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 Normal pressure hydrocephalus (NPH) is a clinical syndrome of gait abnormality, cognitive impairment, and urinary incontinence. Evaluation of CSF dynamics, patterns of fludeoxyglucose (FDG) uptake, and patterns of brain stiffness may aid in the evaluation of challenging cases that lack typical clinical and structural radiographic features. In this episode, Katie Grouse, MD, FAAN, speaks with Aaron Switzer, MD, MSc, author of the article “Radiographic Evaluation of Normal Pressure Hydrocephalus” 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. Switzer is a clinical assistant professor of neurology in the department of clinical neurosciences at the University of Calgary in Calgary, Alberta, Canada. Additional Resources Read the article: Radiographic Evaluation of Normal Pressure Hydrocephalus 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 Aaron Switzer about his article on radiographic evaluation of normal pressure hydrocephalus, which he wrote with Dr Patrice Cogswell. 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. Switzer: Thanks so much for having me, Katie. I'm a neurologist that's working up in Calgary, Alberta, Canada, and I have a special interest in normal pressure hydrocephalus. So, I'm very happy to be here today to talk about the radiographic evaluation of NPH. Dr Grouse: I'm so excited to have you here today. It was really wonderful to read your article. I learned a lot on a topic that is not something that I frequently evaluate in my clinic. So, it's really just a pleasure to have you here to talk about this topic. So, I'd love to start by asking, what is the key message that you hope for neurologists who read your article to take away from it? Dr. Switzer: The diagnosis of NPH can be very difficult, just given the clinical heterogeneity in terms of how people present and what their images look like. And so, I'd like readers to know that detailed review of the patient's imaging can be very helpful to identify those that will clinically improve with shunt surgery. Dr Grouse: There's another really great article in this edition of Continuum that does a really great job delving into the clinical history and exam findings of NPH. So, I don't want to get into that topic necessarily today. However, I'd love to hear how you approach a case of a hypothetical patient, say, where you're suspicious of NPH based on the history and exam. I'd love to talk over how you approach the imaging findings when you obtain an MRI of the brain, as well as any follow-up imaging or testing that you generally recommend. Dr. Switzer: So, I break my approach down into three parts. First, I want to try to identify ventriculomegaly and any signs that would support that, and specifically those that are found in NPH. Secondly, I want to look for any alternative pathology or evidence of alternative pathology to explain the patient's symptoms. And then also evaluate any contraindications for shunt surgery. For the first one, usually I start with measuring Evans index to make sure that it's elevated, but then I want to measure one of the other four measurements that are described in the article, such as posterior colossal angle zed-Evans index---or z-Evans index for the American listeners---to see if there's any other features that can support normal pressure hydrocephalus. It's very important to identify whether there are features of disproportionately enlarged subarachnoid space hydrocephalus, or DESH, which can help identify patients who may respond to shunt surgery. And then if it's really a cloudy clinical picture, it's complicated, it's difficult to know, I would usually go through the full evaluation of the iNPH radscale to calculate a score in order to determine the likelihood that this patient has NPH. So, the second part of my evaluation is to rule out evidence of any alternative pathology to suggest another cause for the patient's symptoms, such as neurodegeneration or cerebrovascular disease. And then the third part of my evaluation is to look for any potential contraindications for shunt surgery, the main one being cerebral microbleed count, as a very high count has been associated with the hemorrhagic complications following shunt surgery. Dr Grouse: You mentioned about your use of the various scales to calculate for NPH, and your article does a great job laying them out and where they can be helpful. Are there any of these scales that can be reasonably relied on to predict the presence of NPH and responsiveness to shunt placement? Dr. Switzer: I think the first thing to acknowledge is that predicting shunt response is still a big problem that is not fully solved in NPH. So, there is not one single imaging feature, or even combination of imaging features, that can reliably predict shunt response. But in my view and in my practice, it's identifying DESH, I think, is really important---so, the disproportionately enlarged subarachnoid space hydrocephalus---as well as measuring the posterior colossal angle. I find those two features to be the most specific. Dr Grouse: Now you mentioned the concept of the NPH subtypes, and while this may be something that many of our listeners are familiar with, I suspect that, like myself when I was reading this article, there are many who maybe have not been keeping up to date on these various subtypes. Could you briefly tell us more about these NPH subtypes? Dr. Switzer: Sure. The Japanese guidelines for NPH have subdivided NPH into three different main categories. So that would be idiopathic, delayed onset congenital, and secondary normal pressure hydrocephalus. And so, I think the first to talk about would be the secondary NPH. We're probably all more familiar with that. That's any sort of pathology that could lead to disruption in CSF dynamics. These are things like, you know, a slow-growing tumor that is obstructing CSF flow or a widespread meningeal process that's reducing absorption of CSF, for instance. So, identifying these can be important because it may offer an alternative treatment for what you're seeing in the patient. The second important one is delayed onset congenital. And when you see an image of one of these subtypes, it's going to be pretty different than the NPH because the ventricles are going to be much larger, the sulcal enfacement is going to be more diffuse. Clinically, you may see that the patients have a higher head circumference. So, the second subtype to know about would be the delayed onset congenital normal pressure hydrocephalus. And when you see an image of one of these subtypes, it's going to be a little different than the imaging of NPH because the ventricles are going to be much larger, the sulcal enfacement is going to be more diffuse. And there are two specific subtypes that I'd like you to know about. The first would be long-standing overt ventriculomegaly of adulthood, or LOVA. And the second would be panventriculomegaly with a wide foramen of magendie and large discernomagna, which is quite a mouthful, so we just call it PAVUM. The importance of identifying these subtypes is that they may be amenable to different types of treatment. For instance, LOVA can be associated with aqueductal stenosis. So, these patients can get better when you treat them with an endoscopic third ventriculostomy, and then you don't need to move ahead with a shunt surgery. And then finally with idiopathic, that's mainly what we're talking about in this article with all of the imaging features. I think the important part about this is that you can have the features of DESH, or you can not have the features of DESH. The way to really define that would be how the patient would respond to a large-volume tap or a lumbar drain in order to define whether they have this idiopathic NPH. Dr Grouse: That's really helpful. And for those of our listeners who are so inclined, there is a wonderful diagram that lays out all these subtypes that you can take a look at. I encourage you to familiarize yourself with these different subtypes. Now it was really interesting to read in your article about some of the older techniques that we used quite some time ago for diagnosing normal pressure hydrocephalus that thankfully we're no longer using, including isotope encephalography and radionuclide cisternography. It certainly made me grateful for how we've come in our diagnostic tools for NPH. What do you think the biggest breakthrough in diagnostic tools that are now clinically available are? Dr. Switzer: You know, definitely the advent of structural imaging was very important for the evaluation of NPH, and specifically the identification of disproportionately enlarged subarachnoid space hydrocephalus, or DESH, in the late nineties has been very helpful for increasing the specificity of diagnosis in NPH. But some of the newer technologies that have become available would be phase-contrast MRI to measure the CSF flow rate through the aqueduct has been very helpful, as well as high spatial resolution T2 imaging to actually image the ventricular system and look for any evidence of expansion of the ventricles or obstruction of CSF flow. Dr Grouse: Regarding the scales that you had referenced earlier, do you think that we can look forward to more of these scales being automatically calculated and reported by various software techniques and radiographic interpretation techniques that are available or going to be available? Dr. Switzer: Definitely yes. And some of these techniques are already in development and used in research settings, and most of them are directed towards automatically detecting the features of DESH. So, that's the high convexity tight sulci, the focally enlarged sulci, and the enlarged Sylvian fissures. And separating the CSF from the brain tissue can help you determine where CSF flow is abnormal throughout the brain and give you a more accurate picture of CSF dynamics. And this, of course, is all automated. So, I do think that's something to keep an eye out for in the future. Dr Grouse: I wanted to ask a little more about the CSF flow dynamics, which I think may be new to a lot of our listeners, or certainly something that we've only more recently become familiar with. Can you tell us more about these advances and how we can apply this information to our evaluations for NPH? Dr. Switzer: So currently, only the two-dimensional phase contrast MRI technique is available on a clinical basis in most centers. This will measure the actual flow rate through the cerebral aqueduct. And so, in NPH, this can be elevated. So that can be a good supporting marker for NPH. In the future, we can look forward to other techniques that will actually look at three-dimensional or volume changes over time and this could give us a more accurate picture of aberrations and CSF dynamics. Dr Grouse: Well, definitely something to look forward to. And on the topic of other sort of more cutting-edge or, I think, less commonly-used technologies, you also mentioned some other imaging modalities, including diffusion imaging, intrathecal gadolinium imaging, nuclear medicine studies, MR elastography, for example. Are any of these modalities particularly promising for NPH evaluations, in your opinion? Do you think any of these will become more popularly used? Dr. Switzer: Yes, I think that diffusion tract imaging and MR elastography are probably the ones to keep your eye out for. They're a little more widely applicable because you just need an MR scanner to acquire the images. It's not invasive like the other techniques mentioned. So, I think it's going to be a lot easier to implement into clinical practice on a wide scale. So, those would be the ones that I would look out for in the future. Dr Grouse: Well, that's really exciting to hear about some of these techniques that are coming that may help us even more with our evaluation. Now on that note, I want to talk a little bit more about how we approach the evaluation and, in your opinion, some of the biggest pitfalls in the evaluation of NPH that you've found in your career. Dr. Switzer: I think there are three of note that I'd like to mention. The first would be overinterpreting the Evans index. So, just because an image shows that there's an elevated Evans index does not necessarily mean that NPH is present. So that's where looking for other corroborating evidence and looking for the clinical features is really important in the evaluation. Second would be misidentifying the focally enlarged sulci as atrophy because when you're looking at a brain with these blebs of CSF space in different parts of the brain, you may want to associate that to neurodegeneration, but that's not necessarily the case. And there are ways to distinguish between the two, and I think that's another common pitfall. And then third would be in regards to the CSF flow rate through the aqueduct. And so, an elevated CSF flow is suggestive of NPH, but the absence of that does not necessarily rule NPH out. So that's another one to be mindful of. Dr Grouse: That's really helpful. And then on the flip side, any tips or tricks or clinical pearls you can share with us that you found to be really helpful for the evaluation of NPH? Dr. Switzer: One thing that I found really helpful is to look for previous imaging, to look if there were features of NPH at that time, and if so, have they evolved over time; because we know that in idiopathic normal pressure hydrocephalus, especially in the dash phenotype, the ventricles can become larger and the effacement of the sulci at the convexity can become more striking over time. And this could be a helpful tool to identify how long that's been there and if it fits with the clinical history. So that's something that I find very helpful. Dr Grouse: Absolutely. When I read that point in your article, I thought that was really helpful and, in fact, I'm guessing something that a lot of us probably aren't doing. And yet many of our patients for one reason or other, probably have had imaging five, ten years prior to their time of evaluation that could be really helpful to look back at to see that evolution. Dr. Switzer: Yes, absolutely. Dr Grouse: It's been such a pleasure to read your article and talk with you about this today. Certainly a very important and helpful topic for, I'm sure, many of our listeners. Dr. Switzer: Thank you so much for having me. Dr Grouse: Again, today I've been interviewing Dr Aaron Switzer about his article on radiographic evaluation of normal pressure hydrocephalus, which he wrote with Dr Patrice Cogswell. 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.

This content has been developed for healthcare professionals only. Patients who seek health information should consult with their physician or relevant patient advocacy groups.For the full presentation, downloadable Practice Aids, slides, and complete CME/MOC/AAPA/IPCE information, and to apply for credit, please visit us at PeerView.com/GWQ865. CME/MOC/AAPA/IPCE credit will be available until June 29, 2026.Cracking the Code of GBA1-Associated Parkinson's Disease and Lysosomal Storage Disorders: Transforming Diagnosis and Management In support of improving patient care, this activity has been planned and implemented by PVI, PeerView Institute for Medical Education, and Gaucher Community Alliance. PVI, PeerView Institute for Medical Education, is jointly accredited by the Accreditation Council for Continuing Medical Education (ACCME), the Accreditation Council for Pharmacy Education (ACPE), and the American Nurses Credentialing Center (ANCC), to provide continuing education for the healthcare team.SupportThis activity is supported by an educational grant from Lilly.Disclosure information is available at the beginning of the video presentation.

