Podcasts about Aan

Hey daar lieve luisteraar, Lou hier. Met een uitzending én een uitnodiging voor Miracle Town. We zijn OPEN. Vanaf vandaag kun je gratis aanmelden via deze link: https://miracle-town.mn.co/plans/1863422?bundle_token=bd49565fbc162d60ba81b4ab4b34a5fc&utm_source=manual Het eerste wat geopend is in Miracle Town is het Miracle Town Café. Aan de Community Table kunnen we met elkaar connecten en alle wonderen delen en tracken en tracen. Je hoeft uiteraard niet deel te nemen aan gesprekken, je mag ook meekijken en luisteren en op de achtergrond blijven. In deze uitzending lees ik een stuk uit de ochtendkronkels en kronieken van mijn journal van vanmorgen voor. Over mijn eigen twijfels en hoe het herlezen van God on a Harley me wederom helpt en inspireert. Met 6 commandments waar jij misschien ook iets aan hebt. Zie ik je daarna in Miracle Town? Praat mee in het Miracle Town Café.

While genetic testing has replaced muscle biopsy in the diagnosis of many genetic myopathies, clinical assessment and the integration of clinical and laboratory findings remain key elements for the diagnosis and treatment of muscle diseases. In this episode, Casey Albin, MD, speaks with Margherita Milone, MD, PhD, FAAN, FANA, author of the article “A Pattern Recognition Approach to Myopathy” in the Continuum® October 2025 Muscle and Neuromuscular Junction Disorders issue. Dr. Albin is a Continuum® Audio interviewer, associate editor of media engagement, and an assistant professor of neurology and neurosurgery at Emory University School of Medicine in Atlanta, Georgia. Dr. Milone is a professor of neurology and the director of the Muscle Pathology Laboratory at Mayo Clinic College of Medicine and Science in Rochester, Minnesota. Additional Resources Read the article: A Pattern Recognition Approach to Myopathy Subscribe to Continuum®: shop.lww.com/Continuum Earn CME (available only to AAN members): continpub.com/AudioCME Continuum® Aloud (verbatim audio-book style recordings of articles available only to Continuum® subscribers): continpub.com/Aloud More about the American Academy of Neurology: aan.com Social Media facebook.com/continuumcme @ContinuumAAN Host: @caseyalbin 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 Albin: Hello, this is Dr Casey Albin. Today I'm interviewing Dr Margherita Milone on her article on a pattern recognition approach to myopathy, which appears in the October 2025 Continuum issue on muscle and neuromuscular junction disorders. Welcome to the podcast, Dr Milone. Thank you so much for joining us. I'll start off by having you introduce yourself to our listeners. Dr Milone: Hello Casey, thank you so much for this interview and for bringing the attention to the article on muscle diseases. So, I'm Margherita Milone. I'm one of the neuromuscular neurologists at Mayo Clinic in Rochester. I have been interested in muscle disorders since I was a neurology resident many years ago. Muscle diseases are the focus of my clinical practice and research interest. Dr Albin: Wonderful. Thank you so much. When I think about myopathies, I generally tend to think of three large buckets: the genetic myopathy, the inflammatory myopathies, and then the necrotizing myopathies. Is that a reasonable approach to conceptualizing these myopathies? Dr Milone: Yeah, the ideology of the myopathies can be quite broad. And yes, we have a large group of genetic muscle diseases, which are the most common. And then we have immune-mediated muscle diseases, which include inflammatory myopathies as well as some form of necrotizing myopathies. Then we have some metabolic myopathies, which could be acquired or could be genetic. And then there are muscle diseases that are due to toxins as well as to infection. Dr Albin: Wow. So, lots of different etiologies. And that really struck me about your article, is that these can present in really heterogeneous ways, and some of them don't really read the rule book. So, we have to have a really high level of suspicion, for someone who's coming in with weakness, to remember to think about a myopathy. One of the things that I like to do is try to take us through a little bit of a case to sort of walk us through how you would approach if someone comes in. So, let's say you get, you know, a forty-year-old woman, and she's presenting with several months of progressive weakness. And she says that even recently she's noted just a little bit of difficulty swallowing. It feels to her like things are getting stuck. What are some of the things when you are approaching the history that would help you tease this to a myopathy instead of so many other things that can cause a patient to be weak? Dr Milone: Yes. So, as you mentioned, people who have a muscle disease have the muscle weakness often, but the muscle weakness is not just specific for a muscle disease. Because you can have a mass weakness in somebody who has a neurogenic paralysis. The problem with diagnosis of muscle diseases is that patients with these disorders have a limited number of symptom and sign that does not match the large heterogeneity of the etiology. So, in someone who has weakness, that weakness could represent a muscle disease, could represent an anterior horn cell disease, could represent a defect of neuromuscular junction. The clinical history of weakness is not sufficient by itself to make you think about a muscle disease. You have to keep that in the differential diagnosis. But your examination will help in corroborating your suspicion of a muscle disease. Let's say if you have a patient, the patient that you described, with six months' history of progressive weakness, dysphagia, and that patient has normal reflexes, and the patient has no clinical evidence for muscle fatigability and no sensory loss, then the probability that that patient has a myopathy increases. Dr Albin: Ah, that's really helpful. I'm hearing a lot of it is actually the lack of other findings. In some ways it's asking, you know, have you experienced numbness and tingling? And if not, that's sort of eliminating that this might not be a neuropathy problem. And then again, that fatigability- obviously fatigability is not specific to a neuromuscular junction, but knowing that is a hallmark of myasthenia, the most common of neuromuscular disorders. Getting that off the table helps you say, okay, well, it's not a neuromuscular junction problem, perhaps. Now we have to think more about, is this a muscle problem itself? Are there any patterns that the patients describe? I have difficulty getting up from a chair, or I have difficulty brushing my hair. When I think of myopathies, I historically have thought of, sort of, more proximal weakness. Is that always true, or not so much? Dr Milone: Yeah. So, there are muscle diseases that involve predominantly proximal weakness. For example, the patient you mentioned earlier could have, for example, an autoimmune muscle disease, a necrotizing autoimmune myopathy; could have, perhaps, dermatomyositis if there are skin changes. But a patient with muscle disease can also present with a different pattern of weakness. So, myopathies can lead to this weakness, and foot drop myopathies can cause- can manifest with the weakness of the calf muscles. So, you may have a patient presenting to the clinic who has no the inability to stand on tiptoes, or you may have a patient who has just facial weakness, who has noted the difficulty sealing their lips on the glasses when they drink and experiencing some drooling in that setting, plus some hand weakness. So, the muscle involved in muscle diseases can vary depending on the underlying cause of the muscle disease. Dr Albin: That's really helpful. So, it really is really keeping an open mind and looking for some supporting features, whether it's bulbar involvement, extraocular eye muscle involvement; looking, you know, is it proximal, is it distal? And then remembering that any of those patterns can also be a muscle problem, even if sometimes we think of distal being more neuropathy and proximal myopathy. Really, there's a host of ranges for this. I really took that away from your article. This is, unfortunately, not just a neat way to box these. We really have to have that broad differential. Let me ask another question about your history. How often do you find that patients complain of, sort of, muscular cramping or muscle pain? And does that help you in terms of deciding what type of myopathy they may have? Dr Milone: Many patients with muscle disease have muscle pain. The muscle pain could signal a presence of inflammation in skeletal muscle, could be the result of overuse from a muscle that is not functioning normally. People who have myotonia experience muscle stiffness and muscle pain. Patients who have a metabolic myopathy usually have exercise-induced muscle pain. But, as we know, muscle pain is also very nonspecific, so we have to try to find out from the patient in what setting the pain specifically occurs. Dr Albin: That's really helpful. So, it's asking a little bit more details about the type of cramping that they have, the type of pain they may be experiencing, to help you refine that differential. Similarly, one of the things that I historically have always associated with myopathies is an elevation in the CK, or the creatinine kinase. How sensitive and specific is that, and how do you as the expert sort of take into account, you know, what their CK may be? Dr Milone: So, this is a very good point. And the elevation of creatine kinase can provide a clue that the patient has a muscle disease, but it is nonspecific for muscle disease because we know that elevation of creatine kinase can occur in the setting of a neurogenic process. For example, we can see elevation of the creatine kinase in patients who have ALS or in patients who have spinal muscular atrophy. And in these patients---for example, those with spinal muscular atrophy---the CK elevation can be also of significantly elevated up to a couple of thousand. Conversely, we can have muscle diseases where the CK elevation does not occur. Examples of these are some genetic muscle disease, but also some acquired muscle diseases. If we think of, for example, cases where inflammation in the muscle occurs in between muscle fibers, more in the interstitium of the muscle, that disease may not lead to significant elevation of the CK. Dr Albin: That's super helpful. So, I'm hearing you say CK may be helpful, but it's neither completely sensitive nor completely specific when we're thinking about myopathic disorders. Dr Milone: You are correct. Dr Albin: Great. So, coming back to our patients, you know, she says that she has this dysphasia. How do bulbar involvement or extraocular eye movement involvement, how do those help narrow your differential? And what sort of disorders are you thinking of for patients who may have that bulbar or extraocular muscle involvement? Dr Milone: Regarding dysphagia, that can occur in the setting of acquired myopathies relatively frequent; for example, in inclusion body myositis or in other forms of inflammatory myopathy. Your patient, I believe, was in their forties, so it's a little bit too young for inclusion body myositis. Involvement of the extraocular muscles is usually much more common in genetic muscle diseases and much less frequent in hereditary muscle disease. So, if there is involvement of the extraocular muscles, and if there is a dysphagia, and if there is a proximal weakness, you may think about oculopharyngeal muscular dystrophy, for example. But obviously, in a patient who has only six months of history, we have to pay attention of the degree of weakness the patient has developed since the symptom onset. Because if the degree of weakness is mild, yes, it could still be a genetic or could be an acquired disease. But if we have a patient who, in six months, from being normal became unable to climb stairs, then we worry much more about an acquired muscle disease. Dr Albin: That's really helpful. So, the time force of this is really important. And when you're trying to think about, do I put this in sort of a hereditary form of muscle disease, thinking more of an indolent core, something that's going to be slowly progressive versus one of those inflammatory or necrotizing pathologies, that's going to be a much more quick onset, rapidly progressive, Do I have that right? Dr Milone: In general, the statement is correct. They tend, acquired muscle disease, to have a faster course compared to a muscular dystrophy. But there are exceptions. There have been patients with immune mediated necrotizing myopathy who have been misdiagnosed as having limb-girdle muscular dystrophy just because the disease has been very slowly progressive, and vice versa. There may be some genetic muscle diseases that can present in a relatively fast way. And one of these is a lipid storage myopathy, where some patients may develop subacutely weakness, dysphagia, and even respiratory difficulties. Dr Albin: Again, I'm hearing you say that we really have to have an open mind that myopathies can present in a whole bunch of different ways with a bunch of different phenotypes. And so, keeping that in mind, once you suspect someone has a myopathy, looking at the testing from the EMG perspective and then maybe laboratory testing, how do you use that information to guide your work up? Dr Milone: The EMG has a crucial role in the diagnosis of muscle diseases. Because, as we said earlier, weakness could be the result of muscle disease or other form of neuromuscular disease. If the EMG study will show evidence of muscle disease supporting your diagnostic hypothesis, now you have to decide, is this an acquired muscle disease or is this a genetic muscle disease? If you think that, based on clinical history of, perhaps, subacute pores, it is more likely that the patient has an acquired muscle disease, then I would request a muscle biopsy. The muscle biopsy will look for structural abnormalities that could help in narrowing down the type of muscle disease that the patient has. Dr Albin: That's really helpful. When we're sending people to get muscle biopsies, are there any tips that you would give the listeners in terms of what site to biopsy or what site, maybe, not to biopsy? Dr Milone: This is a very important point. A muscle biopsy has the highest diagnostic yield if it's done in a muscle that is weak. And because muscle diseases can result in proximal or distal weakness, if your patient has distal weakness, you should really biopsy a distal muscle. However, we do not wish to biopsy a muscle that is too weak, because otherwise the biopsy sample will result just in fibrous and fatty connected tissue. So, we want to biopsy a muscle that has mild to moderate weakness. Dr Albin: Great. So, a little Goldilocks phenomenon: has to be some weak, but not too weak. You got to get just the right feature there. I love that. That's a really good pearl for our listeners to take. What about on the flip side? Let's say you don't think it's an acquired a muscular disease. How are you handling testing in that situation? Dr Milone: If you think the patient has a genetic muscle disease, you pay a lot of attention to the distribution of the weakness. Ask yourself, what is the best pattern that represent the patient's weakness? So, if I have a patient who has facial weakness, dysphagia, muscle cramping, and then on examination represent myotonia, then at that point we can go straight to a genetic test for myotonic dystrophy type one. Dr Albin: That's super helpful. Dr Milone: So, you request directly that generic test and wait for the result. If positive, you will have proof that your diagnostic hypothesis was correct. Dr Albin: You're using the genetic testing to confirm your hypothesis, not just sending a whole panel of them. You're really informing that testing based on the patient's pattern of weakness and the exam findings, and sometimes even the EMG findings as well. Is that correct? Dr Milone: You are correct, and ideally, yes. And this is true for certain muscle diseases. In addition to myotonic dystrophy type one, for example, if you have a patient who has fascial scapulohumeral muscular weakness, you can directly request a test for FSHD. So, the characterization of the clinical phenotype is crucial before selecting the genetic test for diagnosis. Dr Albin: Wonderful. Dr Milone: However, this is not always possible, because you may have a patient who has just a limb-girdle weakness, and the limb-girdle weakness can be limb-girdle muscular dystrophy. But we know that there are many, many types of limb-girdle muscular dystrophies. Therefore, the phenotype is not sufficient to request specific genetic tests for one specific form of a limb-girdle muscular dystrophy. And in those cases, more complex next-generation sequencing panels have a higher chance of providing the answer. Dr Albin: Got it, that makes sense. So, sometimes we're using a specific genetic test; sometimes, it is unfortunate that we just cannot narrow down to one disease that we might be looking for, and we may need a panel in that situation. Dr Milone: You are correct. Dr Albin: Fantastic. Well, as we wrap up, is there anything on the horizon for muscular disorders that you're really excited about? Dr Milone: Yes, there are a lot of exciting studies ongoing for gene therapy, gene editing. So, these studies are very promising for the treatment of genetic muscle disease, and I'm sure there will be therapists that will improve the patient's quality of life and the disease outcome. Dr Albin: It's really exciting. Well, thank you again. Today I've been interviewing Dr Margarita Malone on her article on a pattern recognition approach to myopathy, which appears in the October 2025 Continuum issue on muscle and neuromuscular junction disorders. Be sure to check out Continuum Audio episodes from this and other issues, and thank you to our listeners for joining us today. And thank you, Dr Milone. Dr Milone: Thank you, Casey. Very nice chatting with you about this. Dr Monteith: This is Dr Teshamae Monteith, Associate Editor of Continuum Audio. If you've enjoyed this episode, you'll love the journal, which is full of in-depth and clinically relevant information important for neurology practitioners. Use the link in the episode notes to learn more and subscribe. AAN members, you can get CME for listening to this interview by completing the evaluation at continpub.com/audioCME. Thank you for listening to Continuum Audio.

In this episode, editor in chief Joseph E. Safdieh, MD, FAAN, highlights articles about pegivirus's potential role in Parkinson's disease pathology, the impact of GLP-1 receptor agonistst on idiopathic intracranial hypertension, and the geographic spread of epilepsy specialists.

Aan de slag!Ben jij bereid om te veranderen? Gideon moest in het begin dingen doen waar hij niet geliefd om werd. Durf je God te vertrouwen? Als jij hiertoe bereid bent, wil ik je drie tips geven:Spreek uit naar God dat je bereid bent en dat je naar je volle potentie wilt leven;Verzamel mensen om je heen die je achter je staan, je steunen en je laten groeien;Vertrouw God en durf dingen te doen als je denkt dat God dat van je vraagt.Deze overdenking is geschreven door oud-schrijfster Sanne van Heukelum.

De verkiezingen van 29 oktober gaan over de koers en de toekomst van ons land. En dus over het geld dat we daar voor over hebben en hoe dat bijeen gebracht wordt. De rijksfinanciën en de belastingen zijn dan ook een belangrijk politiek thema. Hoe laat het kabinet-Schoof deze achter? Wat is urgent bij inkomsten en uitgaven van de rijksoverheid? Wat is voor de lange termijn essentieel? Weke plannen van de partijen verdienen daarbij aandacht? En welk Tweede-Kamerlid excelleert op dit wezenlijke terrein? Jaap Jansen en PG Kroeger praten hierover met Djoeke Altena, politiek columnist van Weekblad Fiscaal Recht en website TaxLive. *** Deze aflevering is mede mogelijk gemaakt met donaties van luisteraars die we hiervoor hartelijk danken. Word ook vriend van de show! Help mee aan de bloedvoorziening in Nederland, word bloeddonor op sanquin.nl/geef Heb je belangstelling om in onze podcast te adverteren of ons te sponsoren? Zend ons een mailtje en wij zoeken contact. *** Het financiële beeld dat minister Eelco Heinen (Financiën) nalaat na vijftien maanden kabinet-Schoof lijkt op het eerste gezicht niet onaardig. Maar het begrotingstekort schuurt tegen de grens van 3 procent van het bnp aan en gaat er waarschijnlijk overheen. De staatsschuld daalt niet langer maar schiet omhoog, de komende jaren maskeren fantoomdekkingen een ondeugdelijke begroting, terwijl de noodzakelijke investeringen geschrapt zijn voor consumptieve cadeautjes aan de kiezers. Toezichthoudende organisaties - van Rekenkamer tot Europese Commissie - luiden de noodklok. Djoeke Altena waarschuwt: “Het komende kabinet zal voor noodzakelijke investeringen en hersteloperaties veel geld moeten vinden. Dat kunnen de partijen nu in de campagne maar beter eerlijk toegeven." Het komende kabinet moet zich met spoed buigen over dreigende gaten en niet opgeloste problemen, zoals bij de beruchte Box-3, het 'ravijnjaar' dat de gemeenten bedreigt, de Europese meerjarenbegroting en de lange termijn investeringsfondsen. De vijf staatssecretarissen die in ‘Schoof’ met belastingen en toeslagen belast waren, hebben niet veel gedaan - of kunnen doen. Gelukkig gaat het bij de Belastingdienst zelf de goede kant op, meldt Djoeke Altena. Nog even en de dienst kan grote veranderingen weer aan. Er zijn veel fiscale regelingen die niet doen wat ze zouden moeten doen, maar hardnekkig gehandhaafd worden vanwege deelbelangen. Ook Rekenkamerpresident Pieter Duisenberg wees hier al op. Toch is ook hier door Schoofs kabinet slechts €7 miljoen gesaneerd, hoewel volgens deskundigen 35 miljard euro weggesaneerd zou kunnen worden. Snel kan een nieuw kabinet werk maken van betere fiscale rechtsbescherming. Djoeke Altena wijst op initiatieven van Nina Olson – de voormalige Tax Payer Advocate in Amerika - die in ons land inmiddels zijn overgenomen, zoals het Handvest van Rechten en Plichten. Zoiets kost niets, maar heeft veel impact voor burgers. In de komende kabinetsformatie zouden constructieve partijen een coherente, integrale vereenvoudiging van het fiscaal stelsel moeten afspreken. Niet-werkende fiscale regelingen, duidelijkheid over vermogens en erfenissen en lagere lasten op arbeid en duurzame productie en consumptie zijn al gedegen voorbereid, maar tijdens het kabinet-Schoof blijven liggen. Verdere vertraging is erg kostbaar en geeft bedrijven niet de duidelijkheid waar ze naar snakken. Lezend in de verkiezingsprogramma’s ziet Djoeke Altena opmerkelijke plannen. Zo poogt de PVV de boerenachterban van BBB opzichtig te paaien met fiscale cadeaus en wil ze kunstminnaars juist op kosten jagen. De VVD komt met een serie nieuwe wetten die ondernemers en werkenden moeten helpen. Maar de verfoeide regeldruk wordt daarmee allerminst verminderd. Boeiend is dat veel partijen met eigen plannen komen voor afschaffing van de hypotheekrenteaftrek. De fiscaal specialisten in de Kamer kunnen met doordachte compromissen bijdragen aan de noodzakelijke doorbraken op al deze thema's. Hun inzet is groot, maar ze worden zelden geroemd. Djoeke Altena vertelt dat hier verandering in komt. De Bond voor Belastingbetalers zet vanaf nu jaarlijks de meest effectieve en creatieve volksvertegenwoordiger in het zonnetje. Aan het einde van deze aflevering maakt hij namens de Bond bekend wie de eerste laureaat is… *** Verder luisteren 529 – Schoten voor de boeg in de verkiezingscampagne https://omny.fm/shows/betrouwbare-bronnen/529-schoten-voor-de-boeg 525 –Wat Brainport Eindhoven ons leert en hoe we onze economie nóg toekomstbestendiger kunnen maken https://omny.fm/shows/betrouwbare-bronnen/525-wat-brainport-eindhoven-ons-leert-en-hoe-we-onze-economie-n-g-toekomstbestendiger-maken 516 – Files op het elektriciteitsnet: de energietransitie dreigt slachtoffer te worden van het eigen succes https://art19.com/shows/betrouwbare-bronnen/episodes/54ccc73e-4200-4dbc-87c8-213c70e97491 507 - Het strenge oordeel van Rekenkamerpresident Pieter Duisenberg https://art19.com/shows/betrouwbare-bronnen/episodes/19fb3651-29be-49dd-854b-eeb65ec692ff 501 - Den Haag zonder Omtzigt en een Voorjaarsnota zonder beleid https://art19.com/shows/betrouwbare-bronnen/episodes/03d5c905-9a8d-474c-980c-5e8dd7f209a9 493 - Het belastingkaartenhuis wankelt https://art19.com/shows/betrouwbare-bronnen/episodes/8e0d7872-9be8-439b-94cc-911bf8f7509e 426 - Een doodgewoon meerderheidskabinet met een allesbepalende financiële plaat https://art19.com/shows/betrouwbare-bronnen/episodes/efb48549-3266-405e-8a97-ddc3e6b4e486 382 - 250 jaar Verenigde Staten: de Boston Tea Party en de rechtsbescherming van belastingbetalers in Nederland https://art19.com/shows/betrouwbare-bronnen/episodes/c44ec04f-9408-41be-b5e3-3fab8905ab66 291 – De dubbele jaren van staatssecretaris Marnix van Rij https://art19.com/shows/betrouwbare-bronnen/episodes/2ae6cd4c-9054-4d48-8481-b868182cace2 275 - Nina Olson: Waarom Nederland net als de VS een Taxpayer Advocate moet krijgen https://art19.com/shows/betrouwbare-bronnen/episodes/07aa7c05-edf7-4dac-a292-dd8ba7a2a5d1 247 - Belastingheffing in box 3: hoe de Hoge Raad de wetgever op de vingers tikt en opzadelt met een hels karwei https://art19.com/shows/betrouwbare-bronnen/episodes/cd788cd0-6982-444e-901f-f695ea8e2c79/ 147 – De kindertoeslagaffaire: het ging al mis bij de wetgeving https://art19.com/shows/betrouwbare-bronnen/episodes/b08f3ba1-eb89-4740-a5e7-8d3211038a26 17 - Hoe Rekenkamerpresident Arno Visser de overheid controleert https://art19.com/shows/betrouwbare-bronnen/episodes/9052a9fc-235a-493c-aa5f-104e61d25ddd *** Tijdlijn 00:00:00 – Deel 1 00:29:24 – Deel 2 01:02:15 – deel 3 01:24:13 – Einde See omnystudio.com/listener for privacy information.

