Podcasts about CNS

I sit down with nutrition scientist Dr. Luke Bucci to explore the powerful connection between blood flow, nitric oxide, mitochondrial health, and healthy aging. We discuss why circulation impacts nearly every function in the body, what causes energy levels to decline with age, and how nutrition, exercise, and targeted supplementation may help support long-term vitality. Dr. Bucci also explains the science behind nitric oxide, blood sugar regulation, and the role mitochondria play in keeping us energized and resilient throughout life.Dr. Luke Bucci, PhD, CNS, CCN is the Chief Scientific Officer of Juvenon and a biomedical scientist with more than 40 years of experience in nutrition, dietary supplements, and clinical laboratory science. He earned his PhD in Biomedical Sciences from the University of Texas Health Science Center at Houston and has helped develop numerous patented nutritional products used worldwide. A recognized authority in healthy aging, sports nutrition, omega-3s, probiotics, and dietary supplement science, Dr. Bucci has authored scientific books, taught university-level courses, and received multiple industry awards for his contributions to nutrition and health innovation.Links mentioned during this episode:Juvenon: https://juvenon.com/Free Initial Consultation with Dr. Megan: https://p.bttr.to/3a9lfYkLyons' Share Instagram: www.instagram.com/thelyonsshareJoin Megan's newsletter: www.thelyonsshare.org/newsletter

Life sciences is a hub of dealmaking activity. Over the past year, more than 30 transactions valued at $1 billion or more have crossed the finish line. But the picture in other segments of healthcare is more mixed. At RBC Capital Markets' Global Healthcare Conference in New York, Darren Campili, Global Head of Healthcare Investment Banking, hosts colleagues David Levin, Ahmed Attia and Jason Levitz to explore what's driving deals and where the opportunities are heading.Key PointsHealthcare M&A is strong, with a surge of high-value deals in life sciences.Equity performance is challenging, but investors in life sciences and biotech have seen good outcomes.IPO activity has rebounded; again, life sciences and biotech are most successful.Dealmaking has been largely unaffected by regulatory uncertainty, though challenges remain on reimbursement and MFN pricing.Larger companies believe they have the edge in using AI for profitability and competitiveness.Introductions [00:25]Host Darren Campili, Global Head of Healthcare Investment Banking, introduces the podcast and guests: David Levin, Co-Head of U.S. M&A; Ahmed Attia, Managing Director, Healthcare M&A; and Jason Levitz, Head of Healthcare Equity Capital Markets.M&A strength in healthcare [01:11]The M&A market in life sciences is extremely strong. The number of $1 billion-plus deals has tripled in the past year. There has been significant activity among mid-caps as well as large-cap companies, and a diversity of premiums.Healthcare in the equity markets [13:24]In the broader context of the U.S. equity markets, healthcare is performing poorly, particularly among large-cap medtech and services companies. At the same time, life sciences and biotechs are outperforming, leading to diverse outcomes for investors.IPO activity [15:20]IPO volumes have rebounded after some disappointing years. Deal flow has centered on oncology, I&I, and CNS.Political impact [24:15]Dealmaking has continued despite uncertainty over the FDA. Tariff policy has been a net positive for U.S. inflows as pharma businesses seek U.S. capabilities. Managing reimbursement and Most Favored Nation pricing remains challenging for some.

Life sciences is a hub of dealmaking activity. Over the past year, more than 30 transactions valued at $1 billion or more have crossed the finish line. But the picture in other segments of healthcare is more mixed. At RBC Capital Markets' Global Healthcare Conference in New York, Darren Campili, Global Head of Healthcare Investment Banking, hosts colleagues David Levin, Ahmed Attia and Jason Levitz to explore what's driving deals and where the opportunities are heading.Key PointsHealthcare M&A is strong, with a surge of high-value deals in life sciences.Equity performance is challenging, but investors in life sciences and biotech have seen good outcomes.IPO activity has rebounded; again, life sciences and biotech are most successful.Dealmaking has been largely unaffected by regulatory uncertainty, though challenges remain on reimbursement and MFN pricing.Larger companies believe they have the edge in using AI for profitability and competitiveness.Introductions [00:25]Host Darren Campili, Global Head of Healthcare Investment Banking, introduces the podcast and guests: David Levin, Co-Head of U.S. M&A; Ahmed Attia, Managing Director, Healthcare M&A; and Jason Levitz, Head of Healthcare Equity Capital Markets.M&A strength in healthcare [01:11]The M&A market in life sciences is extremely strong. The number of $1 billion-plus deals has tripled in the past year. There has been significant activity among mid-caps as well as large-cap companies, and a diversity of premiums.Healthcare in the equity markets [13:24]In the broader context of the U.S. equity markets, healthcare is performing poorly, particularly among large-cap medtech and services companies. At the same time, life sciences and biotechs are outperforming, leading to diverse outcomes for investors.IPO activity [15:20]IPO volumes have rebounded after some disappointing years. Deal flow has centered on oncology, I&I, and CNS.Political impact [24:15]Dealmaking has continued despite uncertainty over the FDA. Tariff policy has been a net positive for U.S. inflows as pharma businesses seek U.S. capabilities. Managing reimbursement and Most Favored Nation pricing remains challenging for some.

Mini Episode 1 - airs June 9, 2026 The Wholistic Take: Health News and Trends through a Wholistic Lens The Wholistic Take is a podcast series on the Wholistic Matters Podcast. We explore the latest health news and trends from a wholistic health perspective. The Wholistic Take episodes are shorter in length for easier consumption and timely delivery. We track the latest health news and offer wholistic insights for you to use in clinical practice and for personal care. HOST: Dr. Daina Parent, ND GUEST: Betsy Miller, MS, CNS, RH(AHG), DCN-c In this mini episode, Dr. Daina Parent and Betsy Miller discuss the recent renaming of the condition formerly known as PCOS, know renamed PMOS. They cover what this name change means, why it's important and how it will affect women's healthcare going forward. Parent and Miller emphasize the importance of a holistic approach in managing PMOS symptoms, including lab testing, diet, herbs, nutrients, and lifestyle. Betsy Miller, MS, CNS, RH(AHG), DCN-c is a clinical herbalist and certified nutrition specialist with a passion for women's health, evidence-based medicine and patient-centered care. Over the past 15 years she has devoted herself to building a clinical practice, cultivating critical research skills and teaching herbal medicine at the graduate level. She is the Clinical Product Support Manager at Standard Process and contributes digital education content for the Wholistic Matters website. Podcast Summary 1:35 PCOS is now PMOS – why is this news? 2:55 How the new name will help woman receive the proper diagnosis 4:33 LH:FSH Ratio – when and how to test for these 5:24 Supporting symptoms of PMOS including insulin resistance, ovulation, and hyperandrogenism 6:48 Lab testing, nutrients and herbs for blood sugar regulation 9:57 Menstrual Irregularities – individualized approach paired with labs, nutrients and herbs 14:11 Supporting hyperandrogenism and hirtuism 15:19 How to support fertility challenges 17:24 Diet and lifestyle recommendations for managing PMOS

In this episode of the Oncology Brothers podcast, we discussed challenging cases focused on metastatic non-small cell lung cancer (NSCLC) with common EGFR mutations. Joined by experts Dr. Shirish Gadgeel from the Emory University and Dr. Wade Iams from Tennessee Oncology, the discussion revolved around two real-life patient cases. The first case featured a 54-year-old gentleman with active tobacco use and diffusely metastatic NSCLC, including an isolated brain lesion. The panel explored treatment options, including single-agent osimertinib versus dual combinations of amivantamab-lazertinib and osimertinib-chemotherapy, emphasizing the importance of shared decision-making and considering co-mutations and patient demographics. In the second case, the conversation shifted to supportive care and managing side effects, particularly focusing on skin toxicity associated with amivantamab. The experts shared their proactive approaches to patient education and the significance of monitoring and adjusting treatment plans to enhance patient quality of life.   Key Points: In EGFR-mutated NSCLC with CNS metastases, treatment selection between single-agent osimertinib and combination amivantamab-lazertinib vs. osimertinib-chemotherapy requires individualized consideration of age, co-mutations, extent of disease, and patient preference rather than mutation status alone. Younger patients with CNS disease may benefit from more aggressive upfront combination therapy, while shared decision-making remains central to navigating the expanded efficacy versus increased toxicity trade-off. Dermatologic toxicities associated with amivantamab requires proactive management including supportive care regimen, early dose adjustments and close patient monitoring to maintain treatment continuity. Providing the best available upfront therapy in metastatic EGFR-mutated NSCLC is critical, as sequencing options become more limited at progression. Join us for an insightful discussion on the latest treatment algorithms, the importance of personalized care, and the evolving landscape of NSCLC management.   Listen us on: Spotify: https://open.spotify.com/show/31BXhY9FM4gPWG10WgE11o Apple Podcast: https://podcasts.apple.com/us/podcast/oncology-brothers-practice-changing-cancer-discussions/id1653340966   Follow us on social media: ⁠X/Twitter: https://twitter.com/oncbrothers ⁠Instagram: https://www.instagram.com/oncbrothers Website: https://oncbrothers.com/   Don't forget to subscribe for more episodes featuring conference highlights and challenging cases in oncology! #EGFRMutated, #LungCancer, #ThoracicOncology, #PersonalizedMedicine, #OncologyBrothers

Full Text of Readings The Solemnity of the Most Holy Body and Blood of Christ Lectionary: 167 The Saint of the day is Blessed Franz Jägerstätter Blessed Franz Jägerstätter, an Austrian farmer executed for refusing to fight for Nazi Germany, is pictured in an undated photo. (CNS photo)  Saint of the Day for June 7 (May 20, 1907 – August 9, 1943) Blessed Franz Jägerstätter's Story Called to fight for his country as a Nazi soldier, Franz Jägerstätter eventually refused, and this husband and father of three daughters—Rosalie, Marie and Aloisia—was executed because of it. Born in St. Radegund in Upper Austria, Franz Jägerstätter lost his father during World War I and was adopted after Heinrich Jaegerstaetter married Rosalia Huber. As a young man, he loved to ride his motorcycle and was the natural leader of a gang whose members were arrested in 1934 for brawling. For three years he worked in the mines in another city and then returned to St. Radegund, where he became a farmer, married Franziska and lived his faith with quiet but intense conviction. In 1938, he publicly opposed the German Anschluss–annexation–of Austria. The next year he was drafted into the Austrian army, trained for seven months and then received a deferment. In 1940, Franz was called up again but allowed to return home at the request of the town's mayor. He was in active service between October 1940 and April 1941, but was again deferred. His pastor, other priests, and the bishop of Linz urged him not to refuse to serve if drafted. In February 1943, Franz was called up again and reported to army officials in Enns, Austria. When he refused to take the oath of loyalty to Hitler, he was imprisoned in Linz. Later he volunteered to serve in the medical corps but was not assigned there. During Holy Week Blessed Franz Jägerstätter wrote to his wife: “Easter is coming and, if it should be God's will that we can never again in this world celebrate Easter together in our intimate family circle, we can still look ahead in the happy confidence that, when the eternal Easter morning dawns, no one in our family circle shall be missing—so we can then be permitted to rejoice together forever.” He was transferred in May to a prison in Berlin. Challenged by his attorney that other Catholics were serving in the army, Franz responded, “I can only act on my own conscience. I do not judge anyone. I can only judge myself.” He continued, “I have considered my family. I have prayed and put myself and my family in God's hands. I know that, if I do what I think God wants me to do, he will take care of my family.” On August 8, 1943, Franz wrote to Fransizka: “Dear wife and mother, I thank you once more from my heart for everything that you have done for me in my lifetime, for all the sacrifices that you have borne for me. I beg you to forgive me if I have hurt or offended you, just as I have forgiven everything…My heartfelt greetings for my dear children. I will surely beg the dear God, if I am permitted to enter heaven soon, that he will set aside a little place in heaven for all of you.” Franz Jägerstätter was beheaded and cremated the following day. In 1946, his ashes were reburied in St. Radegund near a memorial inscribed with his name and the names of almost 60 village men who died during their military service. He was beatified in Linz on October 26, 2007. His “spiritual testament” is now in Rome's St. Bartholomew Church as part of a shrine to 20th-century martyrs for their faith. Blessed Franz's liturgical feast is celebrated on August 9. Want to learn more about Blessed Franz Jägerstätter? Click here! Facebook Twitter Pinterest Email Sign Up for Our Daily Newsletter Includes Saint of the Day, Minute Meditations, and Pause + Pray. Saint of the Day, Copyright Franciscan Media

Contributor: Aaron Lessen, MD Educational Pearls:  Back pain is a common presenting complaint in the emergency department. Challenges arise when tailoring care to elderly populations using standard medical therapy: Muscle relaxants carry the risk of CNS depression or anticholinergic effects such as urinary retention and confusion. Pain medications such as opiates have side effects including constipation, respiratory depression, and hypotension. NSAIDs carry a risk of GI bleeding and worsening kidney function with chronic use. A randomized clinical trial assessing the effects of acupuncture on low back pain took 800 adults aged 65 and older with chronic low back pain and placed them into one of three treatment arms: Usual medical care Standard acupuncture consisting of 8–15 treatment sessions over 12 weeks, plus usual medical care Standard acupuncture consisting of 8–15 treatment sessions over 12 weeks, plus 4-6 maintenance sessions during the next 12 weeks, plus usual medical care Using the Roland-Morris Disability Questionnaire (RMDQ) score, they assessed disability at 6 months and 12 months. The study found that those who had undergone treatment with acupuncture had significantly greater improvements in disability related to low back pain compared to the group that was only treated with usual medical care. Acupuncture is not used in the ER, but could represent a relatively safe adjunctive therapy for patients who are not responding to standard medical therapy alone.   References:  American College of Surgeons Committee on Trauma. Best practices guidelines: geriatric trauma management. American College of Surgeons; 2023. Accessed May 27, 2026. https://www.facs.org/media/ubyj2ubl/best-practices-guidelines-geriatric-trauma.pdf DeBar LL, Wellman RD, Justice M, et al. Acupuncture for chronic low back pain in older adults: a randomized clinical trial. JAMA Netw Open. 2025;8(9):e2531348. doi:10.1001/jamanetworkopen.2025.31348 Summarized by Ashley Lyons, OMS3 | Edited by Ashley Lyons & Ahmed Abdel-Hafiz, NREMT-P

We love to hear from our listeners. Send us a message. On this week's episode of the Business of Biotech, Jeff Jonas, M.D., CEO of Tortugas Neuroscience, talks about the company's April 2026 launch and how in-licensed development assets were chosen. Jeff explains his strategy of chasing fast proof of safety and efficacy in humans, not animals, and talks about what product differentiation looks like in brain disorders, from adjusting indication targets to conducting head-to-head trials. He also reflects on the opportunity with psychedelics, RFK Jr.'s quest to curb SSRI prescriptions, the payer landscape in CNS disorders, and more. Access this and hundreds of episodes of the Business of Biotech videocast under the Business of Biotech tab at lifescienceleader.com.  Subscribe to our monthly Business of Biotech newsletter. Get in touch with guest and topic suggestions: ben.comer@lifescienceleader.comFind Ben Comer on LinkedIn: https://www.linkedin.com/in/bencomer/

***"Original Description"*** Hello lovelies. Today on this Saturday evening and night there is again the "Mixmission Clubnight Session" for you, as once that month. The whole thing as usual live on RM FM Techhouse. From 11 p.m. (CET) you will get to hear the exclusive 1 hour guest DJ set of "Miss Manoosh". Mixcloud Link: www.mixcloud.com/ElaManoosh The session is scheduled for 1 a.m. (CET) on a pro forma basis. The CNS will be deep dub, techno and electronica in terms of sound. I wish you a lot of fun listening and watching

This EAUN episode features an interview with the faculty of the hands-on training on erectile dysfunction. Jeannette Verkerk-Geelhoed (NL), MSc, PhD candidate and CNS at St. Antonius Hospital, specialising in male sexual health including erectile dysfunction and Peyronie's disease, is joined by Phil Reynolds (GB), MSc, BSc, HNC, radiographer at Clatterbridge Cancer Centre with a holistic focus on prostate cancer care, and Mariet Lenaers (BE), MSc, BN, prosthetic nurse at Virga Jesse Hospital, specialising in counselling patients undergoing prosthetic treatment.Together, they reflect on the EAUN26 hands-on training session, focusing on the impact of sexual dysfunction in men and what it means for patients and their partners. The discussion highlights both the physical and psychological aspects of erectile dysfunction, as well as the importance of communication and patient education. The faculty also review current treatment options, including oral medication, vacuum devices, intracavernosal injections, and, as a final option, penile prosthesis.For more EAU podcasts, please go to your favourite podcast app and subscribe to our podcast channel for regular updates: Apple Podcasts, Spotify, EAU YouTube channel.

Dr. Hoffman continues his conversation with Dr. Corey Schuler, PhD(c), FNP, DC, CNS, and director of medical affairs at Allergy Research Group.

Dr. Corey Schuler, PhD(c), FNP, DC, CNS, and director of medical affairs at Allergy Research Group, details his paper “Energy Allocation Resilience and Endocrine Integration” in the International Journal of Molecular Sciences. He introduces the Energy Allocation System (EAS), which emphasizes how the body allocates energy—not just produces it—and links many symptoms to impaired bioenergetics and resilience. They discuss mitochondria as energy generators and cellular signaling hubs, the integrated stress response and endocrine coordination (HPA axis, thyroid, gonads), and mitohormesis/eustress (exercise, fasting, heat/cold, circadian “zeitgebers”). Schuler explains nuanced testing for fatigue (diurnal cortisol, CGM patterns, thyroid markers including T3/reverse T3) and a case of a perimenopausal woman where oral contraceptives and cortisol dysregulation affected glucose patterns. They cover mitochondrial support (removing obstacles like pollutants/antibiotics, triglycerides, carnitine, dietary fats, micronutrients) and pacing/sequencing lifestyle interventions.

How does the grit required to finish one of the world's toughest endurance races translate to the delicate work of repairing the human spinal cord? What happens when we stop looking at cells as the cure and start looking at the "secretome"—the potent signals they leave behind? Find out the answers to these questions and more as António Salgado discusses his work and unique trajectory in this episode of Knowledge Pills.From the microscopic signals of Central Nervous System (CNS) regeneration to the high-stakes environment of university leadership, this episode explores the multidisciplinary mindset needed to solve modern mysteries. Professor Salgado explains the shift toward "cell-free" therapies and discusses how close we are to seeing these lab discoveries transition into clinical treatments for conditions like Parkinson's. He outlines why "cross-talk" between biology, engineering, and neuroscience—the core of his ReNEU team—is the only way to tackle complex medical challenges.In this episode, we discuss Prof. Salgado's research at the Life and Health Sciences Research Institute (ICVS) and his dual role as the Vice-Rector for Research and Science Policy at the University of Minho. He offers vital career advice for the next generation of European researchers and reveals how the discipline of long-distance triathlons maintains his mental resilience in a high-stakes academic career.------Learn more about António SalgadoAntónio Salgado is the Vice-Rector for Research and Science Policy at the University of Minho and a Coordinating Investigator at the ICVS. A leading expert in CNS repair, he focuses on developing innovative therapies for Spinal Cord Injury and Parkinson's Disease using Mesenchymal Stem Cell (MSC) secretomes and ECM-like hydrogels. he is the President of the Portuguese Society for Stem Cells and Cell Therapies and has been recognized with the Gulbenkian Award and the Prize Melo e Castro. Beyond the lab, he is a multiple-time triathlete and Ironman finisher.

Recorded last week at Fierce Biotech Week in Boston, this episode of “The Top Line” features a conversation with Kristen Fortney, Ph.D., co-founder and CEO of BioAge Labs. In a conversation with Ayla Ellison, editor-in-chief of Fierce Healthcare and Life Sciences, Fortney discusses the company’s decade-long effort to use human aging data to identify drug targets tied to longevity and age-related disease. She also breaks down BioAge’s oral NLRP3 inhibitor, BGE-102, which the company believes could have applications across cardiovascular, ocular and CNS diseases by targeting inflammation linked to aging biology. The conversation also explores why pharma companies are paying closer attention to aging and exercise biology, how GLP-1 drugs are reshaping conversations around prevention and what the future of aging-related medicine could look like. To learn more about the topics in this episode: BioAge CEO has big plans for 'multi-disease impact' of NLRP3 drug across cardio, ocular and CNS Novartis, BioAge take on age-related diseases in $550M pact What can we learn from 2024’s biotech IPOs? See omnystudio.com/listener for privacy information.