This content has been developed for healthcare professionals only. Patients who seek health information should consult with their physician or relevant patient advocacy groups.For the full presentation, downloadable Practice Aids, slides, and complete CME/MOC/AAPA/IPCE information, and to apply for credit, please visit us at PeerView.com/GWQ865. CME/MOC/AAPA/IPCE credit will be available until June 29, 2026.Cracking the Code of GBA1-Associated Parkinson's Disease and Lysosomal Storage Disorders: Transforming Diagnosis and Management In support of improving patient care, this activity has been planned and implemented by PVI, PeerView Institute for Medical Education, and Gaucher Community Alliance. PVI, PeerView Institute for Medical Education, is jointly accredited by the Accreditation Council for Continuing Medical Education (ACCME), the Accreditation Council for Pharmacy Education (ACPE), and the American Nurses Credentialing Center (ANCC), to provide continuing education for the healthcare team.SupportThis activity is supported by an educational grant from Lilly.Disclosure information is available at the beginning of the video presentation.

In this episode, editor-in-chief Joseph E. Safdieh, MD, FAAN, highlights articles on the association of shortened telomeres on risk for stroke, late-life depression and dementia; affect of research funding cuts on tenure/promotion opportunities; and  herpes zoster vaccine and reduced dementia risk.

Normal pressure hydrocephalus (NPH) is a clinical syndrome characterized by the triad of gait apraxia, cognitive impairment, and bladder dysfunction in the radiographic context of ventriculomegaly and normal intracranial pressure. Accurate diagnosis requires consideration of clinical and imaging signs, complemented by tests to exclude common mimics. In this episode, Lyell Jones, MD, FAAN speaks with Abhay R. Moghekar, MBBS, author of the article “Clinical Features and Diagnosis of Normal Pressure Hydrocephalus” in the Continuum® June 2025 Disorders of CSF Dynamics issue. Dr. Jones is the editor-in-chief of Continuum: Lifelong Learning in Neurology® and is a professor of neurology at Mayo Clinic in Rochester, Minnesota. Dr. Moghekar is an associate professor of neurology at Johns Hopkins University School of Medicine in Baltimore, Maryland. Additional Resources Read the article: Clinical Features and Diagnosis of Normal Pressure Hydrocephalus Subscribe to Continuum®: shop.lww.com/Continuum Earn CME (available only to AAN members): continpub.com/AudioCME Continuum® Aloud (verbatim audio-book style recordings of articles available only to Continuum® subscribers): continpub.com/Aloud More about the American Academy of Neurology: aan.com Social Media facebook.com/continuumcme @ContinuumAAN Host: @LyellJ Full episode transcript available here Dr Jones: This is Dr Lyell Jones, Editor-in-Chief of Continuum. Thank you for listening to Continuum Audio. Be sure to visit the links in the episode notes for information about earning CME, subscribing to the journal, and exclusive access to interviews not featured on the podcast. Dr Jones: This is Dr Lyell Jones, Editor-in-Chief of Continuum: Lifelong Learning in Neurology. Today I'm interviewing Dr Abhay Moghekar, who recently authored an article on the clinical features and diagnosis of normal pressure hydrocephalus for our first-ever issue of Continuum dedicated to disorders of CSF dynamics. Dr Moghekar is an associate professor of neurology and the research director of the Cerebrospinal Fluid Center at Johns Hopkins University in Baltimore, Maryland. Dr Moghekar, welcome, and thank you for joining us today. Why don't you introduce yourself to our listeners? Dr Moghekar: Thank you, Dr Jones. I'm Abhay Moghekar. I'm a neurologist at Hopkins, and I specialize in seeing patients with CSF disorders, of which normal pressure hydrocephalus happens to be the most common. Dr Jones: And let's get right to it. I think most of our listeners who are neurologists in practice have encountered normal pressure hydrocephalus, or NPH; and it's a challenging disorder for all the reasons that you outline in your really outstanding article. If you were going to think of one single most important message to our listeners about recognizing patients with NPH, what would that be? Dr Moghekar: I think I would say there are two important messages. One is that the triad is not sufficient to make the diagnosis, and the triad is not necessary to make the diagnosis. You know these three elements of the triad: cognitive problems, gait problems, bladder control problems are so common in the elderly that if you pick 10 people out in the community that have this triad, it's unlikely that even one of them has true NPH. On the other hand, you don't need all three elements of the triad to make the diagnosis because the order of symptoms matters. Often patients develop gait dysfunction first, then cognitive dysfunction, and then urinary incontinence. If you wait for all three elements of the triad to be present, it may be too late to offer them any clear benefit. And hence, you know, it's neither sufficient nor necessary to make the diagnosis. Dr Jones: That's a really great point. I think most of our listeners are familiar with the fact that, you know, we're taught these classic triads or pentads or whatever, and they're rarely all present. In a way, it's maybe a useful prompt, but it could be distracting or misleading, even in a way, in terms of recognizing the patient. So what clues do you use, Dr Moghekar, to really think that a patient may have NPH? Dr Moghekar: So, there are two important aspects about gait dysfunction. Say somebody comes in with all three elements of the triad. You want to know two things. Which came first? If gate impairment precedes cognitive impairment, it's still very likely that NPH is in the differential. And of the two, which are more- relatively more affected? So, if somebody has very severe dementia and they have a little bit of gait problems, NPH is not as likely. So, is gait affected earlier than cognitive dysfunction, and is it affected to a more severe degree than cognitive dysfunction? And those two things clue me in to the possibility of NPH. You still obviously need to get imaging to make sure that they have large ventricles. One of the problems with imaging is large ventricles are present in so many different patients. Normal aging causes large ventricles. Obviously, many neurodegenerative disorders because of cerebral atrophy will cause large ventricles. And there's an often-used metric called as the events index, which is the ratio of the bitemporal horns- of the frontal horns of the lateral ventricles compared to the maximum diameter of the skull at that level. And if that ratio is more than 0.3, it's often used as a de facto measure of ventriculomegaly. What we've increasingly realized is that this ratio changes with age. And there's an excellent study that used the ADNI database that looked at how this ratio changes by age and sex. So, in fact, we now know that an 85-year-old woman who has an events index of 0.37 which would be considered ventriculomegaly is actually normal for age and sex. So, we need to start adopting these more modern age- and sex-appropriate age cutoffs of ventriculomegaly so as not to overcall everybody with big ventricles as having possible NPH. Dr Jones: That's very helpful. And I do want to come back to this challenge that we've seen in our field of overdiagnosis and underdiagnosis. But I think most of us are familiar with the concept of how hydrocephalus could cause neurologic deficits. But what's the latest on the mechanism of NPH? Why do some patients get this and others don't? Dr Moghekar: Very good question. I don't think we know for sure. And it for a long time we thought it was a plumbing issue. Right? And that's why shunts work. People thought it was impaired CSF absorption, but multiple studies have shown that not to be true. It's likely a combination of impaired cerebral blood flow, biomechanical factors like compliance, and even congenital factors that play a role in the pathogenesis of NPH. And yes, while putting in shunts likely drains CSF, putting in a shunt also definitely changes the compliance of the brain and affects blood flow to the subcortical regions of the brain. So, there are likely multiple mechanisms by which shunts benefit, and hence it's very likely that there's no single explanation for the pathogenesis of NPH. Dr Jones: We explored this in a recent Continuum issue on dementia. Many patients who have cognitive impairment have co-pathologies, multiple different causes. I was interested to read in your article about the genetic risk profile for NPH. It's not something I'd ever really considered in a disorder that is predominantly seen in older patients. Tell us a little more about those genetic risks. Dr Moghekar: Yeah, everyone is aware of the role genetics plays in congenital hydrocephalus, but until recently we were not aware that certain genetic factors may also be relevant to adult-onset normal pressure hydrocephalus. We've suspected this for a long time because nearly half of our patients who come to us to see us in clinic with NPH have head circumferences that are more than 90th percentile for height. And you know, that clearly indicates that this started shortly at the time after birth or soon afterwards. So, we've suspected for a long time that genetic factors play a role, but for a long time there were not enough large studies or well-conducted studies. But recently studies out of Japan and the US have shown mutations in genes like CF43 and CWH43 are disproportionately increased in patients with NPH. So, we are discovering increasingly that there are genetic factors that underlie even adult onset in patients. There are many more waiting to be discovered. Dr Jones: Really fascinating. And obviously getting more insight into the risk and mechanisms would be helpful in identifying these patients potentially earlier. And another thing that I learned in your article that I thought was really interesting, and maybe you can tell us more about it, is the association between normal pressure hydrocephalus and the observation of cervical spinal stenosis, many of whom require decompression. What's behind that association, do you think? Dr Moghekar: That's a very interesting study that was actually done at your institution, at Mayo Clinic, that showed this association. You know, as we all get older, you know, the incidence of cervical stenosis due to osteoarthritis goes up, but the incidence of significant, clinically significant cervical stenosis in the NPH population was much higher than what we would have expected. Whether this is merely an association in a vulnerable population or is it actually causal is not known and will need further study. Dr Jones: It's interesting to speculate, does that stenosis affect the flow of CSF and somehow predispose to a- again, maybe a partial degree for some patients? Dr Moghekar: Yeah, which goes back to the possible hydrodynamic theory of normal pressure hydrocephalus; you know, if it's obstructing normal CSF flow, you know, are the hydrodynamics affected in the brain that in turn could lead to the development of hydrocephalus. Dr Jones: One of the things I really enjoyed about your article, Abhay, was the very strong clinical focus, right? We can't just take an isolated biomarker or radiographic feature and rely on that, right? We really do need to have clinical suspicion, clinical judgment. And I think most of our listeners who've been in practice are familiar with the use and the importance of the large-volume lumbar puncture to determine who may have, and by exclusion not have, NPH, and then who might respond to CSF diversion. And I think those of us who have been in this situation are also familiar with the scenario where you think someone may have NPH and you do a large-volume lumbar puncture and they feel better, but you can't objectively see a difference. How do you make that test useful and objective in your practice? What do you do? Dr Moghekar: Yeah, it's a huge challenge in getting this objective assessment done carefully because you have to remember, you know, subconsciously you're telling the patients, I think you have NPH. I'm going to do this spinal tap, and if you walk better afterwards, you're going to get a shunt and you're going to be cured. And you can imagine the huge placebo response that can elicit in our subjects. So, we always like to see, definitely, did the patient subjectively feel better? Because yes, that's an important metric to consider because we want them to feel better. But we also wanted to be grounded in objective truths. And for that, we need to do different tests of speed, balance and endurance. Not everyone has the resources to do this, but I think it's important to test different domains. Just like for cognition, you know, we just don't test memory, right? We test executive function, language, visuospatial function. Similarly, walking is not just walking, right? It's gait speed, it's balance, and it's endurance. So, you need to ideally test at least most of these different domains for gait and you need to have some kind of clear criteria as to how are you going to define improvement. You know, is a 5% improvement, is a 10% improvement in gait, enough? Is 20%? Where is that cutoff? And as a field, we've not done a great job of coming up with standardized criteria for this. And it varies currently, the practice varies quite significantly from center to center at the current time. Dr Jones: So, one of the nice things you had in your article was helpful tips to be objective if you're in a lower-resource setting. For you, this isn't a common scenario that someone encounters in their practice as opposed to a center that maybe does a large volume of these. What are some relatively straightforward objective measures that a neurologist or someone else might use to determine if someone is improving after a large-volume LP? Dr Moghekar: Yeah, excellent question, Dr Jones, and very practically relevant too. So, you need to at least assess two of the domains that are most affected. One is speed and one is balance. You know, these patients fall ultimately, right, if you don't treat them correctly. In terms of speed, there are two very simple tests that anybody can do within a couple of minutes. One is the timed “up-and-go” test. It's a test that's even recommended by the CDC. It correlates very well with faults and disability and it can be done in any clinic. You just need about ten feet of space and a chair and a stopwatch, and it takes about a minute or slightly more to do that test. And there are objective age-associated norms for the timed up-and-go test, so it's easy to know if your patient is normal or not. The same thing goes for the 10-meter walk test. You do need a slightly longer walkway, but it's a fairly easy and well-standardized test. So, you can do one of those two; you don't need to do both of them. And for balance, you can do the 30-second “sit-to-stand”; and it's literally, again, 30 seconds. You need a chair, and you need somebody to watch the patient and see how many times they can sit up and stand up from a seated position. Then again, good normative data for that. If you want to be a little more sophisticated, you can do the 4-stage balance test. So, I think these are tests that don't add too much time to your daily assessment and can be done with even trained medical assistants in any clinic. And you don't need a trained physical therapist to do these assessments. Dr Jones: Very practical. And again, something that is pretty easily deployed, something we do before and then after the LP. I did see you mentioned in your article the dual timed up-and-go test where it's a simultaneous gait and executive function test. And I've got to be honest with you, Dr Moghekar, I was a little worried if I would pass that test, but that may be beyond the scope of our time today. Actually, how do you do that? How do you do the simultaneous cognitive assessment? Dr Moghekar: So, we asked them to count back from 100, subtracting 3. And we do it particularly in patients who are mildly impaired right? So, if they're already walking really good, but then you give them a cognitive stressor, you know, that will slow them down. So, we reserve it for patients who are high-performing. Dr Jones: That's fantastic. I'm probably aging myself a little here. I have noticed in my career, a little bit of a pendulum swing in terms of the recognition or acceptance of the prevalence of normal pressure hydrocephalus. I recall when I was a resident, many, many people that we saw in clinic had normal pressure hydrocephalus. Then it seemed for a while that it really faded into the background and was much less discussed and much less recognized and diagnosed, and less treated. And now that pendulum seems to have swung back the other way. What's behind that from your perspective? Dr Moghekar: It's an interesting backstory to all of this. When the first article about NPH was published in the Newman Journal of Medicine, it was actually a combined article with both neurologists and neurosurgeons on it. They did describe it as a treatable dementia. And what that did is it opened up the floodgates so that everybody with any kind of dementia started getting shunts left, right, and center. And back then, shunts were not programmable. There were no antibiotic impregnated catheters. So, the incidence of subdural hematomas and shunt-related infections was very high. In fact, one of our esteemed neurologists back then, Houston Merritt, wrote a scathing editorial that Victor and Adam should lose their professorships for writing such an article because the outcomes of these patients were so bad. So, for a very long period of time, neurologists stopped seeing these patients and stopped believing in NPH as a separate entity. And it became the domain of neurosurgeons for over two or three decades, until more recently when randomized trials started being done early on out of Europe. And now there's a big NIH study going on in the US, and these studies showed, in fact, that NPH exists as a true, distinct entity. And finally, neurologists have started getting more interested in the science and understanding the pathophysiology and taking care of these patients compared to the past. Dr Jones: That's really helpful context. And I guess that maybe isn't rare when you have a disorder that doesn't have a simple, straightforward biomarker and is complex in terms of the tests you need to do to support the diagnosis, and the treatment itself is somewhat invasive. So, when you talk to your patients, Dr Moghekar, and you've established the diagnosis and have recommended them for CSF diversion, what do you tell them? And the reason I ask is that you mentioned before we started recording, you had a patient who had a shunt placed and responded well, but continued to respond over time. Tell us a little bit more about what our patients can expect if they do have CSF diversion? Dr Moghekar: When we do the spinal tap and they meet our criteria for improvement and they go on to have a shunt, we tell them that we expect gait improvement definitely, but cognitive improvement may not happen in everyone depending on what time, you know, they showed up for their assessment and intervention. But we definitely expect gait improvement. And we tell them that the minimum gait improvement we can expect is the same degree of improvement they had after their large-volume lumbar puncture, but it can be even more. And as the brain remodels, as the hydrodynamics adapt to these shunts… so, we have patients who continue to improve one year, two years, and even three years into the course of the intervention. So, we're, you know, hopeful. At the same time, we want to be realistic. This is the same population that's at risk for developing neurodegenerative disorders related to aging. So not a small fraction of our patients will also have Alzheimer's disease, for example, or go on to develop Lewy body dementia. And it's the role of the neurologist to pick up on these comorbid conditions. And that's why it's important for us to keep following these patients and not leave them just to the neurosurgeon to follow up. Dr Jones: And what a great note to end on, Dr Moghekar. And again, I want to thank you for joining us, and thank you for such a wonderful discussion and such a fantastic article on the clinical diagnosis of normal pressure hydrocephalus. I learned a lot reading the article, and I learned a lot more today just in the conversation with you. So, thank you for being with us. Dr Moghekar: Happy to do that, Dr Jones. It was a pleasure. Dr Jones: Again, we've been speaking with Dr Abhay Moghekar, author of a wonderful article on the clinical features and diagnosis of NPH in Continuum's first-ever issue dedicated to disorders of CSF dynamics. Please check it out. And thank you to our listeners for joining today. Dr Monteith: This is Dr Teshamae Monteith, Associate Editor of Continuum Audio. If you've enjoyed this episode, you'll love the journal, which is full of in-depth and clinically relevant information important for neurology practitioners. Use the link in the episode notes to learn more and subscribe. AAN members, you can get CME for listening to this interview by completing the evaluation at continpub.com/audioCME. Thank you for listening to Continuum Audio.

