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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.

De strijd tussen Telstar en FC Den Bosch om de finale te halen van de play-offs ligt nog open na de 0-0 in Den Bosch. En zijn de overgebleven ploegen nu in het voor- en nadeel van Willem II dat degradatie probeert te voorkomen? Verder staat Etienne Verhoeff in de AD Voetbalpodcast met Johan Inan uitgebreid stil bij de situatie in Amsterdam. De Ajax-clubwatcher was de laatste dagen getuigen van wat er allemaal gebeurde rondom Francesco Farioli. Aan hem ook de vraag, wat erft zijn opvolger? Lex Lammers vertelt over het kampioenschap in de tweede Bundesliga van FC Köln. Beluister de hele AD Voetbalpodcast nu via AD.nl, de AD App of jouw favoriete podcastplatform.Support the show: https://krant.nl/See omnystudio.com/listener for privacy information.

Wat gebeurt er als je als ogenschijnlijk wit persoon door het leven gaat, maar je familiegeschiedenis een ander verhaal vertelt? Met Liesbeth Smit, Etchica Voorn, Kevin Klein en Anne-Fay Kops.De Surinaamse grootmoeder van journalist en historicus Liesbeth Smit sprak nauwelijks over haar gemengde afkomst. Daardoor bleef het Surinaamse verleden van de familie grotendeels onbesproken, tot Liesbeth – met haar witte huid en blauwe ogen – zelf op zoek ging naar haar familieverleden in Suriname. Naar aanleiding van haar nieuwste boek Aan ons is niets meer te zien, over Smits onzichtbare gemengde afkomst waarvan de wortels in het slavernijverleden in Suriname liggen, gaan we in De Balie in gesprek over de verzwegen bladzijden van ons koloniale verleden en de vaak moeizame zoektocht naar een persoonlijke familiegeschiedenis in Suriname. Wat betekent het om Surinamer te zijn? Wie mag zichzelf een ‘Surinamer' noemen? En welke plaats hebben mensen van gemengde afkomst en huidskleur in het Surinaamse heden en verleden?In samenwerking met Nijgh & van DitmarZie het privacybeleid op https://art19.com/privacy en de privacyverklaring van Californië op https://art19.com/privacy#do-not-sell-my-info Zie het privacybeleid op https://art19.com/privacy en de privacyverklaring van Californië op https://art19.com/privacy#do-not-sell-my-info.

In the second installment of this two-part series, Dr. Stacey Clardy and Dr. Janis Miyasaki discuss how she got involved with the AAN.  Show reference:  https://www.aan.com/news/aan-honors-leader-volunteer-2025-presidents-award  

In deze podcast, aangeboden door oncologie.nu, spreekt prof. dr. Sonja Zweegman met drs. Febe Smits (beiden Amsterdam UMC) over het verhoogde risico op infecties bij patiënten met een multipel myeloom die behandeld worden met CAR T-celtherapie of bispecifieke antilichamen. Aan bod komen het voorkomen en het type infecties tijdens en na behandelingen met de verschillende bispecifieke antistoffen, de beste wijze om infecties te rapporteren, en het voorkomen en de behandeling van de infecties.Referenties Moreau P, et al. N Engl J Med 2022;387:495–505. Chari A, et al. N Engl J Med 2022;387:2232–44. Frerichs KA, et al. Blood Adv 2024;8:194–206. Nooka AK, et al. Cancer 2024;130:886–900. Lancman G, et al. Blood Cancer Discov 2023;4:440–51. Ludwig H, et al. Blood Adv 2024;8:4979–82.

55 procent van de Nederlandse moslims heeft in de afgelopen 5 jaar discriminatie ervaren, zo bleek uit EU-onderzoek naar onze grondrechten. Van beledigingen op straat en het aftrekken van hoofdbedekking tot structurele uitsluiting op de arbeidsmarkt. Ook recent Nederlands onderzoek wees op de ontwrichtende maatschappelijke gevolgen van moslimdiscriminatie. Hoe kunnen we moslimdiscriminatie tegengaan? We gaan in gesprek met Amsterdamse wethouder Touria Meliani, docent burgerschap Bilal Ben Abdelkarim, bestuurslid bij Collectief Jonge Moslims Sana Koulij, advocaat en arabist Maurits Berger, journalist en radio- en tv-presentator Naeeda Aurangzeb, promovendus aan Universiteit Leiden Omer Karaca en met moderator Kashif Amin.Aan het begin van deze eeuw leidden grote gebeurtenissen – waaronder de aanslag op de Twin Towers en de moord op Theo van Gogh – ertoe dat moslims als ‘De Ander' werden gezien. De afgelopen twintig jaar is moslimdiscriminatie steeds zichtbaarder geworden. De verkiezingswinst van de PVV heeft islamhaat verder genormaliseerd in de politiek, en de oorlog in Gaza legt extra druk op de verhoudingen binnen onze samenleving. Dat heeft niet alleen gevolgen voor moslims, maar voor de samenleving als geheel. Hoe doorbreken we de vicieuze cirkel van racisme, uitsluiting en polarisatie? En hoe beïnvloedt de constante stroom aan uitsluiting islamitische Nederlanders?Programmamaker: Rokhaya SeckModerator: Kashif AminMede mogelijk gemaakt door Vfonds.Zie het privacybeleid op https://art19.com/privacy en de privacyverklaring van Californië op https://art19.com/privacy#do-not-sell-my-info.Zie het privacybeleid op https://art19.com/privacy en de privacyverklaring van Californië op https://art19.com/privacy#do-not-sell-my-info.

Aan tafel deze week: Burgemeester van Amsterdam Femke Halsema, oud-generaal Mart de Kruif, politiek leider GroenLinks-PvdA Frans Timmermans, fotograaf Lucas Foglia  Presentatie: Twan Huys  Wil je meer weten over de gasten in Buitenhof? Op onze website vind je meer informatie. Daar kan je deze aflevering ook terugkijken en je vindt er natuurlijk nog veel meer gesprekken:   https://bit.ly/buitenhof-18-mei-25 

Aan de slag!Klamp je vast aan je Redder, en zoek het alle dagen bij Hem alleen. Lees in Zijn Woord en put daar je kracht uit. Moge God je licht zijn, mogen Zijn woorden je vervullen en mag je zo – met een volle lamp – de toekomst tegemoetgaan. En weet dat je in alles – in al je verlangens, je vragen en je hoop – bij Jezus terecht kunt. Zoek Johannes 6:37b maar eens op!Deze overdenking is geschreven door oud-schrijfster Anne-Saar Kunz.

Aan wat geeft Wannes het meeste geld uit? Wanneer heeft hij voor het laatst gehuild? En wat is het verste dat hij zou gaan voor een rol? Maureen & Imane stellen 22 Minuten Stomme Vragen aan Wannes Lacroix en komen er zo achter hoeveel hij durft uitgeven aan zonnebrillen.

Aan de slag!Oefen jezelf in het gelovig bijbellezen. Bedenk dat de woorden kracht in zichzelf hebben en voor jou zijn geschreven.Deze overdenking is geschreven door schrijfster Emmely Post-Spreeuwenberg.

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. 

