to visit the links in the episode notes for information about earning CME, subscribing to the journal, and exclusive access to interviews not featured on the podcast.   Dr. Albin: Hi, all. This is Dr. Casey Albin. Today, I'm interviewing Dr. Reza Seyedsadjadi about his article on the diagnostic approach to neuropathy. This article appears in the October 2026 Continuum issue on peripheral nerve and motor neuron disorders. Welcome to the podcast. I'm so excited to have you here, Dr. Seyedsadjadi. Just love for you to tell us a little bit about yourself and your background and how you got interested in this topic.   Dr. Seyedsadjadi: Hi. Thank you for the kind invitation and the opportunity to contribute to the Continuum. I'm a neuromuscular neurologist. I work here at Mass General Hospital. I got interested in peripheral nerve disease throughout my early training in neurology and continued with the fellowship in neuromuscular disorders, and I've been seeing patients with mostly neuropathy, inherited and acquired neuropathies here in Mass General Hospital.   Dr. Albin: Excellent. And so, you are the perfect person to write this intro article. And so, I always like to start with the basics. The patient comes to you. What are some of the symptoms that you're listening for that help you clue in that this is probably a neuropathy, not somewhere else in the peripheral nerve system?   Dr. Seyedsadjadi: What an excellent question. And it is still difficult to 100% be sure, but overall, I like to put things in different buckets to help you have a pattern recognition with what you think that makes sense to be a neuropathy, a neuronopathy, a radiculopathy. In general, I divide things into positive and negative sensory symptoms in terms of complaints. Positive ones like hyperesthesia, paresthesia, burning, tingling sensation. Negative sensory symptoms are a little bit more tricky, loss of sensation, balance issues. When somebody comes, you have to listen to all of these symptoms in conjunction with the distribution of the symptoms, how they evolve over time, to give you a clue whether this is a neuropathy or just neuropathic symptom related to a different process that could mimic neuropathy. And sometimes it would be difficult to delineate between the two, especially if a patient is very complex, has two different processes going on. But first off, it's good to know if you have positive sensory symptoms, it is more likely that this is a peripheral process than negative sensory symptoms. And some other features that we usually overlook when we see the patient in the clinical setting, especially if it's busy, those are the autonomic complaints that we can talk more about.   Dr. Albin: Yes. And I really wanna double-click on a lot of these features that you brought up. So, I'm hearing you're thinking about not only the symptom quality, but also that pattern of distribution. What about that sort of localized pattern of distribution?   Dr. Seyedsadjadi: Yeah. So typically, the general teaching is that nerves are very long in terms of the course, and when the damage happens to the nerve, the pattern would be a length-dependent pattern, meaning the longest nerve or the tip of the longest nerve will be affected, and this will gradually affect and go more proximally in a symmetrical pattern in more common known types of neuropathy. That's not always true. Sometimes you can have a non-length dependent neuropathy. You can have like an asymmetric neuropathy. But these are all small clues that you can use to see, to help you to narrow your differential diagnosis. So, you can have like a vasculitic neuropathy, which is necessarily not a length-dependent process. It affects one side, not necessarily the other side, and the progression of it, which could be stepwise rather than gradual progression of the disease.   Dr. Albin: I love that. Thinking not only just about the typical numbness and tingling in your fingers and toes, but recognizing that while that is a very common pattern of neuropathic symptoms, that you may have a patchy distribution and that you can still put neuropathy on your differential, even if it's asymmetric and even if it's not starting at tips of the fingers and tips of the toes.   Dr. Seyedsadjadi: Exactly. Nicely summarized.   Dr. Albin: One of the points that I really took away from your article was how sensory symptoms or motor symptoms, whether there's a predominance of one or the other, that actually may have some real importance in helping you think through the underlying process. So, can you tell us a little bit more about that?   Dr. Seyedsadjadi: Exactly. And also, I don't want to confuse this with necessarily involvement of sensory nerves because you can also have positive sensory and negative sensory symptoms. But looking at the signs in terms of how patients present- If you have predominance of, like, motor weakness, you have a patient who comes with the distal upper and lower extremity weakness, but sensory symptoms more than signs, are relatively milder. Obviously, you think more about process that is more chronic, affecting motor nerves more than sensory nerves, or equally at least, you think about more hereditary cases. Whereas when you have more sensory symptoms or predominance of sensory symptoms and less of motor involvement and more recent presentation, you think about more acquired causes of neuropathy. Now, that is not universal because we know that there are acquired neuropathies that affect the motor nerves more than sensory nerves, and we have hereditary neuropathies that purely affect sensory nerves like CANVAS syndrome. But in general, it's good to have, like, a pattern recognition. Now you can more comfortably look for those outliers that would be like a framework that you can approach them by looking for subtle signs and differences that they have from them.   Dr. Albin: I think that's so true of most of what we deal with in neurology. Like, most of neurology is being able to recognize the 75% to 80% that present in the normal typical pattern. But it's learning that for every localization within neurology, there are those variants. They don't read the textbook. But I do love that how if you're thinking about more sensory symptoms and more recent onset, you're generally thinking this is acquired versus that motor really standing out above and beyond the sensory symptoms, thinking more, "Hmm, could this be a hereditary? Should I look a little bit further into the family history?" Great point. And then I heard, especially in our first opening statement, it can be really hard to screen for autonomic symptoms, but that is really a hallmark of neuropathies because the autonomic nervous system is also composed of nerves. So, in a busy clinical environment, how do you suss this out, and what are you asking patients about?   Dr. Seyedsadjadi: It's a great question, I don't think you can never be perfect on that because as you said, in order to do the justice, you really have to go through all systems. One way is to use some of the outcome measures that autonomic symptoms you can ask the patient sort of in ahead of the time. But there are some questions that are more important, and it is difficult to get them from patients if you don't really ask them. And sometimes we shy away for different reasons from those questions. Some of these could be related to the function of the bowel and bladder, erectile dysfunction, specific questions about orthostasis, IBS-like symptoms, early satiety, and some overlap syndrome symptoms like dry eyes and dry mouth could indicate different things. These are the main categories of the questions that you ask. And when you start asking these questions, sometimes patients start adding symptoms, "Oh, I don't have this, but I also have, like, some other dysmotility issue." So, that comes up.   Dr. Albin: Ab

In this episode, Lyell K. Jones Jr, MD, FAAN, speaks with Noah A. Kolb, MD, who served as the guest editor of the October 2026 Peripheral Nerve and Motor Neuron Disorders issue. They provide a preview of the issue, which publishes on October 2, 2026. Dr. Jones is the editor-in-chief of Continuum: Lifelong Learning in Neurology® and is a professor of neurology at Mayo Clinic in Rochester, Minnesota. Dr. Kolb is a professor of neurological sciences at the Robert Larner College of Medicine at the University of Vermont in Burlington, Vermont. Additional Resources Read the issue: continuum.aan.com Subscribe to Continuum®: shop.lww.com/Continuum Continuum® Aloud (verbatim audio-book style recordings of articles available only to Continuum® subscribers): continpub.com/Aloud More about the American Academy of Neurology: aan.com Social Media facebook.com/continuumcme @ContinuumAAN Host: @LyellJ Full episode transcript available here Dr. Jones: The human brain is incredibly complex. That's one of the reasons we like to study it and care for patients with neurologic problems. But to translate cognition into action, we need a functioning sensorimotor and autonomic peripheral nervous system. What do we do when those peripheral systems aren't working? Today, we're speaking with Dr. Noah Kolb, guest editor of our latest issue of Continuum on peripheral nerve and motor neuron disorders.   Dr. Jones: This is Dr. Lyell Jones, Editor-in-Chief of Continuum. Thank you for listening to Continuum Audio. Be sure to visit the links in the episode notes for information about subscribing to the journal, listening to verbatim recordings of the articles, and exclusive access to interviews not featured on the podcast.   Dr. Jones: This is Dr. Lyell Jones, Editor-in-Chief of Continuum: Lifelong Learning in Neurology. Today, I'm interviewing Dr. Noah Kolb, who is Continuum's guest editor for our latest issue on peripheral nerve and motor neuron disorders. Dr. Kolb is a professor of neurology at the University of Vermont Larner College of Medicine in Burlington, Vermont, where he specializes in the care of patients with neuromuscular disorders, including patients with peripheral neuropathy and other immune-mediated neuromuscular diseases. Dr. Kolb, welcome. Thank you for joining us today. Why don't you introduce yourself to our listeners?   Dr. Kolb: Well, thank you very much for having me. Please call me Noah. I've been a longtime listener of Continuum, dating all the way back to when they came on CDs, so it's really a pleasure to be here. Like you said, I'm a neuromuscular doctor up in Vermont. I take care of the whole scope of neuromuscular disease, but kind of wear 3 different hats. I focus my research primarily in chemotherapy-induced neuropathy, but also do other diseases as well. Obviously, see patients clinically, and then I'm an educator as well, so I run the neurology clerkship and the acting AIs for the medical school. So, it's a fun job.   Dr. Jones: Well, thanks for sharing that little bit of history on Continuum Audio, Noah. I got to be honest with you, I don't know if I've ever seen a Continuum Audio CD. If anybody out there in the audience has a Continuum Audio CD, post a picture online and we'll like and share it. I wonder how many of those are still out there. I really appreciate you not just joining us today, Noah, but also putting together this really stellar issue, a very timely update and overview of peripheral nerve and motor neuron disorders. A lot of good topics for us to dig into today. What I'm going to do before we get into questions is ask our audience Continuum Audio's trivia question. Dr. Kolb and I were talking about this before we started recording here. So, the trivia question, just to frame it up a little bit, the transthyretin or TTR protein receives a lot of attention in neuromuscular medicine as the protein behind the most common causes of acquired and familial amyloidosis. But transthyretin is known in clinical settings by a different name and checked for an entirely different reason. So, the trivia question is, what is the other common name for transthyretin? Stick around, and we'll share the answer at the end of our interview. So, let's get right to it. Our listeners know that peripheral neuropathy is common, right? It affects 2 to 3 percent of the general population and 6 to 7 percent of patients who are older than 60. In your mind, Noah, what's the main thing you would like clinicians to know or do differently in the care of these patients?   Dr. Kolb: Yeah, that's a great question. I think it's something that we spend a lot of time teaching our residents and working with our fellows about is understanding the right workup for people presenting with neuropathy because it's very easy to overdo it with more labs and a broader workup than you need. So, when somebody presents with sort of a garden variety neuropathy that doesn't have red flags, the important things to order in terms of a workup are hemoglobin A1C, B12, and SPEP with IFE, potentially serum light chains, and some thyroid studies as well. Because those are really the most common reasons, and then to make sure that they ask the most important historical questions, like about alcohol use, et cetera. If you're going to find a cause for neuropathy, particularly if it's slowly progressive and sensory predominant, oftentimes the answer is found right in that basic workup.   Dr. Jones: Got it. And I think that's very well taken. And I think one of the questions that commonly comes up in the neuromuscular, but also in the broader neurology setting is, when you're evaluating a patient, especially an older patient who has a new onset length-dependent sensorimotor peripheral neuropathy, you've identified the neuropathy, and you're starting to consider what are those potential underlying disorders or risk factors that that neuropathy could be a warning sign of, right? So, you look for metabolic disease, B12 deficiency, paraproteinemia, et cetera. Where do you stop? In what settings do you do more expanded evaluations, genetic testing, et cetera?   Dr. Kolb: Yeah, and I think this kind of goes back a little bit to the last question where the primary focus of the workup that we do is driven by the most common causes. That's why hemoglobin A1C is so important. And so, thinking through what is likely to be the cause in the specific patient setting is kind of really critical. And again, if you don't have red flags, then the labs that we mentioned previously are probably sufficient in terms of a workup. But if there are any of the other red flags, it's really important specifically because there may be treatable causes of neuropathy or things that would affect the prognosis that'd be important to understand earlier so we can make sure we either engage the right therapies or do a broader diagnostic workup. An important part of that is understanding when to use EMG nerve conduction studies and when not to. So obviously, as a neuromuscular doc who does EMGs, I'm very fond of them. But we regularly see patients in our lab who perhaps don't need one. If somebody has a sensory predominant, slowly progressive neuropathy, particularly if you have an etiology, those patients usually don't need an EMG nerve conduction study. When it's asymmetric, when there's prominent weakness, when there's a lot of autonomic symptoms, those are the times when it can be a lot more informative and helpful to try to get an EMG nerve conduction study to see if we can get at what the underlying etiology is.   Dr. Jones: That's very helpful, Noah. Thank you. And so, let's think about a scenario that I think many of our listeners may have encountered in their practice. You're seeing a patient who has a somewhat rapidly progressive, painful neuropathy, which has some small fiber characteristics. They've got a little bit of autonomic dysfunction, and you worry about the possibility of amyloidosis. How do you approach that evaluation and treatment, and why is it important to think about that diagnosis?   Dr. Kolb: Yeah, that's great. It's important to think about that diagnosis because we now have good treatments for AL amyloid and for ATTR-based amyloid. So, because these are treatable disorders, it's really critical that you identify them. And the reality is it's not always straightforward making a diagnosis of amyloid. As you would with any other type of neuropathy, the workup is gonna begin with serum free light chains, SPEP, trying to see if there are any monoclonal gammopathies or elevation in light chains. But importantly, you need to think about what the next diagnostic steps are and understanding how likely those tests are to be abnormal in the setting of amyloid is important as well, because the easier to obtain tests don't have perfect sensitivity. So, once you've moved on kind of from the basic labs, we think about a fat aspirate or a skin biopsy to look and see if there's any evidence of amyloid. But if your clinical suspicion is high enough, it's important to move to a sural nerve biopsy and genetic testing. That's really the best way to confirm this diagnosis.   Dr. Jones: Very helpful. And obviously, that's not just academic, as it might have been at one point. This is something that we now have good disease-modifying therapies for, which leads to another question that I think our listeners may encounter in their practice. When you think about all the available gene tests in panels and other genomic tools that we have to investigate patients, when do you do a broad genetic evaluation for patients with neuropathy?   Dr. Kolb: Yeah, it's a good question. It depends partly on specifically what we're looking for. I think that as with many things in neurology, one of the reasons I got interested in it, and many people did, is we like doing detective work, and the history often lies in the examinatio

