Podcasts about faan

In the first episode of the AAN President's Spotlight series, Dr. Jason Crowell speaks with the new AAN President, Dr. Natalia S. Rost, as she outlines her vision and key priorities for her two-year term. Show references:  https://www.aan.com/about-the-aan/presidents-spotlight

As artificial intelligence (AI) tools become increasingly mainstream, they can potentially transform neurology clinical practice by improving patient care and reducing clinician workload. Critically evaluating these AI tools for clinical practice is important for successful implementation. In this episode, Katie Grouse, MD, FAAN speaks with Peter Hadar, MD, MS, coauthor of the article “Clinical Applications of Artificial Intelligence in Neurology Practice” in the Continuum® April 2025 Neuro-ophthalmology 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. Hadar is an instructor of neurology at Harvard Medical School and an attending physician at the Massachusetts General Hospital in Boston, Massachusetts. Additional Resources Read the article: Clinical Applications of Artificial Intelligence in Neurology Practice 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 Guest: @PeterNHadar 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 Grouse: This is Dr Katie Grouse. Today I'm interviewing Dr Peter Hadar about his article on clinical applications of artificial intelligence in neurology practice, which he wrote with Dr Lydia Moura. This article appears in the April 2025 Continuum issue on neuro-ophthalmology. Welcome to the podcast, and please introduce yourself to our audience. Dr Hadar: Hi, thanks for having me on, Katie. My name is Dr Peter Hadar. I'm currently an instructor over at Mass General Hospital, Harvard Medical School, and I'm excited to talk more about AI and how it's going to change our world, hopefully for the better. Dr Grouse: We're so excited to have you. The application of AI in clinical practice is such an exciting and rapidly developing topic, and I'm so pleased to have you here to talk about your article, which I found to be absolutely fascinating. To start, I'd like to hear what you hope will be the key takeaway from your article with our listeners. Dr Hadar: Yeah, thank you. The main point of the article is that AI in medicine is a tool. It's a wonderful tool that we should be cautiously optimistic about. But the important thing is for doctors, providers to be advocates on their behalf and on behalf of their patients for the appropriate use of this tool, because there are promises and pitfalls just with any tool. And I think in the article we detail a couple ways that it can be used in diagnostics, in clinical documentation, in the workflow, all ways that can really help providers. But sometimes the devil is in the details. So, we get into that as well. Dr Grouse: How did you become interested in AI and its application, specifically in the practice of neurology? Dr Hadar: When I was a kid, as most neurologists are, I was- I nerded out on a lot of sci-fi books, and I was really into Isaac Asimov and some of his robotics, which kind of talks about the philosophy of AI and how AI will be integrated in the future. As I got into neurology, I started doing research neurology and a lot of folks, if you're familiar with AI and machine learning, statistics can overlap a lot with machine learning. So slowly but surely, I started using statistical methods, machine learning methods, in some of my neurology research and kind of what brought me to where I am today. Dr Grouse: And thinking about and talking about AI, could you briefly summarize a few important terms that we might be talking about, such as artificial intelligence, generative AI, machine learning, etcetera? Dr Hadar: It's a little difficult, because some of these terms are nebulous and some of these terms are used in the lay public differently than other folks would use it. But in general, artificial intelligence is kind of the ability of machines or computers to communicate independently. It's similar to as humans would do so. And there are kind of different levels of AI. There's this very hard AI where people are worried about with kind of terminator-full ability to replicate a human, effectively. And there are other forms of narrow AI, which are actually more of what we're talking about today, and where it's very kind of specific, task-based applications of machine learning in which even if it's very complex, the AI tools, the machine learning tools are able to give you a result. And just some other terms, I guess out there. You hear a lot about generative AI. There's a lot of these companies and different algorithms that incorporate generative AI, and that usually kind of creates something, kind of from scratch, based on a lot of data. So, it can create pictures, it can create new text if you just ask it. Other terms that can be used are natural language processing, which is a big part of some of the hospital records. When AI tools read hospital records and can summarize something, if it can translate things. So, it turns human speech into these results that you look for. And I guess other terms like large language models are something that also have come into prominence and they rely a lot on natural language processing, being able to understand human speech, interpret it and come up with the results that you want. Dr Grouse: Thank you, that's really helpful. Building on that, what are some of the current clinical applications of AI that we may already be using in our neurologic practice and may not even be aware that that's what that is? Dr Hadar: It depends on which medical record system you use, but a very common one are some of the clinical alerts that people might get, although some of them are pretty basic and they can say, you know, if the sodium is this level, you get an alert. But sometimes they do incorporate fancier machine learning tools to say, here's a red flag. You really should think about contacting the patient about this. And we can talk about it as well. It might encourage burnout with all the different flags. So, it's not a perfect tool. But these sorts of things, typically in the setting of alerts, are the most common use. Sorry, and another one is in folks who do stroke, there are a lot of stroke algorithms with imaging that can help detect where the strokes occur. And that's a heavy machine learning field of image processing, image analysis for rapid detection of stroke. Dr Grouse: That's really interesting. I think my understanding is that AI has been used specifically for radiology interpretation applications for some time now. Is that right? Dr Hadar: In some ways. Actually, my background is in neuroimaging analysis, and we've been doing a lot of it. I've been doing it for years. There's still a lot of room to go, but it's really getting there in some ways. My suspicion is that in the coming years, it's going to be similar to how anesthesiologists at one point were actively bagging people in the fifties, and then you develop machines that can kind of do it for you. At some point there's going to be a prelim radiology read that is not just done by the resident or fellow, but is done by the machine. And then another radiologist would double check it and make sure. And I think that's going to happen in our lifetime. Dr Grouse: Wow, that's absolutely fascinating. What are some potential applications of AI in neurologic practice that may be most high-yield to improve patient care, patient access, and even reduce physician burnout? Dr Hadar: These are separate sort of questions, but they're all sort of interlinked. I think one of the big aspects of patient care in the last few years, especially with the electronic medical record, is patients have become much more their own advocates and we focus a lot more on patient autonomy. So, they are reaching out to providers outside of appointments. This can kind of lead to physician burnout. You have to answer all these messages through the electronic medical record. And so having, effectively, digital twins of yourself, AI version of yourself, that can answer the questions for the patient on your off times is one of the things that can definitely help with patient care. In terms of access, I think another aspect is having integrated workflows. So, being able to schedule patients efficiently, effectively, where more difficult patients automatically get one-hour appointments, patients who have fewer medical difficulties might get shorter appointments. That's another big improvement. Then finally, in terms of physician burnout, having ambient intelligence where notes can be written on your behalf and you just need to double-check them after allows you to really have a much better relationship with the patients. You can actually talk with them one on one and just focus on kind of the holistic care of the patient. And I think that's- being less of a cog in the machine and focusing on your role as a healer would be actually very helpful with the implementation of some of these AI tools. Dr Grouse: You mentioned ambient technology and specifically ambient documentation. And certainly, this is an area that I feel a lot of excitement about from many physicians, a lot of anticipation to be able to have access to this technology. And you mentioned already some of the potential benefits. What are some of the potential… the big wins, but then also potential drawbacks of ambient documentation? Dr Hadar: Just to kind of summarize, the ambient intelligence idea is using kind of an environmental AI system that, without being very obtrusive, just is able to record, able to detect language and process it, usually into notes. So, effectively like an AI scribe that is not actually in the appointment. So, the clear one is that---and I've seen this as well in my practice---it's very difficult to really engage with the patient and truly listen to what they're saying and form that relationship when you're behind a computer and behind a desk. And having that one-on-one interaction where you just focus on the patient, learn everything, and basically someone else takes notes for you is a very helpful component of it. Some of the drawbacks, though, some of it has to do with the existing technology. It's still not at the stage where it can do everything. It can have errors in writing down the medication, writing down the exact doses. It can't really, at this point, detect some of the apprehensions and some of the nonverbal cues that patients and providers may kind of state. Then there's also the big one where a lot of these are still done by startups and other companies where privacy may be an issue, and a lot of patients may feel very uncomfortable with having ambient intelligence tools introduced into their clinical visit, having a machine basically come between the doctor and the patient. But I think that over time these apprehensions will lessen. A lot of the security will improve and be strengthened, and I think that it's going to be incorporated a lot more into clinical practice. Dr Grouse: Yeah, well, we'll all be really excited to see how that technology develops. It certainly seems like it has a lot of promise. You mentioned in your article a lot about how AI can be used to improve screening for patients for certain types of conditions, and that certainly seems like an obvious win. But as I was reading the article, I couldn't help but worry that, at least in the short term, these tools could translate into more work for busy neurologists and more demand for access, which is, you know, already, you know, big problems in our field. How can tools like these, such as, like, for instance, the AI fundoscopic screening for vascular cognitive risk factors help without adding to these existing burdens? Dr Hadar: It's a very good point. And I think it's one of the central points of why we wanted to write the article is that these AI in medicine, it's, it's a tool like any other. And just like when the electronic medical record came into being, a lot of folks thought that this was going to save a lot of time. And you know, some people would say that it actually worsened things in a way. And when you use these diagnostic screening tools, there is an improvement in efficiency, there is an improvement in patient care. But it's important that doctors, patients advocate for this to be value-based and not revenue-based, necessarily. And it doesn't mean that suddenly the appointments are shorter, that now physicians have to see twice as many patients and then patients just have less of a relationship with their provider. So, it's important to just be able to integrate these tools in an appropriate way in which the provider and the patient both benefit. Dr Grouse: You mentioned earlier about the digital twin. Certainly, in your article you mentioned, you know, that idea along with the idea of the potential of development of virtual chatbot visits or in-person visits with a robot neurologist. And I read all this with equal parts, I think excitement, but horror and and fear. Can you tell us more about what these concepts are, and how far are we from seeing technology like this in our clinics, and maybe even, what are the risks we need to be thinking about with these? Dr Hadar: Yeah. So, I mean, I definitely think that we will see implementation of some of these tools in our lifetime. I'm not sure if we're going to have a full walking, talking robot doing some of the clinical visits. But I do think that, especially as we start doing a lot more virtual visits, it is very easy to imagine that there will be some sort of video AI doctor that can serve as, effectively, a digital twin of me or someone else, that can see patients and diagnose them. The idea behind the digital twin is that it's kind of like an AI version of yourself. So, while you only see one patient, an AI twin can go and see two or three other patients. They could also, if the patients send you messages, can respond to those messages in a way that you would, based on your training and that sort of thing. So, it allows for the ability to be in multiple places at once. One of the risks of this is, I guess, overreliance on the technology, where if you just say, we're just going to have a chatbot do everything for us and then not look at the results, you really run the risk of the chatbot just recommending really bad things. And there is training to be had. Maybe in fifty years the chatbot will be at the same level as a physician, but there's still a lot of room for improvement. I personally, I think that my suspicion as to where things will go are for very simple visits in the future and in our lifetime. If someone is having a cold or something like that and it goes to their primary care physician, a chatbot or something like that may be of really beneficial use. And it'll help segment out the different groups of simple diagnosis, simple treatments can be seen by these robots, these AI, these machine learning tools; and some of the more complex ones, at least for the early implementation of this will be seen by more specialized providers like neurologists and subspecialist neurologists too. Dr Grouse: That certainly seems reasonable, and it does seem that the more simple algorithmic things are always where these technologies will start, but it'll be interesting to see where things can go with more complex areas. Now I wanted to switch gears a little bit in the article- and I thought this was really important because I see it as being certainly one of the bigger drawbacks of AI, is that despite the many benefits of artificial intelligence, AI can unfortunately perpetuate systemic bias. And I'm wondering if you could tell us a little bit more about how this happened? Dr Hadar: I know I'm beating a dead horse on this, but AI is a tool like any other. And the problem with it is that what you put in is very similar to what you get out. And there's this idea in computer science of “garbage in, garbage out”. If you include a lot of data that has a lot of systemic biases already in the data, you're going to get results that perpetuate these things. So, for instance, if in dermatologic practices, if you just had a data set that included people of one skin color or one race and you attempted to train a model that would be able to detect skin cancer lesions, that model may not be easily applicable to people of other races, other ethnicities, other skin colors. And that can be very damaging for care. And it can actually really, really hurt the treatments for a lot of the patients. So that is one of the, kind of, main components of the systemic biases in AI. The way we mitigate them is by being aware of it and actually implementing, I guess, really hard stops on a lot of these tools before they get into practice. Being sure, did your data set include this breakdown of sex and gender, of race and ethnicity? So that the stuff you have in the AI tool is not just a very narrow, focused application, but can be generalized to a large population, not just of one community, one ethnic group, racial group, one country, but can really be generalized throughout the world for many patients. Dr Grouse: The first step is being aware of it, and hopefully these models will be built thoughtfully to help mitigate this as much as possible. I wanted to ask as well, another concern about AI is the safety of private data. And I'm wondering, as we're starting to do things like use ambient documentation, AI scribe, and other types of technologies like this, what can we tell our patients who are concerned about the safety of their personal data collected via these programs, particularly when they're being stored or used with outside companies that aren't even in our own electronic medical records system? Dr Hadar: Yeah, it's a very good question, and I think it's one of the major limitations of the current implementation of AI into clinical practice, because we still don't really have great standards---medical standards, at least---for storing this data, how to analyze this data. And my suspicion is that at some point in the future, we're going to need to have a HIPAA compliance that's going to be updated for the 21st century, that will incorporate the appropriate use of these tools, the appropriate use of these data storage, of data storage beyond just PHI. Because there's a lot more that goes into it. I would say that the important thing for how to implement this, and for patients to be aware of, is being very clear and very open with informed consent. If you're using a company that isn't really transparent about their data security and their data sharing practices, that needs to be clearly stated to the patient. If their data is going to be shared with other people, reanalyzed in a different way, many patients will potentially consider not participating in an AI implementation in clinic. And I think the other key thing is that this should be, at least initially, an opt-in approach as opposed to an opt-out approach. So patients really have- can really decide and have an informed opinion about whether or not they want to participate in the AI implementation in medicine. Dr Grouse: Well, thank you so much for explaining that. And it does certainly sound like there's a lot of development that's going to happen in that space as we are learning more about this and the use of it becomes more prevalent. Now, I also wanted to ask, another good point that you made in your article---and I don't think comes up enough in this area, but likely will as we're using it more---AI has a cost, and some of that cost is just the high amount of data and computational processing needed to use it, as well as the effects on the environment from all this energy usage. Given this drawback of AI, how can we think about potential costs versus the benefits, the more widespread use of this technology? Or how should we be thinking about it? Dr Hadar: It's part of a balance of the costs and benefits, effectively, is that AI---and just to kind of name some of them, when you have these larger data centers that are storing all this data, it requires a lot of energy consumption. It requires actually a lot of water to cool these things because they get really hot. So, these are some of the key environmental factors. And at this point, it's not as extreme as it could be, but you can imagine, as the world transitions towards an AI future, these data centers will become huge, massive, require a lot of energy. And as long as we still use a lot of nonrenewable resources to power our world, our civilization, I think this is going to be very difficult. It's going to allow for more carbon in the atmosphere, potentially more climate change. So, being very clear about using sustainable practices for AI usage, whether it be having data centers specifically use renewable resources, have clear water management guidelines, that sort of thing will allow for AI to grow, but in a sustainable way that doesn't damage our planet. In terms of the financial costs… so, AI is not free. However, on a given computer, if you want to run some basic AI analysis, you can definitely do it on any laptop you have and sometimes even on your phone. But for some of these larger models, kind of the ones that we're talking about in the medical field, it really requires a lot of computational power. And this stuff can be very expensive and can get very expensive very quickly, as anyone who's used any of these web service providers can attest to. So, it's very important to be clear-eyed about problems with implementation because some of these costs can be very prohibitive. You can run thousands and you can quickly rack up a lot of money for some very basic analysis if you want to do it in a very rapid way, in a very effective way. Dr Grouse: That's a great overview. You know, something that I think we're all going to be having to think about a lot more as we're incorporating these technologies. So, important conversations I hope we're all having, and in our institutions as we're making these decisions. I wanted to ask, certainly, as some of our listeners who may be still in the training process are hearing you talk about this and are really excited about AI and implementation of technology in medicine, what would you recommend to people who want to pursue a career in this area as you have done? Dr Hadar: So, I think one of the important things for trainees to understand are, there are different ways that they can incorporate AI into their lives going forward as they become more seasoned doctors. There are clinical ways, there are research ways, there are educational ways. A lot of the research ways, I'm one of the researchers, you can definitely incorporate AI. You can learn online. You can learn through books about how to use machine learning tools to do your analysis, and it can be very helpful. But I think one of the things that is lacking is a clinician who can traverse both the AI and patient care fields and be able to introduce AI in a very effective way that really provides value to the patients and improves the care of patients. So that means if a hospital system that a trainee is eventually part of wants to implement ambient technology, it's important for physicians to understand the risks, the benefits, how they may need to adapt to this. And to really advocate and say, just because we have this ambient technology doesn't mean now we see fifty different patients, and then you're stuck with the same issue of a worse patient-provider relationship. One of the reasons I got into medicine was to have that patient-provider interaction to not only be kind of a cog in the hospital machine, but to really take on a role as a healer and a physician. And one of the benefits of these AI tools is that in putting the machine in medicine, you can also put the humanity back in medicine at times. And I think that's a key component that trainees need to take to heart. Dr Grouse: I really appreciate you going into that, and sounds like there's certainly need. Hoping some of our listeners today will consider careers in pursuing AI and other types of technologies in medicine. I really appreciate you coming to talk with us today. I think this is just such a fascinating topic and an area that everybody's really excited about, and hoping that we'll be seeing more of this in our lives and hopefully improving our clinical practice. Thank you so much for talking to us about your article on AI in clinical neurology. It was a fascinating topic and I learned a lot. Dr Hadar: Thank you very much. I really appreciate the conversation, and I hope that trainees, physicians, and others will gain a lot and really help our patients through this. Dr Grouse: So again, today I've been interviewing Dr Peter Hadar about his article on clinical applications of artificial intelligence in neurology practice, which he wrote with Dr Lydia Moura. This article appears in the most recent issue of Continuum on neuro-ophthalmology. 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. Thank you for listening to Continuum Audio.

Learn the terms healthcare teams use after cancer treatment is complete, and why they hesitate to use the word "cured."  https://bit.ly/3FfnfUxAdvances in cancer diagnosis, screening, and treatment have greatly improved the 5-year survival rates of most people with cancer over the last 30 years. Long-term survivors of cancer are more and more common, and research is increasingly directed at helping people live well after a diagnosis of cancer. But even so, many oncologists still hesitate to use the word “cure” with their patients. We talk with Dr. Jeanne Ford about the difference between the terms No Evidence of Disease (NED), remission, cure, and cancer free.In this Episode: 03:11 | Travel-Vermont and Vermont Chicken Pot Pie04:25 | The Trouble with Using the Phrase "Cancer Free"10:20 | Why We Don't Say Cancer is Cured12:00 | How Dr Ford Explains NED to Her Patients19:17 | What Does "Cure" Really Mean?29:38  | How Do Native Communities Treat the Concept of a Cancer Cure32:51 | The Role of Hope and How to Deliver Honest Information37:28 | Addressing Fear of Recurrence and Uncertainty about Future44:13 | Cancer Survivorship and Surveillance46:03 | Outro#survivor #cancersurvivor #cancerfree #remisssion #NED #cancercured #treatmentfinished #survivorship #oncologynurse #caregiver #palliativecare #everyonedies #everydayisagift #cancerjourneySupport the showGet show notes and resources at our website: every1dies.org. Facebook | Instagram | YouTube | mail@every1dies.org

Neuro-ophthalmic deficits significantly impair quality of life by limiting participation in employment, educational, and recreational activities. Low-vision occupational therapy can improve cognition and mental health by helping patients adjust to visual disturbances. In this episode, Katie Grouse, MD, FAAN, speaks with Sachin Kedar, MD, FAAN, author of the article “Symptomatic Treatment of Neuro-ophthalmic Visual Disturbances” in the Continuum® April 2025 Neuro-ophthalmology 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. Kedar is the Cyrus H Stoner professor of ophthalmology and a professor of neurology at Emory University School of Medicine in Atlanta, Georgia. Additional Resources Read the article: Symptomatic Treatment of Neuro-ophthalmic Visual Disturbances 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: @AIIMS1992 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 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 Sachin Kedar about his article on symptomatic treatment of neuro-ophthalmic visual disturbances, which appears in the April 2025 Continuum issue on neuro-ophthalmology. Welcome to the podcast, and please introduce yourself to our audience. Dr Kedar: Thank you, Katie. This is Sachin Kedar. I'm a neuro-ophthalmologist at Emory University, and I've been doing this for more than fifteen years now. I trained in both neurology and ophthalmology, with a fellowship in neuro-ophthalmology in between. It's a pleasure to be here. Dr Grouse: Well, we are so happy to have you, and I'm just so excited to be discussing this article with you, which I found to be a real treasure trove of useful clinical information on a topic that many find isn't covered enough in their neurologic training. I strongly recommend all of our listeners who work with patients with visual disturbances to check this out. I wanted to start by asking you what you hope will be the main takeaway from this article for our listeners? Dr Kedar: The most important takeaway from this article is, just keep vision on your radar when you are evaluating your patients with neurological disorders. Have a list of a few symptoms, do a basic screening vision, and ask patients about how their vision is impacting the quality of life. Things like activities of daily living, hobbies, whether they can cook, dress, ambulate, drive, read, interact with others. It is very important for us to do so because vision can be impacted by a lot of neurological diseases. Dr Grouse: What in the article do you think would come as the biggest surprise to our listeners? Dr Kedar: The fact that impairment of vision can magnify and amplify neurological deficits in a lot of what we think of as core neurological disorders should come as a surprise to most of the audience. Dr Grouse: On that note, I think it's probably helpful if you could remind us about the types of visual disturbances we should be thinking about and screening for in our patients? Dr Kedar: Patients who have neurological diseases can have a whole host of visual deficits. The simplest ones are deficits of central vision. They can have problems with their visual field. They can have abnormalities of color vision or even contrast sensitivity. A lot of our patients also complain of light sensitivity, eyes feeling tired when they're doing their usual stuff. Some of our patients can have double vision, they can have shaky vision, which leads to their sense of imbalance and maybe a fall risk to them. Dr Grouse: It's really helpful to think about all the different aspects in which vision can be affected, not just sort of the classic loss of vision. Now, your article also serves as a really important reminder, which you alluded to earlier, about how impactful visual disturbances can be on daily activities. Could you elaborate a little further on this, and particularly the various domains that can be affected when there are visual disturbances present? Dr Kedar: So, when I look at how visual disturbances affect quality of life, I look at two broad categories. One is activities of basic daily living. These would be things like, are you able to cook? Are you able to ambulate not just in your home, but in your neighborhood? Are you able to drive to your doctor's appointment or to visit with your family? Are you able to dress yourself appropriately? Are you able to visualize the clothing and choose them appropriately? And then the second category is recreational activities. Are you able to read? Are you able to watch television? Are you able to visit the theatre? Are you able to travel? Are you able to participate in group activities, be it with your family or be it with your social group? It is very important for us to ask our patients if they have problems doing any of this because it really can adversely impact the quality of life. Dr Grouse: I think, certainly with all the things we try to get through talking with our patients, this may not be something that we do spend a lot of time on. So, I think it's it is a good reminder that when we can, being able to ask about these are going to be really important and help us hit on a lot of other things we may not even realize or know to ask about. Now, I was really struck when I was reading your article by the meta-analysis that you had quoted that had showed 47% higher risk of developing dementia among the visually impaired compared to those without visual impairments. Should we be doing more in-depth visual testing on all of our patients with cognitive symptoms? Dr Kedar: This is actually the most interesting part of this article, and kind of hones in on the importance of vision in neurological disorders. Now I want to clarify that patients with visual disorders, it's not a causative influence on dementia, but if you have a patient with an underlying cognitive disorder, any kind of visual disturbance will significantly make it worse. And this has been shown in several studies, both in the neurologic and in the ophthalmological literature. So, I quoted one of the big meta-analysis over there, but studies have clearly shown that if you have these patients and treat them for their visual deficits, their cognitive indices can actually significantly improve. To answer your question, I would say a neurologist should include basic vision screening as part of every single evaluation. Now, I know it's a hard thing in, you know, these days when we are literally running on the hamster wheel, but I can assure you that it won't take you more than 2 to 3 minutes of your time to do this basic screening; in fact, you can have one of your assistants included as part of the vital signs assessment. What are these basic screening tools? Measure the visual acuity for both near and distance. Check and see if their visual field's off with the confrontation. Look at their eye movements. Are they able to move their eyes in all directions? Are the eyes stable when they're trying to fixate on a particular point? I think if you can do these basic things, you will have achieved quite a bit. Dr Grouse: That's really helpful, and thanks for going through some of the standard, or really, you know, solid basic foundation of visual testing we should be thinking about doing. I wanted to move on to some more details about the visual disturbances. You made an excellent point that there are many types of primary ophthalmologic conditions that can cause visual disturbances that we should keep in mind. So maybe not things that we think about a lot on a day-to-day basis, but, you know, are still there and very common. What are some of the most common ones, and when should we be referring them to see an ophthalmologist? Dr Kedar: So, it depends on the age group of your patient population. Now, the majority of us are adult neurologists, and so the kinds of ophthalmic conditions that we see in this population is going to be different from the pediatric age group. So in the adult population, we might see patients with uncorrected refractive error, presbyopia, patients who have cataracts creep on them, they may have glaucoma, they may have macular degeneration, and these tend to have a slightly higher incidence in the older age group. Now for those of us who are taking care of the younger population, uncorrected refractive errors, strabismus and amblyopia tend to be fairly common causes of visual deprivation in this age group. What I would encourage all of our neurologists is, make sure that your patients get a basic eye examination at least once a year. Just like you want them to go to their primary care and get an annual maintenance visit, everybody should go to the ophthalmologist or the optometrist and get a basic examination. And, if you're resourceful enough, have your patients bring a copy of that assessment. Whether it is normal or there's some abnormality, it is going to help you in the management. Dr Grouse: Absolutely. I think that's a great piece of advice, to think of it almost, like, them seeing their primary care doctor, which of course we offer encourage our patients to do, thinking of this as another very important piece of standard primary care. If a patient comes to you reporting difficulty reading due to possible visual disturbances, I'm curious, can you walk us through how you would approach this evaluation? Dr Kedar: It is not a very common presenting complaint of our patients, even in the neuro-ophthalmology clinic. It's a very rare patient that I see who comes and says, I cannot read or, I have difficulty reading. Most of the patients will come saying, oh, I cannot see. And then you have to dig in to find out, what does that actually mean? What can you not see? Is it a problem in your driving? Is it a problem in your reading? Or is it a problem that occurs at all times? Now you asked me, how do you approach this evaluation? One of the things that all of us, whether we are neurologists, ophthalmologists, or neuro-ophthalmologists, forget to do is to actually have the patient read a paragraph, a sentence, when they are in clinic. And that will give you a lot of ideas about what might actually be going wrong with the patient. Now, as far as how do I approach this evaluation, I will do a basic screening examination to make sure that their visual acuity is good for both distance and near. A lot of us tend to do either distance or near and we will miss the other parameter. You want to do a basic confrontation visual field to make sure that they do not have any subtle deficits that's impacting their ability to read. Examine the eye movements, do a fundoscopic examination. Now, once you've done this basic screening, as a neurologist, you already have some idea of whether your patient has a lesion along the visual pathways. If you suspect that this is a problem with, say, the visual pathways, ask your ophthalmology colleague to do a formal visual field assessment, and that'll pick up subtle deficits of central visual field. And lastly, don't forget higher visual function testing or cortical visual function testing. So basically, you're looking for neglect, phenomenon, or simultanagnosia, all of which tends to have an impact on reading. So, in the manuscript I have a schema of how you can approach a patient with reading difficulties, and in that ischemia you will see categories of where things can go wrong during the process of reading. And if you can approach your patient systematically through one of those domains, there's a fairly good chance that you'll be able to pick up a problem. Dr Grouse: Going a little further on to when you do identify problems with loss of central or peripheral vision, what are some strategies for symptomatic management of these types of visual disturbances? Dr Kedar: As a neurologist, if you pick up a problem with the vision, you have to send this patient to an eye care provider. The vast majority of people who have visual disturbances, it's from an eye disease. You know, as I alluded to earlier, it can be something as simple as uncorrected refractive error, and that can be fixed easily. A lot of patients in our older age group will have dry eye syndrome, which means they are unable to adequately lubricate the surface of the eye, and as a result, it degrades the quality of their vision. So, they tend to get intermittent episodes of blurred vision, or they tend to get glare. They tend to get various forms of optical aberration. Patients can have cataracts, patients can have glaucoma or macular degeneration. And in all of those instances, the goal is to treat the underlying disease, optimize the vision, and then see what the residual deficit is. By and large, if a patient has a problem with the central vision, then magnification will help them for activities that they perform at near; say, reading. Now for patients with peripheral vision problem, it's a different entity altogether. Again, once you've identified what the underlying cause is, your first goal is to treat it. So, for example, if your patient has glaucoma, which is affecting peripheral vision, you're going to treat glaucoma to make sure that the visual field does not progress. Now a lot of what happens after that is rehabilitation, and that is always geared towards the specific activities that are affected. Is it reading? Is it ambulating? Is it watching television? Is it driving? And then you can advise as a neurologist, you can advise your occupational therapist or low vision specialist and say, hey, my patient is not able to do this particular activity. Can we help them? Dr Grouse: Moving on from that, I wanted to also hit on your approach when patients have disorders of ocular motility. What are some things you can do for symptomatic management of that? Dr Kedar: So, patients with ocular motility can have two separate symptoms. Two, you know, two disabling symptoms, as they would call it. One is double vision and the other is oscillopsia, or the feeling or the visualization of the environment moving in response to your eyes not being able to stay still. Typically, you would see this in nystagmus. Now, let's start with diplopia. Diplopia is a fairly common presenting complaint for neurologists, ophthalmologists, and the neuro-ophthalmologist. The first aspect in the management of diplopia is to differentiate between monocular diplopia and binocular diplopia. Now, monocular diplopia is when the double vision persists even after covering one eye. And that is never a neurological issue. It's almost always an ophthalmic problem, which means the patient will then have to be assessed by an eye care provider to identify what's causing it. And again, refractive error, cataracts, opacities, they can do it. Now, if the patient is able to see single vision by covering one eye at a time, that's binocular diplopia. Now, in patients with binocular diplopia in the very early stages of the disease, the standard treatment regimen is just monocular occlusion. Cover one eye, the diplopia goes away, and then give it time to improve on its own. So, this is what we would typically do in a patient with, say, acute sixth nerve palsy or fourth nerve palsy or third nerve palsy, maybe expect spontaneous improvement in a few months. Now if the double vision does not improve and persists long term, then the neuro-ophthalmologist or the ophthalmologist will monitor the amount of deviation to see if it fluctuates or if it stays the same. So, what are the treatment options that we have in a patient who absolutely refuses any intervention or is not a candidate for any intervention? Monocular occlusion still remains the viable option. Now, patients who have stable ocular deviation can benefit from using prisms in their glasses, or they can be sent to a surgeon to have a strabismus surgery that can realign their eyes. So, again, a broad answer, but there are options available that we can use. Dr Grouse: Thank you for that overview. I think that's just really helpful to keep in mind as we're working with these patients and thinking about what their options are. And then finally, I wanted to touch on patients with higher-order vision processing and attention difficulties. What are some strategies for them? Dr Kedar: These are frankly the most difficult patients that I get to manage in my clinic, simply because there is no effective therapies for managing them. In fact, I think neurologists are far better at this than ophthalmologists or even neuro-ophthalmologists. In patients with attentional disorders, everything boils down to the underlying cause, whether you can treat it or whether it is a slowly progressive, you know, condition, such as from neurodegenerative diseases. And that tailors our goals towards therapy. The primary goal is for safety. A lot of these patients who have visual disturbances from vision processing or attention, they are at accident and fall risk. They have problems with social interactions. And, importantly, there is a gap of understanding of what's going on, not just from their side but also from the family's side. So, I tend to approach these patients from a safety perspective and social interaction perspective. Now, I have a table listed in the manuscript which will go into details of what the specific things are. But in a nutshell, if your patient has neglect in a specific part of the visual field, they have accident risk on that side. Simple things like walking through a doorway, they can hurt their shoulders or their knees when they bang into the wall on that side because they are unable to judge what's on the other side. Another example would be a patient who has simultanagnosia or a downgaze policy, such as from progressive super nuclear policy. They are unable to look down fast enough, or they are simply unable to look down and appreciate things that are on the floor, and so they can trip and fall. Walking downstairs is also not a huge risk because they are unable to judge distances as they walk down. A lot of what we see in these patients are things that we have to advise occupational therapists and help them improve these safety parameters at home. Another thing that we often forget is patients can inadvertently cause a social incident when they tend to ignore people on their affected side. So, if there is a family gathering, they tend to consistently ignore a group of people who are sitting on the affected side as opposed to the other side. And I've had more than a few patients who've come and said that, I may have offended some of my friends and family. In those instances, it's always helpful when they are in clinic to demonstrate to the family how this can be awkward and how this can be mitigated. So, having everybody sit on one side is a useful strategy. Advise your family and friends before a gathering that, hey, this may happen. And it is not because it is deliberate, but it's because of the medical condition. And that goes a lot, you know, further in helping our patients come out of social isolation because they are also afraid of offending people, you know. And they can also participate socially, and it can overall improve their quality of life. Dr Grouse: That's a really helpful tip, and something I'll keep in mind with my patients with neglect and visual field cuts. Thank you so much for coming to talk with us today. Your article has been so helpful, and I urge everybody listening today to take a look. Dr Kedar: Thank you, Katie. It was wonderful talking to you. Dr Grouse: I've been interviewing Dr Sachin Kedar about his article on symptomatic treatment of neuro-ophthalmic visual disturbances, which appears in the most recent issue of Continuum on neuro-ophthalmology. 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.

Joining John Maytham is Faan van der Walt, CEO of WeBuyCars, a major player in South Africa’s used car space. He shares insights into the risks and realities of buying Chinese vehicles, especially for first-time or budget-conscious buyers. Presenter John Maytham is an actor and author-turned-talk radio veteran and seasoned journalist. His show serves a round-up of local and international news coupled with the latest in business, sport, traffic and weather. The host’s eclectic interests mean the program often surprises the audience with intriguing book reviews and inspiring interviews profiling artists. A daily highlight is Rapid Fire, just after 5:30pm. CapeTalk fans call in, to stump the presenter with their general knowledge questions. Another firm favourite is the humorous Thursday crossing with award-winning journalist Rebecca Davis, called “Plan B”. Thank you for listening to a podcast from Afternoon Drive with John Maytham Listen live on Primedia+ weekdays from 15:00 and 18:00 (SA Time) to Afternoon Drive with John Maytham broadcast on CapeTalk https://buff.ly/NnFM3Nk For more from the show go to https://buff.ly/BSFy4Cn or find all the catch-up podcasts here https://buff.ly/n8nWt4x Subscribe to the CapeTalk Daily and Weekly Newsletters https://buff.ly/sbvVZD5 Follow us on social media: CapeTalk on Facebook: https://www.facebook.com/CapeTalk CapeTalk on TikTok: https://www.tiktok.com/@capetalk CapeTalk on Instagram: https://www.instagram.com/ CapeTalk on X: https://x.com/CapeTalk CapeTalk on YouTube: https://www.youtube.com/@CapeTalk567 See omnystudio.com/listener for privacy information.

