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Aan de slag!Ga deze week de uitdaging aan en begin meteen! Hoe ga je jouw mobielgebruik minderen? Maak het concreet voor jezelf.Heb jij nog een gouden tip? Deel hem hieronder in de reacties.Deze overdenking is geschreven door schrijfster Marijke Gootjes-Verhoeve.
Aan de slag!Kijk eens in je eigen hart: hoe is de afgelopen tijd jouw manier van communiceren met je partner, collega's of vrienden gegaan? Vraag God om je te helpen om zachte, milde woorden te spreken en na te denken over je woorden. Kijk wat het doet in je leven wanneer je probeert deze dingen toe te passen!Deze overdenking is geschreven door schrijfster Marije Dekker-Brandwijk.
Je kunt nog zo gezond eten, maar zolang jouw lichaam stress ervaart, kom je niet in vetverbranding.In deze aflevering ontdek je waarom stress niet alleen mentaal is, maar ook diep in je lichaam plaatsvindt en hoe dat je hormonen, energie en zelfs je humeur beïnvloedt.Na het luisteren weet je:Waarom langdurige stress je vetverbranding letterlijk uitschakeltHoe cortisol jouw hormonen ontregelt en je moe, prikkelbaar of opgeblazen maaktWelke onzichtbare stressoren in je lijf zorgen voor ontregeling Wat je vandaag al kunt doen om je lichaam weer in balans te brengen en energie terug te krijgenEen aflevering vol inzichten die je helpen om niet harder, maar slimmer met je lichaam samen te werken.---
Aan de slag!Zing het lied ‘Neem mijn leven, laat het, Heer'.Deze overdenking is geschreven door schrijfster Naomi Muda.
Wie is de ultieme leider in een wereld vol corruptie en ongelijkheid? Micha wijst op de HEER, de koning die niet uit is op geld of macht, maar op herstel en eenheid. Aan wie denk jij bij de mensen over wie Micha hier spreekt? Bid jij weleens voor de komst van Gods koninkrijk?
00:05:15 - Niels in Japan Van een capsule hotel een bezoek aan MotherBrain: voor het eerst sinds 2019 was Niels in Japan en viel hem op wat er allemaal veranderd was. Ook ontmoette hij wat bijzondere mensen uit de Japanse games industrie rondom zijn bezoek aan BitSummit. 01:17:20 - Michael heeft zijn vakantie in Frankrijk overleefd Michael is veel aan het hardlopen en bouwt op richting een marathon. Ook ging hij van t padje in Frankrijk, wat misschien niet tot de leukste ervaring heeft geleid, maar wel tot een mooie. 01:50:47 - Niels in Zuid-Korea Aansluitend aan zijn reis in Japan ging Niels naar Seoul en Gyeongju in Zuid-Korea om zich te verdiepen in de moderne koffiecultuur, ook bezocht hij een eSports Stadium (02:20:54), en maakte iets zeer onverwachts mee in het Korean Folk Village. 02:37:15 - Niels en K-Pop Het gerucht ging al een tijdje rond dat Niels op het podium stond tijdens een K-Pop optreden. Daarover vertelt hij meer, maar ook heeft hij meegedaan aan een Squid Game en houdt hij tegenwoordig van lekkere zeep. 02:54:12 - Donkey Kong Bananza Michael speelde Donkey Kong Bananza en zegt dat het volgens hem de beste Nintendo game ooit is. Daarnaast speelde hij ook een stukje Arietta of Sprits en wat andere games. 03:03:49 - Ace Attorney Investigations 2, Fire Emblem Engage, Deep Rock Galactic Niels heeft zich in de afgelopen tijd vermaakt met Ace Attorney Investigations 2 Prosecutors Gambit, met Miles Edgeworth in de hoofdrol, nam Fire Emblem Engage mee naar Japan en Zuid-Korea, en speelde online vooral Deep Rock Galactic. 03:18:01 - De laatste Button Bashers aflevering Waarom stopt de Button Bashers Podcast na 13 jaar? Het initiatief kwam van Michael en hij vertelt wat voor hem de redenen waren om er een punt achter te zetten. 04:29:05 - Afsluiting 04:40:30 - Praatje Podcast Om deze laatste Button Bashers Podcast mee af te sluiten is hier nog een toezending van Sven en Johan van Praatje Podcast. Aan alle luisteraars: bedankt voor het luisteren al die jaren! Muziek: - Starcraft 2 - Donkey Kong Bananza Emerald Rush - Mario Golf
Aan de slag!Voorspelbaar, maar ik wil het je niet onthouden: luister naar het liedje 'That's Who I Praise' van Brandon Lake.Verdiep je eventueel in de andere personages die hij noemt.Deze overdenking is geschreven door schrijfster Suzanne Verschoor.
Welkom bij aflevering 2 van seizoen 7 van De Biervrienden Podcast! In onze podcast schuiven regelmatig vrienden en bierliefhebbers aan, maar nog niet eerder hadden we een gast die zelf ook actief is in de wereld van speciaalbier. In deze bijzondere aflevering gaan we in gesprek met Maartje van Bijster Bier. Voor ons een unicum, want vrouwelijke bierkenners én brouwers — die kenden we tot voor kort nog niet. En het belangrijkste natuurlijk: Maartje heeft verschillende batches van haar Double IPA meegenomen om te proeven! Genietend van deze verrukkelijke IPA geeft Maartje ons een kijkje achter de schermen van de wereld van speciaalbier. Aan de keukentafel bespreken we onder andere het ontstaan van Bijster en het verhaal achter de naam, het brouwproces, de speciaalbiermarkt, duurzaamheid, jezelf ontwikkelen als brouwer en plannen voor de toekomst. Een middag vol leuke verhalen en smaakvolle bieren, in gezelschap van goede biervrienden. Kortom: alles waar onze podcast voor staat!
Aan de hand van vele voorbeelden laat Morgan Housel in The Psychology of Money zien wat we allemaal kunnen leren over onze omgang met geld. Uitgegeven door Kosmos Uitgevers Spreker: Jurjen van Loon
‘Prelude' is de opmaat naar het AVROTROS Vrijdagconcert! Gastspreker: sopraan Lilian Farahani Radio Filharmonisch Orkest Groot Omroepkoor Dima Slobodeniouk, dirigent James Burton, koordirigent Ilse Eerens, sopraan Linsey Coppens, mezzosopraan Linard Vrielink, tenor Gerrit Illenberger, bariton Beethoven Meeresstille und glückliche Fahrt Von Weber Missa Sancta nr. 2 ‘Jubelmesse' Brahms Tweede symfonie Meer info & kaarten (https://www.npoklassiek.nl/concerten/4b338fb9-e975-4214-a6f2-3233a2f8b5e7/radio-filharmonisch-orkest-beethoven-en-brahms) In deze podcast vertelt presentator Leonard Evers je iedere week meer over de bijzondere stukken die gaan klinken in TivoliVredenburg én op NPO Klassiek. Dat doet hij samen met verschillende gasten die in de studio aanschuiven. Aan de hand van muziekfragmenten word je warm gemaakt voor de mooie composities die je te wachten staan. Abonneer je nu! Alles over het AVROTROS Vrijdagconcert (https://www.npoklassiek.nl/programmas/avrotros-vrijdagconcert)
Aan de slag!Spreekt het jou aan, het idee van '26 vóór 2026' of ‘6 vóór 2026'? Zo ja, maak dan vandaag vast een beginnetje of kladversie van je lijst. Niet jouw ding, maar wil je wel tijd in Gods Woord doorbrengen? Misschien kun je één ding van het lijstje proberen voor de rest van het jaar.Deze overdenking is geschreven door schrijfster Marieke van der Maaten.
Aan de slag!Ga voor jezelf eens na hoe het je wijnstok erbij staat. Hoe blijf jij dicht bij Jezus, hoe blijf je met Hem verbonden en hoe draag jij vrucht?Deze overdenking is geschreven door oud-schrijfster Anna-Saar Kunz.
Hoger beroep: een tweede kans of juist een groot risico? In deze aflevering van TogaTalks duikt Jady samen met raadsheer Guimet Hansen in de wereld van het hoger beroep bij het gerechtshof. Wat gebeurt er precies als een zaak opnieuw wordt beoordeeld door het gerechtshof? Hoe verschilt een zitting in hoger beroep van die bij de rechtbank? En wat zijn de risico's voor verdachten die in beroep gaan? Guimet, raadsheer bij het gerechtshof in Den Bosch, legt helder uit hoe het hoger beroep in de praktijk werkt, wanneer het loont om in beroep te gaan en wanneer niet, en wat de impact is van nieuwe bewijsmiddelen of getuigenverklaringen. Aan de hand van concrete voorbeelden uit haar carrière – van drugszaken tot moord – bespreekt ze hoe het hof tot een oordeel komt, waarom straffen soms lager óf hoger uitvallen, en welke rol persoonlijke omstandigheden spelen. Tijdpad van de aflevering:(01:13) – Wat is een raadsheer?(02:08) – Hoger beroep uitgelegd(03:37) – Hoger beroep als tweede feitelijke behandeling(04:19) – Nieuwe getuigen en bewijsmiddelen in hoger beroep(06:11) – Verschil tussen liegen door een verdachte en meineed door een getuige(09:36) – Hoe verschilt een zitting bij het hof van de rechtbank?(10:22) – Het voortbouwend appel(13:56) – Het instellen van hoger beroep (15:47) – Waarom hoger beroep soms tot een hogere straf leidt(19:03) – Vrijheid van het hof bij strafoplegging(24:06) – Beslissingsfactoren van de rechter en raadsheer Stukjes van het gesprek op beeld zijn te zien op de Instagram en TikTokpagina van Jady: @JadyCadogan (https://www.instagram.com/jadycadogan?igsh=MTg1cWc5Z2o2MjNyZg%3D%3D&utm_source=qr en https://www.tiktok.com/@jadycadogan?_t=ZG-8zPqjQaKVnd&_r=1). Ook heeft TogaTalks een eigen Instagrampagina @PodcastTogatalks (https://www.instagram.com/podcasttogatalks?igsh=enU5cTUxOTViNmFk&utm_source=qr) en TikTok @TogaTalks (https://www.tiktok.com/@togatalks?_t=ZG-8zPqp57npDd&_r=1). Adverteren in TogaTalks? Mail dan naar hidde@rechtinjeoor.nl. Link naar de video's met Guimet: https://www.instagram.com/reel/C4Q2P-kLi9b/?igsh=MWdzYTFudWw1MXZjOA== (video raadsheer) en https://www.instagram.com/reel/DFIzLkEtlAH/?igsh=MTJ4ZHYxdDloOW9lbg== (video appeleren).
Aan de slag!Luister het lied “Ik weet hoe goed mijn God is” van Reyer.Deze overdenking is geschreven door schrijfster Daniëlle Geneuglijk.
