Podcasts about moyamoya

[REBROADCAST FROM March 18, 2025] In 2016, DJ and producer TOKiMONSTA underwent two brain surgeries for Moyamoya disease, after which she had to relearn how to speak and hear music. In 2019, she became the first Asian-American woman nominated for Best Dance / Electronic Album at the Grammy Awards. Her new album is called Eternal Reverie. She joins us for another installment of "Equalizers: Women in Music Production."

In 2016, DJ and producer TOKiMONSTA underwent two brain surgeries for Moyamoya disease, after which she had to relearn how to speak and hear music. In 2019, she became the first Asian-American woman nominated for Best Dance / Electronic Album at the Grammy Awards. Her new album is called Eternal Reverie. She joins us for another installment of "Equalizers: Women in Music Production."

In this episode, Dr. Kipper shares a deeply personal story about his wife's battle with a rare condition called Moyamoya, which started with a severe headache. We also delve into the impact of social media on the mental health of young people, uncover the hidden dangers of excessive salt intake and its connection to stomach cancer, and offer practical tips for staying safe around the pool. Learn more about your ad choices. Visit megaphone.fm/adchoices

When life throws a curveball, some duck, others catch it and toss it right back. That's Melanie Brown for you, a beacon of hope who turned her neurological battles into powerful narratives of resilience. Throughout our heartwarming conversation, Melanie opens up about her childhood stroke and the rare brain condition Moyamoya. Her story isn't just about survival; it's a melody of joy found in nature, puzzle-solving, and grooving to the nostalgic rhythms of 80s music. She'll have you chuckling with anecdotes from her life, showcasing an infectious positivity that's nothing short of uplifting.Melanie is no stranger to adversity, and she's become an expert at using it as a stepping stone rather than a stumbling block. From the painstaking recovery of motor skills to embracing sports for rehabilitation, her journey is a masterclass in turning challenges into triumphs. The support system of family shines through as Melanie recounts the encouragement she received, fostering a spirit of independence and determination. As a motivational speaker and author, she extends a hand to all, guiding others through the winding roads of their own personal challenges with charm and wisdom.Strap in for an episode that's equal parts inspiring and grounding, as we navigate the struggles that refine us. Melanie doesn't just share her story; she equips us with the tools for our own battles—faith, perseverance, and a positive outlook. She paints trials as preparation for our heavenly roles, blending life advice with spiritual insight. This is more than a podcast; it's a compass pointing towards purpose and contribution, both in this life and the next. Join us and let Melanie Brown's radiant spirit encourage you to face your struggles head-on, with humor, grace, and an eye on the eternal prizes awaiting us. Support the showI enjoy a good cup of coffee like anyone else, you can buy me a cup of coffee, and support the show, here. https://www.buymeacoffee.com/dorseyross Here is another way to support the show. https://www.buzzsprout.com/1754677/supporters/new Find me on Instagram at https://www.instagram.com/dorsey.ross/ Follow me on Facebook at https://www.facebook.com/DROCKROSS/ Check out my ministry website at https://www.dorseyrossministries.com Leave a review https://podcasts.apple.com/us/podcast/dorsey-ross-show/id1495921329

In this first video solocast of season six, I'm excited to share some insights I've gained through the hard challenges of my journey. *Please note that this episode is a video solocast. Please visit my YouTube channel @MelonyBrown to watch it. In 2005, the office supply company, Staples, launched a marketing campaign which introduced the 'easy button.' The easy button would solve frustrating situations. The downfall of the 'easy button' is it trained our culture to be frustrated by anything that was hard, or time-consuming, or took too long to obtain. Going through the drive-thru is easier than preparing a home-cooked meal. Ordering cleaning supplies, wrapping paper, and dog food on Amazon is indeed less-time consuming than making a trip to Target. Unfortunately, the 'easy button' marketing campaign has permeated our mindsets. Not just about our errands but about the hard challenges we face in life. John 16:33 reads, "In this life you will have trouble. Take heart, for I have overcome the world." James 1:2-4 reads, "Consider it pure joy, my brothers and sisters,[a] whenever you face trials of many kinds, because you know that the testing of your faith produces perseverance. Let perseverance finish its work so that you may be mature and complete, not lacking anything." Matthew 19:26 reads, "With man this is impossible, but with God all things are possible.” Jeremiah 32:17 reads, "Nothing is too hard for you." When we are going through hard challenges, we see several of God's responses in each letter of the word hard. H - God helps. Check out these additional verses: 2 Samuel 22:36, 2 Chronicles 32:8, Psalm 46:1, and Psalm 121:1-2. We often don't see God helping us. Hebrews 11:1 reminds us, "Now faith is confidence in what we hope for and assurance about what we do not see." A - God is active.Check out these additional verses:Isaiah 64:4, Deuteronomy 23:14, and 2 Chronicles 36:22. R - We receive many blessings from God. Those blessings are activated by hard challenges, which is often how God strengthens, develops, and grows character traits in us. This one is different from the other three letters. You receive blessings when you accept Jesus' salvation. Challenges activate those blessings, which can lead to your growth. Think fruit of the Spirit from Galatians 5:22-23.D - God directs. Check out these additional verses:Proverbs 20:24, Isaiah 48:17, and 1 Kings 17:9. What is the purpose of hard challenges? Your growth is the purpose of hard. Your growth is what makes hard necessary. Your growth is the outcome of hard. Your growth is valuable because you are invaluable to God. In the last third of this episode, I share several hard challenges I've faced and how those challenges activated my growth. *I do not share this to boast about myself. As Paul said in 1 Corinthians 1:31, "Let the one who boasts boast in the Lord.”2 Corinthians 12:9 reads, "My grace is sufficient for you, for my power is made perfect in weakness.” Therefore I will boast all the more gladly about my weaknesses, so that Christ's power may rest on me." Moyamoya disease is a rare cerebrovascular disease that affects 1 in 2 million people. It is characterized by strokes, mini strokes, and migraines. Philippians 4:7 reads, "And the peace of God, which transcends all understanding, will guard your hearts and your minds in Christ Jesus." Ephesians 6:17 reads, "Take the helmet of salvation and the sword of the Spirit, which is the word of God." My books, Challenges Won't Stop Me and Keep Moving Forward, are available at www.melonybrown.com.books.

Moyamoya disease is a rare neurovascular condition that can affect both children and adults and is caused by progressive narrowing or blockage of the major blood vessels supplying the brain.The result is a lack of necessary blood flow to the brain, which can cause stroke, mini-stroke (TIA – transient ischemic attack) or bleeding into the brain. Numerous tiny vessels develop around the blockage in an attempt to compensate for the lowered blood flow, leading to a smoky appearance of these vessels on imaging. This smoky appearance is what gives the disease its name, as “moyamoya” means puff of smoke in Japanese.Aditya (Adi) Iyer MD, MS, is a fellowship-trained neurosurgeon with a focus on vascular diseases of the brain and spine at Pacific Neuroscience Institute. As one of California's few dual-trained neurosurgeons, Dr. Iyer is able to offer both minimally invasive open surgical techniques as well as incisionless catheter based procedures to treat patients with strokes, aneurysms, AVMs, tumors and pain.

PODCASTE SENIOR: Dr. Francesco Acerbi; PODCASTER JUNIOR: Dr. Nicola Rifino; RAZIONALE: L'arteriopatia Moyamoya è una patologia cerebrovascolare cronica caratterizzata da una progressiva steno-occlusione bilaterale delle arterie carotidi interne e dei suoi rami principali, associata allo sviluppo di una rete collaterale di vasi fragili nelle aree profonde del cervello. I pazienti affetti da questa malattia rara hanno un rischio aumentato di sviluppare ictus ischemici e/o emorragici nel corso della vita. Nonostante nel 2023 siano state pubblicate le linee guida ESO sulla gestione dei pazienti con Moyamoya, questa patologia è ancora poco conosciuta in Italia. Ne parleremo oggi con il Dr. Francesco Acerbi, Responsabile della UOSD Vascolare, Centro di Rivascolarizzazione Neurochirurgica (Neurochirurgia 5) dell'Istituto Neurologico Carlo Besta di Milano, autore delle linee guida europee sull'arteriopatia Moyamoya. Nel corso del nostro podcast, cercheremo di chiarire cosa si intende per arteriopatia Moyamoya, quando è utile porre il sospetto clinico, quali esami sono necessari per la diagnosi, quali trattamenti sono ad oggi disponibili e per quali pazienti l'approccio neurochirurgico può risultare determinante.

Welcome to Season 3, Episode 37 of "Winning Isn't Easy"!

MedLink Neurology Podcast is delighted to feature selected episodes from BrainWaves, courtesy of James E Siegler MD, its originator and host. BrainWaves is an academic audio podcast whose mission is to educate medical providers through clinical cases and topical reviews in neurology, medicine, and the humanities, and episodes originally aired from 2016 to 2021. Originally released: July 18, 2017 If you have sickle cell disease, you have a 1 in 10 chance of experiencing a stroke before college. And if you don't think that's going to hold you back, you don't know stroke. This week on BrainWaves, Dr. Erica Jones shares her experience with the neurologic complications of sickle cell anemia and the latest guidelines for managing patients with this condition. BrainWaves podcasts and online content are intended for medical education only and should not be used to guide medical decision-making in routine clinical practice. REFERENCES Bang OY, Fujimura M, Kim SK. The pathophysiology of Moyamoya disease: an update. J Stroke 2016;18(1):12-20. PMID 26846756“Data & Statistics." Centers for Disease Control and Prevention. Centers for Disease Control and Prevention. Available at: https://www.cdc.gov/datastatistics/index.html. 2016.Gueguen A, Mahevas M, Nzouakou R, et al. Sickle-cell disease stroke throughout life: a retrospective study in an adult referral center. Am J Hematol 2014;89(3):267-72. PMID 24779035Lionnet F, Hammoudi N, Stojanovic KS, et al. Hemoglobin sickle cell disease complications: a clinical study of 179 cases. Haematologica 2012;97(8):1136-41. PMID 22315500Motulsky AG. Frequency of sickling disorders in U.S. blacks. N Engl J Med 1973;288(1):31-3. PMID 4681897Ohene-Frempong K, Weiner SJ, Sleeper LA, et al. Cerebrovascular accidents in sickle cell disease: rates and risk factors. Blood 1998;91(1):288-94. PMID 9414296Scott RM, Smith ER. Moyamoya disease and moyamoya syndrome. N Engl J Med 2009;360(12):1226-37. PMID 19297575Strouse JJ, Lanzkron S, Urrutia V. The epidemiology, evaluation and treatment of stroke in adults with sickle cell disease. Expert Rev Hematol 2011;4(6):597-606. PMID 22077524Switzer JA, Hess DC, Nichols FT, Adams RJ. Pathophysiology and treatment of stroke in sickle-cell disease: present and future. Lancet Neurol 2006;5(6):501-12. PMID 16713922Verduzco LA, Nathan DG. Sickle cell disease and stroke. Blood 2009;114(25):5117-25. PMID 19797523Wang WC, Dwan K. Blood transfusion for preventing primary and secondary stroke in people with sickle cell disease. Cochrane Database Syst Rev 2013;(11):CD003146. PMID 24226646Ware RE, Helms RW; SWiTCH Investigators. Stroke With Transfusions Changing to Hydroxyurea (SWiTCH). Blood 2012;119(17):3925-32. PMID 22318199 We believe that the principles expressed or implied in the podcast remain valid, but certain details may be superseded by evolving knowledge since the episode's original release date.

When Melony Brown was two years old, she had a significant stroke. She did not choose an overcome attitude as a child but her parents instilled it in her. They did not allow her to use lack of coordination, left-sided weakness, or balance issues as an excuse.  Melony is an author, speaker, and host of the Challenges Won't Stop Me podcast. Fighting to overcome life's challenges and thriving is the message she lives by and shares with her audience.  Decades of neurological struggles and brain surgery tried to stop her, but she chose to fight to overcome instead. Learning everything those challenges were meant to teach her and grow in her, Melony desires to encourage, inspire, and motivate women to fight to overcome the challenges intersecting their paths.  With God guiding the way and a backpack filled with your essential gear, you are primed and ready to overcome any challenge that dares to cross your path. It is time to…..JOURNEY ON! Melony shares several stories including an Auschwitz survivor and a young girl who was kidnapped and sex trafficked. After escaping, she had her tattoo removed which branded her as a 'slave'. She started a business helping other women remove these memory scars including tattoos from prison, gang membership, and abuse. You are going to enjoy Melony's interview:   On her podcast, she has interviewed over 135 courageous women who fought to overcome a wide range of challenges.  Be sure to check out her Journey On Quiz.  Click Here to discover your journey personality       Are you prepared to survive when one of life's tough challenges rudely intersects your journey? This journey through life is tough, but you're tougher. In Challenges Won't Stop Me, author, podcaster, and speaker Melony Brown invites you to join her for an eight-mile journey in which you will create a personalized survival guide that will equip and prepare you to survive the rugged terrain that is sure to mark your path. Do not be afraid or discouraged as the master navigator, God, will be with you and fight for you. As you engage and interact with the text, you will color visual symbols, which are reminders of each piece of gear's purpose. discover how Bible characters fought to overcome by consistently using the gear. draw inspiration and encouragement from others who have fought to overcome. reflect and answer questions related to your journey and what you're learning. Melony Brown not only survived several of life's tough challenges, but she also thrived while fighting to overcome those unexpected turns. In Challenges Won't Stop Me, she shares the strength, wisdom, and grit she's gained, as well as all the 135+ overcomers she's interviewed have gained. Their written stories and podcast interviews can be found at www.melonybrown.com. Grab your backpack. Let's fill it with the essential gear you'll need to survive, overcome, and thrive! It's time to JOURNEY ON!

This podcast discusses the preoperative, operative, and postoperative considerations for patients undergoing surgical treatment for moyamoya disease including: anatomy and pathophysiology, clinical presentation, diagnosis, preoperative evaluation, anesthetic management, operative approach, and postoperative care. LEARNING OBJECTIVES Upon listening this podcast, learners will be able to: • Describe the anatomy and pathophysiology of moyamoya disease • Explain the common preoperative evaluation for surgery to treat moyamoya disease • Provide an anesthetic management plan to be used during surgery to treat moyamoya disease • Describe several operative approaches used to treat moyamoya disease • Anticipate the postoperative considerations following surgery to treat moyamoya disease AUTHORS Weston Northam, MD Shilito Clinical Staff Associate Boston Children's Hospital Edward Smith, MD, MBA Director, Pediatric Neurovascular Surgery Boston Children's Hospital Jessica Laird-Gion, MD Clinical Fellow in Pediatrics Boston Children's Hospital Jennifer Perez, MD Associate in Critical Care Medicine, Department of Anesthesiology, Critical Care and Pain Medicine Boston Children's Hospital DATES Initial Publication: October 9, 2023. CITATION Northam W, Laird-Gion J, Soohey R, Marcley S, Marques B, Perez J, Smith ER, Wolbrink TA. Moyamoya. 10/2023. OPENPediatrics. Online Course. https://learn.openpediatrics.org/learn/course/internal/view/elearning/5472/moyamoya-disease. Video: https://youtu.be/2PWwtLTZAUs. Podcast: https://soundcloud.com/openpediatrics/moyamoya-disease/s-H6ggQgYd6xw. Please visit: www.openpediatrics.org OPENPediatrics™ is an interactive digital learning platform for healthcare clinicians sponsored by Boston Children's Hospital and in collaboration with the World Federation of Pediatric Intensive and Critical Care Societies. It is designed to promote the exchange of knowledge between healthcare providers around the world caring for critically ill children in all resource settings. The content includes internationally recognized experts teaching the full range of topics on the care of critically ill children. All content is peer-reviewed and open access-and thus at no expense to the user. For further information on how to enroll, please email: openpediatrics@childrens.harvard.edu Please note: OPENPediatrics does not support nor control any related videos in the sidebar, these are placed by YouTube. We apologize for any inconvenience this may cause.

Vince Murdock is a professional mixed martial arts fighter who came up from difficult circumstances and worked his entire life to get into the UFC. When he finally got the call, a pre-fight brain scan showed he had Moyamoya disease and a life-threatening arterial blockage. Following brain surgery that involved removing a quarter of his skull, Vince's perspective on life radically shifted. He became a father, got into cycling to rehab from surgery and formed an inclusive community, the Enjoy Cycling Club, to counter the elitism and exclusion that's commonplace in competitive cycling. Vince trains at Team Alpha Male under the supervision of multiple former UFC title belt holders and champions including Cody No Love Gabrandt and team founder and owner The California Kid, Urijah Faber. Vince has a unique perspective on life and deep wisdom from the hardships he has persevered through both before and after his surgery. He is a remarkable human and I am deeply grateful for what he shares in this interview. It really moved me. I'm dedicating this episode to my good friend Aaron Burby and his friends and family. Aaron suddenly died from complications related to undiagnosed Moyamoya disease in 2020. He has been with me every day since then and he always will be. Like Vince, Aaron made the people around him feel loved and special, he was a gifted community builder, went full gas after his goals in life and expected the people he loved to give everything to what they valued. Special thanks to past Choose the Hard Way guest Derek Teel from Dialed Health for connecting me to Vince.  This is a special conversation and I'm grateful to be able to share it with you all.    Vince Murdock Instagram  Watch on YouTube Sign up for the Hard Way Newsletter - - - - - - - - - -  Choose The Hard Way Website | Instagram Andrew Vontz LinkedIn Subscribe: Apple Podcasts, Spotify, Google Podcasts, Stitcher

I first met today's guest, Destia, when I was a guest speaker for Lisa Boehm's Hope and Healing Together Community last year. I learned that Destia's son had died of Moyamoya disease, and that, in her grief, Destia was trying to educate the medical community about Moyamoya in order to help save lives. Destia decided to come on the podcast to continue this process of educating people about this rare genetic disorder as well as get to talk about her amazing son. After recording, I often hear back from guests and continue emailing them. In fact, some of my closest friendships today started as those email exchanges. I was a little surprised to hear from Destia, however, as she told me that she was concerned that she didn't show enough emotion during the interview. She wrote, "I am really broken over my son's death two+ years ago, but I might have only shown my gratefulness that we had him as long as we did. In other words, I did not show my deep grief."  I quickly reassured her that I thought it was lovely and that Aaron would be so proud of her, but her words did make me a little sad. They didn't make me sad because I thought the interview was anything but great. It made me sad because all of us as bereaved parents feel so much pressure to show just the right amount of sadness to the world. Over the last 4 years, I know I have occasionally had comments from listeners that they stopped listening for a while because I was not sad enough. I have had other times when I have felt like I have been too emotional during a specific episode. I am actually quite thankful that Destia wrote that to me because it reminds me that all of us show our emotions differently on any given day. I am in a group text of bereaved moms and one of them asked today if there were certain days where we just felt like we were on the verge of tears all day. Many of us quickly responded yes to that question. There are other days, however, when we do feel a bit more 'together'. On those days, we may seem more thankful than sad. Today, I am reminded that both are perfectly fine and completely normal.

As TOKiMONSTA, Jennifer Lee has made a name for herself as a Grammy-nominated music producer, pioneering the L.A. Beat Scene and ranking as one of the top 100 DJs worldwide. Her entire discography has drawn critical praise, collaborating with a long list of artists including Anderson Paak, Earthgang, and Ryuichi Sakamoto, and remixing artists like Sia and Beck. In 2015, Lee was diagnosed with Moyamoya, a rare brain disease that left her unable to communicate or comprehend music, but she persevered through two surgeries and cognitive therapy to make a triumphant comeback at Coachella in 2016. Her first album post-surgery, Lune Rouge, was nominated for ‘Electronic Album of the Year' at the 2019 Grammy Awards. In 2020, she released her fourth full-length album, Oasis Nocturno, showcasing her progression as an artist with a mix of house, funk-soul, and hip-hop. Throughout the pandemic, she continued to innovate by hosting the popular music program Lost Resort on Twitch, collaborating on an NFT collection, and curating a livestream event for Women's History Month. Always looking to combine her creativity with innovation, TOKiMONSTA continues to push boundaries across music, fashion, tech and beyond. Toki has now entered the world of tech having cofounded a music tech start up by the name of “Sona.” The aim of Sona is to democratize music streaming for artists in a world where the pay per stream is not adequate for a musician's cost of living. The protocol and platform will reconstruct the scaffolding of music streaming so that audiences still have access to all the music they desire, while allowing artist's payout to equate to what they truly deserve. In 2022, Sona raised approximately 7 million in funding and is in development. The company is aiming for a mid-2023 launch. In this episode of Takin' Care of Lady Business®, recorded in Ibiza, Spain at the International Music Summit, host Jennifer Justice sits down with special guest TOKiMONSTA, a DJ and music producer who shares her experiences as a woman of color and encourages listeners to lead with their best foot forward, choosing to represent who they really are instead of taking shortcuts. The episode also explores her tech start-up, Sona, which rewards both artists and curators, offers a fairer payment system and uses blockchain technology.    Here is what to expect on this week's show: Sona's plan to revolutionize the music industry with a streaming platform that allows users to stream music for free and invest in artists by buying the streaming rights to their songs. How Sona uses blockchain technology in the music industry to bring transparency and efficiency to the ecosystem for musicians. Challenges for female producers in the music industry, gender bias, fundraising, and democratization in the music industry. Quotes: "With the internet, it kind of opens the floodgates for people to kind of just steal music, and that's really difficult for people who make music... I think technology and music are so intertwined now that it's kind of hard to say that they're two separate entities. Like, they're very linked." - TOKiMONSTA "I never wanted to be a DJ. You know, I wanted to make music. And now it's like I kind of love both and I feel that both are very different and dynamic skills that I've had to learn to kind of work on." - TOKiMONSTA "As far as making music and producing, that's something that came out of just having such a deeply rooted love for music. And then one day, I decided, I think I can do that, you know." – TOKiMONSTA "I feel like the more diversity we have, especially in music, the more interesting it gets because you have all these different perspectives and different ways of thinking.” - TOKiMONSTA https://tokimonsta.com https://sona.stream https://www.internationalmusicsummit.com/   Learn more about your ad choices. Visit megaphone.fm/adchoices

June 2023 Journal Club Podcast Title: MRI/MRA Versus Catheter Angiography for Annual Follow-up of Pediatric Moyamoya Patients: a Cost Outcomes Analysis To read journal article: https://journals.lww.com/neurosurgery/Fulltext/2023/06000/Magnetic_Resonance_Imaging_Angiography_Versus.17.aspx Author: Edward R. Smith Guest Faculty: Cormac O. Maher Resident Planner: Katherine G. Holste Moderator: Rafael A. Vega

Today our guest is Dr. Audrey Fan, Assistant Professor in the Departments of Neurology and Biomedical Engineering. She also serves as co-director of the Imaging Core for UC Davis Health's Alzheimer's Disease Center, an NIH-funded Alzheimer's research center. Dr. Fan is an imaging physicist and translational scientist. She develops novel magnetic resonance imaging (MRI) and positron emission tomography (PET) methods to study brain physiology in cerebrovascular disease and vascular dementia. She has translated new imaging technologies to patient studies in acute stroke, Moyamoya disease and intracranial stenosis. She received her Bachelor's degree from Stanford, then her Ph.D. from the department of Electrical Engineering and Computer Science at MIT. She returned to Stanford for her post-doctoral training, and, recently moved to UC Davis to start up her own lab. Dr. Fan is one of only a handful of researchers who are wielding MRI to non-invasively extract, with ever more effectiveness, useful quantitative information about brain physiology that is also clinically relevant. This includes quantitative blood flow, volume, and oxygenation as well as cerebral metabolic rate and oxygen extraction fraction with a goal to help guide treatment and therapy for stroke, vascular dementia, and other neurovascular disorders. This is such an important area to work in - as MRI is so sensitive to so many physiologic variables with such a broad parameter space. Even at about 40 years old, MRI has untapped potential and clinical efficacy - which Audrey is working to utilize. This conversation gives a great perspective of the unique challenges and opportunities of this exciting subfield of MRI. ~ Episode producers: Omer Faruk Gulban Alfie Wearn ~ Brain Art Artist: Omer Faruk Gulban Title: OHBM22 Brain Art ~ Please send any feedback, guest suggestions, or ideas to ohbm.comcom@gmail.com

On this week's episode of the podcast my new homie Carlie came through to the studio to detail her very unique medical experience. Before Carlie was even in highschool she was diagnosed with an extremely rare disease called Moyamoya. To simplify, it is caused when arteries at the base of brain are blocked. This can lead to increased chance of stroke as well as many other potential issues. Carlie explains in depth her journey through the multiple tests, surgeries, and hospitilizations, that ultimately led to the procedure that ended up allowing her to live the life she has today. She manages to do so while also adding in many jokes and other personal stories that make for a great episode of the podcast. Enjoy.