On this week's show, your host, Justin Mog, scrubs your aural environment of all toxins with two colleagues from the University of Louisville's Center for Integrative Environmental Health Science (CIEHS): Cat Aiton, MSW, is the Community Resource Coordinator for the Community Engagement Core of CIEHS, and Sarah Jump is the Communications & Marketing Specialist. Learn more about the Center at https://louisville.edu/ciehs On the show, we discuss what environmental health is and how we all play a role in either advancing it or detracting from it. We share some practical tips for keeping yourself, your family, and your entire community healthy in the face of a world of dangerous toxins and pollutants. We talk about how the Center is working to reach young people with empowering messages and walking the talk with more sustainable give-aways. You'll also learn about an upcoming Conference for Advancing Participatory Sciences and the importance of Report Back strategies for sharing findings with communities in a language that is meaningful to them. We'll also tell you all about the upcoming Environmental Health Youth Academy that the Center is organizing this summer (https://events.louisville.edu/event/2025-ciehs-cec-environmental-health-summer-youth-academy). The deadline to apply for this free summer series in June 16th and it is open to all high school sophomores, juniors, and seniors. CIEHS will host a two-week Youth Academy focused on environmental health in Louisville, July 14-24! At the end of the academy, participants will receive a certificate and a letter of completion (plus some free sustainable swag), making this a valuable addition to college or job applications. We have limited spots available—only 20 students will be accepted for this exclusive summer program, where you will learn directly from environmental health experts. Applications must be submitted by June 16th! Learn more and apply at https://louisville.edu/ciehs. The schedule for the Youth Academy is as follows: July 14 (In Person with lunch): Introduction to Environmental Health Banrida Wahlang, PhD, UofL Gastroenterology, Hepatology and Nutrition Lu Cai, MD, PhD, UofL Pediatrics, Radiation Oncology, and Pharmacology & Toxicology July 15 (Virtual): Air Quality and Health Petra Haberzettl, PhD, UofL Medicine, Diabetes & Obesity Center July 16 (Virtual): Water & Health Mayukh Banerjee, PhD, UofL Pharmacology & Toxicology July 17 (In Person with lunch): Community-Led Science Ted Smith, PhD, UofL Medicine and Pharmacology/Toxicology Rachel Neal, PhD, UofL Biology Luz Huntington-Moskos, PhD, RN, CPN, FAAN, UofL School of Nursing July 21 (Virtual): Energy & Health Sumedha Rao, Mayor's Office of Sustainability July 22 (Virtual): Mapping the Issues Charlie Zhang, PhD, UofL Geographic & Environmental Sciences, DJ Biddle, Director and Senior Lecturer, UofL Center for Geographic Information System Laura Krauser, UofL's Geographic Information Sciences Research Coordinator July 23 (Virtual): Communicating Sustainability Brent Fryrear, UofL Sustainability Council July 24 (In Person with lunch): Policy Advocacy and Storytelling Dr. Tony Arnold, UofL Law, Urban and Public Affairs, Resilience Justice Project Angela Story, PhD, UofL Anthropology and Director of Anne Braden Institute As always, our feature is followed by your community action calendar for the week, so get your calendars out and get ready to take action for sustainability NOW! Sustainability Now! is hosted by Dr. Justin Mog and airs on Forward Radio, 106.5fm, WFMP-LP Louisville, every Monday at 6pm and repeats Tuesdays at 12am and 10am. Find us at http://forwardradio.org The music in this podcast is courtesy of the local band Appalatin and is used by permission. Explore their delightful music at http://appalatin.com

Die uitvoerende hoof van WeBuyCars, Faan van der Walt, gesels oor die groep se finansiële resultate en die invloed van Chinese motors op die plaaslike mark. Volg RSG Geldsake op Twitter

In this episode, editor-in-chief Joseph E. Safdieh, MD, FAAN, highlights articles about early studies finding dopamine cellular therapies were safe and tolerable for patients with Parkinson's, use of GLP-1 agonists were associated with reduced dementia risks, and the FDA use of accelerated approvals for several neurology drugs are under scrutiny. 

Dysfunction of the supranuclear ocular motor pathways typically causes highly localizable deficits. With sophisticated neuroimaging, it is critical to better understand structure-function relationships and precisely localize pathology within the brain. In this episode, Lyell K. Jones Jr, MD, FAAN, speaks with Gregory P. Van Stavern, MD, author of the article “Supranuclear Disorders of Eye Movements” in the Continuum® April 2025 Neuro-ophthalmology issue. 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. Van Stavern is the Robert C. Drews professor of ophthalmology and visual sciences at Washington University in St Louis, Missouri. Additional Resources Read the article: Internuclear and Supranuclear Disorders of Eye Movements 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: @LyellJ 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 earning CME, subscribing to the journal, and exclusive access to interviews not featured on the podcast. Dr Jones: This is Dr Lyell Jones, Editor-in-Chief of Continuum: Lifelong Learning in Neurology. Today I'm interviewing Dr Gregory Van Stavern, who recently authored an article on intranuclear and supranuclear disorders of eye movements for our latest Continuum issue on neuro-ophthalmology. Dr Van Stavern is the Robert C Drews professor of ophthalmology and visual sciences at Washington University in Saint Louis. Dr Van Stavern, welcome, and thank you for joining us today. Why don't you introduce yourself to our audience? Dr Van Stavern: Hi, my name is Gregory Van Stavern. I'm a neuro-ophthalmologist located in Saint Louis, and I'm pleased to be on this show today. Dr Jones: We appreciate you being here, and obviously, any discussion of the visual system is worthwhile. The visual system is important. It's how most of us and most of our patients navigate the world. Roughly 40% of the brain---you can correct me if I'm wrong---is in some way assigned to our visual system. But it's not just about the sensory experience, right? The afferent visual processing. We also have motor systems of control that align our vision and allow us to accurately direct our vision to visual targets of interest. The circuitry is complex, which I think is intimidating to many of us. It's much easier to see a diagram of that than to describe it on a podcast. But I think this is a good opportunity for us to talk about the ocular motor exam and how it helps us localize lesions and, and better understand diagnoses for certain disorders. So, let's get right to it, Dr Van Stavern. If you had from your article, which is outstanding, a single most important message for our listeners about recognizing or treating patients with ocular motor disorders, what would that message be? Dr Van Stavern: Well, I think if we can basically zoom out a little to the big picture, I think it really emphasizes the continuing importance of the examination. History as well, but the examination. I was reading an article the other day that was essentially downplaying the importance of the physical examination in the modern era with modern imaging techniques and technology. But for neurology, and especially neuro-ophthalmology, the history and the examination should still drive clinical decision-making. And doing a careful assessment of the ocular motor system should be able to tell you exactly where the lesion is located, because it's very easy to order a brain MRI, but the MRI is, like Forrest Gump might say, it's like a box of chocolates. You never know what you're going to find. You may find a lot of things, but because you've done the history and the examination, you can see if whatever lesion is uncovered by the MRI is the lesion that explains what's going on with the patient. So even today, even with the most modern imaging techniques we have, it is still really important to know what you're looking for. And that's where the oculomotor examination can be very helpful. Dr Jones: I did not have Forrest Gump on my bingo card today, Dr Van Stavern, but that's a really good analogy, right? If you order the MRI, you don't know what you're going to get. And then- and if you don't have a really well-formed question, then sometimes you get misleading information, right?  Dr Van Stavern: Exactly. Dr Jones: We'll get into some technology here in a minute, because I think that's relevant for this discussion. I think most of our listeners are going to agree with us that the exam is important in neuro-ophthalmology, and neurology broadly. So, I think you have some sympathetic listeners there. Again, the point of the exam is to localize and then lead to a diagnosis that we can help patients with. When you think about neurologic disorders where the ocular motor exam helps you get to the right diagnosis, obviously disorders of eye movements, but sometimes it's a clue to a broader neurologic syndrome. And you have some nice discussions in your article about the ocular motor clues to Parkinson disease or to progressive supranuclear palsy. Tell us a little more about that. In your practice, which neurologic disorders do you find the ocular motor exam being most helpful? Dr Van Stavern: Well, just a very brief digression. So, I started off being an ophthalmology resident, and I do two years of ophthalmology and then switch to neurology. And during neurology residency, I was debating which subspecialty to go into, and I realized that neuro-ophthalmology touches every other subspecialty in neurology. And it goes back to the fact that the visual system is so pervasive and widely distributed throughout the brain. So, if you have a neurologic disease, there is a very good chance it is going to affect vision, maybe in a minor way or a major way. That's why careful assessment of the visual system, and particularly the oculomotor system, is really helpful for many neurologic diseases. Neuromuscular disease, obviously, myasthenia gravis and certain myopathies affect the eye movements. Neurodegenerative diseases, in particular Parkinson's disease and parkinsonian conditions, often affect the eye movements. And in particular, when you're trying to differentiate, is this classic Parkinson's disease? Or is this progressive supranuclear palsy? Is it some broad spectrum multisystem atrophy? The differences between the eye movement disorders, even allowing for the fact that there's overlap, can really help point in one direction to the other, and again, prevent unnecessary testing, unnecessary treatment, and so on. Dr Jones: Very good. And I think, to follow on a thread from that concept with patients who have movement disorders, in my practice, seeing older patients who have a little bit of restriction of vertical gaze is not that uncommon. And it's more common in patients who have idiopathic Parkinson disease. And then we use that part of the exam to help us screen patients for other neurodegenerative syndromes like progressive nuclear- supranuclear palsy. So, do you have any tips for our listeners to- how to look at, maybe, vertical gaze and say, this is maybe a normal age-related degree of change. This is something that might suggest idiopathic Parkinson disease. Or maybe something a little more progressive and sinister like progressive super nuclear palsy? Dr Van Stavern: Well, I think part of the issue- and it's harder to do this without the visual aspect. One of my colleagues always likes to say for a neurologist, the eye movement exam begins and ends with the neurology benediction, just doing the sign of the cross and checking the eye movements. And that's a good place to start. But I think it's important to remember that all you're looking at is smooth pursuit and range of eye movements, and there's much more to the oculomotor examination than that. There's other aspects of eye movement. Looking at saccades can be really helpful; in particular, classically, saccadic movements are selectively abnormal in PSP versus Parkinson's with progressive supranuclear palsy. Saccades, which are essentially rapid movements of the eyes---up and down, in this case---are going to be affected in downward gaze. So, the patient is going to have more difficulty initiating downward saccades, slower saccades, and less range of movement of saccades in downgaze. Whereas in Parkinson's, it's classically upward eye movements and upgaze. So, I think that's something you won't be able to see if you're just doing, looking at, you know, your classic, look at your eye movements, which are just assessing, smooth pursuit. Looking carefully at the eye movements during fixation can be helpful. Another aspect of many parkinsonian conditions is saccadic intrusions, where there's quick movements or saccades of the eye that are interrupting fixation. Much, much more common in PSP than in Parkinson's disease. The saccadic intrusions are what we call square-wave jerks because of what they look like. Eye movement recordings are much larger amplitude in PSP and other multisystem atrophy diseases than with Parkinson's. And none of these are perfect differentiators, but the constellation of those findings, a patient with slow downwards saccades, very large amplitude, and frequent saccadic intrusions might point you more towards this being PSP rather than Parkinson's. Dr Jones: That's a great pearl, thinking about the saccades in addition to the smooth pursuit. So, thank you for that. And you mentioned eye movement measurements. I think it's simultaneously impressive and a little scary that my phone can tell when I'm looking at it within a few degrees of visual attention. So, I imagine there are automated tools to analyze eye movement. Tell us, what's the state of the art there, and what should our listeners be aware of in terms of tools that are available and what they can and can't do? Dr Van Stavern: Well, I could tell you, I mean, I see neuro-ophthalmic patients with eye movement disorders every day and we do not have any automated tools for eye movement. We have a ton of imaging techniques for imaging the optic nerve and the retina in different ways, but we don't routinely employ eye movement recording devices. The only time we usually do that is in somebody where we suspect they have a central or peripheral vestibular disease and we send them for vestibular testing, for eye movement recordings. There is interest in using- I know, again, sort of another digression, but if you're looking at the HINTS technique, which is described in the chapter to differentiate central from peripheral disease, which is a very easy, useful way to differentiate central from peripheral or peripheral vestibular disease. And again, in the acute setting, is this a stroke or not a stroke? Is it the brain or is it the inner ear? Part of the problem is that if you're deploying this widespread, the people who are doing it may not be sufficiently good enough at doing the test to differentiate, is a positive or negative test? And that's where some people have started introducing this into the emergency room, these eye movement recording devices, to give the- using, potentially, AI and algorithms to help the emergency room physicians say, all right, this looks like a stroke, we need to admit the patient, get an MRI and so on, versus, this is vestibular neuritis or an inner ear problem, treat them symptomatically, follow up as an outpatient. That has not yet been widely employed. It's a similar way that a lot of institutions are having fundus photography and OCT devices placed in the emergency room to aid the emergency room physician for patients who present with acute vision issues. So, I think that could be the future. It probably would be something that would be AI-assisted or AI-driven. But I can tell you at least at our institution and most of the ones I know of, it is not routinely employed yet. Dr Jones: So maybe on the horizon, AI kind of facilitated tools for eye movement disorder interpretation, but it's not ready for prime time yet. Is that a fair summary? Dr Van Stavern: In my opinion, yes. Dr Jones: Good to know. This has struck me every time I've read about ocular motor anatomy and ocular motor disorders, whether they're supranuclear or intranuclear disorders. The anatomy is complex, the circuitry is very complicated. Which means I learn it and then I forget it and then I relearn it. But some of the anatomy isn't even fully understood yet. This is a very complex real estate in the brainstem. Why do you think the neurophysiology and neuroanatomy is not fully clarified yet? And is there anything on the horizon that might clarify some of this anatomy? Dr Van Stavern: The very first time I encountered this topic as an ophthalmology resident and later as a neurology resident, I just couldn't understand how anyone could really understand all of the circuitry involved. And there is a lot of circuitry that is involved in us simply having clear, single binocular vision with the afferent and efferent system working in concert. Even in arch. In my chapter, when you look at the anatomy and physiology of the smooth pursuit system or the vertical gaze pathways, there's a lot of, I'll admit it, there's a lot of hand waving and we don't completely understand it. I think a lot of it has to do with, in the old days, a lot of the anatomy was based on lesions, you know, lesion this area either experimentally or clinically. And that's how you would determine, this is what this region of the brain is responsible for. Although we've gotten more sophisticated with better imaging, with functional connectivity MRI and so on, all of those have limitations. And that's why I still don't think we completely understand all the way this information is integrated and synthesized, and, to get even more big level and esoteric, how this makes its way into our conscious mind. And that has to do with self-awareness and consciousness, which is a whole other kettle of fish. It's just really complicated. I think when I'm at least talking to other neurologists and residents, I try to keep it as simple as possible from a clinical standpoint. If you see someone with an eye movement problem, try to see if you can localize it to which level you're dealing with. Is it a muscle problem? Is it neuromuscular junction? Is it nerve? Is it nucleus? Is it supranuclear? If you can put it at even one of those two levels, you have eliminated huge territories of neurologic real estate, and that will definitely help you target and tailor your workup. So, again, you're not costing the patient in the healthcare system hundreds of thousands of dollars. Dr Jones: Great points in there. And I think, you know, if we can't get it down to the rostral interstitial nucleus of the medial longitudinal fasciculus, if we can get it to the brainstem, I think that's obviously- that's helpful in its own right. And I imagine, Dr Van Stavern, managing patients with persistent ocular motor disorders is a challenge. We take foveation for granted, right, when we can create these single cortical images. And I imagine it's important for daily function and difficult for patients who lose that ability to maintain their ocular alignment. What are some of the clinical tools that you use in your practice that our listeners should be aware of to help patients that have a persistent supranuclear disorder of ocular movement? Dr Van Stavern: Well, I think you tailor your treatment to the symptoms, and if it's directly due to underlying condition, obviously you treat the underlying condition. If they have sixth nerve palsy because of a skull base tumor, obviously you treat the skull base tumor. But from a practical standpoint, I think it depends on what the symptom is, what's causing it, and how much it's affecting their quality of life. And everyone is really different. Some patients have higher levels of tolerance for blurred vision and double vision. For things- for patients who have double vision, depending upon the underlying cause we can sometimes use prisms and glasses. Prisms are simply- a lot of people just think prism is this, like, mystical word that means a lot. It's simply just an optical device that bends light. So, it essentially bends light to allow the eyes- basically, the image to fall on the fovea in both eyes. And whether the prisms help or not is partly dependent upon how large the misalignment is. If somebody has a large degree of misalignment, you're not going to fix that with prism. The amount of prism you'd need to bend the light enough to land on the fovea in both eyes would cause so much blur and distortion that it would essentially be a glorified patch. So, for small ranges of misalignment, prisms are often very helpful, that we can paste over glasses or grind into glasses. For larger degrees of misalignment that- let's say it is due to some skull base tumor or brain stem lesion that is not going to get better, then eye muscle surgery is a very effective option. We usually like to give people a long enough period of time to make sure there's no change before proceeding with eye muscle surgery. Dr Jones: Very helpful. So, prisms will help to a limited extent with misalignment, and then surgery is always an option if it's persistent. That's a good pearl for, I think, our listeners to take away. Dr Van Stavern: And even in those circumstances, even prisms and eye muscle surgery, the goal is primarily to cause single binocular vision and primary gaze at near. Even in those cases, even with the best results, patients are still going to have double vision, eccentric gaze. For most people, that's not a big issue, but we have had a few patients… I had a couple of patients who were truck drivers who were really bothered by the fact that when they look to the left, let's say because it's a 4th nerve palsy on the right, they have double vision. I had a patient who was a golfer who was really, really unhappy with that. Most people are okay with that, but it all depends upon the individual patient and what they use their vision for. Dr Jones: That's a great point. There's not enough neurologists in the world. I know for a fact there are not enough neuro-ophthalmologists in the world, right? There's just not many people that have that dual expertise. You mentioned that you started with ophthalmology and then did neurology training. What do you think the pipeline looks like for neuro-ophthalmology? Do you see growing interest in this among trainees, or unchanged? What are your thoughts about that? Dr Van Stavern: No, that's a continuing discussion we're having within our own field about how to attract more residents into neuro-ophthalmology. And there's been a huge shift. In the past, this was primarily ophthalmology-driven. Most neuro-ophthalmologists were trained in ophthalmology initially before doing a fellowship. The last twenty years, it switched. Now there's an almost 50/50 division between neurologists and ophthalmologists, as more neurologists have become more interested. This is probably a topic more for the ophthalmology equivalent of Continuum. One of the perceptions is this is not a surgical subspecialty, so a lot of ophthalmology residents are disincentivized to pursue it. So, we have tried to change that. You can do neuro-ophthalmology and do eye muscle surgery or general ophthalmology. I think it really depends upon whether you have exposure to a neuro-ophthalmologist during your neurology residency. If you do not have any exposure to neuro-ophthalmology, this field will always seem mysterious, a huge black box, something intimidating, and something that is not appealing to a neurologist. I and most of my colleagues make sure to include neurology residents in our clinic so they at least have exposure to it. Dr Jones: That's a great point. If you never see it, it's hard to envision yourself in that practice. So, a little bit of a self-fulfilling prophecy. If you don't have neuro-ophthalmologists, it's hard to expose that practice to trainees. Dr Van Stavern: And we're also trying; I mean, we make sure to include medical students, bring them to our meetings, present research to try to get them interested in this field at a very early stage. Dr Jones: Dr Van Stavern, great discussion, very helpful. I want to thank you for joining us today. I want to thank you for not just a great podcast, but also just a wonderful article on ocular motor disorders, supranuclear and intranuclear. I learned a lot, and hopefully our listeners did too. Dr Van Stavern: Well, thanks. I really appreciate doing this. And I love Continuum. I learn something new every time I get another issue. Dr Jones: Well, thanks for reading it. And I'll tell you as the editor of Continuum, I learn a lot reading these articles. So, it's really a joy to get to read, up to the minute, cutting-edge clinical content for neurology. Again, we've been speaking with Dr Gregory Van Stavern, author of a fantastic article on intranuclear and supranuclear disorders of eye movements in Continuum's most recent issue on neuro-ophthalmology. Please check it out, 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.

“The signaling and that binding of the MET and the HGF help, in a downstream way, lead to cell proliferation, cell motility, survival, angiogenesis, and also invasion—so all of those key cancer hallmarks. And because of it being on an epithelial cell, it's a really good marker because it's found in many, many different types of cancers, so it makes it what we call kind of a nice actionable mutation,” ONS member Marianne Davies, DNP, ACNP, AOCNP®, FAAN, senior oncology nurse practitioner at Yale Comprehensive Cancer Center in New Haven, CT, told Jaime Weimer, MSN, RN, AGCNS-BS, AOCNS®, manager of oncology nursing practice at ONS, during a conversation about the MET inhibitor drug class. Music Credit: “Fireflies and Stardust” by Kevin MacLeod Licensed under Creative Commons by Attribution 3.0  Earn 0.5 contact hours of nursing continuing professional development (NCPD) by listening to the full recording and completing an evaluation at courses.ons.org by May 9, 2026. The planners and faculty for this episode have no relevant financial relationships with ineligible companies to disclose. ONS is accredited as a provider of nursing continuing professional development by the American Nurses Credentialing Center's Commission on Accreditation. Learning outcome: Learners will report an increase in knowledge related to MET inhibitors. Episode Notes  Complete this evaluation for free NCPD.  ONS Podcast™ episodes: Pharmacology 101 series Episode 330: Stay Up to Date on Safe Handling of Hazardous Drugs ONS Voice articles: Oncology Drug Reference Sheet: Amivantamab-Vmjw Oncology Drug Reference Sheet: Cabozantinib Oncology Drug Reference Sheet: Capmatinib Oncology Drug Reference Sheet: Tepotinib Predictive and Diagnostic Biomarkers: Identifying Variants Helps Providers Tailor Cancer Surveillance Plans and Treatment Selection ONS books: Chemotherapy and Immunotherapy Guidelines and Recommendations for Practice (second edition) Clinical Guide to Antineoplastic Therapy: A Chemotherapy Handbook (fourth edition) Safe Handling of Hazardous Drugs (fourth edition) Telephone Triage for Oncology Nurses (third edition) ONS courses: Safe Handling Basics ONS Biomarker Database ONS Huddle Cards: Monoclonal Antibodies Targeted Therapy ONS Oral Anticancer Medication Learning Library ONS Oral Anticancer Medication Toolkit ONS and NCODA Oral Anticancer Medication Compass Oral Chemotherapy Education Sheets IV Chemotherapy Education Sheets Drugs@FDA To discuss the information in this episode with other oncology nurses, visit the ONS Communities. To find resources for creating an ONS Podcast Club in your chapter or nursing community, visit the ONS Podcast Library. To provide feedback or otherwise reach ONS about the podcast, email pubONSVoice@ons.org. Highlights From This Episode “The MET receptor was actually identified back in 1984. And it was actually identified as an oncogene in osteosarcoma. And so basically what that MET receptor does—it's a tyrosine kinase pathway, and the ligand that it attaches to is something called HGF/SF. That's hepatocyte growth factor/scatter factor. And so this MET pathway tyrosine kinase pathway is really important in tumor cell growth and migration. And it's expressed specifically on epithelial cells, so that's going to really help us in identifying how it can be a pathway for cancer treatments.” TS 1:35 “But in the particular classes, there kind of are some unique things that are with these MET inhibitors. For example, crizotinib, we found early on, causes some vision changes. Patients would report things like floaters or a little bit of blurry vision. For the capmatinib, things like elevation of amylase and lipase, fluid retention and bloating, and hypersensitivity reactions and photosensitivity.” TS 7:36 “Other things to teach for the TKI is the self-management strategies in terms of nausea management and dietary changes for the risk of peripheral edema. Having them do things like maybe doing daily weights, or at least weights every other day, and sometimes doing limb measurements so it can help us really quantify the amount of fluid retention they have. And then from a nursing perspective, meeting with these patients, is to do really good skin inspection. When people have peripheral edema, they're at risk for skin breakdown, and that can lead obviously to infection.” TS 16:06 “The biggest [misconception] is that people assume that all MET mutations are going to be equally responsive to the same targeted therapies, that all of the abnormalities are the same and react the same, and they really don't. We're really diving down and carving that pie thinner and thinner in terms of each individual MET abnormality, in terms of what drugs responds it to and what that means for patient outcomes and prognosis.” TS 25:21

On this compelling episode of NP Pulse: The Voice of the Nurse Practitioner®, Dr. Jessica Peck, DNP, APRN, CPNP-PC, CNE, CNL, FAANP, FAAN, and guest Dr. Ashley Hodges, PhD, CRNP, WHNP-BC, PMHNP-BC, FAANP, FAAN, dive deep into the adolescent mental health crisis, shedding light on the alarming trends affecting today's youth. From the long-term impacts of the COVID-19 pandemic to the pressure of growing up in a hyper-connected digital world, this discussion explores critical risk factors, early warning signs and practical strategies for nurse practitioners (NPs) and families alike. This episode also emphasizes the importance of upstream prevention, holistic care, reducing stigma and integrating mental health support into primary care. Drawing from decades of clinical experience, Jessica and Ashley offer compassionate, expert insight on how to recognize and respond to adolescent mental health challenges, while highlighting resources, screenings and training opportunities for NPs committed to making a difference.

Double vision is a symptom often experienced by patients with neurologic disease. An organized systematic approach to evaluating patients with diplopia needs a foundational understanding of the neuroanatomy and examination of eye movements and ocular alignment. In this episode, Teshamae Monteith, MD, FAAN, speaks with Devin Mackay, MD, FAAN, author of the article “Approach to Diplopia” in the Continuum® April 2025 Neuro-ophthalmology 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. Mackay is an associate professor of neurology, ophthalmology, and clinical neurosurgery at Indiana University School of Medicine in Indianapolis, Indiana. Additional Resources Read the article: Approach to Diplopia Subscribe to Continuum®: shop.lww.com/Continuum Earn CME (available only to AAN members): continpub.com/AudioCME Continuum® Aloud (verbatim audio-book style recordings of articles available only to Continuum® subscribers): continpub.com/Aloud More about the American Academy of Neurology: aan.com Social Media facebook.com/continuumcme @ContinuumAAN Host: @headacheMD Full episode transcript available here Dr 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 Devin Mackay about his article on approach to diplopia, which appears in the April 2025 Continuum issue on neuro-ophthalmology. Welcome to the podcast. How are you? Dr Mackay: Thank you. It's great to be here. Dr Monteith: Congratulations on your article. Dr Mackay: Thank you. I appreciate that. Dr Monteith: Why don't you start off with introducing yourself to our audience? Dr Mackay: So, yeah, my name is Devin Mackay. I'm a neuro-ophthalmologist at Indiana University. I did my residency at what was used to be known as the Partners Healthcare Program in Boston, and I did a fellowship in neuro-ophthalmology in Atlanta. And I've been in practice now for about ten years. Dr Monteith: Oh, wow. Okay. Tell us a little bit about your goals when you were writing the chapter. Dr Mackay: So, my goal with the approach to double vision was really to demystify double vision. I think double vision is something that as trainees, and even as faculty members and practicing neurologists, we really get intimidated by, I think. And it really helps to have a way to approach it that demystifies it and allows us to localize, just like we do with so many other problems in neurology. Dr Monteith: I love that, demystification. So why don't you tell us what got you interested in neuro-ophthalmology? Dr Mackay: Yeah, so neuro-ophthalmology I stumbled on during a rotation during residency. We rotated in different subspecialties of neurology and I did neuro-ophthalmology, and I was just amazed by the exam and how intricate it was, the value of neuroanatomy and localization, the ability to take a complicated problem and kind of approach it as a diagnostic specialist and really unravel the layers of it to make it better. To, you know, figure out what the problem is and make it better. Dr Monteith: Okay, so you had a calling, clearly. Dr Mackay: I sure did. Dr Monteith: You talked about latest developments in neuro-ophthalmology as it relates to diplopia. Why don't you share that with our listeners? Dr Mackay: Yeah. So, you know, double vision is something that's really been around since the beginning of time, essentially. So that part hasn't really changed a lot, but there are some changes that have happened in how we approach double vision. Probably one of the bigger ones has been, we used to teach that with a, you know, patient over the age of fifty with vascular risk factors who had a cranial nerve palsy of cranial nerves 3, 4, or 6, we used to automatically assume that was a microvascular palsy and we just wouldn't do any more testing and we'd just, you know, wait to see how they did. And it turns out we're missing some patients who have significant pathologies, sometimes, with that approach. And so, we've really shifted our teaching with that to emphasize that it's a lot easier to get an MRI, for example, than it ever has been. And it can be important to make sure we're not missing important pathology in patients, even if they have vascular risk factors over the age of fifty and they just have a cranial nerve 3, 4, or 6 palsy. So that's been one change. Dr Monteith: Interesting. And why don't you tell us a little bit about the essential points that you want to get across in the article? Dr Mackay: Yeah. So, I think one is to have a systematic approach to double vision. And a lot of that really revolves around localization. And it even begins with the history that we take from the patients. There's lots of interesting things we can ask about double vision from the patient. For example, the most important thing you can ever ask someone with double vision is, does it go away when you cover either eye? And that really helps us figure out the first question for us as neurologists, which is, is it neurologic or non-neurologic? If it's still there when covering one eye, then it is not neurologic and that's usually a problem for an ophthalmologist to sort out. So that's really number one. And then if it is binocular double vision, then we get into details about, is it horizontal or vertical misalignment? Is it- what makes it better and worse? Is there an associated ptosis or other symptoms? And based on all of that, we can really localize the abnormality with the double vision and get into details about further testing if needed, and so forth. I also love that that approach really reduces our need to rely on things like neuroimaging sometimes when we may not need it, or on other tests. So, I think it really helps us be more efficient and really take better care of patients. Dr Monteith: So definitely that cover/uncover test, top thing there. Your approach- and you mentioned, are you really getting that history, and are there any other kind of key factors when you're approaching diplopia before getting into some of the details? Dr Mackay: Yeah, that's a good question. I think also having some basics of how to examine the patient, because double vision is such a challenging thing. A lot of us aren't as familiar with the exam toolkit, so to speak, of what you would do with a patient with double vision. And so, I go over in the article a bit about a Maddox rod, which is a handy little tool that I always keep in my pocket of my lab coat. It allows you to assign a red line to one eye and a light to the other eye, and you can see if the eyes line up or not. And you don't need any other special equipment, you just need the light in that Maddox rod. That really helps us understand a lot about the pattern of misalignment, which is really important for evaluating double vision. So, for example, if someone has a right 6th nerve palsy, I'll expect a horizontal misalignment of the eyes that worsens when the patient looks to the right and improves when they look to the left. And especially if it's a partial palsy, it's not always easy to see that just by looking at their eye movements. And having a way to really measure the eye alignment and figure out, is it worse or better in certain directions, is really essential to localization, I think, in a lot of cases. Dr Monteith: You caught me. I skipped over that Maddox rod part, even though you spent a lot of time talking about Maddox rods. Kind of skipped over it. So, you're saying that I need one. Dr Mackay: Everyone needs one. I've converted some of our residents here to carry one with them. And yeah, I realize it's a daunting tool at first, but when you have a patient with double vision and their eye movements look normal, I feel like a lot of neurologists are- kind of, their hands seem like they're tied and they're like, oh, I don't know, I don't know what to do at this point. And if you can get some more details with a simple object like that, it can really change things. Dr Monteith: So, we've got to talk to the AAN store and make sure that they have enough of these, because now there's going to be lots of… Dr Mackay: We're going to sell out on Amazon today now because of this podcast. Dr Monteith: Cyber Monday. So, let's talk about the H pattern. And I didn't know it had the- well, yeah, I guess the official name is “H pattern.” In medical school, I mean, that's what I learned. But as a resident and, you know, certainly as an attendee, I see people doing all sorts of things. You're pro-H pattern, but are there other patterns that you also respect? Dr Mackay: It depends on what you're looking for, I think. The reason I like the H pattern is because you get to look at upgaze and downgaze in two different directions. So, you get to look at upgaze and downgaze when looking to the left, and up- and downgaze when looking to the right. And the reason that matters is because vertical movements of the eyes are actually controlled by different eye muscles depending on whether the eye is adducted toward the nose or abducted away from the nose. And so that's why I love the H pattern, is because it allows you to see that. If you just have them look up and down with just a cross pattern, for example, then you really lose that specificity of looking at both the adduction and abduction aspects. So, it's not wrong to do it another way with, like, the cross, for example, but I just think there are some cases where we'll be missing some information, and sometimes that can actually make a difference. Dr Monteith: Well, there you have it. Let's talk a little bit about eliciting diplopia during the neurologic exam. What other things should we be looking out for? Dr Mackay: So, in terms of eliciting diplopia, it really starts with the exam and again, figuring out, are we covering one eye? And figuring out, is this patient still having double vision? It's tricky because sometimes the patients won't even know the answer to that question or they've never done it, they've never covered one eye. And so, if that's the case, I really make them do it in the office with me and it's like, okay, well, are we having double vision right now? Well, great, okay, we are, then we're going to figure this out right now. And we cover one eye and say, is it still double? And that way we can really figure out, are we monocular or binocular? That's always step one. And then if we've established that it's binocular diplopia, then that's when we get into the other details that I mentioned before. And then as far as other things to look for, we're always in tune to other things that are going on in terms of symptoms, like ptosis, or if there's bulbar weakness, or some sensory change or motor problem that seems to be associated with it. Obviously, those will give us clues in the localization as well. Dr Monteith: And what about ocular malalignment? Dr Mackay: Yeah. So ocular malalignment, really, the cardinal symptom of that is going to be double vision. And so, if a patient has a misalignment of the eyes and they don't have double vision, then usually that means either we're wrong and they don't have double vision, or they do have double vision and they, you know, haven't said it correctly. Or it could be that the vision is poor in one eye. Sometimes that can happen. Or, some patients were actually born with an eye misalignment and their brain has learned in a way to kind of tune out or not allow the proper development of vision in one eye. And so that's also known as amblyopia, also known as the lazy eye, some people call it. But that finding can also make someone not experience double vision. But otherwise, if someone's had normal vision kind of throughout their life, they'll usually be pretty aware of when they first notice double vision. It'll be an obvious event for them in in most cases. Dr Monteith: And then the Cogan lid twitch? Dr Mackay: Oh yes, the Cogan lid twitch. So, the Cogan lid twitch is a feature of myasthenia gravis. The way you elicit it is, you have the patient look down. I'm not sure there's a standardization for how long; you want to have it long enough that you're resting the levator muscle, which is the muscle that pulls the upper lid open. And so, you rest that by having them look down for… I usually do about ten or fifteen seconds. And then I have them look up to looking straight forward. And you want to pay careful attention to their lid position as their eye settles in that straight-forward position. What will happen with a Cogan's lid twitch is, the lid will overshoot, and then it'll come back down and settle into its, kind of, proper position. And what we think is happening there is, it's almost like a little mini “rest test” in a way, where you're resting that muscle just long enough to allow some of the neurotransmission to recover. You get a normal contraction of the muscle, but it fades very quickly and comes back down. And that's experienced as a twitch. Dr Monteith: So, the patient can feel it. And it's something you can see? Dr Mackay: Yeah, the patient may not feel it as much. It's usually it's going to be something that the clinician can see if they're looking for it. And I would say that's one of the physical exam findings that can be a hallmark of myasthenia gravis, but certainly not the only one. Some others that we often look for are fatigable ptosis with sustained upgaze. You have the patient look up for a prolonged time and you'll see the lid droop down. So that can be one. Ice pack test is very popular nowadays, and it has pretty good sensitivity and specificity for myasthenia. So, you keep an ice pack over the closed eyes for two minutes and you compare the lid position before and after the ice pack test. And in the vast majority of myasthenia patients, if they have ptosis, the ptosis will have resolved, or at least significantly improved, in those patients. And yet one more sign is, if you find the patient's eye with ptosis and you lift open the eye manually, you'll often see that the other eyelid and the other eye will lower down. So, I'm not sure there's a name for that, but that can be a helpful sign as well. Dr Monteith: Since you're going through some of these, kind of, key features of different neurologic disease, why don't you tell us about a few others? Dr Mackay: Yeah, so another I mentioned in the in the article is measurement of levator function, which is really a test of eyelid strength. And so, that can be helpful if we have- someone has ptosis, or we're not sure if they have ptosis and we're trying to evaluate that to see if it's linked to the double vision, because that really changes the differential if ptosis is part of the clinical situation. So, the way that's measured is you have a patient look down as far as they can. And you get out a little ruler---I usually use a millimeter ruler---and I set the zero of the ruler at the upper lid margin when they're looking down. So, I hold the ruler there, and then I ask the patient to look up as far as they can without moving their head. Where the lid position stops of the upper lid is the new point on the ruler. And so, you measure that and see how much that is. And so, a normal patient may have a value somewhere between, I don't know, twelve or thirteen millimeters up to seventeen or eighteen millimeters, probably, in most cases. Especially if there is an asymmetric lid position, if you find that the levator function is symmetric, then it tells you that the muscle is working fine and that the ptosis is not from the muscle. So then the ptosis may be from dehiscence of the lid margin from the muscle. And so, that's a really common cause of ptosis, and that's often age-related or trauma-related. And we can dismiss that as being part of the symptom constellation of double vision. So, it can be really helpful to clarify, is this a muscle problem, which you'd expect with myasthenia or a third nerve palsy, or is this a mechanical problem with the lid, which is non-neurologic and really should be dismissed? So that can be a really helpful exam tool. Dr Monteith: So, you're just now getting into a little localization. So why don't we kind of start from the most proximal pistol with localization. Give us a little bit of tips. I know they just got to read your article, but give us a few tips. Dr Mackay: So, in terms of most proximal causes, there are supranuclear causes of ocular misalignment. For example, a skew deviation would qualify as that. Anything that's happening from some deficient input before you get to the cranial nerve nuclei, that we would consider supranuclear. So, we also see that with things like progressive supranuclear policy and certain other conditions. And then there can be lesions of the cranial nerve nuclei themselves. So, cranial nerves 3, 4, and 6 all have nuclei, and if they're lesioned they will cause double vision in specific patterns. And then there's also another subgroup, which is known as intranuclear problems with eye alignment. And so, the most common of that is going to be intranuclear ophthalmoplegia. And so that's very common in patients with demyelinating disorders, or it can also happen with strokes and tumors and other causes. And then there's infranuclear problems, which are from the cranial nerve nuclei out, and so those would be the cranial nerves themselves. So that's where your microvascular palsies, any tumor pressing on the nerve in those locations can cause palsies like that, any inflammatory disorder along that course. Then as we get more distal, we get into the orbit, we have the neuromuscular junction---so, the connection between the nerve and the muscle. And of course, that's our myasthenia gravis. And there are rare causes, things like botulinum and tick borne illnesses and certain other things that are more rare. And then, of course, we get to the muscle itself, and there can be different muscular dystrophies, different things like myositis or inflammatory disorders of the orbit or even physical trauma. So, if a patient, you know, had a trauma in trapping an extraocular muscle, that can be a localization. So really, anywhere along that pathway you can have double vision. So, I love to approach it from that perspective to help narrow down the diagnostic possibilities. Dr Monteith: Okay, just like everything? Dr Mackay: Just like all of the rest of the neurology. See, it's not that scary. Dr Monteith: You know, and so, yeah. And then you do a lot more than, you know, a few cranial nerves, right? Dr Mackay: Right. That's right. There's a lot more to double vision than that. I think as neurologists, we get lost if it's not a cranial nerve palsy, we're like, oh, I don't know what this is. And if it's not myasthenia, not a cranial nerve palsy. But it's worth also considering that there are ophthalmologic causes of someone having double vision that we often don't consider. So maybe someone who was born with strabismus, or maybe they have a little bit of a tendency toward an eye misalignment that their brain compensates, for and then it decompensates someday and that now they have a little bit of double vision intermittently, so that those can be causes to consider as well. Dr Monteith: Yeah, well, we'll just have to, you know, request those records from forty years ago. No problem. Dr Mackay: That's right. Dr Monteith: Why don't you also give us a little bit of tip when we're on the wards and we want to teach either a medical student or a resident, or if it's a resident listening, may want to teach a junior resident and seem like a star when approaching a patient with diplopia. Give us some teaching pearls. Dr Mackay: Yeah. So, I would love people teaching more about this at the bedside. I'd say probably the first thing to do would be to equip yourself by recognizing what some of the pertinent questions are to ask someone with double vision. Those things would include, is the double vision worse when looking in a certain direction? Does the double vision go away or not when you cover one eye? What happens when you tilt your head one direction or the other? Is it intermittent or constant? What makes it better? What makes it worse? Those kinds of things can really help us narrow down the possibilities. And then the other thing would be to equip yourself with some tools for examining. And it doesn't have to be physical tools. These can actually be things like, you mentioned the cross-cover test or cover/uncover test. That's described in the article. And I think knowing how to do that properly, knowing how to examine the eye movements properly and how to check for subtle things like a subtle intranuclear ophthalmoplegia, which is also mentioned in the article, being familiar with those things can be a really useful exercise in allowing you to teach others later on. Dr Monteith: Cool. Why don't you tell us about some of the things you're most excited about in the field? Dr Mackay: One of the things about our subspecialty for so long is we really haven't had big data with, you know, big trials and all these things that all the stroke people have. And that's starting to change slowly. There's been, for example, the idiopathic intracranial hypertension treatment trial that was published back in, I think it was 2014. You know, of course we had the optic neuritis treatment trial, back a few decades ago now. Some of the exciting ones coming up, there's going to be a randomized controlled trial looking at different treatments for idiopathic intracranial hypertension that are surgically based. So, for example, comparing venous sinus stenting with optic nerve sheath fenestration. And so, figuring out, is there a best practice for surgical intervention for patients with IIH? So, we're starting to have more trials like that now than I think we've had in the past. And so, it's exciting to get to have an evidence base for some of the things that we recommend and do. Dr Monteith: And what about some of the treatment for diplopia? Like prisms, and where are we with some of that? Dr Mackay: Yeah, great. So, it's a pretty simple concept, but still kind of difficult in practice. I kind of say there are four different ways to treat double vision: you can ignore it, you can patch or cover one eye, you can treat with prisms, and you can treat with eye muscle surgery. And so, those are the main ways other than, of course, treating the underlying disorder if there's a disorder causing double vision. So those are the main ways to treat. In terms of knowing if someone's going to be a candidate for prism therapy, we also have to remember that prisms are really going to be most helpful for when someone's looking straight forward. So, we need to make sure that their double vision is happening when they look straight forward. So, for example, if they're only having double vision looking to the left or to the right, that patient may not benefit from prisms as much as someone who is having double vision when they look straight forward. So that's one thing I look for. And then strabismus surgery is something to be considered if someone is not tolerating prisms and they're not helping and their eye alignment is stable. So, if you think about it, if someone's eye alignment is changing a lot, you're probably not going to want to do surgery for that patient because it's going to keep changing after surgery. And so, if someone's eye alignment is stable for six months or more and they're not getting the benefit they'd like from prisms, then maybe referral to a strabismus surgeon might be something to consider. Dr Monteith: Great. And then, I guess another question is just popping up in my head selfishly. What are your thoughts about patients that get referrals for exercises? Say they have, like, a convergence efficiency or something causing diplopia, maybe after a concussion. Maybe there's not a lot of evidence, but what is your take on exercising? Dr Mackay: Yeah, excellent question. So, there actually is evidence for exercises for convergence insufficiency. So, we know that those do work. Now where exercises are probably not as helpful, or at least not- there isn't an evidence base for them, is really with just about every other kind of eye misalignment in adults. We hear a lot about eye movement therapies for concussion and barely any other acquired misalignment of the eyes as well. And really, the evidence really hasn't shown us that that's helpful; again, with the exception being convergence insufficiency. So, we know that an office-based vision therapy type program for convergence insufficiency does work, but of course it's kind of inconvenient. It can cost money that may or may not be covered by insurance. And so, there are difficulties even with doing that. And so, I often recommend that patients with convergence insufficiency at least try something called pencil push-ups, where they take a pencil at arm's length and they bring it in and exercise that convergence ability. You know, that's a cheap, easy way to try to treat that initially. So yeah, there can be some limited utility for eye muscle exercises in certain conditions. Dr Monteith: My one example. I was- it was fuzzy, but in a different way. So, what do you do for fun? I mean, it sounds like you like to see a lot of eyeballs? Dr Mackay: I do. I like to see a lot of eyeballs. Dr Monteith: When you're not doing these things, what do you do for fun? Dr Mackay: So, people ask me what my hobbies are, and I laugh because my hobby is actually raising children. Dr Monteith: Oh, okay! Dr Mackay: So, my wife and I have eight kids- Dr Monteith: Oh, wow! Dr Mackay: Ages three to thirteen. So, kind of doesn't allow me to have other things right now. I'm sure I'll have more hobbies later on, but no, I really love my kids. And I- they give me plenty to do. There's no shortage of- in fact, they were really, they were really excited about this podcast today. They're so excited that Dad gets to be on a podcast, and so I'm going to have to show this to them later. They're going to be thrilled about it. Dr Monteith: Excellent. Well, thank you so much for being on the podcast. Dr Mackay: Thank you. It's been my pleasure. Dr Monteith: Again, today I've been interviewing Dr Devin Mackay about his article on approach to diplopia, which appears in the most recent issue of Continuum on neuro-ophthalmology. 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.