Aan de slag!Dus, hoe pak je het aan, iets loslaten wat zowat aan je eigen handen zit vastgelijmd?Eerlijk? Ik vind weinig moeilijker dan dat. Het voelt onnatuurlijk om het uit handen te geven. Maar hoe langer je iets vasthoudt, hoe meer het zich nestelt en hoe meer het je afleidt van dat wat God in je leven wil doen.Het enige dat we kunnen doen? Bidden. Bidden of de Heilige Geest ons wil helpen, ertoe wil zetten, wil overreden om los te laten wat we niet los kúnnen laten. We kunnen het niet alleen, hoe graag we onszelf daar ook van overtuigen. De eerste stap is erkennen dat we een probleem hebben, de volgende is het leren loslaten. Bid heel specifiek voor datgene wat je zo in je handen geklemd houdt en zie hoe God aan het werk gaat. Luister ook eens naar 'Have It All' van Bethel, een nummer dat me keer op keer helpt om adem te halen en de controle over te geven.Deze overdenking is geschreven door oud-schrijfster Mandy Wittekoek.

In this episode, Dr. Andy Southerland discusses the Capitol Hill Report from September 8, providing important updates around BrainPAC. Stay updated with what's happening on the hill by visiting aan.com/chr.  Learn how you can get involved with AAN advocacy. 

Genk kroonde zich gisteren tot de ploeg van de provincie Limburg, al zullen de buren uit Sint-Truiden daar hun bedenkingen bij hebben. STVV morste met de kansen en trok aan het kortste eind bij enkele discutabele fases. Genk-coach Thorsten Fink zal er niet om malen. Met het mes op de keel pakt de Duitser drie belangrijke punten in de strijd om Play-Off 1. Aan de andere kant van het Kanaal lijkt de verre inworp terug van weggeweest. Crystal Palace pakte zo de scalp van Liverpool en zo blijven de troepen van Oliver Glasner ongeslagen dit seizoen. Die statistiek kan Napoli niet meer voorleggen na de verloren topper tegen Milan, waar een misnoegde Kevin De Bruyne vroegtijdig werd gewisseld. En zien we Philippe Clement binnenkort op de bank in de Bundesliga? Duitse media linken de voormalige succescoach van Club Brugge aan het zwalpende Borussia Mönchengladbach, dat na 50 minuten 0-6 in het krijt stond tegen Frankfurt.

Send us a textMatteus 7:3-5 “Waarom sien jy die splinter raak wat in jou broer se oog is, maar die balk in jou eie oog merk jy nie op nie? Of hoe kan jy vir jou broer sê: ‘Wag, laat ek die splinter uit jou oog uithaal,' en intussen is daar 'n balk in jou eie oog? Huigelaar! Haal eers die balk uit jou eie oog uit, dan sal jy goed kan sien om die splinter uit jou broer se oog uit te haal. Mense is darem snaakse wesens, nè? Aan die eenkant smag ons na nabyheid, na liefde, na intimiteit, en tog, hoe nader ons aan iemand kom, hoe maklikerkritiseer ons hulle en hoe meer konsentreer ons op hulle swakhede. Hoekom is dit so?Weet jy, Napoleon en Josephine was innig lief vir mekaar. Maar ten spyte van hul liefde, het sy oorheersende geaardheid en haar onvermoë om aan sy verwagtinge te voldoen, gelei tot ernstige konflik en uiteindelik tot ‘n egskeiding. Soos so dikwels die geval is, het hul persoonlike swakhede, hulle aanvanklik opregte toegewyde gevoelens, vernietig.Hoe dikwels het daardie scenario homself deur die eeue in verhoudings afgespeel? En die rede is altyd dieselfde. Jesus het dit so gestel:Matteus 7:3-5 “Waarom sien jy die splinter raak wat in jou broer se oog is, maar die balk in jou eie oog merk jy nie op nie? Of hoe kan jy vir jou broer sê: ‘Wag, laat ek die splinter uit jou oog uithaal,' en intussen is daar 'n balk in jou eie oog? Huigelaar! Haal eers die balk uit jou eie oog uit, dan sal jy goed kan sien om die splinter uit jou broer se oog uit te haal.Hoe nader jy aan iemand kom, hoe makliker is dit om die splinter in hulle oog te sien. Hoe meer irriteer dit jou. Hoe meer aanstoot gee dit jou. En dan voel jy dat die ander persoon moet verander.Huigelaar! Haal eers die balk uit jou eie oog uit, dan sal jy goed kan sien om die splinter uit jou broer se oog uit te haal.Dis God se Woord. Vars … vir jou … vandag. Support the showEnjoying The Content?For the price of a cup of coffee each month, you can enable Christianityworks to reach 10,000+ people with a message about the love of Jesus!DONATE R50 MONTHLY

Korting op vitaily supplementen: vitaily.nl/jasper10 of gebruik de code jasper10 In deze aflevering hoor je mij als gast in de podcast De studieschuld van van Francien Regelink, schrijfster van de boeken Druks 1 en Druks 2. Ik vertel open over mijn schoolcarrière, de hobbels die ik onderweg tegenkwam en waarom ik mijn studie vroegtijdig moest afbreken, met een studieschuld van €15.000 als gevolg. Aan het einde van mijn studie kreeg ik de diagnose ADD, die er uiteindelijk voor zorgde dat mijn studieschuld werd kwijtgescholden. Benieuwd hoe dat precies ging en welke inzichten dit mij heeft gegeven? Luister dan snel naar deze aflevering. Ben jij ook benieuwd of je geld terug kan krijgen van DUO? Download dan dit hoofdstuk: https://duohoofdstuk.nl/duo/ https://francienregelink.nl/

Voel jij je regelmatig overspoeld door stress en heb je het idee dat je emmer ieder moment kan overlopen?In deze aflevering deel ik hoe ik, midden in een verbouwing, een gezin met vier kinderen en een volle agenda, tóch rust en balans weet te bewaren. Ik vertel eerlijk hoe dit vroeger totaal anders was, en welke concrete stappen ik heb gezet om mijn zenuwstelsel te versterken en stress écht te reguleren. Na het luisteren van deze aflevering weet je:Waarom veerkracht begint bij je zenuwstelsel (en hoe je dat voedt en traint)Hoe ik stress letterlijk ontlaad met simpele dagelijkse gewoontesWelke rol voeding, beweging en mindset spelen bij stressregulatieHoe je voorkomt dat je emoties zich opstapelen en je gaat afreagerenEen aflevering vol praktische inzichten en eerlijke verhalen, zodat ook jij kunt ervaren dat een druk leven niet gelijk hoeft te staan aan constante stress. ---

Aan de slag!Welk ‘Ik ben'-woord raakt jou het meest en waarom?Deze overdenking is geschreven door schrijfster Marianne de Bart-van der Lee.

S5, A7 - Romeinen - 1 Deze brief is teamworkHoi, en heel hartelijk welkom bij de Bijbellezen met Jan-podcast. Het is mijn passie om mensen te helpen bij het lezen, begrijpen en geloven van de Bijbel. Op de website bijbellezenmetjan.nl kun je gratis het boek ‘De Bijbel in 1 Dag' downloaden. Daarnaast heb ik bijbelstudies in roman-vorm geschreven. Hierbij maken de personages van alles mee en worstelen ze met geloofsvraagstukken. De Bijbel komt zo hopelijk meer tot leven voor de lezers. Ook kun je met mij de Bijbel in 2 Jaar lezen. Hierbij lezen we twee hoofdstukken per dag, vijf dagen in de week. Daarnaast maak ik korte maar krachtige Bijbellees-challenges over Bijbelboeken of Bijbelse thema's. In de podcast doen we ook zo'n challenge. We staan stil bij de brief die Paulus schreef aan de christenen in Rome. Dit is misschien wel de mooiste brief uit de geschiedenis van de mensheid. Maar het is ook een ingewikkelde brief en het is makkelijk om verkeerde conclusies te trekken. Het lastige van de brieven in de Bijbel is dat ze een moment-opname zijn. Wat is er vooraf gebeurd? Waar reageert de schrijver op? Welke thema's speelden er in die tijd in die plaats? Met andere woorden: wat is de context? Het interessante is dat als je Romeinen wilt doorgronden, je eigenlijk achteraan moet beginnen. Aan het eind van de brief wordt namelijk duidelijk welke groepen er in Rome waren en waarom die op elkaar neerkeken. Als je die context begrijpt, dan begrijp je ook de eerste hoofdstukken van de brief beter. Dus… in deze podcast-serie beginnen we achteraan de brief met Romeinen 16. Ik hoop dat dit prachtige schrijfsel van Paulus daardoor nog meer tot leven komt. Ik wil echt dat het vernieuwend is voor jou en mij. Daarom lees ik ook uit een andere Bijbelvertaling dan gebruikelijk. Meestal lees ik uit de NBV21, maar nu lees ik uit de eigentijdse Bijbelvertaling, de zogeheten EBV. De verschillen tussen beide vertalingen zijn niet groot, maar het staat er toch net iets anders. Of er wordt net een ander woord gebruikt. Uiteraard kun je zelf ook meelezen in een Bijbelvertaling naar keuze. Dus we beginnen achteraan, en ik lees voor uit een andere vertaling. Laten we naar de eerste overdenking gaan.

Als Sinterklaas in 2022 aankomt in Dordrecht, zijn de kinderen natuurlijk door het dolle heen. Maar voor Montussa, het paard van Sinterklaas, is het een zware dag. Agenten zien dat het dier zelfs door zijn benen zakt. Al bij het begin van de intocht zien agenten dat Sinterklaas te zwaar is voor het paard. Zijn benen komen onder de buik van Sinterklaas uit, en ze besluiten er wat van te zeggen. Maar volgens de man die Sinterklaas speelt, is dat niet het moment om het er over te hebben, want de wandeling moet beginnen. Aan het einde van de intocht zakt het dier, met de Sint op zijn rug, zelfs door zijn hoeven. Agenten grijpen in en laten eigenaar Matthijs B. het dier de trailer in begeleiden. Omdat de politie en het Openbaar Ministerie van mening zijn dat er sprake is van dierenmishandeling, moet Matthijs B. zich voor de rechter verantwoorden. Hij wil de zitting niet bijwonen, maar schrijft in een brief dat het dier volgens hem in goede gezondheid verkeert. Rechtbankverslaggever Niels Dekker volgt de zaak namens AD De Dordtenaar: „Als je het paard ziet denk je wel ‘arm beestje’.. Ik denk niet dat Dordrecht Matthijs B. nog gaat inzetten, en er zal extra scherp naar de conditie van het paard van Sinterklaas gekeken worden.’’See omnystudio.com/listener for privacy information.

Aan tafel deze week: politiek journalist Tom-Jan Meeus, partijleider CDA Henri Bontenbal, onderzoeker Josse de Voogd, socioloog Jan Willem Duyvendak, journalist Tim 'S Jongers, Margrite Kalverboer kinderombudsman 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:   https://bit.ly/4gJ1ESv  Deze week was er in de Tweede Kamer een snoeihard debat over de extreemrechtse rellen in Den Haag. Het roept vragen op als: staat de stabiliteit van ons landsbestuur onder druk? En erodeert ons systeem door heftige debatten in de Tweede Kamer? Te gast is Tom-Jan Meeus, politiek redacteur van NRC. Ook met CDA-lijsttrekker Henri Bontenbal praten we over de rellen in Den Haag en het debat wat er donderdag op volgde. Want waren deze rellen politiek en wie is daarvoor dan verantwoordelijk? Ondertussen, je zou het haast vergeten, is de campagne begonnen. Deze week stond wederom in het teken van de angst voor toenemende polarisatie. Maar nu verschijnt het boek Spookkloven van Jan Willem Duyvendak. Dat stelt dat we veel dichterbij elkaar staan dan we denken. En dat kloven in veel gevallen juist zijn áfgenomen. Hoe kan dat? En ís het ook zo? Daarover in Buitenhof: socioloog Jan Willem Duyvendak en electoraal geograaf Josse de Voogd. Kinderen die in armoede opgroeien geven hun leven vaker een onvoldoende concludeert Kinderombudsman Margrite Kalverboer. En de afgelopen tien jaar is hun situatie niet verbeterd ondanks vele pogingen ze te helpen. Wat is er nodig om het tij te keren? We bespreken het met Margrite Kalverboer en publicist en ervaringsdeskundige Tim 'S Jongers.

Aan tafel deze week: politiek journalist Tom-Jan Meeus, partijleider CDA Henri Bontenbal, onderzoeker Josse de Voogd, socioloog Jan Willem Duyvendak, journalist Tim 'S Jongers, Margrite Kalverboer kinderombudsman 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:   https://bit.ly/4gJ1ESv  Deze week was er in de Tweede Kamer een snoeihard debat over de extreemrechtse rellen in Den Haag. Het roept vragen op als: staat de stabiliteit van ons landsbestuur onder druk? En erodeert ons systeem door heftige debatten in de Tweede Kamer? Te gast is Tom-Jan Meeus, politiek redacteur van NRC. Ook met CDA-lijsttrekker Henri Bontenbal praten we over de rellen in Den Haag en het debat wat er donderdag op volgde. Want waren deze rellen politiek en wie is daarvoor dan verantwoordelijk? Ondertussen, je zou het haast vergeten, is de campagne begonnen. Deze week stond wederom in het teken van de angst voor toenemende polarisatie. Maar nu verschijnt het boek Spookkloven van Jan Willem Duyvendak. Dat stelt dat we veel dichterbij elkaar staan dan we denken. En dat kloven in veel gevallen juist zijn áfgenomen. Hoe kan dat? En ís het ook zo? Daarover in Buitenhof: socioloog Jan Willem Duyvendak en electoraal geograaf Josse de Voogd. Kinderen die in armoede opgroeien geven hun leven vaker een onvoldoende concludeert Kinderombudsman Margrite Kalverboer. En de afgelopen tien jaar is hun situatie niet verbeterd ondanks vele pogingen ze te helpen. Wat is er nodig om het tij te keren? We bespreken het met Margrite Kalverboer en publicist en ervaringsdeskundige Tim 'S Jongers.

Aan de slag!Geef niet op om te bidden! Schrijf vandaag je gebed eens op en eindig het in de naam van Jezus, de Verlosser van alle strijd. Lees dit gebed de komende tijd regelmatig door. Blijf zo je verzoek bij God bekendmaken en wacht af hoe God hierin recht zal doen.Deze overdenking is geschreven door schrijfster Joanne van de Vendel.

In de eerste aflevering van Babbelpraat (nee, geen goedkope rip-off van RoddelPraat) spreken Melvin van Haperen en Jens van Kakerken over de moord op Charlie Kirk, de eerste reactie en de weg vooruit. Hoe gaat Pitloos te werk na de moord op Kirk? Waarom komen we juist nú ineens terug? Deels de verkiezingen natuurlijk, maar Kirk speelde een enorme rol. Aan het einde van de aflevering leidt Jens in een gebed (vanuit zijn katholieke geloof) voor de eeuwige rust van Charlie Kirks ziel. O ja, de rellen in Den Haag bij ElsFest van 'Els Rechts' komt ook nog even voorbij, inclusief de verklaring van ChristenUnie samen met verschillende partijen (waaronder CDA, PVV, FVD en JA21). Dit wil je missen!00:00 - Introductie01:13 - Moord op Charlie Kirk03:06 - De weg na Charlie Kirk05:46 - Correctie07:29 - Waarom direct reageren niet altijd goed is09:10 - Mooie effecten10:31 - Erika Kirk vergeeft de moordenaar13:43 - De betekenis van de moord16:13 - De rellen in Den Haag18:11 - Dit helpt rechts niet21:45 - Links schiet in hun voet24:09 - Hypocrisie van links25:21 - Afsluiting26:38 - Bidden voor Charlie Kirk

In deze speciale live-aflevering vanaf de Groene Vloot tijdens het Springtij Congres spreken we met Arjan Keizer, oprichter van Medewerkers voor onze Toekomst. Deze nieuwe beweging roept het bedrijfsleven op om te kiezen voor langetermijnwaarde boven kortetermijnbelangen.De aflevering maakt deel uit van het Leiderschapsprogramma van het Springtij Forum, waarin deelnemers de centrale vraag krijgen voorgelegd: “Wat is jouw bijdrage aan de transitie naar een duurzame samenleving?”Medewerkers voor onze toekomstMedewerkers van grote Nederlandse bedrijven starten nieuwe klimaatbeweging en roepen het bedrijfsleven op tot focus op langetermijnwaarde. 

Aan de slag!Lees Johannes 11:33-36. Welke emoties zie je bij Jezus? Waar raakt dat jou? Breng het bij Jezus zoals het is.Deze overdenking is geschreven door schrijfster Emmely Post-Spreeuwenberg.

Podcast op een plek vol historie, ambitie én toekomst Deze week nam ik een podcast op op een wel héél bijzondere locatie: Landgoed de Olmenhorst – een oase van rust en groen, midden tussen Amsterdam en Den Haag. Aan tafel zaten Amber en Liselotte, de 6e (!) generatie van dit familiebedrijf, en nu aan het roer van een landgoed dat al meer dan 170 jaar bestaat. Twee jonge, ambitieuze vrouwen die het erfgoed niet alleen bewaren, maar ook vernieuwen.

Een nieuwe dag, een nieuwe wanprestatie van Angela de Jong. Aan de andere kant van de oceaan krijgt Trump een tikje van boemerang Kimmel, en reageert met bizarre uitspraken. Terug in ons pittoreske kikkerlandje springt massatoerisme messias Alexander Klöpping in de bres om Amsterdam weer van de Amsterdammers te maken. En FVD krijgt een POWNED-koekje van eigen deeg.See omnystudio.com/listener for privacy information.

Aan tafel zitten Frénk van der Linden, Irene de Kruif en Spraakmaker Laurens Verhagen. Een week vol politieke verontwaardiging over extreemrechts geweld resulteerde gisteren in een vurig debat, dat acht uur duurde. Omdat dát wat lang is voor een journaal vraagt dat om journalistieke keuzes. En dan was er ook opeens een opvallende motie van BBB-leider Caroline van der Plas, hierin pleitte ze voor een asielnoodwet. Dit nieuws zat niet in het overzicht dat Irene de Kruif, politiek verslaggever van RTL Nieuws, maakte. "Ik kijk het debat van A tot Z en dan denk ik wat is de kernboodschap? Wat moet je horen als je om 19:30u de televisie aanzet?" De Kruif vond het verhaal over het pamflet van ChristenUnie-leider Mirjam Bikker en het feit dat de Tweede Kamer zelfs daar niet uit weet te komen, meer veelzeggend dat een motie van Caroline van der Plas "evident een campagnestunt". Journalist Frénk van der Linden vond dat een bijzondere keuze. "Ik begrijp eigenlijk niet zo goed waarom dit is weggelaten uit het item."

‘Prelude' is de opmaat naar het AVROTROS Vrijdagconcert! Gastspreker: cellist David Faber Radio Filharmonisch Orkest Dalia Stasevska, dirigent Anastasia Kobekina, cello Grieg Peer Gynt Suite nr. 2 Elgar Celloconcert Sibelius Vijfde symfonie Meer info & kaarten (https://www.npoklassiek.nl/concerten/6d436738-db30-4bf4-89fe-b69a8e124b08/peer-gynt-en-de-vijfde-van-sibelius) In deze podcast vertelt presentator Leonard Evers je iedere week meer over de bijzondere stukken die gaan klinken in TivoliVredenburg én op NPO Klassiek. Dat doet hij samen met verschillende gasten die in de studio aanschuiven. Aan de hand van muziekfragmenten word je warm gemaakt voor de mooie composities die je te wachten staan. Abonneer je nu! Alles over het AVROTROS Vrijdagconcert (https://www.npoklassiek.nl/programmas/avrotros-vrijdagconcert)

Aan de slag!Luister het lied 'Goodness of God' van CeCe Winans.Deze overdenking is geschreven door schrijfster Linda Aalbers.

