Podcasts about Neurology

In part two of this two-part series, Dr. Stacey Clardy and Dr. Walter Koroshetz discuss ways to empower professionals in the fields of neurology and research. 

We continue our campaign to #EndNeurophobia, with the help of Dr. Aaron Berkowitz. This time, Jeffrey presents a case of headache and diplopia to Vale and Sebastian.  Neurology DDx Schema Jeffrey Shen  Jeffrey is an academic rheumatologist whose early love for guessing TV plot twistswith his parents sparked a lifelong passion forclinical problem solving. He… Read More »Episode 419: Neurology VMR – Headache and diplopia

In part two of this two-part series, Dr. Stacey Clardy talks with Dr. Walter Koroshetz about overcoming funding challenges, the importance of rigor and reputation, unmet needs in neurology, and leveraging AI in neurology research.  Disclosures can be found at Neurology.org.  

In the first part of this two-part series, Dr. Stacey Clardy and Dr. Walter Koroshetz discuss strategies for advancing the fields of neurology and neuroscience research. 

In this week's episode, Brain & Life Podcast co-host Dr. Katy Peters is once again joined by Kristin Flanary, AKA Lady Glaucomflecken, to continue their conversation from last week. Kristin has advanced training in both cognitive neuroscience and social psychology and now is active on social media, podcasts, and comedy shows with her husband, Dr. Glaucomflecken. Kristin shares more about the term “co-survivor” and the importance of thoughtful doctor/patient communication, based on her own lived experiences. Dr. Peters is then joined by Dr. Jessica McFarlin, is an associate professor of neurology at the University of Kentucky Department of Neurology and Chief of the Division of Palliative Care who is trained in both neurocritical care medicine and palliative care medicine. Dr. McFarlin touches on the role of care partners and medical professionals when it comes to the Neurointensive Care Unit.   Additional Resources Lady Glaucomflecken What is the Difference Between Coma, Minimally Conscious State, Persistent Vegetative State, and Brain Death? How to Keep Loved Ones Safe in the Hospital   Other Brain & Life Podcast Episodes on These Topics What is an ICU and Neurologic Critical Care? Tips and a Guide for Everyone Nora McInerny on Moving Forward with Grief  Advocating for a Multiple Sclerosis Diagnosis with Comedian Kellye Howard We want to hear from you! Have a question or want to hear a topic featured on the Brain & Life Podcast? ·       Record a voicemail at 612-928-6206 ·       Email us at BLpodcast@brainandlife.org   Social Media:   Guests: Kristin Flanary @ladyglaucomflecken; Dr. Jessica McFarlin @ukadultneuro Hosts: Dr. Daniel Correa @neurodrcorrea; Dr. Katy Peters @KatyPetersMDPhD

Dr. Bakhtawar Ahmad discuss Ellen Grass the founder of the Grass Instruments Company, which played a vital role in the technological development of EEG in this women history minute. 

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

Send us a textDr. Michael Lebenstein-Gumovski, Ph.D. is Senior Scientific Officer and Neurosurgeon, in the Neurosurgery Department, of the Sklifosovsky Clinical and Research Institute for Emergency Medicine, Moscow, Russian Federation ( https://sklif.mos.ru/ ), where his team is engaged in both neurosurgical and experimental practice, conducting advanced research in the field of spinal cord injury restoration, spinal cord transplantation and head transplantation.The Sklifosovsky Institute for Emergency Medicine is a large multidisciplinary scientific and practical center dealing with problems of emergency medical care, emergency surgery, resuscitation, combined and burn trauma, emergency cardiology and acute poisoning.Since 2013, Dr. Lebenstein-Gumovski has been studying spinal cord injury, and also developing methods for restoring the full functional and morphological repair of the spinal cord.Dr. Lebenstein-Gumovski's work is aimed at studying the effect of fusogens on nervous tissue, developing new methods and techniques for treating spinal cord injury, developing methods for its resection and transplantation. The lab develops and studies various methods of neuroprotection, combining methods to achieve better results and the current focus is the study of combination fusogen-induced (PEG-chitosan, Neuro-PEG) axonal restoration of the spinal cord after its complete transection.Dr. Lebenstein-Gumovski did his doctoral studies in the Department of Neurology and Neurosurgery of the Stavropol State Medical University of the Ministry of Health of the Russian Federation.Dr. Lebenstein-Gumovski is also a Scientific Advisor to Dowell Bio, Inc. ( https://dowell.bio/ ), a start-up company developing his various technologies.Andrei Panferov is the Chief Executive Officer of Dowell Bio, Inc.  Andrei is a deep-tech entrepreneur and does the Russian-English / English-Russian translations during this episode.#MichaelLebensteinGumovski #DowellBio #SklifosovskyClinicalAndResearchInstituteForEmergencyMedicine #Neurosurgery #SpinalCordInjuryRestoration #SpinalCordTransplantation #HeadTransplantation #EmergencyMedicalCare #EmergencySurgery #Resuscitation #Trauma #SpinalCordInjury #Fusogens #PEGChitosan #Neuroscience #SergioCanavero #Chitosan #PolyethyleneGlycol #EyeTransplant #BrainTransplant #ProgressPotentialAndPossibilities #IraPastor #Podcast #Podcaster #Podcasting #ViralPodcast #STEM #Innovation #Science #Technology #ResearchSupport the show

Dr. Paige Kalika discusses the importance of embracing neurodiversity in medicine.  Show reference:  https://jamanetwork.com/journals/jama/article-abstract/2830611 

Here we review Zinc supplements as a treatment for ALS.  These are inexpensive, reasonably safe at certain doses, and are easy to acquire.  They have plausible mechanisms by which they could slow ALS progression.  However, the data from people living with ALS is not very convincing yet.