Send us Fan MailMost autoimmune drugs suppress the immune system broadly - but what if you could selectively remove the antibodies actually causing disease? That's exactly what VYVGART is doing, and it may fundamentally change how we treat conditions like myasthenia gravis and CIDP.Dr. Luc Truyen, M.D., Ph.D., is Chief Medical Officer at argenx ( https://argenx.com/ ), where he leads the company's global clinical development and medical strategy across a rapidly advancing portfolio of immunology and neuromuscular therapies.A neurologist by training, Dr. Truyen brings more than two decades of experience in drug development, with a particular focus on neuroscience, neuroimmunology, and complex CNS disorders. Before joining argenx in 2021, he spent over 20 years at Johnson & Johnson and its pharmaceutical division Janssen Pharmaceuticals, where he held multiple senior leadership roles.Most notably, Dr. Truyen served as Global Head of Development for Neuroscience at Janssen, overseeing early- and late-stage pipelines spanning mood disorders, schizophrenia, and neurodegenerative and neuroinflammatory diseases. He also led global external affairs efforts in Alzheimer's disease, playing key roles in major international collaborations such as the Innovative Medicines Initiative and global dementia platforms.Earlier in his career, Dr. Truyen was Head of R&D and Chief Medical Officer of Janssen Alzheimer Immunotherapy, where he helped guide strategy across research, clinical development, and regulatory functions for novel immunotherapies targeting Alzheimer's disease.At argenx, Dr. Truyen is now helping drive the expansion of VYVGART (efgartigimod), a first-in-class FcRn antagonist, across multiple indications including myasthenia gravis and chronic inflammatory demyelinating polyneuropathy (CIDP), while advancing a broader pipeline aimed at transforming treatment paradigms in autoimmune and neuromuscular diseases.Dr. Truyen earned both his M.D. and Ph.D. in Neurology from the University of Antwerp.#LucTruyen #argenx #VYVGART #efgartigimod #MyastheniaGravis #CIDP #AutoimmuneDisease #Neurology #Biotech #Pharma #DrugDevelopment #FcRn #Immunology #RareDisease #ClinicalTrials #AAN2026 #MedicalInnovation #HealthcareInnovation #BiotechPodcast #LifeSciences #Neuroimmunology #IVIG #PrecisionMedicine #FutureOfMedicineSupport the show

Does GABA Actually Help With Sleep? What the Research Says for Brain Injury Recovery Someone in our community recently asked me about GABA for sleep. They’d seen it recommended online, understood that sleep was critical for their recovery, and wanted to know whether the supplement was worth exploring or just noise. It’s a genuinely good question. And it deserves a proper answer. In this post, I’m going to walk you through what GABA is, what the clinical research actually shows about its effect on sleep, why the blood-brain barrier debate matters (and why it might not derail the whole argument), and what the evidence says about the relationship between sleep and brain recovery. By the end, you’ll have enough to have an informed conversation with your medical team. I’m not a doctor. I’m a three-time haemorrhagic stroke survivor who has spent years researching the science of brain recovery and interviewing hundreds of clinicians and survivors on the Recovery After Stroke podcast. What I offer is a careful read of the evidence, not a clinical prescription. What Is GABA and Why Does It Matter for Sleep? GABA (gamma-aminobutyric acid) is the brain’s primary inhibitory neurotransmitter. If your nervous system were a car, GABA is the brake pedal. It reduces neuronal excitability, quiets cortical arousal, suppresses the brain’s primary arousal centre (the locus coeruleus), and modulates the HPA axis, the stress-response system that drives cortisol. Most sedative medications work by amplifying GABA activity. Benzodiazepines, for instance, bind to GABA-A receptors to increase chloride channel opening, producing their calming effect. GABA isn’t doing something unusual here – it’s doing something fundamental. The question with supplemental oral GABA is more specific: Does taking GABA as a capsule or powder actually produce meaningful neurological effects? What Does the Research Show? Finding 1 — Oral GABA Reduces Sleep Latency (and EEG Can Measure It) A 2015 clinical trial published in the Journal of Nutritional Science and Vitaminology by Yamatsu and colleagues used EEG measurement, actual brainwave monitoring, rather than self-reported sleep questionnaires. One hundred milligrams of oral GABA shortened sleep latency (time to fall asleep) by 5.3 minutes compared to placebo. That might sound modest. But for someone lying awake for 30–40 minutes each night, it’s a meaningful shift. Crucially, this was objective neurophysiological data, not a survey response. (PMID: 26052150) Finding 2 — A 90-Day RCT Showed Improved Sleep Efficiency and Mood A 2024 randomised double-blind placebo-controlled trial published in the Journal of Dietary Supplements (Guimarães et al.) gave 200 mg of GABA daily for 90 days to sedentary overweight women also undergoing an exercise program. The GABA group showed significantly improved Pittsburgh Sleep Quality Index (PSQI) scores, significantly reduced depression scores, and improved heart rate variability, a marker of parasympathetic nervous system activity. The HRV finding is particularly interesting. It suggests GABA may be doing something broader than simply reducing sleep latency – it appears to support the overall physiological state that makes rest restorative. (PMID: 38321713) Finding 3 — But a High-Dose RCT Found No Effect Here’s where intellectual honesty matters. A 2023 Dutch RCT (de Bie et al.) published in the American Journal of Clinical Nutrition gave participants 500 mg of GABA three times daily, 1,500 mg/day total, and found no significant effect on self-reported sleep quality. Fasting plasma GABA wasn’t significantly elevated either, raising real bioavailability questions at that dose. This isn’t a reason to dismiss GABA entirely. It is a reason to pay attention to the dose. The evidence base supports 100–300 mg, not 1,500 mg. Higher is not better, and the non-linear dose response is clinically important. (PMID: 37495019) The Blood-Brain Barrier Debate — and Why the Gut May Be the Point The most common objection to oral GABA supplementation is this: GABA is a zwitterion at physiological pH, meaning it has low lipophilicity and poor predicted ability to cross the blood-brain barrier via passive diffusion. So if it can’t get into the brain directly, how does it produce neurological effects? The emerging explanation involves the gut-brain axis. The enteric nervous system, your gut’s own neural network, has GABA receptors. When oral GABA activates these enteric receptors, it can signal the brain via vagal afferents without needing to cross the BBB at all. Think of it as a side door rather than the front entrance. Supporting this: a 2024 RCT (Li et al.) found that a probiotic strain engineered to increase gut GABA production significantly improved objective sleep duration as measured by wearable devices, alongside reduced cortisol and suppressed HPA axis activity. The mechanism wasn’t direct CNS access – it was gut-brain signalling. (PMID: 39385735) The BBB debate doesn’t negate the clinical effect. It changes how we understand the mechanism. Why Sleep Is Not Optional in Brain Recovery This is the part that I think gets underweighted in recovery conversations — and the research is unambiguous. A 2026 large retrospective cohort study (Muhtar et al., Sleep Medicine) matched over 35,000 stroke patients and found that post-stroke insomnia was associated with a 29% higher risk of post-stroke cognitive impairment and a 30% higher risk of all-cause dementia. The association with Alzheimer’s disease was also significant. (PMID: 41924789) A 2024 observational study from Monash University and Alfred Health (Smith et al.) found that in stroke rehabilitation patients, poor sleep quality was significantly associated with higher fatigue severity and lower salivary BDNF gene expression. BDNF (brain-derived neurotrophic factor) is one of the primary molecular drivers of neuroplasticity. Less BDNF means a less receptive environment for the neurological rewiring that rehab is trying to build. (PMID: 38802847) And then there’s the glymphatic system: the brain’s waste-clearance mechanism that is most active during deep sleep. Poor sleep means reduced clearance of metabolic byproducts, including proteins associated with neurodegeneration. This is not a theoretical risk. It is an active, ongoing process. Sleep is not passive recovery. It is one of the primary mechanisms of recovery. What to Do With This Information Here are three practical steps if you’re exploring GABA for sleep: 1. Measure your sleep baseline first. Use the Pittsburgh Sleep Quality Index (freely available online) before you make any changes. Understanding whether you’re struggling with latency, duration, or quality will determine what you actually need to address. 2. If you trial GABA, choose the right form and dose. Look for PharmaGABA — naturally fermented GABA, derived from Lactobacillus hilgardii, which has the strongest clinical evidence base. A dose of 100–300 mg taken 30–60 minutes before bed is consistent with the positive studies. Avoid very high doses; the null result at 1,500 mg/day is important context. Important drug interaction note: If you are taking benzodiazepines, anticonvulsants (gabapentin, pregabalin, valproate), or any other GABAergic medication, discuss GABA supplementation with your prescriber before adding it. The additive sedative effect is a real risk. The same applies if you drink alcohol regularly. 3. Don’t skip the foundation. Sleep hygiene interventions, consistent sleep and wake times, a dark and cool room, and no screens in the 60 minutes before bed, are consistently among the highest-leverage sleep interventions in the literature. GABA may provide a genuine incremental benefit. But it cannot compensate for a fundamentally disrupted sleep environment. The Bottom Line The evidence for GABA and sleep is more substantive than I expected when I started researching it. The EEG data is real. The 90-day RCT showed meaningful clinical outcomes. The gut-brain axis mechanism is biologically plausible and now has direct RCT support. And the consequences of poor sleep in neurological recovery are not trivial – they are quantifiable, significant, and, to a degree, addressable. GABA is not a guaranteed fix. Individual responses vary. The research is not yet definitive at the level of large multi-centre trials in neurological populations. But as one tool in a comprehensive approach to sleep quality alongside good sleep hygiene, appropriate medical support, and consistent rehabilitation, the case for cautious exploration is reasonable. The next step is a conversation with your neurologist, GP, or rehab physician. Take the research with you if it’s useful. Research References All studies cited in this post are retrievable via PubMed: Yamatsu et al. — GABA sleep latency EEG clinical trial (2015) — PMID: 26052150 Guimarães et al. — GABA 200mg RCT, sleep efficiency + mood (2024) — PMID: 38321713 de Bie et al. — GABA high-dose RCT, null sleep result (2023) — PMID: 37495019 Li et al. — Gut-brain GABA axis and sleep RCT (2024) — PMID: 39385735 Muhtar et al. — Post-stroke insomnia and cognitive decline cohort (2026) — PMID: 41924789 Smith et al. — Sleep, BDNF, and fatigue in stroke rehabilitation (2024) — PMID: 38802847 This post is for educational purposes only and does not constitute medical advice. Always consult a qualified healthcare professional before making changes to your supplementation or treatment plan. If you or someone you care about is recovering from a stroke, brain injury, or any neurological condition, the Recovery After Stroke podcast and this blog exist for you. Subscribe on YouTube @BillGasiamis, or visit Recovery After Stroke to find episodes, resources, and community. The post GABA, Sleep, and Brain Health – Neurological Recovery appeared first on Recovery After Stroke.

Creatine and Microbiomes A new 2026 Cell Metabolism study explores a compelling and increasingly central idea in modern biology: the gut/brain/immune/metabolism axis is not just associative, it is mechanistic. Specifically, Dr. Lu and colleagues investigate how the gut microbiota can directly influence depressive behavior by reshaping systemic and neural metabolism. This is another in a long running list of papers describing the amazing work that bacterial commensal microbes do for us. In this case, our minds and moods. "Although peripheral-brain crosstalk regulates energy metabolism, its role in depression remains unclear. Here, we used metabolic profiling to reveal elevated fecal creatine alongside reduced plasma and cerebrospinal fluid creatine in both patients with depression and mouse depression models. Exogenous creatine produced antidepressant-like effects mediated by gut microbiota. Bifidobacterium pseudolongum was identified as a significantly reduced gut bacterial species in depression, correlating with impaired creatine absorption. Subsequent supplementation with Bifidobacterium enhanced the antidepressant effects of creatine. Mechanistically, B. pseudolongum-derived acetate promoted the creatine transporter (Slc6a8) expression in intestinal epithelial cells via histone acetylation. The Slc6a8 mediated the antidepressant-like effects of creatine. Neuronal creatine deficiency influenced energetic metabolism and neurophysiological function. In patients with depression taking antidepressants, co-administration of creatine and Bifidobacterium increased plasma creatine levels and reduced depression scores. These findings identify the Bifidobacterium-creatine combination as a promising antidepressant strategy and highlight the critical role of gut-brain energy metabolism in depression." "The brain, as an energy-intensive organ, relies on precise metabolic regulation to maintain synaptic plasticity, neurotransmitter synthesis, and stress response systems. Accumulating evidence implicates energy metabolism dysregulation as a hallmark of depression. Neuroimaging studies using positron emission tomography (PET) have identified marked glucose hypometabolism in the medial prefrontal cortex (mPFC) of patients with depression. Cerebral mitochondrial dysfunction and ATP imbalance have been mechanistically linked to depression progression. Notably, emerging studies emphasize the bidirectional interplay between peripheral metabolic signals and central energy regulation, which is fundamental to neural metabolism. Clinical observations such as fatigue, appetite dysregulation, and unexplained weight fluctuations in patients with depression further suggest systemic metabolic disturbances spanning peripheral organs and the CNS.." (Lu et. al. 2026) This is next-level medicine. Mental health can no longer be framed as a disorder of genetics, experience, or circumstance alone. This work opens a clearer window, showing how the microbiome participates as an active partner, shaping brain function through the metabolites it helps produce and deliver. Compounds like creatine are no longer just peripheral players. They become signals, fuel, structure, and information, bridging gut and brain, metabolism and behavior.... and more Enjoy, Dr. M

Epstein–Barr virus (EBV) has become one of the most intensely studied topics in multiple sclerosis research. But how strong is the evidence linking EBV to MS, and could targeting the virus change the future of treatment and prevention? In this episode of the ECTRIMS Podcast, host Brett Drummond speaks with Prof. Gavin Giovannoni and Prof. Tomas Olsson about the evolving science connecting infections, immunity and multiple sclerosis. Together, they explore: Molecular mimicry and how EBV proteins may trigger autoimmune responses Whether EBV contributes to chronic CNS inflammation and disease progression Emerging therapeutic approaches including antivirals, CAR-T cells, and vaccines This conversation examines one of the most important scientific questions in MS research  and the therapeutic possibilities that may emerge from it.

Listen Online: About this episode: Together, The First Lady of Nutrition and James Templeton, CEO of UNI KEY Health, author of I Used to Have Cancer, and a 40+ year stage 4 cancer survivor, tackle one of the most debated questions in health: What is the best diet to beat cancer?Drawing from his personal journey and decades of experience, James shares why he believes diet is the most critical factor in healing—and why removing sugar (including excess carbohydrates) is absolutely essential. He explores the pros and cons of popular approaches like vegan, paleo, keto, and macrobiotic diets, and explains why he ultimately leans toward an anti-fungal, anti-candida style of eating—focused on clean protein, healthy fats, and minimal sugar. Listeners will also hear his take on fermented foods like sauerkraut and kimchi, the role of fruit, and why grains and dairy can be problematic for some individuals.James also reflects on the diet that helped him recover—and why it wasn't the same diet he used to maintain long-term health. This conversation goes beyond theory, offering practical insights on what to eat, what to avoid, and how to think differently about food when it comes to prevention and healing.To learn more about James’ non-profit foundation, check out The Templeton Wellness Foundation at: www.templetonwellness.com . The post The Cancer Diet Debate: What Really Works? With James Templeton first appeared on Ann Louise Gittleman, PhD, CNS.

Synopsis: At the intersection of personal mission and biotech leadership, Rahul Chaturvedi sits down with Catherine Owen Adams, CEO of Acadia Pharmaceuticals, for a deeply personal and strategically rich conversation on leadership, commercialization, and the future of neuropsychiatry. From starting as a pharmacist in the UK to pivoting from R&D into commercial leadership at Johnson & Johnson, rising through Bristol Myers Squibb, and ultimately stepping into her first biotech CEO role at Acadia, Catherine shares how storytelling became the throughline of her career—transforming science into physician trust, investor conviction, and enterprise vision. In this episode, Catherine opens up about the personal family experiences with neurodegenerative disease that made Acadia's focus on CNS and rare disease feel like her “Goldilocks opportunity.” She offers a candid look at the realities of being a first-time CEO, managing investor ecosystems, building the right C-suite, balancing billion-dollar commercial execution with high-risk R&D, and navigating the emotional stakes of developing therapies for Parkinson's disease psychosis, Alzheimer's disease psychosis, Rett syndrome, and beyond. Rahul and Catherine also explore the seismic shifts reshaping biotech—from AI-powered commercialization and patient services to policy advocacy through BIO, FDA modernization, and the strategic pressures facing CNS innovation. This episode is both a masterclass in biotech leadership and a powerful reminder that the best CEOs don't just run companies—they tell stories that move science, markets, and patients forward. Biography: Ms. Owen Adams joined Acadia as Chief Executive Officer and as a member of our Board of Directors in September 2024. Ms. Owen Adams has over 25 years of executive level experience in the pharmaceutical industry. Prior to joining Acadia, Ms. Owen Adams served as Senior Vice President and General Manager, U.S., at Bristol Myers Squibb (BMS), where she led a $20 billion commercial business, overseeing a large and diverse portfolio of promoted brands across Oncology, Cardiovascular, and Immunology. Previously, Ms. Owen Adams held the position of Senior Vice President, Head of Major Markets at BMS, where she led commercial operations leading 6,000 employees across 19 countries in Europe, Japan, and Canada during BMS's merger with Celgene. Prior to her tenure at BMS, Ms. Owen Adams spent 25 years at Johnson & Johnson (J&J), where she held leadership roles across global, U.S., and European business units, with her last position being President, Janssen Immunology U.S. Ms. Owen Adams began her career in R&D and manufacturing at AstraZeneca. Ms. Owen Adams currently serves on the board of directors of Agios Pharmaceuticals, Inc., a publicly held company, and AssistRx, a privately held company. Ms. Owen Adams was formerly on the board of directors and chair of the compensation committee for Optinose PLC, a public specialty pharmaceutical company, and was on the board of directors of Robert Wood Johnson University Hospitals, a non-profit organization. Ms. Owen Adams earned a BSc. in Pharmacy from the University of Manchester, becoming a qualified pharmacist and member of the Royal Pharmaceutical Society (MRPhS).