In ‘Levenslange liefde – Sprookjes bestaan niet' onderzoekt journalist en schrijver Barbara van Beukering op persoonlijke én journalistieke wijze waarom we blijven geloven in de ene ware liefde, terwijl duurzame relaties steeds zeldzamer worden. Aan de hand van gesprekken met deskundigen en haar eigen ervaringen bevraagt ze het romantisch ideaal en de houdbaarheid ervan in deze tijd. Eerder schreef ze de boeken ‘Je kunt het maar éénmaal doen' en Het jaar waarin ik mijn haar verloor'.  Presentatie: Willemijn Veenhoven

In deze aflevering van Money Talks gaan we het hebben over budgetteren. Hoe begin je, wat is slim, en hoe hou je het vol? Hoe krijg je grip op je geld? Budgetteren kan je leren. We gaan samen met de financiële expert Revy Rosalia van Rabobank in gesprek. Hieronder vind je de belangrijkste tips en tools die in de podcast zijn besproken.Wat is eigenlijk budgetteren? Budgetteren betekent dat je kijkt naar wat je verdient en wat je uitgeeft. Dit geeft een goed overzicht van je geld en zorgt voor balans. Dat helpt je om slimme keuzes te maken. Lees meer over budgetteren. Waar geef jij je geld aan uit? Je kunt dit eenvoudig zien in de Rabo App onder Inzicht Je kunt dan precies zien hoeveel geld je uitgeeft aan bijvoorbeeld uit eten gaan. Aan de hand hiervan kun je jouw budget bepalen voor de komende maand. Wil je weten hoe je dit stapsgewijs aanpakt? Lees de 6 stappen om meer inzicht in je geldzaken te krijgen Een simpele budgetmethode is 50/30/20 regel. Je verdeelt de inkomsten (stufi, salaris) in 3 delen: 50% voor vaste lasten (huur, energie, etc), 30% voor persoonlijke uitgaven (kleding, uitgaan) en 20% voor sparen. Hoeveel spaar jij? Een goede vuistregel is om minimaal 10% van je inkomsten opzij te zetten naar je spaarrekening. Een tip is om dit direct na binnenkomst van je salaris automatisch over te maken naar een spaarpotje. Volg Rabobank via haar socials Insta & TikTok 

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.

Wie is Javier Milei? De man die met zijn kettingzaag de bureaucratie van de Argentijnse overheid te lijf ging. Milei is nu anderhalf jaar aan de macht en tegen alle verwachtingen in zijn de eerste economische indicaties goed.  Aan tafel bij Jort Kelder is dr. Susana Menéndez aangeschoven, Latijns-Amerika expert en van origine Argentijnse. Zij schetst voor ons een beeld van het huidige Argentinië en verklaart hoe Milei aan de macht kwam. Ook Edin Mujagic, econoom, is te gast bij Jort. Hij volgt met interesse het Argentijnse libertaire experiment.

Wie is Javier Milei? De man die met zijn kettingzaag de bureaucratie van de Argentijnse overheid te lijf ging. Milei is nu anderhalf jaar aan de macht en tegen alle verwachtingen in zijn de eerste economische indicaties goed.  Aan tafel bij Jort Kelder is dr. Susana Menéndez aangeschoven, Latijns-Amerika expert en van origine Argentijnse. Zij schetst voor ons een beeld van het huidige Argentinië en verklaart hoe Milei aan de macht kwam. Ook Edin Mujagic, econoom, is te gast bij Jort. Hij volgt met interesse het Argentijnse libertaire experiment.

Ook dit WNBA-seizoen maken enkele Belgian Cats de oversteek richting de States. Maar in juni verdedigt België ook z'n Europese titel. Wat mogen we van onze Cats Julie Vanloo, Kyara Linskens en Julie Allemand in Amerika verwachten en komt hun deelname aan het EK in gedrang? We vragen het aan Pascal Angillis, aan de slag in de VS en assistent-bondscoach. Aan ex-Belgian Cat Ann Wauters. Sven Van Camp, de high performance manager van de Cats en Sporza-commentator Christophe Vandegoor.

Op je beeldscherm prijkt een verse aflevering van onze dagelijkse vodcast Gamekings Daily. Elke doordeweekse dag bespreken we in deze podcast en video het laatste nieuws binnen de videogames wereld. In pak-hem-beet 20 minuten gaan Boris en JJ je dit keer helemaal bijpraten. Het hoofdonderwerp van vandaag behelst het gerucht dat Rockstar nog dit jaar de remaster van GTA 4 wil droppen. Daar is nu immers ruimte voor omdat GTA 6 is doorgeschoven naar 26 mei 2026. Tenminste, als die game dan uitkomt. De twee wegen ook het gerucht dat het derde deel uit de Horizon-serie voor 2027 op de planning staat. Daarvoor moet nog wel de online Horizon game uitkomen. Deze twee onderwerpen en meer zie en hoor je in de GK Daily van woensdag 14 mei 2025.'Rockstar wil de GTA 4 remaster nog dit jaar droppen'GK Daily is er maandag, dinsdag, woensdag en donderdag. Op de vijfde werkdag hebben we zoals altijd EvdWL, de uitgebreide podcast over alle ontwikkelingen gedurende die week. In deze editie praten Boris en JJ zoals gezegd over de geruchten die de rondte doen over de remaster van GTA 4 (en Max Payne 3). Nu er in 2025 ruimte is door het uitstel van GTA 6, kan Rockstar deze game daar inplannen. Geloven de twee er in en willen ze die game nog een keer gaan spelen? Opgepoetst en al voor de PS5 en de Xbox Series S en X.Horizon 3 moet in 2027 gaan uitkomenIn het tweede onderwerp praten de twee over de games waar Guerrilla Games mee bezig is. Dan hebben we het over Horizon 3 en de Horizon MMO.  Aan de eerste werken ze zelf en het tweede spel is uitbesteed aan NCSoft. Een insider komt nu met launchwindows voor beide games. Wat zijn die periodes en hoe staan de twee tegenover de twee versies van de bekende Nederlandse franchise. Tot slot bespreken de twee de ontslaggolf die Microsoft op dinsdag doorvoerde.Timestamps:00:00:00 Gamekings Daily van 14 mei00:00:17 Introductie00:06:11 GTA 4 Remastered nog deze zomer naar de PS5 en Xbox00:13:01 Derde deel Horizon moet in 2027 uitkomen

Wat bij het bezoek van Donald Trump aan het Midden-Oosten het meest opvalt is wat hij níet doet: hij slaat Israël over. Het is een bewuste keuze, die niet over het land of volk gaat, maar over Bibi Netanyahu, aan wie Trump opnieuw een keiharde linkse directe uitdeelt. Die kwam net zo hard aan als de met succes beloonde poging die Trump deed om de Amerikaans-Israëlische gijzelaar Edan Alexander te bevrijden. Door rechtstreekse onderhandelingen met Hamas. De rest van de gijzelaars zit nog vast. Aan vreugde over de terugkeer van Alexander ontbrak het in Israël zeker niet. Maar de overgrote meerderheid van het Israëlische volk is razend op Bibi. Dat die het zo ver heeft laten komen dat Trump hem openlijk negeert en dat, buiten Bibi om, één gijzelaar werd bevrijd en de rest niet, is een genadeloze schoffering door Trump van de Israëlische premier. Dit ondanks de sussende commentaren van Trumps medewerkers. De hervatting van de oorlog tegen Hamas, het voornemen om Gaza weer te bezetten, de tragiek van geblokkeerde voedseltransporten – het zijn allemaal kwesties waarmee de meerderheid van de Israëliërs evenzeer worstelt als de buitenwereld. Al liggen de accenten iets anders. Team-Bibi zegt: winnen is belangrijker dan de gijzelaars. De meerderheid van het volk zegt: de gijzelaars zijn belangrijker dan winnen. Waarom delft de meerderheid dan toch het onderspit? Door een situatie die vergelijkbaar is met de Nederlandse. Het kabinet-Schoof leunt op een coalitie van vier partijen, waarvan er bij verkiezingen twee nagenoeg of geheel zouden verdwijnen. Het kabinet-Netanyahu heeft een meerderheid in de Knesset door de steun van enkele extreemrechtse, ultranationalistische partijen. Bij verkiezingen zou de coalitie naar alle waarschijnlijkheid die meerderheid verliezen. Eén probleem: de verkiezingen zijn pas eind oktober volgend jaar. Tenzij het kabinet valt, maar zoals in alle coalitiesystemen gebeurt dat alleen als een van de regeringsfracties de stekker eruit trekt – en die kijken wel uit. Bibi speelt een levensgevaarlijk spel, want ruzie met de Amerikaanse president kan leiden tot sancties. Het geitenpaadje waarvoor Bibi waarschijnlijk kiest is het herstel van voedseltransporten. Dat haalt de grootste druk van de ketel, maar lost niets op. En al zeker niet het lot van de gijzelaars.See omnystudio.com/listener for privacy information.