In part one of this two-part series, Dr. Stacey Clardy talks with Dr. Walter Koroshetz about recent advancements in neurology, emerging genomic therapies, the evolving understanding of long COVID, and current NINDS priorities. Disclosures can be found at Neurology.org. 

Some people living with MS adhere to a treatment plan based exclusively on what we might consider traditional medicine. Others opt for alternative treatments. And, still, others take a whole-person health approach, blending integrative medicine with traditional treatments designed to support an individual's mind and body. Dr. Lynne Shinto joins me to discuss how a whole-person health approach can transform living with MS. Dr. Shinto is a Professor of Neurology and an MS Specialist at the Center for Women's Health at Oregon Health and Science University.   We're also sharing some encouraging news about funding for the National Institutes of Health in 2026. We'll explain the research that has led to the identification of a new and quite different subtype of MS.  We'll tell you about this year's winner of the Rachel Horne Prize for Women's Research in Multiple Sclerosis. The National MS Society's virtual program, New to MS: Navigating Your Journey, takes place in just two days. We have all the details! We have a lot to talk about! Are you ready for RealTalk MS??! This Week: A whole-person health approach to MS care  :22 House Republicans reject President Trump's $20 billion cut to 2026 NIH funding  1:26 Have researchers identified a new MS subtype?  4:16 This year's winner of the Rachel Horne Prize for Women's Research in Multiple Sclerosis   8:27 We're two days away from the National MS Society's New to MS: Navigating Your Journey virtual program  9:53 Dr. Lynne Shinto discusses how taking a whole-person approach to MS care can transform your MS journey 12:04 Share this episode  31:41 Next week's episode   32:01 SHARE THIS EPISODE OF REALTALK MS Just copy this link & paste it into your text or email: https://realtalkms.com/419 ADD YOUR VOICE TO THE CONVERSATION I've always thought about the RealTalk MS podcast as a conversation. And this is your opportunity to join the conversation by sharing your feedback, questions, and suggestions for topics that we can discuss in future podcast episodes. Please shoot me an email or call the RealTalk MS Listener Hotline and share your thoughts! Email: jon@realtalkms.com Phone: (310) 526-2283 And don't forget to join us in the RealTalk MS Facebook group! LINKS If your podcast app doesn't allow you to click on these links, you'll find them in the show notes in the RealTalk MS app or at www.RealTalkMS.com PARTICIPATE: Take the Shaping Tomorrow Together Survey https://s.alchemer.com/s3/Perspectives-on-MS REGISTER: Attend the virtual Shaping Tomorrow Together meeting with the FDA https://nmss.quorum.us/event/25463 SIGN UP: Become an MS Activist https://nationalmssociety.org/advocacy STUDY: Large-Scale Online Assessment Uncovers a Distinct Multiple Sclerosis Subtype with Selective Cognitive Impairment https://nature.com/articles/s41467-025-62156-4 REGISTER: New To MS: Navigating Your Journey https://nationalmssociety.org/understanding-ms/newly-diagnosed/new-to-ms-journey Join the RealTalk MS Facebook Group https://facebook.com/groups/realtalkms Download the RealTalk MS App for iOS Devices https://itunes.apple.com/us/app/realtalk-ms/id1436917200 Download the RealTalk MS App for Android Deviceshttps://play.google.com/store/apps/details?id=tv.wizzard.android.realtalk Give RealTalk MS a rating and review http://www.realtalkms.com/review Follow RealTalk MS on Twitter, @RealTalkMS_jon, and subscribe to our newsletter at our website, RealTalkMS.com. RealTalk MS Episode 419 Guest: Dr. Lynne Shinto Privacy Policy

Dr. Bradley Ong discusses a newly FDA-approved nasal powder formulation for treating debilitating migraine attacks.