In this episode of The Nurse Practitioner Podcast, Julia Rogers, DNP, APRN, CNS, FNP-BC, FAANP and Stephen Ferrara, DNP, FNP, FAANP, FAAN discuss AI and NP practice.

In celebration of Nurses Month, in this episode, recently retired Chief Nursing Officer AnnMarie Papa, DNP, RN, CEN, NE-BC, FAEN, FAAN discusses how nurse leaders can mitigate critical issues facing nurses today, such as burnout, staffing shortages, workplace violence, and a lack of meaningful support. Supporting nurses with compassion is essential to the future of the profession. Rather than placing the burden of resilience on nurses, she advocates for nurse leaders to be authentic, present, and empathetic, asking staff what they truly need. Strong leadership involves humility, mutual elevation between staff and leaders, and tailored approaches that consider generational differences in learning and work preferences. AnnMarie also notes the need for systemic changes including violence prevention through risk assessment and legislation, trauma-informed care, and improved incident reporting processes. She encourages nurses to get involved in policy advocacy and to use storytelling—drawing from their own impactful patient experiences—as a powerful tool to influence change and affirm their purpose. After listening, visit our topical collection on Nurse Wellness for the latest in research and thought leadership promoting self-care for nurses. Transcript

In this episode of Caring Greatly, Dr. Cipriano explains the 2025 International Nurses Day theme, “Our Nurses. Our Future. Caring for Nurses Strengthens Economies.” She describes ICN's call to value, protect and respect nurses as a foundational requirement for patient safety and outcomes, as well as a critical part of supporting the overall welfare of nurses and the organizations for which they work. Dr. Cipriano also outlines ICN's seven-part agenda for sustainable nursing workforce wellbeing and drills into how nursing and institutional leaders can identify opportunities in their scopes of ownership and influence to improve nurse safety and wellbeing.The views and opinions expressed in this podcast are those of the speakers and do not necessarily reflect the views or positions of Stryker.

“We spent time today discussing all the ways that owners can have a positive impact on career growth, whether you're a bedside nurse or just in teaching, research, hospital leadership. More than career growth, I see ONS as kind of a barrier to burnout and a catalyst for professional self-care. I think that no matter what aspect of oncology care you're involved in, it is a difficult and complex specialty. And I think with that can come a lot of challenges and tough days, and ONS brings a sense of community to that and, specifically, a community that is pushing cancer care forward,” ONS member Amy Kaiser, MSN, CPNP-PC, told Nick Escobedo, DNP, RN, OCN®, NE-BC, member of the ONS 50th anniversary committee, during a conversation about the benefits of ONS membership. Escobedo spoke with Kaiser, who joined ONS as a student, and Susan Groenwald, PhD, RN, ANEF, FAAN, a charter ONS member, about how ONS membership and resources have helped them grow in their careers. Music Credit: “Fireflies and Stardust” by Kevin MacLeod Licensed under Creative Commons by Attribution 3.0  Episode Notes  This episode is not eligible for NCPD.  ONS Podcast™ episodes: 50th anniversary series Episode 331: DNP and PhD Collaboration Strategies to Help Advance Oncology Care Episode 327: Journey of a Student Nurse: Choosing Oncology Nursing and the Value of a Professional Home Episode 160: Build Innovative Staff Education Tools and Resources ONS Voice articles: Your ONS Membership Offers You Benefits in Other Organizations, Too Co-Creation Modernizes ONS Chapters to Meet Member Needs ONS book: Cancer Basics (third edition) ONS course: ONS Cancer Basics™ Clinical Journal of Oncology Nursing article: Professional Organization Membership: The Benefits of Increasing Nursing Participation ONS membership ONS chapters ONS Communities Connie Henke Yarbro Oncology Nursing History Center To discuss the information in this episode with other oncology nurses, visit the ONS Communities. To find resources for creating an ONS Podcast Club in your chapter or nursing community, visit the ONS Podcast Library. To provide feedback or otherwise reach ONS about the podcast, email pubONSVoice@ons.org. Highlights From This Episode Groenwald: “ONS was groundbreaking in so many areas. The area that sticks out to me was, I was the board liaison to the standards committee. And so, the development of oncology nursing standards, it was a hallmark and critical to the field and to me and my practice, as well as education. It was very exciting time.” TS 4:18 Kaiser: “I think that my very first introduction to cancer care came from the Cancer Basics course. I think I feel fortunate that I probably was the recipient of a lot of the efforts of Susan, who has pioneered so many of these different oncology resources. I had the benefit of being at school during a time where there were a ton of resources available through ONS.” TS 5:38 Groenwald: “Having attended the meetings and getting involved in some of the committees is where I met people and worked with people. And that became, for me, very vital for doing a book, where it was a contributed book, an edited book [Cancer Nursing: Principles and Practice], so we had lots of different chapters and contributors, but I met them all through ONS. And how we communicated was via the old-fashioned mail and telephone. I didn't even have a computer. We typed the whole manuscript, thousands and thousands of pages, the first couple editions.” TS 12:25 Kaiser: “What's so wonderful about going to [Congress] is everybody there is looking to move oncology nursing forward and meet people and connect and network. And it's this, you know, magical space of people who are meeting and sharing shared experiences, and I got to feel all of that prior to even being an oncology nurse. And I went home from that first conference, immediately discussed with my manager that I wanted to move to the oncology floor, and I did. But it was meeting all of those people and hearing about those career paths that did that for me.” TS 16:42 Kaiser: “I think people who are involved with ONS, I found, are also very, very willing to mentor. I was very fortunate as I was speaking to these people, not even being an oncology nurse, that they were so welcoming and wanted to welcome me into the specialty and wanted to show me how to get involved. So I think it's just taking that very first step of talking to somebody or going to that local chapter meeting, and then the rest of it becomes a lot easier.” TS 19:29 Groenwald: “One thing Amy mentioned that I think is important is that new nurses have so many opportunities. I think it's scary to put forth an abstract to speak at the conference. It's scary, but it's such a great opportunity for anybody at any level in their career. If they have something of interest to share, it's such a great place. I feel like it launched my career in terms of being able to speak in front of people and think critically about things and put together some projects. This all came from my work with ONS.” TS 20:51

This week's episode of Brain & Life Podcast was recorded live at the American Academy of Neurology's annual meeting! Hosts Dr. Daniel Correa and Dr. Katy Peters were joined by Joel Salinas, MD, MBA, MSc, FAAN, Andrea Lendaris, MD, MS, Andrew M. Southerland, MD, FAAN, and Eric J. Seachrist, MD to share what it's like living and practicing neurology with their own neurological condition(s) and neurodiverse perspectives, and explore how their experiences serve as a window into the patient and community perspective.   Additional Resources Neurology®Podcast Switching Roles: A Neuro-oncologist Reflects on his Own Experience with a Brain Tumor   We want to hear from you! Have a question or want to hear a topic featured on the Brain & Life Podcast? ·       Record a voicemail at 612-928-6206 ·       Email us at BLpodcast@brainandlife.org   Social Media:   Hosts: Dr. Daniel Correa @neurodrcorrea; Dr. Katy Peters @KatyPetersMDPhD

In this episode, editor-in-chief Joseph E. Safdieh, MD, FAAN, highlights articles finding microplastics in the brain postmortem linked to dementia, the salary gap between men and women neurologies, and neurologists studying the impact of microgravity on the brain.

Nicholas J. Silvestri, MD, FAAN - From Established to Emerging Therapies: Expert Perspectives on the Latest Evidence Base on FcRn Inhibitors for gMG

Nicholas J. Silvestri, MD, FAAN - From Established to Emerging Therapies: Expert Perspectives on the Latest Evidence Base on FcRn Inhibitors for gMG

Nicholas J. Silvestri, MD, FAAN - From Established to Emerging Therapies: Expert Perspectives on the Latest Evidence Base on FcRn Inhibitors for gMG

Nicholas J. Silvestri, MD, FAAN - From Established to Emerging Therapies: Expert Perspectives on the Latest Evidence Base on FcRn Inhibitors for gMG

Nicholas J. Silvestri, MD, FAAN - From Established to Emerging Therapies: Expert Perspectives on the Latest Evidence Base on FcRn Inhibitors for gMG

Nicholas J. Silvestri, MD, FAAN - From Established to Emerging Therapies: Expert Perspectives on the Latest Evidence Base on FcRn Inhibitors for gMG

The inflammatory and infectious optic neuropathies are a broad, heterogeneous, and common group of diseases producing visual loss. Although many now-distinct syndromes have been previously combined as “typical or atypical optic neuritis,” recent developments highlight the importance of precision terminology as well as an individualized evaluation and treatment approach. In this episode, Gordon Smith, MD, FAAN speaks with Eric Eggenberger, DO, MS, FAAN, author of the article “Optic Neuritis” in the Continuum® April 2025 Neuro-ophthalmology 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. Eggenberger is a professor of ophthalmology, neurology, and neurosurgery at the Mayo Clinic in Jacksonville, Florida. Additional Resources Read the article: Optic Neuritis 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 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 someone who really needs no introduction, Dr Eric Eggenberger, about his article on optic neuritis, which appears in the April 2025 Continuum issue on neuro-ophthalmology. Eric, welcome to the podcast, and maybe you can introduce yourself to our audience. Dr Eggenberger: Thank you. Thanks for having me. So, my name is Eric Eggenberger. I work at Mayo Clinic Florida, and I am involved exclusively in neuro-ophthalmology. Dr Smith: I just had the pleasure, Eric, of talking yesterday with Lindsey De Lott about non-optic neuritis causes of optic neuropathy. And so, I'm going to kind of reference a little bit what I learned yesterday. She was great. I wonder if you might begin by talking a little bit about nomenclature. You talk about the need for use of precise terminology in your article. And yesterday she taught me a lot about the risk of misdiagnosis and other causes of optic neuropathy, and the two seem related. So, I wonder if you can maybe lay the foundation for our conversation by talking about terminology? Dr Eggenberger: I think that's a great point. So, we are in an era now where, instead of lumping all these different diagnoses together, we have learned to split apart some of these clinical entities. And so, I think it's really important that we focus on precise terminology and recognize that all optic neuritis is not the same. And we have very different, distinct clinical pathways for these imaging pathways, treatment pathways, for these different types of optic neuritis, whether that's MS related, whether it's MOG related or aquaporin-4 related. Dr Smith: So, I wonder maybe we can begin by just, you know, giving our listeners wisdom, pearls, and pitfalls about, how do you recognize when someone with a suspected optic neuropathy has optic neuritis versus a noninflammatory optic neuropathy? Dr Eggenberger: So, that's a really important issue because there's a lot of clinical overlap in terms of exam findings. So, for instance, in any optic neuropathy, let's say it's unilateral, you typically are going to see decreases in acuity and field and color, and you're going to see a relative afferent pupillary defect. And then it's really the context that that occurs in that helps us distinguish different disease entities. So, with optic neuritis, typically you're going to have pain. And that's oftentimes going to be in the younger populations compared to some of the other common optic neuropathies we see, like ischemic optic neuropathy, for instance. Dr Smith: Right. So maybe we can talk a little bit about, kind of, your overall diagnostic approach, right? A lot of this is, of course, based on age and context, but young people get ischemic lesions and older people can have inflammatory lesions. So, what's your overall approach to the patient you just described? Let's say it's a forty-eight-year-old woman who comes to the emergency department with subacute unilateral vision loss and there's dyschromatopsia, APD, reduced acuity. And, you know, let's just say a fairly, you know, benign-looking fundoscopic exam. What do you do to evaluate that patient? Dr Eggenberger: In that particular context, I think we're looking at other contextual clues. Is there other vascular risk factors or other things to point you in one direction or the other? One of the important parts you mentioned was the fundus exam. So, we know with ischemic optic neuropathy, 100% of the time with AIOM, you're going to see disc edema. And so, in the context of that story, we want to confirm on our exam an optic neuropathy, and then we can kind of focus on the retrobulbar courses or different types of optic neuropathies. From an exam perspective, in that particular patient we'd be looking to measure the acuity, quantify that. And in the ER, you're not going to be able to do a perfect field, but you'll get some sense of the field and how much field loss there is. And then as you mentioned, the afferent pupillary defect is critical. And we're going to get a little bit of the historical features in terms of pain. With typical retrobulbar optic neuritis, most of those patients are going to experience some pain, and usually it's pain on eye movements. And those would be the clinical things to focus on. Other exposures the patient may or may not have had, any other concomitant conditions, would all help point you in different directions, perhaps, and then we're probably on towards imaging. Dr Smith: Yeah, maybe you can talk a little bit about that? What's the appropriate use of imaging? I mean, presumably the patients, like the one I just threw out there, are pretty much all going to get neuroimaging. What's your approach to that? How do you protocol the study? What should we be looking for? Dr Eggenberger: In our clinic, we would typically be ordering an MRI orbit and brain, and each of those has a specific purpose. The orbit is going to show us the extent of the optic neuropathy. So, we're particularly looking for a longitudinally extensive optic nerve lesion or more than half of the optic nerve involved. And most patients acutely, if it isn't an “itis" situation, we'll see enhancement. And then the MR brain is going to be useful for looking for other evidence of demyelination within the central nervous system. We may at some point get down to doing an MR cord, but I think acutely it's going to be brain and orbit that most of our patients are getting. Dr Smith: Let's say that we did the scan and, sure enough, there's sort of a shorter segment, so less than half the length of the nerve region of enhancement. What's the rest of your diagnostic evaluation look like for that patient? Dr Eggenberger: So, in that particular case, we would look at the remainder of the brain. So, we're looking for other evidence of demyelination and any other contextual clues, systemically that would point you one direction or another. But with a shorter segment involved, one of the more common things we might encounter would be multiple sclerosis-related optic neuritis. Dr Smith: Would you look for aquaporin-4 and MOG in a patient with what appears to be an isolated, uncomplicated short segment optic neuritis? Dr Eggenberger: So, I think it really depends a bit on the context. I would never fault anybody for looking at MOG or an aquaporin-4 in that context because those are really treatment-altering diagnoses, but the yield in this particular case with a short segment involved and depending on the acuity and other features is probably going to be pretty low. Dr Smith: I really liked as an aside- I wasn't going to go there next, but you kind of got me thinking about it, you have a really nice section in your article. Which, all of it's great, but talking about how to manage low titer MOG antibodies. I wonder if you could talk about that because I think that's a lesson, maybe, that is transferable to a lot of other testing that we do. in terms of pre-prior probability and titer and so forth. Dr Eggenberger: Yeah, that's really an important point. So, we've seen this come up a number of times where the MOG antibody is a very good test, but in low titer it has a relatively low positive predictive value, perhaps 50%. In those cases, particularly without a classic clinical context, you have to be extremely alert for some other diagnosis that could mimic what you think is inflammatory demyelinating optic neuritis, but in fact is infectious or some other cause. Dr Smith: Yeah, super, super important and helpful. In terms of aquaporin-4, how does that compare in terms of predictive values, lower titer positive results? Dr Eggenberger: So aquaporin-4, the test has a very high specificity. So, it's quite useful if positive. You have to keep in mind there can be some false negatives, but the test otherwise is quite specific. And that is a diagnosis, you know, we never want to miss. It's a vicious disease. It tends to be a blinding disease, particularly without treatment. Bad things happen when we miss that, and we want to get on that diagnosis early and do pretty aggressive early and prophylactic treatment. Dr Smith: Your article covers not only the common causes of optic neuritis and, you know, MS, isolated optic neuritis, MOGAD NMO, you talk about a bunch of other things. I wonder, in this patient that we've been discussing, in the absence of any other historical information that seems relevant---or maybe you can define what would seem relevant---would you do other evaluation in that individual, other serologic evaluation and so forth, just in terms of diagnosis? Dr Eggenberger: In that particular case, without other red flags, I don't think I would initially. And follow-up is going to give you a lot of this context. So, you'd be on the lookout for other systemic conditions. So, if the patient had some arthropathy, if the patient had any pulmonary disease hints, if there was anything else that could lead you on a broader expedition. But I think in the context of this case, acutely in the ER, I probably wouldn't do a big lab plug for this. I probably would kind of go down the most likely road and start our treatments, and then follow that patient up. Dr Smith: Yeah, I know your article does a really great job, I think, of outlining when do you need to think about some of these less common causes. Well, can we talk about treatment, Eric? Because I want to move on to some other things. But- so, we've got a patient with isolated optic neuritis, nothing else, you know, in terms of the other antibodies we've talked about. What state-of-the-care- or, state-of-the-art treatment for that patient? Dr Eggenberger: So, the acute treatment for these inflammatory, optic neuritis-type cases is very similar Initially. High dose steroids remains kind of the standard. And then, in MS-related optic neuritis, we may or may not see a taper. So many times it's just an acute treatment of three to five days high dose. Whether that's oral or PO, we could institute either depending on the particular case. And then the taper would depend on the potential cause. So, for instance, with these antibody-driven diseases---so with MOG- or particularly with aquaporin-4---if it's a longitudinally extensive region of optic nerve involved, we tend to use a longitudinally extensive taper. And so, we use prednisone in those cases for several months while we're getting everything else set and deciding what the overall course is going to bring. Dr Smith: What about IV versus oral? There must be something about my practice. I was telling this to Lindsey. Every time on our hospital service, we seem to have at least two patients with optic neuropathies, which I always enjoy, but I find it's a little weird to admit someone who's doing just fine otherwise to the hospital with three days of IV SOLU-MEDROL. So, I'm always trying to figure out, like, how can I get this patient home? And your article had the best term I've heard in a long time, which is “SOLU smoothies.” I mean, are there other strategies that you sometimes use, other than just high-dose IV methylprednisolone? Dr Eggenberger: So, I agree with you. It's sometimes hard to admit somebody for just an IV therapy. And we'll do this as an outpatient, high-dose IV, but we'll also use high-dose orals. And in times in the past when there's been methylprednisolone shortage, we've used high-dose oral or IV dexamethasone as well. I think the IV form, although it's the gold standard, the high-dose oral forms have pretty equivalent bioavailability and are pretty tolerable in my experience. And certainly more convenient. Dr Smith: I wonder if we should switch and maybe talk a little bit about aquaporin-4, I mean, you emphasized that this is a vicious disease---I love the way you describe that---and often blinding. What updates do you have in terms of our therapeutic approach to NMO? That's been rapidly evolving of late. Dr Eggenberger: Right, so these are cases we're always going to share with neuroimmunology. And it requires kind of a multidisciplinary approach, in my opinion, for ideal or for best outcomes. And so, all of these patients are going to get put on prophylactic medications. So, this is a disease you just can't leave untreated. Bad stuff will happen for sure. And we now, fortunately, have some approved, FDA-approved medications that can positively impact the course of this disease. So, that's been a welcome addition. Dr Smith: What are the FDA-approved medications at this point for NMO? Dr Eggenberger: So, there are several at this point, and this is an area that's in growth, fortunately. And again, these are cases we're going to be sharing with our neuroimmunology colleagues. So, these are IV medications typically aimed at complement or CD19. And they all are relatively effective at quieting the course of the disease. Dr Smith: Maybe we can talk a little bit about MOG? I think that most of our listeners are probably pretty familiar with aquaporin-4 and NMO, what- maybe you could describe MOG a little bit and the therapeutic approach for patients with MOG-associated disease? Dr Eggenberger: So, MOG has been a real interesting kind of condition to learn more about. We certainly see a lot of MOG, and I'm sure we saw MOG before it was formally described, but I think we just thought it was kind of a benign, maybe monophasic MS type of presentation. But MOG tends to come in with a loss of acuity that kind of rivals aquaporin-4. So, the acuity tends to be pretty, pretty depressed, but it's very steroid-responsive. So, a lot of times these are the patients, you'll see that their vision will start to improve even when they're on the initial few days of the high-dose steroids. And many times we can get their vision back to 20/20 or very close to that. Dr Smith: And do these patients need chronic management? Dr Eggenberger: So, that's an area of controversy to some degree. About 50% of the optic neuritis MOG-related cases are going to have a relapsing course. And because the disease is steroid-responsive, many times we'll follow these patients after a first attack to see if this is the condition that's going to declare itself to be relapsing or if this is just going to be a monophasic kind of presentation of optic neuritis. We don't have great biomarkers to separate patients who are going to be in that 50% monophasic course versus the other half. It'll be relapsing. And so, it depends on the patient. If there's somebody that's, as many of these patients are, been very steroid responsive, they get back to 20/20, we can teach them about the disease so that if they do have a relapse, we can get them high-dose steroids in a relatively rapid fashion and they're otherwise healthy, we're probably going to watch that patient. And if it's somebody that doesn't recover 100%, there's other issues with treating them with high-dose steroids potentially in the future, then we may learn more towards an earlier prophylactic approach in that patient. Dr Smith: And what would that approach look like? Is it different from NMO or using more IVIG or B cell depletion as opposed to complement inhibition, for instance? Dr Eggenberger: In MOG, we know that the B cell depletion strategies don't work as well. And so most times we're turning to IVIG, and we found that pretty effective. That's kind of our go-to at this point. Dr Smith: Eric, it's a joy talking to you and I'd love to keep going about content, but I'll refer our listeners to your outstanding article. I mean, you're such a highly regarded neuro-ophthalmologist and educator. I wonder if you could talk to us about why you've done neuro-ophthalmology, and maybe this is an opportunity for you to convince all of our great residents that are listening or students what's great about being a neuro-ophthalmologist. Dr Eggenberger: I think neuro-ophthalmology is by far the most interesting part of neurology. So, it's an area that I think a lot of general neurologists, in my view, don't get enough of in their residency. But it's kind of the essence of neurology, where in neurology you're localizing down to the millimeter and in neuro-ophthalmology,  we're localizing down to the micron level. We have several new emerging diseases like these varieties of optic neuritis we're focused on. We're learning lots about those. You get to be involved in lots of different areas of neurology. So, we'll see not just demyelinating conditions, we'll see trauma as it relates to the visual system. And we'll see tumor, and we see all different flavors, stroke, and in any piece of neurology, commonly we'll have some vision aspect that we that we get involved in. So, we see a wide variety of conditions. So, I think it's been a really exciting place to be within neurology. And it's rapidly changing at this point. We're getting new therapeutics. So, it's, I think it's a great time to be a neuro-ophthalmologist. Dr Smith: Yeah, listening to you talk and just reflecting on it, it's really true. Neuro-ophthalmology does cover the entire span of neurology, right? I'm a neuromuscular guy and we see a lot of ocular myasthenia, which is another super exciting area. But we've been talking about optic neuritis, and your article talks about infectious causes and the paraneoplastic and a whole host of things. So, you're a great advocate and salesperson for your field. You convinced me. Dr Eggenberger: Efferent neuro-ophthalmology we love, we could talk about ocular myasthenia and other aspects for another hour. And we get involved in all kinds of cases: third nerve palsies, ocular myasthenia, trauma that involves the efferent system, all different aspects. It's really a great subspecialty, and you get to see a bit of all of neurology. Dr Smith: I'm trying to remember who it was, Eric. It was an attending of mine at medical school. I went to medical school at the Mayo Clinic in Rochester, and I want to say it was Manny Gomez, who was a very famous tuberous sclerosis person, who told me that neuro-ophthalmology was the most elegant specialty within neurology. That stuck with me. Thank you so much for joining me today. I really appreciate it. Dr Eggenberger: Thank you. I appreciate it as well. Dr Smith: So again, today I've been interviewing Dr Eric Eggenberger about his really wonderful article on optic neuritis, which appears in the most recent issue of Continuum on neuro-ophthalmology. Be sure to check out Continuum audio episodes from the neuro-ophthalmology and other issues. And listeners, thank you very much 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.

In this episodeof Neurology Today in 5, Neurology Today editor-in-chief Joseph E. Safdieh, MD, FAAN, discusses a large trial that found high-dose Vitamin D reduced MRI evidence of disease activity in patients with clinically isolated syndrome or early relapsing MS; an animal brain map, revealing changes in inflammation, immune activity, and cell repair that preceded the appearance of MS lesions; and a discussion of the challenges and opportunities of using AI in neurology education.