Sleep plays a critical role in brain development, learning, memory, and behavior throughout childhood and adolescence. In this episode, Dr. Kristin Seaborg discusses how sleep architecture changes across development, the impact of sleep disorders on attention, headaches, epilepsy, and neurodevelopmental conditions, and why neurologists should routinely assess sleep in pediatric patients. Learn practical approaches to recognizing sleep problems, including obstructive sleep apnea and insomnia, and how improving sleep can enhance neurologic and cognitive outcomes. In this episode, Casey S. Albin, MD, FAAN, speaks with Kristin Seaborg, MD, author of the article "Sleep in the Developing Brain" in the Continuum® August 2026 Sleep Neurology issue. Dr. Albin is a Continuum® Audio interviewer, associate editor of media engagement, and an assistant professor of neurology and neurosurgery at Emory University School of Medicine in Atlanta, Georgia. Dr. Seaborg is an Assistant Professor in the Department of Neurology at the University of Wisconsin–Madison in Madison, Wisconsin. Additional Resources Read the article: Sleep in the Developing Brain Subscribe to Continuum®: shop.lww.com/Continuum Earn CME (available only to AAN members): continpub.com/AudioCME Continuum® Aloud (verbatim audio-book style recordings of articles available only to Continuum® subscribers): continpub.com/Aloud More about the American Academy of Neurology: aan.com Social Media facebook.com/continuumcme @ContinuumAAN Host: @caseyalbin Guest: @KristinSeaborg  Full episode transcript available here Dr Albin: In neurology and life, we are all looking for the secret to being attentive, focused, and engaged, and we certainly want that for our children. And what if the answer to all of that was just in sleep?  Dr Jones: This is Dr. Lyell Jones, Editor-in-Chief of Continuum. Thank you for listening to Continuum Audio. Be sure to visit the links in the episode notes for information about earning CME, subscribing to the journal, and exclusive access to interviews not featured on the podcast.  Dr Albin: Hello, this is Dr. Casey Albin. Today I'm interviewing Dr. Kristin Seaborg about her article on sleep in the developing brain. This article appears in the August 2026 Continuum issue on the neurology of sleep. Welcome to the podcast, Dr. Seaborg. Thank you so much for being here. I learned a lot from your article. Can you just briefly introduce yourself to the audience?  Dr Seaborg: Sure. Thank you for having me. I'm thrilled to be here. My name is Kristin Seaborg. I'm a pediatric neurologist and sleep neurologist at the University of Wisconsin Medicine. I also run the pediatric sleep neurology clinic at UW Madison.  Dr Albin: That is the perfect person to be writing this article. And every time I read an article about pediatric neurology, I am just so struck that like little tiny humans are not small adults, that they actually have a totally different neurobiology. They are in different stages of development. And this was really a topic that I was not familiar with, and probably for most of our listeners, they're not familiar with as well. And so, I thought we'd maybe just start with some of the basics. What is going on in terms of like pediatric sleep architecture, and how is that different than the adult architecture that we might be m- more familiar with?  Dr Seaborg: Sure. So, a lot of us think that sleep is the thing we do that when, when we're not doing other stuff. But actually, it's completely the opposite. During sleep, our brain is learning and consolidating memory and cleansing what's happened during the day, and that's especially important during infancy and early childhood development, and as a child gets older. If we take infants for an example, fifty percent of their sleep is in a precursor of REM sleep, which we call active sleep, which is much, much more than adults, as opposed to adults have about thirty percent of their sleep in REM sleep. And also, infants need sleep like fifteen to seventeen hours a day. Not all of that is consolidated in one continuous period. They usually sleep over the course of the day, fifteen to seventeen hours, and that sleep time decreases over the course of childhood and adolescence as well.  Dr Albin: Yeah, it's amazing that there's so much more going on. As someone who's had newborns, it feels like, oh my gosh, they're really just sleeping all day. They're not doing anything. But they're doing quite a lot, and that really is so much work for their developing brain. And then one of the things that also really struck me about the article is that as children move from infancy through adolescence, not only is the sleep architecture changing, but the time they go to sleep, the amount of sleep they need, some of the pathology that they may develop, it changes throughout these early years of their life. And so maybe when we are thinking about what patients might come to the clinic with, I assume a lot of parents are kind of concerned like, "Is my child getting enough sleep? Are they sleeping the normal amount? Are they sleeping in the timeframe that would be normal?" Walk us through just in broad strokes, like what is a normal amount of sleep as you go through that pediatric developmental phase?  Dr Seaborg: So that's not a one-sentence answer. And there's a table in the Continuum article.  Dr Albin: Love that.  Dr Seaborg: So, infants sleep like fifteen to seventeen hours, and it's chunked out over the course of the day. Usually they have one consolidated sleep period at night, but then two to three naps during the day. And as you move through early childhood, toddlers and adolescents usually need about fourteen hours of sleep around the time they're one year of age. As they get a little bit older, then they need like eleven to thirteen hours, depending on the child themselves. And then as we move toward like school age, like eight to ten hours of sleep is usually adequate, but especially younger school children need about ten hours of sleep at night. And then the interesting thing that happens in adolescence and early teenage years is that kids need just as much sleep, but they actually naturally fall asleep later because their melatonin is released later. So, it feels like they need to sleep all the time, but actually they just go to sleep later, and when school comes, it's not time or doesn't feel ready for them to wake up. So, adolescents and teens also need about eight to ten hours of sleep a night.  Dr Albin: Right. And I just was struck, you know, we think about it in this article and these issues, we've thought a lot about, I think it'll come up in other podcasts, the importance of daylight savings time and how that actually really is not good for our brains. And I feel so much for these teenagers who are really at a disadvantage because we make them get up early to participate in the world when it's not really aligned with how their natural sleep cycle is, and it feels unfair.  Dr Seaborg: It does. And there's so much to that. So, adolescents have school, and then a lot of time they have like after-school activities, whether that's sports or theater or music or whatever, but that usually happens after school. And then the reality of today's society is they come home, and at least my teenager disconnects or kind of decompresses by looking at her phone forever. And a lot of teenagers and adolescents bring their phone to bed. That exposure to light right up until the time when they want to go to sleep really can disrupt their circadian rhythm too. So they have the natural delayed circadian rhythm, and then they have these lifestyle exposures between activities after school and screens and everything else that really make sleep onset difficult. And so, waking up for school at 6:00 or 7:00 in the morning is really difficult for them.  Dr Albin: Gosh, I feel for that. And I suspect that many patients are coming into the sleep clinic with that exact sort of like my early teen, my preteen, my teenager. They're just exhausted all the time, but they won't fall asleep. They're developing insomnia. It sounds like there's a lot of behavioral changes that need to go along with that. Is that what you're seeing?  Dr Seaborg: Yeah. So, I'm also seeing an kind of a corollary, a lot of kids that come in with headaches because they're not sleeping enough, and they feel awful, or they're coming in with difficulty focusing in school or cognitive fog because they're not sleeping enough, and that they don't always know that that's the chief complaint. But often, as you start asking sleep-related questions, you figure out exactly what's going on. So, their amount they're sleeping and kind of their natural sleep cycle is affecting everything about their life.  Dr Albin: Yeah. It just-- it really struck me that, you know, one of the things that you talk about in the article is that there is, in patients who have neurodevelopmental differences and disorders, they may specifically have some sleep impairment, and they have a neurobiological reason for those sleep changes. But also, like you're saying, sometimes these inattentions or what's diagnosed as ADHD is actually just because they are not sleeping well, and they can't focus. And I imagine that's really hard to tease out. Like, is there something when you're trying to tease that out in the clinic that helps you figure out, is it the dog wagging the tail or the tail wagging the dog?  Dr Seaborg: Sure.  Dr Albin: Which is coming first? Is it, is it really a neurobiology problem where they have nerve developmental disorders and therefore sleep problems, or they have sleep problems causing the symptoms of a nerve developmental disorder?  Dr Seaborg: So, there's so many ways to answer that question. The very first part is you start at the beginning, not only asking the person's chief complaint, lik

Circadian rhythms influence far more than sleep, affecting neurologic disease expression, treatment response, and overall health. In this episode, Dr. Sabra Abbott discusses common circadian rhythm disorders, the health consequences of circadian misalignment, and practical strategies for managing jet lag, shift work, and disrupted sleep-wake schedules. Learn how circadian biology can shape neurologic outcomes and why considering the timing of behaviors, light exposure, and treatments may improve patient care. In this episode, Katie Grouse, MD, FAAN, speaks with Sabra M. Abbott, MD, PhD, author of the article "Circadian Neurology" in the Continuum® August 2026 Sleep Neurology issue. Dr. Grouse is a Continuum® Audio interviewer and a clinical assistant professor at the University of California, San Francisco in San Francisco, California. Dr. Abbott is an Associate Professor of Neurology at Northwestern University Feinberg School of Medicine in Chicago, Illinois. Additional Resources Read the article: Circadian Neurology Subscribe to Continuum®: shop.lww.com/Continuum Earn CME (available only to AAN members): continpub.com/AudioCME Continuum® Aloud (verbatim audio-book style recordings of articles available only to Continuum® subscribers): continpub.com/Aloud More about the American Academy of Neurology: aan.com Social Media facebook.com/continuumcme @ContinuumAAN Full episode transcript available here Dr Grouse: Circadian rhythm disruption affects many of our patients in far-reaching aspects of their general health and has likely personally affected most neurologists at some point in their career. Today, I have the opportunity to interview Dr. Sabra Abbott, who is the author of the latest issue of Continuum on Neurology of Sleep.  Dr Jones: This is Dr. Lyell Jones, Editor-in-Chief of Continuum. Thank you for listening to Continuum Audio. Be sure to visit the links in the episode notes for information about earning CME, subscribing to the journal, and exclusive access to interviews not featured on the podcast.  Dr Grouse: This is Dr. Katie Grouse. Today, I'm interviewing Dr. Sabra Abbott about her article on circadian neurology. This article appears in the August 2026 Continuum issue on Neurology of Sleep. Welcome to the podcast, and please introduce yourself to our audience.  Dr Abbott: Thanks for having me. I'm Dr. Sabra Abbott. I'm an associate professor of neurology at Northwestern, and I'm also director of our circadian medicine clinic.  Dr Grouse: It's really great to have you today. I definitely enjoyed reading your article, and not only did I learn a lot, but I feel like it's really applicable to a lot of topics that come up in clinic when I see patients. Now, I was wondering if you had to choose one key point that readers of your article would take away after reading it, what would it be?  Dr Abbott: I think the most important thing to keep in mind is that time is an important variable in every single thing that we do. And so, it can impact when your patient's disease is at its best and at its worst, and then it also can impact when it's actually most appropriate to provide medications for your patients. There can be times where they may be more impactful and times where they may actually cause more harm for your patients. So, the short answer is think about time always with your patients.  Dr Grouse: On that topic, I was really amazed to learn about the significant health risks associated with circadian misalignment, including even malignancy risks. Can you review some of these risks and why this might be the case?  Dr Abbott: So, I think the risk that we have the most data for is the risk for cancer associated with circadian misalignment, and this comes from a lot of studies that we're looking at patients who are shift workers. The data has actually come back on two separate reviews indicating that shift work could be a probable carcinogen, and we think that that probably comes down to a lot of different factors. So, when you're a shift worker, you are often working in the middle of the night. You may be getting light exposure at a time when you're normally producing melatonin, and that may be one factor that is actually putting you at increased risk for cancer.  