Neste episódio, vamos analisar criticamente o estudo brasileiro publicado no prestigiado periódico Neurology, que virou manchete no mundo todo ao afirmar que sete adoçantes artificiais estariam associados a declínio cognitivo acelerado.À primeira vista, parece alarmante. Mas, quando olhamos com lupa, o estudo se revela um festival de problemas metodológicos e incongruências:É observacional, baseado em questionário de frequência alimentar (FFQ), incapaz de medir miligramas de adoçantes.Foram feitas dezenas de comparações sem ajuste, terreno fértil para falsos positivos.As diferenças absolutas nas curvas são microscópicas, irrelevantes do ponto de vista clínico.Os resultados são cheios de contradições: a mesma substância aparece como “protetora” em um grupo e “prejudicial” em outro.O caso mais bizarro é o da tagatose, um adoçante que sequer é consumido no Brasil, mas que apareceu associado a declínio cognitivo porque os autores usaram uma tabela gringa de composição de alimentos.Até os polióis em miligramas, que não representam consumo real, foram parar nos gráficos como supostos vilões.No fim, o que o estudo mostra não é toxicidade universal dos adoçantes, mas sim que os usuários desses produtos já eram pessoas com mais diabetes, mais hipertensão e maior risco de declínio cognitivo desde o início. É o clássico viés por indicação.Neste episódio, vamos destrinchar cada detalhe, explicar como essas associações espúrias se formam e discutir o perigo de manchetes sensacionalistas que transformam estatística em pânico.Links relacionados:Comida Sem Filtro #27 – “Por Que O Ovo Que Te Faz Bem Hoje Te Mata Amanhã?”Comida Sem Filtro #36 – Assim Fica Difícil, BBCComida Sem Filtro #42 – A Carne QuânticaComida Sem Filtro #46 – Não Caia Em Epidemiologia Nutricional!Comida Sem Filtro #59 – Diretrizes Podem Mudar?Comida Sem Filtro #70 – Adoçantes Artificiais Aumentam Risco Cardiovascular?Comida Sem Filtro #99 – “O Mistério Do Sorvete”Comida Sem Filtro #151 – A Tortura Dos Dados – Parte 1: Os Dados Confessam O Que Você QuiserComida Sem Filtro #152 – A Tortura Dos Dados – Parte 2: Carne Vermelha No MultiversoComida Sem Filtro #153 – A Tortura Dos Dados – Parte3: O Viés De PublicaçãoComida Sem Filtro #175 – Low-Carb Causa Diabetes?Effect of Sibutramine on Cardiovascular Outcomes in Overweight and Obese SubjectsSemaglutide and Cardiovascular Outcomes in Obesity without DiabetesEffects of remote, retroactive intercessory prayer on outcomes in patients with bloodstream infection: randomised controlled trialEstamos no Instagram: ⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠Dr. Souto⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠ - ⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠Sari Fontana⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠ Para ser avisado sobre cada novo episódio e receber os links das matérias mencionadas e as referências bibliográficas por e-mail, cadastre-se gratuitamente em ⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠https://drsouto.com.br/podcast⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠"Dance of the Sugar Plum Fairy"Kevin MacLeod (incompetech.com)Licensed under Creative Commons: By Attribution 3.0⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠http://creativecommons.org/licenses/by/3.0/⁠⁠⁠⁠⁠⁠⁠

In episode 1926, Jack and Miles are joined by actor, musician, and co-host of One of Us, Fin Argus, to discuss… Trump Tried To Drown Out The Epstein Survivor Presser With Jet Flyovers…, Smartphones Are Making Your Hemorrhoids Worse, The Growth of Executive Function Coaches to Fix Our Corporation Ruined Brains and more! LIVE: Reps. Khanna, Massie hold news conference with Epstein survivors Epstein Rape Victim Was Passed on to Donald Trump by Ghislaine Maxwell Smartphones Are Making Your Hemorrhoids Worse White-collar work is breaking people's brains. Some are turning to unorthodox coaches for a fix. LISTEN: Dark Kept Secret by EXUMSee omnystudio.com/listener for privacy information.

In part two of this two-part series, Dr. Stacey Clardy and Dr. Andrew Mammen discuss what's new in the diagnosis and treatment of dermatomyositis. 

In this episode, we discuss the first-in-human gene-based therapy for Lafora disease: A landmark in Pediatric Neurogenetics. Learn more about Berge Minassian, MD 

Also, who are the vigilante group Greater Shankill patrol Angel's?

In part two of this two-part series, Dr. Stacey Clardy talks with Dr. Andrew Mammen about treatment options, real-world case studies, and future directions in myositis research.  Disclosures can be found at Neurology.org. 

In the first part of this two-part series, Dr. Stacey Clardy and Dr. Andrew Mammen discuss the advancements made over the past decade regarding HMGCR antibody-associated myositis and how to treat it. 

Most of us can agree: music is awesome. Regardless of which songs speak to you, music probably plays an important role in your life. The question is, what makes music so powerful? Why does a particular combination of sounds and rhythms grab us and affect us in the way that it does? And is it true that music can help heal patients with Alzheimer's, Parkinson's, PTSD, chronic pain, and more? To help us understand what we're learning about the neuroscience of music and how it can heal and enrich our lives, we're speaking with Daniel Levitin. He's a musician and a producer as well as a neuroscientist and bestselling author. His newest book is "I Heard There was a Secret Chord: Music As Medicine." Learn More:"I Heard There Was a Secret Chord" playlistMenon, V., & Levitin, D. J. (2005). The rewards of music listening: Response and connectivity of the mesolimbic system. NeuroImage.Menon, V. (2023). 20 years of the default mode network: A review and synthesis. Neuron.Salimpoor, V. N., et al. (2013). Interactions between the nucleus accumbens and auditory cortices predict music's reward value. Science.Wang, L., Peng, J.-l., et al. (2022). Effects of rhythmic auditory stimulation on gait and motor function in Parkinson's disease: Systematic review & meta-analysis. Frontiers in Neurology.Zumbansen, A., et al. (2014). Melodic Intonation Therapy: Back to basics for future research. Frontiers in Neurology.Moreno-Morales et al. (2020). Music therapy in the treatment of dementia: Systematic review & meta-analysis. Frontiers in Medicine.Allen, E. J., et al. (2017). Representations of pitch and timbre variation in human auditory cortex. Journal of Neuroscience.Sonos/Apple “Music Makes It Home” study (2016). "This Speaker Company Says Music Makes You Happier." Time Magazine.We want to hear from your neurons! Email us at at neuronspodcast@stanford.eduSend us a text!Thanks for listening! If you're enjoying our show, please take a moment to give us a review on your podcast app of choice and share this episode with your friends. That's how we grow as a show and bring the stories of the frontiers of neuroscience to a wider audience. Learn more about the Wu Tsai Neurosciences Institute at Stanford and follow us on Twitter, Facebook, and LinkedIn.