Eind oktober 2025 is in Nederland het eerste luisterboek van een thriller met AI-stem verschenen. 'Enkele reis Stockholm' van de Zweedse schrijver Kjell Genberg is geïntroduceerd op het Nederlands Thrillerfestival. Alle aanwezigen konden het luisterboek gratis downloaden. Meer dan twintig van hen hebben meegedaan aan een luisterproef. Hadden ze in de gaten te luisteren naar een AI-stem? Dat was bij geen enkele deelnemer aan de proef het geval. De vertaling van Mirjam Jonker en de AI-stem van 'Bastiaan' van Eleven Labs vielen goed in de smaak. Een enkeling vond dat het wel sneller kon, of langzamer, of met meer emotie, of juist minder. Het gevoel van een 'warme stem' die je meevoerde in het verhaal overheerste. De geïnterviewde schrijvers op het festival zouden hun boek aan Bastiaan toevertrouwen, al maakten enkele luisteraars zich zorgen dat sommige menselijke insprekers minder werk zouden krijgen. Luister naar de opnames van de luisterproef en oordeel zelf. Aan het eind zit een verrassing.
Onze noorderburen trekken binnenkort opnieuw naar de stembus. Maar hoe komt dat? En waarom is Geert Wilders een populair politicus? Zou hij het zelfs kunnen schoppen tot premier? Ook het versnipperde politieke landschap valt op. Welke partijen mogen we niet onderschatten? In deze speciale aflevering rond de Nederlandse politiek beantwoorden wij jouw vragen. 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.
Aan de slag!Denk na over hoe jij op God reageert als jouw gebeden niet worden verhoord, zoals je had verwacht of gewild. Wat kun je hierin van Habakuk leren?Deze overdenking is geschreven door schrijfster Daniëlle Geneuglijk.
Aan de vooravond van de verkiezingen zijn politici erg creatief met taal. John & Paul vragen zich af of hun vondsten blijvende impact hebben en het woordenboek zullen halen. Ze bespreken ook een paar bijzondere vormen van lichaamsbeweging.
Kan links weer een factor van betekenis worden? Kun je als liberaal nog bij de VVD terecht? Hoe stevig staat de democratie? Aan de vooravond van de verkiezingen buigen Bas Heijne, Simon van Teutem (De Correspondent), Coen van de Ven (De Groene Amsterdammer) en Amber Wiznitzer (NRC) zich over de kantelpunten in de Nederlandse politiek. In een ultieme poging de kiezer te mobiliseren, kiest links voor een onbestemd gezamenlijk avontuur. Ondertussen verkeren de liberalen van de VVD na hun samenwerking met radicaal-rechts in een vrije val. De traditionele middenpartijen ondergaan een onmiskenbare transformatie – en daarmee neemt het Nederlandse politieke landschap nieuwe vormen aan.Hoe stevig staan vrijheid, gelijkheid en broederschap nog overeind als pijlers van onze democratie, nu de traditionele vertegenwoordigers van die waarden zich op een kantelpunt bevinden? En is de democratie zelf als waarde nog intact in een tijd waarin steeds meer mensen aangeven een ‘sterke leider' ook wel te zien zitten?Over de sprekersBas Heijne (1960) is schrijver en essayist. Voor zijn beschouwende proza ontving hij in 2017 de P.C. Hooft-prijs. Heijne schreef Voor de democratie (Prometheus), een essay over de actualiteit van Perikles' beroemde grafrede, waarin hij de kernwaarden van de Atheense democratie prijst.Simon van Teutem (1997) schrijft voor De Correspondent en Our World in Data over politiek en samenleving. Als PhD-student aan de Universiteit van Oxford onderzoekt hij de groeiende steun voor radicaal-rechts. Hij schreef het boek Waarom een echte liberaal geen VVD stemt (Prometheus)Coen van de Ven (1992) is politiek redacteur van De Groene Amsterdammer. Hij volgde afgelopen jaren intensief de linkse samenwerking tussen PvdA en GroenLinks, wat resulteerde in het boek Een links verhaal (Das Mag)Amber Wiznitzer (1996) is mediajournalist en -columnist. Ze is televisierecensent bij NRC en schrijft een mediacolumn bij Vrij Nederland.Moderator: Frida BoekeProgrammamaker: Veronica BaasZie het privacybeleid op https://art19.com/privacy en de privacyverklaring van Californië op https://art19.com/privacy#do-not-sell-my-info.
Aankomend weekend gaan we er maar weer eens goed voor zitten, als het olympisch schaatsseizoen in Nederland wordt geopend met de Daikin NK Afstanden. Aan de start natuurlijk de vertrouwde namen en teams, maar we gaan ook een nieuw team aan de start zien: Team Staan-CTS GROUP. Dit nieuwe team, onder leiding van Ian Steen en Hein Otterspeer, heeft een aantal interessante schaatsers in de gelederen. Wat verwachten zij van dit debuutseizoen, wat tevens voor de schaatswereld een heel belangrijk seizoen is? We gingen er met Ian Steen over in gesprek. Presentatie: Robert Denneman Foto: Team Staan-CTS GROUP
We leven in een tijd van overvloed, kennis en technologie. We weten meer dan ooit, en toch zijn we zieker dan ooit.We hebben het comfort bereikt waar generaties voor ons van droomden, maar ergens onderweg raakten we het belangrijkste kwijt: de verbinding met ons lichaam, de natuur en ons instinct.In deze aflevering neem ik je mee door de reis van de mens, van de middeleeuwen tot nu, en laat ik zien waarom dit moment een kantelpunt is in onze geschiedenis. Niet om te oordelen, maar om te herinneren wat we zijn vergeten. Dat gezondheid niet ontstaat uit controle, maar uit samenwerking met de natuur.Dit is geen strijd maar een verschuiving.Een revolutie van bewustzijn, gezondheid en verantwoordelijkheid. Een uitnodiging om terug te keren naar wie we in essentie zijn.En jij bent daar onderdeel van.---
Aan de slag!Herken je de vraag: waarom laat God onrecht toe? Herken je onrecht in je eigen leven? Luister naar deze bewerking van Psalm 86 door The Psalm Project en laat je bemoedigen.Deze overdenking is geschreven door schrijfster Joanne van de Vendel.
Aan tafel deze week: Minister van Staat en voormalig secretaris-generaal Jaap de Hoop Scheffer, D66-partijleider Rob Jetten en VVD-partijleider Dilan Yeşilgöz. Presentatie: Twan Huys Wil je meer weten over de gasten in Buitenhof? Op onze website vind je meer informatie. Daar kan je deze aflevering ook terugkijken en je vindt er natuurlijk nog veel meer gesprekken: https://www.vpro.nl/buitenhof/artikelen/buitenhof-26-oktober-2025 Het was opnieuw een heftige week voor Oekraïne. De ontmoeting tussen Trump en Zelensky eindigde in een scheldpartij, Rutte vloog naar Washington om te sussen en Poetin dreigde met een escalatie van de oorlog in Oekraïne, zodra er Tomahawks worden ingezet. Hoe moet een nieuw kabinet omgaan met Oekraïne, met een wispelturige President Trump en hoe herstelt een nieuw kabinet de invloed van Nederland in Europa? Te gast is Minister van Staat en voormalig secretaris-generaal van de NAVO, Jaap de Hoop Scheffer. Hoe denken de partijleiders van de liberale partijen over de toekomst van Nederland? Is er samenwerking mogelijk in deze instabiele geopolitieke tijden die roep om een stabiel kabinet groot maken. Veiligheid en defensie en klimaat vragen om stevige keuzes net als de wooncrisis. Waar staan we nu eigenlijk op dat gebied met nog een paar dagen te gaan voor de Tweede Kamerverkiezingen? VVD-leider Dilan Yeşilgöz en D66-voorman Rob Jetten schuiven aan.
Vandaag een aflevering in de serie "In Stukken". Ein deutsches Requiem van Johannes Brahms wordt in stukken geknipt. Aan de hand van de fragmenten in de mooiste opnames wordt het stuk onder de loep genomen. Panelleden: muziekjournalist Peter van der Lint en mezzosopraan Xenia Meijer.
Aan tafel deze week: Minister van Staat en voormalig secretaris-generaal Jaap de Hoop Scheffer, D66-partijleider Rob Jetten en VVD-partijleider Dilan Yeşilgöz. Presentatie: Twan Huys Wil je meer weten over de gasten in Buitenhof? Op onze website vind je meer informatie. Daar kan je deze aflevering ook terugkijken en je vindt er natuurlijk nog veel meer gesprekken: https://www.vpro.nl/buitenhof/artikelen/buitenhof-26-oktober-2025 Het was opnieuw een heftige week voor Oekraïne. De ontmoeting tussen Trump en Zelensky eindigde in een scheldpartij, Rutte vloog naar Washington om te sussen en Poetin dreigde met een escalatie van de oorlog in Oekraïne, zodra er Tomahawks worden ingezet. Hoe moet een nieuw kabinet omgaan met Oekraïne, met een wispelturige President Trump en hoe herstelt een nieuw kabinet de invloed van Nederland in Europa? Te gast is Minister van Staat en voormalig secretaris-generaal van de NAVO, Jaap de Hoop Scheffer. Hoe denken de partijleiders van de liberale partijen over de toekomst van Nederland? Is er samenwerking mogelijk in deze instabiele geopolitieke tijden die roep om een stabiel kabinet groot maken. Veiligheid en defensie en klimaat vragen om stevige keuzes net als de wooncrisis. Waar staan we nu eigenlijk op dat gebied met nog een paar dagen te gaan voor de Tweede Kamerverkiezingen? VVD-leider Dilan Yeşilgöz en D66-voorman Rob Jetten schuiven aan.
Aan de slag!Wat kan (of moet) jij vandaag loslaten om Hem echt te kunnen volgen?Deze overdenking is geschreven door schrijfster Marianne de Bart-van der Lee.
In deze aflevering neem ik je mee in mijn herstelperiode na een voetoperatie — niet in de medische details, maar in wat die onverwachte stilstand met mijn keuzes, mijn bedrijf en mijn energie heeft gedaan. Ik deel hoe het afzeggen van shows oude patronen zichtbaar maakte, hoe rust een risico kan voelen, en waarom echte groei niet volgt op harder werken maar op afgestemd werken. Je hoort wat er gebeurt wanneer je stopt met duwen en opnieuw begint te kiezen vanuit jezelf — en hoe dat ook financiële ruimte kan opleveren.Aan het eind vertel ik over de masterclass rond print-on-demand met fotograaf Raisa Zwart, als een manier om rust en inkomen tegelijk op te bouwen die plaatsvindt op 10 november om 15u. Wil je mee uit de go-go-go-modus stappen en slimmer gaan verdienen? Schrijf je dan hier in.
