Podcasts about Berkowitz

What is evil—and can even the most depraved among us find redemption? In this profoundly moving conversation, Socrates in the City host Eric Metaxas sits down with Dr. Michael Caparelli, author of Monster Mirror, to explore the dark and sobering case of David Berkowitz—the notorious “Son of Sam” serial killer. Caparelli, who spent over 100 hours interviewing Berkowitz in prison, offers a rare glimpse into the mind of a man who once claimed to be possessed by the devil but now professes a deep Christian faith.See omnystudio.com/listener for privacy information.

What is evil—and can even the most depraved among us find redemption? In this profoundly moving conversation, Socrates in the City host Eric Metaxas sits down with Dr. Michael Caparelli, author of Monster Mirror, to explore the dark and sobering case of David Berkowitz—the notorious “Son of Sam” serial killer. Caparelli, who spent over 100 hours interviewing Berkowitz in prison, offers a rare glimpse into the mind of a man who once claimed to be possessed by the devil but now professes a deep Christian faith.See omnystudio.com/listener for privacy information.

Join Mondo and author Adam Berkowitz as they discuss the latest developments on the red heifers and the Third Temple.

Karen Read Trial Day 25 Recap: Defense Witness Turns on Them, Alleges Defense Member Threatened Her! In a dramatic day inside the Norfolk Superior Court, the Karen Read murder trial took a turn that no one saw coming—when the defense's own witnesses began pushing back. From allegations of witness coercion to a controversial dog bite theory, Day 25 of the trial was packed with explosive revelations and intense courtroom exchanges. Former Canton Police Officer Kelly Dever delivered one of the most impactful testimonies of the trial so far. Dever told the jury that Karen Read's defense team pressured her to testify to a story she knew wasn't true—that she saw Higgins and Berkowitz alone in the garage with Read's SUV. When she refused, she claims they threatened her with perjury. In open court, she directed the accusation directly at defense attorney Alan Jackson. This wasn't a moment of confusion—it was a pointed, emotional standoff that put the defense's tactics under the microscope. Then came Jonathan Diamandis, a friend of former State Trooper Michael Proctor. He confirmed the authenticity of Proctor's now-infamous group chat texts, which were laced with crude, insulting, and misogynistic remarks about Karen Read. But the texts didn't say what the defense needed—they didn't mention any planted evidence, altered reports, or a cover-up. Just hostility. Just bias. And just as easily turned against the defense's credibility as the prosecution's. In the afternoon, the defense called Dr. Marie Russell, a forensic pathologist, to bolster their theory that John O'Keefe's injuries were more consistent with a dog attack than a car crash. But her testimony lacked any physical evidence—no dog DNA, no bite mark match, and no autopsy. The prosecution wasted no time in pointing out that her conclusions were drawn from photos, not science. This video breaks down the legal strategy, expert testimony, and ethical fallout—step by step. #KarenReadTrial #TrueCrime #WitnessCoercion #JohnOKeefe #ForensicEvidence #MichaelProctor #DogBiteDefense #KellyDever #LegalEthics #CourtroomDrama Want to comment and watch this podcast as a video?  Check out our YouTube Channel. https://www.youtube.com/@hiddenkillerspod Instagram https://www.instagram.com/hiddenkillerspod/ Facebook https://www.facebook.com/hiddenkillerspod/ Tik-Tok https://www.tiktok.com/@hiddenkillerspod X Twitter https://x.com/tonybpod Listen Ad-Free On Apple Podcasts Here: https://podcasts.apple.com/us/podcast/true-crime-today-premium-plus-ad-free-advance-episode/id1705422872

Karen Read Trial Day 25 Recap: Defense Witness Turns on Them, Alleges Defense Member Threatened Her! In a dramatic day inside the Norfolk Superior Court, the Karen Read murder trial took a turn that no one saw coming—when the defense's own witnesses began pushing back. From allegations of witness coercion to a controversial dog bite theory, Day 25 of the trial was packed with explosive revelations and intense courtroom exchanges. Former Canton Police Officer Kelly Dever delivered one of the most impactful testimonies of the trial so far. Dever told the jury that Karen Read's defense team pressured her to testify to a story she knew wasn't true—that she saw Higgins and Berkowitz alone in the garage with Read's SUV. When she refused, she claims they threatened her with perjury. In open court, she directed the accusation directly at defense attorney Alan Jackson. This wasn't a moment of confusion—it was a pointed, emotional standoff that put the defense's tactics under the microscope. Then came Jonathan Diamandis, a friend of former State Trooper Michael Proctor. He confirmed the authenticity of Proctor's now-infamous group chat texts, which were laced with crude, insulting, and misogynistic remarks about Karen Read. But the texts didn't say what the defense needed—they didn't mention any planted evidence, altered reports, or a cover-up. Just hostility. Just bias. And just as easily turned against the defense's credibility as the prosecution's. In the afternoon, the defense called Dr. Marie Russell, a forensic pathologist, to bolster their theory that John O'Keefe's injuries were more consistent with a dog attack than a car crash. But her testimony lacked any physical evidence—no dog DNA, no bite mark match, and no autopsy. The prosecution wasted no time in pointing out that her conclusions were drawn from photos, not science. This video breaks down the legal strategy, expert testimony, and ethical fallout—step by step. #KarenReadTrial #TrueCrime #WitnessCoercion #JohnOKeefe #ForensicEvidence #MichaelProctor #DogBiteDefense #KellyDever #LegalEthics #CourtroomDrama Want to comment and watch this podcast as a video?  Check out our YouTube Channel. https://www.youtube.com/@hiddenkillerspod Instagram https://www.instagram.com/hiddenkillerspod/ Facebook https://www.facebook.com/hiddenkillerspod/ Tik-Tok https://www.tiktok.com/@hiddenkillerspod X Twitter https://x.com/tonybpod Listen Ad-Free On Apple Podcasts Here: https://podcasts.apple.com/us/podcast/true-crime-today-premium-plus-ad-free-advance-episode/id1705422872

Karen Read Trial Day 25 Recap: Defense Witness Turns on Them, Alleges Defense Member Threatened Her! In a dramatic day inside the Norfolk Superior Court, the Karen Read murder trial took a turn that no one saw coming—when the defense's own witnesses began pushing back. From allegations of witness coercion to a controversial dog bite theory, Day 25 of the trial was packed with explosive revelations and intense courtroom exchanges. Former Canton Police Officer Kelly Dever delivered one of the most impactful testimonies of the trial so far. Dever told the jury that Karen Read's defense team pressured her to testify to a story she knew wasn't true—that she saw Higgins and Berkowitz alone in the garage with Read's SUV. When she refused, she claims they threatened her with perjury. In open court, she directed the accusation directly at defense attorney Alan Jackson. This wasn't a moment of confusion—it was a pointed, emotional standoff that put the defense's tactics under the microscope. Then came Jonathan Diamandis, a friend of former State Trooper Michael Proctor. He confirmed the authenticity of Proctor's now-infamous group chat texts, which were laced with crude, insulting, and misogynistic remarks about Karen Read. But the texts didn't say what the defense needed—they didn't mention any planted evidence, altered reports, or a cover-up. Just hostility. Just bias. And just as easily turned against the defense's credibility as the prosecution's. In the afternoon, the defense called Dr. Marie Russell, a forensic pathologist, to bolster their theory that John O'Keefe's injuries were more consistent with a dog attack than a car crash. But her testimony lacked any physical evidence—no dog DNA, no bite mark match, and no autopsy. The prosecution wasted no time in pointing out that her conclusions were drawn from photos, not science. This video breaks down the legal strategy, expert testimony, and ethical fallout—step by step. #KarenReadTrial #TrueCrime #WitnessCoercion #JohnOKeefe #ForensicEvidence #MichaelProctor #DogBiteDefense #KellyDever #LegalEthics #CourtroomDrama Want to comment and watch this podcast as a video?  Check out our YouTube Channel. https://www.youtube.com/@hiddenkillerspod Instagram https://www.instagram.com/hiddenkillerspod/ Facebook https://www.facebook.com/hiddenkillerspod/ Tik-Tok https://www.tiktok.com/@hiddenkillerspod X Twitter https://x.com/tonybpod Listen Ad-Free On Apple Podcasts Here: https://podcasts.apple.com/us/podcast/true-crime-today-premium-plus-ad-free-advance-episode/id1705422872

Today Rachel is joined by actress Margaret Berkotwitz about her career in musical theatre roles and her new film THINGS LIKE THIS Check out THINGS LIKE THIS using our affiliate link https://amzn.to/43TDj7G (ad) Pick up WHERE IT ALL BEGAN using our affiliate link https://amzn.to/43oZgM1 (ad) For all our interviews https://www.youtube.com/playlist?list=PLXv4sBF3mPUA_0JZ2r5fxhTRE_-RChCj5 Follow Margaret on instagram https://www.instagram.com/margaret_berkz/?hl=en Join us over on Patreon! http://www.patreon.com/hallmarkies Check out our merch: https://www.teepublic.com/stores/hallmarkies Send us your feedback at feedback@hallmarkiespodcast.com Or call +1 (801) 855-6407 Follow Rachel on twitter twitter.com/rachel_reviews Follow Rachel's blog at http://rachelsreviews.net Follow Rachel's Reviews on youtube https://www.youtube.com/c/rachelsreviews Follow Rachel on facebook www.facebook.com/smilingldsgirl Learn more about your ad choices. Visit megaphone.fm/adchoices

He's seen it all, from the days of hand-written ledgers to artificial intelligence. But one thing remains the same: it's all about people skills. In this episode, Berkowitz Pollack Brant Founder and Executive Chairman Richard Berkowitz shares his takes with SFBJ Editor-in-Chief Mel Melendez.

News headline roundup. The politics of tyranny.  Find us on YouTube. In this episode of The Bulletin, Mike and Clarissa discuss cruelty, the talks between the US and Russia, the bombing of a fertility clinic in California, former president Joe Biden's cancer diagnosis, and the anniversary of George Floyd's death. Then, Mike talks with Roger Berkowitz about the politics of tyranny.  GO DEEPER WITH THE BULLETIN: Join the conversation at our Substack Find us on YouTube. Rate and review the show in your podcast app of choice. ABOUT THE GUEST:  Roger Berkowitz is founder and academic director of the Hannah Arendt Center for Politics and Humanities and professor of politics, philosophy, and human rights at Bard College. Berkowitz is the author of The Gift of Science, the introduction to On Civil Disobedience by Henry David Thoreau and Hannah Arendt, and The Perils of Invention. His writing has appeared in The New York Times, The American Interest, Bookforum, The Forward, The Paris Review online, and Democracy.  ABOUT THE BULLETIN: The Bulletin is a twice-weekly politics and current events show from Christianity Today moderated by Clarissa Moll, with senior commentary from Russell Moore (Christianity Today's editor in chief) and Mike Cosper (director, CT Media). Each week, the show explores current events and breaking news and shares a Christian perspective on issues that are shaping our world. We also offer special one-on-one conversations with writers, artists, and thought leaders whose impact on the world brings important significance to a Christian worldview, like Bono, Sharon McMahon, Harrison Scott Key, Frank Bruni, and more. The Bulletin listeners get 25% off CT. Go to https://orderct.com/THEBULLETIN to learn more. “The Bulletin” is a production of Christianity Today Producer: Clarissa Moll Associate Producer: Alexa Burke Editing and Mix: Kevin Morris Music: Dan Phelps Executive Producers: Erik Petrik and Mike Cosper Senior Producer: Matt Stevens Learn more about your ad choices. Visit podcastchoices.com/adchoices

Truth behind the Crime: Wendy Savino Special guest Frank and Maria DeGennaroWendy Savino is a remarkable woman whose life encompasses both a harrowing encounter with a notorious serial killer and a rich history in the performing arts. ⸻

On today's episode I have comic book writers and filmmakers, Ben and Max Berkowitz!  I first came across the Berkowtiz Brothers almost a year ago when I briefly met them at a signing for their comic book, "The Writer". I'll be honest, I wasn't at the signing for them, but for another comic and decided to pick theirs up while I was there. As soon as I dove in I was hooked! I talked with Max and Ben about growing up on the East Coast, their first introduction to comic books, getting involved with entertainment, earliest influences and the first comics they bought, developing "The Writer" and bringing Josh Gadd on board, pitching to Dark Horse Comics, their social marketing company Not A Billionaire, and so much more! A huge Thank You to Max and Ben for taking the time to join me on the show. I've been wanting to have them on the show for a while now and was thrilled we were able to make it happen. You can pick up the paperback of "The Writer" now, which includes the full story and all of the issues in one book simply by clicking on the links at www.onthemicpodcast.com Make sure to follow the Berkowitz Brothers on all of the links at www.onthemicpodcast.com as well.  Thanks, Ben and Max! Enjoy the episode!  

Paul Berkowitz, director at Hlaziya Solutions, speaks to Lester Kiewit about the latest insights into voter sentiment in South Africa’s metros, based on a recent Brenthurst Foundation survey. He unpacks key trends ahead of the 2026 local government elections, including the Democratic Alliance’s lead in most metros, Cape Town’s strong reputation for good governance, growing support for coalitions despite frustrations with instability, and the rising influence of the uMkhonto weSizwe party in Gauteng. Berkowitz also explores voter preferences for different coalition scenarios and what these findings reveal about the current political mood in the country’s urban centres. Good Morning Cape Town with Lester Kiewit is a podcast of the CapeTalk breakfast show. This programme is your authentic Cape Town wake-up call. Good Morning Cape Town with Lester Kiewit is informative, enlightening and accessible. The team’s ability to spot & share relevant and unusual stories make the programme inclusive and thought-provoking. Don’t miss the popular World View feature at 7:45am daily. Listen out for #LesterInYourLounge which is an outside broadcast – from the home of a listener in a different part of Cape Town - on the first Wednesday of every month. This show introduces you to interesting Capetonians as well as their favourite communities, habits, local personalities and neighbourhood news. Thank you for listening to a podcast from Good Morning Cape Town with Lester Kiewit. Listen live on Primedia+ weekdays between 06:00 and 09:00 (SA Time) to Good Morning CapeTalk with Lester Kiewit broadcast on CapeTalk https://buff.ly/NnFM3Nk For more from the show go to https://buff.ly/xGkqLbT or find all the catch-up podcasts here https://buff.ly/f9Eeb7i Subscribe to the CapeTalk Daily and Weekly Newsletters https://buff.ly/sbvVZD5 Follow us on social media CapeTalk on Facebook: https://www.facebook.com/CapeTalk CapeTalk on TikTok: https://www.tiktok.com/@capetalk CapeTalk on Instagram: https://www.instagram.com/ CapeTalk on X: https://x.com/CapeTalk CapeTalk on YouTube: https://www.youtube.com/@CapeTalk567 See omnystudio.com/listener for privacy information.

On August 10, 1977, the NYPD arrested David Berkowitz for the Son of Sam murders that had terrorized New York City for over a year. Berkowitz confessed to shooting sixteen people and killing six with a .44 caliber Bulldog revolver, and the case was officially closed. Journalist Maury Terry was suspicious of Berkowitz's confession. Spurred by conflicting witness descriptions of the killer and clues overlooked in the investigation, Terry was convinced Berkowitz didn't act alone. Meticulously gathering evidence for a decade, he released his findings in the first edition of The Ultimate Evil. Based upon the evidence he had uncovered, Terry theorized that the Son of Sam attacks were masterminded by a Yonkers-based cult that was responsible for other ritual murders across the country. After Terry's death in 2015, documentary filmmaker Josh Zeman (Cropsey, The Killing Season, Murder Mountain) was given access to Terry's files, which form the basis of his docuseries with Netflix and a companion podcast. Taken together with The Ultimate Evil, which includes a new introduction by Zeman, these works reveal the stunning intersections of power, wealth, privilege, and evil in America—from the Summer of Sam until today.Become a supporter of this podcast: https://www.spreaker.com/podcast/the-opperman-report--1198501/support.

On August 10, 1977, the NYPD arrested David Berkowitz for the Son of Sam murders that had terrorized New York City for over a year. Berkowitz confessed to shooting sixteen people and killing six with a .44 caliber Bulldog revolver, and the case was officially closed. Journalist Maury Terry was suspicious of Berkowitz's confession. Spurred by conflicting witness descriptions of the killer and clues overlooked in the investigation, Terry was convinced Berkowitz didn't act alone. Meticulously gathering evidence for a decade, he released his findings in the first edition of The Ultimate Evil. Based upon the evidence he had uncovered, Terry theorized that the Son of Sam attacks were masterminded by a Yonkers-based cult that was responsible for other ritual murders across the country. After Terry's death in 2015, documentary filmmaker Josh Zeman (Cropsey, The Killing Season, Murder Mountain) was given access to Terry's files, which form the basis of his docuseries with Netflix and a companion podcast. Taken together with The Ultimate Evil, which includes a new introduction by Zeman, these works reveal the stunning intersections of power, wealth, privilege, and evil in America—from the Summer of Sam until today.Become a supporter of this podcast: https://www.spreaker.com/podcast/the-opperman-report--1198501/support.