In this week's episode, Brain & Life Podcast co-host Dr. Katy Peters is joined by Kristin Flanary, AKA Lady Glaucomflecken. Kristin has advanced training in both cognitive neuroscience and social psychology and now is active on social media, podcasts, and comedy shows with her husband, Dr. Glaucomflecken. Kristin shares her unique perspective on the healthcare system, having been a patient, a caregiver, and a co-survivor of her husband's medical challenges, including his two cancer occurrences and a sudden cardiac arrest that led to a stay in the Neurological Intensive Care Unit. Dr. Peters is then joined by Dr. Jessica McFarlin, is an associate professor of neurology at the University of Kentucky Department of Neurology and Chief of the Division of Palliative Care who is trained in both neurocritical care medicine and palliative care medicine. Dr. McFarlin explains how Neurological Intensive Care Units provide life-saving care for patients with severe neurologic injuries, such as strokes and brain trauma. Come back next week for part two to hear more about the term “co-survivor” and the importance of thoughtful doctor/patient communication.   Additional Resources Lady Glaucomflecken What is the Difference Between Coma, Minimally Conscious State, Persistent Vegetative State, and Brain Death? How to Keep Loved Ones Safe in the Hospital   Other Brain & Life Podcast Episodes on These Topics What is an ICU and Neurologic Critical Care? Tips and a Guide for Everyone Nora McInerny on Moving Forward with Grief  Advocating for a Multiple Sclerosis Diagnosis with Comedian Kellye Howard   We want to hear from you! Have a question or want to hear a topic featured on the Brain & Life Podcast? ·       Record a voicemail at 612-928-6206 ·       Email us at BLpodcast@brainandlife.org   Social Media:   Guests: Kristin Flanary @ladyglaucomflecken; Dr. Jessica McFarlin @ukadultneuro Hosts: Dr. Daniel Correa @neurodrcorrea; Dr. Katy Peters @KatyPetersMDPhD

In this episode, editor in chief Joseph E. Safdieh, MD, FAAN, highlights articles about a promising blood test to distinguish Parkinson's disease from dementia with Lewy bodies, how CAR T-cell therapies are showing potential for patients with glioblastoma, and a new wireless electroencephalogram device that can even monitor young children with epilepsy.

The meta‑analysis discussed in this podcast reveals that adults recovering from COVID‑19 without major medical or psychiatric complications experience mild yet statistically significant cognitive deficits - particularly in processing speed, attention, memory, language, and executive function. However, as the main author of this paper tells podcast editor and host, Dr Saima Chaudhry, the impairments generally fall below the threshold for clinical concern, with no evidence of profound neuropsychological dysfunction. Dr Saima Chaudhry is an assistant professor of neurology at the Warren Alpert Medical School, Brown University, Rhode Island, USA. Dr Stephen Aita is a neuropsychologist in the Department of Neurology at the University of South Alabama, Whiddon College of Medicine, Mobile, Alabama, USA. Read the paper on the JNNP website: Neurocognitive and psychiatric outcomes associated with postacute covid 19 infection (doi:10.1136/jnnp-2024-333950).   Please subscribe to the show on Apple Podcasts, Spotify or find it on your platform of choice. Your feedback and reviews are very appreciated. Follow JNNP on twitter: @JNNP_BMJ      

In the September episode of the President's Spotlight, Dr. Jason Crowell and Dr. Natalia Rost highlight this year's AAN Brain Health Summit and discuss the events taking place.  Show reference:  https://www.aan.com/about-the-aan/presidents-spotlight  https://www.aan.com/tools-resources/brain-health/brain-health-summit  

