Podcasts about Neurology

Many people will be familiar with Parkinson's disease: the progressive brain disorder that causes symptoms including tremors and slower movement, leading on to serious cognitive problems. You might not know that it's the fastest-growing neurological condition in the world. Today it affects around 11.8 million people and that's forecast to double by 2030. Dr Sonia Gandhi is one of the scientists working to change that trend. As Professor of Neurology at University College London and Assistant Research Director at the Francis Crick Institute, her work involves using stem cells to build models of the human brain, helping to drive the development of drugs and other therapies for Parkinson's patients.Talking to Professor Jim Al-Khalili, Sonia explains why this destructive condition is on the rise - and the promising routes they're studying to find new ways to tackle it.Presented by Jim Al-Khalili Produced by Lucy Taylor for BBC StudiosFor details of organisations that offer advice and support to anyone affected by Parkinson's Disease, please go online to bbc.co.uk/actionline.

In the final episode of this five-part series, Dr. Paul Crane concludes the measles series by discussing testing and prevention. 

Neurology professor Daniel Weissman on brain farts, Bernie Miklasz on football, and Middle East peace!- h2 full 2060 Mon, 13 Oct 2025 20:59:37 +0000 5Xv2Aq9Ax5PZqvi9mfFO8bTlPKpW6I2q comedy,religion & spirituality,society & culture,news,government The Dave Glover Show comedy,religion & spirituality,society & culture,news,government Neurology professor Daniel Weissman on brain farts, Bernie Miklasz on football, and Middle East peace!- h2 The Dave Glover Show has been driving St. Louis home for over 20 years. Unafraid to discuss virtually any topic, you'll hear Dave and crew's unique perspective on current events, news and politics, and anything and everything in between. © 2025 Audacy, Inc. Comedy Religion & Spirituality Society & Culture News Government False

Dr. Justin Abbatemarco talks with Dr. Jennifer E. Fugate about posterior reversible encephalopathy syndrome (PRES), focusing on its clinical presentation, diagnosis, imaging techniques, and management strategies. Read the related article in The Lancet Neurology.  Disclosures can be found at Neurology.org. 

In the fourth episode of this five-part series, Dr. Paul Crane discusses subacute sclerosing panencephalitis, a serious complication of measles. 

Date: October 3, 2025 Reference: Doheim et al. Meta-Analysis of Randomized Controlled Trials on IV Thrombolysis in Patients With Minor Acute Ischemic Stroke. Neurology 2025 Guest Skeptic: Dr. Casey Parker is a Rural Generalist, Evidence-based medicine enthusiast and Ultrasound Nerd. This episode was recorded live, in beautiful Broome, Australia, at the Spring Seminar on Emergency […] The post SGEM#488: It's Just a Minor Stroke – Should We Still Lyse? first appeared on The Skeptics Guide to Emergency Medicine.

The government just announced a warning label will be added to Tylenol that use during pregnancy may be associated with an increased risk of Autism and ADHD in children..  In this episode, we talk about:—How the makers of Tylenol admitted in their own  internal documents that there is a strong correlation between Tylenol and Autism. —Why Tylenol's interference with the Liver's capability of making Glutathione is the mechanism  behind Tylenol contributing to neurological issues.  And how a rash on babies after giving them Tylenol after vaccination can be a signal that something has gone wrong with the Liver.—The reason Dr. Prather says that Tylenol causes damage to the Kidneys, Liver, and Gut every time you take it.  And the long list of potential harm that Tylenol can cause, including:  Liver damage, Kidney damage, G.I. bleeding, Diarrhea, Vomiting, Heart failure, Heart attacks, Hypertension, Undescended testicles, Asthma, and an increased chance of Cancers like Leukemia. —The benefits of Fever to the body and why Dr. Prather says there is "a tremendous amount of really good things that happen with a Fever."  And why the approach to just suppress a Fever leads to more problems and worse results.—How Fever is an indication of a Neurology issue and can actually reveal a lot of helpful diagnostic information.  And how Chiropractic is the way to deal with Neurological situations, including Fevers.—The chances of seizures from a Fever are not decreased by Tylenol, but Structure-Function Care can help the body avoid seizures by keeping the body in Homeostasis.  And how Tylenol is not only dangerous, but research shows it also has very little effectiveness for pain. —The Spleen-21 Acupuncture point that Dr. Prather's staff immediately request treatment on when they start to feel sick.  And the "really excellent" Elderberry and Vitamin C syrup that is very easy for children to take when they are ill.—Why Dr. Prather says that Homeopathy is "extremely effective for children" and is always safe.  And how it is "the best and safest way to help a child's immune system work better".—The Diathermy treatment Dr. Prather uses in his office to bring immediate relief to crying children with ear infections and "usually clears up the ear discomfort in one session".  And the gentle Galbreath maneuver Dr. Prather teaches Moms to do on their babies to promote ear drainage. —How Dr. Prather says that Autism can be reversed and how he has seen "really strong changes in Autism and ADHD".  And the methods that Holistic Integration uses, such as Craniosacral Therapy, to reverse the damage from the toxicities that cause Autism.http://www.TheVoiceOfHealthRadio.com

Dr. Jessica Ailani and Dr. Kathleen Digre discuss three key updates in the understanding and management of idiopathic intracranial hypertension.  Show references: https://jamanetwork.com/journals/jamaneurology/article-abstract/2836065 https://www.neurology.org/doi/10.1212/WNL.0000000000009312 

Host: Jasmine T. Kency, M.D., Associate Professor of Internal Medicine and Pediatrics at the University of Mississippi Medical Center.Guest: Courtney Huval, M.D., Assistant Professor in the Department of Neurology at the University of Mississippi Medical CenterTopic: Multiple Sclerosis (MS)Email the show: remedy@mpbonline.org. If you enjoy listening to this podcast, please consider contributing to MPB. https://donate.mpbfoundation.org/mspb/podcast. Hosted on Acast. See acast.com/privacy for more information.

Dr. Jessica Ailani talks with Dr. Kathleen Digre about the recognition of symptoms, diagnostic imaging, treatment goals, and the importance of weight loss in managing IIH.  Read the related article in JAMA. Read the related article in Neurology®.  Disclosures can be found at Neurology.org.    

Dr. Andy Southerland and Dr. Amrou Sarraj examine whether general anesthesia (GA) compared with non-GA was associated with better functional outcomes in the SELECT2 trial.  Show reference: https://www.neurology.org/doi/10.1212/WNL.0000000000213819 

In the October episode of the President's Spotlight, Dr. Jason Crowell talks with Dr. Natalia Rost about the crucial role research plays in neurology for clinicians and scientists.  Show reference:  https://www.aan.com/about-the-aan/presidents-spotlight 

