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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.

Beseffen wij de top 50? Aan wie moet Nederland verkocht worden? Like & subscribe als wij Koffietijd moeten kopen. Volg ons op Instagram.Geproduceerd door: Tonny MediaSee omnystudio.com/listener for privacy information.

Aan de slag!Besef jij je weleens hoe rijk je bent? Je bent een erfgenaam van God, een kind van de Koning en je erft Zijn Koninkrijk en een persoonlijke, intieme relatie met God. Als je erover nadenkt is dat heel erg bijzonder!Luister vandaag het lied Royalty van Francesca Battistelli en laat tot je doordringen wie jij bent geworden door het bloed van Jezus.Deze overdenking is geschreven door oud-schrijfster Lydia Hiemstra.

Aan de slag!Lees 1 Johannes 5:14-21 en markeer de vier keer dat er staat: “Wij weten...”Schrijf bij elke ‘Wij weten' op wat dit voor jou persoonlijk betekent. Waarin ervaar jij twijfel, en waar mag je deze waarheid tegenover zetten?Deze overdenking is geschreven door schrijfster Emmely Post-Spreeuwenberg.

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.

Heb jij ook het gevoel dat je lijf soms tegen je schreeuwt, maar je geen idee hebt wat het eigenlijk bedoelt? Of blijven dezelfde klachten, twijfels en blokkades zich herhalen terwijl jij verlangt naar meer energie, helderheid en zelfvertrouwen? Dan is deze aflevering voor jou. Want jouw lichaam praat, en het is tijd dat jij gaat luisteren.In deze aflevering neem ik je mee achter de schermen van mijn eigen proces en ontdek je hoe lichaamssignalen (fysiek én emotioneel) jou de weg kunnen wijzen naar echte verandering. Niet met standaardtips, maar met openheid over mijn eigen worstelingen en inzichten.Na deze aflevering weet jij:Hoe je lichaam via (terugkerende) klachten en emoties met je communiceert, en waarom het belangrijk is die signalen niet te negeren  Dat het proces van samenwerken met je lichaam niet stopt als je klachtenvrij bent, maar juist dan begint  Hoe fysieke klachten zoals huidproblemen, buikklachten en vermoeidheid vaak samenhangen met dieperliggende thema's zoals grenzen stellen, zelfliefde en patronen uit je gezin  Waarom écht luisteren naar je lichaam soms vraagt om ongemakkelijke keuzes en het doorbreken van oud gedrag, maar altijd leidt tot meer vrijheid en balansDurf jij eerlijk te kijken naar waar je nu staat en ben je klaar om de regie eindelijk weer terug te pakken? Zet jezelf op één, druk op play, en ontdek de revolutionaire kracht van jouw lichaamssignalen!

"Ik dacht dat ik m'n prijs moest verlagen…"Ze twijfelde. Aan haar prijs. Aan haar waarde. En eigenlijk… aan zichzelf.Want mensen zeiden: “Te duur.”Dus ging ze schuiven. In de prijs, in de inhoud, in haar energie.Maar wat als het niet je prijs is die in de weg zit?Wat als het je vertrouwen is?In deze aflevering laat ik je zien waarom je klanten niet afhaken op je bedrag, maar op je twijfel.En hoe je je aanbod weer kunt dragen zoals het bedoeld is.Stevig. Duidelijk. Verleidelijk zonder te overtuigen.***

Pieter De Crem is burgemeester af. En hij stapt uit cd&v Oorzaak zijn de illegale praktijken die aan het licht kwamen in zijn gemeente Aalter. Daar werd systematisch gediscrimineerd op vlak van afkomst of origine. Maar welke rechten hebben wens- en draagouders? Na de openlijke kinderwens van Conner Rousseau lijkt dat thema weer 'hot topic' in de Wetstraat. Aan tafel: Bart Eeckhout, Stavros Kelepouris, Joline MaenhoutProductie: Laurens Bervoets (hoorstroom) & Dries VermeulenEindredactie: Sam Feys & Rik Boey Wil je reageren? Mail naar podcasts@demorgen.beSee omnystudio.com/listener for privacy information.

Welkom bij de special MoLo's Makkelijke Maandag! Onze eerste gast is niemand minder dan Martine Heemkerk, ofwel Tienvanwil. Aan de keukentafel van Rebecca kletsen we met haar over het solo moederschap, de keukenprinces die ze is en keuvelen we gezellig door aan de bar terwijl we een makkelijk recept bereiden. Kind kan de was doen!Deze serie wordt gesponsord door HelloFresh. Wil jij het jezelf ook wat makkelijker maken met heerlijke snelle gerechten? Bestel nu je box en ontvang óók de Praatjesmakers-kaartjes in jouw box. Deze zullen de hele maand september te vinden zijn!Wil je adverteren in deze podcast? Stuur dan een mailtje naar adverteren@bienmedia.nlProductie: MIDDLE CHILD MEDIA.Muziek: Soundsright Hosted on Acast. See acast.com/privacy for more information.

Aan de slag!Schrijf elke dag dankpunten op om te ontdekken hoe God voor jou zorgt.Deze overdenking is geschreven door schrijfster Linda Aalbers.

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)

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.

Aan de slag!Hoe stil jij je honger? Denk na over deze vraag en zoek Hem vandaag bewust.Deze overdenking is geschreven door schrijfster Marianne de Bart-van der Lee.

Aan de slag!Probeer de komende tijd eens te bidden samen met je partner. Maak samen een gebedslijst met dank- en bidpunten.Deze overdenking is geschreven door schrijfster Marije Dekker-Brandwijk.

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.

Na een zomer offline keert Ellen terug met een aflevering vol scherpe inzichten, persoonlijke reflectie en krachtige waarheid. Ze deelt hoe ze zichzelf opnieuw aan het heruitvinden is in haar ‘Great Lock-in' – een bewuste periode van groei, herijking en loslaten wat niet meer dient.Aan de hand van een verrassend eerlijke selectie voor haar verjaardagsfeest onderzoekt ze wat het betekent om mensen in je leven toe te laten die écht resoneren met wie je nu bent. Niet wie je vroeger was. Ze maakt korte metten met roddelgedrag, slachtofferschap en de energie van mensen die vooral met hun eigen onzekerheden bezig zijn. Want: “Onzekere mensen zijn gevaarlijk, ze trekken je mee naar beneden.”Ellen laat zien hoe je persoonlijke en energetische groei letterlijk deuren opent. Niet alleen naar feestjes, maar naar kansen, relaties en next-level leiderschap. Ze daagt je uit om te reflecteren op de mensen om je heen, je eigen frequentie en de bergen die je voor jezelf creëert. En ze stelt één simpele maar confronterende vraag: wat als je morgen wakker wordt met geheugenverlies – wie kies je dan om te zijn?Deze aflevering helpt je ontdekken wie je in jouw veld wil toelaten, waar je je energie aan verspilt en hoe je je eigen systeem reset voor een krachtiger einde van het jaar. Verwacht geen oppervlakkige tips, maar eerlijke spiegels die je helpen terug te keren naar je kern en te kiezen voor wie jij wilt zijn in 2026.Ellen werkt achter de schermen aan een toegankelijk digitaal werkboek om je eigen Great Lock-in vorm te gevenTot die tijd kun je starten met haar videocursus of contact opnemen via fullcirclecoaching.beMindset en persoonlijke groei is een ongoing proces. Vergeet je daarom zeker niet te abonneren op deze podcast en laat een review of beoordeling achter via jouw podcast app.Heb je zelf een taboe doorbrekend topic of een vraag aan Ellen? Stuur dan een DM via Instagram of mail naar ellen@fullcirclecoaching.be.

Aan de slag!De vrede van God is geen doel op zichzelf, maar een middel dat je kan beschermen tegen ‘aanvallen' van verdriet, wrok of zorgen. God belooft je steviger te laten wortelen in Jezus, niet per se dat het leven rooskleuriger zal worden. Welke opdracht van Paulus is voor jou? Neem het ter harte en bid, want ‘dan zal de vrede van God, die alle verstand te boven gaat, uw hart en gedachten in Jezus Christus bewaren.'Deze overdenking is geschreven door oud-schrijfster Vivian Straver.