Aan geld geen gebrek meer in de defensie-industrie. Wat staat Nederlandse bedrijven nog in de weg om sneller op te schalen en meer materieel op eigen bodem te produceren? Te gast is Raymond Knops, voorzitter van defensie-branchevereniging NIDV. Gasten in BNR's Big Five van de defensie-industrie: -Gijs Tuinman, staatssecretaris van Defensie -Raymond Knops, voorzitter van defensie-branchevereniging NIDV -Patrick Bolder, defensie analist bij het Haags Centrum voor Strategische Studies -Hadewych Kuiper, manager bij Triodos Investment Management -Miëtta Groeneveld, directeur van het NATO Command & Control Center of ExcellenceSee omnystudio.com/listener for privacy information.

Op 2 mei verschijnt ‘In mijn ogen draag ik wolken', de nieuwe roman van de Afghaans-Nederlandse psychiater en schrijver Forugh Karimi. Aan de hand van Widá, een gevluchte vrouw uit Afghanistan, verweeft Karimi persoonlijke herinnering met recente geschiedenis en onderzoekt ze thema's als schuld, verlies en veerkracht. Eerder schreef ze de boeken ‘Nargis' en ‘De Moeders van Mahipar'.  Presentatie: Eric Corton

Aan tafel deze week: over de oorlog in Gaza directeur Oxfam Novib Michiel Servaes, Palestijns journalist Rita Baroud en schrijvers Maurits de Bruijn en Sinan Çankaya. Hiernaast spreekt Raad voor de rechtspraak voorzitter Henk Naves over de erosie van de rechtstaat.  Presentatie: Maaike Schoon Wil je meer weten over de gasten in Buitenhof? Op onze website vind je meer informatie. Daar kan je deze aflevering ook terugkijken en je vindt er natuurlijk nog veel meer gesprekken: bit.ly/buitenhof-11-mei-25

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.

LES 127Er is geen liefde dan die van God.Jij denkt misschien dat er verschillende soorten liefde mogelijk zijn. Jij denkt misschien dat er een soort liefde is voor dit, en een soort voor dat; een manier om de een lief te hebben, en een andere manier om een ander lief te hebben. Liefde is één. Ze kent geen afzonderlijke delen en geen gradaties, geen soorten of niveaus, geen verschillen en geen onderscheidingen. Ze is zichzelf gelijk, volkomen onveranderlijk. Ze verandert nooit naar gelang de persoon of de omstandigheid. Ze is het Hart van God en tevens van Zijn Zoon.De betekenis van liefde is duister voor ieder die denkt dat liefde veranderen kan. Hij ziet niet in dat veranderlijke liefde nu eenmaal onmogelijk is. En dus denkt hij dat hij nu eens liefhebben, en dan weer haten kan. Hij denkt bovendien dat liefde aan de een kan worden geschonken, en toch zichzelf kan blijven hoewel ze anderen wordt onthouden. Zulke dingen over liefde geloven betekent niet begrijpen wat liefde is. Als ze dergelijke onderscheidingen kon maken, zou ze tussen de rechtvaardige en de zondaar moeten oordelen, en de Zoon van God in afzonderlijke delen waarnemen.Liefde kan niet oordelen. Omdat ze zelf één is, ziet ze alles als één. Haar betekenis ligt in eenheid. En ze moet wel ontgaan aan de denkgeest die denkt dat ze partijdig of gedeeltelijk is. Er is geen liefde dan die van God, en alle liefde is de Zijne. Waar liefde afwezig is regeert geen ander principe. Liefde is een wet zonder tegendeel. Haar heelheid is de kracht die alles bijeenhoudt, de schakel tussen de Vader en de Zoon die Hen beiden voor eeuwig als hetzelfde samenbindt.Geen cursus die tot doel heeft jou te leren je te herinneren wat jij werkelijk bent, kan nalaten te benadrukken dat er nooit een verschil kan zijn tussen wat jij werkelijk bent en wat liefde is. De betekenis van liefde is jouw betekenis en wordt gedeeld door God Zelf. Want wat jij bent, is wat Hij is. Er is geen liefde dan die van Hem, en wat Hij is, is al wat er is. Hemzelf is geen beperking opgelegd, en dus ben jij eveneens onbeperkt.Geen wet waaraan de wereld gehoorzaamt, kan jou helpen de betekenis van liefde te bevatten. Wat de wereld gelooft, werd gemaakt om de betekenis van liefde te verbergen en die duister en geheim te houden. Er is geen enkel principe dat door de wereld hooggehouden wordt, dat niet indruist tegen de waarheid van wat liefde is en wat jij bent.Probeer niet in de wereld jouw Zelf te vinden. Liefde wordt niet gevonden in duisternis en dood. Toch is ze volkomen duidelijk voor ogen die zien en oren die de Stem van de liefde horen. Vandaag oefenen we om je denkgeest vrij te maken van alle wetten waaraan jij denkt te moeten gehoorzamen, van alle beperkingen waaronder je gebukt gaat en alle veranderingen die volgens jou deel uitmaken van het menselijk lot. Vandaag zetten we de allergrootste stap die deze cursus verlangt in je voortgang naar zijn vastgestelde doel.Als je vandaag ook maar het vaagste begrip verkrijgt van wat liefde betekent, heb jij een onmetelijke afstand en een in tijd ontelbaar aantal jaren overbrugd op de weg naar je verlossing. Laten we dan samen vandaag met blijdschap enige tijd aan God geven en begrijpen dat dit het allerbeste gebruik van de tijd is dat er is.Ontsnap vandaag gedurende twee keer vijftien minuten aan elke wet waarin jij nu gelooft. Stel je denkgeest open en rust. Aan de wereld die jou gevangen schijnt te houden, kan iedereen ontsnappen die er niet aan is verknocht. Neem alle waarde terug die jij aan haar povere aanbiedingen en onzinnige geschenken hebt gehecht, en laat de gave van God ze allemaal vervangen.Roep je Vader aan, in de zekerheid dat Zijn Stem zal antwoorden. Hijzelf heeft dit beloofd. En Hijzelf zal een vonk van waarheid in je denkgeest plaatsen, overal waar jij een onjuiste overtuiging of een duister waanbeeld van je eigen werkelijkheid en van wat liefde betekent, opgeeft. Hij zal vandaag door je loze gedachten heenstralen en je helpen de waarheid van de liefde te begrijpen. In liefdevolle mildheid zal Hij bij jou verblijven, wanneer je Zijn Stem toestaat om aan je schone en open denkgeest de betekenis van liefde te leren. En Hij zal de les met Zijn Liefde zegenen.Vandaag vallen de talloze toekomstige jaren van wachten op de verlossing weg tegenover de tijdloosheid van wat jij leert. Laten wij vandaag dankzeggen dat ons een toekomst zoals het verleden blijft bespaard. Vandaag laten we het verleden achter ons, om het voorgoed te vergeten. En we slaan onze ogen op naar een ander heden, waarin een toekomst daagt die in elk opzicht van het verleden verschilt.Deze prille wereld is als een pasgeboren kind. En wij zullen haar in gezondheid en kracht zien groeien om haar zegen uit te stralen over allen die komen leren de wereld aan de kant te zetten waarvan zij dachten dat die was gemaakt in haat om de vijand van de liefde te zijn. Nu zijn zij allen samen met ons bevrijd. Nu zijn zij allen onze broeders in Gods Liefde.We zullen de hele dag door aan hen denken, omdat we geen deel van onszelf kunnen uitsluiten van onze liefde als we ons Zelf willen kennen. Denk minstens drie keer per uur aan iemand die de reis met jou maakt en gekomen is om te leren wat jij leren moet. En zodra hij in je gedachten opkomt, geef hem dan deze boodschap van jouw Zelf:Ik zegen jou, broeder, met de Liefde van God, die ik met jou delen wil.Want ik wil de vreugdevolle les leren dat er geen liefde is dan die van God, van jou, van mij, van iedereen.