Dr Grouse: And certainly, after reading this and hearing all of these things, I'm not surprised that many sleep specialists really dislike daylight savings time, which also is enough of a factor to potentially increase some of these health risks. Do you agree that daylight savings time is something that's contributing to poor health in our population?  Dr Abbott: So, I think it is definitely something that almost all of us want to get rid of, and I think where everybody is in agreement is that we should get rid of these shifts in the spring and the fall. I think the only benefit to those shifts that I see is it does create a time where we start having conversations about your circadian clock, so people become aware of circadian timing twice a year when we have these shifts. Outside of that, that shift back and forth seems to be very problematic. So, we do see both in the fall and the spring an increased risk for car crashes, an increased risk for heart attacks, stroke. People perform worse at work, and so I think in general, we probably should get rid of it. There's a little bit of a debate as to whether we should go to permanent standard time or permanent daylight saving time. I think most sleep and circadian scientists prefer permanent standard time. A lot of people who really like their evening activities prefer permanent daylight saving time, but I think that's also biased by the fact that daylight saving time, everybody has longer days, and I think they want longer days year-round, and you don't get that no matter which way you shift the clock in the winter.  Dr Grouse: That's really interesting. I do see that debate pop up every, I guess twice every year, and I guess there is a silver lining that at least we are all talking about it and thinking about it. I wanted to take a step back about the topic of circadian rhythm disorders in general. Could you just really quickly, like twenty-thousand-foot view, summarize what these main circadian rhythm disorders are?  Dr Abbott: So, at the moment, we primarily think of circadian rhythm disorders in the context of how they impact your sleep-wake timing. And so, at the largest level, we think of them as either intrinsic disorders, so disorders where your internal timing doesn't match up with the environment. The four key disorders there are advanced and delayed sleep wake phase disorders, so you're either earlier or later. You have non-twenty-four, where you actually generally get later and later each day, so it's like you're living on Mars. And then we have irregular, where you have multiple bouts of sleep that happen both night and day. And then the other two are the extrinsic disorders, so these are shift work disorders. So, you may have a normal functioning clock, but the external environment is forcing you to do things you wouldn't normally, or jet lag, where you again have a normal functioning clock, but then you end up having to shift multiple time zones faster than you can adapt to. Now, I think the interesting thing, and we can talk about this more if you want, is that we are moving into thinking of circadian rhythm disorders as being much more than just abnormalities of sleep-wake timing, and I think that's kind of where the future of the field goes.  Dr Grouse: Tell me more about that.  Dr Abbott: So, I think as the article gets into beyond just these kind of classically recognized disorders, we realize that circadian disruption can play a role in almost any other medical disorder that you can experience. And so, we can see circadian disruption as either a symptom or a potential cause of many other disorders. And then also in the optimal care of pretty much any patient, thinking about all of these other factors that they're experiencing on a day-to-day basis, whether it's their light exposure, whether it's the timing of their meals, whether it's the timing of their medications, all of those can play a role in their overall health and improving your ability to care for them.  Dr Grouse: Now, I did find it really fascinating. This was not something that I had really been aware of prior to reading your article about the fact that it really can make a difference about when you time particular medications for particular types of neurologic conditions just related to the circadian rhythm. And really interesting was the epilepsy connection. Can you tell me about how that affects how we should be dosing anti-seizure medication?  Dr Abbott: So, I think the epilepsy connection is an interesting one that definitely needs far more studies. So, at this point, a lot of this data is really coming from observational studies, looking at when patients have received medications and then how good their outcomes are. And in epilepsy, I think a lot of us tend to time anti-seizure medications so that patients get more of them in the evening and lower doses during the daytime. And I think a lot of this has been driven a little bit more by the fact that many of these medications are sedating, so we tend to put the more sedating medications at bedtime. But it turns out that outcomes in patients are actually better if they get higher doses at night and lower doses in the morning. Now, this is sort of theorizing at this point, but it could either be targets of these medications or your ability to uptake these medications across the blood-brain barrier may change with the time of day component. So, at this point, these are still really observational studies, but I think an area where we really need to do a lot more work.  Dr Grouse: Well, I look forward to hearing more about other ways that we'll learn how best to manage our med

Hypersomnia encompasses a group of disorders characterized by excessive daytime sleepiness that can significantly impair quality of life and neurologic function. In this episode, Dr. Margaret Kay-Stacey discusses how to recognize and evaluate hypersomnia, reviews key features of narcolepsy and idiopathic hypersomnia, and highlights the many neurologic conditions associated with excessive sleepiness. Learn practical approaches to diagnosis, treatment, and distinguishing primary hypersomnia disorders from more common causes such as insufficient sleep, sleep apnea, medications, and depression. In this episode, Gordon Smith, MD, FAAN, speaks with Margaret Kay-Stacey, MD, author of the article "Hypersomnia" in the Continuum® August 2026 Sleep Neurology issue. Dr. Smith is a Continuum® Audio interviewer and a professor and chair of neurology at Kenneth and Dianne Wright Distinguished Chair in Clinical and Translational Research at Virginia Commonwealth University in Richmond, Virginia.   Dr. Kay-Stacey is an Assistant Professor of Neurology and Ambulatory Medical Director at the University of Chicago Medical Center in Chicago, Illinois. Additional Resources Read the article: Hypersomnia Subscribe to Continuum®: shop.lww.com/Continuum Earn CME (available only to AAN members): continpub.com/AudioCME Continuum® Aloud (verbatim audio-book style recordings of articles available only to Continuum® subscribers): continpub.com/Aloud More about the American Academy of Neurology: aan.com Social Media facebook.com/continuumcme @ContinuumAAN Host: @GordonSmithMD  Full episode transcript available here Dr Smith: So, what do myotonic dystrophy, Parkinson's disease, and traumatic brain injury have in common? It turns out that each can cause clinically significant and meaningful hypersomnolence. And did you know that narcolepsy has the same population prevalence in the United States as myasthenia gravis, something I commonly see in clinic? If you want to learn more about hypersomnolence and how it impacts the patients you care for and what to do about it, keep listening.  Dr Jones: This is Dr. Lyell Jones, Editor-in-Chief of Continuum. Thank you for listening to Continuum Audio. Be sure to visit the links in the episode notes for information about earning CME, subscribing to the journal, and exclusive access to interviews not featured on the podcast.  Dr Smith: This is Dr. Gordon Smith. Today, I'm interviewing Dr. Meg Kay-Stacey about her article on hypersomnia, which appears in the August 2026 Continuum issue on the neurology of sleep. Meg, welcome to the podcast, and maybe you can begin by just introducing yourself to our audience.  Dr Kay-Stacey: Yeah. Hi, I'm so glad to be here. So, like you said, I'm Meg Kay-Stacey. I'm a sleep neurologist at the University of Chicago. I'm also the AAN's Sleep Section vice chair.  Dr Smith: Awesome. I didn't quite know what to expect in reading your article, except it was gonna be about people who are really sleepy. I was really amazed at how common these problems are, even, we'll get into this, disorders that I think of as being super rare. So, I know our listeners are gonna really enjoy hearing from you. I wonder if you could begin by just defining hypersomnia and maybe give us a flavor for the impact this has on patients who have primary disorders of hypersomnia.  Dr Kay-Stacey: Yeah. I mean, so hypersomnia is really an excessive daytime sleepiness, so a feeling of excessive sleepiness, feeling like they can't stay awake during the day. And these patients' quality of life is quite impacted by these symptoms, and there's lots of different conditions that can cause it, but it can be quite detrimental to day-to-day living.  Dr Smith: I honestly am sleepy a lot cause I work too hard or stay up late, and sleepiness seems to be a very common symptom. How do you sort out when a patient's excessive daytime sleepiness is pathologic related to lifestyle and the extent to which it may be a sleep apnea versus one of the other disorders that we'll talk about?  Dr Kay-Stacey: Yeah. I mean, you really have to take a good history. So as neurologists, we know that, that we have to do that, but particularly a sleep history and really understand, first and foremost, how much sleep the patient is getting. Really important to understand, are they getting adequate sleep at night, right? Because chronic insufficient sleep can cause daytime sleepiness, right? And can make people appear like they might have a primary hypersomnia disorder when in fact they don't. So that's sort of first and foremost, and then it's assessing the other symptoms that they have. So, it's assessing nocturnal symptoms. You mentioned sleep apnea, so assessing for things like snoring and witnessed apneas, nocturia, and then assessing for what the quality of their sleep like. Is it refreshing? Is it not refreshing? How easy or hard is it to wake up in the morning? And then asking them again about daytime symptoms. Are you falling asleep inappropriately at work? Are, you know, you falling asleep while driving? Are you finding it hard to stay awake even after you've had a full night of sleep? To really try to differentiate what the symptoms might be from. And then it's also assessing things, sleep apnea, for example, physical exam findings. You know, are they obese? Do they have a larger neck circumference? Is the airway more crowded? And then we do have some measures, some scales, so there's the Epworth Sleepiness Scale that we'll use that assesses sleepiness, which is kind of a good way to at least initially assess how sleepy a patient might be during the day.  Dr Smith: So that's great, and we'll talk a bit about sleep apnea, I hope. But when I hear hypersomnia, I always think about narcolepsy, and I wonder if maybe we can begin there.  Dr Kay-Stacey: Yeah.  Dr Smith: I was super interested to learn how common this is. About as common as myasthenia gravis. Actually, the population prevalence number is exactly the same as myasthenia. My Monday morning clinic is mostly myasthenia. So how do we recognize narcolepsy? Cause I'm worrying that I'm missing it.  Dr Kay-Stacey: Yeah. So, narcolepsy, you know, there's two types. There's narcolepsy type 1 and narcolepsy type 2. So, narcolepsy type 1 is a little easier because you have cataplexy. But with both conditions, you're gonna see excessive daytime sleepiness. You're gonna ask about things like sleep paralysis, whether or not they're having sleep-related hallucinations, so hypnagogic or hypnopompic hallucinations. Are they having other sort of REM, intrusion phenomenon? You may also hear things like REM behavior disorder, so acting out their dreams at night, and then some degree of, you know, difficulty waking up in the morning, feeling like they need to nap. Naps are often more refreshing in patients with narcolepsy which is a feature that when we talk about idiopathic hypersomnia kind of helps to differentiate them. So, it's really just asking about sleepiness and assessing for these other symptoms that they can have associated with narcolepsy.  Dr Smith: I was also interested to learn that narcolepsy is the most common cause of REM sleep behavior disorder in young patients, which is pretty cool. But I wonder, you used a term that I've never heard of, and I'm betting some of our listeners haven't, which is REM intrusion phenomenon. Could you tell us more about that? Dr Kay-Stacey: Yeah. So, this is the idea that in narcolepsy, your sleep states are sort of, jumbled up, would be the way of thinking of it. You have these phenomenon where REM will persist into wakefulness. So, sleep paralysis is actually a perfect example of that, right? That you wake up and you feel like you're awake, but your body is still paralyzed, you can't move. Cataplexy is similarly a REM intrusion phenomenon, as are these hallucinations that I mentioned, the sleep-related hallucinations.  Dr Smith: So what pearls do you have for recognizing cataplexy? What's the spectrum of cataplexy?  Dr Kay-Stacey: Yeah. So, I think cataplexy, it's associated with emotion, right? And we most commonly think about it being associated with laughter, right, with positive emotion, but it's key to remember that it can happen with negative emotion too, with fright, being upset or angry. And usually when you're asking patients about it, you wanna phrase it to understand, are they having episodes where they feel like they have brief loss of muscle tone? And it can be subtle. It can be a head drop, their mouth opening, a hand dropping something, and it's brief. Usually it's seconds to just a couple of minutes. These aren't prolonged episodes, and they're not losing consciousness. They're awake, they're just having that brief loss of muscle tone.  Dr Smith: So, what about orexin? I'm particularly interested in how often it's necessary to do an LP and look for CSF orexin levels. Is that a common thing in your practice, or do you rely on clinical phenomenology in a, you know, polysomnogram with multiple sleep latency testing to confirm a diagnosis of narcolepsy?  Dr Kay-Stacey: Most commonly, you're gonna still do the PSG and the MSLT, obviously, because it's less invasive than doing the lumbar puncture. There are scenarios, right, where you may consider doing the LP. I think if someone has cataplexy and you're pretty confident in that and they have a positive PSG, MSLT testing done, you know, you really don't need the lumbar puncture, right? But if you're in that gray area that for whatever reason you have a really high suspicion they have narcolepsy, but for whatever reason the PSG, MSLT either couldn't be done or it was inconclusive, then I might think about doing the lumbar puncture. The other scenario is that there are some patients who have to be on REM-suppressing medications, like antidepressants, for example. In those patients, it can confound the re