Sign up for updates on webinars, events, and resources for the Parkinson's community—delivered to your inbox. https://dpf.org/newsletter-signup In the final episode of this three-part series, Connie Carpenter Phinney and Dr. Mark Mapstone explore the emotional and cognitive changes that can occur as Parkinson's progresses. They talk openly about issues like apathy, anxiety, executive function decline, and how these changes can affect relationships, communication, safety, and daily life—including decisions around driving and independence. While the conversation acknowledges grief, frustration, and loss, it also offers insight, practical advice, and strategies for living well through change. This episode is for anyone facing or seeking to understand the emotional and cognitive realities of Parkinson's—people diagnosed, care partners, and clinicians alike. Connie Carpenter Phinney is a co-founder of the Davis Phinney Foundation and has been her husband's care partner for over 25 years. Her background in science combined with her lived experience and curiosity helped shape this conversation with neuropsychologist Dr. Mark Mapstone. Connie is the host of the Foundation's Care Partner Meetup, a monthly virtual meetup for Parkinson's care partners held the first Tuesday of each month. To attend the meetup, sign up here: https://davisphinneyfoundation.org/events/parkinsons-care-partner-meetup/ Dr. Mark Mapstone is Professor of Neurology at the University of California, Irvine School of Medicine. He is a member of the UCI Institute for Memory Impairments and Neurological Disorders and a Fellow of the UCI Center for Neurobiology of Learning and Memory. His research focuses on pre-clinical detection of neurological disease using cognitive tests and biomarkers obtained from blood. He has a special interest in developing strategies to maintain successful cognitive aging. In the clinic, he specializes in cognitive assessment of older adults with suspected brain disease. Dr. Mapstone earned a PhD in Clinical Psychology at Northwestern University and completed fellowship training in Neuropsychology and Experimental Therapeutics at the University of Rochester. He received a Career Development Award from the National Institute on Aging and his research has been funded by the National Institutes of Health, the Michael J. Fox Foundation, and the Department of Defense. This content is possible thanks to the generosity of our listeners. Every day more people are diagnosed with Parkinson's, and this means our work is more important than ever. Please support our work by visiting https://dpf.org/donate. Interested in our Living with Parkinson's Meetup, Care Partner Meetup, or Live Well Today Webinars? Learn how to join. https://dpf.org/webinars

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

In this episode, Dr. Andy Southerland discusses the Capitol Hill Report from October 6th, covering the government shutdown and its potential impact on you and your patients.  Stay updated with what's happening on the hill by visiting aan.com/chr.  Take a minute to email your members of Congress and ensure your voice is heard! 

Clinical trials are essential for improving the lives of those diagnosed with Alzheimer's disease and related dementias. With so many trials out there, it can be difficult for someone who's interested in participating in research to know where to start. Dr. Jonathan Graff-Radford joins the podcast to discuss the ins and outs of clinical trials and the state of Alzheimer's treatments today, as well as share some highlights from his presentation at the National Alzheimer's Coordinating Center's (NACC) 2025 Spring ADRC Meeting. Guest: Jonathan Graff-Radford, MD, behavioral neurologist, associate professor, vice chair, Mayo Clinic Department of Neurology, co-investigator, Mayo Clinic Alzheimer's Disease Research Center Show Notes Read more about Dr. Jonathan Graff-Radford at his profile on Mayo Clinic's website. Listen to part one and part two of our series on preclinical Alzheimer's disease and the AHEAD study with Dr. Reisa Sperling, mentioned at 19:53, on our website. Learn more about the AHEAD study on their website. Learn more about clinical trials in Wisconsin at the UW Clinical Trials Institute's website. Interested in participating in clinical trials? Visit clinicaltrials.gov or Alzheimer's Association's TrialMatch to learn how to get involved. Learn more and register for the 2025 Fall Community Conversation: Addressing Hearing Loss for Better Brain Health on our website. Connect with us Find transcripts and more at our website. Email Dementia Matters: dementiamatters@medicine.wisc.edu Follow us on Facebook and Twitter. Subscribe to the Wisconsin Alzheimer's Disease Research Center's e-newsletter. Enjoy Dementia Matters? Consider making a gift to the Dementia Matters fund through the UW Initiative to End Alzheimer's. All donations go toward outreach and production.

Dr. Andy Southerland talks with Dr. Amrou Sarraj about the importance of understanding anesthesia's impact on patient outcomes, the implications for clinical practice, and future research directions in stroke treatment.  Read the related article in Neurology®.  Disclosures can be found at Neurology.org. 

In the second episode of this two-part series, Dr. Kiran Thakur and Dr. Ava Easton discuss how to get involved in advocacy efforts and policy development related to encephalitis.  Show reference: https://www.thelancet.com/journals/lanmic/article/PIIS2666-5247(25)00057-6/fulltext 

Send us a message with this link, we would love to hear from you. Standard message rates may apply. We unpack myths, the new stepwise approach, and why return to school should come before return to play.• what a concussion is• common and delayed symptoms including mood and sleep changes• immediate sideline steps• why “cocooning” is outdated and how light activity helps• individualized recovery timelines and risk of returning too soon• return-to-learn before return-to-play with simple accommodations• a staircase model for activity and symptom thresholds• helmets vs brain movement and the role of honest reporting• practical tips for coaches, parents, and student athletesCheck out our website, send us an email, share this with a friend or young student athlete who is playing some sports and might get a concussionReferencesBroglio SP, Register-Mihalik JK, Guskiewicz KM, et al. National Athletic Trainers' Association Bridge Statement: Management of Sport-Related Concussion. Journal of Athletic Training. 2024;59(3):225-242. doi:10.4085/1062-6050-0046.22.Centers for Disease Control and Prevention Guideline on the Diagnosis and Management of Mild Traumatic Brain Injury Among Children. Lumba-Brown A, Yeates KO, Sarmiento K, et al. JAMA Pediatrics. 2018;172(11):e182853. doi:10.1001/jamapediatrics.2018.2853.Feiss R, Lutz M, Reiche E, Moody J, Pangelinan M. A Systematic Review of the Effectiveness of Concussion Education Programs for Coaches and Parents of Youth Athletes. International Journal of Environmental Research and Public Health. 2020;17(8):E2665. doi:10.3390/ijerph17082665.Gereige RS, Gross T, Jastaniah E. Individual Medical Emergencies Occurring at School. Pediatrics. 2022;150(1):e2022057987. doi:10.1542/peds.2022-057987.Giza CC, Kutcher JS, Ashwal S, et al. Summary of Evidence-Based Guideline Update: Evaluation and Management of Concussion in Sports: Report of the Guideline Development Subcommittee of the American Academy of Neurology. Neurology. 2013;80(24):2250-2257. doi:10.1212/WNL.0b013e31828d57dd.Halstead ME. What's New With Pediatric Sport Concussions? Pediatrics. 2024;153(1):e2023063881. doi:10.1542/peds.2023-063881.Halstead ME, Walter KD, Moffatt K. Sport-Related Concussion in Children and Adolescents. Pediatrics. 2018;142(6):e20183074. doi:10.1542/peds.2018-3074.Leddy JJ. Sport-Related Concussion. The New England Journal of Medicine. 2025;392(5):483-493. doi:10.1056/NEJMcp2400691.McCrea M, Broglio S, McAllister T, et al. Return to Play and Risk of Repeat Concussion in Collegiate Football Players: Comparative Analysis From the NCAA Concussion Study (1999–2001) and CARE Consortium (2014–2017). British Journal of Sports Medicine. 2020;54(2):102-109. doi:10.1136/bjsports-2019-100579.Scorza KA, Cole W. Current Concepts in Concussion: Initial Evaluation and Management. American Family Physician. 2019;99(7):426-434.Shirley E, Hudspeth LJ, Maynard JR. Managing Sports-Related Concussions From Time of Injury Through Return to Play. The Journal of the American Academy of Orthopaedic Surgeons. 2018;26(13):e279-e286. doi:10.5435/JAAOS-D-16-00684.Zhou H, Ledsky R, Sarmiento K, et al. Parent-Child Communication About ConcussSupport the showSubscribe to Our Newsletter! Production and Content: Edward Delesky, MD & Nicole Aruffo, RNArtwork: Olivia Pawlowski

In part one of this two-part series, Dr. Kiran Thakur and Dr. Ava Easton discuss the World Health Organization's technical brief on encephalitis.  Show reference: https://www.thelancet.com/journals/lanmic/article/PIIS2666-5247(25)00057-6/fulltext  

In this episode, Dr. Peter Gliebus, Chief of Neurology at Marcus Neuroscience Institute, discusses early signs of Alzheimer's, key risk factors, and how new treatments and research are shaping the future of care. He also highlights the importance of caregiver support and a holistic approach to patient well-being.