Advances in immunotherapies for multiple sclerosis and related disorders have increased the risk of infections and raised important questions about vaccination efficacy. This episode reviews infection risks across treatment classes, emphasizes the importance of monitoring and patient education, and discusses optimal vaccine timing to preserve protective immune responses. In this episode, Aaron L. Berkowitz, MD, PhD, FAAN, speaks with Avindra Nath, MBBS, FAAN, coauthor of the article "Infection Risk and Vaccine Considerations in Multiple Sclerosis and Related Disorders" in the Continuum® April 2026 Multiple Sclerosis and Related Disorders issue. Dr. Berkowitz is a Continuum® Audio interviewer and a professor of neurology in the Department of Neurology at the University of California, San Francisco, in San Francisco, California. Dr. Nath is the chief of the Section of Infections of the Nervous System at the National Institute of Neurological Disorders and Stroke, National Institutes of Health, in Bethesda, Maryland Additional Resources Read the article: Infection Risk and Vaccine Considerations in Multiple Sclerosis and Related 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: @AaronLBerkowitz Full episode transcript available here Dr Berkowitz: Over the last decades, there has been a revolution in the treatment of multiple sclerosis, neuromyelitis optica spectrum disorder, and other immune-mediated neurologic conditions with countless new, highly effective medications. However, with every new treatment comes new risks; and in the case of immunomodulatory therapy, many of those risks relate to infection. Today, I have the privilege of talking with an expert on this topic, Dr Avindra Nath, about the infectious risks of treatments for multiple sclerosis and other immune-mediated neurologic disorders.  Dr Jones: This is Dr Lyell Jones, Editor-in-Chief of Continuum. Thank you for listening to Continuum Audio. Be sure to visit the links in the episode notes for information about earning CME, subscribing to the journal, and exclusive access to interviews not featured on the podcast.  Dr Berkowitz: This is Dr Aaron Berkowitz, and today I'm interviewing Dr Avi Nath about his article on vaccine considerations and infection risk in multiple sclerosis and related disorders, which he coauthored with Dr Amit Bar-Or. This article appears in the April 2026 Continuum issue on multiple sclerosis. Welcome to the podcast, Dr Nath, and could you please introduce yourself to our audience?  Dr Nath: Thanks very much for inviting me to this podcast. I'm absolutely delighted to have the opportunity to discuss our areas of interest and expertise related to infections and vaccinations for MS patients. My area has been studying the infections of the nervous system since the beginning of the AIDS pandemic, and over the years and decades, we've developed expertise related to various types of CNS infections. That includes ones that are developing in individuals who have immune compromise due to a variety of different reasons. Dr Berkowitz: Fantastic. Well, glad to have the opportunity to speak with you today. When I was in medical school---and you were my attending, actually, we were just reminiscing, which we probably think was not that long ago, but is now over twenty years ago---there were just two medications for MS, right? Beta interferon and glatiramer acetate. And now we have over a dozen, and it's amazing to think of all the progress in these last two decades, as well as for related diseases like NMO. I don't think we even had the aquaporin-four biomarker, right, when I was working with you as a med student in the early 2000s. Dr Nath: And that certainly dates me a lot.  Dr Berkowitz: Both of us.  Dr Nath: Yeah.  Dr Berkowitz: Of course, with all these new treatments, these have been amazing advances for our patients, right? But these come with new treatment-related risks to monitor for with the immunomodulatory medications for MS and related disorders. And one of those most important risks is that of infection. So, your article reviews the potential infectious complications of medications used to treat MS, NMO, etc, and also covers considerations related to thinking about vaccines in this patient population. So, as the MS treatment landscape grows, I can say as a general neurologist, keeping up with all these medications and what to screen for and what to worry about and when to vaccinate just becomes more challenging every year. And your article has so many helpful tables, some organized by medicine, some organized by- sorry, medication, some organized by infection, some by vaccines. So, this is gonna be a great resource for our providers to print out and tape up in their clinic rooms. We won't be able to get into all the depth and detail that you have in this article today, but I do want to focus on some of the key points here related to the common medications we use for MS and which infections to think about and which vaccine considerations we might need to keep in mind for these medications. But before we delve into the drugs, I just wanna ask you more broadly, you talk in the article about the challenge of patients with immune-mediated diseases who are on immunomodulatory therapy being at risk for both flares of their disease and for infections; and these infections can present somewhat atypically, right, in immunomodulated hosts, to maybe coin a term you can correct me on, because they can't mount the full inflammatory response. So how do you approach new symptoms in patients on these immunomodulatory medicines as far as distinguishing disease flare from a treatment-related infection?  Dr Nath: So, I have to say that although a lot of new treatments have come along for MS, and they've really, you know, improved the outcome tremendously and there are so many different options, it has also kept people like me relevant because they cause a lot of various types of infections, and so keeps me in business all the same. But just as you mentioned, there's so many of them, even I have difficulty keeping track of what does what. So, you do need to be able to refer back to published literature, and the tables, I hope, will be quite useful in that regard. You're absolutely right, and you can get new infections, you can get reactivation of existing infections, and you can get atypical presentations of various types of infections that you may not normally think of. So that presents multiple challenges to the treating physician. The other interesting thing about MS is, just as you mentioned, that you already have CNS lesions to begin with. Now, on top of it, you have an infection, so now how to sort out what is the existing disease and what is the infection, it can again become challenging. But one thing is for sure: all these infections are caused by an organism. So, what you really need to do is, the underlying diagnostic is to demonstrate the presence of the organism. Whether you demonstrate it depending on the infection in the spinal fluid or in the brain or, you know, some peripheral organ system, that is going to be key to making the diagnosis. So, all your clinical acumen is good, but that alone may not be sufficient. Dr Berkowitz: Very good. So, when you see a, a patient now who has a new neurologic symptom in the context of an immune-mediated disease who's on immunomodulatory therapy, what goes through your mind? Are you thinking this disease and this drug, and sort of what are the infections, and does the syndrome match? Or are you thinking, you know, you can't always rely on the imaging to distinguish between, say, a flare of an MS and PML because white matter lesions could look similar? How do you sort of approach this scenario when it comes up?  Dr Nath: So, you're right. You have to keep an open mind so that even though you know some infections are more likely to occur with certain types of medications, that doesn't mean that others cannot occur. So, I think when you first see the patient, you should not jump to conclusions, but rather have an open mind. But yes, for example, your patient is on natalizumab, the chances of PML are going to be high. It's a very interesting drug. It does not cause immune compromise in the periphery, but what it's doing is preventing these cells from getting into the brain. So, because then it's acting at the blood-brain barrier. So that means that organisms that are already present in the brain have an opportunity to get reactivated. Turns out you don't have a lot of organisms in the brain, except JC virus seems to be one of them that does somehow, in some individuals, manage to reside out there. And so that can get reactivated. It can get reactivated in the periphery and then enter the brain, too. So, where the very specific mutations have to occur in that virus in order to take residence in the brain. That would be a suspicion that you might have, and MRI can be useful in, again, helping you think about that possibility. If you have typical lesions involving the U fibers, they're demyelinating, usually you do not have much edema around them because patient is immune compromised, but certainly within the brain in these individuals. And so, then you need to demonstrate the organism. The demonstration of the organism should be in the spinal fluid and not in the blood because in the virus, it can-- is reservoir in the kidneys and in the lymph nodes, and periodically it'll shed into the blood. Detection of the organism in the blood can be a false positive, but in the spinal fluid, it shouldn't be there unless you have an infection. Or if you cause a traumatic tap, I guess, if a patient is viremic, that's a possibility, but those are extremely rare. So at least for PML, that's the way that you would diagnose it. Now, you can develop, for example, if an individual is on fingolimod, you can get a wide variety of infections. Here it's a totally different type of mechanism of action. Here the cells are trapped within the lymph nodes, so that means now your entire periphery is immune compromised, right?  So here you can get viral infections, bacterial infections, fungal infections. So here, if a patient presents with new neurological symptoms, you have to have a really open mind for all these possibilities. Now, let's say a patient was on dimethyl fumarate, and dimethyl fumarate causes neutropenia early on. So here you have to worry about an individual developing bacterial infections, so latent tuberculosis or bacterial meningitis can occur in these individuals. That's something to keep in mind. It's not that other infections cannot occur with dimethyl fumarate, you can see PML and other things too, but the chances of bacterial infections are greater. So, you got to make sure that you draw all the cultures for that purpose. Similarly, if you're on a complement inhibitor, like a C5 inhibitor or the thing that I could use in NMO, there are the chances of meningococcal meningitis. So, these patients, you need to prevaccinate them before you start these kinds of treatments and look for that possibility. When you suspect bacterial infections, particularly acute bacterial meningitis, there time is of essence. Also, in some of the acute viral infections, for example---herpes encephalitis is another one---you have to be so careful, and if you suspect any of them, even if they're with possibly atypical manifestations, you treat first and then diagnose later, and draw all your cultures, whatever you need to, and just treat them. And these infections can also cause cerebral edema, so one has to be careful about doing spinal taps in these individuals. You want some kind of neuroimaging before you do them. In the days when we didn't have neuroimaging, we used to say, "Okay, if your patient has focal neurological signs or is comatose, you don't do it." But these days, you can get imaging very quickly and very easily. All the-- Because of our stroke management, we've learned how to do them so quickly. So, I think there's little excuse not to do imaging and prevent herniation from occurring.  Dr Berkowitz: That's very helpful. So, using the information we know about the drug, and we're going to rapid-fire review some of that in a bit to know what infections the patient is susceptible to, but acknowledging that any patient can get any infection, right? Whether they're on particular medications or not. And then if you're not sure, based on the neuroimaging, which as you said, is helpful, but not always helpful in distinguishing between infections and flares or, as you said, in the case of meningitis, encephalitis, early on at least, especially in immunocompromised or immunomodulated, quote unquote, patient might not see the typical imaging. So really, when safe, getting CSF or cultures, PCRs, and other infectious studies too is really gonna be the definitive diagnostic maneuver here. Is that fair summary across the board?  Dr Nath: I think you said that absolutely right. And you summarized that correctly. And, you know, thing about infection, a lot of neurological diseases are, you know, diagnosed by clinical acumen, like your Parkinson's and Alzheimer's and others. Think about infections is caused by an organism, demonstrate the organism, right? That should be your goal. It doesn't mean that clinical acumen is not important, but here you have an opportunity to demonstrate the organism, so you should depend upon that.  Dr Berkowitz: Okay. Well, you gave us a nice segue by talking about some of the infections to worry about with some of the medications. So what I'd like to do now for the sort of second half of our interview here is to go through some of the more common medications used for MS, and if we have time, for NMO, and just sort of go kind of rapid fire here, and for each medication, if you can tell us the kind of top infectious concerns and whether when to consider them or what screening needs to take place before or during administration of the medication, and then any vaccine considerations we should be aware of. Some of these will obviously be quite short depending on the medicine. So, going back to the two medications I alluded to earlier that were the only ones in play when you and I last saw each other on the wards when I was a medical student, beta interferon, glatiramer acetate, any infections or vaccine considerations with these medications?  Dr Nath: No, I think they're probably your safest medications now as far as immunomodulatory therapies are concerned. These two, and IVIG, if you ever use them, are probably the safest, do not require any vaccine considerations, per se. Dr Berkowitz: Perfect. Okay. So, moving on to fingolimod and others in the sphingosine-one phosphate receptor modulator family, what are the infectious considerations? Any prescreening or vaccination considerations?  Dr Nath: I think all your patients should be prescreened for antibodies to JC virus, because there is a risk for PML, and those who are positive should be closely monitored. So, it's not an absolute contraindication for using these medications, but they just require closer monitoring. With this class of drugs, PML is of consideration. Also, these varicella-zoster virus infection, yeah, with that you can develop zoster encephalitis or myelitis. It can present with motor symptoms as well, which can be atypical. You don't usually see them otherwise in immune-competent individuals. So, varicella-zoster, sometimes you can develop encephalitis, also vasculitis with varicella-zoster, so one has to be careful. So, getting the shingles vaccine can be actually very helpful to prevent these things. And then some patients can even develop herpes simplex encephalitis also, and that can be extremely atypical. So, they don't- they can involve the basal ganglia, can involve the brain stem and cerebellum. So again, your index of suspicion should be very high. Interestingly, although HSV encephalitis has been associated with NMDA receptor encephalitis, those reports of NMDA receptor encephalitis have not been published yet with NMS patients. Not sure why, maybe they just have been missed. But that doesn't seem to be a major concern. And then there are a whole host of other infections that can occur with this class of drugs, and that can include toxo; fungal infections, particularly crypto. There's a case report of histoplasmosis; hepatitis virus, particularly hepatitis C; and then the poxvirus is a good example. You can get molluscum contagiosum; warts with papillomavirus; you can get atypical mycobacteria; and even Kaposi sarcoma, which is HHV8. So, there's a huge variety of infections with the sphingosine one phosphate receptor modulators.  Dr Berkowitz: And any- aside from screening for JC virus before initiating these, any- and then continuing to monitor for JC antibody index, any other considerations as far as labs to send, monitoring before or on the drug or vaccine considerations for patients on fingolimod and the others in this category, siponimod, etcetera?  Dr Nath: Yeah, there are a lot of things to consider. All the details are really available in the chapter if you look at them. But briefly, all the things that one could potentially vaccinate patients for, all these infections I mentioned, one should do so. The timing is critical so that if you can do it before treatment, I think, before starting treatment, that is absolutely important. And you got to give them at least, you know, two to three weeks for these vaccines to take effect before starting your medication. If your patient already arrives on a medication, then you got to play this game of you know, before the next dose, give them again two to three weeks before the next dose and start vaccinating them and get all the vaccines in. Broadly, about the things to worry about the vaccines are you have live vaccines, and you've got the inactivated vaccines or the subunit vaccines. You have to be careful with live vaccines, because if your patient is immunocompromised, that virus can sometimes itself cause harm. For example, you know, yellow fever is one, and there you can develop encephalitis from it. Measles, mumps, rubella, these are all live vaccines. Now, the good thing is that a lot of us have been immunized very early in childhood, but that may not be the case any longer. And so, these things, one has to be very careful with when you're giving live vaccines, that we want to avoid them as much as possible, and individuals are gonna be immune-compromised. But all the others, meningococcus, for example, you should- the HPV vaccines, the varicella zoster vaccines, all these things, you've got to pre-vaccinate and make sure that they have an antibody response to them before starting immunocompromising therapy. Dr Berkowitz: Perfect. Okay, moving on to some of the other orals. What infectious and/or vaccine considerations do we have with teriflunomide?  Dr Nath: Okay, yeah. Teriflunomide is a very interesting drug. It's relatively safe. There is concern about the possibility of varicella zoster infection, people have reported that, and also tuberculosis. But PML is extremely rare, if not at all, and we haven't seen herpes encephalitis quite yet.  Dr Berkowitz: Got it. How about dimethyl fumarate? Dr Nath: Yeah. So dimethyl fumarate is... as I mentioned earlier, it's interesting because it causes this neutropenia. It's transient, but it occurs early on, and these patients can be at risk of PML, although small. They can develop varicella zoster virus infection, herpes encephalitis, and also fungal infections. For example, cryptococcal infection has been reported with dimethyl fumarate. Dr Berkowitz: Okay. We've spoken a bit about natalizumab and PML, and you have extensive information on this in your article, and I'll defer the reader to that. But for natalizumab, what are the key points every neurologist should know about natalizumab and PML as far as from the practical perspective, screening, frequency of screening, when to worry, when to not use natalizumab at all in the first place based on what you find in your screening for JC virus? What are the key points every neurologist should know?  Dr Nath: Uh, yes. You bring up an important point, and that is all patients should be monitored for JC virus. If they're JC virus-negative, so that's your most ideal patient to go on natalizumab, but that doesn't mean they cannot get infected with the virus. In fact, there's an interesting study claiming that, you know, patients, when they get these infusions, they're all sitting in the same room getting infused. Some have JC virus, some don't have JC virus, and so there's the potential that we may be aiding the transmission here in some way or another. The virus is an interesting one. It comes out in urine, and then it's spread through oral contamination, gets into the tonsils, and then spreads from there to your marrow and resides in the kidney and the marrow, as well as the lymph nodes, forever. So, you, you have to monitor these patients to see that during the course, even if they're negative, they could turn out positive. So, every six months or a year, an antibody test should be done on all patients irrespective. If a patient already has antibodies, that's not an absolute contraindication. It just means you've got to monitor them closely for development of new symptoms, and if, whenever there are new symptoms, don't just assume this is due to MS, but just make sure the MRI is done with and without contrast. The- and if there's still a suspicion, that you do a CSF evaluation for JC virus. Just detecting, looking for JC virus in the blood, a rising titer is another thing that can help you. And so, the titer is also important. And the reason you have rising titers is it means that there's an infection that's already occurred in the brain, and the immune system is reacting to that infection by increasing titers. But that alone is not sufficient to make the diagnosis. You still- that gives you an index of suspicion. You've got to then do the MRI and the spinal tap to, you know, be absolutely certain. So, each patient is a little bit different, so the way you monitor them is going to depend on where they are. You know, if they've had prior immunomodulatory therapy before starting natalizumab, or if they're on natalizumab for more than two years, then the chances of PML are much greater, so you may want to monitor them more closely. Uh, they never had any prior immunomodulatory therapy, you're just starting natalizumab, maybe once a year is sufficient. So, I think you've got to tailor it depending on what your risks are for each patient. Dr Berkowitz: Perfect. That's very helpful. And again, you write extensively about PML and natalizumab and PML considerations in your article. So, for a more detailed and in-depth discussion of what we just discussed, definitely hope readers will take a look at your article. Okay. Last but not least---certainly not least, 'cause we're using these probably, it seems, the most commonly in many places I've worked---rituximab, ocrelizumab are B-cell therapies for MS. What are some of the infectious and vaccine considerations related to these infusion medications?  Dr Nath: So, there's concern for PML with anti-B-cell therapies also, maybe not to the same degree as natalizumab, but the same principles should be applied. A lot of people think that these are relatively safe. I don't think so. I think we see enough number of patients on B-cell therapies with PML. So, I would use the same caution because these infections are... you know, can be fatal. So, one should be very careful, even with anti-B-cell therapies. And just with natalizumab, you also have the risk of VZV infection causing shingles. HSV1 has been reported, but there's another interesting complication that has been reported with anti-B-cell therapies, and that is severe West Nile encephalitis. And as mosquitoes-borne diseases are getting more and more prevalent, and we're seeing West Nile cases erupting every summer, I think one's got to be, you know, very cognizant of the fact that this can occur. These patients should take precautions to prevent mosquito bites from occurring and not expose themselves to areas where they could be at risk for it. Unfortunately, there is no vaccine for it and no specific treatment for West Nile. So, all one can do is use prevention strategies for mosquito bites.  Dr Berkowitz: Yeah, I'm glad you mentioned that. I think the only really truly severe neuroinvasive cases I've seen of West Nile virus have indeed been in patients who were being treated with B-cell therapy. Not, if I'm remembering correctly, for immune-mediated disease, but for a lymphoma, so probably other confounding factors there. But yeah, it's a disease we learn about and think about, but I've only seen the most severe cases in patients who had abnormal immune systems, so I'm glad you flagged that. This has been a very helpful discussion, and I've learned a lot from you. I learned a lot from your article, just as I did when you were my attending some 20-something years ago on the wards when I was a medical student. So, it's good to continue learning from you through your writing and research, and today from getting to talk to you again. I encourage our readers to read your article and to bookmark those tables for when these considerations come up for your patients on these immunomodulatory therapies and you're wondering which infections to worry about and how to manage vaccines in this patient population. So again, today I've been interviewing Dr. Avi Nath about his article on vaccine considerations and infection risk in multiple sclerosis and related disorders, which he wrote with Dr. Amit Bar-Or. This article appears in the April 2026 Continuum issue on multiple sclerosis. Be sure to check out Continuum Audio episodes from this and other issues, and thank you again to our listeners for joining today.  Dr Nath: Thank you so much, Aaron, for that wonderful interview, and I'm extremely proud of all your accomplishments over the last 20 years. You've done an amazing job, and it was such a pleasure to see you and to be able to do this interview with you. Thank you again.  Dr Berkowitz: Thanks. That means a lot. I never would have imagined- we won't say 20, how many, but 20-something years ago as the medical student looking up to you and all your expertise on these infections and all of your research that led to so much of our understanding on these, that I would find myself interviewing you two decades later. So, for all the students listening, you never know where you'll end up, but I appreciate your very kind words.  Dr Nath: That's what we hope for all our students. Thank you so much.  Dr Berkowitz: Thanks again.  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.

Welcome to the Oncology Brothers podcast! In this episode, we dived deep into the exciting world of metastatic non-small cell lung cancer (NSCLC) with a focus on targeted mutations in the frontline setting. Listen us on: Spotify: https://open.spotify.com/show/31BXhY9FM4gPWG10WgE11o Apple Podcast: https://podcasts.apple.com/us/podcast/oncology-brothers-practice-changing-cancer-discussions/id1653340966 Follow us on social media: X/Twitter: https://twitter.com/oncbrothers ⁠Instagram: https://www.instagram.com/oncbrothers Website: https://oncbrothers.com/ We were joined by Dr. Eric Singhi from MD Anderson Cancer Center, to discuss the latest advancements in treatment options, including: Common EGFR mutations and the benefits of combination therapies over single-agent osimertinib. The role of CNS involvement in treatment decisions and the importance of patient-centered care. Strategies for managing disease progression and the significance of re-biopsy. Insights into ALK-positive disease, including the efficacy of lorlatinib and alectinib. The latest developments in treating rare mutations like NTRK, MET, RET, and HER2. With a wealth of clinical data and practical insights, this episode is packed with valuable information for oncologists and healthcare professionals. Tune in to learn how to navigate the complexities of NSCLC treatment and improve patient outcomes. Don't forget to subscribe for more discussions on oncology topics and share your thoughts in the comments below! #LungCancer, #TargetedTherapy, #PrecisionMedicine, #NGS, #OncologyBrothers

Episode 42:  30 years of stroke care: What survivors and caregivers need to know now | Stronger After Stroke Stroke care has been transformed over the past three decades, and those advances mean something real for survivors and caregivers navigating recovery right now. In this episode, host Rosa Hart, BSN, R.N., SCRN, sits down with three Norton Neuroscience Institute staff to break down what the 2024 American Heart Association/American Stroke Association updated stroke guidelines mean for you. In this episode: ·      What stroke program certification means for patients ·      The truth about thrombectomy and why calling 911 as soon as possible changes everything ·      What neuroplasticity means for recovery, even years after stroke ·      Therapies backed by strong evidence that many survivors never hear about ·      Why caregivers are now formally part of the standard of care ·      What to do when you live far from a major stroke center Meet the guests: Jessica Sumner, MSN, R.N., CNS, CEN, director of clinical effectiveness and stroke care for Norton Healthcare, leads stroke program certification and statewide quality improvement efforts across Kentucky and Indiana. Jeanette Lanoire, P.T., DPT, NCS, is a physical therapist and board-certified neurologic clinical specialist. She has deep expertise in stroke rehabilitation, movement disorders and community-based neurological wellness. Dimitri Laurent, M.D., is a neurosurgeon and spine surgeon known for making complex surgical information clear and approachable for patients and families. This conversation is not for clinicians. It is for survivors, caregivers and anyone who wants to understand what great stroke care looks like and how to ask for it.   Subscribe to "Stronger After Stroke" for more episodes at the intersection of clinical excellence and real recovery. Want more inspiring stories and real-life resources? Subscribe and share "Stronger After Stroke" with someone who needs a little extra support navigating their recovery. For more support after stroke, check out the programs available virtually and in person through Norton Neuroscience Institute Resource Centers: https://nortonhealthcare.com/services-and-conditions/neurosciences/patient-resources/resource-center/ If you enjoyed this podcast, listen to Norton Healthcare's "MedChat" podcast, available in your favorite podcast app. "MedChat" provides continuing medical education on the go and is targeted toward physicians and clinicians. Norton Healthcare, a not-for-profit health care system, is a leader in serving adult and pediatric patients throughout Greater Louisville, Southern Indiana, the commonwealth of Kentucky and beyond. A strong research program provides access to clinical trials in a multitude of areas. More information about Norton Healthcare is available at NortonHealthcare.com. Date of original release: May 11, 2026

May 7, 2026 - Join us for a discussion with Sarah Laderman, Senior Analyst for Open Nuclear Network, a PAX sapiens programme, on the rollout of a recent series of reports examining North Korea's nuclear program. In conversation with policy director Jonathan Corrado, Laderman discusses a myriad of findings on North Korea's nuclear fuel cycle and weaponisation capabilities, including the research project's development of innovative methodologies to assess an otherwise opaque program. The discussion reviews the high-level findings and unpacks implications for verification, monitoring, and diplomacy. More information on the project findings can be found here. This Global Affairs Canada funded research project was led by VERTIC, in partnership with CNS and RUSI, assisted by Open Nuclear Network. This program is made possible by the generous support of the Korea Foundation and The Korea Society's individual and corporate members. For more information, please visit the link below: https://www.koreasociety.org/policy-and-corporate-programs/2153-north-korea-nuclear

Why is brain cancer so hard to detect and treat - and what if we could change that? In this episode of Rx for Biotech, host Chris Leidli sits down with Marc Hedrick, CEO of Plus Therapeutics, and Russell Bradley, General Manager of CNSide Diagnostics, to explore a new, integrated approach to treating some of the most challenging cancers in medicine: central nervous system (CNS) cancers, including glioblastoma and leptomeningeal metastases. Brain and CNS cancers are among the most difficult to treat because of the blood-brain barrier, which prevents most drugs from reaching tumors. In fact, only a small percentage of therapies can effectively cross into the brain—limiting treatment options and outcomes. Plus Therapeutics is tackling this problem with a novel approach using targeted radiation therapy delivered directly to tumors, bypassing the blood-brain barrier. Their lead program uses a radioactive isotope (rhenium-186) delivered via nanoliposomes, allowing high doses of radiation to reach the tumor while minimizing damage to the rest of the body. At the same time, CNSide Diagnostics is helping physicians detect cancer earlier and monitor treatment response using an advanced cerebrospinal fluid (CSF) diagnostic test. This highly sensitive test can identify even small numbers of tumor cells—helping doctors make faster, more informed treatment decisions. Together, this combination of diagnostics + therapeutics + data represents a new model for precision oncology and personalized cancer care. In this episode, we discuss: • Why brain cancer is so difficult to treat • The role of the blood-brain barrier in limiting therapies • How targeted radiation therapy can improve outcomes • The importance of early detection and diagnostics • How monitoring tumor cells can guide treatment decisions • The future of integrated cancer care (theranostics) This conversation offers a powerful look at how innovation in both treatment and diagnostics could help improve survival and quality of life for patients with some of the most aggressive cancers.