Blue Grass Boogiemen vieren dit jaar hun 35-jarig jubileum. Al die tijd stonden ze aan de Europese top van Bluegrass en traden ze over de hele wereld op met legendes uit binnen- en buitenland. En ze zijn nog lang niet van plan om te stoppen.Aan mandolinespeler en medeoprichter van de band Arnold om in zijn geheugen en fotoalbums te graven voor al zijn speciale ontmoetingen, optredens en andere herinneringen. Verbazing, hilariteit, weemoed, passie en fantastische muziek. Het zit allemaal in deze aflevering.Elvis Presley - Trying to Get to YouHank Williams - I Can't Escape From YouBill Monroe and his Blue Grass Boys - Uncle PenGeorge Jones - The DoorRusty & Doug Kershaw - Louisiana ManJimmy Martin - Hit Parade of LoveInstagram:⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠www.instagram.com/brightlightsandcountrymusic⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠Productie: Martin ter Braake / ⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠www.odepodcast.nl⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠De Bright Lights playlist met alle gedraaide tracks luister je ⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠hier⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠. En door op ⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠deze⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠ link te klikken, kom je terecht bij onze playlist met nieuwe countrytracks.

Vandaag bespreken we het boek Leer denken als Socrates van Donald Robertson. Ondertitel: Filosofie als een manier van leven Engelse titel: How to think like Socrates: Ancient Philosophy as a Way of Life in the modern world (2024) Uitgeverij Ten Have Een indrukwekkend boek. De auteur Donald John Robertson is een in Schotland geboren cognitief-gedragstherapeut en auteur, bekend om zijn werk waarin hij moderne cognitief-gedragstherapie (CGT) integreert met de filosofie van het oude Griekenland en Rome, met name het stoïcisme, waaronder meerdere boeken over Marcus Aurelius en Senneca. Donald J. Robertson - Wikipedia https://en.wikipedia.org/wiki/Donald_J._Robertson  Het bijzondere over de boeken over Socrates en dialogen van Plato me Socrates zijn dat het geen historisch verslag is, maar het zijn ook geen verzinsels. Datzelfde geldt voor dit boek, het is gedramatiseerd en semifictioneel. Het boek gaat over het leven van Socrates, maar minstens zo belangrijk is de rol van zijn leerling Alcibiades in dit boek. Er waren momenten dat ik heel helder had wat ik met dit boek en de Socratische vragen kan doen, en momenten dat ik het kwijt was. Het opvallenste voor mij was de overeenkomsten die je ziet met de huidige wereld, in de politiek, in oorlog. Het verhaal las vaak als een fictie boek waar ik me in deze Griekse tijd waande enkele honderden jaren voor Christus. Daarnaast zitten er verschillende elementen in het boek waar Robertson suggesties geeft hoe je de filosofie, het denken, vragen stellen, en zoeken naar wijsheid kunt toepassen in deze tijd, in je eigen leven. Indeling van het boek: Het socratische probleem Inleiding Het proces De eerste filosoof De vrouwelijke Socrates Het orakel van Apollo De wijste van alle mensen De leeuw van Athene De Peloponnesische Oorlog De Siciliaanse expeditie De val van Athene De Dertig Tirannen De zwanenzang Het boek begint na de inleiding met het proces tegen Socrates waarin hij ter dood wordt veroordeel. Daarna gaat het boek verder over zijn leven en het leven van Alcibiades, tot in het laatste hoofdstuk waarin Phaedo de laatste uren tot aan zijn dood beschrijft. Het socratische probleem Het probleem is dat Socrates zelf niets heeft opgeschreven. De belangrijkste dialogen van Plato met Socrates zijn waarschijnlijk opgeschreven kort na de dood van Socrates. Het zijn de dingen die Plato zich herinnerd. Plato was nog jong bij het overlijden van Socrates en verkeerde waarschijnlijk pas de laatste zes jaar in zijn kring. Volgens deskundigen zitten er veel tegenstrijdigheden in de dialogen en is niet na te gaan wat fictie en wat werklijkheid is. Inleiding Een inleiding in de filosofie, met vele bekende filosofen die na Socrates kwamen en veel hebben gebruikt van zijn manier van vragen stellen. Op pagina 25 en 27 zie je gelijk allerlei gelijkenis met wat er nu gebeurt in de media, met influencers, en in de politiek. Sofisten, mensen die het voral van de rede en beinvloeding van anderen moeten hebben en die veel geld vragen voor het onderricht aan jonge mensen. Of een pandamie, polarisatie, populisme, oligarchie en tirannie. Hier maakt hij ook de connectie met stoicisme. Het proces Een groots proces rondom Socrates met veel rumour waarin ze hem beschuldigen dat hij de goden die door Athene worden herkent, niet herkent, en hij bederft de jeugd. Het deel van het proces gaat vooral over de verdediging van Socrates waarin duidelijk wordt dat voor Socrates wijsheid het belangrijkste is dat de mens heeft te onderzoeken. Wat is wijsheid? Wanneer ben je een goed mens? Aan het einde zie je ook hoe Socrates omgaat met de dood en daar niet bang voor ons en zijn doodstraf niet omzet in een ballingschap. Met zijn vragen laat hij vele ‘wijze' mannen ongemakkelijk voelen, vooral de redenaars. Door zijn vragen praten deze sofisten zich vaak vast. Terwijl Socrates er op uit is dat mensen argumenten inbrengen die aantonen dat hi...

Paroxysmal movement disorders refer to a group of highly heterogeneous disorders that present with attacks of involuntary movements without loss of consciousness. These disorders demonstrate considerable and ever-expanding genetic and clinical heterogeneity, so an accurate clinical diagnosis has key therapeutic implications. In this episode, Kait Nevel, MD, speaks with Abhimanyu Mahajan, MD, MHS, FAAN, author of the article “Paroxysmal Movement Disorders” in the Continuum® August 2025 Movement Disorders issue. Dr. Nevel is a Continuum® Audio interviewer and a neurologist and neuro-oncologist at Indiana University School of Medicine in Indianapolis, Indiana. Dr. Mahajan is an assistant professor of neurology and rehabilitation medicine at the James J. and Joan A. Gardner Family Center for Parkinson's Disease and Movement Disorders at the University of Cincinnati in Cincinnati, Ohio. Additional Resources Read the article: Paroxysmal Movement Disorders 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: @MahajanMD Full episode transcript available here Dr Jones: This is Doctor 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 doctor Abhi Mahajan about his article on diagnosis and management of paroxysmal movement disorders, which appears in the August 2025 Continuum issue on movement disorders. Abhi, welcome to the podcast and please introduce yourself to the audience. Dr Mahajan: Thank you, Kait. Thank you for inviting me. My name is Abhi Mahajan. I'm an assistant professor of neurology and rehabilitation medicine at the University of Cincinnati in Cincinnati, Ohio. I'm happy to be here. Dr Nevel: Wonderful. Well, I'm really excited to talk to you about your article today on this very interesting and unique set of movement disorders. So, before we get into your article a little bit more, I think just kind of the set the stage for the discussion so that we're all on the same page. Could you start us off with some definitions? What are paroxysmal movement disorders? And generally, how do we start to kind of categorize these in our minds? Dr Mahajan: So, the term paroxysmal movement disorders refers to a group of highly heterogeneous disorders. These may present with attacks of involuntary movements, commonly a combination of dystonia and chorea, or ataxia, or both. These movements are typically without loss of consciousness and may follow, may follow, so with or without known triggers. In terms of the classification, these have been classified in a number of ways. Classically, these have been classified based on the trigger. So, if the paroxysmal movement disorder follows activity, these are called kinesigenic, paroxysmal, kinesigenic dyskinesia. If they are not followed by activity, they're called non kinesigenic dyskinesia and then if they've followed prolonged activity or exercise they're called paroxysmal exercise induced dyskinesia. There's a separate but related group of protogynous movement disorders called episodic attacks here that can have their own triggers. Initially this was the classification that was said. Subsequent classifications have placed their focus on the ideology of these attacks that could be familiar or acquired and of course understanding of familiar or genetic causes of paroxysmal movement disorders keeps on expanding and so on and so forth. And more recently, response to pharmacotherapy and specific clinical features have also been introduced into the classification. Dr Nevel: Great, thank you for that. Can you share with us what you think is the most important takeaway from your article for the practicing neurologist? Dr Mahajan: Absolutely. I think it's important to recognize that everything that looks and sounds bizarre should not be dismissed as malingering. Such hyperkinetic and again in quotations, “bizarre movements”. They may appear functional to the untrained eye or the lazy eye. These movements can be diagnosed. Paroxysmal movement disorders can be diagnosed with a good clinical history and exam and may be treated with a lot of success with medications that are readily available and cheap. So, you can actually make a huge amount of difference to your patients' lives by practicing old-school neurology. Dr Nevel: That's great, thank you so much for that. I can imagine that scenario does come up where somebody is thought to have a functional neurological disorder but really has a proximal movement disorder. You mentioned that in your article, how it's important to distinguish between these two, how there can be similarities at times. Do you mind giving us a little bit more in terms of how do we differentiate between functional neurologic disorder and paroxysmal movement disorder? Dr Mahajan: So clinical differentiation of functional neurological disorder from paroxysmal movement disorders, of course it's really important as a management is completely different, but it can be quite challenging. There's certainly an overlap. So, there can be an overlap with presentation, with phenomenology. Paroxysmal nature is common to both of them. In addition, FND and PMD's may commonly share triggers, whether they are movement, physical exercise. Other triggers include emotional stimuli, even touch or auditory stimuli. What makes it even more challenging is that FND's may coexist with other neurological disorders, including paroxysmal movement disorders. However, there are certain specific phenom phenotypic differences that have been reported. So specific presentations, for example the paroxysms may look different. Each paroxysm may look different in functional neurological disorders, specific phenotypes like paroxysmal akinesia. So, these are long duration episodes with eyes closed. Certain kinds of paroxysmal hyperkinesia with ataxia and dystonia have been reported. Of course. More commonly we see PNES of paroxysmal nonepileptic spells or seizures that may be considered paroxysmal movement disorders but represent completely different etiology which is FND. Within the world of movement disorders, functional jerks may resemble propiospinal myoclonus which is a completely different entity. Overall, there are certain things that help separate functional movement disorders from paroxysmal movement disorders, such as an acute onset variable and inconsistent phenomenology. They can be suggestibility, distractibility, entrainment, the use of an EMG may show a B-potential (Bereitschaftspotential) preceding the movement in patients with FND. So, all of these cues are really helpful. Dr Nevel: Great, thanks. When you're seeing a patient who's reporting to these paroxysmal uncontrollable movements, what kind of features of their story really tips you off that this might be a proximal movement disorder? Dr Mahajan: Often these patients have been diagnosed with functional neurological disorders and they come to us. But for me, whenever the patient and or the family talk about episodic movements, I think about these. Honestly, we must be aware that there is a possibility that the movements that the patients are reporting that you may not see in clinic. Maybe there are obvious movement disorders. Specifically, there's certain clues that you should always ask for in the history, for example, ask for the age of onset, a description of movements. Patients typically have videos or families have videos. You may not be able to see them in clinic. The regularity of frequency of these movements, how long the attacks are, is there any family history of or not? On the basis of triggers, whether, as I mentioned before, do these follow exercise? Prolonged exercise? Or neither of the above? What is the presentation in between attacks, which I think is a very important clinical clue. Your examination may be limited to videos, but it's important not just to examine the video which represents the patient during an attack, but in between attacks. That is important. And of course, I suspect we'll get to the treatment, but the treatment can follow just this part, the history and physical exam. It may be refined with further testing, including genetic testing. Dr Nevel: Great. On the note of genetic testing, when you do suspect a diagnosis of paroxysmal movement disorder, what are some key points for the provider to be aware of about genetic testing? How do we go about that? I know that there are lots of different options for genetic testing and it gets complicated. What do you suggest? Dr Mahajan: Traditionally, things were a little bit easier, right, because we had a couple of genes that have been associated with the robust movement disorders. So, genetic testing included single gene testing, testing for PRRT2 followed by SLC2A. And if these were negative, you said, well, this is not a genetic ideology for paroxysmal movement disorders. Of course, with time that has changed. There's an increase in known genes and variants. There is increased genetic entropy. So, the same genetic mutation may present with many phenotypes and different genetic mutations may present with the similar phenotype. Single gene testing is not a high yield approach. Overall genetic investigations for paroxysmal movement disorders use next generation sequencing or whole exome sequence panels which allow for sequencing of multiple genes simultaneously. The reported diagnostic yield with let's say next generation sequencing is around 35 to 50 percent. Specific labs at centers have developed their own panels which may improve the yield of course. In children, microarray may be considered, especially the presentation includes epilepsy or intellectual disability because copy number variations may not be detected by a whole exome sequencing or next generation sequencing. Overall, I will tell you that I'm certainly not an expert in genetics, so whenever you're considering genetic testing, if possible, please utilize the expertise of a genetic counsellor. Families want to know, especially as an understanding of the molecular underpinnings and knowledge about associated mutations or variations keeps on expanding. We need to incorporate their expertise. A variant of unknown significance, which is quite a common result with genetic testing, may not be a variant of unknown significance next year may be reclassified as pathogenic. So, this is extremely important. Dr Nevel: Yeah. That's such a good point. Thank you. And you just mentioned that there are some genetic mutations that can lead to multiple different phenotypes. Seemingly similar phenotypes can be associated with various genetic mutations. What's our understanding of that? Do we have an understanding of that? Why there is this seeming disconnect at times between the specific genetic mutation and the phenotype? Dr Mahajan: That is a tough question to answer for all paroxysmal movement disorders because the answer may be specific to a specific mutation. I think a great example is the CACNA1A mutation. It is a common cause of episodic ataxia type 2. Depending on when the patient presents, you can have a whole gamut of clinical presentations. So, if the patient is 1 year old, the patient can present with epileptic encephalopathy. Two to 5 years, it can be benign paroxysmal torticollis of infancy. Five to 10 years, can present with learning difficulties with absence epilepsy and then of course later, greater than 10 years, with episodic ataxia (type) 2 hemiplegic migraine and then a presentation with progressive ataxia and hemiplegic migraines has also been reported. So not just episodic progressive form of ataxia has also been reported. I think overall these disorders are very rare. They are even more infrequently diagnosed than their prevalence. As such, the point that different genetic mutations present with different phenotypes, or the same genetic mutation I may present with different phenotypes could also represent this part. Understanding of the clinical presentation is really incomplete and forever growing. There's a new case report or case series every other month, which makes this a little bit challenging, but that's all the more reason for learning about them and for constant vigilance for patients who show up to our clinic. Dr Nevel: Yeah, absolutely. What is our current understanding of the associated pathophysiology of these conditions and the pathophysiology relating to the genetics? And then how does that relate to the treatment of these conditions? Dr Mahajan: So, a number of different disease mechanisms have been proposed. Traditionally, these were all thought to be ion channelopathies, but a number of different processes have been proposed now. So, depending on the genetic mutation that you talk about. So certain mutations can involve ion channels such as CACMA1A, ATP1A3. It can involve solute carriers, synaptic vesicle fusion, energy metabolism such as ECHS1, synthesis of neurotransmitters such as GCH1. So, there are multiple processes that may be involved. I think overall for the practicing clinician such as me, I think there is a greater need for us to understand the underlying genetics and associated phenotypes and the molecular mechanisms specifically because these can actually influence treatment decisions, right? So, you mentioned that specific genetic testing understanding of the underlying molecular mechanism can influence specific treatments. As an example, a patient presenting with proximal nocturnal dyskinesia with mutation in the ADCY5 gene may respond beautifully to caffeine. Other examples if you have SLC2A1, so gluc-1 (glucose transporter type 1) mutation, a ketogenic diet may work really well. If you have PDHA1 mutation that may respond to thiamine and so on and so forth. There are certain patients where paroxysmal movement disorders are highly disabling and you may consider deep brain stimulation. That's another reason why it may be important to understand genetic mutations because there is literature on response to DBS with certain mutations versus others. Helps like counselling for patients and families, and of course introduces time, effort, and money spent in additional testing. Dr Nevel: Other than genetic testing, what other diagnostic work up do you consider when you're evaluating patients with a suspected paroxysmal movement disorder? Are there specific things in the history or on exam that would prompt you to do certain testing to look for perhaps other things in your differential when you're first evaluating a patient? Dr Mahajan: In this article, I provide a flow chart that helps me assess these patients as well. I think overall the history taking and neurological exam outside of these paroxysms is really important. So, the clinical exam in between these episodic events, for example, for history, specific examples include, well, when do these paroxysms happen? Do they happen or are they precipitated with meals that might indicate that there's something to do with glucose metabolism? Do they follow exercise? So, a specific example is in Moyamoya disease, they can be limb shaking that follows exercise. So, which gives you a clue to what the etiology could be. Of course, family history is important, but again, talking about the exam in between episodes, you know, this is actually a great point because out– we've talked about genetics, we've talked about idiopathic paroxysmal movement disorders, –but a number of these disorders are because of acquired causes. Well, of course it's important because acquired causes such as autoimmune causes, so multiple sclerosis, ADEM, lupus, LGI1, all of these NMDAR, I mentioned Moyamoya disease and metabolic causes. Of course, you can consider FND as under-acquired as well. But all of these causes have very different treatments and they have very different prognosis. So, I think it's extremely important for us to look into the history with a fine comb and then examine these patients in between these episodes and keep our mind open about acquired causes as well. Dr Nevel: When you evaluate these patients, are you routinely ordering vascular imaging and autoimmune kind of serologies and things like that to evaluate for these other acquired causes or it does it really just depend on the clinical presentation of the patient? Dr Mahajan: It mostly depends on the clinical presentation. I mean, if the exam is let's say completely normal, there are no other risk factors in a thirty year old, then you know, with a normal exam, normal history, no other risk factors. I may not order an MRI of the brain. But if the patient is 55 or 60 (years) with vascular risk factors, then you have to be mindful that this could be a TIA. If the patient has let's say in the 30s and in between these episodes too has basically has a sequel of these paroxysms, then you may want to consider autoimmune. I think the understanding of paraneoplastic, even autoimmune disorders, is expanding as well. So, you know the pattern matters. So, if all of this is subacute started a few months ago, then I have a low threshold for ordering testing for autoimmune and paraneoplastic ideology is simply because it makes such a huge difference in terms of how you approach the treatment and the long-term prognosis. Dr Nevel: Yeah, absolutely. What do you find most challenging about the management of patients with paroxysmal movement disorders? And then also what is most rewarding? Dr Mahajan: I think the answer to both those questions is, is the same. The first thing is there's so much advancement in what we know and how we understand these disorders so regularly that it's really hard to keep on track. Even for this article, it took me a few months to write this article, and between the time and I started and when I ended, there were new papers to include new case reports, case series, right? So, these are rare disorders. So most of our understanding for these disorders comes from case reports and case series, and it's in a constant state of advancement. I think that is the most challenging part, but it's also the most interesting part as well. I think the challenging and interesting part is the heterogeneity of presentation as well. These can involve just one part of your body, your entire body can present with paroxysmal events, with multiple different phenomenologies and they might change over time. So overall, it's highly rewarding to diagnose such patients in clinic. As I said before, you can make a sizeable difference with the medication which is usually inexpensive, which is obviously a great point to mention these days in our health system. But with anti-seizure drugs, you can put the right diagnosis, you can make a huge difference. I just wanted to make a point that this is not minimizing in any way the validity or the importance of diagnosing patients with functional neurological disorders correctly. Both of them are as organic. The importance is the treatment is completely different. So, if you're diagnosing somebody with FND and they do have FND and they get cognitive behavioral therapy and they get better, that's fantastic. But if somebody has paroxysmal movement disorders and they undergo cognitive behavioral therapy and they're not doing well, that doesn't help anybody. Dr Nevel: One hundred percent. As providers, obviously we all want to help our patients and having the correct diagnosis, you know, is the first step. What is most interesting to you about paroxysmal movement disorders? Dr Mahajan: So outside of the above, there are some unanswered questions that I find very interesting. Specifically, the overlap with epilepsy is very interesting, including shared genes, the episodic nature, presence of triggers, therapeutic response to anti-seizure drugs. All of this I think deserves further study. In the clinic, you may find that epilepsy and prognosis for movement disorders may occur in the same individual or in a family. Episodic ataxia has been associated with seizures. Traditionally this dichotomy of an ictal focus. If it's cortical then it's epilepsy, if it's subcortical then it's prognosis for movement disorders. This is thought to be overly simplistic. There can be co-occurrence of seizures and paroxysmal movement disorders in the same patient and that has led to this continuum between these two that has been proposed. This is something that needs to be looked into in more detail. Our colleagues in Epilepsy may scoff this, but there's concept of basal ganglia epilepsy manifesting as paroxysmal movement disorders was proposed in the past. And there was this case report that was published out of Italy where there was ictal discharge from the supplementary sensory motor cortex with a concomitant discharge from the ipsilateral coordinate nucleus in a patient with paroxysmal kinesigenic cardioarthidosis. So again, you know, basal ganglia epilepsy, no matter what you call it, the idea is that there is a clear overlap between these two conditions. And I think that is fascinating. Dr Nevel: Really interesting stuff. Well, thank you so much for chatting with me today. Dr Mahajan: Thank you, Kait. And thank you to the Continuum for inviting me to write this article and for this chance to speak about it. I'm excited about how it turned out, and I hope readers enjoy it as well. Dr Nevel: Today again, I've been interviewing doctor Abhi Mahajan about his article on diagnosis and management of paroxysmal movement disorders, which appears in the August 2025 Continuum issue on movement disorders. I encourage all of our listeners to be sure to check out the Continuum Audio episodes from this and other issues. As always, please read the Continuum articles where you can find a lot more information than what we were able to cover in our discussion today. And thank you for our listeners for joining today. And thank you, Abhi, so much for sharing your knowledge with 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.

