Hypersomnia With Dr. Margaret Kay-Stacey

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 results. And so, if you're not able to stop those for the MSLT testing, then that would be a scenario where I might use the lumbar puncture. Insurance is another reason that, again, if you have some of that inconclusive findings on the PSG, MSLT, that doing the lumbar puncture then can help to confirm the diagnosis, but only useful for type 1 narcolepsy, not type 2.  Dr Smith: And type 2 is like type 1 but without cataplexy?  Dr Kay-Stacey: Exactly. And then you kind of can think of it as sort of on a spectrum, I would say. There's sort of narcolepsy type 1, and there's idiopathic hypersomnia, and narcolepsy type 2 kind of falls in between.  Dr Smith: Do you require the other core features of narcolepsy to make a diagnosis of type 2, like sleep paralysis, hallucinations?  Dr Kay-Stacey: Right. You do. You don't necessarily have to have all of them, but you will see similar features, though most of them are more common in, in type 1 than in type 2.  Dr Smith: So, I'm understanding you need to see, REM intrusion phenomena.  Dr Kay-Stacey: Mm-hmm. Yes.  Dr Smith: I love saying that. Makes me sound like I'm part of the sleep team. Now we're all part of the sleep team, aren't we?  Dr Kay-Stacey: Yeah.  Dr Smith: What about idiopathic hypersomnia? In reading about it and thinking about it, it sounds a lot like narcolepsy without those other features, but there, there are some differences. I wonder if you could give our listeners pearls into how to recognize that as opposed to maybe type 2 narcolepsy.  Dr Kay-Stacey: Yeah. So idiopathic hypersomnia patients are also very sleepy during the day. They're more commonly going to describe that they sleep through the night, often for long hours, and that they wake up and still feel very unrefreshed. They'll have what we call, morning sleep inertia, or some people call it, you know, sleep drunkenness, where when they wake up in the morning, they feel like they're in a haze or a fog. It's really hard to get out of bed. They're often setting multiple alarms. And this is after having a full night of sleep, ten, twelve hours of sleep, and then they just feel tired and sleepy all day. If they nap, their naps will often feel unrefreshing, and when they take naps, they're often longer naps, and then they wake up and again will maybe feel some of that sleep drunkenness or inertia, and it makes it difficult for them to wake up. And then they don't have as many of the REM intrusion phenomena, but you still can sometimes hear things like sleep paralysis or the hallucinations in patients with idiopathic hypersomnia. And so that's where it does get tricky when you're trying to differentiate from narcolepsy. Really, the difference with narcolepsy and idiopathic hypersomnia when you do testing has to do with what you see on the overnight sleep study on the polysomnogram followed by that multiple sleep latency test. In the case of all three conditions, the MSLT should show a mean sleep latency of eight minutes or less. What separates narcolepsy from idiopathic hypersomnia is that in narcolepsy, the expectation's you'll have two or more sleep onset REM periods, so you go into REM sleep very quickly. Whereas in idiopathic hypersomnia, you'll have one sleep onset REM period or less. Traditionally, you'd think of that you wouldn't have any, but you theoretically could have one on that. So, that's sort of one way that we can differentiate the two.  Dr Smith: That's really helpful, actually. Thank you. What about treatment? There are a whole bunch of different medications that you talk about in your article, including, medications that are in the pipeline, which is exciting. What's the treatment approach, maybe starting with narcolepsy?  Dr Kay-Stacey: Yeah. So, with narcolepsy, there are more FDA-approved medications and options then there are for idiopathic hypersomnia, which is, you know, one of the things I hope will change over time with things that are in the pipeline. But with narcolepsy, traditionally often start first with an alerting agent such as modafinil or armodafinil to really help with those daytime symptoms. And then there are a number of other medications that can be used. Sometimes if the armodafinil, modafinil don't work, we'll advance into stimulant medications that are amphetamine containing. At night, there's a medication called sodium oxybate that you can take for narcolepsy. The low sodium oxybate is actually also approved for idiopathic hypersomnia. But sodium oxybate, the idea is that you're taking it at night, and it's helping to reduce the disrupted sleep that occurs in patients with narcolepsy, really kind of enhances slow-wave sleep at night and makes the sleep that patients are getting better quality, which then improves both excessive daytime sleepiness during the day as well as the cataplexy. And then there are some other medications, solrimfetol and pitolisant, that are also used in narcolepsy. I don't wanna necessarily get into the nitty-gritty of all of the mechanisms of action, but definitely read the article to learn more about that. Dr Smith: So that's really helpful. What about cataplexy? Do these medicines also help with cataplexy, or is there a different approach for that symptom?  Dr Kay-Stacey: Yeah. So, sodium oxybate definitely can be used, and the low-dose sodium oxybate can be used to help with the cataplexy. But then we'll also sometimes use medications in the antidepressant category as well. So, SSRIs, SNRIs, and tricyclic antidepressants can all also be used to help in the treatment of cataplexy.  Dr Smith: And how about idiopathic hypersomnia?  Dr Kay-Stacey: Yeah. So, for idiopathic hypersomnia, there are, you know, as I mentioned, less treatment options and not as many things FDA-approved. But, it was exciting, low-dose sodium oxybate was approved for idiopathic hypersomnia, so it's taken at night, similar to how it's used in narcolepsy, and does improve that excessive daytime sleepiness. And then we often will also use some of the other medications off-label, so modafinil, armodafinil, and the stimulant medications. But some of the other meds like the pitolisant and solrimfetol, those are not FDA-approved for the use in idiopathic hypersomnia.  Dr Smith: So, I'm curious if we know what causes these conditions, so narcolepsy type 1, type 2, and idiopathic hypersomnia. I mean, the treatments all seem very kind of neuromodulatory in some way, you know, interacting with the REM system, for instance. What's the current thought regarding mechanism, underlying cause?  Dr Kay-Stacey: So, narcolepsy type 1, it's due to the loss of orexin neurons in the hypothalamus. So that one is sort of the easiest of them that we know that those orexin-producing neurons are lost. There are thoughts that both with narcolepsy 1 and type 2, that there is autoimmune related concept and then also potentially some genetics, though it's not completely clear that it's one mechanism or another. But certainly, easiest is narcolepsy type 1 with that loss of orexin neurons. For idiopathic hypersomnia, we're not exactly sure actually what causes it. Again, some thoughts about maybe there being an autoimmune-related phenomenon for some patients, may begin for them after they've had infection, for example. And then some thoughts that perhaps GABA receptors are impacted in idiopathic hypersomnia.  Dr Smith: Great. Well, that's super helpful, and I'm definitely gonna be on the lookout for narcolepsy. But let me pivot. I wonder if we might play a little bit of a game here. There's so many other things that cause hypersomnia, other disorders and situations, and rather than kind of march through them, I wonder if I could give you a name of a particular neurologic disease or situation and have you provide our listeners just a sentence or two about one thing they should know about hypersomnia in that disorder. You up for it?  Dr Kay-Stacey: Sure.  Dr Smith: So, let's begin with my backyard, myotonic dystrophy.  Dr Kay-Stacey: Yeah. So myotonic dystrophy, we see an association actually with narcolepsy. So, certainly with patients with myotonic dystrophy, you'll see excessive daytime sleepiness, and should be screening them for narcolepsy. You should also be screening them for sleep apnea.  Dr Smith: How about Parkinson's disease?  Dr Kay-Stacey: Parkinson's disease, at least a third of those patients will describe excessive daytime sleepiness. They can also experience sleep attacks during the day, likely has to do with dopaminergic mechanisms.  Dr Smith: So, I'm gonna ask a question in the middle of our game. So, in myotonic dystrophy, it's actually true narcolepsy. So, you would want to screen for that, and then if they meet the criteria, you would treat them similar to we spoke about earlier. All right. How about traumatic brain injury?  Dr Kay-Stacey: Yeah. So traumatic brain injury, very common for patients to experience excessive daytime sleepiness. Those patients will also experience circadian dysregulation. So, when you're interacting, you know, with those patients, you definitely wanna get a good sleep history, understand is there a circadian component, or is it true excessive hypersomnia related to the brain injury?  Dr Smith: How about multiple sclerosis?  Dr Kay-Stacey: So, MS, not as common for it to be hypersomnia per se, more common to hear fatigue in these patients. I do think, again, sleep apnea is probably under-recognized in MS patients, so making sure you're screening for that. But not-- do not classically hear, you know, primary hypersomnia disorders, more so fatigue. But MS fatigue is treated similarly to some of our hypersomnia conditions, often use a modafinil or an armodafinil for that.  Dr Smith: How about medications? Dr Kay-Stacey: So, there's a lot of medications that can cause excessive daytime sleepiness, a lot of medications that we as neurologists give, right? We're very aware that our anti-seizure medications can potentially cause excessive daytime sleepiness. The antidepressants that we use to treat various neuropathic pain conditions and migraines can cause sleepiness. The antidopaminergic medications can cause sleepiness. Benzodiazepines can cause sleepiness. Muscle relaxers can cause sleepiness. So, lots of different, medications that we use to treat neurologic conditions can create sleepiness.  Dr Smith: How about stroke?  Dr Kay-Stacey: Stroke can cause sleepiness too. Also can cause fatigue, and sometimes it can be challenging to differentiate. There's also a higher incidence of sleep apnea in patients with stroke as well, so you definitely wanna make sure that you're screening for that. But yeah, depending on the location of the stroke too, that can also contribute to the sleepiness 'cause if it's anywhere sort of along the ascending reticular activating system, it could cause a problem. Dr Smith: And maybe one more, depression.  Dr Kay-Stacey: Yeah, so depression also can be tricky to differentiate from hypersomnia, and you do really wanna make sure when you're seeing these patients that you're assessing to make sure that it's not the depression that's causing them to be sleepy. You know, patients with depression will often spend long hours in bed and spend a lot of time sleeping, and so you do really kind of have to piece that together and figure out what's what.  Dr Smith: Hey, that was fun, and I think we've probably convinced everyone who's listening to us that they probably should check out and read the article because guaranteed, no matter what you do in neurology, there's something in this article for you. One thing we didn't talk about, one of the kind of eight central causes of hypersomnolence that I thought worth kind of winding up with is insufficient sleep syndrome. I wonder if we might talk about this from the point of view of our listeners. And what advice do you have to neurologists and people who care for patients with brain disease regarding self-care and sleep self-care and not ending up with insufficient sleep syndrome?  Dr Kay-Stacey: Yeah. Great question, and I think I have been thinking a lot about just sleep in general because sleep is so important to brain health, right? I know the AAN has been big proponents of the importance of sleep, and there was lots of talk about it at the annual meeting because of that. You know, the average adult needs somewhere between seven and nine hours of sleep per night. So, if you're getting less than that, you are at risk for insufficient sleep, and that insufficient sleep builds up over time. So, you can't recover from many months or years of insufficient sleep by sleeping for just one night. And so, it is really important to make sleep a priority because when you have chronic insufficient sleep, it can mimic some of these other conditions. You can see narcolepsy-like symptoms where you're falling asleep inappropriately, where it's impacting your quality of life, potentially impacting your ability to drive. So definitely very important to really try to target that seven to nine hours of sleep per night. And I think from a self-care standpoint, if you feel like you are getting that seven to nine hours of sleep per night and you're still feeling sleepy or still feeling unrefreshed or dozing off during the day, then you really should get assessed for an underlying sleep condition that might be causing you to feel that way.  Dr Smith: So, Meg, this has really been such a great conversation, and it's a really great article. I wonder if we might wind up with one more question, which is if there was one thing our listeners should remember from our conversation, other than to kind of wait for their Continuum issue to arrive and immediately read this article, what would it be? What should they remember?  Dr Kay-Stacey: I think that if a patient is telling you that they're sleepy or tired during the day, that you really need to dig in and figure out what it is. Is it something that they themselves are doing that's behaviorally induced? Is it something that's happening with their sleep at night? Or is it an underlying primary hypersomnia condition that you can treat, right? These conditions are treatable, and you can have really a significant impact on quality of life, which is, you know, the best part of our jobs when we can actually make our patients feel better.  Dr Smith: Fantastic. Meg, thank you so much. I know that our listeners really enjoyed this. I know they'll enjoy the article as well. Thank you. Again, today, I've been interviewing Dr. Meg Kay-Stacey about her article on hypersomnia, which appears in the August 2026 Continuum issue on the neurology of sleep. Be sure to check out Continuum Audio episodes from this and other issues, and thanks to you, our listeners, for joining us today.  Dr Monteith: This is Dr. Teshamae Monteith, Associate Editor of Continuum Audio. If you've enjoyed this episode, you'll love the journal, which is full of in-depth and clinically relevant information important for neurology practitioners. Use the link in the episode notes to learn more and subscribe. AAN members, you can get CME for listening to this interview by completing the evaluation at continpub.com/audiocme. Thank you for listening to Continuum Audio. 