Why some lifters go straight to failure with no grinder reps—explained through muscle fiber types, CNS fatigue, and training science. Learn how to push past early failure and unlock more effective reps for hypertrophy. Practical tips to improve effort, bar speed awareness, and get more out of every set. 0:00 Muscle Minds Introduction 1:13 Van Life and Simple Living 3:44 Training Intensity and Bar Speed 7:29 Muscle Fiber Types and Fatigue 27:21 Visualization and Training Techniques 33:50 Psychological Aspects of Training 43:04 Pain Tolerance and Gender Differences 1:02:09 Conclusion and Next Episode Teaser

Listen Online: About this episode: The First Lady of Nutrition recently interviewed Christopher Lee Maher, a retired U.S. Navy SEAL with a powerful story. He explores whether issues like anxiety, persistent patterns, or stress responses may have origins beyond ourselves. In this candid conversation, Christopher shares with Ann Louise how years of unresolved trauma and deeply rooted beliefs led to his body literally shutting down—and what it took to rebuild from the inside out.  They talk about generational patterns, including addiction and alcoholism, and how they can quietly shape your life until you recognize them. Christopher also explains a fascinating turning point that often happens between ages twenty-seven and thirty-one—a time when many people are unknowingly forced to confront the emotional patterns they've carried for years. Move through it, and life can shift. Avoid it, and those same struggles can repeat. He also connects the dots between stress and the body—how it can show up as anxiety, depression, fatigue, or even chronic illness—and why changing your internal “programming” may be one of the most overlooked keys to healing. If you've ever felt stuck in patterns you can't explain… this conversation may give you a completely new way to look at your health—and your future.The post From Trauma to Transformation: The Christopher Lee Maher Story first appeared on Ann Louise Gittleman, PhD, CNS.

Although rare, recognizing NMOSD is crucial for improving patient outcomes through correct diagnostic and treatment approaches. Reports of atypical forms and increasing knowledge of clinical, imaging, and laboratory-specific features are fundamental for the accurate recognition of this condition. Research on targeted therapies and biomarkers measuring and predicting disease activity will improve NMOSD management. In this episode, Gordon Smith, MD, FAAN, speaks with Sara Mariotto, MD, PhD, coauthor of the article "Neuromyelitis Optica Spectrum Disorder" in the Continuum® April 2026 Multiple Sclerosis and Related 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. Mariotto is a neurologist in the Neurology Unit in the Department of Neurosciences, Biomedicine, and Movement Sciences at the University of Verona in Verona, Italy. Additional Resources Read the article: Neuromyelitis Optica Spectrum Disorder Subscribe to Continuum®: shop.lww.com/Continuum Earn CME (available only to AAN members): continpub.com/AudioCME Continuum® Aloud (verbatim audio-book style recordings of articles available only to Continuum® subscribers): continpub.com/Aloud More about the American Academy of Neurology: aan.com Social Media facebook.com/continuumcme @ContinuumAAN Host: @GordonSmithMD Full episode transcript available here Dr Smith: Neurology is an increasingly therapeutic specialty, and across many of our subspecialty areas, lots of new drugs are being approved. Are you interested in learning more about a historically disabling disorder for which we now have a spectrum of new therapies that, if used appropriately and promptly in the right clinical situation, promise to dramatically improve patient outcomes? If so, keep listening. My name's Dr Gordon Smith. Today I'll be talking with Dr Sara Mariotto about her article on neuromyelitis optica spectrum disorder or NMOSD, which she wrote with Dr Romain Marignier. This article appears in the April 2026 Continuum issue on multiple sclerosis.  Dr Jones: This is Dr Lyell Jones, Editor-in-Chief of Continuum. Thank you for listening to Continuum Audio. Be sure to visit the links in the episode notes for information about earning CME, subscribing to the journal, and exclusive access to interviews not featured on the podcast.  Dr Smith: This is Dr Gordon Smith. Today, I'm interviewing Dr Sara Mariotto about her article on neuromyelitis optica spectrum disorder or NMOSD, which she wrote with Dr Romain Marignier. This article appears in the April 2026 Continuum issue on multiple sclerosis. Sara, welcome to the podcast, and maybe you can start by introducing yourself to our audience.  Dr Mariotto: Yes. Thanks, Gordon. I'm Sara Mariotto. I'm a neurologist, and I work at the Neurology Unit, University of Verona, where I do both clinical diagnosis and research into neuroimmunology---so, in particular, autoimmune encephalitis, NMOSD, and MOGAD.  Dr Smith: Well, this is a super exciting area. Whenever I hear about NMOSD, I think of one specific patient I had, and I always think of her when I come across something like your article, which is really fantastic. So, before we dive into the details, I wonder if maybe you can just explain to our listeners who aren't up to speed on what NMOSD is, what the disorder is, and maybe why it's so important that all of our listeners learn how to recognize it quickly and get people started on therapy.  Dr Mariotto: Yes, sure. So, neuromyelitis optica is an inflammatory autoimmune CNS disorder usually associated with aquaporin-4 antibodies, although there are a few cases, around 10%, who can be antibody-negative. And I think it's very much important to have in mind this disease and recognize it because it can be severe, as you pointed out; can present with very severe optic neuritis, myelitis, the brain stem, or area postrema syndrome. So, it can be really severe, affect quite young people around 40 years of age---although it can affect also the pediatric population and elderly people---and, importantly, it can be treated. It's very much important to treat this patient in the acute stage very quickly with steroids or plasma exchange in addition, and then to start a chronic treatment. So, we have treatment for this condition. So, it's very much important to, to recognize it quickly and treat the patient properly.  Dr Smith: So, I wonder if we can talk a little bit about the diagnostic criteria and boundaries of NMOSD, right? So, someone who comes in with bilateral op- severe long segment optic neuritis or long segment myelitis, we think about it. But what are the boundaries? Should we be looking for this, for instance, in someone who comes in with a unilateral optic neuritis or looks like typical multiple sclerosis? Is it important to get aquaporin-4 antibodies in those patients? What do the diagnostic criteria say about this?  Dr Mariotto: So, I wouldn't test aquaporin-4 antibodies in all patients with demyelinating conditions because although aquaporin-4 antibody assay is very specific, as for all assay and all antibody testing---also for MOG antibodies, for example---some false positive results can come out. So, I would suggest to test aquaporin-4 antibodies not in typical MS cases but in those who could be suggestive for not being MS, so in all those cases with atypical optic neuritis and myelitis or other syndromes. For those cases, it's important to test aquaporin-4 antibodies, but I wouldn't test them in all typical, classical MS cases. As I said, it's quite specific, the assay, so it's uncommon to have false positive results, but it can be.  Dr Smith: Serum, CSF, both?  Dr Mariotto: So, for aquaporin-4 antibodies, they're usually present in serum. They can be positive also in the CSF. And there are a few reports of isolated CSF positivity. But if we analyze larger samples volume, then it becomes clear that isolated CSF positivity is so, so rare that it's not recommended to test them in the CSF when serum is negative. So, for aquaporin-4 antibodies, the recommended matrix of testing is serum, which is different for MOG, which is not the topic of our article but is important to mention because MOG antibodies should be tested in serum and CSF. But aquaporin-4, I would recommend to test serum.  Dr Smith: What are the boundaries between MOGAD and NMOSD? And you talked about the differential testing of antibodies, which I was going to ask about. But when should we think of NMOSD relative to MOG? Dr Mariotto: Yeah. There are aspects which are the one mentioned in the criteria, highly suggestive for NMOSD. But the clinical spectrum can be similar to that of MOGAD. Usually, although there are some clinical aspect---like, for example cortical encephalitis or ADEM, which is more typical for MOGAD, or others like area postrema syndrome, which are more typical of NMOSD. The spectrum can be similar among the two conditions, so that's why in our clinical experience, usually they ask both aquaporin-4 and MOG antibodies in patients. It's- for experts, it can be easy to differentiate the two conditions, but for nonexperts can not be so easy.  Dr Smith: Can you define area postrema syndrome? I think not all of our listeners see that every day.  Dr Mariotto: Yeah, sure. This is a syndrome which is highly suggestive of NMOSD. That's why I mention it. And it's characterized by nausea, vomiting, hiccups are known as the syndrome. And it is very, very suggestive because of the expression of aquaporin-4 in that area of NMOSD. That's why I strongly recommend for all patients who comes out to have this syndrome to test for aquaporin-4 antibodies. MOGAD is hardly ever positive for that, so I think that whenever you see a patient with that syndrome, you should think about NMOSD.  Dr Smith: I'm just curious, aquaporin-4 is a water channel, which is kind of an interesting concept. Our conversation, I really want to make sure we give clinically important information to folks, but it's so curious to me at least, how does this actually result in a inflammatory demyelinating syndrome? For a simple neuromuscular guy, what's the immunopathogenesis of this?  Dr Mariotto: Yeah, the immunopathogenesis is quite complicated, as in all CNS disorders. And of course, aquaporin-4 antibodies are the main focus, but they are not the only one. As you said, aquaporin-4 antibodies have a target, this water channel, which is at the basis of the disease, and they are produced by the interplay between T cells, B cells, and plasma cells. But then also eosinophils, macrophages, cytokines, and chemokines are involved, enter the CNS, and then another important component is complement, which is highly activated in this disease. At the end, we have astrocyte damage because astrocytes are the main target of the disease, but also axon and myelin are involved. So, it's a quite complex pathogenesis based on the antibodies, but not only on that.  Dr Smith: And this will become important when we start talking about treatment. There seems to be a recurring theme of long segment demyelination, right? Optic neuritis is typically a large percentage of the length of the optic nerve, and obviously the myelitis se- more than three segments. Do you see other long segment areas of CNS demyelination, corpus callosum or things like that? Any ideas why that is, if that's true?  Dr Mariotto: Of note, this is quite interesting because usually when we have NMOSD, we have a longitudinal involvement, especially of the optic nerve and spinal cord, while brain lesions are quite different. Like, we usually do not have the typical Dawsen fingers-like lesions that we have in MS, for example, or the classical periventricular or subcortical extensive lesions that we can see and we have in mind when we think about MS. In some cases with NMOSD, the brain is completely negative, so we do not see anything. And Dawsen lesion's quite suggestive of NMOSD. So, you're right. I mean, this is related partially to the expression of aquaporin-4, and that's why we have this typical involvement also for area postrema, for example, and maybe also our other examples of clinical aspect that we can see in these conditions. But it's basically linked with the expression of aquaporin-4, which is the main target of the disease. And that's why usually the brain doesn't show so much involvement as we can see in MS, for example.  Dr Smith: I was actually really interested in some of the unusual manifestations or phenotypes, and I don't want to get into arcadia, really, but which of these should our listeners be familiar with that would really suggest that they should be thinking about NMOSD beyond the area postrema and other features that we've already talked about that are part of the core criteria?  Dr Mariotto: Yeah. I mean, I think that the encephalic syndromes or also ADEM, which is most typical of MOGAD but can be observed also in NMOSD or PRES, for example, are syndromes that can be considered in patients with NMOSD. There are the typical ones, which are the ones showed in the criteria, but whenever we have a brainstem involvement or, like, these encephalic syndromes or also PRES, we should think about NMOSD also.  Dr Smith: Another area I was interested in are red flags. In your article, you talk about red flags that might suggest an alternative diagnosis, right? And then this presumably is particularly important in seronegative patients, which 10% is not a reasonably high number, I suppose. What are red flags we should be thinking about for some other diagnosis?  Dr Mariotto: Yeah. I would here mention two very important red flags. The first one is a very hyperacute onset. Usually these conditions, these inflammatory conditions have a subacute onset, so whenever you have a very, very acute onset, you should think about something else. This can occur sometimes also in NMOSD, but hardly ever occur. Like, a very acute myelitis, the first thing we should think about is a vascular origin, for example, with a lot of pain and not about NMOSD, although sometimes the differential diagnosis is not so easy. The second thing is a progression independently of relapses, which hardly ever occur in NMOSD. Usually in NMOSD, we have the onset, and then we have a relapsing disease course. That's why we have to treat patients always and not to stop treatment. But we do not have progression in the meanwhile, while we can have, for example, this in MS. Same thing is for MOGAD. So, these are two things that I think is very much important to keep in mind.  Dr Smith: I want to pivot to talk about treatment because that's been super exciting. But rumor has it there are new diagnostic criteria coming for NMOSD in the next year. I bet you know a bit about those. Can you give our listeners any indication about kind of where the puck is going on this? Not so much what the criteria are specifically, but what sort of diagnostic challenges are the new criteria going to help us with once they come out?  Dr Mariotto: Yeah. So basically, we are working on that, so you will read them in the next future. This is the good point of the conversation on the new criteria. And we work a lot on the definition, on the new definition and nomenclature of NMOSD; on the definition of seronegative NMOSD, which is also quite tricky; and then on the assay we should use to test aquaporin-4 antibodies, and also on potentially new syndromes which should be included into the main feature of the disease. But hopefully you will read about this very soon.  Dr Smith: Looking forward to it. And Continuum Audio listeners, you heard it here first, so thank you. Let's pivot to treatment. This has been super exciting, and I wonder if the way to approach this is to start with acute management and then sort of chronic management. Would that make sense?  Dr Mariotto: Sure.  Dr Smith: Let's say I go on service on Friday, and I have a patient who comes in with positive aquaporin-4 and bilateral optic neuritis. What's the acute approach to managing that patient?  Dr Mariotto: So, the first approach is to administer intravenous steroids, but I would not wait to escalate to plasma exchange. There is quite good evidence that we should treat the patient with additional plasma exchange very quickly, and every day of delay of plasma exchange can cause increased disability. So, we should treat patients with steroids first, and then if we are not satisfied by the recovery, soon start with a plasma exchange. There is also some evidence, although less, for IVIG, but it's important to try to treat them very quickly, even if it's Friday, you know, there is the weekend and so on. But I think it's very much important to start with steroids after excluding other infectious causes or so on, and then to start quickly with plasma exchange. The main problem could be that we do not have the results of the antibody yet.  Dr Smith: Right. So, let me ask that question. You know, let's say my patient comes in on Friday, and clinical syndrome that really looks like NMOSD, and we're waiting for the aquaporin-4. There are many places where it's hard to get plasma exchange over weekends. And so, in that setting, are you better off doing the steroids over the weekend then PLEX on Monday, or should we just give IVIG because maybe it's as good as PLEX? What's your advice there? I'm trying to get ready for Friday because I know one's coming in.  Dr Mariotto: That's true, that's true. Usually they come on Friday or Saturday. I think it's acceptable to have three days of steroids and see how the patient improves, and then after three days to start with plasma exchange. Actually, we have a very good improvement if we start between three and five days after onset. So, I think waiting for three days is acceptable just because we can see if the steroids work properly or not, and then we can quickly start to plasma exchange. But I would not wait, like, 10 days, you know, before starting with a plasma exchange, and I would not wait for antibody results.  Dr Smith: Got it. Super helpful. And I'm actually not joking around, I learned recently that I have a reputation among our residents for having lots of optic neuritis when I'm on service, which I think is sort of karmic justice for being a peripheral nerve expert. But let me ask another question. So, let's say we do that, and the patient gets three or five days of pulse methylprednisolone and five courses of PLEX, and they're not doing well. Do you then just move right along into another agent B cell depletion therapy? I mean, what's your next step in escalation in the acute setting?  Dr Mariotto: I would for sure start to, as you said, with steroids, plasma exchange, and in case IVIG, and then quickly move to chronic treatment. And for patients who are not recovering well, I would think of something which has a quick effect so we can really start treating patients very quickly. There are different options. And all over the world, there are different rules for using immunosuppression in NMOSD. Like in Italy, for example, it's different from US or other countries, Germany, for example. There are different approved treatments and different rules of using them before or after rituximab, for example. We all know that there are treatments approved for NMOSD all over the world. But in some countries, like for example in Italy, we should use rituximab first, and then if it doesn't work, escalate to the approved treatment. I know in the US it's different. But anyway, for a patient who does not improve quickly, I would start with something which has a quick effect on the disease.  Dr Smith: And then rituximab versus inebilizumab, you know, CD20, CD19, what's your advice there? Is one preferable to the other, you know, if we have options to do either?  Dr Mariotto: Yeah. So, between rituximab and inebilizumab, we know that the target, well, is different, but is anyway B cells, so CD19 and CD20. With CD19, we can affect both plasma blast, plasma cells, and B cells. That's why the target is broader. And of note, this is an approved drug, while rituximab is, in most countries, used as off-label treatment.  Dr Smith: So inebilizumab would probably be preferable if we're able to do that.  Dr Mariotto: Unfortunately, there are not so many studies comparing rituximab with the approved drug, which is, of course, a pity, but that's the case. While we have clinical trials for all the approved drugs, and although the trials were designed differently, as we mentioned in the Continuum paper, we can argue something of the comparison between the approved drugs. But it is not so clear the comparison between rituximab and the new drugs, which is also something that we should work on.  Dr Smith: And then for chronic suppressive management, what other options are there?  Dr Mariotto: So, in addition to B cells, target can be interleukin-6, as we know with tocilizumab or satralizumab, and then complement with eculizumab. These drugs are both based on the pathogenesis of the disease. That's why we also discuss it in the paper, which shows a clear involvement of complement, and among cytokines of interleukin-6. So, targeting these made clear that could improve the disease quite well, and that's why they designed some clinical trials on these drugs, which are now approved, as we said, for NMOSD.  Dr Smith: Wow, so many options, and a lot of questions, but limited time. Let me just ask a couple of more. I see a lot of myasthenia patients, and there's a lot of variability, as you know, in patients with myasthenia, the extent to which complement is an important mechanism versus other, you know, important mechanisms. To what extent is response to a complement inhibitor kind of uniform across NMOSD? Or there's some patients who just don't respond to a complement inhibitor and others that respond really well. And then just, I'll just give my second question out is, you know, what about combination therapies for patients who have particularly challenging NMOSD?  Dr Mariotto: So usually these patients have a terrific response to complement inhibitors, and this is also shown by the clinical trials where we saw how eculizumab have a very impressive effect on the disease. And also, maybe this is also your experience, a very quick effect. So that's why there are also thoughts on using it in a very acute stage of the disease. That was what I was thinking about before. But then it has a very huge effect on complement, which is a major factor involved in the pathogenesis of NMOSD also in the chronic disease stage, and that's what also we see from clinical trials. Usually, we prefer to switch treatment from one to another and not to combine them. Of course, in very difficult cases, this can be considered, but the recommendation is to switch from one of these approved drugs to the other, or from rituximab to one of the approved drugs, and try to find out the best for our patient before combining them. Dr Smith: The complement inhibitor trials are breathtaking, at least for me. If I'm trying to convince students to go into neurology, I'll say, "Take a look at that paper," because anyone who claims that we're "diagnose and adios" is so wrong. It's so exciting. So, at a high level, this must have fundamentally changed outcomes for patients. I mean, it's still a difficult disease, but what is the kind of prognosis for that patient I described who comes in, gets the therapy you talked about? What does their long-term outcome look like in this modern therapeutic environment? Dr Mariotto: So, NMOSD is almost always a relapsing disease. That's why, as we mentioned, we have to treat patients always. But the prognosis changes a lot since we were also able to use all these drugs for the disease. So, the prognosis changes if we recognize it properly and early, and if we treat NMOSD properly with immunosuppressives. So, whatever we choose it's important to start it quickly, and this is the only way that we have to improve the prognosis of this disease. We have very active cases, but we have also cases who responds quite well to this immunosuppressive treatment, since now we have, as mentioned, these ones which are very impressive and show incredible results. So, the prognosis of the disease change in the last year, thanks also to the improvement of the diagnosis and of the treatment choices for the disease.  Dr Smith: I'm just... I- maybe my last question, you know, just at a personal level, not only for you as an expert who's caring for these patients, but in the patient community, this must have been a pretty exciting period of time, right? I mean, these, these drugs are coming fast and furious, and what a change. What's the kind of zeitgeist in the community, both your professional community and amongst the patient community about where we are? Dr Mariotto: Yeah, you're right. The last years were defined the years of NMOSD and also MOGAD because we had finally approved drugs which is relevant for all the disease that we treat and changed the landscape of the disease for clinicians, but also for patients. And we have more than one, as we said, so we have more options that we can also discuss with patients to try to choose the best one in terms of activity, but also route of administration or time. Some years ago, we just had rituximab, which is not approved in most of the countries, and now we have different approved drugs. And we improved the diagnosis of the disease thanks to the availability of live cell-based assay. And then we are working a lot also on biomarkers like GFAP, for example, which has been shown to be a very attractive biomarker able to mark disease activity and maybe also prognosis on this disease. So, you're right. I mean, in the last years, the landscape of NMOSD changed a lot.  Dr Smith: Sara, thank you so much for talking with me. I could keep going for another half an hour, but I would be in trouble with my editor, so I think we probably need to wrap it up. But thank you so much. This has been very informative.  Dr Mariotto: My pleasure. Dr Smith: Mine too. Thank you. Again, today I've been interviewing Dr Sara Mariotto about her article on NMOSD, which she wrote with Dr Romain Marignier. This article appears in the April 2026 issue of Continuum on multiple sclerosis. Be sure to check out Continuum Audio episodes from this and other issues, and thanks to you, our listeners, for joining 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.