Insomnia affects neurologic health, quality of life, and daily functioning, but effective treatments are available. In this episode, Dr. Brandon Peters-Mathews discusses a practical approach to evaluating chronic insomnia, highlights the importance of identifying contributing conditions such as sleep apnea and mood disorders, and reviews cognitive behavioral therapy for insomnia (CBT-I), the recommended first-line treatment. Learn how addressing sleep can improve outcomes across a wide range of neurologic disorders. In this episode, Katie Grouse, MD, FAAN, speaks with Brandon R. Peters-Mathews, MD, FAAN, FAASM, author of the article "Insomnia" in the Continuum® August 2026 Sleep Neurology issue. Dr. Grouse is a Continuum® Audio interviewer and a clinical assistant professor at the University of California, San Francisco in San Francisco, California. Dr. Peters-Mathews is the Section Head of Sleep Medicine at Virginia Mason Franciscan Health in Seattle, Washington. Additional Resources Read the article: Insomnia Subscribe to Continuum®: shop.lww.com/Continuum Earn CME (available only to AAN members): continpub.com/AudioCME Continuum® Aloud (verbatim audio-book style recordings of articles available only to Continuum® subscribers): continpub.com/Aloud More about the American Academy of Neurology: aan.com Social Media facebook.com/continuumcme @ContinuumAAN Host: @BrandonPetersMD Full episode transcript available here Dr Grouse: Insomnia may be one of the most common medical issues experienced by patients, yet our knowledge about how to manage it remains limited. Today, I have the opportunity to speak with one of the world's leading experts on sleep disorders, Dr. Brandon Peters-Mathews, about the latest issue of Continuum on Neurology of Sleep.  Dr Jones: This is Dr. Lyell Jones, Editor-in-Chief of Continuum. Thank you for listening to Continuum Audio. Be sure to visit the links in the episode notes for information about earning CME, subscribing to the journal, and exclusive access to interviews not featured on the podcast.  Dr Grouse: This is Dr. Katie Grouse. Today, I'm interviewing Dr. Brandon Peters-Mathews about his article on insomnia. This article appears in the August 2026 Continuum issue on Neurology of Sleep. Welcome to the podcast, and please introduce yourself to our audience.  Dr Peters-Mathews: It's my pleasure to join you, and I'm happy to talk about this article. I think it's an interesting one for most folks. I am a board-certified sleep neurologist. I practice at Virginia Mason Franciscan Health in Seattle. I did my neurology training back at the University of Minnesota and my sleep training at Stanford University. I've been in practice for more than thirteen years at this point. It's hard to believe, but it's exciting to be able to speak with you today.  Dr Grouse: This is definitely an important topic for everybody. Certainly, sleep and the lack of it affects all of our patients, and I can't imagine there's a single clinical neurologist who doesn't have to answer questions and help evaluate patients with this problem, so very high-yield topic for everyone. Now, having read your article, I'm curious if you had to choose one key point that you want the readers of your article to take away after reading it, what would it be?  Dr Peters-Mathews: Emphasize for my patients that insomnia is a condition that we can work through and resolve, that if we really can understand the underlying contributing causes and resolve those issues, we can typically improve sleep. It's a process. It takes time. It takes some attention and, and sometimes even testing to figure out what's going on. But if we can dial into these root causes, we can typically help somebody to sleep much better. As part of that, we often employ a therapy called CBT-I, which we'll talk about here a little bit later. But that also helps us to identify some of these contributing factors that are leading to the poor sleep.  Dr Grouse: And I definitely want to talk more about CBT, it's such an important topic. But even before we get into that, I'd love it if you could just walk us through a hypothetical case of a patient with insomnia. I think the type of patient that I think we've all seen in our clinical practice and somebody who says, "You know, I've had poor sleep. I've had insomnia for many years. I've tried all of the things you're supposed to try. You know, I've tried sleep hygiene. I've tried this. I've tried that. I've tried medications. Nothing seems to work." Could you walk us through how you would evaluate a patient like this and start to consider what to recommend? Dr Peters-Mathews: So, some simple information that we can gather, would be information about when they're trying to go to bed, how long it's taking them to fall asleep initially. If they wake in the night and have trouble getting back to sleep, how often they wake in the night. If they're experiencing early morning awakenings, their final wake time, and when they actually get out of bed in the morning. That gives me a sense of the structure of their sleep pattern and whether or not they might be spending an excessive amount of time in bed for their own sleep need at their current age. The other factors that we might consider are sleep disorders, and typically, I would assess for other symptoms that would point me towards sleep apnea or restless legs and occasionally other disorders of sleep. We wanna make sure we're not missing comorbid conditions that might be affecting that person. These often include mood disorders. Sleep and mood walk hand in hand, and so anxiety and depression are important to identify and treat if present. We also want to make sure someone's not suffering from chronic pain or other conditions that might be impacting their sleep. So, I take a broad approach. I ask the same questions to each patient that comes to see me. I wanna make sure I'm not missing some of these details. And then some of these folks will require testing to further understand their sleep. Others may move on to a different therapy, and long-term may require even other interventions, including medications, to fully resolve their condition.  Dr Grouse: You mentioned in your article circadian rhythm sleep disorders. How often are these really a factor in patients with chronic insomnia? And do you think that's something that we as kind of first-line clinicians should be screening for as well?  Dr Peters-Mathews: So delayed sleep phase syndrome is the most common circadian disorder, and these are folks who are night owls by nature. They often develop their sleep patterns, as teenagers, if not before, and they may fade away in the working years but come back in retirement age. I would say that's a very common condition. It may affect as many as one in ten people. The other circadian disorders are pretty uncommon, so advanced sleep phase syndrome, where somebody is sleepy early and waking too early, that may only affect one in three hundred people. There are other conditions that affect specific populations, like non-twenty-four circadian pattern affects blind people. Typically, half of blind people have that condition. There are conditions that affect the regularity of sleep, so an irregular sleep-wake pattern that might occur more in folks with maybe an advanced dementia. So, there are populations where these conditions can be fairly common, but among the general population, that night owl tendency is by far the most common.  Dr Grouse: That's really helpful. And just taking a step back, why is insomnia bad for us? So, we worry about this in our patients. We know it can make neurologic issues worse. But in general, like, what are the reasons that having poor sleep can affect our health? Dr Peters-Mathews: Yeah, and it's not enough hours, certainly quantity, but also quality of sleep that matters. And I tell people that sleep is a pillar of health, just like nutrition and exercise. It's the other main contributor to our health and well-being. And so, it has its fingers in almost every aspect of our health. Insomnia on its own is a risk factor for other psychiatric conditions, including depression, anxiety, even disorders like bipolar and schizophrenia. Folks with insomnia are more likely to have alcohol or drug abuse issues and are at higher risk for things like chronic pain, suicide and, and social and occupational dysfunction. So, it's a disorder that has a really profound effect on how someone functions during the day, and again, may take a toll on their health over time.  Dr Grouse: That makes sense, and I would assume that there are certain populations within our neurology practices where we should really be attuned to the risk of insomnia. Are there specific populations you'd recommend really make it a habit of screening for insomnia?  Dr Peters-Mathews: I was joking with someone recently that anyone with a neurological nervous system can have issues, impacted by poor sleep. There are certain groups, so chronic headache patients are perhaps one that might warrant a further evaluation and management. Folks with multiple sclerosis or Parkinson's may have physical conditions that lead to more discomfort in sleep, fewer movements of their body in sleep, issues around nocturia that would disturb their sleep. Certainly, those with dementia, Alzheimer's disease and other dementias. Parkinson's and Lewy body dementia overlap a lot, as does multiple system atrophy. That can point us towards other conditions like REM sleep behavior disorder, but also insomnia can be an important feature of those disorders as well. And then folks with stroke often have disturbance to their sleep and may develop insomnia after experiencing a stroke. So those are specific populations where I think the yield is high to be looking for insomnia and other sleep disorders.  Dr Grouse: Yeah, that makes sense. I think a lot of us think

Central sleep apnea is a complex and often underrecognized sleep-related breathing disorder that differs from obstructive sleep apnea by involving reduced respiratory drive rather than upper airway obstruction. In this episode, Dr. Ran Liu reviews the underlying mechanisms of central sleep apnea, including the role of ventilatory control instability, discusses its association with neurologic conditions such as stroke, multiple sclerosis, ALS, and myasthenic disorders, and highlights key considerations for diagnosis and management. Learn how emerging technologies, personalized treatment strategies, and advances in sleep medicine are improving outcomes for patients with this heterogeneous group of disorders. In this episode, Teshamae Monteith, MD, FAAN, speaks with Ran R. Liu, MD, FRCPC, MSc, author of the article "Central Sleep Apnea" in the Continuum® August 2026 Sleep Neurology issue. Dr. Monteith is the associate editor of Continuum® Audio and an associate professor of clinical neurology at the University of Miami Miller School of Medicine in Miami, Florida. Dr. Liu is an Adjunct Clinical Assistant Professor at McMaster University in Hamilton, Canada, and an Adjunct Lecturer at the University of Toronto in Toronto, Canada. Additional Resources Read the article: Central Sleep Apnea Subscribe to Continuum®: shop.lww.com/Continuum Earn CME (available only to AAN members): continpub.com/AudioCME Continuum® Aloud (verbatim audio-book style recordings of articles available only to Continuum® subscribers): continpub.com/Aloud More about the American Academy of Neurology: aan.com Social Media facebook.com/continuumcme @ContinuumAAN Host: @headacheMD Guest: @SleepyNeuroDoc  Full episode transcript available here Dr Monteith: You may be familiar with obstructive sleep apnea, but central sleep apnea is often less understood and frequently underdiagnosed. In this podcast, we break down the key clinical pearls to sharpen your diagnostic reasoning, discuss why central sleep apnea matters, and to explore some of the fascinating advances transforming the field. Dr Jones: This is Dr. Lyell Jones, editor-in-chief of Continuum. Thank you for listening to Continuum Audio. Be sure to visit the links in the episode notes for information about earning CME, subscribing to the journal, and exclusive access to interviews not featured on the podcast.  Dr Monteith: This is Dr. Teshamae Monteith. Today, I'm interviewing Dr. Richard Liu about his article on central sleep apnea. This article appears in the August 2026 Continuum issue on Neurology of Sleep. Welcome to our podcast. How are you?  Dr Liu: Good. Thank you, Dr. Monteith, for having me today.  Dr Monteith: Please introduce yourself to our audience.  Dr Liu: Hello, everybody. My name is Richard Liu. I am a sleep neurologist. I am working out of Toronto at both Sunnybrook Health Science Center and MedSleep. I did my residency at Queen's for neurology and my sleep medicine fellowship at Harvard University.  Dr Monteith: Great. And what got you interested in sleep?  Dr Liu: Thank you very much for asking. For me, sleep medicine is a field where essentially everything is connected. Certainly, impaired sleep can affect many other conditions, including many neurological conditions. And even within sleep medicine, when somebody has a sleep disorder, often the entire system is connected. So as an example, if you have insomnia and fragmented sleep and periodic limb movements of sleep, certainly these conditions can impact sleep apnea. And certainly, for today's topic of central sleep apnea, this is an extremely complicated disorder where it's a very in-depth integration between neurological and respiratory physiology, among other systems as well.  Dr Monteith: So, I guess you're kind of like the cornerstone, sleep being the cornerstone of neurology. Everyone has to sleep. That's for sure. Great. So why don't we talk about what central sleep apnea is, and how prevalent is it as a collective group of disorders compared to obstructive sleep apnea?  Dr Liu: So, one way to think about central sleep apnea is that this is a heterogeneous group of etiology. But the primary concept here for central sleep apnea is that there's a reduction in respiratory drive. This is in contrast to obstructive sleep apnea, where essentially this is some form of airway obstruction in the presence of relatively intact respiratory drive. And of course, there's mixed apneas where they may contain features of both. But of course, now we know that even obstructive sleep apnea, there's a certain degree of drive dependence somewhat blurring these distinctions. The overall prevalence of central sleep apnea is about five to ten percent of all patients with sleep- disorder breathing. And certainly, it could be higher in some neurological conditions, such as things like stroke, multiple sclerosis, and multisystem atrophy.  Dr Monteith: Great. So certainly, it's out there. Why don't you tell us about the objectives of your article?  Dr Liu: Absolutely. Thank you for asking. I think the main objective of this article is really to highlight that central sleep apnea is a complex syndrome resulting from a large group of heterogeneous etiologies. And of course, again, it could be associated with many neurological conditions. And really here, I want to highlight advancements, both medicine and technology, on both the side of diagnosis of central sleep apnea, as well as the multimodal targeted treatment.  Dr Monteith: And what do you want our listeners to take away from this talk and certainly your article? What are the key essential points?  