Hello friends and welcome to The Five By! Your quatriweekly source of rapid-fire board game reviews. 00:00 Sarah - Introduction 00:39 John - Newton (https://boardgamegeek.com/boardgame/244711/newton) Episode 70 (https://thefiveby.fireside.fm/70) Darwin's Journey (https://thefiveby.fireside.fm/160) 06:15 Aaron - Judge Dredd (https://boardgamegeek.com/boardgame/1098/judge-dredd) 11:49 Justin - Fateforge: Chronicles of Kaan (https://boardgamegeek.com/boardgame/363625/fateforge-chronicles-of-kaan) 16:56 Sarah - Dr. Finn's Book of Solo Strategy and Word Games (https://boardgamegeek.com/boardgame/445055/dr-finns-book-of-solo-strategy-and-word-games) 22:02 Jose - Shuffle and Swing (https://boardgamegeek.com/boardgame/414350/shuffle-and-swing) 27:46 Meeple Lady - Outro

Mike Wills speaks to Faan van der Walt, CEO of WeBuyCars, to unpack why Chinese cars are winning over South African drivers. With more than 40 Chinese models now available locally, and prices starting under R280,000, affordability is just part of the story. Backed by premium features, smart technology, and aggressive warranty plans, these vehicles are shaking up both new and used car markets. Presenter John Maytham is an actor and author-turned-talk radio veteran and seasoned journalist. His show serves a round-up of local and international news coupled with the latest in business, sport, traffic and weather. The host’s eclectic interests mean the program often surprises the audience with intriguing book reviews and inspiring interviews profiling artists. A daily highlight is Rapid Fire, just after 5:30pm. CapeTalk fans call in, to stump the presenter with their general knowledge questions. Another firm favourite is the humorous Thursday crossing with award-winning journalist Rebecca Davis, called “Plan B”. Thank you for listening to a podcast from Afternoon Drive with John Maytham Listen live on Primedia+ weekdays from 15:00 and 18:00 (SA Time) to Afternoon Drive with John Maytham broadcast on CapeTalk https://buff.ly/NnFM3Nk For more from the show go to https://buff.ly/BSFy4Cn or find all the catch-up podcasts here https://buff.ly/n8nWt4x Subscribe to the CapeTalk Daily and Weekly Newsletters https://buff.ly/sbvVZD5Follow us on social media:CapeTalk on Facebook: https://www.facebook.com/CapeTalkCapeTalk on TikTok: https://www.tiktok.com/@capetalkCapeTalk on Instagram: https://www.instagram.com/CapeTalk on X: https://x.com/CapeTalkCapeTalk on YouTube: https://www.youtube.com/@CapeTalk567See omnystudio.com/listener for privacy information.

This week on Not Your Granny's Quilt Show, my guest is Carl Brown, PhD, RN, FAAN—also known as QuiltCarl. After a 20-year career in the Army and a lifetime in nursing, Carl is now channeling his energy full-time into fiber art. With a lifelong love of creative hobbies, Carl blends techniques from a range of artists and quilters to develop his own vibrant, expressive style. His mission? To share the joy of quilting and invite others to join the fun. Are you in? Find him at quiltcarl.com or on Instagram @quiltcarl.Want to see more? You can find it here: NYQGS Merch Shop: nygqs.printify.me Patreon: patreon.com/notyourgrannysquiltshow Instagram: https://www.instagram.com/notyourgrannysquiltshow https://www.instagram.com/sweetpeadesigncompany YouTube: https://youtube.com/@notyourgrannysquiltshow Want to be on the show? Send us a message!

In this episode of The Nurse Practitioner Podcast, Margaret Fitzgerald, DNP, FNP-BC, NP-C, FAANP, CSP, FAAN, DCC, FNAP discusses measles, including the recent outbreaks, vaccination, complications, and more.

In this episode of The AJN Podcast, Kerry A. Milner, DNSc, APRN, FNP-BC, EBP-C, Roy Brown, MLIS, AHIP-D, and Ellen Fineout-Overholt, PhD, RN, EBP-C, FNAP, FAAN, discuss their article “Librarian Partnerships in DNP Education,” which appears in AJN’s June 2025 issue. Subscribers to AJN can access the full series and accompanying tools in the repository found here: Evidence-Based Decision-Making Series: Helpful Tools.

What does it mean to age with dignity in today’s healthcare system? What will it take to truly transform how we care for older adults in America? In this episode, the first of a six-part series, we explored the documentary Aging in America: Survive or Thrive, created by the John A. Hartford Foundation. We spoke with Terry Fulmer, PhD, RN, FAAN, president of The John A. Hartford Foundation, to explore the legacy of Dr. Robert Butler and how hospitals are utilizing the “4 Ms” framework (What Matters, Medication, Mentation, Mobility) to enhance care for older adults. We dive into the stark disparities based on income, race, and geography, and highlight programs working to close those gaps. From dementia care models to creative workforce solutions and caregiver support, this conversation offers a hopeful, practical look at reimagining aging in America. Visit johnahartford.org/agefriendly for information about the 4Ms of age-friendly care. Helpful articles and videos can also be found here. Additional resources: Harvard Business Review article on how employers can support family caregivers of older adults The RUSH University Medical Center Caring for Caregivers program My Health Checklist The Reframing Aging Initiative The UCLA Alzheimer's and Dementia Care programSee omnystudio.com/listener for privacy information.

In this episode, editor-in-chief Joseph E. Safdieh, MD, FAAN, highlights articles studies showing persistent fatigue after TIA, the neurologic complications of measles, and the impact of the dismantling of a CDC surveillance program of epilepsy.