We discuss the basics of EEG in the ICU, including when to do it, selecting the appropriate study, and the basics of bedside interpretation, with Carolina B Maciel, MD, MSCR, FAAN, triple boarded in neurology, neurocritical care, and critical care EEG. Learn more at the Intensive Care Academy! Find us on Patreon here! Buy your … Continue reading "Episode 86: EEGs in the ICU with Carolina Maciel"

Optic neuropathies encompass all congenital or acquired conditions affecting the optic nerve and are often a harbinger of systemic and central nervous system disorders. A systematic approach to identifying the clinical manifestations of specific optic neuropathies is imperative for directing diagnostic assessments, formulating tailored treatment regimens, and identifying broader central nervous system and systemic disorders. In this episode, Gordon Smith, MD, FAAN speaks with Lindsey De Lott, MD, MS, author of the article “Optic Neuropathies” in the Continuum® April 2025 Neuro-ophthalmology 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. De Lott is an assistant professor of neurology and ophthalmology at the University of Michigan in Ann Arbor, Michigan. Additional Resources Read the article: Optic Neuropathies Subscribe to Continuum®: shop.lww.com/Continuum Earn CME (available only to AAN members): continpub.com/AudioCME Continuum® Aloud (verbatim audio-book style recordings of articles available only to Continuum® subscribers): continpub.com/Aloud More about the American Academy of Neurology: aan.com Social Media facebook.com/continuumcme @ContinuumAAN Host: @gordonsmithMD Guest: @lindseydelott 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 earning CME, subscribing to the journal, and exclusive access to interviews not featured on the podcast. Dr Smith: Hello, this is Dr Gordon Smith. Today I'm interviewing Dr Lindsey De Lott about her article on optic neuropathies, which appears in the April 2025 Continuum issue on neuro-ophthalmology. Lindsey, welcome to the podcast, and perhaps you can introduce yourself to our audience. Dr De Lott: Thank you, Dr Smith. My name is Lindsey De Lott and I am a neurologist and a neuro-ophthalmologist at the University of Michigan. I also serve as the section lead for the Division of Neuro-Ophthalmology, which is actually part of the ophthalmology department rather than the neurology department. And I spend a good portion of my time as a researcher in health services research, and that's now about 60% of my practice or so. Dr Smith: I'm super excited to spend some time talking with you. One, I'm a Michigan person. As we were chatting before this, I trained with Wayne Cornblath and John Trobe, and it's great to have you. I wonder if we maybe can begin- and by the way, your article is outstanding. It is such a huge topic and it was actually really fun to read, so I encourage our listeners to check it out. But you begin by talking about misdiagnosis as being a common problem in this patient population. I wonder if you can talk through why that is and if you have any pearls or pitfalls in avoiding it? Dr De Lott: Yeah, I think there's been a lot of great research looking at misdiagnosis in specific types of optic neuropathies; in particular, compressive optic neuropathies and optic neuritis. A lot of that work has come out of the group at Emory and the group at Washington University. But a lot of neuro-ophthalmologists across the country really contributed to those data. And one of the statistics that always strikes me is that, you know, for example, in patients with optic nerve sheath meningiomas, something like 70% of them are actually misdiagnosed. And a lot of those errors in diagnosis, whether it's for compressive optic neuropathy or some other type of optic neuropathy, really comes down to the way that physicians are really incorporating elements of the history in the physical. For example, in optic neuritis, we know that physicians tend to anchor pretty heavily on pain in general. And that often tends to lead them astray when optic neuritis was never the diagnosis to begin with. So, it's really overindexing on certain things and not paying attention to other features of the physical exam; for example, say presence of an afferent pupillary defect. So, I think it just really highlights the need to have a really relatively structured approach to patients that you think have an optic neuropathy when you're trying to sort of plan your diagnostic testing and your treatment. Dr Smith: I do maybe five or six weeks on our hospital service each year, and I don't know if it's just a Richmond thing, but there's always at least two people in my week who come in with an optic neuropathy or acute vision loss. How common is this in medical practice? Or neurologic practice, I should say? Dr De Lott: Optic neuropathies themselves… if you look across, unfortunately we don't have any great data that puts together all optic neuropathies and gives us an actual sort of prevalence estimate or an incidence estimate from year to year. We do have some of those data for specific types of optic neuropathies like optic neuritis and NAION, and you're probably looking around five-ish per one hundred thousand. So, these aren't that common, but at the same time they do get funneled to- often to emergency rooms and to neurologists from our ophthalmology colleagues and optometry colleagues in particular. Dr Smith: So, one other question I had before kind of diving into the topic at hand is how facile neurologists need to be in recognizing other causes of acute visual loss. I mean, we see acute visual loss as neurologists, we think optic neuropathy, right? Optic neuritis is sort of the go-to in a younger patient, and NAION in someone older. But what do neurologists need to know about other ophthalmologic causes? So, glaucoma or acute retinal disorders, for instance? Dr De Lott: Yeah, I think it's really important that neurologists are able to distinguish optic neuropathies from other causes of vision loss. And so, I would really encourage the listeners to take a look at the excellent article by Nancy Newman about vision loss in this issue where she really kind of breaks it down into vision loss that is acute and chronic and how you really think through distinguishing optic neuropathies from other causes of vision loss. But it is really important. For example, a patient with a central retinal artery occlusion may potentially be eligible for treatments. And that's very different from a patient with optic neuritis and acute vision loss. So, we want to be able to distinguish these things.  Dr Smith: So maybe we can pivot to that a little bit. Just for our listeners, our focus today is going to be on- not so much on optic neuritis, although obviously we need to talk a little bit about how we differentiate optic neuritis from non-neuritis optic neuropathies. It seems like the two most common situations we encounter are ischemic optic neuropathies and optic neuritis. Maybe you can talk a little bit about how you distinguish these two? I mean, some of it's age, some of it's risk factors, some of it's exam. What's the framework, of let's say, a fifty-year-old person comes into the emergency room with acute vision loss and you're worried about an optic neuropathy? Dr De Lott: The first step whenever you are considering an optic neuropathy is just making sure that the features are present. I think, really going back to your earlier question, making sure that the patient has the features of an optic neuropathy that we expect. So, it's not only vision loss, but it's also the presence of an apparent pupillary defect in a patient with a unilateral optic neuropathy. In a person who has a bilateral optic neuropathy, that apparent pupillary defect may not be present because it is relative. So, you really would have to have asymmetric vision loss between the two eyes. They should also have impairment of their color vision, and they're probably going to have some kind of visual field defect, whether that's central scotoma or an arcuate scotoma or an altitudinal defect that really respects the horizontal meridian. So, you want to make sure that, first and foremost, you've got a patient that really meets most of those- most of those features. And then from there, we're looking at the other features on their history. How acute is the onset of the vision loss? What is the progression over time? Is there pain associated or not associated with the vision loss? What other medical issues does the patient have? And you know, one of the things you already brought up, for example, is, what's the age of the patient? So, I'm going to be much more hesitant to make a diagnosis of optic neuritis in a much older patient or a diagnosis on the other side, of ischemic optic neuropathy, in a much younger patient, unless they have really clear features that push me in that direction. Dr Smith: I wonder if maybe you could talk a little bit about features that would push you away from optic neuritis, because, I mean, people who are over fifty do get optic neuritis- Dr De Lott: They do. Dr Smith: -and people who get ischemic optic neuropathies who are younger. So, what features would push you away from optic neuritis and towards… let's be broad, just a different type of optic neuropathy? Dr De Lott: Sure. We know that most patients with optic neuritis do have pain, but that pain is accompanied---within a few days, typically---with vision loss. So, pain alone going on for a number of days without any visual symptoms or any of those other things I listed, like the afferent papillary defect, the visual field defect, would push me away from optic neuritis. But in general, yes, most optic neuritis is indeed painful. So, the presence of optic disc edema is unfortunately one of those things that an optic neuritis may be present, may not be present, but in somebody with ischemia that is anterior---and that's the most common type of ischemic optic neuropathy, would be anterior ischemic optic neuropathy---they have to have optic disc edema for us to be able to make that diagnosis, and that is a diagnosis of NAION, or nonarteritic ischemic optic neuropathy. An APD in this case, again, that's just a feature of an optic neuropathy. It doesn't really help you to distinguish, individual field defects are going to be relatively similar between them. So then in patients, I'm also looking, like I said, at their history. So, in a patient where I'm entertaining a diagnosis of ischemic optic neuropathy, I want to make sure that they have vascular risk factors or that I'm actually doing things like measuring their blood pressure in the office if they haven't seen a physician recently or checking a lipid panel, hemoglobin A1c, those kinds of things, to look for vascular risk factors. One of the other features on exam that might push me more- again, in a patient with ischemic optic neuropathy, where it might suggest ischemia over optic neuritis, would be some other features on exam like a crowded optic disc that we sometimes will see in patients with ischemic optic neuropathy. I feel like that was a bit of a convoluted answer. Dr Smith: I thought that was a great answer. And when you say crowded optic disc, that's the- is that the “disc at risk”? Dr De Lott: That is the “disk at risk,” yes. So, crowded optic disk is really a disk that is smaller than what we see in the average population, and the average cup to disk ratio is 0.3. So, I think that's where 30% of the disk should be. So, this extra wiggle room, as I sometimes will explain to my patients. Dr Smith: And then, I wonder if you could talk a little bit about more- just more about exam, right? You raised the importance of recognizing optic disc edema. Are there aspects of that disc edema that really steer you away from optic neuritis and towards ischemia-like hemorrhages or whatnot? And then a similar question about the importance of careful visual field testing? Dr De Lott: So, on the whole, optic disc edema is optic disc edema. And you can have very severe optic neuritis with hemorrhages, cotton wool spots, which is essentially just an infarction of the retinal nerve fiber layer either overlying the disc or other parts of the retina. And ischemia, you can have some of the same features. In patients who have giant cell arteritis, which is just one form of anterior ischemic optic neuropathy, patients can have a pallid optic disc edema where the optic disc is swollen and white-looking. But on the whole, swelling is swelling. So, I would caution anyone against using the features of the optic nerve swelling to make any type of, sort of, definitive kind of diagnosis. It's worth keeping in mind, but I just- I would caution against using specific features, optic nerve swelling. And then for visual field testing, there are certain patterns that sometimes can be helpful. I think as I mentioned earlier, in patients with ischemic optic neuropathy, we'll often see an altitudinal defect where either the top half or, more commonly, the bottom half of the vision is lost. And that vision loss in the field corresponds to the area of swelling on the disk, which is really rewarding when you're actually able to see sectoral swelling of the disk. So, say the top half of the disk is swollen and you see a really dense inferior defect. And other types of optic neuropathy such as hereditary optic neuropathies, toxic and nutritional optic neuropathies, they often cause more central field loss. And in patients who have optic neuropathies from elevated intracranial pressure, so papilladema, those folks often have more subtle visual field loss in an arcuate pattern. And it's only once the optic nerves have sustained a pretty significant injury that you start to see other patterns of field loss and actual decline in visual acuity in those patients. I do think a detailed visual field assessment can often be pretty helpful as an adjunct to the rest of the exam. Dr Smith: So, we haven't talked a lot about neuroimaging, and obviously, neuroimaging is really important in patients who have optic neuritis. But how about an older patient in whom you suspect ischemic optic neuropathy? Do those patients all need a MRI scan? And if so, is it orbits and brain? How do you- how do you protocol it? Dr De Lott: You're asking such a good question, totally controversial in in some ways. And so, in patients with ischemic optic neuropathy, if you are confident in your diagnosis: the patient is over the age of fifty, they have all the vascular, you know, they have vascular risk factors. And those vascular risk factors are things like diabetes, hypertension, high blood pressure, hyperlipidemia, obstructive sleep apnea. They have a “disc at risk” in the fellow eye. They don't have pain, they don't have a cancer history. Then doing an MRI of the orbits is probably not necessary to rule out another cause. But if you aren't confident that you have all of those features, then you should absolutely do an MRI of the orbit. The MRI of the brain probably doesn't provide you with much additional information. However, if you are trying to distinguish between an ischemic optic neuropathy and, say, maybe an optic neuritis, in those patients we do recommend MRI orbits and brain imaging because the brain does provide additional information about other CNS demyelinating disorders that might be actually the cause of a patient's optic neuritis. Dr Smith: I wonder if you could talk a little bit about posterior ischemic optic neuropathy. That's much less common, and you mentioned earlier that those patients don't have optic disk edema. So, if there's a patient who has vision loss that- in a similar sort of clinical scenario that you talked about, how do you approach that and under what circumstances do we see patients who have posterior ischemic optic neuropathy? Dr De Lott: So, you're going to most often see patients with posterior ischemic optic neuropathy who, for example, have undergone a recent surgery. These are often associated with things like spinal surgeries, cardiac surgeries. And there are a number of risk factors that are associated with it. Things like blood pressure, drain surgery, the amount of blood loss, positioning of patient. And this is something that the surgeons and anesthesiologists are very sensitive to at this point in time, and many patients are often- this can be part of the normal informed consent process at this point in time since this is something that is well-recognized for specific surgeries. In those patients, though… again, unless you're really certain, for example, maybe the inpatient neurology attending and you've been asked to consult on a patient and it's very clear that they went into surgery normal, they came out of surgery with vision loss, and all the rest of the features really seem to be present. I would recommend that in those cases you think about orbital imaging, making sure you're not missing anything else. Again, unless all of the features really are present- and I think that's one of the themes, definitely, throughout this article, is really the importance of neuroimaging in helping us to distinguish between different types of optic neuropathy. Dr Smith: Yeah, I think one of the things that Eric Eggenberger talks about in his article is the need to use precise nomenclature too, which I plan on talking to him about. But I think having this very structured approach- and your article does it very well, I'll tell our listeners who haven't seen it there's a series of really great tables in the article that outline a lot of these. I wonder, Lindsey, if we can switch to talk about arteritic optic neuropathy. Is that okay? Dr De Lott: Sure. Yeah, absolutely. Dr Smith: How do you sort that out in an older patient who comes in with an ischemic optic neuropathy? Dr De Lott: Yeah. In patients who are over the age of fifty with an ischemic optic neuropathy, we always need to be thinking about giant cell arteritis. It is really a diagnosis we cannot afford to miss. If we do miss it, unfortunately, patients are likely to lose vision in their fellow eye about 1/3 to 1/2 the time. So, it is really one of those emergencies in neuro-ophthalmology and neurology. And so you want to do a thorough review systems for giant cell arteritis symptoms, things like headache, jaw claudication, myalgias, unintentional weight loss, fevers, things of that nature. You also want to check their inflammatory markers to look for evidence of an elevated ESR, elevated C-reactive protein. And then on exam, what you're going to find is that it can cause an anterior ischemic optic neuropathy, as I mentioned earlier. It can cause palette optic disc swelling. But giant cell arteritis can also cause posterior ischemic optic neuropathy. And so, it can be present without any swelling of the optic disc. And in fact, you know, you mentioned one of my mentors, John Trobe, who used to say that in a patient where you're entertaining the idea of posterior ischemic optic neuropathy, who is over the age of fifty with no optic disc swelling, you should be thinking about number one, giant cell arteritis; number two, giant cell arteritis; number three, giant cell arteritis. And so, I think that is a real take-home point is making sure that you're thinking of this diagnosis often in our patients who are over the age of fifty, have to rule it out. Dr Smith: I'll ask maybe a simple question. And presumably just about everyone who you see with a presumed ischemic optic neuropathy, even if they don't have clinical features, you at least check a sed rate. Is that true? Dr De Lott: I do. So, I do routinely check sedimentation rate and C-reactive protein. So, you need to check both. And the reason is that there are some patients who have a positive C-reactive protein but a normal sedimentation rate, so. And vice versa, although that is less common. And so both need to be checked. One other lab that sometimes can be helpful is looking at their CBC. You'll often find these patients with giant cell arteritis have elevated platelet counts. And if you can trend them over time, if you happen to have a patient that's had multiple, you'll see it sort of increasing over time. Dr Smith: I'm just thinking about how you sort things out in the middle, right? I mean, so that not all patients with GCF, sky-high sed rate and CRP…. And I'm just thinking of Dr Trobe's wisdom. So, when you're in an uncertain situation, presumably you go ahead and treat with steroids and move to biopsy. Maybe you can talk a bit about that pathway? Dr De Lott: Yeah, sure. Dr Smith: What's the definitive diagnostic process? Do you- for instance, the sed rate is sky-high, do you still get a biopsy? Dr De Lott: Yes. So, biopsy is still our gold-standard diagnosis here in the United States. I will say that is not the case in all parts of the world. In fact, many parts of Europe are moving toward using other ancillary tests in combination with labs and exam, the history, to make a definitive diagnosis of giant cell arteritis. And those tests are things like temporal artery ultrasound. We also, even though we call it temporal artery ultrasound, we actually need to image not only the temporal arteries but also the axillary arteries. The sensitivity and specificity is actually greater in those cases. And then there's high-resolution imaging of the vessels and the- both the intracranial and extracranial distributions. And both of those have shown some promise in their predictive values of patients actually having giant cell arteritis. One caution I would give to our listeners, though, is that, you know, currently in the US, temporal artery biopsy is still the gold standard. And reading the ultrasounds and the MRIs takes a really experienced radiologist. So, unless you really know the diagnostic accuracy at your institution, again, temporal artery biopsy remains the gold standard here. So, when you are considering giant cell arteritis, start the patient on steroids and- that's high dose, high dose steroids. In patients with vision loss, we use high dose intravenous methylprednisolone and then go ahead and get the biopsy. Dr Smith: Super helpful. And are there other treatments, other than steroids? Maybe how long do you keep people on steroids? And let's say you've got a patient who's, you know, diabetic or has other factors that make you want to avoid the course of steroids. Are there other options available? Dr De Lott: So, in the acute phase steroids are the only option. There is no other option. However, long term, yes, we do pretty quickly put patients on tocilizumab, which is really our first-line treatment. And I do that in conjunction with our rheumatology colleagues, who are incredibly helpful in managing and monitoring the tocilizumab for our patients. But when you're seeing the patients, you know, whether it's in the emergency room or in the hospital, those patients need steroids immediately. There are other steroid-sparing agents that have been tried, but the efficacy is not as good as tocilizumab. So, the American College of Rheumatology is really recommending tocilizumab as our first line steroid-sparing agent at this point. Dr Smith: Outstanding. So again, I will refer our listeners to your article. It's just chock-full of great stuff. This has been a great conversation. Thank you so much for joining me today. Dr De Lott: Thank you, Dr Smith. I really appreciate it.  Dr Smith: The pleasure has been all mine, and I know our listeners will be enjoying this as well. Again, today I've been interviewing Dr Lindsey De Lott about her article on optic neuropathies, which appears in the most recent issue of Continuum on neuro-ophthalmology. Be sure to check out Continuum Audio episodes from this and other issues. I already mentioned Dr Eggenberger and I will be talking about optic neuritis, which will be a great companion to this discussion. Listeners, thank you 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.

Resources for further information: National Council of State Boards of Nursing: https://www.ncsbn.org Find your state’s board of nursing here: https://www.ncsbn.org/membership/us-members/contact-bon.page Nurses Service Organization: https://www.nso.com/risk-management/individuals

Diagnosing and differentiating among the many possible localizations and causes of vision loss is an essential skill for neurologists. The approach to vision loss should include a history and examination geared toward localization, followed by a differential diagnosis based on the likely location of the pathophysiologic process.  In this episode, Aaron Berkowitz, MD, PhD, FAAN speaks with Nancy J. Newman, MD, FAAN, author of the article “Approach to Vision Loss” in the Continuum® April 2025 Neuro-ophthalmology issue.  Dr. Berkowitz is a Continuum® Audio interviewer and a professor of neurology at the University of California San Francisco in the Department of Neurology and a neurohospitalist, general neurologist, and clinician educator at the San Francisco VA Medical Center at the San Francisco General Hospital in San Francisco, California.  Dr. Newman is a professor of ophthalmology and neurology at the Emory University School of Medicine in Atlanta, Georgia.  Additional Resources Read the article: Approach to Vision Loss 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 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 Nancy Newman about her article on the approach to visual loss, which she wrote with Dr Valerie Biousse. This article appears in the April 2025 Continuum issue on neuro-ophthalmology. Welcome to the podcast, Dr Newman. I know you need no introduction, but if you wouldn't mind introducing yourself to our listeners. Dr Newman: Sure. My name's Nancy Newman. I am a neurologist and neuro-ophthalmologist, professor of ophthalmology and neurology at the Emory University School of Medicine in Atlanta, Georgia. Dr Berkowitz: You and your colleague Dr Biousse have written a comprehensive and practical article on the approach to visual loss here. It's fantastic to have this article by two of the world's leading experts and best-known teachers in neuro-ophthalmology. And so, readers of this article will find extremely helpful flow charts, tables and very nuanced clinical discussion about how to make a bedside diagnosis of the cause of visual loss based on the history exam and ancillary testing. We'll talk today about that important topic, and excited to learn from you and for our listeners to learn from you. To begin, let's start broad. Let's say you have a patient presenting with visual loss. What's your framework for the approach to this common chief concern that has such a broad differential diagnosis of localizations and of causes? Where do you start when you hear of visual loss? How do you think about this chief concern? Dr Newman: Well, it's very fun because this is the heart of being a neurologist, isn't it? Nowhere in the nervous system is localization as important as the complaint of vision loss. And so, the key, as any neurologist knows, is to first of all figure out where the problem is. And then you can figure out what it is based on the where, because that will limit the number of possibilities. So, the visual system is quite beautiful in that regard because you really can exquisitely localize based on figuring out where things are. And that starts with the history and then goes to the exam, in particular the first localization. So, you can whittle it down to the more power-for-your-buck question is, is the vision lost in one eye or in two eyes? Because if the vision loss clearly, whether it's transient or persistent, is in only one eye, then you only have to think about the eyeball and the optic nerve on that side. So, think about that. Why would you ever get a brain MRI? I know I'm jumping ahead here, but this is the importance of localization. Because what you really want to know, once you know for sure it's in one eye, is, is it an eyeball problem---which could be anything from the cornea, the lens, the vitreous, the retina---or is it an optic nerve problem? The only caveat is that every once in a while, although we trust our patients, a patient may insist that a homonymous hemianopia, especially when it's transient, is only in the eye with the temporal defect. So that's the only caveat. But if it's in only one eye, it has to be in that side eyeball or optic nerve. And if it's in two eyes, it's either in both eyeballs or optic nerves, or it's chiasmal or retrochiasmal. So that's the initial approach and everything about the history should first be guided by that. Then you can move on to the more nuanced questions that help you with the whats. Once you have your where, you can then figure out what the whats are that fit that particular where. Dr Berkowitz: Fantastic. And your article with Dr Biousse has this very helpful framework, which you alluded to there, that first we figure out, is it monocular or binocular? And we figure out if it's a transient or fixed or permanent deficit. So, you have transient monocular, transient binocular, fixed monocular, fixed binocular. And I encourage our listeners to seek out this article where you have a table for each of those, a flow chart for each of those, that are definitely things people want to have printed out and at their desk or on their phone to use at the bedside. Very helpful. So, we won't be able to go through all of those different clinical presentations in this interview, but let's focus on monocular visual loss. As you just mentioned, this can be an eye problem or an optic nerve problem. So, this could be an ophthalmologic problem or a neurologic problem, right? And sometimes this can be hard to distinguish. So, you mentioned the importance of the history. When you hear a monocular visual loss- and with the caveat, I said you're convinced that this is a monocular visual problem and not a visual field defect that may appear. So, the patient has a monocular deficit, how do you approach the history at trying to get at whether this is an eye problem or an optic nerve problem and what the cause may be? Dr Newman: Absolutely. So, the history at that point tends not to be as helpful as the examination. My mentor used to say if you haven't figured out the answer to the problem after your history, you're in trouble, because that 90% of it is history and 10% is the exam. In the visual system, the exam actually may have even more importance than anywhere else in the neurologic examination. And we need as neurologists to not have too much hubris in this. Because there's a whole specialty on the eyeball. And the ophthalmologists, although a lot of their training is surgical training that that we don't need to have, they also have a lot of expertise in recognizing when it's not a neurologic problem, when it's not an optic neuropathy. And they have all sorts of toys and equipment that can very much help them with that. And as neurologists, we tend not to be as versed in what those toys are and how to use them. So, we have to do what we can do. Your directive thalmoscope, I wouldn't throw it in the garbage, because it's actually helpful to look at the eyeball itself, not just the back of the eye, the optic nerve and retina. And we'll come back to that, but we have in our armamentarium things we can do as neurologists without having an eye doctor's office. These include things like visual acuity and color vision, confrontation, visual fields. Although again, you have to be very humble. Sometimes you're lucky; 30% of the time it's going to show you a defect. It has to be pretty big to pick it up on confrontation fields. And then as we say, looking at the fundus. And you probably know that myself and Dr Biousse have been on somewhat of a crusade to allow the emperor's new clothes to be recognized, which is- most neurologists aren't very comfortable using the direct ophthalmoscope and aren't so comfortable, even if they can use it, seeing what they need to see. It's hard. It's really, really hard. And it's particularly hard without pupillary dilation. And technology has allowed us now with non-mydriatic cameras, cameras that are incredible, even through a small pupil can take magnificent pictures of the back of the eye. And who wouldn't rather have that? And as their cost and availability- the cost goes down and their availability goes up. These cameras should be part of every neurology office and every emergency department. And this isn't futuristic. This is happening already and will continue to happen. But over the next five years or so… well, we're transitioning into that. I think knowing what you can do with the direct ophthalmoscope is important. First of all, if you dial in plus lenses, you can't be an ophthalmologist, but you can see media opacities. If you can't see into the back of the eye, that may be the reason the patient can't see out. And then just seeing if someone has central vision loss in one eye, it's got to be localized either to the media in the axis of vision; or it's in the macula, the very center of the retina; or it's in the optic nerve. So, if you get good at looking at the optic nerve and then try to curb your excitement when you saw it and actually move a little temporally and take a look at the macula, you're looking at the two areas. Again, a lot of ophthalmologists these days don't do much looking with the naked eye. They actually do photography, and they do what's called OCT, optical coherence tomography, which especially for maculopathies, problems in the macula are showing us the pathology so beautifully, things that used to be considered subtle like central serous retinopathy and other macula. So, I think having a real healthy respect for what an eye care provider can do for you to help screen away the ophthalmic causes, it's very, very important to have a patient complaining of central vision loss, even if they have a diagnosis like multiple sclerosis, you expect that they might have an optic neuritis… they can have retinal detachments and other things also. And so, I think every one of these patients should be seen by an eye care provider as well. Dr Berkowitz: Thank you for that overview. And I feel certainly as guilty as charged here as one of many neurologists, I imagine, who wish we were much better and more comfortable with fundoscopy and being confident on what we see. But as you said, it's hard with the direct ophthalmoscope and a non-dilated exam. And it's great that, as you said, these fundus photography techniques and tools are becoming more widely available so that we can get a good look at the fundus. And then we're going to have to learn a lot more about how to interpret those images, right? If we haven't been so confident in our ability to see the fundus and analyze some of the subtle abnormalities that you and your colleagues and our ophthalmology colleagues are more familiar with. So, I appreciate you acknowledging that. And I'm glad to hear that coming down the pipeline, there are going to be some tools to help us there. So, you mentioned some of the things you do at the bedside to try to distinguish between eye and optic nerve. Could you go into those in a little bit more detail here? How do you check the visual fields? For example, some people count fingers, some people wiggle fingers, see when the patient can see. How should we be checking visual fields? And what are some of the other bedside tasks you use to decide this is probably going to end up being in the optic nerve or this seems more like an eye? Dr Newman: Of course. Again, central visual acuity is very important. If somebody is older than fifty, they clearly will need some form of reading glasses. So, keeping a set of plus three glasses from cheapo drugstore in your pocket is very helpful. Have them put on their glasses and have them read an ear card. It's one of the few things you can actually measure and examine. And so that's important. The strongest reflex in the body and I can have it duke it out with the peripheral neurologists if they want to, it's not the knee jerk, it's looking for a relative afferent pupillary defect. Extremely important for neurologists to feel comfortable with that. Remember, you cut an optic nerve, you're not going to have anisocoria. It's not going to cause a big pupil. The pupils are always equal because this is not an efferent problem, it's an afferent problem, an input problem. So basically, if the eye has been injured in the optic nerve and it can't get that information about light back into the brain, well, the endoresfol nuclei, both of them are going to reset at a bigger size. And then when you swing over and shine that light in the good optic nerve, the good eye, then the brain gets all this light and both endoresfol nuclei equally set those pupils back at a smaller size. So that's the test for the relative afferent pupillary defect. When you swing back and forth. Of course, when the light falls on the eye, that's not transmitting light as well to the brain, you're going to see the pupil dilate up. But it's not that that pupil is dilating alone. They both are getting bigger. It's an extremely powerful reflex for a unilateral or asymmetric bilateral optic neuropathy. But what you have to remember, extremely important, is, where does our optic nerve come from? Well, it comes from the retinal ganglion cells. It's the axons of the retinal ganglion cells, which is in the inner retina. And therefore inner retinal disorders such as central retinal artery occlusion, ophthalmic artery occlusion, branch retinal artery occlusion, they will also give a relative afferent pupillary defect because you're affecting the source. And this is extremely important. A retinal detachment will give a relative afferent pupillary defect. So, you can't just assume that it's optic nerve. Luckily for us, those things that also give a relative afferent pupillary defect from a retinal problem cause really bad-looking retinal disease. And you should be able to see it with your direct ophthalmoscope. And if you can't, you definitely will be able to see it with a picture, a photograph, or having an ophthalmologist or optometrist take a look for you. That's really the bedside. You mentioned confrontation visual fields. I still do them, but I am very, very aware that they are not very sensitive. And I have an extremely low threshold to- again, I have something in my office. But if I were a general neurologist, to partner with an eye care specialist who has an automated visual field perimeter in their office because it is much more likely to pick up a deficit. Confrontation fields. Just remember, one eye at a time. Never two eyes at the same time. They overlap with each other. You're going to miss something if you do two eyes open, so one eye at a time. You check their field against your field, so you better be sure your field in that eye is normal. You probably ought to have an automated perimetry test yourself at some point during your career if you're doing that. And remember that the central thirty degrees is subserved by 90% of our fibers neurologically, so really just testing in the four quadrants around fixation within the central 30% is sufficient. You can present fingers, you don't have to wiggle in the periphery unless you want to pick up a retinal detachment. Dr Berkowitz: You mentioned perimetry. You've also mentioned ocular coherence tomography, OCT, other tests. Sometimes we think about it in these cases, is MRI one of the orbits? When do you decide to pursue one or more of those tests based on your history and exam? Dr Newman: So again, it sort of depends on what's available to you, right? Most neurologists don't have a perimeter and don't have an OCT machine. I think if you're worried that you have an optic neuropathy, since we're just speaking about monocular vision loss at this point, again, these are tests that you should get at an office of an eye care specialist if you can. OCT is very helpful specifically in investigating for a macular cause of central vision loss as opposed to an optic nerve cause. It's very, very good at picking up macular problems that would be bad enough to cause a vision problem. In addition, it can give you a look at the thickness of the axons that are about to become the optic nerve. We call it the peripapillary retinal nerve fiber layer. And it actually can look at the thickness of the layer of the retinal ganglion cells without any axons on them in that central area because the axons, the nerve fiber layer, bends away from central vision. So, we can see the best we can see. And remember these are anatomical measurements. So, they will lag, for the ganglion cell layer, three to four weeks behind an injury, and for the retinal nerve fiber, layer usually about six weeks behind an entry. Whereas the functional measurements, such as visual acuity, color vision, visual fields, will be immediate on an injury. So, it's that combination of function and anatomy examination that makes you all-powerful. You're very much helped by the two together and understanding where one will be more helpful than the other. Dr Berkowitz: Let's say we've gotten to the optic nerve as our localization. Many people jump to the assumption it's the optic nerve, it's optic neuritis, because maybe that's the most common diagnosis we learn in medical school. And of course, we have to sometimes, when we're teaching our students or trainees,  say, well, actually, not all optic nerve disease, optic neuritis, we have to remember there's a broader bucket of optic neuropathy. And I remember, probably I didn't hear that term until residency and thought, oh, that's right. I learned optic neuritis. Didn't really learn any of the other causes of optic nerve pathology in medical school. And so, you sort of assume that's the only one. And so you realize, no, optic neuropathy has a differential diagnosis beyond optic neuritis. Neuritis is a common cause. So how do you think about the “what” once you've localized to the optic nerve, how do you think about that? Figure out what the cause of the optic neuropathy is? Dr Newman: Absolutely. And we've been trying to convince neuro-radiologists when they see evidence of optic nerve T2 hyperintensity, that just means damage to the optic nerve from any cause. It's just old damage, and they should not put in their read consistent with optic neuritis. But that's a pet peeve. Anyway, yes, the piece of tissue called the optic nerve can be affected by any category of pathophysiology of disease. And I always suggest that you run your categories in your head so you don't leave one out. Some are going to be more common to be bilateral involvement like toxic or metabolic causes. Others will be more likely unilateral. And so, you just run those guys. So, in my mind, my categories always are compressive-slash-infiltrative, which can be neoplastic or non-neoplastic. For example, an ophthalmic artery aneurysm pressing on an optic nerve, or a thyroid, an enlarged thyroid eye muscle pressing on the optic nerve. So, I have compressive infiltrative, which could be neoplastic or not neoplastic. I have inflammatory, which can be infectious. Some of the ones that can involve the optic nerve are syphilis, cat scratch disease. Or noninfectious, and these are usually your autoimmune such as idiopathic optic neuritis associated with multiple sclerosis, or MOG, or NMO, or even sarcoidosis and inflammation. Next category for me would be vascular, and you can have arterial versus venous in the optic nerve, probably all arterial if we're talking about causes of optic neuropathy. Or you could have arteritic versus nonarteritic with the vascular, the arteritic usually being giant cell arteritis. And the way the optic nerve circulation is, you can have an anterior ischemic optic neuropathy or a posterior ischemic optic neuropathy defined by the presence of disc edema suggesting it's anterior, the front of the optic nerve, or not, suggesting that it's retrobulbar or posterior optic nerve. So what category am I- we mentioned toxic, metabolic nutritional. And there are many causes in those categories of optic neuropathy, usually bilateral. You can have degenerative or inherited. And there are causes of inherited optic neuropathies such as Leber hereditary optic neuropathy and dominant optic atrophy. And then there's a group I call the mechanical optic neuropathies. The obvious one is traumatic, and that can happen in any piece of tissue. And then the other two relate to the particular anatomy of the eyeball and the optic nerve, and the fact that the optic nerve is a card-carrying member of the central nervous system. So, it's not really a nerve by the way, it's a tract. Think about it. Anyway, white matter tract. It is covered by the same fluid and meninges that the rest of the brain. So, what mechanically can happen? Well, you could have an elevated intraocular pressure where that nerve inserts. That's called glaucoma, and that would affect the front of the optic nerve. Or you can have elevated intracranial pressure. And if that's transmitted along the optic nerve, it can make the front of the optic nerve swell. And we call that specifically papilledema, optic disk edema due specifically to raised intracranial pressure. We actually even can have low intraocular pressure cause something called hypotony, and that can actually even give an optic neuropathy the swelling of the optic nerve. So, these are the mechanical. And if you were to just take that list and use it for any piece of tissue anywhere, like the heart or the kidney, you can come up with your own mechanical categories for those, like pericarditis or something like that. And then all those other categories would fit. But of course, the specific causes within that pathophysiology are going to be different based on the piece of tissue that you have. In this case, the optic nerve. Dr Berkowitz: In our final moments here, we've talked a lot about the approach to monocular visual loss. I think most neurologists, once we find a visual field defect, we breathe a sigh of relief that we know we're in our home territory here, somewhere in the visual task base that we've studied very well. I'm not trying to distinguish ocular causes amongst themselves or ocular from optic nerve, which can be very challenging at the bedside. But one topic you cover in your article, which I realized I don't really have a great approach to, is transient binocular visual loss. Briefly here, since we're running out of time, what's your approach to transient binocular visual loss?  Dr Newman: We assume with transient binocular vision loss that we are not dealing with a different experience in each eye, because if you have a different experience in each eye, then you're dealing with bilateral eyeball or optic nerve. But if you're having the same experience in the two eyes, it's equal in the two eyes, then you're located. You're located, usually, retro chiasmally, or even chiasm if you have pituitary apoplexy or something. So, all of these things require imaging, and I want to take one minute to talk about that. If you are sure that you have monocular vision loss, please don't get a brain MRI without contrast. It's really useless. Get a orbital MRI with contrast and fat suppression techniques if you really want to look at the optic nerve. Now, let's say you you're convinced that this is chiasmal or retrochiasmal. Well then, we all know we want to get a brain MRI---again, with and without contrast---to look specifically where we could see something. And so, if it's persistent and you have a homonymous hemianopia, it's easy, you know where to look. Be careful though, optic track can fool you. It's such a small little piece, you may miss it on the MRI, especially in someone with MS. So really look hard. There's very few things that are homonymous hemianopias MRI negative. It may just be that you didn't look carefully enough. And as far as the transient binocular vision loss, again, remember, even if it's persistent, it has to be equal vision in the two eyes. If there's inequality, then you have a superimposed anterior visual pathway problem, meaning in front of the chiasm on the side that's worse. The most common cause of transient binocular vision loss would be a form of migraine. The visual aura of migraine usually is a positive phenomenon, but sometimes you can have a homonymous hemianopic persistent defect that then ebbs and flows and goes away. Usually there's buildup, lasts maybe fifteen minutes and then it goes away, not always followed by a headache. Other things to think of would be transient ischemic attack in the vertebra Basler system, either a homonymous hemianopia or cerebral blindness, what we call cortical blindness. It can be any degree of vision loss, complete or any degree, as long as the two eyes are equal. That should last only minutes. It should be maximum at onset. There should be no buildup the way migraine has it. And it should be gone within less than ten minutes, typically. After fifteen, that's really pushing it. And then you could have seizures. Seizures can actually be the aura of a seizure, the actual ictal phenomenon of a seizure, or a postictal, almost like a todd's paralysis after a seizure. These events are typically bright colors and flashing, and they last usually seconds or just a couple of minutes at most. So, you can probably differentiate them. And then there are the more- less common but more interesting things like hyperglycemia, non-ketonic hyperglycemia can give you transient vision loss from cerebral origin, and other less common things like that. Dr Berkowitz: Fantastic. Although we've talked about many pearls of clinical wisdom here with you today, Dr Newman, this is only a fraction of what we can find in your article with Dr Biousse. We focused here on monocular visual loss and a little bit at the end here on binocular visual loss, transient binocular visual loss. But thank you very much for your article, and thank you very much for taking the time to speak with us today. Again, today I've been interviewing Dr Nancy Newman about her article with Dr Valerie Biousse on the approach to visual loss, which appears in the most recent issue of Continuum on neuro-ophthalmology. Be sure to check out Continuum audio episodes from this and other issues. Thank you so much 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 this 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 of The Nurse Practitioner Podcast, Kerry A. Milner, DNSC, APRN, FNP-BC, EBP-C and Ellen Fineout-Overholt, PhD, RN, EBP-C, FNAP, FAAN explore strategies and opportunities for sharing DNP project impact and lessons learned. (Note: Journal/Author Name Estimator [JANE] mentioned in this episode can be found here – https://jane.biosemantics.org/)