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 of insomnia as almost like, make sure we're not missing this as sort of a mimic of the problem, when in fact it's probably just more part and parcel of the problem and something we need to be thinking about treating as part of their disorder. So helpful to think about it in that light, at least in my own mind. Now, I want to get a little bit back to some of the therapies you've recommended, and I think first just stopping again at sleep hygiene. Your article has a really great list, I think, of sort of like a checklist of actions that people should be taking to make sure that they are managing their sleep hygiene well. And I definitely recommend our listeners look to that. How often do you think that focusing on sleep hygiene helps when you get a patient who says, "Hey, I have got terrible sleep. You know, what do I do?"  Dr Peters-Mathews: It's pretty common for people to have access to this information through their own reading online, and most folks have worked through this by the time they've come to see me, and often a primary care provider or specialist may have given some of this guidance as well. It's pretty rare for them to not recognize something as obvious as having caffeine too late in the day by the time they're coming to my attention. The sleep hygiene generally is used as a control when we do research to look at how something like medication is working or CBT-I might be working. It's the comparative control. It's almost like the null intervention. So, it's not highly effective, and if folks are not finding it helpful, they've made those adjustments to their sleep environment or their habits, and they're continuing to have issues, there's typically more that needs to be done, and that's where CBT-I really comes in as a strong intervention for those people.  Dr Grouse: And then getting on the topic of CBT-I, so helpful. I'm really glad that your article spent a lot of time talking about it as really a truly high-yield, great intervention for insomnia. And I really felt that the question shouldn't be: When is cognitive behavior therapy for insomnia helpful? But like, when isn't it helpful? What are your thoughts about that?  Dr Peters-Mathews: Yeah. I always point out that the American College of Physicians has recommended CBT-I for adult patients as the initial treatment for chronic insomnia even before the use of a medication for nearly ten years. That recommendation came out in July of 2016. So, there are folks who may not be good candidates for it, who may be screened out because of other conditions that they have, and there certainly are folks who don't do as well with CBT-I. And adherence is important. Somebody needs to be able to follow the instructions and apply that to their lives. And certainly, there are a number of things that could interfere with that compliance. I would say untreated anxiety and pain are two things that often trip people up. It's like running a race with a broken leg. Despite their best efforts, if those are not addressed, they will continue to have issues around insomnia. And then one thing that often is unrecognized and may be missed is untreated sleep apnea. That is a common contributor to a chronic insomnia, especially in older folks, women beyond the age of menopause and men even starting in middle age, thirties and forties. We don't want to miss sleep apnea. Even insomnia that's, "I can't fall asleep at the beginning of night," that could still be sleep apnea, so that's something I really emphasize with my patients.  Dr Grouse: Really great reminder about sleep apnea for sure. Something that always is beneficial to make sure we are not missing. Oftentimes I'll bring up a CBT for insomnia, and what is that? Like, what would we actually do, and what is a high-level overview of what happens with CBT-I?  Dr Peters-Mathews: Yeah. So, I generally tell my patients that this is a six-week program. It's a structured program, almost like a boot camp for sleep, in which we are addressing underlying causes, recognizing what those are and, and working through those underlying causes. There is often tracking using a sleep log or sometimes wearable data.To guide decisions that are made in the program. It's very goal-directed, science-based therapy. We often introduce concepts around sleep drive, circadian rhythm dealing with a busy mind at night. There's concepts of mindfulness and relaxation training that are introduced. People often are able to taper or stop using sleeping pills as part of this therapy. And the nice thing is they walk away with a set of skills that they can apply the rest of their lives to sleep more normally. And so, there's good research that suggests even years after someone's completed a CBT-I course, they continue to sleep more normally. They have the tools that they need to sleep better even years beyond that education.  Dr Grouse: You know, this just sounds so great. It almost sounds like why wouldn't someone benefit from this? But of course, like I would imagine many institutions experience, I've definitely run into difficulties with access for my patients for CBT-I, and we have long wait lists. And I imagine there's many places where there just aren't even any specialists that patients can get to, to help with this. What are the resources that our listeners can take advantage of for their patients to get access to these types of therapies?  Dr Peters-Mathews: So, one thing I tried to really emphasize in the article is that there are resources that can be drawn in. I'll give you some examples. So, at our institution, we have three sleep specialists, full-time sleep specialists, who trained at Stanford to become CBT-I specialists, and so we have more resources than probably most institutions would have. We do shared medical appointment workshops so that we can manage the number of patients that we have to see. And, and unfortunately, not everybody has that opportunity. You might plug into resources in your community, and one of the resources I point to in the article is the International Directory that's managed by the University of Pennsylvania that has eight hundred and seventy-five CBT-I specialists listed with contact information, et cetera. And I think that's an amazing opportunity to access this therapy. Unfortunately, there are countries and certainly states that do not have a specialist, that there's no one in the state that provides this therapy. And then we need to extend other resources, and that could be online treatment programs that can be done independently, bibliotherapy, so accessing books that could guide people through the therapy, even accessing other apps and maybe even wearables that pair with an app that could provide some of this guidance. The Veterans Administration worked with Stanford and worked with the National Center for PTSD and developed an app called CBT-I Coach that is free and can be downloaded and, and gives, I think, good education, good guidance. So, there are resources that exist. It's somewhat finding what might work for your individual patient, how they're preferring to access this or their learning preferences. Do they want to read a book or not? And getting them into the right pathway.  Dr Grouse: And I think that gets me into a whole other Pandora's box of the fact that they're already out there in the world are tons of different apps, wearable devices, all sorts of things that promise that they can help us with sleep, some that may have more, I think, data and evidence behind them than others. Do any of these apps or wearables in your mind show promise in our patients helping our patients track and diagnose and manage their insomnia?  Dr Peters-Mathews: Yeah, there's a lot out there, and unfortunately, some of these devices actually can make sleep worse. People can develop a condition called orthosomnia or straight sleep, where they're trying to perfect their sleep and their sleep numbers, their metrics, and the wearables feeding them data that they continue to try to improve upon. And that fixation on those metrics can actually make their sleep quite a bit worse. A lot of these wearables and apps and other resources have not been well-studied. There's not research trials showing outcomes comparing to other standards of care. I would say the basic guidance of CBT-I, which many of these programs are based on, I think will be helpful to the majority of folks who are able to engage and complete that education. A lot of these are not dependent on that sort of framework or structure so that we may not actually be using the standards of CBT-I to try to improve sleep. They may be connecting you with other resources, like listen to this sleep story or this relaxation file or do some meditation, et cetera, which again, may be of some benefit, but it is not the same as a structured CBT-I experience. So, I think there are a few good resources that we highlight within the article, and I think there are probably others coming that may give individuals a more individualized, directed approach to managing their sleep issues. But it's almost like going to the App Store and there's thousands of apps. It's hard to know which one might be most based on science or the most beneficial to that individual.  Dr Grouse: Well, I really appreciate in your article that you did have a great list of apps and things along those lines to try, so I do encourage our listeners to check that out as well. Some really, really great resources there in the article in many different areas. Now, I wanted to turn the conversation to a slightly different thing, which is medications for insomnia. Now, when are medications appropriate for treating insomnia? When should we be thinking about turning to these for our patients?  Dr Peters-Mathews: So again, we would suggest that CBT-I would be first, and that failing improvement with CBT-I, that medications would be extended to a person affected by insomnia. And over-the-counter options as well as prescription medications might be used. Unfortunately, that's not how things unfold in the real world. Many people are jumping to medications first, whether that be an over-the-counter supplement or other medication, or they're seeing primary care and other specialists who's providing them a prescription for sleep aid. So there's data from the CDC going back to twenty twenty that suggests that about six point three percent of adults were taking a sleeping medication every day in the months prior to the survey. And women who were older than sixty five, white women, were more likely to be using a sleeping medication every day. That number was 13.5 percent of those surveyed. So, lots of folks are on medications, and certainly melatonin is widely used. Unfortunately, it's not regulated by the FDA in a sense that we don't have exact concentrations controlled. So, people can take melatonin that has no melatonin in it. They might take melatonin that's forty or more times the dose. There's variance within lots from the same manufacturer. There's a lot of trouble knowing exactly what you're getting when you try to take something like melatonin over the counter. Other sleep aids that we might reach to over the counter, like variants of diphenhydramine or doxylamine, and these are often the PM drugs that we think about. They have risks associated with population-based studies which suggest risk of dementia, risk of falling, risk of mortality with these drugs, especially in older populations. So again, that would give us potentially pause. The prescription medications that we go to, there are some that the American Academy of Sleep Medicine would recommend as more beneficial than harmful, and some are good for both initiating and maintaining sleep. Some have such a short half-life that they're really best as initiation drugs. And then others are better for maintenance of sleep, so reducing awakenings and wakefulness in the night. My own individual take, often people are coming to me on medications, typically over the counter, but often prescriptions, and have even tried and failed many of those medications before they finally come to see a specialist. And so, I don't often reach to medications until I've exhausted CBT-I, until we've completed a sleep test to make sure we're not missing something like sleep apnea, until we've ruled out some other potential contributing causes. But there are patients I have who really will not sleep without medication support and sometimes even multiple medications that work in complementary ways to try to normalize their sleep. And so, in some cases it is necessary, but it is not meant to be a first line for anyone.  Dr Grouse: Yeah, and I think all of our listeners can relate to the fact that we often see patients who've been on sleep medicines for many, many years and take them every night. It's good to know that there is sort of a procedure here to consider and perhaps again, back to the plug to CBT-I as being the right starting point to see if there's some that we can help get off of these meds, although, as you mentioned, maybe not always going to be successful. Well, I really appreciate our conversation about this. It's been really great to read this article about insomnia. Again, I encourage our listeners to check it out. Some really great resources for many different therapies, thinking about other alternative diagnoses and different medical conditions where insomnia really needs to be considered. And I really appreciate you writing this article. It's been a pleasure to talk with you today.  Dr Peters-Mathews: It's my pleasure to share this information with folks, and I hope that you find it useful in your clinical practice or even your personal life as the need arises.  Dr Grouse: Again today, I've been interviewing Dr. Brandon Peters-Mathews about his article on insomnia. This article appears in the August 2026 Continuum issue on Neurology of Sleep. Be sure to check out Continuum Audio episodes from this and other issues, and thank you to our listeners for joining today.  Dr Monteith: This is Dr. Teshamae Monteith, Associate Editor of Continuum Audio. If you've enjoyed this episode, you'll love the journal, which is full of in-depth and clinically relevant information important for neurology practitioners. Use the link in the episode notes to learn more and subscribe. AAN members, you can get CME for listening to this interview by completing the evaluation at continpub.com/audiocme. Thank you for listening to Continuum Audio. 

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 just going to have to read. I don't want them to hear this too much while they're driving or on the treadmill, cause its super high level. But why don't we just start with some very basic factors that we need to know about this circuitry?  Dr Liu: Perhaps I can start with this concept of loop gain, which is the most important concept under hypocarbnic central sleep apnea. For any one of my colleagues who's listening to this, they're probably laughing right now cause they think that loop gain is my favorite word. So, loop gain is an engineering term referring to the sensitivity of a feedback loop. So, in the context of sleep medicine, this is an overly sensitive respiratory control to carbon dioxide and oxygen fluctuation. There are three components. The main one is controller gain. This is a chemosensitivity predominant to CO2. The second is plant gain, which is the lung's effectiveness for carbon dioxide excretion. And the last is what's called the mixing gain. This is circuitry delay from the time the signal travels from the pulmonary artery to the peripheral and central chemoreceptors. So conceptually, one may think, let's say something decreases your ventilation, so for example, apnea or hypopnea. With this, as you can imagine, when you stop breathing, your CO2 builds up, and this builds up according to the curve of the plant gain. And of course, this build of CO2 signal takes time to go from your lung to your chemoreceptor. That's your mixing gain. And of course, here it meets the overly sensitive chemoreceptors. This is your controller gain. As a result, this results in amplification of your ventilation to the initial respiratory disturbance. So, you have a overshoot of ventilation. All of a sudden, you're blowing out too much carbon dioxide, then you become hypocarbnic. At one point, if you blow out way too much carbon dioxide, your CO2 goes below what's called a PCO2 apneic threshold. After this, if your CO2's below, you essentially stop breathing. And of course, after that, you can imagine your CO2s are building up again. So, when this loop goes over and over, you generate what's called a chemoreflex-driven respiratory oscillation, where you create a crescendo, decrescendo-like flow pattern, which is underneath what we see in periodic breathing in central sleep apnea.  Dr Monteith: So, without going into too much detail, what is the key way to target restoration of equilibrium? Are there anatomical targets, physiologic targets that we're trying to manipulate here? Dr Liu: Again, thank you very much for that wonderful question. There's certainly many approaches that we could do to improve the stability of the system. Certainly, there are treatments for ventilation, either CPAP or in the case of hypocarbon central sleep apnea, things like adaptive servo ventilation. There is also medications that we can certainly discuss later that can double down the entire system for loop gain. Positional therapy can help for many of these patients. For the appropriate patient, improving their arousal threshold can actually reduce arousal-induced amplification of loop gain. Many of these patients, again, if appropriate, certainly weight loss may be helpful, and these are among many things that we can potentially do to improve the ventilatory stability of these patients.  Dr Monteith: Okay, great. But let's also talk about the general overall approach to diagnosing, and much of it is by history, as you mentioned. There's also sometimes a need, as you say, to differentiate out how much is obstructive. So, what is the thinking process there when you're approaching a patient?  Dr Liu: So perhaps I can start with in terms of the diagnostic modalities that we could use for this. So, the gold standard for diagnosis of central sleep apnea is still our polysonogram. The home sleep apnea test sometimes may be harder to distinguish between obstructive and central events. In addition, on a PSG, you have EEG. This allows you to assess for sleep quality and arousals, as well as the EMGs, which can help you pick up periodic limb movements of sleep. And of course, all of these things themselves can affect the central sleep apnea and can be a potential treatment factor.  Dr Monteith: Before we get into treatment, can you just give us, like, the top five or six drugs or drug classes we need to look for so that, you know, we can discontinue or try something else for our patients that might be complicating their presentation?  Dr Liu: Certainly medications, in some cases, can help central sleep apnea, but other cases can certainly be a precipitant of central sleep apnea. So, one thing to consider would be opioid medication. They can certainly cause very complicated central sleep apnea, something called ataxic breathing, where you have irregularity to the tidal volume and the rate of breathing. Other medications such as Oxybate, baclofen, valproic acid, gabapentin, all of which can certainly contribute to central sleep apnea. And of course, in the stroke world, something that we should always think about is that Tetagelor can also contribute to central sleep apnea. And outside of this, things like muscle relaxants, anesthetic agents can also be a contributor.  Dr Monteith: Great. Now let's get into some of the treatment.  Dr Liu: I like to divide treatment into targeting a hypercarbnic central sleep apnea and a hypocarbonic central sleep apnea. For hypocarbonic central sleep apnea, the first line is CPAP treatment. But for many patients, CPAP therapy is insufficient. There's also adaptive servo ventilation, which is an advanced device designed for hypocarbonic central sleep apnea. For hypercarbic central sleep apnea, again, first line is CPAP treatment, with more advanced devices being a bilevel therapy as well as volume-assured pressure support ventilation. There are also medications that can reduce loop gain, with the most researched one being acetazolamide. We can also reduce arousal thresholds, which could be appropriate for certain patients. And for certain patients, improving arousal threshold can be helpful as, especially in hypocarbic central sleep apnea, that arousals can amplify loop gain. Weight loss can be helpful for both hyper- and hypocarbonic central sleep apnea, and we have great new medication on the market for this. Other therapy can include supplemental oxygen that can be added to PAP devices, as well as phrenic nerve stimulation, positional therapy, as well as carbon dioxide modulation.  Dr Monteith: Excellent. So, it sounds like there's a lot of opportunity to help patients. Now, what are you most excited about in terms of latest development for detection as well as for intervention?  Dr Liu: Thank you very much. I'm actually excited about many things in sleep medicine. Perhaps the thing that I'm most excited about in detection in sleep medicine would be the wearable technologies. So, these technologies may use photoplethysmography to detect peripheral artertonometry. This is where we're measuring the pulsatile arterial volume signals as a surrogate of cardiac and respiratory function. And when paired, that was often desaturation. With these technologies, we can actually detect the staging, autonomic arousals, and HI. So of course, these technologies do not have flow, and they do not have EEG. But they're very powerful technology that allows us to do multi-night testing from home. And of course, understanding both the potential limitation of these technology in the context of patients can be very useful. In terms of treatment-wise, we're learning so much about the underlying contributing drivers of different forms of central sleep apnea. So again, this is highlighted in my article that many of these patients needs multimodal targeted treatment, both between either a PAP device in addition to other things such as medication, oxygen, positional therapy, and so on.  Dr Monteith: Great. So, I mean, I think there's so much to this field. Your article is very extensive. Thank you very much for writing this. I know it may have taken a bit of time, and I appreciate you being on our podcast.  Dr Liu: Thank you very much.  Dr Monteith: Again today, I've been interviewing Dr. Richard Liu about his article on central sleep apnea. This article appears in the August 2026 Continuum issue on Neurology of Sleep. Be sure to check out Continuum Audio episodes from this and other issues. And thank you to our listeners for joining today.  Dr Monteith: This is Dr. Teshamae Monteith, Associate Editor of Continuum Audio. If you've enjoyed this episode, you'll love the journal, which is full of in-depth and clinically relevant information important for neurology practitioners. Use the link in the episode notes to learn more and subscribe. AAN members, you can get CME for listening to this interview by completing the evaluation at continpub.com/audioCME. Thank you for listening to Continuum Audio. 