Purple Rabbits, slurp that green tea and hunker down for The Neoborn Caveman Show—your marble-mouthed host Neoborn Caveman (me, myself, the gang) unleashing pro-humanity rants on life's raw underbelly. We kick off skewering "irresistible" hobbies—archery? Blacksmithing? Spare me; real pull comes from purpose, like indoor tomatoes barricading your pad against urban poison, not time-wasting fluff. Then, a gut-punch from Des Moines: illegal superintendent Ian Andre Roberts, $300K salary to shove agendas down kids' throats, handpicked by Dem strings, busted fleeing ICE with a loaded handgun and deportation order—laws exist to shield taxpayers, not spotlight squatters. Fist-bump the Florida task force's record haul: 1 million pounds of cartel coke, $11B gutted, 378 million lethal doses dodged—why pity narco scum when they peddle death? Health gut-check: 8-year Neurology probe fingers low/no-cal sweeteners (aspartame, sucralose) as cognition killers, accelerating brain fog—sugar's no satan; brew ginger-honey truth over lab lies. Europe's EES drops October 12: fingerprints and snaps for U.S. travelers, "security" facade for data grabs—control's the import, not the espresso. Cap with life's unscripted churn: still waters rot, gales renew—ditch consumer cages, root real.Music guests are: Broken Colours, Perpacity, Sweet Water, and others.Catch it on your pod platform, fire up patreon.com/theneoborncavemanshow (free fierce), and question the machine. Satire, truths, tunes: slurp, burp, revolt.Key TakeawaysPurpose, Not Pastimes: No room for hobbies—reads, gardens, plants pack purpose, forging shields and souls over aimless arrows.School Scandal Unmasked: Unvetted agendas erode education—taxpayer trust demands vetted voices, not armed interlopers.Sweetener Slow Poison: Artificial zeros hasten memory melts per science—embrace nature's cane, shun corporate cocktails.Biometric Border Trap: EU scans sell safety, deliver surveillance—fingerprint freedom's fade before it sticks.Uncertainty's Edge: Life's flows—winds, rains—vitalize; accept your raw self, skip rivalry, grow unscripted.Soundbites"I don't have time for hobbies. Anything I do, it's serious because I don't have time in my life to waste four meaningless things.""Promiscuity is a bad thing. It's unhealthy, literally unhealthy... Would you be happy for your kid to sleep around? This is a fork spoon is also sexual, right? What about knife?""Don't consume that much and life won't consume you.""It's all about control... Consumption leads towards compliance and compliance will lead to cages.""You don't have to compete with others... Look at the nature. Every tree has the right amount of sunlight next to each other, and they don't necessarily go against each other."Humanity centered satirical takes on the world & news + music - with a marble mouthed host.Free speech marinated in comedy.Supporting Purple Rabbits. Hosted on Acast. See acast.com/privacy for more information.

Dr. Kiran Thakur talks with Dr. Ava Easton about the World Health Organization's technical brief on encephalitis.  Read the related article in The Lancet.  Disclosures can be found at Neurology.org.     

In the third episode of this five-part series, Dr. Paul Crane discusses measles inclusion body encephalitis.     

Victoria says…“That is so gross!”And it might be. If you don't like eggs.My name is Mr. Twenty Twenty.That's the length of a daydream.And daydreams don't manifest.They dissipate.Remember, don't make the Mind Movie Mistake…Because movies feel good then fade away.That's why I am BIG into…One Sip Simple.Watch the video…Notice how I surrendered into a BLINK…That's what we call an Author moment.It's the blink where the Producer…The spark meets the Author…The one who writes the final One Sip Simple scene.The Author writes the final scene.And the final scene is easy…if you begin with,“Wouldn't it be cool?”  And you let it be something - simple and sweet.Anyway… Tat's from Neville Goddard's Four Mighty Ones.More on that later.Reach out if you want more.  I have a really cool little chart you'll love…And I'm writing two books and designing a course on The Core Four right now.So let's get gross.Here's what I do.I crack a duck egg into my cup.Not just any egg.A duck egg.Because I found these wonderful local farmers…A local couple who are amazing.They sell me duck eggs at chicken egg prices.And they're huge.So I crack one into my coffee cup…Then I grab this little gadget — a spring whisk.Four bucks at Kohls's.It's like my best friend.Still grody… Because it's got some egg on it.Anyway. Gross.But here's what I've noticed…Order matters.Cup first.Egg goes in.Spring whisk goes up and down.Thirty-nine seconds.Not less. Not more.Much less, and it's egg-drop soup coffee. Gross.Much more, it gets frothy and never settles. Gross.But at the exact right amount of time?I can feel it.Right then.Ahhh.That release.Then I add the hot water.Shake like hell.And what comes out is glorious.That's why I'm sharing this today.Because manifesting is the same.Same ingredients.Wrong order = gross.Right order = glory.And just like using the spring whisk…Some people stop too soon.Some people go way too long.Both get gross results.Neville gave formulas for a reason.We keep exploring them.Neurology.Biology.Nature.The sacred order shows up everywhere.And here's the deal…Most people won't even bother cracking a duck egg into coffee.Much less test the order.And I'm fine with that.This is just something I enjoy.In the “real” world?I imagined being the Kung Fu King.And suddenly I lost all interest in carbohydrates.And I'm not blaming the diet.I'm not blaming the eggs.What I noticed is this:Two years ago I was functionally crippled.Walking stick.Painkillers.Two hip replacements looming in my future.Now?I do Kung Fu - Wu Shu on the staircases I used to avoid.That tells me something.Not diet.Not time.Not technique.I changed.In the twinkle of an eye.You've got a choice to make today…You can make stuff up on your own.Crack an egg in coffee, slam it back.Gross!Or you can follow Sacred Order.Whisk it just right.Enjoy the richness and gobble up the glory.Same with manifesting.Stop too soon? Soup.  It never feels real.Go too long? Froth.  Because daydreams dissipate.That's the Mind Movie Mistake. Fix that with the first 2 videos at HowToFeelitReal.comAnd if you're ready for some real fun…Go to ManifestingMasteryCourse.com the 90-day adventure.At least grab the free videos at HowToFeelItReal.com.So you don't waste years making up your own recipe…and wondering why it's gross.That's my gift to you today.I'm Mr. Twenty Twenty.You've been enjoying the Power of Imagination Podcast.Where we explore one thing, and one thing only…The wonder-working power of the human imagination.And it all begins with that little Producer moment.“Wouldn't it be cool…”Blink.Producer meets Author.Possibility becomes Proof.And I already feel your comments,your emails, your thank-yous.See ya.

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

The October 2025 Recall features four previously released episodes on topics related to headache. Dr. Jessica Ailani begins the episode with Dr. Kathleen Digre discussing the evolution of spontaneous intracranial hypotension. The episode transitions into a discussion with Dr. Tesha Monteith and Dr. Peter Goadsby about the classification of headaches. In the third episode, Dr. Jessica Ailani is joined by Dr. Francesca Puledda to discuss global recommendations for migraine. The replay concludes with Dr. Jessica Ailani's conversation with Dr. Richard B. Lipton on characterizing PRODROME in migraine. Podcast links: Spontaneous Intracranial Hypotension Updates Understanding the Classification of Headaches and the Science Behind Them Global Recommendations for Migraine Characterizing Prodrome in Migraine Article links: ICHD-4 Editorial International Headache Society Global Practice Recommendations Characterizing Prodrome (Premonitory Phase) in Migraine Disclosures can be found at Neurology.org. 

