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這集我們會談到： 1.匈牙利網路名店的「鵝肝」價格多少？吃起來感受如何？ 2.匈牙利與拉脫維亞的人均GDP差不多，兩地的消費比較如何？ 3.布達區與佩斯區的景點有何差異？匈牙利國家美術館有何特色？ 4.在東歐心存僥倖沒買公車票會如何？無法事後補票、罰款超高！！ 5.匈牙利主要的紀念品為何？辣椒粉、臘肉、貴腐酒！！ 6.捷克布拉格遊客超多，審美疲勞導致旅遊體驗不符預期？？ 7.捷克的教堂超級華麗，教堂內天花板的壁畫超美、雕刻超精緻！ 8.為何天主教的教堂通常較為華麗？背後可能有什麼因素？ 9.捷克的「煙囪捲」如何製作？其主要特色為何？螞蟻人超愛？？ 10.Fana與朋友被斯洛維尼亞人搭訕，斯洛維尼亞有何特色？？ 11.歐洲的火車延遲為大日常，甚至會取消車班！？台鐵優秀多了！！ 【背景介紹】 捷克共和國，通稱捷克，是位於歐洲的共和制國家，也是位於歐洲的內陸國家。南面是奧地利，西面是德國，東北面是波蘭，東面為斯洛伐克。首都在布拉格，素有「百塔之城」美稱，榮列聯合國教科文組織世界文化遺產，同時也是全球最美的城市之一…..。 請贊助我一杯咖啡，感謝您的贊助，讓我們能走得更遠、更久
這集我們會談到： 1.布達佩斯的住宿費用如何？房間大、交通方便還附烤箱！！ 2.國旅住宿有多貴？高雄住宿及國中畢旅的費用大概如何？ 3.國中畢旅費用為何越來越貴？國中老師畢旅晚上在做什麼？ 4.布達佩斯火車站附近的房價大概為何？住宿費用普遍不高？ 5.匈牙利農業博物館—瓦伊達奇城堡，其歷史背景和特色為何？ 6.匈牙利牛肉湯有何特別之處？與羅宋湯有何不同呢？？ 7.身為學生出國遊玩有哪些好處？各展館皆有優惠學生票！！ 8.《藍色多瑙河》圓舞曲的藍色象徵了什麼？實際顏色為何？ 9.在多瑙河搭船遊河花費多少？與台、日遊河花費落差多大？ 10.Fana和朋友在匈牙利被中國人搭訕，有即刻救援既視感！？ 【背景介紹】 匈牙利是位於歐洲的內陸國家。根據地理分區的不同定義，匈牙利被認為處在中歐和東歐，為歐盟中型面積成員國之一。首都和最大城市為布達佩斯，多瑙河沿岸為布達佩斯主要景點之一.…..。 請贊助我一杯咖啡，感謝您的贊助，讓我們能走得更遠、更久
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.
這集我們會談到： 1.Fana對波蘭的整體評價如何？天氣、物價、人民素質皆優？ 2.出國在外，防人之心不可無，請人幫忙拍照其實很危險？ 3.日本旅遊東西遺失經驗談，日本警察非常熱心協助觀光客？ 4.Fana原先對匈牙利之旅有什麼期待？一下公車就遇到小扒手！！ 5.Fana和友人在布達佩斯被吉普賽人糾纏，竟無人伸出援手！？ 6.吉普賽小孩用了哪些招式對付觀光客？主要的目的應該為何？ 7.歐洲人對嬰兒相對友善？東亞國家對育兒相對不友善？？ 8.Fana對匈牙利的第一餐評價如何？早午餐鬆餅搭配炸雞！？ 9.賽切尼溫泉的評價如何？Fana最終為何選擇私人spa池？ 10.抹茶近期在歐洲爆紅，各種飲食都要加抹茶？？ 【背景介紹】 匈牙利是位於歐洲的內陸國家。根據地理分區的不同定義，匈牙利被認為處在中歐和東歐，為歐盟中型面積成員國之一。首都和最大城市為布達佩斯，多瑙河沿岸為布達佩斯主要景點之一.…..。 請贊助我一杯咖啡，感謝您的贊助，讓我們能走得更遠、更久
這集我們會談到： 1.Fana在波蘭華沙的住宿花費如何？最大的困難是沒有電梯！！ 2.歐洲餐廳的開水不見得是免費的，背包客該如何節省開水支出？ 3.華沙的「科學宮」參觀體驗如何？華沙為何比較少老城區？ 4.華沙的「瓦津基宮」有多美？Fana激推華沙當地冰淇淋！！ 5.為了參訪奧斯威辛集中營，Fana如何安排住宿及行程接駁？ 6.比起看書籍和影片，真正到達奧斯威辛集中營有多麼讓人震撼？ 7.克拉科夫的遊客竟比首都華沙來的多，當地的餐點口味如何？？ 8.在外國用餐最大的困擾就是滿滿的碳水和肉，缺少青菜！ 9.Fana在華沙當地的公車一日票票價如何？逃票被抓罰金超高！ 【背景介紹】 奧斯威辛集中營位於波蘭克拉科夫近郊，是二戰時期納粹德國建立的最大集中營。這裡是聯合國教科文組織列名的世界文化遺產，這片土地見證了二戰期間猶太人遭受的極端迫害，超過百萬條生命在此逝去.…..。 請贊助我一杯咖啡，感謝您的贊助，讓我們能走得更遠、更久
這集我們會談到： 1.Fana歷經千辛萬苦，坐了近30個小時的車，終於到達波蘭華沙 2.為何Fana選擇搭乘巴士去華沙？除了金錢考量之外還有什麼因素？ 3.波羅的海三小國是哪三國？愛沙尼亞數位發達，國家有何特色？ 4.拉脫維亞首都里加，老城區與中央市場有何特色？物價如何？ 5.外國人認知的珍奶與台灣的不一樣？充斥著彩色的爆漿珍珠！ 6.亞洲人和歐美人對於觀光旅遊的想法有何不同？玩好玩滿才值得？ 7.歐洲的建築為何那麼美？台灣的建築物在保存上有何限制？ 8.台灣為何常出現醜陋的鐵皮建築？建築物如此雜亂充滿頂樓加蓋？ 9.閒聊：台灣的建築廢棄物能怎麼處理？只能委由私人代收？ 10.Fana到了華沙的第一餐吃了有名的「餃子」，評價如何？ 11.Fana到歐洲參觀了許多教堂，如何快速區分東正教的教堂？ 【背景介紹】 拉脫維亞共和國，通稱拉脫維亞，是位於波羅的海東岸的歐洲東北部國家，是波羅的海國家之一，也是Fana東歐之旅的首個目的地，但在開啟東歐的旅程之前，Fana遇到了哪些問題？整個東歐之旅又有哪些美好的記憶及驚險的經歷？？.…..。 請贊助我一杯咖啡，感謝您的贊助，讓我們能走得更遠、更久
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.