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 important to ask the question about sleep, and if the red flags pop up, to then screen for sleep apnea in particular.  Dr Albin: I think that that's a great point for us to drill down on, and obviously you're a sleep neurologist. You're very used to screening people in the clinic. But say someone comes in, and I'm gonna have you put your former stroke hat on, and say someone comes into the stroke clinic, and you're just making sure that they're optimized on their aspirin or dual antiplatelet therapy, and you're doing secondary risk modification. How would screening for OSA fit into that?  Dr Lee-Iannotti: It would be a part of that screening process to look at preventative ways to prevent strokes, whether it be primary or secondary prevention. So, we did a survey a while back, and it actually showed that 17% of stroke neurologists are screening for sleep apnea. It has quadrupled, fortunately, in the last few years due to public awareness and a lot of education that the AAN has done, in fact. So, at this point, I would say not asking about sleep apnea to a stroke patient is similar to not asking about diabetes.  Dr Albin: So, we really have to be cognizant and conscious about saying, you know, "Do you snore at night? Do you have episodes of apnea, or does someone witness you stop?" Are there things that you ask that maybe I wouldn't be aware and thinking of?  Dr Lee-Iannotti: Those are the right questions, and then very practically, very easy questionnaires to implement that literally take a minute that your nurses or medical assistants can administer to the patient, and the most commonly one that is used in stroke patients is called the STOP BANG, S-T-O-P B-A-N-G, which is a validated questionnaire to screen for symptoms.  Dr Albin: Absolutely. So okay, so this is easy to do. We should all be doing this. If you're not, now's the time. And I suspect if they screen positive, next steps, it can be hard to get into a sleep lab, and we're gonna talk about some workarounds, but I think some of our listeners may never have spent time in the actual sleep lab. So, let's say you refer a patient and you actually can get them in for a gold standard in-lab sleep study. What's gonna happen in that sleep study?  Dr Lee-Iannotti: Yeah. And I just want to preface this by saying that my article hopefully highlights that we've come a long way where we understand that there are many neurologic populations then that can undergo home ambulatory sleep studies with just as much accuracy as an in-lab polysomnogram. But with that, I wanna say an in-lab polysomnogram is actually a highly sophisticated physiologic recording overnight, typically, unless somebody is a day sleeper. So, if I could take a minute to kinda describe the data that we're monitoring throughout the night. There is a limited EEG. We concentrate on frontal, central, occipital leads to look at sleep staging. We have eye leads. We have EMG leads on the chin and the leg. We look at EKG, flow monitors, belt, and then we also do pulse oximetry, snoring mics, and even body position sensors. So, a lot is going on.  Dr Albin: This is incredible. Yeah, it truly is. I mean, this is like... I'm a neurointensivist, and so I think that you have just really outdone what I consider multimodal monitoring in your sleep study patients. I'm not even sure our neuro ICU patients accumulate that much data. All right, so tell me, they go through, and they can get this. But like you said, there's actually a lot of data that you've presented that, you know, not everyone needs to go to the in-lab sleep study. So how do you decide who actually needs to be in a sleep lab versus who can do this at home? And then how do you set them up with getting this done at home?  Dr Lee-Iannotti: Yeah. The home sleep studies are really more accessible ways for us to assess for sleep apnea in our neurologic patients, especially patients who live in very rural areas and don't have access or have very long wait times for an in-lab polysomnogram. With that being said, though, Dr. Albin, I will say that there are a subset of patients who have to go into the lab, and those are patients where you suspect a sleep disorder other than obstructive sleep apnea, so like parasomnias or central sleep apnea, patients with severe cognitive or physical debilitation, like our stroke patients who are hemiplegic and won't be able to apply the home sleep study. But for the most part, I do feel like a home sleep study is a good beginner study to screen the patient. And if there are red flags, then you can always get the in-lab afterwards.  Dr Albin: That's super helpful. And just from a pragmatic standpoint, will insurance cover the home sleep study?  Dr Lee-Iannotti: They will, yes, and it's all about documenting. So, if I could get really practical, for neurologists, it really just requires documenting snoring, for one, whether it's noted by the patient or by their bed partner, and then any form of hypersomnia, which is daytime sleepiness or even a sense of fatigue, having low energy or napping during the day.  Dr Albin: I suspect so many of our patients meet those criterias. That seems, like, wildly simple to do.  Dr Lee-Iannotti: Yes. And if you wanna be the favorite referral person to your sleep neurologist or your sleep specialist, then take another step and do that STOP-Bang. And if you record a score greater than three, that automatically gets them at least a home sleep study.  Dr Albin: It's amazing. And then when you get this data, again, this is really practical, pragmatic stuff, how do you get the report? Does it integrate in your electronic medical record? Does the patient bring it in? How do you get that data back?  Dr Lee-Iannotti: Yeah, so this is where technology is amazing, Dr. Albin. Now we have disposable devices. Sometimes they sync to the WatchPat, or the greater Wi-Fi. So we can get them all through password-protected internet forums that transmits the data, so sometimes the patients don't even have to come back to give us the data. And then we have different forms where we can actually relay the results as well, either through the electronic medical record or through systems themselves to relay those results directly to the patient.  Dr Albin: Yeah, and your article really laid out in beautiful tables, like, all the different devices that are available to patients, and it's honestly mind-blowing how many of these companies and devices exist. So, seems like the world is your oyster in terms of picking from them.  Dr Lee-Iannotti: Absolutely. I think there's... The last time I counted, there was over 20 different home sleep study devices for obstructive sleep apnea. And it's a great thing to have, but sometimes too many choices can be a little bit confusing. So that's where I do say partner with your sleep specialist close by, and they will find the right type of home sleep study device for your particular patient.  Dr Albin: Drilling down a little further, let's say your patient does get diagnosed with OSA. One of the things that really stuck out to me is that there's a whole range of now devices that are new that make this treatment easy so that we can actually prevent and treat neurological conditions by just improving patient sleep. So, walk us through a little bit about how that landscape has changed.  Dr Lee-Iannotti: Sure. And I'll start with the gold standard of treatment, which is still CPAP, which is continuous positive airway pressure. Not only can we monitor the pressure, look at adherence, change the humidification for the patient all remotely through, again, password-protected internet forums, but we can even change the pressure with patients 300-plus miles away.  Dr Albin: Wow.  Dr Lee-Iannotti: It's really cool, right? It prevents patients, especially with significant neurologic debilitation, from having to come into the office for adjustments. The other thing I wanted to mention, Dr. Albin, is for patients, a lot of patients like positive feedback on a daily basis. And a lot of these companies, if you are on CPAP, have come up with a smartphone app that you can look at how many hours you used your CPAP device. They give you a score, and they even tell you how many times you had stoppage of breathing that night.  Dr Albin: I think that this is what's really exciting about where we are in neurology and, like, neurologic care, is we have gotten so much better at getting patients their own data and allowing people to really see that data, integrate lifestyle changes, and see how it impacts them. And that positive feedback loop, I think, is a really powerful tool for our patients to say, "Look, this makes me better," or, "Oh, this makes me worse." I'm just really excited by how much data we can give directly to our patients.  Dr Lee-Iannotti: I agree. It's so empowering. You know, as a CPAP user myself, you want that positive affirmation that all of your efforts at night and cleaning your mask and your machine paid off, and everybody likes to see an A+ on their report card.  Dr Albin: I love that. Now I'm going to ask you on the flip side, I imagine, and I myself am a sleep tracker, like I have my little device and I look at, you know, the score in the morning and I kind of perseverate on like what makes it better, what makes it worse, and I can imagine that sometimes in sleep clinic, people are coming in to you and they have just pages and pages and, you know, they're flipping through all their data from the last year. And I imagine that's pretty overwhelming when you have just the insane amount of data that these devices can generate. So, from another pragmatic, practical standpoint, how are you integrating all that data when someone comes in for a sleep visit?  Dr Lee-Iannotti: I love that question. So first of all, I will say myself, and I think a lot of my sleep colleagues, we love objective data, right? Because it's something that we can see. We can see whether it matches their subject's symptoms. Sometimes it can be a lot of reassurance that, "Look, you actually got more sleep than you thought you did." But sometimes patients will bring in like a month's worth, and that's really hard to analyze, you know, in a 30 or 60-minute visit. So oftentimes what I do is I look at like the last week or last two weeks, and I look at trends. And I think a lot of the apps for whatever device you decide to use have done a really good job in terms of visual graphics to show how much sleep on average you're getting, how much deep sleep or REM sleep or wake-up times that you have. So, I, again, I feel like the technology has really helped us consolidate a lot of data, but also be efficient with the messaging that we relay to our patients.  Dr Albin: Absolutely. And I know personally, at least for the sleep tracker I wear, it also allows you to diary. So, you can say like, "Oh, last night I had a glass of wine," or, "Yesterday I had a really hard workout," or, "I stayed out late with friends," or, "I was on call." Turns out call is really, really bad for my sleep. But it does allow you to sort of track what behaviors, and I wonder how much of that informs what you're counseling patients to do in terms of trying to notice the things that either improve their sleep performance or their subjective feeling of restlessness or restfulness, and how all of that plays into what you're doing in the clinic.  Dr Lee-Iannotti: I love all of those comments. It is validation for the patient. Again, it's empowering for them to look at, what did I do last night to get more REM sleep than the night prior? I want to mention that the best people who do this so well are professional athletes, and they look at, how am I going to cater my day to make sure that I'm sleeping well, that I reduce my risk of injury and concussion and increase my reaction time? And I feel like all of us should do that. That's such a great philosophy, to analyze how we can do things better.  Dr Albin: I love that. This whole issue, but this article in particular, really emphasized to me that sleep, again, it's not a passive time that we're taking a nap. It's a really active form of sort of neurologic healing. There's important removal of toxins through the lymphatics. And like there's a lot happening in sleep, and there are so many more tools that allow us to unpack that sort of peak performance of sleep, which again, sort of is that athletic mentality of like, how can I make this better? Not just to treat a neurologic condition, but also really importantly, to prevent one.  Dr Lee-Iannotti: I often refer to sleep as icing on the cake. With our patients, when you're doing everything right, for example, a multiple sclerosis patient, they're on the right medications, they are exercising, they're participating in rehab, their mood is good, but they're just not getting to the quality-of-life metric that they want to be, it usually is sleep. And if you can add that as a neurologist to your piece of the algorithm to help your patient, it really does improve their quality of life and ultimately their neurologic outcome. I'm a true believer of that.  Dr Albin: I was a true believer. I've been made even more of a true believer through your article and getting to talk to you. I always like to close by asking the person I'm interviewing, what's one really exciting thing in this field? What are you kind of most looking forward to as you think about sleep medicine and its impact in neurology in the next five or 10 years?  Dr Lee-Iannotti: Oh, I love that question, too. So, the thing I'm most excited about in the field of sleep, and specifically sleep neurology, is the power of preventative care. When I did a lot of stroke, I would see young people, older people, healthy people, people with a lot of genetic risk factors come in, and one minute they were totally normal. The second minute, they're paralyzed and can't speak. And for a lot of these patients, I would ask, "Why am I seeing you now? Why couldn't I have seen you 10 years earlier, worked on risk factors, and prevented this outcome?" And I truly believe that is exactly where sleep lies. If you work on sleep, whether you're an adolescent, 20 year old, 30, et cetera, you are ultimately going to prevent horrible cardiovascular, cerebrovascular, neurologic diseases in the long run.  Dr Albin: So important. I really want to direct our listeners back to your article because all of the articles are really practical, but this one in particular looks at how do you do this? What are your options? How do you get this to patients? It really is sort of a step-by-step guidebook on like, A, why this is important, how you should screen, what you should do if someone screens positive for needing to have a sleep study.There's so much more technology that allows really anyone anywhere to have access to the testing that they need to get the right diagnosis, to improve their sleep, to improve their cognitive outcomes, to improve their neurologic health. It's pretty amazing.  Dr Lee-Iannotti: It is amazing. And in the article, I do allude to certain devices and then websites that are very helpful. If I can announce, Dr. Albin, I'm super excited about this. Through work with the American Academy of Sleep Medicine, endorsement with the AAN, we are coming out with a new clinical guideline specifically on home sleep study devices and looking at the validation studies. So, I think that's going to be very helpful. But I hope that everybody after listening to this picks up the phone, call your friendly sleep specialist, and align with them and partner with them. And this will ultimately help your patients, I guarantee it.  Dr Albin: Again, today I've been 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. Be sure to check out Continuum Audio episodes from this and other issues. And thank you to our listeners, and thank you, Dr. Lee-Iannotti, for joining us today. Dr Lee-Iannotti: Thank you.  Dr Monteith: This is Dr. Teshamae Monteith, Associate Editor of Continuum Audio. If you've enjoyed this episode, you'll love the journal, which is full of in-depth and clinically relevant information important for neurology practitioners. Use the link in the episode notes to learn more and subscribe. AAN members, you can get CME for listening to this interview by completing the evaluation at continpub.com/audiocme. Thank you for listening to Continuum Audio. 

