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The current social, political and historical context offers many difficult challenges. We have experienced up close and from a distance awareness of a remarkable number of challenges including the wars, political unrest, growing socioeconomic inequities, climate catastrophe, and human and animal suffering.  These times are also marked by polarized thinking, including among analysts, candidates and in our communities.  An application of a psychoanalytically-informed method that rests on psychoanalytic clinical theory but focuses on group experiences of psycho-historical conflict as it continues in the present is offered as a means to facilitate deep and moving change when there is toxic polarization.    In this episode, Dr. Harriet Wolfe presents a unique application of psychoanalytic thinking.  She describes an interdisciplinary group that is international, intergenerational and diverse that meets periodically to apply analytic thinking to intractable large scale historical group traumas.  This method, called the International Dialogue Initiative includes psychoanalysts but also others (e.g. economists, lawyers, diplomats, historians) who share stories and deeply listen with the purpose of gaining perspective on unmanageable feelings through exploring cases of traumatic residues. While others, including Freud have theorized application of psychoanalysis to groups, this particular use is novel and important in today's times and speaks to how psychoanalysis can be truly psychoanalytic and at the same time be applied to political and social issues. Harriet Wolfe, M.D., is President of the International Psychoanalytical Association, Past President of the American Psychoanalytic Association, Clinical Professor of Psychiatry and Behavioral Sciences at the University of California San Francisco, and Training and Supervising Analyst at the San Francisco Center for Psychoanalysis. Her scholarly interests include clinical applications of psychoanalytic research, organizational processes, female development, and therapeutic action. She has co-authored a number of psychoanalytically informed guided activity workbooks for children, parents and teachers to help children cope with natural and manmade disasters. She has a private practice of psychoanalysis, and individual and couple's psychoanalytic psychotherapy in San Francisco. This Podcast Series, published by the International Psychoanalytical Association, is part of the activities of the IPA Communication Committee and is produced by the IPA Podcast Editorial Team. Co-Editors: Gaetano Pellegrini and Nicolle Zapien. Editing and Post-Production: Massimiliano Guerrieri. To stay informed about the latest podcast releases, please sign up today. A subtitled version of this podcast is available on our YouTube channel: You can download a copy of the paper here.            

Dr. Tracey Woodruff chats with Jake about how drinking, eating and even breathing microplastics are impacting reproductive health, increasing cancer risk and more. They also discuss what can be in our personal lives and in public policy to address these impacts. Dr. Woodruff directs the Program on Reproductive Health & the Environment at the University of California San Francisco.

Our health and the health of our soil are deeply intertwined. Modern agriculture has become heavily dependent on synthetic inputs and industrial practices that strip the land of vitality, and the farmers of agency. Many farmers no longer eat what they grow, suffer from poor health, and experience alarming rates of depression and suicide. But there's a path forward: regenerative farming not only restores soil health and increases nutrient density in food, it also revitalizes rural communities and offers economic resilience. By reconnecting with natural systems and rebuilding diversity in our soil, food, and microbiomes, we reclaim both ecological balance and human well-being. In this episode, I discuss, along with Allen Williams, Dr. Daphne Miller, and Ian Somerhalder the many facets of modern-day farming, including what we need to pay attention to and why we need to reclaim our soil. Allen Williams is a founding partner of Understanding Ag, LLC and the Soil Health Academy, and is a partner in Joyce Farms, Inc. He has consulted with more than 4,000 farmers and ranchers in the US and other countries, on operations ranging from a few acres to over 1 million acres. Allen and his partners pioneered many of the early regenerative agriculture principles and practices and now teach those to farmers globally. He is a “recovering academic,” having served 15 years on the faculty at Louisiana Tech University and Mississippi State University teaching genetics and physiology. Allen has been featured in the Carbon Nation film series, Soil Carbon Cowboys, on the Dr. Oz show, ABC Food Forecast News, and in Kiss The Ground, A Regenerative Secret, The Farmer's Footprint film series, and the Sacred Cow film series.  Dr. Daphne Miller is a practicing family physician, Clinical Professor at the University of California San Francisco, and Founder of the Health from the Soil Up Initiative. She is the author of two books: The Jungle Effect: Healthiest Diets from Around the World and Farmacology: Total Health from the Soil Up. A pioneer in the “Healthy Parks, Healthy People” initiative, Miller helped build linkages between our medical system and our park system and writes her patients “park prescriptions” to get outdoors. She also developed a soil learning lab for health professionals at Paicines Ranch in Hollister California. Ian Somerhalder is an American actor, philanthropist, and entrepreneur. Best known for his iconic roles on "Lost" and "The Vampire Diaries," he is co-founder of The Absorption Company (a revolutionary supplement company formulated for increased absorption) and co-owner of Brother's Bond Bourbon. His recent work includes executive producing the documentary "Common Ground" (2023), which highlights regenerative agriculture's innovative solutions to combat climate change. This episode is brought to you by BIOptimizers. Head to bioptimizers.com/hyman and use code HYMAN10 to save 10%. Full-length episodes can be found here: Can Regenerative Agriculture Reverse Climate Change And Chronic Disease? Why Your Health Depends on the Soil Why Our Farms Hold the Key to a Healthier Future

Recently, sophisticated myelographic techniques to precisely subtype and localize CSF leaks have been developed and refined. These techniques improve the detection of various types of CSF leaks thereby enabling targeted therapies. In this episode, Katie Grouse, MD, FAAN, speaks with Ajay A. Madhavan, MD, author of the article “Radiographic Evaluation of Spontaneous Intracranial Hypotension” in the Continuum® June 2025 Disorders of CSF Dynamics 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. Madhavan is assistant professor of radiology at the Mayo Clinic in Rochester, Minnesota. Additional Resources Read the article: Radiographic Evaluation of Spontaneous Intracranial Hypotension Subscribe to Continuum®: shop.lww.com/Continuum Earn CME (available only to AAN members): continpub.com/AudioCME Continuum® Aloud (verbatim audio-book style recordings of articles available only to Continuum® subscribers): continpub.com/Aloud More about the American Academy of Neurology: aan.com Social Media facebook.com/continuumcme @ContinuumAAN Full episode transcript available here Dr 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 Ajay Madhavan about his article on Radiographic Evaluation of Spontaneous Intracranial Hypotension, which he wrote with Dr Levi Chazen. This article appears in the June 2025 Continuum issue on disorders of CSF dynamics. Welcome to the podcast, and please introduce yourself to our audience. Dr Madhavan:  Hi, thanks a lot, Katie. Yeah, so I'm Ajay Madhaven. I'm a neuroradiologist at the Mayo Clinic in Rochester, Minnesota. I did all my training here, so, I've been here for a long time. And I have a lot of interest in spinal CSF leaks, and I do a lot of that work. And so I'm really excited to be talking about this article with you. Dr Grouse:  I'm really excited too. And in fact, it's such a pleasure to have you here talking today on this topic. I know a lot's changed in this field, and I'm sure many of our listeners are really interested in learning about the developments and imaging techniques to improve detection and treatment of CSF leaks, especially since maybe we've learned about this in training. I want to start by asking you what you think is the most important takeaway from your article. Dr Madhavan:  Yeah, that's a great question. I think---and you kind of already alluded to it---I think the main thing is, I hope people recognize that this field has really changed a lot in the last five to ten years, through a lot of multi-institutional collaboration and also collaboration between different specialties. We've learned a lot about different types of spinal CSF leaks, how we can recognize the disease, particularly the types of myelography that we need to be using to accurately localize and treat these leaks. Those are the things that have really evolved in the last five to ten years, and they've really helped us improve these patients' lives. Dr Grouse:  Can you remind us of the different common types of spinal leaks that can cause spontaneous intracranial hypotension? Dr Madhavan:  Yeah, so there are a number of different spinal CSF leaks, types, and I would say the three most common ones that really most people should try to be aware of and cognizant of are: first, ventral dural tears. So those are, like, just physical holes in the dura. And they're usually caused by little bone spurs that come from the vertebral columns. So, they're often patients who have some degenerative changes in their spine. And those are really very common. Another type of spinal CSF leak that we commonly see is a lateral dural tear. So that's like the same thing in a slightly different location. So instead of being in the front, it's off to the side of the dura laterally. And so, it's also just a hole in the dura. And then the third and most recently discovered type of spinal CSF leak is a CSF-venous fistula. So those are direct connections between the subarachnoid space and little paraspinal vein. And it took us a long time to even realize that this was a real pathology. But now that it's been recognized, we've found that this is actually quite common. So those three types of leaks are probably the three most common that we see. And there's certainly others out there, but I would say over 90% of them fall into one of those three categories. Dr Grouse:  That's a great review, thank you. Just as another quick review, as we talk more about this topic, can you remind us of some of the most common or typical brain imaging findings that you'll see in cases of spontaneous intracranial hypotension? Dr Madhavan:  Yeah, absolutely. So, when you do a brain MRI in a patient who has spontaneous intracranial hypotension, you will usually, though not always, see typical brain MRI abnormalities. And I kind of think of those as falling into three different categories. So, the first one I think of is dural enhancement or thickening. So that's enlargement or engorgement of the dura, the pachymeninges, and enhancement on postgadolinium imaging. So, that's kind of the first category. The second is that, when you lose spinal fluid volume, other things often expand to take up the space. So, for example, you can get distension or enlargement of the dural venous sinuses, and sometimes you can also get subdural food collections or hematomas. They can arise spontaneously. And I kind of think of those as, you know, you, you've lost the cerebrospinal fluid volume and something else is kind of filling up the space. And then the third category is called brain sagging. And that's a constellation of findings where the posterior fossa structures and the pituitary gland in the cell have become abnormal because you've lost the fluid that normally cushions those structures and causes them to float up. For example, the brain stem will sag down, the distance between the mammillary body and the ponds may become reduced. The suprasellar cistern space may be reduced such that the optic chiasm becomes very close to the pituitary gland, and the prepontine cistern may also become reduced in size. And there are various measurements that can be used to determine whether something is subtly abnormal. But just generally speaking, those are really the three categories of brain MRI abnormalities you'll see. Dr Grouse:  That was a great review. And of course, I think in many times when we are thinking about or suspecting this diagnosis, we may be lucky to find those imaging findings to reinforce a diagnosis. Because as it turns out, after reading your article, I was really surprised to find out that in as many as 19% of cases we actually see normal brain imaging, which really was a surprise to me, I have to say. And I think that this really encompasses why spontaneous intercranial hypotension is such a difficult diagnosis to make. I think a lot of us struggle with how far to take the workup when, you know, spontaneous intercranial hypotension is clinically suspected, but multiple imaging studies are normal. Do you have any guidance on how to approach these more difficult cases? Dr Madhavan:  So, that's a really good question. And you know, it's- as you can imagine, that's a topic that comes up in most meetings where people discuss this, and it's been a continued challenge. And so, like you said, about 19 or 20% of patients who have this disease can have a, a normal brain MRI. And we've tried to do some work to figure out why that is and how we can identify patients who still have the disease. And I can just provide, I guess, some tips that have helped me in my clinical practice. One thing is, if I ever see a patient with a normal brain MRI where this disease is clinically suspected---for example, maybe they have orthostatic headaches or other very typical symptoms and we don't know why, but their brain MRI is normal---the first thing I do is I try to look back at their old imaging. So many times, these patients who present to us at Mayo, who, when we do their MRI scan here, their brain MRI looks normal… if you really look back at imaging that they've had done elsewhere---maybe even two to three years prior---at the time their symptoms started, they actually had some abnormalities. So, I might see that a patient, two years ago, had dural enhancement that spontaneously resolved; but now they still have symptoms of SIH and they may still have a CSF leak that we can find and treat, but their brain MRI has, for whatever reason, normalized. So, I always start by looking back at old imaging, and I found that to be very helpful. The other thing is, if you see a patient with a normal brain MRI, it's also important to look at their spine MRI because that can provide clues that might suggest that they could still have a spinal CSF leak. And the two things I look for on the spine MRI: one, if there's any extradural CSF. So, spinal fluid outside of where it's supposed to be within the confines of the subarachnoid space. And you know, really, if you see extradural CSF, you know they probably have a spinal fluid leak somewhere. Even if their brain MRI is normal, that just gives you the information that there is a dural tear probably somewhere. And so, in those patients we'll definitely still proceed to myelography or other testing, even if they have a normal brain MRI. And then the last thing I look for is whether or not they have prominent meningeal diverticula. Patients with CSF venous fistulas almost always have one or more prominent diverticula on their spine along the nerve root sleeves. And that's probably because most of these fistulas come from nerve root sleeve diverticula. We don't completely understand the pathogenesis of CSF venous fistulas, but they're clearly associated with meningeal diverticula. So, if I see a patient who has a normal brain MRI, but I see on their spine MRI that they have many meningeal diverticula that are relatively prominent, that makes me more inclined to be a little bit more aggressive in doing myelography to find a CSF leak. And then I look at other demographic features, too. So, for example, elevated BMI and older age are associated with CSF venous fistulas. So, that can help you determine whether or not it's warranted to go on to more advanced imaging, too. So those are all just a variety of different things that we've used to help us. Dr Grouse:  Thank you for sharing that. I wanted to go on to say that, you know, reading your article, of course, as you mentioned, you alluded to the fact there's lots of new imaging modalities out there. It was very illuminating and just an excellent resource for the options that exist and when they're useful. You did a great job summarizing it. And I encourage our readers to check out your article, to refresh themselves, update themselves on what's happened in this space. And of course, we can't summarize them all today, but I was wondering if you could possibly walk us through a hypothetical case of a patient who comes in with a history very suspicious for SIH? How would you approach this patient? Say you have gotten imaging that suggested that there is a spinal fluid leak and now you have to figure out where it is. Dr Madhavan:  Yeah. So, you know, I think the most typical scenario it'll be a patient who has been seen by one of my excellent neurology colleagues and they've done a brain MRI and they've made the diagnosis through a combination of clinical information and brain MRI finding. And then the next thing we'll do always is, we'll obtain a spine MRI. So, I think of the purpose of the spine MRI as to determine what type of spinal fluid leak they have. On the spine MRI, if you see extradural CSF, those patients essentially always will have a dural tear. And it may be a ventral dural tear or a lateral dural tear. But if you see extradural CSF, that is pretty much what they have. And conversely, if you don't see extradural CSF---if you just see, for example, many meningeal diverticula, but you don't see anything else particularly abnormal---most of those patients have a CSF venous fistula, just common things being common. So I use the spine MRI to determine what type of leak they have. And then the next thing I think about is, okay, I'm going to do a myelogram on this patient. How do I want to position them? Because it turns out that positioning is probably the most important factor for finding these spinal fluid leaks. You have to have the patient positioned correctly to find the leak that you're trying to localize. And so, if I suspect they have a ventral dural tear, I will always position those patients prone for their myelogram. And I might do one of many different types of myelograms. And, you know, the article talks about things like digital subtraction myelography and dynamic CT myelography. And you can find any of these leaks with any of those techniques, but you just have to have the patient positioned correctly. So, if I think I have a ventral dural tear, I'll put them prone for the myelogram. If I think they have a lateral dural tear, I'll put them in the cubitus position for the myelogram. And also, if they- if I think they have a CSF-venous fistula, I'll also put them in the decubitus position. Obviously if you're putting them in the decubitus position, you have to decide whether it's going to be left or right side down. So that may require a two-day exam. Sometimes you don't have to; in many cases, we're able to just do everything in one day. But those are all the different factors I think about when I'm trying to determine how I'm going to work those patients up further. So, I really use the spine MRI chiefly to think about what type of leak they're going to have and how I'm going to plan the myelogram. Dr Grouse:  That's really great. And it's, I think, really nice to emphasize how much the positioning matters in all this, which I think is not something we've been classically taught as far as the diagnosis of spinal leaks. Another thing I'm really interested in your opinion on is, you talked a lot about how to optimize and what can make you successful at diagnosis. I'm curious what you think one of the easiest mistakes to make or, you know, that we should hopefully avoid when treating patients with this disease. Dr Madhavan:  Yeah. And I think, you know, one other thing that's been discussed a lot in this topic… you know, we've talked about the patients with a normal brain MRI. Another barrier or challenge particularly with CSF-venous fistulas is, sometimes they can be very subtle on imaging. So, it's not always you see it very definitive CSF-venous fistula where you can say, like, there's no question, that's a fistula. There are many times where we do a good-quality myelogram and we see something that looks, like, possible for a CSF venous fistula, or probable. If I had to put a number on it, maybe there's a 50 to 70% chance of real. So, in those cases, we end up wondering, like, should we treat this suspected leak? And I think one common mistake  or one thing that needs to be looked at further is, how do we handle these patients where we don't know whether the fistula is real or not? That's usually something where I will have a discussion with the patient, and I'm usually just very upfront with him about my interpretation of the imaging. I'll just tell them, we did a good-quality myelogram. You did a great job. We got good images. I don't see anything definitive, but I see this thing that I think has maybe a 60% chance of being real. And then I'll confer with one of my neurology colleagues and we'll decide whether it's worth treating that or not. And we'll just be very upfront with a patient about whether- about the likelihood of its success and what their long-term prognosis is. And oftentimes we let them make the decision. But I think that remains to be one of the big challenges is, how do we treat these patients who have suspected leaks that are not definitive on imaging. Dr Grouse:  That sounds absolutely like an important area where there can be problems, so I appreciate that insight. I'm interested what you think in your article would come as the biggest surprise to our listeners who may not have kept up as much with all of the changes that have happened in recent years? Dr Madhavan:  One of the things that was certainly, at least, a surprise to me as I was going through my training and learning about this topic is how diverse myelography has really become. You know, when I was a radiology resident, I learned about myelography as this thing that we've been doing for 30 to 40 years. And historically we've used myelograms just to look for degenerative changes: disc bulges, you know, disc herniations and things like that. Now that MRI is more prevalent, we don't use it as much, but it has turned out that it has a very big role in patients with spinal fluid leaks. Furthermore, something that I've learned is just how diverse these different types of myelograms have become. It used to kind of be just that a myelogram is a myelogram is a myelogram, but now we have different types of positioning, different types of equipment that we use. We vary the timing between contrast injection and imaging to optimize success for finding spinal fluid leaks. So, I think many times I talk to people who may not be as familiar with this field and they're surprised at just how diverse that has become and how sophisticated some of the various myelographic techniques have become and how much that really makes a difference in being able to accurately diagnose these patients. Dr Grouse:  Well, I can say it was a surprise to me. Even as someone who does treat quite a few patients with this condition, I was surprised to see the breadth of different options that have become available. And then kind of a follow-up to that, what do you think the current area of controversy is in this area of diagnosis and treatment? Dr Madhavan:  The biggest ones are ones you've sort of already alluded to. So, one big one is, how far do we go in patients who have a normal brain MRI who still have a clinical suspicion of the disease? And sometimes it's really hard, because sometimes you will find patients who clinically have a very strong case for having spontaneous intracranial hypotension. You look at them, they have very acute-onset orthostatic headaches. There's no better explanation for their symptoms that we know of. And it's hard to know what to do with those patients, because some of them want to continue to undergo diagnostic workup, but you can only do so many myelograms and you can only do so much with this diagnostic workup that requires some radiation dose before it becomes very challenging. That's a major point of just, I guess, ongoing research as to what can we do better for that subset of patients. Fortunately, it's not all of them, it's a subset of them, but I think we could help those patients better in the future as we learn more about the disease. So that's one. And the other one is treating these equivocal findings, like I discussed.  And where should our threshold be to treat a patient, and what type of treatment should we do in patients where we don't know whether a leak is real? Should we just do a very noninvasive- relatively noninvasive blood patch? Do we do an embolization where we're leaving a foreign body there? Is it worth sending those patients to surgery? Those are all unanswered questions and things that continue to spark ongoing debate. Dr Grouse:  Do you think that there's going to be any new big breakthroughs, or even, do you know of any big developments on the horizon that we should be keeping our eyes out for? Dr Madhavan:  You know, I think for me the biggest thing is, imaging is dramatically improving. We talked a little bit about photon counting detector CT in our article, and that's one of the newest and best techniques for imaging these patients because it has very, very high resolution, it has a lower radiation dose, it has allowed us to find leaks that we were not able to find before. And there are other high-resolution modalities that are emerging and becoming more accessible to things like cone beam CT which we do in addition to digital subtraction myelography. And on top of that, we've started to use AI-based tools to make images look a lot better. So, there are various AI algorithms that have come out that allow us to remove artifacts from imaging. They help us image patients with a bigger body habitus better without running into a lot of imaging artifacts. They help us reduce noise in imaging. They can just give us better-quality images and aid us in the diagnosis. For me as a radiologist, those are some of the most exciting things. We're finding less invasive ways with less radiation to better diagnose these patients with just better-quality imaging. Dr Grouse:  Well, that is definitely something to be excited about. So, I just want to thank you so much for talking with us today. It's been such an interesting, informative discussion and a real privilege to talk with you about this important topic. Dr Madhavan:  Yeah, thanks so much. I really appreciate the time to talk with you, and I look forward to seeing the article out there and hopefully getting some interesting questions. Dr Grouse:  Again, today I've been interviewing Dr Ajay Madhavan about his article on Radiographic Evaluation of Spontaneous Intracranial Hypotension, which he wrote with Dr Levi Chasen. This article appears in the most recent issue of Continuum on disorders of CSF dynamics. 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.