KABB-pod 06 – innholdsfortegnelse00:00:En liten men viktig appell01:00: Dette får du i KABBpod nummer 603:19: KABB reiste på tur til Tyskland. En vandring i Luther og Bachs fotspor sammen med KABB Norge, Danmark og Syskonbandet, nyt reisebrevet fra sofakroken.23:26: Hvert annet år deles likepersonprisen ut på landsmøte til Norgesblindeforbund, Heidi Haug fikk årets pris.31:22: Informasjon fra KABB Kirkerådet vurderer å kutte driftstøtten til KABB, hør hva generalsekretær Øyvind Woie tenker om dette. 42:38: Forestillingen Med mine øyne kommer snart til Vestlandet nærmere bestemt til Radøy sokn. Gudveig Kartveit er diakon i Sæbø kirke, der forestillingen vises 25. oktober.47:07: Smarte leselister. Hør hvor smart en leselist begynner å bli. Med et enkelt tastetrykk kan du laste ned både aviser og e-bøker direkte til leselisten. Det betyr at du kan ha med deg dagsnyheter, ukeblad og romaner uansett hvor du er.58:34: Tanker om tro med Kristin Sævik Litlere, prost i Fana prosti i Bergen1:05:07: Geir Gundersen, forfatter og teolog, deler fra sitt foredrag på KABBs generalforsamling om hvordan tro og liv formes når man lever med en funksjonsnedsettelse
這集我們會談到： 1.Fana分享俄羅斯近況，出發前往東歐旅遊之前一波三折！？ 2.在俄羅斯有健保看醫生不用錢?公立VS私立醫院哪個較受歡迎？ 3.俄羅斯的就醫流程為何？戰時平民就醫可能面臨何種問題？ 4.Fana前往東歐旅遊前一天急性腸胃炎，嚴重到快昏倒？ 5.俄羅斯要連上社群媒體只能透過VPN，遠離塵囂新生活！ 6.手機成癮的人無法去俄羅斯！！手機養大的孩子會怎樣？ 7.能自己規劃一趟旅程很不容易，需考量許多不同的部分！ 8.利用AI協助規劃行程超方便，但可能會遇到什麼風險？ 9.Fana入境拉脫維亞時遇到什麼問題？差點被拒絕上車！？ 10.Fana歷經波折終於順利搭上車，車程要將近9小時！！ 【背景介紹】 拉脫維亞共和國，通稱拉脫維亞，是位於波羅的海東岸的歐洲東北部國家，是波羅的海國家之一，也是Fana東歐之旅的首個目的地，但在開啟東歐的旅程之前，Fana遇到了哪些問題？整個東歐之旅又有哪些美好的記憶及驚險的經歷？？.…..。 請贊助我一杯咖啡，感謝您的贊助，讓我們能走得更遠、更久
Reporte Urbano. Programa periodístico informativo en radio de interés general. Un recorrido por la actualidad con entrevistas, noticias, opinión, cultura, economía, información, sociedad, espectáculos, comentarios y política. Emisión Principal: Todos los viernes de 10 a 11 horas por AM 1010 y más de 50 retransmisoras en 8 países: España, Colombia, México, EEUU, Costa Rica, Chile, Uruguay, y todo el territorio argentino. Programa periodístico en radio de Roberto VILLALOBOS ATLAS, Cintia NEVES y equipo. 💥Víctor RODRÍGUEZ Transporte 💥Julio PARDO Deportes 💥Víctor LENNIN Psicología 💥Antonio FANÁ Espectáculos 💥Silvana RIDNER Nutrición 💥Walter TELECHEA Trabajo 💥Fabricio GUERRERO Operación Técnica 💥INDESANET Desarrollo Personal Declarado de Interés para la Comunicación Social de la Ciudad Autónoma de Buenos Aires por la Legislatura Porteña. Distinguido por el Premio Latinoamericano "Señal Latina" y por el Premio Nacional "Reina Del Plata" en el rubro Programa Periodístico en Radio. Tags: #Información #Periodismo #Opinión #Actualidad #Entrevistas #Notas #Noticias #Radio #Secciones #Política #Economía #Niños #Infancia #Oyentes #Publicidad #Derecho #DDHH #Cultura #Educación #Vecinos #AyudaSocial #Solidaridad #Salud #Apoyo #Amor #Felicidad, #Efemérides #BolsaDeTrabajo #DadoresDeSangre #Campañas #Historias #Sorteos #Nacionales #Mundiales #Locales #Provinciales #Amigos #Compañeros #Horóscopo #Comunas #Barrios #Justicia #Porteño #Amigos #Lucha #AlienaciónParental #ObstrucciónDeVínculos #ImpedimentoDeContacto #Niñas #Niños #Adolescentes #Infancia #RadioOnLine #RadioEnLínea #RobertoVillalobosAtlas #VAconvos #ReporteUrbano #RadioOrión #CintiaNeves #Ciudad #BuenosAires #Podcast #Ivoox #Spotify #TuneIn #Itunes #Radio #Entrevistas #Nota #VillalobosAtlas #Ayuda
Reporte Urbano. Programa periodístico informativo en radio de interés general. Un recorrido por la actualidad con entrevistas, noticias, opinión, cultura, economía, información, sociedad, espectáculos, comentarios y política. Emisión Principal: Todos los viernes de 10 a 11 horas por AM 1010 y más de 50 retransmisoras en 8 países: España, Colombia, México, EEUU, Costa Rica, Chile, Uruguay, y todo el territorio argentino. Programa periodístico en radio de Roberto VILLALOBOS ATLAS, Cintia NEVES y equipo. 💥Víctor RODRÍGUEZ Transporte 💥Julio PARDO Deportes 💥Víctor LENNIN Psicología 💥Antonio FANÁ Espectáculos 💥Silvana RIDNER Nutrición 💥Walter TELECHEA Trabajo 💥Fabricio GUERRERO Operación Técnica 💥INDESANET Desarrollo Personal Declarado de Interés para la Comunicación Social de la Ciudad Autónoma de Buenos Aires por la Legislatura Porteña. Distinguido por el Premio Latinoamericano "Señal Latina" y por el Premio Nacional "Reina Del Plata" en el rubro Programa Periodístico en Radio. Tags: #Información #Periodismo #Opinión #Actualidad #Entrevistas #Notas #Noticias #Radio #Secciones #Política #Economía #Niños #Infancia #Oyentes #Publicidad #Derecho #DDHH #Cultura #Educación #Vecinos #AyudaSocial #Solidaridad #Salud #Apoyo #Amor #Felicidad, #Efemérides #BolsaDeTrabajo #DadoresDeSangre #Campañas #Historias #Sorteos #Nacionales #Mundiales #Locales #Provinciales #Amigos #Compañeros #Horóscopo #Comunas #Barrios #Justicia #Porteño #Amigos #Lucha #AlienaciónParental #ObstrucciónDeVínculos #ImpedimentoDeContacto #Niñas #Niños #Adolescentes #Infancia #RadioOnLine #RadioEnLínea #RobertoVillalobosAtlas #VAconvos #ReporteUrbano #RadioOrión #CintiaNeves #Ciudad #BuenosAires #Podcast #Ivoox #Spotify #TuneIn #Itunes #Radio #Entrevistas #Nota #VillalobosAtlas #Ayuda
REFLEXIONES IMPROVISADAS http://www.youtube.com/@reflexionesimprovisadas APORTAR 1 DÓLAR AL MES con Paypal: https://www.paypal.com/webapps/billing/plans/subscribe?plan_id=P-7UW227459M544662JM2MVMBA PARA DONAR LA CANTIDAD QUE QUIERAS https://paypal.me/podcastparadormirse Mi número telefónico es +542235208859. Agradecería que me enviaran mensajes de audio para poder reproducir en el podcast y para que nos escuchemos entre todos. Para que todos aquellos que están como vos, escuchando porque no se pueden dormir, sepan que no están solos. También es para que estemos conectados, así que pueden escribirme cuantas veces quieran. Para invitarme un café así sigo despierto grabando más episodios: https://cafecito.app/podcastparadormirse Si vos también te querés suscribir y colaborar económicamente con el podcast: patreon.com/podcastparadormirse Para donar por transferencia (solo argentina): CBU 0140323503420058303116 ALIAS porque Agus me lo pidió: podcastparadormirse Para donar desde el exterior por Wester Union o Paypal, comunicarse por WhatsApp. Mi Instagram es @correapalaciosok Mi Tik Tok es @correapalaciosok Dulces sueños ;) Learn more about your ad choices. Visit megaphone.fm/adchoices
Sabda Tuhan ingatkan bahwa bergantung pada yang fana, hidup jadi gulana merana, bergantung pada Yang Kekal, hidup makin tawakal atasi segala aral.
這集我們會談到： 1.Fana在暑假的尾聲又出國了！這次跑去哪兒玩呢？？ 2.南韓的台灣、中國遊客眾多，如何從對話區分是否台灣人？ 3.日本大城市遊客擠爆！暑假又熱、又擠，淡季去玩比較好？ 4.何謂「觀光公害」？在地居民該如何應對被遊客蠶食的生活圈？ 5.台灣出國人次與來台觀光人次落差有多大？有何隱憂？ 6.沖繩到東京航班很少？來台後轉機竟然比較方便？？ 7.國旅已死！台灣人熱愛出國旅遊，排行前五是哪些國家呢？ 8.出國旅遊最在意什麼？台灣及特旅遊地廁所小點評！ 9.陸客很多的那個時期，台灣的陸客旅行團有何「一條龍」模式？ 10.大阪2025年迎來爆量遊客，當地居民面臨到哪些問題？ 11.據民調統計，日本居民最討厭遊客出現哪些行為？ 【背景介紹】 觀光公害，又稱過度旅遊、超限旅遊，是指旅遊人數過多，造成過度擁擠或堵塞，因此影響當地生活的情形。自從疫情結束後，世界各地旅遊大復甦，許多著名的觀光景點也迎來遊客爆量、影響當地居民生活品質的情況.…..。 請贊助我一杯咖啡，感謝您的贊助，讓我們能走得更遠、更久
Brann og Viking er ute av cupen. Os og Fana meiner dei har funne oppskrifta. Men fråfallet ei utfordring. Store talent forsvinn. Dagens gjestar: Endre Brenne og Ørjan Håland i første omgang. I andre omgang har vi òg med oss Jan-Petter Hauge. Han er trenar for Fana sine juniorar, ei gruppe som gjer det svært skarpt om dagen.For å høre hele episoden må du ha abonnement, det skaffer du deg herEr du abonnent får du tilgang til medlemsfeeden her Hosted on Acast. See acast.com/privacy for more information.