Elke dag kijken er miljoenen mensen naar de ontelbare Nederlandse talkshows. De formule is overal ongeveer hetzelfde. Een tafel met gasten die praten over het nieuws. TV-recensent Amber Wiznitzer is gefascineerd door het format van praatprogramma's. Aan de hand van fragmenten laat ze zien hoe onze talkshows werken. En wat daarvan het effect is op de kijker.Gast: Amber WiznitzerPresentatie: Bram Endedijk Redactie: Cas ReijndersMontage: Gal Tsadok-HaiEindredactie: Nina van HattumCoördinatie: Elze van DrielProductie: Andrea HuntjensHeb je vragen, suggesties of ideeën over onze journalistiek? Mail dan naar onze redactie via podcast@nrc.nl.Zie het privacybeleid op https://art19.com/privacy en de privacyverklaring van Californië op https://art19.com/privacy#do-not-sell-my-info.

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 slides, and complete CME/MOC/NCPD/AAPA information, and to apply for credit, please visit us at PeerView.com/BRK865. CME/MOC/NCPD/AAPA credit will be available until April 29, 2026.Exploring the Promise of Biomarkers and ATTs in Diagnosing and Treating Early Symptomatic Alzheimer's Disease: Key Takeaways From AD/PD 2025 and AAN 2025 In support of improving patient care, 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 slides, and complete CME/MOC/NCPD/AAPA information, and to apply for credit, please visit us at PeerView.com/BRK865. CME/MOC/NCPD/AAPA credit will be available until April 29, 2026.Exploring the Promise of Biomarkers and ATTs in Diagnosing and Treating Early Symptomatic Alzheimer's Disease: Key Takeaways From AD/PD 2025 and AAN 2025 In support of improving patient care, 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 slides, and complete CME/MOC/NCPD/AAPA information, and to apply for credit, please visit us at PeerView.com/BRK865. CME/MOC/NCPD/AAPA credit will be available until April 29, 2026.Exploring the Promise of Biomarkers and ATTs in Diagnosing and Treating Early Symptomatic Alzheimer's Disease: Key Takeaways From AD/PD 2025 and AAN 2025 In support of improving patient care, 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 slides, and complete CME/MOC/NCPD/AAPA information, and to apply for credit, please visit us at PeerView.com/BRK865. CME/MOC/NCPD/AAPA credit will be available until April 29, 2026.Exploring the Promise of Biomarkers and ATTs in Diagnosing and Treating Early Symptomatic Alzheimer's Disease: Key Takeaways From AD/PD 2025 and AAN 2025 In support of improving patient care, 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 slides, and complete CME/MOC/NCPD/AAPA information, and to apply for credit, please visit us at PeerView.com/BRK865. CME/MOC/NCPD/AAPA credit will be available until April 29, 2026.Exploring the Promise of Biomarkers and ATTs in Diagnosing and Treating Early Symptomatic Alzheimer's Disease: Key Takeaways From AD/PD 2025 and AAN 2025 In support of improving patient care, 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 slides, and complete CME/MOC/NCPD/AAPA information, and to apply for credit, please visit us at PeerView.com/BRK865. CME/MOC/NCPD/AAPA credit will be available until April 29, 2026.Exploring the Promise of Biomarkers and ATTs in Diagnosing and Treating Early Symptomatic Alzheimer's Disease: Key Takeaways From AD/PD 2025 and AAN 2025 In support of improving patient care, 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

Wie beelden van de bevrijding oproept denkt aan grote mensenmassa's met vlaggetjes in de hand, colonnes met legervoertuigen en soldaten door de straten en vooral grote blijdschap verlost te zijn van bezetter Nazi-Duitsland. Maar in die meidagen van 1945 gebeurde er veel meer dan dat. De blik op dat deel van de bevrijding is in de afgelopen 80 jaar flink uitgebreid. In Podcast De Dag historicus Tijmen Dokter over de andere kant van de bevrijding. Aan de hand van drie ooggetuigen vertelt hij hoe bijvoorbeeld Joden werden opgevangen na de verschrikkingen die ze meemaakten in de concentratiekampen. Tot in de jaren '60 was er geen oog voor hun leed. Nu komen de verhalen van collaborateurs steeds vaker naar boven, door het openstellen van archieven en mensen die in hun eigen familiegeschiedenis duiken. Dat noemt Dokter goed: ook het perspectief van hen is belangrijk om te vertellen voor de hele maatschappij. Reageren: mail naar dedag@nos.nl Presentatie en montage: Marco Geijtenbeek Redactie: Judith van de Hulsbeek

Huis verkopen, hut kopen en wonen op een cruiseschip. Hoe ziet je leven er dan uit? Aan boord van de Odyssey: „Ik kan me terugtrekken als ik alleen wil zijn.”Gast: Merel ThieStem: Nienke BrinkhuisRedactie: Rogier van ‘t HekMontage: Jan Paul de BondtCoördinatie: Elze van DrielHeb je vragen, suggesties of ideeën over onze journalistiek? Mail dan naar onze redactie via podcast@nrc.nlZie het privacybeleid op https://art19.com/privacy en de privacyverklaring van Californië op https://art19.com/privacy#do-not-sell-my-info.

Aan tafel deze week: Schrijver Arnon Grunberg, hoogleraar Oorlogsrechtsherstel Liesbeth Zegveld, oud-diplomaat Tessa Terpstra, defensiespecialist en hoogleraar Internationale Politiek Carlo Masala  Presentatie: Twan Huys  Wil je meer weten over de gasten in Buitenhof? Op onze website vind je meer informatie. Daar kan je deze aflevering ook terugkijken en je vindt er natuurlijk nog veel meer gesprekken:   Lees meer: https://bit.ly/buitenhof-4-mei-25 

Motorsport: Lando Norris van McLaren hou vol hy is nie bekommerd dat sy spanmaat, Oscar Piastri, die voortou geneem het as nuwe leier in die bestuurderskampioenskap nie. Die Brit het die seisoen se eerste wedren in Australië gewen, terwyl Piastri daarna drie oorwinnings behaal het. Aan die vooraand van hierdie naweek se Miami Grand Prix, is die Australiër nou tien punte voor in die kampioenskap. Norris sê die span werk hard om hom meer gemaklik met die motor te maak:

Aan de vooravond van Dodenherdenking en Bevrijdingsdag herdenken we niet alleen, maar herkennen ook. Dat is leerzaam, maar ook confronterend. Het boek De tien van Den Haag van Stephan Steinmetz is dat zeker in tijden dat ambtenaren worstelen met vragen van loyaliteit. In Amerika bij de omgang met de regering-Trump. En ook in eigen land met vragen over controversieel beleid.Jaap Jansen en PG Kroeger praten met Stephan Steinmetz over de belevenissen van de tien hoogste ambtenaren op de Haagse ministeries toen in mei 1940 Nazi-Duitsland Nederland binnenviel en al na enkele dagen dwong tot capitulatie.***Deze aflevering is mede mogelijk gemaakt met donaties van luisteraars die we hiervoor hartelijk danken. Word ook vriend van de show!Deze aflevering bevat een advertentie van Lendahand.com - gebruik de code betrouwbarebronnen500 bij je eerste investering (geldig t/m 31 mei 2025)Heb je belangstelling om in onze podcast te adverteren of ons te sponsoren? Zend een mailtje naar adverteren@dagennacht.nl en wij zoeken contact.Op sommige podcast-apps kun je niet alles lezen. De complete tekst plus linkjes en een overzicht van al onze eerdere afleveringen vind je hier***Ineens stonden de secretarissen-generaal moederziel alleen, zonder gezamenlijke beleidslijn. Met een naar Londen gevluchte regering die radeloos was en met een vijandige overwinnaar die scherp had afgewogen hoe de Nederlanders te paaien en te onderwerpen. "Maak er het beste van", zei minister Pieter Sjoerds Gerbrandy bij het afscheid tegen zijn SG.Steinmetz vertelt met rijke details hoe de ambtelijke top niet alleen een eigen werkwijze moest vinden - die was er voorheen nauwelijks - maar ook moest leren omgaan met een bezetter die geheel anders te werk ging dan waar men zozeer voor gevreesd werd. Een merkwaardige mengeling van opluchting, daadkracht, argwaan en onbestemde vrees nam de overhand. En stiekem waren 'de tien' zelfs blij dat ze zonder ministers, parlement, verdeelde partijen en verzuilde polder nu eens flink en 'modern' aan de slag konden.Adolf Hitler wilde ‘het Germaanse broedervolk' paaien en de Nederlandse economie inzetten voor zijn oorlogsmachine. Steinmetz laat zien hoe bij alle geruststellend klinkende boodschappen - ook over 'het Jodenvraagstuk'- al in de zomer van 1940 doelgericht werd gewerkt aan de voorbereiding van het maatschappelijk isolement en de ondergang van Joden - ook in Nederland.De tien SG's kozen daarbij voor een lijn van formele samenwerking met de bezetter, om bestuur, economie en grondwettelijke rechten zoveel mogelijk overeind te houden. En ze ontdekten dat ze met de bezetter - onder leiding van Hitlers 'stadhouder' Arthur Seyss-Inquart - één doel deelden: NSB'ers zoveel mogelijk buiten de deur houden.Zo probeerden ze vanuit een defensieve houding te doen wat de vader van Jan de Koning zijn tienerzoon destijds voorhield: 'het onderscheid tussen een greppel en de laatste gracht' in de gaten houden. Dat ze zich met hun houding op ‘een hellend vlak' begaven, beseften sommigen al aan het begin van de bezetting. Anderen hielden zich vast aan hun drijfveer ‘erger te voorkomen'. De sterke man onder de SG's, Hans Hirschfeld, noemde het de principiële keuze tussen 'Gesinnungsethik' en 'Verantwortungsethik', naar de terminologie van Max Weber.Een manier om de dialoog met Seyss-Inquart en zijn staf gaande te houden was het niet agenderen van mogelijke conflictstof, maar wel formele protesten uiten als het niet anders kon. Daarna poogden ze de scherpe kantjes eraf te halen, vaak met procedurele trucjes. Toen Joodse Nederlanders geen parken meer mochten bezoeken, ontstond een hele discussie over de definitie van 'een park'.Intussen kaapte de bezetter een perfectionistisch ambtelijk project dat het mogelijk maakte iedere inwoner nauwkeurig te identificeren en registreren. Stephan Steinmetz laat zien hoe naïef professionalisme, cowboygedrag en gebrek aan toezicht vanuit de top rampzalige gevolgen kreeg.Ondertussen droegen veel Nederlanders op de verjaardag van prins Bernhard een anjer – als stil protest. De aanhankelijkheid aan het Oranjehuis deed Nazi-propagandachef Joseph Goebbels tijdens een bezoek aan Den Haag in woede ontsteken. Steinmetz vertelt buitengewoon beeldend van een confrontatie tussen Hermann Göring en opperbevelhebber Winkelman.De NSB buiten de deur houden lukte uiteindelijk niet. Allengs werden Duitsgezinde SG's in vacatures benoemd. Toch probeerden de resterenden van de oorspronkelijke tien ook met hen erbij het land draaiende te houden. De bezetter besefte dat met name Hirschfeld onmisbaar was voor de economische situatie en de loyaliteit van het bedrijfsleven.Hoogst opmerkelijk - en verrassend actueel - is hoe hij de land- en tuinbouw drastisch aanpakte om mogelijke hongersnood te voorkomen. Niet minder hoe hij zo nodig bruut de confrontatie zocht als geweld dreigde, bijvoorbeeld bij een mijnstaking. "Wilt u kolen of lijken?" zei hij ijskoud tegen de generaals.Na de bevrijding werden de SG's vooral beoordeeld op wat zij hadden gedaan om 'het verzet' te helpen. Dat zij hun taak zagen als 'erger voorkomen', de NSB tegenhouden en 'het land draaiende houden' werd minder zwaar gewogen.Des te opvallender is dat de regering na 1945 Hirschfeld toch hoge posten bleef gunnen. Impliciet besefte men blijkbaar dat "Maak er het beste van" het enige was, dat hem en zijn collega's was meegegeven in onmogelijke omstandigheden.***Verder luisteren322 - 30 januari 1933, een fatale dag voor Duitsland en de wereld105 - Dagelijks leven in Nazi-Duitsland478 - Was Hitler een socialist?314 - Prins Heinrich XIII en het verlangen naar een autoritair Duisland385 - Jan de Koning en het verschil tussen een greppel en de laatste gracht479 - Winston Churchill. Staatsman. Redenaar. Excentriekeling.32 - Churchill en Europa: biografen Andrew Roberts en Felix Klos (vanaf 1 uur 3)300 - Ethische politiek: het bijzondere Nederland met zijn 'moreel hoogstaande opvattingen'441 - Extra zomeraflevering: boekenspecial! (oa over de secretarissen-generaal)186 - Hoe je een ministerie bestuurt, terreur bestrijdt en Poetin op je dak krijgt: Tjibbe Joustra over crisis en controle120 - Roel Bekker: Waarom bij de overheid dingen zo vaak fout gaan489 – Trump, Musk en de aanval op de privacy408 – FBI-chef J. Edgar Hoover, de machtigste ambtenaar van Amerika208 - Max Weber: wetenschap als beroep en politiek als beroep200 - De Heerser: Machiavelli's lessen zijn nog altijd actueel***Tijdlijn00:00:00 – Deel 100:52:00 – Deel 201:38:00 – Deel 302:00:51 – Einde Zie het privacybeleid op https://art19.com/privacy en de privacyverklaring van Californië op https://art19.com/privacy#do-not-sell-my-info.

In de ontmoeting tussen Jezus en Zacheüs ontdekken we de kracht van vergeving. Een rijke tollenaar, door zijn zonden buiten de gemeenschap geplaatst, wordt door genade een nieuw mens. Vergeving herstelt relaties: Aan wie moet jij nog toegeven dat je fouten hebt gemaakt?

Aan de voet van de Pyreneeën, waar bergen het Baskenland omarmen en de wind verhalen van trots en verzet meedraagt, ligt een club die weigert mee te draaien in het circus van miljoenen. Athletic Club is geen gewone voetbalclub. Het is een overtuiging. Een manier van leven. Waar elders met dollars wordt gebouwd, timmert men in Bilbao met bloed, grond en geschiedenis.Sinds 1912 wordt hier een ongekende regel nageleefd: alleen wie Baskisch is — door geboorte of door opvoeding — mag het rood-witte shirt dragen. Geen uitzondering, geen uitvlucht. Geen buitenlandse blikvangers, maar jongens uit de buurt. Geen wereldsterren gekocht, maar karakters gekweekt. In Lezama, een bescheiden trainingscomplex net buiten de stad, wordt voetbal geen truc, maar een traditie.De gevolgen? Een kleinere vijver om uit te vissen. Een hogere druk op elke generatie. Maar ook: een team dat meer is dan een elftal. Het is familie. Van Muniain tot Simón, van Laporte tot Nico Williams — elk van hen is geen product, maar erfgoed. En als de tribunes van San Mamés zingen, dan zingen ze voor zichzelf. Voor zonen van hun eigen grond.De wereld is veranderd. Clubs vervellen elk jaar tot nieuwe versies van zichzelf. Maar Athletic Club bleef zichzelf. Zelfs toen geld lonkte, sterren vertrokken, en de trofeeën uitbleven. Zelfs toen Real Sociedad het opgaf, hield Bilbao vast. Want hier wint niet alleen het team — hier wint het principe.Sommige clubs kopen geschiedenis. Athletic Club schrijft het, generatie na generatie. En zolang het Baskenland ademt, zal het rood-wit van Bilbao nooit te koop zijn. Want sommige voetbalverhalen zijn te heilig om te verkopen.In de podcast verwijzen Bart en Neal naar:Het artikel op VI PRO van Jan Willem Spaans over Athletic Club: https://www.vi.nl/pro/az-opponent-athletic-doet-alles-anders-ons-werk-begint-als-spelers-negen-jaar-zijnZie het privacybeleid op https://art19.com/privacy en de privacyverklaring van Californië op https://art19.com/privacy#do-not-sell-my-info.