On Episode 23 of the Stroke Alert Podcast, host Dr. Negar Asdaghi highlights two articles from the December 2022 issue of Stroke: “Direct, Indirect, and Combined Extracranial-to-Intracranial Bypass for Adult Moyamoya Disease” and “Contemporary Incidence and Burden of Cerebral Venous Sinus Thrombosis in Children of the United States.” She also interviews Drs. Koji Tanaka and Andrew Demchuk about article “Significance of Baseline Ischemic Core Volume on Stroke Outcome After EVT in Patients Age ≥75 Years.” Dr. Negar Asdaghi:         Let's start with some questions. 1) Is direct bypass better than indirect bypass in preventing the future risk of vascular events in adult patients with moyamoya disease? 2) What is the contemporary incidence of cerebral venous sinus thrombosis in the pediatric population? 3) And finally, is endovascular therapy beneficial for patients presenting with a large ischemic core? We have the answers and much more in today's podcast. You're listening to the Stroke Alert Podcast, and this is the best in Stroke. Stay with us. Welcome back to another issue of the Stroke Alert Podcast. My name is Negar Asdaghi. I'm an Associate Professor of Neurology at the University of Miami Miller School of Medicine and your host for the monthly Stroke Alert Podcast. In our final podcast for the year, I'm thrilled to announce that Drs. Nastajjia Krementz and Eric Goldstein have joined our podcast as assistant editors to help us cover the latest and the best in the field of cerebrovascular disorder. And together, here's our article selection to close the year. As part of our Advances in Stroke, in the article titled "Focus on Anticoagulation for Valvular Heart Disease With and Without Atrial Fibrillation," we get an update on current evidence from randomized controlled trials on the use of direct oral anticoagulants or vitamin K antagonists in patients with valvular heart disease that are mechanical valves, moderate to severe mitral stenosis, or bioprosthetic valves from the perspective of stroke physicians. What that means is that data from randomized trials was analyzed based on whether the patient had a prior history of stroke or TIA. In this review, we learned that direct oral anticoagulants may be used in patients with bioprosthetic valves who have atrial fibrillation, although DOACs have never been shown to be superior over vitamin K antagonists. We also learned that vitamin K antagonists should be used in patients with rheumatic moderate to severe mitral valve stenosis or patients with mechanical valves with or without atrial fibrillation and, of course, sometimes during the first few months after either surgical or transcatheter aortic valve replacement in patients without atrial fibrillation. And finally, patients with bioprosthetic valves without AFib don't have any other indications to be treated with anticoagulants should be treated with antiplatelet monotherapy in the long run. In a separate article in this issue of the journal, from Dr. Yang and colleagues from China, we learn about the pathophysiology of radiation-induced brain injury with special attention to radiation-induced vasculopathy. These investigators show that hyperactivity of notch signaling pathway that in normal state is essential in vascular morphogenesis and maintenance of arterial identity actually results in abnormal accumulation and disturbance of vascular smooth muscle cells, resulting in arterial muscularization and arterial dysfunction seen in radiation-induced vasculopathy. What's interesting is that inhibition of the notch signaling pathway in their study resulted not only in a measurable reduction in radiation induced vasculopathy, but also an overall improvement in radiation-induced brain injury as measured by the cognitive function of the mice exposed to radiation in their study. This study takes us a step closer to possible therapeutic options for radiation-induced vasculopathy and radiation-induced brain injury using compounds that can potentially inhibit the notch signaling pathway. As always, I encourage you to review these articles in detail in addition to listening to our podcast. For our interview today, I have a special guest who's not only a prominent researcher and a pioneer in the field of acute stroke therapies, but also, he's an experienced educator who has trained many of the current leaders in the field of vascular neurology and has been influential in shaping the careers of many vascular neurology fellows over the years. Take a listen. Dr. Andrew Demchuk:   I've had the privilege of training fellows. I've been the director since 2004, and we've trained close to 100 fellows in Calgary over 20-some years now. Really, it's frankly an honor and privilege to be able to do that. These individuals come from all over the world. They're here to dedicate themselves to learning a subspecialty really, really well, and it's just a fantastic experience to interact with them all and all their cultures to help them learn those things, and doing it in a fun, enjoyable, comprehensive way. Dr. Negar Asdaghi:         And those are the words of Dr. Andrew Demchuk, who's incidentally my own vascular fellowship director as well. Andrew joins me all the way from Canada to talk about his latest paper on the very hot topic of outcomes of endovascular therapy in patients presenting with a large ischemic core. And true to form, he's accompanied by one of his current vascular fellows. The interview is definitely worth the wait after we review these two articles. Most of us have heard of the term "moyamoya." First described in Japan in 1950s, the term refers to occlusion or stenosis of the terminal portion of the internal carotid artery and is associated with dilated collateral vessels of the proximal middle cerebral artery. These collaterals have a hazy appearance on angiography resembling the puff of smoke, which is Japanese for "moyamoya." Moyamoya is categorized into two broad categories of moyamoya syndrome and moyamoya disease. Syndrome refers to the situations where the occlusion occurs due to another condition. Conditions such as Down syndrome, sickle cell disease, neurofibromatosis type one have all been recognized as associated with moyamoya syndrome. Of course, moyamoya syndrome can occur due to a secondary insult to the blood vessels, anything from radiation vasculopathy, as we reviewed earlier in the podcast, to autoimmune vasculitis, or even good old advanced intracranial atherosclerosis involving the distal ICA region can cause moyamoya syndrome. Now, in contrast to moyamoya syndrome, the term "moyamoya disease" is reserved for individuals with no vascular risk factors or known moyamoya predisposing conditions other than, of course, some potential genetic factors. The most recognized genetic association for moyamoya disease is polymorphism in the ring finger protein 213, or RNF213, gene on chromosome 17. But we also have to keep in mind that the majority of moyamoya disease patients have no identified genetic abnormalities. So, moyamoya is truly a complex condition, and the physicians have to navigate the many possible etiologies that may cause or be associated with this condition. But when it comes to treatment options, we're really limited here. Antiplatelets are generally used and have been shown to reduce mortality in both moyamoya disease and syndrome, and especially cilostazol, which is the favorite antiplatelet therapy of our own assistant editor, Eric, has been shown to be significantly associated with increased survival rate in patients with moyamoya disease. Eric really wanted me to talk about a recently published study out of Korea, which included over 9,000 patients, and that showed that patients treated with cilostazol had a better survival rate than any other antiplatelet therapies. Apart from antiplatelet therapies, medical treatment includes optimizing all other vascular risk factors, which, as we mentioned, are rarely present in this population. So, it all comes down to most cases, at some point, needing surgical treatment, with bypass surgery being the most commonly surgical intervention for this population. Three flavors of bypass are used: indirect, direct, or combination of the two. Indirect bypasses are kind of like long-term investments where the surgeon moves vascular tissue to the surface of the brain in hopes of promoting angiogenesis. Several procedures, such as performing multiple burr holes, pial synangiosis, dural inversion, or omental transposition, among other methods, are used. And broadly speaking, we can think of indirect procedures as angiogenesis-dependent methods, the effect of which takes months to recognize and, in general, are thought to be more efficacious in the pediatric population than the adult population. The direct bypass, in contrast, commonly referred to as extracranial-to-intracranial, or ECIC, bypass, is more of an immediate reward where the surgeon stitches a vessel directly from a donor extracranial branch, typically the superficial temporal artery, to a recipient artery, typically the middle cerebral artery, to provide a direct anastomosis between the two vessels. There are technical variations, of course, especially with regards to the number of donors and recipient arteries used, but essentially this method is an angiogenesis-independent method that results in a quicker revascularization, but it's unclear if this strategy is long lasting. A combination of direct and indirect bypass can also be used. So, the question is, which method is better, especially in the adult population? In this issue of the journal, in the study titled "Direct, Indirect, and Combined ECIC Bypass for Adult Moyamoya Disease," Dr. Nickalus Khan and colleagues report on a meta-analysis and systematic review of those with adult moyamoya disease who underwent either direct, indirect, or a combination bypass. The main study question was whether there's a difference in the rates of early ischemic or hemorrhagic strokes, defined as strokes occurring within 30 days of bypass, or late strokes, defined as strokes occurring after 30 days of bypass, in this population when comparing the different surgical techniques. They also compared the "favorable" outcome rate; however, this outcome was defined in each study between the various broad techniques of direct, indirect, and combined bypass. So, with that, let's take a very quick look at their methodology. They screened more than 4,000 articles and identified 143 articles for their pooled analysis, the majority of articles being from Eastern Asian-based regions, and they had close to 4,000 combined, 4,000 direct, and 4,000 indirect bypass procedures for this analysis. And they had an average follow-up of over three and a half years. So, this is a great sample size for this large, pooled analysis. But they also performed a smaller meta-analysis where they were much more stringent with article selection, excluding pediatric papers, excluding articles containing only one surgical modality, or articles with insufficient outcome data. So, for that meta-analysis, they only had 43 articles qualified and were included in that meta-analysis. So, what did they find? In the larger pooled analysis, a significant benefit in favor of both direct and combined bypass techniques were noted in reduction of early and late ischemic strokes and late intracerebral hemorrhage. Also, a higher rate of that sort of vague favorable outcome was noted with both the direct or combined methods as compared to when indirect bypass techniques were used alone. So, everything in the large, pooled analysis pointed towards the direct bypass or combined technique performing better than all indirect bypass techniques, with only one exception, which was a lower incidence of early intracerebral hemorrhage rate in indirect bypass cases. So, that's one point to keep in mind. The second point was when they compared combined techniques to direct bypass. Overall, these procedures had more or less the same outcomes with the exception that the rate of late ischemic stroke was lower in the combined group than the direct bypass group. So, this is sort of the overall summary of what they found in that large, pooled analysis. When they were much more stringent with their selection criteria, focusing on the smaller meta-analysis portion of the study, what they found was that in the short term, there were no differences in outcomes of any type of stroke between any of these methods. So, basically, people, regardless of the type of bypasses they received, did the same with regards to the risk of intracerebral hemorrhage and ischemic stroke recurrence within the first 30 days after the bypass. But for the late stroke outcomes, whether ischemic or hemorrhagic, those with indirect bypass were nearly twofold more likely to develop late stroke after 30 days compared to those who've undergone the direct bypass. A similar pattern was found comparing combined bypass versus indirect bypass, in general, beyond the 30 days, with combined bypass doing better. Comparing direct versus combined bypass showed no difference regardless of timeframe. So, in summary, overall, it appears that combined or direct bypasses may be the best surgical strategies for treatment of adult patients with moyamoya disease. This study, of course, has many limitations, as does any meta-analysis, but most importantly, the authors focused on moyamoya disease in their analysis. It is presumed, but really unclear if patients with moyamoya syndrome would respond similarly to these different techniques. So, the question is, what surgical procedure are you using at your institution for treatment of adult moyamoya disease patients? And, of course, Eric wanted me to ask if your antiplatelet of choice is cilostazol for this population, yes or no. Leave us your comments, and let us know. Venous sinus thrombosis, or CVST, is a less common form of stroke most commonly affecting women and young individuals. In our past podcast, we've covered many aspects of CVST, especially when it comes to therapy with anticoagulation, anticoagulant of choice, and duration of therapy. In the October podcast, we reviewed a systematic review and meta-analysis comparing direct oral anticoagulants to vitamin K antagonists in the adult patients with CVST. But there are many aspects of this disease that we have not yet covered. For instance, you may ask, how common is this relatively uncommon condition? In the adult population, the incidence of CVST varies depending on the age of individuals studied, and ranges between 1.3 to 2.7 per 100,000 in women between the ages of 31 to 50, which is the adult population at highest risk for this disease. But the incidence of CVST, for instance, in the pediatric population is largely unknown. Some studies suggested an incidence rate of 0.67 per 100,000 in the pediatric population. That's roughly less than half the incidence rate in young female adults, but these reports are from the 1990s and are likely very outdated. Nowadays, many of the pediatric conditions, especially infectious conditions, that can predispose children to CVST are more readily diagnosed and treated. On the other hand, we now perform a lot more imaging than 30 years ago. Our neuroimaging modalities are more accurate, so we are more likely to diagnose CVST than before. So, the question is, what is the contemporary incidence of pediatric cerebral venous sinus thrombosis? In this issue of the journal, in the study titled "Contemporary Incidence and Burden of Cerebral Venous Sinus Thrombosis in Children of the United States," Dr. Fadar Otite and colleagues conducted a retrospective analysis of the New York State Inpatient Database, or SID, from 2006 to 2018, and the National Kids Inpatient Database, referred to as KID, from 2006 to 2019, for all hospitalized CVST cases. KID is the largest publicly-available pediatric inpatient care database in the United States, containing about 3 million pediatric discharges. They included over 700 hospitalized CVST cases from the SID database and 6,100 hospitalizations from the national KID database for the current analysis. And here's what they found. Number one, in terms of significant risk factors associated with CVST, congenital circulatory system anomalies, infections, head trauma, dehydration, and anemia were amongst the top CVST risk factors in the pediatric population. So that's very good to know. Number two, in terms of presentation, seizures were the most common presentation among all pediatric age groups, with close to half of infants with CVST presenting with seizures. Number three, in terms of outcomes, the rate of mortality was twice higher in the infants group as compared to all other age groups. And finally, the overall incidence of CVST, which was the main question of the paper, in this population was 1.1 per 100,000 per year, with a peak incidence during infancy of 6.4 per 100,000 per year. Interestingly, incident admissions also increased annually by 3.8% throughout the study period, which was close to 15 years in this paper. And the national burden of hospitalization dramatically and exponentially grew during the study period. So, here are the top three points from this study. Point one: Girls included less than half of all admissions nationally and statewide, and the overall burden of CVST was higher in boys than girls. That's a dramatic difference between the pediatric and adult populations. Point two: Incidence of CVST in infants was higher than five times that of other age groups at 6.4 per 100,000 compared to overall incidence in children, which was 1.1 per 100,000 people per year. Mortality was also two times higher in infants than in any other age group. And finally, point 3, incident admissions and national burden of hospitalization have dramatically increased over time, but it remains unclear whether true incidence has been on the rise or if simply more cases are recognized nowadays due to heightened awareness of this condition and our advanced neuroimaging capabilities. This study, of course, has some limitations. Data was only obtained on patients admitted, so many patients that may have had CVST but not admitted are not captured in this database. So, in summary, CVST can have catastrophic consequences in children and lead to long-term neurological deficits. Having a high clinical suspicion and early recognition remain crucial for prompt treatment and improved outcomes in this population. Dr. Negar Asdaghi:         Endovascular treatment, or EVT, is an effective method to achieve recanalization and to improve clinical outcomes in ischemic stroke patients with a target vessel occlusion. Both advanced age and having a large infarct volume at the time of presentation are negative predictors of beneficial outcomes post-EVT. Despite this, the neurological benefits of EVT seem to persist across the spectrum of age, and the same has been observed for a range of ischemic core volumes. But it's important to note that, in general, patients presenting with large ischemic core volumes were excluded from the original thrombectomy studies, and currently there's several ongoing trials to determine whether EVT is beneficial for the large core population. Now, the question that everyone is interested in answering is whether there is an actual ischemic core volume beyond which endovascular therapy is either futile or potentially even harmful, and if this magic futile core volume is the same for all patients, or does it differ depending on the age and other factors. In a previous podcast, in an interview with Dr. Osama Zaidat, we learned about that important interaction between the presenting ischemic core volume as measured by ASPECTS score and advanced age in an analysis of patients enrolled in the STRATIS registry. In that study, no one over the age of 75 achieved functional independence post-EVT if the presenting ASPECTS score was under 5 regardless of the angiographic outcomes. In that interview, we also discussed the limitations of STRATIS registry as a non-randomized, single-arm study, and the issues surrounding using ASPECTS score to define ischemic core. In today's podcast, we're going to revisit the important interaction between the presenting ischemic core volume and age while reviewing a pooled analysis of seven endovascular clinical trials in the paper titled "Significance of Baseline Ischemic Core Volume on Stroke Outcome After Endovascular Therapy in Patients Age 75 Years or Older." I'm delighted to be joined today by the first and senior authors of this paper, Drs. Koji Tanaka and Andrew Demchuk. Dr. Tanaka is an Assistant Professor of Neurology at Kyushu University in Japan. With his experience working at the leading center for conducting stroke clinical trials in Osaka, he has now joined the Calgary Stroke Program as a research fellow. And he's accompanied today by his fellowship director, Dr. Demchuk. Dr. Demchuk, of course, needs no introduction to our Stroke readership and our podcast audience. He's a Professor of Neurology at the University of Calgary Cumming School of Medicine. He's a stroke neurologist and a leader in the field of cerebrovascular research who has been involved in multiple clinical studies and randomized trials, including the seminal studies that led to the approval of EVT as the standard of care for treatment of stroke. And, of course, he's a very special guest of this podcast this morning as he was my very own fellowship director. Top of the morning to you both, Andrew and Koji. Welcome to the podcast. Dr. Andrew Demchuk:   Thanks, Negar. It's great to be here. Dr. Koji Tanaka:               Thank you very much for your invitation. That is a great honor to be here. Dr. Negar Asdaghi:         Thank you both. Andrew, let's start with you. Can you please provide us some background on the pooled analysis and the HERMES collaboration, please? Dr. Andrew Demchuk:   Yeah, HERMES is a really, it's been a really fun journey. Years back, when these trials all came out roughly at the same time, right? There was a real quick succession of trials, the MR CLEAN trial was obviously first, and ESCAPE and others quickly followed it. It became very clear to us that it just made total sense to collaborate. And so we got together as a group and decided we will pool the data. We'll do it in a very careful scientific way with basically an independent statistical analysis, and develop a core imaging lab, and really actually share the workload amongst us. I remember one of the really interesting tidbits about HERMES is when we got together, in order, I think, to really build trust in the group, one of the important things we decided early was we were going to have a snake draft. If you don't know what a snake draft is, Negar, it's essentially where you take turns selecting a topic through each of the trials. So, every trialist got an opportunity to pick a topic, and we just went down the list until everyone had their turn, and then we'd start over again and do it again. And I think that really worked very well to be as democratic as possible with this, and as fair. And it really allowed for a lot to get done because whoever was motivated in the collaboration was able to do an analysis. Dr. Negar Asdaghi:         So, what a great summary of this collaboration. So, it's true collaboration between the trialists that basically gave us those seven original randomized trials. Andrew, can I just stay with you, and can you tell us a little bit about the patient population that were enrolled in those trials? Dr. Andrew Demchuk:   Yeah, I think one of the important things to know, and I think a limitation for any kind of analysis like this, is the trials generally were small core trials, right? I mean there are some, MR CLEAN was certainly a more generalized population, but many other trials, including ESCAPE, I mean the "S" and the "C" in ESCAPE is "small core," right? And so a lot of these trials were small core. So, we don't have a lot of data in larger core patients. But, as you can imagine when you do core lab analysis, you realize that some of the stroke patients weren't as small core as we thought they were when we enrolled them. So, there is some sufficient data to hypothesize. I would consider this paper very much hypothesis-generating. So, yeah, it is a limitation to be considered here. I mean, our sample size isn't very large in the big core patients. Dr. Negar Asdaghi:         Perfect. Thank you, Andrew. So, again, a recap for our listeners, that we are looking at pooled analysis of seven original trials of thrombectomy, but keeping in mind that those patients that were enrolled in the trials had, generally speaking, small presenting ischemic core. So, now, Koji, on to you. Can you walk us please through the current study, and what was the premise of it, and who was actually included in this study? Dr. Koji Tanaka:               Yes. In this study, we aimed to evaluate association between baseline ischemic core volume and the benefit of endovascular therapy over the best medical treatment on functional outcomes. Patients were categorized age over 75 years, and less than 75 years old. The primary outcome of interest was a modified Rankin Scale of three or less, and we included 899 patients who underwent this baseline ischemic core volume measurement, which corresponds to 51% of our patients in the HERMES collaboration dataset. Dr. Negar Asdaghi:         All right. So, just a quick recap of what you said. Thank you for this. So, we have 899 patients. Those patients were all included in the HERMES collaboration, but, of course, these are patients in whom we had presenting ischemic core measurements. And that will get me, actually, Koji, to my second question. Can you please walk us through how you did analysis of ischemic core volume measurements in this study? Dr. Koji Tanaka:               In this study, ischemic core volume was measured by CT perfusion in 591 patients and by diffusion-weighted imaging in 309 patients. We defined the ischemic core volume as a relative cerebral blood flow of less than 30% in CT perfusion and diffusion coefficient of less than 620 square micrometers per second in diffusion-weighted imaging. Previous studies showed ASPECTS moderately correlate with ischemic core volume in both CT perfusion and diffusion-weighted imaging. For example, ASPECTS of eight can be considered as ischemic core volume of 20 milliliters. But underlying [inaudible 00:28:21] were different between CT perfusion and diffusion-weighted imaging, and previous studies suggested CT perfusion occasionally overestimates the ischemic core volume was on diffusion-weighted imaging. In this study, the results did not change when analyzing CT perfusion and diffusion-weighted imaging separately. Dr. Andrew Demchuk:   Yeah, that's a really important point Koji makes, is that because we had sort of a, not quite a 50/50 split, we had a 60/40 split of CTP and DWI, we did analyze them separately, and the odds ratios of treatment effect were pretty similar at different core thresholds. So, they're fairly similar when you separate them out, but obviously the methodology is a little different between a CTP and a diffusion. And to Koji's point, he's absolutely right, the CTP has a tendency to slightly overestimate core when you compare to diffusion. Dr. Negar Asdaghi:         Yeah, and thank you. I think you already sort of alluded to what I was going to ask you and Koji, because, in reality, we have different ways of measuring core. We have the ASPECTS score, which is just a quick and dirty way of estimating or guesstimating core, and then we have CT perfusion, and we also have diffusion that sometimes is available to us, but not always. And the question is, in the heat of it, how we're going to measure the volume. With post-processing softwares, with CT perfusion, we get a quick potential ischemic core volume, but we don't have that capability with diffusion even if we did get diffusion. So, I think it's important to know that what Koji mentioned, an ASPECTS of eight can, more or less, in a quick fashion, be thought of as about 20 cc of core. And the other point that Koji raised was that CTP, again, this is sort of ballpark, can tend to overestimate ischemic core if you were to compare that with diffusion-weighted data. So, with that, now we have a study in which we have core volumes, and we're going to look at outcomes from endovascular thrombectomies compared to best medical management and see whether there is a correlation or interaction between ischemic core presentation, especially age. So, my next question would be to Andrew, can you walk us please through the main findings of the paper? Dr. Andrew Demchuk:   The whole goal of this paper was really to understand, are there thresholds in the older patients? When we looked at overall, and Bruce Campbell and the team wrote an important paper with HERMES and the CTP cohort overall, and the sort of message there was if you looked at shift analysis, there wasn't actually a core threshold found at all in HERMES for lack of benefit. There was a benefit across all the core volumes, but, of course, that's all ages. So, we were really interested in looking at the older patients because we felt there's more likelihood the core volume will matter in the elderly than in the younger patient. We know the younger population, it benefits overwhelmingly with EVT, it's hard to even find a core volume threshold. So, that was a premise. Essentially, we had 247 patients over 75 in the overall cohort, of which 98 had EVT. So, it was a decent population, and not a huge sample, but a decent sample. And so we looked at various things. The first thing that was interesting we found was that infarct volumes, the average infarct volume to achieve an mRS three or less, was lower in the older patients, significantly lower, was 23.9 for younger patients under 75 and 10.7 for the older patients. You tend to have much smaller infarcts to achieve good outcome. And so that was kind of interesting, and I think that's been shown by others. Then we got into the weeds to try to figure out, OK, what are these thresholds? And if there's one figure that matters, Negar, you know me to always point out that there's always one figure or table in a paper that's kind of where the money is, where the real learning is, and that's Figure 2 on this paper in my opinion, beautiful figure with four figure A, B, C, and D. And it really sort of nicely highlights these issues and these cutoffs. But what we saw is that in the older patients who received EVT, around 50 mils seemed to be a threshold to achieve zero three, you had to, to see treatment effect, you had to have a baseline infarct volume less than 50 mils for a zero three outcome advantage. For zero four, it was 85 mils. And then we looked at this issue of what we called futility, true futility. And that's a very controversial thing. What is futility, or how do you measure futility? And really, I think, we even had a debate about this as a HERMES group when we were designing the analysis, and we sort of landed on mRS five six. A 90% chance of mRS five six, right? That's quite the bar, right, to say true futility because some people argue mRS four is still not a horrible outcome. Culturally, that is an OK outcome in some situations. But when we did use that five six 90% threshold, it was 132 mils. So, you're getting up to these really large volumes. But here's the catcher in the whole thing, and Koji will probably speak to this a bit more. I don't want to steal his thunder too much, but this issue of reperfusion seemed to matter in this. And we'll come back to that maybe with another question. Reperfusion matters a lot when you think about these thresholds. Dr. Negar Asdaghi:         OK, so, Andrew, a lot of information, I don't know if I need a recap myself to recap, but basically what you mentioned is that for the older patients who received EVT, if we keep our eyes on the outcome of mRS of zero to three, it seems to be the magic core volume for that outcome post-endovascular therapy that it lands on the magic volume of 50 cc core. Did I get that right? Dr. Andrew Demchuk:   That's correct. Dr. Negar Asdaghi:         Then if you're still a bit more lenient with the definitions of what is favorable outcome, what outcomes we're looking at and so on, so forth, for an mRS of five to six, then when we talk about futility of endovascular thrombectomy, the volume that you mentioned, and again I want to ask you this, this volume is for elderly over the age of 75, is 130 mil. Dr. Andrew Demchuk:   132, but yeah, absolutely. But there's a real catcher here, and we need to really emphasize the catcher in this. Dr. Negar Asdaghi:         Okay. I will ask you one more question before I go to Koji, which I'm sure is going to tell us more about that catcher. Andrew, can you please tell us about the factor of time? I feel like that is something that we need to discuss, as well. Your study included patients early on in their stroke onset, but we're talking about an important interaction. The question is, do you think the results of this interaction would be different or impacted by the value of time? Dr. Andrew Demchuk:   Hypothetically? It must, right? I think that that must be the case. We don't have any data specific to this. That would be an interesting Aurora analysis to do. Now, of course, the challenge with late window analysis is, we are really small core in our late window trials, we probably have even a much smaller proportion of large cores. So, to be able to even tackle that question in the late window is, I don't know if we have the data yet, to be honest. But it makes sense that you would expect the thresholds to be a bit lower the later you are in the window. But that is a hypothetical opinion. Dr. Negar Asdaghi:         Right, so, I want to take that and come to Koji. I want to digress a little bit to Koji and see how we can understand the finding of this current analysis of this paper. So, small core patients early on into their onset, we're looking at the interaction between age and their core volume and coming up with numbers 50 cc for the elderly population. If you're looking at the outcome of zero to three or 132, as Andrew pointed out, for an MRS of much higher, four or five. Dr. Andrew Demchuk:   Actually five, six, 90% chance of five, six. So, it's there. It's like almost everybody got five, six, took 132 mils to get there. So, it's like this extreme outcome. Dr. Negar Asdaghi:         Right, so, exactly, and I have to correct it, again, mRS of five or six or dead or almost dead mRS basically. Dr. Andrew Demchuk:   In 90% of patients. Dr. Negar Asdaghi:         90% of patients. So, we have these important numbers here, and I want us to basically understand these numbers in these volumes in the context of the recently published RESCUE-Japan LIMIT study. Can you tell us a little bit about that study and how we can make sense of these volumes in the setting of that paper? Dr. Koji Tanaka:               In the recent RESCUE-Japan LIMIT trial, the median ASPECTS was lower, and baseline ischemic core volume was greater than those in our study. And surprisingly, the median ischemic core volume in that trial was close to our threshold to predict less than 10% of patients achieve a modified Rankin Scale of four or less after endovascular therapy. We thought this is due to much higher complete reperfusion rate in HERMES patient. We have much interest in their additional analysis for outcomes in elderly patients by reperfusion status. This potential benefit of endovascular therapy in the area is promising for the future clinical trials. Dr. Andrew Demchuk:   I think just to add to that, it was actually really interesting, Negar, because when we were analyzing all of this and then the trial came up and it was actually really nice because we're like, OK, how does our data relate to their data? And that's where Table 2 comes in, and it would almost be worth putting on the pod, whatever, I don't know if you have on your podcast website, you have one figure that you can sit there with as you listen to the podcast, because that would be the figure. Dr. Negar Asdaghi:         We'll work on that Andrew, but tell us a little bit more because, really, when I read the trial results, the way I understand it is that people enrolled in RESCUE-Japan that were older than 75, and these are all large core patients, benefited more from endovascular therapy than their younger counterpart. How do I understand that? I don't know how to wrap my head around that finding. Dr. Andrew Demchuk:   You want to try to answer that, and then I'll add? Dr. Koji Tanaka:               As I mentioned previously, we want to know about the exact patient population just only for elderly patients, whether they have a exactly larger ischemic core volume or as well as their functional outcome. How many patients achieved modified Rankin Scale four or less or three or less, or more than five or six? Dr. Andrew Demchuk:   Koji's point's very important. We actually don't have the breakdown of the mRS, so we don't know if they created a lot of fours, or threes, or what. So, that's one issue. But I think that the key to this whole thing is to understand that this is a 2022 trial. HERMES data is essentially a 2015 equivalent where we're looking at a number of clinical trials who roughly ended between 2014, 2016. So, the technology, the technique, the operators, are just at a different level back then than now. And quite frankly, EVT is an improving treatment. We probably don't even fully understand how much, I mean, we're just getting better at it. And I think what's happened here is the reperfusion rates have improved. And our HERMES reperfusion rates, remind me, Koji, I think they're about half, we think, in HERMES, than like the TICI 2bs, threes, are half in HERMES what they got in RESCUE-Japan LIMIT. So, when you achieve successful reperfusion, what were the numbers here? TICI 3 was 43% in the Japan RESCUE LIMIT, and 8.6% in HERMES. Okay, TICI 3s were not ... Now that may be slight differences in core lab interpretation, but we were just starting to get good at 3s. We were getting a lot of 2bs and some 2cs, but we weren't getting a massive number of 3s back in 2015. Well, voilà, now we are, right? We're hitting home runs when we didn't before. And I think that has really shifted the goalposts on the large core. If you open the vessel, they can still do well if they're elderly, but you've got to really open that vessel. And in HERMES, we only did that in a small portion of patients. So, these thresholds are sort of representative of 2015 skill. Dr. Negar Asdaghi:         Golden points, Andrew and Koji, both of you. I want to recap what you mentioned here. A note to all of our audience and listeners that we are looking at an analysis with RESCUE-Japan, an analysis of a 2022 study. And the patient population that were enrolled were also treated much later in terms of time than the patient population that was enrolled in the HERMES collaboration and in all of the trials that contributed to HERMES. So, we've got to remember that EVT is this fluid, ongoing, everyday-improving therapy, from our techniques to everything else, you know, how fast we get patients to the angiosuite. And the point that you raise, I want to repeat that, the percentage or the odds of achieving a perfect reperfusion was, in RESCUE-Japan, was 43% odds of TICI 3 reperfusion, whereas only 8.6%. So, when we're talking about all of these predictive modeling or predictive factors that will tell us who's going to do well, who's not going to do well, it also is predicated on the angiographic success. And perhaps in the earlier trials or even the early study that we covered as part of the STRATIS registry, we put everybody, TICI 3s with TICI 2b or better, whereas nowadays we accept the best, TICI 3s, and maybe that improved percentage in the most recent trial, the RESCUE-Japan, really did what it had to be done for the elderly population to keep that in mind. And Andrew, before we end our interview, I want us to get your top two takeaway messages from this paper. Dr. Andrew Demchuk:   Clearly, elderly patients do better when their strokes are smaller, that we know, compared to younger patients. But it's all about hitting the home run. It's all about hitting the home run. Figure 2C and 2D, you can see that if you achieve that high TICI score, a significant proportion of elderly patients potentially could still benefit, 30–40% reasonable outcomes with bigger cores if you get those high TICI scores. So, it is about hitting the home run in reperfusion in the elderly. You need to go for it, and hopefully you're successful, because if reperfusion isn't successful, then generally the outcomes are not ideal and they certainly worsen as the core volumes become larger, bigger. Dr. Negar Asdaghi:         Before I ended the interview, given Andrew's tremendous experience as a longtime fellowship director and seeing that he was flanked by two of his fellows, one past, myself, and one present, Koji, I had to ask him one final question of what his philosophy is as an educator. Dr. Andrew Demchuk:   I have a sort of philosophy on life with fellows. I always look for the special power in a fellow. I realized a long time ago we're all, we're not perfect, nobody's perfect, I'm not perfect, but there's usually a special power in people, and if you spend the time to get to know them, you identify that special power, and you really help harness it because you know that if they can harness it when they go back to their faculty job, they're going to really contribute something special to their team, right? You can imagine six special powers from six different people in a team. Now you've got a real team, right? If you know what your power is, you know your limitations, but you know where your strengths you can add to the group, and that's what we try to do here when we can. It's not always, you know, special powers, you have to kind of seek them out. But they're there in most people, and that's really important for career down the line. Dr. Negar Asdaghi:         And this concludes our podcast for the December 2022 issue of Stroke. Please be sure to check out this month's table of contents for the full list of publications, including our very interesting Stroke Images series. In this month, we have a case of progressive cervical myelopathy secondary to a dural AV fistula supplied by the anterior inferior cerebellar artery. We also have a separate case of carotid rete mirabile imaged with a four-dimensional flow MRI study. And with these cases, we bring our 2022 Stroke Alert Podcast series to an end. Over the past 12 months, we've ended our podcasts with various inspirational tales. From the moving account of the American runner Steve Prefontaine and the remarkable journey of the Syrian refugee and Olympian swimmer Yusra Mardini, to the discovery of positron and Commander Armstrong's landing on the moon, our podcast stories have but one thing in common, which is the story of human perseverance and consistency in the face of hardship. So, as we end 2022 to start 2023 anew, Andrew's comments on finding that special power in each of us resonate with our resolution to stay alert with Stroke Alert. This program is copyright of the American Heart Association, 2022. The opinions expressed by speakers in this podcast are their own and not necessarily those of the editors or of the American Heart Association. For more, visit AHAjournals.org.