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

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

Professors Karl Friston & Mark Solms, pioneers in the fields of neuroscience, psychology, and theoretical biology, delve into the frontiers of consciousness: "Can We Engineer Artificial Consciousness?". From mimicry to qualia, this historic conversation tackles whether artificial consciousness is achievable - and how. Essential viewing/listening for anyone interested in the mind, AI ethics, and the future of sentience. Subscribe to the channel for more profound discussions!Professor Karl Friston is one of the most highly cited living neuroscientists in history. He is Professor of Neuroscience at University College London and holds Honorary Doctorates from the University of Zurich, University of York and Radboud University. He is the world expert on brain imaging, neuroscience, and theoretical neurobiology, and pioneers the Free-Energy Principle for action and perception, with well-over 300,000 citations. Professor Mark Solms is director of Neuropsychology in the Neuroscience Institute of the University of Cape Town and Groote Schuur Hospital (Departments of Psychology and Neurology), an Honorary Lecturer in Neurosurgery at the Royal London Hospital School of Medicine, an Honorary Fellow of the American College of Psychiatrists, and the President of the South African Psychoanalytical Association. TIMESTAMPS:(0:00) - Introduction (0:45) - Defining Consciousness & Intelligence(8:20) - Minimizing Free Energy + Maximizing Affective States(9:07) - Knowing if Something is Conscious(13:40) - Mimicry & Zombies(17:13) - Homology in Consciousness Inference(21:27) - Functional Criteria for Consciousness(25:10) - Structure vs Function Debate(29:35) - Mortal Computation & Substrate(35:33) - Biological Naturalism vs Functionalism(42:42) - Functional Architectures & Independence(48:34) - Is Artificial Consciousness Possible?(55:12) - Reportability as Empirical Criterion(57:28) - Feeling as Empirical Consciousness(59:40) - Mechanistic Basis of Feeling(1:06:24) - Constraints that Shape Us(1:12:24) - Actively Building Artificial Consciousness (Mark's current project)(1:24:51) - Hedonic Place Preference Test & Ethics(1:30:51) - ConclusionEPISODE LINKS:- Karl's Round 1: https://youtu.be/Kb5X8xOWgpc- Karl's Round 2: https://youtu.be/mqzyKs2Qvug- Karl's Lecture 1: https://youtu.be/Gp9Sqvx4H7w- Karl's Lecture 2: https://youtu.be/Sfjw41TBnRM- Karl's Lecture 3: https://youtu.be/dM3YINvDZsY- Mark's Round 1: https://youtu.be/qqM76ZHIR-o- Mark's Round 2: https://youtu.be/rkbeaxjAZm4CONNECT:- Website: https://tevinnaidu.com - Podcast: https://creators.spotify.com/pod/show/mindbodysolution- YouTube: https://youtube.com/mindbodysolution- Twitter: https://twitter.com/drtevinnaidu- Facebook: https://facebook.com/drtevinnaidu - Instagram: https://instagram.com/drtevinnaidu- LinkedIn: https://linkedin.com/in/drtevinnaidu=============================Disclaimer: The information provided on this channel is for educational purposes only. The content is shared in the spirit of open discourse and does not constitute, nor does it substitute, professional or medical advice. We do not accept any liability for any loss or damage incurred from you acting or not acting as a result of listening/watching any of our contents. You acknowledge that you use the information provided at your own risk. Listeners/viewers are advised to conduct their own research and consult with their own experts in the respective fields.

In part one of this two-part series, Dr. Stacey Clardy talks with Dr. Andrew Mammen about the different types of myositis, approaches to diagnosis, available diagnostic tools, and the evolving roles of MRI and biopsy in clinical practice.  Disclosures can be found at Neurology.org. 

The September 2025 Recall replay highlights four previously released episodes focused on epilepsy. Dr. Halley Alexander begins the series with Dr. Juan Luis Alcala-Zermeno, discussing outcomes of epilepsy surgery in patients with tonic-clonic seizures. She then speaks with Dr. Samuel W. Terman about patients' perceived seizure risk, seizure risk tolerance, and approaches to risk counseling. In the third episode, Dr. Alexander is joined by Dr. Vineet Punia to explore factors influencing the decision to continue or discontinue anti-seizure medications at discharge for patients hospitalized with acute symptomatic seizures. The replay concludes with Dr. Katie Krulisky's conversation with Dr. Leah Blank on how outpatient follow-up impacts readmission rates in older adults with epilepsy or seizures Podcast links:  The Effect of Epilepsy Surgery on Tonic–Clonic Seizures  Patient Perspectives on Antiseizure Medication Discontinuation  Understanding Acute Symptomatic Seizures    Outpatient Follow-Up With 30-Day Readmission After Epilepsy or Seizure Discharge  Article links:  The Effect of Epilepsy Surgery on Tonic–Clonic Seizures Patient Perspectives on Antiseizure Medication Discontinuation  Antiseizure Medication Use and Outcomes After Suspected or Confirmed Acute Symptomatic Seizures Association of Outpatient Follow-Up With 30-Day Readmission After Epilepsy or Seizure Discharge in Medicare Beneficiaries Aged 65 and Older   Disclosures can be found at Neurology.org. 

In the final part of this series, Dr. Jeff Ratliff and Dr. Valtteri Kaasinen discuss how to speak with patients and families when having a conversation about an initial diagnosis of Parkinson disease. Show reference: https://www.neurology.org/doi/10.1212/WNL.0000000000213499  

Dr. Alex Menze and Dr. Christopher J. Klein discuss whether GLP-1RA usage is linked to radiculoplexus neuropathy and common fibular neuropathy.  Show reference: https://www.neurology.org/doi/10.1212/WNL.0000000000213916   

Dr. Alex Menze talks with Dr. Christopher J. Klein about the clinical presentation, diagnosis, and management of diabetic lumbosacral radiculoplexus neuropathy and common fibular neuropathy in the context of GLP-1RA. Read the related article in Neurology®. Disclosures can be found at Neurology.org. 

In part one of this series, Dr. Jeff Ratliff and Dr. Valtteri Kaasinen discuss what this study teaches us about the diagnosis of Parkinson disease once it is given to patients who are subsequently followed over time.  Show reference: https://www.neurology.org/doi/10.1212/WNL.0000000000213499 

In the final episode of this foundational neurology series, Casey Kozak discusses serotonin syndrome. 