Waar gingen de spelers uit de VriendenLoterij Eredivisie en de Keuken Kampioen Divisie heen? Welke landen en clubs waren populair? En valt daar een patroon in te ontdekken? We spreken verder met Jan Hoekstra, keeper van gevallen topclub Girondins de Bordeaux en Bilal Ould-Chikh, die FC Volendam inruilde voor Raja Casablanca, het Ajax van Marokko. Aan tafel bij Yordi Yamali: Anco Jansen en Daan Sutorius. Learn more about your ad choices. Visit podcastchoices.com/adchoices

Aan tafel deze week: partijleider D66 Rob Jetten, partijleider NSC Eddy van Hijum, Juliette Verhoeven beleidsadviseur Save the Children, Karel Hendriks directeur Artsen zonder Grenzen, docent Karim Amghar, journalist Coen van de Ven Presentatie: Joost Vullings 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-7-sept-2025 Zaterdag liep in Den Haag een anti-immigratieprotest op het Malieveld uit de hand. Politieagenten werden belaagd, de A12 werd geblokkeerd en bij het D66-partijkantoor werden ruiten ingegooid. Aan tafel D66-partijleider Rob Jetten en NSC-voorman Eddy van Hijum. Met hen bespreken we ook de Algemene Politieke Beschouwingen. De Tweede Kamer stemde deze week voor de vierde keer tegen de komst van ernstige zieke kinderen uit Gaza. Nederlandse ziekenhuizen, gemeenten en humanitaire organisaties geven aan dat er plek is in de ziekenhuizen. Maar vooralsnog ziet politiek Den Haag meer in opvang in de regio. In de uitzending: Karel Hendriks, directeur van Artsen zonder Grenzen, en Juliette Verhoeven van Save the Children.  Wat hebben influencer Andrew Tate, Gaza, de Maccabi-rellen, de dood van de jonge Lisa en Rivaldo en onze politici met elkaar gemeen? Ze zorgen voor heftige emoties en botsingen in het klaslokaal. Karim Amghar is docent Burgerschap op een MBO en columnist voor Trouw. Hoe heeft hij de polarisatie in het klaslokaal zien toenemen en welke middelen heb je als docent om je leerlingen bij te sturen? Groene Amsterdammer journalist Coen van de Ven volgde vier jaar lang van heel dichtbij de fusie tussen GroenLinks en PvdA. Hij volgde Frans Timmermans in vele zaaltjes door het land, zat met Jesse Klaver en Lilianne Ploumen in haar tuinhuisje en sprak vele prominenten, ook als ze even niet met elkaar wilden praten. Hij schreef het allemaal op in zijn boek Een links verhaal. Van de Ven bij Buitenhof over de linkse samenwerking. Hoe is deze ontstaan? Maar ook: hoe gaat het nu? 

Tics are movements or sounds that are quick, recurrent, and nonrhythmic. They fluctuate over time and can be involuntary or semivoluntary. Although behavioral therapy remains the first-line treatment, modifications to comprehensive behavioral intervention have been developed to make treatment more accessible. In this episode, Casey Albin, MD, speaks with Jessica Frey, MD, author of the article “Tourette Syndrome and Tic Disorders” in the Continuum® August 2025 Movement Disorders issue. Dr. Albin is a Continuum® Audio interviewer, associate editor of media engagement, and an assistant professor of neurology and neurosurgery at Emory University School of Medicine in Atlanta, Georgia. Dr. Frey is an assistant professor of neurology, Movement Disorders Fellowship Program Director, and Neurology Student Clerkship Director at the Rockefeller Neuroscience Institute in the department of neurology at West Virginia University in Morgantown, West Virginia. Additional Resources Read the article: Tourette Syndrome and Tic Disorders Subscribe to Continuum®: shop.lww.com/Continuum Earn CME (available only to AAN members): continpub.com/AudioCME Continuum® Aloud (verbatim audio-book style recordings of articles available only to Continuum® subscribers): continpub.com/Aloud More about the American Academy of Neurology: aan.com Social Media facebook.com/continuumcme @ContinuumAAN Host: @caseyalbin Transcript 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 Albin: Hi all, this is Dr Casey Albin. Today I'm interviewing Dr Jessica Frey about her article Tourette Syndrome and Tic Disorders, which appears in the August 2025 Continuum issue on movement disorders. Dr Frey, thank you so much for being here, and welcome to the podcast. I'd love for you to briefly introduce yourself to our audience. Dr Frey: Thank you for having me here today. My name is Jessica Frey, and I am a movement disorder specialist at West Virginia University. I'm also the movement disorder fellowship director, as well as the neurology clerkship student director. Dr Albin: Dr. Frey, I feel like this was one of the things I actually had no exposure to as a resident. For trainees that kind of want to get a better understanding of how these are managed, what kind of counseling you do, what kind of interventions you're using, how can they get a little bit more exposure? Dr Frey: That's a great question, and I actually had a similar experience to you. I did not see that many patients with Tourette syndrome while I was in my residency training. I got a lot more exposure during my fellowship training, and that's when I actually fell in love with that patient population, caring for them, seeing them be successful. I think it depends on the program that you're in. During the pediatric neurology rotation might be your best bet to getting exposure to patients with Tourette syndrome, since a lot of them are going to be diagnosed when they're quite young, and sometimes they'll even continue to follow through young adulthood in the pediatric neurology clinic. However, up to 20% of patients with Tourette syndrome will have persistent tics during adulthood. And so, I think it is important for neurology trainees to understand how to manage them, understand what resources are out there. So, if you have an interest in that, absolutely try to follow either in the pediatric neurology department, or if you have a movement disorder program that has a Tourette clinic or has a movement disorder specialist who has an interest in Tourette syndrome, definitely try to hang out with them. Get to know that patient population, and educate yourself as much as you're able to educate the patients as well. Dr Albin: Yeah, I think that's fantastic advice. You wrote a fantastic article, and it covers a lot of ground. And I think let's start at some of the basics. When I think of Tourette syndrome and tics, I think of Tourette syndrome having tics, but maybe not all patients who have tics have Tourette syndrome. And so, I was wondering, A, if you could confirm that's true; and then could you tell us a little bit about some of the diagnostic criteria for each of these conditions? Dr Frey: Sure. So, a tic is a phenomenological description. So basically, what you're seeing is a description of a motor or phonic tic, which is a particular type of movement disorder. Tourette syndrome is a very specific diagnosis, and the diagnostic criteria for Tourette syndrome at this point in time is that you need to have had at least one phonic tic and two or more motor tics over the course of at least a year before the age of eighteen. Dr Albin: Got it. So, there's certainly more specific and a lot more criteria for having Tourette syndrome. I was struck in reading your article how many myths there are surrounding Tourette syndrome and tic disorders kind of in general. What's known about the pathophysiology of Tourette syndrome, and what are some common misconceptions about patients who have this disorder? Dr Frey: Yeah, so I think that's a really excellent question because for so many years, Tourette syndrome and tic disorders in general were thought to be psychogenic in origin, even dating back to when they were first described. The history of Tourette syndrome is quite interesting in that, when Tourette---who, you know, it's named after---was working with Charcot, a lot of the initial descriptors were of actual case reports of patients who had more psychogenic descriptions, and eventually they became known as tic disorders as well. It wasn't until the discovery of Haldol and using Haldol as a treatment for tic disorders that people started to change their perception and say, okay, maybe there is actually a neurologic basis for Tourette syndrome. So, in terms of the pathophysiology, it's not completely known, but what we do know about it, we think that there is some sort of hyperactivity in the corticostriatal-thalamocortical circuits. And we think that because of this hyperactivity, it leads to the hyperactive movement disorder. We think similar circuitry is involved in conditions like OCD, or obsessive compulsive disorder; as well as ADHD, or attention deficit hyperactivity disorder. And because of that, we actually do tend to see an overlap between all three of these conditions in both individuals and families. Dr Albin: And hearing all of that, does this all come back to, sort of, dopamine and, sort of, behavioral motivation, or is it different than that? Dr Frey: It's probably more complex than just dopamine, but there is the thought that dopamine does play a role. And even one of the hypotheses regarding the pathophysiology is actually that these tics might start as habits, and then when the habits become more common, they actually reshape the dopaminergic pathways. And each time a tic occurs, there's a little bit of a dopaminergic reward. And so over time, that reshapes those hyperactive pathways and changes the actual circuitry of the brain, leading it to be not just a habit but part of their neurologic makeup. Dr Albin: It's fascinating to hear how that actually might play into our neural circuitry and, over time, rewire our brain. Fascinating. I mean, this is just so interesting how movement disorders play into such behavioral regulation and some comorbid conditions like ADHD and OCD. I thought it would be really helpful, maybe, to our listeners to kind of think through a case that I suspect is becoming more common. So, if it's okay with you, I'll present sort of a hypothetical. Dr Frey: Absolutely. Dr Albin: This is a father bringing in his seventeen-year-old daughter. She's coming into the clinic because she's been demonstrating, over the past four to six weeks, some jerking movement in her right arm. And it's happened multiple times a day. And it was a pretty sudden onset. She had not had any movement like this before, and then several weeks ago, started moving the right hand. And then it became even more disruptive: her right leg was involved, she had some scrunching her face. This is all happening at a time where she was dealing with some stress, maybe a little bit of applications around college that she was having a lot of anxiety about. How do you sort of approach this case if this is someone who comes to your office? Dr Frey: Sure. So, I think the first thing that you want to get is a good solid history, trying to understand, what is the origin of these abnormal movements and what led to the abnormal movements. Now, a key thing here is that in Tourette syndrome, and most physiologic tic syndromes, there's a pretty early onset. So, in Tourette syndrome, the expected age of onset is between the ages of five and seven years old. So, to have kind of acute new abnormal movements as a seventeen-year-old would be very unusual for a new-onset diagnosis of Tourette syndrome. However, there's a couple of things from the history that could help you. One would be, were there ever tics in the past? Because sometimes, when you think retrospectively, a lot of these patients might have had a simple eye-blinking tic or a coughing tic when they were a child. And perhaps they did have Tourette syndrome, a very mild case of it. But because the tics were never that pronounced, they never went to see anyone about it and it was never known that they had Tourette syndrome in the first place. If there is no history like that and the movements are completely new, out of the blue, of course you want to rule out anything acute that could be going on that could be causing that. Looking at the phenomenology of the movements can also be very helpful. When you're looking at abnormal tic movements, you would expect most cases of something like Tourette syndrome to occur first in the midline and go in a rostrocoidal distribution. So, you mostly see things happening with eye blinking, throat clearing, sniffling, neck snapping. These are some of the immediate tics that start to happen. We also usually start to see simple tics, as opposed to complex tics, at the beginning. Now, over the course of time, many patients do develop more complex tics that might involve the arms or the extremities, but that would be unusual to see this as a presenting feature of new-onset Tourette syndrome. Dr Albin: Got it. So, I'm hearing that the history really matters and that sometimes, like those, like, first-onset seizures, I imagine as a neurointensivist, we see a lot of patients who've had seizures who think that they're presenting the first time. And then we go back and we say, well, actually they have had some abnormal movements at night. Sounds like it's very similar with these movement disorders where you have to really go back and ask, well, was there some sniffling? Did they go through a phase where they were grunting frequently? Because I can imagine that many children make those behaviors, and that it may not have registered as something that was cause for concern. Dr Frey: Absolutely. Dr Albin: And then the other thing I heard from you was that the phenomenology really matters and that there is a typical presentation, starting from sort of the face and working the way down. And that can be really helpful. But in this case, the family is quite clear. No, no, no. She's never had movements like this before. This is- nothing like this. We promise you, did not go through a phase where she was coughing or blinking, or, this is all totally new. And the phenomenology, they say, no, no, she did not start with blinking. It definitely started in the arm and then progressed in its complex movements. So, knowing that about her, how does that sort of shape how you move forward with the diagnosis? Dr Frey: Yeah. So, really good question. And this is something that I think really peaked during the Covid-19 pandemic. We saw an influx of patients, especially teenage girls or young adult girls, who basically would come in and have these new, acute-onset, abnormal movements. We weren't sure what to call them initially. There was some discussion of calling them “explosive tic disorder” and things like that. A lot of these actually looked very similar to psychogenic nonepileptic seizures, where they would come into the emergency department and have many abnormal movements that were so severe, that they were having a “tic attack” and couldn't stop the abnormal movements from occurring. And we saw so many of these cases during the Covid-19 pandemic that it eventually became known as a distinctive diagnostic criteria with the name of “functional ticlike behavior”, or FTLB. When we think about functional ticlike behavior, we think that these tics are driven more by anxiety and stress. A lot of times, the backstory of these patients, they were in a very stressful situation, and that's when the abnormal movement started. So, a very similar kind of backstory to patients that might develop psychogenic nonepileptic seizures. These tics were popularized, for lack of a better term, via social media during the Covid-19 pandemic. One article is out there that even has called these functional ticlike behaviors as “a pandemic within a pandemic”, because there was such a strong showing of ticlike behavior in the clinics during the Covid-19 pandemic. Although social media was thought to play a big role in these functional ticlike behaviors, we think that there's probably a little bit more complexity and nuance to why these functional ticlike behaviors develop. There is probably a little bit of a genetic predisposition. There's probably some other psychosocial factors at play. And when we see cases like this, the best thing that you can do is educate your patients about the differences between functional ticlike behaviors and tics that we see associated with conditions like Tourette syndrome. And then the best types of treatments that we have seen thus far are treating any underlying stressors, if any of those exist, as well as cognitive behavioral therapy has been shown to be somewhat helpful. As the Covid-19 pandemic has wound down, we have actually seen a lot less cases in our clinic. And one reason we think is less stressors, less uncertainty for the future, which we think was a driving precipitant of some of these cases. But it also is not as popularized in the media as well. There were a lot of TikTok users in particular, which lent itself to the name “TikTok tic”. These videos are not as viewed or not as popular as they were during the Covid-19 pandemic. One reason being that because we are not all relegated to our homes, constantly looking to online sources of information---just in general, we have kind of not been on the Internet as much as we were during the Covid-19 pandemic---as a society as a whole. Dr Albin: This is really fascinating how the environmental milieu, for lack of a better word, like, really influenced how patients were experiencing, sort of, functional neurologic disorders. In your article you describe really these three baskets of primary tic---which can then be a part of Tourette syndrome---,functional ticlike behaviors---which really were a unique manifestation of stress and anxiety specifically during the Covid-19 pandemic---, and then tics as a manifestation of some either different underlying etiology or medication side effect. So, when do you get concerned about that secondary etiology? Dr Frey: So secondary tics can occur in a variety of instances. I think some of the more common examples would be in genetic disorders. So, Huntington's disease is a really good example. I think we all associate chorea with Huntington's disease. That's probably the most commonly associated phenomenology that we see with Huntington's disease. But we can see a variety of movement disorders in Huntington's, and one of them is tics. So, when we see tics in association with other types of movement disorders, we should be thinking about a possible genetic etiology. If we see tics in association with other neurologic symptoms, such as seizures or cognitive changes, we should be thinking that this is something besides a primary tic disorder. You also mentioned medication use, and it's really important to think about tardive tics. I know we often think about tardive dyskinesia, and the first kind of phenomenology that jumps into our brain is usually chorea because it's those abnormal lip movements, finger movements, toe movements that we see after a patient has been on, for example, an antipsychotic or an antiemetic that has antidopaminergic properties. However, we can see a variety of abnormal movement disorders that occur secondary to antidopaminergic medications, especially after abrupt withdrawal of these antidopaminergic medications. And tics are one of them. There have been cases reported where people that have tardive tics will still report that they have a premonitory urge, as well as a sense of relief after their tics. So, it actually can seem very similar to Tourette syndrome and the tics that people with Tourette syndrome experience on a regular basis. The key here is that the treatment might differ because if it's due to an antidopaminergic medication or abrupt withdrawal of that antidopaminergic medication, you might need to treat it a little bit differently than you would otherwise. Dr Albin: I love that you bring in, it's not just looking at their specific movement disorder that they may be coming to clinic with, that tic disorder, but are there other movement disorders? Has there been a change in their medication history? Have they had cognitive changes? So really emphasizing the importance of that complete and comprehensive neurologic history, neurologic physical exam, to really get the complete picture so that it's not honing in on, oh, this is a primary tic. That's all there is to it, because it could be so much more. I know we're getting close to sort of the end of our time together, but I really wanted to switch to end on talking about treatment. And your article does such a beautiful job of talking about behavioral interventions and really exciting new medical interventions. But I would like to, if you don't mind, have you focus on, what behavioral counseling and what education do you provide for patients and their families? Because I imagine that the neurologist plays a really important role in educating the patient and their family about these disorders. Dr Frey: Absolutely. When we think about treatment, one of the most important things you can do for patients with Tourette syndrome or other primary tic disorders is educate them. This remains true whether it's a primary tic disorder that we see in Tourette syndrome or the functional ticlike behavior that we've discussed here. A lot of times, because there is such a stigma against people with tic disorders and Tourette syndrome, when they hear that they have Tourette syndrome or they are diagnosed with that, sometimes that can be an upsetting diagnosis. And sometimes you have to take time explaining what exactly that means and debunking a lot of the myths that go along with the stigmas associated with Tourette syndrome. I think a lot of times people are under the false assumption that people with Tourette syndrome cannot lead normal lives and cannot hold down jobs and cannot be productive members of society. None of that is true. Most of my patients have great lives, good quality of life, and are able to go about their day-to-day life without any major issues. And one of the reasons for that is we do have a lot of great treatment options available. Another important stigma to break down is that people with tic disorders are doing this for attention or doing this because they are trying to get something from someone else. That is absolutely false. We do think that the tics themselves are semivolitional because people with Tourette syndrome have some degree of control over their tics. They can suppress them for a period of time. But a lot of people with tic disorders and Tourette syndrome will describe their tics as if you're trying to hold onto a sneeze. And you can imagine how uncomfortable it is to hold in a sneeze. We're all able to do it for a period of time, but it's much easier to just allow that sneeze to occur. And a lot of times that's what they are experiencing, too. So, although there is some degree of control, it's not complete control, and they're certainly not doing these tics on purpose or for attention. So that's another important myth to debunk when you're counseling patients and their families. I think the dynamic between young patients that are presenting with their parents or guardians, sometimes that dynamic is a little bit challenging because another faulty assumption is that parents feel they are responsible for having this happen to their child. There used to be a really strong sense that parents were responsible for the tics that occurred in their children, and that is also absolutely not true. Parenting has nothing to do with having the tics or not. We know that this is a neurodevelopmental disorder. The brain is indeed wired differently and it's important to counsel that with the parents, too, so that they understand what tools they need to be successful for their children as well. Dr Albin: I love that. So, it's a lot of partnership with patients and their families. I really like that this is just a wire different, and I hope over time that working together we as neurologists can help break down some of that stigmatization for these patients. This has been an absolutely phenomenal discussion. I have so enjoyed learning from your article. For the listeners out there, there are some really phenomenal tables that go into sort of how to approach this from the office perspective, how to approach it from the treatment perspective. So, thank you again, Dr Jessica Frey, for your article on Tourette syndrome and tic disorders, which appears in the August 2025 Continuum issue on movement disorders. Be sure to check out Continuum Audio episodes from this and other issues, and thank you so much to our listeners for joining us today. Dr Frey: Thank you for having me. Dr Monteith: This is Dr Teshamae Monteith, Associate Editor of Continuum Audio. If you've enjoyed this episode, you'll love the journal, which is full of in-depth and clinically relevant information important for neurology practitioners. Use 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 2006, vlak voordat hij aftrad, trok VN-secretaris-generaal Kofi Annan de stekker uit de Mensenrechten Commissie van de Verenigde Naties. Hij deelde de mening van een groep democratische VN-lidstaten die het bizar vonden dat de commissie vrijwel uitsluitend bestond uit dubieuze landen en meedogenloze dictaturen. Met de oprichting van een nieuwe organisatie, de VN Mensenrechtenraad, hoopten Annan en die groep democratische lidstaten een fatsoenlijke VN-toezichthouder voor mensenrechten te creëren. Nette leden van de Raad, zoals Nederland, zijn altijd gepikeerd als je het beestje bij de naam noemt, maar wat is die Raad een opportunistisch zootje ongeregeld. Een greep uit de 47 lidstaten : Burkina Faso, de Democratische republiek Congo, Eritrea, Libië, Rwanda, Somalië, Soedan, Afghanistan, Azerbeidzjan, China, Koeweit, Qatar, Saoedi-Arabië, El Salvador, Cuba en Venezuela. Landen met een gruwelijke staat van dienst op het gebied van mensenrechten, maar wel andere landen de maat nemen. Ze hebben net onderzoek laten doen waaruit blijkt dat Israël genocide pleegt . Populair onderwerp, dus de media pakken er stevig mee uit. Maar als juist deze Raad het beweert is het even geloofwaardig als wanneer het onderzoek het tegendeel had uitgewezen. Aan de vooravond van de 80ste Algemene Vergadering van de Verenigde Naties kan het geen kwaad om nog eens te beseffen dat de VN een organisatie is zonder ziel. Het is de optelsom van alle 193 lidstaten, die op vrijwel geen enkel gebied een gezamenlijke ideologische overtuiging hebben. Sommige werken samen of hebben bondgenootschappelijke banden, maar daar heeft de VN part noch deel aan. Besluiten van de Algemene Vergadering kunnen symbolisch misschien iets betekenen, maar internationaal-juridisch nooit. En wat koop je voor een symbool? Neem de erkenning van Palestina, door zo’n 150 lidstaten. Als die het echt menen, waarom openen ze dan geen ambassades in Ramallah, en waarom zijn erg geen Palestijnse ambassades in die 150 landen? Bij wie komen de ambassadeurs in Palestina hun geloofsbrieven aanbieden, en waar? Oh ja, nog even over die genocide. Waarom erkent de Nederlandse regering tot de huidige dag de Armeense Genocide niet? 110 jaar geleden vermoordden de Turken anderhalf miljoen Armeniërs. Demissionair premier Schoof onderschrijft de mening van zijn voorgangers. Je moet voorzichtig met de term ‘genocide’ omgaan, vindt hij. ‘Juist als verdediger van het internationaal recht, hoort de Nederlandse regering het mogelijke gebruik van zwaarwegende juridische kwalificatie zeer zorgvuldig te verkennen’. Mooie boodschap voor de Nederlandse vertegenwoordiger bij de VN Mensenrechtenraad.See omnystudio.com/listener for privacy information.