For this episode of Black Hoodie Alchemy, I'm finally covering a topic I have teased here and there since the beginning of the whole show-run! At last, I am covering the sprawling, Charlie-Kelly-in-the-mailroom-style conspiracy theory that suggests that David Berkowitz did not act alone in the Son of Sam Murders of NYC. But make no mistake, this frenzied mailroom vibe comes not from the incredulity of the research, but from the sheer state of mind that tackling all of this topic's many threads will put you into! And let's not forget the fact that Berkowitz was working in a mailroom at the time, and contributed to the whole "going postal" phrase that we have today. Get ready to enter a story that surprisingly finds us diving into real-life theistic Satanism, Scientology and L. Ron Hubbard, Charles Manson, a strange Scientology doom-hippie offshoot called 'The Process Church of the Final Judgment', the dangers of hysterical Satanic Panic, brainwashing, and so much more! There is a lot of hype, hysteria, and leaping-conspiracy-theory conjecture that surrounds this case, but the actual case for the 'Sons of Sam' itself is quite compelling to me. In any case, I work my way through not only the classic tome on the topic, Maury Terry's 'The Ultimate Evil', but I also dissect the docu-series done by award-winning filmmaker Josh Zeman on this same subject, entitled: Sons of Sam: A Descent into Darkness. Not only was Zeman friends with Maury Terry towards the end of his life, but Zeman was the man that Terry willed his entire life's work to -- every document, photo, scribble, phone number... everything. And as an inside scoop, I was able to pick Josh Zeman's brain about this over a Skype call many years ago. While there isn't much he told me that his documentary didn't say, I did get some more direct and explicitly informative answers from him that I share here in the episode.Happy trip down the rabbit hole!Related BHA true crime episodes:The Brazilian PunisherClub Kids & Party MonstersRichard KuklinskiMalachi York's hiphop cultSante Muerte - the good and badIsrael Keyes Alaskan serial killerCartel Black MagiciansSHOW NOTES:NY Times Son of Sam TimelineJosh Zeman filmographySons of Sam: A Descent into Darkness documentaryActual old school Process Church propagandaLove, Sex, Fear, Death - book about the Process ChurchMaury Terry's 'The Ultimate Evil'Declassified FBI investigation into Process ChurchSon of Sam in prisonEd Opperman talks to NYPD Mike CodellaOpperman talks to childhood friend of Carr familyOpperman on History of 'Yonkers Cult'Opperman talks to Carl Denaro, Son of Sam victimLong Island Serial KillingsThis week's featured music -- a truly magnificent sonic assault coming from the strongest underground punk, hardcore, and experimental rock acts around!Salt Style - SaltSouled Out - Doc HammerCarbon Copy - Negative BlastWhen You Force It (Demo) - Zig Mentality

EPISODE 402. Ever wonder why "healthy eating" advice just doesn't seem to fit your brain—or your life? In this jam-packed episode, Katie sits down with neurodivergence nutrition expert Sam Berkowitz MPH, RD, LDN, to unmask the challenges (and unexpected solutions) for neurodivergent folks navigating food, body image, and overwhelming nutrition noise. If you or someone you love struggles with rigid thinking, sensory food aversions, or the stress of diet culture, this conversation just might change how you approach nourishing your body—for good.What We Cover:What neurodivergence really means, how it overlaps with eating challenges, and why a one-size-fits-all approach falls flatHow to break free from all-or-nothing food rules and find structure and flexibility that actually works for unique brainsThe truth about processed foods, sugar, social media fear-mongering—and how to protect your mental (and nutritional) health from all the noiseConnect with Sam:Website | www.unmasked-nutrition.com Podcast | www.unmasked-nutrition.com/blogConnect with Katie:Meal Prep Like a Pro Without Obsessing Over Every Bite | www.katiehake.com/prepJoin our FREE 5-Day Walking Challenge | Walk with Me!Text me your AHA moment from today's episode!

Send us a textAlaska State House Representative for West Anchorage Carolyn Hall got an internship with the Boston Red Sox during her senior year of college in New Hampshire. This led to her dream job working for the team as a videographer during their World Series win in 2004. In 2008 she branched into TV journalism getting her first job with a small local market: KTUU in Anchorage. She covered the Iditarod, Gov. Sarah Palin, Sen. Ted Stevens' trial from DC, and Sen. Lisa Murkowski's 2010 write-in campaign. Hall then worked for a larger TV market in Seattle where she earned an Emmy for her coverage of the Oso Landslide in 2014. After returning to Anchorage, she left broadcast journalism and branched into politics working as communications director for Governor Bill Walker, and at the start of the Covid pandemic, for Anchorage Mayor Ethan Berkowitz. We talk about all of that and how she ended up running for office in today's episode. Watch the video of Carolyn Hall and Ethan Berkowitz leaving Anchorage Assembly Chambers, Aug 12, 2020.

Joining us today are the co-founders of the communications and marketing firm Not A Billionaire and the co-writers of the Jewish fantasy folklore comic series The Writer with actor/co-writer Josh Gad and artist Ariel Olivetti.In their series The Writer, amidst a dark and mysterious turn, comic book writer Stan Siegel's life dives into a neo-Nazi occult nightmare. As demonic chaos and high-speed chases reign, Stan's hunger for answers unveils hidden identities, setting off a desperate race against time in this thrilling saga. To combat the rising tide of terror, Stan must become the hero from his pages.It is our pleasure to welcome Ben & Max Berkowitz onto The Oblivion Bar Podcast!Thank you Oni Press & Endless Comics, Cards & Games for sponsoring The Oblivion Bar PodcastFollow us on InstagramFollow us on ThreadsFollow us on BlueSkyLike us on FacebookConsider supporting us over on PatreonThank you DreamKid for our Oblivion Bar musicThank you KXD Studios for our Oblivion Bar art

On this episode of GoalChat, host Debra Eckerling discusses graphic novels with Ben Berkowitz, co-writer of The Writer, along with his brother, Max, and actor Josh Gad, and cartoonist Chari Pere of the "Unspoken" Cartoonmentary series, among others. According to them, a graphic novel is a book-length work, where you explore themes and stories (Ben) through images and imagery (Chari). It's a quick clean, detailed way to tell a story. Ben and Chari talk about the process of creating a graphic novel, what and who inspires them, their dream projects, and more. Getting Started - Ben: Find the spark that makes you want to run with it - Chari: Be ready to run with it. Some projects are "not yet - Chari: You have an idea, look at other books in that genre, make a summary, turn it into beats, sketch thumbnails, get more and more detailed - Ben: If you are not doing the art, you need to build the team. (The Writer is illustrated by Marvel and DC Comics legend Ariel Olivetti, whom the Berkowitz Brothers pitched via Instagram DM.) Goals - Chari: If you are struggling with an idea, take a noun and an action, and tell a story with that - Ben: Finish something Final Thoughts - Ben: Lean into the spark - Chari: Give yourself permission to do what you want to do to get your ideas out there Learn More About Ben Berkowitz: NotaBillionaire.com Char Pere: ChariPere.com Debra Eckerling: TheDEBMethod.com/blog 52SecretsBook.com Learn more about your ad choices. Visit megaphone.fm/adchoices

Howdy folks of the interwebs! Your host Double J is back with another edition of OpGCD Live! Today, Double J is joined by Jonathan Mitchell, author of "Before Son of Sam: The Submerged History of a Yonkers Cult" - to discuss all things Son of Sam & Maury Terry's investigation as stated in his book "The Ultimate Evil".Jonathan Mitchell has studied the pre-Son of Sam/Yonkers, NY cult activity and has a unique view of the environment that produced the Son of Sam cult.Jonathan also has done an excellent study of the available files of Maury Terry in order to better understand the cast of characters comprising this cult, colloquially known as "Son of Sam" cult. These are the characters not named Berkowitz!This outlying cast of characters comprising this cryptic cult are far more interest'n than David Berkowitz...and some may be just as complicit in the homicides committed by the "Son of Sam" cult, same as Berkowitz.Some of those cast of characters maintained status at the highest levels of society, government, and "national security". Perhaps these are the salient characteristics to understand why we as a public are learning these details decade after the alleged end of the crimes of murder & chaos back in 1977!Anyhow, folks of the interwebs, thank you again for joining me today to get a lil GCD! Enjoy today's podcast discussion on Son of Sam, Yonkers cult activity, The Ultimate Evil, and the Process Church!Enjoy the show! Links for Jonathan Mitchell - throwaways@yahoo.comhttps://jonathandm.substack.com/https://www.amazon.com/Before-Son-Sam...https://x.com/JonathanM1973 Links for JJ - https://linktr.ee/operationgcdLinks discussed in show - https://thepeoplevsdavidberkowitz.com...https://thepeoplevsdavidberkowitz.com...