Book a free consultation call with Robert Sikes on breaking through your Keto or low carb plateau here: https://www.ketobodybuilding.com/callFitness influencers are lying to you about how to build big muscles fast. High intensity training is not the shortcut you think it is. In episode 879 of the Savage Perspective Podcast, host Robert Sikes and guest Dr. Nash Jocic break down high intensity vs high volume training for muscle growth, especially for natural lifters. They cover weekly training splits, recovery, tendons, CNS fatigue, reps and rest times, and why meat and eggs can beat high carbohydrate diets for strength, leanness, and long-term progress.Follow Dr. Jocic on IG: https://www.instagram.com/nash_jocic/Subscribe to his YouTube Channel: https://www.youtube.com/nashjocic888/joinGet Keto Brick: https://www.ketobrick.com/Subscribe to the podcast: https://open.spotify.com/show/42cjJssghqD01bdWBxRYEg?si=1XYKmPXmR4eKw2O9gGCEuQ

Parker Kaleo, PharmD, Pgy2 ID Pharmacy Resident, presents a review of several recent controversies in infectious diseases. He addresses the optimal therapy for refractory MSSA bacteremia, the use of “cidal” versus “bacteriostatic” antimicrobials for severe infections, oral cephalosporins as step down therapy for severe infections, the penetration of cefazolin for CNS infections, and the use of isuvaconazole for Candida albicans infections. The presentation is given in a “confirmed,” “plausible,” or “busted ” format.

We love to hear from our listeners. Send us a message.On Episode 127 of Cell & Gene: The Podcast, Carlos Buesa, Ph.D., Founder and Chairman of the Board at Oryzon talks to Host Erin Harris about how targeting LSD1 is unlocking new treatment approaches across oncology, CNS disorders, and sickle cell disease, with promising early clinical data and a strategy grounded in precision epigenetics.Subscribe to the podcast!Apple  |  Spotify |  YouTubeVisit my website: Cell & GeneConnect with me on LinkedIn

Familiarity with the clinical, MRI, CSF, and serologic features of MOGAD can help neurologists recognize this condition in clinical practice. Awareness of the utility and pitfalls of the MOG antibody test is critical. The current therapeutic approach is guided by retrospective studies and the application of immunotherapies used in other autoimmune neurologic disorders. In this episode, Gordon Smith, MD, FAAN, speaks with Eoin P. Flanagan, MBBCh, coauthor of the article "Myelin Oligodendrocyte Glycoprotein Antibody–Associated Disease" in the Continuum® April 2026 Multiple Sclerosis and Related 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. Flanagan is a professor of neurology and the division chair of the Division of Multiple Sclerosis and Autoimmune Neurology in the Department of Neurology at Mayo Clinic in Rochester, Minnesota. Additional Resources Read the article: Myelin Oligodendrocyte Glycoprotein Antibody–Associated Disease Subscribe to Continuum®: shop.lww.com/Continuum Earn CME (available only to AAN members): continpub.com/AudioCME Continuum® Aloud (verbatim audio-book style recordings of articles available only to Continuum® subscribers): continpub.com/Aloud More about the American Academy of Neurology: aan.com Social Media facebook.com/continuumcme @ContinuumAAN Host: @GordonSmithMD Full episode transcript available here Dr Smith: So, what neurological disorder can cause bilateral optic neuritis, transverse myelitis, ADEM, or can mimic acute flaccid myelitis, intracranial hypertension, viral encephalitis, or cause seizures? Sounds like the great imitator, perhaps. If you want to know and learn more about this syndrome and how you can treat it---and it is very treatable---keep listening. My name is Gordon Smith, and today I have the great opportunity to talk with Dr Eoin Flanagan from the Mayo Clinic on his article on myelin oligodendrocyte glycoprotein antibody associated disease, or MOGAD, which is in the April 2026 issue of Continuum on Multiple Sclerosis and Related Disorders.  Dr Jones: This is Dr Lyell Jones, Editor-in-Chief of Continuum. Thank you for listening to Continuum Audio. Be sure to visit the links in the episode notes for information about earning CME, subscribing to the journal, and exclusive access to interviews not featured on the podcast. Dr Smith: This is Dr Gordon Smith. Today I'm interviewing Dr Eoin Flanagan about his article on myelin oligodendrocyte glycoprotein associated disease, or MOGAD, which appears in the April 2026 Continuum issue on multiple sclerosis and related disorders. Eoin, welcome to the podcast, and please introduce yourself to our audience.  Dr Flanagan: Yeah, thanks so much. I'm Eoin Flanagan. I'm a neurologist at the Mayo Clinic. I'm originally from Ireland. I work in the neuroimmunology lab at the Mayo Clinic, and work and see patients with MS, MOG, and autoimmune disorders here in Rochester, Minnesota.  Dr Smith: Your article is super interesting, I think, and this has been a really rapidly evolving area over the last, you know, many years. We have many more antibodies, and MOG is something that's been around for a while, but we've certainly learned a lot more about it. This is a topic that I think will be familiar to most of our listeners, but I wonder if maybe you can just begin by laying the foundation. Like, what is MOG? What's its typical presentation?   Dr Flanagan: So, MOG is a protein on the surface of the oligodendrocyte or its CNS myelin, and it was always of interest as a potential antibody target, and initially it was investigated in multiple sclerosis. But subsequently, we recognized that the antibodies to MOG have a specific syndrome, of which about a quarter of patients are pediatric and then the remainder are adults. And they can present with a variety of syndromes, probably most commonly optic neuritis, but also acute disseminated encephalomyelitis, or ADEM. Transverse myelitis can also occur, and then some other unusual brain and brainstem cerebellar syndromes can also occur.   Dr Smith: I was really impressed in the very broad phenotypic spectrum of MOG. We'll talk more about that, of course. But I wonder if maybe you can tell us when we should be ordering MOG antibody? Given this broad variability, does anyone who has a CNS demyelinating disease need a MOG assay, only specific phenotypes? What guidance do you have for our listeners?   Dr Flanagan: Yeah. It's a great question. So, I think you have to be a little bit careful because the MOG antibody test is a little bit sticky. So sometimes we can see some low-positive false positives. So, we don't wanna order it in every single patient with classical MS. So, I suppose we'll start with who not to order it in. I think it's also a very optic nerve- and optic neuritis-central disease, so I think you really need to be considering this in a patient with optic neuritis who does not have lesions in the brain suggestive of multiple sclerosis. And then we think about some of the features: if the lesion, the enhancement along the optic nerve is long, if it's bilateral, if there's a lot of optic disc edema accompanying that, we tend to think about MOG antibodies. And then children with demyelinating disease, MOG is over-represented in that cohort, so it accounts for about a third of those. So, if you have a child with CNS demyelinating disease, particularly if they're under twelve, with ADEM presentations or other presentations, you probably want to be ordering the MOG antibody test. And then a longitudinally extensive transverse myelitis in adults, certain types of cerebral phenotypes that we can get into, you would want to consider ordering MOG antibodies too.   Dr Smith: Now, you point out in the article that it's really important that laboratories use the cell-based assay for MOG as opposed to an ELISA, for instance. Is this something folks need to be very attentive to, or are all of the commercial laboratories now using a cell-based assay?   Dr Flanagan: Yeah. I think all of the commercial labs are using cell-based assays, so we don't really get into much of an issue. There are some differences between serum and CSF, so really, serum is the optimal sample to order. There is also some differences between the live cell-based assay and the fixed cell-based assay, where the live cell-based assay may have some advantages in terms of sensitivity. And then CSF is kind of still under evaluation about its role in the condition. So in general, it's a serum test. And then we have to remember that the antibody tends to be highest at the onset, and then it goes down over time. So, if you delay your testing or you're testing a patient long after the condition, it can go negative, for example. So it tends to be highest both around the relapses and particularly at the onset of the condition.   Dr Smith: You mentioned earlier that the test is sticky, which I take to mean that there is some risk for low-titer false positives. How do you navigate that situation? When should we be suspicious about a false positive?   Dr Flanagan: Yeah. I think there's some very useful features that can help you. You know, the main differential diagnosis is going to be multiple sclerosis, particularly in the US, in regions of the northern US where MS is particularly common. So, you really wanna be making sure that if you get a positive result, low positive, that it's not multiple sclerosis. And some of the best discriminating features are CSF oligoclonal bands. They're about 85% in MS and about 15% in MOG, so an easy number to remember, 85 and 15. And then the lesions in MOG, the brain lesions, tend to disappear over time. So, if you have the advantage of that follow-up MRI a year down the line, about 70% of lesions in MOGAD will resolve, while in MS, as we know, the term means multiple scars, so the MS lesions tend to persist over time. So, they are two quite useful features that can help discriminate.   Dr Smith: And how about specific phenotypes or areas of involvement or imaging abnormalities that suggest MOG? One of the things I found really interesting in your article is there are a host of different syndromes that I think had largely been previously described, many of them, that became clear later that these were really tied to MOG antibodies. Presumably, that's helpful in interpreting the antibody assay in that patients who have, perhaps, a borderline low titer, for instance, but have a very typical phenotype are more likely to have MOG than those who have a more clearly MS-type phenotype.   Dr Flanagan: Yeah, absolutely right. Yes. So, there's certain phenotypes that we don't tend to see with MS. The acute disseminated encephalomyelitis, or ADEM, is one that's particularly common in children. And about half of people that have ADEM will be positive for the MOG antibody. So that's a syndrome you need to look out for, which would be often in children, encephalopathy, and they would have multifocal white matter lesions, sometimes involving the gray matter. A second syndrome that was an interesting discovery from a Japanese group was this unilateral cerebral cortical encephalitis, where patients can have this swelling and T2 hyperintensity, often just on one side of the brain. And it's in the cortex, and some of those patients won't have any white matter lesions. And in that situation, it's important to order the MOG antibody, and that seems to be a specific phenotype of MOGAD. But sometimes people don't think about it because the white matter is not involved. So, if you see these patients, they often present with seizures, sometimes they even have fever accompanied by it. And if you see those patients and see this radiological feature, then you really want to consider ordering the MOG antibody too.   Dr Smith: Yeah, I found that really interesting. And I- actually, my next question is perhaps a good follow-up on that, is, what are the diagnostic pitfalls? You give a lot of examples of situations and I think some cases where it's easy to get tripped up and misdiagnose someone who has MOG with another fairly common neurological problem.   Dr Flanagan: Yeah, I think some of the things that can help you when you're determining if the MOG is a true positive or false positive is the level of the antibodies. The super high titers, if it's a clear positive or very strong positive, the likelihood is that that is much more likely to be MOGAD than those low positives just above the cutoff. So that can be useful to help you discriminate from false positives. Those lesions, again, if all the lesions persist over time, that's going to be more suggestive of multiple sclerosis. Other diagnostic pitfalls, I suppose, if it's a syndrome that's not really associated with MOG, like peripheral neuropathy or other syndromes where we'll see some case reports, but usually I would be very cautious about those kind of presentations. So usually, having the antibody at a high level, and then also if they've had other symptoms suggestive of MOGAD, like if a patient has had recurrent optic neuritis and then they have an unusual brain syndrome, or they start out with an unusual brain syndrome and then have recurrent optic neuritis. You know, there are situations that make it more likely if they're having other typical phenotypes of the MOGAD where we can kind of expand the spectrum, but we have to be careful.   Dr Smith: I was really curious about the dynamic imaging findings. And you point this out both in terms of the resolution of imaging findings, but also in that patients who have an acute MOG syndrome often have very rapid evolution of the imaging abnormalities. I'm just curious, you know, why is that, and what do you make of it? Does it have a mechanistic implication, do you think?   Dr Flanagan: I don't think we know for sure. I think there's probably a lot more happening than we see on MRIs sometimes. What sometimes can happen in about 10% of patients is the initial MRI can be normal. We don't tend to see that with multiple sclerosis or NMOSD. Then what we see is it evolving over time. So, at that time, if you do a CSF, you'll often see inflammation, but we don't see the lesions. Now, that might be because the MRI is not very good at picking up cortical involvement. That can be difficult to see in MRI. Or there could be other factors. It could be a functional effect on the MOG but without frank demyelination yet, for example. Or there could be edema that you- myelin edema that you can't see as a lesion yet on MRI. But we do see that if you repeat the MRI, sometimes it'll change a lot. So, you may go from one or two lesions on the first MRI to twenty lesions on the second MRI a week later. So, it does tend to change a lot. And then over time, those lesions also resolve. So, what I say is if it's a very suspicious situation---like a child comes in with new-onset encephalitis, has inflammatory CSF---you might wanna consider repeating that MRI down the line and seeing if it's changing. And then over time, you know, a repeat MRI a year after the onset when there's brain or spinal cord lesions can be very helpful just to make sure you're on the right track, because lots of those lesions will then disappear, and that's a very clear discriminator from multiple sclerosis.   Dr Smith: Yeah, thanks. I mean, I was wondering the same thing about whether that particular feature might imply, you know, a functional abnormality as opposed to more of a structural abnormality. So probably a lot more to learn as we move forward. There are now consensus diagnostic criteria that were published a couple of years ago. I think you've already touched on kind of the general approach, but do you want to speak to those? I found your summary pretty helpful.   Dr Flanagan: Yeah, I think that those criteria are quite useful. They have three main parts to them. The first part is having a characteristic clinical syndrome. So, we talked about ADEM, we talked about cerebral cortical encephalitis, transverse myelitis that's often longitudinally extensive, and optic neuritis being the main syndromes, but sometimes other brainstem or cerebellar involvement can be seen. And then the second part is having a positive MOG antibody. And then there's some caveats there. So, if you have a high positive, then you don't really need any additional supportive criteria. On the other hand, if you're low positive, to get at those sticky antibodies that make sure it's not a false positive, you need some additional supportive clinical or MRI criteria. Or if you're only positive in CSF, you need that additional criteria. You also need to be negative for the aquaporin-4 antibody, because they can overlap clinically. And some of those supportive criteria are things that we talked about a little bit earlier, longer lesions within the optic nerve, bilateral involvement, involvement of the nerve sheath or optic disc edema. This is a situation, MOG antibody disease, where your fundoscope is useful and looking in the back of the eye and seeing swelling, because we don't tend to see that quite as often. It's less common in multiple sclerosis, but we often see prominent edema in MOGAD. And then in the spinal cord, the lesions tend to be central in the cord. Sometimes they form this H sign where it's restricted to the gray matter, and they tend to be longer, sometimes involving the conus. Patients will often have neurogenic bowel or bladder. And then in the brain, deep gray involvement, those large lesions along the cortex with swelling are some of the typical features. And then the final step is exclusion of another diagnosis. Just like with any test that we do in neurology, our final step is going to be to put that into context. So that's just a normal thing that we will always do when we get a group of test results back that we don't know what it means. We have to put it into context. So, make sure it's not multiple sclerosis, everything else does not look like multiple sclerosis, and then you can be on your way to make a diagnosis.   Dr Smith: Definitely encourage listeners to read your article. I guess I say that with every time I- or with everyone I talk to for Continuum Audio, but the images are really fantastic and the cases are fantastic. So, everything you've described is well-illustrated, including really nice schematic sort of diagrams that help differentiate NMO from MOG and MS. So, if you like MRI scans and good imaging frameworks, then this is the article for you.   Dr Flanagan: I think that's true, and the other thing is that the imaging is quite helpful because it takes a while for that antibody to come back. We're lucky at Mayo Clinic, if you work here, it, it comes back faster for you. But for many places, that time of sending it in, so a lot of times you don't know right away. So, looking at scrutinizing that MRI can be very helpful to guide you on your way and to know what you're dealing with and how to approach both the acute treatment and plans to have potentially a steroid taper after the acute treatment and those kind of things that can help guide you in that regard.   Dr Smith: Yeah. So, let's talk about treatment. You know, what's your approach to treating a patient who has an acute demyelinating syndrome related to MOG?   Dr Flanagan: So similar to other things, MOG is very steroid responsive. So, we use high-dose IV methylprednisolone in adults. That would be one gram IV for five days. And then we also will sometimes use oral steroids, twelve hundred and fifty milligrams. That's a bit of a hassle because it's twenty-five fifty-milligram tablets, it doesn't come in a larger tablet version. But it's very helpful to patients because they can get started on it right away. You don't have to set up an infusion center. So, we have used those oral steroids often in people who don't have access to an infusion center, are not in the hospital. And particularly as it's often optic neuritis, some of those patients are seen in the outpatient setting, so we can get in with treatment quickly. In patients where it's more severe, it doesn't recover quickly with steroids, then we would consider escalating to plasma exchange as our second-line treatment, and there's some retrospective data that suggests that plasma exchange can be useful. That's gonna be particularly for those people who don't have that quick response to steroids, or maybe more severe phenotypes like that brain involvement with ADEM or cerebral cortical encephalitis, where those patients might be in the hospital and quite unwell. I will say, we might get on to this, that sometimes MOG can be very, very severe and even fulminant, where there can be increased intracranial pressure, and these patients can be in the ICU, and it can be life-threatening. And so, it's really important to treat those patients aggressively, and some patients have even required hemicraniectomy or additional treatment. Sometimes IL-6 blocking medications have been used in that situation. So, monitoring and treating increased intracranial pressure in those rare patients, probably 2 or 3% that have the very severe attack, is important.   Dr Smith: I think one of the things I found interesting, and then I'd love to get your feedback on this, is that most patients with MOG seem to have a very readily treatable disorder that's monophasic, right? You treat them with steroids, and they do well. On the other extreme, there are these patients that have a much more malignant presentation, and there are some that sound like they benefit from prophylactic or some chronic therapy. What's your approach, right? In MS, we do serial scans to monitor, and obviously, our patients are on, you know, chronic disease-modifying therapy. How do you decide when you're going to provide some sort of prophylactic therapy? How do you monitor it? How long do you continue it?   Dr Flanagan: That's a great point. We don't know for sure yet, but I think for the most part, our approach has been if the patient has a single episode, they recover well from that episode. So, if that's optic neuritis, they're back to twenty/twenty vision. They have recovered well. We don't tend to use chronic maintenance immunotherapy. Sometimes after the first attack, we'll do a little bit of a slow taper, maybe over four, six weeks. We have done longer than that. And then we won't place them on any long-term treatment, because it's about 50% of patients that may have a monophasic disease, so we don't want to treat all those people who are destined never to have another relapse. On the other hand, if a patient had a very severe episode, they're in the ICU, they're intubated, some of those patients then afterwards we will start them at least temporarily on an attack prevention medication for at least a few years to get them through. Some patients will be very fearful of future relapses in that situation. Or if they don't recover well, if they're blind in one eye after an episode and then their other eye is vulnerable, or they're left with some residual deficits neurologically from a myelitis, then we would often sometimes put those patients after the first attack. But most of the time, we're gonna wait and see if they get that second attack, and then once they have the second attack, that is when we would consider a steroid-sparing medication. But I will say that there's no proven medications. We don't have any clinical trial data available yet. So some of those patients with relapsing disease, we'll either try to enroll them in a clinical trial, or we'll use an off-label treatment to try and manage their disease based on what we've learned from neuromyelitis optica or from multiple sclerosis. A few different options seem to be better, and we can maybe get into that too.   Dr Smith: Yeah, let's go there. So, what options are there? You mentioned in more fulminant disease IL-6 inhibitors, and by that I assume you mean tocilizumab, but what are the options when you want to use prophylactic therapy?   Dr Flanagan: So, that tocilizumab can be beneficial in the very acute situation, in that malignant situation. But also as an attack prevention treatment, the IL-6 blockers seem to- some of the retrospective data seems to look like it works reasonably well, so we work and see if we can get that approved. Another medication that can work well is IVIG or subcutaneous immunoglobulin as a maintenance treatment, so we would sometimes give that, like, at least one gram per kilogram once a month. The benefit of that is it doesn't lower your immune system, so there's some advantages there, particularly in people who may be more prone to infections, older people. So, we'll sometimes use that. But we do get into a lot of challenges with insurance coverage, and it can be difficult to get these approved by insurance because we only have retrospective data out there. So then for some patients, if they're in a region where there's a clinical trial available, we might try to enroll them in a clinical trial. And there are some clinical trials underway now, so hopefully in the future we'll be able to have some FDA-approved medications that can have some Class 1 data that we can follow. Because it's hard when you're just following retrospective data or anecdotal reports, it's a little bit difficult to know exactly how well you're doing with your treatments.   Dr Smith: Well, Eoin, I wonder if we could finish up by just looking into the future, right? I mean, it sounds like a fun patient population to take care of because you've got lots of great therapies and can have a durable impact. But sure would be nice to have more evidence-based therapies and an FDA approval. What trials are going on? What's the future look like?   Dr Flanagan: Yep. So, there's some trials going on in the- a couple of worldwide trials. One is on an FCRN blocker called rozanolixizumab, which is kind of like a plasma exchange-type treatment which removes your antibodies, and it's a weekly subcutaneous treatment where adults are enrolled. And the second one is called satralizumab, which is another IL-6 blocking medication. And again, that one's given once monthly under the skin. And the trial for that also includes children down to age eighteen, so for adolescents, too, that can be an option. There are trials, I believe, in Asia for tocilizumab too, and there's one starting in Australia for rituximab. So, the good news is that we're going to have some really good data down the line for lots of different agents, and we'll be able to figure out which treatments work. And this will be really of great benefit to our patients when we get that Class 1 data to kind of guide us on what we should be using and really build on the success of some of the other conditions like neuromyelitis optica spectrum disorder, where we now have four or five approved, medications that work very well.   Dr Smith: Well, Eoin, thank you. This is a great conversation. I will say that it... the topic that I was a little intimidated about. I'm a simple peripheral nerve guy, as you know. But I think moreso than any other Continuum article I've read recently, I'm, like, loaded for bear. I can't wait to go back on the inpatient service and look for some MOG patients, because your article really left me feeling kind of prepared to think through this in a clinical setting. So, thank you for the conversation, and congratulations on a really wonderful piece for Continuum.   Dr Flanagan: Yeah, thanks so much. Always a great honor to be involved in the Continuum, and thanks to all the readers out there.   Dr Monteith: This is Dr. Teshamae Monteith, Associate Editor of Continuum Audio. If you've enjoyed this episode, you'll love the journal, which is full of in-depth and clinically relevant information important for neurology practitioners. Use the link in the episode notes to learn more and subscribe. AAN members, you can get CME for listening to this interview by completing the evaluation at continpub.com/audioCME. Thank you for listening to Continuum Audio.