Idiopathic intracranial hypertension (IIH) is characterized by symptoms and signs of unexplained elevated intracranial pressure (ICP) in an alert and awake patient. The condition has potentially devastating effects on vision, headache burden, increased cardiovascular disease risk, sleep disturbance, and depression.  In this episode, Teshamae Monteith, MD, FAAN speaks with Aileen A. Antonio, MD, FAAN, author of the article “Clinical Features and Diagnosis of Idiopathic Intracranial Hypertension” in the Continuum® June 2025 Disorders of CSF Dynamics issue. Dr. Monteith is the associate editor of Continuum® Audio and an associate professor of clinical neurology at the University of Miami Miller School of Medicine in Miami, Florida. Dr. Antonio is an associate program director of the Hauenstein Neurosciences Residency Program at Trinity Health Grand Rapids and an assistant clinical professor at the Michigan State University College of Osteopathic Medicine in Lansang, Michigan. Additional Resources Read the article: Clinical Features and Diagnosis of Idiopathic Intracranial Hypertension Subscribe to Continuum®: shop.lww.com/Continuum Earn CME (available only to AAN members): continpub.com/AudioCME Continuum® Aloud (verbatim audio-book style recordings of articles available only to Continuum® subscribers): continpub.com/Aloud More about the American Academy of Neurology: aan.com Social Media facebook.com/continuumcme @ContinuumAAN Host: @headacheMD Guest: @aiee_antonio Full episode transcript available here Dr Jones: This is Dr Lyell Jones, Editor-in-Chief of Continuum. Thank you for listening to Continuum Audio. Be sure to visit the links in the episode notes for information about earning CME, subscribing to the journal, and exclusive access to interviews not featured on the podcast. Dr Monteith: Hi, this is Dr Teshamae Monteith. Today I'm interviewing Dr Aileen Antonio about her article on clinical features and diagnosis of idiopathic intracranial hypertension, which appears in the June 2025 Continuum issue on disorders of CSF dynamics.  Hi, how are you? Dr Antonio: Hi, good afternoon. Dr Monteith: Thank you for being on the podcast. Dr Antonio: Thank you for inviting me, and it's such an honor to write for the Continuum. Dr Monteith: So why don't you start off with introducing yourself? Dr Antonio: So as mentioned, I'm Aileen Antonio. I am a neuro-ophthalmologist, dually trained in both ophthalmology and neurology. I'm practicing in Grand Rapids, Michigan Trinity Health, and I'm also the associate program director for our neurology residency program. Dr Monteith: So, it sounds like the residents get a lot of neuro-ophthalmology by chance in your curriculum. Dr Antonio: For sure. They do get fed that a lot. Dr Monteith: So why don't you tell me what the objective of your article was? Dr Antonio: Yes. So idiopathic intracranial hypertension, or IIH, is a condition where there's increased intracranial pressure, but without an obvious cause. And with this article, we want our readers---and our listeners right now---to recognize that the typical symptoms and learning about the IIH diagnostic criteria are key to avoiding errors, overdiagnosis, or sometimes even misdiagnosis or underdiagnosis. Thus, we help make the most of our healthcare resources. Early diagnosis and management are crucial to prevent disability from intractable headaches or even vision loss, and it's also important to know when to refer the patients to the appropriate specialists early on. Dr Monteith: So, it sounds like your central points are really getting that diagnosis early and managing the patients and knowing how to triage patients to reduce morbidity and complications. Is that correct? Dr Antonio: That is correct and very succinct, yes. Dr Monteith: And so, are there any more recent advances in the diagnosis of IIH? Dr Antonio: Yes. And one of the tools that we've been using is what we call the optical coherence tomography. A lot of people, neurologists, physicians, PCP, ER doctors; how many among those physicians are well-versed in doing an eye exam, looking at the optic disc? And this is a great tool because it is noninvasive, it is high resolution imaging technique that allows us to look at the optic nerve without even dilating the eye. And we can measure that retinal nerve fiber layer, or RNFL; and that helps us quantify the swelling that is visible or inherent in that optic nerve. And we can even follow that and monitor that over time. So, this gives us another way of looking at their vision and getting that insight as to how healthy is their vision still, along with the other formal visual tests that we do, including perimetry or visual field testing. And then all of these help in catching potentially early changes, early worsening, that may happen; and then we can intervene more easily. Dr Monteith: Great. So, it sounds like there's a lot of benefits to this newer technology for our patients. Dr Antonio: That is correct. Dr Monteith: So, I read in the article about the increased incidence of IIH, and I have to say that I completely agree with you because I'm seeing so much of it in my clinic, even as a headache specialist. And I had a talk with a colleague who said that the incidence of SIH and IIH are similar. And I was like, there's no way. Because I see, I can see several people with IIH just in one day. That's not uncommon. So, tell me what your thoughts are on the incidence, the rising incidence of IIH; and we understand that it's the condition associated with obesity, but it sounds like you have some other underlying drivers of this problem. Dr Antonio: Yes, that is correct. So, as you mentioned, IIH tends to affect women of childbearing age with obesity. And it's interesting because as you've seen that trend, we see more of these IIH cases recently, which seem to correlate with that rising rate of obesity. And the other thing, too, is that this trend can readily add to the burden of managing IIH, because not only are we dealing with the headaches or the potential loss of vision, but also it adds to the burden of healthcare costs because of the other potential comorbidities that may come with it, like cardiovascular risk factors, PCOS, and sleep apnea. Dr Monteith: So why don't we just talk about the diagnosis of IIH? Dr Antonio: IIH, idiopathic intracranial hypertension, is also called pseudotumor cerebri.  It's essentially a condition where a person experiences increased intracranial pressure, but without any obvious cause. And the tricky part is that the patients, they're usually fully awake and alert. So, there's no obvious tumor, brain tumor or injury that causes the increased ICP. It's really, really important to rule out other conditions that might cause these similar symptoms; again, like brain tumors or even the cerebral venous sinus thrombosis. Many patients will have headaches or visual disturbances like transient visual obscurations---we call them TVOs---or double vision or diplopia. The diplopia is usually related to a sixth nerve palsy or an abducens palsy. Some may also experience some back pain or what we call pulsatile tinnitus, which is that pulse synchronous ringing in their ears. The biggest sign that we see in the clinic would be that papilledema; and papilledema is a term that we only use, specifically use, for those optic nerve edema changes that is only associated with increased intracranial pressure. So, performing of endoscopy and good eye exam is crucial in these patients. We usually use the modified Dandy criteria to diagnose IIH. And again, I cannot emphasize too much that it's really important to rule out other secondary causes to that increased intracranial pressure. So, after that thorough neurologic and eye evaluation with neuroimaging, we do a lumbar puncture to measure the opening pressure and to analyze the cerebrospinal fluid. Dr Monteith: One thing I learned from your article, really just kind of seeing all of the symptoms that you mentioned, the radicular pain, but also- and I think I've seen some papers on this, the cognitive dysfunction associated with IIH. So, it's a broader symptom complex I think than people realize. Dr Antonio: That is correct. Dr Monteith: So, you mentioned TVOs. Tell me, you know, if I was a patient, how would you try and elicit that from me? Dr Antonio: So, I would usually just ask the patient, while you're sitting down just watching TV---some of my patients are even driving as this happens---they would suddenly have these episodes of blacking out of vision, graying out of vision, vision loss, or blurred vision that would just happen, from seconds to less than a minute, usually. And they can happen in one eye or the other eye or both eyes, and even multiple times a day. I had a patient, it was happening 50 times a day for her. It's important to note that there is no pain associated with it most of the time. The other thing too is that it's different from the aura that patients with migraines would have, because those auras are usually scintillating and would have what we call the positive phenomena: the flashing lights, the iridescence, and even the fortification that they see in their vision. So definitely TVOs are not the migraine auras. Sometimes the TVOs can also be triggered by sudden changes in head positions or even a change in posture, like standing up quickly. The difference, though, between that and, like, the graying out of vision or the tunneling vision associated with orthostatic hypotension, is that the orthostatic hypotension would also have that feeling of lightheadedness and dizziness that would come with it. Dr Monteith: Great. So, if someone feels lightheaded, less likely to be a TVO if they're bending down and they have that grain of vision. Dr Antonio: That is correct. Dr Monteith: Definitely see patients like that in clinic. And if they have fluoride IIH, I'm like, I'll call it a TVO; if they don't, I'm like, it's probably more likely to be dizziness-related. And then we also have patient migraines that have blurriness that's nonspecific, not necessarily associated with aura. But I think in those patients, it's usually not seconds long, it's usually probably longer episodes of blurriness. Would you agree there, or…? Dr Antonio: I would agree there, and usually the visual aura would precede the headache that is very characteristic of their migraine, very stereotypical for their migraines. And then it would dissipate slowly over time as well. With TVOs, they're brisk and would not last, usually, more than a minute. Dr Monteith: So, why don't we talk about routine imaging? Obviously, ordering an MRI, and I read also getting an MRV is important. Dr Antonio: It is very important because, one: I would say IIH is also a diagnosis of exclusion. We need to make sure that the increased ICP is not because of a brain tumor or not because of cerebral venous sinus thrombosis. So, it's important to get the MRI of the brain as well as the MRV of the head. Dr Monteith: Do you do that for all patients' MRV, and how often do you add on an orbital study? Dr Antonio: I usually do not add on an orbital study because it's not really going to change my management at that point. I really get that MRI of the brain. Now the MRV, for most of my patients, I would order it already just because the population that I see, I don't want to lose them. And sometimes it's that follow-up, and that is the difficult part; and it's an easy add on to the study that I'm going to order. Again, it depends with the patient population that you have as well, and of course the other symptoms that may come with it. Dr Monteith: So, why don't we talk a little bit about CSF reading and how these set values, because we get people that have readings of 250 millimeters of water quite frequently and very nonspecific, questionable IIH. And so, talk to me about the set value. Dr Antonio: Right. So, the modified Dandy criteria has shown that, again, we consider intracranial pressure to be elevated for adults if it's above 250 millimeters water; and then for kids if it's above 280 millimeters of water. Knowing that these are taken in the left lateral decubitus position, and assuming also that the patients were awake and not sedated during the measurement of the CSF pressure. The important thing to know about that is, sometimes when we get LPs under fluoroscopy or under sedation, then these can cause false elevation because of the hypercapnia that elevated carbon dioxide, and then the hypoventilation that happens when a patient is under sedation. Dr Monteith: You know, sometimes you see people with opening pressures a little bit higher than 25 and they're asymptomatic. Well, the problem with these opening pressure values is that they can vary somewhat even across the day. People around 25, you can be normal, have no symptoms, and have opening pressure around 25- or 250; and so, I'm just asking about your approach to the CSF values. Dr Antonio: So again, at the end of the day, what's important is putting everything together. It's the gestalt of how we look at the patient. I actually had an attending tell me that there is no patient that read the medical textbook. So, the, the important thing, again, is putting everything together. And what I've also seen is that some patients would tell me, oh, I had an opening pressure of 50. Does that mean I'm in a dire situation? And they're so worried and they just attach to numbers. And for me, what's important would be, what are your symptoms? Is your headache, right, really bad, intractable? Number two: are you losing vision, or are you at that cusp where your optic nerve swelling or papilledema is so severe that it may soon lead to vision loss? So, putting all of these together and then getting the neuroimaging, getting the LP. I tell my residents it's like icing on the cake. We know already what we're dealing with, but then when we get that confirmation of that number… and sometimes it's borderline, but this is the art of neurology. This is the art of medicine and putting everything together and making sure that we care and manage it accordingly. Dr Monteith: Let's talk a little bit about IIH without papilledema. Dr Antonio: So, let's backtrack. So, when a patient will fit most of the modified Dandy criteria for IIH, but they don't have the papilledema or they don't have abducens palsy, the diagnosis then becomes tricky. And in these kinds of cases, Dr Friedman and her colleagues, when they did research on this, suggested that we might consider the diagnosis of IIH. And she calls this idiopathic intracranial hypertension without papilledema, IIHWOP. They say that if they meet the other criteria for modified Dandy but show at least three typical findings on MRI---so that flattening of the posterior globe, the tortuosity of the optic nerves, the empty sella or the partially empty sella, and even the narrowing of the transverse venous sinuses---so if you have three of these, then potentially you can call these cases as idiopathic intracranial hypertension without papilledema. Dr Monteith: Plus, the opening pressure elevation. I think that's key, right? Getting that as well. Dr Antonio: Yes. Sometimes IIHWOP may still be a gray area. It's a debate even among neuro-ophthalmologists, and I bet even among the headache specialists. Dr Monteith: Well, I know that I've had some of these conversations, and it's clear that people think this is very much overdiagnosed. So, that's why I wanted to plug in the LP with that as well. Dr Antonio: Right. And again, we have not seen yet whether is, this a spectrum, right? Of that same disease just manifesting differently, or are they just sharing a same pathway and then diverging? But what I want to emphasize also is that the treatment trials that we've had for IIH do not include IIHWOP patients. Dr Monteith: That is an important one. So why don't you wrap this up and tell our listeners what you want them to know? Now's the time. Dr Antonio: So, the- again, with IIH, with idiopathic intracranial hypertension, what is important is that we diagnose these patients early. And I think that some of the issues that come into play in dealing with these patients with IIH is that, one: we may have anchoring bias. Just because we see a female with obesity, of reproductive age, with intractable headaches, it does not always mean that what we're dealing with is IIH. The other thing, too, is that your tools are already available to you in your clinic in diagnosing IIH, short of the opening pressure when you get the lumbar puncture. And I need to emphasize the importance of doing your own fundoscopy and looking for that papilledema in these patients who present to you with intractable headaches or abducens palsy. What I want people to remember is that idiopathic intracranial hypertension is not optic nerve sheath distension. So, these are the stuff that you see on neuroimaging incidentally, not because you sent them, because they have papilledema, or because they have new headaches and other symptoms like that. And the important thing is doing your exam and looking at your patients. Dr Monteith: Today, I've been interviewing Dr Aileen Antonio about her article on clinical features and diagnosis of idiopathic intracranial hypertension, which 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. Thank you again. Dr Antonio: Thank you. Dr Monteith: This is Dr Teshamae Monteith, Associate Editor of Continuum Audio. If you've enjoyed this episode, you'll love the journal, which is full of in-depth and clinically relevant information important for neurology practitioners. Use the link in the episode notes to learn more and subscribe. AAN members, you can get CME for listening to this interview by completing the evaluation at continpub.com/audioCME. Thank you for listening to Continuum Audio.