In the second part of this five-part series, Dr. Paul Crane discusses the early neurologic complications associated with measles.   

Sign up for updates on webinars, events, and resources for the Parkinson's community—delivered to your inbox. https://dpf.org/newsletter-signup In this episode, Connie and Dr. Mapstone dive into the role of neuropsychology in Parkinson's care. They explain what a neuropsychological evaluation is, what to expect during an office or virtual visit, and how results can help guide treatment, daily planning, and care strategies. This episode also discusses why someone might be referred, how testing works, and what insights it can offer for both individuals and families. **This content is possible thanks to the generosity of our listeners. Every day more people are diagnosed with Parkinson's, and this means our work is more important than ever. Please support our work by visiting https://dpf.org/donate.** Connie Carpenter Phinney Connie Carpenter Phinney is a co-founder of the Davis Phinney Foundation and has been her husband's care partner for over 25 years. Her background in science combined with her lived experience and curiosity helped shape this conversation with neuropsychologist Dr. Mark Mapstone. Connie is the host of the Foundation's Care Partner Meetup, a monthly virtual meetup for Parkinson's care partners held the first Tuesday of each month. To attend the meetup, sign up here: https://davisphinneyfoundation.org/events/parkinsons-care-partner-meetup/ Dr. Mark Mapstone Mark Mapstone is Professor of Neurology at the University of California, Irvine School of Medicine. He is a member of the UCI Institute for Memory Impairments and Neurological Disorders and a Fellow of the UCI Center for Neurobiology of Learning and Memory. His research focuses on pre-clinical detection of neurological disease using cognitive tests and biomarkers obtained from blood. He has a special interest in developing strategies to maintain successful cognitive aging. In the clinic, he specializes in cognitive assessment of older adults with suspected brain disease. Dr. Mapstone earned a PhD in Clinical Psychology at Northwestern University and completed fellowship training in Neuropsychology and Experimental Therapeutics at the University of Rochester. He received a Career Development Award from the National Institute on Aging and his research has been funded by the National Institutes of Health, the Michael J. Fox Foundation, and the Department of Defense. Interested in our Living with Parkinson's Meetup, Care Partner Meetup, or Live Well Today Webinars? Learn how to join. https://dpf.org/webinars