In deze editie veel aandacht voor de verkiezingen die volgende week plaatsvinden. Hedy was betrokken bij een klein schandaal rondom verkiezingsposters en geeft uitleg. En hoe kan het dat maar drie partijen een verkiezingsprogramma hebben dat nergens in strijd is met de rechtstaat? Hedy stoort zich eraan dat het in de campagne nauwelijks over buitenland gaat - los van defensie, terwijl Hadassah zich verbaast over de geringe aandacht voor het klimaat.Naar aanleiding van een rechtszaak over kunstsubsidies wordt gekeken naar het belang dat politieke partijen hechten aan cultuur en aan de publieke omroep. In vroeger en nu gaat het over campagne voeren. In Hedy's tijd stond men nog geregeld op de zeepkist én het gaat over de Sacharovprijs voor de vrijheid van denken. Aan het begin van deze aflevering zit trouwens ook nog een niet benoemde vroeger en nu over vrouwen die advies geven over de inrichting van de publieke ruimte. Deze podcast wordt afgesloten met een langzaam afstervende microfoon van Hadassah en een stemadvies van Hedy. Hosted on Acast. See acast.com/privacy for more information.
Aan de slag!Luister eens naar nummers als ‘Deep River – My Home Is Over Jordan', ‘Go down Moses' of ‘Joshua Fit the Battle of Jericho' en lees de tekst ernaast. Bedenk hoe deze vergelijking ook jou tot troost kan zijn!Deze overdenking is geschreven door oud-schrijfster Sara-Maria Smit.
Burgemeesters zien iedere dag met eigen ogen hoe het écht gaat met ons land. Ze merken hoe de druk op het lokale bestuur toeneemt, door onnavolgbaar of ontbrekend beleid uit Den Haag. Ook zien ze de polarisatie toenemen. Plaatsen als Uithoorn, Houten en Eibergen waren de afgelopen weken het toneel van felle demonstraties tegen azc's. Burgers komen meer en meer tegenover elkaar te staan. Hoe houd je als lokale bestuurder ondanks alles de boel bij elkaar? Aan de vooravond van de verkiezingen spreekt Coen Verbraak in 'De publieke tribune' met burgemeesters over de staat van ons land. Hoe verhouden Haagse beloftes zich tot de lokale werkelijkheid? En welk leiderschap heeft ons land de komende jaren nodig? Te gast: Ahmed Marcouch, Yolanda Hoogtanders, Peter Heijkoop en Jaap Velema Presentatie: Coen Verbraak Redactie: Sjoerd Alders, Gea Bruinsma en Arthur Vacca Eindredactie: Sigrid Muusse ℹ️ Meer info? human.nl/dpt ✉️ Reageren? depublieketribune@human.nl
(Advertorial)Deze podcast wordt mede mogelijk gemaakt door AG1:Probeer AG1 nu en ontvang een fles Vitamin D3+K2 en 5 reisverpakkingen (€69 waarde) bij je eerste AG1-abonnementsaankoop op www.drinkag1.com/wielerflits. Slechts voor beperkte tijd! Volledig risicoloos dankzij de 30-daags geld-teruggarantieHet wielerseizoen 2025 zit erop. Nog voordat we aan alle terugblikken beginnen, kijkt de Tour de France alvast vooruit. Eerder deze week werden de parcoursen van de Ronde van Frankrijk voor mannen en vrouwen geopenbaard. Aan de hand daarvan viel er genoeg nieuws te rapen en dat komt allemaal aan bod in de nieuwste aflevering van de WielerFlits Podcast!Het peloton is op vakantie, maar dat geldt niet voor onze verslaggevers Maxim en Youri. Ze hebben de tijd genomen om de Tour-parcoursen onder de loep te nemen. Ze analyseren beide routes uitgebreid en doen een aantal opvallende vaststellingen. Zo zagen ze beiden dat de toprenners niet veel animo hadden om naar de presentatie in Parijs af te reizen, vindt Youri het parcours bij de mannen zelfs wat flets, en stipt Maxim aan dat het merendeel van de etappes relatief kort is. Het hoogtepunt is de dubbele finish op Alpe d'Huez, al is dat eigenlijk niet helemaal waar.Ook kwamen onze verslaggevers tot de conclusie dat er voor sprinters én renners zoals Mathieu van der Poel niet veel eer te behalen valt in de komende editie. Youri gooit vervolgens meteen de knuppel in het hoenderhok. Hij zou niet verbaasd zijn als MVDP besluit om de Tour een jaar over te slaan en zich na het klassieke voorjaar volledig op het mountainbiken te richten. Maxim plaatst daar de kanttekening bij dat zijn ploeg dan wel eerst een tweede naamsponsor zal moeten hebben én dat een deelname aan de Vuelta a España mogelijk een uitdaging kan zijn. Van der Poel reed die wedstrijd nog nooit.Al met al zijn beide mannen het er na een grondige analyse wel over eens dat het parcours van de Tour de France Femmes hen enthousiaster maakt dan die van de mannen. Daarin is de kans overigens wel levensgroot dat we Unibet Rose Rockets terug gaan zien. Precies een jaar geleden stelden we in de WielerFlits Podcast nog dat het de grootste flauwekul was dat we het van origine Nederlandse team nu al in de Tour zouden terugzien, maar verschillende factoren hebben ervoor gezorgd dat ze een wildcard bijna niet kunnen missen. Kortom, alle redenen om te luisteren naar een nieuwe aflevering van de WielerFlits Podcast!
Aan de vooravond van de Tweede Kamerverkiezingen gaan vier politieke partijen met elkaar in discussie tijdens Het Nationale Autodebat bij de Bovag in Bunnik. Kandidaat-Kamerleden debatteren over de belangrijkste thema’s op het gebied van autorijden: betaalbaarheid, elektrisch rijden en bereikbaarheid. Presentatoren Noud Broekhof en Wouter Karssen leiden het debat met leden van vier partijen, en dat zijn: -Wendy van Eijk-Nagel van de VVD -Hanneke Steen van het CDA -Koen Castelein van D66 -Luc Stultiens van GroenLinks-PvdA Bovag-voorzitter Christianne van der Wal en Rogier Kuin, directeur public affairs, hoor je in de nabeschouwing die in het weekend ook online komt. Contact? Een vraag of opmerking? Mail naar autoshow@bnr.nl Of reageer via Spotify, X of Instagram. Meer luisteren? Breek de week | Onze midweekse podcast waarin we het belangrijkste autonieuws bespreken. Luister hier. Petrolheads | Bas van Werven en Carlo Brantsen bespreken op geheel eigen wijze het autonieuws. Abonneer hier. Auto Update | Het laatste autonieuws, met Bas van Werven en Noud Broekhof. Abonneer hier. See omnystudio.com/listener for privacy information.
Aan tafel zitten Nikki van der Naald, Anna Dijkman en Spraakmaker Lotte Prins. Het debat op SBS6 was de eerste keer dat er gedebatteerd kon worden met PVV-leider Geert Wilders. Hij werd hard aangevallen door de andere lijsttrekkers. 'Hij heeft zich even teruggetrokken en het RTL-debat gemist omdat hij zich onveilig voelde. Dat heeft zich niet goed gedaan', stelt Anna Dijkman (journalist Financiële Dagblad). Wilders zelf zag het 'stekelige' debat als een drie-tegen-een, waarbij hij zich hard moest verdedigen tegenover de andere lijsttrekkers van CDA, VVD en GL-PvdA. Gaat hem dat parten spelen, of is dat juist goed voor hem? 'Hij was misschien niet op zijn scherpst, toch denk ik niet dat dit debat hem slecht doet', zegt Niki van der Naald (adjunct-hoofdredacteur van De Gelderlander). 'Hij heeft zijn one-liners kunnen noemen waar mensen op inspringen.'
Aan de slag!Luister en zing mee met Holy Forever van CeCe WinansDeze overdenking is geschreven door schrijfster Linda Aalbers.
In EW Politiek Vandaag bespreken Sam Verbeek en Victor Pak het grote SBS-verkiezingsdebat, waar Geert Wilders na weken van afwezigheid terugkeerde op het podium. Aan een ronde tafel, tegenover Frans Timmermans, Dilan Yesilgöz en Henri Bontenbal, stond hij geïsoleerd als nooit tevoren. De drie trokken eensgezind tegen hem op – soms fel, soms spottend – terwijl Wilders zichtbaar moeite had om zijn oude dominantie terug te vinden. Een debat vol spanning, ritme en verrassend veel humor.EW Politiek Vandaag is je korte update over Nederlandse politiek: wat doet het laatste (geo)politieke nieuws met de bloeddruk op het Binnenhof? Victor Pak (politiek verslaggever) en Sam Verbeek (online redacteur) duiden drie keer per week de impact van Tweede Kamer-debatten, verkiezingen, kabinet en internationale ontwikkelingen (EU, VS, China). Elke maandag, woensdag en vrijdag in je podcastapp én op YouTube. Wil je reageren? Stuur dan je vraag of opmerking naar podcast@ewmagazine.nl. Deel de podcast met vrienden en kennissen en laat een review achter.
Voor onze veiligheid zijn we te afhankelijk van de grillen van Poetin en Trump en voor onze economie van Xi en diezelfde Trump. En in het Midden-Oosten staat Europa aan de zijlijn. Daarover gaan politici van vier partijen in debat in het BNR Buitenlanddebat. Het debat staat onder leiding van Bernard Hammelburg en hij wordt geflankeerd door Michal van der Toorn. Lees ook | BNR tijdens de verkiezingen Aan het debat doen mee: - Derk Boswijk (CDA) - Kati Piri (GroenLinks-Partij van de Arbeid) - Eric van der Burg (VVD) - Anne-Marijke Podt (D66) Luister ook | 'Nederland komt niet zonder kleerscheuren uit Nexperia-rel met China' BNR tijdens de verkiezingen Volg het laatste nieuws over de verkiezingen via bnr.nl/verkiezingen en blijf op de hoogte van alles wat er speelt in de campagne t/m de uitslagenavond. Je vindt hier ook alle andere debatten die BNR organiseert.See omnystudio.com/listener for privacy information.