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 addition to stroke and, and TIA, include Parkinson disease. It can worsen a lot of the motor, cognitive symptoms, sleep disruption that we can see in Parkinson disease. Very common in all causes of dementia, but in particular Alzheimer disease and Lewy body dementia. Very common in neuromuscular conditions. We should definitely have obstructive sleep apnea and all forms of sleep-disordered breathing high on our radar. In conditions like myotonic dystrophy. Charcot-Marie-Tooth is another one where obstructive sleep apnea is very common. Myasthenia gravis, it can worsen the symptoms of that. In particular, a pearl is if somebody has morning weakness in myasthenia gravis, obstructive sleep apnea should be high on your radar. And also, as you mentioned, any forms of headaches. There are some other things too. If somebody has poor seizure control, especially nocturnal seizures, you might have obstructive sleep apnea on your radar as well.  Dr Berkowitz: So, I think you've covered essentially every category of neurologic disease, right? We have cerebrovascular, movement, neurodegenerative, neuromuscular, epilepsy, all conditions where either the disorder itself, such as stroke or the, correct me if I'm wrong, the neurodegenerative disease puts the patient at risk. Or the patient may be at risk for exacerbations of their disease, as you mentioned in myasthenia. I love that pearl. Not fatiguable at the end of the day, but if the patient with myasthenia is telling you they're feeling weaker at the beginning of the day, then think about obstructive sleep apnea and that obstructive sleep apnea worsening control of epilepsy due to poor sleep. So really a lot of bidirectional interactions with this common condition. Okay, so if we're concerned about obstructive sleep apnea, again, myself, a general neurologist speaking perhaps on behalf of other general neurologists, we see a patient with headache or reporting memory loss that we find to be impaired attention, or we see exacerbation of their underlying primary neurologic disease. As you mentioned, we think, "Oh, I've listened to this podcast. I've read Dr. Stahl's article. I should probably be thinking about OSA in this patient, and I should order a sleep study." Now, I admit when I get the sleep study back, I scroll to the bottom, I see they do have obstructive sleep apnea, I'm going to send them over to a sleep specialist. But for the general neurologist, what are some high-yield pearls and some pitfalls to be aware of when we get sleep studies for obstructive sleep apnea, and we are looking at the results? Dr Stahl: The first thing is to understand that there are two main types of sleep studies: in-lab polysomnography and home sleep apnea test. In-lab studies are typically what we consider the more accurate type of study. Main reason for that is that we have EEG, so we can see if someone is awake versus asleep. Most home sleep apnea tests do not utilize EEG, and so when we're looking at respiratory events, apneas or hypopneas, we're looking at over the total recording time rather than the total sleep time. So, we know we're going to capture some time where a person is awake, where we don't have sleep apnea events, and that can be a big amount of time in people with insomnia, poor sleep efficiency. And as a result of that, it can lead to an underestimation of the apnea-hypopnea index. That's really important for people to understand that that means we can end up with a false negative home sleep apnea test, or it can put them in a category of lower severity than what they actually have. And so, if you get a home sleep study report back that's negative for sleep apnea and you remain concerned, you need to go on to do an in-lab study, where about twenty to fifty percent of people will go on to have a positive in-lab study. You can also get false positives with home sleep apnea tests too, and so ideally, we should only be doing home sleep apnea tests in people that are at high risk of having obstructive sleep apnea to decrease our chance of false positive study. When we get that sleep study report, what's important to take a look at? So the main number that we look at currently is the apnea-hypopnea index. The number of apneas, which are full obstructions in that upper airway, or hypopneas, partial obstructions in the upper airway where either there's an oxygen desaturation or an arousal associated with that. Less than five is considered to be normal. Anything five or more gives them a diagnosis of obstructive sleep apnea, and then we stratify them based on the AHI. But it's important to take a look at more than just the apnea-hypopnea index. And while my eyes too on various reports like echocardiograms want to jump to the impression, it is important to take a look at that full report, see what their oxygen levels averaged and what they dipped down to. The arousal index, which is how many times a patient may have woken up briefly throughout the night. Take a look at the histogram, usually an image at the bottom of their report that shows what sleep fragmentation may have been like so that you can take that all in and make that decision. How important are these study findings, and is this a person that would benefit from treatment?  Dr Berkowitz: That's a fantastic overview of sleep studies and some of the highlights to look out for, even if we won't be understanding every detail as you would to know most importantly the caveats about home sleep testing having a fairly high percentage of false negative and false positive results. So being wary if our suspicion is high, and that test is normal or inconclusive to get an in-lab sleep study. And if our suspicion is low or maybe we haven't ordered the test and the patient has had it done elsewhere, and the history doesn't really match up to know that there are false positives on the home studies as well, and again, an in-lab study to settle the diagnosis. Is that right?  Dr Stahl: Yes.  Dr Berkowitz: Okay. Now, for most neurologists, probably if we diagnose OSA, we will be referring the patient to a sleep specialist like yourself for treatment. I think we're all familiar with CPAP and patients being on CPAP. Your article mentions a number of treatment modalities I admit I have not heard of before or maybe heard of in passing, acknowledging most general neurologists are not going to be prescribing or knowing with the nuance that you do as an expert how to decide which treatment a patient would most benefit from or most qualify for. So, can you just give us a broad overview, again, for the general neurologist acknowledging we might see a patient whose past medical history says OSA being treated with fill in the blank. What are the different treatment modalities, and how do you think, just so we can learn from you in broad brush strokes, about particular treatments for particular patients?  Dr Stahl: As you mentioned, most people are familiar with positive airway pressure or PAP therapy, and that does remain our most efficacious treatment. The way I explain it to patients is why PAP therapy is the most effective treatment is it's the only treatment that can take all of the tissues of that upper airway and open them up. Whereas all of our other treatments, we're going to target smaller spaces of that upper airway. So, our first option is if we can get somebody on PAP therapy, we know that that's going to be the best option for the majority. PAP therapy works by basically acting as an air splint to open up the air tissues. Know that masks are not interchangeable. There are masks that cover the nose and go over the nose and mouth and under the nose. Full face masks that cover the nose and mouth, they do typically require higher pressures, also tend to be less comfortable for a lot of patients as well. In addition to different PAP masks, there's different modalities of positive airway pressure therapy too. There are machines that auto-adjust, some that provide fixed pressure, bi-level PAP that provides a higher inspiratory pressure, lower expiratory pressure. Then outside of PAP therapy, there are, as you alluded to, a lot of options and more, continuing to come down the pipeline as well. Mandibular advancement devices or a form of oral appliances has been around for a while. This is device that somebody wears in their mouth. It's preferably customized for their teeth and titratable, meaning that they can make adjustments that pulls their mandible forward in relation to the maxilla in order to pull those tongue tissues further away from the back of the upper airway. That's ideally managed by a qualified sleep dentist or someone that specializes in oral appliance management. Other treatments include surgical options, including hypoglossal nerve stimulation, which is an implanted device that causes the tongue to protrude repetitively throughout their sleep period to hopefully open up the airspace. There's some other surgical options too that open up various places of the upper airway. There's a daytime treatment of obstructive sleep apnea, transoral neuromuscular electrical stimulation that changes the muscle fiber type of the tongue. And then there's some adjunctive treatments that can be helpful too, such as positional therapy, oral facial myofunctional therapy that helps a person breathe better through their nose and may help train the upper airway muscles.  Dr Berkowitz: Great. Well, that's a very helpful overview, and again, I refer our listeners to your article, which talks about all of those modalities in very comprehensive detail. So, Dr. Stahl, as we wrap up our conversation, you have a captive audience of neurologists and neurology trainees here. What would you like to leave us with that every neurologist should know about obstructive sleep apnea?  Dr Stahl: The most important, again, is for neurologists to know that obstructive sleep apnea is so common in your patient population, and it can have a significant negative impact on quality of life and health, including many neurologic conditions. And at the same time, obstructive sleep apnea is very treatable. We have so many options nowadays that we can usually get someone onto adequate treatment. And treatment has that potential to improve several neurologic symptoms and disorders, even at times when you don't think that there's an opportunity to improve symptoms such as say in, headache. So, neurologists really should be screening for signs and symptoms of obstructive sleep apnea, as well as considering testing in high-risk, potentially asymptomatic or minimally symptomatic patients.  Dr Berkowitz: That's a fantastic overview of some of the many pearls that you shared with us today, as well as in your article. So, thank you so much again. Today, I've been interviewing Dr. Stephanie Stahl about her article on obstructive sleep apnea. This article appears in the August 2026 Continuum issue on neurology of sleep. Be sure to check out Continuum Audio episodes from this and other issues. And thank you so much to our listeners for joining today, and thank you again, Dr. Stahl.  Dr Stahl: Thank you again for having me.  Dr Monteith: This is Dr. Teshamae Monteith, Associate Editor of Continuum Audio. If you've enjoyed this episode, you'll love the journal, which is full of in-depth and clinically relevant information important for neurology practitioners. Use the link in the episode notes to learn more and subscribe. AAN members, you can get CME for listening to this interview by completing the evaluation at continpub.com/audioCME. Thank you for listening to Continuum Audio.  