Dr Liu: Thank you very much for asking. I think that one way of looking at central sleep apnea to etiologically divide this into both hypocapnic and hypercapnic central sleep apnea. And of course, loop gain being a major driver for a hypocapnic central sleep apnea, and that one can actually think about hypocapnic central sleep apnea beyond a phenotypic spectrum with obstructive sleep apnea, with many patients having overlapping features of both obstruction and central component. On the other hand, hypercapnic central sleep apnea, often also known as hyperventilation syndrome, can span etiology from chemoreflex dysfunction to a broad range of neuroanatomical localization, such as central nervous system, peripheral nervous system, neuromuscular junction, and muscle disorders.  Dr Monteith: And what are some of the symptoms of central sleep apnea? Do any of them differ from obstructive sleep apnea?  Dr Liu: Thank you for asking, that's an excellent question. So certainly, central sleep apnea symptoms can overlap with obstructive sleep apnea symptoms. And of course, given the large range of underlying etiology, often the CSA symptoms depend on the underlying etiology. There may be less snoring compared to obstructive sleep apnea patients, especially the hypocapnic CSA patients. Of course, these patients, like OSA, may have frequent awakenings, gasping and choking their sleep, and nocturia, and so on.These patients may have daytime sleepiness, insomnia-like symptoms, or they could be asymptomatic. Interestingly, the hypocarbnic central sleep apnea patients, they're a bit more prone to have the insomnia-like symptoms, whereas the hypercarbnic central sleep apnea patients, they tend to have a bit more of the daytime sleepiness and morning headaches.  Dr Monteith: You spoke about some of the neurological disorders that might be associated with central sleep apnea, like stroke and multiple sclerosis. What about some of the more traditional risk factors associated with obstructive sleep apnea or conditions associated with it, like obesity and hypertension? Or does that just mix the picture?  Dr Liu: There is many overlap between risk factors between obstructive sleep apnea and central sleep apnea, and certainly one of the things that I highlight in this article is really that often it's not just black and white, that this could be a spectrum with overlapping disease between both conditions. So certainly, in our neurological world, stroke is the most common thing that may be associated with central sleep apnea. But overall, cardiovascular issues such as heart failure, atrial fibrillation, these things can also be associated with central sleep apnea. And again, from the neurological perspective, if we were to divide from hypocarbnic versus hypercarbnic central sleep apnea, by thinking about the hypercarbic central sleep apnea, again, this is where we're thinking about hypoventilation syndromes. You know, anything that can cause neuromuscular weakness, this is something that we should have a high alarm for, that potentially there may be a hypoventilation component. So, things like any myasthenic syndromes and ALS.  Dr Monteith: Great. Why don't we also talk about the classification? When was the last time central sleep apnea's classification was updated, and what should we know about the classification?  Dr Liu: The most recent classification for central sleep apnea is written in the International Classification of Sleep Disorders, third edition. In this edition, it's classified with six central sleep apnea syndromes. So, these are the CSA with Cheyne-Stoke breathing, CSA due to high altitude periodic breathing, primary CSA, CSA due to medication or substance, CSA due to medical disorder without Cheyne-Stoke breathing, and treatment-emergent central sleep apnea. These classifications more so describe the circumstance of when CSA occurs. A more etiological classification that we can consider would be classifying them by the underlying pathophysiology, which is dividing this from hypercarbnic central sleep apnea versus a hypocarbnic central sleep apnea. Certainly, both set of classification are discussed in this article.  Dr Monteith: Yeah. You discussed at length, the major physiological factors that our audience is ju

Advances in sleep technology are transforming how neurologists identify and manage obstructive sleep apnea, a condition that affects up to 70% of patients with certain neurologic disorders and can negatively impact cognitive and neurologic outcomes if left untreated. In this episode, Dr. Joyce Lee-Iannotti discusses the growing role of wearable and nearable sleep-monitoring devices, when home sleep studies are appropriate, and how emerging technologies are expanding access to diagnosis and treatment. Learn practical strategies for screening patients, interpreting sleep data, and partnering with sleep specialists to improve long-term neurologic health through better sleep. In this episode, Casey S. Albin, MD, FAAN, speaks with Joyce K. Lee-Iannotti, MD, FAAN, FAASM, author of the article "Sleep Diagnostics and Monitoring Technology in Obstructive Sleep Apnea" in the Continuum® August 2026 Sleep Neurology issue. Dr. Albin is a Continuum® Audio interviewer, associate editor of media engagement, and an assistant professor of neurology and neurosurgery at Emory University School of Medicine in Atlanta, Georgia. Dr. Lee-Iannotti is a Professor of Neurology at the Barrow Neurological Institute, University of Arizona College of Medicine, and Creighton School of Medicine in Phoenix, Arizona. Additional Resources Read the article: Sleep Diagnostics and Monitoring Technology in Obstructive Sleep Apnea Subscribe to Continuum®: shop.lww.com/Continuum Earn CME (available only to AAN members): continpub.com/AudioCME Continuum® Aloud (verbatim audio-book style recordings of articles available only to Continuum® subscribers): continpub.com/Aloud More about the American Academy of Neurology: aan.com Social Media facebook.com/continuumcme @ContinuumAAN Host: @caseyalbin Guest: @jleeiannotti Full episode transcript available here Dr Albin: Through the neurology of sleep issue, I think we have all been convinced that we all need better sleep, both for ourselves and for our patients. And fortunately, there is an abundance of new technology that can enable us to diagnose sleep problems, and then also make sure that our patients are getting the rest that's going to give them the best chance at a good cognitive recovery, and improve their cognitive function even if they are not currently suffering from a neurologic condition. Today, I am so excited to dive deeper into this topic.  Dr Jones: This is Dr. Lyell Jones, Editor-in-Chief of Continuum. Thank you for listening to Continuum Audio. Be sure to visit the links in the episode notes for information about earning CME, subscribing to the journal, and exclusive access to interviews not featured on the podcast.  Dr Albin: Hello, this is Dr. Casey Albin. Today I'm interviewing Dr. Joyce Lee-Iannotti about her article on sleep diagnostics and monitoring technology in obstructive sleep apnea. This article appears in the August 2026 Continuum issue on neurology of sleep. Welcome to the podcast, I'd love to just start by having you introduce yourself to our audience.  Dr Lee-Iannotti: Sure. Thank you so much for having me, Dr. Albin. I'm Joyce Lee-Iannotti. I'm a professor of neurology at Barrow Neurological Institute. I am boarded in general neurology, stroke, and sleep, but I spend most of my time in the sleep world, so I jokingly say that I get more sleep doing sleep than I certainly did in stroke.  Dr Albin: Absolutely. I mean, wow, what a fascinating career, and I suspect that we're actually gonna get to some of how all of those pathophysiologies might overlap in the world of sleep. But you had the really exciting task of trying to distill this exciting, rapidly evolving field of sleep diagnostics, and I suspect it's relevant to many of the patients who end up in the neurology clinic, and I suspect that it's actually pretty relevant to many of our listeners who themselves might actually be wearing sleep tracking devices. And all of us probably wonder, well, how can we use that data to improve our own cognitive function and certainly make our patient's life even better? Before we even get into some of the meat and potatoes of this, I thought it would be really helpful for us to define some terms that come up in your article, one of which is wearables. We might figure that out, but the other is nearable. Walk us through what's a wearable, what's a nearable, how are they different?  Dr Lee-Iannotti: I'm happy to do that. First of all, the article is entitled Sleep Diagnostics and Monitoring Technology, and this was a super fun article for me to write because it's very practical, and it's generalizable to everybody. So, I'm going to start with a wearable, and a wearable is really a device that is simply worn on the body. And we're all familiar with wearables like smart watches, they're rings, they're patches, they're headbands, and the most validated form of a wearable that you've probably heard about is actigraphy, which we use in the sleep clinic.  Dr Albin: Tell us a little bit more. So, what is actigraphy? I've heard the word before, but don't actually know what it means.  Dr Lee-Iannotti: Actigraphy has been a tool that we've used in the sleep clinic for a really long time. Traditionally, we used it to monitor circadian rhythm patterns in people who are night owls or morning larks. And then more currently, we actually use it to track sleep patterns in people with suspected narcolepsy. So, before they come in for a sleep study, we actually have them wear an actigraphy for about a week just to get a sense of their sleep duration and their circadian pattern.  Dr Albin: Got it. And what is it monitoring? Our movement or the patterns that we may or may not make?  Dr Lee-Iannotti: It's really based on movement. You're exactly right.  Dr Albin: Cool. Okay, so most of this is based on gold standard monitoring with actigraphy. What other things can be incorporated into these wearable devices?  Dr Lee-Iannotti: Yeah, the technology is really advanced, and every day it changes, which is super exciting. So, on top of movement, these wearables can look at temperature. They can look at even EEG, like limited EEG, heart rate variability, and a really big word that we like to use in sleep technology, which is PPG, or photoplethysmography data, and that's really looking at heart rate variability and oxygenation, saturations, and following those levels as well.  Dr Albin: Wow, so you basically can get most of the data that you might have historically needed to go to a sleep lab to get.  Dr Lee-Iannotti: Most of them. They're still a surrogate. You'll hear me emphasize in the article as well that the gold standard remains the in-lab polysomnogram, but these are good surrogate markers that patients can wear long term to look at trends and patterns.  Dr Albin: Absolutely. And we're gonna unpack a little bit about who specifically those are best for and, really what it gives you in the clinic. But before we jump into that, what's a nearable, and how is that different?  Dr Lee-Iannotti: Yeah. Nearables are really exciting too. So, these are devices that monitor sleep but don't require direct contact on the body. So, these are devices that our patients will use, but it'll be at the bedside table. They're devices that actually go underneath the mattress, or they can be in, like, the ambient environment to detect sleep patterns.  Dr Albin: Oh my gosh. How is it doing that if it's not actually something you're wearing? Dr Lee-Iannotti: I know. It seems a little Big Brother-ish, doesn't it?  Dr Albin: Yes.  Dr Lee-Iannotti: So, they use a technology called radio frequency signals, sometimes radar, sometimes sonar, pressure sensors, even microphones, and they're picking up things like respiration, movement, snoring, and that's how they can decipher sleep patterns.  Dr Albin: Crazy. I mean, I guess the benefit of that is that it's less disruptive to the user 'cause it's not actually on them and having contact with them, and I suspect there's probably some downsides in terms of just it's a more limited data set you're getting.  Dr Lee-Iannotti: Absolutely. Yeah, you're exactly right. It's more convenient because it's not touching them, so, in theory, they're gonna sleep more comfortably. But I would like to think that the most validated forms of devices that we use to track sleep have to have some form of contact with the body, and this technology is new and probably needs a few layers of more sophistication to be as accurate as the wearables.  Dr Albin: Absolutely. I feel like we're going to have this conversation in five, maybe even less than that, years, and this data will have become like, oh, we all have something in our room that's monitoring everything. The world is crazy. All right. One of the places where your article really stood out to me is that sleep diagnostics have really taken off, particularly when we're thinking about obstructive sleep apnea. And I think we all might sort of scratch our heads and be like, "This is a neurology podcast. Why should I, as a neurologist, care about obstructive sleep apnea?" But I think you laid out a very convincing argument in the article. Walk us through why we should care about this.  Dr Lee-Iannotti: Absolutely. So, for neurologists, sleep matters, and I hope that my article translates that. Obstructive sleep apnea, which I'm gonna call OSA, is incredibly common in all of our neurologic patients, whether you see epilepsy, Parkinson's, stroke, Alzheimer's, neuromuscular, or even chronic headache patients. The prevalence of sleep apnea is as high as 70% in these patients.  Dr Albin: Wow. That's incredible. That is an incredibly high number.  Dr Lee-Iannotti: And if I can add, Dr. Albin, there's growing literature in multiple studies across the literature that show that untreated sleep apnea negatively impacts neurologic outcomes in our patients. So, it is really impo