Reporte Urbano. Programa periodístico informativo en radio de interés general. Un recorrido por la actualidad con entrevistas, noticias, opinión, cultura, economía, información, sociedad, espectáculos, comentarios y política. Emisión Principal: Todos los viernes de 10 a 11 horas por AM 1010 y más de 50 retransmisoras en 8 países: España, Colombia, México, EEUU, Costa Rica, Chile, Uruguay, y todo el territorio argentino. Programa periodístico en radio de Roberto VILLALOBOS ATLAS, Cintia NEVES y equipo. 💥Víctor RODRÍGUEZ Transporte 💥Julio PARDO Deportes 💥Víctor LENNIN Psicología 💥Antonio FANÁ Espectáculos 💥Silvana RIDNER Nutrición 💥Walter TELECHEA Trabajo 💥Fabricio GUERRERO Operación Técnica 💥INDESANET Desarrollo Personal Declarado de Interés para la Comunicación Social de la Ciudad Autónoma de Buenos Aires por la Legislatura Porteña. Distinguido por el Premio Latinoamericano "Señal Latina" y por el Premio Nacional "Reina Del Plata" en el rubro Programa Periodístico en Radio. Tags: #Información #Periodismo #Opinión #Actualidad #Entrevistas #Notas #Noticias #Radio #Secciones #Política #Economía #Niños #Infancia #Oyentes #Publicidad #Derecho #DDHH #Cultura #Educación #Vecinos #AyudaSocial #Solidaridad #Salud #Apoyo #Amor #Felicidad, #Efemérides #BolsaDeTrabajo #DadoresDeSangre #Campañas #Historias #Sorteos #Nacionales #Mundiales #Locales #Provinciales #Amigos #Compañeros #Horóscopo #Comunas #Barrios #Justicia #Porteño #Amigos #Lucha #AlienaciónParental #ObstrucciónDeVínculos #ImpedimentoDeContacto #Niñas #Niños #Adolescentes #Infancia #RadioOnLine #RadioEnLínea #RobertoVillalobosAtlas #VAconvos #ReporteUrbano #RadioOrión #CintiaNeves #Ciudad #BuenosAires #Podcast #Ivoox #Spotify #TuneIn #Itunes #Radio #Entrevistas #Nota #VillalobosAtlas #Ayuda
參考書目：《錢先花光，還是命先沒了？》，作者：小梶沙羅，譯者： 陳嫺若 這集我們會談到： 1.日劇《孤獨死又怎樣？》主角對姑姑前後的評價有何差異? 2.《孤獨死又怎樣？》主角姑姑為何會孤獨死?主角也推了一把？ 3.《孤獨死又怎樣？》主角的媽媽與姑姑到老時如何情勢反轉？ 4.年將四十的大齡女子在婚姻市場優勢全無，年老能體面死去嗎？ 5.想體面的死去容易嗎？年紀大了在年老與生病後會面臨何問題？ 6.《錢先花光，還是命先沒了？》，非主要照顧者不懂的現況！！ 7.Fana奶奶可能有失智症狀？？整天說著怎樣奇怪的話呢？ 8.有錢判生，沒錢判死！癌症治療將面臨哪些經濟、照護問題？ 9.《錢先花光，還是命先沒了？》，如何面對老人不講理的問題？ 10.老了天天逛醫院，Joe如何處理長輩生病的各種問題？ 【背景介紹】 《錢先花光，還是命先沒了？》，作者年近60從東京返回千葉縣老家照顧四位90歲的老人，書中以坦白的文字給予照顧者心理上的撫慰、陪伴，知道自己並不孤單…..。 請贊助我一杯咖啡，感謝您的贊助，讓我們能走得更遠、更久
KAJIAN MT AL-KHANSATema: MENCINTAI YANG FANA MELUPAKAN YANG KEKALTerbuka Untuk UmumNarasumber: Ustadzah Hana Eliana, CH, CPHt, CP NLP.Kamis, 11 September 2025 / 18 Rabi'ul Awwal 1447HPukul 08:00 - 11:00 WIBdi Masjid As-Sofia, Bogorمَنْ سَلَكَ طَرِيْقًايَلْتَمِسُ فِيْهِ عِلْمًا,سَهَّلَ اللهُ لَهُ طَرِيْقًا إِلَى الجَنَّةِ . رَوَاهُ مُسْلِم Siapa saja yang menempuh satu jalan (cara) untuk mendapatkan ilmu, maka Allah pasti mudahkan baginya jalan menuju surga." (HR. Muslim) LIVE Streaming: -- Youtube LIVE Event https://youtube.com/live/Nf0ldZFwzds?feature=share-- Youtube: https://youtube.com/@DiMediaTV -- Instagram: @DiMediaTV Podcast: SpotifyMasjid As-Sofia, Jl. RE. Martadinata 46-48, Kel. Ciwaringin, Kota Bogor, Phone: 0811 1226 242, IG @MasjidAsSofia Rekening Donasi:BRI 0387-01-111222-30-1 a.n. Masjid As Sofia (Operasional Masjid) BSI 7265 516 078 a.n. Masjid As Sofia (Operasional Masjid) BSI 7158 607 195 a.n. Masjid As Sofia (Infaq Kajian & Majelis Ilmu)Mari beramal jariyah bagi tersebarnya ilmu, dakwah & perjuangan dijalan Allah melalui donasi biaya operasional dan wakaf peralatan LIVE Streaming, via QRIS atau transfer ke Rekening BSI 7149 665 026 an. DiMediaTV. "Di era informasi sekarang ini penting memanfaatkan media untuk dakwah dan menghadapi opini negatif. Kita manfaatkan semua sarana dan prasana untuk menyiarkan Islam dengan baik, dan lakukan klarifikasi atau membantah jika ada fitnah terhadap Islam." (KH Didin Hafidhuddin).#DiMediaTV #masjidassofia #dimediaradio #DiMedia #AlKhansa #sahabatalkhansa #live #livestream #livestreaming #kajianbogor #kajianislami #kajianmuslimah #nasehatislami #nasehat #infokajianbogor #infokajian #infokajiansunnah #obs #obsstudio #obsstudiolive #obslivestream #obslive #hanaeliana #ustadzahhanaeliana #hipnotherapy Jadikan Dakwah Sebagai Poros dari Aktifitas kita sehari-hari sebagaimana Rasulallah SAW, oleh sebab itu jadikan video ini sebagai amal jariyah dakwah Anda juga dengan cara "Like, Comment, Save, Subscribe & Share" -----
※※本集節目感謝康軒文教事業贊助播出※※ 這集我們會談到： 1.近況更新：Fana終於從俄羅斯回臺灣了！！近期將分享歐洲之旅 2.Joe高中英文家教的gap year有多狂？？騎自行車遊歐亞大陸！ 3.亞洲父母對於「gap year」通常會有哪些說法？男女標準不同？ 4.歐洲與臺灣的治安差距有多大？哪些習慣千萬不能帶過去？ 5.近年詐騙猖獗，竟導致網友海外求助電話被拒接！？ 6.氣候變遷！同為暑假期間，歐洲、日本、台灣氣溫比一比 7.現在國中生多數表示未來不想結婚生子？？原因為何？ 8.結婚才能生子嗎？歐美未婚生子率與東亞國家比一比！！ 9.如何拯救低落的結婚率？衛福部長提出多聯誼引爭議！！ 10.育兒津貼比一比，臺灣與歐美國家社會福利差距為何？ 11.為何育兒津貼愈來愈高，年輕人卻愈來愈不想生呢？ 【背景介紹】 2025年7月臺灣出生人口遠低於死亡人口，已連續55個月出現「生不如死」的趨勢，截至2025年7月底，臺灣人口僅剩2388.8萬人，且65歲以上老年人口已占19.64%，逼近超高齡社會的標準，少子化與高齡化的同步攀升已成為刻不容緩的人口危機.…..。 請贊助我一杯咖啡，感謝您的贊助，讓我們能走得更遠、更久
Hva betyr det for Ap når Rødt og MDG blir så store? Ellers rapporterer vi fra Støre og Stoltenbergs show på Nygårdshøyden, og fra Fana der Høyre-velger i Fana gjemmer seg bak gjerdene. Og så har du ungdommen, da.
Dagens gjest: Bjarg-trenar Torbjørn Birkelund. Bjarg fossar fram – i cup og serie. I Norsk Tipping-ligaen har dei 13 poeng ned til Fana på 2. plass, i NM (2026) slo dei onsdag Sogndal 2-0.For å høre hele episoden må du ha abonnement, det skaffer du deg herEr du abonnent får du tilgang til medlemsfeeden her Hosted on Acast. See acast.com/privacy for more information.