“There have been many changes since the '70s that have shaped the nurse's role in administering chemo, and in supporting patients. The major change early on was the transition from that of nurses mixing chemo to that of pharmacists. Regulatory agencies like NIOSH and OSHA defined chemotherapy as hazardous drugs, and professional organizations became involved, leading to the publication of the joint ASCO and ONS Standards of Safe Handling,” ONS member Scarlott Mueller, MPH, RN, FAAN, secretary of the American Cancer Society Cancer Action Network Board and member of the Oncology Nursing Foundation Capital Campaign Cabinet, told Darcy Burbage, DNP, RN, AOCN®, CBCN®, ONS member and chair of the ONS 50th Anniversary Committee during a conversation about the evolution of chemotherapy treatment. Along with Mueller, Burbage spoke with John Hillson, DNP, NP, Mary Anderson, BSN, RN, OCN®, and Kathleen Shannon-Dorcy, PhD, RN, FAAN, about the changes in radiation, oral chemotherapy, and cellular therapy treatments they have witnessed during their careers. Music Credit: “Fireflies and Stardust” by Kevin MacLeod Licensed under Creative Commons by Attribution 3.0  Episode Notes  This episode is not eligible for NCPD. ONS Podcast™ episodes: 50th anniversary series Episode 330: Stay Up to Date on Safe Handling of Hazardous Drugs Episode 59: Blood and Marrow Transplant Nursing Episode 16: Navigating the Challenges of Oral Chemotherapy ONS Voice article:Safe Handling—We've Come a Long Way, Baby! ONS books: Chemotherapy and Immunotherapy Guidelines and Recommendations for Practice (second edition) Hematopoietic Stem Cell Transplantation: A Manual for Nursing Practice (third edition) Oncology Nurse Navigation: Delivering Patient-Centered Care Across the Continuum (second edition) Safe Handling of Hazardous Drugs (fourth edition) ONS courses: ONS Hematopoietic Stem Cell Transplantation™ ONS/ONCC® Chemotherapy Immunotherapy Certificate™ ONS/ONCC® Radiation Therapy Certificate™ Safe Handling Basics Oral Anticancer Medication Toolkit Oral Anticancer Medication Care Compass Patient education guides created as a collaboration between ONS, HOPA, NCODA, and the Association of Community Cancer Centers: IV Cancer Treatment Education Sheets Oral Chemotherapy Education Sheets Connie Henke Yarbro Oncology Nursing History Center To discuss the information in this episode with other oncology nurses, visit the ONS Communities.  To find resources for creating an ONS Podcast Club in your chapter or nursing community, visit the ONS Podcast Library. To provide feedback or otherwise reach ONS about the podcast, email pubONSVoice@ons.org. Highlights From This Episode Hillson: “I remember as a new grad, from back in '98, walking up to the oncology floor. We had patients with pink labels on the chart and that was the radiation oncology service. I hadn't heard of such a thing before. … I'd gone through nursing school and hospital orientation and unit orientation without ever hearing of these therapies. At the time, both the management and the union had no interest in specialist nurses, and the really weren't any books that were targeting the role. And it was very isolating and frightening. I was very glad to find ONS when I moved to the U.S. Right now, the Oncology Nursing Society Manual for Radiation Oncology, Nursing Practice, and Education, it's in its fifth edition and a sixth is underway. There's nothing else like it. Most books are very much geared towards other professions.” TS 5:34 Mueller: “We mixed our chemo in a very small medication room on the unit, under a horizontal laminar flow hood, which we later discovered should have been a vertical laminar flow hood. Initially, we did not use any personal protective equipment. I remember mixing drugs like bleomycin and getting a little spray that from the vial onto my face. And to this day, I still have a few facial blemishes from that.” TS 14:28 Anderson: “As the increasing number of these actionable mutations continue to grow, so will the number of oral anticancer medications that patients are going to be taking. And we are already seeing that there's multiple combination regimens and complex schedules that the patients have to take. So this role the oral oncolytic nurse and the nursing role, like you said, it cannot be owned by one individual or discipline. So it's not a pharmacist; the pharmacies aren't owning this. The nurses are not owning this. It takes a village.” TS 32:12 Shannon-Dorcy: Then as immunotherapy comes into the picture, we start to learn about [cytokine release syndrome]. All of a sudden, we had no concept that this was a deadly consequence. ONS was on the front lines, convening people across the country together so we could speak to the investigative work with science and find ways that we could intervene, how we can look for signs of it early on with handwriting testing.” TS 39:58

In this episode, Lyell K. Jones Jr, MD, FAAN, speaks with Valérie Biousse, MD, who served as the guest editor of the Continuum® April 2025 Epilepsy issue. They provide a preview of the issue, which publishes on April 3, 2025.   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. Biousse is a professor in the departments of neurology and ophthalmology, as well as the Reunette Harris Chair of Ophthalmic Research, at Emory University in Atlanta, Georgia.  Additional Resources Read the issue: Neuro-ophthalmology Subscribe to Continuum®: shop.lww.com/Continuum More about the American Academy of Neurology: aan.com  Social Media  facebook.com/continuumcme  @ContinuumAAN  Host: @LyellJ  Guest: @vbiouss  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 Jones: This is Dr Lyell Jones, Editor-in-Chief of Continuum: Lifelong Learning in Neurology. Today, I'm interviewing Dr Valerie Biousse, who recently served as Continuum's guest editor for our latest issue on neuro-ophthalmology. Dr Biousse is a professor in the departments of neurology and ophthalmology at Emory University in Atlanta, Georgia where she's also the Renette Harris Chair of Ophthalmic Research. Dr Biousse, welcome and thank you for joining us today. Why don't you introduce yourself to our listeners? Dr Biousse: In addition to what you just mentioned, I would like to highlight that I have a French accent because I was born and raised and went to medical school in France in Saint Pete Pierre, where I trained as a neurologist. And I even practiced as a stroke neurologist and a headache specialist in the big university in Paris before I decided to move to the US to pursue my passion, which was really neuro-ophthalmology. And at the time, it was impossible to get a license in the US, so I had to repeat a residency and became an ophthalmologist. And this is what led me where I am today. Dr Jones: We're fortunate that you did that. I'm glad you did all that extra work because your contributions to the field have obviously been magnificent, especially this issue, which I think is an incredibly important topic for neurologists. This is why we include it in the rotation of Continuum topics. We all know the saying that the eyes are the windows to the soul, but for neurologists they are also the windows to the brain. The only part of the CNS that's visible to us is the optic disc. I think in spite of that, I think neurologists, our readers and our listeners would acknowledge the importance of the ophthalmic exam and respect the importance of that aspect of the neurologic exam. It's an area that feels challenging to us, and many of us, even with lots of years of experience, don't always feel very comfortable with this. So, it's a really important topic and I'm glad you have edited this. And let's start off with, you know, as you've reviewed all these articles from, really, the pinnacle experts in their specific topics in neuro-ophthalmology, as you were editing this issue, Dr Biousse, what would you say is the one biggest, most important practice-changing message about neuro-ophthalmology you would want to convey to our listeners? Dr Biousse: I think its technology, advances in technology. Without any doubt. The ophthalmology world cannot evaluate a patient anymore without access to fundus photography, optical coherence tomography (OCT) of the back of the eye, not just the optic nerve, but the retina. These advantages in technology have completely changed the way we practice ophthalmology. The same applies to neuro-ophthalmology. And these techniques can really help neurologists do a basic eye exam. Dr Jones: So, let's get right into that. And I'm glad you started with that because I still feel, even though I've done it thousands of times, I still feel a little fumbly and awkward when I'm trying to examine and fundus through an undilated pupil, right? And so, this is I think where technology has helped us quantitate with, as you mentioned, OCT, but I think from an accessibility perspective, I think nonmydriatic fundus photography is a very interesting tool for neurologists and non-neurologists.  Tell us how, how does that work and how could neurologists implement that in their practice? Dr Biousse: It's a very important tool that of course neurology should be able to use every day. You can take fundus photographs of the back of the eye without dilating the pupil. The quality of the photographs is usually very good. You only have access to what we call the posterior pole of the eye, so the optic nerves and the macula and the vascular arcade. You don't see the periphery of the retina, but in neuro-ophthalmology or neurology you don't need access to the periphery of the retina, so it doesn't matter. What is remarkable nowadays is that we have access to very highly performing fundus cameras which can take pictures through very, very small pupils or in patients of all ages. You can use it on a two-year-old in a pediatric clinic. You can use it on a much older person who may have a cataract or other eye problems. And what's really new and what this issue highlights is that it's not just that we can take pictures of the back of the eye, we can also perform OCT at the same time using the same camera. So, that's really a complete game changer for neurologists. Dr Jones: And that's extremely helpful. If I'm in a neurology clinic and I would like to use this technology, how would I access that? Do I need special equipment? Can I use my smartphone and an app? How would that work in terms of getting the image but also getting an interpretation of it? Dr Biousse: It all depends on what your ultimate goal is. The fundus cameras, they are like regular cameras or like any technology that would allow you to get brain imaging. The more sophisticated, the better the quality of the image, the more expensive they are. You know, that's the difference between a three-tesla MRI and a head CT. You buy a camera that's more expensive, you're going to have access to much easier cameras and to much higher resolution of images, and therefore you're going to be much happier with the results. So, I always tell people be very careful not to get a tool that is not going to give you the quality of images you need or you may make mistakes. You basically have two big sorts of cameras. You have what we call the tabletop cameras, which is a little more bulky camera, a little more expensive camera that's sitting on the table. The table can be on wheels, so you can move the table to the patient or you can move the patient to the table. That's very convenient in a neurology clinic where most patients are outpatient. It works in the emergency department. It's more difficult at bedside in the hospital. Or you can have a handheld camera, which can be sophisticated, a device that just uses a handheld camera or, as you mentioned, a small camera that you place on your smartphone, or even better, a camera that you can attach to some of the marketed direct ophthalmoscopes. In all situations, you need to be able to transfer those images to your electronic medical records so that you can use them. You can do that with all tabletop cameras, most handheld cameras; you cannot do it with your smartphone. So that gives you an idea of what you can use. So yes, you can have a direct ophthalmoscope with a little camera mounted. This is very inexpensive. It is very useful at bedside for the neurologists who do- who see patients every day, or the resident on call. But if you really want to have a reliable tool in clinic, I always recommend that people buy a tabletop camera that's connected to the electronic medical record. Dr Jones: You know, the photos always make it so much more approachable and accessible than the keyhole view that I get with my direct ophthalmoscope in clinic. And obviously the technology and the tools are part of the story, but also, it's access to the expertise. Right? There are not many neuro-ophthalmologists in the world, and getting access to the experts is a challenge, I think, everywhere, everywhere in the world really. When you think about how technology can expand that---and here I'm getting at AI, which I hesitate to bring up because it feels like we talk about AI a lot---are there tools that you think are here now or will be coming soon that will help clinicians, including neurologists, interpret fundus photography or other neuro-ophthalmologic findings, maybe eye movements, to make that interpretation piece a little more accessible? Dr Biousse: Absolutely. It's going to happen. It's not there yet. OK? I always tell people, AI is very important and it's a big part of our future without any doubt. But to use AI you need pictures. To get pictures, you need a camera. And so I tell people, first you start with the camera, you implement the camera, you incorporate the camera in your electronic medical record. Because if you do that, then the pictures become accessible to everyone, including the ophthalmologist who's maybe offsite and can review the pictures and provide an official interpretation of the pictures to help you. You can also transfer those pictures using secure mode of transfers and not your smartphone text application, which you really don't want to use to transfer medical information. And that's why I insist on the fact that those pictures should definitely appear in the patient's medical record. Otherwise you're going to break HIPAA laws, and that's an issue that comes up quite often. Once you have the pictures in the electronic medical record and once you have the pictures in the camera, you can do three things. You can look at them yourself. And many of my neurology colleagues are very competent at declaring that an optic nerve is normal or an optic nerve is swollen or an optic nerve is pale. And very often that's all we need. You can say, oh, I don't know about that one, and page the ophthalmologist on call, give the patient 's medical record number, have them look at the pictures, provide an interpretation, and that's where you have your answer. And this can be done in real time, live, when you're at bedside, no problem. Or you can use AI as what I call “Diagnostic A.” I always compare it as, imagine if you had a little robot neuro-ophthalmologist in your pocket that you could use at any time by just taking a picture, clicking submit on the AI app. The app will tell you never, it's normal or it's papilledema or it's pale. The app will tell you, the probability of this optic disk of being normal is 99% or the probability that this is papilledema. And when I say papilledema, I mean papilledema from rest intracranial pressure that's incredible as opposed to optic disc edema from an optic neuritis or from an ischemic optic neuropathy. And the app will tell you, the probability that this is papilledema is eighty six percent. The probability that it's normal is zero. The probability that it's another cause of disc edema is whatever. And so, depending on your probability and your brain and your own eyes, because you know how to interpret most fundus photographs, you really can make an immediate diagnosis. So that is not available for clinical use yet because the difficulty with the eye, as you know, is to have it have a deep learning algorithm cleared by the FDA. And that's a real challenge. But many research projects have shown that it can be done. It is very reliable, it works. And we know that such tools can either be either incorporated inside the camera that you use---in which case it's the camera that gives you the answer, which I don't think is the ideal situation because you have one algorithm per camera---or you have the algorithm on the Cloud and your camera immediately transfers in a secure fashion the images to the Cloud and you get your answer that way directly in your electronic medical record. We know it can be done because it happens every day for diabetic retinopathy. Dr Jones: Got it. And so, it'll expand, and obviously there has to be a period of developing trust in it, right? Once it's been validated and it becomes something that people use. And I get the sense that this isn't going to replace the expertise of the people that use these tools or people in neuro-ophthalmology clinics. It really will just augment. Is that a fair statement? Dr Biousse: Absolutely. Similar to what you get when you do an EKG. The EKG machine gives you a tentative interpretation, correct? And when the report is “it's normal,” you really can trust it, it's normal. But when it says it's not normal, this is when you look at it and you ask for a cardiology consultation. That's usually what happens. And so, I really envision such AI tools as, “it's normal,” in which case you don't need a consultation. You don't need to get an ophthalmology consultation to be sure that there is no papilledema in a patient with headache, in a patient with possible cerebrospinal fluid shunt malfunction. You don't need it because if the AI tool tells you it's normal, it's normal. When it's not normal, you still need the expertise of the ophthalmologist or the neuro-ophthalmology. The same applies to the diagnosis of eye movement. So that's a little more difficult to implement because, as you know, to have an AI algorithm, you need to have trained the algorithm with many examples. We have many examples of pathology of the back of the eyes, because that's what we do. We take pictures every day and there are databases of pictures, there are banks of pictures. But how many examples do we have of abnormal line movement in myasthenia, of videos or downbeat nystagmus? You know, even if we pulled all our collections together, we would come up with what, two hundred examples of downbeat nystagmus around the world? That's not enough to train an AI system, and that's why most of the research on eye movement right now is devoted to creating algorithm that mimic abnormal eye movements so that we can make them and then train algorithm which job will be to diagnose the abnormal eye movement. There's an extra difficult step, it's actually quite interesting. But it's going to happen. You would be able to have the patient look at the camera on the computer and get a report about “it's normal” or “the saccades, whatever, are not normal. It's most likely an internucleosomal neuralgia” or “it is downbeat nystagmus.” And that's not, again, science fiction. There are very good groups right now working on this. Dr Jones: That's really fascinating, and that- you anticipated my next question, which is, I think neurologists understand the importance of the ocular motor exam from a localizing perspective, but it's also complex and challenging. And I think that's certainly an area of potential growth. And you make a good point that we need some data to train the models. And until we have these tools, Dr Biousse, that will sort of democratize and provide access through technology to diagnosis and, you know, ultimately management of neuro-ophthalmology disorders, we know that there are gaps in the care of these patients right now in the modern day. In your own practice, in your own work at Emory, what do you see as the biggest gap in practice in caring for these patients?  Dr Biousse: I think there is a lack of confidence amongst many neurologists regarding their ability to perform a basic eye exam and provide a reliable report of their finding. And the same applies to most ophthalmologists. And that's very interesting because we have, often, a large cohort of patients who are in between the two specialties and are getting a little bit lost. The ophthalmologist doesn't know what to do. The neurologist usually knows what to do, but he's not completely sure that it's the right thing to do. And that's where the neuro-ophthalmologist comes in. And when you have a neuro-ophthalmologist right there, it's fantastic, okay? We bridge the two specialties, and we often just translate what the ophthalmologist said to the neurologist or what the neurologist said to the ophthalmologist and suddenly everything becomes clear. But unfortunately, there are not enough neuro-ophthalmologists. There is a definite patient access issue even when there is a neuro-ophthalmologist because not only is there a coverage heterogeneity in the country and in the world, but then everybody is too busy to be able to see a patient right away. And so, this gap impairs the quality of patient care. And this is why despite all this technology, despite the future, despite AI, we teach ophthalmologists and neurologists how to do a neuro-op examination, how to use it for localization, how to use it to increase the value and the power of a good neurologic examination so that nothing is missed. And I'm taking a very simple example. Neurologists see patients with headaches all the time. The vast majority of those headaches are benign headaches. 90% of headache patients are either migraine or tension headache or analgesic abuse headaches, but they are not secondary headache that are life threatening or neurologically threatening. If the patient has papilledema, it's a huge retina that really should prompt immediate workup, immediate prevention of vision loss with the help of the ophthalmologist. And unfortunately, that's often delayed because the patients with headaches do not see eye doctors. They see their primary care providers who does not examine the back of the eye, and then they reach neurology sometimes too late. And when the neurologist is comfortable with the ophthalmoscope, then the papilledema is identified. But when the neurologist is not comfortable with the ophthalmoscope, then the patient is either misdiagnosed or sent to an eye care provider who makes the diagnosis. But there is always a delay in care. You know, most patients end up with a correct diagnosis because people know what to do. But the problem is the delay in appropriate care in those patients. And that's where technology is a complete life-changing experience. And, you know, I want to highlight that I am not blaming neurologists for not looking at the back of the eye with a direct ophthalmoscope without pharmacologic dilation of the pupil. It is not possible to do that reliably. The first thing I learned when I transitioned from a neurologist to an ophthalmologist is that no eye care provider ever attempts to look at the back of the eyes without dilating the pupils because it's too hard. Why do we ask neurologists to do it? It's really unfair, correct? And then the ophthalmoscope is such an archaic tool that gives only a very small portion of the back of the eye and is extraordinarily difficult to use. It's really not fair. And so, until we give the appropriate tools to neurologists, I don't think we should complain about neurologists not being reliable when they look at the back of the eye. It's a major issue.  Dr Jones: I appreciate you giving us some absolution there. I don't think we would ask neurologists to check reflexes but then not give them a reflex hammer, right? So maybe that's the analogy to not dilating the pupil. So, for you and your practice, in our closing minutes here, Dr Biousse, what's the most rewarding thing for you in neuro-ophthalmology? What do you find most rewarding in the care of these patients?  Dr Biousse: Well, I think the most rewarding is the specialty itself. I'm a neurologist at heart. This is where my heart belongs. What's great about those neuro-ophthalmology patients is that it is completely unpredictable. They are unpredictable. They can have anything. I am super specialized because I'm a neuro-ophthalmologist, but I am a general neurologist and I see everything in neurology. So my clinic days are fascinating. I never know what's going to happen. So that's, I think, the most rewarding part of my job as an neuro-ophthalmologist. I'm having fun every day because it's never the same, I never know what's going to happen. But at the same time, we are so useful to those patients. When you use the neuro-ophthalmologic examination, you really can provide exquisite localization of the disease. You're better than the best of the MRIs. And when you know the localization, your differential diagnosis is always right, always correct, and you can really help patients. And then I want to highlight one point that we made sure was covered in this issue of Continuum, which is the symptomatic treatment of patients who have visual disturbances from neurologic disorders. You know, a patient with chronic diplopia is really disabled. A patient with decreased vision cannot function. And being able to treat the diplopia and provide the low vision resources to those patients who do not see well is extremely important for the quality of life of our patients with neurologic disorders. When you don't walk well, if you don't see well, you fall. When you're cognitively impaired, if you don't see well, you are very cognitively impaired. It makes everything worse. When you see double, you cannot function. When you have a homonymous anopia, you should not drive. And so, there is a lot of work in the field of rehabilitation that can greatly enhance the quality of life of those patients. And that really covers the entire field of neurology and is very, very important. Dr Jones: Clearly important work, and very exciting. And your enthusiasm is contagious, Dr Biousse. I can see how much you enjoy this work. And it comes through, I think, in this interview, but I think it also comes through in the articles and the experts that you have. And I'd like to thank you again for joining us today for a great discussion of neuro-ophthalmology. I learned a lot, and hopefully our listeners did too.  Dr Biousse: Thank you very much. I really hope you enjoyed this issue. Dr Jones: Again, we've been speaking with Dr Valerie Biousse, guest editor of Continuum's most recent issue on neuro-ophthalmology. Please check it out, 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 this 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.

     Unlock the secrets of exceptional leadership with BG(R) William T. Bester, RN, MSN, FAAN, as he shares transformative insights from his illustrious 32-year military career. What if leadership is more about breaking down barriers than giving orders? Discover how BG(R) Bester's commitment to removing obstacles, fostering open communication, and embracing the expertise within his teams has shaped his approach to leadership. His candid reflections on avoiding micromanagement and encouraging collaboration will inspire leaders from all backgrounds to rethink how they guide their teams.      Gain a deeper understanding of the power of personal connection in leadership. BG(R) Bester's daily practice of connecting with team members underscores the importance of trust and genuine interest in personal and professional lives. By actively engaging with those he leads, he ensures that their voices are heard, fostering an environment where informed decision-making and committed buy-in thrive. This conversation is a treasure trove of wisdom for anyone seeking to prioritize people and cultivate a setting where trust and collaboration are at the forefront.   Take Home Messages: Empowerment Through Barrier Removal: Effective leadership involves empowering team members by removing obstacles and avoiding micromanagement. This approach fosters a more autonomous and motivated team environment. Inclusive Decision-Making: Engaging those who are directly impacted by decisions in the decision-making process ensures better outcomes and greater buy-in, as it incorporates diverse perspectives and insights. Building Trust Through Personal Engagement: Regular personal engagement with team members builds trust and understanding, allowing leaders to focus on areas that need attention while appreciating what is working well. Transparent Communication During Challenges: In challenging situations, maintaining open and transparent communication helps keep team members informed and focused, alleviating uncertainty and fostering unity. The Importance of Mentorship: Mentorship is a crucial responsibility for leaders, providing guidance and support to junior professionals. This helps them navigate their career paths effectively and builds a culture of continuous learning and development.   Episode Keywords: Brigadier General Bill Bester, leadership insights, military medicine, empowering leadership, Army Nurse Corps, War Docs podcast, empathy in leadership, inclusive teams, micromanagement, open communication, transformative leadership, decision-making process, mentorship in military, trust-building, personal engagement, leadership challenges, leadership philosophy, leadership development, military medical professionals, War Docs series, Jeff Clark   Hashtags: #LeadershipInsights #MilitaryMedicine #EmpoweringLeadership #BrigadierGeneralBester #LeadershipPhilosophy #InclusiveLeadership #EmpathyInLeadership #TrustAndConnection #WarDocsPodcast #OpenCommunication   Honoring the Legacy and Preserving the History of Military Medicine The WarDocs Mission is to honor the legacy, preserve the oral history, and showcase career opportunities, unique expeditionary experiences, and achievements of Military Medicine. We foster patriotism and pride in Who we are, What we do, and, most importantly, How we serve Our Patients, the DoD, and Our Nation.   Find out more and join Team WarDocs at https://www.wardocspodcast.com/ Check our list of previous guest episodes at https://www.wardocspodcast.com/our-guests Subscribe and Like our Videos on our YouTube Channel: https://www.youtube.com/@wardocspodcast Listen to the “What We Are For” Episode 47. https://bit.ly/3r87Afm   WarDocs- The Military Medicine Podcast is a Non-Profit, Tax-exempt-501(c)(3) Veteran Run Organization run by volunteers. All donations are tax-deductible and go to honoring and preserving the history, experiences, successes, and lessons learned in Military Medicine. A tax receipt will be sent to you. WARDOCS documents the experiences, contributions, and innovations of all military medicine Services, ranks, and Corps who are affectionately called "Docs" as a sign of respect, trust, and confidence on and off the battlefield,demonstrating dedication to the medical care of fellow comrades in arms.     Follow Us on Social Media Twitter: @wardocspodcast Facebook: WarDocs Podcast Instagram: @wardocspodcast LinkedIn: WarDocs-The Military Medicine Podcast YouTube Channel: https://www.youtube.com/@wardocspodcast    

CRNAs take pride in the precision and care that goes into every procedure, but what happens when things don't go as planned? In the high-stakes world of healthcare, when something goes wrong, the patient isn't the only one affected. Today we're going to shine a light on Second Victim Syndrome—the emotional trauma healthcare professionals experience following adverse patient events. Joined by Maria van Pelt, PhD, CRNA, CNE, CPPS, FAAN, FAANA and Luci New, DNP, CRNA, FAANA we'll share personal stories and professional insight on this overlooked phenomenon. Here's some of what we discuss in this episode:

Despite advances in epilepsy management, disparities and lack of inclusion of many people with epilepsy are associated with increased morbidity and mortality. Improving awareness and promoting diversity in research participation can advance treatment for underserved populations and improve trust. In this episode, Teshamae Monteith, MD, PhD, FAAN speaks Dave F. Clarke, MBBS, FAES, author of the article “Diversity and Underserved Patient Populations in Epilepsy,” in the Continuum® February 2025 Epilepsy issue. Dr. Monteith is a Continuum® Audio interviewer and an 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. Clarke is the Kozmetsky Family Foundation Endowed Chair of Pediatric Epilepsy and Chief or Comprehensive Pediatric Epilepsy Center, Dell Medical School at the University of Texas at Austin in Austin, Texas. Additional Resources Read the article: Diversity and Underserved Patient Populations in Epilepsy Subscribe to Continuum: shop.lww.com/Continuum Earn CME (available only to AAN members): continpub.com/AudioCME Continuum® Aloud (verbatim audio-book style recordings of articles available only to Continuum® subscribers): continpub.com/Aloud More about the American Academy of Neurology: aan.com Social Media facebook.com/continuumcme @ContinuumAAN Host: @HeadacheMD Full episode transcript available here Dr Jones: This is Dr Lyell Jones, Editor-in-Chief of Continuum, the premier topic-based neurology clinical review and CME journal from the American Academy of Neurology. Thank you for joining us on Continuum Audio, which features conversations with Continuum's guest editors and authors who are the leading experts in their fields. Subscribers to the Continuum Journal can read the full article or listen to verbatim recordings of the article and have access to exclusive interviews not featured on the podcast. Please visit the link in the episode notes for more information on the article, subscribing to the journal, and how to get CME. Dr Monteith: This is Dr Teshamae Monteith. Today I'm interviewing Dr Dave Clarke about his article on diversity and underserved patient populations in epilepsy, which appears in the February 2025 Continuum issue on epilepsy. So why don't you introduce yourself to our audience? Dr Clarke: Sure. My name is Dr Dave Clarke, as alluded to. I'm presently at the University of Texas in Austin, originating from much farther south. I'm from Antigua, but have been here for quite a while working within the field in epilepsy surgery, but more and more getting involved in outreach, access to care, and equity of healthcare in epilepsy. Dr Monteith: And how did you get involved in this kind of work? Dr Clarke: That's an amazing question. You know, I did it in a bit of a inside out fashion. I initially started working in the field and trying to get access to persons in the Caribbean that didn't have any neurological care or investigative studies, but very quickly realized that persons around the corner here in Texas and wherever I've worked have had the exact same problems, getting access via fiscal or otherwise epilepsy care, or geographically getting access, with so few having neurologists close at hand. Therefore, I started working both on a regional, national, and it transcended to a global scale. Dr Monteith: Wow, so you're just everywhere. Dr Clarke: Well, building bridges. I've found building bridges and helping with knowledge and garnering knowledge, you can expand your reach without actually moving, which is quite helpful. Dr Monteith: Yeah. So why don't you tell us why you think this work is so important in issues of diversity, underserved populations, and of course, access to epilepsy care? Dr Clarke: Sure, not a problem. And I think every vested person in this can give you a different spiel as to why they think it's important. So, I'll add in a few facts pertaining to access, but also tell you about why I think personally that it's not only important, but it will improve care for all and improve what you believe you could do for a patient. Because the sad thing is to have a good outcome in the United States presently, we have over three hundred epilepsy centers, but they have about eight or nine states that don't have any epilepsy centers at all. And even within states themselves, people have to travel up to eight hours, i.e., in Texas, to get adequate epilepsy care. So that's one layer. Even if you have a epilepsy center around the corner, independent of just long wait times, if you have a particular race or ethnicity, we've found out that wait may be even longer or you may be referred to a general practitioner moreso than being referred to an epilepsy center. Then you add in layers of insurance or lack thereof, which is a big concern regardless of who you are; poverty, which is a big concern; and the layers just keep adding more. Culture, etcetera, etcetera. If you could just break down some of those barriers, it has been shown quite a few years ago that once you get to an epilepsy center, you can negate some of those factors. You can actually reduce time to access and you can improve care. So, that's why I'm so passionate about this, because something could potentially be done about it. Dr Monteith: That's cool. So, it sounds like you have some strategies, some strategies for us. Dr Clarke: Indeed. And you know, this is a growth and this is a learning curve for me and will be for others. But I think on a very local, one-to-one scale, the initial strategy I would suggest is you have to be a good listener. Because we don't know how, when, where or why people are coming to us for their concerns. And in order to judge someone, if they may not have had a follow-up visit or they may not have gotten to us after five medications, the onus may not have been on that person. In other words, as we learned when we were in medical school, history is extremely important, but social history, cultural history, that's also just as important when we're trying to create bridges. The second major thing that we have to learn is we can't do this alone. So, without others collaborating with us outside of even our fields, the social worker who will engage, the community worker who will discuss the translator for language; unless you treat those persons with respect and engage with those persons to help you to mitigate problems, you'll not get very far. And then we'll talk about more, but the last thing I'll say now is they have so many organizations out there, the Institute of Medicine or the International League Against Epilepsy or members of the American Epilepsy Society, that have ways, ideas, papers, and articles that can help guide you as to how better mitigate many of these problems. Dr Monteith: Great. So, you already mentioned a lot of things. What are some things that you feel absolutely the reader should take away in reading your article? You mentioned already listening skills, the importance of interdisciplinary work, including social work, and that there are strategies that we can use to help reduce some of this access issues. But give me some of the essential points and then we'll dive in. Dr Clarke: OK. I think first and foremost we have to lay the foundation in my mind and realize what exactly is happening. If you are Native American, of African descent, Hispanic, Latinx, geographically not in a region where care can be delivered, choosing one time to epilepsy surgery may be delayed twice, three, four times that of someone of white descent. If you are within certain regions in the US where they may have eight, nine, ten, fourteen epilepsy centers, you may get to that center within two to three years. But if you're in an area where they have no centers at all, or you live in the Dakotas, it may be very difficult to get to an individual that could provide that care for you. That's very, very basic. But a few things have happened a few years ago and even more recently that can help. COVID created this groundswell of ambulatory engagement and ambulatory care. I think that can help to mitigate time to get into that person and improving access. In saying that, there are many obstacles to that, but that's what we have to work towards: that virtual engagement and virtual care. That would suggest in some instances to some persons that it will take away the one-to-one care that you may get with persons coming to you. But I guarantee that you will not lose patients because of this, because there's too big a vacuum. Only 22% of persons that should actually get to epilepsy centers actually get to epilepsy centers. So, I think we can start with that foundation, and you can go to the article and learn a lot more about what the problems are. Because if you don't know what the problems are, you can't come up with solutions. Dr Monteith: Just give us a few of the most persistent inequities and epilepsy care? Dr Clarke: Time to seeing a patient, very persistent. And that's both a disparity, a deficiency, and an inequity. And if you allow me, I'll just explain the slight but subtle difference. So, we know that time to surgery in epilepsy in persons that need epilepsy surgery can be as long as seventeen years. That's for everyone, so that's a deficiency in care. I just mentioned that some sociodemographic populations may not get the same care as someone else, and that's a disparity between one versus the other. Health equity, whether it be from NIH or any other definition, suggests that you should get equitable care between one person and the other. And that brings in not only medical, medicolegal or potential bias, that we may have one person versus the other. So, there's a breakdown as to those different layers that may occur. And in that I'm telling you what some of the potential differences are. Dr Monteith: And so, you mentioned, it comes up, race and ethnicity being a major issue as well as some of the geographic factors. How does that impact diagnosis and really trying to care for our patients? Dr Clarke: So again, I'm going to this article or going to, even. prior articles. It has been shown by many, and most recently in New Jersey, that if you're black, Hispanic, Latin- Latinx, it takes you greater than two times the time to surgery. Reduced time to surgery significantly increases morbidity. It potentially increases mortality, as has been shown by a colleague of mine presently in Calgary. And independent of that, we don't look at the other things, the other socially related things. Driving, inability to work, inability to be adequately educated, the stigma related to that in various cultures, various countries. So, that deficit not only increased the probability of having seizures, but we have to look at the umbrella as to what it does. It significantly impacts quality of life of that individual and, actually, the individuals around them. Dr Monteith: So, what are some of these drivers, and how can we address them, or at least identify them, in our clinic? Dr Clarke: That's a question that's rather difficult to answer. And not because there aren't ideas about it, but there's actually mitigating those ideas or changing those ideas we're just presently trying to do. Although outlines have been given. So, in about 2013, the federal government suggested outlines to improve access and to reduce these inequities. And I'll just give you a few of them. One of those suggestions was related to language and having more improved and readily available translators. Something simple, and that could actually foster discussions and time to better management. Another suggestion was try to train more persons from underserved populations, persons of color. Reason being, it has been shown in the social sciences and it is known in the medical sciences that, if you speak to a person of similar culture, you tend to have a better rapport, you tend to be more compliant, and that track would move forward, and it reduces bias. Now we don't have that presently, and I'm not sure if we'll have that in the near future, although we're trying. So then, within your centers, if you have trainings on cultural sensitivity, or if you have engagements and lectures about how you can engage persons from different populations, those are just some very simple pearls that can improve care. This has been updated several times with the then-Institute of Medicine in 2012, 2013, they came out with, in my mind, a pretty amazing article---but I'm very biased---in which they outline a number of strategic initiatives that could be taken to improve research, improve clinical care, improve health equity through health services research, to move the field forward, and to improve overall care. They updated this in 2020, and it's a part of the 2030 federal initiative not only for epilepsy, but to improve overarching care. All of this is written in bits and pieces and referenced in the article. To add icing on top, the World Health Organization, through advocacy of neurological groups as well as the International League Against Epilepsy and the AES, came out with the Intersectoral Action Plan on Epilepsy and Other Neurological Diseases, which advocates for parallel improvement in overall global care. And the United States have signed on to it, and that have lit a fire to our member organizations like the American Epilepsy Society, American Academy of Neurology, and others, trying to create initiatives to address this here. I started off by saying this was difficult because, you know, we have debated epilepsy care through 1909 when the International League against Epilepsy was founded, and we have continually come up with ways to try and advance care. But this have been the most difficult and critical because there's social dynamics and social history and societal concerns that have negated us moving forward in this direction. But fortunately, I think we're moving in that direction presently. That's my hope. And the main thing we have to do is try to sustain that. Dr Monteith: So, you talked about the importance of these global initiatives, which is huge, and other sectors outside of neurology. Like for example, technology, you spoke about telemedicine. I think you were referring to telemedicine with COVID. What other technologies that are more specific to the field of epilepsy, some of these monitorings that maybe can be done? Dr Clarke: I was just going to just going to jump on that. Thank you so much for asking. Dr Monteith: I have no disclosures in this field. I think it's important and exciting to think how can we increase access and even access to monitoring some of these technologies. That might be expensive, which is another issue, but…. Dr Clarke: So, the main things in epilepsy diagnosis and management: you want to hear from the patient history, you want to see what the seizures look like, and then you want to find ways in which to monitor those seizures. Hearing from the patient, they have these questionnaires that have been out there, and this is local, regional, global, many of them standardized in English and Spanish. Our colleagues in Boston actually created quite a neat one in English and Spanish that some people are using. Ecuador has one. We have created someone- something analogous. And those questionnaires can be sent out virtually and you can retrieve them. But sometimes seeing is believing. So, video uploads of seizures, especially the cell phone, I think has been management-changing for the field of epilepsy. The thing you have to do however, is do that in a HIPAA-compliant way. And several studies are ongoing. In my mind, one of the better studies here was done on the East Coast, but another similar study, to be unnamed, but again, written out in the articles. When you go into these apps, you can actually type in a history and upload a video, but the feed is not only going to you, it may be going to the primary care physician. So, it not only helps in one way in you educating the patient, but you educate that primary care physician and they become extenders and providers. I must add here my colleagues, because we can't do without them. Arguably in some instances, some of the most important persons to refer patients, that's the APPs, the PAs and the nurse practitioners out there, that help to refer patients and share patients with us. So, that's the video uploads they're seeing. But then the other really cool part that we're doing now is the ambulatory world of EEGs. Ceribell, Zeto, to name of few, in which you could potentially put the EEG leads on persons with or without the EEG technologist wirelessly and utilize the clouds to review the EEGs. It's not perfect just yet, but that person that has to travel eight hours away from me, if I could do that and negate that travel when they don't have money to pay for travel or they have some potential legal issues or insurance-related issues and I could read the EEG, discuss with them via telemedicine their care, it actually improves access significantly. I'm going to throw in one small twist that, again, it's not perfect. We're now trying to monitor via autonomic features, heart rate movement and others, for seizures and alert family members, parents, because although about 100,000 people may be affected with epilepsy, we're talking about 500,000 people who are also affected that are caregivers, affiliates, husbands, wives, etcetera. Just picture it: you have a child, let's say three, four years old and every time they have a seizure- or not every time, but 80% of times when they have a seizure, it alerts you via your watch or it alerts you in your room. It actually gives that child a sense of a bit more freedom. It empowers you to do something about it because you can understand here. It potentially negates significant morbidity. I won't stretch it to say SUDEP, but hopefully the time will come when actually it can prevent not only morbidity, but may prevent death. And I think that's the direction we are going in, to use technology to our benefit, but in a HIPAA-compliant way and in a judicious way in order to make sure that we not only don't overtreat, but at the end of the day, we have the patient as number one, meaning everything is vested towards that patient and do no harm. Dr Monteith: Great. One thing you had mentioned earlier was that there are even some simple approaches, efficiency approaches that we can use to try and optimize care for all in our clinics. Give me what I need to know, or do. Give me what I need to do. Dr Clarke: Yeah, I'll get personal as to what we're trying to do here, if you don't mind. The initial thing we did, we actually audited care and time to care delivery. And then we tried to figure out what we could do to improve that access and time to care, triaging, etcetera. A very, very simple thing that can be done, but you have to look at costs, is to have somebody that actually coordinates getting persons in and out of your center. If you are a neurologist that works in private practice, that could potentially be a nurse being associated directly one-and-one with one of the major centers, a third- or fourth-level center. That coordination is key. Educate your nurses about epilepsy care and what the urgent situations are because it will take away a lot of your headache and your midnight calls because they'll be able to know what to do during the day. Video uploads, as I suggested, regardless of the EMR that you have, figure out a way that a family could potentially send a video to you, because that has significantly helped in reducing investigative studies. Triaging appropriately for us to know what patients we can and cannot see. Extenders has helped me significantly, and that's where I'll end. So, as stated, they had many neurologists and epileptologists, and utilizing appropriately trained nurse practitioners or residents, engaging with them equally, and/or social workers and coordinators, are very helpful. So hopefully that's just some low-hanging fruit that can be done to improve that care. Dr Monteith: So why don't you give us some of your major takeaways to how we can improve epilepsy care for all people? Dr Clarke: I've alluded to some already, but I like counts of threes and fives. So, I think one major thing, which in my mind is a major takeaway, is cultural sensitivity. I don't think that can go too far in improving care of persons with epilepsy. The second thing is, if you see a patient that have tried to adequately use medications and they're still having seizures, please triage them. Please send them to a third- or fourth-level epilepsy center and demand that that third- or fourth-level epilepsy center communicate with you, because that patient will eventually come back and see you. The third thing---I said three---: listen to your patients. Because those patients will actually help and tell you what is needed. And I'm not only talking about listening to them medication-wise. I know we have time constraints, but if you can somehow address some of those social needs of the patients, that will also not only improve care, but negate the multiple calls that you may get from a patient. Dr Monteith: You mentioned a lot already. This is really wonderful. But what I really want to know is what you're most hopeful about. Dr Clarke: I have grandiose hopes, I'll tell you. I'll tell you that from the beginning. My hope is when we look at this in ten years and studies are done to look at equitable care, at least when it comes to race, ethnicity, insurance, we'll be able to minimize, if not end, inequitable care. Very similar to the intersectoral action plan in epilepsy by 2030. I'll tell you something that suggests, and I think it's global and definitely regional, the plan suggests that 90% of persons with epilepsy should know about their epilepsy, 80% of persons with epilepsy should be able to receive appropriate care, and 70% of persons with epilepsy should have adequately controlled epilepsy. 90, 80, 70. If we can get close to that, that would be a significant achievement in my mind. So, when I'm chilling out in my home country on a fishing boat, reading EEGs in ten years, if I can read that, that would have been an achievement that not necessarily I would have achieved, but at least hopefully I would have played a very small part in helping to achieve. That's what I think. Dr Monteith: Awesome. Dr Clarke: I appreciate you asking me that, because I've never said it like that before. In my own mind, it actually helped with clarity. Dr Monteith: I ask great questions. Dr Clarke: There you go. Dr Monteith: Thank you so much. I really- I really appreciate your passion for this area. And the work that you do it's really important, as you mentioned, on a regional, national, and certainly on a global level, important to our patients and even some very simple concepts that we may not always think about on a day-to-day basis. Dr Clarke: Oh, I appreciate it. And you know, I'm always open to ideas. So, if others, including listeners, have ideas, please don't hesitate in reaching out. Dr Monteith: I'm sure you're going to get some messages now. Dr Clarke: Awesome. Thank you so much. Dr Monteith: Thank you. I've been interviewing Dr Dave Clarke about his article on diversity and underserved patient populations in epilepsy, which appears in the most recent issue of Continuum on epilepsy. 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 this 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.