Today neuroscientist and psychiatrist Dr. Kieran Fox joins in to talk about the spiritual journey of Albert Einstein.About our guest:Dr. Kieran Fox is a neuroscientist (PhD 2016) and doctor (MD 2023), currently training to be a psychiatrist in the Research Resident Training Program at the University of California San Francisco. His research over the next few years will focus on the neural mechanisms and clinical potential of psychedelic medicines. During medical school, he used intracranial electrical stimulation (neuromodulation) of the human brain to research cognition and emotion in epilepsy patients.

Mifepristone is the first (and extremely safe) in two medications that people will take during a medication abortion—and access to it is under blatant attack in the courts. Dr. Ushma Upadhyay, Public Health Scientist based at University of California San Francisco, and Julia Kaye, Senior Staff Attorney with the ACLU's Reproductive Freedom Project, sit down to talk with us about recent anti-abortion propaganda and how it could be used to shape the FDA's regulations of medication abortion.A past case, Alliance for Hippocratic Medicine v. FDA, was brought by anti-abortion groups to a federal judge in Texas known to have a hostile record against abortion with the goal of challenging the FDA's mifepristone regulations. The Supreme Court ruled that these groups could not challenge the regulations in June 2024. Anti-abortion Attorneys General of Missouri, Kansas, and Idaho are now attempting to revive this litigation, called Missouri v. FDA. Meanwhile, a new report from a Project 2025-backed organization falsely states that 11% of people who have a medication abortion have a serious adverse event. Sec. Kennedy has cited this report as a basis for conducting a “complete review” of the FDA's mifepristone regulations. For more information, check out Boom! Lawyered: https://rewirenewsgroup.com/boom-lawyered/ Support the showFollow Us on Social: Twitter: @rePROsFightBack Instagram: @reprosfbFacebook: rePROs Fight Back Bluesky: @reprosfightback.bsky.social Email us: jennie@reprosfightback.comRate and Review on Apple PodcastThanks for listening & keep fighting back!

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.

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.

When women think about the benefits of menopausal hormone therapy, things like hot flashes, insomnia and vaginal dryness come to mind.  But for many women, bone health is, or should be, at the top of the list.   In this episode, I speak with Dr. Risa Kagan about the role of estrogen, progesterone, and testosterone in bone health. Definition of Low Bone Mass (Osteopenia) and Osteoporosis The Difference Between a T score and a Z score  FRAX- Fracture Risk Assessment Tool When Bone Mass Peaks How to Maximize Bone Health Before Menopause Hits Role of Estrogen in Young Women The Danger Zone- When Most Women Lose the Majority of Their Bone Mass The Role of Birth Control Pills and Prevention of Bone Loss If Exercise is Enough The Relationship Between Hot Flashes and Osteoporosis Bone Loss Post Menopause Impact of Menopausal Estrogen Therapy on Bones Taking Menopausal Hormone Therapy (MHT) in the Absence of Hot Flashes to Protect Bones The Difference Between Bone Density and Bone Quality When it is Appropriate to Take an Anabolic Agent If the TYPE of Estrogen you take matters (Conjugated, Synthetic, Bioidentical) What DOSE of Estrogen is Needed to Prevent Fractures If it is Appropriate to Monitor Estradiol Blood Levels When Taking Transdermal MHT The Target Estradiol Level for Bone Health What Happens to Bone Density When MHT is Discontinued If MHT Should Be Taken Forever If Progestogens Plays a Role in Bone Health The Role of Bazodoxifene (Duovee™) in Bone Health The Role of TESTOSTERONE therapy in Bone Health Another Podcast with Dr. Kagan: When Progesterone is a Problem   Dr. Risa Kagan is a Clinical Professor in the Department of Obstetrics, Gynecology, and Reproductive Sciences at the University of California San Francisco, and a consulting gynecologist with Sutter Health. Dr. Kagan has published over 100 scientific papers  on post menopause bone health and hormone therapy.  Dr. Streicher is on SUBSTACK      DrStreicher.Substack.com Articles Monthly newsletter All COME AGAIN podcast episodes Monthly News Flash Reports on recent research  Monthly Zoom Ask Me Anything Webinar   Information on Dr. Streicher's COME AGAIN Podcast- Sexuality and Orgasm Lauren Streicher MD, is a clinical professor of obstetrics and gynecology at Northwestern University's Feinberg School of Medicine, the founding medical director of the Northwestern Medicine Center for Sexual Medicine and Menopause, and a Senior Research Fellow of The Kinsey Institute, Indiana University. She is a certified menopause practitioner of The Menopause Society. She is the Medical Director of Community Education and Outreach for Midi Health.   Dr. Streicher is the medical correspondent for Chicago's top-rated news program, the WGN Morning News, and has been seen on The Today Show, Good Morning America, The Oprah Winfrey Show, CNN, NPR, Dr. Radio, Nightline, Fox and Friends, The Steve Harvey Show, CBS This Morning, ABC News Now, NBCNightlyNews,20/20, and World News Tonight. She is an expert source for many magazines and serves on the medical advisory board of The Kinsey Institute, Self Magazine, and Prevention Magazine. She writes a regular column for The Ethel by AARP and Prevention Magazine.    LINKS Subscribe To Dr. Streicher's Substack Information About the COME AGAIN Podcast Dr. Streicher's CV and additional bio information To Find a Menopause Clinician and Other Resources  Glossary Of Medical Terminology Books by Lauren Streicher, MD  Slip Sliding Away: Turning Back the Clock on Your Vagina-A gynecologist's guide to eliminating post-menopause dryness and pain Hot Flash Hell: A Gynecologist's Guide to Turning Down the Heat Sex Rx- Hormones, Health, and Your Best Sex Ever The Essential Guide to Hysterectomy                                       Dr. Streicher's Inside Information podcast is for education and information and is not intended to replace medical advice from your personal healthcare clinician. Dr. Streicher disclaims liability for any medical outcomes that may occur because of applying methods suggested or discussed in this podcast.              

Tensions between Robert F. Kennedy Jr. and his employees at the Department of Health and Human Services are mounting, as he made a series of claims about autism this week — contradicting his agency's findings. Plus, President Donald Trump unveiled an executive order to lower drug prices as his administration explores tariffs that could raise them.Shefali Luthra of The 19th, Jessie Hellmann of CQ Roll Call, and Anna Edney of Bloomberg News join KFF Health News' Emmarie Huetteman to discuss these stories and more.Plus, KFF Health News' Julie Rovner interviews two University of California-San Francisco researchers about an upcoming Supreme Court case that could have major ramifications for preventive care. Plus, for “extra credit” the panelists suggest health policy stories they read this week that they think you should read, too: Emmarie Huetteman: KFF Health News' “States Push Medicaid Work Rules, but Few Programs Help Enrollees Find Jobs,” by Sam Whitehead, Phil Galewitz, and Katheryn Houghton. Anna Edney: ProPublica's “Unsanitary Practices Persist at Baby Formula Factory Whose Shutdown Led to Mass Shortages, Workers Say,” by Heather Vogell. Jessie Hellmann: The Hill's “Military's Use of Toxic ‘Forever Chemicals' Leaves Lasting Scars,” by Sharon Udasin and Rachel Frazin. Shefali Luthra: The 19th's “Trump's Push for ‘Beautiful Clean Coal' Could Lead to More Premature Births,” by Jessica Kutz. Visit our website to read a transcript of this episode. Hosted on Acast. See acast.com/privacy for more information.

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.

Guest: Jennie Taylor, MD Defined by the production of 2-hydroxyglutarate, mutant isocitrate dehydrogenase (mIDH) gliomas are diffuse, slow-growing tumors. Managing these tumors requires personalized strategies that consider resectability, histology, and long-term treatment impacts. Dr. Jennie Taylor, Assistant Professor of Neurology and Neurological Surgery at the University of California San Francisco, explains the complexities behind this type of tumor and implications for patient care. Dr. Taylor also spoke about this topic at the 2025 American Academy of Neurology Annual Meeting.

Guest: Jennie Taylor, MD The FDA approval of vorasidenib marks a new era for mutant isocitrate dehydrogenase (mIDH) gliomas. Approved in 2024 for grade 2 tumors after surgery, it doubled progression-free survival in the INDIGO trial. Dr. Jennie Taylor, Associate Professor of Neurology and Neurological Surgery at the University of California San Francisco, dives into the data and explains what questions remain about long-term use and broader applications.

Guest: Jennie Taylor, MD The FDA approval of vorasidenib marks a new era for mutant isocitrate dehydrogenase (mIDH) gliomas. Approved in 2024 for grade 2 tumors after surgery, it doubled progression-free survival in the INDIGO trial. Dr. Jennie Taylor, Associate Professor of Neurology and Neurological Surgery at the University of California San Francisco, dives into the data and explains what questions remain about long-term use and broader applications.

Guest: Jennie Taylor, MD Defined by the production of 2-hydroxyglutarate, mutant isocitrate dehydrogenase (mIDH) gliomas are diffuse, slow-growing tumors. Managing these tumors requires personalized strategies that consider resectability, histology, and long-term treatment impacts. Dr. Jennie Taylor, Assistant Professor of Neurology and Neurological Surgery at the University of California San Francisco, explains the complexities behind this type of tumor and implications for patient care. Dr. Taylor also spoke about this topic at the 2025 American Academy of Neurology Annual Meeting.

Guest: Jennie Taylor, MD Defined by the production of 2-hydroxyglutarate, mutant isocitrate dehydrogenase (mIDH) gliomas are diffuse, slow-growing tumors. Managing these tumors requires personalized strategies that consider resectability, histology, and long-term treatment impacts. Dr. Jennie Taylor, Assistant Professor of Neurology and Neurological Surgery at the University of California San Francisco, explains the complexities behind this type of tumor and implications for patient care. Dr. Taylor also spoke about this topic at the 2025 American Academy of Neurology Annual Meeting.

Guest: Jennie Taylor, MD The FDA approval of vorasidenib marks a new era for mutant isocitrate dehydrogenase (mIDH) gliomas. Approved in 2024 for grade 2 tumors after surgery, it doubled progression-free survival in the INDIGO trial. Dr. Jennie Taylor, Associate Professor of Neurology and Neurological Surgery at the University of California San Francisco, dives into the data and explains what questions remain about long-term use and broader applications.

Get Dr. Mina's free PDF on How to create Healthy Skin Habits here. Download the free eBook 'Skincare Myths Busted' here. Dr. Mina and Dr. Amelia K Hausauer dive deep into the world of Platelet-Rich Plasma (PRP) therapy — breaking down what it is, how it works, and why it's become a go-to in dermatology. From treating hair loss and skin rejuvenation to supporting microneedling, stretch marks, and wound healing, they explore the wide range of applications for PRP. Dr. Hausauer also unpacks the key differences between PRP and Platelet-Rich Fibrin (PRF), shares insight into safety and patient outcomes, and emphasizes the importance of working with a knowledgeable provider. The conversation covers techniques like microneedling with PRP (hello, vampire facial), various injection methods, and the exciting future of regenerative medicine. Whether you're curious about incorporating PRP into your treatments or want a deeper understanding of its potential, this episode is a must-listen.    Key Takeaways: - PRP is derived from the patient's own blood and is rich in signaling molecules. - The field of PRP has evolved significantly over the last decade. - Regeneration is becoming a key focus in modern medicine. - Patients are increasingly interested in natural healing methods. - PRP is most commonly used for hair regrowth and skin treatments. - The effectiveness of PRP can vary based on individual patient factors. - Optimizing platelet levels can enhance PRP treatment outcomes. - Timing and diet can influence the effectiveness of PRP treatments. - Microneedling with PRP can significantly improve skin texture and collagen production. - Injecting PRP can be beneficial for targeted areas like scars and under-eye skin. PRP is most effective when integrated into a comprehensive treatment plan. - Microneedling enhances the release of growth factors from PRP. - Stretch marks can be treated with PRP, often in combination with other modalities. - Safety is paramount; choose a qualified provider for PRP treatments. - PRF differs from PRP in preparation and application, affecting its use. - PRP can accelerate healing in post-surgical and acne scarring cases. - Building a relationship with your provider enhances treatment outcomes. - The medical community is evolving with new regenerative therapies. - PRP has a low risk of allergic reactions due to its autologous nature. - Future advancements in regenerative medicine are promising and exciting. Dr. Amelia K. Hausauer is the Director of Dermatology and Head of Aesthetic Medicine at Aesthetx, a hybrid dermatology and plastic surgery practice in Northern California. She is a key opinion leader for early pipeline innovation and development of multiple injectable and regenerative therapies as well as an active research investigator. Dr. Hausauer spearheaded one of the largest clinical trials using PRP for hair growth and served as the chief editor for Platelet Rich Plasma (PRP) and Microneedling in Aesthetic Medicine. She has published over a dozen articles in peer reviewed journals and teaches throughout the world on cutting-edge techniques in injectable medicine. Earning a bachelor's degree from Stanford University and medical doctorate from University of California San Francisco, Dr. Hausauer completed residency at New York University then an American Society for Dermatologic Surgery cosmetic surgery fellowship.   Follow Dr. Hausauer here: https://www.instagram.com/drhausauer https://www.instagram.com/aesthetxmd https://www.aesthetx.com/   Follow Dr. Mina here:-  https://instagram.com/drminaskin https://www.facebook.com/drminaskin https://www.youtube.com/@drminaskin https://www.linkedin.com/in/drminaskin/ For more great skin care tips, subscribe to The Skin Real Podcast or visit www.theskinreal.com Baucom & Mina Derm Surgery, LLC Email - scheduling@atlantadermsurgery.com Contact - (404) 844-0496 Instagram - https://www.instagram.com/baucomminamd/ Thanks for listening! The content of this podcast is for entertainment, educational, and informational purposes and does not constitute formal medical advice.

In collaboration with the Women in Otolaryngology (WIO) Section of the American Academy of Otolaryngology Head and Neck Surgery. Join Dr. Taylor Standiford Erickson as she discusses pay equity and negotiation as a female surgeon with Dr. Kathy Yaremchuk, Chair Emeritus of the Department of Otolaryngology - Head and Neck Surgery at Henry Ford in Detroit, Michigan, and Dr. Jolie Chang, Professor and Chief of Sleep Surgery in the Department of Otolaryngology - Head and Neck Surgery at the University of California San Francisco.

When you look at a list of the typical symptoms associated with perimenopause, you'd think you were looking at a list of MS symptoms. And, for women living with MS, that's where the confusion begins. With an estimated 30% of the current MS population now in peri- or post-menopause, researchers are beginning to focus on how menopause and MS interact and the best ways to treat symptoms.   Dr. Riley Bove, a neurologist and founding director of the Sex and Gender-Enriched (SAGE) Neurology Program at the University of California San Francisco, joins me to talk about the things you need to know when you're managing MS while you're managing menopause. We'll also tell you about this year's winner of the John Dystel Prize for Multiple Sclerosis Research. We'll share a deeply personal poem written by a friend who's been living with MS since 1988. And we'll tell you about the results of a study that should be a reminder of the importance of starting disease-modifying therapy and the value of early intervention. We have a lot to talk about! Are you ready for RealTalk MS??! This Week: We're in Washington, D.C., at the National MS Society's Public Policy Conference  :22 Dr. Amit-Bar-Or is the winner of the 2025 John Dystel Prize for Multiple Sclerosis Research  2:26 Magician Wayne Dobson's poem  7:07 STUDY: Cognitive impairment is prevalent among people living with untreated MS  10:23 Dr. Riley Bove talks about the things you need to know when you're managing MS while you're managing perimenopause and menopause  14:18 Share this episode  32:56 Have you downloaded the free RealTalk MS app?  33:16 SHARE THIS EPISODE OF REALTALK MS Just copy this link & paste it into your text or email: https://realtalkms.com/395 ADD YOUR VOICE TO THE CONVERSATION I've always thought about the RealTalk MS podcast as a conversation. And this is your opportunity to join the conversation by sharing your feedback, questions, and suggestions for topics that we can discuss in future podcast episodes. Please shoot me an email or call the RealTalk MS Listener Hotline and share your thoughts! Email: jon@realtalkms.com Phone: (310) 526-2283 And don't forget to join us in the RealTalk MS Facebook group! LINKS If your podcast app doesn't allow you to click on these links, you'll find them in the show notes in the RealTalk MS app or at www.RealTalkMS.com Become an MS Activist Web: https://nationalmssociety.org/advocacy Email: msactivist@nmss.org RealTalk MS 2025 ACTRIMS Forum YouTube Playlist https://www.youtube.com/playlist?list=PLATxgj1uHpxNEoc2-9_7-Wzmr96B7wt2C Join the RealTalk MS Facebook Group https://facebook.com/groups/realtalkms Download the RealTalk MS App for iOS Devices https://itunes.apple.com/us/app/realtalk-ms/id1436917200 Download the RealTalk MS App for Android Deviceshttps://play.google.com/store/apps/details?id=tv.wizzard.android.realtalk Give RealTalk MS a rating and review http://www.realtalkms.com/review Follow RealTalk MS on Twitter, @RealTalkMS_jon, and subscribe to our newsletter at our website, RealTalkMS.com. RealTalk MS Episode 395 Guests: Dr. Riley Bove Privacy Policy

What if the most common symptoms of obstructive sleep apnea in women aren't the ones doctors are trained to recognize? In this episode, Dr. Megan Durr, an otolaryngologist from the University of California San Francisco, discusses obstructive sleep apnea in women with host Dr. Gopi Shah.  The doctors explore how symptoms in women differ from men, leading to missed diagnoses. They delve into the lack of literature on the topic and the potential for underrepresented groups to be overlooked. The conversation highlights the need for more inclusive screening tools and the long-term cardiovascular risks women face due to untreated sleep apnea. Dr. Durr emphasizes the importance of better diagnosing and treating sleep apnea in women.  TIMESTAMPS 00:00 - Introduction  00:18 - Recognizing Obstructive Sleep Apnea in Women  00:36 - Pregnancy and Obstructive Sleep Apnea  01:13 - Menopause and Sleep Disorders  01:59 - Underrepresented Groups and OSA 02:47 - Symptoms and Misdiagnosis in Women  04:40 - Screening Questionnaires and Gender Bias  05:59 - Clinical Observations and Gender Disparities  09:39 - Long-term Effects of OSA in Women  CHECK OUT THE FULL EPISODE BackTable ENT Podcast Episode #182 Understanding OSA in Women with Dr. Megan Durr https://www.backtable.com/shows/ent/podcasts/182/understanding-osa-in-women

Originally broadcast February 15, 2024 About 1 in 5 colorectal patients are now under the age of 55, and colorectal cancer is now the leading cause of cancer death for men under age 50 and the second for women under 50. During Colorectal Cancer Awareness Month, we present this encore presentation of our interview with Dr. Alan Venook. Dr. Venook is with the University of California-San Francisco and is one of the nation's leading colorectal cancer researchers. He explained to... Read More Read More The post Colorectal Cancer Rising for Millennials & Gen Z: How to Reverse the Trend appeared first on Healthy Communities Online.

In this podcast, Series 4, Chapter 1, Dr. Barsuk interviews Dr. Roy Soetikno, gastroenterologist, advanced endoscopist, and Professor of Medicine at the University of California San Francisco.  Dr.  Soetikno is internationally renowned for his efforts to disseminate knowledge about simulation-based mastery learning in endoscopy. They discuss Dr. Soetikno's international work on improving endoscopy training through the use of the science of expertise and simulation-based mastery learning.