Andrew Russman, DO, discusses the management and treatment of moyamoya disease in patients with large artery intracranial occlusive disease.

David Langer, MD, is the chair of neurosurgery at Lenox Hill Hospital, vice president of neurosurgery for Northwell Health's Western region. A renowned neurosurgeon and expert in cerebral revascularization, he treats patients who have brain tumors, including acoustic neuromas and meningiomas, and cerebrovascular conditions such aneurysms, arteriovenous malformations (AVMs) and Moyamoya disease. He also treats minimally invasive spine, spinal cord injury and AVMs.“As part of leading and growing our neurosurgery program, I aim to innovate and bring a high level of expertise and energy to my patients,” says Dr. Langer. He was an early adopter of using the exoscope for cerebral bypass surgery. The exoscope projects high-definition, three-dimensional images on a large screen in the operating room, greatly improving the accuracy of procedures.Dr. Langer earned his medical degree and completed a neurosurgical residency at the University of Pennsylvania School of Medicine. He also received mid-career fellowship training in cerebrovascular disease treatment at the University at Buffalo. At Northwell, he practices within a multi-disciplinary team, collaborating with ENT, plastic surgery, psychiatry, radiation oncology, physician assistants and nurses to provide personalized care plans.Dr. Langer is dedicated to teaching the next generation of doctors as a professor of neurosurgery and radiology at the Donald and Barbara Zucker School of Medicine at Hofstra/Northwell. He also values public education and was featured in Lenox Hill—a Netflix Originals docuseries that shadows four doctors as they navigate their daily lives and care for their patients—and frequently contributes to various media outlets on neurosurgery. A technological innovator, Dr. Langer developed Playback Health, a smartphone app designed to enhance the patient experience. He's also an instructor for BRAINTerns, a virtual summer internship program for students worldwide.He is a member the numerous medical societies and has published extensively in peer-reviewed medical journals. He has been a Castle Connelly Top Doctor New York Metro Area (digital guide) for the last several years.“I see patients when they're most vulnerable,” says Dr. Langer. “The most rewarding part of my job is guiding them through not only the physical part of their treatment and recovery, but also the psychological and emotional part.”

In Episode 33 of the Know Stroke Podcast, we were joined by Orlena Skek. Orlena Shek is a former in-house software technology licensing attorney. She lives in the San Francisco Bay Area with her husband and two young children. After experiencing major hemorrhagic stroke in late 2011 due to a rare congenital condition called Moyamoya Disease, she put her law career on hold to focus on her rehab and her family. The numbers that she shares speak for themselves to the long and turbulent journey she went on. 14 ambulance rides within 5 months 6 week hospitalization at Stanford.  3.5 weeks in a medically induced coma 3 different acute rehab hospital stays ranging from Marin to Santa Clara County. Two 10 hour plus brain surgeries, a week apart. One thousand eight hundred paper origami cranes folded by countless co-workers, neighbors, and friends. Some of whom are on the call here tonight.  More than a 100 nights spent hospitalized, away from home.   2 children:1st born pre-Stroke, 2nd born post-Stroke. 1 trip to Las Vegas by myself for a Bachelorette party. Orlena shares with us today that journey and what led her to authoring a book titled "Emerging from the smoke, a collection of warrior voices" This book is a beautiful collection of short poems from 30+ stroke survivors. You can learn more about Orleana's story, and purchase here book here: https://www.storiesofstroke.com/orlena-shek/