On this episode of The Huddle, Wendy Mobley-Bukstein, PharmD, BCACP, CDCES, CHWC, NASM-CPT, FAPhA, FADCES and Debbie Hinnen, APN, BC-ADM, CDCES, FAAN discuss the importance of medication persistence, how to talk to clients about starting and staying on diabetes medications, and strategies to help clients stay consistent with their medication taking. This episode was made possible with support from Lilly, A Medicine Company.Learn more about the latest in diabetes technology on danatech: danatech l Diabetes Technology Education for Healthcare ProfessionalsLearn more about the ADCES7 Self-Care Behaviors: Self-Care Tips (ADCES7)References:Kennedy-Martin, T., Boye, K. S., & Peng, X. (2017). Cost of medication adherence and persistence in type 2 diabetes mellitus: a literature review. Patient Preference and Adherence, 11, 1103–1117. https://doi.org/10.2147/PPA.S136639McGovern, A., Hinton, W., Calderara, S. et al. A Class Comparison of Medication Persistence in People with Type 2 Diabetes: A Retrospective Observational Study. Diabetes Ther 9, 229–242 (2018). https://doi.org/10.1007/s13300-017-0361-5Evans M, Engberg S, Faurby M, Fernandes JDDR, Hudson P, Polonsky W. Adherence to and persistence with antidiabetic medications and associations with clinical and economic outcomes in people with type 2 diabetes mellitus: A systematic literature review. Diabetes Obes Metab. 2022; 24(3): 377-390. doi:10.1111/dom.14603Sabaté E., Adherence to Long-Term Therapies: Evidence for Action, 2003, World Health Organization, Geneva, Switzerland.https://www.ama-assn.org/delivering-care/physician-patient-relationship/8-reasons-patients-dont-take-their-medicationshttps://www.npr.org/sections/health-shots/2017/09/08/549414152/why-do-people-stop-taking-their-meds-cost-is-just-one-reasonhttps://www.adces.org/docs/default-source/handouts/adces7/handout_pwd_adces7_takingmedication.pdf?sfvrsn=4e3f6359_13 Listen to more episodes of The Huddle at adces.org/perspectives/the-huddle-podcast.Learn more about ADCES and the many benefits of membership at adces.org/join.

Lauren Clark (She/Her), PhD, RN, FAAN, is a Professor of Nursing at UCLA, a teacher in the Disability Studies Department, and an Unapologetically Black Unicorn. In this episode, Lauren shares insights from her work and reflects on the groundbreaking legacy of Judy Heumann, a trailblazer in disability advocacy. She discusses how they aim to continue Judy's work through their community partnership project at the Judy Heumann Lab, focusing on the intersectionality of disability, mental health, and immigration/citizenship, and its impact on the campus community. They also explore the concept of “chasms of care,” the importance of language, and the power of community in this work.   Our Judy Heumann Lab: https://dslabs.ucla.edu/chasms-in-the-continuum-of-care-for-people-with-psychiatric-disabilities/ https://dslabs.ucla.edu/labs/heumann-community-partnerships-lab/2023-2/   The overall Judy Heumann Lab initiative: https://dslabs.ucla.edu/labs/heumann-community-partnerships-lab/   UCLA Disability Studies https://www.uei.ucla.edu/academic-programs/disability-studies/   UCLA Disability Studies Inclusion Labs https://dslabs.ucla.edu/disability-studies/   UCLA Disability Studies creates first disability studies major at a California public university https://www.universityofcalifornia.edu/news/ucla-creates-first-disability-studies-major-california-public-university   The National Suicide Prevention Lifeline is now: 988 Suicide and Crisis Lifeline Contact the show: UBU@UnapologeticallyBlackUnicorns.info

Dr. Airica Steed, Ed.D, MBA, RN, CSSMBB, FACHE, FAAN, Chief Executive Officer and Managing Partner at Breakthrough Innovation Partners LLC, joins the podcast to share her perspective on the responsible use of AI in healthcare and the urgent need to address equity gaps. She emphasizes the importance of ensuring health equity is not treated as an afterthought and advocates for a shift toward more proactive, rather than reactive, approaches in healthcare delivery.

“An educated and confident family caregiver who knows what to do in their role is really the absolute best medicine for the care receiver.” Dr. Carolyn Clevenger Do you know extensive research specifically focused on dementia caregivers is being conducted? Are you aware of innovative studies designed to equip family caregivers with navigation skills? Now you will, and you'll be learning about valuable opportunities to strengthen your caregiving journey. We are Sue Ryan and Nancy Treaster. As caregivers for our loved ones with Alzheimer's and other types of dementia, we are continuously learning new ways to support our health and well-being, and that of our care receivers. We recently discovered the groundbreaking dementia caregiver research, the CANDO Study, Dr. Carolyn Clevenger, DNP, RN, GNP-BC, AGPCNP-BC, FAANP, FGSA, FAAN, Professor at the Emory University Nell Hodgson Woodruff School of Nursing is conducting. When most people think about dementia research, they focus on studies involving people living with dementia or pharmaceutical treatments. This crucial area of research focuses on supporting the family caregivers themselves. Dr. Clevenger is a professor and gerontological nurse practitioner who is nationally recognized as an education leader in advanced practice nursing and geriatrics. Carolyn founded, and directs, the comprehensive dementia care model called Integrated Memory Care (IMC), which provides memory and primary care in a single integrated approach for people living with dementia and their care partners. Full Show Notes https://thecaregiversjourney.org/36-learn-to-navigate-support-systems-four-essential-tips-alzheimers-and-other-dementias/ Additional Resources Mentioned Dr. Carolyn Clevenger, a nationally recognized educational leader in advanced practice nursing, geriatrics and gerontology, shares her groundbreaking work on dementia family caregiver education programs that teach new caregivers how to transition into the role and navigate various support systems.For more information about joining this study, visit scholarblogs.emory.edu/CAN-DO/.Savvy Caregiver course: Available face-to-face or online (in-person version includes support group benefits)“Best Programs for Caregivers” website: A collaboration between the Benjamin Rose Institute on Aging and Family Care Alliance featuring only research-proven programs.Support the nonprofit The Caregiver's Journey: https://give.cornerstone.cc/thecaregiversjourney Additional Resources Mentioned Takeaways Tip 1: Understand Different Levels of Care Early Home-Based CareCommunity-Based ProgramsResidential Care Options Key considerations: Each level has different eligibility requirements and payment structuresAvailability varies by state—some follow federal guidelines, others have state regulationsPeople often wait until they desperately need memory care but try to access assisted living instead, creating unnecessary stress Tip 2: Stay Ahead of Financial Challenges Protect your assets while maintaining oversightUnderstand the early warning signsWatch for judgment impairment issues Tip 3: Leverage Legal Support from Elder Law Experts What sets elder law attorneys apartSpecialized dementia expertiseLong-term benefits Tip 4: Take Evidence-Based Classes What makes evidence-based courses effectiveMeasurable outcomes The CAN-DO Study: Training Caregivers as Navigators Dr. Clevenger's current research project, CAN-DO (Caregiver As Navigator Developing Skills Online), trains family caregivers to navigate four critical systems: healthcare, financial, legal, and family systems. Course structure: Six-week online course following three families through different types of dementiaEach day presents real-life scenarios with appropriate responses and preventive measuresVideos from subject matter experts including elder law attorneys, investigators, estate planners, and healthcare providers

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.

"I wanted to be a dolphin trainer... But here I am." - Kelly Guzman  What happens when emergency nurses become healthcare design consultants? In this fascinating episode of Healthcare Interior Design 2.0, host Cheryl Janis sits down with two remarkable guests who made the leap from bedside care to transforming how healthcare spaces are designed. Meet Kelly Guzman, who traded her childhood dreams of training dolphins for a nursing career that began during the 1987 nursing shortage. After years managing emergency departments and clinical services at UCLA Health, Kelly discovered her true calling when tasked with moving entire hospitals into new buildings. Now CEO of Yellow Brick Consulting, she orchestrates complex healthcare facility transitions with military precision - including dress rehearsals with up to 900 staff members testing new spaces before they open. Meet Kevin Meek, whose journey started at age 13 as a hospital candy striper, inspired by the TV show Emergency 51. His design awakening came in 2014 when he walked through a micro hospital under construction and immediately knew it would be an operational nightmare. One complaint to his boss led to a game-changing meeting with architects in Texas, launching his transition from trauma nurse to design consultant. Both Kelly and Kevin have served on the board of the Nursing Institute for Healthcare Design (NIHD), our podcast industry partners. They found their tribe in this organization that connects clinical "unicorns" who felt alone in the design space. The NIHD's mission is to engage and integrate clinical expertise into healthcare facility planning through leadership, education, and advocacy - ensuring that the voices of those who actually work in these spaces are heard in the design process. Together, they've pioneered the concept of "clinically informed design" - and the stories they share will make you question everything you thought you knew about healthcare facility planning. From door handles placed in impossible locations to the eternal struggle of finding space for critical patient information at the bedside, this episode reveals the often hilarious (and sometimes heartbreaking) disconnect between beautiful design and functional reality. In this eye-opening conversation, you'll discover: How two emergency nurses found their calling as healthcare design "unicorns" and why the industry desperately needs more clinical voices The game-changing difference between evidence-based design and clinically informed design (hint: one involves research, the other involves asking the right questions) Why a door paddle eight feet from the door could be a matter of life and death - and other design details that seem obvious once you know them The fascinating world of hospital transition planning, where entire facilities rehearse their opening like a Broadway production How the Nursing Institute for Healthcare Design is connecting clinical expertise with architectural brilliance Real-world horror stories of beautiful spaces that staff absolutely hate to work in Practical strategies for nurses thrust into design meetings and architects wanting to truly engage clinical teams Why post-occupancy evaluations could prevent future design disasters (and why they rarely happen) Discover why nurses are the ultimate design unicorns, learn about the organization connecting clinical voices to design teams nationwide, and find out what happens when a nurse tells a prospective client that they "hate" their gorgeous new facility - with the architect standing right there. Learn more about Kevin Meek: https://www.haskell.com/ Learn more about Kelly Guzman: https://consultyellowbrick.com/ Learn more about The Nursing Institute for Healthcare Design: https://nursingihd.com/. Industry Partners The world is changing quickly. The Center for Health Design is committed to providing the healthcare design and senior living design industries with the latest research, best practices and innovations. The Center can help you solve today's biggest healthcare challenges and make a difference in care, safety, medical outcomes, and the bottom line.  Find out more at healthdesign.org. Additional support for this podcast comes from our industry partners: The American Academy of Healthcare Interior Designers The Nursing Institute for Healthcare Design Learn more about how to become a Certified Healthcare Interior Designer®  by visiting the American Academy of Healthcare Interior Designers at: https://aahid.org/. Connect to a community interested in supporting clinician involvement in design and construction of the built environment by visiting The Nursing Institute for Healthcare Design at https://www.nursingihd.com/ FEATURED PRODUCT The prevention of nosocomial infections is of paramount importance. Did you know that bathrooms and showers – particularly in shared spaces – are a veritable breeding ground for pathogen, some of which we see in the form of mold and the build-up of toxic bio films on surfaces. Body fats and soap scums provide a rich food sauce for micro-organisms such as airborne bacteria Serratia Marcescens, which thrive in humid conditions. We know that people with weakened immune systems are so much more vulnerable to the illnesses associated with infection and let's face it, none of us go into the shower with an expectation that we might get sick. So how do we keep those shower walls clean? Well let's think big – BIG TILES. 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The designer in you will love the incredible options and your specification will deliver the longest & best lifecycle value bar none.