Obstructive sleep apnea affects approximately one in four adults and is especially common among patients with neurologic disorders, including stroke, Parkinson disease, dementia, epilepsy, and neuromuscular conditions. In this episode, Dr. Stephanie Stahl discusses why neurologists should routinely screen for OSA, highlights key symptoms and risk factors, reviews important considerations when interpreting sleep studies, and outlines current treatment options beyond CPAP. Learn how recognizing and treating sleep apnea can improve quality of life, optimize management of neurologic disease, and reduce long-term health risks. In this episode, Aaron L. Berkowitz, MD, PhD, FAAN, speaks with Stephanie M. Stahl, MD, FAASM, author of the article "Obstructive Sleep Apnea" in the Continuum® August 2026 Sleep Neurology issue. Dr. Berkowitz is a Continuum® Audio interviewer and a professor of neurology in the Department of Neurology at the University of California, San Francisco, in San Francisco, California. Dr. Stahl is an Associate Professor of Clinical Medicine and Sleep Medicine Fellowship Program Director at Indiana University School of Medicine in Indianapolis, Indiana, where she also serves as Sleep Laboratory Medical Director in the Division of Pulmonary, Critical Care, Sleep, and Occupational Medicine. Additional Resources Read the article: Obstructive Sleep Apnea Subscribe to Continuum®: shop.lww.com/Continuum Earn CME (available only to AAN members): continpub.com/AudioCME Continuum® Aloud (verbatim audio-book style recordings of articles available only to Continuum® subscribers): continpub.com/Aloud More about the American Academy of Neurology: aan.com Social Media facebook.com/continuumcme @ContinuumAAN Host: @AaronLBerkowitz  Full episode transcript available here Dr Berkowitz: Obstructive sleep apnea is very common. It can cause or contribute to common neurologic symptoms, such as headache and impaired cognition, and it's a risk factor for stroke. And yet, if you're like me, you may not know too much more about sleep apnea than that. Today, I have the pleasure of talking to sleep expert Dr. Stephanie Stahl to learn what every neurologist should know about OSA.  Dr Jones:  This is Dr. Lyell Jones, Editor-in-Chief of Continuum. Thank you for listening to Continuum Audio. Be sure to visit the links in the episode notes for information about earning CME, subscribing to the journal, and exclusive access to interviews not featured on the podcast.  Dr Berkowitz: This is Dr. Aaron Berkowitz. Today I'm interviewing Dr. Stephanie Stahl about her article on obstructive sleep apnea. This article appears in the 2026 Continuum issue on Neurology of Sleep. Welcome to the podcast, Dr. Stahl, and could you please introduce yourself to our audience?  Dr Stahl: Yeah. Thank you for having me. I'm a sleep medicine physician and neurologist and medical director of the Indianapolis Sleep Lab at Indiana University Health. I serve as the director of the Sleep Medicine Fellowship program. I'm faculty advisor for our very first student interest group in sleep medicine at Indiana University School of Medicine. I'm also actively involved in some national leadership roles, including the incoming chair of the American Academy of Sleep Medicine's Education Committee and co-chair of the Academy's Inter-Scorer Reliability Gold Standard Panel. So, I really appreciate this opportunity. I look forward to our discussion.  Dr Berkowitz: Me too, and we appreciate the opportunity too to get to talk to you. You have so much expertise in this area, and I certainly encourage our listeners to look at your article, which is very comprehensive and up to date, and I learned a ton from it. I didn't get much exposure to sleep neurology as a trainee, and I've always worked in academic centers where we have a sleep group and we can refer patients there. So, I have to admit, sleep may probably be the area of neurology I know the least about, and felt like I was learning something new from pretty much every line of your article, and I know our readers will too. So, your article has a lot of excellent detail for our readers on the diagnosis and treatment of this very common condition. But I'd like to keep our interview relatively high level today and focus on the essentials for the practicing general neurologist. So, to start, can you just give us a sense of what obstructive sleep apnea is, and what every neurologist should know about it?  Dr Stahl: Yeah. So obstructive sleep apnea is characterized by either partial or full obstructions in the upper airway. That may sound pretty simple, but this leads to a whole bunch of issues. It leads to oxygen desaturations, arousals from sleep, leading to sleep fragmentation. This can then lead to sympathetic nervous system activation, cerebral hypoperfusion, leading to a whole bunch of symptoms or neurologic conditions.  Dr Berkowitz: Great. And you mentioned this in your article, but just to emphasize, how common is obstructive sleep apnea in the general population?  Dr Stahl: Yeah. So, about a quarter of the general population have obstructive sleep apnea. Much more common in many neurologic conditions.  Dr Berkowitz: Yeah, so very common disorder. We are seeing patients with it quite frequently, whether that's the reason they are seeing us in neurology or not. And this leads to my next question, which is what neurologic symptoms or presenting concerns of a patient should make us think about OSA and the differential diagnosis, and what factors based on the history or the exam or the context would make you suspicious for OSA as the cause of a neurologic symptom? In other words, the patient's presenting with classic symptoms of OSA, and that's why they're seeing a neurologist or seeing a primary care doctor, but is coming for evaluation of, say, headache or other symptoms. And what symptoms would make you think of wanting to consider OSA, and then what aspects of the history or otherwise would make you want to evaluate the patient for OSA?  Dr Stahl: I think a really important takeaway is for neurologists to know that obstructive sleep apnea is very common in neurologic conditions and has that potential to worsen a lot of these conditions or their associated symptoms. And so, it should be on our radar. There are certainly some basic questions and signs and symptoms that we can ask patients about or, or take a look at on exam. And so particular symptoms include snoring. Anybody that snores loudly or frequently, that's a strong risk factor for obstructive sleep apnea. If someone's seeing them stop breathing in their sleep, if they are waking up a lot throughout the night. There are some other symptoms that we may not necessarily attribute upfront to obstructive sleep apnea, such as nocturia, nocturnal reflux, night sweats. There are some daytime symptoms, of course, too, like unrefreshing sleep, daytime sleepiness, morning headaches, an important one in neurology. And then we take a look at the patient's exam. And so, some things that neurologists might want to be thinking about are people with obesity are certainly at a risk for obstructive sleep apnea. But it's also very important to know that someone does not need to have obesity in order to have obstructive sleep apnea. We look at neck size, other morphologic characteristics, such as how much that we can see in the back of their mouth. Can we see their uvula? Does their tongue size appear large in their mouth? And then some other risk factors too, such as male gender, older age, family history, post-menopausal state in women. All that being said, though, sometimes in neurologic conditions, we don't have all of those symptoms or risk factors to be thinking about. And so, in certain neurologic conditions such as stroke where obstructive sleep apnea is very common and has the potential to increase the risk of another stroke, we may need to be thinking about testing these patients even with minimal symptoms or other risk factors.  Dr Berkowitz: That's very helpful. So, you mentioned their headache might be the presenting symptom, right, to a neurologist, and we should certainly be thinking about obstructive sleep apnea as a potential diagnosis, even the cause of the patient's headache, particularly you said patients with morning headache. I often try to think about in patients presenting with, for memory loss, or other cognitive concerns, and that may be due more to inattention from poor sleep, so asking about sleep and symptoms of sleep apnea in those contexts. Are there any other presenting neurologic symptoms not particularly related to sleep? I'm thinking of headache, memory loss, other symptoms that would make you think, "Oh, I should actually screen this patient for sleep apnea also."  Dr Stahl: Yeah, other symptoms to think about in pediatrics, hyperactivity, people that have impaired vigilance, as you alluded to, that poor attention. Sometimes people get misdiagnosed with ADHD, and it's actually just a manifestation of obstructive sleep apnea.  Dr Berkowitz: You alluded to this, Dr. Stahl, that stroke, for example, patients are at higher risk of developing sleep apnea as a result of stroke, and it's also a risk factor for stroke. What other neurologic conditions, primary neurologic diseases, put patients at a higher risk of OSA? And again, similar to the last question I asked you, what are some clues that we should evaluate for? We might be following a patient for their post-stroke care over time and not necessarily thinking about diagnosing a separate condition in them since we're following them for their stroke or their degenerative disease. What are the conditions that put patients at a higher risk of OSA as a result of the condition, and then when would you think about screening them for it?  Dr Stahl: Some particular neurologic conditions where obstructive sleep apnea are very common

In this episode, Lyell K. Jones Jr, MD, FAAN, speaks with Karin G. Johnson, MD, FAAN, who served as the guest editor of the August 2026 Sleep Neurology issue. They provide a preview of the issue, which publishes on August 3, 2026. Dr. Jones is the editor-in-chief of Continuum: Lifelong Learning in Neurology® and is a professor of neurology at Mayo Clinic in Rochester, Minnesota. Dr. Johnson is a Professor in the Department of Neurology at the University of Massachusetts Chan School of Medicine–Baystate and the Sleep Medicine Division Chief at Baystate Medical Center in Springfield, Massachusetts Additional Resources Read the issue: continuum.aan.com Subscribe to Continuum®: shop.lww.com/Continuum Continuum® Aloud (verbatim audio-book style recordings of articles available only to Continuum® subscribers): continpub.com/Aloud More about the American Academy of Neurology: aan.com Social Media facebook.com/continuumcme @ContinuumAAN Host: @LyellJ Guest: @drsleepykarin  Full episode transcript available here Dr Jones: This is Dr. Lyell Jones, Editor-in-Chief of Continuum. Thank you for listening to Continuum Audio. Be sure to visit the links in the episode notes for information about subscribing to the journal, listening to verbatim recordings of the articles, and exclusive access to interviews not featured on the podcast.  Dr Albin: All right, welcome all. For the first time ever in the history of Continuum Audio, we are coming to you live from Chicago here at the AAN annual meeting. And now over to your host, the one and only editor-in-chief, Dr. Lyell Jones.  Dr Jones: Welcome, everybody. My name is Lyell Jones, editor-in-chief of Continuum, and I'm here today with Dr. Karin Johnson, and we're interviewing Dr. Johnson for the upcoming and recently published issue of Continuum on Sleep Neurology. We have been doing Continuum Audio for a while, but we're doing something different this time. As our listeners online can tell, we are recording this for the first time ever with a live studio audience at the American Academy of Neurology annual meeting in Chicago, Illinois. So, this is a fun experience for us. I hope it's been fun so far for you, Dr. Johnson.  Dr Johnson: Great to be here.  Dr Jones: It's great to have you. So, before we get into the interview, I do wanna introduce our team here for the live recording of the podcast. You've already heard Dr. Casey Albin's voice. Dr. Casey Albin is an associate professor of neurology at Emory University. Also serves as one of our associate editors at the journal and one of our Continuum Audio interviewers. So, she's going to be working the crowd today. Let's have a round of applause for Dr. Albin. And our guest of honor today is Dr. Karin Johnson. Dr. Johnson is a professor of neurology at UMass Chan Medical School and, Baystate Medical Center in Massachusetts. She is a world-renowned expert in sleep neurology and is the guest editor for the most recent issue of Continuum on Sleep Neurology. Dr. Johnson, welcome. Why don't you introduce yourself to our audience?  Dr Johnson: You did a great introduction, but I'm a clinical sleep medicine specialist. Spend my days seeing patients, taking care of people with narcolepsy, sleep apnea, restless legs, everything that comes my way. And then I have a side interest in doing sleep medicine advocacy, especially for permanent standard time.  Dr Jones: And we may get to that. I mean, that might be part of our conversation today. So, you've now read all of the articles in this issue, and it's a really great issue. There's a lot of new developments in sleep neurology. There are some updates for clinicians, people who see patients with sleep disorders that I think are, are timely and important updates. You have this unique view because you have just read all of these articles, really good articles by expert authors. When you read through these, Dr. Johnson, what was the biggest, what was the biggest thing that surprised you?  Dr Johnson: I think the biggest surprise for me is just so many changes in, in all of these articles. I realized how easy it was for us to make a journal that is so different from a few years ago. Whether it's Dr. Stahl's obstructive sleep apnea and new ways to think about endotyping sleep apnea that is gonna have treatment implications or the new treatments that are out there like tirzepatide, the changes that we're having with restless leg treatment. I particularly wanted to have a chapter on circadian neurology that Dr. Abbott did a great job really highlighting how if we think about the timing of when we give meds, the timing of when we eat, how that really can help neurological health, brain health, overall health, as well as mental health and cognition, especially as the AAN thinks about brain health as a whole, not just treating our patients, but how we can treat the population of people by improving sleep. I like how we hit on all these different areas in this issue.  Dr Jones: And I don't know how you managed to do it. They're just a small number of articles. We cover a lot of existing territory with well-characterized diseases, with new advances. But there's a lot of new stuff in sleep, and so somehow, it's all packed in there. It's really impressive. One of the things I was gonna ask you about was an evolution, and this has been a number of years now in how we manage restless leg syndrome. When I was training, it was all about dopamine agonists, and that was your first line. And over time, the evidence has supported moving away from that, and now we have more recent guidelines that have come out, and it's really the alpha-two delta-one calcium channel antagonists. How is that transition going? Do you still see people in practice who come in on dopamine agonists? How is that going? How's the field responding to that?  Dr Johnson: That's one of my most frequent restless leg consults. So even though it's been years since I have really initiated dopamine agonists in my patient, every day we get in people often on very high doses of dopamine agonists, and their doctors have just been escalating and escalating these meds over the years, and they come in with horrible augmentation. Their symptoms are much worse than they used to be, happening earlier in the day. And so, trying to get these patients off of these meds that are addictive, the way I like to teach about it is these dopamine agonists are the Fioricets of the sleep world. We know they work great, but in the long run, the patients are gonna be worse overall. And so, it's so hard to get people off these dopamine agonists, just like it's so hard to convince a headache patient that they don't need their Fioricet and that they're gonna be better off if we can get them off of it. What I think has really changed is we have more options to use. So, the alpha-delta-like agonists like gabapentin are now considered first line, but there's a lot of patients who they just don't work well enough with or they don't tolerate. And so, what do you do in that case? It's easy when that works, but and, when that doesn't work, we are being much more aggressive these days with iron replacement, potentially even trying to push ferritin levels in refractory patients up to three hundred, and using IV iron rather than just oral iron to get over the absorption issues to get the brain levels high enough. Motor stimulators, little cuffs that kind of go around the leg and stimulate the peroneal nerve in a certain way that not only can give people immediate relief, but also some data that suggests that over time it actually lessens their restless legs. We have agents like dipyridamole that work on the adenosine system in a sort of new novel pathway at addressing restless legs. And then the opiates, often meds like methadone or Suboxone can be used in some patients. But as we're getting more of these other options, often we don't need to go to those levels because we do have more to work with.  Dr Jones: So, the key point is lots of options. We're not starting with dopamine agonists anymore. And I think the fact that you're still seeing a lot of patients who have been initiated on that probably tells us there's an education gap field that we need to work on. So, another thing that I noticed reading through the issue was, and this feels like a change over the last few years, is the availability and the tendency to use in-home sleep apnea testing as opposed to formal, traditional in-lab. And that feels like a great new option, and maybe that increases and improves availability for patients who need access to the test. But how do you work through that?  Dr Johnson: So, I love in-home testing. We've been using it for over a decade. Other parts of the country where insurances didn't sort of mandate it are now being more mandated. I think the real change happened for a lot of places over the pandemic when labs closed down. But I think it's good because it brings a lot more patients to us. They get tested, they get tested quicker. People who would say, "I would never go into a lab. Oh, I'll do a home study." So, it just does bring more people in, and it gets them to treatment that they need that can really be life-changing. But it's not for everybody. The biggest people are people that have other bad pulmonary issues. If you're on oxygen therapy, you should not be getting a home study. That really should be a group of people that come in the lab. Similarly, if you have bad COPD, you probably should be getting a full in-lab study, so we can get more monitoring. Central sleep apnea is an interesting one. It can be very hard in some cases to differentiate the centrals and obstructive nature as well on a home study. Doesn't mean you can't do a home. So, if it's a person that just can't get an in-lab study easily, maybe you start with the home. If it looks purely obstructive, and you're all set, then you got an answer,