8 april 1721. Voor de kust van Réunion in de Indische Oceaan ligt een zwaar beschadigd schip voor anker - de Nossa Senhora do Cabo. Aan boord: de onderkoning van Goa, de aartsbisschop van Oost-Indië, 200 slaven uit Mozambique, en een schat die vandaag de dag ruim 100 miljoen euro waard zou zijn. Het schip kan zich niet verdedigen - alle 72 kanonnen zijn overboord gegooid na een storm. Dan verschijnen er piratenschepen aan de horizon. Onder leiding van Olivier Levasseur, bijgenaamd "La Buse" - De Buizerd - kapen ze zonder één schot te lossen de rijkste buit in de piratengeschiedenis. Maar het verhaal wordt pas echt mysterieus als negen jaar later Levasseur ter dood wordt veroordeeld voor piraterij . Vlak voor zijn executie gooit Levasseur een cryptogram in de menigte en roept: "Mijn schat voor wie het kan begrijpen!" Nu, 300 jaar later, denken onderzoekers dat ze eindelijk zijn legendarische schip hebben gevonden. Maar de schat zelf? Die ligt misschien nog steeds ergens begraven... Presentator Paul Sanders duikt in het verhaal van de Franse kaper Olivier Levasseur met Will Brouwers, archeoloog en historicus. Hij laat zijn licht schijnen op dit legendarische piratenverhaal. Factor Kuifje is een Paco Podcast productieRedactie en montage: Cornelis van der PlasPresentatie en montage: Paul SandersEindredactie: Annick van der Leeuw-NijlandLuister elke vrijdag een nieuwe aflevering van Factor Kuifje in je podcast-app of in de BNR-app. Download 'm hier voor Android, en hier voor Iphone. See 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.

Hoi, hartelijk welkom bij de Bijbellezen met Jan-podcast. Vandaag een bonus-aflevering. Ik ben bezig met een boek over de geschiedenis van de Bijbel waarin ik het antwoord zoek op cruciale vragen over de betrouwbaarheid van de Bijbel. Als je deze aflevering luistert in de maand september van 2025, dan kun je ook meedoen aan een speciale win actie, waarbij je kans maakt op het winnen van al mijn boeken. Je hoeft alleen maar je e-mailadres in te vullen op bijbellezenmetjan.nl/win. Alle deelnemers krijgen gratis het eBook De Bijbel in 1 Dag. Maar dat is niet enige. Je krijgt ook mijn eBook over de ontstaansgeschiedenis van de Bijbel zodra het af is. Dus ga naar Bijbellezenmetjan.nl/win om kans te maken op de de paperbacks van mijn boeken. Dan krijg je ook later het andere eBook. In deze speciale aflevering wil ik het met je hebben over een belangrijke vraag: is de Bijbel wel Gods Woord? Of is het mensenwerk? Is de Bijbel Gods Woord of mensenwerk? Het gebeurt vaak op momenten dat je het niet verwacht. Bij het koffieapparaat op je werk gaat het gesprek ineens over geloof. Je verzamelt je moed en zegt: ‘In de Bijbel staat…' Nog voor je zin af is, reageert je collega: ‘De Bijbel? Dat vervalste boek? Dat kun je toch niet serieus nemen.' Met je beker in de hand voel je een knoop in je maag. Of je zit bij familie aan tafel. Iemand zegt: ‘Hoe kun je daar nou in geloven? Iedereen weet toch dat bisschoppen in Nicea bepaalden welke boeken erin mochten en welke niet. Ze hielden alleen wat in hun straatje paste.' En dan die filmpjes op social media. Mensen die met stelligheid beweren dat monniken eeuwenlang fouten maakten bij het overschrijven. Soms gaat het nog verder: verhalen over geheime groepen zoals de illuminati die de Bijbel zouden hebben gemanipuleerd. In onze tijd hoor je het steeds opnieuw: de Bijbel zou een sprookjesboek zijn. Een leugen. Een oud wetboek dat achterhaald is. Wat zeggen anderen tegen jou over dat boek waar jij van houdt? Ik ben er zelf ook niet ongevoelig voor. Soms hoor ik dat stemmetje in mijn hoofd: Wat als ze gelijk hebben? Wat als het boek waarin ik geloof, waardoor ik bid om kracht en waarin ik troost vind, niet meer is dan een mensenwerk? Verhalen die door machthebbers zijn aangepast? Alleen al het stellen van die vragen voelt als verraad aan mijn geloof. Maar de vragen zijn er wel. En ze doen pijn, omdat ze raken aan wat ons het meest dierbaar is. De Bijbel is het meest gelezen boek ter wereld, maar ook een boek dat omgeven is door dit soort vragen en complottheorieën. Ze verdwijnen nooit helemaal. Daarom wil ik ze serieus nemen. Durf je het aan om samen met mij op onderzoek te gaan? We beginnen bij de eerste en meest fundamentele vraag: Is de Bijbel Gods Woord, of toch vooral mensenwerk? Waar de vraag vandaan komt Dit spanningsveld bestaat al zo lang als het christendom zelf. Aan de ene kant zijn er gelovigen die zeggen: ‘De Bijbel is door God gegeven. Elk woord, elke komma klopt.' Voor hen voelt twijfelen aan de betrouwbaarheid bijna als verraad. Aan de andere kant staan critici die de Bijbel zien als elk ander oud boek. Zij wijzen op tegenstrijdigheden, op verhalen die historisch niet te controleren zijn, en op teksten die duidelijk uit verschillende tijden komen. ‘Dit is gewoon mensenwerk,' zeggen ze. ‘Oude verhalen die door de eeuwen heen zijn aangepast.' En eerlijk: ze hebben niet helemaal ongelijk. De eerste vijf Bijbelboeken worden vaak aan Mozes toegeschreven. Maar kan dat wel? Hoe kan hij dan zijn eigen dood beschrijven (Deuteronomium 34)? Soms staan er ook zinnen die duidelijk uit een latere tijd komen. Neem Genesis 22:14. Daar lezen we dat Abraham de plaats waar hij zijn zoon bijna offerde ‘De HEER zal erin voorzien' noemt. En dan volgt: ‘Vandaar dat men tot op de dag van vandaag zegt: Op de berg van de HEER zal erin voorzien worden.' Dat klinkt alsof iemand veel later terugkijkt. Daarnaast ontdekten wetenschappers dat er verschillende schrijfstijlen door elkaar heen lopen. Het voelt alsof je een puzzel probeert te leggen waarvan de stukjes niet helemaal passen. Hoe reageren mensen daarop? • Sommige christenen wuiven de vragen weg: ‘Je moet dit gewoon geloven. God kan alles.' Ze doen alsof de Bijbel rechtstreeks uit de hemel is gevallen. Maar dat voelt toch wrang. Alsof je je verstand uit moet zetten. • Anderen gaan de andere kant op: ‘Zie je wel? Het is gewoon mensenwerk. Hooguit kun je er nog wat levenslessen uit halen.' Maar… de Bijbel zelf vertelt hoe hij is ontstaan. Het begin van schrijven in de Bijbel De eerste keer dat God zegt: ‘Schrijf dit op' staat in Exodus 17. Israël trekt net bevrijd uit Egypte door de woestijn. Dan vallen de Amalekieten hen aan. Er volgt een strijd die Israël met Gods hulp wint. Na de overwinning zegt God tegen Mozes: ‘Schrijf dit als herinnering in een boekrol.' Het gaat om dit moment. Dit verhaal van redding. De tweede keer komt een paar hoofdstukken later, in Exodus 24. Mozes is terug van de berg met de Tien Geboden en andere wetten. Hij vertelt het volk wat God gezegd heeft. Zij antwoorden: ‘Alles wat de HEER gesproken heeft, zullen wij doen.' Daarna schrijft Mozes de woorden op. Twee keer schrijven. Twee keer gaat het niet om een neutraal verslag, maar om identiteit en relatie. • Wie zijn wij als volk? • Hoe leven wij met God? Het ene document vertelt het verhaal van redding. Het andere legt vast wat het betekent om Gods volk te zijn. Samen vormen ze de kern van de Bijbel: elke generatie opnieuw leren wie we zijn, waar we vandaan komen, waarom we bestaan, en hoe onze relatie met God eruitziet. Menselijk werk zichtbaar Wie goed leest, ziet overal menselijke sporen. En de Bijbel verbergt dat niet. Neem het laatste hoofdstuk van Deuteronomium. Daar staat hoe Mozes sterft. Hij verdwijnt gewoon. En: ‘Tot op de dag van vandaag is er geen profeet meer opgestaan zoals Mozes.' Duidelijk geschreven vanuit een later moment. Of kijk naar Numeri 21, waar wordt geciteerd uit het ‘Boek van de oorlogen van de HEER'. Het Hebreeuws is daar veel ouder dan de rest. Toch worden deze Bijbelboeken aan Mozes toegeschreven. Mozes werkte dus met bronnen die al bestonden en na zijn dood is er dus nog aan de tekst gewerkt. Ook bij de profeten zie je dit. Jeremia had een secretaris, Baruch, die zijn woorden opschreef. Toen koning Jojakim de eerste boekrol verbrandde, schreef Baruch een tweede versie – en voegde er zelfs meer woorden aan toe. En de Psalmen? We denken vaak aan David, maar er zijn veel andere namen die worden genoemd als psalm-schrijvers: Salomo, Asaf, Ethan, Heman, en zelfs Mozes. Het is een verzameling gedichten en liederen die groeide door de eeuwen heen, met bijdragen van verschillende dichters en zangers. Gods inspiratie door de Geest Toch presenteert de Bijbel zichzelf niet als gewoon mensenwerk. Paulus schrijft aan Timoteüs: ‘Elke Schrift is door God geïnspireerd' (letterlijk: God-ademend). Let op: hij zegt niet dat alleen de schrijvers geïnspireerd waren. Hij zegt dat de teksten zelf God-ademend zijn. Het eindresultaat draagt Gods adem, ook al waren er generaties van mensen bij betrokken. De brief aan de Hebreeën laat dit mooi zien. Daar wordt Psalm 95 twee keer geciteerd. De ene keer staat er: ‘Zoals de Heilige Geest zegt…' De andere keer: ‘Zoals David zegt…' Voor de schrijver was dat geen tegenstelling. Dezelfde tekst heeft zowel een menselijke als een goddelijke auteur. Inspiratie betekent dus niet dat God elk woord dicteerde en mensen alleen maar noteerden. Het betekent dat Gods Geest door mensen en hun culturen heen werkte, door generaties van schrijvers en redacteuren, door het hele proces van ontstaan en overdracht. De spanning tussen God en mens Voor ons kan dit ongemakkelijk zijn. We willen graag weten: wat is precies gebeurd en wat is literaire creativiteit? Zijn de namen die we lezen echt historisch, of soms symbolisch bedoeld? Die spanning is er. En die hoeft niet opgelost te worden. De naam Abel bijvoorbeeld betekent in het Hebreeuws ‘damp'. En inderdaad: hij verdwijnt snel uit het verhaal. Paulus noemt de tovenaars van farao bij naam (Jannes en Jambres), terwijl die namen nergens in Exodus staan. Schrijvers bewaren geschiedenis én geven er creatief vorm aan. De Bijbel schaamt zich daar niet voor. Zoals Jezus volledig mens én volledig God was, zo is de Bijbel volledig menselijk én volledig geïnspireerd. Het is niet ondanks het menselijke element betrouwbaar, maar juist omdat God via hen tot ons spreekt. Een mozaïek van God en mens De Bijbel is geen kant-en-klare download uit de hemel. Het is een mozaïek, opgebouwd door eeuwen heen. Menselijke stemmen en Gods adem, verweven tot één geheel. Mozes schreef. De Levieten bewaarden. Profeten spraken. Schrijvers noteerden. Psalmisten zongen. Redacteuren voegden samen. En door dit alles heen blies Gods Geest zijn adem. Geen ‘dicteerder' die woord voor woord dicteerde. Maar een God die mensen inschakelde, hen meenam, hun stemmen gebruikte. Het resultaat: een boek dat menselijk oogt, maar goddelijk klinkt. Daarom is de vraag ‘Gods Woord of mensenwerk?' verkeerd gesteld. Het is geen óf-óf. Het is én-én. De Bijbel is volledig menselijk én volledig Gods Woord. En precies daardoor spreekt hij vandaag nog met kracht. En dat past bij wie God is. Hij doet zijn werk altijd samen met mensen. • Adam en Eva mochten over de schepping waken. • Noach mocht de ark bouwen. •...