Diagnosing and differentiating among the many possible localizations and causes of vision loss is an essential skill for neurologists. The approach to vision loss should include a history and examination geared toward localization, followed by a differential diagnosis based on the likely location of the pathophysiologic process.  In this episode, Aaron Berkowitz, MD, PhD, FAAN speaks with Nancy J. Newman, MD, FAAN, author of the article “Approach to Vision Loss” in the Continuum® April 2025 Neuro-ophthalmology issue.  Dr. Berkowitz is a Continuum® Audio interviewer and a professor of neurology at the University of California San Francisco in the Department of Neurology and a neurohospitalist, general neurologist, and clinician educator at the San Francisco VA Medical Center at the San Francisco General Hospital in San Francisco, California.  Dr. Newman is a professor of ophthalmology and neurology at the Emory University School of Medicine in Atlanta, Georgia.  Additional Resources Read the article: Approach to Vision Loss Subscribe to Continuum®: shop.lww.com/Continuum  Earn CME (available only to AAN members): continpub.com/AudioCME  Continuum® Aloud (verbatim audio-book style recordings of articles available only to Continuum® subscribers): continpub.com/Aloud More about the American Academy of Neurology: aan.com  Social Media facebook.com/continuumcme  @ContinuumAAN  Host: @AaronLBerkowitz  Full episode transcript available here Dr Jones: This is Dr Lyell Jones, Editor-in-Chief of Continuum. Thank you for listening to Continuum Audio. Be sure to visit the links in the episode notes for information about earning CME subscribing to the journal, and exclusive access to interviews not featured on the podcast. Dr Berkowitz: This is Dr Aaron Berkowitz, and today I'm interviewing Dr Nancy Newman about her article on the approach to visual loss, which she wrote with Dr Valerie Biousse. This article appears in the April 2025 Continuum issue on neuro-ophthalmology. Welcome to the podcast, Dr Newman. I know you need no introduction, but if you wouldn't mind introducing yourself to our listeners. Dr Newman: Sure. My name's Nancy Newman. I am a neurologist and neuro-ophthalmologist, professor of ophthalmology and neurology at the Emory University School of Medicine in Atlanta, Georgia. Dr Berkowitz: You and your colleague Dr Biousse have written a comprehensive and practical article on the approach to visual loss here. It's fantastic to have this article by two of the world's leading experts and best-known teachers in neuro-ophthalmology. And so, readers of this article will find extremely helpful flow charts, tables and very nuanced clinical discussion about how to make a bedside diagnosis of the cause of visual loss based on the history exam and ancillary testing. We'll talk today about that important topic, and excited to learn from you and for our listeners to learn from you. To begin, let's start broad. Let's say you have a patient presenting with visual loss. What's your framework for the approach to this common chief concern that has such a broad differential diagnosis of localizations and of causes? Where do you start when you hear of visual loss? How do you think about this chief concern? Dr Newman: Well, it's very fun because this is the heart of being a neurologist, isn't it? Nowhere in the nervous system is localization as important as the complaint of vision loss. And so, the key, as any neurologist knows, is to first of all figure out where the problem is. And then you can figure out what it is based on the where, because that will limit the number of possibilities. So, the visual system is quite beautiful in that regard because you really can exquisitely localize based on figuring out where things are. And that starts with the history and then goes to the exam, in particular the first localization. So, you can whittle it down to the more power-for-your-buck question is, is the vision lost in one eye or in two eyes? Because if the vision loss clearly, whether it's transient or persistent, is in only one eye, then you only have to think about the eyeball and the optic nerve on that side. So, think about that. Why would you ever get a brain MRI? I know I'm jumping ahead here, but this is the importance of localization. Because what you really want to know, once you know for sure it's in one eye, is, is it an eyeball problem---which could be anything from the cornea, the lens, the vitreous, the retina---or is it an optic nerve problem? The only caveat is that every once in a while, although we trust our patients, a patient may insist that a homonymous hemianopia, especially when it's transient, is only in the eye with the temporal defect. So that's the only caveat. But if it's in only one eye, it has to be in that side eyeball or optic nerve. And if it's in two eyes, it's either in both eyeballs or optic nerves, or it's chiasmal or retrochiasmal. So that's the initial approach and everything about the history should first be guided by that. Then you can move on to the more nuanced questions that help you with the whats. Once you have your where, you can then figure out what the whats are that fit that particular where. Dr Berkowitz: Fantastic. And your article with Dr Biousse has this very helpful framework, which you alluded to there, that first we figure out, is it monocular or binocular? And we figure out if it's a transient or fixed or permanent deficit. So, you have transient monocular, transient binocular, fixed monocular, fixed binocular. And I encourage our listeners to seek out this article where you have a table for each of those, a flow chart for each of those, that are definitely things people want to have printed out and at their desk or on their phone to use at the bedside. Very helpful. So, we won't be able to go through all of those different clinical presentations in this interview, but let's focus on monocular visual loss. As you just mentioned, this can be an eye problem or an optic nerve problem. So, this could be an ophthalmologic problem or a neurologic problem, right? And sometimes this can be hard to distinguish. So, you mentioned the importance of the history. When you hear a monocular visual loss- and with the caveat, I said you're convinced that this is a monocular visual problem and not a visual field defect that may appear. So, the patient has a monocular deficit, how do you approach the history at trying to get at whether this is an eye problem or an optic nerve problem and what the cause may be? Dr Newman: Absolutely. So, the history at that point tends not to be as helpful as the examination. My mentor used to say if you haven't figured out the answer to the problem after your history, you're in trouble, because that 90% of it is history and 10% is the exam. In the visual system, the exam actually may have even more importance than anywhere else in the neurologic examination. And we need as neurologists to not have too much hubris in this. Because there's a whole specialty on the eyeball. And the ophthalmologists, although a lot of their training is surgical training that that we don't need to have, they also have a lot of expertise in recognizing when it's not a neurologic problem, when it's not an optic neuropathy. And they have all sorts of toys and equipment that can very much help them with that. And as neurologists, we tend not to be as versed in what those toys are and how to use them. So, we have to do what we can do. Your directive thalmoscope, I wouldn't throw it in the garbage, because it's actually helpful to look at the eyeball itself, not just the back of the eye, the optic nerve and retina. And we'll come back to that, but we have in our armamentarium things we can do as neurologists without having an eye doctor's office. These include things like visual acuity and color vision, confrontation, visual fields. Although again, you have to be very humble. Sometimes you're lucky; 30% of the time it's going to show you a defect. It has to be pretty big to pick it up on confrontation fields. And then as we say, looking at the fundus. And you probably know that myself and Dr Biousse have been on somewhat of a crusade to allow the emperor's new clothes to be recognized, which is- most neurologists aren't very comfortable using the direct ophthalmoscope and aren't so comfortable, even if they can use it, seeing what they need to see. It's hard. It's really, really hard. And it's particularly hard without pupillary dilation. And technology has allowed us now with non-mydriatic cameras, cameras that are incredible, even through a small pupil can take magnificent pictures of the back of the eye. And who wouldn't rather have that? And as their cost and availability- the cost goes down and their availability goes up. These cameras should be part of every neurology office and every emergency department. And this isn't futuristic. This is happening already and will continue to happen. But over the next five years or so… well, we're transitioning into that. I think knowing what you can do with the direct ophthalmoscope is important. First of all, if you dial in plus lenses, you can't be an ophthalmologist, but you can see media opacities. If you can't see into the back of the eye, that may be the reason the patient can't see out. And then just seeing if someone has central vision loss in one eye, it's got to be localized either to the media in the axis of vision; or it's in the macula, the very center of the retina; or it's in the optic nerve. So, if you get good at looking at the optic nerve and then try to curb your excitement when you saw it and actually move a little temporally and take a look at the macula, you're looking at the two areas. Again, a lot of ophthalmologists these days don't do much looking with the naked eye. They actually do photography, and they do what's called OCT, optical coherence tomography, which especially for maculopathies, problems in the macula are showing us the pathology so beautifully, things that used to be considered subtle like central serous retinopathy and other macula. So, I think having a real healthy respect for what an eye care provider can do for you to help screen away the ophthalmic causes, it's very, very important to have a patient complaining of central vision loss, even if they have a diagnosis like multiple sclerosis, you expect that they might have an optic neuritis… they can have retinal detachments and other things also. And so, I think every one of these patients should be seen by an eye care provider as well. Dr Berkowitz: Thank you for that overview. And I feel certainly as guilty as charged here as one of many neurologists, I imagine, who wish we were much better and more comfortable with fundoscopy and being confident on what we see. But as you said, it's hard with the direct ophthalmoscope and a non-dilated exam. And it's great that, as you said, these fundus photography techniques and tools are becoming more widely available so that we can get a good look at the fundus. And then we're going to have to learn a lot more about how to interpret those images, right? If we haven't been so confident in our ability to see the fundus and analyze some of the subtle abnormalities that you and your colleagues and our ophthalmology colleagues are more familiar with. So, I appreciate you acknowledging that. And I'm glad to hear that coming down the pipeline, there are going to be some tools to help us there. So, you mentioned some of the things you do at the bedside to try to distinguish between eye and optic nerve. Could you go into those in a little bit more detail here? How do you check the visual fields? For example, some people count fingers, some people wiggle fingers, see when the patient can see. How should we be checking visual fields? And what are some of the other bedside tasks you use to decide this is probably going to end up being in the optic nerve or this seems more like an eye? Dr Newman: Of course. Again, central visual acuity is very important. If somebody is older than fifty, they clearly will need some form of reading glasses. So, keeping a set of plus three glasses from cheapo drugstore in your pocket is very helpful. Have them put on their glasses and have them read an ear card. It's one of the few things you can actually measure and examine. And so that's important. The strongest reflex in the body and I can have it duke it out with the peripheral neurologists if they want to, it's not the knee jerk, it's looking for a relative afferent pupillary defect. Extremely important for neurologists to feel comfortable with that. Remember, you cut an optic nerve, you're not going to have anisocoria. It's not going to cause a big pupil. The pupils are always equal because this is not an efferent problem, it's an afferent problem, an input problem. So basically, if the eye has been injured in the optic nerve and it can't get that information about light back into the brain, well, the endoresfol nuclei, both of them are going to reset at a bigger size. And then when you swing over and shine that light in the good optic nerve, the good eye, then the brain gets all this light and both endoresfol nuclei equally set those pupils back at a smaller size. So that's the test for the relative afferent pupillary defect. When you swing back and forth. Of course, when the light falls on the eye, that's not transmitting light as well to the brain, you're going to see the pupil dilate up. But it's not that that pupil is dilating alone. They both are getting bigger. It's an extremely powerful reflex for a unilateral or asymmetric bilateral optic neuropathy. But what you have to remember, extremely important, is, where does our optic nerve come from? Well, it comes from the retinal ganglion cells. It's the axons of the retinal ganglion cells, which is in the inner retina. And therefore inner retinal disorders such as central retinal artery occlusion, ophthalmic artery occlusion, branch retinal artery occlusion, they will also give a relative afferent pupillary defect because you're affecting the source. And this is extremely important. A retinal detachment will give a relative afferent pupillary defect. So, you can't just assume that it's optic nerve. Luckily for us, those things that also give a relative afferent pupillary defect from a retinal problem cause really bad-looking retinal disease. And you should be able to see it with your direct ophthalmoscope. And if you can't, you definitely will be able to see it with a picture, a photograph, or having an ophthalmologist or optometrist take a look for you. That's really the bedside. You mentioned confrontation visual fields. I still do them, but I am very, very aware that they are not very sensitive. And I have an extremely low threshold to- again, I have something in my office. But if I were a general neurologist, to partner with an eye care specialist who has an automated visual field perimeter in their office because it is much more likely to pick up a deficit. Confrontation fields. Just remember, one eye at a time. Never two eyes at the same time. They overlap with each other. You're going to miss something if you do two eyes open, so one eye at a time. You check their field against your field, so you better be sure your field in that eye is normal. You probably ought to have an automated perimetry test yourself at some point during your career if you're doing that. And remember that the central thirty degrees is subserved by 90% of our fibers neurologically, so really just testing in the four quadrants around fixation within the central 30% is sufficient. You can present fingers, you don't have to wiggle in the periphery unless you want to pick up a retinal detachment. Dr Berkowitz: You mentioned perimetry. You've also mentioned ocular coherence tomography, OCT, other tests. Sometimes we think about it in these cases, is MRI one of the orbits? When do you decide to pursue one or more of those tests based on your history and exam? Dr Newman: So again, it sort of depends on what's available to you, right? Most neurologists don't have a perimeter and don't have an OCT machine. I think if you're worried that you have an optic neuropathy, since we're just speaking about monocular vision loss at this point, again, these are tests that you should get at an office of an eye care specialist if you can. OCT is very helpful specifically in investigating for a macular cause of central vision loss as opposed to an optic nerve cause. It's very, very good at picking up macular problems that would be bad enough to cause a vision problem. In addition, it can give you a look at the thickness of the axons that are about to become the optic nerve. We call it the peripapillary retinal nerve fiber layer. And it actually can look at the thickness of the layer of the retinal ganglion cells without any axons on them in that central area because the axons, the nerve fiber layer, bends away from central vision. So, we can see the best we can see. And remember these are anatomical measurements. So, they will lag, for the ganglion cell layer, three to four weeks behind an injury, and for the retinal nerve fiber, layer usually about six weeks behind an entry. Whereas the functional measurements, such as visual acuity, color vision, visual fields, will be immediate on an injury. So, it's that combination of function and anatomy examination that makes you all-powerful. You're very much helped by the two together and understanding where one will be more helpful than the other. Dr Berkowitz: Let's say we've gotten to the optic nerve as our localization. Many people jump to the assumption it's the optic nerve, it's optic neuritis, because maybe that's the most common diagnosis we learn in medical school. And of course, we have to sometimes, when we're teaching our students or trainees,  say, well, actually, not all optic nerve disease, optic neuritis, we have to remember there's a broader bucket of optic neuropathy. And I remember, probably I didn't hear that term until residency and thought, oh, that's right. I learned optic neuritis. Didn't really learn any of the other causes of optic nerve pathology in medical school. And so, you sort of assume that's the only one. And so you realize, no, optic neuropathy has a differential diagnosis beyond optic neuritis. Neuritis is a common cause. So how do you think about the “what” once you've localized to the optic nerve, how do you think about that? Figure out what the cause of the optic neuropathy is? Dr Newman: Absolutely. And we've been trying to convince neuro-radiologists when they see evidence of optic nerve T2 hyperintensity, that just means damage to the optic nerve from any cause. It's just old damage, and they should not put in their read consistent with optic neuritis. But that's a pet peeve. Anyway, yes, the piece of tissue called the optic nerve can be affected by any category of pathophysiology of disease. And I always suggest that you run your categories in your head so you don't leave one out. Some are going to be more common to be bilateral involvement like toxic or metabolic causes. Others will be more likely unilateral. And so, you just run those guys. So, in my mind, my categories always are compressive-slash-infiltrative, which can be neoplastic or non-neoplastic. For example, an ophthalmic artery aneurysm pressing on an optic nerve, or a thyroid, an enlarged thyroid eye muscle pressing on the optic nerve. So, I have compressive infiltrative, which could be neoplastic or not neoplastic. I have inflammatory, which can be infectious. Some of the ones that can involve the optic nerve are syphilis, cat scratch disease. Or noninfectious, and these are usually your autoimmune such as idiopathic optic neuritis associated with multiple sclerosis, or MOG, or NMO, or even sarcoidosis and inflammation. Next category for me would be vascular, and you can have arterial versus venous in the optic nerve, probably all arterial if we're talking about causes of optic neuropathy. Or you could have arteritic versus nonarteritic with the vascular, the arteritic usually being giant cell arteritis. And the way the optic nerve circulation is, you can have an anterior ischemic optic neuropathy or a posterior ischemic optic neuropathy defined by the presence of disc edema suggesting it's anterior, the front of the optic nerve, or not, suggesting that it's retrobulbar or posterior optic nerve. So what category am I- we mentioned toxic, metabolic nutritional. And there are many causes in those categories of optic neuropathy, usually bilateral. You can have degenerative or inherited. And there are causes of inherited optic neuropathies such as Leber hereditary optic neuropathy and dominant optic atrophy. And then there's a group I call the mechanical optic neuropathies. The obvious one is traumatic, and that can happen in any piece of tissue. And then the other two relate to the particular anatomy of the eyeball and the optic nerve, and the fact that the optic nerve is a card-carrying member of the central nervous system. So, it's not really a nerve by the way, it's a tract. Think about it. Anyway, white matter tract. It is covered by the same fluid and meninges that the rest of the brain. So, what mechanically can happen? Well, you could have an elevated intraocular pressure where that nerve inserts. That's called glaucoma, and that would affect the front of the optic nerve. Or you can have elevated intracranial pressure. And if that's transmitted along the optic nerve, it can make the front of the optic nerve swell. And we call that specifically papilledema, optic disk edema due specifically to raised intracranial pressure. We actually even can have low intraocular pressure cause something called hypotony, and that can actually even give an optic neuropathy the swelling of the optic nerve. So, these are the mechanical. And if you were to just take that list and use it for any piece of tissue anywhere, like the heart or the kidney, you can come up with your own mechanical categories for those, like pericarditis or something like that. And then all those other categories would fit. But of course, the specific causes within that pathophysiology are going to be different based on the piece of tissue that you have. In this case, the optic nerve. Dr Berkowitz: In our final moments here, we've talked a lot about the approach to monocular visual loss. I think most neurologists, once we find a visual field defect, we breathe a sigh of relief that we know we're in our home territory here, somewhere in the visual task base that we've studied very well. I'm not trying to distinguish ocular causes amongst themselves or ocular from optic nerve, which can be very challenging at the bedside. But one topic you cover in your article, which I realized I don't really have a great approach to, is transient binocular visual loss. Briefly here, since we're running out of time, what's your approach to transient binocular visual loss?  Dr Newman: We assume with transient binocular vision loss that we are not dealing with a different experience in each eye, because if you have a different experience in each eye, then you're dealing with bilateral eyeball or optic nerve. But if you're having the same experience in the two eyes, it's equal in the two eyes, then you're located. You're located, usually, retro chiasmally, or even chiasm if you have pituitary apoplexy or something. So, all of these things require imaging, and I want to take one minute to talk about that. If you are sure that you have monocular vision loss, please don't get a brain MRI without contrast. It's really useless. Get a orbital MRI with contrast and fat suppression techniques if you really want to look at the optic nerve. Now, let's say you you're convinced that this is chiasmal or retrochiasmal. Well then, we all know we want to get a brain MRI---again, with and without contrast---to look specifically where we could see something. And so, if it's persistent and you have a homonymous hemianopia, it's easy, you know where to look. Be careful though, optic track can fool you. It's such a small little piece, you may miss it on the MRI, especially in someone with MS. So really look hard. There's very few things that are homonymous hemianopias MRI negative. It may just be that you didn't look carefully enough. And as far as the transient binocular vision loss, again, remember, even if it's persistent, it has to be equal vision in the two eyes. If there's inequality, then you have a superimposed anterior visual pathway problem, meaning in front of the chiasm on the side that's worse. The most common cause of transient binocular vision loss would be a form of migraine. The visual aura of migraine usually is a positive phenomenon, but sometimes you can have a homonymous hemianopic persistent defect that then ebbs and flows and goes away. Usually there's buildup, lasts maybe fifteen minutes and then it goes away, not always followed by a headache. Other things to think of would be transient ischemic attack in the vertebra Basler system, either a homonymous hemianopia or cerebral blindness, what we call cortical blindness. It can be any degree of vision loss, complete or any degree, as long as the two eyes are equal. That should last only minutes. It should be maximum at onset. There should be no buildup the way migraine has it. And it should be gone within less than ten minutes, typically. After fifteen, that's really pushing it. And then you could have seizures. Seizures can actually be the aura of a seizure, the actual ictal phenomenon of a seizure, or a postictal, almost like a todd's paralysis after a seizure. These events are typically bright colors and flashing, and they last usually seconds or just a couple of minutes at most. So, you can probably differentiate them. And then there are the more- less common but more interesting things like hyperglycemia, non-ketonic hyperglycemia can give you transient vision loss from cerebral origin, and other less common things like that. Dr Berkowitz: Fantastic. Although we've talked about many pearls of clinical wisdom here with you today, Dr Newman, this is only a fraction of what we can find in your article with Dr Biousse. We focused here on monocular visual loss and a little bit at the end here on binocular visual loss, transient binocular visual loss. But thank you very much for your article, and thank you very much for taking the time to speak with us today. Again, today I've been interviewing Dr Nancy Newman about her article with Dr Valerie Biousse on the approach to visual loss, which appears in the most recent issue of Continuum on neuro-ophthalmology. Be sure to check out Continuum audio episodes from this and other issues. Thank you so much to our listeners for joining us today. Dr Monteith: This is Dr Teshamae Monteith, Associate Editor of Continuum Audio. If you've enjoyed this episode, you'll love the journal, which is full of in-depth and clinically relevant information important for neurology practitioners. Use this link in the episode notes to learn more and subscribe. AAN members, you can get CME for listening to this interview by completing the evaluation at continpub.com/audioCME. Thank you for listening to Continuum Audio.

Subscribe to UnitedHealthcare's Community & State newsletter.Health Affairs' Senior Deputy Editor Rob Lott interviews Seth Berkowitz of the UNC School of Medicine to discuss his recent paper that explores a new approach to help guide research and policy at the intersection of income, food, nutrition, and health. Order the April 2025 issue of Health Affairs.Currently, more than 70 percent of our content is freely available - and we'd like to keep it that way. With your support, we can continue to keep our digital publication Forefront and podcast Subscribe to UnitedHealthcare's Community & State newsletter.

Health Affairs' Jeff Byers welcomes Seth Berkowitz of UNC School of Medicine back to the program to discuss nutrition in the US, the current state of SNAP benefits, and his upcoming paper to be featured in our April 2025 theme issue on food, nutrition, and health.Preorder the April 2024 theme issue of Health Affairs.Join us April 23 for an exclusive Insider virtual event exploring site-neutral payments with health economist and health services researcher Brady Post of Northeastern University and Health Affairs' Meg Winchester.Learn more about Seth's book, Equal Care: Health Equity, Social Democracy, and the Egalitarian State.Related Articles:Tennessee bill could ban candy and soda from SNAP benefits (WJHL)

RED HEIFERS are back in Israel! But what does that mean, exactly? Adam Eliyahu Berkowitz, writer for Israel365News.com and author of the new book Return of the Red Heifers (israel365store.com/products/red-heifers), joins us to explain the significance of the heifers, why they're important, and why a Third Temple isn't necessary to begin the sacrifices on the Temple Mount. We also discuss the historical context of the relationship between Jews and Christians, the role of the Messiah, modern misunderstandings surrounding these topics and the potential for future collaboration between the two faiths.Follow Adam's Substack here: AdamEliyahuBerkowitz.substack.com.