Send us Fan MailPaper Discussed in this Episode: Artificial intelligence in clinical oncology: Multimodal integration and translational development. Ruichong Lin, Zhenhui Zhao, Zhonghai Liu, Jin Kang, Kang Zhang, Xiaoying Huang, Yunfang Yu. Cancer Letters 2026; Volume 649, 218493.Episode Summary: In this journal club deep dive, we explore how cutting-edge AI is fundamentally rewriting the rules of cancer diagnostics. We examine a comprehensive 2026 review on clinical oncology that highlights the shift from narrow, single-modality algorithms to highly sophisticated multimodal AI. We discuss how machines are learning to cross-reference patient charts, genomic data, and medical imaging simultaneously to achieve unprecedented feats—like accurately predicting tumor mutations without ever performing a physical biopsy. Plus, we explore the controversial but necessary world of "computational hallucinations" or synthetic data, which is currently being used to solve diagnostic blind spots.In This Episode, We Cover:• The Fragmentation Bottleneck: Why keeping radiology, pathology, genomics, and clinical history in isolated silos limits our ability to treat the whole patient, and why single-modality AI suffers from severe diagnostic "tunnel vision".• Cross-Modal Attention & Non-Invasive Biopsies: How models like LUCID essentially mimic the deductive reasoning of a multidisciplinary tumor board. By utilizing cross-modal attention mechanisms, LUCID dynamically shifts focus between CT scans, routine labs, and text-based clinical charts to predict EGFR gene mutations in lung cancer entirely non-invasively.• Graph Neural Networks (GNNs) & Tumor Social Networks: A look at the NePSTA framework, which uses GNNs and spatial transcriptomics to treat the tumor microenvironment like a mathematical topology. By mapping the "social network" of cells, it can rapidly molecularly subtype notoriously ambiguous central nervous system (CNS) tumors in minutes.• Computational Hallucinations: Introducing MINIM, a generative AI foundation model that creates statistically valid, photorealistic synthetic medical images (like optical CT or chest X-rays) for rare diseases based on textual descriptions. We discuss how intentionally generating these synthesized images solves the critical "data scarcity" problem and directly improves real-world diagnostic accuracy.• The Reality Check - Distribution Shifts: The dangerous logistical reason why an AI model boasting near-perfect accuracy at a massive urban academic center might fail completely in a rural clinic due to differing scanner calibrations and population demographics. We emphasize why the field must transition away from retrospective "vanity metrics" and toward clinically trustworthy prospective validation.• The Virtual Cell Paradigm: A staggering look into the near future where AI constructs completely accurate, computationally interactive digital twins of a patient's cancer. This framework allows doctors to test different drug regimens and simulate cellular responses mathematically in silico before ever administering medicine to the actual patient.Key Takeaway: Multimodal AI proves that cancer diagnostics must go beyond isolated data points. By dynamically synthesizing highly fragmented clinical information and utilizing synthetic imaging to overcome rare disease data scarcity, AI is pushing oncology into an era of robust, individualized molecular phenotyping. Ultimately, these innovations are replacing risky, invasive testing with precSupport the showGet the "Digital Pathology 101" FREE E-book and join us!

What if one of the biggest health threats on Earth… is something you can't see, taste, or even fully measure yet? In this urgent solo episode, Darin breaks down the rapidly escalating crisis of microplastics and nanoplastics infiltrating our bodies, water systems, and environment. What was once dismissed is now being acknowledged at the highest levels, with government agencies scrambling to understand and contain the damage. From plastics crossing the blood-brain barrier to disrupting hormones and carrying toxic chemicals deep into human tissue, this episode exposes the hidden cost of modern convenience, and more importantly, gives you practical, immediate actions you can take to protect yourself and your family. What You'll Learn Why microplastics are now considered a global health emergency How plastics accumulate in your body and environment The shocking truth about nanoplastics crossing the blood-brain barrier How plastics act as endocrine disruptors affecting hormones The connection between plastics and inflammation, fertility, and disease Why tap water and bottled water are both major exposure sources The role of PFAS ("forever chemicals") in long-term health damage How to filter and detox microplastics from your body Emerging science on breaking down plastics using bacteria and plants Simple, actionable steps to dramatically reduce your exposure Chapters 00:00:00 – Welcome to SuperLife 00:02:12 – Opening: committing to a clean, conscious life 00:02:27 – Fatal conveniences and why awareness matters 00:02:46 – Government officially flags microplastics as a crisis 00:03:04 – $100M+ initiatives to understand plastic contamination 00:03:38 – Microplastics in drinking water and daily exposure 00:04:20 – Plastics found in babies and human brains 00:04:45 – Why we still don't understand the full damage 00:05:08 – Nanoplastics crossing the blood-brain barrier 00:05:33 – Plastics as endocrine disruptors 00:06:02 – Hormonal imbalance, inflammation, and toxicity 00:06:30 – PFAS and the "forever chemical" crisis 00:06:59 – The #1 rule: stop using single-use plastic bottles 00:07:27 – Hidden dangers of "BPA-free" plastics 00:07:58 – Why you can no longer trust tap water 00:08:30 – The importance of high-quality water filtration 00:09:11 – Reverse osmosis systems and best practices 00:10:17 – Detox strategies: sweating and sauna use 00:10:59 – Fiber and plant-based diets binding toxins 00:11:24 – Medicinal mushrooms and beta glucans 00:11:52 – Microbes that break down plastic polymers 00:12:32 – Plant-based flocculants (okra, fenugreek) removing plastics 00:13:20 – Bio-sponges and advanced filtration innovations 00:13:46 – Magnetic separation technology 00:14:27 – Microplastics from clothing and laundry systems 00:15:16 – AI-assisted filtration and regulatory changes 00:15:55 – Light-activated breakdown of plastics 00:16:03 – Boiling water to remove up to 90% of microplastics 00:16:33 – Practical emergency water filtration methods 00:16:59 – Creating a low-toxicity lifestyle at home 00:17:20 – Final message: take control and protect your health 00:17:32 – Outro     Thank You to Our Sponsors Tru Niagen – Boost NAD+ levels for cellular health and longevity. Get 20% off with code DARIN20 at truniagen.com. Shakeology – Shakeology-All in One Nutrition: Get 15% off with code SUPERLIFE at Shakeology.com.     Join the SuperLife Patreon: This is where Darin now shares the deeper work: - weekly voice notes - ingredient trackers - wellness challenges - extended conversations - community accountability - sovereignty practices Join now for only $7.49/month at https://patreon.com/darinolien     Connect with Darin Olien: Website: darinolien.com Instagram: @darinolien Book: Fatal Conveniences Platform & Products: superlife.com New Show: Roadmap to Happiness     Key Takeaway: "We are living in a world where convenience has quietly introduced toxins into nearly every aspect of our lives, but you are not powerless. The moment you become aware, you can take action. And the small choices you make every day: what you drink from, how you filter your water, what you put into your body, can dramatically shift your long-term health and your family's future."     Bibliography/Sources: The News Hook — EPA CCL6 & STOMP Initiative Chemical & Engineering News. (2026, April 3). US government targets microplastics for research and potential drinking-water regulation. American Chemical Society. https://cen.acs.org Environmental Protection Agency. (2026, April 2). EPA takes bold action to ensure drinking water is safe from microplastics, pharmaceuticals, and potential hidden contaminants [Press release]. https://www.epa.gov/newsreleases Environmental Protection Agency & Department of Health and Human Services. (2026, April 2). EPA, HHS announce historic actions to protect Americans from microplastics and safeguard drinking water [Press release]. https://www.epa.gov/newsreleases Inside Climate News. (2026, April 3). EPA flags microplastics as 'priority' water contaminants, but the move doesn't guarantee regulation. https://insideclimatenews.org National Public Radio. (2026, April 2). EPA flags microplastics, pharmaceuticals as contaminants in drinking water. https://www.npr.org STAT News. (2026, April 2). EPA to put microplastics on study list of contaminants in drinking water. https://www.statnews.com The New Lede. (2026, April 2). EPA flags microplastics as 'priority' contaminants in drinking water. https://thenewlede.org U.S. Government. (2026). Public comment docket: EPA-HQ-OW-2022-0946. https://www.regulations.gov The Science — Brain Invasion & Cellular Damage ACS Environment & Health. (2025). Neurotoxicity of micro- and nanoplastics: A comprehensive review of CNS impacts. American Chemical Society. https://pubs.acs.org Journal of Nanobiotechnology. (2025). Maternal nanoplastic exposure led to impaired neuronal development in the fetal cortex. Springer Nature. PubMed Central. (2023). Micro-/nanoplastics breach the blood-brain barrier: Biomolecular corona's role revealed. National Institutes of Health. https://pmc.ncbi.nlm.nih.gov PubMed Central. (2024). A review on micro- and nanoplastics in humans: Translocation of barriers and potential health effects. National Institutes of Health. https://pubmed.ncbi.nlm.nih.gov PubMed Central. (2025). Overall effects of microplastics on brain. National Institutes of Health. https://pmc.ncbi.nlm.nih.gov ScienceDirect. (2025). Mechanisms of micro- and nanoplastics on blood-brain barrier crossing and neurotoxicity. Elsevier. https://www.sciencedirect.com The Science — Endocrine Disruption & Gut Health eClinicalMedicine. (2026). Phthalates attributed to nearly 2 million preterm births globally. The Lancet. Frontiers in Cellular and Infection Microbiology. (2024). Microplastics, human health, and the gut microbiome. Frontiers. https://www.frontiersin.org Frontiers in Endocrinology. (2023). A review of the endocrine disrupting effects of micro and nano plastic in mammals. Frontiers. International Journal of Molecular Sciences. (2025). Micro- and nanoplastics as disruptors of the endocrine system. MDPI. https://www.mdpi.com PubMed Central. (2025). Microplastics, endocrine disruptors, and oxidative stress. National Institutes of Health. Solutions — Filtration & Global Removal Technologies ACS Applied and Environmental Microbiology. (2024). Eco-microbiology: Discovering biochemical enhancers of PET biodegradation by Piscinibacter sakaiensis. American Chemical Society. ACS Omega. (2025). Thermostability and activity improvements of PETase from Ideonella sakaiensis. American Chemical Society. Environmental Science & Technology Letters. (2024). Drinking boiled tap water reduces human intake of nanoplastics and microplastics. American Chemical Society. https://doi.org/10.1021/acs.estlett.4c00081 Srinivasan, R., et al. (2025). Fenugreek and okra polymers as treatment agents for the removal of microplastics from water sources. ACS Omega. https://doi.org/10.1021/acsomega.4c07476 Yoshida, S., et al. (2016). A bacterium that degrades and assimilates poly(ethylene terephthalate). Science.  

The brain health economy is emerging as a critical focus across healthcare and policy both for treating serious neurological and mental health diseases and for increasing brain capital for society. In this episode, Inizio Ignite's Varun Renjen sits down with George Vradenburg, Chairman of the Davos Alzheimer's Collaborative and Harris Eyre, Executive Director of the Global Brain Economy Initiative to explore why it's evolving so rapidly and what it means for life sciences companies.From how the brain health economy is evolving at the global level with growing importance from the World Economic Forum, to CNS trends, and to the impact of initiatives like the Davos Alzheimer's Collaborative and the Davos Brain House, our guests unpack key developments shaping this space. We also examine the role of public-private partnerships and how life sciences companies can better engage.Finally, we look ahead: what does an ideal brain health ecosystem look like—and how can we build it?Panel – Varun Renjen, George Vradenburg, Harris Eyre Recording & Editing – Mike Liberto, Rachel Skonecki For additional discussion, please contact us at TrendingHealth.com. 

Listen Online: About this episode: In this not-to-be-missed interview, The First Lady of Nutrition sits down with Dr. Scott Crawford, her personal practitioner and a leading upper cervical chiropractor, to uncover how a subtle misalignment in the atlas—-the top vertebra that supports the skull—-may be at the root of a wide range of symptoms. With an estimated nearly 65% of people affected by some degree of atlas misalignment, this issue is far more common than most realize. Dr. Crawford explains how it may contribute to headaches, migraines, vertigo, and even behavioral challenges such as ADHD and schizophrenia—while also revealing why “tech neck” is becoming increasingly common in today's screen-driven world. Ann Louise and Dr. Crawford also discuss simple ways to support proper alignment and highlights real-world cases where correcting the atlas led to remarkable improvements in health and well-being.The post Could a Simple Misalignment Change Your Life? first appeared on Ann Louise Gittleman, PhD, CNS.

Jim talks with John Krakauer—professor of neurology and neuroscience, director of the Center for Study of Motor Learning and Brain Repair at Johns Hopkins, and external faculty at SFI—about his 2017 paper "Neuroscience Needs Behavior: Correcting a Reductionist Bias." They discuss defining behavior as ecologically valid goal-directed action within an animal's umwelt, behavioral decomposition being epistemically prior to neural investigation, bipedal running and Sherrington's spinalized cat experiments as illustrations of that decomposition, what a satisfying neural explanation should actually look like, emergence and neuroscientists' resistance to it, the concept of explanatory autonomy and the "wings don't fly, birds do" framing, downward causality and the traffic jam analogy, Sherrington's own epistemic humility about understanding thought, whether consciousness will eventually be explained the way life was or remain permanently fuzzy, the three traditions of studying the nervous system and their persistent tensions, the problem of double-dipping with coarse-grained behavioral language in neural data, "filler verbs" like "involves" and "underlies" that add surplus meaning to a correlation without doing extra explanatory work, everyday pseudo-explanations like dopamine for unhappiness and oxytocin for love, the identity fallacy, LLMs as scientific sparring partners and critical reviewers, Krakauer's vertigo at the current moment and the possibility of retiring if AI generates better intuitions, interpretable AI as a new subject for neuroscience and psychology, Jim's own artificial consciousness project building a rudimentary white-tailed deer, distinguishing consciousness from cognition and sentience, separating the machinery of consciousness from its contents, Nagel's "What Is It Like to Be a Bat?" and echolocation as conscious content, multiple realizability and its being pervasive and fatal to naive reductionism, the mereological fallacy and mirror neurons as ground zero for multiple fallacies, Marr's three levels and the direction of the scientific project from behavioral goal to algorithm to neural implementation, the bradykinesia paper finding that Parkinson's patients move slowly because they want to move more slowly, the C. elegans connectome and the limits of that knowledge, the Jonas and Kording microprocessor paper, and much more. Episode Transcript "Neuroscience Needs Behavior: Correcting a Reductionist Bias", by John Krakauer "What Is It Like to Be a Bat?", by Thomas Nagel "Why Don't We Move Faster?", by Pietro Mazzoni, Anna Hristova, and John Krakauer "Could a Neuroscientist Understand a Microprocessor?", by Eric Jonas and Konrad Kording John Krakauer is currently John C. Malone Professor, Professor of Neurology, Neuroscience, and Physical Medicine and Rehabilitation, and Director of the Brain, Learning, Animation, and Movement Lab at The Johns Hopkins University School of Medicine. He is also an External Professor at the Santa Fe Institute and Director of the Centre for Restorative Neurotechnology at The Champalimaud Centre for the Unknown. His areas of research interest include experimental and computational studies of motor control and motor learning, long-term skill learning and its relation to higher cognitive processes, prediction and mechanisms of motor recovery after stroke, new neuro-rehabilitation approaches including immersive XR gaming with generative AI, robotics and invasive CNS stimulation, and philosophy of mind. He is slowly working on a new book on the mind, intelligence, and AI for Princeton University Press.

Title: CNS Innovation Institute Podcast: Shepherding the Next Generation of Neurosurgical Innovators and Leaders Panelists: David Dornbos, Garni Barkhoudarian, Mohamad Bydon Description: The neurosurgical field continues to evolve at a rapid pace with novel innovations and paradigm-shifting trials coming out nearly constantly. This podcast will highlight the impact of the changing landscape and the new CNS Innovations Institute, which will provide the tools for young innovators to continue to inflect the field in a positive way. This transformative program from the CNS will foster iterative growth in the field and enhance our ability to care for neurosurgical patients.

We discuss this ominous complication of providing local anesthesia. Hosts: Elaine Jonas, MD Brian Gilberti, MD https://media.blubrry.com/coreem/content.blubrry.com/coreem/LAST.mp3 Download Leave a Comment Tags: Critical Care, Toxicology Show Notes I. Pathophysiology & Mechanisms Definition: Systemic toxicity secondary to local anesthetic (LA) via accidental intravascular injection or excessive systemic absorption. Threshold: Occurs when plasma concentration exceeds the safety threshold for cardiac and neural tissue. Agent Profile: Bupivacaine (High Risk) Highly lipophilic with high protein binding. “Fast-on, Slow-off” Kinetics: Strong Na+ channel binding with extremely slow dissociation during diastole. Myocardial Depression: Direct inhibition of Ca2+ release from the sarcoplasmic reticulum, impairing contractility. Low CC:CNS Ratio: The dose required for cardiac collapse is very close to the dose that triggers seizures (narrow safety margin). Contributing Factors: Acidosis/Hypercapnia: Increases the fraction of free drug and promotes ion trapping in the brain/heart; shifts the LA-binding curve toward higher toxicity. Hypoxemia: Exacerbates myocardial depression and lowers seizure threshold. II. Risk Assessment & Prevention Patient-Specific Risk Factors Extremes of Age: Neonates (low α-1-acid glycoprotein) and elderly (reduced clearance). Body Composition: Low muscle mass/frailty (decreased volume of distribution). Organ Dysfunction: Hepatic: Reduced metabolism of amide LAs. Renal: Accumulation of metabolites; risk of metabolic acidosis lowering seizure threshold. Cardiac: Reduced cardiac output slows hepatic delivery/clearance; heart failure patients are more sensitive to Na+ channel blockade. Pregnancy: Increased sensitivity to cardiotoxicity. Procedural Risk Factors Vascularity of Site (Highest to Lowest Risk): Intercostal blocks (highest absorption rate). Caudal/Epidural. Interfascial plane blocks (e.g., TAP block). Psoas compartment/Sciatic. Brachial plexus. Technique: Large volume infiltration, lack of ultrasound, lack of incremental injection. Prevention Mandates Weight-Based Dosing: Lidocaine (Plain): Max 4.5 mg/kg. Lidocaine (with Epi): Max 7 mg/kg. Bupivacaine: Max 2.5–3 mg/kg. Incremental Injection: 3–5 mL aliquots with frequent aspiration. Intravascular Marker: Use Epinephrine (1:200,000) to detect accidental IV placement (HR increase >10 bpmor SBP increase >15 mmHg). III. Clinical Presentation Neurologic Phase (Early to Late) Subjective: Metallic taste, tinnitus, circumoral numbness/tingling. Objective: Visual disturbances, agitation, confusion, tremors. Critical: Generalized tonic-clonic seizures, rapid progression to CNS depression, coma, and apnea. Note: Early phases are often masked in patients receiving midazolam or propofol. Cardiovascular Phase Initial: Hypertension and tachycardia (if epi used) or transient stimulatory phase. Conduction Defects: PR prolongation, QRS widening (classic sign), bundle branch blocks. Dysrhythmias: Bradycardia (most common), VT/VF, PEA, asystole. Contractility: Profound, refractory hypotension and cardiogenic shock. IV. Immediate Management Algorithm Goal: Prevent hypoxia/acidosis and sequester the toxin. 1. Initial Actions Stop Injection: Immediately halt all LA administration. Call for Help: Specify “LAST Protocol” and “Intralipid Kit.” Airway Management: 100% O2​. Hyperventilate slightly if needed to counter respiratory acidosis. Low threshold for intubation (hypoxia/acidosis rapidly worsen LAST). 2. Seizure Control First-line: Benzodiazepines (e.g., Midazolam). Avoid: Propofol if hemodynamically unstable (exacerbates cardiac depression). Neuromuscular Blockers: May be needed for ventilation, but remember they do not stop CNS seizure activity. 3. Lipid Emulsion Therapy 20% Indications: Start at first sign of serious toxicity (airway compromise, seizures, or CV instability). Bolus: 1.5 mL/kg IV over 1 minute. Infusion: 0.25 mL/kg/min immediately following bolus. If Instability Persists: Repeat bolus (up to 2 times). Increase infusion to 0.5 mL/kg/min. Upper Limit: ≈12 mL/kg total dose. 4. Modified ACLS Epinephrine: Use low doses (

In this episode of the Wise Divine Women podcast, Dana Irvine and DANIELLE ARNOLD, MS, CNS, LDN, explore the intricate connections between gut health, hormonal balance, and breast health. They discuss the importance of personalized care through testing, the role of probiotics and digestive enzymes, and the impact of genetics on health outcomes. The conversation emphasizes the need for preventative measures and understanding one's unique health profile to optimize well-being. Danielle is a clinical nutritionist and functional medicine practitioner who supports providers in interpreting functional tests and building microbiome-centered care plans, and she teaches clinical nutrition in an academic setting as well. Together, they are experienced educators who regularly speak with both professional and lay audiences about gut health and the microbiome's role in whole-person care. They can be found online at DesignsforHealth.com.TakeawaysGut health is foundational for overall hormonal balance.Testing is crucial for personalized health care.Probiotics should be tailored to individual needs.Digestive enzymes can significantly improve nutrient absorption.Methylation plays a key role in health and disease prevention.The gallbladder is essential for hormone detoxification.Genetics can inform health strategies but should not be the first step.Lifestyle choices can influence genetic expression.Breast health is closely linked to gut microbiome health.Preventative measures are vital for long-term health.Chapters00:00 Introduction to the Journey of Healing02:53 Understanding Hormonal Health and Its Impact05:36 The Role of Gut Health in Hormonal Balance08:11 Exploring the Connection Between Gut and Breast Health10:51 The Importance of Testing and Personalized Care13:46 Probiotics and Their Role in Gut Health16:40 Digestive Enzymes: A Key to Nutrient Absorption19:11 The Impact of Genetics on Health22:16 Preventive Measures for Breast Health24:47 The Importance of Methylation and Nutrient Absorption27:32 Conclusion and Final ThoughtsIf you're over 40 and feeling:• Tired but wired • Bloated or inflamed • Hormonal and frustrated • Concerned about breast health • Unsure what testing you truly needYou don't need another quick fix. You need clarity.The ⁠Wise Divine Health Clarity Call⁠ is your 1:1 strategy session to uncover root causes and map out your next best steps — whether that's functional testing, thermography, nutrition coaching, or hormone support.