Limb-girdle muscular dystrophies (LGMDs) encompass a group of genetically heterogeneous skeletal muscle disorders. There has been an explosion of newly identified LGMD subtypes in the past decade, and results from preclinical studies and early-stage clinical trials of genetic therapies are promising for future disease-specific treatments. In this episode, Gordon Smith, MD, FAAN, speaks with Teerin Liewluck, MD, FAAN, FANA, author of the article “Limb-Girdle Muscular Dystrophies” in the Continuum® October 2025 Muscle and Neuromuscular Junction Disorders issue. Dr. Smith is a Continuum® Audio interviewer and a professor and chair of neurology at Kenneth and Dianne Wright Distinguished Chair in Clinical and Translational Research at Virginia Commonwealth University in Richmond, Virginia. Dr. Liewluck is a professor of neurology at the Division of Neuromuscular Medicine and Muscle Pathology Laboratory at Mayo Clinic College of Medicine in Rochester, Minnesota. Additional Resources Read the article: Limb-Girdle Muscular Dystrophies Subscribe to Continuum®: shop.lww.com/Continuum Earn CME (available only to AAN members): continpub.com/AudioCME Continuum® Aloud (verbatim audio-book style recordings of articles available only to Continuum® subscribers): continpub.com/Aloud More about the American Academy of Neurology: aan.com Social Media facebook.com/continuumcme @ContinuumAAN Host: @gordonsmithMD Guest: @TLiewluck Full episode transcript available here Dr Jones: This is Dr Lyell Jones, Editor-in-Chief of Continuum. Thank you for listening to Continuum Audio. Be sure to visit the links in the episode notes for information about earning CME, subscribing to the journal, and exclusive access to interviews not featured on the podcast. Dr Smith: This is Dr Gordon Smith with Continuum Audio. Today I'm interviewing Dr Teerin Liewluck, a good friend of mine at the Mayo Clinic, about his article on the limb girdle muscular dystrophies. This article appears in the October 2025 Continuum issue on muscle and neuromuscular junction disorders, a topic that is near and dear to my heart. Teerin, welcome to the podcast, and maybe you can introduce yourself to our listeners. Dr Liewluck: Thank you very much, Gordon, and I want to say hi to all the Continuum fans. So, I'm Dr Teerin Liewluck, I'm the professor of neurology at Mayo Clinic in Rochester, Minnesota. So, my practice focus on all aspects of muscle diseases, both acquired and genetic myopathies. Glad to be here. Dr Smith: I just had the great pleasure of seeing you at a seminar in Houston where you talked about this topic. And so, I'm really primed for this conversation, which I'm very excited about. I find this topic a little hard, and I'm hoping I can learn more from you. And I wonder if, as we get started, recognizing many of our listeners are not in practices focused purely on muscle disease, maybe you can provide some context about why this is important for folks doing general neurology or even general neuromuscular medicine? Why do they need to know about this? Dr Liewluck: Yes, certainly. So, I would say limb girdle muscular dystrophy probably the most complex category of subgroup of muscle diseases because, by itself, it includes thirty-four different subtypes, and the number's still expanding. So, each subtype is very rare. But if you group together, it really have significant number of patients, and these patients present with proximal weakness, very high CK, and these are common patients that can show up in the neurology clinic. So, I think it's very important even for general neurologists to pick up what subtle clues that may lead to the diagnosis because if we are able to provide correct diagnosis for the patients, that's very important for patient management. Dr Smith: So, I wonder if maybe we can talk a little bit about the phenotype, Terran. I mean, your article does a great job of going over the great diversity. And you know, I think many of us here, you know, limb girdle muscular dystrophy and we think of limb girdle weakness, but the phenotypic spectrum is bananas, right? Rhabdomyolysis, limb girdle distal myopathy. I mean, when should our listeners suspect LGMD? Dr Liewluck: Yes, I think by the definition to all the LGMD patients will have limb girdle of proximal weakness and very high CK. So, these are common phenotypes among thirty-four different subtypes. But if it did take into details, they have some subtle differences. In the article, what I try to simplify all these different subtypes that we can categorize at least half of them into three main group that each group the underlying defect sharing among those subtypes and also translate into similar muscles and extra muscular manifestations. You will learn that some of the limb girdle muscular dystrophy may present with rhabdomyolysis. And we typically think of this as metabolic myopathies. But if you have a rhabdomyolysis patient, the CK remain elevated even after the acute episode, that's the key that we need to think this could be LGMD. That's for an example. Dr Smith: So, I wonder if maybe we can start there. I was going to go in a different direction, but this is a good transition. It's easy to see the opportunity to get confused between LGMD or, in that case, a metabolic myopathy or other acquired myopathies. And I think particularly adult neurologists are more accustomed to seeing acquired muscle disease. Are there particular clues that, or pearls that adult neurologists seeing patients with muscle disease can use to recognize when they should be thinking about LGMD given the diverse phenotype? Dr Liewluck: Yes. What I always tell the patient is that there are more than a hundred different types of muscle diseases, but we can easily divide into groups: acquired and genetic or hereditary. So, the acquired disease is when you encounter the patients who present with acute or subacute cause of the weakness, relatively rapidly progressive. But on the opposite, if you encounter the patient who present with a much more slowly progressive cause of weakness over several months or years, you may need to think about genetic disease of the muscle with also including limb-girdle muscular dystrophy. The detailed exam to be able to distinguish between each type of muscular dystrophy. For example, if proximal weakness, certainly limb girdle muscular dystrophy. If a patient has facial weakness, scapular winking, so you would think about facial scapular hematoma dystrophy. So, the slowly progressive cause of weakness, proximal pattern of weakness, CK elevation, should be the point when you think about LGMD. Dr Smith: So, I have a question about diagnostic evaluation. I had a meeting with one of my colleagues, Qihua Fan, who's a great peripheral nerve expert, who also does neuromuscular pathology. And we were talking about how the pathology field has changed so much over the last ten years, and we're doing obviously fewer muscle biopsies. Our way of diagnosing them has changed a lot with the evolution of genetic testing. What's your diagnostic approach? Do you go right to genetic testing? Do you do targeted testing based on phenotype? What words of wisdom do you have there? Dr Liewluck: Yes, so, I mean, being a muscle pathologist myself, it is fair to say that the utility of muscle biopsies when you encounter a patient with suspects that limb girdle muscular dystrophy have reduced over the year. For example, we used to have like fifteen, seventeen hundred muscle biopsies a year; now we do only thirteen hundred biopsies a year. Yes, as you pointed out, the first step in my practice if I suspect LGMD is to go with genetic testing. And I would prefer the last gene panel that not only include the LGMD, but also include all other genetic muscle disease as well as the conjunctive myopic syndrome, because the phenotype can be somehow difficult to distinguish in certain patients. Dr Smith: So, do you ever get a muscle biopsy, Teerin? I mean you obviously do; only thirteen hundred. Holy cow, that's a lot. So, let me reframe my question. When do you get a muscle biopsy in these patients? Dr Liewluck: Muscle biopsy still is present in LGMD patients, it's just we don't use it at the first-tier diagnostic test anymore. So, we typically do it in selected cases after the genetic testing in those that came back inconclusive. As you know, you may run into the variant of unknown significance. You may use the muscle biopsy to see, is there any histopathology or abnormal protein Western blot that may further support the heterogenicity of the VUS. So, we still do it, but it typically comes after genetic testing and only in the selected cases that have inconclusive results or negative genetic testing. Dr Smith: I'd like to ask a question regarding serologic testing for autoantibodies. I refer to a really great case in your article. There are several of them, but this is a patient, a FKRP patient, who was originally thought to have dermatomyositis based on a low-titer ME2 antibody. You guys figured out the correct diagnosis. We send a lot of antibody panels out. Wonder if you have any wisdom, pearls, pitfalls, for how to interpret antibody tests in patients with chronic myopathies? We send a lot of them. And that's the sort of population where we need to be thinking about limb-girdle muscular dystrophies. It's a great case for those, which I hope is everyone who read your article in detail. What do you have to say about that? Dr Liewluck: Yes, so myositis antibodies, we already revolutionized a few of muscle diseases. I recall when I finished my fellowship thirteen years ago, so we don't really have much muscle myositis antibodies to check. But now the panel is expanded. But again, the antibodies alone cannot lead to diagnosis. You need to go back to your clinical. You need to make sure the clinical antibodies findings are matched. For example, if the key that- if the myocytes specific antibodies present only at the low positive title, it's more often to be false positive. So, you need to look carefully back in the patient, the group of phenotypes, and when in doubt we need to do muscle biopsies. Now on the opposite end, the other group of the antibody is the one for necrotizing autoimmune myopathy; or, the other name, immune-mediated necrotizing myopathy. This is the new group that we have learned only just recently that some patients may present as a typical presentation. I mean, when even thinking about the whole testing autoimmune myopathy, we think about those that present with some acute rapidly progressive weakness, maybe has history of sudden exposures. But we have some patients that present with very slowly progressive weakness like muscular dystrophies. So now in my practice, if I encounter a patient I suspect LGMD, in addition to doing genetic testing for LGMD, I also test for necrotizing doing with myopathy antibodies at the same time. And we typically get antibody back within what, a week or two, but projected testing would take a few months. Dr Smith: Yeah. And I guess maybe you could talk a little bit about pitfalls and interpretation of genetic tests, right? I think you have another case in your article, and I've certainly seen this, where a patient is misdiagnosed as having a genetic myopathy, LGMD, based on, let's say, just a misinterpretation of the genetic testing, right? So, I think we need to think of it on both sides. And I like the fact that the clinical aspects of diagnosis really are first and foremost most important. But maybe you can talk about wisdom in terms of interpretation of the genetic panel? Dr Liewluck:Yes. So genetic testing, I think, is a complex issue, particularly for interpretation. And if you're not familiar with