Je krijgt een doorbakken steak op je bord, terwijl je vroeg om een rode, een wijn die naar kattenpies ruikt, of het gerecht van je buurman. Mag je dan klagen? Teun en Yvette vinden van wel - maar wél op de juiste manier. Hoe breng je een klacht? Aan wie? En op welk moment? Je hoort het in Etenstijd!Tips:Gidi Heesakkers over klagenProductie: Meer van ditMuziek: Keez GroentemanWil je adverteren in deze podcast? Stuur een mailtje naar: Adverteerders (direct): adverteren@meervandit.nl(Media)bureaus: adverteren@bienmedia.nl Hosted on Acast. See acast.com/privacy for more information.

Papilledema describes optic disc swelling (usually bilateral) arising from raised intracranial pressure. Due to its serious nature, there is a fear of underdiagnosis; hence, one major stumbling points is correct identification, which typically requires a thorough ocular examination including visual field testing. In this episode, Kait Nevel, MD speaks with Susan P. Mollan, MBChB, PhD, FRCOphth, author of the article “Papilledema” in the Continuum® April 2025 Neuro-ophthalmology issue. Dr. Nevel is a Continuum® Audio interviewer and a neurologist and neuro-oncologist at Indiana University School of Medicine in Indianapolis, Indiana. Dr. Mollan is a professor and neuro-ophthalmology consultant at University Hospitals Birmingham in Birmingham, United Kingdom. Additional Resources Read the article: Papilledema Subscribe to Continuum®: shop.lww.com/Continuum Earn CME (available only to AAN members): continpub.com/AudioCME Continuum® Aloud (verbatim audio-book style recordings of articles available only to Continuum® subscribers): continpub.com/Aloud More about the American Academy of Neurology: aan.com Social Media facebook.com/continuumcme @ContinuumAAN Host: @IUneurodocmom Guest: @DrMollan 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 Nevel: Hello, this is Dr Kait Nevel. Today I'm interviewing Dr Susan Mollan about her article Papilledema Diagnosis and Management, which appears in the April 2025 Continuum issue on neuro-ophthalmology. Susie, welcome to the podcast, and please introduce yourself to our audience. Dr Mollan: Thank you so much, Kait. It's a pleasure to be here today. I'm Susie Mollan, I'm a consultant neuro-ophthalmologist, and I work at University Hospitals Birmingham- and that's in England. Dr Nevel: Wonderful. So glad to be talking to you today about your article. To start us off, can you please share with us what you think is the most important takeaway from your article for the practicing neurologist? Dr Mollan: I think really the most important thing is about examining the fundus and actually trying to visualize the optic nerves. Because as neurologists, you're really acutely trained in examining the cranial nerves, and often people shy away from looking at the eyes. And it can give people such confidence when they're able to really work out straightaway whether there's going to be a problem or there's not going to be a problem with papilledema. And I guess maybe a little bit later on we can talk about the article and tips and tricks for looking at the fundus. But I think that would be my most important thing to take away. Dr Nevel: I'm so glad that you started with that because, you know, that's something that I find with trainees in general, that they often find one of the more daunting or challenging aspects of learning, really, how to do an excellent neurological exam is examining the fundus and feeling confident in diagnosing papilledema. What kind of advice do you give to trainees learning this skill? Dr Mollan: So, it really is practice and always carrying your ophthalmoscope with you. There's lots of different devices that people can choose to buy. But really, if you have a direct ophthalmoscope, get it out in the ward, get it out in clinic. Look at those patients that you'd know have alternative diagnosis, but it gives you that practice. I also invite everybody to come to the eye clinic because we have dilated patients there all the time. We have diabetic retinopathy clinics, and it makes it really easy to start to acquire those skills because I think it's very tricky, because you're getting a highly magnified view of the optic nerve and you've got to sort out in your head what you're actually looking at. I think it's practice. and then use every opportunity to really look at the fundus, and then ask your ophthalmology colleagues whether you can go to clinic. Dr Nevel: Wonderful advice. What do you think is most challenging about the evaluation of papilledema and why? Dr Mollan: I think there are many different aspects that are challenging, and these patients come from lots of different areas. They can come from the family doctor, they can come from an optician or another specialist. A lot of them can have headache. And, as you know, headache is almost ubiquitous in the population. So, trying to pull out the sort of salient symptoms that can go across so many different conditions. There's nothing that's pathognomonic for papilledema other than looking at the optic nerves. So, I think it's difficult because the presentation can be difficult. The actual history can be challenging. There are those rare patients that don't have headache, don't have pulsatile tinnitus, but can still have papilledema. So, I think it- the most challenging thing is actually confirming papilledema. And if you're not able to confirm it, getting that person to somebody who's able to help and confirm or refute papilledema is the most important thing. Dr Nevel: Yeah, right. Because you talk in your article the importance of distinguishing between papilledema and some other diagnoses that can look like papilledema but aren't papilledema. Can you talk about that a little bit? Dr Mollan: Absolutely. I think in the article it's quite nice because we were able to spend a bit of time on a big table going through all the pseudopapilledema diagnoses. So that includes people with shortsightedness, longsightedness, people with optic nerve head drusen. And we've been very fortunate in ophthalmology that we now have 3D imaging of the optic nerve. So, it makes it quite clear to us, when it's pseudopapilledema, it's almost unfair when you're using the direct ophthalmoscope that you don't get a cross sectional image through that optic nerve. So, I'd really sort of recommend people to delve into the article and look at that table because it nicely picks out how you could pick up pseudopapilledema versus papilledema. Dr Nevel: Perfect. In your article, you also talk about what's important to think about in terms of causes of papilledema and what to evaluate for. Can you tell us, you know, when you see someone who you diagnose with papilledema, what do you kind of run through in terms of diagnostic tests and things that you want to make sure you're evaluating for or not missing? Dr Mollan: Yeah. So, I think the first thing is, is once it's confirmed, is making sure it's isolated or whether there's any additional cranial nerve palsies. So that might be particularly important in terms of double vision and a sixth nerve palsy, but also not forgetting things like corneal sensation in the rest of the cranial nerves. I then make sure that we have a blood pressure. And that sounds a bit ridiculous in this day and age because everybody should have a blood pressure coming to clinic or into the emergency room. But sometimes it's overlooked in the panic of thinking, gosh, I need to investigate this person. And if you find that somebody does have malignant hypertension, often what we do is we kind of stop the investigational pathway and go down the route of getting the medics involved to help with lowering the blood pressure to a safe level. I would then always think about my next thing in terms of taking some bloods. I like to rule out anemia because anemia can coexist in a lot of different conditions of raised endocranial pressure. And so, taking some simple blood such as a complete blood count, checking the kidney function, I think is important in that investigational pathway. But you're not really going to stop there. You're going to move on to neuroimaging. It doesn't really matter what you do, whether you do a CT or an MRI, it's just getting that imaging pretty much on the same day as you see the patient. And the key point to that imaging is to do venography. And you want to rule out a venous sinus thrombosis cause that's the one thing that is really going to cause the patient a lot of morbidity. Once your neuroimaging is secure and you're happy, there's no structural lesion or a thrombosis, it's then reviewing that imaging to make sure it's safe to proceed with lumbar puncture. And so, we would recommend the lumbar puncture in the left lateral decubitus position and allowing the patient to be as calm and relaxed as possible to be able to get that accurate opening pressure. Once we get that, we can send the CSF for contents, looking for- making sure they don't have any signs of meningitis or raised protein. And then, really, we're at that point of saying, you know, we should have a secure diagnosis, whether it would be a structural lesion, venous sinus thrombosis, or idiopathic intracranial hypertension. Dr Nevel: Wonderful. Thank you for that really nice overview and, kind of, diagnostic pathway and stepwise thought process in the evaluations that we do. There are several different treatments for papilledema that you go through in your article, ranging from surgical to medication options. When we're taking care of an individual patient, what factors do you use to help guide you in this decision-making process of what treatment is best for the patient and how urgent treatment is? Dr Mollan: I think that's a really important question because there's two things to consider here. One is, what is the underlying diagnosis? Which, hopefully, through the investigational save, you'll have been able to achieve a secure diagnosis. But going along that investigational pathway, which determines the urgency of treatment, is, what's happening with the vision? If we have somebody where we're noting that the vision is affected- and normally it's actually through a formal visual field. And that's really challenging for lots of people to get in the emergency situation because syndromes of raised endocranial pressure often don't cause problems with the visual acuity or the color vision until it's very late. And also, you won't necessarily get a relative afferent papillary defect because often it's bilateral. So I really worry if any of those signs are there in somebody that may have papilledema. And so, a lot rests on that visual field. Now, we're quite good at doing confrontational visual fields, but I would say that most neurologists should be carrying pins to be able to look at the visual fields rather than just pointing fingers and quadrants if you're not able to get a formal visual field early. It's from that I would then determine if the vision is affected, I need to step up what I'm going to do. So, I think the sort of next thing to think about is that sort of vision. So, if we have somebody who, you know, you define as have severe sight loss at the point that you're going through this investigational pathway, you need to get an ophthalmologist or a neuro-ophthalmologist on board to help discuss either the surgery teams as to whether you need to be heading towards an intervention. And there are a number of different types of intervention. And the reason why we discuss it in the article---and we'll also be discussing it in a future issue of Continuum---is there's not high-class evidence