Aan de slag!Probeer vandaag eens wat meer te luisteren en wat minder te spreken. Ervaar wat het voor jou betekent om door God gekend te worden en, in de nabijheid van de goede herder, Hem te volgen.Deze overdenking is geschreven door schrijfster Mathilda van Triest-Cozijnsen.

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.

Het rommelt bij NSC. De partij lijkt in zwaar te verkeren en de vraag rijst of de verkiezingen nog wel haalbaar zijn. Eddy van Hijum, demissionair minister van Sociale Zaken en Werkgelegenheid, is nu de lijsttrekker sinds het vertrek van Nicolien van Vroonhoven en Pieter Omtzigt. In interviews legt hij uit dat Den Haag een "slangenkuil" is en dat de premier geen duidelijke richting heeft aangegeven. "Ik had liever meer antwoorden die naar binnen gericht waren, zoals wat ze beter hadden kunnen doen", reageert Mireille van Ark, adjunct-hoofdredacteur van RTL Nieuws. "We hebben dit vaker gezien bij partijen die ontstaan rondom een persoon en de populariteit van de persoon", zegt programmamaker Kefah Allush. "Ik denk niet dat het te keren is. Als je eenmaal in die negatieve spiraal zit, heb je het daar voortdurend over." Aan tafel zitten Mireille van Ark, Kefah Allush en Spraakmaker Lotte Prins.

In deze podcast staan we stil bij de veranderingen die de wijkaanpak Rookvrij Kennemerland tussen 2021 en 2025 teweeg heeft gebracht bij inwoners van Schalkwijk (Haarlem) en Oosterwijk (Beverwijk/Heemskerk) en bij de betrokken professionals en vrijwilligers. Aan het woord komen twee rookvrij ambassadeurs – van wie er één inmiddels ook rookstopcoach is – die vertellen over hun inzet in de wijk, twee sociaal werkers rookvrij (één uit iedere wijk), een ex-roker voor wie de interventies van de wijkaanpak van grote betekenis zijn geweest, projectleiders van de wijkaanpak (GGD) Lida Samson en Janneke Heys en Inholland onderzoekers Niels Hermens en Lenneke Nieuwenhuizen. Luister naar hun verhalen van verandering, hoop en samenwerking! Wil je meer weten over (de interventies van) Rookvrij Kennemerland? Neem contact op met de GGD Kennemerland: Lida Samson (Lsamson@ggdkennemerland.nl) of Janneke Heys (janneke.heys@vrk.nl)

Aan de slag!Luister aandachtig naar het lied 'The Truth' van Megan Woods.Deze overdenking is geschreven door schrijfster Suzanne Verschoor.

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

Van kindersluiproutes tot sneeuwvrije fietspaden: ontdek hoe verbeelding onze steden fijner kan maken.Hoe maak je een stad écht fijn om in te leven? In zijn boek De Fijne Stad laat Vincent Luyendijk zien hoe verbeelding de sleutel is tot betere, groenere en menselijkere steden. Van sneeuwvrije fietspaden in Finland tot kindersluiproutes in Denemarken: overal zijn inspirerende ideeën te vinden. In ons gesprek hoor je hoe vijf thema's – de bereikbare, actieve, natuurlijke, klimaatbestendige en geleefde stad – handvatten bieden om onze openbare ruimte opnieuw te denken en in te richten.

Aan tafel zitten Arjen Fortuin, Wilma Haan en Spraakmaker Chris de Stoop. Met Jinek, Pauw en De Wit, Lubach, De Slimste Mens en RTL Tonight terug op de buis was het een behoorlijk volle start van het nieuwe tv-seizoen. "Het viel niet mee", reageert Arjen Fortuin, verslaggever bij NRC. Het ging bij de meeste programma's "geen moment over de inhoud van beleid", aldus Fortuin. "We kregen nu een heropvoering van de ruzies van de afgelopen maanden." Ook Wilma Haan, adjunct-hoofdredacteur van NOS Nieuws, had liever het nieuws van de dag besproken gezien dan wat zich afgelopen zomer afspeelde. Fleur Agema zat bij Pauw en De Wit en sprak daar over haar keuze om niet meer kiesbaar te zijn als PVV-lid. "Dat was werken voor Pauw", viel Haan op. "Toen ik keek wie waar zat, wilde ik Agema's verhaal wel horen." 

In deze aflevering neem ik je mee achter de schermen van mijn  miljoenenjaar.  Om transparant met je te delen wat er speelt: cijfers, keuzes en de shifts die nodig zijn om dit level van groei te dragen. Want deze reis draait niet alleen om omzet, maar vooral om wie ik bereid ben te worden. Je ontdekt: Wat mijn cijfers echt zeggen over mijn groei, zowel geaccordeerd als gerealiseerd. En hoe mijn strategie eruit ziet voor de komende periode.  Hoe ik keuzes heb gemaakt en maak die mijn bedrijf op de lange termijn laten werken voor dit jaar. De shifts in mijn identiteit die alles zijn gaan versnellen Waar ik mij op ga focussen voor de komende maanden om naar mijn miljoen omzet te komen.  Aan het einde van deze aflevering weet je hoe jij bouwt aan een bedrijf dat groeit vanuit visie, vertrouwen en strategie. 

Aan de slag!Kijk eens in de Zij Lacht Community op Facebook voor nieuwe contacten/vriendschappen bij jou in de buurt. Luister ook naar ‘I am not alone' van Kari Jobe en laat je vertroosten in je eenzaamheid.Deze overdenking is geschreven door schrijfster Marijke Gootjes-Verhoeve.