this, it's probably best to have your colleagues in genetics that help looking at this together. So, I think the common scenario we encounter is that in those dystrophies that are autosomal recessive, so we expect that the patient needs to have two abnormal copies of the genes to cause the disease. And if patients have only one abnormal copy, they are just a carrier. And commonly we see patients refer to us as much as dystrophy is by having only one abnormal copy. If they are a carrier, they should not have the weakness from that gene abnormality. So, this would be the principle that we really need to adhere. And if you run into those cases, then maybe you need to broaden your differential diagnosis. Dr Smith: I want to go back to the clinical phenomenology, and I've got a admission to make to you, Teerin. And I find it really hard to keep track of these disorders at, you know, thirty-four and climbing a lot of overlap, and it's hard to remember them. And I'm glad that I'm now going to have a Continuum article I can go to and look at the really great tables to sort things out. I'm curious whether you have all these top of mind? Do you have to look at the table too? And how should people who are seeing these patients organize their thoughts about it? I mean, is it important that you memorize all thirty-four plus disorders? How can you group them? What's your overall approach to that? Dr Liewluck: I need to admit that I've not memorize all twenty-four different subtypes, but I think what I triy to do even in my real-life practice is group it all together if you can. For example, I think that the biggest group of these LGMD is what we call alpha-dystroglycanopathies. So, this include already ten different subtypes of recessive LGMD. So alpha-dystroglycan is the core of the dystrophin-associated glycoprotein complex. And it's heavy glycosylated protein. So, the effect in ten different genes can affect the glycosylation or the process of adding sugar chain to this alpha-dystroglycan. And they have similar features in terms of the phenotype. They present with proximal weakness, calf pseudohypertrophy, very high CK, some may have recurrent rhabdomyolysis, and cardiac and rhythmic involvement are very common. This is one major group. Now the second group is the limb-girdle muscular dystrophy due to defective membrane repair, which includes two subtypes is the different and on dopamine five. The common feature in this group is that the weakness can be asymmetric and despite proximal weakness, they can have calf atrophy. On muscle biopsy sometimes you can see a myeloid on the muscle tissues. And the third group is the sarcoglycanopathy, which includes four different subtypes, and the presentation can look like we share. For the rest, sometimes go back to the table. Dr Smith: Thank you for that. And it prompts another question that I always wonder about. Do you have any theories about why such variability in the muscle groups that are involved? I mean, you just brought up dystroglycanopathy, for instance, as something that can cause a very distal predominant myopathy; others do not. Do we at this point now have an understanding given the better genetics that we have on this and work going on in therapeutic development, which I want to get to in a minute, that provides any insight why certain muscle groups are more affected? Dr Liewluck: Very good question, Gordon. And I would say the first question that led me interested in muscle disease---and this happened probably back in 2000 when I just finished medical school---is why, why, why? Why does muscle disease tend to affect proximal muscles? I thought by now, twenty-five years later, we'd have the answer. I don't. I think this, you don't know clearly why muscle diseases, some affect proximal, some affect distal. But the hypothesis is, and probably my personal hypothesis is, that maybe certain proteins may express more in certain muscles and that may affect different phenotypes. But, I mean, dysferlin has very good examples that can confuse us because some patients present with distal weakness, some patients present with proximal weakness, that's by the same gene defect. And in this patient, when we look at the MRI in detail, actually the patterns of fatty replacements in muscle are the same. Even patient who present clinically as a proximal or distal weakness, the imaging studies show the same finding. Bottom line, we don't know. Dr Smith: Yeah, who knew it could be so complex? Teerin, you brought up a really great point that I wanted to ask about, which is muscle MRI scan, right? We're now seeing studies that are doing very broad MR imaging. Do you use some muscle MRI very frequently in your clinical evaluation of these patients? And if so, how? Dr Liewluck: Maybe I don't use it as much as I could, but the most common scenario I use in this setting is when I have the genetic testing come back with the VUS. So, we look at each VUS, each gene in detail. And if anything is suspicious, what I do typically go back to the literature to see if that gene defect in particular has any common pattern of muscle involvement on the MRI. And if there is, I use MRI as one of the two to try to see if I can escalate the pathogenicity of that VUS. Dr Smith: And a VUS is a “Variant of Unknown Significance,” for our listeners. I'm proud that I remember that as a geneticist. These are exciting times in neurology in general, but particularly in an inherited muscle disease. And we're seeing a lot of therapeutic development, a lot going on in Duchenne now. What's the latest in terms of disease-modifying therapeutics and gene therapies in LGMD? Dr Liewluck: Yes. So, there are several precritical and early-phase critical trials for gene therapy for the common lymphoma of muscular dystrophies. For example, the sarcoglycanopathies, and they also have some biochemical therapy that arepossible for the LGMD to FKRP. But there are many things that I expect probably will come into the picture broader or later phase of critical tryouts, and hopefully we have something to offer for the patients similar to patients with Duchenne muscular dystrophy. Dr Smith: What haven't we talked about, I mean, holy cow? There's so much in your article. What's one thing we haven't talked about that our listeners need to hear? Dr Liewluck: Good questions. So, I think we covered all, but often we get patients with proximal weakness and high CK, and they all got labeled as having limb-girdlemuscular dystrophy. What I want to stress is that proximal weakness and high CK is a common feature for muscle diseases, so they need to think broad, need to think about all possibilities. Particularly don't want to miss something treatable. Chronic, slowly progressive cause, as I mentioned earlier, we think more about muscle dystrophy, but at the cranial range, we know that rare patients with necrotic autonomyopathy and present with limb good of weakness at a slowly progressive cost. So, make sure you think about these two when suspecting that LGMD patient diabetic testing has come back inconclusive. Dr Smith: Well, that's very helpful. And fortunately, there's several other articles in this issue of Continuum that help people think through this issue more broadly. Teerin, you certainly don't disappoint. I enjoyed listening to you about a month ago, and I enjoyed reading your article a great deal and enjoy talking to you even more. Thank you very much. Dr Liewluck: Thank you very much, Gordon. Dr Smith: Again, today I've been interviewing Dr Teerin Liewluck about his article on limb-girdle muscular dystrophy, which appears in the October 2025 Continuum issue on muscle and neuromuscular junction disorders. Please be sure to check out Continuum Audio episodes for this and other issues. And thanks to our listeners for joining today. Dr Monteith: This is Dr Teshamae Monteith, Associate Editor of Continuum Audio. If you've enjoyed this episode, you'll love the journal, which is full of in-depth and clinically relevant information important for neurology practitioners. Use the link in the episode notes to learn more and subscribe. AAN members, you can get CME for listening to this interview by completing the evaluation at continpub.com/audioCME. Thank you for listening to Continuum Audio.
In deze speciale aflevering van BNR Beter hoor je het eerste deel van Het Grote Zorgdebat, opgenomen in het Beatrix Theater in Utrecht. Zes politieke partijen kruisen de degens over één van de grootste verkiezingsthema’s van 2025: de toekomst van onze zorg. Dit debat wordt geleid door Donatello Piras, met als sidekick Suse van Kleef. In dit eerste deel gaat het over werken in de zorg – een sector die afstevent op een tekort van ruim 266.000 medewerkers in 2034. Hoe zorgen we dat zorgverleners hun werk met plezier kunnen blijven doen, zonder te bezwijken onder werkdruk en administratie? Aan het woord zijn kandidaat-Kamerleden Harry Bevers (VVD), Sarah Dobbe (SP), Julian Bushoff (GroenLinks-PvdA), Wieke Paulusma (D66), Harmen Krul (CDA) en Vicky Maeijer (PVV). Ze discussiëren over hogere lonen, regeldruk, marktwerking in de zorg, en de vraag: moet zorg nog concurreren – of vooral menselijk blijven?
In deze aflevering onderzoek ik hoe we artiesten, en onszelf, vaak reduceren tot één label, één beeld, één rol. Aan de hand van het verdrietige overlijden van D'Angelo reflecteer ik op creatie, perfectionisme, en wat het betekent om echt te blijven, ook als het niet vlekkeloos is.Ik voelde mwah toen ik dit opnam. Twijfelde of het wel iets waard was. Maar dit is precies in welke fase ik nu zit: blijven maken, blijven delen, ook als het geen meesterwerk is.
Aan tafel deze week: demissionair minister Vincent Karremans, fractievoorzitter SP Jimmy Dijk, fractievoorzitter Volt Laurens Dassen, vredesonderhandelaar Gershon Baskin, oud-China-correspondent Garrie van Pinxteren. 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/3WIuJ7p Het was een bijzondere week voor demissionair minister Vincent Karremansvan Economische Zaken, hij greep stevig in bij chipfabrikant Nexperia. Wat is er precies gebeurd en hebben we nu ruzie met de Chinezen? Ondertussen is de verkiezingscampagne in volle gang. De VVD wil dat Nederland woest aantrekkelijk wordt voor het internationale bedrijfsleven. Hoe gaat Karremans dat met zijn partij voor elkaar krijgen? Nog anderhalve week te gaan tot de Tweede Kamerverkiezingen. Volt-lijsttrekker Laurens Dassen en SP-lijsttrekker Jimmy Dijk hebben beiden grote langetermijnvisies. Hoe kun je je als kleine partij invechten in het campagnegeweld wanneer de leiders van de grote partijen elkaar uitsluiten en over elkaar heen buitelen? Garrie van Pinxteren was jarenlang correspondent in China. Terwijl China de confrontatie zoekt met de Nederlandse overheid, maakt het zich in eigen land op voor een nieuw Vijfjarenplan. De economische langetermijnplanning die de toekomst van China, en een belangrijk deel van de wereldeconomie, bepaalt. Wat betekent dat voor de wereld en wat betekent het voor de Chinezen zelf?
In this episode, editor in chief Joseph E. Safdieh, MD, FAAN, highlights articles about a PET radiotracer that shows intranasally delivered insulin enters the brain, GLP-1s and dementia risk in people with Type 2 diabetes, and how exposure to green space may reduce the risk of neurodevelopmental delays in children.
S5E40 - Een gescheurd toompje en een flinke dosis oversharing halen weer het beste in Mo en Kaj naar boven. Een ordinair potje lullen over seks, haast en pijn. Over haast maakt Kaj zich verder geen zorgen, hij zou het liefst in het bejaardentehuis werken. Small Lulu Momo daarentegen denkt haar weg te vinden tussen het Schiphol-personeel. Aan ambitie geen gebrek.