Aan tafel deze week: partijleider GroenLinks-PvdA Frans Timmermans, admiraal Rob Bauer, econoom Paul Krugman en advocaat Ina Brouwer. 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-14-sept-2025 Nederland gaat niet bepaald door de meest stabiele politieke periode. Welk effect heeft het geharrewar in Den Haag op de ingewikkelde geopolitieke ontwikkelingen? Hoe belangrijk is de steun aan Oekraïne nadat Rusland deze week drones het Poolse luchtruim instuurde? Een gesprek met oppositieleider Frans Timmermans.  Negentien Russische drones in Pools luchtruim. Was dit een vergissing, zoals president Trump opperde, of een doelbewuste actie van president Poetin? Daarover admiraal Rob Bauer. Wat gebeurt er zodra NAVO-luchtruim geschonden wordt, wat is er nodig en zijn wij goed voorbereid? De Amerikaanse Nobelprijswinnaar en econoom Paul Krugman schreef vijfentwintig jaar lang columns voor de New York Times. Ook is hij een fervent criticus van Trump. Met zijn eigen substack nieuwsbrief bereikt hij honderdduizenden lezers met economische analyses. Maar ook met zijn opinie over de staat van de democratie. En advocaat Ina Brouwer schuift aan. Brouwer, zelf oud-corpslid, staat de slachtoffers van de Utrechtse bangalijst bij. Ze zag van dichtbij hoe het uitlekken van foto's, namen en adressen de levens van jonge vrouwen overhoopgooide. Nu vecht ze voor erkenning van de slachtoffers én een cultuuromslag bij het corps.

Ataxia is a neurologic symptom that refers to incoordination of voluntary movement, typically causing gait dysfunction and imbalance. Genetic testing and counseling can be used to identify the type of ataxia and to assess the risk for unaffected family members. In this episode, Katie Grouse, MD, FAAN, speaks with Theresa A. Zesiewicz, MD, FAAN, author of the article “Ataxia” in the Continuum® August 2025 Movement Disorders 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. Zesiewicz is a professor of neurology and director at the University of South Florida Ataxia Research Center, and the medical director at the University of South Florida Movement Disorders Neuromodulation Center at the University of South Florida and at the James A. Haley Veteran's Hospital in Tampa, Florida. Additional Resources Read the article: Ataxia Subscribe to Continuum®: shop.lww.com/Continuum Earn CME (available only to AAN members): continpub.com/AudioCME Continuum® Aloud (verbatim audio-book style recordings of articles available only to Continuum® subscribers): continpub.com/Aloud More about the American Academy of Neurology: aan.com Social Media facebook.com/continuumcme @ContinuumAAN Full episode transcript available here Dr Jones: This is Dr Lyell Jones, Editor-in-Chief of Continuum. Thank you for listening to Continuum Audio. Be sure to visit the links in the episode notes for information about earning CME, subscribing to the journal, and exclusive access to interviews not featured on the podcast. Dr Grouse: This is Dr Katie Grouse. Today I'm interviewing Dr Theresa Zesiewicz about her article on ataxia, which appears in the August 2025 Continuum issue on movement disorders. Welcome to the podcast, and please introduce yourself to our audience.  Dr Zesiewicz: Well, thank you, Dr Grouse. I'm Dr Theresa Zesiewicz, otherwise known as Dr Z, and I'm happy to be here. Dr Grouse: I have to say, I really enjoyed reading your article. It was a really great refresher for myself as a general neurologist on the topic of ataxia and a really great reminder on a great framework to approach diagnosis and management. But I wanted to start off by asking what you feel is the key message that you hope our listeners will take away from reading your article. Dr Zesiewicz: Yes, so, thanks. I think one of the key messages is that there has been an explosion and renaissance of genetic testing in the past 10 years that has really revolutionized the field of ataxia and has made diagnosis easier for us, more manageable, and hopefully will lead to treatments in the future. So, I think that's a major step forward for our field in terms of genetic techniques over the last 10 years, and even over the last 30 years. There's just been so many diseases that have been identified genetically. So, I think that's a really important take-home message. The other take-home message is that the first drug to treat Friedreich's ataxia, called omaveloxolone, came about about two years ago. This was also a really landmark discovery. As you know, a lot of these ataxias are very difficult to treat. Dr Grouse: Now pivoting back to thinking about the approach to diagnosis of ataxia, how does the timeline of the onset of ataxia symptoms inform your approach? Dr Zesiewicz: The timeline is important because ataxia can be acute, subacute or chronic in nature. And the timeline is important because, if it's acute, it may mean that the ataxia took place over seconds to hours. This may mean a toxic problem or a hypoxic problem. Whereas a chronic ataxia can occur over many years, and that can inform more of a neurodegenerative or more of a genetic etiology. So, taking a very detailed history on the patient is very important. Sometimes I ask them, what is the last time you remember that you walked normal? And that can be a wedding, that can be a graduation. Just some timeline, some point, that the patient actually walked correctly before they remember having to hold onto a railing or taking extra steps to make sure that they didn't fall down, that they didn't have imbalance. That sometimes that's a good way to ask the patient when is the last time they had a problem. And they can help you to try to figure out how long these symptoms have been going on. Dr Grouse: I really appreciate that advice. I will say that I agree, it can sometimes be really hard to get patients to really think back to when they really started to notice something was different. So, I like the idea of referencing back to a big event that may be more memorable to them. Now, given that framework of, you know, thinking through the timeline, could you walk us through your approach to the evaluation of a patient who presents to your clinic with that balance difficulties once you've established that? Dr Zesiewicz: Sure. So, the first thing is to determine whether the patient truly has ataxia. So, do they have imbalance? Do they have a wide base gait? That's very important because patients come in frequently to your clinic and they'll have balance problems, but they can have knee issues or hip issues, neuropathy, something like that. And sometimes what we say to the residents and the students is, usually ataxia or cerebellar symptoms go together with other problems, like ocular problems are really common in cerebellar syndromes. Or dysmetria, pass pointing, speech disorder like dysarthria. So, not only do you need to look at the gait, but you should look at the other symptoms surrounding the gait to see if you think that the patient actually has a cerebellar syndrome. Or do they have something like a vestibular ataxia which would have more vertigo? Or do they have a sensory ataxia, which would occur if a person closes his eyes or has more ataxia when he or she is in the dark? So, you have to think about what you're looking at is the cerebellar syndrome. And then once we look to see if the patient truly has a cerebellar syndrome, then we look at the age, we look at---as you said before, the timeline. Is this acute, subacute, or chronic? And usually I think of ataxia as falling into three categories. It's either acquired, it's either hereditary, or it's neurodegenerative. It can be hereditary. And if it's not hereditary, is it acquired, or is it something like a multiple system atrophy or a parkinsonism or something like that? So, we try to put that together and start to narrow down on the diagnosis, thinking about those parameters. Dr Grouse: That's really a helpful way to think through it. And it is true, it can get very complex when patients come in with balance difficulties. There's so many things you need to think about, but that is a great way to think about it. Of course, we know that most people who come in to the Movements Disorders clinic are getting MRI scans of their brains. But I'm curious, in which cases of patients with cerebellar ataxia do you find the MRI to be particularly helpful in the diagnosis? Dr Zesiewicz: So, an MRI can be very important. Not always, but- so, something like multiple system atrophy type C where you may see a hot cross bun sign or a pontine hyperintensity on the T2-weighted image, that would be helpful. But of course, that doesn't make the diagnosis. It's something that may help you with the diagnosis. In FXTAS, which is fragile X tremor/ataxia syndrome, the patient may have the middle cerebellar peduncle sign or the symmetric hyperintensity in the middle cerebellar peduncles, which is often visible but not always. Something like Wernicke's, where you see an abnormality of the mammillary bodies. Wilson's disease, which is quite rare, T2-weighted image may show hyperintensities in the putamen in something like Wilson's disease. Those are the main MRI abnormalities, I think, with ataxia. And then we look at the cerebellum itself. I mean, that seems self-evident, but if you look at a sagittal section of the MRI and you see just a really significant atrophy of the cerebellum, that's going to help you determine whether you really have a cerebellar syndrome. Dr Grouse: That's really encouraging to hear a good message for all of us who sometimes feel like maybe we're missing something. It's good to know that information can always come up down the line to make things more clear. Your article does a great review of spinal cerebellar ataxia, but I found it interesting learning about the more recently described syndrome of SCA 27B. Would you mind telling us more about that and other really common forms of SCA that's good to keep in mind? Dr Zesiewicz: Sure. So, there are now 49 types of spinal cerebellar ataxia that have been identified. The most common are the polyglutamine repeat diseases: so, spinocerebellar ataxia type 3 or type 2, type 6, are probably the most common. One of the most recent spinocerebellar ataxias to be genetically identified and clinically identified is spinocerebellar ataxia 27B. This is caused by a GAA expansion repeat in the first intron of the fibroblast growth factor on chromosome 13. And the symptoms do include ataxia, eye problems, downbeat nystagmus, other nystagmus, vertical, and diplopia. It appears to be a more common form of adult-onset ataxia, and probably more common than was originally thought. It may account for a substantial number of ataxias, like, a substantial percentage of ataxias that we didn't know about. So, this was really a amazing discovery on SCA 27B. Dr Grouse: Now a lot of us I think feel a little anxious when we think about genetic testing for ataxia simply because there's so many forms, things are changing quickly. Do you have a rule of thumb or a kind of a framework that we can think of as we approach how we should be thinking about getting genetic testing for the subset of patients? Dr Zesiewicz: Sure. And I think that this is where age comes into play a lot. So, if you have a child who's 10, 11, or 12 who's having balance problems in the schoolyard, does not have a history of ataxia in the family, the teachers are telling you that the child is not running correctly, they're having problems with physical education, that is someone who you would think about testing for Friedreich's ataxia. A preteen or a child, that would be one thing that would be important to test. When you talk to your patient, it's important to really take a detailed family history. Not just mom or dad, but ethnicity, grandparents, etc. And sometimes, once in a while, you come up with a known spinal cerebellar ataxia. Then you can just test for that. So, if a person is from Portugal or has Portugal background and they have ataxia and the parents had ataxia, you would think of spinal cerebellar ataxia type 3. Or if they're Brazilian, or if the person is from a certain area of Cuba and mom and dad had ataxia and that person has ataxia, you would think of spinal cerebellar ataxia type 2. Or if a person has ataxia and their parent had blindness or visual problems, you may be more likely to think of spinal cerebellar ataxia type 7, for example. If they have that---either they have a known genetic cause in in the family, first degree family, or they come from an area of the world in which we can pinpoint what type we think it is---you can go ahead and get those tests. If not, you can take an ataxia comprehensive panel. Many times now, if you take the panel and the panel is negative, it will reflex to the whole exome gene sequencing, where we're finding really unusual and more rare types of ataxia, which are very interesting. Spinal cerebellar ataxia type 32, spinal cerebellar ataxia type 36, I had a spinal cerebellar ataxia type 15. So, I think you should start with the age, then the family history, then where the person is from. And then, if none of those work out, you can get a comprehensive panel, and then go on to whole exome gene sequencing. Dr Grouse: That's really, really useful. Thank you so much for breaking that down in a really simple way that a lot of us can take with us. Pivoting a little bit now back towards different types of acquired ataxias, what are some typical lab tests that you recommend for that type of workup? Dr Zesiewicz: Again, if there's no genetic history and the person does not appear to have a neurodegenerative disease, we do test for acquired ataxias. Acquired ataxias can be complex. Many times, they are in the autoimmune family. So, what we start with are just basic labs like a CBC or a CMP, but then we tried to look at some of the other abnormalities that could cause ataxia. So, celiac disease, stiff person syndrome. So, you would look at anti-glutamic acid decarboxylase antibodies, Hashimoto's---so, antithyroglobulin antibodies or antithyroperoxidase antibodies would be helpful. You know, in a case of where the patients may have an underlying neoplasm, maybe even a paraneoplastic workup, such as an anti-Hu, anti-Yo, anti-Ri. A person has breast cancer, for example, you may want to take a paraneoplastic panel. I've been getting more of the anti-autoimmune encephalitis panels in some cases, that were- that are very interesting. And then, you know, things that sometimes we forget now like the syphilis test, thyroid-stimulating test, take a B12 and folate, for example. That would be important. Those are some of the labs. We just have on our electronic chart a group of acquired labs for ataxia. If we can't find any other reason, we just go ahead and try to get those. Dr Grouse: Now, I'm curious what you think is the most challenging aspect of diagnosing a patient with cerebellar ataxia? Dr Zesiewicz: So, for those of us who see many of these patients a day, some of the hardest patients are the ones that---regardless of the workup that we do, we've narrowed it down, it's not hereditary. You know, they've been through the whole exome gene sequencing and we've done the acquired ataxia workup. It doesn't appear to be that. And then we've looked for parkinsonism and neurodegenerative diseases, and it doesn't appear to be that either; like, the alpha-synuclein will be negative. Those are the toughest patients, where we think we've done everything and we still don't have the answer. So, I've had patients in whom I've taken care of family members years and years ago, they had a presumed diagnosis, and later on I've seen their children or other family members. And with the advent of the genetic tests that we have, like whole exome gene sequencing, we have now been able to give the patient and the family a definitive diagnosis that they didn't have 25 years ago. So, I would say don't give up hope. Retesting is important, and as science continues and we get more information and we make more landmark discoveries in genetics, you may be better able to diagnose the patient. Dr Grouse: I was wondering if you had any recommendations regarding either some tips and tricks, some pearls of wisdom you can impart to us regarding the work of ataxia, or conversely, any big pitfalls that you can help us avoid? I would love to hear about it. Dr Zesiewicz: Yeah, there's no easy way to treat or diagnose ataxia patients. I've always felt that the more patients you see- and sounds easy, but the more patients you see, the better you're going to become at it, and eventually things are going to fall into place. You'll begin to see similarities in patients, etc. I think it's important not only to make sure that a person has ataxia, but again, look at the other signs and symptoms that may point to ataxia that you'll see in a cerebellar syndrome. I think it's important to do a full neuroexam. If a person has spasticity, that may point you more towards a certain type of ataxia than if a person has no reflexes, for example, that we see in Friedreich's ataxia. Some of the ocular findings are very interesting as well. It's important to know if a person has a tremor. I've seen several Wilson's disease cases in my life with ataxia. They're very important. I think a full neuroexam and also a very detailed history would be very helpful. Dr Grouse: Tell us about some promising developments in the diagnosis and management of ataxia that we should be on the lookout for. Dr Zesiewicz: The first drug for Friedreich's ataxia was FDA-approved two years ago, which was an NRF2 activator, which was extremely exciting and promising. There are also several medications that are now in front of the FDA that may also be very promising and have gone through long clinical trials. There's a medication that's related to riluzole, which is a medication used for amyotrophic lateral sclerosis, that has been through about seven years of testing. That is before the FDA as well for spinal cerebellar ataxia. Friedreich's ataxia has now completed the first cardiac gene therapy program with AAV vectors, which- we're waiting for full results, but that's a cardiac test. But I would assume that in the future, neurological gene therapy is not far behind if we've already done cardiac gene therapy and Friedreich's ataxia. So, you know, some of these AAV vector-based genetic therapies may be very helpful, as well as ASO, antisense oligonucleotides, for example. And I think in the future, other things to think about are the CRISPR/Cas9 technology for potential treatment of ataxia. It is a very exciting time, and some major promising therapies have been realized in the past 2 to 3 years. Dr Grouse: Well, that's really exciting, and we'll all look forward to seeing these becoming more clinically applicable in the future. So, thank you so much for coming to talk with us today. Dr Zesiewicz: Thank you. Dr Grouse: Again, today I've been interviewing Dr Theresa Zesiewicz about her article on ataxia, which appears in the August 2025 Continuum issue on movement disorders. 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.

Aan het Oekraïense front duiken steeds vaker Afrikaanse soldaten op. En opvallend vaak zijn het Kameroeners die aan Russische zijde vechten. Wat drijft hen om te vechten in een oorlog die niet van hen is? Luister naar journalist en documentairemaker Bram Vermeulen. Onze journalistiek steunen? Dat kan het beste met een (digitaal) abonnement op de Volkskrant, daarvoor ga je naar www.volkskrant.nl/podcastactie Presentatie: Pieter KlokRedactie: Corinne van Duin, Lotte Grimbergen, Iris Brans, Julia van Alem en Jasper VeenstraMontage: Rinkie BartelsSee omnystudio.com/listener for privacy information.

Aan tafel deze week: Demissionair minister van Defensie Ruben Brekelmans, burgemeester van Utrecht Sharon Dijksma, directeur van VNG Leonard Geluk, hoofdeconoom van ING Marieke Blom en directeur van het Mauritshuis Martine Gosselink. 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:   https://bit.ly/buitenhof-7-sept-2025 Ruben Brekelmans schuift aan, een dag na het VVD-congres. En na een weerbarstige zomer. Na de PVV vertrok ook NSC uit het kabinet. En dat terwijl het geopolitiek niet bepaald stabieler werd. Het vertrouwen in Den Haag is gedaald tot een dieptepunt. Ook het lokale bestuur in Nederland ergert zich groen en geel aan de chaos in de landelijke politiek. Sharon Dijksma en Leonard Geluk, beiden verbonden aan de Vereniging van Nederlandse Gemeenten, maken zich grote zorgen. De belangrijkste centrale bank in de belangrijkste economie van de wereld staat steeds meer onder druk. Wat betekent dit voor de onafhankelijkheid van deze centrale bank? En voor de economie? Een gesprek met Marieke Blom. En de Nederlandse kunstsector keek deze week met ingehouden adem naar de Verenigde Staten waar president Trump zijn ramkoers op Amerikaanse musea verstevigde. Een gesprek met Martine Gosselink.