Heb jij ook het gevoel dat je altijd aan het geven bent, voor anderen klaarstaat en jezelf soms vergeet? Voel je je vaak leeggetrokken of overprikkeld, terwijl je eigenlijk verlangt naar meer balans, plezier en écht gezien worden? Dan is deze aflevering voor jou!In deze aflevering neem ik je mee in het gelaagde thema van grenzen stellen. Niet alleen in je werk of relaties, maar ook in je eigen lichaam en energie.Je hoort in deze aflevering onder andere:Waarom het negeren van je grenzen fysieke klachten kan veroorzaken, zoals huidproblemen en oververmoeidheidDe verborgen dynamieken waardoor anderen (onbewust) op jouw energie aankoppelen én hoe je dat stoptPraktische voorbeelden hoe je liefdevol "nee" zegt zonder keihard of onmenselijk te wordenHoe je de switch maakt van pleasen en alles dragen naar ontvangen, genieten, en jezelf écht iets gunnenGun jezelf de inzichten en handvatten om gezonde keuzes te maken in geven, ontvangen én genieten. Je lichaam en geest zullen je dankbaar zijn!

Aan tafel zitten Margriet Brandsma, Aimée Kiene en Spraakmaker Maarten Biermans. De NRC en Volkskrant hebben hun voorpagina's vanmorgen aangepast. Bij de NRC ging het om een zwarte pagina met de tekst: 'Zonder verslaggevers gaat het beeld uit Gaza op zwart.' De Volkskrant plaatste een collage van foto's van in Gaza omgekomen journalisten, met de tekst: 'Journalist is in Gaza een dodelijk beroep.' Tegelijkertijd was er een protestactie waarbij burgers om 12 uur, tijdens het nationale luchtalarm in Nederland, hun werk neer te leggen. "De rol van de journalistiek en de vrije pers is ontzettend belangrijk om informatie te krijgen", zegt Aimée Kiene, chef van Volkskrant Magazine. "Het is een belangrijk signaal." Journalist Margriet Brandsma voelt "ongemak" bij de actie, omdat journalisten dit soort middelen tot hun beschikking hebben, in tegenstelling tot andere beroepsgroepen. Tegelijkertijd vindt Brandsma het "ontzettend goed" dat er aandacht is voor dit onderwerp. "Dit gaat over mensenrechten en dat is niet ingewikkeld", zegt Kiene. 

Wat is eigenlijk de beste prijs voor je dienst of product? En hoe speel je slim met bundels, versies en kortingen om je marge en omzet te vergroten? Deze aflevering in het kort: ☑️ Veel ondernemers laten geld liggen met verkeerde prijsstrategieën ☑️ Pricing-hacks van Apple, Netflix en Ryanair die jij ook kunt toepassen ☑️ GreenPT, een ChatGPT-alternatief uit Nederland Een prijskaartje is nooit zomaar een getal. Het zegt iets over je merk, je kwaliteit en je positie in de markt. Toch maken veel ondernemers dezelfde fout: ze baseren hun prijs op kosten of op wat de concurrent vraagt. Daarmee laten ze veel geld liggen. In deze aflevering van schuiven Isabelle van Keulen en Ruben de Lange van Simon-Kucher aan. Dat is een internationaal consultancybedrijf, gespecialiseerd in strategie, marketing, sales en pricing. Zij weten beiden als geen ander hoe je met slimme pricing & packaging meer verkoopt. Luister ook | Nederlandse Airhub levert cruciale technologie voor drones We hebben het over de psychologie van prijzen, van ‘slechts 1 euro per dag' tot een premiumlabel dat vertrouwen uitstraalt. Ook bespreken we waarom A/B-testen onmisbaar zijn, hoe je met bundels en abonnementsvormen extra omzet kunt binnenhalen en waarom korting soms slim is, maar vaak juist funest. Aan de hand van voorbeelden van Apple, Netflix en Ryanair hoor je hoe grote merken hun strategie inzetten en hoe jij dat als ondernemer ook kunt toepassen. Het gesprek zit vol praktische hacks en inzichten, zodat je na het luisteren direct kritisch naar je eigen prijsmodel kijkt. Luister ook | De echo van de Draghi-rapport Remy Gieling bespreekt in zijn update het businessmodel van GreenPT. Dit is een duurzaam AI-chatplatform dat draait op Europese infrastructuur en zich richt op milieuvriendelijke kunstmatige intelligentie. Het maakt gebruik van de modellen Mistral mini en Qwen, die lokaal worden gehost op groene energie. Bijzonder is dat de restwarmte die vrijkomt bij AI-berekeningen wordt hergebruikt om onder meer woningen, zorginstellingen en zwembaden te verwarmen. Het platform wil zo krachtige AI-toepassingen mogelijk maken zonder onnodige energieverspilling en met een zo klein mogelijke ecologische voetafdruk.

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.

Vandaag een aflevering in de serie "In Stukken". Het Strijkoctet van Felix Mendelssohn-Bartholdy wordt in stukken geknipt. Aan de hand van de fragmenten in de mooiste opnames wordt het stuk onder de loep genomen. Panelleden: violist Maria-Paula Majoor en altviolist Francien Schatborn. Deze aflevering is eerder uitgezonden op zondag 26 januari 2025.

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.

Vanavond treffen de Amerikaanse president Donald Trump en zijn Russische collega Poetin elkaar in Alaska. Officieel draait het om mogelijke stappen richting een staakt-het-vuren in de oorlog in Oekraïne. Maar op de achtergrond tekent zich een strategisch machtsspel tussen twee wereldleiders over een mogelijke nieuwe wereldorde. Aan tafel correspondent Olaf Koens, en filosoof en hoogleraar Haroon Sheikh. Presentatie: Sophie Derkzen

Bij opening van de beurs verloor Adyen vandaag 20 procent. Aan het einde van de handelsdag is dat teruggelopen tot een verlies van bijna 5 procent. "De cijfers waren eigenlijk ook helemaal niet zo slecht, redelijk in lijn met de verwachtingen", constateert Robbert Manders van het Antaurus Europe Fund. "Het grote probleem is de groei in de tweede helft van het jaar. Adyen gaat nu uit van 20 in plaats van 24 procent. Het is een duur bedrijf, dus groei in nu eenmaal belangrijk." Wim Zwanenburg van Stroeve Lemberger vindt de reactie op de beurs bij opening ook overdreven. "De schuld gaf Adyen aan de internationale macro-omstandigheden en aan tegenvallende ontwikkelingen in Azië. Visa en Mastercard zijn wel iets andere bedrijven, maar zij hadden daar duidelijk minder last van." Niettemin vindt Wim Adyen een sterke speler in de sector. Hij is er dan ook niet heel negatief over. Anders is dat voor Triodos. De bank kwam met een winstdaling van 52 procent, maar sloot de handelsdag tóch met een piepkleine plus af. Dat zal te maken hebben met de vooruitzichten, waarover de ban redelijk positief was. Het neemt niet weg dat de experts er niet enthousiast over zijn en vinden het bedrijf, als professionele beleggers, ook te klein om in te beleggen. Verder in de podcast aandacht voor onder andere NN Group, Ørsted, Fastned en natuurlijk ook de laatste perikelen omtrent de handelsoorlog. We behandelen de luisteraarsvragen en de experts geven hun tips. Voor Wim is dat een algemene beleggingstip, Robbert tipt een Zwitsers machinebouwbedrijf. 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!See omnystudio.com/listener for privacy information.

Bart Moeyaert ontvangt in oktober de Henriëtte de Beaufortprijs voor zijn autobiografie ‘Een ander leven'. In dit boek neemt hij de lezer mee naar januari 1996, wanneer hij zijn moeder verrast met een driedaagse trip naar Parijs. Aan de hand van brieven, foto's, herinneringen en dagboekfragmenten ontstaat een intiem portret van hun relatie én een openhartig verslag van zijn late coming of age. Eerder in 2024 werd ‘Een ander leven' al uitgeroepen tot Regenboogboek van het jaar. Presentatie: Sarina Vitta