Alexander Pantelyat, MD, FAAN is an associate professor of Neurology at the Johns Hopkins University School of Medicine. He is the founder and director of the Johns Hopkins Atypical Parkinsonism Center, and the co-Founder and Director of the Johns Hopkins Center for Music and Medicine. Dr. Pantelyat's research is focused on the diagnosis and treatment of atypical parkinsonian disorders, such as dementia with Lewy bodies, progressive supranuclear palsy, corticobasal syndrome/degeneration and multiple system atrophy; cognitive aspects of movement disorders; and music-based rehabilitation of neurodegenerative diseaseshttps://www.seniorcareauthorit...

Send us a textMarianne and Jeanna Ford discuss the Hulu Series "Dying for Sex," a true story about a 42 year old woman with recurrent breast cancer. https://bit.ly/3FQcND3Several patients told Dr. Ford she had to watch this. One patient told Jeanna she felt “seen and heard” as this was the first thing to represent what she was going through as a metastatic cancer patient.Why did they find it so powerful? Listen to our interview with Jeanna as she and Marianne discuss the many facets of the terminal metastatic cancer journey that the show explores. In this Episode:03:06 - Road Trip: Maine, Moxy Soda, and Burnt Trailer05:54 - Recipe of the Week: Whoopie Pie06:53 - Discussion of the Hulu Series "Dying for Sex" With Dr. Jeanna Ford45:14 - OutroWhat is “Dying for Sex” About?The series is fairly closely follows the true story of Molly Kochan and her best friend Nikki Boyer. When Molly was diagnosed as terminal with Stage IV Metastatic Breast Cancer at age 42, she realizes for the first time that “life is short” is more than some stupid cliché. With this new ticking-clock hanging over her head Molly make a decision . . . to start living HER LIFE. She leaves her husband and goes on a quest, searching for life's answers via a sexual journey of exploration. She juggles dozens of online suitors and brings kinks and fetishes into the real world, all while dealing with the ups and downs of her cancer treatment.***Spoiler Alert - We Do Discuss The Whole Show***What Does the Show Teach Us?Jeanna and Marianne talk about a lot of points that the episodes cover, from the need for intimacy, end of life wishes, the impact of abuse, communication needs with healthcare team members, and perspectives of not just the person with cancer, but family members, friends, and caregivers.Cancer healthcare teams, mothers, caregivers and terminal cancer patients may all find something they can learn from this series.#cancer #dying #metastaticcancer #terminaldisease #terminalcancer #lastwishes #bucketlist #sex #sexuality #palliativecare #deathdoula #cancercaregiver #everyonedies #everydayisagift Halfway To Dead, A Midlife Spiritual JourneyMidlife is freaking hard. Let's flip the script. Listen on: Apple Podcasts SpotifySupport the showGet show notes and resources at our website: every1dies.org. Facebook | Instagram | YouTube | mail@every1dies.org

In 2017, a fatal medication error shocked the medical world, and its aftermath has left the nursing community forever changed. In this gripping episode, Jeremy and Sharon sit down with RaDonda Vaught, the nurse who was found guilty of two felony charges in 2022. She shares the story of how a routine shift, a medication override, and a system-wide communication failure led to a tragedy — and eventually, criminal prosecution. This is more than a case study in medical error. It's a conversation about system design, transparency, accountability, and what it means to truly support healthcare professionals in moments of crisis. Here's some of what you'll hear in this episode: ⚖️ Criminal charges after a medical error — what happened and why

In this episode, editor-in-chief Joseph E. Safdieh, MD, FAAN, highlights articles studies showing persistent fatigue after TIA, the neurologic complications of measles, and the impact of the dismantling of a CDC surveillance program of epilepsy.