Howdy folks of the interwebs! Your host Double J is back with another edition of OpGCD Live! Today, Double J is joined by Jonathan Mitchell, author of "Before Son of Sam: The Submerged History of a Yonkers Cult" - to discuss all things Son of Sam & Maury Terry's investigation as stated in his book "The Ultimate Evil".Jonathan Mitchell has studied the pre-Son of Sam/Yonkers, NY cult activity and has a unique view of the environment that produced the Son of Sam cult.Jonathan also has done an excellent study of the available files of Maury Terry in order to better understand the cast of characters comprising this cult, colloquially known as "Son of Sam" cult. These are the characters not named Berkowitz!This outlying cast of characters comprising this cryptic cult are far more interest'n than David Berkowitz...and some may be just as complicit in the homicides committed by the "Son of Sam" cult, same as Berkowitz.Some of those cast of characters maintained status at the highest levels of society, government, and "national security". Perhaps these are the salient characteristics to understand why we as a public are learning these details decade after the alleged end of the crimes of murder & chaos back in 1977!Anyhow, folks of the interwebs, thank you again for joining me today to get a lil GCD! Enjoy today's podcast discussion on Son of Sam, Yonkers cult activity, The Ultimate Evil, and the Process Church!Enjoy the show! Links for Jonathan Mitchell - throwaways@yahoo.comhttps://www.amazon.com/Before-Son-Sam-Submerged-History-ebook/dp/B084ZYVM3Jhttps://x.com/JonathanM1973 Links for JJ - https://linktr.ee/operationgcdLinks discussed in show - https://thepeoplevsdavidberkowitz.com/wp-content/uploads/2023/12/IF-MT-Maury-Terry-Files-Maury-Notes-Witness-Flipper-List-Alleged-SoS-Members-Aug-28-1997.pdfhttps://thepeoplevsdavidberkowitz.com/wp-content/uploads/2023/12/C-Conspiracy-Berkowitz-Witness-List-Letter-Apr-5-1996.pdf

03/12/25: Ben Berkowitz is the Managing Editor of Business at Axios, and joins Joel on "News and Views" to talk about tariffs. (Joel Heitkamp is a talk show host on the Mighty 790 KFGO in Fargo-Moorhead. His award-winning program, “News & Views,” can be heard weekdays from 8 – 11 a.m. Follow Joel on X/Twitter @JoelKFGO.)See omnystudio.com/listener for privacy information.

On this episode of Taste Buds with Deb, host Debra Eckerling speaks with Ben and Max Berkowitz aka the Berkowitz Brothers. The award-winning producing and writing duo (NotABillionaire.com) co-wrote the graphic novel, “The Writer,” along with Josh Gad.    “The Writer,” illustrated by Marvel and DC Comics legend Ariel Olivetti (who they pitched via Instagram DM), is a four-issue series, to be released in trade paperback on April 22. The supernatural adventure comic - in the vein of an Indiana Jones story - follows Stan Siegel, a comic book writer whose life unravels when the fantastical worlds that he writes about start bleeding into reality.   “We also added a lot of our family stories into this as well,” Max explains. “We put our mom into the story; it's literally Josh Gad's character's mom.”    Adds Ben, “Our mother's character, Liz, in the book, is constantly pushing food on the characters.”   Ben and Max clearly have strong ties to food.   “ Our family, we always talk about the next meal, even when we're eating a meal,” Max says. “It's always on our mind.”   “For us, food has always been the connector, bringing people from walks of life [together],” Ben says. “When our dad helped build out the family restaurant business … it was made to bring people [together] to enjoy just good, simple fish dishes.”   Whether your family business is fish or creating content, you need to navigate what's most important for work and your home life.   “At the end of the day, what kind of solved most any argument was a great meal,” Ben says. “If anything, it stops people from talking because their mouths were too full of food.”    The Berkowitz Bros talk about how “The Writer” came together, their family food legacy, bagel and other eating habits, and more. They also share their father's famous whitefish salad recipe, which you can get at JewishJournal.com/podcasts.   Check out NABvid.com and follow @BerkowitzBros and @TheWriterComic on Instagram. For more from Taste Buds, subscribe on iTunes and YouTube, and follow @TheDEBMethod on social media.

Ben Berkowitz, managing editor of business at Axios, joins Lisa Dent to discuss the upcoming ‘economic blackout’ movement that has spread across consumers throughout the United States. Berkowitz shares the history of economic blackouts and whether or not they actually work.

Can colleges and secondary schools teach American civics (i.e., an examination of the republic's good and bad experiences) without being jingoistic? Peter Berkowitz, the Hoover Institution's Tad and Dianne Taube senior fellow and teacher of a course in American conservatism that's part of the Stanford Civics Initiative, contends that  “patriotism” isn't necessarily indoctrination. Still, reformers need to look beyond college and the late stages of high school. In a wide-ranging discussion with Volker Senior Fellow (adjunct) “Checker” Finn, Berkowitz suggests that the definition of “civics education” be widened to include core learning at the earliest stages of K-12 and a deeper look at how teachers approach their mission.   Recorded on January 14, 2025.

"Between Two Worlds" (Season 4, Episode 7) welcomes Nancy Gaddy, a performer whose career spans from national theater tours to klezmer music stages. Known for her character "Mrs. Schmaltz" and her latest production "Beyond the Borscht Belt," Gaddy celebrates the evolution of Jewish performance traditions in America.In this conversation, Gaddy shares insights from her journey as a theatrical chameleon - from performing in The Rocky Horror Show to developing her alter ego Belle Burke (formerly Berkowitz). We explore how her current work traces Jewish musical evolution from the Borscht Belt through American popular culture, blending klezmer, jazz, rock, and Latin fusion along the way.The episode illuminates the lasting influence of Borscht Belt entertainment on American comedy and music, while examining how contemporary Jewish performers can honor and reinvent these traditions."On the Bimah" continues to showcase the diversity and depth of contemporary Jewish theatre, guided by your host Danielle Levsky.This podcast is an Alliance for Jewish Theatre program, produced by Danny Debner and Danielle Levsky. Our theme music is by Ilya Levinson and Alex Koffman.

Neuroimaging is a tool to classify and ascertain the etiology of epilepsy in people with first or recurrent unprovoked seizures. In addition, imaging may help predict the response to treatment. To maximize diagnostic power, it is essential to order the correct imaging sequences. In this episode, Aaron Berkowitz, MD, PhD, FAAN speaks with Christopher T. Skidmore, MD, author of the article “Neuroimaging in Epilepsy,” in the Continuum February 2025 Epilepsy issue. Dr. Berkowitz is a Continuum® Audio interviewer and professor of clinical neurology at the University of California, San Francisco Dr. Skidmore is  an associate professor of neurology and vice-chair for clinical affairs at Thomas Jefferson University, Department of Neurology in Philadelphia, Pennsylvania. Additional Resources Read the article: Neuroimaging in Epilepsy Subscribe to Continuum: shop.lww.com/Continuum Earn CME (available only to AAN members): continpub.com/AudioCME Continuum® Aloud (verbatim audio-book style recordings of articles available only to Continuum® subscribers): continpub.com/Aloud More about the American Academy of Neurology: aan.com Social Media facebook.com/continuumcme @ContinuumAAN Host: @AaronLBerkowitz Guest: @ctskidmore  Full episode transcript available here Dr Jones: This is Dr Lyell Jones, Editor-in-Chief of Continuum, the premier topic-based neurology clinical review and CME journal from the American Academy of Neurology. Thank you for joining us on Continuum Audio, which features conversations with Continuum's guest editors and authors who are the leading experts in their fields. Subscribers to the Continuum journal can read the full article or listen to verbatim recordings of the article and have access to exclusive interviews not featured on the podcast. Please visit the link in the episode notes for more information on the article, subscribing to the journal, and how to get CME. Dr Berkowitz: This is Dr Aaron Berkowitz, and today I'm interviewing Dr Christopher Skidmore about his article on neuroimaging in epilepsy, which appears in the February 2025 Continuum issue on epilepsy. Welcome to the podcast, Dr Skidmore. Would you please introduce yourself to our audience?  Dr Skidmore: Thank you for having me today. I'm happy to talk to you, Dr Berkowitz. My name is Christopher Skidmore. I'm an associate professor of neurology at Thomas Jefferson University in Philadelphia. I'm a member of the Jefferson Comprehensive Epilepsy Center and also serve as the vice chair of clinical affairs for the department.  Dr Berkowitz: Thank you very much for joining us and for this fantastic article. It's very comprehensive, detailed, a very helpful review of the various types of brain pathology that can lead to epilepsy with very helpful images and descriptions of some of the more common findings like mesial temporal sclerosis and some of the less common ones such as cortical malformations, heterotopia, ganglioglioma, DNET. So, I encourage all of our listeners to read your article and take a close look at those images. So, hopefully you can recognize some of these findings on patients' neuroimaging studies, or if you're studying for the right or the boards, you can recognize some of these less common congenital malformations that can present in childhood or adulthood with epilepsy. In our interview today, what I'd like to do is focus on some practical tips to approaching, ordering, and reviewing different neuroimaging studies in patients with epilepsy. So to start, what's your approach when you're reviewing an MRI for a patient with a first seizure or epilepsy? What sequence do you begin with and why, how do you proceed through the different sequences and planes? What exactly are you looking for?  Dr Skidmore: It's an important question. And I think to even take a step back, I think it's really important, when we're ordering the MRI, we really need to be specific and make sure that we're mentioning the words seizures and epilepsy because many radiology centers and many medical centers have different imaging protocols for seizure and epilepsy patients as compared to, like, a stroke patient or a brain tumor patient. I think first off, we really need to make sure that's in the order, so that way the radiologist can properly protocol it. Once I get an image, though, I treat an MRI just like I would a CAT scan approach with any patient, which is to always approach it in the same fashion. So, top down, if I'm looking at an axial image. If I'm looking at a coronal image, I might start at the front of the head and go to the back of the head. And I think taking that very organized approach and looking at the whole brain in total first and looking across the flare image, a T2-weighted image and a T1-weighted image in those different planes, I think it's important to look for as many lesions as you can find. And then using your clinical history. I mean, that's the value of being a neurologist, is that we have the clinical history, we have the neurological exam, we have the history of the seizure semiology that can might tell us, hey, this might be a temporal lobe seizure or hey, I'm thinking about a frontal lobe abnormality. And then that's the advantage that we often have over the radiologist that we can then take that history, that exam, and apply it to the imaging study that we're looking at and then really focus in on those areas. But I think it's important, and as I've illustrated in a few of the cases in the chapter, is that don't just focus on that one spot. You really still need to look at the whole brain to see if there's any other abnormalities as well. Dr Berkowitz: Great, that's a very helpful approach. Lots of pearls there for how to look at the imaging in different planes with different sequences, comparing different structures to each other. Correspondent reminder, listeners, to look at your paper. That's certainly a case where a picture is worth a thousand words, isn't it, where we can describe these. But looking at some of the examples in your paper, I think, will be very helpful as well. So, you mentioned mentioning to the neuroradiologist that we're looking for a cause of seizures or epilepsy and epilepsy protocols or MRI. What is sort of the nature of those protocols if there's not a quote unquote “ready-made” one at someone 's center in their practice or in their local MRI center? What types of things can be communicated to the radiologist as far as particular sequences or types of images that are helpful in this scenario? Dr Skidmore: I spent a fair amount of time in the article going over the specific MRI protocol that was designed by the International League Against Epilepsy. But what I look for in an epilepsy protocol is a high-resolution T2 coronal, a T2 flare weighted image that really traverses the entire temporal lobe from the temporal tip all the way back to the most posterior aspects of the temporal lobe, kind of extending into the occipital lobe a little bit. I also want to see a high resolution. In our center, it's usually a T1 coronal image that images the entire brain with a very, very thin slice, and usually around two millimeters with no gaps. As many of our neurology colleagues are aware, when you get a standard MRI of the brain for a stroke or a brain tumor, you're going to have a relatively thick slice, anywhere from five to eight millimeters, and you're actually typically going to have a gap that's about comparable, five to eight millimeters. That works well for large lesions, strokes, and big brain tumors, but for some of the tiny lesions that we're talking about that can cause intractable epilepsy, you can have a focal cortical dysplasia that's literally eight- under eight millimeters in size. And so, making sure you have that nice T1-weighted image, very thin slices with no gaps, I think is critical to make sure we don't miss these more subtle abnormalities. Dr Berkowitz: Some of the entities you describe in your paper may be subtle and more familiar to pediatric neurologists or specialized pediatric neuroradiologists. It may be more challenging for adult neurologists and adult neuradiologists to recognize, such as some of the various congenital brain malformations that you mentioned. What's your approach to looking for these? Which sequences do you focus on, which planes? How do you use the patient 's clinical history and EEG findings to guide your review of the imaging? Dr Skidmore: It's very important, and the reason we're always looking for a lesion---especially in patients that we're thinking about epilepsy surgery---is because we know if there is a lesion, it increases the likelihood that epilepsy surgery is going to be successful. The approach is basically, as I mentioned a little bit before, is take all the information you have available to you. Is the seizure semiology, is it a hyper motor semiology or hyperkinetic semiology suggestive of frontal lobe epilepsy? Or is it a classic abdominal rising aura with automatisms, whether they be manual or oral automatisms, suggesting mesial temporal lobe epilepsy? And so, take that clinical history that you have to help start to hone your eye into those individual locations. But then, once you're kind of looking in these nonlesional cases, you're also then looking at the EEG and where their temporal lobe spikes, where their frontal lobe spikes, you know, using that and pulling that information in. If they saw a neuropsychologist pulling in the information in from the neuropsychological evaluation; if they have severe reductions in verbal memory, you know, focusing on the dominant temporal lobe. So, in a right-handed individual, typically the left temporal lobe. And kind of then really spending a lot of time going slice at a time, very slowly, because in some of these vocal-cortical dysplasias it can be just the blurring of the gray-white margin. What I find easiest is to identify that gray-white margin and almost track it. Like, you use the mouse to kind of track it around and say, can I outline the exact border of the gray white margin in the frontal lobe that I'm interested in or the temporal lobe that I'm interested in, kind of looking for those subtle abnormalities. Often as neurologists, we don't have the luxury of being able to immediately reformat. As I mentioned, our T1 volume acquisition study is done in the coronal plane, but sometimes you might want it in the axial plane. And so, I might reach out to the radiologist and say, hey, can you reformat this in the axial plane because I'm interested in the frontal lobe epilepsy and it's a little bit better at looking at it in that plane? And I'll have them reformat and put it back on the pack so I can look at it in that manner. And so that's a, kind of another strategy is to take what you have, but also then go back to the radiologist and say, I need to look at it this a different way. Can you reformat it for me? Looking for that gray-white matter junction is the nice way to pick up for kind of subtle cortical dysplasias. And then when you see an abnormality, to be able to put the T1, the T2, and the flare image all up next to each other and use the technology built into most of our browsers to put on what's called the localizer mode, where I can highlight a specific spot that I'm seeing on the T1 and then very easily quickly see, what does it look like on the T2? What does it look like on the flare? To kind of quickly decide, is it a true abnormality or am I only seeing it on one slice because of an artifact on that one imaging sequence? And I think that's the biggest kind of key is to make sure, is it an artifact or is it not an artifact? That's kind of the most common thing that we, I think, get confused with.  Dr Berkowitz: So, some very helpful pearls there in terms of reviewing the imaging, being in dialogue with our neuroradiology colleagues to think about potentially reacquiring certain images on certain planes or looking at the images with our neuroradiology colleagues to let them know more about the clinical history and where we're sort of zooming in about possible abnormalities.  Dr Skidmore: I would just add in there that when looking at especially the mesial temporal structures, because of a lot of artifacts that can be present in an individual MRI machine, it's not uncommon that the mesial temporal structure will appear brighter because of an MRI magnet artifact. And so, it's a good key to look at the hippocampus compared to the insula. And so, the hippocampus and the insula should have similar signal characteristics. You're seeing the hippocampus is bright, but the insula  ipsilateral to it's normal intensity. That would suggest that that's probably a true hyperintensity on the flare-weighted image as opposed to if both are bright, unless you're suspecting a hemispheric abnormality, it's more likely to be a kind of artifact in the MRI machine. Dr Berkowitz: Okay. Those are really helpful tips, not just to analyze the hippocampus and medial temporal lobe itself---let's remember our anatomy and the circuit of Papez---and to look at associated structures for supporting evidence of a possible abnormality in the hippocampus itself. It looks like there may be something subtle. We can use some additional information from the image to try to decide if that is real or artifactual, and of course correlating with the clinical picture and EEG. I'd like to talk briefly now about some other imaging modalities that you discuss in your paper, the use of functional imaging such as PET, SPECT and fMRI. Let's talk a bit about each of these. When would you order a PET scan for a patient with epilepsy? What would you be looking for and how would you be using that to make clinical decisions?  Dr Skidmore: Yeah, so these functional imaging modalities are really utilized when we're evaluating somebody that's not responding to medications. So, they're medically intractable, and we're wondering, could they be a candidate for epilepsy surgery? And so, most of these imaging modalities are really relegated to the world of epileptologists at surgical epilepsy centers. I wanted to include them, though, in the article because I do think it's important for general neurologists to understand kind of what they are, because invariably a patient sees me and then they go back to their general neurology and be like, hey, Doctor Skidmore said I had this PET scan abnormality. What do you think? So, I think it's a good idea for general neurologists to kind of understand them. So, probably the oldest that we've utilized is the FDG PET scan, basically looking at fluorodeoxyglucose and the brain's utilization of glucose. As we all remember, again, glucose is the primary molecule for energy and ATP production in the brain. And so basically, by injecting radioactive glucose in the interictal state--- so not during a seizure but in between seizures---areas of the brain that are not taking up the radiotracer will show as being hypometabolic. So, low metabolism. And hypometabolic regions in the interictal state have been associated with onset regions for epileptic seizures. Let's say you have a patient clinical history, you think they have temporal of epilepsy, EEG suggests temporal of epilepsy, but the MRI is nonlesional, meaning there's no abnormality that anybody could appreciate even at a 3 Tesla scanner. We'll get an FDG PET scan and see, is there hypo metabolism in that temporal lobe of interest? And if there is, well, that's been shown through several published papers, that's just as valuable as having an abnormality on the MRI. And so, we often again use these PET scans, especially in nonlesional cases, to try to find that subtle cortical dysplasia. Now you have your nice epilepsy protocol MRI, it says it's nonlesional. You get your PET scan, it shows hypometabolism in a region of the frontal lobe, let's say, in a in a frontal lobe epilepsy case. And then often we go back, we kind of talked about strategy of how you find those subtle lesions. Then you go back and say, well, look, this gyrus specifically on the PET scan said it's abnormal. You end up looking for really subtle, very tiny abnormalities that, even with somebody that's skilled, often at first review gets missed. So, that's how we use the PET scan. The SPECT scan is done typically in the ictal state. So, now somebody's in an epilepsy monitoring unit often, where you're injecting radio tracer at the exact moment that somebody starts having a seizure. And we know when there's increased seizure activity, the increased seizure activity---let's say it's from my right temporal lobe---is going to increase cerebral blood flow transiently to the right temporal lobe. And then if that seizure discharge spreads from the right temporal lobe maybe to the entire right hemisphere and eventually becomes a focal to bilateral tonic chronic seizure by spreading to the other side, the entire brain is going to be hypoperfused at that point. So, if you want to, as soon as the seizure starts, inject that radio tracer to see, where is the blood flow earliest in the seizure? And then we might do an interictal SPECT when you're not having a seizure. Look at, all right, what's the normal blood flow when somebody's not seizing? What's it like when they're having a seizure? And then the area that has increased activity would- might suggest that's where the seizure started from. But we have to be very careful because again, some seizures can spread very rapidly. So, if you delay injecting an injection ten, fifteen, twenty seconds, the seizure could have already propagated to another region of the brain, giving you a false positive in another location. So, you have to be very careful about that modality. I think what's most exciting is the functional MRI because the functional MRI, for many, many centers, is replacing a very old technique called the WADA test. So, in the WADA test, typically you place a catheter angiogram into the internal carotid artery and transiently introduce a sedative medication to put, let's say, the left hemisphere to sleep because you wanted to see what functions were still active in the right hemisphere. And then the surgeon would move the catheter or the right internal carotid artery, and you inject a sedative on that side after the left hemisphere is recovered and see what the left hemisphere can do. And we used that for language dominance, we used that for memory dominance. And while most individuals did fine with angiograms, unfortunately complications do occur and there's injury to the artery, there could be strokes that can- that have happened, which can be quite devastating for the patient. And so, functional MRI is a nice, noninvasive way for us to map out language function, motor function, sensory function, visual function, and is starting to show some usefulness also for mapping out kind of memory function, dominant memory function, meaning verbal memory compared to visual memory. To be able to do those things noninvasively becomes really important because, if we're talking about epilepsy surgery, we want to make you seizure-free but neurologically intact. And so, we need to understand the relationship between where we think the seizures are coming from and where eloquent cortex is so we can properly counsel you and avoid those regions during any planned surgery. Those are the three most common functional imaging modalities that we're using now to supplement the rest of the presurgical work.  Dr Berkowitz: Very helpful. So, these are studies, PET, SPECT, and fMRI, that would really be obtained predominantly in patients in whom epilepsy surgery was being considered to have more precise lesion localization, as well as with the fMRI to get a better sense of how to provide the safest maximal resection of epileptogenic tissue while preserving functions. Dr Skidmore: That's a perfect summary.  Dr Berkowitz: Fantastic. This has been a really helpful interview with Dr Skidmore and a really fantastic article. As I said, a picture is worth a thousand words, so I definitely encourage you to read the article and look at the images of some of the conditions we've been talking about and some of these findings that can be seen on interictal PET or ictal SPECT to get a sense of the visual aspects of what we've been discussing. So again, today I've been interviewing Dr Christopher Skidmore about his article on neuroimaging and epilepsy, which appears in the most recent issue of Continuum on Epilepsy. Be sure to check out Continuum audio episodes from this and other issues. And thank you so much to our listeners for joining us today.  Dr Skidmore: Thank you for having me. Dr Monteith: This is Dr Teshamae Monteith, Associate Editor of Continuum Audio. If you've enjoyed this episode, you'll love the journal, which is full of in-depth and clinically relevant information important for neurology practitioners. Use this link in the episode notes to learn more and subscribe. AAN members, you can get CME for listening to this interview by completing the evaluation at continpub.com/audioCME. Thank you for listening to Continuum Audio.