※※本集節目感謝康軒文教事業贊助播出※※ 這集我們會談到： 1.近況更新：Fana回俄羅斯，順道進行歐洲自由行！！ 2.台灣護照到歐洲國家遊玩有多方便？入境歐盟免簽證！ 3.保加利亞在國中社會科課本僅剩下什麼部份被提及？ 4.近年來歐盟有哪些消息？何國脫歐？哪些國家加入歐元區？ 5.保加利亞為何加入歐元區？主要的原因有哪些？？ 6.加入歐元區可能會有哪些缺點？保加利亞境內反對派意見為何？ 7.加入歐元區對企業與民眾有哪些影響？為何會造成通膨？ 8.交出貨幣自主權後有哪些影響？希臘與冰島的前例為何？ 9.保加利亞加入歐元區根據的條約為何？須達到哪些標準？ 10.若根據馬斯垂克條約，台灣在各方面能否達到加入歐元區標準？ 【背景介紹】 歐洲聯盟（EU）各國財長於2025年7月8日批准保加利亞於2026年1月1日起採用歐元，讓保加利亞成為單一貨幣歐元區（Eurozone）的第21個成員國，加入歐元區可能為該國帶來更多外國觀光客和投資，但亦有許多人擔心通貨膨脹、物價上漲，重蹈過去10年其他歐元區新成員的覆轍…..。 請贊助我一杯咖啡，感謝您的贊助，讓我們能走得更遠、更久
Pedro Corzo, periodista y ex prisionero político entrevista a Ángel de Fana, quien cumplió 20 años de presidio y desde Plantados en el exilio, ayuda a los que luchan en la Isla, a sus familiares y a los presos políticos cubanos.
Reporte Urbano. Programa periodístico informativo en radio de interés general. Un recorrido por la actualidad con entrevistas, noticias, opinión, cultura, economía, información, sociedad, espectáculos, comentarios y política. Emisión Principal: Todos los viernes de 10 a 11 horas por AM 1010 y más de 50 retransmisoras en 8 países: España, Colombia, México, EEUU, Costa Rica, Chile, Uruguay, y todo el territorio argentino. Programa periodístico en radio de Roberto VILLALOBOS ATLAS, Cintia NEVES y equipo. Declarado de Interés para la Comunicación Social de la Ciudad Autónoma de Buenos Aires por la Legislatura Porteña. Distinguido por el Premio Latinoamericano "Señal Latina" y por el Premio Nacional "Reina Del Plata" en el rubro Programa Periodístico en Radio. Tags: #Información #Periodismo #Opinión #Actualidad #Entrevistas #Notas #Noticias #Radio #Secciones #Política #Economía #Niños #Infancia #Oyentes #Publicidad #Derecho #DDHH #Cultura #Educación #Vecinos #AyudaSocial #Solidaridad #Salud #Apoyo #Amor #Felicidad, #Efemérides #BolsaDeTrabajo #DadoresDeSangre #Campañas #Historias #Sorteos #Nacionales #Mundiales #Locales #Provinciales #Amigos #Compañeros #Horóscopo #Comunas #Barrios #Justicia #Porteño #Amigos #Lucha #AlienaciónParental #ObstrucciónDeVínculos #ImpedimentoDeContacto #Niñas #Niños #Adolescentes #Infancia #RadioOnLine #RadioEnLínea #RobertoVillalobosAtlas #VAconvos #ReporteUrbano #RadioOrión #CintiaNeves #Ciudad #BuenosAires #Podcast #Ivoox #Spotify #TuneIn #Itunes #Radio #Entrevistas #Nota #VillalobosAtlas #Ayuda
參考書目：《不平等的錯覺》，作者：湯瑪斯・索威爾，譯者：周宜芳 這集我們會談到： 1.暑假快到了，身邊的人打算去哪些地方旅遊呢？ 2.北極圈與南極相關旅遊討論，可能的交通方式與花費為何？ 3.新竹私立小學生會互相比較嗎？在校用餐有何特色？ 4.Fana暑假返鄉(俄羅斯)後打算到歐洲哪邊旅遊？ 5.窮奢極欲近期影片，為何台、日旅遊人數落差極大？ 6.白俄羅斯適合旅遊嗎？相關的景點主要性質為何？ 7.何謂南非的「Rainbow Nation」？私立小學教了什麼？ 8.南非近年的「轉型正義」，要求白人把土地還回來合理嗎？ 9.《不平等的錯覺》書籍內容簡介，挑戰進步派價值觀！ 【背景介紹】 《不平等的錯覺》這本書是美國保守派經濟大師 湯瑪斯・索威爾的著作，作者試圖打破過度簡化的「社會正義」迷思，並揭露其背後常見的陷阱，作者認為將社會結果的差異過度簡化地歸因於單一因素的話，最終可能導致適得其反的政策結果…..。 請贊助我一杯咖啡，感謝您的贊助，讓我們能走得更遠、更久
Reporte Urbano. Programa periodístico informativo en radio de interés general. Un recorrido por la actualidad con entrevistas, noticias, opinión, cultura, economía, información, sociedad, espectáculos, comentarios y política. Emisión Principal: Todos los viernes de 10 a 11 horas por AM 1010 y más de 50 retransmisoras en 8 países: España, Colombia, México, EEUU, Costa Rica, Chile, Uruguay, y todo el territorio argentino. Programa periodístico en radio de Roberto VILLALOBOS ATLAS, Cintia NEVES y equipo. Declarado de Interés para la Comunicación Social de la Ciudad Autónoma de Buenos Aires por la Legislatura Porteña. Distinguido por el Premio Latinoamericano "Señal Latina" y por el Premio Nacional "Reina Del Plata" en el rubro Programa Periodístico en Radio. Tags: #Información #Periodismo #Opinión #Actualidad #Entrevistas #Notas #Noticias #Radio #Secciones #Política #Economía #Niños #Infancia #Oyentes #Publicidad #Derecho #DDHH #Cultura #Educación #Vecinos #AyudaSocial #Solidaridad #Salud #Apoyo #Amor #Felicidad, #Efemérides #BolsaDeTrabajo #DadoresDeSangre #Campañas #Historias #Sorteos #Nacionales #Mundiales #Locales #Provinciales #Amigos #Compañeros #Horóscopo #Comunas #Barrios #Justicia #Porteño #Amigos #Lucha #AlienaciónParental #ObstrucciónDeVínculos #ImpedimentoDeContacto #Niñas #Niños #Adolescentes #Infancia #RadioOnLine #RadioEnLínea #RobertoVillalobosAtlas #VAconvos #ReporteUrbano #RadioOrión #CintiaNeves #Ciudad #BuenosAires #Podcast #Ivoox #Spotify #TuneIn #Itunes #Radio #Entrevistas #Nota #VillalobosAtlas #Ayuda
The Strictly The Best Bouyon Mix Vol.1 by DJayCee of team Haitian All-StarZ features the sound of Dominica Bouyon music. This infectious genre, straight out of Dominica, is shaking up the global scene. The 2-hour mix is filled with high-energy vibes from start to finish. Song from the following artist: Ridge, Problem Child, Motto, GBM Nutron, HollyG, Asa Bantan, Signal Band, Trilla-G, D0 Production, Fana, Bouzin, Fada, LitleBoy, Reo, LeJuh, hunter, Jab King, litleboy lsbeats767, Klassik Frescobar, blakout prestige, Gootay Wood, Trev Li, TK International, Totally Spice's and many more. {More Music Less Talk}.......Make sure to follow DJayCee on IG: @DJayCeeNYC and @Haitian_All_StarZ
The Strictly The Best Bouyon Mix Vol.1 by DJayCee of team Haitian All-StarZ features the sound of Dominica Bouyon music. This infectious genre, straight out of Dominica, is shaking up the global scene. The 2-hour mix is filled with high-energy vibes from start to finish. Song from the following artist: Ridge, Problem Child, Motto, GBM Nutron, HollyG, Asa Bantan, Signal Band, Trilla-G, D0 Production, Fana, Bouzin, Fada, LitleBoy, Reo, LeJuh, hunter, Jab King, litleboy lsbeats767, Klassik Frescobar, blakout prestige, Gootay Wood, Trev Li, TK International, Totally Spice's and many more. {More Music Less Talk}.......Make sure to follow DJayCee on IG: @DJayCeeNYC and @Haitian_All_StarZ
E le o lagolagoina e le minisita o leoleo i Samoa, Faualo Harry Schuster, le tau'aveina e leoleo i le atunu'u o fana i taimi o fa'atino ai o latou tiute.
E le o lagolagoina e le minisita o leoleo i Samoa, Faualo Harry Schuster, le tau'aveina e leoleo i le atunu'u o fana i taimi o fa'atino ai o latou tiute.