On Episode 20 of the Stroke Alert Podcast, host Dr. Negar Asdaghi highlights two articles from the September 2022 issue of Stroke: “Transdural Revascularization by Multiple Burrhole After Erythropoietin in Stroke Patients With Cerebral Hypoperfusion” and “Silent Infarcts, White Matter Integrity, and Oxygen Metabolic Stress in Young Adults With and Without Sickle Cell Trait.” She also interviews Dr. Timo Uphaus about his article “Revacept, an Inhibitor of Platelet Adhesion in Symptomatic Carotid Stenosis.” Dr. Negar Asdaghi:         Let's start with some questions. 1) Can performing multiple burrholes improve misery perfusion in patients with moyamoya disease? And if yes, how do the results compare to that of a direct EC-IC bypass surgery? 2) The glycoprotein VI antagonist Revacept provides lesion-directed thromboinhibition at the site of atherosclerotic plaque rupture without causing systemic platelet inhibition. In other words, it works where it should work without causing the systemic side effects of antiplatelet therapies. Is Revacept the future of carotid-related stroke treatment? 3) And finally, how should we counsel the family members of a patient with sickle cell anemia who are found to have sickle trait carrier state? Is sickle cell trait a risk factor for development of ischemic stroke?               We're back here with the Stroke Alert Podcast to answer these questions and cover the latest in Stroke because, without a doubt, this is the best in Stroke. Stay with us.               Welcome back to another issue of the Stroke Alert Podcast. My name is Negar Asdaghi. I'm an Associate Professor of Neurology at the University of Miami Miller School of Medicine, and your host for the monthly Stroke Alert Podcast.               For the September 2022 issue of Stroke, we have a number of articles that I'd like to highlight. As part of our International Stroke Early Career and Training section, or the InterSECT series, we have an important article by Drs. Kathryn Hayward and Aaron Davis to discuss the importance of science visualization as a simple, but not a simplistic way to improve scientific communications with the public.               The authors stress that the ability to communicate complex scientific information in an easily understandable format to those unfamiliar with the subject is not an obligation on the part of the scientists, rather, an opportunity for the scientific community to elevate knowledge translation for all.               In a separate article in this issue of the journal, we learned that the presence of early venous filling, or EVF, post-endovascular thrombectomy, defined as presence of contrast opacification of any cerebral vein before the late arterial phase, is an important angiographic marker that has been associated with an increased risk of post-reperfusion hemorrhage and worse clinical outcomes.               In an original contribution, Dr. Wagih Ben Hassen from the Department of Neuroradiology at Université de Paris and colleagues looked at the predictive ability of TAGE score to determine the odds of development of symptomatic intracerebral hemorrhage after thrombectomy. TAGE score, "T "for time from onset to successful recanalization of over 270 minutes, "A" for ASPECTS score either equal or less than five or ASPECTS of six to seven, "G" for blood glucose level of higher than seven millimole per liter, and "E" for EVF, or presence of early venous filling.               The authors found that presence of each of these variables within the TAGE score were independently associated with increased odds of post-thrombectomy symptomatic intracerebral hemorrhage, and together, a higher TAGE score had a great prognostic value in predicting development of reperfusion hemorrhage.               I encourage you to review these articles in detail in addition to listening to our podcast today. Later in the podcast, I have the great pleasure of interviewing Dr. Timo Uphaus from Johannes Gutenberg University in Mainz, Germany, on the results of a phase II clinical trial of symptomatic carotid stenosis patients treated with a novel glycoprotein VI inhibitor, Revacept. But first, with these two articles.               Bypass surgery is often performed for treatment of cerebral hypoperfusion, typically in the setting of chronic cerebral arteriopathies, such as moyamoya disease, moyamoya syndrome, or non-moyamoya steno-occlusive disorders causing perfusion-dependent ischemia.               In the adult population, the direct extracranial to intracranial bypass surgery, also referred to as EC-IC bypass, is the preferred procedure to improve cerebral perfusion as compared to all other currently performed indirect procedures.               This is for many reasons, but one being that direct bypass can immediately improve cerebral blood flow, whereas the indirect methods rely on gradual collateralization and new angiogenesis, a process that's not only slow, but especially in the adult population, is often suboptimal, even if we can wait.               On the other hand, a direct EC-IC bypass requires subspecialized surgical expertise in tertiary levels of stroke, neurosurgical, and neurointensive care, and the procedure could be challenging, especially if it's done in the setting of acute stroke where the patient is neurologically unstable.               Cranial multiple burrhole surgery is a minimally invasive procedure that was actually incidentally discovered to improve transcranial angiogenesis in moyamoya disease.               In 1984, a group of investigators from Japan reported their findings on a pediatric moyamoya case that had bilateral frontal burrholes for a completely different indication, which was drainage of an intraventricular hemorrhage, and three months later, unexpectedly, was found to have marked neurovascularization via the burrholes on the follow-up angiogram. Further experience over the next 30 years, mostly in children, would show that multiple burrholes truly have the potential to provide vascular ingrowth over the entire brain convexity in the ipsilateral hemisphere.               Now, how does this even work? Well, performing burrholes can simply break the barrier, so to speak, between the intracranial space, where there is misery perfusion for whatever the etiology, be Moyamoya or atherosclerotic disease, and the extracranial vascular system that's already overactivated in this setting, and breaking the barrier and disruption of the meninges can stimulate transdural collateralization. But we have to keep in mind that this is not a secure and robust transdural anastomosis that, for example, a direct bypass provides.               So, what do we know about the safety and efficacy of multiple burrhole surgery in the adult population? In this issue of the journal, Dr. Ji Man Hong from the Department of Neurology, School of Medicine, in Ajou University in South Korea and colleagues studied whether performing multiple burrholes, combined with high-dose systemic erythropoietin that's also known to enhance the angiogenetic potential of endothelial cells, improves cerebral perfusion in adult patients with perfusion-dependent acute ischemic stroke.               So, let's look at their study. This was a single-center, prospective, randomized trial, which included 42 patients enrolled within two weeks from their acute ischemic stroke from an intracranial steno-occlusive disorder causing hypoperfusion. The median age of patients was 55 years of age, and median NIH Stroke Scale was under five at presentation. So, this is truly an adult population, obviously, median age was over 50, and a mild stroke population as expected for a bypass cohort. 26% of their cohort had a diagnosis of moyamoya disease, and over 70% had other steno-occlusive disorders, most likely occlusions related to atherosclerosis, although this we cannot know for sure because the exact etiology was not specified in the paper.               Patients were randomized one-to-one to either receive multiple burrholes alone over the area of hemodynamic insufficiency under local anesthesia, or in combination with high-dose systemic erythropoietin, which was administered intravenously at 33,000 units per day for a total of a hundred thousand units administered over three consecutive days. So, everybody got surgery. The treatment group also got erythropoietin, and the control did not receive that. The two groups of patients were similar with regards to demographics, risk factors, stroke severity, and baseline perfusion parameters, and all received comparable stroke care. The primary outcome of the study was the rate of successful revascularization, which was determined on follow-up angiogram at six months.               So, now, on to their findings. So, number one, on their follow-up angio at six months, the combined multiple burrhole and erythropoietin patients had a higher percentage of successful hemispheric and trans-burrhole revascularization rates as compared to those who just had received multiple burrholes. But we have to note that when we look at the details, the rate of excellent revascularization that was defined as improved angiographic reperfusion in greater than 66% of the affected area was only achieved in a third of patients, and only in 23% of multiple burrholes cases alone. Close to half of patients who received both multiple burrholes and erythropoietin had either poor or fair revascularization, which was defined as improvement in angiographic perfusion in less than 33% of the affected area. So, obviously, these are important numbers and percentages to keep in mind as we try to understand the results of the study.               Next finding: In terms of perfusion imaging outcomes, the perfusion parameters were only available in half of their study population. On six months follow-up, the combined group had significant improvement in time-based perfusion parameters in the ipsilateral hemisphere. So, that included improvement in the mean transit time and time-to-peak maps, but not in the cerebral blood flow and cerebral blood volume maps.               Next, in terms of adverse events, there were no significant differences between the two groups in terms of risk of hemorrhage or infarct recurrence and other adverse events. However, in general, a number of important complications were noted in their study, including procedure-related brain hemorrhage in 14% of patients in the combined group and 14% systemic complications in the erythropoietin treated group, which again deserves further assessment.               And finally, I think one of the most important findings of the study was to evaluate serological biomarkers of angiogenesis, including matrix metalloproteinases 2 and 9, vascular endothelial growth factor, granulocyte colony stimulating factor, and interleukin 6. They compared these biomarkers at baseline and then remeasured them again at six months, and the most important finding was that the levels of MMP-9 were significantly increased in patients in whom successful revascularization was achieved, whereas these levels were similar at baseline if we went back and retrospectively divided the group into two groups of patients who would or would not receive successful revascularization at six months. MMP-9 is an important angiographic factor, but whether it can be used as a serological marker of complete revascularization remains to be seen.               So, in summary, what we learned from the study is that the combination of multiple burrholes and erythropoietin therapy is potentially efficacious and possibly safe, though both of these outcomes need further confirmation in larger studies for patients with moyamoya disease and other steno-occlusive disorders causing perfusion dependence. And, in general, it's fair to say that combined approaches in revascularization therapies, be using two indirect approaches, such as the method we just reviewed today, or perhaps combining direct bypass with an indirect approach, may improve the overall revascularization success in this population and may be the way to move forward in the future.               Sickle cell disease refers to an inherited group of hemoglobin disorders characterized by the presence of hemoglobin S either from homozygosity for the sickle mutation resulting in hemoglobin SS or compound heterozygosity with another beta-globin variant, for example, sickle beta thalassemia or hemoglobin SC disease. Now, as we know, even though this is a genetic hemoglobin problem, sickle cell disease creates a multi-system condition, and it's a major risk factor for stroke, with vaso-occlusive events accounting for much of its morbidity and mortality. Now, the question is, if sickle cell disease is a major risk factor for stroke, how about the much more common sickle cell trait carrier state? Sickle cell trait is about 20 times more common than sickle cell disease, is generally considered a benign condition, but some clinical events such as exercise-related injury, renal complications, and venous thromboembolism have been reported to occur more commonly in sickle trait carriers.               If sickle trait is, in fact, a risk factor for ischemia, then it's conceivable that there would be similar, but perhaps to a milder extent, neuroimaging findings of sickle cell disease in individuals with this carrier state. In this issue of the journal, in the study titled "Silent Infarcts, White Matter Integrity, and Oxygen Metabolic Stress in Young Adults With and Without Sickle Cell Trait," Drs. Yan Wang and Andria Ford from the Department of Neurology at Washington University School of Medicine and colleagues report on the results of a prospective multimodal MRI study to measure various cerebrovascular structures, hemodynamic, metabolic functions, and silent infarct burden in young adults with and without sickle cell trait.               So, the cohort composed of 49 healthy young adults without any known risk factors with either hemoglobin AA, which composed their control group with a total of 24 participants, or hemoglobin AS, which gave them their sickle trait cohort with 25 participants. The median age of their participants was 33 years of age, and the groups were matched in regards to age, sex, demographics, and baseline laboratory values, with the exception that the sickle trait group had a higher methemoglobin levels and creatinine concentration as compared to controls. All participants underwent various MR imaging, including ASL perfusion imaging with volumetric analysis and diffusion tensor imaging, and then they compared various values between control and sickle trait group.               Now, let's look at their findings. Number one, as compared to control, participants with the carrier state had similar normalized whole brain gray and white matter volumes. What does normalized volume mean? Well, volume normalization is done in volumetric analysis to adjust for differences in the head size between different participants. So, so far, so good. No differences in size of white or gray matter in those patients who are sickle cell trait carriers.               Next finding, using diffusion tensor imaging, they measured fractional anisotropy and mean diffusivity values for white matter tracts in both groups. Now, we've covered the meanings of fractional anisotropy and mean diffusivity in our podcast a number of times, but just a quick reminder. In general, when we have a structurally organized tissue, such as white matter tracts, the diffusion of hydrogen molecules is unidirectional in these tracts and, therefore, restricted in all other directions as white matter tract is intending to do so.               Now, if we have a disruption to these tracts, for whatever the etiology, we can simply think of this disruption, allowing hydrogen molecules to now freely diffuse in various directions. And this would result in an increase in mean diffusivity values that is determined by diffusion tensor imaging, and a decrease in fractional anisotropy values. And I really want to stress that this is a very simplified formula to understand the values of FA and mean diffusivity for just the white matter tracts. But the damages to the gray matter actually creates differences in FA and mean diffusivity that are a bit different than what I just mentioned for the white matter tracts. Now, we have to keep this in mind if we're reviewing articles that deal with damages to other structures in the brain than the white matter tracts. Now, coming back to our study, for this study, comparing the FA and mean diffusivity values for the white matter tracts, it turns out that these values were similar between those with sickle trait and controlled individuals. So, also good news.               Next, they examined regional white or gray matter or whole brain cerebral blood flow, oxygen extraction fraction, and cerebral metabolic oxygen demand, and similarly found no differences between control and healthy sickle trait carrier adults.               Next finding, in terms of intracranial vascular imaging, there were two asymptomatic aneurysms found in this study, one in each cohort, and they found no differences in the two groups in terms of the prevalence of significant cerebral vasculopathy, which means equal or greater than 50% intracranial stenosis in either groups. So, also very, very good news so far.               Finally, eight people in the control group and 11 people in the carrier group had evidence of silent cerebral ischemia. That is a high percentage. That means that the prevalence of silent ischemia was 33% in the control group versus 44% in the sickle trait group.               This was not statistically different. It's interesting that the authors mentioned that the prevalence of silent ischemia was low, but I think it's actually alarming if we have a cohort of patients with a median age of 33 and found that one in three of them actually have evidence of silent ischemia on neuroimaging. But the good news is that the volumes of these lesions were exceedingly small, under 0.2 mL on volumetric analysis, and not different in size between the two groups. But when they did the analysis restricted to those who had silent ischemia, it turns out that these silent, incidentally found ischemic lesions were ever so slightly larger in those with sickle trait, as compared to the control cohort. The median volume of incidental silent ischemic lesions was 0.29 mL in sickle trait individuals as compared to 0.07 mL in control. So, very small differences, which may or may not become meaningful in larger cohorts.               So, in summary, based on the best neuroimaging capabilities we have to date, we can conclude that unlike sickle cell disease, individuals with sickle trait do not seem to be at an accelerated risk of neurological injury if they are otherwise healthy. But we also have to keep in mind that somehow those incidental cerebral ischemic lesions were ever so slightly bigger in individuals with sickle trait than their control counterparts. And this finding also reminds us of other studies in the literature to suggest that sickle trait may not be a direct risk factor for ischemic stroke, but may be a modifier for increased ischemic risk. For example, in patients with diabetes, those with sickle trait have been found to be at a higher risk of ischemic events, or in the elderly population, individuals with APOE4 genotype have been shown to experience greater cognitive decline if they have sickle trait as compared to their age-matched individuals with the same genotype.               So, the take-home message is that sickle trait is a benign condition, but may be a modifier of brain injury if it's combined with something else or other risk factors. So, it's safe to say that, as always, prevention and treatment of these risk factors are paramount in all, but especially in sickle carrier individuals, to maintain brain health.               It's long been known that patients with carotid disease are at increased risk of first and recurrent ischemic events. The risk of carotid-associated ischemic stroke in each patient is dependent on a number of factors and traditionally predicted by two important pieces of information. Number one, the actual degree of carotid stenosis, and number two, whether or not that carotid artery has already caused an ischemic event, rendering them the designation of symptomatic as opposed to asymptomatic carotid disease. We've also known for some time now that in patients with symptomatic disease, the risk of recurrent stroke is up front. It's quite high, especially in the first two weeks after the index event. More recently, we've learned that there are other factors over and above the absolute degree of carotid stenosis that we should be paying attention to. Features such as plaque morphology, complex plaques with calcified segments of type of soft plaques, and the presence of intraluminal thrombi have all been associated with plaque instability. In these unstable or so-called "hot plaques," further embolization is thought to occur due to activation of circulating platelets by exposed collagen at the site of ruptured plaques.               The presence of microembolic signals, as detected by transcranial Doppler studies, can assist with identifying these active plaques. What is the best antithrombotic regimen in the very hyperacute stage after presentation with acute ischemic stroke? Some of these decisions will depend on the type of presenting symptoms and whether the patient had received acute reperfusion therapies or not, but in routine practice, some patients are treated with dual antiplatelet therapy. Some are on monotherapy alone, especially if there are plans for endarterectomy, and this, in part, is influenced by the surgeon's practice patterns and so on. And some patients are actually treated with anticoagulation either alone or in combination with concurrent antiplatelet therapies. And, of course, we also have the intravenously administered options, the glycoprotein IIb/IIIa inhibitors and the glycoprotein VI antagonists, with growing potentials for usage in the acute setting of ischemic stroke, which are likely more and more to be used in the hyperacute stage of stroke.               In this issue of the journal, in the study titled "Revacept, an Inhibitor of Platelet Adhesion in Symptomatic Carotid Stenosis," we learn about the role of Revacept, a glycoprotein VI antagonist, in patients with symptomatic carotid disease as part of a multicenter phase II randomized trial. I'm joined today by the first author of this randomized study, Dr. Timo Uphaus, all the way from Germany to learn about this newer class of antithrombotic agents and discuss the results of the trial. Dr. Uphaus is an Assistant Professor of Translational Neurology at the Johannes Gutenberg University in Mainz. He's one of the principal investigators of the Revacept randomized trial and is involved in multiple ongoing studies, including the prospective multi-centered German Stroke Registry to evaluate the safety and efficacy of endovascular thrombectomy in clinical practice and the prospective Gutenberg Stroke Study to evaluate biomarkers in patients undergoing endovascular therapy. Welcome to our podcast, Timo. Thank you so much for joining us. Dr. Timo Uphaus:            Great to be with you. Thanks for the invitation. Dr. Negar Asdaghi:         So, we'd like to learn more about Revacept first. How's this agent different from our usual antiplatelet agents? Dr. Timo Uphaus:            Oh, the mechanism of action of Revacept is quite unique, as you already mentioned. In contrast to available agents mediating inhibition of platelet activation in the whole circulation, Revacept is solely inhibiting platelet function really at the site of the plaque rupture. And this is achieved by shielding the exposed collagen after plaque rupture to the bloodstream so that platelets aren't able to be activated at this subendothelial exposed collagen.               And to really go in more mechanistic detail, Revacept is a fragment crystallizable region, also called FC fragment, fused to the glycoprotein VI, short GPVI receptor, which is an endogenous platelet collagen receptor. And this construct binds to the exposed collagen of unstable carotid plaque and acts as a physical barrier, reducing platelet activation, subsequent platelet binding, and aggregation on the carotid plaque. And this collagen-dependent, really, site-specific inhibition of platelet function might be as effective as available agents without side effects due to impairment of systemic platelet function, such as intracerebral hemorrhage. Concerning the administration route, Revacept is administered as an intravenous infusion of about 20 minutes, and, to go in more pharmacological details, Revacept exhibits a half-life of seven to 14 days and can also be administered several times in a row. Dr. Negar Asdaghi:         So, Timo, that's a lot of information, and I'm going to try to summarize it for our listeners. This is a very interesting drug as it works differently than our usual antithrombotics. It's a site-specific antiplatelet agent. So, as you mentioned, it is administered intravenously, but even though it's systemically administered, it goes right where the action is, to the so-called unstable plaque, and prevents the adhesion of platelets to the underlying exposed collagen. So, now, this agent is a newer therapy for us in the field of stroke, but it's not so new for cardiologists. Can you please briefly tell us about the cardiac literature and the current applications of Revacept in patients with, say, acute myocardial infarction or coronary artery disease? Dr. Timo Uphaus:            Well, we all know and experience that coronary and also carotid artery disease are commonly also linked in patients and can also occur simultaneously. And concerning the cardiac literature on Revacept, collagen-dependent platelet inhibition was recently also evaluated in patients with stable coronary artery disease undergoing elective PCI in the ISAR-PLASTER trial. And this was a phase II randomized clinical trial, including more than 300 patients who were allocated to receive either placebo or Revacept. And at the end, Revacept failed to show efficacy for the primary endpoint, which was a composite of death and also myocardial injury. Nonetheless, and this is an important point to mention, is that there were only few bleeding events within this trial and that there were no signs for increased bleeding rates after treatment with Revacept, which is always an issue when you're evaluating a new thrombocyte inhibition. Dr. Negar Asdaghi:         So, just to recap, this agent has been recently studied and as part of a randomized trial in patients undergoing PCI with active coronary disease, and even though the primary results of the ISAR-PLASTER trial was neutral in terms of efficacy, did show us a signal towards safety in terms of bleeding, which is important. So, there seems to be a lot of action happening in the cardiology world. Now, moving from heart to brain, what did we know about the efficacy of Revacept in stroke prior to the current trial? Dr. Timo Uphaus:            So, Revacept was really intensively studied in preclinical animal models, and these are also the basis for this trial now, phase II. And just to give you an example, what was studied in animal models so far, in animal model of a vascular atherosclerosis, Revacept dose twice weekly, over four weeks, was able to improve endothelial dysfunction and also vascular morphology on histology analyses. And importantly, within this study, no influence of Revacept on bleeding time alone, or also in combination with various antiplatelet drugs, could be observed. And another example is a study which made use of middle cerebral artery occlusion, and within this model, treatment with Revacept improved functional outcome, cerebral infarct size, and also edema formation compared to vehicle treatment. And Revacept also showed an effect on immune cell infiltration, which was demonstrated by reduced infiltration of macrophages within the CNS. Dr. Negar Asdaghi:         So, just to recap, there seems to be a lot of positive signal for efficacy of Revacept in patients with an active plaque rupture, whether from the coronary literature or the preclinical studies in stroke, which brings us nicely now to your current study. Please tell us what kinds of patients were included in your trial and the inclusion criteria. Dr. Timo Uphaus:            So, the Revacept/CS/02 study is, as we already mentioned, the first randomized trial examining GPVI inhibition in patients with stroke or symptomatic carotid artery disease as we did. And it is an international, randomized, placebo-control, double-blind, exploratory phase II study with three arm randomization and the treatment groups were placebo, 40 milligram Revacept, and also 120 milligram Revacept. So, we examined two treatment dosages. And who was enrolled in the study, in brief? 148 patients with recent symptomatic carotid artery disease were randomized to receive either high or low dose Revacept or placebo before they underwent then afterwards treatment of this ICA stenosis. It is important to mention that patient characteristics were balanced between these three treatment groups, and also that the treatment regimen was at the discretion of the treating physician, meaning the treatment regimen of the ICA stenosis, which could have been carotid endarterectomy, carotid angioplasty and stenting, and also best medical treatment.               And moving on to inclusion criteria, the initial symptoms qualifying for symptomatic carotid artery disease had to be within the last 30 days prior to screening. And the grading of the ICA stenosis had to be at least 50% according to ECST criteria. And what is some of our pitfall of the study is that the initial study design only included those patients presenting with detection of microembolic signals, which were detected by transcranial Doppler examination at the screening examination. But due to the low percentage of patients who presented with MES at screening, this protocol had to be changed, and all patients in whom transcranial Doppler was possible were then, after this protocol changed, eligible for participation within the study.               And what is the consequence of this protocol change? Well, that the primary efficacy endpoint of the study, which was reduction of microembolic signals after treatment, was no longer accessible, so that it was somehow switched to a number of new ischemic lesions on diffusion-weighted imaging and, therefore, the number of new DWI lesions detectable on MRI performed after the revascularization procedure compared to the MRI at screening served as new, now exploratory efficacy endpoint. And last, with regard to exclusion criteria, patients under dual antiplatelets or anticoagulation, or who received intravenous thrombolysis within the last 48 hours before screening, were eligible. Dr. Negar Asdaghi:         Okay. So, a lot of information again, so I'm going to try to recap it. And also some changes that had to be done during the trial administration, as is always the case for practical reasons. So, we have a trial of symptomatic carotid artery patients. Symptomatic carotid artery defined as percentage of stenosis over 50% in patients that had a relevant TIA or stroke in the past 30 days prior to enrollment, where patients were enrolled into three arms of either placebo or receiving 40 milligram or 120 milligram of Revacept over 20 minutes infusion. And, as you mentioned, just a note that initially the trial only enrolled patients that had a positive microembolic signal as detected by transcranial Doppler, but over the course of the randomization in the trial, this was changed to anyone that had a TCD emboli detection studied prior to randomization. So, with that, I think we're ready to hear about the primary outcomes of the study. Dr. Timo Uphaus:            Concerning this new exploratory efficacy end point, we were able to report a numerical reduction of new diffusion-weighted imaging lesions after treatment with 120 milligram Revacept. This effect was found to be significant within the main statistical analysis, which was a Poisson regression, but was not validated by respective sensitivity analysis, so that these findings at the end needs to be judged with caution. Nonetheless, we see a clear trend that number of new diffusion-weighted imaging lesions is decreased after treatment with 120 milligram Revacept.               And concerning clinical outcomes, we assessed the combined safety and efficacy endpoint, which includes occurrence of ischemic stroke, transient ischemic attack, hemorrhagic stroke, as well as myocardial infarction or necessary coronary intervention deaths and any bleeding complications. And for this combined safety and efficacy endpoint, we observed a 45% risk reduction of the treatment with 120 milligram Revacept compared to placebo treatment over the course of the study. And with a 66% risk reduction, this effect was even more pronounced than the subgroup of patients with more than 70% ICA stenosis. Dr. Negar Asdaghi:         All right. So, just to summarize, on the outcome of reduction of DWI positive lesions, there was a numeric reduction of the number of positive DWI lesions in patients that were enrolled to a higher dose of Revacept. That was not statistically significant in the Poisson regression analysis that you mentioned in the paper. So, this numeric reduction should be judged and needs to be further reevaluated in future studies, but obviously a very positive signal towards efficacy for Revacept. And the high dose Revacept seemed to reduce the combined primary safety and efficacy end points of the study, and that needs statistical analysis. So, very, very, very positive results. If I should say one more time, a very positive results for high dose Revacept in this study.               So, now, moving on, you have discussed a number of subgroup analyses that were pre-specified in the trial. Can you please briefly tell us what we learned from the subgroup analysis? I guess you already alluded to it, over 70% stenosis carotid disease, but I'll let you take away the question. Dr. Timo Uphaus:            Yeah, for sure. So, as you already mentioned, we analyzed subgroups, such as degree of ICA stenosis, prior statin treatment, and also different carotid interventions. And with regard to new diffusion-weighted imaging lesions on follow-up MRI, there were no effect of subgroups on the percentage of patients who suffered from new DWI lesions. However, the combined clinical safety and efficacy end point showed fewer outcome events after treatment with 120 milligram Revacept in the following subgroups: first, degree of ICA stenosis above 70%; second, patients with prior statin therapy; and last, but not least, patients undergoing carotid endarterectomy. Dr. Negar Asdaghi:         So, again, a lot of signal for efficacy of high dose Revacept in these subgroup analyses, specifically for those with a higher grade of stenosis, which are truly the subgroup of patients with carotid disease that are at higher risk of imminent recurrent ischemic events, so, those people at a lower combined safety and efficacy end point, so combined risk of TIA, stroke, hemorrhagic events, as you mentioned. And also there seems to be an improvement or reduction in the total primary outcomes in patients that had plans for endarterectomy. And the way I read it was perhaps that in routine practice, these patients were less likely to be aggressively treated with, for instance, dual antiplatelet therapy, so they really needed that additional push to try to prevent the number of recurrent events until such time that they get their surgical treatment. So, I think we are going to see a lot more in the future on studies of these particular subgroups of patients. Now, just to end the interview, we have two more questions for you, Timo. What should be our top two take-away messages from your study? Dr. Timo Uphaus:            So, I would say, take-home messages are, first, collagen-specific inhibition of GPVI through Revacept in patients with recently symptomatic carotid artery disease, in addition to standard of care medical treatment, is safe without any signs of increased bleeding rates. And second, Revacept showed a trend towards reduction of new ischemic lesions on diffusion-weighted MRI imaging, and altogether, I guess this paves the way for future phase III trials, not only in carotid artery disease, but probably in diseases with underlying rupture plaque embolization pathologies. And maybe I, at the end, I would add that change your primary efficacy endpoint wisely when you're studying a randomized trial. Dr. Negar Asdaghi:         Right? So, a lot of important comments that you made. Very important comment on the site-specific therapies. We are used to giving drugs either intravenously or orally that affects just about everything systemically, has a systemic effect. And many of the adverse events of the drugs that we currently administer are because of those systemic side effects. Here, we have a new therapy that is very site-specific, so it goes right where the problem is. And I think the future of medicine, in general, will be the usage of therapies with such site-specific properties. So, more of that in the future, I'm sure. And you already answered the next question, which was whether there will be a phase III trial for Revacept. So, we look forward to the results of that future randomized trial. So, with that, Dr. Timo Uphaus, it was a pleasure interviewing you on the podcast today. Dr. Timo Uphaus:            Thanks again for the invitation. It's been great talking to you. Dr. Negar Asdaghi:         Thank you.               And this concludes our podcast for the September 2022 issue of Stroke. Please be sure to check out this month's table of contents for the full list of publications, including our Literature Synopsis on the latest developments in reperfusion therapies, covering the results of the newly published AcT randomized trial with a head-to-head comparison of tenecteplase to alteplase in treatment of patients with acute ischemic stroke, to the results of the CHOICE trial on the effects of intra-arterial alteplase following successful thrombectomy. The synopsis is sure a great way to keep updated on the latest in the field.               And now, to end this podcast, I'd like to remind us that September 8 is the International Day of Literacy. Even today, though hard to believe, it's estimated that there are more than 750 million adults around the world who cannot read. Let's think about it for a second. Illiteracy impacts all aspects of life, but especially an individual's health. Studies have shown that people with inadequate literacy have less health-related knowledge, receive less preventative care, have poorer control of their chronic illnesses, and are hospitalized more frequently than others.               But most may not know that illiteracy can also be acquired. How can we lose our ability to read and write? This concept is, of course, far too familiar for stroke neurologists, as a variety of stroke syndromes can cause alexia with agraphia, the very literal acquired illiteracy. So, as the world of education gathers on September 8 to celebrate the basic human right to literacy, in the world of vascular neurology, we celebrate stroke prevention and the right to keep our ability to read and write. And, of course, there's no better way to do so than staying alert with Stroke Alert.               This program is copyright of the American Heart Association, 2022. The opinions expressed by speakers in this podcast are their own and not necessarily those of the editors or of the American Heart Association. For more, visit AHAjournals.org.