In this episode of Going anti-Viral, Dr Michael Saag speaks with Dr Diane Havlir, Professor of Medicine at the University of California San Francisco. Dr Havlir currently serves as Chair of the Scientific Program Committee for the 2025 Conference on Retroviruses and Opportunistic Infections (CROI) and joins Dr Saag to provide a preview of CROI 2025. Dr Havlir provides an overview and history of CROI along with a summary of how the program is developed. Dr Saag and Dr Havlir review why CROI is unique among scientific meetings: leading scientific advances, poster sessions, and the focus on supporting new investigators. They also discuss expected hot topics from CROI such as: HIV treatment and cure, STI prevention, weight management, aging and HIV, as well as pediatric and adolescent care. Dr Saag and Dr Havlir provide an overview of resources that will be available to those who will not attend CROI in person. Finally, they discuss the value of CROI during a challenging time for all involved in the field of HIV research, care, and treatment.0:00 – Introduction1:36 – Overview and history of CROI4:12 – What makes CROI unique6:21 – Discussion of how the CROI program is developed both abstract and invited presentations11:04 – How attendees can interact at CROI12:06 – Features of poster abstract sessions and poster hall13:42 – CROI focus on new investigators17:55 – Hot topics at CROI 202520:45 – Resources for people not attending CROI22:26 – Value of CROI during a challenging time and closing remarksCROI Resources: https://www.croiconference.org/ __________________________________________________Produced by IAS-USA, Going anti–Viral is a podcast for clinicians involved in research and care in HIV, its complications, and other viral infections. This podcast is intended as a technical source of information for specialists in this field, but anyone listening will enjoy learning more about the state of modern medicine around viral infections. Going anti-Viral's host is Dr Michael Saag, a physician, prominent HIV researcher at the University of Alabama at Birmingham, and volunteer IAS–USA board member. In most episodes, Dr Saag interviews an expert in infectious diseases or emerging pandemics about their area of specialty and current developments in the field. Other episodes are drawn from the IAS–USA vast catalogue of panel discussions, Dialogues, and other audio from various meetings and conferences. Email podcast@iasusa.org to send feedback, show suggestions, or questions to be answered on a later episode.Follow Going anti-Viral on: Apple Podcasts YouTubeXFacebookInstagram...

In this episode of the Award-winning PRS Journal Club Podcast, 2025 Resident Ambassadors to the PRS Editorial Board – Christopher Kalmar, Ilana Margulies, and Amanda Sergesketter- and special guest, Edward I. Chang, MD, discuss the following articles from the February 2025 issue: “Avoiding Patient Abandonment: A Pathway to Ethical Resolution in Situations of Untenable Patient–Surgeon Relationships” Prescher, Gudex, Mauch, and Vercler. Read the article for FREE: https://bit.ly/EthicalMngmnt Special guest, Edward I. Chang, MD, who is a board-certified plastic surgeon and Professor in the Department of Plastic Surgery at the University of Texas MD Anderson Cancer Center in Houston, Texas. Dr. Chang trained at the University of California San Francisco for plastic surgery residency, followed by a fellowship in microvascular reconstructive surgery at the University of Texas MD Anderson Cancer Center in Houston, Texas. He was the 2024 ASRM Godina Fellow, currently serves on the editorial board of PRS Journal, and is widely published in reconstructive microsurgery. READ the articles discussed in this podcast as well as free related content: https://bit.ly/JCFeb25Collection

Episode 184: Multiple Myeloma BasicsSub-Interns and future Drs. Di Tran and Jessica Avila explain the symptoms, work up and treatment of multiple myeloma. Written by Di Tran, MSIV, Ross University School of Medicine; Xiyuan Yang, MSIV, American University of the Caribbean. Comments by Jessica Avila, MSIV, American University of the Caribbean. Edits by Hector Arreaza, MD.You are listening to Rio Bravo qWeek Podcast, your weekly dose of knowledge brought to you by the Rio Bravo Family Medicine Residency Program from Bakersfield, California, a UCLA-affiliated program sponsored by Clinica Sierra Vista, Let Us Be Your Healthcare Home. This podcast was created for educational purposes only. Visit your primary care provider for additional medical advice.Di: Hi everyone, this is Di Tran, 4th year medical student from Ross university.  It's a pleasure to be back.  To be honest, this project is a part of teamwork of two medical students, myself and another 4th year, her name is XiYuan.  She came from the AUC. Unfortunately, due to personal matters she was unable to make it to the recording today which makes me feel really sad. Jessica: My name is Jessica Avila, MSIV, American University of the Caribbean.Di: The topic we will present today is Multiple Myeloma. Multiple myeloma is typically a rare disease and it's actually a type of blood cancer that affects plasma cells in the bone marrow.Jessica: Let's start with a case: A 66-year-old male comes to his family doctor for an annual health checkup. He is not in any acute distress but he reports that he has been feeling tired and weaker than usual for the last 3 months. He also noticed that he tends to bruise easily. He has a history of arthritis and chronic joint pain, but he thinks his back pain has gotten worse in the last couple of months. Upon checking his lab values, his family doctor found that he has a calcium level of 10.8 and a creatinine level of 1.2, which has increased from his baseline. Given all that information, what do you think his family doctor is suspecting? And what kind of tests she can order for further evaluation?Di: Those symptoms sound awfully familiar – are we talking about the CRAB? You know, the diagnostic criteria for Multiple Myeloma.Jessica: Exactly! Those are called “myeloma-defining events.” Do you remember what those are?Di: CRAB criteria comes in 4 flavors.  It's HYPERCALCEMIA with >1mg/dL, RENAL INSUFFICIENCY with serum creatinine >2mg/dL, ANEMIA with hemoglobin value 10% plasma cells, PLUS any one or more of the CRAB features, we can make the official diagnosis of multiple myeloma. Di:  Before we go deeper, let's back up a little bit and do a little background.  So, what do we know about the immunoglobulins, also known as antibodies? Back from years of studying from medical school, we know that the plasma cells are the ones that producing the antibodies that help fight infections.  There  are various kinds that come with various functions.  Each antibody is made up of 2 heavy chains and 2 light chains.  For heavy chains, we have A, D, E, G, M and for light chains we have Kappa and Lambda.Jessica: Usually, the 5 possible types of immunoglobulins for heavy chains would be written as IgG, IgA, IgD, IgE, and IgM.  And the most common type in the bloodstream is nonetheless the IgG. Di: What is multiple myeloma? In myeloma, all the abnormal plasma cells make the same type of antibody, the monoclonal antibody.  The cause of myeloma is unknown, but there are lots of studies and evidence that show a number of potential etiologies, including viral, genetic, and exposure to toxic chemicals, especially the Agent Orange, which is a chemical used as herbicide and defoliant. It was used as a chemical warfare by the U.S. military during the Vietnam War from 1961 to 1971.Jessica: We need to order some specific blood tests to see if there is elevated monoclonal proteins in the blood or urine. So, to begin with we'll need to take a very thorough history and physical exam. Next, we'll do labs, such as CBC, basic metabolic panel, calcium, serum beta-2 microglobulin, LDH, total protein, and some not so common tests: serum protein electrophoresis (SPEP), immunofixation of blood or urine (IFE), quantitative immunoglobulins (QIg), serum free light chain assay, and serum heavy/light chain ratio assay.If any of the results is abnormal, we should consider referring our patient to an oncologist.Di: Interesting! I read that Multiple Myeloma symptoms vary in different patients.  In fact, about 10-20% of patients with newly diagnosed myeloma do not have any symptoms at all.   Otherwise, classic symptomatic presentations are weakness, fatigue, increased bruising under the skin, reduced urine output, weakened bones that is likely prone to fractures, etc. And if multiple myeloma is highly suspected, a Bone Marrow biopsy should be done with testing for flow cytometry and fluorescent in situ hybridization (FISH). Actually, if any of the “Biomarkers of malignancy (SLIM)” is met we can also diagnose multiple myeloma even without the CRAB criteria. Jessica: The diagnosis is made if one or more of the following is found: >= 60% of clonal plasma cells on bone marrow biopsy, > 1 lytic bone lesion on MRI that is at least 5mm in size, or a biopsy confirmed plasmacytoma. Di: Imaging comes in at the final step especially if we able to find one or more sites of osteolytic bone destruction > 5mm on an MRI scan.Jessica: What if the bone marrow biopsy returns > 10% of monoclonal plasma cells, but our patient doesn't have either the CRAB or the Biomarker criteria? Di: That's actually a very good question, since Multiple Myeloma is part of a spectrum of plasma cell disorders. That's when smoldering myeloma comes into play. It is a precursor of active multiple myeloma. Smoldering myeloma is further categorized as high-risk or low-risk based on specific criteria.A less severe form is called Monoclonal Gammopathy of Undetermined Significance, or simply MGUS, with < 10% bone marrow involvement. Those are diagnoses we give once we rule out actual multiple myeloma, which are defined by the amount of M-protein in the serum.Jessica:  When to get started on treatment? Multiple Myeloma is on a spectrum of plasma cells proliferative disorders, starting from MGUS to Smoldering Myeloma, to Multiple Myeloma and to  Plasma Cell Leukemia.  Close supervision/active watching is enough for MGUS and low risk Smoldering Myeloma. But once it has progressed to high-risk smoldering myeloma or to active Multiple Myeloma, chemotherapy is usually required. Some situations may require emergent treatment to improve renal function, reduce hypercalcemia, and to prevent potential infections.Di: As of 2024, treatment of Multiple Myeloma comprises the Standard-of-Care approved by the FDA. In fact, the quadruple therapy is a combination of 4 different class of drugs that include a monoclonal antibody, a proteasome inhibitor, an immunomodulatory drug, and a steroid. Jessica: They are Darzalex (daratumumab), Velcade (bortezomib), Revlimid (lenalidomide) and dexamethasone.  Other treatment plans for Multiple Myeloma include chemotherapy, immunotherapy, radiation therapy (for plasmacytomas) and stem cell transplants. The patient will also be on prophylaxis acyclovir and Bactrim while on chemotherapy. Sometimes anticoagulants are also considered because the chemo increases the risk of venous thromboembolic events.Di: Although the disease is incurable, but with the advancing of novel therapies and clinical trials patients with multiple myeloma are able to live longer.  Problem is the majority of patients diagnosed with Multiple Myeloma are older adults (>65), the risk of falling is adding to multiple complications of the disease itself, such as bone density loss, pain, neurological compromises, distress and weakness.  Palliative care may come in help at any point in time throughout the course of treatment but is most often needed at the very end of the course. Jessica, can you give us a conclusion for this episode?Jessica: Multiple Myeloma may not be the most common cancer, but we have to be aware of the symptoms and keep it in our differential diagnosis for patients with bone pain, easy bruising, persistent severe headaches, unexplained renal dysfunction, and remember the CRAB: HyperCalcemia, Renal impairment, Anemia and Bone lesions.Even without trying, every night you go to bed a little wiser. Thanks for listening to Rio Bravo qWeek Podcast. We want to hear from you, send us an email at RioBravoqWeek@clinicasierravista.org, or visit our website riobravofmrp.org/qweek. See you next week! _____________________References:International Myeloma Foundation. (n.d.). International Myeloma Working Group (IMWG) criteria for the diagnosis of multiple myeloma. https://www.myeloma.org/international-myeloma-working-group-imwg-criteria-diagnosis-multiple-myeloma Laubach, J. P. (2024, August 28). Patient education: Multiple myeloma symptoms, diagnosis, and staging (Beyond the Basics). UpToDate. https://www.uptodate.com/contents/multiple-myeloma-symptoms-diagnosis-and-staging-beyond-the-basics.University of California San Francisco. (n.d.). About multiple myeloma. UCSF Helen Diller Family Comprehensive Cancer Center. https://cancer.ucsf.edu/research/multiple-myeloma/about Theme song, Works All The Time by Dominik Schwarzer, YouTube ID: CUBDNERZU8HXUHBS, purchased from https://www.premiumbeat.com/.

In this episode of the Award-winning PRS Journal Club Podcast, 2025 Resident Ambassadors to the PRS Editorial Board – Christopher Kalmar, Ilana Margulies, and Amanda Sergesketter- and special guest, Edward I. Chang, MD, discuss the following articles from the February 2025 issue: “Reliability and Safety of the Superthin Anterolateral Thigh Flap: A Comprehensive Evaluation of Perfusion-Related Complications and Donor-Site Morbidity” by Yoo, Kim, and Lee. Read the article for FREE: https://bit.ly/SuperthinALT Special guest, Edward I. Chang, MD, who is a board-certified plastic surgeon and Professor in the Department of Plastic Surgery at the University of Texas MD Anderson Cancer Center in Houston, Texas. Dr. Chang trained at the University of California San Francisco for plastic surgery residency, followed by a fellowship in microvascular reconstructive surgery at the University of Texas MD Anderson Cancer Center in Houston, Texas. He was the 2024 ASRM Godina Fellow, currently serves on the editorial board of PRS Journal, and is widely published in reconstructive microsurgery. READ the articles discussed in this podcast as well as free related content: https://bit.ly/JCFeb25Collection

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.  

In this episode of the Award-winning PRS Journal Club Podcast, 2025 Resident Ambassadors to the PRS Editorial Board – Christopher Kalmar, Ilana Margulies, and Amanda Sergesketter- and special guest, Edward I. Chang, MD, discuss the following articles from the February 2025 issue: “Contralateral Autologous Augmentation in DIEP Flap Reconstruction: Employing Computed Tomography Angiography and Volumetric Analysis for Preoperative Planning” by Hespe, Sugg, Stein, et al. Read the article for FREE: https://bit.ly/CTAugPlanning Special guest, Edward I. Chang, MD, who is a board-certified plastic surgeon and Professor in the Department of Plastic Surgery at the University of Texas MD Anderson Cancer Center in Houston, Texas. Dr. Chang trained at the University of California San Francisco for plastic surgery residency, followed by a fellowship in microvascular reconstructive surgery at the University of Texas MD Anderson Cancer Center in Houston, Texas. He was the 2024 ASRM Godina Fellow, currently serves on the editorial board of PRS Journal, and is widely published in reconstructive microsurgery. READ the articles discussed in this podcast as well as free related content: https://bit.ly/JCFeb25Collection  

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.

A Buddhist doctor/nun on how we're all addicted to something—and how to reduce craving.Sister Dang Nghiem, MD, (“Sister D”) was born in 1968 in Vietnam during the Tet Offensive, the daughter of a Vietnamese mother and an American soldier. She lost her mother at the age of twelve and immigrated to the United States at the age of seventeen with her brother. Living in various foster homes, she learned English and went on to earn a medical degree from the University of California – San Francisco. After suffering further tragedy and loss, she quit her practice as a doctor to travel to Plum Village monastery in France founded by Zen Master Thich Nhat Hanh, where she was ordained a nun in 2000, and given the name Dang Nghiem, which means adornment with nondiscrimination. She is the author of a memoir, Healing: A Woman's Journey from Doctor to Nun (2010), and Mindfulness as Medicine: A Story of Healing and Spirit (2015).This episode is part of our monthlong Do Life Better series. We talk about:Sister D's Buddhist version of the 12 step program, which is a combination of two canonical buddhist lists: the 4 Noble Truths and the Eightfold PathHow willpower doesn't fit into the Buddhist path of understanding and working with addiction How to change addiction at its rootPractical applications of mindfulnessSelf-compassionThe importance of social supportHer thoughts on our relationships to our phones And moreRelated Episodes:Do Life BetterThis Episode Will Make You Stronger | Sister Dang NghiemThe Science Of Manifestation | James DotySign up for Dan's newsletter hereFollow Dan on social: Instagram, TikTokTen Percent Happier online bookstoreSubscribe to our YouTube ChannelOur favorite playlists on: Anxiety, Sleep, Relationships, Most Popular EpisodesFull Shownotes: https://www.meditatehappier.com/podcast/tph/sister-d-899See Privacy Policy at https://art19.com/privacy and California Privacy Notice at https://art19.com/privacy#do-not-sell-my-info.

It's been five years since the first laboratory-confirmed case of COVID-19 in the U.S., a bleak milestone in the early days of a pandemic that touched the lives of everyone. For the lucky ones, the virus mainly meant more precautions: mask-wearing, the occasional COVID test. But for others, a COVID-19 infection turned into long COVID. This is a chronic condition that lingers long after a COVID infection, and can reduce one's ability to live their day-to-day life.It's been estimated that about 400 million people worldwide have had long COVID. Some researchers say that number is much higher. But there's a lack of research on successful treatments for long COVID.Some patients living with the condition have taken things into their own hands. A recent investigation documented the experiences of 13 long COVID patients who tried taking Paxlovid for longer than the typical 5-day course. The patients had mixed results, adding to a growing body of evidence that there will not be one silver bullet for treating the condition.Joining Ira to talk about the results are two authors of the study, who have both had long COVID for years: Dr. Alison Cohen, assistant professor of epidemiology and biostatistics at the University of California San Francisco, and Dr. Julia Moore Vogel, senior program director at Scripps Research in La Jolla, California.Transcripts for each segment will be available after the show airs on sciencefriday.com. Subscribe to this podcast. Plus, to stay updated on all things science, sign up for Science Friday's newsletters.