Card Talk with Mrs. Doc April 2nd, 2025 brings Bowman Chrome University Basketball, Panini Select Baseball, Vintage Onyx, and Topps Inception Football!
Innovating Food Allergy Care: How Nursing Leadership and Technology Are Transforming Patient Outcomes Join Dr. Olga Kagan, founder of the Food Allergy Nursing Association (FANA), as she shares insights on revolutionizing food allergy care through nursing innovation, technology, and evidence-based practice. Learn how FANA is empowering nurses to lead transformative change in this critical healthcare subspecialty while improving patient outcomes and quality of life. • Discover how nursing leadership is revolutionizing food allergy care through evidence-based practice • Learn strategies for implementing innovative, technology-driven care models in specialty nursing • Understand the impact of nurse-led research and education on patient outcomes in food allergy management To stream our Station live 24/7 visit www.HealthcareNOWRadio.com or ask your Smart Device to “….Play Healthcare NOW Radio”. Find all of our network podcasts on your favorite podcast platforms and be sure to subscribe and like us. Learn more at www.healthcarenowradio.com/listen
Har fått tidenes mest herlige og udugelige hund som spiser oss ut av det meste. Usikker på om han har noen som helst tanker utenom å tygge og spise på alt. Men at det finnes mennesker som ikke hører sine egne tanker, er blitt evig fascinerende og blir mer og mer fokusert på. Så snakker om det, om det elendige språket vi alle kan, engelsk. Om hvor tullete mange kinesere og indere det er. Tungeknekkere. Bittelitt Musk. Og litt annet!Mitt nye show “Tenker Tanker” er ute for salg nå! https://www.ticketmaster.no/artist/christoffer-schjelderup-billetter/983426Billetter til Showet på 5071 i Loddefjord 28. mars kommer snart...Ekstrashow med Jan Tore Kristoffersen der vi tester stoff 2. april i Fana: https://www.ticketmaster.no/event/christoffer-schjeldrup-og-jan-tore-kristoffersen-tester-stoff-tickets/234377091Se hele Specialen "Tro, Hat & Ærlighet" her https://youtu.be/bXPbyBUK3HAFølg meg på facebook: https://www.facebook.com/standupchristofferTwitter: https://twitter.com/CSchjelderupInstagram: https://www.instagram.com/christofferschjelderupTikTok: https://www.tiktok.com/@christofferschjelderup Hosted on Acast. See acast.com/privacy for more information.
Lekte dere "Kyss, Klapp og Klem" på barneskolen og hva f--n var klappet? Er det en internasjonal greie?! Og hva er dine tanker om Luigi Mangione og er han bedre eller verre enn broren til Mario? Det fjases over en lav sko og det kommer snarlig to bonusepisoder på Patreon, så hiv deg gjerne med der.Og kom deg på show! Skal være med på Varmere Våtere Villere-festivalen i Bergen i morgen(fredag den FJORTENDE!!! mars) på Rebel https://ticketco.events/no/nb?pattern=apokalypsen%C3%A5vvvSkal også stikke innom å gjøre et sett på klubbkvelden til Standupbergen https://www.ticketmaster.no/event/klubbkveld-med-stand-up-bergen-tickets/2028756499?language=en-usJeg og Jan Tore skal teste stoff i Fana onsdag 2. april og har satt opp ekstrashow 18:00 - https://www.ticketmaster.no/event/christoffer-schjeldrup-og-jan-tore-kristoffersen-tester-stoff-tickets/234377091Doug Stanhope kommer på Forum Scene og jeg skal varme opp: https://www.ticketmaster.no/event/doug-stanhope-out-of-hibernation-tickets/1480973877?language=en-usMitt nye show “Tenker Tanker” er ute for salg nå! https://www.ticketmaster.no/artist/christoffer-schjelderup-billetter/983426Bli endel av min Patreon her: https://www.patreon.com/skamfrelst Hosted on Acast. See acast.com/privacy for more information.
Hace 50 años que se grabó en Johannesburgo este disco del grupo sudafricano Themba ahora reeditado y del que suenan los cortes 'Themba themba' y 'Fana fana'. Del disco brasileño de la pianista canadiense Rosnes, 'Crossing paths', 'Pra dizer adeus' de Edu Lobo -con la voz del propio Edu-, 'Essa mulher' de Joyce Moreno y Ana Terra -con la voz de Joyce-, 'Trilhos urbano' de Caetano Veloso y 'Amor até o fim' de Gilberto Gil. Y Kurt Elling, el cantante de Chicago, acompañado por el pianista Sullivan Fortner en 'Ana Maria', de Wayne Shorter, y por el pianista Joey Calderazzo en 'Lost in the stars' de Kurt Weill y Maxwell Anderson y 'Stars (Endless stars)' de Fred Hersch y Norma Winstone. Abren la sesión Carlos Malta y Pife Muderno con 'Lero lero' de su disco 'Edu pife' dedicado a Edu Lobo.Escuchar audio
Kjenner du til Streisand-effekten? For nå har vi en historisk mulighet til å fornorske det uttrykket, og hvis du ikke aner hva jeg snakker om så anbefaler jeg voldelig å få med deg siste episode av den ikke i nærheten av prisvinnende podcasten Skamfrelst - norges første humorpodcast fra en av norges mest utrente komikere. Og hvis du vet hva jeg snakker om så anbefales den enda mer!Og hvis du vil på show med Jan Tore og meg i Fana så finner du billetter her: https://www.ticketmaster.no/event/christoffer-schjeldrup-og-jan-tore-kristoffersen-tester-stoff-billetter/1662416664Mitt nye show “Tenker Tanker” er ute for salg nå! https://www.ticketmaster.no/artist/christoffer-schjelderup-billetter/983426Se hele Specialen "Tro, Hat & Ærlighet" her https://youtu.be/bXPbyBUK3HABli endel av min Patreon her: https://www.patreon.com/skamfrelstFølg meg på facebook: https://www.facebook.com/standupchristofferTwitter: https://twitter.com/CSchjelderupInstagram: https://www.instagram.com/christofferschjelderupTikTok: https://www.tiktok.com/@christofferschjelderup Hosted on Acast. See acast.com/privacy for more information.
Oscaren har vært, og Norge fikk sin andre statuett. Kunne blitt mer, men tidligere Hotel Cæsar-skuespiller Mona Fastvold og ektemannen tapte på målstreken for Sean Baker, som tok en Walt Disney og vant fire oscars på en kveld. Gal Gadot kom også litt i fokus, og jeg snakker om det og snøhvit og har masse betraktninger på hollywoodfilmens store aften!Billetter til JTK og meg som tester stoff i Fana: https://www.ticketmaster.no/event/christoffer-schjeldrup-og-jan-tore-kristoffersen-tester-stoff-tickets/1662416664 Hosted on Acast. See acast.com/privacy for more information.
A fluffy episode to chase away some of the blues, whether it be just winter griping or something more serious. Take care of each other and stay safe, everyone! Tune in to hear Ash reconnect with his Snorlax over another Snorlax, some great wordplay and not so gret wordplay, and a tale of people and pokemon working together!