How would you feel if you were diagnosed with a life-threatening illness at the prime of your life? One minute you're at the top of the world, and the next thing you know, you're about to undergo two brain surgeries. Do you get bitter? Scared? No one could blame you if you did. Yet some people manage to see the silver lining and continue to appreciate life in any situation. That's the story we have for you today. Welcome to another episode of The Gift of Failure Podcast. Today's guest is Jennifer Lee, known professionally as TOKiMONSTA. She is a Korean-American record producer and DJ based in Los Angeles. While at the peak of her career, TOKiMONSTA was diagnosed with the debilitating disease Moyamoya, which affected her ability to speak, understand language, and make music. She then had two delicate surgeries and a tough time recovering. But she did it and came back stronger with more appreciation for life. Join us today as we discuss how to find strength and inspiration in a difficult situation. This episode will give you a glimpse into TOKiMONSTA's incredible battle with a rare brain disease and how the experience changed her. “If you listen to a song of mine and it touches you in some kind of way, there's some unspoken bond that we already have.” - TOKiMONSTA   In This Episode: - What does the word FAILURE mean to TOKi? - TOKi talks about her battle with the Moyamoya disease and its effect on her abilities as a musician. - How did TOKi find inspiration in life for the difficulties she had to endure every day while battling the disease? - What does TOKi define as SUCCESS? Would she see things differently if she didn't have the challenges of having a rare disease? - Is there a universal truth to the belief that every difficulty has a silver lining? What does TOKi have to say about this? - What's one thing TOKi wishes everyone knew about? And more… Connect with TOKiMONSTA: -https://tokimonsta.com/ ( Website) -https://www.instagram.com/tokimonsta/ ( Instagram) Connect with Ari: -https://rastegarproperty.com/ ( Website) - https://www.instagram.com/rastegar/ (Instagram) - https://web.facebook.com/rastegarproperty/ (Facebook) - https://www.linkedin.com/company/rastegarproperty/ (LinkedIn)

Summary This week we're joined by professional fighter and Moyamoya survivor, Vince Murdock. Vince has been handed a lot of setbacks in life: a Moyamoya diagnosis led to brain surgery, injuries dogged his career, and a car accident came out of nowhere. Others may have crumpled, but Vince proved his fighting spirit and came back from it all. You won't want to miss this episode as Vince shares parts of his tough childhood and how it has affected raising his son, and the group discusses the merits of alternative medicines, and fighting as universal language and art form. Episode Highlights

In this Point of Doo: Academy, Justin talks about his experience living with Moyamoya Disease. He explains how the disease presented in him, how he was diagnosed, and what treatment options were and are available. Finally, he talks about how his family began their venture in fundraising for Moyamoya Disease research, raising awareness for this rare condition, and how their efforts have directly led to medical advances in the diagnosis, care, and treatment of Moyamoya. https://www.cincinnatichildrens.org/health/m/moyamoya https://www.hopkinsmedicine.org/health/conditions-and-diseases/moyamoya-disease https://rarediseases.org/rare-diseases/moyamoya-disease/ https://www.childrenshospital.org/treatments/pial-synangiosis https://rarediseases.info.nih.gov/diseases/7064/moyamoya-disease http://www.moya-moya.com/ --- This episode is sponsored by · Anchor: The easiest way to make a podcast. https://anchor.fm/app --- Send in a voice message: https://anchor.fm/pointofdoo/message

In this Point of Doo: Academy, Justin talks about his experience living with Moyamoya Disease. He explains how the disease presented in him, how he was diagnosed, and what treatment options were and are available. Finally, he talks about how his family began their venture in fundraising for Moyamoya Disease research, raising awareness for this rare condition, and how their efforts have directly led to medical advances in the diagnosis, care, and treatment of Moyamoya. https://www.cincinnatichildrens.org/health/m/moyamoya https://www.hopkinsmedicine.org/health/conditions-and-diseases/moyamoya-disease https://rarediseases.org/rare-diseases/moyamoya-disease/ https://www.childrenshospital.org/treatments/pial-synangiosis https://rarediseases.info.nih.gov/diseases/7064/moyamoya-disease http://www.moya-moya.com/ --- This episode is sponsored by · Anchor: The easiest way to make a podcast. https://anchor.fm/app --- Send in a voice message: https://anchor.fm/pointofdoo/message

Melbourne’s own character comedian and social media sensation, Ibby Akbar is returning to the stage for a very special encore performance on Thursday, 26 May at the Palais Theatre presented by The Hour Group! Ibby has created a cult following with over 200k fans and boasts over 50M views across his social media platforms, He recently took Australia by storm with his debut live comedy show ‘I Am’ selling out 10 capital city shows around the country. With the election approaching, how would Ibby go about getting your vote? Listen to this episode and discover his "Top 5 Election Issues" with Byron and Perri Lee. Ibby is returning to the stage in his beloved hometown for a final encore performance with all proceeds from the show being donated to the MoyaMoya Charity. The charity is very close to Ibby’s heart, his sister has been personally affected by the MoyaMoya disease. Please join The Byron Cooke Show team at this show - we will all be going! Get your tickets at https://www.ibbyakbar.com/tourSee omnystudio.com/listener for privacy information.

¿Qué es la enfermedad de MoyaMoya? ¿Qué implicaciones puede tener en escolares y en el aprendizaje? En este episodio te contamos algunos aspectos que debes tener en cuenta.