Functional movement disorders are a common clinical concern for neurologists. The principle of “rule-in” diagnosis, which involves demonstrating the difference between voluntary and automatic movement, can be carried through to explanation, triage, and evidence-based multidisciplinary rehabilitation therapy. In this episode, Gordon Smith, MD, FAAN speaks Jon Stone, PhD, MB, ChB, FRCP, an author of the article “Multidisciplinary Treatment for Functional Movement Disorder” in the Continuum® August 2025 Movement Disorders issue. Dr. Smith is a Continuum® Audio interviewer and a professor and chair of neurology at Kenneth and Dianne Wright Distinguished Chair in Clinical and Translational Research at Virginia Commonwealth University in Richmond, Virginia. Dr. Stone is a consultant neurologist and honorary professor of neurology at the Centre for Clinical Brain Sciences at the University of Edinburgh in Edinburgh, United Kingdom. Additional Resources Read the article: Multidisciplinary Treatment for Functional Movement Disorder Subscribe to Continuum®: shop.lww.com/Continuum Continuum® Aloud (verbatim audio-book style recordings of articles available only to Continuum® subscribers): continpub.com/Aloud More about the American Academy of Neurology: aan.com Social Media facebook.com/continuumcme @ContinuumAAN Host: @gordonsmithMD Guest: @jonstoneneuro Full episode transcript available here Dr Jones: This is Dr Lyell Jones, Editor-in-Chief of Continuum. This exclusive Continuum Audio interview is available only to you, our subscribers. We hope you enjoy it. Thank you for listening. Dr Smith: Hello, this is Dr Gordon Smith. Today I've got the great pleasure of interviewing Dr Johnstone about his article on the multidisciplinary treatment for functional neurologic disorder, which he wrote with Dr Alan Carson. This article will appear in the August 2025 Continuum issue on movement disorders. I will say, Jon, that as a Continuum Audio interviewer, I usually take the interviews that come my way, and I'm happy about it. I learn something every time. They're all a lot of fun. But there have been two instances where I go out and actively seek to interview someone, and you are one of them. So, I'm super excited that they allowed me to talk with you today. For those of our listeners who understand or are familiar with FND, Dr Stone is a true luminary and a leader in this, both in clinical care and research. He's also a true humanist. And I have a bit of a bias here, but he was the first awardee of the Ted Burns Humanism in Neurology award, which is a real honor and reflective of your great work. So welcome to the podcast, Jon. Maybe you can introduce yourself to our audience. Dr Stone: Well, thank you so much, Gordon. It was such a pleasure to get that award, the Ted Burns Award, because Ted was such a great character. I think the spirit of his podcasts is seen in the spirit of these podcasts as well. So, I'm a neurologist in Edinburgh in Scotland. I'm from England originally. I'm very much a general neurologist still. I still work full-time. I do general neurology, acute neurology, and I do two FND clinics a week. I have a research group with Alan Carson, who you mentioned; a very clinical research group, and we've been doing that for about 25 years. Dr Smith: I really want to hear more about your clinical approach and how you run the clinic, but I wonder if it would be helpful for you to maybe provide a definition. What's the definition of a functional movement disorder? I mean, I think all of us see these patients, but it's actually nice to have a definition. Dr Stone: You know, that's one of the hardest things to do in any paper on FND. And I'm involved with the FND society, and we're trying to get together a definition. It's very hard to get an overarching definition. But from a movement disorder point of view, I think you're looking at a disorder where there is an impairment of voluntary movement, where you can demonstrate that there is an automatic movement, which is normal in the same movement. I mean, that's a very clumsy way of saying it. Ultimately, it's a disorder that's defined by the clinical features it has; a bit like saying, what is migraine? You know? Or, what is MS? You know, it's very hard to actually say that in a sentence. I think these are disorders of brain function at a very broad level, and particularly with FND disorders, of a sort of higher control of voluntary movement, I would say. Dr Smith: There's so many pearls in this article and others that you've written. One that I really like is that this isn't a diagnosis of exclusion, that this is an affirmative diagnosis that have clear diagnostic signs. And I wonder if you can talk a little bit about the diagnostic process, arriving at an FND diagnosis for a patient. Dr Stone: I think this is probably the most important sort of “switch-around” in the last fifteen, twenty years since I've been involved. It's not new information. You know, all of these diagnostic signs were well known in the 19th century; and in fact, many of them were described then as well. But they were kind of lost knowledge, so that by the time we got to the late nineties, this area---which was called conversion disorder then---it was written down. This is a diagnosis of exclusion that you make when you've ruled everything out. But in fact, we have lots of rule in signs, which I hope most listeners are familiar with. So, if you've got someone with a functional tremor, you would do a tremor entrainment test where you do rhythmic movements of your thumb and forefinger, ask the patient to copy them. It's very important that they copy you rather than make their own movements. And see if their tremor stops briefly, or perhaps entrains to the same rhythm that you're making, or perhaps they just can't make the movement. That might be one example. There's many examples for limb weakness and dystonia. There's a whole lot of stuff to learn there, basically, clinical skills. Dr Smith: You make a really interesting point early on in your article about the importance of the neurological assessment as part of the treatment of the patient. I wonder if you could talk to our listeners about that. Dr Stone: So, I think, you know, there's a perception that- certainly, there was a perception that that the neurologist is there to make a diagnosis. When I was training, the neurologist was there to tell the patient that they didn't have the kind of neurological problem and to go somewhere else. But in fact, that treatment process, when it goes well, I think begins from the moment you greet the patient in the waiting room, shake their hand, look at them. Things like asking the patient about all their symptoms, being the first doctor who's ever been interested in their, you know, horrendous exhaustion or their dizziness. You know, questions that many patients are aware that doctors often aren't very interested in. These are therapeutic opportunities, you know, as well as just taking the history that enable the patient to feel relaxed. They start thinking, oh, this person's actually interested in me. They're more likely to listen to what you've got to say if they get that feeling off you. So, I'd spend a lot of time going through physical symptoms. I go through time asking the patient what they do, and the patients will often tell you what they don't do. They say, I used to do this, I used to go running. Okay, you need to know that, but what do they actually do? Because that's such valuable information for their treatment plan. You know, they list a whole lot of TV shows that they really enjoy, they're probably not depressed. So that's kind of useful information. I also spend a lot of time talking to them about what they think is wrong. Be careful, that they can annoy patients, you know. Well, I've come to you because you're going to tell me what's wrong. But what sort of ideas had you had about what was wrong? I need to know so that I can deal with those ideas that you've had. Is there a particular reason that you're in my clinic today? Were you sent here? Was it your idea? Are there particular treatments that you think would really help you? These all set the scene for what's going to come later in terms of your explanation. And, more importantly, your triaging of the patient. Is this somebody where it's the right time to be embarking on treatment, which is a question we don't always ask yourself, I think. Dr Smith: That's a really great point and kind of segues to my next question, which is- you talked a little bit about this, right? Generally speaking, we have come up with this is a likely diagnosis earlier, midway through the encounter. And you talked a little bit about how to frame the encounter, knowing what's coming up. And then what's coming up is sharing with the patient our opinion. In your article, you point out this should be no different than telling someone they have Parkinson's disease, for instance. What pearls do you have and what pitfalls do you have in how to give the diagnosis? And, you know, a lot of us really weren't trained to do this. What's the right way, and what are the most common land mines that folks step on when they're trying to share this information with patients? Dr Stone: I've been thinking about this for a long time, and I've come to the conclusion that all we need to do with this disorder is stop being weird. What goes wrong? The main pitfall is that people think, oh God, this is FND, this is something a bit weird. It's in a different box to all of the other things and I have to do something weird. And people end up blurting out things like, well, your scan was normal or, you haven't got epilepsy or, you haven't got Parkinson's disease. That's not what you normally do. It's weird. What you normally do is you take a deep breath and you say, I'm sorry to tell you've got Parkinson's disease or, you have this type of dystonia. That's what you normally say. If you follow the normal- what goes wrong is that people don't follow the normal rules. The patient picks up on this. What's going on here? This doctor's telling me what I don't have and then they're starting to talk about some reason why I've got this, like stress, even though I don't- haven't been told what it is yet. You do the normal rules, give it a name, a name that you're comfortable with, preferably as specific as possible: functional tremor, functional dystonia. And then do what you normally do, which is explain to the patient why you think it's this. So, if someone's got Parkinson's, you say, I think you've got Parkinson's because I noticed that you're walking very slowly and you've got a tremor. And these are typical features of Parkinson. And so, you're talking about the features. This is where I think it's the most useful thing that you can do. And the thing that I do when it goes really well and it's gone badly somewhere else, the thing I probably do best, what was most useful, is showing the patient their signs. I don't know if you do that, Gordon, but it's maybe not something that we're used to doing. Dr Smith: Wait, maybe you can talk more about that, and maybe, perhaps, give an example? Talk about how that impacts treatment. I was really impressed about the approach to physical therapy, and treatment of patients really leverages the physical examination findings that we're all well-trained to look for. So maybe explore that a little bit. Dr Stone: Yeah, I think absolutely it does. And I think we've been evolving these thoughts over the last ten or fifteen years. But I started, you know, maybe about twenty years ago, started to show people their tremor entrainment tests. Or their Hoover sign, for example; if you don't know Hoover sign, weakness of hip extension, that comes back to normal when the person's flexing their normal leg, their normal hip. These are sort of diagnostic tricks that we had. Ahen I started writing articles about FND, various senior neurologists said to me, are you sure you should write this stuff down? Patients will find out. I wrote an article with Marc Edwards called “Trick or Treat in Neurology” about fifteen years ago to say that actually, although they're they might seem like tricks, there really are treats for patients because you're bringing the diagnosis into the clinic room. It's not about the normal scan. You can have FND and MS. It's not about the normal scan. It's about what you're seeing in front of you. If you show that patient, yes, you can't move your leg. The more you try, the worse it gets. I can see that. But look, lift up your other leg. Let me show you. Can you see now how strong your leg is? It's such a powerful way of communicating to the patient what's wrong with them diagnostically, giving them that confidence. What it's also doing is showing them the potential for improvement. It's giving them some hope, which they badly need. And, as we'll perhaps talk about, the physio treatment uses that as well because we have to use a different kind of physio for many forms of functional movement disorder, which relies on just glimpsing these little moments of normal function and promoting them, promoting the automatic movement, squashing down that abnormal pattern of voluntary movement that people have got with FND. Dr Smith: So, maybe we can talk about that now. You know, I've got a bunch of other questions to ask you about mechanism and stuff, but let's talk about the approach to physical therapy because it's such a good lead-in and I always worry that our physical therapists aren't knowledgeable about this. So, maybe some examples, you have some really great ones in the article. And then words of wisdom for us as we're engaging physical therapists who may not be familiar with FND, how to kind of build that competency and relationship with the therapist with whom you work. Dr Stone: Some of the stuff is the same. Some of the rehabilitation ideas are similar, thinking about boom and bust activity, which is very common in these patients, or grading activity. That's similar, but some of them are really different. So, if you have a patient with a stroke, the physiotherapist might be very used to getting that person to think and look at their leg to try and help them move, which is part of their