"Un sancerre de Bourgogne SVP". C'est ce qu'on appelle en sommellerie "un briseur de rêves", à savoir un client de grande table qui, sûr de lui, étale au grand jour son ignorance.Pour aborder ce thème et pour bien démarrer cette année 2025, Paul-Louis Coudoumié, sommelier que j'avais déjà reçu dans 20 Divin en 2022 (épisode #35 sur le marché Gris), et créateur de carte de vins pour des tables étoilées, m'a invité à déguster les plats concoctés par ses amis, le chef Gabriel Gras Fernandez et le chef pâtissier Jorice Sardain dans leur restaurant parisien «Fana».Gabriel, formé chez Michel Sarran, Jean-Pierre Vigato et Christain Le Squer, et Jorice, qui a travaillé chez Nicolas Bernardé puis Cédric Grolet au Meurice, se sont rencontrés au Bistrot du 11 à Versailles avant de créer « Fana », ouvert en mai dernier dans le 18ème à Paris.A travers trois belles cuvées sélectionnées par Paul-Louis, nous allons découvrir les plats signature de ce restaurant convivial et revenir sur ces briseurs de rêve, qui ont jalonné le parcours de ces 3 compères.Bonne dégustation
Anti-amyloid therapies provide the first FDA-approved option to alter AD pathology, but an understanding of overall utility and value to patients remains in its infancy. In this episode, Teshamae Monteith, MD, FAAN, speaks with David S. Geldmacher, MD, FACP, FANA, author of the article “Treatment of Alzheimer Disease” in the Continuum® December 2024 Dementia issue. Dr. Monteith is the associate editor of Continuum® Audio and an associate professor of clinical neurology at the University of Miami Miller School of Medicine in Miami, Florida. Dr. Geldmacher is a professor and Warren Family Endowed Chair in Neurology and the director of the Division of Cognitive and Behavioral Neurology, Department of Neurology, Marnix E. Heersink School of Medicine at the University of Alabama at Birmingham in Birmingham, Alabama. Additional Resources Read the article: Treatment of Alzheimer Disease Subscribe to Continuum: shop.lww.com/Continuum Earn CME (available only to AAN members): continpub.com/AudioCME Continuum® Aloud (verbatim audio-book style recordings of articles available only to Continuum® subscribers): continpub.com/Aloud More about the American Academy of Neurology: aan.com Social Media facebook.com/continuumcme @ContinuumAAN Host: @headacheMD Transcript Full interview transcript available here Dr Jones: This is Dr Lyell Jones, Editor-in-Chief of Continuum, the premier topic-based neurology clinical review and CME journal from the American Academy of Neurology. Thank you for joining us on Continuum Audio, which features conversations with Continuum's guest editors and authors who are the leading experts in their fields. Subscribers to the Continuum journal can read the full article or listen to verbatim recordings of the article and have access to exclusive interviews not featured on the podcast. Please visit the link in the episode notes for more information on the article, subscribing to the journal, and how to get CME. Dr Monteith: This is Dr Teshamae Monteith. Today, I'm interviewing Dr David Geldmacher about his article on treatment of Alzheimer's disease, which appears in the December 2024 Continuum issue on dementia. Welcome to our podcast, Dr Geldmacher. How are you? Dr Geldmacher: I'm very well, thank you. It's a pleasure to be here. Dr Monteith: Yeah. So, why don't you introduce yourself to our audience? Dr Geldmacher: Sure. I'm David Geldmacher. I'm a professor of neurology at the University of Alabama in Birmingham and I lead the division of Cognitive and Behavioral Neurology. Dr Monteith: So, I'm really excited about this, to personally learn, and I know that or neurology community is also really excited about this interview. So, why don't we start off with your main objective. Dr Geldmacher: So, my main goal in the article was to review the FDA-approved pharmacologic treatments for dementia. There's lots of ways of thinking about treatment of dementia; psychosocial, caregiver support, and so forth. But I really wanted to focus on the issues of drug treatment because that's what has been our backbone for a long time and now has recently expanded. Dr Monteith: Why don't we talk a little bit about, first of all, the boom in the field? What's that been like? Dr Geldmacher: So, the big change in the field is over the last several years, we've had treatments become available that actually attack the underlying Alzheimer pathology, and that's new and different. For decades, we've been able to treat the symptoms of the disease, but this is the first time we've really been able to get to the root of the pathology and look toward removing amyloid plaques from the brain. Dr Monteith: Let's step back a little bit and talk about the framework of diagnosis and how that leads into the therapeutic potential. I know you're going to dive into some of the biologics, but we should probably talk about the kind of holistic approach to considering the diagnosis. Dr Geldmacher: Sure. So, you know, when someone comes to the clinic with memory complaints, our question we have to ask is, is this neurologic origin, a structural origin like Alzheimer's disease or vascular dementia? Are there complicating factors, the software issues of mood disorders and sleep disorders and pain that can all magnify those symptoms? The clinical reasoning is a critical part of that, but in Alzheimer's disease, typically the problems revolve around difficulty forming new memories of events and activities, the episodic memory. And then it's often accompanied by changes in word finding and semantic knowledge. And those are the things that we look for in the clinic to really point toward an AD diagnosis. And then we support it with exclusion of other causes through blood work and identification of patterns of brain atrophy on MRI. And then most recently in the last couple of years, we've been able to add to that molecular imaging for amyloid with PET scans as well as, most recently, blood-based biomarkers for Alzheimer's pathology. So, it's really been a revolution in the diagnosis over these last several years. Dr Monteith: And when approaching patients or populations of individuals, there seems to be a real full spectrum with looking at the societal burden, the biological impact, of course, risk factors of primary prevention, and now this whole area of brain health and secondary prevention. How do you kind of tie all of this together when talking to patients and family members? Dr Geldmacher: Sure. So, the approaches for brain health apply to everyone. In basically every clinic visited, our brain aging and memory clinic, we reviewed lifestyle approaches to brain health like regular physical exercise, healthy diet, cognitive and social stimulation. And those are fundamental to the approach to everyone, whether they have cognitive impairments that are measurable or not. These are all things that are good for our brain health. And then, you know, focusing on the vascular risk factors in particular and working with the patient and their primary care team to ensure that lipids and blood sugar and blood pressure are all in good healthy ranges and being appropriately treated. Dr Monteith: You know, there's this kind of whole considerations of clinically meaningful endpoints and clinical trials, and even when we're talking to our patients. What would you say the field has kind of identified has the best endpoints in helping patients? Would you call it impaired daily function? Is that like the best hard endpoint? Obviously, there are other things such as caregiver burden, but you know, how do you approach assessing patients? Dr Geldmacher: Defining the endpoints is very difficult. Typically, if we talk to patients and their families, they would like to have better memory or improve memory. How that applies in everyday life actually is daily function. And so, we focus very much on daily function. And when I talk about our therapies, whether they're symptomatic therapies or the new disease-modifying therapies, I really talk about maintenance of function and delays and decline or slowing of decline, helping to foster the person's independence in the activities that they have and be able to sustain that over the longer term. Dr Monteith: And when thinking about diagnosis- and we're going to get into treatments, but when thinking about the diagnosis, and of course, it's full-spectrum from mild cognitive impairment to moderate and severe forms of dementia, but who should have CSF testing and PET imaging? Obviously, these are invasive, somewhat invasive and expensive tests. Should all people that walk in the door that have memory complaints? How do you stratify who should have tests? Dr Geldmacher: I think about this in a big funnel, basically, and the starting point of the funnel, of course, is the person with memory complaints. Then there's that neurologic reasoning. Are these memory complaints consistent with what we expect from the anatomy of Alzheimer's disease, with atrophy in in the hippocampus and temporal lobe? Do they have episodic memory loss or not? That first step is really trying to characterize, do the clinical patterns act like those of Alzheimer's disease or not? And then we follow the Academy of Neurology guidelines, looking for reversible sources of cognitive decline, things like B12 deficiency and depression, sleep disorders and the like, and try to exclude those. We start with structural imaging with everyone, and MRI, typically, that will help us understand vascular burden and patterns of atrophy, looking for things like mesial temporal atrophy or precuneus atrophy that are characteristic of Alzheimer's disease. If those things are all pointing in the direction of AD as opposed to something else, then typically before moving on to CSF or PET scan, we will use blood-based biomarkers, which are one of the big changes in the field in the last year or so, and there are now multiple panels of these available. The downside is they are typically not covered by insurance. On the other hand, they can really help us identify who is likely to have a positive PET scan or positive findings on CSF. We start to provide that counseling and information to the patient before they get to those more definitive tests. We can push people in the other direction. We can say, your blood-based biomarkers are negative or do not indicate AD as the most likely source of your condition now, so let's treat other things. Let's see what else we can focus on. The blood-based biomarkers are now, in our clinic at least, the critical choke point between the routine workout that we've always done on everyone and then the more advanced workup of proving amyloid pathology with CSF or a PET scan. Dr Monteith: How sensitive are those blood biomarkers and how early are they positive? Dr Geldmacher: The sensitivity is generally pretty good, in the ninety plus percent range on average and it depends on which panel. And as you point out, when in the course of symptoms that they're done, we know that they become positive and presymptomatic or asymptomatic people. We're using these kinds of markers to screen people for prevention trials. So, I think when someone is symptomatic, they're a good indicator of the presence or absence of AD pathology. Now that doesn't mean the AD pathology is the sole cause