Recent progress in neurogenetics and molecular pathology has improved our understanding of the complex pathogenetic changes associated with neurodegenerative dementias. In this episode, Katie Grouse, MD, FAAN, speaks with Sonja W. Scholz, MD, PhD, FAAN, an author of the article “Genetics and Neuropathology of Neurodegenerative Dementias,” in the Continuum® December 2024 Dementia 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. Scholz is a senior investigator at the National Institutes of Health in Bethesda, Maryland and an adjunct professor of neurology at Johns Hopkins University in Baltimore, Maryland. Additional Resources Read the article: Genetics and Neuropathology of Neurodegenerative Dementias Subscribe to Continuum: shop.lww.com/Continuum Earn CME (available only to AAN members): continpub.com/AudioCME Continuum® Aloud (verbatim audio-book style recordings of articles available only to Continuum® subscribers): continpub.com/Aloud More about the American Academy of Neurology: aan.com Social Media facebook.com/continuumcme @ContinuumAAN Full episode transcript available here:  Dr 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 Sonia Scholz about her article on genetics and neuropathy of neurodegenerative dementias, which appears in the December 2024 Continuum issue on dementia. Welcome to the podcast, and please introduce yourself to our audience.  Dr Scholz: Thank you so much for inviting me. My name is Sonia Scholz. I'm a neurologist working at the National Institutes of Health. My main focus of research and clinical work are neurodegenerative diseases, and I have a particular interest in using modern genomic tools to understand these diseases and potentially leverage it for new translational applications. Dr Grouse: Sonia, we're really excited to have you today and thanks for joining us.  Dr Scholz: I'm pleased to be here.  Dr Grouse: I'd like to start by asking what you think is the most important message or takeaway point from your article? Dr Scholz: So, this is an article that really captures a very broad and exciting field. So, one thing I wanted to really highlight is that there's a lot of heterogeneity, clinical, pathological, molecular heterogeneity in age-related neurodegenerative dementia syndromes. Our article was really aimed at providing a bird's eye view of the pertinent pathological characteristics, but also important genetic advances and insights and how we can leverage that, particularly in the new physician medicine era, hopefully come up with better treatments and better ways to counsel our patients.  Dr Grouse: What do you think is the most challenging aspect of understanding the genetics and neuropathologic basis of neurodegenerative dementias?  Dr. Scholz: That's a good question. There're many big and challenging questions, but I think one of the things we struggle the most with is really the heterogeneity. I see patients with one and the same Mendelian form of dementia. One patient is in their forties another patient is in their eighties, and the clinical manifestations can be very different from one patient to another. There's a lot of heterogeneity, also, on the pathological level. Not every patient has exactly the same distribution. And so, we're starting to slowly define what the underlying causes are, but it's still quite baffling and quite challenging to put them together and understand them. Dr Grouse: Do you feel that the genome-wide association studies has helped our understanding of these diseases, specifically the heterogeneity? And if so how?  Dr Scholz: That's a great question, but you're talking to a geneticist here. And I definitely would say genome-wide association studies have helped us a lot in identifying what the underlying disease pathways are and what the relationships between neurodegenerative disease entities are. It really also gave us a better understanding of apparently sporadic diseases where genetic factors are still playing a role. And we can leverage that type of knowledge increasingly to highlight high-risk groups, but also, we can increasingly use it to stratify patients for clinical trials, for example. And that's really exciting and there's still a lot of knowledge that we have to garner very quickly, especially in the non-Alzheimer dementia space.  Dr Grouse: You've mentioned, of course, the heterogeneity and these syndromes. And in your article, you go into a lot of the issue of the significant crossover between the genetic links and the neuropathological findings for the various types of neurodegenerative dementias. Do you think that this crossover has been more of a help or a hindrance in better understanding these diseases? Dr Scholz: Yeah, it can be a little bit, you know, challenging to wrap one 's mind around it. But by and large, I think it's actually good news because it highlights that there is a shared biology between many of the neurodegenerative disease entities. And by figuring out which the pathways are that are very often involved, we can prioritize certain targets for therapy development. But we can also be smarter about how we developed treatments. We could repurpose a drug that has been developed for Alzheimer's disease very easily for Lewy body dementia because we increasingly understand the overlap. And we can also leverage new clinical trials design, like basket trials. This is something that has been really transformative in the oncology sphere and now, increasingly, neurodegeneration. We're trying to apply that kind of thinking as well to our patient populations. Dr Grouse: What do you think our listeners will find to be most surprising when they read the article? Dr Scholz: We often present these diseases in our textbooks as these black-and-white entities, but the reality is that there's a lot of overlap. And we also see that co-pathologies are actually the norm and not the exception, and a lot of the molecular risk factors are shared. It's not really surprising. And I think that overlap and crosstalk between the various diseases is something that's a little bit strange to think about, but it actually makes increasingly sense now that we see the genetic risk profiles coming up. Dr Grouse: In reading your article, I was really struck by how many, or how much the prior studies have been lacking in inclusion of different ethno-racial backgrounds in the patients who've been studied. How can this be improved going forward?  Dr Scholz: Yeah, thank you. That's a really important and crucial question, and I think it really takes the collective effort of everybody in the healthcare research community to improve upon that. We need to talk to our patients about genetic testing, about brain donation programs, about referrals to clinical trials, and don't feel shy about reaching out to our colleagues and academic centers, even if you don't have the resources in a smaller institution. We also not only need to engage with the communities, we also need to build up a healthcare research community that has representatives from these various communities. So, it's really a collective effort that we build up and are proactive about building a more equitable healthcare system and research system that works for all of us and that really is going to provide us with the precision medicines that work for everybody. Dr Grouse: What do you think is the biggest debate or controversy related to the genetics and neuropathology of neurodegenerative dementias?  Dr Scholz: Yeah, there are loads of interesting debates, but I think in my field, in particular in the genetics is what to do with risk variance. What is it that I actually communicate to the patient? Obviously, I can learn a lot on the bench and I think I can use a lot of the genetic risk factors for molecular modeling, etc. But to which extent should I share that information? Because genetic information is something that we cannot alter and many of the risk factors are actually mild, that they may never result in disease. And so, communicating risk with patients is something that's very challenging and we used to just steer away from it. But now the discussion is starting to shift a little bit. You know, nowadays we are starting to offer, for example, testing for the APOE4 allele in individuals who are considering antiamyloid therapies. And this really, this is precision medicine in his earliest days because it allows us to stratify patients into those that are high-risk versus low-risk and those that need more frequent follow-up or may be advised not to pursue this treatment. And we're probably going to see more of those discussions and the ethics around it. And it's even harder in an aged population where you know, you may never manifest any of the symptoms despite carrying a lot of these risk deals. Dr Grouse: You mentioned, you know, that testing, APOE4 testing for certain populations when deciding to do the antiamyloid immunotherapies. Apart from that, which I think is a really good example of where genetic testing makes sense, what other scenarios do you think it makes sense at this point in time to recommend genetic testing for symptomatic patients who are concerned about neurodegenerative dementias? Dr Scholz: Yeah. So, I usually have a very frank discussion with patients in whom I suspect the genetic etiology. So those are individuals who have a strong family history, individuals from very early onset of the disease where genetic testing may allow us to establish a molecular diagnosis, individualize and refine our counseling, and potentially get them into targeted clinical trials that may be suitable for that. Those are always very nuanced discussions, but I usually start with those high-risk individuals. Increasingly patients are, even with the apparently sporadic forms, are asking me about it. And then I have a frank discussions about the pros and cons and offer it to the patients who really would like to pursue it.  Dr Grouse: That makes a lot of sense. What about in the case of patients who are asymptomatic but might have high risks because of, well, family members with certain types of neurodegenerative dementias? When would it make sense, if ever, to do genetic testing for them? Dr Scholz: Yeah, that's a that's a tough situation, to be honest. By and large, I would say I would like to understand what the motivation is to learn about the genetic status. If the motivation is something like family planning, future care planning, etc, then it may be a reasonable thing. But I also want to make it very clear upfront that knowing a genetic status, at least aside from APOE status, at least for now, doesn't actually change the clinical management. And I want to make sure patients understand if they are trying to lower their risk, knowing that genetic status is not going to lower their risk. There are other things, brain health habits, that are really important, that patients should double down on: avoiding vascular disease, avoiding traumatic brain injury, excessive alcohol use, etcetera. It's a discussion that really tries to understand the motivations behind the testing. But some patients are very frank and they want to have it. They may want to contribute to the research community, and so in those instances we may offer it, but I also really want to make them understand that knowing a genetic diagnosis may be acceptable to them, but family members who are related to them may not wish to know. And they can really cause a lot of psychological stress that extends beyond the individual. And then that's something to really consider before actually pursuing testing. Dr Grouse: I think that's a really good reminder, especially about how this can even affect people outside of the patient themselves. I think a lot of us don't even think about that. And certainly, our patients may not either. Taking it a step further, thinking about newly available biomarkers, imaging modalities, how should we incorporate the use of these for our patients when we're suspicious of things like Alzheimer's disease or dementia with the Lewy bodies? Dr Scholz: So by and large these biomarkers are used in in the research area, but we can, in a given patient where maybe the clinical presentation is somewhat atypical, we can use it to help with our diagnostic impression. It doesn't get rid of the clinical evaluation, but at least it gives us a little bit more certainty. Here are the you know, the molecular features, the abnormal amyloid tau deposits, for example, that we're there we're detecting supports diagnosis. May also sometimes help in patients where we suspect there could be even the co-pathology going on where we get a mixture of features, where we can counsel the patients and you know, detecting copathologies is something that is certainly challenging. We know that patients who have more pathologies on average are not doing as well as the ones who have relatively pure disease forms. But this is also an area of intense research and as long as it's used judiciously to help with the diagnostic compression, to reduce a diagnostic odyssey, I think there's a lot of potential there to improve the clinical evaluations nowadays. Dr Grouse: It is really exciting to see the options that are opening up as the years go by, which brings me to my next question. There is certainly, as we know, this new category of disease modifying therapies that are available in the form of the anti-amyloid immunotherapies. What else do you think's on the horizon for treatment and prevention, neurodegenerative dementias, going down the road five, ten, fifteen years down the line?  Dr Scholz: Yeah, I think we're entering the era of precision medicine already and we're, we're seeing it already with the anti-amyloid therapies. By and large, I think the standard of care is going to be a multidisciplinary individualized treatment plan that incorporates a more holistic view. It incorporates diet, lifestyle factors, symptomatic management, but also disease modification strategies and potentially even multitarget disease modifying strategies. I think there's a lot more work that we have to do, especially in in the non-Alzheimer's dementia field. But overall, we're becoming much better in refining our diagnostic impression and in treating some of the complications that arise in these very complex diseases.  Dr Grouse: I'm curious, with the future of dementia care and diagnosis being more of a precision medicine model, how do you think this will be possible in an aging population with already, I think, probably a limited access to neurologists even in current state? Dr Scholz: Yeah, this is- these are these are very challenging societal questions. Increasingly, you know, we can use modern technologies such as televisits for follow up, but also, you know, remote monitoring devices. We have to educate the next generation, we need more neurologists, we can't do it alone; but we also need to empower primary care doctors who are usually the first go-to person. And perhaps biomarker testing will become much more common even in the primary care setting. I think overall, you know, we can tackle it by educating the community, empowering participants in various clinical trials, and being flexible of embracing certain new technologies. Dr Grouse: Absolutely. I think that makes a lot of sense and hopefully this will be another call to arms to try to get the word out, get more access to neurology and more people interested and like you said, getting our other colleagues involved and being able to manage it as well.  Dr Scholz: Yeah.  Dr Grouse: I wanted to transition a little bit into learning more about you. How did you become interested in genetics of neurodegenerative dementias? Dr Scholz: Yeah, it's something, it's an interest that has grown gradually. I started out as a neuroscientist in in Austria, where I was fortunate to work with a group that was very strongly involved in Parkinson's disease care. And I was so thrilled to see patients, you know, treated with deep brain stimulation. But yet in the same clinic, I also saw the patients who were not eligible because they had atypical neurodegenerative diseases. And it's the realization that there is such a broad spectrum of diseases that we frankly don't understand very well, that we really need to work with, understand and hopefully develop the treatments with. That's really has resonated with me. And I've since then really built my entire career around it through different countries at the United Kingdom and the United States. And I'm very fortunate to work at the National Institutes of Health, where I can pursue a lot of these research passions and work with interesting patients and colleagues.  Dr Grouse: Well, I've learned a lot today, and I'm sure our listeners would agree. Thank you so much for joining us. It's really been a pleasure speaking with you.  Dr Scholz: Well, thank you so much for allowing me to contribute. And, you know, I hope the review article conveys a lot of the exciting developments in this really challenging field. But there's loads of hope that we will eventually get to the point to tackle these conditions.  Dr Grouse: I encourage all of our listeners to check out Dr Scholz 's article. It is a great overview of these conditions and the genetics and neuropathology underlining them. Again, thank you so much.  Dr Scholz: Thank you for having me. Dr Grouse: Again, today I've been interviewing Dr Sonia Scholz, whose article on genetics and neuropathology of neurodegenerative dementias appears in the most recent issue of Continuum on dementia. 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.