DEATH BY DVD PRESENTS : What's The Deal With Jeremy Berkowitz? An Interview with Jeremy Berkowitz. On this fresh from the grave episode we are proud to bring filmmaker Jeremy Berkowitz to the graveyard to discuss their art! Jeremy is a tremendously talented writer, director and actor and their feature film debut SYDNEY was released early 2025 for all to see. On this episode Jeremy discusses their work, Sydney, what made them want to be an artist and more. We dive deep into into Jeremy's world of art, from his start in stand up comedy to writing directing and starring in a feature film. I am so excited for you all to hear this episode, Jeremy creates dynamic art that drowns you in pure emotion and I truly hope you enjoy this episode and explore their art further. WATCH SYDNEY FOR FREE  : Tap here or copy the link belowhttps://www.sydneythefilm.com/VISIT THE OFFICIAL WEBSITE OF JEREMY BERKOWITZ: Tap here or click the link belowhttps://www.jeremyberkowitz.com/Don't forget, Death By DVD has its very own all original audio drama voiced almost entirely by Death By DVD!DEATH BY DVD PRESENTS : WHO SHOT HANK?The first of its kind, (On this show, at least) an all original narrative audio drama exploring the murder of this shows very host, HANK THE WORLDS GREATEST! Explore WHO SHOT HANK, starting with the MURDER! A Death By DVD New Year Mystery WHO SHOT HANK : PART ONE WHO SHOT HANK : PART TWO WHO SHOT HANK : PART THREE WHO SHOT HANK : PART FOUR WHO SHOT HANK PART 5 : THE BEGINNING OF THE ENDWHO SHOT HANK PART 6 THE FINALE : EXEUNT OMNES Whoah, you're still here?  Check out the official YOUTUBE of Death By DVD and see our brand new program, TRAILER PARK! The greatest movie trailer compilation of all time. Tap here to visit our YOUTUBE or copy and paste the link below : https://www.youtube.com/@DeathByDVD ★ Support this podcast on Patreon ★

Peter recaps his Super Bowl experience, highlighting the behind the scenes moments at Super Bowl Opening Night, Chiefs practice, multiple parties, and the work at the game itself. He, then, welcomes Ron Berkowitz of Berk Communications. Ron works with Michael Rubin and Fanatics, as well as Rao's, and takes us behind the velvet rope and into the biggest, most exclusive events and parties of Super Bowl LIX. See omnystudio.com/listener for privacy information.

Peter recaps his Super Bowl experience, highlighting the behind the scenes moments at Super Bowl Opening Night, Chiefs practice, multiple parties, and the work at the game itself. He, then, welcomes Ron Berkowitz of Berk Communications. Ron works with Michael Rubin and Fanatics, as well as Rao's, and takes us behind the velvet rope and into the biggest, most exclusive events and parties of Super Bowl LIX. See omnystudio.com/listener for privacy information.

What's to be done about immigration? Find us on Youtube. In this episode, Mike Cosper talks with Roger Berkowitz—founder and academic director of the Hannah Arendt Center for Politics and Humanities and professor of politics, philosophy, and human rights at Bard College—to talk about power, populism and the plight of the refugee. It's a conversation not quick with answers but committed to thoughtful engagement with the most important questions. GO DEEPER WITH THE BULLETIN: Everything is on sale! Grab some Bulletin merch. Find us on YouTube. Rate and review the show in your podcast app of choice. ABOUT THE GUEST:  Roger Berkowitz is founder and academic director of the Hannah Arendt Center for Politics and Humanities and professor of politics, philosophy, and human rights at Bard College. Berkowitz is the author of The Gift of Science, the introduction to On Civil Disobedience by Henry David Thoreau and Hannah Arendt, and The Perils of Invention. His writing has appeared in The New York Times, The American Interest, Bookforum, The Forward, The Paris Review online, and Democracy. Berkowitz edits HA: The Journal of the Hannah Arendt Center and the weekly newsletter Amor Mundi. He is the winner of the 2024 Compassion Award given by Con-solatio and the 2019 Hannah Arendt Prize for Political Thought given by the Heinrich Böll Foundation in Bremen, Germany. ABOUT THE BULLETIN: The Bulletin is a weekly (and sometimes more!) current events show from Christianity Today hosted and moderated by Clarissa Moll, with senior commentary from Russell Moore (Christianity Today's editor in chief) and Mike Cosper (director, CT Media). Each week, the show explores current events and breaking news and shares a Christian perspective on issues that are shaping our world. We also offer special one-on-one conversations with writers, artists, and thought leaders whose impact on the world brings important significance to a Christian worldview, like Bono, Sharon McMahon, Harrison Scott Key, Frank Bruni, and more. Learn more about your ad choices. Visit podcastchoices.com/adchoices