to suggest one surgery over another surgery. We may touch on this later. So, we've got our patients with severe visual loss who we need to do something immediately. We may have people where the papilledema is moderate, but the vision isn't particularly affected. They may just have an enlarged blind spot. For those patients, I think we definitely need to be thinking about medical therapy and talking to them about what the underlying cause is. And the commonest medicine to use for raised endocranial pressure in this setting is acetazolamide, a carbonic anhydrous inhibitor. And I think that should be started at the point that you believe somebody has moderate papilledema, with a lot of discussion around the side effects of the medicine that we go into the article and also the fact that a lot of our patients find acetazolamide in an escalating dose challenging. There are some patients with very mild papilledema and no visual change where I might say, hey, I don't think we need to start treatment immediately, but you need to see somebody who understands your disease to talk to you about what's going on. And generally, I would try and get somebody out of the emergency investigational pathway and into a formal clinic as soon as possible. Dr Nevel: Thank you so much for that. One thing that I was wondering that we see clinically is you get a consult for a patient, maybe, who had an isolated episode of vertigo, back to their normal self, completely resolved… but incidentally, somebody ordered an MRI. And that MRI, in the report, it says partially empty sella, slight flattening of the posterior globe, concerns for increased intracranial pressure. What should we be doing with these patients who, you know, normal neurological exam, maybe we can't detect any definite papilledema on our endoscopic exam. What do you think the appropriate pathway is for those patients? Dr Mollan: I think it's really important. The more neuroimaging that we're doing, we're sort of seeing more people with signs that are we don't believe are normal. So, you've mentioned a few, the sort of partially empty sella, empty sella, tortuosity of the optic nerves, flattening of the globes, changes in transverse sinus. And we have quite a nice, again, table in the article that talks about these signs. But they have really low sensitivity for a diagnosis of raised endocranial pressure and isolation. And so, I think it's about understanding the context of which the neuroimaging has been taken, taking a history and going back and visiting that to make sure that they don't have escalating headache. And also, as you said, rechecking the eye nerves to make sure there's no papilledema. I think if you have a good examination with the direct ophthalmoscope and you determine that there's no papilledema, I would be confident to say there's no papilledema. So, I don't think they need to necessarily cry doubt. The ophthalmology offices, we certainly are having quite a few additional referrals, particularly for this, which we kind of called IIH-RAD, where patients are coming to us for this exclusion. And I think, in the intervening time, patients can get very anxious about having a sort of MRI artifact picked up that may necessarily mean a different diagnosis. So, I guess it's a little bit about reassurance, making sure we've taken the appropriate history and performed the examination. And then knowing that actually it's really a number of different signs that you need to be able to confidently diagnose raised ICP, and also the understanding that sometimes when people have these signs, if the ICP reduces, those signs remain. You know, we're learning an awful lot more about MRI imaging and what's normal, what's within normal limits. So, I think reassurance and sensible medical approach. Dr Nevel: Absolutely. In the section in your article on idiopathic intracranial hypertension, you spend a little bit of time talking about how important it is that we sensitively approach the topic of potential weight loss for those patients who are overweight. How do you approach that discussion in your clinic? Because I think it's an important part of the holistic patient care with that condition. Dr Mollan: I think this is one of the things that we've really listened to the patients about over the last number of years where we recognize that in an emergency situation, sometimes we can be quite quick to sort of say, hey, you have idiopathic endocranial hypertension and weight loss is, you know, the best treatment for the condition. And I think in those circumstances, it can be quite distressing to the patient because they feel that there's a lot of stigma attached around weight management. So, we worked with the patient group here at IIH UK to really come up with a way of a signposting to our patients that we have to be honest that there is a link, you know, a strong evidence that weight gain and body shape change can cause someone to fall into a diagnosis of IIH. And we know that weight loss is really effective with this condition. So, I think where I've learned from the patients is trying to use language that's less stigmatizing. I definitely signpost that I'm going to talk about something sensitive. So, I say I'm going to talk about something sensitive and I'm going to say, do you know that this condition is related to body shape change? And I know that if I listen to this podcast in a couple of years, I'm sure my words will have changed. And I think that's part of the process, is learning how to speak to people in an ever-changing language. And they think that sort of signpost that you're going to talk about something sensitive and you're going to talk about body shape change. And then follow up with, are you OK with me talking about this now? Is it something you want to talk about? And the vast majority of people say, yes, let's talk about it. There'll be a few people that don't want to talk about it. And I usually come in quite quickly, say, is it OK if I mention it at the next consultation? Because we have a duty of care to sort of inform our patients, but at the same time we need to take them on that journey to get them back to health, and they need to be really enlisted in that process. Dr Nevel: Yeah, I really appreciate that. These can be really difficult conversations and uncomfortable conversations to have that are really important. And you're right, we have a duty as medical providers to have these conversations or inform our patients, but the way that we approach it can really impact the way patients perceive not only their diagnosis, but the relationship that we have with our patients. And we always want that to be a positive relationship moving forward so that we can best serve our patients. Dr Mollan: I think the other thing as well is making sure that you've got good signposts to the professionals. And that's what I say, because people then say to me, well, you know, kind of what diet should I be on? What should I be doing? And I say, well, actually, I don't have professional experience with that. I'm, I'm very fortunate in my hospital, I'm able to send patients to the endocrine weight management service. I'm also able to send patients to the dietetic service. So, it's finding, really, what suits the patient. Also what's within licensing in your healthcare system to be able to provide. But not being too prescriptive, because when you spend time with weight management professionals, they'll tell you lots of different things about diets that people have championed and actually, in randomized controlled trials, they haven't been effective. I think it's that signpost really. Dr Nevel: Yeah, absolutely. So, could you talk a little bit about what's going on in research in papilledema or in this area, and what do you think is up-and-coming? Dr Mollan: I think there's so much going on. Mainly there's two parts of it. One is image analysis, and we've had some really fantastic work out of the Singapore group Bonsai looking at a machine learning decision support tool. When people take fundal pictures from a normal fundus camera, they're able to say with good certainty, is this papilledema, is this not papilledema? But more importantly, if you talk to the investigators, something that we can't tell when we look in is they're able to, with quite a high level of certainty, say, well, this is base occupying lesion, this is a venous sinus thrombosis, and this is IIH. And you know, I've looked at thousands and thousands of people's eyes and that I can't tell why that is. So, I think the area of research that is most exciting, that will help us all, is this idea about decision support tools. Where, in your emergency pathway, you're putting a fundal camera in that helps you be able to run the image, the retina, and also to try and work out possibly what's going on. I think that's where the future will go. I think we've got many sort of regulatory steps and validation and appropriate location of a learning to go on in that area. So, that's one side of the imaging. I think the other side that I'm really excited about, particularly with some of the work that we've been doing in Birmingham, is about treatment. The surgical treatments, as I talked about earlier… really, there's no high-class evidence. There's a number of different groups that have been trying to do randomized trials, looking at stenting versus shunting. They're so difficult to recruit to in terms of trials. And so, looking at other treatments that can reduce intracranial pressure. We published a small phase two study looking at exenatide, which is a glucagon-like peptide receptor agonist, and it showed in a small group of patients living with IIH that it could reduce the intracranial pressure two and a half hours, twenty-four hours, and also out to three months. And the reason why this is exciting is we would have a really good acute therapy---if it's proven in Phase III trials---for other diseases, so, traumatic brain injury where you have problems controlling ICP. And to be able to do that medically would be a huge breakthrough, I think, for patient care. Dr Nevel: Yeah, really exciting. Looking forward to seeing what comes in the future then. Wonderful. Well, thank you so much for chatting with me today about your article. I really enjoyed learning more from you during our conversation today and from your article, which I encourage all of our listeners to please read. Lots of good information in that article. So again, today I've been interviewing Dr Susie Mollan about her article Papilledema Diagnosis and Management, which appears in the most recent issue of Continuum on neuro-ophthalmology.Please be sure to check out Continuum episodes from this and other issues. And thank you to our listeners for joining us today. Thank you, Susie. Dr Mollan: Thank you so much. 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 deze podcast het tweede deel van het gesprek tussen Bruno, Alex en Bas Nijhuis. Op het erf van de scheidsrechter worden de heren af en toe afgeleid door de vele dieren die er rond lopen, neem bijvoorbeeld Jeroen de pauw of Henk de haan, maar dat zit een goed gesprek niet in de weg.Aan de hand van acht spelsituaties, of eigenlijk ergernissen, van Alex behandelen ze regels, protocollen en verschillen tussen het voetbal in Nederland en het buitenland. Wat gebeurt er? Wat is er afgesproken en hoe ga je ermee om?Een boeiend gesprek, waarin zelfs voor voetbaldier Alex nieuwe dingen te leren vielen.Zie het privacybeleid op https://art19.com/privacy en de privacyverklaring van Californië op https://art19.com/privacy#do-not-sell-my-info.