Katie has had a Cesarean (failure to progress), a VBAC, and most recently, an unmedicated breech VBAC!She talks about the power of mom and baby working together during labor. She is 4'10” and attributes so much of her first successful VBAC to movement. Katie's most recent baby was frank breech throughout her entire pregnancy. After multiple ECV attempts, she exhausted all options to seek out a vaginal breech provider. She was able to work with providers while still advocating for what felt right to her. Though there were some wild twists and turns, this breech vaginal birth showed Katie, yet again, just what her body is capable of! The VBAC Link Blog: Why Babies Go Breech & 5 Things You Can Do About ItThe VBAC Link Blog: ECV and BreechHow to VBAC: The Ultimate Prep Course for ParentsFull Transcript under Episode Details Julie: Welcome, welcome. You are listening to The VBAC Link Podcast. This is Julie Francom here with you today. I'm super excited to be sharing some episodes with you guys this year and helping out Meagan a little bit and keeping things rocking and rolling here at The VBAC Link. I am excited to be back, and I am especially excited to be joined by Katie today who has a really, really incredible story about her three births. Her first was a C-section. Her second was a VBAC, and her third was an unmedicated breech VBAC. I absolutely love hearing stories about vaginal breech birth because I feel like it's something that we need to bring back. It's only fair to offer people options when we have a breech baby. I don't think it should just be an automatic C-section. I'm excited to hear her story. I'm excited to hear her journey to find support in that regard. But first, I'm going to read a review. This review is actually from our VBAC Prep course. If you didn't know, we do have a course preparing you all about all of the things you need to know to get ready for birth after Cesarean. You can find that on our website at thevbaclink.com. But this review on the course is from Heather. She says, “This course was so helpful especially with helping to educate my husband on the safety of VBAC as he had previously been nervous about my choice. We watched all of the videos already, but will also be reviewing the workbook again right before birth. I highly recommend.”I absolutely love that review from Heather because I feel like we get a lot of these comments about people and their partners really being on board and invested after taking the VBAC prep course with their partners. This course is chock-full of information about the safety of VBAC, and different types of birth situations. It talks about different interventions and hospital policies that you might encounter. It talks about the history of VBAC. It talks about all of the statistics and information. It talks about mental prep, physical prep, and all of those things. There are videos. There is an over 100-page workbook. There are actual links to sources, PDFs of studies, and everything you can even imagine. It is in this course. I also highly recommend it. Anyway, thank you, Heather, for that review. All right, let's get rocking and rolling. I am so ready to hear all about Katie's birth stories. Katie is right here snuggling her sweet little baby with her. I cannot wait. I hope we get to hear some little sweet baby noises. They are kind of my favorite. But Katie, go ahead and take it away, my friend. Katie: Yeah, thanks so much for having me. I'm excited to be here and hopefully share some things that I would have loved to have shared with me. So let me just start from the beginning with my first baby 5 years ago. I was planning to have a birth. I wasn't quite sure what it would look like, but I thought I wanted unmedicated. It was my first baby, and I wanted to labor spontaneously. The labor was long, so 3+ days of labor. It ended in me getting to 10 centimeters and pushing. However, due to fatigue and the multiple interventions that I had and the cascade of interventions, I believe, resulted in a diagnosis of failure to progress so I had a C-section. It was, I would say, disappointing to me not because of anything except that I would have loved to continue on my path of vaginal delivery. That wasn't in the cards with this one for me. Then with my second 2.5 years later– oh, I should also say that I was at a teaching hospital. There were lots of people. They were very pro-intervention. You name it, I had it across those 3 days. So 2.5 years later when I got pregnant, I thought, “Okay. I know I want to attempt a VBAC.” My husband, my partner, was so on board. He got a shirt that said, “You've got this.” He was wearing it all of the time. We watched a ton of positive VBAC birth stories on YouTube. We listened to podcasts like this one. We followed all of the things on social media and prepared with an amazing doula. I went into spontaneous labor again and this time, I was sure I wanted– actually, I should say I had a membrane sweep, and then I went into spontaneous labor. I was sure I didn't want interventions for this one. My doula was on board. My partner was on board. I labored at home for quite a while. I came into the hospital. It was the same hospital. That doctor was not so supportive of me attempting a VBAC, however, another OB had said that because of our family planning, I said, “I think I want more kids,” another OB told that OB, “Hey, let's make it as safe as possible to do what she wants, so let her give it a try.” My doctor was semi-supportive, but I came in. I was 9 centimeters. It was unmedicated. I was in there for less than 3 hours. I pushed the baby out with a bar. I was squatting. They didn't even know the baby was out. In fact, the baby started crying, and it felt like minutes or hours in my mind, but it was just a couple of pushes. My doula said, “Baby out. Baby out.” Everyone rushed because they were so surprised because normally, I think, folks labor on their backs, and I had requested a bar. That was pretty amazing. It was just me and my son doing the thing. It was incredible. I remember that OB who was skeptical said, “You did it. You've changed my mind.” So that was exciting. 3 years later to now, I became pregnant with my third baby. I went in for my anatomy scan at 20 weeks, and the ultrasound tech said, “Baby is breech. No big deal. Tons of babies are breech.” Because I have some other health complications, I guess they deemed me as high risk. I went to multiple ultrasounds, so that means I get to see my baby once a month which also meant I continued to see that baby was breech each time. Each time, they kept saying, “Oh, don't worry. Plenty of time. Plenty of time to turn.” As we approached my due date, I was like, “I feel his head. I don't think he's going to turn.” So they started to let me know what type of breech he was. My baby was frank breech. There are a few different types of breech positions which I didn't know prior to this baby, but now I'm very well-versed in the different breech positions. Frank breech is basically a pike position. The feet are by the head, and his little rump was just hanging out in my pelvis. I was also hoping to birth at a birthing center with my doulas. This was different than that learning hospital that I shared because I just wanted a different experience where they were less pushy with interventions. I knew that with my last birth that they used the term “something pelvis”, but anyway, I was ready to do something different with less people in the room. However, when they found out that I was breech, I was told what I think is the stock option which was, “Hey, if baby stays breech, but don't worry, there's plenty of time and he'll probably turn, but this is what we'll do. We'll try an ECV, and if that doesn't work, we'll schedule your C-section. We'll give you an epidural, try the ECV one more time, and that way, you can go right into your planned C-section. But don't worry, we have time. The baby is going to turn.” I left and was like, “I don't want that. My baby is healthy. I'm healthy. I am on the fence about this plan.” Now, I'm 36 weeks so at 37 weeks, I go in. We have the ECV. They give me the shot to relax my uterus. The ECV is the external cephalic version where they put their hands and try to rotate the baby. It was unsuccessful. So I said, “Can we try again?” She looked at me like, “What?” She said, “We'll try again with that epidural when you schedule your C-section.” I said, “No, no, no, no, no. Can we try again?” This is where, I think, that advocacy and that information and research are so important. She said, “Sure. We can try it again.” We scheduled another ECV. I went back in, and it was also unsuccessful with her. She could tell at this point, I was grieving what I thought was the end of this journey for me, and also not necessarily on board with the protocol they had put in place. We planned. I said, “Hey, can I try a different provider?” I know that you can do up to four ECVS. I'm not suggesting that people do that. I just wanted to make sure that I did everything possible for me and baby to have a vaginal birth. They seemed pretty gung-ho about not delivering unless baby was head down. She said, “Sure. We can do that.” That was also unsuccessful. At this point, the OB said, and I appreciated this. They said, “I feel really uncomfortable delivering a breech baby. I think you should go to our sister hospital in a city away if you are considering breech because we don't have a NICU here.” That felt reasonable to me because I had said to her previously, “I hear you, and I hear that protocol with what you're suggesting. I also feel really healthy, and I will absolutely change course if me or baby's health is in jeopardy, but unless that is imminent, I consider breech a variation of normal,” so I didn't necessarily think that was the rationale for the C-section knowing what that recovery is like and knowing that I had a 5 and a 3-year-old back at home. Julie: Oh, I love that so much. I love that they gave you options, and they admitted that they weren't comfortable with it. So many times, doctors will be like, “We don't do breech here.” They don't tell you that it's because they haven't been trained or they're not comfortable with it or it's not safe, they just tell you that's not the protocol, and they don't offer you other options. I really love that, and I love the conversation you had where you were like, “I understand the risks, but however, this is how I feel.” I think that's a really healthy way to go about it on both sides. So, cool. Kudos to your provider. Katie: Yeah. Then that doctor suggested this. It was in the underground world. It wasn't like, “Go to the next place.” She also suggested, “Why don't you consult with UCSF?” That's the University of California San Francisco. That's maybe an hour and 20 minutes with traffic, and it can be up to 3 hours, but they do breech birth there. She referred me to have a consultation with UCSF to talk about breech birth which they are very comfortable with. The consultation was great. The people were really helpful. They also had a lot of requirements for me to deliver there. Those requirements were things like an anatomy scan to ensure that the head and rump sizes were comparable for safety of baby. They wanted me to do a pelvic pelvimetry MRI. Julie: Pelvimetry? Katie: Yes. They said, “You have a proven pelvis,” which is the word I couldn't remember earlier, but because I'm very short– I'm 4'10”--, they just wanted that in this case. I said, “Sure. I'll do all of the things if this is the place where I know I can make that birth plan with you and we can do it.” Then they said, “We also give you an epidural. You'll birth in a birthing room, then we'll transfer you to an OR. You'll have an epidural, and that's in case anything goes wrong.” I fully understand the risk and the why behind that, but given with my first baby, one of the interventions was the epidural and I labored on my back, I wasn't quite confident that was the way baby and I were going to do this because what I found in my second birth is me and baby working together and moving together was what, I think, was all of the difference in the world for us to be able to meet each other. That gave me a little bit of pause, but nonetheless, I was like, “Okay. They are being upfront with me about all of the things I need to do.” I had the anatomy scan. Rump to head ratio was 1:1. It looked great. They were scheduling this MRI for me to take. Now, keep in mind, I'm 38 weeks pregnant now. The other things I was concerned about, or more my husband I should say, was that San Francisco, like I said, is about an hour and 20 minutes away from me. With traffic, it can be 3+ hours. Julie: Oof. I've driven in San Francisco during traffic and let me tell you, it is a nightmare. Katie: Yeah. My husband was like, “What if you don't get there in time? How are we going to make this work?” These were all pauses that we had around it. Nonetheless, we were on this track and UCSF was so helpful and wonderful. I'm so grateful for my provider for recommending this consult. Then my doula, as well as other providers, started sharing information with me. I want to say it's an underground network of knowledge where people aren't advocating for vaginal birth on the record because either the hospitals don't want to or don't condone it for whatever reason. I guess you can guess the reasons whether it's money or policy or education and patriarchy, but there is definitely a need. Breech babies are born all of the time. They said, “There are three providers at that sister hospital (that my doctor had initially recommended that was 15 minutes away) who are experienced with breech.” I thought, “Okay. In the event of an emergency and I went into labor, that's where I want to go.” They had a NICU. They had all of the things that made me want to feel more at ease knowing that we were doing something new to me and to keep myself and my baby safe. I still told the UCSF doctors, “Don't worry. I know I'm 38 weeks, but my other babies came at 40 weeks and 1 day, so I've got 2 weeks. He's cooking for 2 more weeks.” Then, at 38 weeks– Julie: Third babies, man. Third babies. Katie: Right? At 38 weeks, 4 days, I wake up. I should say, sorry. The UCSF doctor also said one other thing to me. She said, “Please do one more ECV, and this time, do a spinal.” I was like, “Ugh, this sounds awful.” But I understood the rationale. The safest way to come out was head down. I wanted to compromise and do everything in my power to do that. She said, “Because they hadn't done a spinal previously, there's data that shows it's more successful.” She shared all of that research with me, so I requested that from my local doctor. My doctor was like, “We don't usually do this,” but to their credit said, “We will. We will absolutely do it.” Keep in mind, I went in. I was like, “I know that this baby is loving where they are at. They are not moving, but if I don't try it, I'll never know.” Knowing the risks of ECVs, and knowing all of these things, I did do that because it was a request of the hospital that was going to be potentially the hospital where I give birth, so I wanted to make sure to follow all of the things. I do that. It was also unsuccessful. Then, now fast forward to 38 weeks and 4 days, I wake up and it's been a couple of days since that ECV. The spinal they give you is on your back. I wake up and I have some stomach cramps. I thought, “Man, this is strange, but it's probably from the ECV,” because in the past, it did cause some cramping for me. Because I had the spinal, I wondered if perhaps it just was residual. In my past labors, all of my laboring started with my back. I had a little bit of back aching, but it was again, I chalked it up to the spinal and just recovering from that. I went about my day. It was right before Halloween. I'm telling my partner, “Let's carve pumpkins.” My 5-year-old had a soccer game. I'm trying to get him ready, and I keep getting these cramps. They start to be regular. I thought, “Oh.” I'm 90% sure I'm in labor. This labor just felt different. Maybe it was because it was a breech baby. Maybe it was because it was a third labor, who knows? But nonetheless, it took me a while to get there. Maybe I was thinking it wasn't happening and willing that 40-week mark. Nonetheless, I was laboring. I texted my doula, and I'm timing my contractions. We had agreed that she would come over earlier this time because the baby was breech. All of the doctors said, “Labor at home. Come in during active labor.” We agreed that I would come in earlier than I did last time because of the circumstances. She comes over. She says, “Where I'm laboring, if the contractions are feeling intense, however, I can talk and laugh in between them,” so we agreed that I might be 5 centimeters. I just started to think, “I've got to lie down. I feel super tired. I had this ECV. I want to keep my energy up,” thinking this could be a long labor. Let me eat something. Then she says, “Just go. Sit on the toilet because your body does something different.” I do that. It's 1:00 in the afternoon now, and my water breaks. My husband was packing the bags to get to the hospital thinking, “Where do we go? Do we go to UCSF? Do we go to that sister hospital?” I say, “My water is broken.” I have another contraction. She's watching it. She was like, “We've got to–”, and I started to feel nauseous which are all signs of labor. Julie: Good signs. Katie: Yes, so she was like, “Let's go. Let's go now.” We get in the car. I think this is funny. It's a little on the side, but my husband had set up the car seat right behind me. I'm laboring. I'm definitely contracting and trying to retract my seat. There is this car seat, so I just remember picking it up and tossing it across the side saying, “Why would you set this up here?” He's looking at me, “Oh, you are really in labor. This is clear.” I'm trying to lay down. He has the GPS set. I am in the car. We get going. It's now between 1:00 and 2:00 on a Saturday. There is a ton of traffic and construction. I'm looking at the GPS and I see 25 minutes to the sister hospital, and to San Francisco was 3 hours. We don't have 3 hours. My doula says, “Where are we going?” I say, “That sister hospital. Let's go.” I also happen to know that there are three doctors there through that grapevine and underground network who are experience at delivering breech babies there, so I thought the odds of me having one of them would be beneficial. I would much rather have had conversations with all of them, but I didn't plan to go there thinking I was going to go to UCSF. We get in the car and are driving in this traffic. I'm just looking at the GPS and at the time ticking down. I'm really quiet which was also strange because with my other births, I was super vocal. My husband and I were thinking, “I'm in labor, but maybe I'm just not as far along, even though my water broke.” I've never been quiet. I was dead silent through this whole thing just staring at this GPS. Then all of a sudden, we're going on a bridge called the Causeway and I looked at him, and I said, “I have to push right now.” Julie: No. Katie: He looks at me and says, “No,” which is not very much– he's a very supportive person. What he meant by this was that we didn't come this far to get this far. We're going to get to this hospital. We are driving, and I just remember internally that I was so quiet going inward. I was talking with my baby, talking with myself and saying, “Okay. We've got to get to the hospital. We didn't come this far to get this far. I'm not having a baby breech unassisted delivery.” That was not something that I was comfortable with. We get off the off-ramp, and we're finding the patient drop-off. I'm contracting and I see the sign, and my husband drives right by it. I look at him right after I contract and I say, “You drove right by the patient drop-off. You have to put on hazards. I have to get out now. I have to push.” He's like, “I can't. We're parking.” So he parked the car, and I was like, “What do you want me to do?” He says, “We've got to walk.” Keep in mind, the parking lot where he went is not right next door. It's a block and a half or two blocks away.Julie: No way.Katie: I just was like, “I can't do this. I can't do this.” He says, “Yes, you can. Yes, you can. You have got this.” So I was like, “Okay. I've got this.” I get up, and I walk. When I start contracting, I'm walking down this busy street. I said, “I have to poop.” I had this big contraction, and I think I possibly poop. I'm just looking at these cars thinking, “Why won't somebody stop and help me?” That's when I channeled back to this idea, at the end of the day, It's just you and your baby. You are the team. I contract. We are going. We finally get to the hospital. I have another contraction. I say, “Run in and tell them to help.” He does. I'm holding on to the railing. This lovely woman with her family sees me. She tells her 13-year-old son, “Get her!” I was standing by myself, definitely in labor.” She says, “Get her a wheelchair!” This amazing 13-year-old does just that as my husband runs back. He gets me this wheelchair. I'm sitting in it, but I can't sit down. Again, I think it's because I've had this bowel movement and maybe I'm in transition. I don't know. We get up and pass security, so security is yelling at us. My husband was like, “I've got to go. We've got to go.” We got to L&D and came in. This amazing nurse midwife welcomes us. I don't know if she saw me not sitting down all of the way in my wheelchair or what, but she yells, “Get her a room right now.” She says, “We're going to deliver this baby.” I say, “My baby is breech. Can you help?”She says, “Call this doctor.” My heart is so relieved because this is one of those three experienced doctors who I know is comfortable with breech delivering. He scrubs out of a C-section, I guess. She helps me take off my pants, and then realizes what I thought was poop was really– it's called rumping as a breech instead of crowning. She was like, “Change of plans. Get on all fours.” I just started laboring. The doctor comes in scrubbed out of that C-section. I know that the nurses are saying, “You're doing great. You're going to meet your baby,” and all of the things that are so wonderful. I couldn't speak more highly of the people in that room at that point. My doula joined us because it took her a minute to find us in all of the mayhem. He tells my partner, “Please make sure she goes on her back.” I had this vision of doing breech without borders on your hands and knees, but given that this doctor was very experienced with breech delivery through this underground network of knowledge, I was like, “Okay. We didn't come this far to get this far. I'll do whatever you want. Let's just see this baby.” I turn around after, my husband said, my baby was halfway out. He sees the legs drop which again, in a frank breech position, that happens. You see the rump, and then you see the back and the legs drop. He sees the rest of the body come out as I'm laboring on my back which I didn't do with my first. I wasn't actually, I didn't know if that was something my body was down for. But here I was delivering this breech baby. Of course, I should have known. Women are amazing. We do amazing things, and our bodies are built for this work. I labored, and then I felt him come out completely. I held my breath for a second because what I do know, and excuse me if this statistic isn't 100% accurate, but my understanding is that 1 out of 7 babies born head down might need resuscitation, but 1 out of 3 babies born breech might need resuscitation. So one of the things I was pausing for at this moment was to hear this sweet baby's voice, and so I just start hearing crying immediately. They tell me that his APGAR score was 9/8 which was exactly the same as my first VBAC. Julie: That's great!Katie: Yeah. They were like, “Baby is great. Baby is healthy.” They put him on me. I was trying to feed, but my cord was short, so low and behold, I have a feeling that the reason he was not interested in turning is because my cord was kind of short. He just was sitting fine where he was at with my posterior placenta up high. He and I sat and met each other. We celebrated. The doctor was so funny. He said, “You keep it interesting. You've had every kind of birth you could possibly have.” Julie: You keep it interesting. Katie: Yeah. Every type of birth you could possibly have. The nurses came in after. They said they wanted to come in and watch because they don't see this. They said, “This is amazing. We wanted to respect your privacy.” But they were so supportive of the whole thing. I just felt elated to have the people in the room and around me who believed in me and my baby as much as we believed in us to make it happen. I should say that I came in at 2:10 to this hospital. I delivered at 2:24. When I say it was fast and this was going quickly when all of those things happened, I wouldn't recommend any of those things. However, I think that advocacy and all of those things like knowing all of the data made me feel prepared to do that. That's my breech delivery story. Julie: I absolutely love that. I love that. I was like, “Aw, dang. Too bad she didn't have her baby in the car.” No, I mean that would not have been ideal for you, but it is a dream birth of mine. I mean, I would have loved to have my own baby in the car. It would have been amazing. I love the stories. One day, I dream of documenting a car delivery, but alas, here I am still waiting. But it's fine. Here's the cool thing. I really love how you navigated your birth. You sought out all of your options. You made a choice that you were comfortable with. You heard the risks that the doctors were telling you about. You acknowledged them, but you also stood up for yourself and your plan. I feel like when you can have that mutual respect where you can trust your provider and your provider can trust you, I feel like that's a great place to be. I love how you adapted and changed plans when needed, but you still stood firm for the things that you wanted. It doesn't always work out like that when you have to change plans, but I love that you had the plan and you navigated it with the twists and turns and all of the things that come with the unpredictabilities of birth. I love how you did all of that. I think it's really important and necessary to have strong opinions about how you want to birth. Like I said before, it doesn't always mean that the strong opinions that you have are going to hold true about what you actually end up getting. I think that the value in having those strong opinions about birth is the things that you learn along the way and the things that enable you to navigate through those changes of plans and things like that. I think that's really, really important for us to be able to have and do and be flexible. I do have a few different blog articles on our website related to breech babies. Now, there's one that is just recently published. It was a few months ago. Well, maybe it will almost be a year ago by the time this episode airs. It talks a lot about ECVs, the external cephalic version, in order to try and manually flip a breech baby. It talks about what ACOG recommends and ACOG's stance on it, things you can do, who is right for it, what may exclude you from having an ECV or attempting one and all of those things. It talks about the safety for VBAC and how it's performed, what it feels like, and all of those things. If you ever want to know about ECV, we have a blog for you. It's called ECV and VBAC: What you Need to Know. It goes into all of that stuff. I definitely recommend looking into it because like we said before, you don't really know your options until you have them, and the more information you have in your arsenal, the easier it's going to be for you to navigate those things. Basically, ECVs are pretty safe for most people. They have a success rate of 60% which is a really cool success rate. It's higher than 50%. You're more likely for it to work than not. Sometimes babies are breech for a reason, and they need to stay that way for some reason. There are really only a few things that exclude you which is excessive vaginal bleeding, placenta previa or accreta, if you have really low levels of amniotic fluid, fetal heart rate issues, if your water's already been born, sometimes providers won't do it that way, or if you have twins or multiples, I think that excludes you. It's listed here, and it makes sense. We've got lots of babies tangled up in there. It's absolutely safe for VBAC as well. We also have a couple more blogs about why babies go breech and some things that you can do about it. I'm sure, Katie, you probably tried all of these things, all of the Spinning Babies protocols, all of the forward-leaning inversions and things like that too that can help. There's another article in here about how to turn your breech baby– 8 ways to flip your baby. Like we said, sometimes babies are breech for a reason and they do not want to turn. I'm just really looking forward to the day where breech can be just a variation of normal again. The biggest problem is that our providers are not learning how to deliver breech babies. It does take a different skill in order to do that. You have to be really hands-off. You have to watch for certain things and depending on the type of breech, there are different techniques that you would use. Those techniques are not being taught. Kudos to your original provider who admitted that they were not comfortable or did not have the knowledge to feel comfortable in delivering a breech baby. I'm excited there are organizations called Reteach Breech, Breech Without Borders, and Dr. Stu. If you know Dr. Stu, he is leading a great mission to bring breech back so that women can have options for delivering their breech babies. So what happens if you don't know your baby is breech and your baby is delivered foot first? You can't just stop and go for a C-section right then. It's impossible. So to deliver breech babies safely no matter the circumstances, the knowledge there is important. I'm hoping that one day, that can be an option for anybody if they want that. All right, Katie, I'm so glad that you joined me today. It was so great hearing your story. I love how it all went. I do not pity you having to drive in San Francisco at traffic time. Yeah. I'm glad everything worked out. Katie: We ended up going to this other hospital closer. Julie: Yeah, yeah. But I mean just ever, not even in labor. Just ever. Katie: Yes. Yes. Julie: All right, Katie. Before we sign off, will you tell me, what is your best piece of advice for somebody preparing for a VBAC?Katie: Oh, I think it is so important to do two things. One, educate yourself and surround yourself around folks who are down with that education and believing in you and baby. What I mean by that is knowing what's happening so you can make those important decisions. You understand what consent looks like. You understand those risks. You understand all of the tips and techniques like in this case of breech and turning that baby, and then making sure that you also are advocating and you have people around you who are advocating, but not so stuck on that that you get stuck. You want to do what's best for you and the baby, but as you said, breech is a variation of normal. I think that being around people who are supportive of you, they don't necessarily have to agree with you, but they are working with you, is just so important to empower you because at the end of the day, it's you and baby doing the thing. People who believe in you as much as you believe in yourself and you believe in your baby are so important to get to that finish line in labor. Julie: Yes. I absolutely love that. You have to have people who believe in you and who are on your side and who will support you even if they don't necessarily understand your decisions. They trust you to make those decisions because that is a huge deal. Katie: And give you the information so that if the information you have is not full or complete, you can reevaluate. You don't know what you don't know until you know. I just think that you need to make sure you take it all in if you can unless you don't know your baby is breech and you find out when you are delivering and you make that snap decision, and it'll be great. Julie: Yes. No, I love that. There's something about people bringing you information especially in a respectful way because I feel like in today's world, when people disagree with others, it's very aggressive and condescending and judgmental. I think it's important that we can disagree respectfully but also bring information if you are concerned or if you have another point of view in a respectful way as well. I think it's received a lot better and I think that's where we can really bring that true change and sway people's opinions. It's if we do that in a respectful and understanding way. Yeah, I appreciate that. Good point, Katie. That was awesome. Okay, well thank you so much for sharing your story with me today. I cannot wait for the whole world to hear it. Katie: Thanks so much for allowing me the space to do it. I hope that women are able to explore their options and do what's right for them and their baby and their families. Julie: Yeah. ClosingWould you like to be a guest on the podcast? Tell us about your experience at thevbaclink.com/share. For more information on all things VBAC including online and in-person VBAC classes, The VBAC Link blog, and Meagan's bio, head over to thevbaclink.com. Congratulations on starting your journey of learning and discovery with The VBAC Link.Support this podcast at — https://redcircle.com/the-vbac-link/donationsAdvertising Inquiries: https://redcircle.com/brands

அமெரிக்காவின் California மாநிலத்தின் San Francisco நகரில் கடந்த மாதம் நடந்த 6வது கேரம் உலகக் கோப்பை போட்டியில் மகளிர் ஒற்றையர் போட்டியில் முதல் பரிசை வென்ற காஸிமா மற்றும் அவரது தகப்பனாரும் அவருடைய பயிற்றுனருமான திரு மேஹபூப் பாஷா அவர்களுடன் உரையாடுகிறார் குலசேகரம் சஞ்சயன்.