On Episode 15 of the Stroke Alert Podcast, host Dr. Negar Asdaghi highlights two articles from the April 2022 issue of Stroke: “Kawasaki Disease May Increase the Risk of Subsequent Cerebrovascular Disease” and “Effect of Moderate and Severe Persistent Hyperglycemia on Outcomes in Patients With Intracerebral Hemorrhage.” She also interviews Dr. François Gros-Louis about his article “Moyamoya Disease Susceptibility Gene RNF213 Regulates Endothelial Barrier Function.” Dr. Negar Asdaghi:                        1) How would you counsel the parent of a child who has just recovered from Kawasaki disease on their child's future risk of having a stroke? 2) Should we or should we not treat stress hyperglycemia in the setting of acute intracerebral hemorrhage? 3) What is the CRISPR-Cas9 gene editing technology? And why, if you haven't heard of it already, you most definitely should be listening to this podcast? We're back here with the April issue of the Stroke Alert Podcast, and this is the latest in Stroke. Stay with us. Dr. Negar Asdaghi:                        Welcome back to another extremely informative Stroke Alert Podcast. My name is Negar Asdaghi. I'm an Associate Professor of Neurology at the University of Miami Miller School of Medicine, and your host for the monthly Stroke Alert Podcast. The April 2022 issue of Stroke contains a range of really exciting papers and topics. In the paper titled "Vascular Response to Spreading Depolarization Predicts Stroke Outcome," we have a really interesting in vivo mouse model of ischemic stroke, looking at the spreading patterns of cortical depolarization and the subsequent vascular response to this by way of hyperemia. The researchers from Zurich University, led by Dr. Binder and colleagues, walk us through how the patterns of hyperemia can actually predict the severity of subsequent ischemic injury. Dr. Negar Asdaghi:                        In a separate paper in this issue of the journal, we're reminded of how the classic NIH Stroke Scale can underestimate the severity of neurological symptoms and outcomes in patients with posterior circulation infarcts. In the paper led by Dr. Alemseged and colleagues, the investigators from the Royal Melbourne Hospital in Australia evaluate the prognostic accuracy of the Posterior NIH Stroke Scale, which is the modified version of the classic NIH Stroke Scale, in predicting the outcomes of patients with posterior circulation infarcts. Dr. Negar Asdaghi:                        I encourage you to review these papers in addition to listening to our podcast today. Later in the podcast, I have the great pleasure of interviewing Dr. François Gros-Louis from Laval University in Quebec to discuss the latest in gene editing technology and how this technology has helped his team unravel the biological function of RNF213 susceptibility gene in Moyamoya disease. But first with these two articles. Dr. Negar Asdaghi:                        Kawasaki disease, which was first described in 1976, is an acute febrile illness predominantly affecting children younger than five years of age. In addition to fever, other clinical signs of the disease include rash, bilateral conjunctival injection, cervical lymphadenopathy, swelling of the hands and feet, and irritation and inflammation of the mouth, lips, and throat. Now, for those of us like me who are adult neurologists, here is a quick review of the pathophysiology of Kawasaki disease. Dr. Negar Asdaghi:                        This is a medium vessel vasculopathy, most significantly affecting the coronary arteries, a vasculopathy that is characterized by three linked pathological processes, necrotizing arteritis, subacute to chronic vasculitis, and luminal myofibroblastic proliferation. So, simply put, these processes can lead to stenotic lesions in various vascular beds, which are affected by this disease. Dr. Negar Asdaghi:                        And as we mentioned earlier, the most recognized vascular blood vessels affected by Kawasaki disease are the coronary arteries, which can lead to myocardial ischemia, infarction, and sudden death in these cases. However, involvement of other vascular beds, including cerebral vessels, are also increasingly reported as part of Kawasaki disease. Dr. Negar Asdaghi:                        So, in the current issue of the journal, Dr. Chien-Heng Lin from the Division of Pediatric Pulmonology at China Medical University Children's Hospital in Taiwan and colleagues studied the subsequent risk of cerebrovascular events in patients with Kawasaki disease. Using the National Health Insurance Research Database of Taiwan, they collected data on 8467 children with Kawasaki disease from 2000 to 2012. And for each child with Kawasaki, data was also collected on four randomly selected non-Kawasaki disease children who were matched with the Kawasaki cohort for sex, urbanization level of residence, and parental occupation. Dr. Negar Asdaghi:                        So, that gave them a sample size of over 33,000 children for their non-Kawasaki cohort. And then they compared the risk of subsequent stroke in children between the two cohorts. The study period for any given patient would end when the said patient was either diagnosed with a cerebrovascular disease or withdrew from the research database. Dr. Negar Asdaghi:                        So, in terms of their demographics, 61% of patients in the Kawasaki group were boys; 88% of the Kawasaki cohort were younger than five years of age. So, here are the findings. Number one, the incident rate of subsequent cerebrovascular disease was 14.7 per hundred thousand person years in the Kawasaki cohort versus only 4.6 per hundred thousand person years in the non-Kawasaki cohort. That's greater than a threefold higher incidence rate of cerebrovascular disorders for children who had Kawasaki disease before. Dr. Negar Asdaghi:                        This finding was independent of other potential confounders, which they adjusted for in their multivariate analysis. Now, the length of follow up was a median of 9.8 years for the entire cohort. And on the issue of time, they found two important associations. The first finding was that when the follow-up time was stratified by five-year periods, Kawasaki disease cohort patients showed a significantly higher risk of developing a stroke within the first five years after being diagnosed. Dr. Negar Asdaghi:                        And the second important association was that when they looked at the age at the time of diagnosis of Kawasaki, children who were younger than five years at the time of diagnosis were at a significantly higher risk of having a future stroke as compared to those who were older than five at the time of diagnosis. Dr. Negar Asdaghi:                        So, simply put, the risk of subsequent stroke was higher in children who acquired the disease at a younger age, and that risk was higher in the first few years after the diagnosis of Kawasaki disease. The authors discuss a number of putative mechanisms to link Kawasaki with stroke. The most important being a cardiac source of embolism that we already alluded to, but other etiologies, including medium vessel cerebral vasculitis, or hypercoagulability in the setting of increased systemic inflammation, and even Kawasaki disease-associated aneurysmal rupture to cause hemorrhagic forms of stroke, are discussed in the paper and should be considered in the correct setting in children with a prior history of this disease. Dr. Negar Asdaghi:                        So, what we learned from this large population-based pediatric study is that Kawasaki disease does indeed increase the risk of subsequent cerebrovascular disorders, and its influence is stronger in children who are diagnosed with this condition under the age of five, and the time period during which the risk of stroke is the highest is within the first five years after the diagnosis. Dr. Negar Asdaghi:                        In the setting of spontaneous intracerebral hemorrhage, or ICH, much research has focused on the association between hypertension and blood pressure-lowering therapies and hematoma expansion and functional outcomes, but a lot less attention relatively has been given to the impact of hyperglycemia and ICH-related outcomes. Dr. Negar Asdaghi:                        The current guidelines state that serum glucose should be monitored and both hypo- and hyperglycemia should be avoided in the setting of ICH. The older studies have given us inconsistent results as to whether or not hyperglycemia can increase the risk of ICH-related mortality. More recent studies have suggested that perhaps persistent hyperglycemia is indeed a predictor of poor neurological outcomes in ICH, but these results come from smaller single-center studies, which require further confirmation. And this confirmation is exactly what Dr. Adnan Qureshi from Zeenat Qureshi Stroke Institute and the Department of Neurology at University of Missouri and colleagues aim to give us in their study titled "Effect of Moderate and Severe Persistent Hyperglycemia on Outcomes in Patients With Intracerebral Hemorrhage." Dr. Negar Asdaghi:                        So, they use data from the ATACH-2 study, and a quick reminder that ATACH-2 was a multicenter randomized control trial of a thousand patients with acute spontaneous intracerebral hemorrhage enrolled within four and a half hours from symptom onset, and patients were randomized to either the intensive blood pressure control treatment arm to maintain their systolic blood pressure goal of 110 to 139 millimeter of mercury versus standard treatment arm, which was keeping their systolic blood pressure above 140, between 140 to 179 millimeter of mercury, in the first 24 hours after randomization. Dr. Negar Asdaghi:                        You will recall that enrollment of ATACH-2 was stopped early because of futility after pre-specified interim analysis. The main results of the trial was published in 2016 in New England Journal of Medicine, and the primary results did not show a lower rate of death or disability in patients assigned to the intensive treatment group. Dr. Negar Asdaghi:                        So, in the current paper, in this current issue of the journal, the authors looked at the glycemic status of the patients enrolled in the trial. As part of the trial, patients had a complete chemistry panel at baseline, 24, 48, and 72 hours from onset. So, they used the glucose measurement from this panel and defined moderate hyperglycemia as serum glucose level of over 140 and under 180 and severe hyperglycemia as serum glucose levels of equal or greater than 180. Dr. Negar Asdaghi:                        Now, persistent hyperglycemia was if two consecutive serum glucose levels were in the moderate or severe categories. And, very simply, they looked at the effects of hyperglycemia on ICH outcomes. And importantly, they evaluated whether hyperglycemia modified the effects of intensive blood pressure reduction on outcomes of ICH. So, of the thousand participants in ATACH-2, 11% had persistent moderate hyperglycemia, and 17% had severe persistent hyperglycemia. Those in the hyperglycemic group were more likely to be diabetic, not surprisingly, more likely to have a history of hypertension and dyslipidemia as compared to the normal glycemic patients. Dr. Negar Asdaghi:                        And here are the results. Number one, serious adverse events were higher in the hyperglycemic groups, whether we're talking about the moderate or the severe hyperglycemic groups. This is despite the fact that the rate of hematoma expansion and perihematomal edema was not different based on the hyperglycemic status. However, the hyperglycemic patients were more likely to have serious adverse events, which were operationally defined as complications that were not expected to have occurred from the study intervention, in this case, the intensive hypertensive therapy, and resulted in either death or prolonged hospitalization or persistent or significant disabilities. Now, serious renal adverse events, which are, of course, expected as a complication for aggressive blood pressure therapy, were also significantly higher in the hyperglycemic category. Dr. Negar Asdaghi:                        Now, their next important finding was that overall, both moderate and severe hyperglycemia was associated with higher odds of 90 days disability or death post-ICH adjusting for typical variables that could predict these outcomes, such as GCS score, hematoma volume, presence or absence of intraventricular hemorrhage, amongst other factors that they accounted for. Dr. Negar Asdaghi:                        Now, number three, this is perhaps the most important finding of the study. Among patients without a preexisting history of diabetes, both moderate and severe hyperglycemia increased the risk of death and disability at 90 days after adjusting for all the potential confounders, but hyperglycemia was not associated with these poor outcomes in those with a prior history of diabetes. I'm going to pause here to let this information sink in. Let's go over them again, stress hyperglycemia in non-diabetics was associated with poor ICH outcomes, but high sugars in diabetics did not predict the same poor outcomes. And finally, they looked at the possible interactions between the glycemic status and the ATACH-2 intervention, which as we alluded to earlier, which was intensive versus standard blood pressure therapy, and it turns out that the intensive systolic blood pressure reduction was indeed associated with a lower rate of hematoma expansion only in patients with normal glycemia, but not in those with moderate or severe hyperglycemia. Dr. Negar Asdaghi:                        So, this is again food for thought. Simply put, if the sugars are not well controlled, it appears that intensive blood pressure control would not lower the rate of hematoma expansion. Blood pressure lowering works when the sugar levels are controlled. So, overall, here are the two simple messages of this study. Number one, hyperglycemia in the acute setting of intracerebral hemorrhage is associated with poor outcomes or death only in those with stress hyperglycemia, meaning in those who have high sugar levels, but are not diabetic. Dr. Negar Asdaghi:                        Number two, there seems to be an important interaction between the acute glycemic status of the patients and how intensive blood pressure control can prevent hematoma expansion, in that intensive BP control is only effective in prevention of hematoma expansion if the sugar levels are normal. So, a lot of thought-provoking and hypothesis-generating findings, and definitely more to come on this topic. Dr. Negar Asdaghi:                        Moyamoya disease, or MMD, is an idiopathic disorder characterized by progressive stenosis of the supraclinoid internal carotid artery and its main branches in subsequent formation of a network of abnormal lenticulostriate collaterals. First described in Japan, the term "Moyamoya" is a Japanese expression for the puff of smoke and describes the characteristic appearance of the tangled and abnormal collateral vessels that are seen in angiography in various stages of the Moyamoya disease. Dr. Negar Asdaghi:                        Epidemiological studies have revealed several risk factors associated with Moyamoya disease, including Asian ethnicity, female gender, and a family history of the disorder. Given that 15% of MMD patients have a family history of this disease, it's not surprising that genetic factors are suspected to underlie its pathogenesis. Now, a polymorphism in the ring finger protein 213, or RNF213, gene on chromosome 17 has been identified as the strongest genetic susceptibility factor for Moyamoya disease specifically in the East Asian population. Dr. Negar Asdaghi:                        But despite the many advances in understanding the pathophysiology of MMD, as well as advances in animal models and genetic studies, to date, none of the animal models of RNF213 have quite replicated the vascular abnormalities that are typically seen in human Moyamoya disease. Dr. Negar Asdaghi:                        The scientists feel that this is related to how little is known about the exact biological function of RNF213 gene and the protein it encodes. So, in the current issue of the journal, in the study titled "Moyamoya Disease Susceptibility Gene RNF213 Regulates Endothelial Barrier Function," Dr. François Gros-Louis from CHU de Québec Research Center at Laval University in Québec and colleagues aim to study the biological functions of RNF213 using a novel genome editing technology by the name of CRISPR-Cas9 technology. Dr. Negar Asdaghi:                        Joining me now is Dr. Gros-Louis himself to discuss the findings of this paper. Dr. Gros-Louis is a Professor of Neurosciences at the Department of Surgery at Laval University. He holds the Canada Research Chair in Brain Disease Modeling and is the Director of the Induced Pluripotent Stem Cell Platform research in Québec. Dr. Negar Asdaghi:                        Good morning, François. Welcome to our podcast. And thank you so much for joining us. Dr. François Gros-Louis:               My pleasure. Dr. Negar Asdaghi:                        François, you have to promise to hold my clinician's hand through this interview as obviously these are some foreign subjects for us, but very excited to learn from your study and learn from you on the association between RNF213 and the pathophysiology of what happens in Moyamoya disease. Now, before we talk about your paper, can you please talk to us about some basic concepts? What is the RNF213 protein? Dr. François Gros-Louis:               Yes. The RNF213 gene is thought to be involved in mediating protein, protein interactions. The protein also contains a domain which is associated with an ATPase activity. This gene is a susceptibility gene for Moyamoya disease, as you mentioned in the introduction, vascular disorder of intracranial arteries. It's encoded in ubiquitously expressed protein. The protein is found to be expressed throughout the cytocell with the partial association in the intracellular membrane and cytoskeleton. Its expression varies according to the tested tissue type or location or cellular types. Dr. François Gros-Louis:               Although the function of RNF213 protein is unknown, studies suggest that it plays a role in the proper development of blood vessels, cell proliferation, and inflammation. Recently, RNF213 has been reported to be associated with angiogenesis. However, little is known about its endogenous function or its pathogenic role in Moyamoya disease. Our results are in line with these results and indicate that RNF213 could also be a key regulator of cerebral endothelial integrity, whose disruption could be an early pathological mechanism leading to Moyamoya disease. Dr. Negar Asdaghi:                        So, just to continue on this, there's quite a bit of research already done on association of the RNF213 gene, that's located, as we noted earlier, on chromosome 17, and basically susceptibility of development of Moyamoya disease. Can you give our listeners a brief overview of this genetic connections and what was known from past research? Dr. François Gros-Louis:               Yeah, there is a couple polymorphism describing this gene, the most frequent, the most prevalent genetic study have identified the variant R4810K, meaning for arginine is replaced by another amino acid at the position of 4810 within the protein. It's a large protein and a large gene and a susceptible gene and a risk factor for developing Moyamoya disease. Dr. François Gros-Louis:               So, people bearing this variant have a higher chance to develop the disease. This is a loss of function variant, also called inactivating mutation, meaning that the mutated gene product have less or no function. So, this variant is found in heterozygous, meaning one copy, or two copy homozygous in Moyamoya disease patients. While patient bearing homozygous mutation develop a more severe disease with earlier age of onset and worse prognosis, patients bearing heterozygous mutation can also develop the disease. Dr. François Gros-Louis:               So, strong evidence suggests that the carrying rate of RNF213 R4810K mutant is closely related and give a higher chance to develop the disease. Interestingly, also with colleagues, we found that there are other variants within this genes leading to what we think is a gain of function mutation have been associated also with other cerebrovascular disease, such as intracranial aneurysms. Dr. Negar Asdaghi:                        So, François, this is very interesting. Let me recap what you mentioned so I know that I understood it. So, this is an interesting gene, this RNF213, and basically evidence shows that mutations in the RNF213, whether it's loss of function or gain of function, both can result in variety of cerebrovascular disorders. And interestingly, the phenotype of the disease when it comes to loss of function of this gene is actually correlated with whether a person is a carrier, homozygous carrier of this gene, loss of function, or heterozygous carrier of the gene. Dr. Negar Asdaghi:                        So, very interesting information for clinicians who treat patients with Moyamoya disease, specifically those who have a family history of Moyamoya disease, so perhaps a higher chance of carrying a genetic susceptibility gene. Now, we want to get to the paper that you published in this issue of the journal, but I think before we talk about your paper, we also have to have a basic understanding of this CRISPR-Cas9 technology, which is the new genome editing technology that you use in your experiments. Can you please give us a little bit of an overview of this technology? Dr. François Gros-Louis:               Yes. CRISPR-Cas9 gene editing is genetic engineering technique in molecular biology by which the genomes of living organisms may be modified. This technology allows genetic material to be added, removed, or altered at particular location in the genome. Several approaches to genome editing have been developed. Recent one is known as CRISPR-Cas9. So, the CRISPR-Cas9 system has generated a lot of excitement in the scientific community because it is faster, cheaper, and more accurate, and also more efficient than other existing genome editing methods. It's clearly revolutionizing the field in research. Dr. Negar Asdaghi:                        So, it's very exciting. It's truly a new chapter in gene targeting research and editing research. So, now we're ready to hear about your study. And I guess the first part of the study was just to look at how various cells in vitro that you used had expressed RNF213. Can you please tell us about the first part of your experiments? Dr. François Gros-Louis:               Yeah. We first wanted to know where the protein is expressed or where the protein is more highly expressed. So, we found by doing immunofluorescence analysis that the RNF213, so we confirmed that it's ubiquitously expressed in the cytoplasm of different cellular types. So, we found that significant difference also in the expression of RNF213 protein levels in several endothelial cells, where we found it's been highly expressed when compared to other endothelial cells isolated from different other body location, meaning outside of the CNS. So, it's highly expressed also when compared to smooth muscle cells or fibroblasts. Dr. Negar Asdaghi:                        Okay. So, just again, to recap for our listeners, this is, this RNF213 protein, is ubiquitously expressed in many different cell types, but you did find a significantly higher expression rates in endothelial cells, specifically those endothelial cells that were derived from cerebrovasculature. So, that's the first exciting part of the experiments that you showed in the study. Now, using the CRISPR-Cas9 technology, you and your team were able to successfully create an in vitro RNF213 knockout model. Can you please tell us about these models and also the main findings of your study? Dr. François Gros-Louis:               Yeah, so taken together, the results we presented in the article indicate that RNF213 could be a key regulator of cerebral, endothelial and tight junctions integrity whose disruption could be an early pathological mechanisms leading to Moyamoya disease. So, we established for the first time an easily reproducible and stable in vitro 3D model generated using the CRISPR-Cas9 gene editing technology. Dr. François Gros-Louis:               This advanced 3D culture approach has emerged as an excellent system to recapitulate histopathological feature reminiscent to disease pathogenesis. So, 3D cell culture approach is different from standard 2D culture, where cells are cultured, monolayered into a Petri dish. And we have results showing that the 3D cell culture system better mimic the in vivo conditions in terms of cell to cell and cell to matrix interaction and lead to histopathological phenotypic feature can be observed in cell culture, in a 3D fashion. Quite interestingly, alongside of providing the first evidence for the role of RNF213, the maintenance of endothelial barrier and the potential implication of this gene in the expression of maturation of tight junctions. So, we define a novel role for PECAM-1 as well in barrier impairment as a part of the disease pathogenic mechanisms. Dr. Negar Asdaghi:                        Okay. And now this is really interesting. So, I wanted to, again, recap some of the important points that you raised here. First of all, your in vitro models are different than the classic in vitro models, where 2D cells were basically grown in a Petri dish. You are trying to, more and more, replicating what happens, for instance, in blood vessels, where you have endothelial cells overlying mesenchymal cells underneath them, so tunica intima and then tunica media, and so you have 3D cells, where various types of cells are overlying each other in a more in vivo representation of what happens in blood vessels, which is truly interesting. Dr. Negar Asdaghi:                        And what you found was, in sort of summary, was that these knockout endothelial cells ended up having abnormal tight junctions and abnormal connectivity, which basically would lead in an in vivo model to abnormal leaky blood brain barrier, if this were truly in the in vivo model. Does that summarize the findings of the paper? Dr. François Gros-Louis:               Yes, perfectly. Dr. Negar Asdaghi:                        Perfect. And so I want to also give us a chance to talk about the important pro-inflammatory aspects of these knockout cells. You did find that a number of cytokines were expressed in excess in those RNF213 deficient cells. Can you please elaborate on those findings? Dr. François Gros-Louis:               So, to further investigate whether inflammation plays an important role in RNF213-associated Moyamoya disease development, we indeed performed experiments to study pro-inflammatory cytokines and analyze the immune secretome profiles of cerebral RNF213 deficient endothelial cells. So, then the cells can secrete different cytokines or different other proteins. So, by analyzing the secretome, we found an end secretion of a few pro-inflammatory cytokines indicating that inflammation may also play a central role in the initiation of the immune response in the pathogenesis of the disease. Dr. Negar Asdaghi:                        So, this is exciting, François. For years, we thought about the pathophysiology of Moyamoya disease as a disorder involving large vessels. And perhaps the initial thought was that it starts with excessive proliferation of smooth muscles within the middle layer of the cerebral blood vessels, in tunica media, and then perhaps subsequently there will be other abnormalities, including the intimal hyperplasia that is classically seen in Moyamoya. Dr. Negar Asdaghi:                        Your study seems to propose a shift in that pathophysiological paradigm, where the problem seems to start from endothelial cells, so inside of the blood vessels and the tunica intima, and then gradually would go out to the middle layers, and, of course, proposes the hyperinflammatory state in the Moyamoya disease as well. So truly interesting. Do you think that that is the new or rather a paradigm shift for pathophysiology of MMD? Dr. François Gros-Louis:               That's a great question. Our results certainly demonstrated that endothelial cells are involving in the disease pathogenesis in Moyamoya disease, but it doesn't exclude the possibility that other cell types might also be involved in the disease pathogenesis. We know, like you mentioned, that a blood vessel is formed by two different cell layers, tunica intima, media, and adventitia, containing, respectively, endothelial cells, smooth muscle cells, and fibroblasts. So which cells are to be blamed in Moyamoya disease is a question of many ongoing results studies over the years. Dr. François Gros-Louis:               So, using tissue-engineered approach to reconstruct small caliber blood vessels, as we developed in my lab, in combination with patient-derived stem cells, in which adult cells isolated from a patient of any individuals can be reprogrammed into stem cells and re-differentiated into different cell types in occurrence, smooth muscle, fibroblasts, or endothelial cells. We would like to generate blood vessels in which each of the different cellular layers will harbor or not, or a combination with RNF213 mutants. So, this will hopefully help us to elucidate this question. Dr. Negar Asdaghi:                        That's perfect. So, François, before we end the interview, I wanted to ask two more questions. So, what should be our top two takeaway messages from your study? Dr. François Gros-Louis:               We believe that the innovative transdisciplinary approach to generate, for the first time, as we describe in the article, an in vitro 3D model recapitulating important diseases features. So, this model could become a unique tool in precision medicine to study Moyamoya disease or other RNF213-associated pathologies. So, our study provides, for the first time, role of RNF213 in the maintenance of blood-brain barrier and the potential implication of RNF213 in the expression and maturation of tight junctions. Taken together, our data define a novel role for PECAM-1 in the blood-brain barrier impairment in Moyamoya disease. Dr. François Gros-Louis:               So, better characterization of each, also this regulated inflammatory molecules, we found taken separately could reveal a crucial information and help elaborate a more precise approach. Hence, this pro-inflammatory signature could be used as a circulatory biomarker for the follow-up of Moyamoya disease patients and to manage an appropriate treatment, according to the pathology progression. Dr. Negar Asdaghi:                        François, this is great. And last, I want to digress a little bit and ask you about the future of gene editing. I think it's important to end our interview with a little bit of a discussion regarding the future of CRISPR-Cas9 technology. In subatomic quantum physics, people talk about the God particles. And I feel that the CRISPR-Cas9 technology is, in a way, like playing God, if you agree. What do you think is the future for gene editing, and how do you see that helping us in terms of treatment of genetic causes of cerebrovascular disorders? Dr. François Gros-Louis:               Yes, gene editing is, like I said, revolutionizing, of course, experimental therapies for genetic disorder and generated excitement for new and improved gene therapies. We can think that it will be possible to correct any gene mutations associated with a disease to reestablish the normal or natural gene function and help treating the targeted diseases. But also, to me, the future of genome editing also resides in optimizing next generation disease models. The use of genome editing, in particular, the CRISPR-Cas9 technology, has extended to potential in generating new personalized model for a number of disorder, not only including Moyamoya disease or other cerebrovascular diseases, but also diseases like Alzheimer's, ALS, or Parkinson's disease, for which obtaining patient sample is difficult. Dr. François Gros-Louis:               No one wants to give up a bit of his brain. So modeling it, this disease, in vitro will be really helpful in combination also gene editing with the stem cells, induced pluripotent stem cells technology, will allow the generation of better model to mimic human disease and reflects the genetic drivers that govern specific pathology. So, the synergy between IPS cell-based model system and gene editing will play a pivotal role in the root of precision medicine and clinical translation in the future. Dr. Negar Asdaghi:                        Dr. François Gros-Louis, it was a pleasure learning from you. And we look forward to the endless possibilities brought by the future of genome editing technology. Dr. François Gros-Louis:               It was a pleasure discussing with you. Dr. Negar Asdaghi:                        Thank you for joining us. Dr. Negar Asdaghi:                        And this concludes our podcast for the April 2022 issue of Stroke. Please be sure to check out this month's table of contents for the full list of publications, including a series of Focused Updates on the topic of blood pressure management in stroke, organized by Dr. Else Sandset. I would also like to draw your attention to two scientific statements from the American Heart Association, which appear in print in the April issue. The first one is titled "Identifying Best Practices to Improve Evaluation and Management of In-Hospital Stroke," and the second one is on the effect of marijuana use on brain health. Dr. Negar Asdaghi:                        And now, to end our podcast, last month, in honor of the 2022 Olympic Games, and to celebrate those with determination to survive and push despite the most difficult of circumstances, we ended our podcast with the story of a refugee Olympic athlete. Dr. Negar Asdaghi:                        Sadly, since our last podcast, the world has seen even darker days of war, mass immigration, displacement, and human suffering. At times like this, we're reminded that although not all of us can help everyone, but at least each of us can do something to help someone, and the comfort in knowing that what we do in the field of medicine, from daily patient care to the scientific work leading to the next medical breakthrough, every action is a step forward in reducing the suffering of another person. And what better way to do this than staying alert with Stroke Alert. Dr. Negar Asdaghi:         This program is copyright of the American Heart Association, 2022. The opinions expressed by speakers in this podcast are their own and not necessarily those of the editors or of the American Heart Association. For more, visit AHAjournals.org.

Sarah Lippett spent eleven years suffering with symptoms from an unknown condition, until she was diagnosed with the rare disease, Moyamoya, at the age of 17. In November 2019 she published her beautiful graphic memoir, A Puff of Smoke, which tells her story using the power of the sequential narrative. Here's a throwback to Lucy's interview with her ahead of the launch. Once you've finished listening watch the follow up video 'Living With It' about what life is like after diagnosis. Sarah spoke to Lucy while shielding in her flat in Edinburgh during the first UK lockdown. She talks about the pandemic and her kidney disease relapse.https://www.youtube.com/watch?v=6m-vSThMtjk&t=1sSarah's website: http://www.crayonlegs.com/When Lucy and Sarah were featured on Woman's Hour: https://www.bbc.co.uk/food/programmes/m000b4whThank you Sarah for being interviewed and Kate Allnutt for doing the editing of my very first interview - Lucy xox

Local boy Jed has been fighting rare brain disease Moyamoya his entire life and this weekend he turns 18! Skypark Cairns are doing $99 bungy and giant swings this Saturday, with $50 from every jump or swing  donated to Moyamoya Australia in Jed's honour.  See omnystudio.com/listener for privacy information.

On this episode of "Behind Diagnoses: Patients", a Peer Med Podcast special series we hear from Sarah Lippett, a UK based artist and author. Her first graphic novel, Stan and Nan, won the Quentin Blake Prize for Best Narrative at the Royal College of Art and was published in 2016 by Jonathan Cape, becoming a Guardian bestseller and 2016 Book of the Year.  Her latest autobiographical work, A Puff of Smoke was published by Jonathan Cape in November 2019 and was supported by an Arts Council England Literary grant. The memoir became an Observer graphic novel of the month, a Guardian graphic novel of 2019, and received accolades from the Herald, It's Nice That and Eye On Design.  Alongside her long form works, Lippett has also created socio-political reportage comics focused on the stories of diverse communities in locations across the UK and abroad. She lectures in Illustration at the University of Edinburgh, and delivers talks on her practice to a variety of audiences both in the UK and internationally. Be sure to subscribe to the Peer Med Podcast on Apple Podcasts, Spotify, Overcast, or wherever you get your podcasts! Follow the Peer  Med Podcast on Instagram @peermedpodcast for more patient stories, disease and inspiring eye-opening content!  Follow Sarah on Instagram: @crayonlegs or check out her website at: www.crayonlegs.com 

In today's Episode, Janice Brown talks to Mica Barrington, a single mom who survived Five strokes that resulted from her Moyamoya Disease.   Mica talks about learning to be independent again, learning to walk and care for her children. She shares her accomplished goals and the new goals she has set for the future.   Conversation Highlights: {1:39}    Introduction of Mica {3:11}    Learning to work {5:00}    Living independently {7:12}    Family encouragement {8:50}    The feeling of being independent and ongoing recovery {11:20}  Future goals {14:00}  Retraining your brain to find the paths it needs {15:30}  3 Ps. Pearl of wisdom, Product recommendations, Practice you use.     Resources: betterhealthandrehab.com https://www.walmart.com/ip/As-Seen-On-TV-Copper-Knife-Medium/936266691

Heidi Romero, CP APMP after a 9-year career in retail optical sales, Heidi Romero joined BMO Harris Bank (then M&I Bank) in 2004 as a Treasury Management Sales Associate for Business customers and Inside Sales. From there she was promoted to a Sales Associate for the Commercial and Mid-Market client base. In 2010 she was promoted to Officer and moved into a Senior Implementation and Portfolio Management role during the M&I/Harris Bank acquisition working with large corporate customers through the merger. In April 2014, Heidi joined the Proposal/RFP Team as a US Proposal Manager for the bank. She was then promoted to Assistant Vice President in January 2016. She has been an active member of APMP since 2014 and achieved her Foundation level accreditation in June 2015, as well as her Practitioner certification in September 2018.Heidi works diligently to instill APMP's best practices and her proposal passion in every opportunity which resonates through her team and the sales process. Heidi is based in Milwaukee, WI.Heidi assisted on the Greater Midwest Chapter (GMC) Events Committee for 3 years, the GMC Marketing Committee for 1 year and as Events Chair most recently in 2020 and 2021.Heidi received her Bachelor of Science in Business Administration with an emphasis in Marketing Management from Carroll College (Waukesha, WI) in 2002 and her Master of Business Administration from Cardinal Stritch University in 2008.Heidi is a Moyamoya (a rare brain artery disease, occurring in less than 1 in 100,000) survivor/warrior since diagnosed in 2014, having had 2 brain artery bypasses in 2014 and 2015 after suffering a stroke on Christmas Eve 2013. She advocates for Moyamoya awareness as often as possible, buddies up with newly diagnosed people in her area and contributed to Faces of Moyamoya Disease, a book launch completed the end of 2020. Additionally, she enjoys reading, writing, shooting darts with her husband of almost 10 years, and instilling a brave warrior, can-do attitude in her daughter Grace (almost 5) and stepson Jeremy (almost 14). More recently, her and her daughter have become interested in geocaching and try to venture out to do that together as frequently as possible.