Essential tremor is the most common movement disorder, although it is often misdiagnosed. A careful history and clinical examination for other neurologic findings, such as bradykinesia, dystonia, or evidence of peripheral neuropathy, can reveal potential alternative etiologies. Knowledge about epidemiology and associated health outcomes is important for counseling and monitoring for physical impairment and disability. In this episode, Lyell Jones, MD, FAAN, speaks with Ludy C. Shih, MD, MMSc, FAAN, author of the article “Essential Tremor” in the Continuum® August 2025 Movement Disorders issue. Dr. Jones is the editor-in-chief of Continuum: Lifelong Learning in Neurology® and is a professor of neurology at Mayo Clinic in Rochester, Minnesota. Dr. Shih is clinical director of the Parkinson's Disease and Movement Disorders Center at Beth Israel Deaconess Medical Center in Boston, Massachusetts. Additional Resources Read the article: Essential Tremor Subscribe to Continuum®: shop.lww.com/Continuum Earn CME (available only to AAN members): continpub.com/AudioCME Continuum® Aloud (verbatim audio-book style recordings of articles available only to Continuum® subscribers): continpub.com/Aloud More about the American Academy of Neurology: aan.com Social Media facebook.com/continuumcme @ContinuumAAN Host: @LyellJ Guest: @ludyshihmd Full episode transcript available here Dr Jones: This is Dr Lyell Jones, Editor-in-Chief of Continuum. Thank you for listening to Continuum Audio. Be sure to visit the links in the episode notes for information about earning CME, subscribing to the journal, and exclusive access to interviews not featured on the podcast. Dr Jones: This is Dr Lyell Jones, Editor-in-Chief of Continuum: Lifelong Learning in Neurology. Today, I'm interviewing Dr Ludy Shih, who recently authored an article on essential tremor for our latest issue of Continuum on movement disorders. Dr Shih is an associate professor of neurology at Harvard Medical School and the clinical director of the Parkinson's Disease and Movement Disorder Center at Beth Israel Deaconess Medical Center in Boston. Dr Shih, welcome, and thank you for joining us today. Why don't you introduce yourself to our listeners? Dr Shih: Thank you, Dr Jones, for having me. It's a real pleasure to be here on the podcast with you. I'm a neurologist, I trained in movement disorders fellowship, and I currently see patients and conduct clinical research. We offer a variety of treatments and diagnostic tests for our patients with movement disorders. And I have developed this interest, a clinical research interest in essential tremor. Dr Jones: And so, as an expert in essential tremor, the perfect person to write such a really spectacular article. And I can't wait for our listeners to hear more about it and our subscribers to read it. And let's get right to it. If you had, Dr Shih, a single most important message for our listeners about caring for patients with essential tremor, what would that message be? Dr Shih: Yeah, I think the takeaway that I've learned over the years is that people with essential tremor do develop quite a few other symptoms. And although we propose that essential tremor is this pure tremor disorder, they can experience a lot of different comorbidities. Now, there is some debate as to whether that is expected for essential tremor or is this some part of another syndrome, which we may talk about later in the interview. But the fact of the matter is, it's not a benign condition and people do experience some disability from it. Dr Jones: And I think that speaks to how the name of this disorder has evolved over time. right? You point out in your article, it used to be called benign essential tremor or benign familial tremor. But it's really not so straightforward as it. And fairly frequently these symptoms, the patient's tremor, can be functionally limiting, correct? Dr Shih: That is correct. In fact, the reason I probably started getting interested in essential tremor was because our center had been doing a lot of deep brain stimulation for essential tremor, which is remarkably effective, especially for tremor that reaches an amplitude that really no oral medication is going to satisfyingly treat. And if you have enough upper limb disability from this very large-amplitude tremor, a surgical option may make a lot of sense for a lot of patients. And yet, how did they get to that point? Do they continue to progress? These were the sort of interesting questions that got raised in my mind as I started to treat these folks. Dr Jones: We'll come back to treatment in just a minute here, because there are many options, and it sounds like the options are expanding. To start with the diagnosis- I mean, this is an extraordinarily common disorder. As you point out, it is the most common movement disorder in the US and maybe the world, and yet it seems to be underrecognized and frequently misdiagnosed. Why do you think that is? Dr Shih: Great question. It's been pretty consistent, with several case series over the decades showing a fairly high rate of quote/unquote “misdiagnosis.” And I think it speaks to two things, probably. One is that once someone sees a postural and kinetic tremor of the arms, immediately they think of essential tremor because it is quite common. But there's a whole host of things that it could actually be. And the biggest one that we also have to factor in is also the heterogeneity of the presentation of Parkinson's disease. Many people, and I think increasingly now these days, can present with not a whole lot of the other symptoms, but may present with an atypical tremor. And it becomes actually a little hard to sort out, well, do they have enough of these other symptoms for me to suspect Parkinson's, or is the nature of their tremor suspicious enough that it would just be so unusual that this stays essential tremor and doesn't eventually develop into Parkinson's disease? And I think those are the questions that we all still grapple with from time to time in some of our clinics. Dr Jones: Probably some other things related to it with, you know, our understanding of the pathophysiology and the availability of tests. And I do want to come back to those questions here in just a minute, but, you know, just the nomenclature of this disorder… I think our clinical listeners are familiar with our tendency in medicine to use words like essential or idiopathic to describe disorders or phenomena where we don't understand the precise underlying mechanism. When I'm working with our trainees, I call these “job-security terms” because it sounds less humbling than “you have a tremor and we don't know what causes it,” right? So, your article does a really nice job outlining the absence of a clear monogenic or Mendelian mechanism for essential tremor. Do you think we'll ever have a eureka moment in neurology for this disorder and maybe give it a different name? Dr Shih: It's a great question. I think as we're learning with a lot of our neurologic diseases---and including, I would even say, Parkinson's disease, to which ET gets compared to a lot---there's already now so much more known complexity to something that has a very specific idea and concept in people's minds. So, I tend to think we'll still be in an area where we'll have a lot of different causes of tremor, but I'm hopeful that we'll uncover some new mechanisms for which treating or addressing that mechanism would take care of the tremor in a way that we haven't been able to make as much progress on in the last few decades as maybe we would have thought given all the advances in in technology. Dr Jones: That's very helpful, and we'll be hopeful for that series of discoveries that lead us to that point. I think many of our listeners will be familiar with the utility---and, I think, even for most insurance companies, approval---for DAT scans to discriminate between essential tremor and Parkinsonian disorders. What about lab work? Are there any other disorders that you commonly screen for in patients who you suspect may have essential tremor? Dr Shih: Yeah, it's a great question. And I think, you know, I'm always mindful that what I'm seeing in my clinic may not always be representative of what's seen in the community or out in practice. I'll give an example. You know, most of the time when people come to the academic Medical Center, they're thinking, gosh, I've tried this or that. I've been on these medicines for the last ten years. But I've had essential tremor for twenty years. We get to benefit a little bit from all that history that's been laid down. And so, it's not as likely you're going to misdiagnose it. But once in a while, you'll get someone with tremor that just started a month ago or just started, you know, 2 or 3 months ago. And you have to still be thinking, well, I've got to get out of the specialist clinic mindset, and think, well, what else really could this be? And so, while it's true for everybody, moreso in those cases, in those recent onset cases, you really got to be looking for things like medications, electrolyte abnormalities, and new-onset thyroid disorder, for example, thyroid toxicosis. Dr Jones: Very helpful. And your article has a wonderful list of the conditions to consider, including the medications that might be used for those conditions that might result or unmask a tremor of a different cause. And I think being open-minded and not anchoring on essential tremor just because it's common, I think is a is a key point here. And another feature in your article that I really enjoyed was your step-by-step approach to tremor. What are those steps? Dr Shih: Well, I think you know first of all, tremor is such common terminology that even lay people, patients, nonclinicians will use the word “tremor.” And so, it can be tempting when the notes on your schedule says referred for tremor to sort of immediately jump to that. I think the first step is, is it tremor? And that's really something that the clinician first has to decide. And I think that's a really important step. A lot of things can look superficially like tremor, and you shouldn't even assume that another clinician knows what tremor looks like as opposed to, say, myoclonus. Or for example a tremor of the mouth; well, it actually could be orolingual or orobuccal dyskinesia, as in tardive dyskinesia. And another one that tremor can look like is ataxia. And so, I think- while they sound obvious to most neurologists, perhaps, I think that---especially in the area of myoclonus, where it can be quite repetitive, quite small amplitude in some conditions---it can really resemble a tremor. And so, there are examples of these where making that first decision of whether it's a tremor or not can really be a good sort of time-out to make sure you're going down the right path to begin with. And I think what's