Vascular cognitive impairment is a common and often underrecognized contributor to cognitive impairment in older individuals, with heterogeneous etiologies requiring individualized treatment strategies.  In this episode, Katie Grouse, MD, FAAN speaks with Lisa C. Silbert, MD, MCR, FAAN, an author of the article “Vascular Cognitive Impairment,” in the Continuum December 2024 Dementia 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. Silbert is is co-director at Oregon Alzheimer's Disease Research Center, a Gibbs Family Endowed professor of neurology, a professor of neurology at Oregon Health & Science University, a staff neurologist, director of Cognitive Care Clinic, and director of the Geriatric Neurology Fellowship Program at Portland Veterans Affairs Health Care System in Portland, Oregon. Additional Resources Read the article: Vascular Cognitive Impairment Subscribe to Continuum: shop.lww.com/Continuum Earn CME (available only to AAN members): continpub.com/AudioCME Continuum® Aloud (verbatim audio-book style recordings of articles available only to Continuum® subscribers): continpub.com/Aloud More about the American Academy of Neurology: aan.com Social Media facebook.com/continuumcme @ContinuumAAN Full 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 Lisa Silbert about her article on vascular cognitive impairment, which is part of the December 2024 Continuum issue on dementia. Welcome to the podcast and please introduce yourself to our audience.  Dr Silbert: Hi Katie. Thanks for having me here today. Like you mentioned, my name is Lisa Silbert. I am a behavioral neurologist at Oregon Health and Science University and my research focus is in the area of vascular contributions to cognitive impairment and dementia. Dr Grouse: It's such a pleasure to have you and I really enjoyed reading your article. Just incredibly relevant, I think, to most practicing general neurologists, and really to any subspecialty. I'd like to start by asking, what do you think is the main takeaway point of your article for our listeners?  Dr Silbert: Yeah. I think, you know, the field of vascular cognitive impairment has changed and evolved over the last several decades. And I would say the main take-home message is that vascular cognitive impairment or vascular dementia is no longer a diagnosis that is only considered in someone who's had acute decline following a clinical stroke. That we have to expand our awareness of vascular contributions to cognitive impairment and consider other forms of the disease that can cause a more subacute or slowly progressive form of cognitive impairment. And there are many, many forms of vascular cognitive impairment that present in a more slowly progressive manner. The other thing I would say as a major take-home message is that we know that cerebrovascular disease is a very common copathology with other forms of dementia and that it lowers one 's threshold for manifesting cognitive impairment in the context of multiple pathologies. And so, in this way, vascular cognitive impairment should be considered as a contributing and potentially modifiable factor in any dementia.  Dr Grouse: I found that last point just really, really fascinating. And also, you know, the reminder that a combination of pathologies are more common than any one. To your initial point, I'm actually curious, could you kind of outline for us how you approach diagnosing vascular cognitive impairment?  Dr Silbert: Yeah. So with everything in neurology, a lot of it comes down to the initial history taking. And so part of the work up always includes a very detailed history of the presentation of cognitive impairment. Any time there is an acute change in cognition, vascular contribution should be considered, particularly if it's in the context of a clinical stroke or some kind of event that might have lowered cerebral blood flow to the brain. And then having said that, I already mentioned there are many forms of vascular cognitive impairment that can mimic neurodegenerative disease in terms of its course. So being more slowly progressive. And so because of that neuroimaging, and in particular MRI, has become an extremely valuable tool in the workup of anyone who presents with cognitive impairment in order to evaluate contributions from cerebral vascular disease. And so, MRI is a really helpful tool when it comes to teasing out what may be contributing to a patient's clinical syndrome, as well as their other comorbid medical issues, including stroke risk factors and other kind of medical conditions that might contribute to reduce cerebral blood flow. Dr Grouse: I'd love to talk a little bit more about that. You know, as is often the case with neurologic disease associated with vascular pathology, the importance of prevention, you know, focusing on prevention of vascular diseases is so important. What are some things that we can make sure to focus on with our patients and, you know, particularly anything new to be aware of in counseling them? Dr Silbert: Yeah, I'm really glad you asked me that question because like I mentioned, you know, cerebral vascular disease is so common, it lowers one's threshold for cognitive impairment in the face of other age-related brain pathologies. And so, it's really important for all of us to focus on preserving our cognitive health, even starting in midlife. And so, there are a number of areas that I counsel my patients on when it comes to preserving cerebral health and maximizing cerebrovascular health. And so, these stem from the American Heart Association's Life's Essential 8 because we know that preserving cardiovascular health is likely going to also preserve cerebral vascular health. And so, some of the things that I'm very commonly discussing with my patients are controlling stroke risk factors such as blood pressure, blood sugars and cholesterol, maintaining a healthy weight, and then also working towards a lifestyle that includes a healthy diet, no smoking, regular exercise. And then new within the last couple years is also the recommendation that people get adequate sleep, which is something that hasn't been focused on previously. Dr Grouse: I was really interested in reading your article to learn about enlarged perivascular spaces and the role as a mediating factor in the interaction between through a vascular dysfunction and development and progression of neurodegenerative pathology. Can you elaborate on this further? Dr Silbert: So, this is an area that's still largely unknown in the field, and it's an area where there's a lot of emerging work being done. The short answer is, we really don't know with great certainty how it directly connects with accumulating Alzheimer's pathology. But there is some evidence to suggest that the perivascular space is involved in the clearance of toxic solutes from the brain, including Alzheimer's disease pathology. And so there's a lot of work looking at how potentially cerebrovascular risk factors might affect the clearance of those toxic solutes through the perivascular space, including pulse pressure changes that might occur with accumulating cerebrovascular disease and other potential contributors. But one thing I can say with more certainty is that the, you know, location of perivascular spaces is thought to help distinguish those who might have cognitive symptoms due to cerebrovascular disease versus due to cerebral amyloid angiopathy. Or I guess I should say location is helpful in terms of recognizing vascular contributions to cognitive impairment that's due to arteriolosclerosis versus that due to cerebral amyloid angiopathy. In so much that… when we see a lot of perivascular spaces in the basal ganglia in the subcortical structures, that is thought to be more associated with arteriolosclerosis and hypertension type related vascular cognitive impairment. Whereas when we see multiple perivascular spaces within the centrum semiovale, that tends to be more associated with cerebral amyloid angiopathy. Dr Grouse: That's so interesting. And on the topic ofcerebral amyloid angiopathy, you did go into this a good deal. And you know, I think I encourage everybody to revisit the article to remind themselves about, you know, the findings that can increase the suspicion of tribal amyloid angiopathy. However, you also talked about transient focal neurologic episodes, which I think is just a great reminder that, you know, these can occur in this setting and definitely not to miss. Tell us more about what to look for with these types of episodes.  Dr Silbert: Transit focal neurologic episodes can be very difficult to tease apart from a transient ischemic attack. And these transient focal neurologic episodes due to CAA can present in a number of different ways. And I think the important take home message for that is that in people who have neuroimaging evidence of CAA to inform them that they are at increased risk for having these focal neurologic episodes and that if they do present to a hospital or an emergency department with any kind of neurologic event, that those treating them are aware that they have evidence of CAA on their neuroimaging because the treatment of course is quite different. So, it's someone presenting with ATIA who has transient neurologic symptoms might be considered urgently to get a thrombolytic or, you know, TPA, whereas someone who has known cerebral amyloid angiopathy or suspected CAA, they likely already have microbleeds on their neuroimaging and in those cases thrombolytics and TPA would be contraindicated and not helpful in terms of the etiology of their neurologic symptoms. Dr Grouse: That's a really good point to make. And I think also in your article you mentioned the use of aspirin if you're suspecting ATIA versus a, you know, a transient amyloid related focal neurologic episode. You know, one you would treat with aspirin and the other one you wouldn't.  Dr Silbert: That's right.  Dr Grouse: Another sort of interesting topic you delved into was cerebral microinfarct and how this can also contribute to vascular impairment. Could you elaborate a little more on that? Dr Silbert: Yeah. So cerebral microinfarcts are kind of the hidden cause of or a hidden cause of vascular cognitive impairment. And it's extremely challenging because by definition they are not visible on routine clinical neuroimaging. It's something that we are more aware of based on pathological studies and neuroimaging studies that have been done at ultra-high field strength like 7T MRI. And so, we are just learning more about how prevalent they are in certain conditions and how we can only look at these after death when we're looking at brain tissue and then go back and realize that these play a significant role in cognitive decline when someone is alive. It's important to understand that we're probably only appreciating kind of the tip of the iceberg when we're evaluating a patient and looking at their neuroimaging. That what we're actually seeing on MRI are only the things that are actually quite relatively big and obvious. And that a lot of these neuroimaging features of vascular cognitive impairment are actually associated with pathologic features that we're missing such as microinfarcts. But the hope is that by treating all individuals, particularly those who already have signs of vascular cognitive impairment, by modulating their stroke risk factors and focusing on maintaining brain health, that those will, interventions will also reduce the incidence of microinfarcts. Dr Grouse: What do you think is the greatest inequity or disparity you see in treating patients with vascular cognitive impairment? Dr Silbert: I think the greatest disparity is- really starts way before I treat a patient. That relates to really focusing on healthy lifestyle factors early in life and being able to, you know, afford fruits and vegetables, and having the advantages of being able to exercise regularly, and just being aware that all of these things are extremely important before older age. So, these are things that, you know, I think more education and awareness and greater access to healthcare will definitely improve access to. Even preventative healthcare is a disparity and not available across all of the population and geographic locations. So, I think of the- all the dementias, vascular cognitive impairment probably has the greatest association with health and social disparities in terms of primary prevention and access to care.  Dr Grouse: All really important things to consider. I have to say when, you know, reading your article, dare I say I came away with a little bit of hope thinking, you know, even with, you know, how little we still, you know, or how much we still need to do to really learn how to fight Alzheimer's and, you know, prevent it and, and, you know, help with its progression. The idea that in so many cases, even just doing what we can to prevent the vascular or cognitive impairment can really help any type of dementia. That was really a strong message for me. Do you mind elaborating on that a little more?  Dr Silbert: No, not at all. I agree. I really am hopeful about the prevention and treatment of dementias and through the treatment and prevention of cerebrovascular disease. I think that is a true reality, just like, you know, as we were discussing before, the treatment and prevention of cerebrovascular disease really should be a part of the treatment of any type of cognitive impairment and recommendations for prevention of cognitive impairment. This is the, you know, one thing we know is largely modifiable and preventable in most cases. I think the, really the key thing is just education and making sure that people understand that these are things that really need to be, they need to be engaged in in midlife and that it's much harder to reverse these- the damages once you have them in later life. Having said that, I do think that there's greater awareness of maintaining healthy lifestyle and maintaining awareness of stroke risk factors. And I think we're already starting to see a reduction in dementia worldwide in several large population-based studies, and probably that is due to more attention to the modifying stroke risk factors. So, I agree with you, it's very encouraging.  Dr Grouse: Is there anything exciting on the horizon that you can tell us about that we should all be keeping our eyes out for? Dr Silbert: Yeah. So, you know, I'm really interested in this connection between vascular cognitive impairment and Alzheimer's disease. And it's a real area of exciting new research. And so I think we're going to have more answers as to how, whether and how, cerebrovascular disease is directly linked to accumulating neurodegenerative disease or neurodegenerative pathologies. The other area that's, I think, really exciting, that's moving forward, is the in the area of blood-based biomarkers for vascular cognitive impairment. As these emerge, we'll be able to really identify those at greatest risk for vascular cognitive impairment, but also identify novel mechanisms that lead to VCI that can be targeted for therapeutic intervention. Dr Grouse: Well, I'm really excited to see what's coming down the pipeline and what more we'll learn in this area. So, thank you so much for everything you've done to contribute to this field. Dr Silbert: Yeah.  Dr Grouse: I wanted to ask a little bit more about you. What drew you to this work?  Dr Silbert: Well, actually, so my very first published manuscript in medical school was a case report and review on MELAS, which is mitochondrial encephalopathy with lactic acidosis and strokelike syndrome. And so, I was really fortunate to have Dr Jose Biller, who is a renowned expert in stroke and cerebrovascular disorders, as my mentor for that paper. And so, that got me really interested in neuroimaging findings of cerebral vascular disease. And so when I was a fellow at Oregon Health and Science University, I was then really fortunate to  be able to work with Jeffrey Kaye's oldest old population. And in working with that population, I really became interested in their neuroimaging findings of these white matter lesions and just realizing how prevalent they were in that population, you know, it just led me to start investigating their clinical significance and etiology, which kind of led me along this path. Dr Grouse: You know, Lisa, thank you so much. I really learned a lot from your article, and I think our listeners will definitely find that it was very helpful for their practice. Thank you so much for joining us. Dr Silbert: Thank you so much, Katie. It's been really fun.  Dr Grouse: Again, today I've been interviewing Dr Lisa Silbert, whose article on vascular cognitive impairment appears in the most recent issue of Continuum on dementia. 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.

Dr. Laurel Mellin is a health psychologist who founded and developed emotional brain training (EBT). She is an associate clinical professor of family and community medicine and pediatrics at the University of California San Francisco. Dr. Mellin has authored papers on the science and efficacy of EBT and is a New York Times bestselling author of four books on the method. Stress and trauma—especially from early childhood—can create survival circuits in the brain, which drive coping mechanisms such as overworking, emotional withdrawal, and unhealthy habits like overeating or excessive perfectionism. Most people, particularly those in their 40s and 50s, often feel emotionally drained and disconnected because of stress. Dr. Laurel describes five levels of stress in the brain, from a calm, connected state (Level 1) to a stressed-out state (Level 5), where the emotional brain takes over. EBT helps shift individuals from a higher stress level to a more positive, calm state, where they can make better decisions.The emotional brain influences decision-making and relationships, and simply relying on logic and hard work isn't enough to address deep emotional needs. Emotional well-being requires addressing the emotional circuits that control our reactions and behaviors. The goal of EBT is to teach individuals how to rewire these circuits for better emotional regulation, so they can improve their mental health, have stronger relationships, and overall life satisfaction.EBT, as Dr Mellin says, helps in weight reducing and her idea with integrative approach—featuring small groups, app support, and telephone coaching—sets it apart from traditional psychotherapy.Let's see what is in our brains so we can live happier lives!Dr. Laurel Mellin is a health psychologist who founded and developed emotional brain training (EBT). She is an associate clinical professor of family and community medicine and pediatrics at the University of California San Francisco. Dr. Mellin has authored papers on the science and efficacy of EBT and is a New York Times bestselling author of four books on the method. Stress and trauma—especially from early childhood—can create survival circuits in the brain, which drive coping mechanisms such as overworking, emotional withdrawal, and unhealthy habits like overeating or excessive perfectionism. Most people, particularly those in their 40s and 50s, often feel emotionally drained and disconnected because of stress. Dr. Laurel describes five levels of stress in the brain, from a calm, connected state (Level 1) to a stressed-out state (Level 5), where the emotional brain takes over. EBT helps shift individuals from a higher stress level to a more positive, calm state, where they can make better decisions.The emotional brain influences decision-making and relationships, and simply relying on logic and hard work isn't enough to address deep emotional needs. Emotional well-being requires addressing the emotional circuits that control our reactions and behaviors. The goal of EBT is to teach individuals how to rewire these circuits for better emotional regulation, so they can improve their mental health, have stronger relationships, and overall life satisfaction.EBT, as Dr Mellin says, helps in weight reducing and her idea with integrative approach—featuring small groups, app support, and telephone coaching—sets it apart from traditional psychotherapy.Let's see what is in our brains so we can live happier lives!Links:Brain Training: www.ebtconnect.netBooks: www.amazon.com/stores/author/B000APE9YS/allbooks Connect with Jennifer: www.jenniferdawncoaching.comRetreats: www.jenniferdawncoaching.com/our-retreatJoin our Academy: www.jenniferdawnacademy.com

With the recent surge in artificial intelligence and machine learning technology, one of the most exciting fields it could revolutionize is health care and, more specifically, the field of cognitive care and research. Dr. Marina Sirota and Alice Tang join the podcast to share their research on how AI could be used to predict one's risk of developing Alzheimer's disease based on their electronic health records. They also discuss what needs to be done to improve these algorithms and other ways this technology could be used in Alzheimer's disease research. Guests: Marina Sirota, PhD, associate professor, University of California San Francisco (UCSF), principal investigator, Sirota Lab, and Alice Tang, MD/PhD student, University of California San Francisco, postdoctoral fellow, Sirota Lab Show Notes Read Alice Tang and Dr. Sirota's study, “Leveraging electronic health records and knowledge networks for Alzheimer's disease prediction and sex-specific biological insights,” online through the journal Nature.. Learn more about Sirota Lab on their website. Learn more about Dr. Sirota on her UCSF profile. Connect with us Find transcripts and more at our website. Email Dementia Matters: dementiamatters@medicine.wisc.edu Follow us on Facebook and Twitter. Subscribe to the Wisconsin Alzheimer's Disease Research Center's e-newsletter. Enjoy Dementia Matters? Consider making a gift to the Dementia Matters fund through the UW Initiative to End Alzheimer's. All donations go toward outreach and production.