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, and you can move on. But if you get back a home study that looks questionably central, they're gonna need to come into that lab. So, if you already know they're high risk because they're on narcotics, cause they have congestive heart failure, it's usually worth going straight to the lab. But again, you may consider a home study based on the patient. Patients that really cannot use the equipment can also be an issue. So, if they've had a debilitating stroke and have no one to help them put on that device, or cognitively they just can't handle the device, they're gonna be someone who's gonna benefit from coming into the lab and getting the help from the techs. So, those are the big populations that you might go starting for a home. And then the other thing that confuses a lot of people, the home is only for diagnostics. It really isn't for treatment. So, I have patients that say, "Oh, like, you can just titrate my CPAP with a home study." No. So if it's a treatment decision where they're not doing well on treatment, or I need to figure out do they need CPAP or BiPAP or IVAPS or one of these more complicated treatments, those are people that are gonna need to come into the lab to get that treatment portion of the evaluation.  Dr Jones: What a great summary. That's like everything I needed to know about who do I need to bring into the lab and who do I think maybe could do an at-home study. Really great. And speaking of devices, I think all of us who see patients in the room here and our listeners out there online have experienced patients, and this feels like a very recent phenomenon to me, are coming in with their commercial at-home wearable device. And they have printouts sometimes, and they show me their phone, and they give me some numbers that I don't really know how to interpret. Reading through this issue, I learned a couple of great new words. I learned about orthosomnia, right? So, people who become so preoccupied with their sleep, it keeps them awake at night, literally, right? I mean, it's a complete paradox. I learned about nearables, so things that aren't necessarily wearables that are just in the room while the patient is sleeping that monitor proxies for sleep quality, sleep stage, and other things. And I frankly, I'm not really sure what to tell patients. So, what do you tell patients who come in with all the data? Like, or how do you tell patients to use these?  Dr Johnson: I think these devices can go both ways. So, I do kind of say the pros and cons of these devices. I think for a lot of patients, they're empowering. It's getting them to think about sleep, to wanna know how good their sleep is. Are they getting enough sleep? So, if it's used in those ways, it's gonna be very helpful. I actually had a patient last week, and they noted that they're having big desats all night and could show me essentially an overnight oximetry data rather than me having to order it, and I had days of data, which sometimes can be too much. But in this case, it's like, oh, when he was on his side that night, he looked a lot better, so I can use that to give advice to the patient about particular treatments. He actually went down to Mexico, and a doctor friend gave him oxygen therapy while he was there randomly. And we could see on the nights that he had the oxygen therapy, it did really help his central sleep apnea pattern. And so that pushed us towards saying, "Let's qualify you for that up here in the States." So, I think in some cases it can give really important data. Now, I saw a posting on social media the other day of someone saying, "Can I get advice on how to improve my REM sleep? My tracker says I have no REM sleep, and I need to do something about it." There's really not data to support needing to do something about it. And so, I do think it can get some people on these wild goose chases, trying to get to a certain percentage of sleep. And these trackers, they're good in a lot of ways, but they're not perfect. He could be getting REM sleep that the tracker on him does not show. You want to relate it to what symptoms are they having. I think they can be very good for trying something out. So, let's say someone, has their tracker telling them they get five hours of sleep, and they try this intervention, and that helps them show that they got the seven hours of sleep, or they went from no REM to REM and it goes in the right direction. It can help give them that positive feedback that something they're trying, is working. But the absolutes for any given patient, it's hard to over-- What does it mean if it says you've got a 50% score versus a 70% score? That may or may not be meaningful in any given person, but again, they can compare themselves to themselves. If they were a lower score and now they're a higher sleep score because they did something that was meaningful, and that goes along with them feeling better, that can help give them that positive feedback to do something good.  Dr Jones: So, a little bit of a mixed picture.  Dr Johnson: Yeah.  Dr Jones: Sometimes they help. Sometimes they distract. Hopefully- Dr Johnson: And as a provider, sometimes it can be overwhelming because they're like, "Come look at my year's worth of data." And you're like, "No."  Dr Jones: Yeah.  Dr Johnson: You know, let me see one page or two pages of data and be like, "Yep, okay, I get it." Dr Jones: Just show of hands in the audience, who in the room wears a sleep device at night, like a ring or a, some kind of sleep monitoring app? That's about half the audience.  Dr Johnson: This is why they're here.  Dr Jones: So that's really helpful, and I think it is. You want to be supported by the data. You want to be supported by evidence and high-quality biometric evidence. Another big trend, and this has been a number of years in the making, is the understanding, Dr. Johnson, of the relationship between sleep physiology and neurodegenerative disease. One of the things I love about neurology is there's still so much left to learn about the normal physiologic functioning of the brain. So glymphatics and other aspects of sleep physiology that we didn't know about a decade or two ago. When you think about how that relationship has developed, sleep physiology, maybe sleep disorders and neurodegenerative disease, how has that changed your approach to talking to patients? Do you counsel patients differently now because of what we understand better about that?  Dr Johnson: Yeah, I mean, we are still limited with our data. We have so many studies that show the associations between whether it's not enough sleep, too much sleep, or having a sleep disorder like obstructive sleep apnea, and that being a risk factor for stroke or Alzheimer's or Parkinson's. But we still sort of lack the treatment trials that necessarily say, "If you treat obstructive sleep apnea, you're gonna have less dementia," or, "You're gonna be less likely to have that stroke." So, we have a lot of physiological studies, a lot of reasons why it makes sense, but we don't have that final, nail in the coffin to say, "If you do this, you'll definitely be better." So, we know certain groups are more at risk. If you have obstructive sleep apnea and you are symptomatic, you seem to have higher cardiovascular risk. If you have a person who's had a stroke and we find a milder case of sleep apnea, and they're someone that's totally asymptomatic. They say, "I sleep fine. I feel fine." There's not great data to say, "If you treat your sleep apnea, you're gonna be less likely to have a stroke." Now, if they come in and they're sleepy and their sleep apnea is really severe, and they have more hypoxic burden, which is also more connected with a lot of these risks, I'm going to say, "I think you are in the higher risk group of sleep apnea people who it's probably gonna be more likely to help your cardiovascular risk, your dementia risk." We can counsel them, and then it's really a personal decision. Some people are like, "No way. I'm never gonna use a CPAP machine, ever." And other people are like, "You know, my mom had a stroke. My dad had Alzheimer's. I want to do every possible thing I can to make it less likely that I have this outcome that I want to avoid." And so, you're going to take that in to, you know, do you want to try this treatment or not? It's a lot easier when you have outcomes that you can follow, like, "If I try CPAP, does my blood pressure get better? Do I stop having AFib attacks?" It's a lot harder when, will I or not get Alzheimer's ten years down the road or have that stroke?  Dr Jones: It's hard to get people to do things for kind of an abstract prevention down the road, but could be important. Are there trials going on that are going to assess this data?  Dr Johnson: Yeah. We currently have a big trial getting people right away, right after their stroke, on CPAP, and not only looking at prevention, but also looking at recovery outcome. It's been running for several years. Hopefully, we'll get enough data to close out the study coming up.  Dr Jones: We'll look forward to that.  Dr Johnson: Yeah.  Dr Jones: So, I'm really excited to get to our audience here, but before we do that, I do want to ask Dr. Johnson one more question. Dr. Johnson is famous for her advocacy for sleep in general, but specifically related to Standard Time. So, let's do a little experiment here. I didn't warn Dr. Johnson about this, so we'll see how she does. She does a ton of advocacy. She's a pro. So, pretend like we're in DC, and I'm a senator, and we just got in an elevator. You're going to give me your elevator pitch on what we should do.  Dr Johnson: So, you know, sleep is one of the few essential things in life. We need to eat, we need to drink, we need to have clean air, and we need to sleep and when we improve sleep, we can improve basically every outcome, whether it's academics, whether it's productivity, whether it's our physical health, our mental health. And the problem is we structure our lives in a way that really keep people, and especially our teenagers, from getting the sleep they need. And one of these structural things we do is permanent daylight savings time. Essentially, what you're doing is you're putting the sun out later, makes it harder to go to bed. I was just talking to someone, the sun's going down at 9:00, and you need to get your kid to sleep at 7:30, 8:00 so they can get the amount of sleep they need. That is almost an impossible task because their circadian rhythms are being pushed later, they can't fall asleep on time. Then you're setting their clocks an hour earlier, so when that alarm clock is going off at 6:00 AM in the morning, it's actually 5:00 AM in the morning. You're squeezing sleep from both sides, and it's basically impossible to get enough sleep. A lot of people think the only problem with daylight savings time is twice a year with the changes, and there are certainly harms related to that. So, a lot of people think if we went to permanent daylight savings time it would be better, and we got rid of those changes. What they don't realize is that permanent circadian misalignment by setting the sun more ahead, at 1:00 to 2:00 instead of at noon causes the sleep and circadian disruption all year round that leads to increased incidents of strokes, of heart attacks, of obesity, of cancer, of suicides, of depression, of worse academic grades. Again, pretty much every outcome you have there that relates to brain health, we have now data that shows that it's worse. And so, we can improve our lives if we can go to permanent Standard Time.  Dr Jones: You convinced me. How about that? If there were any skeptics in the room, I doubt there are any left. We only went to like the fifth floor there, and she... I'm like, "I'm voting for this. Whatever, whatever this bill is, I'm gonna vote for it." So, I'm excited to get to the audience here. Before we get to questions and answers, and we want you to get your questions ready for Dr. Johnson. I do have a couple of trivia questions. And we've been doing this for a little while now on the podcast. The first trivia question actually relates to arts and culture.  Dr Jones: What famous artist used transitions between sleep and wake states to inspire his art? Anybody know?  Guest Speaker 1: Is it Van Gogh?  Dr Jones: Not Van Gogh that I know of. There in the back.  Guest Speaker 2: Picasso.  Dr Jones: Picasso, not that I know of. Right here.  Guest Speaker 3: Salvador Dali.  Dr Jones: Salvador Dali. We have a winner. Thank you for your answer. So apparently, I read this. Salvador Dali would sit in a chair holding onto a metal key and wait until he fell asleep, and it would fall out of his hands and drop into a bowl, and it would wake him up. So, then he would pick it back up, and he would go in and out of sleep trying to generate hypnagogic hallucinations, basically, and he would use that to inspire his art. And you think about his art, maybe that kind of makes sense. All right, now I've got a neurology trivia question. Okay, so maybe we're a little more comfortable with the neurology trivia in here. What is the center in the brain that is responsible for REM sleep atonia?  Guest Speaker 4: The receptor is for erection in the lateral hypothalamus.  Dr Jones: That is not correct. REM sleep atonia. Right here.  Guest Speaker 4: Emilio Malgona, Hyannis, Massachusetts. Dorsal raphe nucleus.  Dr Jones: We'll give you credit for that. Very good. Excellent. So, the-  Dr Johnson: Well, no. That's actually the serotonin. He's talking about another one.  Dr Jones: Oh, I thought I heard, I thought I heard-  Dr Johnson: You heard dorsal  Dr Jones: ... I heard dorsolateral tegmental nucleus of the pod.  Dr Johnson: Not quite.  Dr Jones: You get a prize anyway, sir, just for, just for answering. Thank you very much. All right. So, we're all warmed up here. So, Dr. Albin, what do you think? Should we get some questions from the audience?  Dr Johnson: All right, we've got some questions.  Guest Speaker 5: I have a statement and a question.  Dr Jones: Please tell the podcast your name again, sir.  Guest Speaker 5: Steve Spar, New York City. The tyranny of the morning people. You don't want people, you don't want the sun to go down too late because it'll keep people up longer. I spent my whole life fighting people like you. I am a nighttime person. Why do I have to go to sleep earlier? I want to go to sleep later. I want to wake up later. I don't want to wake up at 7:00 in the morning. I want to wake up at 10:00. There's a certain tyranny that we must use circadian rhythms of the majority, and it persecutes people like me who are night people.  Dr Johnson: So that is a great question.  Guest Speaker 5: What say you?  Dr Johnson: What say me is actually the harms of daylight savings time are actually to the night owls, and don't really affect the morning people. I can still go to sleep on time and get up on time without that pressure of needing to go to work. The night owl people, they can't fall asleep until later. They want to sleep in earlier, but we're forcing them to get up an hour earlier for work and school. And because we're doing daylight savings time, you're not getting the morning light you need, you're getting too much light at night, and you are more sensitive to a delay in your circadian rhythm, which makes you even more of a night owl and increase the degree of social jet lag. So, we actually see that the harms and risks of things like depression, cardiovascular risks are much greater in night owls than they are in normal people or morning larks. And this is again why the risks are the highest for our teenagers, who are essentially all night owls. You're making it harder for them to fall asleep on time. You're making them more and more of a night owl that it becomes more out of line with our standard social schedule. So, what we can do for a night owl is say to our schools, say to life that we want to change our society norms of getting up early. But that has nothing to do with daylight savings time. That has to do with how we make our schedule Dr Jones: All right, next question. And introduce yourself to the audience.  Guest Speaker 6: Sure. I'm Sanjay Rathi from New Haven area, Neurology. Movement disorders, Parkinson's disease, sleep disruptions, sleep-regulating REM, RBD issues, what are your recommendations? And as things get worse, what additional intervention should we do?  Dr Johnson: Yeah, I think it's hard with a lot of our neurodegenerative disorders, it's a two-way sleep. The disorders themselves often worsen sleep quality, have decrease in their sort of circadian amplitudes, and so that can affect sleep ability. And so, trying to do the things that promote sleep, like getting lights down in the evening, keeping things dark and quiet, doing cognitive behavioral sort of therapies if that's needed can all be helpful. Very high incidence of obstructive sleep apnea or other sleep-disordered breathing, whether it's Parkinson's or other neurodegenerative disorders, so evaluating and treating that if need be. And some of these people, especially as they get later on, you may end up considering medication for insomnia because their underlying disorders was causing it and there's, and you're not going to CBTI your way out of it. We do have the new orexin antagonist sleep agents, which are more recommended for older people and probably safer agents than your Z drugs and some of the other sleep meds out there. So, some people should be on some of those meds if their sleep is so disrupted. I've seen some sleep studies where it's basically like wake, sleep, wake, sleep, wake, sleep all night long. And it's like, wow, you really cannot sustain sleep, and we think it's not just a behavioral thing. I think it is part of their underlying Parkinson's and underlying disorders that can really cause major sleep disruption.  Dr Jones: It's a great question. Before we get more from the audience here, Dr. Albin, I'm just curious, you know, you got some questions from online. Don't know if any of those stood out to you. And the other thing is, I think about your practice, Dr. Albin, as a neurointensivist, there's some great content in this issue on how to maintain an adequate sleep environment in the hospital and the importance of that for the acute episode, maybe for some long-term outcomes. When I was reading the article, I didn't really didn't think about the ICU setting. That must be-- what do you do in the ICU?  Dr Albin: Well, we happen to have a question about just that. Dr Jones: Well, there you go  Dr Albin: From Dr. Manners of Baltimore, Maryland. "What meds should I be giving patients in the ICU or the inpatient setting to preserve or recalibrate their sleep-wake cycles? Is there anything that we can do besides just getting them out of bed during the day?"  Dr Johnson: Meds are always hard cause as sleep doctors, we're usually the last one to recommend meds. But there are situations and scenarios where meds may be appropriate. I can't say what's one better than the other, and some of the meds we have probably aren't even available as options in the hospital. So, the, you know, again, the orexin antagonist may be a good class to try to use, but they may not be an option. There was a good study that looked at empowering the patient and whether or not the ICU patients are empowerable. But they give a card to the patients in the hospital and say, "Tell your nurse to turn off my TV and my lights. Do I need all the blood draws all throughout the night, or can it be put off to the morning?" And trying to empower the patient to ask for these things and do some of the behavioral things. And they found that doing that did improve the duration of sleep, did reduce some of the number of awakenings that people ended up having at night. So, I think the ICU is a very particular population where there's a lot of things you can't get rid of. But certainly, turning on the lights, turning off the lights, and trying to limit noises as much as you can, in those night hours, trying to give some sense of a 24-hour day. The other thing is feeding is really important to circadian rhythms. I had a patient that had a brain bleed and, after it, she just her circadian rhythms were just off, and part of it was she was getting tube feeds through the night. So, one of the very first interventions we did was to move her timing of her feeding so that it wasn't in sleep, and that really did help make a difference in getting her back on a pattern, along with light therapy and other behavioral techniques as well.  Dr Jones: It's a great question.  Dr Albin: Absolutely. I mean, I think that validates just that we spend a lot of time actually asking like, "Can we feed people during the day?" Or, "Can we, can we limit the amount of baths that are happening at 3:00 in the morning?" We also had another one from the audience that came from Dr. Lavina Singla of Mississippi, and I think a lot of our patients are asking this question. Is melatonin addictive?  Dr Johnson: Is melatonin safe? Is melatonin addictive? I think with any sleeping aid, people become addictive to what they perceive is the outcome. So, if they said, "This got me to sleep, and now I'm sleeping great, I don't want to come off of it." And so, you get this to meds that are truly addictive, but even meds that aren't felt to have that addiction, there is certainly a behavioral change. And that's a lot of what cognitive behavioral therapy is working with these patients on, is challenging that belief of maybe it isn't the med, maybe it's your internal belief and your worry about doing this. One thing about sleep is sleep happens when you are relaxed and calm and not worried. When you're worried about thinking that thing you're worried about is whether or not you're getting sleep, then you don't sleep. In terms of melatonin, if you don't need to use it, I wouldn't use it. If you are gonna use it, I'd try to use as low doses as possible. Do we know all the risks? We don't know. And especially I think there are potentially more risks in a growing child than, maybe someone who isn't having the same sort of hormonal, needs and growth needs. But then again, if you have, let's say, a kid with autism and melatonin helps him sleep, I'd much rather use melatonin than a lot of other agents, and if that really changes their functionality, that probably is very good for them and better than having them not get sleep. So, I think you have to weigh each individual situation and combine it, especially with the behavioral approaches so that hopefully this is not a long-term addictive thing you're on.  Dr Jones: So, it's complicated. Sounds like it.  Dr Albin: Not a straightforward answer.   Dr Jones: I thought that was gonna be just this hard no, but I guess it is something you have to think about. So, I want to really take a minute here to thank Dr. Karin Johnson, who has been our interviewee for this episode of the Continuum Audio Podcast sleep issue just came out. Really want to encourage our subscribers, our listeners, and our studio audience here to enjoy it. Thank you, Dr. Johnson, for joining us today. I want to give a big round of applause to Dr. Casey Albin for managing this crowd. Thank you to our listeners. Thank you to our subscribers. Thank you to you all for coming today.  Dr Monteith: This is Dr. Teshamae Monteith, Associate Editor of Continuum Audio. If you've enjoyed this episode, you'll love the journal, which is full of in-depth and clinically relevant information important for neurology practitioners. Use the link in the episode notes to learn more and subscribe. Thank you for listening to Continuum Audio.   