Persistent drool rash can be more than just a messy phase. In this episode, we explore how red, irritated cheeks, especially when they flare at certain times of day, may be early clues that a baby's skin barrier is struggling and that deeper eczema-related issues could be developing.We also unpack how signs like cradle cap, colic, diaper rash, flushing with foods, and mucus in stools can fit into a bigger picture. Tune in to learn how to tell the difference between a drool rash, an eczema flare, and a possible allergic reaction, so you can feel more confident about what your baby's skin may be trying to tell you.My guest, Jennifer Brand, MS, MPH, CNS, LDN, is a clinical nutritionist who helps babies and children with chronic rashes get to the root causes of their skin issues. Known for her pediatric skin-focused approach, she is passionate about helping families support healthy skin through her signature method, Rashes Be Gone.⭐️Mentioned in This Episode:- See all the references

Co-hosts Jackie Garlich, OD, FAAO, and Jessilin Quint, OD, FAAO, invite Mila Ioussifova, OD, CNS, FAAO, FOWNS, back on the To the Point podcast to talk about in-office allergy testing. Dr. Ioussifova has built her dry eye and ocular allergy treatment armamentarium over the course of 13 years in practice. She notes that combined, dry eye and ocular allergy can be part of a vicious cycle if the underlying dysregulated immune system isn't addressed—this is where immunotherapy comes in. Dr. Ioussifova covers her in-office pretesting protocol and the billing and reimbursement behind it.

In this episode of The Nurse Practitioner Podcast, Julia Rogers, DNP, APRN, CNS, FNP-BC, FAANP, FAAN; Tracie Kirkland, PhD, DNP, ANP-BC, PPCNP-BC, PNP-BC, FAANP, FAAN; and Cheryl Thaxton, DNP, APRN, CPNP, FNP-BC, CHPPN, ACUE, FPCN, FAANP, FAAN discuss DNP-PhD preparation.

Listen Online: About this episode: In this engaging conversation, The First Lady of Nutrition talks with Dr. David Brownstein—one of the world's leading authorities on iodine—to unpack a topic that's quietly impacting millions. If you've ever been confused about iodine, this is the interview you can't afford to miss. Dr. Brownstein explains why iodine is an essential nutrient the body simply cannot function without, why modern diets are no longer supplying enough, and how iodine levels today are dramatically lower than they were just a few decades ago. He breaks down the critical role iodine plays in thyroid function, breast health, brain health, and even cancer prevention—while addressing the alarming rise in thyroid disorders and thyroid cancer. Ann Louise and Dr. Brownstein also dive into the practical side—what forms of iodine actually work, including the history and clinical relevance of Lugol's Solution, the difference between iodine and iodide, and why a combination approach may be key. They discuss how proper iodine support may reduce the need for thyroid hormone medication in some cases, how much iodine the average adult truly needs, and why individuals with glandular conditions may require more. You'll also learn the best ways to test iodine levels, the surprising dietary factors that enhance iodine absorption, and the far-reaching consequences of deficiency—from fatigue and weight gain to neurological issues. This is a must-listen for anyone serious about optimizing thyroid health and understanding one of the most overlooked nutrients in modern medicine.The post The Iodine Crisis No One Is Talking About first appeared on Ann Louise Gittleman, PhD, CNS.

In this episode, Lyell K. Jones Jr, MD, FAAN, speaks with Andrew J. Solomon, MD, FAAN, who served as the guest editor of the April 2026 Multiple Sclerosis and Related Disorders issue. They provide a preview of the issue, which publishes on April 2, 2026. Dr. Jones is the editor-in-chief of Continuum: Lifelong Learning in Neurology® and is a professor of neurology at Mayo Clinic in Rochester, Minnesota. Dr. Solomon is the Division Chief of Multiple Sclerosis and a Professor in the Larner College of Medicine at the University of Vermont in Burlington, Vermont. Additional Resources Read the issue: continuum.aan.com 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: @LyellJ Full episode transcript available here Dr Jones: It's been more than 150 years since Jean-Martin Charcot first described the disease that we now know as multiple sclerosis. Since then, the tools we have to diagnose and treat this disorder have expanded enormously. So why are the diagnostic criteria for MS. still evolving? Today we're speaking with Dr Andrew Solomon, guest editor of our latest issue of Continuum on MS and related disorders. To learn more about this question and much more. 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 subscribing to the journal, listening to verbatim recordings of the articles, and exclusive access to interviews not featured on the podcast. Dr Jones: This is Dr Lyell Jones, editor in chief of Continuum, Lifelong Learning in Neurology. Today I'm interviewing Dr Andrew Solomon, who is Continuums guest editor for our latest issue of Continuum on multiple sclerosis and related disorders. Dr Solomon is a professor of neurological sciences at the University of Vermont, where he also serves as the division chief of multiple sclerosis. Dr Solomon is an internationally recognized authority on MS, particularly on the diagnostic approach to this complex disorder. Dr Solomon, welcome. Thank you for joining us today. Why don't you introduce yourself to our listeners?  Dr Solomon: Hi, everyone. This is Andy Solomon. It's a pleasure to be here with you. And I feel honored to have helped this collaborative effort that created this important tool for trainees and clinicians in practice, the Continuum issue on multiple sclerosis and related disorders.  Dr Jones: Obviously, we're grateful that you've taken us on. A lot has happened in the world of MS and other neuroinflammatory disorders in the last few years, so lots to update. But as we've done over the last few podcasts, I'm going to start off the interview today, Dr Solomon, with a trivia question. And then we'll come back at the end of the podcast and give the answer. So, the trivia question is this. There are now more than 20 drugs approved by the FDA for the treatment of MS. What was the first disease-modifying therapy approved for MS? And when was it approved? So, don't answer because I know you know the answer. But we'll come back to it at the end of the interview. And our listeners can think about that question. So, let's get right to it. As many of our listeners know, the diagnostic criteria for MS. were recently revised. And you were involved with that revision. So, you're the perfect person to ask what were the major changes in the 2024 McDonald criteria, and why did we need to update them in the first place? Dr Solomon: I'm very excited about the 2024 McDonald criteria, and it was an honor to be part of that process that resulted in that manuscript. When we revise the diagnostic criteria for MS usually it's driven by accumulating data that suggests some changes or revisions might help us diagnose patients either earlier or with more accuracy. And that's certainly the case with this criteria. There was accumulating data that suggested some particular changes were important. You know, there's a lot of expert opinion involved as well. You know, there's many experts who are involved in the collaborative decisions that go into these revisions. And some of the changes in our field also pushed some of the revisions to where maybe there's not as much evidence, but where we felt it would improve care for patients with MS. This criteria, I would argue, is probably one of the most substantial revisions in over 20 years. There's multiple changes that are potentially impactful for the diagnosis of MS. Some very important changes involve the incorporation of new paraclinical tools that we can use to assess the visual pathway, as well as, imaging tools that provide high specificity for MS that we can use to substitute or dissemination in time, for instance, as well as other tools that may allow us to diagnose patients earlier than we would have in prior criteria.  There's also some opportunities with the new criteria to potentially provide access in regions where some tools are more available than others. For instance, the incorporation of Kappa Free Light Chains as a substitute for oligoclonal bands may open up opportunities in regions where expertise for oligoclonal band testing are not available. That's a very qualitative test, whereas Kappa Free Light Chain index is more quantitative, less expensive and may allow CSF testing to be performed to aid the diagnosis of MS in some regions where it wasn't available previously. This criteria provides multiple pathways to the diagnosis of MS, many more than we've had in prior criteria. So, it's important to emphasize that while there's all these new tools and changes that have been incorporated, not every pathway needs to be available where you practice. What it incorporates as flexibility. It is a bit more complex looking at all of these different possibilities, but the point is this flexibility allows clinicians or providers to diagnose MS early with high accuracy based on the tools they have available. Dr Jones: I think it will be a learning curve, right? I think any time we make a change in how clinicians get accustomed to approaching a diagnosis of a disorder, it will take some time for folks to incorporate it. And I see what you mean about the complexity, but I think that's a really great point, that emphasizing the different pathways to the diagnosis is really a strength of the revision, right? Dr Solomon: I agree, I think, you know, in other disorders, particularly if you think about rheumatologic disorders, systemic rheumatologic disorders or inflammatory disorders, where over time we've not had very highly specific and sensitive biomarkers. And we've incorporated a variety of clinical and prior clinical findings, testing, laboratory testing and biopsy and other things to confirm a diagnosis. These approaches to these disorders are sort of a checklist. And I think that clinicians became familiar with that approach and were able to make diagnoses accurately this way. And I think of the new criteria in a similar way. It's not quite amenable to a checklist, but the pathways are sort of simplified with multiple options. Hopefully, using the figures, clinicians can look at the paper and see what tools they have available to help them confirm a diagnosis of MS. I think it's really important to emphasize that the diagnostic criteria for MS still does not discriminate MS from other disorders. Everyone who's listening here, you do, the clinicians do. So, to enter the diagnostic criteria and these pathways, we first have to feel confident that the patient has a clinical presentation and an MRI presentation or MRI findings that are highly suggestive of MS. That aspect of the criteria hasn't changed since, the Schumacher criteria in the 1960s. This concept of no better explanation. So, we still need to know what's typical for MS. And we need to know what signs or symptoms or findings are that might suggest another disorder, because the criteria are really only validated and tested in patients who have these presentations to start with that are typical for MS. A major change in this particular criteria is that we can now diagnose patients who are asymptomatic. Previously just called radiological isolated syndrome. Not every patient with an MRI finding concerning for MS and now being diagnosed with MS. There's other features that, must be present, but even more than before, knowing what the typical appearance of MRI lesions suggestive of MS, it is even more critical now than it was before, because in those patients who have either no symptoms or a nonspecific presentation, if we have an MRI that's highly convincing for MS and some other prior clinical findings, we can make the diagnosis. But we first need to know with some confidence what that MRI should look like.  Dr Jones: So, there is a little circularity when we do these diagnostic criteria. I think our listeners who see patients will be reassured that the clinician is still in the loop. We haven't been automated out of the process yet.  Dr Solomon: We need a highly sensitive and specific biomarker or a set of biomarkers for MS.  We're getting closer with some of these advanced imaging findings like central vein sign and paramagnetic rim lesions. But not every patient can be diagnosed with those. And they're not required for the diagnostic criteria. In lieu of a highly sensitive and specific test. Our clinical acumen, for what we find a neurologic exam. And what we see on imaging in particular, is quite critical for ensuring that the criteria perform as well as we hope they will. Dr Jones: So, you've had the opportunity, the vantage point, to review all of these articles covering a wide variety of topics, MS, other neuroinflammatory disorders like aquaporin‑4–positive neuromyelitis optica spectrum disorder (NMOSD), myelin oligodendrocyte glycoprotein antibody-associated disease, MOGAD. Anything that surprised you in these articles as you were reading through them?  Dr Solomon: I think maybe for listeners, what may be surprising to some of them is that despite guidelines surrounding the use of some of our disease modifying therapies in pregnancy and breastfeeding that are published by regulatory authorities in the United States or Europe or other places, we are making other decisions for patients based on the data we have, the best data we have. Thinking about family planning is really important for us with patients who are newly diagnosed with MS, as well as through the course of their disease. This is a conversation we should be having shortly after diagnosis, because there are strategies we can take to minimize the risk of exposure of DMT around conception and to make plans for how we're going to think about DMT surrounding breastfeeding, to ensure the health of mom and the baby, and reduce risks as much as we can with the knowledge we have. I think in medicine it's quite common for us to use medications off label, right? I mean, so medications are often FDA approved for one indication. And in neurology, for instance, we find a lot of medications after their approval were quite effective for migraine prophylaxis for instance. Right? And so, it's not unusual for us to prescribe medications beyond the label. And I'm not suggesting that we necessarily ignore the advice of our regulatory authorities. But sometimes the data is accumulating really fast around some of these therapies after they're approved. Sometimes we can look towards experts and how we can navigate pregnancy and breastfeeding in MS. Dr Jones: I think that's a great point about the importance of family planning and having to use judgment. I do want to highlight to our listeners and our subscribers a fantastic article in the issue on family planning and MS and other neuroinflammatory disorders. This was written by Dr Ruth Dobson and Dr Kersten Hellwig, and I think it covers a lot of that gray area where we have to use our clinical judgment to manage these diseases in the absence of a regulatory approval. And I think, again, that's an important gap that the issue fills. And really, that's just a wonderfully written article that I think is a must-read. So, we cover lots of topics in this issue. And one of them is again a relatively newly characterized disorder, MOGAD. What's the latest in the world of MOGAD, what should our listeners be aware of? Dr Solomon: I agree, I think we're in an exciting time in CNS inflammatory disease. And this is a recently described disorder. You know, and the diagnostic criteria now is only a few years old. So, I think importantly, readers should be aware of the diagnostic criteria. This is something that, really will help us distinguish this disorder from NO spectrum disorder and MS. There's a key overlap between the MS diagnostic criteria and MOGAD. Two decades ago we saw a pediatric MS included somewhat atypical presentations like bilateral optic neuritis or acute disseminated encephalomyelitis. And we had caveats in our approaches to pediatric presentations of presumed MS, suggesting that there could be something very different than adult MS. Subsequently, we've realized that pediatric MS presents quite similarly to adult MS in terms of its clinical syndromes and MRI appearance, and many of those pediatric patients who had initially been diagnosed with MS and MOGAD. MOGAD is actually probably more common demyelinating syndrome in patients who are under 12 years old. So, the MS diagnostic criteria requires testing for MOG-IgG with a good assay, a cell-based assay, any patient being evaluated under the age of 12 or with a demyelinating syndrome to avoid misdiagnosis.  Dr Jones: Thanks for that. Obviously, MOGAD is one of several disorders that have been more recently characterized and, something that our readers need to be familiar with, and there's plenty of updates within the issue on that and other topics. Okay. So now back to our Continuum audio trivia question. And just to remind our listeners, there are now more than 20 drugs approved by the FDA for the treatment of MS. What was the first disease-modifying therapy approved for MS? And when was it approved? Dr Solomon, do you want to take the honors and answer the question?  Dr Solomon: Sure. It was way back in 1993. You had to get on a wait list, I believe, initially to get on it. There was some sort of lottery, and it was Betaseron.  Dr Jones: Betaseron in 1993, was the first disease-modifying therapy approved by the FDA for the treatment of MS. It just shows how much water under the bridge we've had since then. 1993 was also the first year of the Jurassic Park series of movies. It was the biggest movie of the year, the song of the year in 1993 was "I Will Always Love You" by Whitney Houston. It was also the year you can tell that I look back into 1993 to see what else happened. It was also the first year the World Wide Web became publicly available, which is it kind of puts brackets on the era or the epoch of MS disease modifying therapy. And finally, the Super Bowl champs that year were the Dallas Cowboys, who unfortunately, have not had much luck in Super Bowls since the 1990s. Maybe they will have more opportunities like we've seen with MS therapeutics. So, Dr Solomon, I want to thank you for joining us today. I want to thank you for such a wonderful discussion of the latest in MS. I think the updated diagnostic criteria are really going to be critical for our listeners to understand and incorporate into their practice. Really grateful for your leadership of the issue, putting together a really stellar group of experts for all of our articles and grateful for your time today. Thank you for joining us.  Dr Solomon: Thanks so much for having me. Thank all the other listeners out there for joining us as well. I'm really excited about this issue of Continuum.  Dr Jones: Again, we've been speaking with Dr Andrew Solomon, guest editor of Continuums most recent issue on multiple sclerosis and related disorders. Please check it out. And thank you to our listeners for joining today. Dr Monteith: This is Dr Teshamae Monteith, associate editor of Continuum Audio. If you've enjoyed this episode, you'll love the Journal, which is full of in-depth and clinically relevant information important for neurology practitioners. Use the link in the episode notes to learn more and subscribe. Thank you for listening to Continuum Audio.

Kevin Nash and Sean Oliver are back to tighten things up with a hard-hitting 90 minutes of unfiltered conversation. After hearing the fans' feedback on the "marathon" episodes, Big Sexy and Sean are scaling down the runtime but cranking up the content. This week, the guys dive into the modern obsession with negativity and why it seems easier for people to complain than to give a simple "good job." From the algorithm-driven chaos of social media to the rise of AI-generated content, Kevin reflects on how much the world has changed since the days of "The Upgrade Game" at airport gates with Scott Hall. Speaking of the Bad Guy, Kevin sets the record straight on why he remembers certain dates more vividly than others, leading into a deep dive into wrestling psychology. The guys break down a classic Attitude Era finish involving Stone Cold Steve Austin, Mankind, and The Undertaker, questioning why today's industry often overcomplicates the "layered" finish. Kevin reminisces about his time in the booking room at TNA with Jim Cornet and the Dudley Boyz, explaining the delicate balance between a "Dusty finish" and the clean, impactful storytelling that keeps the crowd hot without "bastardizing" anyone's finisher. Outside the ring, the talk turns to cinema and physical tolls. Sean gives a high recommendation for the 2022 thriller Gold, leading to a discussion on Zac Efron's career-best performance and the "Australian Confusion Era" of film. Meanwhile, Kevin details his latest battle with a smoked CNS and a stubborn psoas muscle, proving that even at nearly 67, he's still outworking guys twenty years his junior. Morgan & Morgan - America's Largest Injury Law Firm. #LAW (529) Tushy-Over 2.5 Million Butts Love TUSHY. Get 10% off TUSHY with the code KLIQ at https://hellotushy.com/KLIQ StopBox-Get firearm security redesigned and save 10% off @StopBoxUSA with code NASH10 at https://www.stopboxusa.com/NASH10 #stopboxpod 00:00 Kliq This #195: 00:57 START 00:57 Back w another action packed 90 minutes! 05:45 The Upgrade game 08:45 How many birthdays do you remember? 11:01 Gold (2022) 16:51 BRACKET CHECK-IN 24:55 "I bet the original Bloodline reunites at Wrestlemania." 30:45 The Curtain Call 34:55 BREAK MORGAN & MORGAN 37:07 MJ in Florida 38:30 RODEO BUILDING 38:59 "Kev, you mentioned your CNS was smoked after leg day." 45:21 Any Daytona gyms that you would recommend? 47:45 NWO as a conspiracy theory 49:59 KTTV 50:54 KEV, I WATCHED RAW… 51:39 Femi standing, Brock retreating again. Backwards? Heat? 55:38 Heyman/Rollins…what will be the resultant match 58:30 Uso involvement in Roman/Punk now--Where can we go w it? Singles turn by Jey? 01:03:45 Dennis Rodman WWE HOF 01:06:56 BREAK TUSHY 01:09:11 DEAR SEXY#01 01:11:40 DEAR SEXY #02 01:15:44 BREAK STOPBOX 01:18:20 ICE at Airports 01:24:49 ASK NASH 01:24:56 NWO 3 pack signed 01:25:31 Sid HOF 01:26:53 VERT How long to tie that knot? 01:28:43 Curtin Call anniversary? 01:29:22 La Parka 01:34:46 Ted Dibiase Jr at Wrestlemania? 01:36:45 OUTRO