Spontaneous intracranial hypotension reflects a disruption of the normal continuous production, circulation, and reabsorption of CSF. Diagnosis requires the recognition of common and uncommon presentations, careful selection and scrutiny of brain and spine imaging, and, frequently, referral to specialist centers.  In this episode, Gordon Smith, MD, FAAN speaks with Jill C. Rau, MD, PhD, author of the article “Clinical Features and Diagnosis of Spontaneous Intracranial Hypotension” in the Continuum® June 2025 Disorders of CSF Dynamics issue. Dr. Smith is a Continuum® Audio interviewer and a professor and chair of neurology at Kenneth and Dianne Wright Distinguished Chair in Clinical and Translational Research at Virginia Commonwealth University in Richmond, Virginia. Dr. Rau is an assistant professor of clinical neurology at the University of Arizona, School of Medicine-Phoenix in Phoenix, Arizona. Additional Resources Read the article: continuumjournal.com Subscribe to Continuum®: shop.lww.com/Continuum Earn CME (available only to AAN members): continpub.com/AudioCME Continuum® Aloud (verbatim audio-book style recordings of articles available only to Continuum® subscribers): continpub.com/Aloud More about the American Academy of Neurology: aan.com Social Media facebook.com/continuumcme @ContinuumAAN Host: @gordonsmithMD Full episode transcript available here Interview with Jill Rau, MD Dr Jones: This is Dr Lyell Jones, Editor-in-Chief of Continuum. Thank you for listening to Continuum Audio. Be sure to visit the links in the episode notes for information about earning CME, subscribing to the journal, and exclusive access to interviews not featured on the podcast. Dr Smith: This is Dr Gordon Smith. Today I'm interviewing Dr Jill Rau about her article on clinical features and diagnosis of spontaneous intracranial hypotension, which she wrote with Dr Jeremy Cutsworth-Gregory from the Mayo Clinic. This article appears in the 2025 Continuum issue on disorders of CSF dynamics. I'm really excited to welcome you to the Continuum podcast. Maybe you can start by just telling our listeners a little bit about yourself? Dr Rau: Hi, thanks for having me. I'm really honored to be here, and I really enjoyed writing the paper with Dr Cutsforth-Gregory. I hope you guys enjoy it. I am the director of headache medicine at the Baba Bay Neuroscience Institute at Honor Health in Scottsdale, Arizona. I'm also currently the chair of the special interest group in CSF Dynamics at the American Headache Society, and I've had a special interest in this field since I first watched Dr Linda Gray speak at a conference where she talked about spinal CSF leaks and their different presentations. And they were so different than what I had been taught in residency. They're not just the post-LP headache. They have such a wide variety of presentations and how devastating they can be, and how much impact there is on someone's life when you find it and fix it. And I've been super interested in the field and involved in research since that time. And, yeah. Love it. Dr Smith: Well, thanks for sharing your story. And as I reflected on our conversation ahead of time and have been thinking about this issue… this is a cool topic, and every time I read one of these manuscripts and have the opportunity to speak with one of the authors, I learn a ton, because this was something that wasn't even on the radar when I trained back in the 1800's. So, really looking forward to the conversation. I wonder if you could really briefly just summarize or remind for everyone the normal physiology about CSF dynamics, you know, production, absorption, and so forth? Dr Rau: So, the CSF is the fluid that surrounds the brain and the spinal cord, and it's contained by the dura, which is like a canvas or a sac that covers that whole brain and spinal cord. And within the ventricles of the brain, the choroid plexus produce CSF. It's constantly producing and then being reabsorbed by the arachnoid granulations and pushed into the venous space, the cerebral sinuses, venous sinuses. And also some absorption and push into the lymphatics that we've just learned about in the past year. This is kind of new data coming out, so always learning more and more about CSF, but we know that it bathes the brain and the spinal cord, helps keep some buoyancy of the brain as well as pushing nutrients in and pulling out metabolic waste. And it sort of keeps the brain in the state of homeostasis that's happy. And so, when there's a disruption of that flow and the amount of fluid there, that disrupts that, that can cause lots of different symptoms and problems for people. Dr Smith: One of the many new things I learned is that even the name of this---spontaneous intracranial hypotension---is misleading. And I think this is clinically relevant, as we'll probably get to in a moment, but can you talk a little bit about this? Is this really like a pressure disorder or a volume disorder? Dr Rau: Yeah. It's almost certainly a volume disorder. We do see in some people that they have low pressure, and it's still part of the diagnostic criteria. But it's there because if you have a low pressure, if you measure an opening pressure and it's below six, if you're measuring it in the spine in the right place, then you have indication that there's low volume. But there's over 50% of people's opening pressure who have a spinal CSF leak, have all the symptoms and can be fixed. So, they have normal pressure in 50% of the people. So, it is an inaccurate term, hypotension, but it was originally discovered because of the thought that it was a low-pressure situation. Some of the findings would suggest low pressure, but ultimately, we are pretty sure it's a low-volume condition. Dr Smith: Another new thing that I learned that really blew me away is how bad this can be. I did a podcast with Mark Burish about cluster, and I was reminded many cluster patients are pushed to the point of suicidal ideation or committing suicide by the severity of pain. And this sounds like for many patients it's equally severe. Can you maybe paint a picture for our listeners why this is so clinically important? Dr Rau: A large number of people, even people who are known to have leaks because they've had them before or they've releaked, they have a lot of brain fog and cognitive impairment. They often have severe headaches when they're upright. So, orthostatic headache is probably the number one most common symptom, and those headaches are one of the worst headaches out there. When people stand up, their fluid is not supporting the brain and there's an intense amount of pain. And so, they spend a large portion of their lives horizontal. And there's associated symptoms with that, it's not just headache pain and brain fog. There's neck pain. There's often subsequent disorders that accompany this, like partial orthostatic tachycardia syndrome. We don't know if that's because of deconditioning or an actual sequela of the disease, but it's a frequent comorbidity. We have patients that have extreme dizziness with their symptoms, but many patients are limited to hours, if that, upright per day, combined, total. And so they live their lives, often, just in the dark, lots of photophobia, sensitive to the light, really unable to function. It's also very hard to find and so underrecognized that a lot of patients, especially if they don't have that really clinical symptom of orthostatic headache. So, it's often missed. So, they're just debilitated. You know, treatments don't work because it's not a migraine and it's not a typical headache. It's a mechanical issue as well as a metabolic issue and not found, not a lot helps it. Dr Smith: So, you know, I have always thought about this as really primarily an orthostatic symptom. I wonder if you can talk about the complexity of this; in particular, kind of how this evolves over time, because it's not quite that simple. And maybe in doing so, you can give our listeners some pearls on when they should be thinking about this disorder? Dr Rau: A large portion of people do have headache with spinal CSF leak, in particular, spontaneous intracranial hypertension- hypotension, excuse me. And that's something to be thought about, is that there are spontaneous conditions where people have either rupture of the dural sac, or an erosion of the dural sac, or a development of a connection between the dura and the venous system. And that is taking away or allowing CSF to escape. In these instances that patients have spontaneous, there may be a different presentation than if they have, like, a postdural puncture or a chronic traumatic or iatrogenic leak. And we're not sure of that yet, but we're looking into that. Still, the largest presentation is headache, and orthostatic headache is very dominant in the headache realm. But over time, patients' brains can compensate for that lack of CSF and start overproducing---or at least we think that's probably what's happening. And you may see a reduction in the orthostatic symptoms over time, and you may see an improvement in the radiographic findings. So, there are some interesting papers that have been published that look at these changes over time, and we do see that sometimes within that first three to four months; this is the most common time to see that change. Other patients may worsen. You may actually see someone going from looking sort of normal radiographically to developing more of a SIH-type of picture on the brain. And so it's not predictable which patients have gone from orthostatic to improvement or the other way around, both radiographically and clinically. So, it can be quite difficult to tell. So, for me, if I have a patient that comes to me and they're struggling with headache… if it's orthostatic, very clearly orthostatic: I lay down, I get considerably better or my headache completely goes away. And then when I stand up, it comes on relatively quickly, within an hour. And sometimes it's a worsening-throughout-the-day type of thing, it's lowest in the morning and it worsens throughout the day. These are the times that it's most obvious to think about CSF leak. Especially if that headache onset relatively suddenly, if it onset after a small trauma. Like I've had patients that say, you know, I was doing yoga and I did some twists and I felt kind of a pop. And then I've had this headache that is horrible when I'm upright but is better when I lay down ever since, you know, since that time. That's kind of a very classic presentation of spinal CSF leak or spontaneous intracranial hypotension. Maybe a less common presentation would be someone who comes to you, they've had a persistent headache for a couple years, they kind of remember it started in March of a couple years ago, but they don't know. Maybe it's, you know, it's a little better when they lay down. It may be a little worse when they're up moving around, but so is migraine, and it's a migrainous headache. But they've tried every migraine drug you can think of. Nothing is responding, nothing helps. I'm always looking at patients who are new daily, persistent headaches and patients who aren't responding to meds even if it's not new daily, but they have just barely any response. I will always go back and examine their brain imaging and get full spine to make sure I'm not missing. And you can never be 100% sure, but it's always good to consider those patients to the best of your ability, if that- have that in the back of your mind. Dr Smith: So obviously, goes without saying, this is something people need to have on their radar and think about. And then we'll talk more about diagnostic tools here in a second. But how common is this? If you're a headache doc, you see a lot of patients who have intractable headaches. And how often do you see this in your headache practice? Now you're- this is your thing, so probably a little more than others, but, you know, how common will someone who sees a lot of headache encounter these patients? Dr Rau: If you see a lot of headache, I mean, currently the thought is it's about 5 in 100,000. That was from a study before we were finding CSF venous fistulas. I think a lot of us think it's more common than that, but it's not super common. We don't have good estimates, but I would guess between 5 and 10 for 100,000 persons, not “persons who come to a tertiary headache clinic with intractable headaches”. So, it's hard to gauge how frequent it is, but I would say it's considerably more frequent than we currently think it is. There's still a group of people with orthostatic headaches that we can't find leaks on; that, once you treat other things that can cause or look for other things that can cause orthostatic headaches. So, there may be even still a pathophysiology out there that is still a leak type. Before 2014, we didn't even know about CSF venous fistulas. And now here we are; like, 50% of them are CSF venous fistulas. So, you know, we're still in a huge learning curve right now. Dr Smith: So, I definitely want to talk about the fistulas in a second. But before moving on, one of the things that I found really interesting is the wide spectrum of clinical phenotype. And we obviously don't have a lot of time to get into all of these different ones, but the one that I was hoping you might talk about---and there's a really great case, and you're on bunch of great case, a great case of this---is brain sagging dementia, not a term I've used before. Can you really briefly just tell our listeners about that, because that's a really interesting story and a great case in your article? Dr Rau: Yeah. So, brain sag dementia is a… almost like an extreme version of a spontaneous intracranial hypotension. Where there is clear brain sag in the imaging---so that's helpful---but the patients present kind of like a frontotemporal dementia. And when this was first started to being determined, you could turn the patient into Trendelenburg, and sometimes they would improve. There are some practitioners that have introduced fluid into the thecal sac and had temporary improvement. Patching has improvement, then they leak again, sometimes  not. But the clinical changes with this have been pretty tremendous to be able to identify that that's a real thing. And in some cases, out of Cedars Sinai, you know, who does a lot of the best research in this, they've had lots of cases where they can't find the leak, but there's clear brain sag that fits with our clinical picture of CSF leaks. So, we're on a learning curve. But yeah, this- they really present. They have disinhibition and cognitive impairment that is very similar to frontotemporal dementia. Dr Smith: Well, so let's talk about what causes this. You mentioned CSF venous fistulas. I mean, that was reported now just over a decade ago, it's pretty amazing. That accounts for about half of cases, if I understand correctly. What are the other causes? And then we'll talk more about therapy in a minute, but what causes this? Dr Rau: So, within the realm of spontaneous, you know, we say it's spontaneous. But the spontaneous cases we account for, they can be tears in the dura, which are usually sort of lateral tears in the dura. They can be little places that rubbed a hole, often on an osteophyte from the spine. They can come from these spinal diverticuli. So, I always describe it to my patients like those balls that have mesh and squishy, and you squeeze them in the- through the mesh, there's the extra little bubbling out. If you think of like the dura bubbling, out in some cases, through the framing of the spine, right where the spinal nerve roots come out, they should poke out like wires from the dura. But in many cases they poke out with this extra dura surrounding them, and we call that spinal diverticuli. And if you imagine like the weakening of where you squeeze that, you know, balloon through your fingers, in those locations, that's a very common place to find a CSF leak, and you can imagine that the integrity of the dura there may be less than it would be if it were not being expanded in that direction. And that's often the most common place we see these CSF venous fistulas. So, you can get minor traumas; like I said, it can be spontaneous, like someone just develops a leak one day. It can be rubbed off, and it can be a development of a connection between the dura and the venous system. There are also iatrogenic causes, but we don't consider them spontaneous. But when you're considering your patients for spontaneous cases, you should consider if they've ever had chronic---even long, long time ago---had any spinal implementation, procedures near the spine, spinal injections, LPs in the past, and especially women who've had epidurals in pregnancy. Dr Smith: All right, so we see a patient, positional severe headache, who meets the clinical criteria. Next step, MRI scan? Dr Rau: Yeah. So, the first thing is always to get the brain MRI with and without contrast. Most places will have a SIH or a spinal CSF leak protocol, but you should get contrast because one of the most pathognomonic findings on brain MRI is that smooth diffuse dural enhancement. And that's a really fantastic thing when you find it, because it's kind of a slam dunk. If you find it, then you will see other findings. It almost never exists alone. But if you see that, it's pretty much a spinal CSF leak. But you're also looking for subdural collections, any indication of brain sag. We do have these new algorithms that have come out in the past couple of years that are helpful. They're not exclusionary---you can have negative findings on the brain and still have spinal CSF leak---but the brain MRI is extremely helpful. If it's positive for the findings, it really does help you nudge you in the direction of further investigations and treatments. Dr Smith: And what about those further investigations and treatments, right? So, you see that there's findings consistent with low pressure, and I guess I should say low intracranial CSF volume. Be that as it may, what's the next step after that? Dr Rau: Depends on where you are and what you can do. I almost always will get a full spine MRI: so, C spine, T spine, and L spine separately. Not, you know, we don't want it all in one picture, because we want to get the full view. And you want to get that with at least T2 highly- heavily T2 weighted with fat saturation in at least the sagittal and axial planes. It's really helpful if you can get it in the coronal planes, but we have to have- often have good talks with your radiologist to get the coronal plane. I spoke about the spinal diverticuli earlier, and I want to clarify a little bit of something. The coronal image will show those really nicely. It's interesting, but 44% of people have those. So just having the spinal diverticuli does not indicate that you have a leak. But if you have a lot of those, there may be more likelihood of having leak than if you don't have any of those. So, I will get all of those and I will look at them myself, but I've been looking at them myself for a long time. But a lot of radiologists in community hospitals, especially not- nonneuroradiologists, but even neuroradiologists, this isn't something that's that everybody's been educated about, and we've been learning so much about it so rapidly in the past ten years. It's not easy to do and it's often missed. And if it's not protocoled properly, the fat saturation's not there, it's very hard to see… you can have a leak and not see it. Even the best people, like- it's not always something that's visible. And these CSF venous fistulas that we talked about are never visible on normal MRI imaging. Nonetheless, I will run those because if I can find a leak---and 90% of the ones that are found on MRI imaging are in the thoracic spine. So that's where I spend the most of my time looking. But if you find it, that's another thing to take to your team to say, hey, look, here it is, let's try and do this, or, let's try and do that, or, I've got more evidence. And there are other findings on the spine; not just the leak, but other findings, sometimes, you can see on spine that maybe help you push you towards, yes, this is probably a leak versus not. Dr Smith: So, your article has a lot of great examples and detail about kind of advanced imaging to, like, find the fistula and what not. I guess I'm thinking most of our listeners are probably practicing in a location where they don't have a team that really focuses on that. So, let's say we do the imaging of the spine and you don't find a clear cause. Is the next step to just do a blood patch? Do you send them to someone like you? What's the practical next step? Dr Rau: Yeah, if your- regardless of whether you find a leak or not, if your clinical acumen is such that you think this patient has a leak or I've treated them for everything else and it's not working and I have at least a high enough suspicion that I think the risk of getting a patch is lower than the benefit that if they got a patch and it worked, I do send my patients for non-directed blood patches, because it currently does take a long time to get them to a center that can do CT myelograms or any kind of advanced imaging to look for sort of a CSF venous fistula or to get treated outside of a nondirected patch. You know, sometimes nondirected patches are beneficial for patients, and there's some good papers out there that sort of explain the low risks of doing these if done properly versus the extreme benefit for patients when it works. And, I mean, I can't tell you how many people come in and tell me how their lives are changed because they finally got a blood patch. And sometimes it works. And it's life-changing for those people. You know, they go back to work. They can interact with their kids again. Before, they didn't know what was wrong, just had this headache that started. So it's worth doing if you have a strong clinical suspicion. Dr Smith: Yeah. I mean, that was great. And, you know, to go back to where we began, this is severe. It's something like 60% of patients with this problem have thought about suicide, right? And you take this patient and cure the problem. I feel really empowered having read the article and talked to you today. And so, I'm ready to go out and look for this. Thank you so much for a really engaging conversation. This has been terrific. Dr Rau: Thank you. I appreciate it. I enjoyed being here. Dr Smith: Again, today I've been interviewing Dr Jill Rau about her article on clinical features and diagnosis of spontaneous intracranial hypotension---which I guess I should say hypovolemia after having talked to you---which she wrote with Dr Jeremy Cutsworth-Gregory. This article appears in the most recent issue of Continuum on disorders of CSF dynamics. Please be sure to check out Continuum Audio episodes from this really interesting issue and other interesting issues. And thank you, our listeners, again for listening to us today. Dr Monteith: This is Dr Teshamae Monteith, Associate Editor of Continuum Audio. If you've enjoyed this episode, you'll love the journal, which is full of in-depth and clinically relevant information important for neurology practitioners. Use the link in the episode notes to learn more and subscribe. AAN members, you can get CME for listening to this interview by completing the evaluation at continpub.com/audioCME. Thank you for listening to Continuum Audio.