rehabilitation. In FND, that makes things worse. That's what's happening in Hoover sign and tremor entrainment sign. Attention towards the limb is making it worse. But if the patient's on board with the diagnosis and understands it, they'll also see what you need to do, then, in the physio is actively use distraction in a very transparent way and say to the patient, look, I think if I get you to do that movement, and I'll film you, I think your movement's going to look better. Wouldn't that be great if we could demonstrate that? And the patient says, yeah, that would be great. We're kind of actively using distraction. We're doing things that would seem a bit strange for someone with other forms of movement disorder. So, the patients, for example, with functional gait disorders who you discover can jog quite well on a treadmill. In fact, that's another diagnostic test. Or they can walk backwards, or they can dance or pretend that they're ice skating, and they have much more fluid movements because their ice skating program in their brain is not corrupted, but their normal walking program is. So, can you then turn ice skating or jogging into normal walking? It's not that complicated, I think. The basic ideas are pretty simple, but it does require some creativity from whoever's doing the therapy because you have to use what the patient's into. So, if the patient used to be a dancer- we had a patient who was a, she was really into ballet dancing. Her ballet was great, but her walking was terrible. So, they used ballet to help her walk again. And that's incredibly satisfying for the therapist as well. So, if you have a therapist who's not sure, there are consensus recommendations. There are videos. One really good success often makes a therapist want to do that again and think, oh, that's interesting. I really helped that patient get better. Dr Smith: For a long time, this has been framed as a mental health issue, conversion disorder, and maybe we can talk a little bit about early life of trauma as a risk factor. But, you know, listening to you talk, it sounds like a brain network problem. Even the word “functional”, to me, it seems a little judgmental. I don't know if this is the best term, but is this really a network problem? Dr Stone: The word “functional”, for most neurologists, sounds judgmental because of what you associate it with. If you think about what the word actually is, it's- it does what it says on the tin. There's a disordered brain function. I mean, it's not a great word. It's the least worst term, in my view. And yes, of course it's a brain network problem, because what other organ is it going to be? You know, that's gone wrong? When software brains go wrong, they go wrong in networks. But I think we have to be careful not to swing that pendulum too far to the other side because the problem here, when we say asking the question, is this a mental health problem or a neurological one, we're just asking the wrong question. We're asking a question that makes no sense. However you try and answer that, you're going to get a stupid answer because the question doesn't make sense. We shouldn't have those categories. It's one organ. And what's so fascinating about FND---and I hope what can incite your sort of curiosity about it---is this disorder which defies this categorization. You see some patients with it, they say, oh, they've got a brain network disorder. Then you meet another patient who was sexually abused for five years by their uncle when they were nine, between nine and fourteen; they developed an incredibly strong dissociative threat response into that experience. They have crippling anxiety, PTSD, interpersonal problems, and their FND is sort of somehow a part of that; part of that experience that they've had. So, to ignore that or to deny or dismiss psychological, psychiatric aspects, is just as bad and just as much a mistake as to dismiss the kind of neurological aspects as well. Dr Smith: I wonder if this would be a good time to go back and talk a little bit about a concept that I found really interesting, and that is FND as a prodromal syndrome before a different neurological problem. So, for instance, FND prodromal to Parkinson's disease. Can you talk to us a little bit about that? I mean, obviously I was familiar with the fact that patients who have nonepileptic seizurelike events often have epileptic seizures, but the idea of FND ahead of Parkinson's was new to me. Dr Stone: So, this is definitely a thing that happens. It's interesting because previously, perhaps, if you saw someone who was referred with a functional tremor---this has happened to me and my colleagues. They send me some with a functional tremor. By the time I see them, it's obvious they've got Parkinson's because it's been a little gap. But it turns out that the diagnosis of functional tremor was wrong. It was just that they've developed that in the prodrome of Parkinson's disease. And if you think about it, it's what you'd expect, really, especially with Parkinson's disease. We know people develop anxiety in the prodrome of Parkinson's for ten, fifteen years before it's part of the prodrome. Anxiety is a very strong risk factor for FND, and they're already developing abnormalities in their brain predisposing them to tremor. So, you put those two things together, why wouldn't people get FND? It is interesting to think about how that's the opposite of seizures, because most people with comorbidity of functional seizures and epilepsy, 99% of the time the epilepsy came first. They had the experience of an epileptic seizure, which is frightening, which evokes strong threat response and has somehow then led to a recapitulation of that experience in a functional seizure. So yeah, it's really interesting how these disorders overlap. We're seeing something similar in early MS where, I think, there's a slight excess of functional symptoms; but as the disease progresses, they often become less, actually. Dr Smith: What is the prognosis with the types of physical therapy? And we haven't really talked about psychological therapy, but what's the success rate? And then what's the relapse rate or risk? Dr Stone: Well, it does depend who they're seeing, because I think---as you said---you're finding difficult to get people in your institution who you feel are comfortable with this. Well, that's a real problem. You know, you want your therapists to know about this condition, so that matters. But I think with a team with a multidisciplinary approach, which might include psychological therapy, physio, OT, I think the message is you can get really good outcomes. You don't want to oversell this to patients, because these treatments are not that good yet. You can get spectacular outcomes. And of course, people always show the videos of those. But in published studies, what you're seeing is that most studies of- case series of rehabilitation, people generally improve. And I think it's reasonable to say to a patient, that we have these treatments, there's a good chance it's going to help you. I can't guarantee it's going to help you. It's going to take a lot of work and this is something we have to do together. So, this is not something you're going to do to the patient, they're going to do it with you. Which is why it's so important to find out, hey, do they agree with you with the diagnosis? And check they do. And is it the right time? It's like when someone needs to lose weight or change any sort of behavior that they've just become ingrained. It's not easy to do. So, I don't know if that helps answer the question. Dr Smith: No, that's great. And you actually got right where I was wanting to go next, which is the idea of timing and acceptance. You brought this up earlier on, right? So, sometimes patients are excited and accepting of having an affirmative diagnosis, but sometimes there's some resistance. How do you manage the situation where you're making this diagnosis, but a patient's resistant to it? Maybe they're fixating on a different disease they think they have, or for whatever reason. How do you handle that in terms of initiating therapy of the overall diagnostic process? Dr Stone: We should, you know, respect people's rights to have whatever views they want about what's wrong with them. And I don't see my job as- I'm not there to change everyone's mind, but I think my job is to present the information to them in a kind of neutral way and say, look, here it is. This is what I think. My experience is, if you do that, most people are willing to listen. There are a few who are not, but most people are. And most of the time when it goes wrong, I have to say it's us and not the patients. But I think you do need to find out if they can have some hope. You can't do rehabilitation without hope, really. That's what you're looking for. I sometimes say to patients, where are you at with this? You know, I know this is a really hard thing to get your head around, you've never heard of it before. It's your own brain going wrong. I know that's weird. How much do you agree with it on a scale of naught to ten? Are you ten like completely agreeing, zero definitely don't? I might say, are you about a three? You know, just to make it easy for them to say, no, I really don't agree with you. Patients are often reluctant to tell you exactly what they're thinking. So, make it easy for them to disagree and then see where they're at. If they're about seven, say, that's good. But you know, it'd be great if you were nine or ten because this is going to be hard. It's painful and difficult, and you need to know that you're not damaging your body. Those sort of conversations are helpful. And even more importantly, is it the right time? Because again, if you explore that with people, if a single mother with four kids and, you know, huge debts and- you know, it's going to be very difficult for them to engage with rehab. So, you have to be realistic about whether it's the right time, too; but keep that hope going regardless. Dr Smith: So, Jon, there's so many things I want to talk to you about, but maybe rather than let me drive it, let me ask you, what's the most important thing that our listeners need to know that I haven't asked you about? Dr Stone: Oh God. I think when people come and visit me, they sometimes, let's go and see this guy who does a lot of FND, and surely, it'll be so easy for him, you know? And I think some of the feedback I've had from visitors is, it's been helpful to watch, to see that it's difficult for me too. You know, this is quite hard work. Patients have lots of things to talk about. Often you don't have enough time to do it in. It's a complicated scenario that you're unravelling. So, it's okay if you find it difficult work. Personally, I think it's very rewarding work, and it's worth doing. It's worth spending the time. I think you only need to have a few patients where they've improved. And sometimes that encounter with the neurologist made a huge difference. Think about whether that is worth it. You know, if you do that with five patients and one or two of them have that amazing, really good response, well, that's probably worth it. It's worth getting out of bed in the morning. I think reflecting on, is this something you want to do and put time and effort into, is worthwhile because I recognize it is challenging at times, and that's okay. Dr Smith: That's a great number needed to treat, five or six. Dr Stone: Exactly. I think it's probably less than that, but… Dr Smith: You're being conservative. Dr Stone: I think deliberately pessimistic; but I think it's more like two or three, yeah. Dr Smith: Let me ask one other question. There's so much more for our listeners in the article. This should be required reading, in my opinion. I think that of most Continuum, but this, I really truly mean it. But I think you've probably inspired a lot of listeners, right? What's the next step? We have a general or comprehensive neurologist working in a community practice who's inspired and wants to engage in the proactive care of the FND patients they see. What's the next step or advice you have for them as they embark on this? It strikes me, like- and I think you said this in the article, it's hard work and it's hard to do by yourself. So, what's the advice for someone to kind of get started? Dr Stone: Yeah, find some friends pretty quick. Though, yeah, your own enthusiasm can take you a long way, you know, especially with we've got much better resources than we have. But it can only take you so far. It's really particularly important, I think, to find somebody, a psychiatrist or psychologist, you can share patients with and have help with. In Edinburgh, that's been very important. I've done all this work with the neuropsychiatrist, Alan Carson. It might be difficult to do that, but just find someone, send them an easy patient, talk to them, teach them some of this stuff about how to manage FND. It turns out it's not that different to what they're already doing. You know, the management of functional seizures, for example, is- or episodic functional movement disorders is very close to managing panic disorder in terms of the principles. If you know a bit about that, you can encourage people around you. And then therapists just love seeing these patients. So, yeah, you can build up slowly, but don't- try not to do it all on your own, I would say. There's a risk of burnout there. Dr Smith: Well, Dr Stone, thank you. You don't disappoint. This has really been a fantastic conversation. I really very much appreciate it. Dr Stone: That's great, Gordon. Thanks so much for your time, yeah. Dr Smith: Well, listeners, again, today I've had the great pleasure of interviewing Dr Jon Stone about his article on the multidisciplinary treatment for functional neurologic disorder, which he wrote with Dr Alan Carson. This article appears in the August 2025 Continuum issue on movement disorders. Please be sure to check out Continuum Audio episodes from this and other issues. And listeners, thank you once again for joining us today. Dr Monteith: This is Dr Teshamae Monteith, Associate Editor of Continuum Audio. We hope you've enjoyed this subscriber-exclusive interview. Thank you for listening.