For certain diagnoses and patients who meet clinical criteria, neuromodulation can provide profound, long-lasting relief that significantly improves quality of life. In this episode, Aaron Berkowitz, MD, PhD, FAAN speaks with Prasad Shirvalkar, MD, PhD, author of the article “Neuromodulation for Neuropathic Pain Syndromes,” in the Continuum® October 2024 Pain Management in Neurology 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. Shirvalkar is an associate professor in the Departments of Anesthesia and Perioperative Care, Neurological Surgery, and Neurology at Weill Institute for Neurosciences at the University of California, San Francisco in San Francisco, California. Additional Resources Read the article: Neuromodulation for Neuropathic Pain Syndromes 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: @PrasadShirvalka 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 Prasad Shirvalkar about his article on neuromodulation for painful neuropathic diseases, which appears in the October 2024 Continuum issue on pain management in neurology. Welcome to the podcast, and if you wouldn't mind, please introducing yourself to our listeners.  Dr Shirvalkar: Thanks, Aaron. Yes, of course. So, my name is Prasad Shirvalkar. I'm an associate professor in anesthesiology, neurology and neurological surgery at UCSF. I am one of those rare neurologists that's actually a pain physician.  Dr Berkowitz: Fantastic. And we're excited to have you here and talk to you more about being a neurologist in in the field of pain. So, you wrote a fascinating article here about current and emerging neuromodulation devices and techniques being used to treat chronic pain. And in our interview today, I'm hoping to learn and for our listeners to learn about these devices and techniques and how to determine which patients may benefit from them. But before we get into some of the clinical aspects here, can you first just give our listeners an overview of the basic principles of how neuromodulation of various regions of the nervous system is thought to reduce pain? Dr Shirvalkar: Yeah, I would love to try. But I will promise you that I will not succeed because I think to a large extent, we don't understand how neuromodulation works to treat pain, to describe or to define neuromodulation. Neuromodulation is often described as using electrical stimuli or a chemical stimuli to alter nervous system activity to really influence local activity, but also kind of distant network activity that might be producing pain. On one level, we don't fully understand how pain arises, specifically how chronic pain arises in the nervous system. It's a huge focus of study from the NIH Heal Initiative and many labs around the world. But acute pain, which is kind of when you stub your toe or you burn your finger, is thought to be quite different from the changes over time and the kind of plasticity that produces emotional, cognitive and sensory dimensions. Really what I think is its own disease, chronic pain, of which there are multiple syndromes when we use neuromodulation, either peripheral nerve stimulation or electrical spinal cord stimulation. One common or predominant theory actually comes from a paper in science from 1967 and people still use it, foundational theory and it's called the gate control theory. Two authors, Melzack and Wall, postulated that at the spinal level, there are, there's a local inhibitory circuit or, you know, there's a local circuit where if you provide input to either peripheral nerves or either spinal cord ascending fibers that to kind of summarize it, there's only so much bandwidth, you know, that nerves can carry. And so that if you literally pass through artificial signals electrically, that you will help gate out or block natural pathological but natural pain signals that might be arising from the periphery or spinal cord. So, you know, one idea is that you are kind of interfering with activity that's arising for chemical neuromodulation. The most common is something known as intrathecal drug infusion drug delivery ITTD for that we quite literally put a catheter in the spinal fluid, you know, at the level of the dorsal horn neurons that we think are responsible for perpetuating or creating the pain. Where's the pain generator? And you really, you can infuse local anesthetic, you can infuse opioids. And what's nice is you avoid a lot of systemic side effects and toxicity because it goes right to the spinal cord, you know, by infusing in the fluid. So there's a couple of modalities, but I will say just, like maybe all of our living experience, pain is in the brain. And so, we don't really understand, I would say, what neuromodulation is doing to the higher spinal or brain levels. Dr Berkowitz: Fascinating topic. And yeah, very interesting to hear both what our current understanding is that some of our current understanding is based on data that's 60 years old and that we're actually probably learning about pain by using these modulation techniques, even though we don't really understand how they might be working. So interesting feedback loop there as well as in as in the as in this land. So, your article very nicely organizes the neuromodulation techniques from peripheral to central. So, encourage our listeners to check out your article. And first before we get into some of the clinical applications, just to give the listeners the lay of the land, can you sort of lay out the devices and techniques available for treating pain at each level of the neuroaxis? We'll get into some of the indications in patient selection in a moment, but just sort of to lay out the landscape. What's available that you and your colleagues can use or implant at different levels when we're thinking of referring patients too? Dr Shirvalkar: Absolutely. So, starting from the least invasive or you know, over the counter patients can purchase themselves a TENS machine. Many folks listening to this have probably tried a TENS machine in the past. And the idea is that you put a couple of pads, at least two. So you have like a dipole or you have a positive and a negative lead and you basically inject some current. So, the pads are attached to a battery and you can put these pads over muscle. If you have areas where myofascial pain or sore muscles, you can put them, frankly, over nerves as well and stimulate nerves that are deeper. Most TENS machines kind of use electrical pulses that occur at different rates. You change the rates, you can change the amplitude and patient can kind of have control for what works best. Then getting slightly more invasive, we can often stimulate electrically peripheral nerves. To do this we implant through a needle, a small wire that consists of anywhere from one electrical contact to four or even eight electrical contact. What I think is particularly cool, like TENS, which is transcutaneous electrical nerve stimulation that goes through the skin. Peripheral nerve stimulation aims to stimulate nerves, but you don't have to be right up against the nerve. So, yeah. We typically do this under an ultrasound and you can visualize a nerve like the sciatic nerve, peroneal nerve, or you know, even if someone has an ulnar or a neuropathy, you know, that's the compression. There's a role obviously for surgery and release, but if they have predominantly pain, it's not related to a mechanical problem per se, you could prevent a wire from a peripheral nerve stimulator as far as one centimeter from a nerve and it'll actually stimulate that that modulated and then, you know, kind of progressing even more deeply. The spinal cord stimulation, SCS, it's probably the most ubiquitous or popular form of neuromodulation for pain. People use it for all kinds of diseases. But what it roughly involves is a trial period, which is a placement of either two cylindrical wires, not directly over the spinal cord, but actually in the epidural space, right? So, it's kind of like when you get an epidural injection or doing labor and delivery, when women get epidural catheters, placing spinal cord stimulator leads in that same potential space outside the dura, and you're stimulating through the dura to actually target the ascending dorsal column fibers. And so, you do a trial period or a test drive where the patients get these wires put in. They're coming out of the skin, they're connected to a battery, and they walk around at home for about a week, take careful notes, check in with them, and they keep a diary or a log about how much it helps. Separately. I will say it's hard to distinguish this, the placebo effect often, but you know, sometimes we want to use the placebo effect in clinical practice, but it is a concern, you know, with such invasive things. But you know, if the trial works well, right, you basically can either keep the leads where they are and place a battery internally. And it's for neurologists. You're familiar with deep brain stimulation. These devices are very similar to DVS devices, but they're specifically made for spinal cord stimulation. And there's now like seven companies that offer manufacturers that offer it, each with their own proprietary algorithm or workflow. But going yet more invasive, there is intrathecal drug delivery, which I mentioned, which involves placement of the spinal catheter and infusion of drug into spinal fluid. You could do a trial for that as well. Keep a patient in the hospital for a few days. You've all probably had experience with lumbar drains. It's something real similar. It just goes the other way. You know, you're infusing drugs, and it could also target peripheral nerves or nerve roots with catheters, and that's often done. And last but not least, there's brain stimulation. Right now, it's all experimental except for some forms of TMS or transcranial magnetic stimulation, which is FDA approved for migraine with aura. There are tens machine type devices, cutaneous like stimulators where you can wear on your head like a crown or with stickers for various sorts of migraines. I don't really talk about them too much in in the article, but if there's a fast field out there for adjunctive therapy as well,  Dr Berkowitz: Fantastic. That's a phenomenal overview. Just so we have the lay on the land of these devices. So, from peripheral essentially have peripheral nerve stimulators, spinal cord stimulators, intrathecal drug delivery devices and then techniques we use in other areas of neurology emerging for pain DBS deep brain stimulation and TMS transcranial magnetic stimulation. OK let's get into some clinical applications now. Let's start with spinal cord stimulators, which - correct me if I'm wrong - seem to be probably the most commonly seen in practice. Which patients can benefit from spinal cord stimulators? When should we think about referring a patient to you and your colleagues for consideration of implantation of one of these spinal cord stimulator devices?  Dr Shirvalkar: So, you know, it's a great question. I would say it's interesting how to define which patients or diagnosis might be appropriate. Technically, spinal cord stimulators are approved for the treatment of most recently diabetic peripheral neuropathy. And so, I think that's a really great category if you have patients who have been failed by more conservative treatments, physical therapy, etcetera, but more commonly even going back, neuropathic low back pain and neuropathic leg pain. And so, you think about it and it's like, how do you define neuropathic pain. Neuropathic pain is kind of broadly defined as any pain that's caused by injury or some kind of lesion in the somatosensory nervous system. We now broaden that to be more than just somatosensory nervous system, but still, what if you can't find a lesion, but the pain still feels or seems neuropathic. Clinically, if something is neuropathic, we often use certain qualitative descriptors to describe that type of pain burning, stabbing, electric light, shooting radiates. There's often hyperpathia, like it lingers and spreads in space and time as opposed to, you know, arthritis, throbbing dull pain or as opposed to muscle pain might be myofascial pain, but sometimes it's hard to tell. So, there aren't great decision tools, I would say to help decide. One of the most common syndromes that we use spinal cord stimulation for is what used to be called failed back surgery syndrome. We never like to, we now try to shy away from explicitly saying something is someone has failed in their clinical treatment. So, the euphemism is now, you know, post-laminectomy syndrome. But in any case, if someone has had back surgery and they still have a nervy or neuropathic type pain, either shooting down their legs and often there's no evidence on MRI or even EMG that that something is wrong, they might be a good candidate, especially if they're relying on long term medications that have side effects or things like full agonist opioids, you know that that might have side effects or contraindication. So, I would say one, it's not a first line treatment. It's usually after you've gone through physical therapy for sure. So, you've gone through tried some medications. Basically, if chronic pain is still impacting your life and your function in a meaningful way that's restricting the things you want to do, then it it's totally appropriate, I think, to think about spinal cord stimulation. And importantly, I will add a huge predictor of final court stimulation success is psychological composition, you know, making sure the person doesn't have any untreated psychological illness and, and actually making sure their expectations going in are realistic. You're not going to cure anyone's pain. You may and that's, you know, a win, but it's very unlikely. And so, give folks the expectation that we hope to reduce your pain by 50% or we want you to list personally, I like functional goals where you say what is your pain preventing you from doing? We want to see if you can do X,Y, and Z during the trial period. Pharmacostimulation right now. Yeah. Biggest indication low back leg pain, Diabetic peripheral neuropathy. There is also an indication for CRPS, complex regional pain syndrome, a lesser, I'd say less common but also very debilitating pain condition. For better or worse. Tertiary quaternary care centers. You often will see spinal cord stem used off label for neuropathic type pain syndromes that are not explicitly better. That may be for example, like a nerve injury that's peripheral, you know, it's not responding. A lot of this off label use is highly variable and, you know, on the whole at a population level not very successful. And so, I think there's been a lot of mixed evidence. So, it's something to be aware about.  Dr Berkowitz: That's a very helpful framework. So, thinking about referring patients to who have most commonly probably the patients with chronic low back pain have undergone surgery, have undergone physical therapy, are on medications, have undergone treatment for any potential psychological psychiatric comorbidities, and yet remain disabled by this pain and have a reasonable expectation and goals that you think would make them a good candidate for the procedure. Are those similar principles to peripheral nerve stimulation I wasn't familiar with that technique, I'm reading your article, so are the principles similar and if so, which particular conditions would potentially benefit from referral for a trial peripheral nerve stimulation as opposed to spinal cord stimulation?  Dr Shirvalkar: Yeah, the principles are similar overall. The peripheral nerve stimulation, you know, neuropathic pain with all the characteristics you listed. Interestingly enough, just like spinal cord stim, most insurances require a psychological evaluation for peripheral nerve stim as well. And we want to make sure again that their expectations are reside, they have good social support and they understand the kind of risks of an invasive device. But also, for peripheral nerve stem, specifically, if someone has a traumatic injury of an individual peripheral nerve, often we will consider it seeing kind of super scapular stimulation. Often with folks who've had shoulder injuries or even sciatic nerve stimulation. I have done a few peroneal nerve stimulations as well as occipital nerve stimulation from migraine, so oxygen nerve stimulation has been studied a lot. So, it's still somewhat controversial, but in the right patient it can actually be really helpful. Dr Berkowitz: Very helpful. So, these are patients who have neuropathic pain, but limited to one peripheral nerve distribution as opposed to the more widespread back associated pains, spine associated pains. Dr Shirvalkar: Yeah, Yeah, that's right. And maybe there's one exception actually to this, which is brachial plexopathy. So, you know, folks who've had something like a brachial plexus avulsion or some kind of traumatic injury to their plexus, there is I think good Class 2 evidence that peripheral nerve stem can work. It falls under the indication. No one is as far as to my knowledge, No one's done an explicit trial, you know PNS randomized controlled trial. Yeah, that's, you know, another area one area where PNS or peripheral nerve stems emerging is actually, believe it or not in myofascial low back pain to actually provide muscle stimulation. There are some, there's a company or two out there that seeks to alter the physiology of the multifidus muscle, one of your spinal stabilizer muscles to really see if that can help low back pain. And they've had some interesting results.  Dr Berkowitz: Very interesting. You mentioned TENS units earlier, transcutaneous electrical nerve stimulation as something a patient could get over the counter. When would you encourage a patient to try TENS and when would you consider TENS inadequate and really be thinking about a peripheral nerve stimulator?  Dr Shirvalkar: Yeah, you know TENS we think of as really appropriate for myofascial pain. Folks who have muscular pain, have clear trigger points or taught muscle bands can often get relief from TENS If you turn a TENS machine up too high, you'll actually see muscle infection. So, there's an optimal level where you actually can turn it up to induce, like, a gentle vibration. And so folks will feel paresthesia and vibrations, and that's kind of the sweet spot. However, I would say if folks have pain that's limited or temporary in time or after a particular activity, TENS can be really helpful. The unfortunate reality is TENS often has very time-limited benefits - just while you're wearing it, you know? So, it's often not enduring. And so that's one of the limitations. Dr Berkowitz: That's helpful to understand. We've talked about the present landscape in your article, also talk a little bit about the future and you alluded to this earlier. Tell us a little bit about some off label emerging techniques that we may see in future use. Who, which types of patients, which conditions might we be referring to you and your colleagues for deep brain stimulation or transcranial magnetic stimulation or motor cortex stimulation? What's coming down the pipeline here?  Dr Shirvalkar: That's a great question. You know, one of my favorite topics is deep brain stimulation. I run the laboratory that studies intracranial signals trying to understand how pain is processed in the brain. But, believe it or not, chronic pain is probably the oldest indication for which DBS has been studied. the first paper came out in 1960, I believe, in France. And you know, the, the original pivotal trials occurred even before the Parkinson's trial and so fell out of favor because in my opinion, I think it was just too hard or too difficult or a problem or too heterogeneous. You know, many things, but there are many central pain syndromes, you know, poststroke pains, there's often pains associated with Parkinson's disease, epilepsy, or other brain disorders for which we just don't have good circuit understanding or good targets. So, I think what's coming down the pipeline is a better personalized target identification, understanding where can we stimulate to actually alleviate pain. The other big trend I think in neuromodulation is using closed loop stimulation which means in contrast to traditional electrical stimulation which is on all the time, you know it's 24/7, set it and forget it. Actually, having stimulation respond or adapt to ongoing physiological signals. So that's something that we're seeing in spinal cord stem, but also trying to develop in deep brain stimulation and noninvasive stimulation. TMS is interestingly approved for neuropathic pain in Europe, but not approved by the FDA in the US. And so I think we may see that coming out of pipeline broader indication. And finally, MR guided focused ultrasound is, is a kind of a brand new technique now. You know, focused ultrasound lesions are being used for essential tremor without even making an incision in the skull or drilling in skull. But there are ways to modulate the brain without lesioning. And, you know, I think a lot of research will be emerging on that in the next five years for, for pain and many other neuronal disorders. Dr Berkowitz: That's fascinating. I didn't know that history that DBS was first studied for pain and now we think of it mostly for Parkinson's and other movement disorders. And now the cycle is coming back around to look at it for pain again. What are some of the targets that are being studied that are thought to have benefit or are being shown by your work and that of others to have benefit as far as DBS targets for, for chronic pain? Dr Shirvalkar: You know, that's a great question. And so, the hard part is finding one target that works for all patients. So, it may actually require personalization and actually understanding what brain circuit phenotypes do you have with regards to your chronic pain and then based on that, what target might we use? But I will say the older targets. Classical targets were periaqueductal gray, which is kind of the opioid center in your brain. You know, it's thought to just release large amounts of endogenous opioids when you stimulate there and then the ventral pusher thalamus, right. So, the sensory ascending system may be through gait control theory interferes with pain, but newer targets the answer singlet there's some interest in in stimulating there again, it doesn't work for everybody. We found some interesting findings with the medial thalamus as well as aspects of the caudate and other basal ganglion nuclei that we hopefully will be publishing soon in a data science paper.  Dr Berkowitz: Fantastic. That's exciting to hear and encourage all of our listeners to check out your article. That goes into a lot more depth than we had time to do in this short interview, both about the science and about the clinical indications, pros and cons, risks and benefits of some of these techniques. So again, today I've been interviewing Dr Prasad Shirvalkar, whose article on neuromodulation for painful neuropathic diseases appears in the most recent issue of Continuum on pain management in neurology. Be sure to check out Continuum Audio episodes from this and other issues. And thank you again to our listeners for joining today.  Dr Shirvalkar: Thank you for having me. It was an honor. 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 heartfelt episode of When the Moment Chooses You, Coach Charlene is joined by Dr. Sheldon Fields, a leader and advocate in nursing and healthcare. Dr. Fields shares his journey and philosophy of "radical grace" and explains why compassion is at the core of true leadership. With over 30 years of experience, Dr. Fields has dedicated his life to making healthcare more inclusive and equitable, especially for historically underserved communities. From his insights on overcoming adversity to his commitment to mentorship and diversity, Dr. Fields emphasizes the importance of leading with humanity, empathy, and understanding. Whether you're in healthcare or simply seeking inspiration on how to lead with kindness and resilience, this episode offers valuable wisdom on the power of grace and compassion in both personal and professional life. #RadicalGrace #CompassionInLeadership #DrSheldonFields #NursingLeadership #InclusiveHealthcare #EmpathyInHealthcare #LeadingWithHumanity #Mentorship #DiversityInNursing #NurseAdvocacy Bio: Sheldon D. Fields PhD, RN, CRNP, FNP-BC, AACRN, FAANP, FNAP, FADLN, FAAN Dr. Fields is Research Professor and inaugural Associate Dean for Equity and Inclusion in the Ross and Carol Nese College of Nursing at Penn State University. He is also founder and CEO of “The S.D.F Group, LLC”, which is a health innovation consultant company. He has over 30 years of experience in the health sector as an educator, researcher, clinician, administrator, consultant, health policy specialist, and entrepreneur / business owner. Dr. Fields is a well-known and respected HIV/AIDS prevention research scientist with a significant focus on young men of color. He is an Advanced AIDS Certified Registered Nurse and a Board-Certified Family Nurse Practitioner. He worked for over a decade as a primary care provider in a federally qualified health center with historically underserved disenfranchised populations. He is a lifetime member of the National Black Nurses Association, Inc., (NBNA) and currently serves as the organization's 14th National President. He was the first ever male Registered Nurse selected for the Robert Wood Johnson Foundation Health Policy Fellowship Program in which he served as a policy adviser to then Senator Barbara Mikulski (D-MD) on the Senate HELP committee during the historic healthcare reform debates and passage of the Affordable Care Act. Dr. Fields is a fellow of the American Academy of Nursing, the American Association of Nurse Practitioners, the National Academies of Practice, and the Academy of Diversity Leaders in Nursing. He is the former dean of the Mervyn M. Dymally School of Nursing at Charles R. Drew University of Medicine and Science, as well as the former dean of the school of Health Professions at New York Institute of Technology. He has held other academic and administrative positions at Binghamton University, University of Rochester, Florida International University, and Long Island University-Brooklyn. Dr. Fields received his Ph.D., in Nursing Science from the University of Pennsylvania, his M.S., in Family Nursing and B.S., in Nursing from Binghamton University. He completed his post-doctoral work in the Center for AIDS Prevention Studies at the University of California San Francisco.  Social Media Links Penn state faculty link: https://www.nursing.psu.edu/directory/fields/ NBNA Officers link: https://www.nbna.org/officers  LinkedIN: https://www.linkedin.com/in/sheldon-d-fields-phd-rn-crnp-fnp-bc-aacrn-fnap-faanp-faan-a5255476/ Wikipedia: https://en.wikipedia.org/wiki/Sheldon_D._Fields

Youtube Version https://youtu.be/HVo0OrT6xic https://amyspeele.com About Amy Amy S. Peele has been an RN since 1974. She discovered her passion for organ donation and transplantation when she started as a transplant coordinator at University of Chicago and enjoyed a thirty-five-year career in transplantation before retiring in 2014 from the University of California San Francisco, one of the largest and most successful transplant programs in the United States. Peele has a love for comedy and improv and graduated from Second City Players Workshop in 1985 in Chicago. She has been writing for over eighteen years. In addition to killing people and using their organs in her murder mysteries, she enjoys meditating, practicing & teaching chair yoga, and swimming.

TOP NEWS | On today's Daily Signal Top News, we break down: Washington Free Beacon reports that Kamala Harris appears to have plagiarized large sections of a Congressional testimony back in 2007. Questions are raised as to why Harris was admitted to the University of California-San Francisco through the school's Legal Education Opportunity Program. A […]

TOP NEWS | On today's Daily Signal Top News, we break down: Washington Free Beacon reports that Kamala Harris appears to have plagiarized large sections of a Congressional testimony back in 2007.  Questions are raised as to why Harris was admitted to the University of California-San Francisco through the school's Legal Education Opportunity Program.  A new USA TODAY/Suffolk University poll out today reports that Donald Trump is leading Harris among Latino voters.  Relevant Links:  https://freebeacon.com/democrats/kamala-harris-plagiarized-pages-of-congressional-testimony-from-a-republican-colleague-plus-a-fictionalized-story-about-human-trafficking/  https://www.dailysignal.com/?p=1112397&preview=true  https://www.cnbc.com/2024/10/22/irs-2025-federal-income-tax-brackets.html  https://tennesseestar.com/kamalafare/warden-admits-biden-harris-doj-has-illegally-imprisoned-steve-bannon-since-october-19/tpappert/2024/10/21/  Listen to other podcasts from The Daily Signal: https://www.dailysignal.com/podcasts/ Get daily conservative news you can trust from our Morning Bell newsletter: DailySignal.com/morningbellsubscription   Listen to more Heritage podcasts: https://www.heritage.org/podcasts Sign up for The Agenda newsletter — the lowdown on top issues conservatives need to know about each week: https://www.heritage.org/agenda