Facioscapulohumeral muscular dystrophy (FSHD) is one of the most common forms of muscular dystrophy, affecting individuals across the lifespan with variable severity. Advances in genetic understanding and therapeutic development have led to an era of promising disease-modifying strategies. In this episode, Katie Grouse, MD FAAN, speaks with Renatta N. Knox, MD, PhD, author of the article “Facioscapulohumeral Muscular Dystrophy” in the Continuum® October 2025 Muscle and Neuromuscular Junction 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. Knox is an assistant professor of neurology in the Division of Pediatric Neurology and Neuromuscular Section at Washington University School of Medicine in St. Louis, Missouri. Additional Resources Read the article: Facioscapulohumeral Muscular Dystrophy 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 Renatta Knox about her article on fascioscapulohumeral muscular dystrophy, which appears in the October 2025 Continuum issue on muscle and neuromuscular junction disorders. Welcome to the podcast, and please introduce yourself to our audience. Dr Knox: Hi Katie, thank you so much for the invitation for the audio interview. I'm looking forward to our conversation. As she mentioned, my name is Renata Knox. It's a pleasure to be here today. Dr Grouse: I'd like to start by asking, what is the key message that you hope your readers will take from your article? Dr Knox: I would say two things. The first is an appreciation and understanding of the unique genetic mechanism that leads to FSHD. And the second is the really exciting therapy landscape that we find ourselves in. So, we're hopeful that there will actually be disease-modifying therapies for FSHD soon. Dr Grouse: We're really looking forward to learning more about that. Now, before we get to that piece, could you just remind us of the clinical manifestations and features that are specific to FSHD? Dr Knox: So, one of the most unique things about FSHD that we see clinically is the pattern of weakness. So, one of the first features is that it's asymmetric. And then there are certain muscle groups that typically are affected, and that's partly where the name comes from. So, we see effects in the face, the limbs, the trunk; and so, those are some of the unique features that we see clinically. Dr Grouse: I'd love it if you could walk us through how you approach diagnosing a patient who presents with proximal weakness where FSHD is in your differential. Dr Knox: Yeah, it's a really great question. So, I would say it depends. So, I actually focus on FSHD in my clinical practice. So, many times patients are referred to me because there's a very high suspicion or there's a known family history of FSHD. So, that's one category of cases. I would say the other category of case is where it's, as you said, maybe more proximal weakness more broadly. Someone that's before me who has a known family history, they really have some of the characteristic physical features---which I'm pretty attuned to, as this is, you know, part of my subspecialty---I'll actually go directly to FSHD genetic testing. And that is one of the unique features of this disease, that the next-generation sequencing panels that are typically used for some of our other muscle diseases, FSHD is not captured on those. So, we actually have to send targeted testing for FSHD to diagnose it. So, that is one category where, again, I have a very high suspicion either based on their clinical presentation and/or a known family history, then I will actually go directly to FSHD-targeted genetic testing. In the second case, where it is one of the conditions that I'm considering among others, I will do more broad testing. So, I will get a CK level to see if there's evidence of muscle breakdown. I'll likely also do one of the next-generation sequencing panels that we have access to, which will allow us to identify, potentially, one to two hundred potential muscle diseases. And then again, if FSHD is higher on my differential in that second group of patients, then I will also send targeted FSHD-specific testing. Dr Grouse: That's really helpful. And I'm wondering if you have any thoughts about common pitfalls that you've seen when providers are trying to work this up? Dr Knox: I don't know if I would say pitfalls. I think I would acknowledge that it's challenging. My subspecialty training in neuromuscular medicine and also gene therapy. And so FSHD is pretty high on my radar. But I would say in neurology in general---and then, you know, the general medical population---,it really isn't something that many people are seeing. So, I would say what patients will communicate to us sometimes is some frustration that maybe it took time to make the diagnosis, but I just have a deep understanding that it's not something that is on many people's radars. And I think, again, it's tricky because it's not picked up on these next-generation sequencing panels, which many of us can send pretty easily. It will be missed. And I will say the biggest pitfall is, again, if you're not thinking about it and you don't send that testing, you actually- it's very difficult to diagnose it. Dr Grouse: Thank you so much for highlighting that. I think there are many people who are not aware that those different panels really aren't picking that up and that they have to test specifically. So, I think that's a great thing for all of us to keep in mind. Are there any tips or tricks to the diagnosis, other than the genetic issues that you mentioned, that sometimes can really bring this diagnosis to the forefront? Dr Knox: I think things that really tip me off to having a higher suspicion for FSHD is facial weakness that we can detect on our exam. Scapular winging---again, there's a small subset of disorders which can impact that. Someone who's presenting with foot drop, you know, with facial weakness, I think definitely about FSHD more. Also, clinically, kind of the presentation or things that they're beginning to have difficulty with is a tip-off. So, if someone is an athlete, like, they're a volleyball player or basketball player and they say, oh, I'm having difficulties, you know, with movements that require them to elevate their arm, which can be a sign of the shoulder weakness that we classically see. Or someone who says, oh, I'm having a harder time shampooing my hair or combing my hair. So those can be tip-offs again, which are basically referencing the type of weakness that they have. Another feature of FSHD which isn't necessarily as broadly appreciated is that pain and fatigue are very common. So, if someone is coming in and saying, actually, I also have a significant amount of fatigue as well or a lot of pain, that's something that can tip me off to it. Hearing loss is something that we can also see in up to 20% of patients with FSHD. So, if they are having those symptoms or saying they're ringing in their ears, these are some things that will make me begin to think about it more. Dr Grouse: Oh, really helpful. I also found it really fascinating reading some of the very FSHD-specific clinical signs, some interesting- some diagrams and pictures as well, that are very specific to the pattern of weakness that develops in FSHD. So, I encourage our listeners to check that out. But are there any highlights from those little clinical pearls that you'd like to point out? Dr Knox: I think the poly-hill sign---so, these are these literal hills that we can see in the shoulders of patients with FSHD---is pretty classic. Popeye arms, which is this older term that we still use that has to do with which muscle groups are preserved versus those that have atrophy. So that's a common feature. And then I would say, really, the asymmetry is something that is a unique feature in FSHD. And again, we did our best to provide good representative images. So again, as you mentioned, Katie, I would really encourage people to look at those images and then think about cases that they may have seen and how similar they are so they can begin to recognize those signs as well. Dr Grouse: Now going back to the genetic topic, the complex genetic underpinnings of FSHD are really well-explained in your article; and again, worth taking a look at to remind ourselves of everything that's of that pathology. Now, I was wondering though, if you could give us a brief overview of how we should approach genetic testing in a suspected case of FSHD? You mentioned some specific panels, but it does sound like there's some more complexity to it as well. Dr Knox: Yes, and I'll just kind of briefly explain that complexity. Part of the thing that we're detecting in the genetic testing is the repeat number. And so, we're actually looking for a contraction in a repeat number. So, not an expansion, which were typical for some of the diseases that we think about, the trinucleotide repeat disorders. And this is why it's not captured in the next-generation sequencing panels, because they do not currently have the ability to do that. And so, again, what the type of testing that I do really depends on my suspicion. So again, if my suspicion is very high for FSHD---they have a family history, they have the classic features---then I will actually go directly to an FSHD-specific testing, which is available from various sources. If, again, it's among different things that I'm thinking about, I will get a CK lab. I typically will also send a next-generation sequencing panel specific for muscle diseases, perhaps muscular dystrophy; again, depending on what I'm thinking about. And then I will also send in a specific FSHD genetic test as well. People are beginning to use whole-genome sequencing, which is capturing some of our true nucleotide repeat disorders and becoming more comprehensive. So, my hope is that as that becomes more standard of care---like, whole-exome sequencing can be gotten pretty routinely now---that it may be easier for us to make some of these diagnoses. Dr Grouse: Well, that's really helpful, and thanks for that overview. Now another thing that you mentioned that I thought was really interesting in your article was that patients with, you know, history of FSHD, perhaps in the family, who are pregnant and want to screen for this disease would not be able to use sort of the more common screening tests like cell-free DNA testing and may have to go to other means to do that. What is generally their route to this type of testing? Dr Knox: Yeah, great question, and really important question for family planning purposes, and it definitely comes up in clinical practice. And so again, because of the unique genetics of FSHD, you actually have to do invasive genetic testing currently to be able to test it. And so that's, you know, amnio or chorio, and then send it to a lab that can perform, again, FSHD-specific testing on the samples that are presented. And there are obviously labs that are capable of doing that and centers that are capable of doing that, but it is not picked up on the cell-free DNA panels that are being very routinely used. You or your provider has to be thinking about it to send that specific testing, similar to our patients that come into clinic and have not yet been diagnosed. Dr Grouse: Once you have the diagnosis, what are our options for therapy? I think it sounds like at this current time, it looks to be mostly supportive. What are some of the supportive care options we should keep in mind? Dr Knox: Yes, so that is definitely accurate. Care today is supportive, but again, we're very excited about the clinical trial and therapy landscape for FSHD. So, I work very closely with my physical therapy colleagues that are in clinic with me. So, we work very closely with physical and occupational therapists to help with supportive measures, adaptive measures, doing assessments, helping our patients to be able to move and exercise safely and effectively. As I mentioned, pain is very common in FSHD and so we can treat that with medications. The most common medication that we use to treat for pain in FSHD are NSAIDs. And then other than that it's really, you know, supportive measures. Do they need to see other subspecialists? There are some surgical options. Those are used very rarely to help with some of the scapular weakness, but typically it's physical therapy, occupational therapy, supportive devices. We treat the pain as we're able to, and then we work with other subspecialists to screen, monitor and support our patients to the best of our ability. Dr Grouse: Well, without further ado, I'd love to hear more about what's coming down the pipeline in clinical trials. What can we look forward to seeing, hopefully, in future years to treat these patients? Dr Knox: Yes. And so, this is actually what got me interested in the neuromuscle space in general is that, because we now for many years have known the genetic cause of many of these disorders as well as some of the underlying mechanisms, we can actually use advances in therapeutics to do what we call targeted therapies. So, rather than treating symptoms or indirect methods or doing kind of broad drug screens---which, again, still do take place and still do have their place---we actually can target mechanisms directly. And so, we know that the underlying biology of FSHD is due to this protein called DUX4 being expressed when it should not be. So, it's what we call a toxic gain of function. And so, the targeted way to address this is to suppress DUX4 expression. And so, kind of broadly speaking, what we're really excited about are a couple of products that are currently in clinical trials right now that actually caused DUX4 suppression to be suppressed. And again, these are targeted pathways. And so, again, the hope is that by doing that, we can hopefully slow the progression of the disease, potentially stop progression of the disease, and potentially reverse. Again, we don't know if that might be possible, but that is one of the hopes. Dr Grouse: Well, that's really exciting, and I know we're all looking forward to more coming down the pipeline soon, and hopefully more things that can really offer some exciting treatments for our patients with this condition. Now, a little more deep-dive into our patients who are diagnosed. You've reviewed some of the treatments currently available and hopefully may someday soon be available. Are there other things that we should be keeping in mind in this population? For instance, screenings that we should be doing for other extramuscular manifestations that we need to be thinking about? Dr Knox: I will answer that question two ways. I think something that's very important to acknowledge is the impact that these diagnoses and these conditions have on our patient practically, psychologically. One of the other unique features of FSHD is, it's autosomal-dominant. So, if it is in a family, you can have many family members who are affected, but the variability is very high. And so, you can have in the same family someone who is wheelchair-dependent, and someone else in the family with the same underlying genetics who has no signs or symptoms or is very mildly affected. And that is something that is definitely challenging for our families and patients to navigate if they're very different than their family members with the same condition. And just navigating the world with a condition that, you know, can be physically debilitating and cause changes to what they're able to do or not able to do, progression is something that's very difficult to handle. So, I think that's one set of things. And we try our best, you know, with my team and my other colleagues in the space, to support our families and patients in the best way that we can. Secondly, there is very important screening that needs to be done for this condition. So, one of the things- and the current guidelines which are actually being updated, the last update was in 2015 is all patients that undergo pulmonary function testing or PFTs. And so that's something we do at baseline and we do at least annually in my practice. Young kids who are presenting very early or patients with certain genetics that we know are more predisposed to extra muscular manifestations, we recommend screening for hearing, which is one of the manifestations, and ophthalmologic exam to look for retinovascular changes, which is one of the manifestations as well. Those are the more common ones that are typically done. There's also some evidence in pediatric patients with very severe manifestations that there may be some cognitive impacts, learning impacts. And so, that is something we're also thinking about screening and supporting our patients in that way. And again, we typically work with these patients in a multidisciplinary team depending on what manifestations and the degrees to which they're impacted by the disorder. Dr Grouse: Thank you so much for that answer. I think a lot of us forget sometimes when we get really focused on what can we do now, that we forget to kind of stop and reflect on sort of the more holistic approach. How is this affecting the patient? How is this affecting the patient's family dynamic, and what other ways are they going through life with this condition that we need to be thinking about? So, I appreciate you bringing that up. I wanted to ask, sort of based on what you're talking about and what you mentioned already, you happened to mention that what initially drew you that to this work was your interest in some of the really exciting breakthroughs in the field. Well, was there anything else that drew you to, specifically, congenital neuromuscular diseases, and FSHD in particular? Dr Knox: I'm a physician scientist by training, and so I would describe myself also as a molecular biologist. So, I love getting into the nitty gritties of disease mechanisms, what genes are doing in bodies, how they function. And so, as I mentioned earlier, in the neuromuscle space, we've known for many years the genetic cause of many of these disorders and have done great, you know, mechanistic work to kind of define why we see the disease. And then now we're at this intersection of that knowledge marrying with these really novel therapeutic approaches, gene therapy approaches, being able to intersect and then in very creative ways actually target diseases very directly. And so, I would say it really is the combination of those two things. FSHD has a really fascinating unique biology, which again, we encourage everyone to read about more in the article. That really drew me to it. I'm very interested in gene regulation, transcription. This is one of the underlying mechanisms that is gone awry in the disorder, and then that being married to advances in therapeutics. So, you could wed those two pieces of information and actually meaningfully impact patient 's lives. And again, that's the real privilege and honor to witness is how these therapies can transform lives. And I saw it happened with this one case for this one disorder when I was a resident where there was no treatment. Young children, unfortunately, would not survive the disease. And then I saw the therapy come be in development and literally change the trajectory. And this is what we're very hopeful for in the FSHD space, that wedding, this wonderful basic science research, translational research, companies working together to develop these therapies that can transform lives. It is just so beautiful to witness and see, and it's something that I get to do. You know, it's a part of my job, so it's a real privilege. Dr Grouse: Well, I have to say, it's really inspiring hearing you talk about it. And I imagine that many neurologists-in-training who are listening to this may be inspired as well and may be convinced to go into this field for that very reason. So, thank you so much for sharing all of this information with us today. I learned a lot, and I think all of our listeners have too. Dr Knox: Thank you. It's really been a pleasure. Dr Grouse: Again, today I've been interviewing Dr Renatta Knox about her article on fascioscapulohumeral muscular dystrophy, which appears in the October 2025 Continuum issue on muscle and neuromuscular junction disorders. Be sure to check out Continuum Audio episodes from this and other issues. And thank you to our listeners for joining 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.