On episode 510 of The Nurse Keith Show nursing and healthcare career podcast, Keith interviews Dr. Karen Myrick, DNP, APRN, FNP, FAANP, FAAN, a nurse practitioner, educator, researcher, author, and leader in nursing education. As Director of Nursing Education and Practice at Springer Publishing, Dr. Myrick focuses on developing innovative learning resources, including video on-demand products that speak to the needs of 21st-century nurses. In the course of their conversation, Keith and Dr. Myrick discuss the importance of certification in the careers of nurse practitioners, and the learning styles, pedagogies, and technologies that support NP success in the spheres of certification and professional advancement. Karen Myrick, DNP, APRN, FNP-BC, ONP-BC, FAANP, FAAN, is a nurse practitioner, educator, researcher, author, and leader in nursing education specializing in orthopedics, sports medicine, and advanced practice training. She practices at Orthopedic Associates of Hartford Urgent Care, providing expert musculoskeletal care. Karen is the Director of Nursing Education and Practice at Springer Publishing, where she develops innovative learning resources, including the FNP and AGNP Video on Demand Review, to support NP students and practicing clinicians. She is also a full tenured professor at multiple universities and serves as Program Director for the Post-Master's Certificate Program in Orthopedics and Sports Medicine at Massachusetts General Hospital Orthopedic Academy. Additionally, she teaches at Plus One Defense Systems, integrating healthcare knowledge with self-defense training. An author of multiple textbooks and a well-published researcher, Karen has received numerous grants and awards for her contributions to nursing and healthcare. A Fellow of the American Association of Nurse Practitioners (FAANP) and the American Academy of Nursing (FAAN), she is dedicated to advancing NP education, research, and clinical excellence This episode of the Nurse Keith Show is brought to you in collaboration with Springer Publishing, who have been delivering award-winning healthcare education and exam prep materials focused on nursing, behavioral health, and the health sciences for more than 70 years. We thank Springer Publishing for their support. Connect with Dr. Karen Myrick and Springer Publishing: Dr. Myrick on LinkedIn SpringerPub.com Contact Nurse Keith about holistic career coaching to elevate your nursing and healthcare career at NurseKeith.com. Keith also offers services as a motivational and keynote speaker and freelance nurse writer. You can always find Keith on LinkedIn. Are you looking for a novel way to empower your career and move forward in life? Keith's wife, Shada McKenzie, is a gifted astrologer and reader of the tarot who combines ancient and modern techniques to provide valuable insights into your motivations, aspirations, and life trajectory, and she offers listeners of The Nurse Keith Show a 10% discount on their first consultation. Contact Shada at TheCircelandtheDot.com or shada@thecircleandthedot.com.

At the seventh BizNews Conference BNC#7, WeBuyCars CEO Faan van der Walt shared the remarkable journey of how he and his brother Dirk turned a small backyard car-trading venture into a multi-billion-rand powerhouse. With no business plan and plenty of hard lessons, they navigated the challenges of scaling, digitalization, and market disruptions. Van der Walt's keynote offered an inside look at the principles, persistence, and pivotal moments that built one of South Africa's most successful automotive businesses. In a Q&A session with Bronwyn Nielsen, Faan van der Walt was joined by WeBuyCars co-founder Dirk van der Walt and they delved deeper into the company's culture, marketing strategy, and challenges of operating in South Africa's tough economic climate. They shared insights on leadership, recruitment, and the transition from a startup to a listed powerhouse. The session also covered the evolution of instant payments, their approach to growth without business plans, and the art of managing risk in a fast-moving industry.

Faan van der Walt, uitvoerende hoof van WeBuyCars, gesels oor hulle planne om motors meganies te laat ondersoek. Volg RSG Geldsake op Twitter

“You can give someone a survivorship care plan, but just giving them doesn't mean that it's going to happen. Maybe there's no information about family history. Or maybe there's information and there's quite a bit of family history, but there's nothing that says, ‘Oh, they were ever had genetic testing,' or ‘Oh, they were ever referred.' So the intent is so good because it's to really take that time out when they're through with active treatment and, you know, try to help give the patient some guidance as to what to expect down the line,” Suzanne Mahon, DNS, RN, AOCN®, AGN-BC, FAAN, professor emeritus at Saint Louis University in Missouri, told Jaime Weimer, MSN, RN, AGCNS-BS, AOCNS®, manager of oncology nursing practice at ONS, during a conversation about breast cancer survivorship.   Music Credit: “Fireflies and Stardust” by Kevin MacLeod  Licensed under Creative Commons by Attribution 3.0   Earn 0.75 contact hours of nursing continuing professional development (NCPD) by listening to the full recording and completing an evaluation at courses.ons.org by March 14, 2027. The planners and faculty for this episode have no relevant financial relationships with ineligible companies to disclose. ONS is accredited as a provider of nursing continuing professional development by the American Nurses Credentialing Center's Commission on Accreditation.  Learning outcome: Learners will report an increase in knowledge related to breast cancer survivorship.  Episode Notes   Complete this evaluation for free NCPD.   Previous ONS Podcast™ site-specific episodes: Episode 350: Breast Cancer Treatment Considerations for Nurses  Episode 348: Breast Cancer Diagnostic Considerations for Nurses  Episode 345: Breast Cancer Screening, Detection, and Disparities  ONS Voice articles: Breast Cancer Prevention, Screening, Diagnosis, Treatment, Side Effect, and Survivorship Considerations  Improve Management of Common Symptoms for Breast Cancer Survivors  Nursing Considerations for Breast Cancer Survivorship Care  Sexual Considerations for Patients With Cancer ONS books:  Breast Care Certification Review (second edition)  Guide to Breast Care for Oncology Nurses  ONS course: Breast Cancer Bundle  ONS Learning Libraries:  Breast Cancer  Genomics and Precision Oncology  Nurse Navigation  Oral Anticancer Medication   Survivorship  ONS Guidelines™ and Symptom Interventions:  Anxiety  Cognitive Impairment  Depression  Fatigue  Clinical Journal of Oncology Nursing article: Survivorship Care: More Than Checking a Box  Clinical Journal of Oncology Nursing supplement: Survivorship Care  American Cancer Society:  Cancer Treatment and Survivorship Facts and Figures  Survivorship: During and After Treatment  Livestrong® Program at the YMCA  National Comprehensive Cancer Network  National Cancer Institute Breast Cancer—Patient Version    To discuss the information in this episode with other oncology nurses, visit the ONS Communities.   To find resources for creating an ONS Podcast Club in your chapter or nursing community, visit the ONS Podcast Library.  To provide feedback or otherwise reach ONS about the podcast, email pubONSVoice@ons.org.  Highlights From This Episode  “I think the biggest thing is to really communicate is that people are living with breast cancer for a long, long periods of time, and a lot of that with really good quality overall.” TS 4:07   “As a general rule, they're going to be seen by the breast surgeon probably every four to six months for a while. After about five years, a lot of times people are ready to say, ‘Okay, annually is okay.' And eventually they may let that drop off. But it also depends on did they have a mastectomy? Did they have breast conserving surgery? And then if they had reconstruction with an implant, how often do they see the plastic surgeon? Because they need to check integrity of the implant. So those schedules are really individualized.” TS 13:24  “When you think about long-term effects, I think you need to kind of think about that survivors can have both acute and long-term chronic effects. And a lot of that depends on the specifics of the treatment they had. I think as oncology nurses, we're used to, ‘We give you this chemotherapy or this agent, and these are the side effects.'” TS 15:36  “The diet issues are huge. And I think we are slow to refer to the dietician, you know, you can get them a couple of consults and because you're saying to them, ‘This is really important. We need you to lose weight or we need you to eat more of this.' Ideally, fruits and vegetables are going to be about half of your plate. And what's the difference between a whole grain and not, less processed foods, making sure that they're getting enough protein. And then once again, really kind of making sure that they're not taking a lot of supplements and extra stuff because we don't really understand all that fully and it could be harmful.” TS 34:53  “Breast cancer is a long, long journey, and I think you should never underestimate the real difference that nurses can make. I think they can ask those tough questions. And I think ask the questions that are important to patients that patients may be reluctant to ask. I think giving patients permission to talk about those less-talked-about symptoms and acknowledge that those symptoms are real and that there are some strategies to mitigate those symptoms.” TS 42:28   

In this episode, Kathy Sanford, DBA, RN, FAAN, Senior Executive Vice President and Chief Nursing Officer at CommonSpirit Health, discusses the health system's innovative approach to nursing, including virtual care models, workforce development, and the next five-year strategic plan. Tune in to hear how CommonSpirit is tackling staffing challenges, enhancing patient care, and preparing for the future of healthcare.

“The response was, in my opinion, sort of overwhelmingly positive. I think all of us old-timers who were at ONS Congress® in 1986 remember those 1,600 nurses waiting in line to enter the ballroom to take that inaugural exam. It takes a while to check in 1,600 people. They kind of all filled up the lobby outside of the ballroom, and then they spilled over down into the escalator, and the escalators had to be turned off,” Cyndi Miller-Murphy, MSN, FAAN, CAE, first executive director of the Oncology Nursing Certification Corporation (ONCC), told Clara Beaver, DNP, RN, AOCNS®, ACNS-BC, ONS member and member of the ONS 50th anniversary committee, during a conversation about the evolution of oncology nursing certification. Beaver spoke with Tony Ellis, MSEd, CAE, ICE-CCP, executive director of ONCC, and Miller-Murphy about the history, current landscape, and future of certification in oncology nursing. Music Credit: “Fireflies and Stardust” by Kevin MacLeod Licensed under Creative Commons by Attribution 3.0  Episode Notes  NCPD contact hours are not available for this episode.  ONS Podcast™ episodes: Episode 254: Oncology Nursing Certification Affects the Entire Cancer Care System Episode 186: Certification Can Fuel Your Leadership Skills and Professional Growth ONS Voice articles: Certification Was a Critical Step Along My Oncology Nursing Career Journey OCN® Certification Test-Taking Tips to Ease Your Anxiety ONS books: Advanced Oncology Nursing Certification Review and Resource Manual (third edition) Breast Care Certification Review (second edition) BMTCN® Certification Review Manual (second edition) Core Curriculum for Oncology Nursing (seventh edition) Study Guide for the Core Curriculum for Oncology Nursing (seventh edition) ONS courses: OCN® Certification Review Bundle ONS AOCNP® Certification Review Bundle™ Clinical Journal of Oncology Nursing article: Findings From the 2023 Radiation Oncology Nursing Role Delineation Study to Shape the Future of the Subspecialty Oncology Certification for Nurses: Joint Position Statement From the Oncology Nursing Society and the Oncology Nursing Certification Corporation ONCC website Connie Henke Yarbro Oncology Nursing History Center To discuss the information in this episode with other oncology nurses, visit the ONS Communities. To find resources for creating an ONS Podcast Club in your chapter or nursing community, visit the ONS Podcast Library. To provide feedback or otherwise reach ONS about the podcast, email pubONSVoice@ons.org. Highlights From This Episode Miller-Murphy: “Oncology nursing is a highly specialized area with a broad, well-defined body of knowledge, and it's essential for employees and healthcare consumers to be able to identify nurses who have demonstrated that they possess the knowledge that's necessary to practice competently in the specialty. Nurses who become certified take that essential step to publicly demonstrate their knowledge. And I believe this makes them a known commodity, so to speak.” TS 1:49 Ellis: “Oncology nursing is an area of high-stakes patient care, and a core purpose of certification is to safeguard the public. This is certainly an area of health care that benefits from having that role of professional certification being played, from the knowledge requirements to the practice hours that a nurse must have, to the performance on the exam and continued competence required to maintain the certification. Our certifications hold nurses to a higher standard, which helps protect the public in the care that they provide.” TS 2:45 Miller-Murphy: “A group of, I think, 200 nurses got together at an American Cancer Society conference back in 1980 to discuss the desire for certification in ontology. Nurses wanted a way to verify their specialized knowledge and skills. They wanted to raise the level of professionalism, and ONS was the most appropriate organization to develop the certifications. And by 1983, a survey of members revealed strong interest in specialty certification in oncology.” TS 5:29 Ellis: “The pace of change in oncology care is really the challenge for certification programs proper right now. There's so many wonderful advances—oncology treatments and drugs that are coming to the market that are being used in non-oncology settings and other advancements in the practice, that keeping up with that change puts pressure on certification programs because they must validate knowledge and practice that has become standard. It has to have been in the practice long enough that whatever the content, whatever the practice is that you're testing on, that there is one single correct answer. So you can't necessarily test on the very latest of what has come to the market or to the practice. The other flipside of that is that pace of change, the new emerging things in the practice create opportunities for other kinds of credentials.” TS 24:31 Ellis: “What we have found is that there are thousands and thousands of oncology nurses that are practicing at a level and doing specialized work beyond the scope of the OCN® body of knowledge—so at the master's level, PhD, especially with the advent of the DNP, and there is work there. And this really came out of our work to update the advanced oncology nurse competencies. … So the new certification is the Advanced Certified Oncology Nurse, or the ACON. In certification, and it is suited for those nurses that are practicing at that higher level.” TS 32:52

Emergency treatment may be necessary after a person's first seizure or at the onset of abnormal acute repetitive (cluster) seizures; it is required for status epilepticus. Treatment for these emergencies is dictated by myriad clinical factors and informed by published guidance as well as emerging research.   In this episode, Lyell K. Jones, MD, FAAN, speaks with David G. Vossler, MD, FAAN, FACNS, FAES, author of the article “First Seizures, Acute Repetitive Seizures, and Status Epilepticus,” in the Continuum® February 2025 Epilepsy issue. 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. Vossler a clinical professor of neurology at the University of Washington School of Medicine in Seattle, Washington. Additional Resources Read the article: First Seizures, Acute Repetitive Seizures, and Status Epilepticus 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: @LyellJ  Full episode transcript available here Dr Jones: This is Dr Lyell Jones, Editor-in-Chief of Continuum, the premier topic-based neurology clinical review and CME journal from the American Academy of Neurology. Thank you for joining us on Continuum Audio, which features conversations with Continuum's guest editors and authors who are the leading experts in their fields. Subscribers to the Continuum journal can read the full article or listen to verbatim recordings of the article and have access to exclusive interviews not featured on the podcast. Please visit the link in the episode notes for more information on the article, subscribing to the journal, and how to get CME. Dr Jones: This is Dr Lyell Jones, Editor-in-Chief of Continuum: Lifelong Learning in Neurology. Today, I'm interviewing Dr Dave Vossler, who has recently authored an article on emergent seizure management, taking care of patients with the first seizure, acute repetitive seizures, and status epilepticus, which is an article in our latest issue of Continuum covering all topics related to epilepsy. Dr Vossler is a neurologist at the University of Washington, where he's a clinical professor of neurology and has an active clinical and research practice in epileptology. Dr Vossler, welcome. Thank you for joining us today. Why don't you introduce yourself to our listeners? Dr Vossler: Thank you very much for the introduction, Lyell. It's a pleasure to speak with you on this podcast, and I hope to go over a lot of important new information in the management of seizure emergencies. As you said, I'm a clinical professor in neurology at University of Washington, been in medicine for many decades now and have published and done research in this area. So, I'm anxious to give you not only my academic experience, but also talk about my own management of patients with status epilepticus over the last four decades. Dr Jones: Yeah, that's fantastic. And I always appreciate hearing from experienced clinicians, and I think our readers and our listeners do appreciate that voice of clinical expertise. And I'll tell you this is a topic, you know, as a neurologist who doesn't see many patients with acute seizure emergencies in my own practice, I think this is a topic that gives many clinicians, including neurologists, some anxiety. Your article, Dr Vossler, is really chock-full of helpful and clinically relevant considerations in the acute management of seizures. So, you now have the full attention of a huge audience of mostly neurologists. What's the one most important practice change that you would like to see in the care of patients with either first or acute prolonged seizures? Dr Vossler: Without a doubt, the most important clinical takeaway with regard to the status epilepticus---and for status epilepticus, many, many clinical trials, research trials have been done over the last couple decades and they all consistently show the same thing, that by and large most patients who have status epilepticus are underdosed and undertreated and treated too slowly in the initial stages of the status epilepticus. And it's important to use full bolus dosages of benzodiazepines to prevent mortality, morbidity, and later disability of these patients. To prevent the respiratory depression, many physicians are afraid to use higher doses of benzodiazepines, even guideline-recommended doses of benzodiazepines for fear of respiratory depression. But it's actually counterintuitive. It turns out that most cases of respiratory depression are due to inadequate doses and due to the status epilepticus itself. We know there's greater mortality, we know there's greater morbidity and we know that there's greater need for higher dose, subsequent, anti-seizure medications, prolonged status, if we don't use the proper doses. So, we'll kind of go over that a little bit, but that is the one clinical takeaway that I really would like our listeners to have. Dr Jones: Let's follow that thread a little bit. Dave, I know obviously we will speak in hypotheticals here. We're not going to talk about actual patients, but I think we've all been in the clinical situation where you have a patient who comes into the emergency room usually who's actively seizing, unknown history, don't know much about the patient, don't know much about the circumstances of the onset of the seizure. But we now have a patient with prolonged convulsive seizures. How do we walk through that? What are the first steps in the management of that patient? Dr Vossler: Yeah, well, I'll try to be brief for the purposes of the podcast. We do, of course, go through all of that in detail in the Continuum article, which hopefully everybody will look at very carefully. Really in the first table, the very first table of the article, I go through the recommended guideline for the American Epilepsy Society on the management of what we call established status epilepticus. The scenario you're talking about is just exactly that: established status epilepticus. It's not sort of evolving or developing status. We're okay they're having a few seizures and we're kind of getting there. No, this patient is now having evidence of convulsive seizure activity and it's continuing or it's repeated seizures without recovery. And so, the first phase is definitely a benzodiazepine and then the second phase is then a longer-acting bolus of a drug like phosphenotoine, valproic acid or levetiracetam. I could get into the details about dosing of the benzodiazepines, but maybe I'll let you guide me on whether we wanted to get into that kind of detail right at the outset. It's going to be a little bit different. For children, its weight-based dosing, but for adults, whether you use lorazepam or you use diazepam or you use midazolam, the doses are a little bit different. But they are standardized, and gets back to this point that I made earlier, we're acting too slow. We're not getting these patients quick enough, for various reasons, and the doses that are most commonly used are below what the guidelines call for. Dr Jones: That's great to know, and I think it's fine for the details to refer our listeners to the article because there are great details in there about a step-by-step approach to the established status epilepticus. The nomenclature and the definitions have evolved, haven't they, Dr Vossler, over time? Refractory status epilepticus, new-onset refractory status epilepticus, super refractory status epilepticus. Tell us about those entities, how they're distinguished and how you approach those. Dr Vossler: That's an important thing to kind of go over. They- in 2015, the International League Against Epilepsy, ILAE, which is, again, our international organization that guides our understanding of all kinds of things epileptic in nature around the world. In 2015 they put out a definition of status epilepticus, but it used to be that patients had thirty minutes of continuous seizure activity or repetitive obvious motor seizures with impairment of awareness and they don't recover impairment between these seizures. And that goes on for thirty minutes. That was the old definition of status epilepticus. Now, the operational definition is five minutes. And I think that's key to understand that, after five minutes of this kind of overt seizure activity, you need to intervene. And that's what's called T1 in the 2015 guideline, the international guideline. There are a bunch of different axes in the classification of status that talk about semiology, etiology, EEG patterns, and what age group you're talking about. We won't really get into those in the Continuum article because that's really more detailed than a clinician really should be. Needing to think about the stages, what we call the stages of status epilepticus that you mentioned and I alluded to earlier are important. And that is sort of new nomenclature, and I think probably general neurologists and most emergency room physicians aren't familiar with those. So, it just briefly goes through those. Developing status epilepticus is where you're starting- the patient's starting to have more frequent seizures, and it's heading essentially in the wrong direction, if you will. Established status epilepticus, as I mentioned, is, you know, this seizure act, convulsive or major, major outward overt seizure activity lasting five minutes or more, at which time therapy needs to begin. Again, getting back to my point, what doesn't happen often enough is we're not- we're intervening too late. Third is refractory status epilepticus, which refers to status epilepticus which continues despite adequate doses of an initial benzodiazepine given parenterally followed by a full loading dose of a single non-sedating anti-seizure medicine, which today includes phosphenotoine IV valproic acid or IV levetiracetam. In the United States, and increasingly around the world, people really are using levetiracetam. First, it has some advantages. There's now proof from a class one NIH-funded trial. We know that these three drugs are equivalent at the full doses that I go over in the article. You have your kind of dealer's choice on those. Phenobarbital, which we used to use and I used as a resident as long as forty years ago, is really a second choice drug because of its sedating and other side effects. But around the world in resource-poor countries phenobarbital can be used and, in a pinch, certainly is an appropriate drug. And then finally, you mentioned super refractory status epilepticus and that's status that's persisting for more than twenty four hours. Now, despite initial benzo and non-sedating anti-seizure medicine, but also lasting more than twenty four hours while receiving an intravenous infusional sedating, anesthetizing anti-seizure medicine like ketamine, propofol, pentobarbital or midazolam drips. Dr Jones: So, it sounds like the definitions have evolved in a way that improves the outcomes, right? To do earlier identification of status epilepticus and more aggressive management, I think that's a great takeaway. If we move all the way to the other end of the spectrum, let's move to the ambulatory setting and we have a patient who comes in and they've had one seizure, they're an adult; one seizure, the first seizure. The key question is, how do we anticipate the risk of future seizures? But walk us through how you talk to that patient, how you evaluate that patient to decide if and when to start anti-seizure medicines. Dr Vossler: Well, it depends a little bit if it's an adult or a child, but the decision making process and the data behind it is pretty robust now. And the decision making process is pretty similar for adults and children, with some differences which I can talk about. First of all, first seizures. I think it's really important to stress that there's been so much research in this area. I'd like to get a cross point that they're not as innocuous as I think many general neurologists might suspect. We know that there is a two- to threefold increased risk of death in children and adults following a first seizure. Moreover, the risk of a second seizure, both in kids and adults, is about 36% two years after that first seizure. It's about 46% five years after that first seizure. It's really pretty substantial. The risk of a second seizure is increased twofold. It doubled in the presence of any kind of a history of prior brain insults that could result in seizures. Could be infections, it could be a prior stroke, it could be prior significant brain trauma. It's also doubled in the presence of an EEG, which shows epileptiform discharges like spikes and sharp waves---and not just a sort of borderline things like sharply contoured rhythmic Theta activity. That's really not what we're talking about. We're talking about overt epileptiform discharges. It's doubled in the presence of lesion that can be seen on imaging studies, and it's doubled in the presence of seizures if that first seizure occurs during sleep. So, we have a number of things that double the risks, above the risk of a second seizure, above that 36% at two years and 46% at five years that I spoke about. And so those things need to be considered when you're counseling a patient about that. Should you be on an anti-seizure medicine after that first seizure? Specifically, to the point of anti-seizure medications, the guideline that was done, the 2015 guideline that was done by the American Academy of Neurology for adults, and the 2003 guideline was actually a practice parameter that was done by the Academy and the American Epilepsy Society for children, are really kind of out of date. They talk about the adverse effects of anti-seizure medications, but when you look back at the studies that were included in developing that practice parameter for kids and guidelines for adults, they are the old drugs: carbamazepine, phenytoin, phenobarbital and valproate. Well, I don't think I need to tell this audience, this well-educated audience, that we don't use those drugs anymore. We are using more modern anti-seizure medicines that have been developed since 1995; things like lamotrigine, levetiracetam, and lecosamide. Those three in particular have very low adverse events. So, the guideline that the Academy, American Academy Neurology and American Epilepsy Society put together for kids and for adults talks about this high adverse event profile. And so, you need to take a look at the risks that I talked about of a seizure recurrence and balance that against adverse effects. But I'm here to tell you that the newer anti-seizure medicines---and by newer I'm talking in the last thirty years since lamotrigine was approved in 1995---these drugs have much better side effect profiles. And I think all epileptologists would agree with that. They're not necessarily more effective, but they are better tolerated. That makes the discussion of the risk of a second seizure, the risk of mortality versus side effects of drugs, it really pushes the risk category higher on the first side and not on the side of drugs. We know that if you take an anti-seizure medicine, you reduce your risk of a second seizure by half. Now, that's not sustained over five years, but over the first two years, you've reduced it by half. In a person who's driving, needs to get to work, has to take the kids to school, whatever, most of my patients are like, yeah, okay, sign me up. These drugs are really pretty well tolerated. There's a substantial risk of a second seizure. So, I'll do that. In a kid,  a child that's, you know, not driving yet, that might be a different discussion. And the parents might say, well, I'd rather not have my son exposed, my daughter exposed to this. They're trying to go to school. They're trying to learn. We don't want to hinder that. We'll wait for a second seizure and then if they have a second seizure, which by the way is, you know, one of the definitions of epilepsy, well then they have epilepsy, then they probably will need to go on the seizure medication. Dr Jones: Great summary, Dr Vossler, and it is worth our audience being aware that the evidence has evolved alongside the improvement in the adverse effect profile. And sounds like your threshold is a little lower to treat then maybe it would have been some time ago, right? Dr Vossler: I would say that's exactly correct in my opinion. Particularly for adults, absolutely. Dr Jones: That's fantastic, Dr Vossler. I imagine there are a lot of aspects of caring for these patients that are challenging, and I imagine many scenarios are actually pretty rewarding. What do you find the most rewarding aspect of caring for patients with acute seizure management? Dr Vossler: Yes, I mean, that is really true. I would say that the most challenging things are treating refractory status epilepticus, but worse yet, new onset refractory status epilepticus and the super refractory status epilepticus, which I talk extensively about or write extensively about in the article and provide a lot of guidance on. Really, those conditions are so challenging because they can go on for such a long time. Patients are hospitalized for a long time. A lot of really good clinical guidance doesn't exist yet. There is a tremendous amount of research in that area which I find exciting, and really there's an amazing amount of international research on that, I think most of our audience probably is unaware of. And certainly, with those conditions, there is a high risk of later disability and mortality. We go through all of that in the article. The rewards really come from helping these people. When someone was super refractory status and it were non- sorry, new onset refractory status epilepticus, has been in the hospital for thirty days, it gets really hard for everybody; the family, the patient. And for us, it wears on us. Yet when they walk out the door, and I've had these people come back to the epilepsy clinic and see me later. We're managing their anti-seizure medications. They've survived. The NORSE patients often have substantial disability. They have cognitive and memory and even some psychiatric disability. But yet we can help them. It's not just management in the hospital, but it's getting to know these people, and I take them from the hospital and see them in my clinic and manage them long-term. I get a lot of great satisfaction out of that. We're hoping to do even better, stop patients' status early and get them to recover with no sequelae. Dr Jones: What a great visual, seeing those patients who have a devastating problem and they come back to clinic and you get the full circle. And what a great place to end. Dr Vossler, thank you so much for joining us, and thank you for such a thorough and fascinating discussion on the importance of understanding and managing patients with the first seizure, acute repetitive seizures, and status epilepticus. Dr Vossler: Thank you very much, Lyell. Dr Jones: Again, we've been speaking with Dr Dave Vossler, author of an article on emergent seizure management, first seizures, acute repetitive seizures and status epilepticus in Continuum's most recent issue on epilepsy. Please check it out, 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 this 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.

Today's discussion with Dr. Joyce Black, Phd, RN, FAAN and her guests, Kelly Moed, MSN, RN, NPD-BC, CSPHP and Charlotte Lisco, BSN, RN, CWON, explores the close connection between safe patient handling and pressure injury prevention. Check out the Episode Note for the key products and resources mentioned. Connect with EHOB for more information about the products discussed in this episode or to speak with the clinical experts featured, reach out to clinical@ehob.com. We hope you enjoy this discussion!