Valentin : “Je ne veux plus avoir peur”“Je décide de commencer une nouvelle aventure”. En 2016, Valentin intègre une école de journalisme. Il part de chez ses parents et découvre Toulouse : “J'arrive dans une ville que je ne connais absolument pas. Elle est grande, c'est immense, c'est super loin de chez mes parents”. Valentin emménage avec un ami du lycée en colocation, c'est le rêve !Mais un soir, il est submergé par une première crise : “Je regarde la télé [...] et j'ai une douleur qui commence à monter crescendo au niveau du cerveau”. S'en suivent d'autres crises, des rendez-vous médicaux et beaucoup de doutes. Quelques mois plus tard le diagnostic tombe : il est atteint d'une maladie auto-immune appelée syndrome de Moyamoya. Dans les faits, “j'ai une bombe à retardement dans le cerveau et on ne peut pas savoir si un jour ça va exploser ou pas”. À peine âgé de 23 ans, comment fait-on pour vivre avec une telle maladie ? Comment réussir à lâcher prise et à profiter de la vie, malgré cette épée de Damoclès au-dessus de soi ? Comment se construire en tant qu'adulte ? Découvrez l'histoire de Valentin dans Élan de vie, un podcast du Crédit Agricole qui donne la parole à celles et à ceux qui ont été touchés par la mort - eux-mêmes ou leur proche - et qui s'en sont relevés. Un podcast qui changera peut-être votre rapport à la vie, à la mort et vous fera découvrir la résilience présente en chacun de nous.Retrouvez tous les autres témoignages d'Elan de vie sur votre application de podcast préférée et sur la chaîne YouTube du Crédit Agricole.Témoignage de Valentin G, janvier 2020. L'objet de ce témoignage est de vous sensibiliser aux conséquences d'un décès prématuré, d'un accident ou d'une maladie. Son contenu reflète l'expérience de son auteur et ne saurait engager le Crédit Agricole. Our GDPR privacy policy was updated on August 8, 2022. Visit acast.com/privacy for more information.

At the age of just 28 years old, Winifred Ling started to experience terrifying episodes of numbness, slurred speech, and minor bouts of stroke. As the symptoms progressed, she began to feel like a walking time-bomb, unsure of when the next attack would come, and would later be diagnosed with the rare cerebrovascular disorder known as Moyamoya disease. In this episode of the Screwed Up Moments Podcast, she shares the details of her experience, and the lasting impact that the diagnosis left on her. Sources: Winifred Ling Blog Stroke Treating strokes: A race against time Music: Theme music for the Screwed Up Moments podcast is the track “A Delicate Moment”, originally composed by Rico Lo of Melodise and performed by Julian Law for this podcast.  Music used in the main body of this episode was provided by Blue Dot Sessions and covered under their blanket license, which you can find at sessions.blue. For full track listing please head over to our show notes at www.fablproductions.com/screwedupmoments

Meet the unflappable Jessie Huggett.  Jessie shares her experience of Moyamoya -  a rare condition in which the blood vessels that supply blood to the brain become narrowed.  You can find Jessie's art here.

In this week’s episode Amanda and Kelly are celebrating World Stroke Day! The ladies welcome the amazing, inspiring and all around badass Lisa Deck. Listen as Lisa shares her stroke story, all of her advocacy work with stroke, rare disease and Moyamoya and being one of the founders of Sisters@Heart. --- This episode is sponsored by · Anchor: The easiest way to make a podcast. https://anchor.fm/app

Novel MR contrast agents, advanced imaging for Moyamoya disease, machine learning for tumor classification, and practical review articles on radiologically isolated syndrome, perfusion MRI and PET for evaluation of gliomas, and new concepts in imaging for deep brain stimulation: Join Dr. Gibbs for the September AJNR podcast. (16:36)

Lisa Deck was a healthy 21-year old a week away from college graduation when her first stroke put her in the hospital. She barely made it to her graduation ceremony. She suffered two more strokes before she turned 25, and after that, a fourth stroke.After serious misdiagnosis and incorrect treatments, she was finally diagnosed with Moyamoya disease, a rare condition without a cure, but it does have a surgical treatment. In this podcast, she shares her diagnostic odyssey, her commitment to advocacy and the value of peer and family support. She also talks about the importance of staying positive and why patients must advocate for themselves.

In this Neuropsych Bite, we brought Joel Kamper, Ph.D., ABPP-CN, back on the podcast to discuss moyamoya, a rare condition that causes transient ischemic attacks and/or repeated strokes.  The term "moyamoya" ("puff of smoke" in Japanese) refers to the smoke-like presentation on angiography.  This is the second episode in a series on rare neurological disorders. Show notes are available at www.NavNeuro.com/55 _________________ If you’d like to support the show, here are a few easy ways: 1) Get APA-approved CE credit for listening to episodes: www.NavNeuro.com/INS  2) Tell your friends and colleagues about it 3) Subscribe (free) and leave an Apple Podcasts rating/review: www.NavNeuro.com/itunes 4) Contribute to the discussion in the comments section of the website (click the episode link listed above) or on Twitter (@NavNeuro)   Thanks for listening, and join us next time as we continue to navigate the brain and behavior! [Note: This podcast and all linked content is intended for general educational purposes only and does not constitute the practice of psychology or any other professional healthcare advice and services. No professional relationship is formed between hosts and listeners. All content is to be used at listeners’ own risk. Users should always seek appropriate medical and psychological care from their licensed healthcare provider.]

“Be patient with yourself. It may take longer than you think.” ~Nilsa Reyna A stroke in your mid-30s. A maze of medical appointments with no answers. 6 years of searching for a diagnosis. Brain surgery. Anxiety. And recovery. Actor, writer, director Nilsa Reyna is creating performances centered around her own health journey with the hope that it helps other people connect with their own stories. May 6th is World Moyamoya Day. Moyamoya is the name of the diagnosis Nilsa finally received. Moyamoya is one of the rarest forms of occlusive cerebrovascular disorders encountered in neurosurgery. The term means a "puff of smoke" coined by a Japanese team who first described the disease because it describes how the blood vessels look on an angiogram. Get the full show notes at http://www.thecreativeimpostor.com/077 Connect with Nilsa www.nilsareyna.com Instagram: @nilsareyna Twitter: @nilsareyna Here are some ways I'd love to connect Send me an email and let me know what you have created from your own trauma or health journey. So no like formal survey or anything. Just email me. You can write it or record a voice memo on your phone and attach it to the email. Join my Facebook Community where we create social support for content creators with inspiring prompts, opportunities for you to share your work, talk about money and more. My favorite hashtags #thecreativeimpostor #creativewomen  Email or Voice (send me a question to answer on the show!) Facebook Group The Creative Impostor Facebook Page @andreaklunder.creative Instagram: @andreaklunder Oh HEY! I'm on LinkedIn now... dropping pro podcasting tips, insights, and stories. Connect with me there and let me know you're a Creative Impostor listener.

Machine learning for detection of intracranial hemorrhage, synthetic MRI of the spine, new techniques for studying neurovascular conflict, cerebrovascular reserve in Moyamoya disease, and rapid identification of brain metastases: join Dr. Gibbs for summaries of these fascinating articles in the September AJNR podcast. (14:14)

This month brings to the show two great Djs from Boston- Xoce and moyamoya. Payum and Jose are doing great things for the techno scene in Boston. Grassroots techno has resurfaced and yet maintaining its underground foundation. At any of their events, you're guaranteed to hear nothing but the deepest and dirtiest of techno, whether it be TRIBÜ, Modular, or Cult.

This month brings to the show two great Djs from Boston- Xoce and moyamoya. Payum and Jose are doing great things for the techno scene in Boston. Grassroots techno has resurfaced and yet maintaining its underground foundation. At any of their events, you're guaranteed to hear nothing but the deepest and dirtiest of techno, whether it be TRIBÜ, Modular, or Cult.

This month brings to the show two great Djs from Boston- Xoce and moyamoya. Payum and Jose are doing great things for the techno scene in Boston. Grassroots techno has resurfaced and yet maintaining its underground foundation. At any of their events, you're guaranteed to hear nothing but the deepest and dirtiest of techno, whether it be TRIBÜ, Modular, or Cult.

Moyamoya is a disease of abnormal blood vessels in the brain that can occur in children. It leads to narrowing and blood clot formation that prevents the brain from getting enough blood. Without treatment, Moyamoya can cause strokes or bleeding into the brain.St. Louis Children's Hospital has a multidisciplinary team of pediatric neurosurgeons, neurologists, pediatricians, neuroradiologists, anesthesiologists, and physicians who work together to protect the brains and development of children with Moyamoya.Joining the show to discuss the Moyamoya program at St. Louis Children's Hospital and when to refer, is Jennifer Strahle MD. She is a Washington University pediatric neurosurgeon at St. Louis Children's Hospital.