Epilepsy classification systems have evolved over the years, with improved categorization of seizure types and adoption of more widely accepted terminologies. A systematic approach to the classification of seizures and epilepsy is essential for the selection of appropriate diagnostic tests and treatment strategies. In this episode, Aaron Berkowitz, MD, FAAN, speaks with Roohi Katyal, MD, author of the article “Classification and Diagnosis of Epilepsy,” in the Continuum February 2025 Epilepsy issue. Dr. Berkowitz is a Continuum® Audio interviewer and a professor of neurology at the University of California San Francisco in the Department of Neurology and a neurohospitalist, general neurologist, and clinician educator at the San Francisco VA Medical Center at the San Francisco General Hospital in San Francisco, California. Dr. Katyal is an assistant professor of neurology and codirector of adult epilepsy at Louisiana State University Health Shreveport in Shreveport, Louisiana. Additional Resources Read the article: Classification and Diagnosis of Epilepsy Subscribe to Continuum: shop.lww.com/Continuum Earn CME (available only to AAN members): continpub.com/AudioCME Continuum® Aloud (verbatim audio-book style recordings of articles available only to Continuum® subscribers): continpub.com/Aloud More about the American Academy of Neurology: aan.com Social Media facebook.com/continuumcme @ContinuumAAN Host: @AaronLBerkowitz Guest: @RoohiKatyal Full episode transcript available here Dr Jones: This is Dr Lyell Jones, Editor-in-Chief of Continuum, the premier topic-based neurology clinical review and CME journal from the American Academy of Neurology. Thank you for joining us on Continuum Audio, which features conversations with Continuum's guest editors and authors who are the leading experts in their fields. Subscribers to the Continuum Journal can read the full article or listen to verbatim recordings of the article and have access to exclusive interviews not featured on the podcast. Please visit the link in the episode notes for more information on the article, subscribing to the journal, and how to get CME. Dr Berkowitz: This is Dr Aaron Berkowitz, and today I'm interviewing Dr Roohi Katyal about her article on classification and diagnosis of epilepsy, which appears in the February 2025 Continuum issue on epilepsy. Welcome to the podcast, Dr Katyal, and could you please introduce yourself to our audience? Dr Katyal: Thank you for having me. I'm very excited to be here. I'm Dr Roohi Katyal. I currently work as Assistant Professor of Neurology at LSU Health Shreveport. Here I also direct our adult epilepsy division at LSU Health along with my colleague, Dr Hotait.  Dr Berkowitz: Fantastic. Well, happy to have you here. Your article is comprehensive, it's practical, and it focused on explaining the most recent International League Against Epilepsy (ILAE) classification of epilepsy and importantly, how to apply it to provide patients with a precise diagnosis of epilepsy and the particular subtype of epilepsy to guide the patient's treatment. There are so many helpful tables and figures that demonstrate all of the concepts and how to apply them at the bedside. So, I encourage our listeners to have a look at your article, even consider maybe screenshotting some of these helpful tables onto their phone or printing them out for handy reference at the bedside and when teaching residents. Your article begins with the current definition of epilepsy. So, I want to ask you about that definition and make sure we're on the same page and understand what it is and what it means, and then talk through a sort of hypothetical patient scenario with you to see how we might apply these in clinical practice. You talked about, in your article, how the new definition of epilepsy from the ILAE allows for the diagnosis of epilepsy in three different scenarios. So, could you tell us what these scenarios are? Dr Katyal: So, epilepsy in general is a chronic condition where there is a recurrent predisposition to having seizures. As you mentioned, epilepsy can be diagnosed in one of three situations. One situation would be where an individual has had two or more unprovoked seizures separated by more than 24 hours. The second situation would be where somebody has had one unprovoked seizure and their risk of having recurrent seizures is high. And the third situation would be where somebody had---where the clinical features could be diagnosis of an epilepsy syndrome. An example of that would be a young child presenting with absence seizures and their EEG showing 3 Hz characteristic generalized spike in with discharges. So that child could be diagnosed with childhood absence epilepsy.  Dr Berkowitz: Perfect. Okay, so we have these three scenarios, and in two of those scenarios, we heard the word unprovoked. Just to make sure everyone's on the same page, let's unpack this word “unprovoked” a little bit. What does it mean for a seizure to be unprovoked versus provoked?  Dr Katyal: So unprovoked would be where we don't have any underlying provoking features. So underlying provoking features are usually reversible causes of epilepsy. These would be underlying electrolyte abnormality, such as hyperglycemia being a common one which can be reversed. And these individuals usually do not need long-term treatment with anti-seizure medications. Dr Berkowitz: Fantastic. Tell me if I have this right, but when I'm teaching residents, I… did it provoked and unprovoked---there's a little confusing, right? Because we use those terms differently in common language than in this context. But a provoked seizure, the provoking factor has to be two things: acute and reversible. Because some people might say, well, the patient has a brain tumor. Didn't the brain tumor provoke the seizure? The brain tumor isn't acute and the brain tumor isn't reversible, so it would be an unprovoked seizure. I always found that confusing when I was learning it, so I try to remind learners I work with that provoked means acute and reversible, and unprovoked means it's not acute and not reversible. Do I have that right? Am I teaching that correctly? Dr Katyal: That's correct. Dr Berkowitz: Great. And then the other important point here. So, I think we were all familiar prior to this new guideline in 2017 that two unprovoked seizures more than twenty-four hours apart, that's epilepsy. That's pretty straightforward. But now, just like we can diagnose MS at the time of the first clinical attack with the right criteria predicting that patient is likely to have relapse, we can say the patient's had a single seizure and already at that time we think they have epilepsy if we think there's a high risk of recurrence, greater than or equal to sixty percent in this guideline, or an epilepsy syndrome. You told us what an epilepsy syndrome is; many of these are pediatric syndromes that we've studied for our boards. What hertz, spike, and wave goes with each one or what types of seizures. But what about this new idea that a person can have epilepsy after a single unprovoked seizure if the recurrence rate is greater than sixty percent? How would we know that the recurrence rate is going to be greater than sixty percent? Dr Katyal: Absolutely. So, the recurrence rate over sixty percent is projected to be over a ten year period. So, more than sixty percent frequency rate in the next ten years. And in general, we usually assess that with a comprehensive analysis and test. So, one part of the comprehensive analysis would be, a very important part would be a careful history taking from the patient. So, a careful history should usually include all the features leading up to the episodes of all the prodromal symptoms and warning signs. And ideally you also want to get an account from a witness who saw the episode as to what the episode itself looked like. And in terms of risk assessment and comprehensive analysis, this should be further supplemented with tests such as EEG, which is really a supportive test, as well as neuroimaging. If you have an individual with a prior history of, let's say, left hemispheric ischemic stroke and now they're presenting with new onset focal aware seizures with right arm clonic activity, this would be a good example to state that their risk of having future seizures is going to be high. Dr Berkowitz: Perfect. Yeah. So, if someone has a single seizure and has a lesion, as you said, most common in high-income countries would be a prior stroke or prior cerebrovascular event, prior head trauma, then we can presume that the risk is going to be high enough that we could call that epilepsy after the first unprovoked seizure. What if it's the first unprovoked seizure and the imaging is unremarkable? There's no explanatory lesion. How would we get to a diagnosis of epilepsy? How would we get to a risk of greater than sixty percent in a nonlesional unprovoked seizure? I should say, no lesion we can see on MRI. Dr Katyal: You know, in those situations an EEG can be very helpful. An EEG may not always show abnormalities, but when it does show abnormalities, it can help us distinguish between focal and generalized epilepsy types, it can help us make the diagnosis of epilepsy in certain cases, and it can also help us diagnose epilepsy syndromes in certain cases.  Dr Berkowitz: Perfect. The teaching I remember from a resident that I'm passing on to my residents, so please let me know if it's correct, is that a routine EEG, a 20-minute EEG after a single unprovoked seizure, this sensitivity is not great, is that right? Around fifty percent is what I was told with a single EEG, is that right? Dr Katyal: Yeah, the sensitivity is not that great. Again, you know, it may not show abnormality in all the situations. It's truly just helpful when we do see abnormalities. And that's what I always tell my patients as well when I see them in clinic. It may be abnormal or it may be normal. But if it does show up normal, that does not rule out the diagnosis of epilepsy. Really have to put all the pieces together and come to that finally diagnosis. Dr Berkowitz: Perfect. Well, in that spirit of putting all the pieces together, let's walk through together a hypothetical case scenario of a 19-year-old patient who presents after a first event that is considered a possible seizure. First, how do you approach the history and exam in this scenario to try to determine if you think this was indeed an epileptic seizure?  Dr Katyal: So, if I'm seeing them in the clinic or in the outpatient setting and they're hopefully presenting with somebody who's already seen the seizure itself, my first question usually is if they had any warning signs or any triggers leading up to the episode. A lot of times, you know, patients may not remember what happened during the episode, but they may remember if they felt anything different just before or the day prior, something different may have happened around that time. Yeah, so they may report that. Then a very important aspect of that would be talking to somebody who has seen the episode, a witness of the episode; and ideally somebody who has seen the onset of the episode as well, because that can give us very important clues as to how the event or the episode started and how it progressed. And then another very important question would be, for the individual who has experienced it, is how they felt after the episode ended. So, you can get some clues as to if they had a clear postictal state. Other important questions would be if they had any tongue biting or if they lost control of their bladder or all those during the episode. This, all those pieces can guide us as to if the seizure was epileptic, or the episode was epileptic or not. Dr Berkowitz: Fantastic. That's very helpful guidance. All right. So, let's say that based on the history, you're relatively convinced that this patient had a generalized tonic clonic seizure and after recovering from the event, you do a detailed neurologic exam. That's completely normal. What's your approach at this point to determining if you think the seizure was provoked or unprovoked, since that's, as you said, a key component of defining whether this patient simply had a seizure, or had a seizure and has epilepsy? Dr Katyal: The important findings would be from the laboratory test that may have been done at the time when the patient first presented with the seizure. So, we want to rule out features like hypoglycemia or other electrolyte abnormalities such as changes in sodium levels or big, big fluctuations there. We also want to rule out any other metabolic causes or other reasons such as alcohol withdrawal, which can be a provoking factor. Because these would be very important to rule out is if we find a provoking reason, then this individual may not need to be on long term anti-seizure medication. So very important to rule that out first.  Dr Berkowitz: Great. So, let's say you get all of your labs and history and toxicology screen and no provoking factors there. We would obtain neuroimaging to see if there's either an acute provoking factor or some type of lesion as we discussed earlier. Let's say in this theoretical case, the labs are normal, the neuroimaging normal. There is no apparent provoking factor, there's no lesion. So, this patient has simply had a single unprovoked seizure. How do we go about now deciding if this patient has epilepsy? How do we try to get ourselves to either an above sixty percent risk and tell this patient they have epilepsy and probably need to be on a medicine, or they have a less than sixty percent risk and that becomes a little more tricky? And we'll talk about that more as well.  Dr Katyal: For in a young patient, especially in a young patient as a nineteen year old as you present, one very important aspect if I get this history would be to ask them about absolutely prior history of similar episodes, which a lot of times they may not have had similar episodes. But then with this age group, you also want to ask about episodes of brief lapses in awareness or episodes of sudden jerking or myoclonic jerking episodes. Because if you have brief lapses of awareness, that could signify an absence seizure in this particular age group. And brief, sudden episodes of myoclonic jerking could be brief myoclonic seizures in this age group. And if we put together, just based on the clinical history, you could diagnose this patient with a very specific epileptic syndrome, which could be juvenile myoclonic epilepsy in the best case. Let's say if you ask about episodes of staring or relapses of awareness, that's not the case, and there's no history of myoclonic jerking episodes or myoclonic seizures, then the next step would be proceeding to more of our supplemental tests, which would be an EEG and neuroimaging. In all cases of new-onset seizure especially should have comprehensive assessment with EEG and neuroimaging to begin with, and we can supplement that with additional tests wherever we need, such as genetic testing and some other more advanced testing.  Dr Berkowitz: That's very helpful. OK, so let's say this particular patient, you talk to them, you talk to their family, no prior history of any types of events like this. No concerns for spells that could---unlike absence, no concern for movements that could sound like myoclonus. So, as you said, we would be looking for those and we could get to part one of the definition. There is more than one spell, even though we're being consulted for one particular event. But let's say this was the only event, we think it's unprovoked, the neuroimaging is normal. So, you said we proceed to an EEG and as you mentioned earlier, if the EEG is abnormal, that's going to tell us if the risk is probably this more than sixty percent and the patient should probably be on a medicine. But common scenario, right, that the patient has an event, they have a full work up, we don't find anything. We're convinced it was a seizure. We get our routine EEG as we said, very good, an affirmative test, but not a perfectly sensitive test. And let's say this person's routine EEG turns out to be normal. So how would you discuss with the patient their risk of a future seizure and the considerations around whether to start an anti-seizure medicine if their work-up has been normal, they've had a single unprovoked seizure, and their EEG is unrevealing? Dr Katyal: And I'm assuming neuroimaging is normal as well in this case? Dr Berkowitz: Correct. Yeah.  Dr Katyal: We have a normal EEG; we have normal neuroimaging as well. So, in this case, you know, it's more of a discussion with the patient. I tell them of that, you know, the risk of seizure may not be higher than sixty percent in this case with all the tests being normal so far and there's no other prior history of similar episodes. So, we have a discussion with them about the risks that can come with future seizures and decide where the medication should be started or not.  Dr Berkowitz: And so how do you approach this discussion? The patient will say, Doctor Katyal, I had one seizure, it was very frightening. I got injured. You told me I can't drive for however many months. One cannot drive in that particular state. But I don't really like taking medicines. What is my risk and what do you think? Should I take a medicine?  Dr Katyal: I'll tell you this because normally I would just have a direct conversation with them, discuss all the facts that we have. We go over the seizure one more time just to make sure we have not missed any similar episodes or any other episodes that may be concerning seizure, which ruled out all the provoking factors, any triggers that may be seen inseizures like this in a young age. And another thing would be to basically have a discussion with them, you know, these are the medication options that we can try. And if there is another seizure, you know, these are the these are the restrictions that would come with it. And it's a very individualized decision, to be honest. That, you know, not everyone may want to start the medication. And you'll also find that some patients who, you know, some individuals are like no,  I want to go back to driving. I don't want to be in this situation again. I would like to try a medication and don't want to ever have a seizure. So, I think it's a very individualized decision and we have a discussion with the patient based on all of these tests. And I would definitely maintain follow-up with them to make sure that, you know, things have not changed and things have---no seizures have recurred in those cases.  Dr Berkowitz: Yeah, great to hear your approach. And similar experience to you, right, where some patients say, I definitely don't want to take the medication, I'll roll the dice and I hope I don't have another seizure. And we say, we hope so also. As you said, let's keep a close eye. And certainly, if you have another seizure, it's going to be a lifelong seizure medicine at that point. And some patients who, as you said, say, wait, I can't drive for months. And if I don't take a medicine and I have a seizure in the last month, I would have to have another period of no driving. Maybe in that case, they would want to start a medicine. That said, we would present that either of these are reasonable options with risks and benefits and these are the medications we would offer and the possible side effects and risk of those, and make a joint decision with the patient. Dr Katyal: Absolutely correct. Mentioned it perfectly well that this is a very individualized decision and a joint decision that we make with the patient.  Dr Berkowitz: Fantastic. Another topic you touch on in your article is the definition of resolved epilepsy. How is that defined in the guidelines?  Dr Katyal: Yes. So, an epilepsy can be considered resolved if an individual has been seizure-free for at least ten years and has been off of IV seizure medications for at least five of those years. Another situation where epilepsy can be considered resolved would be if they have an age-defined epilepsy syndrome and now they are beyond the relevant age group for the syndrome.  Dr Berkowitz: That's very helpful. So again, a very clear definition that's helpful in these guidelines. And yet, as I'm sure you experience your practice, as I do in mine, sometimes a little challenging to apply. So, continuing with our made-up hypothetical patient here, let's say at some point in the subsequent years, they have a second unprovoked seizure, still have a normal EEG but they do go on an anti-seizure medicine. And maybe four or five years later, they're seizure-free on a low dose of an anti-seizure medicine. And they say, you know, do I really still need this medicine? I'd really like to come off of it. What do you think? Is that safe? How do you talk about that with the patient? This definition of ten years and five years off medicine seems to be---and maybe unless someone's seeing a lot of children and young adults, a relatively uncommon scenario. It's we've had a first unprovoked seizure. We never figured out why. We don't really know why they had the seizure. We can't really gauge their subsequent risk. They're on medicines, they don't want to be on them and it's only been a few years, let's say three, four, or five years. How do you frame discussion with the patient? Dr Katyal: Yeah, so that's the definition of being resolved. But in terms of tapering off medications, we can usually consider tapering off medications earlier as well, especially if they've been seizure-free for two or more years. Then again, as we mentioned earlier, it would be a very individualized decision and discussion with the patient, that we could consider tapering off of medication. And we would also want to definitely discuss the risk of breakthrough seizures as we taper off and the risks or the lifestyle modifications that would come with it if they have another breakthrough seizure. So, all those things will go into careful concentration when we decide to taper off, because especially driving restriction may be a big, you know, hard stop for a lot of patients that, you know, now is not a time to taper off medication. So, all of these factors will go into consideration and we could consider tapering off earlier as well.  Dr Berkowitz: That's very helpful. Yeah, as you said, when we're tapering off medications, if that's the direction the patient wants to go during that period, obviously we wouldn't want them to drive, or be up on a ladder, or swimming alone. You said that some patients might say, actually, I'll keep the medicine, whereas some might say, OK, I'll hold off on all these activities and hope that I can be off this medication. I remember epilepsy colleagues quoting to me at one point that all comers, when a patient's been seizure-free for two years, they estimate the risk of relapse, of having another seizure, somewhere around thirty to forty percent. In your expert opinion, is that about what you would quote to a patient as well,. about a thirty to forty percent, all comers? Obviously not someone who's had a history of status epilepticus and has a lesion or a syndrome, but in the sort of common situation of some unprovoked seizures in an adult, we don't have a clear ideology. Is that thirty to forty percent figure, more or less, you would place the risk when you talk to the patient? Or?  Dr Katyal: Yeah, absolutely, especially if the neuroimaging is completely normal, all their EE GS have been normal. They have been in this situation---you have a young patient with two seizures separated by so many years. After three or four years of being on the medication and, you know, the patient has been adhering. There are no more seizures. Thirty to forty percent seems reasonable, and this is what I usually tell them that the risk of, as we taper off medications, that risk is not zero but it's low. And around thirty percent is relatively where we would place the risk at. Dr Berkowitz: We've said in this theoretical case that the EEG is normal. But last question, I've heard some practitioners say that, well, let's say the patient did have an abnormal EEG early on. Not a syndrome, but had maybe a few focal spike wave discharges or sharps and that made you convinced that this patient had epilepsy. But still becomes seizure free for several years. I've heard of some practitioners repeating the EEG before tapering the anti-seizure medicines and I always wonder, would it change anything? It's a brief twenty-minute period. They still have one spike, but I tell them they can't come off. If the spikes are gone, it may be because of the medication, and maybe when I take them off they would have a spike. And how do you use---do you use or how do you use EEG in that decision of whether to taper a medicine? Dr Katyal: Yeah. In general, I would not always use an EEG for considering tapering off medication. Again, it's very individualized decision. I can give you a hypothetical example, but it's a fairly common one, is that if an individual with let's say focal seizures with impaired awareness, they live alone, they live by themselves. Oftentimes they'll say that, I'm not sure if I'm missing any seizures because nobody has seen them. I may or may not be losing awareness, but I'm not too certain. They have not had any definite seizures for history in the last couple of years and are now considering tapering off medication. So, this may be a situation where I may repeat an EEG, and perhaps even considering the longer EEG for them to understand their seizure burden before we decide to taper off medication. But in most situations, especially if we consider the hypothetical situation you had mentioned for the young patient who had to witness seizures separated by several years and then several years without any seizures, that may be a good example to consider tapering off medication, especially considering all the tests that had been normal before then.  Dr Berkowitz: That's very helpful to hear. And of course, this is your expert opinion. As you said, no guidelines and different people practice in different ways, but helpful to hear how you approach this common and challenging scenario for practitioners. Well, I want to thank you again, Dr Katyal. This has been a great opportunity to pick your brain on a theoretical case, but one that I think presents a number of scenarios that a lot of us---myself as a general neurologist, as well as you and your colleagues as epileptologists, we all see in general practice patients with unprovoked seizures and a revealing workup, and how to approach this challenging scenario based on the guidelines and on your expert opinion. I learned a lot from your article. Encourage our readers again to take a look. A lot of very helpful tables, figures, and explanations, some of the concepts we've been discussing. So again, today I've been interviewing Dr Roohi Katyal about her article on classification and diagnosis of epilepsy, which appears in the most recent issue of Continuum on Epilepsy. Be sure to check out Continuum audio episodes from this and other issues. And thank you again so much to our listeners for joining us.  Dr Katyal: Thank you for having me. Dr Monteith: This is Dr Teshamae Monteith, Associate Editor of Continuum Audio. If you've enjoyed this episode, you'll love the journal, which is full of in-depth and clinically relevant information important for neurology practitioners. Use this link in the episode notes to learn more and subscribe. AAN members, you can get CME for listening to this interview by completing the evaluation at continpub.com/audioCME. Thank you for listening to Continuum Audio.