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

In part four of this foundational neurology series, Casey Kozak explores neuroleptic malignant syndrome and highlights key similarities and differences with malignant hyperthermia. 

16 months ago, yoga/meditation/sound teacher Reggie Hubbard had a near-death experience, a major stroke. He visits the podcast to describe the experience of his "neurological storm" and the path of collapse and healing that he's been on ever since, and how it has profoundly affected his views as a practitioner, teacher, and his views of the neurological storm that the United States and the world is currently experiencing. If there's such a thing as a "must-listen" episode of this podcast, this it it.  Reggie Hubbard is a senior political strategist, certified yoga and meditation teacher, and founder of Active Peace Yoga. He bridges the worlds of activism and wellness, helping changemakers cultivate inner peace as a foundation for meaningful civic engagement. His mission is to support activists in finding balance while encouraging the wellness community to become more socially conscious. With a background in global marketing, government relations, and activism, Reggie holds a B.A. in philosophy from Yale and an M.B.A. in international strategy from Vlerick Business School. He turned to yoga in 2014 during a period of deepprofessional adversity, and has since studied with renowned teachers including Faith Hunter, Rod Stryker, Dharma Mittra, and Jack Kornfield. Through Active Peace Yoga, Reggie offers accessible yoga rooted in inclusion and healing, drawing inspiration fromartists like Prince and Jimi Hendrix. His teaching blends movement, meditation, and breathwork with honest conversation and compassion. Following a major stroke, his recovery journey further deepened his commitment to contemplative practice. A passionate advocate for equity in wellness, Reggie advises studios and organizations on diversity and inclusion. He has been featured by Yoga Journal, Kripalu, the Omega Institute, Be Here Now Network, and more. He also supports community programs including Black Boys Om and The Food Group. Reggie currently resides in Maryland. Please support the podcast via Substack and subscribe for free or with small monthly contributions. Additional links and show notes are available there. Paid subscribers will receive occasional extras like guided meditations, extra podcast episodes and more! The Thursday Meditation Group happens each week at 8am ET on Thursdays, and a special guided meditation on Open Awareness in Everyday Life was released this week. Another bonus podcast discussed a mindful take on the Revolutionary Astrology of Summer 2025 with Juliana McCarthy and Ethan Nichtern. These are all available to paid subscribers. You can also subscribe to The Road Home podcast wherever you get your pods (Apple, Spotify,Ethan's Website, etc). Ethan's most recent book, Confidence: Holding Your Seat Through Life's Eight Worldly Winds was just awarded a gold medal in the 2025 Nautilus Book Awards. You can visit Ethan's website to order a signed copy. Please allow two weeks from the time of your order for your copy to arrive. Don't forget to sign up for thee upcoming 5 day retreat at the lovely Garrison Institute Sep 29 - Oct 4, 2025 at this link ! Check out all the cool offerings at our podcast sponsor Dharma Moon, including a free webinar with David Nichtern on why become a meditation teacheron Sep 2th, 2025. Free video courses co-taught by Ethan and others, such as The Three Marks of Existence, are also available for download at Dharma Moon.

Tune into the latest podcast from the American Neurological Association (ANA), ANA Investigates: 75 Years of NINDS. This year marks the 75th anniversary of the National Institute of Neurological Disorders and Stroke (NINDS)—an opportunity to reflect on the institute's past achievements and look ahead to the future of neurological research.  This month, ANA Investigates welcomes Dr. Walter Koroshetz, Director of NINDS, in conversation with Dr. Adeline Goss, Neurohospitalist at Highland Hospital. Dr. Koroshetz joined the institute in 2007 as Deputy Director and became Director in 2015. Before joining the NINDS, he served as Vice Chair of Neurology, Director of Stroke and Neurointensive Care Services at Massachusetts General Hospital, and neurologist in the MGH Huntington's Disease Clinic.   Tune in as they discuss highlights from the NINDS's 75-year history and explore what lies ahead for neurological research and innovation. Guest: Walter J. Koroshetz, MD, FANA Director National Institute of Neurological Disorders and Stroke Interviewer: Adeline Goss, MD Neurohospitalist Highland Hospital Disclosures: None

In this episode of Talk Nerdy, Cara is joined by professor in the Departments of Neurology and Psychiatry and Behavioral Sciences at the UC San Francisco, Dr. Virginia Sturm. They discuss her book: Mysteries of the Social Brain: Understanding Human Behavior Through Science. Follow Virginia: @brainsturming

Dr. Jeff Ratliff talks with Dr. Valtteri Kaasinen about the clinical challenges of diagnosing Parkinson disease and how that diagnosis can evolve over time.  Read the related article in Neurology®.  Disclosures can be found at Neurology.org. 

In part three of this foundational neurology series, Casey Kozak discusses malignant hyperthermia caused by inhaled anesthetics and depolarizing neuromuscular blockers.   