Genetic testing plays a key role in the evaluation of epilepsy patients. With the expanding number of choices for genetic tests and the complexity of interpretation of results, genetic literacy and knowledge of the most common genetic epilepsies are important for high-quality clinical practice. In this episode, Gordon Smith, MD, FAAN speaks Sudha Kilaru Kessler, MD, MSCE, author of the article “Epilepsy Genetics,” in the Continuum February 2025 Epilepsy 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. Kessler is an associate professor of neurology and pediatrics at Perelman School of Medicine at the University of Pennsylvania and Children's Hospital of Philadelphia in Philadelphia, Pennsylvania. ADDITIONAL RESOURCES Read the article: Epilepsy Genetics 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 Academy of Neurology: aan.com SOCIAL MEDIA facebook.com/continuumcme @ContinuumAAN  Host: @gordonsmithMD Full episode transcript available here Dr Jones: This is Dr Lyell Jones, Editor-in-Chief of Continuum, the premier topic-based neurology clinical review and CME journal from the American Academy of Neurology. Thank you for joining us on Continuum Audio, which features conversations with Continuum's guest editors and authors who are the leading experts in their fields. Subscribers to the Continuum journal can read the full article or listen to verbatim recordings of the article and have access to exclusive interviews not featured on the podcast. Please visit the link in the episode notes for more information on the article, subscribing to the journal, and how to get CME. Dr Smith: Hello, this is Dr Gordon Smith. Today I've got the great pleasure of interviewing Dr Sudha Kessler about her article on epilepsy genetics, which appears in the February 2025 Continuum issue on epilepsy. Sudha, welcome to the podcast and please introduce yourself to our audience. Dr Kessler: Oh, thank you so much. I'm Sudha Kessler. I am a pediatric epileptologist here at the Children's Hospital of Philadelphia and the University of Pennsylvania. Dr Smith: Tell us a little bit about yourself. Are you a geneticist too, or how did you get into this particular topic? Dr Kessler: Yes, I want to emphatically say that I am not a geneticist. I'm not an expert in epilepsy genetics at all. I take care of all sorts of patients with epilepsy. I actually do mostly epilepsy surgery-related care. But this part of epilepsy is, every year, increasingly important to our everyday practice. And I think it's fascinating, often a little daunting. I think I was asked to get involved with this article as a non-expert to help translate from the experts to the rest of us. Dr Smith: We're going to get there, because one of the things you do a really good job of in the article is talking about genetic concepts that are germane to everything we do. And I think you're an expert. You do it in a way that I understood. So, I'd like to get there, but- and this is a really hot area. For instance, I really loved your figure that shows the arc of discovery of genetic causes for epilepsy. It's really breathtaking, something we wouldn't have thought possible that long ago. And it's also a lot to digest. And so, I wonder if maybe we can begin by thinking about a framework and, for instance, you talk about these different groups of disorders. And one that seems to be particularly impacted by this unbelievable A-rated discovery. Our developmental and epileptic encephalopathies, or DEEs. What can you tell our listeners about that group of disorders? Dr Kessler: Sure. I think that, you know, most of what we think about in epilepsy genetics now has to do with disorders that are attributable to changes in a single gene. Genetics is obviously much more complicated than that, but that's still where we are in the stage of discovery. And the graph in the article is definitely one to take a look at because it represents the explosion that we've had in our understanding of single gene disorders leading to epilepsy and related manifestations. The DEEs are a group of disorders where any individual disorder is fairly rare, but as a group they are not that rare, and very impactful because they often cause epilepsy at a very young age. And either as a consequence of seizures or as a consequence of the underlying pathophysiology of that gene change, they are typically associated with really significant developmental impairments for a child 's entire life. Dr Smith: My understanding is that there's therapeutic development going on in this space. So, the early recognition of these genetic testing offers the promise of very impactful treatment---like we now do for SMA, for instance---early in the disease course. Dr Kessler: I think that's right. That's one of the most exciting parts of this field is that so much, just around the corner, for drug development, therapy development in this area. And as you can imagine, with a lot of these disorders, earlier intervention is likely to be much more impactful than later intervention when a lot of the developmental consequences are sort of… you know, when the cat 's already out of the bag, so to speak. Dr Smith: Yeah. So, this is really transformational and something that everyone who takes care of kids with epilepsy needs to know about, it seems. So on the other extreme, I guess, there are the self-limited epilepsies. I didn't really know about this in terms of genetic discovery, but can you talk about those disorders? Dr Kessler: Yeah, sure. I mean, I think some of these are the classic childhood epilepsy syndromes that we think about like childhood absence epilepsy or what we used to call benign romantic epilepsy and now call self-limited epilepsy of childhood with centrotemporal spikes. It's a mouthful, shortened to SeLECTS. Those are the epilepsies that occur typically in previously healthy children, that affects them for a few years and often remits so that epilepsy is just age-limited and doesn't continue for life. They clearly have genetic influences because they tend to run in families, but the genetics of them is not generally single gene associated. And so, we haven't actually explained why most of those kids actually get epilepsy. I think that'll be sort of another interesting area of discovery that will help us even understand some really fundamental things about epilepsy, like, why does this syndrome start at this age and tend to resolve by adolescence? Dr Smith: And the other thing I found interesting is disorders that I might have thought going into it would have a defined genetic cause or some of the disorders that there are not. So JME, for instance, or childhood absence, which is a little counterintuitive. Dr Kessler: It's completely counterintuitive. We call them genetic generalized epilepsies, and we know that they run in families, but we still know so little. I would say of all of the disorders that are mentioned in this article, that is the group where I think we have explained the genetic underpinnings the least well. Dr Smith: Yeah. Isn't that interesting? It's… wasn't it Yogi Berra who said, it's hard to predict things, particularly the future? So… Dr Kessler: Yes. Dr Smith: Who would have thought? So, we've talked a lot about kids. What about adults? You know, what role does genetic testing play in adults who have unexplained epilepsy? Dr Kessler: Yeah, I think that that is also a really important emerging area of knowledge. I think many epileptologists may think of genetic epilepsy as being solely pediatric. There are definitely not how many of these disorders can manifest for the first time in adulthood. Not only that, many of our children with childhood onset epilepsy that is due to a genetic problem grow up to become adults and will then need adult epilepsy care. In order to take care of both of those groups, it's really important for all epileptologists, including those that take care of adults, to have some knowledge of the potential impact of genetic testing. And how do you even approach thinking about it? Dr Smith: The message I guess I'm getting is if our listeners take care of patients with epilepsy, no matter how old those patients are, they need to be familiar with this. And the other message I'm getting is, it sounds like there are a lot of patients who really need genetic testing. And this came through in one aspect of your article that I found really interesting, right? So, what are the recommendations on genetic testing? So, the National Society of Genetic Counselors, as I understand it, said everyone needs genetic testing, right? Which I mean, they're genetic counselors, so. Which is great. In the International League Against Epilepsy, they recommended a more targeted approach. So, what's your recommendation? Should we be testing anyone with unexplained epilepsy, or should we be focusing on particular populations? Dr Kessler: Well, I guess I think about it as a gradation. There are certain populations that really deserve genetic testing, where it is going to be absolutely critical. You know, it's very likely that it will be critical knowledge to their care. If you diagnose somebody with epilepsy and you do imaging and that imaging does not reveal an answer, meaning you don't see a tumor or you don't see an old stroke or some other sort of acquired lesion, the next pillar of testing for understanding underlying etiology is genetic testing. That is the point at which I typically send my patients, and that's whether they're refractory or not. I think in the past some people felt that only patients with refractory epilepsy deserve or require testing. I think the reason why not to limit it to that population is that what's on a person's mind with epilepsy, or a family's mind with epilepsy, is what's going to happen to my child or to me in the future? And if genetic testing can shed some light on that, that will have a huge impact on that person's life. Dr Smith: You've got great cases in your article, which, I just want to give you a compliment. The information and entertainment, frankly, for per page: off the charts. It's not a long article, packed with useful information. And, I mean, some of your cases are great examples of patients who are heading down the surgical epilepsy path and you discovered, nope, there's a genetic cause that really impacted their care. What's the yield, right? The number of patients that you send genetic testing on for epilepsy, what percentage come back positive for a relevant sequence variant that you think is either causing or contributing to their epilepsy? Dr Kessler: That's a great question. I think that is actually still in flux because it depends on the population of patients that are being sent for testing, obviously, and then also on what testing is being done. So, I know in at least one large recent meta-analysis, the overall yield was 17%. And somebody hearing that number might think, oh, that's not very high, but it's actually very comparable to the yield for imaging. And we all do MRIs and patients that have new-onset epilepsy where the yield of MRI testing is about 20%  or so. So, quite comparable. And then with children with DEEs, the yield is much, much higher than that. Dr Smith: So, 17% is actually a really great diagnostic yield. When I think of my yield and doing genetic testing on patients who have an axonal CMT phenotype, right? I mean that's better than what I get. So, good for you. That's exciting. Dr Kessler: It's interesting. I think that maybe an assumption might be that you're working somebody up. You do a genetic test, it reveals a difference, and thus surgery is off the table. It's actually quite different than the head, which is that some results may make surgery be even more “on the table” because you might find a gene that is known to be associated with a propensity to vocal cortical dysplasia, for example. And you may take a good second look at that person's MRI imaging or do other imaging to reveal the MRI invisible vocal cortical dysplasia. Dr Smith: Outstanding point. Let's talk a little more about the genetic testing itself. So, we've got all these genes. We understand when to test. What do you do? For instance, last night I just looked at the company that we use for most of our neuromuscular testing and they have a genetic epilepsy next gen panel with, I don't know, three hundred and twenty genes, right? Do you use that kind of panel? Do you go directly to a whole EXO? What's the right approach? Dr Kessler: Yeah, I think that that is quite dynamic right now, meaning that recommendations seem to change often enough that I rely on help. I have the enormous good luck of working here at CHOP where there is a fantastic epilepsy genetics group that I can easily refer to, and I know not everyone has that resource. The current recommendation is to start with an exome if that is available and is covered by that patient's insurance. When exome is not available, then the next best thing is a gene panel. You know, in recent years there have been a lot of sponsored gene panels, meaning free to the patient, administered by a company that then, you know, has other uses for compiled or grouped genetic data. And I think that as long as all of that can be clearly explained to a patient, and- along with all of the other things so you have to explain to a patient before doing genetic testing, about the pluses and minuses of doing it, I think that you sort of go for the best test you can that's available to that patient. Dr Smith: The sponsored programs can be very, very helpful, particularly from a payer or a patient payment perspective. And so, I guess the lesson there is it's great if you got the resources and CHOP to help you decide, but better to get whatever panel you can get than to do nothing; or, of course, refer to a center if you're not comfortable. Dr Kessler: And also, just know that these things change often enough that if it's been a couple of years and you might want to recheck whether the EXO is available to that patient or whether a gene panel can be sent that includes more than they had eight years ago. Dr Smith: So, are there situations to go to the other extreme where you just do targeted sanger sequencing? Like, just sequence the specific gene of interest?  Dr Kessler: Yeah, absolutely. I'm still a big proponent of thinking clinically about a patient. If there are clues in that patient's history, exam, imaging, anything that gives you some sense of the disorder that this patient might have. And I think a classic example would be tuberous sclerosis. If you see an infant who has new onset spasms, you see hypopigmented macules on their skin and their MRI shows a tuber, you know, also known as a focal cortical dysplasia, then sure, send the targeted sequencing for the TSC1 and TSC2 genes. Dr Smith: And Rett syndrome?  Dr Kessler: And Rett syndrome would be another example. And there are many examples where, if you feel like you have a good sense of what the disorder is, I think it's completely acceptable to send the targeted testing.  Dr Smith: So, I'm going to get further down the rabbit hole and get to from easier to harder. I always get confused about things like chromosomal microarrays or, like, karyotypes and rings and stuff like that. What role do these tests play and what do our listeners need to know about them? Dr Kessler: Yeah, I think that it is really important to have at least some knowledge of what each test can't tell you. I tell my medical students at my residence that all the time. With anything in medicine, you should know what you're asking of a test and what answers a test can tell you and can't tell you. It is baseline knowledge before requesting anything. And if you don't know, then it's best to ask. So, chromosomal microarray is used when you think that there is a large-scale derangement in a bunch of genes, meaning there is a whole section of a chromosome missing---that would be deletion, or that that information is duplicated or is turned around in a, you know, in a translocation. That is what- the kinds of things that that test can tell you. I think of doing a microarray when a child has not just epilepsy and intellectual disability, but also has, for example, other organ systems involved, because sections of chromosome can include many, many, many different genes and it can affect the body in larger ways. That's often when I think about that. So, a child with multiple congenital anomalies. Karyotype, which we think of as the most old-fashioned way of looking at our genes, still has some utility because it is useful for looking at a specific situation where the ends of arm of a chromosome get cut off and get sticky and then stick to each other and make a ring. For example, ring chromosome 20 is a disorder which can cause epilepsy, particularly hard-to-treat frontal lobe epilepsy, and that sometimes doesn't show up until adolescence or even early adulthood. That's just one example of something that karyotype can tell you.  Dr Smith: And it goes without saying, but just to emphasize, these are things that you would miss completely on a next generation panel or a next genome? Dr Kessler: That's correct. Because this isn't about sequencing. This is about large structures. You know, with my patients, it's sometimes, I think, very hard to explain. It's hard enough to explain it to other physicians who aren't in genetics, but it's a whole other undertaking to explain it to families who may not have a lot of literacy about cell biology or genetics or, you know, anything related to that. So, I often rely on analogies. And one analogy I use is that if you're- all of your genetic information is like a book, that book is split into chapters and those are the chromosomes. And you can be missing entire paragraphs or have paragraphs duplicated. And that would be the kind of thing that we would be looking for with the chromosomal microarray with sequencing or, you know, with sequencing, we're looking for spelling of words, and we can look at one word at a time. That would be targeted sequencing. Or we can look at many, many words at a time. And that would be next gen sequencing.  Dr Smith: I just want to say that you are the genetic whisperer. You know, translator. I love it.  Dr Kessler: You can continue using it down to the level of explaining the possibility of a variant of unknown significance, which I think is sometimes difficult to explain. So, I often will say, I know how the word color is spelled: C O L O R. But sometimes in other places it will be spelled C O L O U R and that's still the same word, that's still color. That's just what we would call a population variant. If it is spelled C O M O R, that changes meaning; that is not a word, and that is probably a pathogenic variant. But if it gets misspelled and it's K O L O R, then I'm not sure. Could that be a variant that means something different or not. And so that I would call that a variant of unknown significance, meaning its impact is to be determined. Dr Smith: So, I was going to ask you about variant calling, but you'd beat me to the punch. And that's a great metaphor that I will definitely remember. All right, here's another concept that I think people often find challenging, which is read depth. Can you tell us about reading depth or sequence depth?  Dr Kessler: Yes, hopefully I can. Again, not an expert here, but as I understand it, the way next gen sequencing works is that pieces of DNA are getting read. And the number of times any given nucleotide is read in this process is the read depth. It basically just translates to the number of times the processor, the machinery of doing this, pays attention to anyone site. The reason it's important is that the process by which this reading is done can sometimes result in errors. The greater your depth, the more times something is read, the less likely you are to have a mistake.  Dr Smith: In either direction. So, you're presumably less likely to have a false positive or false negative. Yep, again, very well explained. You know, I've got a lot of other questions I want to ask you, but I do want to be respectful of our listeners' time. I wonder if we could pivot a little bit and just let's go back to where we began. Really exciting time, right? Amazing. And you've been doing this long enough. I'm sure you didn't think when you started that it was going to look like this. What does the future look like? I mean, we talked a little bit about therapeutics, but the world's changing fast. Five, ten years from now, what's your hope for that?  Dr Kessler: Oh, that's such a great question. You know, we are at the point with genetic epilepsies that gene-based therapies, either antisense oligonucleotide-based therapies or viral vector-based gene therapies, are actually now being developed and administered in trial situations to actual patients. And so, it always feels like we're on the cusp, but I think actually now we really are on the cusp of having gene-based therapies for genetic epilepsies. I think that there is still so much to sort out, both from basic scientific point and from a practical administering these things to patients and what are the potential long term consequences.For example, unlike medications, which are therapies that you can stop if there are adverse effects, often administering a gene therapy is a one-and-done thing that can't be retracted. Thinking even about the ethical framework of that and the framework of explaining to patients that we don't know the ten, twenty-year consequences of that, is part of the informed consent process, for example. So, there's still so much work that is going to be transformational, not just from the, you know, the big picture, but from developing all, you know, from going through all of these steps to really make these kinds of therapies a reality. Dr Smith: Well, it's really amazing. And, you know, we're seeing this in multiple different areas in neurology. So, well done. You run the child neurology residency program there, I understand. I try to snoop on people before I talk to them because we haven't met before this. And you're obviously a very a very good educator. Thank you so much for talking with me today. I don't spend a lot of time in epilepsy, but every time I do one of these, I kind of want to go back and do something different because it's such a neat field. Thank you.  Dr Kessler: You're welcome. It was my pleasure.  Dr Smith: Again, today I've been interviewing Dr Sudha Kessler about her article on epilepsy genetics, which is truly outstanding. This article appears in the most recent issue of Continuum on epilepsy. Be sure to check out Continuum audio episodes from this and other issues. And thank you, 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 this 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.

Neuroimaging is a tool to classify and ascertain the etiology of epilepsy in people with first or recurrent unprovoked seizures. In addition, imaging may help predict the response to treatment. To maximize diagnostic power, it is essential to order the correct imaging sequences. In this episode, Aaron Berkowitz, MD, PhD, FAAN speaks with Christopher T. Skidmore, MD, author of the article “Neuroimaging in Epilepsy,” in the Continuum February 2025 Epilepsy issue. Dr. Berkowitz is a Continuum® Audio interviewer and professor of clinical neurology at the University of California, San Francisco Dr. Skidmore is  an associate professor of neurology and vice-chair for clinical affairs at Thomas Jefferson University, Department of Neurology in Philadelphia, Pennsylvania. Additional Resources Read the article: Neuroimaging in Epilepsy 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 Guest: @ctskidmore  Full episode transcript available here Dr Jones: This is Dr Lyell Jones, Editor-in-Chief of Continuum, the premier topic-based neurology clinical review and CME journal from the American Academy of Neurology. Thank you for joining us on Continuum Audio, which features conversations with Continuum's guest editors and authors who are the leading experts in their fields. Subscribers to the Continuum journal can read the full article or listen to verbatim recordings of the article and have access to exclusive interviews not featured on the podcast. Please visit the link in the episode notes for more information on the article, subscribing to the journal, and how to get CME. Dr Berkowitz: This is Dr Aaron Berkowitz, and today I'm interviewing Dr Christopher Skidmore about his article on neuroimaging in epilepsy, which appears in the February 2025 Continuum issue on epilepsy. Welcome to the podcast, Dr Skidmore. Would you please introduce yourself to our audience?  Dr Skidmore: Thank you for having me today. I'm happy to talk to you, Dr Berkowitz. My name is Christopher Skidmore. I'm an associate professor of neurology at Thomas Jefferson University in Philadelphia. I'm a member of the Jefferson Comprehensive Epilepsy Center and also serve as the vice chair of clinical affairs for the department.  Dr Berkowitz: Thank you very much for joining us and for this fantastic article. It's very comprehensive, detailed, a very helpful review of the various types of brain pathology that can lead to epilepsy with very helpful images and descriptions of some of the more common findings like mesial temporal sclerosis and some of the less common ones such as cortical malformations, heterotopia, ganglioglioma, DNET. So, I encourage all of our listeners to read your article and take a close look at those images. So, hopefully you can recognize some of these findings on patients' neuroimaging studies, or if you're studying for the right or the boards, you can recognize some of these less common congenital malformations that can present in childhood or adulthood with epilepsy. In our interview today, what I'd like to do is focus on some practical tips to approaching, ordering, and reviewing different neuroimaging studies in patients with epilepsy. So to start, what's your approach when you're reviewing an MRI for a patient with a first seizure or epilepsy? What sequence do you begin with and why, how do you proceed through the different sequences and planes? What exactly are you looking for?  Dr Skidmore: It's an important question. And I think to even take a step back, I think it's really important, when we're ordering the MRI, we really need to be specific and make sure that we're mentioning the words seizures and epilepsy because many radiology centers and many medical centers have different imaging protocols for seizure and epilepsy patients as compared to, like, a stroke patient or a brain tumor patient. I think first off, we really need to make sure that's in the order, so that way the radiologist can properly protocol it. Once I get an image, though, I treat an MRI just like I would a CAT scan approach with any patient, which is to always approach it in the same fashion. So, top down, if I'm looking at an axial image. If I'm looking at a coronal image, I might start at the front of the head and go to the back of the head. And I think taking that very organized approach and looking at the whole brain in total first and looking across the flare image, a T2-weighted image and a T1-weighted image in those different planes, I think it's important to look for as many lesions as you can find. And then using your clinical history. I mean, that's the value of being a neurologist, is that we have the clinical history, we have the neurological exam, we have the history of the seizure semiology that can might tell us, hey, this might be a temporal lobe seizure or hey, I'm thinking about a frontal lobe abnormality. And then that's the advantage that we often have over the radiologist that we can then take that history, that exam, and apply it to the imaging study that we're looking at and then really focus in on those areas. But I think it's important, and as I've illustrated in a few of the cases in the chapter, is that don't just focus on that one spot. You really still need to look at the whole brain to see if there's any other abnormalities as well. Dr Berkowitz: Great, that's a very helpful approach. Lots of pearls there for how to look at the imaging in different planes with different sequences, comparing different structures to each other. Correspondent reminder, listeners, to look at your paper. That's certainly a case where a picture is worth a thousand words, isn't it, where we can describe these. But looking at some of the examples in your paper, I think, will be very helpful as well. So, you mentioned mentioning to the neuroradiologist that we're looking for a cause of seizures or epilepsy and epilepsy protocols or MRI. What is sort of the nature of those protocols if there's not a quote unquote “ready-made” one at someone 's center in their practice or in their local MRI center? What types of things can be communicated to the radiologist as far as particular sequences or types of images that are helpful in this scenario? Dr Skidmore: I spent a fair amount of time in the article going over the specific MRI protocol that was designed by the International League Against Epilepsy. But what I look for in an epilepsy protocol is a high-resolution T2 coronal, a T2 flare weighted image that really traverses the entire temporal lobe from the temporal tip all the way back to the most posterior aspects of the temporal lobe, kind of extending into the occipital lobe a little bit. I also want to see a high resolution. In our center, it's usually a T1 coronal image that images the entire brain with a very, very thin slice, and usually around two millimeters with no gaps. As many of our neurology colleagues are aware, when you get a standard MRI of the brain for a stroke or a brain tumor, you're going to have a relatively thick slice, anywhere from five to eight millimeters, and you're actually typically going to have a gap that's about comparable, five to eight millimeters. That works well for large lesions, strokes, and big brain tumors, but for some of the tiny lesions that we're talking about that can cause intractable epilepsy, you can have a focal cortical dysplasia that's literally eight- under eight millimeters in size. And so, making sure you have that nice T1-weighted image, very thin slices with no gaps, I think is critical to make sure we don't miss these more subtle abnormalities. Dr Berkowitz: Some of the entities you describe in your paper may be subtle and more familiar to pediatric neurologists or specialized pediatric neuroradiologists. It may be more challenging for adult neurologists and adult neuradiologists to recognize, such as some of the various congenital brain malformations that you mentioned. What's your approach to looking for these? Which sequences do you focus on, which planes? How do you use the patient 's clinical history and EEG findings to guide your review of the imaging? Dr Skidmore: It's very important, and the reason we're always looking for a lesion---especially in patients that we're thinking about epilepsy surgery---is because we know if there is a lesion, it increases the likelihood that epilepsy surgery is going to be successful. The approach is basically, as I mentioned a little bit before, is take all the information you have available to you. Is the seizure semiology, is it a hyper motor semiology or hyperkinetic semiology suggestive of frontal lobe epilepsy? Or is it a classic abdominal rising aura with automatisms, whether they be manual or oral automatisms, suggesting mesial temporal lobe epilepsy? And so, take that clinical history that you have to help start to hone your eye into those individual locations. But then, once you're kind of looking in these nonlesional cases, you're also then looking at the EEG and where their temporal lobe spikes, where their frontal lobe spikes, you know, using that and pulling that information in. If they saw a neuropsychologist pulling in the information in from the neuropsychological evaluation; if they have severe reductions in verbal memory, you know, focusing on the dominant temporal lobe. So, in a right-handed individual, typically the left temporal lobe. And kind of then really spending a lot of time going slice at a time, very slowly, because in some of these vocal-cortical dysplasias it can be just the blurring of the gray-white margin. What I find easiest is to identify that gray-white margin and almost track it. Like, you use the mouse to kind of track it around and say, can I outline the exact border of the gray white margin in the frontal lobe that I'm interested in or the temporal lobe that I'm interested in, kind of looking for those subtle abnormalities. Often as neurologists, we don't have the luxury of being able to immediately reformat. As I mentioned, our T1 volume acquisition study is done in the coronal plane, but sometimes you might want it in the axial plane. And so, I might reach out to the radiologist and say, hey, can you reformat this in the axial plane because I'm interested in the frontal lobe epilepsy and it's a little bit better at looking at it in that plane? And I'll have them reformat and put it back on the pack so I can look at it in that manner. And so that's a, kind of another strategy is to take what you have, but also then go back to the radiologist and say, I need to look at it this a different way. Can you reformat it for me? Looking for that gray-white matter junction is the nice way to pick up for kind of subtle cortical dysplasias. And then when you see an abnormality, to be able to put the T1, the T2, and the flare image all up next to each other and use the technology built into most of our browsers to put on what's called the localizer mode, where I can highlight a specific spot that I'm seeing on the T1 and then very easily quickly see, what does it look like on the T2? What does it look like on the flare? To kind of quickly decide, is it a true abnormality or am I only seeing it on one slice because of an artifact on that one imaging sequence? And I think that's the biggest kind of key is to make sure, is it an artifact or is it not an artifact? That's kind of the most common thing that we, I think, get confused with.  Dr Berkowitz: So, some very helpful pearls there in terms of reviewing the imaging, being in dialogue with our neuroradiology colleagues to think about potentially reacquiring certain images on certain planes or looking at the images with our neuroradiology colleagues to let them know more about the clinical history and where we're sort of zooming in about possible abnormalities.  Dr Skidmore: I would just add in there that when looking at especially the mesial temporal structures, because of a lot of artifacts that can be present in an individual MRI machine, it's not uncommon that the mesial temporal structure will appear brighter because of an MRI magnet artifact. And so, it's a good key to look at the hippocampus compared to the insula. And so, the hippocampus and the insula should have similar signal characteristics. You're seeing the hippocampus is bright, but the insula  ipsilateral to it's normal intensity. That would suggest that that's probably a true hyperintensity on the flare-weighted image as opposed to if both are bright, unless you're suspecting a hemispheric abnormality, it's more likely to be a kind of artifact in the MRI machine. Dr Berkowitz: Okay. Those are really helpful tips, not just to analyze the hippocampus and medial temporal lobe itself---let's remember our anatomy and the circuit of Papez---and to look at associated structures for supporting evidence of a possible abnormality in the hippocampus itself. It looks like there may be something subtle. We can use some additional information from the image to try to decide if that is real or artifactual, and of course correlating with the clinical picture and EEG. I'd like to talk briefly now about some other imaging modalities that you discuss in your paper, the use of functional imaging such as PET, SPECT and fMRI. Let's talk a bit about each of these. When would you order a PET scan for a patient with epilepsy? What would you be looking for and how would you be using that to make clinical decisions?  Dr Skidmore: Yeah, so these functional imaging modalities are really utilized when we're evaluating somebody that's not responding to medications. So, they're medically intractable, and we're wondering, could they be a candidate for epilepsy surgery? And so, most of these imaging modalities are really relegated to the world of epileptologists at surgical epilepsy centers. I wanted to include them, though, in the article because I do think it's important for general neurologists to understand kind of what they are, because invariably a patient sees me and then they go back to their general neurology and be like, hey, Doctor Skidmore said I had this PET scan abnormality. What do you think? So, I think it's a good idea for general neurologists to kind of understand them. So, probably the oldest that we've utilized is the FDG PET scan, basically looking at fluorodeoxyglucose and the brain's utilization of glucose. As we all remember, again, glucose is the primary molecule for energy and ATP production in the brain. And so basically, by injecting radioactive glucose in the interictal state--- so not during a seizure but in between seizures---areas of the brain that are not taking up the radiotracer will show as being hypometabolic. So, low metabolism. And hypometabolic regions in the interictal state have been associated with onset regions for epileptic seizures. Let's say you have a patient clinical history, you think they have temporal of epilepsy, EEG suggests temporal of epilepsy, but the MRI is nonlesional, meaning there's no abnormality that anybody could appreciate even at a 3 Tesla scanner. We'll get an FDG PET scan and see, is there hypo metabolism in that temporal lobe of interest? And if there is, well, that's been shown through several published papers, that's just as valuable as having an abnormality on the MRI. And so, we often again use these PET scans, especially in nonlesional cases, to try to find that subtle cortical dysplasia. Now you have your nice epilepsy protocol MRI, it says it's nonlesional. You get your PET scan, it shows hypometabolism in a region of the frontal lobe, let's say, in a in a frontal lobe epilepsy case. And then often we go back, we kind of talked about strategy of how you find those subtle lesions. Then you go back and say, well, look, this gyrus specifically on the PET scan said it's abnormal. You end up looking for really subtle, very tiny abnormalities that, even with somebody that's skilled, often at first review gets missed. So, that's how we use the PET scan. The SPECT scan is done typically in the ictal state. So, now somebody's in an epilepsy monitoring unit often, where you're injecting radio tracer at the exact moment that somebody starts having a seizure. And we know when there's increased seizure activity, the increased seizure activity---let's say it's from my right temporal lobe---is going to increase cerebral blood flow transiently to the right temporal lobe. And then if that seizure discharge spreads from the right temporal lobe maybe to the entire right hemisphere and eventually becomes a focal to bilateral tonic chronic seizure by spreading to the other side, the entire brain is going to be hypoperfused at that point. So, if you want to, as soon as the seizure starts, inject that radio tracer to see, where is the blood flow earliest in the seizure? And then we might do an interictal SPECT when you're not having a seizure. Look at, all right, what's the normal blood flow when somebody's not seizing? What's it like when they're having a seizure? And then the area that has increased activity would- might suggest that's where the seizure started from. But we have to be very careful because again, some seizures can spread very rapidly. So, if you delay injecting an injection ten, fifteen, twenty seconds, the seizure could have already propagated to another region of the brain, giving you a false positive in another location. So, you have to be very careful about that modality. I think what's most exciting is the functional MRI because the functional MRI, for many, many centers, is replacing a very old technique called the WADA test. So, in the WADA test, typically you place a catheter angiogram into the internal carotid artery and transiently introduce a sedative medication to put, let's say, the left hemisphere to sleep because you wanted to see what functions were still active in the right hemisphere. And then the surgeon would move the catheter or the right internal carotid artery, and you inject a sedative on that side after the left hemisphere is recovered and see what the left hemisphere can do. And we used that for language dominance, we used that for memory dominance. And while most individuals did fine with angiograms, unfortunately complications do occur and there's injury to the artery, there could be strokes that can- that have happened, which can be quite devastating for the patient. And so, functional MRI is a nice, noninvasive way for us to map out language function, motor function, sensory function, visual function, and is starting to show some usefulness also for mapping out kind of memory function, dominant memory function, meaning verbal memory compared to visual memory. To be able to do those things noninvasively becomes really important because, if we're talking about epilepsy surgery, we want to make you seizure-free but neurologically intact. And so, we need to understand the relationship between where we think the seizures are coming from and where eloquent cortex is so we can properly counsel you and avoid those regions during any planned surgery. Those are the three most common functional imaging modalities that we're using now to supplement the rest of the presurgical work.  Dr Berkowitz: Very helpful. So, these are studies, PET, SPECT, and fMRI, that would really be obtained predominantly in patients in whom epilepsy surgery was being considered to have more precise lesion localization, as well as with the fMRI to get a better sense of how to provide the safest maximal resection of epileptogenic tissue while preserving functions. Dr Skidmore: That's a perfect summary.  Dr Berkowitz: Fantastic. This has been a really helpful interview with Dr Skidmore and a really fantastic article. As I said, a picture is worth a thousand words, so I definitely encourage you to read the article and look at the images of some of the conditions we've been talking about and some of these findings that can be seen on interictal PET or ictal SPECT to get a sense of the visual aspects of what we've been discussing. So again, today I've been interviewing Dr Christopher Skidmore about his article on neuroimaging and epilepsy, which appears in the most recent issue of Continuum on Epilepsy. Be sure to check out Continuum audio episodes from this and other issues. And thank you so much to our listeners for joining us today.  Dr Skidmore: Thank you 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 this 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.

“This is what totally drives the treatment decisions, and that's why having that pathology report when the nurse is educating the patient is so important, because you can say, well, you have this kind of breast cancer, and this kind of breast cancer is generally treated this way,” Suzanne Mahon, DNS, RN, AOCN®, AGN-BC, FAAN, professor emeritus at Saint Louis University in Missouri, told Jaime Weimer, MSN, RN, AGCNS-BS, AOCNS®, manager of oncology nursing practice at ONS, during a conversation about what oncology nurses need to know about breast cancer treatment.  Music Credit: “Fireflies and Stardust” by Kevin MacLeod  Licensed under Creative Commons by Attribution 3.0   Earn 1.0 contact hours (including 15 minutes of pharmacotherapeutic content) of nursing continuing professional development (NCPD) by listening to the full recording and completing an evaluation at courses.ons.org by February 14, 2027. The planners and faculty for this episode have no relevant financial relationships with ineligible companies to disclose. ONS is accredited as a provider of nursing continuing professional development by the American Nurses Credentialing Center's Commission on Accreditation.  Learning outcome: Learners will report an increase in knowledge related to breast cancer treatment considerations.  Episode Notes   Complete this evaluation for free NCPD. Previous ONS Podcast™ site-specific episodes: ONS Voice articles: Episode 348: Breast Cancer Diagnostic Considerations for Nurses Episode 345: Breast Cancer Screening, Detection, and Disparities ONS Voice articles: An Oncology Nurse's Guide to Cascade Testing  Breast Cancer Prevention, Screening, Diagnosis, Treatment, Side Effect, and Survivorship Considerations  Learn How to Read a Germline Genomic Testing Report  Learn How to Read a Somatic Biomarker Testing Report  Sexual Considerations for Patients With Cancer  ONS books: Breast Care Certification Review (second edition)  Guide to Breast Care for Oncology Nurses  ONS courses: Breast Cancer Bundle  Breast Cancer: Treatment and Symptom Management  ONS Biomarker Database results for breast cancer ONS Next-Generation Sequencing Sample Report  ONS Learning Libraries: Breast Cancer Genomics and Precision Oncology   American Cancer Society: Breast Cancer Facts and Figures  Your Breast Pathology Report: Breast Cancer National Comprehensive Cancer Network   National Cancer Institute Breast Cancer—Patient Version  To discuss the information in this episode with other oncology nurses, visit the ONS Communities.   To find resources for creating an ONS Podcast Club in your chapter or nursing community, visit the ONS Podcast Library.  To provide feedback or otherwise reach ONS about the podcast, email pubONSVoice@ons.org.  Highlights From This Episode  “Local treatment is typically going to consider some kind of surgery with or without radiation, depending on the surgery and the extent of the breast cancer. All women are going to have, and today when you use the word women, individuals assigned female at birth, they are the vast majority of individuals being treated for breast cancer, but for individuals assigned male at birth, there's not near as much research, but generally their treatment is very similar. So that's something to kind of keep in the back of your mind.” TS 2:39  “This is very confusing for patients because they're like, ‘Well, my friend at church had this and why am I getting this and why are they getting something different?' And that is because of the pathology report. So taking that time to explain that with a pathology, I think is really important.” TS 8:31  “When they see the breast surgeon, all individuals are going to have some kind of axillary evaluation.  Now, hopefully it's going to be a sentinel lymph node. So they're going to, at the time of surgery, put a tracer and, you know, they're going to take out maybe one, two, three lymph nodes and hopefully, you know, there is not a lot of disease there. And if that's the case, they're kind of done with that. So the sentinel lymph node evaluation, it's really more to stage and provide that information, but it kind of sets the stage a lot of times for the other treatments selections. And I think people need to realize that this is important. This is a very important procedure.” TS 15:31  “Years ago, when women had a breast mass, they went to the OR and it was biopsied in a frozen section and if it was positive, they had a mastectomy. So women would wake up and they'd be feeling their chest because they're like, ‘What happened here?' And that is not great care. It doesn't give that woman any autonomy, but it was the best that could be done at that point. Now, with the diagnostic where we can do a needle biopsy, they can kind of stop and take a timeout and we can kind of clinically stage that.” TS 17:04  “For women that really desire breast-conserving therapy, they can anticipate that postoperatively at some point, they're going to have treatment to the entire breast, we typically call whole breast radiation, and then they may have a boost. Now, in many, many probably cases, that's going to be over five to six weeks, Monday through Friday. So the treatment itself doesn't take but a couple of minutes, but you have to get to the facility. And even though we streamline check-in processes and whatnot, you have to get undressed, you have to get positioned on the table. So it is a commitment, and it can be disruptive.” TS 24:49  “The hormone-blocking agents are going to be the cornerstone of all those treatments for anyone who has hormone receptor–positive breast cancer. So they are going to take these agents and as you said, they're probably going to take them for 5–10 years. It's quite the journey.” TS 32:33   “I think you need to be mindful that if someone has had germline testing and they've tested positive, they are not only worried about themselves, and they are worried about the rest of their family. That is a big deal. And even though I'll hear mothers say, ‘I feel so guilty, now my daughter has this,' now, I've never heard a daughter come and say, ‘Gosh, I wish my mom hadn't had me because of this.' There's a lot of feeling and emotion that goes on with that, and realize that those individuals are probably going to have fairly complicated management that goes over and above their breast cancer.” TS 41:50 