of their symptoms. And so, we still need to think about those other things like sleep and mood and so forth. But they do point us in the in the direction of Alzheimer's change. Dr Monteith: So why don't we talk about some of the more standard older treatments, and it's also important to leave with kind of some rational approach to when we start and what should we be counseling our patients on. So why don't we start with the older, you know, choline esterase inhibitors and then some of the MDA- I guess there's only one modulator, SEPTA modulator. Dr Geldmacher: So, I've been really fortunate in my career span, the time from the first of those symptomatic agents reaching the market in 1993 to seeing the disease modifying drugs enter the market now. I think most neurologists actually have entered practice after those clinical trials of the colon esterase inhibitors were published. So, one of my goals in this article was to review that primary data and what can we expect from those symptomatic drugs. We know that they are inconsistently effective in mild cognitive impairment, and the Academy of Neurology guidelines says there is not strong evidence to use them in mild cognitive impairment. But in mild AD and beyond, the cholinesterase inhibitors provide meaningful benefits. They delay decline, they can delay nursing home placement. They reduce overall costs of care. So, I think they provide real value. So, in the article I have reviewed what the data looked like on those. My approach is to start with oral Donepezil at five milligrams and increase it to ten in everyone who tolerates the five. If for whatever reason the oral Donepezil is not well tolerated, I'll switch to transdermal rivastigmine to help improve tolerability. There are very few head to head comparisons, but nothing suggests that one of the cholinesterase inhibitors is superior to the other for clinical outcomes, and there's no evidence to support conjoint use of more than one at a time. Should someone be showing decline then on typical cholinesterase inhibitor therapy - and people will, it's often delayed, but the decline will reemerge - then I will add the NMDA receptor, a modulator memantine and titrate that up to full dosing, either 10 mg twice a day for the conventional release or 22 mg extended release. And at that point we're sort of on maximal pharmacologic therapy for Alzheimer's disease. These agents can provide some benefit in other conditions, they're off-label except for Lewy body disease where rivastigmine is labeled. But they can provide benefit across different conditions. And there's some preliminary data, for instance, of acetylcholinesterase inhibitors being helpful in vascular cognitive impairment. So, I will use them, but I expect the greatest response when someone really does follow the patterns of Alzheimer's disease. Dr Monteith: And you have a great chart, by the way, and nice figures looking at some of the meta-analyses on cognitive outcomes as well as functional outcomes. So, thank you for that. Dr Geldmacher: In general, all of those tables favor treatment over placebo in the domains of cognition, daily function, neuropsychiatric symptoms. And it's that consistency of result that lets me know that we really are seeing a drug effect, that it's not a class effect with those, that we really are helping our patients. It's not like some studies are positive and some are negative. They are very consistently positive. Small magnitude, but consistently positive. Dr Monteith: And I know we have a lot of patients coming in where, at least, their caregivers are complaining about agitation, and sleep is also a problem for others. And so how do you help that patient? I know you have a good algorithm that also you included in your article, but why don't you summarize how we should approach these symptoms? Dr Geldmacher: Sure. So, for nonpsychotic agitation, you know, just restlessness, wandering, pacing and so forth, my first choice is an off-label use of citalopram. And there is good clinical trials evidence to support that. if someone has psychotic agitation that is with delusions or hallucinations and so forth, I think we do need to move to the antipsychotic drugs. And the one drug that is now approved for treatment of agitation and Alzheimer's disease does fall into that antipsychotic category, along with its various black box warnings - and that's brexpiprazole. For many of our patients, getting coverage for that agent is difficult. It's not on many formularies. So, it is something I progress toward rather than start with. Similarly, for sleep, there is one approved agent for sleep, that's a dual orexin agonist. And it shows effectiveness, but can have some negative cognitive effects, and so I tend not to start with that either. My first choice when sleep is the primary issue for our patients with dementia is trazodone, and there are some small, limited studies for it's off-label used to enhance sleep. It's safe, inexpensive, often effective, and therefore it's my first choice. Dr Monteith: So, now let's get into the big conversations that everyone is having. Let's talk about the newer disease modifying anti amyloid therapies. Give us a summary dating back 2021 probably, although we can hold the preclinical work, but let's talk about what is available to our patients. Dr Geldmacher: Sure. And the development of anti-amyloid therapies goes all the way back to 1999. So, it's a pretty long course to get us to where we are today. Dr Monteith: Yeah, that's why we limited that. Dr Geldmacher: With that first approved agent with aducanumab in 2021, it received a limited or accelerated approval in FDA parlance. These agents, the aducanumab, lecanemab and donanemab, all approved, are known to remove amyloid pathology from the brain as measured by CSF and/or BIPET. They are amyloid lowering therapies, often called disease-modifying therapies. And across the agents there's some variable results. But if we look at the two with full approval, lecanemab and donanemab, they slow clinical progression by 25% to 35% on average. And that's measured by either cognitive measures or global measures or composite measures, but it's pretty consistent in that range of about one-third slowing. That makes it really difficult to discern in an individual patient, though, because there's so much variability in the progression of the disease already that it can be difficult to tell in one person that these drugs are working. They're also complex to use, so there's a qualification process that involves MRI to exclude things like a high tendency toward hemorrhage. It includes genetic testing for papal E4 status to help us understand the risk for complication, and then once-monthly or twice-monthly infusions with standardized schedule for MRI scanning. So, there's a lot that goes into managing these agents. And they are expensive, and we don't yet know their cost effectiveness. The cost effectiveness of the cholinesterase inhibitors was questioned when they first came out back in the 1990s, and it took five or ten years to really understand that they provided benefit to society and to individuals in those domains of quality of life and return on investment. And we're still learning about that with the disease modifying therapies. Dr Monteith: So, two questions. One, the case that you presented was an individual having symptoms and kind of voiced their desire to be on these therapies. So, people are going to be asking, coming to clinic asking and then of course, they're going to be people that you select out. So, how do you make that decision to recommend this treatment for patients given the potential risk? Dr Geldmacher: We've got some really good guidance from appropriate use recommendation papers for aducanumab and lecanemab, and I'm expecting one from donanemab fairly soon. But the key is to identify individualized risks, and that involves knowing their APOE4 status, knowing their- whether they've had microhemorrhages in the brain previously, and then documenting that they really do have amyloid pathology with something like PET scan to establish those baselines. I talk to people about the burden of twice-monthly infusions or, now with donanemab, once-monthly infusions. And for instance, for someone who's got a working caregiver, getting to an infusion center twice a month can be a significant burden. And then if there are complications, frequent MRI scans and so forth. So, we talk about the burden of entering into this therapeutic pathway. The reality is that people who are qualified generally want it. I have relatively few folks who have said, no, these risks are more than I'm willing to accept. For decades my patients have said, anything you can do to slow this down, I'm willing to try. And now we're seeing that translated to reality with people willing to accept high-risk, high-cost treatments with the chance of slowing their individual progression. Dr Monteith: And how do you select between the two treatments? Dr Geldmacher: So far that's been easy because donanemab's not readily available. Dr Monteith: Outside of clinical trials, right? Dr Geldmacher: Exactly. For prescription use, it's coming in - the first cases have now been infused - but it's not generally available. Nonetheless, what I will do for patients in this is look at the risk tables. So donanemab appears to have in general some higher rates of the Aria complications, amyloid-related imaging anomalies, and some people are going to be more risk tolerant of that for the payoff of potentially faster response. The donanemab trials restructured that. They did their first assessment of effectiveness. I had amyloid removal at six months and a significant proportion of people were eligible to discontinue treatment at six months because their amyloid was below treatable thresholds. So higher risk, perhaps faster action and fewer infusions for donanemab. Lecanemab we have more direct experience with, and between the two of them, the eighteen month outcomes are pretty much the same and indistinguishable. So are we in it for a quick hit, or are we in it for the long race? And different patients and different families will have differing opinions on where they want to accept that risk and burden and so forth. But so far, the data don't indicate a lot of difference in their longer-term outcomes. We still have plenty to learn. Dr Monteith: And so, it sounds like, as you mentioned, we're looking at eighteen months out for kind of a hard outcome, and that there is a lot of variability in response rate. How are you tracking patients- you know about the imaging, so just in terms of clinical outcomes and efficacy? Dr Geldmacher: Sure. So, for Medicare to reimburse on these treatments, people need to be enrolled in a registry program - and there are several of these, CMS runs one of their own. But the requirement for that is, every six months, to do cognitive and functional outcomes through the first two years. Cognitive outcomes are up to the clinician, but things like the mini mental state exam, the MoCA, are appropriate. In our own program, we use something we developed locally called the Alabama Brief Cognitive Screener. As for the cognitive outcomes and then for functional, we use an instrument called the General Activities of Daily Living Scale, but there are many