helpful is to think about some of the clinical definitions of a tremor. And tremor is really rhythmic, it's oscillatory. You should see an agonist and antagonist muscle group moving back and forth, to and fro. And then it's involuntary. And so, I think these descriptors can really help; and to help isolate, if you can describe it in your note, you can probably be more convinced that you're dealing with the tremor. The second step that I would encourage people to really consider: you've established it's a tremor. The most important part exam now becomes, really, the nontremor part of the exam. And it should be really comprehensive to think of what else could be accompanying this, because that's really how we make diagnosis of other things besides essential tremor. There really should be a minimum of evidence of parkinsonism, dystonia, neuropathy, ataxia- and the ataxia could be either from a peripheral or central nervous system etiology. Those are the big four or five things that, you know, I'm very keen to look for and will look pretty much in the head, neck, the axial sort of musculature, as well as the limbs. And I think this is very helpful in terms of identifying cases which turn out to have either, say, well, Parkinson's or even a typical Parkinson disorder; or even a genetic disorder, maybe even something like a fragile X tremor ataxia syndrome; or even a spinal cerebellar ataxia. These cases are rare, but I think if you uncover just enough ataxia, for example, that really shouldn't be there in a person, let's say, who's younger and also doesn't have a long history of tremor; you should be more suspicious that this is not essential tremor that you're dealing with. And then the last thing is, once you've identified the tremor and you're trying to establish, well, what should be done about the tremor, you really have to say what kind of tremor it is so that you can follow it, so you can convey to other people really what the disability is coming from the tremor and how severe the tremor is. So, I think an example of this is, often in the clinic, people will have their patients extend their arms and hands and kind of say, oh, it's an essential tremor, and that's kind of the end of the exam. But it doesn't give you the flavor. Sometimes you'll have a patient come in and have a fairly minimal postural tremor, but then you go out, take those extra few seconds to go grab a cup of water or two cups of water and have them pour or drink. And now all of a sudden you see this tremor is quite large-amplitude and very disabling. Now you have a better appreciation of what you really need to do for this patient, and it might not be present with just these very simple maneuvers that you have at bedside without props and items. And then the severity of it; you know, we're so used to saying mild, moderate, severe. I think what we've done in the Tremor Research Group to use and develop the Essential Tremor Rating Assessment Scale is to get people used to trying to estimate what size the tremor is. And you can do that by taking a ruler or developing a sense of what 1 centimeter, 2 centimeters, 3 centimeters looks like. I think it'd be tremendously helpful too, it's very easy and quick to convey severity in a given patient. Dr Jones: I appreciate you, you know, having a patient-centered approach to the- how this is affecting them and being quantitative in the assessment of the tremor. And that's a great segue to a key question that I run into and I think others run into, which is when to initiate therapy? You know, if you see a patient who, let's say they have a mild tremor or, you know, something that quantitatively is on the mild end of the spectrum, and you have, you know, a series of options… from a medication perspective, you have to say, well, when does this across that threshold of being more likely to benefit the patient than to harm the patient? How do you approach that question? What's your threshold for starting medication? Dr Shih: Yeah. You know, sometimes I will ask, because---and I know this sounds like a strange question---because I feel like my patients will come for a couple of different reasons. Sometimes it's usually one over the other. I think people can get concerned about a symptom of a tremor. So, I actually will ask them, was your goal to just get a sense for what this tremor is caused by? I understand that many people who develop tremor might be concerned it might be something like Parkinson's disease. Or is this also a tremor that is bothering you in day-to-day life? And often you will hear the former. No, I just wanted to get checked out and make sure you don't think it's Parkinson's. It doesn't bother me enough that I want to take medication. They're quite happy with that. And then the second scenario is more the, yeah, no, it bothers me and it's embarrassing. And that's a very common answer you may hear, may be embarrassing, people are noticing. It's funny in that many people with essential tremor don't come to see a doctor or even the neurologist for many years. And they will put up with it for a very long time. And they've adopted all sorts of compensatory strategies, and they've just been able to handle themselves very admirably with this, in some cases, very severe tremor. So, for some of them, it'll take a lot to come to the doctor, and then it becomes clear. They said, I think I'm at the point where I need to do something about this tremor. And so, I think those three buckets are often sort of where my patients fall into. And I think asking them directly will give you a sense of that. But you know, it can be a nice time to try some as-needed doses of something like Propranolol, or if it's something that you know that they're going to need something on day-to-day to get control of the tremor over time, there are other options for that as well. Dr Jones: Seems like a perfect scenario for shared decision-making. Is it bothersome enough to the patient to try the therapy? And I like that suggestion. That's a nice pearl that you could start with an a- needed beta blocker, right, with Propranolol. And this is a question that I think many of us struggle with as well. If you've followed a patient with essential tremor for some time and you've tried different medications and they've either lost effectiveness or have intolerable adverse effects, what is your threshold for referring a patient for at least considering a surgical neurostimulator therapy for their essential tremor? Dr Shih: Yeah, so surgical therapies for tremor have been around for a long time now, since 1997, which was when it was approved by the FDA for essential tremor and Parkinson tremor. And then obviously since then, we have a couple more options in the focus ultrasound thalamotomy, which is a lesioning technique. When you have been on several tremor medications, the list gets smaller and smaller. It- and then chance of likely satisfying benefit from some of these medications can be small and small as you pass through the first and second line agents and these would be the Propranolol and the primidone. And as you say, quite a few patients- it's estimated between 30 to 50% of these patients end up not tolerating these first two medications and end up discontinuing them. Some portion of that might also be due to the fact that some of our patients who have been living with essential tremor for decades now, to the point that their tremor is getting worse, are also getting older. And so, polypharmacy and/or some of the potential side effects of beta blockers and anticonvulsants like primidone may be harder to bear in an older adult. And then as you talk about in the article, there's some level of evidence for topiramate, and then from there a number of anticonvulsants or benzos, which have even weaker evidence for them. It's a personal decision. As I tell folks, look, this is not going to likely extend your life or save your life, but it's a quality of life issue. And of course, if there are other things going on in life that need to be taken care of and they need that kind of care and attention, then, you know, you don't need to be adding this to your plate. But if you are in the position where those other things are actually okay, but quality of life is really affected by your being unable to use your upper limbs in the way that you would like to… A lot of people's hobbies and applications are upper limb-based, and enjoying those things is really important. Then I think that this is something- a conversation that we begin and we begin by talking about yes, there are some risks involved, but fortunately this is the data we have on it, which is a fairly extensive experience in terms of this is the risk of, you know, surgery-related side effects. This is the risk of if you're having stimulation from DBS stimulation-related side effects, which can be adjustable. It's interesting, I was talking with colleagues, you know, after focused ultrasound thalamotomy was approved. That really led more people to come to the clinic and start having these discussions, because that seemed like a very the different sort of approach where hardware wasn't needed, but it was still a surgery. And so, it began that conversation again for a bunch of people to say, you know, what could I do? What could I tolerate? What would I accept in terms of risk and potential benefit? Dr Jones: Well, I think that's a great overview of a disorder where, you know, I think the neurologist's role is really indispensable. Right? I mean, you have to have this conversation not just once, this is a conversation that you have over time. And again, I really want to refer our listeners to this article. It's just a fantastic overview of a common disorder, but one where I think there are probably gaps where we can improve care. And Dr Shih, I want to thank you for joining us, and thank you for such a great discussion on essential tremor. I learned a lot from your article, and I learned even more from the interview today. I suspect our readers and listeners will too. Dr Shih: Well, thank you again for the invitation and the opportunity to kind of spread the word on this really common condition. Dr Jones: Again, we've been speaking with Dr Ludy Shih, author of a fantastic article on essential tremor in Continuum's latest issue on movement disorders. Please check it out, and thank you to our listeners for joining today. Dr Monteith: This is Dr Teshamae Monteith, Associate Editor of Continuum Audio. If you've enjoyed this episode, you'll love the journal, which is full of in-depth and clinically relevant information important for neurology practitioners. Use the link in the episode notes to learn more and subscribe. AAN members, you can get CME for listening to this interview by completing the evaluation at continpub.com/audioCME. Thank you for listening to Continuum Audio.