Send us a textToday, I have a special guest who turned a late-night craving into a multimillion-dollar empire—Seth Berkowitz, the co-founder and CEO of Insomnia Cookies.Seth started his journey as a college student at the University of Pennsylvania, frustrated by the lack of late-night food options. With just a cell phone and a car, he began delivering warm cookies to fellow students, sparking the idea that would eventually grow into a nationwide chain with over 250 locations. From humble beginnings to navigating challenges like near-bankruptcy and evolving business models, Seth's story is one of perseverance and innovation.Join me as we explore how Seth transformed Insomnia Cookies from a side hustle into a beloved brand, sharing insights on entrepreneurship, resilience, and what it takes to succeed in today's competitive landscape. Whether you're an aspiring entrepreneur or simply a cookie lover, this episode is packed with valuable lessons and delicious inspiration.Thanks for listening! If you enjoyed this episode, please leave a 5-star rating along with a brief review. And don't forget to order your BADASS T-shirt here.About MeHey there, I'm Joelly - the Branding Badass. My BADASS superpower is helping you build a brand that matters. From branded merch to keynote speaking, when you work with me, you get results! Need help telling your brand story? Learn more here.To advertise on the show click hereLet's stay connected!instagram - @Branding_BadasslinkedIn - Joelly Goodsonwebsite - BAMKO.NET

Send us a textAs we close Season Six, I think we can all agree we learned a lot from our guests and they seemed to have a good time sharing their expertise with us. I know we all thank them and I in particular thank them for allowing me to interview them and pick their brains! I look forward to sharing more guests with you in Season Seven. Until then, be true to yourself and whenever you can, keep doing the Work, because as we all know, the Work works if you work it!Happy Holidays All! And remember to visit my new podcast website: allthingspilatespodcast.comAbout Darien Gold ~ https://www.dariengold.com, https://www.allthingspilatespodcast.comInstagram: https://www.instagram.com/darien_gold_pilates_expertFacebook: https://www.facebook.com/dariengoldMusic credits ~ Instagram: @theotherjohnmayer Support the show

In today's episode of Let's Talk Business, we are excited to present a compelling conversation with Shulem Berkowitz, an esteemed leadership coach and business strategist. Hosted by Meny Hoffman, this episode dives deep into the intricate journey of transforming from a skilled craftsman to an effective leader. Shulem recounts his own transition from excelling in writing, graphic design, and printing to embracing his role as a leadership coach. His journey underscores the challenges and rewards of moving beyond personal accomplishments to empowering others. Highlighting the fundamental distinctions between consultants, coaches, and therapists, Shulem and Meny explore how each role uniquely contributes to business success. Listeners are taken through practical strategies for overcoming bottlenecks, such as temporarily stepping away from daily operations and identifying delegable tasks. Shulem emphasizes the importance of focusing on the 20% of crucial tasks that leaders must handle themselves and trusting the team with the rest. This episode also sheds light on self-awareness and growth, encouraging leaders to recognize their unique strengths and leverage them effectively. The discussion extends to company culture, where Shulem highlights the necessity of clear communication and value alignment. Drawing parallels between organizational success and the leader's personal development, he illustrates how achieving business goals is intertwined with personal growth and overcoming internal barriers. Whether you're an emerging leader or a seasoned entrepreneur, this episode provides a wealth of knowledge to help you transcend challenges and achieve sustainable growth.   00:06:20 - Learn business, self-transform, understand leadership, empower others 00:08:34 - Consultants guide on business strategies and execution 00:11:04 - PandaDoc streamlines document creation and management 00:14:28 - Transition from craftsman to teacher, guiding others 00:17:40 - Navigating organizational growth while managing uncertainty 00:21:30 - Assess essential tasks by observing absence effects 00:25:20 - Who am I, beyond others' perceptions? 00:28:00 - People struggle with identity, leaders with delegation 00:31:12 - Pursue leadership goals positively, not reactively 00:34:44 - Real understanding and communication ensure company cohesion 00:38:31 - Leadership growth mirrors personal development 00:42:33 - Seek help sooner to alleviate pain and struggles 00:44:33 - Success increases your need for help 00:48:33 - Understand strengths, delegate, align values, seek support   Pratical Pointers  Shulem's journey illustrates the importance of transitioning from a hands-on entrepreneur to an empowering leader. By focusing on enabling team members and embracing leadership roles, individuals can foster business growth and personal development. Recognizing the unique contributions of consultants, coaches, and therapists can help individuals and organizations leverage the right expertise at the right time. This understanding is crucial for overcoming obstacles and achieving organizational goals. Leadership effectiveness is closely tied to self-awareness and continuous personal development. Shulem emphasizes the significance of understanding one's strengths and delegating tasks to create space for strategic leadership. Shulem highlights the necessity of aligning company culture with shared values and clear communication. Leaders should articulate their goals and foster a supportive culture to ensure that team members act in ways that reflect the company's ethos. Shulem's experience underscores the importance of seeking external support and being open to help. Understanding that asking for assistance is a strength rather than a weakness can lead to greater success and continuous growth, both personally and professionally.   PandaDoc Rock Leadership Solutions Sholem's Linkedin

A pragmatic and organized approach is needed to recognize patients with symptomatic Alzheimer Disease in clinical practice, stage the level of impairment, confirm the clinical diagnosis, and apply this information to advance therapeutic decision making. In this episode, Aaron Berkowitz, MD, PhD, FAAN, speaks with Gregory S. Day, MD, MSc, MSCI, FAAN, author of the article “Diagnosing Alzheimer Disease,” in the Continuum December 2024 Dementia issue. Dr. Berkowitz is a Continuum® Audio interviewer associate chief medical information officer at the Cleveland Clinic in Cleveland, Ohio. Dr. Day is an associate professor in the Department of Neurology at Mayo Clinic Florida in Jacksonville, Florida. Additional Resources Read the article: Diagnosing Alzheimer Disease Subscribe to Continuum: shop.lww.com/Continuum Earn CME (available only to AAN members): continpub.com/AudioCME Continuum® Aloud (verbatim audio-book style recordings of articles available only to Continuum® subscribers): continpub.com/Aloud More about the American Academy of Neurology: aan.com Social Media facebook.com/continuumcme @ContinuumAAN Host: @AaronLBerkowitz Guest: @GDay_Neuro Full episode transcript available here Dr Jones: This is Doctor Lyell Jones, Editor-in-Chief of Continuum, the premier topic-based neurology clinical review and CME journal from the American Academy of Neurology. Thank you for joining us on Continuum Audio, which features conversations with Continuum's guest editors and authors, who are the leading experts in their fields. Subscribers to the Continuum journal can read the full article or listen to verbatim recordings of the article and have access to exclusive interviews not featured on the podcast. Please visit the link in the episode notes for more information on the article, subscribing to the journal, and how to get CME. Dr Berkowitz: This is Dr Aaron Berkowitz, and today I have the pleasure of interviewing Dr Gregory Day about his article on Alzheimer disease, which appears in the December 2024 Continuum issue on dementia. Welcome to the podcast, Dr Day. Would you mind introducing yourself to our audience?  Dr Day: Thanks very much, Aaron. I'm Gregg Day. I'm a behavioral neurologist at Mayo Clinic in Jacksonville, Florida, which means that my primary clinical focus is in the assessment of patients presenting typically with memory concerns and dementia in particular. Dr Berkowitz: Fantastic. Well, as we were talking about before the interview, I've heard your voice many times over the Neurology podcast and Continuum podcast. I've always learned a lot from you in this rapidly changing field over the past couple of years, and very excited to have the opportunity to talk to you today and pick your brain a little bit on this very common issue of evaluating patients presenting with memory loss who may have concerns that they have dementia and specifically Alzheimer disease. So, in your article, you provide a comprehensive and practical approach to a patient presenting for evaluation for possible dementia and the question of whether they have Alzheimer disease. The article is really packed with clinical pearls, practical advice. I encourage all of our listeners to read it. In our interview today, I'd like to talk through a theoretical clinical encounter and evaluation so that I and our listeners can learn from your approach to a patient like this. Let's say we have a theoretical patient in their seventies who comes in for evaluation of memory loss and they and/or their family are concerned that this could be Alzheimer disease. How do you approach the history in a patient like that? Dr Day: It's a great way to approach this problem. And if you're reading the article, know that I wrote it really with this question in mind. What would I be doing, what do we typically do, when we're seeing patients coming with new complaints that concern the patient and typically also concern those that know the best? So be that a family member, close friend, adult child. And in your scenario here, this seventy year old individual, we're going to use all the information that we have on hand. First off, really key, if we can, we want to start that visit with someone else in the room. I often say when talking to individuals who come alone that there's a little bit of irony in somebody coming to a memory assessment alone to tell me all the things they forgot. Some patients get the joke, others not so much, but bringing someone with them really enhances the quality of the interview. Very important for us to get reliable information and a collateral source is going to provide that in most scenarios. The other thing that I'm going to start with, I'm going to make sure that I have appropriate time to address this question. We've all had that experience. We're wrapping up a clinical interview, maybe one that's already ran a little bit late and there's that one more thing that's mentioned on the way out the door: I'm really concerned about my memory or I'm concerned about mom 's memory. That's not the opportunity to begin a memory assessment. That's the opportunity to schedule a dedicated visit. So, assuming that we've got someone else in the room with us, we've got our patient of interest, I'm going to approach the history really at the beginning. Seems like an easy thing to say, but so often patients in the room and their caregivers, they've been waiting for this appointment for weeks or months. They want to get it out all out on the table. They're worried we're going to rush them through and not take time to piece it together. And so, they're going to tell you what's going on right now. But the secret to a memory assessment, and particularly getting and arriving at an accurate diagnosis that reflects on and thinks about cause of memory problems, is actually knowing how symptoms began. And so, the usual opening statement for me is going to be: Tell me why you're here, and tell me about the first time or the first symptoms that indicated there was an ongoing problem. And so, going back to the beginning can be very helpful. This article is focused on Alzheimer disease and our clinical approach to the diagnosis of Alzheimer disease. And so, what I'm going to expect in a patient who has a typical presentation of Alzheimer disease is that there may be some disagreement between the patient and the spouse or other partners sitting in the room with me about when symptoms began. If you've got two partners sitting in the room, maybe an adult child and a spouse, there may be disagreement between them. What that tells me is at the onset, those first symptoms, they're hard to pin down. Symptoms typically emerge gradually in patients with symptomatic Alzheimer disease. They may be missed early on, or attributed or contributed to other things going on in the patient's time of life, phase of life. It's okay to let them sort of duke it out a little bit to determine, but really what I'm figuring out here is, are we talking about something that's happened across weeks, months or more likely years? And then I'm going to want to listen to, how did symptoms evolve? What's been the change over time? With Alzheimer disease and most neurodegenerative diseases, we expect gradual onset and gradual progression, things becoming more apparent. And at some point, everyone in the room is going to agree that, well, as of this state, there clearly was a problem. And then we can get into talking about specific symptoms and really begin to pick that apart the way that we traditionally do in any standard neurological assessment. Dr Berkowitz: Fantastic. And so, what are some of the things you're listening for in that history that would clue you in to thinking this patient may indeed be someone who could have Alzheimer's disease and going to require a workup for that diagnosis? Dr Day: It's pretty common when I have new trainees that come to clinic, they just head into the exam room and they sort of try to approach it the way that we would any patient in the emergency department or any other clinical scenario. The challenge with that is that, you know, we're taught to let the patient speak and we're going to let the patient speak - open-ended questions are great - but there's only so many questions you need to sort out if someone has a memory problem. And memory is really only one part, one component, of a thorough cognitive evaluation. And so, I'm going to help by asking specific questions about memory. I'm going to make sure that there is memory challenges there. And whenever possible, I'm going to solicit some examples to back that up, add credibility and sort of structure to the deficits. I'm also going to choose examples that help me to understand how does this concern, or this complaint, how does that actually affect the patient in their day-to-day life? Is it simply something that they're aware of but yet hasn't manifested in a way that their partner knows about? Is it to a level where their partner's actually had to take over their responsibility? It's causing some difficulties, disability even, associated with that. That's going to be important for me as I try to understand that. So, I'll ask questions when it comes to memory, not just, you know, do you forget things, but do you manage your own medications? You remember to take those in the morning? Do you need reminders from your partner? What about appointments; health appointments, social appointments? Are you managing that on your own? Sometimes we need a little bit of imagination here. Partnerships, and particularly those who have been together for a long time, it's natural that different people are going to assume different responsibilities. And so, might have to say, Imagine that you went away for the weekend. Would you worry about your partner remembering to take their medications over that time frame? That can help to really solidify how much of an impact are these challenges having on a day-to-day basis. I may ask questions about events, something that they maybe did a couple of weeks ago. Is the patient likely to remember that event? Are they going to forget details? Maybe the most important of all, with each of these, when there's a yes or an affirmation of a problem, we want to be clear that this represents a change from before. We all have forgetfulness. Happens on a day-to-day basis, and we all pay attention to different details, but what we're concerned about and typically the reasons patients want to come and see us as neurologists is because they've noticed a change. And so, I'm going to focus in on the things that represent a change from before. After I've discussed memory, I think it's really important to talk about the other domains. So, how is judgment affected? Decision-making?  In a practical way, we often see that borne out in financial management, paying the bills. Not just paying them on time and consistently, but making wise choices when it comes to decisions that need to be made. You're out at a restaurant. Can you pay the bill? Can you calculate a tip? Can you do that as quickly and as efficiently as before? Are we starting to see a breakdown in decision-making abilities there? We can sometimes lump in changes in behavior along with judgment as well. The patient that you know, maybe isn't making wise choices, they've picked up the phone and given their social security number out to someone that was calling, seeming to be well-meaning. Or maybe they've made donations to a few more institutions than they would have otherwise? Again, out of- out of order. Again, something that could be atypical for any individual. Looking for behavioral changes along with that as well. And then I'm going to talk about orientation. What's their ability to recognize days of the week, date of the month? Do they get lost? Is there concerns about wayfinding? Thinking about that, which is really a complex integration of some memory, visuospatial processing, judgment, problem solving, as we look to navigate our complex world and find our way from point A to B. And then I like to know, you know, what are they doing outside of the home? What are they doing in the community? How are they maintaining their engagement? Do they go to the store? Do they drive? An important topic that we may need to think about later on in this patient 's assessment. And inside the home? What responsibilities do they maintain there? Are the changes in decision making, memory problems, are they manifesting in any lost abilities inside the home? Cooking being a potentially high-risk activity, but also using typical appliances and interacting with technology, in a way that we are all increasingly, increasingly doing and increasingly reliant on. And last but not least, you know, maybe the one that everyone wants to think about, well, I can still manage all of my own personal care. Well, good news that many of our patients who have early symptoms can manage their own personal care. Their activities of daily living are not the big problem. But we do want to ask about that specifically. And it's not just about getting in the shower, getting clean, getting out, getting your teeth brushed. Do you need reminders to do that? Do you hop in the shower twice because you forgot that you'd already been in there once during the day? And so, asking some more of those probing questions there can give us a little bit more depth to the interview and really does sort of round out the overall comprehensive history taking in a patient with a memory or cognitive concern. Dr Berkowitz: Fantastic. That was a comprehensive master class on how to both sort of ask the general questions, have you noticed problems in fill in the blank memory, judgment, behavior, orientation, navigation and to sort of drill down on what might be specific examples if they're not offered by the patient or partner to try to say, well, in this domain, tell me how this is going or have you noticed any changes because the everyone's starting from a different level cognitively based on many factors. Right? So, to get a sense of really what the change is in any of these functions and how those have impacted the patient's daily life. So, let's say based on the history, the comprehensive history you've just discussed with us, you do find a number of concerning features in the history that do raise concern for dementia, specifically Alzheimer's disease. How do you approach the examination? We have the MoCA, the mini-mental. We have all of these tools that we use. How do you decide the best way to evaluate based on your history to try to get some objective measure to go along with the more subjective aspects of the history that you've ascertained? Dr Day: And you're honing in on a really good point here, that the history is one part of the interview or the assessment. We really want to build a story and potentially and hopefully a consistent story. If there are memory complaints, cognitive complaints from history, from reliable- that are supported by reliable collateral sources, we're going to expect to see deficits on tests that measure those same things. And so, I think that question about what neuropsychological measures or particular bedside tests can we integrate in our assessment is a good one. But I'll say that it's not the end-all-be-all. And so, if you've got a spouse, someone that lives with an individual for twenty or thirty years, and they're telling you that they notice a change in daily activity and it's impairing their day to day function, or where there's been some change or some concern at work, that's going to worry me more than a low score on a cognitive test with a spouse saying they haven't noticed any day-to-day impact. And so, we're going to take everything sort of in concert and take it all together. And it's part of our job as clinicians to try to process that information. But often we're going to see corroborating history that comes from a bedside test. He named a few that our listeners are probably pretty familiar with. I think they're the most common ones that are used. The Mini-Mental State Exam, been in practice for a long time. All the points add up to thirty and seems to give a pretty good sample of various different cognitive functions. The Montreal Cognitive Assessment, another favorite; a little bit more challenging of a test, I think, if we're if we're looking at how people tend to perform on it. And like the MMSE, points add up to thirty and gives a pretty good sample. There are others that are out there as well, some that are available without copyright and easy for use in clinical practice. The Saint Louis Mental Status Exam comes to mind. All these tests that we're willing to consider kind of share that same attribute. They can be done relatively quickly. They should sample various different aspects of function. There should be some component for language reading, spoken, spoken word, naming items, something that's going to involve some kind of executive function or decision making, problem solving. Usually a memory task where you're going to remember a set of words and be asked to recall that again later. So, learn it, encode it, and recall it later on. And then a few other features, I mean, some of them, these tests, most of these tests use some sort of drawing tasks so that we can see visuospatial perception and orientation questions about date, time, location, sort of the standard format. Any of these tests can be used aptly in your practice. You're going to use the one that you're most comfortable with, that you can administer in a reasonable amount of time and that seems to fit with your patient population. And that's the nuance behind these tests. There are many factors that we have to take into account when we're picking one and when we're interpreting the test results. These tests all generally assume that patients have some level of traditional sociocultural education that is westernized for the most part. And so, not great tests for people that aren't well into integrated into the community, maybe newcomers to the United States, those that have English as a second, third, or fourth language, as many of our patients do. Statements like no ifs, ands, or buts may not be familiar to them and may not be as easy to repeat, recall and remember. And so, we want to weigh these considerations. We may need to make some adjustments to the score, but ideally, we're going to use these tests and they're going to show us what we expect and we're going to try to interpret that together with the history that we've already ascertained. When I obtain that history and I'm thinking about memory loss, I'm going to look at the specific domain scores. And so, if I'm using the mini mental state examination thirty point test, but three questions that relate to relate to recall. Apple, penny, table. And so, depending on how our patients do on that test, they could have an overall pretty good score. Twenty seven. Oh, that looks good. You're in the normal range according to many different status. But if I look at that and there's zero out of three on recall, they could not remember those three items, that may support the emergence of a memory problem. That may corroborate that same thing on the MoCA, which uses five-item recall, and other tests in those same parameters. I mentioned some other caveat cities testing. Are patients who are presenting with prominent language deficits important part of cognition. They can't get the words out. They can't frame their sentences. They may really struggle with these tests because a lot of them do require you to both understand verbal instructions and convey verbal instructions. People with prominent visual problems, either visual problems that come because of their neurodegenerative disease and so part of cognition, visual perceptual problems, or people who simply have low vision. Are there difficulties for that? These tests require many people to read and execute motor commands, to draw things, to follow lines and connect dots, all very difficult in that setting. And so, we have to be cautious about how we're interpreting test results in patients who may have some atypical features or may arrive with sort of preexisting conditions that limit our ability to interpret and apply the test to clinical practice.  Dr Berkowitz: Really fantastic overview of these tests, how to use them, how to interpret them. It's not all about the number. As you said, it depends if all the points are lost in one particular domain, that can be salient and then considering, as you said, the patient 's background, their level of education, where English falls in their first language, second, third or fourth, as you said, and then some of the aspects of the MoCA, right, are not always as culturally sensitive since it's a test designed in a particular context. So, let's say your history and exam are now concerning to you, that the patient does indeed have dementia. Tell us a little bit about the next steps in the laboratory neuroimaging evaluation of such a patient?  Dr Day: I've got a history of memory and thinking problems. I've got some corroborating evidence from bedside cognitive testing, a normal neurological exam. This is where we think about, well, what other tests do we need to send our patients for? Blood testing really can be pretty cursory for most patients with a typical presentation who have typical risk factors, and that can include a thyroid study and vitamin B12. So, measuring those in the blood to make sure that there's no other contributions from potential metabolic factors that can worsen, exacerbate cognitive function. And pretty easy to do for the most part, if patients have other things in their history, maybe they come from a high-risk community, maybe they engage in high risk behaviors, I may think about adding on other tests that associate with cognitive decline. We'll think about the role of syphilis, HIV, other infections. But generally, that's when it's driven by history, not a rule of thumb for me in my typical practice. But beyond the blood tests, neuroimaging, some form of structural brain imaging is important. A CT scan will get you by. So, if you have a patient that can't get in the scanner for one reason or another or won't get in the scanner, or you don't have easy access to an MRI, a CT scan can help us in ruling out the biggest things that we're looking for. That's strokes, hemorrhages, and brain masses. So other things that obviously would take us down a very different path, very different diagnosis and very different treatment approach. An MRI, though, is going to be preferred, not only because it gives us a much higher-resolution view, but also because it helps us to see sort of regional areas of atrophy. It's a sensitive scan to look for small vessel disease, tiny strokes, tiny bleeds, microhemorrhages that again might point towards meteorology for us. Of course, it's better at finding those small masses, whether they be metastasis or primary masses, that could give us something else to consider in our diagnostic evaluation. I get an odd question often from patients, well, can you see Alzheimer's disease on an MRI? And the true answer to that is no, you can't. Can we see the signs of Alzheimer's disease? Sure, in some patients, but really what we see on an MRI is a reflection of neurodegeneration. And so, we see evidence of tissue loss and typically in areas that are most often involved early on in Alzheimer's disease. The hippocampus, the entorhinal areas around the hippocampus, we may see atrophy there. We may see biparietal atrophy, and of course, as the disease progresses, we're going to see atrophy distributed throughout other areas of the brain. But if you're looking for atrophy, you've got to have a pretty good idea what's normal for age and what you expect in that patient population. So, I do encourage clinicians who are assessing patients routinely, look at your own images, look at the images for patients with and without cognitive impairment. So we develop a pretty good sense for what can be normal for age, and of course work with our colleagues in radiology who do this for a living and generally do an excellent job at it as well.  Dr Berkowitz: Perfect. So, you're going to look for the so-called reversible causes of dementia with serum labs, structural imaging to either rule out or evaluate for potential structural causes that are not related to a neurodegenerative condition or patterns of regional atrophy suggestive of a neurodegenerative condition, and maybe that will point us in an initial direction. But the field is rapidly expanding with access to FDG-PET, amyloid PET, CSF biomarkers, genetic testing for APOE 4, probably soon to be serum biomarkers. So, patients may ask about this or a general neurologist referring to your clinic may ask, who should get these tests? When should we think about these tests? How do you think about when to send patients for advanced imaging, CSF biomarkers, genetic testing for APOE 4? Dr Day: It's not that patients may ask about this. Patients will ask about this. And you've probably experienced that in your own world as well. They're going to ask about any of these different biomarkers. Certainly, whatever they've recently read or has been covered on television is going to be common fodder for consideration in the clinic environment. It's important to know what tests you can get, what reliable tests that you can get, and to know the differences between some of these tests when making a recommendation or weighing the pros and cons of doing additional testing. I think common practice principles apply here. Let's order tests that are going to change our next steps in some way. And so, if we have a patient, particularly a patient like the one that we've been talking about: seventy something year old, presenting with memory complaints, they're concerned, the family is concerned. We've got that history, physical exam, and now we may need to really hone in on the etiology. Well, I say may need because for that patient it may be enough to know, yeah, I agree, there's a problem here. And I can say it's an amnestic, predominant, gradual-onset progressive cognitive decline. This is probably Alzheimer disease based on your age. And maybe that's all they want to hear. Maybe they're not ready to pursue additional testing or don't see the value or need for additional testing because it's not going to change their perspective on treatment. In that case, it's okay to apply an often underrated test, which is the test of time. Recognizing this is a patient I can follow. I can see them in six months or twelve months, depending on what your clinic schedule allows. If this is Alzheimer disease, I'm going to expect further gradual progression that may affirm the diagnosis. We can think about symptomatic therapies for a patient like that, perhaps Donepezil as an early, early medication that may help with symptoms somewhat and we can leave it at that for the time being. But there's many scenarios where that patient or the family member says, look, I really need to know. We really want this answer. And as you pointed out, there are good tests and increasingly good tests that we have access to.  Dr Berkowitz: Well, that's a very helpful overview of the landscape of more precise diagnostic testing for Alzheimer disease specifically and how you think about which tests to order and when based on your pretest probability and the patient 's candidacy for some of these new potential therapies. To close here, as you said, treatment is discussed in another podcast. There's another article in this issue. So, we won't get into that today. But let's say you have gotten to the end of the diagnostic journey here. You are now convinced the patient does have Alzheimer's disease. How do you present that diagnosis to the patient and their family? Dr Day: I think here we're going to recognize that different styles align with different patients and families, and certainly different clinicians are going to have different approaches. I do tend to take a pretty direct approach. By the time that patients are coming to see me, they've probably already seen another neurologist or at least another physician who's maybe started some of the testing, maybe even built the foundation towards this diagnosis and shared some indications. Certainly, when they look up my profile before they come to see me, they know what I specialize in and so, they may even have done their own research, which has ups and downs in terms of the questions that I'll be faced with at that point in time. The way I like to start is first acknowledging the symptoms. And the symptoms that the patients have shared with me, recognizing if those symptoms are impacting daily life, how they impacted daily life, and usually using that information to synthesize or qualify the diagnosis. Is there cognitive impairment, yes or no? And at what level is that cognitive impairment? Is this mild cognitive impairment? Is this mild dementia? Is it maybe more moderate or severe dementia? So, using those terms directly with patients and explaining the meaning of them. But I then transition in relatively quickly to the important point of not leaving it at the syndrome, but actually thinking about the cause. Because it is cause that patients come to talk about. And if they don't say that directly, they say it in their next question, which is what are we going to do about it and how are we going to treat this? And so, I will use the information I have available at that time to suggest that based on your age, based on the history, the normal physical examination, the performance and the bedside testing that we've done. And hey, that's pretty normal structural imaging or imaging that only shows a little bit of atrophy in a few areas. I think that this condition is most consistent with symptomatic Alzheimer's disease, mild cognitive impairment due to Alzheimer's disease, or mild dementia due to Alzheimer's disease. And then I'll discuss the next options in terms of testing and try to get a feel of what our patients are thinking about when it comes to treatment. Do they want to be on the cutting edge with brand-new therapies that offer potential benefits but counterbalance by pretty substantial risks that warrant individualized discussions? Are they interested in symptomatic therapies? Would that be appropriate for them? And I can usually round out the discussion with advice that works for everyone. And that's where we talk about the importance of brain health. What are the other things that I should be doing, you should be doing, and our patients and their partners should be doing as well to maintain our brain in its best possible state as we hope that we all continue to age and look towards the future where we maintain our cognition as best as possible? And that is still the goal. Even when we're talking to patients who have neurodegenerative diseases that are working against our efforts, we still want to do what we can to treat other problems, to evaluate for other problems that may be contributing to decline and may be amenable to our management as well.  Dr Berkowitz: Well, thank you so much for taking the time to speak with us today. I've learned a lot from your very nuanced and thoughtful approach to taking the history, performing the examination, making sense of cognitive tests and how they fit into the larger picture of the history and examination, and thinking about which patients might be candidates for more advanced imaging as we try to make a precise diagnosis in patients who may be candidates and interested in some of the potential novel therapies, which we both alluded to a few times, but are deferring to another podcast that we'll delve more deeply into that topic in this series. So, thank you so much again, Dr Day. Again, I've been interviewing Dr Gregory Day from the Mayo Clinic, whose article on Alzheimer's disease appears in the most recent issue of Continuum on Dementia. Be sure to check out Continuum Audio episodes from this and other issues. And thank you so much to our listeners for joining today. Dr Monteith: This is Dr Teshamae Monteith, associate editor of Continuum Audio. If you've enjoyed this episode, you'll love the journal, which is full of in-depth and clinically relevant information important for neurology practitioners. Use this link in the episode notes to learn more and subscribe. AAN members, you can get CME for listening to this interview by completing the evaluation at continpub.com/AudioCME. Thank you for listening to Continuum Audio.