Send us a textChristy Kestner, PhD, joins Erich Schramm, MD to discuss her journey from bench scientist to medical communicator. She talks about the importantce of spreading knowledge far and wide, particularly in the current era of massive misinformation. The duo talk about the problem of keeping medical and scientific information in silos and how communicators like Christy Kestner can help other scientists and doctors communicate more effectively with the public and patients alike. Christy Kestner introduces her work at Endosymbiont and her platform at Brain and Beyond to help people understand the complex world of medicine. Dr. Schramm then asks about some of the upcoming neuroscience research, including with brain computer interfaces, ALS, and Alzheimer's treatments.Be a part of advancing science by participating in clinical research.Have a question for Dr. Koren? Email him at askDrKoren@MedEvidence.comListen on SpotifyListen on Apple PodcastsWatch on YouTubeShare with a friend. Rate, Review, and Subscribe to the MedEvidence! podcast to be notified when new episodes are released.Follow us on Social Media:FacebookInstagramX (Formerly Twitter)LinkedInWant to learn more? Checkout our entire library of podcasts, videos, articles and presentations at www.MedEvidence.comMusic: Storyblocks - Corporate InspiredThank you for listening!

In this episode of the Let's Talk Brain Health Podcast, we welcome Dr. Kellyann Niotis, MD, the world's first fellowship-trained preventive neurologist, who shares her insights on early detection and risk reduction for neurodegenerative diseases, including Alzheimer's disease, Parkinson's disease, and Lewy body dementia. Dr. Niotis discusses the emerging field of preventive neurology, the role of blood biomarkers and genetic testing, and the importance of lifestyle choices in maintaining brain health. She also highlights the impact of cholesterol management, sleep studies, and the significance of personalized care approaches. Join us as we dive into a comprehensive discussion about the future of brain health and the proactive steps we can take today for healthier brains tomorrow.00:00 Introduction to Dr. Kellyann Niotis, MD02:47 What is Preventive Neurology?06:08 The Role of Biomarkers in Early Detection13:52 Lifestyle Modifications and Brain Health17:12 Cholesterol and Brain Health24:15 The Impact of Statins on Cognition26:05 Underutilized Tools in Brain Health30:11 Rapid Fire Questions and Final ThoughtsResourcesConnect with Kellyann on Instagram @drkellyannniotis Visit her website ​​and learn more about her new clinic on their websiteResearchLearn more about the research-informed brain health risks mentioned in this episode from the “Dementia prevention, intervention, and care: 2024 report of the Lancet standing Commission” ReportRead more about Dr. Lisa Misconi's research on how estrogen receptors are unregulated in perimenopause in this research article 

In the first part of this five-part series, Dr. Paul Crane discusses the reemergence of measles and outlines steps to take if you suspect someone may have measles. 

Dr. Justin Abbatemarco talks with Dr. Daniel Ontaneda about the 2024 revisions of the McDonald criteria for diagnosing multiple sclerosis.  Read the related article in The Lancet Neurology.  Disclosures can be found at Neurology.org. 

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

The Smart 7 is an award winning daily podcast, in association with METRO that gives you everything you need to know in 7 minutes, at 7am, 7 days a week...With over 19 million downloads and consistently charting, including as No. 1 News Podcast on Spotify, we're a trusted source for people every day and the Sunday 7 won a Gold Award as “Best Conversation Starter” in the International Signal Podcast Awards If you're enjoying it, please follow, share, or even post a review, it all helps...Today's episode includes the following guests:Donald Trump - President of the United States of America Kate Brintworth - Chief Midwifery Officer for NHS EnglandDr Debra Houry - Former Chief Medical Officer and Deputy Director for Programme and Science at America's CDCDoctor Owasi Durrani - Emergency Medical Physician based in Houston TexasWill Guyatt - The Smart 7's Tech Guru Professor Johnny Chan - Atmospheric Scientist at the City University of Hong Kong Antonio Guterres - UN Secretary General Xi Jinping - President of the People's Republic of China Professor Myles Allen - Head of Atmospheric, Oceanic & Planetary Physics at Oxford UniversityProfessor Sarah Tabrizi - Director of University College London Huntington's Disease Centre Professor Edward Wild - Consultant Neurologist at the National Hospital for Neurology and Neurosurgery at UCLH Doctor Chris Van Tulleken - doctor, author and TV presenter Reid Wiseman - NASA Astronaut and Commander of Artemis Moon mission Christine Koch - NASA Astronaut and soon to be the First Woman on the MoonFrank Quevedo - Environmental Scientist and the Executive Director of the South Fork Natural History MuseumContact us over @TheSmart7pod or visit www.thesmart7.com or find out more at www.metro.co.uk Presented by Ciara Revins, written by Liam Thompson, researched by Lucie Lewis and produced by Daft Doris. Hosted on Acast. See acast.com/privacy for more information.