In this episode of the SRNA "Ask the Expert" podcast moderated by Dr. GG deFiebre, Dr. Kyle Blackburn and Dr. Benjamin Greenberg discussed the need for updated diagnostic criteria for myelitis. Dr. Blackburn explained the term myelitis and the importance of precise terminologies for accurate diagnoses and research [00:05:10]. Dr. Greenberg elaborated on the advancements in testing and understanding of associated disorders like NMOSD and MOGAD since 2002 [00:11:10]. Both experts stated that the shift from "transverse myelitis" to "myelitis" will aid future research, treatments, and patient care [00:17:27]. They reassured patients that these changes would essentially refine their care but not alter it dramatically [00:23:40]. They encouraged patients to stay informed and communicate with their healthcare providers about these updates [00:28:58].Kyle Blackburn, MD is an Assistant Professor in the Department of Neurology at UT Southwestern Medical Center in Dallas, Texas. He specializes in neuroimmunology and has clinical interests in antibody-mediated neurologic disorders, including autoimmune encephalitis, epilepsy, and ataxias; neurologic complications of cancers, including paraneoplastic disorders and checkpoint inhibitor/CAR T-cell toxicity; and demyelinating disorders, including sarcoidosis, neuromyelitis optica, myelin oligodendrocyte glycoprotein (MOG)-associated disease, and multiple sclerosis. Dr. Blackburn earned his medical degree at the University of Kentucky College of Medicine. He performed his residency in adult neurology at UT Southwestern, serving his final year as Chief Resident, and stayed to complete a fellowship in neuroimmunology, during which he earned the James T. Lubin Clinician Scientist Award from the Siegel Rare Neuroimmune Association (SRNA). He joined the UT Southwestern faculty in 2020.Benjamin M. Greenberg, M.D., M.H.S. is a Professor and the Cain Denius Scholar in Mobility Disorders in the Department of Neurology at UT Southwestern Medical Center in Dallas, Texas. He currently serves as the Vice Chair of Translational Research and Strategic Initiatives for the Department of Neurology. He is also the interim Director of the Multiple Sclerosis Center and the Director of the Neurosciences Clinical Research Center. In addition, he serves as Director of the Transverse Myelitis and Neuromyelitis Optica Program and the Pediatric Demyelinating Disease Program at Children's Medical Center.Dr. Greenberg earned his medical degree at Baylor College of Medicine before completing an internal medicine internship at Chicago's Rush Presbyterian-St. Luke's Medical Center. He performed his neurology residency at the Johns Hopkins School of Medicine. He also holds an M.H.S. in molecular microbiology and immunology from the Bloomberg School of Public Health, as well as a bachelor's degree in the history of medicine – both from Johns Hopkins. Prior to his recruitment to UT Southwestern in 2009, Dr. Greenberg was on the faculty of the Johns Hopkins Division of Neuroimmunology, serving as the Director of the Encephalitis Center and Co-Director of the nation's first dedicated Transverse Myelitis Center.Dr. Greenberg splits his clinical time between adult and pediatric patients at William P. Clements Jr. and Zale Lipshy University Hospitals, Parkland, and Children's Medical Center. His research focuses on better diagnosing, prognosticating, and treating demyelinating diseases and nervous system infections. He also coordinates clinical trials to evaluate new treatments to prevent neurologic damage and restore function to affected patients. 00:00 Introduction00:58 Overview of Myelitis and Diagnostic Criteria02:57 Historical Context and Importance of Updated Criteria05:10 Challenges with Current Terminology11:10 Changes in Understanding and Diagnostic Approaches17:27 Implications for Patients and Clinical Practice23:40 Impact on Research and Future Directions28:58 Patient Advocacy31:17 Conclusion

Kathryn Moore discusses going into neurology as a second career with neurologists Dr. Jodi Hawes and Dr. Shruti Agashe, former physical therapist and biomedical engineer, respectively. They discuss the reasons for switching, what was easy and what was hard about making the switch, and the things they learned along the way.

Dr. Trey Bateman and Dr. David T. Jones discuss how the StateViewer system leverages FDG-PET imaging and machine learning to improve diagnostic accuracy and clinical decision-making for Alzheimer disease and related disorders. Show reference: https://www.neurology.org/doi/10.1212/WNL.0000000000213831 

Dr. Trey Bateman talks with Dr. David T. Jones about how the StateViewer system leverages FDG-PET imaging and machine learning to improve diagnostic accuracy and clinical decision-making for Alzheimer disease and related disorders. Read the related article in Neurology®.  Disclosures can be found at Neurology.org. 

Dr. Dan Ackerman talks with Dr. Urs Fischer about the optimal timing of anticoagulation after ischemic stroke in patients with atrial fibrillation.  show reference: https://www.thelancet.com/journals/lancet/article/PIIS0140-6736(25)00439-8/fulltext  