(01:30) Deze week organiseerde China een spectaculaire militaire parade om het einde van de Tweede Wereldoorlog te herdenken. Beelden van de militaire parade werden massaal gedeeld door de staatsmedia. Hoe zet China dat oorlogsverleden in voor het huidige Chinese zelfbeeld? Daarover te gast is China-kenner Manya Koetse.     (14:50) De shortlist van de Libris Geschiedenis Prijs 2025    (23:11) De column van Sana Valiulina.    (29:43) Princess Mononoke, Spirited Away en The Boy and the Heron, een paar filmtitels uit dezelfde stal: die van Studio Ghibli. Deze beroemde animatiestudio is 40 jaar, en daarom zijn de films in Nederland in de bioscoop te zien. Wat is de betekenis van deze Japanse studio geweest, en hoe past het in de geschiedenis van anime? Japanoloog Otis Eversteijn vertelt.  (38:45) Deze week krijgen we recensies van Sanne Frequin. Zij bespreekt twee historische boeken en een tentoonstelling:  Floris V ontvoerd en vermoord - een bundel ingeleid door Wim van Anrooij  De middeleeuwen - Dan Jones (vert. Roelof Posthuma)  Artus Quellinus - Beeldhouwer van Amsterdam - tentoonstelling in het Paleis op de Dam    (52:53) Het was de droom van Adolf Hitler; het bouwen van een Führermuseum. Hitler die was afgewezen door de kunstacademie was vastbesloten het grootste museum ter wereld te bouwen. De tot nu toe weinig bekende Duits kunsthistoricus Erhard Göpel speelde een sleutelrol bij het wegroven van de kunst uit bezette gebieden. Wie was Göpel? Hoe slaagde hij erin om schilderijen die de nazi's op het oog hadden te ontfutselen?  Cultuurwetenschapper Ruud Breteler is te gast.  (01:05:05) Deze week de OVT-doc: ‘De Vrolijke Vernietiging' is een project van kunstenaar Maurice Hermans waarin is te zien hoe traumatisch het uitvlakken van de mijngeschiedenis was voor Zuid-Limburg. Er is ‘fantoompijn' in Heerlen, omdat vertrouwde ijkpunten zoals de Lange Jan en de Lange Lies – de hoogste schoorstenen – opeens weg waren en daarmee ook de identiteit van de stad. Hoe kun je verder met een geschiedenis zonder tastbaar houvast?   (01:37:05) Aan de hand van de documentaire De Vrolijke Vernietiging gaan we in gesprek met Casper Gelderblom, wethouder van de Gemeente Heerlen. Veel mensen in deze regio hebben moeite met de energierekening betalen, terwijl de mijnen tijdens de hoogtijdagen van de kolenindustrie recordwinsten behaalden. De burgemeesters willen dat de winsten van de mijnen alsnog terugvloeien naar de regio en hebben de investeerders van de particuliere mijnen een brief gestuurd over de zogenaamde 'ereschuld'.  Meer info: https://www.vpro.nl/ovt/artikelen/ovt-7-september-2025   (https://www.vpro.nl/ovt/artikelen/ovt-7-september-2025%20)

President Trump en First Lady Melania ontvingen gisteravond een select gezelschap van de grootste tech-CEO’s voor een exclusief diner in het Witte Huis. Aan tafel zaten onder meer Mark Zuckerberg (Meta), Tim Cook (Apple), Sundar Pichai (Google), Satya Nadella (Microsoft) en Sam Altman (OpenAI). Ook Bill Gates was aanwezig en zat opvallend naast Melania, die de avond mede organiseerde. Tijdens het diner kregen de CEO’s de kans hun plannen voor investeringen in de VS te presenteren. Trump prees de bedrijven om hun rol in de Amerikaanse economie en kondigde aan dat er “zeer substantiële” heffingen op import van chips aankomen voor bedrijven die niet in de VS produceren of investeren. Opvallend was de afwezigheid van Elon Musk, hij zou naar eigen zeggen wel uitgenodigd zijn maar niet kunnen en stuurde daarom een vertegenwoordiger. Musk was eerder erg hecht met Trump maar de twee hadden afgelopen maanden publiekelijk vooral ruzie op sociale media. Google-ceo Sundar Pichai werd door Trump nog aangesproken op de rechtszaak die een dag eerder beklonken was. Google werd daarin door de Amerikaanse overheid aangeklaagd om een illegale monopolie. De rechter besloot vooral in het voordeel van Google. Ook in deze Tech Update: OpenAI kondigt het OpenAI Jobs Platform aan, een AI-gedreven vacatureplatform dat vanaf midden 2026 moet concurreren met LinkedIn. Daarnaast werkt het bedrijf samen met Broadcom aan een speciale AI-chip voor intern gebruik. Die chip moet ook in 2026 in gebruik genomen worden. Zometeen in De Schaal van Hebben: VanMoof S6See omnystudio.com/listener for privacy information.

De MSCI Emerging Markets Index zit al meer dan een half jaar in de lift. Het is dan ook een ontwikkeling waar beide experts in deze aflevering van BeursTalk op aanslaan. Marc Langeveld van het Antaurus AI Tech Fund legt uit: "De dollar daalt in waarde, niet alleen ten opzichte van de euro, maar wordt ook goedkoper voor opkomende landen. Dat houdt de inflatie daar onder controle." Marc kijkt dan ook met interesse naar techbedrijven in Azië, maar ook in Latijns-Amerika. Koen Bender van Mercurius Vermogensbeheer is eveneens positief, ook vanuit het oogpunt van risicospreiding. "Wij hebben altijd al Emerging Markets in portefeuille gehad voor onze klanten. Dat hoort thuis in een goed gespreide portfolio. Je compenseert er ook de pijn van de zwakke dollar enigszins mee." Wat betreft het sentiment zijn beide experts voorzichtig. Naast de prestaties van bedrijven moet je tegenwoordig de geopolitieke ontwikkelingen ook goed in de gaten houden, het wordt complexer. Dat maakt het dan ook lastig, vinden Marc en Koen, om in dit klimaat harde uitspraken te doen over de ontwikkeling op de beurzen. Verder bespreken we in de podcast onder andere de cijfers van CVC Capital en Saleforce en de aanstaande beursgang van fintechbedrijf Klarna. Uiteraard bespreken we de luisteraarsvragen en geven de experts hun tips. Marc kiest een Amerikaans techbedrijf, Koen tipt een Japans concern. Geniet van de podcast! Let op: alleen het eerste deel is vrij te beluisteren. Wil je de hele podcast (luisteraarsvragen en tips) horen, wordt dan Premium lid van BeursTalk. Dat kost slechts 9,95 per maand, 99 euro voor een heel jaar. Abonneren kan hier! VanEck ETF’s (advertorial) Deze week is ook weer het tweewekelijks gesprek te beluisteren met Martijn Rozemuller, ceo van VanEckETF’s, de partner van BeursTalk. Met Martijn bespreek ik deze week de ontwikkelingen op de energiemarkt en wat dat betekent voor beleggers in ETF's. Aan de ene kant moeten we omschakelen, tegelijkertijd zien we de vraag naar olie en gas nog steeds toenemen. VanEck heeft geen ETF die direct in oliemaatschappijen investeert, maar toch kun je bij VanEck terecht als op de toenemende vraag wilt inspelen. De VanEck Oil Services ETF belegt, de naam zegt het al, bedrijven die diensten verlenen aan de oliesector. Bij een toenemende vraag naar olie, profiteren die bedrijven er ook van. Uiteraard zullen de fossiele bronnen over een aantal decennia uitgeput raken. Vandaar de aandacht, ook van beleggers, voor alternatieve energiebronnen. Martijn legt uit dat VanEck ook voor die transitie klaar is. Zo kun je nu al beleggen in de VanEck Hydrogen Economy ETF en de VanEck Uranium and Nuclear Technologies ETF. Martijn vertelt je de ins en outs van beide producten. Geniet van de podcast! De gepresenteerde informatie door VanEck Asset Management B.V. en de aan haar verbonden en gelieerde bedrijven (samen "VanEck") is enkel bedoeld voor informatie en advertentie doeleinden aan Nederlandse beleggers die Nederlands belastingplichtig zijn en vormt geen juridisch, fiscaal of beleggingsadvies. VanEck Asset Management B.V. is een UCITS-beheerder. Loop geen onnodig risico. Lees de Essentiële Beleggersinformatie of het Essentiële-informatiedocument. Meer informatie? https://www.vaneck.com/nl/nl/See omnystudio.com/listener for privacy information.

Chorea describes involuntary movements that are random, abrupt, and unpredictable, flowing from one body part to another. The most common cause of genetic chorea in adults is Huntington disease, which requires comprehensive, multidisciplinary care as well as support for care partners, who may themselves be diagnosed with the disease. In this episode, Aaron Berkowitz, MD, PhD FAAN speaks with Kathryn P. L. Moore, MD, MSc, author of the article “Huntington Disease and Chorea” in the Continuum® August 2025 Movement Disorders 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 in San Francisco, California. Dr. Moore is an assistant professor and director of the Parkinson's Disease and Movement Disorders Fellowship in the department of neurology at Duke University in Durham, North Carolina. Additional Resources Read the article: Huntington Disease and Chorea Subscribe to Continuum®: shop.lww.com/Continuum Earn CME (available only to AAN members): continpub.com/AudioCME Continuum® Aloud (verbatim audio-book style recordings of articles available only to Continuum® subscribers): continpub.com/Aloud More about the American Academy of Neurology: aan.com Social Media facebook.com/continuumcme @ContinuumAAN Host: @AaronLBerkowitz Guest: @KatiePMooreMD 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 with Continuum Audio, and today I'm interviewing Dr Kathryn Moore about her article on diagnosis and management of Huntington disease and chorea, which appears in the August 2025 Continuum issue on movement disorders. Welcome to the podcast, Dr Moore. Could you please introduce yourself to our audience? Dr Moore: Yeah, thank you so much. I'm so excited to be here. I'm Dr Moore. I'm an assistant professor of neurology at Duke University, where I work as a movement disorder specialist. I run our fellowship there and help with our residency program as well. So, I'm excited to speak with our listeners about chorea today. Dr Berkowitz: Fantastic. And we're excited to talk to you about chorea. So, as a general neurologist myself, I only see chorea pretty rarely compared to other movement disorders like tremor, myoclonus, maybe the occasional tic disorder. And like anything I don't see very often, I always have to look up the differential diagnosis and how to evaluate a patient with chorea. So, I was so glad to read your article. And next time I see a patient with chorea, I know I'll be referring to your article as a great reference to have a framework for how to approach it. I hope our readers will look at all these helpful tables on differential diagnosis based on distribution of chorea in the body, potential etiologies, time course of onset and evolution, associated drug-induced causes, what tests to send. So, I highly recommend our listeners read the article. Keep those tables handy for when a patient comes in with chorea. I'm excited to pick your brain about some of these topics today. First, how do you go about distinguishing chorea from other hyperkinetic movement disorders when you see a patient that you think might have chorea? Dr Moore: One of the wonderful things about being a movement disorder specialist is we spend a lot of time looking at movements and training our brain to make these distinctions. The things that I would be looking out for chorea is involuntary, uncontrolled movements that appear to be brief and flowing from one part of the body to another. So, if you can watch a patient and predict what movements they're going to do, this probably isn't chorea. And it should be flowing from one part of the body to another. So, not staying just in one part of the body or having sustained movements. It can be difficult to distinguish between a tic or dystonia or myoclonus. Those things tend to be more predictable and repetitive than the chorea, which tends to be really random and can look like dancing. Dr Berkowitz: That's very helpful. So, once you've decided the patient has chorea, what's your framework for thinking about the differential diagnosis of the cause of the patient's chorea? Dr Moore: Well, that could be really challenging. The differential for chorea is very broad, and so the two things that I tend to use are age of the patient and acuity of onset. And so, if you're thinking about acute onset of chorea, you're really looking at a structural lesion like a stroke or a systemic issue like infection, hyperglycemia, etc. Where a gradually progressive chorea tends to be genetic in nature. When you're thinking about the difference between a child and an adult, the most common cause of chorea in a child is Sydenham's chorea. And actually, the most common cause of chorea that I tend to see is Parkinson's disease medication. So, if anybody's seen dyskinesia in Parkinson's disease, you've seen chorea. But it's those two things that I'm using, the age of the patient and the acuity. Somewhere in the middle, though---so, if you have subacute onset of chorea---it's important to remember to think about autoimmune conditions or paraneoplastic conditions because these are treatable. Dr Berkowitz: That's very helpful. So, like in any chief concern in neurology, we're using the context like the age and then the time course. And then a number of other helpful points in your article about the distribution of chorea in the body. Any comments you'd like to make about- we have this very helpful table that I thought was very interesting. So, you really get deep into the nuances of chorea and the movement disorder specialist expert level. Are there any aspects of parts of the body affected by chorea or distribution of chorea across the body that help you hone your differential diagnosis? Dr Moore: Certainly. I think where the chorea is located in the body can be helpful, but not as helpful as other conditions where you're localizing a lesion or that sort of thing. Because you can have a systemic cause of chorea that causes a hemichorea; that you can have hyperglycemia causing a hemichorea, or even Sydenham's chorea being a hemichorea. But things that we think about, if the forehead is involved, I would think about Huntington's disease, although this is not pathognomonic. And if it's involving the face or the mouth, you can think about neuroacanthocytosis or, more commonly, tardive dyskinesia. Hemichorea would make me think about some of those systemic issues like hyperglycemia, Sydenham's chorea, those sorts of things, but I would rely more on the historical context and the acuity of presentation than the distribution itself. Dr Berkowitz: Got it. That's very helpful. So those can be helpful features, but not sort of specific for any particular condition. Dr Moore: Exactly. Dr Berkowitz: Yeah, I often see forehead chorea mentioned as sort of specific to Huntington's disease. Since I don't see much Huntington's disease myself, what does forehead chorea look like? What is the forehead doing? How do you recognize that there is chorea of the forehead? It's just sort of hard for me to imagine what it would look like. Dr Moore: It's really tricky. I think seeing the eyebrows go up and down or the brows furrow in an unpredictable way is really what we're looking for. And that can be hard if you're having a conversation. My forehead is certainly animated as we're talking about one of my favorite topics here. One of the tricks that I use with the fellows is to observe the forehead from the side, and there you can see the undulation of the forehead muscles. And that can be helpful as you're looking for these things. I think where it's most helpful to use the forehead is if you're trying to determine if someone with a psychiatric history has tardive dyskinesia or Huntington's disease, because there can be quite a lot of overlap there. And unfortunately, patients can have both conditions. And so, using the forehead movement can be helpful to maybe direct further testing for Huntington's disease. Dr Berkowitz: Oh, wow, that's a very helpful pearl. So, if you see, sort of, diffuse chorea throughout the body and the forehead is involved, to my understanding it may be less specific. But in the context of wondering, is the neuropsychiatric condition and movement disorder related by an underlying cause in the case of seeing orofacial dyskinesias, is the relationship a drug having caused a tardive dyskinesia or is the whole underlying process Huntington's, the absence of forehead might push you a little more towards tardive dyskinesia, presuming there is an appropriate implicated drug and the presence of forehead chorea would really clue you in more to Huntington's. Did I understand that pearl? Dr Moore: That's exactly right, and I'm glad you brought up the point about making sure, if you're considering tardive dyskinesia, that there has been an appropriate drug exposure. Because without that you can't make that diagnosis. Dr Berkowitz: That's a very helpful and interesting pearl, looking at the forehead from the side. That is a movement disorders pearl for sure. Sort of not just looking at the forehead from one angle and trying to figure out what it's doing, but going to look at the patient in profile and trying to sort it out. I love that. Okay. So, based on the differential diagnosis you would have crafted based on whether this is sort of acute, subacute, chronic, the age of the patient, whether it's unilateral, bilateral, which parts of the body. How do you go about the initial evaluation in terms of laboratory testing, imaging, etc.? Dr Moore: Well, certainly in an acute-onset patient, you're going to get a number of labs---and that's listed out for you in the paper---and consider imaging as well, looking for an infarct. One thing our learners will know is that sort of the typical answer to what's the infarct causing hemichorea would be the subthalamic nucleus. But really, those infarcts can be almost anywhere. There are case reports for infarcts in a wide variety of places in the brain leading to hemichorea. So, I think some general blood work and an MRI of the brain is a good place to start. For someone who has a more chronic course of the development of chorea, there are certain labs that I would get---and an MRI, because if you get an MRI and there's heavy metal deposition or other disease, structurally, that indicates a certain condition, that can help you pretty considerably. But otherwise, I'm looking for inflammatory markers, heavy metals, HIV, some general other things that are outlined, to help make sure that I'm not missing something that's treatable before I go down the route of genetic testing. And we may talk about this in a little bit, but if you start out with genetic testing and then you sort of have to back up and do more systemic testing, that can be very disjointed when it comes to good patient care. Dr Berkowitz: That's very helpful. So yeah, if it's acute, obviously this is the most straightforward scenario, acute and unilateral. We're imagining something lesional, as you said, either a stroke or---not sort of sudden, but fast, but not sudden---you might think of another structural lesion. Toxoplasmosis, right, has an affinity for the basal ganglia if you were seeing this in a patient who is immunocompromised. But in a case that, probably as you alluded to, sort of what we would see most commonly in practice, those still relatively rare, sort of subacute to chronic symmetric chorea. There's a long list of tests that are recommended. In your article and in other texts, I've read lupus testing, anti-phospholipid antibodies… but the list is long. I'll refer readers to your article. Out of curiosity as a specialist, how often do you see any of these labs come back revealing any underlying diagnosis in a patient who's otherwise healthy and just has developed chorea and comes to you with that chief concern? I feel like I've sent that mega-workup a few times; I'm obviously a general neurologist, but not nearly as many times as you have been. It's- I can't remember a time where something has come up, maybe an ANA one to forty or something like this that we don't think is relevant. But in your practice, how often do you end up finding a reversible cause in the laboratory testing versus ending up starting to go down the genetic testing route, which we'll talk about in a moment? Dr Moore: It's not common, but it is important that we capture these things. Because for a lot of those laboratory tests, there are treatments that are available, or other health implications if those come back positive. So, the case I think of is a polycythemia vera patient who had diffused subacute onset chorea and was able to be treated, was temporarily managed with medication for her chorea, and as her PV improved, she was able to come off those medications. As I was alluding to before---and I'm sure we'll talk about genetic testing---if you test for HD and it's negative, do you go down the route of additional expensive genetic testing, or do you then circle back and go, oops, I missed this treatable condition? As we talk about genetic testing as well, getting HD testing is a pretty involved process. And so, we want to make sure we are checking all those boxes before we move forward. So, it's not common, but we do catch some treatable conditions, and that's really important not to miss. Dr Berkowitz: That's very interesting. So, you diagnosed that polycythemia vera by blood smear, is that how you make the diagnosis? Dr Moore: Yes. Dr Berkowitz: And is that a once-in-a-career-so-far type of thing, or does that happen time to time? Dr Moore: For me, that's a once-so-far, but I don't doubt that I'll see it again. Dr Berkowitz: Great. And how about lupus and some of these other things we look for in the absence of other systemic features? Have you picked up any of these or heard of colleagues picking up something on laboratory testing? They said, oh, this patient came in for a referral for genetic testing, negative Huntington's disease. And good news, we found polycythemia vera; good news, we found undiagnosed lupus and we reversed it. I'm just curious, epidemiologically, seeing these long lists and not having the subspecialty practice that you do, how often you find a reversible cause like we do for neuropathy all the time, right? Oh, it's diabetes, it's B12---maybe not reversible, but preventing progression---or reversible dementia work up. You get so excited when you find low B12 and you replete the patient's B12, and they get better when they had been concerned they were developing an irreversible condition. How often does one in your subspecialty find a reversible cause on that initial mega-lab screen? Dr Moore: I think it's really uncommon, and maybe the folks that do are caught by someone else that never make it to Huntington's clinic, but I don't tend to see those cases. There are, of course, case reports and well-described in the literature about lupus and movement disorders and things of that nature, but that doesn't come to our clinic on a regular basis for sure. Dr Berkowitz: Got it. That's helpful to hear. Well, we've alluded to genetic testing a number of times now, so let's go ahead and talk about it. A lot of your article focuses on Huntington disease, and I was thinking about---in the course of our medical training in medical school, and then neurology residency, for those of us who don't become movement disorder experts like yourself---we learn a lot about Huntington disease. That's sort of the disease that causes chorea, until we later learned there are a whole number of diseases, not just the reversible causes we've been talking about, but a number of genetic diseases which you expertly reviewing your article. So, what are some of the red flags that suggest to you that a patient with chronically progressive chorea---and whom you're concerned for Huntington's or another genetic cause---what are some things you notice about the history, about the exam, the symptoms, the signs, the syndrome, that suggest to you that, actually, this one looks like it might not turn out to be HD. I think this patient might have something else. And as you have alluded to, how do you approach this? Do you send HD testing, wait for it to come back, and then go forward? Are there genetic panels for certain genetic causes of chorea? Do you skip just a whole exome sequencing, or will you miss some of the trinucleotide repeat conditions? How do you approach this in practice? Dr Moore: I'll try to tackle all that. One thing I will say is that a lot of patients with chorea, regardless of the cause, can look very similar to one another. So, if you're looking at chronic onset chorea, perhaps with some neuropsychiatric features, I'm going to most often think about HD because that's the most common cause. Certainly, as we mentioned before, if there's a lot of tongue protrusion, I would think about the acanthocytic conditions, neurocanthocytosis and McCloud syndrome. But generally in those conditions, we're looking at HD as the most likely cause. Certainly, if there is epilepsy or some other syndromic types of things going on, I may think more broadly. But it's important to know that while HD, as you mentioned, is the cause of chorea, many of our patients will have parkinsonism, tics, dystonia, a whole host of other movement phenomenologies. So, that wouldn't dissuade me from thinking about HD. When we think about the kind of patients that you're describing, upwards of 95% of those people will have Huntington's disease. And the process for genetic testing is fairly involved. The Huntington's Disease Society of America has organized a set of recommendations for providers to go about the process of genetic testing in a safe and supportive way for patients and their families. And so that's referred to in the article because it really is important and was devised by patients and families that are affected by this disease. And so, when we're thinking about genetic testing for HD, if I reveal that you have HD, this potentially affects your children and your parents and your siblings. You can have a lot of implications for the lives and health and finances of your family members. We also know that there is high suicidality in patients with HD, in patients who are at risk for HD; and there's even a higher risk of suicidality in patients who are at risk but test negative for HD. So, we do recommend a supportive environment for these patients and their families. And so, for presymptomatic patients or patients who are at risk and don't have chorea, this involves making sure we have, sort of, our ducks in a row, as it were, when we think about life insurance, and, do you have somebody supportive to be with you through this journey of genetic testing, no matter what the results are? So, oftentimes I'll say to folks, you know, there's this 20-page policy that I encourage you to look at, but there are Huntington's Disease Centers of Excellence across the country that are happy to help you with that process, to make sure that the patients are well supported. This is an individual genetic test because, as you mentioned, it is a CAG repeat disorder. And unfortunately, there is no chorea panel. So, if an HD test comes back negative, what we'll do then is think about what's called the HD phenocopies. As I mentioned before, some of these patients who look like they have HD will have a negative HD test. And so, what do you do then? Well, there's a handful of phenocopies---so, other genetic mutations that cause a very similar presentation. And so, we try to be smart, since there's not a panel, we try to be smart about how we choose which test to do next. So, for instance, there's a condition called DRPLA that is present in an African-American family here in my area, in North Carolina, as well as in Japan. And so, if someone comes from those backgrounds, we may decide that that's the next test that we're going to do. If they are white European descent, we may consider a different genetic test; or if they're sub-Saharan African, we may choose a different one from that. However, even if you do a really thorough job, all those blood tests, all those genetic tests, you will occasionally get patients that you can't find a diagnosis for. And so, it's important to know even when you do a good job, you may still not find the answer. And so, I think trying to do things with this complex of the presentation in a systematic way for yourself so you're not missing something. So, going back to our answer about, how do I look at lupus and polycythemia vera and all of that, to think about it in a systematic way. That when you get to the end and you say, well, I don't have an answer, you know you've tried. Dr Berkowitz: That's very helpful to hear your approach to these challenging scenarios, and also how to approach the potential challenging diagnosis for patients and their families getting this diagnosis, particularly in the presymptomatic phase. And your article touches on this with a lot of nuance and thoughtfulness. So, I encourage our listeners to have a read of that section as well. So, last here, just briefly in our final moments, you discuss in your article the various symptomatic treatments for chorea. We won't have time to go into all the details of all the many treatments you discussed, but just briefly, how do you decide which medication to start in an individual patient with chorea for symptomatic management? What are some of the considerations related to the underlying condition, potential side effect profiles of the particular medications, or any other considerations just broadly, generally, as you think about choosing one of the many medications that can be used to treat chorea? Dr Moore: Certainly. So, there is a group of FDA-approved medications, VMAT2 inhibitors, that we can choose from, or the off-label use of neuroleptics. And so, there's a lot of things that go into that. Some of that is insurance and cost and that sort of thing, and that can play a role. Others are side effects. So, for the VMAT2 inhibitors, they all do have a black box warning from the FDA about suicidality. And so, if a patient does struggle with mental health, has a history of suicidality, psychiatric admissions for that sort of thing, then I would be more cautious about using that medication. All patients are counseled about that, as are their families, to help us give them good support. So, the neuroleptics do not tend to have that side effect and can help with mood as well as the chorea and can be helpful in that way. And some of them, of course, will have beneficial side effects. So, olanzapine may help with appetite, which can be important in this disease. So, the big considerations would be the black box warning and suicidality, as well as, are we trying to just treat chorea or are we treating chorea and neuropsychiatric issues? Dr Berkowitz: Fantastic. Thank you for that overview. And again, for our listeners, there's a lot more detail about all of these medications, how they work, how they're used in different patient populations, their side effects, etc, to be reviewed in your excellent article. Again, today, I've been interviewing Dr Kathryn Moore about her article on diagnosis and management of Huntington's disease in chorea, which appears in the August 2025 Continuum issue on movement disorders. Be sure to check out Continuum Audio episodes from this and other issues. And thank you so much to our listeners for joining today. And thank you again, Dr Moore. Dr Moore: Thanks for having me. Dr Monteith: This is Dr Teshamae Monteith, associate editor of Continuum Audio. If you've enjoyed this episode, you'll love the journal, which is full of in-depth and clinically relevant information important for neurology practitioners. Use the link in the episode notes to learn more and subscribe. AAN members, you can get CME for listening to this interview by completing the evaluation at continpub.com/audioCME. Thank you for listening to Continuum Audio.