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 in terms of quality and precision will be a CT angiography. The caveat there is with CT angiography is that, you know, you use radiation, and the patient has to get iodine. And then under those two, you will have a time-of-flight magnetic resonance angiography, which doesn't use any contrast, but then you lose a little bit of quality in terms of the imaging and some morphological features you might miss. So usually what we do in my practice, I don't wanna do a diagnostic cerebral angiogram, and somebody has to refer an unruptured aneurysm. I try to do CT angiogram as a baseline, see how the aneurysm looks, and then for follow-up, I usually do magnetic resonance an- angiograms with with contrast. If there is a concern that the aneurysm has some dangerous features like it's irregular in shape, it's, it's larger, it's in one of these high-risk locations, might be better just to refer the, the patient to a specialist for a diagnostic cerebral angiography.  Dr Smith: So, you know, there are these scales that you talk about in the article. There's phases in the UIATS that are used to predict rupture risk and guide decision-making. Are these scales that general neurologists or non-vascular neurologists can use to guide care? I'm thinking of like Chad-Baskin, ASBAD, which, you know, all our residents know about. Should we all be familiar with these scores?  Dr Samaniego: I think they're very helpful in the sense that it will give us some guidance. Some of the characteristics of the scale might be up- outdated. For example, like ancestry. Although it's been described more in Japanese and Finnish populations, and North American, not as much as these two other populations. We do see a lot of aneurysms in people from North America and other backgrounds. For example, one of the biggest critiques for the phases is that doesn't take into account smoking history. Smoking that we know is a risk factor. And the other critiques for phases is that, for example, if you are older than seventy years old, you will score one point, which will increase your risk of aneurysm rupturing. Having said that, we do see like tons of aneurysms on younger patients, actually the most productive years of their lives that they rupture. So, it gives you some parameters like the presence of hypertension, the size, as I said, seven or larger, previous history of subarachnoid hemorrhage, and the location of the aneurysm. But it doesn't take into account other factors like smoking or morphological features of the aneurysm. Dr Smith: Now, you mentioned size. I'd like to maybe go back and talk about a case from your article, which I found really impactful. For our listeners, this is a sixty-four-year-old woman who had a five-millimeter ACOM aneurysm. She was imaged serially, didn't change over the time period, and then two years later ruptured with devastating consequence, right? And so that's a small aneurysm. Most aneurysms, I guess, are small aneurysms. I just wonder, when you see a patient like that, how do you handle the discussion regarding risk? And how do you decide when to refer them for an intervention?  Dr Samaniego: Yeah. It's always puzzling when we see these smaller aneurysms. And this example is a typical example of a patient that doesn't follow the rule of seven or larger aneurysm size for rupturing. We see that quite often on aneurysms located in the anterior communicating artery. Just this last week, I treated two patients with similar characteristics, with smaller aneurysms, like average size between four and five, that rupture, and both were located in the anterior communicating artery. So, we know that there is definitely a linear relationship between size and risk and rupture, but we do see a lot of patients that have smaller aneurysms, like three, four, five millimeters that rupture, and we don't really understand very well the, biology of these aneurysms. So, when we see these aneurysms, we try to maximize the characterization of the aneurysm with better imaging, try to see the morphology. And usually when an aneurysm is discovered, what we do for follow-up is a six-month follow-up with some type of imaging, CTA, MRA with contrast, and see if there's has been any change in, on the aneurysm.  Dr Smith: So, is it fair to say that a knowledgeable non-vascular neurologist can safely manage these patients, follow them over time using what they learned from reviewing your article, identify patients who have higher risk aneurysms based on the characteristics you summarize, and refer them to a tertiary center? When I get these, it's easy for me to have our vascular neurosurgeon see them or a vascular neurologist, right? But in a community where you may not have ready access to that subspecialist, is it still important to get all of these patients to a tertiary center? Are there select instances where a community-based general neurologist can follow them and then refer if there's change in size, for instance?  Dr Samaniego: Yeah. I think that everything else that we do in neurology, it's important to do some type of triage in referring some of these patients for further studying and  expert opinion. I think age and size of the aneurysm, age of the patient and size of the aneurysm are huge factors. For example, if we have an older patient in their nineties and has incidentally found two-millimeter aneurysm in a low-risk location like the parathalmic, that patient probably needs to be seen locally. I don't think merits a full workup. As opposed to a younger patient with a three-millimeter aneurysm located in the ACOM. I think that type of patient probably needs to be referred to a tertiary s-stroke center for workup. I mean, most of the time what's gonna happen is that if it's a small aneurysm with benign characteristics, you know, it's gonna be seen by the specialist and they're gonna determine some type of follow-up, which can be done locally.  Dr Smith: So maybe we can pivot a little bit and talk about AVMs, if that's okay. What's your approach to a coincidentally discovered AVM, right? I mean, presumably, we need to think about symptomatic AVMs a little differently, I would think. So maybe we can start with the same scenario we've been talking about. You get an imaging study for something else, and, well, we find an AVM. What's the approach to that situation?  Dr Samaniego: Yeah. AVMs are fascinating vascular lesions because they're very complex, they're very heterogeneous. If we're talking about the morphological features with aneurysms, this, in the case of AVMs, is way more complex in terms of location size. The complexity added to AVMs is that you have a feeding artery, you have a nidus, and then you have draining veins. So, all of these can be very heterogeneous. In case of AVMs, I think those definitely need to be referred to a tertiary center because the management of AVMs is multidisciplinary, even in the tertiary centers. You know, we don't have a magic wand that will say, you know, all these AVMs need to be treated this way. Sometimes they don't even need to be treated because we know from some studies that just watching them will be good enough.  Dr Smith: You raised management of AVMs. Maybe we can go back and talk a little bit about what's the latest in management of aneurysms. You manage aneurysms from soup to nuts and as an endovascular interventional neurologist. What's the latest in management of aneurysms?  Dr Samaniego: The latest is that, which falls within management, is that we have tools that they have not really been validated a hundred percent because we're still understanding the biology of some of these aneurysms. But high-resolution MRI will help us to define if there is some enhancement of the aneurysm. There is the thought that if there is enhancement after the administration of contrast, might be more of an inflammatory process. So that can be used for management, triage, and follow-up of some of these aneurysms. In terms of endovascular treatment, it has been really a revolution of how we treat these lesions. You know, we have a lot of new devices, better catheters to access the aneurysms.There is devices that you can place inside the aneurysm sac and it'll completely shut down flow into the aneurysm. There is other special stents called flow diverters that can take the flow away from the aneurysm and bypassing the aneurysm. So, all of these things have really revolutionized how we treat them. Having said that, you know, there's always a risk with any of these procedures, and that's why we gotta be mindful when we decide to treat these patients with unruptured incidentally found aneurysm.  Dr Smith: I've got just one more question, Edgar, which I kind of led with. You've got training as a vascular neurologist, a neurointensivist, and an interventional neurologist. And you know, Ralph Sacco, as you probably know, used to like to talk about the neurologist, and part of the neurologist was interventional. I wonder what wisdom you have to trainees that are listening to us right now who might be interested in pursuing a career as a neuroendovascular neurologist. What wisdom do you have for them about how to go about doing that?  Dr Samaniego: It has been really rewarding to be part of this process and evolution of treating a stroke and aneurysms and AVMs because I remember when I was a resident at the University of Wisconsin, we only had, like, thrombolysis and only one device for, retrieving some of these clots. But now we have, like, 10 different devices. We have two different indications or two, two different thrombolytics. So, my best advice for trainees that want to pursue neuroendovascular is to get engaged early on, understand very well the biology and the thought process because it's not only a technical field. You have to have really good judgment on when to do and when not to do the procedure, and try to find mentorship. You know, there is a lot of neurointerventional neurologists out there right now. Having a good mentor will really facilitate your career choices and getting into training.  Dr Smith: Well, Edgar, thanks so much. What an exciting conversation. It's just another great example of how exciting neurology is these days. Many exciting advances and innovations, and we just scratched the surface. I encourage all of our listeners to read the article. It's actually really, really informative. So, thank you very much.  Dr Samaniego: Thank you so much, Gordon.  Dr Smith: Again, today I've been interviewing Dr. Edgar Samaniego about his article on unruptured intracranial aneurysms and AVMs. This article appears in the June 2026 issue of Continuum on Cerebrovascular Disease. Be sure to check out other Continuum Audio episodes from this and other issues, and thanks to you, our listeners, for joining us today.  Dr Monteith: This is Dr. Teshamae Monteith, Associate Editor of Continuum Audio. If you've enjoyed this episode, you'll love the journal, which is full of in-depth and clinically relevant information important for neurology practitioners. Use the link in the episode notes to learn more and subscribe. AAN members, you can get CME for listening to this interview by completing the evaluation at continpub.com/audioCME. Thank you for listening to Continuum Audio.