Hey daar lieve luisteraar, Lou hier. Met een uitzending én een uitnodiging voor Miracle Town. We zijn OPEN. Vanaf vandaag kun je gratis aanmelden via deze link: https://miracle-town.mn.co/plans/1863422?bundle_token=bd49565fbc162d60ba81b4ab4b34a5fc&utm_source=manual Het eerste wat geopend is in Miracle Town is het Miracle Town Café. Aan de Community Table kunnen we met elkaar connecten en alle wonderen delen en tracken en tracen. Je hoeft uiteraard niet deel te nemen aan gesprekken, je mag ook meekijken en luisteren en op de achtergrond blijven. In deze uitzending lees ik een stuk uit de ochtendkronkels en kronieken van mijn journal van vanmorgen voor. Over mijn eigen twijfels en hoe het herlezen van God on a Harley me wederom helpt en inspireert. Met 6 commandments waar jij misschien ook iets aan hebt. Zie ik je daarna in Miracle Town? Praat mee in het Miracle Town Café.
Documentairemaker Menna Laura Meijer onderzoekt in de achtdelige serie ‘Fortuyn: On-Hollands' de blijvende erfenis van Pim Fortuyn. De serie belicht hoe zijn gedachtegoed nog altijd doorwerkt in het debat over migratie, tolerantie en identiteit. Aan het woord komen mensen die Fortuyn van dichtbij hebben meegemaakt, waaronder voormalige politieke bondgenoten en tegenstanders, maar ook burgers met uiteenlopende achtergronden die in zijn tijd nauwelijks een stem hadden in het publieke debat. Meijer laat zien hoe Fortuyns opkomst een kantelpunt vormde in de Nederlandse politieke en maatschappelijke geschiedenis. Presentatie: Frénk van der Linden
Het is maandag. De dag dat je weet dat je weer vol aan de bak moet. Het niks doen en heerlijk luieren is passé. Hoogste tijd om de handen uit de mouwen te steken. Dat doen wij bij Gamekings ook. En wel door een nieuwe editie van Brievenmaandag voor je klaar te zetten. Aan de desk bevinden zich Boris, Koos en Shelly. Alle drie ready om de prangende vragen te beantwoorden. En vragen waren er. Volle bak. Zo wilde iemand weten of er nog een nieuwe Advanced Wars uitkomt, een ander vraagt zich af of hij koekoe is geworden omdat hij Fortnite tof vindt en een derde brievenschrijver wil weten of de uitspraak ‘gratis want Game Pass' op dit moment nog wel klopt? Wil je weten wat de antwoorden dan de drie hosts is, check dan de Brievenmaandag van maandag 13 september 2025.'Ik vind Fortnite als volwassen gamer wel leuk'Het wemelde zoals altijd van de vragen in de mailbox en op Discord. Aan de drie presentatoren de verantwoordelijke taak om ze allemaal van een passend antwoord te voorzien. Bijvoorbeeld de vraag hoe je als vader van kids nog aan een gamen kan toekomen? Een vraag die wij, nu een deel van onze doelgroep ouder wordt, vaker tegenkomen. Mooi dus dat onze opperpappie Boris bij deze aflevering in het panel van deskundigen zit. Een andere vraag betreft een probleem wat iemand heeft met zijn PC. Die weigert up te graden naar Windows 11. Weet Koos misschien raad? Je gaat het zien en horen in deze video.Kun je een game die op Game Pass staat nog wel als 'gratis' bestempelen?Dan is er ook een hypothetische vraag. Een die zich ook nog eens afspeelt in de toekomst. Wat als Boris straks de schoonfamilie van een van zijn kids ontmoet en het blijken allemaal paarsharige wereldverbeteraars te zijn? Hoe zou daar mee omgaan? Of kun je niet in de toekomst kijken en heeft het beantwoorden van deze vraag helemaal geen zin?
Aan tafel deze week: voormalig VN-gezant Sigrid Kaag, vicepremier Mona Keijzer, econoom Arnoud Boot, Russische oppositieleider Vladimir Kara-Murza, schrijver Ilja Leonard Pfeijffer. Presentatie: Joost Vullings Wil je meer weten over de gasten in Buitenhof? Op onze website vind je meer informatie. Daar kan je deze aflevering ook terugkijken en je vindt er natuurlijk nog veel meer gesprekken: https://bit.ly/buitenhof-12-okt-25 Sinds vrijdag is er een wapenstilstand in Gaza. Sigrid Kaag was tot voor kort VN-gezant Midden-Oosten en voor de wederopbouw van Gaza. Gaat er een duurzame vrede komen of zit er ergens een adder onder het gras? Vrijdag kwamen de doorrekeningen van de verkiezingsprogramma's door het CPB. Hoogleraar Financiële Markten Arnoud Boot heeft ze bekeken. Hij vertelt in Buitenhof over de haalbaarheid en betaalbaarheid van de plannen én welke tegenstellingen hem opvallen. Mona Keijzer, demissionair minister van Volkshuisvesting en Ruimtelijke Ordening en voor Asiel en Migratie, heeft grote plannen voor de komende jaren als het gaat om wonen maar ook om migratie. Doorpakken zit in haar genen, maar kan dat wel op de manier waarop de BBB dat wil? Wil de BBB weer terugkeren in een nieuw kabinet? En hoe gaat de partij van Keijzer dat voor elkaar krijgen? Vladimir Kara-Murza was samen met Aleksej Navalny de belangrijkste criticus van de Russische president Poetin. Kara-Murza werd twee keer vergiftigd en werd in 2022 gearresteerd en veroordeeld tot 25 jaar strafkamp. Ruim twee jaar zat hij gevangen in Siberië. Vorig jaar kwam hij vrij na een gevangenenruil. We spraken hem eerder deze week over Rusland, oppositievoeren vanuit het buitenland, autocratie en over hoe verandering in Rusland altijd onverwacht komt. En tweeënhalf jaar geleden bracht Ilja Leonard Pfeijffer het boek Alkibiades uit, dat gaat over het verval van de democratie in het oude Athene. Het moest een waarschuwing zijn, want Pfeijffer zag parallellen met het heden. Binnenkort komt de schrijver met de essaybundel Absolute Macht. Hoe staat onze democratie er nu voor volgens Pfeijffer?
While genetic testing has replaced muscle biopsy in the diagnosis of many genetic myopathies, clinical assessment and the integration of clinical and laboratory findings remain key elements for the diagnosis and treatment of muscle diseases. In this episode, Casey Albin, MD, speaks with Margherita Milone, MD, PhD, FAAN, FANA, author of the article “A Pattern Recognition Approach to Myopathy” in the Continuum® October 2025 Muscle and Neuromuscular Junction Disorders issue. Dr. Albin is a Continuum® Audio interviewer, associate editor of media engagement, and an assistant professor of neurology and neurosurgery at Emory University School of Medicine in Atlanta, Georgia. Dr. Milone is a professor of neurology and the director of the Muscle Pathology Laboratory at Mayo Clinic College of Medicine and Science in Rochester, Minnesota. Additional Resources Read the article: A Pattern Recognition Approach to Myopathy Subscribe to Continuum®: shop.lww.com/Continuum Earn CME (available only to AAN members): continpub.com/AudioCME Continuum® Aloud (verbatim audio-book style recordings of articles available only to Continuum® subscribers): continpub.com/Aloud More about the American Academy of Neurology: aan.com Social Media facebook.com/continuumcme @ContinuumAAN Host: @caseyalbin Full episode transcript available here Dr Jones: This is Dr Lyell Jones, Editor-in-Chief of Continuum. Thank you for listening to Continuum Audio. Be sure to visit the links in the episode notes for information about earning CME, subscribing to the journal, and exclusive access to interviews not featured on the podcast. Dr Albin: Hello, this is Dr Casey Albin. Today I'm interviewing Dr Margherita Milone on her article on a pattern recognition approach to myopathy, which appears in the October 2025 Continuum issue on muscle and neuromuscular junction disorders. Welcome to the podcast, Dr Milone. Thank you so much for joining us. I'll start off by having you introduce yourself to our listeners. Dr Milone: Hello Casey, thank you so much for this interview and for bringing the attention to the article on muscle diseases. So, I'm Margherita Milone. I'm one of the neuromuscular neurologists at Mayo Clinic in Rochester. I have been interested in muscle disorders since I was a neurology resident many years ago. Muscle diseases are the focus of my clinical practice and research interest. Dr Albin: Wonderful. Thank you so much. When I think about myopathies, I generally tend to think of three large buckets: the genetic myopathy, the inflammatory myopathies, and then the necrotizing myopathies. Is that a reasonable approach to conceptualizing these myopathies? Dr Milone: Yeah, the ideology of the myopathies can be quite broad. And yes, we have a large group of genetic muscle diseases, which are the most common. And then we have immune-mediated muscle diseases, which include inflammatory myopathies as well as some form of necrotizing myopathies. Then we have some metabolic myopathies, which could be acquired or could be genetic. And then there are muscle diseases that are due to toxins as well as to infection. Dr Albin: Wow. So, lots of different etiologies. And that really struck me about your article, is that these can present in really heterogeneous ways, and some of them don't really read the rule book. So, we have to have a really high level of suspicion, for someone who's coming in with weakness, to remember to think about a myopathy. One of the things that I like to do is try to take us through a little bit of a case to sort of walk us through how you would approach if someone comes in. So, let's say you get, you know, a forty-year-old woman, and she's presenting with several months of progressive weakness. And she says that even recently she's noted just a little bit of difficulty swallowing. It feels to her like things are getting stuck. What are some of the things when you are approaching the history that would help you tease this to a myopathy instead of so many other things that can cause a patient to be weak? Dr Milone: Yes. So, as you mentioned, people who have a muscle disease have the muscle weakness often, but the muscle weakness is not just specific for a muscle disease. Because you can have a mass weakness in somebody who has a neurogenic paralysis. The problem with diagnosis of muscle diseases is that patients with these disorders have a limited number of symptom and sign that does not match the large heterogeneity of the etiology. So, in someone who has weakness, that weakness could represent a muscle disease, could represent an anterior horn cell disease, could represent a defect of neuromuscular junction. The clinical history of weakness is not sufficient by itself to make you think about a muscle disease. You have to keep that in the differential diagnosis. But your examination will help in corroborating your suspicion of a muscle disease. Let's say if you have a patient, the patient that you described, with six months' history of progressive weakness, dysphagia, and that patient has normal reflexes, and the patient has no clinical evidence for muscle fatigability and no sensory loss, then the probability that that patient has a myopathy increases. Dr Albin: Ah, that's really helpful. I'm hearing a lot of it is actually the lack of other findings. In some ways it's asking, you know, have you experienced numbness and tingling? And if not, that's sort of eliminating that this might not be a neuropathy problem. And then again, that fatigability- obviously fatigability is not specific to a neuromuscular junction, but knowing that is a hallmark of myasthenia, the most common of neuromuscular disorders. Getting that off the table helps you say, okay, well, it's not a neuromuscular junction problem, perhaps. Now we have to think more about, is this a muscle problem itself? Are there any patterns that the patients describe? I have difficulty getting up from a chair, or I have difficulty brushing my hair. When I think of myopathies, I historically have thought of, sort of, more proximal weakness. Is that always true, or not so much? Dr Milone: Yeah. So, there are muscle diseases that involve predominantly proximal weakness. For example, the patient you mentioned earlier could have, for example, an