Deze zomer is het 25 jaar geleden dat het Europees Kampioenschap van 2000 in Nederland en België werd gehouden. In deze serie van de Staantribune podcast blikken we terug op elfde editie van het door de UEFA georganiseerde eindtoernooi.  Aan de hand van diverse gasten en verschillende invalshoeken voelt iedereen zich weer voor even terug in die zomer van 2000. In deze allerlaatste aflevering bespreken we met journalist Jurriaan van Wessem de twee finalisten van dit toernooi: Italië en Frankrijk. Uiteraard kan dan de finale in Rotterdam ook niet ontbreken. Jurriaan volgde de voortgang van het toernooi op de voet door in België en Nederland onder meer aanwezig te zijn als verslaggever. Deze podcastserie werd mede mogelijk gemaakt door Kick and Rush. Kick and Rush is een webshop waar iedere voetballiefhebber komt voor zijn of haar unieke en klassieke voetbalshirts en -attributen.Vragen, tips of suggesties over onze podcast zijn altijd welkom: ⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠podcast@staantribune.nl⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠.Word abonnee van hét magazine over voetbalcultuur: ⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠https://staantribune.nl/word-abonnee

Parkinson disease is a neurodegenerative movement disorder that is increasing in prevalence as the population ages. The symptoms and rate of progression are clinically heterogenous, and medical management is focused on the individual needs of the patient. In this episode, Kait Nevel MD, speaks with Ashley Rawls, MD, MS, author of the article “Parkinson Disease” 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. Rawls is an assistant professor at the University of Florida Health, Department of Neurology at the Norman Fixel Institute for Neurological Diseases in Gainesville, Florida Additional Resources Read the article:  Parkinson Disease 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: @DrRawlsMoveMD Full episode transcript available here Dr Jones: This is Dr Lyell Jones, Editor-in-Chief of Continuum. Thank you for listening to Continuum Audio. Be sure to visit the links in the episode notes for information about earning CME, subscribing to the journal, and exclusive access to interviews not featured on the podcast. Dr Nevel: Hello, this is Dr Kait Nevel. Today I'm interviewing Dr Ashley Rawls about her article on Parkinson disease, which appears in the August 2025 Continuum issue on movement disorders. Ashley, welcome to the podcast, and please introduce yourself to the audience. Dr Rawls: Thank you, Kait. Hello everyone, my name is Dr Ashley Rawls. I am a movement disorder specialist at the University of Florida Fixel Institute for Neurologic Diseases in Gainesville, Florida. It's a pleasure to be here. Dr Nevel: Awesome. To start us off talking about your article, can you share what you think is the most important takeaway for the practicing neurologist? Dr Rawls: Yes. I would say that my most important takeaway for this article is that Parkinson disease remains a clinical diagnosis. I think the field has really been advancing and trying to find a biomarker to help with diagnosis through ancillary testing. For example, with the dopamine transporter, the DAT scan, an alpha-synuclein skin biopsy, an alpha-synuclein amplification assay that can happen in blood and CSF. However, I think it's so critical to make sure that you have a very strong history and a very thorough physical exam and use those biomarkers or other testing to help with, kind of, bolstering your thoughts on what's going on with the patient. Dr Nevel: Great. And I can't wait to talk a little bit more about the ancillary testing and how you use that. Before we get to that, can you review with us some of the components of the clinical diagnosis of Parkinson disease? Dr Rawls: Yes. So, when I think about a person that comes in that might have a neurodegenerative disease, I think about two different features, mainly: both motor and Manon motor. So, for my motor features, I'm thinking about resting tremor, bradykinesia---which is fullness of movement with decrement over time---rigidity, and then a specific gait disturbance, a Parkinsonian gait, involving stooped posture, decreased arm swing. They can also have reemergent tremor while walking if they do have tremor as part of their disease process, and also in-block turning as they are walking down the hallway. So, those are my motor features that I look for. So now, when we're talking about a specific diagnosis of Parkinson disease, the one motor feature that you need to have is bradykinesia. The reason why I make sure to speak about bradykinesia, which is slowness of movement with decrement over time, is because people can still have Parkinson disease without having tremor, a resting tremor. So even though that's one of the core cardinal features that most of us will be able to notice very readily, you don't have to necessarily have a resting tremor to be diagnosed with Parkinson' disease. When I talk about nonmotor features, those are going to be the three, particularly the prodromal features that can occur even ten years before people have motor features, can be very prominent early on in the disease process. For example, hyposmia or anosmia for decrease or lack of sense of smell. Another one that we really look for is going to be RBD, or rapid eye movement behavior disorder; or REM behavior disorder, the person acting out their dreams, calling out, flailing their limbs, hitting their bed partner. And then the other one is going to be severe constipation. So those three prodromal nonmotor symptoms of hyposmia/anosmia, RBD or REM behavior disorder, and severe constipation can also make me concerned as a red flag that there is a sort of neurodegenerative issue like a Parkinson disease that may be going on with the patient. Dr Nevel: Great, thank you so much for that overview. While we're talking about the diagnosis, do you mind kind of going back to what you mentioned in the beginning and talking about the ancillary tests that sometimes are used to kind of help, again, bolster that diagnosis of Parkinson disease? You know, like the DAT or the alpha-synuclein skin biopsy. When should we be using those? Should we be getting these on everyone? And what scenarios should we really consider doing one of those tests? Dr Rawls: The scenario in which I would order one of the ancillary testing, particularly like a DAT scan or a skin biopsy, looking for alpha-synuclein is going to be when there are potential red flags or a little bit of confusion in regard to the history and physical that I need to have a little bit more clarification on. For example, if I have a patient that has a history of using dopamine blocking agents, for example, for severe depression; or they have a history of cancer diagnosis and they've been on a dopamine agent like metoclopramide; those I want to be mindful because if they're coming in to see me and they're having the symptoms of Parkinsonism---which is going to be resting tremor, bradykinesia rigidity, or gait disturbance---I need to try to figure out is it potentially due to a medication effect, particularly if they're still on the dopamine blockade medication, or is it something where they're actually having a neurodegenerative illness underneath it, like a Parkinson disease? The other situation that would make me order a DAT skin or a skin biopsy is going to be someone who is coming in that maybe has elements of essential tremor, they have more of a postural or an intention tremor that's very flapping and larger amplitude, and maybe have some mild symptoms and Parkinsonism that might be difficult to distinguish between other musculoskeletal things like arthritis, other imbalance issues from, you know, hip problems or knee problems and what have you. Then I might say, okay, let's see if there is some sort of neurodegeneration underneath this; that may be- that there could be, you know, potentially two elements like a central tremor and Parkinson disease going on. Or is this someone who actually really has Parkinson disease, but there's other factors that are kind of playing into that. Dr Nevel: Great, thank you for that. Gosh, things have really changed over the past fifteen years or so where we have this ancillary testing that we're able to use more, because what you read in the textbook isn't always what you see in clinic. And as you described, there are patients who… it's not as clear cut, and these tests can be helpful. Could you tell us more about the levodopa challenge test? How is this useful in clinical practice? And what are some key points that we should know about when utilizing this strategy for patients who we think have Parkinson disease? Dr Rawls: So, before we had all this ancillary testing with the DAT scan, the skin biopsy, the alpha-synuclein amplification assay, many times if you had a suspicion that a person that had Parkinson disease, but you weren't entirely sure, you would say, hey, listen, let us give you back the dopamine that your body may be missing and see if you have an improvement, in particular in your motor symptom. So, when I talk with my patients, I say, listen, I might have a strong suspicion that you have Parkinson disease. Doing a levodopa trial can not only be diagnostic, but also can be therapeutic as well. So, with this levodopa trial, what I end up doing is saying, okay, we're going to start the medication at a low dose because we are looking to see if you have improvement in three of the main cardinal motor symptoms. Obviously, tremor is much easier for us to see if it gets better. It's very obvious on exam, and the patients are more readily able to see it. Whereas stiffness and slowness is much harder to quantify and try to figure out. Am I stiff and slow because of potential muscle tightness from Parkinson disease, or is it something that's more of a musculoskeletal issue? So, I will tell persons, okay, we're looking for improvement in these three cardinal motor symptoms, and things that we're looking for is getting into and out of a car, into and out of a chair, turning over in bed, seeing how do we navigate ourselves in our daily lives? I give people the example of going through the grocery store, going through a busy airport. Are we able to move better and respond better to different changes in our environment which can give us a better clue of if our stiffness and slowness in particular are being improved with the medication? The other part of this is talking about potential side effects of the carbidopa- of the levodopa in particular. One big thing that I think limits people initially is going to be the nausea, vomiting, potential GI upset when starting this medication initially. So, oftentimes I will find people coming in, oh, you know, my outside doctor started me immediately on one tab of carbidopa/levodopa three times per day. I got nauseous, I threw up, and I never took the medication again. So often times I will start low and go slow because once someone throws up my medication, they are not going to want to take it again---with good reason. So, often times I will ask the patient, hey listen, are you very sensitive to medications? If you are very sensitive, we might start one tablet per day for a week, one tablet twice a day, and then go up until we get to two tablets three times a day if we're talking about carbidopa/levodopa. If someone is not as sensitive then I might go up a little bit quicker. What do we mean when we talk about 600 milligrams per day? So usually, the amount that I use is carbidopa/levodopa, 25/100; so, 100 milligrams being the levodopa portion. Many people just start off at 1 tab 3 times a day, which gives you 300 milligrams of levodopa, and they say, oh, it didn't work, I must not have Parkinson or something else. Well, it just may have been that we did not give an adequate trial and adequate dose to the person. Now if they're not able to tolerate the medication because of the side effects, that's something different. But if they don't have side effects and don't notice a difference, there is room to increase the carbidopa/levodopa or the levodopa replacement that you are using so that you can give it, you know, a very good try to see, is it actually improving resting tremor, bradykinesia and rigidity? Dr Nevel: Yeah, great. Thanks for that. When you diagnose a patient with Parkinson disease, how do you counsel that