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 point for a follow-up, and not much has happened.  Dr Bahouth: That's a really well-put statement. Like I mentioned earlier, we had several focus groups to say, "How's our stroke center doing? How is our comprehensive stroke center doing?" And we realized that we were very comprehensive while the patient was with us, but then the experience of the patient going home was really opposite of receiving comprehensive care. You know, the patient in the hospital said they felt well-supported, surrounded, quite busy all the time, but then they did go home, and this sort of set in that they've had a stroke. And many patients told us, "I just laid in bed because I couldn't quite kind of get through the thought that this has happened to me." And so, in our prior state of our comprehensive stroke system where patients weren't seen for a couple of months after their discharge, patients would tell me, "Well, I'm fine now.  But those first couple of months, I sure wasn't. You know, I was laying in bed. I was crying. I wasn't taking my medicines. I had a lot of despair and fear." Care partners would say, "I wasn't sleeping myself. I was watching to see if another stroke was gonna happen every minute." So, there are a lot of elements that are going on in those first two weeks that really require a specialist to say, "This is normal. This requires more attention," and to really help people get through a lot of the changes that come with stroke and brain injury.  Dr Grouse: Now, your article gave a really great, I think, example, where you had a juxtaposition of a hypothetical patient with a stroke and two very different post-discharge courses, one where they really kind of fell into that vacuum, that post-discharge vacuum, where they didn't get support and had some very disappointing outcomes versus a patient who did have a transitional care program with a lot of support post-discharge, and a lot of obstacles were overcome and problems solved such that the patient could do a lot better. And I encourage our listeners to take a look at it. If you could design and run it, how would your ideal transitional post-stroke program be structured? Like, how would you design it so that it would optimally support these patients?  Dr Bahouth: Yeah, you know, we, um, tangle with this every day in our current transitional stroke program that we call the JSTEP program. We've had several chapters of what we think is ideal for a patient, and thank you for sort of acknowledging that, like, the way those cases were written were really to underscore that we can have a lot of influence for patients. And while they were sort of hypothetical juxtapositions of one another, these are things we literally see every single day for our stroke patients. And people say, "Oh, if only we had done this, we would've caught that, and we would've prevented such-and-so." Some of the indicators of success have been we've really reduced our readmission rates to the hospital. We have decreased our length of stay because the confidence people feel to go home because they're well supported. So there have been indicators of success. But if I could take our program even next level, I would probably include a few other things. So currently, some of the strengths of the program are that a stroke specialist sees a patient within days of their discharge from the hospital, a time where some of those questions are sort of raising for the patient. Maybe a complication is starting to pop up that we can address before it, uh, gets out of hand and requires a readmission. We can tackle some of the fears that patients are having to say, "I wonder if this is normal or not. I better just go to the hospital." So, some of that early touch point by a true stroke specialist is really critical. And that visit only happens because the seed is planted in the hospital, so there really has to be some initiation of the program at the time the patient is in the hospital to say, "This is what you can expect when you leave here. You have someone who's walking this with you. They're a stroke specialist. They're gonna know how to help you navigate." The second part of our program that is a success is our rapid connection to specialties. So, we know that stroke patients are gonna need connection to rehabilitation specialists, physiatrists, the therapists. We know they're gonna need connection to cardiology when atrial fibrillation or heart failure or something is really at an extreme.We know endocrinology might be a part of the patient's story going forward. And so, I think the second success of our program is really alliance with key stakeholders in a stroke patient's life and quick access to having the patient be connected to what it is they need in the moment that we realize that there is a situation at home. The third thing that I think has been really a success of our program is this interprofessional education that we schedule patients for at the time of their discharge, just as any other important healthcare visit. During this interprofessional education session, the patients get to meet dietician, pharmacist, nurse, therapist, where key discussions about healthy behaviors, avoidance of complications after stroke really happen in a group session where there can be a lot of interaction. You know, currently our education happens in a time where the brain is injured, the patient is not sleeping well in the hospital. We have a lot of stress and fear. It's not the perfect time for anyone to receive such important education. So, I think the third really most important thing has been this formalized interprofessional education to really bolster the education that started at the hospital. If I were to really take our program next level, and every day we're considering it, I really think we haven't done a couple of key things. One is we have not really found a way for the care partner to be supported, that the care partner is usually the brave one sitting there with a tight lip and nodding and very, you know, concerned about what's happening and taking close notes. But we really haven't done well to just manage the care partner's needs sort of independently of the patient themselves, sort of help them with the experience of going through this. I think that could benefit both the care partner and the patient by sort of bolstering their sort of emotional consequences of this. And they are really our key partner in the patient's success in the outpatient setting, getting the patient motivated, helping them get to appointments, helping them to adhere with medications. So, I think if we can focus a bit more on the care partner, that might really bolster the long-term effect for patients. And I think finally, behavior change is very complex. Sometimes we're taking a group of patients who may have never exercised and said, "You know, we really... You need to walk several minutes a day. You need to increase your aerobic capacity. We need you to stop smoking." And these are not behavior changes that can just happen with sort of a one-time visit. So, I think we really need to incorporate a lot more of exercise therapy and concepts of people who can sort of coach along the continuum for some of these behavior changes so that we can really promote wellness and a return to health. And I think one final thing that could be additive from a transitional stroke program is really a better way to truly measure recovery for stroke patients, some of those in between the line measures that we're not really getting by a three-month modified Rankin score. I think a transitional stroke care model would really allow us to both insert research and potential other therapies along this time period, but also measure the success of those in a more granular way.  Dr Grouse: Thank you so much for that, and also it was really helpful to get a good overview of, like, what the transitional care program really means, right? Like, what is the structure? What is happening with the patient? So, I think all of that's really helpful. But I can't help but think, listening to all of that, that sounds like while certainly in an ideal state, and I don't think anyone can argue with how helpful that sounds, is it always something that's practical? Can we implement things like this, especially where access is limited, resources are dwindling as far as what patients can get and what evaluations patients can get? Do you think that this is something that can actually be implemented in programs throughout the country? And what are strategies we can consider to try to improve getting some of these resources for our patients?  Dr Bahouth: I think this is such a critical topic. I think that we have, in the medical system, tried to force our healthcare practices into old models of care instead of sort of adopting new ones. And so, I think that, you know, while everyone says, "Wow, that sounds like a very resource-rich program," I would have to stop and push back and say, well, a very resource-rich situation is when a stroke patient, sometimes fifteen to twenty percent of the time, are readmitted to the hospital at a time where hospital beds are at a premium. Maybe we need to turn those dollars of savings of sort of these readmissions and extra length of stay into dollars that we put into sort of this transitional period where we help promote success. So, I think it really becomes more of a value proposition when you talk about it. But that said, of course, we have to make sure that we're a high-value, high-productivity system. So, our current transitional care program uses a telemedicine structure. We know that stroke patients cannot drive in most states after their stroke. We know that their care partners are trying to return to work and normalize. It is very difficult for patients with paralysis, cognitive changes to come back and forth to multiple appointments. In the past, we have tried to make this transitional care program an in-hospital program. I think using the technologies that we have available for telemedicine are critical, especially for this population who have barriers to getting to their appointments. So, I think with a very low resource investment, a transitional care program can be created once you really develop the skills of the, the stroke team to really reach beyond the hospital with the tools that we already have in the hospital and just extend that to the next chapter. It is an investment, most certainly, but I think it's one well worth the investment for the patient's success, their quality of life, as well as some of the value metrics that we judge our hospitals by.  Dr Grouse: Are some of the transitional care codes that CMS has put out in recent years helpful to get some reimbursement for these types of visits?  Dr Bahouth: Absolutely. So, I think that's been a really wonderful policy change that has happened, recognizing the importance of these transitional care models. There are billing codes that allow you to have higher billing than a usual neurology appointment when a patient is within a certain window, meeting certain criteria for their eligibility for such a visit.There are codes that have now been developed and are being more and more utilized to have visits with care partners and realize that the care partner is an important member of the equation of this patient's success. So, there are definitely codes that can be used. I think we're very good in healthcare of delivering a lot of free care, but that's not the nature of the beast these days. We have to really be very aware of our dollars and cents, and so utilizing some of these important codes that I hope only continue to expand to recognize the importance of the transitional period for patients.  Dr Grouse: Now, Mona, I wanted to ask, was there anything that you wish you could have included in this article that didn't make it in?  Dr Bahouth: You know, obviously, um, word limitations are always challenging. I think that the article, I think, does a good job going sort of from beginning to end. I think a deeper section, certainly we have commented on the sort of sociodemographic challenges of a program like this that also relies on a technology like telemedicine in many cases. But there are so many nuances to that conversation that I think that section could have definitely gone on for a much longer period of time to talk about some of the strategies, the strategic ways that we work hard to make sure that these type of transitional care programs are accessible to all, especially the vulnerable who may have challenges with accessing technology. But I will say it is possible. You know, we are in a urban city. We see a lot of patients with various insurance status and access to technologies, and we've had a very high show rate in our post-hospital transitional program, so it can be done with a thought and, uh, care to those vulnerable populations who may need more attention across the transition.  Dr Grouse: Well, I really appreciate all the work you've done in this area, and it sounds like it's an area that will continue to grow as we learn more and hopefully improve. And I really appreciate you taking the time out of your day to talk with us about your article.  Dr Bahouth: Well, thank you for having me, and it's a topic that's near and dear to us, so thanks again for highlighting its importance.  Dr Grouse: Again, today I've been 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. Be sure to check out Continuum Audio episodes from this and other issues, and thank you to our listeners for joining today.  Dr Monteith: This is Dr. Teshamae Monteith, Associate Editor of Continuum Audio. If you've enjoyed this episode, you'll love the journal, which is full of in-depth and clinically relevant information important for neurology practitioners. Use the link in the episode notes to learn more and subscribe. AAN members, you can get CME for listening to this interview by completing the evaluation at continpub.com/audioCME. Thank you for listening to Continuum Audio.

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

Stroke in children and younger adults differs significantly from adult stroke, with varied presentations and a broader range of underlying causes such as congenital heart disease and arteriopathies. This episode highlights key diagnostic considerations and evolving approaches to treatment in these younger populations. In this episode, Aaron L. Berkowitz, MD, PhD, FAAN, speaks with Thalia S. Field, MD, FRCPC, MHSc, coauthor of the article "Stroke in Children and Younger Adults" in the Continuum® June 2026 Cerebrovascular Disease 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. Field is a professor at the University of British Columbia and the Sauder Family Heart and Stroke Professor of Stroke Research, and a stroke neurologist at the Vancouver Stroke Program, Vancouver Coastal Health in Vancouver, British Columbia, Canada. Additional Resources Read the article: Stroke in Children and Younger Adults 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: Most neurologists are used to evaluating and treating adults with stroke since it's one of the most common neurologic conditions. But stroke can also occur in children, in infants, and even in utero. Today, I have the privilege of interviewing Dr. Thalia Field to talk about pediatric stroke.  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, and today I'm interviewing Dr. Thalia Field about her article on stroke in children and younger adults. This article appears in the June 2026 Continuum issue on cerebrovascular disease. Welcome to the podcast, Dr. Field, and could you please introduce yourself to our audience?  Dr Field: Well, thanks so much. It's a pleasure to, uh, be speaking to you. I'm a stroke neurologist, and I treat adults generally. My wonderful colleague, Thivya Selvanathan, who's a neonatal neurologist, co-wrote the chapter with me. We do, unfortunately, have to treat some children with stroke collaboratively and I do advise on those cases. My practice is about one-quarter clinical, so I treat patients with acute stroke, look after them on the wards, see patients in stroke prevention clinic, and the rest of my time is mainly research and some administrative work and teaching. I run the clinical trials program for the Vancouver Stroke Program, and I do research of my own, mainly focused on stroke in younger adults. We previously did a trial and registry on cerebral venous thrombosis, and more recently, I've been running a national study looking at brain health in adults and children with congenital heart disease.  Dr Berkowitz: Fantastic. Wow, that is a lot that you do, and we'll look forward to the results of some of those studies. So, when adults suffer a stroke, they typically present with sudden onset focal neurologic deficits, very common scenario we're consulted on.  And one thing you and your colleague talk about in the article is that strokes can present differently in infants and in young children. Can you talk a little bit about the differing clinical presentations of stroke in the youngest young as compared to our usual experience treating the older adults?  Dr Field: Sure. So, you know, speaking about this as someone who doesn't see the children directly but has had the opportunity to discuss these patients with my colleagues and, like we all do, learn about it during our training, I think one of the distinctions, especially with neonates, is that it's generally not a presentation with focal neurologic deficits. Often these babies will have seizures or encephalopathy as their main presentation, and sometimes we're only finding out after the fact if they're presenting with developmental delay or early preference for handedness and hypotonia, things like that. So, in very young children, that's a distinction. And in older children, there can be sudden onset deficits and, and unfortunately, sometimes these are mistaken for other conditions that are more common in children, like seizures. But sometimes you can have a more indolent course, say, with something like a focal cerebral arteriopathy or something like that. So, it depends on the scenario, but the big difference primarily is in neonates, as far as I understand.  