Wetenschappers gebruiken stamcellen om beter te begrijpen waarom mensen verschillend reageren op ziektes en medicijnen. In het lab helpt een ‘dorp’ van cellen om ziektes na te bootsen en behandelingen te testen – een belangrijke stap richting gepersonaliseerde geneeskunde. In deze aflevering spreekt presentatrice Nina van den Dungen met Joyce van Meurs, hoogleraar populatiegenetica aan het Erasmus MC, en Berend van Meer, medeoprichter van Sync Biosystems. Aan bod komt hoe persoonlijke cellen en genetische verschillen gebruikt kunnen worden om medische behandelingen en medicijnen beter af te stemmen op het individu. Joyce van Meurs is hoofdonderzoeker van het iCELL-project. Daarin worden stamcellen van verschillende mensen opgekweekt tot bijvoorbeeld hersen-, nier- of kraakbeencellen. Zo ontstaat een representatief ‘dorp in een petrischaaltje’ van honderden cellen waarmee onderzoekers kunnen achterhalen waarom bepaalde mensen bijwerkingen krijgen van medicijnen, of juist helemaal niet reageren op een behandeling. Ook biedt het project aanknopingspunten voor een toekomst waarin een ‘DNA-paspoort’ artsen helpt om betere keuzes te maken in de spreekkamer. Berend van Meer werkt aan technologie om de petrischaaltjes in het lab slimmer te maken. Zijn bedrijf ontwikkelt systemen die cellen continu kunnen voeden en prikkelen, waardoor de laboratoriumomgeving meer lijkt op het menselijk lichaam. Hierdoor kunnen onderzoekers nauwkeuriger simuleren hoe medicijnen zich in het lichaam gedragen, bijvoorbeeld bij kinderen met hersenstamkanker. Zo worden modellen in het lab realistischer én betrouwbaarder. Redactie: Stijn GoossensSee omnystudio.com/listener for privacy information.

Aan cijfers geen gebrek. De komende dagen bereikt het cijferseizoen z'n hoogtepunt. Vier van de Magnificent Seven komen met de cijfers, en ook in Nederland komen grote namen zoals Adyen en ASM International langs. Maar echt belangrijk is en blijft Donald Trump, die eindelijk iets te vieren heeft. Hij heeft namelijk de eerste 100 dagen van zijn termijn erop zitten. Voor Han Dieperink van Auréus betekent dat dat ook beleggers iets te vieren hebben. Want volgens hem is de zwaarste periode nu bijna achter de rug. In Beurs in Zicht stomen we je klaar voor de beursweek die je tegemoet gaat. Want soms zie je door de beursbomen het beursbos niet meer. Dat is verleden tijd! Iedere week vertelt een vriend van de show waar jouw focus moet liggen.See omnystudio.com/listener for privacy information.

Vandaag een aflevering in de serie "In Stukken". Die Kunst der Fuge van Johann Sebastian Bach wordt in stukken geknipt. Aan de hand van de fragmenten in de mooiste opnames wordt het stuk onder de loep genomen. Panelleden: fagottist Alban Wesly en klavecinist Tineke Steenbrink.

Aan tafel deze week: Oud-diplomaat Robert Serry, uit Oekraïne Vita Kovalenko, oud-President van de Nederlandsche Bank Nout Wellink, journaliste Sheila Sitalsing  Presentatie: Twan Huys  Wil je meer weten over de gasten in Buitenhof? Op onze website vind je meer informatie. Daar kan je deze aflevering ook terugkijken en je vindt er natuurlijk nog veel meer gesprekken:   https://bit.ly/buitenhof-27-april-25   

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.

Aan tafel deze week: minister van Defensie Ruben Brekelmans, politiekverslaggever Lamyae Aharouay, hoogleraar Alain-Laurent Verbeke, historicus Geert Mak, dat zijn de gasten van #buitenhof op zondag 20 april 2025  Wil je meer weten over de gasten in Buitenhof? Op onze website vind je meer informatie. Daar kan je deze aflevering ook terugkijken en je vindt er natuurlijk nog veel meer gesprekken: https://bit.ly/buitenhof-20-april-2025 

Welcome to the NeurologyLive® Mind Moments® podcast. Tune in to hear leaders in neurology sound off on topics that impact your clinical practice. In this episode, "Sleep and Seizures: Emerging Insights From AAN 2025," Nancy Foldvary-Schaefer, DO, director of the Sleep Disorders Center at Cleveland Clinic, reflected on key sleep-related topics presented at this year's AAN Annual Meeting. She highlighted the growing clinical interest in underrecognized conditions like idiopathic hypersomnia and narcolepsy, stressing the need for better awareness and earlier diagnosis. Foldvary-Schaefer also detailed the development of the Sleep by Cleveland Clinic mobile app, designed to improve screening for common sleep disorders with validated tools and real-time resources. Additionally, she discussed new findings on the prevalence of obstructive sleep apnea in adults with epilepsy, pointing to the importance of routine sleep screening in this population, regardless of seizure severity. Finally, she shared exploratory data on SSRI use and peri-ictal respiratory patterns in epilepsy, offering new perspectives on potential protective mechanisms tied to SUDEP risk. Looking for more neuromuscular discussion? Check out the NeurologyLive® Sleep disorders clinical focus page. Episode Breakdown: 1:00 – Key sleep topics discussed at AAN 2025 and the growing interest in hypersomnia 5:45 – Development and purpose of the SLEEP mobile app by Cleveland Clinic 10:35 – Findings on obstructive sleep apnea prevalence in adults with epilepsy 15:05 – Neurology News Minute 17:10 – The need for sleep disorder screening in epilepsy clinical trials 19:45 – Exploratory findings on SSRI use and respiratory patterns in patients with epilepsy The stories featured in this week's Neurology News Minute, which will give you quick updates on the following developments in neurology, are further detailed here: FDA Approves Pre-Filled Syringe Administration for FcRn Modulator Efgartigimod FDA Approves CT-132 as First Digital Therapeutic for Preventive Treatment of Episodic Migraine FDA Expands Diazepam Nasal Spray Indication to Treat Ages 2 to 5 Thanks for listening to the NeurologyLive® Mind Moments® podcast. To support the show, be sure to rate, review, and subscribe wherever you listen to podcasts. For more neurology news and expert-driven content, visit neurologylive.com.

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

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