Unruptured intracranial aneurysms and arteriovenous malformations are frequently discovered incidentally on neuroimaging, presenting complex decisions around monitoring, referral, and treatment. This episode highlights key risk factors for rupture, the role of imaging in evaluation, and practical approaches to triage and management, including when specialist intervention is warranted. In this episode, Gordon Smith, MD, FAAN, speaks with Edgar Samaniego, MD, FAAN, authors of the article "Unruptured Intracranial Aneurysms and Arteriovenous Malformations" in the Continuum® June 2026 Cerebrovascular Disease issue. Dr. Smith is a Continuum® Audio interviewer and a professor and chair of neurology at Kenneth and Dianne Wright Distinguished Chair in Clinical and Translational Research at Virginia Commonwealth University in Richmond, Virginia. Dr. Samaniego is a professor of neurology, neurosurgery, and radiology and the director of the vascular neurology fellowship at the University of Iowa in Iowa City, Iowa. Additional Resources Read the article: Unruptured Intracranial Aneurysms and Arteriovenous Malformations Subscribe to Continuum®: shop.lww.com/Continuum Earn CME (available only to AAN members): continpub.com/AudioCME Continuum® Aloud (verbatim audio-book style recordings of articles available only to Continuum® subscribers): continpub.com/Aloud More about the American Academy of Neurology: aan.com Social Media facebook.com/continuumcme @ContinuumAAN Host: @GordonSmithMD Guest: @esamaniego Full episode transcript available here Dr Smith: Have you ever ordered an MRI of the brain and found a coincidental unruptured aneurysm or perhaps an arteriovenous malformation? If so, are you up to speed on how to manage this common situation, how to monitor, when to refer, and how to counsel your patients? If your answers to these two questions are yes and or no, then please keep listening.  Dr Jones: This is Dr. Lyell Jones, Editor-in-Chief of Continuum. Thank you for listening to Continuum Audio. Be sure to visit the links in the episode notes for information about earning CME, subscribing to the journal, and exclusive access to interviews not featured on the podcast.  Dr Smith: This is Dr. Gordon Smith. Today, I'm interviewing Dr. Edgar Samaniego about his article on unruptured intracranial aneurysms and arteriovenous malformations. This article appears in the June two thousand twenty-six Continuum issue on cerebrovascular disease. Edgar, welcome to the podcast, and maybe you can briefly introduce yourself to our listeners.  Dr Samaniego: Yeah. Thank you, Gordon. So, I'm an interventional neurologist. I'm practicing at the University of Iowa. I've been in Iowa for the last ten years. I'm originally from Ecuador. Did my residency in Wisconsin, and then I went to Stanford for neuro critical care and stroke. And then I did my neurointerventional fellowship at the Baptist Cardiac and Vascular Institute in Miami.  Dr Smith: You're a triple threat in the world of vascular and critical care, which I want to get to later. But your article's really great. I'll admit one of the first things I do when I read an article for Continuum Audio is I see how long it is. I saw yours was as long as the rest, and I was a little surprised because this sounded like a simple topic. But having read it, it's anything but simple. This is really important and complex stuff. I wonder if maybe you can orient our listeners to the importance of this. We frequently find unruptured aneurysms or vascular malformations on brain imaging that we order for something else. I mean, how common is that, and why do you think our listeners need to be particularly attentive to our conversation today?  Dr Samaniego: It's pretty frequent that we see patients with unruptured brain aneurysms. A lot of times, you know, we do imaging like CT angiograms, or magnetic, resonance angiography. Patients come to the ER with headaches, and we find an unruptured aneurysm. And you know, the question always comes, "What should we do with this aneurysm that we found?" We know that a lot of these aneurysms will not rupture, but the caveat is that when they rupture, like fifty percent of these patients may die or have bad outcomes. So, it's always a puzzling question, you know. What should we do with the aneurysm?  Dr Smith: Well, thanks, Edgar. I mean, this is certainly something that I come across. I'm glad to hear that other people struggle with this as well. What actually is the prevalence of aneurysms in the general population? How common is this?  Dr Samaniego: It's more common than what we think, you know. The, the estimates talk about like one in every fifty people have a brain aneurysm, and about every eighteen minutes an aneurysm will rupture. In the United States, there's approximately thirty thousand ruptures per year. So, there's a significant number of, of patients affected by brain aneurysms. And, and the key thing is that affects usually younger patients who are in the most productive years of their lives. So that's why it shouldn't be ignored, and once we find an aneurysm, we have to have all the information for triaging and deciding on treatment of these aneurysms.  Dr Smith: Well, it's a great way to begin our conversation. I mean, this is not a rare problem. It's a common problem, and there's actually a really great section of the article I'll refer people to about medical malpractice and the importance of recognizing and dealing with this thoughtfully. It's an empowering section, not a scary one, but this is important for our listeners to know about. Pretty high-stakes stuff. Maybe you can orient listeners like me or maybe simple neuromuscular people. What different types of aneurysms are there?  Dr Samaniego: That's the interesting question because there's multiple types of aneurysms, and there is a whole spectrum of aneurysm. When we say aneurysm, you can be talking about a fusiform versus a saccular aneurysm. We tend to classify them based on shape, also location. But the two main classifications for brain aneurysms will be saccular, which, you know, has a sac kind of morphology shape, and then you have the fusiform aneurysms. Those are the main morphological classifications. Then on top of that, you have two other subtypes that you see quite often. The one that we see is mycotic aneurysms that is like a misnomer because it's not a fungal aneurysm. It's just an infectious aneurysm that most of the time we see on the setting of endocarditis. These behave a little bit different than the typical saccular or fusiform aneurysms. And then also you have other more rare types of aneurysms like blister aneurysms that are sometimes located in the anterior wall of the carotid artery. So, you know, within this spectrum, we have those main aneurysms. The typical aneurysms, which can be fusiform or saccular, and also the more atypical, which can be mycotic and also blister-like aneurysms.  Dr Smith: I wonder if you might comment a little bit on the relevance of the type of aneurysm, fusiform, saccular, blister, and then location on rupture risk or prognosis.You have a really great figure about anatomic classification in the article actually that I encourage everyone to check out when they hopefully read it. But what do these characteristics imply for risk?  Dr Samaniego: Yeah. This is very complex question because, you know, entails different characteristics of aneurysms such as shape, the location, morphology. So, we know that some locations, for example, the anterior communicating artery has a high risk of rupturing as opposed to patients such as the part of ophthalmic aneurysm, which are usually located at the origin of the ophthalmic artery in the internal carotid artery. So, by risk of rupturing, the highest risk is usually the anterior communicating. Then you have posterior communicating artery aneurysms, which are usually located in the internal carotid artery, but because of their proximity to the origin of the posterior communicating artery, they're called posterior communicating artery aneurysms. Then you have the posterior circulation aneurysms on top of risk of rupturing is the top of the basilar artery location. Those three are the highest risk for rupturing: ACOM, PCOM, and top of the basilar. In terms of morphology, I always tell my patients, you know, if it's like a nice-looking aneurysm that has this rounded shape is a benign morphology. If you have the aneurysm that's having these Mickey Mouse ears that has these blebs or daughter sacs, those are aneurysms that usually scare us because those are the ones that usually rupture. So that's another criteria, morphology. And then the other criteria would be size. There is this magnificent study called ISUIA, which was published several years ago, and basically what it demonstrated was that aneurysms that are seven millimeters or larger are more likely to rupture versus smaller aneurysms. So those are the three criteria that I'm looking into when talking to patients about morphology, location, size, and the, the shape or morphology of the aneurysm.  Dr Smith: So, let's say a general neurologist or comprehensive neurologist practicing in a community setting in a rural area orders a, let's just say a CT or CTA for a patient with a TIA and finds what looks like an aneurysm. What's the next step in terms of imaging? What's the best next step? I mean, there are a bunch of different imaging modalities. Do you get an MRA? Is it time-of-flight, contrasted? You know, when do you get a DSA and so forth?  Dr Samaniego: Yeah. The first thing to do is to better characterize the aneurysm. Order of more accurate imaging that we can obtain without being invasive with a diagnostic cerebral angiogram. The rest will be a magnetic resonance angiography with contrast that, you know, gives you really good detailed information about the aneurysm. Similar

The period immediately after hospital discharge is a critical yet often overlooked phase in stroke recovery, marked by both heightened vulnerability and opportunities for rapid brain repair. This episode explores the concept of transitional stroke care, emphasizing early specialist follow up, coordinated multidisciplinary support, and targeted interventions to improve outcomes and reduce complications. In this episode, Katie Grouse, MD, FAAN, speaks with Mona N. Bahouth, MD, PhD, FAAN, author of the article "Transitional Stroke Care and the Road to Recovery" in the Continuum® June 2026 Cerebrovascular Disease issue. Dr. Grouse is a Continuum® Audio interviewer and a clinical assistant professor at the University of California, San Francisco in San Francisco, California. Dr. Bahouth is the medical director of the Brain Rescue Unit and an associate professor of neurology at Johns Hopkins School of Medicine in Baltimore, Maryland. Additional Resources Read the article: Transitional Stroke Care and the Road to Recovery Subscribe to Continuum®: shop.lww.com/Continuum Earn CME (available only to AAN members): continpub.com/AudioCME Continuum® Aloud (verbatim audio-book style recordings of articles available only to Continuum® subscribers): continpub.com/Aloud More about the American Academy of Neurology: aan.com Social Media facebook.com/continuumcme @ContinuumAAN Guest: @MonaBahouth Full episode transcript available here Dr Grouse: A lot of attention has been paid to what happens within hours to days of a stroke, but are we missing an equally crucial time in our patient's recovery after their discharge? Today, I have the opportunity to interview Dr. Mona Bahouth about the latest issue of Continuum on cerebrovascular disease.  Dr Jones: This is Dr. Lyell Jones, Editor-in-Chief of Continuum. Thank you for listening to Continuum Audio. Be sure to visit the links in the episode notes for information about earning CME, subscribing to the journal, and exclusive access to interviews not featured on the podcast.  Dr Grouse: This is Dr. Katie Grouse. Today, I'm interviewing Dr. Mona Bahouth about her article on transitional stroke care and the road to recovery. This article appears in the June 2026 Continuum issue on cerebrovascular disease. Welcome to the podcast, and please introduce yourself to our audience.  Dr Bahouth: Thank you for having me. I'm Mona Bahouth. I'm a stroke neurologist in Baltimore, Maryland, and I'm the medical director of our brain rescue unit at the Johns Hopkins Hospital. Great to be with you.  Dr Grouse: Thank you so much. This was a very interesting article. I have to confess going into it, I really didn't know a lot about transitional stroke care and the growing sort of recognition of its importance for stroke recovery and improved outcomes. Can you tell me what the key message from this article is that you really hope that readers will take away after reading it and hopefully integrate into their own patient practices?  Dr Bahouth: Yeah. I would say if there's one overarching message, it is that stroke care has come so far over the last couple of decades. We do so much wonderful life-saving work in the first couple of hours and days after stroke, but we haven't really paid as much attention to what happens once a patient leaves the hospital with this devastating acute disease. And I would just like to say that this article allows us to shine a light on providing a little bit more of a system of care, a more structured system of care that could benefit the patient for the long term, then that will benefit a large population of patients who otherwise may have complications that could cause disability longer in life.  Dr Grouse: Now, Mona, could you tell us in a nutshell, what is transitional stroke care, and why are we needing to focus more of our attention on this to improve patient recovery?  