News for Mid-October Hello Listener! Thank you for listening. If you would like to support the podcast, and keep the lights on, you can support us whenever you use Amazon through the link below: It will not cost you anything extra, and I can not see who purchased what. Or you can become a Fluffle Supporter by donating through Patreon.com at the link below: Patreon/Hare of the Rabbit What's this Patreon? Patreon is an established online platform that allows fans to provide regular financial support to creators. Patreon was created by a musician who needed a easy way for fans to support his band. Please support Hare of the Rabbit Podcast financially by becoming a Patron. Patrons agree to a regular contribution, starting at $1 per month. Patreon.com takes a token amount as a small processing fee, but most of your money will go directly towards supporting the Hare of the Rabbit Podcast. You can change or stop your payments at any time. You can also support by donating through PayPal.com at the link below: Hare of the Rabbit PayPal Thank you for your support, Jeff Hittinger. Busy bunny bussing around London causes commuter commotion https://www.dailydot.com/unclick/bunny-rabbit-bus-london/ Have you heard the one about the London Overground and the hare? One fluffy bunny is going viral after hopping aboard a London bus and casually going for a ride, without an owner in sight. Twitter user Matt Hepburn captured the Petter Cottontail (or Cottontransit, perhaps? Cottontrain?) aboard the bus with a single photo and the only caption that could possibly describe the seriousness and serendipity of the situation: “There’s a rabbit on my bus.” Naturally, the internet wanted to know, where did he come from? And where did he go? Where did he come from, this Cottontail Joe? Well, apparently this li’l bun gets around and was spotted on the Overground once before. Perhaps the bus bunny was bugging out over being a tad bit tardy for a seemingly momentous occasion? Could it have been related to at least one of these bunnies in Manchester? It’s OK though—Hepburn was able to talk to the bunny’s owner, and as it turns out, this is like, a normal day for it. “Apparently he does this often,” Hepburn wrote, stating the owner was sitting a few seats away. However, though it’s not completely clear if the hare is the one who “does this” and rides the bus often, or if the owner rides the bus with the bunny often, but just gives it space. In fact, this “laid back space hippy” of an owner has sparked more questions than answers: If he rides with the rabbit, does he wait for the rabbit’s signal to hop off the bus? If the rabbit rides alone, how does it reach the buttons letting the driver know it would like to get off at the last stop? What circumstances in this world have brought together a bus-riding rabbit and a space hippy? The world may never know.   Steampunk Alice in Wonderland coming to Bristol http://www.itv.com/news/westcountry/2017-09-29/steampunk-alice-in-wonderland-coming-to-bristol/ Rehearsals are gathering pace for a production of Alice in Wonderland... with a twist! The young actors at ITV WEST Television Workshop are bringing a steampunk-themed family version of the classic tale to Bristol next week. The show will be performed by a cast of more than 30 actors aged from 9 to 59. It is suitable for all ages. Alice is bored. Sitting on the riverbank with her Sister who has her head stuck in a book. Again. Nothing exciting ever happens to Alice. Ever. That is, until a sarcastic and frenetic White Rabbit appears with a waistcoat and a pocket watch, obsessing over how late he is. I mean, have you seen a rabbit with a watch before? Alice hasn't! Then he rudely disappears down a rabbit hole... Should Alice stay on the riverbank, bored out of her mind? Or follow him down into a utopia of Steampunk madness - with grinning cats, chaotic twins, mad tea parties and a crazy Queen who's lost some tarts? Boredom loses. Curiosity wins. Welcome to Wonderland. – ITV Television Workshop Alice in Wonderland is being performed at the Redgrave Theatre in Clifton from Tuesday 3rd to Thursday 5th October @ 7.30pm. Tickets are priced at£10/£12 and are available by calling the box office on 0117 3157800 or from the Redgrave website at www.redgravetheatre.com.   Fish and Game to take ownership of New England cottontail habitat http://www.unionleader.com/article/20170928/NEWS01/170929214/-1/mobile?template=mobileart MANCHESTER — The endangered New England cottontail has found a friend in the state Fish and Game Department, which soon is expected to own a prime piece of the rabbit’s habitat. The Fish and Game Department said it is glad to take over ownership of 57 acres of conservation land near the Manchester-Boston Regional Airport, saving the airport about $30,000 a year. “We’re happy to take it,” said Glenn Normandeau, executive director of the New Hampshire Fish and Game Department. “We’re actively doing management at the property to help with the rabbit situation.” The endangered cottontail needs thick shrub cover, which can be found on the site, to avoid predators, which is “pretty much everything,” he said. Airport officials are working to transfer ownership to Fish and Game. Deputy Airport Director Tom Malafronte said the airport was spending $30,000 annually in recent years to maintain the site, including picking up discarded tires and construction materials. In 2001, the airport purchased the property in Manchester and Londonderry for $1.1 million to offset filling in 13 acres of wetlands as part of expanding the southern portion of the airport’s north-south runway more than a decade ago. “Preserving the New England cottontail habitat was an important consideration for NH Fish and Game, and one of the reasons that we felt strongly that they would be best suited to own and manage the property,” Malafronte said. To protect the endangered species, the state has closed off areas of the Merrimack Valley area from Concord south as well as a section of Rochester south to near Exeter from hunting any cottontail rabbit year-round to avoid any confusion. “Just because it’s difficult to tell them apart” from other more populated rabbit species, Normandeau said. The protection means people can’t harm, harass, injure or kill the rabbits, which run 15 to 17 inches long with brown and gray coats. Humans sometimes confuse them with Eastern cottontails. “I’m not aware we’ve ever prosecuted anyone for the taking of a listed species, but we certainly try to discourage it,” said Normandeau, who’s been to the property several times. He called the parcel southwest of the airport “a good wildlife spot in the middle of what’s become a pretty significantly developed area.” The Londonderry-Merrimack area “is definitely one of the hot spots of their existing populations,” Normandeau said. A notice in the Federal Register last week said Fish and Game would “continue to maintain the property in its natural state as a wildlife corridor in perpetuity.” Had homes or businesses been built on that land, it “would probably eliminate the rabbit’s habitat, which in effect means they’re going to disappear, leave the area,” Normandeau said.     The innocent reason Hefner named Playboy girls ‘bunnies’ http://nypost.com/2017/09/28/the-innocent-reason-hefner-named-playboy-girls-bunnies/ Hugh Hefner’s Playboy empire was as famous for its “Bunnies” as it was for its saucy centerfolds. The stunning waitresses, dressed in skin-tight bodices with rabbit ears and tails, became an iconic part of the mogul’s brand — serving at his parties, his clubs and even on his private jet. But have you ever wondered why they were called “Bunnies” in the first place? According to the magazine mogul — who died Wednesday at the age of 91 — the real inspiration behind the Playboy Bunny was a student bar from his college days. When Hefner was a student at Illinois University, in the 1940s, his favorite hangout was a bar called Bunny’s Tavern named after its original owner, Bernard “Bunny” Fitzsimmons. The bar, which opened in 1936, was a favorite for poverty-stricken students because of its 35-cent daily food specials and draft beer for 10 cents a glass. When Hefner set up his Playboy empire, in the 1950s, he came up with his rabbit logo and consequently the Bunny girls as a tribute, which he revealed in a letter to the bar which now hangs on its wall. However, he also admitted that the Bunny costume was a saucy reference to the sexual reputation of rabbits. The iconic costume was designed by Zelda Wynn Valdes and made its formal debut at the opening of the first Playboy Club in Chicago in 1960. Bunnies, who were chosen after a series of auditions, were given designated roles — so they could be a Door Bunny, a Cigarette Bunny, a Floor Bunny or a Playmate Bunny. There were also trained flight attendants, known as Jet Bunnies, who served on the Playboy Big Bunny Jet. Every Bunny went through a strict training regimen and had to be able to identify 143 brands of liquor and know how to garnish 20 cocktails. They also had to master the “Bunny stance” — with legs together, back arched and hips tucked under — as well as the “Bunny perch” for sitting on the back of a chair and the “Bunny dip,” which required them to bend their knees to serve drinks elegantly. Dating customers was forbidden and clients were banned from touching the girls in the clubs.     Giant rabbit, moon sculptures welcome coming Mid-Autumn Festival in Jinan, East China’s Shandong http://www.globaltimes.cn/content/1068642.shtml Inflatable sculptures of a moon and rabbit are displayed on Baihuazhou lake in Jinan, East China’s Shandong Province on September 27, 2017. The illuminated moon model measures six meters tall, while the rabbit stands at a respectable four meters.   Ikea’s Latest Acquisition Will Help Assemble Your Ikea Furniture http://fortune.com/2017/09/28/ikea-task-rabbit/ One of the most popular jobs on TaskRabbit, a service that lets you hire workers for quick gigs, is assembling Ikea furniture. So perhaps it's no surprise that the Swedish retail giant has reportedly acquired the startup for an undisclosed price. TaskRabbit has only a few dozen full-time employees, but it is a platform for a large number of independent contractors who help customers with all sorts of errands, handymen tasks and, of course, furniture assembly. According to tech news site Recode, Ikea will treat TaskRabbit, which is reportedly profitable, as an independent subsidiary and keep on its CEO Stacy Brown-Philpot. Recode sees the deal as a strategic acquisition at a time of rapid change in the world of retail and home delivery: The purchase of TaskRabbit was fueled by Ikea’s need to further bolster its digital customer service capabilities to better compete with rivals likes Amazon, which has stepped up its home goods and installation offerings. The purchase is Ikea’s first step into the on-demand platform space. TaskRabbit had already struck a pilot partnership with Ikea around furniture assembly in the United Kingdom and also had marketed its workers ability to put together Ikea items in the U.S. and elsewhere. TaskRabbit has received investments from a number of prominent venture capital firms, including Shasta Ventures, Lightspeed Venture Partners and Founders Fund. Currently, customers are able to hire "rabbits" in around 40 U.S. cities. TaskRabbit is one of the most high profile of the so-called "gig economy" companies, which connect customers with workers on an independent contractor basis. Other such companies include home cleaning service Handy, and the car-hailing services Uber and lyft. The "gig" business model is popular with investors because it can grow quickly, and allows companies to try to avoid the costs and legal entanglements of hiring staff. In recent years, however, workers on such services have won several court challenges claiming they are not contractors, but are instead employees. Ikea did not immediately respond to a request for comment about the acquisition.     The Peter Rabbit film trailer has been released - and it looks incredible http://www.coventrytelegraph.net/whats-on/film-news/peter-rabbit-film-trailer-been-13676775 The new trailer for the forthcoming Peter Rabbit movie has been released. The jaw-dropping trailer ahead of the CGI/live-action film has left viewers stunned - and fans ready to see it. The film is being shot in Cumbria and takes in the stunning scenery of Windermere and Ambleside that inspired Beatrix Potter to write her stories. Billed by Sony Pictures Animation as a 'contemporary comedy with attitude', it follows the story of Peter Rabbit, the mischievous and adventurous hero who has captivated generations of readers. Starring James Corden as the voice of the titular bunny, Peter Rabbit promises thrills, spills and badgers playing darts with hedgehogs. The film features voice roles played by Corden, Margot Robbie, Daisy Ridley and Elizabeth Debicki, and live-action roles played by Domhnall Gleeson, Rose Byrne and Sam Neill. The film is scheduled to be released on February 9, 2018.   5 Rabbit Cervecería Papi Chulo Bottle Release Details https://thefullpint.com/beer-news/5-rabbit-cerveceria-papi-chulo-bottle-release-details/ (Bedford Park, IL) – At 8.5% abv, Papi Chulo was produced using the Solera method by incorporating 3 vintages blended over 4 years. It is aggressively sour. Acerola, also known as Barbados cherry, is native to Central and South America and is considered a superfood due to its nutritive value and antioxidant powers. If you love sour beers, you do not want to miss this release! 5 Rabbit Papi Chulo The bottle release will take place at our brewery in Bedford Park, on Saturday 10/7/17 at 2pm. These bottles are limited and we will do our best to spread them out as much as possible. We are anticipating to offer 2 bottles per person, however if turnout is larger than expected this number may change. Thank you in advance for understanding.     Short Film Friday: ‘Rabbit’s Blood’ Is The Best Kind Of Weird Read more at Film School Rejects: https://filmschoolrejects.com/short-film-friday-rabbits-blood-best-kind-weird/#ixzz4uJc3hxBW Lynchian” doesn’t really begin to describe it. A stark, darkly funny animation whose styles evoke those of Japan and Eastern Europe, Rabbit’s Blood creates an odd world at the intersection of cartoonishness and realism. The fluctuating colors filling in the clothes combined with the jarringly natural sound design make for an uneasy viewing experience that can create moments of fear and humor as easily as it puts us on edge. Animator Sarina Nihei finds a bit of Don Hertzfeldt and David Lynch, then jostles them together with a repugnant cuteness that’s almost too much to watch. https://vimeo.com/232458407       After the latest supermarket chicken scandal, is it time to reappraise the humble bunny? http://www.devonlive.com/news/devon-news/after-supermarket-chicken-scandal-time-554274 In 1947 the Government came up with a cunning way of measuring inflation. The Retail Price Index took a typical British shopping basket and measured the average cost of its contents. This exercise, carried out annually, allowed statisticians to work out inflation and its effect on the public. Alongside the corned beef, herrings, boiled sweets and cauliflower that typified the diet of the day was wild rabbit. Since the 12 Century, when bunnies were introduced to this country to be raised in managed warrens, they had been a staple of the British diet, particularly in rural areas. We may refer to modern times as “austerity Britain” but with a gourmet burger joint on every corner and supermarket shelves groaning I think the levels of austerity in this country pale into insignificance compared to the post war era, when rabbit would have provided a welcome and tasty protein hit. I’m not sure why rabbit fell out of favor. The deliberate introduction of myxomatosis in an attempt to control burgeoning bunny populations probably had something to do with it, even though this horrible disease apparently doesn’t affect the meat. The introduction of battery farming made the price of poultry tumble, and steadily chicken has replaced rabbit on the nation’s dinner table. With the latest story about dodgy practices at one of the country’s largest processing plants I wonder if it’s time to reappraise the humble bunny. Trendy chefs tell us we’re supposed to eat lean, sustainable, local, organic produce, something our grandparents were doing decades ago when they tucked into a rabbit stew. I was going to describe the Guardian’s revelations about 2 Sisters as shocking, but really only the naive can be even surprised at their undercover reporter’s findings. We all know that cheap meat involves an “ask no questions” pact between producer and consumer. When Aldi sells you a kilo of chicken for £1.79, it’s with a nudge and a wink – we’re getting ridiculously cheap meat – just so long as we don’t glimpse behind the plastic curtains of the processing plants it uses. Evacuee Teddy Neale, 14, with a catch of rabbits on August 10,1944. And the real shame is that while chickens live out pointless and short lives in unpleasant conditions, farmers are obliged by law (The Pests Act 1954 if you’re interested) to kill the rabbits that run wild in the fields next to the battery sheds. There are between 35m and 45m in this country and they breed like, well, rabbits. Yet because there is no longer a market for these animals most will end up buried and rotting – it’s an incredible and epic waste of a natural resource and I think something of a national scandal. So next time you pass a proper butcher why not invest a couple of quid in an animal which has led a wild and free life in a field close to your home?     TOKiMONSTA puts forth her beat-making savvy on ‘Lune Rouge’ after nearly losing it all http://www.nydailynews.com/entertainment/music/tokimonsta-brings-beats-losing-musical-abilities-article-1.3532927 TOKiMONSTA is back — and doing better than ever. The seasoned Los Angeles producer, real name Jennifer Lee, has reemerged with her third full-length record after a tumultuous time in her life — she had two surgeries for a rare brain disorder called Moyamoya she was diagnosed with in 2015. Lee penned an essay detailing her experience regaining the ability to speak as well as comprehend and make music after the surgeries, the first time she publicly addressed her health scare. The artist, whose name translates to rabbit monster (toki means rabbit in Korean), caught up with the Daily News at Panorama over the summer to talk about her love of making beats and “Lune Rouge,” which officially drops Friday. “In a generation where everyone is very playlist-focused, I would say that this album is a playlist of songs for one person,” Lee said. “It represents who I am right now as an artist, how I’ve progressed over the many years that have passed since the last one … I just set the intentions to make the kind of music that makes me happy.” The new music will likely make listeners happy, too. “Lune Rouge” offers 11 hypnotizing tracks suited for the likes of hip-hop and R&B collaborators Yuna, Joey Purp and Isaiah Rashad. MAD creates inflatable pavilion shaped like a rabbit's head https://www.dezeen.com/2017/10/01/mad-inflatable-pavilion-rabbit-ears-beijing-design-week/ For this year's Beijing Design Week, architecture studio MAD has created an inflatable pavilion with two big floppy ears. Beijing-based MAD created the giant-rabbit-shaped pavilion in a hutong – one of the city's old courtyard-house neighbourhoods – near Lama Temple. Titled Wonderland, it is designed to provide a public space where children in the area can meet and play with each other. Beijing Design Week pavilion by MAD architects. The inflatable structure is white and its two lop ears protrude at a jaunty angle. "Through the form of a rabbit, Wonderland brings a carefree spirit and sense of whimsy to this old Beijing neighbourhood," said MAD. "Its playful attitude provides an escape from reality." Beijing Design Week pavilion by MAD architects. At night, the interior of a structure is illuminated with a white light that provides a safe environment for children to socialise. "Surrounded by its soft walls, under the blue sky and green trees, children can play, daydream and drift off into their own fantasy wonderland, in pursuit of happiness," added MAD. Beijing Design Week pavilion by MAD architects. Led by architect Ma Yansong, MAD is best known for projects including the undulating Harbin Opera House, the horseshoe-shaped Sheraton Huzhou Hot Spring Resort and the twisted Absolute Towers. The firm – which ranked at number 61 on the inaugural Dezeen Hot List – is currently working on a variety of projects in California, including the Lucas Museum of Narrative Art, which recently gained approval from Los Angeles city officials. Let sleeping dogs – and their masters – lie http://www.kansas.com/living/health-fitness/article177536371.html President John F. Kennedy’s family had several dogs that cuddled with Caroline and John-John (as well as a beer-swilling rabbit that was a gift from a magician) while they were in Washington. Calvin Coolidge had nine canines lodged in the White House’s family quarters. And the Obamas’ Portuguese water dog, Bo, was allowed to sleep on the bed with the first lady when the president was out of town. Meet the People Rescuing Cuban Cuisine https://www.cntraveler.com/story/meet-the-people-rescuing-cuban-cuisine Even if you’ve never been here, you probably know that only 20 years ago the people on this island just 90 miles from Florida were starving. When the 37-year-old Soto was growing up, during the “special period” when resources vanished after the collapse of the Soviet Union, he and his parents, both government employees, lived on little more than bread, rice, and occasionally beans. Sometimes a meal was simply sugar water. “Cuba has the most complicated relationship with food,” Soto says. “People will tell you there’s no food in Cuba. Or there are no traditions anymore; we lost all our traditions”—of hearty lunches of Caribbean staples like roasted suckling pork or rich gumbos. As food became increasingly scarce, cooking techniques and recipes were forgotten. “And I thought, Even the absence of food is a story about food.” But when he started work on the film two years ago, Soto discovered a new turn in Cuba’s culinary evolution: Young entrepreneurs have picked up the mantle from Nuñez del Valle to open dynamic, pulsating restaurants like O’Reilly 304 and Otramanera that serve lamb burgers and sous vide lobster and innovative takes on standards like pressed pork sandwiches. As the regime has loosened restrictions on private businesses, and as tourists come flooding in from around the world, Cuban cuisine is in the midst of a remarkable renaissance. The question is whether this ambitious new generation of restaurant rookies will chase gastronomic trendiness or help restore and reinterpret all that was lost—the kind of deeply satisfying simplicity that travelers are hungering for today. The difference today is that some can—and that travelers are coming here to eat it, too. “Enrique is the godfather of the new paladares,” says Soto, the Havana-born producer-director of the forthcoming documentary Cuban Food Stories and an expert on the island’s cooking. Back when Nuñez del Valle opened one of the country’s first paladares, or privately owned restaurants, they’d just been legalized by the regime and were limited to 12 seats. Now, La Guarida (“the Animal Den”) has expanded to 100, with an elegant shaded patio that’s drawn the likes of Prince Albert II, Jack Nicholson, and Julian Schnabel—plus today’s young crowd in cool summer garb. After a lunch of lobster ceviche, roasted rabbit with caponata sauce, and pavé of suckling pig with crispy skin, Nuñez del Valle sits down with us for coffee and a selection of Montecristos and Cohibas. His own fat cigar in hand and a glass of Havana Club Selección de Maestros close by, the godfather settles into his chair but doesn’t want to take too much credit for what he’s started. “It’s the new generation that’s trying to do gastronomy differently,” he says in Spanish as Soto translates. “They’re doing a great job of rescuing Cuban cuisine. Like thousands of others, Cano jumped at the chance to list his place on Airbnb, which started operating in Cuba in 2015, and which suddenly turned his relatively modest farm into an ecotourism destination, on the radar of people worldwide. (During my visit, a German-Australian couple happens to be staying in Cano’s $33-a-night one-bedroom cabin. “We love it,” they tell us before setting out on a hike, “though it’s very rustic.”) Cano also puts on epic lunch spreads, given enough notice through Airbnb, centered around a young pig rubbed with garlic and salt and roasted over a wood fire until the skin crackles. As Soto and I watch, Cano plops the cooked pig onto a wooden table and swiftly hacks the meat into hand-size pieces with a machete. His wife, who goes by “China,” then lays out a plastic tablecloth and platters of avocado, black beans, cucumber-and-tomato salad, rice, taro chips, and yucca. We eat overlooking the fields, the thatched tobacco-curing hutch, and chickens pecking at the dirt. It’s a fabulous country spread, made all the more remarkable in that Cano grew all of the food himself—and raised the pig. After our meal, we have coffee from beans he grew, lightened with milk he collected at 5 a.m. Cano then pulls out a white plastic bag filled with tobacco leaves he cultivated and cured, and he rolls us each a cigar. Considering the surroundings and the straight-from-the-field leaf, it rates as the best I’ve ever smoked.   Will the Bunny Park become a housing complex? https://citizen.co.za/news/1681935/will-the-bunny-park-become-a-housing-complex/ The park will keep at least 50 sterilised rabbits. More than 2 000 rabbits were donated from Benoni Bunny Park to Johannesburg Zoo as food for carnivores. Fifty rabbits were, however, left behind at the bunny park so that visitors could enjoy still enjoy them, but they are not happy with current small number of bunnies, Benoni City Times reports. One of the visitors John Priestley wrote to the media as follows: It saddens me greatly to read about the ongoing saga of our beloved Bunny Park. For a facility that has given joy and happiness for decades to so many children, to be limited to 50 sterilised rabbits in an enclosure, is a travesty. A child might as well sit at home and look at pictures of bunnies and farm animals on a computer screen. The fun was when a child could spend a day outdoors running around clutching a carrot trying to feed the ever-elusive rabbit and seeing farm animals up close. The outing, costing no more than a few vegetables, made it accessible to all. Well done to the council for spending money on the park and making it more attractive, but please don’t let the whole concept of a bunny park be destroyed by the ‘experts’. You cannot but wonder if all these changes means authorities have an ulterior motive planned for the future. Perhaps a housing complex?   Age before beauty – Grants bring attention to need for ‘young forests’ in N.H. http://www.concordmonitor.com/young-forests-ecology-environment-cottontail-songbird-12908739 YoungForest.org is the name of a website created by the institute and a number of other organizations to help convince people that healthy forests in New Hampshire and other locations need trees with a mix of ages – even if that requires cutting down a lot of trees now and then so that new ones can grow. “We don’t have a lot of age diversity in our forests,” said Scott Hall, a senior bird conservation biologist for the National Fish and Wildlife Foundation, noting that most of New England’s forest were cut a century ago for logging or farmland and have since grown back. “We have a resilience problem when all the trees you have are 60 to 100 years old. You need more diversity.” The topic came up last week when the NFWF said it was giving about $1.2 million to 10 environmental projects in New England, combined with $1.4 million in contributions from private partners including Eversource. Several projects focused on the effects of successional forests. In ecological circles, “succession” refers to the gradual replacement of one type of ecological community by another in the same area – in this case, that means trees growing up in areas that had been cleared by human activity, fire, flooding from beavers or other causes. Young forests, defined loosely as those with most trees less than two decades old, are valuable for a number of species that depend on the plants, insects and animals drawn to them. Those species include the New England cottontail, a small rabbit that is the target of restoration efforts in southeastern New Hampshire, a project that received $175,000 in NFWF grants. The grants will help UNH researchers study how best to estimate the population of this elusive rabbit in 28,800 acres of restored habitat, using capture-recapture methods and “pellet surveys,” in which piles of rabbit fecal pellets are collected or counted. Getting $103,000 is an ongoing UNH project studying songbird populations in rights of way for power lines, to see how they can function as long, skinny strips of young forest. A summer’s worth of counting and banding songbirds caught in nets underneath Eversource transmission towers in Strafford found at least 68 species in the brushy, tangled growth, according to UNH graduate student Erica Holm, working with professor Matt Tarr. “It seems that the rights of way contribute as many species as a clearcut,” she noted. The counter-intuitive idea of the environmental benefits from huge power-line towers reflects the complexity of creating and maintaining young forests. For one thing, they don’t stay young very long – when the trees get too big, the environmental benefits change. Williamson said the Wildlife Management Institute’s goal is to have 10 percent of forestland in the region be young forest – the best they’ve done so far is 6 percent in some areas. “In 10 or 15 years, it’s going to be gone. This is not something we can do once and stop,” Williamson said. “We’re always thinking, “Where can we go next so I have a constant supply of this habitat?’ ” In New England, that requires dealing with private landowners, convincing them to cut down the mature trees and put up with scrubby, bramble-filled properties that don’t have obvious value. “It’s tough to sell the first three years after a clear cut,” Williamson said. “Commercial forestry has to be the driver on this,” he added, noting the effect of commercial firewood prices on woodlot owners’ decision whether to cut mature trees. “When the firewood market goes down, we just sit on our heels,” he said. But he argued that education can change people’s views about the value of even the ugliest of scrubland. “There was a time when people were afraid of wetlands,” Williamson noted. “Old-growth forests were once regarded as a waste of the value of the forest. Native grasslands – another area that we didn’t use to think had any value.” The grants were awarded through the New England Forests and Rivers Fund, a public-private partnership. Kung fu rabbit game Overgrowth adds story mode in final beta version http://deathrattlesports.com/kung-fu-rabbit-game-overgrowth-adds-story-mode-in-final-beta-version/98623 More than nine years after it was announced, Overgrowth’s surreal mix of wild animals, fast-paced martial arts, stealth, and gore is nearly upon us. The last beta version before a proper release arrived this week, bringing with it the game’s full story mode. Those who have purchased the game early will be able to play through the full campaign now, which sees our rabbit hero Turner fight to protect the island of Lugaru from slavers. Expect hand-to-hand combat that relies upon timing and counters, segments where you sneak through shrubbery, and lots of blood. The amount of gore in the game is emphasized by another tweak in this beta: you can now be impaled by spikes. That means some pretty gory clips of Turner’s limp body sliding down a wooden spear, blood spurting. Other changes will make the game’s different animals more distinct. Cat enemies, for example, can now throw smaller weapons such as daggers, while rats can attach bits of the environment to their head as camouflage. Developer Wolfire Games has fixed lots of bugs, too, and added new settings options including a brightness slider. The full change log is here. Overgrowth is currently £22.99/$29.99 on Steam and the Humble Store. There’s no word on a final release date, but it shouldn’t be too long.   One-Of-A-Kind Rabbit Brings $18,000 At Alderfer Auction https://www.antiquesandthearts.com/one-of-a-kind-rabbit-brings-18000-at-alderfer-auction/   HATFIELD, PENN. —Alderfer Auction conducted a two-day auction of dolls on October 3 – 4 both online and at its auction gallery. On October 4 a bisque-headed rabbit with no ears came to the block with a $500/750 estimate—it went on to sell for $18,000 including premium. “This is a wonderful piece—fashioned after the 1920s ‘Jack Rabbit’ series of books by ‘Uncle Dave,’ David Cory, and published by Grosset & Dunlap,” according to Ranae Gabel of Alderfer Auction. The 18-inch tall, rabbit has big stationary brown eyes and an open smiling mouth. It sports a curly gray wig, cloth body with white leather arms, and individual fingers on its hands. It sports a curly gray wig, cloth body with white leather arms, individual fingers on hands. Dressed in cotton plaid dress, red petticoat, white pantaloons and bonnet, the rabbit has on brown oilcloth heeled shoes. The winning bidder said it was a “one-of-a-kind.” Inclusive art studio hides 200 rabbit sculptures in Rochester parks http://wxxinews.org/post/inclusive-art-studio-hides-200-rabbit-sculptures-rochester-parks Sarah Beren is a licensed creative art therapist and owns Spotted Rabbit, a studio with art classes, art therapy and an apprenticeship program for a population within the disability community she saw was underserved. "I went to a training about job development for them. And I started asking, 'Well, what about these people that need staff with them or are nonverbal who can’t be left alone in the community?' " What she found was hardly anything. To fill this void, Beren created the program, which she says gives people who are highly functional yet can’t quite work independently a purpose, a structured schedule and a job - artists sell their work around Rochester. Ellie Anolik is one of those artists; she said her favorite medium is clay. "I like how you can get mad at it, and you can take it all out on the clay.” Beren said they would like to do more shows and participate in galleries, but many art spaces in the city are more “do it yourself”-type spaces presenting a number of challenges to their artists. Allergies are an issue, or how maintained the buildings are; whether or not snow is plowed in the winter. "A lot of the galleries are on the second floor with no wheelchair accessibility. So we've had a lot of potential partnerships with folks, but then it’s like well, our artist can’t come to her own show opening.” The latest project to come out of the studio, with the help of a Livingston Arts grant, is 200 rabbit sculptures. For seven months, artists molded and glazed and baked 200 rabbits, giving them names and hiding them in 41 parks around Rochester. "The idea was that we would have individuals who don’t normally have an opportunity to make public art, make public art. And then also people who may not have an opportunity to go see art or own a piece of artwork actually be able to find it in their local park, pick it up, and take it home." Beren says they have heard back from only 45 owners who have found rabbits, meaning there are many more out there waiting for a new home. Word of the Week: Sterile Plant of the Week: Bread © Copyrighted

Author Charles Hammond discusses his article Moyamoya Syndrome in South African Children With HIV-1 Infection. Medical student Louisa Chatroux presents the learning topic on neurologic manifestation of HIV In children. Lastly, Dr. Jennifer McGuire discusses what led her to a career in pediatric neurology.  Read Dr. Hammond's article here. 

A discussion about a specific type of brain bleed.

1) Anti-LGI1-associated cognitive impairment: Presentation and long-term outcome2) e-Pearl topic: Moyamoya disease and syndrome3) Topic of the month: Neurology Today story on a published paper titled: Intensive Blood-Pressure Lowering in Patients with Acute Cerebral HemorrhageThis podcast for the Neurology Journal begins and closes with Dr. Robert Gross, Editor-in-Chief, briefly discussing highlighted articles from the print issue of Neurology. In the second segment Dr. Lara Marcuse interviews Drs. Francesc Graus and Josep Dalmau about their paper on the presentation and long-term outcome of anti-LGI1-associated cognitive impairment. Dr. Steve O'Donnell is reading our e-Pearl of the week about Moyamoya disease and syndrome. Dr. Javier Provencio interviews Dr. Adnan Qureshi about a Neurology Today story on his published paper titled: Intensive Blood-Pressure Lowering in Patients with Acute Cerebral Hemorrhage.DISCLOSURES: Dr. Graus serves as an editorial board member of Lancet; receives license fee Payments from Euroimmun for the use of IgLON5 as a diagnostic test; holds a patent for the use of IgLON5 as a diagnostic test.Dr. Dalmau serves as Editor of Neurology®: Neuroimmunology & Neuroinfammation; serves as an Editorial board member of Neurology® and UpToDate; receives royalties from patents for the use of Ma2 and NMDAR as autoantibody tests; is a consult for Advance Medical, receives research support from Euroimmun and the NIH; receives revenue from Euroimmun for the following tests: NMDA receptor autoantibody test, GABA(B)R autoantibody test, GABA(A)R autoantibody test, DPPX autoantibody test and Iglon5 autoantibody test.Dr. O'Donnell serves on the editorial team for the Neurology® Resident and Fellow Section.Dr. Provencio serves as an editorial board member of Journal of Neuroimmunology, serves on the scientific advisory board for Minnetronix, INC. (travel related expenses) and Advanced Circulatory, Inc (travel related expenses); received honoraria from Bard, Inc.; receives royalties from the publication of the book “Family Guide to Surviving the ICU”; receives research support from Bard Inc., Cryothermics INC. and the NIH.

The last music themed episode was such a hit, we interviewed another hometown band! The trio that make up, Moyamoya, guest on the show to talk about instrumental music, the five year process of their debut album, and their upcoming show in October.Support the show (https://www.patreon.com/theshortbox)

As promised, part two from last week! The crew reviews the pilot episode for Gotham, Cesar takes on Thanos and Kiss, Adam talks about his visit at Halloween Horror Nights, and Ice-T makes a cameo! Order the MOYAMOYA album: fortlowell.blogspot.comSupport the show (https://www.patreon.com/theshortbox)

1) Cognition in the minimally-conscious state and 2) Topic of the month: Recent book, Your medical mind: How to decide what is right for you. This podcast for the Neurology Journal begins and closes with Dr. Robert Gross, Editor-in-Chief, briefly discussing highlighted articles from the print issue of Neurology. In the second segment Dr. Thomas Cochrane interviews Dr. Damian Cruse about his paper on etiology and covert cognition in the minimally-conscious state. Dr. Stacey Clardy is reading our e-Pearl of the week about Moyamoya disease. In the next part of the podcast Dr. Ted Burns interviews Drs. Groopman and Hartzband about cognitive errors or biases that can influence our ability to diagnose. Next week, Dr. Burns will interview Drs Groopman and Hartzband about risk-benefit ratios. The participants had nothing to disclose except Drs. Cochrane, Cruse, Clardy, Burns, Groopman and Hartzband.Dr. Cochrane received royalties from the publication of the book First Aid for the Boards: Neurology.Dr. Cruse has received research support from Medical Research Council UK and the Canada Excellence Research Chair Program.Dr. Clardy serves on the editorial team for the Neurology® Resident and Fellow Section. Dr. Burns serves as Podcast Editor for Neurology®; performs EMG studies in his neuromuscular practice (30% effort); and has received research support from the Myasthenia Gravis Foundation of America and Knopp Neurosciences Inc..Dr. Groopman receives royalties from the publication of the book Your Medical Mind.Dr. Hartzband receives royalties from the publication of the book Your Medical Mind.

In this episode, Dr. Hall talks about a who came in with migraines, but actually had a rare genetic disease called Moyamoya. This is a good story to demonstrate that sometimes the most important thing an upper cervical doctor does, is tell you where you need to be.

This Podcast for the Neurology Journal begins and closes with Dr. Robert Gross, Interim Editor-in-Chief, briefly discussing highlighted articles from the print issue of Neurology. In the second segment Dr. David Geldmacher interview Drs. Clifford Jack and Prashanthi Vemuri about their papers on MRI and CSF biomarkers in normal, MCI and AD. In the next segment, Dr. Ryan Overman is reading our e-Pearl of the week about electroencephalography in Moyamoya disease. The next part of the podcast is Dr. Beau Bruce interviews Dr. Dan Moore for our LOTW. In concluding, there is a brief statement where to find other up-to date patient information and current Patient Page. The participants had nothing to disclosure except Dr. Jack is an investigator in clinical trials sponsored by Pfizer, consults for Elan, and is funded by the NIH grant R01-AG11378 and the Alexander Family Alzheimer's Disease Research Professorship of the Mayo Foundation.