Dr. Deanna Saylor and Dr. Senjuti Saha discuss colonialism in global health and the importance of pathogen genomics.  Show reference:  https://www.thelancet.com/journals/landig/article/PIIS2589-7500(24)00091-8/fulltext

Sign up for updates on webinars, events, and resources for the Parkinson's community—delivered to your inbox. https://dpf.org/newsletter-signup In the first episode of our three-part series about neuropsychology and Parkinson's, Connie Carpenter Phinney and Dr. Mark Mapstone explore how brain chemistry, especially dopamine, relates to thinking, movement, and mood in Parkinson's. They break down key terms like cognition and executive function and offer insights into how Parkinson's affects brain systems beyond motor symptoms. This episode lays the groundwork for understanding how the brain works—and what happens when it changes. **This content is possible thanks to the generosity of our listeners. Every day more people are diagnosed with Parkinson's, and this means our work is more important than ever. Please support our work by visiting https://dpf.org/donate.** Interested in our Living with Parkinson's Meetup, Care Partner Meetup, or Live Well Today Webinars? Learn how to join. https://dpf.org/webinars Visit https://dpf.org to learn more about the Davis Phinney Foundation for Parkinson's. Speaker Bios: Connie Carpenter Phinney Connie Carpenter Phinney is a co-founder of the Davis Phinney Foundation and has been her husband's care partner for over 25 years. Her background in science combined with her lived experience and curiosity helped shape this conversation with neuropsychologist Dr. Mark Mapstone. Connie is the host of the Foundation's Care Partner Meetup, a monthly virtual meetup for Parkinson's care partners held the first Tuesday of each month. To attend the meetup, sign up here: https://davisphinneyfoundation.org/events/parkinsons-care-partner-meetup/ Dr. Mark Mapstone Mark Mapstone is Professor of Neurology at the University of California, Irvine School of Medicine. He is a member of the UCI Institute for Memory Impairments and Neurological Disorders and a Fellow of the UCI Center for Neurobiology of Learning and Memory. His research focuses on pre-clinical detection of neurological disease using cognitive tests and biomarkers obtained from blood. He has a special interest in developing strategies to maintain successful cognitive aging. In the clinic, he specializes in cognitive assessment of older adults with suspected brain disease. Dr. Mapstone earned a PhD in Clinical Psychology at Northwestern University and completed fellowship training in Neuropsychology and Experimental Therapeutics at the University of Rochester. He received a Career Development Award from the National Institute on Aging and his research has been funded by the National Institutes of Health, the Michael J. Fox Foundation, and the Department of Defense.

Dr. Deanna Saylor talks with Dr. Senjuti Saha about colonialism in global health and the importance of pathogen genomics.  Read the related article in The Lancet.  Disclosures can be found at Neurology.org. 

In the final episode of this two-part series, Dr. Justin Abbatemarco discusses long-term maintenance therapy options.  Show reference:  https://www.neurology.org/doi/10.1212/CPJ.0000000000200504 

In this week's episode, Brain & Life Podcast host Dr. Daniel Correa is joined by Tiffany Kairos, an epilepsy advocate and founder of the Epilepsy Network, and her husband Chris Kairos. Tiffany shares her journey of living with epilepsy and her recent diagnosis of Functional Neurologic Disorder (FND). Tiffany and Chris delve into their experience managing both conditions, the impact on daily life, and the support systems that help her navigate these experiences. Dr. Correa is then joined by Dr. W. Curt LaFrance, Inaugural Director of Neuropsychiatry and Behavioral Neurology at Rhode Island Hospital, Director of the VA Mind Brain program, and Professor of Psychiatry and Neurology at Brown University. Dr. LaFrance discusses the complexities of FND, the importance of integrating neurology and psychiatry for effective diagnosis and treatment, and the evolution of terminology to reduce stigma and improve patient engagement.   Additional Resources The Epilepsy Network (TEN) What is Functional Neurologic Disorder? Taking Control of Your Seizures Epilepsy Foundation The Anita Kaufman Foundation   Other Brain & Life Podcast Episodes on These Topics JenVon Cherry on Educating Communities of Color About Epilepsy Actor Cameron Boyce's Legacy and Raising Awareness About SUDEP Tiffany Kairos on Finding Her Voice in Epilepsy Advocacy   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: Tiffany Kairos @TiffanyKairos @theepilepsynetwork; Chris Kairos @ka1ro5; Dr. W. Curt LaFrance @brownuniversityhealth Hosts: Dr. Daniel Correa @neurodrcorrea; Dr. Katy Peters @KatyPetersMDPhD

Orla Hardiman, Professor of Neurology at Trinity College and Consultant Neurologist at Beaumont Hospital in Dublin, reacts to a new trial showing success in treating Huntington's Disease

Surprise! Coming to you a few weeks before our Season 11 launch with a BONUS episode to celebrate World FTD Awareness Week. We chatted with Dr. Ryan Darby, director of the Frontotemporal Dementia Clinic in the Department of Neurology at Vanderbilt University Medical Center. He gave us on updates in FTD research - how to get involved & how our advocacy moves research forward.A VERY special thank you to today's sponsor ⁠⁠⁠⁠AVIADOBIO⁠⁠⁠⁠ for making this episode possible! Want more Remember Me? Join us on Patreon⁠⁠⁠⁠⁠⁠You get exclusive content and it's a great way to support the show! ⁠⁠⁠⁠⁠⁠⁠www.patreon.com/remembermecommunity⁠⁠⁠⁠⁠⁠⁠----------If you're curious about anything RM, we'd love to connect with you on ⁠⁠⁠⁠⁠⁠⁠⁠⁠Instagram, and visit ⁠⁠⁠⁠⁠⁠our website at⁠⁠⁠⁠⁠⁠⁠⁠⁠ www.remembermeftd.com⁠⁠⁠⁠⁠⁠⁠⁠⁠, all the latest updates! ------Remember Me Podcast + Community is here to offer hope + human connection for families, caregivers, and individuals impacted by Frontotemporal Dementia (FTD). Always, always accept the good.

In part one of this two-part series, Dr. Justin Abbatemarco discusses what we know and don't know surrounding MOG antibody–associated diseases (MOGADs).  Show reference:  https://www.neurology.org/doi/10.1212/CPJ.0000000000200504 

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

Episode: 2823 Gilles de la Tourette and Hypnotic Crimes.  Today, hypnotic crimes.

In the final part of this three-part series, Dr. Justin Abbatemarco and Drs. John Chen and Smathorn Thakolwiboon discuss how to approach discontinuation of immunotherapy in clinical practice.  Show reference:  https://www.neurology.org/doi/10.1212/WNL.0000000000213903   

In the second part of this two-part series, Dr. Robert Holloway talks with Dr. Carolyn Rennels about legal and ethical considerations, the importance of interdisciplinary support, and the emotional impact on clinicians.  Read the related article in Neurology® Clinical Practice.  Disclosures can be found at Neurology.org. 

In part two of this three-part series, Dr. Justin Abbatemarco and Drs. John Chen and Smathorn Thakolwiboon discuss a long-term maintenance approach for MOGAD.  Show reference:  https://www.neurology.org/doi/10.1212/WNL.0000000000213903  

We live in a culture obsessed with treating symptoms, weight gain, fatigue, high blood pressure, brain fog, poor sleep, as if each were an isolated problem. But what if these struggles aren't the problem at all? What if they're just the flashing check engine lights on the dashboard of your body, pointing to a deeper issue that's been hiding in plain sight: Metabolic Disease. In this episode, Dr. JC Doornick pulls back the curtain on why nearly every chronic health crisis in America today — from obesity and Type 2 diabetes to heart disease, hypertension, and even dementia — can be traced back to metabolic dysfunction. He explains how the healthcare industry profits from keeping us stuck in a never-ending cycle of pills, injections, and quick fixes, rather than empowering us to address the root cause upstream. You'll also learn about Metabolic Synchronization — a practical, upstream approach that helps realign the body and mind through five key foundations: Proper diet & nutrition Proper movement & muscle development Proper sleep Proper education & mental detox Proper community & support This episode is a wake-up call: the lights are flashing, and the choice is yours. Will you keep patching symptoms downstream, or will you finally pop the hood and reclaim control of your health, your mind, and your future?