EEG is the single most useful ancillary test to support the clinical diagnosis of epilepsy, but if used incorrectly it can lead to misdiagnosis and long-term mental and physical health sequelae. Its application requires proper understanding of its limitations and variability of testing results. In this episode, Katie Grouse, MD, FAAN, speaks with Daniel Weber, DO, author of the article “EEG in Epilepsy,” in the Continuum® February 2025 Epilepsy 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. Weber is the director of adult epilepsy and vice chair of clinical affairs at the St. Louis University in St. Louis, Missouri. Additional Resources Read the article: EEG in Epilepsy 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: @drdanielweber Full episode transcript available here Dr Jones: This is Dr Lyell Jones, Editor-in-Chief of Continuum, the premier topic-based neurology clinical review and CME journal from the American Academy of Neurology. Thank you for joining us on Continuum Audio, which features conversations with Continuum's guest editors and authors who are the leading experts in their fields. Subscribers to the Continuum journal can read the full article or listen to verbatim recordings of the article and have access to exclusive interviews not featured on the podcast. Please visit the link in the episode notes for more information on the article, subscribing to the journal, and how to get CME. Dr Grouse: This is Dr Katie Grouse. Today, I'm interviewing Dr Daniel Weber about his article on EEG and epilepsy, which appears in the February 2025 Continuum issue on epilepsy. Welcome to the podcast and please introduce yourself to our audience. Dr Weber: Hi, thanks for having me. My name is Dan Weber and I'm an epileptologist at Saint Louis University. I direct the adult epilepsy program here and also serve as the vice chair for Clinical Affairs. Been my pleasure to work on this article. Dr Grouse: I'm so happy to have you today. I read your article. I found it to be incredibly useful as someone who often orders EEG in the general neurology clinic. So, I wanted to start with asking, what is the most clinically relevant message or takeaway from your article that you'd really like neurologists to know?  Dr Weber: Yes, when I was asked to write this article, I looked back at the previous Continuum on epilepsy and just the general literature. And there's a lot of good articles and books out there on EEG and epilepsy and sort of giving you a primer on what you might see and how to interpret it. So, we wanted to try to go a slightly different direction. This article gives you some of that gives you the background of EEG and some of the basic things that you may see, but the real thrust of it is more about the limitations of EEG in the clinical picture of epilepsy and common things you might avoid. There are some things that we get hammered into our brains in training that aren't always true and there's plenty of examples in the literature to review, and this article sort of tries to encapsulate as many of those as possible in a digestible format. The main takeaway would be that EEG is an extremely helpful tool in the diagnosis of epilepsy, is the best tool we have to help supplement your clinical acumen. But it does not make the diagnosis of epilepsy. And there are certain circumstances when it may not be as helpful as you may have been led to believe in residency. Dr Grouse: Maybe not the most comforting of messages, but certainly an important one, very important to learn more about this. So, we appreciate that. Can you tell us your decision-making process when deciding whether to order a routine EEG, an extended EEG, prolonged ambulatory EEG, or inpatient video EEG? Dr Weber: Sure. So, it's a multi-part question because each one, I think, has a different clinical scenario. In the current state, our best data for estimating risk of recurrence after an initial seizure comes with routine EEG abnormalities. So, often I will order routine EEGs in those scenarios. So new patient presentation, new patients coming in with an initial seizure who want to know what's their risk of recurrence. So, risk stratification, I use a lot of routine EEG for, often sleep deprived if possible to increase the sensitivity. If you'd like, the extended EEG does offer higher sensitivity, or you can repeat the routine EEG if the first routine EEG is nonconclusive. For generally extended EEGs, I tend to order them in my practice if patients have come to see me with a suspected diagnosis of epilepsy but haven't yet had any electrographic confirmation. Maybe they've already had routine EEGs done in the past, so we'll try to obtain just a little more data. The longer-term EEGs I tend to use in different clinical scenarios, in patients usually who already have established diagnosis or people who have become refractory and we haven't yet confirmed their diagnosis. I tend to do inpatient EEGs in those situations. Ambulatory EEGs I do more when there are certain characteristics of the patient or the patient 's presentation that may not fit well on the inpatient side. Patients who are reliant on substances who can't use while they're inpatient and may have withdrawal effects complicating the stay. Or people who have a strong activation component to their epilepsy where activity really draws it out, certain activities that they do at home that they might not do during the inpatient stay. Those are the sorts of people I'll do ambulatory EEGs on. There are a couple other scenarios as well that come up less commonly, but everything has its own little niche. Dr Grouse: That's a really helpful review as we sort of think about which way we want to go as we're working up our patients in the inventory setting. Can you tell me a little more about the difference between sensitivity of, for instance, doing maybe two routine EEGS versus prolonged ambulatory EEG? Dr Weber: Generally speaking, the longer you're recording someone's brain waves, the higher the sensitivity is going to be. So routine EEG is twenty to forty minutes at most places. One of those gives you a certain sensitivity. More of them will give you more sensitivity. And there was a recent study highlighted in the article that compared routine EEGs to initial multi-day ambulatory EEG, and the ambulatory EEG obviously, as would be expected, has a higher sensitivity than either of the routines. So, there may be some cases with that initial evaluation where an ambulatory EEG may be held and we get into that in more detail in the article. But with the caveat, a lot of this article is about limitations, and the data that we have to talk about increased risk of recurrence was based off seeing epileptic form discharges on routine EEG. So you could hypothesize that if you only have one epileptic form discharge in three days on an ambulatory EEG, that may not carry the same recurrent significance as catching one on a twenty minute EEG. But we don't have that knowledge. Dr Grouse: Getting a little bit more into what you mentioned about the limitations, when is the scalp EEG less useful or limited in the evaluation of epilepsy? Dr Weber: So, one thing I see a lot in my residence at here and other places where I've worked is, I get them very excited about EEG and they may order it a bit too much. So, if patients have a known, established diagnosis of epilepsy, electrographically confirmed, and they come in with a breakthrough seizure and they're back to their baseline, there's really not a strong reason to get an EEG. We often seem to in the emergency department as part of our evaluation, but we already know what happened to the patient. The patient's not doing poorly right now, so the EEG is not going to give you any additional information. Just like really any test, you should think, what are the possible outcomes of this test and how would those outcomes alter the care of this patient? And if no outcome is going to affect the care of the patient or give you any additional diagnostic information, then probably don't need to be doing that test. Dr Grouse: This is probably a good segue into asking, what is an area of confusion or common pitfalls that you've seen in the clinical application of EEG and epilepsy? Dr Weber: So, a lot of times on the inpatient service, we'll get longer-term EEGs for patients who are having spells that are occurrent while they're in the ICU or other places or altered in some way, encephalopathic. And these patients will have their spell, and in my report, I'll say that there is not any electrographic correlate. So, there's no EEG finding that goes along with the movement that they're doing that's concerning for a seizure. And that doesn't always mean that it's not an epileptic seizure. An EEG is not a one-hundred-percent tool. Epilepsy and seizures are a clinical diagnosis. The EEG is a helpful tool to guide that diagnosis, but it is not foolproof, so you need to take the whole clinical picture into account. Particularly focal seizures without impaired awareness often can be electrographically silent on surface EEG. If you see something that looks clinically like a seizure but doesn't show up on the EEG, there are circumstances that they get to in the paper a little bit where that can still be an epileptic seizure. And you just have to be aware of the limitations of the tests that you're ordering and always fall back on the clinical skills that you've learned. Dr Grouse: Are there any tips or tricks you can suggest to improve the clinical utility of EEG for diagnosis of epilepsy? And also thinking about the example you just gave, but maybe other cases as well? Dr Weber: Again, definitely need to incorporate EEG as part of a larger picture. The video component of EEG is incredibly helpful. You can't interpret EEG in isolation. Regardless of what the EEG shows, you can't make a diagnosis of epilepsy, but you certainly can be very suspicious of one. So, in those cases where you have a high suspicion for an epileptic seizure and the EEG has not given you any confirmatory evidence, it's really helpful to rely on any clinical expertise that you have access to. So, people who have seen lots of seizures may be helpful in that situation. Getting good recordings, good data to prove yourself one way or the other is helpful and continuing to evaluate. So usually, as I said, focal seizures that don't show up well on the EEG. People who have focal seizures will often have larger seizures if left untreated. So, you can try to admit them to an epilepsy monitoring unit where we try to provoke seizures and try to provoke a larger seizure to help confirm that diagnosis. Dr Grouse: This kind of gets into what we've already reviewed to some degree, but what is the easiest mistake to make (and hopefully avoid) when using EEG to diagnose epilepsy or make other treatment decisions? Dr Weber: I think the easiest, most common mistake I see is overreliance on the test. There's a lot of subjectivity to the interpretation of this test. There are a lot of studies out there on interrater reliability for epilepsy and intrarater reliability for epilepsy. We continue to try to make the findings more objective and get more quantified. The articles talk about our six criteria for epileptiform discharges and have reference to where that came from and the sorts of specificity that each of those criteria lead to. Just because an EEG report has said something, that does not diagnose or negate a clinical diagnosis of epilepsy. It is common for folks with non-epileptic seizures to have a history of reported epileptic form discharges on their EEG. Again, because there is some subjectivity to the test, some abnormal-looking normal variants will pop up and get interpreted as epileptiform discharges. It's important to review the whole patient, as much of the data as you can, and make the best clinical judgment you can of the overall case. Dr Grouse: What is quantitative EEG and how can it be clinically useful? Dr Weber: Now that most EEG is obtained digitally through the use of computer software, we have been able to employ computers to do a lot of the work for us. There are many different ways of looking at the EEG data, but it's all frequency bands over time. The quantitative EEG goal is really to simplify and condense what you're seeing on your normal EEG page into a more digestible format. Lets you look at a larger amount of data faster, which becomes more and more important as we're doing more of these long-term recordings, particularly in the intensive care unit. Quantitative EEG can help you assess a lot of data at a snapshot and get a general sense of what's going on with the patient over the past several hours. It does require some extra training to become familiar with it, but it's training that can be done at all levels. Again, it can help you see more, faster. Obviously, like everything, it has its own limitations. Sometimes the sensitivity and specificity may be a little off from the raw data review, and you should always go back to the raw data anytime there are questions. But it can be helpful to make things faster. Dr Grouse: Do you think you could give me a hypothetical example of a case where this would be something really nice to have?  Dr Weber: The most common example is folks with repetitive seizures in the ICU. If you're just looking at the raw data, you will get a sense of how often the seizures are happening. But if you look at the quantitative data, it sort of compresses that all down to a much smaller snapshot. So you can see much more readily, yes, these are how many seizures were happening. And here's where we gave our intervention; and look, there are fewer seizures after that intervention. So, it can help you assess response to treatment, help you assess just overall volume of seizures in a much more condensed fashion, and you can get through it much faster with the appropriate training. Dr Grouse: Can you tell us about any new developments in EEG that are on the horizon we should be aware of?  Dr Weber: Yeah. So, I think my two favorites, which I highlight in the article, are longer-term recordings---so, there's some companies that are working on subcutaneous EEG. So, implanted EEG electrodes that can stay in your body for the short, long term on the order of year or years and constantly send some EEG data. Obviously, it's not a full montage in most of those cases, but some EEG data that can help you assess long-term trends in epilepsy and long-term response to therapies. I think that's going to be really cool. I think it's very exciting and I think it'll change how we do clinical trials in the future. I think we'll be able to rely less on seizure diaries from folks and more on objective seizure data for patients who have these implanted. But with that will come an ever-increasing amount of data to be reviewed, which leads into the other exciting future trend is AI in the use of interpretations. AI is becoming more and more advanced and there are very exciting articles out on how good AI is getting at interpreting our EEGs. I think soon, in the very near future, the AI platforms will be able to dramatically reduce the amount of time it takes the experts to review an EEG. They'll be able to do a lot of the screening for us and then we can go back, just like I was talking about the quantitative EEG, go back and review segments of the raw data rather than having to review every page of every file, which is quite time consuming. Dr Grouse: Wow, that's really exciting. It certainly does seem like AI is making breakthroughs in just about every area of how we touch the practice of medicine. Exciting to hear that EEG is no exception. Dr Weber: Yeah, I'm fully excited. I think it's going to revolutionize what we're doing and also just greatly expand people's ability to access that level of expertise that the AI will offer. Dr Grouse: I wanted to transition to talking a little bit more about you and your career in neurology. How did you become interested in this area of neurology to begin with? Dr Weber: Yeah, it's sort of a roundabout fashion. So, I started out planning to be a neurointerventionalist, and then I realized that I didn't want that sort of call. For a hot minute in my PGI 3 year. I was planning to be a neuro-ICU doctor. I think that's largely because medicine is all I had been exposed to at that point and the ICU seemed like a very comfortable place. Then as I transitioned into PGI 3 we started doing more electives and outpatient rotations in my residency. And then I was planning on being a movement disorder specialist or an epileptologist, couldn't make up my mind for the longest time. And then I started to like EEG more than I liked watching videos. So, tilted myself towards epilepsy and haven't looked back.  Dr Grouse: Well, I really appreciated you coming to talk with us today about your article. I can't recommend it enough to anyone out there, whoever treats patients with epilepsy or orders the EEGs, I just think it was just incredibly useful. And it was such a pleasure to have you. Dr Weber: Thank you very much for having me, Katie.  Dr Grouse: Again, today I've been interviewing Dr Daniel Weber about his article on EEG and epilepsy, which appears in the most recent issue of Continuum on Epilepsy. 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 this 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.  

Epilepsy classification systems have evolved over the years, with improved categorization of seizure types and adoption of more widely accepted terminologies. A systematic approach to the classification of seizures and epilepsy is essential for the selection of appropriate diagnostic tests and treatment strategies. In this episode, Aaron Berkowitz, MD, FAAN, speaks with Roohi Katyal, MD, author of the article “Classification and Diagnosis of Epilepsy,” in the Continuum February 2025 Epilepsy issue. Dr. Berkowitz is a Continuum® Audio interviewer and a professor of neurology at the University of California San Francisco in the Department of Neurology and a neurohospitalist, general neurologist, and clinician educator at the San Francisco VA Medical Center at the San Francisco General Hospital in San Francisco, California. Dr. Katyal is an assistant professor of neurology and codirector of adult epilepsy at Louisiana State University Health Shreveport in Shreveport, Louisiana. Additional Resources Read the article: Classification and Diagnosis of Epilepsy 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 Guest: @RoohiKatyal Full episode transcript available here Dr Jones: This is Dr Lyell Jones, Editor-in-Chief of Continuum, the premier topic-based neurology clinical review and CME journal from the American Academy of Neurology. Thank you for joining us on Continuum Audio, which features conversations with Continuum's guest editors and authors who are the leading experts in their fields. Subscribers to the Continuum Journal can read the full article or listen to verbatim recordings of the article and have access to exclusive interviews not featured on the podcast. Please visit the link in the episode notes for more information on the article, subscribing to the journal, and how to get CME. Dr Berkowitz: This is Dr Aaron Berkowitz, and today I'm interviewing Dr Roohi Katyal about her article on classification and diagnosis of epilepsy, which appears in the February 2025 Continuum issue on epilepsy. Welcome to the podcast, Dr Katyal, and could you please introduce yourself to our audience? Dr Katyal: Thank you for having me. I'm very excited to be here. I'm Dr Roohi Katyal. I currently work as Assistant Professor of Neurology at LSU Health Shreveport. Here I also direct our adult epilepsy division at LSU Health along with my colleague, Dr Hotait.  Dr Berkowitz: Fantastic. Well, happy to have you here. Your article is comprehensive, it's practical, and it focused on explaining the most recent International League Against Epilepsy (ILAE) classification of epilepsy and importantly, how to apply it to provide patients with a precise diagnosis of epilepsy and the particular subtype of epilepsy to guide the patient's treatment. There are so many helpful tables and figures that demonstrate all of the concepts and how to apply them at the bedside. So, I encourage our listeners to have a look at your article, even consider maybe screenshotting some of these helpful tables onto their phone or printing them out for handy reference at the bedside and when teaching residents. Your article begins with the current definition of epilepsy. So, I want to ask you about that definition and make sure we're on the same page and understand what it is and what it means, and then talk through a sort of hypothetical patient scenario with you to see how we might apply these in clinical practice. You talked about, in your article, how the new definition of epilepsy from the ILAE allows for the diagnosis of epilepsy in three different scenarios. So, could you tell us what these scenarios are? Dr Katyal: So, epilepsy in general is a chronic condition where there is a recurrent predisposition to having seizures. As you mentioned, epilepsy can be diagnosed in one of three situations. One situation would be where an individual has had two or more unprovoked seizures separated by more than 24 hours. The second situation would be where somebody has had one unprovoked seizure and their risk of having recurrent seizures is high. And the third situation would be where somebody had---where the clinical features could be diagnosis of an epilepsy syndrome. An example of that would be a young child presenting with absence seizures and their EEG showing 3 Hz characteristic generalized spike in with discharges. So that child could be diagnosed with childhood absence epilepsy.  Dr Berkowitz: Perfect. Okay, so we have these three scenarios, and in two of those scenarios, we heard the word unprovoked. Just to make sure everyone's on the same page, let's unpack this word “unprovoked” a little bit. What does it mean for a seizure to be unprovoked versus provoked?  Dr Katyal: So unprovoked would be where we don't have any underlying provoking features. So underlying provoking features are usually reversible causes of epilepsy. These would be underlying electrolyte abnormality, such as hyperglycemia being a common one which can be reversed. And these individuals usually do not need long-term treatment with anti-seizure medications. Dr Berkowitz: Fantastic. Tell me if I have this right, but when I'm teaching residents, I… did it provoked and unprovoked---there's a little confusing, right? Because we use those terms differently in common language than in this context. But a provoked seizure, the provoking factor has to be two things: acute and reversible. Because some people might say, well, the patient has a brain tumor. Didn't the brain tumor provoke the seizure? The brain tumor isn't acute and the brain tumor isn't reversible, so it would be an unprovoked seizure. I always found that confusing when I was learning it, so I try to remind learners I work with that provoked means acute and reversible, and unprovoked means it's not acute and not reversible. Do I have that right? Am I teaching that correctly? Dr Katyal: That's correct. Dr Berkowitz: Great. And then the other important point here. So, I think we were all familiar prior to this new guideline in 2017 that two unprovoked seizures more than twenty-four hours apart, that's epilepsy. That's pretty straightforward. But now, just like we can diagnose MS at the time of the first clinical attack with the right criteria predicting that patient is likely to have relapse, we can say the patient's had a single seizure and already at that time we think they have epilepsy if we think there's a high risk of recurrence, greater than or equal to sixty percent in this guideline, or an epilepsy syndrome. You told us what an epilepsy syndrome is; many of these are pediatric syndromes that we've studied for our boards. What hertz, spike, and wave goes with each one or what types of seizures. But what about this new idea that a person can have epilepsy after a single unprovoked seizure if the recurrence rate is greater than sixty percent? How would we know that the recurrence rate is going to be greater than sixty percent? Dr Katyal: Absolutely. So, the recurrence rate over sixty percent is projected to be over a ten year period. So, more than sixty percent frequency rate in the next ten years. And in general, we usually assess that with a comprehensive analysis and test. So, one part of the comprehensive analysis would be, a very important part would be a careful history taking from the patient. So, a careful history should usually include all the features leading up to the episodes of all the prodromal symptoms and warning signs. And ideally you also want to get an account from a witness who saw the episode as to what the episode itself looked like. And in terms of risk assessment and comprehensive analysis, this should be further supplemented with tests such as EEG, which is really a supportive test, as well as neuroimaging. If you have an individual with a prior history of, let's say, left hemispheric ischemic stroke and now they're presenting with new onset focal aware seizures with right arm clonic activity, this would be a good example to state that their risk of having future seizures is going to be high. Dr Berkowitz: Perfect. Yeah. So, if someone has a single seizure and has a lesion, as you said, most common in high-income countries would be a prior stroke or prior cerebrovascular event, prior head trauma, then we can presume that the risk is going to be high enough that we could call that epilepsy after the first unprovoked seizure. What if it's the first unprovoked seizure and the imaging is unremarkable? There's no explanatory lesion. How would we get to a diagnosis of epilepsy? How would we get to a risk of greater than sixty percent in a nonlesional unprovoked seizure? I should say, no lesion we can see on MRI. Dr Katyal: You know, in those situations an EEG can be very helpful. An EEG may not always show abnormalities, but when it does show abnormalities, it can help us distinguish between focal and generalized epilepsy types, it can help us make the diagnosis of epilepsy in certain cases, and it can also help us diagnose epilepsy syndromes in certain cases.  Dr Berkowitz: Perfect. The teaching I remember from a resident that I'm passing on to my residents, so please let me know if it's correct, is that a routine EEG, a 20-minute EEG after a single unprovoked seizure, this sensitivity is not great, is that right? Around fifty percent is what I was told with a single EEG, is that right? Dr Katyal: Yeah, the sensitivity is not that great. Again, you know, it may not show abnormality in all the situations. It's truly just helpful when we do see abnormalities. And that's what I always tell my patients as well when I see them in clinic. It may be abnormal or it may be normal. But if it does show up normal, that does not rule out the diagnosis of epilepsy. Really have to put all the pieces together and come to that finally diagnosis. Dr Berkowitz: Perfect. Well, in that spirit of putting all the pieces together, let's walk through together a hypothetical case scenario of a 19-year-old patient who presents after a first event that is considered a possible seizure. First, how do you approach the history and exam in this scenario to try to determine if you think this was indeed an epileptic seizure?  Dr Katyal: So, if I'm seeing them in the clinic or in the outpatient setting and they're hopefully presenting with somebody who's already seen the seizure itself, my first question usually is if they had any warning signs or any triggers leading up to the episode. A lot of times, you know, patients may not remember what happened during the episode, but they may remember if they felt anything different just before or the day prior, something different may have happened around that time. Yeah, so they may report that. Then a very important aspect of that would be talking to somebody who has seen the episode, a witness of the episode; and ideally somebody who has seen the onset of the episode as well, because that can give us very important clues as to how the event or the episode started and how it progressed. And then another very important question would be, for the individual who has experienced it, is how they felt after the episode ended. So, you can get some clues as to if they had a clear postictal state. Other important questions would be if they had any tongue biting or if they lost control of their bladder or all those during the episode. This, all those pieces can guide us as to if the seizure was epileptic, or the episode was epileptic or not. Dr Berkowitz: Fantastic. That's very helpful guidance. All right. So, let's say that based on the history, you're relatively convinced that this patient had a generalized tonic clonic seizure and after recovering from the event, you do a detailed neurologic exam. That's completely normal. What's your approach at this point to determining if you think the seizure was provoked or unprovoked, since that's, as you said, a key component of defining whether this patient simply had a seizure, or had a seizure and has epilepsy? Dr Katyal: The important findings would be from the laboratory test that may have been done at the time when the patient first presented with the seizure. So, we want to rule out features like hypoglycemia or other electrolyte abnormalities such as changes in sodium levels or big, big fluctuations there. We also want to rule out any other metabolic causes or other reasons such as alcohol withdrawal, which can be a provoking factor. Because these would be very important to rule out is if we find a provoking reason, then this individual may not need to be on long term anti-seizure medication. So very important to rule that out first.  Dr Berkowitz: Great. So, let's say you get all of your labs and history and toxicology screen and no provoking factors there. We would obtain neuroimaging to see if there's either an acute provoking factor or some type of lesion as we discussed earlier. Let's say in this theoretical case, the labs are normal, the neuroimaging normal. There is no apparent provoking factor, there's no lesion. So, this patient has simply had a single unprovoked seizure. How do we go about now deciding if this patient has epilepsy? How do we try to get ourselves to either an above sixty percent risk and tell this patient they have epilepsy and probably need to be on a medicine, or they have a less than sixty percent risk and that becomes a little more tricky? And we'll talk about that more as well.  Dr Katyal: For in a young patient, especially in a young patient as a nineteen year old as you present, one very important aspect if I get this history would be to ask them about absolutely prior history of similar episodes, which a lot of times they may not have had similar episodes. But then with this age group, you also want to ask about episodes of brief lapses in awareness or episodes of sudden jerking or myoclonic jerking episodes. Because if you have brief lapses of awareness, that could signify an absence seizure in this particular age group. And brief, sudden episodes of myoclonic jerking could be brief myoclonic seizures in this age group. And if we put together, just based on the clinical history, you could diagnose this patient with a very specific epileptic syndrome, which could be juvenile myoclonic epilepsy in the best case. Let's say if you ask about episodes of staring or relapses of awareness, that's not the case, and there's no history of myoclonic jerking episodes or myoclonic seizures, then the next step would be proceeding to more of our supplemental tests, which would be an EEG and neuroimaging. In all cases of new-onset seizure especially should have comprehensive assessment with EEG and neuroimaging to begin with, and we can supplement that with additional tests wherever we need, such as genetic testing and some other more advanced testing.  Dr Berkowitz: That's very helpful. OK, so let's say this particular patient, you talk to them, you talk to their family, no prior history of any types of events like this. No concerns for spells that could---unlike absence, no concern for movements that could sound like myoclonus. So, as you said, we would be looking for those and we could get to part one of the definition. There is more than one spell, even though we're being consulted for one particular event. But let's say this was the only event, we think it's unprovoked, the neuroimaging is normal. So, you said we proceed to an EEG and as you mentioned earlier, if the EEG is abnormal, that's going to tell us if the risk is probably this more than sixty percent and the patient should probably be on a medicine. But common scenario, right, that the patient has an event, they have a full work up, we don't find anything. We're convinced it was a seizure. We get our routine EEG as we said, very good, an affirmative test, but not a perfectly sensitive test. And let's say this person's routine EEG turns out to be normal. So how would you discuss with the patient their risk of a future seizure and the considerations around whether to start an anti-seizure medicine if their work-up has been normal, they've had a single unprovoked seizure, and their EEG is unrevealing? Dr Katyal: And I'm assuming neuroimaging is normal as well in this case? Dr Berkowitz: Correct. Yeah.  Dr Katyal: We have a normal EEG; we have normal neuroimaging as well. So, in this case, you know, it's more of a discussion with the patient. I tell them of that, you know, the risk of seizure may not be higher than sixty percent in this case with all the tests being normal so far and there's no other prior history of similar episodes. So, we have a discussion with them about the risks that can come with future seizures and decide where the medication should be started or not.  Dr Berkowitz: And so how do you approach this discussion? The patient will say, Doctor Katyal, I had one seizure, it was very frightening. I got injured. You told me I can't drive for however many months. One cannot drive in that particular state. But I don't really like taking medicines. What is my risk and what do you think? Should I take a medicine?  Dr Katyal: I'll tell you this because normally I would just have a direct conversation with them, discuss all the facts that we have. We go over the seizure one more time just to make sure we have not missed any similar episodes or any other episodes that may be concerning seizure, which ruled out all the provoking factors, any triggers that may be seen inseizures like this in a young age. And another thing would be to basically have a discussion with them, you know, these are the medication options that we can try. And if there is another seizure, you know, these are the these are the restrictions that would come with it. And it's a very individualized decision, to be honest. That, you know, not everyone may want to start the medication. And you'll also find that some patients who, you know, some individuals are like no,  I want to go back to driving. I don't want to be in this situation again. I would like to try a medication and don't want to ever have a seizure. So, I think it's a very individualized decision and we have a discussion with the patient based on all of these tests. And I would definitely maintain follow-up with them to make sure that, you know, things have not changed and things have---no seizures have recurred in those cases.  Dr Berkowitz: Yeah, great to hear your approach. And similar experience to you, right, where some patients say, I definitely don't want to take the medication, I'll roll the dice and I hope I don't have another seizure. And we say, we hope so also. As you said, let's keep a close eye. And certainly, if you have another seizure, it's going to be a lifelong seizure medicine at that point. And some patients who, as you said, say, wait, I can't drive for months. And if I don't take a medicine and I have a seizure in the last month, I would have to have another period of no driving. Maybe in that case, they would want to start a medicine. That said, we would present that either of these are reasonable options with risks and benefits and these are the medications we would offer and the possible side effects and risk of those, and make a joint decision with the patient. Dr Katyal: Absolutely correct. Mentioned it perfectly well that this is a very individualized decision and a joint decision that we make with the patient.  Dr Berkowitz: Fantastic. Another topic you touch on in your article is the definition of resolved epilepsy. How is that defined in the guidelines?  Dr Katyal: Yes. So, an epilepsy can be considered resolved if an individual has been seizure-free for at least ten years and has been off of IV seizure medications for at least five of those years. Another situation where epilepsy can be considered resolved would be if they have an age-defined epilepsy syndrome and now they are beyond the relevant age group for the syndrome.  Dr Berkowitz: That's very helpful. So again, a very clear definition that's helpful in these guidelines. And yet, as I'm sure you experience your practice, as I do in mine, sometimes a little challenging to apply. So, continuing with our made-up hypothetical patient here, let's say at some point in the subsequent years, they have a second unprovoked seizure, still have a normal EEG but they do go on an anti-seizure medicine. And maybe four or five years later, they're seizure-free on a low dose of an anti-seizure medicine. And they say, you know, do I really still need this medicine? I'd really like to come off of it. What do you think? Is that safe? How do you talk about that with the patient? This definition of ten years and five years off medicine seems to be---and maybe unless someone's seeing a lot of children and young adults, a relatively uncommon scenario. It's we've had a first unprovoked seizure. We never figured out why. We don't really know why they had the seizure. We can't really gauge their subsequent risk. They're on medicines, they don't want to be on them and it's only been a few years, let's say three, four, or five years. How do you frame discussion with the patient? Dr Katyal: Yeah, so that's the definition of being resolved. But in terms of tapering off medications, we can usually consider tapering off medications earlier as well, especially if they've been seizure-free for two or more years. Then again, as we mentioned earlier, it would be a very individualized decision and discussion with the patient, that we could consider tapering off of medication. And we would also want to definitely discuss the risk of breakthrough seizures as we taper off and the risks or the lifestyle modifications that would come with it if they have another breakthrough seizure. So, all those things will go into careful concentration when we decide to taper off, because especially driving restriction may be a big, you know, hard stop for a lot of patients that, you know, now is not a time to taper off medication. So, all of these factors will go into consideration and we could consider tapering off earlier as well.  Dr Berkowitz: That's very helpful. Yeah, as you said, when we're tapering off medications, if that's the direction the patient wants to go during that period, obviously we wouldn't want them to drive, or be up on a ladder, or swimming alone. You said that some patients might say, actually, I'll keep the medicine, whereas some might say, OK, I'll hold off on all these activities and hope that I can be off this medication. I remember epilepsy colleagues quoting to me at one point that all comers, when a patient's been seizure-free for two years, they estimate the risk of relapse, of having another seizure, somewhere around thirty to forty percent. In your expert opinion, is that about what you would quote to a patient as well,. about a thirty to forty percent, all comers? Obviously not someone who's had a history of status epilepticus and has a lesion or a syndrome, but in the sort of common situation of some unprovoked seizures in an adult, we don't have a clear ideology. Is that thirty to forty percent figure, more or less, you would place the risk when you talk to the patient? Or?  Dr Katyal: Yeah, absolutely, especially if the neuroimaging is completely normal, all their EE GS have been normal. They have been in this situation---you have a young patient with two seizures separated by so many years. After three or four years of being on the medication and, you know, the patient has been adhering. There are no more seizures. Thirty to forty percent seems reasonable, and this is what I usually tell them that the risk of, as we taper off medications, that risk is not zero but it's low. And around thirty percent is relatively where we would place the risk at. Dr Berkowitz: We've said in this theoretical case that the EEG is normal. But last question, I've heard some practitioners say that, well, let's say the patient did have an abnormal EEG early on. Not a syndrome, but had maybe a few focal spike wave discharges or sharps and that made you convinced that this patient had epilepsy. But still becomes seizure free for several years. I've heard of some practitioners repeating the EEG before tapering the anti-seizure medicines and I always wonder, would it change anything? It's a brief twenty-minute period. They still have one spike, but I tell them they can't come off. If the spikes are gone, it may be because of the medication, and maybe when I take them off they would have a spike. And how do you use---do you use or how do you use EEG in that decision of whether to taper a medicine? Dr Katyal: Yeah. In general, I would not always use an EEG for considering tapering off medication. Again, it's very individualized decision. I can give you a hypothetical example, but it's a fairly common one, is that if an individual with let's say focal seizures with impaired awareness, they live alone, they live by themselves. Oftentimes they'll say that, I'm not sure if I'm missing any seizures because nobody has seen them. I may or may not be losing awareness, but I'm not too certain. They have not had any definite seizures for history in the last couple of years and are now considering tapering off medication. So, this may be a situation where I may repeat an EEG, and perhaps even considering the longer EEG for them to understand their seizure burden before we decide to taper off medication. But in most situations, especially if we consider the hypothetical situation you had mentioned for the young patient who had to witness seizures separated by several years and then several years without any seizures, that may be a good example to consider tapering off medication, especially considering all the tests that had been normal before then.  Dr Berkowitz: That's very helpful to hear. And of course, this is your expert opinion. As you said, no guidelines and different people practice in different ways, but helpful to hear how you approach this common and challenging scenario for practitioners. Well, I want to thank you again, Dr Katyal. This has been a great opportunity to pick your brain on a theoretical case, but one that I think presents a number of scenarios that a lot of us---myself as a general neurologist, as well as you and your colleagues as epileptologists, we all see in general practice patients with unprovoked seizures and a revealing workup, and how to approach this challenging scenario based on the guidelines and on your expert opinion. I learned a lot from your article. Encourage our readers again to take a look. A lot of very helpful tables, figures, and explanations, some of the concepts we've been discussing. So again, today I've been interviewing Dr Roohi Katyal about her article on classification and diagnosis of epilepsy, which appears in the most recent issue of Continuum on Epilepsy. Be sure to check out Continuum audio episodes from this and other issues. And thank you again so much to our listeners for joining us.  Dr Katyal: Thank you 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 this 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.

“We know that some women are going to get called back. And it's just because usually they can't see something clearly enough. And so in most cases, those women are going to get cleared with one or two images, and they're going to say, ‘Oh, we compress that better, we checked it with an ultrasound, we're fine.' That woman can go ahead and go. But we don't want to miss those early breast cancers,” Suzanne Mahon, DNS, RN, AOCN®, AGN-BC, FAAN, professor emeritus at Saint Louis University in Missouri, told Jaime Weimer, MSN, RN, AGCNS-BS, AOCNS®, manager of oncology nursing practice at ONS, during a conversation about what oncology nurses need to know about breast cancer diagnosis.  Music Credit: “Fireflies and Stardust” by Kevin MacLeod  Licensed under Creative Commons by Attribution 3.0   Earn 0.75 contact hours of nursing continuing professional development (NCPD) by listening to the full recording and completing an evaluation at courses.ons.org by January 31, 2027. The planners and faculty for this episode have no relevant financial relationships with ineligible companies to disclose. ONS is accredited as a provider of nursing continuing professional development by the American Nurses Credentialing Center's Commission on Accreditation. Learning outcome: Learners will report an increase in knowledge related to breast cancer diagnostic considerations.  Episode Notes   Complete this evaluation for free NCPD.  Previous ONS Podcast™ site-specific episodes: Episode 345: Breast Cancer Screening, Detection, and Disparities  ONS Voice articles: An Oncology Nurse's Guide to Cascade Testing  Breast Cancer Prevention, Screening, Diagnosis, Treatment, Side Effect, and Survivorship Considerations  ONS books: Breast Care Certification Review (second edition)  Guide to Breast Care for Oncology Nurses  ONS courses: Breast Cancer Bundle  Breast Cancer: Prevention, Detection, and Pathophysiology  ONS Biomarker Database results for breast cancer  ONS Learning Libraries:  Breast Cancer  Genomics and Precision Oncology    American Cancer Society: Early Detection and Diagnosis  Breast Cancer Facts and Figures   Your Breast Pathology Report: Breast Cancer  National Comprehensive Cancer Network    National Cancer Institute Breast Cancer—Patient Version  To discuss the information in this episode with other oncology nurses, visit the ONS Communities.   To find resources for creating an ONS Podcast Club in your chapter or nursing community, visit the ONS Podcast Library.  To provide feedback or otherwise reach ONS about the podcast, email pubONSVoice@ons.org.  Highlights From This Episode  “When a woman gets a callback, that is incredibly anxiety provoking, because they're very scared and they don't know what it means. And I think that's a place where oncology nurses can remind—if it's patients or friends who are asking—that just because you have a call back, doesn't mean you have a malignancy.” TS 8:16  “We also know that when we call somebody back, that's very scary and anxiety provoking. And we don't want to subject women to unnecessary anxiety and stress through the procedure. And if it's too stressful, they won't come back again. That is actually a big harm that we don't want to occur. That's considered an acceptable amount. So we know that some women are going to get called back, and it's just because usually they can't see something clearly enough.” TS 11:26  “I think one of the most important things is to really help that woman understand the biopsy report. So now everybody, with most of the electronic medical records, that woman seeing that biopsy result—maybe before her provider is seeing it, depending on whether they get a chance to call that individual. But, you know, they could get a notification in their medical record, or a new report is available, and they can click on there and they could be looking at something that is very scary, not necessarily a good time, you know, like they're getting ready to do something. And so that is a problem overall with sometimes getting bad news in oncology.” TS 15:09  “Sometimes it's really good [for patients to bring] someone who can just be that set of ears or who can answer those questions, who's emotionally involved but maybe not so emotionally involved, if that makes sense. And I think that that is something we can really encourage people to identify that person who's going to really be able to support them.” TS 16:42  “When we approach a pathology report, the patient, you know, if they open that on their own, they're just going to see breast carcinoma, or they aren't going to look at all of the details of it. They can be quite overwhelming to look at. But I think that it's important to kind of take the patient through it, step by step, and realize that it's often a case of repeated measures—that you might do it and then you might do it again the next day or a day later.” TS 20:55  “Breast cancer care has changed so much over the past few decades. And I think people forget, you know, I've been in the business a long time, but years ago, everybody kind of got the same treatment if they got diagnosed. And we now understand so much about breast cancer treatment, but I think that has come on the shoulders of so, so, so many women who have enrolled in clinical trials to help us understand pathology better, to help us understand the impact of certain treatments. And so I think, first of all, we need to thank those women who have generously contributed to this base of knowledge. And it's a place where those clinical trials have really made a difference.” TS 35:46