This episode's Community Champion Sponsor is Ossur. To learn more about their ‘Responsible for Tomorrow' Sustainability Campaign, and how you can get involved: CLICK HERE---Episode Overview: The future of healthcare delivery demands innovative solutions that maximize physician time and improve patient access. Dr. Lyle Berkowitz, CEO of KeyCare, is leading the charge for how health systems deliver virtual care nationwide. With over two decades of experience as a practicing physician, health system executive, and serial entrepreneur, Dr. Berkowitz brings unique insights into transforming healthcare delivery. As the founder of KeyCare, he's pioneering a new model of virtual care that leverages Epic's EMR platform to create seamless experiences for both providers and patients. While together, Dr. Berkowitz shares how he and his team are building a nationwide network of virtual providers and how KeyCare helps health systems expand access while reducing provider burden. Join us to discover how Dr. Berkowitz and the KeyCare team are bringing their vision to life by offering tech-enabled, team-based care to help reshape healthcare delivery. Let's go!Episode Highlights:Explains how KeyCare achieved one of Epic's fastest implementations by focusing exclusively on virtual care optimizationReveals that recent surveys show two-thirds of patients still prefer telehealth options for routine careIntroduces the concept of "virtualists" as a new specialty, similar to how hospitalists transformed inpatient careChallenges physician shortage assumptions, advocating for tech-enabled teams to expand patient accessEmphasizes how current physician payment models discourage innovation and team-based care approachesAbout our Guest: Lyle Berkowitz, MD, FACP, FHIMSS is a primary care physician, a healthcare innovator, a futurist, a digital health expert and a serial entrepreneur with a passion for creating real world solutions which improve the quality and efficiency of the healthcare system for both patients and physicians.Dr. Berkowitz is the Founder and Chief Executive Officer of KeyCare - a new type of virtual care partner designed to help health systems and others transform how they manage their populations. We do this by offering health systems access to a tech-enabled virtual care team that works on our telehealth-optimized instance of Epic. This allows health systems to augment their workforces and expand virtual care options while ensuring a consistent and high quality experience for their patients. Dr. Berkowitz also has a long history of helping healthcare systems, companies and investors rethink problems and solutions. Special areas of focus include innovation strategies and tactics, digital health technologies, workflow automation, telehealth, electronic medical record optimization, precision medicine, product design, physician leadership, change management, and disruptive thinking (so you can do it to yourself before someone else does it to you!).Links Supporting This Episode:KeyCare website: CLICK HEREDr. Lyle Berkowitz LinkedIn page: CLICK HEREKeyCare LinkedIn page: CLICK HERE Mike Biselli LinkedIn page: CLICK HEREMike Biselli...

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How Donald Trump built a movement. Find us on Youtube. On this deep-dive episode of The Bulletin, Mike Cosper welcomes Roger Berkowitz for a conversation about political movements and what liberals got wrong about MAGA.    GO DEEPER WITH THE BULLETIN: Find Roger's books here. Order Mike Cosper's book The Church in Dark Times (releasing November 19) Follow the show in your podcast app of choice. Find us on YouTube. Rate and review the show in your podcast app of choice. Leave a comment in Spotify with your feedback on the discussion—we may even respond! ABOUT THE GUEST:  Roger Berkowitz is founder and academic director of the Hannah Arendt Center for Politics and Humanities and professor of politics, philosophy, and human rights at Bard College. Berkowitz is the author of a number of books including The Gift of Science: Leibniz and the Modern Legal Tradition, On Civil Disobedience by Henry David Thoreau and Hannah Arendt (forthcoming, 2024), and The Perils of Invention: Lying, Technology, and the Human Condition. His writing has appeared in The New York Times, The American Interest, Bookforum, The Forward, The Paris Review online, Democracy, and many other publications. Berkowitz edits HA: The Journal of the Hannah Arendt Center and the weekly newsletter Amor Mundi. He is the winner of the 2024 Compassion Award given by Con-solatio and the 2019 Hannah Arendt Prize for Political Thought given by the Heinrich Böll Foundation in Bremen, Germany. ABOUT THE BULLETIN: The Bulletin is a weekly (and sometimes more!) current events show from Christianity Today hosted and moderated by Clarissa Moll, with senior commentary from Russell Moore (Christianity Today's editor in chief) and Mike Cosper (director, CT Media). Each week, the show explores current events and breaking news and shares a Christian perspective on issues that are shaping our world. We also offer special one-on-one conversations with writers, artists, and thought leaders whose impact on the world brings important significance to a Christian worldview, like Bono, Sharon McMahon, Harrison Scott Key, Frank Bruni, and more. Learn more about your ad choices. Visit podcastchoices.com/adchoices

In this episode, I sit down with Jennifer Berkowitz to uncover the essentials for planning a successful exit from your business. Jennifer shares her expert insights into the preparation, timing, and strategic decisions that are vital for a smooth and profitable transition. We explore how to align your business for a successful exit by focusing on value, minimizing risks, and setting up sustainable processes. Jennifer provides actionable advice for entrepreneurs at any stage who want to position themselves for the best outcome. Tune in to learn the keys to achieving a successful exit and ensuring your legacy lives on.   Get the show notes for The Keys to a Successful Exit with Jennifer Berkowitz Click to Tweet: Listening to a fantastic episode on Growth Think Tank with #JenniferBerkowitz featuring your host @GeneHammett https://bit.ly/gttJenniferBerkowitz   #successfulexit #GeneHammettPodcast #GHepisode1142 #sellingyourbusiness   Give Growth Think Tank a review on iTunes!

When Seth Berkowitz was in college, he was the cookie guy on campus. He'd grown frustrated that the only food he could get delivered late at night were standards like pizza or Chinese food. He had a sweet tooth, and he craved warm, homemade chocolate chip cookies. So he took matters into his own hands and started making and delivering cookies to students at his school. The operation soon went from a silly side hustle to a real business - and then an all-consuming struggle. But today, after decades of detours, long-shot decisions, and near-bankruptcies, Insomnia Cookies is now a $350 million dollar business.This episode was produced by Alex Cheng with music composed by Ramtin Arablouei. It was edited by Andrea Bruce with research help from Katherine Sypher. Our audio engineers were Robert Rodriguez and Maggie Luthar.You can follow HIBT on Twitter & Instagram and sign up for Guy's free newsletter at guyraz.com.See Privacy Policy at https://art19.com/privacy and California Privacy Notice at https://art19.com/privacy#do-not-sell-my-info.