Dr Berkowitz: Perfect. That's very helpful. So as an adult neurologist, when I think about causes of stroke or teach sort of the categories of causes of stroke to our residents and students, when we think about the evaluation of stroke, I divide them broadly into causes related to the heart, causes related to the blood vessels, and causes related to the blood with, in the adult world, the most common things, of course, being atrial fibrillation for the heart, atherosclerosis for the blood vessels, and then risk factors for atherosclerosis in the blood, diabetes, hyperlipidemia, very rarely picking up a hypercoagulable disorder in the blood column. And reading your article, it seems that, correct me if I'm wrong, stroke in young adults, stroke in the pediatric population can basically be organized into those same broad categories, heart, blood vessels, and blood, just that there's many more conditions on the differential diagnosis that you would consider in young adults to begin with and then children and then neonates as we get into the younger and younger population. So, I'd like to talk about each of these sort of buckets of etiology in turn and ask you about some of the causes we would consider in young adults and children in each of these, and then as they come up, probably ask you more questions about how frequently we find these sorts of things, how frequently they're the cause of stroke treatment, et cetera. So, let's start with the heart. As I said, in adults, we're mostly looking for rhythm disorders, right, atrial fibrillation. Sometimes we'll pick up a patent foramen ovale or PFO or other structural abnormalities, but mostly we're thinking about atrial fibrillation. But reading your paper, I was struck by the huge variety of conditions that you might be looking for in the heart in children or infants with stroke. So, can you tell us a little more about cardiac etiologies of stroke in the young?  Dr Field: Yeah. So, I'd say unlike in older adults, where it tends more often to be a rhythm disorder, in children and adults who are younger, it's primarily a structural cause, and congenital heart disease being the most common. And it changes a little bit from younger adults shifting downwards in age to younger children in terms of the fact that often if we're seeing an adult with stroke related to congenital heart disease, it can be a paradoxical embolism from a previously undiagnosed PFO. Not in all cases, but fortunately this is improving over time. You know, generally people with diagnoses of more severe congenital heart disease are followed up from childhood and people are aware of the diagnosis, and hopefully they're being managed and watched for things like premature arrhythmias or depressed heart function or other things that can develop and require their own distinct antithrombotic management, for example. In young children, however, more severe causes of congenital heart disease tend to more frequently be associated with stroke. And in many cases, those strokes can be early on in life or associated, say, with perioperative complications or other iatrogenic-related causes in, in that way. Again, congenital heart disease can be associated with stroke at, at any point in the life course. But as adult neurologists, most frequently we're seeing very simple lesions like PFO with large shunts, and in children, it tends to be the more complex causes of congenital heart disease.  Dr Berkowitz: Got it. So, let's move on to the blood vessels. Again, in adults, we're usually thinking about atherosclerotic disease, be that of the cervical arteries or of the intracranial arteries. But in your paper, a lot of discussion about the various vasculopathies, arteriopathies that can be cause of stroke in younger adults and in children. Could you talk a little bit more about some of the vasculopathies and vascular conditions that are causes of stroke in the younger population?  Dr Field: Sure. Before I do that, I will say that especially in older younger adults, particularly over the age of thirty-five, and you know, kind of makes me shudder that that's an older younger adult. But, um, in, in any case, certainly conventional vascular risk factors are more common in this population with stroke, especially in those who don't have PFO-associated stroke. Like conventional atherosclerosis, you know, certainly is a cause of stroke in younger adults. But that being said, certainly other vascular causes and vasculopathy in particular is a much more common cause of stroke in younger adults and, and children than it is in older adults. In particular, dissection is an extremely common cause of stroke in younger adults. Generally cervical artery dissection from non-inflammatory vasculopathy, usually on, sometimes on the FMD fibromuscular dysplasia spectrum and, and sometimes, you know, provoked by minor trauma or something post-infectious that may make the vessels a little bit more susceptible. And in younger children, this inflammatory focal cerebral arteriopathy is a distinct cause that is a common cause of stroke in, in young children. There are other causes that can affect the blood vessels, you know, rarer things like vasculitis and vasculopathies that can develop in the context, say, of sickle cell anemia. But in general, as a bucket, vessels are still very important, but the pathology tends to shift.  Dr Berkowitz: Got it. And you, um, alluded to a point that I wanted to ask you about. You mentioned the sort of, there's stroke in the young, and then where do you draw the line at young? Less than sixty, less than thirty-five, and then we've also talked about strokes as young as before the age of birth. Yeah, I'm remembering, is it the Helsinki study, one of the early large series of stroke in younger individuals? I think that, was it eighteen to forty-nine in that or fifty-nine? I don't remember the exact age, but being struck reading that paper as a resident and thinking about the workup for exotic causes we do, right, and when a young patient has a stroke. And correct me if I'm wrong, the most common etiologies of stroke in that series, and I'm curious the other large series yourself have been involved with, have still been vascular risk factors and arrhythmias and things that we, even common, quote unquote, common things in the young, such as dissection or hypercoagulable states. Uh, the things that we sort of tend to think about first are actually less common. But acknowledging that that paper has folks up to the late forties when the vascular risk factors may be, um, unfortunately kicking in earlier, uh, and earlier due to dietary and lifestyle factors. So is that true, or do you have sort of an age cutoff when it's, we say stroke in the young, people sort of think, "Oh, they'd work someone up differently if they're less than sixty, and they have no vascular risk factors or few vascular risk factors." When do we start getting into the kind of younger population where atherosclerosis and cardiac arrhythmias are not number one and two?  Dr Field: I'd say first of all, you and I must have trained around the same time because I was also in my training, really struck by the results of the Helsinki study going, "Wow, I, I really didn't know how much of a role these conventional vascular risk factors still play." And I think we're seeing that information reiterated, unfortunately, like even with higher prevalences and more attributable risk in some of the newer series. There are newer European series looking at stroke in younger adults, and more recently, there's been one that we mentioned in the article from the Florida Stroke Registry. And it's true that generally the burden is in the older younger adults. But what I would say overall in terms of kind of how things guide the workup, you need to look at the patient and consider things. I mean, obviously you don't want to miss things that can be treated differently and identified by tests easily. You know, things like ruling out syphilis or antiphospholipid antibody disease in, in younger patients. You really want to make sure that that's not something that, that you'd miss because, you know, obviously your treatment is going to change. However, certainly we start with the basics for stroke workup in any patient that's coming in. At my center, CT angiography. Some centers it may be MR angiography and echocardiography. We take a careful history. We look at the blood work. We look at the vascular risk factor burden. We find out if there's kind of any worrisome personal history, family history, look at their general health context. I think that really helps to guide how far we go in a particular workup, and it also helps to direct the other investigations and types of follow-up we need to do. For example, if a patient has a fairly suspicious story for dissection, let's say they're getting over a cold, and they went to the gym, and, you know, there was a sudden movement that they did that really produced headache and neck pain, and there's an obvious cervical artery dissection. I'm not going to go too far down testing them for rare infections and doing advanced cardiac imaging unless something shows up on their initial echo, for example. But I will make an effort to do more detailed vascular imaging of the rest of their body, find out careful family history. If there's additional manifestations of a non-inflammatory vasculopathy elsewhere, say consider sending them to medical genetics, or obviously, if this is, you know, a second event, your flags raise even more. So, it really depends on the patient. If I find out that there's, you know, a family history of premature cardiac disease and things like that, you know, obviously we're gonna be keeping a close eye on their cholesterol, making sure that we're not identifying, for example, familial hypercholesterolemia, which is, you know, something that comes up not infrequently where we'll see an LDL in an untreated patient of more than five. I apologize, you're gonna have to do the conversion to American units on that. But there are things we identify and, you know, again, you don't want to fall solely on heuristics and your preconceived notion of, of the patient. You do have to consider the results of the investigations that you do order. But I think you can certainly be mindful in terms of how you direct your workup and in turn, how you direct your follow-up.  Dr Berkowitz: That's great to hear your approach. Yeah, as you said, our approach always begins with the same, coming back to these three categories, right? Doing some type of structural imaging of the heart, rhythm monitoring for the heart, and then vascular imaging of the head and neck. And then I was going to ask you, and you sort of began to answer this question. Yeah. What's next and how far do you go? I think most people think the expanded stroke workup in the young is at a minimum, a TEE if there's been no signal thus far on the original workup. I just mentioned and you spoke about, and then probably hypercoagulable testing and only sending arterial side if there's no shunt and venous and arterial side if there's a shunt. Is that your second pass approach or did I miss anything, or are there other nuances there that are helpful to discuss?  Dr Field: No, I think that's generally in keeping with what I do. I think with TEE being very important. I mean, the first pass are arterial stuff. Really, it's antiphospholipid antibodies and, and making sure there's no cancer. Like you said, only if there's a shunt do I pursue other venous hypercoagulability testing. Again, you [chuckles] kind of reiterate, go through with the history, make sure there's kind of no red flags. And sometimes, obviously, you do your best reasonable job with the first pass workup, and you will find out when someone presents with a second event that it's something very unexpected. Maybe first manifestation, someone with no obvious history and very initially normal-looking imaging, say with, with CATASL or something like Fabry's disease or something where you would consider it if there was kind of a more classical picture. But it wouldn't be something you would do kind of on your first or even second pass workup in the absence of any sort of clinical suspicion, family history, or something along those lines.  Dr Berkowitz: I'm curious just as far as rough percentage. I feel like many of these patients we see it's a patient who's young and who's had a stroke, and the initial first pass has been unremarkable, and we do our TEE, and we do our hypercoagulable workup. Again, antiphospholipid antibodies only if it's-- there's no shunt. And if there's a shunt, adding on some of the venous hypercoagulability protein C, protein S, factor five, Leiden, et cetera. A lot of the times I feel like we don't find anything. What's your sort of general gestalt? Again, as a general neurologist who does a lot of inpatient neurology, I feel like when these cases come up, it's not that common that you say, "Oh, I actually diagnosed protein S deficiency." Or every once in a while, diagnose an antiphospholipid antibody, or you'll find a PFO on TEE. You didn't find on TT. I've maybe found one fibroelastoma in many years. How often do you find something? How often is it just as an adult a cryptogenic stroke in a young adult or child?  Dr Field: So much of what we see is PFO-related, dissection-related, conventional vascular risk factor-related. We do send referrals to medical genetics. Sometimes we'll do testing for rare things like Fabry's or consider other diagnoses. But I mean, those tend to be the exceptions. About one in four to one in five young adults with stroke end up with this cryptogenic label. I like to keep them on my radar for a few reasons. I think, one, it produces tremendous anxiety for them to not have a cause of stroke identified and just to kind of have a generic approach to secondary prevention. So, I think just to kind of keep an eye on them, manage their anxieties each year, make sure there's kind of no updates in, in terms of general secondary preventionAnd sometimes just things dawn on you later or there are new conditions, say things like, you know, DADA2, this, you know, adenosine deaminase deficiency. You know, there are new diagnoses that, that come on the radar. And sometimes treatments change. You know, for example, when I was starting my early career, the evidence hadn't yet been in place for PFO closure, and then all of a sudden, the paradigm completely changed. And you want to make sure that you can get in touch with those patients to reconsider your approach at the time. So I realize that not everybody has the luxury of extended follow-up with their patients, but I think often you can kind of encourage them or their healthcare team or just, you know, patient themselves to keep in touch periodically just to make sure that there haven't been any changes in treatment paradigms or just with your own awareness of particular, you know, diagnoses or, or just kind of readdressing the situation, uh, a year after and seeing if there's anything that may have occurred to you in the interim.  Dr Berkowitz: Perfect. Really illuminating to hear your approach to these challenging cases. And as you said here and then a couple of times, I think, in this interview is in many of these cases it's your first pass, maybe even your second pass, you haven't found anything. And the key is, unfortunately, as distressing as it may be for the patient as well as for us to not have an answer, to just keep following these patients. And sometimes you really can't sort it out until something else happens, either neurologically or systemically, where you say, "Oh, that's what this was." But there would've been no way to know it from the first presentation. So, we've talked a lot about the diagnosis of causes of stroke in younger adults and children. And in the last minute or two here, I just wanted to talk a little bit about treatment. You mentioned early on that you're involved in thrombectomy cases in children. What's the state of evidence or at least state of practice in terms of offering therapies like thrombolysis and thrombectomy in our patient population? I guess it would be under 18, right, who is not studied in the major trials. Do we have evidence and, or in the absence of evidence, what's sort of the, the expert guidance on treating young adults under 18 and children with some of these acute therapies?  Dr Field: So, trying to keep up with the literature on this. You know, certainly the evidence has been more established in a small trial and pediatric registries for use of tPA, tissue plasminogen activator, in children just because, you know, it's been around much longer. In terms of tenecteplase, which I, I really think signifies a, a practice shift in adult stroke because of its, you know, non-inferior efficacy and ease of use and potentially better rates of recanalization over time. In children, to my knowledge, that evidence base is, is limited to case series and anecdotal shifts in availability of drug and, and different practices. So, the evidence base is not particularly strong for tenecteplase in children who are identified within a reasonable amount of time who are still otherwise candidates for thrombolysis, you know, thrombolysis in children. Children who are a little bit older, I think, can't remember the exact age, but generally very young, like neonates, children who are under the age of two, I believe. I would want to double-check that thrombolysis is less commonly used and just because the safety has not really been that well-established. And for thrombectomy, it's now recommended to use thrombectomy in otherwise eligible children in the newest AHA guidelines. It gets a little bit more controversial in very young children. Under the age of six, there's less of an evidence base and, and often it will depend on people's level of comfort in terms of the size of the arteries. It's my understanding that once you get to about age six, the artery diameter is similar to that in fully grown people. But in younger children, I think just because of the catheters, there can be risk of, of injury. So, it's more of a case-by-case conversation with your interventionalist for younger children. And again, the evidence to intervene is not there for very, very young babies, for example.  Dr Berkowitz: That's very helpful to hear the current state of the evidence and the current state of practice, acknowledging, of course, there's not that much evidence, and these are relatively uncommon occurrences, fortunately, for children, but making it challenging for practitioners and practices may, um, vary based on different institutional protocols. So again, today I've been interviewing Dr. Thalia Field about her article on stroke in children and younger adults. This article appears in the June 2026 Continuum issue on cerebrovascular disease. Be sure to check out Continuum Audio episodes from this and other issues. And thank you to our listeners for joining us today.  Dr Monteith: This is Dr. Teshamae Monteith, Associate Editor of Continuum Audio. If you've enjoyed this episode, you'll love the journal, which is full of in-depth and clinically relevant information important for neurology practitioners. Use the link in the episode notes to learn more and subscribe. AAN members, you can get CME for listening to this interview by completing the evaluation at continpub.com/audioCME. Thank you for listening to Continuum Audio.