In the fourth episode of this series, Dr. Andy Southerland discusses the Capitol Hill Report from August 11th, where AAN members met with their local state representatives to discuss making telehealth flexibilities permanent and reforming prior authorization processes. Stay updated with what's happening on the hill by visiting aan.com/chr.  Learn how you can get involved with AAN advocacy. 

Wat is de wereld?De wereld is onjuiste waarneming. Ze is uit dwaling voortgekomen en heeft haar bron niet verlaten. Ze zal niet langer blijven bestaan dan de gedachte die haar heeft voortgebracht wordt gekoesterd. Wanneer de gedachte van afgescheidenheid gewijzigd is in een van ware vergeving, zal de wereld in een heel ander licht worden gezien, een dat tot de waarheid leidt, waarin heel de wereld met al haar dwalingen zal verdwijnen. Nu is haar bron verdwenen en zijn haar gevolgen dat eveneens.De wereld werd gemaakt als een aanval op God. Ze symboliseert angst. En wat is angst anders dan de afwezigheid van liefde? De wereld was aldus bedoeld als een plaats waar God niet binnen kon gaan en waar Zijn Zoon van Hem gescheiden kon zijn. Hier werd waarneming geboren, want kennis zou dergelijke waanzinnige gedachten niet kunnen voortbrengen. Maar ogen bedriegen en oren horen onjuist. Nu worden vergissingen alleszins mogelijk, omdat er geen zekerheid meer is.In plaats daarvan zijn de mechanismen van illusie ontstaan. En die gaan nu vinden wat hun gegeven werd te zoeken. Hun oogmerk is te beantwoorden aan het doel waartoe de wereld werd gemaakt om daarvan te getuigen en dat tot werkelijkheid te maken. Zij zien in haar illusies niets dan een solide basis waarin waarheid bestaat, instandgehouden los van leugens. Maar alles waarvan ze melding maken is slechts een illusie die gescheiden wordt gehouden van de waarheid.Waar het zien werd gemaakt om van de waarheid weg te leiden, kan het ook opnieuw worden gericht. Geluiden worden de roep om God, en aan alle waarneming kan een nieuw doel worden gegeven door Degene die God als Verlosser van de wereld heeft aangesteld. Volg Zijn licht en zie de wereld zoals Hij die beziet. Hoor alleen Zijn Stem in alles wat tot jou spreekt. En laat Hij jou de vrede en zekerheid schenken die jij hebt weggegooid, maar die de Hemel voor jou in Hem heeft bewaard.Laten we niet voldaan rusten voordat de wereld zich bij onze veranderde waarneming aangesloten heeft. Laten we niet tevreden zijn voordat vergeving totaal is gemaakt. En laten we niet proberen onze functie te wijzigen. Wij moeten de wereld verlossen. Want wij die haar gemaakt hebben, moeten haar door de ogen van Christus zien, opdat wat gemaakt was om te sterven tot eeuwig leven kan worden hersteld.LES 245Uw vrede is met mij, Vader. Ik ben veilig.Uw vrede omringt me, Vader. Waar ik ga, vergezelt Uw vrede mij. Zij werpt haar licht op ieder die ik ontmoet. Ik breng haar naar hen die diepongelukkig, die eenzaam en die angstig zijn. Ik schenk Uw vrede aan hen die pijn lijden, of treuren om een verlies, of denken dat ze van hoop en geluk zijn beroofd. Stuur hen naar mij, mijn Vader. Laat mij Uw vrede met me meedragen. Want ik wil Uw Zoon verlossen, zoals dat Uw Wil is, opdat ik mijn Zelf weer herkennen zal.En zo gaan wij in vrede. Aan heel de wereld geven we de boodschap die we hebben ontvangen. En op die manier zullen we de Stem namens God horen, die tot ons spreekt als wij Zijn Woord verkondigen, en wiens Liefde we herkennen doordat we het Woord delen dat Hij ons gegeven heeft.Alle tekst- werk en handboek klassen van Een Cursus in Wonderen met Elbert nu te beluisteren en te bekijken op https://decursusmetelbert.nl

Als tiener leerde ze voedselrestrictie bij de Weight Watchers, wat het voorspelbare begin werd van een strijd met eten. Ze was altijd met eten bezig en bang om aan te komen. Na de diagnose Hashimoto vond ze de weg naar Etenslessen en kon ze voedselrestrictie loslaten. Ze verloor de vijf kilo die ze graag kwijt wilde en haar angst voor aankomen verdween. Wat daarvoor in de plaats kwam vertelt ze tijdens ons gesprek. Aan de hand van herkenbare voorbeelden, laat Louise meerdere laagjes in haar nieuwe relatie met eten aan je zien. Luister naar de Etenslessen van Louise en ga voor de volledige omschrijving naar https://etenslessen.com/ik-kon-slecht-tegen-kritiek/

Progressive supranuclear palsy and corticobasal syndrome are closely related neurodegenerative disorders that present with progressive parkinsonism and multiple other features that overlap clinically and neuropathologically. Early recognition is critical to provide appropriate treatment and supportive care. In this episode, Teshamae Monteith, MD, FAAN speaks with Nikolaus R. McFarland, MD, PhD, FAAN, author of the article “Progressive Supranuclear Palsy and Corticobasal Syndrome” in the Continuum® August 2025 Movement Disorders 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. McFarland is an associate professor of neurology at the University of Florida College of Medicine at the Norman Fixel Institute for Neurological Diseases in Gainesville, Florida. Additional Resources  Read the article: Progressive Supranuclear Palsy and Corticobasal Syndrome 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: Hi, this is Dr Teshamae Monteith. Today I'm interviewing Dr Nikolaus McFarland about his article on progressive supranuclear palsy and cortical basilar syndrome, which appears in the August 2025 Continuum issue on movement disorders. Welcome, how are you? Dr Farland: I'm great. Thank you for inviting me to do this. This is a great opportunity. I had fun putting this article together, and it's part of my passion. Dr Monteith: Yes, I know that. You sit on the board with me in the Florida Society of Neurology and I've seen your lectures. You're very passionate about this. And so why don't you first start off with introducing yourself, and then tell us just a little bit about what got you interested in this field. Dr Farland: I'm Dr Nicholas McFarlane. I'm an associate professor at the University of Florida, and I work at the Norman Fixel Institute for Neurological Diseases. I am a director of a number of different centers. So, I actually direct the cure PSP Center of Care and the MSA Center of Excellence at the University of Florida; I also direct the Huntington's clinic there as well. But for many years my focus has been on atypical parkinsonisms. And, you know, I've treated these patients for years, and one of my focuses is actually these patients who suffer from progressive supranuclear palsy and corticobasal syndrome. So that's kind of what this review is all about. Dr Monteith: You probably were born excited, but I want to know what got you interested in this in particular? Dr Farland: So, what got me interested in this in particular was really the disease and the challenges that's involved in it. So, Parkinson's disease is pretty common, and we see a lot of that in our clinic. Yet many times, roughly about 10 to 15% of my patients present with these atypical disorders. And they're quite fascinating. They present in different ways. They're fairly uncommon. They're complex disorders that progress fairly rapidly, and they have multiple different features. They're sort of exciting to see clinically as a neurologist. I think they're really interesting from an academic standpoint, but also in the standpoint of really trying to bring together sort of a team. We have built a multidisciplinary team here at the University of Florida to take care of these patients. They require a number of folks on that team to take care of them. And so, what's exciting, really, is the challenge of treating these patients. There are very limited numbers of therapies that are available, and the current therapies that we have often really aren't great and over time they fail. And so, part of the challenge is actually doing research. And so, there's actually a lot of new research that's been going on in this field. Recently, there's been some revisions to the clinical criteria to help diagnose these disorders. So, that's really what's exciting. The field is really moving forward fairly rapidly with a number of new diagnostics, therapeutics coming out. And hopefully we can make a real difference for these patients. And so that's what really got me into this field, the challenge of trying to treat these patients, help them, advocate for them and make them better. Dr Monteith: And so, tell me what the essential points of this article. Dr Farland: So, the essential points, really, of this article is: number one, you know, just to recognize the new clinical criteria for both PSP and corticobasal syndrome, the diagnosis for these disorders or the phenotypic spectrum has really expanded over the years. So, we now recognize many different phenotypes of these disorders, and the diagnosis has gotten fairly complicated. And so, one of the goals of this article was to review those new diagnostic criteria and the different phenotypic ways these diseases present. I wanted to discuss, also, some of the neuropathology and clinicopathological overlap that's occurred in these diseases as well as some of the new diagnostic tests that are available. That's definitely growing. Some of the new studies that are out, in terms of research and clinical trials. And then wanted to review some of the approaches for treatment for neurologists. Particularly, we're hoping that, you know, this article educates folks. If you're a general neurologist, we're hoping that recognizing these diseases early on will prompt you to refer these patients to specialty clinics or movement disorder specialists early on so they can get appropriate care, confirm your diagnosis, as well as get them involved in trials if they are available. Dr Monteith: And how has the clinical criteria for PSP and cortical basilar syndrome changed? Dr Farland: I think I already mentioned there's been an evolution of the clinical criteria for PSP. There's new diagnostic criteria that were recently published, and it recognizes the multiple clinical phenotypes and the spectrum of the disease that's out there, which is much broader than we thought about. Corticobasal clinical criteria are the Dr Armstrong criteria from 2013. They have not been updated, but they are in the works of being updated. But it does recognize the classic presentation of corticobasal syndrome, plus a frontal executive predominant and then a variant that actually overlaps with PSP. So, there's a lot more overlap in these two diseases than we originally recognized. Dr Monteith: And so, you spoke a bit about FTD spectrum. So why don't you tell us a little bit about what that is? I know you mentioned multiple phenotypes. Dr Farland: What I really want to say is that both PSP and corticobasal syndrome, they're relatively rare, and what- sort of as to common features, they both are progressive Parkinson disorders, but they have variable features. While they're commonly associated with Parkinson's, they also fit within this frontotemporal lobar spectrum, having features that overlap both clinically and neuropathologically. I just want folks to understand that overlap. One of this pathological overlap here is the predominant Tau pathology in the brain, an increasing recognology- recognition of sort of the pathological heterogeneity within these disorders. So, there's an initial description, a classic of PSP, as Richardson syndrome. But now we recognize there are lots of different features to it and there are different ways it presents, and there's definitely a lot of clinical pathological overlap. Dr Monteith: Why don't we just talk about some red flags for PSP? Dr Farland: Yeah, sure. So, some of the red flags for PSP and even corticobasal syndrome are: number one is rapid progression with early onset of falls, gait difficulty, falling typically backwards, early speech and swallow problems that are more prominent than you see in Parkinson's disease, as well as eye gaze issues. So, ocular motor features, particularly vertical gaze palsy. In particular what we talk about is the supranuclear gaze palsy, and one of the most sensitive features that we've seen with these is downgaze limitation or slowed downgaze, and eventually a full vertical gaze palsy and followed supranuclear gaze palsy. So, there's some of the red flags that we see. So, while we think about the lack of response to levodopa frequently as something that's a red flag for Parkinson's, there are many times that we see Parkinson's patients, and about a quarter of them don't really respond. There's some features that don't respond to levodopa that may not be so specific, but also can be helpful in this disease. Dr Monteith: And what about the red flags for cortical basilar syndrome? Dr Farland: So, for cortical basilar syndrome, some of the red flags again are this rapidly depressive syndrome tends to be, at least in its classical present presentation, more asymmetric in its presentation of parkinsonism, with features including things like dystonic features, okay? For limb dystonia and apraxias---so, inability to do a learned behavior. One of those red flags is a patient who comes in and says, my hand doesn't work anymore, which is something extremely uncommon that you hear in Parkinson's disease. Most of those patients will present, say, I might have a tremor, but they very rarely will tell you that I can't use my hand. So look out for that sign. Dr Monteith: And let's talk a little bit about some of the advances in the fields you mentioned, evolving biomarker and imaging capacities. So, how are these advances useful in helping us understand these conditions, especially when there's so much heterogeneity? Dr Farland: I might start by talking a little bit about some of the clinical criteria that have advanced. Why don't we start there and just discuss some of the advances? I think in PSP, I think, originally we had both probable and possible diagnoses of PSP, and the diagnostic criteria were basically focused on what was what's called “classical PSP” or “Richardson syndrome”. But now we recognize that there are multiple phenotypes. There's an overlap with Parkinsonism that's slower in progression and morphs into PSP, the classical form. There's a frontal behavioral variant where patients present with that frontal behavioral kind of thing. There's a speech-language variant that can overlap with PSP. So they have prominent speech language, potentially even apraxia speech. So, recognition of these different phenotypes is sort of a new thing in this field. There's even overlap with cortical basal syndrome and PSP, and we note that the pathology can overlap as well. So, I think that's one of the things that have changed over time. And these were- recently came out in 2017 in a new publication in the Movement Disorders Society. So, in terms of diagnostic tests as well---and there's been quite a bit of evolution---really still to date, our best diagnostic test is imaging. MRI is really one of our best tests currently. Currently blood tests, spinal fluid, there's new biomarkers in terms of skin… they're still in the research phase and not necessarily very specific yet. So, we rely heavily on imaging still; and for PSP, what we're looking for largely are changes in the brain stem, and particularly focused on the midbrain. So disproportionate midbrain atrophy compared to the pons and the rest of the midbrain is a fairly specific intensive sign for PSP. Whereas in MSA we see more of a pontine atrophy compared to the midbrain. So that can be really helpful, and there are lots of different new measurements that can be done. PET scans are also being used as well. And there are new PET markers, but they still remain kind of research-based, but are becoming more and more prevalent and may be available soon for potential use. Although there's some overlap with PET tracers with Alzheimer's disease and different Tau isoforms. So, something to be wary about, but we will be seeing some of these soon coming out as well. More kind of up-to-date things include things like the spinal fluid as well as even some of the skin biopsies. And I think we've heard some word of recent studies that have come out that potentially in the very near future we might actually have some Tau protein tests that we can look at Tau either in spinal fluid or even in a skin biopsy. But again, still remains research-based and, we still need more information as to whether these tests can be reproducible and how sensitive or specific they are. Dr Monteith: It sounds like, when really approaching these patients, still, it's a lot of back to the history, back to the clinical and some basic imaging that we should be able to identify to distinguish these types of patients, and we're not quite where we need to be yet for biomarker. Dr Farland: I totally agree with you. I think it starts, really, with the clinical exam and that's our main focus here; and understanding some of the new clinical criteria which are more sensitive, but also specific, too. And they're really useful to look at. So, I think reviewing those; patients do progress, following them over time can be really useful. And then for diagnosis, getting imaging if you suspect a patient has an atypical presentation of parkinsonism, to look for signs or features that might be specific for these different disorders. Dr Monteith: Why don't we take a typical case, a typical patient that you would see in clinic, and walk us through the thought process---especially, maybe they presented somewhat early---and the different treatment approaches to helping the patient, and of course their family. Dr Farland: Yeah, sure. So, a typical patient might be someone who comes in with, like, a three year history of progressive gait problems and falling. And let's say the patient says, I'm falling backwards frequently. They may have had, like, a rib fracture, or they hit their head once, and they're describing some speech issues as well. Now they're relying on a walker and family members saying they rarely let them be by themselves. And there may be some slowing of their cognitive function and maybe a bit of withdrawal. So that's a typical patient. So, the approach here is really, what are some of the red flags? I think already you hear a red flag of a rapidly progressive disease. So, Parkinson's disease patients rarely have frequent falls within the first five years. So, this is within three years or less. You're already hearing early onset of gait problems and falling, and particularly falling backwards rather than forwards as often Parkinson's disease patients do. You're hearing early speech problems and maybe a subtle hint of cognitive slowing and some withdrawal. So, a lot of things that sort of are red flags. So, our approach really would be examining this patient really closely. Okay? We'd be listening to the history, looking at the patient. One thing is that some of these patients come in, they may be in a wheelchair already. That's a red flag for us. If they're wearing sunglasses---sometimes we see that patients, they have photosensitivity and they're in a chair and they're wearing sunglasses---you take the glasses off and you look at their face and they have that sort of a facial stare to them---not just the masked face, but the stare---and their eyes really aren't moving. So, another kind of clue, maybe this is probably something atypical, particularly PSP is what I'm thinking about. So, the approach is really, do a thorough exam. I always recommend looking at eye movements and starting with volitional saccades, not giving them a target necessarily, but asking them to look up and then look down. And then particularly look at the speed of downgaze and whether they actually have full versions down, are able to do that. That's probably your most sensitive test for a patient who has PSP. Not the upgaze, which can be- upgaze impairment in older patients can be nonspecific. So, look for that down gaze. So, if I can get out one message, that's one thing that can be easily done and examined fairly quickly for diagnosis of these patients. And then just look for signs of rigidity, bradykinesia, maybe even some myelopraxia, and then look at their gait carefully so that there's a high suspicion. Again, if there's some atypical features, imaging is really important. So, my next step would be probably getting an MRI to evaluate whether- do they have brain somatrophy or other widespread atrophy or other signs? You need to think about your differential diagnosis for some of these patients as well. So, common things are common; vascular disease, you can't have vascular parkinsonism or even signs of NPH. Both of those can present with progressive gait difficulty and falls. So, the gait may look more like Parkinson's rather than ataxic gait that we see in classic PSP, but still they have early gait issues, and that can be a mimicker of PSP, So looking for both of those things in your imaging. Think about sort of autoimmune potentially causes. So, if they have a really rapid progressive cause, there are some rare autoimmune things. There have been recent reports of things like IgLON5, although there's limited cases, but we're doing more screening for some of those autoimmune causes. And then even some infectious causes like Whipples, that are rarely present like this. Okay? And have other signs and features. Dr Monteith: So, let's say you diagnose this patient with PSP and you're assessing the patients to see how you can improve their quality of life. So, what are some potential symptomatic managements that will help our patient? Dr Farland: I recommend for most all of these patients… while the literature indicates that many patients with PSP, and especially corticobasal syndrome, don't respond well to levodopa. So, the classic treatment for parkinsonism. However, we all recommend a trial of levodopa. These patients may respond partially to doses of levodopa, and we try to push the doses a bit higher. So, the recommended trial is usually a dose up to roughly 1000 milligrams of levodopa per day. And give it some time, at least two, if not actually three months of a trial. If not well-tolerated, you can back off. If there's no response at all or no improvement, then slowly back off and taper patients off and ask them to tell you whether they feel like they're actually worsening. So, many patients, sometimes, don't recognize the improvements, or family members don't recognize it until we actually taper them back off. And they may end up saying there are some other things that even recognize. Even some nonmotor benefits can be seen with levodopa. In some cases, we do keep them on levodopa, but levodopa's our best therapy for this. Dopamine agonists, MAO inhibitors, have all been sort of tried and they've been studied, but often don't really help or fail to help benefit these patients and could be fraught with some other side effects. I think many people do also turn to Amantadine as a treatment for Parkinson's, gait problems, freezing, if you see it in these disorders. Yet Amantadine is fraught with issues of side effects, including cognitive issues, and I think is not well-tolerated. But there are the rare patient who actually does respond to this or claims they respond to this. By and large, these patients relentlessly progress, unfortunately. So, beside treatment of other symptoms, I think it's really important to recognize that they require supportive cares and therapy. So, starting those early on and getting your allied healthcares kind of involved. So that includes people like physical, occupational therapy for the gait issues, the falls, occupational therapy for doing daily activities. Speech language pathology can be really a critical player for these because of the early speech and language issues, as well as swallow difficulties. Swallow is compared quickly in these patients. And so, we do recommend the screening evaluation, then often following patients either every six- or even annually, at least, with a swallow evaluation. And we recommend the fluoroscopic-guided kind of modified barium swallow for these patients.  Dr Monteith: And how does that differ if, let's say, the patient had cortical basilar syndrome? What are some of the symptomatic treatments that would be high on your consideration? Dr Farland: So actually, these patients also have a very similar approach, and they often have some overlapping features. Maybe a little bit of difference in terms of the level of apraxia and some dystonic features that you see in corticobasal syndrome. So, as I mentioned earlier that these patients have a more typ- when they present, typically have a more asymmetric presentation. And one of the biggest issues is this limb apraxia. They may have abnormal movements as well as, like, the alien limb-type phenomena as well. So, the focus of therapy, while similar in the sense we focus on the parkinsonism, I do always try levodopa and try to ramp up the doses to see if it benefits. It does often fail, but it's definitely worth trying. The other focus of these patients is trying to treat symptoms. Dystonia, those features… in some cases, we can help; if it's painful or uncomfortable, muscle relaxants can be used. If it's vocal, things like Botox can be really helpful. Often times it is more palliative than actually restorative in terms of function, but still can be really helpful for patients who ask about pain and discomfort and trying to treat. And then of course, again, the focus on our supportive care. We need to build that network and build that team of folks, the therapists, the physical, occupational, and the speech therapist to help them. If they have language problems---like either in PSP or corticobasal---I'll also include my request to a speech language pathologist to work on cognitive function. That's a special, additional thing you have to ask for and then specifically request when you make a referral to a speech language pathologist. Dr Monteith: That is so important. I think keeping the simulation, keeping the social support, and I would probably guess that you would also include screening for sleep and mood disorder. Dr Farland: Absolutely. Mood disorders are really big in these diseases. Patients are suffering terribly. You do hear about labile mood in both of these diseases, particularly PSP; and even what's called pseudobulbar palsy, where the mood is not always congruent with the affect. So they may laugh or cry inappropriately, and particularly the crying can be very disturbing to family and caregivers to see that. And so, treating those things can be really important. So always asking about the mood issues. Depression in particular is something that we're very sensitive about, and there is a higher incidence of suicidal ideations. Asking about that and feeling and making sure that they are in a safe environment can be really important. Dr Monteith: Thank you so much. Dr Farland: Thank you. Dr Monteith: Today I've been interviewing Dr Nikolaus McFarland about his article on progressive supranuclear palsy and cortical basilar syndrome, which appears in the August 2025 Continuum issue on movement disorders. 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.