Dr Bahouth: Yeah. Over the last few years, we've really done a wonderful job of reducing the time that a patient spends in a hospital after stroke care. But in parallel, we have not really changed anything about what we do in the outpatient setting. So, a patient tells us that they come to the hospital with this acute and very scary and disabling disease. They feel that they're the center of the universe at our stroke centers, where we're hustling around them in groups and in interprofessional teams. But then on the day of discharge, they feel that they leave the hospital, and in some of our focus groups, that they kind of go home to a, a dark bedroom where they have to process all of this sort of on their own. It's quite a transition for both patients and their care partners. And here we've been very systematic about how we structure our care in the hospital for stroke patients, but once they leave the hospital, it's been a sort of free-for-all, or the Wild West, as some of my colleagues say. So transitional stroke care is really a way to extend the care that we deliver in the stroke unit to the patient's home or to their next phase of care. We know that stroke patients have 11 handoffs from beginning to end, in average, that they experience through the course of their acute stroke. And so, what we're really trying to do is extend the, the stroke unit to the patient's home or to their next phase of care so that they feel a bit more extension of that specialty care that they were receiving in the hospital. So, it's really a structure, a system.  Dr Grouse: Now, it seems that when we're thinking about the transitional care period, that it really hinges on this idea of sort of the sensitive period of stroke recovery. What is that, and why is that so important, and why do we really need to focus on that specific time?  Dr Bahouth: There are really two reasons that this is a critical period for patients. One is that we know from work in animal models as well as other sort of human early studies that the brain really has its optimal period of efficient brain repair in the first few weeks after stroke, meaning that it's recovering after this injury and figuring out how to reroute some really important brain functions. I would say it's also a critical period because the time period after stroke is a period that all the comorbid conditions that sort of conspired to cause a stroke are sometimes destabilized. And we know that sort of just putting people back on standard regimens for their hypertension, their diabetes, their heart failure doesn't always equate to sort of long-term improved outcomes at a time that the brain itself is going through changes. So, for example, we know that blood flow is critical to the brain. That's what all the hustle is about in the hyperacute period. And for the next couple of weeks after a stroke, autoregulation remains disrupted, so typical treatments of hypertension could have negative consequences for a subpopulation of patients. This management of hypertension needs to continue for a couple of days and weeks after stroke, and therefore, if a patient is discharged from the hospital, really requires a bit more specialty input. We also know that as the brain is trying to repair during the sensitive period, this high period of efficiency, we really want to inject high-intensity, high-quality activities that really improve their recovery. But in our current system in the United States, our transition to the period of rehabilitation is really quite clunky and disrupted and doesn't often happen in a seamless way. So, a true transitional stroke care program really attempts to manage the stroke itself. The comorbid conditions that conspire to cause the stroke, and the expedition of, of rehabilitation that could really jumpstart the recovery period in a more meaningful way.  Dr Grouse: Now, you mentioned hypertension as being sort of a critical factor that can affect the patients during this transitional period or this sensitive period. What are some other factors that can really play a huge part in their long-term outcomes in this really sensitive time?  Dr Bahouth: In our transitional stroke program, in our interprofessional group, we often talk about all of the changes that a patient is required to make at the time of stroke. Typically, they stay in the hospital several days. The patient and their care partner will receive a bolus of instructions about what their new healthier life should look like, and then they're sort of sent off to sort of self-manage without really accepting that that wasn't the perfect time to teach these things. So really, it's all about sort of lifestyle improvement. How do we get into a system of medication adherence when medications are a central portion of a patient's care? It is about managing the cognitive changes that happen after stroke, whether we acknowledge them in the hospital as a main deficit or something that people realize once they get back into the groove of their usual life, and the emotional consequences of stroke for both the patient and their care partner, who are both adjusting to this very scary moment that resulted in a brain injury. So, I think that the things that are focused on are both medical in terms of, you know, what are we doing with the diabetes? Is our glucose at a target range? Have we started wearing our sleep apnea paraphernalia? Are we managing our smoking cessation as much as we should? How have we done with our low-fat diet? Are we taking our medications as prescribed, or was there some cognitive blip that caused a mistake? But also sort of the emotional support that sometimes paralyze patients into sort of saying they cannot handle this transition into a new healthier way of brain recovery.  Dr Grouse: Yes, and it sounds like when patients sort of hit that wall, they almost just give up, right? There's just so many things they have to manage. They're emotionally trying to cope, and then they may eventually get to their neurologist at some poin

Intracerebral hemorrhage carries high morbidity and mortality, but growing evidence highlights meaningful opportunities for prevention, risk reduction, and long-term recovery. This episode covers key strategies, including blood pressure management, interpretation of neuroimaging markers, and individualized decisions around antithrombotic therapy. It also emphasizes the prolonged recovery timeline and the importance of a holistic, patient-centered approach to improving outcomes. In this episode, Casey S. Albin, MD, FAAN, speaks with Wendy C. Ziai, MD, and Vishank A. Shah, MD, coauthors of the article "Intracerebral Hemorrhage" in the Continuum® June 2026 Cerebrovascular Disease issue. Dr. Albin is a Continuum® Audio interviewer, associate editor of media engagement, and an assistant professor of neurology and neurosurgery at Emory University School of Medicine in Atlanta, Georgia. Dr. Ziai is a professor of neurology and critical care medicine at Johns Hopkins University School of Medicine in Baltimore, Maryland. Dr. Shah is an assistant professor of neurology and critical care medicine at Johns Hopkins University School of Medicine in Baltimore, Maryland. Additional Resources Read the article: Intracerebral Hemorrhage Subscribe to Continuum®: shop.lww.com/Continuum Earn CME (available only to AAN members): continpub.com/AudioCME Continuum® Aloud (verbatim audio-book style recordings of articles available only to Continuum® subscribers): continpub.com/Aloud More about the American Academy of Neurology: aan.com Social Media facebook.com/continuumcme @ContinuumAAN Host: @caseyalbin Guest: @VishankShah3 Full episode transcript available here Dr Albin: A patient has suffered an intracerebral hemorrhage. They're taken to the neuro ICU, and they fortunately survive. But the journey does not end there. In fact, in some ways, the journey has just begun. Join us today as we unpack holistic care for ICH patients.  Dr Jones: This is Dr. Lyell Jones, Editor-in-Chief of Continuum. Thank you for listening to Continuum Audio. Be sure to visit the links in the episode notes for information about earning CME, subscribing to the journal, and exclusive access to interviews not featured on the podcast.  Dr Albin: Hello to our audience. This is Dr. Casey Albin. Today, I'm interviewing Dr. Wendy Ziai and Dr. Vishank Shah about their article on intracerebral hemorrhage. This article appears in the April 2026 Continuum issue on cerebrovascular disease. Welcome to the podcast. I am so delighted that both of you are joining. To begin, let's just do a brief introduction of who you are and, and a little bit of how you got interested in the topic.  Dr Ziai: Hi, I'm Wendy Ziai. Thank you for having me on this podcast. I am a professor of neurology at Johns Hopkins. I am a neurointensivist, and I think I got primarily interested in this topic through clinical trials that I have been a part of since my fellowship days.  Dr Shah: Hi, everyone. I'm, uh, Vishank Shah. I am also, uh, very thankful for being invited to be a part of this podcast. I'm also a neurointensivist at Hopkins and the fellowship program director here for neurocritical care, and I'm interested in recovery after ICH, and that's why I'm a part of this work.  Dr Albin: Welcome to you both. It is such a treat for me to get to interview fellow neurointensivist, particularly those who have such a wealth of experience. So, I am delighted to dive into this. All right. So, to set the stage for our audience, intracerebral hemorrhage has long been approached with pessimism. But your article really highlights that there are meaningful advantages in prevention and risk stratification and long-term recovery for these patients. Though you both are neurointensivist, this article really emphasizes primary prevention and the holistic long-term care for the survivors. And so, to begin, Dr. Shah, can you just lay out a little bit for our listeners the scope of intracerebral hemorrhage and its community impact?  Dr Shah: Yeah. So, you know, ICH is the second most common type of stroke. There are more than three million new cases of ICH globally each year, and it accounts for thirty percent of all stroke types, but it is the one that has the highest mortality, with more than forty to fifty percent of the patients dying in the first thirty days, and then continued long-term impact on both functional as well as outcomes, as well as survivorship after the early period. And it also disproportionately impacts lower socioeconomic, and then minority races like Blacks, Asians, as well as Hispanic ethnicity. And so, there's a lot of work that needs to be done to reduce the burden of this disease.  Dr Albin: Absolutely. I mean, these can really be devastating for families, and I really am appreciative of your highlighting that there's a lot of disparities, and there's a lot of work to be done to really increase equity to these patients. I think a lot of this goes into really the AAN's focus on brain health and trying to improve some of what we're doing to maintain brain health. And I really wanted to kind of drill down on this because for ICH, there's a lot that can be done upfront as we think about how do we counsel patients who may walk into the office about strategies to prevent ever becoming an intracerebral hemorrhage patient. So, Dr. Shah, can you walk us through a little bit about what neurologists in the community need to be doing to make sure that no one ends up with us in the neurointensive care unit?  Dr Shah: Yeah, sure. So, I think, you know, one of the most important risk factors is, of course, hypertension and long-standing uncontrolled hypertension. And so really recognizing the need for early onset screening with regular blood pressure monitoring at a very early age, particularly in the races that I discussed earlier. And then I think another big part, obesity, metabolic syndrome, and type two diabetes. And I think there's a lot of interesting new work that with the GLP-1 agonist, you know, in a large multicenter cohort studies showing that patients receiving these had a significantly lower reduction risk of ICH. And so, this might be a really important part that, you know, clinicians need to start increasingly recognizing and using in their practice. And then, of course, other risk factors that are common include smoking, diet high in sodium, exposure to air pollution, both indoor as well as outdoor. And so, mitigating all of these risk factors can also reduce the burden of ICH.  Dr Albin: Absolutely. And I really want to highlight that hypertension plays such an important role and that we as neurointensivist, as community neurologists, really need to be creative about ways that we can help people meet those blood pressure target and meeting people in the community where they are, making sure that they're not suffering from side effects from their medication that would prevent them from sticking with it long term. Dr. Ziai, anything else to add about what we can do in the community?  Dr Ziai: So, we really want to emphasize, even in the acute phase, that patients moving forward need to have targeted interventions to reduce blood pressure, smoking, enhance their physical activity, have a diet that is high in fruits and vegetables and low in alcohol and salt, and then promoting weight loss, of course.  Dr Albin: And Dr. Ziai, I'm gonna ask you a little bit about one of the things that maybe not all of our listeners have heard about is this APOE2, APOE4 genetic risk for intracerebral hemorrhage. What's going on there and, and should clinicians be testing for that? Dr Ziai: That's a great question, and it is not one that we currently test people for at least acute ICH presentation. APOE2 and A4- E4 alleles, these give patients a two to three times higher risk of ICH by increasing cerebral amyloid deposition. And if you happen to have APOE2 carrier ship status, then along with other risk factors like white matter disease and vascular risk factors, these predict the onset of new microbleeds even during very short follow-up periods of about two years. And as we know, having cerebral microbleeds are associated with an increased risk of all strokes, ischemic and ICH, but they are one of many MRI markers of small vessel disease, which along with cortical superficial siderosis, does significantly increase future ICH risk. And so even in people who've never had an ICH, if they happen to have an MRI, it may be reasonable to look at the MRI and incorporate this burden of small vessel disease, and especially these hemorrhagic markers into, uh, decision-making about interventions.  Dr Albin: That's a really excellent point. And so, I think that your article did a really beautiful job of thinking holistically about the patient, incorporating clinical markers of their risk for having ICH, but also those radiographic markers. I'm just gonna ask you to summarize those again one more time because not everyone will be familiar with these. So, when you're looking at an MRI, what are the things that you're particularly clued in on that would increase the patient's risk of future ICH?  Dr Ziai: In the past, what we're looking for really is markers of cerebral amyloid angiopathy, which significantly increase a person's risk for lobar hemorrhage in particular. And so, we have a set of criteria called the Boston Criteria, and there's a new version of these, version 2.0. And these, um, incorporate a number of imaging markers that provide a very high sensitivity and specificity to diagnose CAA after an ICH. But even if someone's never had an ICH, and they evaluate that risk-benefit ratio for different cardiovascular prevention strategies. And so, the markers that we're specifically interested in are, of course, microbleeds. But not just having microbleeds, but are they lobar or are they deep? Lobar having a higher risk for lobar ICH.