Dexmedetomidine — or “Dex” — has become one of the most intriguing and versatile drugs in the anesthesia world. In this episode of Anesthesia Alchemy with hosts Lynn Macksey, MSN, CRNA and Garry Brydges, PhD, DNP, MBA, CRNA, ACNP-BC, FAAN dive deep into the pharmacology, clinical application, and emerging research surrounding this alpha-2 agonist. Here's some of what we discuss in this episode:

Addressing hypertension at the local and global levels requires using validated tools, following the data, and working with patients and policymakers alike. Guest Yvonne Commodore-Mensah, PhD, MHS, RN, FAAN, FAHA, FPCNA describes strategies for clinical practice as well as legislative advocacy for addressing this global healthcare crisis.Resources: Validated blood pressure monitors: validatebp.org PCNA patient education blood pressure resources: pcna.netHigh Blood Pressure: What you need to know (sheet in English & Spanish)Blood Pressure: How do you measure up? (Booklet in English & Spanish)See Privacy Policy at https://art19.com/privacy and California Privacy Notice at https://art19.com/privacy#do-not-sell-my-info.

Jody responds to the American College of Physicians' Annals On Call Podcast episode released on May 19th, 2025.Links:Advanced Practice Clinicians Cannot Replace Primary Care Physicians. Annals On Call Podcast, 5-29-25Physician Assistant and Former PA-Turned-Physician Discuss the State of the Profession. Patients At Risk Podcast, 7-25-21 (Spotify)New Workforce Model Suggests Continued Physician Shortages In Nonprimary Care Specialties (AAMC Article)Christin Giordano McAuliffe. There Is No Substitute for Primary Care Physicians: A Response to the Association of American Medical Colleges' Workforce Model. Ann Intern Med.2025;178:590-591. [Epub 4 March 2025]. doi:10.7326/ANNALS-24-03806University of South Alabama Dual Role NP CurriculumRazavi, Moaven PhD*; O'Reilly-Jacob, Monica RN, PhD, FNP-BC†; Perloff, Jennifer PhD*; Buerhaus, Peter RN, PhD, FAAN, FAANP(h)‡. Drivers of Cost Differences Between Nurse Practitioner and Physician Attributed Medicare Beneficiaries. Medical Care 59(2):p 177-184, February 2021. | DOI: 10.1097/MLR.0000000000001477 McMenamin A, Turi E, Schlak A, Poghosyan L. A Systematic Review of Outcomes Related to Nurse Practitioner-Delivered Primary Care for Multiple Chronic Conditions. Medical Care Research and Review. 2023;80(6):563-581. doi:10.1177/10775587231186720Kippenbrock T, Emory J, Lee P, Odell E, Buron B, Morrison B. A national survey of nurse practitioners' patient satisfaction outcomes. Nurs Outlook. 2019 Nov-Dec;67(6):707-712. doi: 10.1016/j.outlook.2019.04.010. Epub 2019 May 4. PMID: 31607371.Haas, D., Pozehl, B., Alonso, W. W., & Diederich, T. (2023). Patient Satisfaction With a Nurse Practitioner–Led Heart Failure Clinic. Journal for Nurse Practitioners, 19(4), Article 104496. https://doi.org/10.1016/j.nurpra.2022.11.006https://www.techtarget.com/patientengagement/news/366584669/Nurse-Practitioners-Boost-Patient-Satisfaction-Quality-Outcomeshttps://www.aanp.org/advocacy/advocacy-resource/position-statements/quality-of-nurse-practitioner-practicehttps://www.aacnnursing.org/news-data/all-news/rounds-with-leadership-focusing-on-the-outcomes-of-np-practiceStanik-Hutt, J., Newhouse, R. P., White, K. M., Johantgen, M., Bass, E. B., Zangaro, G., Wilson, R., Fountain, L., Steinwachs, D. M., Heindel, L., & Weiner, J. P. (2013). The quality and effectiveness of care provided by nurse practitioners. Journal for Nurse Practitioners, 9(8), 492-500.e13. https://doi.org/10.1016/j.nurpra.2013.07.004Savard I, Al Hakim G, Kilpatrick K. The added value of the nurse practitioner: An evolutionary concept analysis. Nurs Open. 2023 Apr;10(4):2540-2551. doi: 10.1002/nop2.1512. Epub 2022 Dec 17. PMID: 36527435; PMCID: PMC10006655.

In this episode, Dr. Cassandra Vonnes, DNP, GNP-BC, APRN, AOCNP, CPHQ, FAHA, a Gerontological Nurse Practitioner, and member of the GAPNA Communication Team, talks with Dr. Donna M. Fick, PhD, RN, GCNS-BC, FGSA, FAAN, a Professor and Director of the Center for Geriatric Nursing Excellence at the Penn State Ross and Carol Nese College of Nursing. Dr. Fick shares insights into her work on delirium research, validated screening tools like the UB-CAM, and the importance of interdisciplinary care in geriatrics. She also reflects on her recent presidency at the American Geriatrics Society, emphasizing advocacy, inclusivity, and the fight against ageism.Donna M. Fick, PhD, RN, GCNS-BC, FGSA, FAAN, is a Professor and the Director of the Center for Geriatric Nursing Excellence at the Penn State Ross and Carol Nese College of Nursing in University Park, Pennsylvania. Cassandra Vonnes, DNP, GNP-BC, APRN, AOCNP, CPHQ, FAHA, is the Nurses Improving Care for Healthsystem Elders (NICHE) Coordinator, Geriatric Oncology, at the Moffitt Cancer Center, in Tampa, Florida. She is a member of the Gerontological Advanced Practice Nurses Association Communication Team and is a host of the GAPNA Chat podcast series.Discover GAPNA: https://www.gapna.org/Production management by Anthony J. Jannetti, Inc., for the Gerontological Advanced Practice Nurses Association.Opening Music by:Optimistic / Inspirational by Mixaund | https://mixaund.bandcamp.com
Music promoted by https://www.free-stock-music.comClosing Music by:Scott Holmes.http://www.scottholmesmusic.com

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

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

Meet Eleanor, a mom on a mission. When her son was diagnosed with severe food allergies in 2004, Eleanor was launched into a whirlwind of support and advocacy for the food allergy community, eventually leading her to found and lead the Food Allergy and Anaphylaxis Connection Team (FAACT). Alongside the FAACT leadership team, she provides the education, advocacy, awareness, and grassroots outreach needed for the food allergy community through programming available to all. Tune in to hear the story behind Eleanor's incredible efforts and successes and her commitment to inclusivity that drives everything she does.To learn more about FAACT, their amazing resources, and Camp TAG visit: https://www.foodallergyawareness.org/Follow on social media @faactnewsEleanor Garrow-Holding has worked, educated, and advocated in the food allergy community since 2004. She was inspired to start this work after her son, Thomas, was diagnosed with life-threatening food allergies to tree nuts, peanuts, wheat, and sesame; eosinophilic esophagitis (EoE) triggered by milk and wheat; asthma; and environmental allergies. In December 2015, Thomas had a food challenge with wheat and was no longer IgE-allergic to wheat. After a 3-month trial with wheat and another 3-month trial with milk (post wheat) in his diet and upper endoscopies, he has also outgrown the wheat and milk triggers for EoE and is in remission from EoE as of July 2016. Thomas outgrew his peanut allergy in 2016 at age thirteen. In October 2019, at age sixteen, Thomas outgrew almond, sesame, and brazil nut and continues to avoid walnut, cashew, pecan, hazelnut, and pistachio.As CEO of the Food Allergy & Anaphylaxis Connection Team (FAACT), Eleanor provides leadership, development, and implementation for all of FAACT's initiatives and programs, including Camp TAG (The Allergy Gang) – a summer camp for children with food allergies and their siblings that Eleanor founded in 2009. Eleanor has a Bachelor of Healthcare Administration degree from Lewis University in Romeoville, IL, and worked in hospital management for 15 years in Chicago and suburban Chicago prior to working in the nonprofit sector.After Thomas was diagnosed in 2004, Eleanor established a food allergy support group in a southwest Chicago suburb, Parents of Children Having Allergies (POCHA) of Will County, focusing on education and advocacy; chaired the FAAN Walk for Food Allergy in Chicago in 2007 and 2008; was awarded the FAAN Muriel C. Furlong Award for Community Service in 2008; and advocated in the Illinois state legislature on food allergy and Eosinophilic Disorders (EGID, EoE) issues. Thanks to the efforts of Eleanor and other patient advocates, legislation to ensure insurance coverage for elemental formulas was signed into law in 2007 and legislation establishing food allergy management guidelines for Illinois schools was signed into law in 2009.Eleanor joined the Food Allergy & Anaphylaxis Network™ (FAAN) in 2009 as Vice President of Education and Outreach, where she oversaw educational initiatives, all food allergy conferences, the Teen Summit, Camp TAG (The Allergy Gang) now under FAACT's umbrella, a Teen Advisory Group, support group development, and more. She advocated for the Food Allergy & Anaphylaxis Management Act (FAAMA) in Washington, DC, with her son Thomas as part of FAAN's Kids Congress on Capitol Hill and also advocated on Capitol Hill for the School Access to Emergency Epinephrine Act. Eleanor served on the expert panel for the CDC's Voluntary Guidelines for Managing Food Allergies in Schools and Early Care and Education Programs and was a reviewer for the National Association of Education (NEA) Food Allergy Book: What School Employees Need to Know. Eleanor conducted numerous radio, television, and print interviews on food allergy issues and wrote articles for Allergic Living and Living Without magazines. She presented at national and regional conferences about food allergy management in school and restaurant settings and educated personnel in schools and school districts across the country on food allergy management in schools and continues to do so with FAACT.In 2013, Eleanor joined the Cincinnati Center for Eosinophilic Disorders (CCED) as Senior Specialist of Program Management at Cincinnati Children's Hospital and Medical Center. There she led day-to-day clinical operations, clinical research projects, program development, marketing, and development.Eleanor has and continues to educate employees from numerous food industry companies and entertainment venues about food allergies, such as McDonald's Corporation, The Hain Celestial Group, Mars Wrigley, all SeaWorld Parks, and more.Leading the charge at FAACT, Eleanor and the FAACT Leadership Team provides the education, advocacy, awareness, and grassroots outreach needed for the food allergy community. Eleanor serves on the National Peanut Board's Allergy Education Advisory Council, Global Allergy & Airways Patient Platform Board (GAAPP), St. Louis Children's Food Allergy Management & Education (FAME) National Advisory Board, and Association of Food and Drug Officials (AFDO) Food Allergen Control Committee. In August 2015, Eleanor was inducted into The National Association of Professional Women's (NAPW) VIP Professional of the Year Circle for her commitment to healthcare and nonprofit industries. FAACT is The Voice of Food Allergy Awareness. In 2022, Eleanor was a Contributor for The Change Guidebook (3-8-2022, HCI/Simon & Schuster).

Aarti Sarwal, MD, FAAN, FNCS, FCCM, professor of neurology at Virginia Commonwealth University Health System, explores the nuanced intersection of neurology and critical care, offering practical insights for clinicians across disciplines. Dr. Sarwal shares her perspective on the unique challenges of managing neurocritically ill patients, particularly when impairment presents challenges in administering a neurologic examination. She emphasizes that “the brain is the barometer of critical illness,” urging clinicians to prioritize daily neurologic evaluations and integrate neuromonitoring even in non-neurologic ICU populations. Listeners will gain an overview of tools such as continuous EEG, transcranial Doppler, emboli monitoring, and multimodal neuromonitoring platforms, including the role of neuro-ultrasound in expanding point-of-care capabilities. This episode also highlights the need for multidisciplinary collaboration and a shared decision-making model that extends across the continuum of care—from early ICU admission to post-discharge recovery. Listeners will appreciate Dr. Sarwal's reflections on neuroprognostication and the ethical dimensions of care withdrawal, particularly the danger of therapeutic nihilism in patients whose outcomes are uncertain. Referencing a 2023 review she coauthored (Crit Care Med. 2023;51:525-542), Dr. Sarwal outlines a practical framework for neuromonitoring that integrates structural, electrical, vascular, and metabolic insights. This conversation provides a timely and inclusive look at the future of neurocritical care—where technology, teamwork, and training converge to support better patient outcomes.

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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