Spine pain is one of the most common presenting concerns in health care settings. It is important for neurologists to understand strategies for evaluating and managing patients with spine pain. In this episode, Katie Grouse, MD, FAAN, speaks with Vernon B. Williams, MD, FAAN, author of the article “Spine Pain,” in the Continuum October 2024 Pain Management in Neurology issue. Dr. Grouse is a Continuum® Audio interviewer and a clinical assistant professor at the University of California San Francisco in San Francisco, California. Dr. Williams is the director of the Center for Sports Neurology and Pain Medicine at Cedars-Sinai Kerlan-Jobe Institute in Los Angeles, California. Additional Resources Read the article: Spine Pain 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: @VernWilliamsMD Transcript 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 Vernon Williams about his article on spine pain, which appears in the October 2024 Continuum issue on pain management in neurology. Welcome to the podcast, and please introduce yourself to our audience.  Dr Williams: Oh, well, thanks for having me. My name is Vernon Williams and I'm a neurologist here in Southern California. Dr Grouse: So, I want to start off today by asking, what do you feel is the key message from your article? Dr Williams: So, I think the key message is that we want to make sure people understand that there's really a distinction between abnormal imaging, tissue damage, nociception, and this experience of spine pain. So, the concept is that nociception is different from the clinical experience of pain; nociception, meaning the electrical signaling from these, quote unquote, pain generators and that kind of thing. But it's really an incomplete framing. We really want people to understand that the experience of pain is colored by a number of other things, things like genetics, biochemical factors, behavior and psychological factors, social factors, those kinds of things. So that's one of the big messages, this distinction between nociception and this clinical experience of pain.  Dr Grouse: Why do you think it's important for neurology clinicians to read this article? Dr Williams: Well, I think, you know, for one thing, spine pain is very common. So, it is likely that neurologists will encounter patients who come to see them because of that chief complaint. But I think that if we want to really be successful at treating spine-related pain, then we really have to know all of that basic information, the basic knowledge that we came to learn as residents and medical students or what have you. But it's also important to know that that knowledge is necessary, but it's insufficient. You really also have to confront pain from the standpoint of these other things, these other behavioral factors, psychological factors, social factors, and you got to kind of combine those things to be the most successful in treating this very common condition.  Dr Grouse: You know, you mentioned earlier about the difference between tissue damage pain and nociception. I find this to be, you know, a really great lens thinking about these concepts to view this topic and your article specifically. Can you go a little more into what the difference between, specifically, pain and nociception really is? Dr Williams: Yeah. I mean, so when we talk about nociception, in many ways we're talking about the electrical activity. And so, there's the stimulation of these nerves, in the periphery typically, and that electrical signal is transmitted, you know, from those nociceptive fibers into the spinal cord. And it's headed from the first-order neuron to the second-order neuron and axons in the spinal cord and eventually reaches the brain. But essentially the concept is that it's not pain at that point. It's not pain until those signals reach the cortex and they are experienced in some context. And that context really colors whether or not, and to what extent, people experience pain or suffer pain as a result. So, when we think about nociception, we tend to think about kind of tissue damage or the threat of tissue damage. And in clinic, we tend to kind of focus on that and we look for relationships between abnormalities on imaging studies that could be causing those kinds of electrical signals. And we tend to focus less on that second but critical aspect of things, and that's that individual 's personal experience, which is colored by a number of different things: their attention, their expectation, colored by how we interact with them, our verbal and non-verbal communication with them. And again, like we talked about: their history, who are they, their genetics, their behavioral history, their psychological history and those kinds of things. So, it's really this combination of things that we have to be aware of when we're treating spine pain. And I think the tendency is for us to focus on the first half and less on the second half. Dr Grouse: Absolutely. I certainly think our training and our focus on localizing the lesion may in some ways hurt us in that sense because we really focus so much on the first and not so much the second. Would you say that's probably right? Dr Williams: Yeah, I mean, that's part of our heritage as clinicians, particularly neurologists. It's, where's the lesion? And so, what happens when there is no, quote unquote, lesion? What happens if there are multiple potential lesions? And so, these kinds of concepts, I think, become really important, and the context in which you're examining and evaluating that patient becomes important. And I think they are at least as important as the potential pain generator or the nociceptive signal.   Dr Grouse: Now, you mentioned earlier something about sort of how we approach the patient and the language we're putting out, the body language. I found the concept of nocebo and maladaptive pain-related neuroplasticity to be absolutely fascinating when I was reading your article, and I was really surprised to learn that clinicians can really contribute to this effect unknowingly through their body language, verbal language, nonverbal messaging, and even how they're interpreting the test results? When a patient comes to see you with chronic back pain, how do you approach the whole process to minimize this effect and, really, to set the stage for more constructive and therapeutic evaluation? Dr Williams: Yeah, Katie, I think that's… it's tough because our culture is so, you know, it's so ingrained in our culture to look for a structural abnormality as an explanation for an individual 's symptoms. And so, I find myself struggling with that all the time, not only discussing why we're ordering an imaging study, but, if that person comes back and I'm describing to them the abnormalities on that imaging study, I've got to be very careful about describing them in the context of what we expect. And so, I'll typically try to use words like, well, you've got some wear-and-tear changes that we all get, as compared to saying, well, you've got a disc herniation abnormality at L five S one that's causing your pain. That statement could have a negative effect on that individual's framing of what's going on. Maybe that L five S one disc is contributing to their symptoms and maybe it isn't. Maybe it's been there or for years and maybe it's new. And even if it is new, does that mean, in that patient's mind, that now they've got an abnormality that has to be fixed or else they will continue to have pain? And so, kind of trying to keep all of those things in mind is why we want to kind of color that interaction. And I mentioned both verbal and nonverbal interaction and communication with the patient, because I think that they are picking up on all of these signals. Some of them are very obvious and some of them are very subtle. But keep in mind their brains, their nervous systems are primed to interpret all of these signals, both verbal and nonverbal. And that's going to have a downstream - or upstream, I would say - effect on their framing and how they interpret the interaction and what they think it means for them and their future. So, you know, it's kind of a big thing to think about when you- every time you walk in a room, but it's an important thing to think about when we're communicating with patients.  Dr Grouse: It's absolutely fascinating and has really made me go back and think about, gosh, are there ways that I could have done things better to really message this in a more helpful way? And on that note, do you have any tips or tricks on how to put out that that messaging, both verbal and nonverbal; to be, you know, to avoid those pitfalls of kind of reinforcing the wrong message about tissue damage? Dr Williams: Yeah. I mean, so one of the main things is trying to be very purposeful about educating people on the difference between tissue damage or potential tissue damage and pain. And so being careful not to use statements like, well, I think your pain is coming from this disc or this structural abnormality because again, we want to try to separate those things. They are different. I think that, you know, how we discuss imaging studies is very important because you want people to understand that an imaging study is just that. It's anatomy and it doesn't equal function, it doesn't equal what they experience in terms of sensory symptoms and pain. But I think the goal is to try to be very purposeful and maybe even reexamine how we discuss those things or when we discuss those things. One of the things I've found helpful is kind of the order in which I perform my clinical assessment. So traditionally, I was taught, like many, take the history, do the physical examination, and then start to discuss and educate patients. Right? Here's the test I want to order, here's what I think may be going on, so on and so forth. I think in some cases it's more beneficial to take the history and, before the physical examination, discuss what I'm thinking, taking that opportunity to discuss the differences between nociception, tissue damage, the experience of pain, the importance of movement, so on and so forth. And then do the physical examination so that that person has some idea of what is it that he's looking for. How is this going to inform his opinions and recommendations and so on and so forth. But also provide them with the concept that movement, for instance, is safe unless they have certain kinds of red flags on their history. I'm encouraging movement and I'm encouraging them to recognize that some of these movements they may have predicted would have been painful for them actually aren't painful, and they may start to internalize the concept that they can do it once without paying, that probably means that they're not damaging themselves every time they perform that movement. And if they can do one pain-free rep, that's important, and that may counteract the concept that they are damaging themselves every time they move and every time they feel pain, that means that there's tissue damage. So, what we talk about, how we talk about it and even when we talk about it during the course of that evaluation may have some negative or positive effects. And it may be beneficial to kind of think about those things and whether or not our typical approach might be the best or maybe we can improve on that or adjust that, particularly in certain situations and with certain patients. Dr Grouse: That's absolutely fascinating, and great tips I think that all of our listeners will want to incorporate as we're approaching this patient population. You know, in your article, I also wanted to talk about, you mentioned some really interesting treatments for pain is that I think would include, or would, fall under the category of neuromodulation. Can you summarize some of these options for us? Dr Williams: Yeah. I mean, so I think that the concept of neuromodulation, I tend to think of it in a very holistic sense. And so not only focusing on the application of external stimuli and that could be, you know, electrical stimuli, magnetic stimuli, cryo, analgesia, those kinds of things in order to turn up or down nervous system activity, electrical signals, what have you. I think of neuromodulation in a global sense. I think in a way, cognitive restructuring and education, in a way, is a form of neuromodulation. It's affecting how that individual frames the concept of their pain, structural changes versus experience, so on and so forth. But generally, I'm talking about these kinds of things. So, there are some very interesting approaches with electrical stimulation and it doesn't necessarily have to be permanent implantation of a stimulator as we tend to think about with spinal cord stimulation, but there are some interesting temporary peripheral nerve stimulators that that can be very helpful for various kinds of spinal pain. And then there's also these technologies that I find fascinating. Some of them are in the wearables category. So, combining the education and framing and cognitive restructuring with things like virtual reality, there are some interesting programs that combine some predictive modeling with virtual reality, such that an individual has goggles on, they are participating in some activity that requires them to move in a certain direction and move to a certain extent that may or may not match what they are seeing visually in the goggles. So, you can kind of begin to kind of dissociate their expectation of when they may experience pain as a function of their movement from what actually happens. So, these kinds of things, I think, are really interesting ways to augment our traditional approaches to pain, physical therapy, rehabilitation, medications, some kinds of injections, with these additional approaches that really have an effect on the nervous system as opposed to just focusing on what I would call kind of the mechanical anatomy, the joints and the discs and what have you, with traditional approaches. Dr Grouse: It's really exciting to hear about some of these new options that can be tried to help with this neuromodulation and sort of cognitive restructuring. Of course, understanding that there's some things that we do ourselves that do this in the clinic encounter, which I think is a great reminder. I wanted to touch on, in your article, you had mentioned that we really have to be aware as clinicians, that health inequities and disparities and even the social determinants of health have inevitable effects on spine pain. How can our listeners better recognize and ensure equitable care for this patient population, particularly in light of the fact that many of these therapies that we've just been talking about can be difficult to access even in the best circumstances? Dr Williams: Well, you know, thanks for asking that question. I think that's a great question. I think from the standpoint of, you know, health equity and addressing, you know, disparities and that kind of thing, the first thing is to just acknowledge and recognize that these things are present. And even, you know, though we may have the best intentions, there may be scenarios where our practices are affected and our patients are affected by these kinds of things. So, I think the first thing is the acknowledgement. And then the second thing is kind of trying to figure out if there are things that we can do as individual practitioners, or our offices can do or the entities that we interact with, maybe that's a hospital system or what have you to address these kinds of things. So, we know, for instance, from the standpoint of race and ethnicity, there's disparities with respect to African Americans, with Hispanics and other ethnic minorities and the kind of care they receive. We know that access resulting from insurance coverage and geographical limitations, that kind of thing can be significant. And interestingly, it doesn't necessarily mean that the person is uninsured. So, for instance, we will often see individuals who've had work injuries and who are covered by the workers' compensation system have certain limitations placed on what they have access to, often resulting in lots of frustration from those patients. And that's a reality that we sometimes have to work really hard to overcome. Socioeconomic status, provider bias. And again, this is something that we have to kind of do some internal searching to say, hey, am I approaching these individuals on a on a more equal and equitable basis, or am I also subject to some of the biases that that I've been exposed to and trying to overcome that? So, I think that's a huge part of the context. And when we talk about how we learn, whether we're talking about spine pain or anything else, I'm a believer in that kind of cycle of pedagogy that includes content-based information, which is kind of the very basic foundational information, that includes things we can memorize and definitions we can memorize. And that may include things like what we've talked about relative to kind of the nociception and pain pathways, so on and so forth. But then there are concepts, and we've talked about the concept of verbal communication and nonverbal communication, the concept of cognitive restructuring and neuromodulation as an approach. But then context is kind of that last level, probably the most significant level in terms of how we can integrate all this information and really master information. And that context has to do with things like social determinants and disparities and the reality that these things have an effect on how we evaluate and manage patients and the success with which patients can be managed. And so, I appreciate that question, I think it's a great question, because it gets that kind of the reality of what does this look like in real life as opposed to just on the page or just in a textbook. Dr Grouse: Well, that's really helpful and certainly something that we can all keep in mind as we try to be more aware of this, and I like the idea of just acknowledging it and just having it there, knowing that this exists and helping that inform how we approach these patients. I wanted to ask you, what do you think the biggest controversy is currently in the evaluation and management of spine pain? Dr Williams: You know, I think that there's a couple of controversies that are interesting. Nowadays, one of them has to do with the utility of some of the things that have been performed and done most frequently for spine pain, and that's things like epidural injections, facet injections, some of the interventional procedures. There's some controversy among some as to whether or not these things are effective, you know, what role they have in treatment because some people will say, oh, is there any long-term effect from these kinds of procedures? Even patients will sometimes say, hey, listen, I'm not sure if I want an injection because isn't that just temporary, or, isn't that just a band aid? But I think that when we talk about pain from the perspective of it potentially being a progressive disorder and trying to be aggressive with managing pain so that we are less likely to see some of the chronic manifestations that occur with maladaptive neuroplasticity it's important to be aggressive with stopping no subceptive signals, reducing an individual 's experience of pain, optimizing their function, and having a positive effect on the ability to treat and eliminate pain, even if that means with epidural injections or blocks or what have you, as long as they're safe and effective. I think that there are some controversies evolving related to some of the regenerative procedures that have been done for other kinds of musculoskeletal pain. So, for instance, PRP and stem cells, you know, people have been doing those for knees and muscle tears and what have you. And of course, that technology has kind of evolved into potential approaches for spine pain. People are often interested in whether PRP or stem cells may help their spine pain. And so, I think that's another area of potential controversy because there hasn't been a ton of, you know, high-level evidence, although there are some, you know, there's some studies out there and there's some evidence that they may be of benefit. And I think the role of stimulators and implants for axial pain is another area of potential controversy. Those are probably the biggest things in this area of spine pain that are topics of controversy. There are things that have people talked about for years in terms of chiropractic care versus traditional medical care. But I think right now it's the utility of these kinds of interventional procedures, the role of regenerative procedures and injections, and then the role of more aggressive interventions like permanent implantation of stimulators and that kind. Dr Grouse: Is there anything coming on the horizon in the field of managing spine pain that we should be looking out for? Dr Williams: Well, you know, I am still bullish on the concept of neuromodulation and we've talked about that peripheral nerve stimulation, spinal cord stimulation, and then other wearables, VR, so on and so forth. I think that those things will continue to evolve, and I think that technologies continue to evolve that are likely to help with spine related pain. Some of them are very interestingly related to the ability to strengthen multifidus muscles and improve muscular function in individuals with spine pain. But I think that's one area - neuromodulation - that we'll continue to see evolution. I think that- I'm interested to see what the role of regenerative injections and regenerative procedures may play. And then just like every other field of human endeavor, artificial intelligence, machine learning, those kinds of things are likely to have a significant effect on how we diagnose an individuals, on treatment options for various individuals, and even a predicting outcome from various treatment. So those, I think, are examples of areas that we'll see continued growth and evolution with respect to spine pain. Dr Grouse: Well, I'm very excited to see what comes down the pipeline and both vastly more to come, I'm sure. So, thank you so much, Vernon, for joining us. I really enjoyed reading your article. I really enjoyed talking about this topic. I think I've learned a lot and I hope that our listeners will take the time to read this article. It's really, really helpful. Dr Williams: Well, I appreciate the opportunity. I really enjoy participating in this process. The interview was fun, so thanks a lot for having me. I really appreciate it. Dr Grouse: Again, today I've been interviewing Dr Vernon Williams, whose article on spine pain appears in the most recent issue of Continuum on pain management in neurology. 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 Continnpub.com/AudioCME. Thank you for listening to Continuum Audio.

This episode of Going anti-Viral features an IAS–USA Dialogue titled "Latest Update on Urgent Viral Outbreaks," a panel discussion held on October 4, 2024. Dr Carlos del Rio from Emory University serves as moderator and welcomes 3 distinguished panelists: Dr Yvonne Maldonado from Stanford University, Dr Peter Chin-Hong from the University of California San Francisco, and Dr Paul Sax from Brigham and Women's Hospital. The episode covers various pressing topics, including updates on COVID-19, avian flu, mpox, and other viral diseases. Discussions touch on vaccines, their effectiveness, public health approaches, and current research.0:00 – Introduction and overview of ongoing viral outbreaks3:59 – Update on respiratory viruses and vaccination – seasonal flu, RSV, and COVID-1912:17 – Discussion of monoclonal antibody treatment for COVID-1914:15 – Update on the use of Paxlovid for COVID-1918:48 – COVID-19 vaccination – protein vaccines vs. mRNA vaccines22:48 – Update on pertussis28:54 – Discussion of seasonal influenza and vaccination32:55 – Effectiveness of shingles and RSV vaccines 35:57 – Discussion of vaccination during pregnancy40:02 – Audience questions43:04 – Update on H5N1 (avian flu) outbreak52:00 – Update on Marburg virus outbreak in Rwanda55:43 – Discussion of mpox outbreak in central Africa59:29 – Concluding remarks__________________________________________________Produced by IAS-USA, Going anti–Viral is a podcast for clinicians involved in research and care in HIV, its complications, and other viral infections. This podcast is intended as a technical source of information for specialists in this field, but anyone listening will enjoy learning more about the state of modern medicine around viral infections. Going anti-Viral's host is Dr Michael Saag, a physician, prominent HIV researcher at the University of Alabama at Birmingham, and volunteer IAS–USA board member. In most episodes, Dr Saag interviews an expert in infectious diseases or emerging pandemics about their area of specialty and current developments in the field. Other episodes are drawn from the IAS–USA vast catalogue of panel discussions, Dialogues, and other audio from various meetings and conferences. Email podcast@iasusa.org to send feedback, show suggestions, or questions to be answered on a later episode.Follow Going anti-Viral on: Apple Podcasts YouTubeXFacebookInstagram...

Even though highly effective medications are currently available to prevent HIV, there are about 1.3 million new infections worldwide each year. Monica Gandhi, MD, MPH, of the University of California San Francisco joins JAMA Senior Editor Karen E. Lasser, MD, MPH, to discuss preexposure prophylaxis (PrEP) for HIV. Related Content: Preexposure Prophylaxis (PrEP) for HIV What Is Doxycycline Postexposure Prophylaxis?

Support the show to get full episodes and join the Discord community. https://youtu.be/lbKEOdbeqHo The Transmitter is an online publication that aims to deliver useful information, insights and tools to build bridges across neuroscience and advance research. Visit thetransmitter.org to explore the latest neuroscience news and perspectives, written by journalists and scientists. The Transmitter has provided a transcript for this episode. Vijay Namoodiri runs the Nam Lab at the University of California San Francisco, and Ali Mojebi is an assistant professor at the University of Wisconsin-Madison. Ali as been on the podcast before a few times, and he's interested in how neuromodulators like dopamine affect our cognition. And it was Ali who pointed me to Vijay, because of some recent work Vijay has done reassessing how dopamine might function differently than what has become the classic story of dopamine's function as it pertains to learning. The classic story is that dopamine is related to reward prediction errors. That is, dopamine is modulated when you expect reward and don't get it, and/or when you don't expect reward but do get it. Vijay calls this a "prospective" account of dopamine function, since it requires an animal to look into the future to expect a reward. Vijay has shown, however, that a retrospective account of dopamine might better explain lots of know behavioral data. This retrospective account links dopamine to how we understand causes and effects in our ongoing behavior. So in this episode, Vijay gives us a history lesson about dopamine, his newer story and why it has caused a bit of controversy, and how all of this came to be. I happened to be looking at the Transmitter the other day, after I recorded this episode, and low and behold, there was an article titles Reconstructing dopamine's link to reward. Vijay is featured in the article among a handful of other thoughtful researchers who share their work and ideas about this very topic. Vijay wrote his own piece as well: Dopamine and the need for alternative theories. So check out those articles for more views on how the field is reconsidering how dopamine works. Nam Lab. Mohebi & Associates (Ali's Lab). Twitter: @vijay_mkn @mohebial Transmitter Dopamine and the need for alternative theories. Reconstructing dopamine's link to reward. Related papers Mesolimbic dopamine release conveys causal associations. Mesostriatal dopamine is sensitive to changes in specific cue-reward contingencies. What is the state space of the world for real animals? The learning of prospective and retrospective cognitive maps within neural circuits Further reading (Ali's paper): Dopamine transients follow a striatal gradient of reward time horizons. Ali listed a bunch of work on local modulation of DA release: Local control of striatal dopamine release. Synaptic-like axo-axonal transmission from striatal cholinergic interneurons onto dopaminergic fibers. Spatial and temporal scales of dopamine transmission. Striatal dopamine neurotransmission: Regulation of release and uptake. Striatal Dopamine Release Is Triggered by Synchronized Activity in Cholinergic Interneurons. An action potential initiation mechanism in distal axons for the control of dopamine release. Read the transcript, produced by The Transmitter. 0:00 - Intro 3:42 - Dopamine: the history of theories 32:54 - Importance of learning and behavior studies 39:12 - Dopamine and causality 1:06:45 - Controversy over Vijay's findings

This week I sit down with Dr. Elisa Song to discuss her new book, Healthy Kids, Happy Kids. Dr. Song is a graduate of Stanford University with a degree in political Science. She then attended New York University for her medical degree and finally a stop at the University of California San Francisco for pediatric residency training. In her own words, Dr. Song is a holistic pediatrician. She founded Whole Family Wellness, an integrative pediatric practice in Belmont, CA – one of the first and most highly regarded holistic pediatric practices in the country. She created Healthy Kids Happy Kids – dedicated to empowering parents to take charge of their kids' health … naturally! She lectures around the world for the Center for Education and Development in Clinical Homeopathy (CEDH), Academy for Pain Research, Institute for Functional Medicine, and Holistic Pediatric Association, A4M among others. In this interview we look at health through a prevention first lens with a deep look at the intestinal microbiome and nutrition. Dr. Song's immense fund of knowledge is on full display in her book and this interview. Please enjoy my conversation with Dr. Elisa Song, Dr. M

Send us a Text Message.About the guest: Robin Carhart-Harris, PhD is a neuroscientist & psychopharmacologist. His lab at the University of California-San Francisco studies the effects of psychedelics and other drugs on the human brain, using neuroimaging and other approaches.Episode summary: Nick and Dr. Carhart-Harris discuss: psychedelics & the human brain; functional connectivity & entropy in brain patterns; the “entropic brain” hypothesis of psychedelic drug action; psychiatry & depression; psychology, Carl Jung & Sigmund Freud; the FDA's rejection of MDMA-assisted psychotherapy for PTSD; latest research on psychedelics; and more.Related episodes:Anesthesia, Placebo Effects, Consciousness, Subjectivity, MDMA, Ketamine, Opioids, Psychedelics | Boris Heifets | #163DMT, Serotonin, Inflammation, Psychedelics, and Past, Present & Future of Psychedelic Medicine | David & Charles Nichols | #137*This content is never meant to serve as medical advice.Support the Show.All episodes (audio & video), show notes, transcripts, and more at the M&M Substack Try Athletic Greens: Comprehensive & convenient daily nutrition. Free 1-year supply of vitamin D with purchase.Try SiPhox Health—Affordable, at-home bloodwork w/ a comprehensive set of key health marker. Use code TRIKOMES for a 10% discount.Try the Lumen device to optimize your metabolism for weight loss or athletic performance. Use code MIND for 10% off.Learn all the ways you can support my efforts

An explosion of research is painting a clearer picture of how climate change is affecting mental health across the globe. Also, a citizen science project aims to find species that have gone unnoticed by sampling the waters of hundreds of lakes worldwide for environmental DNA.Assessing The Global Mental Health Toll Of Climate ChangeAs the effects of climate change become more visible and widespread, people around the globe are dealing with the mental health impacts. But what are those impacts exactly, and how do they differ between people in different parts of the world? That's been the focus of a rapidly growing area of research, which is seeking to understand the psychological impacts of climate change, sometimes referred to as “eco-anxiety.”Guest host Maggie Koerth is joined by Dr. Alison Hwong, a psychiatry fellow at University of California San Francisco, to talk about what scientists have learned about global eco-anxiety and what strategies they've found to reduce its more harmful effects.Citizen Scientists Will Capture DNA From 800 Lakes In One DayTaking an accurate census of the organisms in an ecosystem is a challenging task—an observer's eyes and ears can't be everywhere. But a new project aims to harness the growing field of environmental DNA (eDNA) to detect species that might escape even the most intrepid ecologists. In the project, volunteers plan to take samples from some 800 lakes around the world on or around May 22, the International Day for Biological Diversity. Those samples will then be sent back to a lab in Zurich, Switzerland, where they'll be analyzed for the tiny traces of DNA that organisms leave behind in the environment.Dr. Kristy Deiner, organizer of the effort, hopes that just as lakes collect water from many streams across an area, they'll also collect those eDNA traces—allowing researchers to paint a picture of the species living across a large area. She talks with SciFri's John Dankosky about the project, and how this type of citizen science can aid the research community.Transcripts for each segment will be available after the show airs on sciencefriday.com. Subscribe to this podcast. Plus, to stay updated on all things science, sign up for Science Friday's newsletters.