other ADL scales that could be used as well. CMS does not mandate specific tests. Since the progression of the disease is variable to begin with, we don't really know how to interpret these results in reference to whether the drug is working, but I can tell a patient or a family member, your scores are stable, or, you have a decline of three points in this test. That's typical for this duration of illness. But there isn't a good way to know whether the drug is working in this person at this time, at least with our current levels of data. Dr Monteith: So, I think we have to talk about health equity, and it sounds like Medicare is reimbursing for some of us. We look at different socioeconomic backgrounds, educational backgrounds, race, ethnicity. Not everyone is aware of these treatments. So, how do we get more patients to become aware of these treatments? And how do we get them to more people to help people? Dr Geldmacher: Yeah, I mean, that's- it's a major, major issue of inequity in our population. We've done some work at UAB looking at the flow of members of minority communities into memory clinics. So, we know that the overall population of, and I'll choose, for an example, blacks and African Americans, that they are represented a much higher rate in our overall UAB treatment population than they are in our memory clinic population. So, they're not even getting to us in the specialty clinic at the same rates as other segments of our population. We also know that blacks and African Americans in our population are not receiving PET scans as often as the overall treatment population. So yes, there are real, real problems with access. There are cultural issues behind this as well. And in many communities, a change in cognition, a loss of memory is an expected part of the aging process rather than recognized as a disease. So, people who come to us from minority communities are often further along in the course of cognitive and functional decline and beyond the point where they might qualify for the disease-modifying therapies, where early AD is the sort of defining boundary. So, I think more awareness and more screening in primary care settings, perhaps more community outreach to let people know that changes in memory that affect daily function are not normal as part of the aging process and should be evaluated for intervention. So, there's lots of places in our healthcare community where we could foster better outreach, better knowledge to get more folks access to the medicines. And this is before we even get to cost. Dr Monteith: Yeah, yeah. And obviously, there's some stigma as well. Dr Geldmacher: That's right. Dr Monteith: Really recognizing what the issues are and diving and asking those questions and funding research that asks those questions, as you mentioned, is really important. And then you have also a nice area where, you know, looking on the impact of treatments on caregiver-related outcomes, and of course ultimately want to keep patients out of nursing homes and prevent death. And so, can you talk a little bit about that? And, you know, mainly the caregiver burden. Dr Geldmacher: So, my research in that area goes back a long way now. But I learned early in the course of therapy that many times the outcome that the family is noticing for symptomatic therapies is not a change in the patient's memory per se, but that there is less work involved in the caregiving. Less time is spent in direct caregiving roles. The patient may shadow less and because they have better independent cognition. I remember one family member once told me, the medicine you started is a godsend because now I can go to the bathroom by myself and he's not pounding on the door saying where are you, where are you. He's able to recall long enough that I'm in the bathroom that I have that moment of privacy. That was very meaningful to me to hear that. So. Dr Monteith: Cool. So why don't you just help us wrap this up and just give us, like, three main takeaway points that we should be getting out of your article? Dr Geldmacher: The three points that I would emphasize from my article is that the symptomatic therapies provide meaningful benefits and measurable, consistent, meaningful benefits. The second is that those benefits extend beyond things like cognitive test scores and into things like caregiver well-being and maintenance of independence in the home environment. And the third is that the disease-modifying therapies are an exciting opportunity to modify the pathology, but we still are learning about their cost effectiveness and their long-term benefit both to individuals and to society. But the only way we're going to learn that is by using them. And that was the experience that we gained from the symptomatic therapies that took use in the community for years before we really began to understand their true value. Dr Monteith: Thank you. That was excellent. And I put you on the spot, too. Dr Geldmacher: No problem. Dr Monteith: Again, today I've been interviewing Dr David Geldmacher, whose article on treatment of Alzheimer's disease appears in the most recent issue of Continuum on Dementia. 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 this link in the episode notes to learn more and subscribe. AAN members, you can get CME for listening to this interview by completing the evaluation at contentpub.com/AudioCME. Thank you for listening to Continuum Audio.
This content has been developed for healthcare professionals only. Patients who seek health information should consult with their physician or relevant patient advocacy groups.For the full presentation, downloadable Practice Aids, slides, and complete CME information, and to apply for credit, please visit us at PeerView.com/TEJ865. CME credit will be available until December 23, 2025.Exploring New Frontiers in Alzheimer's Disease: Early Detection, Emerging Mechanisms, and Therapeutic Advances In support of improving patient care, PVI, PeerView Institute for Medical Education, is jointly accredited by the Accreditation Council for Continuing Medical Education (ACCME), the Accreditation Council for Pharmacy Education (ACPE), and the American Nurses Credentialing Center (ANCC), to provide continuing education for the healthcare team.SupportThis activity is supported by an educational grant from Novo Nordisk Inc.Disclosure information is available at the beginning of the video presentation.
PeerView Neuroscience & Psychiatry CME/CNE/CPE Audio Podcast
This content has been developed for healthcare professionals only. Patients who seek health information should consult with their physician or relevant patient advocacy groups.For the full presentation, downloadable Practice Aids, slides, and complete CME information, and to apply for credit, please visit us at PeerView.com/TEJ865. CME credit will be available until December 23, 2025.Exploring New Frontiers in Alzheimer's Disease: Early Detection, Emerging Mechanisms, and Therapeutic Advances In support of improving patient care, PVI, PeerView Institute for Medical Education, is jointly accredited by the Accreditation Council for Continuing Medical Education (ACCME), the Accreditation Council for Pharmacy Education (ACPE), and the American Nurses Credentialing Center (ANCC), to provide continuing education for the healthcare team.SupportThis activity is supported by an educational grant from Novo Nordisk Inc.Disclosure information is available at the beginning of the video presentation.
PeerView Neuroscience & Psychiatry CME/CNE/CPE Video Podcast
This content has been developed for healthcare professionals only. Patients who seek health information should consult with their physician or relevant patient advocacy groups.For the full presentation, downloadable Practice Aids, slides, and complete CME information, and to apply for credit, please visit us at PeerView.com/TEJ865. CME credit will be available until December 23, 2025.Exploring New Frontiers in Alzheimer's Disease: Early Detection, Emerging Mechanisms, and Therapeutic Advances In support of improving patient care, PVI, PeerView Institute for Medical Education, is jointly accredited by the Accreditation Council for Continuing Medical Education (ACCME), the Accreditation Council for Pharmacy Education (ACPE), and the American Nurses Credentialing Center (ANCC), to provide continuing education for the healthcare team.SupportThis activity is supported by an educational grant from Novo Nordisk Inc.Disclosure information is available at the beginning of the video presentation.
In this episode , we dive into the chilling world of the 2017 horror film "The Ritual" and its dark themes of ancient worship and sacrifice. Inspired by the movie's unsettling lore, we explore real-life stories of rituals and mysterious disappearances. We uncover the shocking serial killings in Fana, Mali, and the eerie disappearance of Dennis Martin, weaving in tales of modern and historical rituals that blur the line between superstition and horror. To balance the darkness, we also delve into the bizarre true story of the infamous “Cocaine Bear” Chapters 00:00 Opening 00:35 Intro and Announcements 1:55 Ritual review: 1:55 7:07 Ancient Rituals 11:58 False accusations of sacrifice 12:51 Vikings 13:39 Modern sacrifice 14:34 Fana Serial Killer 18:15 Missing in the woods 19:00 Denis Martin 23:04 Final Fright - Cocaine Bear 24:24 Closing Resources https://en.natmus.dk/historical-knowledge/denmark/prehistoric-period-until-1050-ad/the-viking-age/religion-magic-death-and-rituals/the-viking-blot-sacrifices/#:~:text=It%20was%20always%20important%20for,fertility%20or%20luck%20in%20battle. https://nypost.com/2020/07/04/why-hundreds-of-people-vanish-into-the-american-wilderness/ https://nypost.com/2023/06/14/us-national-park-visitors-disappearing-without-a-trace/ https://www.britannica.com/topic/human-sacrifice https://www.oxfordbibliographies.com/display/document/obo-9780199791231/obo-9780199791231-0272.xml#:~:text=As for texts about burning,as punishment of the parents. https://www.jstor.org/stable/219450 https://muse.jhu.edu/book/27519/#:~:text=One example, the Ghana Asante,in order to guarantee victory. https://en.wikipedia.org/wiki/Dahomey#Religion https://biblereadingarcheology.com/2016/05/13/did-the-canaanites-sacrifice-their-children/ https://www.ox.ac.uk/news/2014-01-23-ancient-carthaginians-really-did-sacrifice-their-children https://www.ancient-egypt.org/from-a-to-z/h/human-sacrifice.html#:~:text=When examining human sacrifice, the,is therefore not discussed here. https://www.youregypttours.com/egypt-tours-blog/sacrifice-in-ancient-egypt https://en.wikipedia.org/wiki/Disappearance_of_Dennis_Martin#:~:text=Dennis Lloyd Martin (born June,(150 km2) area. https://www.wbir.com/article/news/special-reports/the-vanished/the-vanished-dennis-martin/51-dea1f82d-4bfa-470b-9a69-5b2c603c1510
Na saunoa le sui tauva o le Democratic Party mo le tofi sui peresitene, Tim Walz, ina ua toe tupu mai se osofa'iga i se a'oga i Amerika ua tafanaina ma maliliu ai tamaiti a'oga, o ia ua iso i le tupu pea o nei osofa'iga, ma lau mai le manatua i talosaga o e ua maliliu ma aiga. Ua tatau ona faia se faai'uga faaletulafono i fana.
E 12 tausaga le matua o se tamaititi na fanaina ma maliu ai i se nu'u i Savai'i i le faai'uga o le vaiaso na te'a nei.
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