patient? How do you break that difficult news? And how do you counsel them on what to expect in the future and goals of treatment? I know that's a lot in that question, but it also is a lot that you do in one visit, oftentimes, or at least introduce these kind of concepts to patients in a single visit. Dr Rawls: One thing that I think is helpful for me is trying to understand where the patients and their families are when they come in. Because some of the patients come in and have no prior inkling that they may have a neurodegenerative illness like Parkinson disease. Some of my patients come in and say, I'm here for a second opinion for Parkinson disease. So, then I have an idea of where we are in regard to potential understanding of how to start the conversation going forward. If it is someone who is coming in and has not heard about Parkinson disease, or their family has not been made aware that that's the one reason why they're coming to see a movement disorder specialist, then I will start at the beginning After we finish our history, do a very thorough physical exam, I will talk about things that I heard in the history and that I see on the physical exam that make me concerned for a disease like Parkinson disease. I make sure to tell them where I'm getting my criteria from and not just start off, I think you have Parkinson, here's your medication. I think that's very jarring when you're talking with patients and their families, particularly if they had no idea that this could be a potential diagnosis on the table. Like I said, I will start off with recounting, this is what I've heard in your history that makes me concerned. This is what I've seen on your physical exam that makes me concerned. And I think you have Parkinson disease and here is why. And I'll tell them about the tenants like we discussed about Parkinson disease, both the motor and nonmotor symptoms that we see. So that's kind of the first part is, I make sure to lay it out and then open the room up for some questions and clarification. The other portion of this is that, when I'm talking about counseling the patient, I say, we do not expect Parkinson disease to decrease your lifespan. However, over time, our persons, because it is a neurodegenerative illnesses will accumulate deficits over time. So, more stiffness, more slowness, more walking problems. They may, if they have tremor, the tremor may become worse. If they don't have tremor, they might develop tremor in the future. If we're talking about the nonmotor symptoms that we talk about, the main ones are going to be issues with urinary problems, issues with bowels, and then the other thing is going to be neuropsychiatric issues like anxiety and depression. And those things become more prominent, usually, the nonmotor symptoms later on in the disease process, and then also cognitive impairment as well. I really want to make sure that they have the information that I'm seeing, and if there's anything that they want to correct on their end, as in they're saying, oh wait, well, actually I noticed something else, then that's usually when that comes out around kind of the wrapping-up portion of the visit. So, I think that's really important to, one, be very clear in what I am seeing and if there's red flags, and then tell them, okay this is not going to shorten your lifespan. However, over time, we do have other issues and problems that will arise and we can support you as best as we can through that. The one thing I also been very open with people about is- because our patients will say, is there anything I can do? What can be done? Is there any medication to slow down or stop things? And I let people know that unfortunately, right now there's not an intervention that slows down, stops, or reverses disease progression, with the exception of exercise. Consistent exercise has been found to help to slow down disease progression, okay? And also, it can help to release the dopamine already being made innately in the brain. And also, it can help with our cardiovascular health in the big thing: being balanced. Core strength, quadricep strength. So that's also something that people can work on that they should. And I let people know that exercise is as important as the medications themselves. Dr Nevel: Absolutely. And it's incredible how much they incorporate exercise into their daily lives and get active, people who weren't active before their diagnosis, and how much that can help. One question that I think patients sometimes ask is, when they understand how carbidopa/levodopa works and what the expectations are for that medication, that it's not a disease-modifying medication, but that it can help with their symptoms. And then they kind of hear, well as time goes on, they need higher doses or, you know, it doesn't control their motor symptoms as well. They'll say, okay well, is it better to wait then? Should I wait to start carbidopa/levodopa? Like in my mind, I'm only maybe going to get X amount of time from carbidopa/levodopa. So, I'd rather wait to start it than start it now. What do you say to them and how do you counsel them through that? Dr Rawls: So that is a common question that I do get with my patients. So, I tell people, I'm here for you. And it really depends on how you feel at this time. Because you have to weigh the risks and benefits of the medication itself. If someone who's very, very mild decides to take the medication, they feel nauseous, they're just going to say, hey, listen, it's not for me right now. I don't feel like I need it, and then stop, which is with definitely within their right. But what I always counsel patients as well is to say, the dopamine-producing neurons in the substantia nigra are starting to die over time. That is why we are getting the signs and symptoms of Parkinson disease. At some point, your brain is not going to produce enough dopamine that is needed for you to move when you want to move and not move when you don't want to move. Okay? Giving you at least the motor symptoms of Parkinson disease. With this, it's not that the medication stops working, it's just that you need more dopamine to help replace the dopamine that's being lost. However, the dopamine that you are taking or levodopa that you're taking orally is not going to be released as consistently as it is in your brain on demand and shut off when you don't need it. Hence the reason we get more motor fluctuations. Also, potential side effects in the medication like orthostatic hypertension, hallucinations, impulse control disorders. Because you're having to take more escalating doses, those side effects can become more prominent and also lead us to have to balance between the side effects and the medication itself. So, it's not that the medication does not work, your body needs more of it. Some people will say, oh, well, I want to wait, and I say, that's completely fine. However, my cutoff is basically saying, if you are finding that you, as the person who's afflicted is not able to get up in the morning like you want to, you're avoiding going to walk your dog or working in your garden, you know, because you feel stiff and feel slow; you're avoiding, you know, going out to the community, having lunch with your friends or your family because you're embarrassed by your tremor; this is something that is keeping you from living your life. And that's the time that we need to strongly consider starting the medications. So, a person afflicted will accumulate deficits. However, it's how much the deficits are going to affect you. So, if it's really affecting your life, we have tools and ways to help mitigate that. Dr Nevel: Yeah, absolutely. Are there any aspects of Parkinson disease management that you feel are maybe underrecognized or perhaps underutilized? In other words, you know, are there things that we the listeners should be maybe more aware of or think about offering or recommending to our patients that you think maybe aren't as much as they could be? Dr Rawls: I will say the nonmotor symptoms---in particular the neuropsychiatric symptoms with the anxiety and depression, usually later on disease process but also can be earlier as well---I think that is going to be something that is recognized but maybe undertreated in a lot of our patient population. I think part of that is also the fluctuations in dopamine that are occurring naturally in the person, but also, our patients, oftentimes with their medication regimen, really have to be on the ball taking the medication. If they're even 15 minutes late, 10 minutes late, 5 minutes late, we're now off, and now we're waiting for it to kick in. And so that can cause a lot of anxiousness even throughout the day. And then knowing that slowly over time that they're going to accumulate these motor and nonmotor deficits can definitely be problematic as well. There is obvious reason for this underlying potential anxiety and depression. And while we do talk about that and bring that up, sometimes patients will say, oh well, I don't think it's a problem right now. I don't have to mess with this. But usually at some point it does become an issue that usually the family members will bring up and saying, hey, you know, my loved one is very anxious. Or I've noticed that they're just really disengaged from what's going on in their lives and they are not talking as much, they're not going out as much. Again, that could be a combination of depression/anxiety, but it also can be a physical- a combination of, I'm not physically able to do these things, or, they're much more difficult for me to initiate doing these activities. I always want to be mindful. If my patients come in and they already have a diagnosis of depression or anxiety and they're already being treated by a mental health counselor, provider, or a psychiatrist, then I will work with providers so that we can try to optimize their medication regimen. The other thing is, well, if this is the first time that they're really being seen by someone and talking about their anxiety and depression, then oftentimes I will have them go back to their primary care and see if maybe an SSRI or SNRI will be helpful to try to help with the neuropsychiatric symptoms they may be experiencing. So that's one big one. Another one that I think that might be a little bit underappreciated is going to be drooling. Sometimes I'll come in and see my patients and notice some drooling that's happening with the mouth being open, not being able to initiate the swallowing reflex consistently throughout the day. Or they may be patting their face a lot with a napkin or a towel and then bringing that up and bringing it to light. Oh yeah. I have a lot of drooling while I'm awake. It's on my shirt. It's embarrassing. I feel like it's a little bit too much for me or my family. We have to put a bib on because I'm just drooling all throughout the day. That can really be uncomfortable and cause skin breakdown. It can also be socially embarrassing. So, there are some tools that I talk to people about with drooling. One thing I start with is going to be using sugar-free gum or candy while the person is awake to help initiate the swallow reflex, and sometimes that's all that's needed. There are other agents that can be used---like glycopyrrolate, sublingual atropine drops, and scopolamine patches---that can help with decreasing saliva production. But there can be side effects of making the entire body feel dry, and then also potential cardiac arrhythmias. If those are not helpful or they're contraindicated with the patient, another thing is going to be botulinum toxin injections. So those can be done on the parotid and salivary glands to decrease the amount of saliva that's being produced. So oftentimes people will come to me, because I'm also a botulinum toxin injector. I've been sent by some of my colleagues to inject our persons that have significant sialorrhea. Dr Nevel: Wonderful. Well, thank you so much for chatting with me today about your article. Again, today I've been interviewing Dr Ashley Rawls about her article on Parkinson disease, 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. And thank you, Ashley, for sharing all your knowledge with us today. Dr Rawls: Thank you, Kate, I appreciate your time. And have a great day, everyone. Dr Monteith: This is Dr Teshmae 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 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.