autoimmune muscle disease, a necrotizing autoimmune myopathy; could have, perhaps, dermatomyositis if there are skin changes. But a patient with muscle disease can also present with a different pattern of weakness. So, myopathies can lead to this weakness, and foot drop myopathies can cause- can manifest with the weakness of the calf muscles. So, you may have a patient presenting to the clinic who has no the inability to stand on tiptoes, or you may have a patient who has just facial weakness, who has noted the difficulty sealing their lips on the glasses when they drink and experiencing some drooling in that setting, plus some hand weakness. So, the muscle involved in muscle diseases can vary depending on the underlying cause of the muscle disease. Dr Albin: That's really helpful. So, it really is really keeping an open mind and looking for some supporting features, whether it's bulbar involvement, extraocular eye muscle involvement; looking, you know, is it proximal, is it distal? And then remembering that any of those patterns can also be a muscle problem, even if sometimes we think of distal being more neuropathy and proximal myopathy. Really, there's a host of ranges for this. I really took that away from your article. This is, unfortunately, not just a neat way to box these. We really have to have that broad differential. Let me ask another question about your history. How often do you find that patients complain of, sort of, muscular cramping or muscle pain? And does that help you in terms of deciding what type of myopathy they may have? Dr Milone: Many patients with muscle disease have muscle pain. The muscle pain could signal a presence of inflammation in skeletal muscle, could be the result of overuse from a muscle that is not functioning normally. People who have myotonia experience muscle stiffness and muscle pain. Patients who have a metabolic myopathy usually have exercise-induced muscle pain. But, as we know, muscle pain is also very nonspecific, so we have to try to find out from the patient in what setting the pain specifically occurs. Dr Albin: That's really helpful. So, it's asking a little bit more details about the type of cramping that they have, the type of pain they may be experiencing, to help you refine that differential. Similarly, one of the things that I historically have always associated with myopathies is an elevation in the CK, or the creatinine kinase. How sensitive and specific is that, and how do you as the expert sort of take into account, you know, what their CK may be? Dr Milone: So, this is a very good point. And the elevation of creatine kinase can provide a clue that the patient has a muscle disease, but it is nonspecific for muscle disease because we know that elevation of creatine kinase can occur in the setting of a neurogenic process. For example, we can see elevation of the creatine kinase in patients who have ALS or in patients who have spinal muscular atrophy. And in these patients---for example, those with spinal muscular atrophy---the CK elevation can be also of significantly elevated up to a couple of thousand. Conversely, we can have muscle diseases where the CK elevation does not occur. Examples of these are some genetic muscle disease, but also some acquired muscle diseases. If we think of, for example, cases where inflammation in the muscle occurs in between muscle fibers, more in the interstitium of the muscle, that disease may not lead to significant elevation of the CK. Dr Albin: That's super helpful. So, I'm hearing you say CK may be helpful, but it's neither completely sensitive nor completely specific when we're thinking about myopathic disorders. Dr Milone: You are correct. Dr Albin: Great. So, coming back to our patients, you know, she says that she has this dysphasia. How do bulbar involvement or extraocular eye movement involvement, how do those help narrow your differential? And what sort of disorders are you thinking of for patients who may have that bulbar or extraocular muscle involvement? Dr Milone: Regarding dysphagia, that can occur in the setting of acquired myopathies relatively frequent; for example, in inclusion body myositis or in other forms of inflammatory myopathy. Your patient, I believe, was in their forties, so it's a little bit too young for inclusion body myositis. Involvement of the extraocular muscles is usually much more common in genetic muscle diseases and much less frequent in hereditary muscle disease. So, if there is involvement of the extraocular muscles, and if there is a dysphagia, and if there is a proximal weakness, you may think about oculopharyngeal muscular dystrophy, for example. But obviously, in a patient who has only six months of history, we have to pay attention of the degree of weakness the patient has developed since the symptom onset. Because if the degree of weakness is mild, yes, it could still be a genetic or could be an acquired disease. But if we have a patient who, in six months, from being normal became unable to climb stairs, then we worry much more about an acquired muscle disease. Dr Albin: That's really helpful. So, the time force of this is really important. And when you're trying to think about, do I put this in sort of a hereditary form of muscle disease, thinking more of an indolent core, something that's going to be slowly progressive versus one of those inflammatory or necrotizing pathologies, that's going to be a much more quick onset, rapidly progressive, Do I have that right? Dr Milone: In general, the statement is correct. They tend, acquired muscle disease, to have a faster course compared to a muscular dystrophy. But there are exceptions. There have been patients with immune mediated necrotizing myopathy who have been misdiagnosed as having limb-girdle muscular dystrophy just because the disease has been very slowly progressive, and vice versa. There may be some genetic muscle diseases that can present in a relatively fast way. And one of these is a lipid storage myopathy, where some patients may develop subacutely weakness, dysphagia, and even respiratory difficulties. Dr Albin: Again, I'm hearing you say that we really have to have an open mind that myopathies can present in a whole bunch of different ways with a bunch of different phenotypes. And so, keeping that in mind, once you suspect someone has a myopathy, looking at the testing from the EMG perspective and then maybe laboratory testing, how do you use that information to guide your work up? Dr Milone: The EMG has a crucial role in the diagnosis of muscle diseases. Because, as we said earlier, weakness could be the result of muscle disease or other form of neuromuscular disease. If the EMG study will show evidence of muscle disease supporting your diagnostic hypothesis, now you have to decide, is this an acquired muscle disease or is this a genetic muscle disease? If you think that, based on clinical history of, perhaps, subacute pores, it is more likely that the patient has an acquired muscle disease, then I would request a muscle biopsy. The muscle biopsy will look for structural abnormalities that could help in narrowing down the type of muscle disease that the patient has. Dr Albin: That's really helpful. When we're sending people to get muscle biopsies, are there any tips that you would give the listeners in terms of what site to biopsy or what site, maybe, not to biopsy? Dr Milone: This is a very important point. A muscle biopsy has the highest diagnostic yield if it's done in a muscle that is weak. And because muscle diseases can result in proximal or distal weakness, if your patient has distal weakness, you should really biopsy a distal muscle. However, we do not wish to biopsy a muscle that is too weak, because otherwise the biopsy sample will result just in fibrous and fatty connected tissue. So, we want to biopsy a muscle that has mild to moderate weakness. Dr Albin: Great. So, a little Goldilocks phenomenon: has to be some weak, but not too weak. You got to get just the right feature there. I love that. That's a really good pearl for our listeners to take. What about on the flip side? Let's say you don't think it's an acquired a muscular disease. How are you handling testing in that situation? Dr Milone: If you think the patient has a genetic muscle disease, you pay a lot of attention to the distribution of the weakness. Ask yourself, what is the best pattern that represent the patient's weakness? So, if I have a patient who has facial weakness, dysphagia, muscle cramping, and then on examination represent myotonia, then at that point we can go straight to a genetic test for myotonic dystrophy type one. Dr Albin: That's super helpful. Dr Milone: So, you request directly that generic test and wait for the result. If positive, you will have proof that your diagnostic hypothesis was correct. Dr Albin: You're using the genetic testing to confirm your hypothesis, not just sending a whole panel of them. You're really informing that testing based on the patient's pattern of weakness and the exam findings, and sometimes even the EMG findings as well. Is that correct? Dr Milone: You are correct, and ideally, yes. And this is true for certain muscle diseases. In addition to myotonic dystrophy type one, for example, if you have a patient who has fascial scapulohumeral muscular weakness, you can directly request a test for FSHD. So, the characterization of the clinical phenotype is crucial before selecting the genetic test for diagnosis. Dr Albin: Wonderful. Dr Milone: However, this is not always possible, because you may have a patient who has just a limb-girdle weakness, and the limb-girdle weakness can be limb-girdle muscular dystrophy. But we know that there are many, many types of limb-girdle muscular dystrophies. Therefore, the phenotype is not sufficient to request specific genetic tests for one specific form of a limb-girdle muscular dystrophy. And in those cases, more complex next-generation sequencing panels have a higher chance of providing the answer. Dr Albin: Got it, that makes sense. So, sometimes we're using a specific genetic test; sometimes, it is unfortunate that we just cannot narrow down to one disease that we might be looking for, and we may need a panel in that situation. Dr Milone: You are correct. Dr Albin: Fantastic. Well, as we wrap up, is there anything on the horizon for muscular disorders that you're really excited about? Dr Milone: Yes, there are a lot of exciting studies ongoing for gene therapy, gene editing. So, these studies are very promising for the treatment of genetic muscle disease, and I'm sure there will be therapists that will improve the patient's quality of life and the disease outcome. Dr Albin: It's really exciting. Well, thank you again. Today I've been interviewing Dr Margarita Malone on her article on a pattern recognition approach to myopathy, which appears in the October 2025 Continuum issue on muscle and neuromuscular junction disorders. Be sure to check out Continuum Audio episodes from this and other issues, and thank you to our listeners for joining us today. And thank you, Dr Milone. Dr Milone: Thank you, Casey. Very nice chatting with you about this. Dr Monteith: This is Dr Teshamae Monteith, Associate Editor of Continuum Audio. If you've enjoyed this episode, you'll love the journal, which is full of in-depth and clinically relevant information important for neurology practitioners. Use the link in the episode notes to learn more and subscribe. AAN members, you can get CME for listening to this interview by completing the evaluation at continpub.com/audioCME. Thank you for listening to Continuum Audio.
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