Neurologic complications of substance use may be the first symptoms that lead patients with substance use disorders to seek care. Neurologists have a key role in identifying patients with substance use disorders and connecting them to treatment. In this episode, Lyell K. Jones Jr, MD, FAAN, speaks with Adeline L. Goss, MD, author of the article "Neurologic Complications of Drug and Alcohol Use" in the Continuum® February 2026 Neurology of Systemic Disease issue. Dr. Jones is the editor-in-chief of Continuum: Lifelong Learning in Neurology® and is a professor of neurology at Mayo Clinic in Rochester, Minnesota. Dr. Goss is a neurohospitalist and associate chief of neurology for Highland Hospital in Oakland, California. Additional Resources Read the article: Neurologic Complications of Drug and Alcohol Use Subscribe to Continuum®: shop.lww.com/Continuum Earn CME (available only to AAN members): continpub.com/AudioCME Continuum® Aloud (verbatim audio-book style recordings of articles available only to Continuum® subscribers): continpub.com/Aloud More about the American Academy of Neurology: aan.com Social Media facebook.com/continuumcme @ContinuumAAN Host: @LyellJ Full episode transcript available here Dr Jones: A big part of neurology is solving mysteries. Patients can show up with all kinds of mysterious symptoms. Sometimes the diagnosis comes from within, some internal disruption of neurophysiology. But sometimes the problem is a complication of drug or alcohol use. Today we have the pleasure of speaking with Dr Adeline Goss, who recently authored an article for Continuum on this exact problem, a topic all neurologists need to be familiar with. Dr Jones: This is Dr Lyell Jones, Editor-in-Chief of Continuum. Thank you for listening to Continuum Audio. Be sure to visit the links in the episode notes for information about earning CME, subscribing to the journal, and exclusive access to interviews not featured on the podcast. Dr Jones: This is Dr Lyell Jones, Editor-in-Chief of Continuum: Lifelong Learning in Neurology. Today I'm interviewing Dr Adeline Goss, who recently authored an article on the neurologic complications of drug and alcohol use for our latest issue of Continuum on the neurology of systemic disease. Dr Goss is a neurohospitalist and the associate chief of neurology at Highland Hospital in Oakland, California. She's also an accomplished writer, broadcaster and podcaster. Dr Goss, welcome, and thank you for joining us today. Why don't you introduce yourself to our listeners? Dr Goss: Great to speak with you, Dr Jones. Yes, I'm Adeline. I also go by Addie Goss. Dr Jones: So, before we get into the discussion, we're going to start off today with something fairly new to the podcast, the Continuum Audio trivia question. So, we all know that alcohol and other substances have many potential complications in that use of these substances fluctuates over time. But this one stood out to me from your article, Dr Goss, just for the sheer size of the change. So, for our listeners, here's the question. Accidental exposures to what substance increased a whopping 1,375% between 2017 and 2021? I'll read that again. Accidental exposures to what substance increased 1,375% between 2017 and 2021? So, stick around to the end of our interview for the answer. And let's get right to it, Dr Goss. If you had a single most important message to our listeners from your article, what would it be? Dr Goss: Well, I mean, many of us went into neurology because of the way that neurologic illnesses can be life-changing for patients. And I work as a neurohospitalist at a public hospital in Oakland, California. Many of my patients are admitted for neurologic conditions related to substance use. And when I see my patients later in the discharge clinic, many tell me that the last day that they used meth or the last day they used cocaine, the last day they smoked, was the day they had their stroke or whatever they came into the hospital for. I think the most important message is that hospitalization for a neurologic condition related to substance use can interrupt use patterns, can motivate change. And therefore, as neurologists, we really have an opportunity to connect to our patients and connect our patients to substance use treatment and make a dramatic difference in people's lives in this regard. Dr Jones: I think that's a fantastic point. I enjoyed a point you made in your article---and I can't remember exactly how you phrased it, I won't say it as well---that you think of the syndromes through which alcohol and drug exposures can present. Those syndromes almost always could end up of other primary neurologic disorders. So, put a different way, when a patient presents with a neurologic problem, most of the time an exposure could be on the differential.  And so, we really do have a responsibility as neurologists to be familiar with these. Dr Goss: To be familiar with these and to know how to connect patients to resources to try to get treatment. Dr Jones: Totally agree. And you touched on the public health aspect of this. It's really hard to talk about drug or alcohol use without acknowledging the public health impact particularly of opioids, which has been a crisis for most of this century. Right? And I think most of our listeners will be familiar with the rapid rise in opioid-related deaths. But there might be a glimmer of optimism there. Is what I've seen true, that opioid-related deaths may have plateaued? Dr Goss: So, yes, it's true that opioid-related deaths, overdose deaths in general, have begun to decline, actually, since 2023. And that's in part because overdose deaths really surged early on in the Covid-19 pandemic, in the setting of all of the social disruption, reduced access to services, and social isolation that occurred with the pandemic. But there were really multiple factors there. So, as you mentioned, there was this really rapid rise in illicitly manufactured fentanyl. Fentanyl became a major driver in overdose deaths starting in the mid-2010s. And by the late 2010s, it overtook heroin and prescription opioids as drivers of overdose deaths. And then this just collided with the pandemic in 2020, causing skyrocketing deaths. So, as we know as neurologists, fentanyl is more potent, it's shorter-acting, and it's also cheaper than heroin. It can cost as little as 50 cents or a dollar a pill. Thankfully, as services have rebooted and also as naloxone has become more widely distributed, there has begun to be a decline in opioid overdose-related deaths. So, we're relying on provisional data from the CDC for the most recent years, but that shows about a 24% decline in annual overdose deaths, comparing late 2023 to late 2024. And that's real. That comes out to 70 lives saved per day. Unfortunately, deaths still remain above prepandemic levels, and we're still talking about 87,000 drug overdoses per year. So, I would agree, a glimmer of hope. But we're still seeing overdose as the leading cause of death among young Americans aged 18 to 44. And there's a very long way to go. Dr Jones: 23% is a big number, and that is certainly exciting to think about, but we're still above that long-term secular trend. So, hopefully whatever is happening to bring that down, hopefully it continues. And we talk a lot about- appropriately, we talk a lot about opioid exposures and some of the neurologic presentations of opioid use and toxicity, but alcohol use disorder is the most common substance use disorder, correct? I learned that from your article. And it has been for some time, and it has well-known acute and chronic toxicities. But I think many of us have been taught something of a myth in the acute treatment of patients who may have thiamin deficiency or Wernicke's encephalopathy. Can you tell us a little more about that? Dr Goss: Yeah, sure. So, boy, what is my favorite vitamin? As a neurologist, I think thiamin is my favorite vitamin. Thiamin is a cofactor in- for several enzymes that are involved in glucose catabolism. And it's necessary to synthesize myelin and several neurotransmitters. And as we know, alcohol use disorder leads to reduced nutritional intake and impaired digestion and absorption of nutrients. And this can lead to deficiencies in water-soluble B vitamins, including thiamin, as well as trace elements. The thing about thiamin is that thiamin deficiency often appears first, because the body's stores of thiamin deplete in about 4 to 6 weeks. You know, we're traditionally taught if a patient presents with symptoms concerning for Wernicke's encephalopathy, that if they're also hypoglycemic or just in general, we have to get glucose into them first, because we don't want to tax these thiamin-dependent glucose catabolism pathways. But really, there's no reported case of a single glucose bolus precipitating some dramatic symptomatic thiamin deficiency. It's thought that harm would come potentially from prolonged carbohydrate administration without thiamin. And so, if a patient in front of you is both thiamin deficient and hypoglycemic, you just treat both. You treat both emergently. But it doesn't really matter in what order you do so. Dr Jones: That's good to know that doing the right thing for the patient can involve using either of those in whatever order. And I agree with you, I don't think I've ever hurt anybody by giving them thiamin. It's an easy one to miss and an important one to remember in the right context. And speaking of, and I think a lot about in your article, Dr Goss, I can see a neurologist seeing a patient in the emergency department or in the hospital or even in the clinic thinking about the wonderful points in your article. But we know that when alcohol or substance use enters our mind on the differential, the next impulse is to test for it. And we also know there are pitfalls of drug screening, doing urine drug screens, etc. How do you approach testing when you think about a potential drug-related complication in their differential? Dr Goss: So, like most people, I would start with a urine drug screen for any patient who's presenting with a possible toxidrome or some substance-related neurological presentation. These urine drug screens, they're rapid, they're inexpensive, they're immunoassays for traditional drugs and their metabolites. So, usually amphetamines, cocaine, opiates, plus/minus cannabis. But I think the first thing to note is that they miss entire categories of drugs, and not just drugs that are not in that list. They miss synthetic opioids, including fentanyl. One group is keeping track of this number. So, I have an update for mid-2025. And that's that 30% of U.S. ED overdose encounters as of mid-2025 included fentanyl testing. Only 30% for patients who are presenting with an overdose syndrome. Dr Jones: And that's for one of the most widely used synthetic opioids. So that's really a striking number. Dr Goss: Yeah, one of the most widely used and one with the greatest rate of complications. So, states can make a difference here. In 2022, California passed a law requiring fentanyl testing on hospital urine drug screens and several states have followed. And so that number is rising, the rate of testing for fentanyl. But that's just a really key thing to know, that that one is often missed. Other just important pitfalls, the timing of the urine drug screen matters because for most substances, it only picks up the drug within 24 to 72 hours after the last use. With amphetamines and cocaine going out a couple more days after that, especially in patients who use repeatedly. And then also, notably, there's a risk of false positives. This is especially true with amphetamine use, and beta blockers are one of the drugs that can lead to false positives on an amphetamine test, on a urine drug screen. So, I'll share that I've had several patients who have presented with intracerebral hemorrhage and who tested positive on the emergency department's urine drug screen and who adamantly stated that they do not use amphetamines, they've never used amphetamines, and they didn't ingest anything that could have contained amphetamines. And when we did serum confirmatory testing, in fact, their amphetamine testing was negative, and all those patients had received esmelol or the labetalol in the ED to treat their blood pressure related to their ICH. So false positives can occur with, you know, other medications like decongestants and certain antidepressants. But beta blockers are a key one to know. And then finally, there are just a number of things outside of that short list of substances that I mentioned, including a huge range of novel psychoactive substances that would not be tested for on a standard urine drug screen. And for those, you'd require serum testing, or at some large academic centers or specialty toxicology labs, you can actually do liquid chromatography high-resolution mass spectrometry, with- which is basically unbiased testing for any substance that's present in the patient sample. So, I guess, you know, you asked about my approach. Start with the urine drug screen, but there's no substitute for good history-taking and close examination of your patient's general examination, not just their neurologic presentation. And if patients are presenting with a toxidrome that I would expect would show up on a urine drug screen but it's negative, there are other confirmatory tests that can be sent, although they're often send-out labs and come back in a very delayed fashion. Dr Jones: So, in other words, it's complicated, which usually means it's humbling. And if I'm understanding it correctly, there's the risk of the false positive on the urine drug screen. And then there's the risk of the false negative if we think we're screening for something that might not even be on that initial screen. So, that's a wonderful reminder that these are clinical diagnoses and we have to keep our clinician hats on while we're thinking about how to establish these diagnoses or exclude them. So, back to opioids, Dr Gross. There are some really peculiar neurologic syndromes associated with opioid overdose. Tell us a little about those. Dr Goss: Well, I mean, some of these were described first with heroin. So, we can start with the one that almost anybody has heard of, heroin-associated spongiform leukoencephalopathy, which we know is associated with a practice known as "chasing the dragon," which is inhaling vapors of heroin heated on foil. But we know now that this syndrome can occur with other opioids, including fentanyl. The clinical features are, you know, apathy, cerebellar signs, quadriparesis, parkinsonism, myoclonus, and some patients progress to coma or even death. But on MRI you're seeing, you know, these confluence symmetric white matter diffusion restriction and T2 hyperintensities in the cerebellar white matter and the posterior limb of the internal capsule that spare the subcortical U-fibers. So, you know, I think this is kind of the classic example of something that's symmetric, that has a very obvious and interesting MRI pattern. But as time is passing, we're seeing more and more similar types of syndromes of leukoencephalopathies, but with different clinical presentations and MRI characteristics. So, another of these is CHANTER syndrome. This is an opioid overdose-related presentation where people have stupor and coma. And on the MRI there, you see bilateral symmetric diffusion restriction in the cerebellar cortex, in the hippocampi, in the basal ganglia. And it spares the cerebral cortex. And notably in these cases, patients can progress to cerebellar edema, to obstructive hydrocephalus. And some require suboccipital craniotomy. I had a week recently at Highland Hospital, where I work, where we had two of these cases in the same week, in just a community hospital. And there's a similar syndrome in children known as POUNCE syndrome with profound cerebellar edema, and many patients require posterior decompression. So that's another different distribution of findings with a different outcome. Fortunately, there's a milder sort of phenotype of opioid-associated amnestic syndrome, is what it's been described, where there's primarily DWI changes in the hippocampi and the globus pallidus. So, patients primarily present with an amnestic syndrome, mostly anterograde amnesia. Seeing these in practice, I'm not sure that patients always fall into one bucket or another. But in general, you'll see some degree of symmetric diffusion restriction or symmetric white matter changes that clearly point to a toxic presentation, a toxic syndrome, as opposed to pure anoxia, for example. And it's important to know that because from a prognostic standpoint, anoxic brain injury, which can occur after cardiac arrest and after opioid overdose, can look different than some of these syndromes. Finally, heroin has been associated with myelopathy, but also that's been reported on with fentanyl. So, I think some of these conditions got their reputation from heroin. But as fentanyl has proliferated---and prior to that as prescription opioid, you know, misuse had proliferated---we're seeing similar syndromes with all of the opiates. Dr Jones: And I think it's a good case in point that you can have multifocal disease and it be a manifestation of an intoxication, and I think that's a really good reminder that we have to have many of these syndromes in our differential, we have to be aware of them, otherwise we might miss them or attribute them to another mechanism. Dr Goss, our last issue of Continuum that was dedicated to the neurology of systemic disease came out in 2023, and here we are in 2026 publishing our latest issue, including your article and this podcast. Since 2023, have there been any emerging patterns or novel agents of abuse or misuse out there? Dr Goss: The short answer is yes, and I would say the reason is just the supply is moving at more and more rapid speed. The relationship between the internet and drug supply has really informed what's out there at any given moment. So, the turnover in the market can change in weeks, not in years. And there's all of this distribution through social media and encrypted apps. And then manufacturers are kind of continuously tweaking chemical structures to evade law enforcement. In the process of researching this article, I came across some, I mean, really wild examples. To be clear, these are not- not all these are common substances, but I think the general phenomenon should be known that people can walk into a vape shop or walk into a gas station or meander around online and buy some really weird stuff. So, in 2024, there was this nationwide recall of a product called Diamond Shrooms that was sold online and in smoke and vape shops, and this was billed as, like, a hemp and mushroom mixture. But it led to multiple- I mean, over 100 cases of seizures and agitation and depressed consciousness and a few possible deaths. And when the contents were analyzed, they included psilocybin analogs and pregabalin. I mean, some weird stuff. And so, those have been pulled. But people are constantly inventing and marketing these different substances. I think another example… we all know about nitrous oxide and its association with B12 myopathy. But the use of nitrous oxide has really changed. Companies are selling large canisters online and in vape shops, and they're flavored, like, in blue raspberry flavor. And unfortunately, there's been a rise of nitrous among youth. So, we're seeing not just increased cases of myelopathy, but also a 2025 study in JAMA found a spike in deaths attributed to actual nitrous oxide overdose. And so nitrous, I think, had not been that commonly used a few years ago, but has become more common in the last couple of years. A final one I'll just mention is ketamine. So, ketamine has certainly appeared in reviews of neurological syndromes related to substance use for a long time, and it's also been studied and used off-label for mood disorders in outpatient infusion clinics for some time. But in the pandemic, there was an expansion in telemedicine, as we know, and an associated proliferation of teleclinics that were prescribing very frequent, even daily oral and lozenge and nasal formulations of ketamine, which has led to increased rates of misuse. So, you know, acutely, the syndrome associated with ketamine intoxication is very brief. And often by the time people come to the emergency department, their symptoms have already worn off. But long-term, frequent use of ketamine is really still being studied. There seems to be an association with persistent neuropsychiatric effects like cognitive impairment, psychosis, persistent depressive symptoms. And so, you know, I think it's just important to realize that while the list of substances may look pretty similar to 2023, the use patterns, the distribution patterns are continuing to change. It's hard to keep up. And while alcohol and opioids and stimulants are by far the most common substances that a neurologist is going to encounter in daily practice, there's this ever-expanding range of possible substances that can trigger neurologic syndromes, both acute and chronic. Dr Jones: And I think that might be the best possible plug to read your article, because it is evolving and we have to stay on top of it. And we really can't be complacent with it. So, thank you for that update. Okay, back to our trivia question. Accidental exposures to what substance increased a whopping 1,375% between 2017 and 2021? Dr Goss, what do you think? Dr Goss: That was THC-infused edibles. Specifically, these would be THC-infused substances that are often marketed as looking like candy or snacks or cereal. Exactly what a kid might want to get their hands on. And unfortunately, accidental cannabis exposures in children under age five went up by 1,375% between 2017 and 2021, and 600 of those patients required critical care admission. Dr Jones: Yeah. So, just a mind-blowing number, and obviously something for us to be on the lookout for, especially if you see children in your practice and someone comes in with CNS depression or stupor, it's one to not miss. So that was something I learned in reading your article, among many other things. And Dr Goss, I want to thank you for joining us. I want to thank you for such a great discussion. I learned a lot from reading your article, I learned a lot just from our conversation today, and I suspect our readers and our listeners will too. Dr Goss: What a pleasure. Thank you so much, Dr Jones. Dr Jones: Again, we've been speaking with Dr Adeline Gross, author of a fantastic article on neurologic complications of drug and alcohol use in our latest issue of Continuum on the neurology of systemic disease. Please check it out, and thank you to our listeners for joining 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.

Listen Online: About this episode: In this enlightening conversation, the First Lady of Nutrition sits down with Dr. Ana Maria Mihalcea, board-certified internal medicine physician and award-winning author. Over the past several years, Dr. Mihalcea has been examining the blood of patients suffering from mysterious, unexplained symptoms including long-haul COVID, using dark-field microscopy. She says she has yet to see a truly normal blood sample since the onset of COVID. What she's observing is raising important questions. In this discussion, she explains how dark-field microscopy differs from traditional blood testing and why it can reveal patterns that standard lab work may miss, including blood clumping, strange self-assembling particles, and other abnormalities that may help explain persistent symptoms. Ann Louise and Dr. Mihalcea also explore possible contributing factors and why some people who never contracted COVID or received the vaccine may show similar findings. They also discuss emerging approaches being explored to support recovery—including EDTA therapy, nattokinase, methylene blue, DMSO, grounding, and more. If you're someone who is struggling with unexplained symptoms—particularly after COVID infection—this thought-provoking conversation offers insights you won't want to miss.The post The COVID Effect: When the Blood Doesn't Lie first appeared on Ann Louise Gittleman, PhD, CNS.

Midlife is a time for rebirth… a time to come into who you truly are.  In today's episode, I'm sitting down with the brilliant Dr. Deanna Minich to dive into how this stage of life can bring you to the best version of yourself after years of balancing roles, expectations, and responsibilities.  Dr. Minich shares why midlife is the perfect time to rediscover your voice, clarify your needs, and define your non-negotiables so you can live the next chapter on your own terms.  We're reframing menopause not as an ending, but as the beginning of a powerful second half of life filled with purpose and authenticity.  Ready to reclaim your energy and step into midlife with clarity and confidence?  Tune in here!  Deanna Minich, PhD, MS, CNS, IFMCP Deanna Minich is a nutrition scientist, international lecturer, educator, and author with over 25 years of experience in academia and in the food and dietary supplement industries. She's the Chief Science Officer at Symphony Natural Health, and has written seven books and over 50 scientific publications. Her work aims to help others live well by using therapeutic lifestyle changes that impact their physical, emotional, mental, and spiritual health. IN THIS EPISODE Uncommon signs that you're entering  perimenopause  The importance of musculoskeletal strength in midlife What's really going on with female hormones in perimenopause  Setting boundaries in midlife in your relationships and career Balancing lifestyle changes and hormone replacement therapy for optimal results  How to navigate stress and manage your nervous system Finding your authentic self in perimenopause and beyond How to connect with Dr. Deanna for more midlife expertise  QUOTES “I think it's a really powerful system and I think the best thing for women, no matter if you're going through perimenopause, you're just about to enter, or even if you're post, it's really connecting into that wisdom within that we have as the endocrine system.” “There's no way I could ever do women's health on my own. I want to be connected to a collaborative, to a team, to other people in the space where we rise together and we really get the message out. So that's what I've been doing.” “Here's the message for women: we all need a way to bring ourselves into better coherence, better emotional, mental status, like where we feel in the zone.” RESOURCES MENTIONED Use code ENERGIZED and get 10% off on your Troscription Order http://troscriptions.com/ENERGIZED Dr. Deanna's Website Dr. Deanna on Instagram Dr. Deanna on Facebook Symphony Natural Health Website RELATED EPISODES  724: Age Like A Girl: Why Midlife Women Stop Shrinking and Start Leading with Dr. Mindy Pelz  721: No, It's Not All in Your Head: The Medical Truth About Perimenopause with Dr. Jila Senemar 720: Why No One Talks About Loneliness in Midlife—And Why It's Not Just You  574: The Connection between Trauma, the Immune System, and Autoimmune Disease: Lab Testing and Solutions with Dr. Sara Szal Gottfried

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