In this episode, I sit down with preventative neurologist, Dr. Kellyann Niotis to talk about the importance of brain health. We discuss how to protect our cognitive function and prevent neurodegenerative diseases like Alzheimer's, Dementia, and Parkinson's. Dr. Niotis shares her insights on risk factors, early detection testing, and lifestyle choices that can significantly impact our brain health. I was fortunate enough to do my own preventative testing with her before this episode, so we touch on my experience with concussions, my family history, and how they both impact my own brain health.Key Takeaway / Points:What is preventive neurology and why is it crucial for our long-term health?Innovative testing methods and the importance of early detectionWhy brain health matters starting in your 30s and 40sThe connection between mental health and neurodegenerative diseasesThe role of genetics in brain healthThe link between lifestyle choices and neurodegenerative diseases, plus the effects of alcohol, cannabis, and social media on the brainWhy women are at higher risk for Alzheimer'sHow sleep quality impacts cognitive function and memory consolidationThe importance of diverse experiences and social engagement for brain healthSimple daily habits to boost cognitive functionSponsors:Thrive Market: Go to [ThriveMarket.com/cameron] and start saving today. Sale ends 8/31Crown Maple: Visit CrownMaple.com and use code CAMERON20 at checkout for 20% off your orderArya: Go to Arya.Fyi/Cameron to get 15% off your first orderCotton: Learn more at TheFabricOfOurLives.comLMNT: Right now LMNT is offering a free 8-count Sample Pack of their most popular drink flavors with any purchase. Get yours at DrinkLMNT.com/cameronFollow Dr. Kellyann Niotis:Instagram: @drkellyanniotisWebsite: drkellyanniotis.comFollow me:Instagram: @cameronoaksrogers and @conversationswithcamSubstack: Fill Your CupWebsite: cameronoaksrogers.comTikTok: @cameronoaksrogers and @conversations_with_camYoutube: Cameron RogersSee Privacy Policy at https://art19.com/privacy and California Privacy Notice at https://art19.com/privacy#do-not-sell-my-info.

In today's VETgirl online veterinary continuing education podcast, we interview Dr. Nick Jeffery, BVSc, PhD, MSc, DECVS, DECVN, Professor in Neurology and Neurosurgery from Texas A&M on a recent study by Freeman et al entitled “Percutaneous enzymatic chemonucleolysis of intervertebral disks appears safe and effective in treatment of acute-onset paraparesis and paraplegia in small dogs,” published in JAVMA in March 2025. Can the use of intradiscal chondroitinase ABC (often called "CHASE") injections under fluoroscopic-guidance work as a safe, minimally invasive option for small dogs with acute nonambulatory paraparesis or paraplegia, especially when deep pain perception is intact? If you're a general practitioner who sees a lot of down dogs—and especially if you practice in a Dachshund-heavy region—you'll definitely want to tune in.

Schizophrenia may develop in people of all ages, and the early signs of the disorder vary greatly from person to person. While the symptoms are the same, the presentation of them can change due to age of onset, gender, and severity. Host Rachel Star Withers, a diagnosed schizophrenic, and co-host Gabe Howard explore how the early signs of schizophrenia can present differently and specific behaviors to watch for. Joining them is Dr. Gus Alva, a distinguished fellow of the American Psychiatric Association and board certified by the American Board of Psychiatry and Neurology and the American Board of Geriatrics. As an author and coauthor, Dr. Alva's work has been published in peer-reviewed medical journals, including the International Journal of Geriatric Psychiatry and the Journal of the American Psychiatric Association. He has been featured on numerous media outlets and has served as an expert guest in various television programs, such as CNN News. About Our Guest & Hosts Our guest, Dr. Gus Alva, is a Distinguished Fellow of the American Psychiatric Association. He is also Board Certified by the American Board of Psychiatry and Neurology and the American Board of Geriatrics. He completed his residency training at the University of California, Irvine Medical Center in the Department of Psychiatry and Human Behavior, where he served as chief resident during his final year of residency. He also served as an associate professor and deputy director in the department of psychiatry at U.C. Irvine Medical Center, and he is currently serving as an assistant professor at U.C. Riverside Medical School, Department of Neuroscience. As author or co-author, his work has been published in peer-reviewed medical journals, including the International Journal of Geriatric Psychiatry, The Journal of the American Psychiatric Association, and Clinics in Geriatric Medicine. He has published numerous articles and presented at national and international meetings and conferences. He was the recipient of the First Annual Senior Care Humanitarian Award as Outstanding Physician in Dementia Care and the Physician's Recognition Award by the American Medical Association. He has been featured in numerous media outlets and has served as an expert guest in various television programs, such as CNN News, Inside OC, Salud Es Vida, Despierta America, The Morning Blend, Healthy Body, Healthy Mind. Our host, Rachel Star Withers, (Link: www.rachelstarlive.com) is an entertainer, international speaker, video producer, and schizophrenic. She has appeared on MTV's Ridiculousness, TruTV, NBC's America's Got Talent, Marvel's Black Panther, TUBI's #shockfight, Goliath: Playing with Reality, and is the host of the Healthline podcast “Inside Schizophrenia”. She grew up seeing monsters, hearing people in the walls, and having intense urges to hurt herself. Rachel creates videos documenting her schizophrenia, ways to manage, and letting others like her know they are not alone and can still live an amazing life. She has created a kid's mental health comic line, The Adventures of ____.  (Learn more at this link: https://www.amazon.com/Adventures-Fearless-Unstoppable-Light-Ambitious/dp/B0FHWK4ZHS ) Fun Fact: She has wrestled alligators.  Our cohost, Gabe Howard, is an award-winning writer and speaker who lives with bipolar disorder. He is the author of the popular book, "Mental Illness is an Asshole and other Observations," available from Amazon; signed copies are also available directly from the author. He also hosts the twice Webby honored podcast, Inside Bipolar, with Dr. Nicole Washington. To learn more about Gabe, please visit his website, gabehoward.com. Learn more about your ad choices. Visit megaphone.fm/adchoices