Anita Terpstra is schrijver. Ze studeerde journalistiek en kunstgeschiedenis en debuteerde in 2009 met de thriller ‘Nachtvlucht', dat genomineerd werd voor de Schaduwprijs voor het beste Nederlandstalige thrillerdebuut. Later volgden veelgeprezen thrillers als ‘Anders' en ‘Samen', waarmee ze genomineerd werd voor de Gouden Strop. Daarnaast is Terpstra bekend van non-fictieboeken ‘Het huis vol' en ‘Hiltje' en haar roman ‘De moedermaffia'. Nu verschijnt van haar hand ‘De hoop van Holwerd'. Aan de hand van haar eigen familiegeschiedenis vertelt Anita Terpstra het verhaal van het dorp en zijn inwoners, maar ook dat van Friesland en zijn relatie met de zee. Femke van der Laan gaat met Anita Terpstra in gesprek.

Mensen zijn van nature nieuwsgierig en willen vanalles weten en leren. Hoe komt het dan dat zoveel leerlingen school saai vinden? Ligt het aan de leerstof? Aan de leerkracht? Of aan de leerlingen zelf? Met behulp van UHasselt-pedagoog Katrien Struyven zorgen we ervoor dat studenten en leerlingen dit schooljaar alles (of toch véél ;-)) boeiend vinden!

Multiple system atrophy is a rare, sporadic, adult-onset, progressive, and fatal neurodegenerative disease. Accurate and early diagnosis remains challenging because it presents with a variable combination of symptoms across the autonomic, extrapyramidal, cerebellar, and pyramidal systems. Advances in brain imaging, molecular biomarker research, and efforts to develop disease-modifying agents have shown promise to improve diagnosis and treatment. In this episode, Casey Albin, MD speaks with Tao Xie, MD, PhD, author of the article “Multiple System Atrophy” in the Continuum® August 2025 Movement Disorders issue. Dr. Albin is a Continuum® Audio interviewer, associate editor of media engagement, and an assistant professor of neurology and neurosurgery at Emory University School of Medicine in Atlanta, Georgia. Dr. Xie is director of the Movement Disorder Program, chief of the Neurodegenerative Disease Section in the department of neurology at the University of Chicago Medicine in Chicago, Illinois. Additional Resources Read the article: Multiple System Atrophy Subscribe to Continuum®: shop.lww.com/Continuum Earn CME (available only to AAN members): continpub.com/AudioCME Continuum® Aloud (verbatim audio-book style recordings of articles available only to Continuum® subscribers): continpub.com/Aloud More about the American Academy of Neurology: aan.com Social Media facebook.com/continuumcme @ContinuumAAN Host: @caseyalbin 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 Albin: Hello everyone, this is Dr Casey Albin. Today I'm interviewing Dr Tao Xie about his article on diagnosis and management of multiple system atrophy, which appears in the August 2025 Continuum issue on movement disorders. Welcome to the podcast, and please introduce yourself to our audience. Dr Xie: Thank you so much, Dr Albin. My name is Tao Xie, and sometimes people also call me Tao Z. I'm a mood disorder neurologist, professor of neurology at the University of Chicago. I'm also in charge of the mood disorder program here, and I'm the section chief in the neurodegenerative disease in the Department of Neurology at the University of Chicago Medicine. Thank you for having me, Dr Albin and Dr Okun and the American Academy of Neurology. This is a great honor and pleasure to be involved in this education session. Dr Albin: We are delighted to have you, and thank you so much for the thoughtful approach to the diagnosis and management. I really want to encourage our listeners to check out this article. You know, one of the things that you emphasize is multiple system atrophy is a fairly rare condition. And I suspect that clinicians and trainees who even have a fair amount of exposure to movement disorders may not have encountered that many cases. And so, I was hoping that you could just start us off and walk us through what defines multiple system atrophy, and then maybe a little bit about how it's different from some of the more commonly encountered movement disorders. Dr Xie: This is a really good question, Dr Albin. Indeed, MSA---multisystem atrophy----is a rare disease. It is sporadic, adult-onset, progressive, fatal neurodegenerative disease. By the name MSA, multisystem atrophy. Clinically, it will present with multiple symptoms and signs involving multiple systems, including symptoms of autonomic dysfunction and symptoms of parkinsonism, which is polyresponsive to the levodopa treatment; and the symptom of cerebellar ataxia, and symptom of spasticity and other motor and nonmotor symptoms. And you may be wondering, what is the cause- underlying cause of these symptoms? Anatomically, we can find the area in the basal ganglia striatonigral system, particularly in the putamen and also in the cerebellar pontine inferior, all of the nuclear area and the specific area involved in the autonomic system in the brain stem and spinal cord: all become smaller. We call it atrophy. Because of the atrophy in this area, they are responsible for the symptom of parkinsonism if it is involved in the putamen and the cerebral ataxia, if it's involved in the pons and cerebral peduncle and the cerebellum. And all other area, if it's involved in the autonomic system can cause autonomic symptoms as well. So that's why we call it multisystem atrophy. And then what's the underlying cellular and subcellular pathological, a hallmark that is in fact caused by misfolded alpha-synuclein aggregate in the oligodontia site known as GCI---glial cytoplasmic increasing bodies---in the cells, and sometimes it can also be found in the neuronal cell as well in those areas, as mentioned, which causes the symptom. But clinically, the patient may not present all the symptoms at the same time. So, based on the predominant clinical symptom, if it's mainly levodopa, polyresponsive parkinsonism, then we call it MSAP. If it's mainly cerebellar ataxia, then we call it MSAC. But whether we call it MSP or MSC, they all got to have autonomic dysfunction. And also as the disease progresses, they can also present both phenotypes together. We call that mixed cerebellar ataxia and parkinsonism in the advanced stage of the disease. So, it is really a complicated disease. The complexity and the similarity to other mood disorders, including parkinsonism and the cerebellar ataxia, make it really difficult sometimes, particularly at the early stages of disease, to differentiate one from the other. So, that was challenging not only for other professionals, general neurologists and even for some movement disorder specialists, that could be difficult particularly if you aim to make an accurate and early diagnosis. Dr Albin: Absolutely. That is such a wealth of knowledge here. And I'm going to distill it just a little bit just to make sure that I understand this right. There is alpha-synuclein depositions, and it's really more widespread than one would see maybe in just Parkinson's disease. And with this, you are having patients present with maybe one of two subtypes of their clinical manifestations, either with a Parkinson's-predominant movement disorder pattern or a cerebellar ataxia type movement disorder pattern. Or maybe even mixed, which really, you know, we have to make things quite complicated, but they are all unified and having this shared importance of autonomic features to the diagnosis. Have I got that all sort of correct? Dr Xie: Correct. You really summarize well. Dr Albin: Fantastic. I mean, this is quite a complicated disease. I would pose to you sort of a case, and I imagine this is quite common to what you see in your clinic. And let's say, you know, a seventy-year-old woman comes to your clinic because she has had rigidity and poor balance. And she's had several falls already, almost always from ground level. And her family tells you she's quite woozy whenever she gets up from the chair and she tends to kind of fall over. But they noticed that she's been stiff,and they've actually brought her to their primary care doctor and he thought that she had Parkinson's disease. So, she started levodopa, but they're coming to you because they think that she probably needs a higher dose. It's just not working out very well for her. So how would you sort of take that history and sort of comb through some of the features that might make you more concerned that the patient actually has undiagnosed multiple systems atrophy? Dr Xie: This is a great case, because we oftentimes can encounter similar cases like this in the clinic. First of all, based on the history you described, it sounds like an atypical parkinsonism based on the slowness, rigidity, stiffness; and particularly the early onset of falls, which is very unusual for typical Parkinson disease. It occurs too early. If its loss of balance, postural instability, and fall occurred within three years of disease onset---usually the motor symptom onset---then it raises a red flag to suspect this must be some atypical Parkinson disorders, including multiple system atrophy. Particularly, pou also mentioned that the patient is poorly responsive to their levodopa therapy, which is very unusual because for Parkinson disease, idiopathic Parkinson disease, we typically expect patients would have a great response to the levodopa, particularly in the first 5 to 7 years. So to put it all together, this could be atypical parkinsonism, and I could not rule out the possibility of MSA. Then I need to check more about other symptoms including autonomic dysfunction, such as orthostatic hypertension, which is a blood pressure drop when the patient stands up from a lying-down position, or other autonomic dysfunctions such as urinary incontinence or severe urinary retention. So, in the meantime, I also have to put the other atypical Parkinson disorder on the differential diagnosis, such as PSP---progressive supranuclear palsy---and the DLBD---dementia with Lewy body disease.---Bear this in mind. So, I want to get more history and more thorough bedside assessment to rule in or rule out my diagnosis and differential diagnosis. Dr Albin: That's super helpful. So, looking for early falls, the prominence of autonomic dysfunction, and then that poor levodopa responsiveness while continuing to sort of keep a very broad differential diagnosis? Dr Xie: Correct. Dr Albin: One of the things that I just have to ask, because I so taken by this, is that you say in the article that some of these patients actually have preservation of smell. In medical school, we always learn that our Parkinson's disease patients kind of had that early loss of smell. Do you find that to be clinically relevant? Is that- does that anecdotally help? Dr Xie: This is a very interesting point because we know that the loss of smelling function is a risk effect, a prodromal effect, for the future development of Parkinson disease. But it is not the case for MSA. Strange enough, based on the literature and the studies, it is not common for the patient with MSA to present with anosmia. Some of the patients may have mild to moderate hyposmia, but not to the degree of anosmia. So, this is why even in the more recent diagnosis criteria, the MDS criteria published 2022, it even put the presence of anosmia in the exclusion criteria. So, highlight the importance of the smell function, which is well-preserved for the majority in MSA, into that category. So, this is a really interesting point and very important for us, particularly clinicians, to know the difference in the hyposmia, anosmia between the- we call it the PD, and the dementia Lewy bodies versus MSA. Dr Albin: Fascinating. And just such a cool little tidbit to take with us. So, the family, you know, you're talking to them and they say, oh yes, she has had several fainting episodes and we keep taking her to the primary care doctor because she's had urinary incontinence, and they thought maybe she had urinary tract infections. We've been dealing with that. And you're sort of thinking, hm, this is all kind of coming together, but I imagine it is still quite difficult to make this diagnosis based on history and physical alone. Walk our listeners through sort of how you're using MRI and DAT scan and maybe even some other biomarkers to help sort of solidify that diagnosis. Dr Xie: Yeah, that's a wonderful question. Yeah. First of all, UTI is very common for patients with MSA because of urinary retention, which puts them into a high risk of developing frequent UTI. That, for some patients, could be the very initial presentation of symptoms. In this case, if we check, we say UTI is not present or UTI is present but we treat it, then we check the blood pressure and we do find also hypertension---according to new diagnosis criteria, starting drop is 20mm mercury, but that's- the blood pressure drop is ten within three minutes. And also, in the meantime the patients present persistent urinary incontinence even after UTI was treated. And then the suspicion for MS is really high right at this point. But if you want increased certainty and a comfortable level on your diagnosis, then we also need to look at the brain MRI mark. This is a required according to the most recent MDS diagnosis criteria. The presence of the MRI marker typical for MSA is needed for the diagnosis of clinically established MSA, which holds the highest specificity in the clinical diagnosis. So then, we have- we're back to your question. We do need to look at the brain MRI to see whether evidence suggestive of atrophy around the putamen area, around the cerebellar pontine inferior olive area, is present or not. Dr Albin: Absolutely. That's super helpful. And I think clinicians will really take that to sort of helping to build a case and maybe recognizing some of this atypical Parkinson's disease as a different disease entity. Are there any other biomarkers in the pipeline that you're excited about that may give us even more clarity on this diagnosis? Dr Xie: Oh, yeah. This is a very exciting area. In terms of biomarker for the brain imaging, particularly brain MRI, in fact, today there's a landmark paper just published in the Java Neurology using AI, artificial intelligence or machine learning aid, diagnoses a patient with parkinsonism including Parkinson's disease, MSA, and PSP, with very high diagnostic accuracy ranging from 96% to 98%. And some of the cases even were standard for autopsy, with pathological verification at a very high accurate rate of 93.9%. This is quite amazing and can really open new diagnosis tools for us to diagnose this difficult disease; not only in an area with a bunch of mood disorder experts, but also in the rural area, in the area really in need of mood disorder experts. They can provide tremendous help to provide accurate, early diagnosis. Dr Albin: That's fantastic and I love that, increasing the access to this accurate diagnosis. What can't artificial intelligence do for us? That's just incredible. Dr Xie: And also, you know, this is just one example of how the brain biomarker can help us. Theres other---a fluid biomarker, molecular diagnostic tools, is also available. Just to give you an example, one thing we know over the past couple years is skin biopsy. Through the immunofluorescent reaction, we can detect whether the hallmark of abnormally folded, misfolded, and the phosphorate, the alpha-synuclein aggregate can be found just by this little pinch of skin biopsy. Even more advanced, there's another diagnosis tool we call the SAA, we call the seizure amplification assay, that can even help us to differentiate MSA from other alpha-synucleinopathy, including Parkinson disease and dementia with Lewy bodies. If we get a little sample from CSF, spinal cerebral fluids, even though this is probably still at the early stage, a lot of developments still ongoing, but this, this really shows you how exciting this area is now. We're really in a fast forward-moving path now. Dr Albin: It's really incredible. So, lots coming down the track in, sort of, MRI, but also with CSF diagnosis and skin biopsies. Really hoping that we can hone in some of those tools as they become more and more validated to make this diagnosis. Is that right? Dr Xie: Correct. Dr Albin: Amazing. We can talk all day about how you manage these in the clinic, and I really am going to direct our listeners to go and read your fantastic article, because you do such an elegant job talking about how this takes place in a multidisciplinary setting, if at all possible. But as a neurointensivist, I was telling you, we have so much trouble in the hospital. We have A-lines, and we have the ability to get rapid KUBs to look at Ilias, and we can have many people as lots of diagnosis, and we still have a lot of trouble treating autonomiclike symptoms. Really, really difficult. And so, I just wanted to kind of pick your brain, and I'll start with just the one of orthostatic hypotension. What are some of the tips that you have for, you know, clinicians that are dealing with this? Because I imagine that this is quite difficult to do without patients. Dr Xie: Exactly. This is indeed a very difficult symptom to deal with, particularly at an outpatient setting. But nowadays with the availability of more medication---to give an example, to treat patients with orthostatic hypertension, we have not only midodrine for the cortisol, we also have droxidopa and several others as well. And so, we have more tools at hand to treat the patient with orthostatic hypertension. But I think the key thing here, particularly for us to the patient at the outpatient setting: we need to educate the patient's family well about the natural history of the disease course. And we also need to tell them what's the indication and the potential side effect profile of any medication we prescribe to them so that they can understand what to expect and what to watch for. And in the meantime, we also need to keep really effective and timely communication channels, make sure that the treating physician and our team can be reached at any time when the patient and family need us so that we can be closely monitoring, their response, and also monitoring potential side effects as well to keep up the quality of care in that way. Dr Albin: Yeah, I imagine that that open communication plays a huge role in just making sure that patients are adapting to their symptoms, understanding that they can reach out if they have refractory symptoms, and that- I imagine this takes a lot of fine tuning over time. Dr Xie: Correct. Dr Albin: Well, this has just been such a delight to get to talk to you. I really feel like we could dive even deeper, but I know for the sake of time we have to kind of close out. Are there any final points that you wanted to share with our listeners before we end the interview? Dr Xie: I think for the patients, I want them to know that nowadays with advances in science and technology, particularly given a sample of rapid development in the diagnostic tools and the multidisciplinary and multisystemic approach to treatment, nowadays we can make an early and accurate diagnosis of the MSA, and also, we can provide better treatment. Even though so far it is still symptomatically, mainly, but in the near future we hope we can also discover disease-modifying treatment which can slow down, even pause or prevent the disease from happening. And for the treating physician and care team professionals, I just want them to know that you can make a difference and greatly help the patient and the family through your dedicated care and also through your active learning and innovative research. You can make a difference. Dr Albin: That's amazing and lots of hope for these patients. Right now, you can provide really great care to take care of them, make an early and accurate diagnosis; but on the horizon, there are really several things that are going to move the field forward, which is just so exciting. Again today, I've been really greatly honored and privileged to be able to talk to Dr Tao Xie about his article on diagnosis and management of multiple system atrophy, which appears in the August 2025 Continuum issue on movement disorders. Be sure to check out Continuum Audio episodes for this and other issues. And thank you again to our listeners for joining us today. Dr Xie: Thank you so much for having me. Dr Monteith: This is Dr Teshamae Monteith, Associate Editor of Continuum Audio. If you've enjoyed this episode, you'll love the journal, which is full of in-depth and clinically relevant information important for neurology practitioners. Use the link in the episode notes to learn more and subscribe. AAN members, you can get CME for listening to this interview by completing the evaluation at continpub.com/audioCME. Thank you for listening to Continuum Audio.

Gerbrand Bakker is auteur, columnist en hovenier, en een van de meest vertaalde hedendaagse Nederlandse schrijvers. Zijn (internationale) doorbraak kwam met ‘Boven is het stil' (2006). Het boek werd bekroond met onder meer de toonaangevende International IMPAC Dublin Literary Award, is bewerkt voor toneel en verfilmd, en werd in meer dan dertig landen verkocht. Zijn roman ‘De omweg' stond op de shortlist voor de Libris Literatuur Prijs en werd bekroond met de Independent Foreign Fiction Prize, een voorloper van de International Booker Prize. Zijn meest recente roman is ‘De kapperszoon' (2022). In de autobiografische reeks Privé-domein publiceerde Bakker al drie boeken: ‘Jasper en zijn knecht' (2016), ‘Knecht, alleen' (2020), en ‘Moeder, na vader' (2023). Nu is daar een vierde aan toegevoegd: ‘Aan mij heb je niks'. Femke van der Laan gaat met Gerbrand Bakker in gesprek.

In the August episode of the President's Spotlight, Dr. Jason Crowell and Dr. Natalia Rost discuss the mid-year assessment of AAN's five-year strategic plan.  Show reference:  https://www.aan.com/about-the-aan/presidents-spotlight   

In the third episode of this series, Dr. Andy Southerland discusses the latest Capitol Hill Report, which outlines the 2026 Medicare fee schedule proposal.  Stay updated with what's happening on the hill by visiting aan.com/chr.  Learn how you can get involved with AAN advocacy.